Introduction, Case Study

INTRODUCTION

Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs. Meningitis can be life-threatening because of the inflammation's proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.

Bacterial meningitis remains a serious threat to global health, accounting for an estimated annual 170 000 deaths worldwide.

Three species, Haemophilus influenzae,Streptococcus pneumoniae and Neisseria meningitidis, are responsible for most cases of bacterial meningitis occurring beyond the neonatal period. Since the introduction of H. influenzae type b (Hib) conjugate vaccines, N. meningitidis and S. pneumoniae have become the commonest causes of bacterial meningitis in the world. With the progressive implementation of the conjugated polysaccharide vaccines against pneumococcus, it is likely that N. meningitidis will remain a major agent of meningitis worldwide.

Moreover, N meningitidis is the only bacteria able to generate epidemics of meningitis. Meningococcus serogroups that are responsible for severe meningitis belong to only 6 groups: Nm A, B, C, X, Y and W135.

Group A meningococci are characterized by their propensity to cause large scale epidemics in developing countries, specifically in the countries of the African 'meningitis belt'.

Group B meningococcus (Nm B) is the most important cause of endemic meningitis in industrialized countries, accounting for 30% to 40% of the cases in North America and for up to 80% in some European countries.NmB also can cause severe, persistent epidemics, which begin slowly but may persist for 10 years or longer, as seen in the past in Norway; in Cuba, Brazil and areas of Chile; and currently in New Zealand. Vaccines against groups A, C, Y and W135 include bivalent or plurivalent polysaccharide (PS) and conjugate vaccines, some of which have already been combined with routinely administered vaccines to fit within the EPI regimen. Thus, the introduction of the NmC conjugate vaccines as an addition to routine infant immunization in the UK has had a tremendous impact on the incidence of the disease, resulting in a more than 90% decrease in the number of deaths and clinical cases and a 66% decrease in asymptomatic carriage.

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Because epidemic group A meningococcal meningitis continues to be a major problem in countries of the sub-Saharan meningitis belt, the Meningitis Vaccine Project (MVP), a partnership between the WHO and PATH, has developed a NmA conjugate vaccine, MenAfriVac®. The vaccine has successfully been tested in Phase I, II and II/III clinical trials in India and African countries of the meningitis belt: Mali, The Gambia and Senegal. Serum Institute of India (SII) has received a marketing authorization for export and use of MenAfriVacTM in Africa as single-dose mass vaccination campaigns in 1-29 year olds in the 25 countries of the African belt, a target population of about 250 million people. MenAfriVacTM received WHO prequalification on 23 June 2010 and progressive introduction will be rolled out starting with the 3 hyperendemic countries (Burkina Faso, Mali, Niger) in West Africa in 2010-11.

Group B N. meningitidis, is the only serogroup against which capsular PS vaccines cannot be developed, due to antigenic mimicry with PS in human neurologic tissues. Consequently, vaccine research against Nm B has focused on outer membrane proteins. Vaccines developed in Norway, Cuba or The Netherlands are being used to fight the Nm B epidemics in these countries. However, truly successful development of a broad specificity NmB vaccine is expected to come from a "reverse vaccinology" approach, or 'genome mining'.

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OBJECTIVES

 General Objective

After the discussion of this Case Presentation, the students will be able to deal and care for patients with Bacterial Meningitis integrally by applying their knowledge, skills, and positive attitudes based on what they have learned out of the discussion. Specific Objectives           COGNITIVE 

1. To be able to comprehend the pathophysiology of the patient’s disease.  2. To be able to harness knowledge about the patient’s condition. 3. To be able to determine the purposes of all the medications being

administered to the patient and its actions and mechanism of action. 4. To be able to gather factual information regarding the patient condition. 5. To be able to correlate learned knowledge from the classroom to the

clinical area.  PSYCHOMOTOR 

1. To be able to perform planned nursing interventions.  2. To be able to set priorities and goals in collaborative with the patient. 3. To be able to obtain a nursing health history, conduct physical assessment,

review records, organize and validate data.  4. To be able to realize planned interventions for our patient.  5. To be able to formulate nursing diagnoses and collaborative nursing

statements.

  AFFECTIVE 

1. To be able to establish rapport with the patient and folks.2. To be able to empathize with the patient and folks.3. To be able to address the spiritual needs of the patient.4. To be able to know the patient better and encourage verbalization of fear

and anxiety. 5. To be able to know the feelings of patient towards his condition. 

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PATIENT’S PROFILE

Chief Complaint: Convulsion

Present History of Illness

The patient had cough and colds four days prior to admission. He also had

high grade fever with upward gaggling three days prior to admission. The consult

was done and was admitted for observation. Chest X-ray was done which revealed

Pneumonia in the right lower lobe hence he was started Cefuroxime. There was

persistence of high grade fever with vomiting and remittent convulsive seizure

disorder. Patient was still with absence symptoms hence transferred to this

institution.

Past Medical History of Illness

Last December 2011, patient was admitted to a hospital in Malanday,

Valenzuela City. Then the family of the patient was being referred to San Lazaro

Hospital, a tertiary hospital in Manila. Patient was diagnosed to have bacterial

meningitis. The patient’s parents said that the patient was being comatose for

several weeks (as a result of disease progression), but patient was able to recover

with it.

Family History

The patient’s mother admits that a family history of hypertension on both

father and mother side of the patient.

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Personal and Social History

Patients Name: Maximo Prince Xyron Jay Gregorio

Address: Quiricada St. Sta. Cruz, Manila

Age: 1 6/12

Gender: Male

Civil Status: Child

Birth date: July 3, 2010

Birthplace: Valenzuela City

Religion: Roman Catholic

Nationality: Filipino

Father’s Name: Marlon Maximo

Mother’s Name: Jessa Gregorio Maximo

Admission Date: December 13, 2010

Time: 12:51PM

Department: Pavilion 7

Ward/Room/Bed/Service: FamilyMed-Philhealth Room 2-Bed 20/Pedia

Name of Hospital: San Lazaro Hospital

Hospital No: 000000000636228

Attending Physician: Carmelita A. Alvarez MD

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REVIEW OF SYSTEMS (ROS)

I. SKIN, HAIR and NAILSPresence of pressure ulcer in his left lower occipital area due to prolonged coma,

poor skin turgor and moderate capillary refill is observed during physical examination.

II. HEAD and NECKNo other problem except the pressure ulcer in his head and neck rigidity during

physical assessment, minimal to moderate hydrocephalus and focal minimal edema seen along right temporo-parietal-lobe.

III. EYES Temporary blindness is present, due to meningitis manifested by photophobia.

IV. EARS, NOSE, MOUTH and THROUTNo reported problems in hearing. No trouble eating or swallowing, his still a year

and a half, good formation of teeth.

V. RESPIRATORYShortness of breath is present, present reticular infiltrates seen in right lower

lobes (Pneumonia), no other significant chest findings noted.

VI. BREAST and AXILLAENo reported problems in breast (the patient is a boy) and axillae.

VII. CARDIACHeart and great vessels are normal in size and configuration, no cardiac disease

and never experienced palpitations

VIII. PERIPHERAL VASCULARNo peripheral vascular problem noted, and blood pressure is fine.

IX. GASTROINTESTINALNo other problem except of nausea and vomiting, present in meningitis.

X. URINARYNormal urination but yellowish urine is noted

XI. REPRODUCTIVENo reported problem regarding the reproductive system.

XII. MUSCULOSKELETALDecortication and Decerebration of the upper extremities is observed and the

lower extremities are flexed, difficult to extend and the patient cries when the leg is being extend.

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XIII. NEUROLOGICRemittent convulsion seizure and altered LOC is reported.

DIAGNOSIS

DEFINITIONMeningitis is an inflammation of the membranes (meninges) surrounding your

brain and spinal cord, usually due to the spread of an infection. The swelling associated with meningitis often triggers the "hallmark" signs and symptoms of this condition, including headache, fever and a stiff neck in anyone over the age of 2.

Most cases of meningitis are caused by a viral infection, but bacterial and fungal infections also can lead to meningitis. Depending on the cause of the infection, meningitis can resolve on its own in a couple of weeks — or it can be a life-threatening emergency.

If you suspect that you or someone in your family has meningitis, seek medical care right away. Early treatment can prevent serious complications.

PEDIATRIC BACTERIAL MENINGITIS:

Bacterial meningitis is a life-threatening illness that results from bacterial infection of the meninges. Beyond the neonatal period, the 3 most common organisms that cause acute bacterial meningitis are Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b (Hib). Since the routine use of Hib, conjugate pneumococcal, and conjugate meningococcal vaccines in the United States, the incidence of meningitis has dramatically decreased.

Although S pneumoniae is now the leading cause of community-acquired bacterial meningitis in the United States (1.1 cases per 100,000 population overall), since the introduction of the conjugate pneumococcal vaccine in 2000, the rate of pneumococcal meningitis has declined 59%. The incidence of disease caused by S pneumoniae is highest in children aged 1-23 months and in adults older than 60 years. Predisposing factors include respiratory infection, otitis media, mastoiditis, head trauma, hemoglobinopathy, human immunodeficiency virus (HIV) infection, and other immune deficiency states.

The emergence of penicillin-resistant S pneumoniae has resulted in new challenges in the treatment of bacterial meningitis. Because bacterial meningitis in the neonatal period has its own unique epidemiologic and etiologic features, it is described separately in this article.

ETIOLOGY Escherichia coli meningitis Haemophilus meningitis

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Listeria meningitis Meningococcal meningitis

Meningeal tuberculosis Pneumococcal meningitis

FACTORS

Not completing the childhood vaccine schedule increases your risk of meningitis. So do a few other risk factors:

Age. Most cases of viral meningitis occur in children younger than age 5. In the past, bacterial meningitis also usually affected young children. But since the mid-1980s, as a result of the protection offered by current childhood vaccines, the median age at which bacterial meningitis is diagnosed has shifted from 15 months to 25 years.

Living in a community setting. College students living in dormitories, personnel on military bases, and children in boarding schools and child care facilities are at increased risk of meningococcal meningitis, probably because the bacterium is spread by the respiratory route and tends to spread quickly wherever large groups of susceptible teenagers or young adults congregate.

Pregnancy. If you're pregnant, you're at increased of contracting listeriosis — an infection caused by listeria bacteria, which may also cause meningitis. If you have listeriosis, your unborn baby is at risk, too.

Working with animals. People who work with domestic animals, including dairy farmers and ranchers, have a higher risk of contracting listeria, which can lead to meningitis.

Compromised immune system. Factors that may compromise your immune system — including AIDS, diabetes and use of immunosuppressant drugs — also make you more susceptible to meningitis. Removal of your spleen, an important part of your immune system, also may increase your risk.

SIGNS & SYMPTOMSIt's easy to mistake the early signs and symptoms of meningitis for the flu

(influenza). Meningitis signs and symptoms may develop over several hours or over one or two days and, in anyone over the age of 2, typically include:

High fever Severe headache that isn't easily confused with other types of headache Stiff neck Vomiting or nausea with headache Confusion or difficulty concentrating — in the very young, this may appear as

inability to maintain eye contact Seizures Sleepiness or difficulty waking up

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Sensitivity to light Lack of interest in drinking and eating Skin rash in some cases, such as in viral or meningococcal meningitis

Signs in newbornsNewborns and infants may not have the classic signs and symptoms of headache and stiff neck. Instead, signs of meningitis in this age group may include:

High fever Constant crying Excessive sleepiness or irritability Inactivity or sluggishness Poor feeding A bulge in the soft spot on top of a baby's head (fontanel) Stiffness in a baby's body and neck Seizures

Infants with meningitis may be difficult to comfort, and may even cry harder when picked up.

Medical Management

Antimicrobial Agents

Cephalosporins. Third-generation cephalosporins (cefotaxime or ceftriaxone) are recommended for the treatment of childhood bacterial meningitis (A-I) and for pneumococcal and meningococcal meningitis caused by penicillin- resistant strains (A-III). They are the drugs of choice for empiric therapy in the treatment of H. influenzae type b meningitis, because resistance to chloramphenicol has developed. Third-generation cephalosporins have shown greater efficacy than chloramphenicol (Chloromycetin) and the second-generation cephalosporin cefuroxime (Ceftin). They are effective in meningitis caused by aerobic gram-negative bacilli (A-II), but increasing resistance makes in vitro susceptibility testing crucial. Ceftazidime (Ceptaz) has proved effective in the treatment of Pseudomonas meningitis (A-II). Cefepime (Maxipime), a fourth-generation cephalosporin, has proved safe and effective in the treatment of infants and children with bacterial meningitis, and has been used successfully in patients with bacterial meningitis caused by Enterobacter species and Pseudomonas aeruginosa (A-II).

Vancomycin. The use of vancomycin is not recommended in patients with bacterial meningitis caused by non-resistant strains (E-II). In patients with meningitis caused by penicillin- or cephalosporin-resistant strains it may be used in combination with a third-generation cephalosporin but should not be used

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alone (A-III). If a patient is unresponsive to parenteral administration, intrathecal administration may be considered.

Rifampin. Rifampin should be used only in combination with other antimicrobial agents as resistance develops rapidly when it is used alone. It has been used in combination with a third-generation cephalosporin with or without vancomycin for treatment of pneumococcal meningitis caused by penicillin- or cephalosporin-resistant strains, though data on its efficacy are lacking. The addition of rifampin is recommended only if clinical or bacteriologic response to a susceptible pathogen is delayed (A-III).

Carbapenems. Imipenem (Primaxin) has proved successful, but is not recommended for treatment of meningitis in most patients because of the potential for seizure activity (D-II). Meropenem (Merrem) has less potential for seizure and is recommended as an alternative to cefotaxime and ceftriaxone in the treatment of patients with bacterial meningitis (A-I), and for use in the treatment of meningitis caused by certain gram-negative bacilli (A-III). Although meropenem is effective in treating patients with pneumococcal meningitis caused by penicillin- or cephalosporin-resistant strains, the prevalence of strains with shared resistance may undermine its usefulness (D-II).

Fluoroquinolones. The use of f luoroquinolones in the treatment of bacterial meningitis is recommended when patients are unresponsive to or cannot be given standard antimicrobial therapy, or when meningitis is caused by gram-negative bacilli that are resistant to multiple agents (A-III). Newer fluoroquinolones, such as gatifloxacin (Tequin) and moxifloxacin (Avelox), potentially are useful in treating bacterial meningitis, but should be used only as alternative agents until more evidence is produced (B-II). There are no data on the use of these agents in newborns and children, although they may be considered in these patients when standard therapy is ineffective. Trovafloxacin (Trovan) no longer is used owing to possible liver toxicity.

Nursing Interventions

Assess neurologic function often. Observer level of consciousness (LOC) and signs of increased ICP (plucking at the bedcovers, vomiting, seizures, and a change in motor function and vital signs). Watch for signs for cranial nerve involvement (ptosis, strabismus, and diplopia).

Be especially alert for a temperature increase up to 38. 9o Celsius (102 F), deteriorating LOC, onsent of seizures, and altered respirations, all of which may signal an impending crisis.

Monitor fluid balance. Maintain adequate fluid intake to avoid dehydration, but avoid fluid overload because of the danger of cerebral edema. Measure central venous pressure and intake and output accurately.

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Watch for adverse effects of I.V. antibiotics and other drugs. To avoid infiltration and phlebitis, check I.V. site often and change the sites according to hospital policy.

Position the patient carefully to prevent joint stiffness and neck pain. Turn him often, according to planned positioning schedule. Assist with range-of-motion exercises.

Maintain adequate nutrition and elimination. It may be necessary to provide small, frequent meals or to supplement meals with nasogastric tube or parenteral feedings. To prevent constipation and minimize the risk of increased ICP resulting from straining at stool, give the patient a mild laxative or stool softener.

Ensure the patient’s comfort. Provide mouth care regularly. Maintain a quiet environment. Darkening the room may decrease photophobia. Relieve headache with a nonopioid analgesic, such as aspirin or acetaminophen as ordered.

Provide reassurance and support. The patient may be frightened by his illness and frequent lumbar punctures. If he’s deliberious or confused, attempt to reorient him often. Reassure his family that the delirium and behavior changes caused by meningitis usually disappear. However, fi a severe neurologic deficit appears permanent; refer the patient o a rehabilitation program as soon as the acute phase of this illness has passed.

To help prevent development of meningitis, teach patients with chronic sinusitis or other chronic infections and the importance of proper medical treatment. Follow strict sterile technique when treating patients with head wounds or skull fractures.

Prevention: Give haemophilus influenza type B and pneumococcal vaccines to children. Give meningocococcal vaccine to college students.

Diagnostic Procedures

A. Ideal Laboratory Tests

Cerebrospinal fluid (CSF) analysis. This is a primary diagnostic tool for meningitis. CSF analysis is a group of common tests, and a wide variety of other tests, that can be ordered and performed on a sample of CSF fluid. CSF is collected using a procedure called a lumbar puncture or spinal tap.

Initial CSF tests—the initial basic set of CSF tests that are often performed with suspected infections of the central nervous system include:

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Physical characteristics. Normal CSF appears clear and colorless. The appearance of the sample of CSF is usually compared to a sample of water. In infections, the initial pressure of CSF during collection may be increased, and the sample may appear cloudy due to the presence of white blood cells (WBCs) or microorganisms.

CSF protein. Only a small amount is normally present in CSF because proteins are large molecules and do not cross the blood/brain barrier easily. Increases in protein are commonly seen with meningitis, brain abscess, and neutrophils.

CSF glucose. Normal is about 2/3 the concentration of blood glucose. Glucose levels may decrease when cells that are not normally present use up (metabolize) the glucose. These may include bacteria or cells present due to inflammation (WBCs).

CSF total cell counts. WBCs may be increased with central nervous system (CNS) infections.

CSF WBC differential. Small numbers of lymphocytes, monocytes (and in neonates, neutrophils) are normal in a sample of CSF. There may be:o an increase in neutrophils with a bacterial infection

CSF Gram stain for direct observation of microorganisms

CSF culture and sensitivity for bacteria, fungi, and viruses

Additional or follow-up CSF tests— If any of the initial tests are abnormal, then additional infectious testing may be ordered. This may include one or more of the following: Other CSF antigen tests – depending on which organism(s) are suspected

Specific CSF antibody tests – depending on which organism(s) are suspected

Several other types of CSF testing may occasionally be ordered to help distinguish between viral and bacterial meningitis: CSF lactic acid—often used to distinguish between viral and bacterial

meningitis. The level will usually be increased with bacterial.

CSF C-reactive protein (CRP) is an acute phase reactant and is elevated with inflammation. It is markedly increased with bacterial meningitis. Since it is very sensitive even with early bacterial meningitis, it is often used to distinguish between bacterial and viral meningitis.

Laboratory tests on samples other than CSF—may be ordered along with or following CSF testing and may include: Blood glucose, protein, CBC (Complete Blood Count) – to evaluate and to

compare with CSF levels Blood cultures may be ordered to detect and identify bacteria in the blood.

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Cultures of other parts of the body may be performed to detect the source of the infection that led to meningitis.

CMP (Comprehensive Metabolic Panel) – a group of tests used to evaluate electrolyte balance and organ function. In severe forms of meningitis, monitoring of blood electrolytes may be important; for example, hyponatremia is common in bacterial meningitis, due to a combination of factors including dehydration, the inappropriate excretion of the antidiuretic hormone (SIADH), or overly aggressive intravenous fluid administration.

Non-Laboratory TestsImaging tests may be performed to look for signs of brain inflammation or abnormalities. Brain damage, tumors, bleeding, and abscesses may be detected. Tests may include:

CT (Computed tomography) - is a medical imaging method employing tomography created by computer processing. CT scans may reveal the cause of meningeal infection. Obstructive hydrocephalus can occur with chronic inflammatory changes in the subarachnoid space or in cases of ventricular obstruction. The most important role of CT scanning in imaging patients with meningitis is to identify contraindications to lumbar puncture and complications that require prompt neurosurgical intervention, such as symptomatic hydrocephalus, subdural empyema, and cerebral abscess.

MRI (Magnetic Resonance Imaging) - is a medical imaging technique used in radiology to visualize detailed internal structures. Routine contrast-enhanced brain MRI is the most sensitive modality for the diagnosis of bacterial meningitis because it helps to detect the presence and extent of inflammatory changes in the meninges as well as complications.

A Computed Tomography (CT) scan or Magnetic Resonance Imaging (MRI) scan is used to detect a shift in brain contents (which may lead to herniation) prior to lumbar puncture.

Ultrasonography- is an ultrasound-based diagnostic imaging technique used for visualizing subcutaneous body structures and internal organs for possible pathology or lesions. The role of ultrasonography in patients with bacterial meningitis is limited to the evaluation of complications or deterioration in the patient's clinical situation.

B. Actual Laboratory Findings

Urinalysis Date:

Normal Results Actual Results

Implications/Clinical Significance

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Color Light or pale yellow Yellow AbnormalTransparency Clear Cloudy AbnormalSpecific Gravity 1. 010- 1. 025 1. 1. 015 Normal

Glucose/ Sugar Negative (-) Negative (-) NormalRBC 0- 0- 2/ hpfWBC 40- 50/ hpf

CSF Results Date:

Normal Results

Actual Results

Implications/ Clinical Significance

Albumin 150- 300 mg/ L 361 mg/ L (↑)

Lesion in the choroid plexus or blockage of the flow of CSF; Damage to the blood- brain barrier; Bacterial Meningitis

Glucose 2.75- 4.13 mmol/ L 1. 98 mmol/ L (↓

)

Bacteria used the glucose for energy and mutation/replication.

WBC Neutrophils 0- 5 x 10^6/ L 9 (↑

)Indicates CNS infection, WBC fights the bacteria.

Protein 150- 450 mg/ L 482 mg/ L (↑) Tubercular Meningitis

Transparency Clear/ Colorless CloudyPresence of contamination of bacteria

Hematology Date:

Diagnostic Normal Result Actual Result Implications/ Clinical

SignificanceWBC 4. 8- 10. 8

(10^9/L) 14. 17 (↑) Increased WBC indicates infection

RBC 4.5- 5.9 (10^12/L) 3. 21 (↓)

Decreased in all anemia’s, leukemia, and after hemorrhage when blood volume has been restored

Hgb M- 140- 175 77.5 g/L (↓)

Decreased in various anemia’s, severe or prolonged hemorrhage, and with excessive fluid intake

Hct M- 0.415- 0.504 0. 251 (↓)

Decreased in severe anemia’s; acute massive blood loss

MCV (Mean corpuscular volume)

82- 98 78.06 fL (↓) Decreased in microcytic anemia

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MCH (Mean corpuscular hemoglobin)

28- 33 24.14 pg (↓) Decreased in microcytic anemia

MCHC (Mean corpuscular hemoglobin concentration)

33- 36 30. 92 g/L (↓) Decreased in severe hypochromic anemia

Platelet Count 150- 400 (10^9/L) 271 Normal

RDW 11. 4- 14. 0 18. 93 % (↑)

Increased RDW indicates mixed population of RBCs; immature RBCs tend to be larger.

- Lymphocytes 0. 19- 0. 48 0. 42 Normal

- Eosinophils 0. 02- 0. 08 0. 01 (↓)

Decreased with stress, use of some medications; decreased function in resisting infections.

- Basophils 0. 00- 0. 05 0. 01 Normal- Monocytes 0. 03 – 0. 09 0. 07 Normal

BUN/ Creatinine; Na/ K/ Ca Date:

Normal Results

Actual Results Implications/ Clinical Significance

BUN 2.5- 7. 20 8. 83 mmol/ L (↑)

Increased BUN levels suggest impaired kidney function; d/t acute or chronic kidney disease, damage, or failure; condition that results in decreased blood flow to the kidneys, such as stress, to conditions that cause obstruction of urine flow, or to dehydration.BUN concentrations may be elevated when there is excessive protein breakdown (catabolism), significantly increased protein in the diet, or GI bleeding.

Creatinine 71- 115 42. 80

umol/ L (↓)They can be seen with conditions that result in decreased muscle mass; skeletal muscle necrosis/ atrophy.

Sodium 135- 148 130. 00 mmol/ L (↓)

When the amount of sodium in fluids outside cells drops, water moves into the cells to balance the levels. This causes the cells to swell with too much water. Although most cells can handle this swelling, brain cells cannot, because the skull bones confine them. Brain swelling causes most of the symptoms of HypoNa; Alkali deficit.

Potassium

3. 50- 5. 30

3. 39 mmol/ L (↓)

Critical for normal cell function, neural transmission, membrane stability, bone structure, blood coagulation, and intracellular signaling; GI losses; Vitamin D deficiency.

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Calcium 8. 5- 10. 4 8. 2 mg/ dl (↓)

Cause weakness as cellular processes are impaired; Vitamin D deficiency; Diarrhea; Acute pancreatitis; Nephrosis.

Roentogenological and Ultrasound

There are Reticular infiltrates seen in both lower lobes.Heart and great vessels are normal in size and configuration. No other significant chest findings of note.

- Pneumonia

Computed Tomography (CT) Scan

Multiple plain and contrast enhanced axial images reveal minimal to moderate amount of low density subdural fluid collections or effusions over both fronto- parietal convexities.This measures about 1.5 cm in thickness, on the right side and 1.0 cm on the left which tapers posteriorly.Underlying dural thickening with contrast enhancement ventricles are minimally to moderately dilated due to obstructive hydrocephalus.Focal minimal edema seen along right temporoparietal- lobe.Midline structures not displaced.

Impression:1.) Bilateral subdural effusions, secondary to meningitis.2.) Minimal to moderate communicating hydrocephalus.3.) Diffuse edema in the right temporo- parietal lobe. (Inflammatory or ischemic

process

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ANATOMY and PHYSIOLOGY

Meningitis is characterized by inflammation of the meninges, the thin anatomical structure (3 layers or membranes) that intimately and delicately covers the brain and spinal cord. Specifically, meningitis is an infection within the subarachnoid space, a space between the middle and innermost layers which is also the largest of the 3 spaces and is the main reservoir of CSF). The 3 layers of the meninges are briefly described as follows:

- The Dura mater (Latin: dura, “hard”; mater, “mother”), the outermost layer, is composed of tough, nonelastic, dense connective tissue and adheres to the skull and vertebral column. It is covered on its innermost surface by squamous epithelial cells.

- The Arachnoid (Greek: arachnocides, “like a cob- web”), the middle layer, is composed of dense collagenous and elastic connective tissue, adheres to the dura mater and has delicate spiderweb- like projections (trabeculae) which connect it to the 3rd layer, the pia mater. The arachnoid and its trabeculae are covered with squamous epithelial cells.

- The Pia mater (Latin: pia, “tender”; mater, “mother”), the innermost layer, composed of delicate collagenous and elastic connective tissue and is covered by squamous epithelial cells. It is the only meningeal layer which contacts the CNS, It covers the surfaces of the brain and spinal cord.

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Choroid Plexuses- the sites at which the fluid component of the blood is modified (by secretion and absorption of certain solutes) and secreted into the ventricles.CSF- the modified and secreted fluid, which circulates in the ventricles and the subarachnoid space around the brain and spinal cord and returns to the blood circulatory system through subarachnoid villi that project into the superior sinus, which traverses the inner roof of the skull.In adults, 400 to 600 ml of CSF is produced and recirculated each day. At any given time, the normal CSF volume is 10 to 60 ml in newborns and 100 to 160 ml in adults.

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PATHOPHYSIOLOGY

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Temporal lobe may herniated

through tentoriumIschemia

Necrosis

S/ Sx:- High pitch cry- Fever- Vomiting- Lethargy- Seizure

(Priority: safety)

- Nuchal rigidity/ stiff neck Pressure in brain stem

Predisposing Factors - extreme of ages

- low birth weight baby - prematurity

Precipitating Factors - immunosuppressed

- tobacco use- otitis media/mastoiditis

- viral URI

Streptococcus Pneumoniae

Neisseria MeningitisHaemophilus Influenzae

Decreased Cerebral Blood flow

If not treated

Increased ICP

Inhalation (droplet form)

Enters respiratory tract

Enter circulation

Cross Blood Brain Barrier

Proliferates in Cerebrospinal Fluid

Inflammation of Subarachnoid Space

(Increased WBC, Decreased Glucose, Increased CHON)

Cerebral edema

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Brain deathMeningeal irritation

Kernig’s sign(Cannot extend leg at

the knee when the thigh is flexed because of the stiffness of hamstrings)

Brudzinski’s sign

(When the neck is flexed, the legs are also

flexed)

Cranial nerve compression

Depressed medulla

and underlying function

Respiratory depression/

failure Photophobia

(CN 2)

Cranial nerve

dysfunction

RELATED LITERATURE

Acute bacterial meningitis is one of the most severe infectious diseases, causing neurologic sequelae and accounting for an estimated 171,000 deaths worldwide per year. Although most disease occurs in infants, the societal impact is also important because of the continued high incidence in healthy older children and adolescents. Despite many new antibacterial agents, bacterial meningitis fatality rates remain high, with reported rates between 2% and 30%. Furthermore, permanent sequelae, such as epilepsy, mental retardation, or sensorineural deafness are observed in 10%–20% of those who survive.

The 3 most common etiologic agents are Haemophilus influenzae type b (Hib), Streptococcus pneumoniae, and Neisseria meningitidis, which account for 90% of reported cases of acute bacterial meningitis in infants and children >4 weeks of age. Hib meningitis is a disease affecting primarily young children; most of the cases occur in children 1 month to 3 years of age. The use of Hib conjugate vaccines has reduced the incidence of, or even virtually eliminated, invasive Hib disease in some industrialized countries. S. pneumoniae is a major cause of childhood bacterial meningitis in countries where Hib disease has been eliminated by vaccination. It is the second most frequently reported cause of septic meningitis in some European and sub-Saharan African countries, after meningococcal cases.

N. meningitidis is now considered to be the leading cause of bacterial meningitis in many regions of the world, causing an estimated 1.2 million cases of bacterial meningitis and sepsis worldwide each year. Meningococci are classified into 13 serogroups based on the antigenic properties of their capsular polysaccharide; however, nearly all disease is caused by 5 serogroups: A, B, C, W-135, and Y. The epidemiology of N. meningitidis varies by serogroup; currently, serogroups A, B, and C account for >90% of meningococcal disease worldwide. However, the epidemiologic landscape is constantly changing, and with increasing international travel and cross-border migration, the epidemiology of this disease will remain dynamic. Currently, serogroups A and C predominate throughout Asia and Africa, whereas serogroups B and C are responsible for most cases in Europe and North America. In several countries, including the United States, the proportion of disease caused by serogroup Y has increased over the past decade, where it now accounts for approximately one third of meningococcal cases. Serogroup W-135 has also recently emerged in some parts of the world, primarily in the Middle East and Africa, in some instances causing large epidemics.

The annual Hajj pilgrimage to Mecca is a major international event; ≈2 million people from around the world gather in one place, where the extreme crowding provides an ideal environment for transmission of meningococcal carriage. On several occasions, meningococcal disease outbreaks have subsequently spread

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worldwide by returning pilgrims. A major serogroup A meningococcal disease epidemic occurred in the 1980s, affecting Muslim pilgrims initially, followed by populations in other Middle Eastern and African countries. After this epidemic, Hajj pilgrims were vaccinated with a bivalent (A and C) meningococcal polysaccharide vaccine before entering Saudi Arabia. With the emergence of serogroup W-135 meningococcal disease among Hajj pilgrims in the Middle East during 2000 and 2001, vaccine recommendations for pilgrims were changed to quadrivalent (A, C, W-135, and Y) meningococcal polysaccharide vaccine in 2002.

Global surveillance of confirmed meningococcal cases, including surveillance of the diversity of causative strains, is essential to managing disease and developing vaccines. This study was undertaken to determine the current etiology of bacterial meningitis in Turkey, with particular emphasis on serogroup distribution of meningococci. Turkey is a predominantly Muslim country, and as such epidemics originating at the Hajj may have an effect on the national epidemiology. Although limited epidemiologic studies are available, cases of invasive meningococcal disease as well as carriage of serogroup W-135 have been reported in Turkey. This finding is in contrast to Western Europe, where the incidence of W-135 disease remains low. Turkey has no surveillance system for bacterial meningitis, and exact rates of meningococcal disease and serogroup distribution are unknown. Reliable surveillance data from countries such as Turkey are vital to understand, and better anticipate, the constantly changing landscape of bacterial meningitis and meningococcal disease.

Meningitis cases by geographic region of Turkey. The number of suspected meningitis cases included in the study per region is shown in boldface, with the region-specific estimated incidence rate of laboratory-confirmed...

From February 16, 2005, through February 15, 2006, active surveillance of acute bacterial meningitis among children admitted to 12 participating hospitals was undertaken. Turkey is divided into 7 geographic areas. Twelve health centers in 9 cities located in all of these 7 geographic regions were selected to represent the population characteristics of the country. Two centers from each of the 3 biggest cities and 1 center from each of the other cities were included. Each health center

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served as a referral center for its region in the field of pediatric diseases. The centers serve ≈32% of the entire pediatric population of Turkey. Approval was obtained from the ethical committees of the participating centers and Ministry of Health.

In each hospital, suspected cases of acute bacterial meningitis were identified by a pediatrician, based on the following criteria: any sign of meningitis (fever [axillary measurement >38°C], vomiting [>3 episodes in 24 h], headache, meningeal irritation signs [bulging fontanel, Kernig or Brudzinski signs, or neck stiffness]) in children >1 year of age; fever without any documented source; impaired consciousness (Blantyre Coma Scale <4 if <9 months of age and <5 if >9 months of age); prostration (inability to sit unassisted if >9 months of age or breastfeed if <9 months of age) in those <1 year of age; and seizures (other than those regarded as simple febrile seizures with full recovery within 1 h). For each suspected case, demographic data, predominant clinical signs and symptoms, prior history of use of antimicrobial agent, and laboratory results were recorded by using a standardized case report form.

Cerebrospinal fluid (CSF) samples were obtained from all patients <17 years of age with clinical suspected meningitis. Patient samples were included in further analyses if the CSF had 1) >10 leukocytes/mm3 in the CSF, and/or 2) higher CSF protein levels than normal for the patient’s age, and/or 3) lower CSF glucose levels than normal for the patient’s age. In addition to these patients, all who had a positive CSF culture, PCR, Gram stain, or antigen detection test result were also included in the study. No neonates (<1 month of age) were included in the study since the pathogens of neonatal meningitis were expected to be different than those of the older case-patients.

Statistical AnalysisContinuous variables were compared by the Student t test and categorical

variables with χ2 or Fisher exact tests. A 2-tailed p value <0.05 was considered significant. All statistical analysis was performed with SPSS version 11.5 (SPSS Inc, Chicago, IL, USA).

Meningitis CasesIn total, 408 children were hospitalized with a clinical diagnosis of meningitis

during the study period, and a CSF sample from each patient was obtained. The distribution of these suspected cases according to the geographic regions was as follows: 109 (26.7%) in Southern Anatolia, 74 (18.1%) in Aegean region, 79 (19.6%) in Central Anatolia, 53 (13.0%) in Marmara region, 43 (8.7%) in Eastern Anatolia, 24 (5.9%) in Black Sea region, and 26 (6.4%) in Mediterranean region. The mean age of the 408 children was 4.8 years (standard deviation 4.1 years), and the boy-to-girl ratio was 1.5:1. Of 408 patients diagnosed with acute bacterial meningitis, 20

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(4.9%) died and 14 (5.7%) of these deaths were among patients with laboratory-confirmed cases.

Laboratory-Confirmed Meningitis Cases and Etiology

Distribution of bacteria causing childhood acute bacterial meningitis in different age groups.Neisseria meningitidis was the most common cause of meningitis, and the highest estimated incidence was in children <1 year...

Of the 408 cases, bacterial meningitis was confirmed by PCR, culture, or latex agglutination test in 243 (59.6%) patients. Regional incidence rates of laboratory-confirmed meningitis were estimated as ranging from 1/100,000 population in the Black Sea region to 10.9/100,000 population in the Southeast Anatolia region. Nationwide, the highest incidence was in children 1–12 months of age and was slightly more common in boys. The boy-to-girl ratio of the confirmed cases was 1.3:1, and the age distribution was as shown in.

Overall, the diagnosis of acute bacterial meningitis was confirmed with CSF culture in 41 (17%) of 243 cases, with latex agglutination test in 56 (23%), and with PCR in 243 (100%). Latex agglutination test was positive in 37 cases for N. meningitidis, in 10 cases for Hib, and in 9 cases for S. pneumoniae.

Where data were available, 7 (17%) of 41 cases with positive CSF culture and 111 (54.9%) of 202 cases with negative CSF culture had a history of use of antimicrobial agent(s) before lumbar puncture, which may account for the relatively low diagnosis rate by using this technique. N. meningitidis was reported in 23 cases, S. pneumoniae was reported in 12, and Hib was reported in 6 cases as positive in CSF culture.

Distribution of etiology of acute bacterial meningitis in Turkey detected by using PCR analysis. Of 243 PCR-confirmed cases, 138 (56.5%) were attributable to Neisseria meningitidis, 55 (22.5%) to Streptococcus pneumoniae, and...

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PCR analysis was by far the most reliable method of confirming bacterial meningitis, accounting for all confirmed cases with 243 positive results. In these PCR-positive samples, 138 (56.5%) were attributable to N. meningitidis, 55 (22.5%) to S. pneumoniae, and 50 (20.5%) to Hib. Of the 408 patients, 118 (48.5%) of 243 cases with positive PCR and 96 (58.2%) of 165 cases with negative PCR had received antibacterial drugs in the week before CSF sampling.

In the evaluation of the bacterial agents among the 7 different geographic regions of the country, N. meningitidis was the most common cause of acute bacterial meningitis in all regions except the Mediterranean region, located on the southern coast of Turkey. Here S. pneumoniae were the prominent bacteria, and N. meningitidis were detected in only 2 cases.

Comparison of the incidence of N. meningitidis, S. pneumoniae, and Hib among different age groups demonstrated that N. meningitidiswas the prominent bacterial agent causing acute bacterial meningitis, especially in children <7 years of age. The highest incidence was detected during the first year of life for all 3 bacteria.

CSF findings were recorded for 368 (90.2%) of 408 CSF samples sent to the Central Laboratory. As a mean, in PCR-negative samples, CSF protein level was significantly lower (70.2 vs. 130.4 mg/dL; p = 0.003) and glucose level was significantly higher (55.6 vs. 41.3 mg/dL; p = 0.01) than in PCR-positive samples. Total cell counts were not significantly different in PCR-negative and -positive samples (157.9 and 211.1/mm3; p>0.05), but polymorphonuclear cell count was significantly higher in PCR-positive samples (8,284.3 vs. 38.5/mm3; p = 0.001). Among the PCR-positive samples, total cell and polymorphonuclear cell counts were not significantly different between samples positive for N. meningitidis, S. pneumoniae, and Hib (p>0.05).

Meningococcal EpidemiologyAmong the samples that were positive for N. meningitidis following PCR

analysis, serogroup W-135 was the cause of most infections; 59 (42.7%) cases were serogroup W-135, 43 (31.1%) were serogroup B, 3 (2.2%) were serogroup Y, and 1 (0.7%) was serogroup A. There were no cases with a positive result for serogroup C (this was also the case following analysis of CSF culture-positive samples) and in 32 (23.2%) N. meningitidis–positive samples the serogroup could not be determined by the PCR assay.

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Distribution of predominant Neisseria meningitidis serogroups in different age groups. Serogroups W-135 and B caused 42.7% and 31.1% of all meningococcal infections, respectively. W-135 was the most common cause of meningococcal...

Analysis by age reveals the greatest meningococcal disease incidence is in children <3 years of age, particularly infants <1 year of age. The numbers of cases caused by the 2 most common N. meningitidis serogroups (serogroups W-135 and B) were similar in the most vulnerable age groups (<3 years of age), but W-135 was more common in children 4–16 years of age.

Etiology of confirmed cases of bacterial meningitis in different geographic regions. W-135 was the most prominent Neisseria meningitidis serogroup in the Southeast Anatolia, Aegean, Eastern Anatolia, and Black Sea regions. The...

Etiologic and meningococcal serogroup distribution among the different geographic regions is illustrated in. N. meningitidis serogroup W-135 was more prominent than the other meningococcal serogroups in the Southeast Anatolia, Aegean (Western Turkey), Eastern Anatolia, and Black Sea regions. N. meningitidis serogroup B was much more common in the Marmara region (northwestern Turkey), and in the Central region; the numbers of serogroup B and serogroup W-135 cases were similar. The Mediterranean region had 2 N. meningitidis–positive samples; both were nongroupable by PCR analysis.

Discussion

In this study, 243 cases of laboratory-confirmed acute bacterial meningitis were recorded. Because our study centers provide service to 32% of the population of Turkey, extrapolation from the number of cases recorded suggests that 759 acute bacterial meningitis cases (excluding neonatal cases) per year occur in the whole country. The population of children 1 month through 16 years of age was calculated as 21.6 million. Therefore, the annual incidence of acute bacterial meningitis was estimated as 3.5 cases/100,000/year. Although similar to incidence rates reported from other countries without routine vaccination against N. meningitidis, S. pneumoniae, and Hib, this value likely represents a lower limit estimate of the true disease incidence, given the inherent limitations of hospital-based surveillance. Furthermore, the specific role of these 3 most common bacterial causes of acute bacterial meningitis varies between regions.

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An accurate laboratory confirmation of the etiology in acute bacterial meningitis is essential to provide optimal patient therapy, appropriate case contact management, and reasoned public health actions. Prospectively, it also provides information upon which to base decisions regarding immunization programs, especially for countries without routine vaccination against the main acute bacterial meningitis pathogens. Although bacterial culture is considered to be the standard method, the negative effect of prior antimicrobial drug use on its sensitivity necessitates nonculture techniques for diagnosis. Among nonculture diagnostic tests, PCR is the most accurate and reliable method, especially among patients with a history of antimicrobial drug use before spinal tap. This finding was evident in the present study, in which PCR analysis was the most sensitive method, confirming 243 cases (59.6%) among 408 children meeting the case definition for bacterial meningitis (100% of all cases that were confirmed by any method). Using other methods that are more sensitive may increase the rate of laboratory confirmation.

Several reports review the rates of bacterial causes of acute bacterial meningitis from many different countries, based on CSF cultures. Some factors, such as previous antimicrobial drug treatment, interfere with the recovery of microorganisms from CSF. In our study, bacterial isolation was only possible in 41(16.8%) of 243 of confirmed cases. However, the most important factor for this low positive ratio in culture was likely prior antimicrobial drug use, as 118 case-patients received such treatment before the lumbar puncture (7/41; 17% in culture-positive case-patients and 111 (54.9%) of 202 in culture-negative case-patients). In patients with acute bacterial meningitis, blood cultures can be used in the etiologic diagnosis in up to 80% of cases since the bacteria generally invade meningeal membranes following bacteremia. In our study, however, only 12 (4.9%) of 243 case-patients who had blood culture tests returned positive results. This finding may also be related to the previous antimicrobial drug use.

Previous reports suggested that S. pneumoniae and N. meningitidis serogroups A and B would be the most common bacteria causing acute bacterial meningitis in Turkey. Serogroup W-135 meningococcus was isolated for the first time in Turkey in an asymptomatic healthy preschool child in 2001, and the first patient with meningitis caused by serogroup W-135 was reported in 2003. In this study N. meningitidis, especially serogroup W-135, was responsible for most of the cases observed, with serogroup B the second most common. Only a small number of serogroup A or Y cases were noted, and no serogroup C cases were observed. These data are in contrast to those from many parts of Europe, where serogroups B and C dominate the epidemiologic landscape. In Turkey, meningococcal disease caused by serogroup W-135 has increased from 1 case in 2003 to 59 cases or 42.7% of all laboratory-confirmed N. meningitidis cases in children, in this study, during 2005/06. A dramatic increase in serogroup Y disease

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has been documented in the United States during the last decade, but this has been over a longer period.

Most of the Turkish population is Muslim, and ≈150,000 pilgrims travel annually to Saudi Arabia for the Hajj. Since 2002, all Turkish pilgrims have received a quadrivalent meningococcal polysaccharide vaccine before travel. Although this vaccine generates a robust immune response against serogroup W-135, in contrast to what has been demonstrated for serogroup C meningococcal conjugate vaccines, meningococcal polysaccharide vaccines are not thought to reliably prevent asymptomatic carriage. A study from the United States reported that 0.8% of returning vaccinated pilgrims in 2001 were carrying W-135, whereas no pilgrims carried this serogroup upon departure from the United States. Therefore, the rapid rise in the proportion of cases caused by serogroup W-135 may be attributable to transmission from pilgrims returning from the Hajj carrying this particular serogroup. Although not definitive, this conclusion is further supported by the finding that all serogroup W-135 isolates available for phenotypic characterization were identical to the Hajj-associated clone, W135:2a:P1.5,2. Because strains with this serologic profile have not been uniquely associated with the Hajj outbreak, additional typing data (e.g., multilocus sequence typing or multilocus enzyme electrophoresis), and epidemiologic investigations will be required to support this hypothesis. Therefore, it remains speculative that the increased W-135 disease in Turkey may be caused by spread of Hajj epidemic strain through carriage and transmission by pilgrims.

This study demonstrates the need for good quality, continued surveillance of bacterial meningitis cases, as well as the etiology and epidemiology of the causative bacteria. Only by accurately monitoring meningococcal epidemiology will effective vaccination policies be developed. The bacterial meningitis epidemiologic landscape is not static, and the causative agents change with time and across regions of the world. This study has demonstrated that the relative contribution of serogroup W-135 to the meningococcal disease incidence in Turkey is increasing, which is in contrast to the rest of Europe. Turkey may remain isolated in terms of W-135 disease incidence or it may represent the beginning of epidemiologic change in Eastern Europe. This possibility should be investigated in greater depth and monitored prospectively. Introduction of vaccines can dramatically reduce the meningitis disease incidence, but these vaccines must be targeted against the correct bacteria and, where relevant, the correct bacterial serogroup. The choice of meningococcal conjugate vaccines in Turkey will need to include coverage for serogroup W-135; introduction of such a vaccine would be helpful in protecting the Turkish population from this invasive bacterial meningitis. Moreover, it may also be prudent to switch the meningococcal vaccine used for pilgrims to conjugated vaccine to prevent the carriage of the microorganism by pilgrims.

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DISCHARGE PLANNING

Medications Encourage the family to have a strict compliance with regards to the medication

to attain therapeutic effect Explain to the family the purpose and side effects of the medications so that

they will be aware of its effect Give adequate instructions to the significant others about the importance of the

following medications and dietary regimens so that the patient’s condition can remain stable as soon as possible.

Acetaminophen Acetazolamide Albuterol Sulfate Ceftriaxone Sodium Diazepam Mannitol Meropenem Oxacillin sodium Phenobarbital sodium RIPE

Exercise Teach the significant others on how to perform Passive ROM to improve muscle

strength Instruct the parents to have frequent arm exercise. Educate on proper body

mechanics to enable the patient to relax, be comfortable and prevent strains Instruct the parents to let the client balance his activities with adequate rest

periods

Treatment Educate the parents on the importance of drug and money compliance

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Discuss to the parents the complications of the condition because knowledge about the condition supports learning that will decrease anxiety

Home teaching To promote adherence to the therapeutic programs, teach the following: Take a bath regularly and maintain proper hygiene Take enough rest Environmental sanitation is needed to provide a therapeutic way of curingthe

client’s condition Teach the parents the importance of hand washing to avoid the spread of

infection and avoid recurring of the disease

Out patient Remind the parents that the client must come back to the hospital one week

after, for the follow up check up to confirm if the patient’s condition is really restored. Also, to know if there are complications sited during the check up to know if patient’s condition have worsen or not

Advice the family of the client to report any abnormalities observed to provide immediate medical intervention

Diet Instruct the family to maintain patient’s hydration and give proper nutrition

If indicated: Increase carbohydrates and fibers in the diet

Spirituality Encourage the family to pray together with the client for his fast recovery.

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BIBLIOGRAPHY

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Health and Physical Assessment in Nursing by D’Amico & Barbarito, 1st

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