Coma

Dylan B. M e d l e y , MD James E. Morris, MD, MPH

17

" a n a g e m e n t of Life-Threatening Problems

aragement
i : Assessment i : " " a c r a n i a l Pressure a n d H e r n i a t i o n ; . a t i o n of The Comatose p a t i e n t

Emergency T r e a t m e n t of Specific Disorders Causing Coma Structural Lesions Metabolic Encephalopathies Other Disorders Causing Coma Criteria for Brain D e a t h

ITE MANAGEMENT OF --.-THREATENING PROBLEMS f*=fal Considerations

i: i n e d as the total absence of arousal and aware:i i: least 1 hour associated with injury or funci i c r o n of the ascending reticular activating system ..-.item or bilateral cortical structures. Comatose onstrate no eye opening, speech, or spontafments, and motor activity elicited by painful ::esent) is abnormal or reflexive rather than purma must be differentiated from other pathologic E ;onsciousness such as brain death, vegetative - ::rium, although it may be difficult to do so in jy department.

until administration of empiric therapy for coma. Empiric therapy, often abbreviated by the acronym "D.O.N.T." consists of IV dextrose, supplemental oxygen, IV naloxone, and thiamine. Dextrose (50 mL of 50% solution in adults) reverses coma secondary to hypoglycemia and is indicated if rapid testing of blood glucose is unavailable. Oxygen therapy should be initiated to immediately correct possible hypoxemic induced coma. Naloxone (0.4-2.0 mg IV) rapidly reverses coma and respiratory depression secondary to narcotic overdose but because of short half-life, multiple doses m a y b e required. Thiamine (100 mg IV) is commonly given along with dextrose to avoid precipitating Wernicke encephalopathy in predisposed patients. Flumazenil (0.2 mg/min IV) specifically antagonizes benzodiazepines but is not routinely given empirically as it may precipitate seizures that are then refractory to benzodiazepines. It may be indicated in iatrogenic coma secondary to excess benzodiazepine administration. If coma persists following the administration of naloxone and dextrose, definitive management of airway and breathing should be considered. IV access with two large-bore IVs should be obtained and blood pressure (especially hypotension) managed aggressively. A complete set of vital signs, including temperature and pulse oximetry, is essential to avoid missing coma complicated by severe hypo- or hyperthermia and hypoxia. Cervical spine immobilization should be maintained if there is any suspicion of trauma. A focused

. MANAGEMENT
i - i g e m e n t of the comatose patient involves the :: r.eeded to manage any critically ill patient pre:he emergency department. Immediate assess: support of airway, breathing, and circulation : performed before efforts to diagnose or address : rases of coma are undertaken, with the caveat deration may be given to postponing intubation

 1 k' I?]L' tawSlK-EH

Secure ai rway and establish adequate ventilatior

Pulses pres<

Begin CPR (Chapter 9)

Treat for status epileptious (Chapter 19)

Generalized or focal seizures

No -

Arterial blood gases: P C 0 2 > 60 mm Hg P 0 2 < 60 mm Hg

Body core temper-ature >41 (105.8) or < 32 C (89.6 ~ F ) ! Yes

Yes

No 1. Obtain vital signs 2. Insert intravenous cannula 3. Draw blood for tests 4. Give the following: Glucose, 50 m L of 5 0 % solution intravenously* Thiamine, 5 0 - 1 0 0 mg intravenously Naloxone, 0 . 8 - 2 m g intravenously Patient awakens quickly ( 2 - 3 min.) Yes

Treat for respiratory failure with supplemental oxygen and ventilatory support

Diagnosis: Hypoglycemia (blood glucose <30 mg/dL) or opiate overdose

'Hyperglycemia may increase brain damage from ischemia. If results of blood glucsoe measurements are available and in the normal range, withhold glucose.

A Figure 1 7 - 1 . Approach to the unconscious patient.

Kl

Ov

Lumbar puncture needed immediately in suspected meningoencephalitis if not contraindicated (focal signs, papilledema); otherwise, obtain emergency CT scan.

Supratentorial mass 1. Gradual onset of coma 2. Early hemiparesis and hemihypesthesia 3. Rostral caudal progression of symptoms.

Diagnosis: meningoencephalitis versus subarachnoid hemorrhage

T
Yes Evidence of meningeal irritation No Reassess 1. History, trauma, drugs, seizures, symptoms 2. Physical examination 3. Neurologic examination: pupils, ocular movement, pain response, seizures

Subtentorial mass 1. Abrupt onset of coma 2. Symmetric neurologic deficit 3. Pinpoint pupils or conjugate deviation of gaze

> 71

I
Pinpoint pupils Yes | - No

Repeat naloxone administration.

Metabolic encephalopathy 1. Gradual onset of coma; anteced-ent somnolence or delirium 2. Symmetric neurologic deficit 3. Reactive pupils despite loss of extraocular movements and depreessed respiration 4. Often myoclonus with meningeal I signs or evidence of seizures (active or recent)

TO
71

Diagnosis: Opiate overdose

Diagnosis: 1. Pontine or cerebellar hemorrhage 2. Cholinesterase inhibitor poisoning 3. Miotic eye drops and c o m a of other cause

Psychogenic coma 1. Eyelid tone greater than skeletal muscle tone 2. No roving eye movements 3. Normal response to caloric testing 4. Normal electroencephalogram

-o
73

O C O

H B NM M M H H M M HHS H M MMM M i

Glasgow Coma Scale.

Score 6 5 4 3 2 1 5 4 3 2 1 Adult Follows commands Localizes pain Withdraws to pain Flexion Extension None Oriented Confused speech Inappropriate words Incomprehensible None Wi. Child <5 years Child >5 years Follows commands

Normal spontaneous movements Localizes to supraocular pain (>9 months) Withdraws from nailbed pressure Flexion to supraocular pain Extension to supraocular pain None Age-appropriate speech/vocalizations Less than usual ability; irritable cry Cries to pain Moans to pain No response to pain

Oriented Confused Inappropriate words Incomprehensible

Inane

: a m i n a t i o n should be performed to evaluate for _ : recipitating factors (evidence of drug use, systemic . Obtaining additional history from friends, rela 'inders, and EMS personnel is essential.

: LOGIC ASSESSMENT
r assessment in comatose patients is of p a r a m o u n t and a structured evaluation should be consoon as possible once immediate threats to life addressed. Level of consciousness, cranial nerve )n, and motor examination should be performed.

Lateralizing deficits and a rostrocaudal progression of brainstem dysfunction are seen with structural lesions, while involuntary movements are suggestive of a metabolic cause of coma. Although originally developed for traumatic brain injury, the Glasgow Coma Scale (GCS) has been shown to have predictive value in many different types of coma. Both total and c o m p o n e n t (eye, verbal, motor) scores should be documented (see Table 17-1). Cranial nerve examination (especially pupillary response) is an essential part of the neurologic examination and may assist in determining the level of brainstem dysfunction (see Table 17-2). Normal pupillary function

" " - 2 . Brainstem Reflexes.

Reflex Examination Technique Response to light Normal Response Direct and consensual restriction Eyes move conjugately in direction opposite to head Nystagmus with fast component away from stimulus Eyelid closure Brainstem Location Midbrain Pons Pons Pons Medulla Medulla

tralic
: - rcuiocephaiic

Turn head from side to side Irrigate external auditory canal with cold water Stimulation of cornea Stimulation ol carina Stimulation of soft palate

"eflex
flex

Cough
Symmetric elevation of soft palate

S E C T I O N II

MANAGEMENT OF COMMON EMERGENCY PROBLEMS

Table 1 7 - 3 . Signs of Increased Intracranial Pressure and Herniation Syndromes.

Sign Coma Pupillary dilation Miosis Lateral gaze palsy Hemiparesis Mechanism Compression of midbrain tegmentum Compression of ipsilateral third nerve Compression of the midbrain Stretching of CN VI Compression of contralateral cerebral peduncle Compression of the midbrain Compression of the medulla Compression of the pons or medulla Type of Herniation Uncal, central Uncal Central Central Uncal

Treatment of increased ICP focuses on maintaining cerebral perfusion pressure, defined as mean arterial pre?sure (MAP) m i n u s ICP. The goal is to keep CPP > 70-S m m Hg. The Monro-Kellie principle states that the volume within the skull is fixed and contains three component; brain, blood, and CSF. Increase in the a m o u n t of the>: c o m p o n e n t s (eg, cerebral edema, h e m a t o m a , hydrocephalus) or the addition of other c o m p o n e n t s (eg, t u m c : results in increased ICP. Using this principle, treatment a aimed at either reducing the volume of the components or expanding the volume available t h r o u g h surgical decompression. Emergency department care of herniation consists in tially of p r o m p t recognition and maximizing resuscitat: on Hypoxia and hypotension must be avoided and other ] adverse systemic factors such as hyperglycemia and fe sr treated aggressively. The patient's head should be elevatec a 30 and adequate sedation and analgesia provided. Seiznn ; prophylaxis should be considered, particularly when pari lytics have been given. W h e n available, further treatmefl should be guided by ICP monitoring. In the absence of I CJ monitoring, hyperventilation to a Paco 2 of 30-35 m m rif should be initiated, followed by mannitol (0.25-1.0 c u IV) or hypertonic saline (2 mL/kg of 7.5% solution IN' 1 the ICP remains high and craniectomy is not indicatec ; not available, barbiturates may be used to decrease cerer~i. metabolism and thus cerebral blood flow. Induced hyp thermia to 32-34C has been shown to effectively low otherwise refractory ICP. ent Jiang JY: Clinical study of mild hypothermia treatment inr severe traumatic brain injury. I Neurotrauma 2009;26:3' -99Wi [PMID: 19260782],

Decerebrate posturing Hypertension, bradycardia Abnormal breathing

Central, uncal Central, uncal, cerebellar Central, uncal, cerebellar

and eye movements may be seen in lesions rostral to the midbrain. Pupillary abnormalities (especially unilateral) may be an early indicator of herniation, and pupillary function should be assessed frequently when increased intracranial pressure (ICP) is a concern. Symmetrically reactive pupils that are unusually large or small are commonly secondary to drug ingestions. Motor examination should focus on the presence of movements and whether they are involuntary, reflexive, or purposeful. Purposeful movements such as localization require some degree of cortical processing, while reflexes are stereotypical responses that occur in the absence of cortical input. Structural lesions may result in posturing. Decerebrate posturing, characterized by extension of both upper and lower extremities, is seen in lesions caudal to the midbrain. Decorticate posturing, characterized by flexion of the upper extremities and extension of the lower extremities, is seen in lesions rostral to the midbrain.

FURTHER EVALUATION OF THE COMATOSE PATIENT

The differential diagnosis of coma is broad and i n d u J H primary cerebral disorders (bilateral/diffuse, unilatera. v r i l mass effect, and brain-stem disorders) as well as a n u m : & u I systemic derangements (see Table 17-4).

History
History should be obtained f r o m whatever sources are i able, including friends, bystanders, police, and EMS per- -<| nel. Crucial points include the following: Recent head trauma, even seemingly trivial Drug use (including alcohol), recent or past Past medical history, including a history of seizuresbetes, cirrhosis, or other neurologic disease Medications, including narcotics and benzodiazepinePrecomatose activity and behavior (headache, conr_vomiting)

INCREASED INTRACRANIAL PRESSURE AND HERNIATION

Herniation syndromes result f r o m increased ICP and lead to brainstem compression, manifested by arterial hypertension, bradycardia, and respiratory irregularities (Cushing triad). Herniation may be classified as uncal, central, or cerebellar (see Table 17-3). Increased ICP c o m m o n l y results f r o m a space-occupying lesion such as a t u m o r or hematoma but may also result f r o m cerebral edema secondary to trauma, infection, or severe metabolic derangements.

COMA
^^^^BHlwnwt^-iesiMiM

CHAPTER

17

e 17-4. Etiology of Coma and Altered Consciousness.

cerebral disorders : or diffuse hemispheric disorders lafic brain injury mic rrhagic (subarachnoid hemorrhage, intraventricular emorrhage) . ic-ischernic encephalopathy al venous thrombosis nancy -gitis/encephalitis 'lized or complex partial seizures; status epilepticus :ensive encephalopathy or reversible encephalopathy syndrome disseminated encephalomyelitis cephalus al Hemispheric disorders (with displacement of midline
Tes)

elsewhere on the body is presumptive evidence of head trauma in the comatose patient.

Imaging
Non-contrast head CT is an integral part of the workup for coma that is not obviously related to hypoglycemia, overdose, or other metabolic cause, and should be strongly considered in any patient who remains comatose after dextrose and naloxone. Contrast-enhanced head CT or MRI may be indicated in certain patient populations.

ill

Laboratory Evaluation
Electrolytes, LFTs, CBC, UA, glucose, urine/serum toxicology screens, thyroid function studies, BUN/Cr, and ABG should be obtained early in the evaluation of coma. Lumbar puncture and CSF analysis should be performed if not contraindicated (eg, mass lesions or other evidence of increased ICP) in patients for w h o m the cause of coma is unclear or in w h o m an infectious cause or SAH is suspected. ECG should be obtained and cardiac monitoring instituted to eliminate cardiac arrhythmias as a contributing factor. An EEC should be obtained when possible, especially in intubated patients receiving paralytics and in those for w h o m nonconvulsive status epilepticus is a consideration. Stevens RD, Bhardwaj A: Approach to the comatose patient. Crit Care Med 2006;34:31-41 [PMID: 16374153], Wilber ST: Altered mental status 11 older emergency department patients. Emerg Med Clin North Am 2006; 24:299-316 [PMID: 16584959],

atic (contusions, subdural hematoma, epidural hematoma) 35 hemispheric ischemic stroke -;.ry intracerebral hemorrhage 1 1 -: "= r-ral abscess tumor stem disorders (pons, midbrain) -jrrhage, infarction, tumor, trauma al pontine myelinolysis :ression from cerebellar infarct, hematoma, abscess, tumor - c derangements causing coma ^ c a t i o n overdose/adverse effects .gs of abuse isures (carbon monoxide, heavy metals) lie ::emic inflammatory response syndrome/sepsis

-ipoxia
- rercapnia -.pothermia - .poglycemia -Derglycemic crises (DKA, NHHS) -.po/hypernatremia -.percalcemia -;patic failure Renal failure Wernicke encephalopathy Bdocrine ^hypopituitarism - jrenal insufficiency -.po/hyperthyroidism

EMERGENCY TREATMENT OF SPECIFIC DISORDERS CAUSING COMA STRUCTURAL LESIONS 1. Intracerebral Hemorrhage
See also Chapter 37.

I A L S OF Headache, nausea, vomiting

DIAGNOSIS

Sudden versus gradual onset of coma

Other individuals with similar symptoms

Hypertension Focal neurologic deficit with signs of increased ICP

Physical Examination
Tr.e physical examination (other than the neurologic exami-.ition) should focus on ruling out other threats to life such is hypovolemia and systemic trauma. Evidence of trauma

General Considerations

Intracerebral hemorrhage (ICH) can be classified as primary (unrelated to congenital or acquired lesions) or secondary

S E C T I O N II

MANAGEMENT OF COMMON EMERGENCY PROBLEMS

Table 1 7 - 5 . Primary ICH Syndromes

Location Basal ganglia Thalamus Cerebellum Pons Findings Contralateral motor deficits, gaze paresis, aphasia Contralateral sensory loss Nausea, vomiting, ataxia, nystagmus, AMS, ipsilateral gaze/facial palsy Coma, pinpoint pupils, autonomic Instability, quadriplegia, altered respiratory patterns

obtained for all patients with declining neurological statu; or evidence of hydrocephalus on CT scan. Cerebellar hemorrhages > 3 cm require surgery. Hemorrhages in typical locations may not need further diagnostic evaluation and are rarely amenable to surgery. All patients should be admitted for further care. Broderick J et al: Guidelines for the management of spontaneou; intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group: The American Acadenr. of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke 2007;38:2001-2023 [PMID: 17938297], Hemphill JC. Treating warfarin-related intracerebral hemorrhage: is fresh frozen plasma enough? Stroke 2006;37:6-7 [PMID: 16306461], Rincn F, Mayer SA: Clinical review: Critical care management c: spontaneous intracerebral hemorrhage. Crit Care 2008;12:23~ jl'MID 19108704],

(related to vascular malformations, tumors, or other lesions). The vast majority of primary ICH is related to hypertension and occurs in characteristic areas of the brain: cerebral lobes, basal ganglia, thalamus, pons, and cerebellum. Secondary ICH is m o r e variable in location. Smoking, advanced age, and anticoagulant use are other risk factors for ICH. Early hematoma growth is m o r e c o m m o n than previously thought and is most likely responsible for sudden deterioration within the first 6 hours of initial presentation. Cytotoxic and vasogenic edema surrounding the hemorrhage may result in ischemia and are likely responsible for delayed deterioration.

2. Subdural Hematoma E S S E N T I A L S OF D I A G N O S I S
Headache Confusion Depressed level of consciousness Hyperdense crescent-shaped (biconcave) extra-axial collection of blood on CT scan

Clinical Findings
Presentation is related to the size and location of the h e m o r r h a g e (see Table 17-5). Patients with large areas of h e m o r r h a g e are often comatose on arrival. The m a j o r ity of patients with brainstem or cerebellar h e m o r r h a g e present with a decreased level of consciousness necessitating intubation. Headache is universally present in awake patients and may accompany other signs of increased ICP. Seizures occur in 10% of all ICH b u t in 50% of patients with lobar hemorrhage. Most patients are hypertensive on presentation, even if previously normotensive. N o n - c o n t r a s t CT scan is the diagnostic study of choice with CT angiography being useful in certain patient p o p u lations.

General Considerations
The possibility of subdural h e m a t o m a must be considered in any comatose patient. Trauma is the most c o m m o n cause but in about 25% of cases, there is no history or evidence of trauma. Elderly patients are particularly likely to presen: with absent or trivial trauma. Other risk factors include history of alcoholism, seizures, and coagulopathies.

Treatment and Disposition

Care is primarily supportive and aimed at reducing ICP and controlling blood pressure. Aggressive blood pressure control using IV labetalol, esmolol, or nicardipine should be instituted with a target SBP < 180 m m Hg or MAP < 130 m m Hg. CPP should be maintained > 70. Patients on anticoagulants should receive reversal agents (FFP and vitamin K for warfarin, protamine for heparin) promptly. The use of p r o t h r o m b i n complex concentrate, factor IX complex concentrate, and rFVIIa have been shown to reverse the elevation of the INR very rapidly (often within 1 - 2 hours) and is faster to prepare than FFP. Corticosteroids are contraindicated. P r o m p t neurosurgical consultation should be

Clinical Findings
Symptoms and signs are notoriously nonspecific, nonlocalizing, or absent and may be either stable or rapid/ progressive. The frequency of bilateral hematomas make ; localization of the lesion even m o r e difficult, as does the coexistence of associated cerebral contusion. Hemiparesis when present, is contralateral to the lesion in approximate!'. 60% of cases, and ipsilateral pupillary dilatation occurs ir. approximately 75% of cases. Seizures may occur. When

COMA

associated with trauma, a subdural h e m a t o m a is most :requently f o u n d contracoup to the side of injury. CT scan - the diagnostic study of choice, revealing a hyperdense extra-axial crescent-shaped collection of blood, which rarely .rosses the falx or tentorium. Sub-acute lesions ( 2 - 3 weeks) may appear as isodense, and patients receiving anticoagulation may demonstrate layering of blood in acute-on-chronic 5 jbdural hematoma.

Treatment and Disposition

Immediate neurosurgical consultation is required. In the event a neurosurgeon or CT confirmation of the diagnosis is unavailable and the patient is herniating, a burr hole performed ipsilateral to the area of trauma (or to the dilated pupil if external trauma is not apparent) may be life-saving. Care is otherwise supportive and aimed at decreasing ICP.

Treatment and Disposition

immediate hospitalization and emergency neurosurgical : : r.sultation are indicated. Unstable patients with rapid rrsening (minutes to hours) of their neurologic deficit thought to be due to an expanding subdural h e m a t o m a : ~.ould be treated for increased ICP as discussed previously, ceroids have not been shown to be beneficial.

4. Cerebral Infarction E S S E N T I A L S OF
Hemiparesis Hemisensory losses Aphasia (dominant hemisphere)

DIAGNOSIS

3. Epidural Hematoma E S S E N T I A L S OF
Headache History of trauma with overlying skull fracture Classic lucid interval: "talk and die" .ens-shaped (biconvex) extra-axial collection of blood on CT scan

DIAGNOSIS

General Considerations
The brain swelling of cerebral edema following massive hemispheric infarction can produce contralateral hemispheric compression or transtentorial herniation that will result in coma. Such cerebral swelling becomes maximal 48-72 hours after the infarct.

Clinical Findings
The principal findings are hemiparesis or loss (and aphasia if the dominant hemisphere Evolving transtentorial herniation progresses many hours or several days to stupor and contrast CT scan is the initial diagnostic test of hemisensory is involved). slowly over coma. N o n choice.

General Considerations
: : -ural hematoma is a collection of blood between the dura : the inner table of the skull and occurs almost exclusively n :he setting of trauma. The majority of epidural hemaper-as occur in the temporoparietal region secondary to ; ration of the middle meningeal artery. Occipital epidural - a t o m a s may progress rapidly and extend beneath the rcorium, resulting in apnea.

Treatment and Disposition

Hemicraniectomy may be life-saving in younger patients. Patients who are comatose f r o m massive cerebral infarction have likely progressed to coma secondary to increased ICP rather than the infarction itself, and initial treatment is supportive and aimed at lowering ICP. Blood pressure management is controversial; in severe hypertension (SBP > 220 m m Hg, DBP > 120 m m Hg), IV labetalol or nicardipine are preferred with a goal of reducing the SBP by 15% in first 24 hours.

Clinical Findings
- : : : ms are progressive. The classic presentation of head i followed by a brief loss of consciousness, return _:7tness ("lucid interval"), then worsening headache : smiting with subsequent coma is seen in only 1/5 of I Non-contrast CT scan is the diagnostic study of :. revealing a hyperdense lenticular (biconvex) collec- : f blood that does not cross suture lines, differentiating r : m a subdural hematoma. Ipsilateral pupillary dilation i : mtralateral hemiparesis are ominous findings sugges: : : impending herniation. W h e n associated with trauma, - r . o m a is most frequently f o u n d on the coup side of the

Adams Jr H et al: Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/ American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups. Stroke 2007;38:1655-1711 [PMID: 17515473).

S E C T I O N II

MANAGEMENT OF COMMON EMERGENCY PROBLEMS

5. Basilar Artery Occlusion ESSENTI

PUBS

situations where recanalization may be delayed, "bridging therapy" with IV abciximab has shown to improve survival. Even with aggressive treatment, mortality ranges up to 70%. Hospitalize the patient for treatment and supportive care. Lindsberg PJ, Mattle HP: Therapy of basilar artery occlusion: a systematic analysis comparing intra-arterial and intravenous thrombolysis. Stroke 2006;37:922-928 [PMID: 16439705], Nagel S et al: Therapy of acute basilar artery occlusion: intraarterial thrombolysis alone vs bridging therapy. Stroke 2009;40:140-146 [PMID: 18927446],

Coma, altered mental status Respiratory pattern Irregular Pupillary abnormalities, absent or abnormal horizontal eye movements Hemiparesis, hyperreflexia, positive Babinski sign

General Considerations
Basilar artery thrombosis and embolic occlusion are relatively c o m m o n vascular syndromes that cause coma because of direct involvement of the penetrating arteries supplying the central core of the brain stem. Patients are usually elderly and often have a history of hypertension or transient ischemic attacks or evidence of other atherosclerotic vascular disease.

6. Brain Tumor E S S E N T I A L S OF D I A G N O S I S
Headache Focai weakness Altered mental status Seizures Papilledema CT scan, MRI findings

Clinical Findings
Basilar artery transient ischemic attacks are characterized by (in order of frequency of occurrence) dizziness, diplopia, weakness and ataxia, slurred speech, and nausea and vomiting. Basilar artery occlusion causes coma in half of affected patients, and almost all present with some alteration of consciousness. Focal subtentorial signs are present f r o m the onset, and the respiratory pattern is irregular. Pupillary abnormalities vary with the site of the lesion. Skew deviation of the eyes is c o m m o n . Horizontal eye movements are absent or asymmetric during the doll's eye maneuver or caloric testing. Conjugate eye deviation, if present, is directed away f r o m the side of the lesion and toward the hemiparesis. Vertical eye movements in response to the doll's eye maneuver may be intact. Symmetric or asymmetric motor signs (hemiparesis, hyperreflexia, and Babinski sign) may be present. The classic "locked in syndrome" is characterized by complete quadriplegia, lower cranial nerve palsy, and mutism with retained consciousness and vertical gaze. CT scan of the head with CT angiography is the diagnostic study of choice, with MRA useful in special populations.

General Considerations
Coma is seldom the presenting symptom in primary o: metastatic tumors of the CNS, although coma may resui: from seizures induced by the tumors. Acute bleeding into a t u m o r may also result in coma secondary to a sudder increase in ICP.

Clinical Findings
The patient typically has a history of days to weeks of headache, focal weakness, and altered or depressed consciousneii Papilledema is present in 25% of cases. CT scan (noncontra;: followed by contrast-enhanced if needed) is the initial diagnostic study of choice.

Treatment and Disposition

Glucocorticoids (Dexamethasone 10 m g IV) are remarkably effective at reducing s u r r o u n d i n g edema and shou.: be initiated early in consultation with neurosurgery Hospitalization for supportive care and f u r t h e r evaluatk r is indicated. Roger HP, Butler I, Benzel HC: Neurosurgery in the elder, brain tumors and subdural hematomas. Clin Geriatr Nu2006;22:623-44 [PMID: 16860250],

Treatment and Disposition

C u r r e n t therapy r e c o m m e n d a t i o n is recanalization with intravenous or intra-arterial thrombolytics in combin a t i o n with mechanical m a n i p u l a t i o n , d e p e n d i n g on the institution. While specific guidelines are lacking, time to recanalization is of prognostic importance. In

COMA

7. Brain Abscess

METABOLIC ENCEPHALOPATHIES

Fever (often low grade) Leukocytosis Contrast-enhanced CT scan or AARI findings of intracranial mass

Progressive somnolence Intoxication, toxic delirium Agitation, stupor, coma Headache Symmetric neurologic findings Reactive pupils Hypoventilation, abnormal respiratory pattern Loss of extraocular movements

General Considerations
3rain abscess accounts for only 2% of intracranial masses, rrain abscess should be considered in patients w h o are m m u n o c o m p r o m i s e d w h o develop changes in mentation. Sacterial brain abscesses most c o m m o n l y are the result of contiguous spread of infection f r o m the oropharynx, middle ear, and paranasal sinuses. Cranial t r a u m a and hematogenous spread f r o m distant infection are also causes.

Clinical Findings
Metabolic encephalopathies are characterized by a period of progressive somnolence, intoxication, toxic delirium, or agitation, after which the patient gradually sinks into a stuporous and finally comatose state. Headache is not an initial s y m p t o m of metabolic encephalopathy except in the case of meningitis or poisoning due to organophosphate c o m p o u n d s or carbon monoxide. Neurologic examination fails to reveal focal hemispheric lesions (hemiparesis, hemisensory loss, aphasia) before loss of consciousness. Neurologic findings are symmetric except in some patients with hepatic encephalopathy and hypoglycemic coma, which may be accompanied by focal signs (especially hemiparesis) that may alternate sides. Asterixis may be present. The h a l l m a r k of metabolic encephalopathy is reactive pupils (a m i d b r a i n f u n c t i o n ) in the presence of i m p a i r e d f u n c t i o n of the lower b r a i n stem (eg, hypoventilation, loss of extraocular m o v e m e n t s ) , an anatomically inconsistent set of abnormalities. Respiratory patterns in metabolic c o m a vary widely a n d may help establish the cause of coma.

Clinical Findings
Progression to stupor and coma may be rapid, occurring er days or, rarely, hours. S y m p t o m s include headache 70%), mental status changes (70%), focal neurological : -.its ( > 60%), and seizure (2535%) at time of presentairn. The usual signs of infection are frequently absent. The Emperature is n o r m a l in half of patients, and the white i :od cell count is below 10,000/mL in over o n e - f o u r t h if patients. CT scan (non-contrast followed by contrastinanced if needed) or MRI will reveal almost all abscesses, mbar p u n c t u r e is contra-indicated.

! Treatment and Disposition

late antibiotic therapy early, prior to imaging if pose when the clinical suspicion for CNS infection is high. - rrbiotic choice should cover anaerobes as well as aerobes, | r n c coverage for fungal or other organisms may be indicated ending on the patient's history. Empiric therapy with a i-cr emation of vancomycin 1.0-1.5 g IV plus m e t r o n i d a n e ".5 mg/kg IV plus a third- or fourth-generation cepha" r : rin is indicated. Carbapenems can be used in placed i ihe combination of cephalosporins and metronidazole, rosurgical consultation should be obtained with operaintervention necessary of abscesses > 2.5cm. The use of nds remains controversial and is generally deferred for indication. Seizure prophylaxis should be initiated early Jiir.-g hospitalization.

Treatment and Disposition

T r e a t m e n t depends entirely on the cause of coma. All patients require hospitalization for supportive care a n d specific therapy.

1. Hypoglycemia
See also Chapter 43.

!
i i I, Warren OK. Central nervous system infections: nicnin and brain abscess. Infect Dis Clin N Am 2009;23:609-623 MID: 19665086;.

General Considerations

Unlike other organs, the brain relies mainly on glucose to supply its energy requirements. A b r u p t hypoglycemia rapidly interferes with brain metabolism and quickly produces

S E C T I O N II

MANAGEMENT OF COMMON EMERGENCY PROBLEMS

symptoms. Insulin and oral hypoglycemic drug overdose are the most common causes of hypoglycemia.

of mild hypothermia (~33C) after cardiac arrest has been shown to improve survival and neurological outcome. Hospitalize all patients for diagnosis and treatment. Arrich J, Holzer M, Herkner H, Mllne M: Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev 2009;7:CD004128 [PMID: 19821320],

Clinical Findings
Signs of sympathetic nervous system activity (tachycardia, sweating, and anxiety) may warn patients of impending hypoglycemia, although these signs may be masked by yS-blockers and may be absent in patients with diabetic autonomic neuropathy. Common neurologic abnormalities are delirium, seizures, focal signs that often alternate sides, stupor, and coma. Hypoglycemic coma may be tolerated for 60-90 minutes, but once the stage of flaccidity with hyporeflexia has been reached, glucose administration within 15 minutes is mandatory to avoid irreversible damage.

3. Drug Overdose
See also Chapter 47. Drug overdose is one of the most common causes of coma in patients presenting to the emergency department. Many drugs may be implicated, including sedative-hypnotics, opiates, tricyclic antidepressants, and antiepileptics. Details o: management can be found in Chapter 47.

Treatment and Disposition

Give glucose, 50 mL of 50% solution intravenously (adult dose). Once the diagnosis of hypoglycemia is confirmed by analysis of blood drawn before treatment, give an additional 50 mL as needed or begin an infusion of dextrose 5% in water. Subcutaneous or intramuscular glucagon should be considered in patients in which IV access cannot be obtained. Although case reports of octreotide use in hypoglycemia have been shown to be effective, the indications and dosage have not clearly been defined. Patients should be observed for 1-2 hours after glucose supplementation has been discontinued to ensure that hypoglycemia does not recur before they are discharged from the hospital. In some cases, hospitalization may be necessary, especially if hypoglycemia recurs despite treatment or in the event of long-acting insulin or oral hypoglycemic agent overdose (eg sulfonylureas). Rowden AK, Fasano CJ: Emergency management of oral hypoglycemic drag toxicity. Emerg Med Clin N Am 2007;25:347-356 {PMID: 17482024],

Ethanol Intoxication
Alcohol intoxication produces a metabolic encephalopathy similar to that produced by sedative-hypnotic drugsalthough nystagmus during wakefulness and early impairment of lateral eye movements are not as common. Periphery vasodilatation is a prominent manifestation and produce; tachycardia, hypotension, and hypothermia. In individuals who are not chronic alcoholics, stupo: occurs when blood alcohol levels reach 250-300 mg/dL, anc coma occurs when levels reach 300-400 mg/dL. Becaus: alcohol has significant osmotic pressure (100 mg/dL = 22.4 mOsm), alcohol intoxication is one cause of hyperosmolalm Management is discussed in Chapter 47. Patients shoulc be observed until improvement has occurred with n o r m ^ orientation and judgment, and satisfactory coordination Hospitalize patients who have abnormalities that woulc usually require hospitalization (eg, metabolic abnormalities Wernicke encephalopathy).

2. Hypoxemia Clinical Findings

Hypoxemia produces brain damage only as a result of concomitant cerebral ischemia. Cerebral blood flow diminishes and brain ischemia occurs when the arterial Po 2 falls to 20-45 m m Hg. In cerebral anoxia due to cardiac arrest, where the duration can be timed precisely, 4 - 6 minutes of asystole begins to result in permanent CNS damage. Following asystole, the pupils dilate rapidly and become fixed, and tonic posturing is observed. A few seizure-like tonic-clonic movements are common.

Narcotic Overdose
In narcotic overdose, hypoventilation is almost always present, along with pinpoint pupillary constriction and absen: extraocular movements in response to the doll's eye maneuver. Pinpoint pupils are also associated with other disorderthat must be ruled out: use of miotic eye drops, pontic; hemorrhage, Argyll-Robertson pupils from syphilis, anc organophosphate insecticide poisoning. Narcotic intoxication is confirmed by rapid pupillar> dilation and awakening after administration of a narcoti: antagonist such as naloxone, 2 mg, by rapid IV injection o : intranasally. Note: Patients who have overdosed on certair narcotics (eg, propoxyphene) may not respond to 2 m : and may require 4 mg or more. The duration of action : naloxone varies with the dose and route of administrador (20-90 minutes). Repeat doses are frequently necessan especially following intoxication with long-acting narcotic: (eg, methadone).

Treatment and Disposition

Treatment of hypoxemia depends on the cause. Support cardiac output and maintain arterial Po, above 60 m m Hg by supplemental oxygen or mechanical ventilation. Induction

COMA

Treatment of drug overdose and poisoning is outlined above and discussed in more detail in Chapter 47. Hospitalization should be considered for patients who do not recover completely in the emergency department or who have taken long-acting narcotics. Merlin MA, Saybolt M, Kapitanyan R, Alter SM, Jeges J, Liu J, Calabrese S, Rynn KO, Perritt R, Pryor PW: Intranasal naloxone delivery is an alternative to intravenous naloxone for opioid overdoses. Am I Emerg Med 2010;28:296-303 [PMID: 20223386],

symptoms when serum sodium levels are below 120 mEq/L, and symptoms are c o m m o n with levels below 110 mEq/L. W h e n the serum sodium level falls rapidly, symptoms occur at higher serum sodium levels.

Treatment and Disposition

The diagnosis and treatment of these entities are discussed in Chapter 44. Hospitalization is mandatory in symptomatic patients.

/-Hydroxybutyrate
;/-Hydroxybutyrate is a CNS depressant and can induce coma. The drug has become popular at rave parties and has also been called the "date rape drug." Detection of the drug is difficult, because most of it is eliminated through the lungs. Treatment is primarily supportive and may involve endotracheal intubation. Some patients require hospitalization for prolonged supportive care.

6. Hypothermia/Hyperthermia Clinical Findings

Hypothermia and hyperthermia are associated with symmetric neurologic dysfunction that may progress to coma. All comatose patients must have rectal temperature taken with an extended-range thermometer if the standard thermometer fails to register.

A. Hypothermia
Internal body temperatures below 26C (78.8F) uniformly cause coma; hypothermia with core temperatures above 32C (89.6F) does not cause coma. Body temperatures of 26-32C (78.8-89.6F) are associated with varying degrees of obtundation. Pupillary reaction will be sluggish below 32C (89.6F) and lost below 26.5C (80F).

4. Hepatic Encephalopathy Clinical Findings

Hepatic encephalopathy can occur in patients with severe laite or chronic liver disease. Jaundice need not be present. In n e patient with preexisting liver disease, encephalopathy may :evelop rapidly following an acute insult such as gastrointestinal hemorrhage or infection. Patients with surgical portacaval aunts are especially predisposed to encephalopathy. Mental status is altered and ranges f r o m somnolence to ;elirium or coma. There is increased muscle tone; hyperreflexia is c o m m o n . Prominent asterixis occurs in the somnolent patient. Seizures, either generalized or focal, occur ^frequently. A m m o n i a levels correlate poorly with disease verity. Hyperventilation with respiratory alkalosis is nearly _niversal and may be demonstrated by measuring arterial : ,ood p H . CSF is normal b u t may appear xanthochromic in ratients with serum bilirubin levels higher than 4 - 6 mg/dL.

B. Hyperthermia
Internal body temperatures above 41-42C (105.8-107.6F) are associated with coma and may also rapidly cause permanent brain damage. Seizures are common, especially in children.

Treatment and Disposition

Diagnostic and treatment measures for both hypothermia and hyperthermia are discussed in detail in Chapter 46. Hospitalization is mandatory.

Treatment and Disposition

inergency department care is supportive. Treatment aimed at : rcreasing intestinal ammonia absorption (lactulose, neomycin) maybe initiated but should not take the place of hospitalization : definitive treatment. Studies on induced hypothermia in . rate liver failure are inconclusive to this point. .nil/ RT, Larsen FS: Therapeutic hypothermia for acute liver failure. Crit Care Med 2009;37:S258-264 [PMID: 19535956].

7. Meningoencephalitis
See also Chapter 42

Clinical Findings
The classic triad of fever, neck stiffness, and altered mental status is poorly sensitive for bacterial meningitis (40%). Any patient with altered mental status, seizure, focal neurologic deficit, or evidence of increased ICP should undergo neuroimaging prior to lumbar puncture to minimize the risk of herniation. CSF pleocytosis is c o m m o n although depending on the stage of the disease, the differential may be variable. CSF glucose < 40 mg/dL is more consistent with bacterial meningitis.

5. Hyponatremia
"elirium and seizures are c o m m o n presenting features : hyponatremia. Hyponatremia may cause neurologic

MANAGEMENT OF COMMON EMERGENCY PROBLEMS

Treatment and Disposition

Start antibiotic therapy immediately based on clinical findings, prior to obtaining imaging. Current recommendations are for vancomycin with a third-generation cephalosporin, and dexamethasone (0.6 mg/kg) should be given with or before antibiotic administration. Hospitalization is indicated for all patients with meningitis who present in coma or in w h o m bacterial meningitis cannot be excluded.
Van de Beck D, de Gans ], Mclntyre P, Prasad K: Corticosteroids for acute bacterial meningitis. Cochrane Database Svst Rev 2007;]: CD004405 [PMID: 17253505],

Treatment and Disposition

Emergency department care is supportive. After stabilization, the patient should be admitted or transferred for definitive therapy by neurosurgery for craniotomy and clipping or interventional radiology for coiling. Blood pressure should be treated aggressively to be kept within normal limits untn the aneurysm has been secured. Nimodipine (60 mg), an oraf calcium channel antagonist, is commonly used to preven: delayed vasospasm and can be initiated in the emergenc. department. Bederson JB, Connolly ES Jr, Batjer HH, Dacey RG, Dior JE, Diringer UN, DuiJner JE Jr, Harbaugh RE, Patel AB. Rosenwasser RH; American Heart Association: Guidelines for the management of aneurysmal subarachnoid hemorrhage: statement for healthcare professionals from a: special writing group of the Stroke Council, American Heart Association. Stroke 2009;40:994-1025 [PMID: 19164800],

OTHER DISORDERS CAUSING COMA 1. Subarachnoid Hemorrhage

See also Chapter 37.

Treatmen

2. Seizure
See also Chapter 19. P " : esse postkt

Sudden onset of severe headache Nausea and vomiting Photophobia, visual changes

3 Psychogen
Patient is unresponsive to pain Nonfocal neurologic examination Babinski sign (transient) Todd paralysis Signs of recent seizure: tongue trauma, incontinence, rapidly clearing anion gap lactic acidosis

General Considerations
Aneurysmal subarachnoid hemorrhage (SAH) accounts for 80% of all cases of nontraumatic SAH. Risk factors include cigarette smoking, hypertension, cocaine and alcohol use, first-degree relatives with a history of SAH, female sex, African-American race, and connective tissue disorders.

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Clinical Findings
Typical presentation of SAH involves nausea or vomiting (77%), sudden onset of severe headache (74%), meningismus (35%), photophobia, and may include decreased level of consciousness. A "thunderclap" headache may signify a sentinel leak, and the headache may resolve relatively quickly. The patient may lose consciousness at onset (53%) or may experience a seizure (20%). Retinal hemorrhages may be present on fundoscopic examination and blood pressure is usually markedly elevated. Noncontrast enhanced CT scan of the head is the initial diagnostic study of choice. Because the diagnostic sensitivity of CT scanners is only 98-100% for SAH within the first 12 hours, current recommendations are to follow a negative CT with CSF analysis. If CSF is normal (no xanthochromia, no elevated RBCs), SAH is effectively excluded. Positive or indeterminate CSF findings require CT angiography or traditional angiography to rule out the presence of an aneurysm.

General Considerations
Coma resulting from seizure disorders is usually not a difficult diagnostic problem, because recovery of consciousnes is rapid following the end of the seizure. Prolonged postictal coma (several hours) followed by several days of confusior may occur after status epilepticus, in patients with brain damage (eg, multiple cerebral infarctions, head trauma, encephe litis, mental retardation) and in patients with metabo..encephalopathy that alters consciousness and induces seizure (eg, hyponatremia, hyperglycemia). Nonconvulsive status ep: lepticus is more c o m m o n than previously thought and shoul: be considered in any patient with no other apparent cause : coma, especially in those with a history of seizure disorder.

' " m a l and syi V>rmal Babinst * stagmus witl o r m a l electrof

Clinical Findi
: genic coma i; mide only after s:cal examination examination j; eased muscle to i e n o r m a l dotv The pup i; tonally larger an ements elicited w not be present, 1 reflex.

Clinical Findings
Patients may initially be unresponsive to deep pain anc exhibit sonorous respirations. The neurologic examination usually nonfocal, although Babinski sign may be transien: i

COMA

CHAPTER 17

275

:. Uncommonly, there may be focal abnormalities paralysis) referable anatomically to the focus of selectivity in the brain, er evidence of a recent seizure m a y b e present, such as to the tongue from biting, incontinence, or a rapidly 5 anion gap (lactic) acidosis. The rapid resolution of :n a patient with a witnessed seizure or known seizure t should suggest the diagnosis of the postictal state cause of coma. Coma that is at first thought to be "al but fails to improve should p r o m p t an investigator underlying processes contributing to mental status rision, including metabolic encephalopathy, underlying brain damage, encephalitis, and structural lesion. : ?riate investigations could include measurements of n electrolytes, calcium, and magnesium; CT scan; and ar puncture.

Differentiating Psychogenic Coma from Organic Coma A. Eye Movements

The slow, conjugate roving eye movements of patients in metabolic coma cannot be imitated and, if present, are incompatible with a diagnosis of psychogenic unconsciousness.

B. Eyelid Tone
The slow, often asymmetric and incomplete eyelid closure c o m m o n l y seen in organic forms of coma following passive opening of the lids cannot be mimicked. In addition, the patient with psychogenic coma usually shows some voluntary muscle tone of the eyelids during passive opening by the examiner.

Treatment and Disposition

rment depends on the underlying cause of the seizure, ilert for metabolic causes and treat t h e m appropriately. Ir.apter 19 for details of management. Immediate hos^ation is required for all cases of status epilepticus and j: r.ged postictal coma and for seizures due to metabolic ses that are not quickly correctable.

C. Ice Water Caloric Response

A helpful objective test in diagnosing psychogenic unconsciousness is the caloric test: there is no response at all or tonic deviation to the side of the irrigation in organic coma, but nystagmus occurs in psychogenic coma. Because the quick (return ) phase of nystagmus requires an intact cortex, its presence is incompatible with a diagnosis of true coma.

Psychogenic Coma E S S E N T I A L S OF D I A G N O S I S
- rtient is unresponsive Normal physical examination 1 accid symmetric decreased muscle tone Normal and symmetric reflexes Normal Babinski - Nystagmus with ice water calorics Normal electroencephalogram findings

0. Electroencephalogram
The electroencephalogram in psychogenic coma is that of a normal, awake person. In coma due to other causes, it is invariably abnormal.

f - Treatment and Disposition

Obtain psychiatric consultation. Hospitalization may be required. Bazakis AM, Kunzler C: Altered mental status due to metabolic or endocrine disorders. Emerg Med Clin North Am 2005;23: 901-908 [PMID: 15982551], Chen JW, Wasterlain CG: Status epilepticus: pathophysiology and management in adults. Lancet Neurol 2006;5:246-256 {PMID: 16488380]. f: Marmo EM, Atkinson II, Fulgham JR, Wijdicks EI:: Emerging medical and surgical management strategies in the evaluation and treatment of intracerebral hemorrhage. Mayo Clin Proc 2005;80:420-433 (PMID: 15757025], Mas A: Hepatic encephalopathy: from pathophysiology to treatment. Digestion 2006;73:86-93 [PMID: 16498256], Mayer SA, Brun NC, Broderick J, Davis S, Diringer MN, Skolnick BE, Steiner T; Europe/AustralAsia NovoSeven ICH Trial Investigators: Safety and feasibility of recombinant factor Vila for acute intracerebral hemorrhage. Stroke 2005;36:74-79 [PMID: 1556987)]. Mayer SA, Rincon F: Treatment of intracerebral haemorrhage. Lancet Neurol 2005;4:662-672 |PM1D: 16168935], Rathlev NK, Medzon R, Lowery D, Pollack C, Bracken M, Barest G, Wolfson AB, Hoffman IR, Mower WR: Intracranial

Clinical Findings
rhogenic coma is a diagnosis of exclusion that should made only after careful documentation. The general pttTsical examination should elicit no abnormalities; neug : gic examination generally reveals flaccid, symmetrically :: creased muscle tone, n o r m a l and symmetric reflexes, ec r the n o r m a l downward response to Babinski plantar emulation. The pupils are normal in size ( 2 - 3 m m ) or crasionally larger and respond briskly to light. Lateral eye - : vements elicited with the doll's eye maneuver may or - r v not be present, because visual fixation can suppress a is reflex.

SECTION II

MANAGEMENT OF COMMON EMERGENCY PROBLEMS

Absence of brain-stem reflexes (all of the below): N o pupillary response to light N o oculocephalic reflex (doll's eyes maneuver) N o response to cold water calorics N o corneal reflexes N o jaw reflex N o grimacing to painful stimulus No gag reflex N o cough response to tracheal/bronchial stimulation Apnea over 8 minutes with Pco 2 > 60 m m Hg

Brain death is defined as the irreversible loss of function of the brain, including the brain stem. Before a patient may be evaluated for the diagnosis of brain death, the patient must meet certain criteria: Clinical or neuroimaging evidence of catastrophic CNS event compatible with the clinical diagnosis of brain death Exclusion or correction of medical conditions that may confound clinical assessment: Acid-base disorders Severe electrolyte disorder Endocrinopathies Absence of drug intoxication/poisoning Patient core temperature > 32C (90F)

Confirmatory testing may be used when complicating factors are present such as severe facial trauma, preexisting pupillary abnormalities, or toxic drug levels. Confirmatory tests result in findings that are consistent with brain death and are not diagnostic. The standard confirmatory test; include cerebral angiography," transcranial Doppler ultrasonography, technetium-99m-hexamethylpropyleneamin-. brain scan, and somatosensory-evoked potentials. In some cases these tests may aid in the diagnosis and in others the", may confuse the picture. Documentation of the diagnosis o: brain death should include the cause and irreversibility of the condition, the absence of brain-stem reflexes, the absence o: any motor response to pain, the formal apnea test result and the justification for and results of any confirmatory test; The initial and repeat examinations should be includec Currently most authorities feel that the same criteria above can be used for full-term infants more than 7 days old Criteria for premature and newborns are still unclear. Manno EM, Wijdicks EF: The declaration of death and the withdrawal of care in the neurologic patient. Neurol Clir. 2006;24:159-169 [PMID: 16443137], Wijdicks EF, Rabinstein AA, Manno EM, Atkinson JD: Pronouncir r brain death: contemporary practice and safety of the apnea tes* Neurology 2008;71:1240-1244 [PMID: 18852438],

Once these criteria have been met, the patient can be tested for the diagnosis of brain death. If the patient meets the following criteria, the patient is observed for at least 6 hours and clinical testing is repeated. If patient testing remains unchanged, a diagnosis of brain death can be made. C o m a (unresponsiveness): no cerebral motor response to pain