OBJECTIVES

CENTRAL OBJECTIVE

After the completion of the session the group will acquire knowledge
regarding brain infections, develop a positive attitude towards the caring of
patients with brain infections and understand the basic skills required for the
nursing management of the above condition.

SPECIFIC OBJECTIVES

At the end of the class the group will able to:

1. review the basic anatomy and physiology of central nervous system

2. define meningitis, encephalitis and brain abscess

3. narrate the risk factors and etiology of the brain infections

4. describe the pathophysiology of various brain infections

5. mention the assessment and diagnostic measures of brain infections

6. recognise the medical and surgical management of brain infections

7. understand the nursing management of the condition

8. identify the evidenced based practices utilizing in the disease condition

INTRODUCTION
The infectious disorders of the nervous system include meningitis,
brain abscesses, and various types of encephalitis. The clinical manifestations,
assessment and diagnostic findings as well as medical and nursing management
are related to the specific infectious process. The features of the central nervous
system infections depend upon the location of infection, the causative organism
and whether the infection is acute or chronic. The frequency of these varies
geographically.

ANATOMY AND PHYSIOLOGY

The human nervous system is made up of two main components: the central
nervous system (CNS) and the peripheral nervous system (PNS). The CNS is

1
composed of the brain, the cranial nerves, and the spinal cord. The PNS is made
up of the nerves that exit from the spinal cord at various levels of the spinal
column as well as their tributaries. The autonomic nervous system (divided into
the sympathetic and parasympathetic nervous system) is also considered to be a
part of the PNS and it controls the body's many vegetative (non-voluntary)
functions.

The brain can be subdivided into several distinct regions:

The cerebral hemispheres form the largest part of the brain, occupying the
anterior and middle cranial fossae in the skull and extending backwards over the
tentorium cerebelli. They are made up of the cerebral cortex, the basal ganglia,
tracts of synaptic connections, and the ventricles containing CSF.

The Diencephalon includes the thalamus, hyopthalamus, epithalamus and

subthalamus, and forms the central core of the brain. It is surrounded by the
cerebral hemispheres.

The Midbrain is located at the junction of the middle and posterior cranial
fossae.

The Pons sits in the anterior part of the posterior cranial fossa- the fibres within
the structure connect one cerebral hemisphere with its opposite cerebellar
hemisphere.

The Medulla Oblongata is continuous with the spinal cord, and is responsible
for automatic control of the respiratory and cardiovascular systems.

The Cerebellum overlies the pons and medulla, extending beneath the
tentorium cerebelli and occupying most of the posterior cranial fossa. It is

2
mainly concerned with motor functions that regulate muscle tone, coordination,
and posture.

Meninges: The bony covering around the brain is called the cranium,
which combines with the facial bones to create the skull. The brain and spinal
cord are covered by a tissue known as the meninges, which are made up of three
layers: dura mater, arachnoid layer, and pia mater. The dura mater is a whitish
and nonelastic membrane which, on its outer surface, is attached to the inside of
the cranium. This layer completely covers the brain and the spinal cord and has
two major folds in the brain that are called the falx and the tentorium. The falx
separates the right and left halves of the brain while the tentorium separates the
upper and lower parts of the brain. The arachnoid layer is a thin membrane that
covers the entire brain and is positioned between the dura mater and the pia
mater, and for the most part does not follow the folds of the brain. The pia
mater, which is attached to the surface of the entire brain, follows the folds of
the brain and has many blood vessels that reach deep into the brain. The space
between the arachnoid layer and the pia mater is called the subarachnoid space
and it contains the cerebrospinal fluid.

Cerebrospinal Fluid (CSF): CSF is a clear fluid that surrounds the brain
and spinal cord, and helps to cushion these structures from injury. This fluid is

3
constantly made by structures deep within the brain called the choroid plexus
which is housed inside spaces within the brain called ventricles, after which it
circulates through channels around the spinal cord and brain where is it finally
reabsorbed. If the delicate balance between production and absorption of CSF is
disrupted, then backup of this fluid within the system of ventricles can cause
hydrocephalus.

4
BLOOD SUPPLY TO BRAIN

CIRCLE OF WILLIS

5
BRAIN INFECTIONS
Our brain, the spinal cord, and its surrounding structures could become
infected by a large spectrum of germs (that is, microorganisms). Bacteria and
viruses are the most common offenders. Parasites, fungi, and others can infect
the central nervous system (CNS), although more rarely.

TERMINOLOGY

The infecting germ causes an inflammation of the area invaded.

Depending on the location of the infection, different names are given to the
diseases.

Meningitis is the inflammation of the meninges, the surrounding three-layered

membranes of the brain and spinal cord, and the fluid it is bathed in, called
cerebrospinal fluid (CSF).

Encephalitis is the inflammation of the brain itself.

Myelitis actually means a spinal cord inflammation.

Brain Abscess is an accumulation of infectious material and offending

microorganisms within the CNS.

Organisms may be bacterial, viral, parasitic, fungal, or prion infections of the

central nervous system. Usually, viral meningitis causes milder symptoms.
Viral infections are two to three times more common. Bacterial meningitis is a
very serious disease and may result in a learning disability, speech defects,
hearing loss, seizures, loss of extremity function or amputation, permanent brain
damage, and even death. According to the World Health Organization (WHO)
statistics, up to 15% of the survivors of bacterial meningitis remain with
permanent complications and health issues, as described above.

MENINGITIS
DEFINITION

Meningitis is inflammation of the meninges. The meninges is the collective

name for the three membranes that envelope the brain and spinal cord
(central nervous system), called the dura mater, the arachnoid mater, and the
pia mater. The meninges main function, along with the cerebrospinal fluid is
to protect the central nervous system.
6
 The word "meningitis" comes from the Greek word Menix meaning
"membrane". The suffix "itis" comes from the Greek word itis meaning
"pertaining to". In medical English, the suffix "-itis means"
"inflammation of".

Accordingto Medilexicon's medical dictionary, meningitis is"Inflammation

of the membranes of the brain or spinalcord".

The meninges consists of the dura mater, arachnoid and pia mater

INCIDENCE

Worldwide, bacterial meningitis is common. It continues to be a serious threat

to global health. The most recent statistics published by the WHO in 2010
estimates up to 170,000 annual deaths from bacterial meningitis worldwide. It
particularly affects the African continent, with regular epidemics in sub-Saharan
and West Africa, known as "the meningitis belt."

Risk factors

 Patients with CSF shunts or dural defects (eg staphylococcal).

 Patients who have undergone spinal procedures
 bacterial endocarditis
 diabetes mellitus
 intravenous drug abuse
 renal insufficiency, adrenal insufficiency
 malignancy (increased risk of listerial infection)
 Over crowding increases the risk of outbreaks of meningococcal
meningitis.

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 ETIOLOGY
 Bacterial infections: Meningitis- Pneumococcal, menigococcal,
staphylococcal, Haemophilus influenza, neurosyphilis, brain abscess,
tuberculosis, NesseriaMeningitidis
 Viral infections: meningitis, encephalitis, transverse myelitis, polio
myelitis, rabies
 Prion disease :creutzfeldt-jakob disease
 Protozoal infections: malaria, toxoplasmosis
 Helminthic infections; Schistostomiasis, hydatid disease, cysticercosis.
 Fungal infections: cryptococcal meningitis, candida meningitis.
 Inflammatory conditions: SLE
 Cancer
 Head injuries

PATHOPHYSIOLOGY
Aerosol inhalation of pathogens, blood stream infection, direct injury

Enters the blood stream, it crosses the blood brain barrier and proliferates in the
CSF

The host immune cells stimulates the release of cell wall fragments and
polysaccharides.Cerebral edema that may be vasogenic, cytotoxic or interstial

 Increased blood brain permeability- vasogenic edema

 release of toxic factors from bacteria- swelling of the cellular elements of
brain –Cytotoxic edema
 obstruction of normal pathways of brain- resultant increased CSF out
flow – interstial edema.

the phagocytes rapidly degenerates and disintegrates

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Facilitating inflammation of the sub arachinoid and piamater-Meningeal
irritation

formation of exudate in the sub arachinoid space and ventricular system

fibrosis and adhesions result in obstruction of CSF and hydrocephalus

The cranial vault contain little room for expansion, the inflammation may cause
increased ICP

The CSF circulates through the sub arachinoid space, where the inflammatory
cellular materials enters and accumulate.

CLINICAL FEATURES

1) Fever, headache: The symptom is probably attributable to irritation of

pain sensitive dura and traction on related vascular structures.
2) Altered mental state, unconsciousness, toxic/moribund state: As the
course of the disease progress a deterioration in the level of
consciousness develops. Affected people are in a lethargic state and are
generally unresponsive except for repeated stimulation. They gradually
become unresponsive and lapse in to deep coma state.
3) Shock: signs of shock include tachycardia and/or hypotension,
respiratory distress, altered mental state and poor urine output.
SIGNS OF MENINGEAL IRRITATION

4) Stiff neck (generally not present in children under the age of one year or
in patients with altered mental state), back rigidity, bulging fontanelle (in
infants), photophobia, opisthotonus (if severe). A stiff neck is an early
sign of meningeal irritation. Attempts to flex the neck forward either
actively or passively prove difficult. This resistance is caused by spasms
of the extensor muscles of the neck. Forceful flexion produces severe

9
 pain. The extensor position may be so exaggereated that the patient may
assume the opisthotonos position in bed.
5) Kernig'ssign :Pain and resistance on passive knee extension with hips
fully flexed. Kernig sign is elicited by flexing the upper leg at the hip to a
900 angle and then attempting to extend the knee. In the presence of
meningitis, there is pain and spasm of the hamstrings when an attempt is
made to extend the knee. The pain is caused by inflammation of the
meninges and spinal roots. The spasms are protective mechanism to deter
painful flexion.
6) Brudzinski's sign is described as being positive when both the upper legs
at the hips and the lower legs at the knees are flexed in response to
passive flexion of the neck and head on the chest.
7) Paresis, focal neurological deficits (including cranial nerve involvement
and abnormal pupils).
8) Generalized convulsions: Development of generalized seizures indicates
irritation of the cerebral cortex. Following a seizure transistory paralysis
may be noted. A focal motor seizure may be evident if here is an
accumulation of exudate over one cortical convexity.
9) Increased intracranial pressure: Increased ICP accompanies meningitis
because of purulent exudate, cerebral edema and hydrocephalus.
Papilledema a sign of increased ICP is rare with an acute attack of
meningitis. If it is apparent it is most often associated with a brain
abscess, subdural empyema or venous sinus occlusion. Symptoms of
brain stem pressure are reflected in vital sign changes such as widening of
pulse pressure, decreased pulse and ataxic respirations. Vomiting is a
frequent finding.

If the infection is not aggressively treated or responds poorly to

treatment, the patient becomes subject to herniation syndromes.

10) Cranial nerve dysfunction:Inflammation or vascular changes can

cause cranial nerve dysfunction. The major deficits are ocular palsies
(involving cranial nerve III, IV, VI), facial paresis (cranial nerve VIII)
and deafness and vertigo caused by involvement of cranial nerveVIII.
11) Endocrine disorders: A small percentage of patients develop
hyponatremia( a decrease in serum sodium) and excessive release of the
antidiuretic hormone. There are signs and symptoms of water retension,
along with oliguria and hypervolemia.

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 12) WATERHOUSE-FRIDERICHSEN SYNDROME:

It is the specific complication of meningitis. There is a phase of

meningococcemia often noted before the meningitis is evident or diagnosed.
The combination of signs during this period is eferred to as Waterhouse-
Friderichsen syndrome and includes following

 Chills, fever, headache, malaise and joint and muscle pain

 Petechial haemorrhage or ecchymosis on the skin and mucous membrane
 Hemorrhage can also develop in he adrenal glands and result in adrenal
insufficiency
 Hypotension, cyanosis, respiratory distress and circulatory collapse

ASSESSMENT AND DIAGNOSTIC MEASURES

Meningitiscan diagnosebased on a medical history, a physical exam and certain

diagnostic tests.

Check for signs of infection around the head, ears, throat and the skin along the
spine.

Blood studies

 Complete blood count to detect anemia and infection (by raised WBC
counts)
 Blood culture for diagnosing infection and septicaemia
 Blood glucose to compare it with CSF glucose
 Renal and liver function tests
 Tests to check adequate blood clotting ability
 Blood tests for syphilis if syphilis involvement of meninges is suspected.

Imaging. X-rays and computerized tomography (CT) scans of the head,

chest or sinuses may reveal swelling or inflammation. These tests can also help
your doctor look for infection in other areas of the body that may be associated
with meningitis.Chest X ray to detect lung pathologies like lung abscess,
tuberculosis etc.

Spinal tap (lumbar puncture).The definitive diagnosis of meningitis requires

an analysis of your cerebrospinal fluid (CSF), which is collected during a
procedure known as a spinal tap. In people with meningitis, the CSF fluid often

11
shows a low sugar (glucose) level along with an increased white blood cell
count and increased protein.

CSF analysis to identify the exact bacterium that's causing the illness. If
suspects viral meningitis, a DNA-based test known as polymerase chain
reaction (PCR) amplification or a test to check for antibodies against certain
viruses to check for the specific causes of meningitis. Samples of cerebrospinal
fluid taken from the lumbar puncture are sent to the laboratory for staining with
special dyes that reveal the organism leading to meningitis.

The common stains and tests used are:

Gram stain (to diagnose gram negative Meningococci, E. coli, Pseudomonas

and gram positive staphylococci and Pneumococci)

Ziehl-Neelsen stain (for diagnosing tuberculosis)

cytology (for abnormal cells)

virology (for causative viruses)

glucose, protein, culture (to check for growth of specific bacteria)

rapid antigen screen or polymerase chain reaction (PCR) if available

India ink for Cryptococci (fungal infection)

Urine culture to detect organisms

Nasal swab and stool for virology if viral meningitis is suspected

MEDICAL MANAGEMENT

 Adequate fluid and electrolyte balance must be maintained.Dehydration

and shock are treated with fluid volume expanders
 Frequent assessment of the neurologic status is indicated to detect early
manifestations of increasing ICP and seizures.
 Patient must be watched carefully for changes in neurologic function or
other signs of worsening condition.

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TYPE OF MENINGITIS DRUG

Pneumococcal and meningococcal Pencillin G in divided doses

meningitis 12-15million u/day
HaemophilusInfluenzae meningitis Chloramphenicol in divided doss
100mg/kg/day for 2-3 days
Ampicillin may be used as an
alternative
Enterobacteriaceae (Klebsiella, Gentamicin in divided doses IV
shigella, E coli) 5mg/kg/day
Pseudomonas meningitis Gentamicin, Carbenicillin

Staphylococcus Aureus Oxacillin 10-12g/day

Tuberculous meningitis Combination of drugs

INH- 10mg/kg/day
Rifampicin-600mg/kg
Ethambutol-15mg/kg/day

•Seizures may be treated with intravenous diazepam, 10 mg, or lorazepam, 4

mg, given over 2 minutes and repeated after 15 minutes if seizures persist.
Therapy with these short-acting agents should be followed by a loading dose of
intravenous fosphenytoin given as the equivalent of 10 to 15 mg/kg .Phenytoin
in normal saline at a rate no faster than 50 mg/min. If phenytoin is used rather
than fosphenytoin, the electrocardiogram and blood pressure should be
monitored during administration.

 Increased ICP is treated as necessary.

COMPLICATIONS
 Visual impairment
 Optic neuritis
 Deafness
 Seizure
 Paresis or paralysis
 Hydrocephalus
 Pneumonia
 Endocarditis

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 PREVENTION
 Adequate treatment of infections such as sinusitis, mastoiditis, ear
infections and pneumonia
 Use strict aseptic technique during all intracranial, intraspinal,
mastoid and sinus operations
 Use of strict aseptic technique during procedures
 Prophylactic antibiotics in case of head injuries, and injuries
causing drainage from ear or nose.

ENCEPHALIITIS
DEFINITION
Encephalitis is inflammation of the brain caused by viruses, bacteria, fungi or
viruses are the most common offending organism.

TYPES

Infectious – inflammation occurs as a direct result of an infection, which is

often viral

Post-infectious – inflammation is caused by the immune system reacting to a

previous infection, and can occur days, weeks or sometimes months after the
initial infection

Autoimmune – inflammation is caused by the immune system reacting to a

non-infectious cause, such as a tumour

Chronic – inflammation develops slowly over many months, and can be the
result of a condition such as HIV, though in some cases there is no obvious
cause.

CAUSES

The cause of encephalitis is often unknown, but the most commonly diagnosed
cause is a viral infection. Known causes of encephalitis may include:

 Viruses
 Bacteria: mycobacterium Tuberculosis, syphilis, Leptospiral

14
  Fungi: The presentation of fungal encephalitis is related to geographic
area or to an immune system that is compromised due to disease such as
AIDS or immunosuppressive medications. The main agents are
Cryptococcus neoformans, Histoplasmacapsulatum, Candida.
 Rickettsial infection
 Mycoplasma
 Toxoplasmosis
 Toxic substances: Ingested lead or arsenic, inhaled carbon monoxide.
 Post vaccination encephalitis: Adverse effect of vaccine for measles,
mumps and infectious mononucleosis.
 Neoplasmic

An infection may result in one of two conditions affecting the brain:

Primary encephalitis occurs when a virus or other infectious agent directly

infects the brain. The infection may be concentrated in one area or widespread.
A primary infection may be a reactivation of a virus that had been inactive
(latent) after a previous illness.

Secondary (post-infectious) encephalitis is a faulty immune system reaction in

response to an infection elsewhere in the body.

Common viral causes

 Herpes simplex virus. There are two types of herpes simplex virus
(HSV). HSV type 1 (HSV-1) more commonly causes cold sores or fever
blisters around your mouth, and HSV type 2 (HSV-2) more commonly
causes genital herpes. While HSV-1 encephalitis is rare, it has the
potential to cause significant brain damage or death.
 Other herpes viruses. Other herpes viruses that may cause encephalitis
include the Epstein-Barr virus, which commonly causes infectious
mononucleosis, and the varicella-zoster virus, which commonly causes
chickenpox and shingles.
 Enteroviruses. These viruses include the poliovirus and the
coxsackievirus, which usually causes an illness with flu-like symptoms,
eye inflammation and abdominal pain.
 Mosquito-borne viruses. Arboviruses, or arthropod-borne viruses,
are transmitted by mosquitoes or other blood-sucking insects. Mosquito-
borne viruses can cause infections that include West Nile, La Crosse, St.
Louis, western equine and eastern equine encephalitis. Mosquitoes
15
 transfer the virus from a nonhuman host — such as a bird, chipmunk or
horse — to humans. Symptoms of an infection may appear within a few
days to a couple of weeks after exposure to an arbovirus.
 Tick-borne viruses. The only known tick-transmitted virus that causes
encephalitis is Powassan virus. Symptoms usually appear about a week
after exposure to the virus.
 Rabies virus. Infection with the rabies virus, which is usually transmitted
by a bite from an infected animal, causes a rapid progression to
encephalitis once symptoms begin. The disease causes death if the
infection isn't treated before it reaches the spinal cord and brain.
 Cruetzfelt-Jakob disease: Spongiform encephalopathy characterised
by progressive dementia, dysarthria, spastic weakness of the limbs,
myoclonicjerks and seizures.
 H1N1 (Swine flu) virus:In May 2009, four pediatric patients between the
ages of 7 and 17 years were reported to have neurological involvement in
the setting of H1N1 infection. Patients presented with a flu-like illness,
seizures, or altered mental status. They recovered fully without
neurological sequelae at the time of discharge
 HIV (serious cause):Encephalopathy is the most common CNS
manifestation of HIV infection; occurs in 65% of patients with
HIV/AIDS
 Rabies virus (serious cause): Transmitted to humans through close
contact with rabid animals (bites, scratches, cuts, exposure to mucous
membranes) Incubation period ranges from 20 to 60 days.
 Childhood infections. Common childhood infections such as measles
(rubeola), mumps, and German measles (rubella) are common causes of
secondary encephalitis. These causes are now rare because of the
availability of vaccinations for these diseases.

PATHOPHYSIOLOGY

Causative agents: bacteria, viruses( common agent) , fungus- by direct,

haematogenous or through CSF circulation

Enters the brain parenchyma

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Cellular and humoral immunity get activated

Brain become oedematous (vasogenic, cytotoxic, interstial )

Phagocytes and macrophages hastens the inflammatory response

Necrosis of brain tissue with or without haemorrhage ( focal and general

manifestations of signs and symptoms)

Cerebral edema and inflammation leads to increased ICP

Brain herniation

SIGNS AND SYMPTOMS

 Aphasia or mutism
 Alteration in motor activity- Ataxia, myoclonic movements, nystagmus ,
ocular paralysis
 Stiff neck
 Hemiparesis
 Facial weakness
 Generalized seizures
 A positive Babinski sign and change in tendon reflexes on the affected
side associated with the hemiparesis.
 Severe headache
 Fever
 Altered consciousness
 Confusion or agitation
 Seizures
 Loss of sensation or paralysis in certain areas of the body
 Muscle weakness
 Hallucinations
 Double vision

17
  Perception of foul smells
 Problems with speech or hearing

ASSESSMENT AND DIAGNOSTIC MEASURES

 Medical history (including recent exposure to insects, travel, personality
changes, and contact with unusual animals or illnesses)
 Neurological and general examination
 Blood and urine testsBlood and urine tests are used to isolate and
identify viruses. Enzyme-linked immunosorbent assays (ELISA),
including IgM-capture ELISA (MAC-ELISA) and IgG ELISA, can
identify viruses that cause encephalitis soon after infection. Polymerase
chain reaction (PCR) can identify small amounts of viral DNA.
 Brain imaging.

Brain imaging is often the first test if symptoms and patient history
suggest the possibility of encephalitis. The images may reveal swelling of the
brain or another condition that may be causing the symptoms, such as a tumor.
Technologies may include

 Magnetic resonance imaging (MRI): which can produce detailed

cross-sectional and 3-D images of the brain
 Computerized tomography (CT):which produces cross-sectional
images.
 Spinal tap (lumbar puncture).

In spinal tap, inserts a needle into the lower back (L3-L4 or L5-
L6) to extract cerebrospinal fluid (CSF), the protective fluid that surrounds the
brain and spinal column. A particular profile of blood cells and immune system
proteins can indicate the presence of infection and inflammation in the brain. In
some cases, samples of CSF can be tested in a laboratory to identify the
causative virus or other infectious agent.

Analysis of CSF reveals

o Increased lymphocytes
o Increased protein
o Increased CSF pressure
o Xanthochromia: If haemarrhagic cerebral lesions are present
o Usually normal glucose level

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  CSF culture: It is mainly to isolate the causative organisms.
 Other lab tests

samples of blood, urine, or secretions from the back of the throat.

These can be tested in the laboratory to identify some of the viruses or other
infectious agents that can cause encephalitis.

 Electroencephalogram (EEG).

Electroencephalogram (EEG), a test in which a series of electrodes

are affixed to the scalp. The EEG records the electrical activity of the brain.
Certain abnormal patterns in this activity may be consistent with a diagnosis of
encephalitis.

 Brain biopsy.

Rarely, a procedure to remove a small sample of brain tissue (brain

biopsy) is used if symptoms are worsening, treatments are having no effect, and
there is no working diagnosis. The isolation of HSV from brain tissue obtained
at biopsy has been considered the gold standard for the diagnosis of HSV
encephalitis.

MEDICAL MANAGEMENT
Treatment objectives
1. stop and reverse the process of infection
2. control immediate complications caused by fever, such as seizures or
dehydration
3. prevent long-term complications developing

Encephalitis is a very serious condition and recovery can take months. There is
also a significant risk of developing complications of encephalitis, such as
memory loss, behavioural changes or even death.

Treatment for mild cases mainly consists of:

 Bed rest
 Plenty of fluids
 Anti-inflammatory drugs — such as acetaminophen (Tylenol, others),
ibuprofen (Advil, Motrin, others) and naproxen (Aleve, others) — to
relieve headaches and fever.

19
  Antiviral drugs: More-serious cases of encephalitis usually require
aggressive antiviral treatments. Antiviral drugs commonly used to treat
encephalitis include:

Acyclovir (Zovirax)

Ganciclovir (Cytovene)

aciclovir : is the most widely used treatment for infectious encephalitis.

However, it is only effective in treating cases caused by the herpes simplex
virus or varicella zoster virus. The earlier aciclovir is used, the more successful
it is. Therefore, treatment with aciclovir is usually started while the condition is
being diagnosed. Patient should receive a dose of 10mg/kg of acyclovir IV
every 8hour for a 10 day course. If tests reveal encephalitis is being caused by
something else, alternative treatments will be considered.

Aciclovir works by directly attacking the DNA inside viral cells,

which stops the virus from reproducing and spreading further into the brain. It is
given directly via a tube into a vein (intravenously), usually three times a day
for two to three weeks.

Common side effects of aciclovir include:

 headache
 nausea (feeling sick)
 vomiting
 diarrhoea
 thrombocytopenia

Less common side effects include:

 liver damage
 hallucinations (seeing things that are not real)
 a decrease in the number of white blood cells that are produced by the
bone marrow, which can make you more vulnerable to infection

In rare cases where a bacterial or fungal infection causes encephalitis, treatment

usually consists of antibiotics or antifungal medicines.

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Post-infectious encephalitis: treatment choice

Post-infectious encephalitis is usually treated with injections of

high-dose corticosteroids. This may last several days, depending on the severity
of the condition. Corticosteroids work by calming the immune system (the
body's natural defence against infection and illness). This reduces the levels of
inflammation inside the brain. Some people's symptoms may improve a few
hours after treatment. But in most cases it will take a few days before symptoms
start to improve.

immunoglobulin therapy: contains specific antibodies that help to regulate the

immune system.

Plasmapheresis :If your symptoms do not improve, a therapy called

plasmapheresis may be considered. Plasmapheresis involves gradually passing
your blood through a machine to remove the parts that contain antibodies before
it is returned to your body.

In fungal infection: Amphotericin B is the standard antifungal agent used in

treatment. Dosing depends on the causative organism, and is usually
administered as IV.The most common adverse effects are fever, chills, body
ache and hypotension. Renal insufficiency is a serious side effect of
amphotericin B

Fluconazole or flucystosine may be administered orally in

conjunction with amphotericin B as the maintenance therapy.

Treatment choice ofAutoimmune encephalitis:

Autoimmune encephalitis can be treated with corticosteroids, immunoglobulin

therapy and plasmapheresis. An additional medication known as an
immunosuppressant may also be recommended. Immunosuppressants suppress
your immune system, which should prevent your immune system from
attacking healthy tissue. Cyclosporine is a widely used immunosuppressant in
the treatment of autoimmune encephalitis.

If the immune system is weakened due to a treatment such as

chemotherapy or taking Immunosuppressants, this treatment may be
temporarily withdrawn

21
 There is currently no cure for the
subacutesclerosingpanencephalitis (SSPE) type of chronic encephalitis. Anti-
viral medication can slow its progression, but this condition inevitably proves
fatal within one to two years of receiving a diagnosis.

In HIV infection: Treatment choice

If immune system is weakened due to a HIV infection, a type of

medication known as highly active antiretroviral therapy may be effective.

Some viruses, such as insect-borne viruses, don't respond to these

treatments. However, because the specific virus causing the infection may not
be identified immediately or at all, treatment with acyclovir is often begun
immediately. This drug can be effective against the herpes simplex virus, which
can result in significant complications or death when not treated promptly.

Supportive care

Additional supportive care also is needed in the hospital for people with severe
encephalitis. The care may include:

 Breathing assistance, as well as careful monitoring of breathing and heart

function
 Intravenous fluids to ensure proper hydration and appropriate levels of
essential minerals
 Anti-inflammatory drugs, such as corticosteroids, to help reduce swelling
and pressure within the skull
 Anticonvulsant medications, such as phenytoin (Dilantin), to stop or
prevent seizures.

Follow-up therapy

After the initial illness, it may be necessary to receive additional therapy

depending on the type and severity of complications. This therapy may include:

 Physical therapy to improve strength, flexibility, balance, motor

coordination and mobility
 Occupational therapy to develop everyday skills and to use adaptive
products that help with everyday activities
 Speech therapy to relearn muscle control and coordination to produce
speech

22
  Psychotherapy to learn coping strategies and new behavioral skills to
improve mood disorders or address personality changes — with
medication management if necessary.

Complications of severe encephalitis

Injury to the brain from inflammation can result in a number of

problems. The most severe cases can result in:

 Respiratory arrest
 Coma
 Death

Other complications — varying greatly in severity — may persist for many

months or be permanent:

o Fatigue
o Weakness
o Mood disorders
o Personality changes
o Memory problems
o Intellectual disabilities
o Lack of muscle coordination
o Paralysis
o Hearing or vision defects
o Speech impairments
o epilepsy, a condition that causes repeated seizures

PRIMARY PREVENTION
 Mosquito control in the form of repellents, protective clothing, and
insecticides
 A vaccine against Japanese B encephalitis is now available and is
recommended to people who travel to rural parts of East Asia during the
summer. The licensed monovalent Nakayama vaccine confers protection
against Japanese encephalitis during the first year of administration in a
two-dose schedule. Disease protection by the licensed Nakayama vaccine
1 year after administration is estimated to be close to 95%. Most

23
 countries using the inactivated vaccine today have added annual or tri-
annual booster doses

GUILLAIN BARRE SYNDROME

DEFINITION
Guillain-Barre syndrome (GBS) is an autoimmune disorder. With an
autoimmune disorder, the body's immune system attacks itself. The exact cause
is unknown.

Guillain–Barré syndrome (GBS) sometimes Landry's paralysis or

Guillain–Barré–Strohl syndrome, is an acute polyneuropathy, a disorder
affecting the peripheral nervous system. Ascending paralysis, weakness
beginning in the feet and hands and migrating towards the trunk, is the most
typical symptom, and some subtypes cause change in sensation or pain, as well
as dysfunction of the autonomic nervous system. It can cause life-threatening
complications, in particular if the respiratory muscles are affected or if the
autonomic nervous system is involved. The disease is usually triggered by an
infection.

INCIDENCE

Guillain–Barré syndrome is rare, at one to two cases per 100,000 people

annually, but is the most common cause of acute non-trauma-related paralysis.
The syndrome is named after the French physicians Georges Guillain and Jean
AlexandreBarré, who described it in 1916.

GBS can occur at any age. It is most common in people of both sexes between
ages 30 and 50.

ETIOLOGY

GBS often follows a minor infection, such as a lung infection or

gastrointestinal infection. Most of the time, signs of the infection have
disappeared before the symptoms of GBS begin.

24
 1. Most commonly, infection with campylobacter, a type of bacteria often
found in undercooked food, especially poultry. he most common
infection which precedes the development of Guillain-Barre syndrome is
Campylobacter jejunii - one of the most widespread causes of human
gastroenteritis.

2. GBS may occur with viral infections such as:

 AIDS
 Herpes simplex
 Mononucleosis
 Epstein-Barr virus
 Influenza virus

3.The swine flu vaccination in 1976 may have caused rare cases of GBS.
The swine flu and the regular flu vaccines used today have not caused more
cases of the illness.

4. GBS may also occur with other medical conditions such as:

 Systemic lupus erythematosus

 Hodgkin disease
 After surgery
5. Autoimmune disorder:
In Guillain-Barre syndrome, your immune system — which
usually attacks only foreign material and invading organisms — begins
attacking the nerves that carry signals to your brain. The nerves'
protective covering (myelin sheath) is damaged, and this interferes with
the signalling process, causing weakness, numbness or paralysis.

TYPES

Acute inflammatory demyelinating polyneuropathy

The acute inflammatory demyelinating polyneuropathy (AIDP)

subtype is the most commonly identified form . It is generally preceded by a
bacterial or viral infection. Nearly 40% of patients with AIDP are seropositive
for Campylobacter jejunii. Symptoms generally resolve with remyelination.

25
Acute motor axonal neuropathy

The acute motor axonal neuropathy (AMAN) subtype is a purely

motor disorder that is more prevalent in paediatric age groups. AMAN is
generally characterized by rapidly progressive symmetrical weakness and
causing respiratory failure. Nearly 70-75% of patients with AMAN are
seropositive for Campylobacter.

Prognosis is often quite favourable. Although recovery for many is

rapid, severely disabled patients with AMAN may show improvement over a
period of years. One third of patients with AMAN may actually be
hyperreflexic. Although the mechanism for this hyperreflexia is unclear,
dysfunction of the inhibitory system via spinal interneurons may increase motor
neuron excitability.

Acute motor-sensory axonal neuropathy

Acute motor-sensory axonal neuropathy (AMSAN) is a severe

acute illness differing from AMAN in that it also affects sensory nerves and
roots. Patients are typically adults. Marked muscle wasting is characteristic,
and recovery is poorer .

Miller-Fisher syndrome

Miller-Fisher syndrome (MFS), which is observed in about 5% of

all cases of GBS, classically presents as a triad of ataxia, areflexia, and
ophthalmoplegia. Acute onset of external ophthalmoplegia is a cardinal feature

Acute pan autonomic neuropathy

Acute pan autonomic neuropathy, the rarest GBS variant, involves

the sympathetic and parasympathetic nervous systems. Patients have severe
postural hypotension, bowel and bladder retention, anhidrosis, decreased
salivation and lacrimation, and pupillary abnormalities. Cardiovascular
involvement is common, and dysrhythmias are a significant source of mortality.

Pure sensory GBS

A pure sensory variant of GBS has been typified by a rapid onset

of sensory loss, sensory ataxia, and areflexia in a symmetrical and widespread
pattern of weakness.

26
PATHOPHYSIOLOGY

The pathophysiologic mechanism of an antecedent illness and of GBS can be

typified by Campylobacter jejuniinfections.The virulence of C jejuni is thought
to be based on the presence of specific antigens in its capsule that are shared
with nerves.

An infectious illness in the weeks prior to the onset of GBS.

GBS is a postinfectious, immune-mediated disease.

Cellular and humoral immune mechanisms plays an important role

production of antibodies

Infectious organism contains an aminoacid that mimics the peripheral nerve

myelin protein

The immune system can not distinguish between two proteins

Attacks and destroy the peripheral nerve myelin by cross-react with specific
gangliosides and glycolipids- GM1 and GD1b, (that are distributed throughout
the myelin in the peripheral nervous system.)

resulting in immunologic damage to the peripheral nervous system. This

process has been termed (molecular mimicry- Best accepted theory of cause)

27
multifocal stripping of myelin. Leave the axon unable to support nerve
conduction

results in defects in the propagation of electrical nerve impulses,

with eventual absence or profound delay in conduction, causing flaccid

paralysis.

GBS is a post infectious, immune-mediated disease. Cellular and

humoral immune mechanisms probably play a role in its development. Most
patients report Many of the identified infectious agents are thought to induce
production of antibodies that cross-react with specific gangliosides and
glycolipids, such as GM1 and GD1b, that are distributed throughout the myelin
in the peripheral nervous system.

Immune responses directed against lipopolysaccharide antigens in

the capsule of Campylobacter jejuni result in antibodies that cross-react with
ganglioside GM1 in myelin, resulting in immunologic damage to the peripheral
nervous system. This process has been termed molecular mimicry.

Pathologic findings in GBS include lymphocytic infiltration of

spinal roots and peripheral nerves (cranial nerves may be involved as well),
followed by macrophage-mediated, multifocal stripping of myelin. This
phenomenon results in defects in the propagation of electrical nerve impulses,
with eventual absence or profound delay in conduction, causing flaccid
paralysis. The cell that produces the myelin in the peripheral nervous system is
Schwann cell. In GBS, the Schwann cell is spared, allowing remyelination in
the recovery phase of the disease.

CLINICAL FEATURES

Typically, signs and symptoms emerge a short time after a sore

throat or some minor infectious process.

28
First symptoms - symptoms usually start in the feet and hands and may
eventually make their way further along the limbs. There is more commonly
symmetrical weakness in the lower limbs initially, which rapidly progress in an
ascending fashion. Initial signs and symptoms may include:

 Instability - unsteadiness. Patients often complain of rubbery legs

 Dysesthesias - numbness or tingling
 Muscle weakness, which gets progressively worse
 Weakness or tingling sensations in legs that spread to upper body

Possible later symptoms - In some people, the muscle weakness progresses to:

 Bladder control problems - usually transient (brief). If bladder control

problems are severe, the doctor may suspect a spinal cord disorder.
 Digestive system problems
 Oropharyngeal dysphagia - drooling, or difficulty swallowing and/or
maintaining an open airway
 Difficulty with eye movement and speech
 Facial weakness
 Slow heart rate or low blood pressure
 Temporary paralysis of the legs, arms and face
 Respiratory problems - some patients may require ventilatory assistance.
 Severe pain in lower back
 Pain - a common symptom. Pain is usually a deep aching one, located in
the weakened muscles.
 Sensory loss - less common. If present, it usually takes the form of
position sense (proprioception) and complete loss of deep tendon reflexes
(areflexia). Any loss of pain or temperature sensation is generally very
mild.

MEDICAL MANAGEMENT

Supportive care

Supportive care is the cornerstone of successful management in the

acute patient. Of greatest concern is respiratory failure due to paralysis of the
diaphragm, the muscle most important for breathing. Intubation may be needed
when evidence of impending failure of the muscles of breathing is present –
when the vital capacity (VC) is less than 20 ml/kg, the negative inspiratory
force (NIF) is less negative (i.e., closer to zero) than −25 cmH2O, more than

29
30% decrease in either VC or NIF within 24 hours, rapid progression of
disorder, or autonomic instability.

Patients with Guillain-Barre syndrome will be hospitalized initially

(medical emergency). It is important to monitor the individual's respiration
carefully. If breathing problems are severe he/she may be placed in an ICU
(intensive care unit) and put on a ventilator

According to the National Health Service, the two main initial

treatment options for Guillain-Barre syndrome are intravenous immunoglobulin,
which is safer and easier to give, or plasmapheres (plasma exchange).

Plasmapheresis –

The aim here is to deplete the body of blood plasma without

depleting it of its blood cells. Plasma is the liquid part of blood. In the case of
Guillain-Barre syndrome, the aim is to remove the cells that are attacking the
nerve. Attempting to reduce the body's attack on the nervous system, by
plasmapheresis, filtering antibodies out of the blood stream.Plasmapheresis
hastens recovery when used within four weeks of the onset of symptoms.

Intravenous immunoglobulin–

Concentrated antibodies are injected straight into a vein. The

antibodies are extracted from healthy donors to neutralize harmful antibodies
and inflammation causing disease.Intravenous administration of high dose
immunoglobulin (2g/kg body weight given over 5 days).

REHABILITATION

Following the acute phase, treatment often consists of rehabilitation with the
help of a multidisciplinary team to focus on improving activities of daily living
(ADLs).

 Occupational therapists may offer equipment (such as wheelchair and

special cutlery) to help the patient achieve ADL independence.
 Physiotherapists assist to correct functional movement, avoiding harmful
compensations that might have a negative effect in the long run. Also,
some evidence supports physiotherapy in helping patients with Guillain–
Barré syndrome to regain strength, endurance, and gait quality, as well as

30
 helping them prevent contractures, bedsores, and cardiopulmonary
difficulties.
 Speech and language therapists help regain speaking and swallowing
abilities, especially if the patient was intubated or received a
tracheostomy.

BRAIN ABSCESS
Brain abscess (or cerebral abscess) is an abscess caused by inflammation
and collection of infected material, coming from local (ear infection, dental
abscess, infection of paranasal sinuses, infection of the mastoid air cells of the
temporal bone, epidural abscess) or remote (lung, heart, kidney etc.) infectious
sources, within the brain tissue. The infection may also be introduced through a
skull fracture following a head trauma or surgical procedures. Brain abscess is
usually associated with congenital heart disease in young children. It may occur
at any age but is most frequent in the third decade.

DEFINITION

A brain abscess is a focal suppurative process with in the brain

parenchyma of diversepathogenesis and etiology.

(Braunwald etal, Harrison’s principles of internal medicine)

SUBDURAL EMPYEMA

Subdural empyema is a collection of pus in the space between the dura mater
and the arachnoid membrane. Subdural empyema accouts for about 20% of all
localized intracranial infections.

EPIDURAL ABSCESS

An epidural abscess is defined as a suppurative infection in the

epidural space. This space is located between the dura mater and the overlying
bone. Cranial epidural abscess often crosses the cranial dura along the emissary
veins so subdural empyema is also often present

ETIOLOGY

There are three main ways that a brain abscess can develop:

31
 1) An infection in another part of the skull, such as an ear infection, sinusitis
or dental abscess, spreads directly into the brain
2) An infection in another part of the body, such as the lung infection
pneumonia, spreads into the brain via the blood
3) Trauma, such as a severe head injury, that cracks open the skull allowing
bacteria or fungi to enter the brain

CAUSATIVE ORGANISMS

 S.aureus, streptococci and coliform bacteria. 60% pyogenic brain

abscess are mixed infections
 Gram negative bacilli such as proteus, E coli, klebsiella, Enterobacter
and Pseudomonas aeruginosa
 H. influenza and M. Catarrhalis in acute otitis media
 Toxoplasma gonaddii and fungi (Candida, Aspergillus)- ainly in AIDS
and immune compromised patients

PATHOPHYSIOLOGY

Etiological factors- Contiguous focus of infection, Haematogenous spread,

Following cranial trauma or surgery

Microscopic focus of infection along with microvascular injury, usually within

white matter or at the gray-white junction.

Growth of bacteria within this focus produces a localized encephalitis or

"cerebritis,"

Perivascular inflammatory response surrounding a developing necrotic center

with profound edema( leads to increased ICP)

32
The developing abscess elicits an inflammatory response of lymphocytes and
polymorphonuclear nuclei

liquefaction of purulent material at the center

In latecerebritis maximal extend of wellformed necrotic center and the

appearance of fibroblast and neovascularity in the periphery of the necrotic zone

abscesscapsule forms, consisting of fibroblastalongwith persistent cerebritis

Late capsule formation : thickening of capsule with abundance of reactive

collagen ( Compression of brain parenchyma leads to focal neurologic deficits)

The abscess capsule tends to be thickest on its cortical surface and thinnest
medially

Well encapsulated necrotic focus

33
The abscess tend to expand toward and rupture into the ventricular system

Death in brain abscess may result from brain herniation, caused by the mass
effect of the abscess and its surrounding cerebral edema, or from rupture of the
abscess into the ventricular system.

CLINICAL FEATURES

 The classical clinical triad of brain abscess is fever, headache, and

focal neurologic deficits In most cases, brain abscess presents as a
rapidly or subacutely developing space-occupying lesion, fever or other
signs of active infection may be absent
 Seizures:Approximately one third of patients present with seizures that
are most frequently generalized and are most closely associated with
frontal lobe abscesses
 Nuchal rigidity is present in about 25% of patients
 Papilledema is present in no more than 25% of patients and is frequently
absent in rapidly developing abscesses
 Severe headache:Brain abscess should be considered in any patient
presenting with recent onset of severe headache or with symptoms or
signs of a rapidly developing space-occupying intracranial process.
 Fever is present in only about 50% of patients; even when present, it may
be 38°C or less.
 Nausea and vomiting
 Focal neurologic deficits: Hemiplegia, hemianopsia, cranial nerve
abnormalities.
 Cerebellar abscess manifested as nystagmus, ataxia, vomiting
 Ventricular rupture may be manifested by severe headache and
developing signs of meningeal irritation, and rapid deterioration in
clinical course

ASSESSMENT AND DIAGNOSTIC TECHNIQUES

A history of systemic infection, sinusitis, otitis, carious teeth, drug abuse, or

risk factors for AIDS should increase diagnostic concern.

34
Physical examination for clinical features

Blood studies: The peripheral white blood cell count is normal in 40% of
patients and is elevated above 20,000 cells/mm3 in less than 10% of patients

erythrocyte sedimentation rate is usually minimally elevated but may be normal

C-reactive protein levels are frequently elevated

The patient should be evaluated for remote sources of infection with appropriate
cultures of blood and other fluids such as sputum, pus from sinuses, or material
obtained at myringotomy.

Lumbar punctureis contraindicated in brain abscess: spinal fluid

abnormalities are usually nonspecific, and the procedure itself is accompanied
by a 10% to 18% risk of brain herniation and death

CT Scan: CT is superior to other radiologic techniques in evaluating

teparanasal sinuses, mastoaids along with a chest x ray in all patients with
suspected brain abscess. CT appearance is not specific for brain abscess and
other process including neoplasm, granuloma, cerebral infarction or resolving
haematoma may give a similar finding on CT.The sensitivity of contrast-
enhanced CT may be increased if the scan is repeated 30 to 60 minutes after
contrast infusion. Both MRI and CT will delineate the amount of edema
surrounding the abscess and may also document the presence of accompanying
sinusitis or otitis .

MRI is the diagnostic procedure of choice in suspected brain abscess.MRI

permits multiplanar imaging accentuates the contrast between grey and white
matter and also elucidates pathological changes, Diffusion-weighted MRI or
MR spectroscopy may allow differentiation between brain abscess and tumor
with central necrosis and may also help differentiate between bacterial,
tuberculous, and fungal Contrast-enhanced CT may fail to detect lesions easily
discernible on MRI but should be used if MRI is not available

Abscess biopsy along with culture and sensitivity

35
MEDICAL MANAGEMENT

Before the abscess has become encapsulated and localized, antimicrobial

therapy, accompanied by measures to control increasing intracranial pressure, is
essential.Once an abscess has formed, surgical excision or drainage combined
with prolonged antibiotics (usually 4-8 wk) remains the treatment of choice.
Some neurosurgeons advocate complete evacuation of the abscess, while others
advocate repeated aspirations as indicated

ANTIMICROBIAL AGENTS

Because of the difficulty involved in the penetration of various

antimicrobial agents through the blood-brain barrier, the choice of antibiotics is
restricted, and maximal doses are often necessary.

Suspected Organism Antibiotics for Empiric Therapy of

Brain Abscess

 Streptococci and other Gram-  Penicillin, vancomycin,

positive organisms excluding S ceftriaxone, or cefotaxime
aureus
 Vancomycin, until sensitivity to
 Staphylococcus aureus Oxacillin or Nafcillin is
confirmed. Use vancomycin if
patient is allergic to penicillin

 Gram-negative organisms  Ceftriaxone or cefotaxime

excluding Pseudomonas
aeruginosa

 Pseudomonas aeruginosa  Ceftazidime

 Bacteroides species  Metronidazole

Initial empiric antimicrobial therapy should be based on the

expected etiologic agents according to the likely predisposing conditions, the
primary infection source, and the presumed pathogenesis of abscess formation.
When abscess specimens are available, staining of the material can help guide

36
selection of therapy. Whenever proper cultures are taken and organisms are
isolated and their susceptibility is determined, the initial empiric therapy can be
adjusted to specifically treat the isolated bacteria.

Coverage for streptococci can be attained by a high dose of

penicillin G or a third-generation cephalosporin (eg, cefotaxime, ceftriaxone).
Metronidazole is included to cover penicillin-resistant anaerobes (ie, gram-
negative bacilli). This choice is appropriate for the treatment of an abscess of
oral, otogenic, or sinus origin.

Patients with HIV infection may require therapy for toxoplasmosis.

Penicillin penetrates well into the abscess cavity and is active against non–
beta–lactamase-producing anaerobes and aerobic organisms. However, the
emergence of beta–lactamase-producing organisms limits it use.

Chloramphenicol penetrates well into the intracranial space and is also active
against Haemophilus species, S pneumoniae, and most obligate anaerobes. Its
use has been curtailed dramatically in most US centers because of the
availability of other equally efficacious and less toxic antimicrobial
combinations (ie, cefotaxime plus metronidazole).

Metronidazole penetrates well into the CNS and is not affected by concomitant
corticosteroid therapy. However, it is only active against strict anaerobic
bacteria, and its activity against anaerobic gram-positive anaerobes may be
suboptimal.

Third-generation cephalosporins (eg, cefotaxime, ceftriaxone) generally

provide adequate therapy for aerobic gram-negative organisms as well as
streptococci. If pseudomonads are isolated or anticipated, the parenteral
cephalosporin of choice is a forth generation cephalosporin (ceftazidime or
cefepime).

Aminoglycosides do not penetrate well into the CNS and are relatively less
active because of the anaerobic conditions and the acidic contents of the abscess

Beta-lactamase–resistant penicillins (eg, oxacillin, methicillin, nafcillin)

provide good coverage against methicillin-sensitive S aureus (MSSA).
However, their penetration into the CNS is less than penicillin, and the addition
of rifampin has been shown to be of benefit in staphylococcal meningitis.

37
Because of the risk of methicillin-resistant S aureus (MRSA) infection they
should only be administered to treat culture proved MSSA .

Vancomycin is most effective against MRSA and Staphylococcus epidermidis

as well as aerobic and anaerobic streptococci and Clostridium species.

Antimicrobial that are alternatives to vancomycin include linezolid (600 mg

IV or PO bid), trimethoprim-sulfamethoxazole (5 mg/kg q8-12h), and
daptomycin (6 mg/kg IV qd). Limited data regarding their use in brain abscess
are available.

Caution should be used in administering carbapenems and beta-

lactamases in general, because high doses of these agents may be associated
with seizure activity. Imipenem has been associated with an increased risk of
seizures in patients with brain abscess. Although fluoroquinolones have good
penetration into the CNS, data are limited regarding their use in treating brain
abscesses.

Amphotericin B is administered for Candida, Cryptococcus, and Mucorales

infections; voriconazole for Aspergillus and P boydii infections.

Pyrimethamine and sulfadiazine: T gondii infection

Anticonvulsants: phenytoin, sodium valproate, diazepam

SURGICAL MANAGEMENT

Surgical therapy of brain abscess may involve aspiration or excision

ASPIRATION

Aspiration, particularly under stereotactic CT or MRI guidance, is

becoming increasingly favored because it is less traumatic to the central nervous
system than is excision and carries a lower risk of subsequent seizures.
Aspiration also provides a less traumatic approach to abscesses involving an
eloquent area of the brain or the brainstem. Aspiration removes the purulent
center of the abscess, rendering the abscess more amenable to antibiotic
therapy, and often effectively reduces intracranial pressure. Recurrence of the
abscess may require repeat aspiration.

38
EXICISION

Excision should be considered in large or multi loculated

abscesses, abscesses that do not respond to aspiration and may be necessary in
cases in which ventricular rupture is considered imminent. Excision is also
indicated in cases in which there is a foreign body, in which there is gas within
the abscess, or in abscesses due to Nocardia.

Surgical drainage provides the most optimal therapy. The

procedures used are aspiration through a bur hole and complete excision after
craniotomy. These procedures are also diagnostic and provide material that can
guide antimicrobial therapy

VENTRICULAR SHUNT

Cerebellar abscesses may cause obstructive hydrocephalus and

may hence require placement of a ventricular shunt to avoid further increase in
intracranial pressure .

DEBRIDEMENT OF ABSCESS CAVITY AND VENTRICULAR

LAVAGE WITH ANTIBIOTICS

Although brain abscess with intraventricular rupture has an 80% fatality rate,
survival has been reported following open craniotomy with debridement of
abscess cavity and ventricular lavage, followed by 6 weeks of intravenous
antibiotics, intraventricular gentamicin twice daily for 6 weeks.Although many
neurosurgeons have instilled antibiotics directly into the abscess cavity, the
efficacy of this procedure is not known.Ventricular drainage combined with
administration of intravenous or intrathecal antimicrobials is used to treat brain
abscesses that rupture into the ventricles.

Surgery may be deferred if the abscess is less than 3 cm in

diameter and the patient is neurologically stable. Abscesses treated with
antibiotics alone must be followed with great care, and a follow-up MRI or CT
should be obtained within 24 to 48 hours after initiation of therapy. It is
extremely important to remember that abscesses may enlarge despite antibiotic
therapy .For this reason, frequent follow-up MRI or CT is essential if a decision
is made to treat with antibiotics alone. Intervals between subsequent CT and
MRI studies are determined in part by the patient's neurologic status but should
not be greater than 3 to 5 days in the first 2 weeks.

39
MANAGEMAENT OF SYMPTOMS

 Cerebral edema
 Require emergent treatment with hyperventilation, mannitol, or
dexamethasone.
 Mannitol may be given as a 20% solution with an initial dose of 0.5 to 1.0
g/kg over 10 minutes followed by 0.25 to 0.5 g/kg every 3 to 5 hours.
 The patient should be catheterized before mannitol is begun
 Careful attention should be given to serum electrolytes and osmolality.
 Dexamethasone is effective in reducing vasogenic edema, and a short
course of 10 mg intravenously initially followed by 4 mg intravenously
every 4 to 6 hours should be considered where control of intracranial
pressure is of major concern over time.
 Inappropriate secretion of antidiuretic hormone or development of
diabetes insipidus may require strict attention to fluid and electrolyte
balance.
 Subcutaneous heparin should be considered in patients remaining at bed
rest for extended periods of time.
 Adjacent or remote sources of infection, including sinuses, middle ear,
mastoid, and teeth may also require antibiotic or surgical therapy.
 Seizures may be treated with intravenous diazepam, 10 mg, or
lorazepam, 4 mg, given over 2 minutes and repeated after 15 minutes if
seizures persist. Therapy with these short-acting agents should be
followed by a loading dose of intravenous fosphenytoin given as the
equivalent of 10 to 15 mg/kg phenytoin in normal saline at a rate no faster
than 50 mg/min. If phenytoin is used rather than fosphenytoin, the
electrocardiogram and blood pressure should be monitored during
administration.
 Alternate agents to control seizures include intravenous levetiracetam or
valproic acid.
 Midazolam, propofol, phenobarbital, or other agents may be required to
control seizures unresponsive to phenytoin

40
NURSING MANAGEMENT

Assessment

 Assess vital signs : To denote improvement or deterioration in overall

condition
 Assess neurological signs
 Signs of meningeal irritation- nuchal rigidity, hyperirritability,
photophobia, hyperalgesia
 Assess respiratory function ( auscultate chest, observe chest movement)
 Monitor daily body weight; serum electrolytes; and urine volume,
specific gravity, and osmolality, especially if syndrome of inappropriate
antidiuretic hormone (SIADH) is suspected.
 Assess SPO2 and ABG values.

Nursing Diagnosis

Acute Pain related to nuchal rigidity, muscle aches, immobility and

increased sensitivity to external stimuli secondary to infectious process

Assess location, quality and severity of pain

Elevating the head 300

Maintain a quiet dark room

Administering analgesics as necessary

Adequate rest

Monitor patient’s response to pain and analgesics

Altered cerebral tissue perfusion related to cerebral edema and increased

ICP

Elevate the head of the bed to a 300 angle

Keep the head in a neutral position

Prevent Valsalvamaneuver

Monitor neurological signs

If ICP monitor is available monitor cerebral perfusion pressure

41
Hyperthermia related to infection, inflammation and pressure on the
hypothalamus

Monitor body temperature

Remove excess bed clothes

Provide tepid sponge

Administer antipyretic drugs

Provide high calorie protein rich diet

Administer fluids

Imbalanced nutrition less than body requirement related to increased

metabolic demand secondary to infectious process

Obtain baseline weight of the patient

High calorie protein rich diet

Small and frequent diet

Maintain optimum fluid balance

Monitor electrolytes and haemoglobin

Risk for Injury related to restlessness ,disorientation and seizure secondary

to meningeal irritation

Putting side rails up

Maintain an oral airway

Do not leave the patient alone

Paddled side rails

High risk for Disuse syndrome related to prolonged bed rest

Goal: The patient remains free from risk of pressure ulcers, contractures, deep
vein thrombosis, constipation, urinary stasis, atelectasis and dehydration

Develop a turning and repositioning schedule to prevent skin breakdown

Apply elastic stockings

42
Apply pneumatic compression devices

Institute a bowel training programme

Position the patient to facilitate breathing and patency of airway

Provide a urinary elimination programme

EVIDENCED BASE PRACTICE

Pathogenesis and immune response in tuberculous

meningitis.byIsabel , Rogelio .Cerebral tuberculosis is the most severe type of
extrapulmonary disease that is in developing countries highly predominant in
children. Meningeal tuberculosis is the most common form and usually begins
with respiratory infection followed by early haematogenous dissemination to
extrapulmonary sites involving the brain. In comparison with the lung,
Mycobacterium tuberculosis induces a very different immune response when
infect the central nervous system. Herein, they review several aspects of the
pathogenesis and immune response in pulmonary and cerebral tuberculosis in
humans and experimental models and discuss the implications of this response
in the cerebral infection outcome.

Guillain-Barre syndrome associated with preceding hepatitis E

virus infection. Van den Berg , van der Eijk etal conducted a study. Study was
to determine whether Guillain-Barre syndrome (GBS) is associated with
preceding hepatitis E virus infection. Increased ratio of anti-HEV
immunoglobulin (Ig) M antibodies was found in 10 patients with GBS (5.0%)
compared with 1 healthy control. HEV RNA was detected in blood from 3 of
these patients and additionally in faeces from 1 patient. Seventy percent of anti-
HEV IgM-positive patients had mildly increased liver function tests. The
presence of anti-HEV IgM in patients with GBS was not related to age, sex,
disease severity, or clinical outcome after 6 months.

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WEBSITES

1) www.medicalnewstoday
2) www.Healthcentral.com
3) www.pupmed.com
4) www. neuropathy org
5) www.gbs page

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