An Approach to Neurologic Problems in the Intensive Care Unit

David A. Drachman

Neurologic problems present in the intensive care unit (ICU) in two modes: (a) primary neurologic problems, usually under the care of a neurologist or neurosurgeon, and (b) secondary neurologic complications, occurring in patients with other medical or surgical disorders. Only a handful of common clinical situations bring neurologists and patients together in the ICU, although they may be caused by myriad disease states [1]. These situations include:

Depressed state of consciousness; coma
Altered mental function
Required support of respirations or other vital functions
Monitoring of increased intracranial pressure (ICP), respirations, state of consciousness
Determination of brain death
Prevention of further damage to the central nervous system
Management of seizures or status epilepticus
Evaluation of a neurologic disease that occurs in the course of a severe medical disease
Management of a severe medical disease that develops in the course of a neurologic illness

Patients with primary neurologic problems most commonly have conditions with an identified cause, such as stroke, seizures, Guillain-Barré syndrome, head trauma, or myasthenia gravis. Such patients are admitted to the ICU for close observation and management of vital functions, such as respiration, control of ICP, or arrest of seizure activity. These patients represent the minority of neurologic problems seen in the ICU. Far more frequently the neurologist is called on to evaluate the neurologic complications of medical disease: impairment of consciousness in a patient who has undergone cardiopulmonary resuscitation, development of delirium in an elderly individual with a serious infection, or occurrence of focal neurologic deficits in a patient with a ponderous medical record that reveals long-standing diabetes, renal failure, hypertension, and pulmonary disease.

The questions posed to the neurologic consultant are often imperfectly framed. Background observations regarding the origin, onset, and course of the neurologic abnormality may be unavoidably sparse and the history unavailable. The classic neurologic methodology, which involves a comprehensive history and meticulous examination, is rarely possible in patients encumbered with endotracheal tubes, cardiac monitors, and indwelling arterial and venous lines. For these reasons, neurologists must adopt special strategies to function effectively in the ICU, focusing sharply on the specific question with which they are dealing.

Indications for Neurologic Consultation in the Intensive Care Unit

Depressed State of Consciousness

The patient with the most common of ICU neurologic problems—a depressed state of consciousness, ranging from lethargy to coma—raises a host of questions. Does the patient have a focal brainstem lesion or diffuse cerebral involvement? Is there an anatomic lesion or a metabolic disorder? Have vital brainstem functions been impaired? Is ICP increased?

The most common primary neurologic causes of depressed consciousness include head trauma, intracranial hemorrhage, post cardiac arrest anoxia-ischemia, and less commonly, inapparent seizures. The secondary conditions seen most often are metabolic, such as anoxia, drug intoxication, or diabetic acidosis. Sometimes the diagnosis is evident, as in head trauma; other times determination of the cause of depressed consciousness may present a diagnostic challenge, demanding a race against the clock to avoid irreversible changes. In every case, it is crucial to establish whether depressed consciousness is due to intrinsic brainstem damage, increased ICP, toxins, widespread anoxia or ischemia, or some other less common cause. It is particularly important to sort out rapidly the component(s) that may be treatable.

Examination of the patient with depressed consciousness exemplifies some of the difficulties of neurologic care in the ICU. Details of this examination are described elsewhere [2]. Like the standard neurologic examination, however, it includes evaluation of mental status, cranial nerve functions, motor functions and coordination, reflexes, sensation, and vascular integrity. The observations made must be used to answer the questions posed above, supplemented by appropriate laboratory studies when possible.

A detailed evaluation of memory and cognitive function is rarely possible in patients who are lethargic, and never possible in those who are stuporous or comatose. Instead, the physician must estimate the patient’s responsiveness. Can the patient say any words or respond to commands? Does the patient open his or her eyes? Does the patient groan in response to a painful stimulus or attempt to remove it in a purposeful way? What is the status of the vital functions? Is the respiratory pattern disturbed? The Glasgow Coma Scale score is a simple, but useful, way to document the patient’s sensorium [3].

Cranial nerve evaluations include determination of vision, done by observing how the patient follows a large object or a light, gazes toward right and left visual fields, or blinks to a visual threat. Pupillary size, equality, and responsiveness to light
are assessed. Corneal reflexes, cough, and vibrissal (nasal) reflexes are evaluated. “Doll’s eyes” (vestibulo-ocular) responses are determined by rotation of the head from side to side; if they are absent, ice water caloric testing can be carried out. Facial movements are assessed in response to painful supraorbital stimuli; the gag reflex is tested in the usual fashion.

Motor function is evaluated as completely as possible. All limbs are observed for spontaneous movement and symmetry as well as tremor or other adventitious movements. If no spontaneous movements take place, a pinch or other noxious stimulus can be used to observe purposeful defensive movements. Decerebrate (i.e., four-limb extensor) and decorticate (i.e., upper limbs flexor, lower limbs extensor) rigidity are observed. Tone is assessed passively for spasticity or rigidity. Deep tendon reflexes are checked in the usual way, working around restraints and intravenous tubing. Grasp, suck, snout, and plantar reflexes are evaluated.

Pain is often the only sensory modality that can be tested. The physician must determine whether withdrawal from pinch or pinprick is appropriately defensive or (in the lower extremities) merely part of an exaggerated extensor–plantar response with triple flexion (flexion at hip, knee, and great toe), which may be mistaken for purposeful withdrawal. Finally, the vascular status is evaluated by listening for bruits over the carotid and subclavian arteries, the vertebral arteries, and the orbits.

Such an examination reveals the patient’s state of consciousness, the integrity of brainstem reflexes, and the presence or absence of lateralizing or focal neurologic deficits. The value of the systematic (if limited) neurologic examination cannot be overestimated. For example, in a comatose patient, the finding of decerebrate rigidity that points to significant damage at the level of the pons may be more valuable than many laboratory studies, and unilateral weakness of limbs with ipsilateral hyperreflexia indicates a focal brain disorder rather than a diffuse metabolic problem.

Neurodiagnostic studies are often critical in the analysis of comatose patients in the ICU, but the patient’s immobility and dependence on life support systems present special difficulties. A neuroradiology suite that is distant from the ICU presents additional obstacles. It is frequently difficult to obtain a magnetic resonance imaging scan, computed tomographic scan, or arteriogram on a patient who is dependent on a respirator. Paradoxically, in patients with the most urgent problems, it is often least convenient to obtain the maximum amount of neurodiagnostic information. The decision that a patient is too sick to have the crucial study performed is often incorrect. In such desperate cases, risks must be taken to obtain life-saving information.

Management of the patient with depressed consciousness depends largely on the cause. Techniques for eliminating toxins, reducing ICP, and maintaining vital functions must be applied, depending on the diagnostic context (see Chapter 169).

Altered Mental Function

In patients who remain relatively alert, other organic disorders may affect mental function, producing an often perplexing variety of clinical patterns. These include confusion, delirium, aphasia, and isolated memory impairment. The first question for the physician is whether the patient’s abnormal mental function represents a recent change that is part of the present illness, or instead is part of a long-standing problem. It is also critical to note whether the change developed abruptly (e.g., after surgery or cardiac arrest) or if there is no known precipitating event; and whether it is improving, worsening, or stable.

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