BRAIN AND SPINAL ABSCESSES

A brain abscess is a free or encapsulated collection of infectious material of

brain parenchyma, between the dura and the arachnoid linings (subdural
abscess) or between the dura and the skull (epidural abscess). Spinal
abscesses typically occur in the epidural region.
PATHOPHYSIOLOGY AND ETIOLOGY

Intracranial subdural abscesses, usually due to a streptococcus

organism, are caused by purulent drainage between the dura and
arachnoid. It can result from pus from the meninges, middle ear or
mastoid, sinuses, septicemia, or skull fracture. It occurs most
frequently in children and young adults.
Intracranial epidural abscesses, typically involving an infection of the
cranium, commonly occur due to chronic mastoiditis or sinusitis, head
trauma, or craniotomy. Abscesses may be related to a subdural
empyema (collection of purulent drainage originating from nasal
sinuses, meninges, middle ear, or skull osteomyelitis), meningitis, or
intraparenchymal abscess.
Spinal epidural abscesses occur in the spinal canal external to the
dura. Epidural penetration may seed through the blood and occur from
infected adjacent tissue (eg, infected pressure ulcer), from another
infected site (eg, skin), or contamination from spinal surgery or spinal
instrumentation (eg, lumbar puncture). S. aureus is a frequent
causative agent and the midthoracic vertebrae are most commonly
affected.
Intermedullary abscesses are more common in the pediatric
population, and are associated with lumbosacral dermal sinuses.
Approximately 20% to 30% are cryptic abscesses with no
apparent source of infectious seeding.
In the initial inoculation period, organisms invade the brain
parenchyma resulting in local inflammation and edema. The resulting
cerebritis develops into a necrotic lesion and then becomes
encapsulated.
Fungal brain abscesses are commonly seen in HIV-positive patients and
other populations that are immunosuppressed. Diffuse microabscesses
may occur with infections caused by Candida species.
M. tuberculosis may cause abscesses of pus containing acid-fast bacilli
(AFB) surrounded by a dense capsule. These abscesses are also found
in patients who are HIV-positive or have other immunosuppressive
diseases.

CLINICAL MANIFESTATIONS

Headache is poorly localized with a dull ache.

Increased ICP may result in nausea, vomiting, decreased LOC.
Fever is found in less than 50% of cases.
Neurologic findings such as hemisensory and paresis deficits, aphasia,
ataxia may be present.
Seizures are frequently present.
Dental abscess, sinusitis, and otitis media may be present.
Signs and symptoms of a cerebral subdural empyema include severe
headache, fever, nuchal rigidity, and Kernig's sign (see page 503).
Patients with intracranial epidural abscess commonly present with
fever, lethargy, and severe headache.
Spinal epidural abscesses may be evidenced by severe back pain,
fever, headache, lower extremity weakness or paralysis, nuchal
rigidity, Kernig's sign, and local tenderness.

DIAGNOSTIC EVALUATION

CT scan, MRI with contrast locate the sites of abscess, and follow
evolution and resolution of the suppurative process.
o In the inflammatory stage of cerebritis, imaging reveals a high
signal intensity centrally (inflammation) and peripherally
(edema). When an abscess develops, the capsule becomes
isointense.
o There may be decreased ring enhancement with patients who
are immunosuppressed, which may be due to a lack of
inflammatory response.
o Microabscesses may not be detected by the CT scan or MRI.
o MRI with gadolinium enhancement should be considered to
detect spinal epidural abscesses.
Blood cultures are obtained to identify the organism, positive Gram's
stain, leukocytosis, and elevated erythrocyte sedimentation rate (ESR).
Cultures are obtained from the suspected source of infection, using
stereotaxic needle aspiration or brain surgery, to identify the organism
and sensitivity to antimicrobials.
A metastatic brain abscess may be differentiated from a metastatic
tumor by CT scan or MRI. Abscesses have hypodense centers with a
smooth surrounding capsule, whereas tumors may have irregular
borders and diffuse enhancement.
EEG detects seizure disorders.
Findings in cerebral subdural empyema include increased WBC and
increased pressure of the CSF.

In intracranial epidural abscesses, CT or MRI scans are useful; MRIs are

usually more sensitive. Findings from the CSF may not be definitive. To
avoid transtentorial herniation, lumbar puncture is not indicated until
large cranial masses are ruled out.
Diagnostic findings in spinal epidural abscesses may include increased
WBC and ESR. The CSF may be cloudy. Myelography is typically
abnormal.

MANAGEMENT

With cerebral subdural empyema or intracranial epidural abscesses,

management consists of trephining (drilling through skull to evacuate
purulent material), systemic antibiotics, and treatment of cerebral
edema.
Spinal epidural abscesses may be managed with a laminectomy and
surgical drainage, with antibiotics before and after the procedure. The
abscess site is thoroughly irrigated with antibiotic solution and aerobic
and anaerobic cultures are taken.
Closed stereotaxic needle biopsy, under CT guidance, may be used for
drainage evacuation instead of craniotomy.
Radical surgical dbridement, especially with fungal infections, may
be indicated with antimicrobial therapy.
Initiation of empiric antimicrobial therapy is based on Gram's stain and
the suspected site of origin.Because brain abscesses are frequently
caused by multiple organisms, antimicrobial therapy is directed toward
the most common etiologic agents: streptococci, anaerobic bacteria
(eg, Bacteroides species).
o S. aureus may be suspected if surgical procedures have been
performed.
o Gram-negative bacteria (eg, Clostridium species) should be
suspected if a cranial wound has been contaminated with soil.
o A 6- to 8-week course of parenteral antibiotics is typical, followed
by a 2- to 3-month course of oral antimicrobial therapy.
o Penicillin G, metronidazole, and third-generation cephalosporins
are common therapeutic agents.

Antifungal therapy, such as amphotericin B, is initiated for candidiasis

and other fungal infections.
Antituberculosis pharmacotherapy, such as rifampin, isoniazid, and
pyrazinamide, should be used to treat abscesses containing AFB.
Adjunctive therapy includes corticosteroids and osmotic diuretics to
reduce cerebral edema, and anticonvulsants to manage seizures.

COMPLICATIONS

The brain abscess can rupture into the ventricular space, causing a
sudden increase in the severity of the patient's headache. This
complication is often fatal.
Papilledema may occur in less than 25% of cases, indicating
intracranial hypertension.
Lumbar puncture may be dangerous due to the possibility of brain
stem herniation. Lumbar puncture is also contraindicated if there is a
spinal epidural abscess because pus may be transferred into the
subarachnoid space. Cervical puncture should be considered in such
patients.
Permanent neurologic deficits, such as seizure disorders, visual
defects, hemiparesis, and cranial nerve palsies, may be present.
There is greater mortality if the patient has symptoms of short
duration, has severe mental status changes, and has rapid progression
of neurologic impairment.
Delayed treatment of a spinal epidural abscess may result in
transaction syndrome, in which flaccid paraplegia with sensory loss
occurs at the level of the abscess.
In chronic otitis media, intracranial and intratemporal complications
frequently result from progressive bony erosion, which may expose the
dura, labyrinth, and facial nerves.

NURSING ASSESSMENT

Obtain history of previous infection, immunosuppression, headache,

and related symptoms.

Perform neurologic assessment, including cranial nerve evaluation,

motor, and cognitive status.

NURSING DIAGNOSES

Acute Pain related to cerebral mass

Disturbed Thought Processes related to disease process

Risk for Injury related to neurologic deficits

Anxiety related to surgery, prognosis, and relapse

NURSING INTERVENTIONS
Relieving Pain

Administer pain medications as ordered.

Provide comfort measures, such as quiet environment, positioning with

head slightly elevated, and assistance with hygiene needs.

Provide passive relaxation techniques, such as soft music and

backrubs.

Promoting Thought Processes

Frequently monitor vital signs, LOC, orientation, and seizure activity.

Report changes, which can signal increased ICP, to health care

provider.

Administer medications as ordered, noting response and adverse

reactions.

Prepare patient for repeated diagnostic tests to evaluate response to

therapy and surgery.

Minimizing Neurologic Deficits

Maintain a safe environment with side rails up, call light within reach,
and frequent observation.

Evaluate other cranial nerve function, and report changes.

Refer to occupational therapy, speech therapist, or other rehabilitation

specialist to provide adjunct to nursing rehabilitation.

Reducing Anxiety

Prepare patient and family for surgery when indicated. Encourage

discussion with surgeon to understand risks, benefits of the procedure.

Explain postoperative progression and nursing care (see page 484).

Community and Home Care Considerations

Patient follow-up is essential for sinusitis, otitis media, respiratory

infections, and other infectious processes that may result in a brain
abscess.
Continue with rehabilitation to regain or compensate for neurologic
deficits.
Continue with pharmacologic regimen in community setting.
Observe for recurrence of brain and spinal abscesses.

Patient Education and Health Maintenance

Maintain wellness with vaccinations, immunizations, and overall health.

Reinforce need for dental procedure prophylaxis to avoid dental
abscesses.
Instruct in need for immediate assessment of head wounds.

EVALUATION: EXPECTED OUTCOMES

Verbalizes reduced pain

Oriented to person, place, and time; follows simple commands

No injury related to neurologic deficits

Reduced anxiety regarding disease process and procedures

HERPES SIMPLEX VIRUS ENCEPHALITIS

Encephalitis is an acute inflammatory process of the brain tissue. Herpes

simplex virus (HSV) is the most common cause of acute encephalitis in the
United States (Levitz, 1998). There are two herpes simplex viruses, HSV-1
and HSV-2. HSV-1 typically affects children and adults.
PATHOPHYSIOLOGY
There are two possible modes of HSV-1 infection.
Primary HSV-1 infection of the buccal mucosa occurs, followed by
retrograde spread along the trigeminal nerve to the brain. It is also
believed that latent virus in brain tissue may reactivate and result in
encephalitis (Roos, 1999).
HSV-2 most commonly affects neonates and is discussed in pediatric
textbooks (Gutierrez & Prober, 1998).
CLINICAL MANIFESTATIONS

HSV-1 encephalitis causes

o Inflammation and necrosis in the temporal lobe, frontal lobe, and
limbic system.
o The initial symptoms include fever, headache, confusion, and
behavioral abnormalities (Roos, 1999).
o Focal neurologic symptoms reflect the areas of cerebral
inflammation
o Cerebral necrosis and
o Include behavioral change, focal seizures, dysphasia, hemiparesis,
and altered level of consciousness.
o Focal symptoms are present within 7 days of infection and progress
for 14 to 21 days.

ASSESSMENT AND DIAGNOSTIC FINDINGS

Diagnose HSV Encephalitis:
Neuroimaging studies
MRI is the neuroimaging study of choice in the diagnosis of HSV
encephalitis as it can help identify lesions in the temporal lobe.
The electroencephalography (EEG) demonstrates a specific wave
pattern in 66% of cases of biopsy-proven HSV encephalitis.
CSF examination. CSF reveals a high opening pressure and low glucose
and high protein levels.
Viral cultures are almost always negative.
The polymerase chain reaction (PCR) technique has been used to
diagnose HSV encephalitis (Roos, 1999). PCR will identify the DNA

bands of the HSV specifically. The validity of PCR is very high between
the third and tenth day of symptom onset.
MEDICAL MANAGEMENT
Acyclovir (Zovirax), an antiviral agent, is the medication of choice in
HSV treatment (Karch, 2002). The mode of action is the inhibition of
viral DNA replication. It is usually well tolerated by the patient. To
prevent relapse, treatment should continue for up to 3 weeks. Slow
administration over 1 hour will prevent crystallization of the medication
in the urine. The usual dose of acyclovir is decreased if the patient has
a history of renal insufficiency (Karch, 2002).
In the rare case of acyclovir resistance, foscarnet sodium (Foscavir) is
prescribed (Roos, 1999).
NURSING MANAGEMENT
Assessment of neurologic function is key to monitoring the progression
of disease.
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 level of consciousness require care directed
at injury prevention and safety.
Nursing care addressing patient and family anxiety is ongoing
throughout the illness.
Monitoring of blood chemistry test results.
Monitor I&O. Urinary output will alert the nurse to the presence of renal
complications related to acyclovir therapy.

ARTHROPOD-BORNE VIRUS ENCEPHALITIS

Arthropod vectors transmit several types of viruses that cause encephalitis.
The primary vector in North America is the mosquito. Arbovirus infection
occurs in specific geographic areas during the summer and fall. The four
types of arboviral encephalitis that occur in North America are LaCrosse
encephalitis, St. Louis encephalitis, Western equine encephalitis, and Eastern
equine encephalitis (Roos, 1999).
Pathophysiology
Viral replication occurs at the site of the mosquito bite. If adequate virus is
inoculated, a viremia ensues. The virus gains access to the central nervous
system (CNS) via the cerebral capillaries. It spreads from neuron to neuron,
predominantly affecting the cortical gray matter, the brain stem, and the
thalamus. Meningeal exudates compound the clinical presentation by
irritating the meninges and increasing ICP (Roos, 1999).
Clinical Manifestations

All arboviral encephalitis begins with a flu-like prodrome, but specific

neurologic manifestations depend on the viral type.
LaCrosse encephalitis, for example, may present with focal neurologic
symptoms and seizures. Mortality is low but residual seizures may
occur.
A unique clinical feature of St. Louis encephalitis is SIADH with
hyponatremia. The mortality rate is 10% to 20%.
The clinical manifestations of Eastern equine encephalitis are acute
and carry a high mortality rate of 50% to 75% (Roos, 1999). Although
the clinical manifestations of Western equine encephalitis are
nonspecific, the morbidity rate is high.

Assessment and Diagnostic Findings

Neuroimaging is not useful in diagnosing many types of encephalitis.

In Eastern equine encephalitis, however, CT scan and MRI may reveal
lesions in the basal ganglia and thalamus (Roos, 1999).
The CSF analysis shows a normal glucose level, elevated protein level,
and polymorphonuclear leukocytic pleocytosis. St. Louis, Eastern
equine, and Western equine encephalitis viruses are rarely isolated in
the CSF (Roos, 1999).

The age of the patient is important information in making a specific

viral diagnosis.
o La Crosse virus encephalitis is the most common pediatric
arboviral encephalitis.
o St. Louis encephalitis affects adults over 50 years of age
o Eastern equine encephalitis is not age-specific (Roos, 1999).
o Western equine encephalitis can present as pediatric encephalitis
but is less prevalent.

Medical Management
There is no specific medication for arboviral encephalitis. Medical
management is aimed at controlling seizures and increased ICP (Roos, 1999)
Nursing Management

If the patient is very ill, hospitalization may be required.

The nurse carefully assesses neurologic status and identifies
improvement or deterioration in the patients condition.
Injury prevention is key in light of the potential for falls or seizures.
Arboviral encephalitis may result in death or life-long residual health
issues.
The family will need support and teaching to cope with these
outcomes.
Public education addressing the prevention of arboviral encephalitis is
a key nursing role.
Clothing that provides coverage and insect repellents should be used
in high-risk areas.
Community mosquito control is advocated.