The cause of seizures in the neurosurgical intensive care unit (NICU) can be categorized as emanating from either a primary brain pathology or from physiologic derangements of critical care illness. Patients are typically treated with parenteral antiepileptic drugs. For early onset ICU seizures that are easily controlled, data support limited treatment. Late seizures have a more ominous risk for subsequent epilepsy and should be treated for extended periods of time or indefinitely. This review ends by examining the treatment algorithms for simple seizures and status epilepticus and the role newer antiepileptic use can play in the NICU.
Key points
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Although prophylaxis is often not recommended, prompt treatment of seizures, especially recurrent or prolonged, improves the clinical outcome.
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Seizures occurring in the neurosurgical intensive care unit (NICU) are of diverse structural causes and metabolic disturbances, each with a distinct risk of seizures.
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Several, but not all, new anticonvulsants hold promise as successful agents to treat NICU-related seizures.
Introduction
The neurosurgical intensive care unit (NICU) is a complex environment. Seizures occur more often in this unit than in general or other specialty ICUs, partly because of the patient population but also because of the enhanced neurologic monitoring undertaken in such units with specialty trained personnel. Both primary neurologic as well as non-neurologic causes of seizures may occur, often in combination, leading to complex clinical evaluations to ascertain the probable cause. Therefore, to avoid confusion and frustration, the neurosurgeon, neuro-intensivist, or consulting neurologist should have an algorithmic approach to the problem.
This topic is vast. In this review, the authors present the most common causes of seizures encountered in the NICU, suggest treatment algorithms, and end with the most recent information regarding the newest antiepileptic drugs (AEDs). The interested reader can find additional information in other review articles or specialized textbooks on this subject.
Introduction
The neurosurgical intensive care unit (NICU) is a complex environment. Seizures occur more often in this unit than in general or other specialty ICUs, partly because of the patient population but also because of the enhanced neurologic monitoring undertaken in such units with specialty trained personnel. Both primary neurologic as well as non-neurologic causes of seizures may occur, often in combination, leading to complex clinical evaluations to ascertain the probable cause. Therefore, to avoid confusion and frustration, the neurosurgeon, neuro-intensivist, or consulting neurologist should have an algorithmic approach to the problem.
This topic is vast. In this review, the authors present the most common causes of seizures encountered in the NICU, suggest treatment algorithms, and end with the most recent information regarding the newest antiepileptic drugs (AEDs). The interested reader can find additional information in other review articles or specialized textbooks on this subject.
Incidence
The incidence of seizures in the general ICUs ranges from 3.3% to 34.0%, depending on the ICU population and the detection method. When a routine electroencephalogram (EEG) is used, the incidence is lower than when continuous EEG monitoring is used. Varelas and colleagues reported that out of 129 emergent EEGs ordered in ICUs, 49 (38%) showed some ictal (12%) or interictal (26%) epileptiform activity. Independent variables predicting seizures in the ICU were age, cardiopulmonary arrest, and use of prolonged EEG for detection.
The specific patient population admitted to the ICU may also play a role. For example, in an NICU, 34% of patients had nonconvulsive seizures on continuous EEG, and 76% of them were in nonconvulsive status epilepticus (NCSE).
Cause and pathophysiology
Seizures in the NICU can be caused either by primary neurologic pathology or as a complication of critical illness ( Box 1 ). Although in general ICUs the latter may be more common, in neurologic and neurosurgical patients, structural pathology may be the leading cause. In several patients, however, both can be present. In this case, it is difficult to decide which one of the two is the major contributor, but correcting the nonstructural disorder usually brings seizures under control.
Neurologic pathology
Neurovascular
Ischemic stroke
Hemorrhagic stroke
Subarachnoid hemorrhage
Intracerebral hemorrhage
Arteriovenous malformation
Cerebral sinus thrombosis
Hyperperfusion syndrome
Tumor
Primary
Metastatic
Central nervous system (CNS) infection
Abscess
Meningitis
Encephalitis
Encephalitis (noninfectious)
Paraneoplastic limbic
N-methyl-d-aspartate–receptor antibodies
Nonparaneoplastic limbic
Voltage–gated K+ channel antibodies (VGKC/LGII)
Inflammatory disease
Vasculitis
Acute disseminated encephalomyelitis
Traumatic head injury
Depressed skull fragments
Cerebral contusion
Extra-axial hemorrhage
Subdural hematoma
Epidural hematoma
Hygroma (?)
Primary epilepsy
Primary CNS metabolic disturbance (inherited)
Complications of critical illness
Hypoxia/ischemia
Drug/substance toxicity
Antibiotics
Antiviral agents
Antidepressants
Antipsychotics
Bronchodilators
Local anesthetics
Immunosuppressives
Cocaine
Amphetamines
Phencyclidine
Drug/substance withdrawal
Barbiturates
Benzodiazepines
Opioids
Alcohol
Infection (febrile seizures)
Metabolic abnormalities
Hypophosphatemia
Hyponatremia
Hypoglycemia
Renal/hepatic dysfunction
The mechanisms by which nonstructural abnormalities induce seizures are, in many cases, unknown. Drugs precipitate seizures by either preventing γ-aminobutyric acid (GABA) binding to the GABA A receptor, such as with antibiotics, or via antagonism at the Na + channels, such as with the local anesthetics. Depending on the level of potassium, hyperkalemia may depolarize the neuronal membranes or inactivate the Na + and Ca ++ channels, leading to an increased threshold for membrane depolarization. Hyponatremia and low osmolarity, as a consequence of increased cellular edema and increased neuronal excitability, may also lead to seizures. During alkalosis, increased inward Na + and Ca ++ channel currents and during hypomagnesemia decreased N-methyl-d-aspartate receptor antagonism promote cell depolarization.
Seizures after stroke
Seizures after Ischemic Stroke
The most common cause of seizures in patients older than 60 years is ischemic stroke, although the overall risk is fairly low, ranging from 4.4% to 13.8% depending on the subgroups of patients included in the analysis and the follow-up period. These seizures can be divided into early (24 hours to 4 weeks, depending on the definition used by the study) and late (usually after the first 4 weeks). Early seizures occur in 1.8% to 15.0% of patients and are thought to be caused by excitatory or inhibitory alterations in the penumbral tissue. They are not associated with higher mortality at 1 month and 1 year or with an unfavorable functional outcome, as in a large recent registry from France. Thrombolysis with tissue plasminogen activator (t-PA), however, may lead to worse outcomes in 3 months in the group with seizures compared with the group without seizures. Additionally, patients receiving endovascular treatment and developing early poststroke seizures have worse outcomes and higher mortality compared with seizure-free patients. Late seizures (after 4 weeks) have been reported in 2.5% to 15.0% of poststroke cases and are thought to emanate from gliosis and the development of a meningocerebral cicatrix. These patients with late-onset seizures are at an almost 3 times higher risk for subsequent stroke.
Status epilepticus (SE) comprises one-fourth to one-sixth of poststroke seizures and is significantly correlated with infarcts in the posterior temporal region. Interestingly, if SE is the first epileptic manifestation after stroke, it is usually not followed by other seizures. If, however, SE follows early or late seizures, the chances are high that it will recur as SE or seizures. Using data from the Nationwide Inpatient Sample, Bateman and colleagues estimated that generalized convulsive SE developed in 0.2% of the acute ischemic strokes, in 0.3% of the intracerebral hemorrhages, and was associated with higher rates of adverse outcomes.
Management of patients with ischemic stroke and seizures in the NICU should not be different than that for seizures from other causes. The most recent guidelines from the American Heart Association and the American Stroke Association do not recommend prophylactic use of AEDs and recognize that there are few data pertaining to the efficacy of these drugs in the treatment of poststroke seizures. Some studies report protection from seizures with AEDs only during the period that these drugs are administered but have no carryover effect in preventing late-onset seizures following AED discontinuation. However, some patients may be at a higher risk for seizures, such as those with stroke after cardioembolism (seizures occurring within the first 24 hours), those with high admission glucose or after thrombolysis with t-PA, with large infarcts, cortical involvement or hemorrhagic component, with watershed distributions and affecting temporal and parietal branches of the middle cerebral artery (late seizures) or temporal and occipital branches of the middle cerebral artery (early seizures). Additional factors for poststroke seizures and a possible need for longer AED administration are preexisting dementia, late poststroke seizures (an independent predictor of epilepsy), and SE following poststroke seizures. In a study of 204 patients with stroke-related seizures, seizure recurrence was observed in 13.8% of the early seizure (<15 days), in 54.7% of the late-seizure (1–24 months), and in 34.0% of the very-late-seizure (>24 months) group. Interestingly, 25% of the very late seizures were related to lacunar strokes and very mild disability.
Regarding the choice of AEDs, the available data are also not very helpful; randomized studies comparing AEDs to placebo for primary or secondary prevention of seizures are missing. New-generation AEDs, such as lamotrigine, gabapentin, and levetiracetam, in low doses would be reasonable choices, especially for elderly patients, because of their improved safety profile and fewer interactions with other drugs, including anticoagulants, compared with first-generation AEDs. Topiramate may have additional neuroprotective properties against cerebral ischemia, in contrast with phenytoin, barbiturates, and benzodiazepines, that may have a negative effect on recovery from stroke. Overall, poststroke seizures are usually easily controlled and monotherapy usually suffices.
Seizures after Intracerebral Hemorrhage
The risk for seizures is 2 to 7 times higher with intracerebral hemorrhage (ICH) than with ischemic stroke. This difference was evident in the study by Vespa and colleagues, whereby 28% of patients with ICH developed seizures despite being given prophylactic AEDs. Only 6% of those with ischemic stroke had seizures in the absence of AEDs.
The incidence of post-ICH seizures varies between 0% and 28%, with studies using continuous EEG monitoring (CEEG) reporting higher range percentages. In patients with electrographic seizures, CEEG will detect them within 1 hour in 56% and within 2 days in 94% of the time. Supporting cortical localization as a principal risk, lobar or subcortical ICHs have the highest incidence of seizures; those in the posterior fossa have almost zero. In a large Italian study, hyperlipidemia conferred a lower risk for seizures after ICH. After surgical evacuation of the hematoma, seizures occur even more frequently. In a study of 110 patients with evacuated thrombus, 41.8% of patients had seizures, 29.6% of which were clinical and 16.3% were electrographic. ICH volume, presence of subarachnoid hemorrhage (SAH) and subdural hemorrhage predicted early seizures; subdural hematoma and increased admission international normalized ratio predicted late seizures.
As with ischemic stroke, it is unclear if seizures should be treated prophylactically. The current guidelines suggest administration of AEDs only if clinical or electrographic seizures occur. They also recommend CEEG in patients with depressed mental status out of proportion to the degree of brain injury to detect them. Patients with alcoholism with ICH who have a 3-fold increased risk for SE should also be treated with AEDs that increase GABAergic inhibition (for example, benzodiazepines). If late seizures occur (after 2 weeks from onset), long-term AEDs should be prescribed because of the greater risk of epilepsy. However, it is unknown which AEDs should be used. In a prospective study of 98 patients with ICH, phenytoin (and not levetiracetam) was associated with more fever, worse National Institute of Health’s stroke scale at 14 days, and worse modified Rankin scale up to 3 months. Interestingly, even excluding the 7 patients who did have seizures from the analysis did not change the results.
Seizures after SAH
At the onset of SAH, many patients have motor manifestations and loss of consciousness, which may not be seizures but represent opisthotonos or posturing from acute hydrocephalus or loss of cerebral blood flow momentarily. However, early seizures in 1.1% to 16.0% and late seizures in 5.1% to 14.0% of patients with SAH have also been reported. In a recent review of 25 studies with 7000 patients, early postoperative seizures occurred in 2.3% and late postoperative seizures in 5.5% of patients (on average 7.45 months after the bleed). Late seizures were more likely with middle cerebral artery aneurysms, Hunt/Hess grade III, and clipping. Because rebleeding from an unprotected aneurysm during seizures is a serious concern, most neurosurgeons prefer to administer AEDs until the aneurysm is secured. However, rebleeding may also manifest as a new seizure. Therefore, if there is a prolonged change in the neurologic status or new blood in the ventriculostomy after a seizure, imaging of the brain should be considered. Because CEEG detects NCSE in 8% of patients with SAH, it should be used in those NICU patients with otherwise unexplained coma or neurologic deterioration after SAH or if sedated. In a recent study from Sweden, 7% of sedated patients had seizures, and one was in NCSE for 5 hours.
The therapeutic management of the ruptured aneurysm may also correlate with the incidence of seizures. Coiling, theoretically, may be associated with a lower risk for seizures because of less cortical injury. In a large prospective study, no seizures were witnessed in the periprocedural period (within 30 days) and only 1.7% patients developed late de novo seizures. Further data from the International Subarachnoid Aneurysm Trial have shown a relative risk for seizures of 0.52 with coiling compared with clipping. However, others have found that treatment of only unruptured aneurysms with clipping was associated with a higher risk of seizures or epilepsy compared with coiling, but this difference was not evident in ruptured aneurysms.
The evidence for prophylactic use of AEDs is not compelling. Some experts advocate withholding AEDs on several grounds in the early period because many seizures are unpreventable (occur at onset or during the prehospital period). AED use may precipitate fever, and their use has been correlated to a worse Glasgow Outcome Scale–measured outcome, higher incidence of cerebral vasospasm, neurologic deterioration or cerebral infarction, as well as cognitive and functional disability with phenytoin. Additionally, early perioperative seizures are not predictive of subsequent epilepsy, and such seizures do not lead to a worse outcome after a minimum 1-year follow-up. Others, however, advocate AED use for patients with onset seizures (given only during the hospitalization period), rebleeding, subdural hematoma or cerebral infarction at any time point, thick subarachnoid clot, or just periprocedurally but not after coiling of the aneurysm. In a recent review, a 3-day treatment seems to provide similar seizure prevention with better outcome than longer treatment. The American Heart Association’s most recent guidelines support prophylactic AEDs in the immediate posthemorrhagic period and routine use of AEDs only in patients with high risk for delayed seizures, such as prior seizure, intracerebral hematoma, intractable hypertension, infarction, or middle cerebral artery aneurysm.
It is also unclear which AED should be preferred when seizures occur. Most of the data are derived from phenytoin use, an AED that can reduce the bioavailability of nimodipine, a drug frequently used in these patients. Despite fewer available data, newer AEDs may have a similar or improved profile.
The recently reported association of cortical spreading depolarizations (recorded via electrocorticography) with delayed ischemic neurologic deficits despite the absence of vasospasm, opens new horizons in our understanding of electric epiphenomena after SAH. The clinical improvement with hypertension in patients with SAH and vasospasm may also be related to spreading depolarizations, because, in animals, a reverse correlation between spreading depression and blood pressure has been reported.
Seizures and Cerebral Venous and Sinus Thrombosis
Seizures are very common after cerebral venous and sinus thrombosis, occurring in 29% to 50% of patients, frequently as an inaugural manifestation. Early seizures (within 2 weeks from onset) occur in 34% to 44% of patients and are predicted by presenting seizures, motor or sensory deficits, parenchymal lesion on admission (hemorrhage, infarct, focal edema), and the presence of cortical vein thrombosis. Late seizures occur in 9.5% of patients and may be more common in those patients with early seizures. Although randomized controlled studies for prophylactic use of AEDs are not available, these drugs may be prescribed in those patients at high risk for early seizures because they may be associated with higher morbidity and early mortality. In a recent retrospective study, however, whereby all patients with seizures received AEDs, seizures were not associated with death or 6-month worse outcomes.
Reperfusion-Hyperperfusion Syndrome and Seizures
Reperfusion-hyperperfusion syndrome (RHS) is an uncommon complication of carotid endarterectomy, carotid angioplasty, and stenting. Seizures occur either immediately after revascularization procedures (usually because of distal embolization) or later (7 hours to 14 days) and are considered a delayed manifestation of RHS. Transient periodic lateralizing epileptiform discharges have also been reported after internal carotid stenting in a patient with previous ICH and NCSE after superficial temporal to middle cerebral artery anastomosis, successfully treated with AEDs. The use of prophylactic AEDs remains controversial; early onset seizures are treated almost without exception in addition to tight blood pressure control as an adjunct to a likely procedural complication (ICH, severe edema, ischemic stroke). The management of late seizures also includes AEDs in addition to tight blood pressure control, to a level of equalizing transcranial Doppler-measured velocities ipsilateral and contralateral to the treated carotid artery.
Traumatic brain injury and seizures
The incidence of posttraumatic seizures varies widely, with estimates of 2% to 12% in civilian populations and up to 53% in military populations. Traumatic brain injury (TBI) accounts for 10% to 20% of symptomatic epilepsy in the general population and 5% of epilepsy in general. In a study, however, using CEEG in the NICU, 22% of post-TBI patients had seizures (52% of which were nonconvulsive). One-third of these patients were in SE with minimal clinical signs, such as facial twitching or eye fluttering, and all died. Hippocampal atrophy on volumetric magnetic resonance imaging (MRI), suggesting an anatomic damaging effect, has also been associated with nonconvulsive posttraumatic seizures.
Clinical studies divide seizures into immediate (<24 hours), early (within 1 week, with a seizure incidence of 2.1%–16.9%), or late (with an incidence of 1.9% to >30.0%). Independent risk factors for late seizures or posttraumatic epilepsy include early seizures, coma or loss of consciousness for more than 24 hours, dural penetration, biparietal or multiple contusions, intracranial hemorrhage, depressed skull fracture not surgically treated, and at least one nonreactive pupil. In a recent study, diffuse axonal injury on MRI was not correlated with posttraumatic epilepsy, but cerebral contusions were. Early seizures occur in 25% of patients not treated with AEDs and are associated with seizures immediately following trauma, depressed skull fracture, intracerebral hematoma, or subdural hematoma. The risk is lower (15%–20% range) if the patients had a penetrating head injury, epidural hematoma, cortical contusion, and had a Glasgow Coma scale score of 10 or less. Although early seizures are independently associated with an unfavorable outcome, their effect is much lower than other variables, such as severity of brain injury or older age. Injury surrogate markers have been associated with seizures. In a study of 20 patients with moderate to severe TBI monitored with microdialysis and CEEG, 10 patients had post-TBI seizures, which resulted in episodic increases in intracranial pressure (ICP) and lactate/pyruvate ratio. Both remained elevated beyond postinjury hour 100 in the subgroup with seizures (compared with the subgroup without), suggesting long-lasting effects.
If early and, especially, late posttraumatic seizures occur, AEDs should be used. The treatment of post-TBI seizures in the ICU is not different from the treatment of any other seizures. Prophylactic AED administration is more controversial. In a systematic review of randomized trials, prophylactic AEDs were effective in reducing early seizures; but there was no evidence that they reduced the occurrence of late seizures or had any effect on death and neurologic disability. The current practice parameters by the American Academy of Neurology (AAN) and the Brain Trauma Foundation advocate prophylactic treatment only during the first 7 days from a head injury. Regarding the choice of AEDs, phenytoin has been shown to decrease the incidence of early posttraumatic seizures and be more cost-effective than levetiracetam. Levetiracetam was equally effective as phenytoin in preventing early seizures in a prospective study of 32 patients with severe TBI but was associated with an increased seizure tendency on 1-hour EEG. Valproic acid, compared with phenytoin, did not seem to benefit and actually showed a trend toward higher mortality. Lastly, vagus nerve stimulation may reduce seizures in patients with refractory posttraumatic epilepsy.
Brain tumors and seizures
Many patients admitted to the NICU with brain tumors have seizures (in up to 35% of all tumor cases ) and the incidence is both pathology and location dependent. In high-grade, rapidly progressive tumors, such as glioblastoma, or metastatic tumors, seizures occur in 25% to 35% of cases, which is lower than the reported 70% incidence in slower-growing tumors, such as astrocytomas or meningiomas, and 90% in oligodendrogliomas. The locations with the highest incidence are the temporoparietal regions with cortical gray involvement.
Although patients with brain tumors and seizures should be treated with AEDs, prophylactic treatment is controversial. AEDs may interfere with corticosteroids, chemotherapy, and radiation treatment and induce more frequent and serious allergic reactions in such patients. Therefore, the AAN’s practice parameter does not support prophylactic AEDs in patients with newly diagnosed brain tumors. Postoperatively, patients who have not experienced a seizure should have tapering and discontinuation of AEDs within a week (particularly those patients who are medically stable and have AED-related side effects). Patients who have brain metastases may have less propensity to develop seizures; based on recently published guidelines, they should also not be on prophylactic AEDs.
If seizures occur, the newer-generation AEDs, such as gabapentin, lacosamide, levetiracetam, oxcarbazepine, pregabalin, topiramate, and zonisamide, are preferred because they have fewer drug interactions, especially with chemotherapy, and cause fewer side effects. In a small case series of 25 patients with brain tumor–related epilepsy, oxcarbazepine monotherapy at a mean dosage of 1230 mg/d led to significant improvement in mood and seizure-freedom rate. Perioperative oral or intravenous (IV) levetiracetam administration in patients with primary brain tumors also led to seizure freedom 100% in the presurgery and 84% to 88% in the early late postsurgery phases.
If a primary or metastatic brain tumor is causing SE, a combination of IV phenytoin, IV levetiracetam (median dosage 3 g/d), and by-mouth pregabalin (median dosage 375 mg/d) led to 70% control, on average, 24 hours after the addition of the third AED. In another small case series, pregabalin controlled non-convulsive (NC) seizures or NCSE in 67% of 9 patients with brain tumors.
Older AEDs may also have a role in treating brain tumor–related seizures. In a recent study of patients with glioblastoma, valproic acid improved the survival of patients on temozolomide/radiotherapy compared with those receiving an enzyme-inducing AED or no AED. It is unclear if this valproic effect is through increased temozolomide bioavailability or its action as a histone deacetylase inhibitor.
Drug-induced seizures
Drugs rank low as precipitants of seizures in the NICU. Antibiotics, such as the penicillins, cephalosporins, carbapenems (especially imipenem), aztreonam, fluoroquinolones, isoniazid, and metronidazole, can precipitate seizures when administered intrathecally or at high doses in patients with renal insufficiency or undergoing continuous renal replacement therapy. Peak concentration periods of the drug may also provoke electrographic changes. During infusion of cefepime and CEEG, 23.7% of patients had continuous epileptiform discharges compared with only 3.75% during meropenem infusion. Because of their specific action through GABA receptors, it is important to remember that first-line AEDs should be GABAergic agonists, such as benzodiazepines or barbiturates. In case of isoniazid intoxication, the addition of IV pyridoxine is important because the drug antagonizes B6 transformation to pyridoxal phosphate, an essential cofactor for GABA synthesis.
Intrathecal administration of baclofen may provoke seizures or convulsive or nonconvulsive SE in patients with multiple sclerosis. Similarly, intrathecal absorption of the locally used hemostatic agent tranexamic acid can lead to seizures. These seizures are self-limiting and easily controlled with AEDs.
Rapid opioid withdrawal may provoke seizures, which appear on average, 2 to 4 days following discontinuation. Normeperidine, a metabolite of meperidine, is a strong proconvulsant. This drug should probably be avoided in the NICU.
Electrolyte and metabolic abnormalities
Hyponatremia is the most frequent ICU electrolyte abnormality associated with new-onset seizures (in 18.2% of ICU patients ). Acute hyponatremia is associated with a higher risk for seizures than chronic hyponatremia. Correction of Na + levels is adequate treatment if structural intracranial pathology is not present. The rate of Na + correction with hypertonic solutions can be faster in acute cases (up to 1–2 mEq/L/h of Na + increase until seizures are under control) than in chronic cases, when it should be less than 0.5 mEq/L/h.
Disturbances in glucose levels have become common in NICU patients with implementation of tighter glucose control than in the past. Both focal and generalized seizures can be caused by hyperglycemia and hypoglycemia. Seizures related to nonketotic hyperosmolar hyperglycemia may present as speech arrest, visual disturbances, or be related to limb movement ( reflex seizures ). Seizures associated with hypoglycemia are frequently preceded by signs of sympathetic excitation. There is no role for AEDs, and only correction of the glucose abnormality will bring the seizures under control.
Treatment of NICU seizures
Seizures complicating critically ill neurosurgical patients should not be considered benign phenomena. During seizures or SE, ICP increases in parallel with cerebral blood flow, brain temperature, and lactate/pyruvate ratio and is correlated with dramatic reductions of brain tissue oxygen tension. Although there is no broad acceptance that seizures lead to worse outcomes, most intensivists will treat NICU seizures emergently targeting the ensuing immediate brain metabolic stress and potentially the long-standing secondary effects.
The management of NICU seizures basically follows the same general rules, which guide treatment of noncritically ill patients ( Box 2 ). A new staged approach to the treatment of SE has been proposed and included in Box 2 . Because the NICU admits the most resistant-to-treatment seizures, familiarity of the medical and nursing staff with the process of diagnosis and treatment is essential. Urgency without panic is important when seizures are recurrent or SE is present because the duration of seizures is related to resistance to treatment and overall outcome.
Related posts:
Moderate and Severe Traumatic Brain Injury
Neurocritical Care in Neurosurgery
Managing Subarachnoid Hemorrhage in the Neurocritical Care Unit
Strategies for the Use of Mechanical Ventilation in the Neurologic Intensive Care Unit
Microdialysis in the Neurocritical Care Unit
Parenchymal Brain Oxygen Monitoring in the Neurocritical Care Unit
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