CHAPTER I

1.1.Scenario RC brought his family because of a high fever, fatigue, and decreased consciousness. Arrived at the hospital , temperature was 39.5 C . RC suddenly had a seizure, so directly given diazepam suppo. According to his family, the RC has a fever 3 days, had been given paracetamol but his fever do not heal. RC also complained of head pain and no appetite, RC has never had a seizure before. By RC parents ever Hib immunized once when the baby. CSF : found leukocytosis and purulent, CSF pressure is 350 mm H2O number of cells of 15,000 sel/l,glucose level 16 md/dl. Hematological examination results showed the number of leukocytes is 20.000/mm3. Found in the urine albuminuria, CAST, and red blood cells. Therapy given : infusion D1/4S,Dexamethason inj 3mg 4x1 , Acetazolamide 00mg 3x1 drip, Ampicilin inj 500mg 4x1, Gentamicin inj 40mg 3x1,Paracetamol F syr 4x cth,Diazepam 1 mg ( if fever ).

1.2.CLARIFY TERMS OR CONCEPTS 1. Pleiositosis and purulen Increase leukocytes in the cerebrospinal fluid.Purulen is pus 2. HIB HIB is Haemophilus Influenza type B ,that can cause meningitis,hepatitis B exc. 3. CSF CSF is Cerebrospinal Fluid. 1.3. DETERMINE THE PROBLEM 1. Diagnosis of disease in this scenario? 2. Normal values of laboratory data interpretation? 3. Why RC seizures? 4. Bacteria that cause infection? 5. Meningitis immunization? 6. Indicative of a combination antibiotics? 7. What reactions occur if CSF pressure increases? 8. Pathofisiology and etiology of meningitis ? 9. Management of therapy? 10. Acetazolamid use in meningitis? 11. Dexamethason use in meningitis ?

1.4. BRAINSTORMING 1. Diagnosis of disease in this scenario is meningitis. 2. CSF - Protein = 15 45 mg/dl - Glukosa = 50 75 mg/dl - initial pressure = 70 180 mm - number of cells = 0 5 mononuklear

3. RC seizures because fever not dcrease. 4. Bacteria that cause infection are Meningococcus,H.influenza,Streptococcus Pneumococcus. 5. Immunization meningitis if caused by Hib is Hib immunization. 6. Indicative of combination antibiotic because there are other bacteria. 7. If the CSF pressure increases thereby increasing impulse conduction system so can make patient seizure. 8. Pathofisiology of meningitis Bacteria Nasofaring (because adhesi ) sistemik CSF replikasi

bacteria secrete cytokine

attract neutrophils

enter to CSF

blood vessel

edema / inflammatory manifestations

Etilogy of Meningitis Infection Bacteria Virus Fungi Parasit

9. Giving electrolyte fluids, antipyretics, analgesics for acute meningitis. if the patient is exposed to bacteria (Meningococcus,H.influenza,Streptococcus Pneumococcus ) give antibiotic 7-14 days. 10. Acetazolamide use in meningitis for decrease edema and intracranial pressure. 11. Dexamethason use in meningitis for decrease CSF and intracranial pressure.

1.5. Analyzing the Problem 1. Dose of each drug: Dexamethasone : adjuvant teraphy for decrease intracranial pressure. Inj 3 mg 4x1 Acetazolamide : decrease the cerebrospinal fluid so the intracranial pressure decrease. 100 mg 3x1 drip Ampisilin : antibiotic. Inj 500 mg 4x1 Gentamisin : antibiotic. Inj 40 mg 3x1 Paracetamol F syr : analgetic. Oral : x 250 mg = 187.5 mg 4x1 Diazepam : anticonvulsant. Oral : 1 mg (if fever > 37.8 C) 2. Diagnosis of Meningitis : - brudzinskins neck sign - lumbar puncture 3. Vaccine for Meningitis : - H. Influenza tipe B (HiB) - a few type of pneumococcus

- Meningococcus type C - New active for meningococcus serogroup A,C, W135, and Y

1.6 Learning Objective 1. CSF test to determine a cause of meningitis, virus or bacteria? 2. Empiric antibiotic for meningitis? 3. Definition of D1/4S? 4. Dose for each drugs in this scenario? 5. Vaccine for meningitis + the schedule? 6. Asetazolamid for meningitis?

1.7 Reporting 1. Bacterial Meningitis Glucose (mg/dL) Protein (mg/dL) WBCs (cells/L) Cell differential Culture Opening Pressure : Normal to marked decrease. <40 mg/dL. : (Marked increase) > 250 mg/dL. : >500 (usually > 1000). Early: May be < 100. : Predominance of Neutrophils (PMNs) : Positive : Elevated

Viral Meningitis Glucose (mg/dL) Protein (mg/dL) WBCs (cells/L) Cell differential: Culture: Opening Pressure : Normal (> 40 mg/dL.) : <100 mg/dL (moderate increase) : < 100 cells/L. : Early: neutrophils. Late: lymphocytes. : Negative : Usually normal

2. Recommended Empiric Antibiotics According to Predisposing Factors for Patients With Suspected Bacterial Meningitis

3. D1/4S = 5% Dextrose in 1/4 Strength (25%) Saline is hypertonic solution USES: fluid replacement, replacement of sodium, chloride, and some calories COMPLICATIONS: vein irritation bc of acidic pH, causes agglomeration if used with blood transfusions, hyperglycemia with rapid infusion 4. Dose of each drug: Dexamethasone : adjuvant teraphy for decrease intracranial pressure. Inj 3 mg 4x1 Acetazolamide : decrease the cerebrospinal fluid so the intracranial pressure decrease. 100 mg 3x1 drip Ampisilin : antibiotic. Inj 500 mg 4x1 Gentamisin : antibiotic. Inj 40 mg 3x1 Paracetamol F syr : analgetic. Oral : x 250 mg = 187.5 mg 4x1 Diazepam : anticonvulsant. Oral : 1 mg (if fever > 37.8 C) 5. 2, 4, 8 months, and 1 year 6. Asetazolamide used for adjuvant therapy in meningitis. It indication is for decrease the intracranial pressure by decrease the cerebrospinal fluid.

CHAPTER II

2.1. Problem Background Clinically, meningitis manifests with meningeal symptoms (eg, headache, nuchal rigidity, photophobia), as well as pleocytosis (an increased number of white blood cells) in the cerebrospinal fluid (CSF). Depending on the duration of symptoms, meningitis may be classified as acute or chronic The most common cause of meningeal inflammation is irritation caused by bacterial or viral infections. The organisms usually enter the meninges through the bloodstream from other parts of the body. Most cases of bacterial meningitis are localized over the dorsum of the brain; however, under certain conditions, meningitis may be concentrated at the base of the brain, such as with fungal diseases and tuberculosis. 2.2. Problem Formulation 1. Definision of Meningitis 2. Epidemiology, Etiology and Pathophysiology of Meningitis 3. Treatment of Meningitis 2.3. Purpose of The Problem 1. 2. 3. 4. 5. 6. Students can understand about the disease contained in scenario 2 Students can learn the signs and symptoms of disease in scenario 2 Students can identify the diagnosis of disease in scenario 2 Students can find the results of lab result interpretation of the case Students can understand the use of these drugs Able to know the side effects of these drugs.

CHAPTER III 3.1. Definition of Meningitis Meningitis is inflammation of the coverings around the brain and spinal cord. It is usually caused by an infection. The infection occurs most often in children, teens, and young adults. Also at risk are older adults and people who have long-term health problems, such as a weakened immune system. There are two main kinds of meningitis:

Viral meningitis is fairly common. It usually does not cause serious illness. In severe cases, it can cause prolonged fever and seizures. Bacterial meningitis is not as common but is very serious. It needs to be treated right away to prevent brain damage and death.

3.2. Epidemiology, Etiology and Pathophysiology of Meningitis I. Epidemiology

With almost 8000 cases and 2000 deaths occurring annually, bacterial meningitis continues to be a significant source of morbidity and mortality. The attack rate per year in the United States is reportedly 0.6-4 cases per 100,000 population. Meningococcal meningitis is endemic in parts of Africa, India, and other developing areas. Periodic epidemics occur in the so-called sub-Saharan "meningitis belt," as well as among religious pilgrims traveling to Saudi Arabia for the Hajj. In parts of Africa, widespread epidemics of meningococcal meningitis occur regularly. In 1996, the biggest wave of meningococcal meningitis outbreaks ever recorded arose in West Africa. An estimated 250,000 cases and 25,000 deaths occurred in Niger, Nigeria, Burkina Faso, Chad, and Mali. The incidence of neonatal bacterial meningitis is 0.25-1 case per 1000 live births. In addition, the incidence is 0.15 case per 1000 full-term births and 2.5 cases per 1000 premature births. Approximately 30% of newborns with clinical sepsis have associated bacterial meningitis. The frequency of H influenzae type B (HIB) disease has been markedly reduced, but N meningitidis causes approximately 4 cases per 100,000 children aged 1-23 months. The risk of secondary meningitis is 1% for family contacts and 0.1% for daycare contacts. The rate of meningitis caused by S pneumoniae is 6.5 cases per 100,000 children aged 1-23 months. Previously, HIB, N meningitidis, and S pneumoniae accounted for more than 80% of cases of bacterial meningitis. Since the late 20th century, however, the epidemiology of bacterial meningitis has been substantially changed by multiple developments. An increased incidence of HIV infection worldwide resulted in a correspondingly increased frequency of meningitis caused by encapsulated organisms (primarily S pneumoniae).

Even so, the overall incidence of bacterial meningitis declined from 1.9 to 1.5 cases per 100,000 between 1998 and 2003. This was partially due to the widespread use of the HIB vaccination, which decreased the incidence of HIB meningitis by more than 90% (see Table 3 Changing Epidemiology of Acute Bacterial Meningitis in the United States, below), nearly eliminating it in many developed countries where routine HIB vaccination is used. Because the frequency of bacterial meningitis in children has declined, the condition is becoming more of a disease of adults. The median age for persons with bacterial meningitis was 25 years in 1998, while in 1986, it was 15 months. A total of 255 cases of invasive H influenzae disease among children younger than 5 years were reported to the CDC in 1998, in contrast to 20,000 cases among children in 1987. This shift has reportedly been less dramatic in developing countries, where the use of the HIB vaccine is not as widespread. II. Etiology a) Meningitis caused by Haemophilus influenzae H influenzae is a small, pleomorphic, gram-negative coccobacilli that is frequently found as part of the normal flora in the upper respiratory tract of humans. It can spread from one individual to another by airborne droplets or direct contact with secretions. Meningitis is the most serious acute manifestation of systemic infection with H influenzae. The encapsulated type B strain of this bacterium is the form of H influenzae that most often causes meningitis. The isolation of H influenzae in adults suggests the presence of an underlying medical disorder, such as the following:

Paranasal sinusitis Otitis media Alcoholism CSF leak following head trauma Functional or anatomic asplenia Hypogammaglobulinemia

b) Meningitis caused by Streptococcus pneumoniae S pneumoniae, a gram-positive coccus, is the most common bacterial cause of meningitis. In addition, it is the most common bacterial agent in meningitis associated with basilar skull fracture and CSF leak. It may be associated with other foci of infection, such as pneumonia, sinusitis, or endocarditis (ie, Austrian syndrome). S pneumoniae is a common colonizer of the human nasopharynx (5-10% of healthy adults and 20-40% of healthy children). It causes meningitis by escaping the local host defenses and

phagocytic mechanisms, either through choroid plexus seeding from bacteremia or through direct extension from sinusitis or otitis media. Patients with the following conditions are at increased risk for S pneumoniae meningitis:

Hyposplenism Hypogammaglobulinemia Multiple myeloma Glucocorticoid treatment Defective complement (C1-C4) Diabetes mellitus Renal insufficiency Alcoholism Malnutrition Chronic liver disease

c) Meningitis caused by Streptococcus agalactiae Streptococcus agalactiae (group B streptococci) is a gram-positive coccus that is isolated from the lower gastrointestinal tract. It also colonizes the female genital tract at a rate of 5-40%, which explains why it is the most common (70%) agent of neonatal meningitis. Predisposing risks in adults include the following:

Diabetes mellitus Pregnancy Alcoholism Hepatic failure Renal failure Corticosteroid treatment

In 43% of adult cases, however, no underlying disease is present. d) Meningitis caused by Neisseria meningitides N meningitides is a gram-negative diplococcus that is carried in the nasopharynx of otherwise healthy individuals. It initiates invasion by penetrating the airway epithelial surface. The precise mechanism by which this occurs is unclear, but recent viral or mycoplasmal infection has been reported to disrupt the epithelial surface and facilitate invasion by meningococcus. Most sporadic cases (95-97%) are caused by serogroups B, C, and Y, while the A and C strains are observed in epidemics (< 3% of cases). Currently, it is the leading cause of bacterial meningitis in children and young adults, accounting for 59% of cases. Risk factors for Neisseria meningitis include the following:

Deficiencies in terminal complement components (eg, membrane attack complex, C5C9), which increases attack rates but is associated with surprisingly lower mortality rates Properdin defects that increase the risk of invasive disease Antecedent viral infection, household crowding, chronic medical illness, corticosteroid use, and active or passive smoking Overcrowding, as is observed in college dormitories (college freshmen living in dormitories are at highest risk) and military facilities, which has been reported for a clustering of cases

e) Meningitis caused by Listeria monocytogenes Listeria monocytogenes is a small gram-positive bacillus that causes 8% of bacterial meningitis cases and is associated with one of the highest mortality rates (22%). It is widespread in nature and has been isolated in the human stool of 5% of healthy adults. Most human cases appear to be food-borne. It is a common food contaminant, with a recovery rate of up to 70% from raw meat, vegetables, and meats. Outbreaks have been associated with consumption of contaminated coleslaw, milk, cheese, and alfalfa tablets. At-risk groups include the following:

Pregnant women Infants and children Elderly individuals (>60 y) Patients with alcoholism Adults who are immunosuppressed (eg, steroid use, transplant recipients, patients with acquired immunodeficiency syndrome [AIDS]) Individuals with chronic liver and renal disease Individuals with diabetes Persons with iron-overload conditions (eg, hemochromatosis or transfusion-induced iron overload)

f) Meningitis caused by gram-negative bacilli As a group, gram-negative bacilli can cause meningitis in certain groups of patients. Aerobic gram-negative bacilli include Escherichia coli, Klebsiella pneumoniae, Serratia marcescens, Pseudomonas aeruginosa, and Salmonella species. E coli are a common agent of meningitis among neonates. Other predisposing risk factors for meningitis associated with gram-negative bacilli include the following:

Neurosurgical procedures or intracranial manipulation Old age Immunosuppression

High-grade gram-negative bacillary bacteremia Disseminated strongyloidiasis

Disseminated strongyloidiasis has been reported as a classic cause of gram-negative bacillary bacteremia, as a result of the translocation of gut microflora with the Strongyloides stercoralis larva during hyperinfection syndrome. g) Staphylococcus-associated meningitis Staphylococci species are gram-positive cocci that are part of the normal skin flora. Meningitis caused by staphylococci is associated with the following risk factors:

Status post neurosurgery and post trauma Presence of CSF shunts Infective endocarditis and paraspinal infection

Staphylococcus epidermidis is the most common cause of meningitis in patients with CNS (ie, ventriculoperitoneal) shunts. h) Aseptic meningitis Aseptic meningitis is one of the most common infections of the meninges. As previously mentioned, if appropriate diagnostic methods are performed, a specific viral etiology is identified in 55-70% of cases of aseptic meningitis. However, aseptic meningitis can also be caused by bacteria, fungi, and parasites (see the Table 1 Infectious Agents Causing Aseptic Meningitis Syndrome, below). Importantly, partially treated bacterial meningitis accounts for a large number of meningitis cases with a negative microbiologic workup. III. Pathophysiology

The brain is naturally protected from the body's immune system by a barrier the meninges create between the bloodstream and the brain. Normally, this protection is an advantage because the barrier prevents the body from attacking itself. However, in meningitis, the barrier can become a problem; once bacteria or other organisms have found their way to the brain, they are somewhat isolated from the immune system and can spread. When the body tries to fight the infection, the problem can worsen; blood vessels become leaky and allow fluid, white blood cells, and other infection-fighting particles to enter the meninges and brain. This process, in turn, causes brain swelling and can eventually result in decreasing blood flow to parts of the brain, worsening the symptoms of infection.[8] Depending on the severity of bacterial meningitis, the inflammatory process may remain confined to the subarachnoid space. In less severe forms, the pial barrier is not penetrated, and the underlying parenchyma remains intact. However, in more severe forms of bacterial meningitis, the pial barrier is broken, and the underlying parenchyma is invaded by the

inflammatory process. Thus, bacterial meningitis may lead to widespread cortical destruction, particularly when left untreated. Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process in bacterial meningitis and account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose in patients with this disease. Exudates extend throughout the CSF, particularly to the basal cisterns, damaging cranial nerves (eg, cranial nerve VIII, with resultant hearing loss), obliterating CSF pathways (causing obstructive hydrocephalus), and inducing vasculitis and thrombophlebitis (causing local brain ischemia). Intracranial pressure and cerebral brain fluid

One complication of meningitis is the development of increased intracranial pressure (ICP). The pathophysiology of this complication is complex and may involve many proinflammatory molecules as well as mechanical elements. Interstitial edema (secondary to obstruction of CSF flow, as in hydrocephalus), cytotoxic edema (swelling of cellular elements of the brain through the release of toxic factors from the bacteria and neutrophils), and vasogenic edema (increased blood brain barrier permeability) are all thought to play a role in the development of increased ICP. Without medical intervention, the cycle of decreasing cerebral brain fluid (CBF), worsening cerebral edema, and increasing ICP proceeds unchecked. Ongoing endothelial injury may result in vasospasm and thrombosis, further compromising CBF, and may lead to stenosis of large and small vessels. Systemic hypotension (septic shock) also may impair CBF, and the patient soon dies from systemic complications or from diffuse CNS ischemic injury. Cerebral edema

The increased CSF viscosity resulting from the influx of plasma components into the subarachnoid space and diminished venous outflow lead to interstitial edema, and the products of bacterial degradation, neutrophils, and other cellular activation lead to cytotoxic edema. The ensuing cerebral edema (ie, vasogenic, cytotoxic, interstitial) significantly contributes to intracranial hypertension and a consequent decrease in cerebral blood flow. Anaerobic metabolism ensues, which contributes to increased lactate concentration and hypoglycorrhachia. In addition, hypoglycorrhachia results from decreased glucose transport into the spinal fluid compartment. Eventually, if this uncontrolled process is not modulated by effective treatment, transient neuronal dysfunction or permanent neuronal injury results. The role of cytokines and secondary mediators in bacterial meningitis

Key advances in understanding the pathophysiology of meningitis include insight into the pivotal roles of cytokines (eg, tumor necrosis factor-alpha [TNF-alpha], interleukin [IL]-1), chemokines

(IL-8), and other proinflammatory molecules in the pathogenesis of pleocytosis and neuronal damage during occurrences of bacterial meningitis. Increased CSF concentrations of TNF-alpha, IL-1, IL-6, and IL-8 are characteristic findings in patients with bacterial meningitis. (Cytokine levels, including those of IL-6, TNF-alpha, and interferon-gamma, have been found to be elevated in patients with aseptic meningitis.) The proposed events involving these inflammation mediators in bacterial meningitis begin with the exposure of cells (eg, endothelial cells, leukocytes, microglia, astrocytes, and meningeal macrophages) to bacterial products released during replication and death; this exposure incites the synthesis of cytokines and proinflammatory mediators. Data indicate that this process is likely initiated by the ligation of the bacterial components (eg, peptidoglycan, lipopolysaccharide) to pattern-recognition receptors, such as the Toll-like receptors. TNF-alpha and IL-1 are most prominent among the cytokines that mediate this inflammatory cascade. TNF-alpha is a glycoprotein derived from activated monocyte-macrophages, lymphocytes, astrocytes, and microglial cells. IL-1, previously known as endogenous pyrogen, is also produced primarily by activated mononuclear phagocytes and is responsible for the induction of fever during bacterial infections. Both molecules have been detected in the CSF of individuals with bacterial meningitis. In experimental models of meningitis, they appear early during the course of disease and have been detected within 30-45 minutes of intracisternal endotoxin inoculation. Many secondary mediators, such as IL-6, IL-8, nitric oxide, prostaglandins (PGE2), and platelet activation factor (PAF), are presumed to amplify this inflammatory event, either synergistically or independently. IL-6 induces acute-phase reactants in response to bacterial infection. The chemokine IL-8 mediates neutrophil chemoattractant responses induced by TNF-alpha and IL-1. Nitric oxide is a free radical molecule that can induce cytotoxicity when produced in high amounts. PGE2, a product of cyclo-oxygenase (COX), appears to participate in the induction of increased blood-brain barrier permeability. PAF, with its myriad biologic activities, is believed to mediate the formation of thrombi and the activation of clotting factors within the vasculature. However, the precise roles of all these secondary mediators in meningeal inflammation remain unclear. The net result of the above processes is vascular endothelial injury and increased blood-brain barrier permeability, leading to the entry of many blood components into the subarachnoid space. In many patients, this contributes to vasogenic edema and elevated CSF protein levels. In response to the cytokines and chemotactic molecules, neutrophils migrate from the bloodstream and penetrate the damaged blood-brain barrier, producing the profound neutrophilic pleocytosis characteristic of bacterial meningitis. Bacterial seeding

Bacterial seeding usually occurs by hematogenous spread. Organisms typically enter the meninges through the bloodstream, from other parts of the body. In patients without an

identifiable source of infection, local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source. Many meningitis-causing bacteria are carried in the nose and throat, often without symptoms in the carrier. Most meningeal pathogens are transmitted through the respiratory route, as exemplified by the fact that Neisseria meningitidis (meningococcus) is carried nasopharyngeally and by the nasopharyngeal colonization with Streptococcus pneumoniae (pneumococcus). Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular compartment, presumably by damaging mucosal defenses. Once inside the bloodstream, the infectious agent must escape immune surveillance (eg, antibodies, complementmediated bacterial killing, and neutrophil phagocytosis). Subsequently, hematogenous seeding into distant sites occurs, including the CNS. The specific pathophysiologic mechanisms by which the infectious agents gain access into the subarachnoid space remain unclear. Once inside the CNS, the infectious agents likely survive because host defenses (eg, immunoglobulins, neutrophils, complement components) appear to be limited in this body compartment. The presence and replication of infectious agents remain uncontrolled and incite a cascade of meningeal inflammation. This process of meningeal inflammation has been an area of extensive investigation in recent years that has led to a better understanding of meningitis pathophysiology. Bacterial seeding results in increased permeability of the blood-brain barrier, cerebral edema, and the presence of toxic mediators in the CSF. Inflammations are characterized by polymorphonuclear cell infiltration and extensive fibrinous exudation, which extends throughout the CSF, basal cisterns, and cranial nerves. Acute leptomeningitis results in congestion and hyperemia of the pia-arachnoid and distention of the subarachnoid space by the exudates. Once in the CSF, the paucity of antibodies, complement components, and white blood cells allows the bacterial infection to flourish. Bacterial cell wall components initiate a cascade of complement- and cytokine-mediated events that result in increased permeability of the bloodbrain barrier, cerebral edema, and the presence of toxic mediators in the CSF. 3.3. Treatment of Meningitis Bacterial or severe viral meningitis may require treatment in a hospital, including:

Antibiotics. These medicines usually are given through a vein (intravenously, or IV) to treat meningitis. Antibiotics are given only when bacteria are causing the infection. Giving antibiotics when they are not needed may cause drug resistance. Measures to reduce pressure within the brain. If meningitis is causing pressure within the brain, corticosteroid medicines such as dexamethasone may be given to adults or children. Measures to reduce fever. Medicines such as acetaminophen (Tylenol), fluids, and good room ventilation reduce fever. If you have a high fever, patient also may need a device such as a cooling pad placed on the bed.

Measures to prevent seizures. If patient have seizures, surroundings should be kept quiet and calm. Medicines such as phenobarbital or Dilantin can help stop seizures. Oxygen therapy. Oxygen may be given if patient have trouble breathing and to increase the amount of oxygen in all parts of the body. Oxygen may be delivered by a hood or tent placed over the body, a face mask placed over the nose and mouth, a nose piece (nasal cannula) held loosely under the nose, or, in severe cases, a tube through the mouth into the trachea (windpipe). Monitoring fluids. Patient may need to drink extra liquids because infections increase the body's need for fluids. Increasing liquids also reduces the possibility of dehydration. Liquids are given into a vein (IV) if patient have an infection and are vomiting or are not able to drink enough. Doctors control the amount of fluids given because people with meningitis may develop problems if they have too much or not enough fluid. Monitoring blood chemicals. Frequent blood tests are done to measure essential body chemicals, such as sodium and sugar in the blood.

3.4 SOAP Analysis for Meningitis in This Scenario

Problem medic meningitis

S/O Pleositosis and purulen, CSF =350 mm H2O, Glucose levels 16 mg/dl, Cell count 15.000 cell/ul, Fever and Fatigue

Therapy Infus D1/4S

Analize Supportive therapy

DRP

guidlines Bacterial meningitis in children Bacterial meningitis in children

Dexamethasone Kortikostreroid, inj 3mg 4x1 decreased cerebral edema, anti inflamation Acetazolamide Anti convulsant 100 mg3x1drip Ampicillin inj antibiotic Under dose 500 mg 4x1 Gentamisin inj 40 mg 3x1 Paracetamol F syr 4x cth Diazepam 1 mg ( when fever > 37,8 o C) antibiotic Under dose

Bacterial meningitis in children Bacterial meningitis in children

antipiretik Anti convulsant Bacterial meningitis in children

3.5 Algorithm for Meningitis