STATUS EPILEPTICUS

E-Medicinie Medscape (updated February 19, 2016 ; Author Julie L Roth,

MD Neurologist, Epilepsy and General Neurology, Comprehensive Epilepsy Program,
Rhode Island Hospital; Assistant Professor, Department of Neurology, The Warren
Alpert Medical School of Brown University):
http://emedicine.medscape.com/article/1164462-
overview?pa=SAc9w%2FobCzFq2VBbcUwxjjAVTZ5hjjNKEI41%2BIjqFASg3QGnY3TWyR
HXmcH0O0gBJKjcW6PEagVd%2B1ScnNsJK3Ba6qMPn9v9%2B17kWmU%2BiQA%3D
 STATUS EPILEPTICUS
Status epilepticus (SE) is a common, life-
threatening neurologic disorder that is
essentially an acute, prolonged epileptic crisis.
SE can represent an exacerbation of a
preexisting seizure disorder, the initial
manifestation of a seizure disorder, or an
insult other than a seizure disorder. In patients
with known epilepsy, the most common cause
is a change in medication. Most seizures
terminate spontaneously.
 ETIOLOGY OF SE
Exacerbation of a pre-existing seizure disorder
The initial manifestation of a seizure disorder
Insult other than a seizure disorder.
Toxic / Metabolic that cause cortical structural
damage
MOST COMMON: Change of Medication
 Other Etiologies
Hypoxic injury
Stroke
Tumor
SAH
Head trauma
Drugs (eg, cocaine, theophylline, INH may cause seizures
and is unique in having a specific antidote, pyridoxine (B6)
Alcohol withdrawal
Electrolyte abnormalities (eg, hypo Na, hyper Na,
Hypercalcemia, hep-ench)
Neoplasms
CNS infections (eg, meningitis, brain abscess, encephalitis)
Toxins, notably sympathomimetics
 PATHOPHYSIOLOGY

GLUTAMATE NMDA (N-methyl-D-aspartate)

GABA
 Research with paralyzed and artificially ventilated animals
concluded that neuronal loss after focal or generalized SE is
linked to the abnormal neuronal discharges and not simply to
the systemic effects of the seizures. For example, Meldrum
and Horton demonstrated that prolonged seizure activity
results in pathologic changes after 30 minutes; after 60
minutes, neurons begin to die. The hippocampus seems
especially vulnerable to damage by this mechanism.
These observations parallel findings in human clinical studies,
which have shown that the duration of SE correlates directly
with morbidity and mortality rates. The longer the SE persists,
the more likely that neurons will be damaged by excitatory
neurotransmitters. Sustained seizure activity also
progressively reduces GABA inhibition. On a receptor level,
GABAergic mechanisms fail and seizures become
pharmacoresistent. (EMERGENCY!)
 How to Diagnose
Anamnesis: history of metal exposure, consumtion of
cocaine, INH, Theophylline, Change of meds (b4 OP
NOP)
SS: By clinical history, nonmotor simple partial status
epilepticus involves subjective sensory disturbances,
including the following:
Focal or unilateral paresthesias or numbness
Focal visual changes, usually characterized by flashing
lights
Focal visual obscuration or focal colorful hallucinations
Olfactory or gustatory hallucinations
Gradual loss of uni/bilateral motor-function
History of seizures
Confusion
Twitching
 Systemic Sign and Symptoms
Tachycardia
Cardiac arrhythmias
Hyperglycemia
Rising and lowering of the BP
Hyperthermia
Acidosis
Leukocytosis
Pulmonary Edema (caution)
 Diagnose
Examination for status epilepticus includes the
following:
Generalized convulsive status epilepticus: Typical rhythmic
tonic-clonic activity, impaired consciousness; rarely, may
present as persistent tonic seizure
Status epilepticus due to the use of illicit, or street, drugs:
needle-track marks
Status epilepticus due to possible mass lesion or brain
infection: Papilledema, lateralized neurologic features
Subtle or transformed status epilepticus: Any patient
without improving level of consciousness within 20-30
minutes of cessation of generalized seizure activity
Associated injuries in patients with seizures: May include
tongue lacerations (typically lateral), shoulder dislocations,
head trauma, facial trauma
 Classification
The Luders and Rona semiologic classification
consists of 3 axes, as follows
The type of brain function predominantly
compromised
The body part involved
The evolution over time

The Treiman classification is as follows:

Generalized convulsive status epilepticus
Subtle status epilepticus
Nonconvulsive status epilepticus (eg, absence,
complex partial)
Simple partial status epilepticus
 Test
The workup for potential status epilepticus is similar to that
for any self-limited seizure but is done more expeditiously
to confirm the diagnosis and to abort or limit the seizures.
Stat laboratory studies that should be obtained include the
following:
Glucose and electrolyte levels (including calcium,
magnesium)
Complete blood count
Renal and liver function tests
Toxicologic screening and anticonvulsant drug levels
Arterial blood gas results
Other tests that may be appropriate depending on the clinical
setting include the following:

Electroencephalography: Criterion standard for

diagnosing status epilepticus + neuro consult
Blood cultures
Urinalysis and/or cerebrospinal fluid analysis
Imaging studies
Imaging modalities used to evaluate status
epilepticus may include the following:
CT scanning and/or MRI of the brain
Chest radiography
If a central nervous system infection is suspected,
consider performing a lumbar puncture (after
neuroimaging to rule out potential cerebral
herniation).
 Management
Aggressive treatment is necessary for status epileptics. Clinicians
should not wait for blood level results before administering a
loading dose of phenytoin, regardless of whether the patient is
already taking phenytoin.
Pharmacotherapy
Most patients with status epilepticus who are treated aggressively
with a benzodiazepine, fosphenytoin, and/or phenobarbital
experience complete cessation of their seizures. If status epilepticus
does not stop, general anesthesia is indicated.
Medications used in the treatment of status epilepticus include the
following:
Benzodiazepines (eg, lorazepam, diazepam, midazolam): First-line
agents
Anticonvulsant agents (eg, phenytoin, fosphenytoin)
Barbiturates (eg, phenobarbital, pentobarbital)
Anesthetics (eg, propofol)
 Supportive Theraphy
Supportive care in patients with status epilepticus
includes the following:
Maintenance of vital signs
Airway, breathing, circulation (eg,
hemodynamic/cardiac monitoring)
Respiratory support, with intubation and/or
mechanical ventilation if necessary
Periodic neurologic assessments
Surgery
Surgical intervention for status epilepticus is a last
resort and rarely performed
Ablating a structural abnormality, hemispherectomy,
subpial resction, placement of vagus nerve stimulator
 Prognosis
The longer High Chances of Neurological
deficit or even death
The older High Chances of Neurological
deficit or even death
 Tetanus Seizures
Central of Disease Control and Prevention ;
Available at:
http://www.cdc.gov/tetanus/clinicians.html
 Clostridium tetani (C. tetani) spores usually enters the
body through a wound or breach in the skin. In the
presence of anaerobic (low oxygen) conditions, the
spores germinate.
Toxins are produced and disseminated via blood
stream and lymphatic system. Toxins act at several sites
within the central nervous system, including peripheral
motor end plates, spinal cord, and brain, and in the
sympathetic nervous system.
The typical clinical manifestations of tetanus are
caused when tetanus toxin interferes with release of
neurotransmitters, blocking inhibitor impulses. This
leads to unopposed muscle contraction and spasm.
Seizures may occur, and the autonomic nervous system
may also be affected.
 Symptoms
Headache
Jaw cramping
Sudden, involuntary muscle tightening often in
the stomach (muscle spasms)
Painful muscle stiffness all over the body
Trouble swallowing
Jerking or staring (seizures)
Fever and sweating
High blood pressure and fast heart rate
 Signs and Diagnosis
Tetanus is a clinical syndrome without
confirmatory laboratory tests. The disease is
characterized by painful muscular contractions,
primarily of the masseter and neck muscles,
secondarily of trunk muscles.
A common first sign suggestive of tetanus in
older children and adults is abdominal rigidity,
although rigidity is sometimes confined to the
region of injury. Generalized spasms occur,
frequently induced by sensory stimuli. History of
an injury or apparent portal of entry may be
lacking. The organism is rarely recovered from
the site of infection.
 Clinical Features
The incubation period ranges from 3 to 21 days,
usually about 10 days. In general, the further the
injury site is from the central nervous system, the
longer the incubation period.
A shorter incubation period is associated with
more severe disease, complications, and a higher
chance of death. In neonatal tetanus, symptoms
usually appear from 4 to 14 days after birth,
averaging about 7 days.
 Generalized Tetanus
Generalized tetanus is the most common form, accounting
for more than 80% of cases. Neonatal tetanus usually
occurs because of umbilical stump infections. The most
common initial sign is spasm of the muscles of the jaw or
"lockjaw". This may be followed by painful spasms in other
muscle groups in the neck, trunk, and extremities and by
generalized, seizure-like activity or convulsions in severe
cases. Generalized tetanus can be accompanied by nervous
system abnormalities, as well as a variety of complications
related to severe spasm and prolonged hospitalization. The
clinical course of generalized tetanus is variable and
depends on the degree of prior immunity, the amount of
toxin present, and the age and general health of the
patient. Even with modern intensive care, generalized
tetanus is associated with death rates of 10%20%.
 Localized Tetanus
Localized tetanus is an unusual form of the
disease consisting of muscle spasms in a
confined area close to the site of the injury.
Although localized tetanus often occurs in
people with partial immunity and is usually
mild, progression to generalized tetanus can
occur.
 Cephalic Tetanus
The rarest form, cephalic tetanus, is associated
with lesions of the head or face and has been
described in association with ear infections (otitis
media). The incubation period is short, usually 1
2 days. Unlike generalized and localized tetanus,
cephalic tetanus results in flaccid cranial nerve
palsies rather than spasm. Spasm of the jaw
muscles may also be present. Like localized
tetanus, cephalic tetanus can progress to the
generalized form.
 Complications of Tetanus
Laryngospasms
Fractures
Hypertension
Nosocomial infections
Pulmonary embolism
Aspiration pneumonia
Death
 Other complication of tetanus
Uncontrolled/involuntary muscular contraction of the
vocal cords (laryngospasm)
Break in the bone (fracture)
Hospital-acquired infections
Blockage of the main artery of the lung or one of its
branches by a blood clot that has travelled from
elsewhere in the body through the bloodstream
(pulmonary embolism)
Pneumonia, a lung infection, that develops by
breathing in foreign materials (aspiration pneumonia)
Breathing difficulty, possibly leading to death (10-20%
of cases are fatal)
 Management
Tetanus is a medical emergency requiring:
Hospitalization
Immediate treatment with human tetanus
immune globulin (TIG) (or equine antitoxin)
Tetanus Vaccine
Drugs to control muscle spasms
Aggressive wound care
Antibiotics