Coma

Chapter 59 Coma



Ala Nozari, MD, PhD , Corey R. Fehnel, MD , Lee H. Schwamm, MD, FAHA




1 What is coma, and how is it different from persistent vegetative state (PVS), minimally conscious state (MCS), or locked-in syndrome?




image Coma is a state of profound unresponsiveness caused by structural, metabolic, physiologic, or psychogenic brain dysfunction. The comatose patient is unaware of self and environment and cannot be roused to respond to vigorous stimulation.


image In contrast to coma, patients with PVS are in a state of partial arousal and may briefly alert to sound or visual stimuli. They withdraw to noxious stimuli but are unable to interact or respond voluntarily or in any purposeful way to stimuli. PVS is a chronic condition and thus is typically not assigned unless a patient’s state of altered consciousness persists for more than 30 days.


image Patients in MCS exhibit deliberate or cognitively mediated behavior, may intermittently follow commands, or have intelligible but inconsistent verbal output. Patients may evolve to MCS from coma or PVS.


image Patients with locked-in syndrome have intact cognition but complete paralysis of voluntary muscles in all parts of the body. They traditionally have been able to communicate through code systems by blinking or repeated up-and-down eye movements; however, recent breakthrough technology has allowed some patients to communicate via a human-machine computer interface that allows patients to initiate computer commands with only their thoughts through the use of a surgically embedded microchip in the cerebral cortex.



2 Which are the major categories of disorders or injuries that cause coma?




image Coma can be caused by structural brain injury involving the relay nuclei and connecting fibers of the ascending reticular activation system (ARAS), which extends from upper brainstem through synaptic relays in the rostral intralaminar and thalamic nuclei to the cerebral cortex. The base of pons does not participate in arousal, and lesions such as central pontine myelinolysis do not usually profoundly impair consciousness. Instead, these lesions can interrupt all motor output except vertical eye movements and blinking that are initiated by nuclei in the mesencephalon (locked-in syndrome).


image Mesencephalic and thalamic injuries, for example, as a result of occlusion of the tip of the basilar artery, or bilateral thalamic injuries, may result in somnolence, immobility, and decreased verbal output characteristic for MCS.


image Bihemispheric injuries involving the cortex, white matter, or both may also result in impaired arousal.


image Similarly, an acute unilateral hemispheric or cerebellar mass can lead to coma through destruction of the brain tissue and displacement of the falx and brainstem.


image Physiologic brain dysfunction as a result of generalized tonic-clonic seizures, hypothermia, and poisoning or acute metabolic and endocrine derangements can also lead to coma. Typically, metabolic coma may spare the pupillary light reflex as it causes selected dysfunction of the cortex, whereas brainstem centers that control the pupils are spared. Hypoglycemia or nonketotic hyperosmolar coma, dysnatremia, thyroid storm, myxedema, fulminant hepatic failure, and acute hypopituitarism are examples in this category and should always be considered in a comatose patient. Asterixis, tremor, myoclonus, and foul breath may predominate the examination before these patients become unresponsive.


image Malignant catatonia and psychogenic unresponsiveness should also be considered in all unresponsive patients.


image Acute muscle paralysis (e.g., botulism or other toxins) should also be ruled out, because these patients may be awake and cognitively intact but unable to demonstrate responsiveness.



3 Name common causes of structural brain injury in comatose patients


Structural brain injuries may be caused by the following:



image Bilateral cortical or subcortical infarcts (e.g., as a consequence of cardiac embolization or occlusion of major cerebral vessels)


image Bleeding (e.g., hemorrhagic contusions, epidural or subdural hematoma, subarachnoid hemorrhage)


image Infections (e.g., meningitis, cerebral abscess, subdural empyema, and herpes encephalitis)


image Neoplasm (primary tumors and metastases)


image Vasculitis and leukoencephalopathy, or lateral (acute midline shift of the brain of >1 cm) or downward herniation from mass effect or increased intracranial pressure (ICP) (e.g., massive brain edema, obstructive hydrocephalus)



4 Describe the mechanisms of toxin-induced coma


Depression of neuronal function can be caused by a reduction in the turnover of major neurotransmitters such as acetylcholine, dopamine, and serotonin through the γ-aminobutyric acid–benzodiazepine chloride iodophor receptor complex. Moreover, toxins can result in hypoxia (e.g., through respiratory depression or aspiration) or hypoglycemia (e.g., ethanol, β-blockers, and salicylates) leading to coma. Seizures can also be induced by toxins, as are acute cerebral bleedings, for example, caused by hypertension (cocaine, amphetamine) or coagulation abnormalities. Insulin is a common factor among patients with insulin-dependent diabetes.



5 What are the initial steps in managing a patient with coma?


The immediate approach to the comatose patient includes measures to protect the brain by providing adequate cerebral blood flow and oxygenation, reversing metabolic derangements, and treating potential infections and anatomic or endocrine abnormalities.



image The clinician must ensure that the patient has a patent and protected airway and adequate breathing. Supplemental oxygen should be administered and airway secured by intubating the trachea, if needed.


image Vascular access should be obtained and hypotension corrected with vasopressor agents or fluid administration as required.


image Blood samples should be obtained to rule out infection and metabolic or endocrine abnormalities.


image Generalized seizures should be treated and metabolic abnormalities corrected as soon as possible.


image If the cause of coma is uncertain and hypoglycemia cannot be excluded, 50% dextrose should be administered. Empirical therapy for Wernicke encephalopathy or narcotic or sedative overdose should be considered and thiamine, naloxone, or flumazenil administered if appropriate. Thiamine must be given before dextrose to prevent worsening of Wernicke encephalopathy.


image If increased ICP with mass effect is suspected, the patient should have hyperventilation, mannitol, or hypertonic saline solution administered, and specific surgical measures to evacuate possible mass or hematoma should be initiated.


image If meningitis is suspected, antibiotic treatment should be initiated, and then a computed tomography (CT) scan of the head performed to rule out mass effect or herniation, in combination with laboratory evaluation for coagulopathy or thrombocytopenia before lumbar puncture.

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Jul 6, 2016 | Posted by in CRITICAL CARE | Comments Off on Coma

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