Approach to stupor and coma
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1) Stupor and coma are states of decreased or absent responsiveness that require evaluation to identify potentially reversible causes and provide emergency treatment. 2) The initial approach involves stabilizing vital functions, treating potentially reversible causes, obtaining history, and performing a full neurological examination. 3) Emergency treatment may include supplemental oxygen, IV thiamine, glucose, and antibiotics depending on suspected causes identified from history and examination.
Approach to stupor and coma
- 1. Approach to stupor and coma -Dr. Sachin Adukia
- 2. Definitions Stupor state of baseline unresponsiveness that requires repeated application of vigorous stimuli to achieve arousal. Coma State of complete unresponsiveness to arousal, in which the patient lies with the eyes closed.
- 4. Approach principle all alterations in arousal constitute acute, life-threatening emergencies until vital functions such as BP and oxygenation stabilized, potentially reversible causes of coma treated, underlying cause understood Emergency therapeutic measures, history and exmaination proceed in parallel More than half of all cases of coma are due to diffuse and metabolic brain dysfunction.
- 7. Emergency Therapy quick initial assessment to ensure comatose patient is medically and neurologically stable empirical use of supplemental oxygen, IV thiamine (at least 100 mg), IV 50% dextrose in water (25 g) after a baseline serum glucose Use of IV glucose anoxic brain damage is controversial. Extra glucose may augment local lactic acid production by anaerobic glycolysis and may worsen ischemic or anoxic damage. empirical glucose is still recommended for two reasons : the frequent occurrence of alterations in arousal due to hypoglycemia and the relatively good prognosis for coma due to hypoglycemia when it is treated expeditiously; potentially permanent consequences if it is not treated. By comparison, the prognosis for anoxic or ischemic coma generally is poor and probably will remain poor regardless of glucose supplementation. Thiamine to prevent precipitation of Wernicke encephalopathy.
- 8. Coma usually manifests in one of three ways. Most commonly, as an expected or predictable progression of an underlying illness. focal brainstem infarction with extension barbiturate overdose when the ingested drug cannot be fully removed and begins to cause unresponsiveness Second, as an unpredictable event in whose prior conditions are known to the physician. Arrhythmia who suffers anoxia after a cardiac arrest. sepsis from IV line in a cardiac patient or stroke in hypothyroid patient patient whose medical history is totally unknown to the physician.eg RTA wuth head trauma
- 9. History interviewing relatives, friends, bystanders, or present medical personnel Telephone calls to family members may be helpful. Wallet be checked the circumstances in which the patient was found. drug paraphernalia or empty medicine bottles drug overdose. OHA or insulin in the medicine cabinet or refrigerator hypoglycemia. Antiarrhythmic agents procainamide or quinidine existing CAD with ? MI or unwitnessed arrhythmia may have caused cerebral hypoperfusion, Warfarin, (DVT / PTE) massive ICH Post operative setting - fat embolism, Addisonian crisis, and hypothyroid coma Wernicke encephalopathy, iatrogenic overdose of a narcotic analgesic
- 10. Symptoms before onset of coma headache preceding SAH, chest pain with aortic dissection or AMI shortness of breath from hypoxia, stiff neck in meningoencephalitis, vertigo in brainstem stroke. Nausea and vomiting are common in poisonings, increased ICP. h/o head trauma, drug abuse, seizures, or hemiparesis. ataxia, dysarthria or aphasia, ptosis, pupillary dilatation, or disconjugate gaze may help localize structural lesions
- 11. Examination, decision on emergency Ix and Rx General appearance, T P R BP, breath sounds, best response to stimulation, Pupil size and responsiveness, Posturing or adventitious movements. neck stabilized in all instances of trauma until Cx spine fracture is ruled out Airway immediate therapeutic intervention. Hypotension, marked hypertension, bradycardia, arrhythmias causing fall in BP, Marked hyperthermia, signs of cerebral herniation
- 12. Hyperthermia or meningismus- LP CSF pressure > 500, some recommend leaving the needle in place to monitor pressure and give IV mannitol Can give IV antibiotics and IV steroids pending LP in strong suspicion of meningitis Fundoscopy, CBC, INR, Local c/i- always before LP in coma Blood cultures and throat swabs prior to antibiotic
- 13. Hypotension. MAP < 60 hypovolemia, massive external or internal hemorrhage, myocardial infarction, cardiac tamponade, dissecting aortic aneurysm, intoxication with alcohol or other drugs (especially barbiturates), toxins, Wernicke encephalopathy, Addison disease, and sepsis may have warm extremities Hypertension cerebral infarction, in SAH, certain brainstem infarctions, ICP raised. Cushing’s reflex- ischemia of the pressor area lying beneath the floor of the fourth ventricle. Heart Rate Bradycardia: conduction blocks , certain poisionings, Beta blockers Tachycardia hypovolemia, hyperthyroidism, fever, anemia, toxins and drugs, including cocaine, atropine,
- 14. Temperature in comatose Pure neurogenic hyperthermia is rare, is d/t SAH or hypothalamus lesions. brainstem origin= shivering without sweating. particularly when unilateral, may be s/i deep ICH heatstroke, thyrotoxic crisis, and drug toxicity Hypothermia – reduced cerebral metabolism, EEG silence Sepsis, hypothyroid coma, hypopituitarism, Wernicke encephalopathy, cold exposure, drugs (barbiturates), Central lesions - posterior hypothalamus
- 15. Others Torn clothing Cachexia ALD Fracture skull racoon eyes in ant. Skull # Meningismus – infectious or carcinomatous meningitis, SAH, central or tonsillar herniation Funduscopic examination Grayish deposits around optic disc in lead poisoning. congested and edematous retina in methyl alcohol poisoning, and the disc margin may be blurred. Subhyaloid hemorrhage –consequence of rapid increase in ICP due to subarachnoid hemorrhage (Terson’s syndrome). Papilledema: ICP or hypertensive encephalopathy Otoscopic exam- hemotympanum or CSF otorrhea from a basilar skull # Infections of the middle ear, mastoid, and paranasal sinuses
- 16. Neurological Examination State of Consciousness- auditory, visual, noxious stimuli Supraorbital pressure evokes a response even if afferent pain pathways lost d/t spinal cord lesion or periph. neuropathy blink response to visual threat need not indicate consciousness. apparent coma – ask open or close eyes, look up & down To r/o locked-in state Purposeful movements indicate a milder alteration Vocalization to pain in the early hours of a coma, even if only a grunt light alteration Later, primitive vocalization may be a feature of vegetative state. GCS FOUR score eye response, motor response, brainstem reflexes, respirations
- 18. Pupil Size and Reactivity diencephalic pupils cause small, reactive pupils, Thalamic lesions toxic-metabolic conditions resulting in coma Midbrain lesions produce three types of pupillary abnormality midposition pupils, - fixed to light but react to near vision Dorsal tectal lesions interrupt the pupillary light reflex, fixed, irregular midposition pupils, which may be unequal Nuclear midbrain lesions usually affect both sympathetic and parasympathetic pathways, Wide pupillary dilation, unresponsive to light. Lesions of 3rd nerve fascicle in brainstem, or after brainstem pinpoint pupils- Pontine lesions interrupt sympathetic pathways
- 19. Asymmetry of pupil size may be due to mydriasis of one, such as with 3rd Nr palsy Or miosis of the other, as in Horner syndrome. differentiated by the pupillary reactivity to light and associated neurological signs. A dilated pupil due to a partial third nerve palsy is less reactive a/w extraocular muscle involvement. The pupil in Horner syndrome is reactive sluggishly reactive pupil early s/o uncal herniation, f/b dilation of that pupil and, later, complete 3rd Nr paralysis. common misleading c/o unilateral dilated pupil: mydriatic administration, old ocular trauma or ophthalmic surgery, Carotid artery insufficiency.
- 20. Ocular movement examination Unilateral 3rd Nr palsy - downward and laterally 6th Nr palsy inward deviation- but Poor localisation fourth nerve palsy- subtle deficit, difficult to detect in coma Extraocular nerve palsies often become more apparent with the “doll’s eye maneuver” or cold caloric testing Conjugate lateral eye deviation – d/t ipsilateral lesion in the frontal eye fields Dysconjugate lateral eye movement may result from a sixth nerve palsy in the abducting eye, a third nerve palsy in the adducting eye, or INO Downward deviation- Brainstem lesions- MC is tetctal compression Thalamic and subthalamic lesions produce downward and inward deviation of the eyes- looking at the tip of the nose upward eye deviation- Sleep, seizure, syncope, apnea of Cheyne–Stokes respiration, hemorrhage into the vermis, and brainstem ischemia encephalitis Skew deviation: posterior fossa lesion (brainstem or cerebellar)
- 21. Spontaneous Eye Movements Roving eye movements- Brainstem intact Nystagmus in comatose irritative or epileptogenic supratentorial focus ocular bobbing- classical not pathognomic of pontine lesions Monocular or paretic bobbing – coexisting ocular motor palsy Ocular dipping, also known as inverse ocular bobbing- diffuse cerebral damage Reflex eye movements oculocephalic reflex (doll’s eye phenomenon) caloric (thermal) testing.
- 22. Motor examination in coma Head and eye deviation to one side, with contralateral hemiparesis, suggests a supratentorial lesion, Ipsilateral paralysis - probable brainstem lesion. Decerebrate posturing- Bilateral midbrain or pontine lesions Less commonly, deep metabolic encephalopathies or bilateral supratentorial lesions involving the motor pathways Decorticate posturing occurs with relatively reversible lesions. Unilateral decerebrate or decorticate postures Anywhere in the motor system from cortex to brainstem
- 23. Adventitious movements in the comatose Tonic clonic or other stereotyped movements seizure may be cause of decreased alertness. Myoclonic jerking, - anoxic encephalopathy or metabolic comas, such as hepatic encephalopathy. Rhythmic myoclonus- brainstem injury. Tetany occurs with hypocalcemia. Cerebellar fits of Hughlings Jackson” result from intermittent tonsillar herniation characterized by deterioration of level of arousal, opisthotonos, respiratory rate slowing and irregularity, and pupillary dilatation.
- 24. Toxic- Metabolic Structural •Milder alterations in arousal •waxing and waning of the behavioral state Same level of arousal or progressively deteriorate •Deep, frequent respiration - metabolic abnormalities •Papilledema may occur in metabolic: hypoparathyroidism, lead intoxication, malignant Hypertension Subhyaloid hemorrhage or papilledema are almost pathognomonic •Symmetrical, small, reactive pupils •Except methyl alcohol poisoning, - dilated and unreactive pupils - and hyothermia- fixed pupils Asymmetry in oculomotor function •Roving eye movements with full excursion •Reflex eye movements normally are intact in toxic-metabolic coma, except rarely in phenobarbital or phenytoin intoxication •Myoclonic jerking •Muscle tone symmetrical and normal or decreased asymmetrical muscle tone. Tone - increased, normal or decreased
- 26. Other investigatons ECG EEG- esp in metaolic encephalopahties Also to confirm catatonia, pseudocoma, the locked-in syndrome, PVS, brain death CT or if feasible MRI Evoked potentials Absence of evoked potentials in response to somatosensory stimuli also is highly predictive ofbnonawakening from coma. Intracranial Pressure Monitoring use in treating intracranial HTN following TBI significantly lowers mortality
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