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EPILEPSY : STATUS EPILEPTICUS Definition Status epilepticus is a medical emergency defined as a seizure disorder that persists for 30 minutes or longer, or is repeated frequently enough to prevent recovery of consciousness in between attacks. Status may be generalised or partial, convulsive or non-convulsive. Pathogenesis Continuous or recurrent episodes of neuronal discharge of which the precipitating event is either unknown (idiopathic) or secondary to an insult to the brain, e.g. encephalitis, hypoxic episode, trauma, complex febrile seizures, toxins, hypertension and encephalopathy. Non-compliance and changes in anticonvulsant therapy may also be precipitating factors. After 30 minutes of seizures, the brain begins to suffer from hypoxia, acidosis, depletion of local energy stores, cerebral oedema and structural damage. Complications include hyperpyrexia, respiratory depression, cerebral oedema, inappropriate antidiuretic hormone (ADH) secretion, blood pressure disturbances, acidosis, disturbances of blood glucose, renal failure, and hypoxic, ischaemic damage to brain, myocardium and muscles. Diagnostic criteria Clinical: Seizures lasting 30 minutes or longer, or a series of seizures without complete recovery of consciousness in between attacks. Hyperpyrexia, blood pressure disturbances, cerebral oedema, acidosis, blood glucose disturbances. Investigations: Consider once seizures have been terminated. CT scan or MRI scan may be useful to exclude intracranial pathology. Lumbar puncture may be considered in the absence of increased intracranial pressure or focal neurological signs/seizures. Referral criteria Status epilepticus is a medical emergency. Attempt to control seizures and stabilise the patient before referral. Treatment objectives Control or termination of seizures and prevention of recurrences (maintenance therapy). Prevention of further damage to the brain and other organs. Identification and treatment of underlying cause or precipitating event. Symptomatic and supportive treatment.

Epilepsi Status Epileptikus

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Page 1: Epilepsi Status Epileptikus

EPILEPSY : STATUS EPILEPTICUS

DefinitionStatus epilepticus is a medical emergency defined as a seizuredisorder that persists for 30 minutes or longer, or is repeated frequentlyenough to prevent recovery of consciousness in between attacks.Status may be generalised or partial, convulsive or non-convulsive.

PathogenesisContinuous or recurrent episodes of neuronal discharge of which theprecipitating event is either unknown (idiopathic) or secondary to aninsult to the brain, e.g. encephalitis, hypoxic episode, trauma, complexfebrile seizures, toxins, hypertension and encephalopathy.Non-compliance and changes in anticonvulsant therapy may also beprecipitating factors.

After 30 minutes of seizures, the brain begins to suffer from hypoxia,acidosis, depletion of local energy stores, cerebral oedema andstructural damage.

Complications include hyperpyrexia, respiratory depression, cerebraloedema, inappropriate antidiuretic hormone (ADH) secretion, bloodpressure disturbances, acidosis, disturbances of blood glucose, renalfailure, and hypoxic, ischaemic damage to brain, myocardium andmuscles.

Diagnostic criteriaClinical:

• Seizures lasting 30 minutes or longer, or a series of seizures withoutcomplete recovery of consciousness in between attacks.

• Hyperpyrexia, blood pressure disturbances, cerebral oedema, acidosis,blood glucose disturbances.

Investigations: Consider once seizures have been terminated.• CT scan or MRI scan may be useful to exclude intracranial pathology.• Lumbar puncture may be considered in the absence of increased

intracranial pressure or focal neurological signs/seizures.

Referral criteria

Status epilepticus is a medical emergency.Attempt to control seizures and stabilise the patient before referral.

Treatment objectives• Control or termination of seizures and prevention of recurrences

(maintenance therapy).• Prevention of further damage to the brain and other organs.• Identification and treatment of underlying cause or precipitating event.• Symptomatic and supportive treatment.

Page 2: Epilepsi Status Epileptikus

Treatment guidelines

STATUS EPILEPTICUS

Management Comments

Non-drug treatment Admit to high care or intensive care facility if available.Make the patient comfortable – preferably lying on his/her side.Maintain an open airway.

Identify and treat underlying disorder or precipitatingfactor.

Monitor: Heart rate, respiratory rate, blood pressure, electrolytes, bloodglucose, minerals, acid–base status, blood gases, SaO2, neurologi-cal status, fluid balance, osmolality, anticonvulsant blood levels.

Hyperpyrexia: Tepid water sponges, fan, antipyretics (see drug treatment below).

Oxygenation:

IV fluids:

Cardiovascular andrespiratory support:

Administer 100% oxygen by facemask, nasal cannulae or head boxto maintain SaO2 of ≥ 95%.

Start IV infusion with 5–10% dextrose water; maintenance fluidvolume according to the age of the patient.

Cardiovascular and/or respiratory support if the patient is unable tomaintain blood gases and blood pressure within the normalphysiological range.

Moderate hyperventilation (PaCO2 28–35 mmHg) may be consideredas part of the management of cerebral oedema.

Fluid restriction may be necessary if evidence ofinappropriate ADH secretion (hyponatraemia, lowserum osmolality, high urine osmolality) is present.

1 kPa = 7.5 mmHg; 1 mmHg x 0.133 = 1 kPa

Drug treatmentCerebral oedema: Mannitol, slow IV, 0.25–1 g/kg over 30 minutes, in the absence of

shock.

Anticonvulsanttherapy:

Diazepam, slow IV, 0.2–0.5 mg/kg over 5 minutes.Maximum dose: 1–3 years 10 mg; 3–15 years 15 mg.If response is unsatisfactory, repeat once after 15 minutes.

ORDiazepam, IV given rectally, 0.5–0.75 mg/kg.

If response is unsatisfactory, repeat once after 15 minutes.

Respiratory depression may develop. Consider bagand mask ventilation, or intubate and ventilate.

Page 3: Epilepsi Status Epileptikus

Treatment guidelines: STATUS EPILEPTICUS (continued from previous page)

Management Comments

Anticonvulsanttherapy (continued):

If above measures fail, ADD:Phenobarbital, slow IV, 20 mg/kg over 5 minutes.

If no response after 15 minutes, repeat once 10 mg/kg IV.

Favourable response: Maintenance therapy:Phenobarbital, oral or IV, 5–10 mg/kg/24 hours as a single eveningdose.

If seizures do not cease, ADD:Phenytoin, slow IV, 15–20 mg/kg in 0.9% sodium chloride solution

over 15 minutes with ECG monitoring if possible.Do not give phenytoin IM.

Refractory statusepilepticus:

If all measures fail, give:Thiopental sodium, slow IV, 25–100 mg until seizures stop.

Note: All patients with refractory status epilepticusmust be admitted to an intensive care unit withmonitoring and laboratory services available.Cardiovascular and respiratory support (intubation+ ventilation) will always be necessary.

Metabolic acidosis: Maintain normal acid–base status. If pH ≤ 7.2, give:Sodium bicarbonate 8.5%, IV (diluted to 4.2% with sterile water).

Use formula:HCO3 needed (mmol) = base excess x 0.3 x body mass (kg)

If facilities to assess acid–base status are unavailable, administersodium bicarbonate 4.2% solution, IV, 2 mL/kg as a single dose.

1 mL sodium bicarbonate 8.5% = 1 mmol HCO3

Other biochemicaldisorders:

Correct abnormalities, if present (glucose, calcium and sodium).

Antipyretics: Paracetamol, 10 mg/kg 4–6 hourly via a nasogastric tube.

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EPILEPSY : NEONATAL SEIZURES

DefinitionTypical or atypical seizures occurring in the neonatal period.

PathogenesisNeonatal seizures are usually secondary to a serum biochemicaldisorder or an underlying brain disturbance/injury. They may be subtledue to the relatively underdeveloped cortex, and do not stop when limbsare flexed (as opposed to jitteriness).

The most likely causes are perinatal asphyxia, birth trauma,intracranial haemorrhage, meningitis, hypoglycaemia, hypocalcaemia,hypomagnesaemia, hyponatraemia, and narcotic or alcohol withdrawal.

Diagnostic criteriaCategories of convulsions:

• Subtle seizures: Tonic deviation of the eyes, fluttering of the eyelids,

sucking and chewing movements, ‘swimming’ movements of thearms, ‘cycling’ movements of the legs, apnoea, vasomotor changes.

• Tonic clonic movements.• Focal clonic movements.• Myoclonic movements.• Tonic movements.

Referral criteria• Neonatal convulsions not responding to adequate therapy.• Neonatal convulsions where the underlying cause is unclear.

Treatment objectives• Determination and treatment of the underlying cause/disorder.• Control of seizures with anticonvulsants.• Symptomatic and supportive treatment.

Page 5: Epilepsi Status Epileptikus

Treatment guidelines

NEONATAL SEIZURES

Management Comments

Non-drug treatment Identify and treat the underlying cause (e.g. meningitis, hypoxic-ischaemic encephalopathy).

Ensure an open airway and administer oxygen if necessary.Neutral thermal environment.Adequate nutrition and hydration.Monitor: Respiration, heart rate, blood pressure, blood gases, SaO2,

acid–base status, electrolytes, minerals, blood glucose,haematocrit, body temperature and maintain within acceptedphysiological range.

Follow-up by medical practitioner or at clinic/hospital.

Drug treatmentSeizure control:

Administer phenobarbital AND / OR phenytoin with concomitantmonitoring of cardiorespiratory function.

Phenobarbital: Loading dose: Slow IV, 20 mg/kg over 5 minutes.If seizures persist, administer a further 20 mg/kg IV in aliquots of5–10 mg/kg as required.

Maintenance: Oral or IV, 5–10 mg/kg/24 hours as a single dose or in2 divided doses.

Maintenance anticonvulsant therapy is usuallyconsidered for neonates with underlying braindamage due to hypoxic ischaemic encephalopathy,meningitis, intracranial haemorrhage or birth trauma.Continue until neonate is seizure-free for 2 weeks,then slowly taper to stop.If seizures recur during tapering of anticonvulsant,continue with maintenance therapy.

Phenytoin:If seizures are refractory to phenobarbital, add phenytoin.Loading dose: Slow IV, 15 mg/kg in 0.9% sodium chloride solution

over 15 minutes under ECG control.Maintenance: Oral or IV, 5–8 mg/kg/24 hours in 3 divided doses.

Phenytoin must not be given in glucose/dextrose-containing solutions. To minimise risk of precipitationadminister phenytoin in 0.9% sodium chloride solu-tion, concentration < 4 g/L, and use within 1 hour.

Clonazepam:

Consider clonazepam for seizures refractory to phenobarbitaland phenytoin.

Slow IV, 0.25–0.5 mg. Repeat as required to a maximum of 1 mgper 24 hours.

Maintenance: Oral or IV, 0.5–1 mg per 24 hours in 4 divided doses.

Cardiorespiratory support is usually indicated in thiscategory of infants.

Page 6: Epilepsi Status Epileptikus

Treatment guidelines: NEONATAL SEIZURES (continued from previous page)

Management Comments

Underlying biochemical disorders:

Hypocalcaemia: Serum total calcium ≤ 1.7 mmol/L, or ionised calcium < 0.7 mmol/L.Calcium gluconate 10%, IV, 0.2–0.5mL/kg, diluted 1:4 with 5%

dextrose water. Give preferably under ECG control over 15 minutesor until seizure ceases. Repeat if necessary.

Hypoglycaemia: Serum glucose < 2.5 mmol/LDextrose water, IV bolus, 250–500 mg/kg, followed by dextrose

water, IV, 4–6 mg/kg/minute or more until blood glucose is withinthe physiological range.

Use 50% dextrose water or 10% dextrose water.(250–500 mg/kg = 0.5–1 mL of 50% dextrose)Dilute 50% before administering.

Hypomagnesaemia: Serum magnesium < 0.6 mmol/LMagnesium sulphate 50%, IV, 0.2 mL/kg slowly over 5 minutes as a

single dose.

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INVOLUNTARY MOVEMENTS

DefinitionAbnormal involuntary movements that may mimic seizures.

PathogenesisMost cases of involuntary movements refer to a pathological process ofthe basal ganglia, midbrain and cerebellum. This could be secondary totrauma, infection, tumours, toxins or a degenerative process.

Although some involuntary movements in children may have a benigncourse, they should always be considered as signs of an intracranialpathological process.

Diagnostic criteriaInvoluntary movements include:

• Involuntary contractions that do not move a joint – fasciculation,myoclonus.

• Low amplitude jerking movements – chorea, tics, hemifacial spasms,myoclonus.

• High amplitude jerking movements – ballismus, myoclonus.• Slow writhing movements and abnormal posturing – athetosis,

dystonia.• Rhythmic movements – tremors, myoclonus.

Remember the association of Sydenham’s chorea with rheumatic fever.

Abnormal movements often mimic seizures, but may be distinguishedfrom them in the following ways:

Involuntary moments Seizures

Disappear during sleep. May persist or worsen duringsleep.

More stereotyped and persistent. Less stereotyped and persistent.No loss of consciousness. Often characterised by loss of

consciousness or awareness.No EEG abnormalities. Often accompanied by EEG

abnormalities.

Referral criteriaRefer for exclusion of an intracranial pathological process.

Treatment objectives• Determination and treatment of the underlying cause.• Supportive treatment.

Treatment guidelinesNon-drug treatment and drug treatment depend on the underlyingpathological process.

Page 8: Epilepsi Status Epileptikus

NEUROCYSTICERCOSIS

DefinitionNeurocysticercosis is the commonest parasitic disease affecting thecentral nervous system in children.

PathogenesisNeurocysticercosis is caused by the cysticercal form (larval form) of thepork tapeworm (Taenia solium). Clinical features may vary and arelargely determined by the location and stage of the life cycle of theparasite in the brain. The larvae may locate in the brain parenchyma,intraventricular and meningeal areas, spinal canal/cord and eye, or acombination of these regions. Viable cysticerci incite little inflammatoryresponse, but when they calcify they elicit an increased inflammatoryresponse.

Complications: Cysticerci in the brain may remain dormant or maycause complications such as headache, behavioural disorders, visualdisturbances, seizures, focal neurological deficits, increased intra-cranial pressure, hydrocephalus, meningitis, meningo-encephalitis,spinal cord compression.

Diagnostic criteriaClinical:

• Suspect if children from endemic areas present with neurological

abnormalities such as seizures, raised intracranial pressure/hydro-cephalus, focal neurological deficits, cranial nerve palsies, meningo-encephalitis, meningitis, behavioural disorders, headache.

Investigations:• Positive serological tests for cysticercosis (blood, cerebrospinal fluid).• Computed tomography (CT scan) and/or magnetic resonance imaging

(MRI scan) of brain showing cysts, peri-lesional oedema or calcifi-cation of cysts.

• MRI scan may identify more calcifications and viable cystic lesions thanthe CT Scan.

• Soft tissue radiology (muscles of lower limbs) may demonstratecalcified cysticerci in muscles.

Referral criteria• Neurocysticercosis not responding to adequate therapy.• Neurocysticercosis with complications, such as hydrocephalus.

Treatment objectives• Prevention or early treatment of complications.• Eradication of cysticerci.• Symptomatic and supportive treatment.• Prevention.

Page 9: Epilepsi Status Epileptikus

Treatment guidelines

NEUROCYSTICERCOSIS

Management Comments

Non-drug treatment Prevention – see comments.

Follow-up CT scans and/or MRI scans – may help to assess theresponse to therapy.

Preventative measures include:- prolonged freezing or thorough cooking of beef and

pork to kill the parasite.- thorough washing of fresh fruit and vegetables in

areas endemic for T. solium.- attention to personal hygiene.- provision of proper sanitary facilities.- avoiding the use of human excreta as fertiliser.

Drug treatmentActive disease: See comments.

Praziquantel, oral, 50 mg/kg/24 hours as a single daily dose or individed doses, for 15 days.

ORAlbendazole, oral, 15 mg/kg/24 hours in 3 divided doses for at least

8 days.

Specific drug therapy with praziquantel (oralbendazole) and dexamethasone is reserved forsymptomatic patients with active disseminateddisease with multiple viable brain cysts, widespreadperi-lesional oedema and numerous calcifications.

Albendazole is not registered for neurocysticercosis.

Neurologicalmanifestations:

Dexamethasone, oral or IM, 0.25–0.5 mg/kg/24 hours for 24 hoursprior to praziquantel or albendazole therapy. Continue for theduration of the therapy.

Dexamethasone is used for patients with severeneurological manifestations and raised intracranialpressure.

Inactive disease:

Anticonvulsants:

See comments.

For seizure control, see EPILEPSY, page 88.

Patients with inactive disease (e.g. a single or a fewcalcified brain lesions without viable cysts and peri-lesional oedema) require only symptomatic treat-ment, e.g. appropriate anticonvulsants.

Surgical treatment Ventricular peritoneal shunt procedure for hydrocephalus; removalof cysts.

Page 10: Epilepsi Status Epileptikus

POLYNEUROPATHY(Guillain-Barré Syndrome)

* Notifiable disease

DefinitionGuillain-Barré‚ is the most common polyneuropathy in children,characterised mainly by motor weakness and areflexia (absence oftendon reflexes).

PathogenesisAutoimmune-mediated demyelination is precipitated by a precedingviral or other infection.

Diagnostic criteriaClinical:

• Preceding respiratory tract infection or gastrointestinal infection.• Symmetrical, flaccid muscle weakness with early areflexia.

The muscle weakness may ascend rapidly upwards to involve thetrunk, arms, face and cranial nerves. Bulbar paralysis and respiratoryfailure may develop.

• Autonomic dysfunction.• Relatively mild, or absence of, sensory signs.• Miller-Fisher variant presents with ataxia and ophthalmoplegia.• Guillain-Barré is not to be confused with other more rare causes of

polyneuropathies such as poliomyelitis, transverse myelitis,diphtheria, and botulism.

Poliomyelitis – a rare cause of hypotonia with abrupt onset of weak-ness (often asymmetrical) in association with a febrile illness.

Transverse myelitis – initial flaccid weakness and areflexia, butrapidly progressing to spasticity and hyperreflexia; also a sensorylevel on trunk, and bladder and rectal sphincter involvement.

Botulism (food poisoning caused by Clostridium botulinum, withincubation period of 12–36 hours) – presents with nausea andvomiting, diplopia, dysphagia, dysarthria, weakness and posturalhypotension.

Diphtheria – see page 170.

Investigations:• CSF findings (after 1 week) show elevated protein and no cells or only

a few cells (albumino-cytological dissociation). Glucose is normal.

Referral criteriaGuillain-Barré syndrome with bulbar paralysis and/or early signs ofrespiratory failure.

Treatment objectives• Supportive treatment.• Appropriate treatment of infection/s.• Prevention and early treatment of complications.

Page 11: Epilepsi Status Epileptikus

Treatment guidelines

POLYNEUROPATHY

Management Comments

Non-drug treatment Admit to high care or intensive care unit.Monitor autonomic functions closely – respiratory effort and rate,

forced vital capacity (FVC), blood pressure, heart rate, bulbarfunctions and arterial blood gases.

Ventilation – see comments opposite.Provide adequate nutrition.Bladder and bowel care; pressure-point care.Routine physiotherapy for chest and lower limbs; ankles must be

kept in dorsiflexion.Eyes must be protected and kept moist.Plasmapheresis – seldom used in children.

Notifiable condition.

Ventilation is recommended when:- PCO2 levels start rising;- the FVC or peak expiratory flow rate drops below

12–15 mL/kg body mass;- tachycardia and sweating occur;

- inspiratory efforts are weak.Note: These changes precede hypoxaemia detected

on blood gas analysis, and ventilation should beginbefore frank hypoxaemia occurs. Respiratory toiletmust be impeccable.

Drug treatment Immunoglobulin, IV, 0.4 g/kg as a single daily dose on 5 consecutivedays early in the disease process.

For rapidly progressive ascending paralysis.To be used under supervision of a specialist in anintensive care setting.Immunoglobulin is not registered for this indication.

Secondary infections Treat as indicated.

Page 12: Epilepsi Status Epileptikus

PSYCHOPHARMACOLOGY GUIDELINES IN CHILDREN AND ADOLESCENTS

Effective and safe use of psychiatric drug therapy in children andadolescents is based on:

- a reliable diagnosis;- appropriate administration of the drug therapy (monotherapy,

starting with low dosage and increasing slowly, and periodic re-evaluation for side effects);

- ongoing training in the skills of assessment and diagnosis of childrenand adolescents, taking age and developmental status into account;

- ongoing interaction with patients and their families or caregiversthroughout treatment.

Depressive states in childhood and adolescenceMoods of children and adolescents are especially vulnerable to theinfluence of severe psychosocial stressors such as:

- family discord;- abuse and neglect;- academic failure.

Because children and adolescents do not easily or accurately verbalisetheir affective states, symptoms of these states are hard to recognise.Depressive symptoms and diagnostic criteria are equivalent to thosefound in adults. Children and adolescents with attention deficithyperactivity disorder, oppositional defiant deficit disorder and/orconduct disorder should be screened for mood disorders because of thehigh prevalence of mood disorders.

The following mood disorders are distinguished in children andadolescents: adjustment disorder with depressive mood; substance ormedicine-induced depressive mood disorder; bipolar 1 disorder; major

depressive disorder with of without psychoses (irritable mood andfailure to gain expected weight); dysthymic disorder (one-year period ofirritable mood); cyclothymic disorder (one-year period of numerousmood swings); schizo-affective disorder; and depressive disorder nototherwise specified.The DSM IV criteria for adults apply to children and adolescents, butwith some modifications which should be noted.

Diagnostic criteriaMajor Depressive Episode:The following depressive symptoms are commonly seen:

• Young children and adolescents: Persistence of irritable mood (insteadof depressed mood as in adults); failure to gain expected weight;suicidal ideation; insomnia; diminished ability to concentrate; patientfeels sad/blue/ miserable/unhappy/ ‘a bad feeling inside’.

• Young children: Withdrawn and sad appearance, poor self-esteem,somatic complaints, mood-congruent auditory hallucinations.

• Late adolescence: Severe psychomotor retardation, delusions,pervasive anhedonia, sense of hopelessness, negativistic or frankantisocial behaviour, feelings of restlessness, aggression,reluctance to co-operate, school difficulties.

Referral criteria• Suicidal thoughts and attempted suicide.• Major depressive mood disturbance with psychosis.• Depression not improving on medication (treatment-resistant or

refractory depression).

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Treatment approach

PSYCHOPHARMACOLOGY GUIDELINES IN CHILDREN AND ADOLESCENTS

Management Comments

Non-drug treatment Exclude substance abuse using screening tests (e.g. urine toxicol-ogical screen for cannabis abuse).

Exclude underlying medical conditions (thorough medical andneurological assessment).

Psychotherapy: family therapy, individual psychotherapy, cognitivetherapy, social and problem solving skills, supportive therapy.

Note: Immediate hospitalisation is indicated if patientis suicidal and/or to protect patient against ownimpulsive/dangerous behaviour.

Drug treatment Pharmacotherapy is indicated in major depressive episodes, dysthymic disorders, depressive disorders not otherwisespecified, and bipolar 1 disorders.

Antidepressants: Tricyclic antidepressants, e.g.Imipramine or amitriptyline, oral, < 14 years, 25–75 mg/day,

> 14 years, up to 100 mg/day.

OR (in late adolescence)

Tricyclic antidepressants are the mainstay of thetreatment of depressive disorders.Note: Overdosage with these agents can be fatal.

Caution parents/caregivers to keep medicine out ofreach of children.

Selective serotonin re-uptake inhibitors, e.g. fluoxetine. Fluoxetine is not registered for use in children.

Mood stabilisers: Indications: bipolar disorders in children and adolescents,emotional dyscontrol/aggression, intermittent explosive disorder.

Mood stabilisers should be initiated by a psychiatrist ordesignated specialist only.

Carbamazepine, oral, initially 10 mg/kg/day; may be increased to20–30 mg/kg/24 hours.

OR

Monitor blood levels. Therapeutic range: 4–12 mg/L.Monitor full blood count (FBC) for possible leucopenia.An uncommon reaction is the worsening of theaggressive behaviour and impulsivity in hyperactiveand conduct-disordered children.

Sodium valproate, oral, 20–50 mg/kg/24 hours in 2–3 divideddoses.

Monitor blood levels. Therapeutic range: 50–100 mg/LMonitor liver function for possible liver toxicity.

Page 14: Epilepsi Status Epileptikus

RABIES

* Notifiable disease

DefinitionRabies is a viral infection of the central nervous system.

Pathogenesis and complicationsThe rabies virus is usually introduced by infectious saliva in bitewounds, and travels via the peripheral nerves to the central nervoussystem, where it causes an encephalomyelitis with widespreaddegeneration, demyelination and necrosis of neurons.

The incubation period is variable and is related to the distance of thebite from the head, the severity of the bite and the amount of virus in thewound. It usually varies between 3 days and 3 months.

The pathognomonic sign in the neuronal cytoplasm and dentriticprocesses is the Negri inclusion body.

Diagnostic criteriaClinical:

• History of a bite or contact with an animal with abnormal or unusualbehaviour.

• Prodromal phase: Headache, fever, anxiety, insomnia and malaise.Paraesthesias/numbness and a tingling, burning or cold sensation atthe site of the wound may be early signs.

• Excitation phase: Convulsions, delirium, and painful spasms of thelarynx and pharynx elicited by attempts to swallow food or water(hydrophobia). Later, even the sound, smell or sight of liquid and

food may precipitate spasms. Abnormal behaviour may be present.• Aerophobia may be present and is elicited by fanning a current of air

across the face, causing spasms of the pharyngeal muscles.• Progressive paralysis and coma.

Investigations:• CSF may show pleocytosis and elevated protein, or may be normal.• Positive fluorescent antibody test on brain tissue of the animal.

Type of exposure:First risk category: Touching/feeding animal; licking of intact skin.

(No treatment necessary.)Second risk category: Nibbling of uncovered skin, superficial scratch;

no bleeding or licking of broken skin.Third risk category: Bites or scratches that penetrate the skin and

draw blood; licking of mucous membranes.

Referral criteriaRabies where the diagnosis is uncertain.

Treatment objectives• Preventative measures.• Symptomatic and supportive treatment.

Page 15: Epilepsi Status Epileptikus

Treatment guidelines

RABIES

Management Comments

Non-drug treatmentPost-exposure

prophylaxis:

Prompt cleansing of the bite/wound with soap and water followed byapplication of an antiseptic solution such as povidone iodine 10 %or chlorhexidine 0.05 % in water.

Avoid suturing – use compressive dressing if necessary.Symptomatic and supportive treatment.

The aim is to prevent infection becoming establishedin a patient who has been bitten by an animal withrabies, by cleaning the bite/wound and immunisingthe patient.

Rabies is unlikely if the animal remains alive formore than 10 days. Consult with veterinarian.

Rabies is a notifiable disease.Drug treatment

Post-exposureprophylaxis:

(second and thirdrisk categories)

Unimmunisedpatient:

Human rabies immunoglobulin, 20 IU/kg/dose.Infiltrate as much as anatomically possible subcutaneously at thesite of the wound and into the depth of the wound. The remainderof the dose is injected IM (buttock).

PLUSRabies vaccine (human diploid cell strain virus, HDCV), IM, 1 mL

into the deltoid muscle. Repeat 3, 7, 14, 28 and 90 days afterexposure. (Course of 6 injections.)

Rabies vaccine adsorbed (inactivated) RVA can beused in infants.

Antibiotic therapy: Benzylpenicillin, IV, 200 000 units/kg in 4 divided doses for 5 daysOR

Phenoxymethylpenicillin, oral, < 1 year, 62.5 mg 6 hourly for 5 days,1–6 years, 125 mg 6 hourly for 5 days,> 6 years, 250 mg 6 hourly for 5 days.

Tetanus prophylaxis: Tetanus toxoid, IM, 0.5 mL.

Immunised patient: Rabies vaccine (HDCV), IM, 1 mL. Repeat on day 3 after exposure.No rabies immunoglobulin should be administered.

Only 2 boosters are required after an incident ofexposure to infection — on days 0 and 3.

Frank/confirmedrabies:

Symptomatic and supportive treatment. Specific chemotherapy forrabies is not available.

Immunoglobulin and vaccine are contraindicated infrank rabies.

Pre-exposureprophylaxis

High-risk individuals, veterinarians, health workers, etc.:Rabies vaccine (HDCV), IM, 1 mL, repeated on days 7 and 28.

A single booster dose is given every 2–3 years.

Vaccinate domestic animals; keep them fenced in ortied up. Restrict movement of domestic animalsbetween rabies and non-rabies areas.

Page 16: Epilepsi Status Epileptikus

5. Dermatology

CELLULITIS

DefinitionInfection of the skin and subcutaneous tissue.

Pathogenesis and complicationsAny area of the body may be affected. The port of entry of micro-organisms is often an insect bite, superficial abrasion or penetratingwound. Cellulitis may also be preceded by a skin infection, e.g.impetigo, ecthyma, folliculitis.

There is a rapid, local spread of the infection involving the skin,subcutaneous tissue and lymphatic pathways. Minimal localsuppuration occurs, and the infection may spread to involve otherstructures or enter the bloodstream to cause septicaemia. Cellulitis iscommonly associated with streptococci, H. influenzae type b andsometimes, staphylococci.

Diagnostic criteria• Acutely ill child; fever, malaise.• Involved area is swollen, indurated, erythematous and painful/tender

with regional lymphadenopathy.• If the affected area involves the face, and the area is well demarcated,

very tender and warm with a bright red, swollen appearance andfirm borders, the condition is called erysipelas, and is generallycaused by streptococci.

Referral criteriaCellulitis not responding to adequate therapy.

Treatment objectives• Eradication of the infection.• Symptomatic and supportive treatment.

Page 17: Epilepsi Status Epileptikus

Treatment guidelines

CELLULITIS

Management Comments

Non-drug treatment Ensure adequate nutrition and hydration. Observe for complications, e.g. septicaemia.

Drug treatmentIf streptococci are

suspected:

Benzylpenicillin, IV, 200 000 units/kg/24 hours in 4 divided doses(6 hourly) for 5 days.

ORPhenoxymethylpenicillin, oral, 125–250 mg 6 hourly for 5 days.

Choice of intravenous or oral antibiotics depends onthe severity of the condition.

If staphylococci aresuspected:

Cloxacillin, IV, < 2 years, 62.5–125 mg 6 hourly for 5 days,≥ 2 years, 250–500 mg 6 hourly for 5 days.

ORFlucloxacillin, oral, < 2 years, 62.5 mg 6 hourly for 7 days,

2–10 years, 125 mg 6 hourly for 7 days,> 10 years, 250 mg 6 hourly for 7 days.

If H. influenzae issuspected:

Ampicillin, IV, 50–100 mg/kg/24 hours in 4 divided doses for 5 days.OR

Amoxicillin, oral, < 20 kg, 20–40 mg/kg/24 hours in 3 divided doses,> 20 kg, 250–500 mg 8 hourly, for 5 days.

Penicillin-allergy:

If H. influenzae issuspected:

Erythromycin, oral, 30–50 mg/kg/24 h in 4 divided doses for 5 daysOR

Chloramphenicol, oral or IV, 50−100 mg/kg/24 hours in 4 divideddoses for 5−7days.

If no response to erythromycin suspect H. influenzae.

Analgesics:Severe pain:

Tilidine, oral, 1 drop for each year of age plus 2 drops, 6–8 hourlyfor 48–72 hours. Maximum 10 drops/dose.

ORPethidine, IM or IV, 0.5–2 mg/kg 6–8 hourly for 48–72 hours.

Maximum 6 mg/kg/24 hours.

1 drop = 2.5 mg (50 mg per 0.5 mL = 20 drops)Not recommended for infants < 1 year of age.

Antipyretic/analgesic/anti-inflammatory:

Paracetamol, oral, 10 mg/kg 6 hourly.Ibuprofen, oral, 20 mg/kg/24 hours in 4 divided doses for 72 hours.

(Under 30 kg, maximum 500 mg/day).

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ERYTHEMA MULTIFORME / STEVENS-JOHNSON SYNDROME

DefinitionAcute, vesico-bullous disorder with numerous manifestations on theskin, mucous membranes and, occasionally, internal organs.

PathogenesisPathogenesis is unknown, but erythema multiforme is generallyregarded as a hypersensitivity reaction triggered by drugs(sulphonamides, phenytoin), infections (herpes simplex, Mycoplasma)or exposure to toxic substances.

Complications include conjunctivitis, uveitis, corneal scarring, fluid loss,infections, anaemia, and oesophageal strictures.

Diagnostic criteria• Erythema multiforme minor: Prodromal symptoms are generally

absent. Symmetric crops of skin lesions of diverse morphology,primarily on the extensor surfaces of the arms and legs (oftenincluding soles and palms) with relative sparing of the mucousmembranes and the trunk.

• Iris or target lesions (pathognomonic for erythema multiforme)consisting of a dark centre, an inner pale ring and an erythematousouter border.

• Erythematous macules that evolve into papules, vesicles, bullae,urticarial plaques or patches of confluent erythema. The centre ofthe lesion may be vesicular, purpuric or necrotic.

• Erythema multiforme major (Stevens-Johnson syndrome): Aserious, systemic condition involving the skin and at least twomucous membranes. Eruption may be preceded by non-specificprodromal symptoms like malaise, fever, chills or upper respiratoryinfection. Cutaneous lesions tend to rupture, leaving the skindenuded, with fluid loss, anaemia and high risk of infection.Involvement of oral mucosa is common.

Referral criteria• Erythema multiforme minor or major not responding to adequate

therapy.• Erythema multiforme minor or major with ocular involvement.

Treatment objectives• Avoidance of the triggering event/agent.• Symptomatic and supportive treatment.

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Treatment guidelines

ERYTHEMA MULTIFORME / STEVENS-JOHNSON SYNDROME

Management Comments

Non-drug treatment Frequent mouth washes for oral lesions.Nasogastric feeds if unable to eat. IV alimentation if enteral feeds are

not possible.IV infusion with dextrose-containing paediatric maintenance solution.Cool compresses and wet dressings.Fresh frozen plasma, IV, 20 mL/kg over 4 hours.If anaemic: Blood, IV, 10–20 mL/kg over 2 hours.

Admit to high care or intensive care unit ifavailable.

Examine daily for infection and ocular lesions.Do not puncture bullae or vesicles.

Drug treatment Promethazine, oral, 0.125 mg/kg 6 hourly, ORoral or IV, 0.5 mg/kg as a single dose at night.

Prednisone, oral, 1−2 mg/kg/24 hours as a single dose or in divideddoses. Maximum 60 mg per 24 hours.

ORDexamethasone, IV, 1–2 mg/kg/24 hours in 3 divided doses for 5 days.

Systemic antibiotics:(if infection is

suspected)

Erythromycin, oral, 30–50 mg/kg/24 hours in 4 divided doses for 10days.

ORAmoxicillin, oral, < 20 kg, 20–40 mg/kg/24 hours in 3 divided doses,

> 20 kg, 125–250 mg 8 hourly, for 10 days.

Send blood and skin lesion specimens for cultureand sensitivity before initiating antibiotic therapy.Reassess choice of antibiotic when culture andsensitivity results become available.Use IV antibiotics if the oral route cannot be used.

Analgesics: Tilidine, oral, 1 drop for each year of age plus 2 drops, 6–8 hourly asneeded. Maximum 10 drops/dose.

ORPethidine, IM or IV, 1 mg/kg 6–8 hourly as needed.

1 drop = 2.5 mg (50 mg per 0.5 mL = 20 drops)Not recommended for infants < 1 year of age.

Less severe pain: Paracetamol, oral, 10 mg/kg 6 hourly as needed.

Mouth wash: Chlorhexidine gluconate solution 0.2 %. Rinse mouth as needed. Do not swallow.

Page 20: Epilepsi Status Epileptikus

6. Ear, nose and throat

EPIGLOTTITIS

DefinitionLife-threatening upper airway obstruction at the level of the supraglotticstructures (epiglottis and arytenoids).

PathogenesisAcute infection/inflammation and swelling of the epiglottis and othersupraglottic structures, usually caused by H. influenzae type b.

Epiglottis is an upper airway emergency.

Complications include acute total airway obstruction with hypoxia.

Diagnostic criteria• Acute onset, fever, sore throat, dysphagia, refusal to eat or swallow,

drooling, muffled voice, toxic appearance.

• Position of comfort to protect the upper airway: sitting upright, headforward, open mouth, neck in extension.

• ‘Cherry red’ swollen epiglottis.• Total upper airway obstruction is imminent by the time stridor appears.

Referral criteriaCompromised airway and intubation inevitable.

Treatment objectivesMedical emergency.

• Relieve airway obstruction/secure airway.• Prevent hypoxia.• Treat underlying infection.

Page 21: Epilepsi Status Epileptikus

Treatment guidelines

EPIGLOTTITIS

Management Comments

Non-drug treatment Provide supplemental humidified oxygen and monitor oxygensaturation of haemoglobin (pulse oximeter).Maintain oxygen saturation at ≥ 95%.

Prepare equipment for bag-mask ventilation, endotrachealintubation, needle cricothyrotomy and tracheostomy.

Carefully start an IV line and administer appropriate antibiotic/s.

Airway obstruction: If airway obstructs completely or respiratory arrest occurs, attempt toestablish an airway by any means to prevent hypoxia and death.1) Attempt bag-mask ventilation.2) If unable to ventilate, intubate.3) If unable to intubate, perform needle or surgical cricothyrotomy.

Attempt extubation after 48–72 hours.

After an open airway has been secured:- Take blood for cultures and a swab from the epiglottis for

microscopy, culture and sensitivity.- Monitor heart rate, respiratory rate, blood pressure, and SaO2.- Ensure adequate nutrition and hydration.

Do not interfere with the protective mechanism of thepatient. Allow the child to remain sitting up.Avoid all measures that could agitate the patient;- make no attempt to see the epiglottis;- do not ask for X-rays of neck and chest routinely;- delay blood sampling until after airway is secured.

Under ideal conditions, the patient should beintubated before referral as total airway obstructionmay occur suddenly and quite unpredictably.

If intubation before referral is not possible, transportpatient immediately to a centre where laryngoscopyand intubation/tracheostomy can be performed,preferably under general anaesthesia in anoperating theatre.Inform the hospital before departure.A person able to perform an emergency intubation ortracheostomy must accompany the patient duringtransport.

Drug treatmentAntibiotics: Cefotaxime, IV, 100 mg/kg/24 hours in 3 divided doses (8 hourly) for

7 days.OR

Ampicillin, IV, < 20 kg, 50–100 mg/kg/24 hours in 4 divided doses(6 hourly) for 7 days,

> 20 kg, 250–500 mg 6 hourly for 7 days,plus

Chloramphenicol, IV, 50–100 mg/kg/24 hours in 4 divided doses(6 hourly) for 7 days.

Steroids: Dexamethasone, IV, 1 mg/kg daily as a single dose, until extubation.

Page 22: Epilepsi Status Epileptikus

EPISTAXIS(Nose bleed)

DefinitionNasal bleeding.

PathogenesisNasal bleeding may be spontaneous or precipitated by minor trauma,fever, infection or allergic rhinitis. Bleeding usually arises from a richblood vessel plexus on the caudal part of the septum (Little’s area).Epistaxis may also be a sign of a more serious underlying disorder suchas haemophilia/von Willebrand’s disease, thrombocytopenia, hyper-tension, tumour, or may be due to anticoagulant therapy.

Complications include recurrent epistaxis, anaemia and hypovolaemicshock.

Diagnostic criteria• History of spontaneous nose bleeds.

• Recurrent nose bleeds.• Signs and symptoms of an underlying disorder which may cause

epistaxis.

Referral criteria• Epistaxis caused by a serious underlying disorder.• Epistaxis which fails to respond to treatment.• Recurrent epistaxis.

Treatment objectives• Stop the bleeding.• Identification and treatment of underlying disorder.• Treatment of anaemia and/or shock.

Page 23: Epilepsi Status Epileptikus

Treatment guidelines

EPISTAXIS (Nose bleed)

Management Comments

Non-drug treatmentDigital pressure:

See comments.Apply direct digital pressure to the lower nose over the bleeding site

for 10 minutes; place ice over the nasal bridge.If not effective, clots should be removed by suction or blowing nose.

The child should sit up and lean forward so as not toswallow the blood, and should breathe through themouth.

Local haemostatic:If simple measures fail to control the bleeding:Visualise the bleeding site and insert a small piece of gelatin sponge

or topical thrombin over the bleeding site.

Cauterisation: Cauterise the bleeding point (chemical or electrical cauterisation).

Anterior nasal pack:OR

Anterior nasal packing, using BIPP-coated ribbon gauze soaked in atopical vasoconstrictor such as adrenaline 1:1000.Pack is introduced along the floor of the nose and built up in loopstowards the roof, applying even pressure to the nasal mucosa.

Apply a topical anaesthetic agent before attemptingcauterisation, or perform under general anaesthetic.

Anaesthetise the nasal mucosa with a topicalanaesthetic agent before inserting the anterior nasalpack.

Post nasal pack: If bleeding is from far back, insert a post nasal pack under generalanaesthesia. Pass a catheter through the nose and bring it outthrough the mouth. The post nasal pack (a ball of gauze with tapesattached) is fixed to the oral end of the catheter. The nasal end isthen withdrawn to pull the pack into the mouth. Position the packbehind the soft palate with your finger. Further traction on thecatheter will pull the pack firmly into the back of the nose.

Secure the pack to avoid obstruction of the airway.Leave the pack in place for 24 hours.

Surgical intervention: Surgical intervention if all the above measures fail.

Anaemia: Blood, IV, 10 mL/kg, if anaemic (Hb ≤ 7 g%).

Drug treatment Topical application of a cotton wool plug soaked in a mixture ofadrenaline 1:1000 and lidocaine 1%.

Avoid drugs interfering with platelet function.

Antibiotics: Amoxicillin, oral, 125–250 mg 8 hourly for 7 daysOR, if allergic to penicillin,

Erythromycin, oral, 30–50 mg/kg/24 hours in 4 divided doses for 7 days.

Give antibiotic therapy to patients with a nasal pack.

Page 24: Epilepsi Status Epileptikus

LARYNGOTRACHEOBRONCHITIS, ACUTE VIRAL(CROUP)

DefinitionPotentially life-threatening airway obstruction in children.

PathogenesisViral infection and inflammation of the larynx, vocal cords, subglotticpart of larynx and nearby structures. Viruses responsible for most casesare: para-influenza virus (most common), measles, herpes simplex andadenovirus.Acute viral laryngotracheobronchitis is one of the commonest causes ofstridor in children aged between 6 months and 2 years.

Complications include airway obstruction with hypoxia and respiratoryfailure.

Diagnostic CriteriaClinical:

• Previously healthy child who develops progressive inspiratoryobstruction, with a barking cough and stridor, a day or two after theonset of an upper respiratory tract infection.

• A mild fever may be present. Systemically, the child is not ill andphysical findings are limited to the respiratory system.

• Stridor becomes softer as airway obstruction becomes more severe.The following features suggest a different diagnosis:

- Acute onset of obstruction (foreign body or angioneurotic oedema);- Incomplete immunisation and a membrane in the upper airway

(diphtheria);- Dysphagia, drooling and sitting position (epiglottitis, retropharyn-

geal abscess);- Erythematous rash in a very ill child (staphylococcal disease).

Assessment of severity of airway obstruction

Severity Inspiratoryobstruction

Expiratoryobstruction

Pulsusparadoxus

Grade 1 +

Grade 2 + + (passive expiration)

Grade 3 + + (active expiration usingabdominal muscles)

+

Grade 4 Cyanosis, apathy, marked retractions, impending apnoea

Referral criteria• Grade 3 airway obstruction, not responding to adequate treatment.• Grade 4 airway obstruction.

Under ideal conditions, patient should be intubated before referral.If this is not possible, a person able to perform an emergencyintubation should accompany the patient.

Treatment objectives• Relieve obstruction.• Exclusion of other causes of airway obstruction, such as foreign body,

angioneurotic oedema, epiglottitis and diphtheria.• Prevention of hypoxia and hypercarbia.• Supportive treatment.

Page 25: Epilepsi Status Epileptikus

Treatment guidelines

ACUTE VIRAL LARYNGOTRACHEOBRONCHITIS (CROUP)

Management Comments

Non-drug treatment Admit to high care or intensive care ward, depending on severity.Minimal handling.Keep child comfortable and avoid painful procedures.Maintain adequate hydration.Continue with oral feeds if possible.Monitor oxygen saturation, heart rate, respiratory rate, blood gases

and acid–base status.Supportive treatment.

Note: The early clinical picture of bacterial tracheitis(pseudomembranous croup) is very similar to thatof viral croup. However, instead of gradualimprovement, patients develop high fever, toxicity,and progressive airway obstruction unresponsiveto viral croup therapy.

Bacterial tracheitis treatment includes appropriateintravenous antibiotics. Organisms most commonlyinvolved are S. aureus and S. pneumoniae.

Drug treatmentGrade 1 obstruction: Prednisone, oral, 2 mg/kg as a single dose

ORDexamethasone, IV or IM, 0.5 mg/kg as a single dose.Repeat after 12–24 hours if no improvement.

Observation. Mist therapy may have soothing effect.

Do not give steroids to patients with measles orherpes infection.

Grade 2 obstruction: Steroids as for grade 1 obstruction.Nebulised adrenaline with oxygen, 1 mL adrenaline 1:1000 + 1 mL

0.9% sodium chloride solution. Repeat every 15–30 minutes untilexpiratory obstruction is abolished.

Monitor oxygen saturation and heart rate.

Grade 3 obstruction: Give steroids and nebulised adrenaline inhalations as above.If no improvement within 1 hour, intubate under general anaesthesia

or perform a tracheostomy under general anaesthesia.

Monitor oxygen saturation and heart rate.

Grade 4 obstruction: Give steroids and continue with adrenaline nebulised with 100%warm humidified oxygen.

Emergency intubation or intubation under general anaesthesia ifcircumstances permit.

Antipyretics: Paracetamol, oral, 10 mg/kg 4–6 hourly until fever subsides.

Page 26: Epilepsi Status Epileptikus

OTITIS MEDIA, COMPLICATIONS

DefinitionInfection and inflammation of the middle ear with complications.

PathogenesisPathogenic micro-organisms from the nasopharynx reach the middleear via the eustachian tube. Infection and inflammation may spread toall other adjacent anatomical structures with suppuration, bone necrosisor septic thrombophlebitis. Micro-organisms involved include pneumo-cocci, streptococci, H. influenzae, staphylococci, Pseudomonas, M.catarrhalis, and anaerobes.

Complications include acute mastoiditis, meningitis, extradural abscess,brain abscess (temporal lobe and cerebellum), labyrinthitis, lateralsinus thrombosis, cranial nerve paralysis, petrositis.

Diagnostic criteriaAcute mastoiditis:

• Fever, severe pain, increasing deafness, tenderness over mastoidantrum.

• Swelling in post-auricular area. Pinna is pushed down and forward.• Tympanic membrane is usually perforated with otorrhoea.• Occasionally, pus breaks through the mastoid tip and forms an abscess

in the neck (Bezold’s abscess).• Mastoid X-rays show opacity and air-cell coalescence.

Meningitis – discussed on page 178.

Extradural abscess – usually with clinical features of acute mastoiditis.

Brain abscess (cerebellum or temporal lobe):• Systemic effects of infection: Malaise, pyrexia.• Raised intracranial pressure: headache, drowsiness, confusion,

impaired consciousness, papilloedema, bradycardia, hypertension.• Localising signs (any of the following):

- Cerebellar abscess: neck stiffness, weakness and loss of tone onsame side as abscess, ataxia (falling to same side), intentiontremor with past pointing, dysdiadochokinesis, nystagmus, vertigo.

- Temporal lobe abscess: dysphasia, contralateral upper quadrantichomonymous hemianopia, paralysis contralateral face and arm,rarely leg, hallucinations of taste and smell.

• CT scan and/or MRI scan for confirmation and localisation of theabscess.

Labyrinthitis:• Vertigo, nausea, vomiting, nystagmus towards opposite side, and

deafness.

Lateral sinus thrombosis:• Symptoms and signs may be indistinguishable from those of acute

mastoiditis, with or without features of meningitis or brain abscess.• Compression of the contralateral internal jugular vein may increase

cerebrospinal fluid pressure. No rise in cerebrospinal fluid pressurewith compression of the ipsilateral internal jugular vein.

Facial paralysis/paresis:• Lower motor neuron paresis/paralysis: whole side of face is affected on

the side of pathology; inability to close the eye and upward rolling ofthe eye on the affected side. Drooping of angle of the mouth andloss of nasolabial fold on the affected side; inability to causewrinkles of the forehead on the affected side.

Petrositis:• Diplopia (palsy of lateral rectus eye muscle).• Pain in distribution of trigeminal nerve.

Referral criteria• Otitis media where intracranial suppuration is suspected.• Otitis media with complications not responding to adequate treatment.

Treatment objectives• Eradication of the infection with antibiotics.• Drainage of abscess/pus.• Corrective and/or palliative surgical interventions.• Symptomatic and supportive treatment.

Page 27: Epilepsi Status Epileptikus

Treatment guidelines

OTITIS MEDIA, COMPLICATIONS

Management Comments

Non-drug treatment Ear toilet.

Surgical treatment Corrective and/or palliative surgical interventions such as mastoid-ectomy, drainage of brain abscess through burr hole or craniotomy.

Drug treatment

Mastoiditis:

Initiate treatment with ampicillin + cloxacillin + metronidazole.

Ampicillin, IV, < 20 kg, 50–100 mg/kg/24 hours in 4 divided dosesfor 14 days,

> 20 kg, 250–500 mg 6 hourly for 14 days.PLUS

Cloxacillin, IV, 50–100 mg/kg/24 hours in 4 divided doses for 14 days.PLUS

Metronidazole, oral, 7.5 mg/kg 8 hourly for 14 days.

Suspectedmeningitis or

brain abscess:

Ceftriaxone + cloxacillin + metronidazole.Ceftriaxone, IV or IM, 20–50 mg/kg/24 hours as a single dose or in 2

divided doses for 14 days.PLUS

Cloxacillin, IV, 50–100 mg/kg/24 hours in 4 divided doses for 14 days.PLUS

Metronidazole, oral, 7.5 mg/kg 8 hourly for 14 days.

Collect blood, pus and other specimens for Gramstain, microscopy, culture and sensitivity tests beforeinitiation of antibiotic therapy. Reassess antibiotictherapy as soon as culture results become availableor if response to antibiotic therapy is unsatisfactory.

Complications following acute otitis media areusually caused by Gram-positive organisms.Complications in patients with chronic otitis mediaare usually caused by Gram-negative organisms andanaerobes.

Oral antibiotics: Amoxicillin, oral, < 20 kg, 20–40 mg/kg/24 hours in 3 divided dosesfor 7–14 days,

> 20 kg, 250–500 mg 8 hourly for 7–14 days.

Flucloxacillin, oral, < 2 years, 62.5–125 mg 6 hourly for 7–14 days,> 2 years, 125–500 mg 6 hourly for 7–14 days.

Oral antibiotics may be considered after 7 days of IVantibiotic treatment (except meningitis and brainabscess) if there are clear signs of improvement.If oral antibiotics are considered, replace ampicillinwith amoxicillin, and cloxacillin with flucloxacillin.

Page 28: Epilepsi Status Epileptikus

Treatment guidelines: OTITIS MEDIA, COMPLICATIONS (continued from previous page)

Management Comments

Penicillin allergy: Erythromycin + (clindamycin or metronidazole).Erythromycin, IV or oral, 25–50 mg/kg/24 hours in 4 divided doses

for 14 days.PLUS

Clindamycin, IV or oral, 15–40 mg/kg/24 hours in 4 divided doses,or

Metronidazole, IV or oral, 7.5 mg/kg 8 hourly for 14 days.

Patients allergic to penicillin may also be allergic tocephalosporins and carbapenems.

Suspectedmeningitis or

brain abscess:

Ceftriaxone + (clindamycin or metronidazole).Ceftriaxone, IV or IM, 20–80 mg/kg/24 hours as a single dose or in 2

divided doses for 14 days.PLUS

Clindamycin or metronidazole, dosages above.

Penicillin andcephalosporin

allergy:

Chloramphenicol, oral or IV, 50−100 mg/kg/24 hours in 4 divideddoses for 14 days.

Replace ceftriaxone with chloramphenicol in patientsallergic to penicillin and cephalosporins.

Resistantstaphylococci:

Vancomycin, IV infusion over at least 1 hour, 20 mg/kg 12 hourly for10−14 days.

Monitor vancomycin blood levels.

Pseudomonas: Ceftazidime, IV, 30–150 mg/kg/24 hours in 3 divided doses for 14days.

Analgesic/antipyretic/anti-inflammatory:

Paracetamol, oral, 10 mg/kg 6 hourly.OR

Ibuprofen, oral, 20 mg/kg/24 hours in 3 divided doses for 5 days.(Under 30 kg, maximum 500 mg/day).

Page 29: Epilepsi Status Epileptikus

SINUSITIS, CHRONIC AND COMPLICATED

DefinitionChronic or recurrent inflammation of the paranasal sinuses.

PathogenesisChronic infection and inflammation of the paranasal sinuses, with orwithout complications, may result from an underlying abnormality, e.g.allergic rhinitis, polyp, foreign body, septal deviation, diving sports,immune defect. Causative pathogens include S. pneumoniae, H.influenzae, S. aureus, Moraxella catarrhalis and anaerobes.

Complications include:Spreading of infection to orbital structures: periorbital cellulitis,

subperiosteal or intraorbital abscess.Central nervous system involvement: cavernous sinus thrombosis,

meningitis, epidural, subdural or intracerebral abscess.Bone and soft tissue involvement: osteomyelitis.

Diagnostic criteriaClinical:

• Chronic purulent postnasal drip, nasal congestion, headache, facialpain or percussion tenderness, periorbital swelling, fever.

• Signs and symptoms of complications:- signs of meningeal irritation (neck stiffness, positive Kernig’s and

Brudzinski’s signs);- signs of increased intracranial pressure (hypertension, bradycardia,

papilloedema, headache);

- signs of involvement of orbital structures (periorbital oedema,erythema, chemosis, proptosis, vision loss, ophthalmoplegia);

- signs of brain involvement (neurological signs, ataxia, paresis,paralysis, convulsions, altered level of consciousness).

Investigations:• X-ray or CT scan may show opacities and fluid levels.• CT scan will show if there is involvement of intracranial structures, e.g.

brain abscess.• Pus, cerebrospinal fluid (CSF) and blood for culture and sensitivity

tests. Microscopy and Gram-staining of pus and CSF specimensmay give some indication of the micro-organism/s involved.

Referral criteria

Spread of infection to eye/orbital structures or intracranialstructures/brain necessitates immediate referral.

• Sinusitis not responding to adequate treatment.• Lavage, drainage and other surgical procedures.

Treatment objectives• Identification and treatment of underlying predisposing factors.• Eradication of the infection.• Prevention or early treatment of complications.• Symptomatic and supportive treatment.

Page 30: Epilepsi Status Epileptikus

Treatment guidelines

SINUSITIS, CHRONIC AND COMPLICATED

Management Comments

Non-drug treatment Identify and treat the underlying cause, e.g. nasal allergy. Follow-up by medical practitioner or at clinic/hospital.

See comments.Drug treatment

Less severe cases:(oral antibiotics)

Amoxicillin + flucloxacillin + metronidazole for 10–14 days.Amoxicillin, oral, < 20 kg, 20–40 mg/kg/24 hours in 3 divided doses,

> 20 kg, 250–500 mg 8 hourly.PLUS

Flucloxacillin, oral, < 2 years, 62.5–125 mg 6 hourly,> 2 years, 125–500 mg 6 hourly.

PLUSMetronidazole, oral, 7.5 mg/kg 8 hourly.

Severe sinusitiswithout

complications:

Ampicillin + cloxacillin + metronidazole for 10–14 days.Ampicillin, IV, < 20 kg, 50–100 mg/kg/24 hours in 4 divided doses,

> 20 kg, 250–500 mg 6 hourly.PLUS

Cloxacillin, IV, < 2 years, 62.5–125 mg 6 hourly,> 2 years, 125–500 mg 6 hourly.

PLUSMetronidazole, oral, 7.5 mg/kg 8 hourly.

Sinusitis withintracranial

complications:

Ceftriaxone + metronidazole + vancomycin for 10−14 days.Ceftriaxone, IV, 80 mg/kg/24 hours as a single daily dose. Maximum

4 g per 24 hours.PLUS

Metronidazole, oral, 7.5 mg/kg 8 hourly.PLUS

Vancomycin, IV infusion over at least 1 hour, 20 mg/kg 12 hourly.

Use appropriate antibiotic therapy based on cultureand sensitivity results.Initiate empirically and reassess as soon as cultureand sensitivity results become available or if there isno improvement within 48–72 hours.Intravenous antibiotics are indicated for sinusitis withorbital or intracranial complications and for severesinusitis without complications.Oral antibiotics may be considered after 7 days of IVantibiotics in severe sinusitis without complications, ifthere are clear signs of improvement.

Monitor vancomycin blood levels.

Page 31: Epilepsi Status Epileptikus

Treatment guidelines: SINUSITIS, CHRONIC AND COMPLICATED (continued from previous page)

Management Comments

Sinusitis with orbitalcomplications:

Ceftriaxone + clindamycin for 10−14 days.Ceftriaxone, IV, 80 mg/kg/24 hours as a single daily dose. Maximum

4 g per 24 hours.PLUS

Clindamycin, IV or oral, 25–40 mg/kg/24 hours in 4 divided doses.Clindamycin: Dilute IV infusion to concentrations of≤ 6 mg/mL.

Penicillin / cephalo-sporin allergy:

Sinusitis, less severeand severe without

complications:

Erythromycin + (clindamycin or metronidazole) for 10−14 days.Erythromycin, IV or oral, 25–50 mg/kg/24 hours in 4 divided doses.

PLUSClindamycin, IV or oral, 25–40 mg/kg/24 hours in 4 divided doses,

orMetronidazole, IV or oral, 7.5 mg/kg 8 hourly.

Sinusitis withintracranial/central

nervous systemcomplications:

Vancomycin + metronidazole + chloramphenicol for 10−14 days.Vancomycin, IV infusion over at least 1 hour, 20 mg/kg 12 hourly.

PLUSMetronidazole, IV or oral, 7.5 mg/kg 8 hourly.

PLUSChloramphenicol, oral or IV, 50−100 mg/kg/24 hours in 4 divided

doses.

Monitor vancomycin blood levels.

Sinusitis with orbitalcomplications:

Clindamycin + chloramphenicol for 10–14 days.Clindamycin, IV or oral, 25–40 mg/kg/24 hours in 4 divided doses.

PLUSChloramphenicol, oral or IV, 50−100 mg/kg/24 hours in 4 divided

doses.

Resistantstaphylococci:

Vancomycin, IV infusion over at least 1 hour, 20 mg/kg 12 hourly for10–14 days.

Monitor blood levels.

Page 32: Epilepsi Status Epileptikus

Treatment guidelines: SINUSITIS, CHRONIC AND COMPLICATED (continued from previous page)

Management Comments

Amoxicillin andampicillin resistance:

Amoxicillin and clavulanic acid combination, oral,amoxicillin 20–40 mg/kg/24 hours + clavulanic acid 5 mg/kg/24hours in 3 divided doses for 10–14 days.

Consider oral amoxicillin + clavulanic acid wherethere is evidence that the micro-organism sensitivitypatterns for ampicillin and amoxicillin are becomingless favourable and higher doses are required fortreatment.

Nasal decongestant: Oxymetazoline 0.025% nose drops, 2 drops in each nostril 8 hourlyfor a maximum of 5 days.

Analgesic/antipyretic/anti-inflammatory:

Paracetamol, oral, 10 mg/kg 6 hourly until fever subsides.OR

Ibuprofen, oral, 20 mg/kg/24 hours in 3–4 divided doses for 5 days.(Under 30 kg, maximum 500 mg/day).

Surgical treatment Sinus lavage/wash out, drainage procedures.

Page 33: Epilepsi Status Epileptikus

TONSILLITIS, COMPLICATED(Peritonsillar cellulitis, peritonsillar abscess, retropharyngeal abscess)

DefinitionInfective process involving the tonsils.

PathogenesisInfective process involving the tonsils and peritonsillar tissues causedby bacteria (e.g. beta-haemolytic streptococci, H. influenzae, staphylo-cocci, diphtheroids, anaerobes) and viruses.

Complications:Local complications include peritonsillar cellulitis and abscess

(quinsy), parapharyngeal abscess, retropharyngeal abscess andsuppurative cervical adenitis.

Systemic complications include glomerulonephritis, rheumatic fever,and bacterial endocarditis.

Diagnostic criteriaClinical:

• Pyrexia, headache, malaise.• Sore throat, dysphagia, refusal to eat, drooling.• Earache (referred otalgia).• Tender and enlarged cervical lymph nodes.

• Enlarged hyperaemic tonsils with pus exuding from the crypts.• Signs of peritonsillar abscess: Usually unilateral; soft palate and

uvula on the infected side are oedematous and displaced mediallytowards the uninvolved side.

• Signs of retropharyngeal abscess: Swelling on one side of posteriorpharyngeal wall and hyperextension of the neck.

Investigations:• Lateral X-ray of the neck may show the retropharyngeal space to be

wider than the C4 vertebral body when a retropharyngeal abscess ispresent.

Referral criteriaTonsillitis with local and/or systemic complications not responding toadequate treatment.

Treatment guidelines• Eradication of the offending micro-organism.• Drainage of abscesses.• Symptomatic and supportive treatment.• Tonsillectomy.

Page 34: Epilepsi Status Epileptikus

Treatment guidelines

TONSILLITIS, COMPLICATED (Peritonsillar cellulitis, peritonsillar abscess, retropharyngeal abscess)

Management Comments

Non-drug treatment Abscesses must be drained:- Peritonsillar abscess could be drained by aspiration (needle/

syringe). Intra-oral incision or Quinsy tonsillectomy under generalanaesthesia is preferred in a small child.

- Parapharyngeal abscess bulging in the neck should be drainedexternally.

- Retropharyngeal abscess could be drained by aspiration, butpreferably by intra-oral incision.

- Suppurative cervical adenitis is drained externally.

Tonsillectomy is usually performed 6 weeks afterabscess has been drained or systemic complicationshave settled.

Drug treatmentEmpirical treatment: Initiate treatment with benzylpenicillin and metronidazole, IV, until

culture results are available.

Streptococci: Benzylpenicillin, IV, 250 000 units/kg/24 hours in 4 divided doses for7 days.

ORPhenoxymethylpenicillin, oral, < 5 years, 125 mg 6 hourly for 7 days,

> 5 years, 250 mg 6 hourly for 7 days.

In children who have difficulties in swallowing,administer IV antibiotics until swallowing becomeseasier.

Staphylococci: Cloxacillin, IV, 50–100 mg/kg/24 hours in 4 divided doses for 7 daysOR

Flucloxacillin, oral, < 2 years, 62.5 mg 6 hourly for 7 days,2–5 years, 125 mg 6 hourly for 7 days,> 5 years, 250 mg 6 hourly for 7 days.

Anaerobes: Metronidazole, oral, 7.5 mg/kg 8 hourly for 7 days.

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Treatment guidelines: TONSILLITIS, COMPLICATED (continued from previous page)

Management Comments

H. influenzae: Ampicillin, IV, 50–100 mg/kg/day in 4 divided doses for 7 daysOR

Amoxicillin, oral, < 20 kg, 20–40 mg/kg/24 hours in 3 divided dosesfor 7 days,

> 20 kg, 250 mg 8 hourly for 7 days.

Penicillin allergy:Staphylococci: Clindamycin, IV, 10–40 mg/kg/24 hours in 3 divided doses for 7 days

oral, 15–25 mg/kg/24 hours in 3 divided doses for 7 days.

In children who have difficulties in swallowing,administer IV antibiotics until swallowing becomeseasier.

Streptococci: Erythromycin, oral or IV, 25–50 mg/kg/24 hours in 4 divided dosesfor 7 days.

H. influenzae: Cefotaxime, IV, 50–100 mg/kg/24 hours in 3 divided doses for7 days.

Patients allergic to penicillin may also be allergic tocephalosporins and carbapenems.

Penicillin andcephalosporin allergy

Chloramphenicol, oral or IV, 50−100 mg/kg/24 hours in 4 divideddoses for 7 days.

Analgesic/antipyretic/anti-inflammatory

treatment:

Paracetamol, oral, 10 mg/kg 6 hourly.OR

Ibuprofen, oral, 20 mg/kg/24 hours in 3 divided doses for 3–5 days.(Under 30 kg, maximum 500 mg/day).

Surgical treatment Tonsillectomy – usually performed 6 weeks after abscess has beendrained or systemic complications have settled.