UNIVERSITY OF EASTERN AFRICA, BARATON.

SCHOOOL OF NURSING.

DEPARTMENT OF NURSING.

A PRESENTATION DONE IN PARTIAL FULFILMENT OF

THE REQUIREMENT OF THE COURSE ,CHILD HEALTH CAR
:NRSG328.

STUDENTS DETAILS:

1. Rachael Ogada Anne SOGAAN2111

2. Nzaro Purity Kadzo SNZAPU2111

BACTERIAL ENDOCARDITIS.
Definition
It is an infection or inflammation of the inner lining of the heart (endocardium) or the valves
caused by bacteria.
Causes
 Staphylococcus aureus
 Streptococcus viridans
There are also incidences caused by HACEK group,that is Haemophilus, Actinobacillus,
Cardiobacterium, Eikenella and Kingella.
Risk factors
 Congenital heart disease.
 Artificial heart valves
 Previous history of endocarditis
 Rheumatic heart disease
 Heart transplant with heart valve disease.
 A weak immune system
 Indwelling central venous catheter- Staphylococcus aureus

Pathophysiology
The process starts when there is damage to the valve surface causing alteration in its normal
structure and physiology. This leads to the deposition of platelets and fibrin forming a
nonbacterial thrombotic vegetation. Organism may enter the blood stream from any site of
localized infection. The bacteria attaches itself to the platelet fibrin complex deposits. Since the
bacteria is covered by fibrin, it is protected from neutrophilic attack and in this period, the
bacteria undergoes massive multiplication and the vegetation matures. These bacterial vegetation
cause changes in turbulence around the lesions formed. This turbulent action causes further
trauma to the heart endothelium and the process repeats itself hence proggresing to further
damage to the cardiac muscles.
Endocarditis may occur from routine exposure to bacteremia associated with usual daily
activities such as brushing teeth, although it can also occur after procedures such as dental work,
invasive procedures involving the gastrointestinal or genitourinary tracts, cardiac surgery
especially if synthetic material is used(valves) or from long term indwelling catheters. The most
common causative agents are staphylococcus aureus and streptococcus viridans.
Clinical manifestation
These are very varied and may range from shock and sepsis to vague symptoms that present over
a period of months.
Loss of appetite
Weight loss
Fatigue
Night sweats
Persistent fever: these are usually absent in about 10%
Chills.
Skin manifestations usually due to secondary micro embolization or immunologic phenomenon
Splinter hemorrhages which are blood clots appearing under the finger nails usually linear,
Janeway's lesions are small painless hemorrhagic areas on palms and soles and Osler’s nodes
which are tender pea-sized nodes found at the end of fingers or toes
Petechiae: red spots of blood under the skin
New heart murmur: these have been reported in about 90% but are mostly present in patients
with underlying congenital heart diseases.
Heart failure or valve insufficiency due to an acute onset accompanied by dyspnea on
exhaustion, shortness of breath, lower extremities swelling.
Neurologic involvement due to cerebral infarct
Splenomegaly usually non tender unless it has an infarct or abscesses.
Diagnosis: Modified Duke criteria.
Major criteria
 Blood culture are drawn at different times 12 hours apart to look for infection in the
child’s blood. Typical microorganisms with infective endocarditis from at least 2 positive
cultures.
 Echocardiogram it looks at the structure of the child’s heart and how well it’s working. It
uses sound waves to make a moving picture of the heart. Positive echocardiogram
showing myocardial abscesses or oscillating intracardiac mass on valve or the
surrounding structures.
Minor criteria.
 Predisposing heart condition or IV drug abuser.
 Fever above 38°c
Microbiological evidences: positive blood cultures which fail to meet the major criteria
Vascular phenomena including arterial emboli, Janeway’s lesions, conjunctival hemorrhage,
intracranial hemorrhage.
Immunologic phenomena including glomerulonephritis, Osler’s nodes
Echocardiogram evidence which fail to meet the major criteria but are consistent with infective
endocarditis.
Laboratory work: ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein) will be
elevated.
Definite endocarditis:
2 major criteria or 1 major criteria and 3 minor or 5 minor symptoms.
Possible endocarditis:
1 major and 1 minor or 3 minor criteria.
Medical management.
Ibuprofen PO for the fever and chills.
Requires IV antibiotics over 2-6 weeks delivered through a peak line.
In case of valve damage, valve repair or replacement may be necessary.
Flucloxacillin/ methicillin and gentamicin. If the S.aureus is methicillin resistant, use
vancomycin and gentamicin combination.
Gentamicin is stopped after the first 2 weeks of commencing treatment due to its adverse side
effects to the child’s developing organs especially the kidney and liver.
PO Amoxicillin 50mg/kg
PO Azithromycin/ Clarithromycin 15mg/kg
PO Clindamycin 20mg/kg
Nursing management
Ensure bed rest.
Ensure salt restriction.
Give diuretics when indicated.
Monitor vitals especially blood pressure, pulse, temperature which provides baseline data to
monitor progress.
Listen to heart sounds to be able to detect any new heart murmurs
Position patient is semi fowler’s position to decrease oxygen consumption.
Monitor fluid input and output to eliminate any undetected water retention.
Prevention
For any patient who recovers from the illness should take prophylactic antibiotics before any
dental or surgical procedures
Nursing diagnosis.
Decreased cardiac output related to valvular dysfunction as evidenced by tachycardia, cyanosis,
shortness of breath, reduced activity.
Impaired gaseous exchange related low oxygen perfusion as evidenced by shortness of breath,
use of accessory muscles and dyspnea.
Decreased cardiac output related to fluid overload in heart as evidenced by tachycardia, heart
murmur.
Activity intolerance related to fatigue as evidenced by patient verbalizing weakness,need to rest
after short period of activity.
References.
Johnson. Y Joyce, Keagh Jim Pediatric nursing demystified: a self-teaching guide. 1 ST Edition
McGraw-Hill Professional (2009) Ppaperback.