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.

Fever develops in 25% to 50% of NICU patients. Fifty-two percent of fevers were explained by an infectious etiology, with pulmonary pathology being most predominant.¹⁴ Infectious causes should be aggressively sought (chest radiograph; blood, urine, and sputum cultures), but noninfectious causes of fever may occur and include reaction to blood products, deep venous thrombosis (DVT), drug fever, postsurgical local tissue injury, pulmonary embolism (PE), and central fever with its extreme autonomic storms (episodes of profuse sweating, tachycardia, tachypnea, and bronchial hypersecretion). Subarachnoid hemorrhage, intraventricular hemorrhage, and posterior fossa surgery can lead to a sterile inflammatory meningitis characterized by a progressive increase in cerebrospinal fluid (CSF) white blood cell counts and hypoglycorrhachia. Penicillins and phenytoin are the most common causes of drug-induced fever.¹⁵ DVT occurs in 9% of NICU patients and should be monitored with lower extremity ultrasonography.

The systemic inflammatory response syndrome may be diagnosed when fever is associated with tachypnea, tachycardia, or leukocytosis in the absence of detectable infection.¹⁶

Pneumonia is the most common nosocomial infection in critically ill neurological patients, and approximately half of all nosocomial infections are associated with mechanical ventilation. The rate of pneumonia increases 5- to 20-fold in intubated patients and with the duration of mechanical ventilation.¹⁷ Empirical antibiotic therapy is typically used at the first signs of infection. In general, early infections (<3 days) require coverage for Staphylococcus aureus, Haemophilus influenzae, Streptococcus pneumoniae, and nonpseudomonal gram-negative rods. Patients with late infections require double coverage for resistant Pseudomonas or Acinetobacter and treatment with vancomycin for methicillin-resistant S. aureus. Treatment should be modified after culture and sensitivity results are available. The duration of treatment with an effective agent should range from 7 to 14 days.

Urinary tract infections commonly develop after chronic indwelling bladder catheterization. After 10 days, nearly 50% of all catheterized patients have significant bacteriuria.¹⁸ Because asymptomatic bacterial colonization is extremely common, treatment should be reserved for patients with pyuria (>10 cells/mm³) and fever and leukocytosis. Early uncomplicated urinary tract infection can be treated with sulfamethoxazole/trimethoprim or fluoroquinolone for 7 days. Treatment should be guided by the results of culture and sensitivity testing. Changing the catheter before treatment of infection may reduce the rate of secondary infection.¹⁹

Ventriculostomy-related infection is rare, with the incidence of ventriculostomy-related meningitis or ventriculitis being approximately 8%.²⁰ A combination of ceftazidime and vancomycin is the preferred regimen for empirical coverage. The infected catheter should be removed and treatment given for a minimum of 14 days.

Initial management of fever includes the administration of acetaminophen, but even high doses may not be effective. Currently, fever is aggressively treated with water-circulating cooling pads, and a feedback mechanism in the device secures a constant core temperature. A clinical trial comparing a simple cooling blanket with administration of acetaminophen for controlling fever found a 30% failure rate with both modes of treatment.²¹ The use of cooling pads with constant temperature control was shown to be superior to simple cooling blankets for the management of fever.²²

Assessment of Seizures

Acute injury to cortical structures can elicit seizures. Seizures may be focal or generalized, single or continuous. Patients with a new hemispheric mass may be susceptible to the development of epilepsia partialis continua or generalized status epilepticus. Most frequently, seizures occur within the first days after injury. Repeated seizures without recovery of consciousness constitute status epilepticus, which is a neurological emergency and thus needs to be treated aggressively. Tonic-clonic status epilepticus is commonly defined as repetitive seizures without full recovery between episodes, usually with seizure intervals of 5 to 10 minutes. Status epilepticus may begin with adversive movements of the head and eyes, flexion of the ipsilateral arm, extension of the ipsilateral leg, and repeated vocalizations. Over time, both the tonic and clonic phases decrease in duration in patients with continuing seizures, and they may even fade into solitary multifocal twitches in all limbs. Status epilepticus remains a difficult diagnosis to make and hard to differentiate from postictal stupor. Emergency electroencephalography (EEG) is needed before proceeding with the use of second-line agents such as propofol or midazolam.

Seizures may affect other systems and cause cardiac and pulmonary complications. Rhabdomyolysis may potentially lead to acute renal failure if not recognized. Metabolic (lactic) acidosis occurs because of excessive muscular contraction, which results in depletion of glycogen and anaerobic glycolysis and thus the promotion of lactic acid formation from pyruvic acid (Fig. 24-3).

FIGURE 24-3 Systemic effects of status epilepticus.

Nonconvulsive status epilepticus is very difficult to diagnose and is probably less common. It frequently follows a clearly defined generalized tonic-clonic seizure or occurs in elderly patients with a major irreversible brain injury. Clinical hallmarks are a decrease in the level of consciousness or fluctuation in responsiveness. Patients may have fluttering of the eyelids or eye deviation as the only signs of nonconvulsive status epilepticus.

Management of seizures begins with aspiration precautions. Respiratory support with manual bagging is commonly sufficient, but progression to status epilepticus requires mechanical ventilation and placement of a central line.

Benzodiazepines—in particular, lorazepam—are the preferred first-line drugs for acute control of tonic-clonic seizures. Lorazepam terminates seizures in more than 80% of patients.²³

Intravenous administration of phenytoin or fosphenytoin usually follows treatment with benzodiazepines. Newer alternative drugs such as levetiracetam have fewer side effects and are now available as intravenous and oral formulations. Data are insufficient to use levetiracetam for the treatment of status epilepticus, but it remains a preferable drug in patients with single seizures. The recent Food and Drug Administration acceptance of intravenous levetiracetam (15-minute intravenous infusion of 1000 mg) may increase its role in the treatment of refractory status epilepticus, but levetiracetam has been effective mostly in patients with nonconvulsive or focal status epilepticus.

Failure of lorazepam and fosphenytoin in adequate doses to control seizures indicates transition to refractory status epilepticus. The different approaches for refractory status epilepticus have seldom been compared in a prospective controlled study. At this point, either increasing doses of barbiturates or midazolam should be used for treatment.²⁴ Propofol is another alternative, but high doses are needed. Propofol infusion syndrome, or sudden cardiovascular collapse with metabolic acidosis, is a serious complication that limits the routine use of this otherwise very effective medication.²⁵ Drugs used for seizures and status epilepticus are presented in Table 24-3.

Assessment of Nutritional Needs

Early feeding of the gut to ensure adequate nutrition is part of daily care. Outcome studies in patients with severe strokes and head injury suggest that early nutritional support reduces mortality and the incidence of nosocomial infections.^26–28 The main goal of nutrition should be to preserve muscle mass and provide adequate fluids, minerals, and fats.^29,30

Malnutrition should be recognized during emergency admission of patients with severe head injury or fulminant meningitis, conditions that are more prevalent in alcoholics and illegal drug users. Vitamin B₁ (thiamine) deficiency might lead to the development of Wernicke-Korsakoff syndrome (confusional state, horizontal and vertical nystagmus, gaze palsy, and ataxia of gait). Intravenous administration of thiamine (100 mg intravenously initially and then 100 mg daily for 5 to 7 days) prevents the development of Wernicke-Korsakoff syndrome after carbohydrate loads.

Malnutrition causes significant lung malfunction by impairing the respiratory muscles, decreasing the respiratory drive, and diminishing lung defense mechanisms. At the same time, overfeeding with excessive carbohydrate calories may lead to hypercapnia, which reduces the success of weaning. Caloric needs can be estimated by weight and approximate 25 to 30 kcal/kg per day. The nutritional needs of patients with critical neurological illness should be calculated with the Harris-Benedict formula to obtain the basal energy expenditure (BEE) in calories. The Harris-Benedict equations are based on weight in kilograms, height in centimeters, and age in years. For men, BEE = 66.5 + (13.75 × weight) + (5.003 × height) − (6.775 × age), and for women, BEE = 655.1 + (9.563 × kg) + (1.850 × cm) − (4.676 × age).

The integrity of the gut is maintained by enteral feeding and greatly challenged by parenteral nutrition. It is prudent to consider postpyloric feeding in patients with neurological catastrophes because gastric atony increases the risk for aspiration. However, drug absorption in the jejunum may be unreliable. Enteral feeding should preferably be carried out by continuous infusion with a volumetric pump. Current protocols recommend that feeding start at 25 mL/hr and the volume be increased by 25 mL/hr every 4 hours until the goal of nutrition is achieved.³¹ In patients with a gastric residual volume of greater than 250 mL, feeding should be withheld for 4 hours and then restarted at the same rate but with a more gradual increase. Problems with enteral feeding are frequent and include diarrhea, nausea, and abdominal distention.

Gastrostomy placement should be considered in patients with a prolonged need for enteral nutrition because of impaired swallowing mechanisms. Gastrostomy should also be considered if recovery from dysphagia is not anticipated for 2 to 3 weeks.

Parenteral nutrition is rarely used in the NICU. It is much more complex, has the potential for more complications, and requires close monitoring of laboratory values. Energy requirements are again estimated with the Harris-Benedict equation. Mechanical or metabolic complications occur in about 50% of patients undergoing parenteral nutrition.

Assessment of Prophylaxis and Need for Anticoagulation

Patients with acute brain injury and hemiparesis have a higher incidence of DVT because of lack of mobility of the affected limb. Clinically apparent DVT was reported in 2% to 5% of patients with ischemic stroke,^30,32 whereas subclinical DVT occurred in 28% to 73%, mostly in the paralyzed extremity.³³

No observational studies are available to clarify the incidence of DVT in patients with intracerebral hemorrhage. One study demonstrated that DVT was detected at day 10 in 16% of patients wearing elastic stockings alone.³⁴ In another study, 5% of patients with intracranial hemorrhage died of PE within the first 30 days.³⁵

Only general recommendations can be made for postoperative neurosurgical patients. The most recent consensus statement published by the American College of Chest Physicians in 2004 recommended mechanical methods (intermittent pneumatic compression with or without elastic stockings) as the standard of care.³⁶ The use of unfractionated heparin was left to the discretion of the physician, but the use of low-molecular-weight heparin was discouraged.³⁶ Only one randomized clinical trial compared low-dose unfractionated heparin with no prophylaxis in craniotomy patients and found an 85% reduction in DVT in heparinized patients.³⁷

The use of DVT prophylaxis in patients with traumatic head injury is another challenging situation. Several studies have tried to address the safety of anticoagulation in patients with recent hemorrhagic contusions. One study demonstrated no increased risk for hemorrhage in patients treated with unfractionated heparin within 72 hours.³⁸ Another comprehensive study of 150 patients with hemorrhagic traumatic brain injury tested enoxaparin, 30 mg twice daily subcutaneously, starting 26.5 ± 11.5 hours after head injury. Overall, 23% of the patients demonstrated progression of the hemorrhagic lesion on CT. Nineteen percent had enlarging lesions before anticoagulation, but only 4% demonstrated an increase after initiation of anticoagulation. In 8% of patients who underwent craniotomy, hemorrhagic complications developed and required reoperation.³⁹ These studies emphasize the potential dangers with the use of unfractionated heparin, and no definitive recommendation can be made.

Full anticoagulation is indicated for patients with cardioembolic strokes, acute DVT, or PE. It might be considered in patients with critical stenosis or acute occlusion of the carotid artery.⁴⁰ Anticoagulation is used frequently in patients with high-grade basilar artery stenosis or recent basilar artery occlusion despite a virtual lack of any evidence of effectiveness. Anticoagulation is resumed in patients with a mechanical heart valve and recent cerebral hematoma, usually after a 10- to 14-day interval.

The weight-based nomogram for the use of intravenous heparin has been shown to be more effective than the standard-care nomogram.⁴¹ Heparin boluses are not recommended in neurological patients because of the increased incidence of intracerebral hemorrhage. The activated partial thromboplastin time (aPTT) is used to monitor heparin therapy closely, with values ranging from 1.5 to 2.0 times the baseline aPTT (50 to 75 seconds) being recommended. Bleeding is possible at any location with heparin but frequently occurs in the gastrointestinal tract as a result of stress ulcers. Bilateral adrenal hemorrhage might be manifested as sudden shock without any evidence of overt blood loss.⁴² Retroperitoneal hemorrhage should be considered in patients with a rapid decrease in hematocrit, in those with labile blood pressure, and especially when a recent cerebral angiogram or endovascular procedure has been performed. Thrombocytopenia secondary to the development of heparin-induced antibodies is another well-established complication. It is usually delayed by 5 to 10 days after the initiation of heparin therapy and might be associated with hemorrhagic and ischemic complications.^43,44

Assessment of Intracranial Pressure

Intracranial pressure (ICP) is tightly controlled. According to the Monro-Kellie model, overall intracranial volume is constant because of the rigidity of skull, which does not permit any expansion. An increase in the volume of any component leads to a compensatory decrease in other components or eventual displacement of brain tissue through the tentorial opening or foramen of Magnum and possibly brainstem displacement and loss of brainstem function. Several compensatory mechanisms may prevent this complication. First, CSF may shift from the ventricular or subarachnoid space into the spinal compartment. Second, reduction of intracranial blood volume is achieved by collapse of veins and dural sinuses and by changes in the diameter of cerebral vessels. If the limits of the compensatory mechanisms are exceeded, a minimal increase in intracranial volume will lead to a precipitous rise in ICP (Fig. 24-4).

FIGURE 24-4 Pressure-volume curve. Zone 1, fully compensated for an increase in volume; zone 2, failing compensatory mechanisms with a slow rise in intracranial pressure (ICP); zone 3, exponential rise in ICP indicating absent compensation with shifting of brain tissue occurring.

Autoregulation is usually severely impaired in patients with acute neurological injury. Severe diffuse traumatic brain injury, aneurysmal subarachnoid hemorrhage, diffuse brain infection, or any type of bilateral global cerebral injury may virtually eliminate any autoregulation and thus compensatory mechanisms for control of ICP.

Monitoring of ICP is an integral function of the NICU. Indications for placement of ICP monitors include a coma from severe traumatic brain injury, and massive cerebral edema from infarction. ICP can be reduced by decreasing total intracranial volume, which is achieved by withdrawal of CSF via ventricular drainage, reduction of cerebral tissue volume (osmotic dehydration), or removal or decompression of an intracranial mass.⁴⁵

Head position should be neutral to reduce any possible compression of the jugular veins. Head elevation of 30 degrees is considered standard.⁴⁶ Patients should be made comfortable, and pain, bladder distention, and agitation should be avoided because these factors might increase ICP.

The patient should be maintained in a euvolemic state. Hypovolemia caused by fluid restriction does not have an impact on ICP but may result in hypotension and unnecessary risk to already compromised brain tissue.

Hyperventilation is one method of reducing ICP. Hypocapnia causes cerebral vasoconstriction, which in turn reduces cerebral blood flow. This effect is maintained for several hours, after which it becomes ineffective because of compensatory rapid buffering of alkalotic CSF.⁴⁷ Moreover, monitoring of brain tissue oxygenation has demonstrated that even a small reduction in PCO₂ causes a decrease in cerebral oxygenation in comatose patients.⁴⁸ Aggressive hyperventilation might thus decrease cerebral blood flow to levels approaching ischemia. Consequently, hyperventilation should be used only as a bridging measure while other means of ICP control are being instituted.

Osmotic diuresis is the mainstay of medical therapy for elevated ICP. The most widely used diuretic agents for the treatment of increased ICP are mannitol and hypertonic saline. The basic mechanism of this intervention is transport of extracellular water to the intravascular space.⁴⁹ Mannitol not only facilitates the movement of extracellular water but also might increase CSF absorption. This osmotic gradient remains the overriding mechanism, but other mechanisms of action are increased cerebral blood flow from transient hypervolemia and hemodilution resulting in a decrease in blood viscosity.⁵⁰ Cerebral blood volume, however, remains much the same as the result of a compensatory reflex vasoconstriction of the cerebral arterioles. Mannitol is typically used in a 20% solution, and the agent is excreted through the kidneys. The initial dose is 1 g/kg, which is then tapered to 0.25 to 0.5 g/kg. Rarely, higher doses (up to 2 g/kg) are needed to reduce ICP. The effect is apparent within 15 minutes, and failure to respond to mannitol is a sign of poor compliance and failing compensatory mechanisms. Not infrequently, it is a reason for decompressive surgery to allow more volume expansion within the skull. The maximal effect lasts about 60 minutes. The adverse reactions of mannitol, including congestive heart failure and profound pulmonary edema, are a result of rapid intravascular expansion.

Failure of mannitol to control ICP should lead to a trial of hypertonic saline. In a recent retrospective study, hypertonic saline was effective in 75% of patients deteriorating from increased ICP.⁵¹ Hypertonic saline can be administered only by central venous access, especially when given in more concentrated solutions. Brief hypotension, caused by a sudden reduction in peripheral vascular resistance in reaction to a sudden osmotic load, is the most common side effect of administration of hypertonic saline and can be avoided by slow administration lasting 10 to 15 minutes. No cases of central pontine myelinolysis were documented after treatment with a 23.4% solution.⁵¹ Cardiac arrhythmia is another potential complication of this treatment.

Failure to respond to osmotic agents might lead to the use of barbiturates. Barbiturates are useful in reducing ICP even in patients resistant to standard medical and surgical therapies. This treatment is far from benign, however, and is associated with multiple complications, including myocardial depression, infections, hypotension, and skin breakdown. Vasopressors are commonly needed to maintain blood pressure and cerebral perfusion pressure. Suppression of the EEG to the level of burst suppression is often needed to achieve adequate ICP control, and this requires high doses. Therapy is usually maintained for several days until stabilization of the clinical situation. Barbiturate therapy can be withdrawn slowly by reducing the infusion rate by 50% each day, but because of a very prolonged half-life, improvement in consciousness may not occur for 7 to 10 days.

Monitoring of Deterioration After Acute Brain Injury

One of the most distinctive tasks in the NICU is monitoring for neurological decline, and the burden is on the neurosciences nursing staff. Their assessment will lead to further evaluation and often initial measures to prevent further worsening.

Brain function can currently be evaluated with the use of monitors for ICP, brain tissue oxygenation, and microdialysis, and each of these devices may signal neuronal distress. Video-EEG monitoring may be used in patients with a fluctuating level of consciousness after a single seizure and to titrate antiepileptic drugs. However, most NICUs will have to rely on repeated expert neurological examination and neuroimaging.

Deterioration in a patient with an acute brain injury is disease specific but predictable. Examples are shown in Table 24-4. In many instances, neurological deterioration is due to further displacement of brain tissue and, eventually, brainstem displacement. A lateral shift in brain tissue distorts the thalamus and mesencephalon. These patients have a decline in consciousness (thalamus-mesencephalon). A unilateral fixed dilated (varying from a difference of 2 to 5 mm) pupil is seen early and can be followed by bilateral fixed pupils. The pontine reflexes remain intact. This course, however, can be mimicked by acute lesions in the thalamus that suddenly extend asymmetrically to the mesencephalon (e.g., a thalamic hemorrhage). Lesions in the cerebellum may produce compression of the brainstem, but more often at the pontine level. Most notable is a predominance of pontine signs with possible bilateral miosis and loss of both corneal reflexes and the oculocephalic reflex. Frequent episodes of bradycardia with or without hypertension may occur (Cushing’s sign). A mass located more centrally will distort the thalamus and mesencephalon in a vertical plane and cause fixed midposition (4 to 6 mm) pupils initially. Asymmetric compression of the mesencephalon with anisocoria and a larger pupil or an oval-shaped pupil on the side with the lesion may be seen. Motor responses vary from decorticate to extensor responses, sometimes even with variation throughout the day and no evidence of other signs of deterioration. In patients with a gaze preference toward the expanding mass, gaze may reverse as a result of thalamic compression. Brief episodes of periodic lateral gaze may occur. Further vertical displacement of the entire thalamus-mesencephalon pontine structure may take place, but only after the upper brainstem has been destroyed directly from compression. It may occur with bilateral thalamic compression as a result of diffuse brain edema. Patients who lose all brainstem reflexes generally lose their pontomesencephalic reflexes at onset and medulla function later. A common progression is the appearance of flaccidity and no motor response with loss of the pontomesencephalic reflexes and, finally, failure to trigger the ventilator indicative of brain death.

TABLE 24-4 Causes of Clinical Deterioration in Selected Disorders

Fluctuating consciousness with transient eye deviation and frequently eye fluttering may indicate seizures. There is evidence that seizures, when monitored 24 hours a day for several days after head injury, may be more common than appreciated, and in any such patient EEG monitoring is warranted. Patients with cortical ischemic and hemorrhagic lesions, encephalitis, and major tumor surgery are at high risk.

Serial CT remains the most useful method of monitoring structural CNS lesions. Portable CT may be even more helpful, but no comparative studies have yet been performed. CT is able to document enlargement of the ventricles, signs of a mass effect with further displacement of the pineal gland and septum pellucidum, obliteration of the basal cisterns and sulcal effacement, compression of the brainstem, and intraventricular extension of hemorrhage, among other signs of a changing lesion.

Conclusion

Care of critically ill neurological patients is not a simple combination of critical care and neurological assessment, but an amalgamated treatment plan that is specific for the cause of the injury. Surely, many of the intensive care principles apply to acutely ill neurological patients, but some specific interventions are available for this category of patients. There has been better understanding of medical and neurosurgical care of critically ill neurological patients. There has also been better understanding of the mechanisms of clinical deterioration and ways to recognize them. Our approach to critically ill neurological and neurosurgical patients is to avoid further injury, which might not only reduce recovery potential but also shift patients into a permanently disabled category.