Approach to the comatose patient

Abstract

Coma and other states of impaired consciousness are signs of extensive dysfunction or injury involving the brainstem, diencephalon, or cerebral cortex and are associated with a substantial risk of death and disability. Management of impaired consciousness includes prompt stabilization of vital physiologic functions to prevent secondary neurologic injury, etiological diagnosis, and the institution of brain-directed therapeutic or preventive measures. Neurologic prognosis is determined by the underlying etiology and may be predicted by the combination of clinical signs and electrophysiological tests.

The essential neurological examination of the unconscious patient in the emergency room

“…Despite being recommended in reviews about the approach to the comatose patient (e.g., Stevens & Bhardwaj, 2006; Stevens, Cadena, & Pineda, 2015), fundoscopy was rated lowest by our neurologists. Reasons are speculative only: As fundoscopy may be a useful examination step in the approach to the awake patient with acute headache in the ED to stratify further diagnostic steps (Sachdeva et al., 2018), its role for acute coma is unclear, as the development of papilledema as the most relevant finding in the comatose patient is usually to be expectable at least in the range of several hours and therefore may not be helpful in the clarification of the etiology of acute coma.…”

“…Because this condition represents a medical emergency, quick assessment of the unconscious patient's airway, breathing, and circulation should also be accompanied by a swift neurological examination (NE) (Stevens & Bhardwaj, 2006; Stevens, Cadena, & Pineda, 2015). While the medical history and focused presenting of the patient can each provide clues about the etiology of the coma, the results of the NE can greatly facilitate this process by providing important information about the site of the underlying lesion or pathophysiological process (i.e., increased intracranial pressure, infection, etc.).…”

“…Scientific publications (e.g., Stevens & Bhardwaj, 2006; Stevens et al., 2015) as well as neurology (Bender, Remi, Feddersen, & Fesl, 2012; Biller, Gruener, & Brazis, 2011; Delank & Gehlen, 2015; Fuller, 2013; Hacke, 2016; Mattle & Mumenthaler, 2015; Posner, Saper, Schiff, & Plum, 2007; Urban, 2012) or emergency medicine (Marx, Hockberger, & Walls, 2013; Tintinalli, Stapczynski, Ma, Meckler, & Cline, 2010) textbooks often describe the NE of the unconscious patient as a complex procedure that includes a multitude of elaborate features. It should be noted, however, that these appraisals are based on the opinions of just a few experts, mostly tracing back to the approaches described either by Plum and Posner, which was first published in 1966 (Plum & Posner, 1966), or C. M. Fisher's work (Fisher, 1969) published in 1969.…”

“…The most commonly applied approach to the NE aims to differentiate between focal asymmetric clinical deficits, primarily located in the motor system, and nonfocal symmetric findings; this can then help determine the underlying cause of the symptoms as being a localized structural brain lesion/functional disturbance (e.g., ischemic or epileptic) vs. nonstructural events (e.g., toxic‐metabolic), respectively (Stevens & Bhardwaj, 2006; Stevens et al., 2015). However, severe neurological diseases such as meningitis, subarachnoid hemorrhage, or basilar artery occlusion (including top of the basilar syndrome) often present with coma, either without focal asymmetric deficits, or with bilateral symmetric deficits (Caplan, 1980; Mattle, Arnold, Lindsberg, Schonewille, & Schroth, 2011; Schwarz, Egelhof, Schwab, & Hacke, 1997).…”

Brain Death: Assessment, Controversy, and Confounding Factors

“…Consciousness or responsiveness (wakefulness) reflects intact function of neurotransmitters and the ascending reticular activating system connecting the pons, thalamus, and midbrain with the diencephalon and cerebral cortex. [22][23][24][25] Loss of cerebral hemispheric function is evidenced by total loss of consciousness, unresponsiveness to all stimulation mediated above the spinal cord, and lack of arousal, awareness, and sleep-wake cycles. 22,26,27 Unresponsiveness to noxious stimuli can be assessed by using stimuli such as a sternal rub or pressure on the supraorbital notch or temporomandibular joint or both.…”