infection of cns

8/13/2019 Infection of CNS

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INFECTION OF CNS AND ENERGY PROTEIN MALNUTRITION

CHAPTER I

INTRODUCTION

1.1. BackgroundIn 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


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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. ObjectiveThe 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.


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CHAPTER II

LITERATURE REVIEW

2.1. Central Nervous System InfectionAcute 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

andEhrlichia) 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. MeningitisMeningitis 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


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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


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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, meningococcusandPneumococcus. 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 tuberculosisspecies and virus.3Meningitis

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


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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.

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

Picture 2.2. Brudzinski Sign and Kernig Sign


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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 3rdor 6th cranial nerve palsy with a depressed level of consciousness, or

hypertension and bradycardia with respiratory abnormalities.

2. severe cardiopulmonary compromise requiring prompt resuscitativemeasures 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. EnchepalitisEncephalitis 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.


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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


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.


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- Isodens or hypodense lesions are round ring, nodular or homogeneouspatterns and worsen by contrast, places predilection hemisphere (gray-

white 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 orhomogeneous 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 ofleukocytes.

- 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. MeningoencephalitisMeningoencephalitis 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


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. TreatmentThe 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 ofH. influenzaetype b produce -lactamases and therefore are resistant to

ampicillin. These -lactamase-producing strains remain sensitive to the extended-

spectrum 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 trimethoprim-

sulfamethoxazole is an alternative treatment forL. 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 herpeszostervaricella:

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 .

- ToxoplasmosisSulfadiasin 100 mg / kg orally for 1 month

Pirimetasin 1 mg / kg orally for 1 month

Spiramycin 3 x 500 mg / day

- AmebiasisRifampicin 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. ComplicationCollections 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. PrognosisAppropriate 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 GlomerulonephritisAcute 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. EtiologyAcute 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. PathologyAs 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 manifestationsThe 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. DiagnosisUrinalysis 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. ComplicationsPotential complications include heart failure, hyperkalemia,

hyperphosphatemia, hypocalcemia, asidosis, seizures, and urecemia.14

2.2.6. TreatmentManagement 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. PrognosisComplete 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 Energi (Kkal)

0-6 bulan 550

7-12 bulan 650

1-3 tahun 1000

4-6 tahun 1550

7-9 tahun 1800

2.3.1. MarasmusMarasmus 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

Picture 2.5. Marasmus(Source:http://www.childclinic.net)

2.3.2. KwashiorkorKwashiorkor occurs mainly due to not taking enough protein. In patients

suffering from kwashiorkor, the child will experience growth retardation, mental
http://www.childclinic.net/http://www.childclinic.net/http://www.childclinic.net/http://www.childclinic.net/


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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 Assessment2.3.3.1.Anthropometric

Anthropometric measurements most often used to measure growth

disorders. Anthropometry is widely used because it is practical with a non-

invasive approach to measure the nutritional status of an individual or society.

Anthropometric measures are body weight (BW), body height (BH), mid upper
http://adam.about.com/http://adam.about.com/http://adam.about.com/http://adam.about.com/


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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 short-

term 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 Standard Deviation Nutritional Status

BW/A 2 SD

-2 until +2 SD

< -2 until -3 SD< -3 SD

Nutritional excess

Nutritional normal

Nutritional lackMalnutrition

BH/A -2 until +2 SD

< -2 SD

Normal

BW/BH 2 SD

-2 until +2 SD

< -2 until -3 SD

< -3 SD

Overweight

Normal

Underweight

Over underweught


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2.3.4. TreatmentThe treatment for malnutrition children always based on 5 (five) event

management children with malnutrition.21

a. CONDITION: IIf Found: - Shock (shock)

- Letargis- vomiting / diarrhea / dehydration

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)

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 fluidsame 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 F-

75, F-75 given every 3 hours (the remainder via NGT)

If no diarrhea / vomiting / minimal edema and children can spend the F-75, change granting to 4 hours

b. CONDITION: IIIf Found: - Letargis

- vomiting / diarrhea / dehydrationImmediately:

Give 10% glucose bolus iv, 5 ml / KgBW Glucose / sugar 10% through NGT, 50 ml

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 1hour, 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 F-

75, F-75 give every 3 hours

Diarrhea / vomiting, edema is reduced, the child can spent the F-75, F-75administration change into every 4 hours

c. CONDITION: IIIIf Found: - vomiting / diarrhea / dehydration


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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, ifworse (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 toevery 4 hours

d. CONDITION: IVIf Found: Letargis

Immediately:

give 10% glucose bolus iv, 5 ml / KgBW Glucose or lar. sugar 10%through NGT, 50 ml


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


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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: VIf Not Found: - Shock (shock)

- Letargis- vomiting / diarrhea / dehydration

Immediately:

give 50 ml of glucose / lar. Sugar 10% oral Record the pulse, breathing frequency, awareness

37


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)

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


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CHAPTER III

CASE REPORT

Name : DN

Age : 4 years 6 months

Sex : Female

Date of Admission : September, 13th 2013

Main Complaint : Loss of consciousness

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

started with the feeling of sleepy. Seizures (-), history of seizures (+). Seizures happened3 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 : Patient was referred from RSUD Kumpulan Pane Tebing

Tinggi by pediatrician.

History of drugs : paracetamol, 2 bags of blood transfusion

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 (-).


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History of growth and development : 4months - baby started raising her head

, 8 monthsbaby started sitting, 1.5 yearsbaby 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 : 10 kg ( ideal body weight 11kg)

Height : 83 cm

BB/TB : -2 < Z score < -1

Arm measurement : 11 cm

Presens status

Sens: GCS 8 (E2V2M4), Blood pressure: 110/70 mmHg, Body temperature: 38.5oC,

Pulse: 110 bpm, Respiratory rate: 60 bpm.

Localized status

1. Head : Oedem at face and eyes. Eyes: Light reflexes (+/+), isochoricpupil, pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Mouth :

normal, Nose: pernafasan cuping hidung (+).

2. Neck : Lymph node enlargement (-)3. Thorax : Symmetrical fusiformis, suprasternal, epigastria, intercostal

retraction (+). HR: 110 bpm, regular, murmur (-), RR: 60 bpm, regular,

crackles (-/-)

4. Abdomen : Soepel, enlargement (+), Peristaltic (+) N. Liver: palpated 5cmbelow arcus costae. Spleen: Schuffner I-II. Renal: undeterminate. Turgor : good

5. Extremities : Pulse 110 bpm, regular, adequate pressure and volume, warm acral,CRT


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Laboratory Result:

September, 13th 2013Complete blood count(CBC)

Hemoglobin (HGB) g% 13.70 11.3-14.1

Eritrosit (RBC) 106/ mm

3 5.01 4.40-4.48

Leukosit (WBC) 10 / mm 25.36 4.5- 13.5

Hematokrit % 43.30 3741

Trombosit (PLT) 10 / mm 355 217-497

MCV fL 86.40 81-95

MCH Pg 27.30 25-29

MCHC g% 31.60 29-31

RDW % 18.40 11.614.8MPV fL 8.90 7.2-10.0

PCT % 0.32

PDW fL 9.6

WBC Count

Neutrofil % 72.70 3780

Limfosit % 19.80 2040

Monosit % 7.30 28

Eosinofil % 0.00 16

Basofil % 0.200 01

Neutrofil Absolut 10 /L 18.43 2.4 - 7.3

Limfosit Absolut 10 /L 5.03 1.7 - 5.1

Monosit Absolut 103/L 1.86 0.2 - 0.6

Eosinofil Absolut 103/L 0.00 0.10 - 0.30

Basofil Absolut 10 /L 0.04 0 - 0.1

Laboratory Result:September, 13th 2013

Blood gas analysis Unit Value Normal value

pH 7.462 7.35-7.45

pCO2 mmHg 22.7 38-42

pO2 mmHG 163.6 85-100

HCO3 mmol/L 15.8 22-26

Total CO2 mmol/L 16.5 19-25

BE mmol/L -6.1 (-2)-(+2)

O2 saturation % 99.5 95-100

Liver function test

Albumin g/dL 3.0 3.8-5.4


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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 + dd/ -GNA + hypertension

stageI

- intracranial hemmorhage -SN

Working Diagnosis

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

Carbohydrate metabolism

Glukosa ad random mg/dl 64.90


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- 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 Lymph node enlargement (-), nuchal rigidity (+)

Thorax 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

Extremities Pulse 120 bpm, regular, adequate pressure and volume, warm acral, CRT


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

Planning:

- Head CT scan- MRI- LP- C3, ASTO, CRP- Blood culture


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O:Sens: GCS 12 (E3V3M4), Temp: 37 oC TD 130/80 mmHgHead Oedem at face and eyes. Eyes: Light reflexes (+/+), isochoric pupil, pale

conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: fixed, Mouth :

Normal appearance.

Neck Lymph node enlargement (-), nuchal rigidity (+)







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Planning:

- Head CT scan- MRI- LP- C3, ASTO, CRP- Blood culture


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conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: fixed, Mouth :

Normal appearance.

Neck Lymph node enlargement (-),nuchal rigidity (+)







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Planning:

- Head CT scan- MRI- LP- C3, ASTO, CRP

Laboratorium result:

-

Total cholestrol/ TG (mg/dL) : 195/300- Cholestrol HDL/LDL (mg/dL) : 35/157- Ureum/ creatinine (mg/dL) : 35.6/0.18- Na/K/Cl (mEq/L) : 141/3/107- ASTO :


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Neck Lymph node enlargement (-)







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Planning:

- Head CT scan- MRI- LP


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Planning:



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O:Sens: GCS 13 (E4V4M5), Temp: 37 oC TD 130/80 mmHgHead Oedem at face and eyes diminished. Eyes: Light reflexes (+/+), isochoric pupil,

pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: NGT fixed,









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Planning:



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S:loss of consciousness (-)


pale conjunctiva palpebra inferior (-/-), icteric (-/-), Ear: normal, Nose: normal,



Thorax Symmetrical fusiformis, Epigastria retraction (-). HR: 100 bpm, reguler, murmur (-






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Planning:



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September, 21st 2013












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Planning:



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September, 22nd 2013










`Extremities Pulse 100 bpm, regular, adequate pressure and volume, warm acral, CRT


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Planning:



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September, 23rd 2013


O:Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 100/70 mmHgHead Face: normal. Eyes: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra

inferior (-/-), icteric (-/-), Ear: normal, Nose: normal, Mouth : Normal appearance.



), RR: 24 bpm, regular, Crackles (-/-).





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Albumin : 3.7 g/dL

Head CT scan result : There is no infarct, SOL, or hemorrhage.

Advice : Contrast IV CT Scan


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O:Sens: GCS 15 (E4V5M6), Temp: 37 oC TD 100/70 mmHgHead Face: normal, oldman face (-). Eyes: Light reflexes (+/+), isochoric pupil, pale

conjunctiva palpebra inferior (-/-), icteric (-/-), sunken eyes (-/-). Ear: normal,

Nose: normal, Mouth : Normal appearance.



), RR: 24 bpm, regular, Crackles (-/-). Widened ribs gap





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Planning:

- MRI- LP



O:Sens: GCS 15 (E4V5M6), Temp: 37oC TD 100/70 mmHg

Head Face: normal, oldman face (-). Eyes: Light reflexes (+/+), isochoric pupil, pale





), RR: 24 bpm, regular, Crackles (-/-).Widened ribs gap


Spleen: Schuffner I-II, Renal: undeterminate.



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Planning:

- MRI- LP



O:Sens: GCS 15 (E4V5M6), Temp: 37oC TD 100/70 mmHg

Head Face: normal, oldman face(-). Eyes: Light reflexes (+/+), isochoric pupil, pale





), RR: 24 bpm, regular, Crackles (-/-). Widened muscle gaps.





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- 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 )


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CHAPTER IV

DISCUSSION AND SUMMARY

Infection of the central nervous system and the surrounding tissue is a life-

threatening 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


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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.

infection of cns

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