auses of coma

I. Symmetrical, nonstructural
Toxins
Lead
Thallium
Mushrooms
Cyanide
Methanol
Ethylene glycol
Carbon monoxide
Drugs
Sedatives
Barbiturates*
II. Symmetrical, structural
Other hypnotics
Supratentorial
Tranquilizers
Bilateral internal carotid occlusion
Bromides
Bilateral anterior cerebral artery occlusion
Alcohol
Sagittal sinus thrombosis
Opiates
Subarachnoid hemorrhage
Paraldehyde
Thalamic hemorrhage*
Salicylate
Trauma-contusion, concussion*
Psychotropics
Hydrocephalus
Anticholinergics
Infratentorial
Amphetamines
Basilar occlusion*
Lithium
Midline brainstem tumor
Phencylidine
Pontine hemorrhage*
Monoamine oxidase inhibitors
Central pontine myelinolysis
Metabolic
III. Asymmetrical, structural
Hypoxia
Supratentorial
Hypercapnia
Thrombotic thrombocytopenic purpura
Hypernatremia*
Disseminated intravascular coagulation
Hypoglycemia*
Nonbacterial thrombotic endocarditis (marantic endocarditis)
Hypergylcemic nonketotic coma
Subacute bacterial endocarditis
Diabetic ketoacidosis
Fat emboli
Lactic acidosis
Unilateral hemispheric mass (tumor, abscess, bleed) with
Hypercalcemia herniation
Hypocalcemia Subdural hemorrhage bilateral
Hypermagnesemia Intracerebral bleed
Hyperthermia Pituitary apoplexy
Hypothermia Massive or bilateral supratentorial infarction
Reye's encephalopathy Multifocal leukoencephalopathy
Aminoacidemia Creutzfeldt-Jakob disease
Wernicke's encephalopathy Adrenal leukodystrophy
Porphyria Cerebral vasculitis
Hepatic encephalopathy* Cerebral abscess
Uremia Subdural empyema
Dialysis encephalopathy Thrombophlebitis
Addisonian crisis Multiple sclerosis
Hypothyroidism Leukoencephalopathy associated with chemotherapy
Infections Acute disseminated encephalomyelitis
Bacterial meningitis Infratentorial
Viral encephalitis Brainstem infarction
Postinfectious encephalomyelitis Brainstem hemorrhage
Syphilis Brainstem thrombencephalitis
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
Heat stroke

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:
Mannitol
For possible nonconvulsive status:
Lorazepam
Phenytoin or equivalent

Common poisoning syndromes (toxidromes)

Examples of toxic
Toxidrome Mental status Pupils Vital signs Other manifestations
agents
Hyperthermia,
tachycardia, Cocaine, amphetamines,
Hyperalert,
hypertension, cathinones, ephedrine,
agitation, Diaphoresis, tremors,
Sympathomimetic Mydriasis widened pulse pseudoephedrine,
hallucinations, hyperreflexia, seizures
pressure, phenylpropanolamine,
paranoia
tachypnea, theophylline, caffeine
hyperpnea
Antihistamines, tricyclic
Hypervigilance, Dry flushed skin, dry
antidepressants,
agitation, Hyperthermia, mucous membranes,
cyclobenzaprine,
hallucinations, tachycardia, decreased bowel
Anticholinergic Mydriasis orphenadrine,
delirium with hypertension, sounds, urinary
antiparkinson agents,
mumbling speech, tachypnea retention, myoclonus,
antispasmodics,
coma choreoathetosis,
phenothiazines,
 picking behavior, atropine, scopolamine,
seizures (rare) belladonna alkaloids (eg,
Jimson Weed)
Hallucinations,
Phencyclidine, LSD,
perceptual Hyperthermia,
mescaline, psilocybin,
distortions, Mydriasis tachycardia,
Hallucinogenic Nystagmus designer amphetamines
depersonalization, (usually) hypertension,
(eg, MDMA ["Ecstasy"],
synesthesia, tachypnea
MDEA)
agitation
Bradypnea,
apnea Opioids (eg, heroin,
characteristic; Hyporeflexia, morphine, methadone,
CNS depression,
Opioid Miosis May develop: pulmonary edema, oxycodone,
coma
hypothermia, needle marks hydromorphone),
bradycardia, diphenoxylate
hypotension
Often normal,
but may Benzodiazepines,
develop: barbiturates,
CNS depression,
hypothermia, carisoprodol,
Sedative-hypnotic confusion, stupor, Variable Hyporeflexia
bradycardia, meprobamate,
coma
hypotension, glutethimide, alcohols,
apnea, zolpidem
bradypnea
Salivation, urinary
and fecal
incontinence, Organophosphate and
Bradycardia, diarrhea, emesis, carbamate insecticides,
hypertension diaphoresis, nerve agents, nicotine,
Cholinergic Confusion, coma Miosis orhypotension, lacrimation, GI pilocarpine,
tachypnea or cramps, physostigmine,
bradypnea bronchoconstriction, edrophonium,
muscle fasciculations bethanechol, urecholine
and weakness,
seizures
Tremor, myoclonus,
Hyperthermia, MAOIs alone or with:
hyperreflexia, clonus,
Serotonin Confusion, tachycardia, SSRIs, meperidine,
Mydriasis diaphoresis, flushing,
syndrome agitation, coma hypertension, dextromethorphan,
trismus, rigidity,
tachypnea TCAs, L-tryptophan
diarrhea
LSD: lysergic acid diethylamide; CNS: central nervous system; GI: gastrointestinal; MAOI: monoamine oxidase
inhibitor; SSRI: serotonin reuptake inhibitor; TCA: tricyclic antidepressant.
Graphic 71268 Version 16.0

Glasgow Coma Scale (GCS)

Score
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
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
Total

impaired responsiveness (or are unresponsive) to external stimulation , difficult to

arouse or unarousable.

The ascending reticular activating system in the upper pons and midbrain is integral to
inducing and maintaining alertness.Injury to the cerebral hemispheres can also produce
coma, but in this case, the involvement is necessarily bilateral and diffuse, or if
unilateral, large enough to exert remote effects on the contralateral hemisphere or
brainstem. Coma in toxic, metabolic, and infectious etiologies and hypothermia is
produced by impair oxygen or substrate delivery

Questions to ask time course abrupt (eg, subarachnoid hemorrhage, seizure), gradual
(eg, brain tumor), or fluctuating (eg, recurring seizures, subdural hematoma, metabolic
encephalopathy)? Did focal signs or symptoms precede the loss of consciousness? .
Transient visual symptoms, previous neurologic episodes recent illness ,altered
behavior or function recently, prescription or nonprescription drugs ,medical or
psychiatric conditions, history of alcohol or drug abuse?

Vital signs Extreme hypertension : reversible posterior leukoencephalopathy

syndrome, hypertensive encephalopathy, or hemorrhage. Hypotension : circulatory
failure, drugs or Addison's disease. Hyperthermia :infection; heat stroke, or
anticholinergic intoxication. Hypothermia accidental (cold exposure), primary
(hypothalamic dysfunction as in Wernicke's encephalopathy or tumor), or secondary
(eg, adrenal failure, hypothyroidism, sepsis, drug or alcohol intoxication).

Ventilatory pattern hypo or hyperventilation / Cheyne-Stokes respirations (a pattern

of periodic waxing then waning hyperpnea, followed by brief apnea) / irregular
respirations with progression of downward herniation /Apneustic breathing (in which
there is a prolonged inspiratory phase or end-inspiratory pause) is rare and usually
attributed to pontine tegmental lesions.

Cutaneous and mucosal abnormalities Bruises : head trauma, "raccoon eye"

(periorbital ecchymosis). Battle's sign (bruising over the mastoid) are signs of
basal skull fracture. Petechiae and ecchymoses in bleeding diatheses (eg,
thrombocytopenia, disseminated intravascular coagulation), some infections (eg,
meningococcal septicemia, Rocky Mountain spotted fever), and certain
vasculitides. Subungual (splinter) and conjunctival hemorrhages sometimes seen
 in endocarditis. Petechiae confined to the head and neck may be found after
convulsive seizures
Perspiration is common in fevers, hypoglycemia, and pheochromocytoma.
Bullous lesions are characteristic of barbiturate intoxication (coma
blisters).Jaundice . cherry red color, especially of the lips and mucous
membranes, suggests carbon monoxide intoxication. Pallor may suggest uremia,
myxedema, or severe anemia .Needle tracks, tongue bitten .Cerebrospinal fluid
rhinorrhea can occur with skull fracture, and is important to recognize, as
recurrent pyogenic meningitis can occur. Meningeal signs

NEUROLOGIC EXAMINATION Level of consciousness .GCS . Spontaneous

behavior and responses to stimuli .Arousability by noise (eg, shouting in the ear) and
somatosensory stimulation. Pressing on the supraorbital nerve (medial aspect of the
supraorbital ridge) or the angle of the jaw, or squeezing the trapezius .

Motor examination muscle tone, spontaneous and elicited movements and reflexes.
Asymmetries : hemiplegia of the non-moving side, implying a lesion affecting the
opposite cerebral hemisphere or upper brainstem. Purposeful movements include
crossing the midline, approaching the stimulus, pushing the examiner's hand away or
actively withdrawing from the stimulus. Decorticate posturing indicates dysfucntion in
cerebral cortical level or below Decerebrate posturing traditionally implies
dysfunction below the red nucleus, . Reflex posturing can occur in deep metabolic coma
or hypoglycemia. Muscle tone is generally not affected by most metabolic conditions.
Bilateral rigidity seen in in neuroleptic malignant syndrome, malignant hyperthermia,
Multifocal myoclonus, brief, random, asynchronous muscle jerks in limbs, trunk, or
face, strongly suggest a metabolic or toxic Tremor and asterixis in metabolic More
subtle myoclonic twitches of the facial muscles or fingers, more synchronous or
rhythmic movements, or spontaneous nystagmus in nonconvulsive status epilepticus.

Pupillary light reflex is each eye individually to evaluate direct and consensual
responsesWith an expanding supratentorial mass and/or a lateral shift in the
supratentorial compartment : unilateral, the ipsilateral pupil is dilated and unreactive
directly and consensually, but the contralateral pupil reacts to light shone in either eye..
When bilateral, there is neither a direct nor consensual response, the pupils are
symmetrically enlarged, and the eyes are deviated outward.
 In transtentorial herniation, after initial dilation and loss of light reactivity, pupils
become somewhat reduced in size (4 to 5 mm) and remain unreactive; they are called
midposition and fixed. Typically, the pupils are spared in metabolic and toxic
conditions, In severe sedative drug overdose or in hypothermia, the pupils are
midposition and fixed and can mimic brain death. Lesions in the pontine tegmentum
can produce very small (<1 to 2 mm) pupils in which a light response is barely
perceptible, so-called pontine pupils.

Eye movements Large cerebral lesions produce a persistent conjugate deviation of the
eyes toward the side of the lesion (contralateral to limb paralysis). Persistent eye
deviation, especially if accompanied by nystagmus, may also suggest seizures; in this
case, the eye deviation is away from the side of the lesion. Lateral and downward eye
deviation (usually with pupillary involvement) suggests oculomotor involvement of the
nerve or midbrain nuclei, while medial deviation suggests sixth nerve palsy.

In the comatose patient, bilateral conjugate roving eye movements that appear full
indicate an intact brainstem and further reflex testing is not required. In the absence of
this do horizontal eye movements testing with vestibuloocular reflexes (VORs):

In the oculocephalic maneuver (or doll's eyes), the head is abruptly rotated from one
side to the other in the horizontal plane. When the oculocephalic reflex is present
(positive doll's eyes), the eyes do not turn with the head, but in the opposite direction, as
if the patient is maintaining visual fixation on a single point in space.

Caloric testing of the oculovestibular reflex .The head or upper torso is inclined 30
degrees up from the horizontal and inject at least 50 mL of ice water is injected into the
ear canal using a syringe with a small catheter attached. A normal response is sustained
deviation of both eyes toward the ear being stimulated. Five minutes should elapse
before testing the other side.

A cold caloric response is also present in conscious people, producing not only
deviation of the eyes toward the stimulated ear, but also nystagmus , severe vertigo,
nausea, and vomiting. If nystagmus occurs, the patient is awake and not truly in coma;
this can be a useful confirmatory test for psychogenic unresponsiveness. However, the
presence of nystagmus with caloric stimulation can also be seen in akinetic mutism and
less profound coma
Vertical eye movements can be tested either by moving the head and neck in the vertical plane or
injecting ice water (causes the eyes to deviate downward in the unconscious patient) or warm water
(seven degrees above body temperature - causes the eyes to deviate upwards) into both ear canals
simultaneously.

With brainstem lesions, both VORs are often absent or abnormal. If pupillary sizes and reflexes are
normal and one eye abducts and the other fails to adduct, this indicates disruption in the pons. Upper
midbrain lesions, affecting the third cranial nerve nuclei, may also lead to abduction without adduction
(but usually with pupillary involvement). Pontine involvement of the sixth nerve nuclei may selectively
affect abduction. Profound toxic or metabolic pathology can also disrupt the VORs, usually the
oculocephalic reflex primarily. Abnormalities are generally symmetric and equally affect abduction and
adduction. Absent caloric responses with normal pupillary reflexes raises the possibility of Wernicke's
encephalopathy, which selectively involves the VOR, sparing other brainstem reflexes or some cases
benzodiazepines intox .

Corneal reflex both orbicularis oculi muscles contract when either cornea is touched. The reflex can
be suppressed acutely contralateral to a large, acute cerebral lesion, and intrinsic brainstem lesions. Loss
of the corneal reflex is also an index of the depth of metabolic or toxic coma; bilaterally brisk corneal
reflexes suggest the patient is only mildly narcotized.

Herniation syndromes Transtentorial herniation can occur with expanding mass lesions (eg,
intracerebral, subdural, or epidural hemorrhage, large ischemic stroke, abscess, tumor, obstructive
hydrocephalus). Initial impairment of consciousness usually related to lateral rather than downward
displacement. Horizontal shifts of midline structures, especially the pineal body of greater than 8 mm are
associated with some impairment of consciousness; patients with shifts of >11 mm are usually comatose
Further shifts in brain structures can lead to downward, transtentorial herniation .While the sequence is
relatively predictable, the timing is not; deterioration can be precipitous. 2 variants central herniation and
uncal herniation syndrome. In uncal herniation , laterally directed compressive forces lead to asymmetric
herniation of the temporal uncus with ipsilateral 3 rd nerve palsy (pupillary dilation, downward and
outward eye deviation prior to diencephalic signs, then loss of reactivity of the contralateral pupil from
midbrain damage. Hemiplegia due to compression of the cortical spinal tract in the midbrain often
follows immediately and then sequence of central herniation,
Brainstem lesions infarction or hemorrhage of the upper pons and/or midbrain.. Osmotic demyelination syndrome
and 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..

Metabolic coma A cardinal feature of metabolic coma is the symmetrical nature of the neurologic deficits.
Exceptions occur 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 metab coma.

CONDITIONS MISTAKEN FOR COMA

Locked-in syndrome : focal injury to the base of the pons, usually by embolic occlusion of the basilar artery .
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.. 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

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. This 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 (including response to cold caloric stimulation), and postural reflexes usually remain
intact.

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. The presence of
nystagmus with caloric stimulation in an apparently comatose patient supports a diagnosis of psychogenic
unresponsiveness

DIAGNOSIS CT head, LP ,CBC, CMP ,coag, lactate, drug screen , ethyl alcohol, acetaminophen, , salicylates,
methanol,osmolality ,adrenal and thyroid function tests,blood cultures,blood smear Carboxyhemoglobin CT head is
very sensitive for structural causes of coma, including subarachnoid hemorrhage other intracranial hemorrhage acute
hydrocephalus, tumors, marked cerebral edema, and large ischemic strokes. CT angiography if brainstem stroke is
suspected. MRI is better in 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 Electroencephalography Nonconvulsive status epilepticus (NCSE) usually occurs in pt with alternative
explanations for coma, including stroke, trauma, and anoxic brain injury, organ failure, drug toxicity, alcohol and
benzodiazepine withdrawal, and other metabolic disturbances

MANAGEMENT Patients with a GCS of 8 or less usually require endotracheal intubation to protect the airway. If
hypotension (mean arterial BP of <70 mmHg) use volume expanders or vasopressors or both. With severe
hypertension (mean arterial BP of >130 mmHg) repeated labetalol (5 to 20 mg boluses as needed) . 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. Use naloxone (0.4 to 2.0 mg IV) and flumazenil treatment only in the setting of known or strongly
suspected drug If a herniation syndrome is evident clinically or appears imminent based on computed tomography
(CT) findings, urgent treatment with mannitol (1 g/kg IV) and hyperventilation. 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 2 g/day IV in four divided doses) or viral encephalitis
(acyclovir 10 mg/kg IV every eight hours) 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.