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Coma

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coma

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Coma

  1. 1. COMAMUHAMMAD ABD ELMONEIM
  2. 2. DEFINING COMA"unarousable unresponsiveness"•Defined coma as a state of unresponsiveness in which thepatient lies with his eyes closed and cannot be aroused torespond appropriately to stimuli even with vigorous Stimulation•The patient may grimace in response to painful stimuli and limbsmay demonstrate stereotyped withdrawal responses, but thepatient does not make localized responses or discrete defensivemovements
  3. 3. • 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
  4. 4. ETIOLOGIES ANDPATHOPHYSIOLOGY •The ascending reticular activating system (ARAS) is a networkof neurons originating in the tegmentum of the upper pons andmidbrain, believed to be integral to inducing and maintainingalertness•These neurons project to structures in the diencephalon,including the thalamus and hypothalamus, and from there to thecerebral cortex•Alterations in alertness can be produced by focal lesions withinthe upper brainstem by directly damaging the ARAS•Injury to the cerebral hemispheres can also produce coma, butin this case, the involvement is necessarily bilateral and diffuse,or if unilateral, large enough to exert remote effects on thecontralateral hemisphere or brainstem
  5. 5. • 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
  6. 6. • 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
  7. 7. Assessment of coma•Coma is an acute, life threatening situation. Evaluation must beswift, comprehensive, and undertaken while urgent steps aretaken 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
  8. 8. Assessment of coma • 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?
  9. 9. 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
  10. 10. 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
  11. 11. 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
  12. 12. Assessment of coma NEUROLOGIC EXAMINATION •Level of consciousness •Motor responses •Brainstem reflexes: • Pupillary light • Ocular motility • Corneal reflexes
  13. 13. 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
  14. 14. 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 examiners hand away or actively withdrawing from the stimulus
  15. 15. 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
  16. 16. 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
  17. 17. Assessment of coma Brainstem reflexes Pupils •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
  18. 18. Assessment of coma
  19. 19. Assessment of coma (A) Cingulate herniation  (B) Uncal herniation (C) Tonsillar herniation
  20. 20. • Lesions above the thalamus and below the pons preserve pupillary reactions
  21. 21. Eye movements•Ocular pathways run from the mid brain to the pons, thus normalreflex eye movements imply that the pontomedullary junction tothe level of the ocular motor nucleus in the mid brain is intact•In the comatose patient, bilateral conjugate roving eyemovements that appear full indicate an intact brainstem andfurther reflex testing is not required•In addition the oculomotor nerve is susceptible to compressionin tentorial herniation
  22. 22. 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
  23. 23. 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 ofmetabolic or toxic coma; bilaterally brisk corneal reflexessuggest the patient is only mildly narcotized. Absent cornealreflexes 24 hours after cardiac arrest is usually, but notinvariably, an indication of poor prognosis (assuming the patienthas not been sedated). Corneal reflexes may also be reduced orabsent at baseline in elderly or diabetic patients
  24. 24. SUMMARY ANDRECOMMENDATIONS•Stupor and coma are alterations in arousal; these are neurologicemergencies•Causes of coma are diverse and include structural brain diseaseand systemic disease. Cerebrovascular disease, trauma,metabolic derangements, and intoxications are the most commonetiologies•A complete history and physical examination can provide valuableclues as to the underlying etiology•The neurologic examination in coma patients includes assessmentof arousal, motor examination, and cranial nerve reflexes.Important findings are abnormal reflexes that indicate dysfunctionin specific regions of the brainstem, or a consistent asymmetrybetween right- and left-sided responses, which indicates structuralbrain pathology as a cause•Evaluation and early therapeutic interventions should proceedpromptly, even simultaneously. An algorithm for urgent evaluation
  25. 25. References•Stupor and coma in adults • Author G Bryan Young, MD, FRCPC • Section Editors Michael J Aminoff, MD, DSc Robert S Hockberger, MD, FACEP • Deputy Editor Janet L Wilterdink, MD

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