(1)
Division of Pulmonary and Critical Care Medicine, Eastern Virginia Medical School, Norfolk, VA, USA
Keywords
SeizuresStatus epilepticusDilantinLevetiracetamBenzodiazepinesNon-convulsant status epilepticusSeizures in the ICU
Seizures are common neurological complications in medical and postsurgical ICU patients and commonly arise from coexisting conditions associated with critical illness. Most seizures occur in ICU patients who did not have prior seizures or neurologic pathology as part of the primary admitting diagnosis. In general ICUs, metabolic abnormalities have been reported to account for 33 % of seizures, drug withdrawal for 33 %, drug toxicity for 14.5 %, and stroke for 9–39 % [1]. Hypoglycemia should always be excluded as this is imminently treatable and delayed diagnosis is associated with significant neurological injury. Status epilepticus as an admitting diagnosis is much less common than seizures occurring as a complication during the course of critical illness [2]. Most seizures that occur in the ICU setting manifest as generalized tonic-clonic convulsions.
It is important to emphasize that “all that shakes” is not a seizure [3]! Abnormal movements and “jerkiness” are common in ICU patients especially those with delirium. The distinction between seizures and abnormal movements is crucial as anti-epileptic drugs (AEDs) are not indicated in those with abnormal movements and can cause further sedation and delirium in an already susceptible patient population. Seizures are unlikely in patients with jerking movements who are alert and responsive; these patients should NOT be treated with AEDs. In cases of diagnostic uncertainty bedside EEG-video recordings and a neurology consult are recommended. Benbadis et al. reviewed EEG-video recordings obtained for “possible seizures” in 52 ICU patients [3]. In this study only 14 patients (27 %) had epileptic seizures. Tremor-like movements, multifocal myoclonic jerks, and other abnormal movements were diagnosed in the 73 % of patients without seizures.
Seizures Occurring as a Complication of Critical Illness
(a)
Drug/substance toxicity
Antibiotics
Carbapenems, esp. imipenem
Penicillins
Cephalosporins
Aztreonam
Fluoroquinolones
metronidazole
Antidepressants
Tricyclics
bupropion
Antipsychotics
chlorpromazine
Immunosuppressants
tacrolimus
cyclosporine
Other
Theophylline
Cocaine
Amphetamines
(b)
Drug/substance withdrawal
Alcohol
Barbiturates
Benzodiazepines
Opioids
(c)
Metabolic
Hypoglycemia
hypocalcemia
Hypophosphatemia
Hyponatremia
Renal failure
(d)
Eclampsia
(e)
Posterior reversible encephalopathy syndrome (PRESS)
Seizures from Primary Neurological Disease
“Primary” epilepsy with poor compliance (subtherapeutic AED levels)
Previous stroke
Acute ischemic stroke
Intracerebral hemorrhage
Intracranial tumor
Cortical primary
Cortical metastatic
Traumatic head injury
Cerebral sinus thrombosis
Encephalitis
Meningitis
Brain abscess
Non-infectious encephalitis
NMDA-receptor antibody
Paraneoplastic limbic
Anoxic-Hypoxic brain injury
Cerebral vasculitis
Management
Many seizures manifest as single, self-limited episodes. Such occurrences serve to alert the intensivist that a metabolic, drug or structural problems exists. The first step is to terminate the ictal activity followed by an evaluation as to the cause of the seizure. Neuro-imaging (CT scan) is always required to exclude a structural lesion even in the context of an identifiable metabolic/drug etiology. An EEG is required in patients who do not fully regain conscious (see Sect. “Status Epilepticus”) and in those patients whose level of consciousness is difficult to assess (due to sedation, underlying disease, etc.).
Seizure Therapy
Acute termination of ictal activity
Lorazepam 0.05–0.1 mg/kg
Midazolam 0.05–0.2 mg/kg
Treatment of underlying cause
Prophylaxis if risk persists (consult neurology)
Levetiracetam (drug of choice). Levetiracetam (Keppra) has distinct advantages over the other intravenous and oral anticonvulsants in the critically ill as it has few drug interactions and is usually well tolerated.
Valproic acid
Status Epilepticus
Status epilepticus is a relatively common condition. It accounts for 3–5 % of all ED admissions for seizure disorders and occurs in 2–16 % of all epilepsy patients [4]. Status epilepticus is a major medical emergency associated with significant morbidity and a mortality of up to 76 % in elderly patients with refractory status epileptics [5]. This clinical entity requires prompt management. The complications of status epilepticus include cardiac dysrhythmias, derangements of metabolic and autonomic function, neurogenic pulmonary edema, hyperthermia, rhabdomyolysis, and pulmonary aspiration. Permanent neurological damage occurs with prolonged uncontrolled convulsive activity.
Status epilepticus has previously been defined as continuous seizure activity lasting 30 min or as two or more discrete seizures between which consciousness is not fully regained [6]. Lowenstein, Bleck and Macdonald have proposed that status epilepticus be defined as a continuous, generalized, convulsive seizure lasting greater than five minutes or two or more seizures during which the patients does not return to baseline consciousness [7]. The rationale for this revised definition is based on the fact that a typical, generalized tonic-clonic seizure rarely lasts longer than 5 min, spontaneous termination becomes less likely in seizures greater than 5 min and the longer the seizure continues the more difficult the seizure becomes to control with antiepileptic drugs and the greater the degree of neuronal damage [8]. This definition is consistent with common clinical practice in which it would be unreasonable to wait 30 min before initiating antiepileptic drug therapy.
Refractory status epilepticus is usually defined as seizures lasting longer than 2 h, or seizures recurring at a rate of two or more episodes per hour without recovery to baseline between seizures, despite treatment with conventional antiepileptic drugs. However, from a clinical perspective it is preferable to consider refractory status epilepticus as any patient who has failed first-line therapy [8]. Status epilepticus may be classified by the presence of motor convulsions (convulsive status epilepticus) or their absence (non-convulsive status epilepticus). They may be further divided into status epilepticus that affects the whole brain (generalized status epilepticus) or only part of the brain (partial status epilepticus) [6]. Status epilepticus appears to be more frequent among males, blacks and the aged.
Etiology
In many patients with a pre-existent seizure disorder no obvious precipitating factor can be determined. A fall in serum levels of AEDs due to poor compliance with medications or due to increased clearance associated with concurrent illness has been implicated in some patients. Adult patients with a new diagnosis of epilepsy may first present in status epilepticus.
Common Causes of Status Epilepticus Include
Anti-epileptic drug non-compliance
Alcohol related
Cerebrovascular accidents
Drug toxicity
cephalosporins
carbapenems
penicillins
ciprofloxacin
tacrolimus
cyclosporine
theophylline
cocaine
Central nervous system infections
Meningitis
Encephalitis
Central nervous system tumors (primary or secondary)
Metabolic disturbances (i.e., electrolyte abnormalities, uremia)
Head trauma
Cerebral anoxia/hypoxia
Hypoglycemia
Pathophysiology
It is likely that ineffective recruitment of inhibitory neurons together with excessive neuronal excitation play a role in the initiation and propagation of the electrical disturbance occurring in status epilepticus. A growing body of basic science and clinical observation supports the concept that status epilepticus becomes more difficult to control as its duration increases. It is been postulated that this may occur due to a mechanistic shift from inadequate GABAergic inhibitory receptor-mediated transmission to excessive NMDA excitatory receptor mediated transmission [1]. Furthermore, as status epilepticus progresses, the GABAA receptors are internalized and become functionally inactivated, conferring benzodiazepine resistance, which is believed to be a major cause of treatment failure. This may explain why benzodiazepines (GABAergic receptor agonists) are very effective AEDs during the early period of status epilepticus however they become less effective as time passes [1]. In humans and experimental animals, sustained seizures cause selective neuronal loss in vulnerable regions such as the hippocampus, cortex and thalamus. The degree of neuronal injury is closely related to the duration of seizures, underscoring the importance of rapid control of status epilepticus.
Complications of Generalized Status Epilepticus
Systemic
Acidosis
Hyperthermia
Rhabdomyolysis
Renal failure
ArrhythmiasRelated posts:
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