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College of Nursing

Silliman University
Dumaguete City, Philippines

Care of Pediatric Patients with Kawasakis Disease

Submitted by: Alna Shelah F. Ibaez

COLLEGE OF NURSING
Silliman University Dumaguete City

Resource Unit on the Care of Patients with Kawasakis Disease


Placement: NCM 105, Level IV 1st semester Time Allotment: 1 hour Topic Description: This topic deals on the care of pediatric patients with Kawasaki Disease. It emphasizes on the utilization of nursing process on the whole duration of care. It also includes the clinical manifestation, diagnostic aids, the medical management and nursing management of Kawasakis Disease. Central Objective: At the end of 1-hour ward class, the learners shall gain knowledge, demonstrate beginning skills and manifest a positive attitude and values in the care of a pediatric patient who is experiencing Kawasakis Disease.
Specific Objectives At the end of the discussion the learners/participants will: Content T. A. T/L Activities Evaluation

a. Define Kawasaki Disease in his/her own undersatnding at a 75% level of competency.

I.

Overview

Kawasaki Disease, otherwise known as mucocutaneous lymph node syndrome, is an acute, self limiting vasculitis that resolves in 6 to 8 weeks. It was first described by Dr. Thomisakyu Kawasaki in 1967. Without treatment, approximately 20% to 25% of children 1 min with this illness will develop cardiac sequelae. Damage to the blood vessels that supply the heart muscle (the coronary arteries) and damage to the heart muscle itself can occur. The most common sequelae are ecstasia (dilation) of the coronary arteries, or aneurysm formation.

Lecture with PowerPoint Presentation

Oral Evaluation 1. In your own understanding, define Kawasakis Disease.

II. b. Review comprehensively the structures and parts of Cardiovascular system and state each function at 75% level of competency.

Human Anatomy and Physiology

Video Presentation Oral Evaluation 1. Give the most important parts of the circulatory system. 2. Give major of the Circulatory system.

The Circulatory System The circulatory system is responsible for the transport of water and dissolved materials 3 mins throughout the body, including oxygen, carbon dioxide, nutrients, and waste. The circulatory system transports oxygen from the lungs and nutrients from the digestive tract to every cell in the body, allowing for the continuation of cell metabolism. The circulatory system also transports the waste products of cell metabolism to the lungs and kidneys where they can be expelled from the body. Without this important function toxic substances would quickly build up in the body. Anatomy of the Circulatory System The human circulatory system is organized into two major circulations. Each has its own pump with both pumps being incorporated into a single organthe heart. The two sides of the human heart are separated by partitions, the interatrial septum and the interventricular septum. Both septa are complete so that the two sides are anatomically and functionally separate pumping units. The right side of the heart pumps blood through the pulmonary circulation (the lungs) while the left side of the heart pumps blood through the systemic circulation (the body). The human heart is a specialized, four-chambered muscle that maintains the blood flow in the circulatory system. It lies immediately behind the sternum, or breastbone, and between the lungs. The apex, or bottom of the heart, is tilted to the left side. At rest, the heart pumps about 59 cc (2 oz) of blood per beat and 5 l (5 qt) per minute. During exercise it pumps 120220 cc (4-7.3 oz) of blood per beat and 20-30 l (21-32 qt) per minute. The adult human heart is about the size of a fist and weighs about 250-350 gm (9 oz). The human heart begins beating early in fetal life and continues regular beating throughout the life span of the individual. If the heart stops beating for more than 3 or 4 minutes

permanent brain damage may occur. Blood flow to the heart muscle itself also depends on the continued beating of the heart and if this flow is stopped for more than a few minutes, as in a heart attack, the heart muscle may be damaged to such a great extent that it may be irreversibly stopped. The heart is made up of two muscle masses. One of these forms the two atria (the upper chambers) of the heart, and the other forms the two ventricles (the lower chambers). Both atria contract or relax at the same time, as do both ventricles. An electrical impulse called an action potential is generated at regular intervals in a specialized region of the right atrium called the sinoauricular (or sinoatrial, or SA) node. Since the two atria form a single muscular unit, the action potential will spread over the atria. A fraction of a second later, having been triggered by the action potential, the atrial muscle contracts. The ventricles form a single muscle mass separate from the atria. When the atrial action potential reaches the juncture of the atria and the ventricles, the atrioventricular or AV node (another specialized region for conduction) conducts the impulse. After a slight delay, the impulse is passed by way of yet another bundle of muscle fibers (the Bundle of His and the Purkinje system.) Contraction of the ventricle quickly follows the onset of its action potential. From this pattern it can be seen that both atria will contract simultaneously and that both ventricles will contract simultaneously, with a brief delay between the contraction of the two parts of the heart. The electrical stimulus that leads to contraction of the heart muscle thus originates in the heart itself, in the sinoatrial node (SA node), which is also known as the heart's pacemaker. This node, which lies just in front of the opening of the superior vena cava, measures no more than a few millimeters. It consists of heart cells that emit regular impulses. Because of this spontaneous discharge of the sinoatrial node, the heart muscle is automated. A completely isolated heart can contract on its own as long as its metabolic processes remain intact. The rate at which the cells of the SA node discharge is externally influenced through the

autonomic nervous system, which sends nerve branches to the heart. Through their stimulatory and inhibitory influences they determine the resultant heart rate. In adults at rest this is between 60 and 74 beats a minute. In infants and young children it may be between 100 and 120 beats a minute. Tension, exertion, or fever may cause the rate of the heart to vary between 55 and 200 beats a minute. Coronary Circulation The coronary arteries supply blood to the heart muscle. These vessels originate from the aorta immediately after the aortic valve and branch out through the heart muscle. The coronary veins transport the deoxygenated blood from the heart muscle to the right atrium. The heart's energy supply is almost completely dependent on these coronary vessels. When the coronary vessels become blocked, as in arteriosclerosis or hardening of the arteries, blood flow to the cardiac muscle is compromised. This is when the common "bypass surgery" is performed where the coronary arteries are "bypassed" by replacing them with, for example, a vein from the leg. A "double bypass" is when two coronary arteries are bypassed. A "triple bypass" is when three are bypassed, etc. The Heartbeat The heart muscle pumps the blood through the body by means of rhythmical contractions (systole) and relaxations or dilations (diastole). The heart's left and right halves work almost synchronously. When the ventricles contract (systole), the valves between the atria and the ventricles close as the result of increasing pressure, and the valves to the pulmonary artery and the aorta open. When the ventricles become flaccid during diastole, and the pressure decreases, the reverse process takes place. The Pulmonary Circulation From the right atrium the blood passes to the right ventricle through the tricuspid valve, which consists of three flaps (or cusps) of tissue. The tricuspid valve remains open during diastole, or ventricular filling. When the ventricle contracts, the valve closes, sealing the opening and preventing backflow into the right atrium. Five cords attached to small muscles,

called papillary muscles, on the ventricles' inner surface prevent the valves' flaps from being forced backward. From the right ventricle blood is pumped through the pulmonary or semilunar valve, which has three half-moon-shaped flaps, into the pulmonary artery. This valve prevents backflow from the artery into the right ventricle. From the pulmonary artery blood is pumped to the lungs where it releases carbon dioxide and picks up oxygen. The Systemic Circulation From the lungs, the blood is returned to the heart through pulmonary veins, two from each lung. From the pulmonary veins the blood enters the left atrium and then passes through the mitral valve to the left ventricle. As the ventricles contract, the mitral valve prevents backflow of blood into the left atrium, and blood is driven through the aortic valve into the aorta, the major artery that supplies blood to the entire body. The aortic valve, like the pulmonary valve, has a semilunar shape. The aorta has many branches, which carry the blood to various parts of the body. Each of these branches in turn has branches, and these branches divide, and so on until there are literally millions of small blood vessels. The smallest of these on the arterial side of the circulation are called arterioles. They contain a great deal of smooth muscle, and because of their ability to constrict or dilate, they play a major role in regulating blood flow through the tissues.

The Blood The blood transports life-supporting food and oxygen to every cell of the body and removes their waste products. It also helps to maintain body temperature, transports hormones, and fights infections. The brain cells in particular are very dependent on a constant supply of oxygen. If the circulation to the brain is stopped, death shortly follows.

Blood has two main constituents. The cells, or corpuscles, comprise about 45 percent, and the liquid portion, or plasma, in which the cells are suspended comprises 55 percent. The blood cells comprise three main types: red blood cells, or erythrocytes; white blood cells, or leukocytes, which in turn are of many different types; and platelets, or thrombocytes. Each type of cell has its own individual functions in the body. The plasma is a complex colorless solution, about 90 percent water, that carries different ions and molecules including proteins, enzymes, hormones, nutrients, waste materials such as urea, and fibrinogen, the protein that aids in clotting. Red Blood Cells The red blood cells are tiny, round, biconcave disks, averaging about 7.5 microns (0.003 in) in diameter. A normal-sized man has about 5 l (5.3 qt) of blood in his body, containing more than 25 trillion red cells. Because the normal life span of red cells in the circulation is only about 120 days, more than 200 billion cells are normally destroyed each day by the spleen and must be replaced. Red blood cells, as well as most white cells and platelets, are made by the bone marrow. The main function of the red blood cells is to transport oxygen from the lungs to the tissues and to transport carbon dioxide, one of the chief waste products, it to the lungs for release from the body. The substance in the red blood cells that is largely responsible for their ability to carry oxygen and carbon dioxide is hemoglobin, the material that gives the cells their red color. It is a protein complex comprising many linked amino acids, and occupies almost the entire volume of a red blood cell. Essential to its structure and function is the mineral iron. Platelets Platelets, or thrombocytes, are much smaller than the red blood cells. They are round or biconcave disks and are normally about 30 to 40 times more numerous than the white blood cells. The platelets' primary function is to stop bleeding. When tissue is damaged, the

platelets aggregate in clumps to obstruct blood flow. Plasma The plasma is more than 90 percent water and contains a large number of substances, many essential to life. Its major solute is a mixture of proteins. The most abundant plasma protein is albumin. The globulins are even larger protein molecules than albumin and are of many chemical structures and functions. The antibodies, produced by lymphocytes, are globulins and are carried throughout the body, where many of them fight bacteria and viruses. An important function of plasma is to transport nutrients to the tissues. Glucose, for example, absorbed from the intestines, constitutes a major source of body energy. Some of the plasma proteins and fats, or lipids, are also used by the tissues for cell growth and energy. Minerals essential to body function, although present only in trace amounts, are other important elements of the plasma. The calcium ion, for example, is essential to the building of bone, as is phosphorus. Calcium is also essential to the clotting of blood. Copper is another necessary component of the plasma. Cerebral circulation Cerebral circulation refers to the movement of blood through the network of blood vessels supplying the brain. The arteries deliver oxygenated blood, glucose and other nutrients to the brain and the veins carry deoxygenated blood back to the heart, removing carbon dioxide, lactic acid, and other metabolic products. Since the brain is very vulnerable to compromises in its blood supply, the cerebral circulatory system has many safeguards. Failure of these safeguards results in cerebrovascular accidents, commonly known as strokes. The amount of blood that the cerebral circulation carries is known as cerebral blood flow. The presence of gravitational fields or accelerations also determine variations in the movement and distribution of blood in the brain, such as when suspended upside-down. There are two main pairs of arteries that supply the cerebral arteries and the cerebellum:
y

Internal carotid arteries: These large arteries are the left and right branches of the

common carotid arteries in the neck which enter the skull, as opposed to the external carotid branches which supply the facial tissues. The internal carotid artery branches into the anterior cerebral artery and continues to form the middle cerebral artery Vertebral arteries. These smaller arteries branch from the subclavian arteries which primarily supply the shoulders, lateral chest and arms. Within the cranium the two vertebral arteries fuse into the basilar artery, which supplies the midbrain, cerebellum, and usually branches into the posterior cerebral artery.

Both internal carotid arteries, within and along the floor of the cerebral vault, are interconnected via the anterior communicating artery. Additionally, both internal carotid arteries are interconnected with the basilar artery via bilateral posterior communicating arteries. The Circle of Willis, long considered to be an important anatomic vascular formation, provides backup circulation to the brain. In case one of the supply arteries is occluded, the Circle of Willis provides interconnections between the internal carotid arteries and basilar artery along the floor of the cerebral vault, providing blood to tissues that would otherwise become ischemic. Cerebral venous drainage The venous drainage of the cerebrum can be separated into two subdivisions: superficial and deep. The superficial system is composed of dural venous sinuses, which have wall composed of dura mater as opposed to a traditional vein. The dural sinuses are, therefore located on the surface of the cerebrum. The most prominent of these sinuses is the Superior sagittal sinus which flows in the sagittal plane under the midline of the cerebral vault, posteriorly and inferiorly to the torcula, forming the Confluence of sinuses, where the superficial drainage joins with the sinus the primarily drains the deep venous system. From here, two transverse sinuses bifurcate and travel laterally and inferiorly in an S-shaped curve that forms the sigmoid sinuses which go on to form the two jugular veins. In the neck, the jugular veins parallel the upward course of the carotid arteries and drain blood into the vena cava. The deep venous drainage is primarily composed of traditional veins inside the deep structures of the brain, which join behind the midbrain to form the Vein of Galen. This vein

merges with the Inferior sagittal sinus to form the Straight sinus which then joins the superficial venous system mentioned above at the Confluence of sinuses. The Renal Circulation The kidneys continuously cleanse the blood and adjust its composition, so it is not surprising that they have a very rich blood supply. Under normal resting conditions, the large renal arteries deliver approximately one-fourth of the total systemic cardiac output (about 1200 ml) to the kidneys each minute. The renal arteries issue at right angles from the abdominal aorta between the first and second lumbar vertebrae. Because the aorta lies to the left of the midline, the right renal artery is longer than the left. As each renal artery approaches a kidney, it divides into five segmental arteries that enter the hilus. Within the renal sinus, each segmental artery branches into several lobar arteries. These then divide to form several interlobar arteries, which pass between the medullary pyramids toward the cortex. At the medulla-cortex juncture, the interlobar arteries branch into the arcuate arteries that arch over the bases of the medullary pyramids. Small interlobar arteries radiate outward from the arcuate arteries to supply the cortical tissue. More than 90% of the blood entering the kidneys perfuses the cortex, which constraints the bulk of the nephrons, the structural unit and functional unit of the kidneys. Veins of the kidney pretty much trace the pathway of the arterial supply in reverse. Blood leaving the renal cortex drains sequentially into the interlobular, arcuate, interlobar, and finally, the renal veins. The renal veins issue form the kidneys and empty into the inferior vena cava. Since the inferior vena cava lies to the right of the vertebral column, the left renal vein is about as long as the right.

III.

Etiology and Risk Factors

Kawasaki disease is primarily a condition of young children. Eighty percent of cases are seen in children younger than 5 years of age, with incidents peaking in the toddler age group. Males are affected slightly more than females. It occurs 1.5 to 1.7 times more

frequent in males. Its peak incidence is during winter and spring. Infants younger than 1 year old are at great risk for heart involvement. Recent data have suggested that children older 5 years of age are also at risk of developing cardiac sequelae, perhaps because KD is often not suspected in older children, which leads to delayed diagnosis of the treatment. The etiology of KD remains unconfirmed. Although KD is not spread by person to person contact, several factors support an infectious cause. It is often seen in geographic and seasonal outbreaks with most cases reported in late winter and early spring. KD is also a pediatric illness, which suggests the development of passive immunity. Because an etiologic agent has not been found, some experts believe that the illness may represent a final common pathway for more than one potential agent. IV. Pathophysiology

c. Identify the different risk factors that may contribute to the occurrence of Kawasaki Disease at 75% level of competency.

Kawasaki Disease (KD) involves widespread inflammation of the small and medium sized blood vessels with the coronary arteries being the most susceptible to damage. During the acute stage of the illness, there is a progressive inflammation of the small vessels 3 (capillaries, venules, arterioles), along with pancarditis. This inflammation is reflected in mins clinical signs and symptoms as well as laboratory test results, which show an elevation in the markers of inflammation (C reactive level and erythrocyte sedimentation rate) in the acute illness. This vasculitis progresses to the medium size muscular arteries, potentially damaging the walls and leading to the formation of coronary artery aneurysm in some children. Initial evidence of enlargement of the coronary arteries can be detected as early as day 7 of illness. Affected vessels continue to increase and generally reach their largest diameter approximately 4 to 6 weeks from the onset of fever. Longer duration of fever (most likely reflecting the severity of inflammation) is strongly associated with the development of aneurysms. Aneurysms of the peripheral vessels (axillary, brachial, iliac, cervical and renal arteries) can occur, although this is very rare and is usually seen only in children who have large coronary aneurysms. In the acute phase, myocarditis (inflammation of the myocardium) is usually present. Decreased LV function is maybe seen in the echocardiogram, but children do not often have clinical signs and symptoms of heart failure, and ventricular function often usually improves after the administration of IV immunoglobulin (IVIG). The systemic inflammation gradually subsides and eventually

Socialized discussion with concept map Oral Evaluation 1. Give at least 2 risk factors for Kawasakis Disease

ceases in 6 to 8 weeks. d. Understand clearly the Pathophysiology of Kawasakis Disease Over time, affected vessels may try to heal through multiplication of cells in the vessels, in an attempt to restore a normal diameter. The process is called myointimal proliferation. Even if the lumen size is restored, however, the vessel size is never completely 10 normal again. The affected vessel walls are thicker, and are subject to scarring and mins calcification, especially in the distal ends of the aneurysms. Almost all of the morbidity and mortality resulting from KD is caused by cardiac complications. Coronary thrombosis may result from sluggish blood flow, in a dilated or aneurismal vessel. Over the years, stenosis and scarring may lead to impeded blood flow, which predisposed the patient to myocardial ischemia or infarction.

Socialized discussion with concept map

Oral Evaluation 1. Briefly describe the Pathophysiology of Kawasakis Disease.

V.

Clinical Manifestations

KD manifests in three phases: Acute, Subacute and Convalescent. The acute phase begins with an abrupt onset of high fever that is unresponsive to antibiotics and antipyretics. Over the next week or so, diagnostic symptoms become evident. The bulbar conjunctivas of the eyes become reddened with clearing around the iris (limbal sparing). The eyes are generally dry without significant drainage. Inflammation of the pharynx and the oral mucosa develops with red crackes lips with the characteristic Strawberry tongue (the normal coating of the tongue sloughs off leaving the large papilla exposed, so that the tongue resembles a strawberry). The rash of KD differs from child to child but is never vesicular. It is most often accentuated in the perineum. Often, the areas affected by the rash desquamate. In addition, the childs hands and feet become edematous and the palms and soles become very erythematous. The child may have cervical lymphadenopathy (at least single node of 1.5 or larger). The node is usually not very tender or red. During this stage, the child is typically very irritable and inconsolable. Approximately one third of patients will develop a temporary arthritis beginning in the small joints. Cardiac manifestations during this period include myocarditis with resultant ECG changes, decreased LV function, pericardial effusion and mitral regurgitation. Generally, these findings are subclinical, but occasionally children with poor function present with symptoms of cardiogenic shock. On physical examination,

the child is maybe tachycardic with with a gallop rhythm. The coronary arteries may begin to show enlargement during this phase. The subacute phase begins with the resolution of the fever and lasts until all outward clinical signs of KD have disappeared. If changes in coronary arteries occur, enlargement or dilation is generally evident by echocardiography during the second week of illness. Thrombocytosis and hypercoagulability in children with expanding aneurysms and disrupted blood flow place the child at risk for coronary thrombosis. During this period the child often has the characteristic periungal desquamation (peeling that begins under the fingertips and toes) of the hands and feet. Arthritis may be evident during this phase and usually affects the 5mins larger weight-bearing joints. Irritability persists during this period. In the convalescent phase, all of the clinical signs of KD have resolved. The laboratory values, however, have not yet returned to normal. The C-reactive protein level and erythrocyte sedimentation rate remain elevated which reflects lingering inflammation. Thrombocytosis may still be present. Arthritis may continue into this stage, and coronary complications may remain a concern, because coronary dimensions peak 4 to 6 weeks from the onset of illness. This phase is complete when all blood values return to normal (6 to 8 weeks after onset). At the end of this stage, parents report that the child appears to have to return to normal in terms of temperament, energy, and appetite. Cardiac Involvement. The most serious complication of KD is the potential for myocardial infarction in children with aneurysm formation. Ischemia generally results from thrombotic occlusion or stenotic occlusion of a coronary aneurysm. The group at higher risk for thrombus is children with giant (larger than 8mm in diameter). Symptoms of acute myocardial infarction in young children may be subtle and may include abdominal pain, vomiting, restlessness, inconsolable crying, pallor, and shock. Complaints of chest pain are more typical in older children. VI. Diagnosis

e. Identify the phases of the manifestation of Kawasakis disease and correctly describe in their own understanding the clinical manifestations of Kawasakis Disease in each phases.

Socialized discussion with concept map Oral Evaluation 1. What are the phases of the manifestation of Kawasakis Disease? 2. What are the different clinical manifestations in each phase?

Currently no specific diagnostic test exists for KD. Therefore, the diagnosis is established on the basis of clinical findings and associated laboratory results.

Several associated laboratory findings, when combined with clinical data, can be helpful in making the diagnosis. The typical child with KD is anemic and has leukocytosis with a shift to the left (increased immature white blood cells) during the acute phase. Thrombocytosis with hypercoagulability becomes evident in the subacute phase and peaks approximately 3 weeks after the onset of fever. An elevated erythrocyte sedimentation rate and C-reactive protein level reflect ongoing inflammation and generally persists for 6-8 weeks. The erythrocyte sedimentation rate can be further elevated by the administration of IVIG and therefore useful to measure C-reactive protein level as another indicator of inflammation. Microscopic urinalysis reveals a sterile pyuria with mononuclear cells. This will not be evident with a regular dipstick test, because the white blood cells are not polymorphnuclear neutrophils. A transient elevation of liver enzyme levels typically occurs, reflecting inflammation of the liver. Examination of the cerebrospinal fluid may give evidence of aseptic meningitis (presence of inflammatory cells). Albumin levels may be lower than normal. Echocardiograms are used to monitor myocardial and coronary artery status. A baseline echocardiogram should be obtained at the time of diagnosis for comparison with future studies. In addition, follow-up echocardiograms should be performed at approximately 2 weeks after the onset and again at 6to 8 weeks from the onset of fever to determine the diameter of the coronary arteries as well as LV contractility and valvular function. If cardiac involvement is evident, or if the child has continued fever or required retreatment, more frequent studies to assess coronary dimensions may be indicated.

f. Identify at least 5 diagnostic aids in detecting Kawasakis Disease.

VII.

Therapeutic Management Socialized discussion with concept map

The current treatment of KD includes high dose IVIG along with salicylate therapy. High dose IVIG has been shown to reduce the duration of fever and the incidence of coronary artery abnormalities when given within the first 10 days of illness. A single large 5 mins infusion of 2g/kg over 10 to 12 hours is recommended. Aspirin is given initially in an anti-inflammatory dosage (80 to 100 mg/kg/day in

divided doses every 6 hours) to control fever and symptoms of inflammation. The duration of therapy varies among institutions. Once fever has subsided, and the child has been afebrile for 48 to 72 hours, the aspirin dosage is generally decreased to an antiplatelet dosage (3to 5 mg/kg/day). Low dosage aspirin is continued in patients without echocardiogram evidence of coronary abnormalities until the platelet count has returned to normal. If the child develops coronary abnormalities, low-dose antiplatelet salicylate therapy is continued indefinitely. Additional anticoagulatory therapy, such as warfarin administration, maybe indicated in children with giant aneurysms (larger than 8mm), who are at the greatest risk for morbidity and mortality. Prognosis. Most children with KD recover fully after treatment. When cardiovascular complications occur, however, serious morbidity occurs. Death occurs rarely (0.3%) and almost always results from ischemia caused by coronary thrombosis or stenosis. Children with coronary abnormalities are followed with periodic ECG, echocardiography, myocardial perfusion testing at rest and during exercise, and/or cardiac magnetic resonance imaging based on their individual risk and the availability of various testing modalities. Although the echocardiography is very sensitive in visualizing cardiac dilatation, it does not detect the presence of stenosis of the coronary arteries. Cardiac catheterization of the coronary arteries remains gold standard and maybe performed in children who still have significant abnormalities after 1 year and in situations in which myocardial ischemia is suspected from the results of noninvasive testing. A rare sequel of KD is sensorineural hearing loss. If decreased hearing is suspected, the child should undergo audiologic testing. g. Briefly describe the therapeutic management for Kawasaki Disease at a 75% level of competency Bear in mind that children who has cardiac complications should have a close 5 mins monitoring of cholesterol levels and Blood pressure levels and these children should be encouraged to lead a heart-healthy lifestyle in terms of diet, exercise, and avoidance of smoking.

Oral Evaluation 1. Give 5 diagnostic aids for Kawasakis Disease.

Socialized discussion with concept map

Oral Evaluation

VIII.

Nursing Care Management

The nursing care of management of children with Kawasaki disease is challenging. Inpatient care focuses on symptomatic relief, emotional support, diagnostic assistance, medication administration, and education of the child and the family. In the initial phase the nurse must monitor the childs cardiac status carefully. Intake and output and daily weight measurement are recorded. Although the child may be reluctant to eat and therefore maybe partially dehydrated, fluids need to be administered with care because of the usual findings of myocarditis. The child should be assessed frequently for signs of congested heart failure, including decreased urinary output, gallop rhythm, tachycardia, and respiratory distress. Cardiac monitoring is suggested in the following cases: before the initial ECG and echocardiogram are recorded and shown to be normal, during the infusion of IV alpha-globulin (because of the large fluid load), in children younger than 1 year of age, and in any child with cardiac symptoms. Sedation is generally required before echocardiography in children younger than 2.5 to 3 years of age, because child must remain still for 1 hour. Nursing care focuses primarily on symptomatic relief. To minimize skin discomfort, application of cool cloths and unscented lotions, and use of soft, loose clothing are helpful. During the acute phase, mouth care, including application of lubricating ointment in the lips, is important for the mucosal inflammation. Clear liquids and soft foods can be offered. Temperature must be carefully monitored. It is important to document temperature just before aspirin administration, because the occurrence of fever reflects on going inflammation and may indicate the need for further treatment. In situations in which temperature is very high, acetaminophen is maybe given in addition to high dose aspirin. If arthritis develops, passive-range-of-motion exercises maybe indicated and can be done most easily during the childs bath. The administration of alpha-globulin should follow the same guidelines for administration of any blood product, with frequent monitoring of vital signs. Patients much be watched for allergic reactions. Cardiac status must be monitored because of the large fluid

1. Give the possible therapeutic management for Kawasakis Disease.

h. Identify the nursing management for Kawasakis Disease at 75% level of competency.

being administered to patients who have subclinical myocarditis or diminished left ventricle function. Patency of the IV line is checked because extravasation can result in tissue damage. Hypercoagulability and venous fragility often make it difficult to maintain IV access in children with KD. Patient irritability is perhaps the most challenging problem. These children need to be 10 placed in a quiet environment that promotes adequate rest. Their parents need to be mins supported in their efforts to comfort an often inconsolable child. They may need time away from their child, and nurses can often provide respite care for the family. Parents need to understand that irritability is a hallmark of KD and that they need not feel guilty or embarrassed about their childs behavior. Discharge teaching. Parents need accurate information about the usual course of KD, including the importance of follow-up monitoring and the circumstances under which that should contact their practitioner. Irritability is likely to persist up to 2 months after the onset of symptoms. Peeling of the hands and feet are painless and occurs primarily in the second or third weeks. Arthritis, especially for the larger weight-bearing joints, may persist for several weeks. Children are typically most stiff in the mornings, during cold weathers and after naps. Passive range-of-motion exercises in the bathtub are often helpful in increasing flexibility. Although arthritis in KD is always temporary, it can be severe enough that some children require treatment with an antiarthritic agent once they are no longer on high dose aspirin. Despite treatment with IVIG, some children develop recurrent fever and symptoms, which necessitate retreatment with IVIG (2g/kg) in approximately 10% of children. Parents should be educated about recrudescent illness after discharge and to contact their physician or practitioner if there is any increase in temperature. Parents also need to be instructed about administration of salicylates and, if the child if the child is receiving high dosages, made aware of the signs of toxicity- ringing in the ears (tinnitus), headache, dizziness and confusion. The only side effect of low-dose aspirin is easy bruising. In addition, the aspirin should be stopped and the practitioner notified if the child is exposed to chickenpox or influenza because of the drugs possible association with Reye

Socialized discussion with concept map

Oral Evaluation 1. Identify various nursing management for Kawasakis Disease.

syndrome. All parents should understand the unlikely but real possibility of myocardial infarction as well as the signs and symptoms of cardiac ischemia in a child. At the time of hospital discharge, the final cardiac sequelae are generally not full known, because changes in the in the coronary arteries occur over the first 4 to 6 weeks after the onset of KD. In addition, the parents of children with known severe coronary artery sequelae should be taught cardiopulmonary resuscitation. Finally, children with coronary abnormalities require indefinite antiplatelet therapy with low-dose aspirin or other anticoagulants. In such cases, contact sports should be avoided, and yearly administration of influenza vaccine is indicated. The administration of measles-mumps-rubella vaccine should be delayed for 11 months after the administration of IVIG because the body might not produce the appropriate number of anti-bodies. In addition, the varicella vaccine should not be given for at least 11 months after IVIG therapy.

IX.

Nursing Diagnoses and Interventions

1. Altered Comfort: Acute Pain related to swelling of the lymph nodes and inflammation of the joints         Investigate reports of pain, noting location and intensity(scale of 010). Note precipitating factors and nonverbal pain cues. Recommend/provide firm mattress or bedboard, small pillow. Elevate linens with bed cradle as needed Suggest patient assume position of comfort while in bed or sitting in chair. Promote bedrest as indicated. Place/monitor use of pillows, sandbags, trochanter rolls, splints, braces. Encourage frequent changes of position. Assist patient to move in bed, supporting affected joints above and below, avoiding jerky movements. Recommend that patient take warm bath or shower on arising and/or at bedtime. Apply warm, moist compresses to affected joints several times a day. Monitor water temperature of compress, baths, and so on. Provide gentle massage. Encourage use of stress management techniques, e.g., progressive relaxation, biofeedback, visualization, guided imagery, self-hypnosis, and controlled breathing. Provide Therapeutic Touch.

  

Involve in diversional activities appropriate for individual situation. Medicate before planned activities/exercises as indicated. Administer medications as indicated, e.g. Salicylates, e.g., aspirin (ASA)

2. Hyperthermia  Monitor patient temperature (degree and pattern); note shaking chills/profuse diaphoresis.  Monitor environmental temperature; limit/add bed linens as indicated  Provide tepid sponge baths; avoid use of alcohol.  Increase fluid intake if not contraindicted.  Administer antipyretics, e.g., acetylsalicylic acid (ASA) (aspirin), acetaminophen (Tylenol).  Provide cooling blanket. 3. Impaired Skin Integrity related to presence of skin erythema and desquamation secondary to hyperthermia.  Inspect skin, tissues, and mucous membranes routinely.  Assess nutritional status and initiate corrective measures as indicated. Provide balanced diet, e.g., adequate protein, vitamins, and minerals.  Maintain strict skin hygiene, using mild, non detergent soap (if any), drying gently and thoroughly, and lubricating with lotion or emollient. Change position frequently in bed and chair. Recommend 10 min of exercise each hour and/or perform passive ROM.  Keep sheets and bedclothes clean, dry, and free from wrinkles, crumbs, and other irritating material. Limit exposure to temperature extremes/use of heating pad or ice pack. 8  Keep nails cut short and smooth mins  Use lotion, softening cream on feet

i.

Give 2 possible Nursing Diagnoses for Kawasaki Disease and give at least 5 interventions for each.

Lecture with PowerPoint Presentation

Oral Evaluation 1. Give 2 nursing diagnoses for Kawasakis Disease. 2. Give 5 interventions for the identified Nursing diagnosis.

20-30 item Quiz at 75% level of competency

References: Hockenberry, M. & David, W. (2007). Wongs Nursing Care of Infants and Children. 5th Ed. U.S.A.: Mosby, Elsevier Inc. Marieb, E.N. (2001). Essentials of Human Anatomy & Physiology. (5th ed.) Pearson Education Inc. South Asia. Pilliteri, A. (2007). Maternal and Child Health Nursing. (5th ed.). Lippincott Williams and Wilkins McCance, K.L. &Huether, S.E.(2006).Pathophysiology: the biologic basis for disease in adults and children. (5th ed) U.S.A: Mosby, Elsevier, Inc.