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CHAPTER 168: Altered Mental Status and Coma 1137 Altered Mental Status and Coma M. Kathryn Mutter J. Stephen Huff INTRODUCTION Altered mental status and coma are broad clinical categories used to describe disorders of arousal and content of consciousness. Arousal behaviors include wakefulness and basic alerting. Content of con sciousness includes awareness, memory, language, reasoning, spatial relationship integration, emotions, complex attention, and the myriad integration processes that make us human. Delirium, dementia, and coma may each affect consciousness, but their clinical presentations are distinct. Prompt and accurate differentiation between the three conditions is essential for appropriate management in the ED setting. Coma is characterized by failure of both arousal and content functions of consciousness. The altered states of delirium and dementia have multiple effects on neuropsychological function to varying degrees. While delirium refers to an acute state of fluctuating attention and change in cognition, dementia is a chronic disorder of deteriorating cognition, with or without behavioral disturbances. Psychiatric disorders and altered mental states may share features such as hallucinations or delusions. Some distinctions between the different states are summarized in Table 168-1. DELIRIUM  INTRODUCTION Delirium, acute encephalopathy, and other synonyms all refer to an abrupt disorder characterized by impairment of attention and cogni tion. While delirium may present at any age, it is much more prevalent in older adults. The literature suggests that at least 1 out of 10 elderly ED patients and at least 1 out of 4 elderly hospitalized patients have delirium at the time of admission. 1-4 Emergency physicians may fail to recognize delirium in three out of four of such cases. 3,4 Given evidence that delirium in ED patients is associated with an increase in morbidity, mortality, and hospital length of stay, the Society for Academic Emer gency Medicine Geriatric Task Force has recommended that formal cognitive assessment should be a quality indicator in emergency care of the elderly. 3,5-7  PATHOPHYSIOLOGY The pathologic mechanisms leading to delirium are complex and are thought to involve impairments in neuronal connectivity and plasticity, leading to “acute brain failure. ” 3,8 There are five general causes9: 1. Primary intracranial disease 2. Systemic diseases secondarily affecting the CNS 3. Exogenous toxins (including prescribed pharmacotherapies) 4. Drug withdrawal and pain 5. Major trauma or surgery  CLINICAL FEATURES Delirium typically develops over days. Disordered attention and acute fluctuating course are the hallmarks of the condition, which may also affect cognition, level of consciousness, language, and perception. Activity levels may be either increased or decreased. The patient may fluctuate rapidly between hypoactive and hyperactive states. Symptoms may be intermittent, and it is not unusual for different caregivers to witness completely different behaviors within a brief time span. Sleep-wake cycles are often disrupted. Tremor, asterixis, tachycardia, sweating, hypertension, or emotional outbursts may be present. Hallucinations tend to be visual, although auditory hallucinations can also occur. 1,2,10  DIAGNOSIS Since delirium is a clinical diagnosis, a thorough history and physi cal examination are key for obtaining findings indicative of possible delirium.

ardia, sweating, hypertension, or emotional outbursts may be present. Hallucinations tend to be visual, although auditory hallucinations can also occur. 1,2,10  DIAGNOSIS Since delirium is a clinical diagnosis, a thorough history and physi cal examination are key for obtaining findings indicative of possible delirium. Eliciting a history from caregivers, spouse, or other family members is the primary method for diagnosing delirium. 1,2,10 Compared to the patient’s baseline, the acute onset of attention deficits and cognitive abnormalities, fluctuating in course, is virtually diagnostic of delirium. One important tool for detecting delirium is the mental status examination and other cognitive screening instruments. 11,12 The Mini-Mental State Examination is historically the standard against which many shorter and less cumbersome tools have been tested. 12 The Geriatric Emergency Department Guidelines recommend a combination of screening tests: the highly sensitive Delirium Triage Screen (incorporates the Richmond Agitation-Sedation Scale) and the highly specific Brief Confusion Assessment Method 13 (Figure 168-1). Evaluate medication history, including both over-the-counter medi cations and prescribed medications, in detail. Check for drug interac tions. Assess for an underlying process, such as infection, metabolic derangement, or trauma. Basic ancillary testing should include serum electrolyte levels, hepatic and renal studies, urinalysis, CBC, and a chest radiograph. Order a head CT if a mass lesion such as subdural hematoma is suspected; follow this by performing a lumbar puncture if meningitis or subarachnoid hemorrhage is considered. Depression may resemble hypoactive delirium, with withdrawal, slowed speech, and poor results on cognitive testing present in both conditions. However, rapid fluctuation of symptoms is common in delirium but generally absent in depression. Patients with depression are oriented and able to perform commands. An unusual cause of an altered mental state, but one suspected to be underrecognized, is nonconvulsive status epilepticus, or complex partial status epilepticus. This twilight state may persist for hours or even months. Suspicion and electroencephalography are required for recognition. (See Chapter 171, “Seizures and Status Epilepticus in Adults, ” for further discussion of nonconvulsive status epilepticus.)  TREATMENT Direct treatment toward the underlying cause(s). Common medical causes of delirium are listed in Table 168-2. Multiple causes may be present in a given patient. Nonpharmacologic approaches to delirium are the standard of care. Environmental manipulations such as adequate lighting, psychoso cial support, re-orientation activities, and mobilization may be help ful in enhancing the patient’s ability to interpret the surroundings correctly. 2,9,10,13 In the elderly, physical restraints are inadvisable except as a last resort and are associated with worse outcomes. 14 In circumstances of risk of harm to self or others, the use of antipsychotics may be indicated. However, the efficacy of antipsychotics in treating delirium CHAPTER TABLE 168-1 Features of Delirium, Dementia, and Psychiatric Disorder Characteristic Delirium Dementia Psychiatric Disorder Onset Over days Insidious Sudden Course over 24 h Fluctuating Stable Stable Consciousness Reduced or hyperalert Alert Alert Attention Disordered Normal May be disordered Cognition Disordered Impaired May be impaired Orientation Impaired Often impaired May be impaired Hallucinations Visual and/or auditory Often absent Usually auditory Delusions Transient, poorly organized Usually absent Sustained Movements Asterixis, tremor may be present Often absent Absent Tintinalli_Sec14_p1101-1186.indd 1137 8/2/19 12:08 PM

ired May be impaired Orientation Impaired Often impaired May be impaired Hallucinations Visual and/or auditory Often absent Usually auditory Delusions Transient, poorly organized Usually absent Sustained Movements Asterixis, tremor may be present Often absent Absent Tintinalli_Sec14_p1101-1186.indd 1137 8/2/19 12:08 PM 1138 SECTION 14: Neurology in older adults remains controversial.15 Haloperidol is a frequent initial choice at a dose of 5 to 10 milligrams PO, IM, or IV , with reduced dosing of 1 to 2 milligrams in older adults. Repeat at 20- to 30-minute intervals as needed. In younger patients, benzodiazepines, such as lorazepam, 0.5 to 2.0 milligrams PO, IM, or IV , may be used in combination with haloperidol. Guidelines recommend avoiding benzodiazepines in the elderly. 14,16 Chapter 287, “ Acute Agitation, ” provides further discussion on management of agitation.  DISPOSITION AND FOLLOW-UP Admit the patient with delirium to the hospital for further treatment and additional diagnostic testing, unless a readily reversible cause for the acute mental status change is discovered and treatment initiated. This decision is individualized with consideration of patient characteristics, the resources in the home or healthcare facility, and the patient’s safety. DEMENTIA  INTRODUCTION Dementia is a chronic, major neurocognitive disorder entailing a grad ual loss of mental capacity. Executive, social, and cognitive abilities deteriorate, and behavioral problems can develop. The most frequent causes of dementia include Alzheimer’s disease and vascular dementia. Dementia with Lewy bodies is the second most common neurodegenerative FIGURE 168-1. Delirium Triage Screen (DTS) and Brief Confusion Assessment Method (bCAM). RASS = Richmond Agitation-Sedation Scale. [Reproduced with permission from XOS Technologies, Inc. dba XOS Digital, Atlanta, GA.] bCAM negative No Delirium bCAM negative No Delirium bCAM negative No Delirium Confirmation: Highly specific Feature 1 - Altered mental status or fluctuating course Feature 2 - Inattention “Can you name the months backward from December to July?” Feature 3 - Altered level of consciousness? RASS Feature 4 - Disorganized thinking Command: “Hold up this many fingers” (Hold up two fingers). “Now do the same thing with the other hand” (Do not demonstrate). 1) Will a stone float on water? 2) Are there fish in the sea? 3) Does 1 pound weigh more than 2 pounds? 4) Can you use a hammer to pound a nail? bCAM positive DELIRIUM PRESENT Yes >1 error Yes 0 or 1 error errors Any errors Rule-Out screen: Highly sensitive Altered level of consciousness RASS Inattention “Can you spell the word ‘lunch’ backward?” ED-DTS negative No delirium DTS positive confirm with bCAM >1 error Yes 0 or 1 error Tintinalli_Sec14_p1101-1186.indd 1138 8/2/19 12:08 PM

PRESENT Yes >1 error Yes 0 or 1 error errors Any errors Rule-Out screen: Highly sensitive Altered level of consciousness RASS Inattention “Can you spell the word ‘lunch’ backward?” ED-DTS negative No delirium DTS positive confirm with bCAM >1 error Yes 0 or 1 error Tintinalli_Sec14_p1101-1186.indd 1138 8/2/19 12:08 PM CHAPTER 168: Altered Mental Status and Coma 1139 dementia after Alzheimer’s. However, other, more treatable disorders may cause or simulate dementia. The typical course of dementia involves insidious symptom onset. The abrupt onset of symptoms or rapidly progressive symptoms should prompt a search for other diagnoses, including delirium. Presentation to the ED is usually precipitated by a sentinel event. Hallucinations, delusions, repetitive behaviors, depression, and anxiety are all common.  PATHOPHYSIOLOGY Most cases of dementia in the United States are due to Alzheimer’s disease, a neurodegenerative disorder of imprecise etiology. The pathophysiology is complex, with neuritic or amyloid plaques of tau protein and neurofibrillary tangles. However, the relationship between these findings and the clinical syndrome of Alzheimer’s disease is incompletely understood. 17 Other neurodegenerative diseases have their own unique pathologies. Vascular dementia accounts for the next largest number of dementia cases. The pathology is that of cerebrovascular disease with multiple infarctions, not all of which may have been clinically apparent. A listing of different types of dementia is provided in Table 168-3.  CLINICAL FEATURES Clinical features of dementia vary depending on etiology. Whereas visual hallucinations are a cardinal feature of dementia with Lewy bod ies, perceptual disturbances may or may not be present in Alzheimer’s or vascular dementia. In many dementias, impairment of short-term memory is gradual and progressive, with relative preservation of remote memories. Language function can be affected in any dementia subtype, but is most common in frontotemporal dementia and later stages of Alzheimer’s disease. Generally, dementia is staged according to degree of decline in global function. Individuals with mild cognitive impairment often have intact activities of daily living and instrumental activities of daily living, whereas those who meet criteria for dementia have some measure of functional deficit. Patients with vascular dementia often show similar neurocognitive symptoms but may have chronic neurologic physical deficits from prior cerebrovascular accidents. Furthermore, vascular dementia often coex ists with Alzheimer’s disease.  DIAGNOSIS General physical examination does not determine the diagnosis of dementia but may be helpful in identifying associated causes. 19 The presence of focal neurologic signs may suggest vascular dementia or a mass lesion. Increased motor tone, rigidity, or a shuffling gait may suggest Parkinsonian-related dementia. Consider normal-pressure hydrocephalus if urinary incontinence and gait disturbance develop early in the disease process. The recommended screening method by the Geriatric Emergency Department Guidelines is to first screen for delirium with the Delirium Triage Screen and Brief Confusion Assessment Method combined, and then screen for dementia using the Short Blessed Test. 13,20 Laboratory assessment in the ED may include a CBC, comprehensive metabolic profile, urinalysis, and possibly thyroid function tests and chest radiography. Outpatient evaluation may include serum vitamin 12 level, serologic testing for syphilis (in patients at risk), erythrocyte sedimentation rate, serum folate level, and human immunodeficiency virus testing.

ude a CBC, comprehensive metabolic profile, urinalysis, and possibly thyroid function tests and chest radiography. Outpatient evaluation may include serum vitamin 12 level, serologic testing for syphilis (in patients at risk), erythrocyte sedimentation rate, serum folate level, and human immunodeficiency virus testing. 21 Consider CT or MRI imaging in the ED when clinically TABLE 168-2 Important Medical Causes of Delirium Infectious Pneumonia Urinary tract infection Meningitis or encephalitis Sepsis Metabolic/toxic Hypoglycemia Alcohol ingestion Electrolyte abnormalities Hepatic encephalopathy Thyroid disorders Alcohol or drug withdrawal Neurologic Stroke or transient ischemic attack Seizure or postictal state Subarachnoid hemorrhage Intracranial hemorrhage CNS mass lesion Subdural hematoma Cardiopulmonary Congestive heart failure Myocardial infarction Pulmonary embolism Hypoxia or carbon dioxide narcosis Drug related Anticholinergic drugs Alcohol or drug withdrawal Sedatives—hypnotics Narcotic analgesics Selective serotonin or serotonin-norepinephrine reuptake inhibitors Polypharmacy TABLE 168-3 Classification of Dementia by Cause Degenerative •  Alzheimer’s  disease •  Dementia  with Lewy bodies •  Huntington’s  disease •  Parkinson’s  disease Vascular •  Multiple  infarcts •  Hypoperfusion  (cardiac arrest, profound hypotension, others) •  Subdural  hematoma •  Subarachnoid  hemorrhage Infectious •  Meningitis  (sequelae of bacterial, fungal, or tubercular) •  Neurosyphilis •  Viral  encephalitis (herpes, human immunodeficiency virus), Creutzfeldt-Jakob disease Inflammatory •  Systemic  lupus erythematosus •  Demyelinating  disease, others Neoplastic •  Primary  tumors and metastatic disease •  Carcinomatous  meningitis •  Paraneoplastic  syndromes Traumatic •  Traumatic  brain injury •  Subdural  hematoma Toxic •  Alcohol •  Medications  (anticholinergics, polypharmacy) Metabolic •  Vitamin  B12 or folate deficiency •  Thyroid  disease •  Uremia,  others Psychiatric •  Depression  (pseudodementia) Hydrocephalic •  Normal-pressure  hydrocephalus (communicating hydrocephalus) •  Noncommunicating  hydrocephalus Tintinalli_Sec14_p1101-1186.indd 1139 8/2/19 12:08 PM

inergics, polypharmacy) Metabolic •  Vitamin  B12 or folate deficiency •  Thyroid  disease •  Uremia,  others Psychiatric •  Depression  (pseudodementia) Hydrocephalic •  Normal-pressure  hydrocephalus (communicating hydrocephalus) •  Noncommunicating  hydrocephalus Tintinalli_Sec14_p1101-1186.indd 1139 8/2/19 12:08 PM 1140 SECTION 14: Neurology indicated (e.g., if there is concern for normal pressure hydrocephalus or new stroke). Diagnosis of probable vascular dementia requires signs of cerebro vascular disease. The relationship between stroke and cognitive decline are usually temporally related. A fluctuating, stepped course suggests vascular dementia. The possibility of a concurrent medical condition suddenly caus ing cognitive functioning to deteriorate should be strongly considered and often is the thrust of investigation in the ED. Urinary tract infection, congestive heart failure, and hypothyroidism are just a few of the conditions that may cause a patient with mild dementia to show rapid decline. The symptoms overlap with those of delirium, as dis cussed earlier in the “Clinical Features” section under “Delirium, ” and the two conditions may overlap. 2,10 In the differential diagnosis, consider the so-called treatable causes of dementia (included in Table 168-3) and impairment in cognitive function caused by depression (pseudodementia). Additionally, behavioral and psychiatric symptoms of dementia (e.g., depression, anxiety, agitation, hallucination) may prompt a visit to the ED.  TREATMENT The behavioral and psychiatric symptoms of dementia are ideally managed by nonpharmacologic measures. There are three main categories to consider when targeting with interventions: (1) unmet needs, such as unrecognized pain; (2) learned behaviors, such as a behavior that elicits a desired response; and (3) environmental vulnerability and stress sensitivity, such as an aggressive behavior due to fear from a new situation. Atypical and conventional antipsychotic drugs carry a black box warning against use for behavioral and psychiatric symptoms of dementia, due to an increased risk in mortality. Reserve consideration of anti psychotic use for patients with significant risk of harm to self and others. Coordinate treatment with caregivers who are in a position to monitor the patient’s behavior patterns over time. Treatment of vascular dementia is limited to treatment of risk factors, including hypertension. Normal pressure hydrocephalus is suggested by the presence of excessively large ventricles on head CT and can prompt consideration of a trial of lumbar puncture with cerebrospinal fluid drainage or ventricular shunting.  DISPOSITION AND FOLLOW-UP A new diagnosis of dementia may be entertained in the ED, but the depth of the required diagnostic evaluation usually exceeds the time available during the ED visit. A decision to admit or to arrange an out patient diagnosis should occur after the major and urgent differential diagnostic possibilities have been eliminated. Direct attention toward the presence of delirium or a treatable cause of dementia. Consider hospital admission if comorbid medical problems, a rapidly progressive or atypical clinical course, or an unsafe or uncertain home situation exists. COMA  INTRODUCTION Coma is a state of reduced alertness and responsiveness from which the patient cannot be aroused. 23,24 The Glasgow Coma Scale (Table 168-4; see also Chapter 257, “Head Trauma”) is a widely used clinical scoring system for alterations in consciousness. Advantages are the simplicity of the scoring system and assessment of separate verbal, motor, and eye-opening functions. Disadvantages include lack of acknowledgment of hemiparesis or other focal motor signs and lack of testing of higher cognitive functions.

sed clinical scoring system for alterations in consciousness. Advantages are the simplicity of the scoring system and assessment of separate verbal, motor, and eye-opening functions. Disadvantages include lack of acknowledgment of hemiparesis or other focal motor signs and lack of testing of higher cognitive functions. Interrater variability has been noted in assessments using the Glasgow Coma Scale. 25 Another coma scale, the FOUR (Full Outline of Unresponsiveness) score, has been used in intensive care units and has the advantages of assessing simple brainstem functions and respiratory patterns, as well as eye and motor responses. 26 Causes of coma likely to be encountered in the ED are noted in Table 168-5.  PATHOPHYSIOLOGY The pathophysiology of coma is complex. Coma can result from defi ciency of substrates needed for neuronal function (as with hypoglycemia or hypoxia). With systemic causes, the brain is globally affected, and signs that localize dysfunction to a specific area of the brainstem or cortex are usually lacking. With primary CNS causes, coma may result from a brainstem disorder such as hemorrhage or from bilateral corti cal dysfunction. Signs localizing to specific areas of CNS dysfunction such as hemiparesis or cranial nerve abnormalities may be present. Unilateral hemispheric disease, such as stroke, should not alone result in coma. The function of the brainstem and/or both hemispheres must be impaired for unresponsiveness to occur. The herniation syndromes are models for alterations of consciousness, but their mechanisms are unknown. In uncal herniation syndrome, the medial temporal lobe shifts to compress the upper brainstem, which results in progressive drowsiness followed by unresponsiveness. 24,27 The ipsilateral pupil is sluggish, eventually becoming dilated and nonreactive as the third cranial nerve is compressed by the medial temporal lobe. Hemiparesis may develop ipsilateral to the mass from compression of the descending motor tracts in the opposite cerebral peduncle. Central herniation syndrome is characterized by progressive loss of consciousness, loss of brainstem reflexes, decorticate posturing, and irregular TABLE 168-4 Glasgow Coma Scale Component Score Adult Child <5 y Child >5 y Motor 6 Follows commands Localizes pain Withdraws to pain Flexion Extension None Normal spontaneous movements Localizes to supraocular pain (>9 mo) Withdraws from nail bed pressure Flexion to supraocular pain Extension to supraocular pain None Follows commands Verbal 5 Oriented Confused speech Inappropriate words Incomprehensible 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 Eye opening 4 Spontaneous To command To pain None Spontaneous To voice To pain None

Confused speech Inappropriate words Incomprehensible 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 Eye opening 4 Spontaneous To command To pain None Spontaneous To voice To pain None Tintinalli_Sec14_p1101-1186.indd 1140 8/2/19 12:08 PM

Confused speech Inappropriate words Incomprehensible 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 Eye opening 4 Spontaneous To command To pain None Spontaneous To voice To pain None Tintinalli_Sec14_p1101-1186.indd 1140 8/2/19 12:08 PM CHAPTER 168: Altered Mental Status and Coma 1141 respiration.24 Because midline shift without herniation, as demonstrated by neuroimaging, seems to correlate with a decreased level of consciousness, vascular compression due to local cerebral edema or local increased intracranial pressure (ICP) may be an underlying mechanism for these syndromes. A diffuse increase in ICP can cause diffuse CNS dysfunction. Cerebral blood flow is constant at mean arterial pressures of 50 to 100 mm Hg due to the process of cerebral autoregulation. At mean arterial pressures outside this range, cerebral blood flow may be reduced, and diffuse ischemia may develop. Cerebral perfusion pressure is equal to the mean arterial pressure minus the ICP (cerebral perfusion pressure = mean arterial pressure – ICP). In extreme uncontrolled elevation of the ICP , cerebral perfusion pressure is diminished as the ICP approaches the mean arterial pressure, which causes brain ischemia. Particularly in unresponsive patients with a history of seizures, the possibility of ongoing nonconvulsive seizures must be considered. Subtle status epilepticus or ictal coma may represent transformed generalized convulsive status epilepticus. Electrical seizures may continue in the absence of clinical seizures.  CLINICAL FEATURES The clinical features of coma vary with both the depth of coma and the cause. For example, a patient in a coma with a hemispheric hemor rhage and midline shift may have decreased muscle tone on the side of the hemiparesis. The eyes may conjugately deviate toward the side of the hemorrhage. With expansion of the hemorrhage and surrounding edema, increase in ICP , or brainstem compression, unresponsiveness may progress to a complete loss of motor tone and loss of the ocular findings as well. A variety of abnormal breathing patterns may be seen in the comatose patient. 24 They offer little information in the acute setting. Pupillary findings, the results of other cranial nerve evaluation, hemiparesis, and response to stimulation are all parts of the clinical picture that need assessment. These findings can assign the cause of the coma into a probable general category—diffuse CNS dysfunction (toxic-metabolic coma) or focal CNS dysfunction (structural coma). A further division of structural coma into hemispheric (supratentorial) or posterior fossa (infratentorial) coma is often possible at the bedside. Toxic-Metabolic Coma Many different toxic and metabolic condi tions cause coma. The diffuse CNS dysfunction is reflected by the lack of focal physical examination findings that point to a specific region of brain dysfunction. For example, in toxic-metabolic coma, if the patient demonstrates either spontaneous movements or reflex posturing, the movements are symmetric without evidence of hemiparesis. Muscle stretch reflexes, if present, are symmetric. Pupillary response is gener ally preserved in toxic-metabolic coma. Typically, the pupils are small but reactive. If extraocular movements are present, they are symmetric. If extraocular movements are absent, however, this sign is of no value in differentiating toxic-metabolic from structural coma. A notable excep tion is severe sedative poisoning as from barbiturates; the pupils may be large, extraocular movements absent, muscles flaccid, and the patient apneic, which simulates the appearance of brain death.

ts are absent, however, this sign is of no value in differentiating toxic-metabolic from structural coma. A notable excep tion is severe sedative poisoning as from barbiturates; the pupils may be large, extraocular movements absent, muscles flaccid, and the patient apneic, which simulates the appearance of brain death. Coma From Supratentorial Lesions Coma caused by lesions of the hemispheres, or supratentorial masses, may present with progressive hemiparesis or asymmetric muscle tone and reflexes. The hemiparesis may be suspected with asymmetric responses to stimuli or asymmetric extensor or flexor postures. Uncal herniation syndrome, as described earlier in “Pathophysiology, ” is an example of a supratentorial syndrome. Frequently, however, large acute supratentorial lesions are seen without the features consistent with temporal lobe herniation. Coma without lateralizing signs may result from decreased cerebral perfusion secondary to increased ICP . Reflex changes in blood pressure and heart rate may be observed with increased ICP or brainstem compression. Hypertension and bradycardia in a comatose patient may represent the Cushing reflex from increased ICP . Coma From Infratentorial Lesions Posterior fossa or infratentorial lesions compose another structural coma syndrome. An expanding lesion, such as cerebellar hemorrhage or infarction, may cause abrupt coma, abnormal extensor posturing, loss of pupillary reflexes, and loss of extraocular movements. The anatomy of the posterior fossa leaves little room for accommodating an expanding mass. Early brain stem compression with loss of brainstem reflexes may develop rapidly. Another infratentorial cause of coma is pontine hemorrhage, which may present with the unique signs of pinpoint-sized pupils. Pseudocoma Pseudocoma or psychogenic coma is occasionally encountered and may present a perplexing clinical problem. Adequate history taking and observation of responses to stimulation reveal find ings that differ from those in the syndromes described in the previous sections. Pupillary responses, extraocular movements, muscle tone, and reflexes are shown to be intact on careful examination. Tests of par ticular value include responses to manual eye opening (there should be little or no resistance in the truly unresponsive patient) and extraocular movements. Specifically, if avoidance of gaze is consistently seen with the patient always looking away from the examiner, or if nystagmus is demonstrated with caloric vestibular testing, this is strong evidence for nonphysiologic or feigned unresponsiveness.  DIAGNOSIS In the approach to the comatose patient, perform stabilization, diag nosis, and treatment actions simultaneously. Examination, laboratory procedures, and neuroimaging allow differentiation between structural and metabolic causes of coma in almost all patients in the ED.

siologic or feigned unresponsiveness.  DIAGNOSIS In the approach to the comatose patient, perform stabilization, diag nosis, and treatment actions simultaneously. Examination, laboratory procedures, and neuroimaging allow differentiation between structural and metabolic causes of coma in almost all patients in the ED. History and physical examination findings allow that initial assignment in many TABLE 168-5 Differential Diagnosis of Coma Coma from causes affecting the brain diffusely •  Encephalopathies •  Hypoxic  encephalopathy •  Metabolic  encephalopathy •  Hypertensive  encephalopathy •  Hypoglycemia •  Hyperosmolar  state (e.g., hyperglycemia) •  Electrolyte  abnormalities (e.g., hypernatremia or hyponatremia, hypercalcemia) •  Organ  system failure •  Hepatic  encephalopathy •  Uremia/renal  failure •  Endocrine  (e.g., Addison’s disease, hypothyroidism, etc.) •  Hypoxia •  Carbon  dioxide narcosis •  Toxins •  Drug  reactions (e.g., neuroleptic malignant syndrome) •  Environmental  causes—hypothermia, hyperthermia •  Deficiency  state—Wernicke’s encephalopathy •  Sepsis Coma from primary CNS disease or trauma •  Direct  CNS trauma •  Diffuse  axonal injury •  Subdural  hematoma •  Epidural  hematoma •  Vascular  disease •  Intraparenchymal  hemorrhage (hemispheric, basal ganglia, brainstem, cerebellar) •  Subarachnoid  hemorrhage •  Infarction •  Hemispheric,  brainstem •  CNS  infections •  Neoplasms •  Seizures •  Nonconvulsive  status epilepticus •  Postictal  state Tintinalli_Sec14_p1101-1186.indd 1141 8/2/19 12:08 PM