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1 NEW CONCEPTS IN THE MANAGEMENT OF MALARIA. 2 INTRODUCTION Malaria is an ancient scourge of humanity. Although almost eradicated from the industrialized.

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Presentation on theme: "1 NEW CONCEPTS IN THE MANAGEMENT OF MALARIA. 2 INTRODUCTION Malaria is an ancient scourge of humanity. Although almost eradicated from the industrialized."— Presentation transcript:


2 2 INTRODUCTION Malaria is an ancient scourge of humanity. Although almost eradicated from the industrialized nations, malaria continues to extract a heavy toll of life and health in a substantial part of the world. Almost half the world's population lives in countries where the disease is endemic, and almost every country in the world encounters imported malaria. Malaria is the number one cause of morbidity in the countries of Africa and one of the major contributors to childhood deaths and the leading cause of mortality in the vulnerable group (children less than five years and pregnant women) in Sub-Saharan Africa.

3 3 The WHO estimated that about 2100 million people are at risk from Malaria, and the disease kills about 2 million people every year. (Half of these being children less than 5 years old). In addition, 3000 people die from malaria each day, ten new cases occurring every second. Malaria is reported to account for ten percent of Africa’s disease burden. Five hundred and fifty cases are estimated to occur annually (75% stable transmission, 17% epidemic, 8% unstable transmission and non- malarial transmission areas). Incidentally, 80% of malaria cases and 90% of deaths are recorded in Africa. They die because they lack access to health care, life-saving drugs and insecticide- treated –bednets.

4 4

5 5 ETIOLOGY Malaria in humans is caused by plasmodium..The species include P falciparum; P. malariae, P. ovale, P. vivax. Transmission depends on the presence of and relationship between the three epidemiological factors. Reservoir- man (for human plasmodia) Agent of Infection- gametocytes of plasmodium Vector of transmission- Anopheles mosquito

6 6

7 7 ETIOLOGY contd It is however worthy of note that transmission of the parasite can also be transplacentally acquired and by blood transfusion

8 8 PATTERNS OF MALARIA ENDEMICITY Stable Malaria- Malaria is transmitted all year round, but may have seasonal variation. Adults living here may acquire some immunity and are hence unlikely to develop severe malaria Unstable Malaria- It is characterized by intermittent transmission that may be bi- annual or variable epidemic due to poor immunity against malaria Malaria free-areas- No immunity whatsoever, hence all are prone to severe malaria

9 9 PROBLEMS OF MALARIA -Increase in school absentism -Low Birth Weight of babies of Infected mothers with risk of mortality in children, -Adolescents and pregnant women - Increasing resistance to commonly used drugs -Poor reporting

10 10 CLINICAL FEATURES PATHOPHYSIOLOGY LIFE CYCLE Consist of 2 phases 1.)Asexual Phase 2.)Sexual Phase These phases should however be well understood because various drugs used in the management of malaria are directed at specific forms of parasite in the two phases.

11 11 ASEXUAL PHASE The bite of an infected mosquito introduces asexual forms of the parasite, called sporozoites, into the bloodstream. Sporozoites enter the hepatocytes and form schizonts, which are also asexual forms. Schizonts undergo a process of maturation and multiplication known as preerythrocytic or hepatic schizogony. 1.The bite of an infected mosquito introduces

12 12 In Plasmodium vivax and Plasmodium ovale infection, some sporozoites convert to dormant forms called hypnozoites, which can cause disease after months or years. Preerythrocytic schizogony takes 6-16 days, and results in the host cell bursting and releasing thousands of merozoites into the blood.

13 13 Relapses and recrudescences occur and may vary depending on the species of Plasmodium involved. P vivax and P ovale both give rise to hypnozoites in the liver. P vivax malaria may relapse for up to 3 years and P ovale for 1-1.5 years. P falciparum and P malariae do not form hypnozoites, so they do not have true relapses

14 14 However, the disease recrudesces because of surviving erythrocytic forms. While P falciparum can recrudesce for up to 1 year, P malariae may continue to cause clinical malarial attacks even 20 years after the original infection. Only the sporozoites (introduced by the mosquitoes themselves) can penetrate the liver cells.

15 15 Thus, if malaria is acquired by blood transfusion or transplacentally, no infection of the liver occurs and relapses do not occur.

16 16 Merozoites enter the erythrocytes and initiate another asexual reproductive cycle, known as erythrocytic schizogony. The parasite passes successively through the stages of trophozoite and schizont, ultimately giving rise to several merozoites. On maturation of these merozoites, the erythrocyte ruptures, releasing the merozoites and multiple antigenic and pyrogenic substances into the bloodstream.

17 17 These pyrogens stimulate the blood macrophages and endothelial cells to produce cytokines, the cause of fever. These merozoites again infect new erythrocytes. After a few cycles of this erythrocytic schizogony, some merozoites differentiate into the sexual forms: the male and female gametocytes.

18 18 SEXUAL PHASE The merozoites destined to become male and female gametes differentiate into micro gametes and macro gametes respectively. Further development results in the formation of male and female gametocytes, when taken up by mosquito during a blood feed, the male and the female gametes fuse in the stomach of the mosquito.A Zygote is formed which develop through stages of ookinetes, oocytes and sporozoites. The latter moves to the salivary gland of the mosquito where they are inoculated into man to recommence the asexual cycle.

19 19 Incubation Period Incubation period in malaria covers the time between infection and the first appearance of clinical signs. The length of the incubation period is usually between 9 and 30 days, depending on the infecting species (shortest for P.falciparum, longer for P.malariae). In some strains of P.vivax (P.v.hibernans) the incubation period may last some 8-9 months

20 20 RISK FACTORS 1 ENVIRONMENTAL FATORS The environment in Nigeria is favourable for transmission Rain the amount of rain and the number of rainy days are important- 10 cm Low Altitude 200m meters above sea level High temperature20-28 0C High humidity60% 2. RACIAL FACTOR: People of all races are affected, with some exceptions. People of West African origin who do not have the Duffy blood group are not susceptible to P vivax malaria.

21 21 3. AGE FACTOR: Partial immunity is developed after repeated attacks of malaria. Thus, older children and adults often have asymptomatic parasitemia, i.e, presence of plasmodia in the bloodstream without clinical manifestations of malaria. Most deaths resulting from malaria occur in children younger than 5 years. 4. NUTRITIONAL FACTOR: Ironically malnourished children are noticed to have a lower incidence of cerebral malaria due to reduced amounts of ICAM-1 and CD46 on their cerebral endothelial cells to which the P. falciparum infected red blood cells bind

22 22 OTHERS Socio-economic conditions like large scale population movements eg labour force coming from endemic areas to develop project areas. Immune status as in Pregnancy

23 23 CLASSIFICATION OF MALARIA Malaria can be classified into two main types –Simple / uncomplicated malaria.: This is a type of malaria that has no life threatening manifestation –Severe / complicated malaria.: Malaria with life threatening manifestation and complication.

24 24 CLINICAL FEATURES OF SIMPLE / UNCOMPLICATED MALARIA It is often an acute disease, which clinically normally presents with Fever. Chills Profuse sweating Headache Aching joints General discomfort

25 25 CLINICAL FETAURES OF SEVERE MALARIA A change of behaviour (confusion or drowsiness) Altered consciousness or coma+++ Multiple convulsions+++ Hypoglycemia++ Severe Anaemia (haematocrit <20% or HB <5g/dl)++ Haemoglobinuria (coca-cola coloured urine)+ Jaundice+ Prostration+++ Acidosis+ Oliguria or acute renal failure± Difficulty in breathing or pulmonary oedema± Circulation collapse or shock+ Bleeding tendency± Hyperpyrexia++ Hyperparasitemia++ Persistent vomiting++ An individual patient may have any one or any combination of complications listed above



28 28 DIAGNOSIS History: General information as age, place of residence, history of travel within and outside the country Main manifestation is FEVER. Clinical features vary from asymptomatic to mild to severe disease Enquire about the following symptoms: Characteristic history of fever associated with chills (feeling cold in older children), rigors (shaking of the body), or history of fever within the last two days prior to presentation, headache, joint weakness or tiredness Also ask for the symptoms of other common childhood diseases -cough, diarrhoea, ear pain and skin rashes within the last three months

29 29 Physical Examination -Increased body temperature >37.20C -Pallor -Enlarged spleen ± liver * In children under five, a clinical diagnosis is often sufficient for uncomplicated malaria. This is to forestall undue delay in commencing treatment. Malaria can be rapidly fatal in this age group.

30 30 Management Establish an intravenous infusion Correct hypoglycemia if present; 10% DW IV, 2- 3 ml/kg over 1-2 minutes. Recheck blood glucose after 30 minutes and throughout course of management. Assess fluid req. based on patients weight and set up appropriate volume to run in 1st 4 hours Add the correct antimalarial drug in the correct dose according to the patients weight to the infusion fluid

31 31 Reduce body temperature give paracetamol orally 20mg/kg/ dose give paracetamol suppository tepid sponge expose to fan Control convulsions use paraldehyde IM 0.1 ml/kg /yr of life up to 5 mls IV diazepam (titrated) 7.).Consider the need for blood transfusion (PCV <15% /Hb <5gm/dl) –8.) Decide whether a urinary catheter should be passed

32 32. Lab Studies: Take samples for PCV, E&U, blood smear for MP, LP, WBC, ESR Examination of blood smear Demonstration of the parasite in a smear of the blood definitely establishes the presence of malaria.

33 33 The presence of the asexual form must be established A negative finding on examination does not rule out malaria. Only 50% of children with malaria are smear positive, even on repeated examination. A positive finding on examination does not confirm malaria, especially in patients from an endemic area, in whom asymptomatic parasitemia often exists. Both thick and thin films are essential. If the parasitemia is light, a thin film examination may miss the diagnosis. Thick films save time in diagnosis of scanty infections but make species identification of the parasite difficult. Blood sample must be examined 8-12 hourly and only 3 consecutive negative samples are acceptable

34 34 Criteria suggestive of P. falciparum infection Prominent non-pigmented ring forms Double chromatin Diagnostic crescent shaped gametocytes The infected red cells are not enlarged and are without the pink stippling (Schuffner dots).

35 35 Enumeration of malaria parasite In addition to definitive diagnosis of malaria and diagnosis of the specie of malaria parasites, microscopical examination also enables their number in a unit volume of blood to be determined. This becomes important for diagnosis, prognosis and follow-up. OTHER TESTS INCLUDE Serological tests Dipstick tests Molecular biological detection tests Lumbar puncture is indicated to rule out meningitis in cerebral malaria and febrile seizures with malaria. Severe P falciparum malaria is often associated with hypoglycemia. Lower blood glucose levels are associated with higher mortality rates.

36 36 PREVIOUS NATIONAL ANTIMALARIA TREATMENT GUIDELINES The latest (2006) management guideline was released few weeks ago by WHO. The policy currently in use in Nigeria was adopted Feb, 2005. It is however important to highlight previous antimalarial drugs that were used before 2005. These drugs are grouped into 2 ; For simple / uncomplicated malaria For severe / complicated malaria

37 37 Previous Classification of drugs for Simple malaria First line drugs- chloroquine Second line drugs- Amodiaquine, sulphadoxine+Pyrimethamine(Fansidar) Third line drugs- Mefloquine,Halofantrine,Artemisinin and its derivatives

38 38 CHLOROQUINE. This was given orally and first dose in the presence of an health worker Dose 1ST DAY: 10mg/kg 2nd DAY: 10mg/kg 3 rd DAY: 5mg/kg It was effective against the erythrocytic forms of the parasite. It is not effective against hypnozoites. However, P falciparum developed widespread resistance to chloroquine. It was only given parenterally where there was repeated vomiting despite measures to reduce vomiting Interactions there were possible delayed or reduced absorption with co administration of antacids containing magnesium; cimetidine may increase serum levels of chloroquine (possibly other 4-aminoquinolones) Pregnancy - Safety for use during pregnancy was not established

39 39 SULFADOXINE/PYRIMETHAMINE (SP). was used as a second line drug in CQ sensitive areas but as an alternative to first line in CQ resistant areas or in Px unable to tolerate CQ. Cannot be used in potentially severe cases being slowly acting It has no activity against hypnozoites and gametocytes. It is contra indicated in pregnancy. c.)HALOFANTHRINE was a 3rd line drug in CQ and SP failures. It is cardio toxic. Its absorption may be erratic following oral administration but better absorbed after a fatty food. was contraindicated in involvement of a cardiac disease.

40 40 d.) Artemisinin & its derivatives. their use was restricted to the management of severe malaria were used as 3rd line drugs in CQ failure, SP failure orally. Monotherapy was given over 5-7 days and compliance was ensured.

41 41 PRIMAQUINE It was the only drug in clinical use that destroyed hypnozoites of both P vivax and P ovale, and so was used for the radical cure of the relapsing malarias. It is also gametocidal against all 4 species of human plasmodia and was used to render patients noninfectious. Contraindicated in G6PD deficiency. Other drugs used- proguanil, tetracycline, quinidine and erythromycin. e.) Combination therapy used include Artemisinin+ SP Artemisinin+ mefloquine SP+ Chloroquine SP+ Quinine

42 42 DRUGS FOR SEVERE MALARIA DRUGS FOR SEVERE MALARIA A. Quinine[IV or IM] 20mg/kg in 4.3% dextrose in 0.18 normal saline over 4 hours. Then, 12 hours after the start of the loading dose, give 10mg\kg over 4 hours every 12 hours until the patient can tolerate orally. Change to Quinine tablets 10mg\kg every 8hours to complete 7 days of treatment or give a single dose of SP. SUMMARY DAY 1- 30-40mg\kg DAY 2- 30mg\kg DAY 3- 15mg\kg IM sites- anterior thighs.

43 43 B. Artemisinin derivatives As an alternative to quinine in the treatment of severe malaria. Dosage Artesunate: 2.4mg\kg IV bolus, repeat 1.2mg\kg after 12 hours and then 1.2mg\kg daily for 6 days. The daily dose was changed to oral if the patient is able to swallow. Artemether: 3.2mg\kg loading IM, followed by 1.6mg\kg daily for 6days. The daily dose was changed to oral if the patient is able to swallow.


45 45 If our previous modalities of treatment were as effective as it used to be, today we will not be talking about the need for change to a different modality of treatment. Recent estimates of the global malaria burden have shown increasing levels of malaria morbidity and mortality, reflecting the deteriorating malaria situation in Africa. Taking note of the very high morbidity and mortality rate as well as the huge economic burden malaria has caused Africa, African leaders met in yr 2000 at Abuja to declare and rededicate themselves to reducing the burden of malaria in Africa by at least half by year 2010 through “ROLL BACK MALARIA” PROGRAMME.

46 46 Key among the factors contributing to the increasing malaria mortality and morbidity is the widespread resistance of Plasmodium falciparum to inexpensive monotherapies, such as. sulfadoxine–pyrimethamine (SP), amodiaquine, and chloroquine, which still remains the cheapest and most affordable drug. Drug resistance has been implicated in the spread of malaria to new areas and re-emergence of malaria in areas where the disease had been eradicated. P falciparum still remains the commonest cause of malaria in Nigeria.

47 47 DRUG RESISTANCE Drug resistance in malaria is the ability of the parasite strain to survive or multiply despite the administration and absorption of a drug given in doses equal to or higher than those usually recommended but within the limit of tolerance of the subject. This definition was later modified to specify that the drug in question must “gain access to the parasite or the infected red blood cell for the duration of the time necessary for its normal action

48 48 A distinction must be made between a failure to clear malarial parasitaemia and true antimalarial drug resistance. While drug resistance can cause treatment failure, not all treatment failure is due to drug resistance. Causes of Treatment failure include Incorrect Dosing Poor Compliance to duration of dosing Regimen Poor Drug Quality Drug interaction Poor absorption Presumptive treatment for malaria Misdiagnosis non absorption of the right dose e.g. in frequent vomiting Handling and storage of the drugs

49 49 Mechanisms of antimalarial resistance In general, resistance appears to occur through spontaneous mutations that confer reduced sensitivity to a given drug or class of drugs. For some drugs, only a single point mutation is required to confer resistance, while for other drugs, multiple mutations appear to be required. Provided the mutations are not deleterious to the survival or reproduction of the parasite, drug pressure will remove susceptible parasites while resistant parasites survive.

50 50 Chloroquine Resistance Chloroquine resistance has been reported from all falciparum endemic areas with the exception of Central America and the Caribbean. In Africa, Chloroquine resistance was first detected in Tanzania, in the late 1970s and has since spread and intensified across the continent..

51 51 MECHANISM As the malaria parasite digest haemoglobin large amount of a toxic by product (haeme) is formed. The parasite polymerises this toxic by-product in its food vacuole, producing non-toxic haemozoin (malaria pigment). Resistance of P falciparum to chloroquine is related to an increase capacity of the parasite to expel chloroquine at a rate that does not allow chloroquine to reach levels required for inhibition of haem polymerization. This chloroquine efflux occurs at a rate of 40 to 50 times faster among resistant parasites than sensitive ones. Further evidence supporting this mechanism is provided by the fact that chloroquine resistance can be reversed by drugs which interfere with this efflux system. It is unclear whether parasite resistance to other quinoline antimalarials (amodiaquine, mefloquine, halofantrine, and quinine) occurs via similar mechanisms

52 52 Quinine Despite widespread use of quinine, resistance levels are low, and quinine is still generally effective. It however still remains the first drug of choice for the treatment of severe falciparum malaria in many countries. Although decreasing sensitivity has been observed in some parts of south-east Asia. Artemisininn and its derivatives Confirmed resistance to Artemisinin and its derivatives (artemether, artesunate, and dihydroartemisinin) has not been reported even in areas of multi drug resistance. These drugs are so valuable and it is essential that they be protected from resistance development by its combination with longer-acting antimalarias such as mefloquine, lumefantrine and amodiaquine.

53 53 GRADING OF DRUG RESISTANCE OF ASEXUAL PARASITES TO SCHIZONTOCIDAL DRUGS There is said to be sensitivity[S] to an antimalarial drug if THE ASEXUAL PARASITES DISAPPEAR BY DAY 6 AND NO RECRUDESCENCE BY DAY14. Resistance proper is in 3 part;R1, R11 & R111 R1 Early—if the asexual parasites disappear by day 6 but reappears by day7 Late----if it reappears by day 14 R11—asexual parasitemia decrease to 25% of the original within 1st 48hrs of treatment but no clearance. R111--- if asexual parasitemia decrease by < 75% within 48hrs or it continues to rise.

54 54 Criteria for antimalarial treatment policy change These malaria treatment guidelines recommend that antimalarial treatment Policy should be changed at treatment failure rates considerably lower than those recommended previously. It is now recommended that a change of first-line treatment should be initiated if the total failure proportion exceeds 10%.

55 55 However, it is acknowledged that a decision to change may be influenced by a number of additional factors, including the prevalence and geographical distribution of reported treatment failures, health service provider and/or patient dissatisfaction with the treatment, the political and economical context, and the availability of affordable alternatives to the commonly used treatment. Review and change of the antimalarial treatment policy should be initiated when the cure rate with the current recommended medicine falls below 90% (as assessed through monitoring of therapeutic efficacy). A new recommended antimalarial medicine adopted as policy 95% as assessed in clinical trials.  should have an average cure rate


57 57 NEW CONCEPT IN THE MANAGEMENT OF MALARIA RECALL: The problems of DR. has led to an in morbidity and mortality and worsened the economic burden of the African continent. A survey by the WHO revealed that 9 out of every 10 people who suffer malaria are from Africa 5 of which are from sub- Saharan Africa. This prompted the Abuja declaration on ROLL BACK MALARIA [RBM] in Africa (April 2000 at the African summit). The FG adopted the WHO recommended treatment guidelines for 2005, this entails RBM, ACT and the use of ITN (Prevention).It is however important to inform us that the New Treatment Guidelines was released by the WHO, Jan 2006. This guideline is slightly different from the management guideline adopted by the Federal Government in 2005. The differences shall be highlighted as I proceed.

58 58 National Anti-malarial treatment guideline 2005. This will be taken as follows: 1a. Artemisinin-based combination therapy (ACT) -Poly- therapy 1b. Compare ACT with other previous treatment e.g. Chloroquine-based, Monotherapy with artemisinin and other anti-malaria combination therapy 2. RBM 3. Prevention Aim: To offer highly effective anti-malarials. The main determinants of change are therapeutic efficacy and consequent effectiveness of anti-malarial in use.

59 59 Recommended Treatment Of Malaria A. Treatment of simple uncomplicated malaria Objectives: 1 -Cure of infection, prevent progression from simple to severe malaria and prevent additional morbidity associated with treatment failure. 2 -Prevent the infection from being transmitted 3 -Prevent emergence of DR to anti-malariaL drugs The treatment of choice for uncomplicated malaria is Artemisinin Based Combination Therapy (ACT). This consist the use of an artemisinin derivative and another effective antimalarial medicine. Recommended ACT for uncomplicated malaria Artemether- Lumefanthrine (Coartem)

60 60 Weight (Age group) 5 – 14kg (6month – 3 years) 15 -24kg (4 – 8 years) 25 – 34kg (9 – 14 years) > 35kg (> 14 years) Number of tablets / dose 1 tablet BD x 3 days 2 tablets BD x 3 days 3 tablets BD x 3 days 4 tablets BD x 3 days

61 61. Absorption of the drug is aided by food If the patient shows evidence of inadequate clinical response, do the following : Evaluate the patient and review diagnosis Exclude sub-optimal dosing or inadequate intake. E.g. vomiting of drug Seek confirmatory test

62 62 Other ACT available Artesunate 4mg/kg + amodiaquine (10mgbase/kg) daily for 3 days) Artesunate 4mg/kg once daily for 3 days + mefloquine (25mgbase/kg) i.e. 15mg/kg – day 2, 10mg/kg – day 3. Mono-therapy with dihydro-artemisinin, and other artemisinin derivatives are not recommended.

63 63 Follow up 1. Patient should return if a. Fever > 2 days after commencement of treatment b. Immediately if condition gets worse or develop signs of severe disease. 2. When the patient returns a. Check that they complied with the treatment as advised b. Repeat or do blood smear for malaria parasites c. Do a complete assessment to exclude any other possible cause of fever

64 64 Treatment of uncomplicated malaria in special Groups 1. Children < 3 months (5kg) – risk of dying 1. Give oral quinine (20mg/kg) and other supportive therapy 2. Also refer to the table on ACT in children. 2. Pregnant women (high mortality of fetus and mother) Quinine is recommended for the treatment of malaria in the 1st, 2nd and 3rd trimester. The use of ACT’s in the 1st trimester is contraindicated because of its possible teratogenic effect on embryogenic neuronal development * Slight modification has been effected here in the 2006 recommendation.

65 65 1st Trimester – Give Quinine +- clindamycin Other safe ones are proguanil, SP, CQ, Pyrimethamine, if there is no DR 2nd and 3rd trimesters - ACT is preferred to quinine because Quinine induces hypoglycemia - Give ACT Parenterally - It may otherwise give Quinine +- Clindamycin for 7 days

66 66 Treatment of Complicated Malaria - Urgent Treatment - Specific Treatment Recall: Severe malaria is a medical emergency requiring in- patient care as Deaths can either result from a direct effect of this disease or the complications Objectives 10- Attend to the immediate threats - prevent neurological deficit - save a life of a ill pregnant mother 20- Prevent recrudescence - Avoidance of minor adverse effects

67 67 Urgent Treatment Treat Coma – ABCD of resuscitation Convulsion – give 0.1ml/kg paraldehyde IM,if convulsion continue give IM phenobarbitone 10- 15mg/kg Severe dehydration or shock- give 20-30 ml/kg normal saline and reassess Severe anaemia –urgent blood transfusion using packed cells (10ml/kg), partially packed (15ml/kg)

68 68 Specific anti-malarial treatment Quinine – a cinchona alkaloid administered by either IV or IM route (Loading dose of 20mg/kg in 4.3% dextrose or 0.18% normal saline or 5% Dextrose over 4 hours Maintenance Dose 12hours after the onset of the stat dose i.e. 8 hours after the end of the loading dose give 10mg/kg over 4 hours, every 12 hours until the patient is able to take orally. Change to quinine tablets 10mg/kg every 8 hours to complete 7 days of treatment If the patient require quinine for > 48 hours, maintenance dose to 5mg/kg, 8 hourly. - don’t give loading dose if patient has received quinine or mefloquine in the last 24 hours. For IM quinine don’t give on the buttocks but on the anterior thigh Dilute total dose with sterile normal saline to 60mg/ml, 8 hours after give 10mg/kg 8 hourly for 7 days.

69 69 Artemisinin derivatives can be used on alternatives to quinine for severe malaria. 1.Artesunate 2.4mg/kg IV Bolus, repeat 1.2mg/kg after 12 hrs Take 1.2mg/kg daily for 6days Once patient can tolerate oral medication, give a full dose of A.L(Coartem). Patient advice to eat because food promotes the drug absorption 2.Artemether 3.2mg/kg loading IM 1.6mg/kg daily for 6days Change to AL once patient can tolerate oral medication

70 70 pre-referral Tx. The role of death for severe malaria is greatest in the first 24hrs.A patient must get rapid access to a health facility where parenteral treatment and other supportive care can be given safely and as appropriate. Pre-referral treatment with rectal artesunate or artemisinin should be used

71 71 Table showing the different dosages for initial Tx of Acute malaria in paediatric patient (2-5years Weight (Kg) AgeArtesunate Dosage Regimen Single dose 5-8.9kg0-12mths50mg One 50mg suppository 9-19kg12-42mths100mg One 100mg suppository 20-29kg43-60mths200mg One 100mg + one 50mg suppository 30-39kg6-13years300mg Three 100mg suppository >40kg>14 years400mg 400mg suppository

72 72 * Management of Treatment Failure as recommended by the 2006 treatment guideline 1.) Confirm diagnosis parasitologically a) Blood slide exam b) HRP2 – based tests 2.) Treat Give Quinine 10mg/kg TID + Tetracycline (if not younger than 5yrs) for 7days Give Artesunate 2mg/kg one per day + tetracycline (4mg/kg QID) or Doxycycline (3.5mg/kg once per day)

73 73 ROLL BACK MALARIA -Is a global partnership founded in July 21, 1998 with the goal of reducing by ½ the world’s malaria burden by year 2010. Objectives -Support to endemic countries in development National health sector -Develop a broader health sector -Encourage the needed human of financial investment for health system development Goals -To help the malaria burden of 1998 by 2010 -Expand the use of already known effective intervention -Support under which leach to more effective intervention -Encourage research for better intervention

74 74 RMB advocates for -Early diagnosis and prompt Treatment (EDPT) -Insecticide-treated acts and other materials -Education, enlightenment -Prevention and Treatment Roll Back Malaria in Africa -3000children die everyday and malaria kills an African child every 40sees. -Cost of tackling malaria = and 2billion per year Total economic loss (GDP) = 12 billion per year > 300 million acute cause per year -> 1million death worldwide General Objective of RMB in Africa -To significant decrease the global burden of malaria through interventions adapted to local needs by reinforcement of the health sector.

75 75 RMB in Nigeria Objectives -Prevent and reduce malaria death (cause fatality & malaria) -Reduce malaria morbidity &Reduce the duration of illness Approaches of achieving these objectives -accessibility of the total population at risk to prompt diagnosis and -Adequate treatment -Clinical recognition and management of treatment failures -Health education *Chemoprophylaxis is not advocated for those residing in endemic zones. -Public awareness of the appropriate use of antimalarial days -Collection and analysis of making data and monitoring of action taken. -Initial and in-service training of health worker in the current anti- malarial activities - Research operation to deal with implementation and managerial issues

76 76 Emphasis - Health education & prevention - Early diagnostic (prompt treatment) - Prevention - Counsel patients about illness and treatment. - Mosquito screening device in the house - Use of ITN Other preventive measures still remain relevant: -Clearing of bushes, even broad leaves of banana breeds mosquito when they collect water -Proper disposal of empty containers e.g. cans, pots, bottles. -ensure free flowing gutters by unclogging them.


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