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Coma
- 2. Anatomy related to coma
- 5. Common causes of coma
- 6. INTRODUCTIONAlert being alert reflects an underlying, well- functioning cerebral cortex, brainstem, and reticular activating system lethargy In a deeper level of unconsciousness, lethargic patients remain with their eyes closed and appear asleep; however, with stimulation, they open their eyes and temporarily assume an alert state. Even when aroused, these patients are typically inattentive, disoriented, and cognitively impaired. Causes Sleep deprivation 1. toxic-metabolic aberrations 2. large destructive lesions 3. increased intracranial pressure Conditions that cause An aspect of delirium (“toxic- metabolic encephalopathy.’’) Stupor Stuporous patients remain unarousable with their eyes closed. They respond with only rudimentary motor or verbal responses to verbal or tactile stimuli. Causes 1. metabolic aberrations 2. structural lesions • Structural lesions usually also produce lateralized signs, such as hemiparesis. 3. increased intracranial pressure L e v e l o f u n c o n s c i o u s n e s s
- 7. Introduction continuesComa • Coma , which can be graded by the Glasgow Coma Scale • Is the most profound depression of consciousness. • Comatose patients always have closed eyes, make little or no verbal responses, and move their limbs just reflexively. • This profound depth of unconsciousness reflects profound disturbance of both cerebra l hemispheres or the brainstem. • Sometimes the patient returns from coma to the locked-in syndrome, PVS, or minimally responsive state.
- 8. Locked-In Syndrome Among the innumerable patients who have sustained strokes or other structural lesions and appear completely incapacitated. Presentation Patients are mute, quadriplegic, bedridden, and totally dependent on caregivers. however, these patients remain alert, have intact cognitive capacity, and can communicate by moving their eyes. their completely disabled body encases (locks -in) an intact mind Pathophysiology Usually results from an infarction of the base or ventral surface of the pons (basis pontis) or medulla (bulb), usually because a thrombosis or embolus has occluded a branch of the basilar artery. Bulbar palsy and bilateral interruption of the corticospinal tracts render patients mute and quadriplegic. They almost always require tracheostomy, ventilator support, and feeding tubes.
- 9. Despite the devastating neurologic damage, the upper brainstem, bulb’s dorsal surface (including the reticular activating system), and cerebral cortex remain intact the physiologic circuits between the cerebral cortex and upper brainstem, including the thalamus, continue to reverberate patients retain normal cognition, affective capacity, and, given sufficient clues, a sleep-wake cycle. relatively normal EEG. Although otherwise almost totally paralyzed, patients can still purposefully move their eyes and eyelids. Causes Several peripheral nervous system (PNS) diseases & bulbar lesions myasthenia gravis ALS Guillain-Barre´ syndrome other PNS illnesses
- 10. Management The medical, social, and legal management of locked-in syndrome patients should be based on their being cognizant. They can remain alert and comprehend people talking and reading to them. They can convey their wishes, including decisions regarding their care. Prognosis Although locked-in syndrome patients who have suffered a brainstem infarction partially recover, their overall prognosis is poor. In contrast, patients debilitated from a PNS illnesses often fully recover
- 11. Persistent Vegetative State Extensive cerebral damage, in either children or adults, may cause the persistent vegetative state (PVS) Much more common than the locked-in syndrome. Difference between lock-in syndrome and PVS PVS patients, unlike those in a locked-in syndrome, lack self- awareness and cognizance of their surroundings, have lost all cognitive capacity, and cannot communicate in any manner. Similarities between Locked-in syndrome and PVS They are both bedridden with quadriparesis and incontinence. Causes Acute, massive cerebral insults, including: Major traumatic brain injury Cerebral anoxia from cardiac arrest or drug overdose Profound hypoglycemia Massive strokes Progression of neurodegenerative illnesses, such as Alzheimer’s disease Childhood onset metabolic disorders. After 1 month of existing in a vegetative state, patients fall into the category of persistent vegetative state
- 12. Presentation In what might constitute a misleading appearance these patients seem alert with open eyes retain sleep-wake periods breathe without respirators withdraw a limb from noxious stimulation maintain hypothalamic and brainstem reflexes (vegetative functions) Their eyes, moving spontaneously and randomly, may momentarily fix on a face or reflexively turn toward voices or other sounds The vegetative activity and seeming wakefulness are rudimentary. With their lack of consciousness, patients in the PVS can neither perceive pain nor suffer
- 13. Minimally Responsive State Patients have lost almost their entire cognitive capacity and voluntary movements They require complete bodily care. But retain a fragment of mental function Unlike patients in the PVS, ones in the minimally responsive state are conscious and interactive— albeit in the smallest ways—with their environment, visitors, or family members. Nevertheless, their reactions are only miniscule, inconsistent, and liable to be ‘‘seen’’ only by wishful relatives. Patients at least follow simple requests Causes similar to PVS
- 14. Catatonia A marked psychomotor disturbance that may involve decreased motor activity, decreased engagement during interview or physical examination, or excessive and peculiar motor activity. Diagnosis The presence of 3 or more of 12 psychomotor features in the diagnostic criteria for catatonia associated with another mental disorder and catatonic disorder due to another medical condition. Treatment Benzodiazepines ECT
- 15. Management strategy or algorithm
- 16. History Obtained from who ever accompanies the patient FOCUSED NEUROLOGIC EXAMINATION motor responses to stimuli respiratory patterns pupils, and eye movements, classic monograph, Plum and Posner General examination
- 17. Practical Pearls in the Physical Examination of the Comatose Patient System Positive Finding Body temperature •Fever (implies infection or heatstroke) •Hypothermia (cold exposure, sepsis, cardiac arrest, hypothyroidism, hypoglycemia) Peripheral pulses •Asymmetry of pulses suggests dissecting aortic aneurysm. Head and scalp •External signs of trauma (e.g., mastoid ecchymoses consistent with Battle sign) •Ears and nose are examined for blood or CSF.
- 18. Breath •Acetone •Alcohol •Fetor hepaticus Optic fundi •Papilledema (suggests elevated ICP), hypertensive or diabetic retinopathy, retinal ischemia •Roth spots (suggests endocarditis) •Subhyaloid hemorrhages (suggests subarachnoid hemorrhage) Neck •Resistance to passive neck flexion but not to turning suggests meningitis, subarachnoid hemorrhage, or foramen magnum herniation. •Resistance to manipulation in all directions suggests bone or joint disease, including fracture. Urinary or fecal incontinenc •May signify an unwitnessed seizure, especially in patients who subsequently awaken
- 19. Skin, nails, and mucous membra nes •Pallor •Cherry redness (carbon monoxide poisoning) •Cyanosis •Jaundice •Sweating •Uremic frost •Myxedema (dry, flaky, cool skin) •Petechiae •Dehydration •Decubiti •Signs of trauma
Editor's Notes
- Other words used to describe coma include -confused -Stuporous -agitated -unresponsive -comatose -delirous -unconcious
- Summery Physicians might examine stroke victims (and those with severe, extensive PNS disease) for the locked-in syndrome if they are unable to speak or move their limbs but have their eyelids open and can voluntarily look from side to side. The physician should ask these patients to blink a certain number of times. If they respond, a system of communication can be developed. (One patient communicated freely using eyelid blinks in Morse code.) If patients can blink meaningfully, the physician should test their ability to see and calculate. Afterward, physicians can undertake detailed mental status testing.
- Course Following acute insults, most patients are typically comatose for days to weeks before entering a vegetative state. Patients with neurodegenerative illnesses usually slip into a PVS without first entering coma. Once patients have been in PVS from head trauma for 1 year or from degenerative illness for 3 months, they have no realistic chance of recovery.
- Summery Beyond its heart-wrenching neurologic aspects, PVS raises important ethical and legal considerations. Acting on patients’ living wills or other directions that they ‘‘not live like a vegetable,’’ their relatives have sought to discontinue nutrition and artificial supports. Several well-known legal cases have explored the limits of maintaining PVS patients in accordance with their wishes or in the absence of any known wish. In general, the courts have allowed the health care proxy or closest relative to make decisions regarding the patient in the vegetative state, including removing food and nutrition
- Unlike patients in the PVS, ones in the minimally responsive state are conscious and interactive—albeit in the smallest ways—with their environment, visitors, or family members. Nevertheless, their reactions are only miniscule, inconsistent, and liable to be ‘‘seen’’ only by wishful relatives.
- Medical causes neurological conditions (e.g., neoplasms, head trauma, cerebrovascular disease, encephalitis) metabolic conditions (e.g., hypercalcemia, hepatic encephalopathy, homocystinuria, diabetic ketoacidosis).
- Initial management of the comatose patient should always focus on the ABCs: airway, breathing, and circulation. Assuring a patent airway, securing adequate ventilation, and restoring or maintaining circulation should take precedence, as it does with any critically ill patient. Vascular access needs to be obtained as soon as possible and may include central venous access and large bore peripheral access. Detection and treatment of immediately life-threatening systemic conditions may include stopping a hemorrhage; supporting the circulation by administration of fluids, blood products, or pressors; intubation when necessary (e.g., to prevent aspiration in a patient who is vomiting); and obtaining an electrocardiogram to detect dangerous arrhythmias. Fingerstick glucose should be obtained immediately and if in doubt, 50% dextrose should be given intravenously with parenteral thiamine. (Administering glucose alone to a thiamine-deficient patient can precipitate Wernicke-Korsakoff syndrome.) When opiate overdose is a possibility, naloxone hydrochloride (Narcan) 0.4 mg IV is given. If trauma is suspected, damage to internal organs and cervical fracture should be assumed until radiographs determine otherwise and emergency ultrasound scanning (i.e., focused assessment with sonography for trauma [FAST]) or other imaging has ruled out major internal bleeding or organ injury.
- In their classic monograph, Plum and Posner divided the causes of coma into supra- and infratentorial structural lesions and diffuse or metabolic diseases. 1. Motor Responses Appearance: The patient is observed to assess respiration, limb position, and spontaneous movements. Myoclonus or seizures may be subtle (e.g., twitching of one or two fingers or the corner of the mouth). More florid movements, such as facial grimacing, jaw gyrations, tongue protrusion, or complex repetitive limb movements, may defy ready interpretation. Asymmetric movements or postures may signify either focal seizures or hemiparesis. Tone: Assessment of motor tone is crucial in the examination of coma. Asymmetry of muscle tone suggests a structural lesion, but it is not always clear which side is abnormal. Gegenhalten, or paratonia, is variable resistance to passive movement that often increases with the velocity of the movement; it is attributed to diffuse forebrain dysfunction and is often accompanied by a grasp reflex. Rigidity is present throughout the entire range of movement, is often seen in combination with cogwheeling, and usually indicates basal ganglia dysfunction (e.g., parkinsonism) or symptomatic hydrocephalus. Spasticity has a characteristic “catch” midway through passive movement and indicates corticospinal pathway dysfunction. Acute transtentorial herniation often produces exaggerated lower extremity spasticity and clonus. 2. Respiration In Cheyne-Stokes respiration (CSR), periods of hyperventilation and apnea alternate in a crescendo-decrescendo fashion. The hyperpneic phase is usually longer than the apneic, so arterial gases tend to show respiratory alkalosis. CSR occurs with bilateral cerebral disease or metabolic encephalopathy. It usually signifies that the patient is not in imminent danger. Long-cycle CSR, with brief periods of apnea occurring every 1 to 2 minutes, is a stable breathing pattern and does not imply impending respiratory arrest. Conversely, “short-cycle CSR” (cluster breathing) with less smooth waxing and waning is often an ominous sign of a posterior fossa lesion or dangerously elevated ICP. Sustained hyperventilation is usually due to metabolic acidosis, pulmonary congestion, hepatic encephalopathy, or during acute herniation. Rarely, it is the result of a lesion in the rostral brain stem. Apneustic breathing, consisting of long inspiratory pauses, is seen with pontine lesions, especially infarction; it occurs infrequently with metabolic coma or transtentorial herniation. Respiration having a variably irregular rate and amplitude (ataxic breathing) indicates medullary damage and may progress to apnea, which also occurs abruptly in acute posterior fossa lesions. Loss of automatic respiration with preserved voluntary breathing (Ondine curse) occurs with medullary lesions; as the patient becomes less alert, apnea may be fatal. Other ominous respiratory signs are end-expiratory pushing (e.g., coughing) and “fish-mouthing” (i.e., lower jaw depression with inspiration). Stertorous breathing (i.e., inspiratory noise) is a sign of airway obstruction. Pupils Pupillary abnormalities in coma may reflect an imbalance between input from the parasympathetic and sympathetic nervous systems or lesions of both. Although many people have slight pupillary inequality, anisocoria should be considered pathologic in a comatose patient. Retinal or optic nerve damage does not cause anisocoria, even though there is an afferent pupillary defect. Parasympathetic lesions (e.g., oculomotor nerve compression in uncal herniation or after rupture of an internal carotid artery aneurysm) cause pupillary enlargement and, ultimately, full dilation with loss of reactivity to light. Sympathetic lesions, either intraparenchymal (e.g., hypothalamic injury or lateral medullary infarction) or extraparenchymal (e.g., invasion of the superior cervical ganglion by lung cancer), cause Horner syndrome with miosis. With involvement of both systems (e.g., midbrain destruction), one or both pupils are in mid position and are unreactive. Small but reactive pupils following pontine hemorrhage are the result of damage to descending intra-axial sympathetic pathways. With few exceptions, metabolic disease does not cause unequal or unreactive pupils. Fixed, dilated pupils after diffuse anoxia -ischemia denote a bad prognosis. Anticholinergic drugs, including glutethimide, amitriptyline, and antiparkinsonian agents, abolish pupillary reactivity. Hypothermia and severe barbiturate intoxication may cause not only fixed pupils but also a reversible picture that mimics brain death. Bilateral or unilateral pupillary dilation and nonreactivity may accompany (or briefly follow) a seizure. In opiate overdose, miosis may be so severe that a very bright light and a magnifying glass are necessary to detect reactivity. Some pupillary abnormalities are local in origin (e.g., trauma or synechiae). Eyelids and Eye Movements Spontaneous blinking may occur with or without purposeful limb movements. Eyes that are conjugately deviated away from hemiparetic limbs indicate a destructive cerebral lesion on the side toward which the eyes are directed. Eyes turned toward paretic limbs may indicate a pontine lesion, an adversive seizure, or the wrong-way gaze paresis of thalamic hemorrhage. Eyes that are dysconjugate while at rest may indicate paresis of individual muscles, internuclear ophthalmoplegia, or preexisting tropia or phoria. When the brain stem is intact, the eyes may rove irregularly from side to side with a slow, smooth velocity; jerky movements suggest saccades and relative wakefulness. Repetitive smooth excursions of the eyes first to one side and then to the other, with 2- to 3-second pauses in each direction (periodic alternating or ping-pong gaze), may follow bilateral cerebral infarction or cerebellar hemorrhage with an intact brain stem.