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
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
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
DENGUE FEVER
Nursing Care:
Watch for bleeding:
 Nosebleed – cold compress over forehead
 Melena – cold compress over stomach area,
avoid eating dark colored foods
 Gingival bleeding – offer ice chips, use soft
bristle toothbrush
 Hematemesis - NPO
 Observe for signs of shock
DENGUE FEVER
Prevention: DOH CLEAN Program
C – hemically treated mosquito nets
L – arvae eating fish
E – nvironmental sanitation (4pm habit)
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) is a
laboratory 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. This test is 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
 Caused by Leptospira interrogans
spirochetes
 Affects farm animals- cattle, pig, horses,
rats
 Source of infection: urine of rats

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 Mode of transmission: 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

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 Leptospirosis
Population at risk:
1. Farmers
2. Sewage workers
3. Miners
4. Slaughterhouse workers
5. People living in manila (due to floods)

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

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 Leptospirosis
Clinical Manifestation
 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
 Anicteric – low grade fever, meningeal
manifestation (convulsion, disorientation)
 Icteric (Weil’s syndrome) – jaundice, hemorrhages,
hepatomegaly, renal involvement (RF)

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 Convalescence stage-
 Relapse may occur during 4th to 5th weeks

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 Leptospirosis
Dx:
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

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 Leptospirosis
Nursing Care:
1. Symptomatic and supportive
2. Monitor urine output

Preventive
1. Eradicate rats – environmental sanitation, rat
poisons
2. Avoid wading in contaminated pool of water/
swamps
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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
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 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


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 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.

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 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
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