Acs0811 Coma, Cognitive Impairment, And Seizures

© 2008 B C Decker Inc All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 11 COMA, COGNITIVE IMPAIRMENT, AND SEIZURES — 1

11 COMA, COGNITIVE IMPAIRMENT,
AND SEIZURES
Maxim D. Hammer, M.D.

Coma is the neurologist’s favorite consultation: the history is First, the term unresponsive may be applied to a patient who is
usually straightforward, the neurologic examination is focused, actually fully conscious but is unable or unwilling to respond ver-
and the differential diagnosis is limited. A good neurologic bally. For example, a patient with aphasia (a common manifesta-
examination, in combination with a thoughtful battery of tests, tion of stroke) may be awake, alert, and aware, yet unable to speak.
will invariably achieve the correct diagnosis. It is vital for the As another example, a patient who is in a locked-in state (either
intensivist to become equally comfortable with the rapid assess- from a brain stem injury or from generalized muscle paralysis) is
ment of coma. Once initial stabilization of the patient has been fully conscious but cannot speak and cannot communicate except
achieved, management of coma is determined by the specific through subtle eye movements. Finally, patients with a psychiatric
causative condition or conditions present. Rapid recognition of disorder may present with a so-called functional coma while
potentially reversible causes of coma (e.g., basilar artery occlu- remaining fully conscious; simple examination techniques quickly
sion [BAO], nonconvulsive status epilepticus, and herniation), reveal that they are completely awake.
followed by the appropriate emergency consultations, can often Second, the term unresponsive may be applied to a patient who has
prevent or reduce morbidity and mortality. a waxing-and-waning level of wakefulness.This fluctuation between
This chapter is intended as a practical, rational, and efficient wakefulness and coma is what defines delirium, and it is invariably
approach to the diagnosis and management of coma. To that caused by infection, metabolic disturbances, or alcohol withdrawal.
end, an algorithmic approach to diagnosis is formulated, gener- Third, the term unresponsive may be applied to a patient who
al treatment measures for comatose patients are outlined, specif- truly is not even awake. In this sense, the term could of course be
ic causes of coma are reviewed, and prognostic issues are consid- applied to a person who is simply asleep, but for the purposes of
ered. Detailed discussions of neuroanatomy and cranial nerve this chapter, it should be understood as referring to a patient who
pathways, which are readily available elsewhere,1 are intentional- is comatose.
ly omitted, as are detailed descriptions of specific treatment of
SPECTRUM OF COMA
individual causes of coma (other than BAO, status epilepticus,
cardiac arrest, increased intracranial pressure [IICP], and cer- Patients who are not aware, alert, or even awake (except for those
tain metabolic derangements). who are simply asleep) fall somewhere along the spectrum of
coma. This spectrum reflects varying levels of impairment of the
response to stimuli. On the high end of the spectrum, for example,
Classification of Levels of Consciousness is the patient who can be aroused (albeit perhaps only temporari-
ly) by the sound of a voice. Somewhat farther down is the patient
AWAKENESS, ALERTNESS, AND AWARENESS
who can be temporarily aroused by a painful stimulus. Farther
A patient’s level of consciousness can usefully be described in down still is the patient who cannot be aroused by a painful stim-
terms of the three As of consciousness: Awake, Alert, and Aware. ulus but at least exhibits some motor response to it. On the low end
To be awake means to be fully roused and thus not asleep. To be
alert means to be able to pay attention to one’s environment or to
an examiner. Finally, to be aware means to have an understanding
of oneself and one’s environment. Being oriented is a manifesta- Aware
tion of being aware of one’s environment.
A person who is awake, alert, and aware may be said to be fully
conscious [see Figure 1]. One who is awake and alert but has lost Alert
awareness is severely demented. Someone who is merely awake
and not alert or aware is delirious. A delirious patient’s level of
wakefulness may wax and wane. A person who is not awake, alert,
or aware either is asleep (in which case he or she can be rendered Awake
awake—i.e., is arousable) or is somewhere along the so-called
spectrum of coma (see below). Sleep, Delirium Dementia, Normal Adult
Admittedly, describing patients simply in terms of awakeness, Coma Infant Consciousness
alertness, and awareness omits many important nuances; never- Consciousness
theless, it is an excellent and easily reproducible way of assessing
Figure 1 Awareness depends on alertness, which in turn
level of consciousness.
depends on arousal (i.e., how awake one is). Normally cognizant
UNRESPONSIVE PATIENT adults are aware of themselves and their environment. Persons
who have lost awareness but retain alertness and wakefulness may
The term unresponsive is used frequently, but often in a vague be characterized as severely demented. Persons who have lost
manner that does not yield a clear meaning. Fortunately, in the alertness are delirious by definition, though their level of wakeful-
setting of coma management, there are only three possible mean- ness may wax and wane. Finally, persons who are not aware,
ings that need be considered [see Figure 2]. alert, or awake may be either asleep or in a coma.


Unresponsive patient requires evaluation

Assess level of consciousness.

Patient is fully conscious Patient is not alert or aware and exhibits Patient is not awake, alert, or aware
(awake, alert, and aware) waxing-and-waning awakeness
Determine whether patient is arousable.
Patient is aphasic, faking, or in Patient is delirious as a result of infection
a locked-in state. or metabolic derangement.

Figure 2 In the evaluation of an unresponsive patient, it should
be kept in mind that the patient may be fully conscious (e.g., an Patient is not arousable
Patient is arousable
aphasic stroke victim), delirious, asleep, or comatose.
Patient is asleep or Patient is comatose [see
delirious. Figure 3].

of the spectrum is the patient who has no motor response to a HISTORY
painful stimulus; this is the generally accepted definition of coma.
The ideal historian is a person who knows the patient well.
The terms lethargy, stupor, and obtundation, though widely
Optimally, if the coma was of sudden onset, a witness was present
used, have come to signify different things to different people.
who can describe what occurred. A history of trauma, drug use,
Accordingly, to ensure precise communication, it is perhaps advis-
medications, recent febrile illness, heart disease, organ failure, or
able to employ clear clinical patient descriptions rather than rely
seizures often rapidly leads to the correct diagnosis [see Table 2].
on these particular terms.
Typically, the most challenging cases are those patients who are
“found down”; such cases necessitate a clear diagnostic approach
Initial Stabilization that begins with the physical and neurologic examinations.
The first step in dealing with coma is to stabilize the patient by FOCUSED NEUROLOGIC EXAMINATION
addressing the ABCs of resuscitation (Airway, Breathing, and There are two good reasons for performing a neurologic exam-
Circulation). The patient’s airway must be cleared of all foreign ination on a coma patient. First, such an examination allows the
material, and the patency of the airway must be verified.The spon- physician to assign the patient a Glasgow Coma Scale (GCS) score
taneous rate and rhythm of respiration should be noted. [see Table 3], which may be used in making decisions about the
Endotracheal intubation is indicated in patients who are dyspneic, necessity for intubation and which provides an objective means of
hypoventilating, or vomiting uncontrollably. If a patient is to be following (at least superficially) the patient’s neurologic status.
intubated, however, it is extremely helpful first to obtain a focused Second, the neurologic examination may quickly yield important
neurologic examination (which can be done in 60 seconds) diagnostic information.
because the information that can be gained from this examination A complete and exhaustive neurologic examination is totally
will be lost when the patient is paralyzed for the intubation. unnecessary. For the purposes of evaluating coma, a focused neu-
Hyperventilation with a bag and mask and 100% oxygen should rologic examination is preferable, being both valuable and rapid (~
be performed before intubation to ensure adequate oxygenation 60 seconds). If intubation is indicated, the coma examination
during the procedure. If there is any possibility of cervical spine should be performed quickly before sedative and paralytic agents
injury, intubation should be delayed, if possible, until fracture can are given. This examination addresses a number of key findings
be ruled out radiographically. [see Table 4], but in general, it may be thought of as assessing four
Circulation must be vigorously supported, especially in the set- neurologic variables: (1) spontaneous movements (~ 15 seconds),
ting of brain injury or hypoxia.This is accomplished by inserting a (2) pupillary response (~ 15 seconds), (3) ocular motility (~ 15 sec-
large-bore I.V. or central venous catheter and infusing isotonic flu- onds), and (4) motor response (~ 15 seconds). A reflex hammer is
ids or volume expanders. The use of solutions containing free not needed.
water (e.g., 5% dextrose in water) should be avoided, especially in Spontaneous movements should be observed over a period of
the setting of brain injury or stroke, because such solutions have 10 to 20 seconds. Generalized seizures may present as tonic or
the potential to increase cerebral edema. tonic-clonic movements of one or both sides. Tonic seizures are
characterized by sustained contractions with upper-extremity flex-
ion and lower-extremity extension.Tonic-clonic seizures are char-
Clinical Evaluation
acterized by tonic contractures alternating with periods of muscle
As the patient is being stabilized, evaluation should be initiated. atonia, resulting in rhythmic contractions. Myoclonus consists of
A witness or someone else capable of providing a history should motor jerks that are sudden, brief, shocklike, and randomly dis-
be sought. The differential diagnosis of coma is wide but limited tributed; it may be seen in patients with hypoxic-ischemic enceph-
[see Table 1]. Clues from the history, the focused neurologic exam- alopathy (e.g., after cardiac arrest) or other metabolic distur-
ination, and the general physical examination are often helpful and bances. Other findings (e.g., a flaccid arm that hangs down the
sometimes diagnostic [see Figure 3]. side of the stretcher or a leg that is extorted) may be indicative of


hemiparesis. The motor response to pain can be tested and the pupils are generally resistant to metabolic insult); they also
assigned a GCS score. Asymmetry should be noted. indicate the integrity of the brain stem [see Table 5]. The origin of
Pupillary responses are important in that their presence or the reticular activating system (RAS), the so-called on switch of
absence distinguishes structural from metabolic coma (because consciousness, may be physically located adjacent to the brain
stem nuclei that control pupillary response.
The pathways that control ocular motility also lie adjacent to
Table 1 Differential Diagnosis of Coma the RAS. Roving eye movements usually indicate that the brain
stem is intact and that a metabolic problem is affecting the brain.
Potential Cause of Coma Differential Diagnosis Minimal or absent eye movement in conjunction with reactive
pupils also typically signifies a metabolic process. Gaze deviation
Large brain stem stroke (with or without basilar may indicate a stroke: a cortical stroke will cause the eyes to look
artery occlusion) toward the damaged side of the brain, whereas a pontine stroke
Massive stroke or hemorrhage with mass effect
will cause the eyes to look away from the damaged side of the
Subarachnoid hemorrhage
Cerebrovascular
Subdural or epidural hematoma
pons. Gaze deviation may also signify an ongoing seizure: the eyes
Hypoxic-ischemic encephalopathy after cardiac look away from the hemisphere in which the seizure is occurring
arrest or, after the seizure is over, toward the postictal hemisphere.
Hypertensive encephalopathy Vertical disconjugation of the eyes (skew deviation) is indicative of
Cardiac arrest
brain stem disease and frequently occurs during basilar artery
Cardiac dysrhythmia thrombosis. Ocular bobbing (rapid downward movements with a
Cardiovascular Congestive heart failure slow drift back to the original position) is occasionally seen in the
Hypotension setting of extensive pontine damage.
Myocardial infarction
GENERAL PHYSICAL EXAMINATION
Bacteremia or sepsis
Meningitis
Blood pressure, heart rate, and cardiac rhythm are key to the diag-
Infectious
Encephalitis (e.g., herpesvirus, arbovirus) nosis of the various cardiovascular and hemodynamic causes of coma
[see Table 1]. Hypothermia is noted in cases of exposure, drowning,
Multiple severe concussions (diffuse axonal injury, methanol poisoning, and septic shock. Hyperthermia is obviously
second-hit syndrome)
Subdural or epidural hematoma
suggestive of an ongoing infectious process. A stiff neck is often
Traumatic
Multiple contusions caused by meningeal irritability resulting from infection or inflamma-
Penetrating head injury tion; it may be indicative of meningitis, but it also may be the only
physical sign of subarachnoid hemorrhage. Various other physical
Alcohol intoxication/withdrawal findings may be observed in comatose patients as well [see Table 5].
Opiate intoxication
A rise in intracranial pressure (ICP) occurs with any space-occu-
Anesthesia
Overdose
pying lesion in the calvaria. Signs of rising ICP include increasing
Antianxiety agents or antidepressants blood pressure, decreasing heart rate, and slowing or periodic res-
Anticholinergics piration (Cushing phenomenon). Papilledema caused by IICP
Anticonvulsants usually takes weeks to develop and is seldom a presenting sign.
Toxic Antihistamines
Insulin
Lithium Management
Neuroleptics
Opiates GENERAL MEASURES, TRIAGE, AND TEST BATTERY
Salicylates
As emergency management is being provided, laboratory stud-
Sedatives
ies should be obtained, including serum electrolyte, calcium, mag-
Hyperglycemia or hypoglycemia nesium, phosphorus, blood urea nitrogen (BUN), and creatinine
Diabetic ketoacidosis levels, as well as liver function tests. A complete blood count
Hyperosmolar nonketotic coma (CBC), a urinalysis, and a urine toxicity screen should also be
Hypernatremia or hyponatremia obtained. A lumbar puncture should be performed only if menin-
Osmotic demyelination syndrome: central pon-
Metabolic tine myelinolysis gitis is suspected on the basis of clinical examination.
Hepatic failure The so-called coma cocktail—consisting of dextrose, naloxone,
Renal failure and thiamine—is administered if the cause of coma is not immedi-
Hypoxia or hypercarbia ately apparent from the brief history and physical examination; the
Hypothermia addition of flumazenil is considered if benzodiazepine overdose is
Grand mal status epilepticus
suspected [see Table 6].2,3 It should be kept in mind that adminis-
Epileptic Nonconvulsive status epilepticus tering dextrose to a thiamine-depleted patient (especially one who
Postictal state is malnourished or alcoholic) may precipitate the Wernicke-
Korsakoff syndrome. As a rule, therefore, thiamine should always
Massive stroke or hemorrhage with mass effect be given before dextrose.
Mass
Tumor or abscess with mass effect
Any comatose patient with focal signs on the coma examination
Hematologic Thrombotic thrombocytopenic purpura should undergo head CT scanning. Any patient with signs of
meningitis on the physical examination should receive emergency
Conversion
Psychiatric Malingering
antibiotic therapy. When drug overdose or toxin ingestion is sus-
pected, activated charcoal, 50 to 100 mg (with or without gastric


Comatose patient requires evaluation and treatment

Stabilize patient (ABCs).
Obtain focused history [see Table 2].
Perform focused neurologic (coma) examination [see Tables 3 and 4].
Perform general physical examination [see Table 5].

Likely cause of coma is not immediately Likely cause of coma is immediately
apparent from clinical evaluation apparent from clinical evaluation

Give coma cocktail: thiamine, naloxone, and Manage specific cause of coma as
dextrose, along with flumazenil if benzodiazepine appropriate.
overdose is suspected [see Table 6].
Restore acid-base balance.

Patient has focal signs and Patient has elevated T°, with or
coma of sudden onset without meningism

Treat patient for stroke [see 6:1 Stroke Treat patient for any infection present.
and Transient Ischemic Attack].

Patient is in status epilepticus Patient exhibits Cushing Patient shows evidence of
phenomenon and has focal signs having experienced cardiac
leading to CT scan arrest
Give first-line agent: lorazepam I.V. in 2 mg increments,
3 min apart, to maximum dose of 8 g. (Alternative
first-line agent: diazepam, 10–20 mg.) Treat patient for increased ICP: Treat according to ACLS guidelines,
hyperventilation; mannitol, 0.25 mg/kg employing hypothermia.
If coma is refractory to lorazepam, give second-line
q. 4–6 hr; neurosurgery.
agent: fosphenytoin, 20 mg/kg I.V., at a rate of
100–150 mg/min. (Alternative second-line agent:
phenytoin, 20 mg/kg I.V., at a rate of up to 50 mg/min.)
If coma is refractory to fosphenytoin, give third-line Figure 3 Depicted is an algorithmic approach to the most
agent: pentobarbital, 5–12 mg/kg I.V., then 1 mg/kg/hr; common causes of acute coma.
or midazolam, 0.1–0.3 mg/kg bolus, then 0.05–0.2
mg/kg/hr; or propofol, 3–5 mg/kg, then 1–15 mg/kg/hr.
(Levetiracetam may also be considered.)

lavage), should be given to prevent systemic absorption. As noted, A typical case scenario for BAO, occasionally heard by stroke
flumazenil may be given for suspected benzodiazepine overdose neurologists, is as follows. A patient presents with double vision,
and may produce dramatic arousal; however, this agent is con- followed hours later by ataxia. This may prompt an emergency
traindicated in patients taking tricyclic antidepressants because of department (ED) visit.The patient is admitted to the hospital but,
an increased risk of seizures. on the nursing unit, becomes suddenly unresponsive and needs
Once the recommended general treatment measures have been intubation for airway protection. In another typical scenario, a
carried out, the next step is to look for and address specific caus- patient who has just undergone cardiac catheterization becomes
es of coma. suddenly unresponsive on the angiography table but is hemody-
namically stable.
MANAGEMENT OF SPECIFIC CAUSES OF COMA
A comatose patient with BAO usually manifests obvious clini-
cal signs of brain stem injury, such as quadriparesis, skew devia-
Basilar Artery Occlusion tion, and diminished gag reflex (many physicians report that intu-
BAO is an uncommon cause of stroke but also an underrec- bation is unexpectedly easy). On occasion, CT scanning may
ognized one. Morbidity and mortality are high, with only about reveal an apparently hyperdense basilar artery [see Figure 4]; imag-
15% to 45% of victims surviving.4 BAO may be caused by ing of the posterior circulation invariably reveals the problem.
embolism (most often from the heart but sometimes from the Management of BAO should be aimed at immediate recanaliza-
vertebral arteries), by intrinsic atherothrombosis, or by verte- tion of the occluded artery. Thrombolysis, either intravenous
bral dissection. It frequently presents with a stepwise accumu- (with tissue plasminogen activator) or intra-arterial (with uroki-
lation of neurologic deficits that culminates in a coma. nase or mechanical clot disruption), may be lifesaving.


As noted, patients with extensive brain stem injury resulting Table 3 Glasgow Coma Scale
from BAO often die. Some enter what is known as the locked-in
state, in which they remain conscious but are unable to move,
Test Response Score
breathe, or swallow. Occasionally, patients retain the capacity for
subtle eye movements or eye blinking and thus are able to com- Spontaneous 4
municate through yes/no responses to questions. Most stroke neu- To verbal command 3
rologists consider the locked-in state a fate worse than death. Eye opening (E)
To pain 2
Seizures None 1

A seizure disorder can cause coma in two different ways. First, Obedience to verbal command 6
the coma may be the initial manifestation of the immediate post- Localization of painful stimulus 5
ictal state after a generalized seizure. In such cases, the coma
Flexion withdrawal response to pain 4
resolves rapidly, and further management is unnecessary.The dura- Best motor
response Abnormal flexion response to pain 3
tion of the postictal coma may be directly correlated with patient (arm) (M) (decorticate rigidity)
age and inversely correlated with baseline functional status. Extension response to pain 2
Second, coma may develop when multiple generalized seizures (decerebrate rigidity)
occur in succession and there is not enough time between seizures None 1
to allow patients to recover.The resulting state is status epilepticus.
Generalized convulsive status epilepticus (GCSE) may be Oriented conversation 5
defined either as (1) continuous seizure activity lasting longer than Disoriented conversation 4
5 minutes or as (2) two or more discrete generalized seizures Best verbal
response (V) Inappropriate words 3
between which there is incomplete recovery of consciousness. Incomprehensible sounds 2
GCSE is most frequently the result of noncompliance with an None 1
antiepileptic drug regimen, alcohol use or withdrawal, or drug tox-
icity. Less common causes include CNS infection, a cerebral Total (E + M + V) 3–15
tumor, trauma, refractory epilepsy, stroke, metabolic disorders,
and cardiac arrest. If untreated, GCSE leads to cerebral edema,
herniation, and death.
A tonic-clonic seizure begins with a tonic contraction that lasts
as long as 30 seconds, followed by several minutes of repeated
Table 2 Coma History muscle contractions, loss of pupillary response to light, sweating,
tachycardia, excessive bronchial secretion, and marked hyperten-
Questions to Be Asked Possible Causes to Be Considered sion. Repeated seizures cause lactic and respiratory acidosis, rhab-
domyolysis and myoglobinuria, aspiration and pulmonary edema,
Is there a witness? [If no, see Table 4.] shoulder dislocations, rib fractures, and cardiac dysrhythmias.The
Stroke
neuronal damage induces an inflammatory response, and if
If stepwise deterioration, consider BAO seizures continue, cerebral edema ensues.
Was it sudden? In the treatment of GCSE, the aim is not to stop the body from
Seizure
Cardiac arrest convulsing but to stop the abnormal cerebral electrical activity
immediately. The longer GCSE continues, the more refractory it
Traumatic brain injury
will be to treatment. Paralytics mask (but do not prevent) the
Subarachnoid hemorrhage
Was there trauma?
Subdural or epidural hematoma with mass effect
seizures; therefore, intubation and paralysis should be avoided if
and herniation possible.
Like all other coma victims, patients with GCSE should first be
Recreational drug overdose
stabilized [see Initial Stabilization, above]. I.V. access should then
Opioids, alcohol
Has there been drug use?
Prescription drug overdose
be obtained. Glucose should be given empirically, along with thi-
If so, which drugs? amine, and blood should be drawn and sent for laboratory tests
Opioids, benzodiazepines, barbiturates,
anticholinergics (including anticonvulsant levels).
Anticonvulsant management of status epilepticus is discussed in
Was there a recent febrile Meningitis or encephalitis
illness? Bacteremia or sepsis
detail elsewhere5,6 and so need only be summarized here.The first-
line treatment for GCSE consists of administration of lorazepam
Cardiac arrest [see Figure 3]. Although there is no significant difference between
Myocardial infarction the benzodiazepines with respect to rapidity of seizure control,
Is there a history of heart Congestive heart failure
disease? lorazepam is thought to bind more tightly to brain receptors and
Cardiac dysrhythmia
thus is believed to have a longer duration of action. Lorazepam is
Hypotension
given in 2 mg increments 3 minutes apart to a maximum dose of
Is there a history of organ Renal failure 8 mg before another agent is tried [see Table 7]. Diazepam may be
failure? Hepatic failure employed as an alternative.The second-line agent is fosphenytoin,
Postictal from single seizure 20 mg/kg at up to 150 mg/min I.V.; phenytoin may be given as an
Is there a history of alternative. If the patient does not respond to either lorazepam or
seizures? Convulsive status epilepticus
Nonconvulsive status epilepticus fosphenytoin, a third-line agent—pentobarbital, midazolam, or
propofol—should be given in a continuous infusion. Of the three
BAO—basilar artery occlusion third-line choices, midazolam may be the most effective, and it


Table 4 Focused Neurologic Examination (Coma Examination)

Neurologic Variable Findings Likely Cause of Coma
Assessed

Rhythmic movements Seizure
Spontaneous movement
(15 sec) Random jerks (myoclonus) Hypoxic-ischemic encephalopathy

Unilateral fixed and dilated pupil Brain herniation (mass)
Posterior communicating artery aneurysm

Midposition unreactive pupils Midbrain lesion

Pinpoint unreactive pupils Pontine lesion
Pupillary response
(15 sec) Small and sluggishly reactive pupils Drug intoxication

Large and unreactive pupils Atropine

Barbiturates, paralytics, lidocaine, phenothiazines, methanol,
Unreactive pupils
aminoglycoside antibiotics, hypothermia

Roving eye movements Metabolic insult to brain; brain stem is intact

Stroke (eyes look toward damaged side of brain)
Gaze deviation Seizure (eyes look away from side of brain producing
seizure)
Ocular motility (15 sec)
Skew deviation BAO

Ocular bobbing Extensive damage to pons

Unilateral weakness Structural injury (e.g., stroke)

Herniation (mass)
Motor response (15 sec) Posturing (flexor or extensor)
Extensive cortical injury

certainly has the lowest side effect profile. Levetiracetam has also Committee on Resuscitation issued a guideline statement con-
been successfully employed to treat some refractory cases of taining the following recommendation: “Unconscious adult
GCSE.7,8 patients with spontaneous circulation after out-of-hospital car-
The goal of therapy is to achieve a burst-suppression pattern on diac arrest should be cooled to 32° C to 34° C for 12 to 24
electroencephalography for 12 to 24 hours before any attempt is hours when the initial rhythm was VF. Such cooling may also be
made to taper medications. beneficial for other rhythms or in-hospital cardiac arrest.”12 This
recommendation has spurred the implementation of hypother-
Increased Intracranial Pressure mia for resuscitation of cardiac arrest victims in many hospital
If IICP is suspected on the basis of clinical examination and centers.
herniation is identified, treatment must be initiated immediately.9
Medical management of IICP is a temporizing measure, aimed at Metabolic Derangements
slowing the process of herniation until the problem can be correct- Intoxication Many comatose patients who are seen in the
ed neurosurgically. ED are suffering from an overdose of alcohol, narcotics, sedatives,
The head of the patient’s bed should be elevated to an angle of or some combination thereof. Most of these drugs induce depres-
30° to 45° to facilitate venous return from the head. If the patient sion of respiration and cardiovascular function, which is a major
is intubated, hyperventilation to bring the carbon dioxide tension cause of mortality in comatose patients. Anticipation and early
below 25 mm Hg will rapidly, but only transiently, lower the ICP. treatment of these complications may alleviate their effects. Early
Mannitol, 0.25 mg/kg every 4 to 6 hours, will also control IICP intubation, respiratory support, and maintenance of normal
temporarily. Steroids may be used in the setting of tumors or blood pressure are essential. Gastric lavage is effective when
abscesses of the brain. In most cases of IICP, the eventual treat- ingestion of a drug is discovered no more than 4 hours after the
ment is neurosurgical decompression. event (except in the case of salicylates, which may be removed in
substantial amounts as long as 10 hours after ingestion).
Cardiac Arrest Accordingly, in most cases of drug overdose, little is gained by
Cardiac arrest, if ongoing, is treated according to advanced performing gastric lavage more than 4 hours after ingestion,
cardiac life support (ACLS) guidelines. Several preliminary unless the patient has been in shock and consequently manifests
studies on the use of hypothermia for brain resuscitation after delayed gastric emptying and slowed absorption. When a patient
ventricular fibrillation (VF) cardiac arrest led to the publication is comatose or uncooperative, however, the examiner is rarely able
of two randomized, controlled clinical trials in back-to-back to determine the exact time of ingestion; thus, gastric lavage is
issues of the New England Journal of Medicine in 2002.10,11 Both almost always indicated in this situation.
trials clearly demonstrated that hypothermia significantly Patients are intubated with a cuffed endotracheal tube (to
improved survival and neurologic outcomes. As a result, the protect the airway from aspirated gastric contents) and placed
Advanced Life Support Task Force of the International Liaison in the left lateral decubitus position (to allow pooling of the gas-


Table 5 General Physical Examination If hypoglycemic coma is prolonged, it may result in permanent
brain damage. Therefore, initial management involves urgent
restoration of the patient to a euglycemic state.This may be accom-
Physical Variable Finding and Possible Causative Condition plished through I.V. injection of glucose.Traditionally, injection of
Assessed
an ampule (50 ml) of a 50% solution is prescribed; however, this
Signs of trauma around head/neck measure frequently results in loss of the peripheral I.V. site used.
Jaundice Alternatively, 250 ml of a 10% dextrose solution is rapidly inject-
Hepatic failure ed; this measure provides the same amount of dextrose without
Skin Exanthema causing any loss of venous access. If necessary, infusion of a 5%
Viral infection dextrose solution may be continued subsequently. As noted [see
Petechial rash General Measures, Triage, and Test Battery, above], if the patient
Meningococcal infection
is thiamine depleted, 100 mg of thiamine should be given before
Brudzinski or Kernig sign dextrose so as not to precipitate Wernicke-Korsakoff syndrome.
Head and neck Meningitis, meningoencephalitis Further treatment consists of prevention, in the form of educat-
Subarachnoid hemorrhage ing patients in the use of insulin and encouraging them to carry
Fever
glucose tablets or sweets with them at all times. A supply of
Infection (meningitis, encephalitis, bacteremia, glucagon (1 g I.M.) that can be administered by relatives may also
sepsis) be stored at home.
Hypothermia
Temperature Exposure Diabetic ketotic coma Because patients who are comatose
Intoxication (alcohol, benzodiazepine, barbiturate) as a result of diabetic ketoacidosis often present in a profoundly
Myxedema coma
dehydrated state, treatment must be initiated as soon as possible.
Sepsis
The following are the key components of the management of dia-
Alcohol intoxication betic ketoacidosis.
Fetor hepaticus
Hepatic failure 1. Replacement of fluid losses (the average fluid loss is approxi-
Breath mately 7 L).
Uriniferous smell
Uremia 2. Normalization of electrolyte levels and careful monitoring of
Ketoacidosis serum potassium.
3. Restoration of acid-base balance (bicarbonate infusion is
Hypotension
Shock
reserved for severe cases).
Sepsis
Intoxication
Blood pressure
Myocardial infarction
Addison disease
Hypertension
Hypertensive encephalopathy

Cardiac conduction and Dysrhythmia
rhythm (ECG) Acute myocardial infarction

Hepatomegaly
Abdomen
Splenomegaly

tric contents) with the head down. Lavage is then performed
with copious amounts of fluid until the returned fluid is clear.
After evacuation, a slurry containing 10 g of activated charcoal
in 30 to 50 ml is instilled into the stomach via a nasogastric
tube. After lavage, cathartic agents may be used to shorten the
transit time through the GI tract and thus to decrease absorp-
tion of the ingested material. Diuresis (saline, ionized, or
osmotic), dialysis, and charcoal hemoperfusion all facilitate
excretion of toxins. Specific antidotes exist for several common
intoxicants; however, discussion of these antidotes is beyond
the scope of this chapter.

Hypoglycemic coma Symptomatic hypoglycemia may
occur when plasma glucose levels fall below 45 mg/dl.
Symptoms may range from jitteriness with palpitations and
diaphoresis to focal neurologic symptoms mimicking ischemic Figure 4 In this noncontrast head CT scan, the basilar artery,
stroke to frank coma. The most common predisposing cause is which runs ventral to the pons and the lower midbrain, appears
diabetes; other common causes include alcoholism, hepatic fail- hyperdense. In the setting of acute coma, this finding suggests
ure, and renal failure. BAO.


Table 6 Coma Cocktail

Drug Indications Dosing (Adults) Potential Adverse Effects

Anaphylactoid reaction
Wernicke-Korsakoff syndrome
Thiamine 100 mg I.V. over 5 min Hypotension
Ethylene glycol ingestion
Angioedema

50–100 ml of 50% dextrose I.V.
Symptomatic hypoglycemia Alternatively, 250 ml of 10% dextrose Phlebitis
Dextrose Altered mental status without ability to (to prevent the phlebitis that fre- Cellulitis
rapidly obtain serum glucose level quently occurs with administration
of 50% dextrose)

0.1 mg I.V. initially (I.V. route is more
effective than subcutaneous or Hypersensitivity reaction
endotracheal), aimed at producing
subtle improvement in ventilation Precipitation of sudden narcotic withdrawal syndrome
Reversal of CNS depression and respi-
Repeat doses given in 2–3 min inter- (If heroin has been tainted with scopolamine, withdrawal of
Naloxone ratory depression caused by over-
vals, increased very slowly each opioid can precipitate anticholinergic crisis)
dose of opioid medication
time Lung injury, hypertension, and cardiac dysrhythmias (rarely
If no response after total dose of 10 reported)
mg, opioid toxicity ruled out

0.2 mg I.V. over 30 sec
Contraindicated in patient experiencing seizure
If no response, 0.3 mg I.V. over 30 sec
Flumazenil Benzodiazepine overdose Benzodiazepine withdrawal, which may cause seizures and
If still no response, 0.5 mg I.V. every autonomic dysfunction
30 sec to maximum dose of 3 mg

4. Correction of insulin deﬁciency (4 to 6 U/hr). er, that meticulous rehydration be performed, given that many
5. Replenishment of energy stores (e.g., through dextrose infu- patients with this condition are elderly.
sion with insulin coverage until the patient can resume oral
feeding).
6. Investigation to identify an underlying cause (infection is Vegetative State
common). Approximately 10% to 12% of comatose patients eventually
lapse into a vegetative state (VS).Whereas comatose patients have
Hyperglycemic hyperosmolar nonketotic coma Manage- closed eyes and do not respond to pain, VS patients have sponta-
ment of hyperosmolar nonketotic coma is essentially the same as neous eye opening according to sleep-wake cycles and may have
that of diabetic ketotic coma. It is particularly important, howev- minimal, purposeless movement. Speciﬁcally, the diagnosis of VS

Table 7 Drugs Used to Treat Status Epilepticus

Drug Priority of Use Dosing Potential Adverse Effect

2 mg increments I.V. 3 min Respiratory depression
Lorazepam First-line agent apart to maximum of 8 mg Hypotension

Respiratory depression
Diazepam Alternative first-line agent 10 mg I.V., 1 or 2 doses
Hypotension

Dysrhythmia
Fosphenytoin Second-line agent 20 mg/kg, 150 mg/min
Hypotension

Dysrhythmia
Phenytoin Alternative second-line agent 20 mg/kg, 50 mg/min Hypotension
(Risk is lower than with fosphenytoin)

Poor WBC chemotaxis
Pentobarbital Third-line agent 5–12 mg/kg, 1–10 mg/kg/hr Paralysis of respiratory cilia
Poikilothermia

0.1–0.3 mg/kg, 0.05–2.0 Tachyphylaxis
Midazolam Third-line agent mg/kg/hr Death (mortality lower than with propofol)

Recurrent seizures after abrupt discontinuance
Hypotension
Propofol Third-line agent 3–5 mg/kg, 1–15 mg/kg/hr Hypertriglyceridemia
Anemia
Death (mortality higher than with midazolam)

WBC—white blood cell


can be made if there is intermittent wakefulness (sleep-wake Prognosis
cycles); no evidence of awareness of self or environment or ability At least 50% of patients who are in traumatic VS will recover
to interact with others; no evidence of sustained, reproducible, consciousness within 1 year, compared with only 15% of patients
purposeful, or voluntary behavioral responses to external stimuli; in nontraumatic VS. In one series, 69% of nontraumatic VS
no evidence of language comprehension or expression; and suffi- patients died, 20% survived with severe disability, and 8% survived
ciently preserved hypothalamic and brain stem autonomic func- without severe disability. Indicators of poor prognosis in nontrau-
tion to permit survival with medical and nursing care.VS that per- matic VS patients include the absence of pupillary reflexes for 24
sists for more than 1 month is referred to as a persistent vegetative hours after the event; no withdrawal from painful stimuli after 72
state (PVS); PVS that lasts for 1 year or longer is considered per- hours; the absence of roving eye movements after 7 days; and the
manent VS.13,14 absence of motor response to noxious stimuli after 72 hours.15-17

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