Assessment of Impaired Consciousness

Neurologists and neurosurgeons have a singular aptitude for the assessment and correct interpretation of impaired consciousness. Because consciousness is often decreased in patients with acute CNS lesions,¹ a brief review of the processes underlying abnormal consciousness is warranted. One of the critical anatomic elements that maintain or, more strictly speaking, activate consciousness has been defined under the term ascending reticular activating system. This neuronal system, located in the caudal brainstem, connects to the thalamus. These synapsing fibers extend from the entry of the trigeminal nerve in the midpons to the thalamus, which in turn loops fibers to the cortex and back, thereby creating a thalamic-cortical circuitry. Coma can be expected when destructive or compressive lesions interrupt these synapsing fibers. Therefore, a structural lesion in the pons or mesencephalon can interrupt cortical stimulation and generate an altered state of consciousness. Common lesions are occlusion of the basilar artery, which causes ischemia of major portions of the brainstem; pontine hemorrhage involving the tegmentum; and compression of the brainstem from acute, mostly hemorrhagic cerebellar lesions.

The next level of interruption in this circuit is the thalamus, as long as lesions involve both thalami. Bilateral lesions in the thalamus are commonly due to infarcts resulting from occlusion of the top of the basilar artery, occlusion of the deep cerebral veins, extension of midbrain-pontine hemorrhage to the thalamus, or occlusion of thalamic perforators secondary to fulminant meningitis.

Lesions of the cerebral hemisphere (cortex or white matter) reduce alertness only if present bilaterally (e.g., anoxic-ischemic cortical laminar necrosis or massive demyelination in patients with acute disseminated encephalomyelitis). With unilateral lesions, the cause of impaired consciousness may be either a mass effect from shifting of tissue or associated hydrocephalus (e.g., cerebral parenchymal hematoma extending into the ventricular system).

These anatomic principles have been proved correct over many years and will help in understanding the patient’s level of consciousness. Any discrepancy should point to another cause or a confounding factor (e.g., depressed consciousness in an intoxicated patient with a hemorrhagic lesion without mass effect).

Thus, disturbances in arousal lead to diminished alertness. Altered arousal involves an altered state of awareness, and these two components are interrelated but sometimes dissociated. One can be awake and aware (normal vigilance), awake but not aware (persistent vegetative state), and not awake and not aware (coma or brain death).¹

Neurological examination starts with assessment of responsiveness of the patient, and the simple reaction to painful stimuli is often one of the most important tests. Absent eye opening, vertical eye movements, or blinking (locked-in syndrome) and absent motor response to a voice command lead to the application of noxious stimuli. These stimuli should be limited to three known and reliable stimuli (compression of the supraorbital nerve, nail bed, and temporomandibular joints). The response of the patient to these stimuli is the first step in determining the depth of coma (Fig. 24-1).

FIGURE 24-1 Examples of reliable noxious stimuli (see text).

There have been attempts to further grade impaired consciousness. The Glasgow Coma Scale (GCS) has been used widely, but limitations have been recognized (e.g., inability to assess verbal component in intubated patients, no assessment of brainstem reflexes). Alternative coma scales floundered mostly because they did not appreciate the essential components of clinical examination, the scales were too complicated to be useful in day-to-day practice, and many lacked rigorous validation. There has been a need for a more comprehensive, yet simple-to-use coma scale that would help in communication and monitoring of comatose patients.

We have developed and validated a new coma scale, the FOUR score, and tested it for accuracy when used by neurologists, emergency physicians, and medical intensivists.^3–5 We compared ratings by residents and nursing staff specialists from all intensive care units (ICUs) and found a high degree of agreement. In this scale (Fig. 24-2) there is no assessment of verbal response, which at least in the GCS, is more a measure of orientation than alertness. The FOUR score is more useful in intubated, critically ill patients. This scale identifies different levels of coma but also locked-in syndrome, uncal herniation, and brain death. The FOUR score can be summed, and the summed scores reasonably correlate with certain degrees of impaired consciousness (alert, 16; drowsy, 12; stupor, 8; coma, 4; brain death, 0). However, it is better to describe the separate components when communicating (e.g., “this patient with traumatic brain injury has his eyes open but does not track a finger, has intact pupil and corneal reflexes, localizes to pain, is intubated, and triggers the ventilator”).

FIGURE 24-2 FOUR score. Eye response: 4 = eyelids open or opened, tracking, or blinking to a command; 3 = eyelids open but not tracking; 2 = eyelids closed but open to a loud voice; 1 = eyelids closed but open to pain; 0 = eyelids remain closed with pain. Motor response: 4 = thumbs-up, fist, or peace sign; 3 = localizing to pain; 2 = flexion response to pain; 1 = extension response to pain; 0 = no response to pain or generalized myoclonus status. Brainstem reflexes: 4 = pupil and corneal reflexes present; 3 = one pupil wide and fixed; 2 = pupil or corneal reflexes absent; 1 = pupil and corneal reflexes absent; 0 = absent pupil, corneal, and cough reflex. Respiration: 4 = not intubated, regular breathing pattern; 3 = not intubated, Cheyne-Stokes breathing pattern; 2 = not intubated, irregular breathing; 1 = breathes above ventilatory rate; 0 = breathes at ventilator rate or apnea.

The FOUR score has been received well and is currently used or being piloted in ICUs. After initial assessment of the depth of coma, a more detailed examination follows, including a comprehensive assessment of brainstem reflexes, eye movements in particular. The eyes should be evaluated for spontaneous movement, position of the eyes with eyelid opening, and movement after turning the head or irrigation of the ear with cold water. Abnormal motor movements, pathologic reflexes, and tone are noted. With these neurological findings it should be possible to localize the lesion to three main parts of the brain—both hemispheres (or thalamus), the brainstem, or the cerebellum; key findings are shown in Table 24-1. These findings are then combined with findings on computed tomography (CT) and lead to a tailored differential diagnosis. Causes of impaired consciousness in patients in the NICU are mostly structural, secondary to postictal stupor, or, less commonly, due to acute metabolic derangements or the use of toxic substances, drugs, alcohol, or sedatives.

TABLE 24-1 Main Areas of Lesion Localization in Coma with Common Clinical Pointers

Assessment of the Airway and Need for Mechanical Ventilation

Management of the airway and mechanical ventilation is different in critically ill neurosurgical patients. First, many young patients admitted to the NICU have normal baseline pulmonary function, unlike patients routinely admitted to medical intensive care with exacerbation of chronic pulmonary problems or newly acquired pulmonary disease. Second, the mode of mechanical ventilation in acutely ill neurosurgical patients is often limited to intermittent mandatory ventilation or assist/control mode and much less often pressure control, inverse ratio or permissive hypercapnia, or prone ventilation. Third, ventilator dependency is much less common, and except for patients with high cervical cord injury or other polytrauma, most acutely ill neurological patients can later be weaned off ventilatory support.

As with any acute illness, expeditious securing of the airway is the main priority. An obstructed airway should be managed immediately, and one can assume that any amount of hypoxia in the injured brain could add further damage to the brain. Much of the injury, however, occurs outside the hospital setting, such as in a patient found face down, and failure to improve can be attributed to coexisting anoxic-ischemic brain damage.

Endotracheal intubation should be performed in patients who cannot protect their airway, in those who may have aspirated gastric contents, and certainly in those with decreased alertness during which airway obstruction may occur.

Depression of the level of consciousness is not an absolute indication for mechanical ventilation. Intubated patients with acute CNS disease are generally able to maintain efficient gas exchange. However, patients with abnormal breathing patterns that result in inadequate oxygen delivery and hypercapnia need to be mechanically ventilated. Noninvasive mechanical ventilation (BiPAP) is a reasonable option in many postoperative patients with marginal oxygenation.⁶ In any patient on mechanical ventilation, a “ventilator bundle” is ordered (head elevation 30 degrees; peptic ulcer and venous thromboembolism prophylaxis).⁷ Intubation after a seizure is not usually necessary if the airway is not obstructed.

Most patients with acute neurosurgical illness can be supported with intermittent mandatory ventilation and pressure support ventilation. Many patients can be quickly transitioned to a continuous positive airway pressure mode if there are few and clear secretions and no pulmonary infection, aspiration, or edema.

Early tracheostomy should be considered when prolonged mechanical ventilation is anticipated, but the timing of tracheostomy is controversial. Potential serious complications and cosmetic disfiguration should strongly influence this decision. At the same time, placement of a tracheostomy will lead to better patient comfort, more effective tracheal suctioning, and perhaps a decrease in the considerable risk for tracheolaryngeal stenosis from prolonged intubation. Tracheostomy may reduce pulmonary complications and shorten the ICU stay. Generally, tracheostomy is considered after 2 or 3 weeks of mechanical ventilation, but it could be performed much earlier in comatose patients with severe brain injury and no prospects for early recovery if continued ICU care is desired. However, the majority of patients with acute stroke or intracerebral hemorrhage are liberated from the ventilator within 2 to 3 weeks, and therefore tracheostomy should be postponed. Many ICUs have resorted to the use of percutaneous dilation tracheostomy (Ciaglia Blue Rhino), which can easily be done at the bedside. The major complication is loss of the airway and massive subcutaneous emphysema associated with tracheal perforation, but the procedure is safe in experienced hands when using bronchoscopy. In other patients, open surgical tracheostomy is combined with percutaneous endoscopic gastrostomy in the same setting.

Assessment of Volume Status and Blood Pressure

Very few patients admitted to the NICU are euvolemic, and correction of volume status is one the first steps in the management of critically ill neurological or neurosurgical patients.

Hypovolemia is a potential clinical problem in all patients with acute CNS illness. Hypovolemia triggers at least three physiologic pathways—antidiuretic hormone, renin, and norepinephrine—all facilitators of sodium reabsorption, but these mechanisms may not be sufficient. Failure to recognize the inability of patients with depressed consciousness to signal thirst may lead to rapid loss of intravascular volume. In addition, insensible losses associated with fever or emesis are commonly underestimated. Hypovolemia may go unnoticed for some time, until the patient is placed on mechanical ventilation with positive pressure support, which will result in reduction of venous return, decreased cardiac output, and hypotension.

Initial correction of hypovolemia should be done with crystalloids (normal saline). Glucose-containing solutions may precipitate increased lactate production and secondary brain injury.

Insensitive losses should be taken into consideration when calculating fluid deficits. Gastrointestinal losses average 250 mL/day, and evaporation of fluid through the skin and lungs accounts for losses of 750 mL/day. Fever increases evaporation and can lead to losses of 500 mL/°C above normal.

Monitoring of volume status should include laboratory values (Table 24-2), with serial body weight and fluid balance being the most practical indicators. Patient with adequate fluid balance should have a hematocrit of less than 55%, an osmolality of less than 350 mOsm, and a serum sodium concentration of less than 150 mEq/L. Any higher values should signal dehydration.

TABLE 24-2 Indicators of Volume Status in Patients with Acute Neurologic Illness

From Wijdicks EFM. The Practice of Emergency and Critical Care Neurology. New York: Oxford University Press; 2010.

Increased blood pressure is very common in patients with acute neurological injury. Hypertension has traditionally been explained as a stress response that exacerbates any preexisting hypertension or a compensatory (Cushing’s) response to global ischemia. It is common with acute lesions in the posterior fossa and may be accompanied by bradycardia. Causes of increased blood pressure, however, may include pain, anxiety, agitation, and bucking on the ventilator. Unsustained surging hypertension could increase cerebral edema, expand cerebral hematoma, and cause congestive heart failure.

Hypertension has been arbitrarily defined as systolic blood pressure of 180 mm Hg or greater and mean arterial blood pressure of 120 mm Hg or greater. There are very few data on the need for blood pressure control and the best pharmaceutical agents in patients with acute neurological illness. In most patients in the NICU, acute hypertension is treated with a labetalol bolus of 20 to 40 mg and hydralazine, 20 mg (when patients have significant bradycardia). Recalcitrant hypertension may be treated with nicardipine by titrating up from a starting dose of 5 mg/hr while closely monitoring for hours via an arterial line. Recently, a study in China suggested that aggressive lowering of blood pressure with urapidil and furosemide to a systolic pressure of 140 mm Hg is safe and may possibly reduce expansion of intracerebral hemorrhage.⁸ It remains very uncertain whether outcome is affected by this measure, however.

How to best manage blood pressure in patients with aneurysmal subarachnoid hemorrhage is not known. Most neurosurgeons feel comfortable only if systolic blood pressure is maintained at less than 180 mm Hg, particularly in patients with an unsecured aneurysm. The relationship between blood pressure and rebleeding has not been established. A recent study suggested that systolic blood pressure above 160 mm Hg is associated with an increased risk for rebleeding, but many of these studies have poorly defined rebleeding.⁹

Postoperative hypertension is best managed by treatment of pain (mostly fentanyl), hypoxemia, and volume overload, if present.¹⁰

Assessment of Infection Potential

Fever is a key clinical sign that mostly signals infection. Fever is also associated with poor outcome after ischemic stroke,¹¹ intracerebral hemorrhage,¹² and aneurysmal subarachnoid hemorrhage,¹³ but the pathophysiologic effects of increased brain temperature on neuronal function are not well understood.