Brainstem lesions — Coma from a primary brainstem process usually occurs in the setting of infarction or
hemorrhage of the upper pons and/or midbrain [
11
]. Central pontine myelinolysis or brainstem encephalitis are
other causes. Bilateral long tract involvement is usual and may manifest with flaccid quadriparesis or
decerebrate posturing. Eye movements may be notably asymmetric or absent and pupils are classically small.
It is critical to ensure that these patients are not locked-in. (See
'Conditions mistaken for coma'
below.) In a
case series of nine patients with brainstem stroke, four developed hyperthermia just prior to their death in the
absence of identified infection [
11
].
Metabolic coma — A cardinal feature of metabolic coma is the symmetrical nature of the neurologic
deficits. Exceptions occur; in particular, hypo- and hyperglycemia are frequently associated with lateralized
motor findings. Fluctuations in the examination are common. Tremor, asterixis, and multifocal myoclonus,
strongly suggest metabolic coma. Muscle tone is usually decreased; decerebrate posturing is less common in
metabolic coma, but may occur. Pupils may appear abnormal but almost always are symmetric and constrict
with light. Suppression of VORs and corneal reflex occur with very deep metabolic coma.
Toxic syndromes — Drug overdoses or poisonings often appear similar to metabolic coma, but may be
associated with distinctive clinical features (
table 6
). (See
"General approach to drug poisoning in adults"
.)
CONDITIONS MISTAKEN FOR COMA — Some conditions that appear to be coma but are not include the
locked-in syndrome, akinetic mutism, and psychogenic unresponsiveness:
Locked-in syndrome — The locked-in syndrome is a consequence of a focal injury to the base of the pons,
usually by embolic occlusion of the basilar artery [
12,13
]. Consciousness is preserved; however, the patient
cannot move muscles in the limbs, trunk, or face, except that voluntary blinking and vertical eye movements
remain intact. Patients with this syndrome have been mistakenly believed to be unconscious [
14,15
]. The
locked-in syndrome may sometimes be mimicked by a severe upper spinal cord lesion, a motor neuropathy,
myopathy, neuromuscular junction disease, or extreme muscular rigidity (as in severe Parkinsonism or the
neuroleptic malignant syndrome). A careful neurologic examination can usually distinguish between these
entities and true coma. (See
"Locked-in syndrome"
.)
Akinetic mutism — A lack of motor response in an awake individual might arise from injury to the prefrontal
or premotor (including supplementary motor) areas responsible for initiating movements [
16,17
]. This
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executive problem is called akinetic mutism. The patient follows with the eyes but does not initiate other
movements or obey commands. The patient's tone, reflexes, and postural reflexes usually remain intact.
Psychogenic unresponsiveness — Patients with psychogenic unresponsiveness often resist passive eye
opening, roll over when tickled to avoid the stimulus, turn the eyes towards the floor regardless of which side
they are lying on, or demonstrate nonepileptic seizures. Catatonia is distinguished from coma by the patient's
preserved ability to maintain posture, even to sit or stand.
DIAGNOSIS — The goal of diagnostic testing in a patient in coma is to identify treatable conditions (infection,
metabolic abnormalities, seizures, intoxications/overdose, surgical lesions). Because neurologic recovery is
often reliant on early treatment, testing must proceed rapidly in concert with the clinical evaluation (
table 1
).
Investigations almost always include laboratory testing and neuroimaging. Some patients require lumbar
puncture and electroencephalography (EEG). Testing should be prioritized according to the clinical presentation.
Caveats include:
The presence of papilledema or focal neurologic deficits suggesting a structural etiology mandate an
urgent head computed tomography (CT) scan, particularly if the clinical presentation suggests an acute
stroke, expanding mass lesion, and/or herniation syndrome.
Fever suggesting bacterial meningitis or viral encephalitis mandates an urgent lumbar puncture.
Neuroimaging prior to lumbar puncture in a comatose patient is recommended (see
"Clinical features and
diagnosis of acute bacterial meningitis in adults", section on 'Lumbar puncture'
) [
18
].
Laboratory tests — Screening laboratory tests for patients presenting in coma of uncertain cause include:
Complete blood count
Serum electrolytes, calcium, magnesium, phosphate, glucose, urea, creatinine, and liver function tests
Arterial blood gas
Prothrombin and partial thromboplastin time
Drug screen (usually done on urine and serum), including ethyl alcohol,
acetaminophen
, opiates,
benzodiazepines, barbiturates, salicylates, cocaine, amphetamines, ethylene glycol, and methanol
In selected patients, when other conditions are suspected or if the cause of coma remains obscure, further
laboratory testing is required:
Adrenal and thyroid function tests
Blood cultures
Blood smear: screen for thrombotic thrombocytopenic purpura (fragmented erythrocytes, elevated serum
lactate dehydrogenase) or disseminated intravascular coagulation (DIC) (D-dimer and fibrinogen
determination); consider antiphospholipid determination if a coagulation problem is suspected
Carboxyhemoglobin if carbon monoxide poisoning is suggested (patient found in a burning building or in
a stationary automobile)
Serum drug concentrations for specific drugs
Neuroimaging — Computed tomography (CT), allowing for quick assessment of intracranial structural
changes, is usually the test of choice for the initial evaluation of a coma patient. Except for focal brainstem
lesions, it is very sensitive for structural causes of coma, including subarachnoid hemorrhage (95 percent in
early presentation), other intracranial hemorrhage (essentially 100 percent), acute hydrocephalus, tumors,
marked cerebral edema, and large ischemic strokes. CT angiography (where available) can be a helpful
addition that allows assessment of the intra and extracranial arterial and venous circulation, particularly when
brainstem stroke is suspected.
CT is inferior to magnetic resonance imaging (MRI) for detecting abnormalities in patients with herpes simplex
encephalitis, early ischemic strokes (especially involving the brainstem), multiple small hemorrhages or white
matter tract disruption associated with traumatic diffuse axonal injury, anoxic-ischemic damage from cardiac
arrest, and most disorders affecting the white matter [
19
]. However, MRI takes longer to perform than CT,
requires the patient to be farther from monitoring personnel, and may be problematic for the unstable patient.
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In general, CT is the test of choice for initial evaluation. Follow-up MRI is recommended when CT and other
testing do not explain, or incompletely explain, the clinical picture [
19
].
Lumbar puncture — Evaluation of cerebrospinal fluid (CSF) is a necessary part of the urgent evaluation of a
patient with suspected infection of the central nervous system. In a patient with altered level of consciousness,
neuroimaging to exclude an intracranial mass lesion is required prior to lumbar puncture (LP) in order to avoid
precipitating transtentorial herniation. Coagulation test results should also be obtained beforehand. (See
"Lumbar puncture: Technique; indications; contraindications; and complications in adults"
.)
Because there might be some delay in obtaining CSF, empiric antimicrobial treatment is recommended when
the diagnosis of bacterial meningitis or herpes encephalitis is strongly suspected; as early treatment improves
prognosis of these conditions (see
'Management'
below). Treatment may impair the diagnostic sensitivity of
CSF cultures but should not affect other tests (WBC, gram stain, PCR). Blood cultures should be obtained prior
to antibiotic intervention, as they have a 50 to 75 percent yield in bacterial meningitis [
20-22
]. (See
"Clinical
features and diagnosis of acute bacterial meningitis in adults", section on 'Blood cultures'
.)
CSF is also useful to exclude subarachnoid hemorrhage when CT is normal and the diagnosis remains suspect,
and may be helpful in the diagnosis of less common infections, as well as demyelinating, inflammatory, and
neoplastic conditions (eg, meningeal lymphomatosis or carcinomatosis).
Electroencephalography — In the comatose patient, EEG is used primarily to detect seizures [
23
]. If the
patient has clinical finding suggestive of nonconvulsive seizures (see
'Motor examination'
above), or if the
cause of coma remains obscure after other testing, then an EEG is indicated.
In one series, 236 patients without overt seizure activity received an EEG as part of a coma evaluation; 8
percent had nonconvulsive status epilepticus (NCSE) [
24
]. These patients had alternative explanations for
coma, including stroke, trauma, and anoxic brain injury. NCSE also occurs in the setting of organ failure, drug
toxicity, alcohol and benzodiazepine withdrawal, and other metabolic disturbances [
25-27
]. Prolonged or
continuous EEG monitoring increases the yield for detecting nonconvulsive seizures; however, it is not clear
that this influences outcome [
28-32
].
In the setting of severe medical illness, NCSE presents a difficult diagnostic and treatment challenge. While
subtle signs may suggest the diagnosis (see
'Motor examination'
above), NCSE can often only be detected and
verified by EEG. A high index of suspicion for the diagnosis is required, as the underlying illness may often be
deemed a sufficient explanation for altered sensorium.
Other, nonepileptiform, EEG findings can be helpful in the diagnosis of coma [
23,33
]. Diffusely disorganized,
slowed background rhythms confirm an impression of toxic metabolic encephalopathy, while strongly lateralized
findings suggest structural disease. More rhythmic, slow EEG patterns, such as the classic triphasic waves of
hepatic encephalopathy, sometimes present a challenge in differentiating from seizures. The triphasic wave
pattern is not specific for hepatic encephalopathy, and can occur in other metabolic encephalopathies as well.
Periodic lateralized epileptiform discharges (PLEDS) are classically associated with herpes encephalitis, but may
also occur in acute structural lesions, as well as in other central nervous system infections, hypoxic ischemic
encephalopathy, and other metabolic diseases [
34,35
].
In some patients with coma, 8 to 12 Hz activity is seen; this resembles normal alpha rhythm, but extends
beyond the posterior cerebral regions and does not react to stimuli [
33
]. This so-called "alpha coma" is
associated with pontine lesions, and has also been described with hypoxic ischemic encephalopathy following
cardiac arrest, traumatic brain injury, and drug overdose. This should not be confused with a normal EEG
pattern, which suggests a psychogenic origin for the patient's unresponsiveness.
EEG can also be helpful in determining the prognosis of victims of cardiac arrest, however, somatosensory
evoked potential testing is more prognostically definitive [
35
]. (See
"Hypoxic-ischemic brain injury"
.)
Continuous EEG may also be helpful in showing the effects of treatment, eg, for seizures or vasospasm and in
monitoring the depth of anesthesia in the ICU [
36
].
MANAGEMENT — In the emergency department (ED), basic care should be done in concert with the clinical
and laboratory investigations mentioned above (
table 1
).
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The primacy of ABCs (airway, breathing, and circulation) applies to cases of coma. Vital signs should be
taken, an initial Glasgow Coma Scale score (GCS) established (
table 5
), and a set of arterial blood gases,
along with the other blood and urine tests (see
'Laboratory tests'
above), sent to the laboratory.
Patients with a GCS of 8 or less usually require endotracheal intubation to protect the airway. This can
sometimes be avoided, eg, in patients with large hemispheric strokes or alcohol withdrawal seizures.
Intubation is also advised in the presence of hypoxemia (oxygen saturation of <90 percent), recent
vomiting, or poor cough or gag reflex. Oxygen supplementation is often needed, whether or not assisted
ventilation is required.
It is best to treat hypotension (mean arterial BP of <70 mmHg) with volume expanders or vasopressors
or both. With severe hypertension (mean arterial BP of >130 mmHg) repeated doses of intravenous
labetalol
(5 to 20 mg boluses as needed) are often adequate for initial stabilization. A 12-lead
electrocardiogram should be done.
It is recommended to give 25 g of dextrose (as 50 mL of a 50 percent dextrose solution) while waiting
for the blood tests, if the cause of coma is unknown. Thiamine, 100 mg, should be given with or
preceding the glucose in any patient who may be malnourished (to treat or to prevent precipitating acute
Wernicke's encephalopathy).
While the use of a coma cocktail consisting of glucose, thiamine,
naloxone
, and
flumazenil
has been
promoted, a systemic review of trials considering outcome and adverse effects, suggested that it was
reasonable to use glucose and thiamine in unselected patients, but that naloxone (0.4 to 2.0 mg IV) and
flumazenil treatment should be used only in the setting of known or strongly suspected drug overdose
[
37
]. Gastric lavage and
activated charcoal
are also often recommended for suspected ingestions. This
topic is discussed in more detail separately. (See
"General approach to drug poisoning in adults"
.)
If a herniation syndrome is evident clinically or appears imminent based on computed tomography (CT)
findings, urgent treatment is recommended. This includes administration of
mannitol
(1 g/kg IV) and
hyperventilation. (See
"Evaluation and management of elevated intracranial pressure in adults"
.)
Hyperthermia (T>38.5 degrees C) can contribute to brain damage in cases of ischemia; efforts to lower
fever with antipyretics and/or cooling blankets should be administered immediately. Empiric antibiotic
and antiviral therapy are recommended if bacterial meningitis (eg,
ceftriaxone
2 g IV every 12 hours
and
vancomycin
vancomycin 2 g/day IV in four divided doses) or viral encephalitis (
acyclovir
10 mg/kg
IV every eight hours) are among the suspected entities. These should be continued until these conditions
have been excluded. (See
"Clinical features and diagnosis of acute bacterial meningitis in adults", section
on 'If LP is delayed'
and
"Herpes simplex virus type 1 encephalitis", section on 'Treatment'
.)
Since hypothermia has neuroprotective effects in patients with cardiac arrest, only extreme hypothermia
(<33ºC) should be treated. Efforts to search for and correct its cause are more helpful than to
vigorously raise the body temperature to the normal range.
If the patient has had a seizure, treatment with
phenytoin
or
fosphenytoin
(15-20 mg/kg phenytoin
equivalent IV) is recommended. If nonconvulsive seizures are suspected and an electroencephalogram
(EEG) is not available, a therapeutic trial of phenytoin or
lorazepam
(1 to 2 mg IV) is reasonable.
Definitive therapy depends on establishing the precise diagnosis (sometimes more than one). Monitoring
of the course of the patient, looking for improvement, worsening, and complications, follows, along with
establishing a prognosis and communicating this to families.
PROGNOSIS — Coma is a transitional state that rarely lasts more than several weeks, except in cases of
ongoing sedative therapies or protracted sepsis. Patients either recover or evolve into brain death or a
persistent vegetative or minimally conscious state. (See
"Hypoxic-ischemic brain injury", section on 'Persistent
vegetative state'
.)
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The prognosis depends on the underlying etiology, as well as the severity of the insult and other premorbid
factors, including age. (See
"Hypoxic-ischemic brain injury"
and
"Acute toxic-metabolic encephalopathy in
adults", section on 'Prognosis'
.)
Glasgow coma scale — The Glasgow coma scale (GCS) grades coma severity according to three categories of
responsiveness: eye opening, motor, and verbal responses (
table 5
). With good interobserver reliability and
ease of use, the admission GCS has been linked to prognosis prediction for a number of conditions, including
traumatic brain injury, subarachnoid hemorrhage, and bacterial meningitis [
22,38-40
]. Intubation and use of
sedating drugs interfere with its utility; for this reason, it is useful to obtain a GCS on admission prior to these
interventions. The GCS is not useful for the diagnosis of coma.
An alternative scale, the FOUR score, has been proposed that may have greater utility in coma diagnosis,
primarily by including a brainstem examination [
41
]. However, this lacks the long track record of the GCS in
predicting prognosis and is more complicated to perform, which may be a barrier for nonneurologists.
SUMMARY AND RECOMMENDATIONS — Stupor and coma are alterations in arousal; these are neurologic
emergencies.
Causes of coma are diverse and include structural brain disease and systemic disease. Cerebrovascular
disease, trauma, metabolic derangements, and intoxications are the most common etiologies. (See
'Etiologies and pathophysiology'
above.)
A complete history and physical examination can provide valuable clues as to the underlying etiology.
(See
'History'
above and
'General examination'
above.)
The neurologic examination in coma patients includes assessment of arousal, motor examination, and
cranial nerve reflexes. Important findings are abnormal reflexes that indicate dysfunction in specific
regions of the brainstem, or a consistent asymmetry between right- and left-sided responses, which
indicates structural brain pathology as a cause. (See
'Neurologic examination'
above.)
Evaluation and early therapeutic interventions should proceed promptly, even simultaneously. An
algorithm for urgent evaluation and management is recommended (
table 1
).
Use of UpToDate is subject to the
Subscription and License Agreement
.
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GRAPHICS
Emergent evaluation and management of stupor and coma in adults
EVALUATION
Vital signs and general examination
Neurologic examination and GCS
Screening laboratories (CBC, glucose selectrolyes, BUN, creatinine, PT, PTT, ABG, LFTs, drug screen)
ECG
Head CT scan: prioritize emergent if focal neurologic signs, papilledema, fever
Lumbar puncture: prioritize emergent after CT scan if fever, elevated WBC, meningismus; otherwise do
according to level of suspicion for diagnosis or if cause remains obscure
EEG: for possible nonconvulsive seizure, or if diagnosis remains obscure
Other laboratory tests: blood cultures, adrenal and thyroid tests, coagulation tests, carboxyhemoglobin,
specific drug concentrations - do according to level of suspicion for diagnosis or if cause remains obscure
Brain MRI with DWI, if cause remains obscure
MANAGEMENT
ABCs:
Intubate if GCS ≤8
Stabilize CSpine
Supplement O2
IV access
Blood pressure support as needed
Glucose 50 percent IV 50 mL (after blood drawn, before results back)
Thiamine 100 mg IV
Treat definite seizures with phenytoin or equivalent
Consider empiric treatments:
For possible infection:
Ceftriaxone and Vancomycin
Acyclovir
For possible ingestion:
Naloxone
Flumazenil
Gastric lavage/activated charcoal
For possible increased ICP:
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Mannitol
For possible nonconvulsive status:
Lorazepam
Phenytoin or equivalent
GCS: Glasgow coma scale; CBC: complete blood count; BUN: blood urea nitrogen; PT: prothrombin time; PTT:
partial thromboplastin time; ABG: arterial blood gas; LFT: liver function tests; ECG: electrocardiogram; CT:
computed tomography; WBC: white blood cells; EEG: electroencephalography; MRI: magnetic resonance imaging;
DWI: diffusion weighted imaging; ICP: intracranial pressure.
Causes of coma
I. Symetrical, nonstructural
Toxins
Lead
Thallium
Mushrooms
Cyanide
Methanol
Ethylene glycol
Carbon monoxide
Drugs
Sedatives
Barbiturates*
Other hypnotics
Tranquilizers
Bromides
Alcohol
Opiates
Paraldehyde
Salicylate
Psychotropics
Anticholinergics
Amphetamines
Lithium
Phencylidine
Monoamine oxidase inhibitors
Metabolic
Hypoxia
Hypercapnia
Hypernatremia*
II. Symetrical, structural
Supratentorial
Bilateral internal carotid occlusion
Bilateral anterior cerebral artery occlusion
Sagittal sinus thrombosis
Subarachnoid hemorrhage
Thalamic hemorrhage*
Trauma-contusion, concussion*
Hydrocephalus
Infratentorial
Basilar occlusion*
Midline brainstem tumor
Pontine hemorrhage*
Central pontine myelinolysis
III. Asymetrical, structural
Supratentorial
Thrombotic thrombocytopenic purpura•
Disseminated intravascular coagulation
Nonbacterial thrombotic endocarditis (marantic
endocarditis)
Subacute bacterial endocarditis
Fat emboli
Unilateral hemispheric mass (tumor, abscess,
bleed) with herniation
Subdural hemorrhage bilateral
Intracerebral bleed
Pituitary apoplexy•
Massive or bilateral supratentorial infarction
Multifocal leukoencephalopathy
Creutzfeldt-Jakob disease
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Hypoglycemia*
Hypergylcemic nonketotic coma
Diabetic ketoacidosis
Lactic acidosis
Hypercalcemia
Hypocalcemia
Hypermagnesemia
Hyperthermia
Hypothermia
Reye's encephalopathy
Aminoacidemia
Wernicke's encephalopathy
Porphyria
Hepatic encephalopathy*
Uremia
Dialysis encephalopathy
Addisonian crisis
Hypothyroidism
Infections
Bacterial meningitis
Viral encephalitis
Postinfectious encephalomyelitis
Syphilis
Sepsis
Typhoid fever
Malaria
Waterhouse-Friderichsen syndrome
Psychiatric
Catatonia
Other
Postictal seizure*
Diffuse ischemia (myocardial infarction, heart
failure, arrhythmia)
Hypotension
Fat embolism*
Hypertensive encephalopathy
Hypothyroidism
Nonconvulsive status epilepticus
Adrenal leukodystrophy
Cerebral vasculitis
Cerebral abscess
Subdural empyema
Thrombophlebitis•
Multiple sclerosis
Leukoencephalopathy associated with
chemotherapy
Acute disseminated encephalomyelitis
Infratentorial
Brainstem infarction
Brainstem hemorrhage
Brainstem thrombencephalitis
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Heat stroke
* Relatively common asymmetrical presentation.
• Relatively symmetrical presentation.
Reproduced with permission from: Berger, Joseph R. Clinical Approach to
Stupor and Coma. In: Neurology in Clinical Practice: Principles of diagnosis and Management, 4th ed, Bradley,
WG, Daroff, RB, Fenichel, GM, Jankovic, J (Eds), Butterworth Heinmann, Philadelphia, PA 2004. p.46. Copyright ©
2004 Elsevier.
Ventilatory and arterial blood gas patterns in coma
Breathing
pattern
Metabolic
pattern
pH, PaCO2,
HCO3
Specific conditions
Hyperventilation
Metabolic
acidosis
pH <7.3, PaCO2
<30 mmHg,
HCO3 <17
mmol/L
Uremia, diabetic ketoacidosis, lactic acidosis,
salicylates, methanol, ethylene glycol
Hyperventilation
Respiratory
alkalosis
pH >7.45, PaCO2
<30 mmHg,
HCO3 >17
mmol/L
Hepatic failure, acute sepsis, acute salicylate
intoxication, cardiopulmonary states with
hypoxemia, psychogenic causes
Hypoventilation
Respiratory
acidosis
pH <7.35 (if
acute), PaCO2
>90 mmHg,
HCO3 >17
mmol/L
Respiratory failure from central (eg, brain or spinal
cord) or peripheral nervous system disease, chest
conditions or deformities. Coma only with severe
hypercarbia.
Hypoventilation
Metabolic
alkalosis
pH> 7.45, PaCO2
>45 mmHg,
HCO3 >30
mmol/L
Vomiting, alkali ingestion. Usually no impairment of
consciousness; if so, suspect psychogenic
unresponsiveness or additional cause.
Skin lesions and rashes in coma
Lesion or
rash
Possible cause
Antecubital
needle marks
Opiate drug abuse
Pale skin
Anemia or hemorrhage
Sallow, puffy
appearance
Hypopituitarism
Hypermelanosis
(increased
pigment)
Porphyria, Addison's disease, chronic nutritional deficiency, disseminated malignant
melanoma, chemotherapy
Generalized
cyanosis
Hypoxemia or carbon dioxide poisoning
Grayish-blue
cyanosis
Methemoglobin (analine or nitrobenzene) intoxication
Localized
cyanosis
Arterial emboli or vasculitis
Cherry-red skin
Carbon monoxide poisoning
Icterus
Hepatic dysfunction or hemolytic anemia
Stupor and coma in adults
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Petechiae
Disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, drugs
Ecchymosis
Trauma, corticosteroid use, abnormal coagulation from liver disease or anticoagulants
Telangiectasia
Chronic alcoholism, occasionally vascular malformations of the brain
Vesicular rash
Herpes simplex, varicella, Bechet's disease, or drugs
Petechial-
purpuric rash
Meningococcemia, other bacterial sepsis (rarely), gonococcemia, staphylococcemia,
pseudomonas, subacute bacterial endocarditis, allergic vasculitis, purpura fulminans,
Rocky Mountain spotted fever, typhus, fat emboli
Macular-
papular rash
Typhus, candida, cryptococcus, toxoplasmosis, subacute bacterial endocarditis,
staphylococcal toxic shock, typhoid, leptospirosis, pseudomona sepsis, immunological
disorders (systemic lupus erythematosus, dermatomyositis, serum sickness)
Ecthyma
gangrenosum
Necrotic eschar often seen in the anogenital or axillary area in Pseudomonas sepsis
Splinter
hemorrhages
Linear hemorrhages under the nail, seen in subacute bacterial endocarditis, anemia,
leukemia, and sepsis
Osler's nodes
Purplish or erythematous painful, tender nodules on palms and soles, seen in subacute
bacterial endocarditis
Gangrene of
digits'
extremities
Emboli to larger peripheral arteries
Pigmented
macules
Tuberous sclerosis, neurofibromatosis
Reproduced with permission from: Berger, Joseph R. Clinical Approach to Stupor and Coma. In: Neurology in
Clinical Practice: Principles of Diagnosis and Mangement, 4th ed, Bradley, WG, Daroff, RB, Fenichel, GM, Jankovic,
J (Eds), Butterworth Heinmann, Philadelphia, PA 2004. p.51. Copyright © 2004 Elsevier.
Transtentorial herniation
Stupor and coma in adults
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Data from Pulm, F, Posner, JB. The Diagnosis of Stupor and Coma III. FA Davis,
Philadelphia 1982. p. 103.
Glasgow coma scale
Eye opening
Spontaneous
4
Response to verbal command
3
Response to pain
2
No eye opening
1
Best verbal response
Oriented
5
Confused
4
Inappropriate words
3
Incomprehensible sounds
2
No verbal response
1
Stupor and coma in adults
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Best motor response
Obeys commands
6
Localizing response to pain
5
Withdrawal response to pain
4
Flexion to pain
3
Extension to pain
2
No motor response
1
The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of three
parameters: best eye response (E), best verbal response (V), and best motor response (M). The
components of the GCS should be recorded individually; for example, E2V3M4 results in a GCS
score of 9. A score of 13 or higher correlates with mild brain injury; a score of 9 to 12 correlates
with moderate injury; and a score of 8 or less represents severe brain injury.
Decorticate/decerebrate postures
Toxidromes
Toxidrome
Mental status
Pupils
Vital signs
Other
manifestations
Examples of
toxic agents
Sympathomimetic
Hyperalert,
agitation,
hallucinations,
Mydriasis
Hyperthermia,
tachycardia,
hypertension,
Diaphoresis,
tremors,
hyperreflexia,
Cocaine,
amphetamines,
ephedrine,
Stupor and coma in adults
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paranoia
widened pulse
pressure,
tachypnea,
hyperpnea
seizures
pseudoephedrine,
phenylpropanolamine,
theophylline, caffeine
Anticholinergic
Hypervigilance,
agitation,
hallucinations,
delirium with
mumbling
speech, coma
Mydriasis
Hyperthermia,
tachycardia,
hypertension,
tachypnea
Dry flushed skin,
dry mucous
membranes,
decreased bowel
sounds, urinary
retention,
myoclonus,
choreoathetosis,
picking behavior,
seizures (rare)
Antihistamines,
tricyclic
antidepressants,
cyclobenzaprine,
orphenadrine,
antiparkinson agents,
antispasmodics,
phenothiazines,
atropine,
scopolamine,
belladonna alkaloids
(eg, Jimson Weed)
Hallucinogenic
Hallucinations,
perceptual
distortions,
depersonalization,
synesthesia,
agitation
Mydriasis
(usually)
Hyperthermia,
tachycardia,
hypertension,
tachypnea
Nystagmus
Phencyclidine, LSD,
mescaline, psilocybin,
designer
amphetamines (eg,
MDMA, MDEA)
Opioid
CNS depression,
coma
Miosis
Hypothermia,
bradycardia,
hypotension,
hypopnea,
bradypnea
Hyporeflexia,
pulmonary edema,
needle marks
Opiates (eg, heroin,
morphine,
methadone,
oxycodone,
hydromorphone),
diphenoxylate
Sedative-
hypnotic
CNS depression,
confusion, stupor,
coma
Miosis
(usually)
Hypothermia,
bradycardia,
hypotension,
hypopnea,
bradypnea
Hyporeflexia
Benzodiazepines,
barbiturates,
carisoprodol,
meprobamate,
glutethimide,
alcohols, zolpidem
Cholinergic
Confusion, coma
Miosis
Bradycardia,
hypertension
orhypotension,
tachypneaor
bradypnea
Salivation, urinary
and fecal
incontinence,
diarrhea, emesis,
diaphoresis,
lacrimation, GI
cramps,
bronchoconstriction,
muscle
fasciculations and
weakness, seizures
Organophosphate and
carbamate
insecticides, nerve
agents, nicotine,
pilocarpine,
physostigmine,
edrophonium,
bethanechol,
urecholine
Serotonin
syndrome
Confusion,
agitation, coma
Mydriasis
Hyperthermia,
tachycardia,
hypertension,
tachypnea
Tremor, myoclonus,
hyperreflexia,
clonus, diaphoresis,
flushing, trismus,
rigidity, diarrhea
MAOIs alone or with:
SSRIs, meperidine,
dextromethorphan,
TCAs, L-tryptophan
Tricyclic
antidepressant
Confusion,
agitation, coma
Mydriasis
Hyperthermia,
tachycardia,
hypertension
then
hypotension,
hypopnea
Seizures,
myoclonus,
choreoathetosis,
cardiac arrhythmias
and conduction
disturbances
Amitriptyline,
nortriptyline,
imipramine,
clomipramine,
desipramine, doxepin
Oculocephalic and caloric response
Stupor and coma in adults
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Oculocephalic (doll's eyes) response: This test should not be
performed if a cervical spine injury is suspected. Observe the motion
of the eyes while passively moving the head. In a comatose patient,
conjugate movement of the eyes in the direction opposite to the
head movement is expected. An absent or asymmetric response in
an unconscious patient implies brain stem dysfunction. Caloric
response: After visually checking that the tympanic membrane is
intact, ice cold water is used to irrigate the ear canal and should
produce a slow conjugate deviation toward the irrigated side. An
absent or asymmetric response indicates brain stem dysfunction.
Adapted from: Bateman, DE. Neurologic assessment of coma. J Neurol Neurosurg
Psychiatry 2001; 71 Suppl 1:13.
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