MENINGITIS NURSING

DEFINITION OF MENINGITIS

DEFINITION

It is the inflammation of the meninges covering of the brain. It can be divided into main two types….

Bacterial meningitis viral meningitis

Bacterial meningitis is often severe and is considered a potential medical emergency. If left untreated, bacterial meningitis may be fatal or cause serious long-term complications. Because bacterial meningitis can progress rapidly, it is important to identify the bacteria and begin antibiotic treatment as soon as possible.

Bacterial infection in the ears, mouth, or sinuses can spread directly to the brain and spinal cord. Some types of bacteria are transmitted from person to person through secretions from the mouth and nose.

Viral meningitis, also called aseptic meningitis, is the most common type. It is rarely fatal and usually resolves with treatment. Meningitis develops in fewer than 1 in 1000 people who are infected with one of the viruses associated with the condition

Fungal meningitis develops in patients with conditions that compromise the effectiveness of their immune systems (e.g.,HIV ,AIDS, lupus, diabetes). Fungal meningitis occurs in 10% of patients with AIDS. Cryptococcus neoformans and Candida albicans are commonly involved in fungal meningitis.

MENINGITIS

The brain and spinal cord are relatively well protected from infective agents by the bone of the skull and vertebral column, meninges, and blood brain barrier. This shield does have some weak point, such as air sinuses and the thick bone of the mastoid process. Almost any pathogenic micro organism can invade the nervous system and related structures. Neurologic infection syndrome may be categorized according to the main area for involvement or by causative mechanism. Meningitis, encephalitis, and brain abscess are the most common inflammatory condition of the brain and spinal cord. Inflammation can cause by bacteria, viruses, fungi, and chemicals. CNS infection may occur via blood streams.

BACTERIAL MENINGITIS

BACTERIAL MENINGITIS

Surrounding the brain and spinal cord are three protective membranes or meninges: dura mater, arachnoid membrane, and the pia matter. Bacterial meningitis primarily cause inflammation of the leptomeninges (pia mater and arachinoid) and involve the cerebrospinal fluid in the subarahinoid space. Meningitis may result from four known causes bacteria, viruses, parasites, and fungi. The infection can acute, subacute, or chronic with the patient presentation depend on the type of organism. Bacterial meningitis continues to be a series cause of morbidity and mortality.

ETILOGY AND EPIDIMILOGY

Bacterial meningitis is a common infectious disease that has been diagnosed throughout the world. It is affect the very young, the very old, and immunosuppressed persons. Approximately 2400 – 3000 cases of bacterial meningitis occur in the United States each year. According to Center of Disease Condition and Prevention (CDC) more than 300 people die in each year from this disease. When this infection occurs, it has significantly high case fatality rate in healthy adolescents. This factor alone makes the disease frightening. The cause’s brain damage, organ failure, and multiple amputation from the toxin the meningococcal organism produces. When epidemic of bacterial meningitis, especially meningococcal meningitis, occurs in a community.

CAUSES OF BATERIAL MENINGITIS

  • Streptococcus pneumonia (44%)
  • Neisseria meningitides (16%)
  • Group B streptococci (8%)
  • Staphylococci (6%)
  • Haemophilus influenzae type (5%)
  • Gram negative enteric bacillici (4%)

PATHOPHYSIOLOGY

The Meningitis can be transmitted through in four ways

  • Airborne droplet passed from infected individuals through sneezing, coughing, or kissing, or droplet passed along through the saliva and transmitted via drinks, cigarettes, or utensils
  • Direct contamination, such as a penetrating head injury or surgical procedure.
  • The blood stream such as from pneumonia,
  • Direct innansion or meningeal membrane such as in a brain abscess.

To survive and effectively penetrate the meninges, the bacteria must first able to surive with in the vasculture and overcome additional host defense.

After successful bacterial invasion, the inflammatory response become wide spread and involves the piaarachinoid, CSF, and ventricles, it does not usually involve adjacent parenchymal brain tissue. A purulent exudates forms and is circulated quickly throughout the CSF that surrounds the brain and spinal cord. These exudates are particularly attracted to the base of the brain, the sheaths of the cranial and spinal nerves, and perivascular space of the cortex. The bacterial and exudates can create vasuculare congestions by plugging arachinoid villi. The obstruction of CSF flow and decreased CSF reabsorption can lead to increased intracranial pressure, brain herniation, and death.

Two defense processes that can alter the ability of the of the body to fight bacterial meningitis effectively are

  • Deficient CSF complement level, which directly interfere with opzonization and effecent pahgocytosis of bacteria,
  • Low serum immunoglobulin G (IgE) concentration which decrease the brains ability to protect itself.

Both of these processes contribute to host deficiency at the outset of bacterial meningitis . the uncontrolled invasion of bacteria in to the leptomeninsges and subarachinoid space creates increased meningial blood flow, with neutrophils coming to the defense and imgrating into the sub arachinoid he space. After phagocytosis, the process in which certain cells engulf and dispose of microorganism and cell debris, neutorphil contribute to the exdates as the y rapidly disintegrate and add to the purulent matter the role of neutrophils in the process .

CLINICAL ASSESSMENT

The clinical assessment of adults which bacterial meningitis require a through neurologic assessments. The clinical assessment often reveals a classic clinical presentation of the following


  • Alter level of consciousness that ranges from confusion, comparativeness, and drowsiness to coma
  • Cranial nerve palsies (II,IV, VI,VII, VIII)
  • Meningial irritation : Kerning’s sing, Brudzinki’s sign, and photophobia
  • Fever as high as 1030F and (chills , headache, and nuchal rigidity is the common symptoms)
  • Nausea , vomiting and irritability,
  • Photophobia, nystagmus, abnormal eye movement
  • Rash in approximately 70% of patient
  • Seizures
  • Rapid respiration and respiratory failure.
  • Shock: sepsis, hypotension, cool, clammy skin

Nuchal rigidity: resistance to flexion in the neck. Particularly very yung and old agers

Brudzinski’s sings : A positive Brudzinski's sign can usually be elicited 24 hours after the onset of meningitis, a life-threatening disorder. Accompanying findings may include headache, a positive Kernig's sign, nuchal rigidity, irritability or restlessness, deep stupor or coma, vertigo, fever (high or low, depending on the severity of the infection), chills, malaise, hyperalgesia, muscular hypotonia, opisthotonos, symmetrical deep tendon reflexes, papilledema, ocular and facial palsies, nausea and vomiting, photophobia, diplopia, and unequal, sluggish pupils. As ICP rises, arterial hypertension, bradycardia, widened pulse pressure, Cheyne-Stokes or Kussmaul's respirations, and coma may develop.

it is elicited by passively flexing the patients head and neck into the chest, a positive Brudzinski’ signs result in involuntary flexion of lips and legs

Kerning’s signs : A reliable early indicator and tool used to diagnose meningeal irritation, Kernig’s sign elicits both resistance and hamstring muscle pain when the examiner attempts to extend the knee while the hip and knee are both flexed 90 degrees. However, when the patient’s thigh isn’t flexed on the abdomen, he’s usually able to completely extend his leg. This sign is usually elicited in meningitis or subarachnoid hemorrhage. With these potentially life-threatening disorders, hamstring muscle resistance results from stretching the blood- or exudate-irritated meninges surrounding spinal nerve roots. Read more at it is the inability to extent the leg when the tight is flexed on the abdomen which result from inflamed meninges and spinal roots. It is identified by the flexing the patient’s upper leg at the hip to a 90 degree angle and then attempting to extent the leg at the knee.

DIAGNOSTIC EVALUATIONS

COMPUTED TONOGRAPHY (CT) OR MAGNETIC RESONACE IMAGING (MRI)

  • LUMBAR PUNCTURE (LP): in patients with coma, if meningitis is suspected, a CT scan should be done as soon as possible followed by an LP to obtain CSF. CSF analysis is the most crucial diagnostic test and is the gold standard for diagnosis. It includes

Pressure

Cell count

Glucose

Lactic acid

Protein concentration

  • TWO SET OF BLOOD CULTURES SHOULD BE OBTAINED BEFORE ANTIBIOTIC ARE ADMINISTERED
  • URINE CULTURE
  • ARTERIAL BLOOD GASES

MANAGEMENT

EMERGENCY DEPARTMENT

The patients who present to the emergency department with suspected bacterial meningitis require immediate triage, diagnosis, and treatment. The urgent need for treatment in the first management priority for the patients with bacterial meningitis. Antibiotic treatment should be

Started with in the 30 minutes. The antibiotic should be according to the result of the blood culture. After administration of the antibiotic therapy, the search begin for the offending organism via the patient’s history, physical examination, and CSF and blood culture. In addition to controlling the infection process, treatment goal must be include preventing further brain insult from the possible complication of cerebral edema, hemorrhage, hydrocephalus, inflammation, and seizure

ACUTE CARE

Once the emergency department protocol has been completed, the patient is transferred to the intensive care unit for acute care and close monitoring and observation. During the acute phase of bacterial meningitis the therapy may include

  • Intravenous mannitol to treat rapid elevations is ICP
  • IV fluids monitoring and CSF drainage via external ventricular drain if ICP is elevated
  • Bed rest with head of bed elevated 30 to 45 degree.
  • Intubation and hyperventilation to maintain the PaCO2 between 25 and 35 mm of Hg
  • Blood and CSF culture
  • Antibiotic therapy
  • Seizure precaution and anticonvulsant therapy
  • Pain assessment and appropriate pain management
  • Fever management

As the acute inflammatory period subsides the patient require close monitoring to prevent secondary complication.

POST ACUTE AND NONACUTE CARE

Patient who are fortunate enough to be diagnosed and treated early may be transferred to the post acute setting for follow up. The therapies will continued with the close monitoring for potential complication. As the patient is stabilized, supportive therapy is continued in preparation for discharge, with explanation regarding the treatment and medication

REHABILITAION AND HOME CARE

For patients requiring additional care, and rehabilitation. Supportive therapy may be include physical therapy, occupational therapy, speech therapy and rehabilitation. The family support and education provided to help the family cop with complication, particularly if one or more of the patient’s extremities were amputated.

TUBERCULAR MENINGITIS

TUBERCULAR MENIGITIS

TUBERCULAR MENIGITIS is the most common and serious form of CNS tuberculosis. It is responsible for grave morbidity and mortality statistics in underdeveloped country. Currently the annual incidence is approximately 10 million worldwide. Children under age 5 and adult under age 40 are most often affected, but TB meningitis may affect any age group. The patient may require prolonged hospitalization, and significant danger of death or irreversible brain death.

PATHOPHYSIOLOGY

TB meningitis involves the basal meninges, cerebrum, and spinal meninges. It nearly always preceded by the invasion of Tuberculosis elsewhere in the body, often the lung. Brain or spinal subpial tuberculomas are the likely route through which tubercle bacilli enter the CSF. When the tuberculoma erode the pia, mycobacteria enter the CSF and meningitis follow.

The exudate that forms as a result of the bacterial invasion is located predominantly in the basilar cisterns and surrounds the cranial nerves and major blood vessels at the base of the brain. As the basilar cisterns become filled with the purulent exudates, the flow of CSF is blocked, and an obstructive hydrocephalus may develop. The exudates is also blocks the reabsorption of CSF by arachinoid granulation, which results in communicating hydrocephalus.

CLINICAL MANIFESTATION

  • Long history of symptoms, which may have been present for 2 weeks to 3 months before the onset of meningitis
  • Level of consciousness : confusion with significant behavioral changes that may progress to coma
  • Pupil : large and sluggish
  • Common initial symptoms: headache, fever, nausea, vomiting, irritability, difficulty sleeping and fatigue.
  • Headache: may increase intensity
  • Motor status: involuntary movement not uncommon, may progress to hemiplagia
  • Cranial nerve paralysis: especially CNs III and IV
  • Papilledema
  • Increased ICP : with meinigial inflammation and advancing disease progress
  • Stiff neck ( nuchal rigidity)
  • Seizures
  • Fever: Temperature above 102.20F
  • Vital signs: possible increase pulse and irregular respiration

DIAGNOSTIC EVALUATION

Lumbar puncture: examine the CSF and TB organism, increased protein, decreased glucose level, increased pressure,

Chest X ray

Tuberculin skin test

CT / MRI to detect associated complication (area of infraction, increased ICP)

TREATMENT

ACUTE CARE

Depending on the severity of the patient’s symptoms, the individual may brought to emergency care, after treatment in Emergency Department, the patient is transferred to acute care to continue management. The most significant factor in producing a favorable outcome depends on the early identification of the offending tubercle bacilli and rapid initiation of an effective anti tuberculosis therapy. A 90% of recovery is possible with early diagnosis and treatment

PHARAMCOLOGICAL MANEGEMENT

Several drugs, each with special features, are used in the treatment of TB meningitis. After pharmacological therapy, clinical improvement usually follows within 2 weeks. Depending on the severity of disease process, TB meningitis may require treatment for 6 months to 2 years

¨ ISONIAZID

It is usually given in 300 mg/day dosage, is perhaps the most significant drug in the medication treatment program of TB meningitis. It is exceptional CSF penetration and low toxicity and relatively affordable. Pyroxidine is administered in 10 mg / day dosages along with isoniazid to prevent peripheral neuropathy because of the inhibitory effect that isoniazid has on the action of pyridoxine.

¨ PYRIZINAMIDE

It is important in the treatment of TB meningitis because of its unique bactericidal activity. Pyrizinamide has a sterilizing effect on tubercle bacilli in acidic environment and effectively penetrates the CSF. It is given in dosage of 35mg/kg/day

¨ RIFAMPCIN

It is used to prevent relapses because of its inhibitory effects on bacilli during spurts of metabolic activity. Adverse reaction to rifampicin is not uncommon. The overall efficacy of rifampicin in the TB meningitis treatment is currently uncertain.

¨ ETHAMBUTOL

At dosage of 15 to 25 mg /kg/day inhibit the growth of micro bacteria. Often it is used as a second line drug for situations in which other drug cannot be prescribed. Ethambutol is used for first 2 months of therapy because of its limited ability to maintain effective penetration of CSF after the initial inflammatory process. One potential side effect of ethambutol therapy is optic neuritis, which is manifested as impaired visual acuity and red-green color blindness and should assessed weekly forth duration of treatment.

¨ STREPTOMYCIN

Another drug is used to treat TB meningitis, is usually limited to the first 2 to 3 months of treatments because its ability to penetrate the CSF depend on meningial inflammation. Streptomycin is an ototoxic drug, is usually administered intramuscularly. The therapy continues for at least one year. It is discontinued if dizziness or hearing loss occurs because of the possibility of permanent deafness

¨ Corticosteroids ( dexamethasone, prednisone)

It may be used to decrease inflammation and cerebral edema to prevent arichinoditis in the acute stage the disease. When patient is discharge, extensive education is needed for patient compliance with the medication regimen.

VIRAL MENINGITIS

VIRAL MENINTITIS

Patient with viral or aseptic meningitis may have similar symptoms. It is more common in males than females and four times more common in children who are age 1 or old. Viral meningitis is nonpurulent inflammatory process that is confined to meninges, choroid plexus and other region of brain.

Viral meningitis is caused by various viruses, such as

  • Coxsackie viruses,
  • Mumps virus
  • Viruses of lymphocytic choriomeningitis

The characteristic symptom may include

  • Malaise
  • Fever (low grade)
  • Nausea
  • Abdominal pain
  • Stiffness of neck

The patient requires a comprehensive history and complete neurological examination

The neurodiagnostic studies are the same as those used to diagnose bacterial meningitis. When laboratory results report viral antibodies, bacterial meningitis can be ruled out and supportive therapy provided. The CSF analysis from the LP usually reveals a characteristic normal glucose. Blood culture is negative.

NON ACUTE AND HOME CARE

The treatment is supportive, when pain relief for headache and reassurance that most patients usually experience a benign clinical course that is short and uncomplicated with the full recovery expected. If the patient experience any motor deficit, rehabilitation can be prescribed and patient discharged with instructions and follow up clinic or office appointment.

NURSING MANEGEMENT

The patient may be critically ill, therefore so many of the nursing interventions are collaborative with those of the physician, respiratory therapist, and other member of the health team. The patient’s prognosis may develop on the supportive care provided.

Neurologic status and vital signs are continually assessed, pulse oximetry and arterial blood gas values are used to quickly identify the need for respiratory support as the increasing ICP compromises the brain stem. Insertion of a cuffed end tracheal tube and mechanical ventilation may be necessary to maintain adequate tissue oxygenation.

Arterial blood pressures are monitored to assess for incipient shock, which precede cardiac or respiratory failure. Rapid intravenous ( IV) fluid replacement may be prescribed, but care is taken to fluid overload. Fever also will increase the workload of the heart and cerebral metabolism. ICP will increase in response to increased cerebral metabolic demand. Therefore, measure are taken into reduce body temperature as quickly as possible.

The other important components of nursing management

  • Monitor body weight, serum electrolytes, and urine volume, specific gravity, and osmolality.
  • Protecting the patient from injury secondary to seizure activity or altered level of consciousness
  • Preventing complications associated with immobility, such as pressure ulcer and pneumonia.
  • Instituting droplet precautions until 24 hours after the initiation of antibiotic therapy

An important aspect of the nurses role is to support the patient and to assist the family in identifying others who can be supportive to them during the crisis

NURSING DIAGNOSIS OF MENINGITIS

NURSING DIAGNOSIS

  1. 1. Disturbed thought process related to increased intracranial pressure and cognitive changes with orientation and problem solving.
  2. 2. Pain related to headache or other signs of discomfort
  3. 3. Self care deficit, bathing/ hygiene related to mental status changes and inability to perform ACLs independently
  4. 4. Sensory perceptual disturbance (visual, auditory, or tacticle) related to cranial nerve involvement as evidenced by alteration in sensation
  5. 5. Impaired physical mobility related to motor deficit

Disturbed thought process related to increased intracranial pressure and cognitive changes with orientation and problem solving.

Interventions

  • Assess the level of consciousness (LOC) using Glasgow coma scale
  • Monitor orientation and reorients necessary
  • Observe patients reaction to simple commands such as ”rise your hand”
  • Monitor patients capability as activities increases

Pain related to headache or other signs of discomfort

Interventions

  • Assess the pain using a scale of 0 - 10 or a face scale, if patient is unable to participate, observe for pain behaviors such as restlessness, grimacing, or moaning
  • Monitor the vital signs
  • Administer appropriate pain medication as ordered
  • Keep head of bed elevated at least 30 degrees
  • Provide alternative comfort measures such as dim, lights , a quiet environment and positioning for comfort


Self care deficit, bathing/ hygiene related to mental status changes and inability to perform ACLs independently

Interventions

  • Assess what the patient was able to do prior to admission
  • Provide all supplies and equipment for hygiene and bath
  • Encourage the patient to perform activities at own pace.
  • Teach and encourage family to participate with care


Sensory perceptual disturbance (visual, auditory, or tacticle) related to cranial nerve involvement as evidenced by alteration in sensation

Interventions

  • Monitor patient’s ability to perceive stimuli
  • Turn the patient and assess skin every 2 hour while in bed, provide moisturizer as needed.
  • Protect bony prominence
  • Assist the patient out of bed and into a different environment
  • Teach the patient to monitor own position and skin, and to direct position changes.

Impaired physical mobility related to motor deficit

Interventions

  • Assess the degree of mobility limitation
  • Turn patient every 1-2 hour
  • Position patient in correct body alignment
  • Perform range of motion exercise, consult physical therapy as ordered
  • Consult occupational therapist to assist the patient in learning to perform ADLs

MENINGITIS COMPLICATIONS

COMPLICATION

Resolution of meningitis depends on how quickly and effectively the disease is treated. Some individual experience no lasting effect. While other patient have permanent neurologic deficit

Cranial nerve damage may lead the patient blind or deaf.

Cognitive deficit ranging from memory impairment to profound learning disabilities may occur

Seizures may continue to occur even after the acute phase of illness has passed.

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