MENINGITIS

Meningitis

Is an inflammation of the meninges, the protective membranes that surround the brain and spinal cord. Meningitis is classified as aseptic or septic.

In aseptic Meningtis, bacteria are not the cause of the inflammation; the cause is viral or secondary to lymphoma, leukemia or brain abscess.

Septic meningitis refers to meningitis cause by bacteria most commonly neisseria meningitidis although haemophilus influenzae and streptococcus pneumoniae are also causative agents.Factors that increase the risk for developing bacterial meningitis include tobacco use and viral upper respiratory infection because they increase the amount of droplets production.

Otitis media and mastoiditis increase the risk of bacterial meningitis because the bacteria can cross the epithelium membrane and enter the subarachnoid space. Persons with immune system deficiencies are also at greater risk for developing bacterial meningitis.

Pathophysiology:

Causative organism enter blood stream and causes blood brain barrier

Infection inflammation of the meningitis and subarachnoid space and pia mater nerves

Headache ICP, visual impairment death paralysis, hydrocephalus, Septic shock

Signs and Symptoms: -headache

-fever (frequently initial symptoms) Clinical Manifestation:

-nuchal rigidity -positive Kernig’s sign -positive Brudzinski’s sign -photophobia -skin lesions -disorientation and memory impairment -lethargy, unresponsiveness and coma -seizures - increase ICP -purulent exudates -brain stem herniation -shock -signs of disseminated intravascular coagulopathy

Assessment and Diagnostic Findings:

-diagnostic testing to identify causetive organism -gram staining of CSF and blood -presence of polysaccharide in CSF

Medical Management:

-antibiotic that crosses blood brain barrier -penicillin (ampicillin, piperacillin) -cephalosporins (ceftriaxone sodium, cefotaxime sodium) -vancomycin hydrochloride or combined with rifampin -dexamethasone -fluid volume expanders -phenytoin (dilantin)

Nursing Management: -neurologic status and vital signs are continually assess -pulse oximetry & arterial blood gas values identify need for respiratory

support -cuffed endotracheal tube (or tracheotomy) -mechanical ventilation -arterial blood pressure monitoring -IV fluid replacement -monitor body weight, serum electrolytes -protect patient from injury secondary to seizure or altered level of

consciousness -prevent complication associated with immobility such as pressure ulcer

& pneumonia -instituting droplet precaution until 24 hours after initiation of antibiotic

therapy -diet: small frequent feedings, high protein diet

Complication: -endocarditis, conjunctivitis

BRAIN ABSCESS

Brain Abscess - is a collection of infection material within the tissue of the brain.

PathophysiologyInfection

From the different part

Of the body

Hematologic spread

Brain

Penetrating head wound

Invasion of the brain

Formation a collection of exudates

Brain tissue

Brain abscess

Clinical Manifestation

1. Subjective a. Headache – usually worse in the morning is the most prevailing symptom.b. Malaisec. Anorexia

2. Objective

a. feverb. vomitingc. weight lossd. focal defect based on site:

1.vision loss – decrease vision reflect the area of the brain2.paresis3.seizures – observed4.personality changes

Assessing for Brain Abscess

Sign / Symptoms

1. Frontal Lobe- Hemipakesis

- Aphasia (expessive - Seizures - Frontal headache

2. Temporal Lobe - Localized headache - Changes in vision - Facial weakness - Aphasia

3. Cerebellar Abscess - Occipital headache - Ataxia ( inability to coordinate movement )

-Nystagmus (rhythm, involuntary movement of the eye)

Diagnostic Finding

A. Magnetic Resonance Imaging (MRI) scan-is useful to obtain image of the brain stem and posterior fossa if

an abscess is suspected in these areas.

B. Computed Tomography (CT) scan-is invaluable in locating the site of the abscess, after the evolution and resolution of supportive lesions and in determining the optional time for surgical intervention

Medical Management

Treatment is ahead at controlling increased ICF draining the abscess and providing antimicrobial therapy directed at the abscess and primary sources of infection.The choice of the specific antibiotics medication is based on culture and sensitivity testing and directed at the causative organism.

Nursing Intervention

Focuses to assess the neurologic status, administering medication, assessing the response to treatment and providing supportive care.

Assess and document the responses to medication

Closely monitored when corticosteroids are prescribed

Administrating of insulin or electrolyte replacement may be required to return these values to normal or acceptable level.

The nurse must assess the family’s ability to express distress at the patient’s condition cope with the patient illness and deficits and obtain support.

Test Result:

- Blood Laboratory- Blood Glucose- Serum potassium level

Pharmacologic

Antibiotics Medications

-to penetrate the blood brain barrier and reach the abscess.

Corticosteroids

-to help reduce the inflammatory cerebral edema if shows evidence of an increasing neulogic deficit

Anti seizure Medication

-to prevent or treat seizures

Therapeutic Intervention

1. Large doses of antibiotics 2. In Severe cases, a craniotomy may be performed to allow removal of the abscess. 3. Anti convulsants to control seizure

ENCEPHALITIS

ENCEPHALITIS

DEFINITIONEncephalitis is an inflammatory disease involving part or all of the nervous

system resulting in abnormal function of the brain and the spinal cord. It is an acute inflammatory process of the brain tissue.

CAUSESThe cause of encephalitis is most often a viral infection. Some examples include

herpes viruses; arboviruses transmitted by mosquitoes, ticks and other insects; and rabies transmitted through animal bites.

Encephalitis takes two forms, categorized by the two ways that viruses can infect your brain:

Primary encephalitis. This occurs when a virus directly invades your brain and spinal cord. It can happen to people at any time of the year (sporadic

encephalitis), or it can be part of an outbreak (epidemic encephalitis).Secondary (post-infectious) encephalitis. This form occurs when a virus first infects another part of your body and secondarily enters your brain.

Also, bacterial infections, such as Lyme disease, can sometimes lead to encephalitis, as can parasitic infections, such as toxoplasmosis (in people with weakened immune systems).

Here are some of the more common causes of encephalitis:

CHILDHOOD INFECTIONS

In rare instances, secondary encephalitis occurs after vaccine-preventable childhood viral infections, including:

Measles (rubeola) Mumps Rubella (German measles)

In such cases, encephalitis may be due to hypersensitivity — an overreaction of your immune system to a foreign substance.

HERPES VIRUSES

Some herpes viruses that cause common infections may also cause encephalitis. These include:

• Herpes simplex virus. There are two types of herpes simplex virus (HSV) infections.

-HSV type 1 (HSV-1) more commonly causes cold sores or fever blisters around your mouth. HSV-1 is the most important cause of fatal sporadic encephalitis in the United States, but it's also rare.

-HSV type 2 (HSV-2) more commonly causes genital herpes.

• Varicella-zoster virus. This virus is responsible for chickenpox and shingles. It can cause encephalitis in adults and children, but tends to be mild.

• Epstein-Barr virus. This herpes virus causes infectious mononucleosis (mono). If encephalitis develops, it's usually mild, but can be fatal in a small number of cases.

PATHOPHYSIOLOGY

Herpes Simplex Virus 1

Retrograde intraneuronal path from olfactory and trigeminal

nerves to the brain

Viruses reactivate in the brain tissue

ENCEPHALITIS

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Neuroimaging studies• Electroencephalography (EEG)• Demonstrates periodic high-voltage spikes originating in the temporal lobe.• CSF examination• Lumbar puncture often reveals high opening pressure and low glucose and high protein levels in CSF samples.• Magnetic Resonance Imaging (MRI) – study of choice for detection of early changes caused by HSV1.

(The study will show edema in the temporal lobe).• Viral cultures are always negative.• Polymerase chain reaction (PCR) test

• The standard test for early diagnosis of HSV1 in the CSF.• The validity of PCR is very high between the third and tenth days after symptom onset,

CLINICAL MANIFESTATIONS

• Inflammation and hemorrhagic necrosis of the temporal lobe

• Fever, headache and confusion (initial symptoms)

• Focal seizures

•Hemiparesis

•Dysphagia

•Altered LOC

MEDICAL MANAGEMENT

•Acyclovir (Zovirax) - an antiviral agent, the medication of choice in the treatment of HSV. - early administration of this drug improves the prognosis associated with HSV-1 encephalitis.

- the mode of action is inhibition of viral DNA replication.

- it is well tolerated by the patients. - dose is decreased if the patient has a history of

renal insufficiency.•Treatment should be continued up to 3 weeks to prevent relapse.

•Slow IV administration over 1 hour prevents crystallization of the medication in the urine.

NURSING MANAGEMENT

• Assessment of the neurologic function is the key to monitoring the progression of disease.

• Provide comfort measures to reduce headache include dimming the lights, limiting noise, and administering analgesic agents.

• Opioid analgesic medications may mask neurologic symptoms; therefore, they are used cautiously.

• Focal seizures and altered LOC require care directed at injury prevention and safety.

• Nursing care addressing the patient and family anxieties is ongoing through the illness.

•Monitoring of blood chemistry test results and urinary output will alert the nurse to the presence of renal complications related to acyclovir therapy.

ARTHROPOD-BORNE VIRUS ENCEPHALITIS

Mosquito is the primary vector in North America, birds are the primary host and humans are the secondary host.

Argosies infection (transmitted by arthropod vectors) occurs in specific geographic areas during the summer and fall.

In the United States, West Nile and St. Louis are the most common types of arboviral encephalitis; both are members of the Japanese encephalitis soregroup.

ARBOVIRUSES

Viruses that are transmitted by mosquitoes and ticks (arboviruses) have, in recent years, produced well-publicized encephalitis epidemics. Here's how the transmission cycle works:

Organisms that transmit disease from one animal host to another are called vectors. Mosquitoes are vectors for the transmission of encephalitis from small creatures — usually birds and rodents — to humans.

In the United States, the following types of mosquito-borne encephalitis occur:

• Eastern equine encephalitis. This infection generally afflicts horses and birds, especially birds that live near freshwater swamps. It can also affect humans, although fewer than 10 cases are reported in most years. Eastern equine encephalitis outbreaks occur most commonly in the eastern United States. Symptoms of eastern equine encephalitis usually appear four to 10 days after a bite by an infected mosquito.

• Western equine encephalitis. Most reports of western equine encephalitis come from the central and western Plains of the United States. Like eastern equine encephalitis, this infection affects horses and, rarely, humans. It flourishes in birds that live near irrigated fields and farming areas. Symptoms appear between five and 10 days after a bite. Western equine encephalitis is less likely to be fatal than is its eastern cousin, but can result in brain damage and other major complications, particularly in infants.

• St. Louis encephalitis. This virus is transmitted to mosquitoes by birds. The mosquito vector of St. Louis encephalitis breeds in areas of standing water, including polluted pools, roadside ditches and containers such as birdbaths, flowerpots and discarded tires. Symptoms appear within a week to 10 days. Although many young people have mild or no symptoms when infected, the disease can be severe in adults older than 60.

• La Crosse encephalitis. This virus is named for La Crosse, Wis., where the virus was first recognized in 1963. It's most common in the hardwood forest areas of the Upper Midwest and in Appalachia. Unlike other forms of viral encephalitis, this virus is passed to mosquitoes from chipmunks and squirrels. Symptoms appear five to 15 days after a bite by an infected mosquito.

• West Nile encephalitis. This virus first appeared in the United States in 1999 and spread across most of the country over the next several years. It's also found in Africa and the Middle East and in parts of Europe, Russia, India and Indonesia. The virus is similar to other encephalitis viruses in that birds are its main animal hosts. However, in rare cases, it's possible for the disease to spread from person to person through organ transplant, blood transfusions or breast-feeding, or from mother to unborn child. Symptoms of West Nile encephalitis are generally mild, but the disease can be severe, especially in older adults and those with weakened immune systems. Symptoms appear within five to 15 days of being bitten by an infected mosquito.

PATHOPHYSIOLOGY

Mosquito bite

Viral Replication

Viremia

CNS access of virus

ENCEPHALITIS

CLINICAL MANIFESTATIONS

• Early flu-like symptoms but specific neurologic manifestations depend on the viral type

•SIADH with hyponatremia (unique clinical feature of St. Louis encephalitis.

• Maculopapular or morbilliform rash on the neck, trunks, arms, and legs and flaccid paralysis (specific feature of West Nile encephalitis)

• Parkinsonian-like movements, reflecting in inflammation of the basal gangliaSeizures, a poor prognosis indicator

ASSESSMENT AND DIAGNOSTIC FINDINGS

•After a brief febrile prodrome, neurologic symptoms will reflect the area of the brain involved.

•Neuroimaging studies

•CSF examination/evaluation and serum cultures

•Immunoglobulin M antibodies (West Nile virus are observed in serum and CSF.

•Magnetic Resonance Imaging (MRI) scan– demonstrates inflammation of the basal ganglia (in St. Louis encephalitis) and inflammation in the periventricular area (in West Nile encephalitis).

•Polymerase chain reaction (PCR) evaluation

•Demonstrate viral RNA

MEDICAL MANAGEMENT

• Controlling the seizures and the increase ICP.

• Studies indicate that interferon may be useful in treating St. Louis encephalitis.

• Ribavirin and interferon alpha-2b show some effect against West

• Nile virus but not been evaluated in controlled studies.

• Neuropsychiatric complications, such as emotional outburst and other behavioral changes, occur frequently.

• Vaccine decreases the risk of requiring West Nile encephalitis.

NURSING MANAGEMENT

• Assessment of the neurologic status of the patient.

• Identification of the improvement or deterioration in the patient’s condition.

• Injury prevention is the key in light of the potential for falls or seizures.

• Supporting and teaching to cope with the outcomes are needed by the patient’s family. • Public education addressing the prevention of arboviral encephalitis are essential. • Clothing that provides coverage and insect repellents containing 25% to 30% diethyltoluamide (DEET) should be used on exposed clothing and skin in high risk areas to decrease mosquito and tick bites.

• Blood donation centers –screen all blood for West Nile virus.

FUNGAL ENCEPHALITIS

Fungal infection of the CNS occurs rarely in healthy people. The presentation of fungal encephalitis is related to geographic area or to an immune system that is compromised due to disease or immunosuppressive medication.

Causative organism –usually Cryptococcus neoformans (exposure to bird droppings and maybe seen in bird handlers) or blastomycer dermatitidis (risk for coal miners, construction workers and farmers --South Eastern United States, Ohio St.

Lawrence, Mississippi and River basins). Other fungi that cause neurologic infection include:

Histoplasma capsulatum, Aspergillus fumigatus, Candida and Coccidioides immitis (California, Arizona, New Mexico and Texas).

PATHOPHYSIOLOGY

Inhalation of fungal spores

Vague respiratory symptoms or pneumonitis

Fungemia

Spreads in CNS

ENCEPHALITIS

CLINICAL MANIFESTATIONS

• Fever

• Malaise

• Headache • Meningeal Signs

• Change in LOC or Cranial Nerve Dysfunction

• Increase ICP related to hydrocephalus often occur

• Specific skin lesion (C.Neoformans and C.Immitis)

• Seizures (H.Capsulatum)

• Ischemic or hemorrhagic strokes (A.Fugimatus)

ASSESSMENT AND DIAGNOSTIC FINDINGS

A history of immunosuppression associated with AIDS or use of immunosuppressive medications may indicate fungal disease of the brain.CSF exam usually demonstrate elevated white cells and protein levels; glucose levels are decreased.

C.Immitus and H.Capsulatum will demonstrate fungal antibodies in serologic test.

C.Neoformans is easily identified in CSF in fungal cultures. Candida may be cultured from the blood or CSF.

B. Dermatitidis – cisternal or ventricular cultures of CSF are needed to be obtained.

A. Fungimatus is difficult to isolate in CSF and is diagnosed by LUNG BIOPSY.

Neuroimaging is used to identify CNS changes related to fungal infection.MRI is the study of choice; it demonstrates areas of hemorrhage, abscess, or enhanced meninges indicating inflammation.

MEDICAL MANAGEMENT

• Management of neurologic consequences of infection.

• Seizures are controlled by standard antiseizure medications.

• Increase ICP is controlled by repeated lumbar punctures or shunting of CSF.

• Antifungal therapy until the infection is controlled.

• Maintenance dose of medications for indefinite period.

• Amphotericin B is the standard antifungal agent used in treatment.

• Fluconazole (Diflucan) or Flucytosine (Ancobon) may be administered orally in conjunction with Amphotericin B as maintenance therapy.

-- Flucytosine should have leucocyte and platelet counts monitored regularly.

NURSING MANAGEMENT

• Early identification of increase ICP is necessary to ensure early control and management.

• Administering noniopiod analgesics, limiting environmental stimuli, and positioning may optimize patient comfort.

• Administering diphenhydramine (Benadryl) and acetaminophen (Tylenol) approximately 30 minutes before giving amphotericin B may prevent flu-like side effects.

• Increasing levels of serum creatinine and blood urea nitrogen (BUN) may alert the nurse to the development of renal insufficiency and the need to address the patient’s renal status.

• Providing support assists the patient and family to cope with the illness.

• Work-up of patient for immunodeficiency disease such as AIDS may put additional stress on the family.

• Mobilizing community support systems for the patient and family, because the recovery may be long.