Transcript Acute stroke

NEUROLOGICAL
EMERGENCIES
Medical coma
Traumatic brain injury
Acute stroke
Delirium
Acute behaviour disturbances and their management
Tonic-clonic status epilepticus
Raised intracranial pressure
Management of subarachnoid haemorrhage
Cerebral infection
Acute spinal cord compression
Acute neuromuscular respiratory paralysis
coma
The Anatomy and Physiology of Coma
Almost all instances of diminished alertness can be traced to widespread abnormalities of the
cerebral hemispheres or to reduced activity of a special thalamocortical alerting system termed the
reticular activating system (RAS).
The proper functioning of this system, its ascending projections to the cortex, and the cortex itself
are required to maintain alertness and coherence of thought.
It follows that the principal causes of coma are (1) lesions that damage the RAS in the upper
midbrain or its projections; (2) destruction of large portions of both cerebral hemispheres; and (3)
suppression of reticulocerebral function by drugs, toxins, or metabolic derangements such as
hypoglycemia, anoxia, uremia, and hepatic failure.
Pupillary enlargement with loss of light reaction and loss of vertical and adduction movements of
the eyes suggests that the lesion is in the upper brainstem.
Conversely, preservation of pupillary light reactivity and of eye movements absolves the upper
brainstem and indicates that widespread structural lesions or metabolic suppression of the cerebral
hemispheres is responsible for coma
Confusion.
“Disturbance of consciousness characterised by impaired capacity to think clearly and to
perceive, respond to and remember current stimuli; there is also disorientation.”
Confusion involves a generalised disturbance of cortical cerebral function which is usually
associated with considerable electroencephalographic (EEG) abnormality.
Intervening state between normal consciousness and confusion, that of “clouding of
consciousness”.
Delirium.
“A state of much disturbed consciousness with motor restlessness, transient hallucinations,
Disorientation and delusions.”
Obtundation
. “A disturbance of alertness associated with psychomotor retardation.”
Stupor.
“A state in which the patient, though not unconscious, exhibits little or no spontaneous
activity.” Although the individual appears to be asleep he or she will awaken to vigorous
stimulation but show limited motor activities and usually fail to speak.
Coma.
“A state of unrousable psychologic unresponsiveness in which the subject lies with eyes closed
and shows no psychologically understandable response to external stimulus or inner need.”
This may be shortened to “a state of unrousable unresponsiveness” which implies both the
defect in arousal and in awareness of self or environment manifest as an inability to respond.
Vegetative state.
“A clinical condition of unawareness of self and environment in which the patient breathes
spontaneously, has a stable circulation and shows cycles of eye closure and eye opening which may
simulate sleep and waking.
This may be a transient stage in the recovery from coma or it may persist until death.”
When the cortex of the cerebral hemispheres of the brain recovers more slowly than the brain stem
or when the cortex is irreversibly damaged there will arise a situation in which the patient enters a
vegetative state without cognitive function.
This may be a transient phase through which patients in coma pass as they recover or deteriorate but,
commonly after anoxic injuries to the brain, a state develops in which the brain stem recovers
function but the cerebral hemispheres are not capable of recovery. This is the “persistent vegetative
state”
Akinetic mutism.
This term has been used to define a similar condition of unresponsiveness but apparent
alertness together with reactive alpha and theta EEG rhythms in response to stimuli.
The major difference from the vegetative state, in which there is tone in the muscles
and extensor or flexor responses, is that patients with akinetic mutism have flaccid tone and are
unresponsive to peripheral pain.
It is thought that this state is due to bilateral frontal lobe lesions, diffuse cortical lesions, or lesions of
the deep grey matter.
The locked-in syndrome.
a de-efferented state caused by a bilateral ventral pontine lesion involving damage to the corticospinal, cortico-pontine, and cortico-bulbar tracts.
The patient has total paralysis below the level of the third nerve nuclei and, although able to open,
elevate and depress the eyes, has no horizontal eye movements and no other voluntary movements.
The diagnosis depends upon the clinician being able to recognise that the patient can open the eyes
voluntarily and allow them to close and can signal assent or dissent, responding numerically by
allowing the eyelids to fall.
Similar states are occasionally seen in patients with severe polyneuropathy, myasthenia gravis, and
after the use of neuromuscular blocking agents
Pseudo-coma.
Rarely, patients who appear in coma without structural, metabolic, toxic, or psychiatric disorder
being apparent can be shown by tests of brain stem function to have intact brain stem activity and
corticopontine projections and not to be in coma.
Coma Due to Metabolic Disorders
Cerebral neurons are fully dependent on cerebral blood flow (CBF) and the delivery of oxygen and
glucose.
CBF is 75 mL per 100g/min in gray matter and 30 mL per 100 g/min in white matter (mean 55
mL per 100 g/min);
oxygen consumption is 3.5 mL per 100 g/min, and glucose utilization is 5 mg per 100 g/min.
Brain stores of glucose provide energy for 2 minutes after blood flow is interrupted, and oxygen
stores last 8–10 seconds after the cessation of blood flow.
Simultaneous hypoxia and ischemia exhaust glucose more rapidly.
Unlike hypoxia-ischemia, which causes neuronal destruction, most metabolic disorders such as
hypoglycemia, hyponatremia, hyperosmolarity, hypercapnia, hypercalcemia, and hepatic and renal
failure cause only minor neuropathologic changes. The causes of the reversible effects of these
conditions on the brain are not understood but may result from impaired energy supplies, changes in
ion fluxes across neuronal membranes, and neurotransmitter abnormalities.
Coma and seizures are common accompaniments of large shifts in sodium and water balance in the
brain
These changes in osmolarity arise from systemic medical disorders, including diabetic ketoacidosis,
the nonketotic hyperosmolar state, and hyponatremia from any cause (e.g., water intoxication,
excessive secretion of antidiuretic hormone, or atrial natriuretic peptides).
Sodium levels <125 mmol/L induce confusion, and <115 mmol/L are associated with coma and
convulsions.
In hyperosmolar coma, the serum osmolarity is generally >350 mosmol/L.
Hypercapnia depresses the level of consciousness in proportion to the rise in carbon dioxide (co2)
tension in the blood.
In all of these metabolic encephalopathies, the degree of neurologic change depends to a large extent on the rapidity
with which the serum changes occur.
reflect derangements of CNS biochemistry, membrane function, and neurotransmitters.
Differential Diagnosis of Coma
1. Diseases that cause no focal or lateralizing neurologic signs, usually with normal brainstem
functions; CT scan and cellular content of the CSF are normal
a. Intoxications: alcohol, sedative drugs, opiates, etc.
b. Metabolic disturbances: anoxia, hyponatremia, hypernatremia, hypercalcemia, diabetic
acidosis, nonketotic hyperosmolar hyperglycemia, hypoglycemia, uremia, hepatic coma,
hypercarbia, addisonian crisis, hypo- and hyperthyroid states, profound nutritional deficiency
c. Severe systemic infections: pneumonia, septicemia, typhoid fever, malaria, WaterhouseFriderichsen syndrome
d. Shock from any cause
e. Postseizure states, status epilepticus, subclinical epilepsy
f. Hypertensive encephalopathy, eclampsia
g. Severe hyperthermia, hypothermia
h. Concussion
i. Acute hydrocephalus
2. Diseases that cause meningeal irritation with or without fever, and with an excess of WBCs or
RBCs in the CSF, usually without focal or lateralizing cerebral or brainstem signs; CT or MRI shows
no mass lesion
a. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous malformation, trauma
b. Acute bacterial meningitis
c. Viral encephalitis
d. Miscellaneous: fat embolism, cholesterol embolism, carcinomatous and lymphomatous
meningitis, etc.
3. Diseases that cause focal brainstem or lateralizing cere-bral signs, with or without changes in the
CSF; CT and MRI are abnormal
a. Hemispheral hemorrhage (basal ganglionic, thalamic) or infarction (large middle cerebral artery
territory) with secondary brainstem compression
b. Brainstem infarction due to basilar artery thrombosis or embolism
c. Brain abscess, subdural empyema
d. Epidural and subdural hemorrhage, brain contusion
e. Brain tumor with surrounding edema
f. Cerebellar and pontine hemorrhage and infarction
g. Widespread traumatic brain injury
h. Metabolic coma (see above) with preexisting focal damage
i. Miscellaneous: Cortical vein thrombosis, herpes simplex encephalitis, multiple cerebral emboli
due to bacterial endocarditis, acute hemorrhagic leukoencephalitis, acute disseminated
(postinfectious) encephalomyelitis, thrombotic thrombocytopenic purpura, cerebral vasculitis,
gliomatosis cerebri, pituitary apoplexy, intravascular lymphoma, etc.
Approach to the Patient: Coma
History
In many cases, the cause of coma is immediately evident (e.g., trauma, cardiac arrest, or reported
drug ingestion). In the remainder, certain points are especially useful:
(1) the circumstances and rapidity with which neurologic symptoms developed;
(1) the antecedent symptoms (confusion, weakness, headache, fever, seizures, dizziness, double
vision, or vomiting);
(1) the use of medications, illicit drugs, or alcohol; and
(1) chronic liver, kidney, lung, heart, or other medical disease. Direct interrogation of family,
observers, and ambulance technicians on the scene, in person or by telephone, is an important
part of the evaluation.
General Physical Examination
Fever suggests a systemic infection, bacterial meningitis, encephalitis, heat stroke, neuroleptic
malignant syndrome, malignant hyperthermia due to anesthetics or anticholinergic drug
intoxication; only rarely is it attributable to a lesion that has disturbed hypothalamic
temperature-regulating centers ("central fever"). A slight elevation in temperature may follow
vigorous convulsions.
Hypothermia is observed with exposure; alcoholic, barbiturate, sedative, or phenothiazine
intoxication; hypoglycemia; peripheral circulatory failure; or extreme hypothyroidism.
Hypothermia itself causes coma only when the temperature is <31°C (87.8°F).
Tachypnea may indicate systemic acidosis or pneumonia or rarely infiltration of the brain with
lymphoma.
Aberrant respiratory patterns that reflect brainstem disorders are discussed below.
Marked hypertension suggests hypertensive encephalopathy, but it may also be secondary to a
rapid rise in intracranial pressure (ICP) (the Cushing response) most often after cerebral
hemorrhage or head injury.
Hypotension is characteristic of coma from alcohol or barbiturate intoxication, internal hemorrhage,
myocardial infarction, sepsis, profound hypothyroidism, or Addisonian crisis.
The funduscopic examination can detect subarachnoid hemorrhage (subhyaloid hemorrhages),
hypertensive encephalopathy (exudates, hemorrhages, vessel-crossing changes, papilledema), and
increased ICP (papilledema).
Cutaneouspetechiae suggest thrombotic thrombocytopenic purpura, meningococcemia, or a bleeding
diathesis associated with an intracerebral hemorrhage.
Cyanosis, reddish or anemic skin coloration are other indications of an underlying systemic disease
responsible for the coma.
Neurologic Examination
The patient should first be observed without intervention by the examiner. Tossing about in the bed,
reaching up toward the face, crossing legs, yawning, swallowing, coughing, or moaning reflect a
drowsy state that is close to normal awakeness.
Lack of restless movements on one side or an outturned leg suggests a hemiplegia. Intermittent
twitching movements of a foot, finger, or facial muscle may be the only sign of seizures.
Multifocal myoclonus almost always indicates a metabolic disorder, particularly uremia, anoxia, drug
intoxication (especially with lithium or haloperidol), or a prion disease .
In a drowsy and confused patient, bilateral asterixis is a certain sign of metabolic encephalopathy or
drug intoxication.
Decorticate rigidity and decerebrate rigidity, or "posturing," describe stereotyped arm and leg movements
occurring spontaneously or elicited by sensory stimulation.
Flexion of the elbows and wrists and supination of the arm (decortication) suggests bilateral damage
rostral to the midbrain,
whereas extension of the elbows and wrists with pronation (decerebration) indicates damage to
motor tracts in the midbrain or caudal diencephalon.
The less frequent combination of arm extension with leg flexion or flaccid legs is associated with
lesions in the pons.
In fact, acute and widespread disorders of any type, regardless of location, frequently cause limb
extension, and almost all extensor posturing becomes predominantly flexor as time passes
Pupillary Signs
Reactive and round pupils of midsize (2.5–5 mm) essentially exclude midbrain damage, either
primary or secondary to compression.
One enlarged and poorly reactive pupil (>6 mm) signifies compression or stretching of the third
nerve from the effects of a cerebral mass above.
Enlargement of the pupil contralateral to a hemispheral mass may occur but is infrequent.
An oval and slightly eccentric pupil is a transitional sign that accompanies early midbrain–third nerve
compression.
The most extreme pupillary sign, bilaterally dilated and unreactive pupils, indicates severe midbrain
damage, usually from compression by a supratentorial mass.
Ingestion of drugs with anticholinergic activity, the use of mydriatic eye drops, and direct ocular
trauma are among the causes of misleading pupillary enlargement
Ocular Movements
Horizontal divergence of the eyes at rest is normal in drowsiness. As coma deepens, the ocular axes
may become parallel again.
Spontaneous eye movements in coma often take the form of conjugate horizontal roving.
This finding alone exonerates damage in the midbrain and pons and has the same significance as
normal reflex eye movements .
Conjugate horizontal ocular deviation to one side indicates damage to the pons on the opposite side
or alternatively, to the frontal lobe on the same side. This phenomenon is summarized by the
following maxim: The eyes look toward a hemispheral lesion and away from a brainstem lesion
. The eyes may occasionally turn paradoxically away from the side of a deep hemispheral lesion
("wrong-way eyes").
The eyes turn down and inward with thalamic and upper midbrain lesions, typically thalamic
hemorrhage.
.
"Ocular bobbing" describes brisk downward and slow upward movements of the eyes associated
with loss of horizontal eye movements and is diagnostic of bilateral pontine damage, usually from
thrombosis of the basilar artery.
"Ocular dipping" is a slower, arrhythmic downward movement followed by a faster upward
movement in patients with normal reflex horizontal gaze; it indicates diffuse cortical anoxic damage
Respiratory Patterns
These are of less localizing value in comparison to other brainstem signs.
Shallow, slow, but regular breathing suggests metabolic or drug depression.
Cheyne-Stokes respiration in its classic cyclic form, ending with a brief apneic period, signifies
bihemispheral damage or metabolic suppression and commonly accompanies light coma.
Rapid, deep (Kussmaul) breathing usually implies metabolic acidosis but may also occur with
pontomesencephalic lesions.
Tachypnea occurs with lymphoma of the CNS.
Agonal gasps are the result of lower brainstem (medullary) damage and are recognized as the
terminal respiratory pattern of severe brain damage.
Laboratory Studies and Imaging
chemical-toxicologic analysis of blood and urine,
cranial CT or MRI,
EEG, and CSF examination.
Arterial blood gas analysis
Toxicologic analysis
The EEG
Lumbar puncture
. Blood culture
Treatment: Coma
The immediate goal in a comatose patient is prevention of further nervous system damage.
Hypotension, hypoglycemia, hypercalcemia, hypoxia, hypercapnia, and hyperthermia should be
corrected rapidly.
An oropharyngeal airway is adequate to keep the pharynx open in a drowsy patient who is breathing
normally.
Tracheal intubation is indicated if there is apnea, upper airway obstruction, hypoventilation, or
emesis, or if the patient is liable to aspirate because of coma.
Mechanical ventilation is required if there is hypoventilation or a need to induce hypocapnia in order
to lower ICP.
IV access is established, and naloxone and dextrose are administered if narcotic overdose or
hypoglycemia are possibilities; thiamine is given along with glucose to avoid provoking Wernicke's
disease in malnourished patients.
In cases of suspected basilar thrombosis with brainstem ischemia, IV heparin or a thrombolytic
agent is often utilized, after cerebral hemorrhage has been excluded by a neuroimaging study.
The use of benzodiazepine antagonists offers some prospect of improvement after overdose of
soporific drugs and has transient benefit in hepatic encephalopathy.
Administration of hypotonic solutions should be monitored carefully in any serious acute brain
illness because of the potential for exacerbating brain swelling.
Cervical spine injuries must not be overlooked, particularly before attempting intubation or
evaluation of oculocephalic responses.
Fever and meningismus indicate an urgent need for examination of the CSF to diagnose meningitis.
If the lumbar puncture in a case of suspected meningitis is delayed, an antibiotic such as a thirdgeneration cephalosporin may be administered, preferably after obtaining blood cultures.
Establish the routine care of an unconscious patient regard-less of the cause
(a) Observations: assessment every 15–30 minutes of vital functions, pupils and Glasgow Coma
Scale, to monitor improvement or deterioration in the patient’s condition.
(b) Airway, ventilation, blood gases.
(c) Blood pressure, to maintain adequate perfusion of the body, particularly of the brain and kidneys
.
(d) Fluid and electrolyte balance.
(e) Nutrition and hydration.
(f) Avoidance of sedative or strong analgesic drugs.
(g) General nursing care of eyes, mouth, bladder, bowels, skin and pressure areas, passive limb
mobilization to prevent venous stagnation and contractures, chest physiotherapy
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Traumatic brain injury
General Medical Measures
If coma persists for more than 48 h, a nasogastric tube should be passed and fluids and nutrition
givenby this route.
Agents that reduce gastric acid production—or theequivalent, antacids by stomach tube to keep
gastric acidity at apH above 3.5—are of value in preventing gastric hemorrhage.
Theprophylactic use of anticonvulsant drugs, as discussed earlier, un-der “Posttraumatic Epilepsy,”
has recently been favored, but thereis no evidence that delayed epileptic seizures are reduced Only if
there has been a seizure are anti-convulsants given.
Restlessness is controlled by diazepam or a similar sedative,but only if careful nursing fails to quiet
the patient and provide sleep for a few hours at a time..
Fever is counteracted by antipyretics such as ac-etaminophen, and, if necessary, by a cooling blanket.
The use of morphine or bromocriptine to quiet episodes of vigorous extensor posturing and
accompanying adrenergic activity
decompressive craniectomy
Acute stroke
Swallowing, hydration, and nutrition
Glycaemic control
Pyrexia
Pressure areas
Bladder management
Venous thromboembolism prophylaxis
Epileptic seizures
Treatment of acute ischaemic stroke
Thrombolysis
Anticoagulant
Cardiovascular changes in late status epilepticus
Pulmonary hypertension and oedema are frequent, even in the presence of systemic hypotension.
Pulmonary artery pressures can rise to dangerous levels, well in excess of the osmotic pressure of
blood, causing oedema and stretch injuries to lung capillaries.
Cardiac arrhythmias in status epilepticus are the result of direct seizure-related autonomic
activation, catecholamine release, hypoglycaemia, lactic acidosis, electrolyte disturbance, or
cardiotoxic therapy.
The autonomic effects are sometimes caused by simultaneous discharges in sympathetic and
parasympathetic pathways.
Intravenous sedatives depress cardiac function, and the drug effects can be potentiated by preexisting compromise of cardiac function.
In spite of the greatly increased demand, cardiac output can fall due to decreasing left ventricular
contractility and stroke volume,20 causing cardiac failure.
noradrenaline and epinephrine release also contributes to the cardiac dysfunction, arrhythmia,
and tachycardia.
Hyperpyrexia
acidosis (including lactic acidosis), hypoglycaemia, hypo/ hyperkalaemia, and hyponatraemia
Lactic acidosis is almost invariable in major status epilepticus, from its onset, due to
neuronal and muscle activity, the acceleration of glycolysis,tissue hypoxia, impaired respiration,
and catecholamine release.
Acute tubular necrosis due to myoglobinuria or dehydration, and occasionally fulminant renal
failure, may occur.
Hepatic failure is a not uncommon terminal event in status epilepticus, due to other
physiological disturbances, drug treatment, or underlying disease.
Rhabdomyolysis, resulting from persistent convulsive movements, can develop early in status
epilepticus and precipitate renal failure if severe, and can be prevented by artificial ventilation
and paralysing drugs.
Disseminated intravascular coagulation is another rare but serious complication of status
epilepticus, which usually requires urgent therapy.
Medical complications in tonic-clonic status epilepticus
Cerebral
Hypoxic/metabolic cerebral damage
Seizure-induced cerebral damage
Cerebral oedema and raised intracranial pressure
Cerebral venous thrombosis
Cerebral haemorrhage and infarction
Cardiovascular, respiratory, and autonomic
Hypotension
Hypertension
Cardiac failure, tachy- and bradyarrhythmia, arrest
Cardiogenic shock
Respiratory failure
Disturbances of respiratory rate and rhythm, apnoea
Pulmonary oedema, hypertension, embolism
Pneumonia, aspiration
Hyperpyrexia
Sweating, hypersecretion, tracheobronchial obstruction
Peripheral ischaemia
Metabolic
Dehydration
Electrolyte disturbance (especially hyponatraemia, hyperkalaemia,
hypoglycaemia)
Acute renal failure (especially acute tubular necrosis)
Acute hepatic failure
Acute pancreatitis
Other
Disseminated intravascular coagulopathy/multiorgan failure
Rhabdomyolysis
Fractures
Infections (especially pulmonary, skin, urinary)
Thrombophlebitis, dermal injury
General measures
For the new patient presenting as an emergency in status epilepticus, it is helpful to plan therapy in
a series of progressive phases
. General measures
1 (0–10 minutes)
Assess cardiorespiratory function
Secure airway and resuscitate
Administer oxygen
2 (0–60 minutes)
Institute regular monitoring
Emergency antiepileptic drug therapy
Set up intravenous lines
Emergency investigations
Administer glucose (50 ml of 50% solution) and/or intravenous thiamine (250 mg) as high potency
intravenous Pabrinex where appropriate
Treat acidosis if severe
3 (0–60/90 minutes)
Establish aetiology
Identify and treat medical complications
Pressor therapy where appropriate
4 (30–90 minutes)
Transfer to intensive care Establish intensive care and EEG monitoring
Initiate seizure and EEG monitoring
Initiate intracranial pressure monitoring where appropriate
Initiate long term, maintenance, antiepileptic therapy
These four stages should be followed chronologically; the first and second within 10 minutes, and
stage 4 (transfer to intensive care unit) in most settings within 60–90 minutes of presentation.
Suggested emergency antiepileptic drug regimen for status in newly presenting adult patients
Premonitory stage (pre-hospital)
Diazepam 10–20 mg given rectally, repeated once 15 minutes later if status continues to threaten
If seizures continue, treat as below Early status
Lorazepam (IV) 0·07 mg/kg (usually a 4 mg bolus, repeated once
after 10–20 minutes; rate not critical)
If seizures continue 30 minutes after first injection, treat as below
Established status
Phenytoin infusion at a dose of 15–18 mg/kg at a maximum rate of 50 mg/min or fosphenytoin
infusion at a dose of 15–20 mg
PE/kg at a maximum rate of 100 mg PE/minute and/or
Phenobarbitone bolus of 10 mg/kg at a rate of 100 mg/min
(usually 700 mg over seven minutes in an adult)
Refractory status
General anaesthesia, with propofol, midazolam, or thiopentone.
Anaesthetic continued for 12–24 hours after the last clinical or electrographic seizure, then dose
tapered
In the above scheme, the refractory stage (general anaesthesia) is reached 60/90 minutes after the
initial therapy. This scheme is suitable for usual clinical hospital settings. In some situations,
general anaesthesia should be initiated earlier and, occasionally, should be delayed.
Common reasons for the failure of emergency drug therapy to control seizures in status
epilepticus
Inadequate emergency antiepileptic drug therapy (especially the administration of drugs at too low
a dose)
Failure to initiate maintenance antiepileptic drug therapy (seizures will recur as the effect of
emergency drug treatment wears off)
Hypoxia, hypotension, cardiorespiratory failure, metabolic disturbance
Failure to identify the underlying cause
Failure to identify other medical complications (including hyperthermia, disseminated intravascular
coagulation, hepatic failure)
Misdiagnosis (pseudostatus epilepticus is a common differential diagnosis that is often missed)
Cerebral infection
Viral causes of cerebral infection
Meningitis
Enteroviruses
Encephalitis
Herpes simplex
Echo
Varicella zoster virus
Polio
Cytomegalovirus
Coxsackie
Epstein–Barr virus
Herpes simplex 2
HIV
Lymphocytic choriomeningitis virus
Mumps
Varicella zoster virus
Measles
Mumps
Rabies
HIV
Arboviruses
Bacterial meningitis: causal organisms
Neonates
Gram negative bacilli
Streptococci (usually group B)
Listeria monocytogenes
Children
Meningococci
Pneumococci
Adults
Pneumococci
Meningococci
Staphylococci
Listeria monocytogenes
Streptococci
Mycobacterium tuberculosis can affect children and adults
Bacteria linked to underlying causes of meningitis
Cause
Diabetes mellitus
Organism
Pneumococci
Staphylococci
Gram negative bacilli
Alcohol
Pneumococci
Sickle cell disease
Pneumococci
Skull fracture
Dural fistula/CSF leak
CNS shunt
Pregnancy/childbirth
Gram negative bacilli
Staphylococci
Pneumococci
Gram negative bacilli
Staphylococcus epidermidis
Listeria
Streptococci
Cell mediated immune defect
Humoral immune defect
Neutropenia
Listeria
Pneumococci
Haemophilus
Meningococci
Pseudomonas
Management of cerebral infection
• Cerebral infection may be due to meningitis, encephalitis, or focalspace occupation.
• Viral meningitis must be distinguished from partly treated bacterial and other causes of aseptic
meningitis.
• Viral encephalitis in the UK and Europe is usually due to herpes simplex which must be treated
quickly with intravenous acyclovir.
However other causes must be considered including, especially in other parts of the world, rabies
and arborviruses.
• At seroconversion HIV infection may cause aseptic meningoencephalitis and later it may cause
HIV encephalopathy.
AIDS is associated with cytomegalovirus, toxoplasmosis, progressive multifocal
leukoencephalopathy, and tuberculosis.
• Bacterial meningitis is a serious neurological emergency. The commonest causative organisms,
except in neonates and the elderly, are Neisseria meningitidis and Streptococcus pneumoniae.
Immediate treatment should be given to adult patients with ceftriaxone.
• Cerebral malaria is fatal in 25–50% of cases. Patients with febrile illnesses returning from malarial
areas should be suspected of having malaria. Quinine is the drug of choice for severe malaria.
• Cerebral abscess may be caused by a wide variety of organisms but Streptococci are the
commonest in non-immunocompromised hosts. Most patients require surgical drainage and
empirical treatment with antibiotics. These usually include a third generation cephalosporin,
metranidazole, and, if Staphylococci are suspected, vancomycin.
Cerebral sarcoid. Gadolinium-enhanced MRIof the brain.
Sarcoid lesions coat the base of the brain and cerebellum and surround the pituitary stalk.
The patient had pulmonary sarcoid, marked abulia, and panhypopituitarism.