Miscellaneous Neurologic Problems in the Intensive Care Unit

Jing Ji

Ann L. Mitchell

Nancy M. Fontneau

A wide variety of neurologic problems may confront the physician in the intensive care unit (ICU), including several important disorders for which basic information is not readily available. These include

Suicidal hanging, electrical shock, acute carbon monoxide poisoning, and decompression sickness, which present so blatantly that the diagnosis is rarely in question, yet the range of clinical manifestations and their management may be unanticipated.
Cerebral fat embolism, which is often not initially suspected if other surgical or medical issues take precedence.
Singultus (hiccups), which is an all too common secondary problem that may further weaken the severely ill patient.
Compression neuropathies, which may complicate prolonged bed rest.

Suicidal Hanging

Hanging is the second most common means of committing suicide in the United States [1]. Introduced in fifth-century England, hanging proceeded to become the official form of execution. Early on, there was no exact procedure, and most hangings resulted in slow strangulation [2]. Changes in techniques, such that the victim dropped at least his height and the hangman’s knot being placed in the submental location, produced a consistently fatal bilateral axis-pedicle fracture, resulting in complete herniation of the disc and severance of the ligaments between C2 and C3 [3]. This injury causes almost immediate death by destroying the cardiac and respiratory centers, lacerating the carotid artery, and injuring the pharynx [2,3].

Suicidal hangings are rarely so expert, and death usually results from strangulation due to interruption of cerebral blood flow [4]. A minimal amount of compression occludes the jugular veins, while an increased force occludes the carotid arteries [5,6]. A much larger force is necessary to arrest blood flow in the vertebral arteries [5]. Pressure on the jugular veins from the noose results in venous obstruction and stagnation of cerebral blood flow, causing hypoxia and loss of consciousness [3]. Cervical muscle tone then decreases, allowing airway obstruction and arterial compression, further worsening hypoxia [3]. In addition, external compression of the carotid bodies or vagal sheath can increase parasympathetic tone, whereas pressure on the pericarotid area stimulates sympathetic tone; either can result in cardiac arrest [4,5]. The altered autonomic tone may also cause a release of catecholamines, resulting in neurogenic pulmonary edema, as well as affect the respiratory smooth muscle tone, causing respiratory acidosis and a further insult to cerebral oxygenation [3].

If blood flow is quickly restored, full recovery can often be expected. If the blood flow is interrupted for more than a few minutes, however, hypoxia causes cell death and cytotoxic and vasogenic edema, with increased intracranial pressure. There is selective vulnerability of the cerebral cortex (particularly the pyramidal cell layer), the globus pallidus, thalamus, hippocampus, and the cerebellar Purkinje cells to anoxia and ischemia.

Diagnosis

Although the diagnosis is rarely in doubt, the patient may show a range of findings, varying from rope burns to coma. In the immediate posthanging period, the patient most commonly shows evidence of an altered level of consciousness, ranging from restlessness, delirium, or violence to lethargy, stupor, or coma. Seizures, and rarely status epilepticus, may occur [4,5]. Hyperthermia may be present because of hypoxic damage to the hypothalamus [6]. Injury to the neck blood vessels occurs in 40% of patients, resulting in carotid dissection, thrombus formation, and distal ischemic infarcts [7]. Venous occlusion may lead to venous congestion, venous ischemia, and hemorrhage [8]. Development of the acute respiratory distress syndrome may result from central nervous system (CNS) catecholamine release, causing constriction of the pulmonary venules [3]. In incomplete hanging, the patient may also show signs of laryngeal and pharyngeal edema, resulting in hoarseness, dysphagia, and stridor [3,8]. Although infrequent in suicidal hangings, fracture of the odontoid and injury to the spinal cord may occur.

Careful neurologic examination should be performed, with particular attention to alterations in the level of consciousness and evidence of spinal cord injury, such as paraparesis, quadriparesis, or urinary retention. There should be frequent monitoring of vital signs for evidence of autonomic instability and stridor. Initial laboratory evaluations should include radiographs of the cervical spine, arterial blood gas determination, electrocardiogram, and cardiac monitoring. CT angiogram should also be considered if suspicious for dissection of the carotid artery [9].

Neuroimaging of the brain may be quite variable, from a normal head computed tomography (CT) scan in many patients, to evidence of edema, hemorrhage, and ischemia. Due to decreased blood flow and the resultant hypoxia, edema may be seen in the white matter tracts [10]. Subcortical and subarachnoid hemorrhages may result from venous occlusion, while ischemic insults may result from venous or arterial occlusion, particularly in the areas of greatest vulnerability: the basal ganglia, cortex, thalamus, and hippocampus [11].

Treatment

The patient may appear dead but might still be resuscitable. Patients quickly lose consciousness with hanging attempts, but may still have cardiac and respiratory function or can quickly regain these with prompt cardiopulmonary resuscitation (CPR). The goals of treatment are to maintain an adequate level of cerebral oxygenation, to decrease the raised intracranial pressure, and to monitor and treat any cardiac arrhythmias or respiratory distress that may develop. In hangings, the mechanical trauma induced by strangulation can also cause hemorrhage and edema in the paratracheal and laryngeal areas and result in a delayed but significant airway obstruction at any time within the first 24 hours. Endotracheal intubation may be required if there is evidence of hypoxia due to acute respiratory distress syndrome, airway obstruction, or increased intracranial pressure [8].

Other concerns in victims of hangings include fractures and thrombi. A fracture of the odontoid requires immediate neurosurgical or orthopedic intervention to stabilize the cervical spine and protect the cord from injury. A carotid thrombus requires prompt vascular intervention to remove the clot and restore patency and blood flow. In addition, assessing the patient for other evidence of self-inflicted injuries and intoxications is also warranted, as is a complete psychiatric evaluation once the patient is able to cooperate.

Course

The prognosis for recovery is not immediately apparent with the first neurologic examination. Many patients have made a full recovery despite an initial Glasgow Coma Scale (GCS) score of 3 [4]. However, the fatality rate for suicidal hangings may range from 60% to 70% [12]. Indicators for a good recovery include a hanging time of less than 5 minutes, a heartbeat present at the scene or in the emergency room, CPR initiated at the scene, a GCS score greater than 3, and an incomplete circumferential ligature [4]. Predictors of a poorer prognosis include evidence of cardiopulmonary arrest, a spontaneous respiratory rate less than 4 per minute, need for intubation, and neurogenic pulmonary edema [5].

Other neurologic sequelae can become manifest either in the immediate posthanging period or after a relatively asymptomatic latent period. The individual may show evidence of a confusional state, a circumscribed retrograde amnesia, Korsakoff’s syndrome, or even progressive dementia [8]. Transient hemiparesis, aphasia, abnormal movements, motor restlessness, and myoclonic jerks also can characterize this period [8]. Ear numbness may result from injury to the greater auricular nerve [13]. Three more severe outcomes have also been observed: (a) comatose state with minor neurologic improvement
and death; (b) early neurologic recovery, followed by cerebral edema with uncontrollable uncal herniation and severe morbidity or mortality; and (c) complete neurologic recovery, followed by delayed encephalopathy and death [3]. Most patients who survive recover to variable degrees.

Electrical Injuries

Approximately 4,000 injuries and 1,000 deaths from electrical shock occur annually in the United States. Most fatalities occur in the workplace, but one third result from contact with household current [14]. Approximately 400 people per year are affected by lightning strikes, with one-third of victims dying due to their exposure [15].

Pathophysiology

Electrical and lightning injuries are exceedingly variable and dependent on a number of factors. Current flowing between two potentials, or amperage, is equal to the voltage divided by the resistance to current flow (I = V/R). Current is generated by either an electrical source or a lightning strike. Current may be direct (DC), as with lightning, or alternating (AC), as with most household appliances. Alternating current has a tendency to produce tetanic contractions that prevent voluntary release from the current source, thus prolonging the electrical contact time and increasing the potential for injury. Higher voltages, such as those that occur with lightning or with contact with high-voltage conductors, produce more severe injuries than those due to low voltages. Wet skin and tissues high in water content provide low resistance to current flow and are at a higher risk for injury, while tissues high in fat and air, such as hollow organs, provide high resistance. Nerves and blood vessels have lower than expected resistances, and thus are more sensitive to electrical injury than their water content would suggest [16]. Other variables that affect the severity of damage include the current pathway (i.e., whether it involves the heart, diaphragm, spinal cord, or brain), the area of current contact and exit, and the duration of contact [16].

In addition, lightning injuries are classified according to the type of exposure [17]. “Direct strikes” involve direct contact between the lightning bolt and the highest point of the victim, often the head. “Side flash” involves the spread of electricity from the lightning bolt to a nearby object and then to the patient. Side flash victims are typically exposed to less voltage and current than with a direct strike. Finally, “stride current” involves the spread of electricity from the lightning bolt to the ground and then through contact points in the patient. Stride current patients are more likely to experience spinal cord injuries, as the current crosses through the spinal cord from one limb to another.

Neurologic Complications of Electrical and Lightning Injuries

Neurologic sequelae of electrical injuries affect both the central and peripheral nervous systems, with both immediate and long-term difficulties.

Immediate Effects

Immediate neurologic effects of electrical injuries are noted throughout the neuraxis. Ten percent to 50% of patients experience a brief loss of consciousness, as well as headache, retrograde amnesia, and confusion [18]. Patients with electrical and lightning injuries to the head may also suffer subarachnoid or parenchymal hemorrhages, particularly in the basal ganglia and brainstem [19]. In patients who suffer cardiac or respiratory arrest, posthypoxic encephalopathy may develop in “watershed” areas of the cerebral cortex. Less commonly, patients may present with cerebral infarction or a temporary cerebellar syndrome [19].

Catecholamine release may result in autonomic dysfunction, as evidenced by transitory hypertension, tachycardia, diaphoresis, vasoconstriction of the extremities, and fixed and dilated pupils [20]. Thus, lightning strike victims should receive full resuscitative efforts despite pupillary changes, as these may not indicate brainstem dysfunction. Lightning strike victims may also suffer “keraunoparalysis,” a self-limited paralysis more often involving the lower extremities, accompanied by a lack of peripheral pulses, pale and cold extremities, and variable paresthesias [19]. Keraunoparalysis is presumably due to localized vasospasm from catecholamine release.

Acute spinal cord injuries are also seen, particularly with stride current injuries. The spectrum of spinal cord injuries includes paralysis, spasticity, autonomic dysfunction, and, later, chronic pain and pressure ulcers [19]. Acute neuropathies are typically not seen with lightning strikes, but may be seen with electrical injuries in association with compartment syndromes, local burns, or vascular injury [21]. Both electrical and lightning strike victims are vulnerable to the subacute development of cataracts, while lightning strike patients are peculiarly susceptible to tympanic membrane rupture, vertigo, and hearing loss [22,23].

Delayed Effects

Delayed effects of electrical and lightning injuries may also span the neuraxis. Recognized neuropsychiatric effects include depression, posttraumatic stress disorder, fatigue, irritability, and memory and concentration difficulties [24]. Movement disorders have also been described, such as transient dystonias, torticollis, and parkinsonism [19]. Delayed ophthalmologic and otologic consequences include cataracts, conductive and sensorineural hearing loss, and vertigo [22,23]. Delayed autonomic dysfunction may manifest as reflex sympathetic dystrophy, presenting as a limb with burning pain, cutaneous vasoconstriction, swelling, and sweating [20]. Prolonged and permanent spinal cord abnormalities may become manifest in the delayed development of a myelopathy or a motor neuronopathy [14,25]. Peripheral neuropathies may result from compression due to scarring and fibrosis from the original injury or delayed ischemia due to vascular occlusion [26]. Peripheral neuropathies are more likely to occur in areas directly involved by the electrical current, but may also occur in limbs that were not seemingly in the current path [27].

Evaluation

Initial evaluation of the electrical- or lightning-injured patient involves assessment of the scene and evaluation of safety. Disconnect electrical sources before evaluating the patient. Contrary to conventional mythology, lightning-strike victims are not electrically charged and may be examined immediately.

Assessment of cardiopulmonary status is essential, as many victims suffer cardiopulmonary arrest and may recover well if CPR is initiated promptly. Cardiac arrhythmias and asystole commonly accompany these injuries, as does respiratory arrest due to passage of current through the brainstem respiratory centers. Stabilization of the spine is also essential, due to potential spinal cord injuries and fractures from falls.

Neurologic Examination

The neurologic examination should begin with assessment of the level of consciousness. Initially, many patients are
comatose, but this is often brief and followed by a period of confusion and amnesia, lasting hours to days [28]. Seizures are uncommon. The cranial nerve examination may reveal fixed and dilated pupils, blindness, papilledema, partial hearing loss, and tinnitus. Rupture of the tympanic membranes may also be present with lightning injuries to the head. Evaluation of the motor system for focal weakness and reflex changes may indicate cerebral injuries, myelopathy, or neuropathy. Cerebral lesions, due to hemorrhage or infarction, may result in contralateral hemiparesis. Spinal cord injuries are more common in the cervical region and produce paraparesis or quadriparesis. Peripheral nerve injuries in the immediate assessment are typically located in areas of extensive burns. Sensory loss is less frequent than motor deficits and is maximal in burned areas.

Laboratory Evaluation

Laboratory evaluations should be focused on the known complications of electrical and lightning injuries. Serial determinations of electrolytes, renal function, and hematocrit are essential for assessing adequate fluid replacement. Serum creatine kinase and urinary myoglobin are useful measures of muscle necrosis. Arterial blood gases may reveal a metabolic acidosis. Electrocardiogram (ECG) and cardiac monitoring are used in patients with cardiopulmonary arrest or with known current pathways through the thorax, as delayed cardiac arrhythmias may develop. Radiologic examinations of the long bones, spine, and skull are indicated when fractures or deep burns are suspected based on the history and physical examination. Magnetic resonance imaging (MRI) or myelography may be used to assess spinal cord damage if signs of myelopathy are present. Cranial imaging is indicated when there is prolonged alteration of consciousness and may reveal intracranial hemorrhages, cerebral edema, or the effect of diffuse cerebral hypoxia. The electroencephalogram (EEG) is also useful to rule out status epilepticus in patients with prolonged unconsciousness. The EEG background may remain slow even when the mental status has returned to baseline. Nerve conduction studies and electromyography may be useful in localizing and following axonal and demyelinating electrical injuries to the peripheral nerves and plexi, although they are not generally used in the acute evaluation.

Management

Evaluation and treatment of medical concerns are essential for good neurologic recovery. Efforts should focus on circulatory volume, hydration status, renal function, acidosis, and electrolyte balance. Because high-voltage electric shock victims usually have myoglobinuria secondary to burns and deep tissue injury, their fluid needs are similar to those of crush injuries. Central venous pressure monitoring is usually needed, and urine output should be maintained at greater than 50 mL per hour. Alkalinization of the urine and osmotic diuresis with mannitol also help to prevent myoglobin nephropathy.

Extensive burns due to direct current or clothing ignition are best treated in specialized burn units. At times, skin grafts are required. Debridement of necrotic muscle and fasciotomy are sometimes necessary to prevent secondary ischemia from a compartment syndrome. Amputation is required if there is significant necrosis. In these patients, arteriography may assist in identifying the level of viability. Tetanus prophylaxis and prevention of superinfection are also needed. Spine and long-bone fractures require stabilization.

Recurrent seizures are treated with phenytoin (18 to 20 mg per kg loading dose followed by 5 to 7 mg per kg per day). Other antiepileptics, such as levetiracetam, could also be considered. Because fluid restriction is contraindicated, patients with signs of increased intracranial pressure require osmotic diuresis with mannitol. Intracranial pressure monitoring may be useful in patients with cerebral edema. Specific treatment for electrical spinal cord injuries is not available, and early institution of physical therapy is recommended. In patients with cardiac arrest, the hypothermia protocol could be considered.

Prognosis

Prognosis is difficult to ascertain for electrical injuries to the nervous system. Patients with deficits at presentation frequently recover fully, whereas those with delayed onset of neurologic deficits may have syndromes that progress over months to years.

Carbon Monoxide Poisoning

Carbon monoxide is a colorless, tasteless, odorless gas that may give no warning of its presence. It is normally present in the atmosphere in a concentration of less than 0.001%, but a concentration of 0.1% can be lethal [29]. Carbon monoxide is found in automobile exhaust, fires, water heaters, charcoal-burning grills, methylene chloride, volcanic gas, and cigarette smoke. It is also endogenously formed from the degradation of hemoglobin, resulting in baseline carboxyhemoglobin saturation between 1% and 3% [29]. Smoking can raise the endogenous level to 6% to 7% saturation [29]. Carbon monoxide poisoning may occur in the acute and chronic setting. For further information on the pathogenesis, diagnosis, and treatment of carbon monoxide poisoning, see Chapter 64.

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