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serum should also be saved for future analysis especially if the cause of the status epilepticus
is uncertain. Other investigations depend on the clinical circumstances.

Intravenous glucose and thiamine. If hypoglycaemia is suspected, 50 ml of a 50% glucose
solution should be given immediately by intravenous injection. If there is a history of
alcoholism, or other compromised nutritional states, 250 mg of thiamine (for example, as the
high potency intravenous formulation of Pabrinex, 10 ml of which contains 250 mg) should
also be given intravenously. This is particularly important if glucose has been administered,
as a glucose infusion increases the risk of Wernicke’s encephalopathy in susceptible patients.
Intravenous high-dose thiamine should be given slowly (for example, 10 ml of high potency
Pabrinex over 10 minutes), with facilities for treating anaphylaxis. Routine glucose
administration in non-hypoglycaemic patients should be avoided as there is some evidence
that this can aggravate neuronal damage.

Acidosis. If acidosis is severe, the administration of bicarbonate has been advocated in the
hope of preventing shock, and mitigating the effects of hypotension and low cerebral
bloodflow. In most cases, however, this is unnecessary and more effective is the rapid control
of respiration and abolition of motor seizure activity.

3rd stage (060/90 minutes)

Establish aetiology. The range of causes of status epilepticus depends primarily on age and
the presence or absence of established epilepsy. The investigations required depend on
clinical circumstances; CT or MRI and CSF examination are often required. The latter should
be carried out only with facilities for resuscitation available as intracranial pressure is often
elevated in status epilepticus. If the status epilepticus has been precipitated by drug
withdrawal, the immediate restitution of the withdrawn drug will usually rapidly terminate
the status epilepticus.

Physiological changes and medical complications. The physiological changes of
uncompensated status epilepticus may require specific therapy. Active treatment is most
commonly required for: hypoxia, hypotension, raised intracranial pressure, pulmonary
oedema and hypertension, cardiac arrhythmias, cardiac failure, lactic acidosis, hyperpyrexia,
hypoglycaemia, electrolyte disturbance, acute hepatic or renal failure, rhabdomyolysis, or
disseminated intravascular coagulation.

Pressor therapy. Failure to correct hypotension can lead to significant cerebral ischaemia and
so blood pressure should be maintained by correcting hypovolaemia and if necessary through
the use of pressor agents such as adrenaline, noradrenaline and dobutamine. These agents are
almost invariably required in patients sedated with barbiturate anaesthesia.

4th stage (3090 minutes)

Intensive care. If seizures are continuing in spite of the measures taken above, the patient
must be transferred to an intensive care environment.

Intensive care monitoring. In severe established status epilepticus, intensive monitoring may
be required, including: intra-arterial blood pressure, capnography, oximetry, central venous
and pulmonary artery pressure monitoring.

Magnesium. Although effective in preventing eclampsia, there is no evidence to suggest that
increasing magnesium serum concentrations to supranormal levels has any benefit in status
epilepticus. Indeed, such a policy can result in motor paralysis, difficulty in detecting clinical
seizure activity and hypotension. However, serum magnesium can be low in alcoholics and