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 Definition: The condition where one seizure follows another without recovery of consciousness. It may be convulsive or non convulsive.

 Emergency evaluation of seizures:

 History – look out for history of trauma, previous seizures, drugs or alcohol use, current medications.

 Physical examination

 vital signs such as pulse rate and rhythm (to rule out dangerous cardiac arrhythmia, cardiac arrest), blood pressure (rule out hypotension and shock), body temperature (rule out hyperthermia 41 – 42°C).

 papilloedema, focal neurological signs

 heart murmur

 look for evidence of systemic disease

 Laboratory and special investigations

 serum glucose: either hypoglycemia or hyperglycemia

 arterial blood gases: hypoxia, hypercapnia, acidosis

 ECG: cardiac arrhythmia

 serum electrolytes: hyponatremia or hypernatremia

 full blood count

 serum calcium and magnesium levels

 hepatic and renal function studies

 lumbar puncture

 CT scan brain

 blood and urine samples for toxicology studies (if indicated)

 Treatment - therapeutic aims are towards rapid termination of seizures and the prevention and treatment of associated complications.

 Place an oropharyngeal airway (Guedel) to prevent the tongue from falling back and to facilitate suction. Do not force when fitting. Place it in between seizures.

 High flow oxygen to correct hypoxia. The un-coordinated respiratory efforts together with increased metabolism requires oxygen at high flow rates.

 Rule out hypoglycaemia. Use a test strip to determine the blood glucose.

 i.v diazepam 5mg/min. Pause at 10 mg and at each subsequent 5 mg to assess the effects. Maximum bolus dose is 20 mg. The dose may be repeated if necessary after 30 minutes. Risk of hypotension and respiratory depression with high doses. Be prepared for mechanical ventilation.

Diazepam may be given per rectum if an IV line is not immediately available.

IV diazepam infusion may be given without dilution at 2 to 4 mg per hour.

Watch for respiratory depression. DO NOT give i.m diazepam as absorption is slow and erratic.

 Anticonvulsant agents

 i.v phenytoin – to be given in saline of 100 ml at a loading dose of 10-15 mg/kg at a rate no faster than 50 mg/minute. IV maintenance at 100 mg every 8 hourly. Monitor the BP closely for hypotension. ECG monitoring is required.

 i.v sodium valproate 1.2 gm is given bolus followed by maintenance dose of 400 mg every 8 hours.

 i.v phenobarbitone is given at a loading dose of 200 mg over one hour.

Further i.v doses of 100 – 200 mg can be given until the seizure stop and has to be titrated according to blood pressure measurement and respiratory rate

 Consider paralysis and mechanical ventilation if seizures persistent. It is important to continue with anticonvulsants as seizure activity may persist despite the paralysis. EEG monitoring is useful if available to assess the effectiveness of the anticonvulsants in inhibiting the abnormal cerebral discharge.

 Monitor electrolytes - metabolic acidosis is likely with prolonged seizures.

NaHCO3 may be required for correction. Amount of NaHCO3 (mmol/l) = 1/3 x BW (kg) x base deficit.

 Acute renal failure may rarely result from rhabdomyolysis and myoglobinuria.

If myoglobinuria is present treat with I/V fluids, mannitol or frusemide to establish good urine output and prevent acute renal failure.

 Cerebral oedema may complicate prolonged seizures.

7. Tetanus

 Definition - a potentially fatal disease caused by Clostridium tetani. The organism produces tetanospasmin which blocks the function of inhibitory neurons hence increasing reflex excitability of motor nerves.

 The injury allowing the Clostridium tetani spores to enter the body may be trivial.

 Incubation period – refers to time interval from injury to first symptom. This period varies greatly from one to three months. Generally, it is less than 14 days. The shorter the incubation period, the worse the prognosis.

 Period of onset – it is the time interval between the first symptom and the first spasm. The shorter the interval, the worse the prognosis.

 Clinical presentation

 rigidity – occurs in all cases. Ranges from ―stiff‖ jaw muscles, risus sardonicus, neck stiffness, abdominal rigidity to opisthotonus in extreme cases.

 reflex spasms – these are sudden exacerbation of underlying rigidity. Whole groups of muscles suddenly contract and this will impede respiration.

Spasms may be rapidly recurrent and this will seriously embarrass respiration.

 the patient is generally most severely ill in the first 6 weeks.

 coughing while drinking or eating or dysphagia is an important symptom which indicates serious disease. There is risk of laryngospasm and a tracheostomy is required.

 spontaneous recovery occurs from the tenth day onwards. Laryngeal spasms may occur suddenly and must be looked for.

 The diagnosis is based on clinical features.

 Complications - the principal problem is respiratory complications from spasms, aspiration and pneumonia. Severe cases may be complicated by:

 heart failure, pulmonary oedema

 autonomic dysfunction - tachy or bradycardia, sweating, ileus,

 hyperpyrexia

 deep vein thrombosis (DVT)

 syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH)

 Treatment

 Passive immunization with human anti-tetanus immunoglobulin. Given as early as possible. It is effective only against circulating toxin. Toxin which has already reached the CNS is unaffected.

 prophylactic dose: i.m 250 to 500 units

 treatment dose: i.m 3000 to 6000 units (there is doubt about the efficiency of passive immunisation in established tetanus. It is however routinely given).

 Wound - this is cleared and any narcotic tissue debrided.

 Antibiotics - Clostridium tetani is sensitive to:

 i.v Benzyl Penicillin: 1 – 3 Mega every 6 hours.

 Erythromycin or tetracycline is given if allergic to penicillin

 Control spasms - infusion of diazepam at 1mg to 4 mg per hour with or without i.m chlorporomazine 50 mg 4 to 6 hourly is adequate to control most cases of mild tetanus. These patients should be nursed in a quiet darkened room to minimize external stimuli.

 Laryngospasm may be treated with i.v chlorpromazine 100 mg or with paralysis, intubation and mechanical ventilation. The use of tacheostomy circumvents this risk.

 Severe spasms and patients with respiratory embarrassment will require paralysis and mechanical ventilation. A tracheostomy is usually required.

Patients are paralysed for at least 10-14 days. Most patients start to recover by the 3rd week of illness.

 Supportive measures – this is very important as patients die from complications of tetanus rather than from the spasms or rigidity.

 chest physiotherapy and care of airway.

 parenteral nutrition or feeding via a naso-gastric tube if airway is secured.

 ensure normal arterial blood gases and electrolytes

 autonomic dysfunction - sympathetic overactivity is treated with labetolol. Parasympathetic over activity is treated with atropine.

 treat intercurrent infection.

 s.c low molecular weight heparin for deep vein thrombosis (DVT) prophylaxis.

 Active immunisation with anti-tetanus toxoid (ATT) - natural immunity does not occur after tetanus as immunizing dose is higher than the fatal dose of tetanus toxin. Active immunisation with 0.5 ml the toxoid must be given preferably at convalescence and then at 6 weeks and 6 months later. Immunity lasts for 5 years and booster doses are then required. If ATT is given during the acute illness, passive immunisation with immunoglobulins must be given at a different site.

8. Gullain Barre Syndrome (Acute Inflammatory Demyelinating