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MODULE-1: HISTORY OF VETERINARY MEDICINE

Learning objectives

 To know about how the art and science of animal healing eveolved in India and around the
globe.
 To understand the contributions of Indians for the development of Veterinary Medicine and
Animal Health Care as well as the international contributions for the animal health care.
 History repeats itself! At the end, the learner must be able to evolve himself / herself for a
dedicated carrier, following the innovations of the past and endeavouring to innovate further
for a better future.

HISTORY OF VETRINARY MEDICINE IN INDIA

The World's First Animal Hospital was established in India(Emperor Asoka's Period).The Practice of
Animal Healing, existed in India even centuries prior to the Emperor Asoka's regime, as evident from
the life of the ancient saints of the Tamil Kingdoms & Dravidian Civilizations and from the Rishi’s &
Sadhu’s of Aryan Civilizations in Northern India. Keeping these rich traditions alive for several
centuries and even today, the Indian Subcontinent boasts one of the richest biodiversity of animal
and plant life in India.
Father of Veterinary Medicine - RENATUS VEGETIUS (450-500 A.D.)

Why the Indian Veterinary History is important...

 According to Somvanshi's Documentation(2006)on Indian History of

Veterinary Medicine, Cattle husbandry was well developed during the
Rigvedic period (1500–1000 BC)
 Atharvaveda provided an interesting information about ailments of
animals, herbal medicines, and cure of diseases.
 Shalihotra, the first known veterinarian of the world, was an expert in
horse husbandry and medicine and composed a text Haya Ayurveda.
 Sage Palakapya was an expert dealing with elephants and composed a
text Gaja Ayurveda.
 In Mahabharata period (1000 BC), Nakula and Sahadeva, the two
Pandava brothers were experts of horse and cattle husbandry,
respectively.
 Lord Krishna was an expert caretaker and conservator of cow
husbandry. Gokul and Mathura were famous for excellent breeds of
cows, high milk production, quality curd, butter, and other products.
 Buddha was a great protector of all kinds of animals and birds
(including game) in ancient India as he preached lessons of non-violence
to masses.
 Graeco-Romans imported livestock from India after invasion by Alexander.
These descriptions are available in Indika, a book authored by
Megasthenes, the ambassador of Seleucus Nikator, king of Mecedonia in the
court of Chandragupta Maurya.
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 The great king Ashoka (300 BC) erected the first known veterinary hospitals
of the world. He arranged cultivation of herbal medicines for men and
animals in his empire and adjoining kingdoms.
 In a famous text, the Arthashastra (science of economics) composed by
Kautilya, the guide and political advisor of emperor Chandragupta Maurya, a
lot of information is available about different animal (elephant, horse, and
cow) departments, grazing lands, rules of meat science, livestock products
like skin and fur, and veterinary jurisprudence. This knowledge flourished
during the great Hindu kings of the Gupta period up to 800 AD before Islamic
followers invaded India.

HISTORICAL DEVELOPMENTS IN HARAPPAN PERIOD & VEDIC

AGE

Historical Developments in Harappan Culture

Excavations of Harappa in Montgomeri district, Punjab and Mohenjo- daro in Larkana district, Sin
People of Indus Valley civilization were familiar with dogs, bulls, sheep, goats, buffaloes, horses, an
Fish was their main animal food. These people were fond of mutton, beef, chicken, and meat of tor

Historical Developments in Vedic age

 A lot of information is available on keeping of animals in the Vedic Age in the Rigveda, which
is the oldest holy book of Aryans. In Rigveda, animals were considered as wealth. Aryans
maintained their cattle on pastures, which were near to their dwellings. They cut the jungles
and grazed cattle there. The cows were milked thrice a day. Castration of males was practiced
and oxen were used for farm transport. It appears that Aryans preferred cows. Buffalo was
not a commonly used animal by them. They kept dogs for guarding houses and for hunting of
boars. Sheep were kept mostly for wool and goats for milk. Oxen were used for plowing and
irrigation also. The cow has been defined as aghanya, i.e., not to be killed, indicating the high
sanctity of the cow in the Vedic period. In Rigveda, barley, sugarcane, and leftovers of sesame
after extraction of oil were used for feeding of animals.
 Masters of philosophy searched the secrets of life and the universe and developed “cow
science”. Virtually “cow science” is a unique gift of India to the whole world. Learned people
of ancient India considered that whole cow family or “gau vansh” was essential for existence
of humanity, its protection, nourishment, development, and culture. Cow milk provided
special energy, strength, and intelligence. Cow dung and urine nourished agriculture
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farming. Bullock power helped in development of techniques in agriculture like carrying

draft,
transportation, and cottage industry. Skin from dead animals supported the leather industry
and handicrafts. Therefore, cow husbandry was always core-point in the Indian lifestyle and
economy during the Vedic period.

ANIMAL AYURVEDA & DEVELOPMENTS DURING EPIC ERA

Animal Ayurveda in Vedic period

 The Vedic Society in India was dominated by the ‘cow culture’ and Vedic people adored the
cow and regarded it as the source of their good fortune, happiness, and good health (Rigveda
6.28.1, 6).
 It is believed that the religious priests, who had the responsibility of maintaining cattle, were
the first animal healers or veterinarians.
 A number of Vedic hymns indicate medicinal values of the herbs and it is likely that these
priests were also apt to it and used their medical knowledge to keep the sacred cattle free
from ailments.
 The Atharvaveda mentions about healing herbs and drugs. The Ayurveda (the science of life)
deals with the knowledge of medicine possessed by the Vedic saints.

Epic period

 Ramayana is the oldest literature of Sanskrit, although no written history is available of that
period. The treatment of various ailments using medicinal herbs and surgical procedures are
described at length.
 Various uses of oil as preservative and treatment are mentioned.
 Surgical procedures like caesarean section, hysterectomy, etc. were known to be performed
by trained vaidhyas or physicians.
 Fruit juices, flower extracts, and wines made from fruits were said to have great medicinal
properties.
 Medicinal herbs like arjuna (Terminalia arjuna), kutaja (Holarrhena antidysenterica),
kadamba (Anthocephalus cadamba), sarja (Vateria indica), neem (Azadirachta indica),
ashoka (Saraca asoca), asana (Pterocarpus marsupium), etc. were used widely to cure
ailments of men and animals.
 Diseases like leprosy, tuberculosis, mental disorders, etc. were described along with
treatment. The herbs found in the mountains of Kanchanjunga and Kailash (now in China)
are said to possess good medicinal quality.

DEVELOPMENTS IN MAURYAN AGE AND THEIR INTERNATIONAL RELEVA

Historical Developments in Mauryan Age

 Animal husbandry made great progress in the Mauryan age (322–232 BC). The Mauryan age
preceded the period of Buddha and Mahavir, who preached non-violence towards animals.
 The earliest Buddhist text “Suttanipata” describes cattle as a giver of food, beauty, and
happiness (annada, vannada, and sukhada) and therefore deserves to be protected.
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 According to Kautilya’s Arthashastra, cow was a worshiped animal. It was one of the first
duties of the King to worship the cow with her calf and bull. The killing of cow was a deadly
sin.
 Buffalo also became a recognized dairy animal by this period.
 In the Arthashastra, goat has been described as an important milch animal like cows and
buffaloes. Sheep were raised for wool.
 According to Arthashastra, in a breeding herd, 4 bulls should be provided for every 10
cows/buffaloes. Feeding of animals on pasture was the main practice. It was the duty of the
King to identify and provide enough land for pastures near each village. The Gopa (village
accountant) was supposed to keep the details of the pasturelands. \
 In Arthashastra, there is separate mention of capital punishment for stealing or hurting a
cow. When a person caused a bull to fight with another bull, he was fined. If any person
injured a bull, he was heavily fined. Similiar punishents were also describe in Code of
Hamurabhi (Egypt)

 Veterinary services were essential services during the Mauryan period. In this period, asses
were used to carry loads. Horses were used to yoke different kinds of chariots like festival
chariots, battle chariots, and traveling chariots. In the stables, different kinds of horses were
kept separately. Horses were regularly trained for warfare. There were horses of many
breeds.
 Arthashastra has graded them as best, middle, and ordinary quality. Thoroughbred horses
were recommended parched rice, drippings, minced meat, red rice-powder, and grasses.
Mules have also been mentioned in Arthashastra, indicating their presence in the Mauryan
period. Elephants were very important animals in the Mauryan period. They were used in
warfare, as they were very useful for storming fortresses; breaking upon massive doors and to
move even in dense forests and marshy lands. There were about 6000 elephants with Nandas
and 9000 with Chandragupta Maurya. Elephants for war and riding were housed inside the
fort. Whoever killed an elephant was sentenced to death. Tusks of an elephant were
considered precious.

ASOKA PERIOD

The Golden Era for Veterinary Medicine in the Ancient Word

 The present-day Veterinary Council of India adopted its insignia, the sculpture of a bull and a
part of the text of the stone edict from the period of Emperor Ashoka (around 300 BC),
which projected the veterinary profession as its “best heritage”.
 Ashoka, the grandson of Chandragupta, who turned to Buddhism after Kalinga war gave
veterinary science a new turn in India. It is described that the first veterinary hospital existed
in Ashoka’s regime.The ‘Baniyan Hospital’ of Suratis is believed to be one of them, which
consisted of a large piece of land enclosed by high walls. Provision for keeping indoor
patients was made inside to accommodate animals.

Animal Surgery

 From primitive therapeutics, the early man turned to primitive surgery. “Susruta Samhita” is
the earliest known work dealing with surgery. According to evidence with Indian scholars,
Dhanvantari’s direct disciple Susruta belonged to 600 BC.
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 He made great improvement in the general techniques of surgery and performed many new
and major operations. Susruta Samhita testifies to the great scientific knowledge of the
ancient Indian surgeons.
 It was translated into Arabic before the end of 800 AD and was called ‘Kitab-Show-Shoon-a-
Hindi’ or ‘Kitab-i-Susrud’; Cellars translated into Latin and Hassler into German. The
students were taught surgical techniques first on dummies and later on dead bodies. Before
Susruta’s time, knowledge and practice of surgery in India was more or less of the same
standard as in contemporary civilizations like Egypt, Mesopotamia, and Greece.
 Almost all aspects of surgery were dealt in ancient medical veterinary treatises. Some of these
aspects were preliminary surgical methods, dressing and bandaging of wounds, symptoms to
predict prognosis of the surgical cases, etc. Special methods include application of cautery,
removal of foreign bodies and obstructions, surgical grafting, and treatment of fractures,
dislocations, and fistula. Methods of suturing and plastering and duties of physicians,
surgeons, and nurses have been dealt in detail. General principles of surgery described
include preparatory measures and principal measures (including surgery and post-operative
measures). However, there appears to be no mention of anaesthetic techniques. Surgical
treatment of animal disease was very much developed during Vedic period. Skilful surgeons
treated animals with precision and great perfection. Various techniques of surgical
operations along with instruments have been dealt in detail in Shalihotra’s and Palakapya’s
works. Treatment of sinus fistula, burns and scalds, snakebite, fractures, ailments of
ligaments/tendons, dystocia, removal of dead foetus, extraction of teeth and fractures were
routinely done during Vedic period (Singh, 2002b).

The Animal Haealth Care & Treatise on Animal Health

 Animals received good medical care in ancient India. Physicians treating human beings were
also trained in the care of animals. Indian medical treatises like Charaka Samhita, Susruta
Samhita, and Harita Samhita contain chapters or references about care of diseased as well as
healthy animals. There were, however, physicians who specialized only in the care of animals
or in one class of animals only; the greatest of them was Shalihotra, first known veterinarian
of the world and the father of Indian veterinary sciences. The treatment of animal diseases in
ancient India was well developed and carried out with great care and precision by well-
trained personnel.
 The treatment of animal diseases using Ayurvedic medicine has been mentioned in Agni
Purana, Atri-Samhita, Matsya Purana and many other texts. The treatment of a variety of
ailments: infection of horns, ears, tooth, throat, heart, and navel, rheumatism, haemorrhagic
enteritis, dysentery, digestive ailments, cold, parasitic/verminous diseases, stomach worms,
rabies, abscess, anaemia, wounds, medicines to increase milk production, epistasis,
retention of urine, urinary colic, constipation, lacrimation, arthritis, rhinitis, sprain,
haematuria, and skin infection has been given in detail (Somvanshi, 1993).

ETHNO VETERINARY MEDICINE AND FOOD SAFETY IN ANCIENT INDIA

Ethno Veterinary Medicine

 Before the advent of modern allopathic system of medicine, it seems possible that the healing
art was almost the same throughout the world including India. This system of medicine has
given the term ethno-medicine (when implied to human treatment) and ethno-veterinary
medicine (in the context of animal treatment). In India, ethno-veterinary practices were in
vogue since time immemorial. In ancient India, the Vedic literature, particularly Atharvaveda
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is a repository of traditional medicine including prescriptions for treatment of animal

diseases. Scriptures such as Skanda Purana, Devi Purana, Matsya Purana, Agni Purana,
Garuda Purana, Linga Purana, and books written by Charaka, Susruta, Palakapya (1000 BC),
and Shalihotra (2350 BC) documented treatment of animal diseases using medicinal plants.
Vedic texts also describe divine healing powers. Yajurveda cites importance of growth and
development of medicinal plants and Atharvaveda mentions about the value of medicines in
curing the diseases. Shalihotra undoubtedly appears to be the first veterinarian of pre-
historic times. The ancient Indians were so apt with the knowledge of herbals, even
Alexander acquired some of the skills used by Indians, particularly for treatment of
snakebite.

Food Safety in Ancient India

 Although milk, fruits, vegetables, and grains formed bulk of their food, Vedic Indians were
meat eaters. Slaughter of animals was more or less a sacrificial act. Goat and sheep meat
were consumed by men and offered to their gods. During Rigveda, cow slaughter was
banned. However, horseflesh was eaten occasionally at the time of religious sacrifice called
Ashvamegha yagna. Dogs were used for hunting wild boars. In later Vedic period, meat
eating was fairly common but killing of cow was a deadly sin. Vedic Aryans did not prefer fish
while the Indus Valley people had a special liking.
 During Ashoka period, non-violence or ahimsa was a policy of the state but meat eating was
not banned. Slaughterhouse was located at a distant place towards south of the palace and
regulated by a superintendent. Pregnant or milking goat, sheep, pig, and piglets up to 6
months of age were banned from slaughter. Butchers selling meat derived from sick or dead
animals and adulterated or spoiled meat were severely punished. This shows that meat
science had a sound basis in ancient India.

ELEPHANT MEDICINE, EQUINE & BOVINE MEDICINE - THE ANCIENT INDI

Elephant Medicine or Gaja Ayurveda

 Palakapya, an ultimate authority on elephant medicine belonged to the Rigvedic period

2000–4000 BC. The Gautam Samhita, the Ashva Ayurveda, and Hastya Ayurveda are the
only treatises on animal science till now. Palakapya wrote Hastya Ayurveda or Gaja Ayurveda
dealing with elephant medicine and dedicated to Lord Ganesha. Elephant medicine and
surgery were divided into four parts by Palakapya, viz., Maha Rogsthan or major diseases,
Ksudra Rogasthan or minor diseases, Salyasthan or surgery, and materia medica-diet and
hygiene. He classified various ailments of elephants into: Adhyatmika (physical) and
Agantuka (accidental or incidental); physical classes of ailments were called Manasa (caused
by mental diseases) and Dosaja [caused by disorder of bodily humors – vata (air), pitta (bile),
and kapha (phlegm)]. Hastya Ayurveda also mentions about anatomy of elephant, treatment
of different kinds of diseases, training of elephant, and also classification of elephants on the
basis of a number of characteristics.

Equine Medicine or Haya Ayurveda

 There is no legend of horses in the seal of Mohanjo-daro, Harappa, Kalibangan and in Indus
Valley culture. Amongst 18 gems recovered in Samudramanthan by gods and demons, the
horse named Ucchasrava was possibly the first known horse of puranik (ancient) India. The
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Aryans introduced horses for rapid transportation. Pack, riding, chariot, war, race, and even
plowing horses were frequently mentioned in the Vedic age (1500–1000 BC). The Aryans
took advantage of the trained horses to march into the fertile land of Iran and Mesopotamia.
The Aryan chariot (ratha) is depicted at Sanchi. In the later Vedic period (1000–600 BC),
Buddhist period (600 BC), and Mauryan period (400 BC), the use of horses was well
documented. In the Mauryan age (322–232 BC), equine husbandry made tremendous
progress and these were used for riding and for war.
 The royal horses were under the charge of a superintendent of horses (Asva adhyakacha),
who used to register the breed, age, color, and place of origin. Detailed accounts of housing
and feeding of horses were mentioned in Arthashastra. Veterinary doctors and horse trainers
were assigned free endowment. In the Gupta dynasty (300–550 AD), horses were given more
importance than elephants in Samudragupta’s army because of their speed and easy
maneuvrability. He also performed Ashvamedha yagna to proclaim his imperial power and
issued a gold coin depicting a horse. Skandagupta (455–467 AD) was shattered by Huns, who
were expert horse riders. The Kannauj empire (606–647 AD) has also been mentioned to use
saddled horses in warfare.

Bovine Husbandry , Health Care and Medicine

 Cows were regarded as wealth and were the backbone of the economy of ancient Indians, i.e.,
Aryans. Wars were fought for acquiring cows. Cattle were one of the most frequently used
animals described in Vedas. Cows were regarded as mother (“Gau-mata”) and referred to as
Aghanya. Prayers were offered to Agni (God of Fire) to kill with his flame all those evil
dwellers, who stole milk of cows. Those demons may not get the nectar (milk of cows).
Voluminous treatises are also available on cows, e.g., ‘Gau Ayurveda’. During Pauranik
period, cow (Kamdhenu) emerged out of Samudra manthan, was considered so valuable that
devatas fought with demons and acquired them.
 Mantras in Vedas (Shala Nirman and Goshth Suktas of Atharvaveda) describe that the
animal houses (Goshth) and their management were of good quality. Pashu Samvardhan
Sukta of Atharvaveda indicates that Vrihaspati Deva knew the animal behavior and
management well. Cows were high milk-yielders and were milked thrice a day by women
(Duhitras). They knew the animal feeding practices and fed them with dry hay and green
fodder. The herb arundhati (a climber, not identified) not only treated several disease
conditions but also increased milk yield in cows. Prayers were offered to Aditi Deva to
discover medicines for health improvement of humans and calves. It shows that Aditi was
one of the researchers of medicine. Treatment of weak, infertile, and unproductive cows for
making them productive was well described. Castration of males by crushing the testicles
between two stones was also practiced.

Cow prosperity and protection

 Cow worship, cow keeping, and cow protection were the three stages through which the
prosperity of the mother cow occurred from time to time. Beef eating in ancient India has
been a controversial subject. Due to availability of natural facilities of breeding, feeding, and
grazing, cattle flourished in the ancient times. Cow prosperity started declining with
increasing human population and socioeconomic conflict. In case of buffalo, it is the utility of
the buffalo that has increased its prospects.

Legends of cow-bulls in coins of ancient India

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 In ancient India, cow was addressed as “Gau-mata” or mother cow. Rulers from 600 BC
used to inscribe pictures of bulls (rarely cows) on coins, which show their importance and
utility. Round coins (occasionally rectangular or square) weighing 5–7 g made up of copper,
silver, lead, or gold were used as currency. The best and rare inscription of cow was seen in
the coins of King Anshu Verma, ruler of ancient republic of Lichavvi (Nepal). Inscriptions of
standing right facing (rarely left facing) humped bulls are seen on the coins of punch-mark,
Airan, Audumbar, Ayodhya, Kaushambi, Saatvahan, Ujjaini, Chatrapa, Yaudhey, Krishnaraj
(Kalchuri), etc.

Buffalo

 Reference of buffaloes in the form of a furious demon, Mahishasur and docile beast, the ride
of death God Yamraj has been made in the prehistoric ancient Indian literature. Taming and
domestication of buffalo has been mentioned during the epic era of Ramayana and
Mahabharata and true domestication during the Indus Valley civilization. Several types of
buffaloes have been described in different parts. The Indian subcontinent is the richest
habitat of riverine buffaloes (dairy) whereas East and Southeast Asian countries are
dominated by draft type swamp buffaloes. In South India buffaloes were used for plowing
lands after which they wallow in the pond to reduce tiredness. Buffalo keeping was a symbol
of prosperity in Southern India.

Goat

 Goats and sheep were first domesticated near Iraq and United Arab Emirates 8700 years
ago, much earlier than the advent of agriculture. People who belong to Chalcolithic age
were found in the Indian states of Madhya Pradesh, Maharastra, and Rajasthan and they
reared goats and other animals. Goats were domesticated earlier, and served mankind for
longer period for their milk and other products.
 During Pre-Harappan period, wild ancestors of goats were found in barren hills of
Baluchistan and Western Sindh. Gaddi goats resembling the ancestral wild goats are still
used for carrying goods in the higher Himalayan region of India. The greatest artistic
creations of Harappan culture are seals resembling goats, which greatly supported the animal
husbandry in Indus Valley civilization. Goats serve mankind providing meat, milk, fiber and
therefore, appropriately called poor man’s cow.

Sheep

 Sheep was domesticated about 8700 BC. The original center of domestication was the Aralo-
Caspian steppe and Turkestan. From there, sheep keeping spread early into Iran and later
into Mesopotamia and Baluchistan. The sheep kept in India, Tibet, and other countries of
East and South Asia were of western derivation and basically of Urial stock.
 In India, sheep keeping was practiced evidently from Pre-Harappan period through to
Mauryan Age. The dominant form of sheep rearing still remained of nomadic nature.
Domestication of sheep, besides ensuring a permanent meat supply, also improved the
supply of skin, hair (wool), fat, and bones. Although these animal by-products are available
from other sources, production of wool, however, remained a monopoly of the sheep. Sheep
rearing is an exclusive occupation of a class of herders traditionally marked out as a
pastoral caste.

Fowl
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 People of the Indus Valley civilization were quite familiar with domesticated fowl. In the
seals of the Indus Valley, two Sonarati red cocks with fighting gesture were identified. At the
same place, small pieces of earthen hen toys were recovered. One of these birds, which was
adjoining to feed pot, was considered as hen. This indicates that captive breeding of birds
was practiced during those days.
 Domestic fowl was also found in Harrappa. From this place, two earthen birds (one male and
the other female) were recovered. From Kanhudaro also, small-sized figures of birds
belonging to the family of domestic fowl were recovered. Possibly these were the images of
quails. It is accepted that Indus Valley people kept birds for games and breeding for meat,
possibly started afterwards. When Aryans invaded India around 2500 BC, they appreciated
cocks.
 Cock is mentioned in Atharvaveda and Yajurveda, but not in Rigveda. During 1000 BC,
eating hen meat was prohibited, possibly for religious reasons. The study of Northwest
Indian coins indicates that cocks were favored. During 310 BC, Softitus, a Prince of Punjab
presented a few silver coins to Alexander, which had legends of cocks along with spur.
Satyamitra (100–200 AD) engraved fowl on coins with palm leaves. During this period, India
had trade with Western Asia, Arabia, and Egypt through sea and land route, which was
instrumental in the dissemination of red jungle fowl throughout the world.

SCOPE OF VETERINARY MEDICINE

Clinical practice

 All veterinarians have a professional responsibility to the community and an

important part to play in the economic and social well being of the nation. The
primary responsibility of veterinarians in practice is to serve the public
through the provision of high quality care for the health and welfare of their
animals, whether these animals are kept as pets or for leisure activities, are
working animals, farm livestock, or wildlife.
 Veterinary practices are distributed through the country in towns and rural areas.
These may involve one veterinarian working on their own but, more commonly,
several veterinarians work together. The type of practice varies according to the
location. In large cities, for example, practices may deal only with companion
animals such as dogs, cats and caged birds. This is commonly referred to as
'small animal' or 'companion animal' practice. In farming areas, the emphasis is
on farm livestock such as cattle, sheep, deer and pigs, although other animals
such as dogs, cats and horses will also be dealt with ('large animal' or 'mixed'
practice). Some practices, particularly in areas where there are large numbers of
horses, may deal mainly or solely with them ('equine practice').
 Veterinarians in clinical practice in today generally operate from well-equipped
clinics containing x-ray equipment, surgery and animal hospital facilities and
laboratory equipment for conducting clinical pathology. There are also private
and government-run laboratories that provide diagnostic services for
practitioners through the testing of samples of various kinds from their animal
patients. These can be for bacteriology, parasitology, virology, pathology,
biochemistry and so on. These laboratories commonly employ veterinarians
with advanced training.
 Clinical practice offers an interesting career with plenty of variety. Apart
from other veterinary skills, it requires an ability to assess facts in
investigating
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outbreaks of disease in order to arrive at a satisfactory diagnosis. Common sense,

independence and the ability to work with people of the farming community or
other animal owners are necessary. The graduate engaged in this work has ample
opportunity to exercise and extend knowledge and practical skills gained during
university education.

Some special characteristics of particular types of practice

 Large animal (Farm animal) practice

o Diagnosing and treating disease in individual animals is an important part
of all clinical practice and in some cases it is the major concern. In farm
animal practice, however, the veterinarian has additional responsibilities
centred on the flocks and herds that make up farming enterprises.
Veterinarians have an important contribution to make to the productivity
of these flocks and herds by assisting with the planning and development
of flock and herd health programmes, monitoring the health status and
production of the animals, often working in collaboration with other
animal production advisers. Veterinarians in these practices also have an
important part to play in national disease control and eradication
schemes, in maintaining the quality of animal products in keeping a
lookout for exotic diseases or pests that may be brought into the country
and in ensuring and promoting animal welfare.
 Equine Practice
o Some private practitioners practice only in the care of horses, which makes
a valuable contribution to the economy. Success in racing requires
absolute fitness and by helping to achieve this, veterinarians have
significantly contributed to the outstanding reputation of gallopers and
trotters. They also play an important part in keeping horses that are used
for other sporting and leisure activities fit and well.
 Companion Animal Practice
o In larger towns and cities, ample opportunity exists for restriction of
practice to companion animal work including cats, dogs and other family
pets. Most urban small animal practices use similar techniques to those
available at a public hospital. In the field of medicine this involves the
diagnosis and treatment of such widely differing diseases as diabetes,
dysentery, and cancer. Abdominal, thoracic and orthopaedic surgery is
routine, although some procedures require specialised equipment that not
every practice may have. The use of techniques such as blood transfusion,
fluid therapy and advanced procedures for repairing bone fractures are
examples of skills that can be expected of a veterinarian providing surgical
services. Within companion animal practice, specialisation is becoming
increasingly common so that specialist veterinary ophthalmologists,
dermatologists, behaviourists and surgeons accept referrals from other
companion animal veterinarians.

Food Safety Authority

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 This newly setup authority sets standards for food safety for exports of animal
(and horticultural) products, and for meat and dairy products for domestic
consumption. It is a food safety assurance organisation that provides food
evaluation, verification, and certification services to the food production
industries. It is concerned with quality control and hygiene in meat and other
animal products. Many veterinarians can work in meat processing
establishments and are responsible for the standards of hygiene and meat
inspection in meat processing establishments to ensure that meat and meat
products are fit for human consumption, and can be certified for export or
domestic consumption.

Ministry of Agriculture and Forestry

 There are many career opportunities for veterinarians in the Ministry

of Agriculture and Forestry in various cadres.

Veterinary Diagnostic Services

 Diagnostic Services are provided by government and privately owned

laboratories. They are staffed by veterinarians, with advanced training in
disciplines such as diagnostic pathology, microbiology, virology,
parasitology, clinical biochemistry and haematology.

Veterinary Education

 An important employer of veterinary graduates is the education sector, with the

different kinds of Veterinary and Animal Science Programmes , being the major
employer in this area. Veterinary staff are responsible for most aspects of the
training of BVSc undergraduates, diploma students and postgraduate
veterinary studies up to doctoral level. An important aspect of the work of the
staff is the conduct of research and supervision of postgraduate student
research.

Veterinary Research and Technical Services in Industry

 As you would expect in any economy which is so firmly based on animal

production, a considerable industry exists in certain packets of India(eg. Poultry
in Namakkal District of Tamilnadu) to provide veterinary pharmaceuticals,
feedstuffs, and other aids to the maintenance of animal health and production.
This industry requires the professional skills of veterinarians, and there are
posts available in such fields as technical advisory services and research. Many
of these can lead to senior executive management roles.

International Veterinary Science & Service

 There are development projects for livestock industries in overseas countries.

A number of veterinarians are involved in projects concerned with this
development, with some projects being on a very large scale.
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 A veterinary degree can lead to a great diversity of other careers including

employment in animal welfare, conservation biology, specialist clinic
construction, animal feed formulation and manufacture, and zoological
parks.

Other career opportunities

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COMMON QUESTIONS
 Who is the Father of Veterinary Medicine?
 Who is the Father of Clinical Medicine?
 Describe about Code of Hamurabi?
 Briefly describe about Ancient Indian contributions in Veterinary Medicine.
 What are the treatise on animal health from ancient India?

MODULE-2: CONCEPTS OF ANIMAL DISEASES

Learning objectives

 To understand the concept of disease and to know about the various theories regarding the
disease.
 To learn the evolution of disease concept from the age old humoral theory to the current
concept of diseases.

WHAT DOES DISEASE MEANS?

Disease is defined as an abnormal condition affecting the body of an organism. It is also a

pathological condition of a part, organ or system of an organism that results from different causes
like infection, genetic defect or environmental stress.

The term disease have a variety of definition, but it has a common concept. It is a term for any
condition that impairs normal functioning of an organism or body. Not just human beings alone; but
also the Plants and animals have diseases.

Diseases are classified into three categories:

 Intrinsic,
 Extrinsic and
 Unknown origin.
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Intrinsic is defined as coming from within the body and is more familiar to us now a days.
Examples of intrinsic diseases are autoimmune disorders, cancers, stress-related, hereditary and
conditions resulting from malnutrition.

Extrinsic or infectious simply means coming from the outside or external organism such as
parvovirus, distemper and many others. Extrinsic diseases are diseases that are triggered by external
factors like bacterial organisms, which entered into body and affect the normal function of healthy
organisms inside.

The third category is of unknown origin, like Alzheimer's disease in Human beings. Until now
doctors and scientist failed to know the main cause of Alzheimer's disease and this is greatly affecting
elderly human population. Some of the animal examples included Pyrexia of Unkown Origin(PUO).

CONCEPT OF ANIMAL DISEASES

 Disease is the result of complex interactions (some would say imbalance) between the triad
of the agent (toxic or infectious), the host and the environment. The components of this
interaction differ depending upon the specific circumstances of each group of affected
animals. Particularly for agricultural animals, this triad is strongly influenced by husbandry
and management factors, which are often the most important. For vector-borne diseases,
vector factors are also linked to the other factors.
 Recognizing the different components of this triad is important because they are the
source of opportunities to reduce disease at multiple points in the transmission cycle. A
common mistake is to focus on only one aspect of the triad for disease control or
prevention and to overlook the others.
 Examination of the past historical and contemporary writings on disease suggested that
disease concepts were viewed as causal networks that represent relations among the
symptoms, causes, and treatment of a disease. Conceptual change concerning disease is
primarily driven by changes in causal theories about diseases.
 The most famous thories on diseases include
o The Humoral Theory
o The Contagion Theory &
o Germ Theory
 All of which were now superseded by the current medical advances.
 Ancient Greek viewed of diseases, whose concepts are closely connected to the humoral
theory of the causes of disease. The same view dominated european medical thought until the
development of the germ theory of disease, which was first hinted at in the sixteenth century
but not developed and generally accepted until the nineteenth.
 Fracastoro, an Italian physician, wrote the first important work on contagion in 1546, but the
modern germ theory of disease developed with the research of Pasteur, Lister, Koch, and
others in the 1860s and 1870s.
 Transition from the humoral to the germ theory of disease required a major conceptual
revolution, involving many kinds of conceptual change including a fundamental shift in how
diseases are classified. Less radical conceptual changes occurred in the twentieth century
with the discovery of genetic, nutritional, and immunological causes of disease.

Agent Factor Examples

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 Dose
 Environmental hardiness
 Virulence (microbial)
 Infectivity (microbial)
 Toxicity (poisons)

Host Factor Examples

 Innate resistance (e.g. gastric barrier, mucocilliary transport mechanism)

 Previous exposure
 Passive immune status (neonates)
 Vaccination status and response
 Age
 Gender
 Behavior (e.g. mutual grooming, dominance, pica)
 Production status (e.g., lactating vs. non-lactating)
 Reproductive status (e.g., pregnant vs. non-pregnant, sterile vs. intact)
 Genetics

Intrinsic (non-changeable in the individual)

 Age is very important because the risk of many diseases change widely over the animals life
time due to underlying physiological changes that are associated with age. Neonates are very
susceptible to many enteric and respiratory infections but resistance increases as the animals
mature. As immune function declines with advanced age, susceptibility begins increasing
again.
 Clinical disease due to ubiquitous agents, such as the viral scour agents, can be reduced by
delaying the neonate's exposure to the agent (innate resistance increases with age) and
reducing the infectious dose by changing the environmental factors.
 Due to genetics different breeds have different risks for diseases, such as hip dysplasia in
German Shepherds. Within breeds, some infectious diseases occur due to underlying genetic
defects (e.g., Holstein BLAD, Arab CID, Quarter Horse HPP).

Extrinsic (changeable in the individual)

 Intact bitches are at risk of pyometra and mammary gland tumors than spayed (excluding
stump pyometras) are not. Intact dogs behave differently than non-intact dogs, tending to
roam more and thus being at higher risk of being hit by cars and of acquiring communicable
infectious diseases.
 Vaccination increases an individual’s resistance to disease but the protection is not absolute
for most biologics.

Environmental Factor Examples

 Animal stocking density

 Animal movement between groups
 Housing (e.g. ventilation, sanitation)
 Environmental conditions (e.g. temperature, humidity, wind velocity, precipitation)
 Nutrition (protein, energy and macromineral and micromineral adequacy)
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 Many infectious agents are susceptible to the ultraviolet (UV) in direct sunlight and to
desiccation. Many infectious agents survive for long periods in damp environments.
 Strangles (Strep. equi) in horses appears to occur more frequently during damp cold weather.
This is likely because the agent is able to survive longer in damp environments.
 Salmonellosis in all animals including humans occurs more frequently during summer than
during other times of the year. This is likely because the agent is able to replicate to infectious
doses in moist feedstuffs at summer temperatures.
 Bluetongue virus grows more rapidly in Cuilicoides variipennis at higher temperatures. A
strong association has been shown between bluetongue infection in cattle and both
temperature and rainfall.
 These factors interact in complex ways that are often under the control of man.
 Eg: Increased animal density may lead to increased microbial load in the environment, a roof
may prevent exposure of microbe to killing UV, low ventilation may increase humidity from
animal respiration which in turn increases environmental survival of the organism which in
turn increases exposure dose and infects more animals.
 It has been said that:
o "Bovine mastitis is a disease of man with signs in the cow."
o "Bad management will overwhelm the best immunology."

The "Iceberg" Concept

 In outbreaks of most disease in animal groups, both clinical cases (the tip of the iceberg) and
subclinical cases (unobserved beneath the ocean surface) are present in the group.
 For many infectious agents, particularly those that are endemic, more of the infections in a
group are subclinical (silent) than are clinical. For some exceptions, such as rabies, few if any
subclinical infections occur and almost all if not all clinical infections end in death. This
iceberg concept of severity distribution also holds for most induced, non-infectious diseases
affecting a group, such as hypomagnesemia, ketosis and hypocalcemia. Disease in an
individual is often evidence of a group phenomena because the factors that caused the
disease in that individual are usually affecting others adversely as well.
 For most groups, the response to the host-agent-environment interaction that results in
disease is usually not an either / or, black or white phenomenon. Instead, it is usually a
continuum, with different individuals expressing different degrees of severity at different
times as determined by the unique combinations of agent – host – environment risk factors
that they experience. For each problem outbreak, the "shape" of this iceberg (the proportion
affected, the proportion of the affected that become clinical and the proportion of these that
die) at any point in time depends on the specific combination of agent, host, environment,
vector (if one is involved), and human husbandry / management factors acting in that
specific situation.
 Because these factors change over time (e.g., animal immune responses eliminate the
infection, humans change their management practices, the environment changes both
seasonally, day-to-day and year-to-year), this "shape" changes over time. This does make
outbreak investigation and problem solving both challenging and rewarding for the
clinician.
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HIPPOCRATES AND THE HUMORAL THEORY

 The quotes from Hippocratic treatises concisely summarized the humoral
theory:
o The human body contains blood, phlegm, yellow bile, and black bile.
These are the things that make up its constitution and cause its pains
and health. Health is primarily a state in which these constituent
substances are in the correct proportion to each other, both in strength
and quantity, and are well mixed.
o All human diseases arise from bile and phlegm; the bile and phlegm
produce diseases when, inside the body, one of them becomes too moist,
too dry, too hot, or too cold; they become this way from foods and
drinks, from exertions and wounds, from smell, sound, sight, and
venery, and from heat and cold.
 Diseases arise because of humoral imbalances. For example, too much bile can
produce various fevers, and too much phlegm can cause epilepsy or angina.
Imbalances arise from natural causes such as heredity (phlegmatic parents
have phlegmatic children), regimen (diet and other behavior), and climate
(temperature, wind, and moisture conditions).
 Different kinds of imbalance produce different diseases with symptoms and
development that were acutely observed by the Hippocratics. They described in
detail not only the symptoms of patients with a particular disease, but also the
ways that the patients tended to develop toward recovery or death.
 The course of a disease was affected by the development of a particular humor,
producing crises that signaled basic changes in patient outcome. Fevers were
classified as tertian, quartan, and so on based on the number of days before a
crisis occurred.

FRACASTRO AND THE CONTAGION THEORY

 Fracastoro, the Italian Physician suggested that the persons can contract infections
even if their humors are normally balanced. He defined a contagion as a "corruption
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which develops in the substance of a combination, passes from one thing to another,
and is originally caused by infection of the imperceptible particles".
 He called the particles the seminaria (seeds or seedlets) of contagion. He described
how contagion can occur by direct contact, by indirect contact via clothes and
other substances, and by long-distance transmission. In addition, he stated that
diseases can arise within an individual spontaneously.

PASTEUR, LISTER, KOCH AND THE GERM THEORY

 The germ theory viewed diseases in terms of a causal network similar to that of
Fracastoro, but with much more detail about the nature of germs and possible
treatments. The Hippocratics were largely confined to a taxonomy of diseases
in terms of symptoms, and Fracastoro' theory allowed only a limited causal
classification based on kinds of contagion; but the germ theory of disease
made possible a detailed and clinically powerful taxonomy of diseases in terms
of their microbial causes. Today, infectious diseases are typically classified as
bacterial (e.g. tuberculosis,), viral (e.g. herpes), protozoal (e.g. trypanosomes),
and so on.

CURRENT CONCEPTS OF ANIMAL / HUMAN DISEASES

 While many diseases are infectious, research in the twentieth century has revealed other
kinds of cause of disease: genetic, nutritional, immunological, metabolic, and cytological. The
Hippocratics saw some traits such as being phlegmatic as hereditary, but the first
demonstration of the genetic basis of a disease was Archibald Garrod's work on alkaptonuria
in 1901. Many other kinds of genetic disorders have been identified, and in recent years
genetic engineering has offered the possibility of new kinds of treatment for such disorders.
 Hippocrates placed great emphasis on diet as a factor on disease, and the value of citrus
fruits in preventing scurvy was established in 1747, but identification of vitamin C as a
nutritional requisite of health occurred only in 1932. Diseases caused by nutritional
deficiencies can easily be treated by providing the missing vitamins or other nutrient.
 Knowledge of the immune system advanced rapidly in the 1950s, making possible the
understanding of diseases that arise from attacks by the immune system on the body's own
organs, as occurs in diseases such as lupus erythematosus.
 Metabolic disorders such as diabetes have become increasingly understood as knowledge
increases of the physiology of organs such as the pancreas, but causality in such cases is
complex, involving an interaction of hereditary and environmental factors.
 Similarly, although knowledge is developing rapidly concerning the nature of the cells and
genes involved in the growth of cancers, the causal interactions are enormously complex
and hard to identify.
 Currently the authoritative Textbooks of Medicine are divided into parts that implicitly
classify diseases in two complementary respects: organ systems and pathogenesis. Most of
these are organized around physiological systems, such as the cardiovascular and respiratory
systems. But there are also parts that group diseases in terms of pathogenetic mechanisms
that can affect various organ systems: oncology, metabolic diseases, nutritional diseases,
infectious diseases, and so on. Some diseases are naturally discussed in more than one part,
as when myocarditis occurs both under cardiovascular diseases and infectious diseases.
Modern medical classification thus blends two overlapping taxonomies of disease.
o Cardiovascular diseases
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o Respiratory diseases
o Renal diseases
o Gastrointestinal diseases
o Diseases of the liver, gall bladder, and bile ducts
o Hematologic diseases
o Oncology
o Metabolic diseases
o Nutritional diseases
o Endocrine and reproductive diseases
o Diseases of the bone and bone mineral metabolism
o Diseases of the immune system
o Musculoskeletal and connective tissue diseases
o Infectious diseases
o HIV and associate disorders
o Diseases caused by protozoa and metazoa
o Neurology
o Eye diseases
o Skin diseases
 The shift from the humoral to the germ theory of disease required a conceptual revolution:
the old conceptual and explanatory system was replaced by a radically different one. In
contrast, the development in the twentieth century of concepts of genetic, nutritional,
immunological, and metabolic diseases were relatively conservative extensions of the
nineteenth century ideas: new causes were introduced without denying that the germ theory
was right about the causes of diseases to which it had been applied.

COMMON QUESTIONS

1. What are the components of the

triad pertaining to a disease?
2. Explain about the iceberg concept,
endemic stability concept and the
herd immunity concept?
3. Define prognosis and its importance
in clinical practice?
4. Enlist the various records
maintained in a veterinary hospital
and the advantages of maintaining
them.

MODULE-3: CONCEPTS OF DISEASE - DIAGNOSIS,

DIFFERENTIAL DIAGNOSIS AND PROGNOSIS
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Learning objectives

 To understand concept of
diagnosis
 To know how to make a
differential diagnosis
 To understand arriving at a
diagnosis
 To know how to decide
upon the prognosis

CONCEPT OF DIAGNOSIS

 A Veterinary health care provider's job is to know the animal body and its functions in terms
of normality (homeostasis). The four cornerstones of diagnostic medicine, each essential for
understanding homeostasis, are: anatomy (the structure of the human body), physiology
(how the body works), pathology (what can go wrong with the anatomy and physiology) and
psychology (thought and behavior). Once the provider knows what is normal and can
measure the patient's current condition against those norms, she or he can then determine
the patient's particular departure from homeostasis and the degree of departure. This is
called the diagnosis.
 Once a diagnosis has been reached, the health care provider is able to propose a management
plan, which will include treatment as well as plans for follow-up. From this point on, in
addition to treating the patient's condition, the provider educates the patient about the
causes, progression, outcomes, and possible treatments of his ailments, as well as providing
advice for maintaining health.

Diagnostic procedures

 The diagnostic process is fluid in which the provider gathers information from the patient
and others, from a physical examination of the patient, and from medical tests performed
upon the patient.
 There are a number of techniques used by providers to obtain a correct diagnosis:
o Exhaustive method
o Every possible question is asked and all possible data is collected.
o Algorithmic method
o The provider follows the steps of a proven strategy.
o Pattern-recognition method
o The provider uses experience to recognise a pattern of clinical characteristics.

Differential diagnosis

 The health care provider uses the hypothetico-deductive method, a systematic, problem-
focused method of inquiry.
 The advanced clinician uses a combination of the pattern-recognition and hypothetico-
deductive approaches.
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 The presence of some medical conditions cannot be established with complete confidence
from examination or testing. Diagnosis is therefore by elimination of other reasonable
possibilities, referred to as the diagnosis of exclusion.
 The process of diagnosis begins when the animal owner with the animal patient consults the
animal health provider and presents a set of complaints (symptoms). If the patient is
unconscious, this condition is the de facto complaint. The provider then obtains further
information from the patient owner and from those who know the animal patient, if present,
about the animal patient's symptoms, their previous state of health, living conditions, and so
forth.
 Rather than consider the myriad diseases that could afflict the patient, the provider narrows
down the possibilities to their illnesses likely to account for the apparent symptoms, making
a list of only those disease (conditions) that could account for what is wrong with the patient.
These are generally ranked in order of probability.
 The provider then conducts a physical examination of the animal patient, studies the
patient's medical record, and asks further questions in an effort to rule out as many of the
potential conditions as possible. When the list is narrowed down to a single condition, this is
called the differential diagnosis and provides the basis for a hypothesis of what is ailing the
patient.
 Unless the provider is certain of the condition present, further medical tests are performed or
scheduled such as medical imaging, in part to confirm or disprove the diagnosis but also to
document the patient's status to keep the patient's medical history up to date. Consultations
with other providers and specialists in the field may be sought. If unexpected findings are
made during this process, the initial hypothesis may be ruled out and the provider must then
consider other hypotheses.
 Despite all of these complexities, most animal patient consultations are relatively brief,
because many diseases are obvious, or the providers experience may enable him or her to
recognize the condition quickly. Another factor is that the decision tree is used for most
diagnostic hypothesis testing are relatively short.
 Once the provider has completed the diagnosis, the prognosis is explained to the patient and
a treatment plan is proposed which includes therapy and follow-up consultations and tests to
monitor the condition and the progress of the treatment, if needed, usually according to the
medical guideline provided by the vetrinary medical field on the treatment of the particular
illness.
 Treatment itself may indicate a need for review of the diagnosis if there is a failure to respond
to treatments that would normally work.
 A laboratory diagnosis is either a substitution or complement to the diagnosis made by
examination of the patient. For instance, a proper diagnosis of infectious diseases usually
requires both an examination of symptoms, as well as laboratory characteristics of the
pathogen involved.

CONCEPT OF DIFFERENTIAL DIAGNOSIS

 In Veterinary Medicine, differential diagnosis (abbreviated DDx, ddx, DD, or ΔΔ) is a

systematic method used to identify unknowns. This method, essentially a process of
elimination, is used by physicians, physician assistants, and other trained medical
professionals to diagnose the specific disease in a patient.
 Not all veterinary medical diagnoses are differential ones: some diagnoses merely name a set
of signs and symptoms that may have more than one possible cause, and some diagnoses are
based on intuition or estimations of likelihood.
 Careful differential diagnosis involves first making a list of possible diagnoses, then
attempting to remove diagnoses from the list until at most one diagnosis remains. In some
cases, there will remain no diagnosis; this suggests the physician has made an error, or that
the true diagnosis is unknown to medicine. Removing diagnoses from the list is done by
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making observations and using tests that should have different results, depending on which
diagnosis is correct.
 In Veterinary Medicine, differential diagnosis is the process whereby a given condition or
circumstance, called the presenting problem or chief complaint, is examined in terms of
underlying causal factors and concurrent phenomena as discerned by appropriate
disciplinary perspectives and according to several theoretical paradigms or frames of
reference, and compared to known categories of pathology or exceptionality.

Differential diagnosis allows the physician to

 More clearly understand the condition or circumstance

 Assess reasonable prognosis
 Eliminate any imminently life-threatening conditions
 Plan treatment or intervention for the condition or circumstance
 Enable the patient and the family to integrate the condition or circumstance into their lives,
until the condition or circumstance may be ameliorated, if possible.
 If the patient's condition does not improve as anticipated when the treatment or therapy for
the disease or disorder has been applied, the diagnosis must be reassessed.
 The method of differential diagnosis is based on the idea that one begins by first considering
the most common diagnosis first: a head cold versus meningitis, for example. As a reminder,
medical students are taught the adage, "When you hear hoofbeats, don't look for zebras,"
which means look for the simplest, most common explanation first. Only after the simplest
diagnosis has been ruled out should the clinician consider more complex or exotic
diagnoses.
 At one time doctors ordered only particular blood tests, but now a full blood chemistry
profile is standard, which can speed up the process of diagnosis as well as uncover sub-
clinical conditions.
 With the advent of better radiological studies like MRI and the wider use of nuclear
medicine, it has become more likely that unexpected findings will emerge and will be further
studied, though such findings may not be supported by further investigation.
 Such findings are a valuable tool but not infallible; often it still takes a veterinary physician
or veterinary medical team to track down either a more common illness with a rare
presentation or a rare illness with symptoms suggestive of many other conditions.
Sometimes a definitive diagnosis might take years.

CONCEPT OF PROGNOSIS

 Prognosis is a veterinary medical term to describe the likely outcome of an illness. When
applied to large populations, prognostic estimates can be very accurate: for example the
statement "45% of patients with severe septic shock will die within 28 days" can be made
with some confidence, because previous research found that this proportion of patients died.
However, it is much more difficult to translate this into a prognosis for an individual patient:
additional information is needed to determine whether a patient belongs to the 45% who will
succumb, or to the 55% who survive. A complete prognosis includes expected time, function,
and a description of the disease course such as progressive decline, intermittent crisis, or
sudden, unpredictable crisis.
 Prognosis tells about

o The expected course of a disease.

o The patient's chance of recovery.
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 The prognosis predicts the outcome of a disease and therefore the future for the patient, for
example, good / favourable /unfavourable /grave etc. The word prognosis comes from the
Greek prognostikos (of knowledge beforehand). It combines pro (before) and gnosis (a
knowing). Hippocrates used the word prognosis, much as we do today, to mean a foretelling
of the course of a disease.

CLINICAL DIAGNOSIS

 Clinical diagnosis is the science of clinical methods of examination of animals in order to

identify the affected organ or system that is the cause of disease.
 Externally visible or appreciable changes in the body of an animal or one of its organs is an
indicator of disease. The recognition of such changes using inspection, palpation, percussion
or auscultation is called clinical or physical examination.
 Physical examination is an integral part of clinical diagnosis, which is crucial for
the management of disease conditions.
 The determination of the causes of disease may be termed aetiological diagnosis whereas
symptomatic diagnosis is used when the cause of the disease cannot be determined.

Some definitions

 Symptoms are any visible functional disturbances of various body systems (e.g. increased
body temperature).
 Syndrome , a group of clinical signs that constitute a group of diseases that cannot be
traced to a single aetiological factor (e.g. feline urologic syndrome).
 Prognosis , anticipating the outcome of the disease or condition (e.g. recovery or death).
 Three main categories should be taken into account when clinically examining the animal,
these are:
o Case history.
o Examination of the environment.
o Examination of the animal.

CLINICAL EXAMINATION - MODEL RECORD

GENERAL METHODS OF EXAMINATION

 These include inspection, palpation, percussion and auscultation.

Inspection

 Means observing the animal from a distance, simple and widely used in veterinary medicine
it helps obtaining an idea about the general characters of diseased animal.
 The following information can be obtained by inspecting the animal:
o General demeanor, posture and gait.
o Body score of the animal (thin, emaciated, obese).
o Depression, anxiety or frenzy.
o Skin diseases and lesions.
o Lameness.
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o Abnormal odour.
o Type of respiration, rate and rhythm.
 Inspection should always be performed in daylight except in emergency where artificial light
may be used.

Palpation

 Using the sense of touch to obtain information about the organs examined, this is called
direct palpation. Indirect palpation can sometimes be used by means of a probe.
 When palpating an organ or a lesion, the following information can be obtained:
o Sensitivity (pain and tenderness)
o Temperature (hot, cold or normal)
o Consistency (resilient, doughy, firm, hard, fluctuating or emphysematous).

Percussion

 Obtaining information about internal organs using a plexor and pleximeter (indirect
percussion) or using the fingers (direct percussion).
 Tapping on the area of examination and noting the sound is used to obtain information about
the physical condition of certain organs.
 It also reveals the sensitivity of this organ.
 Percussive sounds
o Resonant
 This is the sound heard over a normal lung and indicates presence of air in
tissues.
o Tympanic
 Sound produced by percussion over a hollow organ containing gas (e.g.
Rumen).
o Dull
 The sound heard in case of percussion of solid tissues containing no air.
 A change of percussive sound (e.g. change from resonant to dull over the
lung area) indicates disease of the organ.

Auscultation

 Listening to sounds produced by the functional activity of an organ.

 Organs that can be auscultated are
o The heart.
o The lungs.
o The rumen.
 Direct auscultation is performed by using the ear, whereas indirect auscultation is
performed by means of a stethoscope.

COMMON QUESTIONS

 What are the cornerstones of a diagnosis?

 What are the techniques used by the clinician to make a diagnosis?
 Explain the basis for forming a differential diagnosis?
 What advantages of forming a differential diagnosis ?
 Define the following: clinical diagnosis, symptoms, syndrome and prognosis?
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 Explain briefly about the general methods of examination?

MODULE-4: GENERAL AND SYSTEMIC STATES - I

Learning objectives

 To understand the concepts of the generalized states affecting all body systems
 To know about their clinical findings, diagnosis and treatment
 To know about medical management pertaining to the general systemic
states such as
o Hypothermia
o Hyperthermia
o Fever
o Electrolyte Imbalnces
o Acid-Base Disorders

HYPOTHERMIA

 Hypothermia is a lowering of the body's temperature in animals or human beings.

 At a rectal temperature of less than 28 C (82 F), the ability to regain normal temperature is
lost, but the animal will continue to survive if external heat is applied and the temperature
returns to normal. It is important to observe and measure the vital signs: pulse, breathing,
mental status and rectal temperature.
 To know the severity of hypothermia is valuable to decide the re-warming technique to be
used for treatment.
 On the basis of body temperature, hypothermia can be classified as Mild (86 -89 F or 30 - 32
C), Moderate (71- 77 F or 22 -25 C) and Severe (32- 46.5 or 0 - 8 C). There are three
rewarming techniques (Passive external, Active external, and Active internal) which should
be used according to severity of hypothermia.
 When the skin or blood is cooled enough to lower the body temperature in non-hibernating
animals, the metabolic and physiological processes slow down. In the hypothermic state,
the oxygen need of cells, particularly neurons is greatly reduced, and the circulation can be
stopped for relatively long periods.
 At a rectal temperature of less than 28 C (82 F), the ability to regain normal temperature is
lost, but animal will continue to survive if external heat is applied and the temperature
returns to normal. Hypothermia is a condition of general body cooling in contrast to
frostbite, which is localized.
 A fall in body temperature can be due to accidental exposure to external cold, effect of
drugs, or failure of internal temperature regulating mechanisms.
 The simplest way to determine whether the patient is hypothermic or not, is to assess body
temperature by placing a bare hand against the skin (preferably in axilla or groin region) of
the patient. If the skin feels warm, hypothermia is unlikely.
 Patients with cold skin should have rectal temperatures taken with a low reading
thermometer.

What to expect in a hypothermic animal?

 As the body core temperature drops, more body systems suffer from the effects of cold.
 The signs and symptoms can assess the presence and severity of hypothermia.
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 In the cold patient, a rectal temperature is one of the most important signs and is useful for
assessing and treating hypothermia, however there is a tremendous variability in
physiological responses at specific temperatures among individuals and species.
 Once it is established that an animal is hypothermic it is important to observe and measure
the following most important signs: pulse (slow to none); breathing (slow to none); mental
status (responsive to unconsciousness); cold skin; low rectal temperature.
 Severally hypothermic animals may have other problems, which are not easily detected.
e.g. change in blood chemistry; irregular heart beat; dehydration; difference in temperature
between deep body tissues and superficial body tissues.

Classification on the basis of severity

 On the basis of body temperature, hypothermia can be classified as Mild (86 -89 F or 30 - 32
C), Moderate (71- 77 F or 22 -25 C) and Severe (32- 46.5 or 0 - 8 C).

Management of a hypothermic animal

 The primary goals in the treatment and handling of a hypothermic animal are: keep the
animal alive by warming, avoid any further exposure to cold, and then transport the animal
to a site of complete veterinary care.
 In order to treat the hypothermic animal appropriately, one should first know that
the animal is in fact hypothermic.
 If so, then the severity of hypothermia e.g. mild, moderate or severe.
 Once this is determined, one has to decide the re-warming technique to be used for
treatment.

EXAMINATION OF HYPOTHERMIC ANIMAL

 To examine a hypothermic animal, one should proceed as follows:

o Attention to ABCD:
 A. Airway;
 B. Breathing;
 C. Circulation;
 D. Degrees.
o One should make sure that the animal has an open airway, is breathing, and has a
heart beat and assess rectal temperature.
 Brief history (e.g. duration of exposure, regarding circumstances in which animal found etc.).
 Brief physical examination including
o feel of body temperature
o level of consciousness and neurological examination
o cardio-pulmonary examination
o associated trauma
o weight of animal
 Depending upon the availability of staff and equipment, chest x-ray, urinalysis, complete
blood work, and arterial blood gases are also recommended.
 If there is a high probability that the animal is severely hypothermic, breathing and heart rate
may be slow, shallow and very hard to detect, therefore, take a full minute or more to
measure these vital signs.
 Hypothermic patients with any measurable pulse or respiration obviously do not require
Cardio - pulmonary Resuscitation (CPR). However, if both pulse/heart beat and respiration
are absent then commence CPR.
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 Evaluate the animal's level of consciousness, size of pupil, ability to respond if conscious and
ability to walk.
 When any of these characteristics are abnormal, suspect severe hypothermia and treat
accordingly.
 While treating the hypothermic animal, also check the animal for other possible injuries. The
best chances of recovery are as a result of early diagnosis and treatment.
 In accidental hypothermia, the animal should be brought into a heated environment and
allowed to warm slowly to its normal temperature. Rewarming and maintenance of normal
body temperature can be accomplished externally or internally (see Rewarming techniques).
 Neonates not only require rewarming but careful attention to nutrition should also be given.

Mild Hypothermia

 Prevent further heat loss, insulate from the ground, protect from the wind, cover the head
and neck, and move the animal to a warm environment. Rewarming through the application
of insulated heat packs to high heat loss areas such as head, neck, between legs, side of chest
wall to prevent heat loss. Consider warm showers and warm bath, if the patient is alert (see
passive external and active external rewarming techniques)

Moderate Hypothermia

 Keep the patient warm e.g. warm bottles, blankets, immerse patient in tub of warm water.
 Continue rewarming efforts until animal's core temperature is restored to normal (see
active external rewarming methods).

Severe Hypothermia

 Animal in severe hypothermic state, can erroneously thought to be dead as no pulse, no

heart rate, and no respiration is apparent. It is wise to follow the same criteria as in human
medicine which suggests " the hypothermic patient is not dead until the patient is warm and
dead."
 Animals with severe hypothermia should be treated by putting heat directly into the core
areas (see active rewarming methods).
 If the heart beat and respiration is not detectable after checking for up to 1 minute then
commence CPR: Mouth to mouth or mouth to mask breathing during CPR is best
because this provides warm, humidified air or oxygen.
 One can also use an apparatus to ventilate the animal with 100% heated, humidified air or
oxygen.
 Reassess the animal's physical status periodically while performing CPR.
o CPR is less likely to have a significant effect on the survival of a hypothermic animal,
if
 The animal has been under the water for more than 1 hour.
 The animal with a core temperature below 60 F (15.5 C).
 The animal is frozen e.g. ice formation in the airway.
 The animal's chest wall is so stiff that compression is impossible

 Treatment that stimulates peripheral circulation (i.e. wrapping in a blanket, massaging

extremities etc.) must be avoided in cases of severe hypothermia.
 These activities will likely increase flow of cold blood from the periphery (muscle pumping)
which can cause after drop, increasing the depth of hypothermia in critical core tissues,
especially the heart.
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 Stimulating the peripheral circulation also reduces the blood volume in the body core,
causing rewarming shock, which increases the workload on the heart.
 The blood returning from the periphery can also include metabolic waste products that can
cause a fatal heart arrhythmia.

REWARMING TECHNIQUES

 There are three classes of rewarming techniques:

Passive external

 The animal's own metabolic processes continue to produce heat spontaneously so no external
heat is required.
 Shivering is an example of thermogenesis.
 This is simplest and slowest rewarming method but is sufficient for mild hypothermic
patients.

Active external

 This system includes warm water baths, hot water bottles, blankets, heating pads, radiant
heaters.
 This method of rewarming is safe only for mild hypothermia because externally applied heat
stimulates peripheral circulation.

Active internal

 These rewarming methods are usually more complex and need to be carried out
by professionals (Veterinarians/Animal health technicians).
 These include inhalation rewarming (ventilation of patient with heated, humidified air or
oxygen), circulation of heated fluids (40.5 - 43.5 C) in body cavities (gastric, thoracic and
peritoneal lavage), and heated intra venous solutions preferably dextrose as this provides
energy to meet increased metabolic demands (contribute little heat due to vasoconstriction in
cold extremities).
 Inhalation rewarming is the only method, which can be used by a layman and does not
require much training (mouth to mouth breathing). Inhalation of warm-saturated air
delivers heat directly to the lungs and heart.
 The brain is also warmed from this blood flow and from conductive heat flow from
the respiratory and nasal cavities.
 This method also assists in re-hydration as an added benefit.

PRECAUTIONS

Precautions while treating hypothermic animals

 Be cautious about assuming that animal can not be resuscitated. As in resuscitation, a

positive attitude is important.
 The hypothermic animal may appear to be beyond help because of, skin and
membrane colors, pupil dilatation and depressed vital signs.
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 Avoid direct application of hot objects or excessive pressure (e.g. uninsulated hot water
bottles, tourniquets etc.).
 Ensure that items such as oxygen and fluids coming into contact with the animal are
warmed.
 Do not put severely hypothermic animal in a shower or bath.
 Drug treatments are not useful in treating severe hypothermic animals since the cold heart
will not respond as expected.
 If administered, drugs will not be metabolized normally by the liver and kidneys; instead
these will accumulate in the body and become active as it warms.
 Do not use Lactated Ringers because the hypothermic liver may not be able to metabolize
the lactate normally.
 Do not administer cold fluids.

HYPERTHERMIA

 Hyperthermia is an elevated body temperature in mammals. The effects of hyperthermia, or

heat stroke, if left untreated, can cause permanent internal organ damage or even death.
 Hyperthermia is an elevated body temperature due to failed thermoregulation.
 Hyperthermia occurs when the body produces or absorbs more heat than it can dissipate.
 When the elevated body temperatures are sufficiently high, hyperthermia is a medical
emergency and requires immediate treatment to prevent disability and death.
 The most common causes are heat stroke and adverse reactions to drugs.
 Heat stroke is an acute condition of hyperthermia that is caused by prolonged exposure to
excessive heat and/or humidity.
 The heat-regulating mechanisms of the body eventually become overwhelmed and unable to
effectively deal with the heat, causing the body temperature to climb uncontrollably.
 Hyperthermia is a relatively rare side effect of many drugs, particularly those that affect the
central nervous system.
 Malignant hyperthermia is a rare complication of some types of general anesthesia.
 Hyperthermia can be created artificially by drugs or medical devices.
 Hyperthermia therapy may be used to treat some kinds of cancer and other conditions, most
commonly in conjunction with radiotherapy.
 Hyperthermia differs from fever in the mechanism that causes the elevated body
temperatures: a fever is caused by a change in the body's temperature set-point.

Signs and Symptoms

 Hot, dry skin is a typical sign of hyperthermia.An inability to cool the body through
perspiration causes the skin to feel dry.
 Other signs and symptoms vary depending on the cause. The dehydration associated with
heat stroke can produce vomiting, and low blood pressure. This can lead to fainting or
dizziness, especially if the person stands suddenly.
 In the case of severe heat stroke, the animal or person may become confused or hostile, and
may seem intoxicated.
 Heart rate and respiration rate will increase (tachycardia and tachypnea) as blood pressure
drops and the heart attempts to supply enough oxygen to the body.
 The decrease in blood pressure can then cause blood vessels to contract, resulting in a pale or
bluish skin color in advanced cases of heat stroke.
 Some, especially young animals, may have seizures. Eventually, as body organs begin to fail,
unconsciousness and coma will result.
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Heat Stroke

 Heat stroke is due to an environmental exposure to heat, resulting in an abnormally high

body temperature.
 In severe cases, temperatures can exceed 40 °C (104 °F).
 Heat stroke may be exertional or non-exertional, depending on whether the animal or person
has been exercising in the heat.
 Significant physical exertion on a very hot day can generate heat beyond a healthy body's
ability to cool itself, because the heat and humidity of the environment reduces the efficiency
of the body's normal cooling mechanisms.
 Other factors, such as drinking too little water, can exacerbate the condition.
 Non-exertional heat stroke is typically precipitated by medications that reduce vasodilation,
sweating, and other heat-loss mechanisms, such as anticholingeric drugs, antihistamines,
and diuretics.
 In this situation, the body's tolerance for the excessive environmental temperatures can be
too limited to cope with the heat, even while resting.

Diagnostic Approach

 Hyperthermia is generally diagnosed in the presence of an unexpectedly high body

temperature and a history that suggests hyperthermia instead of a fever.
 Most commonly this means that the elevated temperature has appeared in a animal that was
working in a hot, humid environment (eg. equine heat stroke) or that was taking a drug for
which hyperthermia is a known side effect (drug-induced hyperthermia).
 If fever-reducing drugs lower the body temperature, even if the temperature does not return
entirely to normal, then hyperthermia is excluded.

Prevention & Mitigation

 In cases where heat stress is caused by physical exertion, hot environments or wearing
protective equipment it can be prevented or mitigated by taking frequent rest breaks, staying
hydrated and carefully monitoring body temperature. However, in situations demanding
prolonged exposure to a hot environment or wearing protective equipment, a personal
cooling system is required as a matter of health and safety.
 A variety of active or passive technologies personal cooling systems exist which can be
categorized by their power sources and whether they are animal or vehicle-mounted.

Treatment

 Treatment for hyperthermia depends on its cause, as the underlying cause must be corrected.
 Mild hyperthemia caused by exertion on a hot day might be adequately treated through
measures, such as allowing to drink more water and resting in a cool place.
 Hyperthermia that results from drug exposures is frequently treated by cessation of that
drug, and occasionally by other drugs to counteract them. Fever-reducing drugs such as
paracetamol and aspirin have no value in treating hyperthermia.
 When the body temperature is significantly elevated, mechanical methods of cooling are used
to remove heat from the body and to restore the body's ability to regulate its own
temperatures.
 Passive cooling techniques, such as resting in a cool, shady area and removing clothing can
be applied immediately.
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 Active cooling methods, such as sponging the head, neck, and trunk with cool water, remove
heat from the body and thereby speed the body's return to normal temperatures.
 Making the animal to drink water and turning a fan or dehumidifying air conditioning unit
on the affected animal may improve the effectiveness of the body's evaporative cooling
mechanisms (sweating).
 Placing the animal in a bigger bathtub or pool of tepid or cool water (immersion method) can
remove a significant amount of heat in a relatively short period of time. However, immersion
in very cold water is counterproductive, as it causes vasoconstriction in the skin and thereby
prevents heat from escaping the body core.
 In exertional heat stroke, studies have shown that although there are practical limitations,
cool water immersion is the most effective cooling technique and the biggest predictor of
outcome is degree and duration of hyperthermia.No superior cooling method found for
nonexertional heat stroke.
 When the body temperature reaches about 40 C, or if the affected animal is unconscious or
showing signs of confusion, hyperthermia is considered a medical emergency that requires
treatment in a proper veterinary medical facility.
 In a veterinary hospital, more aggressive cooling measures are available, including
intravenous hydration, gastric lavage with iced saline, and even hemodialysis to cool the
blood.

FEVER

 Fever (also known as pyrexia or controlled hyperthermia) is a common medical sign

characterized by an elevation of temperature above the normal range due to an increase
in the body temperature regulatory set-point.This increase in set-point triggers increased
muscle tone and shivering.
 As an animal's temperature increases there is generally a feeling of cold despite an increasing
body temperature.
 Once the new temperature is reached there is a feeling of warmth.
 A fever is one of the body's immune responses which attempts to neutralize a bacterial or
viral infection.
 A fever can be caused by many different conditions ranging from benign to potentially
serious.
 With the exception of very high temperatures, treatment to reduce fever is often not
necessary; however, antipyretic medications can be effective at lowering the temperature,
and this may improve the affected person's comfort.
 Fever differs from uncontrolled hyperthermia, usually just referred to as hyperthermia, in
that hyperthermia is an increase in body temperature over the body's thermoregulatory set-
point, due to excessive heat production and/or insufficient thermoregulation.

Classification/Types of Fever
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 Fever continues - A
 Fever continues to abrupt onset and remission - B
 Fever remittent - C
 Intermittent fever - D
 Undulant fever - E
 Relapsing fever - F

Hyperpyrexia

 Hyperpyrexia is a fever with an extreme elevation of body temperature greater than or equal
to 41.5 °C (106.7 °F).[12] Such a high temperature is considered a veterinary medical
emergency as it may indicate a serious underlying condition or lead to significant side
effects.
 The most common cause is a intracranial hemorrhage. Other possible causes include
sepsis,malignant syndrome, drug effects, serotonin syndrome, and thyroid storm.
 Infections are the most common cause of fevers as the temperature rises other causes
become more common.
 Hyperpyrexia differs from hyperthermia in that in hyperpyrexia the body's temperature
regulation mechanism sets the body temperature above the normal temperature, then
generates heat to achieve this temperature, while in hyperthermia the body temperature rises
above its set point.

Pathophysiology

 Temperature is ultimately regulated in the hypothalamus. A trigger of the fever, called a

pyrogen, causes a release of prostaglandin E2 (PGE2). PGE2 then in turn acts on the
hypothalamus, which generates a systemic response back to the rest of the body, causing
heat-creating effects to match a new temperature level.
 In many respects, the hypothalamus works like a thermostat.When the set point is raised, the
body increases its temperature through both active generation of heat and retaining heat.
Vasoconstriction both reduces heat loss through the skin and causes the person to feel cold.
 The liver produces extra heat. If these measures are insufficient to make the blood
temperature in the brain match the new setting in the hypothalamus, then shivering begins,
to use muscle movements to produce more heat.
 When the fever stops, and the hypothalamic setting is set lower, the reverse of these
processes (vasodilation, end of shivering and nonshivering heat production) and sweating
are used to cool the body to the new, lower setting.
 This contrasts with hyperthermia, in which the normal setting remains, and the body
overheats through undesirable retention of excess heat or over-production of
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heat.Hyperthermia is usually the result of an excessively hot environment (heat stroke) or an

adverse reaction to drugs.
 Fever can be differentiated from hyperthermia by the circumstances surrounding it and its
response to anti-pyretic medications.

Pyrogens

 A pyrogen is a substance that induces fever. These can be either internal (endogenous) or
external (exogenous) to the body.
 The bacterial substance lipopolysaccharide (LPS), present in the cell wall of some bacteria, is
an example of an exogenous pyrogen.
 Pyrogenicity can vary, as in extreme examples some bacterial pyrogens known as
superantigens can cause rapid and dangerous fevers.
 Depyrogenation may be achieved through filtration, distillation, chromatography,
or inactivation.

Endogenous Pyrogens

 Cytokines (especially interleukin 1) are a part of the innate immune system, are produced by
phagocytic cells, and cause the increase in the thermoregulatory set-point in the
hypothalamus. Other examples of endogenous pyrogens are interleukin 6 (IL-6), and tumor
necrosis factor-alpha.
 These cytokine factors are released into general circulation where they migrate to the
circumventricular organs of the brain due to easier absorption caused by the blood-brain
barrier's reduced filtration action there. The cytokine factors then bind with endothelial
receptors on vessel walls, or interact with local microglial cells. When these cytokine factors
bind, the arachidonic acid pathway is then activated.

Exogenous Pyrogens

 One model for the mechanism of fever caused by exogenous pyrogens includes LPS, which is
a cell wall component of gram-negative bacteria.
 An immunological protein called lipopolysaccharide-binding protein (LBP) binds to LPS.
 The LBP–LPS complex then binds to the CD14 receptor of a nearby macrophage.
 This binding results in the synthesis and release of various endogenous cytokine factors, such
as interleukin 1 (IL-1), interleukin 6 (IL-6), and the tumor necrosis factor-alpha.
 In other words, exogenous factors cause release of endogenous factors, which, in
turn, activate the arachidonic acid pathway.

PGE2 release

 PGE2 release comes from the arachidonic acid pathway.

 This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2),
cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase. These enzymes ultimately
mediate the synthesis and release of PGE2.
 PGE2 is the ultimate mediator of the febrile response. The set-point temperature of the body
will remain elevated until PGE2 is no longer present. PGE2 acts on neurons in the preoptic
area (POA) through the prostaglandin E receptor 3 (EP3).
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 EP3-expressing neurons in the POA innervate the dorsomedial hypothalamus (DMH), the
rostral raphe pallidus nucleus in the medulla oblongata (rRPa) and the paraventricular
nucleus (PVN) of the hypothalamus .
 Fever signals sent to the DMH and rRPa lead to stimulation of the sympathetic output
system, which evokes non-shivering thermogenesis to produce body heat and skin
vasoconstriction to decrease heat loss from the body surface.
 It is presumed that the innervation from the POA to the PVN mediates the neuroendocrine
effects of fever through the pathway involving pituitary gland and various endocrine organs.

Hypothalamus

 The brain ultimately orchestrates heat effector mechanisms via the autonomic nervous
system. These may be:
 Increased heat production by
o Increased muscle tone, shivering and hormones like epinephrine.
o Prevention of heat loss, such as vasoconstriction.
 The autonomic nervous system may also activate brown adipose tissue to produce heat (non-
exercise-associated thermogenesis, also known as non-shivering thermogenesis), but this
seems mostly important for babies.
 Increased heart rate and vasoconstriction contribute to increased blood pressure in fever.

EPHEMERAL FEVER OR THREE DAY FEVER

 Ephemeral fever is an insect-transmitted, noncontagious, viral disease of cattle and buffalo.

Inapparent infections can develop in goats also.

Etiology

 Ephemeral fever virus is classified as a Rhabdovirus (single-stranded, negative sense RNA).

 It is best isolated from infected cattle by inoculation of mosquito ( Aedes albopictus ) cell
cultures with defibrinated blood, followed by transfer to baby hamster kidney (BHK-21) or
monkey kidney (Vero) cell cultures after 15 days.
 The virus can be transmitted from infected to susceptible cattle by IV inoculation; as little as
0.005 mL of blood collected during the febrile stage is infective.
 Although the virus has been recovered from several Culicoides species and from Anopheline
and Culicine mosquito species collected in the field, the identity of the major vectors has
not been proved. Transmission by contact or fomites does not occur, and the virus does not
appear to persist in recovered cattle.
 Most recovered cattle have a lifelong immunity.
 The prevalence, geographic range, and severity of the disease vary from year to year, and
epidemics occur periodically.
 During epidemics, onset is rapid; many animals are affected within days or 2-3 wk.
 Ephemeral fever is most prevalent in the wet season in the tropics and in summer to early
autumn in the subtropics or temperate regions (when conditions favor multiplication of
biting insects); it disappears abruptly in winter.
 Morbidity may be as high as 80%; overall mortality is usually 1-2%, although it can be higher
in lactating cows, bulls in good condition, and fat steers (10-30%).

Clinical Findings
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 Signs, which occur suddenly and vary in severity, include biphasic to polyphasic fever,
shivering, inappetence, lacrimation, serous nasal discharge, drooling, dyspnea, atony
of forestomachs, depression, stiffness and lameness, and a sudden decrease in milk
yield.
 Affected cattle may become recumbent and paralyzed for 8 hr to >1 wk.
 After recovery, milk production often fails to return to normal levels until the next lactation.
Abortion, with total loss of the season’s lactation, occurs in ~5% of cows pregnant for 8-9 mo.
 The virus does not appear to cross the placenta or affect the fertility of the cow.
 Bulls, heavy cattle, and high-lactating dairy cows are the most severely affected, but
spontaneous recovery usually occurs within a few days.
 More insidious losses may result from decreased muscle mass and lowered fertility in bulls.

Diagnosis

 Diagnosis is based almost entirely on clinical signs in an epidemic.

 All clinical cases have a neutrophilia with the presence of many immature forms, although
this is not pathognomonic.
 Laboratory confirmation is by serology, rarely by virus isolation.
 Whole blood should be collected from sick and apparently healthy cattle in affected herds.
 Samples must be sufficient to provide 2 air-dried blood smears, 5 mL in anticoagulant (not
EDTA), and 20 mL for serum.
 Isolated viruses are identified by neutralization tests using specific ephemeral fever
virus antisera and by ELISA using specific monoclonal antibodies.
 The neutralization test and the blocking ELISA are recommended for antibody detection and
give similar results.
 A 4-fold rise in antibody titer between paired sera collected 2-3 wk apart confirms infection.

Treatment and Control

 Complete rest is the most effective treatment, and recovering animals should not be stressed
or worked because relapse is likely.
 Anti-inflammatory drugs given early and in repeated doses for 2-3 days are effective.
 Oral dosing should be avoided unless the swallowing reflex is functional. Signs
of hypocalcemia are treated as for milk fever .
 Antibiotic treatment to control secondary infection and rehydration with isotonic fluids may
be warranted.

PYREXIA OF UNKNOWN ORIGIN (PUO)

 In both veterinary patients, fever may indicate infectious, inflammatory, immune-mediated,

or neoplastic disease.
 In most cases, the history and physical examination reveal the cause of the fever, or the fever
resolves spontaneously or in response to antibiotic therapy.
 However, in a small percentage of patients, the cause of fever is not readily apparent, and the
problem becomes persistent or recurrent.
 These patients are said to have pyrexia of unknown origin (PUO).
 The classical PUO is defined as fever >101ºF (38.3ºC) on several occasions over a period >2-
3 wk with no diagnosis established after 3 outpatient visits or 3 days in the hospital.

Body Temperature Regulation

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 Body temperature is regulated by the hypothalamus. This area of the brain acts as a
thermostat to maintain temperature as close as possible to a normal set-point.
 The hypothalamus receives input from internal and external thermoreceptors, and it
activates physiologic and behavioral activities that influence heat production, heat loss, and
heat gain.
 Hyperthermia refers to any increase in body temperature above the normal range.
 Fever is a particular form of hyperthermia in which the heat loss and heat gain mechanisms
are adjusted to maintain body temperature at a higher hypothalamic set-point; thus, fever is
essentially a regulated hyperthermia.
 In nonfebrile cases of hyperthermia (eg, heat stroke, exercise-induced hyperthermia,
malignant hyperthermia, seizure), body temperature is elevated by abnormal and
unregulated heat loss, heat gain, or heat production, and the hypothalamic set-point is not
altered.
 Depending on their severity, these conditions can potentially result in body temperatures
³106ºF (41.1ºC).
 In comparison, most patients with true fever have body temperatures in the range of 103-
106ºF (39.5-41.1ºC).
 Elevation of the hypothalamic set-point may be initiated by exogenous pyrogens, which
include drugs, toxins, and viral or bacterial products (eg, endotoxin).
 These pyrogenic stimuli lead to the release of cytokines, termed endogenous pyrogens, from
inflammatory cells.
 Ultimately, locally synthesized prostaglandin E2 in the hypothalamus is responsible for
elevating the set-point, resulting in fever.

TOP

Etiology and Pathogenesis

 PUO may be defined as fever that does not resolve spontaneously in the period expected for
self-limited infection and for which a cause cannot be found despite considerable diagnostic
effort.
 This excludes patients that respond to antibiotic therapy (and do not relapse) and patients in
which the cause of fever is determined from initial history, physical examination, or
laboratory tests, or in which fever resolves spontaneously.
 Infectious, immune-mediated, and neoplastic disease are the most common causes of PUO in
dogs.
 In a study of 101 dogs with fever, 22% had immune-mediated diseases, 22% primary bone
marrow abnormalities, 16% infectious diseases, 9.5% neoplasia, 11.5% miscellaneous
conditions, and 19% had genuine FUO.
 In cats, the cause is more likely to be infectious, but there are fewer published data on
feline cases compared with canine cases.
 In a case series of horses with PUO, 43% had infectious disease, 22% had neoplasia, 6.5% had
immune-mediated disease, 19% had miscellaneous causes, and in 9.5% the cause was not
determined.
 In farm animals, the most likely causes of PUO are infectious or inflammatory diseases such
as pneumonia, peritonitis, abscesses, endocarditis, metritis, mastitis, polyarthritis, and
pyelonephritis.

Diagnosis
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 The key to diagnosis of PUO is to develop and follow a systematic plan that allows for the
detection of both common and uncommon causes of fever.
 Clients should be informed that diagnosis of PUO may require considerable time and
patience and may demand more advanced or expensive diagnostic tests. Nevertheless, simple
and inexpensive tests may also reveal diagnostic clues that eventually point to the cause of
the fever.
 A staged or tiered approach to diagnosis can assist in choosing appropriate tests.
 The first stage should include history, physical examination, ophthalmic and neurologic
examinations, CBC, fibrinogen, serum chemistry profile, urinalysis and urine culture, feline
leukemia virus and feline immunodeficiency virus tests (cats), and usually thoracic and
abdominal radiographs in small animals.
 In the second stage, some first-stage tests may be repeated (particularly the physical
examination) and additional specialized tests are performed.
 These may be dictated by abnormal findings in the first stage of testing or may be
determined by consideration of the most common known causes of PUO.
 Tests included in this stage include blood cultures, arthrocentesis, abdominal ultrasound,
lymph node aspiration, aspiration of other organs or masses, analysis of body fluids (eg, fluid
from body cavities, milk samples, reproductive tract secretions), fecal culture,
echocardiography (in the presence of a murmur), long-bone and joint radiographs, contrast
radiographs, and serology.
 The third stage again may repeat earlier tests, as well as additional specialized procedures.
 These procedures are most likely to be chosen on the basis of previous findings, but may also
be considered when all previous testing has been unrewarding.
 Examples include echocardiography (in the absence of a murmur), dental radiographs, bone
marrow aspiration, bronchoscopy and bronchoalveolar lavage, CSF analysis, computed
tomography (CT), MRI, laparoscopy, thoracoscopy, biopsies, exploratory surgery, or trial
therapy.

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History and Physical Examination

 Epidemiologic characteristics such as vaccination, parasite control, and travel history should
always be reviewed.
 The response to previous medications should be determined, as well as the presence of
illness in other animals or humans.
 Clients should be questioned carefully about specific clinical signs as these may help
localize the source of the fever.
 The physical examination should be detailed and repeated frequently.

CBC and Serum Chemistry Profile

 The CBC and chemistry changes in FUO patients are often nonspecific, but may suggest
further diagnostic tests.
 The CBC should always be accompanied by blood smear evaluation to detect parasites or
morphologic changes.

Urine Culture
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 This test is always indicated to evaluate FUO in small animals, regardless of the appearance
of the urine sediment.

Radiography and Advanced Imaging

 Thoracic and abdominal radiographs are useful screening tools for the early localization of
fever.
 Skeletal radiographs and contrast radiographs may subsequently be considered, depending
on initial findings.
 For example, myelography may be used to investigate back pain.
 The use of advanced techniques such as CT and MRI is determined by the results of initial
diagnostic testing or by consideration of the body system of interest, eg, MRI is particularly
useful for evaluating the CNS.

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Ultrasonography and Echocardiography

 Abdominal ultrasound may reveal a source of fever in the abdomen, such as neoplasia,
peritonitis, pancreatitis, or abscesses.
 The thoracic cavity, limbs, and retrobulbar areas may also be examined by ultrasound.
 Echocardiography is indicated at the early stages of evaluation of the PUO patient with a
murmur.
 This may aid in the detection of endocarditis, although this diagnosis should also be based on
signalment, onset of the heart murmur, and blood culture results.

Bone Marrow Evaluation

 Bone marrow cytology and histology should be evaluated in any patient with unexplained
CBC abnormalities.
 Bone marrow disease is a common cause of FUO in small animals; therefore, bone marrow
aspiration should also be included in the second stage of diagnostic testing in these
patients.

Arthrocentesis

 Because immune-mediated polyarthritis is a common cause of FUO in dogs, arthrocentesis is

included in the second stage of diagnostic testing in this species, even if the joints are normal
on palpation.
 Some dogs with steroid-responsive meningitis-arteritis also have concurrent immune-
mediated polyarthritis; therefore, arthrocentesis should be performed in dogs with spinal
pain.
 Infectious polyarthritis is more commonly recognized in large animals, in which
arthrocentesis is an important diagnostic test.

Blood Culture

 Blood cultures are recommended in all patients with unexplained fever.

 The techniques used should allow the collection of adequately large volumes of blood under
aseptic conditions.
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 If the size of the patient allows collecting more than one blood culture set, using
appropriately sized aerobic and anaerobic bottles increases the sensitivity and specificity of
the test.

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Serology

 Serologic tests are available for the diagnosis of many infectious diseases and some immune-
mediated disorders.
 Selection should be based on the signalment, clinical signs, and epidemiologic characteristics
of the patient.
 Interpretation of test results requires an understanding of disease prevalence, vaccination
history, and sensitivity and specificity of the test.
 The use of immune panels or autoantibody screens in small animal patients with FUO is
discouraged.
 Neither antinuclear antibody or rheumatoid factor titers alone are sensitive or specific
enough to diagnose systemic lupus erythematosus or rheumatoid arthritis,
respectively.

Microbiology, Cytology, and Histology

 Fine-needle aspirates are safe and simple to obtain from effusions, masses, nodules, organs,
tissues, and body fluids.
 Fluids should be examined cytologically and also submitted for microbiologic testing.
 Tissue biopsies are generally obtained in the second or third stages of diagnostic testing, after
clinical signs or initial diagnostic tests have localized the fever.
 When biopsies are obtained, sufficient samples should be submitted for histopathology,
appropriate culture (aerobic and anaerobic, fungal, mycoplasmal, mycobacterial, etc), and
special stains. If exploratory surgery is performed, biopsies should be obtained from
several sites.

Treatment

 In some PUO cases a specific diagnosis is not reached, or diagnostic testing is discontinued,
leading to consideration of therapy in the absence of a diagnosis.
 Options include antibiotics, antifungal agents, and anti-inflammatory or immunosuppressive
therapy (usually with corticosteroids).

 Trial therapy may resolve the patient’s clinical signs or may confirm a presumptive diagnosis,
but it is also associated with significant risk.
 Before pursuing a therapeutic trial, the client should be informed of the potential risks and
should be committed to careful monitoring of the patient for an appropriate length of
time.
 The therapeutic trial should be based on a tentative diagnosis and should define the
parameters to be followed and the criteria used to determine treatment success or failure.
 In true fever, the elevation in body temperature is regulated; therefore, cooling methods
such as water baths work against the body’s own regulatory mechanisms.
 It is also likely that fever itself has some beneficial effects, particularly in infectious diseases.
 However, fever can lead to anorexia, lethargy, and dehydration.
 Thus, PUO patients may benefit from IV fluid therapy or from the use of antipyretic
medications.
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 Examples include NSAID such as aspirin, carprofen, ketoprofen, and meloxicam (small
animals) and flunixin meglumine or phenylbutazone (large animals).

ELECTROLYTE IMBALANCES-CONCEPTS

Elecrolytes

 Major concepts
o Electrolyte concentrations in serum are the net result of:
 intake
 excretion
 shifts between the ICF and ECF
 must consider hydration state with [Na+] and [Cl-]

REPRESENTATIVE ELECTROLYTE CONCENTRATIONS

IN THE BODY FLUID COMPARTMENTS (mEg/L)

Extracellular
Electrolytes Intracellular Fluid Interstitial ntravascular
Fluid

Cations - - - -
Sodium 15 147 142 -
Potassium 155 4 5 5
Calcium 2 2.5 - -
Magnesium 27 1 2 -
Anions - - - -
Bicarbonate 10 30 27 -
Chloride 1 114 103 -
Phosphate 100 2 2 -
Sulfate 20 1 1 -
Organic acids 1 7.5 - 5
Protein 62 0 16 -
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 Major functions of electrolytes

o Na+
 - H2O conservation (osmotic effect in kidney tubules)
 As a measure of hydration status
 hypothalmic osmoreceptors
 renal volume receptors
o Cl-
 Gastric fluid (HCl)
 linked to the renal generation of HCO3-

volume effects

 hypovolemia - ↑ pituitary antidiuretic hormone (ADH)* → ↑ CT H2O resorption

 hypervolemia - ↓ pituitary antidiuretic hormone (ADH)* → ↓ CT H2O resorption

Note : *at atrial and carotid baroreceptors (ADH)

 hypoosmolality:
o inhibit thirst centers → ↓ H2O intake
o CT H2O resorption↑ ADH* →
 hyperosmolality
o stimulate thirst centers → ↑ H2O intake
o ↑ ADH* → ↑ CT H2O resorption

Note : * at hypothalmic osmoreceptors

SPECIFIC IMBALANCES

Sodium

 Approximately 1/2 of the total body concentration of sodium is found in ECF.

 The quantity of sodium in the body is controlled by dietary intake and loss.
 The most important route for sodium excretion is through the kidney. Most
sodium presented to renal tubules is reabsorbed in a process controlled by
aldosterone.
 Renal reabsorption of sodium requires an equivalent passage of hydrogen or potassium ions
in the opposite direction.
 Sodium is also lost in sweat and in digestive tract secretions.
 In carnivores and most herbivores, sodium is reabsorbed in the lower intestinal tract.
 In herbivores with large quantities of fluid in the feces, such as the cow and the horse, there
may be considerable fecal loss of sodium.
 A decrease in plasma sodium concentration (hyponatremia) occurs most frequently because
of excessive sodium loss.
 from the gastrointestinal tract through diarrhea or vomition
 in renal disease in which the sodium conservation mechanism is operating deficiently
because of tubular damage
 Hyponatremia may occur with hyperglycemia due to increased sodium excretion to prevent
hyperosmolarity.
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 An increase in plasma sodium concentration (hypernatremia) is rare and can occur

when there is restricted water intake with excessive sodium intake, in advanced chronic
renal failure with a low glomerular filtration rate, and with primary hyperaldosteronism.

Potassium

 Potassium concentration is low in ECF and high in most cells of the body.
 Most potassium is excreted by the kidneys through glomerular filtration and tubular
secretion.
 Aldosterone facilitates excretion of potassium since it causes increased sodium reabsorption
by promoting the exchange of sodium in tubular fluid for potassium in the tubular cell.
 Potassium excretion by the kidneys is also controlled by competition between potassium
and hydrogen ions for reabsorption.
 Alterations in serum potassium levels occur when there is a disturbance in the equilibrium
between potassium in the ICF and potassium in the ECF.
 In alkalosis, potassium moves into the cell in exchange for hydrogen ions and may cause
hypokalemia.
 In acidosis, potassium moves out of the cell in exchange for hydrogen ions and may cause
hyperkalemia.
 Plasma potassium increases about 0.6 mEq/L for each 0.1 unit decrease in blood pH.
Therefore, if an acidotic animal has a normal plasma potassium level, it should be considered
hypokalemic and corrective therapy should be initiated.
 In addition to its role in maintaining the tonicity of the ICF, potassium is of great importance
in the mechanism of neuromuscular transmission.
 Low concentrations of K+ in the ECF result in profound muscular weakness
and ECG abnormalities.
 High concentration of K+ in the ECF (10-12 mEq/L) result in severe myocardial
disturbances and death due to cardiac arrest.

Chloride

 Chloride concentration is low in ICF and high in ECF.

 Excretion, absorption and distribution of chloride are passive processes in association with
active sodium transport.
 Unusual reduction in chloride concentration in the absence of comparable change in sodium,
usually reflects sequestration of gastric juice in the stomach or vomiting.

Bicarbonate

 Bicarbonate is mostly of endogenous origin in that it comes from the hydration of carbon
dioxide to carbonic acid which then dissociates to bicarbonate and hydrogen ions.
 Bicarbonate is lost through secretions to the digestive tract and in the urine.
 Bicarbonate levels are regulated by respiratory and metabolic (kidney) processes.

ACID-BASE BALANCE AND DISORDERS

Major concepts
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 Acidosis and alkalosis refer to the pathophysiologic process that cause net accumulation of
acid or alkali (base) in the body
 Acidemia and alkalemia refer specifically to the pH of the blood
 Buffer - a substance that is able to take up or release H+ so that drastic changes in [H+] are
minimized; a depot for H+.

Physiologically relevant buffer systems

 Bicarbonate (HCO3-/H2CO3) – most important quantitatively; easily measured;

 Can be effectively regulated in response to acidosis or alkalosis through Mmtabolic (renal) or
respiratory (lung) compensation
 Red cell hemoglobin
 Plasma and intracellular proteins
 Organic and inorganic phosphates (HPO42-, / H2PO4-)
 Bone carbonate (CO32-)

Bicarbonate system

CO2 + H2O → H2CO3 → H+ + HCO3-

Respiratory Metabolic
Component Component

 Measurements of the above components, and more, are performed on a blood gas analyzer
 CO2 - Respiratory Acid; HCO3- - Metabolic Base
 Samples are collected in a heparinized syringe with the needle closed with a rubber stopper
to prevent exposure to air
 Analysis should be done within minutes
 Analytes of a standard blood gas include pH, pCO2, HCO3-, TCO2, pO2, and Base Excess
(BE)

pH

 pH is necessary to determine if the patient is acidemic or alkalemic

 Remember that small changes in pH represent large changes in [H+] since it is measured on
an logarithmic scale

pCO2

 Partial pressure of CO2 dissolved in plasma (mmHg)

 Respiratory component – regulated by the lungs
 Respiratory acidosis is characterized by ↑ pCO2 (hypercapnia) caused by
alveolar hypoventilation
 Respiratory alkalosis is characterized by ↓ pCO2 (hypocapnia) caused by alveolar
hyperventilation

HCO3-
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 Bicarbonate concentration (mmol/L)

 Metabolic component – regulated by the kidney
 Metabolic acidosis is characterized by ↓ [HCO3-], due either to HCO3- loss or HCO3-
buffering of acid (titration)
 Metabolic alkalosis is characterized by ↑ [HCO3-], due to H+ loss or rarely iatrogenic HCO3-
administration
 pH [H+] Primary Compensatory
 Metabolic acidosis ↓ ↑ ↓ [HCO3-] ↓ pCO2
 Metabolic alkalosis ↑ ↓ ↑ [HCO3-] ↑ pCO2
 Respiratory acidosis ↓ ↑ ↑ pCO2 ↑

[HCO3-] Respiratory alkalosis ↑ ↓ ↓ pCO2 ↓

[HCO3-]

Total CO2 (TCO2)

 TCO2 ~ HCO3- ; TCO2 ≠ pCO2

 TCO2 is the sum of all substances in serum which can be converted to CO2 gas after the
addition of a strong acid; dissolved CO2, H2CO3, and HCO3-
 Approximately 95% of TCO2 is HCO3-
 Can be performed on serum/plasma and may be run several hours after collection; however,
values will decrease over longer periods

Anion gap (AG) = (Na+ + K+) − (HCO3- + Cl-)

 Represents the major electrolytes in serum

 Law of electroneutrality → all anionic charges = all cationic charges
 AG measures the major electrolytes and compares to reference range

Abnormal AG - change in an ion(s) not normally present to that degree or at all in health

In practice is used to detect unmeasured anions :

 lactic acid
 ketoacids
 uremic acids (PO42-, SO42-, and citrate)
 ethylene glycol metabolites (glycolate and oxalate)
 massive rhabdomyolysis (PO42- and lactic acid)
 ↓ AG is rare and not likely of clinical significance; substantial hypoalbuminemia can lower
AG somewhat.

Metabolic Acidosis

 Addition of H+ (unmeasured acids):

o ↑AG, normochloremic -
o organic acids:
o lactic acidosis (hypoxia)
o ketoacidosis (DKA, ketosis)
o anionic toxins: (ethylene glycol, salicylate, methanol, paraldehyde, etc.)
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 Decreased removal of H+:

o inorganic acids:
o PO42-, SO42-, citrate (renal failure, urinary obstruction, uroabdomen)
o renal distal tubular acidosis
 HCO3- loss:
o normal AG, hyperchloremic
o GI (diarrhea, vomiting, sequestration, salivation in ruminants)
o renal proximal tubular acidosis

respiratory compensation (immediate) → hyperventilation → ↓ pCO2

Metabolic Alkalosis

 Loss of H+:
o hypochloremic
o GI (vomiting, pyloric obstruction, abomasal displacement)
 Addition of HCO3-:
o iatrogenic with fluid administration (NaHCO3, lactate, citrate)

respiratory compensation (immediate) → hypoventilation → ↑ pCO2

Respiratory acidosis

↑ pCO2 from hypoventilation: Iinhibition or dysfunction of medullary respiratory center

 drugs (anesthetics, sedatives, narcotics)

 brain stem disease
 alkalemia
 inhibition or dysfunction of respiratory muscles (tick paralysis, tetanus, botulism,
myasthenia gravis, hypokalemia, succinylcholine
 upper airway dysfunction (foreign body, vomitus)
 impaired gas exchange (lung/thoracic disease)
 inappropriate mechanical ventilation

metabolic compensation (days) → ↑ H+ secretion and ↑ HCO3- production

Respiratory Alkalosis

 ↓ pCO2 from hyperventilation

o altered respiratory control (fear, convulsions, fever, heat exposure, hepatic
encephalopathy)
o hypoxemia (lung disease, hypotension)
o inappropriate mechanical ventilation
 Metabolic compensation (days) → ↓ H+ secretion and ↓ HCO3- production
 Mixed acid/base - coexistence of multiple primary acid/base abnormalities
 Compensating responses to simple acid-base disturbances do not correct pH to normal

First type
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 A normal pH with abnormal HCO3- and/or pCO2 represents a mixed acid/base disturbance.
e.g. HBC → uroabdomen + extremely painful (panting):
o Low normal pH
↓ [HCO3-]
↓ pCO2
↑ AG
o Uroabdomen → primary metabolic acidosis
o Panting → primary respiratory alkalosis
 An extremely high or low pH can occur if the [HCO3-] and pCO2 levels go in opposite
directions, i.e. both representing primary acidoses or both representing primary
alkaloses.
 These can be grave situations.

COMMON QUESTIONS

1. What are the basic factors affecting the electrolyte balance?

2. What are the functions of the electrolytes?
3. Define respiratory acidosis and alkalosis?
4. Define hypothermia, how is it classified, enumerate the consequences of hypothermia?
5. Explain breifly the management of hypothermia?
6. What are the different forms of rewarming techniques used, explain ?
7. What is hyperthermia, explain briefly the various causes for heat stroke and its medical
management?
8. What is the difference between hyperthermia and fever? Describe the pathophysiology of
fever?
9. Enumerate the clinical findings of ephemeral fever, how to diagnose the condition and what
is the line of treatment for the disease?
10. Define pyrexia of unknown origin, explain the pathogenesis and line of treatment to be
followed?

MODULE-5: GENERAL AND SYSTEMIC STATES - II

Learning objectives

 To know about their clinical findings, diagnosis and treatment of common generel systemic
states such as septicemia and shock.
 To know about the medical management pertaining to the general systemic states such as
o Septecemia
o Toxaemia
o Shock
o Dehydration

SEPTICEMIA

 Septicemia is the presence of bacteria in the blood (bacteremia) and is often associated with
severe infections.

Causes

 Septicemia is a serious, life-threatening infection that gets worse very quickly.

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 It can arise from infections throughout the body, including infections in the lungs, abdomen,
and urinary tract.
 It may come before or at the same time as infections of the bone (osteomyelitis), central
nervous system (meningitis), heart (endocarditis), or other tissues.

Symptoms

 Septicemia can begin with spiking fevers, chills, rapid breathing, and rapid heart rate.
 The symptoms rapidly progress to shock with fever or decreased body temperature
(hypothermia), falling blood pressure, confusion or other changes in mental status, and
blood clotting problems that lead to a specific type of red spots on the skin (petechiae and
ecchymosis).
 There may be decreased or no urine output.

Examinations and Tests

 A physical examination may show:

 Low blood pressure
 Low body temperature or fever
 Signs of associated disease (such as meningitis, epiglottitis, pneumonia, or cellulitis)

Tests that can confirm infection include

 Blood culture
 Blood gases
 CBC
 Clotting studies
 PT
 PTT
 Fibrinogen levels
 CSF culture
 Culture of any suspect skin lesion
 Platelet count
 Urine culture

Treatment

 Septicemia is a serious condition that requires a vetrinary hospital stay.

 The animal patient may be admitted to an intensive care unit (ICU).
 Fluids and medicines are to be given by IV to maintain the blood pressure.
 Oxygenneeds to be be given. Antibiotics are used to treat the infection.
 Plasma or other blood products may be given to correct any clotting abnormalities.

Prognosis

 What to expect depends on the organism involved and how quickly the patient is hospitalized
and treatment begins.
 The death rate is high -- more than 50% for some organisms.
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Possible Complications

 Septicemia can rapidly lead to adult respiratory distress syndrome (ARDS), septic shock, and
death.
 Septicemia associated with meningococci can lead to shock or adrenal collapse.

Prevention

 Appropriate treatment of localized infections can prevent septicemia.

 In certain cases, animals who are in close contact with someothers with septicemia may be
prescribed preventative antibiotics.

SEPTICEMIA IN EQUINE NEONATES

 Septicemia is a systemic disease involving the presence and persistence of bacteria or their
toxins in the blood.

 The condition implies an extensive, whole body insult from a single or multiple sources of
infection.

Etiology and Pathogenesis

 The predominant bacteria involved in neonatal foal septicemia are the gram-negative
organisms Escherichia coli , Klebsiella spp , Enterobacter spp , Actinobacillus spp , and
Pseudomonas spp .
 About 50% of infections also involve gram-positive bacteria, with Streptococcus spp being
the most common isolates.
 Anaerobic pathogens are involved in 30% of cases.
 The routes of entry for these bacteria include the placenta, umbilicus, lungs, and GI tract.
 Clinical Signs of septicemia and septic shock mainly result from the release of endotoxins
related to gram-positive infections.
 Endotoxins stimulate macrophages to release an array of cytokines (eg, IL-6, IL-1, TNF-α)
and activate pro-inflammatory enzymes (eg, phospholipase A2).
 Together, these factors lead to signs of inflammation such as fever, vasodilation,
hypoglycemia, myocardial depression, procoagulant activity, and eventually
disseminated intravascular coagulation (DIC).
 Bacterial infection accounts for nearly one third of all foal mortality. Septicemia is the second
most common problem of equine neonates, second only to failure of passive transfer of
maternal antibodies.
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 Certain immunologic and management factors predispose foals to septicemia. Although foals
can respond immunologically in utero to bacterial or viral infections, their ability to do so is
less than that of adults.
 The major risk factor for septicemia in foals is failure to receive an adequate quality and
quantity of colostral antibodies.
 Other factors that influence disease incidence include unsanitary environmental conditions,
gestational age of the foal (prematurity), health and condition of the dam, difficulty of
parturition, and the presence of new pathogens in the environment against which the mare
has no antibodies.

Clinical Findings

 Clinical signs largely depend on the stage of the animal’s illness and the primary body
systems involved.
 Frequently affected organ systems include the umbilical remnants, CNS, respiratory,
cardiovascular, musculoskeletal, renal, ophthalmic, hepatobiliary, and GI organs.
 Foals in the early stages of sepsis display some degree of depression and lethargy and may lie
down more than usual.
 The mare’s udder is often distended with milk, indicating that the foal is not nursing with
normal frequency.
 In the advanced stage of illness (septic shock), foals are severely depressed, recumbent,
dehydrated, and tachycardic.
 The mucous membranes are muddy, and hypotension, which manifests clinically as
cold extremities, thready pulse, and poor capillary refill time, is evident.
 Foals may be hyper- or hypothermic. In septicemia, bacteria spread hematogenously to
various organs, such as the lungs, intestines, eyes, CNS, bones, and joints.
 The foal may show evidence of single or multiple organ dysfunction. Sepsis can manifest as
respiratory distress, pneumonia, diarrhea, uveitis, meningitis, osteomyelitis, or septic
arthritis.

Diagnosis

 A good perinatal history and physical examination can provide clues in the diagnosis.
 Depending on the specific organ systems involved, an umbilical, abdominal, and synovial
ultrasound examination; arterial blood gas analysis; arthrocentesis; cerebrospinal centesis;
and chest, abdominal, and distal limb radiographs may be indicated. Advanced diagnostic
imaging techniques (eg, computed tomography of the distal limbs) may further serve as a
prognostic aid.
 Septic foals are often neutropenic with a high ratio of band to segmented neutrophils.
 The neutrophils may exhibit toxic changes, which are highly suggestive of sepsis. Foals
<24 hr old are often hypoglycemic.
 Fibrinogen levels >600 mg/dL in a foal <24 hr old is indicative of an in utero infection.
 Other chemistry abnormalities that may be evident include azotemia due to inadequate renal
perfusion and increased bilirubin secondary to endotoxin damage to the liver.
 A high anion gap (>20 mEq/L), hypoxemia, hypercapnia, and a mixed respiratory and
metabolic acidosis may be found on arterial blood gas analysis.
 Because of the high correlation between failure of passive transfer of antibodies and
septicemia, serum IgG levels should be measured in any questionably sick equine neonate.
IgG levels <200 mg/dL indicate complete failure of passive transfer of maternal antibodies.
IgG levels >800 mg/dL are optimal.
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 A definitive diagnosis of neonatal sepsis is based on clinical signs, laboratory data, and
evidence of failure of passive antibody transfer. These data can be combined to determine
the animal’s sepsis score, which helps synthesize laboratory results into a coherent whole.
 A positive blood culture also correlates to sepsis, but a negative culture does not rule out the
possibility of infection.
 Differential diagnoses include hypoxic ischemic encephalopathy (Hypoxic Ischemic
Encephalopathy: Introduction), hypoglycemia, hypothermia, neonatal isoerythrolysis
(Hemolytic Anemia), white muscle disease (Nutritional Myopathy of Calves and Lambs),
prematurity, neonatal pneumonia, and uroperitoneum (Uroperitoneum in Foals).

Treatment

 Foals suspected of being septic should be placed on broad-spectrum antibiotics active against
both gram-positive and gram-negative organisms.
 Penicillin (22,000 IU/kg, IV, qid) in combination with amikacin sulfate (20-25 mg/kg, IV,
sid) provides good initial coverage until culture results are available.
 Metronidazole (10-15 mg/kg, PO or IV, tid) may be necessary if an anaerobic infection (eg,
Clostridium ) is suspected.
 A third- generation cephalosporin (eg, ceftiofur, 4.4-6 mg/kg, IV, bid-qid) may be used as a
broad-spectrum agent in patients with compromised renal function.
 In all cases of neonatal sepsis, immunologic support, in the form of IV plasma transfusions
(1-2 L), to raise the IgG levels to >800 mg/dL is important.
 Effective IV fluid therapy is needed to combat endotoxic shock.
 Foals may require 100 mL/kg/day of maintenance therapy using polyionic isotonic
crystalloid fluids (eg, lactated Ringer’s solution) after fluids have been administered for
shock. Because many foals are hypoglycemic, dextrose should be added to make a 2.5-5%
dextrose solution.
 Isotonic bicarbonate solution may be given to help correct moderate to severe metabolic
acidosis, but can worsen respiratory acidosis.
 In these cases, mechanical ventilation should be used to decrease PaCO2 before giving
bicarbonate.
 Treatment with hyperimmune antiendotoxin serum should be considered in patients with
endotoxemia.
 Antiprostaglandin drugs counteract several of the clinical and hemodynamic changes
associated with endotoxemia and septic shock.
 Low doses of flunixin meglumine (0.25 mg/kg, IV, tid) may help reduce signs of
endotoxemia.
 Additionally, administration of low doses of polymyxin B (6,000 IU/kg, diluted in 300-500
mL of saline, slow IV) is an investigational treatment used to neutralize systemic
endotoxin.
 Because sepsis creates a catabolic state in the foal, nutritional support is important.
 If the foal is not nursing adequately, it should be fed mare’s milk or a milk substitute at 15-
25% of its body weight over each 24-hr period. An indwelling nasogastric tube should be
placed in foals with a decreased suckle reflex.
 Parenteral nutrition may also be helpful to provide adequate nutrients.
 Administration of gastric protectants (eg, ranitidine, cimetidine, omeprazole) has been
proposed as an adjunct therapy in sick neonates.
 System-specific therapy includes lavaging septic joints with sterile fluids and providing nasal
oxygen (2-10 L/min) or ventilation for foals with septic pneumonia.
 Corneal ulceration may be treated with low doses of topical atropine (although it may cause
ileus), NSAID, and broad-spectrum topical antimicrobials. Entropion generally requires
mattress sutures of the lower eyelid.
 Surgical removal of infected umbilical remnants may be indicated.
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 Recovery from neonatal sepsis depends on the severity and manifestation of the infection.
 Current survival rates are 50-65% in referral centers. A minimum of 1-4 wk of intensive care
should be expected.
 Early recognition and intensive treatment of neonatal sepsis improves the outcome.
 If the foal survives the initial problems, it has the potential of becoming a healthy and useful
adult.

TOXEMIA

 Toxemia is a generic term for the presence of toxins in the blood. It is not necessarily the
same as Bacteremia.
 The toxins released by bacteria can enter the blood stream and can move throughout the
body without any bacteria entering the blood stream.
 Pre-eclampsia, a serious condition in pregnancy that involves hypertension and proteinuria,
may be caused by toxemia.

Septicemic Disease (Colisepticemia)

 Septicemia caused by Escherichia coli is a common disease of calves, and to a lesser extent
lambs, <1 wk old.
 It may present with signs of acute septicemia or as a chronic bacteremia with localization.
 The disease is caused by specific serotypes of E coli that possess virulence factors enabling
them to cross mucosal surfaces and produce bacteremia and septicemia.
 However, the main determinant of the disease is deficiency of circulating immunoglobulins
as the result of a failure in passive transfer of colostral immunoglobulin; septicemic disease
due to invasion by E coli occurs only in immunoglobulin-deficient calves.
 Colisepticemia is seen during the first week of life, most commonly at 2-5 days of age.
 Chronic disease with localization can be seen up to 2 wk of age. The disease is usually
sporadic and is more common in dairy than beef calves.

Transmission and Pathogenesis

 Invasion occurs primarily through the nasal and oropharyngeal mucosa but can also occur
across the intestine or via the umbilicus and umbilical veins.
 There is a period of subclinical bacteremia that, with virulent strains, is followed by rapid
development of septicemia and death from endotoxemic shock.
 A more prolonged course, with localization of infection, polyarthritis, meningitis, and less
commonly uveitis and nephritis, is seen with less virulent strains.
 Chronic disease also develops in calves that have acquired marginal levels of circulating
immunoglobulin.
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 The organism is excreted in nasal and oral secretions, urine, and feces; excretion begins
during the preclinical bacteremic stage.
 Initial infection can be acquired from a contaminated environment.
 In groups of calves, transmission is by direct nose-to-nose contact, urinary and respiratory
aerosols, or as the result of navel-sucking or fecal-oral contact.

Clinical Findings and Diagnosis

 In the acute disease, the clinical course is short (3-8 hr), and signs are related to the
development of septic shock.
 Pyrexia is not prominent, and the rectal temperature may be subnormal.
 Listlessness and an early loss of interest in sucking are followed by depression, poor response
to external stimuli, collapse, recumbency, and coma.
 Tachycardia, a poor pulse pressure, and a prolonged capillary refill time are seen.
 The feces are loose and mucoid, but severe diarrhea is not seen in uncomplicated cases.
 Mortality approaches 100%. With a more prolonged clinical course, the infection may
localize.
 Polyarthritis and meningitis are common; tremor, hyperesthesia, opisthotonos, and
convulsions are seen occasionally, but stupor and coma are more common.
 A moderate but significant leukocytosis and neutrophilia are seen early, but leukopenia is
marked in the terminal stages.
 The joint fluid contains increased inflammatory cells and protein, and the CSF
shows pleocytosis and an increased protein concentration; organisms may be
evident on microscopic examination.
 Less commonly, other bacteria, including other Enterobacteriaceae, Streptococcus spp , and
Pasteurella spp , produce septicemic disease in young calves.
 These organisms are more common in sporadic cases than as causes of outbreaks.
 They produce similar clinical disease, but they can be differentiated by culture.
 As with colisepticemia, the primary determinant of these infections is a failure of
passive transfer of immunoglobulins.
 The diagnosis is based on history and clinical findings, demonstration of a severe deficiency
of circulating IgG, and ultimately, demonstration of the organism in the blood or tissues.
 Zinc sulfate or total protein estimation can be used for rapid estimation of IgG ( Nutritional
Requirements).

Treatment

 Treatment requires aggressive use of antibiotics.

 Because there is no time for sensitivity testing, the initial choice should be a bactericidal drug
that has a high probability of efficacy against gram-negative organisms.
 Antibacterial therapy should be coupled with aggressive fluid, drug, and other therapy for
endotoxic shock. Mortality is high despite aggressive treatment.

Control and Prevention

 Calves that acquire adequate concentrations of immunoglobulin from colostrum are resistant
to colisepticemia.
 Therefore, prevention depends primarily on management practices that ensure an adequate
and early intake of colostrum.
 The adequacy of the farm’s practice of feeding colostrum should be monitored, and corrective
strategies applied as required.
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 In dairy herds, natural sucking does not guarantee adequate concentrations of circulating
immunoglobulins, and calves should be fed 2-4 L of first-milking colostrum, using a nipple
bottle or an esophageal feeder, within 2 hr of birth, followed by a second feeding at 12 hr.
 The circulating concentration of immunoglobulin required to protect against colisepticemia
is low; however, high concentrations of circulating immunoglobulins are desirable because
they decrease susceptibility to other neonatal infectious diseases.
 When natural colostrum is not available for a newborn calf, commercial colostrum
substitutes containing 25 g IgG will provide sufficient immunoglobulin for protection against
colisepticemia if fed early in the absorptive period.
 Plasma containing at least 4 g and preferably 8 g IgG, administered parenterally, will provide
some protection for older calves that have not been fed colostrum and are unable to absorb
immunoglobulins from the intestine.
 Small-volume hyperimmune serum is of benefit only when it contains antibody specific to
the particular serotype associated with an outbreak.
 The risk of early infection should be minimized by hygiene in the calving area
and disinfection of the navel at birth.
 To minimize transmission, calves reared indoors should be in separate pens (without
contact) or reared in calf hutches.

PRINCIPLES OF ANTIMICROBIAL THERAPY

Penicillins

 β-Lactams. G+, easy G-, anaerobes. Bactericidal. Inhibit cell wall synthesis. Safe. Elimated
via kidney, good for UTIs.
 Natural penicillins – G+, poor G-, spirochetes, destroyed by penicillinase. PenG and PenV.
Penicillinase-resistant penicillins – Penicillinase producing G+ cocci, esp. Staphylococcus.

 Cloxacillin, dicloxacillin. Aminopenicillins – Broad spectrum, ↑ G- activity. Ampicillin,

amoxicillin. Extended spectrum penicillins – addl G- activity, Pseudomonas.
 Carbenicillin, ticarcillin, piperacillin. Potentiated penicillins - Developed to inactivate β-
lactamases.
 Clavomox, timentin. Don’t use penicillins in rodents and lagomorphs; elimination of G+ gut
flora can lead to fatal colibacillosis.

Cephalosporins

 β-Lactams. G+, some G- (more with each generation), anaerobes. Bactericidal. β-lactam
antibiotics. Inhibit cell wall synthesis.
 More effective against actively growing bacteria. Classifications – 1st generation
cepholosporins include cephalothin, cefazolin, cephapirin, cephadine, cephalexin, cefadroxil.
Activity against most G+, poor G- activity. 2nd generation cepholosporins - not very popular,
same G+ activity, expanded G-. 3rd generation cepholosporins – same G+ activity, much
expanded G- activity; cefotaxime, moxolactom, cefoperazone, ceftiofur (BRD, no withdrawal
time).

Aminoglycosides

 1° G- aerobes. Some G+. Pseudomonas, staphylococcus, atypical

mycobacterium (nocardia/actinomyces).
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 Irreversibly bind to 30S ribosomal unit and inhibits protein synthesis. Bactericidal.
 Includes amikacin (SID, parvo pups), gentamicin, neomycin, and spectinomycin.
 Inactive against fungi, viruses and most anaerobic bacteria. Accumulate in inner ear and
kidneys.
 Elimination via glomerular filtration. Adverse Effects – Nephrotoxic.
 Casts in urine, increased BUN and Cr. Nephrotoxicity reversible when drug discontinued.
Ototoxic. 8th cranial nerve toxicity.
 Auditory and vestibular symptoms may be irreversible.

Fluoroquinolones

 Good G- aerobes, facultative anaerobes, atypical mycobacterium, chlamydia,

mycoplasma, ehrilichia, BRD.
 Bactericidal. DNA gyrase inhibitor, prevent DNA synthesis. Enrofloxacin (SID, prostate,
RMSF, deethylated to cipro), ciprofloxacin. Variable activity against Streptococci – not
recommended. Contraindicated in young animals due to cartilage defects. Baytril associated
with blindness in cats.

Sulfonamides

 G+, easy G-, anaerobes; nocardia and actinomyces. Bacteriostatic.

 Inhibit folic acid pathway (PABA/pteridine not converted to DHFA). Broad spectrum.
 Many bacteria have developed resistance. Potentiated sulfonamides – TMPS.
 Bactericidal, inhibits bacterial thymidine synthesis in folic acid pathway.
 Excellent tissue distribution. Most drug side effects of all Abs, allergic reactions, hepatotoxic,
KCS, hypothroidism, crystalluria, thyrotoxic, anemia, BM toxicity (aplastic anemia,
thrombocytopenia hypoprothrombinemia).

Tetracyclines

 G+, easy G-, Mycoplasma, spirochetes, chlamydia, Rickettsia, Hemobartonella, Brucellosis.

Bacteriostatic.
 Inhibits protein synthesis by binding to the 30S ribosomal unit. Safe.
 Prostate. Includes doxycycline (biliary excretion), oxytetracycline, tetracycline. Resistance ↑.
 May cause esophagitis. Chloramphenicol – G+, G-. Bacteriostatic.
 Binds to the 50S ribosomal subunit preventing protein synthesis.
 Penetrates everything. Can cause aplastic anemia in humans.

Lincosomides

 G+ aerobes, anaerobes. No G-. Often combo w/ aminoglycosides. Lincomycin, clindamycin.

 Bacteriostatic or bactericidal. Bind to the 50S ribosomal subunit.
 Distribute well, biliary elimination. Contraindicated in rabbits, rodents, horses, ruminants
due to serious GI effects.

Macrolides

 G+, selected G-. Bacteriostatic. Bind 50S ribosomal subunit. [ ] in alveolar macrophages,
great for pulmonary infections.
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 Erythromycin, tylosin, tilmicosin. Erythromycin is used in the treatment of Rhodococcus

equi in combo w/ rifampin.
 Can cause increase in GI motility. Tilmicosin – used in BRD; CV toxicity in primates,
horses, swine.

Metronidazole

 Bactericidal and antiprotozoal. Obligate anaerobes.

 Disrupts DNA and nucleic acid synthesis. Immunolmodulator in IBD.

Rifampin

 Bactericidal or bacteriostatic. Inhibits DNA-dependent RNA polymerase.

 Used for treatment of Rhodococcus equi in combo w/ erythromycin.

Antifungal Agents

Amphotericin B

 Polyene macrolide. Binds to fungal sterols, altering permeability of membrane.

 Fungistatic. Dimorphic fungi (histo, blasto, crypto, coccidio).
 Because of the risk of severe toxicity reserved for disseminated, progressive, potentially fatal
fungal infections. Nephrotoxic, anaphylactoid.

Imidazoles

 Fungistatic. Inhibit ergosterol/steroid synthesis (blocks cytochrome p450), ↑ cell membrane

permeability, ↓ cell membrane fluidity.
 Use for dermatophytes, yeast, dimorphic fungi. Impairs steroid sythesis, so sometimes
used in hyperadrenocorticism and prostate diz.
 Ketaconazole – Fairly safe (hepatotoxicity), give w/ food. Short t½. Not got w/ dimorphic
fungi, esp. blasto.
 Itraconazole – more effective spectrum. Fluconazole – Crosses BBB.

Flucytosine

 Ancoban. Inhibits DNA synthesis (antimetabolite, competes with uracil, interfering with
pyrimidine metabolism and protein synthesis).
 Limited spectrum - Cryptococcus, Candida. Rapid absorption, excellent distribution.
Synergistic effect with amphotericin B.
 Adverse effects include BM depression (pancytopenia), GI disturbances, rashes, oral
ulceration, increased liver enzymes.

Griseofulvin

 Inhibits fungal mitosis by disrupting mitotic spindle, inhibit nucleic acid and fungal wall
sythesis.
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 Limited to dermatophytes only. Give w/ fatty food to ↑ absorption. [ ] in keratin. Side effects
include GI, teratogenic and carcinogenic at ↑ doses, bone marrow dyscrasias.
 Do not give to pregnant animals.

Antiseptic Agents

 Agents applied to the body vs. disinfectants which are used on inanimate objects.

Alcohol

 Protein denaturation. 70% is effective against G+ and G- bacteria.

 Good bactericidal, fungicidal, virucidal. Most rapid acting but least residual action.
 Fast kill, defatting agent. Evaporates quickly. 2 min for max effect. May be drying or
irritating.
 May cause cytotoxicity. Often used in combo w/ povidone iodine.

Chlorhexidine

 Cytoplasmic membrane disruption. 0.05% soln effective against Gram+ and Gram-.
 Persists on skin to give cumulative antibacterial effect. Less irritating.
 Not inactivated by organic matter. 0.05% is 1:40 dilution, most bactericidal and least toxic to
tissues.

Hydrogen peroxide

 Poor antiseptic. Short-acting germicidal effect through release of nascent O2, irreversibly
alters proteins.
 Effective sporicide. Effervescent action mechanically removes pus and bacteria.

Iodine

 One of most potent antiseptics. Bactericidal, virucidal, fungicidal. Takes 15 min for sporicidal
action.
 Organic matter inactivates free I in PI. Iodine Soln USP has little to no stinging on broken
skin.
 Iodine tincture USP (I in alcohol) is even more effective, but stings and irritates skin.
 Rare HPS rxns. Povidone iodine often used in conjunction w/ alcohol. Use PI in 0.1 to 1% [ ];
more dilure solns have ↑ free I and faster, potent bactericidal activity.
 Dilute stock solution 1:100 or 1:10. Don’t use I scrub on open wounds –damage tissue and ↑
infection.

Iodophors

 Betadine. Aqueous complex of iodine, less bactericidal but also less irritating. Gram-, gram+.
 Do not require repeated application for optimal antimicrobial effect.
 Contact time 10 min for max effect.

Hexachlorophene
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 Gram+ bacteria. Only effective after days of use once film deposition on skin, long contact
time.
 CNS toxin if absorbed, esp in young. Not used much anymore.

Quaternary ammonium compounds

 Changes in cell membrane permeability. G+.

 Inactivated by organic debris and soaps. Not recommended.

DEHYDRATION - CONCEPTS AND ASSESSMENT

Dehydration is one of the most commonest general systemic state, encountered in majority of the
diosders /diseases and Fluid therapy is the most imporntant therapeutic strategy, not only in day to
day veterinary practice, but also as a cornerstone in emergency and critical care medicine practice.

Body Fluid Distribution

 The total body water ranges from 55-70% of the lean body weight. In the average adult dog
the total body water is about 60%. Thus in a 15 Kg dog the total body water will equal about 9
liters.
 Total body water is distributed into 2 main compartments:
o The intracellular fluid space, and
o The extracellular fluid space.
 About 66% of the total body water resides in the intracellular fluid space and 33% in the
extracellular fluid space.
 The extracellular fluid space is further subdivided into two fluid containing compartments:
o The interstitial space (containing 75% of the extracellular fluid space water) and
o The intravascular space (containing 25% of the extracellular fluid space water).
 When water is added to one compartment, it distributes evenly across the total body water
and the amount of volume added to any given compartment, is proportional to its fractional
representation of the total body water. Thus, if one liter of free water is placed in the
intravascular space, there will be a minimal increase in the intravascular volume after
equilibrium takes place. In fact, approximately 30 minutes after rapid volume infusion of free
water, only 1/10th of the volume infused remains in the intravascular space.

FLUID MOVEMENT
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 A. Into and out of cells. Determined by concentration gradient in freely diffusible substances
(ie: urea)
o Tonicity dictates water movement in “nonpermeable” substances. (ie: Na/K,
proteins)
 B. Between vascular and interstitial spaces
 C. Governed by starling forces
 D. Influenced by integrity of capillary endothelium (inflammation causes increased vascular
permeability).
 E. Forces favoring fluid into vessel (reabsorbtion)
o Tissue hydrostatic pressure
o Plasma oncotic pressure
 F. Forces favoring fluid out of vessel (filtration)
o Vascular hydrostatic pressure
o Tissue oncotic pressure
 G. Net: Filtration at arteriolar end of capillary, reabsorption at venule end (also some fluid
goes into lymphatic system).

DETERMINING THE PERCENTAGE OF DEHYDRATION

 The percentage of dehydration can be subjectively estimated based on the presence and
degree of loss of body weight, mucous membrane dryness, decreased skin turgor, sunken
eyes, and altered mentation. These parameters are largely subjective because they can also be
affected by decreased body fat and increased age.

Estimated Physical Examination Findings

Percentage
Dehydration
<5 History of fluid loss but no findings on physical
examination
5 Dry oral mucous membranes but no panting or
pathological tachycardia
7 Mild to moderate decreased skin turgor, dry oral mucous
membranes, slight tachycardia, and normal pulse pressure.
Moderate to marked degree of decreased skin turgor, dry
10 oral mucous membranes, tachycardia, and decreased pulse
pressure.
12 Marked loss of skin turgor, dry oral mucous membranes,
and significant signs of shock.

 The more severe stages of dehydration are also accompanied by signs of hypovolemic shock.
Other factors, including hemorrhage and third spacing of body fluids, can also result in a
decrease in intravascular circulating volume, resulting in signs of hypovolemia.
 Severe hypovolemia resulting in more than a 15% depletion of effective circulating volume
leads to a transcompartmental fluid shift from the interstitial to the intravascular
compartments, which occurs within one hour of fluid loss.6 When fluid loss is so severe
that
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intravascular fluid volume is affected, hypovolemia can result in tachycardia, prolonged

capillary refill time, decreased urine output, and hypotension.
 The vascular space is sensitive to changes in the amount of circulating volume. During states
of normovolemia, baroreceptors in the carotid body and aortic arch sense vascular wall
tension and send pulsatile continuous feedback via vagal afferent stimuli to decrease heart
rate.
 In the early stages of hypovolemic shock, the baroreceptors sense a decrease in vascular wall
stretch or tension and blunt the tonic vagal stimulation. This allows sympathetic tone to
increase heart rate and contractility in an attempt to normalize cardiac output.
 Later, decreased blood flow and sodium delivery to receptors in the juxtaglomerular
apparatus activate the renin-angiotensin-aldosterone axis, stimulating sodium and fluid
retention to replenish intravascular fluid volume.

DEHYDRATION : CORRECTING FLUID IMBALANCES

CORRECTING FLUID IMBALANCES

 When there are clinical signs of hypovolemic shock, intravascular fluids must be replaced
immediately. Calculated fluid volumes for patients in shock are 90 ml/kg for dogs and 44
ml/kg for cats. A simple guideline to follow in day to day practice is to replace one-fourth of
the calculated fluid volume as rapidly as possible and then reassess perfusion parameters
including heart rate, blood pressure, capillary refill time, and urine output.
 About 80% of the volume of crystalloid fluid infused will re-equilibrate and leave the
intravascular space within one hour of administration. A constant-rate infusion of a
crystalloid fluid is recommended to provide continuous fluid support in patients that are
dehydrated and have ongoing losses. In some cases, the fluid required to restore
intravascular and interstitial volume can cause hemodilution and dilution of oncotically
active plasma proteins, resulting in interstitial edema formation. In such cases, a
combination of a crystalloid fluid along with a colloid-containing fluid can help restore
oncotic pressure and prevent interstitial edema.
 Once immediate life-threatening fluid deficits are replaced, provide additional fluid based on
the estimated percentage of dehydration and maintenance needs. Basic dehydration
estimates can be calculated based on the fact that 1 ml water weighs about 1 g and by using
the following formula:
 Body weight in kg × estimated percent dehydration × 1,000 ml/L
 This formula helps to determine the amount of fluid deficit in liters. A frequent mistake
when replenishing fluid deficits is to arbitrarily multiply a patient's daily water requirement
by a factor of two or three to replenish intravascular and interstitial deficits. This practice
frequently underestimates a patient's fluid needs and does little to treat volume depletion
and interstitial dehydration. Instead, it is better to use the formula above and add the result
to daily maintenance fluid requirements and ongoing losses.
 Eighty percent of the calculated fluid deficit can be replaced in the first 24 hours. More rapid
administration of an animal's estimated fluid deficit can result in diuresis and loss of the
fluid administered. After successfully treating hypovolemic shock and replacing fluid deficits
estimated based on the percentage of dehydration, we need to administer only maintenance
fluids until the animal can maintain hydration on its own, provided no signs of dehydration
or ongoing excessive fluid losses are present. An objective way to assess whether the fluid
volume is adequate is to evaluate body weight regularly throughout the day. Acute weight
loss is commonly associated with fluid loss and can be used to determine whether the patient
is at risk of becoming dehydrated again.
 Vomiting results in loss of H2O, H+, Cl-, Na+, K+, and HCO3-. If vomit is primarily stomach
contents, 1o loss is HCl, H2O.
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 Most vomit includes proximal duodenal contents, therefore HCO3- also lost.
 Conclusion: H2O is consistently lost in vomiting, other electrolytes/acid base are best
assayed.
 Diarrhea results in loss of H2O and electrolytes, resulting in dehydration,
electrolyte depletion/imbalance, acid-base imbalance, and shock.
 Intestinal contents are basically ECF; also can lose large amounts of K+.
 Fluid losses from diarrhea can be particularly severe in the cow and horse (salmonellosis,
neonatal calf diarrhea).
 The primary acid-base disturbance is metabolic acidosis.

Plasma osmolality

 Ratio of body solute to body water.

Effective circulating volume

 Part ECF in the vascular space Depends on SNS, angiotensin II, and renal sodium excretion.
 Regulates by increasing vasoconstriction, and renal sodium resorption (RATS).
 Hypovolemia causes activation of RATS. If < 5%, PE is normal. If 5%, dry mm but no
panting. If 7%, decreased skin turgor, dry mm, mild tachycardia.
 If 10%, dec skin turgor, tachycardia, dry mm, dec pulse pressure.
 If > 12%, marked loss of skin turgor, dry mm, shock.
 In mild dehydration, s/c route (isotonic fluids, max. 5 to 10 ml/lb at each injection site).
 Need multiple sites. I/p route is quick, easy but can cause dyspnea. IV route indicated with
dehydration < 7%.

Amount of fluid

 The deficit volume - only 75% to 80% of the deficit should be replaced during the first 24
hours, as it can worsen dehydration.
 Total Deficit Replacement Volume (24 hrs) = Deficit Volume(% dehydration x body weight
(lb/kg) x 454/1000 x 0.80) + Maint. Volume

Maintenance volumes

 2/3 sensible (urine and feces) and 1/3 insensible (panting or sweating). (30 X BWKg) + 70.
 A 22-lb (10 kg) dog, 7% dehydrated will need - Volume (ml) required = deficit volume +
maintenance volume= [0.07 x 22 lb x 454 x 0.80] + [(10 x 30) + 70]= [560] + [370] = 930
ml

Continuing losses during the replacement

 Estimate the volume of fluid loss and then double this estimate.
 How to know if animal is receiving an inadequate fluid volume.
 If the animal is losing body weight while being given crystalloid fluids, the animal is likely
receiving inadequate volumes of fluid.
 One group of patients where body weight may fool you is in animals that are third-spacing
fluids (peritonitis, pyometritis, pleural effusions).
 In these animals the animal may still be dehydrated but the body weight may not
have changed.
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 Additionally, if renal function is adequate, an animal which is dehydrated will have a urine
specific gravity above 1.025.

Clinical signs of overhydration

 Increased serous nasal discharge, followed by chemosis, and finally pulmonary congestion
will be ausculated before edema ensues.
 Clinically, pulmonary edema is the terminal event of overhydration!
o non-respiratory acidosis (HCO -3). may result from: excess ingestion of H+, decreased
elimination of H+ (renal), increased production of H+ (anaerobic metabolism), or
increased elimination of HCO -3. It is the most common acid-base disturbance in
dogs, cats, and horses.
o non-respiratory alkalosis ( HCO -) excess ingestion of HCO -, excess admin. of HCO -
3 3 3
, excess loss of H+ (vomiting), or sequestration of H+ (functional 3rd space loss). This
acid-base disturbance is common in the cow (displaced abomasum).
o respiratory acidosis (CO2) hypoventilation. This is common in the anesthetized horse.
o respiratory alkalosis (CO2). hyperventilation, pain, excitement, and artificial
ventilation that is excessive.

 Shock therapy with crystalloid fluid: (no head trauma or pulmonary edema) - Dog – 90
mL/kg/hour. Cat – 60 mL/kg/hour
 Blood transfusion (PCV < 20%): 20 ml/kg fresh whole blood. 15-30 ml/kg Oxyglobin.
 Shock therapy for head trauma or pulmonary contusions: Hypertonic saline + Hetastarch or
dextran. Total dose = 5 ml/kg. Draw up 1/3 volume as 23% saline, 2/3 as colloid.
 Small volume resuscitation: 5ml/kg IV hetastarch or dextran. Repeat every 5-10 minutes
until HR, pulses and color improves.
 Crystalloids: Run very fast. Doesn’t stay in vascular space, so need to give 3-4 times what
they have lost.
 Avoid in animals w/ interstitial edema (head trauma, pulmonary contusions,
hypoproteinemia).
 RL - Buffered pH of about 7.4 which is good for acidosis, The lactate is converted to
bicarb for acidosis, Lactate is metbolized in the liver and has calcium.
 Avoid in cows (alkalosis). Normalsol R - Buffered pH of about 7.4 which is good for acidosis,
The acetate in normalsol R is converted to bicarb for acidosis.

 Colloids: Help in retention of fluid in the vascular space. Increases oncotic pressure b/c are
not filtered in the glomerulus. Give smaller volume to restore circulation.

Indications

 Hypoproteinemia, 3rd space loss, Head trauma, pulmonary edema, leaky capillaries, SIRS.
 Eg. Hetastarch, Dextran 70, Whole blood – if PCV drops below 20% and TP < 3.5 (1 mL of
blood per pound will raise hematocrit 1%) then give 20 mL/kg,

Oxyglobin

 Same as above at a rate of 15-30 ml/kg, Whole plasma

 If there is evidence of ongoing blood loss into the abdominal cavity, a snug compressive
bandage should be applied, being careful not to impair respiration.
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NEONATAL DIARRHEA

 Diarrhea is the most important disease of neonatal calves and results in the greatest
economic loss due to disease in this age group in both dairy and beef calves.

 Neonatal diarrhea in calves is a complex, multifactorial condition with factors such as

pathogen exposure, strain variation, environmental and management conditions, nutritional
state and immune status playing a major role in production of disease.
 Most of these factors are related to biosecurity in the calf rearing area and must
be considered before developing a treatment plan for individual cases of the
disease.

 Diarrhea is an increase in frequency, volume or fluidity of bowel movements.

 Fluidity is much less important in cattle than in other species.
 Cattle normally produce 15-28 Kg of feces per day that is 75-85% water.
 Mechanisms of diarrhea are one of more of the following: Malabsorption- decreased or
damaged cellular absorptive area; Osmotic- increased number of particles within the lumen
of the bowel holds water; Secretory- cyclic AMP and prostaglandin mediate active secretion
into the bowel; Abnormal motility- increased or decreased transit time; Hydrostatic-
increased blood to lumen pressure gradient such as with cardiac problems or inflammatory
bowel disease.
 Pathogenesis of diarrhea is related to either increased secretion or decreased absorption.
 The normal bovine GI system absorbs only slightly more than what is secreted per day.
 Normal secretory amounts are equal to, or exceed the extracellular fluid amounts.
 Clinical signs of diarrhea are associated with dehydration, acidosis, depression, failure to
nurse, weight loss, cardiac arrhythmias, sepsis and endotoxemia.
 Dehydration should be scored as a percentage of body weight and results in profound loss of
circulatory volume.
 Acidosis increases vascular resistance, impairs cardiac function, and blocks catecholamine
action.
 Hyperkalemia causes cardiac arrhythmias due to myocardial potassium imbalances.
 Shock and sepsis occur frequently in severe diarrheic cases. Signs of sepsis in calves include
hypopion, arthritis, hyperesthesia, rigid neck, fever, and scleral injection.
 Remember that calves are born and raised in a wide diversity of environments and housing
condition, which will affect the risk of enteric infectious disease.
 Ventilation is inadequate in many cases resulting in high humidity. Vermin such as flies and
rodents are often present in high numbers and these vectors can become a significant factor
in disease transmission.
 The most frequently recognized agents causing calf diarrhea include E. coli, rotavirus,
coronavirus, cryptosporidia, coccidia and Salmonella.
 With the exceptions of Salmonella and specific strains of E. coli these organisms are
ubiquitous in the environment and present within the GI tract of most healthy, mature cattle
without clinical signs of infection.
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SHOCK

 Shock is inadequate cellular respiration due to inadequate tissue perfusion, due to any
number of causes It is defined as oxygen delivery to the tissue that is insufficient to meet
tissue requirements. This may be due to altered hemodynamics, such that the circulatory
system is unable to provide adequate pressure to drive perfusion. Or, shock can occur when
tissues are receiving adequate flow, but there is either not enough oxygen in the blood or the
tissues are unable to extract and utilize the oxygen.

 Shock is a syndrome of clinical signs that has multiple underlying causes.

 Classically, the signs that indicate the shock state are:
o Tachycardia (although bradycardia often occurs in cats)
o Tachypnea
o Pale mucous membranes
o Cold extremities
o Poor peripheral pulses
o Altered mentation

Brief Pathophysiology

 Shock is genearlly associated with a decrease in cardiac output, venous return, and arterial
blood pressure (sepsis is an important exception to this rule).
 The decrease in CO and MABP may lead to a self-perpetuating cycle and downward spiral.
The ¯ CO and ¯ MABP stimulate the sympathetics, baroreceptors, and the renin-angiotensin
system in an attempt to restore MABP.
 Stimulation of these systems results in an heart rate and intense vasoconstriction. The result
of the vasoconstriction and ¯ MABP is ¯ capillary perfusion resulting in deterioration of the
microcirculation, stasis of blood, endothelial damage, capillary permeability, development of
microthrombi, and disseminated intravascular coagulation. The resultant tissue ischemia
results in cellular hypoxia and anaerobic metabolism.
 Anaerobic metabolism is energy inefficient (94% energy loss) and associated with a lactic
acidosis, metabolic acidosis, ¯ cell function, and tissue autolysis. All of these results tend to
further depress cardiac output and blood pressure, thus worsening the shock cycle.
 The clinically observed effects of vasoconstriction are:
 Decreased blood flow to skin causes cold skin temperature
 Decreased blood flow to splanchnic vasculature leads to GI hypermotility, followed by stasis
and mucosal necrosis ® bacterial proliferation, absorption of bacteria, toxins, etc., and septic
shock
 Decreased renal blood flow results in decreased urine output, renal ischemia, tubular
necrosis
 Decreased blood flow to liver (hepatic artery, portal vein) leads to anaerobic metabolism and
the resultant clostridia, toxins
 Decreased blood flow to pancreas results in MDF
 Initially, peripheral vascular beds will vasoconstrict to shunt flow to the "essential organs"
(brain and heart). This results in reduced perfusion and oxygen delivery to the affected
vascular beds.
 In the dog, the GI tract is considered the shock organ since it takes the brunt of
vasoconstriction. Unless shock is rapidly reversed, tissue beds enter an anaerobic state.
 The products of cellular metabolism build up in tissues, including lactate, acids, nitric oxide,
CO2 and adenosine. As ATP stores decrease, membrane pumps are unable to maintain
electrochemical gradients, leading to cellular edema.
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 Over time, cellular death will occur, resulting in cell lysis, inflammation, free radical
formation and local activation of coagulation. As the by-products of cellular metabolism
continue to accumulate, these local factors can eventually overwhelm the vasoconstriction
induced by the sympathetic nervous system. This results in vasodilation, systemic
hypotension, decompensate, and entry of metabolic byproducts, cytokines, free radical and
activated white blood cells into systemic circulation.
 Many compensatory mechanisms are induced in the shock state. The goals of the
compensatory mechanisms are to maintain perfusion to the core organs and restore vascular
volume. These include:
o Mobilization of fluid from the interstitial to intravascular space. This occurs primarily
in shock states with low blood volume, especially hypovolemic shock, but can
potentially occur in all shock states.
o Activation of the sympathetic nervous system (SNS). This results in release of
norepinephrine and epinephrine. There are many effects of the SNS, including
tachycardia, vasoconstriction which may preferentially affect certain tissue beds, and
positive inotropy. Activation of the SNS also results in retention of sodium (and
therefore water) by the kidneys.
o Activation of the renin-angiotensin-aldosterone system (RAAS). This results in
multiple effects, the most important (and immediate) of which are retention of
sodium and water by the kidneys, and peripheral vasoconstriction.
o Release of Antidiuretic hormone (ADH). This results in retention of water and urine
concentration. ADH is also a powerful vasoconstrictor.

Stages of shock

 The earliest stage of shock is the compensated phase. During this period of time,
compensatory mechanisms are able to maintain blood flow to the important organs through
peripheral vasoconstriction. Clinical signs are the "classic" signs of shock, and include pale
mucous membranes, poor pulse quality and cold extremities secondary to vasoconstriction.
Tachycardia is a result of SNS activation, as the body tries to maintain cardiac output. Blood
pressure is usually normal to high as a result of vasoconstriction. Remember that the overall
goal of compensation is to maintain blood pressure, and a normal blood pressure does NOT
mean that perfusion is normal.
 Over time, the body is either able to "fix" the blood volume and return to normal
homeostasis, or it goes into decompensated shock. This phase occurs when local tissue beds
that were vasoconstricted begin to vasodilate. Vasodilation leads to pooling of blood and
maldistribution of flow to "non-essential" organs. Clinical signs include grey mucous
membranes, bradycardia, loss of vasomotor tone leading to hypotension, and severely altered
mentation. The patient is often stuporous to comatose. Ventricular arrhythmias can be seen
on an ECG. It is important to realize that the progression from compensated to
decompensated shock can occur over minutes to hours depending on the cause and severity
of injury, and that patients can present anywhere along this spectrum.
 Cats present a special challenge since they do not always display the classic signs of shock
like dogs do. The shocky cat often presents with bradycardia, hypothermia and hypotension,
even in the early stages of shock. The causes for this are unknown, although it is documented
that cats have species specific alterations in vascular tone and in vascular response to injury.
 Treatment of the decompensated shock patient may result in resolution of clinical signs of
shock, but the patient may decompensate again soon after resuscitation. This is the result of
inflammatory mediators and free radicals being flushed back into systemic circulation,
setting up DIC and the systemic inflammatory response syndrome, and eventually multi-
organ dysfunction. In short, there was simply too much tissue damage to fix despite
appropriate shock therapy.
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STAGES OF SHOCK

 The earliest stage of shock is the compensated phase. During this period of time,
compensatory mechanisms are able to maintain blood flow to the important organs through
peripheral vasoconstriction.
 Clinical signs are the "classic" signs of shock, and include pale mucous membranes, poor
pulse quality and cold extremities secondary to vasoconstriction. Tachycardia is a result of
SNS activation, as the body tries to maintain cardiac output. Blood pressure is usually
normal to high as a result of vasoconstriction.
 Remember that the overall goal of compensation is to maintain blood pressure, and a normal
blood pressure does NOT mean that perfusion is normal.
 Over time, the body is either able to "fix" the blood volume and return to normal
homeostasis, or it goes into decompensated shock. This phase occurs when local tissue beds
that were vasoconstricted begin to vasodilate.
 Vasodilation leads to pooling of blood and maldistribution of flow to "non-essential" organs.
Clinical signs include grey mucous membranes, bradycardia, loss of vasomotor tone leading
to hypotension, and severely altered mentation.
 The patient is often stuporous to comatose. Ventricular arrhythmias can be seen on an ECG.
It is important to realize that the progression from compensated to decompensated shock
can occur over minutes to hours depending on the cause and severity of injury, and that
patients can present anywhere along this spectrum.
 Cats present a special challenge since they do not always display the classic signs of shock
like dogs do. The shocky cat often presents with bradycardia, hypothermia and hypotension,
even in the early stages of shock. The causes for this are unknown, although it is documented
that cats have species specific alterations in vascular tone and in vascular response to injury.
 Treatment of the decompensated shock patient may result in resolution of clinical signs of
shock, but the patient may decompensate again soon after resuscitation.
 This is the result of inflammatory mediators and free radicals being flushed back into
systemic circulation, setting up DIC and the systemic inflammatory response syndrome, and
eventually multi-organ dysfunction. In short, there was simply too much tissue damage to fix
despite appropriate shock therapy.

CAUSES AND CLASSIFICATION OF SHOCK

 Multiple classification systems and etiologies of shock have been described. The
classic approach will be used here

Hypovolemic shock

 It is one of the most common etiologies, and means that blood volume is low. This can be due
to two major causes: hemorrhage (either external or internal) and dehydration. Dehydration
does not always cause hypovolemia, but in severe cases can lead to it. The categories of
hemorrhagic shock are listed below:
Cardiogenic shock
 It occurs when the heart is unable to put enough blood forward to maintain perfusion and
oxygen delivery. Examples of cardiogenic shock include dilated cardiomyopathy, mitral
regurgitation and myocardial failure Obstructive shock
 It occurs when there is an obstruction to flow. Usually this is an obstruction to venous return,
although arterial obstruction (such as with a saddle thrombus) can also cause obstructive
shock. GDV, pericardial effusion, venous thrombosis and tension pneumothorax are all
causes of obstructive shock.
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Distributive shock

 It is a combination of various types of shock. (Mal)distributive shock usually occurs as a

result of sepsis, although anaphylaxis can cause it as well. The hallmark of distributive shock
is peripheral vasodilation and vascular pooling.
 The patient may have red instead of pale mucous membranes.
 Patients with septic shock may also have elements of hypovolemia (from fluid losses or
tissue edema), cardiogenic (from myocardial dysfunction) and obstructive (from DIC)
shocks.

Hypoxemic and anemic shock

 It occurs when there is insufficient oxygen content to meet tissue needs. This can be that
there are not enough red blood cells to carry the oxygen (anemic), or that the oxygen cannot
get into the blood (hypoxemic). Hypoxemic shock is usually the result of pulmonary
pathology.

Neurogenic shock

 It is a specialized form of distributive shock. Massive sympathetic release causes severe

systemic vasoconstriction, which results in decreased forward flow and signs of shock despite
adequate blood volume.
 Causes are severe spinal cord or CNS injury, head trauma, status epilepticus, strangulation
and airway obstruction.

Metabolic shock

 It is caused when the cells have sufficient oxygen for normal metabolism, but are unable to
use that oxygen. This is usually the result of disruption of the Krebs cycle or the electron
transport chain.
 Causes include hypoglycemia, cyanide toxicity or mitochondrial dysfunction (as occurs with
sepsis).

MANAGEMENT OF SHOCK

 Management of shock depends on rapid determination of the underlying cause. The causes
and treatment principles of the various shock categories are listed below.
o Hypovolemic shock can be treated by replacing blood volume, either with
crystalloids, colloids, or blood products as indicated. More information on this will be
presented in the next session.
o Cardiogenic shock can be treated by reducing vascular volume (Furosemide 2mg/kg
in dog; 1mg/kg in cats; PRN), causing peripheral vasodilation if indicated
(nitroglycerin) or improving inotropy (Dobutamine).
o Obstructive shock can only be treated by relieving the obstruction, whether that is by
decompressing the GDV, tapping the pericardial effusion or the pneumothorax, or
otherwise de-obstructing flow. Vascular loading with IV fluids can also be of benefit,
especially if decreased regional blood flow is the cause of shock (as occurs with
GDV).
o Distributive shock can be very difficult to diagnose and treat. If vasodilation and
hypotension are present, treatment with vasopressors (such as dopamine,
vasopressin or norepinephrine infusions) can be beneficial. These patients may also
respond to fluid loading, which is the first line treatment for septic shock.
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o Anemic or hypoxemic shock can be treated with relative ease. RBC transfusions or
Oxyglobin can be given in cases of anemia shock (more on this later). Hypoxemic
shock will usually respond to supplemental oxygen, although mechanical ventilation
may be indicated in more severe cases.
o Neurogenic shock is difficult to treat. The only known treatment is to treat the
underlying cause. This may include administration of mannitol 1 g/kg IV or
hypertonic saline in case of head trauma or CNS disease to reduce intracranial
pressure.
o Treatment of metabolic shock is also aimed at correcting the underlying cause. Give
dextrose 0.5g/kg IV bolus for hypoglycemia, but otherwise treatment is symptomatic
and supportive.
 In Practice scenario, unfortunately, the cause of shock is not always readily apparent. With
the exception of cardiogenic shock, it is never wrong to try an IV bolus of crystalloids. The
"shock dose" of crystalloids should be given in ¼ - 1/3 aliquots over a 10-15 minute period. If
cardiogenic shock is suspected (heart murmur on auscultation +/- crackles), a test dose of
furosemide can be administered. The test dose for dogs is 2 mg/kg IV or IM, and for cats is 1
mg/kg IV or IM. IV fluids should not be routinely administered in cardiogenic shock.

SUPPORTIVE THERAPY FOR SHOCK

Steroids

 The proposed benefit of steroids include stabilization of lysosomal membranes, prevention of

lipid peroxidation, scavenging and stabilization of free radicals, and maintenance of
adrenoreceptor function.
 Disadvantages are many, and include alterations of GI blood flow (especially in an already
compromised GI tract), immunosuppression, vasodilation, and impaired wound healing.
Multiple studies have failed to show any benefit of high dose steroid administration in any
shock state. Low dose steroid administration (at physiologic doses) may be beneficial in
anaphylactic or septic shock.

Antibiotics

 They should be administered only when indicated. In dogs, severe shock states are associated
with GI tract hypoperfusion. This may cause ischemia-induced sloughing of the mucosal
barrier, which allows bacteria to translocate from the gut lumen to the blood vessels. This
often manifests as raspberry jam-like diarrhea which may have flecks of mucosa. If bloody
diarrhea accompanies shock, broad spectrum antibiotics may be indicated.

Analgesia

 It is always indicated if shock is accompanied by pain. The physiologic response to pain is

similar to that to shock, in that SNS activation causes tachycardia and peripheral
vasoconstriction.
 Not administering opioids can make shock resuscitation more difficult since the physical
manifestations of the pain response can easily be confused with prolonged shock. If the
animal seems painful, opioids should be administered.
 The opioids are typically cardiovascularly sparing and can be titrated to effect.
Hydromorphone, oxymorphone, buprenorphine, fentanyl or morphine (except in cats) can
all be used with success.
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 Butorphanol is generally not sufficient for treatment of severe pain. NSAIDs should be
avoided in the shocky dog due to alterations in GI blood flow.

MONITORING OF SHOCK

 Shock resuscitation is aimed at improving tissue oxygen delivery such that homeostasis can
be maintained. Therapy should always be titrated to effect and halted once the endpoints of
resuscitation are achieved.
 Over-zealous fluid administration can cause more harm than good, and complete shock
volumes should not be given unless necessary. Therefore, it is important to constantly
monitor endpoints of resuscitation during shock therapy. These include:

Heart rate

 This is the easiest modality to measure. For the patient in compensated shock, the heart rate
should decrease during resuscitation. In cats, heart rate should increase to normal if
presented with bradycardia. Unfortunately, ongoing pain or stress can obscure the response
to therapy.

Pulse quality

 This should improve with shock therapy. However, pulse quality is a relatively imprecise
indicator of blood pressure since pulse pressure is merely the difference between the systolic
and diastolic pressures. A normal pulse quality does not mean that the animal is fine, but a
poor pulse quality usually indicates ongoing issues.

Mucous membrane color

 MM color reflects the degree of tissue perfusion. If there is on-going vasoconstriction, MM

color will remain poor. However, vasodilatory conditions such as sepsis may cause normal
color even in the face of severe shock. Additionally, ongoing pain can contribute to peripheral
vasoconstriction even without shock.

Mental status

 Improvements in mentation often lag behind normalization of other parameters, so it should

not be used as the sole measure of shock resuscitation. However, improvements in mentation
are expected as shock is resolved. Mental status can be difficult to asses in patients with CNS
disease or head trauma.

Arterial blood pressure

 This modality is one of the most frequently used to assess shock states, but the astute
clinician also should realize the limitations of blood pressure measurement.
 A normal blood pressure does not mean that the patient is fine, and an abnormal blood
pressure definitely means that something is not right. Out of all parameters, blood pressure
is the most protected by compensation for shock.
 Normalization of blood in conjunction with normalization of heart rate, mucous membrane
color and mentation indicate the shock resuscitation has been successful.
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PCV/TS

 These are insensitive indicators of shock resuscitation. Even with severe blood loss,
redistribution of fluid from the interstitial to intravascular compartments takes time.
 Further changes in PCV will occur with fluid administration, or PCV can be falsely elevated
due to splenic contraction. PCV can be useful for determining the need for blood
transfusions.

Urine output and specific gravity

 Urine output is an excellent indicator of renal blood flow, provided that the patient does not
have pre-existing renal disease. The normal urine output for a patient on IV fluids is 1-2
ml/kg/hr.
 The well-hydrated patient should have a urine SG of 1.012-1.020. Unfortunately, shock states
can cause acute renal failure or impaired concentrated ability, which limit the usefulness of
this as a monitoring tool.
 Additionally, evidence of good renal perfusion does not necessarily equal normal perfusion in
other tissues.

Acid-base balance

 Shock states are usually associated with metabolic acidosis. Successful treatment of shock
should cause an improvement in pH and base excess back towards normal. Failure of base
excess to return to normal is associated with a worse prognosis.

Lactate

 This is a good marker of tissue perfusion, especially in the GI tract. Lactate is produced by
tissues undergoing anaerobic metabolism. Remember that the measured value is the
balanced between lactate production and clearance.
 Decreased clearance (i.e., liver disease) can cause elevations in lactate. Additionally, severely
underperfused tissue can have lactate trapped, resulting in falsely low blood concentrations.
Lactate has been shown to be an important prognostic marker. Failure to reduce lactate
concentrations have been strongly correlated with a worse prognosis for multiple diseases.
The important point is that multiple parameters should be assessed to judge response to
shock resuscitation. No single marker has been shown to be strongly correlated with
successful treatment, therefore, the entire patient should be reassessed frequently (every 10-
15 minutes) during the resuscitation period.

COMMON QUESTIONS

1. Differentiate between septicemia and toxemia.

2. What are the complications of septicemia. Enumerate the measures used to control toxemia?
3. What is the line of treatment for septicemia?
4. Explain about fluid therapy?
5. What are the mechanisms of diarrhea?
6. Define hyperpnoea,polypnoea and oligopnoea?
7. Explain the different variations of the color of the mucus membranes and its significance.
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MODULE-6: DISEASES OF DIGESTIVE SYSTEM-I

Learning objectives

 In this section, discussion will be made on vomiting, regurgitation, simple indigestion and
ruminal parakeratosis

VOMITING

 Forceful ejection of contents of the stomach and the proximal small intestine through
the mouth is called vomiting
 True vomiting occurs in monogastric animals. True vomiting is not a feature of gastric
diseases in horses.
o The strong cardiac sphincter inhibits the release of stomach contents
o The soft palate and epiglottis combine to affect a seal between the oral and nasal
parts of the pharynx. Hence the stomach contents are discharged through the nasal
cavities and not through the mouth in case of vomiting in horses.

Vomiting

 Coordinated vigorous contraction of abdominal, thoracic and diaphragmatic muscle with

resultant forceful ejection of vomitus from the mouth is called vomiting
 Nausea: outward sign of nausea include depression, shivering, hiding, yawning and
lip licking.
 Retching is second phase of vomiting and consists of forceful contractions of the abdominal
muscles and diaphragm occurring with the glottis closed to produce negative intrathoracic
pressure and positive abdominal pressure. These pressure changes are associated with
movement of gastric contents into a dilated esophagus.

PATHWAYS OF VOMITING

 When the vomitus passes through the pharyngeal cavity, nasopharynx and glottis are closed
to prevent aspiration.
 Emetic center : Located in medulla oblongata in brain.
o Receptors located throughout the abdominal viscera. Diseases or irritation of the
gastro intestinal tract, other abdominal organs or peritoneum stimulate vomiting
through vagal afferent pathways
o Receptors in kidney, uterus, urinary bladder send afferent impulses through
sympathetic nerves
o Receptors in pharynx, tonsillar fossae through afferent fibers of the glassopharyngeal
nerve.
o CNS disease through direct extension of inflammatory stimuli, hydrocephalus or
space occupying lesions. CSF increase, cereblral edema, infection, neoplasia.
o Fear, stress or pain: Stimulation of higher centers in cerebro cortex- psychogenic
vomiting
o Cyclic vomiting in dog is associated with an autonomic / visceral epilepsy arising
from limbic region.

CLINICAL APPROACH TO VOMITING

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Clinical approach

 History: gagging, coughing, regurgitation, dysphagia

 Young unvaccinated animal- check for infectious diseases- parvo/CD vaccination/ travel/
medical problem/ medication/ NSAID
 Age of the animal - assess– weaning- vascular ring anomaly; projectile- gastric outflow
obstruction
 Breed: GDVin deep chested dogs- Setter boxer, GSD; pyloric stenosis in brachycephalic
breeds- boxer
 Check for Ingestion of toxins/ foreign bodies
 Rule out Systemic diseases/ metabolic diseases, polyuria/ polydipsia, weight loss-
ketoacidosis, renal failure
 Assess vomiting episode: duration frequency, relationship with eating/ drinking, description
of the vomitus
 Dietary clue: type of diet, change- adverse reaction to food.
 Vomitus with fecal odour- low intestinal obstruction or SIBO
 Bile in vomitus- no pyloric obstruction
 Blood in vomitus: fresh bright red or digested blood that has coffee ground appearance- GI
erosion / ulceration.
 Hematemesis- metabolic related ulcers uremia, NSAID, gastric neoplasms.
 Examination of oral cavity: icteric mm, uremic breath, ulceration or linear foreign body
around the base of the tongue.
 Fever- infectious/ inflammatory process.
 Bradycardia or cardia arrhythmia sign of metabolic disturbance
 Abdomen palpated for distension and tympany (GDV) effusion

Hematology

 Neutrophilia with left shift- sepsis or inflammatory disease - pyometra

General treatment and management of vomiting animal

 To correct / remove the primary cause

 To control vomiting episode- alleviating further loss of fluid and electrolytes
 To correct fluid and electrolyte or acid- base disturbances.
 NPO (Nothing per os) for 24 hrs
 After 12 hrs offer small amount of water or ice cubes
 After 24 hrs if water is tolerated, introduce bland carbohydrate== cooked rice, lean minced
beef, chicken, cottage cheese, baby food. Avoid diet high in fat/ protein
 Initially split total daily requirement into 3-4 small meals
 Fluid therapy- loss of sodium, potassium chloride; hypokalemia with metabolic acidosis
 PCV total protein - animal’ s dehydration status
 Anaemia- bleeding GI lesions, CRF
 Lipase/ amylase- pancreatitis - acute vomiting/ pain - plain radiograph are inconclusive
 Urinalysis: fractional excretion of sodium
 pH of vomitus - regurgitation - alkaline; vomitus- acidic
 ECG- hypoadrenocorticism vomiting is associated with bradycardia and signs of hypovolemic
shock
 Radiography/ Endoscopy/ laparotomy
 Leukopenia (with or without left shift) gram-negative sepsis salmonella/ viral infection
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VOMITUS IN DOG

Frothy vomitus Vomitus with blood Bilious vomiting

Praying posture Acute vomiting

Dog with Chronic Vomitting Severely emaciated dog

PATHOPHYSIOLOGY
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 Other causes
 Physaloptera – lymphocytic, plasmocytic gastritis
 Pythium (fungal), Insidiosum – Pyo granulomatous gastitis
 Helicobacter
 Enterogastric reflex

DIAGNOSIS

 Clinical Signs

 Ultrasonography

DIFFERENTIAL DIAGNOSIS

 Dietary indiscretion
 Ingested grass materials: grass or house plants
 Chemical irritation or Toxins like herbicides, cleaning materials, heavy materials.
 Drugs : Aspirin, NSAID’s, glucocorticoids
 Viral infections : Parvo virus
 Bacterial infections : Helicobacter
 Parasites : Physanoptesa, Ollulanus tricuspis
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 Systemic disorder : ureamia, liner diseases, neurological diseases, sepsis

 Gastric / Pyloric Obstruction: -foreign body, neoplasms or polyps.
 Hepatic diseases
 Renal failure
 Neurologic -spinal cord diseases in dogs receiving corticosteroids.
 Most cell tumours
 Gastrinoma

TREATMENT I

Treatment

 NPO. Rest
 Without food and water for atleast 24 hrs
 If vomiting resolves – bland diet
 Double cooked chicked with rice
 Gradually introduce normal diet.
 Balanced electrolyte solution
 Potassium supplements if there is hypokalemia
 Metabolic acidosis
 Antiemeties:- for symptomatic control and prevention of furher fluid and electrolyte loss

Phenothiazine Derivatives

 Chlorpromazine - 0.5 mg/kg BW s/c, i/, i/v q 6-8 hrs

 Prochlorperazine - 0.5 mg/kg BW s/c, i/, i/v q 6-8 hrs
 Metaclopromide – 0.2 to 0.4 mg/kg BW, oral, i/m. o/c q 8 hrs
 (or) 1-2 mg/kg BW as constant rate infusion q 24 hrs.
 Promotes gastric emptying, increases tone and amplitude of gastric contraction
and relaxation of pylorus.

Serotonin Antagonists

 Ondansetron – 0.1-0.2 mg/kg BW s/c q 8 hrs

(or)- 0.5 mg/kg i/v as a loading dose and

- 0.5 mg/kg i/v q 1 hr as maintenance dose.

TREATMENT

H2 blockers – decreased gastric acid secretion

 Cimetidine – 5-10 mg/kg BW PO. i/v, q 6-8 hrs

 Ranitidine - 2 mg/kg BW PO, i/v, q 8-12 hrs
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 Famotidine – 0.5 – 1 mg/kg BW PO, i/v, q 12-24 hrs

 Nizatidine - 2.5 – 5 mg / kg BW PO, q 24 hrs
 Sucralfate
o 1 g total dose for large dogs
o 0.5 g total dose for small dogs

Proton Pump Inhibitors

 Omeprazole - 0.7-1 mg/kg BW PO, q 12-24 hrs

 Pantaprazole - 0.7 – 1 mg/kg BW PO or i/v, q 24 hrs

Prostaglandin analogues

 Misoprostol - 3-5 mg/kg BW PO, q 6 hrs

 7.5 – 10 mg/kg BW
 Cizapride – 0.25 – 0.5 mg/kg BW PO, q 6-12 hrs
 Tegaserod – 0.05 – 0.1 mg/kg BW PO
 Erythromycin – 0.5-1 mg/kg BW PO, q 8 hrs
 Antacids: Gelusil – 5-10 ml PO, q 4-6 hrs

REGURGITATION

 Regurgitation is the expulsion through the mouth or nasal cavities of feed, saliva and other
substances, which have not yet reached the stomach.
 Regurgitation of rumen contents through the mouth in cattle is abnormal and is associated
with loss of tone of cardia or inflammation of the cardia
 Naso gastric regurgitation or gastric reflux occurs in the horse. Stomach contents flow into
the esophagus and usually into the nasopharynx and nasal cavities due to distension of the
stomach with fluid.
 Gastric reflux in the horse can be elicited by nasogastric intubation. Spontaneous reflux of
stomach contents is indicative of high volume and high-pressure fluid distension of the
stomach.

Causes

 Terminal vomiting in horse with gastric dilatation

 Vomiting in cattle is really regurgitation occurring in
o Third stage milk fever
o Arsenic poisoning
o Poisoning by plants
o Administration of large quantities of fluids into the rumen
o Cud dropping associated with abnormality of the cardia
 Regurgitation in all diseases causing dysphagia or paralysis of swallowing.

SIMPLE INDIGESTION

Causes
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 Dietary abnormalities of minor degree like

o Indigestible Roughage, particularly when protein intake is low,
o Moldy, overheated and frosted
o Moderate excesses of grain and concentrate intake.
o Prolonged or Heavy oral dosing with antimicrobials

Primary atony

 Dietary abnormalities
 Increase or decrease pH of the contents:
 Accumulation of indigestible food
 Putrefaction of protein Production of toxic amides and amines - histamine

Clinical findings

 Reduction in appetite
 Milk yield is reduced to a lesser extent.
 Mild depression and dullness.
 Rumination ceases and depressed ruminal movements - in frequency and amplitude
 Rumen larger than normal with mild abdominal pain and Discomfort
 Moderate tympany with doughy rumen
 Dry Feces and quantity reduced. 24 hrs later feces are softer and voluminous and
malodorous.
 No systemic reaction.
 Spontaneously recovery or with simple treatment

Clinical Pathology

 Urine: ketone, SAT and cellulosed digestion test, pH test are done in rumen fluid.
 DD : Acetonemia, TRP, Acidosis, LDA, RDA, Abomasal volvulus, vagal indigestion,
phytobezoars, secondary ruminal atony
 Treatment
o Most cases recover spontaneously.
o Feeding of good quality palatable hay
o Rumenatorics: containing nux vomica, ginger and tartar emetic in powder form.
o Parasympathomimetics:
 Caramylcholine chloride, physostigmine and neostigmine are used.
Neostigmine @ 2.5 mg/45 kg BW used.
 Metoclopromide : for hypomotility associated with vagal nerve damage.
 Epsom salts 0.5 to 1.0 kg/ adult cow
 Magnesium hydroxide @ 400g/ adult cow in acidic conditions
 Acetic acid or vinegar 5- 10 l in rumen alkalinity.
o Reconstition of ruminal microflora

RUMINAL PARAKERATOSIS

Parakeratosis of ruminal epithelium

 Caused by lowered pH and increased VFA

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 Papillae are enlarged, leathery, dark in color and adhere to form clumps.
 Increase in the thickness of the cornified epithelium especially on the dorsal surface of
rumen about the level of the fluid ruminal contents.

INDIGESTION IN CALVES FED MILK REPLACERS

Ruminal drinkers

 Occurs in veal calf characterized by recurrent ruminal tympany, inappetence, unthriftiness,

and clay like feces.
 After being placed on milk diet and fed with a bucket.

Cause

 Insufficient closure of reticular groove while drinking milk.

 Milk enter rumen decreasing the pH of rumen and increasing lactate concentration
 Clinical recovery occurs after retuning to normal feeding. eg weaning onto hay and
concentrates.

Clinical signs

 Temperature, Heart rate, Respiratory rate normal.

 Unthrifty calf.
 Increase in size especially in the ventral half of the abdomen with fluid splashing sound on
ballottment.
 Auscultation of LPF reveals fluid splashing sound when calf is drinking.
 Foul greyish white fluid siphoned off the rumen.
 Casein clot.
 Treated by inducing them to suck on the herdsman's fingers while they are being fed a small
quantity of cows' whole milk or Milk replace.

MODULE-7: DISEASES OF DIGESTIVE SYSTEM-II

Learning objectives

 Under this section, bloat and its management will be discussed.

RUMINAL TYMPANY

 Ruminal tympany is the excessive retention of gases of fermentation with abnormal

distension of the rumen and reticulum. The gas may be in the free form or persistent foam
mixed with the rumen contents.

Types-Primary bloat/ Frothy bloat : Production of stable foam traps the normal gases of
fermentation in the rumen. There is inhibition of coalescence of the small gas bubbles and increase
in the intra ruminal pressure as eructation do not occur
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 Secondary bloat/ Free gas bloat: due to physical obstruction of oesophagus or failure of
eructation mechanism

FROTHY BLOAT

Primary ruminal tympany (frothy bloat)

 Inhibition of Coalescence of the small gas bubbles

 Production of stable foam

Pasture bloat

 The vital factor is the frothiness of ruminal contents. The stable dispersion of feed particles
are responsible for the frothiness. There is also slower clearance of ruminal contents that
enhances microbial activity and gas production. Soluble leaf protein may contribute to
frothiness.

Feedlot bloat

 Feedlot bloat is due to feeding finely ground grain. High carbohydrate content increases
encapsulated bacteria that produce slimes. The slime entraps the gases of fermentation.
Maximum stability of foam occurs at pH of about 6.

ETIOLOGY- SECONDARY BLOAT

Free gas bloat

 Physical obstruction to eructation occurs in esophageal obstruction (foreign body), stenosis

of esophagus or pressure outside the esophagus such as Tuberculous lymphadenitis or bovine
viral leucosis, bronchial lymph node enlargement or obstruction of cardia)
 Interference with esophageal groove function as in vagal indigestion or DH, tetanus or
carcinoma, Actinomyces bovis, granulomatous lesion near esophageal groove papillomata

EPIDEMIOLOGY

 Lush young and leaves containing high concentration of soluble protein are dangerous.
 Outbreaks of feedlot bloat are usually of the frothy bloat
 Sporadic: Free gas type and secondary to lesions which cause dysfunction of eructation.

Bloating forages

 Alfalfa, red clover, white clover, young green pasture with high protein content.

Non-bloating forages
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 Bloat safe forages contain tannins, which bind with soluble proteins and inhibit
microbial digestion
 Grazing very succulent pasture –immature rapidly growing legumes in the pre bloom stage

Risks

 Herbage at vegetative to prebud stages of growth

 Liberal administration of urea to pasture, high intake of glucose, calcium and magnesium
and high nitrogen intake.
 Cool temperature delay the maturation and extend the vegetative growth phase of forage
crops and optimize conditions for bloat
 Salivary protein bSP30 is correlated with susceptibility to bloat

CLINICAL SIGNS - PRIMARY BLOAT

Primary pasture

 Signs may develop Within 15 minutes after going on to bloat producing pasture. The entire
abdomen is enlarged with obvious distension of the upper left para lumbar fossa. Discomfort
with the animal may standing and lying down frequently, kicking at its abdomen and rolling.
Dyspea, open mouth breathing, protrusion of tongue, salivation and extension of the head,
increased respiratory rate are noticed.
 Mild bloat : LPF is distended , no distress, 5-7 cm of skin over the LPF may be easily grasped
and tented
 Moderate bloat: Animal is Anxious and uncomfortable, and the skin over the LPF is usually
taut
 Severe bloat: Distension of both sides of the abdomen, breathing through mouth and
protusion of tongue. Animals are uncomfortable, anxious and staggering. Skin is very tense
and cannot be grasped and tented.
 Trocarization or passage of stomach tube releases only small amounts of gas.
 Sudden death in some animals

CLINICAL SIGNS - SECONDARY BLOAT

Secondary bloat

 Excess gas as a free gas cap on top of ruminal contents. There is initial increase in frequency
and strength of contraction and later atony. There is release of large quantities of gas
when stomach tube is passed or trocarization is done.
 If esophageal obstruction is present the same may be detected while the stomach tube is
passed.
 Marked elevation of heart rate, systolic murmur and dyspea are noticed.

Laboratory findings

 Non specific

Differenial Diagnosis
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 Vagus indigestion
 Tetanus
 Carcinoma and papillomata of the esophageal groove and reticulum;
 Actinobacillosis of the reticulum

TREATMENT

First aid emergency measures

 Emergency rumenotomy in severe cases with gross ruminal distension, mouth breathing
with protrusion of tongue and staggering.
 An incision of about 10-20 cm in length over the LPF through the skin, abdominal
musculature and directly into the rumen.

Trocar and cannula

 2.5 cm in diameter. If trocar is successful in reducing the pressure, antifoaming agents are
used.
 Promotion of saliva: A stick is tied in the mouth like a bit to promote the production
of excessive saliva
 Drenching of sodium bicarbonate 150-200 g in one liter of water or any non-toxic oil.
 Stomach tube: Passage of tube -2 cm in diameter in free gas bloat, Anti foaming agents can
be administered with the tube in rumen.

Feedlot bloat

 Swellers/ moderate cases of bloat, will resolve if the cattle are made to walk.
 Antifoaming agents: Non-toxic oil, non biodegradable - 250 to 500 ml per animal is used.
 Detergent such as dioctyl sodium sulfosuccinate.
 Synthetic surfactant like polaxalene at 25-50 g is recommended
 Alcohol ethoxylate are more effective and faster than oil.

PREVENTION AND CONTROL

 Restricting the grazing to 20 minutes at a time Prior feeding of dry scabrous hay particularly
cereal hay and straw
 Choice of forages: Seeding cultivated pastures to grass-legume mixtures is the most effective.
 In a grass- legume mixture a legume content of 50% is suggested as the maximum bloat safe
level.
 High energy and high protein supplement increases the incidence of bloat.
 Use of condensed tannins (proanthocynanidins) : @ 5g/kg DM of CT is necessary to prevent
bloat

Antifoaming agents

 Individual drenching: twice daily dose of 60- 120 ml of oil;Method to be adopted if practical
utility is observed under field conditions
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Application to flanks

 Types of oil: most vegetable oils, mineral oil and emulsion tallow are effective. Choice
depends on availability and cost. This procedure is followed in foreign countries and may be
tried in India if feasible.

Synthetic non-ionic surfactant

 Polaxalene: surface-active agent polyoxythylene polyoxypropylene block polymer effectively

used for prevention of legume pasture @ 2g/100 kg BW.
 Alcohol ethoxylate detergents: foam-reducing qualities, better palatability. Blocks containing
10% alcohol ethoxylate @ 17-19 g daily consumption.

Feedlot bloat

 Roughage in ration: feedlot high level grain rations should contain at least 10-15% roughage,
which is cut or chopped and mixed into a complete feed.

Dietary salt

 4% salt to feedlot has been recommended.

MODULE-8: DISEASES OF DIGESTIVE SYSTEM-III

Learning objectives

 Details about acidosis in cattle, LDA and RDA will be discussed.

RUMINAL LACTACIDOSIS

Etiology

 The sudden ingestion of toxic doses of carbohydrate rich feed such as grain
 Ruminating cattle, sheep susceptible; most common in feedlot cattle
 Animals fed low energy rations
 A gradual change during a period of 3-5 weeks from forage ration to high energy lactation
rations
 Feeding excessive quantities of concentrate and Insufficient forages result in fiber deficient
ration
 Feeding of excessive amounts of rapidly fermentable carbohydrates.
 Due to breakdown in feed mill/ handling facilities
 Accidental ingestion.
 Morbidity 10-50 %.
 Case fatality may be up to 90% in untreated cases and 30-40% in treated cases.
 Wheat barleycorn grains, Finely Ground Grain are more toxic. Oats and sorghum grain are
least toxic
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CLINICAL SIGNS

 Speed of onset of illness varies with the nature of feed, being more rapid With ground feed
than whole grain.
 Severity increases with the amount of Feed taken.
 Within few hours of engorgement: Distended rumen, abdominal discomfort, Kicking at belly.
 Mild form: anorectic, bright and alert and soft feces and reduced ruminal movements.
Rumination absent and begin to eat normally after 3-4 days.
 Severe form: within 24- 48 hrs animals become recumbent, staggering and stand-alone.
Anorectic, apathetic, depressed. Grinding of Teeth and do not drink water, noticed in sheep,
but cattle engorge with water if it is readily available.
 Depression, dehydration, inactivity, weakness, abdominal distension, Temp below normal,
increased H/R. Shallow respiration. Diarrhoea is profuse with kernels of grain. Dehydration
is severe and progressive. Anuria is a common finding
 Pitched tinkling and gurgling sounds are audible in auscultation. Ruminal Fluid is milky
green to olive brown color and has pungent acid smell. pH of rumen is below 5.
 Severely affected animal: Staggering drunken gait and impaired eyesight. They bump into
object and palpebral reflex sluggish. Acute laminitis with animal lame in all four feet
 Recumbency after 48 hrs. Lie quietly with heads turned into the flank. A rapid onset of
recumbency suggests an unfavorable prognosis. Evidence of improvement include fall in
H/R
, rise in temp, return of ruminal movements and passage of large amount of soft feces.
 Mycotic rumentitis may occur
 Chronic laminitis for severe months or weeks or abortion in pregnant cattle
 Sub acute ruminal acidosis in dairy cattle; laminitis, intermittent diarrhea, Sub optimal feed
intake, liver abscess, haemoptysis, epistaxis and pulmonary haemorrhage. Laminitis is
characterized by ridges in dorsal hoof wall, sole ulceration white line lesion, sole hemorrhage
end misshapen hooves.

DIAGNOSIS

Clinical pathology

 Ruminal pH less than 5.

 Absence of Ruminal protozoa.
 Gram-negative bacterial flora replaced by Gram-positive bacteria.
 Hematocrit rise from 30-32 to 50- 60 %
 Blood lactate and inorganic phosphate levels increased
 Blood pH and bicarbonate reduced
 Hypocalcaemia due to malabsorption. ( 6- 8 mg/dl)
 Urine pH fall to 5 and concentrated

Necropsy findings

 Acute cases: Content of rumen and reticulum are thin and porridge like and have typical
odor of fermentation.
 Cornified epithelium is mushy and easily wiped off leaving dark hemorrhagic surface
beneath. These are restricted to ventral half of the sacs. Abomasitis, pronounced thickening,
darkening of blood and visceral vein stand out prominently.
 Fungal hepatitis and ischemic nephrosis are noticed
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Differential diagnosis

 Parturient paresis
 Peracute coliform mastitis
 Acute diffuse peritonitis
 Simple indigestion

TREATMENT

 Correction of ruminal and systemic acidosis and prevention of further lactic acid production.
 Restoration of fluid and electrolyte loses and maintenance of circulating blood volume
 Restoration of fore stomach and intestinal motility to normal.

Prevention of further access to feed

 Not providing water for 12- 24 hours orally

 Supply of good quality of palatable hay ½ the quantity of daily ration
 Exercise to promote movement of ingesta through digestive tract.
 After 18- 24 hours those cattle which continue to eat hay may be allowed to free access of
water.

Rumenotomy

 In severe cases (recumbency severe depression, hypothermia, prominent ruminal distension

with fluid, H/R 110-130/mt and pH of 5 or below)

Sodium bicarbonate

 Systemic acidosis is treated with IV solutions of 5% sodium bicarbonate @ 5l for 450 kg

animal over a period of 30 minutes. Followed by 1.3% sodium bicarbonate at150ml/kg body
weight IV over next 6-12 hrs.
 Following rumenotomy, and fluid therapy animal show improved muscular strength and
begin to urinate within one hour and attempt to stand within 6-12 hrs.

Rumen lavage

 In less severe cases standing depressed H/R 90-100/mt moderate distension and pH 5-6.
Warm water is pumped until LPF is distended and rumen is allowed to empty by gravity
flow.
 Alkalinizing agents: 500g of Mg hydroxide per 450 kg animal or Ma oxide in 10 litres of
warm water pumped into rumen and kneading done.

Ancillary therapy

 Antihistamines for laminitis, NSAID for shock therapy, thiamin or brewer’s yeast to
promote lactic acid metabolism, parasympathomimetic for stimulation of gut motility.
Calcium borogluconate for hypocalcemia.
 Oral tetracycline to control growth of lactic acid producing bacteria .
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 Following treatment the animals should begin eating hay by third day and some ruminal
movements should be present, pass large quantities of feces and maintain hydration.

PREVENTION AND CONTROL

 Gradual period of adaptation

 Small incremental increases in grain
 Usage of dietary buffer: 2% sodium bicarbonate, sodium bentonite or limestone Or usage of
10% alfalfa hay

Ionophores

 Salinomycin, monensin and lasalocid provides protective effect. Laidlomycin reduces the
severity of acidosis.
 Ionophores alters VFA profile in the rumen and increases the propionate production
 Decreases the population of S. bovis in rumen
 Clearance of lactate from rumen and increases ruminal pH
 Decreases ruminal methanogenesis, ruminal ammonia and decreaes blood levels of ketone
bodies.

LEFT - SIDE DISPLACEMENT OF THE ABOMASUM

Etioloy

 Multifactorial.
 Hypomotility and gaseous distension of the abomasum- prerequisite for displacement of
abomasum
 Feeding of high levels of concentrate to dairy cattle

Occurrence

 Most commonly in large-sized, high-producing adult dairy cows immediately after

parturition.
 Case fatality : 21% in cows with LDA and diarrhea than in cows with LDA and normal feces
(8%).

LEFT - SIDE DISPLACEMENT OF THE ABOMASUM

Dietary risk factors

 Negative energy balance prepartum, High body condition scores, suboptimal feed
management, prepartum diets containing >1.65 Mcal of NE/kg of DM, winter and summer
seasons, high genetic merit, and low parity hepatic lipidosis
 High-level grain feeding
 A crude fiber concentration < 16-17% in the diet of dairy cows
 Feeding rations high in carbohydrates,
 Inadequate levels of roughage
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ANIMAL RISK FACTORS

 Greatest risk at 4-7 years of age.

 Dairy cattle and Female cattle were at a higher risk
 Occurs throughout the year
 Parturition, atonic or distended abomasum-common precipitating factors
 Concurrent diseases
 Pre-existing subclinical ketosis
 Hypocalcemia
 Genetic predisposition
 Unusual activity, including jumping

PATHOGENESIS

 The atonic gas-filled abomasum gets displaced under the rumen and upward along the left
abdominal wall
 The fundus, greater curvature of the abomasum, pylorus and duodenum, omasum, reticulum
and liver are also displaced to varying degrees. A reduced rumen volume in the immediate
postpartum period allows this displacement to occur.
 Leads to rupture of the attachment of the greater omentum to the abomasum.
 Compression of the abomasum causing a decrease in the volume of the organ and
interference with normal movements.
 Metabolic alkalosis with hypochloremia and hypokalemia
 Secondary ketosis, abomasal ulceration and adhesions may occur

CLINICAL SIGNS

 Inappetence, or anorexia, a marked drop in milk production and varying degrees of ketosis.
 The left lateral abdomen appears 'slab-sided'
 Temperature, heart rate and respirations are within normal ranges.
 The feces are reduced in volume and softer than normal but diarrhea may occur.
 Ruminal movements decreased in frequency and intensity
 Rumen pack is palpable in the left paralumbar fossa.
 Rumen sounds not be audible over an area anterior to the fossa .

Other clinical features

 Rectal examination
o A sense of emptiness in the upper right abdomen is appreciated.
o The rumen is usually smaller than expected
o The distended abomasum may palpable to the left of the rumen..
 Anterior displacement of abomasum
o The characteristic LDA pings cannot be elicited over the typical region.
o Normal rumen contractions can be heard in LPF.
o Gurgling sounds may be audible just behind and above the heart and on both sides of
the thorax.
o The distended abomasum can be felt between the reticulum and diaphragm, if a
rumenotomy is done
 Atrial fibrillation
o A paroxysmal atrial fibrillation
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Course of LOA

 The course of an LDA is highly variable. -several weeks or even a few months.

DIAGNOSIS

 Diagnosis is based on clinical signs. It should be diferentiated from

o Simple indigestion
o Primary ketosis
o Traumatic reticuloperitonitis
o Vagus indigestion
o Fat cow syndrome at parturition

LDA

TREATMENT

 Right paramedian abomasopexy and right paralumbar fossa omentopexy are used for cor-
recting left displacement of the abomasum.

Closed suture techniques

 In the blind suture technique, the precise location of insertion of the sutures is unknown.
 Complications: peritonitis, cellulitis, abomasal displacement or evisceration, complete
forestomach obstruction, and thrombophelebitis of the subcutaneous abdominal vein

Roll-and-toggle procedure

 Rolling the cow

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 The cow is cast and laid on her back, then rolled vigorously to the right and the roll stopped
abruptly

Treatment of ketosis

 Parenteral dextrose
 Oral propylene glycol

RIGHT - SIDE DISPLACEMENT OF THE ABOMASUM (RDA) AND ABOMASAL

Etiology

 Atony is the precursor of dilatation and displacement, and consequently abomasal volvulus.

Occurrence and incidence

 Lactating dairy cows: within the period 3-6 weeks after calving. Calves: occurs in young
calves from a few weeks of age up to 6 months

Risk factors

 Feeding of high levels of grain to high producing dairy cows in early lactation .
 The risk increased with increasing age,
 Dairy cattle are at a much higher risk than beef cattle.
 The case fatality rate for abomasal volvulus - 23.5%

PATHOGENESIS

Dilatation and displacement phase

 Abomasal atony occurs initially, resulting in the accumulation of fluid and gas in the viscus
 This leads to gradual distension and displacement in a caudal direction on the right side
(dilatation phase).
 There is continuous secretion of hydrochloric acid, sodium chloride, and potassium into the
abomasum. These causes gradual distension and the secreations do not evacuate into the
duodenum.
 Leading to dehydration and metabolic alkalosis with hypochloremia and hypokalemia.
 Increased luminal pressure cause mucosal injury by local vascular occlusion and affect the
prognosis.
 In complicated cases : hemoconcentration, hypovolemia and dehydration and marked
metabolic alkalosis with a severely distended abomasum.
 Severe and prolonged abomasal volvulus: paradoxic aciduria with metabolic alkalosis
associated with abomasal disease.

Volvulus phase
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 The distended abomasum twists in a clockwise or anticlockwise (viewed from the right side)
direction in a vertical plane around a horizontal axis.
 Degreeof volvulus is of 180-270* causing a acute obstruction with local circulatory
impairment and ischemic necrosis of the abomasum.
 Sometimes abomasum and omasum are distended and form a loop with the cranial part of
the duodenum. Pressure and tension damage to the ventral vagal nerve trunk and to the
blood vessels are responsible for the poor prognosis in severe cases

CLINICAL SIGNS

Dilatation and displacement phase

 History of calving within the last few weeks, inappetence, decreased milk production; the
feces are reduced in amount and are abnormal.
 Anorexia, depression, dehydration, no interest in feed, increased thirst and sometimes
muscular weakness.
 The temperature is usually normaland the respirations are usually within the normal range.
The heart rate will vary from normal to 100/min
 The mucous membrances are usually pale and dry.
 The reticulorumen is atonic and the rumen pack feel excessively doughy. The distended abo-
masum is detectable as a tense viscus on palpation immediately behind and below the right
costal arch.
 Ballottement of the middle third of the right lateral abdomen immediately behind the right
costal arch along with simultaneous auscultation reveals fluid-splashing sounds suggesting a
fluid-filled viscus.
 Percussion and simultaneous auscultation over the right middle to upper third of the
abdomen commonly elicits a characteristic high-pitched ping.

Volvulus phase

 The clinical findings more severe than during the dilatation phase.
 The abdomen is visibly distended, depression , weakness and dehydration
 The heart rate is 100-120/min, and respirations are increased
 Recumbency with a grossly distended abdomen and grunting may occur
 Rectal examination reveals the partially distended abomasum . In the volvulus phase, the
distended tense viscus is usually palpable in the right abdomen anywhere from the upper to
the lower quadrant.
 The feces are usually scant, soft and dark in color. The soft feces must not be mistaken for
diarrhea.
 Death usually occurs in 48-96 hours from shock and dehydration.
 Rupture of the abomasum may occur and cause sudden death.

Acute abomasal volvulus (adult cattle)

 A sudden onset of abdominal pain with kicking at the abdomen, depression of the back and
crouching.
 The heart rate is usually increased to 100-120/min, the temperature is subnormal, and there
is peripheral circulatory failure.
 Mucous membranes are pale, dry and cool.
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 Abdomen is grossly distended on the right side and auscultation and percussion reveal the
tympanitic sounds of a gas-filled viscus.
 Fluid-splashing sounds are audible on percussion.
 Paracentesis of the distended abomasum -large quantities of bloodtinged fluid with a pH of
2-4.
 The distended abomasum palpated on rectal examination
 The feces are scant, soft become blood-stained or melenic

Acute abomasal volvulus (calves)

 A sudden onset of anorexia, acute abdominal pain with kicking at the belly, depression of the
back, bellowing and straining.
 H/R 120-160/min, the abdomen is distended and tense
 Auscultation and percussion over the right abdomen reveal distinct high-pitched pings.
 Palpation behind the right costal arch reveals a tense viscus.

CLINICAL PATHOLOGY

Serum biochemistry

 Hemoconcentration, metabolic alkalosis, hypochloremia and hypokalemia.

 The severity of volvulus can be classified according to the amount of fluid in the abomasum
and the concentration of serum chloride and the heart rate:
o Group 1 - abomasum distended principally with gas
o Group 2 - abomasum distended with gas and fluid, and surgical reduction possible
without removal of fluid
o Group 3 - abomasum distended with gas and fluid, 1-29 L of fluid removed before
reduction of abomasum
o Group 4 - abomasum distended with gas and fluid, more than 30 L of fluid removed
before reduction of torsion.
 Cows classified as group 3 or 4 or those having presurgical chloride levels equal to or
below 79 rnEq/L (79 mmollL) or pulse rates equal to or greater than 100/min have a poor
prognosis.

Urinalysis

 Paradoxic aciduria

Hemogram

 The total and differential leukocyte count --a stress reaction in the early stages, and in the
later stages of volvulus there is leukopenia with a neutropenia and degenerative left shift

Abomasocentesis

 Centesis of the distended abomasum will yield large quantities of fluid without protozoa
and a pH of 2-4.
 The fluid may be serosanguineous when volvulus is present.
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Prognostic Indicators

 An anion gap of 30 rnEq/L - poor prognosis and more accurate than either serum chloride or
base excess values.
 The surgical and postoperative findings in cattle with abomasal volvulus are good prognostic
indicators of outcome.
 Cattle with omasal-abomasal volvulus have a worse prognosis than those without omasal
involvement.
 Large abomasal fluid volume, venous thrombosis, and blue or black abomasal color before
decompression are all indicative of a poor prognosis.
 Postoperatively decreased gastrointestinal motility is an unfavorable prognostic sign.

DIAGNOSIS

 Diagnosis is based on clinical signs and physical findings. Ultrasonography is used nowadays
to diagnose displacement of abomasum. The condition should be differentiated from the
following:
 Impaction of the abomasum associated with vagus indigestion. Pings are not present in
abomasal impaction.

Abomasal ulceration

 A laparotomy may be required to distinguish between them Subacute abomasal ulceration

with moderate dilatation of the abomasum.
 The presence of melena suggests abomasal ulcers but these may be present as secondary
complications in dilatation and right-side displacement

Cecal torsion

 Distension of the right flank, tympanitic sounds on auscultation and percussion,

 Cecum can be palpated on rectal examination, as a long (60-80 cm), usually easily movable,
cylindrical, tense tube (10-20 cm in diameter), with a blind sac

Fetal hydrops

 Bilateral distension of the lower abdomen and an enlarged gravid uterus palpable on rectal
examination

Chronic or subacute traumatic reticuloperitonitis.

 The feces are usually firm and dry, the abdomen is gaunt and a mild fever may be present. A
laparotomy is necessary to make the diagnosis.
 Abdominocentesis may be useful.

RDA APPROACH
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PINGS IN RIGHT ABDOMEN

Dilatation and right-side displacement of the abomasum

 Ping is usually audible between the 9th and 12th ribs extending from the costochondral
junction of the ribs to their proximal third aspects.

Abomasal volvulus:

 Ping is larger than that of the rightside displacement and extends more cranially and
caudally. The ventral border of the ping area is horizontal because of the level of fluid within
the abomasum

Cecal dilatation:

 Ping is confined to the dorsal paralumbar fossa and caudal one or two intercostal spaces.

Intestinal obstruction:

 Presence of multiple, small areas of ping varying in pitch and intensity

Dilatation of descending colon and rectum:

 Ping in the right caudal abdomen just ventral to the transverse processes of the vertebrae

Pneumoperitoneum:

 Pings audible over a wide area of the dorsal third of the abdomen bilaterally.

TREATMENT

Medical therapy for mild cases

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 Empirical treatment with 500 mL of 25% calcium borogluconate IV.

 Offered good quality hay but no grain for 3-5 days and monitored daily.
 Surgical correction not be necessary if the appetite and movements of the alimentary tract
return to normal in a few days. The ping in the right abdomen may gradually become smaller
in 2-3 days and eventually disappear.
 The cow will usually not regain her appetite until the abomasal atony has been corrected.
 A combination of hyoscine-butyl bromide and dipyrone and fasting followed .

Deflation of distended abomasum in calves

 Gas is removed from a grossly distended (bloated) abomasum of calves as an emergency

measure.
 The calf is placed in dorsal recumbency and the abdomen is punctured with a 16 gauge 12 cm
hypodermic needle at the highest point of the distended abdomen between the umbilicus and
the xiphoid.
 fluid therapy is given

Surgical correction

 Right flank laparotomy for drainage of the distended abomasum and correction of the
volvulus is done
 Intensive fluid therapy is preoperatively and for several days postoperatively to correct the
dehydration, metabolic alkalosis and to restore normal abomasal motility.
 Rumen transplants to restore rumen function

Fluid and electrolyte therapy

 Dehydration, metabolic alkalosis, hypochloremia and hypokalemia ae present. Balanced

electrolyte solutions containing sodium, chloride, potassium, calcium and a source of
glucose are to be given.
 A mixture of 2 L of isotonic saline (0.85%), 1 L of isotonic potassium chloride (1.1%) and 1 L
isotonic dextrose (5%) given at the rate of 4-6 L/hour IV is also recommended and reliable.

Acidifying solutions

 Isotonic solutions -potassium chloride and ammonium chloride (KCI 108 g, NH4Cl 80 g,
H20 20 L) will correct the alkalosis. This solution can be given IV at the rate 20 L over 4
hours to a 450 kg cow. Followed by the use of balanced electrolyte solutions at the rate of 1
00-150 mL/kg BW over a 24 hour period.

Oral therapy

 A mixture of sodium chloride (50-100 g), potassium chloride (50 g) and ammonium chloride
(50-100 g) is given orally daily postoperatively along with the parenteral fluids

MODULE-9: DISEASES OF DIGESTIVE SYSTEM-IV

Learning objectives
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 In this section, enteritis in animals and megaoesophagus in dogs will be discussed.

ENTERITIS

 Gastric dilatation and volvulus, small intestinal bacterial overgrowth, megacolon, proctitis
and colitis will be discussed under this head

PATHOGENESIS

Mechanism of diarrhea

o Osmotic diarrhoea
o Exudative diarrhoea
o Secretory diarrhoea
o Abnormal intestinal motility

Osmotic diarrhoea

 Substances within the lumen of the intestine increase the osmotic pressure .
 E.g. saline purgatives, overfeeding indigestible feeds and disaccharides deficiencies.
Incomplete digestion and accumulation of large quantities of undigested material
 Epitheliotropic viruses E.g. TGF virus, rotavirus, and corona virus: selective destruction of
villous absorptive cells, villous atrophy loss of digestive and absorptive capacities, diarrhoea,
crypt hyperplasia and recovery.

Exudative diarrhea

 Acute or chronic inflammation or necrosis of the intestinal mucosa resulting in increase in

fluid production, inflammatory products, E.g diseases caused by bacteria, viruses, fungi,
protozoa, chemical agents and tumors. Salmonellosis, swine dysentery, bovine virus
diarrhoea and inorganic poisoning.

Secretory diarrhoea

 A secretory absorptive imbalance results in a large net increase in fluid secretion with
little structural change in the mucosal cells. The enterotoxin elaborated by E. coli results
in intestinal hypersecretion. The integrity of the mucosal structure is maintained and the
secreted fluid is isotonic electrolyte rich alkaline and free of exudates.

Abnormal intestinal motility

 Hyperexcitability, convulsions and the stress of unexpected sudden confinement may result
in diarrhea
 Reduced intestinal absorption due to rapid passage of intestinal fluids in an otherwise
normal intestines.

CLINICAL SIGNS
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 Major clinical finding is diarrhea.

 Dehydration, abdominal pain, septicemia and toxemia with fever.
 In acute enteritis, feces are soft or fluid in consistency and unpleasant odor.
 Contain blood, fibrinous casts and mucus/ foreign material –sand.
 Color of feces- pale yellow; sometimes frank blood; hematochezia or melena.
 Distribution of the feces on animal’s perineum:

Systemic changes

 Septicaemia, toxaemia and fever .

 Increase in body temperature, dehydration, tachycardia or bradycardia and arrhythmia.
 Abdominal pain in heavy inorganic metal poisoning and in acute salmonellosis.
 Increased peristalsis and fluid rushing sounds

Chronic enteritis

 Feces are soft homogenous in consistency,

 Considerable mucus and do not have abnormal odor.
 Progressive weight loss and runting are common.
 Hypoproteinemia and subcutaneous edema.
 In terminal ileitis there is usually chronic progressive weight loss and mild diarrhea.

CLINICAL PATHOLOGY

Clinical pathology

 Fecal examination -causative bacteria, helminthes, protozoa, viruses, and chemical agents.
 Necropsy on selected early-untreated cases of acute diarrhea,
moconcentration, metabolic acidosis, and decreases in plasma bicarbonate, hyponatremia, hypochloremia and hypo
 Digestion and absorption tests: for investigation of chronic malabsorptive conditions
 Intestinal biopsy for definitive diagnosis of lymphosarcoma, granulomatous enteritis and JD.

Last modified: Wednesday, 22 February 2012, 10:33 AM

TREATMENT

 Removal of the causative agent;

 Specific treatment - intestinal helminthiasis with anthelmintics, antiprotozoan agents against
diseases like coccidiosis and antimicrobial agents against bacterial enteritis.

Antimicrobials:

 Orally or parenterally or both. Oral preparation should not be used for more than 3 days
to avoid superinfection.
 Mass medication for the treatment of outbreaks of specific infectious enteritis.
 If the cause is dietary, the feed should be removed until the animal has fully recovered.

Intestinal protectants and adsorbents:

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 Kaolin and pectin mixtures

Antidiarrheal drug: antimotility drugs

Antisecretory drug: treatment of hypersecretory activity of enterotoxin. Loperamide hydrochloride.

Anti secretory drugs include chlorpromazine, opiates atropine and prostaglandin inhibitors.
Loperamide should not be given in cats.

Control

 Reduce infection pressure

 Ensure adequate non specific resistance by adequate colostrums intake
 Vaccinate for those diseases for which there is an effective vaccine
 Minimize Managemental and environmental stressors.

MEGAESOPHAGUS

 Megaesophagus refers to esophageal dilation and hypomotility.

 It can be a primary disorder or secondary to esophageal obstruction or neuromuscular
dysfunction.

Causes

 Congenital idiopathic megaesophagus

 Esophageal obstruction—esophageal foreign body, stricture, neoplasia, granuloma, vascular
ring anomalies (e.g., persistent right aortic arch), periesophageal compression
 Neurologic and neuromuscular diseases—myasthenia gravis (focal or generalized),
polymyositis (including systemic lupus erythematosus [SLE]),
polyneuritis/polyradiculoneuritis, botulism, dysautonomia, central nervous system (CNS)
disorders, degenerative, infectious/inflammatory, neoplasia, traumatic disorders of the
brainstem and spinal cord, bilateral vagal damage.
 Miscellaneous—esophagitis, hypothyroidism, hypoadrenocorticism, thymoma (with
secondarily acquired myasthenia gravis), toxicosis (lead, thallium,
acetylcholinesterase inhibitors)

PATHOPHYSIOLOGY

 Esophageal motility is decreased or absent,

 Resulting in accumulation and retention of food and liquid in the esophagus.
 Reflex esophageal motility begins when food stimulates sensory afferents in the esophageal
mucosa, which then sends afferent messages to the brainstem swallowing center via the
vagus nerve.
 Efferent messages from lower motor neurons in the nucleus ambiguus travel via the vagus to
stimulate contraction of esophageal striated and smooth muscle.
 Lesions anywhere along this pathway, including the myoneural junction, may result in
esophageal hypomotility and distention.

 Hereditary in wire-haired fox terriers and miniature schnauzers

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 Familial predispositions reported in the German shepherd, Newfoundland, Great dane, Irish
setter, Sharpei, Pug, Greyhound, and Siamese cats.
 Congenital megaesophagus—signs of regurgitation first appear at weaning
 Acquired forms—reported most often in young adults to middle-aged animals.

CLINICAL SIGNS

History

 Regurgitation of food and water

 weight loss or poor growth
 hypersalivation and
 a gurgling sound with swallowing
 coughing
 mucopurulent nasal discharge
 dyspnea with concurrent aspiration pneumonia

Clinical findings

 Occasionally normal
 regurgitation
 weight loss
 auscultation of retained fluid and food in the esophagus,
 halitosis
 ptyalism
 bulging of the esophagus at the thoracic inlet
 pain associated with palpation of the cervical esophagus
 respiratory crackles
 tachypnea
 pyrexia
 myalgia
 muscle weakness, muscle atrophy, hyporeflexia
 proprioceptive and postural deficits
 autonomic disorders (mydriasis with loss of pupillary light reflex
 dry nasal and ocular mucous membranes, diarrhea, bradycardia)
 cranial nerve deficits (especially cranial nerves VI, IX, and X)
 paresis or paralysis, and mentation changes.

RADIOGRAPH - MEGAOESOPHAGUS
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 Radiograph: Barium stasis in the oesophagus

DIAGNOSIS

Differential diagnosis

 Obstructive pharyngeal disease (foreign bodies, inflammation, neoplasia, cricopharyngeal

achalasia) and
 palate disorders may produce regurgitation with normal esophageal motility.
 Pharyngeal pain and dysphagia often occur with obstructive pharyngeal disease.

Laboratory investigation

 No characteristic findings
 Hyponatremia and hyperkalemia suggest hypoadrenocorticism.
 Hypercholesterolemia is usually present with hypothyroidism.
 Acetylcholine receptor antibody titers to screen for acquired myasthenia gravis
 Antinuclear antibody titers to evaluate for SLE
 ACTH stimulation to evaluate adrenal function
 Free T4/TSH level to evaluate thyroid function
 Blood lead and cholinesterase levels to evaluate for toxicity

Radiograph

 Survey Thoracic Radiographs

o Esophagus dilated with gas, fluid, or ingesta
o The trachea is often displaced ventrally by the distended esophagus.
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Other Diagnostic procedures

 Endoscopy—can use to visualize a dilated esophagus, foreign bodies, neoplasia, and

esophagitis;
 Fecal examination for Spirocerca lupi ova

TREATMENT

 Feeding in upright position (45–90° angle to the floor) and maintaining position for 10–15
min following feeding
 Feeding a gruel reduces regurgitation
 Patients with severe regurgitation are fed via gastrotomy tube
 There is risk of aspiration pneumonia
 Surgery may be necessary to remove esophageal foreign bodies or neoplasia or correct
vascular ring anomalies
 No drugs are commonly used to treat megaosophagus alone
 Treatment directed at the underlying disease or associated conditions (e.g., aspiration
pneumonia)
 Sucralfate (0.5–1.0 g/dog PO q8h), H2 blockers (e.g., famotidine 0.5 mg/kg PO q12–24h in
dogs) or omeprazole (0.7 mg/kg PO q24h in dogs) can be used if reflux esophagitis is
present
 Metoclopramide (0.2–0.5 mg/kg PO q6–8h in dogs)
 Broad-spectrum antibiotics—necessary for patients with aspiration pneumonia
 Immunosuppressive agents for immune-mediated diseases
 Prednisone and acetylcholinesterase inhibitors (pyridostigmine) are used to treat myasthenia
gravis
 Cisapride (0.1–0.5 mg/kg PO q8–12h in dogs)

MODULE-10: DISEASES OF DIGESTIVE SYSTEM-V

Learning objectives

 Gastric dilatation and volvulus, small intestinal bacterial overgrowth, megacolon, proctitis
and colitis will be discussed under this head

GASTRIC DILATATION AND VOLVULUS (GDV)

 A syndrome of dogs in which the stomach dilates and twists around its central
axis, resulting in complex local and systemic pathologic and physiologic
changes

 Can be due to pyloric outflow obstruction, gastric myoelectric abnormalities, dynamic

movement of the stomach following ingestion of food or water, and aerophagia.

 Activity following ingestion of large quantities of food or water

 Any intense activity or stress (including hospitalization and surgery)

PATHOPHYSIOLOGY
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 Fluid or ingesta accumulates in the stomach (due to a mechanical or functional obstruction

of the gastroesophageal and pyloric orifices)
 Twisting of the stomach may occur without dilation.
 The stomach twists in a clockwise or counterclockwise direction.
 Direct gastric damage and multiple systemic abnormalities occur secondary to ischemia and
reperfusion injury.
 Acute clinical signs, which include hypovolemic shock and cardiovascular failure.
 Reperfusion injury

CLINICAL SIGNS

History

 Nonproductive retching
 Ptyalism
 Progressive abdominal distension
 Weakness or collapse
 Depression
 Frequent belching

Clinical Findings

 Tympanic cranial abdomen

 Tachycardia
 Tachypnea
 Rectal body temperature may vary widely.
 Signs of hypovolemic shock

DIAGNOSIS

Differential diagnosis

 Gastric dilation without torsion—due to overdistension, usually from ingesting excessive

quantities of food
 Intestinal volvulus
 sSplenic torsion
 Abdominal effusion or
 Haemorrhage
 Non-GDV conditions

Laboratory findings

 Expect hemogram abnormalities consistent with acute inflammation and

hemoconcentration/shock
 Electrolyte abnormalities and acid–base alterations are common.
 high urine specific gravity

Imaging
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 Abdominal radiography—a “double bubble” compartmentalized stomach is considered

pathognomonic.
 Dorsoventral view—the pylorus may be shifted toward, or located in, the left cranial
abdomen.

Diagnostic procedures

 Abdominocentesis and cytology may help determine if perforation has occurred.

TREATMENT

 Shock/fluid therapy == isotonic fluids at the rate of 90 mL/kg within the first 30–60 min
 Use of colloid solutions to restore cardiorespiratory function.
 gastric decompression by orogastric intubation
 Decompression by trocarization and indwelling catheters
 Immediate surgery is indicated in patients unresponsive to cardiorespiratory stabilization
and in all patients following successful stabilization.
 Severely restrict activity prior to surgery and for a minimum of 10–14 days postsurgery

 Corticosteroids such as dexamethasone sodium phosphate (5 mg/kg slow IV) or

prednisolone sodium succinate (22 mg/kg slow IV
 Cefazolin sodium (20–35 mg/kg IV q8h or every 2 h interoperatively) or cefoxitin sodium
(30 mg/kg IV q6–8h).
 H2-receptor antagonists may ameliorate or prevent gastric ulceration (e.g., famotidine 0.5
mg/kg IV or PO q12–24h; ranitidine 1.0 mg/kg IV or PO q12h).

SMALL INTESTINAL BACTERIAL OVERGROWTH (SIBO)

 An increased number of bacteria in the small intestine causes small intestinal dysfunction
 Almost any bacteria may be responsible
 SIBO differs from colonization of the alimentary tract by known pathogenic bacteria with
virulence factors (i.e., Salmonella spp., Campylobacter jejuni, etc.) or overgrowth of
toxigenic Clostridium perfringens in the colon.

ETIOLOGY

 Idiopathic
 Altered small intestinal anatomy—blind or stagnant loops, partial obstruction
 Exocrine pancreatic insufficiency (EPI)
 Hypochlorhydria or achlorhydria—spontaneous or iatrogenic
 Immunodeficiency and preexisting intestinal disease—suggested, but unproven

PATHOPHYSIOLOGY

 When the natural defenses fail and excessive bacteria persist in the upper small intestine,
 Because the species and numbers of bacteria in the small intestine may vary between and
even within patients, pathophysiology is not consistent.
 Purported mechanisms include deconjugation of bile acids, dehydroxylation of fatty acids,
formation of alcohols, and destruction of brush border enzymes.
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 Anaerobic bacteria (e.g., Bacteroides spp. and Clostridium spp.) have been considered more
likely to cause pathology than many aerobic bacteria; SIBO can cause protein-losing
enteropathy.

SIGNS

 Weight loss may occur despite a reasonable appetite—principal sign

 Small bowel diarrhea (e.g., no mucus or blood in the feces, no tenesmus)—common
 Vomiting and borborygmus—occasional/variable
 May wax and wane or be consistent
 May be evidence of diarrhea
 Intestinal thickening is unexpected unless other infiltrative intestinal disease is also present.
 Signs typical of infection (i.e., fever, depression) are unexpected.

DIAGNOSIS

Differential diagnosis

EPI - Exocrine pancreatic insufficiency

Malabsorption due to any cause—

 IBD- InflammatoryBowel Disease

 alimentary lymphoma,
 lymphangiectasia,
 dietary intolerance/allergy,
 giardiasis,
 IBD may mimic and/or be associated with SIBO.
 Intestinal parasites (especially Giardia)

Laboratory investigations

 Hypoalbuminemia—rare;
 Quantitated Culture
o Aerobic and anaerobic bacteria from fasted, upper intestinal fluid—the “gold
standard”

TREATMENT

 Highly digestible, restricted in fat

 Antigen-restricted diets recommended if concurrent dietary intolerance/allergy is suspected.
 Broad-spectrum, orally administered antibiotics effective against both aerobic and anaerobic
bacteria are preferred.
 Tetracycline (20 mg/kg PO q12h)—good initial choice;
 Tylosin (40–80 mg/kg/day PO divided q12h)
 Amoxicillin (20 mg/kg PO q12h) or amoxcillin with clavulanate (22 mg/kg PO q12h)—
 Metronidazole (10–15 mg/kg PO q12h)
 Drugs that do not kill anaerobic bacteria (e.g., neomycin) may be less effective.
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MEGACOLON

 A condition of persistent increased large bowel diameter associated with chronic

constipation/obstipation and low-to-absent colonic motility.

ETIOLOGY

1. Idiopathic—cats
2. Mechanical obstruction—pelvic fracture malunion, foreign body or improper diet,
stricture, pseudocoprostasis, prostatic disease, perineal hernia, neoplasia, anal or rectal
atresia
3. Causes of dyschezia—anorectal disease, trauma
4. Metabolic disorders—hypokalemia, severe dehydration
5. Drugs—vincristine, barium, antacids, sucralfate, anticholinergics
6. Neurologic/neuromuscular disease—congenital abnormalities of the caudal spine,
paraplegia, spinal cord disease, intervertebral disk disease, dysautonomia, sacral nerve
disease, sacral nerve trauma, trauma to colonic innervation

Risk factors

 Conditions leading to inability to posture or rectoanal pain

 Prior pelvic fractures
 Possible association with low physical activity and obesity
 Perineal hernias

PATHOPHYSIOLOGY

 Acquired megacolon results from chronic retention of fecal material that leads to
colonic absorption of fecal water and solidified fecal concretions.
 Prolonged distension of the colon results in irreversible changes in colonic motility that leads
to colonic inertia.

CLINICAL SIGNS

 Idiopathic megacolon—typically a chronic/recurrent problem; signs often present for months

to years.
 Constipation/obstipation
 Tenesmus with small or no fecal volume
 Hard, dry feces
 Infrequent defecation
 Small amount of diarrhea (often mucoid) may occur after prolonged tenesmus.
 Weight loss
 Abdominal palpation reveals an enlarged colon with a hard fecal mass.
 Dehydration

DIAGNOSIS

Differential diagnosis
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 Lymphoma,
 Carcinoma,
 Intussusception
 Dysuria/stranguria
 Colitis

Laboratory investigation

 Elevated packed cell volume, total protein and stress leukogram

 Electrolyte abnormalities
 Urinalysis—to confirm normal renal function in dehydrated animals and to rule out lower
urinary tract disease as a differential diagnosis

Imaging

 Abdominal/pelvic radiographs
 Enlarged, fecal-filled colon on plain abdominal radiographs
 Abdominal ultrasound
 Colonoscopy to rule out mural or intraluminal obstructive lesions

TREATMENT

 Manual evacuation of the colon using warm water enemas, water-soluble jelly, and gentle
extraction of feces with a gloved finger or sponge forceps;
 Most patients require parenteral fluid support to correct dehydration.
 Encourage activity and exercise.
 Many patients require a low-residue-producing diet; bulk-forming fiber diets can worsen or
lead to recurrence of colonic fecal distension.
 A high-fiber diet is occassionally helpful.
 Cisapride, a prokinetic GI drug (dogs, 0.1–0.5 mg/kg PO q8–12h; cats, 2.5–10.0 mg/cat q8–
12h)
 Stool softeners (e.g., lactulose, 1 mL/4.5 kg PO q8–12h to effect)
 Broad-spectrum prophylactic antibiotics

COLITIS AND PROCTITIS

Definition

 Colitis—inflammation of the colon

 Proctitis—inflammation of the rectum

ETIOLOGY

 Infectious—Trichuris vulpis, Ancylostoma caninum, Entamoeba histolytica, Balantidium

coli, Giardia spp., Trichomonas spp., Cryptosporidium spp., Salmonella spp, Clostridium
spp., Campylobacter spp., Yersinia enterocolitica, Escherichia coli, Prototheca,
Histoplasma capsulatum, and pythiosis/phycomycosis
 Traumatic—foreign body and abrasive material
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 Uraemia
 Segmental—secondary to chronic pancreatitis (transverse colitis)
 Allergic—dietary protein and possibly bacterial protein
 Inflammatory/immune—lymphoplasmacytic, eosinophilic, granulomatous, and histiocytic

PATHOPHYSIOLOGY

 Inflammation of the colon causes accumulation of inflammatory cytokines, disrupts tight

junctions between epithelial cells, stimulates colonic secretion, stimulates goblet cell
secretion of mucus, and disrupts motility.
 These mechanisms reduce the ability of the colon to absorb water and store feces; which
causes frequent diarrhea, often with mucus or blood.

CLINICAL SIGNS

Historical Findings

 Feces vary from semiformed to liquid

 High frequency of defaecation with small fecal volume
 Often demonstrate prolonged tenesmus after defecation
 Chronic diarrhea often with mucus or blood; cats may have formed feces with hematochezia.
 Vomiting in dogs
 Weight loss is rare.

DIAGNOSIS

Differential diagnosis

 Neoplasia—lymphoma and adenocarcinoma

 Irritable bowel syndrome
 Rectocolonic polyps
 Cecal inversion
 Ileocecocolic intussusception

CBC/Biochemistry/Urinalysis

 Results usually normal; neutrophilia with a left shift is possible; eosinophilia occasionally
observed in eosinophilic colitis, parasitism, and pythiosis/phycomycosis
 Mild microcytic, hypochromic anemia may occur in some patients with persistent bleeding.
 Rare hyperglobulinemia in some patients (especially cats) with chronic disease.

Other laboratory tests

 Examination of fecal floatation, direct fecal smear, bacterial culture, or fungal culture
(Pythium) may reveal an infectious cause.
 Feces may test positive for Clostridium perfringens toxin.
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Imaging

 Abdominal radiographs—usually normal

 Barium enema—may reveal mucosal irregularities or filling defects in severely affected
patients, but this procedure is time-consuming and not cost-effective
 Abdominal ultrasonography—may reveal masses, diffuse thickening, or altered architecture;
can perform guided biopsies or fine-needle aspiration

Other diagnostic procedures

 Colonoscopy with biopsy—technique of choice for diagnosis; may see disappearance of

submucosal blood vessels, granular appearance of mucosa, hyperemia, excessive mucus,
ulceration, pinpoint hemorrhage (small ulcerations), or mass
 Always take multiple biopsy specimens because the extent of mucosal change does not
necessarily reflect severity or absence of disease.

Pathologic findings

 Gross findings as described

 Histopathologic findings depend on the histologic type of colitis—lymphoplasmacytic,
eosinophilic, granulomatous, or histiocytic; hyperplastic mucosa may be seen with irritable
bowel syndrome; various infectious agents may be seen with special stains.

TREATMENT

Appropriate health care

 Outpatient medical management unless diarrhea is severe enough to cause dehydration.

Nursing care

 Give dehydrated patients balanced electrolyte solution with potassium, intravenously,

subcutaneously, or orally.

Diet

 Patients with acute colitis can be fasted for 24–48 h.

 Try a hypoallergenic diet in patients with inflammatory colitis; use a commercial or home-
prepared diet that contains a protein to which the dog or cat has not been exposed.
 Fiber supplementation with poorly fermented fiber (e.g., bran and a -cellulose) is
recommended to increase fecal bulk, improve colonic muscle contractility, and bind
fecal water to produce formed feces.
 Some fermentable fiber (e.g., psyllium or a diet containing beet pulp or
fructooligosaccharides) may be beneficial—short-chain fatty acids produced by fermentation
may help the colon heal and restore normal colonic bacterial flora.

Client education
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 Treatment may be intermittent and long-term in patients with inflammatory/immune

colitis, and repeated recurrence is seen in some cases, especially those with the histiocytic
and granulomatous forms.
 Granulomatous and histiocytic colitis, pythiosis/phycomycosis, and protothecal colitis
respond poorly to medical treatment; surgery may be necessary.

Surgical considerations

 Segments of colon severely affected by fibrosis from chronic inflammation and subsequent
stricture formation may need surgical excision, especially in patients with the granulomatous
form of the disease; cecal inversion, ileocecocolic intussusception require surgical
intervention; pythiosis/phycomycosis often requires surgical excision or debulking.

Medications - Drugs of choice

 Antimicrobial Drugs
o Trichuris, Ancylostoma , and Giardia—fenbendazole (50 mg/kg PO q24h for 3 days,
repeat in 3 months)
o Entamoeba, Balantidium, Giardia , and Trichomonas—metronidazole (25 mg/kg PO
q12h for 5–7 days)
o Salmonella —treatment is controversial because a carrier state can be induced; in
patients with systemic involvement, choose the antibiotic on the basis of bacterial
culture and sensitivity testing (e.g., enrofloxacin, chloramphenicol, or trimethoprim-
sulfa).
o Clostridium —metronidazole (10–15 mg/kg PO q12h for 5–14 days) or tylosin (10–15
mg/kg PO q12h for 7 days)
o Campylobacter —erythromycin (30–40 mg/kg PO q24h for 5 days) or tylosin (45
mg/kg PO q24h for 5 days)
o Yersinia and E. coli—choose the drug on the basis of bacterial culture and sensitivity
testing
o Prototheca —no known treatment
o Histoplasma —itraconazole (dogs, 5 mg/kg PO q24h; cats, 5 mg/kg PO q12 h; several
months of therapy is necessary); amphotericin B (0.25–0.5 mg/kg slow IV q48h up
to cumulative dose of 4–8 mg/kg) in advanced cases
o Pythiosis/phycomycosis—ABLC (dilute in 5% dextrose to 1 mg/mL, give 3 mg/kg IV
Monday-Wednesday-Friday for 9 treatments)
 Antiinflammatory and Immunosuppressive Drugs for Inflammatory/Immune Colitis
o Sulfasalazine (dogs, 25–40 mg/kg PO q8h for 2–4 weeks; cats, 20 mg/kg PO q12h for
2 weeks)
o Corticosteroids—prednisone (dogs, 1–2 mg/kg PO q24h; cats, 2–4 mg/kg PO q24h;
taper dosage slowly over 4–6 months once clinical remission is achieved)
o Azathioprine (dogs, 1 mg/kg PO q24h for 2 weeks followed by alternate-day
administration; cats, 0.3 mg/kg PO q24h for 3–4 months)
o Sulfasalazine—drug of choice for plasmacytic lymphocytic colitis
o Prednisone and azathioprine are indicated only in eosinophilic colitis
and severe plasmacytic lymphocytic colitis that does not respond to sulfasalazine
o Reexamine the diagnosis carefully in dogs that do not respond to sulfasalazine
treatment in 4 weeks; the need for chronic maintenance therapy means that an
underlying cause (e.g., C. perfringens infection) may have been missed.
 Motility Modifiers (Symptomatic Relief Only)
o Loperamide (0.1 mg/kg PO q8–12h)
o Diphenoxylate (0.1–0.2 mg/kg PO q8h)
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o Paregoric (0.06 mg/kg PO q8–12h)

o Propantheline bromide (0.25–0.5 mg/kg PO q8h) if colonic spasm is contributing to
clinical signs

MODULE-11: DISEASES OF DIGESTIVE SYSTEM-VI

Learning objectives

 Colic in horses wll be discussed in this section.

COLIC IN HORSE

 Gastrointestinal diseases causing signs of abdominal pain in horses

 It is frequent and one of the main cause of the death in horses.
 It may be acute, chronic or recurrent.

Etiology

 Impaction of stomach or intestine

 Mural or extramural blockage of stomach or intestine
 Dilatation of stomach or intestine
 Intestinal spasms
 Paralytic ileus
 Gastric reflux
 Peritonitis and other inflammatory conditions of stomach or intestine
 Verminous arteritis of mesenteric vessels
 Intusususception
 Torsion or strangulation of intestine

PATHOGENESIS

 In obstructive type there will be reduced flow of ingesta with subsequent distention and pain
and in severe cases ischemia and rupture of the part.
 Endotoxaemia due to intestinal stasis and cardiovascular collapse
 Pain due to distention and following gastrointestinal dysfunction, impairment of barrier
function of intestine, ischemia of intestinal wall, endotoxaemia and hypovolemia resultng in
cardiovascular collapse, shock and death.

CLINICAL SIGNS

 Signs of abdominal pain

 Flank watching, flank biting
 Pawing and frequent lying down
 Kicking at the abdomen
 Protrusion of penis
 Sham drinking of water
 ‘Saw horse’ stance
 Frequent attempts of urinate and defecate and rolling
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 Tachycardia
 Polypnoea
 Tympanic gut sounds
 Abdominal distention
 Cool extremities and frequent sweating in severe cases
 Pinging sound in combined auscultation and percussion of intestinal area.
 Colonic impaction, distention or displacement on per rectal examination

CLINICAL DIAGNOSIS

Clinical pathology

 Hemoconcentration
 Azotemia
 Metabolic acidosis
 Increased total protein concentration in peritoneal fluid.

Diagnosis

 Clinical signs
 Ultrasonography
 Radiology

Differential diagnosis

 Laminitis
 Pleuritis
 Enterocolitis
 Rhabdomyolysis
 Obstructive urolithiasis
 Uroperitoneum
 Uterine torsion
 Peritonitis
 Cholelithiasis
 Ovulation and ovarian pain
 Esophageal obstruction
 Proximal enteritis
 Gastric ulceration
 Anthrax testicular torsion
 Lactation tetany
 Tetanus
 Rabies
 Botulism
 Grass sickness
 Psychogenic colic

TREATMENT

 Treatment of each case of colic varies according to nature and severity.

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 Principles of treatment involves

o Provision of analgesia (NSAIDS or opiates)
o Correction of fluid – electrolyte and acid base abnormalities.
o Gastrointestinal lubrication and administration of stool softners
o Treatment of underlying disease.
o Trocarisation and surgical treatment.

MODULE-12: DISEASES OF DIGESTIVE SYSTEM-VII

Learning objectives

 Traumatic pericarditis in cattle will be discussed in this section.

TRAUMATIC RETICULO PERITONITIS

 Traumatic reticulo peritonitis, is caused by the ingestion and migration of a foreign body in
the reticulum.
o Cattle are more likely to ingest foreign bodies than small ruminants.
o Foreign body may be metallic object, such as a piece of wire or a nail, often
greater than 2.5 cm in length.
o The majority of affected cattle are dairy cattle and are older than 2 years of age.
o A large number of adult dairy cattle have metallic foreign bodies in their
reticulum without signs of clinical disease.
o Tenesmus or a gravid uterus, causes migration of the foreign body into the reticular
wall

CLINICAL SIGNS

 Signs of acute, localized peritonitis including anorexia, fever, tachypnea, and an arched
stance with abducted elbows
 Muffled heart sounds, jugular pulses, and brisket edema secondary to congestive heart
failure caused by pericarditis
 A significant population of affected cattle develops chronic or subclinical TRP that is not as
easily diagnosed as acute TRP.
 Clinical signs associated with chronic peritonitis include anorexia, unthriftiness,
decreased milk production, rumen hypomotility, and a change in manure consistency.
 The most appropriate laboratory tests for diagnosing TRP are the complete blood count
(CBC), serum biochemical profile, and abdominocentesis.

CLINICAL PATHOLOGY

Complete blood count

 Cattle with persistent purulent inflammation have leukocyte counts ranging from 4,000-
15,000/µL, with neutrophilia.
 A degenerative left shift (band neutrophils outnumbering segmented neutrophils).
Cattle with acute diffuse peritonitis will also have a degenerative left shift. In chronic
cases, a mature neutrophilia is common.
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 Neutrophil counts in these individuals are often greater than 4,000/µL. Affected cattle also
will show hyperfibrinogenemia, with fibrinogen concentrations greater than 1,000 mg/dL.
 Fibrinogen is an acute phase protein, and in cattle it may be the best indicator of acute
inflammation because fibrinogen concentrations often increase prior to development of
neutrophilia.
 Hematology data can be used to detect inflammation, but generally cannot identify a specific
cause of inflammatory disease. Other tests may be useful in differentiating between different
inflammatory diseases, such as TRP

Serum biochemical profile

 The most common chemistry abnormality associated with TRP is hyperproteinemia with a
hyperglobulinemia. Some authors suggest that a total serum protein concentration greater
than 10 mg/dL is highly suggestive of TRP.
 In one study of cattle suspected of having TRP that also had a total plasma protein
concentration of 100 g/L (10mg/dL) had an 83% chance of having TRP, 83% of the cattle
with a total plasma protein concentration of 10 mg/dL had TRP.
 Other chemistry abnormalities associated with TRP may include hypochloremia,
hypokalemia, and metabolic alkalosis; these abnormalities occur secondary to ruminal
hypomotility and/or vagal indigestion. Hypochloremic metabolic alkalosis may occur due to
sequestration of hydrochloric acid in the rumen caused by rumen stasis or vagal indigestion.
 Hypokalemia is caused primarily by anorexia, but may be potentiated slightly by ion
exchange caused by the alkalosis and/or abomasal reflux into the rumen. With alkalosis,
intracellular H+ ions can be exchanged for extracellular K+ ions, decreasing serum potassium
concentrations. This effect is minor compared to the K+ ion shifts associated with acidosis.

Abdominocentesis

 Normal peritoneal fluid of an adult cow is straw-colored, clear, and odorless. Protein and
fibrinogen concentrations can vary from 1.0-3.0 g/dL and 100-500 g/dL, respectively. The
nucleated cell count should be less than 10,000 cells/µL.
 The majority of nucleated cells are non-degenerate neutrophils and mononuclear cells.
 Turbid samples or samples containing gross pus or fibrin are indicative of peritonitis.
 It is, however, normal for bovine peritoneal fluid to clot upon standing. Nucleated cell count,
cell percentages, and character of cells present are suggestive of disease.
 If a sample contains immature, degenerative, or toxic neutrophils purulent peritonitis is
present.
 Purulent peritonitis is indicated by an abdominal fluid sample with greater than 40%
neutrophils. The presence of intracellular bacteria and/or degenerate neutrophils indicates
septic peritonitis.

DIFFERENTIAL DIAGNOSIS

 Other causes of peritonitis or abdominal pain for a definitive diagnosis.

 Perforating abomasal ulcer.
 Indigestion
 Ketosis.

TREATMENT AND PREVENTION

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Treatment

 Reticular foreign bodies often migrate back into the lumen of the reticulum,
conservative treatment can have good results.
 Conservative treatment: instillation of a magnet to recover or immobilize the metal foreign
body
 Affected cattle should be administered with systemic antibiotic for 3-7 days (penicillin,
ceftiofur, ampicillin, or tetracycline).
 Stall rest and other supportive therapy
 Re-evaluated in 48-72 hours.
 An exploratory laparotomy/rumenotomy is indicated for removal of the foreign body.

Prevention

 Cattle should be kept away from construction sites

 Crop fields should be monitored for metal debris.
 Processed feed passed over magnets to recover any magnetic foreign bodies prior to being fed
to cattle.

MODULE-13: DISEASES OF PERITONEUM

Learning objectives

 Peritonitis and ascites will be discussed under this head.

PERITONITIS

 Inflammation of the peritoneum is accompanied by abdominal fever, toxaemia and reduction

in the amount of feces.

Etiology

 Peritonitis occur as a primary disease or secondarily as part of an etiologically specific

disease.
 Primary disease – it results most commonly from injury of the serosal surfaces of
the alimentary tract within the abdomen.

ETIOLOGY

Cattle

 TRP
 Perforation or leakage of abomasal ulcer
 Necrosis and rupture of abomasal wall after abomasal volvolus
 Rumenitis of cattle
 Complication of caesarean section
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 Rupture of vagina during coitus

 Deposition of semen into the peritoneum
 Chemical peritonitis
 Transection of small intestine
 Intraperitoneal injection of non-sterile solutions
 Spontaneous uterine rupture during parturition or dystocia
 Sadistic rupture of vagina
 Spontaneous rupture of rectum at calving
 As part of specific disease such as tuberculosis.

Horses

 Secondary to infectious chemical or parasitic peritoneal injuries

 Complication after abdominal surgery
 Rupture of dorsal sac of cecum or colon at foaling
 Cecal rupture in foals subjected to anaesthesia and gastric endoscopy
 NSAID
 Rectal rupture or tear
 Extension from a retroperitoneal infection
 Gastric erosion or rupture related to ulceration
 Leakage from a cecal perforation
 Spontaneous gastric rupture

Pigs

 Ileal perforation
 Haemophilus suis

Sheep:

 Spread from intestinal wall

 Serositis- arthritis
 Faulty asepsis at laparotomy, peritoneal injection trocarization for tympany of rumen or
cecum
 Leakage through wall infracted gut segment

PATHOGENESIS

Toxaemia and septicemia

 Toxins produced by bacteria are absorbed readily through the peritoneum. Toxaemia is
important factor in the production of clinical illness

Acute diffuse peritonitis

 Toxaemia is profound
 Endotoxic shock due to absorption of toxins from the gut contents.
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 Cows which suffer penetration of the reticular wall at calving

Shock and hemorrhage

 The shock by sudden deposition of gut contents or infected uterine contents into the
peritoneal cavity
 Hemorrhage resulting from the rupture are significant contributors

Abdominal Pain

 Animal adopts an arched back posture

 Shows evidence of pain on palpation of the abdominal wall.
 Humped up posture

Paralytic ileus

 Reflex inhibition of alimentary tract tone and movement.

 Sequel to intestinal obstruction and to traumatic abdominal surgery.
 The net effect is functional obstruction of the intestine and complete absence of feces.
 Accumulation of fluid exudates.

Adhesions

 Trauma results in serosanguineous exudates, which contain fibrinogen and plasminogen.

 Intraabdominal fibrin deposition and adhesion formations

CLINICAL FINDINGS

Acute and subacute peritonitis

 Inappetence and anorexia

 Toxaemia usually with a fever
 Increase in heart rate and respiratory rates.
 Grunting at the end of each expiratory movements.
 The feces are characteristically scant dark and like small fecal balls accompanied by thick
jelly like mucus.
 The feces may alternatively have a thick sludge like consistency and be tenacious and difficult
to remove a rubber glove and have foul smell.
 In acute peritonitis, ruminal contractions are reduced or absent while in chronic peritonitis
the contractions are weaker than normal.
 Intestinal stasis – absence of intestinal peristaltic sounds on auscultation.
 Disinclination to move, disinclination to lie down, lying down with great care and
grunting with pain.
 Arched back, gait is shuffling and cautious with the back held rigid and arched.
 Grunting at each step and during urination and defecation.
 Sudden movements are avoided and there is absence of kicking or bellowing or licking the
coat
 Pinching of withers, pole test is positive
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 Can palpate distended saggy thick walled loops of intestine in some cases.

Peracute diffuse peritonitis

 Profound toxaemia.
 There is severe weakness, depression and circulatory failure.
 Recumbent, subnormal temperature, high heart rate and weak pulse.
 No abdominal pain is evidenced spontaneously or on palpation of the abdominal wall.

Chronic peritonitis

 Adhesions
 Chronic syndrome of indigestion and toxaemia

DIAGNOSIS

Leukopenia neutropenia and degenerative left shift in acute diffuse peritonitis.


 There is toxic granulation of neutrophils.
 Normal total leukocyte count or slight increase with regenerative left shift- In acute local peritonitis
and differential count may be normal or there may be leukocytosis with marked neutrophilia and in increase in tota
lymphocytes and monocytes In chronic
 Analysis of peritoneal fluid

Diagnosis

Abnormal feces – in amount and composition


 Alimentary tract stasis
 Abdominal pain
 Abnormalities of intestine on rectal examination
 Fibrinous or fibrous adhesions on rectal e examination
 Abnormal peritoneal fluid with an increased leukocyte count collected by paracentesis
 Normal or low blood leukocyte count with a degenerative left shift

TREATMENT

 Antimicrobials: broad spectrum antibiotics IV or IM ;

 Administration of antimicrobials into the peritoneal cavity.
 Fluid and electrolyte
 NSAID flunixin meglumine- 0.25 to 1.1 mg /kg BW every 8-12 hrs
 Lavage: peritoneal lavage with large volumes of fluid containing antimicrobials

ASCITES
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 The escape of fluid, either transudate or exudate, into the abdominal cavity between the
parietal and visceral peritoneum
 Ascites can be caused by the following:
o CHF and associated interference in venous return
o Depletion of plasma proteins —protein-losing nephropathy or enteropathy
o Obstruction of the vena cava or portal vein, or lymphatic drainage due to neoplastic
occlusion
o Overt neoplastic effusion
o Peritonitis—infective or inflammatory
o Electrolyte imbalance, especially hypernatremia
o Liver cirrhosis

CLINICAL SIGNS

Signalment

 Dogs and cats

 No species or breed predisposition

Signs

 Episodic weakness
 Lethargy
 Abdominal fullness
 Abdominal discomfort when palpated
 Dyspnea from abdominal distension or associated pleural effusion
 Anorexia
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 Vomiting
 Weight gain
 Scrotal or penile edema
 Groaning when lying down

ICTERUS
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DIFFERENTIAL DIAGNOSIS

 Differentiating Abdominal Distension Without Effusion

 Organomegaly—hepatomegaly, splenomegaly, renomegaly, and hydrometra
 Abdominal neoplasia
 Pregnancy
 Bladder distension
 Obesity
 Gastric dilatation
 Differentiating Diseases
 Transudate—nephrotic syndrome, cirrhosis of liver, right-sided CHF, hypoproteinemia, and
ruptured bladder
 Exudate—peritonitis, abdominal neoplasia, and hemorrhage

CLINICAL PATHOLOGY

CBC/Biochemistry/Urinalysis

 Neutrophilic leukocytosis occurs in patients with systemic infection.

 Albumin is low in patients with impaired liver synthesis, gastrointestinal loss, or renal loss.
 Cholesterol is low in patients with impaired liver synthesis

Liver Enzymes

 Low to normal in patients with impaired liver synthesis

 High in patients with liver inflammation, hyperadrenocorticism, gallbladder obstruction, and
chronic passive congestion

Total and Direct Bilirubin

 Low to normal in patients with impaired liver synthesis

 High in patients with biliary obstruction caused by tumor, gallbladder distension, or
obstruction

BUN and Creatinine

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 High in patients with renal failure

 BUN low in patients with impaired liver synthesis or

hyperadrenocorticism Glucose- Low in patients with impaired liver synthesis

Other laboratory tests

 To detect proteinuria—urinary protein:creatinine ratio (normal < 0.5:1)

ASCITIC FLUID EVALUATION

 Exfoliative cytologic examination and bacterial culture and antibiotic sensitivity—remove

approximately 3–5 mL of abdominal fluid via aseptic technique.

Transudate

 Clear and colorless

 Protein < 2.5 g/dL
 Specific gravity < 1.018
 Cells < 1000/mm3—neutrophils and mesothelial cells

Modified Transudate

 Red or pink; may be slightly cloudy

 Protein 2.5–5.0 g/dL
 Specific gravity > 1.018
 Cells < 5000/mm3—neutrophils, mesothelial cells, erythrocytes, and lymphocytes

Exudate (Nonseptic)

 Pink or white; cloudy

 Protein 2.5–5.0 g/dL
 Specific gravity > 1.018
 Cells 5,000–50,000/mm3—neutrophils, mesothelial cells, macrophages, erythrocytes, and
lymphocytes

Exudate (Septic)

 Red, white, or yellow; cloudy

 Protein > 4.0 g/dL
 Specific gravity > 1.018
 Cells 5,000–100,000/mm3—neutrophils, mesothelial cells, macrophages, erythrocytes,
lymphocytes, and bacteria

Hemorrhage

 Red; spun supernatant clear and sediment red

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 Protein > 5.5 g/dL

 Specific gravity 1.007–1.027
 Cells consistent with peripheral blood
 Does not clot

Chyle

 Pink, straw, or white

 Protein 2.5–7.0 g/dL
 Specific gravity 1.007–> 1.040
 Cells < 10,000/mm3—neutrophils, mesothelial cells, and large population of small
lymphocytes
 Other—fluid in tube separates into creamlike layer when refrigerated; fat droplets stain with
Sudan III.

Pseudochyle

 White
 Protein > 2.5 g/dL
 Specific gravity 1.007–1.040
 Cells < 10,000/mm3—neutrophils, mesothelial cells, and small lymphocytes
 Other—fluid in tube does not separate into creamlike layer when refrigerated; does not
stain with Sudan III.

Urine

 Clear to pale yellow

 Protein > 2.5 g/dL
 Specific gravity 1.000–> 1.040
 Cells 5,000–50,000/mm3—neutrophils, erythrocytes, lymphocytes, and macrophages
 Other—if the urinary bladder ruptured < 12 h before, urinary glucose and protein could be
negative; if bladder ruptured > 12 h before, urine becomes a dialysis medium with
ultrafiltrate of plasma, and urine contains glucose and protein.

Bile

 Slightly cloudy and yellow

 Protein > 2.5 g/dL
 Specific gravity > 1.018
 Cells 5,000–750,000/mm3—neutrophils, erythrocytes, macrophages, and lymphocytes
 Other—bilirubin confirmed by urine dipstick; nonicteric patient may have gallbladder
rupture, biliary tree leakage, or rupture in the proximal bowel.

SPECIAL INVESTIGATION

ECG

 May reveal Reduced R amplitude suggestive of fluid accumulation

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 Chamber enlargement

ECG - Reduced R ECG- Deep S wave ECG- Deep Q wave

amplitude
Imaging

 Thoracic and abdominal radiography is sometimes helpful.

 Left: Radiograph of thorax and abdomen -cardiomegally and ascites

 Right : Radiograph of the abdomen- ascites- typical ground glass appearance
 Ultrasonography of the liver, spleen, pancreas, kidney, bladder, and abdomen can
often determine cause.
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Ultrasonogram of the abdomen: Liver lobe and ascitic fluid

Ultrasonogram of the abdomen: Liver tumour and ascites

Ultrasonogram of the liver showing hepatic congestion

TREATMENT
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 If patients are markedly uncomfortable or become more dyspneic with stress, removal of
fluid is done.
 Dietary salt restriction may help control transudate fluid accumulation due to CHF, cirrhosis,
or hypoproteinemia.
 Corrective surgery is often indicated, followed by specific therapeutic management (e.g.,
patient with splenic tumor: tumor removed, abdominal bleeding controlled, blood
transfusion administered).

Dog with ascites

Before Treatment After Treatment

Before Treatment After Treatment

SPECIFIC TREATMENT

Medications - Drugs and Fluids

 Lactated Ringer's solution or 0.9% NaC with KCl (20-30 mEq/L) and B-complex vitamins (2
ml/L) added. Glucose should be added if hypoglycemia is present.
 For Hepatic Encephalopathy
o Lactulose (1 ml/kg PO q8h)
o Antibioticsmetronidazole (7.5 mg/kg PO q8h), ampicillin (20 mg/kg PO q8h),
or neomycin (20 mg/kg PO q8h)
 For Ascites
o Sodium: restricted diet
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o Diuretics: spironolactone (1-2 mg/kg PO q12h) or furosemide (1-2 mg/kg PO q12h)

o Repeated abdominocentesis in patients refractory to diet and diuretics
 For Hemorrhage
o Fresh whole blood transfusion.
 For Fibrosis
o Prednisone (1 mg/kg PO q24h-q48h)
o Colchicine (0.03 mg/kg PO q24h)
o d-penicillamine (10-15 mg/kg PO q12h)
 Altered Bile Acid Dynamics
o Ursodiol (10-15 mg/kg PO q24h)

Contraindications

 Diuretics may worsen hepatoencephalopathy if prerenal azotemia results.

 Prednisone should not be used in animals with secondary infection.
 The following drugs should be avoided if
possible: chloramphenicol , tetracycline , clindamycin , meperidine , pentazocine , aspirin , a
nd azathioprine .

Nephrotic syndrome

 ACE inhibitor such as enalapril (0.5 mg/kg q24h)

Treatment of Edema and Ascites

 Cage rest and dietary sodium restriction

 Paracentesis and diuretics
 Dietary management

MODULE-14: DISEASES OF LIVER AND PANCREAS - I

Learning objectives

 In this section let us learn about the enzyme profile related to liver.

LIVER ENZYME PROFILING

 The biochemical parameters used to assess liver pathology may be divided into two classes:
the enzymes that reflect liver damage and/or cholestasis and the indicators of liver function
(bile acids, ammonia, albumin etc.). Serum enzyme screening for hepatobiliary disease is
common in veterinary practice.
 Clinical signs associated with liver disease are wide-ranging and often non-specific, and
consequently laboratory profiles are often run in patients that have a constellation of clinical
signs that includes one or more of those seen in liver disease.

ALANINE AMINOTRANSFERASE (ALT)

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 ALT is accepted as being essentially liver specific in the dog. Peak serum activity is
proportional to the number of hepatocytes affected, but gives no indication as to whether
the disease is diffuse or focal, and does not reflect the severity of the disease or its
reversibility.
 The reported plasma half life is of the order of two-and-a-half days, implying that, after
serum peak levels, a halving every 2 to 3 days is a good prognostic indicator.

ALKALINE PHOSPHATASE (ALP)

 The presence of several isoenzymes and a unique sensitivity to drug and cholestatic induction
by de novo synthesis, solubilization from membranes by bile salts and/or elution from
membranes, is reported to make ALP a test of relatively low specificity. However, its clinical
utility arises from its reported sensitivity in detecting hepatobiliary disease.
 Interpretation of results in "sick" dogs, that do not have canine Cushing's disease, is often
confounded by the difficult-to-predict effect of endogenously produced and/or iatrogenically
administered corticosteroids.

GAMMA - GLUTAMYL TRANSPEPTIDASE (GGT)

 Although present in many tissues, the majority of serum GGT is derived from the liver.
Although abundant in renal tubular epithelium, it is accepted that serum levels are not
elevated after kidney damage as the released enzyme is lost in the renal filtrate. Activity
usually parallels that of ALP, but it is perhaps less influenced by hepatocyte necrosis and
more by biliary epithelium disease.
 It appears that serum GGT is more specific (87%) than serum ALP (51%) in the detection of
hepatobiliary disease, but less sensitive (50%) than ALP (80%) . The
measurement/interpretation of ALP and GGT in series improves the specificity markedly
from 46% to 91%.

GLUTAMATE DEHYDROGENASE (GLD)

 GLD is a mitochondrial enzyme, and therefore requires fairly substantial cell damage before
it is released Increased GLD is reported to be a fairly specific indicator of liver damage.
Although abundant in renal tubular epithelium, it is accepted that serum levels are not
elevated after kidney damage as the released enzyme is lost in the renal filtrate. Sensitivity of
this enzyme for hepatic disease is reported to be high at 92%, and it is believed to
reflect necrosis of hepatocytes.

ASPARATE AMINOTRANSFERASE TRANSAMINASE (AST)

 Two AST isoenzymes are found, one cytosolic and one mitochondrial. The half life is reported
to be about 12 hours in dogs. This enzyme is released into the blood with increased cell
membrane permeability and cellular necrosis (when the mitochondrial isoenzyme is
released).
 Like ALT, the magnitude of increase said to be proportional to the number of hepatocytes
injured but does not indicate the functional status of the organ. It is reported to be a good
indicator of degree of necrosis as well as a good screening test with a sensitivity of 88%.
 Since AST is found in many organs, including muscle, heart and liver it is not a specific
indicator of hepatic damage and if elevations occur in the absence of elevations of ALT,
measurement of serum Creatine kinase, a muscle specific enzyme, may be required to rule
out muscle damage.
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 Since AST does not appear to have an advantage over ALT as a marker of hepatocyte damage
in terms of liver specificity, its value as an additional test should be questioned. It is not
routinely used to assess hepatic injury in dogs as it does not appear to have an advantage
over ALT as a marker of hepatocyte damage. However, AST was increased in 2/3 of 14 dogs
with hepatic abscesses. In the late stages of hepatic lipidosis when the lipid accumulation
becomes excessive, AST is reported to elevate.
 Increased AST is reported to be a sensitive indicator of metastatic (secondary) liver disease in
dogs. The author's institution does not, generally, make use of this enzyme in dogs,
preferring to rely on ALT and ALP.
 Until time-and-while a novel serum, liver-specific enzyme is proposed, the use of ALT and
ALP (with the possible occasional use of GDH), probably supplies the average veterinary
clinician with sufficient information about hepatocyte integrity, cholestasis and steroid
induction provided that the limited sensitivity and poor predictive value are borne in
mind.

MODULE-15: DISEASES OF LIVER AND PANCREAS - II

Learning objectives

 Diabetes mellitus, exocrine pancreatic insufficiency and hepatic encephalopathy are

discussed in this section

PATHOGENESIS OF DIABETES MELLITUS (DM)

 Autoimmune destruction of pancreatic β cells may be the cause of type 1 DM (formerly called
insulin-dependent DM).
 The etiology of type 2 DM is less clear, and is characterized by an inadequate secretion and
an altered action of insulin.
 Type 3 DM, also called secondary DM, results from other diseases, hormonal influences or
medications causing a decrease of insulin secretion or an altered action of insulin (pancreatic
neoplasia, pancreatitis, cortisol, growth hormone, etc ...).
 Transient DM: Resolution of DM seems to be closely related to a rigorous control of blood
glucose and can be definitive or transitional and last a period of months or yearS

DIAGNOSIS

 Clinical signs are polyuria/polydipsia, polyphagia and weight loss.

 Anorexia, lethargy, vomiting, and diarrhea
 Occasionally a plantigrade stance may be observed in cats.
 Dogs can present with cataracts.
 Hyperglycemia associated with glucosuria.
 When clinical signs are not typical, the diagnosis becomes more difficult to confirm. In these
cases, repeated measurement of blood glucose, or determination of fructosamine is done
 A complete blood count, biochemical analysis, and urinalysis

MANAGEMENT

Treatment of DM has several goals:

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 to reestablish glycemia in order to eliminate clinical signs of polyuria/polydipsia and

polyphagia,
 to prevent complications related to diabetes, and
 to avoid hypoglycemia.
 Treatment in dogs should always be based on insulin therapy. Ovariohysterectomy in intact
bitches developing DM is recommended.

DIET - FEEDING SCHEDULE

 Appropriate commercial diet, for each patient, either to favor weight loss in obese patients or
to ensure weight gain in thin patients.
 Palatability and acceptance of the diet are considered.
 Semi-moist diets or diets containing simple carbohydrates are to be avoided.
 The feeding schedule is adjusted if needed in light of the results of the blood glucose curve.
 Pets that are used to 'nibble' or 'graze' should be allowed to do so even when diabetic.

INSULIN THERAPY

 Insulin is classified in 3 categories: short- (regular), intermediate-(lente, NPH, Caninsulin®)

and long-acting (ultralente or PZI in the USA) preparations.
 Concentrations frequently available are 100 U/ml or 40 U/ml,
 In cats: initial recommended dosage varies from 0.25 to 0.5 U/kg, i.e., 1 to 3 U per cat.
 In dogs: initial recommended dosage is around 0.5 U/kg 2x/day with an intermediate
insulin.

Client education is paramount:

 they must be informed of the clinical signs of hypoglycemia (lethargy, trembling, seizures)
 how to store and administer the insulin.
 Usually 3 to 4 visits at one-week intervals are usually required to obtain an adequate control
of the diabetes.
 Home blood glucose monitoring has to be done

HYPOGLYCEMIC AGENTS

 Second generation sulfonyureas (glipizide/glyburide) cause the release of preformed insulin

by pancreatic β cells and also increase peripheral utilization of insulin. For these medications
to be effective, pancreatic β cells need to be functional (type 2 DM).
 If the cat is generally well, weight loss is mild, is not ketoacidotic and does not have a
peripheral polyneuropathy; hypoglycemic agents can be tried. Glipizide (2.5 mg 2x/day) or
glyburide (2.5 mg 2x/day) are available in many countries.
 Other hypoglycemic agents --eg metformin, acarbose, troglitazone and vanadium are also
used
 Dosage for acarbose is 12.5-20 mg/meal in dogs and cats.

EXOCRINE PANCREATIC INSUFFICIENCY

 Syndrome that is characterized by a lack of effective pancreatic exocrine secretion in the

small intestine.
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 The most common cause of EPI in dogs is pancreatic acinar atrophy (PAA).
 A familiar predisposition exists in German Shepherd dogs, collies and English setters.
 Chronic pancreatitis, repeated episodes of acute or subacute pancreatitis and pancreatic
neoplasia are also reported as a cause of canine EPI.
 In cats chronic pancreatitis is the most common cause of EPI.
 Malassimilation of nutrients, small intestinal bacterial overgrowth, morphologic and
functional changes of small intestine are produced as a result of EPI.

HISTORY AND CLINICAL SIGNS

 History and clinical signs of small bowel diarrhoea with voluminous, semiformed, yellowish
or gray feces,
 Polyphagia, pica especially in young dogs with inherited EPI,
 Extreme weight loss,
 Intestinal borborygmus, and
 Dermatological problems such as poor coat and seborrhoea sicca.
 Anorexia

CLINICAL PATHOLOGY

 Routine haematology results within normal limits.

 Serum alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase are
mildly increased .
 Concurrent hyperglycemia or abnormal glucose tolerance test
 Some dogs have subnormal cobalamin and high folate concentration.
 Serum vitamin E and A concentrations are decreased in dogs, while serum vitamin K is
decreased in some cats with EPI.

TRYPSIN - LIKE IMMUNOREACTIVITY

 Measurement of serum trypsin-like immunoreactivity (cTLI) by radioimmunoassay.

 The cTLI is a species and pancreas specific test and determines trypsin and trypsinogen that
have entered the blood from pancreas.
 The values of TLI test are characteristic and help in differentiating EPI of small intestinal
diseases.
 Low-fasting serum cTLI concentrations (< 2.5 μg/L) are typical of EPI.
 Reference range of TLI in normal dogs is 5.0 to 35 μg/L. cTLI values between 2.5-5 μg/L are
indicative of early phase of EPI, before severe destruction of exocrine pancreas.
 A new fecal test for diagnosis of EPI is based on the determination of fecal elastase activity
using the ELISA method. It is also a species and pancreas--specific test. A single fecal sample
is sufficient and values less than 10 μg/g are suggestive of EPI.
 The fasting serum feline TLI test (fTLI) : Values of less than 8 μg/L are suggestive of
EPI. fTLI values between 8-17 μg/L are indicative of early phase of EPI.

MANAGEMENT

 Dietary modification and pancreatic enzyme supplementation.

 A highly digestible, lowfat, low-fiber diet has been shown to ameliorate clinical signs of EPI.
 Dietary supplementation of medium-chain triglyceride oil (2 ml/meal every other day)
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 Powdered pancreatic extracts (2 teaspoons/20 kg BW/meal for dogs, 0-1 teaspoon/cat/meal

for cats)
 The powdered form of pancreatic extracts is more suitable compared to the enteric-coated
tablets, capsules or raw-chopped pancreas.
 Dogs and cats with EPI require parenteral cobalamin, vitamin K and oral vitamin E
supplementation.
 Inadequate enzyme supplementation may be a cause of treatment EPI failure. In these cases
reevaluation of dose is indicated. Lipase is acid-sensitive enzyme.
 In some dogs with EPI the enzyme supplementation must followed by an antacid
administration (ranitidine, cimetidine).
 Small intestinal bacterial overgrowth and/or inflammatory small intestinal
diseas: Metronidazole and/or prednisone administration

HEPATIC ENCEPHALOPATHY

 A metabolic disorder affecting the CNS and

 Developing secondary to advanced hepatic disease

Causes

 PSVA (dogs)—usually single large intrahepatic or extrahepatic vessels

 Acquired portosystemic shunting—occurs with diseases that induce portal hypertension
(cirrhosis; intrahepatic arteriovenous fistula; fibrosis;
 Acute hepatic failure—induced by drugs, toxins, or infection

Risk factors

 Alkalosis
 Hypokalemia
 Certain anesthetics and sedatives
 Gastrointestinal bleeding—most common precipitating cause
 Transfusion of stored blood products containing high concentrations of ammonia
 Infections
 Constipation
 Methionine

PATHOPHYSIOLOGY

 Complex pathophysiologic state with a multifactorial origin

 Ammonia as the putative neurotoxin with or without other synergistic toxins;
 Alteration in monoamine or catecholamine neurotransmitters as a result of perturbed
aromatic amino acid metabolism;
 Alteration in amino acid neurotransmitters, GABA, and/or glutamate; increased cerebral
levels of an endogenous benzodiazepine-like substance

 PSVA—usually in purebred dogs;

 PSVA—usually young dogs
 Acquired liver disease resulting in acquired portosystemic shunting—dogs and cats of any
age
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CLINICAL SIGNS

 Neurologic—may be related to meal ingestion

 Dramatic temporary resolution—may occur after initiating antibiotic therapy
 Prolonged recovery from sedation or anesthesia
 Cats and dogs similar; important differences noted below

 Episodic abnormalities

Disorientation—aimless wandering; compulsive pacing; head pressing


 Polyuria or polydipsia
 Amaurotic blindness
 Seizures
 Coma
 Ptyalism; seizures; aggression; disorientation; ataxia; stupor --CAT
frequent in dogs than in cats—compulsive behavior (head pressing, circling, aimless wandering); vomiting; diarrhea
polydipsia --dog

Physical Examination Findings

 PSVA—stunted growth (less common in cats);

 Copper-colored eyes (cats)
 Ptyalism (cats)
 Depression
 Disorientation
 Palpable urolith

DIAGNOSIS

Differential diagnosis

 Lead toxicity
 Urinary tract infection—cystic calculi
 Intestinal parasitism
 Primary gastrointestinal disease
 Hypoglycemia
 Toxoplasmosis
 Congenital CNS disease or malformation—hydrocephalus; storage diseases
 Acute ethylene glycol toxicity
 Rabies
 CNS neoplasia
 Canine distemper
 Thiamine deficiency—Wernicke encephalopathy
 Drug intoxication
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CBC/Biochemistry/Urinalysis


o Acquired portosystemic shunting and PSVA—RBC microcytosis
o Poikilocytosis
o Leukogram—reflects specific liver disease or causal conditions
o Hypoalbuminemia
o ALT and ALP—high; may be normal or only slightly high with PSVA or end-stage
cirrhosis
o BUN—low; reflects hepatic urea cycle dysfunction, protein-restricted diet, polyuria or
polydipsia associated with increased GFR
o Creatinine—low; reflects reduced muscle mass, hepatic synthetic failure, and polyuria
or polydipsia causing increased GFR
o Hypoglycemia—especially in young dogs with PSVA; fulminant hepatic failure; end-
stage cirrhosis
 Urinalysis
o Ammonium biurate crystalluria

Imaging

 Abdominal radiography—reveal a small liver in dogs; less reliable in cats

 Abdominal ultrasonography—may identify PSVA, acquired portosystemic shunting,
intrahepatic arteriovenous fistula, or echogenic patterns consistent with acquired liver
disorders may note a relatively hypovascular liver in dogs with microvascular hepatoportal
dysplasia

TREATMENT

 Depends on underlying condition

 PSVA—surgical correction

 Fluids—0.9% saline or Ringer with 2.5%–5.0% dextrose and 20–30 mEq of potassium
chloride/L; do not use lactate with fulminant hepatic failure (rare); use sodium-restricted
fluids with acquired liver disease with acquired portosystemic shunting and ascites.
 Colloids—may be essential with low albumin (< 1.5 g/dL); use fresh-frozen plasma rather
than synthetic colloids.
 Minimize exposure to drugs that require hepatic biotransformation or elimination.

Diet

 Adequate calories—avoid catabolism

 Dietary protein restriction—cornerstone of medical management for chronic disease; only as
needed to ameliorate signs; dairy and vegetable proteins best tolerated
 Good-quality vitamin supplement (without methionine)—vitamin metabolism often
perturbed with liver dysfunction

Drugs of choice
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 Antibiotics—spectrum against intestinal flora (aerobic and anaerobic); nonabsorbable

(neomycin, 10–20 mg/kg PO q8–12h); local and systemic (metronidazole, 7.5–10 mg/kg
q12h); used in combination with lactulose
 Nonabsorbable-fermented carbohydrates—lactulose, lactitol, or lactose (if lactase
deficient); lactulose most commonly used (starting dose, 0.5–1 mL/kg given two or three
times daily);
 Enemas—cleansing (warmed polyionic fluids) mechanically clean the colon (10–15 mL/kg);
lactulose, lactitol, or lactose diluted 1:2 in water; neomycin in water (do not exceed oral
dose); diluted Betadine (1:10, rinse well after 15 min); diluted vinegar (diluted 1:10 in
water)

MODULE-16: DISEASES OF RESPIRATORY SYSTEM -I

Learning objectives

 To learn about the principles of respiratory dysfunction and the manifestations of the
respiratory diseases.
 To understand and to perform clinical examination of an animal for the diagnosis of
respiratory tract diseases.
 To understand the clinical presentation, diagnosis and management of common upper
respiratory tract diseases.

PRINCIPLES OF RESPIRATORY INSUFFICIENCY

Anoxia

Definition

It means failure of the tissues to receive an adequate supply of oxygen

Types of anoxia

 Anoxic Anoxia
o Occurs when there is defective oxygenation of the blood in the pulmonary circulation.
o It is usually caused by primary disease of the respiratory tract.
 Anemic Anoxia
o Occurs when there is a deficiency of hemoglobin per unit volume of the blood.
o The percentage saturation of the available hemoglobin & oxygen tension are normal,
but the oxygen carrying capacity of the blood is reduced. It is usually caused by
anemia due to any cause.”e.g.”poisoning by nitrites or carbon monoxide .
 Stagnant Anoxia
o Occurs when the rate of blood flow through the capillaries is reduced.
o It usually occurs in cases of congestive heart failure, peripheral circulatory
failure& venous obstruction.
 Histotoxic Anoxia
o Occurs when the blood is fully oxygenated, but because of the failure of the “tissue
oxidation system,” the tissues can not take up oxygen .
o It usually occurs as a result of cyanide poisoning.
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Special causes of Anoxic Anoxia

 When the oxygen tension of the inspired air is too low, that it can not oxygenate the
pulmonary blood.
 Any lesion or dysfunction of the respiratory tract reducing the supply of alveolar air such as :
o Pneumonia.
o Pulmonary atelectasis.
o Pneumothorax.
o Pulmonary edema &congestion.
o Any decrease in the chest movement due to pain in the chest wall.
o Obstruction of air passage by accumulation of the exudates.
 Depression of the respiratory center by drugs or toxins.
 Congenital defects of the heart & large blood vessels, when mixing of arterial & venous blood
occurs through shunts between the two circulation.
 Paralysis of respiratory muscles.
 Botulism.
 Tetanus.
 Strychnine poisoning.

Complications of anoxia

 Increase in depth of respiratory movement “hyperpenea” which is mediated by

chemoreceptors in the aortic arch & parorecptors in the carotid sinus.
 Stimulation of splenic contraction.
 Erythropoiesis in the bone marrow.
 Increased heart rate.
 Signs of dysfunction of various organs appears, cerebral anoxia, myocardial
dysfunction, renal and hepatic dysfunctions as well as reduction in motility and
secretory activity of alimentary tract.

Carbon Dioxide Retention “Hypercapnia”

 It means that there is an accumulation of CO2 in the blood and tissues which cannot be
eliminated via the lungs and that is due to respiratory insufficiency. This Co2 stimulates the
respiratory center.

Respiratory Failure

 Respiratory movements are controlled by respiratory center in the medulla & this center is
controlled by afferent impulses from cerebral cortex, heat regulatory center in the
hypothalamus, stretch receptors in lungs via the vagus & from chemoreceptors in the carotid
body.
 The activity of respiratory center is also regulated by: pH, oxygen & carbon dioxid tensions of
the cranial arterial supply. So, stimulation of the above afferent nerves may cause reflex
changes in respiration & causing stimulation of the pain fibers.

Definition
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 Respiratory failure is the terminal stage of respiratory insufficiency, in which the activity of
respiratory center is diminished to the point where the movement of respiratory muscles is
completely stopped.

Types & causes

 Respiratory failure may be tachypenic, dyspneic, a sphyxial or paralytic depending on the

primary disease.
 A- Asphexial respiratory failure:

Causes

 Pneumonia.
 Pulmonary odema.
 Upper respiratory tract obstruction.

Clinical signs

 Hypercapnia
 Stimulate respiratory center
 Stimulation respiration
 Anoxia.
 Gasping. Apnea
 Death

Causes

 Poisoning with respiratory center depressants.

 Nervous shock.
 Acute heart failure.
 Hemorrhage.

Clinical signs

 Variable degree of dyspnea & gasping.

 Paralysis of the respiratory center Ø shallow respiration & less frequent then complete stop
of respiration .
 Tachypneic respiratory failure

Causes

 Increased pulmonary ventilation "hypoxia " but no carbon dioxide retention "acapnio".

Clinical signs

 Because of the lack of carbon dioxide to stimulate the respiratory movement; Rapid &
shallow respiratory & shallow tachypnea are evident.
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Treatment of respiratory failure

 In paralytic type - Stimulants of respiratory center are given.

 In asphyxyial type - Oxygen is provided.
 In tachypneic type - Oxygen & CO2 are provided.

PRINCIPLE MANIFESTATIONS OF RESPIRATORY INSUFFICIENCY

 The principal manifestations of respiratory dysfunction are those, which derive from anoxia.

Hyperpnea and dyspnea

 Hyperpnea is defined as increased pulmonary ventilation.

 Dyspnea means difficulty of respiratory.

Causes

 Anoxia.
 Hypercapnia arising most commonly from diseases of respiratory tract.
o Congestion of the pleura leads to rapid & shallow respiration.
o Pulmonary emphysema " caused by anoxic anoxia ".
o Cardiac dyspnea results from backward failure of the left ventricle with congestion &
edema of the lungs. Stagnant anoxia play a role in the production of this type of
dyspnea .
o Acidosis causes liberation of CO2 and stimulation of respiratory center results in
dyspnea .
o Encephalitis causes neurogenic dyspnea.

Clinical signs

 Abnormalities of respiratory cycle such as prolongation of expiration than inspiration.

 Abnormal movements of the two sides of the chest.
 Evidence of pain during respiratory movement.
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Cyanosis

 Definition
o It is a bluish discoloration of the skin, conjunctiva & visible mucosa.
 Causes
o Increased amounts of reduced hemoglobin in the blood. It occurs only when the Hb
concentration of the blood is normal & there is incomplete oxygenation of
hemoglobin.
o It occurs in all cases of anoxic anoxia , stagnant anoxia . but not in anemic
anoxia because there is insufficient hemoglobin .
o Polythemia, congenital cardiac defect & heart diseases .
 Diagnosis
o The bluish discoloration should disappear when pressure is exerted on skin or
mucosa & blood flow is stopped temporarily. Mat haemoglobinaemia is accompanied
by discoloration of the skin & mucosa but color is more brown than blue.

Cough

 It is a sudden expulsion of the air from the lung preceded by deep inspiration & it is initiated
by irritation of the respiratory mucosa of the air passages. It has a primary expulsive
function. It is an important sign indicating the presence of primary or secondary disease of
the respiratory system.

Nasal discharge

 Abnormal nasal discharge is usually an indication of respiratory diseases. Mucoid or

purulent discharge indicates the presence of inflammation in the nasal cavities or paranasal
sinus. Frothy exudates indicates pulmonary congestion or odema.
 Small amount of serofrothy exudates in equine infectious anemia and infectious
equine pneumonia.
 Color may be greenish in gangrene, yellowish rusty in pnumonia &pleurisy.
 Amount could be slight in T.B., profuse in rhinitis or intermittent in sinusitis.
 Odour may be offensive in gangrene, bad in cyanosis.

Abnormal respiratory sounds

 These are abnormal sounds produced from the lung, bronchi, bronchioles & pleura. These
sounds may be classified into rales & frictional sounds.
 Rales
o Are abnormal respiratory sounds indicating the presence of secretions or aspired
fluids in the bronchi & bronchioles. These fluids include "exudates, transudate, blood
& aspired fluid". According to the viscosity of the secretion, rales may be dry or moist
and cripitant.

EXAMINATION OF THE RESPIRATORY SYSTEM-I

 Respiratory system signs are induced by infectious as well as non-infectious causes; therefore
its examination is of particular clinical importance.
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Principle manifestations of respiratory insufficiency

o Hyperpnoea, dyspnoea
o Cyanosis
o Cough
o Nasal discharge

The main methods of examination of respiratory system are inspection, palpation, percussion and
auscultation.

 Inspection: Determines the respiratory movement, rhythm, quality and type

of respiration. Symmetry and form of thorax are also determined by
inspection.
 Palpation: Sensitivity of the larynx, trachea and thorax are determined by
palpation.
 Percussion: Used to determine the physical condition of the lungs and pleura.
 Auscultation: For detection of the condition of mucosa, lumen of trachea and
bronchi changes of alveoli, pleura and the presence or absence of exudate.

ROUTINE EXAMINATION OF RESPIRATORY SYSTEM

Nasal discharge and expired air

 In healthy animals, small amount of mucous is found in the nasal cavity. In equine, following
severe exercise, watery mucous can be seen dripping from the nostrils.
 Pathologically, may contain detached destroyed tissues, transudate, blood or saliva.
Unilateral nasal discharge is seen in unilateral localized affection of the nose or adjacent
structure. Bilateral nasal discharge occurs in bilateral affection of the bronchi, diseases of
pharynx, oesophagus and stomach (vomiting).
 The amount of nasal discharge increases in acute nasal catarrh, malignant head catarrh in
rumenants and swine infectious rhinitis. Reduced amount is noted in chronic catarrh of
upper respiratory tract (URT), bronchitis and pheumonia and in pulmonary tuberculosis in
ruminants.
 The consistency depends on the pathological changes; serous discharge which is watery in
consistency, colorless, transparent is seen in acute diseases of respiratory tract. Secondary
infection may turn it into mucous or mucopurulent discharge.
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 Seromucoid discharge is slightly more viscous than serous discharge. It maybe colorless or
grayish in cases of late stages of acute nasal catarrh or bronchitis and laryngitis. The color is
derived from presence of small numbers of leukocytes in the discharge.
 Purulent discharge is liquid, non-transparent, yellow or greenish in color. It is present in
cases of abscesses opening in the respiratory tract. Bloody discharge is a main sign of trauma
of capillaries of URT, pulmonary infarction, haemorrhagic diathesis in horses and in anthrax
in ruminants.
 All the above-mentioned types of discharge have no characteristic odour except for purulent
discharge, which has a characteristic rancid odour.
 In pulmonary oedema, haemorrhage and chronic bronchitis, nasal discharge may contain air,
which results in the foamy character of the discharge. In diseases or paralysis of the pharynx,
nasal discharge maybe mixed with saliva and food particles.
 Microscopical examination of the nasal discharge detects epithelial cells, leukocytes,
erythrocytes, fibrin, elastic fibers, crystals of fatty acids, parasitic ova, fungi and various
microorganisms. Elastic fibers are seen in pulmonary gangrene and opened tuberculous
nodules.

Examination of the nostrils and nasal mucous membranes

 This is preferably carried out in daylight to facilitate detection of the color of mucous
membranes. Nasal mucous membranes may become hyperaemic in acute nasal
catarrh (rhinitis).
 Cyanosis maybe seen in venous congestion, cardiac insufficiency, dyspnoea, disturbance of
gas metabolism accompanying insufficient oxidation of the blood.
 Anaemia results in pale mucous membranes. Chronic nasal catarrh also results in pale
mucous membranes. Jaundice (yellowish discoloration of mucous membranes) is seen in
hepatic diseases, acute infectious anaemia and leptospirosis.

Other lesions or abnormalities of nasal mucous membranes

 Wounds resulting from trauma.

 Ulcers resulting in loss of epithelial layer and
 tissue destruction as seen in acute or chronic nasal catarrh or haemorrhagic diathesis in
equines. In these cases the ulcers are superficial whereas deep ulcers are seen in glanders.
 Neoplasia as in sarcoma and carcinoma.
 Oedema of the nasal cavity in severe diseases (malignant head catarrh in cattle).
 Facial nerve paralysis in horses results in a change in the shape of nostrils, as they become
elongated and drawn downwards.

Examination of the para-nasal sinuses

 Inspection, palpation and percussion are all useful in examination of para-nasal sinuses. In
special cases, rhino-laryngeoscopy and X-rays are also used.
 Inspection reveals uni- or bilateral enlargement or asymmetry of the head in cases of acute
sinusitis. Tumors may also result in asymmetry of sinuses. Rickets and osteomalacia both
cause bony deformities.
 Palpation is useful in determining the sensitivity and consistency of bones. In acute
inflammation the examined area is hot and painful.
 Normal sinuses give tympanic sound on percussion; dull sound is heard if the sinuses are
largely filled with exudate, in cases of bone degeneration and tumors.
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Examination of the larynx and trachea

 Inspection is used to detect enlargement of the area of larynx and trachea through
edematous swelling. Inflammatory swelling at the area of larynx is seen in cases of severe
form of laryngitis, anthrax in ruminants, malignant oedema and atypical forms of strangles
in horses.
 Traumatic pericarditis in ruminants may cause non-inflammatory oedema in the
submaxillary space that may extend to the area of larynx and trachea.
 In sheep, oedematous swelling is often seen in helmenthiasis (Dictycaulus and Fascioliasis).
 In cases of increased sensitivity of the larynx (laryngitis), cough is induced by applying
pressure on the first three tracheal rings. Pressure on tracheal rings results in irritation of the
larynx and therefore results in induced cough reflex.
 Bronchial sound is heard by auscultation over the area of the trachea; this sound is also
referred to as tracheal, laryngeal and bronchia sound. In cases of bronchitis or trachitis, the
sound is intensified. Stenosis of URT in cases of laryngeal oedema and tumours results in
stenotic sounds. If the larynx or trachea is filled with liquid exudate, rales also are heard. The
character and strength of rales vary according to the amount and type of exudate.
 Laryngeoscopy is helpful for detection of tumours, oedema and character of mucous
membranes.

Cough

 This is a reflex action to irritation of respiratory passages due to any cause. Examples of
causes or inducers of cough are dust, inspiration of food particles, inflammation of mucosal
lining, inhalation of various gases (chlorine or ammonia), or from exposure to cold.
 Cough described based on strength and character. Strong cough occurs when inspiration is
deep. Weak cough occurs in difficult expiration where the animal is unable to cough actively;
this is seen in pulmonary emphysema, pneumonia and exudative pleuritis.
 Character of cough depends on production of exudate and could be described as either
moist (productive) or dry (unproductive) cough. Moist cough is seen in acute inflammatory
conditions of the respiratory tract where there is accumulation of a large amount of mucous.
Dry cough occurs in chronic respiratory diseases or in acute dry bronchitis.
 Frequency of cough depends on the degree of irritation of mucous membranes; it may be
single, continuous or periodic. Cough may also be painful or painless. It is painful in acute
laryngitis, tracheitis, bronchitis, pleuritis and peritonitis. In chronic inflammation of URT,
cough is painless. However, evaluation of pain in animals is often very difficult as this is a
subjective sign.

Examination of sputum

 Mucous and other inflammatory substances are expelled out of the respiratory system via
the mouth or the nostrils following productive cough. These expelled materials are termed
sputum.
 Microscopic or bacteriological examination of sputum is helpful in detection of causative
agents of the respiratory infection or disease. Sputum is collected by inducing cough
artificially or by introduction of a swab.

Other methods of examination

 Other methods are also used for examination of the respiratory system such as, X-rays and
bronchoscopy. These methods are of great importance in the diagnosis of various forms of
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pneumonia and pleurisy in all species of domestic animals. Emphysema and tuberculosis are
also diagnosed using these methods.
 Rhinoscopy and laryneoscopy for examination of the nasal cavity and pharynx.
 Microscopic examination of nasal discharge, swabs, sputum, faeces (lung worm).
 Paracentesis of thoracic cavity is of value when fluid is present in the thoracic cavity for
drainage, treatment and cytological examination.

EXAMINATION OF THE THORAX

 The thorax must be first examined by inspection to assess its form and shape. Unilateral
narrowing of the thorax occurs in pleuritic diseases after absorption of exudate whereas
bilateral narrowing occurs in tuberculosis, and in rickets.
 Bilateral enlargement (barrel shape) of the thorax is seen in bilateral alveolar emphysema,
and bilateral exudative pleuritis. Unilateral enlargement of the thorax maybe seen in
unilateral exudative pleuritis, pneumothorax and unilateral pneumonia.
 Palpation for assessing the sensitivity of the thorax and its temperature. Hotness and pain
occurs in acute inflammatory conditions and pleuritis.
 Direct or indirect percussion is an important method of examination in small and large
animals (dogs, cats, and ruminants, equines respectively). For percussion of thorax, the vet
must first determine the area of percussion.
 On percussion of the thoracic wall, the area must be divided into upper, middle and lower
thirds. The most intensive pulmonary sound is heard on percussion of the middle third
where the thoracic wall is somewhat thin, curvature of the ribs is large and airwaves are deep.
In the upper third, the heavy musculature hinders clear resonant sound of the lungs.

Changes in area of percussion

 Increased area of percussion is seen when the size of lung tissue increases, presence of large
amount of air in the lungs as in alveolar emphysema, various forms of pneumonia and in
cases of unilateral pneumonia and pneumothorax there is a unilateral increase in the area
of lung percussion.
 Decreased area of lung percussion is seen in animals with acute gastric dilatation, tympany of
the intestine, ruminal tympany and in cases of presence of fluids in the thoracic cavity.
 Normally in most animal species percussion over the lung area results in resonant sound; in
very small animals it is more of a tympanic sound.

Abnormal percussive sounds

 Loud resonant sound (e.g. emphysema and pneumothorax).

 Tympanic sound; when a part of lung tissues are surrounded by solidified tissue or exudate,
which isolates it from its environment. This occurs in the following conditions
o In early and late stages of fibrinous pneumonia.
o In catarrhal pneumonia.
o In pulmonary oedema and atelectasis.
o In presence of small or large tumors which surround lungs.
o In prolapse of the bowel into the thoracic cavity in diaphragmatic hernia.
 Dull sound is heard when lung tissue becomes dense. This occurs in
o Pneumonic hepatization.
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o Tuberculosis and metastatic pneumonia.

o Tumors.

Notes of practical importance

 Changes in the character of the percussion sound is detectable only when a lesion is present
in a considerable size and is superficially situated.
 A pain reaction maybe produced by percussion. This is indicated by the animal kicking or
biting or even shying away from the examiner; vocalization in cases of dogs and cats.
 Percussion may also induce cough in cases of pneumonia, bronchitis and pleurisy.
 Differentiation between increased density of the lungs and that due to the presence of fluid in
pleural sacs is determined as follows
o Increased density of the lungs in pneumonia, the area of dullness has an irregular
outline, the cardiac impulse is palpable, heart sounds are clearly audible outside the
cardiac area, abnormal bronchial or other sounds are often heard during auscultation
(rales or frictional sounds).
o Presence of fluid in the pleural cavity (e.g. exudative pleurisy, hydrothorax) results in
an area of dullness that has a horizontal delimitation, which changes when the
posture of the animal is altered.
o Auscultation is carried out to assess sounds produced during breathing when the air
enters the lung. The sound normally heard on the healthy lung is termed vesicular
murmur. This sounds like the soft pronunciation of the letter “V”. It begins with the
inspiration, increasing as the inspiration continues, becomes fainter and shorter
having the character of a softly aspirated “F” at expiration.
o An exaggerated vesicular murmur occurs
o If the respiration is intensified.
o Physiological or pathological dyspnoea.
o In bronchitis where the lumen of the bronchi are either swollen, or filled with
exudate.

Adiminished vesicular murmur occurs in

o Thickened, swollen or neoplastic thoracic wall.

o In severe bronchitis.
 Complete absence of vesicular murmur occurs if plural exudate or tumours have replaced the
lung tissue. Rarely occurs in severe vesicular pulmonary emphysema, or complete occlusion
of a bronchus preventing access of air into a certain portion of the lung.

Rales

 These are abnormal respiratory sounds indicate presence of respiratory disease; if the
bronchi or a cavern in the lung contain movable exudate.

Types of rales include

 Moist rales
o If the bronchi contain light fluid (pus, liquid exudate or blood). Bronchitis with
varying degrees result in moist rales.
 Crepitant rales
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o Fine cracking noises. They originate from a separation at respiration of the adhering
walls of the bronchi and vesicles. They appear in bronchitis, pulmonary oedema and
in early stages of fibrinous pneumonia.
 Dry rales
o In cases of swelling of mucous membranes, or presence of tough bronchial secretion
of small quantity. These result in rough mucous membranes, projecting irregularities,
which vibrate during inspiration and expiration.
o Sounds maybe humming, hissing or whistling in character. Dry rales are seen in
chronic bronchitis, compression of the bronchi by nodules (tuberculosis, chronic
pneumonia) and tumours.
o Presence of peristaltic sounds in the thoracic cavity indicates ruptured diaphragm
and protrusion of the intestine into the thoracic cavity. In contrast to the lung
sounds, they are not synchronous with inspiration and expiration.
 Pleuritic frictional sounds
o In cases of surface of pleura becomes rough and dry due to presence of inflammatory
deposits, frictional sounds are heard. Pleuritic frictional sounds occur in dry or
fibrinous pleuritis only. It is most frequently heard in contagious pleuro-pneumonia
of horse and ox.
o Summary of the differences between rales and frictional sounds.

Rales Frictional sounds

More pronounced at inspiration than Heard at both inspiration and expiration regularly (i.e.
expiration associa with respiratory cycle).
Removed or modified by cough Cough does not affect its presence
Painful
RESPIRATORY SOUNDS ON AUSCULTUTION

 The normal respiratory sound heard over the respiratory area consists of vesicular sound &
bronchial sound.

 Vesicular respiratory sound "vesicular murmur" The vesicular murmur resemble the sound produced
when the letter "V" is whispered softly & it occurs during inspiration, but during expiration the
vesicular murmur changes its character& resembles the sound of the letter "F".
 The vesicular murmur may be exaggerated or feeble "soft".
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Exaggerated vesicular sound

 Increased respiratory frequency "polypnea".

 Increased depth of respiration "hyperpnea".
 Occurs normally in young animals.

Feeble vesicular sound

 Thickening of thoracic wall & pleura due to any cause

 Reduced air content of the lung as in early stages of pneumonia.
 In old animals.
 Hydrothorax, hemothorax & pulmonary neoplasms.

Bronchial respiratory sound

 It resembles the sound produced by the letter "CH". It is heard clearly in small animals and
very lean old animals but in large animals it is less distinct.

 The occurrences of bronchial sound in the lung are indicating of a diseased condition.
 It is audible when the lung contains less air with increase in the structural density of the
inflammatory area which acts as a good conductor of the sound as in cases of hydrothorax,
hemthorax & pleurisy "Exudative stage".
 Cripitant rales
o Occurs when the bronchial mucosa is sufficiently swollen & affection extends to
involve the alveoli. So, opposing walls become adherent to one another but the
stream of air still pass through small communication between them it resembles the
sound produced by rubbing a tuft of hair held between fingers close to the ear. It
occurs in cases of:
 Bronchiolitis.
 Early stages of pneumonia.
 Pulmonary odema.

Frictional sound
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 Normally the visceral & parietal pleura glide smoothly over each other, since both
membranes are smooth & lubricated by clear lymph like fluid, when these surfaces are
dry, frictional sound occurs.
 It resembles the sound produced by rubbing two pieces of leather against each other or by
pressing the finger against the ear & stretching the finger nail of other hand. It occurs in
cases of:
o Preexudative stage of pleurisy.
o Pericarditis.

Emphysematous sound (Harch sound), or (Sharp sound)

 Resembles the sound produced by collection of a piece of paper between fingers & hand.

Girgling sound

 Resembles sound produced by gases & air bubbles, as in cases of diaphragmatic hernia (in
the chest) &bloat (in the rumen).
 Moist rales: Occurs when the bronchi & bronchioles contains thin watery mucous secretions,
they are obtaining as when air is drawn from the end of the tube under the surface of water,
so it is called bubbling sound. According to the site of affection moist rales are classified
into:-
o A-Fine moist rales : Occurs when the terminal parts of respiratory tract "alveoli" are
involved. They are of unfavorable prognosis.
o B-Coarse moist rales : Occurs when the affections are confined to the bronchi &
bronchioles only. It occurs in cases of:
 Bronchitis "acute".
 Bronchiolitis.
 Bronchopneumonia.
 Aspiration "drenching pneumonia".
 Hydrothorax.
 Haemothorax.
 Exudative stage of pleurisy.
 Dry rales
o Dry rales are heard when air is forced through the bronchial tube which is partially
thickened by the thick consistency exudate as by the severe swelling of the mucous
membrane. It resembles the sound produced by the movement of two tightly
stretched papers against each other. It occurs in cases of:
 Early acute stages of bronchitis.
 Chronic bronchitis.
 T.B

DISEASES OF THE UPPER REPIRATORY TRACT

Rhinitis "Coryza Or Nasal Cattarah"

 Definition
o Rhinitis means inflammation of the mucous membrane of the nose and usually
involving the upper part of the trachea, it may be acute, chronic, croupous or
follicular.
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 Etiology
o Primary causes
 Inhalation of irritant vapour as ammonia or chlorides.
 Presence of foreign bodies in the nose as dust particles.
o Secondary causes
 Sudden exposure from hot to cold, this well reduce the resistance of the body
& enable the M.O. which are normally inhabitant or commensals, in the
upper respiratory tract as strept., staph., coryne. & pasteurella, to become
pathogenic, active and then attack the mucous membrane.
 Extension of inflammation from other parts of respiratory tract as laryngitis
or even pharyngitis.
 Bold causes, "in the course of some diseases as"
 Glanders.
 Strarngles.
 Meliodosis of sheep.
 Necrotic rhinitis of sheep.
 Viral causes
 Malignant catarrhal fever of cattle.
 Mucosal disease.
 Render pest.
 Blue tongue disease.
 Infectious bovine rhinotracheitis.(I.B.R.).
 Equine viral rhinopneumonietis.
 Swine influenza.
 Parasitic causes
 Ostrus ovis of sheep.
 Blood flukes as Shestsoma Nasalis of cattle.

Fungal Aspirigillosis of dogs

Allergic condition

 Pathogenesis
o Rhinitis is usually of minor importance except when the nasal discharge rises up and
block the nostril. Its major importance arises when it accompanies some specific
infectious disease.
 Clinical signs
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o Redness and swelling of mucous membrane of the nose.

o Bilateral nasal discharge which usually begins watery in character then mucopurualnt
& purulent.
o Swelling of the submaxillary L.N.
o Difficulty of swallowing "dysphagia".
o Sometimes the discharge rises up and blocks the nose leading to a condition of
"snorting".
o When there is irritation the animal rubs its nose against any hard objects.
o There may be lacrimation and bleeding.
 Prognosis
o Favorable but when the causes are not treated it leads to chronic rhinitis.
 Diagnosis
o Clinical findings.
o Sudden onset.
o The character of the discharge which usually begins watery. When the animal rubs its
nose against objects, ulcerations & abrasions well be formed.
 Complications
o Chronic rhinitis may extend to other parts as nasal sinus giving rise to sinusitis.
o Enlargement of submaxilary L.N.
o Conjunctivitis specially in sheep.
o Extension of the inflammation to the lung.
 P.M. findings
o Rhinitis is not a fatal disease, although the animal may die from a Specific disease in
which rhinitis is a prominent lesions.
 Treatment
o Put the animal in a well ventilated space away from draughts.
o Complete rest of the animal & give only laxative, easily digestive food.
o Irrigate the nostrils with Sodium bicarbonate (1% solution).
o Apply medicated steam inhalation, but contraindicated to be used in milk and meat
producing animals.
o Put Vaseline on the upper lip of the animal.

Chronic Rhinitis

 This disease takes more longer time than the acute type & it means that the case was either
acute type and neglected or the stimuli acted slowly till it produces the condition
 Etiology
o Neglected acute cases of rhinitis.
o Accompanied with some chronic diseases of respiratory tract as chronic alveolar
emphysema of horses as well as glander & T.B.
 Clinical signs
o Mucoid nasal discharge, sometimes it may be transparent in color.
o The mucous membrane of the nose is swollen & bluish or brownish.
o Sometimes there is stenosis of the nasal cavities, due to swelling of the mucous
membrane, accompanied by snorting which is due to breathing from the mouth.
o There may be ulcers & abrasions on the surface of the nose, due to the fact that the
animal shakes its head and tries to get rid of the discharge by rubbing the nostrils
against objects.
 Diagnosis & differential diagnosis
o Chronic rhinitis need care in its diagnosis, since some infectious disease gives the
same symptoms as
o Glanders
 The nasal discharge is unilateral.
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 Non inflammatory swelling of the submaxillary lymph node.

 Ulceration & abrasions in the nostrils.
 Positive Malline Test.
o Strangles
 The submaxillary lvmph node is inflammed and tend to form abscess.
o Sinusitis
 On percussion, there well be dull sound with severe painful response.
 The nasal discharge is unilateral & is intermittent.
o Infections of the teeth
 Careful examination of the teeth with smelling of the mouth will be helpful in
differentiation.
o Tuberculosis (TB)
 Must be excluded by application of Tuberclin Test.

Differentiation between acute & chronic rhinitis

Acute rhinitis Chronic rhinitis

Watery nasal discharge
Mucous memb. Is swollen &
redden
Swelling of the submaxillary L.N.
Stenosis of the nostril
Mucoid nasal discharge
Mucous m. is swollen &bluish
Swelling of submaxillary L.N.followed by
dysphagia
The animal rubs its nose against objects

 Treatment: As acute rhinitis but takes more longer time.

Croupous Rhinitis

 Definition
o It means inflammation of the mucous membrane of the nose with the formation of
pseudomembrane.
 Etiology
o Inhalation of irritant vapour as gases, hot fumes or smoke.
o Some m.o. as bacillus necrophorus.
 Clinical signs
o Exactly as acute rhinitis with inflammation of the mucous membrane & appearance
of same grayish patchs on the m.ms. Or yellow false membrane which lastly sheds off,
leaving a bleeding surface, and scares.
o The nasal discharge contain shreds of the mucous membrane which distinguishes
this type from the acute type.
o Swelling of the submaxillary lymph gland.
o There may be slight rise in the body temperature.
 Prognosis
o Recovery within one week.
 Treatment
o As acute rhinitis but, for the rise of the body temp. give a course of antibiotics &
antipyretic & isolate the diseased animals.
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Follicular Rhinitis

 Definition
o It means inflammation of the mucous membrane of nose with the formation of
pustules which later on forms ulcers. The inflammation may involve the maxillary
gland & often the sebaceous gland.
 Etiology
o Streptococcus equi.
 Clinical signs
o Swelling of the mucous membrane of the nose with formation of small nodules on
the septum nasi "flea bite" size which increase in size & number & becomes yellowish
in color.
o The adjacent nodules will coalesce forming bigger nodules which ruptured leaving a
bright red erosions" heal in few days".
o The regional lymph glands & lymph .v. become swollen & enlarged forming
thick cords & sometimes suppurates.
o Conjunctivitis.
 Diagnosis
o Differentiate between this type and Glander & Pox.
 Prognosis
o Recovery takes place within 2-3 weeks.
 Treatment
o Medicated steam inhalation.
o Injection of antibiotics such is
 Streptopenicid.
 Oxytetracyclines.
 Local application of iodine ointment on the affected area.

Differentiation between cruopous & follicular rhinitis

Crupous rhinitis Follicular rhinitis

Definition  It means inflammation of the
mucous membrane with the
 It means inflammation of the mucous formation of pastules
membrane with formation of pseudo-
membrane

Etiology  Streptococcus equi

 Inhalation of irritant gases

 M.Os as Bacillus Necrophrus

Susceptibility: Equines & Bovines Equines

Clinical signs  Swelling of the mucous
membrane with appearance of
 Nasal discharge contain shreds of small nodules
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pseudomembrane  Enlargment of the regional L.N

 Swelling of submaxillary L.N. forming thick cord
 Presence of yellow false membrane on  Conjunctivitis
the mucous membrane

Prognosis: Recovery in one week Recovery in 2-3 weeks

Diagnosis: From symptoms
Treatment
 As acute rhinitis, but in case of rise
of body temperature give a course of
antibiotics & isolate the animals.
Different from Pox & Glander
 Medicated steam inhalation
 Course of antibiotics
 Local application of ointments.

OBSTRUCTION OF THE NASAL

CAVITY

 Obstruction of nasal cavities is rare in farm animals.

Etiology

 Acute rhinitis
 Granulomatous lesions caused by a fungus “ Rhinosporidium”
 Lesions caused by blood flukes “Schistosoma nasalis”
 Foreign bodies entering the nasal cavities when the animal rubbing its nose against objects to
relieve irritation of acute allergic rhinitis
 Neoplasms of olfactory mucosa
 Lesions usually occur in the posterior nares & are usually unilateral & may be bilateral
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Clinical findings

 In cattle & pigs there is severe inspiratory dyspnea

 The animal is excited & breathes through mouth
 Loud noise “sound” occurs in each inspiration
 Serious bloody stained nasal discharge “when there is foreign bodies, or purulent
exudative nasal discharge when there is allergic rhinitis”
 Snorting & shaking of head

Treatment

 Treat the cause & remove the foreign bodies by a long forceps if it is accessible
 Administration of iodine preparation in chronic nasal obstruction as pot.iodide or sodium
iodide

EPISTAXIS

Definition

 It means bleeding from nostrils or from nasal sinuses

Etiology

 Primary cause
o Bad use of the tracheal tube
o Traumatic injury of the nose, head, frontal nasal bore as will as sinuses
o May be congenital
o Over exhaustion of race horse
o May occur without any apparent cause
 Secondary cause
o Ulceration of the nose & septum nasi as in case of glanders in equine
o Puncture of parasite in infection diseases as anthrax & hemorrhagic septicemia

Other causes

 Diseases of mucosa of the upper respiratory tract nasal cavity nasoparynx or guttural pouch
 Erosion of the mucosa occurs in glanders & in granulomatous & neoplastic lesions in the
nasal cavities.
 By entry of foreign body in acute allergic rhinitis, or by accidental injury to the facial bones.
 Purpuric diseases as purpura hemorhagica, sweet clover poisoning, braken fern poisoning &
in congestive heart failure.

Clinical findings

 There is bleeding from nostrils either unilateral or bilateral. Blood is bright red in color, or
may be mixed with mucous in case of glanders
 It may be scanty & stop by itself or profuse & the bleeding is profuse.
 Pulse is rapid & weak & pale mucous membrane & anemia, loss of condition & death.
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Diagnosis & differential diagnosis

 Try to lactate the site of injury using endoscope

 Unilateral bleeding is usually of nasal origin.
 Bilateral bleeding is usually of nasal passage origin.
 Bleeding caused by ulcers in the nostrils (Glanders) blood s scanty & mixed with mucous.
 You have to identify the origin of epistaxis as following:
o a-Blood from nostrils ® bright red.
o b-Blood coming from lung ® bright red & frothy.
o c-Blood coming from stomach ® brownish red and acidic in reaction & mixed with
ingesta.

Treatment

 Complete rest of the animal & keep it quite

 Apply cold compresses on the head particularly on the frontal nasal bone & nose.
 Apply astringent solution on the affected nostrils as:
o Alum solution 2% or tannic acid 2%.
o Piece of gauze soaked with adrenaline 2%.
 In case of bilateral bleeding apply tracheotomy & plug the two nostrils with a piece of gauze
soaked in adrenaline
 Inject vitamin K to accelerate coagulation “ ½ -3 ml /20 lb.B.W.
 Inject calcium chloride 10% 100 cc s/c.
 Treat the cause if it is secondry epistaxis.
 Fluid therapy “ Glucose sol. 20% I/V about one litre” or normal physiological saline 500 ml
I/V.

TRACHEAL COLLAPSE

Collapsing Trachea ( Canine)

 Etiology unknown.
 Most common in toy & miniature breeds.
 Clinical signs include:
o nonproductive, honking & chronic cough.
o Frequently obese with concurrent cardoivascular / pulmonary disease (chronic
bronchitis).

Treatment:
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 Weight loss,
 Restrict exercise,
 Reduce excitement/stress,
 Medications:
o Antitussives,
o Antibiotics,
o Bronchodilators,
o Corticosteroids.

COUGH

Cough (Canine)

 Etiology: Nasal cavity and sinuses diseases with postnasal drip

 Pharyngeal & Laryngeal disorders:
o Trauma
o Foreign bodies
o Infections (bact, viral, fungal, paras)
o Neoplasia
o Laryngeal pralysis
o Everting laryngeal saccules
o Laryngeal collapse

Tracheal & lower airway disorders

 Trauma
 F.B.
 Allergy
 Infection
o Viral (distemper, parainfluenze [dogs] herpes & calici [cats])
o Bacterial (Bordatella bronchisepticum)
o Parasitic (Filaroides, Capillaria sp.)
 Anomalies (collapse, hypoplasia, 1o cilliary dyskinesia,
 segmental stenosis)
 Bronchiectasis

Pulmonary parenchymal disorders

 Trauma,
 Allergy (pulmonary infiltrates w/ eosinophillia),
 Infection
 Viral
 Bact
 Fungal (Blastomyces, Crytococcus, Aspergillus)
 Protozoal (Toxoplasmosis, Pneumocystis)
 Parasitic (Filaroides, Dirofilaria, Paragonimus)
 Neoplasia (1o or 2o)

Cardiac Disorders
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 Pulmonary edema
 Left atrial enlargement (Causing bronchial compression

Mediastinal Disorders (causing airway compression)

 Lymphosarcoma (esp cats)

 Thymomas
 Tracheobronchial lymphadenopathy

MODULE-17: DISEASES OF RESPIRATORY SYSTEM -II

Learning objectives

 To learn about the following diseases in domestic animals

o Larynx
o Pharynx
o Trachea
 To learn about the guttural pouch diseases in horses, its treatment as well as management
 To know in detail about the following diseases, their clinical signs, diagnosis and treatment
o Feline upper respiratory tract disease
o Infectious bovine rhinotracheitisis

DISEASES OF THE LARYNX

Laryngitis

Laryngitis, an inflammation of the mucosa or cartilages of the larynx, may result from upper
respiratory tract infection or by direct irritation from inhalation of dust, smoke, or irritating gas;
foreign bodies; or the trauma of intubation, excess vocalization, or in livestock, by injury from roping
or restraint devices. Laryngitis may accompany infectious bronchitis in horses. Edema is seen.
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 Laryngeal chondropathy is a suppurative condition of the cartilage matrix that principally

affects the arytenoid cartilages; it is believed to result from microbial infection. Initially,
there is often acute laryngeal inflammation. Later, there is progressive enlargement of the
cartilages that commonly results in a fixed upper airway obstruction with stertorous
breathing and reduced exercise tolerance.
 Clinical Signs: Harsh dry cough initially and soft, moist painful later on. Cough can be
induced by pressure on the larynx, exposure to cold or dusty air, swallowing coarse food or
cold water, and attempts to administer medicines.
 Diagnosis: clinical signs, laryngoscopy.
 Treatment: Tracheotomy tube, NSAIDs and corticosteroids, systemic antibiotics, diuretic
drugs, tx of primary disease, avoidance of causes.
 Laryngeal paralysis middle aged to older, large breeds of dogs – dry cough, voice changes,
noisy breathing, stridor and collapse. Diagnosi: Laryngoscopy. Traetment- Surgical.

DYSPNEA

 Inspiratory dyspnea results from upper respiratory disorders. Associated with a prolonged
and noisy inspiratory effort. Conditions include stenotic nares, nasal cavity obstruction,
nasopharyngeal polyp (cats), elongated or edematous soft plate, laryngeal disease, cervical
tracheal disease, etc.

 Expiratory dyspnea results from lower respiratory tract disorders. Inspiratory and
expiratory dyspnea is present in animals with lower airway or pulmonary parenchymal
disease. These include thoracic tracheal disease, pneumonia, pulmonary edema, pulmonary
thromboembolism, pulmonary contusions, pulmonary neoplasia, and pulmonary
granulomatosis.
 Rapid and shallow respiration with muffled breath sounds on auscultation is present with
restrictive or pleural space disorders. These include pleural effusion, pneumothorax,
congenital thoracic wall abnormalities, thoracic wall trauma, thoracic wall or mediastinal
neoplasia, diaphragmatic hernia, extreme obesity, marked ascites, severe hepatomegaly,
large intraabdominal mass, severe gastric distention. Miscellaneous disorders include
anemia, methemoglobinemia, cyanosis, compensation for metabolic acidosis, heatstroke,
damage to CNS, neuromuscular weakness, pain
 Diagnosis: from detailed history and radiographs.
 Treatment: First stabilize animal, then elimination of primary cause.

EXERCISE INDUCED PULMONARY HEMORRHAGE

 Blood from lungs (caudodorsal lung field) as consequence of exercise.

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 Horses with a history of repeated bouts of severe EIPH have extensive bronchiolitis in the
dorsal regions of the caudal lobe with concurrent bronchial arterial neovascularization,
interstitial fibrosis, and sequestration of macrophages containing hemosiderin
(hemosiderophages).
 Endoscopy (60-90 min after exercise), see blood in airways . If you suspect EIPH but can not
do endoscopy, examine TB asp for hemosidin containing macrophages.
 Differential Diagnosis: Guttural pouch mycosis and ethmoidal hematoma.
 Therapy: ineffective. Symptomatic. Frusemide, conjugated estrogens, vitamin K, and vitamin
C used for prevention but not very effective.

FELINE UPPER RESPIRATORY DISEASE COMPLEX

ified by rhinitis, conjunctivitis, lacrimation, salivation, oral ulcerations. By feline viral rhinotracheitis (herpes) and fe
umonitis (chlamydia) and mycoplasma are less important.

al Rhinotracheitis – Herpesvirus. Affects conjuctiva and nasal passages. Fever, sneezing, bilateral conjunctivitis, rh
ating fever. Oro nasal discharge (s → p). Excitement or movement induces sneezing. Ulcerative stomatitis, ulcerativ
debilitated cats. Treatment corneal ulcers with topical acyclovir. Lysine. Avoid sec inf. Vax.
civirus – Loves oral mucosa and Lower respiratory tract. Ulceration of oral mucosa. Serous rhinitis, bilateral conjun

roduce alt leg lameness with pain and fever in kittens which resolves on its own. May occur with Feline calici virus v
iratory tract signs.
umonitis – Chlamydia - Chronic, low grade conjunctivitis (one eye initially, other eye later). Diagnosis by Giemsa st
s. Treatment with tetracycline.
ma – Severe edema of conjunctiva and a less severe rhinitis. Diagnosis as chlamydia. Extracellular coccoid bodies on
ells.

GUTTERAL POUCH DISORDERS

ouch Empyema - Pus in the guttural pouch. Inspisated pus = chondroids. Usually culture S. zooepidemicus. Develop
infection in horses, can also develop 2° to congenital tympany. Affects horses of any age. See chondroids on rads. E
roids, place indwelling cath, flush, lavage. Surg via viborg’s triangle, get chondroids out, leave drainage.
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Pouch Mycosis - Caused by a fungal infection of the gutteral pouch, usually Aspergillus. Unilateral epistaxis due to f
rnal or external carotid. Hemorrhage may be fatal. Treat as an emergency, is life threatening. Clinical signs 2° to da
d arteries within gutteral pouch mucosa. Dysphagia, Horner's syndrome, laryngeal hemiplegia, dorsal displacement
opy, check both pouches. Treatment is surgical, hyovertebrotomy. Occlude blood blow on both sides of lesion so no r
using balloon-tipped catheter. Ddx – ethmoid hematoma.

Pouch Tympany - Distention of the guttural pouch with air in young horses (days to 1 y.o). Nonpainful swelling, ma
a, aspiration. Rads or needle decompression to dx. Sx – viborg’s triangle, excise medial lamina of eustachian tube, fe
septum between pouches. Good px if no aspiration.

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ASPERGILLOSIS

 It is an inhaled fungus and causes the most common nasal fungal infection in dogs (A.
fumigatus), especially in dolichocephalics. Urinary aspergillosis occurs in German shepherd
dogs. Systemically it is a respiratory disease.

 Causes pulmonary infections in birds and death in penguins, mycotic abortion in cattle,
gutteral pouch mycosis in horses, infections of the nasal and paranasal tissues of dogs.
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 Clinical signs and lesions in birds include yellow nodules in respiratory passages, etc. It eats
away at turbinates.
 Treatment with Itraconazole and others. Flush nasal cavity with Clortrimazole.

ATROPHIC RHINITIS

Atrophic Rhinintis

 One of the causes of Atrophic Rhinitis is atrophy of the turbinates. Pure B. bronchiseptica
infections are self-limiting. (lesions heal and there is little to no effect on performance or
growth).
 Piglets infected soon after birth from carrier dam. When infected with pasteurella
multocida, will result in atrophy of the nasal turbinates. B. bronchiseptica also causes
whooping cough.Carried in the nasal cavity of an asymptomatic carrier sow. Horizontal
transmission among piglets may occur.
 Clinical disease occur in very young piglets. The organism colonizes bronchi and
bronchioles. Endotoxins and exotoxins diffuse into the lung tissue causing vascular damage
and fibrosis. Mortality up to 30%. Anterioventral hemorrhagic consolidation in a lobular
pattern (checkerboard).
 Diagnosis: bacterial culture.
 Treatment with oxytetracycline, sulfonamides and others.

CALF DIPTHERIA - NECROTIC LARYNGITIS

 It is caused by Fusobacterium necrophorum and its necrotizing edotoxin.

 Clinial Signs: moist, painful cough, severe inspiratory dyspnea with open-mouth breathing &
head and neck extended, ptyalism, bilateral purulent nasal discharge, fetid breath odor, fever
(106 F/ 41.1 C).
 Lesions: Necrotic ulcers of the larynx (behind vocal cords on vocal process of arytenoids).
 Diagnosis: based on History, Clinical Signs, Laryngoscope.
 Traetment: Sulfonamides, NSAIDS, isolation, & supportive therapy. Treat Early &
Aggresively!

OBSTRUCTIVE PULMONARY DISEASE

 Chronic Obstructive Pulmonary Disease - “COPD” is a coomon disease of equines and also
called as Heaves/ Asthma.
 Allergic reaction thought to initiate the disese.
 It's prevalence increases with age.
Inflammation, chronic bronchoconstriction, thickened bronchi. Increased expiratory effort,
exercise intolerance, cough and afebrile is the disease nature.
 Diagnosis: Endoscopy, Tracheo bronchial aspiration, thoracic auscultation of expiratory
wheezes.
 Traetment with environmental changes, antiinflammatories, steroids, bronchodilators.

MODULE-18: DISEASES OF RESPIRATORY SYSTEM - III

Learning objectives
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 To learn about and understand common respiratory diseases such as Bacterial pnuemonia
and Bovine Respiratory diseases.
 To learn about and understand common respiratory diseases such as small animal
respiratory disorders, drug therapy in small animal respiratory disorders and about pleural
effusion.

BOVINE RESPIRATORY DISEASE

 Bovine respiratory disease is not a single entity nor is it attributable to a single cause. Three
different categories of problems occur in affected cattle.
 Bovine respiratory disease complex (BRDC) is the most common and most devastating form.
This is commonly called “shipping fever” or enzootic calf pneumonia. Acute interstitial
pneumonia also occurs and is most commonly associated with toxins. The third form of
disease in metastatic pneumonia that occurs as a result of septicemic conditions such as
discussed in the GI section.

 Bovine respiratory disease complex refers to bacterial bronchopneumonias that may are may
not be complicated by previous or concurrent viral or mycoplasma infections. Numerous
bacteria can be isolated from the lungs of affected cattle.
 In cattle the most important bacterial pathogen is Mannheimia hemolytica, with Pasturella
multocida and Hemophilus somnus playing lesser roles. These organisms play the same role
in pathogenesis in younger calves and Mycoplasma spp. are of additional concern.

Viral pathogens are implicated in the BRDC even though the final pulmonary pathology is caused by
the previously mentioned bacteria.

 The primary viruses involved include herpesvirus 1 (IBR), parainfluenza type 3 (PI3),
respiratory syncytial virus (BRSV), and bovine viral diarrhea virus (BVD). Other viruses may
cause lesser disease at times but these four are the most problematic for producers and
veterinarians.
 These viruses infect the upper respiratory tract resulting in rhinitis, tracheitis and
bronchitis. Their ability to cause direct pulmonary disease is limited except for BRSV.
However, all of these pathogens predispose the lung to bacterial infection and
bronchopneumonia by compromising the respiratory tract defense mechanisms.
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 The persistence of pathogens in the environment obviously contributes to exposure. Survival

times of the pathogens depend on many factors including the amount of organic material
present, moisture, sunlight and exposure to disinfectants.
 Survival times for most viral pathogens are on the order of minutes to several hours, while
bacterial pathogens may be longer. Airborne transmission of a typical virus can occur over
distances of about 4 meters, although some viruses are capable of survival over several miles.
The complexity of the problem is increased by the knowledge that survival varies between
different strains of the same pathogen.
 Ventilation improvement is an important means of reducing pathogen concentration. As
pathogen load increases in the air, ventilation provides less protection against infection.
 Increased animal activity increases dust exposure and ventilation rate, effort and tidal
volume, which in increases the amount of pathogen shed by infected animals and the amount
of pathogen inhaled by susceptible animals. The increased dust exposure also will adversely
affect the mucociliary clearance and respiratory defense mechanisms.

PNEUMONIA - CAUSES AND PATHOGENESIS

 Pneumonia is the inflammation of the pulmonary parenchyma usually accompanied by

inflammation of the bronchioles and often by pleurisy. It is manifested clinically by an
increase in respiratory rate, cough, abnormal breath sound on auscultation and in most
bacterial pneumonia, by evidence of toxemia.

Causes:

Cattle:

 Pneumonic pasteurellosis (Shipping fever). Pasteurella hemolytica, P.multocida with or

without parainfluenza –3 virus (PI3).
 Enzootic pneumonia of calve: PI3, adenoviruse 1,2, and 3 Rhinovirus, Bovine Syncytial
Virsus (BSV), reoviruses, Bovine herpes virus l (BSV virus) plus chlamydia spp. Mycoplasma
spp. Pasteurella spp. Corynebacterium pyogenes, Strept spp. and bedsomia spp.
(Actinobacillus actinoides).
 Viral Pneumonia of yearling and adult cattle is caused by either PI3 or adenoviruses.
 Contagious bovine pleuropneumonia caused by Mycoplasma mycoides.
 Atypical interstitial pneumonia.
 Massive infestation with ascarid larvae.
 Lungworm pneumonia (Dictycolus viviparous).
 Klebsiella pneumonia infection in calves and nursing cows suffering from mastitis caused by
this organism.
 Sporadically in T.B. (Mycobacterium bovis).
 Sporadically in calf Diphtheria (Spherous necropherous).
 Hemophilus somnus, possibly in young cattle affected with the more common septicemic
form of the disease. Its role as primary cause is uncertain.

Sheep:

 Pneumonic pasteurellosis (Pasteurella sp.) as acute primary pneumonia in feedlot lambs,

or secondary to PI3 or Chlamedia spp.
 Newborn lambs: Uncommonly Strept. Zooepidemicus, Salmonella abortus ovis.
 Mycoplasma spp. (Severe pneumonia).
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 Symptomless pneumonia without secondary infection adenovirus, RSV, reovirus

Mycoplasma sp.
 Corynebacterium pseudotuberculosis (sporadic).
 Melioidosis (Pseudomonus pseudomallei).
 Lungworm pneumonia (Dictycolus filarial).
 Progressive interstitial pneumonia.

Goats:

 Pleuropneumonia caused by mycoplasma strain F38 or M.Capri is a devastating disease.

 Chronic interstitial pneumonia with pulmonale as common sequel by a number of
mycoplasma spp. M . mycoides var. mycoids appears to be the most commonly recorded.
 Rotavirus infection.

Pathogenesis:

 Under normal condition the major airway and the lung parenchyma prevent the entry of and
neutralize or remove injurious agents, so that the lung contains very few, if any organism
beyond the terminal lung agents.
 Many infections of the respiratory tract originate from aerosolized particles carrying
infectious agents, which arise external to or within the respiratory tract. Thus the
pathogenesis of respiratory infections is related to the depletion of particles and infectious.
Lung clearance mechanism:-
 The major defense mechanisms of the respiratory tract include aerodynamic filtration by
the nasal cavities, sneezing, local nasal antibody, the laryngeal mechanism, the alveolar
macrophages and the systemic and local antibody systems.
 Anything which interferes with the clearance of particles from the upper mucous will
interfere with the clearance of particles from the upper respiratory tract. The cough reflex
provide an important mechanism by which excess secretions and inflammatory exudates
from the lungs and major airway can be removed from the airway and disposed of by
expectoration or swallowing.
 In animal with relatively normal lugs, coughing represents a very effective means of expelling
materials. In the presence of severe trachitis and pneumonia, coughing may results in
retrograde movements of infected material to the terminal respiratory bronchioles and
actually promotes spread of the infection to distal parts of the lungs.
 The lung clearance mechanism may be affected by a concurrent viral infection. This may
have major implication in the control of some of the common infectious respiratory disease
of farm animals.

PNEUMONIA - CLINICAL FINDINGS

 Rapid, shallow respiration is the cardinal signs of early pneumonia, dyspnea occurring in the
later stages.
 Polypnoea may be quite maker with only minor pneumonic lesions and the rapidity of the
respiration is an inaccurate guide to the degree of pulmonary involvement.
 Cough is other important sign (the type of the cough varies with the type of the lesion).
Bronchopneumonia is usually accompanied by a moist painful cough, interstitial pneumonia
by frequent, dry, backing cough, often in paroxysms.
 Cyanosis is not a common signs and occurs only when large of the lung are affected.
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 A nasal discharge may or may not be present in the bronchioles whether or not there is
accompanying inflammation of the upper respiratory tract.
 The odour of the breath may be informative. It may have an odour of the decay when there is
a large accumulation of inspissated pus present in the air passages, or putrid, especially in
horses, when pulmonary gangrene is present.
 Auscultation of the thorax before and after coughing may detect exudate in the air passages.
 By auscultation in the early congestive stage of bronchopneumonia and interstitial
pneumonia the vascular murmur is increased. Moist rales develop in broncho- pneumonia as
bronchiolar exudation increases but in uncomplicated interstitial pneumonia, clear, harsh
bronchial tones are audible.
 Consolidation also causes increased audibility of the heart sounds. When pleurisy is also
present it causes a pleuritic friction rub in the early stages and muffling of the pulmonary
sounds in the late exudative stages. Consolidation can be detected also by precussion of the
thorax or by tracheal percussion.
 There may be an observable difference in the amount of movement in the two side of the
chest if the degree of consolidation is much greater in one lung. Additional signs evident in
pneumonia include fever of variable severity, anorexia, depression, and an increase in pulse
rate.

PNEUMONIA-TREATMENT

 In specific infection, isolation of affected animals and careful surveillance of the remainder of
the group to detect cases on the early stages should accompany the administration of the
specific antibacterial drugs or biological preparations to affected animals.
 The choice of antibacterial agents will depend on the tentative diagnosis, the experience with
drugs in previous cases and the results of the drug sensitivity tests.
 The common bacterial pneumonia of all species will usually recover quickly (24 hr.) if
treated with an adequate dose of the drug of choice early in the course of the disease.
 Animals with severe pneumonia will require daily treatment for the several days until
recovery occurs.
 Those with bacterial pneumonia and toxemia must be treated early on an individual basis.
Each case should be identified and carefully monitored for failure to recover.
 Antimicrobial agents in a long acting base may be used to provide therapy over a 4-6 day
period instead of the daily administration of the shorter-acting preparations. However, the
blood level from the long-acting preparations are not as high as the shorter-acting
preparations and may not be as effective in severely affected animals.
 There is no specific treatment for the viral pneumonia because viral and mycoplasmal
pneumonia are commonly complicated by secondary bacterial infections. It is common
practice to treat acute viral and mycoplasmal pneumonia with antibacterial until recovery is
apparent. In outbreaks of pneumonia where many animals are affected and new cases occur
each day for several days, the use of mass medication of the feed and / or water supplies
should be considered.
 Mass medication may assist in the early treatment of subclinical pneumonia and is a labor-
saving method of providing convalescent therapy to animals which have been treated
individual. Corticosteroids have been used for their anti-inflammatory. Effect in the
treatment of acute pneumonia. However, there is no clinical evidence that they are beneficial.
Affected animals should be housed in warm, well-ventilated, draft-free accommodation,
provided with ample, fresh water, and light nourishing food.
 During convalescence condition, the return to work or exposure to bad or cold weather
should be avoided. If the animal does not eat, oral or parentral force-feeding should be
initiated. If fluids are given intravenously care should be exercised in the speed with which
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they are administered. Injection at too rapid rate may cause overload on the heart ventricle
and death may occur due to acute heart failure.
 Supportive treatment may include the provision of O2 supply to be available especially in
the critical stages when hypoxia is evident. In foals, the oxygen can be administered through
an intranasal tube passed back to the nasopharynx and delivered at the rate of about 3
liters / min. for several hours. Expectorants may be of value in chronic cases and during
convalescence.

EQUINE PNEUMONIA

Equines

 Rhodococcus (Corynebacterium) equi cause severe pneumonia and may be endemic on

some farms. Also maybe secondary to viral diseases.
 Acute bronchointerstitial pneumonia affects foals 1 wk to 8 months old, and the etiology is
unknown. R. equi and P. aeruginosa have been identified. Marked by acute or peracute onset,
respiratory distress, cyanosis, reluctance to eat, septicemia, DIC, increased fibrinogen
concentrations, radiographs showing increased alveolar and neutrophilic leucocytosis.
 Diagnosis: Culture of bronchoalveolar lavage or a tracheal wash (nasal swabs not
recommended because of resident microflora). The diagnosis of respiratory infections is
usually based on a combination of history and results from clinical, endoscopic,
radiographic, and in some cases, ultrasonographic examinations.
 Treatment: Antibioticsbs (eg, penicillin, potentiated sulfonamide& bronchodilators.

EXAINATION OF A SMALL ANIMAL PATIENT FOR RESPIRATORY DISEASES

Complete physical exam indicated

 Observe posture
 Note elbows abduction, if any, as an attempt to maximize intrathoracic space
 External nares discharge; Mucosa – colour
 Soft palate - length, turgidity
 Chest contour, breath for ketone

PALPATE for abnornalilties in Larynx, Trachea

Elicit cough

 Subcutaneous emphysema
 Congenital defects of thorax
 Cardiac thrill - heart disease

AUSCULTATION

Perform systematically

 Classify sounds from heart, trachea, Bronchi, lungs, chest cavity
 Moist, dry, insp./expiatory
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PERCUSSION - Finger or Instrument based

 Can detect change in density or location

 Fluid line, consolidation of lungs, etc.
 Must know:
o Normal density
o Normal location
o Applied Anatomy

HISTORY/AMAMNESIS

Age - Viral disease in young


Neoplasia in middle and old

 Breed - Brachycephalic -- Upper Respiraory tract problems
 Toy - high incidence of collapse trachea
o Dolichocephalic and mesocephalic -nasal tumors
 Sex – Females: Mammary Tumors – Metastasis
 Geographic Origin
 Present Environment - Trauma - More in unconfined
 Infectious in kennel boarders
 Vaccination and heart worm status
 Gets worse inside than outside or vise versa - allergy

Prior Medical Problems - Relationships

Neoplasia -metastasis, e.g. osteosarcoma, etc.


 Previous viral disease and present bact. pneumonia
revious smoke inhalation, Bact. pneumonia tracheobronchitis may have lead to present bronchiectasis / Pulmonary

Current Complaint & Last known period of normalcy

 Onset, acute dyspnea, rales, pulmonary edema in a young indoor dog - Electrocution?
ession - slow progressive cough in old dog; Cardiogenic Intermittent signs - vomiting, diarrhea, weight loss - Canine
 Previous treatment – Antibiotics for chronic bronchitis?
 Present Status - weight loss, attitude, exercise tolerance.

CLASSIFICATION OF BREATH SOUNDS

Normal

 Vesicular - rustling over periphery. Inspiratory / Expiratory

 Bronchial - harsher, over trachea and anterior chest.

Abnormal/Adventitious

 Crackling - fluid accumulation or fibrosis

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 Wheeze - mostly during exp. high pitch

 Ronchi - low pitch. Stridor - Insp. wheeze
 Pleural friction rub - creaky leather sound

CLINICAL RESPIRATORY SIGNS VERSUS ANATOMIC LOCATION

 Pharynx : Salivation, gaging, retching, stridor

 Nasal Cavity : Discharge, snorting, sneezing N. rubbing
 Larynx : Gagging, dyspnea, stridor, occasional cough
 Trachea : Harsh, resonant cough followed by gag
 Bronchi/Bronchioles : Cough followed by gag
 Alveoli : Tachypnea, dyspnea, cough-yes/no
 Pleural Effusion : Tachypnea, dyspnea.

SIGNS OF RESPIRATORY DISEASES IN SMALL ANIMALS

Cardinal Signs of Respiratory Diseases

 Cough, Hemoptysis
 Dyspnea, Cyanosis
 Abnormal Secretions
 Noisy Breathing, Tachypnea
 Sneezing, Wheezing
 Change in voice, body posture

Nonspecific Systemic Signs

 Fever, anorexia, fatigue

 Lethargy, weight loss
 Others

Cough

 Sudden forced Expiration after deep Insp. on closed epiglottis

 Protective reflex. Clears Tracheo-bronchial Tree.
 Afferent arm: from irritated mucosa of Pharynx (glossopharyngeal N) Larynx, Trachea,
Bronchi, pleura (Vagus) cough centre in Medulla Oblongata.
 Efferent Arm through sympathetic trunk & cervico-thoracic motor nerve to intrinisic and
accessory muscles of respiration.

Etiology of Cough

 Inflammation - Pharyngitis, Bronchiectasis

 C.V. disorder - L. Heart failure
 Trauma, Physical Agents - Foreign body, Smoke
 Neoplasia - Primary or secondary
 Allergic disorders - Bronchial Asthma
 Parasitism - Larva Migration, D. Immitis - Filaroides, Paragonimus
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Cough - Potential Harmful Effects

 Dissemination of Infection.
 Rupture of Lung Abscess
 Rupture of Pleural Adhesions.
 General Weakness, Malaise, Fatigue

Clinical Signs - Upper Respiratory Diseases

 Sneezing
 Cough
 Nasal Discharge
 Facial Swelling
 Stertorous breathing
 Voice Change
 Inspiratory dyspnea
 Loud upper Resp. Sounds

Clinical Signs - Lower Respiratory Diseases

 Cough, Nasal discharge

 Inspiratory / Expiratory dyspnea
 Hyperpnea
 Abnormal Lung Sounds
 Rapid shallow respiration

Sneezing

 Forced expiration after deep inspiration on open epiglottis.

o Rids the nasal passages of irritants
o Occasional sneezing is normal, esp. in Hairy faced breeds. eg. Lhasa,
 Prolonged episodes - F.B. allergy, viral diseases.
 Bleeding & discharge - Trauma, Destructive Lesion

Nasal Discharge

 Serous - Mucoid Viral Diseases, Allergy, irritants

 Purulent - Chronic Infections
 Mixed with Blood - destructive Lesion
 Unilateral - Sudden - Foreign Bodies.
 Insidious - Tumor, Fungal

Stertorous Breathing

 Obstruction
 Nasal & Pharyngeal Disease
 Inspiratory Wheezing-Laryngeal or URD.
 Honking/Rattling - Tracheal Collapse
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Abnormal Secretions - Tracheobrochial Tree

 Mostly Swallowed
 Vomited out following coughing as mucoid watery material
 Purulent sputum - Pneumonia, bronchiectasis
 Hemoptysis - Thoracic trauma, Diroflariasis, Pulmonary edema, Lung tumors, Lung worms
F.B.

Dysepena Labored or difficult breathing

 Severe signs - Respire with open mouth, cyanosis, pallor or injection of mucosa
 Main causes
o Stimulus for ventilation e.g. Hypoxemia, Acidemia, Fever.
o Ventilatory Capacity e.g. Resistance to airflow, Weak Respiration

Causes of Dyspnea

 Obstruction of air passages - Inflammatory.

 Restrictive Lung volume – Diseases like Diaphragmatic Hernia (DH).
 Primary Diseases of Lungs - Emphysema
 C.V. and anemic disorders - Anemia
 Nervous Emotional disorders - Fear
 Metabolic disorders - Acidosis, hepatic coma.

DRUG THERAPHY IN RESPIRATORY DISEASES

Drug Therapy in Respiratory Diseases

 Purpose: To maintain Normal Ventilation, Reflexes and Secretion

 Pre-requist: An accurate diagnosis
 Choice: Perform Surgery -DH.
o - Medicate if, Bacterial Pneumonia.
o - Do nothing, if viral infections.

Medical Treatment

Must Consider

What is medically possible

 Benefits of Treatment
 Potential risk to the patient
 Pathophysiology of Respiratory Tract Inflammations

Mucokinetic Therapy

 Mucokineses achieved by:

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Thinning Viscous Secretions

o
Improving ciliary activity
o
o Improving air way mechanics
o Water most valable Agents
 Mist (steam)
 Vapor (aerosols) Mouth
 Caution - Bronchospasm with (a) & (b).
o Agents - water, Saline. 2% Propylene glycol 2 ml
o Acetylcysteine - Breaks mucoprotein mol. 2 to 5 ml, 10% Sol for nebulization
o Sod. Bicarb 2.5% for nebulization natural proteases, Adhesiveness Resp. secretion by osmotic effect
o thanol - Surface tension of Resp. T.
o Eucalyptus, menthol and camphor - ?

Oral Mucokinetic Agents (Expectorants)

Reflex stimulation of vagal efferents to Bronchial gland through gastric mucosa.

 ral W.K. Salt sol. - Ammonium bicarbonate

 Amm. chloride, KI, Sodium bicarbonates NaCL
 Volatile oil
 Phenolic Compounds - Creosol, G. Guaiacolate.

Aerosol Therapy

 uspension of a liquid as fine particles dispersed in a gas. Idea particle size 2-4 u
 A plastic bag tapped to the neck and a nubulizer attached at one cut corner

BRONCHOSPASM THERAPY

A. Sympathomimetic dilators (long acting)


o B 2 stimulator preferred
o Ephedrine: Mod B 2 , slight B 1 &
o Metaproterenol: B 2 , B 1 &
o Salbutamol: specific B 2
 Phosphodiesterase inhibitors - Xanthines
o Preserve AMO. Intercellular messenger eg., Theophylline and aminophylline
o Relax brochial M. Cardiac output

Antitussive Therapy

 Depress cough than totally supress.

o Act peripherally - irritation, block receptors e.g. Benzons
o Act Centrally
 Narcotic antitussives - codeine, hydrocodone
 Non-narcotics - Benzonatate, dextromethorphan
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Decongestant Therapy

When specific etio. lacking


 Antihistamines - chlorpheniramine
 Alpha adrenergic sympathomimetics
 Cause vasoconstriction. Rebound congestion?
 e.g. Phenylephrine, phenylpropanolamine

Antimicrobial Therapy

large mole AB (Gents - Erythro.) have better blood - bronchial penetration then small mole AB - (Penicilline, C
 Topical Antibiotic - not effective in tracheobronchial tree

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SPECIFIC REPIRATORY DISORDERS

Therapy of Specific Respiratory Disorders Bronchitis and Small Airway

Disorders Acute Bronchitis

 Inflammatory bronchi
 Clinical signs - retching, paroxysmal coughing
 Antibiotic no value, humidification and oral water helpful
 Expectorants arc of little value
 Spontaneous recovery

Chronic Bronchitis

 2 consecutive months in a year

o Squamous metaplasia of bronchial M.
o Loss of ciliated cells
o Proliferation of goblet cells
 Treatment - Aerosols, AB, Bronchodilators
 Oral expectorants. Antitussives at night

Bronchopneumonia

 Bacterial pneumonia - AB doses through complete recovery

o - Humidification of air

Pulmonory Infiltrates with Eosinoophilis

 Allergic etio Transtracheal wash diagnosis Eosinophilia. No bacterial growth in culture

 Prednisone 1mg/lb/day - NED calculated
 Give E O D mornings to dogs

Small Airway Disease & Emphysema

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 Signs - wheezing, coughing, expir. effort

 Bronchodilators, corticosteroids as treatment
 Antibiotics if infectious component present
 Emphysema - distension of air spaces
 Distal to terminal bronchioles with destruction of alveolar septa.
 Antibiotics and Bronchodilators as Treatment.

RHININTIS AND SINUITIS

Acute Rhinitis

Traumatic (Sharp or Blunt)

 Etio - Auto, Bullet, Bites, Kicks, F.B.

 Symp. - Epistaxis, sneezing, snorting
 Bony fractures
 Open mouth breathing deformity
 Dx - MDB, X-ray, Rhinoscopy, Exploratory
 Rx - Epistaxis - Sedation, confinement. Ice packs
 Gauge packing, Deformity -surgery
 FB - Removal, reverse flushing

Viral Rhinitis/Bact. Rhinitis

 Etio - viral CD, Adeno, Herpes, Reo, Influenza

o Bact.- Bordetella, Mycoplasma, Spirochetes
 Symp.- Fever, sneezing, nasal discharge, tracheitis, bronchitis, cough
 Dx. - MDB, symptoms, dried nasal secretions
 Rx. - TLC, remove dried secretions
o Instill 4-6 drops of broad spect. AB TID
o Phenylophrine 0.2% I/N TID

Chronic Rhinitis/Sinusitis

 Etio - Following acute, allegic

o Sec. bact. staph, strep, prote.
o Mycotic, - aspergillus, crypto,
o BP - Dolicocephalic, collie
o Parasitic - Linguatula serrata
 Pneumonyssys Caninum
o Caranassialtooth abscess
 Symp - Sneezing, nasal discharge, U/B
 Smearing, conjestion, stertorous breathing
 Facial deformity
 Dx - MDB, x-ray, Rhinoscopy, Cytology, Culture
 Rx - Bact. - revelent AB
 Mycotic - Surgery, currettage, 1% lugols + 90 mg/lb, TDD, of 5-FC, QID for 3 m.
 Neoplasia - surgery and currettage, radiation
 Parasitic - Self limiting confine in a cage with a dichlorvos strip in it
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 Carnassial tooth - Extraction, AB

TONSILLAR AND LARYNGEAL DISORDERS

Tonsillar and Laryngeal Disorders

Tonsilitis

 Palastine Tonsils, Pharyn, Tonsil

o Prevent micro organism entry
o Help formation of lymphocytes
o Infected tonsils provide nidus for dissemination of infection
o Tonsillar hyperplasia normal in pups

Acute Tonsillitis

 Etio - Bact. strep. hemolyticus common

 Symp - Hyperplasia to hyperemia
 Necrotic focci to grayish exudate
o Anorexia, dysphagia, emesis, fever, pain, drooling. lymph N.
 Dx - Clinical signs - Inspec & Palpation, Culture
 Rx - AB, paint with KMNO 4 , 10% AgHO 3 ,
 Iodinated glycerine, Boroglycerine

Chronic Tonsillitis

 Etio - Sequlae to acute, or CD

o More in mature and older dogs
 Signs - Same as acute
 Dx - same as acute
 Rx - Tonsillectomy, medical

Tonsillar Neoplasms

 Etiopath - Epitheliomas, Sq. cell. carc.

 Regional spread to lymph N.
 Signs - Same as in acute tonsillitis size, hemorrhage
 Dx - Inspec. palp. Cytology, Biopsy
 Rx - Surgery, radiation. Chest x-ray

Laryngitis

 Etiopath - Excess barking, irritation, virus

o From surrounding area
 Signs - Change in voice, fever? coughing at deglutation, drooling?
 Dx - MDB, gurgling sound on ausc.
 Rx - Control barking, AB
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Laryngeal Edema/Stenosis/Fract.

 Etiopath - Following surgery, brachyceph.

o Trauma - bite
 Signs - Snoring, Insp. dyspnea, gurgling
 Wheezing as in laryngitis
 Dx - MDS
 Rx - Proper breathing, steroids
 Surgery, Tranquilizers, diuretics, AB

Laryngeal Neoplasia

 Etiopath - Uncommon, polyp. Adenoma

 Adenocarc., mast cell, lymphosarc.
 Signs - Change in voice, cough, wheezing, etc.
 Dx - MDB, cytology, biopsy
 Rx - Surgery

LARYNGEAL PARALYSIS

Laryngeal Paralysis(dogs)

 Failure of glottic cleft to open

 C/S: Dyspnea (inspire), Cyanosis, Voice difference, coughing, upper respiratory obstruction,
exercise intolerance, stertorious sound (gurgling), open mouth breathing.
 Dx: Laryngoscope=> hyperhemia, edema, no abduction on inspire.
 U/S, THS, EMG and nerve conductivity
 Histopathology: mild to moderate type 1 and 2 myofiber atrophy
 Tx: Emergency tracheostotomy
 Steroid (edema)
 Sx enlargement of glottic cleft
 Unilateral arytenoids lateralization
 Partial laryngectomy
 Castellated laryngofissure and vocal fold resect
 Soloxine if low T4

TRACHEAL DISORDERS

Trachea

 Non collapsible cylinderical structure

 35 incomplete cartilage rings
 Cervical and thoracic trachea
 Thoracic affected by pleural pressures

Trecheitis

 Etio - Viral, bact., parasitic, irritative

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o Adeno, herpes, perainfluenza, CD. Virus

o Sec. bac. coli. strep, pseudo, bordetella
 Parasitic: Aelurostronglus, Capillaria,
 Crenosome, Oslerus D.
o Inhalation of irritative gases, smoke, etc.
 Signs - Gagging cough, earlier non-product.
o Affects younger < 1 yr dogs
o Anorexia, fever, depression, cough on palp. harsh sound on auscult.
 Leucocytosis
 Dx - MDB, CBC, culture, cytology (T.W)
 Rx - On cause, cough suppresents, AB; I/T.
 Bronchodilators, vapor humidification
 Levamisole, Benzimidazoles.

Collapsed Trachea

 Etio - Congenital, trauma, DV compression

o Toy or minature breeds, chi, Yorke
 Signs - Honking cough, cyanosis, dyspnea
 Dx - BP, signs, MDB, x-ray, fluroscopy
 Rx - Symptomatic, reduce wt. cough suppresent
o Acute case oxygen therapy. Surgery

Tracheal Neoplasia

 Etiopath - Uncommon, osteosarc, carci.,

o Chondroma, osteochond.
 Signs - Cough, gagging, dyspnea, cyanosis
 Dx - MDB, T. wash, cytology, endoscopy
 Rx - Surgery, Chemotherapy

BRONCHITIS AND BRONCHIECTASIS

Bronchitis

Acute Bronchitis

 Etio - Infectious, Non-infectious, Irritative

o Infectious Tracheobronchitis (kennel cough)
 Very imprecise term
 Etio - Virus - CD, CAV -2, CPI (Simian V 5 )
o Mycoplasma and Bacteria
 Signs - Kennel problem in unideal Hygiene
o Transmission through masopharynx.
 cough, dry/moist, hacking paloxysmal
 gagging, expectoration
o Excitement, change in temp, humidity, palpation may elicit cough
o mild cases, runny eyes, tonsilitis
o x-ray - mild Broncho Pneumonia
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 Severe form - fever (103 0 - 104 0 ) anorexia

 mild or no cough. Mucoid/MP
 nasal discharge. Tonsilitis,Pneumonia
 Dx - MDB, x-ray, vaccinations, bronchial
 wash - Intranuclear Inclusions
o R/o - CD, ICH, Mycoses.
 Rx - Confinement, isolation, antitussive
 ihydrocodainone 5ml/20lb Q.I.D.
 AB against Gram - Ve. Chloramph.
 Cephalosporins, Gentamicin
 Nembulizers. Bronchodilators.
 Isuprel Comp. Elexir 2ml/10lb T.I.D.
 TLC and supportive therapy

Chronic Bronchitis

 Etio - Viral, Bact, Allergy, Mycoses, neoplasia, C.V.

 Signs - More common in > 4 yrs. Persistant Harsh cough with retching
o Productive moist. Moist rales on Ausc.
 Dx - MDB., x-ray, cBC, - "Stress". Bronchoscopy
 Cytology, culture
 Rx - Control/Cure - AB, Bronchodilators, expect.
 Antitussive Prednisilone 0.5 mg/lb/day
o TLC, Humidification, Hembulization.
o Treat the cause

Bronchiectasis

 Persistant abn. dilation of Bronchi/Bronchioles

 Both Saccular and Cylindrical dilations
 Etio - Sequela to Chr. Bronchitis, F.B, Pulmonary.
 Fibrosis, Neoplasia
o Destruction of Wall, collection of Mucous, no collateral ventilation
 Cillia and elastic muscular component destroyed.
 Distortion & Fibrosis of the lumen, dilation, pooling
o Etra/Intra lumminal obs. same pathogenesis
 Signs - History of persistant tracheo Br. Alg. Br. Pneum.
o Early, dry and non Prod. cough, later prod. Hemoptysis
o Auscultation rales like Chr. Br., Anorexia depression, fever
 Dx - MDB, Br. scopy, Culture, Br. wash, - Inflam. Resp.
 x-ray - fibrosis, peribronchial thickening, atelectasis,
 consolid.
o Absence of N. branching Pattern. doughnets
 Rx - Symp. like chr. Br. Control-yes, cure -no.

PULMONARY OEDEMA

Pulmonary Edema

 Accumalation of Extravascular Fluid

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 Etiopath - Alteration in a capillary Endo, Basement Memb. alveolar epithelium, interstial

 Comp. Pulm. Lympaties
o Physical forces like, hydrostatic Press. in caps.
 Hydro. P in Interstitium. Obs. lymphatics
 Cap. Osmotic P. Osmotic P in Interstitum
o Pours in alveoli and terminal Bronchiole
o Dyspena, Tachypnea, - metabolic Acidosis
 Etio - Cardiogenic - Lt. heart Failure. Cardiomyopathy non cardiogenic - Hypoalbuminemia,
diffuse Neop.
o Iatrogenic overhydration & left heart & Renal failure
o Viral and Bact Infections, Anaphylaxis
o Toxicosis - Phosgene, ANTU, Paraquat, Venoms
o Neurogenic, I/cranial P. - acute onset
o Electric shock, Aspiration of Irritants, DIC, Thoracic Trauma
 Signs - Tachypnea, dyspnea, moist cough, Harsh rales. Cyanosis, Nemoptysis
o Muffled Heart sounds
 Dx - MDB, x-ray
 Rx - Acute - Treat as emergency. Oxy. Diuretics
o Bronchodilators, correct acidosis
o Lasix/mg/lb/v TID; Digoxin. 0/mg/lb po.
 Ammophyllin % mg/lb/TID.

PNEUMONIA AND EMPOHYSEMA

Pneumonia

 Classify - Broncho. Lobar., Intgerstitial, Br. Vascular, Thromboemoblic,

 Granulomatous, Atelectasis
 Etiopath - Physical, chemical, biological agents
 damage resp. mucosa, Inflam, reduced cilliary activity, fluid accumulation, Pneumonia
o - Ecoli, Pseudo, Pasteu. Proteus, Strep, Staph
 Bordetella. Virus, Fungal.
 Parasitic - A. Abstrusus, P. Kellicott
 Signs - Anorexia, depression, dehydration, fever
 Prod. cough, Rhinitis, Sinusitis, Conjectivitis, moist roles on Auscultation. Dyspnea, activity.
 Dx - MDB, Leukocytosis, "Stress response" degenerative left shift. Metabolic and Resp.
acidosis. x-ray-alveolar pattern
o - Culture & Sensitivity through Bronchial wash or Percutaneous route
 Rx - Same as in chr. Bronchitis, AB. through clinical recovery Anthilminitics

Pulmonary Infilterates with Eosinophils

 Etiopath - Unknown, Hypersensitivity, Biroflariasis

 Chr. Pneumonia. Auto immune disease
 Signs - A Chr. dry cough, anorexia, fever, dyspnea, wheezing, resp, failure
 Dx - Eosinophilia, Eosinophilic Infilterate,
 Leukocytesis, neutrophilia, x-ray, diffuse
 alveolar Infilt. and Peri-Bronchial thickening
 Rx - Symp. relief, prednisolone C.l mg/lb/day Bid.
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Emphysema

 Over distension of distal alveoli

 Etio - Obst. of Bronchioles, trapping of air weakening of airways and narrowing.
 Signs -Obscure, expiratory dyspnes, Barrel chest, Abducted Elbows
 Dx - X-ray R/o Pneumothorax, Bullae Formation. Pneum
 Rx - as in Chr. Bronchitis

PLEURAL EFFUSIONS

 Etiopath - Altered homeastasis of Plearal Fluids

o Sign of a disease not a disease itself.
o Primary Pleural disease -Mesotheliomas
o Second eg. conjestive H. Failure, Kypoproteinemia.
 Signs - Variable comprimised lung expansion
o Labored breathing Abd. breathing, mouth breathing
o Abducted elbowsm change in postures, NonProd. cough
 Dx - MDB, X-ray, hemograms, Urinalysis, BUN, TP, SGPT.
o Thoracocentesis, Chest tube, Fluid Analysis, Culture
o CK. Benjamin "Clinical Path" for fluid analysis
 Rx - On cause, Hydrothorax - removal of fluid Dry Pleuritis - AB, chest
 Bandage, Antitussives, Purulent Pleuritis - Thoracocentesis,
 Continuous aspiration. Chylothorax - Surgical ligation,
 Nemothorax - blood transfusion, Exploratory thoracotemy.

MODULE-19: DISEASES OF CARDIOVASCULAR SYSTEM - I

Learning objectives

 To know about clinical signs, diagnosis and treatment of

o Congestive heart failure
o Acute heart failure
o Canine cardiomyopathy
 To know about the significance of pericardial effusion in animals.

PRINCIPLES OF HEART FAILURE

 Heart failure and Shock are both manifestations of circulatory failure.

 Heart failure, a deficit in myocardial performance, is characterized by the inability of the
heart to adequately pump the blood presented to it.
 In shock, there is an inadequate venous return to the heart, usually as a result of peripheral
circulatory failure.

Functional response to Cardiac Disease

 The circulatory system has multiple responsibilities including the transport of oxygen &
nutrients to the tissues; the transport of carbon dioxide & other products of metabolism
to
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the lungs and kidneys; the distribution of hormones and other substances that regulate cell
function; and maintaining the adequacy of thermoregulation and urine formation.
 Circulatory control is affected by multiple regulatory systems which generally ensure an
adequate capillary blood flow to meet the varying metabolic requirement of various organs,
tissues and cells.
 Circulatory adjustments are affected by neural and chemical mechanisms that change the
caliber of arterioles and other resistance vessels, that vary the rate and stroke out put of the
heart, that increase or decrease blood storage in the capacitance venous vessels, and that in
certain specific situations create alterations in the caliber and permeability of capillaries.
 It is readily apparent that other organs of the body are affected when heart function is
impaired, even before congestive heart failure becomes clinically apparent. Therefore, many
of the signs of congestive heart failure have their basis in organs other than the heart, and the
same signs can be produced by other causes when the heart is normal. The involvement of
multiple organs in heart disease may be either compensatory functions to maintain
homeostasis or functional derangements brought on by circulatory insufficiency.
 In animals with heart disease, the maximal sustainable cardiac output is usually reduced
because the cardiovascular reserve capacity is being used even at rest. The importance of the
components of the cardiovascular reserve becomes apparent in understanding the functional
response to heart disease.

UNDERSTANDING THE FUNCTIONAL RESPONSE TO HEART DISEASE

The importance of the components of the cardiovascular reserve becomes apparent in understanding
the functional response to heart disease. The following factors must be considered (and their
limitations).

1. Venus oxygen reserve

2. The maximus effective heart rate
3. The stroke-volume reserve
4. Cardiac work and efficiency
5. Coronary vascular reserve
6. Cardiac enlargement

Venous Oxygen Reserve

 Exercise taxes the cardiovascular reserve and serves as a model to define its component. The
amount of exercise or activity that can be performed over any extended period of time is
limited by the maximal capacity of the cardiovascular system to deliver oxygen to the
tissues.
 The amount of oxygen consumed by the tissues is limited by the cardiac output and by the
amount of oxygen extracted from each increment of blood. Therefore, oxygen availability to
tissues is dependent upon cardiac output and the magnitude of the arterial-venous oxygen
difference.
 Typically, each 100 ml of arterial blood contains l9cc of oxygen. At rest, mixed venous blood
contains about 14cc of oxygen per l00ml. Oxygen extraction increases progressively with
exercise so that at maximal levels of exertion, 75% of the oxygen may be removed from the
blood passing through the systemic capillaries.
 The venous oxygen reserve can be depleted to this extent only if extraction increases in both
active and inactive tissues. Vasoconstriction during exertion diverts blood flow from the skin,
kidneys, gastrointestinal tract, and spleen, making more oxygen available for active muscles.
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Heart Rate

 Heart rate is the most liable factor in the cardiac reserve an increase in heart rate in the
principle means by which cardiac output is increased in response to an increased demand for
blood flow. The maximal effective increase in heart rate is approximately two and one half
times the normal rate for that animal.
 Example: In the dog the resting rate is about 70 beats per minute, however the heart rate in
this species is capable of increasing its maximum cardiac output effectively up to 180 beats
per minute. Beyond this rate. Tachycardia results.
 Increased heart rate usually do not occur as isolated events, but rather as part of a
coordinated cardiovascular response of autonomic (sympathetic) nervous system origin.

Stroke Volume

 Mean the amount of blood the heart ejects with each beat. When the normal resting heart
contracts, it empties by only one half. Thus it can theoretically increase its output by
emptying to a greater degree or utilizing the systolic reserve volume.

Efficiency of the Myocardium

 The efficiency of the myocardium is the amount of useful work performed divided by the
total energy expended. Thus, myocardial efficiency may improve in the normal animal during
exercise since useful work is increased more than myocardial oxygen consumption. In
congestive heart failure, the efficiency of energy conversion is reduced at rest and declines
further during exercise.

Coronary Vascular Reserve

 The amount of oxygen available to the myocardium depends upon the coronary blood flow
and the arterial-venous oxygen difference.
 The normal heart, even at rest extracts most of the oxygen available to it. (Therefore, the
myocardium has very little coronary venous oxygen reserve).

Cardiac Enlargement

 Hypertrophy
 Dilatation
o Both maybe due to a physiologic compensatory mechanisms which enables the heart
to adapt to an increased work load.
 Compensatory mechanisms (most are self limiting)

a. Tachycardic

b. Chamber dilatation

c. Wall hypertrophy
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CONGESTIVE HEART FAILURE

 The failure of the heart to adequately pump blood is the simplest definition of cardiac failure.
 Congestive heart failure is the clinical syndrome initiated by myocardial dysfunction or
failure and is characterized by pulmonary or systemic venous congestion or both and low
cardiac output.
 The Congestive aspects of heart failure results from the body’s attempts to compensate for a
low cardiac output principally by sympathetic reflexes and by the renal retention of fluid.
 Indeed, these compensatory mechanisms frequently determine whether cardiac disease is
clinically detectable or not, and they form the basis for many diagnostic and therapeutic
considerations.
 Fluid retention - a low cardiac output can cause anuria, and the urinary output is generally
less when the cardiac output is below normal. Similarly, the relationship between cardiac
disease and the accumulation of edema and accites has long been recognized, as has the
causal relationship between increased salt intake and the progressive accumulation of fluid
in congestive heart failure.

Clinical Manifestations of CHF

Clinical signs of Left Heart Failure

 Mainly pulmonary components, which on exertion causes

 Cough
 Orthopnea
 Paroxysmal dyspnea or cardiac asthma
 Cyanosis
 Hemoptysis
 Varying degrees of pulmonary edema
o Animal with left ventricular failure are frequently reported to develop respiratory
distress while lying down resting. This is due to the escape of fluid into the tissues as
a result of daily activity which is reabsorbed while resting, thus expanding, the
blood volume and creating respiratory distress. The term Orthopnea applies for this
occurrence, such patients present with a history of not resting well during, the night.

Clinical Signs of Right Side Heart Failure

 Generalized systemic venous congestion

 Distension of the jugular veins and other superficial veins
 Hepatic & splenic enlargement
 Effusion of fluid in serous cavities
 Subcutaneous edema
o Other features of congestive heart failure when there is generalized distention of the
superficial veins.
o Due to the increase in the central venous press with right heart failure. The jugular
veins remain distended even when the head is elevated.

Hepatomegaly and Splenomegaly

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 Hepatomegaly and Splenomegaly are consequences of chronically elevated systemic venous

pressure. Hepatic function test are usually moderately elevated (SGPT) which is central
lobular necrosis. Also noted are mild to moderate elevation in the SGOT test, alkaline
phosphatase and urobilinogen levels.

Ascites

 Ascites in the dog, is a very common occurrence and tends to develop long before
subcutaneous edema becomes apparent. The ascites fluid that in right heart failure is initially
a transudate with a specific gravity below l.018. With chronic ascites the fluid frequently
becomes blood tinged and the specific gravity may rise above l.018.

TREATMENT OF CONGESTIVE HEART FAILURE (CHF)

ation of approaches is usually involved for successful management of C.H.F. The veterinarian must consider all etiol
all associated organ structures which may be involved.

The practical approach when C.H.F. is present, is

to decrease exercise,

 to decrease sodium intake,
 to mechanically remove excess fluid from the body cavities,
 to provide sedation if needed,
 proper nutrition,
 bronchodilatation and
 supplemental oxygen as needed.
o Additionally, the use of cardiac glycosides (digitalis) and diuretics are the backbone of pharmacologic ther

The beneficial effects of digitalis

 Increases the force of myocardial contraction causing the ventricle to empty more completely, resulting in
 An increased stroke volume and cardiac output
 Improved renal hemodynamies with a resultant diuresis
 The loss of excessive fluids
 Decreased venous pressure and a reduction in the diastolic volume
 Decrease in the heart rate
There is no fixed dosage rate for the administration of cardiac glycosides, each patient must be individually assess
ndamental principles of digitalization is to administer the drug until the desired therapeutic affect is achieved or un
intoxication appear.

Last modified: Tuesday, 5 June 2012, 06:02 PM

CLINICAL ASSESSMENT OF CARDIOVASCULAR SYSTEM

The circulatory system consists of two main functional units, the heart and the blood vessels. The
function of the cardiovascular system is to maintain the normal exchange of oxygen, carbon dioxide,
electrolytes, nutrients, fluids and excretory products between blood and tissues.
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Area of examination of the heart in equines and ruminants

Area Equines Ruminants

Base From 2nd to 6th intercostal space From 3rd to 6th rib
Apex Half an inch from the last sternal segment One inch from the
diaphragm
Posterior Opposite to the 6th rib Opposite to the 5th rib
border
Left surface Composed of left ventricle and extends from Extends from 3rd to
3rd to 6th rib 4th rib
Right surface Extends from 3rd to 4th rib Not examined

Position of valves

 Mitral valves
o Examined on the left side in the 5th intercostals space, 4 inches above the sternal
extremity of 5th rib.
 Tricuspid valves
o Present on the right side in the 3rd intercostals space and 3 inches above the sternal
extremity of the 4th rib.
 Aortic semi-lunar valve
o Present on the left side in the 4th intercostals space level with the shoulder point.
 Pulmonary semi-lunar valve
o Present on the left side in the 3rd intercostals space at the level of olecranon process
of the ulna.
o Examination of the circulatory system includes examining the heart, pulse and
blood vessels.
o Chest movement is noticeable in small and young animals (normal animals). Visible
evidence of cardiac activity is noted in over-exertion, haemolytic anaemia and some
cardiac diseases.
o The strength of cardiac impulse can be determined by placing the palm of the hand
over the cardiac area on the left side.
o The point of maximum impact is increased in area and displaced posteriorly in
cardiac hypertrophy or dilatation associated with insufficiency or anaemia; anteriorly
in ascitis, hepatomegally, distention of stomach or intestine with food or gases. It
cannot be palpated when the heart has been displaced away from the thoracic wall as
in serous pericarditis, pleurisy, hydropericaritis, hydrothorax and mediastinal or
pulmonary neoplasia or hydatosis.
o The character of heart sounds and presence of abnormal sounds is detected by
auscultation. Two main sounds must be differentiated:
o The first heart sound is dull, loud and prolonged. Followed immediately by the
second heart sound, which is shorter and sharper. The second heart sound is followed
by a pause. The first heart sound is the result of contraction of the cardiac muscle
together with closure of the atrio-ventricular valves. It corresponds to the phase of
cardiac systole and is referred to as systolic sound. The second heart sound is
produced by closure of the semi-lunar valves. It occurs during the cardiac diastole
and is therefore termed the diastolic sound.
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o When the heart rate is slow, the first and the second sounds are readily recognized by
their characteristic and by the fact that the first sound occurs after a pause whereas
the second sound occurs directly after the first. If the heart rate is increased, the
sounds cannot be easily distinguished from each other. In these cases, palpating the
wall and detecting which sound coincides with the apex beat with help distinguish
systolic sound.

Abnormal heart sounds

 Abnormal heart rate

o Increased rate with loud sounds occur in cardiac hypertrophy, anaemia,
febrile conditions, exertion.
o Decreased rate with weak sounds occur in cardiac insufficiency, congestive heart
failure, all conditions in which the heart is displaced away from the thoracic wall or
fluid is present in the pleural or pericardial sac (hydro pericardium, hydrothorax and
pleurisy).
 Abnormalities in intensity of heart sounds
o The intensity of the first heart sound is related to the force of the ventricular
contraction, so that it is increased in ventricular hypertrophy and decreased in
myocardial weakness.
o The intensity of the second heart sound is dependent upon the arterial and
pulmonary blood pressures. Accentuation of the second heart sound is usually the
result of an increase in the backpressure of the blood against the closed valves. This
occurs when the blood is expelled from the ventricles with greater force than usual
producing a variable degree of hypertension. This hypertension is observed in
bronchitis, pneumonia and pulmonary emphysema, which result in increased
resistance in the pulmonary circulation. Less often, the accentuated second heart
sound involves the aortic valve at which instance it is attributable to increased
resistance in the systemic circulation as in renal disease.
 Reduplication of the heart sounds
o Reduplication of the first sound occurs in elevated blood pressure and in
asynchronous contraction of the ventricles. This is observed in disturbance in the
conductivity of one branch of the bundle of hiss or severe damage of the myocardium
(myocarditis).
o Reduplication of the second heart sound occurs when the semi-lunar valves fail to
close simultaneously, seen in pulmonary hypertension where the pulmonary semi-
lunar valves are rarely closed. Reduplication also occurs in asynchronous ventricular
contraction.

Other abnormal heart sounds

 These may replace one or both heart sounds or accompany them. They may originate from
the cavities of the heart or from the pericardium. Those that arise from the inside of the heart
are classified as murmurs and are caused by endocardial lesions such as valvular vegetation
or adhesions, valvular insufficiency and by abnormal orifices such as ventricular septal
defect.
 Cardiac murmurs caused by these conditions maybe hissing, humming, whirring or vibrant
in tone. Such sounds are produced by stenosis of the valvular orifice or insufficiency of the
valves.
 Theoretically there are eight possible separate valvular defects but several of the possibilities
are extremely rare in animals. The murmur arising from stenosis is produced when the
valve
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is open and that of insufficiency when the valve is closed. Valvular endocardial murmurs are
caused by chronic valvular endocarditis, cardiac dilatation, acute endocarditis and neoplasia.
 Endocardial murmurs occur during either systole or diastole. Systolic murmurs indicated
either stenosis of the semi-lunar orifices or insufficiency of the atrioventricular valves.
Diastolic murmurs suggest the opposite; either stenosis of the atrioventricular orifice or
insufficiency of the semi-lunar valves. These endocardial murmurs are heard at the site of the
valve.
 The continuous machinery murmur of the patent ductus arteriosus maybe heard during both
systole and diastole over a wide area of the thorax but most intensely in the 3 rd left
intercostals space in the region of the pulmonary valve.
 Murmurs that originate at the valves or other cardiac structures are classified as organic
murmurs, whereas those that occur in the absence of primary heart disease are known as
functional murmurs (non-organic).
 Functional murmurs are best heard in anaemia where the reduction of haemoglobin and
red blood cells, the oxygen-carrying capacity of the blood is greatly reduced, with the result
that the circulation time is shortened in an attempt to prevent tissue anoxia, this leads to
increased heart rate.
 Functional murmurs are usually systolic, rather faint and organic murmurs in contrast
are loud and maybe either systolic or diastolic, audible at a precise phase of the cardiac
cycle.

Pericardial sounds

 Frictional sound is heard at the beginning of pericarditis where its surface becomes rough
and dry. The exudation into the pericardial sac results in presence of fluid that sets in motion
by the movement of the heart; the heart sounds then becomes muffled.
 Appearance of gas on the surface of fluid in the pericardial sac results in presence of tinkling
or splashing sounds. These sounds are observed in traumatic pericarditis in cattle.

CONGESTIVE HEART FAILURE

Etiology

 Valuvular disease
o Endocarditis
o Congential valvular detects
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o Valve or chordae tendinae rupture

 Myocardial disease
o Myocarditis
o Myocardial degeneration
o Cardiomyopathy, congenital, hereditary
 Pericardial disease
o Pericarditis
o Cardiac tamponade
 Blood pressure increase
o Pulmonary hypertension, e.g. high altitude disease, cor pulmonale
 Congenital shunts, constriction
o Septal defects
o Fibro-elastrosis
o Aorta coaretation
o Patent ductus arteriosus

Clinical findings

 Left side failure

o Resting respiratory rate, depth increased
o Cough
o Moist crackles at lung base
o Dull percussion note over ventral lungs
o Dyspnea, cynaosis at rest
o Possibly murmur referable to left AV or aortic valves
 Right side failure
o Listlessness depression
o Reluctant to walk
o Shuffling, staggery under, eventual recumbency
o Anasarca ventrally under the jaw, down the neck and under the abdomen
o Ascites
o Hydrothorax
o Possibly palpable enlargement of liver beyond right costal arch
o Urine volume small, concentrated, minor albuminuria
o Profuse diarrhea terminally
o Anroexia
o Condition lost, weight may increase due to edema
o Jugglar vein distension (other veins also)
o Abnormally high and visible jugular pulse
o Epistaxis in some horses
o Hydropericardium
 Progenosis
o Horses with rhythm defects capable of surviving
o Rarely survive; survival is with permanently reduced cardiac reseve

Clinical pathology

 Increased venous pressure

 Paracentesis from all body cavities; fluid is edema transudate but has high protein content
due to anoxic damage to capillary walls
 Proteinuria
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Dignosis

 Resembles
o Peritonitis
o Bladder rupture
o Liver fibrosis
o Hypoproteinenmia
o Urine accumulation is ventral abdominal wall due to urethral perforation
o Edema of late pregnancy in mares and cows involving perineum udder edema,
ventral abdominal wall
o Pulmonary edema occurs also in
 Acute bovine pulmonary emphysema and edema
o Organophosphorous compound poisoning
o Jugular engorgement also caused by space occupying thoracic lesions, e.g. thymus
lymphosarcoma

Treatment

 Limited value in cattle because lesions not reparable. Impractical in all species because rest-
of-life treatment not eminently practicable
o Digoxin orally or intravenously in horses; intravenously only in cattle. Not
intramuscular in any species.
o Horse: I/V loading dose 1.0-1.5 mg/100 kg then maintenance dose every 24 hours at
half the dose. Oral loading dose; 7 mg /100 kg, plus daily maintenance oral doses at
hall the rate.
o Cattle and sheep: I/V loading dose 2.2 mg/ 100 kg, then maintenance doses 0.34
mg/ 100 kg every 4 hours. Any animals under treatment, require daily potassium
chloride (100g cattle, 30g horses) if not eating, with blood potassium levels being
monitored
o Furosemide (0.25-1.0 mg/kg for horses, 2.5-5.0 mg/kg for cattle) when edema a
problem; also reduce salt intake
o Stall rest

CONGESTIVE HEART FAILURE-DIAGNOSIS

Diagnosis

 History
o The patient may or many not have a history of a previous problem. The patient may
or may not be an medication. The patient may have a dry and harsh cough, especially
at night, in the early morning, or after exercise. The patient may be restless at night,
have orthopnea, exercise intolerance, syncope, respiratory distress
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 Clinical signs
o Left-sided heart failure:dyspnea, tachypnea, coughing, cyanosis, hemoptysis,
murmur or arrhythmia, cardiac cachexia, cardiogenic shock, pulmonary edema
, fever.
o Right-sided heart failure: possibly pleural effusion, muffled heart sounds, pericardial
effusion, ascries, distended jugular veins with visible pulsations, pallor, synope.

 Laboratory tests
o CBC, electrolytes, BUN, ALT, Alk, Phos, serum thyroxin levels, heart worm
microfilaria or immunologic tests, urinalysis.

 Throacic radiographs
o Cardiomegaly. With left-sided heart failure, may see dorsal displacement-
Cardiomegaly and pulmonary edema. With right-sided heart failure, may see pleural
effusion, engored caudal vena cava, and hepatomegaly.

 Echoradiography
o May see mitral or tricuspid regurgitation, dilated cardiac chambers, thickened
ventricular walls, pericardinal effusion, or dilated pulmonary vessels.

Prognosis

 The prognosis is fair to grave.

CONGESTIVE HEART FAILURE: TREATMENT STRATEGIES

Treatment

 Inform the client of the diagnosis, prognosis, and cost of the treatment.
 Intravenous fluid therapy with cardiac disease
o The indications for intravenous fluid therapy include
 Cardiogentic shock.
 Dehydration.
 Drug-induced hypotension.
 Renal failure.
 Moderate to severe hypokalemia.
 Anorexia.
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 Vomitting.
 Concurrent metabolic or infectious diseases.
 Need of a vehicle for constant rate drug infusions.
o Although Dextrose Saline or 2.5% dextrose in 0.45% Nacl are usually recommended
due to their lower sodium content, these fluids are controversial. They supply free
water and may actually increase cellular edema. 0.9% NaCl, in small volumes, 30-45
ml/kg/day, may be a more appropriate fluid with which to re-establish normal
circulating plasma volume in hypovolemic patients.
o Once the circulating plasma administer D5W or 2.5% dextrose in 0.45% NaCl at the
rate of 20-40 ml/kg/day.
o If the patient is receiving diuretics prior to admission and requires
maintenance intravenous fluid therapy, continue diuretic therapy.
o If the patient presents in cardiogentic shock, administer intravenous fluids and
intropic support until renal perfusion and the circulating plasma volume are
restored, then begin diretic therapy.
o Discontinue fluid therapy and administer diuretics if fluid overload occurs.
o Monitor the patient’s body weight, mucous membrane color, pulse rate and quality,
respiratory rate and effort, and thoracic auscultation several times a day to monitor
fluid therapy.
o Also evaluate urine output, blood gas analysis, indirect blood pressure
measurements, central venous pressure, PCWP, serum urea nitrogen, serum
creatinine, ECG and thoracic radiographs.
 If the patient is dyspneic but not cyanotic
o Place an intravenous catheter.
o Hospitalize the patient for observation.
o Administer furosemide ,2-6mg/kg IV,q6-8th or bumetanide, 0.05-0.05 mg/kg IV or
Po as needed for severe pulmonary edema (Caution: Must monitor serum potassium
levels and maintain with IV fluids to prevent excessive fluid and potassium
depletion).
o Evaluate the need for intravenous fluid therapy.
 If the patient is cyanotic
o Place the patient in an oxygen cage, administer oxygen via nebulizer, consider
nebulization of 20-35% ethyl alcohol if the patient has severe pulmonary
edema.
o Place an intravenous catheter.
o Administer furosemide, 2-6mg/kg IV in dogs, q1-2h, 1-4 mg/kg in cats, q1-2h, until
effective diutresis is established and respiratory rate decreases. Then decrease the
dose of furosemide to 4 mg/kg in dogs and 2mg/kg in cats q2-8h . An alternative loop
diuretic is bumetanide, 0.05-0.2 mg/kg IV or PO as needed, if furosemide appears to
be ineffective.
o Furosemide can also be administered as a constant rate infusion in refractory
patients, 3-8µg/kg/min CRI IV.
o If furosemide is ineffective, administer a thiazide diuretic, such as chlorthiazide, 20-
40 mg/kg PO q12h.
o Evaluate the need for intravenous fluid therapy.
o If the patient is in immediate need of oxygen , has pulmonary venous engorgement or
wheezes are auculted, administer aminophylline, 5-10 mg/kg IV, IM or PO q 8h, or
terbutaline, 0.01 mg/kg SC q4th or 1.25-5.0 mg PO q8-12h.
o Place a nasal oxygen catheter, administer nebulized nasal oxygen
o Administer morphine sulfate , 0.2mg/kg SC or IM, if needed for anxiety and
arteriolar dilatation.
 Cardiogenic shock
o The signs are dyspnea, tachycardia, decreased capillary refill time, decreased
pulse strength, possibly hypothermia.
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o Administer intravenous fluids. 2.5% dextrose in 0.45% NaCL at the rate of 30-45
ml/kg/day is usually appropriate. Consider the administration of Hetastarch, 5ml/kg
IV boluses, re-evaluate CVP , repeat up to a dose of 20 ml/kg to increase the
circulating plasma volume and control pulmonary edema.
o Administer furosemide, 2-6 mg/kg IV in dogs, q1-2h, 1-4mg/kg in cats, q1-2h,until
effective diuresis is established and respiratory rate decreases. Then decrease the
dose of furosemide to 4mg/kg in dogs and 2 mg/kg in cats as needed. If
furosemide appears to be effective.
o Furosemide can also be administered as a constant rate infusion in refractory
patients, 3-8 µg/kg/min CRI IV.
o If furosemide is ineffective, adminster a thaiazide diuretic, such as chlorthiazide, 20-
40 mg/kg PO q12h.
o If the patient is in immediate need of oxygen , has pulmonary venous engorgement or
wheezes are auscuted, administer aminophylline 5-10 mg/kg IV, IM or PO, q8th , or
terbutaline, 0.01 mg/kg q4th or 1.25-5.0 mg POq8-12th.
o Place a nasal oxygen catheter, administer nebulized nasal oxygen
o Administer morphine sulfate, 0.2 mg/kg SC or IM, if needed for anxiety and arterior
dilation.
 Vasodilator therapy
o Niytoglycerin cream: 0.25-2.0 inches, applied to a clipped area on the thorax or on
the abdomen , q4-6h, especially for pulmonary edema (venous dilator). Wear gloves
during application, use a tongue depressor to apply and cover the area with tape.
Avoid contact with the applicator’s skin. The dose for cats is 0.25-0.5 inch
cutaneously 86-8h, every other day.
o Captopril: 0.25-2 mg/kg PO q8-24th, (Arteriolar and venous dilator)
o Enalaprill: 0.25-2 mg/kg PO q8-12th. (dogs), 2-6 mg PO q12th (cats).
o Hydralzaine: 0.5-3 mg/kg PO q12h (Arteriolar dilator). Use caution and monitor
closely as hydralazine can induce marked vasodilation, decreased blood pressure, and
increased heart rate. Clinical affect occurs within 1h. Start with the low dose and
gradually increase as needed.
o Sodium nitroprusside (arteriolar and venous dilator): if unresponsive to all the other
treatment, administer sodium nitroprusside, up to 1-10µ/kg/min IV in the dog; 0.25-
5 µg/kg/min IV in the cat.
 If the patient has cardimyopathy or low cardiac output, use a positive
inotropic agent
o Dobutamine: 5-20 µg/kg/min IV infusion in dogs ,2.5-10µg/kg/min in cats. (High
doses or prolonged use can cause seizures in cats). Avoid in cats with hypertrophic
cardiomyopathy.
 (wt.inkg)x(no.of µg/kg/min) = no. of mg to add to 250 ml D5W at drip rate of
15 ml/hr.
 Must protect from light.
 See affect within 3-5 min.
o Sodium nitroprusside treatment; very potent arterial dilator
 Must use only after using dobutamine.
 Must put in separate line from dobutamine.
 Start at 2µg/kg/mg/min. (Dose = 1-10µg/kg/min IV in the dog 0.25-
5µg/kg/min IV in the cat.)
 Usually see and hear effects within 15-20 min of the right dosage.
 Administer at a rate of 15ml/h.
 Very sensitive to light, must cover the entire IV line.
 Monitor blood pressure.
o Monitor CVE, maintain between 5-12 cm H2O
 Normal CVP is 0-5 cm H2O
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 A CVP of 8-11 cm H2O is considered to be the optimal right ventricular filing

pressure in the presence of heart failure.
 Values above 16 cm H2O usually associated with ascites.
 Elevated CVP measurements may indicates catheter malfunction, right heart
failure, or intravascular volume overload.
 Left heart failure in the absence of right heart failure does not change the
CVP
 Monitor urine output, minimum is 1-2 ml/kg/h

ACUTE HEART FAILURE

Etiology

 Cardiac tamponade
 Aortic or pulmonary arterial rupture
 Myocarditis
 Nutritional deficiency myopathy
 Plant poisoning myopathy
 Electrocution, lightning strike
 Latrogenic intravenous injection calcium, potassium solutions, xyaline
 Aortic valve rupture
 Anaphylaxis
 Induction stage of halothane or barbiturate anesthesia

Clinical findings

 Acute syndrome
o Commonest during exercise or excitement; a significant cause of death in horses
during training or tracing
o Dyspnea
o Staggering, falling, recumbency
o Marked mucosal pallor
o Sporadic, incordinated limb movements; short of actual convulsions
o Bradycardia, tachycardia or heart sounds absent
o No pulse
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o Death within minutes, with deep, asphyxial gaps

 Subacute syndrome
o Course 12-24 hours
o Tachycardia , often tachyarththmia
o Severe dyspnea
o Lung base crackles
o Hydrothorax, ascites in those with longer course
o Clinical pathology
o Not applicable in most cases
o Elevated serum levels of creatine kinase, aspartase aminotransferase, lactate
dehydrogenase

Diagnosis

 Acute cases resemble other causes of sudden death. Less acute cases resemble:
o Congestive heart failure
o Pulmonary edema
o Pneumonia

Treatment

 Usually impractical because of short course.

CANINE CARDIOMYOPATHY

Dilatted form

 The dilated form is the most common form. It occurs in large breed dogs, 3-7 years of age
 Diagnosis
o History
 Lethargy , cough , exercise intolerance, anorexia , abdominal swelling.
o Physical exam
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 Pulses weak, pulses deficits, harsh lung sounds, dyspnea, ascites, pale
mucous membranes, cardiac cachexia.
o Throacic radiographs
 May possibly see generalized cardiomegaly, pulmonary edema, pleural
effusion.
o Echocardiongraphy
 Ventricular and artial dilatation, with depressed myocardial systolic function,
mitral or tricuspid regurgitation, decreased aortic ejection velocity.
 Prognosis
o The prognosis is guarded to grave. The average life span after diagnosis is 6 months
to 2 years.
 Treatment
o Inform the client of the diagnosis, prognosis, and cost of the treatment.
o Immediate stabilization.
 Place an IV catheter. Evaluate PCV/TP,BUN.
 Administer furosemide, 2-6 mg/kg q8h; or bumetanide, 0.05-0.2 mg/kg/IV
or PO, as needed for severe pulmonary edema (Caution: Most monitor serum
potassium levels and maintain with IV fluids to prevent excessive fluid and
potassium depletion)
 Administer a bronchodilator
 Aminophylline 5-10 mg/kg slow IV,PO q6-8h.
 Theophylline , 4-8 mg/kg PO q6-8h.
 Long-acting theophylline (Theo-Dut*), 10-25 mg/kg q12h.
 Terbutaline (Brethine*), 1.25 mg/PO q8-12h or 0.01 mg/kg q4h.
 Albuteral (Proventil*), 0.02-0.05 mg/kg q8h.
 Administer nasal oxygen, apply an Elizabethan collar for hood oxygenation,
or place the patient in an oxygen cage, possibly with 35% ethyl alchol (mix
53.5 ml 100 proof Vodka with 100 ml sterile water in the nebulizer).
 Consider the administration of morphine, 0.1-1mg/kg SC.
 Consider the application of nitroglycerine cream, 0.25-2 inches q4-6h rubbed
on clipped skin on the thorax or abdomen (wear a glove and use a tongue
depressor). Cover the area with nonpremeable tape to prevent inadvertent
administration to the patient health care provider.
o After stabilization
 Throacic, radiogrphs-generalized cardiomegaly, pulmonary, pleural effusion.
 ECG- variable, possible artial fibrillation, wide QRS complexes, numerous
other changes may be observed. Treat arrhythmias as indicated.
 Consider the administration of digoxin, 0.0025 mg/lb PO q12h * Maximum
doses: Doberman = 0.375 mg/day, other breeds =0.500 mg/day.
 Administer furosemide, 2 mg / day, oher breeds = 0.500 mg / day.
 Administer an angiotensin-converting enzyme (ACE) inhibitor
 Captopril, 0.25 - 1 mg / kg PO q8 - 12h.
 Enalapril, 0.5 mg/kg PO q12-24h.
 Diltiazem, 1-2 mg/kg PO q812h.
 Administer β-adrenergic(beta-adrenergic)-blocking medication
 Sotolol (Betapace@), 1.0-5.0 mg/kg PO q12h.
 Metoprolol (Lopressor@) ,0.5-1.0 mg/kg PO q8th.
 Atenolol (Tenormin@), 0.5.-1.0 mg/kg PO q8h.
 Dobutamine, 5-20 µg/kg/min IV infusion. Positive inotropic agent
 (Wt in kg)x(no of µg/kg/min) = no of mg to add to 250ml D5W at a
drip rate of 15ml/h.
 Must protect from light.
 See effect within 3-5 min.
 Offer a sodium-restricted diet such as Hills h/d@ and water.
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 Consider supplementation with L-carnitrine, 1-2 g q8-12h PO, and taruine

500 mg/kg PO q12h.
 Administer conservative intravenous fluids with 5% destrose in water or 2.5%
destrose in 0.45% Nacl at 0.5-0.75 times maintenance rates.
o Arrhythmias-treat accordingly

Hypertrophic form

 Diagnosis
o History
 Sudden death, often asymptomatic, or left heart failure.
o Physical exam
 In the small number of symptomatic dogs, dyspnea, moist rales and ascities is
observed.
o ECG
 Possible heart blocks.
o Thoracic radiographs
 Possible cardiomegaly (Caution: Plain radiographs may not differentiate
between the hypertrophic and the dilated forms.)
o Echoradiography
 Left artial enlargement, thickening of the interventicular septum and/or left
ventricular free wall.
 Prognosis
o The prognosis is guarded to grave.
 Treatment
o Inform the client of the diagnosis, prognosis, and cost of the treatment.
o Place an intravenous catheter.
o Administer oxygen as needed.
o Administer propranolol (Inderal@) , 0.04-0.06 mg/kg q8h, or 0.2-1 mg/kg PO q8th
o Restrict exercise, excitement, stress.
o Administer furosemide or bumetanide.
o Digitalis is not indicated

PERIPHERAL CIRCULATORY FAILURE

Etiology

 Hypovolemic failure
o Hemorrhagic anemia
o Dehydration
 Distributive failure (including vasogenic shock)
o Severe burns injury
o Surgical shock after extensive surgery or trauma
o At uterine prolapse
o Too sudden reduction of pressure in body cavity
o Severe pain as in equine colic
 Non-toxic general vasogenic shock
o Hypocalcemia as in milk fever
 Toxic and septic shock
o Endotoxemia
o Exotoxins, eg. Gangrenous mastitis, acute diffuse peritonitis
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Clinical findings

 Depression, dullness, coma terminally

 Muscle weakness,
 Subnormal temperature
 Tachycardia
 Small amplitude, low pressure pulse
 Skin coll
 Mucosal pallor, prolonged capillary refill time
 Muzzle dry
 Shallow respiration, rapid rate
 Anorexia, thirst in some
 Clonic convulstion in a few
 Reversal relatively easy provided no toxic component

Clinical pathology

 Arterial blood pressure reduced from 120 to 60 mmHg

 Disseminated intravascular coagulation
 Other parameters indicative or primary condition, e.g. leukocytosis, hemoconcentration,
anemia, hypocalcemia
 Metabolic acidosis in untreated peripheral circulatory failure

Diagnosis

 Resembles
o Shock
o Dehydration
o Hemorrhagic anemia

Treatment

 Restoration of the circulating blood volume by

o Plasma in cases of shock when plasma protein concentration < 3.5 g / dl
o Isotonic fluids required in cases of dehydration where PCV > 40 %
o Fluid replacement continued until urine flow rate restored to normal or PCV reduced
to <40% or central venous pressure < 5 cm H2O
o Specific bicarbonate therapy when blood pH < 7.1
o Blood transfusion in cases of hemorrhagic anemia where PCV < 12%
o Large does of corticosteroids (dexamethazone 5 – 10 mg / kg or methylprednisolone
30 mg / kg may be beneficial

PERICARDIAL EFFUSION

Etiology
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 Neoplasia of the heart base, or pericardium

o Right atrial hemangiosarcoma.
o Chemodectoma.
o Metastatic adenocarcinoma.
o Lymphoma.
o Thynoma
o Undifferentiated carcinoma.
 Idiopathic pericardial hemorrhage.
 Congestive heart failure
 Peritoneopericardial diaphragmatic hernia.
 Pericardial cysts.

 Infectious pericarditis
o Bacterial (Actinomyces and Nocardia spp.).
o Fungal (coccidioidomycosis).
o Vital
o Trypanosomal
 Noninfectious pericarditis (uremia).
 Cardiac rupture.
 External chest trauma.
 Foreign bodies ( foxtails, grass awns, etc.).
 Hypoalbuminemia
 Anticoagulant rodenticide toxicity.
 Other coagulopathies
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Diagnosis

 History
o The most common cause of pericardial effusion; right artrial hemangiosarcoms most
commonly occurs in large breed eggs, particularly the German shepherd and golden
retriever, five years of age or older. Feline infectious peritonitis is the most common
cause in cats, so carefully evaluate cattery cats and outdoor cats.
o Weakness, exercise intolerance, lethargy dyspnea and abdominal distension are
common client complaints.

 Physical exam
o Weakness.
o Dyspnea
o Ascites and /or pleural effusion.
o Weak and thready femoral pulses.
o Muffled heart sounds and muffled respiratory sounds.
o Jugular pulse and peripheral venous distension.
o Sinus tachycardia.
o May have hepatomegaly.
o Cachexia

 Thoracic radiographs
o Pleural, hepatomegaly and ascites may be seen. If there is significant fluid
accumulation in the pericardium, an enlarged globoid or mound heart shadow may
be seen. Tracheal elevation may be observed, especially if a heart base neoplastic
mass is present. Distension of the caudial vena cava and underperfusion of the
pulmonary vasculature may also be observed.

 ECG
o Sinus tachycardia, decreased R-wave amplitude with electrical alternans.

 CVP
o The patients’s CVP is often>12 cm H2O.

 Echocardiography
o A fluid filled space is visible surrounding the heart, between the parietal pericardium
and the epicardium. In severe cases of cardiac tamponade, the right atrium and
ventricle may appear collapsed. Masses may be observed, as well as cardiac
disorders.

 Laboratory findings
o Routine CBC and serum biochemical profile is usually nonspecific , but may show
hypoproteinmia, anemia, leukocytosis, possibly elevated hepatic enzymes due to
congestion or mild azotemia if there is impairment of renal perfusion. Serum titers
for FIP; coccidioidomycosis, ehrlichiosis and other infectious diseases could be
measured. Thrombocytopenia, coagulation disorders, and erythrocyte abnormalities
may be seen hamangiosarcoma.

Prognosis

 The prognosis is guarded to poor, depending upon the underlying etiology

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Treatment

 Inform the client of the diagnosis, prognosis , and cost of the treatment.
 Place an intravenous catheter, administer intravenous fluids if in shock.
 Perform pericardiocentesis if serious cardiac tamponade exists
o Position the patient in either lateral or sternal recumbency.
o Clip and surgically prepare the right 5th or 6th intercostal space just above the
costochondral junction.
o Attach ECG leads to the patient.
o Administer a lidocaine local anesthetic block.
o Use an intravenous catheter of sufficient length and diameter (8-French, 9 cm) to
pentrate the pericardial sac
o Perform pericardicentesis by carefully advancing the catheter through the
intercostal space and into the pericardial sac.
o Monitor the ECG continuously.
o Once pericardial fluid is obtained, advance the catheter over the stylet, attach
extension tubing a three-way stopcock and a large 35-60 ml syring.
o Apply gentle suction and remove as much fluid as possible.
o Save a sample of any fluid obtained.
o If there is active , acute pericardial hemorrhage, the fluid will have a PCV similar to
blood and will have clots in it.
o To determine whether blood aspirated is actually from the pericardial sac rather than
a cardiac chamber, compare the PCV to that of peripheral blood. In active, chronic
hemorrhage will have a lower PCV and will not clot when placed in a red-top
collection tube.
 Administer Vitamin K, and fresh-frozen plasma or whole blood to treat anticoagulant
rodenticide toxicity.
 Treat heart failure if that is the underlying etiology.
 Avoid the use of diuretics, unless indicated in the treatment of heart failure.
 Afterload-and preload-reducing agents (including ACE inhibitors) should be avoided.
 Surgical exploratory of the thorax and pericardiectomy will allow for detection of small
masses, the collection of biopsy specimens, and avoidance of cardiac tamponade.
o Treat infectious pericardial disease with the appropriate antimicrobial agent.
o Actinomyces spp-penicillins.
o Nocardia spp-potentiated sulfonamides.
o Coccidioidomycosis-ketoconazole, itraconazole, fluconazole, or amphotericin B.
 Treatment of neoplastic pericardial disease with the appropriate chemotherapeutic agents
can be directed based on the biopsy results.

BLOOD PRESSURE

Arterial blood pressure

 Indirect measurement practicable only in the horse by application of sphygmomanometer to

the tail and measurement of pressure in ventral coccygeal artery
 Mean systolic/diastolic pressures in the coccygeal artery in normal horses are 112-77 mm Hg
 Raising or lowering head significantly alters pressure
 Hypertension in horses occurs in
 Epistaxis
 Laminitis
 Painful lower limb fractures
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 Intestinal obstruction

Intracardiac blood pressure

 Cardiac catheterization can provide evidence of blood pressure in each of the heart chambers
and in the larger vessels.
 Abnormalities can provide conclusive diagnostic information about such disease as
congenital cardiac, artial or large vessel defects.
 Largely supplanted by the less hazardous echocardiography

MODULE-20: DISEASES OF CARDIOVASCULAR SYSTEM - II

Learning objectives

 To understand about cardiac arrhythmias, their clinical presentation and management

 To diagnose and manage congenital diseases of the cardiovascular system
 To learn about valvular disorders and endocarditis.
 To understand the action of common cardiac drugs.