Pro ject Re por t





Submitted By:

September, 2007

zahid ali Doctor of Pharmacy

Department of Pharmacy University of Peshawar

Submitted By: Zahid ali
This project is submitted to the Department of Pharmacy in Partial fulfillment of the requirements for the degree of doctor of pharmacy (Pharm. D Condensed Course)

(Morning Shift)


Department of Pharmacy University of Peshawar


This Effort is dedicated to My Lovely Parents who took pains to educate me.

Project approval
This project entitled malaria in the specialty of pulmonalogy ward in Khyber teaching Hospital Peshawar, prepared by zahid ali submitted to the Department of Pharmacy for the fulfillment of the requirements for the degree of Doctor of Pharmacy is hereby approved for submission.

Hospital Chief Pharmacist: ______________________________

Approved & Supervised by: ______________________________ Prof. Dr. Raza khan Department of Pharmacy, University of Peshawar.


_____________________________ Prof. Dr. Zafar Iqbal Department of Pharmacy, University of Peshawar.

External Examiner:


Table of contents S.No Contents

Page No


Title page


Summary of the project


Aims & Objectives




Result / Finding


Clinical pharmacy








Introduction The term “clinical pharmacy” has been developed principally in the field of Hospital Pharmacy where it is widely used. Definitions A number of definitions have been put forward but there does not appear to be a structured practice that can be called as clinical pharmacy. Some of these definitions are: United Kingdom Clinical Pharmacy Association Clinical pharmacy is the knowledge skills, and attitudes needed to contribute to patient care or to deliver pharmaceutical care. OR Clinical pharmacy is a health science discipline in which pharmacist provides patient care that optimizes medication therapy and

promotes health, wellness, and disease prevention. The Clinical Recourse and Audit Group of Scottish Office Department of Health:

Clinical pharmacy is a discipline concerned with the application of pharmaceutical expertise to help maximize drug efficiency and minimize drug toxicity and expenditure. American College of Pharmacy Clinical pharmacy is a health science specialty which embodies the application, by the pharmacist, of scientific principles of

pharmacology, toxicology, pharmacokinetics and therapeutics to the care of patient. OR The area of the pharmacy concerned with the science and, practice of rational medication use However as an essence of all those definitions, clinical pharmacy involves pharmacists playing a role in a way that medicines are used to treat patients rather than to merely supplying medicines to patients according to the prescriptions of other health care

professionals (such as doctors).

The Emergence of Clinical Pharmacy in Advance Countries The concept of clinical Pharmacy arose as a result of a number of different factors including: • Development of sub disciplines n hospital pharmacy since the 1920’s. • • • • The growth of clinical pharmacology since the 1940’s. Innovative. Teaching programs. The decline of pharmacology instructions in medical schools. To some extent, pharmacy ‘took over an aspect partially abandoned by physicians. . • Over burdened by patients dad and explosion of new drugs, physicians turned to pharmacists more and more for drug information, especially with in institutional settings.

Clinical Role of Pharmacist in Advance Countries Clinical pharmacy works in collaboration with the doctors, nurses and other health care professionals to help ensure that medicines are used safely, effectively and in cost-effective manner. Some of his roles are:


Dispensing of Medications i) ii) Receipt and interpretation of prescription. Performance / supervision of the dispensing.

2. Prescription Monitoring for: i) ii) iii) iv) v) Medication errors. * Drug interactions. Side effects and d drug reactions. Allergic manifestations and hypersensitivity Contraindications.

3. Prescribing Advice to Medical Staff in i) ii) iii) iv) v) vi) vii) Choice of medicine and use. .Method/route of ministration. Possible side effects. Interaction with other medication and with food. Pharmacokinetic monitoring. Drug therapy monitoring. Parenteral Nutrition.

4. Drug History Taking

i) Obtaining information on all medication, a patient is t ii) Assessment of patient compliance with prescribed treatment. 5. Patient Counseling on Medicines i) Helping patient to understand the method of taking their medicines. ii) Answering any other questions. iii) Supply of aid to patients, to take their medicines correctly. 6. Answering Medicines Information Queries i) Being expert on & dug, pharmacist can answer more complicated queries. ii) Provide references for the prescriber. iii) May run a telephonic help line. 7. Treatment Guidance Collaborate with other health professionals to produce guid on more appropriate use of medicines. 8. Medicines Management Work with budget holders and senior clinicians to ensure that resources for medicines are efficiently used.

9. Clinical Audit i) Contribute to the audit program of medicines. ii) Also collaborate in multidisciplinary audits. 10. Education and Training of Staff Contribute to the education and training of students and staff within pharmacy and from other health care disciplines.

CONCLUSION: The clinical pharmacist does not make decisions concerned with diagnosis. Although, the doctor will determine the drug therapy, the pharmacist can help particularize the medication to be used. The senior medical practitioners are expected to know more about the range of drugs used within their own specialty the pharmacist can contribute to the choice of drug regimen, particularly in a position when more than one condition is being treated. The ph can help decide about the dosage form and the best route of administration of a medicine which the clinician has prescribed. The pharmacist is also expected to take the specific responsibility for dosage calculation. In none of these aspects, the. pharmacist is practicing the clinical role of the doctor. On contrary, the presence pf pharmacist permits the doctor to use the pharmacist’s knowledge & experience to be better informed in prescribing decisions. Thus, the contribution of the pharmacist is additive to, and not a substitute for that of a doctor. It has been shown from the study that clinical pharmacist can incorporate his valuable comments in avoiding the Irrational drug prescribing, irrational drug usage, irrational dispensing, the practices of poIypharmacy, interactions of drugs with other drug moity, appropriate drug the in cases of antibiotics to enhance patient compliance and to correct the pharmacy problems in-the prescribed

drugs. It is therefore suggested that specialized pharmacist in clinical pharmacy practice should be provided to each unit to prevent such types of problems. There pharmacist should be handed over the duties of management of drug therapy provision of drug —drug and drug food interactions, improve patient compliance through patient counseling and patient education although the senior practioner are expected to know more about the range of drug used with their own specialty, the pharmacist can contribute to the choice of drug regimen, practical in a position in which more than one conditions are being treated. The pharmacist can help about the dosage form and the best route of administration, which the clinician has prescribed. the pharmacist is also expected to take the specific responsibility for dosage calculation. In none of these aspects, the pharmacist is practicing the clinical role of the doctor. On contrary the presence of pharmacist permits the doctor to use the pharmacist knowledge and presence to be better informed in prescribing decisions.

SUMMERY OF THE PROJECT Clinical pharmacy includes II performed by pharmacist practicing in hospital, community pharmacies, nursing homes, clinics and any other settings. Where medicines are prescribed and used.” The purpose of this clinical clerkship is to ensure the safe, effective and economic use of medicines. These studies were conducted. Under the supervisor of chief pharmacist. There is direct interaction of trainee clinical pharmacist with the doctors and patients. This project was assigned to find out various level in Govt. Hospital where the clinical pharmacist can play a vital role for the

improvement of health care setting. For this purpose, data was collected and evaluated by stud various books of pharmacology and clinical medicine. The Clinical Pharmacy clerkship is designed to integrate the

knowledge from previous didactic courses in pharmacology, clinical chemistry & pathophysiology for application encountered in Clinical practice. At the completion of this clerkship the student would be able to; • Appropriately and effectively communicate with other health care professionals and patients to assure complete and

accurate information concerning drug therapy and patient’s response. • Effectively’ obtain the necessary information from the patients and other health care providers to ensure appropriate drug treatment • • Correctly interpret the disease state, signs, and Symptoms. Utilize laboratory data for both diagnosis and monitoring of drug therapy. • • • Identify therapeutic end points. Formulate a rational drug treatment plan. Consistently demonstrate proper documentation of

pharmaceutical care activities. • Interpret, describe and apply pathophysiology and therapeutics of the minimum knowledge based on diseased states into patient care activities. • Understand, interpret, critically’ evaluate and apply in clinical context primary literature encountered during the Clinical Pharmacy clerkship. The studies reveal that in about 30% of patient are malarial Infected.

Malaria is an infectious disease caused by the parasite called Plasmodium. There are four identified species of this parasite causing human malaria, namely, Plasmodium vivax, P. falciparum, P. ovale and P. malaria. It is transmitted by the female anopheles mosquito. It is a disease that can be treated in just 48 hours, yet it can cause fatal complications if the diagnosis and treatment are delayed. It is reemerging as the # 1 Infectious Killers and it is the Number 1 Priority Tropical Disease of the World Health Organization. MALARIA IS A MAJOR GLOBAL HEALTH PROBLEM Malaria affects more than 2400 million people, over 40% of the world's population, in more than 100 countries in the tropical countries. conditions distribution.

The for

tropics the



breeding and

and hence

living this



Every year 300 million to 500 million people suffer from this disease (90% of them in sub-Saharan Africa, two thirds of the remaining cases occur in six countries- India, Brazil, Sri Lanka, Vietnam, Colombia and Pakistan etc).

WHO forecasts a 16% growth in malaria cases annually.

About 1.5 million to 3 million people die of malaria every year (85% of these occur in Africa), accounting for about 4-5% of all fatalities in the world.

One child dies of malaria somewhere in Africa every 20 sec., and there is one malarial death every 12 sec somewhere in the world.

• •

Malaria kills in 1 year what AIDS killed in 15 years. Malaria ranks third among the major infectious diseases in causing pneumococcal acute respiratory infections and

tuberculosis. It is expected that by the turn of the century malaria would be the number one infectious killer disease in the world.
• •

Every year 30000 visitors to endemic areas develop malaria. Estimated global annual cost (in 1995) for malaria: US$ 2 billion (direct and indirect costs, including loss of labour).

Estimated annual expenditure on malaria research, prevention and treatment: $ 84 million.

Malaria was nearly eradicated from most parts of the world by the early 60's, owing largely to concerted anti malarial campaigns world over under the guidance of the World Health Organization.

Malaria is probably one of the oldest diseases known to mankind that has had profound impact on our history. But for malaria, the outcomes of many a wars and destinies of many a kings would have been different. It has been responsible for the decline of nations and crushing military defeats, often having caused more casualties than the weapons themselves. For centuries it prevented any economic development in vast regions of the earth. It continues to be a huge social, economical and health problem, particularly in the tropical countries. History of malaria and its terrible effects is as ancient as the history of civilization, therefore history of mankind itself. Malaria was linked with poisonous vapors of swamps or stagnant water on the ground since time immemorial. This probable

relationship was so firmly established that it gave the two most frequently used names to the disease malaria, later shortened to one word malaria, and paludisme. The term malaria (from the Italian mala “bad” and aria “air”) was used by the Italians to describe the cause of intermittent fevers associated with exposure to marsh air or miasma. The word was introduced to English by Horace Walpole, who wrote in 1740 about a “horrid thing called malaria that comes to Rome every summer and kills one.” The term malaria, without the

apostrophe, evolved into the name of the disease only in the 20th century. Up to that point the various intermittent fevers had been called jungle fever, marsh fever, paludal fever, or swamp fever.

Diagnosis of malaria involves identification of malaria parasite or its antigens/products in the blood of the patient. Although this seems simple, the efficacy test of the diagnosis is subject to many factors. The diagnosis of malaria is confirmed by blood tests and can be divided into microscopic and non-microscopic tests.

For nearly a hundred years, the direct microscopic visualization of the parasite on the thick and/or thin blood smears has been the accepted method for the diagnosis of malaria in most settings, from the clinical laboratory to the field surveys. The careful examination of a wellprepared and well-stained blood film currently remains the "gold standard" for malaria diagnosis. The microscopic tests involve staining and direct visualization of the parasite under the microscope.

1. Peripheral smear study 2. Quantitative Buffy Coat (QBC) test Non-Microscopic Tests Several attempts have been made to take the malaria diagnosis out of the realm of the microscope and the microscopist. These tests involve identification of the parasitic antigen or the antiplasmodial antibodies or the parasitic metabolic production. Rapid Diagnostic Tests (RDTs) 1. Para Sight F test 2. OptiMal Assay 3. The immuno chromatographic test (ICT Malaria P. f. test) 4. Polymerase Chain Reaction 5. Detection of antibodies by Radio immuno assay,

immunofluorescence or enzyme immuno assay The simplest and surest test is the time-honoured peripheral smear study for malarial parasites. None of the other newer tests have surpassed the 'gold standard' peripheral smear study. Remember this:

Ask for MP test in all cases of fever and related symptoms and also whenever there is high level of suspicion.

MP test can be done at any time. Do not wait for typical symptoms like chills, vomiting and high grade fever.

A negative test DOES NOT rule out malaria. Repeated tests may have to be done in all doubtful cases. Duration of the illness, level of parasitemia, expertise of the technician and the method of examination may all have a bearing on the result of the M.P. test.

Peripheral smear study for malarial parasites - The MP test Peripheral smear study for malarial parasites is the gold standard in diagnosing malarial infection. It involves collection of a blood smear, its staining with Romanowsky stains and examination of the Red Blood Cells for intracellular malarial parasites. Thick and thin smears are usually prepared. Thick smears are used to identify the parasites and thin smears for identifying the species. Staining methods: An experienced technician can detect as few as 5 parasites/µl in a thick film and 200/µl in a thin film.

Malaria is a febrile illness characterized by fever and related symptoms. However it is very important to remember that malaria is not a simple disease of fever, chills and rigors. In fact, in a malarious area, it can present with such varied and dramatic manifestations that malaria may have to be considered as a differential diagnosis for almost all the clinical problems! Malaria is a great imitator and trickster, particularly in areas where it is endemic. All the clinical features of malaria are caused by the erythrocytic schizogony in the blood. The growing parasite progressively

consumes and degrades intracellular proteins, principally hemoglobin, resulting in formation of the 'malarial pigment' and hemolysis of the infected red cell. This also alters the transport properties of the red cell membrane, and the red cell becomes more spherical and less deformable. The rupture of red blood cells by merozoites releases certain factors and toxins (such as red cell membrane lipid, glycosyl phosphatidyl inositol anchor of a parasite membrane protein), which could directly induce the release of cytokines such as TNF and interleukin-1 from macrophages, resulting in chills and high grade fever. This occurs once in 48 hours, corresponding to the erythrocytic cycle. In the initial stages of the illness, this classical pattern may not

be seen because there could be multiple groups (broods) of the parasite developing at different times, and as the disease progresses, these broods synchronise and the classical pattern of alternate day fever is established. It has been observed that in primary attack of malaria, the symptoms may appear with lesser degree of parasitemia or even with submicroscopic parasitemia. However, in subsequent attacks and relapses, a much higher degree of parasitemia is needed for onset of symptoms. Further, there may be great individual variations with regard to the degree of parasitemia required to induce the symptoms. The first symptoms of malaria after the pre-patent period (period between inoculation and symptoms, the time when the sporozoites undergo schizogony in the liver) are called the primary attack. It is usually atypical and may resemble any febrile illness. As the disease gets established, the patient starts getting relapse of symptoms at regular intervals of 48-72 hours. The primary attack may

spontaneously abort in some patients and the patient may suffer from relapses of the clinical illness periodically after 8-10 days owing to the persisting blood forms of the parasite. These are called as short term relapses (recrudescences). Some patients will get long term relapses after a gap of 20-60 days or more and these are due to the reactivation of the hypnozoites in the liver in case of vivax









recrudescences can occur due to persistent infection in the blood.

While most of the clinical manifestations of malaria are caused by the malarial infection per se, high grade fever as well as the side effects of anti malarial therapy can also contribute to the clinical

manifestations. All these may act in unison, further confusing the picture. In some cases, secondary infections like pneumonia or urinary tract infection can add to the woes. All these facts should always be kept in mind. Typical features: The characteristic, text-book picture of malarial illness is not commonly seen. It includes three stages viz. Cold stage, Hot stage and Sweating stage. The febrile episode starts with shaking chills, usually at mid-day between 11 a.m. to 12 noon, and this lasts from 15 minutes to 1 hour (the cold stage), followed by high grade fever, even reaching above 1060 F, which lasts 2 to 6 hours (the hot stage). This is followed by profuse sweating and the fever gradually subsides over 2-4 hours. These typical features are seen after the infection gets established for about a week. The febrile paroxysms are usually accompanied by head aches, vomiting, delirium, anxiety

and restlessness. These are as a rule transient and disappear with normalization of the temperature. In vivax malaria, this typical pattern of fever recurs once every 48 hours and this is called as Benign Tertian malaria. Similar pattern may be seen in ovale malaria too (Ovale tertian malaria). In falciparum infection (Malignant tertian malaria), this pattern may not be seen often and the paroxysms tend to be more frequent (Subtertian). In P. malariae infection, the relapses occur once every 72 hours and it is called Quartan malaria.

In an endemic area, malaria often presents with atypical manifestations Atypical features are more common in the following situations: Falciparum malaria Early infection Patients at extremes of age Patients who are immune-compromised (extremes of age, malnourished, AIDS, tuberculosis, cancers, on

• • • •

immunosuppressive therapy etc.)

Patients on chemoprophylaxis for malaria

• • •

Patients who have had recurrent attacks of malaria Patients with end stage organ failure Last but not the least, pregnancy.

Atypical fever: In an endemic area, it is rather unusual to find cases with typical fever pattern. Some patients may not have fever at all and may present with other symptoms listed below. Many present with fever of various patterns - low grade to high grade, with or without chills, intermittent to continuous, or even as cases of prolonged fever. In the initial stages of the illness, fever may be quotidian, with more than one spike per day and this is due to the development of multiple broods of the parasite. As the disease progresses, these broods get synchronized and the fever tends to be more uniform. However in cases of P. falciparum malaria and mixed infections, this pattern of multiple spikes may continue. Headache: Headache may be a presenting feature of malaria, with or without fever. It can be unilateral or bilateral. Some times the headache could be so intense that it may mimic intra-cranial infections or intra-cranial space occupying lesions. It may also mimic migraine, sinusitis etc. Presence of projectile vomiting, papilloedema, neck stiffness and focal neurological signs would suggest other possibilities.

Body ache, back ache and joint pains: These symptoms are fairly common in malaria. These can occur even during the prodromal period and at that stage these are generally ignored and diagnosis of malaria is impossible owing to lack of peripheral parasitemia. They are also common malaria accompaniments may present of only the with malaria these paroxysm. symptoms,


particularly in cases of recurrent malaria. Dizziness, vertigo: Some patients may present with dizziness or vertigo, with or without fever. They may also have associated vomiting and/or diarrhoea. This may mimic labyrinthitis, Menniere's disease, vertebro-basilar insufficiency etc. Rarely patients may present with swaying and cerebellar signs. Drugs like chloroquine, quinine, mefloquine and halofantrine can also cause dizziness, vertigo, and tinnitus. Altered behaviour, acute psychosis: Patients may present with altered behaviour, mood changes, hallucinosis or even acute

psychosis, with or without fever. Malaria may be detected accidentally in such cases and they improve completely with anti malarial therapy. Altered behaviour may also be due to high grade fever or drugs. Antimalarial drugs like chloroquine, quinine, mefloquine and







delirium or even frank psychosis. Altered sensorium: Patients with P. falciparum malaria may present with altered sensorium due to severe infection, hypoglycemia, electrolyte imbalance due to vomiting or diarrhoea (particularly the elderly), diagnosis hyperpyrexia, will include subclinical acute convulsions etc. Differential metabolic



encephalopathy etc. As a rule of the thumb, malaria should be considered a possibility in all cases of acute neuropsychiatric syndromes and in cases of proven malaria, other possibilities should be considered in the presence of papilloedema, increasesd ICT, neck stiffness and focal deficits. Convulsions, coma: Patients with cerebral malaria present with generalised seizures and deep unarousable coma. Sometimes one single fit can precipitate deep, unarousable coma. These could also be due to hypoglycemia and all patients presenting with these

manifestations should be administered 25-50% dextrose immediately. Drugs like chloroquine, quinine, mefloquine and halofantrine may also trigger convulsions. Cough: Cough may be a presenting feature of malaria, particularly P. falciparum infection. Patient may have pharyngeal congestion and

features of mild bronchitis. Patients who have persistent cough and/or fever even after clearance of parasitemia should be evaluated for secondary bacterial pneumonias/ bronchopneumonia and

bronchitis. Breathlessness: In severe falciparum malaria, patients may present with history of breathlessness, due to either severe anemia or noncardiogenic pulmonary oedema. Secondary respiratory tract infections and lactic acidosis are other rarer causes for tachypnoea and/or breathlessness in these patients. Patients with pre-existing cardiovascular or pulmonary compromise may deteriorate or even die if they suffer from severe malaria. Chest pain: Acute retrosternal or precordial pain may be presenting feature of malaria. It may radiate to the left or right shoulder tips or arms. It is due to rapid increase in the splenic size and perisplenitis. This pain may mimic acute myocardial infarction, pleurisy, neuralgia etc. Coupled with breathlessness, sweating and hypotension (algid malaria), the picture will very closely resemble that of acute MI. Acute abdomen: Patients can present with acute abdominal pain, guarding and rigidity, mimicking bowel perforation, acute

appendicitis, acute cholecystitis, ureteric colic etc.

One such patient presented with pain abdomen and vomiting with low grade fever, and on examination had tenderness in the right lower abdomen. He was posted for appendicectomy. Pre operative blood test revealed P. falciparum malaria and he recovered completely with anti malarials! Weakness: Sometimes patients may present with history of

weakness, malaise and prostration. On examination they may have significant pallor, hypotension, dehydration etc. Algid malaria may present like this and the patient may not have fever at all. Chloroquine is also known to cause profound muscular weakness and a new disease called macrophagic myofaciitis has been described in patients receiving chloroquine. Vomiting and diarrhoea: Malaria can present as a case of acute gastroenteritis with profuse vomiting and watery diarrhoea (Choleraic form). Vomiting is very common in malaria and is due to high grade fever, the disease itself or even drugs. Vomiting may pose problems in administering antimalarial treatment. These could also be due to drugs like chloroquine and due to secondary bacterial or amebic colitis. Jaundice: Patients may present with history of yellowish

discoloration of eyes and urine. Mild jaundice is fairly common in

malaria and may be seen in 20-40% of the cases. Deeper jaundice with serum bilirubin of more than 3 mg/dL is seen in severe P. falciparum malaria and is associated with anemia, hyperparasitemia and malarial hepatitis with elevated serum enzymes. Malaria must be considered as a differential diagnosis for all cases of jaundice in a malarious area. Pallor: Severe anemia can be a presenting feature of malaria. It is usually normocytic normochromic. It may pose special problems in pregnancy and in children. Pre-existing nutritional anemia may be aggravated by malaria. Puffiness of lids: Occasionally patients may present with puffiness of lids, with or without renal dysfunction. Secondary infections: Malaria produces significant immune

suppression and this can result in secondary infections. Common among them are pneumonia, aspiration bronchopneumonia (in the elderly), urinary tract infection, colitis etc. Meningitis and enteric fever have also been reported. In falciparum malaria, severe infection can lead to septicaemic shock (algid malaria). Persistence of fever, neutrophilic leucocytosis and focal signs of infection should always alert the clinician to this possibility of secondary infections.

Hepatosplenomegaly: Patients can present with enlargement of liver and/or spleen, tender or non-tender, with or without fever. Rapid enlargement of spleen or liver in malaria can cause acute pain in the abdomen or chest. Generally, organomegaly is noticed in the second week of malarial it illness. may be However, present in cases of relapse in or





compromised patients splenomegaly may be absent. In pregnancy, particularly second half, splenomegaly may be smaller or an enlarged spleen may regress in size due to immune suppression. Although splenomegaly is a cardinal sign of malaria, absence of splenomegaly does not rule out the possibility of malaria. Combinations of the above: Patients can frequently present with various combinations of the above mentioned symptoms and signs, further confusing the picture. This list is not exhaustive and malaria may present in many other ways. In all the above listed situations, patients may not have associated fever, thus confusing the picture. In some, fever may follow these symptoms. Therefore, one should not wait for the typical symptoms of malaria to get a blood test done; it is always better to do a smear whenever reasonable doubt exists.

1. Presence of any of the complications of P. falciparum malaria viz. altered sensorium; convulsions; coma; jaundice; severe anemia; hypotension; prostration; hyperpyrexia; renal failure etc. 2. Atypical presentation. 3. Not responding to chloroquine therapy within 48 hours. 4. Recurrence within 2 weeks.

Plasmodium vivax malaria is usually more common than P.

falciparum malaria and rarely causes any complications. Also, almost all cases of P. vivax malaria respond to Chloroquine and resistance to this drug has been reported only in sporadic cases in Irian Jaya, Myanmar, Papua New Guinea and Vanuatu. Therefore, P. vivax malaria should be treated with chloroquine and primaquine ONLY. However, in areas where P. falciparum malaria is also seen in significant numbers, there is always a chance of mixed infection. Further, in some cases, the tests for malarial parasite may reveal only P. vivax infection. This is particularly important if QBC method has been used for identifying the infection, wherein species identification

is rather difficult. Therefore, all cases of P. vivax malaria should be carefully observed during initial stages of treatment and if there are any signs of not improving or deterioration, a possible co-infection with P. falciparum should be considered. After 6 days of treatment, a repeat test for malarial parasites should be done to confirm clearance of parasitemia.

Treatment of P. vivax malaria: A flow chart Chloroquine + Primaquine After 48 hours

Clinical Recovery Continue treatment

Status quo / worse the Suspect P. falciparum, repeat MP test at 48 hrs. (A thin smear examination is better for species

Repeat the MP test identification and for assessing parasite count) on the 6th day




causes of fever, may be in association

with malaria. P. falciparum P. vivax Treat possibly chloroquine resistant as If the patient has typical malarial

complications, treat as P. falciparum;

otherwise, wait.


Plasmodium falciparum malaria is the cause of all the mortality and most of the morbidity in malaria. It can present with atypical features, it can cause dramatic complications and to add to the woes, treatment may be rendered difficult by resistance to antimalarial drugs. Treatment of P. falciparum malaria therefore is different from that of other types of malaria. It depends on the severity of infection, status of the host and drug sensitivity pattern in the locality. In view of the seriousness of the problem and synergistic toxicity of antimalarial drugs, the drugs should be properly chosen right at the start of the treatment. Changing the drugs or adding of drugs halfway through the treatment only complicates the issue and adds to the adverse effects of treatment. Although blood schizonticidal drugs like chloroquine are enough to give a radical cure of the falciparum infection, Primaquine should be administered to all patients as a gametocytocidal drug to prevent the spread of this potentially lethal infection. However, primaquine should not be used concurrently with quinine and mefloquine and it is contraindicated in pregnancy and lactation. In cases of severe P. falciparum malaria, only parenteral drugs should be used. And in all such cases, it is safer to presume drug resistance and start on drugs other than chloroquine, because waiting for a response to chloroquine may prove costly for the patient.

In cases of resistant P. falciparum malaria, it is better to use two antimalarial drugs. Various combinations have been tried, but it is advisable to use one rapid acting drug and another slow acting drug in combination. In places where the QBC test is widely used for diagnosis of malarial infection, it is better to get a thin smear examined for assessing parasite count in all positive cases of P. falciparum malaria. This simple test would help in assessing the severity of the infection, in monitoring response to treatment, and in identifying cases of resistance. Treatment of P. falciparum malaria - A flow chart Uncomplicated andComplicated and chloroquine chloroquine sensitive sensitive Tab. Chloroquine + PrimaquineInj. Chloroquine + Primaquine single dose After 48 hours Better; parasite countStatus quo/ worse; parasite single dose

reduced by >75% count reduced by <75% Continue Consider resistance Drugs for chloroquine resistant malaria Uncomplicated andComplicated and Chloroquine Chloroquine resistant resistant Use any one of the following1. Inj.Quinine combinations: 1. Tab. Quinine + Pyrimethamine/Sulphadoxine Tab.2. Inj. Quinine + Tetracycline / +



2. Tab. Quinine + Tetracycline3. Inj. Artemether / Arteether / /doxycycline 3. Tab. Artesunate + Tab. Artesunate + Mefloquine.

Mefloquine 4.Tab. Mefloquine +


All cases of P. falciparum malaria, particularly in the nonimmune and high-risk population, should be monitored for complications. Clinical parameters: Vital signs, hydration, intake/output, level of sensorium, pallor, jaundice. hourly blood glucose (to detect

Lab. parameters: 4

hypoglycemia); 12 hourly hemoglobin, P.C.V. (to assess hemolysis); 12 hourly parasite count (to assess response); 24 hourly S. creatinine, S. bilirubin. Follow-up MP tests In all cases of P. falciparum malaria, follow-up MP tests should be done on the 6th and 28th days after treatment. The 6th day smear is done to assess clearance of parasitemia and 28th day smear is done to identify recrudescence.

6th day smear: If the parasite is sensitive to the drugs that have been used, then the parasitemia should clear within 7 days. However, gametocytes may be found on the smear and this does not require any treatment; if primaquine has not been given, it can be given now. Persistence of ring forms of the parasite indicates incomplete clearance and hence drug resistance. These cases should be retreated accordingly with other anti malarial drugs. 28th day smear: If the parasite is not completely eradicated due to partial resistance, then the 28th day smear will be positive. All such cases should be re-treated with other antimalarial drugs. Primaquine should be re-administered in these cases to destroy freshly formed gametocytes. The National Malaria Eradication Programme in India recommends repeat smears on 6-7th, 14th, 21st, and 28th days of treatment to identify resistance and recrudescence. Combinations of Antimalarial Drugs Early and effective chemotherapy for malaria has a pivotal role in reducing morbidity and mortality especially since a vaccine is unlikely to emerge within the next decade. Multidrug resistance has been reported from most parts of the world and as a result, monotherapy or some of the available combination chemotherapies for malaria are either ineffective or less effective. New antimalarial regimens are, therefore, urgently needed and antimalarial combination

chemotherapy is widely advocated. Antimalarial combinations can increase efficacy, shorten duration of treatment (and hence increase compliance), and decrease the risk of resistant parasites arising through mutation during therapy. Combination therapy with antimalarial drugs is the simultaneous use of two or more blood schizontocidal drugs with independent modes of action and different biochemical targets in the parasite. The concept of combination therapy is based on the synergistic or additive potential of two or more drugs, to improve therapeutic efficacy and also delay the development of resistance to the individual

components of the combination. Artemisinin based combinations are known to improve cure rates, reduce the development of resistance and they might decrease transmission of drug-resistant parasites. The total effect of

artemisinin combinations (which can be simultaneous or sequential) is to reduce the chance of parasite recrudescence, reduce the withinpatient selection pressure, and prevent transmission.

Antimalarial Drug Combinations Artemisinin based combinations Artesunate + Chloroquine Efficacy Very high chloroquine failure rates (>60%) and sub-optimal efficacy of the combination (85% Status cure rate) Not approved; Not a viable option in areas with pre-existing moderate to high levels of P.

falciparum resistance to Chloroquine Artesunate + Amodiaquine Efficacy and Better efficacy than amodiaquine alone (cure rate advantages >90%); Well tolerated Disadvantages ?Neutropenia; Pharmacokinetic mismatch Dose Artesunate 4mg/kg and amodiaquine 10mg base/ kg once a day 3 days Approved


Artesunate + Mefloquine Efficacy and In use for many years and the first-line treatment advantages in several parts of SE Asia Disadvantages Pharmacokinetic mismatch; neuropsychiatric effects,

Mefloquine cardiotoxic

induced effects,

incidents of vomiting in children; but combination with artesunate results in less adverse reactions than the use of mefloquine alone Artesunate (4mg/kg once daily) for 3 days + mefloquine (25mg base/kg) as a split dose of 15mg/kg on Day 2 and 10mg/kg on Day 3. (Alternatively 8mg/kg mefloquine daily for three


Non-Artemisinin based Combinations Sulfadoxine-pyrimethamine based combinations Sulfadoxine-pyrimethamine (SP) Efficacy and Single dose; Cheap advantages Disadvantages Drug resistance; Serious adverse effects Dose Sulfadoxine 25mg/kg and Pyrimethamine


1.25mg/kg as single dose Not approved; Considered as single drug

SP + Chloroquine Advantages Cheap; Similar pharmacokinetic profiles, with varied modes of action on different biochemical targets in the parasite Disadvantages Drug resistance; Serious adverse effects to SP Dose Chloroquine 25mg/kg over 3 days; SP single dose as above Not approved; an be used where resistance to SP is


not a problem SP + Amodiaquine Advantages Similar pharmacokinetic profiles Disadvantages Adverse effects of amodiaquine and SP Dose Amodiaquine 10mg/kg daily for 3 days; SP single dose as above Approved (In







amodiaquine and SP remain high - countries in West Africa) SP + Quinine Advantages Effective where resistance to SP is not a problem

Disadvantages Drug resistance; Serious adverse effects Dose Quinine 15mg/kg 12 hourly for 3 days; SP single dose as above Not approved


SP + Mefloquin (FansimefTM) Advantages Fixed dose pill, single dose Disadvantages Not an additive or synergistic combination; Each drug has a different pharmacokinetic profile;

Dose Status

Expensive; Resistance known Mefloquine 15mg/kg and SP as above single dose Not approved; Not recommended for general use

since 1990 Atovaquone + Proguanil (MalaroneTM) Advantages Synergistic activity; Good safety and tolerability in children and adults Disadvantages High cost; Restricted availability; Contra-indicated in case of hypersensitivity or renal insufficiency Atovaquone 20mg/kg and Proguanil 8mg/kg once daily for 3 days Approved; Highly efficacious against P. falciparum, including strains that are resistant to chloroquine and mefloquine, with cure rates of 94-100% Chlorproguanil + Dapsone (LapDapTM) Advantages Well tolerated; Efficacious Disadvantages Dapsone induced methaemoglobinaemia and



haemolysis in G6PD deficiency; Potential crossresistance with SP Chlorproguanil 2mg/kg





once daily for 3 days Status Approved Quinine based Combinations Quinine + Tetracycline Advantages Efficacious Disadvantages 7-day course, multiple doses daily; Cinchonism; Tetracyclines contraindicated in children and


pregnant women; Emergence of resistance Quinine 10mg/kg 8 hourly and Tetracycline 4mg/kg 6 hourly for 7 days Not approved; Difficult to recommend as a first-line


treatment for uncomplicated malaria Quinine + Clindamycin Advantages Good efficacy; Safe in children and women; Lesser risk of resistance Disadvantages Cinchonism Dose Quinine 15mg/kg 12 hourly and




5mg/kg 12 hourly for 3 days Not approved

New Combinations Piperaquine + Dihydroartemisinin



(ArtecomTM) and ArtecomTM plus Primaquine (CV8TM) (CV = China-Viet Nam) Advantages Efficacy consistently above 93% Disadvantages Animal toxicology studies indicate additive toxicity; No serious adverse events observed in human studies


Trials; May prove to be more affordable

Chlorproguanil+ Dapsone + Artesunate (CDATM or Lapdap plusTM ) Status

No adequate data available yet

Fosmidomycin+ Clindamycin Advantages Both drugs act on the parasite's apicoplast; Rapid clearance and 100% cure rates reported Trials on


Dose and Administration of Antimalarial Drugs






All cases of P. vivax malaria and uncomplicated cases of P. falciparum malaria are treated with oral drugs. Chloroquine is the ONLY drug used for P. vivax malaria, because resistance to chloroquine in P. vivax malaria is almost unknown (only sporadic reports). Most cases of P. falciparum malaria can also be treated with chloroquine alone, however, in areas with known resistance to chloroquine, it is safer to combine chloroquine with another oral antimalarial like

pyrimethamine/ sulphadoxine. Primaquine should be used in both types of malaria for radical treatment. Dose of commonly used antimalarial drugs

Dose of Chloroquine (as base) (Each 250 mg tabletDose of Dose of

contains 150 mg base andPrimaquine Age in years 1st 2nd 3rd 4th each 5 ml of suspension contains 50 mg base) P. P. vivax/ falciparu mixed dose* dose dose dose m Single (for 14 dose days)** Nil mg 150 1-5 mg 300 5-9 mg 450 9-14 mg 600 >14 *1st mg 300 mg 300 mg 300 mg 225 mg 225 mg 225 10 mg 30 mg 75 mg 75 mg 75 mg 2.5 mg 7.5 mg 150 150 150 5 mg 15 mg mg mg Nil

Pyri/Sulpha (Of 25+500

mg tablet)

37.5 0-1 75 mg


37.5 1/4 tablet

1/2 tablet

1 tablet

2 tablets

15 mg 45 mg 3 tablets mg mg mg mg dose of chloroquine should always be larger to obtain sufficient

blood levels, in view of large volume of distribution. ** The National Malaria Eradication Programme in India recommends a 5 day course of primaquine instead of 14 days.



for1st dose 2nd dose After

3rd dose

4th dose

chloroquine If the patient comes in the morning and treatment can beStat.

6After 24After 48 hours hours

hours started by mid-day If the patient comes in the

After 12After 24After 36 afternoon and treatment isStat hours started by evening If the patient is coming from a Stat far off place and /or if the MP hours hours

(as2nd and 3rd doses

After 48 presump together after 24 test report is available only next hours tive) hours day Parenteral Chloroquine: Parenteral chloroquine may be needed in patients with complicated, yet drug sensitive, P. falciparum malaria and in case of persistent vomiting. 10 mg / kg (max.600mg) in isotonic fluid, over 8 Intravenous hours; followed by 15 mg / kg (max.900mg) over infusion 24 hours. Intramuscular 3.5 mg of base/ kg (max.200 mg) every 6 hours or or 2.5 mg of base/ kg (max.150mg) every 4 hours. injection can cause fatal

subcutaneous (Intramuscular

injections hypotension, especially in children) Treatment of complicated/ chloroquine resistant P. falciparum malaria

It is safer to treat cases of severe P. falciparum malaria as chloroquine resistant, unless one is very certain about the sensitivity. It is better to use two drugs, one rapid acting and one slower acting. Severe malaria should always be treated with parenteral antimalarials to ensure adequate treatment. Quinine In intensive care unit: 7mg of salt/kg over 30 minutes., followed immediately by 10mg/kg diluted in 10ml/kg isotonic fluid over 4 hours; after 4 hour interval, 10mg/ kg over 4 hours, repeated every 812 hours until patient can swallow. OR 20mg of salt/kg diluted in 10 ml/kg isotonic fluid, infused Intravenous over 4 hrs; then 10 mg of salt / kg over 4 hrs, every 8-12 hrs until patient can swallow. Children: 24 mg of salt/kg diluted in 10 ml/kg isotonic fluid, infused over 4 hrs; then 12mg of salt/kg over 4 hrs, every 8-12 hrs until patient can swallow. 20mg of salt/kg diluted to 60 mg/ml by deep i.m. Intramuscular injection, (divided into two sites); then 10mg of salt/kg every 8 hours. Adults: 600mg of salt 3 times a day for 7 days (max. of 1800mg/day) Children: Approximately 10mg/kg 3


times a day for 7 days. In areas where resistance to quinine is known or suspected, add single dose of pyrimethamine/ sulphadoxine OR Tetracycline or Doxycycline for 7 days (for non-pregnant adults only) Artemisinin derivatives Preparation Dose and administration Artemether: IM: (Availability: 3.2mg/kg as loading dose, followed by

1.6mg/kg daily, until patient is able to swallow or

80 mg/ml Inj. for 5 days. (Maximum dose: 480 mg in adults and and cap.) 40 mg 9.6mg/kg in children.)

Oral: 160mg in two doses on the first day, then 80 mg/day for total 5 days

Arteether: (Availability: 150mg/2 injection)

Adults: 150mg IM once daily for 3 consecutive days. Children: 3 mg/kg once daily for 3

ml consecutive days.

Artesunate: Injection: The powder should be reconstituted in (Availability: 1 ml of 5% sodium bicarbonate and then further

60mg powder diluted with isotonic saline or 5% dextrose (to a with 1 ml of total of 3 ml for im and 6 ml for iv use). 5% sodium Dose: 2.4mg/kg on the first day (additional 1.2 mg/kg after 4 hours in case of severe falciparum

bicarbonate ampoule

for malaria), followed by 1.2 mg/kg daily until patient


and is able to swallow or for a maximum of 7 days.

50 mg tablet) Oral: 100 mg on the first day, followed by 50 mg/ day for 7 days. Other drugs Drug Mefloquine Dose 15-25 mg/kg (max. of 1500 mg), given as two doses, 6-8 hrs apart 250 mg 4 times a day for 7 days (for patients > 8 years and non-pregnant) 100 mg twice a day for 7 days (for patients > 8 years and non-pregnant)



Most blood schizonticidal drugs prevent the development of the forthcoming erythrocytic cycle of parasitic development and hence have no or little effect on the ongoing cycle that is already causing fever. Therefore, it would take at least 48 hours for the treatment to be effective. In severe P. falciparum malaria, oral antimalarials should not be used. Vomiting, poor general health, poor compliance, erratic G.I. absorption due to splanchnic vasculopathy etc. make oral therapy less reliable. Therefore, use only parenteral antimalarials. This also means that oral only antimalarials like Mefloquine and Halofantrine have no place in treating severe falciparum malaria.

In all cases of P. falciparum malaria, the antimalarial drugs should be chosen depending on the severity of the illness and the sensitivity pattern in the locality. Changing the drugs or adding the drugs in between is not advisable. Most antimalarial drugs have a long plasma half-life. Therefore, adding similar drugs half way through the treatment will only add to the adverse effects and not to the therapeutic benefit. The following combinations should therefore be avoided, concurrently or within a short interval: (1.) Chloroquine + Quinine (2.) Chloroquine + Mefloquine (3.) Quinine + Mefloquine (5.) Quinine + Primaquine (6.) Quinine + Halofantrine (7.) Mefloquine + Primaquine (8.) Administration of Primaquine and Pyrimethamine/sulphadoxine on the same day is also not advisable. Both sulpha and primaquine can precipitate hemolytic crisis in patients with Glucose 6-phosphate dehydrogenase deficiency. Do not exceed the maximum recommended dose of antimalarial drugs. All antimalarial drugs have a narrow safety range and excess dose may lead to adverse effects. Moreover, larger dose does not offer any superior antimalarial effect. Primaquine should be administered to ALL cases of malaria as radical treatment except in the following situations where it is

contraindicated: (i.) Pregnancy and lactation (ii.) Infants below one

year of age. In these two categories, chloroquine should be given every week as a suppressive chemoprophylaxis to prevent relapse of vivax malaria. When these patients are fit for administration of primaquine, they should be given full therapeutic dose of chloroquine as well as primaquine. (iii.) Patients with known Glucose 6-phosphate dehydrogenase deficiency (iv.) Concurrently with quinine, mefloquine and halofantrine (v.) It should not be used on the same day with sulphadoxine. In such cases it can be given the next day. Do not misuse the newer antimalarial drugs. We need to preserve them for future. Research into newer antimalarial drugs is scanty and the parasite is fast developing resistance even for newer drugs. Thus if we deplete the newer drugs by misusing them, we may not have anything left for treating ALL DRUG RESISTANT malaria in the nottoo-far-future. Therefore, newer anti malarial drugs should be used only when definitely indicated and not indiscriminately. These drugs should be used ONLY when parasite index or other methods PROVE drug resistant malaria. In addition, artemisinin derivatives can be used in cases of hyperparasitemia or life-threatening complications on account of their ability to clear the parasitemia earlier compared to other anti malarial drugs.

1. To detect, report and follow up drug reactions, drug interactions and patient compliance. 2. To work with health care professional to minimize the risk and maximize the clinical effects of medication. 3. To communicate with health care professional to seek knowledge and to give information about drugs. 4. To educate patient about appropriate administration of the drug. 5. Consistently demonstrate proper documentation of

pharmaceutical care activities. 6. 7. To encoverage the rational use of drug. To improve the patient disease state by therapeutic drug monitoring to increase the efficacy of drug.

Patient Name: Age: Sex: Bed: Address: Date of birth: Chief complaint Pain in abdomen Fever Vomiting Burning maturation 3 weeks 3 weeks 3 weeks 5 days Asad Bad Shah s/o Saleem Khan 18 years Male 11 Karak 28-08-2007

History of present illness According to the patient he is suffering from high grade fever which is at different intervals and not associated with chills. Thus is a history of Abdominal pain and vomiting and burning macturation. Family history D.M, H.TN and TB not significance History of post illness No surgery, no hospitalization Socioeconomic status General physical examination

Anemia (-ve), jaundice (-ve), B.P 120/80, pulse rate 90/mint temperature 102Fo Systemic examination Respiratory system normal Nervous system normal G.I.T clear History based diagnosis Malaria fever Investigation M.P, widal, blood culture etc Test investigation Test HBs Ag HCV SGPT Billurbin Hb Platelet count TLC DLC Lymphocytes Esinophil Monocytes Polymorpus Neutrophil Medication history Inf. Quinine sulphate 900mg 35% 03% 02% 60% 25% Result -ve -ve 38 u/l 0.9 u/l 12 g / dl 210,000 9800

25-45% 4-6% 1-6% 40-75%

+ 500ml D/ Saline + 5-Hypertence Inf. Quinine 600 mg in D/ Saline + 5 Hypertence Inj. Bestrix 2g i/v Inf. D/S IL I/V Inf. Plabolyte i/v Tab paradal Result / finding Drug interactions No drug interaction is reported Adverse drug reaction Loss of epetite Bad test Compliance

State give TDS OD State thin OD State given 2 805

The patient is complaining with the current drug therapy. Cautions: Quinine use with caution in patient with cardiac arrhythmia and myastehmia gravisa Discussion The patient is admitted with fever, chills, and vomiting. The prescribe therapy should improve the patient. Comments The patient is vomiting but then is no prescribed the anti – emelic e.g motilliun etc. for relief.

Patient Name: Age: Sex: Bed: Date of birth: Address: Chief complaint Fever high grade Continuous Known epileptic 3 weeks 3 weeks 15 weeks Basmeena 30 years Female 8 24-08-07 Zargar abad peshawar

History of present illness The patient developed high grade fever 3 days back the patient developed seizure and pits. Her whole body shavered and rigid then started vibrating moments sizne she is un-concious and ptis are occurs every 5-10 minuts. Family history D.M, H.TN and TB not significance History of post illness Epilepsy from 15 years

Socioeconomic status Poor General physical examination Anemia (-ve), jaundice (-ve), B.P 130/80, pulse rate 85/mint temperature 100Fo Systemic examination Respiratory system normal Nervous system normal G.I.T clear History based diagnosis Epilepsy and Malaria Investigation M.P+ve Widal –ve Test Hbs Ag: HCV SGPT BB -ve -ve 40u/c 0.8g/dl

RESULT / FINDINGS Drug interaction No drug interaction is reported

Adverse drug reactions The moxation tachycardia Epival Bestrix somnolence insomonic depressun hypertension lnucesed epatite thrombcyte GIT disturbance

pain in injection site

Compliance The patient is complaining with current drug therapy Action : Discussion: The patient is admitted iwht high grade fever, pits, and the prescribe therapy should improve the patient. Comments bestirx administered with caution in pencillin ellergy

Medication history Inj epival

2nd day medication

3rd day medication

Patient : Age: Sex: Bed: Address: Malik Aman 28 Male 17 Charsadda 30-08-07

Date of admission:

Present complaint Fever 18 days Loss motion 5 days Drows ness 2 days History of present illness According to the father of patient he will be onset of high grade fever with chill and reger back in Wazirastan 15 days ago. For the last two days he become drowzee and disoriented no history of vomiting; dirrhoea or pain, no history of cough headache and local treatment in charsadda. Past drug history No history of allergy to any drug Personal history

Herone General physical examination BP 120/60; pluserate 80/min; anemia –ve, jaundice –ve, lymphode no palpable GIT soft smooth. History based diagnosis Cerebral malaria; Investigation CSF examination, CT-Scan, chest x-ray, blood culture, Blood CP.

Test investigation Blood sugar Blood urea Serum creatinine Sodium Potassium Chloride Billuribin SGPT Alkaline Phosphatase H.B Plate let count TLC CHEMICAL EXAMINATION Protein Glucose 55 50 144mg/dl 48mg/dl 1.1mg.dl 132 4.8 101 0.7mg/dl 24u/L 95 u/l 12.5gm/dl 2,15,000 9950

Prescribed medication Quinine 600mg i/v TDS

Infusion plabolyte i/v in 100ml TDS pladox Inj. Rocifen 3g i/v Result / finding Drug interaction No drug interaction is reported Adverse drug reaction No adverse drug reaction are observed Compliance The patient is complaining with the current drug therapy Caution Ceftriaxone should be avoided in neonate due interference in billurbin metabolism Discussion The patient in admitted with fever loss motion, drowsiness, confusion the prescribe therapy should improve the condition of patient. The patient is discharge with good prognosis. OD

Patient : Age: Sex: Bed: Malik Aman 70 Male 17


Kabul 28-08-07

Date of admission:

Present complaint Fever 15 days Disorientation and confusion – 15 days fits – 15 days History of present illness Fever was not associated with chill and regor can not speaked, confused, unable to walke and there is tremer in his limb. Urinary incontinence there is post epileptic drowsiness present. Past history: Was admitted in Kabul hosp for same problem was relieved for 2 days but aggravated the. Past drug history No history of allergy to antibiotic General physical examination Pulse rate 100, BP= 130/70 respiratory system deformity

pigmentation none, movement normal, percussion normal breath should normal. Alimentary system Shape scophid, liver, spleen kidney impalpalote ascites not present, hernia not present. History based diagnosis

Acute meningitis Cerebral malaria; Test investigation CSF examination, CT-Scan, Chest X-ray, Blood culture, Blood CP. Blood sugar Urea Creatinine Sodium Potassium Chloride Billuribin SGPT Alkaline Phosphatase Prescribed medication Dose 1 x TDS BDs BD 2Xsos ITDS BD 166mg/dl 59mg/dl 1.2mg.dl 134 4.9 104 0.6mg/dl 21 u/l 90 u/l

Inj. Quinine 600mg i/v Inf. plabolite i/v in 100ml pladox Inj. Zanatc ½ Tab. Panadol Extra Tab. Tegral 200mg Tab. Decadron 2cci/v

Result / finding Drug interaction No drug interaction is reported with the prescribed drug therapy. Adverse drug reaction Vomiting Compliance The patient is complaining with the current drug therapy

Caution Ceftriaxone should be avoided in neonate due interference in billurbin metabolism Discussion The patient in admitted with fever loss motion, drowsiness, confusion the prescribe therapy should improve the condition of patient. The patient is discharge with good prognosis.

Patient : Age: Sex: Bed: Address: Sofia Bibi 25 Female 40 Peshawar

Present complaint Headache Vomiting Fever Pregnancy Present History 15 2 15 days 5 months

According to the attendeant of patient she is having headache for the last 15 days. It is associated with vomiting she is also fever, patient was very irritable. She has been coming to gynecology doctor for many times for therapy. Patient is very irritable to communication. Past drug history Pregnant Past treatment Antimalerial Ciproxin Cefixime Socio economic states Satisfactory Family history No DM, Hypertension History base diagnosis Meningitis General physical examination B.P 130/80 Pulse rate 87 /min Local examination Neck stiffness

Investigation CSF examination, CT-Scan, Chest X-ray, Blood culture, Blood CP. Test investigation SGPT Billurbin H.B Platelete count TLC Blood urea Creatinine Blood sugar Alkaline Phosphatase Chemical examination Protein 40mg/dl 41 u/l 0.6U/L 11.2 mg/dl 210000 9650 39.5 1.8 150/u/l 150 mgu/l

Prescribed medication Inj. Quinine 600mg i/v Inf. Rociphen 3gm i/v Inj. Dormicum I/V Result / finding Drug interaction No drug interaction Is reported Adverse drug reaction No adverse drug reaction was observed Compliance TDS OD SOS

The patient is complaining with the current drug therapy Caution Ceftriaxone should be avoided in neonate due interference in billurbin metabolism Discussion The patient in admitted with fever loss motion, drowsiness, confusion the prescribe therapy should improve the condition of patient. The patient is discharge with good prognosis.

Patient Name: Age: Sex: Bed Address: Date of Admission: Chief complaint Fever, chills from last 15 days Dry coiugh from last 2 weeks Loss of eptits Nausea Islam Gul 26 Male 15 Bunir 21/08/07

History of present illness According to the pateitn he has high grade fever and cough from 2 weeks and he cosnet to a doctor and local hospital and use the following drugs. d/ saline 1000ml state artem D.S 2+2+2 for 3 days syp calpol s.o.s the patient not re-covered with it and refered to LRH medical B ward.

History of past illness The patient is suffered from malaria 3 years back. General physical examination Anemia = -ve BP 12/80 102Fo Jaundice –ve pulse rate 90 /minte


Systemic examination Respiratory system normal Nervous system normal GIT Normal History of based diagnosis Malaria fever

Test investigation Test Hbs Ag HCV SGPT Billurubin Hb Platelet count TLC Medication history Inj. QUININE 60MG IN 100ml TDS pladex i/v Inf. Rocipin 1g i/v Tab. Posnton Fort 22-08-2007 BD SOS Result -ve -ve 35 u/l 0.9 u/l 13.g /dl 215000 9700

Inj. Bestrix 1 gm BD Inf. Quinine 600mg in 500 ml TDS d/w i/v Tab pnadol RESULT / FINDINGS Cost effectivness : rociphin 1gm Rs. 477, Macter, Rs. 149 Drug interaction Quinine increased the risk of ventricular arrythemia when given with pimozide or thioridazine Pre – caution Quieinien in pregnancy with high dose in tetrogenic Adverse drug reaction or side effect 2+TDS

Quienine: cinchonism = visual disturbance Hypoglycemia after i/v administrator

Over dose Rociepin 1 gm is OD according to BNF but in prescription is BD Compliance The patient is compliance with given medication Discussion The patient improve form fever , chills, etc.


1. 2. 3. British National formulary (BNF)-51st Edition. Clinical Medicine by Kumar and Clark 5th edition. Pharmaceutical practice by A.J Winfield and R.M.E Richards 3rd ed. 4. 5. 6. 7. 8. basic and clinical pharmacology by Bertam G.Katzung 9th ed. Short textbook of pathology by Mohd. Inam Dansih. Pakistan guide, 2006 ed. phrma guide 2006 ed. The practice of community pharmacy in Remington. The science nad practice of pharmacy 20th national book

foundation. 9. 10. 11. Current medical diagnosis and treatment 2006. Clinical medicine fourth edi. Drug information hand book

Websites 12. 13. 14. 15. 16. www.nytimes.vom.