Malaria is an infectious disease caused by Plasmodium parasites. It can become severe or complicated if asexual forms of P. falciparum are present in the blood along with complications like severe anemia, cerebral malaria, respiratory distress, shock, or bleeding tendencies. Those most at risk include young children, pregnant women, non-immune adults, and those with underlying conditions like sickle cell disease. Treatment for complicated malaria involves intravenous or intramuscular quinine along with managing any complications present. Common complications include cerebral malaria, severe anemia, hypoglycemia, respiratory distress, shock, hyperpyrexia, and bleeding tendencies. Proper management is needed to address these complications and prevent high mortality rates.

1. Dr. Kyalema Samuel

2. Definition:
 Malaria is a clinical disease (collection of
symptoms and signs) due to infection by asexual
forms of the parasites Plasmodium falciparum, P.
vivax, P. ovale, P. malariae.
 Malaria is regarded as severe or complicated if
there are asexual forms of P. falciparum in blood
plus one or more of the following complications:
- Severe normocytic anaemia
- Cerebral malaria
- Pulmonary edema/Respiratory distress
- Shock/Circulatory collapse

3. - Bleeding tendency/DIC
- Thrombocytopenia
- Acidosis
- Hypoglycaemia
- Hyperparasitaemia
- Hyperpyrexia
- Jaundice
- Haemoglobinuria
- Severe vomiting
- Generalised convulsions
- Fluid and electrolyte disturbances

4. Who gets complicated malaria?
 Children between 3months and 5 years
(Children below 3 mo are protected by maternal
anti malarial antibodies and fetal hemoglobin
which is resistant to Plasmodia)
 Pregnant women especially prime and
secundigravidas
 Adults in hypoendemic areas
 Non immune immigrants into the area
 Persons with RBC abnormalities e.g. Sickle cell
disease, G6PD deficiency.

5. Specific treatment:
 Intravenous/ Intramuscular Quinine 10mg/Kg body
weight every 8 hours till the patient can take orally
(usually 1 – 3 days), then oral quinine 10mg/kg 8
hourly to complete 7 days of treatment.
 Always assess children for all complications and
manage them at the same time
 Take the child’s weight before administering any
treatment.

6. COMPLICATIONS:
1) Cerebral Malaria:
Definition:
 Presence of unrousable coma (motor, verbal and
eye response) or altered consciousness for over
30 minutes with asexual parasitaemia in the
absence of other causes of coma.
Pathophysiology:
 Seizures and coma: Intracranial sequestration of
metabolically active parasites, cerebral hypoxia,
increased intracranial pressure, cerebral edema,
hypoglycaemia, hyponatremia.

7. Clinical features:
 Coma/ altered consciousness
 Convulsions (60 – 80%)
 Hypertonic posturing (decorticate or decerebrate
rigidity, opisthotonos)
 Pupillary changes
 Absent corneal reflexes
 Abnormal respiratory pattern (Kussmaul’s,
Cheyne-Stokes, periodic apnoea)
 Gaze abnormalities (eyes wide open, conjugate
gaze deviation, nystagmus)

8. Blantyre Coma Scale:
Best Response Score
Best Motor Response:
• Localise painful stimuli
• Withdraws from a painful stimulus
• Extends/No response
2
1
0
Best Verbal Response:
• Normal cry
• Abnormal cry/ moan
• No response
2
1
0
Eye movements:
• Follows mother’s face/ moving object
• Unfocused gaze/ Does not follow mother’s
face
1
0

9.  Total score = sum of individual scores from the
three categories; (Max = 5, Min = 0)
 Coma = BCS score of 3 or less
 Standard painful stimulus is firm pressure on a
nailbed, sternum, supraorbital rigde
Management:
 Manage Airway, Breathing and Circulation
 Place child in lateral position and turn them 2
hourly
 Nasogastric tube to empty stomach in first 2 hours
to avoid aspiration, then for feeding

10.  Intravenous access for drugs and maintenance
fluids; avoid fluid overload
 Check blood sugar and treat hypoglycaemia
 Intravenous quinine
 Lumbar puncture for CSF analysis
 Monitor and record vital signs at least every 4
hours (BP, Pulse, RR, Temp, Level of
consciousness)
Outcome:
 Mortality rate 15 – 30%
 9–12% are discharged with neurological sequalae,
half of these recover fully within 4-6 weeks

11. 2) Severe anaemia:
 Packed Cell Volume =/< 15%
 Haemoglobin =/< 5 g/dl
 If MCV is normal Hb = 1/3 PCV. This is altered by
micro/macrocytosis
Pathophysiology:
 Haemolysis/ destruction of parasitised RBCs at
merogony or by erythrophagocytosis in the spleen
 Unparasitised RBCs also have a shorter lifespan
during malaria infection
 Preexisting Iron deficiency or hemoglobinopathies
 Dyserythropoiesis

12. Features:
 Severe pallor of mucous membranes, palms and
soles
 Respiratory distress (deep, laboured breathing)
 Hyperdynamic circulation (gallop rhythm, tachycardia,
hepatomegaly, pulmonary edema)
 Confusion, restlessnes, come, retinal hemorrhages
Management:
 Do PCV or Hb estimation, Thick and thin film
 If Hb =/< 4g/dl, transfuse. If Hb >4 but <6g/dl, with
features of cardiac failure, hyperparasitaemia,
respiratory distress, impaired consciousness;
tranfuse.

13.  Transfuse with packed cells 10 – 15ml/Kg or
whole blood 20ml/Kg over 2 -3 hours
 A diuretic is not often required but IV furosemide
(1-2mg/Kg) may be given be given if there fluid
overload
 Folic acid and/or iron at discharge
Outcome:
 Mortality rate is 4.7 – 16% but is higher if severe
anemia occurs with other complications like
cerebral malaria and respiratory distress

14. 3) Hypoglycaemia:
 Very common in children who have been
undernourished, those below 3 years, those with
convulsions and in 10 – 20% of those with
cerebral malaria
Pathophysiology:
a) Pretreatment:
 Impaired gluconeogenesis
 Accelerated metabolism
 Reduced food intake
 Parasite glucose consumption

15. b) During treatment:
 Quinine stimulates insulin secretion. Rapid
infusions of quinine (>10mg/kg in 1 hour) can
precipitate hypoglycaemia
Features:
 Blood glucose =/< 2.5 mmol/l
 Convulsions/ altered consciousness
 Sweating,
 Extreme weakness

16. Management:
 Check random blood sugar before and even after
correcting hypoglycaemia
 Intravenous dextrose 10% infusion or bolus push
of 5ml/kg
 Feed the patient
 Prepare a solution of sugar which may be given by
NGTube
Outcome:
 Mortality of pretreatment hypoglycemia in children
with cerebral malaria is 22 – 37%
 Recurrent hypoglycaemia has a 71% mortality

17. 4) Respiratory distress:
Features:
 Alae nasi flaring
 Chest/ subcostal recessions
 Use of accessory muscles of respiration
 Deep acidotic breathing
 Grunting
Pathophysiology:
 Metabolic acidosis (PH < 7.3) from anaerobic
glycolysis
 Pulmonary edema
 Anaemia, Hypogylcamia

18. Management:
 Correct reversible causes of acidosis; Anaemia,
dehydration, hypoglycaemia, treat convulsions
 Prop the child up in bed
 +/- oxygen
Outcome:
 Mortality is up to 19%

19. 5) Shock:
 A systolic BP of 50mmhg or less signifies shock.
Children may have cold clammy cyanotic skin;
constricted peripheral veins and a rapid feeble
pulse.
 Circulatory collapse may result from a
complicating gram negative septicaemia,
hypovolaemia from dehydration, pulmonary
edema or metabolic acidosis.
 Possible foci of infection should be sought e.g.
lungs, urinary tract, meninges, intravenous lines
and sites.

20. Management:
 Correct hypovolaemia with normal saline or
appropriate plasma expander
 Take blood for culture and sensitivity, and start
broad spectrum antibiotics which can be modified
when results are available.

21. 6) Hyperpyrexia:
 Axillary temperature of 39o
C and above
Pathophysiolgy:
 Release of metabolites and cytokines from red
blood cell breakdown leading to elevation of the
hypothalamic set point
 Rapid rise in temp may lead to febrile
convulsions.
Management:
 Antipyretics – Paracetamol 10mg/kg rectally or
orally
 Tepid sponging, fanning

22. 7) DIC/Bleeding tendency:
 Bleeding from gums, epistaxis, petechiae,
subconjunctival haemorrhages, and sometimes
GI bleeding may occur.
 Thrombocytopenia is common in falciparum
malaria, often without other coagulation
abnormalities and resolves soon after treatment
Management:
 Transfusion with blood, platelets, clotting factors
 Vitamin K

23. MANAGEMENT OF CONVULSIONS
 These are either febrile convulsions or due to
cerebral malaria.
 Management includes:
- Airway: Lie child in left lateral position, clear the
airway of secretions, put nothinb in the mouth
- Breathing: Ensure child is breathing, +/- ambu
bag
- Circulation: IV access,
- Dextrose: Quick random blood sugar, then give a
slow push of dextrose 10% 5ml/kg

24. - Give diazepam per rectal 0.25 - 0.5mg/kg
- If convulsions recur, repeat another dose of
diazepam and then start intravenous
Phenobarbitone 10mg/kg loading dose given as a
slow push over 5-10min,and continue with
oral/NGT phenobarbitone 5mg/kg once a day for
up to 5 days.
- Monitor random blood sugar and feed the child
- When the convulsion is controlled, do an LP for
CSF analysis to rule out Meningitis

25. QUININE
 Intravenous Quinine is the drug of choice for the
treatment of complicated malaria
 Presentation: IV/IM Quinine dihydrochloride
300mg/ml, 2ml ampoule
 Dosage: 10mg/kg 8 hourly
 Administration:
- Intravenously: slow infusion of 10mg/kg in
10ml/kg of 5% dextrose solution ran over 4 hours
8hourly till the patient can take orally, then give
oral quinine 10mg/kg to complete 7 days

26. - Intramuscular quinine is administered in dilutions of
100mg per ml into the anterior thigh, if the total dose
to be gives exceeds 3ml or 300mg, then divide the
dose into twoo and give each half in either thigh.
 Bioavailability of iv, im and oral quinine is comparable.
Side effects:
 Cinchonism: Tinnitus, headache, nausea, visual
disturbances
 Others: Vertigo, reduced hearing, blurred vision,
diplopia
 Cardiac: Prolongation of QT interval, AV block, sinus
arrest, vetricular tachycardia
 Hypoglycamia.

27. Reference:
 WHO, 2000: Management of severe malaria
 Toto ward protocals MRRH
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