223.

Define peptic ulcer disease

It’s a disorder due to discontinuation of gastrointestinal intestinal tract ( the stomach and and the
duodenum) as a result of gastric acid or pepsin which may extend to the lower esophagus, jejunum and
can extend into the muscularis propria .

224. What is the difference between gastric ulcer and duodenal ulcer?

GASTRIC ULCER

 Usually in the lesser curvature of the stomach

 Symptoms increases with meals
 More in females
 May lead to weight loss
 Less common to duodenal ulcer
While;
DUODENAL ULCER
 Usually in the duodenal bulb
 Symptoms relieved with meals
 Symptoms occurs between meals and nocturnal
 More in males
 May lead to weight gain
 More common than gastric ullcer

225. List the risk factors for peptic ulcer disease

1. Helicopters bacteria pylori ( most commonest cause)

EFFECTS:

i) Produces grease that breaks down urea to ammonia acid which protects the mucosa
layer from gastric acid
ii) Produces toxins ( cagA and vacA) that causes inflammation

iii) it has a flagellum for movement into the gastric epithelium

2. NSAIDS ( 2nd most commonest cause) ;

EFFECTS; Wears off the mucus layer of the GIT

 Blocks protective factor prostaglandin via cox 1 enzyme
1. Decreased mucus production
2. Decreased bicarbonate production
3. Decreased mucosal blood flow
 The following worsens the effects
1. High doses of NSAIDS
2. Prolong use
3. Corticosteroids
4. > 70 years old
5. Female
 3. First degree relative with peptic ulcer disease

3. Emigrant from developed nation

4. African American/ Hispanics

226. List the clinical features of peptic ulcer disease

i) Epigastric pain
ii) Heart burn
iii) Nausea and vomiting
iv) Bloating
v) Dark stools
vi) Hematemesis

227. List the alarming features of peptic ulcer disease

i) Unintentional weight loss

ii) Progressive dysphagia
iii) Overt GI bleeding
iv) Recurrent emesis
v) Family history of upper GI bleeding
vi) Iron deficiency anemia
vii) Malignancy

228. List the investigations done for peptic ulcer disease

1. Endoscopy ( gold standard)

Indications
i) >50 years old
ii) New onset dyspepsia
iii) Any alarming feature regardless of age
2. Helicopter pylori assay
o Blood
o Breath
o Stool
3. Stool microscopy
4. Abdominal Xray
5. CT scan
6. Barium meal or follow through

229. Management of peptic ulcer disease

i) If bleeding
o Endoscopic injections, clamping and catheterization of the bleeding vessels
ii) Proton pump inhibitors reduces gastric acid secretion e.g omeprazole, pantoprazole,
esoprazole, rabeprazole
 iii) Histamine receptor blockers reduces gastric acid secretion
iv) Antacid forms a protective layer e g bismuth sulphate
v) Triple regimen;
 PPI + CLARITHROMYCIN + METRONIDAZOLE /AMOXICILLIN
vi) Quadriple regimen;
 Triple regimen + Bismuth sulphate but no metronidazole
 PPI + levofloxacin /amoxicillin + bismuth sulphate
vii) Dietary modifications; stop NSAIDS , smoking and alcohol
viii) Surgery;
 Vagotomy
 Partial gastrectomy
Indications for surgery
a) Unresponsive to medical treatment
b) Non compliance
c) High risk for developing complications
d) Refractory PUD ; ulcer >5mm in diameter, that doesn’t heal 8-12 weeks of
PPI treatment
Causes of Refractory PUD
i) Persistent H.pylori infection
ii) Continous use of NSAIDS
iii) Significant morbidity that impairs ulcer healing

230. List the complications of peptic ulcer disease

i) Bleeding
ii) Perforation
iii) Gastric outlet obstruction

231. List the 4 differentials of peptic ulcer disease

i) Gastritis
ii) Gastro esophageal reflux disease
iii) Gastric cancer
iv) Pancreatitis

234. Define the following terms

 Asexual cycle: → The life cycle of the malaria parasite in the host from merozoite
invasion of red blood cells to schizont rupture (merozoite →ring stage→
trophozoite → schizont → merozoites) with approximate duration of ;
1. 24 hrs - plasmodium knowlesi
2. 48 hrs - Plasmodium Falciparum ,Ovale , Vivax
3. 72 hrs – Plasmodium Malariae
 Cerebral Malaria:
Severe Plasmodium falciparum , with coma (Glasgow coma scale < 11, Blantyre
coma scale < 3); malaria with coma persisting for > 30 min after a seizure.
 Cure : Elimination of the malaria parasites that caused the treated illness
 Drug resistance: The ability of a parasite strain to survive and/or to multiply
despite the administration and absorption of a drug given in doses equal to or
higher than those usually recommended, provided the exposure is adequate.
Resistance to antimalarial agents arises because of the selection of parasites with
genetic changes (mutations or gene amplifications) that confer reduced
susceptibility
 Gametocytes: The sexual stages of malaria parasites that infect anopheline
mosquitoes when taken up during a blood meal
 Hyperparasitaemia: A high density of parasites in the blood, which increases the
risk of deterioration to severe malaria (although the risk varies in different
endemic areas according to the level of transmission) and of antimalarial drug
resistance and subsequent treatment failure.
The term is used to refer to
1. a parasite density > 4% ( Patients with knowlesi P. falciparum ∼ 200
000/µL)
2. parasite densities > 10% and patients with parasite densities > 100
000/µL ( ∼ P. 2%) are considered to have severe malaria even if they do
not have evidence of vital organ dysfunction
 Malaria pigment (hemozoin): A dark brown granular material product
formed by malaria parasites as a by- product of hemoglobin digestion
 The pigment is evident in mature trophozoites and schizonts
and may also be phagocytosed by monocytes, macrophages and
polymorphonuclear neutrophils

 Preerythrocytic development: The development of the malaria parasite when it

first enters the host when after inoculation into a human by a female
anopheline mosquito, sporozoites invade hepatocytes in the host liver and
multiply there for 512 days, forming hepatic schizonts, which then burst,
liberating merozoites into the bloodstream, where they subsequently invade red
blood cells.
 Radical cure: This term refers to both cure of blood killing hypnozoites (in P.
vivax and P. ovale stage infection and prevention of relapses by infections only)
 Recrudescence: Recurrence of asexual parasitemia following antimalarial
treatment comprising the same genotype(s) that caused the original illness;
this results from incomplete clearance of asexual parasitemia because of
inadequate or ineffective treatment, but must be distinguished from re infection
(usually determined by molecular genotyping in endemic areas) and note that
recrudescence is different from relapse in P. vivax and P. ovale infections
 Recurrence: Recurrence of asexual parasitemia after treatment, due to
recrudescence, relapse ( P. Vivax and Ovale infections only) or a new infection
 Relapse: Recurrence of asexual parasitemia in P. vivax and P. ovale P. malaria
deriving from persisting liver stages; occurs when the bloodstage infection has
been eliminated but hypnozoites persist in the liver and mature to form
 hepatic schizonts, which after an interval of weeks or months, burst and
liberate merozoites into the bloodstream
 Ring stage: Young, usually ringshaped, intraerythrocytic malaria parasites before
malaria pigment is evident by microscopy
 Schizont: Mature malaria parasite in host liver cells (hepatic schizont) or red
blood cells (erythrocytic schizont) that is undergoing nuclear division by a
process called schizogony
 Severe anemia: Hemoglobin concentration of < 5 g/100 mL (haematocrit <
15%) in children less than 12 y old
 Severe falciparum malaria: Acute falciparum malaria with signs of severity
and/or evidence of vital organ dysfunction
 Sporozoite: Motile malaria parasite that is infective to humans inoculated by a
feeding female anopheline mosquito that then invades hepatocytes.
 Trophozoite: The stage of development of malaria parasites growing within host
red blood cells from the ring stage to just before nuclear division with mature
trophozoites containing visible malaria pigment
 Uncomplicated malaria: Symptomatic malaria parasitemia with no signs of
severity and/or evidence of vital organ dysfunction

235. What is malaria?

Malaria is a potentially fatal infection caused by the parasite Plasmodium species and one of the
significant health problems of humans

236. List 5 types of malaria species

1. Plasmodium Falciparum - Tropical Africa , southeast Asia, western Pacific

2. Plasmodium vivax – South America , south east Asia, western Pacific

3. Plasmodium ovale wallickeri, Plasmodium ovale curtisi } P. Ovale - Tropical Africa

4. Plasmodium malariae – May occur in all malaria areas, but the prevalence rate is low
5. Plasmodium knowlesi – Southeast Asia

Areas where malaria is endemic;

 Central America
 South America
 Hispaniola
 Sub Saharan Africa
 Indian subcontinent
 South east Asia
 Middle east Asia
 Oceania
1. The dominant vector specie in Africa is - Anopheles gambiae complex
2. Breeding habitat for Anopheles- water
3. 512 Recognized Anopheles species- 50 provisionally designated
237. List the risk factors for malaria

1. Children less than 5 years old

2. Pregnant women
3. Non immune visitors

238. On the basis of splenomegaly prevalence rate in children 2-9 years old , Define the 4 endemicity
areas based on the malariometric indices

1. Holo-endemic areas : where the splenomegaly prevalence is >75%

2. Hyper – endemic areas : 51-75%
3. Meso- endemic areas : 11-51%
4. Hypo- endemic areas : <11%

239. List the routes of transmission of malaria species

1. Bite of female Anopheles mosquitoes

2. Blood transfusion
3. Maternal fetal transmission

240. What is the pathogenesis of malaria

1. On the human skin; Bite of female Anopheles mosquitoes

2. Injection of sprorozoites into the bloodstream within minutes
3. Transported in to the liver to infect the hepatocytes ( LIVER PHASE )
4. Within the phase of 7 – 10 days asexual replication of sprorozoites to form schizonts
(ASYMPTOMATIC )
5. Schizonts emerges from the liver to form merozoites
6. Merozoites enters into the bloodstream to infect the red blood cells and multiply
7. The red blood cells ruptures and releases products (SYMPTOMATIC)
8. Merozoites released infects other red blood cells
9. The cytokines released from the ruptured red blood cells are responsible for the symptomatic
manifestations of malaria ( headache, fever, rigors, vomiting, diarrhoea, anorexia, tiredness,
muscle aches and joints)
10. Also, the plasmodial DNA is also highly pro inflammatory and can induce cytokinemia and
fever
11. Hemozin presents plasmodial DNA during parasite development within the red blood cells to
interact intracellularly with the Toll like Receptor -9, to release Pro- inflammatory cytokines that
inturns induce COX 2 upregulating prostaglandins leading to the induction of fever
12. Hemozin as been linked to induce apoptosis in developing erythroid cells in the bone marrow
causing anemia

241. List the clinical features of malaria

The signs and symptoms are not specific they include

1. Fever
2. Headache
3. Malaise
 4. Weakness
5. Gastrointestinal distress( nausea , vomiting, diarrhea)
6. Neurological complaints ( dizziness, disorientation, confusion, coma)
7. Back pain
8. Chills
9. Cough
10. Features of severe malaria

242. What is the difference between uncomplicated malaria and complicated malaria

Uncomplicated malaria is defined as symptoms present ( fever) but no clinical or laboratory features to
indicate severity or vital dysfunction

While

Complicated typically occurs due to delayed treatment of uncomplicated malaria and is defined as
clinical or laboratory evidence of vital dysfunction

243. What is the difference between asymptomatic and symptomatic malaria infection

Asymptomatic malaria infection is defined as positive malaria smear or other diagnostic test without
symptoms of malaria

While

Symptomatic malaria infection is defined as positive malaria smear with symptoms of malaria ( fever )

245. List the complications of malaria

1. Cerebral malaria – symptoms are similar to toxic encephalopathy

2. Seizures – secondary to hypoglycemia or cerebral malaria
3. Renal failure – 30% non immune adults suffer acute kidney injury
4. Hemoglobinuria ( black water fever)-
 Passage of dark urine( Madeira - wine coloured urine)
 Hemolysis
 Hemoglobinemia
 Hemoglobinuria
 Hemozinuria
5. Non cardiogenic pulmonary edema – common in pregnant women and fatal in 80% of patients
6. Severe hypoglycemia - often in young children and pregnant women, difficult to diagnose
7. Lactic acidosis -
 occurs from clogged microvasculature with P. Falciparum
 the venous lactate = 45mg/dl
 Poor prognosis
8. Hemolysis- leads to severe anemia and jaundice
 9. Bleeding ( coagulopathy)
In pregnancy as a result of decreased immune function and placenta sequestration of
P.falciparum parasites
10. Anemia – severe in pregnant women
11. Fetal complications – premature birth, risk of miscarriage ( 1 st trimester) ,low birth weight,
anemia and death
( the final common pathway for severe malaria can include respiratory distress, hepato renal
failure, shock and coma)

246. List the guiding principles for malaria treatment

1. The choice of drug regimen for treatment depends on:

i. Clinical status of the patient
ii. Type of malaria specie
iii. Area where infection was acquired
iv. Drug resistance status
v. Pregnancy status
vi. History of drug allergies
vii. Other Medications taken by the patient
2. Early diagnosis and prompt treatment
i. Within 24-48 hrs of onset of malaria symptoms
ii. In all cases of suspected malaria confirm diagnosis using the parasitological test
or rapid diagnostic test
3. Use of Combination therapy – this improves efficacy , prevents or delay resistance
4. Rational use of antimalarial –
a. To reduce spread of drug resistance
b. Limit wastage
c. Ensure effective management of febrile illness
5. Appropriate weight based dosing – prolong therapeutic life of medicines

247. List the laboratory tests done for malaria

1. Microscopic examination
a. Thick blood films – Parasite detection and and quantification
b. Thin blood films- specie identification
c. Results should be available within 2 hours
d. Negative blood smears- diagnosis of malaria unlikely
e. In non immune individuals :
 they may be symptomatic with very low parasite densities which may initially be
undetectable
 Blood tests should be repeated every 12- 24 hours for a total of 3 sets to rule
out malaria
i. Malaria Positive Slides: Malaria parasite seen (MPS) clearly stating the
parasite stage
 1 ii. Negative malaria slides: No Malaria Parasite seen

iii. Parasite Quantification: Number of parasite counted /µl of blood

2. Polymerase chain reaction PCR based techniques and
3. Multiplex bead assay- for diagnosis under special circumstances and research purposes to
monitor drug resistance Drug therapeutic efficacy testing or therapeutic efficacy testing
4. Urine malaria test device and automated diagnostic medicines– Novel test under research
evaluation
5. Malaria rapid diagnostic test – detects specific antigens (proteins) Produced by the malaria
parasites
 mRDTs are lateral flow immunochromatographic antigen detection tests which rely
on the capture of dye antibodies to produce a visible band on a strip of nitrocellulose
labelled
 They detect the presence of clinically significant malaria infection
 The sensitivities and specificities of RDTs are variable, and their vulnerability to high
temperatures and humidity is an important constraint
TYPES OF RAPID DIAGNOSTIC TESTS
1. Plasmodium falciparum histidine rich protein 2 (PfHRP2) based test detects
the presence of the plasmodium protein (PfHRP2) whether dead or alive
 There could be some false positives as they persist after death of
the parasite for up to five weeks
2. Enzyme based tests including Plasmodium dehydrogenase (pLDH) and
aldolase lactate based tests detect all Plasmodium species as these enzymes
are part of the glycolytic process
 The parasites must be viable for the test to be positive

• Most RDTs have a sensitivity of ≥ 95% at parasite densities of 200/ μ l of blood

• Malaria RDT results should be available within 20 minutes

• The patient who has been treated for malaria within two weeks should not be
subjected to mRDT; instead microscopy is recommended

• Reporting Technique in using mRDTs:

ii. RDTs Positive should be reported as: POS

iii. ii. RDTs Negative should be reported as: NEG

248. Define severe malaria

Defined as one or more of the following, occurring in the absence of an identified alternative
cause, and in the presence of P. falciparum asexual parasitemia

1.Impaired consciousness :

A Glasgow Coma Score <11 in adults or a Blantyre Coma Score <3 in children

2.Prostration :

Generalized weakness so that the person is unable to sit, stand or walk without assistance
3. Severe hypoglycaemia : Blood or plasma glucose <2.2mmol/L (<40mg/dL).

4. Severe malarial anemia :

A hemoglobin concentration < 5g/dL or a hematocrit of < 15% in children <12 years of age
< 7g/dl and <20% respectively in adults a parasite count >10,000/ μL

5.Renal impairment (acute kidney injury):

Plasma or serum creatinine >265 μ mol/L (3mg/dL) or blood urea > 20 mmol/L

6. Acidosis :

• A base deficit of >8 meq/L or, if unavailable, a plasma bicarbonate of <15mmol/L or

venous plasma lactate > 5 mmol/L.

 Severe acidosis manifests clinically as respiratory distress- rapid, deep and labored
breathing.

7. Multiple convulsions :

 More than two episodes within 24 hours

8. Jaundice:

 Plasma or serum bilirubin > 50μmol/L (3mg/dL) together with a parasite count >100,000/ mL

9. Pulmonary oedema:

 Radiologically confirmed, or oxygen saturation < 90% on room air or respiratory rate
>30/minute
 often with chest in drawing and crepitations on auscultation

10. Significant bleeding (DIC):

including recurrent or prolonged bleeding from nose, gums or venepuncture sites; hematemesis or

melaena.

11. Shock:

 Compensated shock is defined as capillary refill ≥3 seconds or temperature gradient on leg (mid
to proximal limb), but no hypotension
 Decompensated shock is defined as systolic blood pressure less than 70 mmHg in children or
<80 mm Hg in adults with evidence of impaired perfusion (cool peripheries or prolonged
capillary refill)

12. Hyperparasitaemia:

 Red blood cell P. falciparum parasitemia >10% or malaria parasite density of ≥200,000
parasite/µl of blood.( This definition is variable depending on the level of malaria
transmission)
 Severe vivax malaria is defined as above but with no parasite density thresholds
  Severe knowlesi malaria is also defined as above with two differences:

• P. knowlesi hyperparasitaemia:

1. Parasite density >100,000/µL

2. Jaundice and parasite density >20,000/µL

249. List the population at risk for severe malaria

1. Children <5years

2. Adolescents in regions with low malaria transmission

3. Pregnant women especially the 1 st and 2nd pregnancy

4. People with sickle cell disease

5. People returning or coming from malaria free areas

6. People who have had a splenectomy and the immunosuppressed

250. Treatment of Uncomplicated Malaria

1. Diagnosis through rapid diagnostic tests or microscopy is recommended in all

cases according to the National Malaria Policy in Nigeria except rarely in
children under the age of 5 years where treatment for malaria may be started if
diagnostic tests are not immediately available.

2. Treat with an Artemisinin-based Combination Therapy (ACT)

° ACTs are medicines consisting of an artemisinin derivative and
another effective long acting schizonticidal antimalarial medicine
3. The recommended ACTs are:
i) artemether plus lumefantrine (AL)
 Recommended in Nigeria as medicine of choice for
uncomplicated malaria
 AL strengths: 20mg/120mg; 40mg/240mg; and 80mg/480mg
 The new higher strengths provide for less pill burden per dose

Weight(kg) No of tablets/dose No of tablets/dose No of tablets/dose

(20/ 120mg/Tab ) (40/ 240mg/Tab ) (80/480mg/Tab)

5 - <15kg 1 Tab twice daily NA NA

×3days

15- <25kg 2 Tabs twice daily 1 Tab twice daily NA

×3 days ×3days
 25 -<35kg 3 Tabs twice daily NA NA
×3days

>35kg 4 Tabs twice daily 2 Tabs twice daily 1 Tab twice daily

(Adults) ×3days ×3days ×3days

ii) artesunate plus amodiaquine (AA)

 Recommended in Nigeria as medicine of choice for
uncomplicated malaria
 Not used in pregnancy

Weight / Age Tablet strength Dosage Regimen

a. 4.5kg - 9kg 50/135mg 1 Tab once daily for 3days

1 – 5 years

b. >18kg 100/270mg 1 Tab once daily for 3days

6 -13 years

c. >36kg 100/270mg 2 Tabs once daily for 3days

> 14years

iii) artesunate plus mefloquine (AM)

 Should be avoided if patient has cerebral malaria because of
the increased risk of seizures , encephalopathy and psychosis
iv) dihydroartemisinin plus piperaquine (DHP)
 Recommended in Nigeria as medicine of choice for
uncomplicated malaria
 Not taken with High fatty meals ,drug has high lipid solubility
and increases therapeutic levels.

Weight 120/ 160mg Tablet 40/320mg Tablet

5 - < 8kg 1 Tab once daily × 3days _

½
8- < 11kg 1 Tab once daily × 3days _

11- <17kg _ 1 Tab once daily ×3days

½
17 - < 25kg _ 1 Tab once daily × 3days

25 - <36 kg _ 2 Tabs once daily ×3days

36 - < 60kg _ 3 Tabs once daily ×3days

60 -< 80kg _ 4 Tabs once daily ×3days

> 80kg _ 5 Tabs once daily ×3days

v) artesunate plus pyronaridine (PA)

 Recommended in Nigeria as medicine of choice for
uncomplicated malaria
 20mg artesunate and 60mg Pyronaridine Tetraphosphate
 Administered with or without food

Weight No of satchets or tablets Regimen

5 - < 8kg 1 Sachet Daily × 3days

8- < 15kg 2 Sachets Daily × 3days

15- <20kg 3 Sachet Daily × 3days

20 - < 24kg 1 Tablet Daily × 3days

24 - <45kg 2 Tablets Daily × 3days

45 - < 65kg 3 Tablets Daily × 3days

> 65kg 4 Tablets Daily × 3days

vi) artesunate plus sulfadoxine/pyrimethamine

4. Tafenoquine used for anti relapse treatment for vivax malaria
5. Antipyretic measures
i) if body temperature is >38.5°c
ii) Advise care giver to
a. Take off unnecessary clothing
b. Tepid sponge the child with a towel soaked in lukewarm water

iii) In children;

 Give paracetamol; 10 - 15mg/kg every 6 – 8 hours, or when

necessary but not exceeding 4 doses in 24hours

iv) In adults;

 Give 500-1000 mg of paracetamol every 6-8 hours, or when

necessary but not exceeding 4 doses in 24 hours

6. For persistent vomiting

 If a patient vomits within 30 minutes of taking the medicine,

repeat the dose
  If the patient vomits again he should be managed with
parenteral antimalarial until the vomiting stops and thereafter
completes normal course of ACT.

7. Febrile Seizures

• If a patient has a seizure and does not recover within 30 minutes

from the seizure, it should be considered as severe malaria

8. In pregnancy

i. Treat pregnant women with uncomplicated P. falciparum

malaria during the first trimester with
7 days of oral Quinine + Clindamycin
ii. Where Quinine is not available or adherence to Quinine is not
assured, treat with ACTs
iii. Second and Third Trimesters and Lactating Mothers should
be treated with recommended ACTs for uncomplicated malaria

251 Treatment of severe malaria

1. For children <20kg

 IV/ IM Artesunate 3mg/kg body weight ( BW) on admission at Time O , then at 12hr and
24hr, Then once a day is the recommended treatment
2. For children >20kg and adults
 IV /IM Artesunate 2.4mg/kg Body weight (BW) on admission at Time 0, then at 12 hr and
24 hr, Then once a day is the recommended treatment
3. There is no upper limit to the total dose of artesunate
4. If parenteral artesunate is not available
 Give IM Arthemeter 3.2mg/kg per body weight on admission
 Then 1.6mg/kg Body weight per day
5. IV / divided IM injection Quinine 20mg salt /kg body weight on admission
 Then 10mg/kg per body weight every 8 hours
 Infusion rate should not exceed 5mg/salt /kg body weight per hour
6. Note: Give parenteral antimalarial in the treatment of severe malaria for a minimum of 24 hours
once started ( irrespective of the patient’s ability to tolerate oral medications earlier)
7. Thereafter, complete treatment by giving a complete course of the recommended ACT
8. The recommended dose of QUININE
a. Its given IV or IM
b. In children
 Give a loading dose of 20mg/kg of Quinine dihydrochloride salt
Diluted in 10ml/kg of 4.3% dextrose in 0.18% saline or 5% dextrose over a
period of 4 hours
 Then 12 hours after the loading dose ;
 □ Give 10mg salt/kg infusion over 4 hours every 8 hours until patient is
able to take orally.
 Subsequently give a full dose of recommended ACT
 Pre - referral treatment - a single rectal dose ( 10mg/kg) before referral
c. In Adults
 Give a loading dose of Quinine dihydrochloride 20mg/kg to a maximum of 1.2g
 Diluted in 10mg/kg 5% dextrose saline by IV infusion for over 4 hours
 8 hours after the start of the loading dose;

□ Give 10mg/kg salt to a maximum of 600mg over 4 hours every 8 hours

until patient is able to tolerate orally

 Then give a full dose of recommended ACT

 Intramuscular Quinine ;
- Where IV access is not possible
- Give a loading dose of IM Quinine
dihydrochloride
- Dilute to 60mg/ml
- Continue with a maintenance dose of 10ml/kg
8hourly until the patient is able to tolerate
orally
- Monitor glucose level especially for IM Quinine

252. Management of complications of malaria

a. COMA OR UNCONSCIOUS PATIENT

1. Ensure airway is patent; gentle suction nostrils and the oropharynx

2. Make sure the patient is breathing
3. Nurse the patient lying on the side or with the head sideways
4. Insert a Nasogastric tube
5. Establish an intravenous line for giving drugs and fluids
6. Correct hypoglycemia
 Children ; 0.5ml/kg of 50% dextrose diluted to 10- 15% IV
 Adults; 25ml of 50% dextrose IV
7. Where intravenous access is not possible, give dextrose or any sugar solution through the
Nasogastric tube

b. CONVULSIONS

1. Ensure patent airway and ensure patient is breathing

2. Correct hypoglycemia

3. In children ; Give rectal diazepam 0.5mg/kg or paraldehyde 0.1ml/kg

 If convulsions continues give IM phenobarbitone 10-15mg/ kg

3. In Adults; Give IV diazepam 10mg
C. SEVERE DEHYDRATION OR SHOCK

1. Give 20-30ml/kg of normal saline and re access the patient within 30 minutes to decide on the
next fluid requirement according to the degree of dehydration

2. After corrections of the fluid deficit it is important to reduce the maintenance fluid to 2/3rds of the
required volume when the patient is well hydrated.

d. SEVERE ANEMIA

1. Give blood transfusion to patients with severe anemia .

2. The blood must be screened against blood borne pathogens such as HIV, Viral Hepatitis etc.

3. Use packed cells ( 10ml/kg in children ) or whole blood ( with preceding parenteral frusemide to avoid
cardiovascular overload)

4. Where blood is not available give pre referral treatment and refer urgently to a health facility with
blood transfusion services

e. HYPER PYREXIA

1. In children

 Avoid overclothing
 Tepid sponge ( wipe the body with a towel soaked in lukewarm water)
 If temperature is >39.5°c give antipyretics such as paracetamol

f. PULMONARY EDEMA

1. Prop up the patient at an angle of 45 degrees .

2. Give oxygen and IV frusemide 2-4mg/kg.

3. Stop IV fluids and exclude other causes of pulmonary edema

g. ACUTE KIDNEY INJURY

1. If patient is dehydrated give fluids at 20ml/kg of normal saline and challenge

with IV frusemide 1-2mg/kg.

2. Monitor fluid input and fluid output

3. If the patient doesn’t pass urine within the next 24 hours refer for peritoneal or hemodialysis

4. Exclude the pre renal causes of AKI

h. SPONTANEOUS BLEEDING AND COAGULOPATHY

1. Transfuse with screened fresh whole blood (cryoprecipitate , fresh frozen plasma and whole blood
if available)

2. Give vitamin K injection

 3. Where facilities for blood transfusion is not available refer urgently.

I. METABOLIC ACIDOSIS

1. Exclude or treat hypoglycemia , hypovolemia and sepsis

2. If severe add hemofiltration or hemodialysis.

j. BACTERIAL MENINGITIS AND SEPSIS

1. If meningitis or sepsis is suspected in addition to severe malaria and cannot be immediately

excluded by lumbar puncture , appropriate antibiotics should also be given.

2. Any other severe disease identified should be treated accordingly.

253. Chemoprevention of malaria

1. Preventive chemotherapy is different from chemoprophylaxis for travelers and non immune
individuals
2. Chemoprophylaxis is the use of sub-therapeutic doses of anti malarial to prevent the
development of malaria .
3. Chemo preventive therapies includes
a. Intermittent preventive treatment of pregnant women (IPTp)
b. Intermittent preventive treatment of infants ( IPTi) also known as perennial malaria
chemoprevention( PMC)
c. Seasonal chemoprevention (SMC)

4. Objective; prevent malaria illness by maintaining therapeutic drug levels in the blood
throughout the period of greatest malaria risk

5. Malaria vaccine ( Mosquirix ) – another preventive tool

 Piloted by WHO in 3 different African countries; Ghana ,Kenya and malawi, will be
deployed in Nigeria for approved use in 2023

a. Intermittent preventive treatment of pregnant women (IPTp)

1. Sulfadoxine/pyrimethamine (SP) ( FANSIDAR )

 Should be give as a single adult dose of 3 tablets
 Each tablet containing 500mg sulfadoxine and 25mg pyrimethamine
 Therefore , Giving the total required dosage 1500mg/ 75mg
sulfadoxine/pyrimethamine by Directly Observed Therapy ( DOT) at scheduled
antenatal contacts
 The first dose of IPTp-SP should be given at quickening ( as early as possible in the 2 nd
trimister)
 A minimum of 3 doses given 4 weeks apart is currently recommended
  In malaria endemic countries like Nigeria it us used to prevent the adverse effects of
malaria in pregnancy
 At the same time, folic acid is required as a daily dose to prevent the occurrence of
neural tube defects (NTDs)
 Sulfadoxine/pyrimethamine and folic acid 5mg are not to be used together because
they counter balance each other which is undesirable
 Studies have shown that low dose folic acid supplementation at 0.4- 1.0mg per day is
in consequential as it is not detrimental to the course of pregnancy
 Pregnant women who are HIV Positive and are on Co- trimoxazole ( septrin)
chemoprophylaxis should not receive IPTp-SP to avoid sulphonamide overdose
 Co- trimoxazole is an alternative for chemoprevention
 Another preventive measure is to promote the use of Long Lasting Insecticidal Nets
(LLINS) in National guidelines for Diagnosis and Treatment of Malaria in Pregnancy
 early diagnosis and prompt case management is recommended as part of the
control measures of Malaria in Pregnancy (MIP).

b. Intermittent preventive treatment of infants ( IPTi ) also known as perennial

malaria chemoprevention( PMC)
 Now perennial malaria chemoprevention
 WHO recommends PMC as an intervention against P.falciparum in infants
 perennial malaria chemoprevention (PMC) ;
This is defined as the administration of a full therapeutic course of
sulfadoxine/pyrimethamine ( fansidar ) through the immunization program at
defined intervals corresponding to routine vaccination schedules to infants at risk of
malaria usually at 10weeks , 14 weeks and approximately 9 months .
 Its role hasn’t been implemented in Nigeria , However pilot studies are planned to
determine its role in prevention of malaria among infants

d. Seasonal chemoprevention (SMC)

 This is defined as the intermittent administration of full treatment courses of an anti
malarial medicine during the peak of raining season ( July to October) to prevent
malaria illness
 Objective; To maintain therapeutic antimalarial drug concentrations in the blood
throughout the period of greatest risk .
 It is recommended in areas of highly seasonal malaria transmission throughout the
Sahel – Sub region
 A complete treatment course of sulfadoxine/pyrimethamine(fansidar)plus
Amodiaquine( AQ) should be given in children aged 3-59 months at monthly
intervals.
Beginning at the start of the transmission season , up to a maximum of four doses
during the transmission season ( provided that both drugs retain sufficient
antimalarial efficacy)
  AGE DOSAGE
a. Infants 3-11 months old
- 1 Tablet of a 76.5mg dispersible tablet of
Amodiaquine given once daily for 3 days .
- A single dose of half a 500/25mg Tablet of
sulfadoxine/pyrimethamine
b. Children 12 -59 months
- A full tablet of 153mg dispersible Tablet of
Amodiaquine base given once daily for 3 days.
- A single dose of a full Tablet of 500/25mg of
sulfadoxine/pyrimethamine

• The Target areas for implementation are those in malaria transmission and the
majority >60% of clinical malaria cases occur during a short period of about 4 months

• In Nigeria the states where seasonal chemoprevention( SMC) implementation is

recommended are

o Bauchi
o Borno
o Jigawa
o Kano
o Kastina
o Kebbi
o Sokoto
o Yobe
o Zamfara

• Seasonal chemoprevention SMC shouldn not be considered for

1. A child with acute febrile illness or to severely ill children unable to take
oral medications
2. An HIV positive child receiving cotrimoxazole prophylaxis
3. A child who has received a dose of either Sulfadoxine/pyrimethamine or
Amodiaquine during the past months
4. A child is who is allergic to sulfadoxine/pyrimethamine or Amodiaquine
5. Children who are being administered PMC

● CHEMOPREVENTION OF SICKLE CELL ANEMIA PATIENT

a. The current practice among health care practitioners in Nigeria is to give

proguanil to individuals with sickle cell anemia and counsel them to sleep under
long Lasting Insecticidal Nets (LLIN)
b. While SCA patients need chemoprophylaxis, the evidence based on the
clear benefits of proguanil at the drug of choice has been equivocal
Other molecules and chemoprevention strategies are being tried to inform
better drug selection
 c. Sickle cell anemia individuals with suspicion of malaria should report to
the facilities for prompt diagnosis and treatment

254. Chemoprophylaxis for Non immune visitors

1. The recommended chemoprophylaxis for nonimmune visitors should be available in the

visitor’s country of origin

2.Doses should be taken prior to arrival in Nigeria and continued during the stay and two weeks
following departure from Nigeria

3.The following options are recommended for use in Nigeria:

- Mefloquine
o Given at a dose of 5mg/mg weekly
o Approximately 250mg of base in an
adult weekly
o Should be started 2-3 weeks prior to
arrival
o Weekly in the country
o Then 2-3weeks after departure

- Atovaquone-Proguanil
o It’s a fixed dose combination that is
administered daily
o Commencing 1-2 days prior to arrival
o Then continue through out the stay
o Thereafter 7days after departure

Its is given according to body weight as Weight Total daily Dosage Regimen
shown below (kg) dose
11 - 20 kg 62.5mg/25mg 1 Daily
paediatric
Tablet
21 - 30 kg 125mg/50mg 2 As a single
paediatrics daily dose
Tablets
31 - 40 kg 187.5mg/75mg 3 As a single
paediatrics daily dose
Tablets
>40kg 250mg/100mg 1 Adult As a single
strength daily dose
dose
4. For nonimmune visitors who develop acute malaria, institute the guidelines on
management of severe malaria for prompt treatment in centres equipped to treat severe
malaria.

255. Discuss the treatment failure of malaria

1. Treatment failure refers to failure to clear parasitemia after administration of antimalarial

treatment and / or failure of resolution clinical symptoms
2. Causes of Treatment failure

i) Incorrect dosing
ii) problem of treatment compliance
iii) poor drug quality
iv) Interactions with other drugs
v) Compromised drug absorption
vi)