1

INFECTION OF CNS AND ENERGY PROTEIN MALNUTRITION

CHAPTER I INTRODUCTION

1.1.

Background In developing countries and in developed countries, infectious diseases are

still an important medical problem because the death rate is still quite high. Among the most dangerous infectious disease is an infection of CNS (CNS) belong to it meningitis and encephalitis. Meningitis synonymous with leptomeningitis which means the existence of a brain infection that involves the arachnoid membrane and piamater while encephalitis is an infection of the brain parenchyma tissue. Diseases of central nervous system infection had a mortality rate above 50%, if a person survived brain infection generally have disabilities ranging from paralysis and coma. Central nervous system is the most protected part of the body or the most recent hit, so when the brain is exposed to the infection will very likely affect other organs in the body and its functions become impaired. In the other hand Glomerulonephritis is a major cause of end stage renal failure and high rates of morbidity in children. Glomerulonephritis terminology used here is to show that the first and primary abnormality occurs in the glomerulus, not in other renal structures. Indonesia in 1995, reported 170 patients treated at a teaching hospital in 12 months. Most patients treated in Surabaya (26.5%), followed by a row in Jakarta (24.7%), London (17.6%), and Palembang (8.2%). Male patients and female versus 2: 1 and the highest in children aged between 6-8 years (40.6%). Glomerulonephritis symptoms can take place suddenly (acute) or chronic (chronic) often not known because not cause symptoms. Symptoms may include nausea, anemia (anemia), or hypertension. Common symptoms such as swollen

eyelids, pee a little, and red in color, usually accompanied by hypertension. The disease is generally (about 80%) recovered spontaneously, 10% became chronic, and 10% fatal. Meanwhile Malnutrition remains a problem in some countries. Previously recorded one of three children in the world died every year because of poor nutritional quality. Of Health Department data showed at least 3.5 million children die every year due to malnutrition and poor food quality, supported also by malnutrition during still inside the womb. This can result in damage that can not be repaired by the time children get older. Dr.Bruce Cogill, a nutrition expert from the UN agency UNICEF said that the global issue of malnutrition is now a problem that must be addressed. Malnutrition problem have not been solved till today. In some region, malnutrition cases emerge and become hot news. Malnutrition cases on pre-school child have influenced for their growth and development, especially on their brain that cause their inteligency is lower than those whose not suppered.

1.2.

Objective The aim of this study is to explore more about the theoretical aspects on

central nervous system infection, acute glomerulonephritis and marasmus kwarshiorkor on children, and to integrate the theory and assessment of cases in daily life.

CHAPTER II LITERATURE REVIEW

2.1.

Central Nervous System Infection Acute infection of the central nervous system (CNS) is the most common

cause of fever associated with signs and symptoms of CNS disease in children. Infection may be caused by virtually any microbe, the specific pathogen being influenced by the age and immune status of the host and the epidemiology of the pathogen. In general, viral infections of the CNS are much more common than bacterial infections, which, in turn, are more common than fungal and parasitic infections. Infections caused by rickettsiae (e.g., Rocky Mountain spotted fever and Ehrlichia) are relatively uncommon but assume important roles under certain epidemiologic circumstances. Mycoplasma spp also can cause infections of the CNS, although their precise contribution often is difficult to determine.1 Classification of nervous system infection by the affected inflamed organs did not provide clinically meaningful grip. Inflammation of the peripheral nerves called neuritis, the meninges is called meningitis, the network called myelitis and spinal cord to the brain known as encephalitis. Otherwise the distribution of CNS infection by type of microbes that can infected directly explain the disease diagnosis.2

2.1.1. Meningitis Meningitis is an inflammation of the meninges that cause the stimulation of the meninges symptoms such as headache, stiff neck, photophobia accompanied by an increase in the number of leukocytes in the cerebrospinal fluid (CSF). Based on the duration of symptoms, meningitis can be divided into acute and chronic. Provide clinical manifestations of acute meningitis in a span of hours

to days, whereas chronic meningitis onset and duration of weeks to months. In

many cases, clinical symptoms of meningitis are overlap varies etiology.3 Picture 2.1. Anatomy of cranial meningeal layer

Meningitis is divided into two groups based on changes the cerebrospinal fluid is serous meningitis and purulent meningitis. Serous meningitis characterized by the number of cells and proteins with elevated cerebrospinal fluid clear. The most common cause is a germ Tuberculosis and virus. Purulent meningitis or bacterial meningitis is meningitis which is acute and produce pus and exudates form is not caused by bacteria specific or virus. Meningococcus meningitis is purulent meningitis the most frequently occurs.4 Microbe transmission can occur by direct contact and droplet infection from sufferers or exposed to spray saliva, sputum, snot, sneezing and throat fluids of patients.5 Respiratory tract is a major port d'entree on the transmission of this disease. The bacteria is spread to others through air exchange of respiratory and throat secretions coming hematogenous (through the blood stream) into the cerebrospinal fluid in it and multiply, causing inflammation of the meninges and the brain.6 Meningitis can be caused by viral, bacterial, rickettsial, fungal, worms and protozoa. The most common cause is a virus and bacteria. Meningitis caused by bacteria result in more fatal than other causes of meningitis due to the mechanism

of brain damage and disruption caused by bacteria or bacterial products more severe.3 Infectious Agent purulent meningitis have a tendency in certain age groups, neonate group most often caused by E.coli, S.beta monositogenes hemolytic and Listeria . Under 5 years age group (toddlers) caused by H.influenzae, meningococcus and Pneumococcus. 5-20 years age group is caused by Haemophilus influenzae, Neisseria meningitidis and Streptococcus

Pneumococcus, and in the adult ( > 20 years ) caused by the meningococcus, Pneumococcus, Stafilocccus, Streptococcus and Listeria.7 The most common microbe that caused serous meningitis tuberculosis species and virus.3 Meningitis caused by the virus have a better prognosis, likely benign and can heal itself. Cause of viral meningitis is most often found in the Mumpsvirus, echovirus, and Coxsackie virus, while Herpes simplex, Herpes zooster, and enteroviruses rarely cause aseptic meningitis (viral).8

Clinical Manifestation The onset of acute meningitis has two predominant patterns. The more dramatic and, fortunately, less common presentation is sudden onset with rapidly progressive manifestations of shock, purpura, disseminated intravascular coagulation (DIC), and reduced levels of consciousness frequently resulting in death within 24 hr. More often, meningitis is preceded by several days of fever accompanied by upper respiratory tract or gastrointestinal symptoms, followed by nonspecific signs of CNS infection such as increasing lethargy and irritability. The signs and symptoms of meningitis are related to the nonspecific findings associated with a systemic infection and to manifestations of meningeal irritation. Nonspecific findings include fever, anorexia and poor feeding, symptoms of upper respiratory tract infection, myalgias, arthralgias, tachycardia, hypotension, and various cutaneous signs, such as petechiae, purpura, or an erythematous macular rash. Meningeal irritation is manifested as nuchal rigidity, back pain, Kernig sign (flexion of the hip 90 degrees with subsequent pain with extension of the leg), and Brudzinski sign (involuntary flexion of the knees and hips after passive flexion of the neck while supine). In some children, particularly

in those younger than 12-18 mo, Kernig and Brudzinski signs are not consistently present. Increased ICP is suggested by headache, emesis, bulging fontanel or diastasis (widening) of the sutures, oculomotor or abducens nerve paralysis, hypertension with bradycardia, apnea or hyperventilation, decorticate or decerebrate posturing, stupor, coma, or signs of herniation. Papilledema is uncommon in uncomplicated meningitis and should suggest a more chronic process, such as the presence of an intracranial abscess, subdural empyema, or occlusion of a dural venous sinus. Focal neurologic signs usually are due to vascular occlusion. Cranial neuropathies of the ocular, oculomotor, abducens, facial, and auditory nerves also may be due to focal inflammation. Overall, about 10-20% of children with bacterial meningitis have focal neurologic signs.

Picture 2.2. Brudzinski Sign and Kernig Sign

Seizures (focal or generalized) due to cerebritis, infarction, or electrolyte disturbances occur in 20-30% of patients with meningitis. Seizures that occur on presentation or within the first 4 days of onset are usually of no prognostic significance. Seizures that persist after the 4th day of illness and those that are difficult to treat may be associated with a poor prognosis. Alterations of mental status are common among patients with meningitis and may be due to increased ICP, cerebritis, or hypotension; manifestations include irritability, lethargy, stupor, obtundation, and coma. Comatose patients have a poor prognosis. Additional manifestations of meningitis include photophobia and tache crbrale, which is elicited by stroking the skin with a blunt object and observing a raised red streak within 30-60 sec.1

Diagnosis The diagnosis of acute pyogenic meningitis is confirmed by analysis of the CSF, which typically reveals microorganisms on Gram stain and culture, a neutrophilic pleocytosis, elevated protein, and reduced glucose concentrations. LP should be performed when bacterial meningitis is suspected. Contraindications for an immediate LP include: 1. Evidence of increased ICP (other than a bulging fontanel), such as 3rd or 6th cranial nerve palsy with a depressed level of consciousness, or hypertension and bradycardia with respiratory abnormalities. 2. severe cardiopulmonary compromise requiring prompt resuscitative measures for shock or in patients in whom positioning for the LP would further compromise cardiopulmonary function; and (3) infection of the skin overlying the site of the LP. Thrombocytopenia is a relative contraindication for LP. If an LP is delayed, empirical antibiotic therapy should be initiated. CT scanning for evidence of a brain abscess or increased ICP also should not delay therapy. LP may be performed after increased ICP has been treated or a brain abscess has been excluded. Blood cultures should be performed in all patients with suspected meningitis. Blood cultures reveal the responsible bacteria in 80-90% of cases of meningitis.1

2.1.2. Enchepalitis Encephalitis is inflammation of the brain tissue which can be caused by a variety of microorganisms such as bacteria, viruses, parasites, fungus and rickets. In general, symptoms of encephalitis include fever, seizures, and decreased consciousness. This disease can be found at all ages ranging from children to adults.

Encephalitis occurs in two forms, namely primary form and a secondary form. Primary encephalitis involves direct viral infection of the brain and spinal cord. While secondary encephalitis, a viral infection first occurs elsewhere in the body and then to the brain.9

Etiology The most frequent cause of encephalitis is a viral infection. Some examples include: Herpes virus Arbovirus transmitted by mosquitoes tick and other insects Rabies is transmitted through an animal bite Bacterial and parasitic infections such as toxoplasmosis can cause encephalitis in people who have weakened immune systems.9

Clinical Manifestation In general, symptoms of encephalitis triad: 1. fever 2. convulsions 3. decreased awareness When developing a cerebral abscess will arise common symptoms of infection with signs of increased intracranial pressure, namely: chronic headache and progressive, vomiting, blurred vision, seizures, decreased consciousness. On examination there may be edema papil edema. Signs of neurological deficits depend on the location and extent of the abscess.9

Diagnosis Radiologic test: 1. CT-Scan10 CT may show hypodense on contrast pre-post contrast hyperdensity on one or both temporal lobes, edema / mass and sometimes contrast enhancement.

Isodens or hypodense lesions are round ring, nodular or homogeneous patterns and worsen by contrast, places predilection hemisphere (graywhite junction).

Bias found edema cerebry. Sometimes accompanied by signs of bleeding.

Picture 2.3. CT scan of the brain in a girl with Rasmussen's encephalitis 2. MRI11,12 Usually bilateral pathological changes in the medial temporal lobe and inferior frontal lobe portion (the lesion). Hipointens isointens lesions are round or ring, nodular or homogeneous patterns and worsen by contrast, places predilection hemisphere (gray-white junction), on T1WI. Hiperintens lesions on T2WI and the flair looks hiperintens.

Picture 2.4. herpes simplex type 1 encephalitis in a 11 years old child.

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Laboratory tests: Complete blood examination, was found to increase the number of leukocytes. Examination of cerebrospinal fluid: clear fluid, cell count above normal, counts dominated by lymphocytes, normal protein and glucose or increased Other tests: - EEG obtained a picture of declining or slowing activity.

2.1.3. Meningoencephalitis Meningoencephalitis is an acute inflammatory process involving the meninges and, to a variable degree, brain tissue. These infections are relatively common and may be caused by a number of different agents. The CSF is characterized by pleocytosis and the absence of microorganisms on Gram stain and routine bacterial culture. In most instances, the infections are self-limited. Enteroviruses cause more than 80% of all cases of meningoencephalitis. Enteroviruses are small RNA-containing viruses; more than 80 serotypes have been identified. The severity of disease ranges from mild, self-limited illness with primarily meningeal involvement to severe encephalitis with death or significant sequelae.1

Clinical Manifestation The progression and severity of disease are determined by the relative degree of meningeal and parenchymal involvement, which in part is determined by the specific etiology. However, the clinical course resulting from infection with the same pathogen varies widely. Some children may appear to be mildly affected initially, only to lapse into coma and die suddenly. In others, the illness may be ushered in by high fever, violent convulsions interspersed with bizarre movements, and hallucinations alternating with brief periods of clarity, followed by complete recovery.

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Diagnosis The CSF contains from a few to several thousand cells per cubic millimeter. Early in the disease, the cells are often polymorphonuclear; later, mononuclear cells predominate. This change in cellular type is often demonstrated in CSF samples obtained as little as 8-12 hr apart. The protein concentration in CSF tends to be normal or slightly elevated, but concentrations may be very high if brain destruction is extensive, such as that caused by HSV encephalitis. The glucose level is usually normal, although with certain viruses, for example, mumps, a substantial depression of CSF glucose concentrations may be observed. The CSF should be cultured for viruses, bacteria, fungi, and mycobacteria; in some instances, special examinations are indicated for protozoa, Mycoplasma, and other pathogens. The success of isolating viruses from the CSF of children with viral meningoencephalitis is determined by the time in the clinical course that the specimen is obtained, the specific etiologic agent, whether the infection is a meningitic as opposed to a localized encephalitic process, and the skill of the diagnostic laboratory. Isolating a virus is most likely early in the illness, and the enteroviruses tend to be the easiest to isolate, although recovery of these agents from the CSF rarely exceeds 70%. To increase the likelihood of identifying the putative viral pathogen, specimens for culture also should be obtained from nasopharyngeal swabs, feces, and urine. Although isolating a virus from one or more of these sites does not prove causality, it is highly suggestive. Other tests of potential value in the evaluation of patients with suspected viral meningoencephalitis include an electroencephalogram (EEG) and

neuroimaging studies. The EEG typically shows diffuse slow-wave activity, usually without focal changes. Neuroimaging studies (CT or MRI) may show swelling of the brain parenchyma. Focal seizures or focal findings on EEG or CT or MRI, especially involving the temporal lobes, suggest HSV encephalitis.

2.1.4. Treatment The initial (empirical) choice of therapy for meningitis in

immunocompetent infants and children is primarily determined by the antibiotic

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susceptibilities of S. pneumoniae. Selected antibiotics should achieve bactericidal levels in the CSF. Although there are substantial geographic differences in the frequency of resistance of S. pneumoniae to antibiotics, rates are increasing throughout the world. In the United States, 25-50% of strains of S. pneumoniae are currently resistant to penicillin; relative resistance (MIC, 0.1-1.0 ug/mL) is more common than high-level resistance (MIC 2.0 ug/mL). Resistance to cefotaxime and ceftriaxone also is evident in up to 25% of isolates. In contrast, most strains of N. meningitidis are sensitive to penicillin and cephalosporins, although rare resistant isolates have been reported. Approximately 30-40% of isolates of H. influenzae type b produce -lactamases and therefore are resistant to ampicillin. These -lactamase-producing strains remain sensitive to the extendedspectrum cephalosporins. Based on the substantial rate of resistance of S. pneumoniae to -lactam drugs recommended empirical therapy is vancomycin (60 mg/kg/24 hr, given every 6 hr) in combination with either of the third-generation cephalosporins, cefotaxime (200 mg/kg/24 hr, given every 6 hr) or ceftriaxone (100 mg/kg/24 hr administered once per day or 50 mg/kg/dose, given every 12 hr). Patients allergic to -lactam antibiotics can be treated with chloramphenicol, 100 mg/kg/24 hr, given every 6 hr. If L. monocytogenes infection is suspected, as in infants 1-2 mo old or patients with a T-lymphocyte deficiency, ampicillin (200 mg/kg/24 hr, given every 6 hr) should be given with ceftriaxone or cefotaxime because cephalosporins are inactive against L. monocytogenes. Intravenous trimethoprimsulfamethoxazole is an alternative treatment for L. monocytogenes. If a patient is immunocompromised and gram-negative bacterial meningitis is suspected, initial therapy might include ceftazidime and an aminoglycoside.1 For encephalitis: 1. Encephalitis supurativa Ampisillin 4 x 3-4 g orally for 10 days . Cloramphenicol 4 x 1g/24 hours intravenously for 10 days .

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2. Encephalitis syphilis Penicillin G 12-24 million units / day 6 divided doses for 14 days Procaine penicillin G 2.4 million units / day intra muskulat + 4 x 500mg oral probenecid for 14 days . When penicillin allergy : 4 x Tetracycline 500 mg orally for 30 days Erythromycin 4 x 500 mg orally for 30 days Cloramfenicol 4 x 1 g intravenously for 6 weeks Seftriaxon 2 g intravenous / intra muscular for 14 days .

3. Encephalitis virus Treatment of symptomatic Analgesic and antipyretic : Mefenamic acid 4 x 500 mg Anticonvulsi : Phenitoin 50 mg / ml intravenous 2 times daily . Antiviral treatment is given on the cause of viral encephalitis with herpes zoster varicella: Asiclovir 10 mg / kg intravenously 3 times daily for 10 days or 200 mg orally every 4 hours for 10 days . 4. Encephalitis due to parasite Cerebral Malaria Quinine 10 mg / KgBW in infusion for 4 hours , every 8 hours until visible improvements . Toxoplasmosis Sulfadiasin 100 mg / kg orally for 1 month Pirimetasin 1 mg / kg orally for 1 month Spiramycin 3 x 500 mg / day Amebiasis Rifampicin 8 mg / kg / day . 5. Encephalitis due to fungus Amphotericin 0,1 - 0,25 g / kg / day intravenously 2 days at least 6 weeks Miconazole 30 mg / kg intravenously for 6 weeks.

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6. Riketsiosis cerebral Cloramphenicol 4 x 1 g intravenously for 10 days 4x Tetracycline 500 mg orally for 10 days.

2.1.5. Complication Collections of fluid in the subdural space develop in 10-30% of patients with meningitis and are asymptomatic in 85-90% of patients. Subdural effusions are especially common in infants. Symptomatic subdural effusions may result in a bulging fontanel, diastasis of sutures, enlarging head circumference, emesis, seizures, fever, and abnormal results of cranial transillumination. CT or MRI scanning confirms the presence of a subdural effusion. In the presence of increased ICP or a depressed level of consciousness, symptomatic subdural effusion should be treated by aspiration through the open fontanel. Fever alone is not an indication for aspiration. Possible complications for encephalitis include encephalitis seizures, brain damage that causes loss of sensation, coordination and control in certain body areas, and / or difficulty speaking, and death. Membranes covering the brain and attach (meninges) may also be involved, and it can become inflamed membranes (meningoencephalitis).1

2.1.6. Prognosis Appropriate recognition, prompt antibiotic therapy, and supportive care have reduced the mortality of bacterial meningitis after the neonatal period to less than 10%. The highest mortality rates are observed with pneumococcal meningitis. Severe neurodevelopmental sequelae may occur in 10-20% of patients recovering from bacterial meningitis, and as many as 50% have some, albeit subtle, neurobehavioral morbidity. The prognosis is poorest among infants younger than 6 mo and in those with more than 106 colony-forming units of bacteria/mL in their CSF. Those with seizures occurring more than 4 days into therapy or with coma or focal neurologic signs on presentation have an increased

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risk of long-term sequelae. There does not appear to be a correlation between duration of symptoms before diagnosis of meningitis and outcome.1 The mortality rate for encephalitis ranged between 35-50%. Patients whose treatment is delayed or not given antiviral (in encephalitis Herpes Simplex) high death rate could reach 70-80%. Early treatment with acyclovir will lower the mortality to 28%. 6 Approximately 25% of patients died in the acute stage of encephalitis. Patients who lived his 20-40% will have complications or sequelae. 6 Sequelae is more common and more severe in untreated encephalitis. Treatment delay of more than 4 days gave a poor prognosis, as well as coma. Coma patients often died or recovered with severe sequel. Many cases of encephalitis is an infection and faster recovery usually mild encephalitis usually go without residual neurological problems. And 10% of all encephalitis deaths from infection or complications from secondary infection.

2.2.

Acute Glomerulonephritis Acute glomerulonephritis is commonly caused after streptococcus

infection. Acute glomerulonephritis post-streptococcus is a nephritic syndrome with the characteristics of hematuria, edema, hypertension, and diminished renal function. These signs appear after infection, usually caused by Sreptococcus beta hemolyticus group A at upper respiratory tract or at skin. Acute

glomerulonephritis post-streptococcus is the most commonly found acute glomerulonephritis post-infection. Abnormality of renal function caused by deposition of immune complex at glomerular basal membrane that eventually caused inflammation reaction.13

2.2.1. Etiology Acute postsreptococcal glomerulonephritis follows infection of the throat or skin by certain nephrtogenic strains of group A -hemolytic streptococci. The factors that allow only certain strains of streptococci to be nephritogenic remain unclear. Post streptococcal glomerulonephritis commonly follows streptococcal

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pharyngitis during cold weather months and streptococcal skin infections or pyoderma during warm weather months. Although epidemics of nephritis have been described in association with both throat (serotype 12) and skin (serotype 49) infections, this disease is most commonly sporadic.14

2.2.2. Pathology As in most forms of acute glomerulonephritis, the kidneys appear symmetrically enlarged. On loght microscopy, all glomeruli appear enlarged and show diffise mesangial cell proliferation with an increase in mesangial matrix. Polymorphonuclear leukocytes are common in glomeruli during the early stage of the disease. Crescents and interstitial inflammation may be seen in severe cases. These changes are not specific for poststreptococcal glomerulonephritis. Immunofluorescence microscopy reveals lumpy-bumpy deposits of

immunoglobulin and complement on the glomerular basement membrane (GBM) and in the mesangium. On electron microscopy, elecrton-dense deposits, or humps, are observed on the epithelial side of the GBM.13

2.2.3. Clinical manifestations The typical patient develops an acute nephritic syndrome 1-2 weeks after an antecedent streptococcal pharyngitis or 3-6 weeks after a streptococcal pyoderma. The severity of renal involvement varies from asmptomatic microscopic hematuria with normal renal function to acute renal failure. Depending on the severity of renal involvement, patients may develop various degrees of edema, hypertension, and oliguria. Patients may develop

encephalopathy and/or heart failure owing to hypertension or hypervolemia. Encephalopathy may also result directly from the toxic effects of the streptococcal bacteria on the central nervous system. Edema typically results from salt and water retention and nephrotic syndrome may develop in 10-20% of cases. Specific symptoms such as malaise, lethargy, abdominal or flank pain, and fever are common. Acute subglottic edema and airway compromis has also been reported. The acute phase generally resolves within 6-8 weeks. Although urinary protein

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excretion and hypertension usually normalize by 4-6 weeks after onset, persistent microscopic hematuria may persist for 1-2 years after the initial presentation.15

2.2.4. Diagnosis Urinalysis demonstrates red blood cells (RBCs), frequently in association with RBC casts, proteinuria, and PMN leukocytes. A mild normochromic anemia may be present from hemodilution and low-grade hemolysis. The serum C3 level is usually redused in acute phase and returns to normal 6-8 weeks after onset. Confirmation of the diagnosis requires clear evidence of invasive streptococcal infection ( positive throat culture). On the other hand, a rising antibody toter to streptococcal antigens confirms a recent streptococcal infection. The differential diagnosis of poststreptococcal glomerulonephritis includes nephrotic syndrome, IgA nephropathy, systemic lupus erythematosus nephritis, or trauma.15

2.2.5. Complications Potential complications include heart failure, hyperkalemia, hyperphosphatemia, hypocalcemia, asidosis, seizures, and urecemia.14

2.2.6. Treatment Management is directed at treating the acute effects of renal insufficiency and hypertension. Although a 10-day course of systemic antibiotic therapy with penicillin is recommended to limit the spread of the nephritogenic organisms, antibiotic therapy does not affect the natural history of glomerulonephritis. Sodium restriction, diuresis, and pharmacotherapy with calcium channel antagonists, vasodilators, or ACEI are standard therapies used to treat hypertension.15

2.2.7. Prognosis Complete recovery occurs in more than 95% of children with acute poststreptococcal glomerulonephritis. Mortality in the acute stage can be avoided

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by appropriate management of acute renal failure, cardiac failure, and hypertension. Reccurences are extremely rare.15

2.3.

Protein Energy Malnutrition (PEM) Malnutrition is the condition where the body does not obtain adequate

nutrition. Malnutrition also can be known as condition which caused by imbalance between caloric intake with energy needs to maintain health.16 Protein energy malnutrition can be divided into two main causes, primer malnutrition and secondary malnutrition. Primer malnutrition is the condition which caused by inadequate of protein or caloric intake. Secondary malnutrition is caused by increase needed of energy accompanied by the decrease of absorption, and/or increase loss of protein and energy from the body. Protein energy malnutrition can occur due to several factors that simultaneously cause the disease, such as social and economic factors like for example the problem of poverty and environmental factors which the resident is crowded and dirty. In addition, feeding of Breast Milk and inadequate supplementary food is also a problem of cause of the occurrence PEM.17 Severity and classification of PEM parameters can be measured using anthropometric indicators. Indicator of weight to height (weight / height) can be used as a guide in determining the current nutritional status and height-for-age (TB / U) is used as a clue about the state of nutrition of the past. Department of Health (2000) recommends standard WHO-NCHS for use as raw anthropometry in Indonesian. PEM if the child is said to suffer under -2 Z-score of each indicator.18 Clinically, PEM can be distributed to the three types, namely, kwashiorkor, marasmus, and marasmik-kwashiorkor. Marasmus occurs because of insufficient energy intake while kwashiorkor occurs mainly due to insufficient protein intake. While marasmik-kwashiorkor type which is a combination between the symptoms of marasmus and kwashiorkor.17

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Table 2.1. Daily Needed Energy Umur 0-6 bulan 7-12 bulan 1-3 tahun 4-6 tahun 7-9 tahun 2.3.1. Marasmus Marasmus occurs because of insufficient energy intake. In patients suffering from marasmus, growth will be reduced or stopped, often wakes up at night time, constipation or diarrhea. Diarrhea in patients with marasmus will be seen of dark green patches that consist of a little bit of mucus and feces. Disorder of the skin is skin turgor will disappear and the patient looks wrinkled. If the symptoms get severe fat on the cheek will disappear and the patient's face looks like an old man. Superficial veins will be obvious, large sunken fontanel, prominent cheekbones and chin and eyes look big and deep, widened ribs gap. Stomach bulging or sunken look with a clear picture of the gut and looks atrophy.19 Energi (Kkal) 550 650 1000 1550 1800

Picture 2.5. Marasmus (Source: http://www.childclinic.net ) 2.3.2. Kwashiorkor Kwashiorkor occurs mainly due to not taking enough protein. In patients suffering from kwashiorkor, the child will experience growth retardation, mental

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changes that the patient is usually whiny and at an advanced stage to be apathetic and most patients found edema. Additionally, the patient will experience gastrointestinal symptoms such as anorexia and diarrhea. This may be due to malfunctioning of liver, pancreas and intestines. Kwashiorkor patients hair is easily removed and painlessly. In patients with an advanced stage, the hair will look dull, dry, smooth, sparse and white. Patients have dry skin with show lines deeper and wider. Typical skin change is crazy pavement dermatosis which are patches of white or pink with black edges and is found in the body that are often under pressure and moist. At abdomen palpation found hepatomegaly, rubbery, slippery surfaces, and sharp edges. Also found mild anemia and chemical abnormalities that low levels of serum albumin and globulin levels were normal or slightly elevated.19

Picture 2.6. Kwashiorkor (Source : http://adam.about.com ) 2.3.3. Nutritional Status Assessment 2.3.3.1.Anthropometric Anthropometric measurements most often used to measure growth disorders. Anthropometry is widely used because it is practical with a noninvasive approach to measure the nutritional status of an individual or society. Anthropometric measures are body weight (BW), body height (BH), mid upper

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arm circumference (MUAC), circle head and the fat layer under the skin using a certain size and standard. Anthropometric indices most commonly used is BW/A, BH/A and BW/BH. BW/A index can be used to recognize the problem of low weight for age specific. Excess BW/A is certainly familiar to both acute malnutrition and/or chronic, although the BW/A index can not distinguish patients suffering from acute or chronic malnutrition. Index BH/A can be used to know definitely that chronic malnutrition problems. For children under two years, length-age is used as the term BH/A is used for children two years and above. Low BH/A index indicating the impaired growth. Index BW/BH used to know for sure acute malnutrition experienced or recently time. BW/BH is useful for measuring shortterm effects of malnutrition due to illness or dietary changes.20 Severity and classification of PEM parameters can be measured using anthropometric indicators. Indicator of body weight to body height (BW/BH) can be used as a guide in determining the current nutritional status and height-for-age (BH/A) is used as a clue about the state of nutrition of the past. Department of Health (2000), based in Bogor Nutrition Expert Meeting 19-20 January and in Semarang on 24-26 May of 2000, WHO-NCHS standard is recommended for use as raw anthropometric in Indonesia.18

Table. 2.2. Severity and Classification of PEM Index BW/A Standard Deviation 2 SD -2 until +2 SD < -2 until -3 SD < -3 SD -2 until +2 SD < -2 SD 2 SD -2 until +2 SD < -2 until -3 SD < -3 SD Nutritional Status Nutritional excess Nutritional normal Nutritional lack Malnutrition Normal Overweight Normal Underweight Over underweught

BH/A BW/BH

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2.3.4. Treatment The treatment for malnutrition children always based on 5 (five) event management children with malnutrition.21 a. CONDITION: I If Found: - Shock (shock) immediately: Replace the oxygen 1 -2 l / min Infusion of Ringer Lactate and Dextrose / glucose 10% with a ratio of 1: 1 (RLG 5%) 10% glucose iv bolus, a dose of 5 ml / KgBW together with ReSoMal 5 ml / KgBW / NGT (Naso Gastric Tube) Letargis vomiting / diarrhea / dehydration

I Hours: Forward granting RLG 5% as much as 15 ml / KgBW for 1 hour or 5 drops / min / KgBW 24 Record the pulse, breathing frequency of every 30 minutes for 1 hour

Second hour: Pulse rise and fell breath frequency, continue with the drops of the fluid same for 1 hour Give the child according to ability ReSoMal Record the pulse, breathing frequency of every 30 minutes for 1 hour II The pulse is still weak, and breathing frequency continue to remain high iv fluid administration the dose was reduced to 1 drop macro / min / kg (4 mL / kg / hour). When can not afford refer to the hospital. The next 10 hours: Record the pulse, breathing frequency every 1 hour When the administration of iv finished (not yet revoked), give ReSoMal and F-75

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Breastfeed after administration of F-75 When you are rehydrating, stop ReSoMal, continue F-75 every 2 hours If diarrhea / vomiting decreased, edema reduced, children can spend the F75, F-75 given every 3 hours (the remainder via NGT) If no diarrhea / vomiting / minimal edema and children can spend the F75, change granting to 4 hours

b. CONDITION: II If Found: Immediately: Give 10% glucose bolus iv, 5 ml / KgBW Glucose / sugar 10% through NGT, 50 ml Letargis vomiting / diarrhea / dehydration

2 hours of the first: ReSoMal oral / nasogastric tube every 30 minutes, 5 ml / kg / administration Record the pulse rate, breathing frequency and administration ReSoMal every 30 minutes

The next 10 hours If improved, continue providing alternating ReSoMal with F-75 every 1 hour, and if worse (shock) I immediately infusion according to plan, without giving glucose bolus Record the pulse rate, breathing frequency every 1 hour When you have no rehydration and diarrhea, stop ReSoMal, forward F-75 every 2 hours. Give ReSoMal any diarrhea. Breastfeed between giving the F-75 Diarrhea and vomiting is reduced, children are able to spent most of the F75, F-75 give every 3 hours Diarrhea / vomiting, edema is reduced, the child can spent the F-75, F-75 administration change into every 4 hours c. CONDITION: III If Found: vomiting / diarrhea / dehydration

24

Immediately: give 50 ml of glucose or sugar solution 10% (oral / NGT)

2 hours of the first: Give ReSoMal oral / nasogastric tube every 30 minutes, 5 ml /KgBW/gift Record pulse, breathing frequency and give ReSoMal each

The next 10 hours: If improved, continue with alternating ReSoMal F-75 every 1 hour, if worse (shock) infusion soon Ist plan accordingly (without glucose bolus) Record the pulse rate, breathing frequency: When you have no rehydration and diarrhea, stop ReSoMal, forward F-75 every 2 hours. If there is rehydration and diarrhea, give ReSoMal any diarrhea Breastfeed between giving the F-75 When diarrhea / vomiting decreased, F-75 can be spent, change the provision of F-75 to be every 3 hours If there is no diarrhea and child can spend F-75, F-75 provision change to every 4 hours d. CONDITION: IV If Found: Immediately: give 10% glucose bolus iv, 5 ml / KgBW Glucose or lar. sugar 10% through NGT, 50 ml 2 hours of the first: F-75 every 30 minutes, a quarter dose every 2 hours (NGT) Record pulse, breathing frequency Reorder the F-75 every 30 minutes (NGT) Record pulse, breathing frequency, awareness and input F-75 every 30 minutes The next 10 hours: F-75 every 2 hours (oral / NGT) Record the pulse, breathing frequency, awareness, give F-75 every 1 hour Letargis

25

Children can spend most of the F-75, change to every 3 hours provision Breastfeed between giving the F-75 Children can spend the F-75, change into each 4 hours

e. CONDITION: V If Not Found: - Shock (shock) Immediately: 37 2 hours of the first: F-75 every 30 minutes for 2 hours according to BB Record pulse, breathing frequency, awareness and intake F-75 every 30 minutes (Table 6, I book it. 12) give 50 ml of glucose / lar. Sugar 10% oral Record the pulse, breathing frequency, awareness Letargis vomiting / diarrhea / dehydration

The next 10 hours: Forward F-75 every 2 hours (Table F-75 with/without edema Record the pulse, breathing frequency, intake of F-75 Breastfeed between giving the F-75 Edema is reduced, children may spend most of the F-75, change it to every 3 hours minimal edema and children can spend the F-75, change to every 4 hours

26

CHAPTER III CASE REPORT Name Age Sex Date of Admission : DN : 4 years 6 months : Female : September, 13th 2013

Main Complaint History

: Loss of consciousness

: Patient lost her consciousness 6 days ago, happened gradually and

started with the feeling of sleepy. Seizures (-), history of seizures (+). Seizures happened 3 days ago, happened only once with 20 minutes duration. While seizures happened, patients hand and foot were rigid, eyes were wide open upwards. After seizures happened, patient were sleepy. Shortness of breath (+). History of shortness of breath (+) 4 days ago and worsened one day before admitted to RSHAM Medan. Shortness of breath is not associated with activity and weather. Shortness of breath is not relieved by changing position. Fever (+). History of fever (+) since 2 weeks ago. Fever with high degree and lowered by consumption of antifever drugs. History of recurrent fever (+) in these 2 months, fever was intermittent. H istory of painful swallowing was discovered about two months ago. Oedem (+) happened 3 days ago. Oedem at the eyes and foot happened together. History of oedem (-). Loss of weight since a week ago. Loss of appetite (+). Vomit (-). Diarrhea (-). History of pale face (+) a week ago, history of spontaneous bleeding (-). Urination (+) normal, defecation (+) normal. History of oliguria (-), history of flesh coloured urine (-), history of sandy urine (-). History of disease Tinggi by pediatrician. History of drugs : paracetamol, 2 bags of blood transfusion : Patient was referred from RSUD Kumpulan Pane Tebing

History of birth : Spontaneous birth with the help of midwife, cried immediately, cyanosis (-), body weight 2800gr. History of pregnancy : fourth baby, age of the mother during pregnancy is 33 years old, fever (-), hypertension (-), DM (-), history of taking medications (-).

27

History of growth and development : 4months - baby started raising her head , 8 months baby started sitting, 1.5 years baby started walking and can only say papa and mama, 3.5 years baby started to jump and can talk well. History of Feeding: 0-6 months of breastfeeding, 6months-1,5 year old breastfeeding + porridge, 1,5 years old till now plate of rice with side dish, 3x/day. History of immunization : Complete

Physical Examination Body weight Height BB/TB Arm measurement Presens status Sens: GCS 8 (E2V2M4), Blood pressure: 110/70 mmHg, Body temperature: 38.5 oC, Pulse: 110 bpm, Respiratory rate: 60 bpm. : 10 kg ( ideal body weight 11kg) : 83 cm : -2 < Z score < -1 : 11 cm

Localized status 1. Head : Oedem at face and eyes. Eyes: Light reflexes (+/+), isochoric

pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Mouth : normal, Nose: pernafasan cuping hidung (+). 2. Neck 3. Thorax : Lymph node enlargement (-) : Symmetrical fusiformis, suprasternal, epigastria, intercostal regular, murmur (-), RR: 60 bpm, regular,

retraction (+). HR: 110 bpm, crackles (-/-) 4. Abdomen

: Soepel, enlargement (+), Peristaltic (+) N. Liver: palpated 5cm

below arcus costae. Spleen: Schuffner I-II. Renal: undeterminate. Turgor : good 5. Extremities : Pulse 110 bpm, regular, adequate pressure and volume, warm acral, CRT <3. 6. Anogenital : female, normal.

28

Laboratory Result: September, 13th 2013

Complete blood count(CBC) Hemoglobin (HGB) Eritrosit (RBC) Leukosit (WBC) Hematokrit Trombosit (PLT) MCV MCH MCHC RDW MPV PCT PDW WBC Count Neutrofil Limfosit Monosit Eosinofil Basofil Neutrofil Absolut Limfosit Absolut Monosit Absolut Eosinofil Absolut Basofil Absolut g% 106/ mm3 103/ mm3 % 103/ mm3 fL Pg g% % fL % fL % % % % % 103/L 103/L 103/L 103/L 103/L 13.70 5.01 25.36 43.30 355 86.40 27.30 31.60 18.40 8.90 0.32 9.6 72.70 19.80 7.30 0.00 0.200 18.43 5.03 1.86 0.00 0.04 11.3-14.1 4.40-4.48 4.5- 13.5 37 41 217-497 81-95 25-29 29-31 11.6 14.8 7.2-10.0

37 80 20 40 28 16 01 2.4 - 7.3 1.7 - 5.1 0.2 - 0.6 0.10 - 0.30 0 - 0.1

Laboratory Result: September, 13th 2013

Blood gas analysis pH pCO2 pO2 HCO3 Total CO2 BE O2 saturation Liver function test Albumin Unit mmHg mmHG mmol/L mmol/L mmol/L % g/dL Value 7.462 22.7 163.6 15.8 16.5 -6.1 99.5 3.0 Normal value 7.35-7.45 38-42 85-100 22-26 19-25 (-2)-(+2) 95-100 3.8-5.4

29

Carbohydrate metabolism Glukosa ad random Renal Ureum Kreatinin Electrolytes Natrium (Na) Kalium (K) Klorida (Cl)

mg/dl mg/dl mg/dl mEq/L mEq/L mEq/L

64.90 57.40 0.28 144 4.4 109

<200 <50 0.31-0.47 135-155 3.6-5.5 96-106

Dipstick urine: leu (-), Nit (-), Uro (0.2), Pro (), pH (6), blood () SG (1.010), Ket (+), bil(-), glu (-)

Differential Diagnosis

Loss of consciousness ec dd/ - CNS infection stageI - intracranial hemmorhage

Working Diagnosis

+ dd/ -GNA + hypertension

-SN

Loss of consciousness ec CNS infection + GNA + hypertension stage I

Treatment O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30 Inj. Ceftriaxone 1g/12hours/IV in 20 cc NaCl 0.9% finished in 20 minutes (skin test) Paracetamol 3x100mg Diet MBRG 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure Put NGT

Planning Consult Hematooncology division, nefrology division Head CT scan MRI

30

LP C3, ASTO, CRP Blood culture FOLLOW UP

September, 14th 2013 S: loss of consciousness (+) O: Sens: GCS 12 (E3V3M4), Temp: 37.9 oC TD 140/100 mmHg Head Oedem at face and eyes. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: NGT fixed, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-), nuchal rigidity (+) Symmetrical fusiformis, Epigastria retraction (+). HR: 120 bpm, reguler, murmur (), RR: 40 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 120 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Excitatory meningeal + Physiological reflex:APR/KPR +/+ normal Pathological reflex: Babinsky -/-, Oppenheim -/-

Extremities

A: Loss of consciousness ec dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30

+ dd/ -GNA + hypertension stageI -SN

Inj. Ceftriaxone 1g/12hours/IV in 20 cc NaCl 0.9% finished in 20 minutes (H1) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametason 0.75 mg/6 hours/IV Paracetamol 3x100mg Diet SV 1000kkal with 20gr protein

31

Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

Planning: Head CT scan MRI LP C3, ASTO, CRP Blood culture

32

September, 15th 2013 S: loss of consciousness (+) O: Sens: GCS 12 (E3V3M4), Temp: 37 oC TD 130/80 mmHg Head Oedem at face and eyes. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: fixed, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-), nuchal rigidity (+) Symmetrical fusiformis, Epigastria retraction (+). HR: 120 bpm, reguler, murmur (), RR: 36 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 120 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Excitatory meningeal + Physiological reflex:APR/KPR +/+ normal Pathological reflex: Babinsky -/-, Oppenheim -/-

Extremities

A: Loss of consciousness ec dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30

+ dd/ -GNA + hypertension stageI -SN

Inj. Ceftriaxone 1g/12hours/IV in 20 cc NaCl 0.9% finished in 20 minutes (H2) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Paracetamol 3x100mg Diet SV 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

33

Planning: Head CT scan MRI LP C3, ASTO, CRP Blood culture

34

September, 16th 2013 S: loss of consciousness (+) O: Sens: GCS 12 (E3V3M4), Temp: 37 oC TD 130/80 mmHg Head Oedem at face and eyes. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: fixed, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-),nuchal rigidity (+) Symmetrical fusiformis, Epigastria retraction (+). HR: 110 bpm, reguler, murmur (), RR: 36 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 110 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Excitatory meningeal + Physiological reflex:APR/KPR +/+ normal Pathological reflex: Babinsky -/-, Oppenheim -/-

Extremities

A: Loss of consciousness ec dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30 Inj. Ceftriaxone 1g/12hours/IV (H3) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Paracetamol 3x100mg Diet SV 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

+ dd/ -GNA + hypertension stageI -SN

35

Planning: Head CT scan MRI LP C3, ASTO, CRP

Laboratorium result: Total cholestrol/ TG (mg/dL) Cholestrol HDL/LDL (mg/dL) Ureum/ creatinine (mg/dL) Na/K/Cl (mEq/L) ASTO CRP Blood culture : 195/300 : 35/157 : 35.6/0.18 : 141/3/107 : <200 : negative : there is no bacterial growth

36

September, 17th 2013 S: loss of consciousness (+) O: Sens: GCS 12 (E4V3M5), Temp: 37 oC TD 130/80 mmHg Head Oedem at face and eyes. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: NGT fixed, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (+). HR: 100 bpm, reguler, murmur (), RR: 28 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Excitatory meningeal Physiological reflex:APR/KPR +/+ normal Pathological reflex: Babinsky -/-, Oppenheim -/-

Extremities

A: Loss of consciousness ec dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30 Inj. Ceftriaxone 1g/12hours/IV (H4) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Paracetamol 3x100mg Diet SV 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

+ dd/ -GNA + hypertension stageI -SN

37

Planning: Head CT scan MRI LP

38

September, 18th 2013 S: loss of consciousness (+) O: Sens: GCS 12 (E4V3M5), Temp: 37 oC TD 130/80 mmHg Head Oedem at face and eyes. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: NGT fixed, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (+). HR: 100 bpm, reguler, murmur (), RR: 24 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Excitatory meningeal Physiological reflex:APR/KPR +/+ normal Pathological reflex: Babinsky -/-, Oppenheim -/-

Extremities

A: Loss of consciousness ec dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30 Inj. Ceftriaxone 1g/12hours/IV (H5) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Paracetamol 3x100mg Diet SV 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

+ dd/ -GNA + hypertension stageI -SN

39

Planning: Head CT scan MRI LP

40

September, 19th 2013 S: loss of consciousness (+) O: Sens: GCS 13 (E4V4M5), Temp: 37 oC TD 130/80 mmHg Head Oedem at face and eyes diminished. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: NGT fixed, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (+). HR: 100 bpm, reguler, murmur (), RR: 22 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Rangsang meningeal + Refleks fisiologis: APR/KPR +/+ normal Refleks patologis: Babinsky -/-, Oppenheim -/-

Extremities

A: Loss of consciousness ec dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Elevasi kepala 30 Inj. Ceftriaxone 1g/12hours/IV (H6) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Paracetamol 3x100mg Diet SV 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

+ dd/ -GNA + hypertension stageI -SN

41

Planning: Head CT scan MRI LP

42

September, 20th 2013 S: loss of consciousness (-) O: Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 130/80 mmHg Head Oedem at face and eyes diminished. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: normal, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (-). HR: 100 bpm, reguler, murmur (), RR: 22 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3.

Extremities

A: dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30

+ dd/ -GNA + hypertension stage I -SN

Inj. Ceftriaxone 1g/12hours/IV (H7) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Paracetamol 3x100mg Diet MII 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

43

Planning: Head CT scan MRI LP

44

September, 21st 2013 S: loss of consciousness (-) O: Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 130/80 mmHg Head Oedem at face and eyes diminished. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: normal, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (-). HR: 100 bpm, reguler, murmur (), RR: 22 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3.

Extremities

A: dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30

+ dd/ -GNA + hypertension stage I -SN

Inj. Ceftriaxone 1g/12hours/IV (H8) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Paracetamol 3x100mg Diet MB 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

45

Planning: Head CT scan MRI LP

46

September, 22nd 2013 S: loss of consciousness (-) O: Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 130/80 mmHg Head Oedem at face and eyes diminished. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: normal, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (-). HR: 100 bpm, reguler, murmur (), RR: 24 bpm, regular, Crackles (-/-)

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3.

`Extremities

A: dd/ - CNS infection - intracranial hemmorhage

T: O2 L/i nasal canule IVFD D5% 20gtt/i Head elevation 30

+ dd/ -GNA + hypertension stage I -SN

Inj. Ceftriaxone 1g/12hours/IV(H9) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Paracetamol 3x100mg Diet MB 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day Watch out blood pressure

47

Planning: Head CT scan MRI LP

48

September, 23rd 2013 S: loss of consciousness (-) O: Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 100/70 mmHg Head Face: normal. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: normal, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (-). HR: 100 bpm, reguler, murmur (), RR: 24 bpm, regular, Crackles (-/-).

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3

Extremities

A: dd/ - CNS infection - intracranial hemmorhage

T: Threeway fixed

+ dd/ -GNA + hypertension stage I -SN

Inj. Ceftriaxone 1g/12hours/IV(H10) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Diet MB 1000kkal with 20gr protein Balance liquid / 6 hours Urinalisa / day

Planning: MRI LP

Leukocyte

: 19.21 x 103 /mm3

49

Albumin Head CT scan result Advice

: 3.7 g/dL : There is no infarct, SOL, or hemorrhage. : Contrast IV CT Scan

50

September, 24th 2013 S: loss of consciousness (-) O: Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 100/70 mmHg Head Face: normal, oldman face (-). Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), sunken eyes (-/-). Ear: normal, Nose: normal, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (-). HR: 100 bpm, reguler, murmur (), RR: 24 bpm, regular, Crackles (-/-). Widened ribs gap

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Lost of subcutaneous fat, muscles hypotrophy.

Extremities

A: dd/ - CNS infection - intracranial hemmorhage

T: - Threeway fixed -

+ dd/ -GNA + marasmus kwarshiorkor -SN

Inj. Ceftriaxone 1g/12hours/IV(H11) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Multivitamin tanpa Fe 1xcth1 Cotrimoxazole 1xcth1 Asam folat 1x1g Diet F75 160cc per 3 hours with mineral mix 3.2cc Balance liquid / 6 hours Urinalisa / day

51

Planning: MRI LP

September, 25th 2013 S: loss of consciousness (-) O: Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 100/70 mmHg Head Face: normal, oldman face (-). Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), sunken eyes (-/-). Ear: normal, Nose: normal, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (-). HR: 100 bpm, reguler, murmur (), RR: 24 bpm, regular, Crackles (-/-).Widened ribs gap

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate. Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Lost of subcutaneous fat, muscles hypotrophy.

Extremities

A: dd/ - CNS infection - intracranial hemmorhage

T: Threeway fixed

+ dd/ -GNA + marasmus kwarshiorkor -SN

Inj. Ceftriaxone 1g/12hours/IV(H12) Inj. Ranitidine 10mg/8hours/IV Inj. Dexametasone 0.75mg/6hours/IV Multivitamin tanpa Fe 1xcth1 Cotrimoxazole 1xcth1 Asam folat 1x1g Diet F100 160cc per 3 hours with mineral mix 3.2cc Balance liquid / 6 hours Urinalisa / day

52

Planning: MRI LP

September, 26th 2013 S: loss of consciousness (-) O: Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 100/70 mmHg Head Face: normal, oldman face(-). Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), sunken eyes (-/-). Ear: normal, Nose: normal, Mouth : Normal appearance. Neck Thorax Lymph node enlargement (-) Symmetrical fusiformis, Epigastria retraction (-). HR: 100 bpm, reguler, murmur (), RR: 24 bpm, regular, Crackles (-/-). Widened muscle gaps.

Abdomen

Soepel, enlargement (+), Peristaltic(+) N, Liver: palpated 5cm below arcus costae, Spleen: Schuffner I-II, Renal: undeterminate Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT <3. Lost of subcutaneous fat, muscles hypotrophy.

Extremities

A: dd/ - CNS infection - intracranial hemmorhage

T: Threeway fixed

+ dd/ -GNA + marasmus kwarshiorkor -SN

Inj. Ceftriaxone 1g/12hours/IV(H13) Inj. Ranitidine 10mg/8hours/IV Multivitamin tanpa Fe 1xcth1

53

Cotrimoxazole 1xcth1 Asam folat 1x1mg Diet F100 160cc per 3 jam dengan mineral mix 3.2cc Balance liquid / 6 hours Urinalisa / day

Patient went back home at her own request. ( 26th September 2013 )

54

CHAPTER IV DISCUSSION AND SUMMARY

Infection of the central nervous system and the surrounding tissue is a lifethreatening condition. Prognosis depends on the identification of the place and the type of pathogen that causes inflammation that can be given anti -biotic treatment is effective as soon as possible. Therefore analysis of CSF, biopsy, and laboratory analysis is the Gold standard for identifying pathogens causing meningitis, neuroimaging is a very important examination to describe the location of lesions in the brain and spinal cord. Picture of the pattern of lesions determine the proper diagnosis and determine the treatment of subsequent therapy. In particular, neuroimaging has a very important role in opportunistic diseases, not only for diagnosis, but also for monitoring response to therapy. Glomerulonephritis is a kidney disease with a glomerular inflammation and cell proliferation. Inflammation was mainly due to immunological mechanisms leading to glomerular pathology by mechanisms that are still unclear. In children, most cases of acute glomerulonephritis is post-infection, most commonly beta-hemolytic streptococcal infection group A. Of the development of renal biopsy technique per-cutaneous, examination by electron microscopy and immunofluorescent and serological examination, acute post-streptococcal glomerulonephritis has been known as one example of immune complex disease. This disease is a classic example of an acute nephritic syndrome with onset gross hematuria, edema, hypertension and acute renal insufficiency. Although the disease can heal itself with the perfect healing, in a small proportion of cases of acute renal failure can occur that require monitoring. Malnutrition will lead to failure of physical growth, mental development and intelligence, lowered productivity, increased morbidity and mortality. The relationship between nutrition and infectious diseases is highly correlated relationship. Protein-calorie malnutrition has a significant negative impact on the various components of the immune system. Malnourished children have less good immune response, making it more susceptible to infectious diseases. Infection

55

then leads to inflammation and worsening nutritional status, which aggravate the immune system. Poor immune system is directly proportional to the decrease in defense functions of the digestive system, skin, and respiratory muscle function decline. In these patients symptoms of central nervous system infection was found such as, lost of consciousness, positive meningeal stimulation. History of painful swallowing also found about two months ago. The patient also had hypertension, and the result obtained from the urine dipstick was positive. Based on the clinical symptoms signs of malnutrition was found such as widened ribs gap, loss of subcutaneous fat, muscle hypotrophy, and enlarged abdomen. Therefore, this patient was diagnosed with central nervous system infection + acute glomerulonephritis + malnutrition marasmus kwarshiorkor.