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David L. Ginsburg, M.D. Associate Professor of Neurology University of Nevada School of Medicine

Status Epilepticus. Approx. 152,000 cases per year, resulting in 42,000 deaths and an inpatient cost of $3.8 to $7 billion per year.Bimodal distribution, most frequent during first year of life and after age 60Most common cause in adults subtherapeutic anticonvulsant levels and stroke (ischemic or

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David L. Ginsburg, M.D. Associate Professor of Neurology University of Nevada School of Medicine

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    1. David L. Ginsburg, M.D. Associate Professor of Neurology University of Nevada School of Medicine

    2. Status Epilepticus Approx. 152,000 cases per year, resulting in 42,000 deaths and an inpatient cost of $3.8 to $7 billion per year. Bimodal distribution, most frequent during first year of life and after age 60 Most common cause in adults subtherapeutic anticonvulsant levels and stroke (ischemic or hemorrhagic)

    3. Status Epilepticus Mortality rates: 3% in children, 26% in adults, 38% in elderly. Primary determinants of mortality duration of seizures, age at onset, and etiology Patients with anoxia and stroke had a very high mortality rate independent of other variables

    4. Status Epilepticus Patients in alcohol withdrawal and low AED level had a relatively low mortality rate Cognitive decline following SE, as documented by neuropsychometric testing, is a well-established end result of prolonged secondarily generalized and partial status epilepticus

    5. Definition Two or more sequential seizures without full recovery of consciousness between seizures, or more than 30 minutes of continuous seizure activity. Various classifications, including generalized (tonic-clonic, myoclonic, absence, atonic, akinetic) vs. partial (simple or complex).

    6. Etiologies Causes of SE in 280 Patients from Medical College of Virginia: Anticonvulsant Withdrawal 21% Alcohol Withdrawal 18% Anoxia 2% Hypotension 4% Cerebrovascular Disease 21% Hemorrhage 7%

    7. Etiologies Metabolic Disorders 13% Infectious Disorders 4% Tumors 3% Other 7%

    8. Systemic Complications Metabolic: lactic acidosis, hypercapnia, hyperglycemia, hyperkalemia, hyponatremia, CSF/serum leukocytosis Renal: Acute Renal Failure from Rhabdomyolysis, myoglobinuria Autonomic: hyperpyrexia, failure of cerebral autoregulation, vomitting, incontinence Cardiac/Respiratory: hypoxia, arrythmia, pneumonia, high output cardiac failure

    9. Management Imaging with computed tomography is recommended after stabilization of the airway and circulation. If imaging is negative, lumbar puncture is required to rule out infectious etiologies.

    10. Management Electroencephalography (EEG) is extremely useful, but underutilized, in the diagnosis and management of status epilepticus. Although overt convulsive status epilepticus is readily diagnosed, EEG can establish the diagnosis in less obvious circumstances.

    11. Management EEG also can help to confirm that an episode of status epilepticus has ended, particularly when questions arise about the possibility of recurrent episodes of more subtle seizures.

    12. EEG

    13. Treatment Protocol for Management of Status Epilepticus At: zero minutes Initiate general systemic support of the airway (insert nasal airway or intubate if needed) Check blood pressure. Begin nasal oxygen. Monitor ECG and respiration. Check temperature frequently. Obtain history. Perform neurologic examination.

    14. Treatment Protocol Send sample serum for evaluation of electrolytes, blood urea nitrogen, glucose level, complete blood cell count, toxic drug screen, and anticonvulsant levels; check arterial blood gas values. Start IV line containing isotonic saline at a low infusion rate. Inject 50 mL of 50 percent glucose IV and 100 mg of thiamine IV or IM. Call EEG laboratory to start recording as soon as feasible

    15. Treatment Protocol Administer lorazepam (Ativan) at 0.1 to 0.15 mg per kg IV (2 mg per minute); Lorazepam has emerged as the preferred benzodiazepine for acute management of status epilepticus. Lorazepam differs from diazepam in two important respects. It is less lipid-soluble than diazepam, with a distribution half-life of two to three hours versus 15 minutes for diazepam. Therefore, it should have a longer duration of clinical effect. Lorazepam also binds the GABAergic receptor more tightly than diazepam, resulting in a longer duration of action. The anticonvulsant effects of lorazepam last six to 12 hours, and the typical dose ranges from 4 to 8 mg.

    16. Treatment Protocol If seizures persist, administer fosphenytoin (Cerebyx) at 18 mg per kg IV (150 mg per minute, with an additional 7 mg per kg if seizures continue). At: 20 to 30 minutes, if seizures persist, intubate, insert bladder catheter, start EEG recording, check temperature.

    17. Treatment Protocol Administer phenobarbital in a loading dose of 20 mg per kg IV (100 mg per minute). Because high-dose phenobarbital is sedating, airway protection is an important consideration, and aspiration is a major concern. Intravenous phenobarbital also is associated with systemic hypotension.

    18. Treatment Protocol At: 40 to 60 minutes, if seizures persist, begin pentobarbital infusion at 5 mg per kg IV initial dose, then IV push until seizures have stopped, using EEG monitoring; continue pentobarbital infusion at 1 mg per kg per hour; slow infusion rate every four to six hours to determine if seizures have stopped, with EEG guidance; monitor blood pressure and respiration carefully. Support blood pressure with pressors if needed.

    19. Treatment Protocol or Begin midazolam (Versed) at 0.2 mg per kg, then at a dosage of 0.75 to 10 mg per kg per minute, titrated to EEG monitoring.

    20. Treatment Protocol or Begin propofol (Diprivan) at 1 to 2 mg per kg loading dose, followed by 2 to 10 mg per kg per hour. Adjust maintenance dosage on the basis of EEG monitoring.

    21. Spinal Cord Compression

    22. Spinal Cord Compression Approximately 85% to 90% of cases of epidural spinal cord compressions (ESCC) are due to metastates, 20% of which are the initial manifestation of malignancy. The most prevalent metastatic neoplasms are breast, lung, prostate and kidney tumors, and lymphoma. Primary spinal neoplasms are encountered far less frequently in adults than in children. Multiple myeloma is the most common of these tumors in adults.

    23. Spinal Cord Compression Epidural spinal cord compression from metastatic cancer is common and serious but potentially treatable. This complication affects the thoracic spine in approximately two thirds of patients, the lumbosacral spine in about one fifth of patients and the cervical spine in the remainder of patients.

    24. Spinal Cord Compression Less common etiologies include spinal epidural abscess, spinal epidural hematoma, and central disc herniation. Disc herniation resulting in compression below the termination of the spinal cord is termed the cauda equina syndrome.

    25. Spinal Cord Compression Risk factors for abscess include IV drug abuse, recent bacterial infection, or recent procedure known to cause bacteremia Patients with epidural hematoma usually have a history of recent spinal procedure or trauma. An epidural hematoma can also develop in a patient who is prone to bleeding because of, for example, anticoagulant therapy

    26. Clinical Features Back pain in 83-95% of patients, and usually precedes neurologic symptoms by an average of 7 weeks. The pain produced by spinal neoplasm is often worse when the patient is at rest and may even awaken the patient from a sound sleep. Most common neurologic symptom is motor weakness, affecting 60-85% of patients at the time of diagnosis

    27. Clinical Features ESCC typically causes symmetric lower extremity findings. For spinal cord lesions, the neurologic examination usually reveals symmetric weakness with either flaccidity and hyporeflexia (if the diagnosis is made early) or spasticity and hyperreflexia (if the diagnosis is made later). In cauda equina syndrome, hyporeflexia. Sensory findings include bilateral ascending paresthesias, saddle anesthesia, and unilateral paresthesias in a radicular distribution.

    28. Clinical Features Saddle anesthesia highly suggestive of cauda equina syndrome. Bowel or bladder dysfunction is frequently a late finding in spinal cord compression.

    29. Evaluation Laboratory Tests CBC with differential, ESR, UA. The findings of the clinical evaluation may indicate the need for other specific tests, such as a serum calcium level, a uric acid level, electrophoresis of serum and urine for light chains, and a prostate-specific antigen level. Laboratory tests are particularly useful when infection or malignancy is considered to be a possible cause of the spinal pathology.

    30. Evaluation Plain films inadequate, as 10-17% of patients with ESCC have normal plain films CT and radionuclide bone scans may provide information about spinal metastases, but neither can clearly image the spinal cord or epidural space.

    31. Evaluation Myelography and MRI are the two definitive imaging modalities for ESCC Myelography may be combined with CT to provide better anatomic detail, but is invasive. It may be performed relatively quickly, and has added benefit of CSF analysis

    32. Evaluation Myelography is being replaced by MRI in many institutions MRI can provide information regarding masses that are not compressing the spine. Myelography is imaging modality of choice for patients with contraindications to MRI (e.g., pacemaker)

    33. Treatment For patients with cauda equina syndrome, early lumbar laminectomy with discectomy has been shown to improve outcome when performed within 48 hours. Patients with spinal epidural abscess and signs of compression require surgical drainage. Ideally, this should be accomplished within 24 hours of presentation. Patients should be started on broad spectrum antibiotics while awaiting intervention.

    34. Treatment Management of the patient who has epidural spinal cord compression secondary to mtastastes requires consultation with a radiation oncologist in addition to the surgical subspecialties. Frequently, radiotherapy alone results in improvement in symptoms. Patients who have malignant spinal cord compression should be given systemic steroids. High-dose steroids have been reported to improve rates of postradiation ambulation. Steroid administration for nonmalignant spinal cord compression is controversial and remains a current topic of debate.

    35. Treatment Radiation therapy is the standard approach. Surgery is indicated if the diagnosis is in doubt, a tissue diagnosis is required, the spine is unstable or neurologic deterioration is severe, rapid and progressive. Surgery is also indicated if decompression by radiation therapy is not expected to become effective in time to save a patient from severely disabling neurologic deficits.

    36. References Arce D, Sass P, Abul-Khoudoud H - Am Fam Physician. 2001 Aug 15;64(4):631-8. Sirven JI - Am Fam Physician. 2003 Aug 1;68(3):469-76. Winters ME - Med Clin North Am - 01-MAY-2006; 90(3): 505-23.

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