Coma

61


Coma





Concept and Terminology of Impaired Consciousness


Alteration of consciousness is a frequent admission diagnosis to critical care services. Most patients require immediate and often extensive diagnostic workup as both time to diagnosis and treatment initiation are decisive factors for brain recovery. To the public, the portrayal of coma is overly optimistic as 89% of “comatose” patients in a meta-analysis of 64 characters in American soap dramas regained consciousness and around 92% “survived” coma.1 In contrast, medical experience does not compare as favorably, as only about 50% of patients survive in an unselected coma population.2–4 Therefore, defining coma in a succinct and operational manner will provide a deeper understanding of the depth of brain injury and avoid miscommunications and unrealistic prognostications.


Consciousness can be viewed as the patient’s responses to internal and external stimulation and his or her awareness of self and the environment. These two basic components of consciousness, arousal and awareness, are clinically used to classify the state of consciousness, but, strictly speaking, the qualitative examination of arousal should be separated from the quantitative assessment of the patient’s self- and environmental awareness and cognitive function. These interdependent components are regulated by different neuroanatomic domains within the central nervous system. Arousal and ensuing wakefulness are tightly dependent on the network function of the ascending reticular activating system (ARAS), namely, the midbrain reticular formation, mesencephalic nucleus and tegmentum, thalamic intralaminar (centromedian) nucleus, and dorsal hypothalamus. These build a network of brainstem and diencephalic centers with a strong connection to the cerebral cortices. Self-awareness and the spectrum of cognitive interactions with the environment are the purview of the hemispheres. Simplistically, the hemispheres are structured into three functional systems: units that receive, process, and store sensory information; units that generate and regulate motor activity; and units responsible for programming, regulating, and verifying actions. These three functional systems operate as an intercortical network; relate, as a whole, to the experience of awareness; and allow cognitive performance. The partition of arousal network and intercortical (cognitive) network implies that the level of self-awareness and cognitive performance cannot be examined in a patient with lack of arousal. In other words, in a person with a quantitatively reduced state of consciousness, the qualitative assessment of the content of consciousness is not possible. Practically speaking, the assessment of content (i.e., testing a patient’s cognitive abilities and thinking) should be done after the best level of arousal has been achieved. A fully aroused person can express completely normal or deficient awareness and cognitive performance. Conversely, failure of arousal renders it impossible to test awareness and cognition.


When evaluating a patient’s mental status, the state of consciousness should be viewed as a continuum ranging from the patient who has full alertness and cognitive lucidity to the deeply comatose patient; it is not an all-or-nothing phenomenon.5 An all-or-nothing approach limits the interpretation of remaining brain function and, hence, diagnostic certainty. Furthermore, the duration and time development of coma are helpful diagnostic features and should complement the quantitative and qualitative assessment of consciousness. Standard classification systems categorize consciousness based on systematic testing of arousal, awareness, and content. Table 61.1 classifies various abnormalities of consciousness, and the following section delineates clinically important syndromes.



In the awake state, the examination allows the clinician to test a person for the degree of self-awareness and intactness of cognitive function. Drowsiness, sleepiness, and lethargy resemble reduced spontaneous physical and mental activities in a person who cannot sustain wakefulness without repeated external stimulation. They are somewhat comparable to the experience of lighter sleep, though drowsy patients almost always have reduced attention and concentration and some degree of associated mild confusion. Although sleep and pathologic states of consciousness share common features—for instance, the sleeping person is unaware of his or her resembling unconsciousness—quick reversal to full consciousness is a classic feature of sleep.


A stuporous patient (from Latin stupure, meaning “insensible”) requires repeated, stronger stimuli to show some arousal, and these patients may or may not open their eyes. Full arousal and alertness are not achieved and with continuing external stimulation, restlessness and stereotypic motor responses are observed, but without the appropriate cognitive interactions. A deep stuporous state closer to coma is differentiated by European clinicians and is referred to as sopor (from Latin sopor, meaning “deep sleep”).


Coma (from Greek κimageµα, or “deep sleep”) is a continuous state of unresponsiveness identified by an inability to arouse to vigorous (noxious) external or internal stimuli. The degree of coma can differ; lighter stages (sometimes denoted as semicoma) can be identified by brief moaning to strong stimulation and associated observed changes in autonomic function; whereas the deepest coma examination shows an absence of any response, including brainstem reflex responses (i.e., lack of oculo- and pupillomotoric responses). Some cyclic autonomic activity such as the sleep-wake cycle and changes in motor tone may coexist. A detailed discussion of coma is provided in the classic textbook by Plum and Posner.6


The vegetative state is characterized by the complete absence of behavioral evidence for self- or environmental awareness. This state can follow coma and identifies a state in which brainstem and diencephalic (thalamic) activity is present to a degree that clinical signs of spontaneous or stimulus-induced arousal and sleep-wake cycles are observed. Patients often show blink responses to light; intermittent eye movements (sometimes erroneously interpreted as following objects or looking at family members); stimulus-sensitive automatisms such as swallowing, bruxism, and moaning; or primitive motor responses. If this state lasts longer than 30 days, it is referred to as persistent vegetative state (PVS) and is used as a descriptive clinical syndrome rather than a disease-specific entity. The most common causes include cardiac arrest, head trauma, severe brain infections, and various causes of thalamic injury. Vegetative states can also be seen in the terminal phase of degenerative illnesses such as Alzheimer’s disease. Ambiguous terms for PVS such as apallic syndrome and neocortical death should be avoided.2,7


Minimal conscious state can be diagnosed in patients displaying some but often inconsistent behavioral evidence of awareness of the environment, but they cannot communicate their content and are unable to follow instructions reliably.8 It describes a large group of patients who are different from vegetative patients in that they demonstrate some signs of awareness of themselves and their surroundings, albeit inconsistently.


As mentioned earlier, the time progression and persistence of the impairment can be used to further classify abnormalities of consciousness. Delirium is classified as a mental disorder because it involves a fluctuating level of consciousness and pervasive impairment in mental, behavioral, and emotional functioning. It is commonly acute in onset and short in duration and is frequently correlated to a specific etiology such as medications, anesthesia, or sleep deprivation. The criteria for delirium listed in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) include a disturbance of consciousness with reduced the ability to sustain or shift attention and focus. In our experience, attention and concentration deficits are always present in delirious patients and accompanied by a variable degree of cognitive dysfunction unattributed to preexisting dementia. The dysfunctions of this acute syndrome include memory deficits, disorientation, disturbance of language and situational perception, and disorganized behavior. Other delirium markers are its acute onset and tendency to fluctuate along a spectrum of hyperactive (i.e., agitation, restlessness, emotional labiality), hypoactive (withdrawal, flat affect, apathy, decreased responsiveness), or mixed presentations. Concurrent or sequential appearance of features of both hyper- and hypoactive states is not unusual. The history, physical examination, and ancillary test results frequently indicate that the disturbance is caused by an underlying medical or situational condition.


Dementia is a chronic condition in which content of consciousness is affected initially, but in advanced stages reduced levels of arousal are seen. Dementia is generally progressive and affects memory and at least two other cognitive domains such as language, executive function, planning motor tasks, and recognition. Dementing illnesses include a variety of intrinsic degenerative diseases of the cerebral hemispheres, but they also result from many other causes such as traumatic brain injury and hydrocephalus. The underlying etiology can be reversible (i.e., after correction of a vitamin deficiency) or irreversible (Lewy body dementia). Additionally, disease progression can be highly variable, lasting weeks to years, often with fluctuating severity, or be static after the initial impact injury. Anxiety, depression, and agitation may alternate and greatly complicate the disease course. The anatomically affected neurologic structures are commonly a result of bihemispheric cortical dysfunction; however, subcortical structures (i.e., vascular dementia from multifocal small vessel disease) can also represent the predominant pathology.


Akinetic mutism is a silent, alert-appearing immobility of a patient with injury to the hypothalamus or basal forebrain. It manifests as apparent depressed levels of consciousness in a patient with well-formed sleep-wake cycles and with little or no evidence of awareness or spontaneous motor activity. Various etiologies can present or lead to an akinetic mute state, and it is imperative to have a rigorous neurologic examination and careful review of neuroimaging and electroencephalography (EEG). The term locked-in syndrome was introduced by Plum and Posner to describe the quadriplegia and anarthria resulting from the disruption of corticospinal and corticobulbar pathways, respectively. The extent of the deficits in patients with locked-in syndromes can vary, but these patients are aware of the environment and can hear and understand what is discussed around them. They may retain some ability of oculomotor (i.e., ability to open eyes) or other residual cranial nerve function. These patients are also anarthric or severely dysarthric with varying degrees of motor deficits ranging from complete quadriplegia to quadriparesis. As consciousness is preserved, communication is possible using vertical or lateral eye movements or blinking of the eyelid to signal yes/no responses. The majority of cases are caused by basilar artery occlusion leading to brainstem infarction in the ventral pons, yet numerous other etiologies have been described. Abulia (from the Greek meaning “lack of will”) is an apathetic state in which the patient is awake, has normal sleep-wake cycle, and is very slow to respond to stimuli. Mental function is usually normal when tested with sufficient stimulation. It is secondary to bilateral frontal lobe disease and in severe instances may mimic or progress to akinetic mutism.



Neuroanatomy, Neurotransmitter, and Pathology


Consciousness, which consists of three main parts, largely depends on the integrity of brain structure for arousal (Fig. 61.1). The ascending reticular activating system (ARAS) is the lowest order arousal system, consisting of a set of brainstem nuclei located within the brainstem and interconnected by neuronal circuits. The ARAS relays arousal signals to the more rostral thalami, which, in turn, act as hemispheric gatekeepers of arousal and regulate consciousness and sleep-wake transitions. In turn, thalamic activated cerebral cortices allow cognitive processing, which then determines the overall content of consciousness.6 Structural damage to or metabolic-chemical derangements of any or all of these elements will affect consciousness. Important components of the ARAS9–11 include the midbrain reticular formation, mesencephalic nuclei (dorsal raphe nucleus, pedunculopontine tegmental nucleus, locus coeruleus), and ventral tegmental areas. Those areas have rich connections to thalamic intralaminar nuclei and further frontally reaching projections to the tuberomammillary nucleus, lateral hypothalamus, and basal forebrain.



The ascending arousal system of the brainstem contains different neurotransmitter systems. Main cholinergic projections include the ascending mesopontine tegmental and basal forebrain pathways projecting to the thalami and to virtually all subcortical and cortical structures. These projections usually function as synaptic facilitators but at times can act as depressors of transmission.12 Glutamate is the main transmitter influencing the firing patterns of tegmental cholinergic neurons.13 The adrenergic component of the ARAS is closely associated with the noradrenergic neurons of the midbrain locus coeruleus. It runs in parallel with cholinergic projections rostrally to the cortical areas but also descends caudally within the spinal cord.14 Hypocretin/orexin neurons within the hypothalamus activate both adrenergic and cholinergic pathways and coordinate activity of the entire ARAS system, enhancing complementary and synergistic control of arousal and locomotion.15 Histamine-releasing cells from the hypothalamus and tuberomammillary neurons are active during the qualitative activation needed for cognition and EEG activation, but they remain silent during sleep.16–18


The main inhibitor of the arousal system is γ-aminobutyric acid (GABA), without which normal sleep does not occur. The GABAergic circuitry is located in the midbrain and pons, but its activity is regulated and sustained by forebrain structures.19 It is thought that the GABAergic system’s main function is to contain and channel the spread of arousal, both spontaneously and in response to a stimulus. GABAergic processes are responsible for the occurrence of paradoxical sleep (deep sleep characterized by a brain wave pattern similar to that of wakefulness, rapid eye movements, and heavier breathing but without motor responses). The name “waking neurons” has been given to the serotonergic dorsal raphe nucleus in the midbrain,20 which receives convergent excitatory input from the noradrenaline, histamine, and hypocretin/orexin arousal systems21,22 as the main activator of the ARAS. Cortical signals that pass through the striatum (caudate and putamen) are refined by the action of dopamine. Dopaminergic neurons are tonically active and stimulate or inhibit cortical neurons depending on various environmental influences (pain, hunger, etc.).23,24 It is thought that many sensory signals that reach conscious awareness pass through this basal ganglia loop with dopamine as the modulating neurotransmitter. Koch and colleagues suggested that coalitions of neurons compete to dominate conscious thoughts and activities at any given time point and, hence, dopaminergic innervation may facilitate the transient domination of conscious awareness by certain sets of neuron coalitions.25 Therefore, it seems that arousal is an event with a defined time distribution, which is tightly orchestrated by a few key neurotransmitters. As we know, there is no singular “arousal neurotransmitter.”10,26



Pathology Seen in Patients with Impaired Consciousness


There are four major pathologies that can cause severe, acute, and global reductions of consciousness.6,27 (1) One of these pathologies is the presence of diffuse, global, or extensive multifocal bilateral dysfunction of the cerebral cortex. In this injury mechanism, the cortical gray matter is diffusely impaired and so are cortical-subcortical excitatory feedback loops. The clinical examination will reveal disinhibited autonomic brainstem reflexes, which have also been described as “reticular shock.” (2) Another is injury to the paramedian gray matter from the level of the nucleus parabrachialis of the pons (tegmentum) and reaching to the midbrain pretectal areas and ventral posterior hypothalamus. An injury of this type damages the ascending arousal system and normal cortical activation. The affected structures are predominantly the paramedian gray matter, extending rostrally from the level of the nucleus parabrachialis of the pons (tegmentum) and reaching rostrally as far as the adjacent pretectal area and ventral posterior hypothalamus. (3) The widespread disconnection of the cortex from subcortical activating mechanisms acts pathophysiologically to produce effects similar to both of the previously mentioned conditions. (4) Finally, cortical and subcortical arousal mechanisms can be affected by a variety of diffuse disorders and to various degrees—for example, metabolic encephalopathy in a patient with acute liver failure.



Approach to Coma


The initial approach to stupor and coma is based on the principle that all alterations in arousal are acute, life-threatening emergencies. Urgent steps are required to prevent or minimize permanent brain damage from reversible causes. Patient evaluation and treatment must occur simultaneously. Serial examinations with accurate documentation are necessary to determine a change in the patient’s status. Accordingly, management decisions (therapeutic and diagnostic) must be made. The clinical approach to an unconscious patient entails the following steps: (1) emergency treatment; (2) history (from relatives, friends, and emergency medical personnel); (3) general physical examination; (4) neurologic profile, the key to categorizing the nature of coma; and (5) specific management.



Emergency Management


Initial assessment must focus on vital signs to determine appropriate resuscitation measures; diagnostic processes can occur later. Urgent and sometimes empiric therapy must be given to avoid additional brain insults.



Oxygenation and Intubation


Oxygenation must be ensured by establishing an airway for ventilation of the lungs. The threshold for intubation should be low in a comatose patient, even if respiratory function is sufficient for proper ventilation and oxygenation. The level of consciousness may deteriorate, and breathing may decompensate suddenly and unexpectedly. An open airway must be ensured and protected from aspiration of vomitus and blood. If severe neck injury is a possibility or has not been excluded, intubation should be performed by the most skilled practitioner without extension of the patient’s neck. Mask-bag-assisted ventilation should continue during the examination if necessary. Signs of arousal include dilated, reactive pupils, copious tears, diaphoresis, tachycardia, and systemic hypertension.


A brief neurologic examination is mandatory before any sedative or paralytic required for intubation is administered. The key points of a rapid neurologic examination are the following:28



The preferred route of emergency intubation is orotracheal, which can be performed rapidly, safely, and reliably with inline stabilization of the neck in patients with suspected cervical spine injury. Intubation causes intense reflexive cardiovascular stimulation that may lead to a deleterious elevation of intracranial pressure (ICP). Therefore, the patient should be adequately sedated. Etomidate is the preferred sedative in patients with suspected ICP elevation as it reliably facilitates induction in less than 1 minute with a duration of action of 4 to 6 minutes. Propofol is another anesthetic agent that does not increase ICP; however, its hypotensive effects, which can ultimately decrease cerebral perfusion pressure, often limit its use. Both medications result in a dose-dependent decrease of cerebral metabolic rate that reduces cerebral blood flow and ICP. Ketamine has a fast onset, but it may elevate ICP and should generally be avoided. Midazolam can alter the patient’s mental status and may prohibit a postintubation examination.



Respiration/PEEP


The effect of positive end expiratory pressure (PEEP) on ICP is only partly predictable for a number of reasons. Lung and pleural pressures are transmitted to the cerebrospinal fluid (CSF) column through intravertebral spaces and the vertebral venous plexus, and to the jugular venous system through the superior vena cava. The effect of PEEP on ICP depends on both intracranial and pulmonary compliance and changes over time. ICP responses are not limited to PEEP but also relate to mean airway pressure, which can be elevated by many factors other than PEEP, including peak airway pressure and inspiratory time. Furthermore, the position of the patient’s head and upper body can significantly affect ICP. A nasogastric tube should be placed to facilitate gastric lavage, decompression, and to reduce the risks for aspiration.



Circulation


Circulation must be maintained at a level always ensuring adequate cerebral perfusion pressure. In any patient with suspected brain injury, resuscitation fluids include isotonic solutions such as normal saline or lactated Ringer’s solution. An initial systemic mean arterial pressure (MAP) of approximately 100 mm Hg is adequate and safe for most patients (unless intracranial bleeding is suspected). Because cerebral perfusion pressure (CPP) equals the difference between MAP and ICP, CPP-matching ICP therapy targets a CPP from 60 to 70 mm Hg in most instances. Invasive ICP monitoring is mandatory if ICP elevations are suspected. While obtaining venous access, blood samples should be collected for anticipated tests. Hypotension may be treated by replacing blood and volume losses and vasoactive agents may be utilized (if volume and cardiac status is adequate) to maintain target MAP and systolic blood pressures. Hypertension should be aggressively managed with intravenous antihypertensive agents that do not elevate ICP by their vasodilatory effects. Thus labetalol and nicardipine are generally preferred and commonly used for managing uncontrolled hypertension. In most cases, including patients with intracranial hemorrhage, systolic and diastolic blood pressures of less than 160 mm Hg and 90 mm Hg, respectively, are tolerated and maintained. Urine output should be at least 0.5 mL/kg/hour and accurate measurement requires bladder catheterization.




Seizures


Repeated generalized seizures such as impact seizures invariably lead to secondary brain injury and should be treated aggressively with an intravenous benzodiazepine. Lorazepam, in 4-mg doses administered at 2 mg/min, has become the preferred agent due to its longer duration of action; however diazepam and midazolam are effective alternatives. Subsequent seizure control is maintained with an intravenous antiepileptic. Although there is no proven drug of choice, first-line agents generally include phenytoin (15 to 20 mg/kg intravenous (IV) bolus at a maximum rate of 50 mg/min), fosphenytoin (15- to 20-mg PE/kg IV bolus at a maximum rate of 150 mg/min), or valproic acid (20- to 40-mg/kg IV bolus). Fosphenytoin is often selected due to its faster rate of administration and lower risk of hypotension (as it is not formulated with propylene glycol). Drug levels for these agents should be drawn following the loading dose and maintenance dosing should be initiated. Corrected total target levels for phenytoin (and fosphenytoin) are 15 to 20 mcg/mL; free levels can be drawn in patients who are critically ill or have low protein stores with a target of 1.5 to 2 mcg/mL. Valproic acid target levels are 50-100 mcg/mL. Seizure breakthrough requires immediate administration of benzodiazepines and loading of a second anticonvulsant. Continuous video EEG monitoring is frequently employed to detect nonconvulsive seizures.



Sedation and Paralysis


Sedation is often required to facilitate comfort with respiratory support, to counteract agitation, or to treat elevated ICP. Short-acting medications given as continuous infusions such as propofol or dexmedetomidine are preferred. However, deeper sedation, especially in patients with seizures, may require a midazolam infusion. Because of the accumulation of its active metabolite in patients with renal dysfunction, extended durations of midazolam should be avoided or interrupted if possible. Sedation should be titrated to a predefined goal using a validated sedation scale. The Richmond Agitation Sedation Scale (RASS) is commonly used and a goal range of 0 (alert and calm) to −2 (light sedation, briefly awakens with eye contact to voice) is appropriate for most patients. Hourly interruption of sedation is needed to obtain serial neurologic examinations, except in paralyzed patients or those in whom awakening leads to deterioration of ICP. Additional analgesia (i.e., intravenous intermittent morphine [2 to 4 mg every 3 to 4 hours] or a fentanyl infusion) is often needed in postoperative patients or patients with traumatic injuries. Patients with critically high ICP should be paralyzed as part of the treatment regimen for increased intracranial hypertension, but only after initiation of both a sedative and analgesic.



Reversal of Drug Overdose


Drug overdose is the largest single cause (30%) of coma in the emergency department. Most drug overdoses are treated by supportive measures alone. Certain antagonists, however, specifically reverse the effects of coma-producing drugs. Intravenous naloxone (0.4 to 2 mg) is used as “test” antidote for opiate-induced coma, and it acts as a µ-receptor antagonist. Caution is needed as the reversal of narcotic effect may precipitate acute withdrawal in an opiate addict. In suspected opiate coma, the minimum naloxone dose (not completely reversal) should be given to establish the diagnosis by pupillary dilation and to reverse depressed breathing and consciousness. Due to its short half-life, patients who respond to naloxone reversal may require additional doses or a continuous infusion to avoid rebound sedation and respiratory depression. Intravenous flumazenil antagonizes benzodiazepine-induced coma and can be administered in 0.2-mg doses every minute for a maximum of 1 mg. In patients who initially respond to flumazenil reversal but experience recurrent sedation, flumazenil 1 mg may be redosed every 20 minutes with a max of 3 mg/hour.29 Careful consideration should be given prior to administration of flumazenil as patients may experience benzodiazepine-withdrawal seizures. Thus, whereas naloxone is commonly used with minimal serious adverse effects, the use of flumazenil should be restricted to select, low-risk cases. The sedative effects of drugs with anticholinergic properties, particularly tricyclic antidepressants, can be reversed with 1 to 2 mg physostigmine intravenously (duration of action about 45 to 60 minutes). Pretreatment with 0.5 mg atropine will reduce the risk for symptomatic bradycardia. Of note, only full awakening is characteristic of an anticholinergic drug overdose because physostigmine has nonspecific arousal properties.



Body Temperature


Hyperthermia is detrimental in brain injury as it increases brain metabolic demands and facilitates secondary brain injury.30 Elevated temperature greater than 104° F (40° C) requires immediate, lifesaving cooling measures, even before the underlying cause is determined and treated. In 2002, two research groups independently published that lowering the body temperature to 33° C for 12 or 24 hours in comatose survivors of cardiac arrest resulted in nearly doubling the number of patients being discharged home or to rehabilitation. Generally speaking, no patient with acute brain injury should be allowed to be hyperthermic, and modern technology provides a variety types of noninvasive and invasive cooling equipment suitable to maintain any target core temperature desired. Core temperatures of less than 93° F (34° C) on admission should be slowly elevated to above 35° C to reduce the risks of unwanted side effects from uncontrolled, persistent hypothermia.




Physical Examination


A systematic, detailed examination is necessary when approaching a comatose patient (Box 61.1, Table 61.2). Important findings include evidence of trauma, acute or chronic medical illnesses, ingestion of drugs (needle marks, alcohol breath), and the presence of nuchal rigidity.



Box 61.1   Neurologic Profile


A Modified Glasgow Coma Scale



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As outlined earlier, an in-depth physical and neurologic examination followed by serial neurologic evaluations (i.e., hourly) is the most important, indispensable, and readily available method of assessing a comatose patient.31 However, in coma patients the examination remains limited in detecting changes in brain function. Nevertheless, the astute clinician will carefully evaluate for changes in findings (i.e., the appearance of new asymmetry in examination or focal deficits, progressive loss of brainstem reflexes, or loss of reflex motor responses). Finding progression of impairment is of immense clinical value as it indicates a new or worsening “intracranial emergency” demanding immediate clarification and stabilization. Skilled neurologic examination is challenging and provides a limited surveillance window of brain tissue at risk. Intracranial monitoring and, if needed, repeated head imaging have become the standard of care in neurocritical care units.


The differential diagnosis of a comatose patient is supported by the patient’s risk factor profile, activity at symptom onset, and disease progression. Acute, devastating headaches with nausea and vomiting quickly followed by impaired consciousness in a hypertensive patient with a history of smoking should be rapidly worked up for subarachnoid or intracerebral hemorrhage. Deterioration of consciousness hours after head injury necessitates immediate exclusion of newly emerging, delayed intracranial hematoma with intracranial pressure crisis. In contrast, the slow progression of a focal neurologic deficit evolving to generalized depressed consciousness in an elderly individual directs toward an intracranial metastasis with secondary seizures. Increased intracranial pressure is a common denominator of many acute and subacute central nervous system (CNS) injuries. Typical manifestations include headaches from the dural stretch of trigeminal (V) sensory fibers; intractable nausea and recurrent vomiting often associated with visual disturbances; some neurologic deficits on detailed examination; and, in later stages, reduction in level of alertness.


When performing the neurologic examination, monitoring vital signs can be utilized as part of the autonomic nervous system evaluation. For example, appearance of systolic hypertension, vagal bradycardia, and respiratory irregularity is known as Cushing’s triad and indicates increased ICP. In addition, changes in the pattern of respiration in a spontaneously breathing patient can help localize the level of injury. Abnormalities of respiration can range from apnea to hyperpnea with undulating crescendo-decrescendo patterns as well as complete irregularity of breathing with erratic pauses that finally terminate in complete apnea. This “autonomic survey” and observing for spontaneous patient movements are followed by the assessment of a patient’s level of arousal. The reduction in response to external stimulations provides the basis for commonly used classification schemes such as the Glasgow Coma Scale (GCS). If the patient’s level of alertness permits, then orientation, attention and concentration span and intactness of cognitive functions are examined next. This is followed by a detailed assessment of cranial nerve, motor, and peripheral reflex status. Optic nerve head edema (papilledema) is an important and, if present, a reliable manifestation of raised ICP. Additional findings of increased ICP on fundoscopy include venous engorgement, loss of venous pulsation, optic disk hemorrhage with increased disk diameter, and blurring of its margins. Compression of the third nerve is a result of a variety of intracranial processes, including uncal herniation and aneurysms of the posterior communicating artery. It is identified by pupillary dilatation, ptosis, and various degrees of ophthalmoparesis except for abduction and intorsion-depression. A sixth nerve palsy, typically a nonlocalizing sign, is identified by abduction deficit and is seen in patients with elevated ICP or hydrocephalus and stretching of the nerve but is also present in patients with intrinsic brainstem injury (i.e., strokes). Patients with acute intracranial mass lesions and increased ICP commonly develop herniation syndromes—that is, shifting of brain tissue from areas with higher regional ICP toward areas with normal ICP. If the mass lesion is predominantly located within one hemisphere, the main force vector will shift the brain primarily laterally across the midline and toward the opposite hemisphere as it impresses on the upper brainstem and thalamic structures during lateral displacement. More centrally located mass lesions (i.e., acute, obstructive hydrocephalus or global brain swelling as seen in fulminant encephalitis or hepatic encephalopathy) will to the contrary lead primarily to downward herniation with the main force vector impressing upon the brainstem. Different herniation syndromes have different clinical presentations and therapeutic approaches. When intracranial hypertension remains uncontrolled and escalates uniformly central, downward herniation occurs involving increasingly more brainstem structures in a rostrocaudal fashion. The terminal event is complete brainstem destruction resulting invariably in brain death. During this course, progressive loss of brainstem reflexes can be determined on examination and at this stage, the patient is deeply comatose. Injury to the fifth cranial nerve nucleus within the pons results in loss of the corneal reflex. A vestibulocochlear nerve nucleus compromise results in loss of the oculocephalic reflex and manifests as “doll’s eyes” or the inability to maintain eye position as the head moves. Medullary injury with damage to the ninth and tenth nerves results in loss of lower cranial nerve reflexes including the absence of gag and cough reflexes.


Ipsilateral hemiparesis indicates the possibility of uncal herniation causing compression of the contralateral cerebral peduncle as temporal lobe tissue herniates into the space between the tentorium and brainstem. For example, a left-sided subdural hematoma causing temporal herniation pushes the opposite cerebral peduncle and its motor fibers against the right tentorial edge (right-sided Kernohan’s notch) leading to a hemiparesis on the same side as the hemispheric lesion. Posturing is involuntary flexion or extension of the arms or legs spontaneously or elicited by stimulation, and it is included in the Glasgow Coma Scale as a measure of the severity of brain injury. Three types of posturing can be observed depending on the level of brain injury: decorticate (flexor), decerebrate (extensor), and opisthotonos (body arching along the craniospinal axis) posturing. Injury involving the brainstem above or below the red nucleus in the midbrain leads to decorticate and decerebrate posturing, respectively. Of note, flexion or extension can be witnessed either unilaterally or bilaterally, is sometimes seen only intermittently, and can involve one or all extremities. Decorticate posturing commonly indicates damage of the cerebral hemispheres, the internal capsule, and the thalamus, possibly also involving the uppermost brainstem. Decerebrate posturing is involuntary extension of both upper (elbow) and lower extremities indicating brainstem damage below the midbrain. Progression from decorticate to decerebrate posturing is indicative of progressive transtentorial herniation. Opisthotonic posturing is an infrequently encountered sign seen with severe brainstem injury or extrapyramidal lesions involving the axial muscles. Importantly, increasing downward pressure leads to dysfunction first at the level of the diencephalon (i.e., thalami), next affecting the upper and middle sections of the brainstem (midbrain and pons), and ultimately impeding medullary function leading to deep coma without any reflexes or motor responses (flaccidity). Once complete rostrocaudal herniation has occurred, the patient is brain dead.



Assessment of Coma: General Aspects


Correctly characterizing disorders of consciousness continues to pose interesting clinical questions and diagnostic challenges with important ethical consequences (Box 61.2). Not only may an individual patient acutely fluctuate in his or her examination findings, but recovery may take place over prolonged time periods, necessitating constant reassessments. To address this uncertainty, standardized neurobehavioral assessments have become the best tool for categorizing coma and its transitional stages. Predicting long-term outcome has significantly improved when utilizing standardized assessments. Generally speaking, clinical and electrophysiologic markers of coma and its transitional states remain unsatisfactory. The reader is reminded that larger observational studies identified a high rate of misdiagnoses (>40%),32 especially in patients in vegetative state, when assessment is made on clinical grounds only.



Box 61.2   Characteristics of Categories in Coma



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Jun 4, 2016 | Posted by in CRITICAL CARE | Comments Off on Coma

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