Neurologic Emergencies

Tricia Y. Ting

Lisa M. Shulman

key points

Status epilepticus may present with convulsions or nonconvulsive altered mental status.Treatment must be rapidly initiated to achieve early seizure termination for best outcome.
Delirium, or encephalopathy, may be caused by acute medical conditions that demand emergency medical or surgical treatment for infection (i.e., herpes encephalitis), structural abnormalities (i.e., intracranial hematoma, cerebellar stroke), or toxic-metabolic etiologies (i.e., drug intoxication, thiamine deficiency).
Other central nervous system emergencies that may require neurosurgical intervention include acute intracranial hypertension and spinal cord compression.
Increasing weakness in peripheral nervous system disorders, such as myasthenia gravis and Guillain-Barré syndrome, carries the risk of acute respiratory failure. For this reason, inpatient observation and treatment are warranted.
Neuroleptic malignant syndrome is best treated by discontinuation of dopamine-blocking antipsychotic medications.

Neurologic emergencies are encountered frequently in the practice of medicine, and, if unrecognized, they may progress rapidly to permanent neurologic disability or death. The topics included in this chapter represent the more common and treatable conditions that non-neurologists may likely encounter. Cerebrovascular emergencies are discussed separately in Chapter 7.

CENTRAL NERVOUS SYSTEM

Status Epilepticus

Most epileptic seizures are self-limiting, lasting only seconds to minutes. Seizures that become prolonged or repetitive with impaired recovery of consciousness are at risk of evolving into status epilepticus (SE), a serious medical emergency.
SE is not uncommon, affecting approximately 50 patients per 100,000 population yearly with a mortality rate estimated at up to 20% in adults. Long-term morbidity from SE includes chronic epilepsy, cognitive dysfunction, and focal neurologic deficits.

The point at which a seizure may be defined as SE has been a matter of debate over the past decade. Physiologic evidence for neuronal damage in animal studies formerly led to the definition of SE as any seizure or intermittent seizures without recovery of consciousness lasting for 30 minutes or longer. More recently, however, clinical experience has broadened the definition of SE to continuous or repeated seizure activity without return of consciousness for longer than 5 minutes. The shortened time frame reflects a general push for initiating treatment earlier to minimize the potential morbidity and mortality. Longer seizure duration has been associated with a poorer outcome, and the longer a seizure remains untreated, the more difficult it becomes to abort.

▪ SPECIAL CLINICAL POINT: To optimize patient outcome by earlier treatment, the working definition of SE should be ongoing or repetitive seizures without recovery of consciousness for >5 minutes.

The most common type of SE carrying the greatest risk of morbidity and mortality is generalized convulsive SE. The seizures are usually easy to recognize clinically as tonic-clonic convulsions of the extremities with complete loss of consciousness. However, generalized convulsive SE may progress over time from overt convulsions to more subtle physical activity such as mild focal twitching or ocular deviation before further evolving to only generalized electrical activity with persistent loss of consciousness but absence of all physical manifestations. There is a risk of delayed recognition of generalized SE when patients present to the emergency room without overt tonic- clonic movements, so clinicians must be aware of the signs of nonconvulsive as well as convulsive SE.

Nonconvulsive SE is a more heterogeneous category that includes absence SE and complex partial SE. Both forms of nonconvulsive SE are characterized by confusion or other altered mental status with minimal motor manifestations. Patients may exhibit blinking, automatisms, or fluctuating bizarre behavior. Evidence from an electroencephalogram (EEG) is important to support the diagnosis of nonconvulsive SE and sometimes, but not always, can help differentiate between absence and complex partial SE. EEG findings may vary from generalized epileptiform discharges to focal discharges or generalized activity with a focal predominance. Absence SE is believed to have little long-term neurologic sequelae. Whether complex partial SE carries a risk of significant neurologic morbidity remains controversial. Although several series documented no lasting neurologic deficits in patients following complex partial SE, there are others that reported long-term morbidity, particularly in those whose seizures were precipitated by acute neurologic disorders. Nevertheless, there is widespread agreement that patients with nonconvulsive SE should be treated quickly and aggressively to avoid potential adverse outcomes.

Morbidity and mortality from SE are a result of multiple factors including central nervous system (CNS) damage from the causative illness or acute insult that precipitated SE, the metabolic consequences of prolonged convulsive SE, and the neuronal excitotoxic effects of prolonged electrical seizure activity. It is recognized that continuous electrical activity for more than 60 minutes, even while correcting for SE-associated metabolic derangements, can result in hippocampal damage and probably in more widespread brain damage as well. Excitotoxic neuronal injury may be compounded by significant systemic manifestations including hypoxemia, metabolic and respiratory acidosis, hyperglycemia, hyperthermia, and blood pressure fluctuation. With more prolonged SE, rhabdomyolysis from prolonged muscle activity and significant sodium and potassium derangements may develop along with renal failure.
Cardiac arrhythmias may occur from CNS dysregulation, electrolyte abnormalities, or even medications used in the treatment of SE. Laboratory investigations commonly demonstrate a peripheral leukocytosis, an acidotic pH, and a mild cerebrospinal fluid (CSF) pleocytosis.

The general principles to minimize the morbidity and mortality associated with SE are early diagnosis, early intervention, and prompt identification and management of concurrent medical and surgical conditions, including potential etiologies. The three most common precipitants of SE in adults are withdrawal from anticonvulsive medications, alcohol withdrawal, and cerebral infarction. Metabolic derangements such as hyponatremia, hyperglycemia or hypoglycemia, hypocalcemia, hepatic failure, and renal failure account for 10% to 15% of the cases reported. Other recognized etiologies of SE include anoxia, hypotension, CNS infections (meningitis, abscess, encephalitis), tumors, trauma, and drug overdose.

Treatment of SE

It has been established that earlier treatment of SE leads to better patient outcome. To this end, the past decade has seen many options investigated for the prehospital treatment of SE and acute repetitive seizures by first-responders— medical personnel and family members of at-risk patients. Concern for respiratory compromise from treatment administered out of the hospital, moreover, has not been substantiated in clinical trials. In fact, a prehospital SE study found the rates of respiratory or circulatory complications after treatment were highest in a placebo group.

Accepted prehospital options for early SE therapy are currently limited to a rectal benzodiazepine gel (diazepam), particularly for nonmedically trained persons, and intravenous (IV) benzodiazepine administration by health care professionals (Table 5.1). Alternative routes of drug administration, including intramuscular (midazolam), buccal, and nasal routes, are under investigation. Prehospital benzodiazepine dosing should be repeated once if necessary to abort continued seizure activity after initial dosing, but activation of emergency services and transfer to an emergency department should then be considered in such cases.

▪ SPECIAL CLINICAL POINT: Rescue therapy that patients can take at home, such a benzodiazepine, can be prescribed for patients with epilepsy who are at high risk for prolonged or acute repetitive seizures and SE.

Generalized convulsive SE is a medical emergency and should be managed in the emergency department or intensive care unit (ICU) where aggressive measures to provide life support and terminate seizure activity may be best performed. The first steps are to assess vital signs and evaluate oxygenation. An oral or nasopharyngeal airway is inserted, nasotracheal suction is performed, and supplemental oxygen is administered if necessary. Oxygenation is evaluated by clinical examination, pulse oximetry, and arterial blood gas determination. Establishing two intravenous (IV) lines is the next priority, providing a backup IV access as well as allowing parallel delivery of IV glucose, medications, and fluids with IV anticonvulsant therapy. Simultaneously, venous blood is drawn for a complete blood count, electrolytes, glucose, calcium, magnesium, blood urea nitrogen, liver function tests, anticonvulsant drug levels, toxicology screen, and ethanol level. An IV bolus of 50 mL of 50% glucose and thiamine (1 mg/kg) is administered as soon as the IV access is established. Electrocardiographic (ECG) monitoring is instituted immediately, and vital signs are monitored throughout the treatment protocol. Electrographic seizure activity may persist in up to 15% of patients even after anticonvulsant therapy has suppressed all signs of clinical seizure activity. Moreover, seizure activity becomes difficult to assess clinically when patients receive long-acting neuromuscular paralytic agents for endotracheal intubation or when anesthesia is induced for treatment of refractory SE. EEG monitoring, therefore, should begin at the earliest possible opportunity. It should be emphasized, however, that lack of
immediate EEG monitoring should never delay therapy for suspected SE.

TABLE 5.1 Management of Status Epilepticus

Objectives	Time Frame	Intervention
Prehospital treatment (nonmedical persons)	>5 minute	1.	Recognize SE or acute repetitive seizures
Prehospital treatment (nonmedical persons)		2.	Safety measures, lie patient on side, nothing inserted in mouth
		3.	Check blood glucose if appropriate
		4.	Treat with rescue benzodiazepine:
			Adults: Diazepam 10 mg rectally
			Children: Diazepam 0.5 mg/kg rectally
		Repeat once if needed and activate emergency services for continued seizure activity
Prehospital (medical personnel) or initial in-hospital treatment	5 to 20 minute	1.	Recognize SE
		2.	Assess vital signs and oxygenation
		3.	Insert oral airway and administer oxygen if necessary
		4.	Establish two IV lines
		5.	Draw blood for CBC, electrolytes, glucose, calcium, magnesium, BUN, LFTs, anticonvulsant levels, toxicology screen, and ethanol level
		6.	Begin ECG and EEG^a monitoring
		7.	Administer IV bolus of thiamine 1 mg/kg and 50 mL of 50% glucose
		8.	Treat with benzodiazepine:
			Adults: Lorazepam IV 4 mg bolus or Diazepam IV 10 mg
			Children: Lorazepam IV 0.1 mg/kg (maximum 4 mg) or
			Diazepam IV 0.3 mg/kg (maximum 10 mg)
In-hospital treatment/ED setting (second stage SE)	20 to 60 minute	1.	Treat with longer-acting AED:
In-hospital treatment/ED setting (second stage SE)			Fosphenytoin IV 15-18 mg PE/kg at a rate of 150 PE/min or Phenytoin IV 15-18 mg/kg at maximum rate of 50 mg/min, or in children, Phenobarbital^b IV 15-20 mg/kg at maximum rate of 100 mg/min
		2.	Monitor blood pressure, ECG, and respirations
Treatment of refractory SE/ICU setting	>60 minute	1.	If seizures persist, consider transfer to an intensive care unit. Perform elective endotracheal intubation
Treatment of refractory SE/ICU setting		2.	Treat with general anesthesia:
			Midazolam, 0.2 mg/kg boluses, maximum 2 mg/kg then, infusion rate 0.05-2 mg/kg/hr, or in adults:
			Propofol, 1-2 mg/kg boluses, maximum 10 mg/kg, then infusion rate 2-10 mg/kg/hr, or
			Pentobarbital, 10-15 mg/kg, then infusion rate 0.5-1 mg/kg/hr, or
			Thiopental, 3-5 mg/kg bolus, then infusion rate, 3-5 mg/kg/hr
		3.	Titrate anesthetic to burst-suppression pattern on EEG for 24 to 48 hours, then gradually taper infusion rate while monitoring for seizure activity
		4.	If clinical or electrographic seizure activity is observed, repeat the anesthetic induction
Prevention and treatment of complications of SE	Throughout	1.	Monitor vital signs
Prevention and treatment of complications of SE		2.	Monitor volume status
		3.	Maintain airway and prevent aspiration
		4.	Review laboratory information and treat accordingly
Identification of cause of SE	Throughout	1.	Obtain history from relatives and friends
		2.	Obtain head CT, when indicated
		3.	Perform lumbar puncture, when indicated
		4.	Initiate IV antibiotic or antiviral coverage when meningitis or encephalitis is suspected
Prevention of recurrence of SE	Following cessation of seizure activity	1.	Monitor anticonvulsant levels
Prevention of recurrence of SE	Following cessation of seizure activity	2.	Initiate daily therapy with appropriate anticonvulsant(s)
		3.	Educate patient and family to ensure medication compliance
CBC, complete blood count; BUN, blood urea nitrogen; LFTs, liver function tests; SE, status epilepticus; ICU, intensive care unit; PE, phosphenytoin sodium equivalents.
^aAt earliest availability.
^bThird-line therapy (after anesthetics) in some protocols.

Termination of seizure activity is the focus of SE treatment, and benzodiazepines, generally lorazepam or diazepam, are the first-line agents (Table 5.1 details drug dosing). Lorazepam is preferable to diazepam because of a longer duration of action and, consequently, a lower seizure-relapse rate. Benzodiazepine therapy is often followed by treatment with a longer-acting antiepileptic drug (AED), traditionally phenytoin IV. Phenytoin IV should be infused at a rate no faster than 50 mg/min because of the risk of hypotension and cardiac dysrhythmias. ECG and frequent blood pressure monitoring are essential. If hypotension or bradycardia develops, the rate of administration can be decreased or the infusion can be held until the vital signs stabilize. Phenytoin IV should never be delivered by an automatic infusion pump to an unattended patient. Phosphenytoin, a prodrug that is
converted to phenytoin, has gained favor over parenteral phenytoin where available. Dosage is expressed in phosphenytoin sodium equivalents (PE) for ease of transition from more familiar phenytoin dosing. By virtue of its solubility, phosphenytoin does not require the addition of propylene glycol as a vehicle, which is thought to cause most of the clinically significant hypotension, arrhythmias, and local injection reactions of phenytoin administration. Absence of these side effects allows for a faster rate of infusion of phosphenytoin, up to 150 mg PE/min, with peak concentrations within 10 minutes after infusion. Phosphenytoin offers the additional advantage of intramuscular injection in those patients without IV access; therapeutic plasma concentrations are reached within 30 minutes by this route. Phosphenytoin is considerably more expensive than phenytoin, but, in fact, may be more cost-effective as a
result of a reduced need for adverse event management.

If seizures persist, phenobarbital IV traditionally has been used as a second-line agent, after benzodiazepines and phenytoin have failed. However, phenobarbital may result in respiratory depression, prolonged sedation, or severe hypotension. This adverse side effect profile has relegated the barbiturate to the status of a thirdline agent in some SE treatment algorithms. If phenobarbital IV is used, elective endotracheal intubation is recommended before initiation of the infusion. Valproate IV has become available for use in treating SE, with loading doses of 15 to 20 mg/kg infused at a rate of 3 to 6 mg/kg/min. Its safety profile suggests usefulness as a secondline agent, particularly in patients who are hemodynamically unstable. However, clinical experience with valproate in this capacity remains limited, and it is absent from many standard SE treatment protocols.

Approximately 30% of patients with SE will have ongoing seizures resistant to standard loading doses of anticonvulsant medications, thus requiring therapy for “refractory SE.” Anesthetic doses of benzodiazepines, short-acting barbiturates, or propofol are the third-line agents used to treat refractory SE, although some investigators have proposed resorting to these drugs as second-line agents in place of phenobarbital IV. Midazolam is a well-tolerated, short-acting benzodiazepine that causes fewer problems with hypotension. An alternative to more costly midazolam is propofol, a nonbarbiturate, anesthetic agent. A disadvantage of this therapy is the potential for developing “propofol-infusion syndrome,” characterized by hypotension, lipidemia, metabolic acidosis, renal failure, and cardiovascular collapse. Finally, pentobarbital and thiopental sodium are shortacting barbiturates that may be used in treating refractory SE. Prolonged elimination and the potential immunosuppressive propensity of these agents are potential disadvantages.

EEG monitoring is important in the management of refractory SE. Although the necessary depth and duration of anesthesia for treatment of refractory SE has not been standardized, anesthetics typically are titrated to produce a burst-suppression pattern on the EEG for 24 to 48 hours. After this time, the infusion rate is decreased gradually. If electrographic or clinical seizures emerge, induction is repeated at progressively longer intervals.

The prevention and management of complications of SE is ongoing throughout the treatment protocol. Hypertension, hyperthermia, and acidosis require attention, but effective treatment of SE should reverse these problems. Hypotension can be a direct consequence of prolonged SE or, alternatively, the effect of anticonvulsant medication, volume depletion, trauma, or cardiovascular disease. The potential risks of rhabdomyolysis, aspiration pneumonia, or traumatic injury as a result of seizure activity also must be recognized and prevented if possible.

The management of SE cannot be separated from the exigency of identifying the underlying cause. Obtaining historical information from the patient’s family, friends, or medical records may reveal a pattern of noncompliance with medication or a recurrent history of alcohol withdrawal. Reports of acute neurologic deficits or febrile illness may further help guide appropriate diagnostic evaluation. A head computed tomography (CT) should be considered, with and without contrast (if renal function and allergies permit), to exclude the possibilities of neoplasm, cerebrovascular infarction, intracerebral hemorrhage, and traumatic injury. Following CT, lumbar puncture may be indicated. It should be noted that the CSF can reveal a moderate pleocytosis (up to 150 white blood cells) and an increase in CSF protein (up to 100 mg/dl) following persistent seizure activity. Nonetheless, if there is any suspicion of meningitis, antibiotic therapy should be started promptly and appropriate cultures should be sent for evaluation.

Upon successful treatment of SE, careful attention to initiating a daily dosing schedule of one or more anticonvulsants and monitoring the total and free serum drug levels will help
prevent recurrence of seizure activity. In the coming years, the development of novel routes of administration for established drugs as well as new anticonvulsant and neuroprotective agents holds promise for further reducing the morbidity and mortality of SE.

ACUTE ALTERATION OF MENTAL STATUS

An acute alteration of mental status is the most common neurobehavioral disorder seen in hospitalized patients. It is characterized by a sudden change in cognition with impaired attention that may fluctuate; it is potentially reversible; and it is not a result of preexisting dementia.

A well-known form of acute alteration of mental status is delirium. The Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM IV), delineates the following clinical criteria for the diagnosis of delirium: inattention, change in cognition, acute and fluctuating course, and evidence of a medical cause. Subtypes of delirium have been described and categorized by overall psychomotor activity and arousal level. These subtypes include hyperactive, hypoactive, and mixed delirium. Hyperactive delirium is dominated by hyperarousal, hallucinations, and agitation, whereas hypoactive delirium is characterized by lethargy, confusion, and sedation. Although specific etiologies do not consistently coincide with certain subtypes, there do appear to be some trends associating causes with clinical subtypes. For instance, patients with alcohol and benzodiazepine withdrawal typically appear more hyperaroused, whereas those with a metabolic disorder tend toward hypoactivity. Categorizing patients into general subtypes may be helpful prognostically. Investigators found that patients with hypoactive delirium had longer hospitalizations with increased risk of developing pressure ulcers, whereas their hyperactive counterparts incurred an increased risk of falls.

An unexplained acute alteration of mental status due to a medical condition (delirium) must be differentiated from a psychiatric disorder, and even in patients with known psychiatric illness, several evaluations of possible causes of delirium are important to perform. The differential diagnosis of delirium is extensive and can be divided into several broad etiologic categories: infections, structural lesions, toxic-metabolic causes (drug-related, hypoxia, hypoglycemia, hepatic and renal disease, electrolyte abnormalities, thiamine deficiency, etc.), and postictal states. The term “encephalopathy” is frequently substituted for delirium to describe diffusely abnormal brain function from a medical cause (i.e., toxic-metabolic encephalopathy). A psychiatric disorder should only be considered after underlying, potentially life-threatening, medical causes are properly excluded. Several of the more important causes of altered mental status that require special attention are discussed below.

Herpes simplex encephalitis (HSE) is one of the most common, potentially fatal infections of the brain associated with an acute altered mental state. HSE is usually associated with herpes simplex virus (HSV)-1 in adults and children from either primary infection or virus reactivation. The virus causes inflammation of the brain parenchyma, necrosis, and hemorrhage, particularly in the temporal and orbitofrontal lobes. Patients are often ill-appearing with fever, headache, meningitis, focal neurologic deficits such as hemiparesis and aphasia, confusion, and seizures (both partial and secondarily generalized). The clinical course of a patient with HSE may decline precipitously to obtundation, coma, and death if left untreated. For this reason, treatment with IV acyclovir (10 mg/kg every 8 hours for at least 14 days) should be initiated promptly in anyone suspected of having HSE. The risk of acyclovir is low but does include bone marrow suppression, liver and renal toxicities.

▪ SPECIAL CLINICAL POINT: In patients suspected of having herpes simplex encephalitis (HSE), empiric treatment with acyclovir, even prior to completion of diagnostic testing, is warranted due to the high risk of morbidity and mortality from delayed treatment.

Diagnostic testing for HSE should include a brain magnetic resonance imaging (MRI)
(or HCT if not available) and CSF sampling (including HSV PCR analysis). MRI may show edema particularly in the temporal and frontal regions, often with associated hemorrhage. Opening pressure of the lumbar puncture may be elevated, and the CSF may mimic an aseptic meningitis with a mildly decreased glucose, mildly elevated protein, pleocytosis (with lymphocytes and some neutrophils) as well as many red blood cells (RBCs) and xanthrochromia due to hemorrhagic necrosis of the brain parenchyma. A traumatic lumbar puncture may falsely elevate RBCs in the CSF; therefore, cell counts should be sent on the first and last tubes collected to aid interpretation. The sensitivity and specificity of PCR of CSF for HSV is high. It is, therefore, appropriate to consider discontinuation of acyclovir initiated empirically in patients who are later found to have a negative PCR result.

An EEG is frequently indicated in patients with HSE exhibiting overt seizures or an alteration in their mental status without return to their baseline. Seizures are particularly common with temporal lobe lesions, such as seen with HSE. The EEG may show areas of focal slowing or focal epileptiform discharges with temporal predominance, often superimposed upon an abnormal diffusely slowed background. Classically, the focal sharp wave abnormalities in HSE are periodic, lateralized, epileptiform discharges (PLEDs), though this is not specific for HSE. Patients who recover from HSE are at somewhat higher risk for later developing epilepsy. AED therapy is appropriate in the management of HSE for the treatment of seizures and in those at high risk for seizures based on the EEG.

Intracranial hematoma should be considered in any patient with a recent history of head trauma and an acute change in mental status, particularly with headache or focal neurologic deficits. A patient with a spontaneous intracerebral or subarachnoid hemorrhage may have a similar acute presentation requiring emergency intervention. These neurologic emergencies, however, are more aptly discussed in the context of cerebrovascular disease (see Chapter 7).

Chronic subdural hematomas, especially in older patients, may result from blunt head trauma and develop slowly over weeks to months, presenting clinically with cognitive decline that can be easily mistaken for dementia. Like the elderly, patients with coagulopathies and alcoholism have a higher risk for subdural hematomas. Acute epidural and subdural hematomas may develop within just minutes to hours after head trauma. Younger patients and those with skull fractures are at greater risk for epidural hematomas, most commonly from tearing arterial vessels. Headache, vomiting, seizures, and focal deficits may progress rapidly to bradycardia, apnea, and coma in a patient with an expanding epidural hematoma coinciding with increasing intracranial pressure and cerebral herniation.

▪ SPECIAL CLINICAL POINT: A falsely reassuring “lucid interval” may be seen following head injury in a patient with an epidural hematoma who has a transient recovery of mental status after initial impact, only to have rapid neurologic decline minutes to hours later with hematoma expansion.

Patients, thus, presenting after head injury with headache or altered mental status should have an unenhanced head CT as soon as possible and be kept under close surveillance with frequent neurologic evaluations. If necessary, emergency transfer to a trauma center for decompression should be arranged.

Cerebellar stroke, either infarction or hemorrhage, is an acute structural lesion not to be overlooked due to the potentially devastating neurologic outcome. Patients may present with any combination of headache, nausea, vomiting, vertigo, clumsiness, ataxia, and dysarthria, or may present early on in coma. The difficulty in managing acute cerebellar stroke lies in predicting who will deteriorate, deciding which treatment options are needed, and electing when to proceed with surgery. There is as yet no definitive protocol for the management of
patients with acute cerebellar stroke. Clinicians generally must rely upon both the overall clinical picture as well as neuroimaging features to guide their decision-making. A deteriorating level of consciousness, gaze palsy, or signs of herniation along with findings on HCT (i.e., effacement of the fourth ventricle, presence of hydrocephalus, size of cerebellar hemorrhage, and evidence of brainstem infarction) may help determine the primary mechanism(s) of clinical decline and, thus, the best therapeutic approach.

▪ SPECIAL CLINICAL POINT: An observation period of 72 to 96 hours in a neurologic intensive care unit is generally recommended for patients with acute cerebellar stroke to enable early detection of a deterioration in neurologic status and, if necessary, emergency surgical intervention.

Several mechanisms may account for the neurologic deterioration seen in cerebellar stroke. These include obstructive hydrocephalus from fourth ventricle compression, direct brainstem compression from mass effect, upward herniation of the cerebellar vermis through the tentorial notch, and irreversible brainstem infarction. In cases of acute hydrocephalus without brainstem compression (clinically or on imaging), ventriculostomy alone may be adequate. However, if there is no clinical improvement, a posterior fossa decompressive craniectomy may be required as a staged approach following ventriculostomy. In cases of direct brainstem compression or when there is a rapid neurologic decline, a suboccipital craniectomy with hematoma evacuation or resection of infarcted tissue is indicated. Additionally, cerebellar hemorrhages more than 3 cm in diameter usually require surgical evacuation.

Metabolic encephalopathies are common acquired causes of acute alteration in mental status, a diverse group of neurologic disorders defined by an alteration of mental status resulting from failure of organs other than the brain. Cerebral dysfunction may result from three basic mechanisms: deficiency of a necessary metabolic substrate (e.g., hypoglycemia), disruption of the internal environment of the brain (e.g., dehydration), or the presence of a toxin or accumulation of a metabolic waste product (e.g., drug intoxication or uremia). Hepatic and uremic encephalopathies are common metabolic causes of mental status change in hospitalized patients. Disorders of glucose regulation; osmolarity/sodium homeostasis; and derangement of calcium, magnesium, and phosphorous levels are also frequent offenders. Endocrine encephalopathies seen in Cushing syndrome, Addison disease, and thyroid disease are less common and may be overlooked.

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