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    CONVULSIONS

    DEFINITIONS

    1.   Acute generalized convulsion: paroxysmal discharge of cerebral
         neurons resulting in a brief clinical phenomenon characterized by
         loss of consciousness and generalized involuntary tonic and
         clonic contractions of the skeletal muscles.

    2.   Acute focal convulsion: paroxysmal discharge of localized central
         neurons (e.g. petit mal, temporal, focal motor).

    3.   Status epilepticus: continued unremitting convulsions or several
         consecutive episodes without intervening restoration of
         consciousness.

    TOXIC CAUSES

     Pharmaceuticals
         Antihistamines
         Camphor
         Carbamazepine
         Carbon monoxide
         Chlorambucil
         Cyclic antidepressants
         Cyclosporine 
         Ergot alkaloids 
         Hypoglycaemic agents 
         Isoniazid
         Lithium salts 
         Local anaesthetics 
         Mefenamic acid
         Metronidazole
         Nicotine
         Penicillin
         Pentazocine 
         Pethidine (meperidine)
         Phenothiazines
         Physostigmine
         Propoxyphene
         Salicylates
         Xanthine derivatives (theophylline, caffeine)

     Drugs of abuse
         Amphetamines and derivatives (e.g. MDMA/"ecstasy")
         Cocaine
         PCP (phencyclidine)

     Pesticides
         Carbamates
         Organochlorines
         Organophosphorus compounds
         Strychnine

     Others
         Hyperbaric oxygen
         Ethanol and sedative-hypnotic drug withdrawal syndrome 
         Heavy metals (e.g., lead in children)

    NON-TOXIC CAUSES

     Structural
         Haemorrhage
         Tumour
         Trauma

     Non-structural
         Cardiac arrhythmia
         Fever
         Hypoxia 
         Hypoglycaemia
         Infection 
         Metabolic 

    CLINICAL FEATURES

    Toxic convulsions are characterized by generalized involuntary tonic
    and clonic contractions of skeletal muscles.  There may be evidence of
    physical injury (e.g.: tongue biting) and/or incontinence. The
    post-convulsive state may be associated with coma or altered CNS
    function ("Todd's paralysis"). 

    Acute complications may include pulmonary aspiration of gastric
    contents, hypoventilation, hypoxia, metabolic acidosis, cardiac
    arrhythmias, rhabdomyolysis, and sudden death. 

    DIFFERENTIAL DIAGNOSIS

    Abnormal movements (dyskinesia, myoclonic jerking, dystonic reactions)
    Muscular hyperactivity and/or rigidity 
    Malingering, hysteria (pseudoseizures)
    Tetany or tetanus
    Fasciculations due to organophosphorus or carbamate poisoning

    RELEVANT INVESTIGATIONS

    The following investigations should be performed routinely:
         Blood glucose 
         Serum electrolytes including calcium

    Additional tests that may be clinically relevant include:
         Arterial blood gases 
         Cerebrospinal fluid analysis 
         Creatine phosphokinase 
         CT Scan head
         EEG 
         Serum magnesium

         Serum anticonvulsant concentrations 
         Toxicological screening.

    TREATMENT

    Most toxic convulsions are brief, lasting from a few seconds to a few
    minutes, and usually do not require pharmacological intervention. 
    However, if the seizure is prolonged, or if status epilepticus
    supervenes, urgent medical intervention is required.  Status
    epilepticus is an acute medical emergency.  Suggested treatment
    protocols for adults and children are as follows:

     Initial Management 

    Protect patient from self-inflicted injury; remove false teeth if
    present; establish a clear airway and give high flow oxygen by mask. 
    Place the patient in lateral semiprone position.  Establish
    intravenous access.

     Glucose.  If rapid bedside glucose measurement indicates low blood
    sugar, administer intravenous  glucose (adults: 25 g IV; children:
    0.5 to 1 g/kg IV, as 25% dextrose).

     Benzodiazepines:  (Note - patients should be carefully monitored for
    evidence of respiratory depression and hypotension during
    administration.)

    1.   Give  Diazepam 10 mg intravenously (0.15 to 0.25 mg/kg) over
         1 minute.  If convulsions continue, give a further 10 mg over 1
         minute. This may be repeated if necessary.   Diazepam may be
         given IM, but absorption is erratic and this route is not
         recommended. Rectal administration has been used in children
         (0.5 mg/kg) when IV access is not readily available. 

    2.    Lorazepam (0.1 mg/kg IV at 1 to 2 mg/minute up to a maximum of
         10 mg) or  Clonazepam (0.5 to 1mg IV) may be used instead of
         diazepam.  Also consider  midazolam, which is rapidly absorbed
         after intramuscular administration (IM dose: 0.1-0.2 mg/kg). 

    If convulsions are difficult to control with large doses of
    benzodiazapines, the following drugs may be considered:

     Phenobarbitone (Phenobarbital) 15 mg/kg intravenously slowly (e.g.
    2 mg/kg/min). Repeat doses may be given, up to a total dose of
    30 mg/kg. Monitor blood pressure and heart rate during infusion. 
    Hypotension may occur.  Observation of respiratory state is mandatory
    and assisted ventilation may be required.

     Phenytoin.  As an alternative to phenobarbitone, administer
     phenytoin 15 to 20 mg/kg body weight IV in 0.9% normal saline (1 g
    in 250 mL), to be given no faster than 50 mg/kg/minute.  Monitor
    cardiac rhythm and blood pressure. Rapid infusion of intravenous

    phenytoin may cause acute hypotension, AV block, or asystole. (Note:
    phenytoin is not effective for patients with seizures caused by
    theophylline and may be dangerous in patients with tricyclic
    antidepressant overdose).

     Thiopentone. If control of convulsions is not achieved with the
    preceding drugs, general anaesthesia with  thiopentone should be
    instituted (adult dose: 500mg diluted in 20 mL administered
    intravenously over 2 to 3 minutes or until the convulsion stops.
    Consider maintenance infusion at 2 to 4g/24hrs). Mechanical
    ventilation is required, and heart rate and blood pressure should be
    monitored. 

    Note: If neuromuscular relaxants are given to control muscular
    hyperactivity, EEG monitoring must be instituted because CNS seizures
    may continue without external manifestations.

     Pyridoxine. If isoniazid overdose is suspected, administer
     Pyridoxine, 1g IV for each gram of isoniazid ingested (or 4 to 5g IV
    empirically).

     Thiamine. In alcoholic or malnourished patients, consider 
     Thiamine 100 mg IV or IM.

    CLINICAL COURSE AND MONITORING

    Toxic seizures are usually self-limited.  Monitoring of vital signs
    and neurological status is required until the patient is fully
    conscious and convulsion-free. 

    LONG-TERM COMPLICATIONS

    Permanent neurologic deficit may result from prolonged convulsions or
    acute respiratory failure and hypoxia.

    AUTHOR(S)/REVIEWERS

    Authors:       Poisons Unit, London, United Kingdom.
    Reviewers:     Sao Paulo 9/94, Cardiff 3/95, Berlin 10/95; Cardiff
                   9/96: V. Afanasiev, M. Burger, T. Della Puppa,
                   L. Fruchtengarten, K. Olsen, J. Szajewski).