Neurologic Assessment and Prognosis after Cardiopulmonary Arrest

Chapter 69


Neurologic Assessment and Prognosis after Cardiopulmonary Arrest image



Advances in cardiopulmonary resuscitation (CPR), emergency medical systems, and intensive care have been associated with increased rates of return of spontaneous circulation (ROSC) after cardiac arrest. The neurologic prognosis for survivors, however, remains poor. Approximately 80% of survivors are initially comatose. Of those who survive beyond hospital discharge, good neurologic recovery occurs in only 10% to 30%, and less than 10% resume their former lifestyle. The primary determinant of outcome in survivors of cardiac arrest is the degree of functional neurologic recovery. A wide spectrum of possible neurologic outcomes exists, ranging from brain death to complete recovery. Familiarity with the natural history of cardiac arrest and prognostic indicators of neurologic recovery is essential for clinicians in intensive care units (ICUs) in order to advise families about goals of further care that respect the patient’s preferences and values.


This chapter describes the natural history, clinical neurologic assessment, and prognosis of comatose survivors of cardiac arrest. Predictors of outcome are disease specific; prognostic indicators used for patients with cardiac arrest cannot reliably be applied to patients with coma from other causes, such as trauma, stroke, and toxic or metabolic derangements.



States of Consciousness after Cardiac Arrest


The central nervous system (CNS) is exquisitely vulnerable to ischemia and circulatory arrest. Brain injury from global ischemia or circulatory arrest is termed hypoxic-ischemic encephalopathy. Cognitive, motor, and sensory abnormalities develop and recover after cardiac arrest with tremendous variability in rate and degree. In general, when recovery occurs, brain stem functions return in a caudal-to-rostral progression. First to return are spontaneous respirations and other cranial nerve reflexes. This is followed by the appearance of extensor (decerebrate) posturing, then flexor (decorticate) posturing, and intermittent electrical cortical activity. Defensive motor or verbal responses and increasing levels of consciousness are last to appear. Level of consciousness is frequently used to gauge recovery in the ICU.


States of consciousness fall along a spectrum, with coma at one end and normal consciousness at the other. Patients who are in coma exhibit no responses to external stimuli other than reflexive behavior. Their eyes are closed and sleep-wake cycles are absent. Coma is usually prolonged—lasting for at least hours to days, but rarely permanent—eventually progressing either to death or to a higher level of consciousness. In the United States, brain death (death by neurologic criteria) refers to the irreversible cessation of whole-brain activity and is legally equivalent to cardiac death. Brain death is a clinical diagnosis whose cardinal features are coma, apnea, and absence of all other brain stem reflexes (Chapter 68). Those who recover from coma progress through a vegetative state, which is distinguished from coma by the presence of episodic eye opening and sleep-wake cycles. Patients in a vegetative state may turn their heads to auditory or tactile stimuli and may produce unintelligible sounds; however, they do not follow commands or exhibit purposeful movements, such as pulling a limb away from painful stimuli. When the vegetative state lasts for more than one month it is termed a persistent vegetative state, and when it lasts for more than one year it is termed a permanent vegetative state. Those who recover further enter a minimally conscious state, characterized by limited awareness of and responsiveness to their environment. In this state, patients inconsistently may track visual stimuli with their eyes, obey simple commands, reach for objects, and at times exhibit purposeful behavior such as crying or smiling. Although somewhat artificial, categorizing level of consciousness may be helpful in assessing the severity of brain injury and in charting the course of neurologic recovery.




Determination of Neurologic Prognosis after Cardiac Arrest


Predicting neurologic outcome after cardiac arrest is challenging. The only reliable predictor of good recovery is rapid awakening after resuscitation (i.e., within minutes to hours). Studies have focused primarily on predictors of poor outcome. Importantly, few studies have included patients treated with therapeutic hypothermia, which is now recognized as the standard of care. This section addresses traditional methods of prognostication and also covers what is currently understood about prognostication in cardiac arrest patients who have been treated with hypothermia.


Many studies have assessed predictors of outcome in the comatose patient after CPR. Most have been retrospective analyses of a cohort of patients. The outcomes measured have usually been overall patient survival and neurologic recovery. The degrees of recovery and level of neurologic function were defined similarly (Table 69.1). Predictors of outcome that have been studied include neurologic signs followed sequentially postarrest, circumstances of arrest, electrophysiologic studies, brain imaging, and biochemical markers.





Level of Consciousness


Assessment of level of consciousness begins with observation. Patients who exhibit spontaneous eye opening, verbalization attempts, moaning, tossing, reaching, leg crossing, yawning, coughing, or swallowing have a higher level of consciousness than those who do not. The examiner should next assess the patient’s response to a series of stimuli that escalate in intensity. The patient’s name should be called loudly. If there is no response, the examiner should stimulate the patient by gently shaking him. If this produces no response, the examiner must use a noxious stimulus, such as pressure to the supraorbital ridge, nail beds, or sternum, or nasal tickle with a cotton wisp. Responses such as grimacing, eye opening, grunting, or verbalization should be documented. Motor responses provide information not only about sensation and limb strength but also about level of consciousness. The examiner should note whether stimuli produce “purposeful,” or nonstereotyped limb movements—such as reaching toward the site of stimulation (“localization”). This implies a degree of intact cortical function. Stereotyped limb movements are generally mediated by brain and spinal reflexes and do not require cortical input. Examples include extension and internal rotation of the limbs (decerebrate posturing), upper extremity flexion (decorticate posturing), and flexion at the ankle, knee, and hip (“triple-flexion”).



Brain Stem Function


Brain stem integrity is assessed by examination of the cranial nerves. The pupillary light reflex involves cranial nerves II and III and evaluates midbrain function. Pupillary size, shape, and reactivity to light should be noted. The pupils are normally round, have equal diameters, and briskly constrict when illuminated. In general, abnormalities of the pupillary light reflex suggest a structural abnormality. However, drugs that are frequently administered during resuscitation and in the ICU may also affect the pupillary light reflex. Bilaterally fixed and dilated pupils are seen with brain death but also with anticholinergic medications, such as atropine. Hyperadrenergic states (e.g., pain, anxiety, cocaine intoxication) produce bilaterally large and reactive pupils. Reactive pinpoint (< 1 mm) pupils are observed with opioid usage or intoxication. Pupil size, shape, and reactivity might provide clues to the presence of intoxicants that might otherwise confound neurologic assessment.


Cranial nerve II (optic nerve) should also be evaluated by direct visualization. A funduscopic examination should be performed to look for signs of intracranial hypertension. Papilledema is swelling of the optic nerve head from increased intracranial pressure. It is almost always bilateral and may be accompanied by retinal hemorrhages, exudates, cotton wool spots, and ultimately by enlargement of the optic cup. Papilledema develops over hours to days. Its absence, therefore, does not imply normal intracranial pressure, especially in the acute setting. Pulsatility of the retinal veins strongly suggests normal intracranial pressure, whereas the absence of pulsatility is noninformative.


Eye position and spontaneous movements should be noted. Horizontal or vertical misalignment of the eyes should be documented as well as spontaneous roving or rhythmic and repetitive vertical movements. Regions of cortex in the frontal and parietal lobes (“eye fields”) mediate conjugate deviation of the eyes toward the contralateral side. Lateral deviation of both eyes therefore indicates a destructive lesion in the ipsilateral cortex or, as may be more common after cardiac arrest, an excitatory focus (seizure) in the contralateral hemisphere. Dysconjugate gaze is frequently seen in sedated patients and usually represents unmasking of a latent esophoria or exophoria. Roving or slow to-and-fro eye movements imply functional integrity of the brain stem. There is a high incidence of nonconvulsive seizures in comatose patients after cardiac arrest, and jerking movements of the eyes or a forced conjugate deviation may be the only clinical evidence of seizure activity.


If spontaneous eye movements are absent, then an oculocephalic response (“doll’s eyes”) should be sought by turning the head rapidly both horizontally and vertically. The oculocephalic reflex interrogates function of the vestibular nuclei (pons) and its connections to the ocular motor nuclei (midbrain and pons). This maneuver should not be performed on patients with known or suspected cervical spine instability. Normally the eyes move opposite the direction of head turning. If an oculocephalic response cannot be elicited, then an oculovestibular (“cold-caloric”) response is sought. First, the tympanic membrane should be visualized to ensure that it is intact and unobstructed. The head of the bed should be set at a 30-degree angle to align the patient’s horizontal semicircular canals parallel to the floor. Then, using an angiocatheter or a butterfly catheter without the needle, 30 to 60 mL of ice-cold water are instilled into the external auditory canal against the tympanic membrane. This inhibits the ipsilateral vestibular system and normally causes the eyes first to move slowly toward the ipsilateral ear and then to jerk quickly toward the contralateral ear. The initial slow response is mediated by the unopposed contralateral vestibular system in the brain stem, and the subsequent corrective nystagmus is mediated by the cortical eye fields. With bilateral cortical dysfunction and an intact brain stem, slow tonic deviation of the eyes toward the ipsilateral ear is observed and is not followed by contralateral nystagmus. Complete absence of any response indicates diffuse brain stem dysfunction and may be seen in cardiac arrest patients during late stages of transtentorial herniation, barbiturate intoxication, or brain death.


The corneal reflex evaluates cranial nerves V and VII (pons) and is tested by gently touching the cornea of each eye with a drop of saline or a cotton wisp and observing for bilateral eyelid closure. The cough and gag reflexes and spontaneous respirations are mediated by the medulla. The cough reflex may be evaluated by stimulation of the carina with a suction catheter. The gag reflex is tested by stimulation of the posterior pharynx (with a tongue depressor or cotton swab) or by gently tugging on the endotracheal tube. To determine whether spontaneous respirations are present, the patient should be observed for overbreathing the ventilator (i.e., breathing at a respiratory rate higher than the rate set for the ventilator) and pressure tracings should be examined for spontaneous (patient) effort. Breathing patterns are discussed later.

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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Neurologic Assessment and Prognosis after Cardiopulmonary Arrest

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