Neurological Emergencies In The Pediatric ICU

Harry Abram, M.D.; David Hammond, M.D.; Daniel Shanks, M.D.; and William Turk; M.D.
Drs. Harry Abram, David Hammond, Daniel Shanks, and William Turk
are from the Division of Neurology at Nemours Children's Clinic, Jacksonville, Florida
 and are on faculty of the Mayo Medical School.

Acute neurological symptoms are relatively common in infants and children. In many cases timely evaluation and therapy can prevent or reduce both morbidity and mortality from many neurological disorders. Management of acute neurological disorders in children often requires the simultaneous performance of many tasks including stabilization of vital functions, assessment of systemic and etiological factors, physical examination, and performance of diagnostic studies as a prelude to localization of the neurological insult and specific therapeutic intervention. This paper discusses management of three common neurological emergencies: status epilepticus, coma, and acute weakness and the role of neurophysiological testing and monitoring in the Pediatric ICU.

Status Epilepticus

Status epilepticus (SE) is a common neurological emergency estimated to have an incidence between 50,000 and 150,000 cases per year with the highest rates of occurrence in young children and the elderly. While mortality from SE in children is uncommon, there can be substantial acute and chronic morbidity which may be prevented by appropriate and timely therapy.

Traditionally status epilepticus is defined as continuous seizure activity lasting for 30 minutes or longer or intermittent seizures from which the patient does not regain consciousness. Any type of seizure may present as SE, although the most common presentation is generalized convulsive SE which is easily identified. SE can have a less dramatic presentation with minimal motor movement associated with unresponsiveness which has been called "subtle SE." The latter may be the initial presentation of the SE or evolve following prolonged convulsive SE. Nonconvulsive SE can also occur in absence or partial seizure disorders where the major manifestation may be a prolonged confusional state or repetitive focal tonic-clonic activity. Rarely pseudoseizures may present as apparent SE but usually can be differentiated by clinical assessment. If in doubt as to whether a patient is in a state of subtle convulsive or nonconvulsive SE, treatment should be guided by simultaneous EEG monitoring.

A number of precipitants of SE in children have been identified with fever and changes in antiepileptic drug regimen being most common. SE may also commonly be the initial presentation of an idiopathic seizure disorder. In the initial assessment of a patient with SE, potential precipitants should be identified as this may influence acute management. It should be noted that tumors and trauma are relatively infrequent causes of SE and usually easily identifiable. Thus, in the initial management of patients with SE, emphasis should be placed on stopping the seizure activity and assessing possible precipitants prior to automatically obtaining a CT or MRI scan.

When a child presents with suspected SE, the diagnosis should be confirmed and immediate monitoring of the ABC's of life support initiated. Simultaneously the patient should be screened for potential precipitants such as fever, trauma, preexisting epilepsy or systemic disorders. Blood samples should be obtained for serum glucose, electrolytes, calcium, CBC, anticonvulsant levels and toxicology screens. Glucose should be immediately assessed as IV access is obtained.

A number of AED's are useful in stopping status epilepticus and the most important principles are to: 1) use an AED that is effective for SE; 2) use an appropriate dose and route of administration; 3) know the pharmacokinetics and pharmacodynamics of the AED used; and 4) anticipate the potential side-effects of the AED, particularly respiratory depression or hypotension, so appropriate intervention can be initiated. A number of treatment protocols have been developed. In 1993 the Epilepsy Foundation of American convened a working group that published recommended guidelines that are the basis for most treatment protocols in use today¹ (See Table 1).

Of the available effective AED's for SE, most authorities initiate therapy with either diazepam or lorazepam. Both drugs quickly enter the brain and may be effective in several minutes. For stopping SE there is no convincing evidence that either benzodiazepine is more effective and their major side-effects of respiratory depression, hypotension and sedation are similar. However, diazepam is highly lipid soluble and is quickly redistributed to other tissues causing brain and serum concentrations to fall rapidly. Thus, the anticonvulsant effect of diazepam is short-lived and most patients will require immediate administration of a longer acting AED. For this reason, lorazepam, which has a longer duration of action up to 8-16 hours, is our preferred agent for treatment of SE.

Should the initial dose of either diazepam or lorazepam not stop the SE, it is usually repeated after 5 minutes. If the SE persists after a second dose of benzodiazepine (BZP) we then begin a second AED. Commonly used second AED's are phenytoin (PHT) and phenobarbital (PB). Either of these agents given in appropriate does will control SE, although they may take 10-30 minutes to be effective. Of the two AED's, PHT has become the preferred second drug due to its' relative lack of sedative side effects compared to PB. This is particularly important in assessing the patient after cessation of SE as many children who receive large doses of PB are often

lethargic for several days. This may make it difficult to determine if the child has an underlying acute encephalopathy as the precipitant or result of their SE. Traditionally, PB has been the third agent given in an initial dose of 10mg/kg with repeated boluses up to a cumulative dose of 40mg/kg or even higher according to some authorities.

Recently phosphenytoin (FPHT) has become available as a treatment option for IV therapy of SE. Phosphenytoin is a prodrug that is converted to PHT with a conversion half-life of 8 to 15 minutes. The major reported advantage of FPHT over PHT is a more favorable vehicle that does not contain propylene glycol and has a pH of between 8.6-9.0 as opposed to 11-12 for PHT. This allows FPHT to be administered in dextrose containing IV solutions at a more rapid rate. As the pH is more physiological there is less risk of soft tissue injury with extravasation at the IV site. The elimination of propylene glycol from the vehicle is thought to also reduce the incidence of hypotension. Both drugs are equally effective in stopping SE and selection between them should be based on ease of administration, side-effects and cost issues.

If SE has not stopped after administration of a BZP and PHT or PB the patient has usually been seizing for at least one hour. At this point SE may become life threatening. Options at this point are a continuous benzodiazepine infusion with either valium or midazolam², propofol, pentabarbital or general anesthesia with halothane or isoflurane and neuromuscular blockade. An intravenous preparation of sodium valproate has recently been marketed, but has not been approved for treatment of SE.

The cornerstone of treatment for SE remains appropriate doses of intravenously administered medications. However, in some situations, intravenous access cannot be obtained and other routes must be considered. Rectal diazepam given as a liquid solution (IV formulation) is rapidly absorbed within ten minutes and achieves potentially therapeutic serum levels. Lorazepam is poorly absorbed rectally and generally is not efficacious this route. Intramuscular administration of Valium produces lower serum levels than rectal administration and is not effective in the treatment of SE. PHT should not be given IM due to crystallization and discomfort at the injection site with erratic and delayed absorption. However, PPHT can be administered IM and produce therapeutic levels within 30 minutes, although the absorption is slower than when administered IV. There is little information regarding the efficacy and safety of intraosseous infusion of AED's and this route should be used only when other routes are not available. Intranasal adminstration of midazolam has been suggested as an effective route of administration and is being further evaluated.

Over the past several decades the morbidity and mortality of SE in children appears to have decreased. Aicardi and Chevrie³ in 1970 reported 11% mortality and frequent permanent neurological morbidity in children with SE. Review of their report and many subsequent reports^4-5 suggest that outcome in SE is primarily a function of the etiology of the status. In the absence of an acute severe or progressive neurological disorder the morbidity and mortality of SE is very low.^6-7

Coma

Coma and altered consciousness can be caused by a large variety of disorders which alter central nervous system (CNS) function. Consciousness requires intact function of the cerebral hemispheres. Coma can occur in processes which adversely affect both of the cerebral hemispheres directly or with dysfunction of the ascending reticular activating system (ARAS). The ARAS is an ill-defined group of neurons extending from the rostral medulla to the midbrain which has a primary role in arousal of the cerebral cortex. Whereas large bilateral lesions are required to produce coma in the cerebral hemispheres, small lesions in critical areas of the brainstem may produce pronounced changes of consciousness.

There is a continuum of altered consciousness and this can be subdivided depending on the degree of severity. Plum and Posner⁸ subdivide this continuum into clouding of consciousness, delirium, obtundation, stupor and coma. While specific definitions have been suggested for each of these states, they are not uniformly applied and easily confused. Thus, for clinical management and communication we encourage clinicians not to rely on single word descriptions of a patient with altered mental status. Instead, the patients' state should be carefully described including: orientation, verbal output, eye opening and response to environmental stimuli. Useful in quantitating these observations is the Glasgow Coma Scale which measures and provides a numerical score for three parameters: motor responses, eye opening and verbal response. Developed to look at outcome in patients with head trauma, the GCS should be cautiously applied as a prognostic measure in patients with metabolic or toxic CNS insults.

The evaluation and management of coma should be approached as a medical emergency. First, medical stability should be ensured. Unless the possibility of trauma can be excluded, the cervical spine should remain stabilized until appropriate radiological evaluation excludes injury. Further evaluation ensues as a combination of history, physical examination and treatment which must occur concurrently and requires a team of caregivers.^9-10 When the cause of coma is known (e.g. medication ingestion, near drowning, etc.) work-up is more limited and treatment can be immediately focused.

The differential diagnosis of coma is extensive and can be divided into the following broad categories: metabolic, infectious, parainfectious, trauma, epilepsy, and vascular. An extensive discussion of all the entities is beyond the scope of this paper. The most important causes will be highlighted to provide a basis for evaluation of a comatose patient.

Various metabolic disorders can produce altered levels of consciousness. Hyperglycemia is seen in diabetic ketoacidosis and history of diabetes is generally readily available. However, this can occur as the presenting feature of insulin dependent diabetes. Hypoglycemia can be seen in a variety of conditions¹¹. Other metabolic derangements include hypernatremia, hyponatremia, hyperammonemia, uremia and carbon monoxide poisoning. The latter should be considered in victims of smoke inhalation and when multiple individuals from a given environment are symptomatic. The possibility of medication ingestion should be considered in toddlers as an accidental phenomenon, and in older individuals as suicide attempts. Acute lead intoxication produces encephalopathy and seizures, especially in preschool age children.

Infectious etiologies include meningitis and encephalitis. The constellation of fever, seizures and encephalopathy should be considered encephalitis until proven otherwise. If there is strong clinical suspicion of acute bacterial meningitis or sepsis based upon the initial history and examination, broad-spectrum intravenous antibiotics should instituted immediately.

The presentation of coma due to trauma usually has an apparent history and physical evidence, however, shaken baby syndrome may present with little external evidence of trauma. Head CT scan will show areas of intracranial bleeding. In the absence of adequate history of trauma, complex skull fractures and retinal hemorrhages are diagnostic of child abuse¹².

Once stabilized, the initial studies to be done consist of basic chemistries, blood gas, ammonia, screen for toxins, complete blood count, and blood culture. Because the standard toxin screen varies among laboratories, it is important to know which compounds are assayed by your lab. The lab should be notified if a specific toxin or medication is suspected. When indicated, carbon monoxide, serum lead level and tests for inborn errors of metabolism can be considered. Although many of the tests for inborn errors will not be helpful in the acute management, some of these disorders are intermittent and evaluation is more informative when performed during a symptomatic period.

Neuroimaging should be done, except when medical instability jeopardizes transport or an established diagnosis suggests otherwise. Head CT is often the initial study of choice. CT is readily available, quickly performed and is very sensitive for intracranial hemorrhage, skull fractures and hydrocephalus, but may not visualize early infarcts, encephalitis or posterior fossa pathology. A brain MRI scan, which better defines the pathology, can be performed electively at a later stage. Intravenous antibiotic administration should never be held pending neuroimaging if meningitis is suspected. Lumbar puncture should be strongly considered if the patient is stable and there is no evidence of increased intracranial pressure, but may be deferred pending neuroimaging results.

Acute Paralysis

Acute weakness in children is seen in a wide variety of disorders. At the time of presentation, the clinical approach involves: a) stabilization of cardiopulmonary function; b) localization of the site of dysfunction within the neuraxis; c) diagnostic testing as indicated by (b); and d) supportive and specific treatment. A number of reviews are available.^13-15

Localization can usually be approximated by history and exam. The presence of marked asymmetry of weakness, upper motor neurons signs (increased tone, hyperreflexia, and extensor plantars), and/or focal cranial nerve or sensory signs suggest central nervous system disease, as distinct from disorders of the motor unit (anterior horn cell, peripheral nerve, neuromuscular synapse, and muscle). While subacute myelopathy typically results in upper motor neuron signs, acute myelopathy often presents with lower motor neuron signs (flaccidity, diminished or absent reflexes, and mute or flexor plantars). A myelopathy is further strongly suggested by the occurrence of a sensory level and bowel and bladder sphincter dysfunction, although sensory abnormalities may be mild if the anterior cord is predominantly affected. If a myelopathy is suspected, magnetic resonance imaging (MRI) of the relevant region of the spinal cord must be performed promptly to identify lesions requiring neurosurgical intervention in order to optimize the chances for recovery of function. Motor unit disorders, the subject of the remainder of this section, are suggested by bilateral weakness, with lower motor neuron signs, and the absence of marked sensory and bowel and bladder changes. The more common disorders include: anterior horn cell dysfunction due to enteroviral infection; peripheral nerve involvement by acute inflammatory demyelinating polyradiculoneuropathy (AIDP; Guillain-Barre syndrome); neuromuscular transmission defects including myasthenia, botulism, and anticholinesterase poisoning; and inflammatory, electrolyte, and ion channel disorders of muscle.

The enteroviruses coxsackievirus and echovirus may produce a syndrome virtually identical to that caused by poliovirus, the latter now very rare. Upper respiratory or gastrointestinal symptoms are followed by myalgias, and a rapidly progressive, asymmetric weakness with lower motor neuron signs. Cerebrospinal fluid (CSF) pleocytosis of approximately 50-200 cells / microliter, present within several days, helps distinguish the disorder from AIDP. Viral culture or serology can confirm the diagnosis.

Complications of enteroviral anterior horn cell dysfunction, as well as some of the other disorders discussed below, include respiratory failure and aspiration due to bulbar involvement. In contrast to primary pulmonary disease, in motor unit respiratory weakness clinical evaluation and arterial blood gases may not be sensitive enough to detect incipient respiratory failure, which may evolve over a matter of hours. Serial measurement of vital capacity and inspiratory and expiratory pressures, as adjuncts to clinical monitoring, are more sensitive. While the respiratory care of each patient must be individualized, a progressive fall in pulmonary function indicates the possible need for intubation even before hypoxemia or hypercapnea have developed. A decline in vital capacity to less than 15 ml / kg body weight has been suggested as a criterion for intubation. When bulbar involvement results in swallowing difficulty, steps should be taken to prevent aspiration pneumonia .

The most common cause of severe acute weakness in children is AIDP. In about 50% of cases, an infection, surgery, or other immunologic stressor precedes onset of weakness by a matter of weeks. Essentially symmetric weakness, which typically ascends from the distal lower extremities but may begin in the arms, reaches its maximum within two to four weeks. Facial weakness, which may be asymmetric, occurs in approximately half of the cases, with swallowing difficulties in a smaller percentage. Sensory symptoms, especially paresthesias and pain, are generally mild. Diffuse areflexia is the rule, although distal areflexia with hyporeflexia at biceps and patellar tendons may be seen in milder cases. Two disorders that mimic AIDP include porphyria and tick paralysis. Laboratory findings in AIDP include elevated CSF protein, without pleocytosis after the first week. Nerve conduction studies show conduction block and slowed conduction velocities, and are often abnormal before the elevation of CSF protein. Patients should be closely monitored in an intensive care unit because of the risk of respiratory insufficiency and of autonomic dysfunction. In addition to supportive care, immunotherapy with plasma exchange or intravenous immunoglobulin is given if there is loss of independent ambulation or respiratory insufficiency.

Disorders of neuromuscular transmission include myasthenia gravis. While typically presenting with the subacute development of fatiguable weakness, myasthenia may present as acute generalized weakness when insults which otherwise would have a minor impact on neuromuscular transmission are superimposed. These include acute intercurrent illness; certain medications such as aminoglycoside antibiotics, phenytoin, anticholinergics, procainamide, and succinylcholine; metabolic disturbances including hypermagnesemia, hypocalcemia, and hyper- or hypokalemia; and surgery. Nerve conduction studies, including repetitive stimulation, are helpful acutely in localizing the disorder to the neuromuscular synapse. When positive, the presence of aceytlcholine receptor antibodies confirms the diagnosis. Amelioration of the weakness by edrophonium (Tensilon), a rapidly acting acetylchloinesterase inhibitor, is suggestive, though not diagnostic, of myasthenia. Respiratory support (see above) and immunotherapy with plasma exchange are the mainstays of immediate treatment.

Organophosphate pesticide poisoning, which may occur via oral ingestion or skin penetration, impairs cholinesterase, leading to excessive acetylcholine at muscarinic and nicotinic sites. Prominent muscarinic symptoms are an important clue to the diagnosis: vomiting, diarrhea, abdominal cramps, sweating, hypersalivation, lacrimation, blurred vision, broncho-constriction, arrhythmias, shock, and changes in mental status. At the neuromuscular junction, depolarizing blockade results in diffuse weakness, often with fasciculations. Decreased erythrocyte acetylcholinesterase activity confirms the diagnosis. Muscarinic complications are treated with atropine, while pralidoxin reactivates acetylcholinesterase in most cases.

It is important to correctly diagnose botulism, another disorder of the neuromuscular synapse, since specific antitoxin is available. In infants, the symptoms of poor feeding, constipation, listlessness and hypotonia are unfortunately nonspecific, so a high index of suspicion is required. A history of ingestion of potentially contaminated foodstuff, in particular honey, supports the diagnosis. In older children, nausea and vomiting followed by visual changes and dysphagia are important diagnostic clues. Decreased pupillary response to light and ophthalmoparesis occur in some but not all cases. In both infantile and childhood cases, respiratory insufficiency often occurs prior to extremity weakness (see above). Treatment includes respiratory support and antitoxin.

Myopathic causes of acute weakness include electrolyte disorders, ion channel dysfunction, and inflammatory muscle diseases. Hypokalemia severe enough to cause significant weakness has been associated with diuretics, amphotericin B and laxatives. Hyperkalemia may result in weakness when potassium levels are in excess of seven mEq / liter. Poorly nourished patients who develop severe hypophosphatemia (less than one mg / dl) are often profoundly weak. Disorders of skeletal muscle sodium channel (potassium-sensitive or hyperkalemic periodic paralysis) and calcium channel (hypokalemic periodic paralysis) present in childhood with acute weakness. Clues to the diagnosis of a channelopathy include an autosomal dominant family history, the transient nature of the weakness, recurrence of similar episodes, and onset after a period of rest or sleep. Diagnosis is aided by measurement of serum potassium level, nerve conduction studies and EMG, and provocative tests. Dermatomyositis and polymyositis may present with acute weakness. Erythema and edema of the periorbital area and the extensor surfaces provide an important clue to dermatomyositis. However, fulminant cases may present with fever, myalgias, and arthralgias, but no rash, with the subsequent development of weakness. Elevations of creatine kinase, antinuclear antibodies, and typical EMG abnormalities support the diagnosis of inflammatory muscle disease. Immunotherapy is with high-dose corticosteroids.

Neurophysiology In The ICU

The role of neurophysiology in the ICU is characterized by advancing technology and expanding uses. An EEG is a recording of the brain's electrical activity. It is linked to cerebral metabolism and is a highly sensitive indicator of cerebral dysfunction. There are four main areas where the EEG can be of value in the ICU: 1) assisting in diagnosis; 2) guiding therapy; 3) monitoring the central nervous system; and 4) establishing a prognosis.

In diagnosis, the EEG can have several roles particularly in encephalopathic or comatose patients. The EEG will distinguish true coma from psychogenic coma or apparent coma from a locked-in syndrome. In both of these cases, the EEG will reveal a normal awake pattern. The EEG is useful in defining the depth and cause of toxic-metabolic encephalopathies. Certain patterns may indicate a specific etiology. For example, excessive fast activity is common in overdose of sedative-hypnotic medications and a pattern of triphasic waves is seen with hepatic dysfunction and less commonly with renal failure and anoxia. Herpes Simplex encephalitis, often a very difficult diagnosis to make early in a patient's course, has a very characteristic pattern of periodic sharp waves localized to the temporal lobe. An EEG should be obtained early in any patient suspected to have this diagnosis. Finally, the EEG is extremely useful in identification of non-convulsive status epilepticus, particularly when the cause of an acute confusional state or coma is not apparent and there are no clinical features to suggest seizure activity¹⁶.

In addition to diagnostic utility, EEG can assist in other decision making. In status epilepticus, EEG monitoring can help avoid under treatment and overtreatment. Undertreatment may lead to metabolic acidosis, rhabdomyolysis and neuronal death. Overtreatment is common and may result in iatrogenic respiratory failure and cardiovascular collapse. Often critically ill patients have involuntary and semipurposeful movements, which might mimic a seizure. These include tremors, myoclonus, spasms, and posturing. The EEG is useful in distinguishing these movements from epileptic seizures. In addition, EEG guidance is required for barbiturate-induced "burst suppression" coma which has been used for management of refractory increased intracranial pressure.

In the ICU, careful monitoring of the cardiovascular and pulmonary status is routinely performed in-patients with various catheters, transducers, digital readouts and alarms. The goal of such monitoring is to extend the powers of observation in order to detect deterioration at a reversible stage so that appropiate intervention can occur. However, the brain is only monitored by "neuro checks" which are subjectively performed on an intermittent basis predominantly by nursing staff. This is often inadequate, for if an abnormality is noted, such as a unilateral dilated pupil, intervention is often too late. The difficulties of such clinical monitoring are amplified when sedative medication and neuromuscular paralytics are given.

EEG has been a useful monitor of the central nervous system when the patient is not easily clinically assessed and has been proven to detect potential injuries at a reversible stage. The EEG is very sensitive to ischemia and hypoxia and can detect neuronal dysfunction at a reversible point and furthermore is able to localize, to a certain degree, the area of pathology. EEG abnormalities begin when cerebral blood flow drops to 20-25 ml/100 g/min. Cell death does not occur till flow falls below 12 ml/100 g/min. This window underlies the value of EEG monitoring in carotid and cardiac surgery where changes in the EEG can warn the surgeon and anesthesiologist of critical drops in cerebral perfusion. Similar applications exist in ICU patients with acute intracranial ischemic or hemorrhagic events in which cerebral blood flow may be precarious.

The role of EEG in the intensive care unit is gaining increasing attention as the need to more effectively monitor the nervous system is recognized. However the complexity of EEG monitoring can be intimidating for the non-neurologists. Newer methods for simplifying the data have included digital EEG, compressed spectral analysis and topographic brain mapping. These allow the vast amount of complex data to be simplified, easily retrieved, and rapidly reviewed even by non-neurologists. However expert EEG supervision must be readily available as a multitude of pitfalls can transpire which can seriously limit the validity of the data recorded. Digitalized real-time EEG best meets the current logistical challenges of the ICU. Current hard drives can easily store over 24 hours of continuous EEG data, thus eliminating the reams of paper which were required in the past. This data can easily be remotely transmitted, in a real-time fashion, to offsite monitors where it can then be reviewed by a neurologist.

Reliable and early prediction of neurological outcome remains a challenge for the intensivist especially following an hypoxic-ischemic event. It would be ideal to distinguish between hopelessly ill patients where further intensive care is expensive and futile, from those where vigorous treatment might result in a reasonable outcome. An ideal predictor would be objective, reproducible, non-invasive, portable, independent of therapies, and be accurate with negligible false pessimism. EEG and evoked potentials have many of these attributes.

Evoked potentials commonly performed in the ICU include brainstem-evoked potentials (BAER's) and somatosensory evoked potentials (SSEP's). BAER's are a collection of waveforms produced by the central auditory pathway which are highly resistant to sedative medications and neuromuscular paralytic agents. SSEP's are a series of potentials recorded from the brainstem and cerebral cortex following stimulation of a peripheral nerve such as the median nerve. They are able to assess a larger portion of the nervous system than a BAER and are also negligibly affected by sedative medications.

Brainstem evoked potentials have a limited role in assessing prognosis, in that only a small portion of the neuroaxis, the central auditory pathway, is monitored. Cortical function is not reflected, and patients with profound cortical injury, hence a poor outcome, may have normal BAER's. In addition, peripheral hearing must be assured. Thus in patients with pre-existing severe deafness or in head trauma victims who might have suffered cochlear injury, absence of BAER's may be attributed to peripheral factors. However, in all other settings, absence of BAER's is indicative of severe structural brainstem pathology and a strong prediction of a poor outcome.

Somatosensory evoked potentials are of greater prognostic value then BAER's in that both brainstem and cortical function are assessed. Absence of cortical SSEP's bilaterally is an accurate and reliable marker of widespread cortical necrosis and remains one of the best prognostic rules: outcome will be persistent vegetative state at best.¹⁷ In addition, unlike BAER's where a normal study has no predictive value, normal SSEP's should be reassuring and encourage continual vigorous treatment. Electroencephalography has a more established role in prognosticating in the ICU and more commonly performed. The integrity of both cortical and subcortical structures is assessed. A normal or near-normal EEG is suggestive of a favorable outcome. In addition, the presence of sleep activity and the demonstration of reactivity to environmental stimuli are generally favorable indicators. Other patterns, such as an isoelectric pattern or burst suppression pattern are of grave significance. Though very sensitive to clinical deterioration, the main limitation of EEG in the ICU is lack of specificity. Hypothermia and sedative medications may artificially mimic a grave prognostic pattern. The prognostic value of EEG is increased if the etiology of coma is known, it is performed at least six hours after cerebral injury, if sedative medications are minimized, and the abnormalities persist on serial recordings.

There has been debate whether EEG and EP's provide superior indicators of prognosis when compared to the history and exam. These studies can provide important independent objective evidence and can corroborate or refute clinical impressions. These studies must not be used in isolation, and should be placed in context with the entire clinical picture.

In summary, EEG and evoked potentials can be very helpful in the ICU when the clinical evaluation of a patient is difficult, especially those at risk for neurological deterioration, when the etiology for an altered state of consciousness is unclear, and when early objective prognostic indicators are sought after central nervous system injury. Advances in technology, especially digitalized computerized EEG, has made such monitoring feasible and more readily available.¹⁸

REFERENCES

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September, 1998/ Jacksonville Medicine

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