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Malaria in Pregnancy (MIP)
Abdalla Mutwakil Gamal
House Officer
Department of Obstetrics and Gynecology
Alakadimiy Charity Hospital
Khartoum, Sudan
17-08-2017
Contents
• The case.
• Differential diagnosis of jaundice in pregnancy.
• Malaria in pregnancy.
THE CASE
Our Patient
• 22-Years-Old.
• From Sinaar
• G1-P0-A0.
• LMP: Uncertain.
• Ultrasound estimated GA=30wks.
• Ultrasound estimated date of delivery =8-10-
2017.
Presentation
• On Sunday 30-7-2017.
• Fever (9 days duration).
• Yellowish discoloration of eyes with urine and
stool becoming darker (9 days duration).
Before admission
to Sinaar hospital
• 21st and 22nd of
July.
In Sinaar hospital
• From the 23rd
till the 27th of
July.
After Sinaar
hospital
• From the 27th
till the 29th of
July
Before admission to Sinaar hospital
• 21st and 22nd of July
• Symptoms:
– Fever, sweating and shivering.
– Yellowish discoloration of sclera, dark urine and dark
stool
– Bilateral loin pain, suprapublic pain and burning on
micturation
– Vomiting
• On the 22nd of July:
– BFFM +ve.
In Sinaar hospital - Day 1 (23rd July):
– Admission.
– Fluids (N/S and D5).
– Pantodac.
– Hyoscine butylbromide, Metoclopramide (given
10pm after paint complained of epigastric pain).
• Investigations:
– WBCs =17 x 103 (Neutrophils 66%, Lymphocytes 16%,
Eosinophils 6%).
– HB =7.6 (MCV 89 fl).
– Platelets = 176
– ICT for malaria +ve.
– Pelvic Ultrasound: single viable fetus. USEGA=29wks.
Normal heart, liquor, movement, lower posterior
placenta, cephalic presentation. Conclusion: Normal
USG of pregnancy.
– Abdomen USG: Normal apart from mild dilatation of
renal pelvis bilaterally
In Sinaar hospital - Day 2 (24th July):
• Given:
– Artemisinin
– 1 unit of blood
In Sinaar hospital - Day 3 (25th July):
• Patient said that the doctors discussed with
her the possibility of terminating the
pregnancy but she refused.
In Sinaar hospital - Day 4 (26th July):
• Patient developed shortness of breath and
bilateral lower limb swelling. Couldn’t sleep at
night.
• Chest was clear on examination
• Given O2 and lasix.
In Sinaar hospital - Day 5 (27th July):
• Patient refused to receive quinine and another
unit of blood and left hospital against medical
advice.
• Investigations:
– Blood urea = 58
– S.creatinine = 3.5
– RBS= 74
– WBCs = 22.1 (Neutro = 82%, lympho = 8.8%, esoino=3)
– HB = 8.5 (MCV =82.2)
– Platelets = 266.
After Sinaar hospital
• The patient was at home and received some
herbal treatment for her condition but her
symptoms worsened and she was brought to
Khartoum.
During her stay
in our unit
• 30th of July
In the ICU
• From the 31st
of July till
the 5th of
August
Back to our
unit
• From the 6th
of August till
13th of
August
During her stay in our unit – Day 1
• Came to the outpatient clinic on our duty on the 30th of
July at 12:50pm.
• Complains:
– Fever, sweating and shivering were still present.
– Yellowish discoloration of sclera, dark urine and dark stool
increased.
– Bilateral loin pain, suprapubic pain and burning on
micturation was present.
– Vomiting stopped, but epigastric pain was present.
– drowziness.
– Lower limbs swelling and shortness of breath increased.
• Looked ill, was jaundiced, had pallor and was in
pain and confused. Had tachycardia (130bpm)
and tachypnea (40/min). BP=110/50 mmhg,
abdomen was distended, bilateral lower limb
edema was present.
• Was admitted, put on O2 and catheterized, input
and output chart was started, patient was given
one unit of blood and IV maxil was started.
• Investigation’s samples were sent and urgent
Medical consultation was requested.
• General urine:
– Protein: +++
– Bilirubin: +
– Color: Deep yellow
– Pus cells: uncountable
• CBC:
– WBCs: 33.1 (neutro 91%, Lympho 6.4%)
– HB: 7.2 (MCV 61)
– Platelets: 249
• Bl group: O Rh+ve
• RBS: 357 (?)
• RFTs & electrolytes:
– Blood Urea: 131
– S.Creatinine: 6.1
– Na+: 125
– K+:3.0
• LFTs:
– T.bilirubin: 10.4 (Direct Bilirubin: 8.4)
– AST: 102
– ALT: 240
– ALP: 222
– Total protein: 6
– Albumin: 3.7
• Virology (HIV, HBV, HCV): -ve
• Abdomen and pelvis USG:
– Liver: Mildly enlarged measuring 16.5cm with normal
echogenicity and smooth texture, no focal lesions.
– Kidneys: Both are mildly enlarged (RT=12.6x6.7cm and
LT=12.5x6.3cm) with decreased cortical echogenicity
and promninent pyramids, no stones, masses or
obstructive changes. Features suggestive of acute
renal disease for clinical correlation.
– GB, CBD, UB, Pancreas, Spleen: are normal
– Uterus: Single viable fetus, cpehlaic presentation,
posterior placenta, average liquor, USEGA=30wks.
USEDD=6/10/2017.
• Medical consultation plan was:
– Input and Output charts
– Daily RFTs and electrolytes.
– Abdomen USG
– UG
• Patient level of consciousness was decreasing,
sample for urgent random blood sugar was
withdrawn and the patient was given D50. RBS
result was found to be 40mg/dl.
• Patient was admitted in the ICU.
In the ICU – Day 1 (31st July):
• Dx after assessment:
– ?HELLP ? Severe Malaria, Acute Kidney Injury, Sepsis and liver
failure
• Management plan:
– IV fluids
– Dexamethasone IV
– Flagyl
– Fortum
– Quinine
– Pantoprazol
– Ca+2 Gluconate
– Vitamin K
• RBS 4 hourly
• Daily RFTs, electrolytes, CBC and bleeding
profile.
• Input and output charts
• Hepatitis C antibody
• Patient BP during ICU stay:
Date Day in ICU Lowest BP Highest BP Notes
31 – 7 - 2017 Day 1 110/60 127/82 Dialysis Done
1 – 8 - 2017 Day 2 93/75 120/87 Dialysis done
2 – 8 - 2017 Day 3 137/95 168/102 Dialysis done
3 – 8 - 2017 Day 4 109/72 142/89
4 – 8 - 2017 Day 5 140/99 162/105
5 – 8 - 2017 Day 6 136/82 150/87
• CBC during ICU stay:
Date Day in ICU WBCs HB Platelets
31 – 7 - 2017 Day 1 25.5 7.7 163
1 – 8 - 2017 Day 2 29.5 7.8 138
2 – 8 - 2017 Day 3
3 – 8 - 2017 Day 4 Given blood
4 – 8 - 2017 Day 5 18.4 8.2 144
5 – 8 - 2017 Day 6 15.7 8 219
• Renal functions and electrolytes during ICU
stay
Date Day in ICU Cr Urea Na+ K+ Notes
31 – 7 Day 1 6.7 168 123 3 Dialysis Done
1 – 8 Day 2 4.9 122 131 2.1 Dialysis Done
2 – 8 Day 3 3.1 71 134 2.8 Dialysis Done
3 – 8 Day 4 2.2 42 134 2.8
4 – 8 Day 5 2.9 73 131 4.0
5 – 8 Day 6 3.2 76 134 5.4
• Liver functions during ICU stay:
Date Day in ICU T.Bili / D.Bili AST ALT ALP T.ptn Alb
31 – 7 Day 1
1 – 8 Day 2
2 – 8 Day 3 3.3 (3.2) 47 25 151 5.4 1.9
3 – 8 Day 4
4 – 8 Day 5
5 – 8 Day 6
Back to our unit
• No new complains.
• No further Fever, sweating, shivering, and
shortness of breath.
• Lower limbs swelling is less. Yellowish
discoloration of the eyes decreased. Urine and
stool color was becoming closer to normal
than before.
• Patient BP In our department:
Date Day in our
department
Lowest BP
6 – 8 Day 1
7 – 8 Day 2
8 – 8 Day 3 140/90
9 – 8 Day 4 130/90
10 - 8 Day 5 130/90
11 - 8 Day 6 120/80
12 - 8 Day 7
13 - 8 Day 8
• CBC In our department :
Date Day in our
department
WBCs HB Platelets
6 – 8 Day 1
7 – 8 Day 2
8 – 8 Day 3
9 – 8 Day 4 8.2 8.1 221
10 - 8 Day 5
11 - 8 Day 6
12 - 8 Day 7
13 - 8 Day 8
• Renal functions and electrolytes In our
department
Date Day in our
department
Cr Urea Na+ K+
6 – 8 Day 1 3.2 87 136 4.5
7 – 8 Day 2 3.7 87 136 4.5
8 – 8 Day 3 2.2 - - -
9 – 8 Day 4 1.7 - - -
10 - 8 Day 5 1.2 31 139 3.1
11 - 8 Day 6
12 - 8 Day 7 0.5
13 - 8 Day 8 0.5 16 137 3.0
• Liver functions In our department :
Date Day in our
department
T.Bili / D.Bili AST ALT ALP T.ptn Alb
6 – 8 Day 1
7 – 8 Day 2
8 – 8 Day 3
9 – 8 Day 4
10 - 8 Day 5 1.2 / 1.0 16 11 176 6.0 2.5
11 - 8 Day 6
12 - 8 Day 7
13 - 8 Day 8
On discharge:
• Complains: None
• Physical Examination: No abnormality detected
• Pregnancy Ultrasound: Normal pregnancy
• Latest investigations:
CBC RFTs LFTs BFFM
WBCs = 8.2 Creatinine = 0.5 T.Bilrubin = 1.2 -ve
HB = 8.1 Urea = 16 D.Bilirubin = 1.0
Platelets = 221 Na+ = 137 AST = 16
K+ = 3.0 ALT = 11
ALP = 176
T.Protein = 6
Albumin = 2.5
DIFFERENTIAL DIAGNOSIS OF
JAUNDICE IN PREGNANCY
• Yellow discoloration
of skin, conjunctiva,
sclera and mucosa
associated with rise
in serum bilirubin
above 2mg/dl
( normal 0.2-01mg/dl)
Latent jaundice:1-2mg/dl
PSYSIOLOGY OF BILIRUBIN
• Incidence: 1 to 4/1000 deliveries.
• Grade of jaundice:
 Mild: bilirubin <6mg%
 Moderate 6-15mg%
 Severe >16mg%
Cause of jaundice during pregnancy
Liver disease unique to
pregnancy
• Acute fatty liver of
pregnancy.
• Intrahepatic cholestasis of
pregnancy.
• Pre-eclampsia, eclampsia,
HELLP syndrome.
• Hyperemesis gravidarum
Coincidental occurrence of
liver disease in pregnancy
• Acute viral hepatitis.
• Hemolytic jaundice.
• Cholelithiasis.
• Drug induced
• Obstructive jaundice
Acute Hepatitis ICP HELLP AFLP
Trimester Any Trimester Third Third Third
Presenting
symptoms
Fever, Jaundice Pruritus
HTN, Nausea,
Vomiting,Pain
Nausea,
Vomiting,Pain
ALT & AST Markedly high
Normal to Mild
rise
Moderately high Moderately high
Alkaline
Phospatase
Normal to mild
rise
High Normal Normal
Platelets Normal Normal Low Normal
Fetal
Complications
Infection with
HBV & HCV
Prematurity,
IUGR, FD
IUGR,
Prematurity
Prematurity
Maternal
Complications
Acute liver
failure(HEV)
None
Thrombocytope
nia, septicemia,
DIC
Acute liver
failure
MALARIA IN PREGNANCY
Outline
• Epidemiology
• Clinical features
• Complications
• Management of MIP
Epidemiology
• It leads to 7.5 million cases and 35,000 deaths
every year in Sudan (2000 estimates).
• Plasmodium falciparum is incriminated in
>90% of cases. P. vivax, P. ovale and P.
malariae are responsible of the rest.
• Anopheles arabiensis is the main vector
together with A. gambiae and A.funestus
Malaria and pregnancy
• In the Sudan each year more than 1.2 million women become
pregnant, of those 750,000 are in areas with high malaria
Transmission.
• 25 million pregnant African women in endemic areas yearly
Malaria is more frequent and complicated during pregnancy In
malaria-endemic areas, malaria during pregnancy accounts for:
– Up to 15% of maternal anaemia
– 8-14% of low birth weight
– 30% of "preventable" low birth weight
– 3-8% of infant death
Clinical features
The common manifestations of malaria in pregnancy, articularly in the
second half of pregnancy include the following:
1. Fever with more paroxysms in the second half of pregnancy due to
immuno-suppression.
2. Anaemia is a common presentation and it could be due to:
haemolysis of parasitized RBCs; increased demands of pregnancy;
or profound haemolysis that may aggravate folate deficiency.
Anaemia is more common and severe between 16 -29 weeks, and
pre-existing iron and folate deficiency can exacerbate it and vice
versa. Anaemia increases the risk of perinatal mortality and
maternal morbidity and mortality, the risk of pulmonary oedema,
and the risk of postpartum haemorrhage is also higher.
3. Splenomegaly may be present but variable in size; and preexisting
large spleen may regress in size in pregnancy.
4. Acute pulmonary oedema is a more common and serious
complication of MIP compared to non-pregnant population. It is
more common in the second and third trimesters. However, it can
occur immediately postpartum due to: the auto-transfusion of
placental blood with high proportion of parasitized RBCs and the
sudden increase in the peripheral vascular resistance after delivery.
5. Hypoglycaemia is another complication of severe malaria and is due
to: Increased demand of glucose due to hypercatabolic state and
infecting parasite Hypoglycaemic response to starvation Increased
response of pancreatic islets to secretary stimuli.
Hypoglycaemia presents with symptoms
similar to those of malaria. Abnormal
behaviour, convulsions and sudden loss of
consciousness are also symptoms of cerebral
malaria.
6. Secondary infections such as urinary tract
infection, pneumonias… etc. are more
common due to immunosuppression.
Complications and effects of MIP:
During pregnancy:
• Frequency and severity are greater than in non-pregnant
• Severe anaemia is common
• Hyperpyrexia leading to abortion, preterm labour, intra-
uterine foetal death and macerated stillbirth.
• Hypoglycaemia
• Transplacental infection leading to congenital malaria and
neonatal death.
• Spontaneous abortion, premature birth, stillbirth, placental
insufficiency and intrauterine growth retardation (IUGR),
low birth weight and foetal distress.
During labour:
• Precipitated labour
• Postpartum haemorrhage
During puerperium:
• Puerperal pyrexia
• Difficulty in lactation.
Risks to the foetus:
High grade fever, placental insufficiency, hypoglycaemia,
anaemia and other complications can adversely affect the
foetus. Spontaneous abortions, premature birth, stillbirth,
placental insufficiency and IUGR, low birth weight, and
foetal distress are problems observed during foetal growth.
Transplacental spread to the foetus can result in congenital
malaria, which is very rare.
The placental barrier and maternal IgG antibodies, which
cross the placenta, may protect the foetus to some extent.
Congenital malaria
is more common in the non-immune population
and the incidence goes up during the epidemic of
malaria. Foetal Quinine level is about one third of
simultaneous maternal level and this
subtherapeutic drug level does not cure the
infection in the foetus. All four species can cause
congenital malaria. The newborn can present
with fever, irritability, feeding problems,
hepatosplenomegaly, anaemia, and jaundice. The
diagnosis can be confirmed by smear for malaria
parasite.
Diagnosing Malaria
Case definition of Uncomplicated Malaria (UM):
• Suspected malaria: Malaria is suspected when a
patient presents with fever (or history of fever)
and other symptoms and signs suggestive of
malaria (e.g. headache, vomiting, sweating). The
health care worker in this case, has to exclude
clinically other common causes of fever in his
area, such as: tonsillitis, , chest infection,
measles, abscess, urinary tract infection, etc…
• Confirmed malaria:
A malaria case is confirmed by demonstration of
asexual forms (trophozoite stage) of the
parasite in the thick or thin peripheral blood
film or by rapid diagnostic test in the presence
of fever.
• Clinical malaria:
For management of malaria in children, in facilities with integrated
management of childhood illnesses (IMCI) trained personnel,
and where there are no facilities for laboratory diagnosis, the health
worker should deal with the child according to IMCI guidelines
. According to IMCI «Any febrile child (by history,
temperature of ≥37.5oC or feeling hot) in any area should be
managed as having malaria after exclusion of other obvious causes
of fever (tonsillitis, measles, abscess, urinary tract infection or acute
respiratory infection….)
For management of malaria in adult and children more than 5 years
old and where there is a malaria risk but there is no facilities for
laboratory diagnosis it is reasonable to assume that the patient
has clinical malaria when there is no other obvious reason for fever
Severe Malaria
Case definition of severe malaria (SM):
Severe malaria is defined as malaria due to P.
falciparum infection that is sufficiently serious
to be an immediate threat to life. It is a
medical emergency, which requires
hospitalization.
Who gets severe malaria?
Any infection with P. falciparum can become severe if
treatment is delayed or inadequate. Those who are most at
risk are:
• Children (especially those who are in areas of high
endemicity – south of Sudan) aged from 6 months to 6
years.
• Indigenous pregnant women, especially primigravidae.
• People of all ages in areas of low endemicity (north Sudan).
• People returning to endemic areas after a few years
absence.
• Visitors (of any age) from non-endemic areas.
The health worker should regard a patient as having severe malaria if he or
she has one or more (mostly seen in combination) of the conditions listed
in the table below (WHO 2000).
Diagnosis of malaria
1) Clinical diagnosis
2) Blood film
– Can take any time (or at the height of fever)
– 3 consecutive days
– Giemsa-stained Thick film andThin film
• Thick film for MP positive or not
• Thick film facilitates the diagnosis of low level
parasitemia
• Thin film is essential
• to confirm the diagnosis,
• to identify the species of parasite, &
• to quantify the parasite load by counting the
% of infected RBCs
• P. falciparum  only ring forms may be found in
early stage
• Other species  all stages of erythrocytic cycle may
be found
• Gametocyte appears after about 2 wks, and persist
despite tx and are harmless, except that they are the
source by which more mosquitos become infected
Thick film &Thin film
Thick and Thin film
• parasites are not detected at times
in peripheral smear :
•
a. sequestration deep vascular bed
b. partially treated patients
c. prophylactic antimalarial t/t
d. inexperienced technician
e. poor quality staining
3) Rapid Diagnosis Tests (RDT) by ICT
Rapid diagnosis for falciparum
– Parasight-F test based upon HRP 2 (Histidine rich
protein 2)
Rapid diagnosis for falciparum and vivax
– LDH coted OptiMAL test kits
– Test positive  1 band in vivax and 2 bands in
falciparum
– Test took only 5 min
– Sensitivity 100%, specificity 96%
• Importance of ICT
– Rapid Dx
– Can get Dx in MP negative cerebral malaria
– Can differentiate falciparum and vivax
– Suitable for microscopists less experienced in
examining blood films
4) QBC MalariaTest (Quantitative Buffy Coat)
• Fluorescence microscopy-
based malaria diagnostic
test
• Increased sensitivity over
traditionalGiemsa thick film
methods
• In > 90% of cases, the
species of parasite can also
be identified.
• Simply fill a capillary tube
with a patient sample 
coat with acridine orange
(fluorescent dye) 
centrifuge  place under a
fluorescent microscope
5) DNA detection (PCR)
• Used mainly in research
• Useful for determining whether a patient has
• a recrudescence of the same malaria parasite or
• a re-infection with a new parasite
Management of MIP:
This includes:
• treatment of malaria
• management of complications
• and management of labour.
Treatment of malaria:
• Ideally the patient should be admitted when it is possible. Assess
the severity of the condition by general examination: palor,
jaundice, blood pressure, temperature, haemoglobin level and
parasite count.
• SGPT, serum bilirubin, serum creatinine and blood sugar may also
need to be assessed.
• Monitor the maternal and foetal vital parameters 34- hourly and
monitor the fluid intake/output daily.
• Choose the drug according to the severity of the disease and
gestational age.
• Avoid overdosing and under dosing with the drugs; avoid fluid
overload or dehydration
Treatment of UM in pregnancy:
A - In the first trimester:
Oral Quinine is safe and is the first line of
treatment throughout pregnancy. The dose is
10 mg salt/Kg body weight, administered 8-
hourly for 7 days.
B – In the second and third trimester:
• Oral Quinine 10mg/kg administered 8 hourly for 7
days. Or
• Oral Quinine for 3 days 10mg/kg administered 8 hourly
followed by sulfadoxine–pyrimethamine in the full
treatment dose. Or
• A combination of artesunate tabs (AS) 4mg/kg and SP
(AS + SP) on the first day, followed by 2 further days of
AS 4mg/kg
Management of severe malaria during pregnancy:
In the management of severe malaria in pregnancy especial concern must be
paid to: anaemia, hypoglycemia and pulmonary oedema.
• Quinine dihydrochloride, Quinine hydrochloride or Quinine sulphate is the
first line of treatment all through during pregnancy. The dose is 10 mg
salt/Kg body weight 8-hourly for 7 days. Start with IV Quinine in 10%
glucose infusion or 5% glucose in normal saline; if for some reason
Quinine can not be given by infusion, Quinine dihydrochloride can be
given in the same dosage by IM injection diluted with sterile normal saline
to a concentration of 60 mg/ml. The dose should be divided into two
halves and injected into both anterior upper thighs, and shift to oral as
soon as possible. In case there is no 10% glucose concentration give one
bottle of 5% glucose before administration of Quinine; be careful not to
induce pulmonary oedema. Random blood sugar should be done before
and after Quinine administration.
• Or Quinine 10 mg/Kg body weight 8 hourly
for at least 3 days (IV or IM) and shift to
(AS+SP) as soon as the patient can take orally;
this is of course in the second and third
trimesters.
• Or Artemether IM 3.2 mg/Kg body weight in
the first day (divided to two doses 12 hours
apart) followed by 1.6 mg/Kg daily for the
next 6 days in the second and third trimesters.
Management of complications:
• Pulmonary oedema: careful fluid management, back rest elevation,
diuretics and ventilation if needed.
• Hypoglycaemia: 25 -50% dextrose, 50 -100 ml IV (1ml/kg) followed
by 10% dextrose as a continuous infusion. Blood sugar should be
monitored every 4 -6 hours where possible.
• Anaemia: packed cell should be transfused if Hb <5 g/dL.
• Renal failure: it could be pre-renal due to unrecognized
dehydration or renal due to severe parasitaemia. Management
involves careful management, diuretics and dialysis if needed.
• Septicaemic shock or algid malaria: administration of third
generation of cephalosporin, monitoring of vital parameters (blood
pressure) and fluid replacement when required (systolic <90mmHg)
Management in labour:
Falciparum malaria and higher fever induce uterine contractions,
resulting in premature labour. The frequency and intensity of the
contractions is related to the degree of the fever. Foetal distress
is the commonly recognized complication. Lower the temperature
of the woman by using tepid sponging or antipyretics such as
paracetamol. Adequate fluid management and careful monitoring
in labour are mandatory.
The table below summaries the use of antimalarial
drugs for MIP and puerperium.
Important remarks:
• Severe malaria (SM) cases should be managed at hospitals. So health
workers at the peripheral units should refer patients immediately. Pre-
referral treatment is recommended.
• Attention should be given to the general management (good nursing care)
of the patient as for the specific treatment.
• Early recognition, referral and early institution of the appropriate
management at hospital are of paramount importance in the reduction of
deaths attributed to malaria.
• Case fatality rate (CFR) is a useful indicator for hospital i.e. higher CFR
indicates inadequate case management at hospital level or late
presentation which would identify a communication need for the
community.
CFR = No. malaria deaths ÷ No. of admitted malaria cases × 100
General management of the patient
with SM:
The health worker (medical doctor, medical
assistant or the nurse) on duty should
consider the following (8 + 8 + 4) points in
the management of the patients with severe
malaria:
• Immediate measures (8).
• Searching for and managing complications
(8).
• Monitoring the case (4).
Do the following 8 immediate measures:
1. Start resuscitation, particularly maintenance of a patent airway.
2. Establish IV line.
3. Make a thick blood smear for immediate malaria parasite count. RDTs can
be useful in certain areas
4. Classify the degree of dehydration, assess patient’s fluid requirements and
correct accordingly.
5. Control fever if the axillary temperature is 38.5ºC or above: Tepid sponge,
fanning and oral or rectal paracetamol (15mg/kg every 4 to 6 hours)
6. Control convulsions: Maintain airway, treat with rectal diazepam
(0.5mg/kg) or slow IV diazepam (0.3mg/kg, maximum 10mg in an adult).
Also correct hypoglycaemia and electrolytes
7. Detect and treat Hypoglycaemia: Hypoglycaemia can be
induced by high parasitaemia, fasting and quinine therapy.
Hypoglycaemia can recur especially in pregnant women and
children. If blood glucose ≤2.2mmol/l or ≤ 40mg/dl; give
1ml/kg of 50% dextrose IV, diluted with an equal volume of
0.9% Saline, give slowly over 35- minutes. Follow with 10%
dextrose infusion at 5ml/kg/hr. I f there is no test for blood
glucose, treat as if the patient is hypoglycaemic;
8. Start Quinine IV or Artemether IM (if not accessible, Quinine
I.M. or Artesunate suppositories can be administered; notably
in case of hyperparasitaemia). imbalance if it is present.
Look and deal with the following 8 complications:
1. Shock, algid malaria: if Systolic Bp <50mmHg in children 15- yrs or <80
mmHg in >5yrs, suspect Gram-negative septicaemia. In such case take
blood samples for culture. Give parentral broad-spectrum antimicrobials.
Correct haemodynamic disturbances. Treat with: 30ml/kg 0.9% Saline IV in
1hour, then, reassess. Give oxygen if possible
2. Consider the need for blood transfusion: Assess the degree of palor (no
palor, some palor or severe palor). Look for signs of severe anaemia such
as very pale mucous membranes, respiratory distress and a rapid pulse.
Note: The decision to transfuse with blood should not only be based on low
laboratory values but as a guide Hct <15% or Hb <5 g/dL Transfuse blood if
there is:
* Cardio respiratory symptoms e.g. severe anaemia.
* PCV <20 or Hb <5g/dL.
3. In case of metabolic acidosis: Exclude and treat hypoglycemia,
hypovolaemia and gram negative septicaemia. Give isotonic saline
20 ml/Kg of body weight rapidly or screened whole blood 10ml/Kg
over 30 minutes if haemoglobin is <5 g/dl.
4. If there is spontaneous bleeding and coagulopathy: Transfuse
screened fresh whole blood or clotting factors; give vitamin K 10 mg
IV per day for adult, 1 mg/day for infant, 2 -3 mg/day for children,
and 5 -10 mg/day for adolescent. Vitamin K should be given SC or
IV.
5. Acute renal failure: Special efforts should be given to detection of
symptoms and signs suggestive of renal failure. Exclude
dehydration; maintain strict fluid balance; carry out dialysis if
indicated.
6. Malarial hemoglobinuria (black-water fever): Due to
excessive destruction of RBCs which leads to jaundice
and low Hb level. Continue with suitable antimalarial
treatment; transfuse screened fresh blood if needed.
7. Acute pulmonary oedema:
May be due to malaria itself. Prevent by avoiding excessive
rehydration. Treatment -prop patient up, give oxygen
100%. If pulmonary oedema is due to over-hydration,
stop intravenous fluids, give a diuretic (frusemide I.V. in a
dose of 40 mg for adult and 0.5 -1 mg/Kg/dose for
children) or withdraw 3 ml/Kg of blood by venesection
into a donor bag.
.
8. Exclude common infections/conditions that
present like severe malaria:
Perform urinalysis for urinary tract infection; lumbar
puncture for meningoencephalitis in unconscious
patients (unless contraindicated); white blood cell
count for other infections and chest x-ray for
bronchopneumonia.
Monitor considering the following 4 points:
1. Level of consciousness: If there is an altered level of consciousness
use Glasgow or Blantyre coma scales to assess progress every 6
hours until the patient retained full consciousness.
2. Fluid input/output: Detect dehydration and avoid fluid overload.
prevent pulmonary oedema.
3. Vital signs: Monitor vital signs every 6 hours to detect
complications of severe malaria. If pulmonary oedema develops
(rapid respiratory rate and deep laboured breathing) stop all IV
fluids except quinine and call medical officer/ clinical officer for
management
4. Level of parasitaemia: Determine the parasite count daily to
monitor the therapeutic effect of treatment. Stop when there is no
detectable parasitaemia.
Educate the patient and relatives about
compliance with a full course of treatment,
home prevention of malaria and the sequelae
of severe malaria. Wait for the patient to
recover before counselling.
Specific treatment of patients with SM:
Pre-referral treatment at peripheral units:
In most of the rural settings of the Sudan, it is usual to see
patients
with SM seeking care at the primary health care units. The
health personnel in these units should refer the patients to
the nearest hospital. Pre-referral treatment should be
given. This could be Quinine IM or artesunate
suppositories as follows:
• Quinine IM
The dose of IM Quinine is 10 mg salt/kg body weight given after
dilution with sterile normal saline or distilled water to a
• concentration of 60 mg/ml; the dose is
divided into 2 halves and injected into both
anterior upper thighs.
If referral does not occur after 8 hours repeat the dose.
Don,t keep the patients more than 24 hours
• Artesunate suppositories
Artesunate rectal capsules/suppositories, 10 mg/Kg
(available in form of 50 mg or 200 mg per rectocap),
should be given rectally as soon as possible, once the
diagnosis of malaria is made. If the rectal capsule is
expelled within the first hour, another rectal capsule
should be inserted immediately
If after 24 hours the patient has not been
referred to hospital and is still unable to take
oral medication, a second dose should be
repeated
Hospital treatment:
• Treatment with quinine:
Quinine dihydrochloride, Quinine hydrochloride or
Quinine sulphate is the drug of choice for the
treatment of severe malaria. Quinine can be
given in one of the 3 ways depending on the
patient conditions and according to the level of
health facility.
A - Quinine for 7 days:
Start with Quinine infusion, the dose is 10 mg
salt/kg body weight preferably in 5% Glucose, 5%
glucose in normal saline, or in 10% glucose given
over four hours duration every 8 hours (with a
rate of 15 drops/min for adult) with a maximum
dose of 600 mg. Shift to the oral quinine as soon
as the patient can take oral medication and
continue for 7 days
B - Quinine IM:
If the IV route is not possible, Quinine can be given
in the same dose by intramuscular injection
diluted with sterile normal saline or distilled
water to a concentration of 60 mg/ml as a pre-
referral dose. The dose should be divided into
two halves and injected into both anterior upper
thighs. Shift to the oral Quinine as soon as the
patient can take oral medication.
C - Quinine for at least 3 days and then first-line:
It is observed that compliance to oral Quinine
sometimes is not good. Alternative option is to
give Quinine IV or IM for at least 3 days at
hospital and then shift to the first-line treatment
(AS+SP) if the patient can take oral medication.
Ensure patient takes full oral course (AS+SP).
Quinine side effects:
The commonest are nausea, vomiting and tinnitus. Over-dose
causes headache, dizziness, severe CNS disturbance and
delirium. The most serious side effect is hypoglycemia.
Hypoglycemia can be induced by Quinine itself (as it is found
to stimulate insulin release), marked parasitaemia (as it increases
glucose consumption) and fasting (as the ill patient may not be
able to take foods or drinks particularly in children and pregnant
women).
Rapid intravenous administration of Quinine can precipitate
hypotension and fatal cardiovascular toxicity.
Treatment with Artemether injection (ARM):
The drug is available in injectable form (80 mg/ml
for adult and 40 mg/ml for children). In Sudan
ARM injection (monotherapy) is recommended
only for the treatment of severe malaria in
facilities where the full 7-day course can be
administered. If ARM monotherapy is
administered for less than 7 days, radical cure will
not be achieved.
The drug can be administered by one of two regimens; the first one is
preferable:
• Artemether IM, 1.6 mg/Kg initially, and again after 12 hours on the
first day.Then 1.6 mg/Kg daily for at least 3 days (total of 4 days of
IM ARM).Then the first-line treatment (AS+SP) if the patient can
take oral medication.
• Artemether IM, 1.6 mg/Kg initially, and again after 12 hours on the
first day. Then 1.6 mg/Kg daily for the next 6 days giving a total of 8
doses.
Side effects in general are mild and include headache, vomiting,
abdominal pain; itching and minor non-specific ECG changes
(Nonspecific ST changes and 1st degree atrioventricular block).
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Malaria in Pregnancy Guide

  • 1. Malaria in Pregnancy (MIP) Abdalla Mutwakil Gamal House Officer Department of Obstetrics and Gynecology Alakadimiy Charity Hospital Khartoum, Sudan 17-08-2017
  • 2. Contents • The case. • Differential diagnosis of jaundice in pregnancy. • Malaria in pregnancy.
  • 4. Our Patient • 22-Years-Old. • From Sinaar • G1-P0-A0. • LMP: Uncertain. • Ultrasound estimated GA=30wks. • Ultrasound estimated date of delivery =8-10- 2017.
  • 5. Presentation • On Sunday 30-7-2017. • Fever (9 days duration). • Yellowish discoloration of eyes with urine and stool becoming darker (9 days duration).
  • 6. Before admission to Sinaar hospital • 21st and 22nd of July. In Sinaar hospital • From the 23rd till the 27th of July. After Sinaar hospital • From the 27th till the 29th of July
  • 7. Before admission to Sinaar hospital • 21st and 22nd of July • Symptoms: – Fever, sweating and shivering. – Yellowish discoloration of sclera, dark urine and dark stool – Bilateral loin pain, suprapublic pain and burning on micturation – Vomiting • On the 22nd of July: – BFFM +ve.
  • 8. In Sinaar hospital - Day 1 (23rd July): – Admission. – Fluids (N/S and D5). – Pantodac. – Hyoscine butylbromide, Metoclopramide (given 10pm after paint complained of epigastric pain).
  • 9. • Investigations: – WBCs =17 x 103 (Neutrophils 66%, Lymphocytes 16%, Eosinophils 6%). – HB =7.6 (MCV 89 fl). – Platelets = 176 – ICT for malaria +ve. – Pelvic Ultrasound: single viable fetus. USEGA=29wks. Normal heart, liquor, movement, lower posterior placenta, cephalic presentation. Conclusion: Normal USG of pregnancy. – Abdomen USG: Normal apart from mild dilatation of renal pelvis bilaterally
  • 10. In Sinaar hospital - Day 2 (24th July): • Given: – Artemisinin – 1 unit of blood
  • 11. In Sinaar hospital - Day 3 (25th July): • Patient said that the doctors discussed with her the possibility of terminating the pregnancy but she refused.
  • 12. In Sinaar hospital - Day 4 (26th July): • Patient developed shortness of breath and bilateral lower limb swelling. Couldn’t sleep at night. • Chest was clear on examination • Given O2 and lasix.
  • 13. In Sinaar hospital - Day 5 (27th July): • Patient refused to receive quinine and another unit of blood and left hospital against medical advice. • Investigations: – Blood urea = 58 – S.creatinine = 3.5 – RBS= 74 – WBCs = 22.1 (Neutro = 82%, lympho = 8.8%, esoino=3) – HB = 8.5 (MCV =82.2) – Platelets = 266.
  • 14. After Sinaar hospital • The patient was at home and received some herbal treatment for her condition but her symptoms worsened and she was brought to Khartoum.
  • 15. During her stay in our unit • 30th of July In the ICU • From the 31st of July till the 5th of August Back to our unit • From the 6th of August till 13th of August
  • 16. During her stay in our unit – Day 1 • Came to the outpatient clinic on our duty on the 30th of July at 12:50pm. • Complains: – Fever, sweating and shivering were still present. – Yellowish discoloration of sclera, dark urine and dark stool increased. – Bilateral loin pain, suprapubic pain and burning on micturation was present. – Vomiting stopped, but epigastric pain was present. – drowziness. – Lower limbs swelling and shortness of breath increased.
  • 17. • Looked ill, was jaundiced, had pallor and was in pain and confused. Had tachycardia (130bpm) and tachypnea (40/min). BP=110/50 mmhg, abdomen was distended, bilateral lower limb edema was present. • Was admitted, put on O2 and catheterized, input and output chart was started, patient was given one unit of blood and IV maxil was started. • Investigation’s samples were sent and urgent Medical consultation was requested.
  • 18. • General urine: – Protein: +++ – Bilirubin: + – Color: Deep yellow – Pus cells: uncountable • CBC: – WBCs: 33.1 (neutro 91%, Lympho 6.4%) – HB: 7.2 (MCV 61) – Platelets: 249 • Bl group: O Rh+ve
  • 19. • RBS: 357 (?) • RFTs & electrolytes: – Blood Urea: 131 – S.Creatinine: 6.1 – Na+: 125 – K+:3.0 • LFTs: – T.bilirubin: 10.4 (Direct Bilirubin: 8.4) – AST: 102 – ALT: 240 – ALP: 222 – Total protein: 6 – Albumin: 3.7 • Virology (HIV, HBV, HCV): -ve
  • 20. • Abdomen and pelvis USG: – Liver: Mildly enlarged measuring 16.5cm with normal echogenicity and smooth texture, no focal lesions. – Kidneys: Both are mildly enlarged (RT=12.6x6.7cm and LT=12.5x6.3cm) with decreased cortical echogenicity and promninent pyramids, no stones, masses or obstructive changes. Features suggestive of acute renal disease for clinical correlation. – GB, CBD, UB, Pancreas, Spleen: are normal – Uterus: Single viable fetus, cpehlaic presentation, posterior placenta, average liquor, USEGA=30wks. USEDD=6/10/2017.
  • 21. • Medical consultation plan was: – Input and Output charts – Daily RFTs and electrolytes. – Abdomen USG – UG
  • 22. • Patient level of consciousness was decreasing, sample for urgent random blood sugar was withdrawn and the patient was given D50. RBS result was found to be 40mg/dl. • Patient was admitted in the ICU.
  • 23. In the ICU – Day 1 (31st July): • Dx after assessment: – ?HELLP ? Severe Malaria, Acute Kidney Injury, Sepsis and liver failure • Management plan: – IV fluids – Dexamethasone IV – Flagyl – Fortum – Quinine – Pantoprazol – Ca+2 Gluconate – Vitamin K
  • 24. • RBS 4 hourly • Daily RFTs, electrolytes, CBC and bleeding profile. • Input and output charts • Hepatitis C antibody
  • 25. • Patient BP during ICU stay: Date Day in ICU Lowest BP Highest BP Notes 31 – 7 - 2017 Day 1 110/60 127/82 Dialysis Done 1 – 8 - 2017 Day 2 93/75 120/87 Dialysis done 2 – 8 - 2017 Day 3 137/95 168/102 Dialysis done 3 – 8 - 2017 Day 4 109/72 142/89 4 – 8 - 2017 Day 5 140/99 162/105 5 – 8 - 2017 Day 6 136/82 150/87
  • 26. • CBC during ICU stay: Date Day in ICU WBCs HB Platelets 31 – 7 - 2017 Day 1 25.5 7.7 163 1 – 8 - 2017 Day 2 29.5 7.8 138 2 – 8 - 2017 Day 3 3 – 8 - 2017 Day 4 Given blood 4 – 8 - 2017 Day 5 18.4 8.2 144 5 – 8 - 2017 Day 6 15.7 8 219
  • 27. • Renal functions and electrolytes during ICU stay Date Day in ICU Cr Urea Na+ K+ Notes 31 – 7 Day 1 6.7 168 123 3 Dialysis Done 1 – 8 Day 2 4.9 122 131 2.1 Dialysis Done 2 – 8 Day 3 3.1 71 134 2.8 Dialysis Done 3 – 8 Day 4 2.2 42 134 2.8 4 – 8 Day 5 2.9 73 131 4.0 5 – 8 Day 6 3.2 76 134 5.4
  • 28. • Liver functions during ICU stay: Date Day in ICU T.Bili / D.Bili AST ALT ALP T.ptn Alb 31 – 7 Day 1 1 – 8 Day 2 2 – 8 Day 3 3.3 (3.2) 47 25 151 5.4 1.9 3 – 8 Day 4 4 – 8 Day 5 5 – 8 Day 6
  • 29. Back to our unit • No new complains. • No further Fever, sweating, shivering, and shortness of breath. • Lower limbs swelling is less. Yellowish discoloration of the eyes decreased. Urine and stool color was becoming closer to normal than before.
  • 30. • Patient BP In our department: Date Day in our department Lowest BP 6 – 8 Day 1 7 – 8 Day 2 8 – 8 Day 3 140/90 9 – 8 Day 4 130/90 10 - 8 Day 5 130/90 11 - 8 Day 6 120/80 12 - 8 Day 7 13 - 8 Day 8
  • 31. • CBC In our department : Date Day in our department WBCs HB Platelets 6 – 8 Day 1 7 – 8 Day 2 8 – 8 Day 3 9 – 8 Day 4 8.2 8.1 221 10 - 8 Day 5 11 - 8 Day 6 12 - 8 Day 7 13 - 8 Day 8
  • 32. • Renal functions and electrolytes In our department Date Day in our department Cr Urea Na+ K+ 6 – 8 Day 1 3.2 87 136 4.5 7 – 8 Day 2 3.7 87 136 4.5 8 – 8 Day 3 2.2 - - - 9 – 8 Day 4 1.7 - - - 10 - 8 Day 5 1.2 31 139 3.1 11 - 8 Day 6 12 - 8 Day 7 0.5 13 - 8 Day 8 0.5 16 137 3.0
  • 33. • Liver functions In our department : Date Day in our department T.Bili / D.Bili AST ALT ALP T.ptn Alb 6 – 8 Day 1 7 – 8 Day 2 8 – 8 Day 3 9 – 8 Day 4 10 - 8 Day 5 1.2 / 1.0 16 11 176 6.0 2.5 11 - 8 Day 6 12 - 8 Day 7 13 - 8 Day 8
  • 34. On discharge: • Complains: None • Physical Examination: No abnormality detected • Pregnancy Ultrasound: Normal pregnancy • Latest investigations: CBC RFTs LFTs BFFM WBCs = 8.2 Creatinine = 0.5 T.Bilrubin = 1.2 -ve HB = 8.1 Urea = 16 D.Bilirubin = 1.0 Platelets = 221 Na+ = 137 AST = 16 K+ = 3.0 ALT = 11 ALP = 176 T.Protein = 6 Albumin = 2.5
  • 36. • Yellow discoloration of skin, conjunctiva, sclera and mucosa associated with rise in serum bilirubin above 2mg/dl ( normal 0.2-01mg/dl) Latent jaundice:1-2mg/dl
  • 38. • Incidence: 1 to 4/1000 deliveries. • Grade of jaundice:  Mild: bilirubin <6mg%  Moderate 6-15mg%  Severe >16mg%
  • 39. Cause of jaundice during pregnancy Liver disease unique to pregnancy • Acute fatty liver of pregnancy. • Intrahepatic cholestasis of pregnancy. • Pre-eclampsia, eclampsia, HELLP syndrome. • Hyperemesis gravidarum Coincidental occurrence of liver disease in pregnancy • Acute viral hepatitis. • Hemolytic jaundice. • Cholelithiasis. • Drug induced • Obstructive jaundice
  • 40. Acute Hepatitis ICP HELLP AFLP Trimester Any Trimester Third Third Third Presenting symptoms Fever, Jaundice Pruritus HTN, Nausea, Vomiting,Pain Nausea, Vomiting,Pain ALT & AST Markedly high Normal to Mild rise Moderately high Moderately high Alkaline Phospatase Normal to mild rise High Normal Normal Platelets Normal Normal Low Normal Fetal Complications Infection with HBV & HCV Prematurity, IUGR, FD IUGR, Prematurity Prematurity Maternal Complications Acute liver failure(HEV) None Thrombocytope nia, septicemia, DIC Acute liver failure
  • 42.
  • 43. Outline • Epidemiology • Clinical features • Complications • Management of MIP
  • 45. • It leads to 7.5 million cases and 35,000 deaths every year in Sudan (2000 estimates). • Plasmodium falciparum is incriminated in >90% of cases. P. vivax, P. ovale and P. malariae are responsible of the rest. • Anopheles arabiensis is the main vector together with A. gambiae and A.funestus
  • 46. Malaria and pregnancy • In the Sudan each year more than 1.2 million women become pregnant, of those 750,000 are in areas with high malaria Transmission. • 25 million pregnant African women in endemic areas yearly Malaria is more frequent and complicated during pregnancy In malaria-endemic areas, malaria during pregnancy accounts for: – Up to 15% of maternal anaemia – 8-14% of low birth weight – 30% of "preventable" low birth weight – 3-8% of infant death
  • 47. Clinical features The common manifestations of malaria in pregnancy, articularly in the second half of pregnancy include the following: 1. Fever with more paroxysms in the second half of pregnancy due to immuno-suppression. 2. Anaemia is a common presentation and it could be due to: haemolysis of parasitized RBCs; increased demands of pregnancy; or profound haemolysis that may aggravate folate deficiency. Anaemia is more common and severe between 16 -29 weeks, and pre-existing iron and folate deficiency can exacerbate it and vice versa. Anaemia increases the risk of perinatal mortality and maternal morbidity and mortality, the risk of pulmonary oedema, and the risk of postpartum haemorrhage is also higher.
  • 48. 3. Splenomegaly may be present but variable in size; and preexisting large spleen may regress in size in pregnancy. 4. Acute pulmonary oedema is a more common and serious complication of MIP compared to non-pregnant population. It is more common in the second and third trimesters. However, it can occur immediately postpartum due to: the auto-transfusion of placental blood with high proportion of parasitized RBCs and the sudden increase in the peripheral vascular resistance after delivery. 5. Hypoglycaemia is another complication of severe malaria and is due to: Increased demand of glucose due to hypercatabolic state and infecting parasite Hypoglycaemic response to starvation Increased response of pancreatic islets to secretary stimuli.
  • 49. Hypoglycaemia presents with symptoms similar to those of malaria. Abnormal behaviour, convulsions and sudden loss of consciousness are also symptoms of cerebral malaria. 6. Secondary infections such as urinary tract infection, pneumonias… etc. are more common due to immunosuppression.
  • 50. Complications and effects of MIP: During pregnancy: • Frequency and severity are greater than in non-pregnant • Severe anaemia is common • Hyperpyrexia leading to abortion, preterm labour, intra- uterine foetal death and macerated stillbirth. • Hypoglycaemia • Transplacental infection leading to congenital malaria and neonatal death. • Spontaneous abortion, premature birth, stillbirth, placental insufficiency and intrauterine growth retardation (IUGR), low birth weight and foetal distress.
  • 51. During labour: • Precipitated labour • Postpartum haemorrhage During puerperium: • Puerperal pyrexia • Difficulty in lactation.
  • 52. Risks to the foetus: High grade fever, placental insufficiency, hypoglycaemia, anaemia and other complications can adversely affect the foetus. Spontaneous abortions, premature birth, stillbirth, placental insufficiency and IUGR, low birth weight, and foetal distress are problems observed during foetal growth. Transplacental spread to the foetus can result in congenital malaria, which is very rare. The placental barrier and maternal IgG antibodies, which cross the placenta, may protect the foetus to some extent. Congenital malaria
  • 53. is more common in the non-immune population and the incidence goes up during the epidemic of malaria. Foetal Quinine level is about one third of simultaneous maternal level and this subtherapeutic drug level does not cure the infection in the foetus. All four species can cause congenital malaria. The newborn can present with fever, irritability, feeding problems, hepatosplenomegaly, anaemia, and jaundice. The diagnosis can be confirmed by smear for malaria parasite.
  • 54. Diagnosing Malaria Case definition of Uncomplicated Malaria (UM): • Suspected malaria: Malaria is suspected when a patient presents with fever (or history of fever) and other symptoms and signs suggestive of malaria (e.g. headache, vomiting, sweating). The health care worker in this case, has to exclude clinically other common causes of fever in his area, such as: tonsillitis, , chest infection, measles, abscess, urinary tract infection, etc…
  • 55. • Confirmed malaria: A malaria case is confirmed by demonstration of asexual forms (trophozoite stage) of the parasite in the thick or thin peripheral blood film or by rapid diagnostic test in the presence of fever.
  • 56. • Clinical malaria: For management of malaria in children, in facilities with integrated management of childhood illnesses (IMCI) trained personnel, and where there are no facilities for laboratory diagnosis, the health worker should deal with the child according to IMCI guidelines . According to IMCI «Any febrile child (by history, temperature of ≥37.5oC or feeling hot) in any area should be managed as having malaria after exclusion of other obvious causes of fever (tonsillitis, measles, abscess, urinary tract infection or acute respiratory infection….) For management of malaria in adult and children more than 5 years old and where there is a malaria risk but there is no facilities for laboratory diagnosis it is reasonable to assume that the patient has clinical malaria when there is no other obvious reason for fever
  • 57. Severe Malaria Case definition of severe malaria (SM): Severe malaria is defined as malaria due to P. falciparum infection that is sufficiently serious to be an immediate threat to life. It is a medical emergency, which requires hospitalization.
  • 58. Who gets severe malaria? Any infection with P. falciparum can become severe if treatment is delayed or inadequate. Those who are most at risk are: • Children (especially those who are in areas of high endemicity – south of Sudan) aged from 6 months to 6 years. • Indigenous pregnant women, especially primigravidae. • People of all ages in areas of low endemicity (north Sudan). • People returning to endemic areas after a few years absence. • Visitors (of any age) from non-endemic areas.
  • 59. The health worker should regard a patient as having severe malaria if he or she has one or more (mostly seen in combination) of the conditions listed in the table below (WHO 2000).
  • 60. Diagnosis of malaria 1) Clinical diagnosis 2) Blood film – Can take any time (or at the height of fever) – 3 consecutive days – Giemsa-stained Thick film andThin film
  • 61. • Thick film for MP positive or not • Thick film facilitates the diagnosis of low level parasitemia • Thin film is essential • to confirm the diagnosis, • to identify the species of parasite, & • to quantify the parasite load by counting the % of infected RBCs • P. falciparum  only ring forms may be found in early stage • Other species  all stages of erythrocytic cycle may be found • Gametocyte appears after about 2 wks, and persist despite tx and are harmless, except that they are the source by which more mosquitos become infected Thick film &Thin film
  • 63. • parasites are not detected at times in peripheral smear : • a. sequestration deep vascular bed b. partially treated patients c. prophylactic antimalarial t/t d. inexperienced technician e. poor quality staining
  • 64. 3) Rapid Diagnosis Tests (RDT) by ICT Rapid diagnosis for falciparum – Parasight-F test based upon HRP 2 (Histidine rich protein 2) Rapid diagnosis for falciparum and vivax – LDH coted OptiMAL test kits – Test positive  1 band in vivax and 2 bands in falciparum – Test took only 5 min – Sensitivity 100%, specificity 96% • Importance of ICT – Rapid Dx – Can get Dx in MP negative cerebral malaria – Can differentiate falciparum and vivax – Suitable for microscopists less experienced in examining blood films
  • 65.
  • 66. 4) QBC MalariaTest (Quantitative Buffy Coat) • Fluorescence microscopy- based malaria diagnostic test • Increased sensitivity over traditionalGiemsa thick film methods • In > 90% of cases, the species of parasite can also be identified. • Simply fill a capillary tube with a patient sample  coat with acridine orange (fluorescent dye)  centrifuge  place under a fluorescent microscope
  • 67. 5) DNA detection (PCR) • Used mainly in research • Useful for determining whether a patient has • a recrudescence of the same malaria parasite or • a re-infection with a new parasite
  • 68.
  • 69.
  • 70. Management of MIP: This includes: • treatment of malaria • management of complications • and management of labour.
  • 71. Treatment of malaria: • Ideally the patient should be admitted when it is possible. Assess the severity of the condition by general examination: palor, jaundice, blood pressure, temperature, haemoglobin level and parasite count. • SGPT, serum bilirubin, serum creatinine and blood sugar may also need to be assessed. • Monitor the maternal and foetal vital parameters 34- hourly and monitor the fluid intake/output daily. • Choose the drug according to the severity of the disease and gestational age. • Avoid overdosing and under dosing with the drugs; avoid fluid overload or dehydration
  • 72. Treatment of UM in pregnancy: A - In the first trimester: Oral Quinine is safe and is the first line of treatment throughout pregnancy. The dose is 10 mg salt/Kg body weight, administered 8- hourly for 7 days.
  • 73. B – In the second and third trimester: • Oral Quinine 10mg/kg administered 8 hourly for 7 days. Or • Oral Quinine for 3 days 10mg/kg administered 8 hourly followed by sulfadoxine–pyrimethamine in the full treatment dose. Or • A combination of artesunate tabs (AS) 4mg/kg and SP (AS + SP) on the first day, followed by 2 further days of AS 4mg/kg
  • 74. Management of severe malaria during pregnancy: In the management of severe malaria in pregnancy especial concern must be paid to: anaemia, hypoglycemia and pulmonary oedema. • Quinine dihydrochloride, Quinine hydrochloride or Quinine sulphate is the first line of treatment all through during pregnancy. The dose is 10 mg salt/Kg body weight 8-hourly for 7 days. Start with IV Quinine in 10% glucose infusion or 5% glucose in normal saline; if for some reason Quinine can not be given by infusion, Quinine dihydrochloride can be given in the same dosage by IM injection diluted with sterile normal saline to a concentration of 60 mg/ml. The dose should be divided into two halves and injected into both anterior upper thighs, and shift to oral as soon as possible. In case there is no 10% glucose concentration give one bottle of 5% glucose before administration of Quinine; be careful not to induce pulmonary oedema. Random blood sugar should be done before and after Quinine administration.
  • 75. • Or Quinine 10 mg/Kg body weight 8 hourly for at least 3 days (IV or IM) and shift to (AS+SP) as soon as the patient can take orally; this is of course in the second and third trimesters. • Or Artemether IM 3.2 mg/Kg body weight in the first day (divided to two doses 12 hours apart) followed by 1.6 mg/Kg daily for the next 6 days in the second and third trimesters.
  • 76. Management of complications: • Pulmonary oedema: careful fluid management, back rest elevation, diuretics and ventilation if needed. • Hypoglycaemia: 25 -50% dextrose, 50 -100 ml IV (1ml/kg) followed by 10% dextrose as a continuous infusion. Blood sugar should be monitored every 4 -6 hours where possible. • Anaemia: packed cell should be transfused if Hb <5 g/dL. • Renal failure: it could be pre-renal due to unrecognized dehydration or renal due to severe parasitaemia. Management involves careful management, diuretics and dialysis if needed. • Septicaemic shock or algid malaria: administration of third generation of cephalosporin, monitoring of vital parameters (blood pressure) and fluid replacement when required (systolic <90mmHg)
  • 77. Management in labour: Falciparum malaria and higher fever induce uterine contractions, resulting in premature labour. The frequency and intensity of the contractions is related to the degree of the fever. Foetal distress is the commonly recognized complication. Lower the temperature of the woman by using tepid sponging or antipyretics such as paracetamol. Adequate fluid management and careful monitoring in labour are mandatory.
  • 78. The table below summaries the use of antimalarial drugs for MIP and puerperium.
  • 79. Important remarks: • Severe malaria (SM) cases should be managed at hospitals. So health workers at the peripheral units should refer patients immediately. Pre- referral treatment is recommended. • Attention should be given to the general management (good nursing care) of the patient as for the specific treatment. • Early recognition, referral and early institution of the appropriate management at hospital are of paramount importance in the reduction of deaths attributed to malaria. • Case fatality rate (CFR) is a useful indicator for hospital i.e. higher CFR indicates inadequate case management at hospital level or late presentation which would identify a communication need for the community. CFR = No. malaria deaths ÷ No. of admitted malaria cases × 100
  • 80. General management of the patient with SM: The health worker (medical doctor, medical assistant or the nurse) on duty should consider the following (8 + 8 + 4) points in the management of the patients with severe malaria: • Immediate measures (8). • Searching for and managing complications (8). • Monitoring the case (4).
  • 81. Do the following 8 immediate measures: 1. Start resuscitation, particularly maintenance of a patent airway. 2. Establish IV line. 3. Make a thick blood smear for immediate malaria parasite count. RDTs can be useful in certain areas 4. Classify the degree of dehydration, assess patient’s fluid requirements and correct accordingly. 5. Control fever if the axillary temperature is 38.5ºC or above: Tepid sponge, fanning and oral or rectal paracetamol (15mg/kg every 4 to 6 hours) 6. Control convulsions: Maintain airway, treat with rectal diazepam (0.5mg/kg) or slow IV diazepam (0.3mg/kg, maximum 10mg in an adult). Also correct hypoglycaemia and electrolytes
  • 82. 7. Detect and treat Hypoglycaemia: Hypoglycaemia can be induced by high parasitaemia, fasting and quinine therapy. Hypoglycaemia can recur especially in pregnant women and children. If blood glucose ≤2.2mmol/l or ≤ 40mg/dl; give 1ml/kg of 50% dextrose IV, diluted with an equal volume of 0.9% Saline, give slowly over 35- minutes. Follow with 10% dextrose infusion at 5ml/kg/hr. I f there is no test for blood glucose, treat as if the patient is hypoglycaemic; 8. Start Quinine IV or Artemether IM (if not accessible, Quinine I.M. or Artesunate suppositories can be administered; notably in case of hyperparasitaemia). imbalance if it is present.
  • 83. Look and deal with the following 8 complications: 1. Shock, algid malaria: if Systolic Bp <50mmHg in children 15- yrs or <80 mmHg in >5yrs, suspect Gram-negative septicaemia. In such case take blood samples for culture. Give parentral broad-spectrum antimicrobials. Correct haemodynamic disturbances. Treat with: 30ml/kg 0.9% Saline IV in 1hour, then, reassess. Give oxygen if possible 2. Consider the need for blood transfusion: Assess the degree of palor (no palor, some palor or severe palor). Look for signs of severe anaemia such as very pale mucous membranes, respiratory distress and a rapid pulse. Note: The decision to transfuse with blood should not only be based on low laboratory values but as a guide Hct <15% or Hb <5 g/dL Transfuse blood if there is: * Cardio respiratory symptoms e.g. severe anaemia. * PCV <20 or Hb <5g/dL.
  • 84. 3. In case of metabolic acidosis: Exclude and treat hypoglycemia, hypovolaemia and gram negative septicaemia. Give isotonic saline 20 ml/Kg of body weight rapidly or screened whole blood 10ml/Kg over 30 minutes if haemoglobin is <5 g/dl. 4. If there is spontaneous bleeding and coagulopathy: Transfuse screened fresh whole blood or clotting factors; give vitamin K 10 mg IV per day for adult, 1 mg/day for infant, 2 -3 mg/day for children, and 5 -10 mg/day for adolescent. Vitamin K should be given SC or IV. 5. Acute renal failure: Special efforts should be given to detection of symptoms and signs suggestive of renal failure. Exclude dehydration; maintain strict fluid balance; carry out dialysis if indicated.
  • 85. 6. Malarial hemoglobinuria (black-water fever): Due to excessive destruction of RBCs which leads to jaundice and low Hb level. Continue with suitable antimalarial treatment; transfuse screened fresh blood if needed. 7. Acute pulmonary oedema: May be due to malaria itself. Prevent by avoiding excessive rehydration. Treatment -prop patient up, give oxygen 100%. If pulmonary oedema is due to over-hydration, stop intravenous fluids, give a diuretic (frusemide I.V. in a dose of 40 mg for adult and 0.5 -1 mg/Kg/dose for children) or withdraw 3 ml/Kg of blood by venesection into a donor bag.
  • 86. . 8. Exclude common infections/conditions that present like severe malaria: Perform urinalysis for urinary tract infection; lumbar puncture for meningoencephalitis in unconscious patients (unless contraindicated); white blood cell count for other infections and chest x-ray for bronchopneumonia.
  • 87. Monitor considering the following 4 points: 1. Level of consciousness: If there is an altered level of consciousness use Glasgow or Blantyre coma scales to assess progress every 6 hours until the patient retained full consciousness. 2. Fluid input/output: Detect dehydration and avoid fluid overload. prevent pulmonary oedema. 3. Vital signs: Monitor vital signs every 6 hours to detect complications of severe malaria. If pulmonary oedema develops (rapid respiratory rate and deep laboured breathing) stop all IV fluids except quinine and call medical officer/ clinical officer for management 4. Level of parasitaemia: Determine the parasite count daily to monitor the therapeutic effect of treatment. Stop when there is no detectable parasitaemia.
  • 88. Educate the patient and relatives about compliance with a full course of treatment, home prevention of malaria and the sequelae of severe malaria. Wait for the patient to recover before counselling.
  • 89. Specific treatment of patients with SM: Pre-referral treatment at peripheral units: In most of the rural settings of the Sudan, it is usual to see patients with SM seeking care at the primary health care units. The health personnel in these units should refer the patients to the nearest hospital. Pre-referral treatment should be given. This could be Quinine IM or artesunate suppositories as follows: • Quinine IM The dose of IM Quinine is 10 mg salt/kg body weight given after dilution with sterile normal saline or distilled water to a
  • 90. • concentration of 60 mg/ml; the dose is divided into 2 halves and injected into both anterior upper thighs. If referral does not occur after 8 hours repeat the dose. Don,t keep the patients more than 24 hours
  • 91. • Artesunate suppositories Artesunate rectal capsules/suppositories, 10 mg/Kg (available in form of 50 mg or 200 mg per rectocap), should be given rectally as soon as possible, once the diagnosis of malaria is made. If the rectal capsule is expelled within the first hour, another rectal capsule should be inserted immediately If after 24 hours the patient has not been referred to hospital and is still unable to take oral medication, a second dose should be repeated
  • 92. Hospital treatment: • Treatment with quinine: Quinine dihydrochloride, Quinine hydrochloride or Quinine sulphate is the drug of choice for the treatment of severe malaria. Quinine can be given in one of the 3 ways depending on the patient conditions and according to the level of health facility.
  • 93. A - Quinine for 7 days: Start with Quinine infusion, the dose is 10 mg salt/kg body weight preferably in 5% Glucose, 5% glucose in normal saline, or in 10% glucose given over four hours duration every 8 hours (with a rate of 15 drops/min for adult) with a maximum dose of 600 mg. Shift to the oral quinine as soon as the patient can take oral medication and continue for 7 days
  • 94. B - Quinine IM: If the IV route is not possible, Quinine can be given in the same dose by intramuscular injection diluted with sterile normal saline or distilled water to a concentration of 60 mg/ml as a pre- referral dose. The dose should be divided into two halves and injected into both anterior upper thighs. Shift to the oral Quinine as soon as the patient can take oral medication.
  • 95. C - Quinine for at least 3 days and then first-line: It is observed that compliance to oral Quinine sometimes is not good. Alternative option is to give Quinine IV or IM for at least 3 days at hospital and then shift to the first-line treatment (AS+SP) if the patient can take oral medication. Ensure patient takes full oral course (AS+SP).
  • 96. Quinine side effects: The commonest are nausea, vomiting and tinnitus. Over-dose causes headache, dizziness, severe CNS disturbance and delirium. The most serious side effect is hypoglycemia. Hypoglycemia can be induced by Quinine itself (as it is found to stimulate insulin release), marked parasitaemia (as it increases glucose consumption) and fasting (as the ill patient may not be able to take foods or drinks particularly in children and pregnant women). Rapid intravenous administration of Quinine can precipitate hypotension and fatal cardiovascular toxicity.
  • 97. Treatment with Artemether injection (ARM): The drug is available in injectable form (80 mg/ml for adult and 40 mg/ml for children). In Sudan ARM injection (monotherapy) is recommended only for the treatment of severe malaria in facilities where the full 7-day course can be administered. If ARM monotherapy is administered for less than 7 days, radical cure will not be achieved.
  • 98. The drug can be administered by one of two regimens; the first one is preferable: • Artemether IM, 1.6 mg/Kg initially, and again after 12 hours on the first day.Then 1.6 mg/Kg daily for at least 3 days (total of 4 days of IM ARM).Then the first-line treatment (AS+SP) if the patient can take oral medication. • Artemether IM, 1.6 mg/Kg initially, and again after 12 hours on the first day. Then 1.6 mg/Kg daily for the next 6 days giving a total of 8 doses. Side effects in general are mild and include headache, vomiting, abdominal pain; itching and minor non-specific ECG changes (Nonspecific ST changes and 1st degree atrioventricular block).