MODULE-1: INTRODUCTION, HISTORY AND DEVELOPMENT

OF VETERINARY SURGERY, CLASSIFICATION AND SURGICAL

TERMINOLOGIES

Learning objectives

This module deals with

 History of surgery
 Classification
 General surgery principles
 Pre and post-operative considerations

HISTORY OF ANAESTHESIA

 300 B.C. Juice of mandrake plant was used during Alexandrian

period. Egyptians induced unconsciousness by compression of the carotid arteries. In
following centuries various plants containing opium and atropine likecompounds were
used.
 1540, Paracelsus administered ether to chickens.
 1771, Joseph Priestley isolated and identified depholgisticated air-oxygen and
depholgisticated Nitrous oxide.
 1825, Hentry Hill Hickman performed surgeries on experimental animals by
inducing asphyxiation using carbon dioxide.
 1831, Chloroform was discovered independently by Von Liebig, Souberian and
Guthrie.
 1846 William Thomas Green Morton (1819-1868) demonstrated the use of ether as
anaesthetic for the removal of tumor in humans. Later ether was patented as Lethon.
Morton deserves the chief credit for the introduction of ether as anaesthetic agent.
 1846, Chloroform was used first in animals by Flourens.
 1847, Horace Wells (1815-1848) though lived only a for short duration, published
valuable information through his news letter “A History of the discovery of the
application of Nitrous oxide gas, Ether and other vapours to surgical operations”.
 1857, John Snow administered chloroform to Queen Victoria during the delivery of
her eighth son Prince Leopold and later it became popular.
 Sir William Macewen (1847-1924) Pioneer of oral and nasolaryngeal intubation in
diphtheria patients as an alternative to tracheotomy using rubber, gum elastic catheters
and metal and flexometalic tubes. Later he administered chloroform and air through the
tubes for induction of anaesthesia.
 William Stewart Halsted (1852-1922) Famous surgeon proposed the “Principles of
Surgery” originated nerve block techniques like blocking brachial plexus, nerves of the
face, internal pudental nerve and posterior tibital nerve using cocaine in 1886.

Classification of surgery

DEFINITION
 Surgery is a branch of Medicine, in which manipulative and other modalities are used in
treating injuries, deformities and diseases.
 The word surgery originated from a Greek word “CHEIR” meaning “HAND”, and
“ERGON” meaning “WORK” German language it is called CHIRURGIA.

FUNCTIONS OF A SURGEON

 A surgeon mainly deals with

o Repair of tissues. Example: Treating a lacerated wound.
o Reconstruction of tissues. Example: Suturing divided tendons and nerves.
o Control of infection. Example: Post pharyngeal abscess.
o Prevent spread of malignancy. Example: Tumours of lung.
o Alter or correct structural and functional disorders.Example: Correction of
knuckling of fetlocks (Structural disorder).
o Removal of harmful or useless parts. Example:Gangrenous limb, gangrenous
bowel.

REASONS FOR SURGERY

 To save life of an animal.

 To prolong life of an animal.
 To hasten recovery from an injury.
 For elimination of disease process. Example: removal of a benign tumour.
 For cosmetic reasons.
 For correction of deformities.
 For replacement of a part by an artificial one.
 To make an animal sociality acceptable. Example: Castration in a male cat.
 To aid in diagnosis. Example: Exploratory laparotomy.
 For investigation in research work. Example: Rumen fistulation.

OBJECTIVES OF SURGERY

 Restoration of functions to as near normalcy as possible.

 To eliminate life threating maladies (choke, intestinal obstruction).
 Removal of diseased part - gangrenous tail
 Removal of foreign bodies - rumenotomy
 To hasten recovery process - wounds and fractures
 To make the animals to less dangerous - debudding
 For economic reasons - e.g.,castration in pigs, cattle etc.,to improve the live body weight
 For aesthetic purposes - removal of supernumerary teat
 To replace the organs - Organ transplantation
 For confirming diagnosis - exploratory laparotomy

BASED ON NATURE OF SURGERY

 General surgery: Is carried out to restore the normal function of the body without
substituting or discarding any part of the body. (Restorative Surgery)
 Extirpative surgery: Involves removal of a part e.g.,ovariohysterectomy, eyeball
  Plastic surgery: To restore the destructive part which includes reconstructive surgery (a
structure is reconstructed) e.g., skin grafting and cosmetic surgery (which improves
appearance) e.g. docking, ear cropping etc.
 Replacement surgery
 Physiological surgery - Portosystemic shunt
 Diagnostic surgery
 Exploratory surgery

CLASSIFICATION BASED ON REGIONS/SYSTEMS INVOLVED

 Specialization on particular system examples

o Thoracic surgery
o Cardiovascular surgery
o Orthopaedic surgery
o Ophthalmic surgery
o Neuro surgery
o Urogenital surgery

CLASSIFICATION BASED ON INSTRUMENT/APPLIANCES USED

 General surgery - Is used when in a procedure common surgical instruments are used
 Micro surgery - Magnification facilities are used for specialized surgical procedures.
 Cryosurgery - Involves controlled use of substances like liquid nitrogen which produces
freezing temperatures to destroyed abnormal tissues.
 Electro surgery - Electricity is converted into heat to incise tissue.
 Laser surgery - Laser beams are used to cut or destroy diseased tissue
 Ultra sonic surgery - High frequency waves are used to destroy particular tissue or a
substance (lithotripsy)
 Endoscopic surgery - involves use of rigid and flexible scope e.g., laparoscope,
arthroscope, bronchoscope

TENETS OF HALSTED

HALSTED described certain essential principles for wound healing. These include:

 Gentle handling of tissues to avoid unnecessary trauma

 Aseptic procedures to control infection
 Anatomical dissection of tissues with sharp instruments. Avoid damage to major blood
vessels and nerves
 Control haemorrhage with fine, non-irritating suture material in small quantities
 Obliteration of dead spaces to avoid accumulation of blood and exudates which favour
pus formation
 Use of Minimum suture material
 Avoidance of suture Tension
 Immobilisation - Give rest to the operated part and to the patient

G A A C O M T I - accronymn
 CLASSIFICATION OF PHYSICAL STATUS

 It reflects an attempt to define the condition of the animal and thereby surgeon becomes
alert to problems which may occur during anesthesia and surgery.
 Physical status may be of
o Good
o Fair
o Poor
o Extremely poor
o Emergency good
o Emergency poor
o Moribund condition

The patient

IDENTIFICATION

 Identification is important due to veterolegal cases

 Extension of preoperative medication when owner is not available
 To prepare operative site
 To avoid chances of wrong animal being operated
 To avoid mixing of radiographs

HISTORY

 Information provided by the owner may prove highly beneficial since an animal cannot
describe the ailment.
 A surgeon should have experience and analytical power to extract valuable information
as an owner may provide misleading history.
 A simple language without technical terms should be used while extracting information.
 An approach of through questioning with tact and generation without irritating the
owner may provide better results.
 Clinical signs recorded by owner, probable duration of the disease, status of pregnancy ,
date of last parturition and status of milk yield should be recorded.
 Information should also be gained regarding the treatment previously received by the
animal
 The conflicting points of history should be sorted out logically to gather reliable
information.
 Even though history provided by the owner may be useful it is not a substitute for careful
clinical examination.
 If history and clinical examination are at variance, it is better to depend upon the
examination.

PREPARATION OF PATIENT

 Make the patient an indoor one to accustom with the environment of ward In ruminants
rest for couple of hours lowers the stress(Travel of animal long distances on feet)
 Emergency case should be attempted immediately General physical examinations should
be carried to assess prognosis.
 Severe dehydration and debilitation with prominent ribs indicate poor prognosis if
general anaesthesia or major surgery is indicated.
 Rough and hard coat .
 Sunken eyes
 Prolonged lateral recumbency
o Colour of the mucous membrane and capillary refill time are the
o useful aids in dealing seriously ill patients
 Rectal temperature, pulse and respirations should be recorded
 Palpation, percussion and auscultation help to arrive diagnosis
 In a febrile state surgery should be postponed
 Paracentesis of swelling and cavities for differential diagnosis
 Laboratory procedures – Pathological tests and their correction for treatment
 Radiography
 Fluid therapy particularly in case of dehydrated and worm infested animals.
 With holding of feed and water
 Large animals: 24 - 48 Hrs ; 12 - 24 hrs
 Small animals : 12 Hrs ; 4 - 6 hrs
 Administration of laxative, purgative or enema for 2-3 days before operation to evacuate
the bowels and fit for general anesthesia (not recommended in Ruminants)

Preparation of operation site

DAY BEFORE OPERATION

 Clipping of long hairs by scissors or by shaving the animals. Before shaving some soapy
solution should be used
 Washing the area by non-irritant antiseptic lotion like Savlon liquid
 Washing by plain water and rubbing gently by cotton or swab gauge
 Again washing by running water
 Evaporative type of antiseptic wash or lotion should be applied locally
 Covering the site by sterile gauge and bandage for the next day of operation

DAY OF OPERATION

 Again wash with antisepti

 clotion and shaving
 Application of alcohol
 At the time of operation the animal should be brought to the operation table

PREPARATION OF THE SURGEON

 Surgeon dresses should be changed in preparation room

 Infection from the nose and mouth should be prevented by using caps and musk
 Shoes of surgical team should be changed
 Hands upto elbow should be scrubbed for at least 5 minutes with soap and running
water. Nails should be cut and scrubbed with nail brush or gauge. Hands should be
immersed in cetrimide solution or rinse with surgical spirit (70% alcohol)
 While putting on gloves the outer surface of the gloves should not touch with the hands

LOCATION

 It is always preferable to do surgery in an operation theater if feasibility exists where

routine professional and manual help in and equally available.

PLANNING

 A surgeon must know the structure to be incised and handled in any surgical procedure
and so be thoroughly familier with surgical anatomy.
 If doubt, available literature should be consulted.
 Anatomical structure should be reviewed on a cadaver. (Major surgery)
 The surgeon should also ensure that the equipments, instruments, drugs and other items
required during an operation have been arranged properly.
 A better approach is to mentally visualize the operation to be done and make a check list
of all items required.
 Necessary assistance required for restraint of the animal should be arranged.
 Getting a risk note signed from the owner even for a simple operation is essential.
 A proper planning avoids wastage of time and energy immediately, before and during
surgery.

MAINTENANCE OF RECORDS

 A surgeon must keep records of each and every aspects of a case.

 The case sheets should be such that there can be stored for future reference and use.
 Description of the patient identification marks, owners name and address, history of the
case clinical findings type of surgical and postoperative treatment and the outcome
should be recorded.
 Records can be analyzed to work out incidence of various diseases in an area and also to
judge the efficany of the treatment measures adopted.
 Records will help to identity the technical areas of difficulty

Post operative care and management

SHIFTING OF PATIENT IN THE WARD

 Immediately after major operation, the patient should be gently removed from operation
table.
 Unconscious patient should be placed in the bed of surgical ward with slightly lowered
down the head except in brain surgery operation cases.
 It prevents cerebral ischemia, vomition and helps to remove tracheobronchial secretion.

POST-OPERATIVE MEDICATION

 According to severity of pain, analgesic drugs should be given to control pain which may
originate from the operation site.
 Restlessness can be controlled by the application of sedative or tranquilizer.
 Routine broad or narrow spectrum antibiotic should be given.
 Antiemetics may be given to prevent vomition.
 Supportive therapy with fluid and vitamins should be resorted too.
o Oral intake of food and fluid is restricted for 12-24 hours after major operation.
o Liquid diet should be given at second day.
o Semisolid food should be given from forth day.
o Solid food should be given after 8th day of operation.
o Food must be free from fat and some vitamins, enzymes should be added.

POST-OPERATIVE DIET

 Oral intake of food and fluid is restricted for 12-24 hours after major operation.
 Liquid diet should be given at second day.
 Semisolid food should be given from forth day.
 Solid food should be given after 8th day of operation.
 Food must be free from fat and some vitamins, enzymes should be added.

POST-OPERATIVE EXCERCISE

 Exercise means walking which should be accomplished for 2-3 hours per day.
 The time and distance of walking depend upon the severity of patient.

POST-OPERATIVE DRESSING

 Dressing should be done on 3rd, 5th and 7th post-operative days to visualize the condition
of operative site.
 The area should be washed with antiseptic lotion and rebandaged for proper healing.

RELEASE FROM THE WARD

 Skin sutures should be removed between 8-10th day of post-operative days according to
the condition.
 Operative site should be treated with topical antibiotics and covered by light bandages.

FOLLOWED BY CHECK UP

 The surgeon advised the attendants that the patients must be checked by him for a
certain days.
 MODULE-2: ASEPSIS AND ANTISEPSIS - THEIR APPLICATION
IN VETERINARY SURGERY, SURGICAL RISK AND JUDGMENT

Learning objectives

This module deals with

 Terminology
 Sterilization techniques for surgical materials and instruments
 Preoperative Considerations
 Factors Influencing Surgical Risk

TERMINOLOGY

 Asepsis - being free of disease-producing microorganisms.

 Contaminated - dirty, unclean, soiled with germs.
 Disinfection - the process of destroying most, but not all, pathogenic organisms.
 Medical Asepsis - the practice used to remove or destroy pathogens and to prevent
their spread from one person or place to another person or place, clean technique.
 Microorganism - a living body so small that it can only be seen with the aid of a
microscope.
 Sterilize - to kill all microorganisms including spores.
 Antisepsis: is the destruction of micro organisms but not bacterial spores on living
tissue.
 Antibiotic: A substance derived from mould or bacteria that inhibit the growth of other
micro-organisms.
 Astringent: Causes contraction of tissues and so arrests haemorrhage.
 Styptic: Astringent, haemostatic agent used externally to stop flow of blood.
 Haemostatic: Arresting flow of blood within a vessel.
 Sterilization: Complete elimination of microbial viability including both the vegetative
forms of bacteria and spores process by which an article can be rendered free from all
forms of living microbes including bacteria, fungi and their spores and viruses.

STERILIZATION TECHNIQUES FOR SURGICAL MATERIALS

AND INSTRUMENTS

 Two general categories of sterilization methods can be grouped under.

o Physical sterilization
 Thermal
 Filtration
 Radiation
o Chemical sterilization
 Germicidal solutions Glutral dehyde, Beta propiolactone
 Ethylene oxide

THERMAL
  Steam sterilization is the most commonly employed method of sterilization of
instruments and equipment.
 Different types of autoclaves are
o pressure steam sterilizer
o steam pressure sterilizer
o vacuum steam sterilizer
o dressing sterilizer
o gravity displacement sterilizer

Points to be considered

 Instrument packs are positioned vertically (on edge ) and longitudinally in autoclave
 A 13 minutes sterilizing cycle (exposure to saturated stem at 1210C) is a safe minimum
required
 Large linen packs require 30 minutes at 1210C
 Once sterilized, sterile packs should be stored in closed cabinets. All packs should be
dated.
 Sharp instruments ¾ scissors, needles; surgical instruments can be sterilized by this
method.

Dry heat sterilization

 Dry heat destroys microorganisms primarily by oxidation process.

 It is used to sterilize those materials for which moist heat cannot be used either due to
deleterious effects on the material or material being impermeable to steam e.g: oils,
powders, glass surgicals etc.
 Slow process and long exposure time at a high temperature is required as spores are
relatively resistance to dry heat.

Methods

 Direct exposure of instruments to flame – not reliable.

 Hot air oven – most common method.
 An exposure to dry heat at a temperature of 1600C for 60 min will achieve sterilization
equal to that of moist heat at 1210C for 15 min, at 151 lbs pressure.

Temperature time combinations for dry heat sterilization

 1200c for 8.0 hours

 1400c for 2.5 hours
 1600c for 60 minutes
 1700c for 40 minutes
 Exposure time relates to the time after specific temperature has been achieved and don’t
include heating lags.
 Clean gowns, paper wrapped material, swabs, Petridis – 1200c for 8 hours
 Stainless steel lens and glass ware – 1600c for 60 min

FILTRATION
  Filtration is used in air conditioning system to remove particles as small as 0.3 µm in
diameter and also used to filter-sterilize heat labile solutions.

RADIATION

 Ultraviolet light is used for surface sterilization.

 Ionizing radiations, Beta and cathode rays are used to sterilize heat sensitive
prepackaged surgical materials.
 Example: Surgical mask - to produce two fold effect.

CHEMICAL AGENT

 An ideal chemical agent should have following properties

o kill all pathogenic microorganism
o work effectively in short period of time
o exert residual action
o not corrode, dry or stain
o be stable, odorless, non toxic
o be effective in presence of organic matter
o not be inactivated by other concurrently used chemicals

Agents in solution form

Alcohol

 Ethyl alcohol (70%), Isopropyl alcohol (90%) are commonly used

 Presence of water easily denatures the protein.
o 70% alcohol is more qermicidal than absolute alcohol.
o Isoprophyl alcohol is more bacterial than ethyl alcohol
 Sterilization can be done by immensities continuously. Eg: Needles.

Aldehyde

 Formaldehyde and flutasaldehyde (cidex, parvo cide )

Formaldehyde

 Available as formalin 37% solution of formaldehyde and water.

 Used as gas for fumigation.
 Irritant to skin and mucous membranes.
o Oxidizing agent e.g. Halogens
 Inorganic Iodine compounds
 Organic Iodine compounds
o Surfactants – Soaps, detergents,
o Phenolic derivatives - carbolic acid

Chemical sterilization by gases

 Ethylene oxide acts by inactivating the DNA molecules in the microbial cells thus
preventing cell reproduction. Temperature - 120 to 140F
 Eg: ethylene oxide, formal dehyde and beta propiolatone (generally used)
 Sharp edged instruments – Scalpel blades, hypodermic needles.

PREOPERATIVE CONSIDERATIONS

 A surgeon must keep certain considerations in mind before undertaking surgery.

 Preoperative considerations may relate to the owner, patient and Surgeon.

THE OWNER

 Owner is the custodian and provider of the animals need and therefore he has a legal
right over his animal.
 A veterinarian is legally answerable to the owner.
 The owner must be well informed about the diseases, proposed surgical treatment and
the possible outcome.
 The owner must be convinced that every thing being done is in the interest of the animal
patient.
 Owner – patient – Surgeon relationship becomes very important in veterinary profession
to maintain a good rapport.
 The whole approach towards the owner should be based on the logic and sound
reasoning.
 In Eastern countries the relationship may at times be more influenced by personnel &
religious sentiments of the owner, the myths of taboos of the region.
 Incertain instances the owner may strictly forbid the use of a knife or other cutting
instrument on the animal.
 A surgeon may be approached for surgery when it is not feasible. Ex. Multiple fractue of
pelvis.
 A surgeon must also consider 1. Economic aspects of the case 2. Surgical risk involved
3.Ethics and centiments of the owner.
 After weighing each aspect carefully, the surgeon should make a decision and
communicate the same to the owner in a confident and convincing tone.
 It is the ethical and legal duty of the surgeon to inform the owner about surgical risk in
advance.

SURGICAL RISK

 The term risk is used to describe the animal’s potentiality for surviving anesthesia and
surgery.
 To reduce the risk to minimum is of surgeons concern and alert to problems that may
arise during anesthesia and surgery.

FACTORS INFLUENCING SURGICAL RISK

 Haemorrage and shock

 Fluid and electrolyte imbalances
 Acidosis and alkalosis
 Anemia and hypovolaemia
 Malnutrition and hypoproteinemia
 Pulmonary and cardiovascular complication
 Hepatic insufficiency
 Renal and adrenal diseases
 Obesity of the patient
 Extreme of age - complication in both very old and very young animals

HOW SURGICAL RISK IS DETERMINED

 Detailed history of animals

 Physical status and condition of animal
 Individuality
 Clinical examination of the patient including general, systemic and special examination
 Essential laboratory examination including routine examination of stool, urine and
blood (clotting time, bleeding time, total count, differential lecucocytic count,
hemoglobin %, packed cell volume)
 On the basis of magnitude of operation, nature of aliment with foresaid findings, the risk
of patient is evaluated

ADJUNCTS AND SAFEGAURDS

 These are
o Evaluation of operative risk
o Recognition and correction of preoperative deficits
o Prevention of intra-operative and postoperative complication before they develop
o Resuscitation and after care of surgical patient

SURGICAL JUDGEMENT

 Surgical judgment is something that can be developed only over a period of time, the
length of time depending on the surgeon’s exposure to many and varied cases.
 A Surgeon who continuously makes the same errors can never develop sound judgment.
 When examination and diagnosis favours or indication for surgical treatment then
decision must be made about:
o Feasibility of performing surgery in consideration to the animal’s condition.
o When to under take surgery
 Feasibility of performing surgery entirely depends of the evaluation of the patient but the
proper timing of operation is more of a problem in clinical judgment then the decision as
to performance.
 The decision must be based on the circumstances and the optimum condition of the
patient for surgery.
 Such type of decision as to wheather and when to undertake surgery is applicable both
for emergency and elective surgery.
 In elective surgery certain preoperative schedule should be carefully followed and
evaluated.
o Careful recorded history
o Detailed physical examination
o Essential laboratory test
o Radiographic study where necessary
  Other diagnostic test like ultrasonography, computed tomography, doppler study,
magnetic resonance imaging etc., wherever required
 Emergency surgical operations are those where there is serious injury or massive
internal hemorrhage which may endanger the life of the patient.
 In such cases the preoperative preparation must be limited to be rare essential.
 It is never justified to omit the details of a careful recorded history and careful physical
examination treatment of preoperative preparation of emergency cases.
 Resuscitation, emptying of stomach, empting of bladder by catheterization should be
considered as general rule, if necessary.

MODULE-3: SHOCK AND ITS MANAGEMENT

Learning objectives

This module deals with

 Definition and Classification of Shock

 Pathophysiology of Shock
 Symptoms and Treatment of Shock
 Types of Intravenous Fluids

DEFINITION

 A recent veterinary textbook defines shock as "the clinical state resulting from an
inadequate supply of oxygen to the tissues or an inability of the tissues to properly use
oxygen." This deprives the organs and tissues of oxygen (carried in the blood) and allows
the buildup of waste products.
 Shock can result in serious damage or even death.
 Many attempts have been made to define shock, but because it is such a complex
disorder, no single definition has been successful.

CLASSIFICATION

 There are four general categories of shock: hypovolemic, cardiogenic, septic and
vasogenic shock.
o Hypovolemic shock is the result of inadequate intravascular circulatory volume
commonly resulting from haemorrhage, fluid loss in excess of intake, or third
spacing of body fluids.
 A. Acute blood loss: - Major laceration, ruptured abdominal or thoracic
organs, surgical procedures.
 B. Fluid loss:- Severe vomiting, diarrhea, burns
 C. Fluid sequestration: - Massive tissue trauma, especially crushing
injuries.
o Cardiogenic shock occurs from cardiac insufficiency with lowered cardiac output.
 It may result from:
 · Inherent heart diseases such as arrhythmias, myocardial trauma etc.
 · Extracardiac diseases such as cardiac tamponade, tension
pneumothorax.
  The circulatory failure is central in origin.
o Septic or endotoxic shock occurs from massive infection caused by gram negative
microbes. Various diseases which can cause this type of shock are peritonitis,
pyometra, haemorrhagic gastroenteritis, intestinal strangulation, or volvulus,
pericarditis, mastitis, osteomyelitis etc.
o Vasogenic shock occurs either due to extensive vasoconstriction or extensive
vasodilatation. Direct action of toxic substance on blood vessels produces
dilatation of blood vessels. It leads to decreased resistance and increased capacity
of vascular bed.
 Pain or extensive handling and traction of the viscera – massive
vasoconstriction
 Deep anaesthesia or spinal injury – extensive vasodilatation
 Anaphylactic shock occurs due to antigen-antibody reaction and resultant
histamine release. Histamine leads to increased permeability and massive
vasodilatation.

PATHOPHYSIOLOGY OF SHOCK

 Although the nature of shock vary, the fundamental sequence of events is essentially the
same in all forms of shock:
o Some precipitating cause decreases cardiac output and blood pressure
o Stimulation of sympathoadrenal system leads to peripheral vasoconstriction and
shunting of blood away from the skin and intestinal viscera
o Heart rate and myocardial contractility increases, leading to cardiac output
o Simultaneously there is increased release of ADH, activation of rennin-
angiotensin system and release of aldosterone which ultimately helps to conserve
water and sodium through the kidneys.
 In microvascular level certain compensatory changes become less reversible as shock
persists and provide a positive feedback.
o There is lowered oxygen delivery to tissue due to sympathetic constriction of
arteriole and pre-capillary sphincters.
o Development of cellular anoxia with release of lactic acid.
o Permeability of cell membrane increases with release of lysozymes
o Capillary stasis and decreased capillary pH triggers vascular pulling and
decreased venous return to heart.
o Hypercoagulability also occurs, which may leads to disseminated intravascular
coagulopathy (DIC).
 The end result in all forms of shock is cardiac failure ultimately leading to death.
 SYMPTOMS OF SHOCK

 It is easy to recognize fully established shock; but it is difficult in early or compensated

shock.
 Shock is dynamic and not a static process.
 Physical examination findings associated with hypovolemic and cardiogenic shock
include:
o Tachycardia
o Tachypnea
o Pallor of mucous membrane
o Prolongation of the capillary refill time and decrease pulse quality
o Heart murmurs or arrhythmias (not absolute)
 Laboratory findings during shock shows lowered red blood cells, haematocrit and plasma
proteins; and elevated blood urea nitrogen (BUN).
 Other signs include weakness, restlessness, and depression, reduced urine output, coma
and dilation of pupils.

TREATMENT

 The most important goals in the treatment of shock include:

o quickly diagnosing the patient's state of shock;
o quickly intervening to halt the underlying condition (stopping bleeding, re-
starting the heart, giving antibiotics to combat an infection, etc.);
o treating the effects of shock (low oxygen, increased acid in the blood, activation of
the blood clotting system);
o and supporting vital functions (blood pressure, urine flow, heart function).
 Patent airway should be ensured by intubating animal if collapsed or comatose. Oxygen
should be delivered via musk, cannula or endotracheal tube.
 Haemorrhage, if any, should be controlled by direct pressure, bandages, tourniquet or
ligation.
 Fluid theraphy: A multi electrolyte, sodium containing crystalloid replacement solution
is usually the fluid of choice; plasma and whole blood have obvious advantages.

TYPES OF INTRAVENOUS FLUIDS

 Crystalloid: Dextrose or electrolyte solutions increase intravascular and interstitial fluid

volume: Isotonic .9% NaCl, lactated Ringers Hypotonic (5% dextrose in water, 45%
NaCl).
 Colloids: Do not diffuse easily through capillary walls Fluids stay in vascular
compartment; increase osmotic pressure: albumin, plasma protein and dextran.
 Blood and blood products: Treatment of hemorrhage Restore coagulation properties.
 Glucocorticoid: the role of glucocorticoid in shock state has remained debatable even in
man and small animal. Beneficial effects (dexamethasone @10mg/kg, prednisolone @
30mg/kg) include: increase in cardiac output, decrease in peripheral resistance, increase
in metabolism of lactic acid, improved efficiency of glycolytic enzymes, stabilization of
lysosomal enzymes and interference with endotoxin- induced immune reaction.
 Vasoactive drugs are used to modify sympathetic and adrenal responses. Dopamine is
most popular vasoactive drugs used in shock.
 Sodium bicarbonate is indicated to counteract metabolic acidosis caused by
accumulation of lactic acid in shock state.
 Broad spectrum antibiotics are indicated to combat wide-ranging secondary bacterial
infection and diuretics for over dehydration or poor urine output.
 Drugs acting on cardiovascular system are also indicated to improve blood pressure and
to stimulate blood flow. Digitalis and adrenaline are drug of choice in this case.
 The animal should be kept in a warm and well ventilated room without exposing direct
heat.
 Thrombolytic therapy (drugs that dissolve clots as they form) may be considered in the
case of myocardial infarction or pulmonary embolism.
 Treatment with antioxidants that help rid the body of free radicals (harmful by-products
of the oxidative process) may protect against some types of shock.
 o Carnitine may be helpful in treating cardiogenic, septic, and hypovolemic shock.
o Coenzyme Q10 (CoQ10), an antioxidant, may be beneficial in treating
hypovolemic and septic shock.
o Glutamine added to parenteral nutrition may protect the intestines and prevent
complications from septic shock.
o N-acetylcysteine (NAC) improved the immune system response in septic shock
caused by endotoxins (toxins released from bacterial cells).
o Omega-3 fatty acids compared with omega-6 fatty acids may protect against the
harmful effects of septic shock.
o Vitamins B3 and B 12 -nicotinamide (a form of vitamin B3) may help protect
against bacterial endotoxin that causes septic shock.

MODULE-4: HAEMORRHAGE AND ITS MANAGEMENT

Learning objectives

This module deals with

 Haemorrhage and its Classification

 Etiology
 Symptoms
 Haemostasis

HAEMORRHAGE

 Haemorrhage means escape of blood from an artery, vein or capillary to extravascular

space.
 The complete loss of blood is referred to as exsanguination.

CLASSIFICATION

 External haemorrhage
 Internal haemorrhage
 Depending on the time of occurrence
 Depending on the source of haemorrhage
o External haemorrhage occurs from open wounds or cut wounds that is visible on
the outside of the body
o Example
 Epistaxis – bleeding from nose.
 Haematuria: Blood in urine.
 Haematemesis- vomiting fresh blood .
 Haemoptysis – coughing up blood from the lungs .
 Melena - presence of blood in faeces.
o Internal haemorrhage is bleeding occurring inside the body . It may be caused by
high blood pressure (by causing blood vessel rupture) or other forms of injury,
especially high speed deceleration occurring during an automobile accident ,
 which can cause organ rupture. When blood is collected in a newly formed cavity
called as Haematoma.
o Example:
 Haemometra - haemorrhage into uterus
 Haemopleura - haemorrhage into pleural cavity
 Haemoperitoneum - haemorrhage into peritoneal cavity
 Haematocele - haemorrhage in to tunica vaginalis
 Haemarthrosis - haemorrhage into a joint
 Haematomyelia - haemorrhage into spinal cord
 Petechiae - Pinpoint haemorrhages on skin and subcutis
 Ecchymosis - haemorrhagic spots on skin and subcutis.
o Depending on the time of occurrence
 Primary haemorrhage occurs immediately after injury.
 Reactionary haemorrhage occurs within 24hours after the primary
bleeding has been arrested due to mechanical disturbance of clot in vessel
or due to slipping of the ligature.
 Secondary haemorrhage occurs after about a week or more due to septic
disintegration of clot or due to sloughing of portion of vessel because of a
septic or gangrenous lesion.
o Depending on the source of haemorrhage: Arterial, Venous and Capillary

Characteristics Arterial Venous Capillary

Color Bright red Dark red Red
Flow Jets (Jerks) Continuous slow and steady oozing
Spurting / pulsating flows freely
Of force cardiac side peripheral side(distal ) wound
ETIOLOGY

 Trauma - blunt trauma (e.g. fall, motor vehicle accident), laceration, or penetrating
trauma (e.g. knife or gun).
 Necrosis and ulcerations of blood vessel wall
 Infection and subsequent release of toxins of microorganism
 Aneurysm ( weaknesses in blood vessels )
 Increased blood pressure
 Lack of oxygen and nutrition.
 Anaphylactic shock
 Deficiencies of coagulation factors.
 Deficiency diseases
o Haemophilia
o Thrombocytopenia
o Deficiency of vitamin C, vitamin K
o Plant toxins (sweat Clover)

SYMPTOMS

 Bleeding from injured blood vessel

 Skin and mucous membrane become pale, cold and moist
  Patient feels thirsty
 Air hunger
 Thready pulse
 Hypotension
 Low hemoglobin and red blood cells
 Severe bleeding leads to shock

HAEMOSTASIS

 Haemostasis may be defined as complex interaction between vessels, platelets,

coagulation factors, coagulation inhibitors and fibrinolytic proteins to maintain the
blood within the vascular compartment in a fluid state.

Methods of haemostasis

 Bleeding should be addressed in calm and controlled manner. Gentle digital pressure on
the point of haemorrhage provides an extremely effective temporary haemostasis in
minor bleeding.
 Pressure haemostasis: A dressing, typically made of gauze, should be applied. The tissue
should be gently blotted rather than wiped (Wiping causes abrasion and dislodges blood
clots that have formed).
 Haemostatic forceps: Crushing of tissues at the point of application leads to clot
formation inside the vessel adjoining the ruptured ends of the inner coats. This can be
done using artery forceps.
 Diathermy: Cauterization of vessel is usually performed by Mono polar coagulation and
bipolar coagulation. Arteries less than 1mm and veins 2mm diameter causes vessel wall
to shrink and lumen occlude by thrombosis.
 Ligation is the ideal method of controlling bleeding from a vessel which can be
accomplished first by grasping the vessel followed by putting a ligature. Vascular clips
made of titanium or stainless steel is also used for ligation.
 Tourniquet: A cord should be tied around an extremity (limb, tail, penis etc.) and
proximal to bleeding area to control bleeding (not more than one hour 20 to 60
minutes). The use of a tourniquet is not advised in most cases, as it can lead to
unnecessary necrosis or even loss of a limb.
 Topical agents like Fibrin adhesives, oxidized cellulose (regenerated), absorbable
collagen fibrils, and gelatin sponge with or without thrombus are also helpful for
arresting bleeding from small vessels. Bleeding from drilled cut or chipped edges of bone
can be controlled by using bone wax plugs physically.
 Application of Tr. Benzoin, Liq. Ferri perchlor, collodion, ice, cold water etc. can be
successfully used for controlling bleeding from small vessels.
 Bleeding from unidentified points of vessels in a wound cavity can be controlled
by packing or plugging the cavity with sterilized gauze pieces (tampon). Tamponing
favours coagulation of blood by exerting pressure in the area.
 Adrenalin, a vasoconstrictor agent when applied topically controls bleeding especially
from a small bleeding vessel.
 Administration of vitamin K (Kapillin), calcium and other coagulation factors may have
remarkable effect in controlling haemorrhage.
 MODULE-5: FLUID THERAPY IN SURGICAL EVENTS

Learning objectives

This module deals with

 Fluid infusion and

 Uses

FLUID INFUSION

Fluids

 Routine administration of multielectrolyte containing crystalloid replacement solutions

at the rate of 10 ml/kg/hr plus 2 to 3 times the volume of estimated blood loss will satisfy
the requirement during surgery.
 During major procedures it can be increased upto 20 ml/kg. Lactated Ringer’s is
preferred over other solutions during shock.

During anaemia

 If the PCV less than 20% blood transfusion is indicated and if the serum protein is less
than 3 to 3.5 g/dl further volume replacement is done using plasma or synthetic colloidal
is administered.
 Blood volume is calculated as 8 to 10% of the body weight in dogs (45% cells and 55%
plasma) and 6% in cats(36% cells and 64% plasma).
 Blood transfusion is indicated in dogs whose preanaesthetic haemtocrit is less than 30 to
34% and in cats less than 25 to 29%.
 If the blood loss is more than 10% during surgery blood transfusion is necessary.
 Blood and plasma transfusion is done based on the following formula.
o Amount of donor blood needed (ml) = Recipient blood volume in ml x
((Desired PCV - Patient PCV) / PCV of donar blood)
o Amount of donor plasma needed (ml) = Recipient plasma volume in ml x
((Desired TSP - Patient TSP) / TSP of donar blood)

FLUIDS AND THEIR USE

Isotonic crystalloids

 Indications
o To maintain plasma volume in uncomplicated anaesthetized cases.
o To replace deficits in dehydration
o To restore interstitial fluid status
o To promote diuresis
 Disadvantages
o Large volume of administration coupled with migration into interstitial spaces
may result in oedema
 o Produce haemodilution in anaemic patients

Hypertonic crystalloids

 Indications
o Expansion of plasma volume
o Used in the intial treatment of shock
o Administered intraoperatively during cardiac surgery
o To prevent tissue oedema from the conventional therapy
o These agents increase the plasma volume; cardiac output and improves the blood
pressure. They increase the myocardial contractility
o Improve the microcirculatory blood flow by decreasing the systemic vascular
resistance, lowering the blood viscosity and reducing the size of the endothelial
cells.
 Disadvantages
o Induce hypernatraemia, hyperchloraemia, hypdokalaemia, hypermolarity and
metabolic acidosis
o May induce mild cellular dehydration
o Uncontrolled bleeding will become worsen due to the rapid increase in blood
pressure.

Synthetic colloid solution

 Indications
o Hypoproteinemia and hypoalbuminemia
o Blood loss
o Hypovolemia
o Sepsis
o Persistent hypotension
o Does not cross the capillary walls hence will have sustained effect
o No risk of transmission of infectious diseases as compared with plasma and less
expensive
 Disadvantages
o Induce pulmonary oedema in patients with permeable capillaries
o May induce circulatory over load
o May induce coagulation disorders due to dilution of platelets, precipitation of
coagulation factors, increased fibrinolytic activity and decreased functional von
willebrand factor.

MODULE-6: DIFFERENTIAL DIAGNOSIS AND SURGICAL

TREATMENT OF ABSCESS, TUMORS, CYST AND HAEMATOMA

Learning objectives

This module deals with

 Definition of abscess and its Parts
 Classification of abscess
 Etiology and Treatment of abscess
 Tumors and its Types
 Incidence, Treatment and Diagnosis of tumors
 Cyst
 Diagnosis and Treatment

DEFINITION

 Abscesses are circumscribed collections of purulent material (pus) in a cavity, found in

several species of animals in a variety of locations.
 This purulent inflammation is usually caused by one of four pyogenic (pus producing)
bacteria: Corynebacterium, Pseudomonas, Streptococcus and Staphylococcus.

PARTS OF AN ABSCESS

 Abscess consists of a wall, pyogenic membrane and pus (Liquor puris).

 The pyogenic membrane that lies between the wall and pus, controls spread of infection,
and helps in phagocytosis and granulation tissue formation.

CONTENTS OF PUS AND ITS CHARACTER

 Pus contains necrosed tissue, dead bacteria, leukocytes and proteins of blood and tissues.
 Pus cells mainly consist of polymorphonuclear leukocytes along with a few mononuclear
cells.
 Pus is alkaline in nature and yellow in colour.
 Pus serum will not clot, since the fibrin of exudates is digested by the proteolytic
enzymes of the leukocytes.

CLASSIFICATION OF ABSCESS

 Abscess may be classified as:

o Acute Abscess (Hot abscess): Inflammatory symptoms are more active.
o Chronic Abscess (Cold abscess): Inflammatory symptoms are less active.
 Chronic abscess may be:
 Hard with inspissated pus,or
 Soft with liquid pus and thin abscess wall.
o Superficial or deep abscess: based on location.

ETIOLOGY OF ABSCESS

 Pyogenic organisms like Staphylococci, Streptococci, Escherichia coli and Pseudomonas

aeruginosa.
 Specific organisms like Corynebacterium pyogenes, Actinomyces bovis etc.
 Chemicals like mercuric chloride and Zinc chloride.
 COMMON SEATS OF ABSCESS FORMATION

 Cattle: Yoke, udder and prominences

 Horses: Shoulders, sub-maxillary and post pharyngeal lymph nodes.
 Dogs: Anal region, and mammary glands.

ACUTE ABSCESS

 Acute abscess forms in 3 to 5 days following infection.

 In long duration abscess, the liquid part is absorbed and the solid part is left. This is
called Inspissated Pus.

Symptoms

 Acute superficial abscess appears as a local painful swelling.

 The dead tissues and dead inflammatory cells are continuously thrown into the cavity
which leads to a gradual increase in the amount of pus.
 Thus the abscess enlarges till it reaches the surface of skin or mucous membrane.
 The center of abscess becomes soft (pointing) and later ruptures, discharging pus.
 Local acute inflammatory symptoms without fever are observed in superficial abscess.
 Deep abscess has no local symptoms, but fever and pain on manipulation of the part are
evident.

CHRONIC ABSCESS (Cold abscess)

 A chronic abscess develops slowly without any inflammatory symptoms.

 It may be painless or slightly painful.
 Primary chronic abscess usually occurs from repeated injuries and observed on the
prominences of limbs and ribs due to bed sores.
 Secondary chronic abscess develops in the course of various local affections.
 Chronic abscess may be hard in consistency surrounded by fibrous tissue and containing
small amount of pus or it may be soft and thin walled with comparatively larger amount
of pus.

TREATMENT

 Treatment should correspond to the stage of development of an abscess.

 In time, abscesses may become inactive or enclosed (sterile); the body defenses having
killed all of the causative bacteria.
 The accumulated pus, with no route of escape, will slowly become liquefied and be
absorbed.
o Measures to accelerate maturation of abscess by using liniments, fomentations
and mild blisters.
o Once mature, abscess must be early cleared up of pus by aspiration and
subsequent washing of the purulent cavity.
o The abscess should be opened by syme’s abscess knife or a scalpel at the place of
pointing. The pus should be drained and the cavity is to be irrigated with a mild
antiseptic lotion. In cases where the pointing of abscess is not at a dependent
 Part, then drainage will not be perfect. A counter opening is made at the most
ventral part (dependent Part) of the abscess.
o Tincture of Iodine soaked gauge is be packed to keep the openings patent. This
should be changed once in 24 hours. The quantity of gauze used to pack the
abscess cavity has to be reduced daily as the cavity is being filled up by
granulation tissue. Gauze soaked with 0.5% silver nitrate is best against most of
the micro-organisms.
o Further therapy is the same as that of a granulating wound.
o A chronic abscess is converted into an acute abscess by applying blisters, and
then treated as acute abscess. Sometimes the chronic abscess is enucleated under
local infiltration analgesia, and the skin is sutured.
 Cellulitis or Phlegmon is diffuse, suppurative spreading inflammation of loose
connective tissue, with predominance of necrotic events over suppurative.
 Pustule is a circumscribed cavity with pus, situated in epidermis.
 Furuncle or Boil is suppurative inflammation of hair follicle or a sebaceous gland due
to Staphylococcus aureus. A group of furuncles is called Furunculosis.
 Carbuncle is small boil, which drains to outside by multiple small openings. It is caused
by Streptococci and Staphylococci.
 Acne is an abscess of sebaceous gland. It appears as single or multiple pustules
containing grayish white pus. Antiseptic ointments externally and systemic penicillin
gives good relief.
 Empyema is collection of pus in a body cavity. Example: Empyema of frontal sinus,
empyema of joint.
 Antibioma is a clinical condition resulting from improper treatment of an abscess.

TUMORS (Neoplasm)

 The term neoplasm is a Greek word used primarily for new formations or new growths.
 Tumour may be defined as “an abnormal mass of tissue, the growth of which extends
uncontrolled, in comparison to the normal tissue and persists in the same excess even
after cessation of the stimuli which evoked the change.”

TYPES OF TUMOR
Benign Malignant
Grow slowly Grow rapidly
Locally grow to great size Create metastases
Don’t invade the neighboring tissue Invade and destroy neighboring tissues.
Usually do not return after surgical removal Recurrence after surgical removal
INCIDENCE

 Tumors are more common in canines.

o Skin - Common in older dogs (often benign) but much less common in cats
(malignant).
o Breast - Fifty percent of all breast tumors in dogs and 85% of all breast tumors in
cats are malignant.
 Testicles - Testicular tumors are rare in cats and common in dogs, especially
o
those with retained testes.
o Bone - Bone tumors are most commonly observed in large breed dogs and rarely
in cats. The most common sites are leg bones, near joints.
o Head and Neck - Cancer of the mouth is common in dogs and less common in
cats. A mass on the gums, bleeding, odor, or difficult eating are signs to watch for.
 Horse and cattle are more often affected than sheep, pig and goat.
o Fibropapillomatosis of the skin, mucosa of mouth, esophagus and urogenital
organs are often seen in domestic animals. Fibroma is more common in horses,
cattle and dogs.
 Old animals are affected more commonly than young ones.

VARIETIES OF TUMORS
Tissue of origin Name of tumor Cell type
Mesenchymal Fibroma Fibrous connective tissue
tumors
Chondroma Cartilaginous tissue
Osteoma Bony tissue
Odontoma Tooth substances
Myoma muscular tissue
Myxoma Cardiac skeleton
Lipoma Adipose tissue
Neuroma Nerve cells and fibers
Leiomyoma Smooth muscle
Rhabdomyoma Skeletal tissue
Haemangioma Blood vessels
Meningioma Meninges
Teratoma Germ cells
Epithelial tumors Papilloma Skin or mucous
membrane
Adenoma Glandular epithelium
Basal cell tumour Basal cell of skin
Hepatocellur adenoma Hepatocytes
Glomus tumour Melanocytes
Blood cells Non-Hodgkin lymphoma and Hodgkin Lymphoid cells
lymphoma
Leukemia Hematopoietic cells
DIAGNOSIS
 Clinical examination – location, size and consistency
 Radiography – bones and vascular organs.
 Biopsy – exploratory cytology

TREATMENT

 Prophylactic treatment is undertaken either to reduce the anticipated incidence rate of

a particular tumor type or the rate of recurrence of a neoplastic disease after therapy.
o Mammary tumors in bitch – Spaying between 6 and 12 months of age will greatly
reduce the risk of breast cancer. Surgery is the treatment of choice for this type of
cancer.
o Benign vaginal tumor – ovariotomy
o Testicular tumors (Seminoma and sertole cell tumour) - Castration
 Definitive excision refers to use of surgery as the sole treatment procedure without
adjunctive radiotherapy or chemotherapy.
o Local excision: The removal of a neoplastic mass with the minimal amount of
surrounding normal tissue.
o Wide local excision: Removal of a significant predetermined margin of
surrounding tissues together with the primary mass.
o Radical local excision: Removes of a tumor with anatomically extensive margins
of tissue extending into fasuil planes which are wndistrubed by the primary
growth of the tumor us termed radical local excision or compartmental excision.
Eg: sarcomas.
 Palliative treatment: A procedure that remarkably improves an animal’s quality of life
by providing pain relief, or relieving poor function, despite the presence of unsolved
systemic neoplastic disease.
o Eg: Limb amputation – osteosarcoma
o Spleenectomy – Bleeding haemorrhage of sarcoma
 Apart from surgery and chemotherapy, radiation, cryosurgery (freezing), hyperthermia
(heating) or immunotherapy can be effectively used to treat cancers. Combination
therapy is commonly employed.

CYST

 A cyst is a closed sac having a distinct inner lining of secreting membrane.

 They may contain air, fluids, or semi-solid material.
 Cyst may contain a solid structure like tooth (dentigerous cyst) or hair (dermoid cyst)
also.
 The outer wall of a cyst is called as ‘capsule’.
 Most of the cysts are benign in nature, but some may produce symptoms due to their size
and /or location.
 Size of a cyst may vary from a small grape to a football.
 Cysts can arise anywhere in the body,
o Common example listed below:
 Chalazion cyst (eyelid)
 Retention Cyst (gland like salivary cyst)
 Dentigerous Cyst (associated with the crowns of non-erupted teeth)
 Exudation Cyst (Hydrocoele).
 Dermoid (misplaced embryonic tissue).
  Encapsulation cyst (around foreign bodies and parasites. Ex:
Cystecercosis)
 Neoplastic (Cyst adenoma).
 Ganglion cyst (hand/foot joints and tendons)
 Glial Cyst (in the brain)
 Distension cyst: (Follicular cyst of ovary, cystic distension of a joint
bursa).
 Meibomian cyst (eyelid)
 Ovarian cyst (ovaries, functional and pathological)
 Renal cyst (kidneys)
 Sebaceous cyst (sac below skin)

DIAGNOSIS

 Cysts are generally non-inflammatory in nature and develop slowly with well defined
periphery.
 On palpation fluid filled cyst fluctuates uniformly while cysts with solid mass fluctuates
en-masse.

TREATMENT

 Puncture and evacuate the contents of cyst and inject an irritant solution like Tr. iodine
to destroy the smooth lining membrane and setting up inflammation.
 Use of setton to drain cyst is a good practice.
 Surgical excision of the cyst is the preferred option. Intact cyst is carefully dissected and
removed from the surrounding tissue in possible cases.

DIFFERENTIAL DIAGNOSIS

An abscess must be differentiated from the following conditions:

 Cyst
o Slow in development as compared to an abscess.
o Soft and fluctuates uniformly, but not hard at periphery.
o No inflammatory symptoms.
o No pain sensation.
 Haematoma
o Forms due to coagulation of blood or serum.
o Doughy on palpation and forms immediately following an injury.
o Does not point like an abscess.
o No pain sensation.
 Hernia
o History of recent injury and swelling.
o Hernial ring can be palpated.
 Tumour
o Uniformly hard in consistency.
o Exploratory puncture with needle may reveal blood.
o No pain sensation.
o Does not point like an abscess.
 MODULE-7: NECROSIS, GANGRENE, ULCER AND BURNS

Learning objectives

This module deals with the classification, etiology, clinical signs, diagnosis and treatment of:

 Necrosis
 Gangrene,
 Ulcer,
 Burns and
 Frostbite.

NECROSIS

 Necrosis means death of tissue in the body. This occurs when enough blood is not
supplied to the tissue, whether from injury, radiation, or chemicals.
 Necrosis is not reversible.

CLASSIFICATION

 Avascular necrosis is a disease resulting from the temporary or permanent loss of the
blood supply to the bones. Without blood, the bone tissue dies and causes the bone to
collapse. This disease also is known as osteonecrosis, aseptic necrosis, and ischemic bone
necrosis
 Coagulative necrosis is typically seen in hypoxic environments (e.g. myocardial
infarction , infarct of the spleen ).
 Liquefactive necrosis is usually associated with cellular destruction and pus formation
(e.g. pneumonia ).
 Haemorrhagic necrosis is due to blockage of the venous drainage of an organ or tissue
(e.g. in testicular torsion ).
 Caseous necrosis is a specific form of coagulation necrosis typically caused by
mycobacteria (e.g. tuberculosis ).
 Fatty necrosis results from the action of lipases on fatty tissues (e.g. acute pancreatitis ,
mammary tissue necrosis).
 Fibrinoid necrosis is caused by immune -mediated vascular damage. It is marked by
deposition of fibrin -like proteinaceous material in arterial walls.

ETIOLOGY

 There are many causes of necrosis including injury, infection, cancer, infarction, toxins
and inflammation .
 Severe damage to one essential system in the cell leads to secondary damage to other
systems, a so-called "cascade of effects".
 Necrosis can arise from lack of proper care to a wound site.
o Physical agents like excessive heat or cold.
o Mechanical injuries that crush or cut off blood supply.
o Loss of blood supply cuts off oxygen may be due to passive hyperemia with
sluggish flow of nutrients and deficient oxygenation (volvulus, strangulated
 hernia) and ischemia ( decreased blood supply to a part) due to thrombus or
embolism; compression of an artery, and ergot poisoning

GANGRENE

 Gangrene is necrosis and subsequent decay of body tissues caused by infection or

thrombosis or lack of blood flow.
 It is usually the result of critically insufficient blood supply sometimes caused by injury
and subsequent contamination with bacteria. This condition is most common in the
extremities .

ETIOLOGY

 The main factors in gangrene are loss of blood supply, and later invasion of the part by
micro-organisms.
 Gangrene may be caused by:
o Direct damage to tissues which include:
 Mechanical compression or interference with blood and nerve supply to a
part of the body or an organ while lying on a hard floor. Example: bed-
sores; sit-fast.
 Physical agents like application of heat and cold. Example: burns, frost-
bite.
 Action of acids, alkali and other chemicals producing dry gangrene and
moist gangrene.
 Impaction of intestine in the hernial ring and infestation with pathogenic
microbes especially with anaerobic infection.
o Indirect changes in tissues due to cardiac, venous, arterial or nervous affections
like:
 Ergot intoxication, which causes spasmodic narrowing of arterioles and
leads to dry gangrene of extremities. It is commonly seen in feet of cattle.
 Diabetic gangrene narrows arteries and sugar in tissues, favours bacterial
growth.
 Senile gangrene i.e. arteriosclerosis in old age, which narrows lumen of
blood vessels.

COMMON SITES OF AFFECTION

 Extremities like legs, ears, tail, wattle and combs. It is mostly due to freezing or ergot
poisoning.
 Mammary gland: Staphylococcal mastitis produces necrosis due to toxins or thrombosis
of mammary vessels.
 Involvement of lung due to wrong drenching of medicines, improper passage of stomach
tube or severe lung infection.
 Intestines in equines are commonly involved either with infarction due to verminous
thrombosis of anterior mesenteric artery; or due to acute, local passive hyperaemia
produced by intestinal torsion, volvulus or intussusceptions.
 CLASSIFICATION, ETIOLOGY AND SIGNS OF GANGRENE
Type Etiology Characteristic signs
Wet Sudden interruption of blood  Affected tissue may
gangrene, flow such as due to burns, appear badly
or moist freezing, injury or blood clot. bruised, swollen or
gangrene Wet gangrene spreads very blistered.
quickly and can be fatal.  May also become
infected.
 No clear line
between healthy
and affected tissue.

Dry Insufficient blood flow through  Affected tissue

gangrene the arteries such as due to becomes shriveled,
atherosclerosis or blood clots. It dry and blackish or
usually doesn't involve bacterial greenish colour.
infection.  cold to touch

Gas Infection with certain types of  Swelling around

gangrene bacteria, such as clostridium. It skin due to
typically occurs at the site of a exudates and gas
recent injury or surgery. The formation.
bacteria rapidly destroy muscle  Skin initially looks
and surrounding tissue. pale and then turns
dark red or purple
in color.
 Offensive odour of
exudates.

DIAGNOSIS

 Diagnosis of gangrene will be based on a combination of

o History (recent trauma, surgery, cancer, or chronic disease).
o Physical examination
o Results of blood and other laboratory tests (presence and extent of infection).

TREATMENT

Treatment should be directed to:

 Prevention of cause and extension of gangrene.

 Debridement: Removal of dead, damaged, or infected tissue to improve the healing
potential of the remaining healthy tissue.
 Application of warm antiseptic fomentations to relieve pain.
 Surgical excision or amputation of a limb or organ.
 Antibiotics alone are not effective because they do not penetrate ischemic muscles
sufficiently. However, penicillin is given as an adjuvant treatment to surgery.
 In addition to surgery and antibiotics, hyperbaric oxygen therapy (HBOT) is used that
inhibit the growth and kill the anaerobic organisms.

ULCER

 An ulcer is a localised defect in the continuity of an epithelial surface without any

tendency to heal.
 It is usually associated with an inflamed base of granulation tissue with or without
necrotic slough.
 The majority is chronically inflamed; the slough at their base represents inadequate
drainage.
 Acutely inflamed ulcers may have an outer rim of cellulitis.
 Ulcer must be differentiated from erosion which is an epithelial defect with loss of
superficial layers, but the basal layers are intact.

CLASSIFICATION

 Iatrogenic ulcers: wound breakdown post-operatively and in irritant fluid extravasating.

 Non-specific ulcers: Ex; Traumatic ulcers including secondary stress ulcers.
 Specific ulcers: as observed in tuberculosis, ulcerative lymphangitis, and glanders.
 Malignant ulcers observed in skin and gastrointestinal tract.
 Ischemic ulcers or Decubitus ulcers: These are due to continuous pressure which
interferes with supply of nutrition to local tissues leading to pressure or bed sores.
 Infective ulcers: primary e.g. viral, tuberculosis, and secondary e.g. due to drainage of
deep focus.
 Neuropathic ulcer e.g. in diabetes

ETIOLOGY

 Repeated and continuous irritation of wound. Example: Traumatic ulcer, bed sore.
 Secondary infection of the site by bacteria, fungus or virus with which the tissues cannot
effectively combat.
 Insufficiency of nerve and blood supply to the part.
 Presence of necrotic tissue or foreign body in a wound.
 Specific diseases like tuberculosis, glanders, and ulcerative lymphangitis.
 Presence of neoplasm. Example: Rodent ulcer.

COMMON SITES OF ULCERATION

 Cattle: yoke
 Horse: saddle place, elbow, limbs.
 Dog: root of tail, tip of ears, and cornea of eye.
 SYMPTOMS

 The edge of ulcer may be raised or in level with the surrounding skin and rugged.
 The center of the lesion may be flat or concave, and may show necrotic spots.
 Granulations are pale or blue in colour depending upon the form.
 The discharge may be serous, purulent or grayish.

TREATMENT

The specific treatment of an ulcer is dependent on the subtype.

 Elimination of the cause adversely affecting the course of ulcerative disease and
stimulation of regenerative processes at the affected site.
 Astringent or caustic applications for ulcers with excessive or unhealthy granulations.
E.g. copper sulphate, silver nitrate, carbolic acid.
 Thermo-cautery with red hot iron to destroy unhealthy tissue which promotes
granulation and cicatrisation.
 Bier’s hyperaemic treatment.
 Antibiotics are only indicated for infected ulcers in which there is evidence of spread
around the margin e.g. a cellulitic rim and there may be ongoing systemic infection e.g.
tuberculosis.
 Exposure to ultra – violet rays to stimulate circulation and to destroy micro-organisms.
 For large deficits or prolonged ulcers with little evidence of healing, further surgical
intervention may be indicated e.g. skin grafts and rotational flaps.

BURN AND SCALD

 Burn is an injury of integuments and underlying tissues, occurring due to high

temperature or chemical substances.
 Burn may be defined as tissue changes that occur on excessive absorption of heat by
skin.
 Scald is an injury caused by hot liquids or stream.
 Scald is likely to be more injurious than because of the hot liquid may penetrate into the
deeper part of tissues.

CLASSIFICATION

According to the depth and severity of burn:

 First Degree (Superficial): epidermis is affected and transient erythema, sometimes

vesicle formation and desquamation of the epidermis occurs. Epidermal burns look red,
are painful and heal rapidly.
 Second degree burn (partial thickness burn): Here, depth extends to the mid dermis.
Loss of epidermis is complete. Capillaries and venules in the dermis is dilated, congested
and exude plasma. There is erythema, coagulative necrosis of epidermal cells and vesicle
formation. Healing is rapid and complete by the regeneration of epithelium unless there
is involvement of secondary infection.
  Third degree burn (Full thickness): is characterized by coagulation of epidermis and
dermis. Severe edema of the sub cutis develops and dry gangrene of the damaged tissue
occurs. The epidermis is desiccated and charred with presence of black layer in skin.
Permanent scarring occurs due to healing by granulation. Full thickness burn is
insensitive to pain because of damage of cutaneous nerve endings.
 Fourth degree: Here, subcutaneous fascia and deeper tissue like muscles, bones etc are
involved. The clinical features are similar to those described in third degree burn. Repair
is by scar formation preceded by sloughing of the necrotic tissue.

CAUSES

The following may cause burn:

 Thermal injuries
o Direct heat
o Flame
o Scalding
 Electrical burns
o Electrical cord exposure
o Lightning

Chemical burns

 Injuries caused by chemicals like strong acids and alkalis, solvents, petroleum distillates
and hot tars are referred to as chemical burns.
 The chemical produces localized necrosis of skin and deeper tissues with which it comes
in contact.
 The degree of tissue destruction depends on the strength of the chemical and the
duration of contact.
 Chemical causes local coagulation of proteins and necrosis.

CLINICAL SIGNS

Thermal burns

 Superficial-hyperemia, desquamation and pain.

 Partial thickness- exudation, pain, decreased sensitivity.
 Full thickness- White, black or brown, leathery escher, subcutaneous edema and little or
no pain.

Electrical burns

 No pain
 Well-circumscribed cold, blood less, pale yellow lesion.

Chemical burns
 Line of demarcation between dead and healthy tissue
 Devitalized tissues may get infected
 Formation of ulcer which heals gradually

TREATMENT

 The therapeutic measures must be aimed at

o termination of painful stimuli and improvement of the nervous system function
for avoiding shock;
o reduction of autointoxication;
o prevention of infection;
o promotion of rejection of coagulated Skin and tissues;
o creation of favorable conditions for regeneration of skin
 Anti-shock measures are to be provided to prevent shock that may arise as burn
complication.
 Burn may lead to renal failure and fatty infiltration of liver thus appropriate care should
be extended to combat the complication.
 Local treatment of burns should include:
o Application of ice (3-17ºc) pack wrapped in a soft towel and cold water for 30
minutes or covers it with wet towels. This also helps to remove caustic substances
(acid or alkali) if these are the cause.
o Hair should be removed and gently clean from the site. Necrotic tissue should be
debrided. The area should be swabbed with weak vinegar (half water, half
vinegar) using cotton wool or cloth.
o Topical antibacterial ointments may be applied to prevent the animal from post
burn sepsis. Several topical commercial products like Aloevera cream, Silver
sulphadiazine cream (Indo-Pharma), Silver nitrate 0.5% Solution, chlorhexidine
0.5% Solution, gentamycin sulphate 0.1% cream, povidone iodine cream can be
used. Soothing and protective preparations like Badional gel (Bayer), Caladryl
cream (Park Davis), Burnol (Knoll) may be used as burn dressing.
o Drugs like gentian violet, picric acid, acriflavin and tannic acid should not be
used as far as possible as they delay the healing process by damaging the living
cells.
o Analgesic should be given to reduce pain.
o Hypovolemic shock and acidosis are to be prevented by supplementation of large
quantities of fluid (Dextrose 5%) including 4% sodium bicarbonate.
o The treatment in chemical burns should include washing with lots of plain water
and neutralization of the offending chemicals. Acids can be neutralized with 2-3%
solution of sodium carbonate or milk, while alkali with 2% vinegar, citric or boric
acid. Finally soothing ointment like olive oil may be applied. If shock occurs, keep
the animal warm with heating pads or hot water bottles and a blanket of heavy
coat. A burn patient (pet) should be provided with ample warm fluids to drink
and this may be given in the form of milk or glucose water.

FROST BITE

 Frost bite is injury of tissues due to the action of a low temperature on them.
 The condition is rare in animals because they can withstand cold temperature due to
their hairy coats and will instinctively seek shelter from inclement weather.
 Udder and teats are commonly frozen in cows during exercise on frosty winter days.
Besides the prepuce, penis and scrotum in horses, snout of pig, comb and wattles of
birds, tip of the ear and scrotum of dogs, tail and distal extremities in other animals are
commonly affected.
 It usually occurs in a low temperature but it can also ensue in prolonged action of wet
moderate above zero temperature (3-7ºc) since heat conductance of the skin is increased
and heat emission is intensified by it.

CAUSES

 Exposure to cold or chilling environment.

 Contact with cold metal, glass, and liquids.
 Iatrogenic freezing with cryogens like liquid nitrogen and nitrous oxide etc.

CLASSIFICATION AND PATHOPHYSIOLOGY

 Various degrees of frost bite recognized are:

o Mild: contraction of blood vessels (parts appear white) —> paralytic dilatation of
blood vessels —> engorgement of vessels —> parts appear red and swollen —>
thawing —> severe pain
o Moderately severe: Below 0oC temperature for longer period than mild —>
injury of Blood vessels —> inflammation of the tissues —> redness of epidermis
together with certain amount of necrosis and blister formation —> desquamation
o Severe: Temperature falls for lower than freezing point —> impaired circulation
of blood and lymph —> parts undergoes necrosis and gangrene may ensue

CLINICAL SIGNS

 Loss of sensation in the affected part.

 Cyanotic or pale appearance of frozen part.
 Moderate edemas, pain and very cold to touch.
 Shivering.
 In neglected cases, necrosis and sloughing of skin.

TREATMENT

 Withdrawal from cold

 Warming of frost bitten extremities, and restoration of blood and lymph circulation:
Frozen animals must be immediately put in a warm housing to restore body core
temperature. Hot water bag or hot pad may be used for warming; frozen parts should be
bathed in increasingly warm water until pink colour is restored.

DRUGS

 Prevention of infection with systemic antibiotics

 Fluid therapy with dextrose should be considered.
 Analgesics may be provided to prevent self-trauma.
 Artificial respiration should be provided to frozen animals.
  The frozen tissue should not be massaged.
 Necrosed tissue if there should be removed. Amputation of frozen part if necessary
should be carried out
 Diet: High protein, high caloric diet and vitamins should be instituted.

MODULE-8: WOUND - CLASSIFICATION, SYMPTOMS,

DIAGNOSIS AND TREATMENT

Learning objectives

This module deals with

 Wound and its classification

 Symptoms of wound
 Phases of wound healing
 Factors affecting wound healing

INTRODUCTION

 A wound is a separation or discontinuity of soft tissues caused by trauma, surgery or

noxious physical agents.

CLASSIFICATION OF WOUND

Open or external wound

 There is discontinuity in the skin and other covering tissues to a varying depth.
 In closed or interstitial wound, only deeper tissues, barring the skin or mucous
membrane are damaged.

Closed wound/ internal wound

 Contusion is injury to the skin without any break in the continuity of tissue surface. It is
caused by blunt objects and the subcutaneous tissues, muscles; nerves are damaged to a
varying degree.
 According to the severity and extent of tissue damage it may be of:
o First degree with rupture of capillary vessels of the skin and subcutaneous tissue.
o Second degree with rupture of larger vessels leading to haematoma formation.
o Third degree with major damage of tissues leading to gangrene formation.

Open wounds

 Incised wounds are caused by sharp cutting instruments such as knives, scalpels,
fragments of glass etc with minimum loss to tissue, edges are regular, bleeds freely and
painful.
 Lacerated wounds are caused by tearing of tissues with torn and uneven edges. Wounds
have irregular jagged borders and loss of tissue is limited to skin and subcutaneous
tissue e.g.: barbed wire.
 Penetrating wounds are types of deep wounds communicating with cavities like
abdomen, thorax, and joints etc. e.g.: stab wounds.
 Perforating wound is having two opening, one of entrance and other of exit.
 Punctured wound are caused by sharp pointed objects like nails relatively with a small
opening. There might be presence of infection/ foreign particles deep into the wound
with inadequate opening for drainage. Ex: Stab wounds.
 Gunshot wound is produced by various forms of firearms e.g. injuries caused by bullet.
 Abrasions are superficial damage to the skin, generally not deeper than the epidermis.
 Avulsion occurs when an entire structure or part of it is forcibly pulled away. Explosions,
gunshots, and animal bites may cause avulsions.
 Bite wounds are caused by snake; dog or wild animals bite with significant degree of
tissue damage.
 Virulent wounds are caused by bacteria or virus leading to formation of pustules or
vesicles e.g.: FMD, anthrax.
 Granulating wound is one in which there is a tendency to heal within expected time.
 Aseptic wound is surgical wound made under aseptic conditions where chances of
bacterial contamination are negligible.
 Contaminated wound is one where there is presence of micro organisms.
 Infected/ septic wound: A contaminated wound may become infected after a period of 6
-8 hours where bacterial multiplication may occur and liberation of their toxin.

SYMPTOMS OF WOUND

 Localized pain and bleeding.

 Gaping of the lips of wound.
 Weakness, paralysis or a loss of function in a dependent portion.
 Febrile disturbances in severe septic wound.
 Neuritis extending along the course of the nerve involved in the wound.

PHASES OF WOUND HEALING

 Wound healing involves a complex series of interactions between different cell types,
cytokine mediators, and the extracellular matrix.
 The phases of normal wound healing include hemostasis, inflammation, proliferation,
and remodeling.
 Each phase of wound healing is distinct, although the wound healing process is
continuous, with each phase overlapping the next.
 Before the advent of modern veterinary practice, many soft tissue injuries healed with
time.
 The difference that the modern veterinary practice has made is that the more severe
injuries that would have killed the animal are now manageable; the deformity and
infection that often accompanies natural unaided tissue healing can be avoided or
minimized.
 The Four phases of wound healing are
o Haemostasis
o Inflammatory phase
o Proliferative phase
 o Wound remodeling

HAEMOSTASIS

 Tissue injury initiates a response that first clears the wound of devitalized tissue and
foreign material, setting the stage for subsequent tissue healing and regeneration.
 The initial vascular response involves a brief and transient period of vasoconstriction
and hemostasis.
 A 5-10 minute period of intense vasoconstriction is followed by active vasodilatation
accompanied by an increase in capillary permeability.
 Platelets aggregated within a fibrin clot secrete a variety of growth factors and cytokines
that set the stage for an orderly series of events leading to tissue repair.

INFLAMMATORY PHASE

 The second phase of wound healing i.e. the inflammatory phase lasts for 1-3 days in
uninfected wounds.
o Classic signs include the following:
 Redness (rubor)
 Swelling (tumor)
 Pain ( dolor)
 Heat (calor)
 Loss of function (function laesa)
o Process
 The inflammatory response increases vascular permeability, resulting in
migration of neutrophils and monocytes into the surrounding tissue. The
neutrophils engulf debris and microorganisms, providing the first line of
defense against infection. Neutrophil migration ceases after the first few
days post-injury if the wound is not contaminated. If this acute
inflammatory phase persists, due to wound hypoxia, infection, nutritional
deficiencies, medication use, or other factors related to the patient’s
immune response, it can interfere with the late inflammatory phase.
 In the late inflammatory phase, monocytes converted in the tissue to
macrophages, which digest and kill bacterial pathogens, scavenge tissue
debris and destroy remaining neutrophils. Macrophages begin the
transition from wound inflammation to wound repair by secreting a
variety of chemotactic and growth factors that stimulate cell migration,
proliferation, and formation of the tissue matrix.

PROLIFERATIVE PHASE

 The subsequent proliferative phase is dominated by the formation of granulation tissue

and epithelialization.
o Its duration is dependent on the size of the wound.
o Chemotactic and growth factors released from platelets and macrophages
stimulate the migration and activation of wound fibroblasts that produce a
variety of substances essential to wound repair, including glycosaminoglycans
(mainly hyaluronic acid, chondroitin-4-sulfate, dermatan sulfate, and heparan
sulfate) and collagen.
 o These form an amorphous, gel-like connective tissue matrix necessary for cell
migration.
 New capillary growth must accompany the advancing fibroblasts into the wound to
provide metabolic needs.
o Collagen synthesis and cross-linkage is responsible for vascular integrity and
strength of new capillary beds.
o Improper cross-linkage of collagen fibers has been responsible for nonspecific
post-operative bleeding in patients with normal coagulation parameters.
o Early in the proliferation phase fibroblast activity is limited to cellular replication
and migration.
o Around the third day after wounding the growing mass of fibroblast cells begin to
synthesize and secrete measurable amounts of collagen.
o Collagen levels rise continually for approximately three weeks.
o The amount of collagen secreted during this period determines the tensile
strength of the wound.

WOUND REMODELING

 The final phase of wound healing i.e. remodeling develops 3 weeks following injury and
continues up to two years, achieving 40-70 percent of the strength of undamaged tissue
at four weeks.
 This phase is characterized by reorganization of new collagen fibers, forming a more
organized lattice structure that progressively continues to increase wound tensile
strength.
 The strength of scar tissue formed in this phase is less than the surrounding normal
tissue.

COMPLICATIONS OF WOUND HEALING

 Wound dehiscence is the splitting and separation of previously closed wound layers.
Evisceration is protrusion of viscera through the wound. Eventration is protrusion of the
bowels from the abdomen. The main causes responsible for these conditions include
improper surgical technique and the local and systemic factors described below.
Dehiscence usually occurs 3-5 days after surgery before collagen deposition. The
characteristics features include incisional swelling, discolouration, necrosis and unusual
exudation.
 Haemorrhage due to rupture of blood vessels can lead to development of hemorrhagic
shock and ultimately death.
 Traumatic neuralgia is the pain perceived at or around the vicinity of wound. Primary
traumatic neuralgia persist for prolong period whereas secondary one appear during
cicatrisation.
 Septicemia and pyemia are the common complications of wound healing cause by the
bacterial toxins due to massive infection and may lead to endotoxic shock.
 Traumatic fever is the resultant of pyrogen release from neutrophils and injured body
tissue.
 Haematoma (accumulation of blood in the Subcutis) or seroma (accumulation of serum
in the dead space) may occur due to rupture of blood vessels following injury.
 Sinus (draining tract from a suppurative cavity to the surface) may develop due to
presence of necrotic tissue debris and foreign bodies.
 Fistula (abnormal passage between two internal organs) may develop due to paucity of
drainage from a purulent cavity.
 Cellulitis is inflammation of the connective tissues presenting as oedema, redness, pain
and heat often with hardness.
 Exuberant granulation tissue (proud flesh) is granulation tissue which grows above the
level of the surrounding skin (overgranulation), preventing epithelial cells from growing
across the wound.
 Tetanus may develop due to Clostridium tetani infection particularly in deep penetrating
and punctured wound. Caprine, equine and camalidae are more susceptible to tetanus.
 Adhesions are the major post-operative complication following abdominal surgery due to
rough handling of viscera.
 Traumatic emphysema arises due to punctured wounds of the respiratory or
gastrointestinal tract where gas or air accumulate in and around the wound area.
 Venous thrombosis and embolism may occur when fat tissue accidentally entered in the
circulation.
 Gas gangrene may develop.

FACTORS AFFECTING WOUND HEALING

 Local factors
 Systemic factors
 Medication
 Systemic diseases

LOCAL FACTORS

 Good surgical technique is warranted for proper wound healing if Halsted’s principles
are followed. The principles include:
o Gentle handling of tissue.
o Aseptic surgical technique
o Perfect hemostasis and preservation of blood supply to the wound area.
o Close tissue approximation and obliteration of dead space
o Removal of necrotic and devitalized tissue.
 Tissue vascularity ensures oxygenation and nutrients which is essential for wound
healing. Oxygen influences angiogenesis, epithelialization and resistance to infection.
 Infection is one of the major factors which retard the wound healing significantly as it
prolongs the inflammatory phase, disrupts the normal clotting mechanisms, promotes
disordered leukocyte function and ultimately prevents the development of new blood
vessels and formation of granulation tissue.
 Topical medications promote wound healing by minimizing bacterial infection.
However, certain antimicrobial agents and local anesthetics delay the healing process by
destroying cellular elements of wound.
 Lavage and dressings accelerate wound healing by protecting healing tissue. Lavage
with sterile isotonic solutions like normal saline decreases the concentration of the
microorganisms mechanically and aids in healing process. Nonadherent, moist dressing
triggers epithelisation whereas adherent gauge dressing mechanically debride the
contaminated wound.
 Presence of foreign bodies such as tissue debris, dirt, soil, sequestrum, or nonabsorbable
braided suture materials delay the healing process by exacerbating the inflammatory
response and inciting infection.
 Obliteration of dead space and prevention of fluid accumulation promote migration of
reparative cells and minimizing the risk of infection during wound healing.
 Ionizing radiation retards wound healing by decreasing fibroblast formation, collagen
synthesis and neovascularisation within fortnight of surgery.
 Movement of the wound site prolongs the healing process as movement can disrupt cell
migration, neovascularisation and formation of early ground substances of the wound.
 Mutilation of the wound not only disturbs the healing but also complicate by creating
evisceration like condition.

SYSTEMIC FACTORS

 Advanced age retards healing because of reduced skin elasticity and collagen
replacement. The immune system also declines with age making patients more
susceptible to infection. Older animals are also susceptible to other chronic diseases,
which affect their circulation and oxygenation to the wound bed as compared to young.
 Nutrition plays a pivotal role in wound healing process.
 Protein is required for all the phases of wound healing, particularly important for
collagen synthesis. Hypoproteinemia slows healing by decreasing wound tensile
strength, delaying fibroplasia and producing edema.
 Glucose balance is essential for wound healing. Hyperglycemia delay wound healing.
 Iron is required to transport oxygen.
 Minerals like zinc, copper are important for enzyme systems and immune systems. Zinc
deficiency contributes to delay epithelisation and disruption in granulation tissue
formation by inhibiting fibroblastic cellular proliferation.
 Vitamins A and B complex are responsible for supporting epithelialization and collagen
formation. It is also important for the inflammatory phase of wound healing.
 Vitamin C is essential for formation of intercellular cementing substances as it is needed
for hydroxylation of the lysine and proline moieties of collagen.
 Carbohydrates and fats: These provide the energy required for cell function. When the
patient does not have enough, the body breaks down protein to meet the energy needs.
Fatty acids are essential for wound healing.

MEDICATION

 Anti-inflammatory, cytotoxic, immunosuppressive and anticoagulant drugs all reduce

healing rates.
o Anti-inflammatory drugs like corticosteroids if used in long term and at higher
doses impair the inflammatory phase, decrease fibroplasia, collagen synthesis
and neovascularisation.
o Chemotherapeutic agents like methotrexate, doxorubicin and cyclophosphamide
delay the wound healing process by inhibiting cell division or collagen synthesis.
In addition, healing process is adversely affected by depressing immune function,
epithelialization and contraction.
o Anticoagulant drugs retard the healing by interrupting clotting mechanism and
thus making a wound more prone to infection due to presence of blood clots.
o Most NSAIDs lower resistance to infection and ultimately delay healing.

SYSTEMIC DISEASES
  Systemic diseases like malignancy, uncontrolled diabetes, renal and hepatic disturbances
delay healing process.
 A malignancy in the body retards wound healing by altering metabolism, producing
chachexia, and minimizing inflammatory cell division.
 Uremia delays fibroblastic proliferation, granulation tissue formation, epithelial
proliferation and subsequently strength of healing wund.
 In patients with uncontrolled diabetes, there is delayed healing as hyperglycemia impairs
collagen formation, neovascularisation, granulocytes cell functions and ultimately
leading to wound dehiscence.

CLINICAL SIGNS OF INFECTION

 Local pain/tenderness
 Local swelling/oedema
 Increased exudate
 Frank pus
 Wound breakdown
 Pyrexia
 Delayed healing
 Change in appearance of granulation tissue
 Bridging of epithelial tissue
 Abnormal smell

MANAGEMENT OF WOUNDS

 Humans have always been faced with the dilemma of how to treat wounds.
 Many diverse and interesting approaches to wound management have been applied
throughout medical history. Thirty years ago physicians believed pus in a wound was
laudable and anxiously awaited its arrival; surgeons today attempt every conceivable
means to prevent its presence.
o Contusions: are treated with cold and astringent applications to minimize
extravasation.
o Haematomas: when small get absorbed other wise they may have to be opened
and treated.
o Open wounds: surgical or aseptic wound, contaminated and septic wound or
infected wounds.

Surgical or aseptic wounds

 A surgical wound made with all aseptic precautions in a non infected tissue is an aseptic
wound.
 Surgeon should avoid drying of the tissue, excessive trauma and haemorrhage – lower
the wound infection.
 Prophylaxis against tetanus.
 Dependent drainage should be provided if haemotoma or seroma formation is expected.
 Suture should be supported upto healing time 8 -14 days
 Systemic use of specific antibiotics as a therapeutic or prophylactic measure.
 Local application of Fly repellents – hot summer months.
 The patient and the affected injured part should be kept at rest.
Contaminated wound

 A fresh wound gets contaminated when it is more than 4 -5 days old.

 The principal therapeutic strategies of the open and contaminated wound are to convert
it into a clean closed wound.

WOUND CLEANSING PROTOCOL

 Wound cleansing is a clean - not sterile – procedure. Not all wounds require cleaning.

Reasons to clean a wound

 Presence of:
o Foreign bodies
o Debris e.g. slough, residue from hydrocolloid dressings
o Purulent exudate i.e. infection

EQUIPMENT

 Clean basin - basin for this purpose must be washed with soapy water, rinsed and dried
before use.
 Warm tap water is required otherwise cold water may reduce the temperature of the
wound surface to a degree where cell mitosis will not recommence for up to 4 hours.
 Gauze / soft wash cloth: Contaminated wound, where possible, immerse and clean.
Otherwise, the soaked wash cloth must be squeezed over it allowing the water to wash
over it. Non-fiber shedding gauze should be used where foreign bodies remain. This is
not a routine practice as it redistributes bacteria, is painful and causes trauma to healing
cells
 Disposable gloves (clean but not sterile)
o The following procedures should be meticulously adhered:
 A sterile gauze pad should be placed over the wound followed by shaving
the surrounding skin and finally, cleaning the edges of wound with a
detergent soap and water.
 The surrounding area should be draped with a sterile one.
 The wound area should be prepared for surgical debridement by gentle
irrigation with lukewarm isotonic saline solution.
 Devitalized and ragged skin edges, nonviable and heavily contaminated
tissues should be removed.
 Again the wound area should be exposed by gentle traction and carefully
irrigated.
 After cleansing, dry surrounding skin but not the wound itself.
 The operative field should be again prepared by placing sterile gauze over
the wound and redraping the surrounding area.
 Capillary and venous oozing should be controlled by gentle pressure and
ligating blood vessels if necessary.
 Wound closure should be done either by suture without drainage or
placing a small rubber drain into the depths of the wound and other end
in the skin margin.
  The wound may be loosely packed with petrolatum-impregnated gauze
and sutured at a later date (delayed primary closure).

SEPTIC WOUND OR INFECTED WOUND

Basic principles of infected wound treatment strategies

 Debridement: Thorough debridement is most essential to manage septic wounds which

will provide easy access to the wound depth.
o All necrotic tissue debris and foreign materials should be removed until clean,
healthy tissue margin of the wound are achieved.
o Infected wound should not be plugged or closed unless infection is well
controlled for primary healing but should be left to heal by secondary healing.
 Lavage: after removal of the necrotic debris, the wound and its periphery should be
copiously irrigated with warm normal saline or water and soap or 2% hydrogen per
oxide.
o Volume and nature of lavage fluid depends on the degree of gross contamination
and size of the wound.
o Addition of antibiotics or antiseptics is not required when large volume of fluid is
used as improper concentrations of such drugs may have deleterious effect to the
wound healing process.
 Wound drainage can be achieved by using Penrose drains, plastic or rubber tubes or
open drainage with bandage support. The aim is to reduce fluid accumulation, dead
space, hematoma and seroma. The following guidelines should be observed:
o Dependent drainage of wound exudate should be provided if possible so that
gravity will aid drainage of the exudate.
o The incision for drainage should be placed in the most direct route possible and
away from anastomotic sites, tendon and major vessels. They may cause pressure
necrosis.
o Soft, petrolatum based antiseptic gauze should be used to keep the wound edges
apart.
o Incision to place the drain should be made within the zone of reaction; avoid
cutting into non-infected areas. The drain exit site should be prepared in an
aseptic manner and should be covered with sterile bandages to prevent
premature removal or loss of the drain and to access the nature of the exudate.
o Through and through drainage should not be used.
o Usually drain should be removed after 24-48 hrs. ( insert picture).
 Antimicrobial therapy: Selection of the antimicrobial agent should be based on culture
and antibiotic sensitivity test. However, empirical antimicrobial agents should be
advocated in life–threatening infections that exists or develops while awaiting culture
and sensitivity results (48-72 hrs). In most cases, animals with existing wound infection
are treated initially with loading dose of intravenous medication. Antimicrobial therapy
should be continued for 10-14 days.
 Sterile protective bandaging is a good practice to avoid hospital infection, colonization
of the wound by opportunistic organisms and to prevent environmental contamination
with the infective agent.

MODULE-9: PREANAESTHETIC CONSIDERATIONS AND

PREANAESTHETICS
Learning objectives

This module deals with

 Anticholinergics
 Transquilizers or neuroleptics
 Phenothiazine derivatives
 Butyrophenones
 Benzodiazepines
 Sedatives
 Alpha 2 adrenergic agonist
 Chloral hydrate
 Opioid agents
 Agonists
 Partial Agonists/Antagonists

PREMEDICATION

 Premedication and selection of premedicants are important components of safe

anaesthetic protocol in tailoring anaesthetic regimen suitable for species, breeds, age and
disease status.

Aims of premedication

 To reduce fear and calm the patient,

 To reduce distress during restraining and minor manipulations like placement of
catheters,
 To produce pre, intra and post operative analgesia,
 To reduce salivary secretion and airway secretion,
 To decrease the total quantity or amount of the major anaesthetic drug,
 To reduce the delecterious side effects of the major anaesthetic drug,
 To provide smooth induction,
 To reduce intra operative complications like vomiting and regurgitation and
 To provide safe and smooth recovery.

CLASSIFICATION OF PREMEDICAMENTS

 The premedicants used in veterinary anaesthesia are classified as follows based on their
properties.

S.No. Premedicaments Examples

1. Anticholinergics Atropine sulphate, Glycopyrrolate
2. Transquilizers or neuroleptics Chlorpromazine, Acepromazine,
trith promaziae promethorine
Phenothiazine derivatives
 Butyrophenones Droperidol, Azaperone

Benzodiazepines Diazepam, Medazolam,

Zaazepur clamazolam
3. Sedatives Xylazine, Detomidine,Meditomedine

Alpha 2 adrenergic agonist Ranifidiae

Chloral hydrate
4. Opioid agents Morphine, Meperidine

Agonists Pentazocaine, Butorphenol

Partial Agonists/Antagonists
ANTICHOLINERGICS

 Anticholinergic premedicants are atropine sulphate, scopolamine and glycopyrrolate.

Atropine sulphate is a natural product widely available invarious plants like Atropa
belladonna.
 It is also found in Jimson weed. Scopolamine is not used in veterinary practice.
 Glylcopyrrolate is a synthetic quaternary ammonium compound.
 These agents are competitive of acetylcholine (Ach) hence attenuate the physiological
responses of parasympathetic nerve impules.

CLINICAL PROPERTIES AND USES

 These agents are administered to

o suppress the vagal tone
o reduce salivary and bronchial secretions.
 Anticholinergic premedication is contraindicated in ruminants as the salivary and
bronchial secretions will become more viscid and block the airway. They also induce
ruminal atony. But their use is justified and recommended along with anaesthetics and
adjuncts, which cause excessive salivation and bradycardia (eg. Xylazine).
 Though the routine use of these drugs has decreased in anaesthetic protocols, their use is
still recommended in patients with preexciting bradycardia or in combination with drugs
anticipated to cause bradycardia. In animals with preexciting bradycardia they increase
the cardiac out put.
 Herbivores are more resistant to anticholinergics.
 They increase the heart rate by blocking vagal tone on S.A node. The increase in heart
rate is associated with increased myocardial oxygen consumption, hence contraindicated
in animals with pre exciting tachycardia, heart failure and cardomyopathies.
 Large dose of atropine may cause dilatation of cutaneous vessels due to the effect on the
cholinergic receptors of the vascular smooth muscles (Atropine flush).
 Decrease salivary secretion, gastric acid secretion and gastrointestinal motility.
 Decrease bronchial secretion, dilate bronchi and increase the pulmonary dead space.
 Induce mydriasis due to the cholinergic blockade of iris and ciliary body and paralyze
accommodation reflex (cycloplegia) resulting in photophobia and blurred vision.
 Indicated in eye surgeries whether performed under local or general anaesthesia to
prevent oculo-cardiac reflex.
 Relax the urinary tract smooth muscles and tend to cause urinary retention.
 Excessive dose of atropine and scopolamine may induce hallucination, excitement and
seizures. And this central stimulation is not noticed after administration of
glycopyrrolate, as it does not cross the blood-brain barrier. Due to this property
glycopyrrolate is considered as a usefulo premedicant in equine anaesthesia.
 The undesirable effects of atropine and glycopyrrolate can be reversed with neostigmine
or physostigmine.

ADVANTAGE AND DISADVANTAGES OF ATROPINE AND

GLYCOPYRROLATE
Drug Advantages Disadvantages
Atropine  Less expensive,  may induce variety of
sulphate  Tachycardia is not cardia arrythmias if
extreme as in myocardial oxygen demand
glycopyrrolate is not satisfied.
 Indicated in animals  Iduces bradycardia initially
requiring immediate if administered through
treatment for intravenous route due to
bradycardia due to its the stimulation of vagal
quick action. nuclei in the medulla:
hence intravenous
administration is
contraindicated for
caesarian section in
bitches.

Glycopyrrolate  Less dose (0.44 mg of  Not completely effective in

atropine is equivalent to preventing sialorrhea
0.11 mg of glycopyrrolate
in intravenous route).
 Controls bradycardia
effectively.
 Indicated in caesarian
section as it does not
cross the placental
barrier and causes
excessive increase in the
heart rate of neonates.
 Effectively controls
gastric acidic pH and
avoids aspiration of
gastric acidic secretion.
 Causes less intestinal
stasis hence indicated in
 equine anaesthetic
regimen to reduce the
incidences of post
anaesthetic colic due to
ileus.

CLINICAL DOSES
Species Atropine Glycopyrrolate
Horses 0.02 – 0.05 mg/kg S.C/I.M 0.02 mg/kg S.C/IM
Goats 0.20 mg/kg I.M 0.01 mg/kg I.M
Pigs 0.3—1.8 mg total dose
0.02—0.05 mg/kg S.C/I.M 0.01—0.02 mg/kg S.C/I.M/I.V
Dogs
0.02 – 0.02 mg/kg I.V
0.02 – 0.1 mg/kg S.C/I.V 0.02—0.02 mg/kg S.C/I.M./I.V
Cats
0.01 – 0.02 mg/kg I.V

PHENOTHIAZINE DERIVATIVES

 Phenothiazine derivatives are basically three ring structures in which two benzene rings
are linked by a sulphur and nitrogen atom.
 The steriochemical model of phenothiazine derivatives is similar to epinephrine,
norepinephrine and dopamine.
 They act on the central nervous system by depressing the brain stem and connections of
the cerebral cortex.
 These agents increase the dopamine and norepinephrine turn over in the brain and block
the peripheral actions of catecholamines at alpha 1 receptors.
 These agents are weak anticholinergics and have extrapyramidal stimulating properties.
 Acepromazine maleate, triflupromazine hydrochloride, chlorpromazine, promazine,
promethazine and methotrimeprazine are the commonly used phenothiazines. Among
these agents acepromazine, triflupromazine and chlorpromazine are used in veterinary
anaesthesia.

CLINICAL PROPERTIES AND USES

 Produce sedation, general calming and reduction in motor activity

 Antagonize dopamine excitatory chemoceptors and suppress vomiting.
 At high doses and some times in clinical doses induce extrapyramidal signs such as
rigidity, tremors and catalepsy. Hence contraindicated in patients;
 o With the previous history of epilepsy,
o Undergoing myelographic procedures
o With the history of recent intake of organophophorus drugs or toxicity
 Pulmonary functions are maintained following the administration of phenothiazines
except slight depression in respiratory rate
 Induce urine production due to the suppression of antidiuretic hormone
 Animals undergoing intradermal allergic tests should not be administered with
phenothiazines as they are potent antihistaninics
 Depletes catecholamines of the thermoregulatory center and render the animal’s body
temperature susceptible to the changes in the environmental temperature.
 Tranquilization with phenothiazines is contraindicated in animals undergoing epidural,
spinal or segmental anaesthesia. Following induction of regional anaesthesia there will
be vasodilation in the anaesthestised part of the body and this effect is compensated by
the vasoconstriction in the unanaesthetized parts of the body to maintain cardiac out
put. This response is abolished by the generalized vasodilationinduced by
phenothiazines.

CLINICAL DOSES
Drug Dose
Acepromazine Dogs = 0.03 – 0.05 mg/kg I.V, 0.03 – 0.05 mg/kg I.M.

Cats = 0.03 – 0.05 mg/kg I.V, 0.03 – 0.1 mg/kg I.M.

Horses = 0.02 – 0.05 mg/kg I.V, 0.04 – 0.09 mg/kg I.M.

Cattle = 0.02 – 0.05 mg/kg i.V, 0.04 – 0.09 mg/kg I.M.

Pigs = 0.1 mg/kg I.M.

Chlorpromazine Dogs = 0.55 – 4.4 mg/kg I.V, 1.1 – 6.6 mg/kg I.M.

Cats = 0.55 – 4.4 mg/kg I.V, 2.2 – 6.6 mg/kg I.M

Horses = 1.1 – 2.2 mg/kg I.M.

Cattle = 0.2 – 1.1 mg/kg I.V, 0.2 – 2.2 mg/kg I.M.

Sheep = 0.55 – 4.4 mg/kg I.V, 2.2 – 6.6 mg/kg I.M.

Goats = 0.55 – 4.4 mg/kg I.V, 2.2 – 6.6 mg/kg I.M.

Pigs = 1.0 – 2.0 mg/kg I.M.

Promazine Horses = 0.44 – 1.1 mg/kg I.V/I.M.

Cattle = 0.44 – 1.1 mg/kg I.V/I.M.

Goats = 0.44 – 1.1 mg/kg I.V/I.M.

 Sheep = 0.44 – 1.1 mg/kg I.V/I.M.

Pigs = 0.44 – 1.1 mg/kg I.V, 0.44 – 4.0 mg/kg I.M.

Triflupromazine Dogs = 1.00 mg/kg
BUTYROPHENONES

 Butyrophenones have similar properties like phenothiazines.

 They block the central actions of dopamine and norepinephrine.
 They are more likely to produce extrapyramidal signs like tremors, rigidity and catalepsy
in clinical doses hence not popular.
 Droperidol, fluanisone, azaperone and lenperone are the butyrophenones used in
anaesthesia.
 They are potent antiemetics and even prevent drug induced vomiting produced by opioid
analgesics by acting on the chemoemetic trigger zone. Hence used as neuroleptic
analgesics in anaesthetic regimen.
 Butyrophenones have less cardiac depressive effects and the hypotension produced by
the agents can easily be reversed with phenylephrine.
 They induce minimal changes in respiratory parameters.

DRUGS AND DOSES

 Droperidol
o It is available in combination with an opioid analgesic, fentanyl citrate. (0.4 mg of
fentanyl citrate and 20 mg of droperidol per ml = Innovar vet) This combination
produces profound analgesia for 30 minutes and sedation for a considerable time
in dogs.
o In cats it may induce undesirable central nervous system stimulation.
o Other effects noticed after administration are panting, aggression upto 48 hours
after recovery, defecation and salivation. Naloxone - 0.04 mg/kg mixed with 4-
aminopyridine - 0.5 mg/kg intravenously reverse the side effects of droperidol-
fentanyl combination.
o Clinical dose
 Dogs 0.05 – 0.1 mg/kg I.M
 Cats 0.10 – 0.11 mg/kg S.C
 Pigs 0.10 – 0.4 mg/kg I.M
 Azaperone
o It is widely used in pigs for control and transportation. In pigs it is administered
prior to metomidate. Azaperone sometimes produce muscle tremors, sweating
and excitement in horses hence it is unsuitable for equine anaesthesia.
o Clinical dose - Pigs = 0.4 – 1.2 mg/kg I.M (low dose),2.0 mg/kg I.M (medium
dose), 4.0 mg/kg I.M (high dose)
 Fluanisone
o It is available in combination with fentanyl citrate. (0.315 mg of fentanyl and 10
mg of fluanisone = Hypnorm).
o This combination is contraindicated in patients with respiratory, renal and
hepatic diseases. Naloxone is the reversal agent for this combination.
o Clinical dose - Dogs = 5 mg/kg along with 0.1 mg/kg of fentanyl citrate
(neuroleptanalgesia).
 BENZODIAZEPINES

 Benzodiazepines exerts their effects by binding to a specific binding site on aminobutyric

acid (GABA) receptor.
 They do not have analgesic property.
 These agents are good anxiolytics, hypnotics and anticovulsants.
 They have minimal respiratory and cardiovascular depression.
 These agents produce muscle relaxation.
 Diazepam, midazolam, climazolam and zolazepam are the commonly used
benzodiazepines.
 These agents are combined with opioid analgesics and dissociative anaesthetics.

DIAZEPAM

 Diazepam is used to treat status epilepticus in dogs, cats and human.

 It can not be used as a sole sedative agent in dogs and cats.
 In horses it produces excitation if used as a sole sedative premedicant hence combined
with xylazine.
 It decreases the release of catecholamines and act as antidysrhythmic agent.
 It is used as an effective appetite stimulant in dogs and cats at the dose of 0.05 – 0.40
mg/kg Oral/I.M.
 In human it causes congenital anomalies if administered during the first trimester of
pregnancy. And the significance of this is not clear in veterinary practice.
 It is absorbed by plastic materials hence storage in plastic syringes, infusion bags and
infusion tubes are not advisable.
 Rapid intravenous injection may cause thrombosis.
 Dose
o Dogs 0.1 – 0.5 mg/kg I.V, 0.3 – 0.5 mg/kg I.M.
o Cats 0.05 – 0.4 mg/kg I.V, 0.3 – 1.0 mg/kg I.M.
o Horses 0.02 – 0.04 mg/kg I.V
o Foals 0.1 – 0.2 mg/kg I.V
o Cattle 0.1 mg/kg I.V
o Goat 0.1 – 0.1 mg/kg I.V
o Pigs 1.0 mg/kg I.V

MIDAZOLAM AND CLIMAZOLAM

 Midazolam
o It is twice as potent as diazepam.
o Can be administered as premedicant to thiopentone, ketamine and propofol
anaesthesia.
o It is metabolized in the liver rapidly hence less cumulative can be stored in
aquane solution in plastic container upto 100 hours without loss of potency.
o Dose - Dogs & cats = 0.07 – 0.22 mg/kg I.M/I.V
 Climazolam
o It is a potent benzodiazepine, has variety of use in cattle, sheep, horses and dogs.
o In horses the drug is combined with other premedicants and anaesthetics as it
may produce excitement and muscle weakness.
o Dose
 Dogs = 1.0 – 1.5 mg/kg in combination with 5.15 mg/kg of fentanyl I.V
  Horses 0.05 – 0.2 mg/kg I.V
 Cattle 0.5 – 1.1 mg/kg I.M
 Sheep & goats 0.5 – 1.1 mg/kg I.M
 Pigs 0.5 – 1.0 mg/kg I.M
 Chicken 5.5 – 11.0 mg/kg I.M

ZOLAZEPAM AND FLUMAZENIL

 Zolazepam
o It is marketed in combination with dissociative drugs like tiletamine (250 mgs of
tiletamine and250 mgs of zolazepam in lyophilized form). For dose calculation
the two drugs are considered as one product (500 mg).
o Dose
 Dogs 6.6 - 9.9 mg/kg I.M, 2.0 - 43 mg/kg I.V
 Cats 6.0 - 11.9 mg/kg.I.M.
 Flumazenil
o The actions of all benzodiazepines can be reversed or antagonized with
flumazenil at the dose of 0.1 mg/kg I.V.

ALPHA 2 ADRENERGIC AGONIST

 Alpha 2 adrenergic agonists are referred as sedative analgesics.

 The popular agents are xylazine hydrochloride, detomidine, meditomidine and
romifidine.

XYLAZINE HYDROCHLORIDE

 Xylazine is a sedative analgestic having alpha 2 adrenergic agonist activity.

 It produces dose-related depression of the central nervous system.
 The duration of analgesic activity is 15 – 30 minutes and the sedation is for 1-2 hours.
 Ruminants are more sensitive to xylazine. One tenth of the dose used in horses and dogs
induce sedation and recumbency in cattle.
 In horses it is a reliable sedative and the horse will be in standing position in clinical
doses. Drooping of head and buckling of hind limbs are commonly noticed in horses. The
clinical dose through intravenous route is 1.1 mg/kg. Further increase in the dose will not
increase the intensity of sedation, only the duration will be increased.
 Emesis is common in dogs and cats after xylazine injection due to the stimulation of
central emetic center.
 Produces muscle relaxation, which is attributed to decrease in intraneural and synaptic
transmission in the central nervous system.
 Xylazine is used in the treatment of equine colic for pain relief. But it must be used with
caution as it may mask the clinical signs and may aggravate ileus.
 Xylazine induce profound depression of cardiovascular system. Bradycardia, decreased
cardiac out put, hypotension and and increase in central venous pressure are noticed. It
also often produces A.V block. Intravenous administration causes a transient increase in
blood pressure. Administration of anticholinergies as premedicants reduce the incidence
of bradycardia and even the bradycardia that occurs after administration of xylazine can
be reversed with atropine (0.045 mg/kg initially and followed by 0.01 mg/kg
intravenously).
  It is contraindicated in branchycephalic breeds, older dogs and in intestinal obstruction.
 It increases the sensitivity of myocardium to the circulating catecholamines. Cardiac
dysrhythmias may occur if used along with halothane.
 In ruminants it reduces the gastrointestinal and ruminal motility with relaxation of
cardia oesophageal sphincter. This favors ruminal tympany and regurgitation.
 Xylazine has oxytocic property and increase the intrauterine pressure hence it may
induce abortion in pregnant animals. Increase in intrauterine pressure may cause
embryo/ovum ejection if administered in embryo/ovum transplantation.
 Thermoregulation is depressed following xylazine administration and the animal may
become hypothermic or hyperthermic depending on the ambient temperature.
 Xylazine is used as epidural anaesthetic because of the presence of alpha receptors in the
spinal cord and its structural similarity with lidocaine.
 Other effects
o Excessive urine production because of the suppression of antidiuretic hormone
o Salivation
o Hyperglycemia
 Dose
o Horse 1.1 mg/kg I.V/IM
o Dogs & cats 0.2 --- 1.1 mg/kg I.V/I.M/.S.C
o Cattle, sheep & goats
 0.05 – 0.08 mg/kg I.M. standing restraint
 0.1 – 0.3 mg/kg I.M. recumbency and prolonged
 0.1 – 0.2 mg/kg I.V recumbency
o Pigs
 1.0 – 2.0 mg/kg I.V
 Upto 4.0 mg/kg I.M.
o Epidural 0.07 – 0.17 mg/kg in 5.0 to 10.0 ml of saline

OTHER AGENTS

Detomidine

 Detomidine is a potent alpha 2-adrenaergic agonist mainly used in horses and cattle.
 Advantages of these drugs
o Does not stimulate pituitary adrenocortical adrenocortical axis hence stress is
less.
o Can be administered in pregnant animals
o Can be administered in animals which are not fasted
o It is very effective in relieving pain from colic in horses.
o Provides standing restrain in cattle at the dose of 10 to 20 µg/kg I.V
o Dose (not recommended in dogs cats and wild felines): Horse, Cattle, Sheep &
Goats 10 - 40 µg/kg I.V

Meditomidine

 It is a potent alpha 2 adrenergic agonist used in small animal anaesthesia. The other
properties are similar to xylazine.
 Dose
o Dogs 0.01 - 0.04 mg/kg I.V/I.M/S.C
o Cats 0.04 - 0.08 mg/kg I.V/I.M/S.C
 o Cattle 0.01 - 0.02 mg/kg I.V

Romifidine (Sedivet)

 It is developed from clonidine and has alpha 2 adrenergic agonistic action. Used in
horses and maximum sedation is achieved at the dose of 80 µg/kg I.V

SPECIFIC REVERSAL AGENTS

Alpha 2 antagonists

 Yohimbine hydrochloride
o It is a specific reversal agent for xylazine and detomidine.
o It is an alpha 2 adrenergic blocking agent used at the dose of 0.1 mg/kg I.V.
o It is often combined with 4-aminopyridine (0.04 mg/kg) for better results.
o Yohimbine is used in the treatment of equine colic due to ileus.
o It reverses the gastrointestinal stasis produced by xylazine.
 Atipamezole
o It is used to reverse the effects of meditomidine at the dose of 0.04 – 0.5 mg/kg
I.V.
 Doxapram
o It is not a specific reversal agent to alpha 2 adrenergic agonists but offer certain
beneficial effects due to its central nervous system stimulation and respiratory
stimulation.

CHLORAL HYDRATE

 Chloral hydrate is used as a reliable sedative hypnotic in cattle and horses.

 It is less expensive and still perfectly acceptable sedative agent.
 It has deeply penetrating aromatic odour and is bitter in taste.
 The central nervous system depression is due to its metabolic product namely 2,2,2
trichloro ethanol, hence the sedative effect is prolonged even after cessation of
administration.
 It does not have analgesic property.
 Trichloro ethanol conjucates with glucuronic acid to urochloralic acid and excreted.
 Chloral hydrate depresses the motor and sensory responses at sedative dose and
produces cerebral and medullary center depression at anaesthetic dose resulting in
muscle relaxation and depression of cardiac and respiratory system.
 In cattle it can be drenched preferably through stomach tube, at the dose of 30 to 120
grams dissolved as 1 in 20 solution in water.
 Bullls that are uncontrollable and free in the yard can be controlled by water deprivation
for brief period and allowing them to drink chloral hydrate dissolved water (90 to 120
grams in 12 litres of water).
 Chloral hydrate is administered as 10% solution intravenously in cattle at the dose of 80
to 90 mg/kg.
 Chloral hydrate is combined with magnesium sulphate at 2:1 or 3:1 ratio (weight) and
administered in cattle.
 It is combined with magnesium sulphate and pentobarbital and administered to horses
(Equithesin mixture).
 Intravenous dose of chloral hydrate in horses
o Chloral hydrate alone 5 to 10 mg/kg for mild sedation and hypnosis, 20 to 40
mg/kg for moderate sedation and hypnosis, 50 to 75 mg/kg for profound
sedation and hypnosis and 150 to 250 mg/kg for anaesthesia.
o Chloral hydrate 100 mg/kg and thiopentone 1.5 to 2 mg/kg
o Chloral hydrate 100 mg/kg and ketamine 1.5 to 2 mg/kg
o Promazine 0.6 to 0.8 mg/kg, 7% chloral hydrate 20 to 40 mg/kg and thiopentone
5 to 7 mg/kg
o Acepromazine 0.04 to 0.08 mg/kg, 7% chloral hydrate 20 to 40 mg/kg and
thiamylal 2 to 4 mg/kg.
o Xylazine 0.4 to 0.6 mg/kg, 7% chloral hydrate 20 to 40 mg/kg and thiamylal 1 to
2 mg/kg.
 Disadvantages of chloral hydrate
o Prolonged hangover with ataxia and stupor
o Perivascular administration causes pain, swelling and necrosis
o Induces abortion in mares

Opioids

Pure agonists
PURE AGONISTS - MORPHINE

 Morphine
o Morphine is derived from the dried milky exudates of the unripe seed
capsules of the opium poppy (Papaver somniferum).
o The exudates contains 3-25% of morphine, 5% noscapine and 0.8%
papaverine.
o The laboratory synthesis of morphine is different hence still it is derived from
opium poppy. The laboratory synthetic agents are codeine, heroin
(dimorphine = diacetylmorphine) and oxymorphine.
o Morphine acts and produces
 Analgesia
 Drowsiness
 Produce nausea and vomiting by stimulating chemoceptor trigger zone
for vomiting. It induces dopaminergic excitement in cats, horses, pigs,
dogs and cattle.
 Induce respiratory depression
 Depress cough
 The effects on myocardium are not significant; but produce increase in
vagal tone and slowing of heart.
 Morphine is used as a postoperative analgesic for pain relief in
veterinary practice.
 Morphine decreases motility of stomach with increase of antral
portion. Initial use may cause defecation and chronic use will result in
constipation.
  It is absorbed from the gut and oral mucosa.
 It is used in the treatment of congestive heart failure to relieve pain
and decrease after load.
 Preservative free morphine can be administered epidurally to relieve
pain.
 Dose
o Horses Morphine gives good results in horses if administered after xylazine
sedation. Xylazine 1.0 mg/kg I.V and morphine 0.6 mg/kg I.V
o Dogs 0.2 – 0.5 mg/kg ( total dose not exceeding 10 mg ) I.M/I.V
o Cats 0.05 – 0.1 mg/kg S.C/I.M. must be administered with caution because it
may induce CNS stimulation. Hence must be used with suitable tranquilizer.
o Morphine is administered after administration of Acepromazine.
Acepromazine 0.1 mg/kg I.M. and Morphine 0.6 mg/kg I.M.

PATHADINE, MEPERIDINE AND OXYMORPHONE

 Pathadine
o Pathadine is a vagolytic and negative inotropic drug at clinical doses.
o It reduces salivation and respiratory secretion without inducing vomiting and
defecation.
o Pathadine induces histamine release if administered through intravenous route.
o Dose
 Dogs = 2 - 6.5 mg/kg S.C/I.M
 Catls = 2 - 4.4 mg/kg S.C/I.M
 Meperidine
o It is a synthetic product, less potent (one tenth of morphine) and used in dogs
and cats.
o Intravenous administration causes release of histamine hence most often used
along with acepromazine. (Phenothiazines are potent antihistaminics)
o Dose: Dogs and Cats 2-5 mg/kg I.M
 Oxymorphone
o Oxymorphone is a synthetic derivative having 10 times greater potency than
morphine.
o It is widely used in dogs and cats for its analgesic property. Analgesia lasts for 4
hours.
o It does not cause histamine release as meperidine.
o It is used popularly in small animal anaesthesia due to its analgesic and lack of
release of histamine.
o The only limitation with drug is stimulation of vagus leading to bradyarrhythmias
and it can be reduced or prevented with the use of antichlinergic agents in the
protocol.
o It is also administered epiduraly to control pain in the hindquarters (0.025 - 0.05
mg/kg).
o Dose
 Dogs 0.05 - 0.2 mg/kg I.V/I.M/S.C (total dose not exceeding 4.5 mg)
 Cats 0.05 - 0.4 mg/kg I.V/I.M/S.C
 Horses 0.02 - 0.03 mg/kg I.V/I.M.

FENTANYL CITRATE AND ETORPHINE

Fentanyl citrate

 Fentanyl is a synthetic opioid product related to phenylpiperidines.

 Its analgesic property is 80 times greater than morphine.
 Cardiac out put, heart rate, respiratory rate and arterial oxygen tension (PaO2) are
reduced following administration of fentanyl.
 Fentanyl citrate is available alone, or in combination with droperidol (Innovar vet
contains 0.4 mg of fentanyl and 20 mg of droperidol per milliliter) or fluanisone.
(Hypnorm contains 0.315 mg of fentanyl and 10 mg of fluanisone per milliliter)
Fentanyl combinations provides good intra operative analgesia.
 In dogs and primates it produces sedation and myosis whereas in horses it produces
excitement and mydriasis. It is not recommended in cats.
 Dose - Dogs 0.01 - 0.02 mg/kg I.M/I.V. (see butyrophenones for other doses).
 The other synthetic pure agonists are afentanil, sufentanil, lofentanil and
carfentanil.

Etorphine

 Etorphine is a potent synthetic morphine derivative. Its general properties are

similar to morphine.
 The dose of etorphine is 0.5 mg/500 g B.W
 Etorphine is an extremely long acting agent whose effects are maintained by
enterohepatic recycling.
 The action of this drug can only be terminated by the administration of the specific
antagonist Diprenorphine.
 In clinical dose etorphine along may produce initial excitement hence it is marketed
in combination with phenothiazine derivatives. Separate combinations are available
for large and small animals. Each pack of the marketed drug will be having two
components. 1-Immobilon and 2-Revivon.
 Preparation
 Immobilon L A contains Etorphine 2.45 mg/ml and acepromazine 10 mg/ml
 Immobilon S A contains Etorphine 0.074 mg/ml and Methotrimeprazine 18 mg/ml
 Revivon L A contains Diprenorphine 3.0 mg/ml
 Revivon S A contains Diprenorphine 0.272 mg/ml
 This mixture is popularly used to capture elephants and giraffes
 Not recommended for domesticated and wild felines
 Etorphine is extremely potent in human and any accidental injection may cause
death if not treated with naloxone or diprenorphine.

Partial agonists
PENTAZOCAINE, BUTORPHENOL TARTRATE AND
BUPRENORPHINE

Pentazocaine

 It is used as an analgesic.
  In human it causes dysphoria and hallucination and pentazocaine is developed to
prevent drug abuse.
 In clinical doses it produces pulmonary vascular resistance.
 In horses it is used in the treatment of colic and administered at the rate of 0.33
mg/kg I.V.
 Dose -3 mg/kg for 1 to 3 hours of analgesia.
 Penlog -Duration of analgesia 3-4 hour .
 Onset 1 min – one hour

Butorphenol tartrate

 Butorphenol is used in horses, cats and dogs.

 It produces sedation, analgesia and increase in pulmonary vascular resistance.
 Dose
o Horse = 0.1 mg/kg I.V
o Dogs = 0.2 – 0.8 mg/kg I.M/S.C
o Cats = 0.2 – 0.4 mg/kg I.V/I.M/S.C
o Onset 1 mint – 15 mint I.V. rapid

Buprenorphine

 Respiratory depression is more and often treated with intermittent positive pressure
ventilation.
 Dose
o Horses = 6 - 10 µg/kg
o Dogs = 0.01 - 0.02 mg/kg S.C/I.M/I.V
o Cats = 0.005 - 0.02 mg/kg S.C/I.M

PURE ANTAGONISTS

 Naloxone hydrochloride, nalorphine hydrochloride and diprenoorphine are the opioid

pure antagonists used for the reversal of the effects of pure agonists and partial agonists.
 In horses naloxone is used in the control of crib biting.
o Dose
 Naloxone
 Dogs and cats = 0.04 - 0.1 mg/kg I.V/I.M/S.C
 Horses 0.005 = 0.2 mg/kg I.V
 Diprenorphine
 Dogs & Cats = 0.0272 mg/kg I.V
 Horse = 0.02 - 0.03 mg/kg I.V

MODULE-10: LOCAL ANALGESIA/ANAESTHESIA

Learning objectives

This module deals with

  Local anaesthetics
 Regional analgesia of limbs

INTRODUCTION

 Varieties of minor and major surgical procedures canbe accomplished in domestic

animals under local and regional anaesthesia, depending on the species, breed,
temperament of the animal, health status of the animal and magnitude of the
producedures.

LOCAL ANAESTHETICS

Cocaine

 It is an extract from the leaves of Erythroxylon coca.

 It is an irritant and toxic in small doses.
 The toxic manifestations include clonic convulsions, loss of consciousness and paralysis
of medullary centres.
 The maximum dose is 780 mg in horses, 120mg in large dogs, 45 mg in small dogs and 15
mg in cats.
 Cocaine was used as a doping agent in horses.
 The lethal dose is 15 mg/kg.
 Cocaine is withdrawn from the injectable forms due to its toxicity.
 Only topical preparations are available for eye(4% solution) and nasal and laryngeal
areas (10 to 20% solutions).

Procaine hydrochloride

 It is a short acting local anaesthetic derived from ester.

 It is detoxified in the blood and liver rapidly.
 The margin of safety is high in terms of convulsive dose (35 mg/kg in cats).
 In clinical practice it is administered intravenously to relieve pain in fire injured
patients.
 It is also used as adjunct to thiopentone sodium to maintain anaesthesia.
 Procaine is combined with adrenaline 1 in 100000 to potentiate its anaesthetic action.

Lidocaine hydrochloride

 It is a fast acting amide local anaesthetic detoxified in the liver.

 The convulsive dose is 15 mg/kg in cats.
 Goats are extremely sensitive to lignocaine. The total dose should never be exceeded 10
mg/kg in any route. The toxic manifestations in goats are excitation, tonic clonic
convulsions, opisthotonus, respiratory depression, cardiac arrest and death.
 Lignocaine is combined with general anaesthetics, which does not posses convulsive
properties as an ajunct (See injectable anaesthetics).
 It is often combined with thiopentone due to its dysrhythmic property and protective
action on myocardium.
  In clinical practice adrenaline free lignocaine is administered intravenously at the rate of
0.25 mg/kg in cats and 2 mg/kg in dogs to control cardiac arrhythmia due to myocardial
ischemia.
 The local anaesthetic preparationis marketed in combination with adrenaline 1 in
200000. It is also available as 2% jelly and 2.5% and 5% viscous ointments. The duration
of action is two hours.

Bupivacaine hydrochloride

 Bupivacaine is a fast and long acting amide derivative.

 Its margin of safety is less.
 The convulsive dose in cats is 3.4 to 5 mg/kg.
 Intravenous administration induces mdyocardial depression.
 Bupivacaine associated ventricular dysrhythmia are due to prolonged inhibition of
sedum conductance in the cardiac muscles.
 It is not combined with general anaesthetics.
 High molecular weight substance like dextran is added to prolong the durationof action
in obstetrical anaesthesia.

POTENTIATION OF LOCAL ANAESTHETICS

 Epinephrine/Adrenaline - 1 in 1000000 or 1 in 200000 is added to increase the

intensity and duration of action.
 Hyaluronidase - It increases the diffusion of local anaesthetics and favours quick onset
of action. It is added at the rate of 150 TRU (Turbidity reducing unit) Addition of
hyaluronidase will reduce the duration of action.
 Dextran - High molecular weight substance is added to reduce the rate of absorption and
increase the duration of action.

SURFACE ANALGESIA

 Surface anaesthesia includes topical analgesia of skin, eye and mucous membrane of
nose, mouth, penis,vulva, urethra and rectrum and intra – synovial analgesia.

TOPICAL ANALGESIA

 Ice, ethyl chloride spray, ether spray and carbonic acid snow are used to achieve
superficial analgesia of the skin.
 Absorbent cotton or gauze soaked in 4% procaine or 2% lignocaine is often used on
superficial aberrations of the skin and eczematous lesions to alleviate pain.
 Lignocaine 4% and proxymetacaine 5% (Ophthaine) are used as topical anaesthetics for
eye.
 Analgesia of mucous membrane is induced for examination, catheterization or
intubation.
 The commercial preparation containing lignocaine with carboxymethyl cellulose is
applied on mucous membrane.
 This preparation is also used to lubricate catheters and endotracheal tubes. Lignocaine
4% is sprayed on nasal or oral mucous membrane to achieve analgesia.
  In horses 60 ml of lignocaine 1% can be administered intra rectally to reduce the
discomfort during examination.

INTRA-SYNOVIAL ANALGESIA

 Intra-synovial analgesia is induced to relieve pain arising from the joint and tendon
sheath.
 Often it is used in the diagnosis of lameness in horses.
 Strict aseptic precautions muse bt adopted prior to injection.
 Inadvertent introduction of infection will be disastrous.
 If the needle is placed into the synovial cavity one can notice synovial fluid at the hub of
the needle.
 Some quantity of synovial fluid is aspirated before injection into a distended synovial
cavity.
 The intra-synovial injection techniques in horses are

Distal interphalangeal (coffin) joint

 Site - in the midline approximately one centimeter proximal to the coronary band with
the needle angled slightly steeply than at right angles to the skin.
 Needle and volume 19 G x1”, 5 - 8 ml.

Proximal interphalangeal (pastern) joint

 Site - Pastern joint is situated approximately 1 cm below an imaginary line through the
attachment of the collateral ligaments to the first phalanx.
 The joint is entered near the midpoint on the dorsal midline approximately 3 cm
proximal to the coronary band with the needle pointing obliquely downwards and
inwards.
 Needle and volume 20 Gx 1”, 5 - 8 ml

Metacarpophalangeal (fetlock) joint

 Site - The fetlock joint is entered in the triangular space formed by the third metacarpal
bone, the proximal sesamoid bone and the suspensory ligament. Can be performed with
the limb weight bearing.
 Needle and volume 20 G x 1”, 10 ml

Digital flexor tendor sheath

 Site - Usually performed onlyd in the presence of synovival distension. The site of
injection is the most prominent distended part of the sheath on the lateral aspect of the
digital flex or tendons just proximal to the fetlock.
 Needle and volume 20G x 1”, 10ml

Carpal joints
  Site - The two carpal joints into which inje3ction can be performed. (mid carpal joint and
antebranchiocarpal joint). The mid carpal joint opens with the proximal
(antebrachiocarpal joint) between the third and and fourth carpal bones hence does not
require separate injection. The joints can be entered on the dorsal aspect of the flexed
limb just lateral to the extensor carpiradialis tendon.
 Needle and volume 20G x 1”, 10 ml.

Elbow joint

 Site - The elbow joint can be entered either in front or behind its lateral ligament. To
enter in front of the ligament the needle is inserted just under themargin of the lateral
condyle of the humerus.
 Needle and volume 19G x 2”, 15 ml.

Shoulder joint

 Site - The shoulder joint is entered horizontally between the anterior and posterior part
of lateral tuberosity of the humerous.
 Needle and volume 19G x 3.5”, 20 ml

Tarsometatarsal joint

 Site - Over the head of the fourth metactarsal bone and fourth tarsal bone
 Needle and volume 20G x 1”, 5 ml

Stifle joint

 Site -This joint has three synovial sacs, one in the femoropatellararticulation and two,
one medial and one lateral in the femoro-tibial artibulation.
 Femoro-patellar sac can be entered on either side of the middle patellar ligament.
 Medial sac of the femoro-tibial articulation can be entered between the patellar ligament
and the medial femoro-tibhial ligament.
 Lateral sac of the femoro-tibial articulation can be entered behind the lateral patellar
ligament. Another route is between the lateral femoro-tibial ligament and the common
tendon of the long digital extensor and the peroneus tertius.
 Needle and volume 18G x 2”, 20 ml each sac.

Hip joint

 Site - Can be performed in standing horse. The needle is inserted between the anterior
and posterior parts of the trochantger major.
 Needle and volume 2 mm x 15 cm

INFILTRATION ANAESTHESIA

 In this procedure the nerve ending is desensitized at the actual site of operation.
 Depending on the duration one can use procaine, lignocaine or bupivacaine.
  This form of analgesia is useful in the treatment of wound, skin incision, extirpation of
superficial tumors.
 Following disinfection of the skin 0.5 to 1 ml of local anaesthetic is injected intradermally
before injecting into deeper tissues. This called as an intradermal skin wheal.
 Small circular wheals are created for catheterization of vessesl.
 A linear continuous wheal can be produced by the use of a longer needle with single prick
and it reduces the number of pricks in case of paravertibral nerve block.
 There are two types of infilteration anaesthesia
o Line block
o Field block

LINE BLOCK

 The needle is inserted parallel to the skin incision and for every 1 cm area of incision 1 ml
of the local anaesthetic solution is deposited.
 The needle is withdrawn gently as the solution is deposited.
 If the length of the incision is longer than the length of the needle the needle can be
inserted at the mid point of incision to preent multiple pricks.

FIELD BLOCK

Field block

 Making walls of desensitized areas enclosing the operation or incisional site.

Production of a cup

 A cup of desensitized area is produced by making fan wise injection.

Inveted “L” block

 Two lenior infiltration at right angle in the form of an inverted “L” desensitizes the flank
region in cattle.

Ring block

 Used in the extremities like limb for amputation of digit in cattle or in teat for teat
surgery. Infiltration is done proximal to the site of operation.

Inverted “V” block

 This is an another alternative method for ring block normally done in teat for the repair
of teat fistula.

Local anaesthesia of fracture

  Lignocaine is directly injected into the haematoma of fracture site with through aseptic
precautions to relieve pain and favours closed method of reduction.

REGIONAL INTRAVENOUS ANAESTHESIA

 This technique is used for amputation of limbs and digits.

 A tight tourniquet or blood pressure measuring cuff is placed proximal to the site of
operation to block venous drainage.
 Procaine or lignocaine is injected into the engorged superficial vein so as to facilitiate the
retrograde flow of blood and deposition and infiltration of local anaesthetic into the
tissues.
 Bupivaccaine is not normally used in this technique due to its myocardial effects.
 Analgesia lasts as long as the cuff or tourniquet is in place and maintains the pressure
above the systolic blood pressure.

INFRA ORBITAL NERVE BLOCK

Nerve

 Infra orbital nerve is the division of trigeminal nerve.

 It supplies sensory nerve to the first and second molar (PM 1 & 2), canine and incisors as
it passes the canal.
 After emerging from the canal it supplies sensory fibres to the upper lip, cheek, nostrils
and lower part of the face.

Site and technique

 The nerve can be blocked either as it passes the canal or after emerging from the canal
using a 19 G x 5 cm needle.
 The infra orbital foramen is located about one half the distance and 2.5 cm dorsal to a
line connecting the nasomaxillary notch and the rostral end of the facial crest in horse.
 In dogs the infra orbital foramen is situated in front of the anterior margin of the PM 4
where it can be palpated.
 Its better to have the tip of the needle slightly curved to enter into the canal, 0.5 to 2 ml
may be required in dogs and 10 ml in large animals.

Area desensitized

 The skin of the lip, face of the side upto the level of the foramen is desensitized if blocked
at the level of the foramen. If it is blocked in side the canal in addition to the above
structures PM 1 & 2, canine, and incisors with their alveoli and gum and the skin upto
the inner canthus of the eye.

MANDIBULAR NERVE BLOCK

Nerve
  Mandibular nerve is the alveolar branch of mandibular division of the 5 th cranial nerve. It
enters the mandibular foramen at the medial aspect of the vertical ramus of the
mandible. Then it passes through the mandibular canal and supplies sensory dental and
alveolar branches to the side. After emerging out it is called as mental nerve and it
supplies to the lower lip.

Site and technique

 The nerve can be blocked as it enters the mandibular foramen or as it emerges out from
the mental foramen.
 Mandibular block: The mandibular foramen is located opposite to the point of
intersection of a line passing vertically downwards from the lateral canthus of the eye
and another line extending backward from the tables of the mandibular teeth. The site is
selected medially 3 cm below the temperomandibular articulation on the posterior
boarder of the mandible. 4 to 6 ml of the solution is deposited using along spinal needle.
 Mental block: Mental foramen is easily located on the lateral aspect of the jaw below the
angle of the lip (in the middle of the interdental space) 3 to 5 ml of the solution is
deposited.

SUPRA ORBITAL NERVE BLOCK

Nerve

 Supra orbital nerve (frontal nerve) is a sensory terminal branch of the ophthalmic
division of 5th cranial nerve. It emerges from the orbit through the foramen accompanied
with the artery. It supplies sensory fibres to the upper lip andpartof the skin on the
forehead.

Site and technique

 The foramen is palpated as a pit like depression midway between the upper and lower
borders of the supra orbital process close to the frontal bone (about 6-cm dorsal to the
medial canthus) 5 ml of the solution is injected with 19G x 2.5 cm needle.
 Successful block desensitizes the upper eyelid and the frontal region. Dogs do not have
supra orbital foramen.
 The frontal nerve leaves the orbit medial to the ligament.

CORNUAL NERVE BLOCK

Cattle

 Cornual nerve is a branch of lacrimal (zygomaticotemporal) division of ophthalmic

division of trigeminal nerve.
 It supplies sensory fibres to the horn corium and the skin around the base of the horn.
 The nerve passes through theperiorbital tissues dorsally and then runs along the frontal
crest to the base of the horn.
Goats

 In goats the horn is supplied by the corneal branch of lacrimal (zygomaticotemporal)

nerve and corneal branch of infratrochlear nerve.
 The infratrochlear nerve emerges from the orbit dorsomedially.

SITE AND TECHNIQUE

Cattle

 As the nerve run from the orbit to the base of the horn it becomes more and more
superficial.
 The block is done more easily 2 to 3 cm below the base of the horn with 5 to 10 ml of 2%
lignocaine.
 In cattle with large horn a second injection is given about 1 cm behind the first to block
the posterior division of the nerve.

Goats

 The lacrimal branch can be blocked half way between the lateral canthus and the lateral
base of the horn.
 The infratrochlear branch can be blocked half way between the medial canthus and the
medial base of the horn.
 To amputate the horn at the base it is better to provide sedation, as this block will not
desensitize the perostium and sinus mucous membrane.

RETROBULBAR NERVE BLOCK

 Auriculopalpebral branch of the facial nerve - motor nerve (VII)

 Oculomotor (III), trochlear (IV), and abducens (VI) nerves – motor innervation to the
ocular muscles
 Maxillary branch of the trigeminal nerve (V) - sensory innervation to lower eyelid, soft
palate, the nasal cavity, maxilla maxillary sinus and adjoining bones and the region
supplied by the infraorbital nerve.
 Ophthalmic branch of the trigeminal nerve - sensory innervation to the upper eye lid,
third eyelid, medial canthus, caudal part of nasal septum, cornea and sclera and the
frontal sinus
 Optic nerve (II)
 For enucleation of eyeball all these nerves are blocked to achieve analgesia of the eye
and orbit and immobilization of the globe.

SITE AND TECHNIQUE

 All these nerves except the optic nerve pass through foramen orbital.
 Anaesthetic solution is deposited anterior to the foramen.
 The notch formed by the supraorbital process, zygomatic arch and the coronoid process
of the mandible is located and a 18G x 7 to 11 cm needle is inserted directed towards the
opposite side last upper premolar until it reaches the pterygopalatine fossa.
 Deposit 15 ml of the solution. An additional 10 to 15 ml can be deposited slightly
caudodorsally as the needle is withdrawn.
 This block does not provide desensitization of eyelids, hence for extirpation of eye ball in
addition to this the auriculopalpebral nerve block and infiltration of eyelids mut be
carried out.

PARAVERTIBRAL NERVE BLOCK

 This regional anaesthesia is very important for bovine laparotomy.

 The dorsal and ventral nerve roots of last thoracic (T13) and first and second lumbar (L 1
& 2) spinal nerves are blocked as they emerge from the intervertibral foramen.
 If analgesia of caudal paralumbar area is required additionally the third lumbar (L3) is
blocked which result in weakness of the hind limb.

SITE AND TECHNIQUE

 Each nerve is blocked immediately in front of the cranial border of the transverse
process of the succeeding lumbar vertebra.
 The last thoracic nerve is blocked half way between the last rib and the transverse
process of the first lumbar vertebra about 5 cm from mid line.
 The first and second lumbar nerves can be blocked at the posterior edge of the transverse
process of the corresponding vertebrae about 5 cm from the mid line.
 The needle pricks are made through the subcutaneous wheals, to penetrate the
intertransverse ligaments and 15 ml of local anaesthetic is deposited below the ligament
and another 5 ml above the ligament.
 Successful block shows analgesia of flank, paralysis of flank muscles, increase in the
temperature of flank, and scoliosis towards the desensitized side.
 In horses the block is performed on T 18, L1 and L2.

EPIDURAL ANALGESIA

 Epidural space is that compartment between the duramater and the bony and
ligamentous wall of the spinal canal.
 This space is filled with extradural fat, internal vertebral plexus of veins and the spinal
nerves.
 Injection of local anaesthetics will desensitize the nerves.
 Normally the site is preferred after the end of cona medularis of the spinal cord.

SITE OF INJECTION IN DIFFERENT SPECIES

o Bovine - Sacrococcygeal junction between I & II coccygeal vertebrae

o Equine - Between I & II coccygeal vertebrae
o Canine - Lumbosacral space
o Swine - Lumbosacral space
o Sheep and Goats - Lumbosacral space
 The terms high (anterior) and low (posterior) are often used to describe the level of
block.
 If the block extends the segment from where the sciatic nerves arises (second sacral and
more cranial segments) the block is termed as anterior epidural.
  The anterior epidural is achieved by increasing the volume of local anaesthetic injected.
 In high epidural or anterior epidural the animal will be recumbent and the motor
functions will be lost.

TECHNIQUE

Cattle and horse

 The exact position of the sacrococcygeal junction or the space between the first and
second coccygeal vertebrae cn be located by palpating the borders with simultaneous
pumping of the tail.
 3 ml of 2% lignocaine with epinephrine is injected incows for low epidural which will
induce paralysis of tail, and analgesia of perineum rectum, and the inner aspect of the
thigh.
 Higher dose upto 120 ml of 2% lignocaine is administered in adult cow to achieve high
epidural in which the cow will be recumbent for more than 4 hours.
 Sympathetic blockade and hypotension are common in high epidural.
 In horses low epidural is induced using 5 to 7 ml of 2% lignocaine.
 Analgesia of rectum tail, distal colon, bladder, and reproductive organs are produced.

Swine

 The site of needle placement is on the midline, just caudal to the transverse line between
the cranial prominences of the wing of the ilium on either side.
 A 20G x 8 cm needle is inserted caudal to this line at an angle of 20 caudal to the
perpendicular.
 Local anaesthetic is injected at the rate of 1 dml for every 10 kg. Hypotension and death
are more common in pigs following epidural analgesia.

Dogs

 The site of injection is lumbosacral space which is located in the middle just behind the
line joining the highest points of these crests.
 Some time the local anaesthetic is administered between sacrococcygeal or I and II
coccygeal vertebrae for docking.
 The compliation of epidural anaesthesia includes hypotension, respiratory collapse due
to the block on higher levels, clonic spasms, convulsions (goats are more sensitive),
pareses or paralyses due to infection and fistula formation.

INTERNAL PUDENTAL NERVE BLOCK

 This block is commonly done to induce relaxation and analgesia of penis to aid in
examination and treatment in cattle.
 The lesser sciatic foramen is located by rectal palpation as a circumscribed depression in
the sciatic ligament.
 The internal pudental nerve is found a finger width dorsal to the pulsating pudental
artery.
 The block is done bilaterally on both the sides.
 The ischorectal fossa is prepared aseptically and an 18G x 8 to 10 cm needle is inserted
and directed towards the nerve under rectal guidance 20 to 25 ml of local anaesthetic is
deposited and the process is repeated on the other side.
 Penile relation and cutaneous analgesia over the anus, perineum, posterior medial thigh
and urethral opening are achieved.

ANALGESIA FOR CASTRATION

 Analgesia can be provided by injecting local anaesthetic into the spermatic cord or
directly into the testicle. The incisional site must be infiltrated subcutaneously on the
scrotum.

Regional analgesia of limbs

BRANCHIAL PLEXUS BLOCK

 This block is mainly induced in dogs.

 Successful analgesia will show all the symptoms of radial paralysis.
 The brachial plexus in the dog is best blocked on its lateral recumbancy.
 First the costochondral junction of the first rib is located by moving the upper limb.
 An 8 to 10 cm long needle is inserted towards the costochondral junction.
 If the leg is held, as in the normal positionthe correct site of needle insertion will be
medial to the shoulder joint directed parallel to the vertebral column.
 After reaching the costochondral junction the needle is withdrawn 0.5 to 1 cm, then
aspirated to ascertain that no blood vessel is punctured.
 1 to 10 ml of 2%lignocaine is injected depending on the size of the dog.

MEDIAN AND ULNAR NERVE BLOCK

 Median and ulnar nerve block will desensitize the carpus and structure distal to it.
 Median nerve is blocked at the caudomedial borner of the radius just distal to the
superficial pectoral muscle.
 The nerve lies cranial to the median artery and vein. Skin desensitization involves only
the medial aspect of the pasern.
 Ulnar nerve is blocked in the groove on the palmar aspect of the antebrachium between
the ulnaris lateralis and the flexor carpi ulnaris muscles, 10 cm proximal to the accessory
carpal bone at a depth of 1 to 2 cm.
 Skin desensitization occurs on the dorsal aspect of the proximal metacarpus.
 Needle and volume 20G x 1”, 10 to 15 ml on each site.

TIBIAL AND PERONEAL NERVE BLOCK

  Tibial and peroneal nerve block will eliminate deep sensation from the hock and
structures distal to it.
 Tibial nerve is blocked just caudal to the deep digital flexor tendon and cranial to the
Achilles tendon about 10 cm proximal to the top of the tuber calcis on the medial aspect
of the limb beneath the fascia.
 Skin sensation is usually lost between the bulb of the heel.
 Peroneal nerve is blocked between the long and lateral digital extensor tendons on the
lateral aspect of the crust, 10 cm proximal to the lateral malleolus.
 The peroneal nerve has deep and superficial branches.
 10-ml of 2% lignocaine is injected around the deep branch and 5 ml around the
superficial branch as the needle is withdrawn.
 Needle and volume 19G x 2”, 20 ml on each site.

PALMAR/PLANTAR DIGITAL NERVE BLOCK

 The palmar/plantar nerve is desensitized in the palmar region of the pastern joint
medially and laterally.
 Palmar nerve is formed by the fusion of the terminal branch of ulnar nerve and the
terminal branch of median nerve
 Plantar nerve is the result of bifurcation of the tibial nerve.
 Needle and volume 20 to 25 G x 2.5 cm, 2 ml on each site.
 The area of desensitization includes pastern and one third of the hoof with portions of
navicular area.

MODULE-11: GENERAL ANAESTHESIA - INJECTABLE AGENTS

Learning objectives

This module deals with

 Introduction to injectable anaesthetics

 Routes of administration
 Advantages and disadvantages of injectable anaesthetics
 Classification of injectable anaesthetics

INTRODUCTION

 Injectable anaesthetics can be administered through various routes.

 The equipment required for administration of injectable anaesthetics is minimal.
 Following are the commonly used equipments
o Syringes
o Needles
o Butterfly needles
o Intravenous catheters.
 Two types of intravenous catheters are available; they are
 Through the needle catheters
 Over the needle catheters. Through the needle catheters are long
and used for long term administration of fluids. 12 to 16 gauge 5¼
 inch catheters are used in large animals and 18 to 22 gauge
catheters are used in small animals. (Refer Anaesthetic
equipment)
o Infusion controllers and Syringe devises (refer Anaesthetic Equipment).

ROUTES OF ADMINISTRATION

 Intravenous e.g. thiopentone in horses

 Intramuscular e.g. ketamine in dogs
 Intraperitonial e.g. thiopentone in cats
 Intrathoracic e.g. thiopentone in cats
 Intratesticular e.g. pentobarbitone in pigs for castration
 Subcutaneous e.g. droperidol – fentanyl in cats

ADVANTAGE AND DISADVANTAGE

Advantages

 Simple to administer
 Have rapid onset of action
 Useful as induction agents
 Does not irritate the airways
 Non explosive and inflammable
 Does not pollute the theatre
 Controls convulsions

Disadvantages

 May induce tissue damage if not injected through appropriate route (thiopentone if
administered perivascularly induce severe tissue reaction and accidental administration
of xylazine through carotid artery may cause fatal).
 Excess dose administered without calculating the dose or patient evaluation may cause
toxicity. It may not be possible to recover the patient without the use of specific
reversal/antagonistic agents, oxygen supplementation, intermittent positive pressure
ventilation and other life saving supports.

CLASSIFICATION OF INJECTABLE ANAESTHETICS

Main category Examples
Barbiturates  Thiobarbiturate e.g. thiopentone sodium, thiamylal
sodium
 Methylated oxybarbiturate e.g. methohexitone sodium
 Oxybarbiturate e.g. phentobarbital sodium

Dissociative anaesthetics  Ketamine hydrochloride

 Titatamine
  Phencylidine

Steroid anaesthetics  Combination of Alphaxalone and alphadolone e.g.

Saffan, Althesin

Imidazole derivatives  Etomidate

 Metomidate

Alkylphenols  Propofol

Opioid synthetic analgesics  Fentanyl citrate

 Alfentanil
 Sufentanil
 Lofentanil
 Etorphine

Neuroleptanaesthetic mixture  Droperidol and Fentanyl

 Fluanisone and Fentanyl
 Etorphine combinations

Centrally acting muscle  Glyceryl Quaiacolate

relaxants

Chloral hydrate -

Barbiturates
ULTRA SHORT ACTING

 The commonly used ultra short acting barbiturates are thiopentone sodium , thiamylol
sodium and methohexitone sodium.
o Thiopentone and thiamylal - thiobarbiturates
o Methohexitone - oxybarbiturate.
 These agents are strong alkalies (11 -12 pH) and the alkalinity is due to the addition of
sodium carbonate. Following administration, the blood buffers neutralize the sodium
carbonate. Thiopental and thiamylal are converted into acid form, which bind with the
plasma protein particularly with albumin fraction. The narcotic and anaesthetic action is
induced by the unbound fraction. These agents produce dose dependent action varyhing
from hypnosis to general anaesthesia.
 o Binding with protein depends on the drug concentration and the ptotein level.
Hence care must be taken in calculating the dose of thiopentone, thiamylal and
methohexitone for hypoprotinemic animals. Unbound fractions will be more and
may cause profound depression.
o These agents produce unconsciousness in 30 to 90 seconds as they cross the
blood-brain barrier in one arm-brain circulation. The duration of anaesthesia
varies from 5 to 15 minutes.
o The recovery from anaesthesia is not due to the detoxification, biotransformation
and elimination, it is due to distribution. From the blood it moves to the highly
vascularised tissues and from there slowly redistributed to less vascularised
tissues. Initially the concentration in the fat will be more. If fluids are
administered during recovery the redistributed fractions may be mobilized into
the circulation resulting in further deepening of anaesthesia. The distribution
depends on the speed and quantity injected. A small quantity injected rapidly as a
bolus will produce high plasma and brain concentration resulting in narcosis and
the recovery will be faster.
o The amount of thiopentone and thiamylal required to produce anaesthesia vary
from 10 to 18 mg/kg in small animals and 6 to 10 mg/kg in large animals.
Anaesthesia is induced by administering half of the calculated as a bolus followed
by slow incremental doses to abolish pedal reflex. Thiopentone and thiamylal are
administered as 1 to 5% solutions in dogs and cats and 5 to 10% solutions in
horses and cattle.
o Methohexitone is administered as 1% solution in small animals and as 6% in
large animals. The dose is 3 to 5 mg/kg intravenously.

CARDIOVASCULAR AND RESPIRATORY EFFECTS

 Cardiovascular effects
o Barbiturates are potent cardiovascular depressants.
o They increase the heart rate and peripheral resistance with reduction in cardiac
out put and increasein central venous pressure.
o These actions are due to the reflex action secondary to the stimulation of
baroreceptors and chemoreceptors and myocardial hypoxia.
o Myocardial hypoxia may result in cardiac arrhythmia, bigeminy, premature
ventricular contraction and depression/elevation/slurring of S-T segment.
o Administration of oxygen will prevent further manifestations.
o Lidocaine can be administered to control ventricular arrhythmia and it can act as
a useful adjunct if incorporated in the anaesthetic regimen.
o It prevents and corrects ventricular arrhythmia and reduce the requirement of
barbiturates. Separate syringes must be used for administration to prevent the
formation of precipitation.
 Respiratory effects
o Ultrashort acting barbiturates induce severe respiratory depression even at
clinical doses.
o Rapid administration results in apnea during induction.
o The changes are reduction in respiratory volume, tidal and minute volume. If
respiratory arrest is noticed it must be managed with oxygen supplementation
and mechnical ventilation.
 o Artificial respiration by compressing the chest and stimulation of respiratory
reflex may help to over come apnea but may not be as effective as oxygen
supplementation.
o Thiopentone protects the ischemic brain hence used in patients with brain injury
and in cardiopulmonary bypass anaesthesia. Thiopentone is used as an induction
agent in patients suffering from epilepsy.
o These agents are metabolized in the liver and to a less extend in kidney, brain and
in other tissues. They are eliminated as alcohols, ketones, phenols and carboxylic
acids through urine. Microsomal enzymes of the liver get elevated following
administration of barbiturates.
o These agents do not cause prolonged decrease in gastrointestinal motility. They
produce sufficient muscle relaxation required for minor surgery.
o Barbiturates readily cross the placental barrier and depress fetus. However the
amount of thiopentone transferred is not large enough to be detrimental to the
neonate at birth.

CONCURRENT USE OF OTHER DRUGS AND BENEFITS

 Antichlolinergics
o Anticholinergics are administered to reduce salivation and prevent bradycardia.
In horses anticholinergics can be administered if they are fasted for 6 to 8 hours.
o Atropine sulphate - Dogs & Cats = 0.044 mg/kg S.C/I.M, 0.022 mg/kg I.V
o Glycopyrorolate - Dogs & Cats = 0.011 mg/kg I.M.
 Tranquilizers
o Tranquilizers are administered to reduce the anxiety and the dose of the
anaesthetic drugs
o Triflupromazine - Dogs & Cats = 1.0 mg/kg I.V
o Acepromazine - Dogs & Cats = 0.1 - 0.2 mg/kg I.M., Horses = 0.06 - 0.1 mg/kg
I.V/I.M.
o Chlorpromazine - Dogs & Cats = 1.1 - 2.2 mg/kg I.V/I.M.
o Xylazine
 Dogs = 0.22 - 1.1 mg/kg I.V, 0.55—2.2 mg/kg I.M.
 Cats = 0.5 - 1.1 mg/kg I.M.
 Horses = 0.5 - 1.0 mg/kg I.V
 Cattle 0.1 – 0.2 mg/kg I.V (combine anticholinergics)
o Diazepam - Dogs & Cats 0.04 mg/kg I.V
 Neuraleptanalgesics
o Not safe to combine with barbiturates as the combined effects will be extreme
bradycardia, hypotension and cardiac arrest.
 Narcotics
o Narcotics markedly reduce the dose of barbiturates.
o Morphine - Dogs 0.11 – 0.66 mg/kg S.C, Cats not recommended
o Methadone - Dogs 0.11 – 0.55 mg/kg I.M/I.V, Cats not recommended
o Oxymorphine - Dogs 0.22 mg/kg I.V/I.M/S.C, Cats 0.88 --- 3.3 mg total dose
I.V/I.M/S.C
o Pentozocaine - Dogs & Cats 2.2 – 3.3 mg/kg I.M./S.C
o Innovar vet - Dogs 1 ml/7 to 9 kg I.M. , Cats not recommended
 Muscle relaxants
o In large animals centrally acting muscle relaxant glyceryl quaiacolate
(Guaifenisin) is combined with barbiturates. 2 to 3 grams of thiopentone is added
to 50 grams of glyceryl guaiacolate and 5% solution of glyceryl quaiacolate is
 prepared using 5% dextrose solution. Anaesthesia can be induced by the
intravenous administration of the solution at the rate of 1 to 2 ml/kg in horses.
o In dogs succinyl choline, pancuronium, gallamine and other products can be
combined with barbiturates. Oxygen administration and intermittent positive
pressure ventilation are essential to maintain respiratory and cardiovascular
functions.
 Procaine and lidocaine
o Procaine hydrochloride and lidocaine hydrochloride can be combined with
thiopentone and thiamylol. They should not be mixed in the same syringe
because the local anaesthetics are acidic and barbiturates are alkaline. Every time
the needle or the catheter must be flushed with normal saline before
administration of each agent.
o Advantages
 Analgesia, Reduce the dose of barbiturates to 50% , Protects the
myocardium and brain from ischemic changes, Act as antidysrhythmic
agents and Provide good muscle relaxation.

LONG ACTING BARBITURATES

 Pentobarbital sodium is the long acting barbiturate used in anaesthesia and is marketed
in vials containing 50 mg/ml and 65 mg/ml. Use of pentobarbital is restricted to small
animal and swine anaeshesia. The standard solution is diluted and given intravenously.
 Dose - Dogs & cats 20 - 30 mg/kg without premedication 10 - 20 mg/kg with
premedication. For continuous infusion an initial loading dose of 2 - 5 mg/kg is given
followed by 1 - 2 mg/kg/hr.
 A special preparation containing 240 mg/ml of pentobarbital is available and is used for
euthanasia of animals. For euthanasia it is administered at the rate of 48 mg/kg (1
ml/5kg). This solution is often used to castrate large boars. The solution is administered
deep into both the testicles at a dose not exceeding 24 mg/kg. Castration is performed
immediately after reaching light stage of anaesthesia by ligation of the cord and
emasculation. The testicles must be disposed carefully otherwise dogs may get access
and die due to poisoning.

DISSOCIATIVE ANAESTHETICS

 Ketamine hydrochloride and tilatamine are the commonly used dissociative anesthetics
in veterinary field.
 Phencyclidine is another cyclohexamine product withdrawn from use because of drug
abuse.
 The dissociative anaesthesia is characterized by
o Profound amnesia, superficial analgesia and catalepsy
o Involuntary spontaneous movements
o Persistence of reflexes like swallowing, pharyngeal palpebral and corneal
o Large dose may induce convulsions
o Lack of muscle relaxation

KETAMINE
 Ketamine is a popular anaestheic used in veterinary and human anaesthesia due to its
wide margin of safety and compatibility with other agents.
 It was first synthezied in 1963 and introduced in human anaesthesia in 1965 and in
veterinary anaesthesia in 1970.
 Ketamine alters the central nervous system activity to sensory impulses without blocking
it at spinal cord or brain stem levels.
 It allows the impulses to reach the cortical receiving areas but not perceived because of
the depression and dissociation of limbic system and other cortical association areas.
 It can cause seizures even in patients not known to be epileptic and may occur even after
24 hours administrations.
 The depression effects of ketamine are determined in the central nucleus of thalamus,
neocorticothalamic axis and nociceptive cells in the medial medullary reticular
formation.
 Cardiovascular effects - Ketamine increases heart rate, cardiac out put, peripheral
vascular resistance, systemic and pulmonary blood pressure, cardiac contractility and
myocardial oxygen consumption. The cardiovascular stimulation is attributed to
o Stimulation of sympathetic discharge
o Vagolytic activity and
o Negative inotropic effects on heart.
 Respiratory effects - The effect of ketamine on respiratory functions are increase in
respiratory rate with or without decrease in tidal volume. Also the partial arterial carbon
dioxide level (PaO2) will increase with reduction in partial arterial oxygen level (PaCo2).
 Muscle relaxation will be poor hence must be used with other drugs which produce
muscle relaxation.
 It induces copious salivation and lacrimation. Salivation can be controlled by the prior
administration of anticholinergics.
 Ketamine is metabolized in the liver and certain amount is excreted as unchanged
through urine.
 Decreases total RBC counts due to the sequestration of RBCs in the spleen
 Classical stress leukogram; leukocytosis with lymphopenia and neutrophilia can be
observed following ketamine administration.
 Induces hyperglycaemia
 Contraindicated in patients with increased intracranial pressure or in patients who are
undergoing brain or spinal cord surgery as it increases the cerebrospinal fluid flow and
pressure.
 Not recommended for intraocular surgery as it increases the blood pressure and
intraocular pressure.
 Ketamine maintains the uterine blood flow hence can be a useful alternative for
thiopentone in cardio vascular
 The aims of combining ketamine with other agents are to achieve
o Muscle relaxation
o Eliminate side effects like salivation and recovery delirium.
o Improve visceral analgesia and
o Prolong the period of anaesthesia

DOSE RATE OF KETAMINE

 Cats
o In cats the dose of ketamine is 10 - 30 mg/kg I.M. If it is combined with
narcotics, tranquilizers or sedatives the dose can be reduced to 5 - 15 mg/kg I.M.
and 2- 5 mg/kg I.V.
 o The standard protocols are
 Xylazine 1.0 mg/kg I.M. and Ketamine 20 --- 25 mg/kg I.M.
 Acepromazine 0.1 mg/kg I.M. and Ketamine 20 --- 25 mg/kg I.M.
 Midazolam 0.2 mg/kg I.M. and Ketamine 10 mg/kg I.M
 Midazolam 0.2 mg/kg I.V and Ketamine 5 mg/kg I.V
 Meditomidine 80 µg/kg I.M. and Ketamine 2.5 – 7.5 mg/kg I.M.
 Meditomidine 40 µg/kg I.V and Ketamine 1.25 mg/kg I.V
 Butorphenol 0.4 mg/kg I.M, Meditomidine 40 µg/kg I.M. and
Ketamine 5 mg/kg I.M.
 Butorphenol 0.1 mg/kg I.V. Meditomidine 40 µg/kg I.M. and
Ketamine 1.25 mg/kg I.V
 Dogs
o Xylazine 1 - 2 mg/kg I.M (lower dose in larger dogs) and Ketamine 10 mg/kg
IM/IV
o Diazepam 0.2 - 5 mg/kg I.V and Ketamine 5 mg/kg I.V
o Meditomidine 40 µg/kg I.M. and Ketamine 5- 7.5 mg/kg I.M.
o Butorphenol 0.1 mg/kg I.M, Meditomidine 25 µg/kg I.M. and Ketamine 5 mg/kg
I.M. 15 minutes later.
 Horses
o Xylazine 1.1 mg/kg I.V and 4 to 5 minutes after Ketamine 2.2 mg/kg I.V. To
prolong the anaesthesia half of the initial dose of both the drugs must be repeated
at every 10 to 20 minutes. Diazepam at the rate of 0.22 mg/kg I.V can be
combined to reduce muscle fasciculation. Often glyceryl quaiacolate is combined
with xylazine and ketamine at the rate of 50 mg/kg I.V and even administered as
mixture to maintain anaesthesia and this mixture gives good muscle relaxation.
 Detomidine 20 µg/kg I.V and Ketamine 2.2 mg/kg I.V
 Promazine 1.0 mg/kg and Ketamine 1.5 – 2.0 mg/kg I.V
 Acepromazine 0.05 – 09.10 mg/kg and Ketamine 2.2 mg/kg I.V
 Cattle
o Xylazine 0.1 mg/kg and Ketamine 2 - 5 mg/kg I.V
o Detomidine 20 µg/kg and Ketamine 2 - 5 mg/kg I.V
 Sheep and Goats
o Xylazine 0.04 - 0.06 mg/kg and Ketamine 2.2 - 4.4 mg/hg I.V
o Detomidine 40 µg/kg and Ketamine 2.2 - 4.4 mg/kg I.V
 Pigs
o Xylazine 2 mg/kg, Oxymorphone 0.075 mg/kg and Ketamine 2 mg/kg I.V
o Acepromazine 0.4 mg/kg and after 30 minutes Ketamine 15 mg/kg I.M.
o Acepromazine 0.44mg/kg, Xylazine 2.2mg/kg and Ketamine 1230 mg/kg I.M
o (Further maintenance is done with a mixture containing 0.5 to 1 ml of xylazine
(100mg/ml) and 1 ml of ketamine (100mg/ml).

TILATAMINE

 Tilatamine is closely related to ketamine and is two to three times potent than ketamine.
 It induces muscle rigidity and tonic-clonic convulsions if administered alone hence it is
marketed in combination with a benzodiazepine Zolazepam.
 (Telozol in USA and Zoletil in Australia) It contains 250 mgs of tilatamine and 250 mgs
of zolazepam. This combination provides muscle relaxation and a dissociative state of
anaesthesia in dogs, cats and wild animals. Its use in horses may result in potential
severe reactions. Premedication with xylazine minimizes the adverse reactions in horses.
 Animals anaesthetized with telozol – zolazepam will respond to palpebral, laryngeal,
pharyngeal, pedal and pinnal reflexes. Salivation is more marked and can be controlled
by the use of anticholinergic premedication. Anticolinergic premedicationis very
important while using this combination
 Dossage
o Cat @ 7 - 15 mg/kg I.M; 5 - 10 mg/kg I.V
o Dog @ 10 - 15mg/kg I.M; 5 - 7 mg/kg I.V
o Horses
o Xylazine 0.5 - 1.0 mg/kg
o Tilatamine zolazepam 0.5 - 1.0 mg/.kg I.V

STEROID ANAESTHETIC

 Combination of alphaxalone and alphadolone is marketed as Saffan (in veterinary) and

Althesin (in human).
 Alphaxalone is insoluble in water and can be dissolved in Cremophor EL
(polyoxyethylated caster oil).
 Alphadolone is another steroid which has hypnotic property and increase the solubility
of alphaxalone in cremophor.
 Each milliliter of Saffan contains 9 mgs of alphaxalone and 3 mgs of alphadolone. This
preparation is viscid and the pH is around 7.
 Saffan froths in syringes due to the presence of cremophor EL and is miscible with water.
 Low solubility of these steroids in water made them less popular.
 Saffan is used in cats.
 In dogs it induces histamine release and causes severe hypotension hence not
recommended in dogs.
 It selectively decreases cerebral oxygen consumption to a greater extend by reducing the
blood flow. Indicated in cats with head injuries.
 Retching, vomiting and twitching of facial muscles may occur during induction.
 In cats it does not induce significant change in cardiac index and systemic vascular
resistance.
 It induces respiratory depression.
 It poduces good muscle relaxation.
 It can be used in cats for caesarian section because the neonates are less depressed at the
dose of 4.0 mg/kg. Some trials have been conducted on dogs for caesarian section. All
the dogs were given prior anti histaminic medication and premedicated with
phenothiazines.
 It may cause oedema of ear pinnae and paws in cats due to histamine release.
 It has got week antioestrogenic effect
 It may induce laryngeal oedema
 In horses it produce excitement for upto 30 minutes during induction and recovery is
associated with marked tactile and hyperaesthesia, twitching and violent kicking. It is
not recommended in horses.
 Dose
o Cats 4 - 6 mg/kg I.M/I.V
o Pigs 4 - 6 mg/kg I.V
o Pig neonates 2 - 3 mg/kg I.V
o Sheep 1.65 - 3 mg/kg I.V

IMIDAZOLE DERIVATIVES
Metomidate

 Metomidate is a non-barbiturate crystalline power belonging to imidazole group.

 In room temperaturethedissolved solution is stable only 24 hours.
 Metomidate has hypnotic and central muscle relaxant property, but does not have
analgesic property hence oftencombined with fentanyl or azaperone premedication.
 It is mainly used in pigs and birds.
 In horses it was used with azaperone (0.2 – 0.8 mg/kg) at the rate of 3.5 mg/kg I.V.
Recovery was violent. It is not recommended in horses.
 Dose
 Birds 3 - 20 mg/kg I.M

Etomidate

 Etomidate is a white crystalline power available as 20 mg dissolved in 10 ml of a mixture

containing 35% propylene glycol and 65% water (v/v).
 Intravenous injection is associatred with high incidence of spontaneous movements,
involuntary muscle tremors and hypertonus.
 Premedication with fentanyl or diazepam reduces the side effects.
 It induces less cardiovascular depression and does not release histamine. Hence it is
used in dogs for caesarian section at the dose of 1.5 - 3.0 mg/kg I.V along with diazepam
(0.2 mg/kg I.V total dose not exceeding 5 mg).
 Etomidate is recommended in high risk allergic patients who had exhibited or are
expected to exhibit severe anaphylactic responses.
 Etomidate like thiobarbiturates decrease the circulating cortisol concentration in
hyperadrenocortism, hence can be used as safe induction agent in these patients.

ALKYLPHENOLS

 Propofol is a lipophilic alkylphenol (2-6 diisoprophylphenol) becoming popular in

human and veterinary anaesthesia.
 It is an oil at room temperature and can not be injected hence was formulated with
Cremaphor EL (polyoxyethylated casteroil) as vehicle.Cremaphor EL as with other
agents induced histamine release in human and animals. Now the vehicle is changed and
reformulated with a parental nutritional agent called as Intralipid which contains
soybean oil, glycerol and purified egg phosphatide.
 The new formulation is milky in colour. The vehicle added favors bacterial growth hence
the open ampule after 6 to 12 hours must be discarded.
 Propofol induce rapid loss of unconsciousness in 20 to 40 seconds after I.V.
administration due to its lipophilic nature.
 It crosses the blood-brain barrier in one arm-brain circulation and further redistributed
from plasma, brain and well-perfused tissues to less perfused tissues as thiopentone.
 Recovery periods are shorter without any undesirable side effects in propofol anaesthesia
half of the calculated dose in infused as a bolus and the remaining half is administered in
a slow phase.
 Propofol can be administered in continuous infusion to maintain anaesthesia.
 It is conjugated in the liver and metabolized as glucuronide and sulphate and excreted in
urine.
 Cardiovascular effects - Propofol induce 20 to 40% reduction in arterial blood pressure
due to reduction in cardiac output and systemic vascular resistance. Its use is cautioned
in dogs with serious volume depletion.
 Respiratory effects - Propofol induce apnea and greater respiratory depression.
 Propofol does not affect hepatic and renal functions
 It can be used for long term sedation and anaesthesia in intensive care patients, as it
does not alter adrenocortical function.
 It reduces the intraocular pressure hence can be used in patients undergoing intraocular
procedures
 Propofol is a good induction agent for caesarian section in dogs and cats. It reported that
the puppies were bright and the mother was alert enough to care the puppies
immediately following recovery.
 It is a safe anaesthetic in branchycephalic breeds of dogs.
 Dose
o Dogs
 3 - 4 mg/kg I.V. in premedicated,
 5 - 6.5 mg/kg I.V. in Unpremedicated (continuous infusion 0.4 – 0.6
mg/kg/minute)
o Cats
 8 mg/kg I.V. inunpremedicated (continuous infusion 0.51 mg/kg/minute)
o Horses
 2.0 mg/kg with xylazine 0.5 mg/kg I.V.(continuous infusion 0.2
mg/kg/minute)
o Sheep and goats = 3 - 4 mg/kg I.V
o Rabbit = 7.5 - 15 mg/kg I.V
o Mouse = 26 mg/kg I.V
o Birds = 1-15 mg/kg I.V
o Reptiles = 10 mg/kg

Opioids

PURE AGONISTS - MORPHINE

 Morphine is derived from the dried milky exudates of the unripe seed capsules of the
opium poppy (Papaver somniferum).
 The exudates contains 3-25% of morphine, 5% noscapine and 0.8% papaverine.
 The laboratory synthesis of morphine is different hence still it is derived from opium
poppy. The laboratory synthetic agents are codeine, heroin (dimorphine =
diacetylmorphine) and oxymorphine.
 Morphine acts and produces
o Analgesia
o Drowsiness
o Produce nausea and vomiting by stimulating chemoceptor trigger zone for
vomiting. It induces dopaminergic excitement in cats, horses, pigs, dogs and
cattle.
 o Induce respiratory depression
o Depress cough
o The effects on myocardium are not significant; but produce increase in vagal tone
and slowing of heart.
o Morphine is used as a postoperative analgesic for pain relief in veterinary
practice.
o Morphine decreases motility of stomach with increase of antral portion. Initial
use may cause defecation and chronic use will result in constipation.
o It is absorbed from the gut and oral mucosa.
o It is used in the treatment of congestive heart failure to relieve pain and decrease
after load.
o Preservative free morphine can be administered epidurally to relieve pain.
 Dose
o Horses Morphine gives good results in horses if administered after xylazine
sedation. Xylazine 1.0 mg/kg I.V and morphine 0.6 mg/kg I.V
o Dogs 0.2 – 0.5 mg/kg (total dose not exceeding 10 mg) I.M/I.V
o Cats 0.05 – 0.1 mg/kg S.C/I.M. must be administered with caution because it
may induce CNS stimulation. Hence must be used with suitable tranquilizer.
o Morphine is administered after administration of Acepromazine. Acepromazine
0.1 mg/kg I.M. and Morphine 0.6 mg/kg I.M.

PATHADINE, MEPERIDINE AND OXYMORPHONE

 Pathadine
o Pathadine is a vagolytic and negative inotropic drug at clinical doses.
o It reduces salivation and respiratory secretion without inducing vomiting and
defecation.
o Pathadine induces histamine release if administered through intravenous route.
o Dose
 Dogs = 2 - 6.5 mg/kg S.C/I.M
 Catls = 2 - 4.4 mg/kg S.C/I.M
 Meperidine
o It is a synthetic product, less potent (one tenth of morphine) and used in dogs
and cats.
o Intravenous administration causes release of histamine hence most often used
along with acepromazine. (Phenothiazines are potent antihistaminics)
o Dose: Dogs and Cats 2-5 mg/kg I.M
 Oxymorphone
o Oxymorphone is a synthetic derivative having 10 times greater potency than
morphine.
o It is widely used in dogs and cats for its analgesic property. Analgesia lasts for 4
hours.
o It does not cause histamine release as meperidine.
o It is used popularly in small animal anaesthesia due to its analgesic and lack of
release of histamine.
o The only limitation with drug is stimulation of vagus leading to bradyarrhythmias
and it can be reduced or prevented with the use of antichlinergic agents in the
protocol.
o It is also administered epiduraly to control pain in the hindquarters (0.025 - 0.05
mg/kg).
o Dose
  Dogs 0.05 - 0.2 mg/kg I.V/I.M/S.C (total dose not exceeding 4.5 mg)
 Cats 0.05 - 0.4 mg/kg I.V/I.M/S.C
 Horses 0.02 - 0.03 mg/kg I.V/I.M.

FENTANYL CITRATE AND ETORPHINE

Fentanyl citrate

 Fentanyl is a synthetic opioid product related to phenylpiperidines.

 Its analgesic property is 80 times greater than morphine.
 Cardiac out put, heart rate, respiratory rate and arterial oxygen tension (PaO2) are
reduced following administration of fentanyl.
 Fentanyl citrate is available alone, or in combination with droperidol (Innovar vet
contains 0.4 mg of fentanyl and 20 mg of droperidol per milliliter) or fluanisone.
(Hypnorm contains 0.315 mg of fentanyl and 10 mg of fluanisone per milliliter) Fentanyl
combinations provides good intra operative analgesia.
 In dogs and primates it produces sedation and myosis whereas in horses it produces
excitement and mydriasis. It is not recommended in cats.
 Dose - Dogs 0.01 - 0.02 mg/kg I.M/I.V. (see butyrophenones for other doses).
 The other synthetic pure agonists are afentanil, sufentanil, lofentanil and carfentanil.

Etorphine

 Etorphine is a potent synthetic morphine derivative. Its general properties are similar to
morphine.
 The dose of etorphine is 0.5 mg/500 g B.W
 Etorphine is an extremely long acting agent whose effects are maintained by
enterohepatic recycling.
 The action of this drug can only be terminated by the administration of the specific
antagonist Diprenorphine.
 In clinical dose etorphine along may produce initial excitement hence it is marketed in
combination with phenothiazine derivatives. Separate combinations are available for
large and small animals. Each pack of the marketed drug will be having two components.
1-Immobilon and 2-Revivon.

Preparation

 Immobilon L A contains Etorphine 2.45 mg/ml and acepromazine 10 mg/ml

 Immobilon S A contains Etorphine 0.074 mg/ml and Methotrimeprazine 18 mg/ml
 Revivon L A contains Diprenorphine 3.0 mg/ml
 Revivon S A contains Diprenorphine 0.272 mg/ml
 This mixture is popularly used to capture elephants and giraffes
 Not recommended for domesticated and wild felines
 Etorphine is extremely potent in human and any accidental injection may cause death if
not treated with naloxone or diprenorphine.

PENTAZOCAINE, BUTORPHENOL TARTRATE AND

BUPRENORPHINE
 Pentazocaine
o It is used as an analgesic.
o In human it causes dysphoria and hallucination and pentazocaine is developed to
prevent drug abuse.
o In clinical doses it produces pulmonary vascular resistance.
o In horses it is used in the treatment of colic and administered at the rate of 0.33
mg/kg I.V.
o Dose -3 mg/kg for 1 to 3 hours of analgesia.
o Penlog -Duration of analgesia 3-4 hour .Onset 1 min – one hour
 Butorphenol tartrate
o Butorphenol is used in horses, cats and dogs.
o It produces sedation, analgesia and increase in pulmonary vascular resistance.
o Dose
 Horse = 0.1 mg/kg I.V
 Dogs = 0.2 – 0.8 mg/kg I.M/S.C
 Cats = 0.2 – 0.4 mg/kg I.V/I.M/S.C
 Onset 1 mint – 15 mint I.V. rapid
 Buprenorphine
o Respiratory depression is more and often treated with intermittent positive
pressure ventilation.
o Dose
 Horses = 6 - 10 µg/kg
 Dogs = 0.01 - 0.02 mg/kg S.C/I.M/I.V
 Cats = 0.005 - 0.02 mg/kg S.C/I.M

PURE ANTAGONISTS

 Naloxone hydrochloride, nalorphine hydrochloride and diprenoorphine are the opioid

pure antagonists used for the reversal of the effects of pure agonists and partial agonists.
 In horses naloxone is used in the control of crib biting.
 Dose
o Naloxone
 Dogs and cats = 0.04 - 0.1 mg/kg I.V/I.M/S.C
 Horses 0.005 = 0.2 mg/kg I.V
o Diprenorphine
 Dogs & Cats = 0.0272 mg/kg I.V
 Horse = 0.02 - 0.03 mg/kg I.V

CENTRALLY ACTING MUSCLE RELAXANTS (guaifenisin)

 Glyceryl quaiacolate ether (Guaifenisin) is the centrally acting muscle relaxant and it acts
on the internuncial neurons of the spinal cord.
 It affects the polysynaptic reflexes more than monosynaptic reflexes hence it has got
little action on the diaphragm.
 It does not influence the respiratory centers in brain. Diaphragmatic muscle is composed
of mainly striated titanic fibers and not striated tonic fibers; hence GGE does not affect
the diaphragm.
 It also induces sedation and hypnosis due to its action on the reticular formation of the
brain stem.
  It has got bactericidal action. In practice, it is administered as 5% (50 mg/ml) solution in
5% dextrose.
 Concentration greater than 10% is irritant to body tissues and caninduce heamolysis.
GGE dissolves readily in 5% dextrose if warmed slightly.
 GGE is used in combination with other agents in 5% dextrose solution as induction and
maintenance agent. These mixtures are administered after routine premedication.
 The maximum dose of GGE is 90 to 100 mg/kg and if this dose is exceeded it will cause
spasm, hypertonicity of muscles and cardiac arrest.
 GGE does not cross the placental barrier due to its high molecular weight.

Horses

 GGE 50 mg/ml (5% solution) in 5% dextrose mixed with xylazine 0.5 mg/ml and
ketamine 1.0 mg/ml is the routinely used mixture in horses.
 Induction is achieved at the dose rate of 1.1 ml/kg and further maintenance is done with
this mixture at the rate of 2.75 ml/kg/hour. Alternatively induction can be done using
xylazine (1.1 mg/kg I.V) and ketamine (2.2 mg/kgIV) andfurther maintenance can be
done with this mixture.
 GGE can be combined with thiopentone or thiamylal (1-3 grams) and administered in
horses (See barbiturates)

Cattle

 GGE 50 mg/ml (5% solution) in 5% dextrose mixed with xylazine 0.05 mg/ml and
ketamine 1.0 mg/ml is the mixture used in cattle. 1.0 ml/kg I.V is administered for
induction and further maintenance can be done with this mixture.

CHLORAL HYDRATE

 Chloral hydrate is used as a reliable sedative hypnotic in cattle and horses.

 It is less expensive and still perfectly acceptable sedative agent.
 It has deeply penetrating aromatic odour and is bitter in taste.
 The central nervous system depression is due to its metabolic product namely 2,2,2
trichloro ethanol, hence the sedative effect is prolonged even after cessation of
administration.
 It does not have analgesic property.
 Trichloro ethanol conjucates with glucuronic acid to urochloralic acid and excreted.
 Chloral hydrate depresses the motor and sensory responses at sedative dose and
produces cerebral and medullary center depression at anaesthetic dose resulting in
muscle relaxation and depression of cardiac and respiratory system.
 In cattle it can be drenched preferably through stomach tube, at the dose of 30 to 120
grams dissolved as 1 in 20 solution in water.
 Bullls that are uncontrollable and free in the yard can be controlled by water deprivation
for brief period and allowing them to drink chloral hydrate dissolved water (90 to 120
grams in 12 litres of water).
 Chloral hydrate is administered as 10% solution intravenously in cattle at the dose of 80
to 90 mg/kg.
 Chloral hydrate is combined with magnesium sulphate at 2:1 or 3:1 ratio (weight) and
administered in cattle.
  It is combined with magnesium sulphate and pentobarbital and administered to horses
(Equithesin mixture).
 Intravenous dose of chloral hydrate in horses
o Chloral hydrate alone 5 to 10 mg/kg for mild sedation and hypnosis, 20 to 40
mg/kg for moderate sedation and hypnosis, 50 to 75 mg/kg for profound
sedation and hypnosis and 150 to 250 mg/kg for anaesthesia.
o Chloral hydrate 100 mg/kg and thiopentone 1.5 to 2 mg/kg
o Chloral hydrate 100 mg/kg and ketamine 1.5 to 2 mg/kg
o Promazine 0.6 to 0.8 mg/kg, 7% chloral hydrate 20 to 40 mg/kg and thiopentone
5 to 7 mg/kg
o Acepromazine 0.04 to 0.08 mg/kg, 7% chloral hydrate 20 to 40 mg/kg and
thiamylal 2 to 4 mg/kg.
o Xylazine 0.4 to 0.6 mg/kg, 7% chloral hydrate 20 to 40 mg/kg and thiamylal 1 to
2 mg/kg.
 Disadvantages of chloral hydrate
o Prolonged hangover with ataxia and stupor
o Perivascular administration causes pain, swelling and necrosis
o Induces abortion in mares

MODULE-12: GENERAL ANAESTHESIA - INHALANT

ANAESTHETIC AGENTS AND MAINTENANCE

Learning objectives

This module deals with

 Inhalant Anaesthetic Agents and

 Its Maintenance

INTRODUCTION

 The inhalant anaesthetics are chloroform, ether, trilene, cyclopropane, enflurane,

desflurane, halothane, isoflurane and sevaflurane.
 Their uptake and distribution determine the anaesthetic action of these inhalant agents.
 The uptake and distribution depends on
 Solubility coefficient - At any given temperature the mass of a gas dissolved in a solution
(i.e. its concentration in the solution) varies directly with its tension and is governed by
the solubility of the gas in the particular solvent. For example the blood gas partition
coefficient of nitrous oxide is 0.47. This means that there will be 47 parts of nitrous oxide
inblood for every 100 parts of nitrous oxide per unit volume (litre) of alveolar air. The
solubility of most of the inhalant agents in brain and other tissues except fat are almost
common as that of blood. That means the tissue – blood partition coefficient will be
almost the same. Whereas halothane is almost 60 times more soluble in fat than other
tissues; hence the blood partial coefficient will be lesser than the fat. Brain – lipid (fat)
coefficient will be almost equal (2.6) because of the lipid nature of brain.
 Blood flow - The inhaled anaesthetic gas is diluted in the residual air when it enters
pulmonary ventilation and then distributed to alveolar membrane. From alveolar
membrane two types of diffusion take place. The major diffusion process takes place into
the pulmonary blood (pulmonary circulation) and it reaches equilibrium with alveolar
tension immediately. The second process occurs across the capillary membrane of the
lung into the interstitial fluid, then to the cells through the cell membrane and finally
into the venous blood leaving the lung (bronchial circulation). In thismanner the arterial
and venous tension of the anaesthetic slowly increases towards the ventual equilibrium
with the inspired air.
 Solubility of inhalant anaesthetic is defined as a concentration distribution ratio between
alveolar concentration and the tissue concentration. The solubility of inhalant
anaesthetics influences the induction and recovery time. Methoxyflurane is highly
soluble than isoflurane in the body tissues hence the induction and recovery will be slow.
 Mininimum alveolar concentration (MAC) - MAC is the concentration of the inhalant
anaesthetic in the alveoli to produce lack of response in 50% of the subjects to a standard
stimulus. This term is used to mention the potency of the anaesthetic. The MAC of each
inhalant anaesthetic varies in each species.
 The other factors are
o Physical and chemical properties of the agent
o Absorption
o Pulmoanry blood flow
o Cardia output perfusion
o Lipid content of tissues
o Final elimiantion

NITROUS OXIDE

 Nitrous oxide is the oldest anaesthetic gas available as liquid at room temperature in
cylinders (See anaesthetic equipment).
 Its MAC is more than 100% in animals (Dogs 188%, Cats 255%).
 It has got good analgesic property and combining narcotics, which interact selectively
with opiate receptor endorphin system, potentiates the analgesia.
 Nitrous oxide is used as the principle anaesthetic at a level of 80% in combination with
20% oxygen for dental extraction in human. In veterinary anaesthesia, it is combined
with other injectable and inhalant agents.
 It is used as fresh gas source or carrier gas. It helps in additional uptake of the inhalant
agent and potentiate the desirable effects at a minimal concentration of the inhalant
agent (Second gas effect).
 It is eliminated rapidly from the body because of low partition coefficient and relatively
insoluble nature.
 Nitrous oxide moves rapidly through tissues faster than carbon dioxide and diffuses into
the closed cavities filled with gas such as pneumothorax and distended intestinal loops
due to obstruction or strangulation and induces detrimental effects by inducing further
distension.
 It is not used in ruminants, as it will diffuse into the rumen and results in distension and
increase in transdiaphragmatic pressure. In horses prolonged administration induce
distension of bowels and increase in transdiaphragmatic pressure.
 It induces tachypnoea at higher concentration due to direct central stimulation.
 During recovery it may induce diffusion hypoxia following prolonged administration.
The outward movement of nitrous oxide from the alveoli reduce the alveolar partial
pressure of oxygen. The expired air may contain more than 10% of nitrous oxde. In older
 animals and animals maintained for a longer duration with nitrous oxide must be
supplemented with oxygen.
 Prolonged exposure to nitrous oxide causes bone marrow depression due to depletion of
Vit.B12. Hence it can cause occupational hazards to humans. The theatre environment
must have less than 25 ppm of nitrous oxide.
 Nitrous oxide is administered at 66 to 70% of the total inspired air. Oxygen is given at
30% concentration.

DIETHYL ETHER

 It is a colourless, highly volatile and inflammable liquid with a boiling point 35oC.
 One pound of ether mixed in air can given 277 cubic feet of flammable mixture. The
ignition temperature is 304 C.
 The MAC is 1.92%.
 It gives an irritating vapour and may cause salivation if not premedicated with
anticholinergics.
 In low concentration the vagal activity is decreased and at higher concentration it induce
arrhythmia.
 Catecholamine level increases following ether administration.
 The use of ether is decreased due to its explosive and inflammable nature.
 Health hazards are more in human exposed to ether for a prolonged period.

METHOXYFLURANE

 Methoxyflurane is a halogen-substituted ethyl ether (O2,2-dichloro-1,1 difluoro ethyl

methyl ether).
 Its boiling point is 104oC and is non-flammable and nonexplosive. Its molecular weight is
165.9 and the specific gravity is 1.41 at 25oC.
 It has fruity odour and an antioxidant butylated hydroxyflurane is added for stability.
 This antioxidant may accumulate in the vaporizer wick hence methoxyflurane vaporizer
must be often cleaned and rinsed with diethyl ether.
 The MAC is 0.23.
 It reacts with metal, rubber and soda lime, and decomposes if exposed to ultraviolet
light.
 Methoxyflurane induce dose dependent central nervous system depression. Though it
can be used to mask induction, its better to induce with injectable anaesthetics.
 It does not alter the cardiac function much except slight hypotension, which is associated
with reduction in cardiac contractility, and cardiac out put.
 Concurrent use of epinephrine and adrenaline are contraindicated as methoxyflurane
sensitizes the myocardium to the actions of catecholamines.
 Compared to halothane the sensitization and cardiac arrhythmia are less.
 Methoxyflurane reduce the minute volume and induces respiratory acidosis.
 It is highly soluble in fat hence recovery will be prolonged in obese patients.
 Biotransformation of methoxyflurane results in fluoride ions, which are potent toxic
agents to kidneys and is further aggravated by the concurrent use of tetracycline.
Methoxyflurane is contraindicated in patients with renal disease.
 In veterinary practice its use is restricted to small animals.
 It can be used in most of the breathing circuits with oxygen and nitrous oxide.

HALOTHANE
 Halothane is colourless volatile liquid with aboiling point of 50.2oC and the vapour
pressure is 244.1 mmHg at 20oC.
 It is non-flammable and nonexplosive.
 Halothane is a potent anaesthetic with a molecular weight of 197.4 and specific gravity
1.86 at 25oC.
 Halothane reacts with metal and soda lime and decomposes if exposed to ultra violet
light.
 It is marketed in amphor coloured bottles with thymol.
 The MAC varies in various species.
o Dogs 0.87%,
o Cats 0.75%,
o Horses 0.9%
o Pigs 1.25%
 The MAC is reduced when combined with agents like morphine (reduced 84%),
alfentanil (48%), xylazine and nitrous oxide.
 Halothane reduces cerebrospinal fluid production and pressure hence can be used in
patients undergoing brain and spinal cord surgeries and in patients with increased
intracranial pressure.
 It suppress adrenal cortical hormone release by 50% due to its action and inhibition on
the carrier - mediated transport system of choline.
 Halothane depress cardiac out put,mean arterial pressure and coronary blood flow.
 Halothane decreases arrhythmogenic thresholds and sensitizes the myocardium for the
actions of catecholamines. Exogenous administration of epinephrine or adrenaline
induces cardiac arrhythmia and ventricular stand still.
 It induces AV shunts (arterio-venous shunts) and is further aggrevated by hypoxia. (21 to
22%) thus resulting in ventilation perfusion mismatch. Oxygen exchange is further
reduced in patients with pulmonary diseases.
 The minute volume decreases during halothane anaesthesia due to the decreased
contractility of inspiratory muscles.
 Halothane induces hepatic hypoxia. In ponics following halothane anaesthesia 138%
increase in plasma bilirubin excretion, 16% reduction in plasma bilirubin and 46%
reduction in biliary bile acid concentration was noticed. Centrilobular necrosis is the
toxic manifestation induced by halothane in liver. The incidencesof hepatic necrosis are
higher in goats following halothane anaesthesia.
 Halothane undergoes biotransformation in the liver. The metabolic products or the
intermediary products induce allergic and toxic responses similar to autoimmune
diseases. The metabolic intermediary products bind with the bivalent genes responsible
for self-protein synthesis in the liver. Following binding the genes will alter the coding
and non-self protein will be synthesized which may result in allergy, anaphylaxis or
autoimmune like diseases.
 Experimental studies revealed that halothane has got teratogenic and mutogenic
properties. In human the rate of successful deliveries following embryo transfer or
gamete intra fallopian transfer were less as compared with isoflurane. Initial conception
rate was high followed by higher incidence of aborption.
 Halothane suppress the number and activity of natural killer cells (NK cells) and produce
immune suppression, thus favouring higher incidences of post anaesthetic infection.
This property is taken as an advantage in patients undergoing tissue transplantation. It’s
better to revaccinate horses with tetanus toxoid following halothane exposure.

ISOFLURANE
 Isoflurane is the new inhalant anaesthetic widely used in human anaesthesia.
 It is relatively insoluble hence induction and recovery are quick.
 It is non-inflammable and does not react with metal, rubber or soda lime.
 It does not decomposed if exposed to ultra violet light.
 Its vapour pressure is almost equal to halothane hence halothane vaporizers can be used
after cleaning thymol. It has got pungent odour.
 It provides cardiac stability. Reduction in blood pressure is noticed during isoflurane
anaesthesia due to the reduction in peripheral vascular resistance, not due to myocardial
depression as in halothane. It increase the myocardial perfusion by reducing the
coronary vascular resistance. It has little or no action on sensitizing the myocardium for
the actions of catecholamines. Hence it is recommended in patients with cardiac
diseases.
 It does not interfere with of central autoregulation of blood pressure, hence indicated in
patients with head injures.
 It has better muscle relaxation property than halothane and does not promote
convulsions.
 It induces more respiratory depression than halothane and results in hypoventilation.
 Only 2% are metabolized in the liver due to its relative insolubility, hence recommended
in patients with liver diseases.

SEOFLURANE

 It is the newest inhalant anaesthetic used in humans. Still trials are conducted in
veterinary anaesthesia.

PROPERTIES OF INHALANT ANAESTHETICS

Property Halothane Isoflurane Sevoflurane
Formula CBrCIH-CF3 CF3-CHCl-O-CF2H CFH2-O-(CF3)2
Type Halogenated Ether Ether
Molecular weight 197.4 184.5 187.0
Sp.gr. 1.86 1.50
Preservative Thymal Not required Not required
Reaction
Soda lime Yes No Yes
U.V. Light Yes No
Metal Yes No No
Boiling point C@ 760 mm Hg 50.2 48.5
-Vaplour pressure (mm hg) 243, 32% 239, 31%
 MAC OF COMMONLY USED INHALANTS
Agent Dogs Cats Horses
Halothane 0.86 0.98 0.88
Enflurane 2.2 2.37 2.12
Isoflurane 1.28 1.63 1.31
Methoxyflurane 0.23 0.23 -
Nitrous oxide 188.0 255.0 -

MODULE-13: MONITORING ANAESTHESIA

Learning objectives

This module deals with

 Pre operative patient monitoring

 History
 Physical and Clinical Examination
 Functions of CNS, Cardio vascular, Pulmonary during anaesthesia monitoring

INTRODUCTION

 Pre, intra and post operative monitoring are most important for the final out come of
anaesthesia and surgery.
 The monitoring procedures are aimed to assess the functions of cardiovalscular,
pulmonary and CNS and body temperature, fluid and electrolyte balances.
 Intraoperative monitoring must be carefully done because during this stage the
anaesthetic drug will act on various compensatory mechanisms and surgery will be
having its effects on physiology and anatomy of the patient (See Table - 1 and Table -
2 for parameters).

TABLE 1

 Normal physiological, cardiovascular, respiratory and hematobiochemical parameters of

domestic animals (Dog, cat, horse and cattle)

Parameters Dogs Cats Horses Cattle

Rect. Temp 0C 37.5 - 39.2 37.8 - 39.2 37 - 38 38 - 39
Heart rate/min 70 - 110 115 - 200 35 - 60 70 - 120
Cardiac output ml/kg 100 - 200 120 30 - 45 80 - 240
Blood vol.ml/kg 75 - 90 47 - 66 65 - 70 60 - 100
Blood pressure mm of Hg
Systolic 120 - 140 120 - 140 90 - 130 120 - 150
Diastolic 80 - 100 80 - 100 65 - 85 75 - 100
Mean 100 - 110 100 - 110 85 - 120 90 - 120
Resp. rate/min 10 - 30 24 - 42 8 - 20 15 - 35
Tidal volume ml/kg
Minute volume ml/dkg/min 170 - 350 200 - 350 150 - 600
PaO2 mm Hg >100 >100 85 - 90 80 - 110
PaCO2 mm Hg 28 - 49 35 - 49 38 - 40 30 - 50
pH 7.27 - 7.46 7.25 - 7.43 7.40 - 7.45 7.34 - 7.45
HCO3 mmol/lit 20 - 25 17 - 22 24 - 32 20 - 28
Hb g/dl 14 - 17.5 8 - 15 11 - 19 8 - 16
RBC x 10 cu.mm 10 7
WBC x 10 cu.mm 9 - 13 10 - 15 5.5 - 12.5 7 - 10
N% 65 - 70 55 - 60 50 - 60 25 - 30
L% 20 - 25 30 - 35 30 - 40 60 - 65
E% 2-5 2-5 2-5 2-5
M% 5 5 5-6 5
B% <1 <1 <1 <1
PCV % 40 - 55 25 - 45 32 - 52 24 - 46
ESR mm/hr 1-5 7 - 27 2 - 12 2-4
T.S. Protein g/dl 6 - 7.8 6 - 7.5 6 - 8.5 6.7 - 7.5
Albumin g/L 26 - 37 30 - 35.5
Globulin g/L 26.4 - 40.4 30 - 34.8
Fibrinogen mg/ml 200 - 400 50 - 30 400 300 - 700
Blood glucose mg/ml 65 - 118 70 - 110 75 - 115 45 - 75
BUN mg/ml 10 - 28 20 - 30 10 - 25 25 - 30
Creatinine mg/ml 0.44 - 1.32 0.7 - 1.59 1.0 - 2.4 0.84 - 1.77
Total cholesterol mmol/l 3.5 - 6.99 2.46 - 3.37 1.94 - 3.89 2.07 - 3.11
 ALT (GPT) IU/L 21 - 102 6 - 83 3 - 23 14 - 30
AST (GOT) IU/L 23 - 66 26 - 43 226 - 366 78 - 132
Lactate dehydrogenase IU/L 45 - 233 63 - 273 100 - 412 692 - 445
Creatinine kinase IU/L 14 - 460 100 - 850 97 - 188 150 - 450
Sorbitol dehydrogenase IU/L 4 - 20 6 - 30
Sodium mEq/L 130 - 143
Chloride mEq/L 98 - 109
Potassium mmol/L 4.37 - 5.35 4 - 4.5 2.2 - 4.1 3.9 - 5.8
Calcium mg/L 10.3 - 13.3
Icterus index,unit 2-5 2-5 5 - 20 5 - 15
Bile acids umol/L 0-5 0-5 5 - 28 20 - 80
Bilirubin mmol/L (total) 1.71 - 8.55 2.57 - 8.55 7.1 - 34.2 0.17 - 8.55
Cortisol nmol/L 27 - 188 9 - 71 36 - 81 17 +/-2

TABLE 2

 Normal physiological, cardiovascular, respiratory and haematobiochemical parameters

of domestic animals (Sheep, goat and pig)

Parameters sheep goat pig

Rec. temperature 37 - 40 38 - 40 38 - 40
Heart rate/min 70 - 130 70 - 130 60 - 200
Cardiac output ml/kg 110 - 160 60 - 230 66 - 184
Blood vol. ml/kg 55 - 70 55 - 90 50 - 100
Blood pressure mm Hg
Systolic 80 - 120 80 - 120 80 - 120
Diastolic 60 - 80 60 - 80 60 - 80
Mean 80 - 110 90 - 120 75 - 100
Resp.rate/min 15 - 40 15 - 25 10 - 45
Tidal vol.ml/kg 7-8 7-8 11
Minute vol.ml/kg/min 100 - 133 300 - 400
PaO2 mm Hg 75 - 100 85 - 95 75 - 80
PaCO2 mm Hg 30 - 40 33 - 38 30 - 40
Ph 7.43 - 7.53 7.42 - 7.48 7.38 - 7.50
Bicarboante mmol/L 21 - 28 24 - 27
Hb g/dl 8 - 16 8 - 14 10 - 16
RBC x / cumm 11 7
WBC x /cu.mm 7 - 10 8 - 12 15 - 122
N% 25 - 30 35 - 40 30 - 35
L% 60 - 65 50 - 55 55 - 60
M% 5 5 5-6
E% 2-5 2-5 2-5
B% <1 <1 <1
PCV % 30 - 46 20 - 38 32 - 50
T.S. Protein g/dl 6-8 6.5 - 7.5 6.7 - 7.5
Albumin g/L 24 - 30 27 - 39 79 - 89
Globulin g/L 35 - 57 27 - 49 52 - 64
Fibrinogen mg/ml 100 - 500 100 - 400 100 - 500
Blood glucose mg/dl 50 - 80 50 - 75 85 - 150
BUN mg/dl 8 - 20 10 - 20 10 - 30
Creatinine mg/ml 1.6 - 1.68 0.884 - 1.59 1.41 - 1.50
T.cholesterol mg/dl 1.35 - 1.97 2.07 - 3.37 0.93 - 1.40
ALT (GPT) IU/L 24 - 83 31 - 58
AST (GOT) IU/L 167 - 513 32 - 84
Lactate dehydrogenase IU/L 238 - 440 123 - 392 380 - 634
Potassium mmol/L 3.9 - 5.4 3.5 - 6.7 4.4 - 6.7
Icterus index (unit) 2-5 2-5 2-5
Total Bilirubin mmol/I 1.71 - 8.55 0 - .71 0 - 1.71
Cortisol nmol/L 62+/-10 65+/-8 82+/-3

PRE OPERATIVE PATIENT MONITORING

  Preoperative assessment of the patient is done for the safe administration and
maintenance of anaesthesia.
 It will help in tailoring a suitable anaesthetic regimen suitable for the patient.
 The importance of preoperative assessment
o To prepare the patient for safe administration of anaesthesia
o To assess the cardiovascular, pulmonary, hepatic, renal functions and haemato
biochemical and electrolyte balances (eg. In diabetic patients half of the insulin
dose is administered after stabilization).

HISTORY

Identification

 Identification includes the details of species, breed, sex, age and other identification
marks.

Main complaint

 The main complaint is detected to find out whether the disease condition will interfere
with the normal anaesthetic practice and to tailor suitable anaesthetic regimen.

History of the present illness

 Details of the duration of illness, clinical signs and severity of illness are collected.

Previous medical history

 This includes the collection of detils regarding the previous illness, medication,
vaccination, deworming, anaesthetics administered, poisoning, application of
cetoparasiticide etc., (e.g thiopentone is used as induction agent in patients with the
history of epilepsy, horse that suffered from myocarditis will be an anaesthetic risk
patient.

PHYSICAL AND CLINICAL EXAMINATION

 Physically examination includes general body condition, palpatin, percussion,

auscultation, measurement of heart, pulse and respiratory rates, examination of lymph
nodes, rectal temperature, appearance of the mucous membrane, reflex status,
integument, location of the lesion and weight of the animal.
 Weight calculation
o Horse = (Heart girth cm- 63.7)/0.38 = body weight in Kg.

Systemic examination

 Systemic examination includes the assessment of cardiovascular, pulmonary, hepatic,

renal gastrointestinal, central nervous system, endocrine and musculoskeletal functions.
Presurgical laboratory examination

 It includes the determination of a complete blood count and total plasma protein.

Further tests

 Includes ECG, X-rays and other special examinations.

INDIRECT MONITORING

 Indirect monitoring of CNS function is assessed by the reflex status. The reflex status is
modified by the stages of anaesthesia, drugs used and cerebral blood flow.
 The following reflexes are assessed
o Pedal reflex
o Palpebral reflex
o Corneal refle
o Lacrimation
o Yawning
o Swallowing reflex
o Laryngeal reflex
o Anal reflex
o Pupillary reflex
o Eyeball position
o Hearing sense

CNS Function
PEDAL REFLEX

 This reflex is elicited by applying firm pressure on the interdigital skin in dogs and cats,
squeezing the claws to gather in cattle and swains and firm pressure on the pastern on
horses.
 This relfex is abolished in stage III anaesthesia.
 Pedal reflex is reliable in barbiturate anaesthesia to assess the depth of anaesthesia,
where as with halogenated inhalants it disappears even in the light plane of anaesthesia.

PALPEBRAL REFLEX

 Tapping the skin at the medial canthus or running the finger along the eyelashes
stimulates this reflex.
 It is abolished in the light plane of anaesthesia in dogs where as in horses sluggish
response can be noticed even at surgical plane of anaesthesia when inhalants are used.
 Palpebral reflex is not abolished during ketamine anaesthesia

CORNEAL REFLEX
  This reflex is stimulated by gentle palpation of the cornes on the lateral aspect.
 The response is observed by the closure of eyelids.
 In horses absence of corneal reflex indicates deep plane of anaesthesia, in dogs its not
reliable and in cattleit may be abolished by repeated stimulation.
 Corneal reflex is not abolished during ketamine anaesthesia.

LACRIMATION AND YAWNING

Lacrimation

 In horses and cattle lacrimation is reduced during deep plane of anaesthesia, leading to
drying of cornea. It may result in keratitis and ulceration. Sterile mineral oil or plain eye
ointment must be instilled to prevent corneal ulcer.

Yawning

 Dogs under light plane of anaesthesia yawn when the mouth is opened.

SWALLOWING AND LARYNGEAL REFLEX

Swallowing reflex

 This reflex disappears at the light plane of anaesthesia with exception of young foals.
This reflex is protected in ketamine anaesthesia.

Laryngeal reflex

 This reflex is abolished in the light plane anaesthesia except with ketamine induction. In
cats local anaesthetic is sprayed on the larynx to prevent laryngeal spasm before
intubation.

ANAL REFLEX

 This reflex is abolished in the middle of III stage of anaesthesia in dogs and cats.
 In horses it is abolished soon after induction with ketamine.
 This reflex is elicited by sudden gentle manipulation of the anus and the response will be
sphincter contraction.

PUPILLARY REFLEX

 In general the pupil in unpremedicated animals will dialate during early excitement
phase and then constricts progressively upto surgical anaesthesia.
 Again the pulil will dialate as the animal enters into the IV stage of anaesthesia
(progressive medullary paralysis) followed by respiratory and cardiac arrest.
 Premedicants alter the papillary reflex.
 E.g. Atropine induces pupillary dialatation and narcotics induce constriction in dogs.
 EYEBALL POSITION

 The position of eyeball depends on the species and the anaesthetic used.
 In small animals the eyeball rotates medially and ventrally in the early stages and then
centrally placed at plane I surgical anaesthesia when inhalants like halothane or
isoflurance is used.
 In horses under halothane anaesthesia nystagmus is common during light plane of
anaesthesia and it is centrally placed at the surgical plane of anaesthesia.
 In ruminants the eyeball rotates ventrally in light plane of anaesthesia, then gradually
rotates dorsally and finally fix to the central position.

OTHER REFLEXES

Muscle relaxation

 It will be modified with the use of anaesthetics and muscle relaxants.

 In small animals the jaw tone is used as the criteria of muscle relaxation and anaesthetic
dept.

Hearing sense

 It is the last sense to disappear during induction and the first sense to reappear during
recovery.

ELECTROENCEPHALOGRAPH

 The normal EEG pattern is low voltage high frequency activity in the activated state of
brain.
 During cerebral hypoxia, hypoglycemia, hypothermia, hyponatremia and at excessive
depth of anaesthesia it becomes high voltage and low frequency.
 Then it become isoelectric (burst suppression) as the condition worsened and finally
becomes complete inactive.
 Intracranial pressure also provides valuable information regarding the cardiovascular
and pulmonary system and underlying disease.

Cardio vascular function

HEART RATE

 Heart rate can be monitored by using stethoscope, electronic stethoscope, oesophageal

stethoscope, electronic heart rate meters, elecrocardiography and Doppler blood flow
detector.
 Heart rates below 50 to 60 bpm in dogs and cats, 25 bpm in horses and ruminants is
considered to be low heart rate.
  Heart rate above 250bpm in dogs, 300 bpm in cats, 75 bpm in horses and ruminants are
considered as high heart rate.
 The alteration in heart rate must be simultaneously compared with cardiac output and
blood pressure.

BRADYCARDIA

 Bradycardia may arise due to

o Excessive depth of anaesthesia
o Excessive vagal tone (often increased by intubation vasovagal reflex and traction
of abdominal organs)
o Terminal hypoxia
o Endogenous and exogenous toxaemias
o Conduction disturbances in myocardium
o Hyperkalaemia
o Hypothyroidism

Treatment

o Administration of atropine or glycopyrrolate.

o Dopamine 2.5 to 20ug/kg/min (40 to 200 mg in 250 to 500 ml of 5% dextrose or
saline )I.V.
o Dobutamine 2.5 to 20 ug/kg/min (20 to 200 mg in 250 to 500 ml of 5% dextrose
or saline)I.V.
o Mephenteramine 0.1 to 0.75 mg/kg I.V. duration 15 to 30 minutes
o Ephedrine 0.05 to 0.5 mg/kg I.V. duration 15 to 30 minutes.
o Isoproterenol 5 to 10 ug/kg/min (0.4 ti 1.0 mg in 250 to 500 ml of 5% dextrose or
saline )I.V.

TACHYCARDIA

 Tachycardia m ay arise due to

o Light level of anaesthesia
o Hypovolaemia
o Hypoxia
o Hypercarbia
o Hyperthyroidism
 Normally pulse rate may either be equal or slightly deficit of heart rate because all the
contraction may not produce palpable effective wave and waves may overlap.
 The abnormal conditions which causes deficit of pulse rates are
o Premature contraction,
o Variable diastolic ventricular filling
o Electromechanical dissociation of heart.

HEART RHYTHM

 Supraventricular and ventricular ectopic pacemaker activities are common during

general anaesthesia. The other arrhythmia are sinus bradycardia, tachycardia and
 atrioventricular conduction block and all these conditions may response to the treatment
suggested for bradycadia.
 Other forms of arrhythmia
o Premature atrial contraction
o Premature ventricular contraction
o Pacemaker actrivity
o Bundle branch blocks
 Premature ventricular contraction may progressively lead to ventricular tachycardia and
fibrillation.
 The atrial and ventricular premature contraction may be caused by
o Too light level of anaesthesia (due to the release of catecholamines) or due to
deep plane or anaesthesia (due to hypoxia and hypercapnia)
o Hypoxia and hypercapnia
o Hypovolaemia and hypotension
o Exogenous catecholamine therapy
o Digitalis toxicity potentiated by hypokalemia
o Hypokalemia potentiated by respiratory or metablic alkalosis or insulin therapy
o Hypercalcemia potentiated by respiratory acidosis
o Anaesthetics sensitizing the myocardium for the actions of catecholamine activity
(halothane and xylazine)
o Endocarditis and myocarditis
o Endocardial stimulation by the catheters or epicardial stimulation by the tubes or
surgery
o High preload or afterload
o Severe hypothermia
o End stages of visceral organs function
o Increased intracranial pressure and intracranial diseases
 If the premature ventricular contraction is persistent with heart rate exceeding 180 to
200 the following treatments must immediately be adopted.
o Check the oxygen supply and maximize the inspired oxygen level. (10 ml/kg/min
in circle system and 200 ml/kg/min in nonbreathing system)
o Institute intermittent positive pressure ventilation
o Start fluid aministration
o Discontinue the agents which results or lower the threshold for the onset of
arrhythmia.
o Administer anyone of the following.
 Lignocaine 1 to 5 mg/kg I.V.
 Procainamide 1 to 5 mg/kg I.V
 Propranolon 0.05 to 0.3 mg/kg I.V
 Verapamil 0.05 to 0.15 mg/kg I.V
 The other ECTG abnormalities are
o Change in the rhythm
o Change in the configuration of PQRST
o Absence of P wave or shortened P – R interval (Right ventricular hypertrophy,
Bundle branch block and ventricular premature contraction all will show bizarre
– locking ORS
o Abnormal T wave (tent shaped) due to hyperkalemia and hypoxia
o Depressedor elevatedor slurred S – T segment due to myocardial hypoxia.

ECG lead placement in anaesthetized animal (LEAD II)

  Small animals

RA Right arm or any where on the body rostral to the heart

LL Left hind leg or any where on the body caudal to the heart
LA Left arm or any where on the body (ground)

 Large animals

RA Right arm or low on the chest towards the sternum (negative pole)
LL Left hind leg or on the chest above the spine of scapula (Positive pole)
LA Left arm or on the neck (ground)
VENTRICULAR PERFORMANCE

 Ventricular performance is the contractile force of the heart, and can be assessed by the
loudness on auscultation using ordinary stethoscope or oesophageal stethoscope or heart
sound amplifier.
 Diminished heart sound is due to hyproventilation, myocardial weakness, hypoxia,
anaesthetics, severe metabolic disturbances, endo and exogenous foxins, execessive or
insufficient end-diastolic filling volume.
 Ventricular performance can be improved by
o Dopamine 2.5 to 20 ug/kg/min (40 to 200 mg in 250 to 500 ml of 5% dexotrose
or saline)
o Dobutamine 2.5 to 20 ug/kg/min (40 to 250 to 500 ml of 5% dextrose or saline)
o Mephenteramine 0.1 to 0.75 mg/kg/I.V
o Calcium chloride 10% 0.1 mg/kg. I.V.
o Digitalis
o Amrinone (new inotropic agent ) 0.75 to 3 mg/kg I.V (peak effect in 10 minutes
and the duration is 30 to 120 minutes)

CARDIAC OUTPUT

 Cardiac output can be measured by dye dilution technique or thermodilution technique.

 Indocyanian green a dye is injected into the right atrium at a known concentration.
 The change in the concentration at the down stream (pulmonary artery or aorta) is
measured and the cardiac output is calculated.
 In thermodilution technique iced saline or saline in room temperature is administered in
the right atrium and change in the temperature is assesses at downstream using
thermodilution catheter located in the pulmonary artery.
 The thermodilution catheter is inserted into the right atrium through jugular vein using
fluoroscopy or blindly (flow directional balloon catheters are used for blind methods).
 The causes for reduced cardiac output
o Insufficient venous return
o Ventricular restrictive diseases (hypertrophy, pericardial tamponade or
pericardial fibrosis)
o Decreased contractility
o Excessive bradycardiaand arrhythmis
o Regurgitation and retrograde flow
o Stnosis
o Positive inotropic drugs are administered to correct the cardiac output.
 PERIPHERAL PERFUSION

 It is assessed by the collur of the mucous membrane and the capillary refill time.
 The normal capillary refill time is less than 2 seconds.
 Pale mucous membrane and prolonged refill time are due to reduction in perfusion.
 The other methods to asses the peripheral perfusion is by the use of ultrasonic Doppler,
electromagnetic flow probes, radionuclide imagery, nuclear magnetic resonance and
position emission tomography.
 The reasons for reduced peripheral perfusion
o Stress induced increase in sympathetic tone
o Hypovolemia
o Low cardiac output
o Fear and pain
o Exogenous alpha – Receptor agonist catecholamine therapy.

BLOOD PRESSURE

 Blood pressure is one of the important parameter to be monitored during anaesthesia

because adequate blood pressure is needed to perfuse the brain and heart.
 A minimum 50 to 60 mm of Hg mean arterial blood pressure (MAP) is to be maintained
for coronary and cerebral perfusion.
 Arterial blood pressure can be measured by
o Direct and Indirect techniques in animals.
 Indirect technique
o In indirect technique a cuff is placed snugly around the limb or tail and inflacted
until the blood flow is occluded.
o The extraluminal pressure just to occlude the blow is considered as the pressure,
which is above the systolic pressure. As the cuff pressure is reduced the flow will
restore.
o The flow can be assessed by direct palpation of the artery (only for systolic
pressure) or by auscultation for Korotkoff sounds.
o The first sound represents systolic pressure and the muffing or disappearance of
the sound represents the diastolic pressure.
o Pediatric cuffs are well suited for veterinary use.
o Cuff Placement
 Dogs above the elbow
 Horses Coceygeal artery
 Sheep and goats above the elbow or around the tibia
 Direct technique
o direct method of blood pressure measurement is done by catheterization of a
suitable artery and connecting it to an aneroid manometer to assess the mean
arterial pressure.
o A transducer is placed in machines to record both diastolic and systolic pressure.
o Catheterization of artery
 Dogs femoral artery, dorso metatarsal artery,l lingual artery
 Horses Facial artery, metatarsal artery, common digital artery
 Cattle Middle coccygeal artery, median auricular artery
 Sheep & goat Auricular artery
 Cat Superficial musculocutaneous branch of femoral artery.
 o The normal systolic, diastolic and mean arterial pressure is 100 to 160, 60 to 100
and 80 to 120 mm of Hg respectively. Systolic pressure below 80 and mean
arterial pressure below 60 mm of Hg are considered as hypotension and will
result in poor cerebral and coronary perfusion.
o The mean arterial pressure can be calculated from systolic and diastolic pressure
using the formula:
o MAP in mm of Hg + Diastolic + ((Systolic –
diastolic)/3)
o The mean blood pressure is not the half of the total of systolic and diastolic
pressure. The MAP is always close to the diastolic pressure. The difference
between the systolic and diastolic pressure is called as pulse pressure.

TREATMENT OF HYPOTENSION

 Discontinue the anaesthetics and adjuncts, which induces hypotension and use the
agents like diazepam and ketamine.
 Lactated Ringer’s 10 to 40 ml/kg is administered over a period of 10 to 30 minutes.
 Multielectrolyte sodium containing crystalloid replacement solutions can be
administered routinely at the rate of 10 ml/kg/hr plus 2 to 3 times the volume of
estimated blood loss. During major procedures like thoracotomy, fracture repair and
laparotomy it can be increasedupto 20 ml/kg.
 During anemia and hypoproteinemia crystalloid solutions are not administered. If the
PCV is less than 20% blood is indicated and if the total serum protein is less than 3 to 3.5
g/dl further volume replacementis done only by plasma or dextran.
 Sympathomimetic drugs are used in extreme hypotension with caution and continuous
monitoring as they may induce cardiac arrhythmia.
 (See Anaesthetic emergenices)

CENTRAL VENOUS PRESSURE

 Central venous pressure (CVP) is the luminal pressure of the intra thoracic anterior vena
cava or right atrium.
 The central venous catheters are positioned through percutaneous catheterization of
jugular vein.
 The zero level of the manometer is maintained at the heart level.
 The nomal CVP is 0 to 10 cm of H2O in small animals, t to 15 cm of H2O in awake
horses, 25 to 35 cm of H2O in anaesthetized recumbent horses and 5 to 10 cm ofH2O in
cattle, sheep and goats.
 Increase in CVP could be noticed in reduced cardiac output vascconstriction and
hypervolemia.
 CVP decreases during vasodilatation, hypovolemia and obstruction to venous return.
 Fluid therapy is indicated when increase in CVP is noticed with heart failure.

PULMONARY ARTERY PRESSURE AND WEDGE PRESSURE

 Pulmonary artery and wedge pressures indicate the functional capacity of the left side of
the heart.
 A flow directional balloon catheter is inserted into the jugular vein to pass the right
atrium, right ventricle to reach the pulmonary artery bifurcation.
 Pulmonary wedge pressure is recorded when the balloon is in inflated condition and
pulmonary artery pressure isrecorded when the balloon is in deflated condition.
 Normal pulmonary artery systolic and diastolic pressures are 20 to 40 mm Hg and 5 to
10 mm Hg respectively.
 The pulmonary wedge pressure is 3 to 8 mm Hg. Pulmonary artery diastolic pressure will
almost be equal to wedge pressure.
 Increase in pulmonary artery and wedge pressure is observed during positive pressure
ventilation, mitral insufficiency and excess pulmonary venous pressure.
 During spontaneous ventilation the pulmonary artery and wedge pressure will decrease.

Pulmonary function
RESPIRATORY RATE

 Carbon dioxide is the primary chemical stimulant of respiratory centers to maintain

normal respiratory pattern.
 Hypocapnia in anaesthetized patients may resulting apnea.
 In anaesthetized patients each respiration must be long and large to satisfy the
ventilatory requirement and oxygen demand.

BRADYPNEA

 The reasons for bradypnea are

 Cerebral oedema, neoplasia or haematoma.
 Anaesthetic depression and hypoxia
 Medullary dysfunction
 The altered breathing patterns are
o Apnea due to medullary dysfunction
o Diaphargmatic breathing: during respiration the diaphragmatic component
precedes and thoracic component.
o Cheyne – Stokes breathing: It is characterized by cyclic hyperventilation and
hypoventilation due to the delay in medullary response to changing carbon
dioxide tension.
o Biot’s breathing: characterized by cyclic hypoventilation and apnea and this
pattern is also a sign of serous medullary disturbance.
o Apneustic breathing: This pattern is associatedwithbrain stem disease and is
commonly seen in ketamine anaesthesia.
o Agnoal gasps: Characterized by periodic retraction of the hyoid apparatus and
gasping through the mouth may or may not associate with diaphragmatic
contraction.
 During surgical procedures apnea may develop due to
o Spinal cord oedema secondary to CSF tapping
o Injection of contrast agents for myelography
o Due to neuromuscular blocking agents
o Deep anaesthesia.
 TACHYPNEA

 Elevated respiratory rate (tachypnea) may be associated with normoventilation or

hypoventilation.
 Reasons for tachypnea
o Hypercapnia
o Hypoxia
o Hypotension
o Hyperthermia
o Too light level of anaesthesia inducestachypnea and hyperventilation
o Too deep anaesthesia induces tachypnea and hypoventilation
o Airway obstruction resultsiln tachypnea and hypoventilation
o Pneumothorax, hydrothorax, chylothorax, haemothorax and diaphragmatic
hernia
o Space occupying abdominal lesions such as gastric/intestinal tympany, ascitis,
neoplastic mass, gravid uterus and pyometra
o Atelectasis and airway collapse
o Anesthetic drugs like ketamine, diazepam and certain narcotics.

Treatment

o Proper intubation
o Articifial ventilation oncein 30 seconds in case of apnea
o Institution of intermittent positive pressure ventilation
o Sighing of the patient once every minute (squeezing the rebreathing bag)

NATURE OF VENTILATORY EFFORT

 The normal respiratory effort is smooth, easy, regular and comprised of thoracic and
diaphragmatic movements.
 The abnormal ventilatory efforts are
o Exaggerated breathing effort- indicative of respiratory stimulation.
o Stertorous- indicative of upper airway obstruction
o Wheezing- indicative of lower airway narrowing
o Crepitation- indicative of fluid bubbling sound
o Intercostal retraction during inspiration- indicative of upper airway obstruction
o Predominance of diaphragmatic component during inspiration-indicative of deep
anaesthesia.

COLOR OF MUCOUS MEMBRANE

 Cyanosis indicates severe hypoxemia.

 If cyanosisis noticed during anaesthesia immediately the oxygen supply must be checked
for the correct delivery.
 The oxygen is supplied at the rate of 10 ml/kg/min in circle system and 20 ml/kg/min in
nonrebreathing system.
 The other reasons for cyanosis are shock, hypothermia, cardiac arrest and intrathoracic
lesions.
  Drugs like acetaminophen induces cyanosis in cats and benzocaine induces cyanosis in
dogs and cats.

VENTILOMETRY

 Measurement of ventilation volume is ventilometry.

 Visual observation suggests the volume roughly.
 Ventilometers are fitted on the expiratory side of the breathing circuit will indicate the
tidal and minute volume.
 The normal ventilation is 150 to 250 ml/kg/min. Minute volume below 100 ml.kg/min is
considered as hypoventilation and above 300 ml/kg/min as hyperventilation.

BLOOD GAS

 Arterial blood is collected in 2 ml heparinized syringe with 22 to 25 gauge needle and the
needle is corked or the needle guard is replaced immediately.
 The syringe is kept in ice and sends for analysis using blood gas analyzer.

Partial pressure of carbon dioxide (PaCO2)

 The normal PaCO2 is 35 to 45 mm Hg.

 PaCO2 less than 35 mm Hg indicates hyperventilation.
 PaCO2 above 45 mm Hg indicates hypoventilation. PaCO.
 PaCO2 above 60 mm Hg indicates severe respiratory acidosis
 PaCO2 less than 20mm Hg indicates severe respiratory alkalosis and decreased cerebral
blood flow
 PvCO2 (venous) will be 2 to 5 mm Hg greater than PaCO2.
 PaCO2 indicates the ventilatory status of the patient
 PaCO2 level can be used to calculate the alveolar partial pressure of oxygen (PAO2) using
the formula
o PAO2 = FiO2 x ( P B – P H20 ) – PaCO2 / R
 FI02 – Fractional concentration of inspired oxygen (normal air contains 21% oxygen
hence it is 0.21.
 PB – Barometric pressure (normally 760 mm Hg at sea level) given in the blood gas
report.
 PH20 – Water vapour pressure (47 mm Hg when the air is fully saturated at 37oC) given
in the blood gas report.
 R - Respiratory quotient, it is a constant, which is equal to 0.8 (ratio of carbon dioxide
production to oxygen consumption)

Partial pressure of oxygen (PaO2)

 The normal PaO2 is 90 to 100 mm Hg.

 Pa02 less than 60 mm Hg indicates hypoxia and hypoventilation
 Animals breathing enriched oxygen mixture will be having higher Pa02
 Pa02 indicates the oxygenating capability of the lung
 METABOLIC ACIDOSIS

 The pH will indicate the metabolic acidosis and is attributed to the lactic acidosis
secondary to inadequate tissue perfusion due to vasoconstriction, hypotension,
hyperthermia or infusion of acidotic fluids.
 Bicarbonate is administered only for the patients having bicarbonate deficit, not for all
acidotic conditions.
 The amount of bicarbonate in mEq to be administered is calculated as base or
bicarbonate deficit x 0.3 x body weight in kg (approximately 1 to 5 mEg/kg).
 The commercially available bicarbonate powder is equal to 12 mEq per grams.
 Bicarbonate solution must be administered slowly because rapid administration may
cause alkalemia, hypokalemia, decreased ionized calcium, hypotension, nausea,
vomiting, collapse and even cardiac arrest.

Temperature and urine output

TEMPERATURE

 Recording body temperature is important in anaesthetized patients as it indicates the

systemic function.
 The temperature can be recorded at deep rectum, cervical oesphagus, pharynx and under
the tongue.
 During anaesthesia drop in temperature could be noticed due to the reduction in
metabolic rate.
 Premedicants like acepromazine deplete the catecholamine in the thermoregulatory
center and render the animal to pick up the environmental temperlature.(See
hypothermia and hyperthermia in Anaesthetic complication)

URINE OUTPUT

 It is an indirect assessment of visceral perfusion. Urinary catheters are placed aseptically

and the urine is collected.
 The normal expected urine output in anaesthetized animals is 1 to 2 ml/kg/hr.
 If the urine output is reduced lactated Ringer’s is administered at the rate of 20 to 40
ml/kg rapidly to induce diuresis.
 The other agents administered to induce diuresis are
o Furosemide 5 mg/kg diuresis occurs in 5 to 10 minutes
o Glucose, Mannitol (0.5 g/kg over 20 to 30 minutes) as infusion
o Dopamine 1 to 5 µg/kg/min.

MODULE-14: ANAESTHETIC EMERGENCIES AND THEIR

MANAGEMENT

Learning objectives
This module deals with

 Bradycardia
 Tachycardia
 Shock
 Signs of CPR
 Treatment for CPR
 Drugs used in CPR

REASONS FOR ANAESTHETIC EMERGENCIES

 Human error
o Not familiar with the equipment and anaesthetic drug and its action,
miscalculation of dose, incorrect route of administration and wrong medications.
 Equipment problems
o Failure to deliver oxygen, empty cylinders, misconnected gas lines and kinked or
plugged endotracheal tubes.
 Ventilatory problems
o Hypoventilation due to anaesthetic over dose, hyperventilation due to inadequate
anaesthesia and ventilatory depression.
 Circulatory problems
o Hypotension, bradycardia, tachycardia and shock.

BRADYCARDIA

 Bradycardia may arise due to

o Excessive depth of anaesthesia
o Excessive vagal tone (often increased by intubation vasovagal reflex and traction
of abdominal organs)
o Terminal hypoxia
o Endogenous and exogenous toxaemias
o Conduction disturbances in myocardium
o Hyperkalaemia
o Hypothyroidism

Treatment

o Administration of atropine or glycopyrrolate.

o Dopamine 2.5 to 20ug/kg/min (40 to 200 mg in 250 to 500 ml of 5% dextrose or
saline )I.V.
o Dobutamine 2.5 to 20 ug/kg/min (20 to 200 mg in 250 to 500 ml of 5% dextrose
or saline)I.V.
o Mephenteramine 0.1 to 0.75 mg/kg I.V. duration 15 to 30 minutes
o Ephedrine 0.05 to 0.5 mg/kg I.V. duration 15 to 30 minutes.
o Isoproterenol 5 to 10 ug/kg/min (0.4 ti 1.0 mg in 250 to 500 ml of 5% dextrose or
saline )I.V.

Reasons for intraoperative bradycardia

  Due to increase in vagal tone
o Difficulty in intubation
o Deep abdominal surgery
o Intraocular surgery
o Neck and thoracic surgery
o Effect of anaesthetics
o Premedication with atropine or glycopyrrolate will control this
o condition.
 Non vagal bradycardia
o Excessive depth of anaesthesia
o Hypoxia
o Hypothermia
o Hyperkalemia

TACHYCARDIA

 Tachycardia may arise due to

o Light level of anaesthesia
o Hypovolaemia
o Hypoxia
o Hypercarbia
o Hyperthyroidism
 Normally pulse rate may either be equal or slightly deficit of heart rate because all the
contraction may not produce palpable effective wave and waves may overlap.
 The abnormal conditions which causes deficit of pulse rates are
o Premature contraction,
o Variable diastolic ventricular filling
o Electromechanical dissociation of heart.
 Heart rate above 180 per minute in dogs and above 200 per minute in cats are
considered as tachycardia.

SHOCK

 Shock is defined as inadequate blood flow to the vital organs or the inability of the body
cells to metabolize nutrients normally.
 The tissue perfusion depends on the cardiac function, circulatory volume and integrity of
vascular function.
 Shock can be classified as
o Hypovolemic shock
o Cardiogenic shock
o Vasculogenic shock
o Hyperdynamic shock
o Hypodynamic shock

HYPOVOLEMIC SHOCK

Causes
  Due to inadequate volume of fluids or blood due to the loss of whole blood, plasma or
loss of water and electrolytes
 Loss of blood in accident
 Loss of polasma protein into inflamed body cavities
 Loss of fluid and electrolytes in diarrhea

Symptoms

 Depressed, dull and lack luster/lusterless eyes

 Pale or white or blue mucous membrane
 Reduced capillary refill time
 Cold extremities
 Tachycardia
 Fast and weak pulse
 Elevated respiratory rate
 Reduced body temperature

CARDIOGENIC SHOCK

Causes

 Occurs when the heart fails to pump adequate blood to maintain perfusion. Failure could
be due to reduced venous filling and reduced cardiac output. This condition is common
in small animals.
 Cardiac tamponade
 Rupture of chordae tendinae
 Toxic myocardial depression
 Cardiac arrhythmia
 Severe prolonged systemic vascular resistance

Symptoms

 Depressed, dull and lack luster/lusterless eyes

 Pale or white or blue mucous membrane
 Reduced capillary refill time
 Cold extremities
 Tachycardia
 Fast and weak pulse
 Elevated respiratory rate
 Reduced body temperature
 Distended pulsating peripheral veins
 Hepatomagaly
 Peripheral oedema
 Cardiac dysrhythmia
 Heart murmurs

VASCULOGENIC SHOCK
Causes

 The vessels supplying the blood to the tissues are affected and the perfusion is reduced
 Arteriolar constriction
 Prolonged sympathetic stimulation
 Vasomotor paralysis due to head injuries
 Endotoxic and septic shock can also be categorized under vasculogenic shock as the
toxins produce vasodilation due to the release of histamine, bradykinin and
prostoglandins.

HYPERDYNAMIC SHOCK

Causes

 An early stage of septic shock is an example of hyperdynamic shock.

Signs

Stage I

 Increase in cardiac output

 Decrease in arteriovenous oxygen difference
 Decrease in systemic vascular resistance
 Blood pressure may be normal or reduced
 Oxygen utilization at cellular level is reduced

Stage 2

 Cardiac output may be normal

 Hypotension
 Respiratory acidosis with metabolic alkalosis
 Elevated heart rate

Stage 3

 Reduction in cardiac out put

 Elevated heart rate
 Increased difference in arteriovenous oxygen level
 Increase in systemic vascular resistance
 Hypotension
 Brick red mucous membrane due to peripheral vasodilation
 Pyrexia due to toxins and damaged leukocytes

HYPODYNAMIC SHOCK

 It occurs at the terminal stage of sepsis or during the absorption of toxins. This can be
otherwise called as fourth stage of septic shock.
  Hypodynamic shock is common in large animal practice. E.g. terminal stage of horses
with colic and cow with coliform mastitis.

Signs

 Myocardial depression
 Maldistribution of blood volume
 High peripheral resistance
 Endothelial damage
 Infarcts in vital organs
 Acute respiratory failure and hypoxaemia

SIGNS OF CPR

 No ausculatatable heart sound

 No palpable pulse
 Cyanotic mucous membrane
 Dilated pupil
 No ventilatory attempts or agonal gasps
 Unconsciousness
 It is really a true emergency condition, which is to be treated immediately within a
period of 2 to 3 minutes.
 The basic life support in cardio pulmonary resuscitation(CPR) is the optimal
management of airway(A), Breathing(B) and circdulation(C). Otherwise called as ABC of
CPR.

AIRWAY

 The head must be immediately extended

 If not intubated intubate the animal immediately.
 Examine for the possible obstruction of the airway with food materials or kinked
endotracheal tube
 In emergency perform tracheostomy to maintain airway patent
 In case of bronchospasm treat the animal with aminophylline 5 mg/kg I.V.

TREATMENT OF CPR

Airway

 The head must be immediately extended

 If not intubated intubate the animal immediately.
 Examine for the possible obstruction of the airway with food materials or kinked
endotracheal tube
 In emergency perform tracheostomy to maintain airway patent
 In case of bronchospasm treat the animal with aminophylline 5 mg/kg I.V.

Breathing
  Institute artificial respiration using rebreathing bag or mechanical ventilators at the rate
of 12 to 20 breaths per minute.
 Supply 100% oxygen
 Or use Ambu type resuscitation bag (using room air 21% oxygen) or mouth to
endotracheal or mouth to muzzle procedures to maintain breathing
 Analeptic agents like doxapram can be administered at the rate of 1 mg/kg I.V.
 The other agents are specific alpha 2 antagonist (yohimbine) and opioid pure antagonists
(naloxone) (See premedication).

Circulation

 External cardiac massage by chest compression at the rate of 90 to 120 per minute. In
dogs the chest compression can be attempted by placing the hands on either side of the
chest. In cats the forefinger and the thumb is used.
 Open cardiac massage is done at the rare of 60 to 100 per minute. If surgery is
performed in the thorax its easy to provide open chest massage. During abdominal
procedures if emergency occurs the thoracic cavity can be entered through the
diaphragm.
 Defibrillation - The defibrillation is done using external or internal paddles of cardiac
defibrillators. The power setting depends on the weight of the animals. In small animals
the heart is defibrillated at the rate of 1 to 10 J/kg using external paddles and 0.1 to 1
J/kg using internal paddles.

DRUGS USED IN CPR

Calcium solutions

 Administered as inotropic agent or in hypocalemic agent. (halothane decreases calcium

availability in heart muscles.
 It strengthens the myocardial contraction. Dose Calcium chloride 10% solution at the
rate of 0.1 mg/kg I.V, Calcium gluconate 10% solution at the rate of 0.5 mg/kg I.V.

Dobutamine

 It is a sympathomimetic amine, whichstimulates beta 1 and beta 2 adrenergic receptors

and to a lesser extend alpha 1 receptor.
 It decreases peripheral vascular resistance and increases cardiac output, blood pressure
and tissue perfusion.
 Rapid intravenous administration may cause cardiac dysrhythmias.
 Dose 0.25 to 20 µg/kg/min in small animals and 0.5 to 2.0 µg/kg/min in large animals
(40 to 200 mg in 250 to 500 ml of 5% dextrose or saline).

Ephedrine

 It stimulates beta 1, beta 2 and alpha 1 receptors.

 The cardiac output and blood pressure are increased.
 It is indicated in mild to moderate hypotension.
  Dose 0.05 to 0.5 mg/kg I.V in small animals and 0.022 to 0.66 mg/kg I.V in large
animals as a bolus.

Isoproternol

 It is a sympathomimetic amine, which stimulates beta 1, beta 2 and adrenergic receptors

located in the heart, bronchialsmooth muscles, skeletal muscle vasculature and
alimentary tract.
 It decreases peripheral vascular resistance, diastolic blood pressure and mean arterial
pressure and increases cardiac output and systolic blood pressure.

Epinephrine

 It is a sympathomimetic amine that stimulates alpha 1, 2 and beta 2 adrenergic

receptors.
 It dilates the vasculature of muscles and constricts cutaneous, mucosal and renal
vasculature.
 The systolic, MAP andpulmonary blood pressures are increased following
administration.
 It can cause dysrhythmia if administered during halothane anaesthesia.
 It is administered at a dose of 5 ml of a 1 in 1000 solution for a 454 kg horse.
 In extreme condition it is administered through intracardiac route.

Doxapram (Dopram)

 It is a nonspecific analeptic agent used to act on the peripheral chemoreceptors. Dose.

0.55 mg/kg I.V. to reverse the effect of xylazine it is administered at the rate of 1.0 mg/kg
I.V.

Sodium bicarbonate

 It is a buffer aids in reversing metabolic acidonin. Dose mEq of HCO3 = 0.3 x base deficit
(mEq/L) x Body weight.

Coricosteroids

 These group of agents increases the glucose production, induce hypdokalemia by sodium
retention.
 They have inotropic effect on the heart and maintain vasomotor response and suppress
the adrenal gland.
 Indicated in shock and malignant hyperthermia.

Lignocaine

 Indicated in premature ventricular contraction.

 Only the epinephrine free preparation is used.
  Dose 0.5 to 2 mg/kg in large animals and 1 to 5 mg/kg in small animals followed by 40 to
60 µg/kg/min I.V. It is contraindicated in slow ventricular rate combined with sinus
arrest, sinoatrial block or atrioventricular block.

MODULE-15: NEUROLEPTANALGESIA

Learning objectives

This module deals with

 Neuroleptanaesthetics and its clinical doses

PHENOTHIAZINE DERIVATIVES

Phenothiazine derivatives

 Phenothiazine derivatives are basically three ring structures in which two benzene rings
are linked by a sulphur and nitrogen atom.
 The steriochemical model of phenothiazine derivatives is similar to epinephrine,
norepinephrine and dopamine.
 They act on the central nervous system by depressing the brain stem and connections of
the cerebral cortex.
 These agents increase the dopamine and norepinephrine turn over in the brain and block
the peripheral actions of catecholamines at alpha 1 receptors.
 These agents are weak anticholinergics and have extrapyramidal stimulating properties.
 Acepromazine maleate, triflupromazine hydrochloride, chlorpromazine, promazine,
promethazine and methotrimeprazine are the commonly used phenothiazines. Among
these agents acepromazine, triflupromazine and chlorpromazine are used in veterinary
anaesthesia.

Clinical properties and uses

 Produce sedation, general calming and reduction in motor activity

 Antagonize dopamine excitatory chemoceptors and suppress vomiting.
 At high doses and some times in clinical doses induce extrapyramidal signs such as
rigidity, tremors and catalepsy. Hence contraindicated in patients;
o With the previous history of epilepsy,
o Undergoing myelographic procedures
o With the history of recent intake of organophophorus drugs or toxicity
 Pulmonary functions are maintained following the administration of phenothiazines
except slight depression in respiratory rate
 Induce urine production due to the suppression of antidiuretic hormone
 Animals undergoing intradermal allergic tests should not be administered with
phenothiazines as they are potent antihistaninics
 Depletes catecholamines of the thermoregulatory center and render the animal’s body
temperature susceptible to the changes in the environmental temperature.
 Tranquilization with phenothiazines is contraindicated in animals undergoing epidural,
spinal or segmental anaesthesia. Following induction of regional anaesthesia there will
 be vasodilation in the anaesthestised part of the body and this effect is compensated by
the vasoconstriction in the unanaesthetized parts of the body to maintain cardiac out
put. This response is abolished by the generalized vasodilationinduced by
phenothiazines.

CLINICAL DOSES OF PHENOTHIAZINE DERIVATIVES

Drug Dose
Acepromazine  Dogs = 0.03 – 0.05 mg/kg I.V, 0.03 – 0.05 mg/kg I.M.
 Cats = 0.03 – 0.05 mg/kg I.V, 0.03 – 0.1 mg/kg I.M.
 Horses = 0.02 – 0.05 mg/kg I.V, 0.04 – 0.09 mg/kg I.M.
 Cattle = 0.02 – 0.05 mg/kg i.V, 0.04 – 0.09 mg/kg I.M.
 Pigs = 0.1 mg/kg I.M.

Chlorpromazine  Dogs = 0.55 – 4.4 mg/kg I.V, 1.1 – 6.6 mg/kg I.M. Cats = 0.55 –
4.4 mg/kg I.V, 2.2 – 6.6 mg/kg I.M
 Horses = 1.1 – 2.2 mg/kg I.M.
 Cattle = 0.2 – 1.1 mg/kg I.V, 0.2 – 2.2 mg/kg I.M.
 Sheep = 0.55 – 4.4 mg/kg I.V, 2.2 – 6.6 mg/kg I.M.
 Goats = 0.55 – 4.4 mg/kg I.V, 2.2 – 6.6 mg/kg I.M.
 Pigs = 1.0 – 2.0 mg/kg I.M.

Promazine  Horses = 0.44 – 1.1 mg/kg I.V/I.M.

 Cattle = 0.44 – 1.1 mg/kg I.V/I.M.
 Goats = 0.44 – 1.1 mg/kg I.V/I.M.
 Sheep = 0.44 – 1.1 mg/kg I.V/I.M.
 Pigs = 0.44 – 1.1 mg/kg I.V, 0.44 – 4.0 mg/kg I.M.

Triflupromazine  Dogs = 1.00 mg/kg

MODULE-16: ELECTRO ANAESTHESIA, ACUPUNCTURE

AND HYPOTHERMIC ANAESTHESIA

Learning objectives

This module deals with

 Acupuncture
 Electronarcosis
 Hypothermia

ACUPUNCTURE - INTRODUCTION

 Acupuncture (AP) can be used to obtain pain relief in clinical disorders or as an

alternative or complementary method of inducing pain control during surgical
procedures. AP analgesia (AA) is a misnomer. It should really be called AP hypoalgesia.
 It is a pain inhibition phenomenon caused by stimulation of peripheral nerves via certain
AP points.
 The degree of pain inhibition may be complete or partial. In vet surgery, the AA
technique, if applied carefully, often is sufficient to allow surgery without the use of other
anaesthetics. Consciousness is retained throughout the operation but many animals
become slightly drowsy (as if slightly sedated) during and for a short time after AA
stimulation. All other sensations (touch, traction, pressure, tickle etc) and reflexes (to
sight or sound stimuli, fear, traction etc) are intact. AA can be induced by
simple AP (manual twirling of the needles) but it is more common to use electrical
stimulation (ES) via the needles. In this case the technique is called Electro-APanalgesia
(EAA).
 In emergencies a slight degree of hypo-algesia can be obtained in humans and animals
by heavy digital pressure over the correct AP/nerve points. This method may have
application in time of war or national disasters, when anaesthetists and anaesthetics may
not be available. AA also can be induced by other stimuli, such as injection or electro-
static fields applied to the points. Since the late 1980s, research on uses of low-power
(cold) Laser as an AA stimulus is ongoing, with some positive results. However, it is too
early to attempt to assess that method.
 Stimuli via the AA points are carried in the peripheral sensory nerves to the spinal cord.
They reach the midbrain via the ascending spino-thalamic tracts. In the midbrain the
ascending signals cause release of endorphin, serotonin and other neurotransmitters
which activate a "descending inhibition mechanism" and prevent the "pain signals" from
the surgical area from reaching the cerebral cortex. Thus, AA can be said to "close"
various "pain gates" in the nervous system. These gates are thought to be located in the
spinal cord, thalamus and possibly other areas. The result is that the human (and,
presumably, the animal) patient can feel the knife, the touch and traction etc but does
not "feel pain".
 Stimulation-Produced-Analgesia (SPA): Since the 1970s, western researchers, working
independently of the Chinese, found that various types of stimuli applied indirectly or
directly to the nervous system can reduce or abolish clinical and operative pain.
Transcutaneous Electro-Stimulation Analgesia (TESA) has been used in childbirth in the
human female and is somewhat comparable to EAA. Dorsal Column Stimulation (DCS)
of the spinal cord has been used in intractable pain in humans. ES via electrodes
implanted in specific sites in human or animal brain can induce a high degree of
analgesia, usually involving the entire body. Direct ES of human thalamic or spinal areas
can abolish clinical pain. Vaginal stimulation (electrical or mechanical) can cause potent
whole-body analgesia in rats.

TYPES OF OPERATIONS UNDER AA

 Since the mid 1970s, major surgery has been done in animals under AA as the sole
analgesic agent in many countries in the West. These include France, Germany, Austria,
Belgium, USA, Canada and Australia.
 Workers in Eastern countries such as China, Japan, Taiwan etc have used the method for
many years. The animal species involved include horses, mules, donkeys, cattle, sheep,
goats, pigs, monkeys, dogs, cats, rats, cavies, guinea pigs and mice.
 Types of surgery successfully done in animals include:
o caesarean section, ovario-hysterectomy;
o gastric and intestinal surgery;
o nephrectomy;
o removal of mammary and skin tumours;
 o surgery of the eye, ear, anal and vaginal region, limbs and teats;
o surgery on the lip, oesophagus, trachea, frontal sinuses;
o rumen;
o navel hernia repair;
o surgery on the bladder and urethra;
o orthopaedic surgery (bones, joints);
o removal of parotid and submaxillary glands;
o castration, orchidopexy, inguinal hernia.
 The late Dr. Westermayer's method for reposition of the prolapsed uterus has been
mentioned already, as has AP therapy for the relief of dystocia.

EQUIPMENT AND METHODS OF RESTRAINT FOR AA

Equipment

 Most AA is done using electrostimulation (ES) through needles in the correct points
(Electro-AP analgesia = EAA). The choice of points will be discussed later. Many
different types of electrostimulator are on the market. Some are made in China, others in
Japan, USA, Canada, Europe and Australia etc.
 The equipment should be strong, portable and battery-operated. It should have outputs
for at least 8 electrodes. There is little standardization of equipment. Newer models for
human use would be adequate for EAA in animals. It is safer to use models which deliver
a bipolar waveform, (+) and (-), at each electrode. This prevents the development of
serious electrolytic lesions which could arise if a monopolar waveform was used for long
periods, as in prolonged surgery.
 The Model 71-3 General Purpose Electro-AP Apparatus is suitable for AA as well as AP
therapy. I had 8 teeth extracted and 8 teeth filled under EAA with the Model 71-3. I used
mainly ChiaChe (ST06) plus Earlobe "Dental Analgesia Point" on the affected side.
Needles were inserted 12-20 mm in the points. Voltage was increased slowly to
maximum tolerance (anaesthesia mode, dense-disperse waveform). Occasionally
adjustable waveform at 5-10 Hz was used.
 After 30 minutes of induction, the output was usually at a setting of 4-5 on a 10 point
scale. When heavy needle-probing of the gum caused no pain, dentistry could begin.
Dental fillings under EAA were uneventful except in deep root fillings. If "nerve pain"
arose, turning up the voltage usually controlled it.
 Extraction was painless or caused minimal pain in 5/8 cases but 3/8 extractions caused
moderate to severe pain but were completed without the use of drug analgesia. An
impacted wisdom-tooth required 10 minutes of very strong rocking to remove it from its
socket. There was rather severe pressure-pain with that attempt but I was able to tolerate
it without asking for another anaesthetic. My dentist told me that most patients could
not have had the tooth removed unless they had general anaesthesia.
 In human patients, Caesarean section has been done in Japan using electro-static or
electromagnetic fields around the hands and feet. The apparatus used does not appear to
have been tested in Europe or America. Childbirth has been helped in 60-80% of women
treated by transcutaneous ES analgesia (TESA) of the thoraco-lumbo-sacral region. The
apparatus used was the Travisens, available from Dan Sjo Elektronik AB, Box 144-17224,
Sundbyberg, Sweden. TESA does not appear to have been tested in animals.

Restraint for AA in animals

 Surgery under AA requires adequate restraint because consciousness and all sensations
and reflexes (except those of pain) are retained.
In large animals, operations under AA may be performed with the animal in the standing
position or in dorsal, lateral or ventral recumbency, depending on the type of operation
and whether or not the animal is quiet. Horses and nervous cattle should be knocked by
ropes or a short-acting knock-down anaesthetic. Nervous animals may be given a
tranquilliser i/v.
 Recumbent animals should be roped securely and an attendant should ensure that the
head is kept down. A blindfold over the animal's eyes helps to avoid fright by visual
stimuli. Unnecessary noise, movement and fuss should be kept to a minimum.
 The standing position may be used for surgery in quiet cattle. An attendant may hold the
nose and the animal should be restrained in a suitable cattle crate, or ropes may be used
through rings in the wall to keep the animal in one position. Kicking may be prevented
by the usual methods as applied in operations under local anaesthesia.
 Small animals are normally operated on in lateral, dorsal or ventral recumbency. If a
special operation-harness is not available they are restrained by tying bandages from the
hocks and elbows to suitable anchor-points on the operating table. Dogs are excellent
subjects for AA but it is advisable to tie a tape bandage around the jaws to prevent biting.
It helps if the owner or an attendant talks to the dog and comforts the animal from time
to time during surgery. Cats are difficult animals to handle and some vets who have tried
AA in cats have ceased to use the technique in this species.

AA TECHNIQUES IN LARGE AND SMALL ANIMALS

 Electro-AP analgesia (EAA) is the most common method used. When the animal is
properly restrained, AP needles are placed to the correct depth in the AA points related
to the operation site.
 The stimulator is checked to ensure that the power switch is off. The output leads are
then connected to the needles. Do not connect the leads from one output across the
thoracic or posterior cervical region. This is especially advisable if the instrument uses
(+) and (-) electrodes. In this case the correct connection would be as in the diagram on
the next page.
 An output circuit placed across the thorax may interfere with cardiac function and may,
on rare occasions, cause cardiac arrest. Tape or suture the needles firmly in position.
Otherwise, they are liable to become dislodged by muscle twitches induced by the
stimulation, or by struggling in nervous animals.
 When the needles are in position, the output controls are checked to ensure they are set
at zero. Attach the leads and turn on the power switch.
 Turn up the output controls slowly until the needles begin to twitch in time with the
frequency of the stimulator. Increase the output voltage from each control to the
maximum tolerance of the patient. At that point, the animal indicates a degree of
discomfort or pain (restlessness, defensive reaction, struggling, vocalisation etc). Reduce
the output to a "strong but acceptable level" (that which can be tolerated without obvious
discomfort). Excessive stimulation reduces the EAA effect and to weak a stimulus may
induce little or no analgesia. Note: A needle can not twitch unless it is embedded in
reactive muscle. As long as one of a pair is twitching, the paired needle is also receiving a
similar stimulus. Needles may not twitch in points such as GV26.
 If output voltage is too high at such points, the animal will indicate discomfort. In that
case, reduce the output to the tolerance of the patient. Every 5 minutes or so, after
switch-on, the operation site is tested for analgesia using rat-tooth forceps, towel clip,
 clamp or pin prick. Initially, full sensitivity to pain is present, as indicated by local
muscle twitch or guarding, vocalisation or defence reactions/struggling.
 After 5-10 minutes, the response to pain stimulus decreases. After 20-40 minutes, in
successful cases, the animal makes no response to strong pain stimuli in and around the
operation site. The operation may then commence.
 Pain stimuli may exceed the hypoalgesia (thereby inducing pain response by the animal)
at certain stages of the operation, especially during incision and suturing of the skin,
serosa (peritoneum, pleura etc) and incision of periosteum and nerves. During these
stages of the operation the frequency or output voltage should be increased. This is
normally sufficient to counteract the pain.
 Occasionally (in those animals which respond poorly to AA) it may be necessary to use
small volumes of local anaesthetic injection or spray at these stages. In the first few
minutes after stimulation begins it is usual for the animal to show a mild stress reaction
(dilated pupils, increased blood pressure, faster respiration and heart rate). These
quickly return to normal or near normal levels, and should remain at this level during
the operation.
 Studies of EEG patterns in animals under AA indicate that brain waves are in the alpha
range (8-13 cycle per second) i.e., similar to those of drowsiness or light sleep. However,
the animals are still conscious and can eat or drink and (in dogs) wag the tail if petted by
someone they know. Because sight and hearing are unaffected (pupil reflex is also
intact), unnecessary noise should be avoided and a blindfold may be desirable.
 Pupillary dilation and salivation occurs in some animals. If salivation is excessive or
retching/vomiting occurs, this usually indicates that excessive traction on
mesentery/internal organs is the cause. This may be partly counteracted by increase in
frequency or output of the AA stimuli.

ELECTRO NARCOSIS

 Since the end of the last century many investigations with electroanaesthesia have been
performed in animals and man. The interest in this method of anaesthesia has emerged
because anaesthesia is achieved immediately after the onset of the current and the
recovery is very rapid after cutting off of the current. Recently a battery operated
appuratus became available (Feenix Stockstill) for application of electroanaesthesia and
electroimmobilisation under field conditions, and an experiment was conducted with 10
calves, 10 sheep, and 9 pigs, which were equipped with EEG and ECG electrodes. to
check the analgesic and other practical effects of the apparatus. The duration of current
administration was 20 minutes. Three animals of each species were used as control
animals.
 In all animals, during administration of the current, the breathing movements appeared
to be somewhat impaired. The body temperature, the plasma cortisol level, and the pulse
rate were raised durring the current administration. Moreover, the pulse rate was
irregular.
 The corneal reflex remained positive in all animals, and the reaction to painful stimuli
was positive in 15 out of 29 experimental animals. The body temperature, pulse rate, and
plasma cortisol level remained constant in the control animals. Before and after
administration of the current the electroencephalogram recordings were similar, except
in one calf and one sheep, both of which showed patterns suggesting a decreased
consciousness.
 The electrocardiogram recordings showed pronounced changes in cardiac activity. In one
pig the heart activity stopped some minutes after the onset of the current. Changes in the
 electroencephalogram and electrocardiogram were not observed in the control animals
during their treatment.
 The results suggest that the apparatus did not cause electroanaesthesia or electrosleep
but had mainly an electroimmobilising effect on the experimental animals. Because of
the dubious effects on the animals' welfare, the use of such an apparatus cannot be
recommended.

HYPOTHERMIA

 Hypothermia may develop in animals anesthetized in a cool environment. A decrease in

temperature of 1-3ºC below normal has been demonstrated to provide substantial
protection against cerebral ischemia and hypoxaemia in anaesthetized dogs. Life
threatening cardiovascular depression may develop when the temperature decreases
below 32.8ºC.
 Rectal or esophageal temperature should be monitored at regular intervals during
inhalation anesthesia , during protracted total intravenous anesthesia and during
recovery from anesthesia. Basically ,the causes consists of a reduction in heat production
by the animal , usually coupled with an increased heat loss.
 It is very difficult to influence production of heat but care should be taken not to wet the
animal excessively to reduce evaporative heat losses, placing the animal on a warm
surface and covering with blankets , drapes , wrapping of extremities with towel and
blanket and plastic insulation or hot air circulating devices.
 Respiratory heat losses are increased when animal breathes cold dry gas from non-
rebreathing system, such losses are reduced by the use of rebreathing circuits,and also
maintaining low flow rate and attachment of humidifier to endotracheal tube. Fluids to
be administered i.v. should be warm.

The adverse effects of perianaesthetic hypothermia are

1. Impaired cardiovascular function.

2. Hypoventilation
3. Decreased metabolism and detoxification of anesthetic drugs
4. Weakness during recovery
5. Decreased resistance to infection
6. Increased incidence of surgical wound infection
7. Increased postoperative protein catabolism

MODULE-17: MUSCLE RELAXANTS

Learning objectives

This module deals with

 Physiology of neuromuscular transmission

 Reversal of Neuromuscular Blockade
 Ventilation

INTRODUCTION
 Anaesthesia is comprised of narcosis, analgesia and muscle relaxation.
 Muscle relaxation is best achieved by the administration of neuromuscular blocking
agents.
 Use of neuromuscular blocking agents
 To provide the muscle relaxant component of anaesthesia
 To minimize the dose of general anaesthetics
 To provide easy access to the deep structures in the abdomen
 To aid in intubation without laryngeal spasm
 To prevent fighting the ventilator during controlled ventilation
 To help removal of foreign bodies from the proximal portion of oesophagus as it is
composed of striated muscles.
 To aid in reducing the luxated joints
 To ensure immobility of the patient during delicate surgery
 To stabilize the eyeball in central position during ophthalmic surgery

PHYSIOLOGY OF NEUROMUSCULAR TRANSMISSION

 The large myelinated nerve from the ventral horn of the spinal cord carries impulses to
the muscles. It carries stimuli to several muscle fibres that must be activated for
contraction.
 As the nerve approaches the muscle cell its branches lose their myelin sheaths and the
terminal ends lie in grooves on the surface of the muscle fibre and are covered by
Schwann cell. The area where the nerve ending lies close to the proximity of the muscle
fibre is called neuromuscular junction.
 The muscle fibre membrane forms the groove and the grooves are deeply corrugatede
and called as secondary clefts. The small gap between the nerve fibre terminal and the
muscle membrane is 60 nm wide and is called as junctional cleft. The areas of secondary
cleft are rich in mitochondira.
 The action potential traveling along the motor fibre produces depolarization of the nerve
terminal and triggers the release of acetylcholine, which crosses the junctional cleft to
stimulate nicotinic-cholinoceptors of the post synaptic muscle membrane.
 Acetylcholine is synthesized from choline and acetate in the presence of an enzyme
acetyltransferase. The acetylcholine molecules are present as uniform sized vesicles near
the presynaptic membrane and these areas are called as active zones.
 When acetylcholine is released it travels a minimum distance across the junctional cleft
to reach the receptors. Interaction between the receptor and acetylcholine triggers an
end plate potential, which is converted into muscle action potential leading
tocontraction. After activating the receptor the acetylcholine is rapidly hydrolysed to
choline and acetate. The drugs used for neuromuscular blockade are classified into
o depolarizing muscle relaxants
o nondepolarizing muscle relaxants.

DEPOLARIZING MUSCLE RELAXANTS

 Depolarizing drugs produce intial muscle fasciculations and their action is rapid.
Depolarized muscles are unresponsive to other stimuli such as electrical stimulation.
Their action is not reversed by anticholinesterases. In partial paralysis neuromuscular
monitoring slow depression of muscle twitch, no fade and no post titanic facilitation are
noticed. The only drug used in this group is suxamethonium chloride (Succinyl choline).
It is hydrolysed by cholinesterase and pseudocholineesterase into choline and succinic
 acid. Cholinesterase is synthesized in the liver. Hence liver damage, cachexia and
malnutrition may prolong the action of suxamethonium. Organophosphorous
compounds (use as ectoparasiti-cides) decrease the action of pseudocholinesterase,
hence not recommended in patients recently exposed to such agents.
 Isoflurane, respiratory alkalosis, hypothermia and magnesium ions potentiate the effect
of suxamethonium. Its effects are antagonized by halothane, acidosis and
nondepolarizing drugs.
 Its administration is associated with the release of potassium into the blood from the
muscles, which may result in cardiac irregularities. However prolonged administration
results in decrease in serum potassium level.
 In dogs 0.3 mg/kg intravenously produces muscle relaxation and it extends upto 25 to
30 minutes. Repeat dose may result in dual block (nondepolarizing) which can be
reversed with anticholinesterase drugs.

NONDEPOALRIZING MUSCLE RELAXANTS

 These drugs do not produce muscle fasciculations and are slow in action. Their effects
can be reversed using anticholinesterase.
 The relaxed muscles will response to other stimuli such as electrical stimuli.
 During partial paralysis monitoring it shows fade andpost titanic facilitation followed by
exhaustion and depression of muscle twitch.
 Acidosis, magnesium slats and volatile anaesthetics potentiate the action of these agents.
 Nondepolarizing drugs are either quaternary ammonium or steroid compounds.
 The following are nondepolarising muscle relaxing agents
o Tubocurarine chloride
o Gallamine triethiodide
o Pancuronium bromide
o Vecuronium bromide
o Atracurium besylate

TUBOCURARINE CHLORIDE

 Tubocurarine is derived from Chondrodendron tomentosum tree. Not recommended in

dogs due to its profound cardiac defects/effects.

GALLAMINE TRIETHIODIDE

 It has atropine like action on the heart.

 It also blocks the muscarinic effects of acetylcholine and acts directly on the B receptors
resulting in tachycardia and rise in blood pressure which may lead to greater blood loss
during surgery.
 This drug is excreted through kidney hence not indicated in patients with renal diseases.
 Dose - 1 mg/kg I.V, Duration: around 29 minutes.

PANCURONIUM BROMIDE

 It is an amino-steroid having no steroidal effects.

 Only 30% is metabolises and the rest is excreted unchanged through bile (10%) and the
reaming through the kidney.
 It is contraindicated in patients having renal and hepatic diseases.
 It has minimal effects on cardiovascular system and some times produces rise in heart
rate.
 Dose 0.06 mg/kg I.V, Duration around 31 minutes.

VECURONIUM BROMIDE

 It is a steroidal agent supplied in lyophilized form and soluble in water (stable for 24
hour only).
 Its duration of action is less than pancuronium.
 The drug is primarily excreted through bile in an unchanged form hence can not be used
in patients with hepatic diseases and recommended in patients with renal disorders.
 It has got minimal cardiovascular effects and does not release histamine.
 Dose 0.1 mg/kg I.V., Duration 18 to 25 minutes.

ATRACURIUM BESYLATE

 It is a novel muscle relaxant, which does not depend on body system tometabolize.
 It is broken down by a self-destruction process known as Hofmann elimination. It is a
safer drug for cardiac and renal patients.
 It is administered with caution inpatients with the history of anaphylaxis as it may
release histamine.
 Dose: 0.5 mg/kg I.V, duration around 40 minutes further maintenance can be done with
incrementaldose (0.2 mg/kg) or by continuous infusion (0.5 mg/kg/hr).

CISATRACURIUM BESYLATE

 This drug is 5 times potent than atracurium, has no cardiovascular effects, does not
release histamine, and is eliminated by Hofmann effects.
 No clinical literature is available on its use in veterinary anaesthesia.
 The other nondepolarizing drugs are mivacurium, rocuronium and doxacurium.

REVERSAL OF NEUROMUSCULAR BLOCKADE

 Reversal of nondepolarizing drugs is achieved by establishing high concentration of

acetylcholine at the binding site.
 It is achieved by the administration of certain drugs, which will inhibit cholinesterase,
and the drugs are pyridostigmine, edrophonium and neostigmine.
 In clinical condition reversal is attempted when at least two twitches are present.
 Atropine (0.04 mg/kg) or glycopyrrolate (0.01 mg/kg) administered intravenously
atleast one minute prior to the administration of reversal agent to block the muscarinic
effects of acetylcholine.
 Neostigmine 0.1 mg/kg I.V or Edrophoniumj 1.0 mg/kg I.V.
 Intermittent positive pressure is discontinued only after achieving train of four
responses (all must be of equal force).
 The action of neuromuscular blocking agents are potentiated and prolonged by
aminoglycoside antibiotics e.g. streptomycin, gentamicin, and tobramycin by decreasing
the release of acetylcholine. Calcium can be given prophylactically in these patients. The
 other antibiotics include polypeptide antibiotics like tetracycline, lincomycin and
metronidazole.

VENTILATION

 There following are the different types of ventilation

o Spontaneous ventilation
o Assisted ventilation
o Controlled ventilation
o Intermittent positive pressure ventilation

TYPES OF VENTILATION

Spontaneous ventilation

 It refers to breathing without any assistance from mechanical ventilator or the

anaesthetist squeezing the rebreathing bag.
 Spontaneous ventilation can be abolished by hyperventilation.

Assisted ventilation

 The patient initiates the respiration but the tidal volume is increased or assistedby the
ventilator or by squeezing the rebreathing bag.

Controlled ventilation

 The total breathing function of the patient is done entirely by a mechanical ventilator or
by the squeezing of rebreathing bag.

Intermittent positive pressure ventilation

 This is a technique used in controlled ventilation or assisted ventilation to force air into
the lung during inspiration and lower it to atmospheric pressure or slightly below during
expiration.

USES

 To provide ventilation during neuromuscular blockade and respiratory muscle paralysis

due to toxins.
 To maintain near normal acid base status and oxygenation during long surgical
procedures.
 To reduce ventilation-perfusion mismatch during prolonged periods of anaesthesia.
 To provide controlled respiration during thoracotomy. Intermittent positive pressure
ventilation is essential to maintain pulmonary function in dogs, cats and in horses during
open thorax as their mediastinum is incomplete. (fenestrated mediastinum). In cattle,
sheep and goats the mediastinumis complete (unfenestrated mediastinum) hence
thoracotomy can be performed in one side with out the need of ventilator. But still use of
 intermittent positive pressure in these animals also helps in maintaining
cardiopulmonary parameters.
 Used in patients whose respiratory centre is depressed by drugs, increased intracranial
pressure, cerebral ischemia, and cardiac or respiratory arrest.
 Used in thoracic diseases, which affect the negative pressure of the thorax. (-5 cm of H2O
during expiration and -12 cm of H2O during inspiration) eg. Diaphragmatic hernia,
pleural effusion, pneumothorax.
 Used in patients having inadequate respiratory exchange due to obstruction or
pulmonary oedema.
 Guidelines
o Volume, pressure, rate and inspiratory: expiratory ratio must be properly set in
the ventilators.
 Volume
o Small animals 10 to 20 ml/kg
o Large animals 10 to 15 ml/kg (maximum limit is for open thorax)
 Pressure
o 15 to 30 cm of H20
 Rate per minute
o Dogs 8--- 14
o Cats 10---14
o Horses 6 --- 10
o Cow 6 --- 10
o Sheep & goats 8 --- 12
o Pigs 8 --- 12
 Inspiratory: Expiratory ratio
o It should be 1:2 or 1:3 to minimize the interference with venous return the
inspiratory time is kept shorter than expiratory time.

MODULE-18: GENERAL PRINCIPLES OF CHEMICAL

RESTRAINT OF WILD AND ZOO ANIMALS

Learning objectives

This module deals with

 Chemical Immobilization of Wild Animals

CHEMICAL IMMOBILIZATION OF WILD ANIMALS

 Wild animals are chemically restrained for the following reasons

o Animal translocation and transportation
o To study the ecology and population estimate
o For veterinary studies
o To relieve wild animals in distress
o Control of animals causing distress to the public
 Various devices used for injecting the drug from a distance are drug darts, projectile
syringes (short range, long range, and extra long range), blow gun rifle, blow pipe, and
stick syringe.
Primates

 Ketamine – 5-20 mg /kg intramuscular

 Xylazine 2 mg/kg intramuscular

Chimpanzee

 Ketamine 10-15 mg/kg body weight

 Xylazine 2 mg/kg

Kangaroo

 Xylazine 8 mg/kg body weight and Ketamine 3 mg/kg combination

 Thiopentone less than 20 mg/kg body weight

Antelope

 Xylazine 0.23 mg /kg and Ketamine 11.54 mg/kg body weight combination

Deer

 Xylazine 0.89-8.0 mg/kg body weight

 Ketamine 10-20 mg/kg body weight

Camels

 Xylazine 0.27-0.51 mg/kg intramuscular

Bears

 Xylazine 2-4 mg/kg and Ketamine 4.5-9mg/kg (Combination)

Bison

 Chloral hydrate 250mg/kg body weight

Elephant

 Asian elephant 100-175 mg Xylazine (total dose)

 Etorphine-Acepromazine combination (2.4 mg/ml-Etorphine and 10mg/ml of
Acepromazine per ml) Dose 1 ml/4 feet of shoulder height

Reptiles

 Ketamine 20 mg/kg intramuscular

  Xylazine 1 mg/kg

Snakes

 Ketamine 50-130 mg/kg intramuscular

 Tiletamine 10-20 mg/kg intramuscular

MODULE-19: ANAESTHESIA OF LABORATORY ANIMALS

Learning objectives

This module deals with

 Injectable Anesthesia
 Inhalant Anesthesia
 Gas Delivery Systems
 Anesthetic Machine
 Preparation, Monitoring and Maintenance of normal physiology

INJECTABLE ANESTHESIA

 Anesthetic induction using injectable anesthetics is fairly simple. It involves

admininsistration of the drug and monitoring the depth of anesthesia. Supportive care
may be needed. Maintenance of injectable anesthesia can be through repeated bolus
doses of the drug or through a constant infusion. Infusion rates are calculated based on
the clearance time of the drug. Bolus dosing is simpler. Typically, 1/2 of the original dose
is given for repeat doses.
 Injectable anesthetics can be administered by various routes depending upon the specific
compound. The most frequently used routes of administration in laboratory animals are
intraperitoneal, intramuscular and intravenous. Less frequently used routes, among
others, are intrathoracic, oral and rectal. Techniques are described below. Contact RAR
at 624-9100 for training materials on handling animals and administering injections.

Intravenous(IV)

 Method - An appropriate vein must be selected. For large animals, the saphenous,
cephalic or jugular veins are best. For rodents, the tail veins are best. For rabbits and
swine, ear veins may be used. The vein is held off proximal to the venipuncture site. The
vessel may be stroked with a finger to stimulate blood flow into it. The needle is inserted
at a 30-45° angle to the vessel. Then the needle is lowered to align with the longitudinal
axis of the vessel and advanced slightly. Draw back. If blood appears in the hub of the
needle, the drug may be injected. If not, try redirecting the needle (before you pull it out
of the skin) and repeat. You may need to try several times while learning. Using a new,
sharp needle for each stick, even if it is the same animal, will improve your chances for
success. Once the needle is withdrawn, it is necessary to put pressure on the vessel to
prevent bleeding.
 Advantages - rapid delivery of drug, ability to titrate dose, irritating substances may be
given IV
  Disadvantages - small veins are hard to access (i.e. small animals), restraint is critical,
developing skill in venipuncture takes experience

Intramuscular(IM)

 Method - Insert the needle into a large muscle mass. Draw back slightly. If blood is
aspirated, you are in a blood vessel. Redirect the needle. When the needle is placed
correctly, inject the drug. The best muscle masses to use are for small animals, the caudal
thigh muscles. For larger animals, the lateral dorsal spinal muscles or the cranial or
caudal thigh muscles may be used. When administering into thigh muscles, inject from
the lateral aspect, or if from the caudal aspect, direct the needle slightly lateral. This will
help avoid injecting into the sciatic nerve.
 Advantages - Fairly rapid absorption, technique is simple
 Disadvantages - IM injections are painful, small volumes are necessary, the animal may
try to bite or escape

Intraperitoneal (IP)

 Method - The animal is usually restrained in dorsal recumbency. The drug may be
injected anywhere in the caudal 2/3 of the abdomen. However, it is best to try to avoid
the left side in rodents and rabbits because of the presence of the cecum. After the needle
is inserted, draw back. If anything is aspirated, you have likely hit the viscera. Withdraw
and get a new needle before trying again. If the needle is placed correctly the drug may
be injected.
 Advantages - relatively large volumes may be injected (0.5 ml in mice, 2 ml in rats, etc.)
 Disadvantages - technique is more difficult than IM injections, drug may be
administered into the viscera resulting in no effect or in a complication.

Subcutaneous (SQ)

 Method - Pinch an area of loose skin. Inject into the center of the "tent" created by
pinching.
 Advantages - Technique is the simplest of any, large volumes may be given (basically as
much as the tent of skin will hold that doesn't cause discomfort to the animal)
 Disadvantages - Irritating substances cannot be given this way, absorption is slow

INHALANT ANESTHESIA

 Induction of inhalation anesthesia can be difficult. Anesthetic gases are irritating to eyes
and nasal passages. Animals may resist as they begin to lose consciousness or they may
stop breathing temporarily. For this reason induction using a mask or nose cone held
over the animal's nose can only be performed on smaller or non-fractious animals. In
smaller animals gas can be delivered into an induction chamber large enough to contain
the entire animal. Induction via a nose cone or chamber requires delivery of the
anesthetic gas at 2-3x MAC. Frequently an injectable anesthetic is used to induce
anesthesia and the inhalation agent is used for maintenance.
 Maintenance of inhalation anesthesia is normally accomplished by delivering
approximately 1.2 MAC to an animal via a mask or nose cone, or directly into the lungs
via an endotracheal tube. Intubation is recommended whevever possible, particularly
 when a procedure will be prolonged. Endotracheal access is essential to provide
ventilation support.

GAS DELIVERY SYSTEMS

 The most complicated aspect of using inhalant anesthesia is the delivery system. A
delivery system must provide the anesthetic gas to the animal at a known and constant
rate.
 It must also ensure that animals receive adequate oxygen. There are several types of
delivery systems typically used in laboratory animals.

ANESTHETIC MACHINE

 The best method of delivering an inhalant anesthetic is with an anesthetic machine.

These machines precisely mix the gas with air or oxygen and can be easily adjusted.
Machines can vary in construction and design. Anesthetic machines typically require
more training to learn to operate.
 Anesthetic concentration is accomplished by sets of mixing valves or a precision
vaporizer. Vaporizers are easier to use but are very expensive. Vaporizers are calibrated
for the specific anesthetic gas to be used.
 Anesthesia circuits can be re-breathing or non-rebreathing.
o Re-breathing circuits include typical circle systems used in large animals. The
gas/oxygen mixture is delivered to the animal via a one-way valve. When the
animal breathes out the gas passes out another valve attached to a y-piece. This is
passed over a carbon dioxide absorbent and then back into the system. Additional
gas and oxygen are continuously delivered to replace that lost.
o Re-breathing circuits conserve anesthetic gas and the animal's body heat. The
CO2 absorbent must be replaced regularly.
o Non-rebreathing circuits are primarily used for smaller animals that cannot cycle
the valves in a re-breathing system. With newer machines non-rebreathing
circuits are normally only necessary for rodents and birds. In older machines
with metal valves a non-rebreathing circuit may be necessary for rabbits and cats
as well. A Bain system is the most common non-rebreathing circuit available.
o The non-rebreathing circuit is attached to the same anesthetic supply as used for
a re-breathing system. However, the exhaust line is connected directly to the
waste gas scavenging system.
o Non-rebreathing circuits depend on gas and oxygen being delivered at a higher
pressure than is present in the exhaust line. This tends to increase anesthetic
usage and can increase body heat loss in the patient.
 Anesthesia machines must have a waste gas scavenging system. Normally the exhaust
line on a non-rebreating system or the pop-off valve on a re-breathing system is
connected to a vacuum line or to the building exhaust. Other scavenging systems can be
used, contact RAR at 624-9100 or Environmental Health & Safety at 626-5804 for
further information on anesthetic delivery systems.

Apparatus for rodent anesthesia

 Left: a non-re-breathing nose cone that can be used with a large animal anesthetic
machine; Middle: a typical drop system closed anesthetic chamber; Right: a gas
scavenging system that can be used with a drop system.

PREPARATION, MONITORING AND MAINTENANCE OF

NORMAL PHYSIOLOGY

 A variety of things must be done to prepare for anesthesia. Once animals are under
anesthesia they must be monitored closely while they are anesthetized to ensure that
they do not become too deep and die, and to ensure that they do not become too light
and experience pain from the surgical procedure.
 Normal physiologic functions such as body temperature, respiration and cardiovascular
function must also be monitored and supported while the animal is anesthetized.
 For all major surgical procedures on non-rodent mammals, an intra-operative anesthesia
record must be kept and included with the surgeon's reports as part of the animal's
record. The anesthetist must be prepared to handle emergencies if they occur.

PREPARATION

 Withhold food and water from large animals for 12 h prior to anesthesia and from
small animals for 2 h to prevent regurgitation and aspiration. It is not necessary to
withhold food and water from rodents prior to anesthesia. Prolonged food or water
deprivation are distressful to animals and are rarely necessary. Please consult RAR's
policy for fasting requests.
 Have all drugs and equipment ready before the animal is anesthetized. You may
not have time to look for things once the animal is under.
 Have an assistant: Anesthesia takes time to perform and monitor. A person should be
available to assist so the surgeon does not have to break sterility to monitor the animal or
administer medications.
 Premedication with atropine or glycopyrrolate (anticholinergics) may reduce the
respiratory tract secretions in some animals
 Protect the eyes from drying out using an ophthalmic ointment and protect them from
being contaminated with surgical scrub solutions. Also protect pressure points, such as
bony protrusions, from pressure necrosis or peripheral nerve damage by providing
padding between the animal and the table.

RESPIRATION

 Most anesthetics cause direct depression of the respiratory center in the brain and
reduce ventilation. This is complicated by other factors that may interfere with
respiration. When an animal is in lateral recumbency the lung that is down is being
compressed by the rest of the body. Likewise, animals in dorsal recumbency may
experience compression of the diaphragm by abdominal viscera.
 The airway may be compromised by regurgitated food or pharyngeal and tracheal
secretions that normally would be removed by reflex swallowing or coughing. These
reflexes are lost during anesthesia. There are several ways to monitor and support the
ventilation of an anesthetized animal.
 Intubate the trachea whenever possible, even if injectable anesthetics are being used.
Intubation can be achieved on animals as small as a rat. This will prevent aspiration
pneumonia and allow you to assist respiration if the animal stops breathing. Contact
RAR at 624-9100 for training materials.
 Assist respiration during the procedure. This can be done with a mechanical
ventilator. However, mechanical ventilation is rarely needed (unless a thoracotomy or
diaphragmectomy is being performed) and can be detrimental to the animal if over-
done. Attaching an AMBU bag to the endotracheal tube or using an anesthetic machine's
rebreathing bag will allow you to administer a deep breath every 2-5 min during the
procedure. This will inflate all areas of the lungs and improve gas exchange. If the animal
is not intubated, ventilation can be performed using a nose cone or face mask.
 Monitor respiratory function throughout the procedure and recovery.
o Monitor respiratory rate and depth (compare to normal for your species. You can
expect them to be slightly decreased). Observe chest movement, or use a
stethoscope or esophageal stethoscope.
o Monitor the color of the mucous membranes (gums, conjunctiva, vulvar mucosa).
A bluish color means the animal is not getting enough oxygen- ventilate!
o Red-tinged foam present in the airway along with dyspnea (difficulty breathing)
may indicate pulmonary edema. This can result from overventilation or
overhydration. A diuretic like furosemide can be administered, but prognosis is
poor.
o Sophisticated respiratory monitoring can be achieved by measuring blood gasses,
or expired oxygen and carbon dioxide concentration or by use of a pulse
oximeter.

FLUID THERAPY

 Many anesthetics have direct effects on the heart or vasculature, decreasing cardiac
output and blood pressure. This is further complicated by increased fluid requirements
during anesthesia and surgery that may result in hypovolemia.
 Fluid requirements are increased because: breathing dry, cold oxygen (if inhalant
anesthesia is used) increases respiratory fluid loss; the animal has not received its
normal fluid intake since it was fasted; fluid may be lost through hemorrhage or
 exposure of moist viscera to room air; many anesthetics are metabolized in the kidney
(creating a slight diuresis minimizes renal toxicity).
 To minimize the effects of surgery and anesthesia on hydration:
o Place an intravenous catheter whenever possible to provide access for fluids
and medications
o Supplement fluids, intravenously if possible; otherwise intraperitoneally or
subcutaneously
 Fluid should be supplemented at the rate of 5-10 ml/kg/hour during
anesthesia
 Monitor hydration status- Overhydration results in frequent urination
and pulmonary edema, underhydrationresults in sticky mucous
membranes, loss of skin elasticity, the eyes sinking into the orbit, decrease
in blood pressure and increase in heart rate
 To replace blood loss with saline or lactated ringers, administer 3X the
volume of blood lost by slow IV drip. Monitor the hematocrit. If it drops
below 20%, whole blood replacement may be necessary.
 Monitor cardiovascular function by monitoring one or more of the following:
o Mucous membrane color and capillary refill time (the time it takes for the
mucous membranes to regain their normal color after pressure is applied)
o Heart rate and rhythm - stethescope or esophageal stethoscope
o Pulse rate and pressure - using your fingers
o Blood pressure - arterial catheter or Doppler cuff required
o ECG - If the animal has pale mucous membranes, the capillary refill time is
greater than 2 seconds, or if the other cardiovascular parameters are out of
normal range (determine normal for the species you are using!) you may have a
cardiovascular emergency. Increasing the rate of intravenous fluid
administration will improve cardiac output temporarily. However the depth of
anesthesia will need to be reduced and if there is a primary cardiac problem it
will require specific treatment. Consult with an RAR veterinarian for more
information on anesthetic emergencies.

THERMOREGULATION

 Animals frequently become hypothermic during anesthesia because of inhalation of cold

gases, exposure of body cavities to the room air, and loss of normal thermoregulatory
mechanisms and behaviors.
 Hypothermia depresses all physiologic functions, including respiration and cardiac
function, slows the metabolism of anesthetics and results in prolonged recoveries.
 All of these can contribute to anesthetic death. Hyperthermia is less common, but may
occur because of excessive application of heat, hot surgery lights or malignant
hyperthermia in genetically pre-disposed animals. To thermoregulate your patient:
o Monitor the body temperature frequently using a thermometer during the
procedure and during anesthetic recovery. While animal normals vary from
species- to-species, in general, when body temperature drops below 99° F, an
animal is considered hypothermic. Below 95-96° F an animal cannot regain
normal body temperature without supplementation.
o Prevent heat loss by insulating cold surfaces with a blanket
o Prevent heat loss during gas anesthesia by utilizing low flow techniques that
conserve heat
o Supplement heat with a thermal blanket (keep blanket temperature below 40
C to prevent burns!) or with pre-warmed fluids
 o Treat hyperthermia by administering intravenous fluids or applying water to
foot pads or exposed skin. Only use an ice bath as a last resort, as it may cause
cardiovascular shock.

MONITORING ANESTHESIA

Monitoring anesthesia

 The depth of anesthesia must be monitored carefully. Animals that are too light will
experience pain and may move during the procedure. Animals that are too deep run
the risk of experiencing cardiopulmonary arrest. If an animal is too light the
anesthesia should be supplemented, if too deep, animals on gas anesthesia can be
turned down.
 Animals given injectable anesthetics can not be lightened directly. Instead
respiratory and cardiovascular support must be administered until the anesthetic is
metabolized and the animal begins to lighten on its own.
 To monitor the depth of anesthesia, perform the following:
o Reflexes - these reflexes disappear as the animal becomes deeper in the
following order:
 Palpebral reflex - touching the eyelids causes blinking. The animal is
light if it is blinking.
 Toe pinch reflex - pinching the toe or foot web will cause a pain
response. If the animal withdraws the toe it is not deep enough. If it
doesn't, it is not sensing pain.
 Corneal reflex- touching the cornea of the eye with a tuft of cotton
results in a blink. Once the animal has lost its corneal reflex, it is too
deep.
o Muscle tone increases as the depth of anesthesia decreases, unless the
animal is receiving a cataleptic drug like ketamine in the absence of a
sedative. Test muscle tone by pulling on the lower jaw or a limb. Rigid tone
indicates inadequate depth of anesthesia.

Monitor cardiopulmonary function and body temperature

  As an animal becomes too deeply anesthetized, respiration and cardiac output
decrease, resulting in poor blood oxygenation and tissue perfusion and decreased
blood pressure and temperature. Likewise, elevations in heart rate and blood
pressure may be indications that an animal may be feeling pain and is anesthetized
too lightly. Monitor as previously described.

Anesthetic Dose (mg/kg) Indications

Emergency Drugs
Doxopram (Dopram) 1-5 IV (10x in Respiratory stimulant, for complete
farm animals) respiratory arrest only, use with CPR
Furosemide (Lasix) 2- IV, IM For pulmonary edema. Administer as needed
Naloxone (Narcan) 0.04 IV For reversal of narcotic sedation or respiratory
depression
Yohimbine 0.1-0.15 IV Reversal of xylazine or detomidine sedation
Atropine 0.02-0.04 IV For bradycardia
Epinephrine 0.1 ml/kg IV, IT, For cardiac arrest only. Administer IV,
(1:1000) IC, IM intratracheal or intracardiac and perform
cardiac massage
Lidocaine 2, IV (0.5 mg/kg For diagnosed ventricular tachycardia only.
in cats) Administer to effect and monitor

Recovery

 Monotoring and support must continue until the animal is completely recovered
from anesthesia. Complete recovery means the animal is able to hold itself in a
normal upright position, has returned to normal body temperature and all
physiological indices are within normal limits.
 Anesthetic recovery can be rapid for gas agents and short anesthetic episodes.
Recovery time can be prolonged if animals were under for a long time or if injectable
agents were used.

MODULE-20: PRODUCTION AND PROPERTIES OF X – RAYS

Learning objectives

This module deals with

 Types of X-ray apparatus

 Parts of X-ray machine
 Production of X-rays
 Properties of X-rays
 BASIC INTERACTION OF X-RAY WITH MATTER

 For an x-ray examination, the part to be examined is kept between the x-ray source and
an x-ray film. Thus the x-ray beam emitted by the machine traverse through the part to
be examined to reach the film, carrying useful information that is recorded as a image on
the film. While passing through the patient.
 Some x-rays are differentially transmitted through the patient carrying
information.Some photons are absorbed and least to exist.
 Some are deviated from their course as scatter radiation which decreases the quality of a
radiograph by causing fog on the film.X ray photon can interact with matter in five ways
of which the Photoelectric effect and Compton effect are important in diagnostic
radiology.
o Coherent scattering
o Photoelectric effect
o Compton effect
o Pair production
o Photo disfiguration

Photoelectric effect

 The effect is mostly produced when x-ray photos interact with inner shell electrons of a
atom (KLM). It occurs more with low energy incident photons and high atomic numbers
element, provided that the photons have sufficient energy to over come electron building
energy with atom.

Compton effect

 As an incident photon encountered a free electron of the outer shall of the atom, the
photon travel in a new direction as scatter radiation.Compton effect produce almost all
the surface radiation encountered is diagnostic radiology.It is the major radiation
hazzard y fluorspar examinations.
 Photon defected at a narrow angle is electron to reach the film being exposed to cause
fog.When an incident photon with energy slightly greater than the binding energy of a k
shell electron encounter the scatter, the k shell electron is affected from its shell. The
photon disappears as most of its energy is utilized to over come the binding energy of k
shell electron.
 The free electron flies off as photoelectron. Another electron from an adjacent or outer
shell of another atom immediately fills in to the void created by an ejected electron. As
this electron drops in to the created void, it gives off energy is the form of
characteristicradiation.

Uses in diagnostic radiology

 Contrast of the image is enhanced.

 No scatter radiation – Excellent quality of radiology
 Increases radiation ion of patient.

TYPES OF X-RAY APPARATUS

Portable apparatus

 Portable x-ray machines are widely used in veterinary practise.

 The advantages are
o They are less than other types of machines.
o They need little maintanence.
o They can be operated from any 15 A electrical point .
o They can be easily transported.
o They are light and easily manoeuvered .
 The disadvantages is their low milliamperage necessitates longer exposure time and it
predisposes to movement blur. Maximum output is 70 - 90 Kv and 15-30 mA.
 Uses
o Suitable for x-raying of limbs below stifle and elbow of large animals and
abdomen and skeletal system of small animals.

Mobile x-ray apparatus

 In machines of this type the transformer are larger to permit higher output and hence
cannot be transported easily. They are mounted on wheels , and are cumbersome to use
for restive animals. The output varies from 40-60 mA and 90Kv. (the maximum of 125
kv and 300mA)
 Uses
o Can be used for large animal for radiographing head , neck, and limbs and this
machine is quite useful for small animal practices

Fixed x-ray apparatus

 This machine requires transformer which have to be built in the room and special
electric connection (3 phase). The output ranges from 300 - 1000mA and 120-200kv.
This type of mahcines are suitable only for big institutions because of high expenses
involved. Suitable for both large animal and small animal radiography.

Properties of x-ray beam

 X-rays are invisible to eye & travel at high speed & at straight lines
 They can penetrate objects depending on atomic no, density, thickness of the material
 Photographic effect - on photographic emulsions x-rays ionises silver halides on the
photo film
 Fluoroscent effect - certain chemicals such as zinc sulphide, calcium tungstate etc
fluoresce when exposed to x-rays & emit green or blue light. This effect is utilised to
intensify the x-ray effect by using intensifying screen in the x-ray cassetes.
 Biological effect - x-rays ionises the atoms & bring about disturbances in the cells by
chemical activity which may cause either destruction or activation or mutation.

Collimation of X-ray beam

  The x-rays because of diverting property is capable of extending to a considerable width.
So the X-ray machine incorporate some mean to collimate or restrict the beam. The
purpose is three fold & they are
o To prevent unnecessary radiations of the patients or persons restraining the
animals
o To reduce the scattered radiations.
o To minimize genetrical distortion.
 This is done by using cones or light beam diaphragm in a semi-darkened room.

PARTS OF X-RAY MACHINE

 It consists of four main parts

o X-ray tube,
o Transformers,
o Tube stand and
o Control panel.

X-ray tube

 An X-ray tube consists of a large thermionic diode glass tube which has been
evacuated to produce a high vaccum and in to which are sealed two electrodes, the
cathode (-) and the anode (+).
 Stationary or rotating is placed 1 - 3 cm apart. The glass tube is made of borosilicate
to with stand high temperature generated inside.
 The passage of a high kilo voltage electric current across the electrodes results in the
production of X-rays.
 The glass tube isfitted in to an oil filled casing and the whole assembly is housed in a
metal encased with lead covering with a small opening for the useful X-rays to exit
after filtration.
 The vacuum in the tube creates a free flow for the electron beam and also prevents
oxidation of cathode filament.
 This also increases tube life. The oil in the tube helps to dissipate heat apart from
acting as a electrical insulator.
 Cathode
o The negative electrode consists of tungsten filament and a focussing cup and
it serves as the source of electrons. Tungsten is preferred because of its high
melting point ( 3370 c) and high atomic number.The tube current is
measured in milliampereage and decides the number of electrons flowing per
second from the filament to the target.
o Modern machines have two filaments made of tungsten -rhenium alloy to
increase the thermionic emission efficiency and hence the tube life. Focussing
cup is a concave cup made of nickel or molybdenum and its function is to
restrict the electron cloud to a small beam.
o Immediately prior to making an x ray exposure the filament is heated to
create an electron cloud by a low voltage current (average about 10 volts and
 amperege about 3-5.)The tube current decides the quantity or intensity of the
x rays produced and also can be altered in the control panel.
 Anode
o Anode is the target made up of thin sheet of tungsten embedded in a copper
block serves to obstruct the electrons to make them give up their energy. As
99 % of it is converted in to heat, the heat produced at the target is rapidly
transferred to the copper block and hence to the oil. The anode angle differs
according to individual tube design and may vary between 10 deg and 20 deg
and the size of the focal spot may vary from 0.3mm to 2 mm.
o It is important that the x ray beam should arise from the smallest practical
portion of the anode. This area is often termed as target or focal spot.
o Larger x ray tubes possess rotating anode to with stand the heat generated
due to large exposure.
o There are two types of anode - stationary and rotating.
o The stationary one is used in dental x ray machines.

Transformers

 This consists of an auto transformer, a step down or filament transformer and a high
tension transformer.
 A auto transformer corrects the fluctuations in input voltage, step down transformer
permits the suitably reduced current to the cathode, and the high tension
transformer produces a high voltage current for the production of x rays.

Tube stand

 This is to support the x ray tube during the exposure.

Control panel

 This contains the meters switches, on and off voltameter, kilovoltage selector, milli
amperage selector the timer, and exposure button.

PRODUCTION OF X-RAYS

 X rays are produced by energy conversion when a fast moving streams of electrons is
suddenly decelerated in the target anode of the x-ray tube,or by bombarding a tungsten
target with an electron beam it gives up some of electron of its energy .
 Most of the energy (over 99A) will be transformed into heat; the reminder of the energy
will be converted into x-rays.
 As x-ray beam passes thriough the patient differential absorption takes place depending
on the tissue density and shadowgraph is obtained.

Electron orbits and energy level

  Electrons are negatively charged particles revolving round the nucleus.Since an atom is
electrically neutral in its normal state, it must contain an equal number of protons and
electrons.
 The atom resembles a tiny planetary system with the nucleus as the sun and the
electrons as the orbiting planets.
 X rays are generated by two different process when high speed electrons lose energy in
the target of the x ray tube due to radiative interaction.

Characteristic radiation or Line radiation

 When the projectile electron interacts with the electron in the K shell of the traget atom
rather than the electron in the outer shell it results in the ejection of electron in the K
shell if the energy of the projectile electron exceeds the binding energy of the ejected
electron. This results in transient electron vacancy in the K shell into which an electron
from the outer shell or from another atom falls and this process continues till the atom
becomes stable. This shifting of electrons results in emission of X-ray photon which
possoses an energy equal to the difference between the binding energies of the electrons
involved. Hence the X-ray photon energy is characterisitic of the shells involved in an
element and so called as characteristic radiation.

Bremstrahlung radiation or Breaking radiation

 When the projectile electron approaches the nucleus of the atom avoiding the orbital
electrons, it slows down, due to the opposite charges, and gets difflected from its original
course. During this the incident electron loses its kinetic energy, due to its slow down,
and this loss of kinetic energy is emitted as X-ray photon.
 The X-ray produced by this type is called bremstrahlung or breaking radiation. The
incident electron may also collide with the nucleus at times, converting all its kinetic
energy to a single X-ray photon.

TYPES OF X-RAY APPARATUS

 X-rays remain the main domain in diagnosis although various other imaging specialities
were later explored and being practiced.
 The main reason behind this is the cost of the equipment involved in the latest imaging
techiniques. This makes use of X-rays for its wide application amd so also its potential
harmful effects. Hence physics of X-ray production and priciples involved must be
explained.
 Matter in the universe is a substance made up of mass and occupies space. Einstein law
of conversion of energy states matter and energy can neither created nor destroyed as its
mass, energy or charge remain unchanged Like matter, energy may exist is many forms
eg: Kinetic energy, electric energy, potential energy, chemical energy, nuclear energy,
heat energy, electro magnetic energy etc. energy of one form can easily be converted into
another form. For example X-rays are produced in X-ray machine from electrical energy.

MODULE-21: FACTORS INFLUENCING PRODUCTION OF X-

RAYS
Learning objectives

This module deals with

 Factors affecting radiographic quality

FACTORS AFFECTING RADIOGRAPHIC QUALITY

 An good diagnostic radiograph is one is which there excellent details, correct density
and the proper scale of contrast. The proper use of various radiographic exposure
factors KVP, mA Time and FFD are employed.

Detail

 Detail is the degree of definitions of an object on a radiograph. Good detail is the true
reproductions of an object. The factors affecting the detail are:
o Shorter Focal Spot film distance. (FFD)
o Closeness of the object to the film.
o Use of intensifying screen.
o Movement of either the patient, cassette on movement of the machine.
o Screens, film contrast.
o Over exposure or under exposure.
o Focal spot size.
o Any condition fogging the film will bring out loss of detail.

Density

 Radiographic density is determined by the amount of light absorbed by an exposed

x-ray film and is a measure of the degree of blackness of the film.
 Radiographic density is affected by te subject density which the weight per unit
volume of different body constituents.
 The density of the radiograph varies directly with milliamperage, provided all other
factors remains constant.
 Higher milliamperage produces more x-rays and thus more density and lower
milliamperage results is less density. Radiographic density varies directly with
exposure time.Radiographic contrast is the difference in density between the image
of parts or structures on the radiograph.

Contrast

 Contrast is the difference between blacks, grays and whites. There can be long scale
contrast and short scale contrast. Radiographic contrast varies inversely with the
kilovoltage. The lower the kv produces a radiograph with a “short scale of contrast”.
Secondary radiation and scattered radiations causes lack of contrast. Improper
 development of film and use of warm developer cause lack of contrast.To get good
radiograph in veterinary patients the following technique should be followed
o Fastest exposure time possible (To prevent movement blur)
o Higher kvp.
o Constant distance
o Constant milliamperage

Viewing of the radiograph

 Radiograph should be viewed on a good, evenly lit viewing box, in a semi darkened
room.
 Over exposed film should be viewed against bright light. Though provisional
diagnosis can be given on a wet film, it is advisable to wait till the film is dry, before
giving final diagnosis.
 When viewing radiographs of the dorsoventral or ventrodorsal or skull, the left side
of the film should be facing the viewers right side and when viewing the lateral views
it would be better that the anterior aspect should be directed towards the left side of
the viewers. Always follow the same conventions.
 To give radiological interpretation the viewer must have a comprehensive data of
clinical and physical examinations and also have a knowledge of the range of
radiological animal anatomy and for this a library of normal films taken in the
standard position is an asset.

MODULE-22: PRINCIPLES OF VIEWING AND INTERPRETING X

- RAY FILMS

Learning objectives

This module deals with

 Handling of X-rays
 Viewing of X-rays
 Interpretation of X-rays

HANDLING, VIEWING AND INTERPRETATION OF X-RAYS

Handling

 Cassettes with exposed film should be opened in a dark room and the film is removed by
holding the corners. The film is loaded in a suitable size cassette and stored in lead lined
boxes.
 The loaded cassettes and the exposed film cassettes are kept with radiopaque surface
upwards. Unexposed film boxes are always kept in lead lined boxes.

Viewing
  Radiography should be viewed on a good evenly lit viewing box in a semi darkened room.
 Dorsoventral chest, ventrodorsal abdomen or skulls are viewed with a right side of the
film facing the viewer’s left side.
 Lateral view radiographs are viewed by placing it facing left. Radiographs of extremities
are viewed with lateral aspect on left side of the viewer.

Interpretation

 The three important factors to be considered before interpreting a radiograph are

o Case history,
o Physical examination and
o Correct radiographic technique.

Radiographic diagnosis

 Radiographic diagnosis consists of two parts namely location of the lesion and
classification of the lesion. Location of the lesion requires knowledge of normal
radiographic anatomy, basic radiographic signs in terms of changes such as size,
architecture, contour, density, position and function. A systematic and methodical
examination of each radiograph will prevent overlooking unexpected lesion.

Classification of Lesion

 The lesions in the radiograph are classified as developmental, metabolic, traumatic,

infectious, neoplastic, and degenerative.

MODULE-23: RADIOGRAPHIC LESIONS - THORAX

Learning objectives

This module deals with

 Radiological pathology of thorax

RADIOLOGICAL PATHOLOGY OF THORAX

Cardiomegaly

 Outline of the heart becomes more rounded.

 Occupies a much larger area of the thorax.
 Trachea and major blood vessels are seen displaced.
 Posterior border of heart becomes straighter.
 Cardiac silhouette in contact with sternum and diaphragm.

Bronchitis
  Slight increase in the radio-density of the bronchial tree

Pneumonia

 Areas of increased density of lung substance.

 Areas of consolidation can be visualized

Pneumothorax

 Collapse of the lungs.

 Presence of air in the pleural cavity
 Floating heart shadow

Fluid in the pleural cavity

 Fluid shadow will be masking the structures in the thorax.

 Fluid level appears as area of increased density.
 Typical leafy appearance

Diaphragmatic Hernia

 Disappearance of the normal diaphragm line.

 Displacement of lungs and visualization of part of GI tract in thoracic cavity.

Tuberculosis

 Areas of opacity in lung parenchyma

 Recognition of cavitations and calcified nodules in the lung parenchyma or pleura.

MODULE-24: RADIOGRAPHIC LESIONS - ABDOMEN

Learning objectives

This module deals with

 Radiological pathology of abdomen

RADIOLOGICAL PATHOLOGY OF ABDOMEN

Gastric torsion

 Greatly distended gas filled organ occupying the major portion of the anterior abdomen.
Compartmentalization of stomach.

Oesophageal achalasia
  Distended organ occupying the upper half of the chest in the lateral view
 Dorsoventral view-distended organ projecting beyond the shadow of the spine

Oesophageal foreign body

 Thickening of the oesophageal wall

 Increased density from that of the surrounding tissues.

Pyloric Obstruction

 Enlargement of the stomach

 Accumulation of fluids/material (accumulation of barium) in pyloric area.

Intussusceptions

 Sausage shaped mass with increased density

 Thin layer of gas outlining the layers of intussusceptions
 Barium enema- ‘coiled watch spring’ pattern.

Hydronephrosis

 Large mass with a smooth outline in the anterior abdomen filled with fluids, with
appearance of homogenous density

Kidney calculi

 Small irregular dense areas roughly central to the kidney outline

Cystic calculi

 Radiopaque cystic calculi easily visualized slightly radiopaque calculi can be

demonstrated by using penumo cystography.

Prostate enlargement

 Relatively dense mass just anterior and ventral to the pelvic brim in the position
normally occupied by the bladder, which is displaced anteriorly.

Metritis and pyometra

 Slight thickening and enlargement of uterus- may be uniformly tubular or sacculated.

 Displacement of the colon.

MODULE-25: RADIOGRAPHIC LESIONS - LIMBS

Learning objectives

This module deals with

 Radiological pathology of bones and joints

RADIOLOGICAL PATHOLGY OF BONES AND JOINTS

Radiographic signs of bone diseases

 Altered contour of the bone

 Altered size of the bone
 Decreased one density
 Change in trabecular pattern

Radiographic signs of joint diseases

 Widening or narrowing of the joint space

 Cystic changes
 Swollen joint capsule-soft tissue swelling

Osteoporosis

 Diminished density of the bone.

Small animals

 Hip dysplasia
o Bony exostosis, new bone formation involving acetabulum- thickened
disorganized appearance of the femoral neck-remodeling and flattening of the
femoral head.
 Hip dislocation
o Abnormal width of intra articular space.
 Long bone fractures
o Disruption of the continuity of a bone

MODULE-26: CONTRAST RADIOGRAPHY - CLASSIFICATION,

MATERIALS, INDICATIONS AND CONTRA INDICATION

Learning objectives

This module deals with

 Contrast radiography and its classification

 Intravascular contrast agents and contrast radiography
 CONTRAST RADIOGRAPHY - CLASSIFICATIONS

 Radiography is founded upon the principle that an object when exposed to an incident x-
ray beam will absorb a part of the x-ray beam and a part willpenetrate the object and
interact with the film. Radiodense objects absorb larger percentage of the x-rays than
radiolucent objects resulting in less film exposure and the recording of white object
image.
 In other words, the absorption of x-ray by the tissues of the body, and thus their
radidensity, depends upon the atomic weight of the principal substances of which the
tissues are composed. That means absorption capacity of an organ or object is directly
proportional to the number of orbital electrons in the atom of the molecule of the
absorbing material (atomic number). Comparison of equal volumes of different
tissues/with their densities.

Density

 Barium - 56
 Bone - 14 (Average)
 Muscle, Organ, fluid
 Soft tissue 7.4 (Average)
 Fat - 6.3
 Gas (Air) - 1 to 2
 The differences in density (radiographic contrast) between bones, muscles, fat and gas
form the basis of plain film radiography. Ex: Kidney is seen clearly in a plain radiography
if there is perirenal fat around the organ. Bone is clearer because of surrounding soft
tissues.
 But the kidney pelvic is not visible or the mucous pattern of bladder or stomach are not
seen normally due to lack of contrast.
 Artificial methods of delineating such organs are required and so a suitable contrast
medium is employed. The contrast medium may have either high atomic weight and
provide positive contrast or a low atomic weight and provide negative contrast. Examples
of positive contrast media re Barium sulphate, organic iodine compounds. Examples of
negative contrast media area co2, o2 and N20 or atmospheric air.

Positive contrast agents

 Positive contrast agents can be precisely classified and may be divided into five main
groups.
 Agents used for the demonstration of Alimentary tract.
 The substance used for this purpose should be insoluble and non absorbable and inert.
The substance used routinely for this purpose is barium sulphate.

Water soluble agents

 These form the largest single group of contrast agents. The ideal criteria for the contrast
media included in this group are that they should be (1) opaque to x-rays and they all
contain iodine (2) pharmacologically inert (3) very water soluble so that they can be
injected at high concentrations (4) chemically stable so that the iodine is not released in
the body (5) rapidly excreted by the kidneys; (6) of low viscosity for injecting quickly
 through a small catheter and (7) of low toxicity and irritancy so that large quantities can
be employed.
 The conventional water soluble contrast media are ionic and are therefore hypertonic
and their osmolality ranges from 4 to 7 of that of blood. The newer low osmolar non-
ionic contrast agents have ratio 3 contrast as compared to the conventional high osmolar
ionic contrast agents which have only ratio 16. Contrast property. Ex: Conray, Urografin
(Ionic agent); Iohexol, Iopamidol metrizamide (non-ionic)
 Agents excreated selectively through biliary system to study the gall bladder, after
absorption from alimentary system or intravascular injection. Ex: Biligrafin and Ipodate
calcium powder (solu-Biloptin) (Scheringe).

Viscous and oily agents

 These agents are developed to overcome immediate climination which occure with the
water soluble preparation. Viscous solution are used to demonstrate bronchial tree and
the uterus.
 Oily solutions are used in those situation in which it is essential to avoid even the
slightest local irritation once introduced they are slowly climinated.

Radiographic quality

 Gaseous agents: Are those most frequently employed. They are cheap easy to administer
and are comparatively safer.

INTRAVASCULAR CONTRAST AGENTS AND CONTRAST

RADIOGRAPY
CONVENTIONAL IONIC MEDIA
Generic name Proprietary name
Meglumine iothalamate Conray-280
Sodium iothalamate Conray-420
Meglumine diatrizoate Urografin-150
Sodium diatrizoate Urografin-370
NEW LOW OSMOLAR NON-IONIC MEDIA
Metrizamide Amipaque
Iopamidol Niopam
Iohexol Omnipaque

Angiography

 The radiographic demonstration of the vascular system by the injection of a water

soluble organic iodide compound into a suitable vessel. Specialized techniques
o Arteriography-Arteries
o Venography-Veins
o Aortography-aorta
o Portal venography–Portal vein
o Angiocardiography-Heart and vessels
o Cerebral angiography–Cerebral vessels
Technique

 Contrast agents are injected rapidly by means of a syringe of an appropriate volume

connected to a hypodermic needle or cannula or catheter which is inserted into a suitable
blood vessel. Radiographs are taken immediately on completion of the injection.

MODULE-27: CONTRAST RADIOGRAPHY - THORAX AND

ABDOMEN

Learning objectives

This module deals with

 Radiography of alimentary tract

RADIOGRAPHY OF ALIMENTARY TRACT

Indications

 To reveal obstruction of the alimentary tract. Ex: Tumour or stenosis.

 To find out distorsion of the wall of alimentary tract such as enlargement. Ex: Dilatation
of stomach or oesophagus.
 To find out displacement of the alimentary tract. Ex: Hernia.
 To reveallesions in the wall of the alimentary tract. Ex: Neoplasms – Ulcer.

Procedure

 Oesophaqus
o No preparation is required. Take plain radiography and administer Barium
sulphate paste about 50 to 100 Gms. Orally (Braium Swallow) and taken with
lateral and ventrodorsal projections immediately after administration.
o Normal oesophequs should not retain bacium. Only a thin streak of barium
indicating the position of the oesophegus and outlining the mucous surface is
seen as normal oesophagus is a collapsed tubular structure.
 Stomach
o 50 to 100% suspension of about 15 to 100 ml. Is given orally observed under
fluoroscopy or x-rays are taken at regular intervals 10 minutes, 30 mts, 1 hr. and
4 hrs. etc. at different angles like left lateral, right lateral, ventro dorsal and
oblique if necessary to demonstratethe different areas of stomach and mucosal
surface.
o The stomach should be empty by starving overnight or by administering laxative
or enema if necessary.
o Normal stomach start emptying the barium within minutes after the
administration. Space occupying lesions or obstructive lesions can be easily
demonstrated.
 Small Intestine
 o To promote easy passage of the contrast agent 25% suspension is preferred.
Repeated x-rays at interals could demonstrate lesions inside or outside the
intestine easily. Intestinal motility can be assessed.
 Large Intestine
o To demonstrate large intestine barium is best given by enema. Double contrast
gastrography or colonography can be obtained by combining air (negative
contrast agent)
 The functional and anatomical abnormalities could be better assessed by means of
flucroscopy apparatus, if available.

MODULE-28: CONTRAST RADIOGRAPHY - URINARY SYSTEM

AND SPINAL CORD

Learning objectives

This module deals with

 Myelography
 Urography

MYELOGRAPHY

Indication

 To outline the neural canal

 To demonstrate disc lesions and other space occupying lesions.
 Contrast agents used
o Oily fluid containing 40% iodine (Ex. Myodil).
o Water soluble: Metrizamide soluble. Iohexol, Iopamidol solution.

Technique

 Cysterna puncture
 Lumbar puncture
 Under general anaesthesia the contrast agent is injected into the sub-arachnoid space. In
the first method cisterna magna is punctured and in the second method sub-arachnoid
puncture is made using a spinal needle between 4th and 5th Lumbar vertebral space in
lateral recumbent position.If myodil is used the quantity is 0.5 to 2 ml. Per animal.
 The animal may be positioned in an inclined plane for easy flow caudally. Pictures are
taken at 5 mts. And 10 mts. Interval under lateral and ventrodorsal projection. If
Metrizamide or any other water soluble agent is used, 0.3 ml. To 0.5 ml/kg.body wt. Is
injected into the subarachnoid space and x-rays are taken immediately.
 The advantage of the new water soluble non-ionic solution is that it gives better
visualization of the spinal canal and the agent gets eliminated within few hours. In the
case of oily agents the contrast material will tend to globulate and remain in the canal for
longer period causing at times undesirable side effects.
 UROGRAPHY: (PYELOGRAPHY AND CYSTOGRAPHY)

Intravenous urography (Intravenous pyelography, IVP)

 Pyelography is used to demonstrate kidney shadow when it cannot be demonstrated in a

straight radiography.
 To show the presence or absence of lesions in the renal pelvis.
 To get a rough indications about renal function.
 Contrast agents used
o Ionic contrast agents such as sodium Iothalamate (conray-420); Meglumine
Iothelamate (conray-280); Sodium and Meglumine diatrizoate (Uregrafin 60% or
76%); Sodium diatrizoed (Hypoque). Non-ionic contrast agents such as Iohexol
(Omnipaque-300); Iopamidol (Niopem) Metrizamide have also been used.
 Dosage: To give better demonstration upto 600 mg to 1200 mg/kg. Body weight may be
administered I/V usually 1 to 2 ml/kg. Body weight.
 Preparation: With hold food for 24 hrs. and water for 12 hrs. Empty the bowels with
enemata. Anaesthesis as optional
 Technique
o Inject the dyeasa single bolus I/V by taking about 1 minute. Straight firms may be
taken before injection and subsequent to injection at 1 mt. 5 mts., 10 mts. And 20
mts. With ventrodorsal and lateral projections. Use of a compression bandge over
the abdomen will enhance the clarity of renal pelvis and ureter.
o This technique is popularly known as intravenous pyelography or excretory
urography. Another method to carry out this procedure is to mix the contrast
agent about 1200 mg/kg. With 150 to 250 ml. Of normal saline and given by drip
taking about 20 to 40 mt. Time to give more accurate evidence of kidney function
and is a safer method.

Cystography

 Indications
1. To recogrise radiolucent small calculi
2. To demonstrate space occupying lesions in the bladder.
3. To demonstrate abnormal prostate gland.
 Preparation: The G.I. tract should be empty. Iodine compund 10 to 20% about 40 to 100
ml. Are employed after catheterizing the bladder.
 Procedure: After evacuating the bladder, inject the contrast agent either iodine solution
or air (100 to 300 ml). Radiography is taken (lateral & ventrodorsal projections). For
double contrast small quantity of iodine solution followed by air may be used for better
visualization of the interior of bladder.

MODULE-29: BIOLOGICAL EFFECTS OF RADIATION,

RADIATION HAZARDS AND THEIR SAFETY MEASURES

Learning objectives

This module deals with

  Biological effects of radiation
 Radiation hazards and safety measures

RADIATION HAZARDS AND ADOPTION OF SAFETY

INCREASERS

Dangers of radiations

 Ionising radiation used in diagnostic radiography is potentially harmful and if proper

protective measure are taken the risk is small compared with the benefit to the patient.
 Certain tissues especially those which contains many multiplying cells, such as blood
forming organs (bone marrow, lymphoid tissue, spleen), the gonads, embryos and cetain
tumours are radiosensitive.
 X-rays have long term effect of producing Cancer, long after irradiation injury has
healed.

MODULE-30: ULTRASONOGRAPHY - PRINCIPLES AND ITS

APPLICATION IN VETERINARY PRACTICE

Learning objectives

This module deals with

 Principles of ultrasonography
 Properties of ultrasound waves
 Different modes of echo display

PRINCIPLES OF ULTRA SONOGRAPHY

Introduction

Medical sonography is the only diagnostic imaging modality that does not use electromagnetic
radiation. Modern ultrasound instruments are highly sophisticated pieces of equipment. A basic
understanding of the physics of ultrasound, its interactions with tissue and the functions of the
controls are important while using the machines. In 1957 – Ian Donald invented – scanner or
diagnostic ultrasound.

What is ultrasound?

 Sound waves of frequencies greater than audible to the human ear i.e greater than 20-
20,000 Hz. is called Ultrasound waves. Diagnostic ultrasound uses frequencies between
1 to 10 MHz
 A sound wave travels in a pulse or a wave and when it is reflected back it becomes an
Echo and this pulse-echo principle, is used for ultrasound imaging. A transducer is a
 device that converts one form of energy to another. The piezoelectrical crystal in an
ultrasound transducer generates a pulse. When this crystal is stimulated electrically it
changes its shape and produces sound waves of a particular frequency. Mechanical
transducers are devices where the movement of crystals suspended in a coupling
medium generates ultrasound.where as electronic transducers also called array
transducers do not have intrernal coupling medium and are fired electronically.

How is ultrasound generated?

 When a high voltage electrical current is applied crystals in the transducer are vibrated
and this is called piezo electric effect.
 A sound wave travels in a pulse and when it is reflected back it becomes an Echo.
 It is this pulse-echo principle, which is used for ultrasound imaging. A pulse is generated
by one or more piezoelectrical crystal in an ultrasound transducer.
 When this crystal is stimulated electrically it changes its shape and produces sound
waves of a particular frequency.
 As the transducer is placed in close contact with the body surface through a coupling
medium it undergoes continuous modification, which occurs through three processes
those are absorption, reflection and scattering.
 By means of the echo principle, an image can be produced on the display of the scanner
which relates to the acaustic independence of tissues encountered by the ultrasound
beam and the depth / distance of tissue interfaces.

PROPERTIES OF ULTRASOUND WAVES

 Frequency, wavelength and velocity are parameters used to describe the sound waves.
 Diagnostic ultrasound frequency ranges between 2 mega Hertz and 13 mega Hertz.
 Wave length is the distance travelled by the sound in one cycle and is expressed in
millimeters and is important for image resolution.
 Velocity is the rate at which sound travels through an acoustic medium. As a rule it is
greatest in solids, lower in liquids and lowest in gases.Medically sound waves travel
fastest in bone and slowest in gas filled structures.
 This causes a problem for diagnostic ultrasound machines, because they use the average
velocity of sound in soft tissue 1540m/s.

Interaction of ultrasound with matter

 Absorption: It occurs when the tissues absorb heat energy in the sound beam.
Absorption process forms the basis of therapeutic ultrasound.
 Reflection: The reflection gives rise to an echo and forms the basis for ultrasound
scanning. Interfaces between tissues of different acoustic impedence give rise to different
echoes. These echoes are converted by piezoelectric effect into electrical signals and
displayed onto a oscilloscope screen.
 Scattering: It occurs when the beam encounters an interface that is irregular and smaller
than the sound beam. The portion of the beam than interacts with this interface is
scattered in all directions. Since the scattering interfaces are small, only a small portion
of the beam is involved. Once the echoes are converted into electrical signals, these are
processed and transformed into a visual display of the measure of the amplitude of the
echo. This is known as echo quantification.
Generation of images on the display

 Two basic shapes of ultrasound images are encountered: images made in sector fashion
are pie shaped and linear fashion are rectangular
 Images are usually generated from the systemic scanner converter or frame store which
processes the reflected ultrasound in to a form required for screen presentation.
 Information is displayed regarding distance and amplitude. Each echo position is
represented as a dot on the screen. Thus a two dimensional image is generated.
 The brightness of each dot is related to the amplitude of the reflection and is referred as
a grey scale display.
 Resolution is the ability of the ultrasound machines to distinguish echoes on the basis of
time, space and strength.
o Axial resolution: Ability to differentiate two objects lying closely together in the
direction of the beam.
o Lateral resolution: Ability to different the two objects lying side by side. The
ultrasound beam is refracted when it enters a tissue of different acoustical
density.
 The image of refraction depends on the relative velocity of sound in the two tissues.
 Depth of sound wave penetration varies inversely with frequency.

DIFFERENT MODES OF ECHO DISPLAY

Different modes of echo display

 Different modes of echo display are Brightness mode, B – mode B scan or grey scale used
commonly for abdominal scanning and cardiac imaging.
 Static B mode: Transducer is moved in the scanning plane by hand.
 Real time B mode: Sound beam automatically and rapidly moves in the scan plane. In
this method the image is continuously updated to allow movement.
 Motion mode: M–mode mainly used for echocardiography.
 A MODE or amplitude mode is simplest form of display. It displays two parameters of
the echoes in the form of spikes, ie., distance from the transducer and the amplitude. The
horizontal line shows the distance and the amplitude is depicted on the vertical line. It is
used for ocular biometry.

Different types of basic probes

 Linear curvilinear and sector probes

 Transducers are classified based on the location of crystals on the scan head. When
elements are located at the end of the probe they are called end fire transducers and they
are used in abdominal and cardiac scanning. Side fire trasducers are used for intracavity
scanning like large animal reproductive scanning.

Doppler ultrasonography

 The pitch of a siren in a train changes with the proximity of the train movement, due to
difference in the sound wave frequency, called Doppler shift, the principle used in
 imaging the direction and velocity of blood flow. It was first proposed by Johann
Christian Andreas Doppler in 1842.
 Four Doppler modes are used in medical ultra sonography. They are Continous wave
Doppler, pulsed wave Doppler colour Doppler and power Doppler.

MODULE-31: RADIATION THERAPY - PRINCIPLES, ISOTOPES

AND THEIR USES IN DIAGNOSIS AND THERAPY

Learning objectives

This module deals with

 Radiation therapy and its methods

 Complications 0f radiation therapy

RADIATION THERAPY - INTRODUCTION

 Radiation therapy for the treatment of neoplasm of domestic animals has been used
since the discovery of X-ray. Dr. R. Eberlin was the first to report on the use of
radiotherapy in veterinary practice.
 Radiotherapy is usually indicated for localised solid neoplasm’s that cannot be excised
completely. It is not indicated if neoplasm has the potential of high incidence of
metastasis.
 The other indication are :
1. When surgery is expected to or has already failed.
2. When the regional or distant metastasis not occurred.
3. When radical surgery is unable to remove whole of the neoplasm.
4. When bulk of the neoplasm needs reduction in size so that it can subsequently be
removed surgically.
 Radiotherapy is not done by a single dose, rather multiple treatments are given over a
period of time, termed fractioned therapy. In animals, it is usually in 10-12 fractions of a
radiation dose of 4-5 Gy each time, usually three times per week.

METHODS OF RADIOTHERAPY

Teletherapy

 The radiation source is kept at a distance from the lesion. It is of four types
o Superficial X-ray therapy: Given through X-ray machine with energy range of 60-
100 keV.
o Deep X-ray therapy: Given through X-ray machine with energy range of 100- 200
keV.
o Super voltage therapy: Provided through (i) X-ray machine having linear
accelerator or betatron or cyclotron, (ii) isotropic X-ray machine with cobalt or
cesium. It is used in deep and substantial lesions
o Particulate beam therapy: Electron, neutron or proton beam can also be used as a
mode of teletherapy.
Brachytherapy

 It is the therapeutic use of radioisotope either within the interstitium or on the surface of
a neoplasm. The isotopes used are 198 Au , 60 Co, 125 K. Specific methods of
brachytherapy are
o Interstitial brachytherapy: Sources of radiation are within the interstitium of the
neoplasm.
o Pliesotherapy: It is surface brachytherapy for superficial lesions.
o Systemic brachytherapy: 132 I and 32 P can be used systemically. It is used in
extensive lesions and specific malignant conditions.

COMPLICATIONS OF RADIOTHERAPY

 Complications of radiotherapy are

o Immediate (minute to days): epilation, erythema , hematological depression and
GI disturbances and chromosomal aberration.
o Latent (months to years): leukemia , life span shortening , cancer, lethal gene
expression etc.

MODULE-32: SCAN AND MRI - PRINCIPLES AND THEIR

APPLICATION

Learning objectives

This module deals with

 Digital Radiography (DR)

 Computed Tomography (CT)
 Magnetic Resonance Imaging (MRI)
 Nuclear Medicine

DIGITAL RADIOGRAPHY (DR)

Basic principles

 DR involves translating x-ray energy into an electric signal that is in turn converted to
digital data (numbers). The process may be direct, indirect, or hybrid. In direct DR, the
x-ray energy is converted directly into an electrical signal. In indirect DR, the x-ray
energy is first converted to light by using a phosphorescent plate; the light is then
converted to an electrical pulse.
 The data are recorded on a plate, which is connected to a computer, and the x-ray image
is available for viewing almost immediately after exposure. It can then be stored or
printed out. Hybrid radiographic processes record the output of the phosphorescent
plate with a system similar to that found in a digital camera. CR and DR systems have a
number of advantages compared with film screen systems.
 The linear response of digital systems to the x-ray exposure means that these systems are
relatively forgiving of errors in radiographic technique. However, the quality of DR
 images depends on software processing to produce a degree of contrast that is familiar to
the reader. DR and CR images are stored on a computer hard drive and should be saved
as DICOM (Digital Imaging and Communication in Medicine) files. Some form of backup
device is recommended, ideally at another location.
 The images may be quite large files, but they can be easily transmitted to a remote
location for review by a radiologist or other specialist. These images may be manipulated
in multiple ways, including adjusting brightness and contrast, applying sharpening
filters, inverting the image, and magnifying part or all of the image.

COMPUTED TOMOGRAPHY (CT)

Basic principles

 CT is an imaging method that uses the principles of tomography. Tomography is the

demonstration of a slice through the body displayed without interference from structures
lying above or below the level under examination.
 CT uses x-rays generated by a high-output x-ray tube. The tube is mounted on a gantry
opposite a series of detectors. The tube and the detectors rotate in unison around the
subject under examination. A fan-shaped beam of x-rays passes through the body at a
predetermined level.
 The pattern of x-rays that reaches the detectors is recorded—a projection. The entire
gantry assembly is then rotated slightly, and the procedure is repeated, generating a new
projection. A series of such projections is obtained, completely encompassing the body
under examination.
 A computer uses complex mathematical formulas to create an image from the series of
projections. This image represents a slice of the body at the level under examination.
 The advantage of CT is its ability to distinguish different types of soft tissue, such as
brain white and gray matter or liver and gallbladder. CT achieves this degree of contrast
by being able to measure very fine differences in the ability of tissues to stop x-rays
passing through them.
 CT images are digital, and a computer is used for viewing. The gray scale can be adjusted
to highlight specific features such as bone or soft tissue (windowing). In CT imaging,
tissues and structures are described in terms of attenuation, which is a measure of the
capacity of a tissue to stop x-rays. Attenuation is equivalent to radiopacity in
radiography. The appearance of a tissue is defined in relation to some reference tissue or
its expected normal appearance. Thus isoattenuating means having the same
attenuation and would be displayed as the same shade of gray. If the tissue attenuates or
stops the x-rays less than the reference tissue or less than expected, it is described
as hypoattenuating and is portrayed as a darker shade of gray.
 The term hyperattenuating is used to describe tissues with more attenuation than
expected. These terms are relative rather than absolute, and the reference tissue or
structure is usually stated. Superimposed structures are eliminated. Iodinated contrast
agents such as those used for myelography or excretory urography may be used by
intravenous injection.
 Lesions with abnormal circulation may show marked contrast enhancement after such
injections. In viewing CT images, brightness and contrast are adjusted to highlight
specific structures. CT can resolve far greater contrast than can be displayed on a
monitor or appreciated by the human eye. Therefore the gray scale of the image is
adjusted to assign useful grays to tissues with varying levels of attenuation, referred to as
the window.
  A lung window will show detail within the lungs, but almost all other structures appear
white with little detail. A bone window will display detail of skeletal structures such as
cortex and trabeculae, whereas soft tissues appear gray with little detail and lungs appear
quite black. A soft tissue window shows good contrast and detail within soft tissue
structures such as the liver.
 Hepatic veins can be distinguished from the gallbladder and other soft tissues, whereas
bone appears white and lungs dark. CT may be used to image almost any body part.
Among the more common applications are diseases of the nasal cavity, sinuses, and ears.
It may also be used to evaluate the spine, brain, joints, lungs, mediastinum, pleural
cavity, and abdominal masses

MAGNETIC RESONANCE IMAGING (MRI)

Basic principles

 Unlike CT, no ionizing radiation is used in magnetic resonance imaging (MRI). MRI uses
hydrogen atoms to generate an image. Hydrogen is universally distributed in the body,
principally in water molecules. Hydrogen atoms are essentially spinning protons and
have an electrical charge. Each atom acts as a tiny bar magnet. Under normal
circumstances, these tiny magnets are arranged randomly.
 MRI uses relatively strong magnetic fields, ranging from 0.05 to 3.0 tesla in clinical use.
In a strong magnetic field, a small majority of the protons will be forced to point in the
direction of the field while spinning at a specific rate.
 A radio signal pulse at the same frequency as the spin of the protons will knock them out
of their equilibrium state. As the protons return to their original state, they release
energy in the form of a radio signal, effectively an echo of the original pulse used to
disturb the protons. This signal is collected by a scanner, processed, and displayed.
 Smaller gradient magnetic fields are used to localize signals from specific blocks of
tissue. Whereas CT offers good soft tissue detail, the contrast seen with MRI is superb.
Different sequences of radiopulses can be used to emphasize different tissue
characteristics. Manipulation of the parameters such as the timing and duration of the
radiopulse and the interval before an echo is recorded is used to highlight tissue features.
 MRI has superb contrast resolution in soft tissues and is very sensitive to changes such
as edema and hemorrhage. Signal intensity is used to describe the appearance of tissues
in MRI, just as attenuation is in CT imaging.
 It is a relative measure of the radio signal generated by tissues in response to the
stimulating radio energy pulse. If something is termed isointense, it has the same
appearance as some reference tissue—for example, a mass might be isointense to the
gray matter of the brain.
 Hypointense means less signal and appears darker, whereas hyperintense means more
signal and a brighter appearance. As in CT, these terms are relative and must be defined
in relation to the expected normal appearance, reference tissue, or appearance before the
use of contrast.
 Bones, ligaments, and tendons appear quite dark on all image sequences because they
have very little water content and therefore very little hydrogen to generate a signal.
Nonetheless, MRI can provide useful data about these structures.
 Like CT, MRI uses contrast agents that enhance lesion visibility. However, in the case of
MRI, the agents are based on gadolinium, which alters the local magnetic field and
changes signal intensity.
  Lesions that accumulate gadolinium appear bright (hyperintense) with some sequences.
MRI is capable of distinguishing or resolving objects of approximately 1 mm in size,
which is termed spatial resolution. This is similar to CT but compares poorly to
radiographic systems, which can resolve objects of 0.1 mm in size. MRI has excellent
contrast, showing different soft tissues as distinct shades of gray, which creates the
impression of much finer detail.
 Unlike CT, which is limited to images in the plane of the gantry, images can be obtained
in any plane, so slices can be varied infinitely to highlight lesions. MRI applications
include imaging disease of the central nervous system, nasal cavity and sinuses, joints,
and the abdomen.

NUCLEAR MEDICINE (SCINTIGRAPHY)

Basic principles

 Scintigraphy is a branch of nuclear medicine. It is an imaging technique in

which radionuclides (radioactive elements emitting gamma rays) are administered to a
subject.
 The radionuclides are attached to chemicals to form radiopharmaceuticals that
accumulate in the tissue of interest. Mostradiopharmaceuticals are analogues of
physiologic substances or biologic organic molecules. Their presence, and their
concentration, can be detected by gamma-ray detection equipment—usually a gamma
ray camera.
 The gamma rays are converted by the camera into signals from which a computer
produces a digital format that is used to construct an image of the area under
examination. Nuclear medicine images are described in terms of uptake of the
radiopharmaceutical.
 The degree of uptake is subjectively assessed in some techniques, while in others
quantitative analysis is performed. In this way normal and abnormal tissues can be
identified by the selective accumulation of the radioactive substances within them.

MODULE-33: ECOCARDIOGRAPHY - PRINCIPLES AND ITS

APPLICATION

Learning objectives

This module deals with

 Doppler Ultrasound
 Types of Doppler Ultrasound
 Applications of Doppler Ultrasound

DOPPLER ULTRASOUND

 A Doppler ultrasound test uses reflected sound waves to see how blood flows through a
blood vessel. It helps to evaluate blood flow through major arteries and veins, such as
those of the legs and neck.
  It can show blocked or reduced blood flow through narrowing in the major arteries of the
neck that could cause a stroke. It also can reveal blood clots in leg veins (deep vein
thrombosis, or DVT) that could break loose and block blood flow to the lungs
(pulmonary embolism).
 During pregnancy, Doppler ultrasound may be used to look at blood flow in an unborn
baby (fetus) to check the health of the fetus.
 During Doppler ultrasound, a handheld instrument (transducer) is passed lightly over
the skin above a blood vessel. The transducer sends and receives sound waves that are
amplified through a microphone. The sound waves bounce off solid objects, including
blood cells.
 The movement of blood cells causes a change in pitch of the reflected sound waves
(called the Doppler effect). If there is no blood flow, the pitch does not change.
 Information from the reflected sound waves can be processed by a computer to provide
graphs or pictures that represent the flow of blood through the blood vessels. These
graphs or pictures can be saved for future review or evaluation. See a picture of a
Doppler ultrasound.

TYPES OF DOPPLER ULTRASOUND

The basic types of Doppler ultrasound are

 "Bedside" or continuous wave Doppler: This type uses the change in pitch of the sound
waves to provide information about blood flow through a blood vessel. The veterinarian
listens to the sounds produced by the transducer to evaluate the blood flow through an
area that may be blocked or narrowed. This type of ultrasound can be done at the
bedside in the hospital with a portable machine to provide a fast estimate of the extent of
blood vessel damage or disease.
 Duplex Doppler: Duplex Doppler ultrasound uses standard ultrasound methods to
produce a picture of a blood vessel and the surrounding organs. Also, a computer
converts the Doppler sounds into a graph that gives information about the speed and
direction of blood flow through the blood vessel being evaluated.
 Color Doppler: Color Doppler uses standard ultrasound methods to produce a picture of
a blood vessel. Also, a computer converts the Doppler sounds into colors that are
overlaid on the image of the blood vessel and that represent the speed and direction of
blood flow through the vessel. Power Doppler is a special type of color Doppler. Power
Doppler can get some images that are hard or impossible to get using standard color
Doppler. Power Doppler is most commonly used to evaluate blood flow through vessels
within solid organs.

APPLICATIONS OF DOPPLER ULTRASOUND

 Non-invasive
 Generally painless
 Does not use radiation
 Can show if you have any blocked arteries in neck, arms, abdomen, coronary arteries and
limbs
 Can show if you have any blood clots in the veins in limbs
 Can show the amount and speed of blood flow in your veins and arteries
 Can be used instead of some more invasive procedures further reading
 MODULE-34: PRINCIPLES AND APPLICATIONS OF
SCINTIGRAPHY, GAMMA CAMERA, XERORADIOGRAPHY AND
DOPPLER

Learning objectives

This module deals with

 Nuclear Scintigraphy

NUCLEAR SCINTIGRAPHY

 Scintigraphy ("scint," Latin scintilla, spark) is a form of diagnostic test used in nuclear
medicine, wherein radioisotopes (here called radiopharmaceuticals ) are taken
internally, and the emitted radiation is captured by external detectors (gamma cameras)
to form two-dimensional images.
 The principle is based on the use of pharmaceutical labelled with radioisotope which
after entry into the blood stream get localised in particular tissue or organ. Thus the
localisation of radioisotope can be detected by using camera due to emission of gamma
rays. Most widely used radioisotope is Technetium-99m. This isotope has the advantage
of a short half life of 6hrs and thus animal can be discharged next day after the scan . in
addition, radiation exposure is minimum.
 The distribution of the labelled isotope can be detected by a gamma camera or a hand
held detector. In both the case sodium iodide crystalis used which absorbs gamma rays
emitted by the radioisotope from the patient and converts it to light flashes. The light is
converted to an electrical impulse. This impulse is shown on a oscilloscope or converted
to an image. Image can be produced in colours or in a grey colour.
 A scan appears as a image formed of dots. The interpretation is based on the appearance
of increased (hot spots) or decreased (cold spots) radioactivity region. Active process
produces hot spots where as cold spots observed in case of abscess.
 It is mainly used to detect functional disorders of kidney, liver , GI tract, lungs thyroid
glands etc. Using this technique it is easier to detect localised increase or decrease in
bone turn over as a result of trauma or disease. Any inflammatory or pathological
process that causes increased bone activity can be diagnosed by scintigraphy. Usefull in
diagnosing occult lameness. It has also been used to study renal, cardiac, lung functions ,
images of vertebral column and detecting the neoplasms.
 Problems associated with scintigraphy are
1. Cost of the gamma camera
2. Precise and strict safety precautions required.
3. Non specificity to the aetiology and difficulty encountered some times in
interpreting the scan especially skeletal system