COMA

MUHAMMAD ABD ELMONEIM

DEFINING COMA "unarousable unresponsiveness"

•Defined coma as a state of unresponsiveness in which the patient lies with his eyes closed and cannot be aroused to respond appropriately to stimuli even with vigorous Stimulation

•The patient may grimace in response to painful stimuli and limbs may demonstrate stereotyped withdrawal responses, but the patient does not make localized responses or discrete defensive movements

• The terms stupor, lethargy, and obtundation refer to states between alertness and coma

• An alteration in arousal represents an acute, life threatening emergency, requiring prompt intervention for preservation of life and brain function

ETIOLOGIES AND PATHOPHYSIOLOGY 

•The ascending reticular activating system (ARAS) is a network of neurons originating in the tegmentum of the upper pons and midbrain, believed to be integral to inducing and maintaining alertness

•These neurons project to structures in the diencephalon, including the thalamus and hypothalamus, and from there to the cerebral cortex

•Alterations in alertness can be produced by focal lesions within the upper brainstem by directly damaging the ARAS

•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

• Magnetic resonance imaging (MRI) studies have indicated that coma in supratentorial mass lesions occurs both with lateral forces on the contralateral hemisphere and with downward, brainstem compression

• Lesions below the level of the pons do not normally result in coma

• Drugs and metabolic disease produce coma by a depression of both cortex and ascending reticular activating system function

• Anatomically, dysfunction of one of the following three areas of the brain can cause coma: • The brainstem reticular activating system (RAS)• Bilateral frontal lobes• Bilateral temporal lobes

are all sufficient to cause coma

Assessment of coma

•Coma is an acute, life threatening situation. Evaluation must be swift, comprehensive, and undertaken while urgent steps are taken to minimize further neurological damage

•Emergency management should include: • Resuscitation with support of cardiovascular and

respiratory system• Correction of immediate metabolic upset, notably control

of blood glucose and thiamine if indicated; control of seizures and body temperature; any specific treatments—for example, naloxone for opiate overdose

• History—through friend, family or emergency medical personnel

• General physical examination

• Neurological assessment—to define the nature of coma • where is the lesion responsible for coma?• what is its nature?• what is it doing?

Assessment of coma

• Neurological diagnosis is based on history, thoughtful examination, and the appropriate choice of investigations

• This is essential, as there is little point in performing a cranial computed tomographic (CT) scan in a patient in hypoglycaemic coma where urgent correction of the metabolic disorder is paramount and any delay—for example, waiting for a scan—is unacceptable

Assessment of coma

• The approach to clinical evaluation is used to categorise coma into:• Coma without focal signs or meningism. This is the most

common form of coma and results from anoxic-ischaemic, metabolic, toxic, and drug induced insults, infections, and post ictal states

• Coma without focal signs with meningism. This results from subarachnoid haemorrhage, meningitis, and meningoencephalitis

• Coma with focal signs. This results from intracranial haemorrhage, infarction, tumour or abscess

Assessment of coma

Keep in mind

•Multifocal structural pathology, such as venous sinus thrombosis, bilateral subdural haematomas, vasculitis or meningitis, can present with coma without focal signs or meningism and so mimic toxic or metabolic pathologies

•Conversely, any toxic/metabolic cause for coma may be associated with focal findings—for example, hypoglycaemic or hepatic encephalopathy

•Also focal signs may be the consequence of pre-existing structural disease; in the septicaemic patient with a previous lacunar infarct, for example, the focal neurology may be mistakenly accepted as signs of the current illness

Assessment of coma

NEUROLOGIC EXAMINATION

•Level of consciousness

•Motor responses

•Brainstem reflexes: • Pupillary light• Ocular motility • Corneal reflexes

Assessment of coma

Level of consciousness

•Arousability is assessed 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, may have a higher yield than the more commonly used sternal rub and nailed pressure

•Important responses include vocalization, eye opening, and limb movement

Assessment of coma

Motor examination

•Muscle tone, spontaneous and elicited movements and reflexes

•Asymmetries of these often indicate a 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

Assessment of coma

• Decorticate posturing consists of upper-extremity adduction and flexion at the elbows, wrists, and fingers, together with lower-extremity extension, which includes extension and adduction at the hip, extension at the knee, and plantar flexion and inversion at the ankle . This occurs with dysfunction at the cerebral cortical level or below and may reflect a "release" of other spinal pathways

• Decerebrate posturing consists of upper-extremity extension, adduction, and pronation together with lower-extremity extension and traditionally implies dysfunction below the red nucleus, allowing the vestibulospinal tract to predominate

Assessment of coma

Motor response to pain. (A) Left hemisphere lesion. The two figures illustrate localisation of pain with the left hand and flexion (left hand figure) or extension (right hand figure) on the right

(B) Subcortical: unilateral left sided lesion exerting a variable contralateral effect. The figures illustrate flexion to pain with the left hand with either extension (right hand figure) or flexion with the right and hyperextension in both lower limbs

(C) Midbrain upper pontine: a bilateral upper and lower limb extension response

(D) Lower pontine/medullary: a bilateral extensor upper limb posture with either flaccidity or minimal diminished flexor response in lower limbs

Brainstem reflexesPupils •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

•Pupil size and symmetry should be noted as well. Pupils are normally between 3 to 7 mm in diameter and equal, although about 20 percent of normal individuals have up to 1 mm difference in pupillary size. Typically, the pupils are spared in metabolic and toxic conditions, except in certain toxic syndromes, which are associated with either miosis or mydriasis

•In severe sedative drug overdose or in hypothermia, the pupils are midposition and fixed; this syndrome can mimic brain death

•Lesions in the pontine tegmentum, which selectively disrupt sympathetic outflow, can produce very small (<1 to 2 mm) pupils in which a light response is barely perceptible, so-called pontine pupils. Opiate overdose can also produce this sign

Assessment of coma

Assessment of coma

Assessment of coma

(A) Cingulate herniation

 (B) Uncal herniation

(C) Tonsillar herniation

• Lesions above the thalamus and below the pons preserve pupillary reactions

Eye movements

•Ocular pathways run from the mid brain to the pons, thus normal reflex eye movements imply that the pontomedullary junction to the level of the ocular motor nucleus in the mid brain is intact

•In the comatose patient, bilateral conjugate roving eye movements that appear full indicate an intact brainstem and further reflex testing is not required

•In addition the oculomotor nerve is susceptible to compression in tentorial herniation

Oculocephalic and caloric response

This reflex is usually suppressed (and therefore not tested) in conscious patients

If nystagmus occurs, the patient is awake and not truly in coma; this can be a useful confirmatory test for psychogenic unresponsiveness

Corneal reflex 

The reflex can be suppressed acutely contralateral to a large, acute cerebral lesion, and also with 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. Absent corneal reflexes 24 hours after cardiac arrest is usually, but not invariably, an indication of poor prognosis (assuming the patient has not been sedated). Corneal reflexes may also be reduced or absent at baseline in elderly or diabetic patients

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

•A complete history and physical examination can provide valuable clues as to the underlying etiology

•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

•Evaluation and early therapeutic interventions should proceed promptly, even simultaneously. An algorithm for urgent evaluation and management is recommended

References

•Stupor and coma in adults• Author

G Bryan Young, MD, FRCPC• Section Editors

Michael J Aminoff, MD, DScRobert S Hockberger, MD, FACEP

• Deputy EditorJanet L Wilterdink, MD