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Handbook of Clinical Neurology, Vol.

140 (3rd series)


Critical Care Neurology, Part I
E.F.M. Wijdicks and A.H. Kramer, Editors
http://dx.doi.org/10.1016/B978-0-444-63600-3.00008-8
© 2017 Elsevier B.V. All rights reserved

Chapter 8

Management of the comatose patient


E.F.M. WIJDICKS*
Division of Critical Care Neurology, Mayo Clinic and Neurosciences Intensive Care Unit, Mayo Clinic Campus, Saint Marys
Hospital, Rochester, MN, USA

Abstract
Coma has many causes but there are a few urgent ones in clinical practice. Management must start with
establishing the cause and an attempt to reverse or attenuate some of the damage. This may include early
neurosurgical intervention, efforts to reduce brain tissue shift and raised intracranial pressure, correction of
markedly abnormal laboratory abnormalities, and administration of available antidotes. Supporting the
patient’s vital signs, susceptible to major fluctuations in a changing situation, remains the most crucial
aspect of management.
Management of the comatose patient is in an intensive care unit and neurointensivists are very often
involved. This chapter summarizes the principles of caring for the comatose patient and everything a neu-
rologist would need to know. The basic principles of neurologic assessment of the comatose patient have
not changed, but better organization can be achieved by grouping comatose patients according to specific
circumstances and findings on neuroimaging. Ongoing supportive care involves especially aggressive
prevention of medical complications associated with mechanical ventilation and prolonged immobility.
Waiting for recovery—and many do- is often all that is left. Neurorehabilitation of the comatose patient
is underdeveloped and may not be effective. There are, as of yet, few proven options for neurostimulation
in comatose patients.

INTRODUCTION expanding mass lesion causing shift of the thalamus or


Management of the comatose patient is divided into two brainstem, acute obstructive hydrocephalus, and central
major priorities. First, the cause should be elucidated, nervous system (CNS) infection (Wijdicks, 2010, 2014;
so that attempts can be made to reverse it. Second, these Salottolo et al., 2016). Any acute metabolic arrangement
extremely vulnerable patients should be protected requires correction, albeit slowly in some situations (i.e.,
in every possible way. This includes appropriate airway acute hyponatremia). Seizures and nonconvulsive status
management, adequate oxygenation, and possibly epilepticus need urgent treatment. The evaluation of the
mechanical ventilation. Other abnormal vital signs should comatose patient usually runs through a logical sequence,
also be corrected, such as blood pressure and temperature. starting with initial medical support, detailed examination
Each of these simple mundane tasks is essential in the of the patient, finding the cause of coma, and treatment.
initial hours of care. In patients brought to the emergency Using a combination of neurologic findings and neuroim-
department, coma can be due to traumatic brain injury, aging, clinicians can elucidate the cause of coma. Because
cerebral or cerebellar hemorrhage, acute basilar artery of its specialization, there are good reasons to involve a
embolus, anoxic-ischemic brain injury after cardiopul- neurologist in the assessment of coma in patients admitted
monary resuscitation, and drug overdose. Once the cause to general intensive care units (Wijdicks, 2016).
of coma is established, management should proceed The management of the comatose patient is multidis-
quickly. This is most pertinent in patients with an ciplinary from the onset, with many specialties and allied

*Correspondence to: Eelco F.M. Wijdicks, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester MN 55905, USA.
E-mail: wijde@mayo.edu
118 E.F.M. WIJDICKS
healthcare workers involved. This chapter provides the epidemic” and many survivors have long-term anoxic
main essentials for care and treatment, not only in the brain injury. The presentation of a comatose patient in spe-
acute stage, but also in the weeks and sadly sometimes cialized hospital wards and units may also narrow the dif-
months or years ahead. ferential diagnosis of acute coma. It is highly unusual for
patients who have been admitted to general medical or sur-
CAUSES OF COMA AND PREVALENCE gical wards to suddenly deteriorate and become comatose.
Acute coma in the hospital is occasionally a reason for a
For the physician trying to make sense of it all, there
rapid response team call, and acute metabolic disturbances
are multifarious causes of coma, but, after an initial eval-
or an unintentional drug overdose (e.g. post operative opi-
uation, physicians often have narrowed the range of pos-
oid treatment) remain most likely. Acute hypo- or hyper-
sibilities. In the initial evaluation of the comatose patient
glycemia is also often a cause for immediate alarm, but is
with no apparent cause, the medical history becomes more
usually recognized quickly and corrected. In our experi-
important and often cues the physician towards a possible
ence, only a small fraction of comatose patients have no
explanation. Questions that should be asked to family
clear explanation on computed tomography (CT) scan
members or bystanders – when appropriate – are shown
or after lumbar puncture (Edlow et al., 2014). In some
in Table 8.1. However, the cause of coma clearly depends
patients, early magnetic resonance imaging (MRI) has
on where the patient is seen first. Assessing a patient in a
been diagnostic in demonstrating posterior reversible
transplant intensive care unit (ICU) is a different environ-
encephalopathy syndrome, fat embolization syndrome
ment than consulting in a medical ICU or coronary care
(Mijalski et al., 2015), infarcts in the brainstem and
unit. Consultation in surgical ICUs for coma is relatively
thalamus, or acute demyelination disease such as acute
frequent and involves questions about failure to awaken or
disseminated encephalomyelitis (ADEM) or osmotic
acute coma in the setting of critical illness. Moreover, the
demyelination. In many others, coma may be a result of
nature of the primary illness for which the patient is admit-
an unwitnessed seizure, illicit drug use, or other toxins.
ted may provide sufficient leads. It is likely to be true that
intoxications are the predominant cause of coma in
patients arriving in the emergency department. Neverthe- NEUROPATHOPHYSIOLOGY
less, comatose patients may present to the emergency
Coma is a result of dysfunction or damage of structures
department with no known cause, clinical course and little
that allow normal wakefulness and awareness. Wakeful-
documentation (Stevens et al., 2015). Many emergency
ness is mostly driven by the ascending reticular forma-
departments in the world are in the midst of a “fentanyl
tion in the brainstem. Becoming aware and thus
understanding content requires the thinking parts of
Table 8.1 the cortex, including the associative parietal areas and
frontal lobe. Comatose patients are neither awake nor
Questions to ask in coma of uncertain etiology
aware (even if sporadic functional MRI signals may sug-
Could there have been trauma or assault? gest otherwise). Coma may deteriorate to brain death in
Was the patient breathing when the response team arrived? about 5–10% and simply implies that all brainstem
Was there noticeable blood loss? reflexes are permanently lost, including the ability to
Did the patient use antibiotics for infection? generate a breath. Hypotension almost always occurs,
Was there a rapid onset of fever and headache?
but the spinal cord may increase sympathetic tone just
Was a cardiac arrest documented? How long did the efforts last
enough to maintain a pressure which allows circulation.
before resumption of circulation?
Has the patient had prior episodes of diabetic ketoacidosis, or The clinical diagnosis of brain death is conservative and
severe hypoglycemia, and has there been a recent change in defines a clear point of no return. Once all brainstem
insulin medications? reflexes are absent in a demonstrably apneic comatose
Is the patient known to have atrial fibrillation or other cardiac patient, with no confounding circumstances, recovery
disease and be using anticoagulation or has it recently been does not occur and then fullfills criteria for a neurologic
discontinued? determination of death (Wijdicks 2001, 2011, 2017). In
Was hypertension poorly controlled? comatose patients with preserved brainstem reflexes,
What other pills or over-the-counter drugs does the patient have long-term support with a gastrostomy tube for feeding
access to? and possibly a tracheostomy and mechanical ventilator
Has the patient had prior suicide attempts, a psychiatric
is feasible. Patients in a persistent vegetative state
consultation, and are there problems at work?
(PVS) may be kept alive for decades with no improve-
Has anyone complained about the patient’s drinking habits?
Has the patient used medications that may increase heat ment in awareness. Patients in a minimally conscious
production, such as salicylate drugs with sympathicomimetics state may stay in this condition for years or improve mar-
such as cocaine, amphetamines, or ecstasy? ginally. Each of these conditions can be linked to certain
degrees of brain injury, but a neuropathologist cannot
MANAGEMENT OF THE COMATOSE PATIENT 119
Table 8.2
Classification and causes of coma

Structural brain injury Basilar artery occlusion and brainstem infarct


Cerebral hemisphere Central pontine myelinolysis
UNILATERAL (WITH DISPLACEMENT)
Brainstem contusion
Intraparenchymal hematoma
CEREBELLUM (WITH DISPLACEMENT OF BRAINSTEM)
Middle cerebral artery ischemic stroke
Cerebellar infarct
Intracranial venous thrombosis
Cerebellar hematoma
Hemorrhagic contusion
Cerebellar abscess
Cerebral abscess
Cerebellar glioma
Brain tumor
Acute metabolic-endocrine disturbance
Subdural or epidural hematoma
Hypoglycemia
BILATERAL
Hyperglycemia (nonketotic hyperosmolar)
Subarachnoid hemorrhage
Hyponatremia
Multiple traumatic brain contusions
Hypernatremia
Penetrating traumatic brain injury
Hypocalcemia
Anoxic-ischemic encephalopathy
Acute hypothyroidism
Multiple cerebral infarcts
Acute panhypopituitarism
Bilateral thalamic infarcts
Acute uremia
Lymphoma
Hyperammonemia
Encephalitis
Hypercapnia
Gliomatosis
Diffuse physiologic brain dysfunction
Acute disseminated encephalomyelitis
Generalized tonic-clonic seizures
Cerebral edema
Poisoning, illicit drug use
Multiple brain metastases
Hypothermia
Acute hydrocephalus
Gas inhalation
Acute leukoencephalopathy
Acute catatonia
Posterior reversible encephalopathy syndrome
Malignant neuroleptic syndrome
Air or fat embolism
Functional Coma
BRAINSTEM
Pseudostatus epilepticus
Pontine hemorrhage
Eyes closed unresponsiveness to stimuli

predict the clinical state after grading the degree of injury. overwhelming ischemia, necrosis of all cortical layers
The neuropathology associated with coma is summa- is seen. In most patients, hypoxic-ischemic injury spares
rized in Table 8.2. the brainstem clinically, but necrosis may occur, espe-
The neuropathology associated with disorders caus- cially in the inferior colliculi and tegmental nuclei. Sus-
ing acute or prolonged coma has been well characterized. tained absence of brainstem reflexes after cardiac arrest is
Several fatal neurologic disorders causing coma have relatively uncommon.
come to autopsy and -mostly in the past-have allowed Few patients with CT-proven catastrophic stroke
detailed description of the underlying pathology. come to autopsy. The destruction and mass effect are evi-
The neuropathology of hypoxic-ischemic injury is a dent. In patients with large thalamic hemorrhage, blood
result of damage to the most vulnerable sites, including has tracked deep into the brainstem. In other patients,
the first and second frontal gyrus, globus pallidus, cornu edema may have caused further deterioration. Edema
ammonis, and the cerebellar cortex affecting predomi- around an intracerebral hematoma peaks after several
nantly the Purkinje cells. The ischemic alterations in days. Edema is a multiphase event and is caused by clot
the cornu ammonis involve the CA1 and CA4 sectors. retraction, movement of serum into ambient tissue, fol-
The hippocampus becomes ischemic in CA1 areas after lowed by activation of coagulation cascade and throm-
several minutes of global ischemia. The CA4 region bus, and finally erythrocyte lysis with toxicity from
requires only minimal ischemic insult for these cells to hemoglobin. Edema is perpetuated by disruption of the
become damaged. Necrosis of the globus pallidus points blood–brain barrier, as well as inflammation and
to major anoxic-ischemic injury, and is also a common activation of the complement system. Increased produc-
manifestation of carbon monoxide poisoning. tion of matrix metalloproteinase iron may also exacer-
The pathologic changes of anoxic-ischemic injury bate cerebral edema.
are typically in the watershed zones and therefore The neuropathology of traumatic brain injury is
also involve the posterior cerebral regions. With diverse but often multiple contusions and subdural
120 E.F.M. WIJDICKS
hematomas are identified at autopsy, localized on cortical Fungal encephalitis may be difficult to detect micro-
surfaces. Diffuse axonal injury is caused by rotational scopically on routine stains, and the fungus may also be
acceleration following an impact to the head. On gross challenging to culture. Aspergillus fumigatus infection of
examination, hemorrhages of the corpus callosum and the CNS is aggressive and destructive. At autopsy, both
cerebellar peduncle region are often seen, and there infarcts and hemorrhages can be found due to
may also be hemorrhages in the deeper structures. angioinvasion.
So-called “gliding contusions” can sometimes be found In acute demyelinated leukoencephalopathies, the
in the parasagittal white matter. Small hemorrhagic shear acute changes are edema with fibrinoid necrosis of blood
lesions are also commonly found in the hemispheric vessels, and also infiltration of neutrophils, mononuclear
white matter, perpendicular to the cortical ribbon. Tissue inflammatory cells, sometimes with regions of hemor-
tear hemorrhages are mostly concentrated in the midline rhage (particularly in acute hemorrhagic leukoencepha-
structures, such as the corpus callosum, septum pelluci- lopathy). Another inflammatory demyelinating disease
dum, fornix, midbrain, pons, and hippocampus. Trau- is ADEM, resulting in symmetric subcortical white-
matic brain injury is often in the medial basal cortical matter lesions. Multiple sclerosis may present with an
areas of the temporal lobes, in the margins of the base acute mass (tumefactive form of Marburg syndrome).
of the cerebellar peduncles, due to pressure on the tentor- Next to marked demyelinization, the neuropathology
ial ridge, and on top of the corpus callosum, due to inden- findings in this variant are characterized by macro-
tation by the free edge of the falx cerebri. phages, large glial cells with mitosis, and chromatin frag-
The neuropathology of bacterial meningitis is fairly mentation (Creutzfeldt cells).
characteristic and immediately apparent. At autopsy, Coma due to intoxication or poisoning is usually acci-
purulent meningitis is revealed by pus and yellow and dental, but can occur intentionally in the setting of suicide
green deposits on the leptomeninges. Generally, the pus or homicide. Many neurotoxins produce no apparent neu-
follows the distribution of the meningeal blood vessels. ropathologic changes in the CNS. In some, such as lithium
Depending on the time elapsed before death, microscopic poisoning, more specific abnormalities are seen, such as
features include neutrophils, macrophages, and fibrin in spongiform changes in the thalamus, midbrain, and cere-
the subarachnoid space. Arteritis associated with severe bellum, with significant damage to the Purkinje cells
forms of meningitis has now been recognized as one of (explaining cerebellar ataxia during presentation). Thal-
the most important secondary complications leading to lium (used in many rat poisons) produces cerebral edema
ischemic strokes and much worse outcome, including with multiple white matter and cerebellar hemorrhages,
prolonged coma. Fulminant meningitis may show cere- but also degenerative changes in the cerebral cortex, hypo-
bral edema and relatively little exudate. Acute bacterial thalamic nuclei, and olivary complex. An important foren-
meningitis may be a surprising finding in patients who sic question is whether death occurred from carbon
died rapidly, when no real opportunity for the physician monoxide poisoning. The morphology is fairly character-
existed to obtain cerebrospinal fluid. istic, with bright redness of brain sections at autopsy that
Similarly, fulminant viral encephalitis may cause remain after fixation. Often a significant brightness of the
early demise and can be confirmed at autopsy. The find- dura is seen at exposure of the brain. There is bilateral
ings are generally nonspecific, showing clusters of necrosis of the globus pallidus and pars reticulata of the
inflammatory changes. In some regions, there is perivas- substantia nigra. Cortical laminar necrosis and involve-
cular chronic inflammation with microglial nodules and ment of both hippocampi are expected.
neuronophagia. The most common etiology is herpes Acute fatal alcohol intoxication remains nonspecific,
simplex virus encephalitis, which is characterized by but brain edema and congestion can be found. Equally
hemorrhagic necrosis, specifically involving the tempo- rare is documented neuropathologic confirmation of
ral lobes, insula, and posterior orbitofrontal cortex. Cow- Wernicke–Korsakoff syndrome, with its characteristic
dry A intranuclear inclusions can be found in herpes changes that involve atrophy of the mammillary bodies,
simplex virus encephalitis. When ultrastructural findings periventricular hemorrhages, and also astrogliosis and
are examined, viral particles with hexagonal features and capillary proliferation in more chronic cases. Far more
a central nucleoid are found. Polymerase chain reaction likely in alcoholics are multiple intracranial hemorrhages,
amplification of viral DNA in cerebrospinal fluid has particularly subdural and parenchymal hemorrhages.
long replaced brain biopsy in making the diagnosis.
Cytomegalovirus encephalitis is more commonly seen
NEUROLOGIC EXAMINATION OF THE
in patients who have been infected with the human
COMATOSE PATIENT
immunodeficiency virus. Cytomegalovirus has typical
microscopic findings of scattered cytomegalic cells with The primary goal of the neurologic examination in an
intracytoplasmic viral inclusion. The absence of an unresponsive patient is to localize the lesion and thereby
inflammatory infiltrate is notable in these infections. narrow the differential diagnosis. The examination
MANAGEMENT OF THE COMATOSE PATIENT 121
should proceed in a stepwise fashion and is familiar to involving the CNs or the pathways connecting them
the neurologist. and thus are indicative of brainstem functioning. Pupil
Pending a more comprehensive neurologic examina- size, shape and reactivity should be examined. Small
tion, the depth of coma can be assessed using a coma scale. pupils could be secondary to a pontine lesion that inter-
The Glasgow Coma Scale (GCS) is the most common of rupts descending sympathetic outflow. The most com-
such scales and originally developed for victims of trau- mon cause of small pupils is prior use of opioids (on
matic brain injury, and to improve transfer of patients, it the streets, it is most often heroin; in the hospital, it is
consists of three parts: eye opening, best motor response, overuse of opioids and can be related to errors with
and best verbal response (Teasdale and Jennett, 1974). patient-controlled analgesia pumps or opioid patches).
Each component is graded on a different scale (maximum Dilated (>8 mm) pupils are due to disruption of CN
4 for eyes, 5 for verbal, and 6 for motor) and the summation III, secondary to either a mesencephalic injury or lesion
of the scores is used to communicate the depth of coma. of the peripheral nerve. Drugs and other toxins such as
The minimum score is 3 and the maximum 15. Although amphetamines or lidocaine can also result in bilaterally
not useful in the diagnosis of coma, the GCS has been dilated pupils, and must be excluded through the
shown to have acceptable interobserver reliability through patient’s history and laboratory testing. Midsize, fixed
a wide range of trained providers, and has predictive value pupils are seen in severe midbrain lesions that can be sec-
for outcomes in aneurysmal subarachnoid hemorrhage, ondary to herniation and are frequently the first sign of
traumatic brain injury, and comatose survivors of cardiac impending loss of all brainstem reflexes (Fig. 8.2).
arrest. However, the GCS does not account for the presence In addition to pupil size and reactivity, any deviation
or absence of brainstem reflexes and does not detect other of one or both eyes should also be noted. Spontaneous
highly relevant changes in the neurologic examination, eye movements, including “ping-pong” eyes or ocular
findings that could be instrumental in determining a dipping, generally indicate bihemispheric dysfunction.
patient’s prognosis. GCS is reduced to a raw motor scale Ocular bobbing, described as a rapid downward devia-
if a patient is intubated and has facial injury with swelling. tion of the eyes followed by a slow upward movement,
To address the shortcomings of the GCS, the Full Out- typically implies a pontine lesion. Bihemispheric dys-
line of UnResponsiveness (FOUR) score was developed function can also lead to the classic “roving eye
(Fig. 8.1). To simplify scoring, the FOUR score includes movements,” though metabolic processes and various
four components – eyes, motor, brainstem, and toxicities can also be responsible. Rather than support-
respiratory – that are each graded on a scale from 0 to ing particular localization or a specific disease process,
4, producing a maximum combined total score of 16. roving eye movements indicate that the brainstem is
With an equal to higher interrater reliability than the relatively intact (Table 8.3). The oculocephalic reflex
GCS, as well as validation in multiple patient popula- deserves special mention as several brainstem structures
tions, the FOUR score has proven to be an important ini- are assessed simultaneously. In a patient with a nor-
tial tool in the evaluation of comatose patients. Perhaps mally functioning brainstem, eyes will move in a direc-
because of its greater emphasis on brainstem reflexes tion opposite the head movement and appear to remain
and respiratory patterns, the FOUR score has also been fixated on a point in space (much like a doll’s eyes). If a
shown to have greater predictive value in terms of even- lesion disrupts any of the structures or pathways
tual progression towards more severe injury, especially involved in the reflex, including CNs III, IV, and VI,
in patients with low GCS scores, or the relatively ubiq- or the medial longitudinal fasciculus, the eyes will
uitous GCS score of 3 T, which is commonly reported move along with the head, remaining in midposition
by paramedics following intubation in the field after sed- with respect to the orbits.
atives and paralytics have been given. Brainstem damage Tonic deviation of the eyes, typically in the horizontal
and failure to maintain adequate ventilation are reflec- plane, may indicate an ipsilateral hemispheric lesion
tions of injury severity. The FOUR score does not con- affecting the frontal eye fields or a contralateral pontine
tain a verbal component, and can be measured with lesion. Differentiation between a hemispheric lesion and a
equal accuracy in intubated and nonintubated ICU pontine lesion can be difficult in comatose patients as
patients. The FOUR score can be used to evaluate for hemiparesis is typically not apparent. However, the oculo-
clinical progression with serial examinations in patients cephalic maneuver will be able to overcome gaze
with intracranial mass lesions. preference from a cortical lesion, since the pontine and
midbrain structures responsible for the reflex remain intact.
Horizontal deviation can also be seen with noncon-
Cranial nerves
vulsive status epilepticus, and may be one of the few
A more formal neurologic evaluation of an unresponsive signs to indicate the need for an emergent electroenceph-
patient typically begins with the cranial nerves (CNs). alogram (EEG). Skew deviation implies a brainstem
Dysfunction of any of these reflexes implies a lesion injury.
122 E.F.M. WIJDICKS

Fig. 8.1. The Full Outline of UnResponsiveness (FOUR) score. Used with the permission of Mayo foundation for Medical
Education and Research. All rights reserved.
Eye response (E) Brainstem reflexes (B)
4 ¼ eyelids open or opened, tracking, or blinking to command 4 ¼ pupil and corneal reflexes present
3 ¼ eyelids open but not tracking 3 ¼ one pupil wide and fixed
2 ¼ eyelids closed but open to loud voice 2 ¼ pupil or corneal reflexes absent
1 ¼ eyelids closed but open to pain 1 ¼ pupil and corneal reflexes absent
0 ¼ eyelids remain closed with pain 0 ¼ absent pupil, corneal, and cough reflex
Motor response (M) Respiration (R)
4 ¼ thumbs-up, fist, or peace sign 4 ¼ not intubated, regular breathing pattern
3 ¼ localizing to pain 3 ¼ not intubated, Cheyne–Stokes breathing pattern
2 ¼ flexion response to pain 2 ¼ not intubated, irregular breathing pattern
1 ¼ extension response to pain 1 ¼ breathes above ventilatory rate
0 ¼ no response to pain or generalized myoclonus status 0 ¼ breathes at ventilator rate or apnea

A fundoscopic examination should also be performed Further testing of the CNs is accomplished through
once the external examination of the eyes has been the various reflexes, including the corneal, gag, and
completed. Vitreous hemorrhage, often subhyaloid in cough, but these are the least helpful with localization.
location, can be indicative of subarachnoid hemor- Midbrain and pontine lesions can cause central neuro-
rhage. Fundoscopy may also reveal the presence of genic hyperventilation. Pontine lesions can cause cluster
papilledema. Though often cited as a manifestation of breathing (brief episodes of tachypnea punctuated by
acutely increased intracranial pressure in subarachnoid brief spells of apnea). Lower pontine and medullary
hemorrhage or acute meningitis, papilledema is more lesions can produce ataxic breathing or apnea. Sighs
commonly seen with slowly progressive processes such or yawns can herald a decrease in level of consciousness
as an enlarging intracranial mass, and may also be seen resulting from rapidly increasing intracranial pressure.
with severe hypertensive crisis causing posterior revers-
ible encephalopathy syndrome. The presence of venous
Motor responses
pulsations suggests normal intracranial pressure, but
their absence is less useful. Measuring the optic nerve Testing of the motor system in an unresponsive patient
sheath with bedside ultrasound using a high-frequency typically involves applying a noxious stimulus to the
probe is reported to estimate intracranial pressure with supraorbital nerve or the temporomandibular joint, and
some accuracy. This method could be a noninvasive assessing the patient’s reaction. Possible responses
way to detect raised intracranial pressure, allowing ear- include a localizing response, in which the patient reaches
lier and more rational therapeutic interventions, but bet- towards the stimulus, reflexive responses such as decorti-
ter validation is needed. cate or decerebrate posturing, or no response at all.
MANAGEMENT OF THE COMATOSE PATIENT 123

Fig. 8.2. Pathways of commonly used brainstem reflexes in assessment of coma. Used with the permission of Mayo foundation for
Medical Education and Research. All rights reserved.

Table 8.3 posturing reflexes have purportedly been useful in lesion


Relevant eye movements in coma examination
localization, these responses can be seen with either focal
lesions or global conditions affecting the nervous system.
Type of movement Lesion location It is also not uncommon for both responses to be present
in the same patient at the same time. Given this, the
Periodic alternating gaze (lateral Bihemispheric, presence of decerebrate or decorticate posturing has rel-
deviation every few minutes, left midbrain, vermis atively little utility in prognostication until the underly-
and right) ing etiology is found.
Ping-pong (lateral deviation every Bihemispheric, In addition to movements in response to stimulation,
few seconds, left and right) vermis spontaneous movements can also be seen in unrespon-
Convergence nystagmus (bilateral Mesencephalon sive patients, the classic example being generalized
abduction, slow with rapid jerk
myoclonus. Although a predictor of poor outcome
back)
Retractory nystagmus (retraction Mesencephalon
following cardiac arrest and resulting anoxic-ischemic
orbit) injury, generalized myoclonus status can also be seen
Bobbing (rapid down, slow up) Pons with various intoxications, including lithium, cephalo-
Dipping (slow down, rapid up) Bihemispheric sporins, and pesticides.

Classifying coma syndromes


Decorticate posturing involves a slow flexion of the
elbow, wrists, and fingers, whereas decerebrate posturing Combinations of physical findings characterize hernia-
is defined as adduction and internal rotation of the shoul- tion syndromes and their dynamic changes can be used
der with arm extension and wrist pronation. Although to recognize progression of mass effect (Table 8.4).
124 E.F.M. WIJDICKS
Table 8.4 peduncle compression), weakness ipsilateral to the
Coma syndromes lesion can also be falsely localizing. Although increased
access to CT has diminished the influence of these false
Bilateral hemispheric Spontaneous eye movements localizing signs, they might still be relevant in hospitals
(roving, dipping, ping-pong, without CT availability, especially if the treating physi-
nystagmoid jerks) cian is contemplating burrhole trephination. An awake,
Upward or downward eye
alert patient with a dilated pupil is unlikely to have
deviation
uncal herniation as a cause of the anisocoria, but I have
Intact oculovestibular reflexes
Intact pupillary and corneal seen a partial oculomotor palsy in a relatively awake
reflexes patient with an acute subdural hematoma. Sixth-nerve
Variable motor responses palsy from high or low intracranial pressure is also
Adventitious limb movements nonlocalizing.
(subtle manifestations of If progressive neurologic disease associated with
seizures, myoclonus, mass effect goes untreated, brainstem reflexes might fail
asterixis) in a caudal direction. Fixed pupils (midbrain) are fol-
Brainstem displacement Anisocoria or unilateral fixed lowed by disappearance of corneal reflexes and oculoce-
from a hemispheric and dilated pupil phalic responses (pons), followed by loss of cough
mass (predominant lateral
response, the development of apnea, and loss of vascular
displacement)
tone (medulla). It defines brain death. Neurologists
Midposition fixed pupils
(predominant downward and neurosurgeons have come to realize that when all
displacement) brain stem reflexes are absent in a demonstrable apneic
Extensor or flexor posturing patient—and nothing else could explain it—it is
Central hyperventilation irreversible and it is the end of it.
(diencephalic) Combinations of physical findings can also character-
Brainstem displacement Direction-changing or vertical ize toxic syndromes. Pinpoint pupils with hypoventila-
from a cerebellar mass nystagmus from the tion suggest opioids. Hypertension, tachycardia, and
cerebellar lesion vertical or rotatory nystagmus suggest a dissociative
Ocular bobbing agent, such as ketamine or phencyclidine. Increased sal-
Absent corneal reflexes with
ivation, lacrimation, bronchial secretions, diaphoresis,
intact pupillary reflexes
and incontinence suggest cholinergic agents. Sedative-
Extensor or flexor posturing
Facial or abducens nerve palsy hypnotic toxicity produces more varied symptoms,
Skew deviation (vertical including normal vital signs (benzodiazepines), apnea
misalignment of eyes) and circulatory collapse (barbiturates), and seizures
Internuclear ophthalmoplegia (gamma hydroxybutyrate).
Intrinsic brainstem lesion Vertical nystagmus or bobbing
Miosis (with pontine lesions)
Internuclear ophthalmoplegia LABORATORY TESTS AND
Variable pupillary and corneal NEUROIMAGING
reflexes (can both be absent) The initial assessment of comatose patients generally
Absent oculocephalic and
includes measurement of serum glucose, complete blood
oculovestibular responses
count, coagulation factors, electrolytes, blood urea nitro-
Extensor or flexor posturing
Ataxic breathing gen (BUN) and creatinine, liver panel, thyroid function,
(pontomedullary damage) serum ammonia, and a venous blood gas (Moore and
Wijdicks, 2013). Blood should be cultured if infection
is suspected. The value of toxicologic testing for ethanol
and drugs of abuse is questionable, and poisoning
Transtentorial herniation classically presents with a remains a clinical diagnosis. Routine toxicologic testing
dilated pupil ipsilateral to the compressive lesion (ipsi- rarely changes acute management.
lateral CNIII damage) with contralateral hemiplegia In patients with metabolic acidosis, a widened
(ipsilateral cerebral peduncle compression causing anion gap suggests one of four mechanisms (ketones,
contralateral motor findings). However, either compo- uremia, lactate, toxins). Ketosis can occur in diabetes,
nent can be reversed. In up to 10% of cases, the dilated alcohol misuse, or starvation. Uremia generally pro-
pupil is contralateral (falsely localizing). Because of the duces acidosis only in later stages. Increased serum lac-
Kernohan notch phenomenon (contralateral cerebral tate can occur in sepsis, hypoperfusion, Wernicke’s
MANAGEMENT OF THE COMATOSE PATIENT 125
encephalopathy, or with toxins such as cyanide. Toxins MRI is far more revealing in demonstrating anoxic-
can also produce acidosis by other mechanisms (car- ischemic injury to the brain. MRI is also superior in
boxylic acid derivatives in ingestion of methanol or eth- documenting acute demyelination, the presence of pus
ylene glycol, pyroglutamic acid in massive ingestion of or blood, encephalitis (predominantly herpes simplex
acetaminophen), or a combination of mechanisms virus or limbic encephalitis), and meningitis or ventricu-
(salicylates). litis. Fat embolism is often clearly seen on early MRI.
At most institutions, the CT scan is the fastest and Sagittal and coronal MRI images are particularly helpful
most readily available imaging modality. In the evalua- to view brain tissue shifts and brainstem displacement.
tion of an unresponsive patient, CT scans are excellent Fluid-attenuated inversion recovery (FLAIR)
at detecting hydrocephalus, brain edema or intracranial sequences and DWI are the most useful MRI modalities
hemorrhage, with a sensitivity and specificity approach- in patients with unexplained coma. MRI usually includes
ing 100% in conditions such as acute (<12 hours since T1- and T2-weighted images and diffusion-weighted
onset) subarachnoid hemorrhage. Limitations of CT imaging (DWI) with mapping of the apparent diffusion
include poor visualization of the posterior fossa second- coefficient (ADC). DWI measures diffusion of water
ary to bone artifact, as well as reduced anatomic through tissue; under pathologic circumstances, water
differentiation in comparison to MRI, which may allow accumulates, and in ischemic lesions the decrease in
precise determination of etiology. ADC is shown as a hyperintense region on DWI.
MRI scans provide greater definition of cortical and Several studies have found that increased signal inten-
subcortical structures and may show cortical injury, sity on FLAIR in the cerebrospinal fluid compartment
laminar necrosis, or white-matter disease that is not can indicate subarachnoid hemorrhage or purulent exu-
apparent on a CT scan. Magnetic resonance angiogra- date in meningitis. The hyperintensity on FLAIR is
phy allows for excellent visualization of the arterial sys- explained by the presence of increased protein or pleocy-
tem and is an appropriate method for visualization of tosis and will decrease T1 relaxation time.
suspected acute basilar artery occlusion; however, this
may not be possible at all institutions. In such instances,
CT angiogram or conventional angiography can also MANAGEMENT OF THE COMATOSE
allow for rapid visualization of the arterial system. PATIENT
The major drawbacks of MRI scans include accessibil- The chance of a favorable outcome in the care of acute
ity, cost, and time necessary to complete the scan but brain injury leading to coma can be easily diminished
modern neurology cannot and should not do without if general principles of high-quality intensive care are
it. It has resolved many unclear situations in acute not aggressively attended to. An immobile mechanically
neurology. ventilated patient fed through a percutaneous gastrotomy
Hypodensity on CT in comatose patients indicates (PEG) (Fig. 8.3) requires vigilance, specialized nursing
infarction, edema, and tumor. Very low density indicates care, and stewardship. Every day, infections may present,
air, mostly from penetrating injury. Hyperdensity indicates skin may break down, and fluid shifts may cause
hemorrhage or calcification. However, in patients with rapid imbalance of homeostasis. Drugs (particularly
early diffuse cerebral edema (e.g., anoxic-ischemic antibiotics) have potential short- and long-term adverse
encephalopathy), the arteries in the basal cisterns are more effects. Adequate management of eye, mouth, and skin
clearly seen against a hypodense background and may at compression sites requires frequent change of linens,
falsely suggest subarachnoid blood (pseudo-subarachnoid
hemorrhage). Contrast CT in the acute setting is rarely per-
formed, but could show a ring-enhancing lesion in a
poorly defined hypodense area and indicate an abscess
or glioma. Epidural or subdural empyema is also much
better imaged with contrast, but in all these cases uncer-
tainties in interpretation are best resolved with MRI.
A normal CT scan is expected in comatose patients seen
immediately after cardiac or respiratory resuscitation,
asphyxia, near drowning, most poisonings and intoxica-
tions, and acute metabolic disturbance or endocrine
crises. CT scans are not sensitive enough to document
abnormalities in these conditions, but abnormalities may
become apparent later when the patient remains deeply Fig. 8.3. Tracheostomy allowing speech for recovering
comatose. patients.
126 E.F.M. WIJDICKS
patches, and protective pads. Splinting of extremities faecalis or faecium, Staphylococcus aureus, Klebsiella
may be needed to avoid contractures. There are few hard pneumoniae, Acinetobacter baumannii, Pseudomonas
data to support any of these interventions. The hard truth aeruginosa, and Enterobacter cloacae. Clostridium
is that maintenance of a comatose patient is fraught with difficile infections are also on the rise, particularly in
difficulties. patients with long hospital stays. The dilemma faced
Inability to close eyelids completely after trauma and, by treating physicians is that delayed initiation of antibi-
in particular, nocturnal lagophthalmos are risk factors for otics increases mortality, yet combination therapies to
conjunctivitis and corneal erosion (Lavrijsen et al., broaden the spectrum may lead to antibiotic resistance.
2005). Polyethylene moisture chambers are required to Antibiotic therapy is complex and often changing as a
prevent early epithelial breakdown, but some patients result of infectious disease consultation.
may have to be treated with lateral tarsorrhaphy. Fila- Fever in comatose patients is mostly caused by
mentary keratopathy is a common dry-eye syndrome in infections. Lingering infections have to be excluded
patients in prolonged coma. Prolonged eyelid contact before attributing fever to the brain injury. However,
with the cornea and reduced blinking impair lacrimal Paroxysmal sympathetic hyperactivity (PSH) syndrome
fluid turnover and may be contributing factors. is a commonly seen in “unexplained” fever of comatose
Tracheostomy reduces pulmonary complications and patients. PSH or dysautonomic storming all too fre-
provides easier access for pulmonary toilet. Tracheos- quently remains unrecognized and untreated. These
tomy will reduce length of stay, but it should generally spells are most common in young patients with diffuse
be postponed until approximately 2 weeks in patients axonal traumatic brain injury, but can occur with any
who can potentially be liberated from the ventilator if major brain injury. Episodes of PSH can begin during
they show early signs of substantial neurologic improve- the acute phase, often in comatose patients,
ment (Fig. 8.4). Gradually, after the patient is weaned off and continue into the rehabilitation phase. Patients
the ventilator, the tracheostomy can be closed, including become tachycardic, hypertensive (with widened pulse
in patients with prolonged unconsciousness. Pulmonary pressure), tachypneic, febrile, diaphoretic, and often
care involves frequent culturing of sputum when secre- develop markedly increased tone, which may result in
tions change in color and texture and immediate anti- dystonic posturing. Pupillary dilatation, piloerection,
biotic coverage to treat pneumonia and sepsis. Pleural and skin flushing can also be seen. The manifestations
effusions are frequent as a manifestation of anasarca of PSH respond best to bolus doses of morphine sulfate
and large pleural collections may need to be drained. (2–8 mg intravenously). This favorable response is not
Gastrointestinal problems vary from gastroparesis to related to the analgesic effect of opiates, but rather to
paralytic ileus, resulting in distension of the colon and modulation of central pathways that are responsible
increased risk of perforation. Daily bowel care may for the autonomic dysfunction. The response to mor-
include motility agents. phine is rapid and quite reliable in aborting spells of
The most common healthcare-related infections PSH. Other effective medications for the treatment of
are pneumonia, urinary tract infections, or infections PSH include noncardioselective beta-blockers (such
of indwelling venous catheters. Potentially difficult as propranolol), clonidine, and dexmedetomidine (cen-
to eradicate microorganisms include Enterococcus tral alpha 2-receptor agonists), bromocriptine (a dopa-
mine D2-receptor agonist), baclofen (a GABAB
receptor agonist), benzodiazepines (GABAA receptor
agonist), and gabapentin (which binds GABA receptors
and voltage-gated calcium channels in the dorsal horn
of the spinal cord). In our experience, beta-blockers
and clonidine are useful in controlling the tachycardia
and hypertension, but less so for the dystonia. Baclofen
and benzodiazepines (especially diazepam) do cause
muscle relaxation, but may not improve the other
hypersympathetic features.
Continuous volume replacement is needed for long-
term care. The adequate intravascular status is deter-
mined by satisfactory organ perfusion (urinary output,
capillary refill, cold or warm extremities, blood lactate,
and mixed venous oxygen saturation). Tissue edema
may form over time, possibly as a result of overzealous
Fig. 8.4. Percutaneous gastrostomy. fluid administration (e.g., failure to adjust intravenous
MANAGEMENT OF THE COMATOSE PATIENT 127
fluid rate while advancing enteral nutrition, failure to Table 8.5
concentrate medications). Volume depletion is less com- Daily concerns in care of the comatose patient
mon in the longterm but may occur, especially when
extravascular compartment is expanded by sepsis. Hypo- Lungs Mechanical ventilation settings
tonic crystalloids, such as lactated Ringer’s or half nor- Weaning option
mal saline, should be avoided in traumatic brain injury. Tracheostomy care
Chest X-ray for infiltrates
Albumin (5%) is a good volume expander, and may have
Heart Cardiac arrhythmias
a role in sepsis resuscitation, but the safety in acute brain
Electrocardiogram changes
injury is unclear and may be deleterious in traumatic (i.e., QT prolongation)
brain injury. In patients who have developed oliguria Inotropes/vasopressors/beta blockade
and a rise in BUN (BUN/creatinine ratio > 20), dehydra- Gastrointestinal Oropharyngeal hygiene
tion is very likely and should result in discontinuation of Nutrition and choice of formula
all diuretics and administration of normal saline. Targets glucose/insulin drips
Nutrition is eventually provided through a PEG Bowel motility assistance
(Fig. 8.3), which is very safe. A study of 674 patients Bladder Indwelling catheter
reported only 2% of patient experienced reversible compli- Urine analysis
cations (Iizuka and Reding, 2005). Complications include Skin Decubitus
Conjunctiva/eye care
wound infection, leakage, peritonitis, self-extubation or
Prophylaxis Unfractionated heparin
hemorrhage in the first weeks of placement. The risk of
Surveillance ultrasound of venous system
gastrointestinal hemorrhage may be increased. Compared Gastrointestinal prophylaxis
with nasogastric tubes, gastroesophageal reflux is lower in Fever control
patients with a PEG. Access Peripheral catheter
A bowel care regimen should be initiated. Bowel Peripherally inserted central catheter
incontinence is often present, and the task is to keep Subclavian
the skin clean and dry. Diarrhea may have many causes, Peripheral intravenous
but can be attributed to certain nutritional formulas and Medication Medication reconciliation
resolve with reducing fiber content. Antibiotics, as well Antibiotic stop dates
as Escherichia coli or Clostridium difficile infections, are Drug–drug interaction
Sedation/analgesia needs
other possible causes of diarrhea. Failure to pass stool, or
marble-like stools, should be treated with rectal enema or
manual removal. Glycerol suppository can be helpful, neomycin and polymyxin. The long-term care of the
but senna (10 mL) and lactulose (20 mL) are common comatose patient is summarized in Table 8.5.
maintenance therapies. Comatose patients are at risk of
adynamic ileus. Marked abdominal distension and
auscultatory silence are early signs. Metoclopramide
NEUROREHABILITATION
(10 mg IV) or erythromycin (500 mg orally) can be very
effective to resolve the bowel distension. When a patient awakens from coma, neurorehabilitation
Nosocomial urinary tract infections will likely occur can be considered. Criteria to admit patients to rehabili-
in comatose patients with long-term indwelling cathe- tation centers have been developed. Most generally,
ters. Bacteriuria involves Escherichia coli and Pseudo- patients are not eligible if: (1) there are continuous med-
monas aeruginosa in two-thirds of all cases, with less ical concerns that may lead to an unstable situation; (2) it
frequent pathogens, including Enterococcus spp., Acine- is unlikely that the patient will be able to improve or
tobacter spp., Klebsiella spp., and Proteus spp. Increased make progress in daily therapy sessions; and (3) there
risk for bacteriuria in patients admitted to ICU is con- is no support system after the patient returns home. Cen-
veyed by female gender (short urethra and flora contam- ters for Medicare and Medicaid Services (CMS) criteria
ination), length of ICU stay, antibiotic use, and duration are most often applied, as they determine reimbursement.
of catheterization; thus, they are to some degree unavoi- In addition to the patient having brain-related limiting
dable. The types of drainage systems, aseptic handling, neurologic impairment, the need for multidisciplinary
and other avoidance measures have been successful in therapies, and the capability to participate and benefit
reducing infection rates. This includes preventing the from an intensive intervention (i.e.,  3 hours of daily
catheter tubing from kinking, regular emptying of collec- therapy), CMS requires that: (1) the patient has active
tion bag, maintaining drainage systems below level of medical problems that require physician attendance;
bladder, appropriate meatal care, and use of silver- (2) the patient has needs specific to specialized rehabil-
impregnated urinary catheters or vesical irrigation with itation nursing; and (3) this care cannot be provided in
128 E.F.M. WIJDICKS
a less intense medical environment (nursing home). Are there therapeutic options in patients with impaired
Neurorehabilitation can only function well with a large consciousness? Treatment of minimally conscious state
staff that includes physiatrists, neuropsychologists, has mostly been of interest, and now data suggest that
speech therapists, occupational and recreational thera- amantadine 100 mg twice daily for 2 weeks followed by
pists, rehabilitation nurse specialists, social workers, 150 mg twice daily at week 3 and 200 mg twice daily at
and vocational case counselors. This multidisciplinary week 4 accelerates recovery in traumatic brain injury. Zol-
team should be carefully orchestrated and often involves pidem (10 mg) trial may be administered, but the response
a case manager involved in coordinating care. Programs is variable and mostly absent. Others have tried fluoxetine
usually involve activities for several hours a day, 5 days (selective serotonin reuptake inhibitor) 20 mg daily, with
a week. Functional independence is best achieved if some effect in motor response. Methylphenidate is a
patients can enter these programs within the first dopaminergic agent that improves processing speed,
6 months after acute brain injury. Substantial evidence attention, and possibly memory. Another dopaminergic
for remedial interventions involving attention, memory, drug (bromocriptine) and a selective norepinephrine reup-
social communication skills, and executive function take inhibitor (atomoxetine) have been considered in post-
remains wanting. concussional cognitive impairment, but not in minimally
Rating of improvement of patients with disorders of conscious state.
consciousness is needed not only to better measure range Interest in deep-brain stimulation has rekindled,
of behaviors, but also to assist in research on prognosis in and bipolar stimulation of thalamic nuclei has been con-
patients with severe brain injury. It has been known that sidered, with variable results. Recent data in 3 patients
probabilistic models improve accuracy when compared have not shown clinically evident improvement in
to clinical prediction, but there continues to be an uncer- consciousness (Magrassi et al., 2016). There is also little
tainty about the most meaningful and interpretable score. evidence that these treatments produce harm in these vul-
There is no shortage of scales assessing patients and nerable adults (who, I hasten to add, are human beings).
major competition for practical use. Current scales that On the other hand, one can see that these patients may
are used in practice and research studies are Functional become perceived as a “neglected” group of patients,
Independence Measure (FIM), Disability Rating Scale while there truly may not be much offered here that will
(DRS), Glasgow Outcome Scale, Cerebral Performance lead to improved functional outcome. It remains unexa-
Scale, Glasgow Outcome Extended Scale, Neurobeha- mined if increased awareness of a major neurologic
vior Rating Scale-Revised and, more recently, Neuro- handicap causes more agony to the patient, who is
logic Outcome Scale for Traumatic Brain Injury. now becoming more fully aware of the ordeal.
Outcome measures in rehabilitation most commonly
are considered in relation to the International Classifica-
OUTCOME PREDICTION
tion of Functioning, Disability and Health realms of
impairment (how the examination is different from nor- Outcome prediction in coma is only possible with disease
mal), activity limitations (so-called activities of daily liv- entities followed for a substantial amount of time, usually
ing and instrumental activities of daily living), and 6–12 months. Outcome prediction may not be reliable in
restrictions to participation (e.g., personal, family, voca- young patients who have shown enormous resilience and
tional, community roles). The National Institutes of surprising improvement in functioning. There are some
Health toolbox, Patient-Reported Outcomes Measure- important facts to keep in mind: approximately 50% of
ment Information System (PROMIS) measures, Activity poor-grade patients with an aneurysmal subarachnoid
Measure for Post-Acute Care (AM-PAC), and Traumatic hemorrhage improve over time; over 80% of comatose
Brain Injury Quality of Life (TBI-QOL) are examples of patients with traumatic brain injury awaken; but fewer
current measures. than 10% of patients who remain comatose 1–2 days
Although the FIM is most widely used, the DRS has after an anoxic-ischemic event improve to better grades
been used in research studies and requires eight items. of consciousness (Greer et al., 2013).
The total scores vary from 0 to 30 (a vegetative state Prolonged unconsciousness is uncommon, mostly
has a score of 22 or more, and 30 indicates death). The because patients who remain comatose die. This is often
first three items are the GCS (lowest number is here because of an intercurrent event (e.g., severe sepsis or
0 rather than 1), and the other scores are for self-care decubitus ulcers), but also because family members wish
activities and level of functioning (physically, mentally, no further life-sustaining interventions as a result of an
emotionally, and socially). The interrater reliability is advance directive (advance directives, used in many
good, as is the comparison of ratings by family members countries, are legal documents in which patients have
and rehabilitation professionals. determined what actions should be taken if they are no
MANAGEMENT OF THE COMATOSE PATIENT 129
longer able to make decisions due to illness or incapac- Lavrijsen J, vaqn Rens G, van den Bosch H (2005).
ity). No neurologist wants to deprive the patient or family Filamentary keratopathy as a chronic problem in the
of hope or the potential for recovery. Still, families may long-term care of patients in a vegetative state. Cornea
decide to proceed with withdrawal of life support, even in 24: 620–622.
Magrassi L, Maggioni G, Pistarini C et al. (2016 Jan 8). Results
the setting of some uncertainty. The prospect of a
of a prospective study (CATS) on the effects of thalamic
severely disabled person, even if the chance is realistic,
stimulation in minimally conscious and vegetative state
might not be commensurate with the patient’s wishes. If patients. J Neurosurg 1–10.
the patient stays on a ventilator and cannot return home, it Mijalski C, Lovett A, Mahajan R et al. (2015). Cerebral
may not be the quality of life everyone has hoped for. fat embolism: a case of rapid-onset coma. Stroke 46:
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The massive destruction in the cortical layers and thala- patient: clinical approach and diagnosis. Semin Neurol
mus at autopsy, absence of operational modular networks 33: 110–120.
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tion in glucose metabolism on positron emission tomog- operative neurosurgical management in patients with
extra-axial mass lesion and Glasgow Coma Scale of 3 is
raphy, and markedly depressed EEG in postresuscitation
associated with survival benefit: a propensity matched
PVS are all test results that confirm a clinical examina-
analysis. Injury 47: 70–76.
tion showing a nonsapient being. The general rule Stevens RD, Cadena RS, Pineda J (2015). Emergency neuro-
remains that if the clinical findings of PVS are still logical life support: approach to the patient with coma.
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