Treating seizures in the intensive care unit (ICU) has much in common with treatment in the emergency department, but seizure care in the ICU branches out from acute assessment, emergent therapy, and triage to more prolonged care, in-depth diagnosis, prognostication, and definitive care planning. (See Approach to epilepsy)
The goal of therapy in the ICU is to suppress seizures and obtain a good patient outcome. The over-riding principle of ICU seizure care is that, barring therapeutic misadventure, the outcome ultimately is determined by how sick the patient is rather than by nuances of care. The ICU patient is subjected to factors that lower the seizure threshold. Although aggressive treatment with antiepileptic drugs (AEDs) reverses this, some conditions (e.g., end-stage organ failure) can only be treated by improving or compensating for decreased organ function. In acute renal failure, for instance, rapid recovery of function or emergent hemodialysis must occur if seizures are to be stopped. In cases in which recovery or replacement of function is not an option, such as status epilepticus and fulminant hepatic failure in patients who are not candidates for liver transplantation, physicians may still choose to follow treatment protocols for status epilepticus, although with little hope of ultimately affecting outcome.
Protocols for the treatment of status epilepticus are discussed elsewhere. Challenges to seizure care that are uncommon outside of the ICU include sepsis, acute brain injury, organ failure, and coma.
Seizures in the septic patient most commonly originate from hypotension, metabolic dysfunction, electrolyte disturbances, infection, or other factors directly related to the cause or consequences of the underlying disorder. In many cases, a patient may have an underlying predisposition to seizures, such as an old cerebral infarct, small-vessel vascular disease, or, less commonly, a neurodegenerative disorder.
As with all ICU patients, the focus should be on addressing the underlying cause or sequela of sepsis rather than on the seizures themselves. The specific choice of AED in these patients is not usually as crucial as the care with which the AED is given. These patients may be exquisitely sensitive to the hypotensive side effects of IV phenytoin or benzodiazepines, so these agents usually must be given much more slowly than in individuals who do not have sepsis. Interactions with steroid medications must be considered, if they have been prescribed. Finally, it is important to be aware of hepatic dysfunction in these individuals early in the course of treatment, as it may alter the choice of AED.
Seizures are frequently seen in patients with acute brain injury. Prophylactic therapy with an AED reduces the incidence of seizures, although only in the first week after acute head trauma.36 There has been some interest in investigating the use of AEDs to interfere with epileptogenesis and inhibit the development of spontaneous seizures after acute brain injury, but most of these studies have not yielded encouraging results. Studies of newer AEDs for cerebral protection, such as topiramate, are under consideration.
Other types of brain injury that are associated with a higher incidence of seizures include:
It is not common to administer prophylactic therapy to patients with these conditions, unless the risk of harm from a single seizure is quite high, such as with cerebral edema. The risks of administering AEDs to these individuals usually outweigh the benefits, but each patient must be considered individually.
Individuals with organ failure are common in the ICU. This group has a much higher risk of acute seizures. Considerations regarding therapy (especially the choice and dosage of AEDs) must be carefully considered with respect to the particular systems affected.
Survival in these patients is primarily dictated by the underlying causes of the conditions and how ill they are (e.g., the number of organ systems failing), rather than by the aggressiveness of seizure treatment.41 This applies whether the patient is experiencing convulsive or nonconvulsive status epilepticus, intermittent jerking movements, or impaired consciousness with EEG patterns suggestive of seizures. In the most ill patients, benzodiazepine use was statistically associated with an increased mortality, however.
Convulsive or definitive partial seizures usually should be treated with adequate levels of a single AED, with add-on therapy if necessary. Aggressive pharmacologic treatment of more nonspecific, generalized EEG patterns in these patients is not recommended, as it has not been demonstrated to improve clinical outcome.
The comatose patient provides a great challenge to clinicians, particularly in diagnosing and treating seizures. Mechanical ventilators, continuous sedation, and paralytic agents make it difficult to diagnose seizures, although one study has indicated that the prevalence of undetected seizures and status epilepticus is high.43 The threshold for ordering routine EEGs and bedside, continuous EEG monitoring should be low in these patients, particularly in the case of those with a history of epilepsy or a predisposition to it.
Therapy is aimed first toward suppressing clinical seizures. Then, suppression of electrographic seizures is accomplished, when possible. Escalating therapy to suppress interictal epileptiform activity on the EEG is generally considered counterproductive in these patients, however. Periodic lateralizing epileptiform discharges usually fall into this category, unless they evolve into frank clinical seizures. The risks of aggressive treatment (e.g., AED-induced hypotension, cardiac dysrhythmias, or rash) often outweighs potential benefits when isolated electrographic seizures are:
Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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