MENINGITIS
Introduction
Meninges are the protective membranes that surround the brain and spinal cord. The meninges
are the three membranes (the outermost dura mater, middle arachnoid mater and the innermost
pia mater) that cover the brain and spinal cord. Meningitis can occur when fluid (CSF)
surrounding the meninges becomes infected.
Definition: meningitis can be defined as the inflammation of the meninges or infection of the
pia, arachnoid mater and the cerebrospinal fluid filled subarachnoid space.
Types of meningitis
Meningitis can be of bacterial, viral and fungal origin. Viral and bacterial meningitis are the most
common causes of meningitis. Fungal meningitis is less common.
Viral Meningitis: the most common type of meningitis. Viruses in Enterovirus category cause
85% of cases. These are common during summer. These viruses include:
- Coxsackievirus A
- Coxsackievirus B
- Echoviruses
Viruses in enterovirus category cause about 10-15 million per year, but only a small
percentage who get infected will develop meningitis.
Other viruses that can cause meningitis include: West Nile virus, influenza, mumps, HIV,
measles, herpes viruses and Coltivirus, which causes Colorado tick fever.
ii. Bacterial Meningitis: is contagious and caused by infection from certain bacteria. About 5 to
40 percent of children and 29 to 50 percent of adults with this condition die, even with proper
treatments.
The most common types of bacteria that caused bacterial meningitis are:
- Streptococcus Pneumoniae: this is typically found in the respiratory tract, sinuses and
nasal cavity causing Pneumococcal Meningitis.
- Neisseria meningitides: which is spread through saliva and other respiratory fluids and
causes Meningococcal Meningitis.
- Haemophilus Influenza: which cause not only meningitis but infection of the blood,
inflammation of the windpipe, cellulitis and infectious arthritis.
- Listeria Monocytogenesis: which are foodborne bacteria
- Staphylococcus Aereus: which is typically found on the skin and in the respiratory tract
causing Staphylococcal Meningitis
iii. Fungal Meningitis: is a rare type of meningitis. It is caused by a fungus that infects body and
then spread through bloodstream to the brain or spinal cord.
People with weak immune system are more likely to develop fungal meningitis. This include
people with HIV and Cancer.
The most common funguses related to fungal meningitis include:
Cryptococcus: which is inhaled from dirt or soil that is contaminated with bird droppings.
Blastomyces: another type of fungus found in soil.
Histoplasma: which is found in environments that are heavily contaminated with bats or bird
droppings.
Coccidioides: which found in soil in specific areas of the U.S. southwest and south and central
America.
iv. Parasitic Meningitis: this is less common than viral or bacterial meningitis. It is caused by
parasites that are found in dirt, feces, and on some animals and food like snails, raw fish, poultry
or produce.
Eosinophilic meningitis: which is caused by
- Angiostrongylus cantonensis
- Baylisascaris procyonis
- Gnathostoma spinigerum
Amoebic Meningitis: a life threatening type of infection.
- Naegleria fowleri.
V. Non-infectious Meningitis: meningitis caused by other medical conditions or treatments.
These include:
lupus, head injury, brain surgery, cancer and certain medications.
Mode of Infection
Mode of infection can be through:
- Infectious agents via blood or choroid plexus
- Direct invasion from contagious tissues such as otitis media, osteomyelitis, upper
respiratory tract infection.
- Accidental contamination during certain procedures such as lumber puncture,
administration of spinal anaesthesia and head injury.
Incubation period
This depends on the causative organisms but it is usually between 48 hours.
Meningococcal meningitis has a very rapid onset and death can occur in 8-12 hours.
Haemophilus meningitis has insidious onset with patient becoming worse over a period of 4-5
days.
Pathophysiology
When the micro-organisms gain entrance into the body through any means, it travels through the
blood stream into brain and cross the blood brain barrier to the meninges especially the CSF
filled space (subarachnoid space) and spinal cord. On getting into the subarachnoid space they
proliferate faster in order to increase their number. This brings about an inflammatory response
which lead to oedema, there will also be an increase blood supply especially the neutrophils to
the affected areas in order to engulf the invaded micro-organisms and halt their proliferations.
The host immune response will further stimulate the release of cell wall fragments and
lipopolysaccharides thereby facilitating the inflammation of the subarachnoid and pia mater
which causes fever.
Meningitis of bacterial origin makes the CSF to become cloudy and purulent thereby prevent the
absorption of CSF giving rise to its accumulation. Because the cranium is rigid has little room
for expansion, accumulation of CSF, increase blood supply and oedema of the meninges will
bring about an increase in intracranial pressure since equilibrium cannot be maintained. Raised
ICP causes headache which is usually throbbing, toxins released by the causative organisms
causes nausea and vomiting. In response to the micro-organisms and their toxins, the
reticuloendothelial organs produce more WBC to combat this infection causing leukocytosis.
Involvements of the heat regulating centre of the hypothalamus further increases the body
temperature and caused convulsion in children and fits in adults. Irritation of the optic centre
caused photophobia, irritation of hearing centre will cause phonophobia. irritation of the spinal
nerves causes spasms of the muscle neck and caused severe neck pain leading to stiffness of the
neck. The involvements of the mid-brain make the patient become confused, drowsy and may
lose consciousness.
Clinical manifestations
The initial symptoms of meningitis are headache and fever. Fever tends to remain high
throughout the course of the illness. The headache is usually throbbing and severe.
Cardinal signs common to all types of meningitis are:
- Nuchal rigidity (stiff neck) – this is an early sign. Any attempts at flexion of the head are
difficult because of the spasms in the muscles of the neck.
- Positive kernig’s sign – when the patient is lying with the thigh flexed on the abdomen,
the leg cannot be completely extended.
- Positive Brudzinki’s sign – when the patient’s neck is flexed, flexion of the knees and
hips is produced. When the lower extremity of one side is passively flexed, a similar
movement is seen on the opposite extremity.
- Photophobia and phonophobia
- Nausea and vomiting
- Conculsions in children and fits in adults
- Rashes if it is N. meningitis, skin lesion may develop, ranging from a petechial rash with
purpuric lesions to large areas of ecchymosis.
- Disorientation and Memory impairment
- Raised ICP
- Septicemia in bacterial meningitis, shock and sign of Disseminated Intravascular
Coagulopathy (DIC).
- Lethargy, unresponsiveness and coma may develop
- In meningitis of bacterial origin death may occur within few hours of after onset of the
infections.
Assessments and Diagnostic Findings
- Clinical presentations
- Smear and Culture to determine the causative organisms
- Cytologic examination of CSF (lumber puncture)- this will show low glucose level along
with an increase in white blood cell count and protein. The presence of polysaccharides
antigen in CSF is an indication of bacterial meningitis.
- CSF becomes cloudy and the pressure is higher than normal (120-130mm of water).
- Chemical analysis will show an increased value of electrolyte, protein and carbohydrate.
- Imaging: CT Scan or MRI of the head may show swelling or inflammation
- X-rays or CT Scan of the chest or sinuses may show infection in other areas that may be
associated with meningitis.
Nursing and Medical Managements
Medical Managements
Successful outcome depends on the early administration of an antibiotic that crosses the blood
brain barrier into the subarachnoid space in sufficient concentration to halt the multiplication of
bacteria. The treatment of meningitis depends on the types of meningitis.
Bacterial meningitis
Acute bacterial meningitis must be treated immediately with intravenous antibiotics that is strong
enough to cross the blood brain barrier in order to halt the multiplications of the bacterial. This
helps to ensure recovery and reduce risk of complications.
Viral meningitis
Antibiotics cannot cure viral meningitis; most cases improve on their own in several weeks.
Symptomatic treatment is the option here.
Treatment of mild viral meningitis includes:
Bed rest
Plenty of fluid volume expanders
Analgesics and antipyretics to reduce fever and relief body aches.
Fungal meningitis: anti-fungal medications such as
Tuberculosis meningitis: a combination of specific antibiotics
Non-infectious meningitis due to auto-immune disease or allergic reaction may be treated with
corticosteroids. In some cases, the condition can resolve on its own.
General Medical Managements
- Penicillin antibiotics – ampicillin, piperacillin or cephalosporin e.g. ceftriaxone sodium,
cefotaxime sodium may be used.
- Vancomycin Hydrochloride alone or in combination with rifampin may be used if
resistant strains of bacteria are identified. High dose of appropriate antibiotics are
administered intravenously.
- Dexamethasone has been shown to be beneficial as adjunct therapy in the treatment of
acute bacterial and pneumococcal meningitis. It is administered 15-20 minutes before the
first dose of antibiotics and every 6 hours for the next four days. Dexamethasone
improves the outcome in adults and does not increase the risk for gastro – intestinal
bleeding.
- Phenytoin to control seizures which may occur early in the course of the disease.
- Antipyretics and analgesics – suppository ASA, I/m Pcm 600mg 6hourly.
Nursing Managements
1. Admission: - the patients should be admitted on a simple hospital bed with side rails and
nurse in a dark and quiet room because of photophobia and phonophobia.
2. Observations: - neurologic status and vital signs are continually monitored. Pulse
oximetry and blood gas values must be assessed to identify the need for respiratory
support. Fever increases the workload of the heart and cerebral metabolism; measure
must be taken to reduce it.
- Arterial blood pressure is monitored to assess for incipient shock, which precedes cardiac
or respiratory failure.
3. Ventilation: - to maintain adequate tissue oxygenation insertion of a cuffed endotracheal
tube may be necessary.
4. Parenteral fluid: - because of body fluid and electrolytes loss from vomiting which
resulted into dehydration, rapid replacement of i/v fluid is essential. Care should be taken
to prevent fluid overload.
5. Nutrition: - patients may be fed with fortified pap with about 100 ml 4hourly through
NG- Tube.
6. Protect the patient from injury secondary to seizure activity and altered level of
consciousness.
7. Monitor serum electrolytes, urine volume, specific gravity and osmolality especially if
syndrome of inappropriate anti-diuretic hormone is suspected.
8. Skin care: - prevent complications with immobility such as pressure ulcers and
pneumonia.
9. Institute infection control precautions; until 24 hours after initiation of antibiotics therapy
oral and nasal discharge is considered infectious.
10. Nurses’ role is to support the family and assist them in identifying others who can be
supportive to them during crisis. Periodic family visits are essential to facilitate coping oc
patient and family.
Complications
- Visual impairment
- Deafness
- Seizures
- Paralysis
- Hydrocephalus
- Septic shock
- Death
Prognosis
Prognosis depends on the causative organisms, the severity of the infection and illness and the
timeliness of treatment.
Nursing diagnosis
- Ineffective cerebral tissue perfusion related to cerebral oedema
- Risk for Imbalanced temperature related to infection
- Potential for impaired gas exchange related to hypoventilation, aspiration and immobility.
- Risk for impaired skin integrity related to immobility, pressure and incontinence.
- Risk for ineffective breathing pattern related to unconsciousness.
ENCEPHALITIS
Definition
Encephalitis is an acute inflammatory condition process of the brain tissue.
Causes
Encephalitis could be caused by fungus, viruses or parasites, autoimmune disorders and certain
medications.
Types
- Viral Encephalitis e.g. herpes simplex virus, rabies virus, polio virus and measles virus.
- Bacterial encephalitis can be caused by bacterial meningitis, parasitic, protozoan
infestations such as malaria.
- Limbic encephalitis- inflammatory disease confined to the limbic system of the brain.
- Autoimmune encephalitis e.g. Antibody mediated anti-N- Methyl-D-aspartate receptor
encephalitis and Rasmussen encephalitis.
- Encephalitis lethargica – this type of encephalitis has no known cause.
VIRAL ENCEPHALITIS
There are two types of herpes simplex viruses HSV-1 and HSV- 2. HSV-1 typically affects
children and adults. HSV- 2 most commonly affects neonates.
Clinical Manifestations
- Inflammation and hemorrhagic necrosis of the temporal lobe
- Fever
- Headache
- Confusion
- Behavioral changes
- Dysphasia
- Focal seizures
- Hemiparesis
- Altered level of consciousness.
Assessment and Diagnostic Findings
- MRI- to detect early changes caused by HSV-1 and oedema in the temporal lobe.
- Electroencephalography (EEG) – usually demonstrate periodic high voltage spikes
originating in the temporal lobe.
- CSF Examination – reveals a high opening pressure (100-180 mmH 2O when lying, 200-
300 mmH2O when sitting), low glucose (Normal CSF glucose level 50-80mg/dl) and high
protein (Normal CSF Protein level 15-45mg/dl).
Medical Management
- Anti-viral medication e.g. Acyclovir, early administration improves prognosis. To
prevent relapse treatment should be continued for up to three weeks
- Anticonvulsants e.g. phenytoin or epanutin.
- Corticosteroids e. g. Dexamethazone.
Nursing Management
- Assessment of Neurologic function
- Monitoring blood chemistry test results and urinary output to alert the nurse to the
presence of renal complications.
- Comfort measures to reduce headache e.g. dimming of light, limiting noise and
administration of analgesic agents e.g. pethidine.
- Focal seizures and altered level of consciousness require care directed at injury
prevention and safety.
- Psychological supports to allay fear and anxiety.
ARTHROPOD-BORNE ENCEPHALITIS
Arthropod vectors transmit several types of viruses that cause encephalitis. Primary vector is
Aedes mosquitoes while human is the secondary host.
Pathophysiology
Viral replication occurs at the site of mosquito bite, the host immune response attempts to control
viral replications. If the host immune response is inadequate, viremia ensue. The virus will gain
access to the CNS via cerebral capillaries resulting into encephalitis. It is further spread from
neuron to neuron predominantly affecting the cortical grey mater, the brain stem and the
thalamus. Meningeal exudates compound the clinical presentations by irritating the meninges
and thus raised the Intra- Cranial Pressure.
Clinical Manifestations
- Fever
- Headache
- Malaise
- Rash on the neck, arm, trunk and legs
- Fatigue
- Seizures
- Flaccid paralysis
- Rarely, vomiting and heamorrhagic fever
Diagnostic Investigations
- Clinical presentation of symptoms
- Epidemiological history of the location where infection occurred
Definitive Diagnosis
- Blood tests e.g. serologic and or virologic technique such as Enzyme –Linked
Immunosorbent Assay (ELISA).
- CSF evaluation
- MRI- will demonstrates inflammation of the basal ganglia and peri-ventricular area.
Management
Arbovirus encephalitis are viral diseases, so antibiotics are not an effective form of treatment and
no effective antiviral drugs have been discovered yet.
Treatment is supportive and symptomatic one to deal with problems such as oedema, loss of the
automatic activity of the brain and other treatable complications such as bacterial pneumonia.
Nursing Management
Hospitalization may be required if the patient is very ill
- Careful assessment of neurologic status is crucial in identifying improvement and
deterioration in the patient’s condition.
- Institution of measure to prevent patient from sustaining an injury.
- Psychological support and teaching to cope with complications such as life-long residual
issues e.g. neurologic deficits and seizures.
- Public education addressing the prevention of arbovirus encephalitis is a key role of
nurses especially public health nurses.
Preventive Measures
- Vector control measure especially mosquitoes habitat control such as draining of
swamps, removal of other pools and stagnant water.
- Use of insecticides.
- Sleeping inside mosquitoes’ nets
- Wearing protective clothing.
- Applying insect repellent such as permethrin and Diethyl-toluamide (DEET) to the cloth
and exposed area of the skin.
FUNGUS ENCEPHALITIS
This is rare in healthy people. The presentation of fungal encephalitis is related to geographical
area or to an immune-suppressive medication.
Causes
It can be caused by the following types of fungus: -
- Candida: - Candida albicans which is the most common cause of CNS infection.
- Coccidioides
- Histoplasma Capsulatum
- Blastomyces
- Cryptococcus Neoformans or Blastomyces Dermatitids
- Aspergillus which account for 5% of CNS fungal infection.
Risk Factors
People with weak immune system are the most at risk e.g. individuals taking immune-
suppressive medications such as cancer patients, HIV/AIDS patients, premature babies with very
low birth weight and the elderly.
Pathophysiology
The fungal spores enter the body via inhalation. They initially infect the lungs causing vague
respiratory symptoms such as pneumonitis. The fungi may enter the blood stream causing
fungemia. If the fungemia overwhelms the individuals’ immune system, the fungus spread to the
CNS. The fungal invasion may cause meningitis encephalitis or brain abscess.
Clinical manifestations
- Fever
- Stiff neck
- Photophobia
- Nausea and vomiting
- Altered mental status
- Malaise
- Symptoms of Increased Intracranial Pressure related to hydrocephalus often occur.
Diagnostic Findings
- History of immune-suppression associated with HIV/AIDS, or use of immune-
suppressive medications.
- Occupational or travel history.
- Serology tests- to identify the causative organisms especially infection caused by H.
Capsulatum and Coccidioides.
- CSF analysis will demonstrate elevated white blood cells and protein level but decreased
glucose levels.
- MRI- will demonstrate areas of haemmorrhage, abscess or enhanced meninges indicating
inflammation.
Management.
- Management is directed at the causative fungus and the neurologic consequences of the
infection.
- Seizures are controlled by standard anti-seizures medications such as phenobarbitone,
phenytoin or epanutin.
- Increased ICP is controlled by repeated lumber puncture of shunting of CSF.
- Antifungal agents are administered for a specific period of time e.g. I/V Amphotericin B
- Fluconazole or flucytosine may be administered orally in conjunction with Amphotericin
B.
Nursing Managements.
Aim: Early identification of Increased ICP to ensure early control and management.
- Administration of Non-opioid analgesics e.g. Aspirin 300mg.
- Administration of Diphenhydramine and acetaminophen 30 minutes before Amphotericin
B.
- There may be need to reduce the dose if patients show signs of renal insufficiency.
Increased levels of serum creatinine and blood urea nitrogen (BUN) signals development
of renal insufficiency and the need to address it.
- Psychological supports should be given to the patient so as to cope with the illness. Also,
work up of the patient for immune deficiency diseases such as HIV/AIDS may put
additional stress on the family.
