Paediatrics

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Common child health problems

 Malaria
 Malnutrition
 Diarrhea
 Upper respiratory tract infections e.g. cough &pneumonia
 Skin infections
 Neonatal infections
 All immunizable diseases
 Mumps
 Chicken pox
 Worm infestations
Etc.
Main groups of diseases with their causes
Disease group Cause Examples
Genetic Inherited Sickle cell disease
Asthma
Deficiency Intake of inadequate essential PEM
nutrients Anaemia
Environmental - Mostly by - TB
microorganisms - Tetanus
- Can be social factor - Depression
- Physical factor - Anxiety
- Economic factor
Degenerative - due to wear and tear of - arthritis
the body - heart failure
Metabolic - due to disorders of bio- - diabetes
chemicals in the body
Malignancy - change in cell growth - cancer of cervix
due to known or - cancer of liver
unknown cause

DISEASES OF RESPIRATORY SYSTEM


PNEUMONIA

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Definition
(i)This is an inflammation of the alveoli of the lungs which becomes
airless and solid with exudate
(ii)Is an inflammatory condition of the lung caused by infection,
usually bacterial or viral.
There are many numbers of different types, causes and possible
methods of classification.
Aetiologically, they can be divided into two groups:
I. Non – specific pneumonia e.g. Lobar: in which the disease is caused
by specific pathogenic micro organisms
ii. Non – specific or aspiration pneumonia: in which some
abnormality in the respiratory system predisposes to the invasion of
the lungs by virulent organisms. In this form the infection reaches the
lungs by aspiration.

Pathology
As a result of the infection, the alveoli become filled with serous fluid
and with inflammatory cells. The area of the lung involved is said to
have gone consolidation.
As recovery takes place in the alveoli, the inflammatory material is
coughed up: in the early stages this sputum often contains many red
cells and is rusty in appearance. Later as the white cells invade the
alveolar exudate, the sputum becomes yellow and purulent.

Lobar (Pneumococcal) pneumonia

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Exciting causes
Pneumococcus or Klebsiella bacilli
Predisposing causes
 Chills
 Malnutrition
 HIV infection
 Pre-existing lung or heart disease
 Renal failure
 Diabetes
 Rarely alcoholic excess
 The elderly
Clinical features
The clinical presentation depends on the type and the causative
organism.
 Onset Is Sudden, With A High Fever Often 39 – 40 o C and Is
Often Accompanied By
 Shivering Attack,
 Vomiting And
 Convulsions in Children.
 Malaise,
 Anorexia,
 Headache And
 Aching Pain in The Limbs
Presentation

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 Chest pain: a severe pain in the chest over the affected lobe of
the lung may be present owing to the frequently accompanying
pleurisy. This pain characteristically catches the breathing so
that the patient is nervous of taking a deep breath.
 Cough: there is a short painful cough, dry at first later
productive with rusty sputum or frank blood. The sputum is very
thick and tenacious. For this reason, also the cough which is
always present is always present is short and suppressed.
 Respiration: the respirations are rapid about over 60b/m in
children. Alae nasal may be seen to move with respiration.
 The pulse rate rises but not to same extend as respiration.
 Herpes labialis: the face is flushed and herpes febrile is very
commonly present on the lips and cheeks. Herpes labialis is
most commonly associated with lobar pneumonia or common
cold.
 Cyanosis: in severe cases the breathing may be very distressed
and cyanosis is present. In these severe attack’s delirium may
also occur.
 Physical findings
On examination with the stethoscope, typical alteration in breath
sounds over the consolidated lobe may be heard.
 Chest X-ray
May be carried out too confirm the diagnosis and will show the
solid (consolidated) lobe.

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Diagnosis
Sputum for AAFBs, culture and sensitivity and bacteriological
examination
Management
Nursing care
Admission
 The patient should be propped up in bed in a comfortable
upright position, in a well-ventilated room.
 Sputum mug provided and the patient is encouraged to cough up
the sputum and the patient should be disturbed as little as
possible.
 Tepid sponging done as frequently as possible if the temperature
exceeds 39.5oC.
 Oxygen administered when there is cyanosis and dyspnoea
 Psychological treatment
 Reassure the parents/caretaker of the child about the condition
 Physiotherapy patients may be required to carry out breathing
exercises by giving them balloons to blow in air for several
times in a day, movement of the legs and to cough up sputum.
 Postural drainage is carried out in the morning and afternoon.
 Diet: in early stages should consist of liquids and semisolids
graduating to normal.
 General nursing care.

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Treatment
 Benzyl penicillin 50,000 IU/kg IM every 6 hours for 2 days.
Then PPF 800,000 IU IM once daily for 5days.
 If pleuritic pain makes breathing difficult, non-steroidal anti-
inflammatory agents e.g. aspirin or ibuprofen may be needed.
Complications
Pulmonary complications
 Infection may spread to the other wards
 Delayed resolution leading to pyothorax and lung abscess
 Bronchiectasis
 There may be underlying lung cancer, PTB, fibrosis and
Atelectasis
Pleural complications
 Sterile pleural effusion which may be small and requires no
treatment since it causes no symptom.
 Empyema: especially when inflammation of the pleura goes to
suppuration accompanied by fever.
Cardiovascular
 Peripheral circulatory failure
 Acute pneumococcal pericarditis and endocarditis
 Cardiac failure as a result of distressed myocardium
 Venous thrombosis in the lower limbs
Neurological complications
 Meningism common in children
 Pneumococcal meningitis

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BRONCHOPNEUMONIA
This is the inflammation of the terminal bronchioles and air sacs due
to various organisms.
Causes (see treatment guidelines)
Predisposing conditions
 Infectious fevers such as measles and whooping cough in
children.
 Age especially children and elderly
 Dry or dusty conditions especially the dry months of the year,
the old and the frail are liable to respiratory infection leading to
the development of pneumonia
 Congestion of the lungs as a result of CCF
 Collection of sputum following a general anaesthetic

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TUBERCULOSIS
This is the name given to the illness caused by infection with tubercle
bacillus.
There are two types of tubercle bacillus:
 The human type: which is endemic in man and can be spread
from person to person
 Bovine type: occurs in cattle but can be spread to man by
drinking contaminated milk or eating an undercooked food.
TB can affect many parts of the body. The lungs are the organs most
commonly affected, but TB can also affect the glands,
meninges, bones, kidneys, joints, abdomen or ovaries.
Clinical types
 Pulmonary TB or open lung TB
 Non – pulmonary TB or extra-pulmonary TB.
PULMONARY TUBERCULOSIS
This is an infection of the lungs due to tubercle bacilli
(mycobacterium tuberculosis)
Causes
Exciting – tubercle bacilli
Predisposing factors
i-Natural resistance: it is common in people with low resistance to
TB
ii-Acquired immunity

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 The nature and the effect of a person who had a primary TB and
has recovered and given acquired immunity is likely to develop
active TB
 Massive infection and re-infection are quite common in children
especially by infected parents or in overcrowded environment
 Age and sex: TB tend to affect young people more since they
live together especially females
 Poor housing associated with overcrowding increases the risks
of massive infection and re – infection
 The disease tends to occur more frequently in poor community
 Certain occupation has direct influence over the occurrence of
PTB e.g. nurses lab technicians and doctors
 Certain medical conditions affecting individual patients e.g.
DM, measles, malnutrition, whooping cough and HIV/AIDS
 Bad habits such as random spitting, sneezing or coughing
Mode of spread
 Contact with tuberculous sputum
 Inhalation of sputum which may be expectorated by careless
individuals so that it dries up and the TB bacilli accumulates in
the dust to be inhaled
 Drinking contaminated milk from TB cows
 Direct inhalation from mothers especially children

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Clinical features
 Clinical Features of a Constitutional Disorders with Loss Of
 Weight,
 Loss of Appetite,
 Malaise,
 Low Graded (Hectic/Habitual) Fevers,
 Profuse Night Sweats
 And Fatigue
 A Persistent Cough Lasting for More Than Three Weeks
 Haemoptysis: There May Be Bloodstained Sputum or Sudden
Coughing Up of Bright Red Blood Due to Erosion of An Artery
in The Cavity
 Chest Pain
 Patient Who Present with Pneumonia but Fail to Respond
Completely to Antibiotics May Have Underlying Chronic TB
 Pleural Effusion May Also Occur.

Investigations
 Chest X-ray
 Sputum for AAFBs and culture
 Blood: full Hemograms especially ESR and lymphocytes

Management

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Nursing care
Rest:
The patient is admitted in TB (Sanatorium) ward, isolated and kept in
bed until the acute symptoms have subsided.
Notification should be done to the DDHS or the relevant authorities.
The majority of these patients are ambulant throughout the course of
treatment and some of them remain at work.
Isolation
The patients who are excreting tubercle bacilli are potentially sick and
should be isolated though most of them are treated as outpatients.
Those admitted should be isolated or sanatorium treated for at least 2
months until when the sputum is negative on three consecutive tests.
Health education is done on all aspects of prevention, control and
compliance to treatment.
Fresh air
It is necessary that the patient should be kept in an open room.
Windows opened day and night and should not be closed for any cold
or rain or fever or any other symptoms
Diet
Patients who are undergoing treatment in sanatorium are provided
with varying and satisfying diet adequate to maintain body weight. A
high protein diet with plenty of fluids is given orally.
Weekly assessment of weight.

Gradual exercise

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When early symptoms have entirely disappeared under the influence
of chemotherapy, the patient should be put on gradual exercise by
means of which the activity of the pulmonary circulation is slowly
and gradually increased. The exercise should start with a short walk
and slow pace, gradually lengthened until the patient can cover 5km
without ill effect.
Gradual labour
This is begun soon after the patient can carry some simple work for
himself. In sanatorium, the course of graduated outdoor labour starts
with slight work or washing until he is able to do a heavy independent
work. Should acute symptoms return the patient is returned and
confine to bed.
Chemotherapy
The country has adopted community – based TB care with DOT
(directly observed short course).
The requirements for adequate chemotherapy are:
 An appropriate combination of ant-tuberculous medications to
convert from smear positive to smear negative and to prevent
the development of resistance to those medications
 Prescribed in the correct dosage
 Taken regularly by the patient
 For a sufficient period to prevent relapse.

The treatment is divided into:

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 An initial (intensive) phase of 2 – 3 months since an initial
course of four medications has the advantage of being more
effective in eliminating micro-organisms and in minimising the
influence of micro-organisms which are resistant to medications.
 A second continuation phase of 4 – 6 months, depending on the
drug combination used. This ensures that the patient is
permanently cured and does not relapse after completion of
treatment. The continuation phase does not require as many
medications but requires a sufficient duration to ensure success.

TB treatment regimens are expressed in a standard format e.g.


2 EHRZ / 6 EH where:
 Letters represent abbreviated drug names
 Numbers show the duration in months
 / shows the division between treatment phases
Drugs used are:
E = ethambutol H = isoniazid R = rifampicin
S = streptomycin Z = pyrazinamide

Short Course TB Treatment Regimens

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Patient category Initial Continuation
(Type of TB) phase phase
1. Any form of TB in children
2 HRZ 4 HR
NB. The number preceding the first letter indicates the duration in
months of chemotherapy

Daily Drug Doses (in mg) by body weight


Drug Weight (kg)
5 -10 11 - 20 21 - 30 31 - 50 > 50
Streptomycin (S) 250 500 500 750 1,000
Isoniazid (H) 100 100 200 300 300
Rifampicine (R) 150 150 300 450 600
Pyrazinamide (Z) 500 500 1,000 1,500 2,000
Ethambutol (E) - - - 800 1,200

Note
 streptomycin: for patients >40 years and <50kg should be given
750mg instead of 1g
 Ethambutol: is not recommended for children <6years

Preventive and control measures


 Early detection of cases and tracing of contacts

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 Prompt and adequate treatment with anti TB drugs till cure is
achieved
 Isolation of sputum – positive patients
 Avoidance of over crowding
 Drinking properly boiled milk
 BCG immunisation to all children
 Good nutrition
Complications
 Massive haemoptysis i.e. coughing up >250 ml of blood per
episode
 Spontaneous pneumothorax
 Pleural effusion
 TB peritonitis
 TB meningitis
 Bone TB

ASTHMA
BRONCHIAL ASTHMA

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This is an Immunological allergic disease characterised by chronic
inflammation of the lower airways, the end result of which can be
permanent structural damage in the lungs. It consists of attacks of
reversible narrowing of the small airways causing difficulty in
breathing, with expiratory wheezing. This restriction of the airways is
not permanent and is due to:
 Bronchospasm: due to tightness of the constricting muscles of
the smaller bronchi
 Congestion and thickening of the lining of the bronchial tree:
due to oedema of the mucous membrane of the bronchi
 Secretion of large amount of mucus into the bronchial tree.
Incidence
More common in children and adolescents although it may occur in
early adulthood.

Aetiology/causes
The exact cause of asthma is not known; neither is the reason for its
increasing incidence. However, there are many factors, which can
cause or precipitate an asthmatic attack
 Unknown factor: asthma can begin later in life and is sometimes
called intrinsic asthma.
 Allergy: asthmatic attacks can occur as a manifestation of
hypersensitivity to certain foreign substances. This type of
asthma begins usually in childhood or adolescence. Allergy
means an excessive reaction to certain environmental substances

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and these include pollens, animal hairs, house dust, face
powders, perfumes or sudden exposure to cold air. Other factors
include certain foods such as eggs, milk, beans, chocolate or
taking drugs such as Aspirin.
 Psychological disturbance: anxiety, worrying emotional stress
and undue exercises. Other patients develop an attack due to
conditioned reflex e.g. a sight of an artificial rose may
precipitate an attack.
 Infections: any upper respiratory tract infection, even a heavy
cold, can set off an attack in an asthmatic subject.
Clinical features
 Onset: the attack of asthma usually begins fairly sudden with
wheezing and a sense of tightness in the chest.
 Dyspnoea: the patient experiences intense dyspnoea. Expiration
becomes conscious and exhausting in comparison to inspiration,
which is short and gasping. Use of accessory muscles of respiration
may occur
 Wheeze: there is wheezing on expiration and this aggravates the
dyspnoea. The patient adopts an upright position fixing the shoulder
girdle to assist the accessory muscles of respiration. Expiration is
prolonged with high - pitched wheezes throughout the lungs.
 Cough: the patient coughs up copious viscid sputum.
 In severe cases, restlessness, anxiety, tachycardia, and cyanosis
usually present as a later sign. The duration of the attacks varies
considerably, usually for a few hours.

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STATUS ASTHMATICUS
This is the term used to describe a severe and persistent attack of
asthma sometimes continuing for many hours or even days. This is
associated with extreme respiratory distress and arterial hypoxaemia.
The patient becomes exhausted and demoralised due to lack os sleep
and the physical effort of breathing. There is often a cough with thick,
tenacious sputum. Cyanosis and sweating with a rapid pulse rate and
sometimes low BP. This can lead to mental confusion due to lack of
oxygen or even to coma with a fatal outcome.

Physical signs in the chest


 During paroxysm, the chest is held near the position of full
inspiration. The percussion note may be hyper resonant.
 Between paroxysms there are usually no abnormal physical
signs except in patients with chronic asthma, who are seldom without
rhonchi. Severe asthma starting I childhood usually causes a
“pigeon’s” chest deformity.

Investigations
 Chest X-ray

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 Pulmonary function test: forced expiratory volume in 1 second
(FEV1), forced vital capacity (FVC) or peak expiratory flow rate
(PEFR).
 Skin sensitivity test

Management
The following measures may be of value in the management of
patients with bronchial asthma
 Reduction to exposure to relevant allergens
 Hypo sensitisation which may prevent damaging antigen –
antibody reactions
 Drugs such as bronchodilators or corticosteroids which control
or suppress clinical manifestation of asthma
 Measures to counter the effect of aggravating factors such as
infection, exercise and emotional stress.
1.Avoidance of allergens
There are a few instances in which a single allergen can be identified
as the cause of attacks of asthma. These include pollens, mites, animal
dander, drugs such as aspirin and certain articles of the diet. Attempts
should be made to avoid such allergens.

2.Hypo sensitisation

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This involves the subcutaneous injection of initially very small, but
gradually increasing doses of extracts of allergens believed to be
responsible for the patient’s asthma.
3.Drugs which control or suppress the clinical manifestation of
asthma
 General principles: it is important to distinguish between
bronchodilators which have a direct and immediate effect on airflow
obstruction, and corticosteroids which relive or prevent airflow
obstruction indirectly by their less rapid anti-inflammatory action. IV
aminophylline is often an effective treatment for severe acute asthma.
 Episodic asthma: where episodes of asthma are mild and
infrequent, they can be controlled by inhalation by a bronchodilator
inhaler e.g. Salbutamol inhaler prn as required. When the episodes are
more frequent, this should be supplemented by regular prophylactic
measure such as corticosteroids.
General management
Whether the patient suffers from episodic or chronic asthma, the
following general principles are essential to successful management:
 The nature of the disease and the action of various drugs must
be explained to every patient.
 The patient should be taught how to recognise ‘danger signs’
such as failure to respond to bronchodilator aerosol, and how to deal
with them.

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 All patients must be taught how to use the various types of
inhaler. If they are unable to use one type efficiently, another type
should be substituted.
 It is as important to secure patient compliance in the dosage of
aerosols as of tablets. Excessive use of a bronchodilator aerosol is as
much the fault of the prescriber as it is of the patient.
Drugs
Uncontrolled asthma
Adult and children > 12 years
Treat as an out – patient
 Give salbutamol 5mg by nebuliser or inhaler 2 puffs (200μg)
every 10 minutes for 30 – 60 minutes. Monitor response 30 minutes
after the dose.
 If the patient says s/he feels better, give Prednisolone 30 – 60mg
as single dose or in 2 – 3divided doses.
Acute severe asthma
This is treated as an emergency.
 Oxygen 40 – 60%
 Give salbutamol 5mg by nebuliser or 2 inhaler puffs (200μg)
every 2 – 5minutes for 20 puffs
 Prednisolone 30 – 60mg single dose or hydrocortisone 200mg
IV bolus stat
 Monitor response 30 minutes after the nebuliser

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Life threatening asthma (status asthmatics)
This should be treated as an emergency and requires constant
supervision, sometimes in an intensive care unit.
 Steroids are lifesaving and should be given in adequate dosage
from the moment it is clear that previous remedies have been
ineffective.
 Regular bronchodilators are given by nebuliser
 Intravenous therapy may take the form of infusions of
aminophylline
 Oxygen should be given by nasal catheter.
 In no condition is good nursing care more important. Patients in
status asthmaticus are frightened and exhausted and exhausted and the
nurse can do much to give reassurance and emotional support as well
as to see to the physical comforts. It is important to make sure that an
adequate intake of fluid is maintained and the patient is encouraged to
take a light diet.

Medicines
 Immediately give Prednisolone 30 – 60mg single dose or
hydrocortisone 200mg IV bolus stat. When the patient improves, taper
off the dose of Prednisolone gradually.
 Oxygen 40 – 60%
 Salbutamol 500 micrograms SC or aminophylline 250mg slow
IV bolus, but not with patients already taking oral theophylline.

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 If there is suspicion of infection (fever, purulent yellow
sputum), add 7 – 10 days course of an antibiotic e.g.
 Amoxicillin 500mg every 8 hours. Child: 15mg/kg per dose OR
 Cotrimoxazole 480mg every 12 hours. Child: 24mg/kg per
dose
 Alternative in severe infection:
 Benzyl penicillin 1 – 2 MU IV or IM every 6 hours for 5days.
Child: 50,000 IU/kg per dose.

Preventive measures
Allergy
Careful questioning of the patient is the best way of finding out what
factors bring about the attack and consequently how to avoid them.
When asthma appears to be due to hypersensitivity to an inhalant or
ingestant, an attempt should be made to remove the suspected
substance from the patient’s environment.
Infections
Asthmatics should be started on antibiotics as soon as there is
evidence of URTI. Emotional disturbance (factors)

This should be controlled since emotional factors can precipitate


asthma. The social and psychological background of the patient
should be considered and discussed.
Occasionally the advice of a psychiatrist may be necessary.

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CONDITIONS OF CARDIOVASICULAR SYSTEM
ANAEMIA
Definition: is a state in which there is a reduction in the number of
red blood cell or in the amount of Hemoglobin or alteration in the
shape or size of the red blood cell. This reduction can be acute in
origin as seen in
 epistaxis,
 Hemoptysis,
 hematemesis,
 post-partum hemorrhage,
 accidents that cause blood vessels and internal organs to rupture.
It may be chronic because of the underlying conditions such as:
 hemorrhoids,
 cancers,
 ulcers,
 hookworm infestations,
 menorrhagia (abnormally heavy bleeding during menstruation),
 schistosomiasis, etc.
The normal amount of blood in circulation in an adult is
6000mls/6litres and when this amount is reduced, it is called anemia.
The normal number of red blood cells in an adult body is, 4.5-
5millions/mm3 in females, and 5-5.5millions/mm3 in adult men and
when this is low is also called anemia. The normal shape of the red
blood cell is circular and biconcave and allows the cell to pass

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through the blood vessel without any problem. Any abnormality
causes collusion and injuries. The normal size of the red blood cell is
about 7 microns in diameter and any megaloblastic size becomes
difficult to pass through small blood vessels and they are immature in
nature liable to breakages easily. The normal Hb in an adult is adult
man is 14-17g/dl/100ml, and in females = 12-16g/dl/100ml and for
children is higher because the red bone marrows have higher
manufacture rate and anything lower than that cannot carry oxygen
efficiently to all the body cells and the vital organs.
Classification of anemias:
A. According to onset:
- acute e.g.
a) trauma,
b) child birth,
c) surgery, etc.
- chronic type of anemia.
a) hemorrhoids,
b) cancers,
c) ulcers,
d) hookworm infestations, menorrhagia (abnormally heavy
bleeding during menstruation), schistosomiasis, etc.
B. According to the cause:
1. Due to excessive blood loss: acute hypovolemic/post
hemorrhagic type of anemia or anemia due to chronic blood loss.

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2. Due to reduced red blood cell production from the red bone
marrow: as a result of deficiency factors:
 iron deficiency anemia or megaloblastic anemia from deficient
vitamin B12 and folic acid
 pernicious anemia from lack of intrinsic factor that is necessary for
the absorption of vitamin B12.
 anemias of bone marrow failure (hypoplastic anemia) falls in this
classification
 bone marrow cancer or infections,
 fibrosis of the bone marrow
 irradiations
 drugs that destroy the bone marrow
 the chronic diseases.
3. Due to excessive destruction of the red blood cells/hemolytic
anemias: especially from factors outside the red blood cell such as
 trauma,
 chemical agents and drugs/toxic anemia or aplastic anemia,
 infectious agents,
 auto-immune disorders,
 systemic diseases.
4. Due to defective Hemoglobin production and abnormalities in
the Hb: as in sickle cell disease.
 vitamin B12,
 folic acid,
 iron and vitamin C,

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 pernicious anemia from lack of intrinsic factor needed for B 12
absorption. Red blood cell hemolysis from:
 parasites,
 drugs,
 toxins,
 abnormal shapes,
 enlarged spleen,
 trauma, etc.
C. According to the morphologic features/shapes and sizes:
 Anemia where the size and shape of the red blood cells appear
normal. It is called normocytic/normochromic anemia where the
cause is mainly from acute blood loss as seen in acute
hemorrhagic anemia, anemia in pregnancy or in chronic illness
like cancer.
 Macrocytic anemia: where the red blood cell is seen abnormally
large, i.e. = 9 microns in diameter, more than the 7microns in
the normal size. This is seen in deficiency anemias where the
red blood cells remain abnormally large from failure to mature
because of lack of vitamin B12, folic acid and lack of intrinsic
factor. The megaloblasts will be seen.
 Microcytic anemia: this is an abnormal size of the erythrocyte,
i.e. < 6 microns in size as seen in chronic diseases.
 Hypochromic anemia: the erythrocyte appears pale because of
abnormally low Hb content as seen in iron deficiency anemia.

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 Sickle cell anemia: the erythrocyte is sickle –shaped/crescent or
moon-shaped due to presence of an abnormal HbS.
TYPES OF ANEMIAS:
1. Hypovolemic/hemorrhagic anemia: this follows bleeding
internally or externally from any cause, i.e. spontaneous rupture of an
aneurysm, hemorrhagic disorders. When blood is lost a lot, the body
quickly pulls water from tissues outside the blood vessels in an
attempt to fill them up and to maintain the blood pressure. As a result,
the blood is diluted and percentage of RBS is reduced. The body’s
oxygen carrying capacity falls and a person goes into heart attack,
stroke or death.
2. Hemolytic anemia:
 The parasites rupture the red blood cells and reduce the oxygen
carrying capacity.
 Big spleen disease/hyperactive spleen. The spleen may be enlarged
due to many disorders and usually the old red blood cells are
destroyed in the spleen, liver or bone marrow. The spleen traps the
red blood cells and the larger it becomes; the more the red blood cells
are destroyed.
 Obstacles of the blood vessels cause more red blood cell breakage as
they knock against the obstruction. Abnormalities inside the blood
vessels such as aneurysms (pocket in a weakened blood vessel wall),
or in artificial valves, or high blood pressure in the narrow blood
vessels, cause cells to rupture.

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 Antibodies bind to the red blood cells and make the immune system
to break down those cells (autoimmune reactions) when they mistake
these cells as foreign bodies.
 Abnormal shapes of the red blood cells make them to knock the
walls of the blood vessels and break. Sometimes the red blood cells
are deformed, have weak membranes that break easily, or lack the
enzymes needed to function properly and maintain the flexibility that
enables them to travel through the narrow blood vessels as seen in
inherited spherocytosis(inherited disorder in which the normally disk-
shaped red blood cells become spherical in shape), or hereditary
eliptocytosis (red blood cells are oval rather than disk-shaped),or
absence G6PD = GLUCOSE-6-PHOSPHATE DEHYDROGENASE-
an enzyme that helps process glucose in a red blood cell to produce
glutathione which helps to prevent the cell from breaking down(it is
an inherited disorder which affects mainly males).
 Toxins from bacteria and drugs cause the red blood cells to break
down.
 Abnormalities of the Hemoglobin where these red blood cells that
contain abnormal Hb may become misshapen or unable to carry or
deliver an adequate supply of oxygen.
3. Deficiency anemias/nutritional deficiency anemias:
 Iron deficiency anemia: this follows less iron intake in foods that
are rich in iron or if not properly absorbed from the gut wall due:
- to chronic diarrhea,
- malabsorption syndrome,

29
- partial or complete gastrectomy
- clay/pica eating (this causes iron to precipitate as an insoluble
substance within the intestinal tract),
- more loss from excessive bleeding as seen in acute or chronic
bleeding or from gastro intestinal tract bleeding as seen in peptic
ulcers, hiatus hernia, gastritis, cancer, hemorrhoids, diverticula,
salicylates poisoning or in blood donation as one gives away blood
to someone else. Iron is important for formation of Hb within the
red blood cell.
 Megaloblastic anemia: this is due to deficiency of vitamin B 12
(cyanocobalamin/antianemic/extrinsic factor), and folic acid.
Vitamin B12 and folic acid are important for the normal RBC
maturation and for conduction of nerve impulses.
- When food rich in these vitamins are not taken in enough quantities
- if the intestinal bacteria do not produce them,
- if they cannot be absorbed because of lack of intrinsic factor,
- if metabolic disturbances such as pregnancy, hyperthyroidism,
cancer may increase the need for these vitamins to create
deficiency states, the megaloblasts are seen in blood and the red
bone marrow.
 Pernicious anemia: this is due to lack of intrinsic factor especially
if there is atrophy of the glandular mucosa secreting the gastric
juice and the intrinsic factor from the stomach wall. This leads to
less reabsorption of vitamin B12 from the intestinal wall leading to
megaloblastic anemia.

30
 Aplastic anemia/bone marrow failure anemia: aplastic means =
having arrested/deficient development. It is a deficiency of
circulating RBCs owing to the arrested development of red cells
within the bone marrow.
- The cause of this deficient development is unknown but may be
attributed to:
- chromosomal abnormalities,
- tumors,
- exposure to myelotoxins (toxins to the bone marrow) as seen in
large doses of radiant energy rays,
- from drugs such as sulphonamides, anticonvulsants, and
antibiotics-CAF.
 Hypo plastic anemia: reduced production of RBCs: by the red
bone marrow due to the aplastic factors.
Signs and symptoms of anemia/according to types:
Hypovolemic anemia:
 Restlessness, dizziness, fainting, thirst, pallor(extreme),
sweating(excessively), rapid thread pulse, low blood pressure
that continuous dropping, rapid deep breathing at first that
becomes shallow with time, severe headache, disorientation
(sign of cerebral anoxia), severe weakness.
 Dyspnea: this is very common in severe cases where the heart
fails to compensate for the reduction of the oxygen carrying
capacity, therefore heart failure develops.

31
 For internal bleeding: fever, pain in the area of bleeding due to
pressure/distention of tissues and symptoms of organ
displacement as in hemothorax/mediastinal shift.
 Signs and symptoms of shock that becomes irreversible if
nothing is done quickly and death ensures.
 On RBC count and Hb estimation immediately, they are
deceptively high due to hemoconcentration from compensatory
mechanism of vasoconstriction in shock and loss of plasma
volume but after treatment of shock and the extra cellular fluids
entering into the vessels in 1-2 days, on blood examination, the
Hb will be abnormally low plus the RBC count because they
will be few circulating in the added fluid.
Deficiency anemia:
 Patient may appear asymptomatic in mild cases.
 In more severe cases especially if deficiency is due to rapid
blood loss, then the signs and symptoms of hypovolemic anemia
are all there.
 Palpitations, dizziness and sensitivity to cold are present
because of the effects on the heart and brain.
 In chronic cases, patients develop brittle hair and nails and the
nail beds are cracked and spoon-shaped (koilonychias).
 In severe cases, patients develop ulceration of the mucous
membranes as seen in stomatitis, glossitis (atrophic-smooth
irritated tongue = tongue sored and smooth), loss of skin
pigmentation, angular stomatitis.

32
 A craving for non-foods such as ice, dirt or pure starch (pica).
 Sometimes palpable spleen.
 General weakness and tiredness.
 Edema of the ankle joints and lower limbs as a result of heart
failure.
Hemolytic anemia:
 All the general signs and symptoms are there plus the following
other signs and symptoms:
 Jaundice (yellowness of the skin and eyes) due to abnormally
large amounts of bilirubin accumulation within the blood from
excessive destruction of RBCs.
 Spleno-hepatomegally and hyperplasia of the bone marrows.
This is because the reticuloendothelium in the spleen, liver, and
bone marrow become hyperactive because of increased demands
upon them to breakdown the defective RBCs.
 Cholelithiasis (pigment gallstones). This comes about as
pigments/stones develop from accumulation of bilirubin in the
gall bladder from the excessively destroyed RBCs.
 Febrile states in case of parasitic destruction of red blood cells.
 Dyspnea from decreased oxygen-carrying capacity
General signs and symptoms of anemia:
 General body weakness
 Pale mucous membranes
 Drowsiness and dizziness
 Lack of concentration

33
 Palpitations
 Blurring of vision
 Insomnia
 Oedema of the ankles
 Cardiac failure
 Angina pectoris
 Headache
Signs and symptoms of pernicious anemia:
The gastric mucous fails to produce intrinsic factor in the stomach
required, i.e., Vit. B12 which a raw material required in making the
red blood cell and it is hereditary and comes on at the age of 45 to
65 years.
The following are the signs and symptoms.
 The onset is gradual
 All general signs of anemia are present
 Soreness of the tongue which is inflamed and remains smooth
 Patient looks pale
 Occasionally the patient develops diarrhea and gets constipated
 Enlarged spleen
 Patient loses appetite
 Patient loses weight and energy
 Patient has epigastric discomfort
 There is tingling and numbness
 Gait disturbance/ataxia
Investigations:

34
 Signs and symptoms based on clinical presentation.
 Blood for Hb, grouping and cross-matching, red blood cell
count, FBC, etc.
 blood shows reduced number of red blood cells and low Hb.
These two are cardinal signs.
 Investigate the underlying cause such as bone marrow puncture
to reveal the size and shape, any other infection or parasitic
infection (Bs x MPs, stool analysis for hookworm infestation),
etc.
 RBCs are present but immature and keeps dying off (pernicious
anemia)
Diagnosis:
 History from the patient
 Signs and symptoms
 Blood investigations
 Stool for hookworm examination and amoebic cyst examinations,
for schistosomiasis and for occult blood
 Sickle cell test
Management of anemia:
This depends on the type of anemia in question. Usually hemorrhagic
and hemolytic anemias are the most severe type of anemia and they
need urgent attention. Deficiency anemia becomes only severe after
taking some times unless it is iron deficiency anemia due to severe
blood loss from acute bleeding.
Aims of management:

35
 Save life of the patient when in shock or in respiratory distress
(resuscitation of the patient).
 Treat the underlying cause if urgent as in blood loss/hemolysis.
 Increase the oxygen carrying capacity by administering blood.
 Replace the missing factors (dietary replacement)
 Offer patients comfort/relieve symptoms.
 Prevent complications
 Patient’s rehabilitation in preparation for discharge/develop for
chronic anemic patients realistic, practical, lifelong plans.
Specific management of the different types of Anemias:
Anemia due to blood loss:
1.Reception:
 In an emergency department or straight in a medical ward on a
couch.
 Quickly assess for ABC and act accordingly.
 Provide warmth to the patient.
 Stop the bleeding by clamping the artery/vein or by digital
pressure, packing the site, elevating the part (limb or head).
 Put up the i.v line and give fluids through it esp. NS to raise the
blood pressure rapidly (1000mls) and call the doctor immediately and
tell him the amount of fluid you have given.
 Administer oxygen (3-5l/min) and tell the doctor, if there is
need for it.
 Position the patient in desired position if shocked or dyspneic.
 Reassure the relatives and the patient to calm him down.

36
 Take the history and other vital observations including the level
of consciousness
2.Doctor’s orders:
 Investigations such as Hb, grouping and cross-matching, bs x
mps, CBC if necessary.
 Admit for complete bed rest in a medical ward to lower the
patient’s oxygen requirements and to reduce strain on the heart and
lungs.
 Blood transfusion is done accordingly and controls the Hb level
after 24 hours of treatment.
 Surgical ligature of the broken blood vessels (patient’s
preparation by the nurse).
 Give a well-balanced diet full of iron from food sources like
liver, meat, kidneys; egg yolk, green vegetables, fruits and alcoholic
drinks.
 Give oral iron tablets 200mg o.d x 1/12.
 In chronic blood loss, investigate the cause.
Deficiency anemia:
 Dietary supplements full of folic acid and iron and vitamins B 12.
This is aimed at replacing the missing factors.
 Oral iron sulphate 200mg b.d with food for 3 months and child
6mg/kg in 2-3 divided doses. All pregnant mothers should receive
these tablets (iron and folic acid) daily orally. Folic acid is given
5mg 8-12 hourly for 3 months
 Transfuse with packed cell.

37
 Treat the underlying cause, e.g. malaria, hookworm infestation,
RTI, etc.
 For vitamin B12 deficiency, parenteral vitamin B12
therapy(hydroxychobalamine), 1mg o.d or weekly until the blood
levels of the vitamin returns to normal, then changed to once
weekly for life. BT with packed cells is imperative when the Hb
falls to 4mg/dl.
Hemolytic anemia:
 Remove/treat the cause such as drugs, diseases such as malaria.
 Blood transfusion.
 In persistent anemia in chronic ill health, splenectomy is done.
 Prevent the cause of anemia if possible.
Other nursing management/general management:
 Complete bed rest: is essential for lowering the patient’s oxygen
requirements and for reducing strain on the heart and lungs. For
those who are mildly anemic, frequent rest is important. An
extremely weak patient needs to be helped in doing everything.
 Skin care: frequent turning in severely anemic patients prevents
skin break down since there is already reduction in amount of
circulating blood cells and plasma, these parts receive less oxygen
and they are easy to die.
 Diet: should be high in proteins, iron and vitamins for these are
needed for red blood cell formation. The diet should be light, well
balanced, served in small bits. Later health advice may be given on
dietary requirements.

38
 Mouth care: this is done frequently because these patients suffer
from mouth sores/tongue sores. The patient should be told to brush
with a soft bristle brush, and rinse the mouth 2 hourly with the
mouth wash.
 Transfusions: this is done only when necessary and not routinely
because of the danger of reactions and complications. The
following precautions are taken during blood transfusion:
 giving blood very slowly to avoid transfusion reaction and
cardiac overload
 , check the pulse rate 15 minutes every time to check for
tachycardia which indicates that the heart I s overworking as a
pump,
 examine the patient’s neck veins signifying cardiac overload,
 observe for respiratory distress and listen for sound rales to
detect pulmonary congestion,
 stop the BT when the pulse rate is over 120b/m.
 Oxygen therapy: especially in severely anemic patients who
need additional oxygen since the blood in them is so little that it
is not able to carry the required volume. Oxygen therapy helps
to prevent tissue hypoxia and also lessens the work of the heart
as it struggles to compensate for the deficiency of oxygen
carrying Hemoglobin.
 Protection of patient from chilling and burns: this is because
of poor circulation anemic patients always feel cold and those
with pernicious anemia suffer from decreased sensitivity to heat

39
such that a heating device may burn them before they are aware
of the condition.
 Isolation: these patients who are severely anemic are typically
exhausted and debilitated and they easily develop infections.
They are reversed barrier nursed to protect them from infections
from infectious sources.
Complications of anemia:
 Heart failure due to tachycardia.
 Brain damage due to less oxygen supply to the brain.
 Abortion and intra uterine fetal death due to less supply to the
fetus.
 Low resistance to infections.
 Growth retardation and loss of weight.
 Other organic failures such as liver, kidneys, etc.

40
SICKLE CELL DISEASE (HB SS DISEASE):
Definition:
Is a chronic hereditary hemolytic blood disorder characterized by
sickle-shaped red blood cells primarily affecting black population in
the world. It is characterized by the presence in the patient’s red blood
cells, of an abnormal type of Hemoglobin (Hb S) instead of the
normal type (HbA). Normal people without any sickle cell problem
have Hb AA, sickle cell traits/carriers have Hb AS and about 25-40%
of their red blood cells carry the abnormal HbS, while those with
sickle cell disease have Hb SS and their red blood cells carry about
80-100% of the abnormal HbS.
These cells assume a sickle or crescent shape when oxygen
amount/concentration in the blood decreases. Once they sickle, they
are destroyed in thousands as they attempt to circulate through the
body’s smaller vessels.
PATHOLOGY:
The disease is attributed to a chemical defect (substitution of one of
the amino acids that forms the hemoglobin) within the protein chains
(alpha and beta chains) that form the normal hemoglobin. This single
substitution of one of the amino acids that forms the Hemoglobin with
a different type greatly alters the properties of that Hemoglobin
molecule by changing its electrical charge and making it less soluble
and more prone to cause clamping/crystallization of the alpha and
beta chains when oxygen level in blood falls. As a consequence of
intermolecular rearrangement, HbS are formed instead of HbA which

41
is normal. Crystallization within the red blood cells distorts their
shape and they take on the characteristic appearance of sickles. Other
abnormal Hbs can be formed apart from HbS, e.g. HbC, or HbD, but
the most common is Hbs

42
MALE (Normal Hb AA) FEMALE (carrier of sickle cell
trait HbAS)
Hb A A Hb A S

MA +FA
= OAA
MA +FS
= OAS
MA +FA
= OAA
MA +FS
= OAS

This means that 50%


of offsprings
Have normal Hb and
50% are carriers of sickle cell trait
having mild or no
Attacks of sickle cell
crisis

43
MALE (Carrier Hb AS) FEMALE (carrier of sickle cell
trait HbAS)
Hb A S Hb A S

MA +FA
= OAA
MA +FS
= OAS
MS +FA
= OAS
MS +FS
= OSS

This means that 25%


of offsprings
Have normal Hb and
50% have
Offsprings who are
carriers and 25%
Of the children will be
sicklers and
Will be experiencing
sickle cell crisis

44
MALE (Sickler Hb SS) FEMALE (Sickler HbSS)
Hb S S Hb S S

MS +FS
= OSS
MS +FS
= OSS
MS +FS
= OSS
MS +FS
= OSS

This means 100% of


the offsprings
Are sicklers. Parents
need genetic
counselling

45
PRECIPITATING FACTORS OF SICKLE CELL
ATTACK/CRISIS:
1.HYPOXIA: hypoxia develops in persons with HbS whenever they
are exposed to low oxygen tensions as a result of:
 Climbing to High Altitudes,
 Flying in Non-Pressurized Planes,
 Exercising Strenuously,
 Undergoing Anesthesia Without Receiving Adequate Oxygenation
 In Suffocated Rooms,
 Polluted Atmosphere,
 When Swimming and Diving into The Waters. Deoxygenation of
Blood Rapidly Affects the Hbs.
2.ELEVATED BLOOD VISCOSITY:
 If the patient is heavily dehydrated from vomiting, diarrhoea,
 Excessive sweating from exercises/fever following infections,
 Bleeding,
 Taking diuretics, the blood becomes thicker and coupled with
concentration of misshapen cells in circulation from hypoxia, the
viscosity is worsened, and the sickle cells tend to pack together or
“log jam” within the smaller blood vessels. As a result of
occlusion of these small blood vessels, severe hypoxia develops
which in turn causes more red blood cells to sickle. The cycle
continues and as this worsens, thrombosis and infarction develop
and the surrounding tissues become necrotic. The most sensitively
affected organs are the brain and the kidneys, heart, lungs, skin

46
bone marrow, spleen and penis as the destroyed red blood cells
are collected and blocked in them from thrombosis.
3.ANXIETY AND COLD WEATHER:
 Emotional upsets interfere with breathing = lowers oxygen intake,
and
 Coldness reduces circulation by constricting the peripheral vessels
precipitating reduced blood flow to the affected parts and
breakdown of the abnormal red blood cells occur, triggering the
hemolytic reactions.
4.OTHER STRESSFUL CONDITIONS THAT PRECIPITATE
THE DISEASE: these include:
 Pregnancy,
 Surgery,
 Infections, And
 Trauma.
The sudden worsening of Sickling from any of the above factors drags
a patient to a crisis which is serious and life-threatening.
TYPES OF SICKLE CELL DISEASE:
a. ASYMPTOMATIC: this is sickle cell trait/carrier that
does not suffer any sign and symptoms but carries the gene
of an abnormal HbS in his genetic makeup.

b. SEVERE TYPE/SICKLE CELL DISEASE: this is the


type where there are persistent hemolytic anemic attacks
with periodic episodes of painful crisis. It is the one mostly

47
referred to as sickle cell disease. This is more severe in
children than in adults especially from 4 months to 12-14
years old and for those who survive this period, the
symptoms reduce as they move to adulthood.

SICKLE CELL CRISIS: these are divided into 3.


1.Painful crisis: this is the most common type and is due to occlusion
of small arterioles and venules by the abnormal shaped cells. The pain
is mostly severe and throbbing in nature and may be confined to the
abdomen, musculoskeletal systems, brain, lungs or heart
2.Aplastic crisis: this occurs when the process of erythroblast
division/maturation is depressed from blocked red bone marrow by
the abnormal thrombotic clots or from other cause of bone marrow
depression.
3.Hemolytic crisis: this involves rapid decrease in the number of red
blood cells from cell breakdown.
4.sequestration crisis: this is when there is too much pulling of blood
from the liver and the spleen leading to hepatosplenomegaly.

SIGNS AND SYMPTOMS:


These majorly come from hemolysis, thrombosis and infarction.
Hemolytic symptoms and signs:
 High fever which is persistent despite administration of
antipyretics and antimalarial.

48
 Severe pallor of the mucous membrane and chronic lowered Hb
controls after transfusions.
 Severe dyspnea from low oxygen carrying capacity.
 Restlessness, dizziness, fainting, thirst, pallor (extreme), sweating
(excessively), rapid thread pulse, low blood pressure that
continuous dropping, rapid deep breathing at first that becomes
shallow with time, severe headache, disorientation (sign of cerebral
anoxia), severe weakness.
 Jaundice (yellowness of the skin and eyes) due to abnormally large
amounts of bilirubin accumulation within the blood from excessive
destruction of RBCs.
 Spleno-hepatomegally and hyperplasia of the bone marrows. This
is because the reticuloendothelium in the spleen, liver, and bone
marrow become hyperactive because of increased demands upon
them to breakdown the defective RBCs.
 Cholelithiasis (pigment gallstones). This comes about as
pigments/stones develop from accumulation of bilirubin in the gall
bladder from the excessively destroyed RBS.
 Because of chronic anemia, there is fatigue, reduced exercised
tolerance, susceptibility to infection, Cardiomyopathies which may
later lead to heart failure with its symptoms and signs.
Aplastic signs and symptoms:
 Finger and toe nail clubbing (dactylitis) and swollen joints due
to hyperactivity of the bone marrows to produce more red blood
cells.

49
 Swollen skull-frontal (“towered skull), from enlargement of the
skull bones. This is sometimes described as “typical facial
appearance and bossing-from distorted skull”. This also brings
about prominent molar teeth and protuberances
Thrombotic and infarction signs and symptoms:
 Severe pain in the joints and bone marrow from clots, lack of
oxygen and nutrients (throbbing in nature).
 Abdominal pain from occlusion of mesenteric vessels may lead to
acute abdomen.
 Thin legs and arms (muscle wasting) and poor growth rate/growth
retardation and delayed puberty occurs from insufficient supply of
food and oxygen to the muscles due to persistent haemolysis and
blocking of blood vessels and from persistent ill health and
repeated admissions.
 Development of leg ulcers results from cell death and tissue
necrosis from thrombosis and infarction.
 Visual changes and pain from accumulated sickle cells in the eye
vessels.

DIAGNOSIS:
 Blood for Sickling test.
 Skull x-ray will show skull abnormalities.
 Hb. erythropoiesis (viewing of barbicels in an electric field
towards the anode or cathode) to check for the red blood cell
movement within the blood vessels.

50
DIFFERENTIAL DIAGNOSES:
 Osteomyelitis.
 Arthritis/rheumatoid arthritis.
 Other causes of anemia.
 Other conditions causing jaundice.
MANAGEMENT:
Since there is no cure for sickle cell disease, the management is only
aimed at alleviating symptoms, prevent the precipitating factors and
making the patient comfortable always. There is no known method of
changing the genetic constitution of an individual and therefore, no
means of curing the disease.
Resuscitative mgt:
 Reception: ABC assessment and immediate action taken.
 Good positioning and oxygen if dyspneic.
 Brief history taking and observations and informing doctor.
 Doctor’s orders: Hb, gp, &x-m, Sickling test and others
urgently.
 blood transfusions immediately.
Other management at acute stage/hemolytic symptomatic relief:
 Admission in a pediatric/medical ward for complete bed rest in a
well-made occupied/admission bed in a room with enough fresh air
in a comfortable position.
 Reduce the fever by giving antimalarial, antipyretics, tepid
sponging, plenty of fluids, remove any extra linen, fan the patient
with fresh air, open the adjacent windows.

51
 Treat dehydration by administering i.v fluids as per doctor’s order
in order to reduce blood viscosity
 Treat the offending infections as per the laboratory and doctor’s
order by giving parenteral antibiotics.
Thrombotic and infarction symptomatic relief/pain and skin
management:
 Give pain killers/strong ones like pethidine, then later reduce to
diclofenac and mild paracetamol.
 Support the joints with pillows and the bony prominences to
reduce the pain.
 Frequent turning of the patient.
 Range of movement exercises when pain subsides to prevent
joint stiffness and to keep the muscle tone.
 Apply bed cradle to keep off bed linen from the painful joints.
 Remove any constrictive clothing.
Other general nursing care:
 Counseling of the parents on how to prevent the predisposing
factors and on genetic counseling.
 Good feeding to encourage tissue building and wound healing if
there are ulcers from tissue death.
 Wound dressing and later skin grafting may be performed.
 Continuous monitoring of hemoglobin level and the general
observations especially the patient’s activity levels, any discomfort
from altered vital signs, circulation to the extremities, pain and
joint movements.

52
 Give folic acid 5-10mg 8hourly for 7 days and for sickle cell
mothers daily until delivery.
Complications of sickle cell disease:
 Severe anemia from hemolysis.
 Stroke from thrombosis in one of the blood vessels supplying
the brain.
 Organic failure: heart, liver, kidney due to reduced blood
volume from dehydration, anemia, excessive iron storage for the
liver.

53
CONDITIONS OF GASTRO INTESTINAL TRACT
1.JAUNDICE (ICTERUS)
Jaundice also known as icterus, is a yellow discolouration of the skin,
sclera and mucous membranes caused by elevation of bilirubin levels
in the blood.
Classification of jaundice
1. Haemolytic jaundice (Prehepatic)
This occurs when red blood cells are destroyed at a rate exceeds the
liver’s ability to remove bilirubin from the blood. Haemolytic
jaundice is seen in pernicious anaemia, sickle disease and transfusion
reactions.

2. Obstructive or intrahepatic or extrahepatic jaundice


This occurs when the flow of bile to the duodenum is obstructed. The
obstruction can be intrahepatic or extrahepatic.
Intrahepatic obstruction is obstruction of bile ductules within the
liver.
Extrahepatic obstruction results from an obstruction to the flow of
bile through the common bile duct.
Causes of intrahepatic cholestasis or jaundice
 Viral hepatitis
 Drugs e.g. chlorpromazine
 In some cases, cirrhosis
 Cholangitis (inflammation of the bile ducts)

54
 Infiltration of the liver e.g. by carcinoma
 Rare disorders e.g. biliary cirrhosis

Causes of extrahepatic jaundice


 Gall-stones in the common bile duct
 Carcinoma of the head of the pancreas, ampulla of Vater or
rarely the bile duct
 Fibrosis and stricture of the bile duct
 Obstruction and pressure on the ducts from outside by tumours
or enlarged lymph glands.
3. Hepatocellular or infective or toxic jaundice
This is associated with the damage to the parenchymal cells of the
liver by toxic or infective agents. The liver cells are unable to
metabolise bilirubin because of infection, chemical or drug toxicity,
or hepatocytes necrosis. The power to transfer bilirubin from blood to
the biliary canal is diminished. The cells become oedematous and the
bilirubin is retained in blood.
Causes
 Infections with viruses of infective hepatitis A and B
 Other infections such as yellow fever, lactospirosis and
septicaemia.
 Poisonous substances e.g. drugs
 As a consequence of primary defect in bilirubin transport within
the liver and conditions such as physical jaundice of the new born
(icterus gravis fetalis).

55
Clinical manifestations
 The patient with jaundice has yellow discolouration of the skin
and mucous membranes. General skin colour may range from a
light-yellow tint to a deep bronze colour.
 Pruritis occurs when bile salts which are an irritant is deposited
in the skin.
 Because bile is not entering the small intestine in normal
quantities, the stool is lighter in colour progressing to clay
colour.
 Urine becomes dark or deep orange in colour owing to the
presence of bilirubin.
 Lack of bile salts reaching the bowel means that vitamin K
cannot be absorbed. This leads to Prothrombin deficiency and a
prolonged blood clotting time.
 Liver cell damage in long-standing obstruction.
Other symptoms include:
 Chills, headache and malaise
 Nausea, vomiting, anorexia and diarrhoea
 Upper abdominal pain
 Tender hepatomegaly
Treatment (No specific medical treatment)
1. Treatment of the causative factors
In most cases, nothing can be done to eliminate the cause of the
disease. It is important to detect the drugs including hepatitis so that

56
the drug can be stopped and the patient warned to avoid its use in
future.
2. Bed rest
When the symptoms are marked, the patient is strictly confined to bed
thereafter; young patients may go up and about taking care only to
avoid heavy exertion.
For those whom the risk of hepatitis may be greater, rest should be
prolonged unless symptoms and signs disappears and liver function
test has returned almost to normal.
3. Diet
A good diet containing high calories are recommended. Because of
anorexia and nausea, a light diet supplemented with fluids sweet
drinks and glucose is usually accepted.
Also, a good intake of protein is should be encouraged. If vomiting is
severe, IV glucose and fluids may be required for a few days.
4. Drugs
Prednisolone may be given provided the hepatic function test is
negative.
Drugs metabolised in the liver should avoided e.g. sedatives or
hypnotics.

57
2.STOMATITIS
This is an inflammation of the mucous membrane of the mouth.
It may be acute or chronic depending on the cause. It could come
from infectious origin or as symptom of a systemic disease or from
any other cause.
Causes
1.Viral: measles virus and herpes simplex type 1 causes an acute
stomatitis and recurrent cold sores.
2.Bacterial: e.g. bacilli, and spirochetes this is a rare form of
stomatitis but may occur in malnourished patients and those with poor
dentition. Vincent’s stomatitis which is due to a number of organisms
such as fusiform bacteria, spirochetes, streptococci, staphylococci, etc
results in necrotizing ulcerative gingivitis and severe oral ulceration.
3.Fungal: the commonest is candida albicans. This may accompany
prolonged use of antibiotics which destroy normal flora of the mouth
and allow the fungus to grow. It is also seen in immunosuppressed
patients.

58
4.Non-infective: Aphthous stomatitis-canker sore: is a recurrent and
chronic painful ulceration of the mouth of unknown cause, possibly
secondary to systemic disease, trauma, stress, etc.
5.Nutritional deficiency: e.g. lack of vitamin A which is obtained
from fish liver oils, beef, liver, egg yolk, butter, cream, dark green
leafy vegetables, yellow vegetables and fruits. Vitamin A is necessary
for normal vision, healthy skin and other surface tissues, defence
against infections, thus causing hardening and drying, peeling of the
skin and inner mucous lining.
6.mechanical causes: trauma from jagged teeth, wrongly fitting
dentures, biting the cheeks, chemical irritation from spiced foods,
mouth washes, alcohol, drug allergy, mouth breathing-dries the
mouth.
7.Dehydration: when there is severe febrile attacks, vomiting,
diarrhoea, etc.
Clinical features
 Inflammation of the tongue and mucous membrane of the
mouth. The tongue is red, raw and painful including the mucous
membrane of the mouth.
 The patient complaints of soreness and difficulty with eating
and sometimes speaking.
 One loses interest in eating because of pain and a foul breathe.
 Excessive salivation is very prominent.
 Visible ulcers on the gum, palate and lips.

59
 White plaques or thrush can be seen in babies and
HIV/debilitated patients.
 Swelling and bleeding of gums
Investigation
 Swab the mouth for microscopy, C&S of bacteria and fungi.
 Blood for Rapid Plasma Regain (RPR) test, HIV serology.
Management
 Wash the mouth with salt solution
-dissolve 5ml spoonful of salt in a cup of warm water or hydrogen
peroxide solution 6%
-add 15 ml to a cup (200ml) of warm water
 Repeat this mouth wash 3 times daily
 Apply gentian violet solution 0.5% every 8 hours
 Continue treatment until healing takes place
 Treat the cause if known: antifungal = nystatin tablets-1-2 to be
chewed then swallowed, or suspension 6 hourly 100000i.u/ml x 10
days or Ketoconazole 200mg o.d x 5 days. Antibiotics according to
culture and sensitivity results
 Plenty of oral fluids followed by oral care.
Complications:
 Spread to the middle ear-otitis media
 Parotitis
 Digestive disturbances

60
3.GINGIVITIS:
Definition:
This is inflammation of the gum due neglected mouth care.
Causes: as for the mouth. Poor mouth hygiene leads to accumulation
of food remains, bacteria which coats the teeth and gums.
Pathology:
Due to decomposition and rotting of the plague, the mouth smells,
inflammation occurs, and the gum becomes pink, reddish, swollen
and becomes movable and detached from the teeth instead of being
firm and tight against the teeth. When one brushes or eats, the gum
often bleeds and ulceration occurs.
Signs and symptoms:
 Gum is red, swollen and ulcerate
 Bleeds easily when touched
 Difficulty in eating, drinking and speech due to pain
 Fever, swelling of the cervical nodes

61
Differential diagnoses: dental abscess, swelling from trauma, acute
stomatitis, oral thrush or chemical oral ulcers.
Management:
 In the absence of systemic signs and symptoms, microbial
therapy is not indicated.
 Oral hygiene as in stomatitis.
 5 day antibiotic therapy; phenoxy methyl penicillin 500mg 6
hourly or 10-20mg/kg/dose or PPF 1mu i.m o.d or 50000i.u/kg
or Metronidazole 400mg 12 hourly-10-12.5mg/kg/dose but
contraindicated in pregnancy or erythromycin 250mg 6 hourly
or 7.5mg/kg/dose indicated in penicillin allergic patients.

Prevention:
 Oral hygiene: to regularly clean the teeth to remove plague at
least 2 times daily but preferably after every meal, avoid sweets
and soft drinks, regular visits to the dentist, good nutrition and
increase in vitamin C intake.

62
4.DENTAL CARIES/CAVITIES:
Definition: dental caries are decayed areas in the teeth from a process
that gradually dissolves a tooth’s hard outer surface and progresses
towards the interior.
For decay to occur there must be a susceptible tooth that has relatively
little fluoride, or pronounced pits, grooves or fissures that retain
plague. There must also be acid producing bacteria like streptococcus
mutans and food especially the sugars.
Causes:
 Soft enamel of poor quality from defective formation in
childhood as a result of vitamin deficiency in the diet.
 Lack of fluoride in the drinking water and drugs such as
tetracycline intake causes the problem.
 Failure to carry out efficient dental hygiene. This permits the
accumulation of food debris btn the teeth especially sweets and

63
multiplication of decay causing bacteria that produce acid which
erodes the enamel and exposes the delicate organs of the teeth.
 Trauma to the gum and teeth from accidents, fights, gun-shots,
tooth removal, etc.

Pathology: a combination of bacteria, food rich in sugars and a tooth


with cavities or groove or fissure or with less fluoride. Coating of the
tooth occurs. An acid is produced within 20 minutes which dissolves
and destroys the enamel, goes to the dentine, up to the pulp cavity if
untreated, and thus can now spread systemically causing rheumatic
fever, endocarditis, etc.
Signs and symptoms:
 Tooth ache not only from pain but also from exposed roots
when chewing or if there is fracture of the teeth.
 Cavity on the enamel causes no pain but pain only starts if the
dentine is exposed. One feels pain only when drinking
something cold. This indicates the pulp is still un touched and
can be rescued by treatment.
 A cavity that reaches the pulp causes irreversible damage. Pain
is there throughout even when the stimulus is removed.
 Tooth becomes sensitive when a patient bites anything, or when
the tongue presses on it or finger touches it, just because the
infection has spread beyond the roots

64
 This later leads to abscess formation which causes swelling to
the adjacent gum or spread more broadly to the jaw and drains
into the mouth or even the skin near the jaw.
Diagnosis:
 clinically,
 sensitivity test-cold/hot substances-foods or liquid and
 x-ray for traumatic teeth.
Treatment:
 Regular visits to the dental surgeon so that minor caries can be
detected and filled in,
 Antibiotics for systemic spread control and
 Drainage of the abscess.
Prevention:
 Oral hygiene,
 Avoidance of tetracycline intake.
 More intakes of calcium salt and vitamins.

65
5.GLOSSITIS:
Definition:
Is the inflammation of the tongue and it can occur together with
stomatitis but can also be seen in several illnesses such as anemias-
deficiency type.
The appearance of the tongue indicates the state of the digestive
system function and the progress of febrile or other disorders. This
can be detected from the size and shape of the tongue, movement,
condition of the surface and its appearance.
Causes:
 Central nervous system disorders where the nerves supplying
the tongue are affected. The tongue becomes painful and
inflamed.

66
 Lack of iron, folic acid and vitamins to maintain the mucous
membrane covering the surface
 Chronic alcoholism and drugs which have the burning effects on
the tongue surface.
 Other associated GIT disorders such as stomatitis, gastritis,
constipation, dental caries, appendicitis, Cholecystitis, tonsillitis,
intestinal obstruction, general peritonitis, Anaemias, etc.
NB: Treatment: as for stomatitis

6.DIARRHOEA
This is the increased frequency of passage of abnormally liquid stools
3 or more times in 24 hours. It results from an excessive amount of
water in the intestinal contents, from changes in intestinal motility or
a combination of the two.
Diarrhoea may be acute or chronic (persistent).
Causes
Acute
 Acute gastroenteritis
 Infective gastroenteritis
 Food poisoning

67
 Chemical poisoning as in mercury poison and prolonged use of
oral antibiotics and aperients
 Alcoholic excess
 Appendicitis in some patients
 Specific intestinal infections e.g. enteric fevers (salmonellosis),
protozoal infections such as giardiasis and amoebic dysentery,
shigellosis, cholera, viral infection with enterovirus, worm
infestations (strogyloides).
 Infectious diseases e.g. measles, malaria and other fever causing
conditions.
 Anxiety mainly due to fear.
 Unhygienic feeding methods

Chronic
 Inflammatory diseases
- Ulcerative colitis
- Crohn’s disease
- Diverticulitis
- Tuberculosis

 Carcinoma of the colon


 Coeliac disease and tropical sprue (deficient absorption of food due
diseased small intestine.
 Vitamin B deficiency

68
 Thyrotoxicosis
 Irritable bowel syndrome
 Malnutrition e.g. kwashiorkor.
Symptoms and signs of diarrhoea
 Loose watery stools
 Abdominal cramping
 Appearance of mucus, blood or fat in stool
 Urgency such that involuntary expulsion of stool may occur if
there is any delay in reaching the toilet
 Tenesmus
 Per anal discomfort
 Often there is also a feeling that the rectum has not been
completely emptied
 Signs and symptoms of dehydration
 Signs of malnutrition if diarrhoea persists for more than 14 days.
Investigations
Stool for microscopy
Management
Aims of management
 Identify and treat the cause
 Prevent or correct dehydration
Management of dehydration children
Movement with treatment Plan A, B and C is based on an assessment
of the degree of dehydration according to the key clinical signs.

Signs Degree of dehydration


None/ Mild Some Severe
General condition Well, alert 69 irritable
Restless, Lethargic or unconscious or
very drowsy
Eyes Not sunken Sunken Sunken
Clinical features of dehydration in children (Parameters for
assessing dehydration)
Plan A (No dehydration and for prevention)
Counsel the mother on the three rules of Home Treatment
- Extra fluids, continue feeding, when to return
Give extra fluids as much as the child can take
Advise the mother to:
Continue/increase breastfeeding
-If the child is exclusively breastfed, give ORS or clean water in
addition to milk
-If the child is not exclusively breastfed, give one or more of ORS,
soup, rice water, yoghurt drinks or clean water
In addition to the usual fluid intake, give ORS after each loose
stool or episode of vomiting: <2years: 50-100mL; 2 years and over
100 – 200ml
-Give the mother 2 packets to use at home
-Giving ORS is especially important if the child has been treated with
Plan B or Plan C during current visit
-Give frequent small sips from a cup
-If the child vomits, wait for 10 minutes and then give more slowly
In a child with high fever or respiratory distress, give plenty of
fluids to counter the increased fluid losses in these conditions
Continue giving extra fluids as well as ORS until the diarrhoea or
other cause of dehydration stops
Counsel the mother on:

70
Correct breastfeeding and other feeding during sickness or health
How to maintain her own health
When to return to the health worker

Plan B (Some dehydration)


Give ORS in the following amounts during the first four hours:

Age <4 4 – 12 13 – 24 25 – 60
(mth)
Weight <6 6 – 9.9 10 – 11.9 12 – 19
(kg)
ORS 200 – 400 – 700 – 900 -
(mL) 400 700 900 1400

NB:
X- Only use the child age when you do not know the age
X- You can also calculate the approximate amount of ORS to give a
child in the first 4 hours as weight (kg) X 75mL
Show the mother how to give ORS
-Give frequent small sips from a cup
-If the child wants more than is shown on the table, give more as
required
-If the child vomits, wait 10 minutes, then continue more slowly.
For infants <6 months who are not breastfed, also give 100 –
200mL of clean water during the first 4 hours

71
Reassess patient frequently (every 30 – 60 minutes) for
classification of dehydration and selection of treatment plan.
After 4 hours
Reassess the patient
Classify the degree of dehydration
Select the appropriate Treatment Plan A; B or C
Begin feeding the child in the clinic
If the mother must leave before completing the child’s treatment:
Show her how to prepare ORS at home and how much ORS to give
to finish the 4- hour treatment
Give her enough packets to complete this and two more to complete
Plan A at home
Counsel the mother on the three rules of home treatment - extra
fluids, continue feeding, when to return.
Plan C (severe dehydration)
a) if you are able to give IV fluids:
Set up an IV fluids line immediately. If the child can drink, give
ORS while the drip is set up.
Give 100ml/kg, of compound sodium lactate infusion (Hartman’s
solution or Ringer’s Lactate solution) or half – strength Darrow’s
solution in glucose 2.5% or sodium chloride infusion 0.9%. Divide
the IV fluids as follows:
Age First give 30mL/kg in
Then give 70mL/kg in

72
Infants (<12 months) 1 hour*
5 hours*
Children (2mths – 5yrs) 30 minutes* 2 ½ hours*

* Repeat once if radial pulse is still very weak/undetectable


Reassess the patient frequently (every 30 – 60 minutes) for
classification of dehydration and selection of Treatment Plan
As soon as the patient can drink usually after 2 – 4hours in infants or
1 – 2hours in children:
Also give ORS 5mL/kg/hour
Continue to reassess the patient frequently, classify the degree of
dehydration and select appropriate Plan A, B or C and continue
treatment.
b) If you are unable to give IV fluids but IV treatment is available
nearby (i.e. within 30 minutes):
Refer urgently for IV treatment
If the child can drink:
Provide the mother with ORS and show her how to give frequent
sips during the trip to the referral facility
c) If you are unable to give IV fluids and this therapy is not available
nearby (i.e. not within 30 minutes) but you can use a NGT or the child
can drink:
Start rehydration with ORS by NGT or by mouth: give 20
mL/kg/hour for 6 hours (total = 120ml/kg)
Reassess the child every 1 – 2 hours:

73
-If there is repeated vomiting or increasing abdominal distension, give
the ORS more slowly.
-If hydration status is not improving within 30 minutes, refer the child
urgently for IV therapy.
After 6 hours, reassess the child
Classify the degree of dehydration
Select appropriate Plan A, B or C to continue treatment.
Note:
If possible, observe the child for at least 6 hours after rehydration to
ensure that the can correctly use ORS to maintain hydration.

MANAGEMENT IN OLDER CHILDREN AND ADULTS


Assess the level of dehydration using the table below
Clinical Degree of dehydration
Mild Moderate* Severe*
feature
General Thirsty, Thirsty, Generally conscious,
appeara alert alert anxious, cold
nce extremities, clammy,
cyanosis, wrinkly skin
of fingers, muscle
cramps, dizzy if
standing
Pulse Normal Rapid Rapid, thready,
sometimes absent
Respirat Normal Deep, Deep and rapid

74
ion may be
rapid
Systolic Normal Normal Low, may be
BP unmeasurrable
Skin Returns Returns Returns very slowly (> 2
pinch rapidly slowly seconds)
Eyes Normal Sunken Very sunken
Tears Present Absent Absent
Mucous Moist Dry Very dry
membra
nes
Urine Normal Reduced, Anuria, empty bladder
output dark
urine
*At least 2 of the above signs must be present.
Rehydrate the patient as follows:
Degree of Rehydrat Route Volume to
dehydratio ion fluid give in first 4
n hrs
Mild ORS Oral 25mL/kg
Moderate ORS Oral 50mL/kg (3)
Severe Ringer’s IV 50mL/kg (5)
Lactate

Notes on the Table

75
 Volumes shown are guidelines only – if necessary, volumes can
be increased or the initial high rate of administration maintained
until clinical improvement occurs.
 As well as ORS, other fluids such as soup, fruit juice and clean
water may be given.
 Initially adults can usually take up to 750mL of ORS/hour
 If sodium lactate compound (SLC) IV infusion (Ringer lactate)
is not available, use half – strength (HS) Darrow’s solution in
glucose 2.5% or sodium chloride infusion 0.9%. However, both
are less effective.
 In severe dehydration, give IV fluids as rapidly as possible at
first until radial pulse can be felt then slow down the rate of
administration.
 Volumes that can be given over the first 24 hours (60kg adult)
are as follows:

Time period Volume of IV


fluid
First 1L
hour
Next 3 2L
hours
Next 20 3L
hours

76
 After 4 hours, evaluate rehydration in terms of clinical signs and
not in terms of volumes of fluids given
 As soon as signs of dehydration have gone, start fluid
maintenance therapy with as much alternating ORS and water as the
patient wants to avoid hypernatremia
 Continue with this for as long as the cause of original
dehydration persists.

Note:
Continued nutrition is important – there is no physiological reason to
discontinue food during treatment for dehydration.

77
SYSTEMIC DISEASES OF CENTRAL NERVIOUS

1. MENINGITIS
Definition
This is the inflammation of the meninges esp. the pia and arachnoid and the
CSF between them.
Etiology
It can be caused by various organisms.
1) Viruses eg mumps, measles and herpes simplex
2) Bacteria e.g. streptococcal pneumonae, hemophilia influenza, Neisseria,
staphylococcus auras.
Note: Neisseria meningitides cause epidemics meningococcal meningitides, e-
coli are the commonest causes of meningitis in the new born.
Klebsella pneumonia, mycobacterium tuberculin which causes Tb meningitis.
3) Fungus cryptococcal neoformans which is common in HIV patients
4) Protozoa amoeba and toxoplasma Gondi
Classification of meningitis
1. Pyogenic meningitis (bacterial meningitis) it’s usually caused by pus
forming organism such as Cryptococcus peumoniae, meningococcal
meningitis which is caused by Neisseria meningitides.
2. Aseptic meningitis like that one caused by viruses.
3. Acute meningitis like meningococcal meningitis
4. Chronic meningitis like Tb meningitis
Mode of spread
 Haematogenous spread from respiratory tract infection such Neisseria
meningitides which is a normal flora in the nose.
 Penetrating wounds on the scalp e.g. open head injury

78
 It can occur secondary to lumber puncture if aseptic measures are not
taken.
 Brain abscesses
 Ascending infection secondary to sinusitis or mastoids
Predisposing factors
 Malnutrition
 Overcrowding or poor ventilation
 Epidemics with measles and mumps
Signs and symptoms
 On set is sudden
 High fever
 Nausea and vomiting
 Photophobia
 Neck rigidity
 Bulging of the fontanels
 Convulsion
 There may be papillary edema
 Positive kerning’s sign (in ability to flex the knee while the hip is flexed
900)
 Opthotonus (when the person lies on the bed and the back is arched)
 Signs of ICP e.g.
- Reduced level of consciousness
- Mental confusion
- Drowsiness etc.
Investigation
The most important investigation is lumber puncture for CSF analysis.
Management of bacterial meningitis
The management of the baby with meningitis depends very much on supportive
care given. The patient with bacterial meningitis is very ill and the combination
of fever, dehydration, cerebral edema will predispose the patient to convulsions,
airway obstruction and respiratory failure.
Admission
This is neonatal emergency admit on ICU and establish positive nurse patient
relationship, inform the doctor, protect the bed with the rails in case of
convulsions, ensure dim light in the room to relieve discomfort from the
photophobia, the room should be well ventilated and quiet.
Position
Semi-prone if the baby is unconscious to maintain clear air way.
Observations

79
Vital observation such as TPR ¼ hourly, ½ hourly then 4 hourly when the
condition has improved esp. temperature
Physical observation observes for convulsion, asses for cranial nerve damage,
assess ICP, asses for neurological status using Glasgow coma scale.
Investigations
 LP for CSF analysis
 BS for malaria to r/o malaria parasites
Specific nursing care
- Maintain clear air way if the baby is convulsing
- Access an IV line for fluids and medication
- Fever must be vigorously managed because it increases cerebral edema
and frequency of seizure by tepid sponging, antipyretics e.g. paracetamol
- Administer prescribed drugs as ordered by the doctor such as
 dexamethasone to reduce cerebral edema,
 analgesics, and
 anticonvulsants
 Antibiotics such as ceftriaxone
 Iv fluids e.g. dextrose and normal saline
 Maintain strict fluid input and output balance
Nursing care
- Diet give balanced diet easily digestible, high protein , calories and fluids
pass NGT if un able to feed orally
- Care of bowel and bladder regularly
- Exercises start with passive exercise later active.
- Psychotherapy reassures the mother about the child’s condition.
- Advice on discharge
 Avoid over crowding
 Give all the medications as prescribed
 Avoid sleeping in poorly ventilated house
 Come back for review
Prevention
 Immunization is very important in epidemic areas
 Health educate on the dangers of sleeping in poorly ventilated houses
 Give prophylactic treatments to contact cases e.g. cepro
 Report all the meningitis cases to DHO
 Careful surveillance should be done
Complications
- Hearing loss
- Blindness
- Cranial nerve dysfunction

80
- Cerebral abscess
- Subdural empyema
- Hydrocephalus
- Epilepsy
- Mental retardation

2. INTRACRANIAL DAMAGE/CEREBRAL INJURIES (PALSY)

Definition

This is damage to the brain due to, too much pressure with quick or sudden
compression of the fetal head.

Structures involved

 The flexi celebri: a folder of Dura matter between the two cerebral
hemisphere is liable to be torn.
 The tentorium cerebral also a fold of the Dura mater which is between
the cerebrum and cerebellum. The bone between the parietal bone and
occipital bone is also liable to break usually happens in upward moulding
in persistent occipital posterior.
 Large veins running underneath these membranes are likely to be torn
e.g. the great vein of galen may tear when the tentorium gets torn and the
usual source of bleeding.
Predisposing causes

1. Prematurity
A premature baby is most likely to have cerebral damage because;

 The skull bones are soft


 The sutures are wide
 The cerebral blood vessels and tissues are very delicate.
2. Obstructed labour
3. Instrumental delivery

81
Real causes

1. Prolonged anoxia
2. Trauma due to compression of fetal head as in;
 Excessive moulding caused by contracted pelvis, large babies, and
occipital posterior.
 Rapid pelvic floor i.e. rapid compression in precipitate labour, after
come head of a breech.
 Upward moulding occurs in; after face to pubis, and after head of a
breech.

3. EPILEPSY
Definition:
This is recurrent, episodic, paroxysmal, transient disturbance of the brain
function due to abnormal or excessive electrical activity of the neurones often
associated with impaired or loss of consciousness.
Or its brief cerebral disorder associated with altered consciousness due to
excessive electrical discharges.
Causes
 May be idiopathic
 Post infective
 Familial tendencies
 Infections like cerebral malaria
 Head injuries or brain damage
 Vascular abnormalities
Classifications
a) Generalized e.g.{tonic colonic seizures (grandimal) and absent seizures
(petitmal)}
b) Partial e.g. { simple (no unconsciousness) and complex
(unconsciousness)}
Clinical manifestations of;
1. Generalized tonic and clonic seizure(grandimal)

82
 On set is abrupt
 Dizziness
 Stiffness of the body
 Falls on the ground
 Biting of the tong
 Frothy discharge in the mouth due to in ability to swallow saliva
 Ineffective breathing due to spasm of respiratory muscles
 Pulse becomes weak and irregular
 Jerking body movement
 Child becomes sleepy and confused or exhausted
2. Status epilepticus
Definition
Is the state of continues or recurrent seizures that are prolonged for more than
30 minutes or occur in series without regaining consciousness in between the
attacks.
Its medical or pediatric emergencies.
Management
Management of convulsive disorder depends on the cause identified.
The management is mainly done with the drug, diet therapy and surgery if
indicated, emotional support, psychosocial rehabilitation and vocational
guidance are also very important. Long term management may need supervision
and explanation about treatment compliance.
Drug therapy
Commonly drugs used are phenytoin, carbamazepine, phenobarbtone, diazepam
etc. success of treatment depends on the regularity in taking the drugs,
Nursing care
 Ensure safety during seizures by protecting the child from injury
- Remove hard and sharp objects and place the patient on the floor or on
the bed with side rails
- Monitor vital signs regularly
 Prevention of respiration arrest and aspiration

83
- Loosen the tight clothes on the neck
- Don’t put anything in the mouth
- Don’t restrict the body movement
- Clear airway by suctioning and put the child with the head turned to one
side.
 Promote socialization
- Advice the parents to allow the child to perform the normal life as
possible with some restricted activities like climbing high, avoid
swimming and exhausting activities.
 Promote self esteem
- Explanation on self-care and promoting independence
 Proved health education on the following
- Continue with medication
- Restricted activities
- Misconceptions about the disease

84
4. MENTAL RETARDATION

Definition;
Mental retardation is subaverage intellectual ability present from birth or early
infancy.
The people with mental retardation has a lower intellectual development than
normal, and difficulties in learning and social adaptation.
About 3% of the total population is mentally retarded.
Causes
Intelligence is determined by both hereditary and environment. In most cases of
mental retardation, the causes are unknown. But several conditions during
women’s pregnancy can cause or contribute to mental retardation in her child
common ones include.
 Use of drugs
 Excessive consumption of alcohol
 Radiation therapy
 Poor nutrition
 Certain viral infections such as German measles (rubella)
 Chromosomal abnormalities e.g. down syndrome, and common causes of
mental retardation.
 Difficulties associated with prematurity.
 Asphyxia (low level of oxygen)

Levels of mental retardation


Levels IQ Ability at pre- Ability at school age Ability at adult
school
85
age(birth-5yrs) (6-20yrs) age 21yrs older
Mild 52-68 – Can – Can learn up – Can
develop to about the 6th usually
social and grade level by achieve
communic late teens enough
ation skills – Can be guided social and
– Muscle towards the vocational
coordinati social skills for
on are conformity self-
slightly – Can be support.
impaired educated – But may
– Often not need
diagnosed guidance
until later and
age assistance
during
times of
unusual
social or
economic
stress
Moderate 36-51 – Can talk – Can learn – May
or learn to some social achieve
communic and self-
ate occupational support by
– Social skills performin
awareness – Progression g
is poor beyond the 2nd unskilled
– Muscle grade level in or
coordinati school work is semiskille
on is fair unlikely d work
– Profit in under
training sheltered
self-help conditions
.
– Needs
supervisio
n and
guidance
when
under

86
mild
social or
economic
stress
Severe 20-35 – Can say a – Can talk or – May
few words learn to contribute
– Able to communicate partially
learn some – Can learn to self-
self-help simple health care under
skills habits complete
– Have few – Benefits from supervisio
or no habit training n
expressive – Can
skills develop
– Muscle some
coordinati useful
on poor self-
protection
skills in
controlled
environme
nt.
Profound 19- – Extremely – Some muscle – Some
below retarded coordination muscle
– Little – Unlikely to coordinati
muscle walk or talk on and
coordinati speech
on – May
– Needs achieve
nursing very
care limited
self-care
– Needs
nursing
care

Prevention of mental retardation


1) Genetic counseling to parents of mentally retarded child which gives
them knowledge on the causes of mental retardation to avoid having more
mental retarded children in future.

87
2) Diagnosis of mental retardation before birth gives parents options of
abortion and subsequent family planning practices.
3) Vaccination against rubella infection which is one of the causes of mental
retardation.
4) Amniocentesis and chorionic villus samples are diagnostic tests to detect
number of abnormalities such as genetic abnormalities, spinal cord or
brain defects in babies.
Treatment for mental retarded child
The primary care doctor in the consultation with number of specialists, develop
comprehensive individualized program for child with mental retardation
 A child with development delays should be started on an early
intervention program as soon as the diagnosis is made.
 Emotional support of the family is an integral part of the program.
 A child with retardation usually does best living at home or at community
based residence and if possible attending a normal day care center or
preschool program
 Psychological support to the families, which may also need help with
burdens of daily care in order to prevent disruption or discord in the
family.
A retarded adult can be provided with long term residence in an apartment,
cluster, hostel, or nursing home

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5. NEONATAL TETANUS

Definition This is acute, preventable but often fatal disease of the central
nervous system caused by clostridium tetani which is characterized by painful
muscular rigidity primarily involves the masseter muscles and neck muscles.

Pathophysiology

 The organism lives in the gut of an animal such as the cows, sheep, and
goats as a normal flora. The organisms are passed in the dung of the
animal into the soil in form of spores when the human beings with open
wound comes into conduct with it, it gets entry. At the site of entry the
tetanus bacilli multiplies and produce toxins known as ( exotoxins) which
passes to motor nerves up to spinal cord and brain causing severe
irritation of the nerve cells, which results into violent contraction
(spasms) of muscles.
Incubation period

3-14 days in the new born babies. Although the symptoms may occur within 24
hours they may progress for as long as 8days.

Incidence

 Common in babies born before arrival to the hospital


 In homes where domestic animals are kept

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Mode of spread

In the new born babies, it passes through the umbilical cord, through the
wounds and scratches.

Predisposing factors

 Cutting babies cord with reeds, unsterilized razorblades or broken bottles


in the villages
 Application of native medicines on the cord or wound or any cut
 Use of dirty dressings
 Application of cow dung on the umbilical cord
 Application of powder on the cord
 Cutting babies cord with contaminated scissors and using unsterile
equipment during 2nd stage of labour

Signs and symptoms

Cardinal Signs and symptoms

 At the site of entry, the tetanus bacilli multiply and produce toxins which
pass to motor nerves up to spinal cord and brain causing severe irritation
of the nerve cells, which results into violent contraction (spasms) of
muscles.
 Painful stiffness of the jaw and neck muscles
 Severe spasms of the jaw muscles (lock jaw/trismus) make the mouth to
become difficult to open accompanied by difficult in swallowing i.e.
(dysphagia), difficult in speaking (aphasia).
 Raised eye brows
 Mouth corners pulled outside causing a facial muscle paralysis (false
smile)
 Opisthotonos (tetanus spasms the head is retracted, the back is arched
with the great rigidity of the muscles of the neck and the back).
 Photophobia (sensitive to light).
Other signs and symptoms

 Sign of infection are present i.e. inflammation of the nearby areas (the
cord)
 Wetness of the cord
 Offensive smell
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 Pus discharge form the cord
 Loss of weight due to starvation
 Temperature may be high or subnormal
 Headache may be present in older children
 Retention of urine due to spasm of urethral sphincter muscles
 Rapid pulse which may be irregular
Management
Management at maternity Centre
 Receive the mother and the baby and take brief history
 Keep the air way clear
 Sedate the baby with: diazepam 0.5mg/kg body weight,
phenobarb:2.5mg/kg or chlorohydrate30-60mgs
 Then send the patient with the note to the hospital
 Give antibiotics like crystalline penicillin 50,000 iu/kg body weight every
12hours until you get the baby to hospital.
Hospital management
Aims

 Neutralize the toxins in circulation


 Preventing and controlling of the spasms
 Prevent complication
Admission

Admission is in the intensive care unit where close and constant observation and
equipment for monitoring and respiratory support are readily available.

A quiet environment should be ensured to reduce external stimuli. The infant is


handled as little as possible and extra effort taken to avoid any sudden or loud
noise to prevent convulsions.

Medical treatment

 Dr. Orders sedatives according to his/her choice i.e. diazepam 0.5mg/kg


body weight or phenobarbital 2.5mg/kg/body weight
Normally these sedatives are given every after 6hours at an interval of 3 hours.
Therefore, only two types are used.
 The dose may be increased according to the severity of the spasms and
gradually decreased as the spasms become less frequent and mild.
 Anti-tetanus serum is ordered by the doctor doe 50,000 iu for babies,
100,000 iu for older children given intramuscularly as initial dose.
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 Antibiotic treatment with penicillin G (alternatively erythromycin or
tetracycline in older children with allergy to penicillin) is given when the
child is fully sedated.
Nursing care given

The aim is to control and eliminate stimulation of the muscle spasms from
sound, light, and touch.

 Environment
 A dark room is ideal but still sufficient light is essential so that the child
can carefully be observed.

 Observations
 Take observations such as temperature 2 time a day or 4hourly if raised,
pulse and respirations are done 4hourly and spasms are observed for
frequency and duration.
 Any severity should be reported, observe the part which are affected and
the cause of the spasm
 Record everything noted
Note: muscle relaxants and sedative can cause respiratory depression; therefore,
the child must be assessed for excessive central nervous system depression.

Oxygen saturation is monitored and when needed blood gases (oxygen and
carbon dioxide) are obtained frequently to evaluate respiratory status.

 Hygiene
- Top tailing is done daily
- Oral care done 4hourly
- In case of neonate care of the cord is done with daily cleaning with
normal saline.
 Diet and feeding
- Hydration involves monitoring an iv infusion
- A nasogastric tube is passed and expressed breast milk is given to the
neonate. Most of the drugs (oral) can be given through the tube.
This tube can be passed when the baby is sedated.

 Care of the bladder and bowel


Ensure that baby and the older child empties the bladder and bowel.

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 Treatment
Prescribed medications are administered such as sedatives or muscle relaxants
to help reduce tetanic muscle and prevent convulsions.

 Advice on discharge
- Bring the child for review
- Take back the baby for YCC immunization
- Continue breast feeding
- Observe hygiene
Prevention
 Health education on the following
- Discourage delivery in the villages
- Danger of use of native medicines on the cord
- Provision of adequate training and equipment for indigenous midwives to
decrease incidence of tetanus as well as of other neonatal infections
 Encourage mother to deliver at the hospital
 Encourage mothers to move with delivery kits
 Personal hygiene is emphasized
 Immunize all women at the child bearing age
 Ensure safe and clean practices during child birth
 Avoid smearing the flow with the cow dung on the floor
 Clean and aseptic Wound dressing
 Complications
- Fractures of the spine or other bone may occur as a result of the spasms
and convulsions.
- Pneumonia
- Brain damage
- Growth retardation
- Exhaustion
- Respiratory failure
- Retention of urine
- Death due to
 Obstruction of airway by saliva
 Spasms of the larynx which completely closes the airway
 Involvement of the bronchial secretions and some instances resulting
in cessations of breathing

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DISEASES OF GENTO-URINARY TRACT:
Definition
Is the infection of the urinary system commonly occurring in females compared
to men: ratio of 5:1. it involves the kidneys, ureter, bladder and urethra.

Pathogenesis:
 It is usually an ascending infection of colonic micro-organisms, i.e. those
normal flora of the colon. This occurs if there is faecal contamination of
the urinary urethral meatus.
 Organisms multiply in situation of stasis of urine. It can also occur due to
haematogenous spread of organisms.

Risk factors for developing urinary tract infection:


 Female because they have shorter urethra
 Uncircumcised males
 Sexual intercourse which is unprotected
 Catheterisation: this must be done aseptically and also depending on the
duration of the catheter stay in situ
 Obstructive uropathy, i.e. obstruction in the flow of urine as in urethral
stricture and enlarged prostate glands.
 Neuropathic bladder, that is, when there is no more contractility of the
bladder and the commonest cause is diabetes mellitus.
 Spill over of glucose into the kidneys and excretion in urine > 180mg/dl

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 Vesico-ureteric reflux disease where urine regurgitates into the kidneys
from the bladder and ureters. This commonly occurs in old age
neuropathy >60 years.
 Pregnancy: commonly women get UTI as the uterus constricts the urethra
or reduces the bladder capacity, thus causing urine stasis. It is usually
unilateral especially on the right side.
 Hygiene: when cleaning the anus from posterior to anterior aspect.

Clinical features: as for pyelonephritis:


 Abdominal pain from the lateral aspect
 Fever associated with rigors
 Nausea and vomiting
 Malaise, that is, general unwellness
 On examination, there is tenderness on the flank side of the kidneys.

Investigation:
 Urinalysis for pus cells and casts of WBCs.
Management:
 Phorogenous antibiotics like ciprofloxacin, best choice for UTI, Amoxil,
gentamycin + ampicillin 500mg 6 hourly.
 Pyelonephritic patients are commonly very sick so they are given i.v
gentamycin 160mg o.d and i.v ciprofloxacin 200mg bd for 5 days, i.v
ceftriaxone 1-gram o.d for 5 days
 i.v fluids to flash the kidneys, ureters, bladder and urethra and to prevent
precipitation of drugs.
 Analgesics for pain like Panadol 1g tds for 3 days.
 Identify the possible risk factor for UTI if DM, then treat it. Encourage
the patient to reduce on the risk factors.
Complications:
 Urethral scarring
 Urethral stricture
 Recurrent urethritis

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1.URETHRITIS:
Definition
Is inflammation of the urethra
Caused
By gram negative organisms such as E. coli, which is responsible of 75-90% of
UTI. Others include: proteus, klebsiella, staphylococcus aureus and
saprophyticus; viruses such as adeno virus, murbag and Ebola viruses which
commonly cause cystitis. Viral UTI presents with haematuria.
Signs and symptoms
 Dysuria,
 Incontinence of urine,
 Stress incontinence.

2.CYSTITIS
Definition
This is the inflammation of the bladder which usually result from the invasion
of bacteria into the urinary tract.
 In the female patient, bacteria that enter the urinary tract usually originate
from either the rectum or the vagina and ascend upward via the urethra.
 In the male, cystitis is usually the result of an existing problem in the
urinary tract such as prostatitis or benign prostatic hypertrophy.
Incidence
More common in women than men and it is due to the length of the female
urethra and the proximity of the meatus to the vagina and the rectum

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Causes
Bacterial infection e.g. E. coli from the colon
Pathology
When bacteria enter the bladder, they adhere to and multiply in the bladder’s
mucosal surface. As the infection intensifies, the surface of the bladder becomes
reddened and oedematous; areas of ulceration also develop. Symptoms of pain
and urinary urgency result when urine comes in contact with the irritated
surface of the bladder. This irritation is exacerbated when the bladder becomes
slightly distended with urine.
Clinical manifestations
 Supra pubic (lower abdominal) pain usually burning in nature
 Tenderness on palpation
 Lower back and abdominal pain when passing urine
 Urge incontinence: the patient cannot wait if the place is far to pass urine.
She can pass urine on her clothes
 Frequent urination more than before and the colour is deep yellow or dark
and also during the night. This is different from the clear urine passed by
DM patient.
 In severe infection, there may be retention of urine
 Dysuria: pain on micturition
 Pyuria
 Haematuria is not uncommon
 Urine often has strong odour
 features of obstructive uropathy.

Investigation
 Midstream specimen of urine for microscopy of pus cells, RBCs, protein,
WBCs, C&S
 ultrasound in the abdomen showing thickening of the bladder wall.

Management
 Ensure an increased oral intake of up to 3000 ml/day because a more
dilute urine lessens the irritation to the bladder.
 Encourage voiding at regular intervals. Frequent bladder emptying
decreases intravascular irritation and prevents stasis of urine.
 Alkalinise the urine with oral sodium bicarbonate solution 5% (dissolve
5g in 100ml water) twice a day.

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 Cotrimoxazole 1.92g (4 tablets of 480mg) single dose. Child 48mg/kg
single dose
 Or Ciprofloxacin 500mg single dose. Child 10 – 15mg/kg single dose
 for viral cystitis: give ampicillin 500mg 6 hourly i.v for 3 days + i.v
gentamycin 80-160mg bd for 3 days.
 If no response or recurrent infections:
 Do not continue to treat blindly
 Refer for investigation of C&S and further management
Prevention
 Improve personal/genital/perineal hygiene
 Avoid sharing of bathing basins, towels, soap

3.PYELONEPHRITIS
This is an infection of the upper urinary tract involving one or both kidneys (but
not usually involving the glomeruli) which may extend to the bladder. This is an
ascending infection and pathogenic organisms usually reach the kidneys from
the bladder via an incompetent urethral vesicle junction. The condition may be
acute or chronic.
ACUTE PYELONEPHRITIS
Causes
Exciting or causative organisms
 E. Coli
 Streptococci
 Staphylococci
 Pseudomonas
Conditions causing obstruction associated with urinary stasis
 Enlarged prostate
 Pressure from the pregnant uterus
 Uterine fibroids pressing of the ureters
 Urethral stricture
Others
 Incomplete emptying of the bladder in neurological conditions
 Recent instrumentation of the urinary tract as in catheterisation
Symptoms and signs
 The patient complains of persistent ache (pain) which may radiate from
the renal angle to the iliac fossa and sometimes to the suprapubic area.

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 Fever with chills and general malaise accompanied by nausea, vomiting
and diarrhoea. Sometimes rigor may accompany the fever.
 Dysuria and frequency of micturition.
 Urine contain pus, bacteria and white blood cells.
 Upon examination, there is tenderness in the area of the costovertebral
(renal angle).

CHRONIC PYELONEPHRITIS
This follows acute Pyelonephritis which has not been adequately treated. It
produces chronic ill health and may cause hypertension when both kidneys are
involved. It is the commonest cause of death in renal failure in young patients.
Causes
As for acute
Clinical pictures
 Patients with chronic Pyelonephritis are usually asymptomatic.
 A dull aching pain in the loin may be present
 Proteinuria and oedema may occur
 Fever and malaise
 Frequency and dysuria on and off
Differential diagnosis
 Appendicitis
 Salpingitis
 Cholecystitis
Investigations
 Urine: microscopy for pus cells and organisms, C&S of midstream
specimen of urine
 Blood: full count, C&S, urea and electrolytes
 IV urography.
Management
 Ensure adequate fluid intake to irrigate the bladder and dilute the
bacterial concentrations

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 Ensure perianal hygiene
 Regular complete emptying of the bladder and /or double voiding
(additional attempt to empty the bladder after the initial urine flow
ceases)
 Chemotherapy
Paracetamol 1g (10mg/kg) 8 hourly for pain and fever
Cotrimoxazole 960mg every 12 hours for 10 – 14days. Child 24mg/kg per
dose OR
Amoxicillin 500mg every 8hours for 10 – 14days. Child 15mg/kg per dose
In severe cases or if no response to the above treatment in 48hours give:
Ampicillin 1 – 2g IV or IM every 6hours for 7 – 14 days. Child 50mg/kg per
dose
Plus, gentamycin 2.5mg/kg IV/IM every 8 hours for 7days. Reduce dose in
renal impairment.
Following initial response to the parenteral therapy consider change to
Ciprofloxacin 750mg every 12hours for the rest of the course

Complications
 If the diagnosis is missed in acute stage, the infection may become
chronic
 Both cases lead to progressive renal scarring and destruction and may
result to a small atrophic scar non – functioning kidney

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4.ACUTE GLOMERULONEPHRITIS
Definition
This is characterised by diffused inflammation of the renal cortex (glomeruli) of
both kidneys.
This is inflammation of the glomerulus.
Causes
 Its onset is usually secondary to infection of the upper respiratory tract,
most commonly caused by beta – haemolytic streptococci (post
streptococcal infection)
 malaria parasites (falciparum malariae)
 It may be a result of the primary infection elsewhere in the body and be
caused by primary staphylococcus, pneumococcus or a virus
 It is thought to be due to an abnormal immune reaction to infection
Incidence
Glomerulonephritis can occur at any age; it has a higher incidence in males than
in females. It is common in the young and the peak age is 7-10 years.
Adolescents and young adults are also commonly affected by the acute
glomerulonephritis.
Pathogenesis:
 An occurrence of a streptococcal infection which can either be sore throat
or a skin infection.

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 There follows an immune response which is mounted against the
streptococcal infection (a specific antibody is produced against
streptococci)
 These antibodies destroy the glomerulus because it resembles the
antigens of the streptococci. This usually occurs 2-3 weeks after the
streptococcal infection has taken place.
 The destruction of the glomerulus permits the red blood cells which is
passed in urine as haematuria and pus-cells, RBC casts. The destruction
further causes reduction in the filtration process and reduced ultra
filtration stimulates angiotensin I release which in turn is changed to
angiotensin II which causes constriction of arterioles, hence increasing
total arteriolar resistance, leading to elevation of blood pressure.
 Angiotensin release further causes production of aldosterone which
causes reabsorption of sodium and water, leading to increase in cardiac
output and elevation of blood pressure.

Symptoms and signs


 The onset is usually sudden with history of sore throat or skin infection,
elevated temperature, headache and vomiting.
 The patient presents with body swellings of the face and lower
extremities which tends to become worse in the mornings on waking up
with elevation of hypostatic pressure.
 does not cause ascites
 Costovertebral angle tenderness and flank pain likened to renal colic.
 Urinary changes:
- Decreased urinary output and dark in colour
- Microscopic haematuria making the urine to appear dark, concentrated
and smoky
- Albumin is always present in large amounts
- Casts may be present and can be seen

 Hypertension often develops. In severe cases, it may be extremely high


with severe headache, palpitations, easy fatigability, visual disturbances,
vomiting and convulsions (hypertensive encephalopathy).
 features of cardiac failure

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 As the disease progresses, the patient experiences shortness of breath,
lethargy and anorexia.
Investigations
 Urine: protein, microscopy for pus cells, red blood cells, red blood cell
casts, proteins negative, glucose negative.
 Blood: urea and Creatinine levels, and electrolytes
 Ultrasound scan of the kidneys: size, shape of the kidneys
 blood pressure
 Throat and skin swab where indicated for C&S
Management
The disease is usually self-limiting and the majority of patients may recover
spontaneously.
 Rest:
The patient should be nursed in a complete bed rest in a warm well-ventilated
room. Even ambulation a short distance must be restricted until the kidneys
have had time to heal and there is little or no protein and blood in the urine.

 Dietary regulations (Diet regimen)


Protein should be restricted in the diet, adequate calorie from carbohydrates and
fats ensures minimum protein breakdown. About 20 – 40g of protein daily will
be adequate.
 Fluids and electrolytes
Assess the patient frequently for signs and symptoms of fluid overload. Daily
weighing of the patient. Fluids must be restricted to 1500mls in 24hrs when
oedema and oliguria is present. An intake and output chart must be kept and the
urine examined daily for albumin, RBCs and casts.
 Food
Should be given in such quantities as the patient desires but consisting mainly
of carbohydrates and fats.
 Salts
Should not be used in cooking or added to food (salt free diet).
If oedema is severe, no salt diet should be given.
Avoid or use with caution any drugs excreted in by the kidney
 Chemotherapy
Treat any continuing hypertension (Ref UCG 2003 page 168), e.g. captopril
25mg o.d daily + calcium channel blocker like nipedipine

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diuretics to reduce blood volume and oedema in turn
Treat primary streptococcal infection with a 10day course of
- Phenoxy methyl penicillin 500mg every 6hours. Child: 10 – 20mg per
dose Or Amoxicillin 500mg every 8hours. Child: 15mg/kg per dose.
- If allergic to penicillin give erythromycin every 6hours. Child: 15mg/kg
per dose
- Prophylactic treatment: penicillin every month or erythromycin in case of
allergy to the penicillin.

Prognosis: is always poor with acute glomerulonephritis than with nephritic


syndrome
Prevention
 Energetic treatment of throat and skin infections
 Avoid overcrowding
 Adequate ventilation in dwellings.
Complications:
 Congestive cardiac failure
 Renal failure
 Nephritic syndrome

The patient may have both nephritic syndrome and acute glomerulonephritis
and they are called to have nephritic nephritis and the prognosis is poor.

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5.NEPHROTIC SYNDROME
Definition
Is a collection of symptoms caused by many diseases that affect the kidneys,
resulting in severe, prolonged loss of protein in the urine, decreased blood levels
of proteins especially albumin, retention of excess salt and water in the body
and increased levels of fats in the blood.
It is a renal disease characterized by proteinuria, hypoproteinaemia, oedema,
hyperlipidaemia.
Incidence
Nephrotic syndrome can occur at any age but usually, more children are
affected than adults. In children between 18 months and 4 years, with the peak
age of 2-6 years in young adolescents, young adults and children more than 1
year, more boys are affected than girls (ratio of 2:1).
90% of nephrotic syndrome are idiopathic while 10% is due to
glomerulonephritis.
Causes
Are usually unknown but could be due to the following predisposing factors
Disease
 Amyloidosis

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 Cancers
 Diabetes mellitus
 HIV (common in black people who have the disease)
 Leukaemia
 Lymphomas
 Systemic lupus erythematosus
 Glomerulopathies
Drugs
 Aspirin-like analgesics
 Heroin taken IV
Allergies
 Insect bites
 Sunlight
 Poisons
Rarely congenital

Pathogenesis:
There is increased permeability of the glomerulus because of the loss of
negative change in glycoproteins at the glomerulus which causes exudation of
proteins from the glomerulus into the tubules. The protein lost in the urine is
albumin.
Loss of protein in urine cause low concentration of proteins in the blood
circulation which is hyperproteinaemia.
Hyperproteinaemia causes a reduction of oncotic pressure. A low oncotic
pressure in turn causes the loss of the fluid from the vessels into the tissue
hence, oedema.
Exudation from the blood vessels to the tissues causes hypovolaemia which
leads to the reduced blood supply to the kidneys. The low perfusion of the
kidneys stimulates the release of angiotensin I from the kidneys which is
converted to angiotensin II in the liver which in turn causes constriction of the
efferent arterioles in the kidneys so that more fluids is regulated into the
glomerulus causing further loss of proteins in the urine.
Angiotensin II also causes the release of aldosterone at the distal collecting
tubule and distal convoluted tubule to cause re-absorption of sodium ions and
water back into circulation which worsens the oedema.

107
Hyperproteinaemia stimulates the liver to produce more proteins which include:
albumin, glycoprotein and lipoproteins and other factors of coagulation. There
is also decreased production of lipase which causes the accumulation of lipids in
the circulation and it is called hyperlipidaemia.

Signs and symptoms


Early symptoms include
 Loss of appetite and a generally sick feeling
 body swelling: begins from the face, feet and eventually to the rest of the
body. The swelling is normally worse in the morning and gets well at the
course of the day. Swelling of tissues from excess salt and fluid retention
(generalised anasarca). Ascites and shortness of breath. Puffy eyelids.
The fluid causing tissue swelling moves round, accumulating in the
eyelids in the morning and in the ankles after walking.
 Abdominal pain and muscle wasting
 Other symptoms include swelling of the knees and in men, the scrotum
 Low or normal BP (normotensive or hypotensive)
 Urine output may decrease and kidney failure may develop. The colour of
urine is normal and no microscopic haematuria.
 Urine contains a high level of proteins
 A low plasma albumin due to the loss of albumin in the urine
 High cholesterol level
 some degree of fever may be experienced.
Investigation
As for acute glomerulonephritis plus serum protein and cholesterol
 urinalysis: urine protein is always above +++ or ++++
 24hour urine volume/collection: collect the urine over 24 hours and add
the volume (urine output is 0.5-1ml/kg/hour.
 24hour urine protein: will be about 2gms
 Blood: do serum albumin and lipid profile. There will be high lipid and
low serum proteins in blood.
Management
 Give a high protein diet
 Restrict salt intake in the diet in an attempt to reduce water retention
 Restrict water/fluid intake
 Monitor intake and output and keep FBC up-to-date

108
 daily 24hour urine collection: the amount should be able to rise with each
day to show improvement
 do urine protein test until the protein is negative
 Daily weighing and recording to assess the oedema
Treatment
 This is aimed at the underlying cause. Detect treatable causes and treat
accordingly.
 If there are clinical signs of/suspected infection give antibiotics as in
acute glomerulonephritis.
 If the patient from the area of endemic Schistosomiasis give praziquantel
40mg/kg single dose.
 If no cause can be found give symptomatic treatment in the form of:
 If the oedema is severe give
 Furosemide 40 –80mg each morning to induce diuresis. Child: 1
–2mg/kg per dose.
Note:
 Use of furosemide is not routine in children
 Only give if oedema is interfering with breathing or urination
 Carefully watch out for electrolyte imbalance and hypovolemic shock
 Prednisolone 1-2mg/kg daily (max 60mg)
- Continue until no further Proteinuria (around 6-8 weeks)
- Gradually reduce the dose after the first four weeks e.g. reduce by
0.5mg/kg per day each week.
 When oedema has subsided and if still hypertensive, give appropriate
antihypertensives.
 If no improvement after 4 weeks or patient relapses, refer for
management. Nephritic syndrome tends to relapse, i.e. he may relapse
more than 3 times in 12 months.
 Give prophylactic antibiotics.

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6.RENAL FAILURE
Definition
Is a state in which the kidneys’ function is no longer able to maintain the body’s
chemistry within normal limits A patient is said to be in renal failure when
his/her renal function is inadequate to maintain the volume and composition of
his internal environment. It may occur suddenly as an acute and gradually over
years as chronic.
It is the failure of the kidneys which is usually occurring in days or weeks
characterized by reduced volume of urine. The normal urine output is
1ml/kg/hr.

ACUTE RENAL FAILURE


ARF occurs suddenly and is often reversible. It generally follows an ischaemic
or toxic trauma to the kidney. Recovery is dependent on the cause and
underlying disease process.

Causes
This can be classified into three functional groups:

110
I. Pre-renal failure:
These cause hypo perfusion to the kidneys:
This is caused by interference with the renal blood flow. The kidney is
dependent on an adequate blood flow to maintain its function. A decrease in
perfusion results in decreased glomerular filtration. The renal function is
impaired without parenchyma damage and the impairment is rapidly reversible
with fluid therapy. The causes of pre-renal failure include:
 Extracellular fluid deficits as in shock and dehydration
 hypovolaemia as seen in injuries, burns, etc.
 Decreased cardiac output such as in CCF, pericardial tamponade and
acute pulmonary embolism
 Decreased vascular resistance as in anaesthesia and hepatorenal syndrome
 Vascular obstruction as in dissecting aneurysm and bilateral renal artery
occlusion
 renal artery Stenosis.
II. Intrinsic renal failure;
This means that there is a problem within the kidneys themselves that
interferes with the functions.
This is divided into two groups:
a) Acute tubular necrosis (ATN)
The major causes of acute tubular necrosis include:
 Nephrotoxic agents: this include organic solvents (e.g. carbon
tetrachloride), drugs (e.g. amphotericin, gentamycin, kanamycin and
sulphonamides) and poisons/heavy metals (e.g. mercuric chloride)
 Postoperative: high risk cases include major abdominal surgery in
patients over 50 years, major surgery in jaundiced patients and biliary
tract sepsis
 Mismatched blood transfusion: The Hb which is released from the RBCs
is very toxic to the kidney causing severe destruction to the parenchymal
cells
 Crush injury: severe muscle injury allows myologlobin to escape from
the cells and this like haemoglobin is very toxic to the kidneys.
 Acute glomerulonephritis
 Acute interstitial nephritis
 Septic abortion: ANT may result from a complicating septicaemia or
from drugs used to induce the abortion.

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 Acute haemorrhage: examples include gastrointestinal haemorrhage and
PPH
 Extensive burns: ATN may be related to hypovolaemia, infection and
DIC.
 Unrelieved severe pre-renal failure: multivariant analysis of risk factors
identifies hypotension, excess aminoglycosides as highly significant
especially.
b) Other causes
 Bilateral cortical necrosis
 Malignant hypertension
 Severe pyelonephritis
III. Post renal failure
This is caused by obstruction to the flow of urine from the renal tubules to the
urethral meatus. The obstruction may be caused by:
 Urethral or bladder cancer
 urethral stricture
 phimosis
 Renal calculi
 Atony of bladder
 Prostatic hyperplasia or cancer
 Cervical cancer
 Post-surgical or traumatic interruption

Pathology
Acute renal failure is caused by two main mechanisms:
1) ischaemic changes to renal cells or
2) renal changes as a result of toxic substances.
Ischaemia may be a result of decreased perfusion leading to the death of renal
cells and compromised renal function. Toxic substances decrease renal function
by attacking the renal cell membranes and destroying their ability to maintain
haemostasis. In this case both kidneys as a rule are affected equally.
Clinical presentation
 The onset is sudden and the individual appears acutely ill.
 The patient may exhibit either oliguria or anuria
 Fluid overload is exhibited by oedema and hypertension when the intake
of fluids exceeds the urinary output and insensible losses. When the

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overload becomes severe, the signs and symptoms of CCF and pulmonary
oedema are present.
 Retention of electrolytes and metabolic waste such as urea and Creatinine
produce a group of symptoms known as uraemia (azotaemia). These
include nausea, vomiting, fatigue, drowsiness, twitching and shortness of
breath. Confusion, convulsions, coma or gastrointestinal bleeding may
also be present.
 Pericarditis may also develop as a result of irritation of the pericardium
by the build-up of metabolic wastes.
 The course of renal failure is usually characterised by several phases.
 The onset phase is the period from the precipitating event to the onset of
symptoms.
 The oliguric phase occurs from the onset of symptoms, lasting as long as
8 weeks. The longer this phase lasts the worse the prognosis. The patient
is acutely ill at this time.
 The diuretic phase is marked by a levelling of blood urea nitrogen
(BUN) level and a return to glomerular filtration. The urine output may
be greater 2000 ml/day and dehydration can occur. The
 The final phase is that of recovery. This phase lasts 3 to 12 months.

ENDEMICS AND EPIDEMICS


1. MEASLES
Objectives
1) Definition
2) Causes
3) Mode of spread
4) Incubation period
5) Incidence
6) Signs and symptoms
7) Treatment
8) Complications
9) Prevention
Definition
Measles rubeola is an acute febrile eruptive infection caused viruses. Its most
common in childhood

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Cause
Its caused by virus known as rubeola virus
Mode of spread
Its spread through air droplets when coughing and sneezing
Incubation period is 10days
Incidence
The maximum incidence is between 6months to 5years
The attacks are most common in winter and spring when it spreads among
children inform of epidemics.
Signs and symptoms
Measles present in two stages
 Catarrhal stage
This is the stage when rashes have not appeared
They present as follows
 Onset is acute with fever
 Coryza
 Sneezing
 Redness of the conjunctiva
 Swelling of the eye lids
 Watery eyes
 Cough
 Hoarseness of the voice
 Photophobia (fear to see light/reaction to light)
 Koplik spots (typical)
 Child appears miserable
 Irritability
 Increased temperature of 380c-390c until rashes appear
 Exanthemataus stage
Usually appear on the 4th day of illness and this is the stage when rashes appear.
 Rashes appear on the fore head and behind the ears soon spreads all over
the body.
 Fever increases on appearance of rashes and subsides
 Dark red macular or maculopapular rashes which are numerous.
 Rashes fully erupts then gradually fades followed by peel of the skin.

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Treatment/management
Treatment of measles depends on the severity
If the measles is uncomplicated treat as OPD case and do the following,
- Ensure adequate fluid intake and good feeding
- Reduce temperature by tepid sponging
- Give antipyretics to lower fever like paracetamol
- Give single dose of oral vitamin A caps 200,000iu
- Advice the mother to give extra meals for 5day
- Make follow up
In case of complicated measles
-Admit the child in the hospital on isolation unit or ward
-Give balanced diet with protein and energy rich foods
-Observe for the signs of pneumonia
-If stomatitis is present clean the mouth 4-6hourly daily
-If there is gastro enteritis give plenty of oral fluids
-If convulsions rule out malaria/meningitis and give muscle relaxants like
phenorbabitone
- If conjunctivitis, give oral vitamin A caps 200,000iu and CAF eye drops
- Treat otitis media with PPF for 5days
- Reduce temperature by giving antipyretics like paracetamol and tepid
sponging
- Advice the mother of extra-meals.
Complications
 Broncho pneumonia (responsible for death)
 Febrile convulsion
 Stomatitis
 Appendicitis
 Encephalitis
 Otitis media
 Conjunctivitis /corneal ulceration
 Malnutrition (kwashiorkor)
 Laryngitis
Prevention
Through immunisation of all children with measles vaccines
NB: measles that can be transmitted from mother to child during pregnancy is
called German measles caused by rubella virus

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2. MALARIA
Objectives
1) Definition
2) Causes
3) Types of plasmodium
4) Mode of spread (transmission)
5) Pathogenesis (life cycle)
6) Signs and symptoms
7) Diagnosis
8) Treatment
9) Complication
10) Prevention
Definition
Malaria is an acute infective febrile illness caused by protozoa of plasmodium
genus (spp)
Causes

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Malaria is caused by a parasite of the genus plasmodium
Types of plasmodium species
 Plasmodium falciparum
 Plasmodium vivax
 Plasmodium ovale
 Plasmodium malarae
 Plasmodium knawel
Mode of transmission or spread
The parasite is transmitted to human by the bite from female anopheles
mosquitoes

Life cycle of mosquitoes in man

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Life cycle of malaria in both mosquitoes and man

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Malaria is transmitted by female anopheles’ mosquitoes which
requires blood for the development of its eggs.
In mosquitoes
Sexual reproduction
The male and female gametocytes develop into gametes and then
fuse in the stomach of the mosquito to form zygote, this develops
into mobile ookinete which migrate through the wall of stomach
to form oocyst. Oocyst matures and release sporozoites which
migrates to the salivary glands of mosquito ready for delivery in
the next meal.
Illustrated below
Gametocytes gametes zygote ookinate oocyst
sporozoites salivary gland
In human
1. Sporozoites in the mosquito salivary glands are injected
into the host via proboscis of mosquito.

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They quickly migrate to the liver and are only in circulation for
30minutes.
2. Hepatic (liver) stage
Sporozoites are taken up by the Kuepfer cells of the liver and
then pass through into hepatocytes or liver cells there it develops
into hepatic schizonts releasing thousands of merozoites in to the
general circulation this takes about 9-14days
3. Erythrocytic (blood stage)
The merozoites released from the liver cells invade the red blood
cells and then develop within the red blood cells forming rings
(immature trophozoits) into blood schizonts then rapture the
red blood cell releasing numerous merozoites which invade new
red blood cells. It’s this part of cycle where signs and symptoms
are seen.
4. Gametocytes
At an unknown stage or time in the red blood cells cycle sexual
forms develop and are in turn responsible for the survival and
transmission of parasites. The female and male gametocytes
circulate for a few weeks and are taken up by feeding
mosquitoes.
Signs and Symptoms include;
 Fever chills
 General malaise
 Joint pain
 Back pain
 Nausea and vomiting
 Headache
 Diarrhoea
 Dizziness
 High temperature
 Rigors
 Splenomegaly
 Convulsion
 Anaemia

FEVER

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Definition
Is alteration of body temperature
Stages of fever
 Cold stage
- Temperature rises
- Shivering
- Lasts for 1-2 hours
 Hot stage
- Temperature is high (400c)
- The skin is dry and hot
- Severe headache
- Often nausea/vomiting
- Lasts for 3-4hours
 Sweating stage
- Temperature falls rapidly
- Patient sweats profusely
- Lasts for 2-4hours
- Patient is relieved but exhausted
Diagnosis
 Clinical presentation
 Lab investigations eg RDT and BSXMPs
Differential diagnosis
 Viral infection
 Early measles
 Otitis media
 Meningitis
 Upper respiratory tract infection
 Relapsing fever
Treatment
The treatment of malaria depends on the severity
Its categorised into two i.e.
Uncomplicated malaria and complicated or severe malaria.

Medication – first line treatment for uncomplicated malaria


Artemisinin combination therapy (ACT)

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1. Coartem (Artemether 20mg and Lumefantrine 120mg).
Four tablets given x 6 doses for adults– at diagnosis, then
at 8, 24, 36, 48 and 60 hours.
2. Artesunate and
3. Amodiaquine Four tablets x 6 doses as above
Medication – second line treatment for severe or complicated malaria.
1. Dihydroartemisinin and
2. Piperaquine (Duocotecxin) 3 tablets given daily for 3 days (adults)
3. Quinine – used where ACT is not available or contra-indicated
Give 10mg/kg IV over 4 hours in 5% glucose solution allow the patient to rest
for 4 hours for period 24hours. Then Change to oral syrup/tablets when patient
can drink for six days.
Side effects
 hypoglycaemia,
 deafness,
 cardiac arrhythmias,
 headache.
 Bitter taste.
4. Artemeter 1.5mg/kg im twice
5. Artesunate 2.4mg/kg iv
NB: antimalarial which are injectable should only be given to patients who
cannot take oral medication or who are seriously ill.

Nursing care management


 Reduction of temperature by tepid sponging
 Diet
 Oral care
 Eliminations
 Observations
 Hygiene
 Advice on discharge.
Complications
 Severe anaemia
 Hypoglycaemia
 Convulsion
 Major organ failure
 Splenomegaly
 Recurrent infection e.g. pneumonia, septicaemia
 Abortion
 IUFD

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 Growth retardation
Prevention
 Clear the bushes around home
 Open channel for stagnant waters
 Sleep under insecticide treated net
 Provision of prophylaxis
 Use of mosquito repellents
 Close windows and doors before 6pm
 Wear long sleeved shirts and trousers in the evening
 Application of oil on the water surfaces to destroy mosquito lavers.

3. TYPHOID FEVER
Objectives
1) Definition
2) Causes

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3) Mode of spread
4) Incubation
5) Pathology
6) Signs and symptoms
7) Diagnosis
8) Treatment
9) Complications
10) Prevention
Definition
Typhoid fever is an infection caused by salmonella typhii
It is a gram negative bacillus which causes the disease by liberating the
enterotoxin
Mode of spread
The bacilli enter the GIT through infected water, food, and milk. human carriers
excrete the organisms in the faeces or urine and if proper hygiene and sanitation
are lacking contamination of water food may result.
Incubation period
It takes about 10-14days
The bacilli localise mainly in the lymphoid tissues of the small intestine,
initially they cause inflammation (swelling) and subsequently ulceration. These
ulcers may bleed or perforate from the intestine bacillus enter the blood stream
and cause septicaemia with fever. The bacteria may also affect the gall bladder;
the heart may be affected by bacterial toxins.
Signs and symptoms
in the first week
 Onset is gradual
 General body malaise
 Headache
 Drowsiness
 Arching in the limbs
 Temperature rises in stepladder pattern
 Epistaxis
 Diarrhoea in children
 Vomiting
 Bradycardia

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In the end of first week
Rashes appear on the abdomen, consisting of small round red areas (rose spots)
which fades with pressure
In the second week (7th-10th day)
 Spleen is palpable
 Constipation is succeeded by diarrhoea
 Abdominal distention with tenderness at the right iliac fossa
 Bronchitis may develop
 Delirium
By the end of the second week the patient is gravely ill if no antibiotics is
started.

In the 3rd week


 Toxins increase and patient may go into coma and die
 Bleeding from intestines or perforations.
Prognosis is good if treated early.
Diagnosis
 Blood for culture (70-90%) during first week
 Stool for urine culture (10-15%) positive in the first one week and 75% in
the 3rd week
 Widal reaction useful for supporting clinical diagnosis
Treatment
 Isolation
 Nurse the patient in isolation
 Use disposable eating utensils
 Use urinals/ bed pans
 Disinfection of equipment
 Use protective gears like gloves
 Use barrier nursing
Supportive treatments
 Good nursing care and attention to nutrition requirement
 Give low residue foods which is easily digestible
 Avoid enema and laxatives because of danger of haemorrhage or
perforation.
 Avoid salicylates because it may cause gastritis
 Give paracetamol and do tepid sponging to reduce temperature.
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Curative treatment
 Iv ceftriaxone 75mg/kg od daily for 5-7 days
 Ciprofloxacin 125-250mg twice daily for 5-14 days
 Chloramphenicol 125-250mg 6hourly for 14 days
 Azithromycin 20mg/kg od for 5-7days
Complications
 Perforations
 Haemorrhage if localised may require surgery.
 Mental illness
 Anaemia
 Peritonitis
 Shock
Prevention
 Immunisation with typhoid paratyphoid vaccines given at one-month
interval recommended at the age of 5-6 years given subcutaneously, two
booster doses are given at the age of 10-16 years.
 Good public sanitation
Therefore, a yearly booster is required to maintain immunity

4. CHOLERA
Objectives
1) Definition
2) Causes (aetiology)
3) Mode of spread
4) Incidence
5) Pathology
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6) Incubation period
7) Signs and symptoms
8) Diagnosis
9) Treatment (management)
10) prevention
Definition
cholera is an acute intestinal disease characterised by sudden onset of profuse
watery stool, vomiting, rapid dehydration and circulatory collapse.
Causes
Cholera is caused by vibro-cholerae comma shaped bacillus gram-negative very
small curved mobile organisms.
Mode of transmission
Through faecal-oral route but almost all cholera infections are water borne.
The organism survives up to two weeks in fresh water and up to 8weeks in salt
water

Water

Faeces/vomitus mouth

Food

Incidence
The disease is endemic in countries of Asia and Africa
Pathology
Cholera vibrio multiply in the lumen of the intestine and by the action of
powerful enterotoxin liberated by them, the cholera organisms induce
outpouring of profuse alkaline small bowel fluid. There is mild to severe
fulminating diarrhoea leading to rapid dehydration and electrolyte imbalance.
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Incubation period
Few hours to 5days
Signs and symptoms
The typical cases of cholera present in three stages
The first stage
lasts for 3-12hours and the following signs are present.
 Profuse watery stool pour from the patient soon faecal matter disappears
from the stool which becomes almost clear fluid with the flakes of mucus
giving the classical rice-water appearance.
 Vomiting follows the diarrhoea at first food is vomited soon after only
rice-water is vomited.
 Severe abdominal pain (cramp)
 Severe muscle cramp (limbs) because of salt lost.
In the 2nd stage
 Dehydration is noticed and collapse
 Body is cold
 Skin is dry and inelastic
 Blood pressure is low or unreportable
 The pulse rate is rapid and feeble
 Urine production stops
 Patient may die of shock
In the 3rd stage
 This is the stage of recovery, either spontaneously or with treatment.
 Diarrhoea decreases
 Patient is able to drink or take fluids
 General condition improves

Management and treatment


- Patient with cholera can be admitted to temporary hospital (school or
church)
- Strict isolation is not necessary as only the vomitus and stool are
infective, which should be properly disposed and disinfected.
- Hospital equipment should be cleaned with disinfectants and sterilised.
- Patients are treated on cholera bed with hole through which the stool
continues to pass into the bucket and measured.

128
- Essential cure of cholera is rehydration this even without any drug will
save many cholera cases if started in time.
- Start iv infusion which should run very fast until the pulse and blood
pressure stabilises.
- Monitor the pulse, blood pressure and neck vein and pulmonary oedema.
- Maintain fluid balance chart.
NB: 60kg patient is given 8-10litres of fluids
1-2litres is given within the first 20minutes then the remaining is given over
2hours and the fluid is given at the rate of 50-100mls/minute and ringers lactate
is fluid of choice because it contains Na131, K15, Cl111.
 After vomiting has stopped by iv rehydration give oral fluids every hour,
and the patient is made to drink up to 500mls orally every hour.
The three days’ treatment with;
 Tetracycline 250mg 6hourly for 3days
 Cotrimoxazole 240-480mg twice daily for 3days
 Doxycycline 100mg single dose eradicates vibrio from the stool and
reduces number of stools.
 Chlorpromazine 25mg 6hourly reduces intestinal secretions and fluid
loss.
 Health education on discharge
Diagnosis
Stool culture and sensitivity for correct selection of antibiotics
Prevention and control
 Immunisation
 Personal hygiene provides some protection
 Health education to the communities
 Disinfection and sterilisation instruments used on cholera patients and
 Disinfection of the stool and vomitus.
 Chlorination of water sources
 Boil drinking water
 Inspection of foods and food stores and handlers
 Chemoprophylaxis to cholera attendants with tetracycline.

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5. BACILLARY DYSENTERY
Objectives
1) Definition
2) Causes
3) Mode of spread
4) Incidence
5) Clinical presentation
6) Diagnosis
7) Management/treatment

130
8) Prevention
Definition
This is an acute diarrhoeal disease characterised by blood in stools, fever,
vomiting and abdominal cramps.
Another name for dysentery is shigellosis
Causes
 Bacillary dysentery is caused by non-mobile gram-negative bacilli of
shigella spices
The most frequent responsible spice for out breaks include;
 Shigella sonnei
 Shigella dysenteriae
 Shigella Flexner
Incidence
 Areas where sanitary conditions are poor
 In dry season
Factors influencing occurrence of bacillary dysentery
 Poor methods of disposal of faeces
 In availability of water
 Increased number of flies
 Seasonal changes and nutrition (rain season)
 Poor personal and house hold hygiene
 Low immunity due to malnutrition
 Overcrowded areas like prisons
Clinical presentation
 Incubation period is 1-4 days
 Onset is sudden with fever
 Colicky abdominal pain
 Faecal bloody diarrhoea with mucus
 Tenesmus (painful contraction of sphincter ani)
 Continues and irresistible urge to defecate
 Vomiting
 Headache
 General malaise
 Patient becomes weak and dehydrated
Diagnosis
 Stool examination shows RBC mucus

131
 Stool culture is positive for shigella
 Blood picture shows increased number of WBCs
 Sigmoidoscopy examination reveals diffuse mucosal inflammation and
multiple ulceration
Management/treatment
 The patient with dysentery needs to be managed in isolation, and use
disposable eating utensils
 Barrier nursing is encouraged
 Disposable napkins should be used and destroyed
 Supportive therapy informs of iv fluids replacement commonly normal
saline, antipyretics for fever, and antispasmodics for colicky abdominal
pain
 Bowel rest is an important measure
 Antibiotics such as ampicillin is ABC of choice given in the dose of
2gms/24hrs in four divided doses for 3-5days in adults
 In children 50-100mg/kg per day
 Tetracycline and cotrimoxazole are other effective ABCs
Nb: the patient is considered free from infection till three successive stool
cultures are negative.
Prevention and control
 Prevention of bacillary dysentery depends on stopping the faecal-oral
transmission like:
 Proper public sanitation
 Personal hygiene
 Health education to public about the mode of spread

Complications
 Water and electrolyte depletion
 Arthritis
 Disaccharides deficiency (frequent stool even after clinical cure).

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TUMOURS IN CHILDREN
1. Burkitt’s lymphoma
Definition
This is cancer of lymphatic system particularly B lymphocytes found in
germinal centre
It is named after Denis parsons Burkitt, surgeon who described the disease in
1958 while working in equatorial Africa.
The overall cure rate for Burkitt in developed countries is about 90% but worse
in low income countries.
Burkitt is uncommon in adults where it has worse prognosis
Causes
133
Burkitt lymphoma is caused by Epstein Barr virus
Classification
Current Burkitt lymphoma can be divided into three main clinical variants
a) Endemic
b) Sporadic
c) Immunodeficient associated variants
1. Endemic (African variant) most common occurs in children living in
malaria endemic regions of the world e.g. equatorial Africa, brazil,
The disease is characteristically involving the jaw or other facial bone, ovaries,
kidney, breast, distal ileum and cecum.
2. Sporadic type (non-African variant) this is commonly found in the
patients where malaria is not endemic which accounts for 30-50%of the
childhood lymphomas jaws are less commonly involved ileocecal region
is common site.
3. Immunodeficiency is usually associated with HIV infections or those
who are taking immunosuppressive drugs
Incidence
 Mostly affecting the children
 Rarely the adults
 More in males than the females
 Common in immunocompromised people like those with HIV infections
 Its high in north America, middle east and south America.

Signs and symptoms


 Weight loss
 Fever
 Night sweat
In sporadic and HIV patients
 Abdominal pain swelling
 Distortion of facial bones
 Night sweats
 Intestinal obstruction
 Enlarged thyroid
 Enlarged tonsils
In endemics
 Swelling and distortion of facial bones
 Rapid growth of lymphoid
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 Enlarged lymphoid are none tender
 Tumours grow extremely quickly
Diagnosis
 Medical history
 Physical examination
 Biopsy of bone and spinal fluids
Treatment
The treatment modalities include
a. Chemotherapy
 Vincristine
 Methotrexate
 Cyclophosphamide
 Cytarabine
 Dororubian
 Etoposide
The above drugs are injected directly in spinal fluid to prevent spread of cancer
in CNS
b. Radiotherapy

2. Brain tumours
Definition;
Brain tumour is abnormal cell growth within the brain
Types
Brain tumours are grouped into two types these include
1. Malignant or cancerous tumours
2. Benign tumours
Malignant tumours can be divided into;
a. Primary tumours these are tumours that start within the brain
b. Secondary tumours that have spread from somewhere else known as brain
metastasis
Causes
The causes of most brain tumours are unknown

135
Risk factors include
 Inherited neurofibromatosis
 Exposure to vinyl chloride
 Epstein Barr virus
 Ionizing radiation
Signs and symptoms
All types of brain tumours may produce symptoms that vary depending on the
part of the brain involved.
They include;
a. Frontal lobe
 Poor reasoning
 Inappropriate social behaviour
 Personality changes
 Poor planning
 Decreased production of the speeches
b. Temporal lobe
 Poor memory
 Loss of hearing
 Difficult in language comprehension
c. Parietal lobe
 Poor interpretation of language
 Reduced sense of touch, pain, and vision
d. Occipital lobe
 Poor or loss of vision
e. Brain stem
 Affects the blood pressure, swallowing and heart beat
Others include
Headache due to increased intracranial pressure which is worse in the morning
and goes away with vomiting
 Seizures
 Visual problem
 Vomiting
 Mental changes
 Difficult in walking
 Difficult in speaking
 Unconsciousness as the condition progresses
The most common type of tumour in children is malignant medulloblastoma

136
Diagnosis
 Medical examination with
 CT scan
 MRI
 Biopsy based on the findings
Treatment
Treatment may include combination of surgery, radiation therapy and
chemotherapy
When brain tumour is diagnosed medical team will be formed to assess the
treatment options presented by the leading surgeon to patients and relatives.
Neurosurgeon takes time to observe and evaluation of the neoplasm before
proposing the management plan to the patient and relatives.
These various type of treatments are available depending on the neoplasm type,
location and may be combined to give the best chances of survival.
Surgery
Complete or partial resection of the tumour with objective of removing as many
tumour cell as possible.

Radiotherapy
The most commonly used treatment for brain tumours, the tumours are
irradiated with beta, x-ray or gamma rays.
Chemotherapy
Is the treatment option for cancer however it is not always used to treat brain
tumour because of blood brain barrier which can prevent some drugs from
reaching the cancerous cells?
Variety of experimental therapies are available through clinical presentations
like;
 Anticonvulsants may be needed if seizures occur
 Dexamethasone and furosemide may be used to decrease swelling around
the tumours.

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3. Wilms tumour
Definition
This is cancer of the kidney typically occurs in the children sometimes known
as nephroblastoma
It was described by German surgeon in 1867-1918 known as Dr max Wilms
Incidence
 Approximately 500 cases are diagnosed in united states annually
 75% occur in normal children
 25% in developmental abnormalities
 It is highly responsive to treatment with 90% of patients surviving at least
five years
Signs and symptoms
 Painless, palpable abdominal mass
 Loss of appetite
 Abdominal pain
 Fever
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 Nausea and vomiting
 Haematuria
 High blood pressure
Diagnosis
 Clinical examination ultra sound scan
 CT scan
 MRI
Biopsy is not typically performed due to risk of creating fragments of cancer
tissues and seeding the abdomen with malignant cells.
Stages
Staging is the standard way to describe the extent of spread of Wilms tumour
and to determine prognosis and treatments.
The staging is based on anatomical finding and tumour cells pathology.
Stage 1 (43% of the cases)
 The tumour is limited to the kidney and completed excised
 Surface of the renal capsule is intact
 Tumour is not ruptured or biopsied (opened)
 No involvement of extra renal spaces
 No residual tumours apparent beyond the margins of excision
 Metastasis of tumours to the lymph nodes not identified.
Stage 2 (23% of the cases)
 Tumour extends beyond the kidney but completely excised
 No residual tumour apparent at or beyond the margins of excision
 Any of the following conditions may also exist
 Tumour involving blood vessels of renal sinus outside parenchyma
 Involves renal sinus soft tissues

Stage 3 (20% of cases)


 In operable primary tumours
 Lymph node metastasis
 Tumour is present at surgical margins
Stage 4(10% of the cases)
Presence of haematogenous metastasis (lung, liver, bone or brain) or lymph
node metastasis outside the abdominal pelvic region.
Stage 5 (5% of cases)

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Is defined as a bilateral renal involvement at the time of initial diagnosis.

CONDITIONS OF EYE AND EAR IN CHILDREN

1) OPTHALMIA NEONATORUM
Definition; is a purulent discharge from the eyes of an infant within the 1st 21
days of life.
Causative organisms
1) Staphylococci the most common and it happens when a midwife touches
the baby’s eyes or face with unwashed dirty hand. Also using dirty water
for cleaning baby’s face and eyes.
2) Gonococci the common this occurs when the baby’s eye is infected from
infected mothers. This infection may collect around the eye lids when the
baby opens the eye the bacteria gains entry.
3) Streptococci and e-coli occasionally the midwife may be souse of
infection when she has URTI i.e. during talking, sneezing and coughing,
and using unsterilized bowels and swabs.
4) Viruses the dust from atmosphere containing bacteria and viruses may
also infect the baby.
5) Pneumococci are rare
Predisposing causes

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1) Prematurity
The premature babies have low immunity to resist against infection and in the
1st few weeks these babies do not have tears to wash away the dusts and
bacterias.
2) Early rupture of membranes
Though it’s very rare when aseptic techniques are not employed during 2nd stage
of labour.
3) Flies

Signs
 Sticky-watery discharge from the eyes about 2nd and 3rd day but if the
infection is due to gonorrhea the signs may appear within 12-24 hours.
 The eye lids become red, swollen, and tightly closed.
 Yellowed fluid then pus.
Prevention
1) During pregnancy
 Examine patients regularly for vaginal discharges
 Ensure adequate treatment for patients with vaginal discharge
 Correct all mal presentations and mal positions.
 Treat and control all those conditions that can lead to prematurity.
 Prevention and treatment of anemia.
 Health education to the mothers on importance of hygiene.
2) During labour
 Use sterile equipment
 Proper washing of the hands before touching the baby’s eyes
 Isolation of the mothers with pus discharge in labour
 Mothers who had early rapture of membranes over 12th hours should be
given prophylactic antibiotics.
 Use one swab for one eye during cleaning of the eye of the baby.
3) After birth
 Wash your hand before/between handling the baby
 Instruct the baby not to touch the eyes of the baby without washing
hands.
 Never allow the bath water to touch the baby’s face.
 Use prophylactic antibiotics esp. instilling of eye drops
Treatment at (maternity Centre)

141
 Admit and isolate the baby from the rest, lay the baby on the side which
is having infected eye, should be nursed under mosquito net to prevent
flies and disinfect all the equipment used for the baby and should be kept
separate.
 Clean your hands and swab the eyes with normal saline or boiled cooled
water.
 Put antibiotic eye ointment in both eyes. If not available use penicillin
umbrella i.e. dilute crystalline penicillin 100,000i.u Vail with 4mls of
sterile water and use syringe to drop 5 drops in each eye. If 500,000i.u
vial dilute with 20mls of sterile water drop;
- 5 drops every 5minutes 6 times
- 5 drops every 10minutes 6 times
- 5 drops every 30minutes 6 times
- 5 drops every 1 hour for 3days
 Give crystalline penicillin 50,000i.u/kg im 12hourly for 7 days.
 Advise the patient to go to hospital to be tested for gonorrhea.
 Give the general nursing care like hygiene, feeding, observation, and
bowel/bladder care.
Hospital management
 Doctor is notified who may order eye swab for culture and sensitivity
 Instillation of penicillin may be ordered as in maternity in case of
gonococci infections
 Doctor may order soluble penicillin 50000-100000i.u im every 4-6 hours
 Neomycin and tetracycline eye ointments are ordered to prevent eye lid
from becoming adherent.
 Nursing care is as in maternity Centre.

Complication
 In neglected cases corneal ulcer occurs causing poor sight
 Blindness
Conjunctivitis with the pus in new born baby
(Opthlamia neonatorum)
Purulent discharge in the eyes of the new born baby

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Taking history and examine

Rx for the baby Rx for the mother Rx for the partner

 Always wear gloves  Ceftriaxone  Ciprofloxacin


 Cover the inflamed eye 2gms stat 500mgs stat
with the gauze before  Erythromycin  Septrine 5tabs bd for
you open the eye for 500mgs for 3days
your own protection 7days PLUS
 Clean the eye with  Doxy 100mg bd
saline or water apply for 7days
Teo hourly for 24hours  Or tetracycline
and 8houly for 10days 500mg 6hourly
PLUS for 7days
ceftriaxone125mgim
stat or erythromycin
15mg/kg 6hourly for 2
weeks

NB: Health educate them on the following


 Drug compliance
 Schedule for retune visit
 Provide mother and the partner with the condoms and counsel on the risk
behaviors

143
2) CONJUNCTIVITIS
Objectives
1) Definition
2) Signs and symptoms
3) Diagnosis
4) Treatment
Definition
This is an inflammation of the conjunctiva usually caused by virus, bacteria or
an allergy
Conjunctiva can be inflamed by an allergic reaction to dust or pollen. It can also
be irritated by wind, dust, smoke and other types of air pollution also common
cold.
Sometimes conjunctivitis can last for months or years.
This type of conjunctivitis may be caused by conditions in which eye lids turn
out wards (ectropion) or in ward (entropion)
Signs and symptoms
 Blood shot

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 Discharges appear in eyes (discharge may be thick or creamy in bacterial
infection, and clear in viral infection).
 Swelling of eye lids
 Itching especially in allergic reactions
Diagnosis
 Occurs in cold or allergies
 It’s less painful
 Blood vessels are closely on the Irish part of the eye
 Does not affect the vision
Treatment/management
Depends on the cause
 The eye lids should be gently bathed with tap water and clean washed
cloth to keep them clean and free of discharges.
 Antibiotics eye ointment in case of bacterial infections.
 Antihistamines taken orally may relieve the itching and irritation
 Wash the hands before and after bathing the eyes and application of
medicine.
 Use one washed cloth on each eye to avoid cross infection.
 Surgery may be indicated to correct the alignment of the eye lids or to
open clogged tear ducts.
Gonococcal conjunctivitis
New-borns can acquire gonococcal conjunctivitis from their mother while
passing through the birth canal for this reason all the new born babies should get
antibiotic eye ointment
Adults may also contract gonococcal conjunctivitis during sexual intercourse
when infected semen reaches the eyes.
Signs and symptoms
 Incubation period is between 12-48hours
 Eye is reddish
 Painful
 Corneal ulceration if not treated
 Perforated eye balls
 Blindness
 Development of abscess
Treatment/management
Treat with antibiotic tablets, eye drops, and injections.

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3) TRACHOMA (granular conjunctivitis or Egyptian
ophthalmia)
Definition
This is prolonged infection of the conjunctivitis caused by bacterium chlamydia
trachomatis
Incidence
 Common in poverty-stricken parts of the dry, hot meditarania countries
and far east.
 Occurs among the native Americans
 Among people in the mountain areas of southern united states
Mode of transmission
Trachoma is contagious in the early stages and may be transmitted by;
 Eye to eye contact
 By house flies
 By contaminated towels and handkerchiefs
Signs and symptoms
In early stage
 Conjunctiva is inflamed
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 Reddened conjunctiva
 Irritations with itching
 Discharge appears
In late stages
 Cornea becomes scarred
 Eye lashes turn inward
 Impaired vision
Investigation
 Eye swab for culture and sensitivity
Treatment/management
 Application of antibiotic eye ointment e.g. tetracycline, erythromycin for
4-6 weeks alternatively
 Or antibiotics can be taken orally
 Surgery may be indicated if the condition causes deformities of eye lids
or cornea

4) OTITIS MEDIA
Otitis media can be acute or chronic
1) Acute otitis media
Definition
Acute otitis media is a bacterial or viral infection of the meddle ear.
Incidence
Although this disorder can develop in people of all ages, its most common in
the young children particularly those between ages of 3months -3years.
Usually this disorder develops as complication of common cold, viruses and
bacteria from the throat can reach the middle ear through Eustachian tube or
occasionally through the blood stream
Viral otitis media usually follows bacterial otitis media
Signs and symptoms
 Persistent ear pain
 Temporary hearing loss
 Increased temperature
 Chill

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 On examination ear drum is inflamed and bulged
 There is discharge when ear drug rapture which is bloody at first, changes
to clear fluid and finally pus
 Nausea and vomiting
 Diarrhoea
Diagnosis
 Clinical presentations
 Ear discharge is send for culture and sensitivity
Treatment/management
 Antibiotic treatment can be given orally the drug of choice is amoxicillin
 Antihistamines are given in case of allergies
 If ear drum is bulged doctor may perform myringotomy to open the ear
drum to allow fluids to drain from the ear drum.
2) Chronic otitis media
Definition
This is long standing infection causing by permanent hole (perforation) in the
ear drum
Causes
 Acute otitis media
 Blockage of Eustachian tubes
 Injury to the ear from the object entering the ear
 Sudden change of air pressure in the ear
Treatment/management
 Thorough cleaning of the ear canal and the middle ear with suction and
dry cotton swab
 Instil a solution of acetic acid with hydrocortzone in the ear
 Oral antibiotics such as amoxyciciline is given after culture and
sensitivity is done
 Ear drum can be repaired in condition called tenpanoplasty

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PAEDIATRIC HIV/AIDS
Introduction
• HIV is the greatest health crisis the world faces today.
• Estimated 40million people living with HIV
• 2.7 million children under 15 years are estimated to be infected with HIV
• 570,000 children died of AIDS in 2005
• Children account for 18% of the 3.1 million AIDS deaths
Only 40,000 or 4% of the approximately one million people now on treatment
are children
Etiology
Caused by the Human Immunodefiency virus
Types I and II
Type I - Worldwide
Type II - Common in West African
Transmission
 Majority (90%) infected children acquire the infection through MTCT
This occurs during pregnancy, delivery and breastfeeding, in absence of
any intervention, the risk of MTCT is 15 – 30% in non-breast-feeding
populations Breastfeeding increases the risk by 5 – 20% to a total of 20 –
45%.

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Other Means of Transmission
 Blood transfusions, blood products and organ/tissue transplants
 Contaminated needles
 Scarification marks?
 Sexual intercourse
Factors that contributes to MTCT
(Maternal)
 High maternal HIV RNA level
 Low maternal CD4+ T-lymphocyte count
 Chorioamnionitis
 Maternal vitamin A deficiency and malnutrition
 Co-exciting sexually transmitted disease
 Urea of antiretroviral therapy
 Clinical states of mother
 Intrapartum hemorrhage
 Vaginal delivery with tears
 Artificial rapture of membranes
 Episiotomy

Transmission Through Breastfeeding


Risk is 14% if sero conversion occurs before birth
Risk is 29% if during breastfeeding
Highest in the first 6 months of life but continues throughout breastfeeding
Transmission risk increased by
 Seroconversion during breastfeeding
 Mastitis/breast abscess
 Bleeding nipples
 High plasma viral load
 Oral thrush in baby
 Mixed feeding (including breast milk)
Prevention of MTCT
1. In 1997, a joint WHO, UNAIDS, and UNICEF policy Statement called
for giving women access to voluntary counseling and testing and
information to allow them make informed decisions regarding infant
feeding.
2. – (WHO) If a woman has tested positive when replacement feeding is
affordable, feasible, acceptable, sustainable and safe (AFASS) avoidance
of breastfeeding is recommended Otherwise, exclusive breastfeeding is
recommended. It should be short with abrupt cessation Mixed feeding is
discouraged as its promotes transmission
3. Pregnant women who need ARV treatment should receive it in
accordance with WHO guidelines

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4. HIV – infected pregnant women who do not have indication for ARV
treatment or do not have access to treatment should be offered ARV
prophylaxis to prevent MTCT using one of the several regimens know to
be safe.
Treatment for pregnant women/infant during pregnancy/infant
ZDV from 28wks of pregnancy + single dose NVP during labour and single
dose NVP and one week ZDV for infant.
Nevirapine tab 200mg given to the mother during labour and the syrup 2mg/kg
given to baby within 72 hours of life reduces transmission by half
CLINICAL FEATURES
CNS
 microcephaly
 progressive neurological deterioration or spastic encephalopathy
 developmental delay/regression
 predisposition to CNS infections

Respiratory System
 Recurrent infections (pneumonia, sinusitis, otitis media)
 Tuberculosis
 Pneumocystis carinii pneumonia or lymphoid interstitial pneumonitis

CVS
 cardiomyopathy with congestive cardiac failure

GIT
 AIDS enteropathy (malabsorption, infections with various pathogens)
leads to chronic diarrhea resulting in failure to thrive
 Abdominal pains,
 dysphagia,
 chronic hepatitis or
 pancreatitis

Renal (urinary system)


 AIDS nephropathy: the most common presentation being nephrotic
syndrome
 urogenital warts

Skin
 Eczema
 candida infections
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Opportunistic infections
 pneumocystis carinii pneumonia
 Cryptosporidium
 Epstein Barr Virus
 Measles
 Cryptococcus meningitis
 Toxoplasmosis
 Malignancy
- Non-Hodgkin’s Lymphoma
- Primary CNS lymphoma
 Kaposi sarcoma
WHO CLINICAL CASE DEFINITION OF PAEDIATRIC AIDS
2 major + 2 minor Criteria
major signs
 Weight loss of failure to thrive
 Chronic diarrhea > 1 month
 Prolonged fever > 1 month

minor signs
 Generalized lymphadenopathy
 Oropharyngeal candidiasis
 Recurrent common infections
 Generalized dermatitis
 Recurrent invasive bacterial infection
 Confirmed maternal HIV infection

CDC Immunologic categories based on CD4+ and % Total lymphocyte


counts

< 1yr 1 – 5years


Categories
No  1500 >1000
 25%
Suppression >25%
Moderate 750 – 1499 500 – 999
Suppression 15 – 24% 15 – 24%

152
Severe <750 <500
Suppression <15% <15%

Diagnosis of HIV Infection


 Diagnosis of HIV infected children over 18months can be made by
antibody test (ELISA and confirmatory tests)
 Specific diagnosis in children less than15 -18months can be made by
virology tests
- HIV DNA polymerase chain reaction (PCR)
- HIV RNA Assay
- Standard and immune complex dissociated p24 antigen
- Viral culture
Tests should be performed at
 48 hours of age
 14 days
 1 – 2 months
 3 – 6 months

153
NB: HIV infection is absent if there are 2 or more negative viral tests between
the age 1 month and 6 months
HIV infection is present if there are 2 positive viral tests on 2 separate blood
samples regardless of age
In the absence of virology tests
 2 or more negative antibody tests performed by the age of over 6
months with an interval of at least 1 month between tests reasonably
excludes HIV infection in exposed children
 A reactive HIV antibody test at >18 months followed by a positive
confirmatory test definitely indicates HIV infection.
TREATMENT MODALITIES
 Antiretroviral therapy
 Treatment of acute bacterial infections
 Prophylaxis and treatment of opportunistic infections
 Maintenance of good nutrition
 Immunization
 Management of AIDS – defining illnesses
 Psychological support for the family
 Palliative care for the terminally ill child
Antiretroviral Therapy
Goal
Is to maximally suppress viral replication to on detectable levels for as long as
possible The antiretroviral drugs fall under 4 major categories
Categories of antiretroviral therapy
 Nucleoside reverse transcriptase inhibitors (NRTIs)
ZDV, ddI, 3TC, d4T
 Non-nucleoside RTIs, Nevirapine, Efavirenz
 Protease inhibitors: Nelfinavir, Ritonavir
 Fusion inhibitors: Enfuvirtide
When to initiate ARV
All HIV infected children less than 12 months
Clinical AIDS
Mild to moderate clinical symptoms
Mild to moderate immunosuppression
Good response to 2NRT1s +1 protease inhibitor
Some studies have shown comparable result with 2NRT1s + 1 NNRT1
Immunization
 All HIV-exposed infants should be fully immunized
 Infected and symptomatic infants should receive all vaccines including
measles and hepatitis B but not BCG or Yellow fever vaccine

154
 Infected and symptomatic children should receive IPV instead of OPV
Issues and Challenges
 Difficulties in Diagnosis
 Lack of appropriate formulations
 Difficulties in dosing
 Cost of Formulations
 Lack of trained manpower to deliver care & support
 Special needs of children affected & infected by HIV/ AIDS

INTEGRATED MANAGEMENT OF CHILDHOOD ILLNESS (IMCI)


Background
Each year nearly 7 million children die before the age of 5 years from 5 main
causes: Malnutrition, Pneumonia, Preterm birth complications, Diarrhea and
Malaria
Affordable Effective Interventions
Estimate of percentage of < 5yrs deaths that could be prevented (if there was
universal access to this intervention)
interventions Percentages
• Exclusive breast-feeding 13%
• Insecticide treated bed nets 7%
• Immunization (measles/Hib) 6%
• Antibiotics for pneumonia 6%
• ORS for children with diarrhea 15%
• Antimalarial 5%
• TOTAL 52%
The Role of Nutrition
• Malnutrition is responsible for 30-50% child deaths globally
• Maternal under nutrition contributes to 800,000 neonatal deaths
annually through small for gestational age births
• A severely malnourished child is
- 6 times more likely to die from diarrhea

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- 9 times more likely to die from pneumonia
Current average position in Africa
• 40% exclusively breast fed till 2 months and then 20% between 2-5
months
• Only 30% of children with pneumonia receive the antibiotics they
need
• IMCI (Integrated Management of Childhood Illness)
• Introduced in 1997 by WHO and UNICEF with the aim of
prevention, or early detection and treatment of the leading causes of
under 5 death
• Integrates preventative and curative aspects of treatment
emphasizing prevention of disease through immunization, hygiene
and improved nutrition
• Syndromic approach recognizing that children in the developing
world often suffer from more than one diagnosis
• Also seeks to reduce childhood morbidity and mortality by
improving family and community practices for the home
management of illness, and case management skills of health
workers
IMCI in Practice
What's the age of the child?
 Birth – 2 months
 2 months – 5 years
• Step 1 – Assess the child
(2months – 5 years)
Assess child by asking career questions and simple focused examination for
main symptoms and danger signs? (3 things to ask, 1 to look for)
Check for general danger signs
Step1 – Assess the child
(2months – 5 years) for
 Cough or Difficulty in breathing
ASK
How long cough has been present for?
- If > 30 days = chronic
- Count respiratory rate: Number of breaths in one minute
- Fast breathing:
< 2months = 60 breaths/minute
2 – 12 months = 50 breaths/minute
12 months – 5 years = 40 breaths/minute
LOOK

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- chest in drawing (subcostal recession)
- Look and listen for stridor
Step 2 – Classify the Child
 Diarrhea
ASK:
- For how long the diarrhea has been? (Diarrhea > 14 days = Persistent)
- Is there blood in the stool?
LOOK:
- Look at the child’s general condition (restless/irritable, lethargic)
- Look for sunken eyes
- Offer the child something to drink (Drinking eagerly/thirsty, drinking
poorly, Not able to drink)
- Pinch the skin of the abdomen – look to see if skin pinch goes back
immediately, slowly and very slowly (> 2 seconds)
• Classify Diarrhea (dehydration)
• If no dehydration uses plan A to treat diarrhea if same dehydration
uses plan B and if severely dehydrated use plan C.
 Fever
• Classify fever in high malaria risk areaReferurgently
• Fever in high or low malaria area
 Measlesurgently
• Measles now or in past 3 months classify
 Ear problem
ASK:
- Who long has been the ear pain?
- If there is ear discharge?
LOOK & FEEL:
- Pus from ear?
- Tender swelling behind ear (mastoiditis)?
- Refer urgently if ?mastoiditis, start cotrimoxazole
- Ear discharge <14days & ear pain: cotrimoxazole for 5days, wick the
ear, and do HIV test
- Ear discharge >14days: wick the ear (+ quinolone ear drops), do HIV
test.
 Under nutrition definitions
ASK
• Does the child have one or more of the following conditions:
Pneumonia, Persistent Diarrhea, Ear discharge, Very low weight for
age

157
• If so, look for oral thrush, parotid enlargement, generalized
persistent lymphadenopathy
LOOK FOR
- Stunting: height for age less than 3SD below mean
- Wasting: weight for height less than 3SD below median = severe acute
malnutrition.
- Children with bilateral oedema if not due to liver/kidney/heart disease
also have severe acute malnutrition (they have lost fat & muscle but not
weight because of fluid retention)
• Quick screen for possible malnutrition age 6months-5yr: mid upper
arm circumference < 13.5cm.
• <11.5cm= likely severe acute malnutrition
• Weight for age is a composite of long term & current nutrition,
weight for height is a better measure of current nutrition
Step 3 Classify and Treat
• In high HIV setting
When checking for malnutrition and anemia, also check for HIV infection
• Has the mother or child had an HIV test?
Step 4 - Counsel the Mother
- Explain how to care for child at home (hand-washing, sanitation, ITN’s,)
and
- how to give treatment (ORS, oral medications)
- Counsel about feeding and fluids advise to increase fluid during illness
- Advise when to return
Using process: ask, praise, advice, check
Step 5 - Follow-up
Advantages of IMCI
 Accurately identifies childhood illness in out-patient setting
 Ensures appropriate combined treatment of major illnesses
 Strengthens caretaker counselling
 Speeds referral of severely ill children
 Provides preventive services

Hospital Triage of children


Up to 50% of children dying in hospital die in first 24 hours
Some will die waiting to be seen
Some can only be saved if treatment starts immediately
Triage = ‘Sorting’ process quickly sorting children into those with emergency,
priority and non-urgent signs

158
Emergency Signs ABCCD
A or B-obstructed airway, child not breathing, cyanosis, very fast breathing or
severe chest in drawing
C-Circulation Problem
C-Coma or convulsing
D-Diarrhea with dehydration –( 2 of these; sunken eyes, slow skin pinch,
lethargy)
Management of Airway or breathing problem
• Obstructed breathing (noisy)
• Central cyanosis
• Severe respiratory distress: fast breathing, in drawing, OR
weak/absent breathing
1. Remove any visible secretions or foreign body from mouth
2. If suspected FB aspiration(choking) give backslaps & chest (baby)
or abdominal (older child) thrusts
3. Open the airway: <1yr neutral, >1yr neck extended
4. Give oxygen
5. If conscious & not in shock put in sitting position
6. Diagnose & treat underlying cause
Management of Circulation problem
Cold hands AND weak and fast pulse AND capillary refill time >3 seconds
- If bleeding apply direct pressure to stop bleeding
- Give oxygen
- Keep child warm
- If no severe acute malnutrition, give IV 20ml/kg Ringer’s lactate or
normal saline quickly, (give intraosseous if IV is impossible) If no
improvement repeat it up to 2x. If SAM avoid iv fluids
- If pale check Hb, if <6 transfuse 20ml/kg whole blood
- Diagnose & treat underlying cause
Management of Coma or Convulsions
- Open the airway, & place in recovery position
- Give 5ml/kg of 10% dextrose (same as 1ml/kg of 50% dextrose diluted)
- If convulsing now give oxygen & diazepam rectally or slow i-v
- Diagnose & treat the underlying cause
Priority Signs (3T’s, 3P’s, 3R’s MOB)
3T’S
- Tiny baby (Age < 2 months)
- Temperature high,

159
- Trauma or other surgical condition (e.g. suspected fracture)
3P’S
 Pallor
 Pain
 Poisoning
3R’S
 Restless, lethargic, irritable child
 Referral from another health Centre/hospital
 Respiratory distress
MOB
 Malnutrition/Severe Wasting (MUAC<11.5cm)
 Oedema of both feet
 Major Burn

SURGICAL CONDITIONS IN CHILDREN


1. OESOPHAGEAL ATRESIA
During the intra-uterine life between 4 and 8 weeks the laryngotracheal groove
develops into the larynx, trachea and beginning lung tissues. The esophageal
lumen forms parallel to this.
A number of anomalies may occur if trachea and esophagus are affected by
teratogen that does not allow the two organs to separate but remain connected.

Oesophageal atresia is obstruction of the esophagus.

The fine usual types of esophageal atresia that occur are:

 The esophagus ends in a blind pouch


There is tracheoesophageal fistula between the distal part of the esophagus and
the trachea (A)

 The esophagus ends in a blind pouch; there is no connection to the


trachea (B)
 A fistula is present between an otherwise normal esophagus and trachea
(C)
 The esophagus ends in blind pouch. A fistula connects the blind pouch of
the proximal esophagus to the trachea (D)

160
 There is blind end portion of the esophagus; fistula are present between
both widely spaced segments of the esophagus and the trachea (E)
Signs and symptoms

 Polyhydramnios (excessive amniotic fluid) a fetus with


tracheoesophageal atresia cannot swallow, so the amount of amniotic
fluid can grow abnormally large.
 Infants are born preterm because of hydrominous.
 The infant will cough and become cyanotic and have obvious difficult
breathing as fluids is aspirated
 Excessive accumulation of saliva and mucus in the mouth and pharynx
because there is a development anomaly with blind ending esophageal
pouch
Diagnosis

Whenever atresia is suspected, affirm catheter should be passed to test for


gastric acid. If it travels less than 10cm atresia is suspected.

If not diagnosed prior to the first feed, the baby will cough and regurgitate the
feed into the trachea and the baby will become cyanosed.

Chest x-ray will usually confirm esophageal atresia, air in the stomach indicates
presence of fistula.

Management

 Emergency surgery for the infants with tracheoesophageal fistula to


prevent the development of pneumonia
 Surgery consists of closing of the fistula and anastomosing the
esophageal segments.
Nursing care

The baby is nursed in propped position and nil per mouth

Frequent aspiration of air passages and mouth

Complications

Respiratory infections e.g. pneumonia

Delay in operation will result into starvation, dehydration and death of the baby.

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2. INTUSSUSCEPTION
Definition;
Is the invagination of the portion of the bowel into the other
Causes
– Vigorous peristalsis which may be due to swelling of lymphatic tissues in
the gut
– Malignant tumors in the gut
Incidence
Common in children between 4-9months
Signs and symptoms
 History of colicky abdominal pain of sudden on set
 Blood stained stool which is called red currant jelly stool.
 Vomiting and abdominal distension
 On physical examination there is a mass on the colon, its first felt in the
right hypochondria later on the left side of the abdomen.
 On rectal examination there may be nothing but the examining finger
may be blood stained.
 Later dehydration, and
 shock occurs
Management
1. Conservative treatment
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 Is effective in early cases when there is no swelling found.
 Barium enema under x-ray control which will force the invagination back
by pressure
 Plenty of fluids given either iv or orally is necessary
2. Surgical treatment
 It may be simple reduction of the loop and decompression
 If gangrenous or grossly swollen, resection and anastomosis.
Pre-operative care
– Child is admitted in paediatric surgical ward
– Parents are reassured condition explained and consent form signed
– Observations are taken such as temperature, respiration and pulse plus
general condition assessed in relation to abdominal swelling, anemia, and
weight.
– NGT is passed and aspiration is started
– Sedatives are given to the patient to calm down e.g. diazepam 2.5mg IM
– Iv fluids are set up
– Blood taken for grouping and x-matching
– If the swelling is small or absent, child is prepared for barium enema
which may decompress the invaginated colon and release the obstruction.
– If the intussusception has been released, NGT, and IV fluids are
discontinued then oral feeds are started.
– In advanced phases, the patient is prepared for operating theatre.
– Pre-medications are given e.g. atropine 0.3mg IM to prevent secretions.
Post-operative care
– Iv fluids are continued until feeding is started
– Sanction is continued until bowel sounds are heard and aspirations is
decreased
– Clear fluids are started soon after bowel sounds have been heard with no
abdominal distention and vomiting.
– Accurate aspirates are measured to maintain the lost fluid.
– Note any sign of peritonitis and shock such as changes in vital signs,
colour of the patient and abdominal distention, smell and discharge from
the incision site.
General nursing care
1. Hygiene such as daily bed bath, change of linen PRN and changing of the
position 2hrly treat pressure are as 4hrly and give oral care.
2. Diet regular feeds if breast feeding continues with other sub-feeds.
3. Weigh the baby on alternative days to see if the baby is gaining or not.
4. Bladder is observed for proper functioning.
5. Drugs e.g. Analgesics are given to relief pain and Antibiotics also give to
prevent infection

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6. Stitches may be removed on the 7th-8th day and discharge may be
considered if improved.
7. Prognosis is usually 100% good in most cases.
Complications
 Incisional hernia
 Reoccurrence of the condition
 Adhesions peritonitis
 Peritonitis
 Paralytic ileus

3.PYLORIC STENOSIS
Definition;
This is obstruction of the stomach outlet due to excessive thickening of the
pyloric sphincter.
This may occur as a malformation in anew born infants.
Signs and symptoms
 At birth the infant is apparently quite fit
 Projectile vomiting and deterioration of the general condition occurs after
2-3weeks (vomitus is plenty in quantity)
 There is rapid weight loss
 Dehydration sets in, which makes the face wized.
 Tetany may develop if vomiting is severe.
 On palpation there is a mass felt at the epigastrium.
 Visible peristalsis may be present
 The child is constipated.
Treatment
Medical treatment
– Gastric lavage with normal saline to wash out stagnant stomach content.
This may be necessary once or twice daily.
– An antispasmodic drug is administered to relax the muscles e.g. cumydrin
1ml of 1/1000 solution 20minutes before each feed).
Surgical treatment
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In most cases surgical treatment is now the treatment of choice as medical
treatment is tedious and never certain.
Ramstad’s operation is done
Pre-operative care
 Admit in pediatrics surgical ward
 Establish nurse patient relationship and reassure the parents
 An iv fluid is put up of n/saline or dextrose
 Investigations e.g. blood for Hb grouping and x-matching
 Gastric lavage is carried out with n/saline before the operation. The
stomach is emptied and the NGT is left in situ.
 Patient taken for operation and operation is taken through the muscle of
pylorus.
Post-operative care
 Post-operative bed is made
 Patient is put gently in the bed in recumbent position with head turned to
one side.
 Care of the tube is done i.e. IV, NGT, drainage tube
 Observations e.g. TPR are taken and recorded
 Feeding cane start after 4hours after operation unless the mucosa has
been in advertently opened by surgeon then he may order feed to be
withheld for 24hours.
 The feeding regimen is as follows; -

Hours post-operatively Amount Type of feed


4 4mls Glucose water
6 4mls Feed
8 8mls Glucose water
10 8mls Feed
12 16mls Glucose water
14 16mls Feed
16 32mls Glucose water
18 32mls Feed
20 48mls Glucose water

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Feeds are continued two hourly for about the next six hours and gradually
increased to 90mls every 3hours depending on the age and weight of the baby.
Should any feed be vomited it is repeated in two hours rather than preceding to
the next stage.
– Hygiene
– Elimination
– Rest and sleep
– Exercise
– Rehabilitation
– Discharge
Following successful operation, the child grows up normally without further
problems in adulthood.

3. IMPERFORATED ANUS
Definition;
This is stricture of anus this occurs during the 7th week of intrauterine life
The upper bowel elongates to the pouch and combines with a pouch invigilating
from the perineum.
There may be no rectum or anus or rectum may be there but no opening
The anal sphincter may be enclosed by a membrane.
Signs and symptoms
 The condition may be diagnosed during prenatal sonogram
 On inspection of the a new born it reveals that no anus is present
 The abdomen becomes distended and
 Baby will start vomiting within 48hours.
 There is no meconium seen at birth.
Management
1. Degree of difficulty in repair
If the rectum end is close to the perineum below or at the level of the levator ani
muscle and anal sphincter is formed, repair involves simple anastomosis of the
separated bowel segment
2. The repair becomes complicated if the end of the rectum is at a distance
from the perineum (above the levator ani muscle) the surgeon may create
temporary colostomy

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4. VOLVULUS
Definition;
It’s twisting of the bowel by itself. It nips the mesentery supplying the twisted
portion so blood supply leading to gangrene.
Peritonitis may occur as result most common in sigmoid colon.
Signs and symptoms
 Complete constipation
 Early vomiting though the obstruction is in the lower part
 Distention of the abdomen flatulence
 Restlessness due to distention
 Breathlessness as a result of gaseous distention
Diagnosis /investigations
5. Abdominal x-ray shows huge gas shadow inform of an inverted “V’’ out
lining the distended loop
6. Sigmoidoscopy done to see to see the sigmoid flexure.
7. Barium enema
8. Blood for Hb grouping and x-matching.
Management
Pre-operative management
 Admit in surgical ward in a warm bed
 Reassure the mother and create good nurse patient relationship
 Resuscitate the baby with iv fluids if the baby has being vomiting

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 Pass NGT and aspirate the gastric contents
 Ensure that the child passes urine
 Doctor is informed who comes to assess the condition of the baby
 The mother is explained the condition and she consents for the operation
 The child is prepared for operating theatre.
 In the operating theatre doctor may carry out sigmoidoscopy and untwist
the volvulus if the bowel is not gangrenous and the child is taken back to
the ward.
 If sigmoidoscopy and volvulus fails to untwist then laparotomy is done
 If the volvulus untwists and the colon is found to be gangrenous the
resection and anastomosis is performed
Post-operative management
Is like any other laparotomy

CONGENITAL MALFORMATIONS IN CHILDREN

Definition of congenital abnormality

Is any defect in form, structure or function or it is a malformation of the fetus


which is present at birth and can be detected on examination of the new born
after 1 hour of the birth. They can be determined before or during birth or
recognized later in early life. Some disorders however may remain
unrecognized.

Causes

Why some fetal tissues develop abnormally is not fully known but the following
factors are thought to be responsible.

Predisposing Factors

 Maternal age
The risk of having a baby with an abnormality increases with the maternal age
e.g. women above the age of 35 are more at risk of having babies with downs
syndrome

 Paternal age
Though men can father children up to the age of 90years of age, increase in
paternal age has been linked to dwarfism.
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 Nutritional factors
 Anoxia or hypoxia in utero
This may seriously affect the growing brain cells if the mother’s blood is
insufficient in oxygen in conditions like serious cardiac diseases, general
anesthesia, and partial placental separation as may occur in threatened abortion.

Causes of congenital abnormalities

 Chromosome and gene abnormalities


Each human cell carries a print for reproduction in the form of 44 chromosomes
(autosome) and two sex chromosomes. Each chromosome comprises of genes.
Should anything occur in formation of gametes, the defect is transmitted via the
genes in the ovum or spermatozoa then some abnormalities like downs
syndrome, an encephally, cleft palate and cleft lip.

 Teratogenic causes
A teratogen is an agent that arises and affects the wellbeing of the fetus.

Factors that influences the effects produced by the teratogen are such as
gestational age at the exposure, length of exposure and toxicity of exposure.

Agents such as large concentration of vitamin A, anticonvulsants, tetracycline,


streptomycin and substances e.g. alcohol nicotine from passive and active
smokers.

 Environmental factors
This occurs in embryonic stage where by the tissues are affected by deprivation
of oxygen or vital substances.

 Physical and chemical agents


a) Radiation; Diagnostic abdominal radiology x-ray should be avoided
during the 1st 30 weeks of pregnancy where growth and development of
the developing fetus can be affected.
b) Chemicals such as pesticides
c) Ineffective agents; Drugs like streptomycin and tetracycline
d) Infections like viral infections i.e. HIV, toxoplasmosis, rubella,
cytomegallo virus, herpes/histoplasmosis, syphilis (TORCHES)
e) Maternal diseases; like hypertension, DM, kidney diseases and
cardiovascular diseases.

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f) Abnormalities of the placenta and the cord; which tend to lead to
oxygen and nutrient deprivation hence causing abnormalities of fetus.
g) Abnormal implantation of the ovum
How do these abnormalities occur?

1) Failure of tissues to engage to each other


2) Failure of an organ to form during organogenesis
3) Failure of canalization e.g. biliary tract, imperforated anus
4) Failure of organs to separate e.g. synduct (two digits fuse together), horse
shoe kidney.
5) Pressure on fetal limbs e.g. clubbed foot
6) Failure to rotate during intra uterine life due to limited space in the uterus.

Examples of The Abnormalities

1) Hydrocephalus
This is when there is an excess of (CSF) in the ventricles or the subarachnoid
space. CSF is found in the first and second ventricles of the brain.

Causes

Hydrocephalus can happen if the CSF is blocked because of the way your
child’s brain is formed. This is called congenital.

The real cause is not known

It’s believed that maternal infection such as toxoplasmosis or infant meningitis


may be factors.

An excess of CSF in the new born occurs for one of the three main reasons: -

 Over production of fluid by a choroid plexus in the 1st and 2nd ventricle.
 Obstruction of the passage of the fluid in the narrow aqueduct of syllis
(most common cause) non-communicating hydrocephalus.
 An interference with the absorption of CSF from the sub arachnoid space
if apportion of sub arachnoid is removed. (communicating
hydrocephalus)
Hydrocephalus that are caused by any other reasons are called acquired
hydrocephalus

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 Reasons for acquired hydrocephalus include;
 Head injury
 Intraventricular hemorrhage
 Brain infection
 Brain tumor
This hydrocephalus occurs in approximately 3 to4 per 1000 births.

Signs during pregnancy

 The presentation is cephalic but with a high head and it feels soft, none
ballotable and big.
 During 2nd stage of labour may be somehow prolonged because shoulder
must dilate further to allow the passage of the shoulders.
 Assisted delivery may be required.

Signs after birth

 A high-pitched irritable cry if associated with the infection or high rate of


accumulation of the fluid.
 Head growth that is larger than the normal
 Bulging of the fontanels that may be soft or firm.
 Wider sutures
 The eye that seems to look down all the time (sunset eyes). the white part
of the eye can be seen above coloured part.
 Delayed development
 Poor eating
 Sleepiness
 Irritability
In older children

Signs of increased intracranial pressure such as;

 Altered consciousness
 Headache
 Irritability
 Change in personality
 Decreased appetite
 Vomiting
 Blurred vision (double vision).

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Management Of Hydrocephalus

Is aimed at examination of the child looking for signs and symptoms of


hydrocephalus and imaging tests

This depends on the assessment of ventricular dilatation.

Diagnosis

 Cranial US
 CT scan
 MRI scan
Treatment

The treatment depends on its cause and the extent (on assessment of ventricular
dilatation). In most cases it’s surgical.

Aims

 To relieve raised ICP


 To minimize the risk of neurological damage.
1. If the hydrocephalus is due to over production of CSF, (Diamox) diuretics
may be prescribed to promote the excretion.
If over production is due to tumor it should be removed to provide the solution.

2. If the cause is due to obstruction, a shunting procedure is done


A shunting involves threading a thin polythene catheter under the skin from the
ventricles to the peritoneum where absorption takes place across the peritoneal
membrane into the body circulation.

Nursing Care

Preoperative Nursing Care

a) Admit and record subjective and objective data (take history).


b) Assessment
 head circumference,
 fontanels,
 cranial suture,
 level of consciousness
 check for irritability

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 altered feeding habits
 high pitched cry
 Firmly support the head and neck when holding the child.
 Provide skin care for the head to prevent breakdown
 Give small, frequent feeding to decrease the risk of vomiting
 Encourage parental new born bonding
 Teach the family about the management required for the disorder.
 Treatment is surgical by direct removal of an obstruction and insertion of
shunt to provide primary drainage of the CSF to an extra cranial
compartment, usually peritoneum (ventriculoperitoneal shunt)
Post-Operative Nursing Care

Depending on the child’s condition nurse in ICU or beside nursing station.

 Patient is placed in a lateral or prone position


 Record the vital signs and CNS observations and head circumference.
 Assess for the signs of increased ICP and check the following; head
circumference(daily), anterior fontanel for size and fullness and behavior
 Administer prescribed medicines which may include antibiotics to
prevent infections and analgesics to control pain.
 Provide light diet in order to avoid straining of the bowel.
 Dress the wound and cover it with wet dressing
a) Provide shunt care
Monitor for shunt infection and malfunction which may be characterized by
rapid onset of vomiting, severe headache, irritability, lethargy, fever, redness
along the shunt tract, and fluid around the shunt valve.

b) Teach home care


 Encourage the child to participate in age-appropriate activities as
tolerated.
 Encourage the parents to provide as normal life’s as possible. Remind the
parent and child that conduct sport is prohibited.
 Explain how to recognize the signs and symptoms of increased ICP.
Some signs include changes in school performance, intermittent headache
and mild behavior changes.
 Arrange the child to have frequent developmental screenings and routine
medical checkups.
Prevention

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 Screening women of child bearing age for syphilis
 Take folic acid early enough during early antenatal periods.
 Pregnant epileptic women should be given double dose of folic acid
because anticonvulsants interfere with the metabolism of folic acid.
 Educate the women of child bearing age to take folic acid.
Complications

 The major complication of shunt are infection usually from


staphylococcus epidermis or (staphylococcus aureus)
 Over drainage leads to slit ventricle syndrome
 Subdural hematoma caused by too much rapid reduction of CSF.
 peritonitis
 Perforation of organs
 Abdominal abscess
 Fistulas
 Hernia

2. Anencephaly

This is absence of cerebral hemispheres (the fore brain and skull vault and
secondary distortion of the face and the ear). It occurs when the upper end of the
neural tube fails to close in early intrauterine life.

Symptoms

 Absence of the skull


 Absence of the brain (cerebral hemisphere and cerebellum)
 Heart defect
 Facial feature abnormalities
Effects in labour

 Under developed head does not engage so dilatation of cervix is very


slow.
 Many infants present in breech
 Children with this abnormality do not survive because they have no
cerebral function.
 The respiration and cardiac centers are located in the intact medulla;
however they may survive for several days after birth.
Treatment

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There is no current treatment for it.

Prevention

It is important for the women who may get pregnant to get enough folic acid.
There is good evidence that folic acid can reduce the risk of certain birth
defects, including anencephaly.

Women who are pregnant or planning to become pregnant should take


multivitamin and folic acid every day. Many foods are now fortified with folic
acid to help the to prevent these kind of birth defects.

Getting enough folic acid can reduce the chance of neural tube defects by 50%.

3. Microcephaly
This is a condition or disorder in which brain growth is so slow that it fails more
than three standard deviation below normal on growth charts. The head is
inappropriately small for length and weight of the infant.

Causes

It’s usually unknown but associated with mental retardation.

 Disorder in brain development


 Intrauterine infections such as rubella, cytomegalovirus, or toxoplasmosis
 Severe malnutrition or anoxia in early infancy (pregnancy).
Signs

 The fontanels are either closed or very small.


 The head is less than normal
 The infant generally cognitively challenged because of lack of
functioning brain tissues.
NB: The baby does not survive.

4. Spinal Bifida
This is malformation of spine where there is failure of fusion of the vertebral
foramina which may or not lead to protrusion of the meninges with or without
the spinal cord.

It occurs mostly in the 5th lumber or 1st sacral level but may occur at any point
along the spinal canal. It’s one of the commonest abnormalities.

Incidence

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Can occur in any sex

Causes

Folic acid deficiency

Types

 Spinal bifida occulta


 Meningocele
 Meningomyelocele

a) Spinal bifida occulta


Is very slight, marked by dimpling of the skin, no swelling, a hairy patch or
birth mark. The bone defect can be seen by radiology

Signs

 There is no spinal cord involved


 Some children develop convulsion
 Bladder problem otherwise its generally asymptomatic
b) Meningocele
This is when the meninges containing CSF protrudes through the defect or
unformed vertebrae.

The anomaly usually appears protruding approximately at the size of an orange.

Signs and symptoms

 Cystic
 Completely covered by the skin
 No CSF leakage
 No paraplegia
Treatment

Surgery in the first few days of life.

c) Meningomyelocele
This is protrusion of meninges and spinal cord through the vertebrae.

It’s more common and serious.

Symptoms

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 Cystic
 Not completely covered by the skin
 There is CSF leakage.
 There is paraplegia
 Associated with hydrocephalus and skeletal abnormalities.
Treatment

Early surgery gives better prognosis (suture to the skin avoids CSF leakage) but
usually there is extensive paralysis of the trunk and the limbs, severe deformity,
paralysis and insensitivity of the bowel and bladder.

Involuntary movement may be present

Surgery is only indicated to the severely handicapped infants after careful


assessment of the abnormality and neurological state of infants in the first few
days of life.

Nursing care

 The baby should be nursed in prone or lateral position to prevent pressure


on the affected part.
 Dressing of the wound with the sterile none adhesive dressing.
Complication

 Infection of the wound


 Meningitis
 Rupture leading to hemorrhage and subdural hemorrhage.

5. Encephalocele
An encephalocele is a herniation of the meninges and brain through the skull.

The disorder occurs most often in the occipital area of the skull but may occur
as nasal or nasopharyngeal disorder.

Encephalocele is covered fully by the skin but may be open and covered by
Dura.

Treatment

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Encephalocele involves immediate surgery to replace the contents that are
replaceable and to close the skin disorder to prevent infection.

Nursing care

The baby is nursed in prone position

Dressing should be done and kept in position by crepe bandage.

Physical and Developmental Gastrointestinal System

They include;

 Ankyloglossia (tongue tie)


 Thyroglossal cyst
 Cleft lip and palate
 Tracheoesophageal atresia and fistula
 Omphalocele
 Gastroschisis
 Intestinal obstruction
 Meconium plug syndrome
 Imperforated Anus

I. Ankyloglossia (Tongue Tie)


Is an abnormal restriction of the tongue caused by an abnormally tight frenulum
(membrane under the tongue).

Signs and symptoms

 Failure to protrude or elevate the tongue


 Suckling difficulties related to inability to clear food from the mouth
 Difficult latching on the breast
Management

When mild reassurance is done

If tongue is unable to move between the gum, check surgery may be prescribed
(frenectomy) can be done.

II. Thyroglossal cyst


Is an opening to the anterior surface of the neck?

Management

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Cyst is surgically removed to avoid future infection of the space.

Complication

Can turn into thyroid cancer in later life.

III. Cleft Lip and Palate


Cleft lip is more common in boys than in girls. This is due to fusion of the
palate.

It can be bilateral or unilateral.

a) Cleft palate
This is an opening of the palate is usually on the middle line and involve the
anterior hard palate.

Management

 If the condition is discovered while the infant is still in the utero fetal
surgery can repair the condition.
 If discovered after birth. Surgical repair is done shortly thereafter
between 2-10 weeks of age.
 The optimal time for repair of cleft palate is at 15 to 18 months of age.
 Soft palate is at 3 to 6 months as recommended.
i. Esophageal Atresia and Tracheoesophageal Fistula
During intra uterine life, between 4 and 8 weeks laryngotracheal groove
develops into the larynx, trachea and beginning lung tissue. The esophageal
lumen forms parallel to this.

A number of anomalies may occur if trachea and esophagus are affected by


teratogen that does not allow the two organs to separate but remain connected.

Esophageal atresia is obstruction of the esophagus.

The fine usual types of esophageal atresia that occur are:

 The esophagus ends in a blind pouch


There is tracheoesophageal fistula between the distal part of the esophagus and
the trachea (A)

 The esophagus ends in a blind pouch; there is no connection to the


trachea (B)

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 A fistula is present between an otherwise normal esophagus and trachea
(C)
 The esophagus ends in blind pouch. A fistula connects the blind pouch of
the proximal esophagus to the trachea (D)
 There is blind end portion of the esophagus; fistula are present between
both widely spaced segments of the esophagus and the trachea (E)
Signs and symptoms

 Polyhydramnios (excessive amniotic fluid) a fetus with


tracheoesophageal atresia cannot swallow, so the amount of amniotic
fluid can grow abnormally large.
 Infants are born preterm because of hydramnios.
 The infant will cough and become cyanotic and have obvious difficult
breathing as fluids is aspirated
 Excessive accumulation of saliva and mucus in the mouth and pharynx
because there is a development anomaly with blind ending esophageal
pouch
Diagnosis

Whenever atresia is suspected, affirm catheter should be passed to test for


gastric acid. If it travels less than 10cm atresia is suspected.

If not diagnosed prior to the first feed, the baby will cough and regurgitate the
feed into the trachea and the baby will become cyanosed.

Chest x-ray will usually confirm esophageal atresia, air in the stomach indicates
presence of fistula.

Management

 Emergency surgery for the infants with tracheoesophageal fistula to


prevent the development of pneumonia
 Surgery consists of closing of the fistula and anastomosing the
esophageal segments.
Nursing care

The baby is nursed in propped position and nil per mouth

Frequent aspiration of air passages and mouth

Complications

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Respiratory infections e.g. pneumonia

Delay in operation will result into starvation, dehydration and death of the baby.

ii. Omphalocele
This is protruding of abdominal contents through the abdominal wall at the
point of the junction of the umbilical cord and abdomen.

The herniated organs are usually the intestines but they may include the
stomach and liver.

When the defect is less than 4cm it’s termed as hernia but when greater than
4cm it’s a true omphalocele.

This condition occurs because at approximately 6 to 8 weeks of intra uterine


life. The fetal abdominal contents grow faster than the fetal abdomen.

The occurrence is associated with chromosomal deviations.

Signs and symptoms

 Presence is obvious on the inspection at birth


Management

 If identified during pregnancy by sonography caesarian birth may be


considered.
 Most infants will have surgery within 24 hours to replace the bowel
before the thin membrane surrounding it gets ruptured.
iii. Gastroschisis
Is a condition similar to omphalocele except the abdominal disorder is distant
from the umbilicus, usually to the right and the abdominal organs are not
contained by the membrane but rather spill freely from the abdomen.

iv. Intestinal Obstruction


This is failure of canalization of the intestines during utero, it may be an atresia
(complete closure) or stenosis (narrowing) of the fetal bowel. The most
common site of occurrence is in the duodenum.

Signs and symptoms

 Persistent vomiting; milk vomited first then bile later


 The upper part of the abdomen may be distended
 Meconium is passed but no any other stool is passed.

181
Management

 Intravenous therapy is necessary to restore lost fluid.


 Pass NGT and leave it open to prevent gastrointestinal distention
 Surgery is prescribed immediately

v. Meconium Plug Syndrome


This is extremely hard portion of meconium that has completely blocked the
intestinal lumen causing bowel obstruction

Signs and symptoms

Abdominal distention and vomiting which may occur after 24 hours of age.

Management

Administration of saline enema which causes enough peristalsis to expel the


plug.

vi. Imperforated anus


Imperforated anus is stricture of the anus during the 7th week intrauterine life

Signs and symptoms

 The condition may be diagnosed during prenatal sonogram


 On inspection of the new born there is no anus present.
 The abdomen becomes distended and child begins to vomit within 48
hours.
Management

Repair is done

Physical and Developmental Disorders Of The Skeletal System

1. Amelia: This is total absence of the limbs due to thalidomide.

2. Ectromelia: this is partial absence of the limbs it’s most common.

3. Polydactyl (extra digitals): this means extra toes or fingers if the digit is
attached by skin it can be tied with the string but if it has bone refer to doctor
for surgery

4. Syndactyl: this is fusing of the two digits (webbing) together. This may
require surgery.

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5. Talipes or club foot: this is abnormal position of the feet due to pressure in
the uterus. These are of two forms i.e. talipes equinovarus (inversion) or inside
and talipes calcanovalo (everted) outwards.

9. CONGENITAL HEART DISEASES


Definition it refers to a range of possible heart defects.
The following are the congenital heart defects
1) Aortic valve stenosis
This is unknown and serious type of congenital heart defect. It accounts for 5%
of the cases of heart defects.
In aortic valve stenosis, aortic valves that controls the flow of blood out of the
main pumping chamber of the heart (left ventricle) to the body’s main artery
(aorta) is narrowed.
This affects the flow of oxygen rich blood away from the heart towards the rest
of the body may result into left ventricle muscle thickening because the pump
has to work harder.
2) Coarctation of aorta
This is where main artery (the aorta) has narrowed which means less blood can
flow through it.
Coarctation accounts for 10% cases of congenital heart disease. It occurs by its
self or with other types of heart defects. Most commonly ventricular septal
defect or patent ductus arteriosus.
In around half of all the cases the narrowing can be severe and will require
treatment shortly after birth.
3) Epstein’s anomaly
This is where the valve on the right side of the heart (tricuspid valve), which
separates the right atrium from right ventricle, does not develop properly.
That means blood can flow in a wrong way within the heart and the right
ventricle may be smaller and less effective than the normal.
This accounts for about 1% of the congenital heart defects.

4) Patent ductus arteriosus


Is a rare type of congenital heart disease affecting around 5 in 100,000 babies.
As baby develop in the womb, a blood vessel called ductus arteriosus connects
the pulmonary artery directly to the aorta, the ductus arteriosus diverts blood
away from the lungs (which isn’t working well before birth) to the aorta.
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Patent ductus arteriosus is where this connection does not close after birth as it’s
supposed to. This means the extra blood is pumped into the lungs, force the
heart and the lungs to work harder.
5) Pulmonary valve stenosis
This is heart defect where the pulmonary valve which controls the flow of blood
out of the right heart pumping chamber (right ventricle) to the lungs are
narrower than the normal.
This means that the right heart pump has to work harder to push the blood
through the narrowed valve to get in to the lungs.
Pulmonary valve stenosis accounts for 10% of the defects.
6) Atrial septal defects
This where there is a hole between the two collecting chambers of the heart i.e.
left and right atrium. It’s the common and affects 2 in 1000 babies.
When this defect is there extra blood flows through the defect in to stretch and
enlarge the heart.
7) Ventricular septal defects
Occurs when there is a hole between 2 pumping chambers of the heart i.e. left
and right ventricle.
This means extra blood flows through the hole from the left to right ventricle
due to pressure difference between them.
The extra blood goes to the lungs and causing high blood pressure in the lungs
and stretches on the left side pump chamber.
Small holes often close by themselves but larger ones need surgery for closing
it.
8) Single ventricle defects
This is where only one of the pumping chamber (ventricle) develop properly.
Without treatment this defect can be fatal within a few weeks of birth.
a) Hypo plastic left heart syndrome.
Is a rare type of heart defect where left side of the heart doesn’t develop
properly and is too small, this results in no enough oxygenated blood getting
through to the body
b) Tricuspid atresia
Is where the tricuspid valve of the heart hasn’t formed properly. It’s estimated
that 10 babies out of 100,000 babies are affected by tricuspid atresia.
9) Tetralogy of Fallot
Is a combination of several defects affecting 3 in every 10,000 babies.
The defects making up the tetralogy of Fallot are;

184
 Ventricular septal defect (is a hole between left and right ventricle)
 Pulmonary stenosis (narrowing of the pulmonary valve)
 Right ventricular hypertrophy (muscle of the right ventricle is thickened)
 Displaced aorta (where aorta is not in its usual position coming out).
As a result of this combination of defects oxygenated and non-oxygenated
blood mixes, causing the overall amount of oxygen in the blood to be lower
than normal. This may cause the baby to appear blue (cyanosed) at times.
10) Total (or partial) anomalous pulmonary venous connection.
(TAPVC)
Occurs when the four veins that take oxygenated blood from lungs to the left
side of the heart are not connected in the normal way, instead are connected to
the right side of the heart.
Sometimes, only some of the four veins are connected abnormally which is
known as partial (PAPVC).
Its uncommon type affecting around 7 in 100,000 babies.
11) Transposition of the great arteries.
Is relatively common accounting for around 5% of the cases.
Is where pulmonary artery (lung artery) and main body artery (aorta) are
swapped over and are connected to wrong pumping chamber.
This leads to blood that’s low in oxygen being pumped around the body.

12) Truncus arteriosus


Is where two main artery (pulmonary artery and aorta don’t develop properly
and remain as a single vessel. This results into too much flow of blood to the
lungs, which over time can cause breathing difficulties and damage blood
vessels inside the lungs.
It’s fatal within a year of birth if not treated.
Others include the following;
 Tricuspid valve regurgitation (insufficiency). is leakage of tricuspid
valve each time the right ventricle contracts.
 Aortic valve regurgitation. this is leakage of aortic valve each time the
left ventricle relaxes.
 Mitral valve prolapses. is when the mitral valve bulges into the left
atrium during ventricular contraction, sometimes allows leakage of some
blood into the atrium.
 Mitral valve regurgitation. is leakage back through mitral valve each
time the left ventricle contracts.

185
 Mitral valve stenosis. Is narrowing of the valve that increases resistance
to blood flow from left atrium to left ventricle.

FRACTURES
By the end of this topic students should be able to;
1) Define fracture
2) Types of fracture
3) Anatomical varieties of fracture
4) Causes of fracture
5) Predisposing factors to facture
6) Signs and symptoms of fracture
7) First aid management of fracture
Definition
A fracture is complete or incomplete break in continuity of a bone tissue.
Types of fracture
Fracture has mainly two types
1. Simple or closed fracture it when bone breaks tissue breaks and there
is no external communication and the skin remains intact.
2. Compound or open fracture it is when bone breaks and there is an
opening/skin damaged and there is danger of infections and its
surgical emergency.
Anatomical varieties
a) Pathogenical fracture caused by infection e.g. osteomyelitis
b) Green stick fracture this when the bone tissue bends and part of it
remains intact, commonly seen in children because their bones are not
yet fully ossified but cartilages
c) Oblique /slant fracture bone breaks in slanting manner
d) Transverse fracture breaks in transverse form
e) Impacted fracture bone breaks and the broken ends over rid each
other
f) Communited fracture is when the bone is crushed into small pieces and
there is danger of injuring the neighbouring organs
g) Depressed fracture this pertains to bones of the skull

Causes of fracture
186
The main causes of fracture are as follows;
 Direct violence: this is when the bone breaks at the point of impact or
force.
 Indirect violence: this is when the break is away from the point of
impact or force e.g. fall on palm and the collar bone breaks
 Muscular violence or contraction this is when there are strong
abnormal muscle contractions then may go into spasms e.g. fracture of
patella
 Infections (pathogenic) these can be congenital when bone tissues are
infected, inflamed and deprived of nutrients and its weak e.g. in
osteomyelitis and poliomyelitis
Predisposing factors to fracture
The following the predisposing factors to fractures
1. Age
2. Diet- poor nutrition
3. Slippery floor
4. Vigorous exercises
5. Occupational hazards
6. Diseases e.g. sickle cell disease

Signs and symptoms of fracture


• There is pain
• Loss of function
• Unusual mobility/ movement
• Swelling
• Deformities
• Irregularity
• Crepitus-noise
• Tenderness
• Shortening
PLUSDICT
First aid management of fracture
• Advice the casualty to keep still not to move the affected part
• Assess the general condition of the person
• Remove the tight clothes on the affected part
• If there is bleeding flash the wound with clean water and cover with
clean cloth
• Apply pressure to control bleeding
• Immobilise the fractured part
• reassure the person if conscious and the relatives
• Arrange for the transport
• As you wait for the transport check the vital signs, level of
consciousness
• Escort the casualty when transport arrives

187
BURNS AND SCALDS
By the end of this lesson students should be able to;
1. Define burns and scalds
2. Causes of burns and scalds
3. Classify burns
4. Types of burns and their features
5. First aid management of burns.
Definition
• Burns are destruction of body tissues caused by dry heat.
• Scalds are destruction of body tissues caused by wet heat.
Causes of burns
• Lightening
• Electricity
• X-ray radiation
• Friction
• Open flame
• Dry chemicals e.g. sulphuric acid
• Etc.
Causes of scalds
• Boiled water
• Boiled milk
• Boiled cooking oil
• Steam from boiling water
Types of burns
a) Dry burns
Caused by fire flames, cigarettes and hot electrical appliances
b) Dry frictions burn
Is caused by either skin rubbing against anything or fast-moving object against
the skin e.g. rope
c) Scalds
Caused by steam or hot liquids including fats
d) Cold burns
As a result of contact with metal in freezing conditions or with freezing agents
such as liquid oxygen and nitrogen
e) Chemical burns
Caused by acids, alkalis used in industries and domestic cleaning products

188
f) Electrical burns
This may be as a result of electrical current
g) Radiation burns
May be caused by sun light either direct or reflected from bright surface, over
exposure to x-ray and radioactive substances.

Classification of burns
1. Depth
Burns are described as superficial, partial thickness and full thickness (formerly
as first, second, third, and fourth degree burns)
 Superficial burns
 Involves only the outer layer of epithelium and
 result in blisters and erythema (redness of skin)
 They are painful as nerve endings are affected
 Usually they heal in few days
 First (1st) degree burn (erythema) this involves epidermis only no blisters
formed.
 Partial thickness burns cause deeper layer of epidermis and dermis
 They form blisters and are painful
 Such burns heal within 1-4weeks
 Care must be taken to prevent infections
 It is Second (2nd) degree burn epidermis and dermis
 Full thickness burns
 involve complete destruction of the skin including the germinal layer.
 Third (3rd) degree burn which involves epidermis, dermis, subcutaneous
and muscles.
 Fourth (4th) degree burn which involves epidermis, dermis, subcutaneous
layer, muscle layers, tendon and bones.
2. Extent
Classically the extent of burn is calculated by using the rule-of-nine.
This divides the body into areas.
For an adult
 Head -9%
 Arm-9% each (times 2) =18%
 Trunk (back and chest)-36%
 Perineum -1%
 Each leg-18% (times 2) =36%
Totalling=100%

189
Calculating burnt area percentage in children
Use rule of seven for calculating the percentage burn area in children.
Features of superficial burn
 They are painful
 The form blisters
 They heal easily if not infected
 The hair follicles are not affected or damaged
 The burned part becomes reddish in colour/erythema
Features of deep burn
 They are no blisters formed
 They are painless because of damage to the nerves
 No epithelial tissue is left
 Muscle are damaged and bones exposed
 Numbness felt in the affected area or site
 Burned part can easily be infected
 Heals slowly
 Healing takes place by scar formation
 it may need skin grafting
 It may result into deformities and contractures
General signs and symptoms of burns
 Severe pain due to exposure of nerve endings
 History of involvement of the above cause
 Blisters formed due to vasoconstriction/vasodilatation
 Redness for the complete loss of the skin
 Acute circulatory failure leading to hypovolemic shock and
neurogenic shock.
 Loss of function of the part
 Dehydration due to oozing of the body fluids
 Oozing of the fluids from the site
 Reduced urine out put
 Irritability
 Skin discolouration and etc.
First aid Management of burns
i. Call for help
ii. Put off the souse of fire
iii. If possible, wrap him/her in the blanket to stop the flame
iv. Remove the casualty from the cause or cause from the casualty
v. Keep the casualty worm to prevent heat loss.
vi. Ensure clear air way
vii. Cool the burnt are with cold water to reduce pain
viii. Reassure the casualty and the relatives
i. Do not break the blisters
ii. Do not apply oil or ointment on the burnt area.

190
iii. Immobilise the burnt limb
iv. Arrange for the transport to hospital
v. If not in shock give frequent oral fluids to drink
vi. Then when transport arrives escort the casualty to the hospital

Cautions to be taken
• Do not allow the casualty to run away.
• Do not allow him/her to inhale the smock.
• Do not place ice directly on the burnt area because it can damage the
nerves.
• Don’t prick or break blisters
• Don’t remove piece of cloths that are attached to the skin.
• Do not pull away any skin folds.

191
HOME ACCIDENTS
Definition
Home accident is sudden and unexpected occurrence or happening that causes
harm to the body.
Causes of home accidents
 Hot objects e.g. fire, oven and liquids
 Sharp objects e.g. knife, razor blade and needles
 Water kept in open saucepans can cause drowning
 Smooth and rough floor
 Open cooking places can cause fire out break
 Electricity and electrical appliances
 Furniture at home
 Compound with pot holes and stones
 Drugs being left to children reach
 Bath rooms
 Toilets/latrine
 Chocking
 Lightening
People at risk of getting burns
• People who are venerable to home accidents
I. Elderly
II. Children
III. Blind
IV. Deaf
V. Epileptic
VI. Babies
VII. Alcohol brewers
VIII. Leprosy patients
Prevention of home accidents
• Proper storage of sharps e.g. knife etc.
• Keep drugs out of reach of children
• Always switch of electricity and its appliances
• Insulate electrical wires
• Compounds should be levelled
• Keep floor clean
• Over water in the big saucepans
• Proper handling of the sharps
• Observe meal times and avoid eating in darkness
192
• Have raised fire place especial the ovens
• Use good materials for construction of building
• Always protect the venerable like epileptic from fire and water bodies.
BURNS AND SCALDS
• By the end of this lesson students should be able to;
1. Define burns and scalds
2. Causes of burns and scalds
3. Classify burns
4. Types of burns and their features
5. First aid management of burns.
Definition
• Burns are destruction of body tissues caused by dry heat.
• Scalds are destruction of body tissues caused by wet heat.
Causes of burns
• Lightening
• Electricity
• X-ray radiation
• Friction
• Open flame
• Dry chemicals e.g. sulphuric acid
• Etc.
Causes of scalds
• Boiled water
• Boiled milk
• Boiled cooking oil
• Steam from boiling water
• Etc.
Classification of burns
• Burns are classified according to;
1) Degree of burn
According to the degree of burns burns have four degrees
st
a. First (1 ) degree burn (erythema) this involves epidermis only
no blisters formed.
nd
b. Second (2 ) degree burn involves epidermis and dermis and
blisters are present.
rd.
c. Third 3 degree burn which involves epidermis, dermis,
subcutaneous and muscles.
th
d. Fourth (4 ) degree burn which involves epidermis, dermis,
subcutaneous layer, muscle layers, tendon and bones.
2) Extent of burn
this classification of burn is divided into two

193
a) Superficial burn this sub classification of burn involves first and
second degree burns
In this type of burn epithelial tissues are left for regeneration
b) Deep burn this type of burn involves third and fourth degree
burns
Here total thickness of the skin is burned.
Types of burns
There are two types of burns these include;
• superficial burn
• Deep burn as explained in the previous slide above.
Features of superficial burn
 They are painful
 The form blisters
 They heal easily if not infected
 The hair follicles are not affected or damaged
 The burned part becomes reddish in colour/erythema

Features of deep burn


 They are no blisters formed
 They are painless because of damage to the nerves
 No epithelial tissue is left
 Muscle are damaged and bones exposed
 Numbness felt in the affected area or site
 Burned part can easily be infected
 Heals slowly
 Healing takes place by scar formation
 it may need skin grafting
 It may result into deformities and contractures
General signs and symptoms of burns
 Severe pain due to exposure of nerve endings
 History of involvement of the above cause
 Blisters formed due to vasoconstriction/vasodilatation
 Redness for the complete care provided for infected children and
their familiesloss of the skin
 Acute circulatory failure leading to hypovolemic shock and
neurogenic shock.
 Loss of function of the part
 Dehydration due to oozing of the body fluids
 Oozing of the fluids from the site
 Reduced urine out put
 Irritability

194
 Skin discolouration and etc.
First aid Management of burns
i. Call for help
ii. Put off the souse of fire
iii. If possible, wrap him/her in the blanket to stop the flame
iv. Remove the casualty from the cause or cause from the casualty
v. Keep the casualty worm to prevent heat loss.
vi. Ensure clear air way
vii. Cool the burnt are with cold water to reduce pain
viii. Reassure the casualty and the relatives
i. Do not break the blisters
ii. Do not apply oil or ointment on the burnt area.
iii. Immobilise the burnt limb
iv. Arrange for the transport to hospital
v. If not in shock give frequent oral fluids to drink
vi. Then when transport arrives escort the casualty to the hospital
Cautions to be taken
• Do not allow the casualty to run away.
• Do not allow him/her to inhale the smock.
• Do not place ice directly on the burnt area because it can damage the
nerves.
• Don’t prick or break blisters
• Don’t remove piece of cloths that are attached to the skin.
• Do not pull away any skin folds.

195

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