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CHAPTER 16 Depressed Consciousness
and Coma
Benjamin S. Bassin and Jeremy L. Cooke
PERSPECTIVE
Epidemiology
Depressed mental status represents an alteration in arousal and is
a common presenting complaint in the emergency department
(ED). This presentation can be the manifestation of a wide spectrum of diseases, with the degree of impairment ranging along a
continuum from sleepiness to decreased alertness to frank coma.
The differential diagnosis of stupor and coma is broad and diverse
(Table 16-1) but can usually be categorized into metabolic and
systemic, structural, or psychogenic causes. The majority of cases
are caused by metabolic or systemic derangements, whereas the
remainder are usually caused by structural lesions. Psychogenic
presentations are much less common. The differential diagnosis
for depressed level of consciousness often overlaps with that for
confusion (see Chapter 17). Frequently, diagnosis and management occur simultaneously, and a structured systematic approach
is used. A thorough grasp of the underlying pathophysiology
leading to the acute depressed mental state will lead to timely
diagnosis and treatment.
Pathophysiology
Consciousness is defined as the awareness of one’s self or sur­
roundings; it includes the properties of arousal and cognition.
Alterations in arousal frequently are described as levels of consciousness, although they actually refer to dynamic points on a
continuum ranging from fully alert to stuporous to comatose
or complete unconsciousness. Conversely, cognition frequently
refers to states of consciousness or awareness and is defined as the
combination of orientation, the accurate perception of what is
experienced; judgment, the ability to process input data to generate
more meaningful information; and memory, the ability to store
and retrieve information. There are many examples of medical
states that alter cognition, including confusion, inattention, delusions, and dementia. However, these states do not depress the
level of arousal and therefore are discussed in other chapters in
this book.
The ascending reticular activating system (ARAS) is the neuroanatomic structure primarily responsible for arousal and cortical
activation. It is located in the paramedian tegmental zone in the
dorsal part of the brainstem (Fig. 16-1). The input of somatic and
sensory stimuli to the cerebral cortex is controlled by the ARAS
and functions to initiate arousal from sleep. The brain’s cognition
centers are located primarily in the cerebral cortex and serve to
determine the content of consciousness.
Insults to the cerebral cortex or brainstem can each independently cause depressed consciousness or coma. These structures
142
are vulnerable to metabolic derangements, toxins, or mechanical
injury. Typically, both cerebral hemispheres need to be affected to
induce coma, and this also depends on the size and speed of progression of the insult. Localized, unilateral lesions in the cerebral
cortex usually do not induce depressed consciousness or coma
even if other cognitive functions are impaired. In contrast, a completely intact brainstem is necessary for arousal. Small focal lesions
in the brainstem can affect the ARAS. If the ARAS is impaired, the
cerebral cortex cannot be aroused, and depressed consciousness
or coma occurs.
DIAGNOSTIC APPROACH
Differential Considerations
Potential causes of depressed consciousness can be divided into a
few general categories. Metabolic or systemic causes of coma can
include hypoxia, hypoperfusion, infection, toxic drug effects, or
electrolyte disturbances. Hypoxia can be the result of congestive
heart failure (CHF), pulmonary embolism, carbon monoxide
poisoning, or severe pulmonary compromise such as occurs in
chronic obstructive pulmonary disease (COPD), cystic fibrosis,
and asthma. The various causes of shock can result in global
hypoperfusion states leading to depression of consciousness.
These include anaphylactic, septic, hypovolemic, cardiogenic, and
neurogenic origins of shock. Each type of shock has its own
unique characteristics, which are detailed in other chapters. Infection, both systemic (sepsis) and focal, can be another general cause
of depressed consciousness. This is particularly true if central
nervous system (CNS) structures are involved, as in meningitis,
encephalitis, or CNS abscess. Toxic drug effects ranging from recreational drug use and intentional overdoses to therapeutic doses
with adverse side effects are common general causes of depressed
consciousness seen in the ED. In the elderly, adverse side effects
from prescription medications are common. In addition, electrolyte and glucose abnormalities can be caused by multiple conditions, including diabetes, renal dysfunction, malignancy, and
medication interactions or dosage errors.
Head trauma, stroke, tumor, and infection are the most common
structural causes of coma and depressed consciousness. Traumatic
causes can include subdural and epidural hematomas, intraparenchymal or subarachnoid hemorrhage, or simply contusion or concussion. Strokes occur with embolic, thrombotic, or hemorrhagic
mechanisms, but it is extremely unusual for ischemic (i.e., nonhemorrhagic) stroke to depress consciousness unless a massive
insult to both hemispheres has occurred (e.g., diffuse severe cerebral edema after a massive infarct) or a high-grade basilar artery
stenosis or occlusion is present.1 Depression of consciousness with
CNS infections may be caused by mass effect and is common with
Chapter 16 / Depressed Consciousness and Coma 143
Table 16-1
Differential Diagnosis
ORGAN SYSTEM
CRITICAL DIAGNOSES
EMERGENT DIAGNOSES
NONEMERGENT DIAGNOSES
Neurologic or CNS
Hemorrhage
• Subarachnoid
• Pontine
• Cerebellar
• Intracerebral
Ischemic stroke
Status epilepticus
Acute hydrocephalus
Subdural hematoma
Epidural hematoma
Acute hydrocephalus
Primary brain tumor
Metastatic disease
Venous sinus thrombosis
CNS vasculitis
Pseudotumor cerebri
Seizures (limited)
Concussion or contusion
Infectious
Bacterial meningitis
Encephalitis
Septic shock
Brain abscess
Viral meningitis
Sepsis from other sources
Metabolic
Hypoglycemia
Hyperglycemia (DKA, HONK)
Thiamine deficiency
(Wernicke-Korsakoff syndrome)
Hyponatremia or hypernatremia
Hypocalcemia or hypercalcemia
Hyperammonemia
Myxedema coma
Thyrotoxicosis
Uremia
Porphyria
Hypophosphatemia
Hypomagnesemia or hypermagnesemia
Hypoparathyroidism or hyperparathyroidism
Toxic
Carbon monoxide
Cyanide
Heroin or opiates
Beta-blockers
Calcium channel blockers
Cardiac glycosides (digoxin)
Tricyclic antidepressant
Alcohol
Benzodiazepines
Cocaine, amphetamines
γ-Hydroxybutyrate (GHB)
Isoniazid
Organophosphates
Acetaminophen
Anticonvulsants
Aspirin
Lithium
PCP
SSRIs
Marijuana
LSD
Mushrooms
NSAIDs
Environmental
High-altitude cerebral edema
Heat stroke
Hypothermia
Malignant hyperthermia
Neuroleptic malignant syndrome
Dysbarism
Pulmonary, hypoxia
Anaphylaxis
Pulmonary embolus
Asthma, COPD
Cardiovascular
Acute MI
Aortic dissection
Cardiogenic shock
Cardiac tamponade
Hypovolemic shock
Hypertensive crisis
Malignant arrhythmia
Congestive heart failure
Anemia
CNS, central nervous system; COPD, chronic obstructive pulmonary disease; DKA, diabetic ketoacidosis; HONK, hyperosmolar nonketotic coma; LSD, lysergic acid diethylamide;
MI, myocardial infarction; NSAIDs, nonsteroidal anti-inflammatory drugs; PCP, phencyclidine; SSRIs, selective serotonin reuptake inhibitors.
severe bacterial meningitis, cerebral abscess or empyema, or parasitic mass. Malignancies, whether primary or metastatic, can cause
depressed consciousness if the tumor mass elevates intracranial
pressure (ICP) or reduces cerebral blood flow, or if surrounding
edema develops rapidly.
Special consideration should be given to specific populations of
patients. The elderly, in particular, are susceptible to alterations in
therapeutic medication dosage and drug-drug interactions. Even
seemingly minor infections, such as urinary tract infections, upper
respiratory infections, or viral gastroenteritis, may cause altered
mental status (see Chapter 13), depressed consciousness, or
coma. In addition, immunocompromised patients with acquired
immunodeficiency syndrome (AIDS) or those undergoing
chemotherapy treatments for transplants, and patients with
malignancy or immunologic disease are vulnerable to a multitude
of opportunistic infections not commonly seen in the general
patient population.
The clinical evaluation and stabilization of patients with
depressed consciousness occur simultaneously with the diagnosis
in the ED. The differential diagnosis of depression of consciousness is extensive but can be greatly simplified by focusing attention
on the distinguishing characteristics of the available patient
history and physical examination (Box 16-1).2 Approaching the
patient’s presentation systematically, beginning with a broad differential diagnosis, usually allows development of a short list of
likely diagnoses early in the encounter.
144 PART I ◆ Fundamental Clinical Concepts / Section Two • Cardinal Presentations
Medial geniculate body
Inferior brachium
Optic tract
Pulvinar
Pineal body
Optic commissure
Superior colliculi
Inferior colliculi
Peduncle of
cerebrum
Frenulum veli
Trochlear nerve
Lateral lemniscus
Superior peduncle
Oculomotor nerve
Pons
Trigeminal nerves
Middle peduncle
Rhomboid fossa
Acoustic nerve
Facial nerve
Abducent nerve
Clava
Figure 16-1. Brainstem anatomy. (Adapted
Hypoglossal nerve
Glossopharyngeal
and vagus nerves
from Adams J: Emergency Medicine.
Philadelphia: Elsevier; 2008.)
BOX 16-1
Structural Etiology of Altered Mental Status
and Coma
Trauma
Subdural hematoma
Epidural hematoma
Cerebral concussion or contusion
Stroke Syndromes
Embolism
Cardiac (atrial fibrillation, endocarditis)
Paradoxical (fat embolus)
Thrombosis
Cerebral venous sinus thrombosis
Hemorrhage
Subarachnoid hemorrhage (SAH)
Pontine hemorrhage
Cerebellar hemorrhage
Intracerebral hemorrhage
Tumor
Brainstem tumors
Metastatic disease
Angiomas
Pituitary apoplexy
Acute hydrocephalus
Infection
Subdural empyema or abscess
Pivotal Findings
History
Chief complaints relating to depressed consciousness vary widely.
Family members may report the patient as being more difficult to
arouse from sleep or less interactive. Often, family members or
friends have alerted emergency medical services after the patient
is “found down” or unarousable even with vigorous stimulation.
Often, information from alternate sources guides the diagnostic
workup. Common sources of information include family members,
neighbors, prehospital personnel, law enforcement, and nursing
home staff.3 They may know of preceding symptoms such as
headache, nausea, vomiting, or fever. Key historical information
includes the rate of symptom onset, a history of trauma, exposure
to drugs or toxins, or new medications or change in dosage.
Rate of symptom onset is important, as an abrupt onset of
decreased alertness may suggest structural phenomena or vascular
insult, whereas a gradual onset would be more indicative of the
slow, indolent course frequently seen with toxic, metabolic, or
infectious causes. Family members usually have some knowledge
regarding the patient’s past medical history, which may include
diabetes, liver or renal disease, vascular disease such as hypertension, coronary disease, stroke or transient ischemic attacks, malignancy, seizures, immunocompromised states such as human
immunodeficiency virus (HIV) infection, sickle cell disease, organ
transplantation, or psychiatric illness. Family members may also
be able to relay additional diagnostic clues such as rate of onset or
waxing-waning characteristics of the patient’s symptoms.
In addition, previous medical records should be reviewed
whenever possible to augment or confirm the information provided. Items with the patient such as a card in the wallet containing lists of medical conditions and/or medications or a medical
alert bracelet or necklace can provide valuable information. If the
patient’s historical baseline mental status cannot be established,
the current presentation is assumed to be an acute change.4
Causes of depression of consciousness vary with patient age
(Box 16-2). The elderly are particularly vulnerable to infectious
causes, medication changes, and alterations in their living environments. Young adults and adolescents are more likely to be
affected after recreational drug use or trauma. Accidental toxic
ingestions are often seen in younger children. In infants, infectious
Chapter 16 / Depressed Consciousness and Coma 145
BOX 16-2
Common Age-Related Etiology of Altered
Mental Status
Infant
Infection
Trauma, abuse
Metabolic
Child
Toxic ingestion
Adolescent or Young Adult
Toxic ingestion
Recreational drug use
Trauma
Elderly
Medication changes
Over-the-counter medications
Infection
Alterations in living environment
Stroke
causes of depressed consciousness are most common; however,
trauma secondary to physical abuse and metabolic derangements
from inborn errors of metabolism can be seen.5
Physical Examination
The severity of presenting symptoms dictates the speed needed for
stabilization and diagnosis. After necessary stabilization measures
have been instituted (e.g., intubation of the frankly comatose
patient), a systematic physical examination is conducted. Level of
consciousness is determined by the patient’s ability to speak in full,
coherent sentences and to respond appropriately to the examiner.
A rapid, directed neurologic screening examination can determine
whether the patient has a significant focal motor deficit. The presence of a distinctive odor on the breath, although uncommon, can
cue the examiner to the presence of alcohol, ketones (diabetic
or alcoholic ketoacidosis), or bitter almonds (cyanide toxicity).
Undressing the patient completely permits evaluation for signs
of trauma or skin lesions suggesting overwhelming infection or
needle track marks.
Significant hypotension with depressed consciousness suggests
shock with resultant cerebral hypoperfusion, and both causes and
therapy should be addressed immediately. Hypertension can be
seen as a result of subarachnoid hemorrhage or cerebral or brainstem infarction or may be secondary to any condition resulting in
increased ICP. Late-stage, severe elevation in ICP can cause bradycardia and hypertension, also known as the Cushing reflex. This
is an ominous sign and is seen most commonly in lesions affecting
the posterior fossa and in children. Bradycardia is also seen in
medication overdoses such as with beta-blockers, calcium channel
blockers, cardiac glycosides, and clonidine. Myocardial conduction blocks may also cause severe bradycardia, hypotension, and
subsequent stupor or coma. Tachycardia has a broad differential
in the altered patient and can be the result of hypovolemia, fever,
severe anemia, thyrotoxicosis, and drugs such as anticholinergics
and stimulants. Both hypothermia and hyperthermia can result in
altered mental status whether from infectious, structural, toxic or
metabolic, or environmental causes. Hyperventilation, Kussmaul’s
or Cheyne-Stokes breathing, agonal breathing, apnea, or other
alterations in respiratory patterns can suggest primary CNS
abnormalities or toxic or metabolic derangements. Changes in
respiratory patterns can be challenging for the clinician in an
unresponsive patient, as they can represent the sequelae of a
primary CNS insult or compensation for an underlying toxic or
metabolic process.
BOX 16-3
Glasgow Coma Scale
Eye opening
Verbal response
Adult
Pediatric
Motor response
Spontaneous
To voice
To pain
None
Oriented
Confused
Inappropriate words
Incomprehensible words
None
Appropriate
Cries, consolable
Persistently irritable
Restless, agitated
None
Obeys commands
Localizes pain
Withdraws to pain
Flexion to pain
Extension to pain
None
Score
4
3
2
1
5
4
3
2
1
5
4
3
2
1
6
5
4
3
2
1
Immediately after an assessment of the patient’s vital signs, a
head-to-toe physical examination is performed.6 A methodical
and complete head and neck examination is conducted, with particular emphasis on examination of the pupillary reflexes and
eye movements (see later discussion) and any indications of
head trauma, including hemotympanum, periorbital ecchymosis,
Battle’s sign, scalp hematoma, or CSF otorrhea or rhinorrhea. The
hydration of the mucous membranes may give clues to specific
toxidromes. Laceration or bruising of the tongue may indicate a
recent seizure.
Examination of the neck should focus on evidence of meningismus, which can be seen in meningitis, subarachnoid hemorrhage, and some cases of herniation. The cervical spine should be
immobilized if there are signs of neck trauma, such as cervical
spine tenderness or evidence of blunt external trauma, or if the
history indicates a potential mechanism for neck injury. Stridor
indicates respiratory distress typically from infection, allergic reaction, or foreign body aspiration. Presence of a goiter may indicate
underlying thyroid pathology.
Cardiopulmonary examination should focus on respiratory
effort, ventilatory patterns, presence of arrhythmia or murmurs,
cardiac output, and the presence of injury. Potentially helpful
abdominal findings include hepatosplenomegaly, pulsatile masses,
ecchymosis, or sequelae of liver failure such as ascites, caput
medusa, or spider angiomata. Gross blood, purulent drainage,
or retained foreign bodies should be sought on genitourinary
and rectal examination. In the absence or presence of signs of
trauma, lesions on the skin such as rashes, signs of drug use
(needle tracks or medication patches), or embolic phenomena can
be differential clues.
A systematic neurologic examination, with particular attention
paid to the eyes, is the most useful tool in differentiating a structural from a systemic or metabolic cause of depressed consciousness or coma. A head-to-toe approach is a proven strategy. This
should include evaluation of the patient’s Glasgow Coma Scale
(GCS) score (Box 16-3), level of alertness, cranial nerves, strength,
reflexes, and cerebellar functions with emphasis on gait, pronator
drift, finger-to-nose, heel-to-shin, rapid alternating movements,
and Romberg testing. The GCS measures the best motor and
verbal responses and the degree of stimulus required to elicit eye
146 PART I ◆ Fundamental Clinical Concepts / Section Two • Cardinal Presentations
opening and is measured serially, as level of consciousness frequently is dynamic after the initial insult and subsequent response
to therapy. The GCS does not differentiate among causes of altered
mental status or coma or assess cognition but is useful in monitoring changes in mental status when serial examinations are performed and serves as an objective reference for communicating
with consultants.7 A change of two or more points in serial GCS
testing represents a significant change.
Discovery of a focal neurologic deficit is suggestive of a structural cause. Particular attention should be paid to a focused eye
examination, during which a helpful amount of information can
be obtained. Unilateral dilatation of a pupil (“blown pupil”) and
loss of reactivity in a comatose patient are ominous signs of uncal
herniation and necessitate immediate neurosurgical consultation
and intervention. Papilledema, which may indicate increased ICP
or retinal hemorrhages associated with trauma, can be identified
on funduscopic examination. The eye examination should also
include testing of eye movements, which are coordinated by the
medial longitudinal fasciculus located in the brainstem and ocular
centers located in the cerebral cortex. Cranial nerves III, IV, and
VI are responsible for control of the extraocular muscles. Cranial
nerve III paralysis results in a persistently abducted eye, whereas
a persistently adducted eye is caused by paralysis of cranial nerve
VI. In the setting of trauma, a unilateral third cranial nerve palsy
suggests an ipsilateral compressive lesion such as seen with epidural hematoma. Cranial nerve VI palsies are often nonlocalizing, as
the nerve has a long intracranial course and compressive forces
from intracranial mass effects (e.g., tumor, traumatic hematoma,
increased ICP) may compromise cranial nerve function anywhere
in its course. Horizontal disconjugate gaze is an important finding
and is commonly seen in patients who are sedated, drowsy, or
intoxicated. Disconjugate gaze found in the vertical plane is usually
more serious and suggests cerebellar or pontine dysfunction.
Normal ocular motility suggests that a significant portion of the
brainstem remains intact.
Oculocephalic (doll’s eyes) and oculovestibular reflex testing are
useful in looking at the functional integrity of the brainstem.
These tests, if results are negative, make structural lesions in the
brainstem very unlikely as the source of the patient’s altered
mental status.
If there are no contraindications, such as suspected cervical
spine injury, oculocephalic testing is accomplished by observing
the patient’s eye movements while the head is turned from side
to side. Patients who exhibit a maintained forward gaze despite
head turning (doll’s eye reflex) are unlikely to have a brainstemmediated cause of coma. If the eyes remain in a fixed position
within the orbits, turning in unison with the head, brainstem
dysfunction is suggested. Oculovestibular or “cold water caloric”
testing is a more sensitive test for brainstem involvement and
cannot voluntarily be resisted (Fig. 16-2). After elevation of the
patient’s head to 30 degrees (this can be done in patients whose
cervical spine is not cleared by placing the bed in the reverse
Trendelenburg position), 10 to 30 mL of ice water is used to irrigate the external auditory canal. Tympanic membrane perforation
and cerumen impaction should be ruled out before this test is
performed. In patients who have an intact brainstem, the response
is a slow conjugate deviation of gaze toward the side of the cold
water stimulus for 30 to 120 seconds. The reflex is short-lived and
followed by corrective fast beats of nystagmus toward the midline.
This corrective nystagmus is described by the mnemonic COWS,
which stands for “cold-opposite, warm-same.” If there is no
response to the irrigation, brainstem dysfunction is possible.
Recently, literature on the phenomenon of basilar artery
stenosis or occlusion manifesting as depressed consciousness or
coma has increasingly been published. A review of the Lausanne
Stroke Registry showed that 100% of patients with poor outcome
from high-grade basilar stenosis or occlusion had either stupor or
Ice water
irrigation
right ear
Alert wakefulness (nystagmus with rapid
movement opposite side of cold stimulation)
Bilateral cerebral
hemisphere dysfunction
Left MLF dysfunction
Brainstem dysfunction
Left oculomotor
nerve dysfunction
Figure 16-2. Oculocephalogyric (caloric) responses to various central
nervous system pathologic conditions. MLF, medial longitudinal
fasciculus.
coma or the triad of pupillary abnormalities, dysarthria, and
bulbar findings on presentation.1
Ancillary Testing (Refer to Table 16-2)
Laboratory Studies
Bedside glucose testing definitively confirms or excludes hypoglycemia and can frequently limit further extensive metabolic testing
in diabetic or intoxicated patients. Serum electrolytes and renal
function measurement identify the presence of a metabolic acidosis, anion gap, uremia, or derangements in sodium or potassium.
Changes in serum calcium can be a marker for metastatic disease,
and severe hypercalcemia can cause altered mental status. Arterial
blood gas analysis rapidly assesses acid-base status and the presence of hypercarbia or hypoxia and allows calculation of arterialalveolar gradient in conditions in which shunting is suspected.
Carbon monoxide (CO)–oximetry can be added to confirm methemoglobinemia or carbon monoxide exposure.
A urine dip test is a quick way to screen for the presence of
ketones, the spilling of glucose as seen in hyperosmolar states, or
infection, which can frequently precipitate changes in mentation,
especially in the elderly. Urinalysis itself provides valuable information regarding hydration status (specific gravity) and the possible presence of calcium oxalate crystals in the setting of ethylene
glycol ingestion. Urine drug testing may confirm a suspected
ingestion or be helpful if another cause is not readily apparent.
Chapter 16 / Depressed Consciousness and Coma 147
Table 16-2
Ancillary Testing in the Altered Patient
TEST
FINDING
POTENTIAL DIAGNOSIS
Hypoxemia
Hypercarbia
Metabolic vs. respiratory acidosis
Pulmonary embolus, intracranial event, central hypoventilation, CHF
Laboratory
ABGs
A-a Gradient
Obstructive or restrictive pulmonary condition, high altitude cerebral edema,
intracerebral process
Multiple—DKA, toxic ingestion, sepsis, respiratory failure
Pulmonary embolus
Electrolytes
Carboxyhemoglobin—elevated
Sodium—increased
Sodium—decreased
Carbon monoxide exposure (consider cyanide in inhalational exposure)
Dehydration, diuretic overuse, diabetes insipidus, osmotic diuresis
Adrenal insufficiency, CHF, cirrhosis, DKA, infant formula dilution, myxedema
coma, renal failure, SIADH
BUN, creatinine, glucose
Complete blood count
Bicarbonate—decreased
Calcium—elevated
BUN, creatinine-elevated
Glucose-elevated
Decreased
WBCs—elevated
WBCs—decreased
Hgb and Hct—elevated
Hgb and Hct—decreased
Platelets—elevated
Platelets—decreased
Metabolic acidosis—multiple causes (anion vs. non–anion gap)
Malignancy, hyperparathyroidism, thyrotoxicosis
Acute renal failure, uremia
DKA, hyperosmolar hyperglycemic state (HHS)
Alcohol abuse, cirrhosis, insulin overdose, sepsis
Nonspecific—infection, inflammation, steroids, stress
Immunocompromised—malignancy, drug, alcohol, or viral marrow suppression
Polycythemia
Severe anemia
Hereditary thrombocytosis, acute phase reactant
Sepsis, DIC, intracranial hemorrhage
Coagulation
ammonia
PT and INR—elevated
Elevated
Bleeding dyscrasias, liver disease, warfarin use
Hepatic encephalopathy, valproic acid toxicity, inborn errors of metabolism
Thyroid studies
Elevated
Decreased
WBCs—elevated
Thyrotoxicosis
Myxedema coma
Meningitis
Cerebrospinal fluid
RBCs—elevated
Specific gravity—elevated
Subarachnoid hemorrhage
Dehydration
Urinalysis
WBCs, leukocyte esterase, nitrites
RBCs—elevated
Glucosuria
Calcium oxalate crystals
Urinary tract Infection
Retroperitoneal hemorrhage
DKA, HHS
Ethylene glycol ingestion
Ingestion
Urine drug screen
Multiple possibilities
Imaging
Head CT—non-contrast
Head CT—contrast
CT angiography or venography
MRI
Chest radiograph
Ultrasound
Other Studies
ECG
EEG
Blood
Enlarged ventricles
Mass or edema
Mass or edema
Ring-enhancing lesion
Vascular clot
Vascular dilation
Hypoperfusion
Mass
Meningeal enhancement
Consolidation or mass
Pulmonary edema
Radiolucency, mediastinal shift
Widened mediastinum
Hampton’s hump, Westermark’s
sign
Intra-abdominal blood
ST segment changes, Q waves
T wave inversions
Abnormal intervals
Osborne wave (J wave)
Right-sided heart strain
Multiple findings
Intracerebral hemorrhage, epidural hematoma, subdural hematoma,
subarachnoid hemorrhage, hemorrhagic stroke
Obstructive hydrocephalus, shunt malfunction
Ischemic stroke, tumor, or metastatic disease
Tumor, metastatic disease
Abscess
Basilar or vertebral artery occlusion or stenosis, venous sinus thrombosis
Aneurysm, arteriovenous malformation,
Ischemic stroke, basilar or vertebral artery occlusion or stenosis, venous sinus
thrombosis
Tumor, metastatic disease, abscess (superior to CT for posterior fossa lesions)
Meningitis, encephalitis, neurosarcoidosis, carcinomatosis, post–lumbar puncture
Pneumonia, tumor, foreign body
CHF, cardiogenic shock
Pneumothorax
Aortic dissection
Pulmonary embolus
Ruptured abdominal aortic aneurysm; spleen, kidney, or liver laceration (trauma)
Ischemia or infarction
Ischemia, intracerebral hemorrhage
Conduction blocks, drug ingestion, electrolyte abnormality
Hypothermia
Pulmonary embolus
Status epilepticus (convulsive or nonconvulsive)
ABGs, arterial blood gases; BUN, blood urea nitrogen; CHF, congestive heart failure; CT, computed tomography; DIC, disseminated intravascular coagulation; DKA, diabetic
ketoacidosis; ECG, electrocardiogram; EEG, electroencephalogram; Hct, hematocrit; Hgb, hemoglobin; INR, international normalized ratio; MRI, magnetic resonance imaging;
PT, prothrombin time; RBCs, red blood cells; SIADH, syndrome of inappropriate antidiuretic hormone secretion; WBCs, white blood cells.
148 PART I ◆ Fundamental Clinical Concepts / Section Two • Cardinal Presentations
A complete blood count can be useful. Although an elevated
white blood cell count can be a marker for infection, it is nonspecific and rarely helpful in discerning a toxic or metabolic cause.
An abnormally low white blood cell count, however, suggests an
immunocompromised state and should urgently direct clinical
investigation toward an infectious cause. Profound anemia may be
seen from witnessed or occult blood loss. Thrombocytopenia can
be a marker for sepsis, intracranial hemorrhage, or disseminated
intravascular coagulation.
Elevated results from serum coagulation studies can be a marker
for bleeding dyscrasias, liver disease, or supratherapeutic levels
of anticoagulation drugs. Both platelets and coagulation studies
should be checked before invasive procedures are performed at
noncompressible sites such as lumbar punctures and central
venous access, if the patient’s condition allows.
Serum ammonia levels are controversial and have not been
shown to be a reliable marker for the cause of depressed consciousness. Although usually associated with severe liver disease,
ammonia levels can be elevated in other conditions such as valproic acid toxicity and inborn errors of metabolism and can be
normal in patients with hepatic encephalopathy.8 Thyroid function studies can help confirm myxedema coma or thyrotoxicosis.
When CNS pathology such as infection or hemorrhage is suggested but not seen on neuroimaging studies, cerebrospinal fluid
analysis is undertaken.
Imaging Studies
Noncontrast computed tomography (CT) of the brain is the
initial imaging modality of choice in the setting of depressed
consciousness and coma. In the majority of ED settings, it is
available and quickly obtained, and this makes CT more suitable
than other imaging tests for the patient with borderline hemodynamic instability. Brain CT is sufficiently sensitive to detect most
intracranial hemorrhages that are large enough to cause coma. In
addition, the presence of hydrocephalus can quickly be assessed.
Despite its utility, linear artifacts created by the thick skull base
can limit the view of the posterior fossa on CT. In this case, magnetic resonance imaging (MRI) of the brain is generally much
better for identifying structural lesions in this region. However,
this modality is less practical in most ED settings because of its
cost, limited availability, and duration of acquiring each study,
which consequently limits the ability to monitor or access the
unstable patient.4
Contrast-enhanced CT may be used if a tumor, metastatic
disease, or intracerebral infection is suspected. CT or magnetic
resonance angiography or venography may be available in larger
tertiary care centers for use in the diagnosis and/or treatment of
intracerebral aneurysms, arteriovenous malformations, cerebral
venous sinus thrombosis, or basilar or vertebral artery stenosis
or occlusion.
Plain radiography may identify severe pneumonia or acute
respiratory distress syndrome. In ingestions, it may rarely reveal
specific types of heavy metals such as mercury, iron, or lead in the
pediatric population or packages of ingested illicit substances in
body packers or stuffers.
Additional Testing
Electrocardiograms (ECGs) can reveal cardiac ischemia, conduction blocks, or arrhythmia or can help corroborate certain ingestions (tricyclic antidepressants), electrolyte abnormalities (e.g.,
potassium, calcium), or hypothermia. If nonconvulsive status epilepticus is suggested, or if a patient with status epilepticus has
required neuromuscular blockade, continuous electroencephalographic monitoring, if available, can provide key information
about the patient’s status and guide therapy.
DIAGNOSTIC ALGORITHM
Critical diagnoses to consider are listed in Table 16-1.
Information gathered from the history and physical examination of the patient with depressed consciousness is used to direct
the approach to diagnostic testing. Most often, this information
points toward a systemic or metabolic cause rather than a structural cause. Neuroimaging studies are performed early in patients
with suspected structural causes but should not precede treatment
of quickly reversible conditions such as opioid overdose or hypoglycemia. Systemic or metabolic causes of depressed consciousness
and coma are most often found on analysis of laboratory studies.
Consequently, in the undifferentiated patient, diagnostic tests
should be performed in parallel whenever possible to avoid unnecessary delays in initiation of treatment.
Similarly, owing to the severe morbidity and mortality associated with many causes of depressed consciousness and the ability
for rapid reversal of several conditions, initial stabilization, treatment, and assessment are performed simultaneously. A logical
approach to the history, physical examination, and diagnostic
testing is presented in Figure 16-3.
EMPIRICAL MANAGEMENT
Initial establishment of airway, breathing, and circulation (ABCs)
is of primary importance in stabilizing the patient with altered
mental status. Initiation of intravenous access combined with the
administration of oxygen and continuous telemetry monitoring
should happen concomitantly within the first few minutes of the
patient’s arrival.2 In patients with a GCS score lower than 8, intubation is indicated unless the coma is readily reversible, such as
that caused by hypoglycemia or opioid overdose (see Chapter 1).
All patients should receive a thorough neurologic examination
before sedation and chemical paralysis for intubation. Trauma
patients require spinal immobilization in addition to indicated
fluid resuscitation.
Reversible causes of the patient’s condition should be sought
concomitantly with initial stabilization. Administration of the
components of the “coma cocktail,” which include dextrose,
naloxone, and thiamine, can quickly reverse the alterations in
mental status caused by hypoglycemia, narcotic overdose, and
thiamine deficiency, respectively, and can substantially narrow
the differential diagnosis. Bedside capillary blood glucose, blood,
and urine studies should be sent while ECG and emergent noncontrast head CT are ordered. Further therapy and workup will
be dictated by the patient’s history and physical examination.
Specific attention should be given to identifying the focal neurologic abnormalities, including pupillary reflexes and pathologic
eye movements that suggest mass effect or depressed brainstem
function, prompting neuroimaging and evaluation by a neurosurgeon. Empirical administration of mannitol and elevation of
the head of the bed are indicated when there is clear evidence of
transtentorial herniation (see Chapters 41 and 101). In patients
with compromised brainstem function who lack evidence of herniation, investigation of possible exposure to toxins or metabolic
imbalances should proceed with consideration of basilar artery or
bilateral vertebral artery occlusion requiring CT or magnetic resonance angiography. Basilar stenosis or occlusion is one of the
few stroke syndromes that can manifest as stupor or coma, and
administration of antiplatelet, anticoagulation and thrombolytic
agents should be considered in consultation with a neurologist or
stroke team.
In patients who demonstrate normal brainstem function, the
workup proceeds as supportive care is provided. When an infectious cause is suggested, empirical administration of a broadspectrum antibiotic should not be delayed for lumbar puncture
or other diagnostic tools.9 Lesions or masses found on brain
Chapter 16 / Depressed Consciousness and Coma 149
Initial assessment:
Vital signs
Airway, breathing, circulation
IV, oxygen, monitor
Bedside glucose
Narcan
No gag reflex, GCS < 8
RSI
History/suggestion
of trauma?
Yes
No
History/suspicion
of infection?
C-spine
immobilization
Yes
Signs of impending herniation?
• Cushing’s response (↑ BP, ↓ HR)
• Unilateral blown pupil
Yes
No
IV antibiotics
Consider
steroids
Toxic/metabolic
workup
ECG
CT
CT
Toxic/metabolic
etiology?
No
Elevate head
Neurosurgery consult
↑ RR (PCO2 ~ 35 mm Hg)
Mannitol
Craniotomy/ventriculostomy
CT/OR
CT
Yes
Lesion
on CT?
Lesion
on CT?
Yes
Yes
No
Neurosurgery
consult
OR
Neurosurgery
consult
OR
Toxic/
metabolic
etiology?
Yes
Treat
appropriately
No
Treat
appropriately
Lumbar
puncture
Yes
Continue
antibiotics
Admit to ICU
Neurology
consult
Lesion
on CT?
Yes
Lumbar
puncture
No
Neurosurgery
consult
OR
Infection?
No
No
Hemorrhage?
No
Toxic/
metabolic
workup
Lumbar
puncture
Yes
Neurosurgery
consult
Angiography
OR
No
Anoxia
CVA
MRI
Neurology
consult
Figure 16-3. Algorithm for diagnostic approach to altered mental status and coma. BP, blood pressure; C-spine, cervical spine; CT, computed
tomography of brain; CVA, cerebrovascular accident; HR, heart rate; ICU, intensive care unit; IV, intravenous; OR, operating room; RR, respiration
rate; RSI, rapid sequence intubation. (Adapted from Adams J: Emergency Medicine. Philadelphia: Elsevier; 2008.)
150 PART I ◆ Fundamental Clinical Concepts / Section Two • Cardinal Presentations
imaging should prompt evaluation by a neurosurgeon and, if indicated, early operative intervention. In patients in whom a toxic
ingestion is possible, activated charcoal is of little benefit in most
cases. Specific toxin antidotes, if indicated, can be given, with
consultation with a local or regional poison center when required.
Early hemodialysis after consultation with a nephrologist should
also be considered in patients who have toxic or metabolic abnormalities amenable to this therapy.
DISPOSITION
Patients with structural lesions on imaging require immediate
neurosurgical consultation and frequently will require operative
intervention. Patients are urgently transferred to a center with
neurosurgical capabilities once hemodynamically stabilized if
these services are not available at the site of initial patient
presentation.
The vast majority of patients with depressed consciousness or
coma require admission to the hospital for further treatment and
workup. Some patients who have returned to their baseline mental
status after reversal of hypoglycemia or opioid overdose may be
suitable for discharge directly from the ED or ED observation unit
after a period of observation. Patients with alcohol or recreational
drug intoxication and no other discernible cause of altered mental
status can be discharged when they are clinically sober.
The references for this chapter can be found online by
accessing the accompanying Expert Consult website.
Chapter 16 / Depressed Consciousness and Coma 150.e1
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