Lapkas Anak (Prof Dr. Hj. Bidasari)

8/10/2019 Lapkas Anak (Prof Dr. Hj. Bidasari)

1/74

CHAPTER 1

INTRODUCTION

1.1. Background

Malnutrition can be defined as a state of nutrition in which deficiency or excess of energy,

protein, and other nutrients causes measurable adverse effects on tissue and body form and

function, and clinical outcome. Malnutrition can be of the acute, chronic or mixed type.

Acute malnutrition is the type that usually occurs in illness, but children with underlying

chronic diseases whoare admitted to the hospital because of an acute illness can also presentwith chronic malnutrition. Anthropometric variables are used to define nutritional status

worldwide but various classification systems and cutoff points are used to define

malnutrition. One such classification method includes kwashiorkor and marasmus. These

terms were originally established to describe syndromes of protein-energy malnutrition in

children in developing countries. The most used classification system was that described by

Waterlow, in which acute and chronic malnutrition were divided into four stages, on the basis

of the actual weight to the 50th percentile of Weight For Height for acute malnutrition and

the actual height to the 50th percentile for height for chronic malnutrition.

Childhood malnutrition is a disease of relevance and importance to public health. These

children exhibit elevated morbidity and increased prevalence of hospital admissions. When

admitted to the hospital they are not generally subjected to anthropometric assessment and do

not, therefore, receive nutritional support. Hospital acquired malnutrition is caused by a

reduction in the hospitalized children nutritional intake and increase in their calorie

requirements as a result of morbidity. There is an identified number of contributing factors tothe widespread existence of under nutrition among hospitalized child and sometimes leads to

exacerbation of his or her nutritional status.

Examples are interference with meal times by ward rounds, investigations and procedures.

Nil-by-mouth orders may be used inappropriately or prolonged unnecessarily. A patient

may be kept nil-by mouth all morning only to find that their treatment has been cancelled or

delayed. In addition, many drugs cause anorexia, taste changes, nausea, vomiting or

constipation, thereby reducing food intake. The psychological outcome of hospitalized


2/74

children remains little studied and poorly understood. Children have been observed to be

anxious, withdrawn, fearful, restless, and angry or demonstrate hostile behaviors and

therefore, contributing to malnutrition.

Cholestasis is defined as reduced bile flow and abnormal accumulation of conjugated

bilirubin, indicating impaired hepatobiliary function. Conjugated bilirubin is considered

abnormal if it is 1 mg/dl or above when the total bilirubin is less than 5 mg/dl or more than 20

percent of the total bilirubin when the total is above 5 mg/dl.

Cholestasis occurs in approximately 1 in 2,500 births. Biliary atresia and neonatal hepatitis

account for most cases. The other etiologies of cholestasis are numerous and include

anatomic obstruction (such as bile sludging and choledochal cyst), infection (such as urinary

tract infection and CMV), metabolic disorders (such as galactosemia and tyrosinemia),

genetic disorders (such as alpha-1 antitrypsin deficiency, cystic fibrosis and Alagille

syndrome), endocrine dysfunction (such as hypothyroidism and panhypopituitarism) and

toxins (such as TPN).

The primary care physician is critically important in the evaluation of the jaundiced infant. It

is recommended that all infants with persistent jaundice beyond 2 weeks old be assessed with

a fractionated bilirubin. In healthy breast-fed infants with no signs of cholestasis, thisinvestigation can be postponed until 3 weeks old. If conjugated hyperbilirubinemia is present,

prompt referral to a pediatric gastroenterologist for further evaluation is imperative.

Developmental Disability/Delay (DD) is present when functional aspects of a childs

development in one or more domains are significantly delayed compared to the expected

level for age. These functional aspects are gross/fine motor, speech/language, cognition,

social/personal, and activities of daily living. Global Developmental Delay (GDD) is a subset

of Developmental Disability/Delay, defined as significant delay in two or more

developmental domains. However, this is reserved for children less than 5 years old. An

estimated 12-16% of children have a developmental and/or behavior disorder.


3/74

CHAPTER 2

LITERATURE REVIEW

2.1. HOSPITAL ACQUIRED MALNUTRITION

2.1.1. DEFINITION

Malnutrition can be defined as a state of nutrition in which deficiency or excess of

energy, protein, and other nutrients causes measurable adverse effects on tissue andbody

form and function, and clinical outcome.The World Health Organization (WHO) defines

malnutrition as the cellular imbalance between the supply of nutrients and energy and the

bodys demand for them to ensure growth, maintenance, and specific functions. This

dynamic imbalance of nutrients affects children differently than adults and can have profound

implications for the developing child.

The most used classification system was that described by Waterlow,1 in which acute

and chronic malnutrition were divided into four stages, on the basis of the actual weight

to the 50th percentile of WFH for acute malnutrition and the actual height to the 50th

percentile for height for chronic malnutrition.

In 1992, the international statistical classification of disease and related health

problems used weight, expressed as SD scores, to define the probability of malnutrition.

For example, an SD score between 1 and 2 (representing 13.5% of the reference

population) indicates a probability of mild malnutrition and an SD score of less than

2 indicates a probability of severe malnutrition (2.3%). This statistical approach does

not use weight-for-height index and does not define the reference population. In 1999, theWorld Health Organization

2 recommended an additional classification for malnutrition in

children, which became widely used. The likelihood of malnutrition is defined using a

cutoff point of 2 SD. A child with a SD score between 1 and 2 is no longer defined

as malnourished. According to these WHO criteria, a SD score for WFH between 3 and

2 can be considered as moderate malnutrition and a SD score below 3 as severe

malnutrition.


4/74

Acute malnutrition (severe and moderate) is defined as one of the following:

WFH SD score less than 2,

WFH less than 80% of the median,

% ideal body WFH less than 80,

WFH less than 5th percentile,

BMI SD score less than 2.

Chronic malnutrition is defined as:

Height for age (HFA) SD score less than 2,

HFA less than 90% of the median,

HFA less than 5th percentile.


5/74

Hospital acquired malnutrition refers to nutrient imbalance acquired during hospitalization

and may occur with or without pre-existing malnutrition, or malnutrition that was present

prior to hospital admission. The mechanisms of nutrient imbalance in illness-related

malnutrition include decreased nutrient intake, altered utilization, increased nutrient losses, or

increased nutrient requirements (hyper metabolism) not matched by intake.

2.2 CAUSES

Hospital acquired malnutrition occurs largely among children admitted to hospital with an

underlying disease.

Cardiac disease

Cardiac cachexia refers to a syndrome of protein-energy malnutrition seen in patients

with chronic cardiac disease. A high prevalence percentage of low WFH is reported

most commonly in patients with chronic congestive failure, chronic shunt hypoxemia and

nosocomial postoperative acute and chronic states. Various studies3-5among children

with various cardiac diseases (e.g. congenital heart disease, idiopathic dilated

cardiomyopathy) showed prevalence rates between 18 and 64% on admission. The

highest rates were found in cardiac surgical patients and in children with congenital

heart diseases and left-to-right shunt.

Cystic fibrosis

Malnutrition is an extremely substantial complicating factor in patients with cystic

fibrosis. A poor nutritional status is a negative prognostic factor and malnutrition and

deterioration of lung function are interrelated and inter- dependent. Substantial

improvements in medical management including nutritional therapy have been made.

In the USA, in 1999, it was reported that 24% of the cystic fibrosis patients had a weight

less than the 5th percentile. In a very large study in the USA6, children below 1

year and above 10 years appeared tobe at more risk of acute malnutrition than children

aged 110 years.

Malignancy

Malnutrition in childhood cancer is a common and serious problem. Besides the

previously mentioned con- sequences of malnutrition, it is associated with adecreased tolerance to chemotherapy. Although malnutrition is not uniformly found in


6/74

all pediatric malignancies, certain types of malignancies are at high nutritional risk (solid

tumors, medulloblastoma, acute nonlymphocytic leukemia, and multiple relapse

leukemia). Furthermore, marked differences in the prevalence of malnutrition will be

found between children on therapy and those off therapy. The use of body weight to

assess nutritional status in pediatric cancer patients has been misleading because of the

confounding effects of tumor mass. Up to 50% of pediatric patients with malignancies

were reported to be undernourished. Recently, a study6reported a prevalence rate of

9.1% acute malnutrition (


7/74

Neurological disorders

In general, poor nutritional status and growth is often seen in children with

neurological disorders. It is advocated to use specific weight charts for specific diseases

such as Duchennes muscular dystrophy. The preciseprevalence varies depending on

the criterion by which malnutrition is defined, the degree of mental retardation, the

presence of associated problems, treatment administered, and socioeconomic and family

environment. In a study, eight different criteria were used to define the nutritional

status of mentally retarded children on the basis of anthropometric variables. The

prevalence of malnutrition increased with age, increasing intelligence quotient deficit and

cerebralpalsy.

In children with Duchenne muscular dystrophy, malnutrition occurs after the age of 14

years, involving 54% of boys at about 18 years of age. Evaluating developmentally

disabled children is often difficult because they do not fit into normal standards for

assessment. In children with cerebral palsy, malnutrition is associated with the degree

of feeding dysfunction. A s t u d y found in a mixed population7, using the criterion

less than 80% WFH, malnutrition in 24% of the children with mental retardation.

In conclusion, a summary was given of the prevalence of malnutrition in a selection ofchildren with an underlying disease. The main finding is that malnutrition is still

highly prevalent in children with an underlying disease. In children with chronic

inflammatory diseases such as chronic kidney disease, both acute and chronic mal-

nutrition remain highly prevalent, probably due to the ongoing inflammatory state. For

diseases such as inflammatory bowel disease and AIDS, the nutritional status is also

dependent on the degree of inflammation

2.3 PATHOGENESIS

Inflammatory conditions may increase requirements for nutrients while promoting a nutrient-

wasting catabolic state. Illness-related malnutrition is associated with an inflammatory

component. Inflammation promotes skeletal muscle breakdown, mediated by a cytokine-

driven pathway. Critical illness or injury promotes an acute inflammatory response that has a

rapid catabolic effect on lean body mass. The acute phase inflammatory response isassociated with elevated resting energy expenditure and nitrogen excretion and thereby


8/74

energy and protein requirements, respectively. Nutrition supplementation alone only partly

reverses or prevents muscle protein loss in active inflammatory states. The anorexia that

accompanies inflammation will promote further loss of lean tissue if nutrition intake is

inadequate. Over the past decade, it has become increasingly evident that the

pathophysiology of disease or injury-associated malnutrition invariably includes acute or

chronic inflammation that affects body composition and biological function.

The inflammatory condition may be short-lived or chronic in nature with the severity being

influenced by the progression and extent of underlying illness/disease condition. Loss of

muscle mass and function may occur insidiously in the chronic disease state over months to

years. It is important to recognize the presence or absence of a systemic inflammatory

response in the malnourished state, as it affects the response to intervention. In the absence of

inflammation, as seen in malnutrition due to starvation, appropriate nutrient interventions

may be successful in treating malnutrition. On the other hand, the presence of inflammation

may limit the effectiveness of nutrition interventions, and the associated malnutrition may

compromise the clinical response to medical therapy. If inflammation is present, then it is

useful to clarify whether it is mild, moderate, or severe and transient or sustained. The

recently proposed adult malnutrition definition has suggested that acute disease- related

malnutrition is probably associated with a severe degree of inflammation and chronic disease-related malnutrition with a mild to moderate degree of inflammation.

However, the role of inflammation and currently available inflammatory markers, such as C-

reactive protein (CRP) or erythrocyte sedimentation rate, in classifying pediatric malnutrition

severity has not been adequately described.

Inflammatory cytokines can impair growth via multiple pathways. Anorexia, skeletal muscle

catabolism, and cachexia affect the growth plate via insulin-like growth factor 1 (IGF-1)

independent or IGF-1dependent pathways.The inhibitory effects of tumor necrosis factor

(TNF-)and interleukin (IL)1 on the growth plate are reversed by antiIL-1 and anti

TNF-. The effect of TNF- on IL-6 transcription and circulating leptin level may be

reversed by infliximab. In pediatric Crohns disease, growth retardation may result from a

complex interaction between nutrition status, inflammation, disease severity, and genotype,

which causes resistance to the effects of growth hormone. Elevated serum concentration of

CRP is one of the most common nontraditional markers used to stratify cardiovascular risk,

and it has been used to identify patients with chronic inflammation as it reflects a pro-


9/74

inflammatory state. IL-6 concentrations may be an important marker of early inflammatory

response with serial levels correlating with nutrition status in critically ill children.Although

there is no doubt about the association between inflammatory state and nutrition recovery, the

precise nature of this relationship remains elusive.

2.4 PREVENTION

To prevent malnutrition and especially hospital-acquired malnutrition, the risk of

nutritional depletion needs tobe identified at the time of admission so that appropriate

nutritional intervention can be initiated at an early stage. Routine nutritional screening is

rarely carried out inpediatric patients due to the lack of a simple and valid nutritional

screening tool. Only two screening tools have been published since 2000 to identify

children at risk of malnutrition. Sermet-Gaudelus et al.8described a simple pediatric

nutritional risk score, which is suitable for routine use to identify patients at risk of

malnutrition during hospitalization. Nutritional risk was assessed prospectively in 296

children by evaluating various factors within 48 h of admission. Multivariate analysis

indicated that food intake less than 50%, pain, and grades 2 and 3 pathologic

conditions were associated with weight loss of more than 2%. These significant risk

factors were scored (one point for food intake


10/74

divided children into the three groups with significantly different mean values for

various anthropometric measures. SGNA was considered a valid tool for assessing

nutritional status in children and identifying those at higher risk of nutrition-associated

complications and prolonged hospitalizations. Both methods described by Sermet-

Gaudelus et al. and Secker and Jeejeebhoy link nutritional status to outcome. Both

methods have their limitations in use. The tool of Sermet-Gaudelus et al. needs a period

of 48 h after admission to complete and the study results of Secker and Jeejeebhoywere

not based on a single assessor but were a composite of the data of five asessors. For both

methods, skilled staff are necessary and theprocedures seem to be time-consuming.

3.1. CHOLESTASIS

3.1.1. DEFINITION

Neonatal cholestasisis defined as impaired canalicular biliary flow resulting in accumulation

of biliary substances (bilirubin, bile acids and cholesterol) in blood and extrahepatic tissues.

Jaundice is a common clinical finding in the first 1 to 2 weeks after birth and usually

resolves spontaneously. Any infant who is jaundiced beyond 2 to 3 weeks after birth needs

further evaluation to rule out neonatal cholestasis.10

3.1.2. PATHOPHYSIOLOGY

The normal process of bile production involves two mainprocesses: uptake ofbile acids by

hepatocytes from the blood and excretion of bile acids into the biliary canaliculus. Uptake of

bile acids from sinusoidal blood is an active process at the sinusoidal membrane of the

hepatocytes. Na taurocholate cotransporting polypeptide (NTCP) and organic anion trans-

porting proteins (OATP) are the two main receptors involved in the uptake of conjugated bile

acids by the liver cells. These receptors are also responsible for the transport of other an- ions

like drugs and toxins through the hepatocellular membrane. At the biliary canaliculus, bile

salt export pump (BSEP) and the multidrug resistant proteins MRP2 and MDR3 are

involved in the secretion of bile acids into bile. These pumps are present in the canalicular

membrane.

In newborn infants, the biliary system is both structurally and functionally immature making

them more susceptible to cholestasis. In hepatitis and sepsis, there is down regulation of the


11/74

NTCP and OATP receptors resulting in decreased bile production and cholestasis. Various

genetic defects in the transporter proteins have been recognized in familial cholestasis

syndromes, eg, mutation of BSEP gene in progressive familial intrahepatic cholestasis type 2

(PFIC), defect in the MDR3 in PFIC type 3.

3.1.3 CLASSIFICATION

The differential diagnosis of neonatal cholestasis is extensive and can be classified based on

the anatomic location of the pathology into extrahepatic and intrahepatic causes. Biliary

atresia and choledochal cyst are examples of extrahepatic

causes while common intrahepatic causes include idiopathic neonatal hepatitis, infections,

1-antitrypsin deficiency and other metabolic disorders.The different causes of cholestasis can

also divided into broad etiological categories like infectious, metabolic, toxic, chromosomal,

vascular disorders and bile duct anomalies.

The causes of cholestasis are as below:

1) Idiopathic neonatal hepatitis

2) Infections

Viral

Cytomegalovirus

Rubella

Reovirus3

Adenovirus Coxsackie

Virus Human herpes

Virus 6

Varicella zoster

Herpes simplex

Parvovirus

Hepatitis B and C

Human immuno-deficiency virus


12/74

Bacterial

Sepsis

Urinary tract infection

Syphilis Listeriosis

Tuberculosis

Parasitic

Toxoplasmosis

Malaria

Bile duct anomalies

Biliary atresia

Choledochal cyst

Alagille syndrome

Non syndromicbile duct paucity

Inspissatedbile syndrome

Caroli syndrome

Choledocholithiasis

Neonatal sclerosing cholangitis

Spontaneous bile duct perforation

Metabolic disorders

1-antitrypsin deficiency

Galactosemia

Glycogen storage disorder type IV

Cystic fibrosis

Hemochromatosis

Tyrosinemia Arginase deficiency

Zellwegers syndrome

Dubin-Johnson syndrome

Rotor syndrome

Niemann Pick disease, type C

Gauchers disease

Bile acid synthetic disorders


13/74

Progressive familial intrahepatic cholestasis

North American Indian familial cholestasis

Aagenaes syndrome

X-linked adreno-leukodystrophy Endocrinopathies

Hypothyroidism

Hypopituitarism (Septo-optic dysplasia)

Chromosomal disorders

Turners syndrome

Trisomy 18

Trisomy 21

Trisomy 13

Cat-eye syndrome

Donahues syndrome (Leprechauns)

Toxic

Parenteral nutrition

Fetal alcohol syndrome

Drugs

Vascular

Budd-Chiari syndrome

Neonatal asphyxia

Congestive heart failure

Neoplastic

Neonatal leukemia

Histiocytosis X

Neuroblastoma

Hepatoblastoma

Erythrophagocytic lymphohistiocytosis

Miscellaneous

Neonatal lupus erythematosus

Le foie vide(infantile hepatic non regenerativedisorder)

Indianchildhoodcirrhosis


14/74

3.1.4 CLINICAL PRESENTATIONS

An infant with cholestasis usually presents with prolonged jaundice, pale stools and dark

urine. Acholic stools are a cardinal feature of cholestasis and should be promptly evaluated.

Some infants may present with signs of coagulopathy due to deficiency of clotting factors or

vitamin K deficiency. Neurological abnormalities like irritability, lethargy, seizures and poor

feeding may indicate either sepsis or metabolic disorders.

Physical examination is remarkable for jaundice. Hepatomegaly is common. Splenomegaly

may be seen in infants with advanced liver disease. Other physical findings may include

growth retardation seen in congenital infections and syndromic facial dysmorphisms.

Choledochal cyst can present as a mass in the right upper quadrant

3.1.5 DIAGNOSIS

Any infant presenting with jaundice beyond 2 weeks after birth should be immediately

evaluated for cholestasis. A detailed history (including family history, pregnancy and

delivery history and postnatal course) and physical examination could provide clues to a

specific diagnosis. Breast- fed infants who can be reliably monitored and have an

otherwise normal history and physical examination should be reevaluated at 3

weeks of age and if still jaundiced, have fractionated serum bilirubin levels checked at that

time.Once cholestasis is established, further investigations should be done in a stepwise

manner to establish the specific cause of cholestasis. The investigations should first rule out

conditions requiring immediate intervention like sepsis, metabolic disorders like

galactosemia, glycogen storage disorders and other endocrinopathies. Once they have

been excluded, the next step is to look for biliary atresia. It is important to establish or

rule out biliary atresia early because of better prognosis if the patient undergoes surgical

intervention before 60 days of life. If biliary atresia has been excluded, further

investigations should be done to establish the cause of intrahepatic cholestasis. The

potentially extensive evaluation of an infant with cholestasis should be individualized to

efficiently and promptly establish a diagnosis.


15/74


16/74

3.1.6 Management

Medical management of cholestasis is mostly supportive and does not alter the natural course

of the disease. It is aimed mostly at treating the complications of chronic cholestasis like

pruritus, malabsorption and nutritional deficiencies andportal hypertension.10

4.1 GLOBAL DEVELOPMENTAL DELAY

4.1.1 DEFINITION

Developmental Disability/Delay (DD) is present when functional aspects of a childs

development in one or more domains are significantly delayed compared to the expected

level for age. These functional aspects are gross/fine motor, speech/language, cognition,

social/personal, and activities of daily living. Global Developmental Delay (GDD) is a subset

of Developmental Disability/Delay, defined as significant delay in two or more

developmental domains.

Children with developmental delays often are identified early in life, because they fall

significantly behind their age-mates in meeting developmental milestones. For example, a

young child may be slow to roll over, to understand his or her name, or to exhibit fine motor

skills. Parents of infants often worry when their second child takes longer than the first to

display a specific ability. In fact, the range of ages within which an infant should be able to

perform any given skill is broad. Differences in personality can also result in variations in

developmental progress. Nevertheless, special educators and medical doctors find that the

behaviors and abilities of children who have developmental delays are well outside the age

ranges for almost every developmental benchmark.


17/74

Identifying a child with a developmental delay involves going through a set of evaluative

processes, including intelligence tests, developmental scales, adaptive behavior evaluations,

and tests of general knowledge. Evaluation tools such as intelligence tests and behavioral

scales are normed on a large sample of the population over a long period of time, and the

scores from these sample assessments are distributed along a curve, offering a picture of how

the measured attributes occur in the general population.

Figure 4.1 illustrates a bell curve (or normal curve), the graphic shape that depicts scores on

any standardized measure. On such a curve, the mean (average) score falls in the middle, and

a statistical measure called a standard deviation is used to indicate the distance of a given

score from the mean. When educational evaluators describe children with developmental

delays, they are talking about children whose assessment scores fall at least two standard

deviations below the mean. As you can see from the figure, this means that the childrens

scores are lower than those of 95 percent of the population used to establish the norms for the

test.

4.1.2.CAUSES

The primary cause for developmental delays in school-aged children is genetic abnormalities.

For example, phenylketonuria (PKU) is a single-gene disorder also referred to as an inborn

error of metabolism. PKU leads to mental retardation and other developmental delays if

untreated in infancy because the body is unable to produce proteins or enzymes needed to

convert certain toxic chemicals into nontoxic products or to transport substances from one

place to another (Glanze, 1996). Infants with untreated PKU appear to develop typically for


18/74

the first few months of life, but by twelve months of age most of them will have a significant

developmental delay and will be diagnosed with mental retardation before they start school.

Down syndrome is an example of a chromosomal disorder. Chromosomal disorders happen

sporadically and are caused by too many or too few chromosomes or by a change in structure

of a chromosome. In the case of Down syndrome, the children have recognizable physical

characteristics and limited intellectual endowment because of the presence of an extra

chromosome 21.

Similarly, fragile X syndrome arises from a single gene located on the X (female)

chromosome. It is the leading inherited cause of mental retardation.

Other causes of developmental delays include these:

Problems during pregnancy. Use of alcohol or drugs by a pregnant mother can cause

mental retardation and developmental delays in the child. Research suggests that

smoking also increases the risk of developmental delays. Other risks include

malnutrition, certain environmental contaminants, and illnesses of the mother during

pregnancy, such as toxoplasmosis, cytomegalovirus, rubella, and syphilis. Pregnantwomen who are infected with HIV may pass the virus to their child, leading to future

neurological damage.

Problems at birth. Although any birth condition of unusual stress may injure the

infants brain, prematurity and low birth weight predict serious problems more often

than any other conditions.

Problems after birth. Childhood diseases such as whooping cough, chicken pox,

measles, and HIB disease (which may lead to meningitis and encephalitis) can

damage the brain, as can accidents such as a blow to the head or near drowning. Lead,

mercury, and other environmental toxins can cause irreparable damage to the brain

and nervous system. It is important to note that some children with developmental

delays have problems caused by abuse or neglect. Although accidents and injuries can

result in brain damage, it is often difficult to determine whether the childs problems

existed prior to the accident.

Measured by both intelligence and adaptive behavior measures, approximately 1 percent of

the general population has developmental delays. According to states data reported to the


19/74


20/74

4.1.4 MANAGEMENT

Management of children with developmental delays are usually in the form of therapy. The

therapies are

Occupational and physical therapy. Therapy can help children with motor skills (such

as increasing range of motion and fine motor skills); perceptual skills (for instance,

helping a child track an object in two- or three-dimensional space); and social-

emotional skills (working in groups and taking turns). Occupational therapy also

focuses on the use of adaptive and assistive technologies.

Speech/language therapy.This type of therapy can help children with articulation and

expressive disorders; it also boosts receptive language skills.

Psychotherapy and psychiatric therapy. Broadly speaking, psychological therapy

helps children with the process of recognizing, defining, and overcoming

psychological and interpersonal difficulties. School psychologists are also responsible

for administering many of the assessment inventories mentioned earlier. Psychiatrists

have medical credentials and are responsible for managing any medication therapy the

child may receive for psychological issues, such as anxiety, depression, and sleep

disorders.


21/74

CHAPTER 3

CASE REPORT

Name : AD

Age : 1 years 11 month

Sex : Male

Date of Admission : Augusts, 16th 2013

Main complain: Yellowish pigmentation throughout the body. Patient has been experiencing

this approximately 1 week ago before visiting the hospital. Initially, it started on both eyes,

spreading on face and throughout the body. Fever was found about 1 week ago, not too high

and subsided with medication. Convulsion or seizure was not found. Patient was found

shivering during fever.

Patient was also suffering from diarrhea since 3 days ago, with a frequency of less than 3

times a day. The consistency of the feces was watery with residues. It was slimy indicating

the presence of mucus. However, blood was not found.

Patient's urine was in a colour similar with dark tea (dark and brownish) since 1 week ago.

At the time of the physical examination, patient is unable to face down and lift his head. He is

only able to tilt his head to the left and right.

Patient was given food and drinks through NGT because he is not able to eat and drink

properly with his mouth.

History of previous illness: Patient was treated in a hospital before at the age of 3 months

old with the diagnose of coagulated blood due to trauma and had an head operation.

Physical Examination

Body weight : 5.5kg

Height : 53.4 cm


22/74

Presence status

Sens. Compos Mentis, Body temperature: 36.5 oC, Pulse: 152 bpm, Respiratory Rate: 40bpm.

Locali zed status

1.

Head : Microcephalic Eye : Light reflexes(+/+), isochoric pupil, conjunctiva

palpebra inferior ane (+/+), icteric (+/+) , Ear : Normal appereance ,

Mouth : Sianosis (-), Nose: Normal appereance.

2.Neck : Lymph node enlargement (-)

3. Thorax : Icteric (+) Symmetrical fusiformis. Epigastria retraction (-).

HR:152bpm, regular, murmur (+) systolic grade III-IV HR: 40bpm,

regular. Crackles (-/-), interposed rib clearly visible

4. Abdomen : Distention (+), symmetrical, Decreased tenderness, Peristaltic

movement normal. Liver: palpable 3cm from costal margin,

concentration kenyal, flat surface, Pain(-). Spleen : Normal

5.Extremities : Pulse 152 bpm, regular, adequate pressure and volume, warm

extremities, CRT< 2.

Working Diagnosis : Cholestasis Jaundice + Global Development delay + Microchepaly

Diffential Diagnosis : - Cholestasis Jaundice + Global Development Delay + Microchepaly

- Suspected of hepatitis

- Suspected of sepsis

- Microchepaly

Medication : IVFD D 5% NaCl 0.2 25% 20gtt/I micro


23/74

Follow Up

August, 16th 2013

S:Yellowish skin colour on the whole body (+)

O:Sens: CM, Temp: 37 oC

Head Microsefali ,Eye : Light reflexes(+/+), isochoric pupil, pale conjunctiva

palpebra inferior (-/-), icteric (+/+) , Ear : Normal appereance ,Mouth :

Sianosis (-), Nose: Normal appereance Face icteric (+)

Thorax Ikteric (+), Symmetrical fusiformis. Retracsi (-).

HR: 139 bpm, reguler, murmur (-)

RR: 28 bpm, reguler. Crackles (-/-)

Abdomen Icteric (+), symmetrical, Decreased tenderness, Peristaltic (-). Liver:

palpable 4cm from costal margin, sharp edge, flat surface, Pain(-)Spleen:normal

Extremities Pulse 139 bpm, regular, adequate pressure and volume, warm acral, CRT1 bulan : 0,2-1,0

4-6 hari : 0,1 -12,6

3 hari : 0,7 -12,7

2 hari : 1,3-11,3

< 1 hari :

Bilirubin

Direct

19,39 Mg/dl 0-0,2

HBsAg NEgatif

TV:

0.01

Negatif Indeks : =0,13

Alkaline

Phospatase

2515 U/L P: 53-128 W:42-98

SGOT 121 U/L P:


26/74

Laboratory Result:August,5th 2013

Blood Gases

Ph 7.174 7.35-7.45

pCO2 mmHg 60.8 38-42pO2 mmHg 164.3 85-42

Bikarbonat (HCO3) mmol/L 21.9 22-26

Total CO2 mmol/L 23.7 19-25

Kelebihan Basa (BE) Mmol/L -6.6 (-2)-(+2)

Saturasi % 98.6 95-100

Carbohydrate

metabolism

Glukosa ad random Mg/dl 362.00


27/74

August, 17th 2013

S:yellowish skin colour on the whole body (+)

O:Sens: CM, Temp: 37 oC

Head Microsefali ,Eye : Light reflexes(+/+), isochoric pupil, pale conjunctiva

palpebra inferior (-/-), icteric (+/+) , Ear : Normal appereance ,Mouth :Sianosis (-), Nose: Normal appereance Face icteric (+),

Thorax Ikteric (+), Symmetrical fusiformis. Retracsi (-).

HR: 132 bpm, reguler, murmur (-)

RR: 36 bpm, reguler. Crackles (-/-),

Abdomen Icteric (+), symmetrical, Decreased tenderness, Peristaltic (-). Liver:

palpable 3cm from costal margin, sharp edge, flat surface, Pain(-)

Spleen:Normal

Extremities Pulse 132 bpm, regular, adequate pressure and volume, warm acral, CRT

Documents

Lapkas Anak (Prof Dr. Hj. Bidasari)