Pro ject Re por t

On

CLINIC AL PHA RMACY

CLER KSHIP
In
IN KH YB ER
HAYAT SHAHEED TEACHING
TEAC HING HOSPITAL
PESH AW AR, N- W .-F .-P .
Submitted By:
ziaullah zahid ali

Doctor of Pharmacy
September, 2007

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

Department of Pharmacy
University of Peshawar

DEDICATED TO MY PARENTS

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.

Chairman: _____________________________

Prof. Dr. Zafar Iqbal

Department of Pharmacy,
University of Peshawar.

External Examiner: ______________________________

Table of contents
S.No Contents Page No

1. Title page

2. Summary of the project

3. Aims & Objectives

4. Methodology

5. Result / Finding

6. Clinical pharmacy

7. Conclusion

8. Acknowledgment

9. References
 CLINICAL PHARMACY

UNIVERSITY OF PESHAWAR

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:

I Dispensing of Medications

i) Receipt and interpretation of prescription.

ii) Performance / supervision of the dispensing.

2. Prescription Monitoring for:

i) Medication errors. *

ii) Drug interactions.

iii) Side effects and d drug reactions.

iv) Allergic manifestations and hypersensitivity

v) Contraindications.

3. Prescribing Advice to Medical Staff in

i) Choice of medicine and use.

ii) .Method/route of ministration.

iii) Possible side effects.

iv) Interaction with other medication and with food.

v) Pharmacokinetic monitoring.

vi) Drug therapy monitoring.

vii) 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.
WHAT IS MALARIA

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 re-

emerging 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. The tropics provide ideal breeding and living

conditions for the anopheles mosquito, and hence this

distribution.

• 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.

HISTORY OF MALARIA

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

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.

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 well-

prepared 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.

CLINICAL FEATURES OF MALARIA

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

and ovale malaria. In falciparum and malariae infections,

recrudescences can occur due to persistent infection in the blood.

MANIFESTATIONS OF ACUTE MALARIAL ILLNESS

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 (Sub-

tertian). In P. malariae infection, the relapses occur once every 72

hours and it is called Quartan malaria.

ATYPICAL FEATURES:

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 accompaniments of the malaria paroxysm.

Sometimes, malaria may present only with these 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

halofantrine can cause restlessness, hallucinations, confusion,

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), hyperpyrexia, subclinical convulsions etc. Differential

diagnosis will include acute encephalitis, meningitis, 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 non-

cardiogenic 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 cardio-

vascular 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 illness. However, in cases of relapse or

recrudescence, it may be present earlier. Also, in immune

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.

CLINICAL FEATURES SUGGESTING P. FALCIPARUM

INFECTION:

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.

TREATMENT OF P. VIVAX MALARIA

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 Status quo / worse

Continue the Suspect P. falciparum, repeat MP test at 48 hrs.

treatment (A thin smear examination is better for species

Repeat the MP test identification and for assessing parasite count)

on the 6th day

NEGATIVE POSITIVE POSITIVE NEGATIVE

Cured See below Consider other

causes of fever, may

be in association

with malaria.
P. falciparum P. vivax
Treat as If the patient has

possibly typical malarial

chloroquine complications, treat

resistant as P. falciparum;

otherwise, wait.
TREATMENT OF P. FALCIPARUM MALARIA
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 half-

way 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 single dose

After 48 hours

Better; parasite countStatus quo/ worse; parasite

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: Pyrimethamine/Sulphadoxine

1. Tab. Quinine + Tab.2. Inj. Quinine + Tetracycline /

Pyrimethamine/ Sulfa.Doxycycline

2. Tab. Quinine + Tetracycline3. Inj. Artemether / Arteether /

/doxycycline Artesunate + Mefloquine.

3. Tab. Artesunate + Tab.

Mefloquine

4.Tab. Mefloquine +

Pyrimethamine/Sulpha.
MONITORING CASES OF P. FALCIPARUM MALARIA

All cases of P. falciparum malaria, particularly in the non-

immune and high-risk population, should be monitored for

complications.
Clinical Vital signs, hydration, intake/output, level of

parameters: sensorium, pallor, jaundice.

Lab. parameters: 4 hourly blood glucose (to detect

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 re-

treated 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 within-

patient 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%

cure rate)
Status 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

Status 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; Mefloquine induced

neuropsychiatric effects, cardiotoxic effects,

incidents of vomiting in children; but combination

with artesunate results in less adverse reactions

than the use of mefloquine alone

Dose 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

Status 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
Status 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
Status Approved (In areas where efficacy of both

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
Status 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;

Expensive; Resistance known

Dose Mefloquine 15mg/kg and SP as above single dose
Status 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

Dose Atovaquone 20mg/kg and Proguanil 8mg/kg once

daily for 3 days

Status 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 cross-

resistance with SP
Dose Chlorproguanil 2mg/kg and Dapsone 2·5mg/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

Dose Quinine 10mg/kg 8 hourly and Tetracycline 4mg/kg

6 hourly for 7 days

Status Not approved; Difficult to recommend as a first-line

treatment for uncomplicated malaria

Quinine + Clindamycin
Advantages Good efficacy; Safe in children and pregnant

women; Lesser risk of resistance

Disadvantages Cinchonism
Dose Quinine 15mg/kg 12 hourly and Clindamycin

5mg/kg 12 hourly for 3 days

Status Not approved

New Combinations
Piperaquine + Dihydroartemisinin + Trimethoprim

(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
Status 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

Status Trials on
Dose and Administration of Antimalarial Drugs

DRUGS FOR TREATMENT OF UNCOMPLICATED

MALARIA

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

contains 150 mg base andPrimaquine

Dose of
Age each 5 ml of suspension
Pyri/Sulpha
in contains 50 mg base)
(Of 25+500
P.
years
P. mg tablet)
vivax/
1st 2nd 3rd 4th falciparu
mixed
dose* dose dose dose m Single
(for 14
dose
days)**
37.5 37.5 37.5
0-1 75 mg Nil Nil 1/4 tablet
mg mg mg
150
1-5 75 mg 75 mg 75 mg 2.5 mg 7.5 mg 1/2 tablet
mg
300 150 150 150
5-9 5 mg 15 mg 1 tablet
mg mg mg mg
450 225 225 225
9-14 10 mg 30 mg 2 tablets
mg mg mg mg
600 300 300 300
>14 15 mg 45 mg 3 tablets
mg mg mg mg
*1st 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.

Dose spacing for1st dose 2nd 3rd 4th dose

chloroquine dose dose

If the patient comes in the
After 6After 24After 48
morning and treatment can beStat.
hours hours hours
started by mid-day
If the patient comes in the
After 12After 24After 36
afternoon and treatment isStat
hours hours hours
started by evening
If the patient is coming from a
Stat (as2nd and 3rd doses
far off place and /or if the MP 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.

subcutaneous (Intramuscular injection can cause fatal

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 8-

12 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.

Oral 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: 3.2mg/kg as loading dose, followed by

(Availability: 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 40 mg 9.6mg/kg in children.)

cap.) Oral: 160mg in two doses on the first day, then

80 mg/day for total 5 days

Arteether: Adults: 150mg IM once daily for 3 consecutive

(Availability: days. Children: 3 mg/kg once daily for 3

150mg/2 ml consecutive days.

injection)
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

bicarbonate mg/kg after 4 hours in case of severe falciparum

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

injection 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 Dose
Mefloquine 15-25 mg/kg (max. of 1500 mg), given as two

doses, 6-8 hrs apart

Tetracycline 250 mg 4 times a day for 7 days (for patients > 8

years and non-pregnant)

Doxycycline 100 mg twice a day for 7 days (for patients > 8

years and non-pregnant)

IMPORTANT

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 not-

too-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.

AIMS AND OBJECTIVES

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. To encoverage the rational use of drug.

7. To improve the patient disease state by therapeutic drug

monitoring to increase the efficacy of drug.

CASE HISTORY NO.1

Patient Name: Asad Bad Shah s/o Saleem Khan

Age: 18 years

Sex: Male

Bed: 11

Address: Karak

Date of birth: 28-08-2007

Chief complaint

Pain in abdomen 3 weeks

Fever 3 weeks

Vomiting 3 weeks

Burning maturation 5 days

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 Result
HBs Ag -ve
HCV -ve
SGPT 38 u/l
Billurbin 0.9 u/l
Hb 12 g / dl
Platelet count 210,000
TLC 9800
DLC

Lymphocytes 35% 25-45%

Esinophil 03% 4-6%
Monocytes 02% 1-6%
Polymorpus 60% 40-75%
Neutrophil 25%

Medication history

Inf. Quinine sulphate 900mg

+ 500ml D/ Saline State give

+ 5-Hypertence
Inf. Quinine 600 mg in D/ Saline TDS

+ 5 Hypertence
Inj. Bestrix 2g i/v OD
Inf. D/S IL I/V State thin OD
Inf. Plabolyte i/v State given
Tab paradal 2 805

Result / finding

Drug interactions

No drug interaction is reported

Adverse drug reaction

Loss of epetite

Bad test

Compliance

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.

CASE HISTORY NO2

Patient Name: Basmeena

Age: 30 years

Sex: Female

Bed: 8

Date of birth: 24-08-07

Address: Zargar abad peshawar

Chief complaint

Fever high grade 3 weeks

Continuous 3 weeks

Known epileptic 15 weeks

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: -ve

HCV -ve

SGPT 40u/c

BB 0.8g/dl

RESULT / FINDINGS

Drug interaction

No drug interaction is reported

Adverse drug reactions

The moxation tachycardia insomonic depressun hypertension

Epival somnolence lnucesed epatite thrombcyte

Bestrix pain in injection site GIT disturbance

Compliance

The patient is complaining with current drug therapy

Action : bestirx administered with caution in pencillin ellergy

Discussion:

The patient is admitted iwht high grade fever, pits, and the prescribe

therapy should improve the patient.

Comments

Medication history

Inj epival

2nd day medication

3rd day medication

CASE HISTORY NO. 3

Patient : Malik Aman

Age: 28

Sex: Male

Bed: 17

Address: Charsadda

Date of admission: 30-08-07

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 144mg/dl

Blood urea 48mg/dl
Serum creatinine 1.1mg.dl
Sodium 132
Potassium 4.8
Chloride 101
Billuribin 0.7mg/dl
SGPT 24u/L
Alkaline Phosphatase 95 u/l
H.B 12.5gm/dl
Plate let count 2,15,000
TLC 9950

CHEMICAL EXAMINATION

Protein 55

Glucose 50

Prescribed medication

Quinine 600mg i/v TDS

Infusion plabolyte i/v in 100ml TDS

pladox
Inj. Rocifen 3g i/v OD

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.

CASE HISTORY NO. 4

Patient : Malik Aman

Age: 70

Sex: Male

Bed: 17
Address: Kabul

Date of admission: 28-08-07

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 166mg/dl

Urea 59mg/dl
Creatinine 1.2mg.dl
Sodium 134
Potassium 4.9
Chloride 104
Billuribin 0.6mg/dl
SGPT 21 u/l
Alkaline Phosphatase 90 u/l

Prescribed medication

Dose
Inj. Quinine 600mg i/v 1 x TDS
Inf. plabolite i/v in 100ml pladox BDs
Inj. Zanatc ½ BD
Tab. Panadol Extra 2Xsos
Tab. Tegral 200mg ITDS
Tab. Decadron 2cci/v BD

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.

CASE HISTORY NO. 5

Patient : Sofia Bibi

Age: 25

Sex: Female

Bed: 40

Address: Peshawar

Present complaint

Headache 15

Vomiting 2

Fever 15 days

Pregnancy 5 months

Present History
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 41 u/l
Billurbin 0.6U/L
H.B 11.2 mg/dl
Platelete count 210000
TLC 9650
Blood urea 39.5
Creatinine 1.8
Blood sugar 150/u/l
Alkaline Phosphatase 150 mgu/l

Chemical examination

Protein 40mg/dl

Prescribed medication

Inj. Quinine 600mg i/v TDS

Inf. Rociphen 3gm i/v OD
Inj. Dormicum I/V SOS

Result / finding

Drug interaction

No drug interaction Is reported

Adverse drug reaction

No adverse drug reaction was 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.

HISTORY NO. 6

Patient Name: Islam Gul

Age: 26

Sex: Male

Bed 15

Address: Bunir

Date of Admission: 21/08/07

Chief complaint

Fever, chills from last 15 days

Dry coiugh from last 2 weeks

Loss of eptits

Nausea
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 Jaundice –ve

BP 12/80 pulse rate 90 /minte

Temperature 102Fo

Systemic examination

Respiratory system normal

Nervous system normal

GIT Normal

History of based diagnosis

Malaria fever
Test investigation

Test Result
Hbs Ag -ve
HCV -ve
SGPT 35 u/l
Billurubin 0.9 u/l
Hb 13.g /dl
Platelet count 215000
TLC 9700

Medication history

Inj. QUININE 60MG IN 100ml TDS

pladex i/v
Inf. Rocipin 1g i/v BD
Tab. Posnton Fort SOS
22-08-2007

Inj. Bestrix 1 gm BD
Inf. Quinine 600mg in 500 ml TDS

d/w i/v
Tab pnadol 2+TDS

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

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.

ACKNOWLEDGMENT
 REFERENCES

1. British National formulary (BNF)-51st Edition.

2. Clinical Medicine by Kumar and Clark 5th edition.

3. Pharmaceutical practice by A.J Winfield and R.M.E Richards

3rd ed.

4. basic and clinical pharmacology by Bertam G.Katzung 9th ed.

5. Short textbook of pathology by Mohd. Inam Dansih.

6. Pakistan guide, 2006 ed.

7. phrma guide 2006 ed.

8. The practice of community pharmacy in Remington. The

science nad practice of pharmacy 20th national book

foundation.

9. Current medical diagnosis and treatment 2006.

10. Clinical medicine fourth edi.

11. Drug information hand book

Websites

12. www.malariasite.com/malaria

13. www.idph.state.il.us/health/infect/reportids/nmen.htm.

14. www.who.int/entity/esr/resources/publication.

15. www.nytimes.vom.

16. www.freefromhunger.org