ORAL REVALIDA NCM1O5 JMCD

KAWASAKI DISEASE
Definition: an acute febrile vasculitic syndrome. It was first described in 1967
by Dr. Tomisaku Kawasaki in Japan.
Anatomy and physiology:

Etiology: Idiopathic, Genetic, Autoimmune response

Symptomatology
Stage I Acute Febrile Phase (First 10 days)

High, spiking fever for 5 days or more.

Bilateral conjunctival injection.

Oropharyngeal erythema, Strawberry tongue, or red dry lips.

Erythema and edema of hands and feet, periungal desquamation.

Erythematous generalized rash.

Cervical lymphadenopathy greather than 0.6 inch (1.5cm)

Stage II Subacute Phase (Days 11 to 25)

Acute symptoms of stage I subside as temperature returns

normal. The child remains irritable and anorectic.

Dry, cracked lips with fissures.

Desquamation of toes and fingers.

Coronary thrombus, aneurysm, myocardial infarction, and heart

failure.

Thrombocytosis peaks at 2 weeks.

Stage III Convalescent Phase (Until sedimentation rate and platelet count
normalize)

The child appears well.

Transverse grooves of fingers and toenails (Beaus lines).

Coronary thrombosis, aneurysms may occur.

Medical Management
Labs

Based on s/s

Electrocardiogram, echocardiogram, cardiac catheterization, and

angiocardiography

CBC leukocytosis during acute stage.

Erythrocytes and hemoglobin slight decrease.

Platelet count increased during second to fourth week of illness.

IgM, IgA, IgG, and IgF transiently elevated.

Treatment

Immunoglobulin

Methotrexate or cyclophosphamide: In IVIG-resistant cases

Aspirin
Prognosis
With prompt treatment, the prognosis is good.
If left untreated

Clinically significant heart failure or myocardial dysfunction

(unlikely to occur once fever is resolved)

Diffuse coronary artery ectasia and aneurysm formation, giant

aneurysm (internal luminal diameter 8 mm)

Myocarditis (common but rarely causes chronic heart failure)

Rupture of coronary artery aneurysms with hemopericardium

Nursing Diagnosis

Elevated body temperature

Impaired skin integrity

Activity intolerance

Pain related swollen joints

Risk for decreased cardiac output related to accumulation of fluid

in the pericardial sac
Nursing management
1. Monitor pain level and childs response to analgesics.
2. Institute continual cardiac monitoring and assessment for
complications; report arrhythmias.
3. Take vital signs as directed by condition; report abnormalities.
4. Assess for signs of myocarditis (tachycardia, gallop rhythm, chest
pain).
5. Monitor for heart failure (dyspnea, nasal flaring, grunting, retractions,
cyanosis, orthopnea, crackles, moist respirations, distended jugular
veins, edema).
6. Closely monitor intake and output, and administer oral and I.V fluids as
ordered.
7. Monitor hydration staus by checking skin turgor, weight, urinary output,
specific gravity, and presence of tears.
8. Observe mouth and skin frequently for signs of infection.
9. Perform comfort measures related to the eyes.

Conjunctivities can cause photosensitivity, so darken the room,

offer sunglasses.

Apply cool compress.

Discourage rubbing the eyes.

10. Monitor temperature every 4 hours. Provide sponge bath if temperature
above normal.

ORAL REVALIDA NCM1O5 JMCD

HEPATITIS B
Definition: Hepatitis B is an infectious disease caused by the hepatitis B virus
(HBV) which affects the liver.
Anatomy and physiology

R hypochondriac region
Largest internal organ
Produce proteins and blood clotting factors, bile
Stores
vitamin B12,
folic acid,
iron required to make red blood cells,
vitamin A for vision,
vitamin D for calcium absorption, and
vitamin K to help blood to clot properly.

Etiology

HBV, bodily fluids, sexual intercourse, IV drug abuse

Symptomatology
Icteric Hepatitis

Anorexia

Nausea

Vomiting

Low-grade fever

Myalgia

Fatigability
fulminant and subfulminant hepatitis

Hepatic encephalopathy

Jaundice

Somnolence

Mental confusion

Coma

Ascites

Gastrointestinal bleeding
Laboratories

Alanine aminotransferase and/or aspartate aminotransferase

levels

Alkaline phosphatase levels

Gamma-glutamyl transpeptidase levels

Total and direct serum bilirubin levels

Albumin level

Hematologic and coagulation studies (eg, platelet count, complete

blood count [CBC], international normalized ratio)

Ammonia levels

Erythrocyte sedimentation rate

Serologic tests

Hepatitis B surface antigen (HBsAg)

Hepatitis B e antigen (HBeAg)

Hepatitis B core antibody (anti-HBc) immunoglobulin M (IgM)

anti-HBc IgG

Hepatitis B e antibody (anti-HBe)

hepatitis B virus (HBV) deoxyribonucleic acid (DNA)

Imaging studies

Abdominal ultrasonography

Abdominal computed tomography (CT) scanning

Abdominal magnetic resonance imaging (MRI)

Treatment

Alpha interferon

Tenofovir (Nucleos(t)ide reverse transcriptase inhibitors)

Entecavir
Prophylaxis

Hepa B vaccine

Immunoglobulin
Prognosis
Patients who have lost the hepatitis B e antigen (HBeAg) and in whom
hepatitis B virus (HBV) DNA is undetectable have an improved clinical
outcome, as characterized by the following:

Slower rate of disease progression

Prolonged survival without complications

Reduced rate of HCC and cirrhosis

Clinical and biochemical improvement after decompensation

Complications: Hepatocellular carcinoma and cirrhosis
Nursing Diagnosis
1. Imbalanced Nutrition, Less Than Body Requirements
relate to: discomfort in the right upper quadrant
2. Acute pain
related to: swelling of the liver, the inflamed liver and portal vein dam.
3. Hyperthermia
related to: invasion agent in blood circulation secondary to liver inflammation
4. Fatigue
related to: chronic inflammatory process secondary to hepatitis
5. Risk for skin integrity and tissue damage
related to: pruritus secondary to the accumulation of the pigment bilirubin in
the bile salts
Nursing management
1. Monitor I&O, compare with periodic weight. Note enteric losses:
vomiting and diarrhea.
Provides information about replacement
needs and effects of therapy.
2.

Assess vital signs, peripheral pulses, capillary refill, skin turgor, and
mucous membranes. Indicators of circulating volume and perfusion.

3.

Check for ascites or edema formation. Measure abdominal girth as

indicated.
Useful in monitoring progression and resolution of fluid
shifts.

4.

Observe for signs of bleeding: hematuria, melena, ecchymosis, oozing

from gums, puncture sites Prothrombin levels are reduced and
coagulation times prolonged when vitamin K absorption is altered in GI
tract and synthesis of prothrombin is decreased in affected liver.

5.

Monitor periodic laboratory values: Hb/Hct, Na, albumin, and clotting

times.
Reflects hydration and identifies sodium
retention/protein deficits, which may lead to edema formation. Deficits
in clotting potentiate risk of bleeding and hemorrhage.

6.

Administer antidiarrheal agents: diphenoxylate with atropine (Lomotil).

Reduces fluid and electrolyte loss from GI tract.

ORAL REVALIDA NCM1O5 JMCD

7.

Provide IV fluids (usually glucose), electrolytes. Protein hydrolysates.

Provides fluid and electrolyte replacement in acute toxic state.

8.

dminister medications as indicated: Vitamin K Correction of albumin

and protein deficits can aid in return of fluid from tissues to the
circulatory system. Because absorption is altered, supplementation
may prevent coagulation problems, which may occur if clotting factors
and prothrombin time (PT) is depressed.