DD KOMA

KOMA DIENSEFALIK
1. Intracerebral Hemorrhage
tanda khas:
• Headache, nausea, vomiting
• Hypertension
• Focal neurologic deficit with signs of increased ICP
Intracerebral hemorrhage (ICH) can be classified as:
a. primary (unrelated to congenital or acquired lesions)
related to hypertension and occurs in characteristic areas of the brain: deep white matter, basal ganglia,
thalamus, pons, and cerebellum
b. secondary (related to vascular malformations, tumors, or other lesions).
more variable in location. caused by: Smoking, advanced age, and anticoagulant use are other risk
factors for ICH
Clinical Findings
Table 1. Primary ICH syndromes
Location Findings
Basal ganglia Contralateral motor deficits, gaze paresis, aphasia
Thalamus Contralateral sensory loss
Cerebellum Nausea, vomiting, ataxia, nystagmus, AMS, ipsilateral gaze/facial palsy
Pons Coma, pinpoint pupils, autonomic instability, quadriplegia, altered respiratory
patterns
- Patients with large areas of hemorrhage are often comatose on arrival.
- Headache is universally present in awake patients and may accompany other signs of increased ICP.
- Seizures occur in 10% of all ICH but in 50% of patients with lobar hemorrhage.
- Most patients are hypertensive on presentation, even if previously normotensive.
- CT scan is the diagnostic study of choice.
Treatment & Disposition
Care is primarily supportive and aimed at reducing ICP and controlling blood pressure. Aggressive blood
pressure control using IV labetalol should be instituted, with a target MAP <130 mm Hg for patients with a
history of hypertension. CPP should be maintained above 70. Patients on anticoagulants should receive
reversal agents (FFP and vitamin K for warfarin, protamine for heparin) promptly. Activated factor VII may
be beneficial in all cases, including noncoagulopathic ICH, but is not yet approved for this indication.
Hemorrhages in typical locations may not need further diagnostic evaluation and are rarely amenable to
surgery. Younger patients with no clear source of hemorrhage should be considered for cerebral
angiography and possible surgery. Symptomatic cerebellar hemorrhage requires surgery. All patients
should be admitted for further care.

2. Subdural Hematoma
ESSENTIALS OF DIAGNOSIS
• Headache
• Confusion
• Depressed level of consciousness
• Hyperdense crescent-shaped (biconcave) extra-axial collection of blood on CT scan
General Considerations
The possibility of subdural hematoma must be considered in any comatose patient. Trauma is the most
common cause, but in about 25% of cases, there is no history or evidence of trauma. Elderly patients are
particularly likely to present with absent or trivial trauma.
Clinical Findings
Symptoms and signs are notoriously nonspecific, nonlocalizing, or absent and may be either stable or
rapidly progressive. The frequency of bilateral hematomas makes localization of the lesion even more
difficult, as does the coexistence of associated cerebral contusion. Hemiparesis, when present, is
contralateral to the lesion in approximately 60% of cases, and ipsilateral pupillary dilatation occurs in
approximately 75% of cases. Seizures may occur. CT scan is the diagnostic study of choice, revealing a
hyperdense extra-axial crescent-shaped collection of blood, which rarely crosses the falx or tentorium.
Subacute lesions may appear as isodense, and patients receiving anticoagulation may demonstrate layering
of blood in acute-on-chronic subdural hematoma.
Treatment & Disposition
 Immediate hospitalization and emergency neurosurgical consultation are indicated. Unstable patients with
rapid worsening (minutes to hours) of their neurologic deficit thought to be due to an expanding subdural
hematoma should be treated for increased ICP as discussed previously. Steroids have not been shown to be
beneficial.

3. Epidural Hematoma
ESSENTIALS OF DIAGNOSIS
• Headache
• History of trauma with overlying skull fracture
• Classic lucid interval: "talk and die"
• Lens-shaped (biconvex) extra-axial collection of blood on CT scan
General Considerations
Epidural hematoma is a collection of blood between the dura and the inner table of the skull and occurs
almost exclusively in the setting of trauma. The majority of epidural hematomas occur in the
temporoparietal region secondary to laceration of the middle meningeal artery. Occipital epidural
hematomas may progress rapidly and extend beneath the tentorium, resulting in apnea.
Clinical Findings
Symptoms are progressive. The classic presentation of head trauma followed by a brief loss of
consciousness, return to alertness, then worsening headache and vomiting with subsequent coma is seen in
only 1/5 of patients. CT scan is the diagnostic study of choice, revealing a hyperdense lenticular (biconvex)
collection of blood that does not cross suture lines, differentiating it from a subdural hematoma. Ipsilateral
pupillary dilation and contralateral hemiparesis are ominous findings suggestive of impending herniation.
Treatment & Disposition
Immediate neurosurgical consultation is required. In the event a neurosurgeon or CT confirmation of the
diagnosis is unavailable and the patient is herniating, a burr hole performed ipsilateral to the area of
trauma (or to the dilated pupil if external trauma is not apparent) may be life-saving. Care is otherwise
supportive and aimed at decreasing ICP.

4. Cerebral Infarction
ESSENTIALS OF DIAGNOSIS
• Hemiparesis
• Hemisensory losses
• Aphasia (dominant hemisphere)
General Considerations
The brain swelling of cerebral edema following massive hemispheric infarction can produce contralateral
hemispheric compression or transtentorial herniation that will result in coma. Such cerebral swelling
becomes maximal 48-72 hours after the infarct.
Clinical Findings
The principal findings are hemiparesis or hemisensory loss (and aphasia if the dominant hemisphere is
involved). Evolving transtentorial herniation progresses slowly over many hours or several days to stupor
and coma.
Treatment & Disposition
Hemicraniectomy may be life-saving in younger patients. Patients who are comatose from massive cerebral
infarction have likely progressed to coma secondary to increased ICP rather than the infarction itself, and
initial treatment is supportive and aimed at lowering ICP. Blood pressure management is controversial; in
severe arterial hypertension (MAP >120 mm Hg), IV β-blockers (e.g., labetalol) are preferred over
nitroprusside to reduce the MAP up to 25%.

5. Basilar Artery Occlusion

ESSENTIALS OF DIAGNOSIS
• Coma, altered mental status
• Respiratory pattern irregular
• Pupillary abnormalities, absent or abnormal horizontal eye movements
• Hemiparesis, hyperreflexia, positive Babinski sign
General Considerations
Basilar artery thrombosis and embolic occlusion are relatively common vascular syndromes that cause
coma because of direct involvement of the penetrating arteries supplying the central core of the brain stem.
Patients are usually elderly and often have a history of hypertension or transient ischemic attacks or
evidence of other atherosclerotic vascular disease.
 Clinical Findings
Basilar artery transient ischemic attacks are characterized by (in order of frequency of occurrence)
dizziness, diplopia, weakness and ataxia, slurred speech, and nausea and vomiting. Basilar artery occlusion
causes coma in half of affected patients, and almost all present with some alteration of consciousness. Focal
subtentorial signs are present from the onset, and the respiratory pattern is irregular. Pupillary
abnormalities vary with the site of the lesion and include poorly reactive pupils of normal size (3 mm),
pupils fixed in mid position (5 mm), or pinpoint pupils. Skew deviation of the eyes is common. Horizontal
eye movements are absent or asymmetric during the doll's eye maneuver or caloric testing. Conjugate eye
deviation, if present, is directed away from the side of the lesion and toward the hemiparesis. Vertical eye
movements in response to the doll's eye maneuver may be intact. Symmetric or asymmetric motor signs
(hemiparesis, hyperreflexia, and Babinski sign) may be present. The CSF is free of blood.
Treatment & Disposition
Current opinion supports anticoagulation for progressive subtotal lesions, although evidence for the
efficacy of this treatment is inconclusive. Hospitalize the patient for treatment and supportive care. The
prognosis varies directly with the degree of brain-stem injury.

6. Brain Tumor
ESSENTIALS OF DIAGNOSIS
• Headache
• Focal weakness
• Altered mental status
• Seizures
• Papilledema
• CT scan, MRI findings
General Considerations
Coma is seldom the presenting symptom in primary or metastatic tumors of the CNS, although coma may
result from seizures induced by the tumors. Acute bleeding into a tumor may also result in coma secondary
to a sudden increase in ICP.
Clinical Findings
The patient typically has a history of days to weeks of headache, focal weakness, and altered or depressed
consciousness. Papilledema is present in 25% of cases. CT scan (noncontrast followed by contrast-
enhanced if needed) is the initial diagnostic study of choice.
Treatment & Disposition
Glucocorticoids are remarkably effective at reducing surrounding edema and should be initiated early in
consultation with neurosurgery. Hospitalization for supportive care and further evaluation is indicated.

7. Brain Abscess
ESSENTIALS OF DIAGNOSIS
• Fever (often low grade)
• Leukocytosis
• Contrast-enhanced CT scan or MRI findings of intracranial mass
General Considerations
Brain abscess accounts for only 2% of intracranial masses. Brain abscess should be considered in patients
who are immunocompromised who develop changes in mentation. Opportunistic organisms and
hematogenous seeding from dental infections is becoming more common.
Clinical Findings
Progression to stupor and coma may be rapid, occurring over days or, rarely, hours. Often the usual signs of
infection are absent. The temperature is normal in half of patients, and the white blood cell count is below
10,000/mL in over one-fourth of patients. CT scan (non-contrast followed by contrast-enhanced if needed)
or MRI will reveal almost all abscesses. Lumbar puncture is contra-indicated.
Treatment & Disposition
Initiate antibiotic therapy early, prior to imaging if possible when the clinical suspicion for CNS infection is
high. Antibiotic choice should cover anaerobes as well as aerobes, and coverage for fungal or other
organisms may be indicated depending on the patient's history. Empiric therapy with a combination of
vancomycin 1.0-1.5 g IV plus metronidazole 7.5 mg/kg IV plus a third- or fourth-generation cephalosporin
is indicated. Neurosurgical consultation and hospitalization are necessary, although many surgeons will
defer intervention initially.
METABOLIC ENCEPHALOPATHIES
ESSENTIALS OF DIAGNOSIS
• Progressive somnolence
• Intoxication, toxic delirium
• Agitation, stupor, coma
• Headache
• Symmetric neurologic findings
• Reactive pupils
• Hypoventilation, abnormal respiratory pattern
• Loss of extraocular movements
Clinical Findings
Metabolic encephalopathies are characterized by a period of progressive somnolence, intoxication, toxic
delirium, or agitation, after which the patient gradually sinks into a stuporous and finally comatose state.
Headache is not an initial symptom of metabolic encephalopathy except in the case of meningitis or poisoning
due to organophosphate compounds or carbon monoxide.
Neurologic examination fails to reveal focal hemispheric lesions (hemiparesis, hemisensory loss, aphasia)
before loss of consciousness. Neurologic findings are symmetric except in some patients with hepatic
encephalopathy and hypoglycemic coma, which may be accompanied by focal signs (especially hemiparesis)
that may alternate sides. Asterixis may be present.
The hallmark of metabolic encephalopathy is reactive pupils (a midbrain function) in the presence of impaired
function of the lower brain stem (e.g., hypoventilation, loss of extraocular movements), an anatomically
inconsistent set of abnormalities. Respiratory patterns in metabolic coma vary widely and may help establish
the cause of coma.
Treatment & Disposition
Treatment depends entirely on the cause of coma. All patients require hospitalization for supportive care and
specific therapy.
penyebab metabolic encephalopathy
1. Hypoglycemia
General Considerations
Abrupt hypoglycemia rapidly interferes with brain metabolism and quickly produces symptoms. Insulin
and oral hypoglycemic drug overdose are the most common causes of hypoglycemia.
Clinical Findings
Signs of sympathetic nervous system activity (tachycardia, sweating, and anxiety) may warn patients of
impending hypoglycemia, although these signs may be masked by β-blockers and may be absent in patients
with diabetic autonomic neuropathy. Common neurologic abnormalities are delirium, seizures, focal signs
that often alternate sides, stupor, and coma. Hypoglycemic coma may be tolerated for 60-90 minutes, but
once the stage of flaccidity with hyporeflexia has been reached, glucose administration within 15 minutes is
mandatory to avoid irreversible damage.
Treatment & Disposition
Give glucose, 50 mL of 50% solution intravenously (adult dose). Once the diagnosis of hypoglycemia is
confirmed by analysis of blood drawn before treatment, give an additional 50 mL as needed or begin an
infusion of dextrose 5% in water. Patients should be observed for 1-2 hours after glucose supplementation
has been discontinued to ensure that hypoglycemia does not recur before they are discharged from the
hospital. In some cases, hospitalization may be necessary, especially if hypoglycemia recurs despite
treatment or in the event of long-acting insulin or oral hypoglycemic agent overdose.

2. Hypoxemia
Clinical Findings
Hypoxemia produces brain damage only as a result of concomitant cerebral ischemia. Cerebral blood flow
diminishes and brain ischemia occurs when the arterial Po2 falls to 20-45 mm Hg. In cerebral anoxia due to
cardiac arrest, where the duration can be timed precisely, 4-6 minutes of asystole begins to result in
permanent CNS damage. Following asystole, the pupils dilate rapidly and become fixed, and tonic posturing
is observed. A few seizure-like tonic-clonic movements are common.
Treatment & Disposition
Treatment of hypoxemia depends on the cause. Support cardiac output and maintain arterial Po2 above 60
mm Hg by supplemental oxygen or mechanical ventilation. Hospitalize all patients for diagnosis and
treatment.

3. Drug Overdose
 Introduction
Drug overdose is one of the most common causes of coma in patients presenting to the emergency
department. Many drugs may be implicated, including sedative-hypnotics, opiates, tricyclic antidepressants,
and antiepileptics.
 Alcohol Intoxication
Alcohol intoxication produces a metabolic encephalopathy similar to that produced by sedative-
hypnotic drugs, although nystagmus during wakefulness and early impairment of lateral eye
movements are not as common. Peripheral vasodilatation is a prominent manifestation and produces
tachycardia, hypotension, and hypothermia.
In individuals who are not chronic alcoholics, stupor occurs when blood alcohol levels reach 250-300
mg/dL, and coma occurs when levels reach 300-400 mg/dL. Because alcohol has significant osmotic
pressure (100 mg/dL = 22.4 mOsm), alcohol intoxication is one cause of hyperosmolality.
Management is discussed in Chapter 45. Patients should be observed until improvement has occurred
with normal orientation and judgment, and satisfactory coordination. Hospitalize patients who have
abnormalities that would usually require hospitalization (e.g., metabolic abnormalities, Wernicke
encephalopathy).
 Narcotic Overdose
In narcotic overdose, hypoventilation is almost always present, along with pinpoint pupillary
constriction and absent extraocular movements in response to the doll's eye maneuver. Pinpoint pupils
are also associated with other disorders that must be ruled out: use of miotic eye drops, pontine
hemorrhage, Argyll-Robertson pupils from syphilis, and organophosphate insecticide poisoning.
Narcotic intoxication is confirmed by rapid pupillary dilation and awakening after administration of a
narcotic antagonist such as naloxone, 2 mg, by rapid IV injection. Note: Patients who have overdosed on
certain narcotics (e.g., propoxyphene) may not respond to 2 mg and may require 4 mg or more. The
duration of action of naloxone varies with the dose and route of administration. Repeat doses are
frequently necessary, especially following intoxication with long-acting narcotics (e.g., methadone).
 Gamma-Hydroxybutyrate
Gamma-Hydroxybutyrate is a CNS depressant and can induce coma. The drug has become popular at
rave parties and has also been called the "date rape drug." Detection of the drug is difficult, because
most of it is eliminated through the lungs. Treatment is primarily supportive and may involve
endotracheal intubation. Some patients require hospitalization for prolonged supportive care.

4. Hepatic Encephalopathy
Clinical Findings
Hepatic encephalopathy can occur in patients with severe acute or chronic liver disease. Jaundice need not
be present. In the patient with preexisting liver disease, encephalopathy may develop rapidly following an
acute insult such as gastrointestinal hemorrhage or infection. Patients with surgical portacaval shunts are
especially predisposed to encephalopathy.
Mental status is altered and ranges from somnolence to delirium or coma. There is increased muscle tone;
hyperreflexia is common. Prominent asterixis occurs in the somnolent patient. Seizures—generalized or
focal—occur infrequently. Ammonia levels correlate poorly with disease severity. Hyperventilation with
respiratory alkalosis is nearly universal and may be demonstrated by measuring arterial blood pH. CSF is
normal but may appear xanthochromic in patients with serum bilirubin levels higher than 4-6 mg/dL.
Treatment & Disposition
Emergency department care is supportive. Treatment aimed at decreasing intestinal ammonia absorption
(lactulose, neomycin) may be initiated but should not take the place of hospitalization for definitive
treatment.

5. Hyponatremia
Introduction
Delirium and seizures are common presenting features of hyponatremia. Hyponatremia may cause
neurologic symptoms when serum sodium levels are below 120 mEq/L, and symptoms are common with
levels below 110 mEq/L. When the serum sodium level falls rapidly, symptoms occur at higher serum
sodium levels.

6. Hypothermia Hyperthermia
Clinical Findings
 Hypothermia and hyperthermia are associated with symmetric neurologic dysfunction that may progress
to coma. All comatose patients must have rectal temperature taken with an extended-range thermometer if
the standard thermometer fails to register.
 Hypothermia
Internal body temperatures below 26°C (78.8°F) uniformly cause coma; hypothermia with core
temperatures above 32°C (89.6°F) does not cause coma. Body temperatures of 26°C-32°C (78.8°F-
89.6°F) are associated with varying degrees of obtundation. Pupillary reaction will be sluggish below
32°C (89.6°F) and lost below 26.5°C (80°F).
 Hyperthermia
Internal body temperatures above 41°C-42°C (105.8°F-107.6°F) are associated with coma and may also
rapidly cause permanent brain damage. Seizures are common, especially in children.

7. Meningoencephalitis
Clinical Findings
The classic triad of fever, neck stiffness, and altered mental status is poorly sensitive for bacterial
meningitis. Any patient with altered mental status, seizure, focal neurologic deficit, or evidence of increased
ICP should undergo neuroimaging prior to lumbar puncture to minimize the risk of herniation. CSF
pleocytosis is common although depending on the stage of the disease, the differential may be variable. CSF
glucose <40 mg/dL is more consistent with bacterial meningitis. See Chapter 40 for further information
regarding meningitis.
Treatment & Disposition
Start antibiotic therapy immediately based on clinical findings, prior to obtaining imaging. Current
recommendations are for vancomycin with a third-generation cephalosporin, and dexamethasone should
be given at or before antibiotic administration. Hospitalization is indicated for all patients with meningitis
who present in coma or in whom bacterial meningitis cannot be excluded.

OTHER DISORDERS CAUSING COMA

1. Subarachnoid Hemorrhage
ESSENTIALS OF DIAGNOSIS
• Sudden onset of severe headache
• Nausea and vomiting
• Photophobia, visual changes
General Considerations
Aneurysmal subarachnoid hemorrhage (SAH) accounts for 80% of all cases of nontraumatic SAH. Risk
factors include cigarette smoking, hypertension, cocaine and alcohol use, first-degree relatives with a
history of SAH, female sex, African-American race, and connective tissue disorders.
Clinical Findings
Typical presentation of SAH involves sudden onset of severe headache, nausea, vomiting, meningismus,
photophobia, and may include decreased level of consciousness. A "thunderclap" headache may signify a
sentinel leak, and the headache may resolve relatively quickly. The patient may lose consciousness at onset
or may experience a seizure. Retinal hemorrhages may be present on fundoscopic examination and blood
pressure is usually markedly elevated. Noncontrast CT scan of the head is the initial diagnostic study of
choice. The presence of blood in the subarachnoid space warrants a CT angiogram (CTA) or traditional
cerebral angiography. Although the sensitivity of fourth-generation CT scanners is 95-99% for SAH (100%
within the first 12 hours), current recommendations are to follow a negative CT with CSF analysis. If CSF is
normal (no xanthochromia, no elevated RBCs), SAH is effectively excluded. Positive or indeterminate CSF
findings require either CTA or cerebral angiography to rule out the presence of an aneurysm.
Treatment & Disposition
Emergency department care is supportive. After stabilization, the patient should be admitted or transferred
for definitive therapy by neurosurgery for craniotomy and clipping or interventional radiology for coiling.
Blood pressure should be treated aggressively to be kept within normal limits until the aneurysm has been
secured. Nimodipine, an oral calcium channel antagonist, is commonly used to prevent delayed vasospasm
but is not commonly initiated in the emergency department.

2. Seizure
ESSENTIALS OF DIAGNOSIS
• Patient is unresponsive to pain
• Nonfocal neurologic examination
• Babinski sign (transient)
 • Todd paralysis
• Signs of recent seizure: tongue trauma, incontinence, rapidly clearing anion gap lactic acidosis
General Considerations
Coma resulting from seizure disorders is usually not a difficult diagnostic problem, because recovery of
consciousness is rapid following the end of the seizure. Prolonged postictal coma (several hours) followed
by several days of confusion may occur after status epilepticus, in patients with brain damage (e.g., multiple
cerebral infarctions, head trauma, encephalitis, mental retardation) and in patients with metabolic
encephalopathy that alters consciousness and induces seizures (e.g., hyponatremia, hyperglycemia).
Nonconvulsive status epilepticus is more common than previously thought and should be considered in any
patient with no other apparent cause of coma, especially in those with a history of seizure disorder.
Clinical Findings
Patients may initially be unresponsive to deep pain and exhibit sonorous respirations. The neurologic
examination is usually nonfocal, although Babinski sign may be transiently present. Uncommonly, there
may be focal abnormalities (Todd paralysis) referable anatomically to the focus of seizure activity in the
brain.
Other evidence of a recent seizure may be present, such as trauma to the tongue from biting, incontinence,
or a rapidly clearing anion gap (lactic) acidosis. The rapid resolution of coma in a patient with a witnessed
seizure or known seizure disorder should suggest the diagnosis of the postictal state as the cause of coma.
Coma that is at first thought to be postictal but fails to improve should prompt an investigation for
underlying processes contributing to mental status depression, including metabolic encephalopathy,
underlying diffuse brain damage, encephalitis, and structural lesion. Appropriate investigations could
include measurements of serum electrolytes, calcium, and magnesium; CT scan; and lumbar puncture.
Treatment & Disposition
Treatment depends on the underlying cause of the seizure. Be alert for metabolic causes and treat them
appropriately.

3. Psychogenic Coma
ESSENTIALS OF DIAGNOSIS
• Patient is unresponsive
• Normal physical examination
• Flaccid symmetric decreased muscle tone
• Normal and symmetric reflexes
• Normal Babinski
• Nystagmus with ice water calorics
• Normal electroencephalogram findings
Clinical Findings
Psychogenic coma is a diagnosis of exclusion that should be made only after careful documentation. The
general physical examination should elicit no abnormalities; neurologic examination generally reveals
flaccid, symmetrically decreased muscle tone, normal and symmetric reflexes, and the normal downward
response to Babinski plantar stimulation. The pupils are normal in size (2-3 mm) or occasionally larger and
respond briskly to light. Lateral eye movements elicited with the doll's eye maneuver may or may not be
present, because visual fixation can suppress this reflex.
Differentiating Psychogenic Coma from Organic Coma
a. Eye Movements
The slow, conjugate roving eye movements of patients in metabolic coma cannot be imitated and, if
present, are incompatible with a diagnosis of psychogenic unconsciousness.
b. Eyelid Tone
The slow, often asymmetric and incomplete eyelid closure commonly seen in organic forms of coma
following passive opening of the lids cannot be mimicked. In addition, the patient with psychogenic
coma usually shows some voluntary muscle tone of the eyelids during passive opening by the examiner.
c. Ice Water Caloric Response
A helpful objective test in diagnosing psychogenic unconsciousness is the caloric test: there is no
response at all or tonic deviation to the side of the irrigation in organic coma, but nystagmus occurs in
psychogenic coma. Because the quick (return) phase of nystagmus requires an intact cortex, its
presence is incompatible with a diagnosis of true coma.
d. Electroencephalogram
The electroencephalogram in psychogenic coma is that of a normal, awake person. In coma due to other
causes, it is invariably abnormal.
Treatment & Disposition Obtain psychiatric consultation. Hospitalization may be required.