TITLE

__________
HARRIET P. VALEROS, RN MAN
St. Luke’s College of Nursing
NURSING CARE OF PATIENT WITH DISEASE OF THE

CIRCULATORY SYSTEM
 Lecture outline

• Dengue Hemorrhagic Fever

• Malaria
• Leptospirosis
• Encephalitis
• Filariasis
 DENGUE FEVER
Tropical disease caused by different strains of
dengue virus which are transmitted by
mosquitoes
Synonyms: Dandy Fever, Break bone fever
Etiology:
Arthropod-Borne virus (arbovirus)
belonging to the family Flaviviridae
4 serotypes (DENV1, 2, 3, 4)
Incubation Period: 4-6 days
Vectors:
Aedes aegypti
Aedes albopictus- tiger mosquito
Culex fatigans
Characteristics of Aedes aegypti:
– Low-flying
– Day-biting
– Breeds on stagnant water
– Urban areas
– Has white stripes on the legs
 pathogenesis
• Infectious virus is deposited in the skin via vector
• There is marked increase in vascular permeability,
hemoconcentration, thrombocytopenia with
increased agglutinability
• Hypovolemic shock that resulted from increased
permeability of the vascular endothelium and loss
of plasma from the intravascular space
 DENGUE
FEVER
Manifestations of patients with DHF
depends on its grade
1. Grade I
- High grade fever (3-5 days)
- Headache, peri-orbital pain
- Joint & bone pain
- Abdominal pain
- Nausea & vomiting
- Petechial formation
Herman’s sign –
generalized flushing of
the skin
 DENGUE FEVER
2. Grade II - signs & symptoms of grade I + bleeding
- Epistaxis
- GI bleeding
- Gum bleeding
3. Grade III – grade II + circulatory failure
- Cold, clammy skin
- Altered VS – decreased BP, rapid, weak pulse,
increased RR
4. Grade IV – grade III + hypovolemic shock (profound
bleeding)
 DENGUE FEVER
Diagnostic tests:
1. Tourniquet test (Rumpel-
Leede test)
- presumptive test that
checks for capillary
fragility
- pedia: 3-5 mins; adults:
5-10 mins
+ if > 20 petechiae
formation in 1 square
inch
 Diagnostics
• 2. NS1 antigen, DENGUE DUO
• 3. Platelet count (decreased)
• 4. Hematocrit
 DENGUE FEVER
Treatment:
Symtomatic and supportive
1. Oral fluids and electrolyte
2. Antipyretics (don’t use aspirin)
3. Platelet transfusion
4. Convulsions – Dilantin
5. bleeding- FFP, Platelet conc
 Nursing Care:

Watch for bleeding:

Nosebleed – cold compress over forehead

DENGUE Melena – cold compress over stomach area,

avoid eating dark colored foods

FEVER Gingival bleeding – offer ice chips, use soft

bristle toothbrush

Hematemesis - NPO

Observe for signs of shock

 C – hemically treated mosquito nets

L – arvae eating fish

Prevention:
DOH CLEAN E – nvironmental sanitation (4pm
habit)
Program
A – ntimosquito soaps (basil,
citronel)

N – atural mosquito repellants

(neem tree, eucalyptus, oregano)
 MALARIA
Synonyms: Ague, “King of Tropical Diseases”
Infectious disease that is arthropod-borne,
characterized by chills followed by fever
occurring regular intervals
Caused by the protozoan Plasmodium
Vector: Female anopheles mosquito
– Night biting
– Breeds in clear, slow-moving water
(rural areas)
 Anopheles mosquito
• Brown in color and bigger than othert
mosquito
• Night biting mosquito
• Usually does not bite a person in motion
• Assumes 36 degrees when alights a wall,
curtain, trees
• Breeds in clear ,flowing, shaded streams,
usually in the mountains
 MALARIA
Species of plasmodium
1. P. vivax - causes benign tertian malaria
2. P. falciparum – malignant tertian malaria
- Most frequently encountered here ff by
vivax; most fatal; multiplies rapidly
3. P. malariae – less frequent; causes quartan
malaria
4. P. ovale – rarely seen
 MALARIA
Incubation Period:
P. falciparum: 12-14 days
P. vivax/ovale: 13-17 days
P. malariae: 28-30 days

Period of Communicability:
Infective as long as
gametocytes & asexual
forms remain in blood
Malaria Life Cycle
Mosquito – Sexual cycle
(Sporogony) - sporozoites

Human – Asexual cycle

(Schizogony) – schizonts
and merozoits
 MALARIA
Stages of Malaria
1. Cold stage –
- Chilling manifestations (10-15 mins)
nursing responsibility: provide warmth to
patient
> Add clothing
> Warm drinks
> Hot water bags
> Socks
 MALARIA
2. Hot stage
– Characterized by fever, headache, abdominal pain &
vomiting
- Lasts for 4-6 hours
Nursing responsibility: lower body temperature
> TSB
> Light, loose clothing
> Antipyretics
 MALARIA
3. Diaphoretic stage
– Excessive sweating/ feeling of weakness due to the
past stages px underwent
Nursing Responsibility:
-Keep patient comfortable with dry, warm clothes,
replace fluid loss.
-Monitor V/S
-Diet high calories, vitamins and minerals
-Fluid and electrolytes balance
 MALARIA
Complications of P. falciparum
- Cerebral malaria – delirium, coma, death
- Severe hemolytic anemia
- Pulmonary edema
- Shock
 MALARIA
Diagnostic Examination:
1. Malarial Smear- collect at the peak of fever-
The classic and most used diagnostic test for
malaria is the blood smear on a microscope
slide that is stained (Giemsa stain) to show
the parasites inside red blood cells
2. Quantitative Buffy Coat (QBC)- rapid test for
malaria
 Quantitative Buffy Coat (QBC)
• test to detect infection with malaria or other blood
parasites: the blood is taken in a QBC capillary tube
which is coated with acridine orange (a fluorescent
dye) and centrifuged;
• the fluorescing parasites can then be observed under
ultraviolet light at the interface between red blood
cells and buffy coat.
• more sensitive than the conventional thick smear
and in >90% of cases, the species of parasite can also
be identified.
Treatment:
Anti-malarial agents
-Chloroquine (drug of Choice)
-Quinine- neurologic toxicity, muscular
twitching, delirium, convulsion
-Primaquine
-Fansidar
 MALARIA
Preventive
1. Advise malaria chemopropylaxis when
travelling to malaria endemic areas
2. Limit dusk to dawn exposure, wear
protective clothing, sleep under mosquito
nets and use topical repellents
 Leptospirosis (orange eye)
Synonyms: Mud fever, Swamp fever,
Canicola fever, Weil’s Disease, Swine
herd’s Disease, Ictero-Hemorrhagia
Causative agent: Leptospira interrogans
spirochetes
Affects farm animals- cattle, pig, horses,
rats
Source of infection: urine of rats

32
• MOT: Skin penetration, through direct
contact with urine, blood or tissue from an
infected animal.
can enter through broken skin or through the
soft tissues on the inside of the mouth, nose
or eyes.
• Can be transmitted by the semen of
infected animal
• Human to human transmission is very rare
33
 Leptospirosis
Population at risk:
1. Farmers
2. Sewage workers
3. Miners
4. Slaughterhouse
workers
5. People living in
manila (due to
floods)

34
AFFECTED ORGANS
• multiplies in the bloodstream and
invade liver resulting in jaundice
• Eyes- iritis, due to liver
involvement, giving an orange
colored slera
• Kidneys- inflammation of the
nephrons and tubular necrosis
resulting in renal failure
• Muscles- pain

36
 Septicemic/ septic stage – high fever 4-
7 days, headache, N/V, abdominal pain,
joint pain, respiratory distress

Immune or toxic stage- with or without

jaundice- 4-30 days
Clinical
• Anicteric – low grade fever, meningeal
Manifestations manifestation (convulsion, disorientation)
• Icteric (Weil’s syndrome) – jaundice,
hemorrhages, hepatomegaly, renal involvement
(RF)

Convalescence stage-
Relapse may occur during 4th to 5th
weeks
37
 Diagnostics
:
BLOOD EXAMINATION
LAT- Leptospira Agglutination Test
LAAT- Leptospira Antigen-Antibody Test
Liver function test.
BUN CREATINE

Tx:
Antibiotics: penicillin, doxycycline,Tetracycline (not given to
< 8 yrs old and pregnant women)
***Do not give calcium- rich foods (tetracycline binds with
calcium)
Prophylaxis- doxy 100 mg p.o q12 x 7 days
38
 Leptospirosis
Nursing Care:
1. Symptomatic and
supportive
2. Monitor urine output

Preventive
3. Eradicate rats –
environmental sanitation,
rat poisons
4. Avoid wading in
contaminated pool of
water/ swamps

39
JAPANESE ENCEPHALITIS
• Synonym: Brain fever  one of a group of mosquito-
borne virus diseases that can affect the central
nervous system
• Arbovirus is short for arthropod-borne virus. --
group of viruses that are spread by certain
invertebrate animals (arthropods), most
commonly blood-sucking insects    
Causes inflammation of the brain
MOT: Mosquito bite (Culex)
Causative agent - Culex trieantorhynchus
The incubation period is 4 to 21 days.
 Encephalitis
• uncommon but serious condition in which the brain
becomes inflamed resulting from either a viral infection or
due to the body’s own immune system mistakenly attacking
brain tissue.
• It can be life threatening and requires urgent treatment in
hospital.
• very young and very old are most at risk.
• sometimes starts off with flu-like symptoms, such as a high
temperature and headache.
 TYPES
• Primary encephalitis occurs when a virus directly infects the
brain and spinal cord.
• three main categories of viruses:
• (1) Common viruses, including HSV (herpes simplex
• virus) and EBV (Epstein-Barr virus);
• (2) Childhood viruses, including measles and mumps, (3)
Arboviruses (spread by mosquitoes, ticks, and other
insects), including Japanese encephalitis,
\West Nile encephalitis, and tick-borne encephalitis.
• Secondary encephalitis occurs when an infection starts
elsewhere in the body and then travels to the brain.
• caused by a complication of a viral infection. Symptoms
start to appear days or even weeks after the initial infection.
• The patient’s immune system treats healthy brain cells as
foreign organisms and attacks them
• Japanese Encephalitis
• generally begins with fever, nausea, chills, and
headache, vomiting with stiffness/ neurologic
manifestations within 24 hours,
• dizziness, conjunctivitis, arthralgia, myalgia
• decreased IQ and serious brain damage.
• The symptoms rapidly worsen, with signs and symptoms
of rigidity, ataxia, speech difficulties, ocular palsy, flaccid
paralysis and there may be seizures, confusion, and loss of
consciousness, and even coma.
Clinical Manifestations- s/s appears after 6-8
days after bite
Altered Level of consciousness - lethargic
Fever, chills and vomiting
Convulsion
Signs of neurologic damage
 JAPANESE ENCEPHALITIS

Diagnosis:
- lumbar puncture
- EEG
Medical Management:
-      patient is treated symptomatically
Nursing Care:
- same as meningitis
Preventive Measure:
- eradicate mosquito thru DOH program
Vaccination of equine or swine
 management
• Symptomatic and supportive management
• (1) Provide comfort – keep patient in a quiet, well ventilated
room; encourage oral hygiene and bed bath.
• (2) Prevent from complications – turn the patient
at least every 2 hours
increase oral fluid intake, encourage high caloric diet,
• moisten lips with mineral oil.
• (3) Monitor intake and output.
• The prevention are identification of vectors and eliminating breeding
grounds, destruction of larvae, screening homes, and use of
 Medical Management
• Anticonvulsant for seizure
• Mannitol to decrease ICP
• Corticosteroids
• Paracetamol
• Mechanical ventilation
 Filariasis (elephantiasis)
• Parasitic disease caused by microscopic,
threadlike african eye worm
• Adult worm can live in human lymphatic
system and would cause disfigurement,
disability
• Causative organism- wuchereria bancrofti-
thread worm 4-5cms long and affects lymph
nodes and lymph vessels of the legs, arms
vulva and breast
• MOT- transferred person to person with
circulating microfilariae by mosquito bites
54
 pathogenesis
transferred person to person with circulating
microfilariae by mosquito bites
Adult worm lives for 7 years in the lymph vessels,
mate and releases microfilaria in the blood stream
Damages the kidneys, collects fluid in arms, breast
leg and genital area
Bacterial infection and skin hardens and thickens-
elephantiasis
•

55
• Elephantiasis occurs in the chronic stage of
lymphatic filariasis due to the obstruction of
lymphatic vessels by filariae.
• After invasion into lymph vessels, third stage
larvae grow to maturity in the lymphatic
system, mainly in and around the
genitourinary system.

56
• Dx- circulating filarial antigen (CFA)
• MANAGEMENT-
• Health education- control mosquito
• Tx- ivermectin, albendazole or
diethylcarbamazine (DEC)to eliminate larvae
and its reproduction
• Sx to remove surplus tissue to drain fluid
around the damaged lymphatic vessels
57
58
 Schistosomiasis
acute and chronic disease caused by parasitic worms.
caused by blood flukes (trematode worms) of the genus
Schistosoma.
• People are infected during routine agricultural,
domestic, occupational, and recreational activities,
which expose them to infested water.
• Lack of hygiene and certain play habits of school-aged
children such as swimming or fishing in infested water
make them especially vulnerable to infection.
 Schistosomiasis
Synonyms: Snail fever, Bilharzia, Blood
fluke
Etiologic agent: Schistosoma japonicum
, S. mansoni, S. hematobium
Incubation Period: 2-6 weeks to 2 months
MOT: Skin penetration of free-swimming
fork-tailed cercariae, ingestion of
contaminated water
60
S. Japonicum-infects the intestinal tract, also
known as oriental schistosomiasis
s. mansoni- affects intestinal tract and common
is Africa
S. Haematobium – affects urinary tract and
common in Middle east like Iraq and Iran

61
 Sources of infection
• Feces of infected person
• Dogs, pigs, carabaos, monkeys and wild rats
have been found to be infected and can serve
as a host
• Transmitted through intermediary host a tiny
snail called Oncomelania quadrasi-
• Thrives in riverbanks, creeks, swamps, clings to
grasses, hyacinths, bamboo and loves sandy
loamy soil

62
 Infection and Transmission
• People become infected when larval forms of the parasite –
released by freshwater snails – penetrate the skin during
contact with infested water.
• Transmission occurs when people suffering from
schistosomiasis contaminate freshwater sources with their
excreta containing parasite eggs, which hatch in water.
• the larvae develop into adult schistosomes. Adult worms
live in the blood vessels where the females release eggs.
Some of the eggs are passed out of the body in the feces or
urine to continue the parasite’s lifecycle.
• Others become trapped in body tissues, causing immune
reactions and progressive damage to organs.
63
64
65
 Manifestations:
1. Itchiness at the site of penetration
“swimmer’s itch”
2. Low grade Fever, myalgia and cough
3. Dysentery –like symptoms
4. Emaciations from chronic disease
5. Hepatomegaly, splenomegaly,
lymphadenopathy
Enlarged abdomen because of inflamed liver,
resulting from the accumulation of eggs in
the organ
66
67
 complications
 Liver cirrhosis/portal hypertension
 Ascites
 Heart failure
 Fibrosis of the bladder and ureter
 Renal failure
 genital lesions, vaginal bleeding, pain during
sexual intercourse, and nodules in the vulva.
 pathology of the seminal vesicles, prostate
 Cerebral schistosomiasis

68
Diagnosis:
Schistosomiasis
Stool exam – look for egg of parasite, kato katz technique
Blood exam – COPT (circumoval precipitin test)
ELISA
Treatment: effective only when given early at the course of
disease
Praziquantel (Biltricide) = 30 mg/kg BID
Fuadin IM OR IV

Preventive measures:
Snail Control (Oncomelania quadrasi) – use of
molluscides
Environmental Sanitation – proper disposal of excretion

69
 RABIES

 Synonyms: Hydrophobia, Lyssa, La Rage

 Causative agent : Rhabdovirus (has a special affinity
to the CNS) causing encephalitis
 Primarily a disease of animals (dogs, cats and other
mammals)
 MOT: Bite, abrasion or lick on
a damaged skin or mucous
membrane
 RABIES

- is a vaccine-preventable viral disease that transmits

from mammals to humans that causes acute
encephalitis
- Once clinical symptoms appear, rabies is virtually
100% fatal.
- 99% of cases, domestic dogs are responsible for
rabies virus transmission to humans
- spreads to people and animals through bites or
scratches, usually via saliva.
 RABIES
2 Stages of Manifestations(animal)
1. Dumb stage- complete change in
disposition (withdrawn, stays in one
corner, quite-depressive behavior,
hyperactive, walks to and fro- manic
behavior)
2. Furious stage- easily agitated; bites,
fearful look, drooling of saliva, animal
expected to die.
 Manifestations in Humans
Incubation period is 10 days up to 15 years
(longest record is 21 years)
3 stages of manifestations
1. Prodromal/Invasive stage- numbness on site,
sore throat, flu – like symptoms, marked
insomnia, restless, copious salivation,
irritable, apprehensive, with slight
photosensitivity, sensitive to sound and temp.
Pain in the site bite. Aches and body pain
 RABIES
2. Excitement stage- aerophobia, hydrophobia,
px fears water due to laryngospasm, difficulty
in swallowing, profuse drooling
Marked excitation and apprehension
Nuchal rigidity, convulsions, delirium
If the patient survives this phase, patient
deteriorates rapidly and enters to terminal phase
 RABIES
3. Paralytic stage- spasms stops but paralysis will set
in starting from toes up, done in a matter of
minutes.
Death occurs due to respiratory paralysis and cardiac
failure
*Death expected in 24 hours from invasive to
paralytic stage
*Rabies is preventable but not curable.
 Diagnosis: established largely from history of animal
bite
 Observation of dog for 10 days – dead or w/ behavior
changes w/in 10 days (rabid)
Virus culture and isolation of saliva and throat
Flourescent rabies antibody (FRA)- MOST
DEFINITIVE DIAGNOSIS
diagnostic tools are not suitable for detecting
rabies infection before the onset of clinical
disease, and unless the rabies-specific signs
of hydrophobia or aerophobia are present
Brain Biopsy – negri bodies
Negri bodies
Management:
RABIES
1. Wash the wound immediately with soap and water,
povidone iodine for 15 minutes.
2. Do not cover or suture the wound. If suturing is
necessary, ensure that RIG has been applied locally
Management of Biting animal:
3. Capture the animal and keep under veterinary
surveillance
a. If animal remains healthy in 10 days
b. If animal dies
Management: POSTEXPOSURE PROPHYLAXIS (PEP)
consists of a dose of human rabies immune globulin (HRIG)
and rabies vaccine given on the day of the rabies
exposure, and then a dose of vaccine given again on days
3, 7, and 14.
For people who have never been vaccinated against rabies,
postexposure prophylaxis (PEP) should always include
administration of both HRIG and rabies vaccine.
Combination of HRIG and vaccine is recommended for both
bite and non-bite exposures, regardless of the interval
between exposure and initiation of treatment.
 RABIES
Management
2 types of vaccines administered
A. Active
q  PVCV: purified vero cell vaccine (verorab)
: 0.50 cc/vial (IM) .1cc (ID)
Site: Deltoid or Vastus lateralis
Schedule: Verorab:
Day 0: 2 vials-1 vial for each site
Day 7: 1 vial
Day 21: 1 vial
Day 90: booster dose of 1 vial in case dog dies in
10 days
 RABIES

A. Active
q  Purified duck embryo
IM deltoid or SubQ OD for 14 days
1. Lyssavac N – no skin test, cloudy
solution
2. Lyssavac plain – with skin test, pink
in color
 RABIES
B. Passive immunization:
q  For immediate effect
q  Given up to 7 days after being bitten,
q  Deep IM at buttocks area
q  Single dose
qAnimal Serum (ERIG) equine rabies immunoglobulin
Eg. ARS (antirabies serum); HyperRAB
Skin testing done 40 IU/kg body weight
qHuman serum (HRIG) human rabies immunoglobulin
(administered only once at the start of anti rabies prophylaxis)
E.g. Rabuman; Imogam
Skin testing not necessary; 20 IU/kg body weight.
 Nursing care of patients with Rabies
 Provide a dim & quiet environment
 Room should be away from sub-utility rooms (area for
washing: avoid sound of water)
 Restrain patient even before aggressive behavior sets
in
 Wear protective barriers
Prevention
 Immunization of animals
 All animals should be caged or chained
 Stay away from stray animals
Thank You!