CODE: NRS 511

COURSE TITLE: COMMUNITY HEALTH NURSING PRACTICE I

A CASE STUDY ON SEVERE MALARIA

A CASE STUDY CARRIED OUT IN PRIMARY HEALTH CARE
BUKURU EXPRESS, JOS SOUTH PLATEAU STATE, NIGERIA

FORWARDED TO
THE DEPARTMENT OF NURSING SCIENCE, COLLEGE OF
MEDICAL SCIENCES, UNIVERSITY OF JOS
IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE
AWARD OF BACHELOR OF NURSING SCIENCE (BNSC.) DEGREE

DATE

30 AUGUST, 2017

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 CERTIFICATION PAGE

This is to certify that (GWOTT REUBEN CHUNGWOM ELENDU JENIFER

UGBEDE ICHADO MASOK BWEHFA ISAAC) of the department of Nursing

Science, Faculty of Medical Science, University of Jos, carried out this study under

my supervision (MR M.J MAFUYAI) and submitted to the department of Nursing

Science University of Jos in partial fulfilment of the requirement for the award

Bachelor Degree in Nursing Science

……………………… ………………………
MR MANGAI JOSEPH MAFUYAI
DATE
Supervisor

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 ACKOWLEDGMENT

We wish to extend our profound gratitude to God Almighty for giving us the Grace to

start and finish this course despite all odds, all Honour and Glory to His Holy Name

our profound gratitude also goes to my supervisor, MR MANGAI who made out time

from his tight schedule to supervise this work. Thank you very much sir.

Our appreciation also extends to our families and loved ones God bless u all.

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 TABLE OF CONTENTS

Title page .................................................................................................................................... i

Certification ...............................................................................................................................ii

Acknowledgement .................................................................................................................... iii

Table of contents ....................................................................................................................... iv

CHAPTER ONE

1.0 INTRODUCTION ........................................................................................................... 1

1.1 OBJECTIVE OF THE STUDY .................................................................................... 2

1.2 SPECIFIC OBJECTIVE ................................................................................................ 2

1.3 PATIENTS PARTICULARS/ DEMOGRAPHY ........................................................ 2

1.4 PRESENTING COMPLAINTS .................................................................................... 3

1.5 PROGNOSIS ................................................................................................................... 4

CHAPTER TWO

LITRATURE REVIEW

2.1 DEFINITION ................................................................................................................... 5

2.2 A BRIEF HISTORY OF MALARIA ............................................................................. 5

2.3 AETIOLOGY .................................................................................................................. 6

2.4 PATHOPHYSIOLOGY .................................................................................................. 9

2.5 INCUBATION ................................................................................................................ 13

2.6 CLINICAL MANIFESTATION.................................................................................... 14

2.7 DRUG .............................................................................................................................. 15

2.8 DIAGONOSIS ................................................................................................................ 16

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2.9 MANAGEMENT ............................................................................................................ 17

2.10 COMPLICATIONS ........................................................................................................ 18

CHAPTER THREE

3.1 MEDICAL CARE OF PATIENT .................................................................................. 23

3.2 NURSING CARE OF THE PATIENT ........................................................................ 23

3.3 TABULATION OF DRUGS GIVEN TO MISS G. R ................................................. 24

3.4 COMPLICATIONS OF THE PATIENT..................................................................... 25

3.5 NURSING CARE PLAN OF MISS B.M DATE: 30/08/2017 .................................... 25

CHAPTER FOUR

DAILY PROGRESS WITH NURSING INTERVENTION

4.1 DAILY PROGRESS OF PATIENT .............................................................................. 27

4.2 HEALTH EDUCATION ................................................................................................ 27

4.3 DISCHARGE SUMMARY............................................................................................ 27

4.4 ADVICE ON DISCHARGE .......................................................................................... 28

4.5 HOME VISIT.................................................................................................................. 28

CHAPTER FIVE

5.1 SUMMARY ..................................................................................................................... 29

5.2 CONCLUTION .............................................................................................................. 29

5.3 RECOMMENDATION ................................................................................................. 30

REFERENCES .............................................................................................................. 31

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 CHAPTER ONE

1.0 INTRODUCTION

Malaria, which widely occurs in tropical areas, is a potentially life-threatening

condition caused by infection with Plasmodium protozoa transmitted by an infective

female Anopheles mosquito vector. Malaria is a severe condition that causes high

fever and chills. It is gotten from a bite by an infected mosquito. Malaria is rare in the

United States. It is most often found in Africa, Southern Asia, Central America, and

South America.

Malaria is preventable and curable, and increased efforts are dramatically reducing the

malaria burden in many places. Between 2010 and 2015, malaria incidence among

populations at risk (the rate of new cases) fell by 21% globally. In that same period,

malaria mortality rates among populations at risk fell by 29% globally among all age

groups, and by 35% among children under 5. Sub-Saharan Africa carries a

disproportionately high share of the global malaria burden. In 2015, the region was

home to 90% of malaria cases and 92% of malaria deaths.

We choose severe malaria as our case study during community clinical posting at

Bukuru express Primary Health Care (PHC). We found out the case when the patient

was first admitted into the PHC 15/08/2017 in the ward room on bed 3, the patient

was brought by her mother and siblings. The patient is a 9year old B.M a primary 3

pupil of the government primary school at gyel bukuru. She presented with the history

of chills, headache, tiredness, nausea, vomiting with bitter taste and diarrhea of two

days which equals to 48 hours duration but at arrival which is the third day patient

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was brought in not conscious, severe breathing difficulties and when several

investigation were performed patient has low blood hemoglobin ( severe anemia). The

blood test shows the presence of P. falciparum parasites. .

1.1 OBJECTIVE OF THE STUDY

The objectives of this study can be broadly divided into:

GENENRAL OBJECTIVE:

To provide knowledge about malaria in relation to the condition of the client,

including history, assessment, treatment and management.

1.2 SPECIFIC OBJECTIVE

 To define severe malaria and identify the cause of the disease process
 To identify the life cycle of malaria
 To identify the diagnoses procedure
 To understand the pharmacological treatment.
 To examine and correlate actual assessment of the patient with severe malaria
 To appreciate nursing interventions to put in to practise in rendering care.
1.3 PATIENTS PARTICULARS/ DEMOGRAPHY

The patient bio data are as thus:

Name: B.M

Age: 9 years

Gender: Female

State of origin: Plateau State

Nationality: Nigeria
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Tribe: Berom

Religion: Christianity

Occupation: Student

Address: Behind COCIN church Gyel.

Marital status: Single

Admission status: involuntarily

Number of admission: 1

Diagnosis: Severe Malaria.

1.4 PRESENTING COMPLAINTS

A 9 year old primary school student right handed, English, Hausa and Berom

speaking, Christian , admitted into the PHC with complaints of :

 Chills
 Headache
 Tiredness
 Nausea
 Vomiting with bitter taste
 Diarrhoea

 Unconscious

 Difficulty breathing

 severe anemia

 Blood test shows the presence of P. falciparum parasites. .

A female child, dark in complexion was brought into the PHC wearing a yellow top

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and a blue trouser looking averagely neat and hair fairly kept.

1.5 PROGNOSIS

Most patients with uncomplicated malaria exhibit marked improvement within 48

hours after the initiation of treatment and are fever free after 96 hours. P. falciparum

infection carries a poor prognosis with a high mortality rate if untreated. However, if

the infection is diagnosed early and treated appropriately, the prognosis is excellent.

Physician in charge

Miss B.M has since been admitted and managed in the ward room of the Primary

Health Care facility by the most senior Community Nurse on duty.

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 CHAPTER TWO

LITRATURE REVIEW

2.1 Definition

Malaria is a human disease that is caused by sporozoan parasites (genus plasmodium)

in the red blood cells, is transmitted by the bite of anopheline mosquitoes; and is

characterized by periodic attacks of chills and fever (www.merriam-webster.com).

You cannot get malaria just by being near a person who has the disease.

2.2 A BRIEF HISTORY OF MALARIA

Malaria occupies a unique place in the annals of history. Over millennia, its victim s

have included Neolithic dwellers, early Chinese and Greeks, princes and paupers. In

the 20th century alone, malaria claimed between 150 million and 300 million lives,

accounting for 2 to 5 percent of all deaths (Carter and Mendis, 2002). Although its

chief sufferers today are the poor of sub-Saharan Africa, Asia, the Amazon basin, and

other tropical regions, 40 percent of the world's population still lives in areas where

malaria is transmitted.

Ancient writings and artifacts testify to malaria's long reign. Clay tablets with

cuneiform script from Mesopotamia mention deadly periodic fevers suggestive of

malaria. Malaria antigen was recently detected in Egyptian remains dating from 3200

and 1304 BC (Miller et al., 1994). Indian writings of the Vedic period (1500 to 800

BC) called malaria the “king of diseases.” In 270 BC, the Chinese medical canon

known as the Nei Chin linked tertian (every third day) and quartan (every fourth day)

fevers with enlargement of the spleen (a common finding in malaria), and blamed

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malaria's headaches, chills, and fevers on three demons—one carrying a hammer,

another pail of water, and the third a stove (Bruce-Chwatt, 1988). The Greek poet

Homer (circa 750 BC) mentions malaria in The Iliad, as does Aristophanes (445-385

BC) in The Wasps, and Aristotle (384-322 BC), Plato (428-347 BC), and Sophocles

(496-406 BC). You may be able to prevent malaria by taking medicine before, during,

and after travel to an area where malaria is present. But using medicine to prevent

malaria doesn't always work. This is partly due to the parasites being resistant to some

medicines in some parts of the world.

2.3 AETIOLOGY

Malaria is a protozoal infection (Kumar et al, a. 2009), which can be caused by

several Plasmodium species: P. falciparum, P. vivax, P. ovale, P. malariae and P.

knowlesi (Perkins et al, 2011). Malaria is most commonly transmitted through female

mosquitoes of the Anopheles genus, but can also be transmitted congenitally or

through contaminated blood, for example via blood transfusion or used needles

(Goering et al, 2007). When malaria is transmitted through mosquito bites,

Plasmodium parasites in the form of sporozoites are transferred from the mosquito’s

salivary glands into the person’s bloodstream. The parasites are incorporated by

hepatocytes in the liver, where a maturation process results in schizonts. When the

hepatocyte ruptures, the schizont divides into thousands of merozoites (Goering et al,

2007). These merozoites invade erythrocytes, where they mature into either

trophozoites or gametocytes. The trophozoites of the different species can be

differentiated using microscopic examination (Kumar et al, b. 2007). The trophozoites

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then develop into schizonts, which later rupture and result in more merozoites that can

invade new erythrocytes, thus repeating the cycle. Gametocytes stay inside the

erythrocytes until they are taken up by a mosquito, which is then re-infected; the life-

cycle is complete, with new sporozoites stored inside the mosquito’s salivary glands.

In addition to the stages described above, P. vivax and P. ovale have dormant stages,

hypnocytes, which remain in the liver (Goering et al, 2007).

The Plasmodium life cycle is reliant on the Anopheles mosquito as a vector and an

adequate temperature. Therefore, the geographical distribution of malaria is

determined by the distribution of the Anopheles mosquitoes, as well as areas having

the correct climate. The transmission has traditionally remained at altitudes below

2000 m (Kumar et al, a. 2009). However, in recent years there has been increased

malarial transmission in areas of higher altitudes in Africa, which may be a result of

climate change resulting in increased temperatures in high-altitude areas (McMicheal,

2003). According to the World Health Organization (WHO), malaria transmission

intensity can be divided in four different categories: holoendemic, hyperendemic,

mesoendemic and hypoendemic. Holoendemic includes areas with perennial

transmission of high intensity, where the prevalence of parasitaemia among infants is

above 75%. Hyperendemic includes areas with seasonal transmission of high

intensity, defined as prevalence of parasitaemia above 50% in children between 2–9

years of age. Mesoendemic includes areas with intermediate transmission, defined as

prevalence of parasitaemia in 11–50% of children between 2–9 years of age. Finally,

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hypoendemic includes areas where malaria transmission is low, defined as prevalence

of parasitaemia below 10% in children between 2–9 years of age (WHO, 2002). The

level of transmission intensity can be simplified further into high, moderate and low

transmission areas. High transmission areas include holoendemic and hyperendemic

areas, while moderate corresponds to mesoendemic area and low to hypoendemic area

(WHO, 2010).

Individuals with malaria typically acquired the infection in an endemic area following

a mosquito bite. Cases of infection secondary to transfusion of infected blood are

extremely rare. The risk of infection depends on the intensity of malaria transmission

and the use of precautions, such as bed nets, diethyl-meta-toluamide (DEET), and

malaria prophylaxis.

The outcome of infection depends on host immunity. Individuals with immunity can

spontaneously clear the parasites. In those without immunity, the parasites continue to

expand the infection. P falciparum infection can result in death. A small percentage of

parasites become gametocytes, which undergo sexual reproduction when taken up by

the mosquito. These can develop into infective sporozoites, which continue the

transmission cycle after a blood meal in a new host.

The mechanisms that underlie immunity remain poorly defined. Additionally,

individuals who develop immunity to malaria who then leave the endemic area may

lose protection. Travelers who return to an endemic area should be warned that

waning of immunity may increase their risk of developing several malaria if

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reinfected. These travelers returning to endemic areas are a special population,

sometimes termed visiting friends and relatives (VFRs).

2.4 PATHOPHYSIOLOGY

When malaria infected erythrocytes rupture, merozoites and digestive vacuoles are

released. These vacuoles contain haemozoin, a pigment by-product of haemoglobin

digestion; this pigment activates both the complement system and the coagulation

system, which turns the focus of the immune system away from the merozoites. The

immune response induces cytokine release leading to phagocytation of vacuoles

(Dasari and Bhakdi, 2012), and can result in splenomegaly (Kumar et al, b. 2007).

Each erythrocyte cycle lasts about 48 hours in P. vivax, P. ovale and P. falciparum, and

72 hours in P. malariae (Kumar et al, a. 2009). P. knowlesi has an erythrocyte cycle of

about 24 hours (WHO, 2012). The malaria-infected erythrocytes by P. falciparum

have changed cell surfaces, which affects the interaction with endothelial cells by

making the infected erythrocytes adhere to the vessel walls (Kumar et al, b. 2007).

Research has shown that the Plasmodium species reduces human immune response

towards itself, and through this down-modulation impairs the development of

immunity against malaria. The acquired immunity protects only against clinical

malaria, allowing asymptomatic parasitaemia. Even this degree of immunity takes

years to develop, and requires frequent re-infection over a long time period (Hafalla et

al, 2011). As the immunity depends on exposure, the degree of protection is affected

by the transmission intensity in the area. A correlation between the median parasite

density in febrile patients and transmission intensity has been seen. While 95% of

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febrile patients with P. falciparum had over 200 parasites per microlitre blood in a

high transmission setting, the same number for settings with lower transmission was

90–95%. P. vivax tends to have higher parasite densities than P. falciparum (WHO,

2010).

Plasmodium life cycle (figure 1)

Plasmodium species that infect humans

Until recently, there were four plasmodium species that were considered responsible

for malaria disease in humans: P. vivax, P. falciparum, P. ovale and P. malariae. In

2008, P. knowlesi, a species that used to infect exclusively apes of the genous
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Macaque, was recognised by WHO as the fifth plasmodium species that infect

humans.

Transmission routes

The main mode of transmission of the disease is by bites from infected Anopheles

mosquitoes that have previously had a blood meal from an individual with

parasitemia. Less common routes of transmission are via infected blood transfusion,

transplantation, infected needles, and from a mother to her fetus during pregnancy.

Plasmodium life cycle

The life cycle (Figure 1) is almost the same for all the five species that infect humans

and follows three stages:

(I) Infection of a human with sporozoites

(II) Asexual reproduction

(III) Sexual reproduction

The two first stages take place exclusively into the human body, while the third one

starts in the human body and is completed into the mosquito organism

The human infection begins when an infected female anopheles mosquito bites a

person and injects infected with sporozoites saliva into the blood circulation. That is

the first life stage of plasmodium (stage of infection).

The next stage in malaria life cycle is the one of asexual reproduction that is divided

into different phases: the pre- erythrocytic (or better, exoerythrocytic) and the

erythrocytic phase. Within only 30- 60 minutes after the parasites inoculation,

sporozoites find their way through blood circulation to their first target, the liver. The

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sporozoites enter the liver cells and start dividing leading to schizonts creation in 6- 7

days. Each schizont gives birth to thousands of merozoites (exoerythrocytic

schizogony) that are then released into the blood stream marking the end of the

exoerythrocytic phase of the asexual reproductive stage.

It is worth mentioning that, concerning P. vivax and P. ovale, sporozoites may not

follow the reproduction step and stay dormant (hypnozoites) in the liver; they may be

activated after a long time leading to relapses entering the blood stream (as

merozoites) after weeks, months or even years. The exoerythrocytic phase is not

pathogenic and does not produce symptoms or signs of the disease. Its duration is not

the same for all parasite species.

Merozoites released into the blood stream, are directed towards their second target,

the red blood cells (RBCs). As they invade into the cells, they mark the beginning of

the erythrocytic phase. The first stage after invasion is a ring stage that evolves into a

trophozoite. The trophozoites are not able to digest the haem so they convert it in

haemozoine and digest the globin that is used as a source of aminoacids for their

reproduction. The next cellular stage is the erythrocytic schizont (initially immature

and then mature schizont). Each mature schizont gives birth to new generation

merozoites (erythrocytic schizogony) that, after RBCs rupture, are released in the

blood stream in order to invade other RBCs. This is when parasitaemia occurs and

cinical manifestations appear. The liver phase occurs only once while the erythrocytic

phase undergoes multiple cycles; the merozoites release after each cycle creates the

febrile waves.

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A second scenario into the RBCs is the parasite differentiation into male and female

gametocytes that is a non-pathogenic form of parasite. When a female anopheles

mosquito bites an infected person, it takes up these gametocytes with the blood meal

(mosquitoes can be infected only if they have a meal during the period that

gametocytes circulate in the human’s blood). The gametocytes, then, mature and

become microgametes (male) and macrogametes (female) during a process known as

gametogenesis. The time needed for the gametocytes to mature differs for each

plasmodium species: 3- 4 days for P. vivax and P. ovale, 6- 8 days for P. malariae and

8- 10 days for P. falciparum.

In the mosquito gut, the microgamete nucleus divides three times producing eight

nuclei; each nucleus fertilizes a macrogamete forming a zygote. The zygote, after the

fusion of nuclei and the fertilization, becomes the so- called ookinete. The ookinete,

then, penetrates the midgut wall of the mosquito, where it encysts into a formation

called oocyst. Inside the oocyst, the ookinete nucleus divides to produce thousands of

sporozoites (sporogony). That is the end of the third stage (stage of sexual

reproduction/ sporogony). Sporogony lasts 8- 15 days.

The oocyst ruptures and the sporozoites are released inside the mosquito cavity and

find their way to its salivary glands but only few hundreds of sporozoites manage to

enter. Thus, when the above mentioned infected mosquito takes a blood meal, it

injects its infected saliva into the next victim marking the beginning of a new cycle.

2.5 INCUBATION

Each Plasmodium species has a specific incubation period. Reviews of travelers

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returning from endemic areas have reported that P falciparum infection typically

develops within one month of exposure, thereby establishing the basis for continuing

antimalarial prophylaxis for 4 weeks upon return from an endemic area. This should

be emphasized to the patient to enhance posttravel compliance.

Rarely, P falciparum causes initial infection up to a year later. P vivax and P ovale

may emerge weeks to months after the initial infection. In addition, P vivax and P

ovale have a hypnozoite form, during which the parasite can linger in the liver for

months before emerging and inducing recurrence after the initial infection. In addition

to treating the organism in infected blood, treating the hypnozoite form with a second

agent (primaquine) is critical to prevent relapse from this latent liver stage.

When P vivax and P ovale are transmitted via blood rather than by mosquito, no latent

hypnozoite phase occurs and treatment with primaquine is not necessary, as it is the

sporozoites that form hypnozoites in infected hepatocytes.

2.6 CLINICAL MANIFESTATION

The classic symptom of malaria is high fever spikes every third or fourth day,

depending on the Plasmodium species (Kumar et al, a.2009). This classic fluctuation

is caused by the erythrocyte cycle, but this pattern is not always distinctive. The

fluctuations are less marked with falciparum malaria, and the temperature changes can

be more irregular with all species during the first days of illness. Common symptoms

in addition to fever include vomiting and headache (Kumar et al, a. 2009). The

clinical manifestation is rarely distinctive (Crawley et al, 2010), and even fever is not

always consistent. The lack of fever is not necessarily a sign of mild disease. For

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instance, in one African trial, children between 8 months and 4 years of age without

fever or a history of fever had a higher mortality rate than the febrile children among

admitted children with confirmed malaria (Schellenberg et al, 1999). Muhe et al.

observed that splenomegaly, pallor and history of chills were statistically increased in

patients with parasitaemia. They further theorized that detection of splenomegaly and

pallor could increase the probability of making the correct diagnosis when used by

health workers when other diagnostic possibilities are unavailable (Muhe et al, 1999).

In Tanzania, a trial based on children admitted with malaria infection found pallor in

59% and splenomegaly in 56% of children between 1 and 7 months of age. The

association was weaker in older children, where the signs were present in only 31%

and 39%, respectively (Schellenberg et al, 1999). In their review over symptoms and

signs connected to malaria, Chandramohan et al. found that the clinical aspect alone

was not sufficient to separate malaria from other febrile illnesses. They also found

that predictors associated with malaria differed between locations (Chandramohan et

al. 2002). Most malaria infections cause symptoms like the flu, such as a high fever,

chills, and muscle pain. Symptoms tend to come and go in cycles. Some types of

malaria may cause more serious problems, such as damage to the heart, lungs,

kidneys, or brain. These types can be deadly.

2.7 DRUG

There are a limited number of antimalarial compounds which can be used to treat or

prevent malaria. The most widely used are quinine and its derivatives (chloroquine,

amodiaquine, primaquine and mefloquine), antifolate (proguanil, chlorproguanil,

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pyrimethamine, and trimethoprim) and sulfa (dapsone, sulfalene, sulfamethoxazole,

sulfadoxine, and others) combination drugs, as well as artemisinin and its derivatives

(artesunate, arteether, artelinate, artemether, dihydroartemisinin). Antibiotics such as

tetracycline and its derivatives (doxycycline) can also be used for treatment and

prophylaxis in combination with quinine. As a result of widespread drug resistance,

many malaria endemic regions have shifted to ACT where artemisinin is partnered

with a drug with long half life such as mefloquine or lumefantrine, (Mutabingwa and

Adamu, 2013).

Other effective drug combinations such as atovaquone-proguanil (MalaroneTM) are

also available but their use is compromised by high costs. The use of combination

therapy, especially when partner drugs have different mechanisms of action has the

potential of acting synergistically allowing rapid parasite clearance and at the same

time inhibiting the development of resistance to either of the components.

2.8 DIAGONOSIS

Early diagnosis and treatment of malaria reduces disease and prevents deaths. It also

contributes to reducing malaria transmission. In April 2015, WHO that recommends

that all cases of suspected malaria be confirmed using parasite-based diagnostic

testing (either microscopy or rapid diagnostic test) before administering medication.

Results of parasitological confirmation can be available in 30 minutes or less.

Treatment, solely on the basis of symptoms should only be considered when a

parasitological diagnosis is not possible. More detailed recommendations are

available in the (WHO, 2015).

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2.9 MANAGEMENT

Early malaria case detection and prompt treatment with safe and effective antimalarial

drugs still remains the mainstay of malaria case management (Winstanley, 2000). If

not properly managed, either due to missed or delayed diagnoses, malaria may

progress from mild through complicated to severe disease. Case management usually

depends on the severity of infection, age, therapeutic efficacy of the antimalarial drug

as well as their costs and availability (White, a. 1996). Gestational age is also an

important issue to consider prior to prescription of any drugs due to potential risks of

harming the embryo/foetus (Nosten et al. 2006).

Antimalarial drugs work by disrupting processes or metabolic pathways in different

sub- cellular organelles and most of them target the erythrocytic stages. For effective

treatment, antimalarial drugs must be fast acting, highly potent against blood stage

parasites, with minimal toxicity and should be readily available and affordable to

residents of endemic regions (Greenwood et al. 2008).

During pregnancy, uncomplicated malaria is treated by quinine as the first line (in

order to avoid risk of harming the embryo/foetus) and artesunate for seven days if this

treatment fails for infections occurring in the first trimester. In the second and third

trimester, first line treatment is usually an ACT known to be effective in the area or

artesunate and clindamycin or quinine and clindamycin. For the Tanzanian setting,

treatment is either by artemether lumefantrine (ALU) for uncomplicated malaria and

intravenous quinine for severe malaria. Elsewhere, severe malaria during the second

and third trimester is treated by parenteral artesunate instead of quinine whereas

23
during the first trimester parenteral quinine is used (WHO, 2010).

Recent studies have shown parenteral artesunate is more effective than quinine in

resolving fever and parasite clearance for severe malaria cases in children (PrayGod et

al. 2008). Quinine is used during pregnancy despite side effects such as quinine-

induced hyperinsulinaemic hypoglycaemia that necessitates careful monitoring of

glucose level (Pasvol et al. 2005; White et al. b. 1983). As a strategy to prevent

adverse pregnancy outcomes due to malaria infection during pregnancy, all pregnant

women visiting the antenatal clinics (ANC) are given intermittent preventive

treatment using sulfadoxine pyrimethamine (IPTp-SP). This is in accordance to the

WHO recommendations on malaria prevention during pregnancy. Generally

medicines usually can treat the illness. But some malaria parasites may survive

because they are in your liver or they are resistant to the medicine.The best available

treatment, particularly for P. falciparum malaria, is artemisinin-based combination

therapy (ACT) (WHO, 2013).

2.10 COMPLICATIONS

Roca-Feltrer et al. estimated the incidence of severe malaria to be 5.7/1000 per year

among children below five years of age in malaria endemic areas (Roca-feltrer et al.

2008). Patients with severe falciparum infections often have high parasite counts, and

may develop severe symptoms from several organ systems (Craweley et al. 2010).

The severity of the disease may increase in a short time-span, especially in children

where the situation can deteriorate within hours (Kumar et al. a. 2009. Schellenberg et

al. found that among malarial admissions, half of the mortality cases died within the

24
first 24 hours (Schellenberg et al. 1999).

A multicenter study from WHO have measured the prevalence of different clinical

features in children with severe falciparum malaria. They found that 54.1% had severe

anaemia, 17.7% had cerebral malaria and 13.2% hypoglycaemia, while jaundice and

respiratory distress were present in less than 2% (WHO, b. 2012). Kidney failure,

metabolic acidosis and high lactate levels have also been associated with severe

malaria (Perkins et al. 2011).

Cerebral malaria is a clinical syndrome where the patient has reduced consciousness

that can develop into coma or death (Kumar et al. 2009). Clinical manifestations

connected to impaired consciousness include convulsions, reduced response to painful

stimuli, abnormal motor posturing and increased intracranial pressure (WHO, a.

2012).

Among the children with known outcome 14 days after they were admitted for severe

falciparum malaria, almost 10% had died and 1.7% had neurological sequelae. Most

of the children made a full recovery. In that study, the case-fatality rate of cerebral

malaria was estimated at 17.7% (WHO, b. 2012). Epilepsy may also be a late sequela

to cerebral malaria, which can appear months after the illness itself. It has been

estimated that as many as 10% of children with cerebral malaria may go on to develop

epilepsy (WHO, a. 2012).

Severe anaemia has been associated with malaria infection (Calis et al. 2008). Malaria

infection cause anaemia through destruction of infected and uninfected erythrocytes,

25
insufficient erythropoiesis, folate depletion and reduced proportion of red blood cells

in the circulation, through sequestration and splenomegaly (Kumar et al. a. 2009).

Perkins et al. claims that the most important cause of severe anaemia with P.

falciparum is suppression of the erythropoiesis (Perkins et al. 2011). The anaemia may

develop rapidly or be of a more chronic character (WHO, a. 2012), the latter caused

by persistent infections (WHO, 2001).

Hansbroek et al. observed reduced erythrocyte production in almost half of the

children with severe anaemia. A fifth of these had another mechanism causing

anaemia in addition to the reduced erythrocyte production. For those who tested

positive for malaria, the proportion with failure to produce erythrocytes was 42.1%. In

this study, they also found that to reverse the production deficit, all the aetiological

components should be addressed (Boele et al. 2010), which may include bacteraemia,

hookworm infection, HIV infection or vitamin deficiency (Calis et al. 2008).

Schellenberg et al. found that hypoglycaemia was an independent risk factor for

mortality among children admitted to the hospital because of malaria (Schellenberg et

al. 1999). Hypoglycaemia has also been estimated to double the mortality in children

when accompanying cerebral malaria or severe anaemia (WHO, 2012).

Even though P. falciparum is responsible for most of mortality from severe malaria,

other species may progress in severity as well. There are many similarities between

severe infections caused by P. falciparum and P. vivax, though the latter is less

common (WHO, a. 2012). Vivax malaria often includes respiratory symptoms, and

patients with severe disease may develop acute respiratory distress syndrome

26
(ARDS). Increased alveolar permeability through cytokine release is believed to be

the mechanism for this. Severe vivax malaria may also progress to coma, though this

is rare. As the mechanism for falciparum malaria is connected to its sequestration, the

mechanisms for vivax- induced coma are more uncertain. Vivax malaria resulting in

renal failure has also been described (Anstey et al. 2009). As P. vivax has hypnozoites,

relapse of infection is common. These relapses make the chronic complications to

malaria infections, such as anaemia, more severe (Anstey et al. 2009). Severe malaria

caused by P. knowlesi is similar to severe falciparum malaria, but without affecting

consciousness (WHO, 2012).

27
 CHAPTER THREE

1. Intergumentary System:

A) Skin

 skin dryness

 Increase skin pallor

 Increased skin fragility

 Increased perspiration

B) Hair

 Thinning of scalp hair

 Slower nail and growth

C) Muscle Mass

 Decrease in muscle mass and weight gain.

2. Neuromuscular System.

 Decreased power of skeletal/muscle

 Occasionally impaired balance.

3 Respiratory System

 Difficulty breathing

4. Cardiovascular System.

 Tachycardia

 decrease in blood (anaemia)

5. Gastrointestinal System

28
  there is signs of constipation and diarrhoea

6. Urogenital System

 Dysuria

 Urinary urgency and frequency

3.1 MEDICAL CARE OF PATIENT

 Artemisinin-based combination therapy (ACT)

 Panadol half to one tablet every 4-6 hours

 Psychotherapy

 Rehabilitation

3.2 NURSING CARE OF THE PATIENT

 Admit the patient on a comfortable bed

 Assess patient vital signs

 Make the environment suitable for her age.

 Provide a caring, therapeutic environment.

 Establish rapport with the patient.

 Encourage her to eat and bathed.

 Administered prescribed drugs such as Artemisinin-based combination therapy

(ACT), Panadol and others as prescribed

 Tepid sponge where and necessary

3.3 TABULATION OF DRUGS GIVEN TO MISS G. R

NAME GROUP ROUTE INDICATION SIDE EFFECT NURSING
OF IMPLICATIONS
29
DRUG
ACT Antimalarial oral To treat Advice on
malaria  Headache increase on water
 Tachycardia intake.
 Arrhythmias
 Blurred vision
 Dry mouth
 Drowsiness
 Dizziness
 Loss of appetite
,nausea

Panadol Antipyretics Oral or To reduce Liver damage Avoid excessive

I.M body intake
temperature
B Oral To Improve Eat food and
complex feeding drink water often

3.4 COMPLICATIONS OF THE PATIENT

Patient has not developed any complication during the cause of management,

she responded well to all her treatments.

30
 3.5 NURSING CARE PLAN OF MISS G. R DATE: 16/12/2016
NURSING DIAGONESES OBJECTIVES INTERVENTION RATIONALE EVALUATION
Ineffective breathing pattern Patient will breath at the rate of  Monitor vital signs  To provide ongoing Patient breath with ease
related to disease severity evidence 18-22 times per minute within and auscultate data on patients between 18-22 times per
by difficulty to breath well. 48 hours of admission. lungs every 2-4 response to therapy minutes within 48 hours of
hours.  To assess admission.
 Monitor arterial oxygenation status.
blood gases if  To maximize lung
prescribed expansion.
 Position patients in
semi-flowlers or
other comfortable
position for
breathing.
Altered nutrition less than body Patient will eat at least of meal  Monitor weight  It serve as indicators Patient eat more than ¾ of meal
requirement related to anorexia, served at any time from second and laboratory of patients response served from second day of
dietary restrictions nausea loss of day of nursing intervention. values to treatment intensive nursing intervention.
nutrients from vomiting and  Administer total  To provide
impaired digestion evidence by parenteral nutrition carbohydrates and
body weakness if prescribed aminoacides to
 Implement prevent negative
measures to reduce nitrogen balance
pain and nausea  To increase patient
 Provide oral care desire to eat
before and after  Helps to decrease
meals foul taste and odour
that inhibit appetite.
Anxiety related to the new Patient fear will be allay  Put patient in a  Comfortable bed help Patients fear was allayed
environment evidence by crying throughout hospitalization. good comfortable to relax patient throughout hospitalization.
bed thereby reducing the
 Create good anxiety.
rapport with the  Creating good
patient rapport with the child

31
 Reassure patient will helps the child to
and the parent that trust the nurse better.
with good  It makes patient to
medication and her comply with drugs
compliance with thereby hastening her
drugs will improve treatment and relief
her status soon. anxiety.

32
 CHAPTER FOUR

DAILY PROGRESS WITH NURSING INTERVENTION

4.1 DAILY PROGRESS OF PATIENT

Day 1- 15/08/2017 patient body temperature is reduced but not stable.

Day 2- 16/08/2017 Patient temperature is stable; she eats well and talks

about home.

Day 3-17/08/2017 Patient was discharged home and given take home

medications

4.2 HEALTH EDUCATION

 The family members should a close look on the child and report any abnormal

changes, elevated temperature etc

 The relatives should always make nutritive food available and clean water for

drinking.

 Give the patient bath when the temperature is high.

 Tepid sponge patient whenever the temperature is high and how to do it

 Parent should ensure the child sleeps under treated mosquito net at home.

4.3 DISCHARGE SUMMARY

 Nil fresh complaint today

 Temperature is now stable

 Sleeps and eats well

 Discharged home on Tabs

 To be seen at the clinic in a week time.

33
4.4 ADVICE ON DISCHARGE

 Educate the family about the impact of untreated body temperature on

the individual and functional ability

 Tell the client and family to report any similar signs and symptoms

 Educate the family about what do whenever the temperature gets high

before coming to the PHC.

 Inform the family to come back if there is abnormal rapid change.

 Tell clients and family about the need to continue medication and

discuss with and when to come back to the PHC.

 Advice the family to ensure the child sleeps under treated mosquito net at

home.

4.5 HOME VISIT

 Sleeps well

 Eats well and takes a lot of fluid especially water.

 Relate well with family members and functions well.

34
 CHAPTER FIVE

5.1 SUMMARY

B.M is a 9 year old student that was brought into the PHC by her mother and siblings,

she is a new patient of the PHC diagnosed with severe malaria on 15/08/2017. Until

the incidence she has been physically active and relate well with family and friends.

This admission is her first hospitalization. Since admission, Miss B. M condition has

gradually improved.

She was discharge on 17th, August 2017, communicating normal, with good appetite

and responding well to treatment.

5.2 CONCLUTION

In summary, severe malaria is a serious disease condition that demands specialist

assessment and management. This work reviews that severe malaria is treatable but

when the treatment is delayed can cause organs damage and can even lead to death.

Early diagnosis and treatment is essential as it prevent major complications from

occurring.

The disease affects more pregnant women, children and the aged, focus has recently

shifted from cure to prevention of the disease (WHO 2013). Treated nets are made

available to reduce contact with the vectors, Environmental sanitation is encouraged

to destroy breeding spaces for the vectors and antimalarial medications are made

available for pregnant women in mild doses. It will cause less to prevent than to cure.

35
5.3 RECOMMENDATION

To prevent relapse of the condition and to provide long term monitoring, the

following are recommended:

 The healthcare provider should be adequate in various PHC.

 More PHC should be built in larger communities.

 The government should play its part by increasing numbers of treated nets and

it accessibility.

 The government alone side other non-governmental organization should

support the financial expenses of malaria such as making some drugs available

and free.

 Seminars for the general public on the need to support and participant in the

eradication of malaria by environmental sanitation.

 Awareness should also be done on the important of the used of treated nets.

 More Research should be conducted on these conditions.

36
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