MINIROUND PRESENTATION

BY WARD 3C

NEONATAL SEPSIS.

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 CONTENTS.
PART 1: HISTORY.
PART 2: PHYSICAL EXAMINATION.
PART 3: DISCUSSION

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 PART 1: HISTORY.
We are presenting baby Rosemary
Wanjiru, a 14 day old male infant born to a
22 year old now para 3+0 on the 6th of Feb
2006 via emergency cesarian section
following premature labour with bleeding
per vagina in a woman with two previous
scars. The neonate had an APGAR score
of 5/1,7/5,8/10 and a birth weight of
1950g.
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 Hpi….
The mother was well until 3 weeks ago when
she presented to KNH with a complaint of
abdominal pain of sudden onset, burning in
nature, originating at the scar of the previous
C/S and radiating to the back. The mother was
put on Hyoscine, Tramadol, and Salbutamol.
Six days later she had per vaginal bleeding and
had the emergency CS performed. The
membranes had not ruptured and the state of
the liquor was therefore not known.
There was no history of trauma, high blood
pressure, or heavy exertion during pregnancy.

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 Hpi….
On delivery the baby was suctioned, bagged,
cleaned and dried.
He was admitted to the NBU due to respiratory
distress, prematurity at 32 weeks (by U/s) and
rhesus negativity of the mother.
There was grunting, flaring of the alae nasi and
subcostal and intercostal recession. The
respiratory rate was 64 breaths per minute.

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 Hpi….
The primitive reflexes were all
depressed. The following interventions
were undertaken;
a) Placed in an incubator.
b) Given oxygen by hood.
c) 0.5mg of vitamin K stat.
d) 80ml/ 24hours of iv 10% dextrose.
e) Xpen and gentamycin.
18 hours after birth he was noted to be
jaundiced.
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 Hpi….
Day 2:
Mild jaundice, RR 80/min, HR 156bpm, Temp
37.8oC
Blood culture results showed enterecoccus spp
sensitive to vancomycin, augmentin,
ciprofloxacin, gentamicin, and resisitant to
nalidixic acid and amoxicillin
FHG: WBC count of 27.0 x 109/l, Neutrophil
73.1%, hb 11.0g/dl, platelet count of 108 x 10 9/l
PBF: Polychromasia, nucleated RBCs, and
reactive neutrophil leucocytosis.

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 Hpi….
Day 3:
Jaundiced, RR 60/min, HR 160bpm,Temp 37.2oC
CNS: poor reflexes
trophic feeds were introduced (5 mls)
Phototherapy was started
DCT test was negative
Day 4:
Jaundiced, RR 80/min, HR 136bpm, Temp 36.5oC
LFTs: Albumin 26g/l (35-52g/l), AST 206 IU/l (10-37),
ALT and GGT were within ref range

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 Hpi….
Day 5:
Weight had reduced to 1850g, Jaundiced,
RR 64/min, HR 166bpm, Temp 36.3oC
SCR still present
FHG: WBC count of 33.0 x 109/l,
Neutrophil 70%
EBM increased to 8ml/feed

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 Hpi….
Day 7:
Weight had reduced to 1750g, mild pallor, petechiae,
jaundice spread to trunk and extremities, RR 60/min, HR
160bpm, Temp 37.7oC Splenomegally of 2cm
Neonatal responses were weak
Abs Changed to Fortum and Amikacin
FHG: WBC count of 9.85 x 109/l, Neutrophil 56.2%, HB
8.19g/dl, platelet count of 31.7 x 109/l
GXM (O +ve)
Blood transfusion of 40mls whole blood was done
PCV & Bilirubin tests were requested but the sample was
reportedly insufficient

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 Hpi….
Day 8:
Wt 1750g, Jaundiced, RR 59/min, HR 152bpm, Temp 36.6oC, EBM increased
to 21ml/feed
Bilirubin (Total 361.8 umols/l [0-17umol/l], Direct 226.1 umols/l [0-3.4umol/l])
Day 10:
Wt 1850g, Jaundiced, RR 60/min, HR 160bpm, Temp 36.0oC
EBM increased from 27ml/feed to 35ml/feed
Baby noted to be active
Day 11:
RR 50/min, HR 168bpm, jaundice had increased, Hmegally 4cm below CM
Day 14:
RR 84/min, HR 160bpm, Temp 36.2oC. Skin exfoliative, Pallor,
Splenomegally 3cm below CM
EBM increased to 45ml/feed
Do PCV and GXM

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 ANTENATAL HISTORY.
The mother had a history of a UTI in August 2005 for which she
was given antibiotics (amoxicillin) in a clinic. A pregnancy test
was done on the same urine specimen and revealed that she was
pregnant.

The mother attended antenatal clinic once at Kasarani in

December. The antenatal profile was as follows;

a) Blood group was O negative.

b) Haemoglobin was 12.6g/dl.
c) HIV negative.
d) VDRL negative.
e) ICT negative.

She also received multivitamins.

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 OBGYN HISTORY.
The mother attained her menarche at 13
years. Her menstrual cycles are regular
and occur every 21 days. Usually last for
2 days.

History of contraception use from 2 ½

years ago in the form of injections of Depo
(DMPA) every 3 months. She failed to get
her injection in April.

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 OBGYN HISTORY…..
Her first child was born in 2001 at 42 weeks
gestation via CS due to craniopelvic
disproportion and died 2 days post delivery due
to birth asphyxia. Rhogam (RhIG) was not
administered.

Her 2nd child was born in 2002 at 36 weeks

gestation via emergency CS due to pre-
eclampsia. He has no history of jaundice in the
neonatal period. He is alive and well and is 3 ½
years old. Rhogam was given after the second
delivery.

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FAMILY SOCIAL HISTORY.
The mother is a housewife married to a 27
year old hawker.
They reside in Kasarani. Neither of them
drink or smoke.
There is no history of hypertension,
diabetes or asthma in the family.

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 PART TWO: PHYSICAL
EXAMINATION
GENERAL EXAM
The baby was sick looking, lying in an
incubator under an oxygen hood and a
phototherapy lamp. There was an iv line in
the right arm through which 10% dextrose,
normal saline and potassium chloride were
being infused.
RR 62/minute. HR 176 bpm and the
temperature was 36.70 C. There was no
pallor, no cyanosis, no oedema.

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 GENERAL EXAM……………

Jaundice on the sclera and mucous membranes.

The skin was pink in colour with scaling over the
trunk and extremities. Sclerema was prominent
on the lower limbs. There was wasting.
Capillary refill was 3 sec.
Mild dehydration (slight sinking of the anterior
fontanelle)
The weight was 1850g i.e. at the 50th percentile.
The length was 43cm i.e. above 10th percentile
and the head circumference was 32cm i.e. at the
50th percentile.

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 S/E-THE HEAD.
The anterior fontanelle was 3cm by 2cm
and the posterior fontanelle was 1cm by
1cm. Moulding was present.
No facial dysmorphic features or visible
injuries.
There was no eye discharge.

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 HEAD………
Both nostrils were patent, with no septal deviations and
no discharge.

The ears were in the normal position; the cartilage was

soft and had instant recoil.

The palate was continuous and the tongue was of

normal size. There was no drooling and no oral thrush.

No masses were felt in the neck. There was no webbing

or shortening

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 RESPIRATORY SYSTEM.
The chest was of normal shape and
symmetrrical.
There was Subcostal and intercostal indrawing.
There was no flaring of the alae nasi and no
expiratory grunting.
The trachea was central.
Breast tissue was present and was of a diameter
of 5mm.
On auscultation, there was bilateral air entry and
vesicular breath sounds were heard. No added
sounds were heard.

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 CVS.
The precordium was not active.

The apex beat was in the 4th ICS, left

MCL. All the pulses were present. They
were regular and of normal volume.

S1 and S2 were heard. No murmurs

heard.
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 PER ABDOMEN.
Was not distended and was moving with
respiration. The umbilicus was well ligatured and
dry with no pus, no hyperemia.

The abdomen was soft. The spleen was

enlarged at 4cm below the costal margin. The
liver edge was palpated 2cm below the costal
margin. No masses were felt. The anal opening
was patent.
Bowel sounds were heard.

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 GENITALIA.
Normal male genitalia. Rugae were
present on the scrotum.

The testicles were palpated in the

scrotum.

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 NEUROLOGICAL
The neonate responded poorly to handling. He was
lying in the flexed position. There was spontaneous
symmetrical movement of all the limbs.
Tone was normal in all the limbs.
The primitive reflexes were as follows;

a) Grasp reflex was present but weak.

b) Rooting reflex was absent.
c) Sucking reflex was absent.
d) Placing reflex was present.
e) Tonic neck reflex was absent
f) The stepping and Moro’s reflexes not done

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 GESTATIONAL AGE
ASSESSMENT.
According to the Dubowitz Scoring system
the gestational age was 35 weeks.

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 IMPRESSION
Neonatal Sepsis and neonatal jaundice
in a preterm

Differential diagnosis
a) Neonatal hepatitis
b) Bone marrow depression
c) Red cell enzyme abnormality e.g. G6PDH def
d) Immune thrombocytopenia

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PART 3: DISCUSSION.

NEONATAL SEPSIS

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 DEFINITION

Invasive bacterial infection that occurs in

the first 4wks of life. It is the systemic
response to infection in newborn infants
that includes tachypnoea, tachycardia,
hyperthermia, hypothermia, neutropenia
and leucocytosis.

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 EPIDEMIOLOGY.
Bacterial infections are the primary
cause in 10-20% of neonatal deaths.
Low birth weight infants develop serious
bacterial infection five times more often
than full term babies. The incidence is
1:500 to 1:1600 live births. The highest
rates are seen in lower socioeconomic
groups. Males are at higher risk than
females.
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 CLASSIFICATION.
a) Early onset:
Is from birth to 7 days. It begins in utero due to GUTorganisms. The main
causative agents include;
• GBS.
• [Link].
• Klebsiella.
• L. monocytogenes.
• H. influenzae.
Risk factors for infection include;

• Preterms.
• Vaginal colonization by GBS.
• Prolonged rupture of membranes(18-24hrs).
• Amnionitis.
• Maternal fever or leucocytosis.
• Fetal tachycardia.

Most infected infants and preterms will show non-specific cardiorespiratory

signs such as grunting, tachypnoea and cyanosis.
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 CLASSIFICATION….
b) Late onset (8-14 days): There are
increased neurological features e.g.
twitching.

c) Nosocomial (more than 1wk): Due to

long hospital stay. Present with
bradycardia, temperature instability,
lethargy and apnoea.

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 RISK FACTORS

a) Age; prematures are at greater risk than full

term infants due to immaturity of humoral and
cellular immune factors(esp if less than 30wks
where even maternal antibodies are not yet
acquired)

b) Associated disease states; malignancy,

nephrotic syndrome, galactosemia, iv drug
abuse, paraplegia, gonococcal gut infection,
contact with N. meningitidis and H. influenzae.
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 RISK FACTORS…..
c) Medical procedures; indwelling intravascular
catheters, indwelling urinary catheters,
endotracheal intubation, ventriculoatrial
shunts, continous peritoneal dialysis, surgery,
prosthetic heart valves, newborn resuscitation.

d) Obstetrics and gynaecology; prolonged or

premature membrane rupture , maternal
bleeding (placenta previa, abruptio placentae).

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 RISK FACTORS…..

e) Toxemia; precipitous delivery, maternal

infection e.g. UTI, endometritis.

NB; in a newborn with perinatal complications,

NNS is diagnosed in the first 5 days of life.
Infants without history of predisposing factors
during birth get sepsis in 2wks of age due to
nosocomial infection. NNS in 72hrs after birth
is associated with greater mortality.

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 CAUSATIVE ORGANISMS.

a) Viral; CMV, HSV, RSV, VZV, rubella virus, parvovirus,

adenovirus, echovirus, influenza A and B, parainfluenzae,
enterovirus.

b) Fungal; candida species.

c) Protozoal; plasmodium, toxoplasma gondii, trypanosoma cruzi.

d) Bacterial; [Link], pseudomonas, H. influenzae,

[Link],enterococci, group A Streps., S. aureus, T.
pallidum, GBS, N. meningitidis, enteric bacteria, L.
monocytogenes, S. epidermidis and salmonella.

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 MODE OF SPREAD.

a) Exposure of neonate to the environment.

b) Neonates sharing incubators.
c) Haematogenous spread.
d) Infected amniotic fluid inhalation.
e) Passage of infant through an infected
birth canal

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 Mode of acquisition

Clustering of neonatal bacterial infection

in perinatal period that are aquired during
labour and delivery. Haematogenous and
transplacental dissemination of maternal
infection occurs through invasion of fetal
circulation by contamination of superficial
chorionic vessels, fetal aspiration or
swallowing contaminated amniotic fluid.

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STATE OF PRETERM INFANT
IMMUNITY

In premature infants, the levels of IgG are

lower than in the full term infant. (IgM in an
infant signifies intrauterine infection since it
cannot cross the placental barrier) .
Complement factors are reduced. WBC are
immature and increased in number. The
reticular endothelial system is immature.
Natural Killer Cells and cytokines are also
reduced.
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 SIGNS AND SYMPTOMS.

a) General; fever, temperature instability, poor feeding,

oedema.

b) GIT; abdominal distension, vomiting, diarrhoea,

hepatomegally, splenomegally.

c) RS; apnoea, dyspnoea, tachypnoea, retractions, flaring

of alae nasi, grunting, cyanosis.

d) Renal; oliguria.

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 SIGNS AND SYMPTOMS….
e) CVS; pallor, mottling, cold and clammy skin,
tachycardia, hypotension.

e) CNS; irritability, lethargy, tremors, seizures,

hyporeflexia, hypotonia, abnormal Moro’s
reflex, bulging anterior fontanelle, high pitched
cry.

f) Skin; petechiae, purpura, jaundice.

g) Haematological; bleeding.

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 COMPLICATIONS.

a) Respiratory failure.
b) Pulmonary hypertension.
c) Cardiac failure.
d) Shock.
e) Renal failure.
f) Liver dysfunction.
g) Cerebral oedema.
h) Thrombosis.

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 INVESTIGATIONS.

a) Haemogram shows reduced haemoglobin levels in infection, increased

RBC counts, neutropenia, thrombocytopenia. The IT ratio would indicate
sepsis if is greater than 0.18, where the normal is equal to or less than
0.15.

b) Blood sugar and blood culture.

c) Urine culture and Urinalysis.

d) CXR in respiratory distress.

e) CSF culture and microscopy

f) Abdominal U/s

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 MANAGEMENT

a) Monitor vital signs, urine output and blood pressure.

b) Supportive care; rehydrate with iv fluids, electrolyte

replacement, provide thermal neutral environment.

c) Definitive treatment; antibiotics are required.

Crystalline penicillin and gentamicin are used. A third
generation cephalosporin can substitute the penicillin.
Other aminoglycosides can also be used.

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 PROGNOSIS

With early diagnosis and treatment, infants

are not likely to experience long-term
health problems associated with neonatal
sepsis; however, if early signs and/or risk
factors are missed, the mortality rate
increases. Residual neurologic damage
occurs in 15-30% of neonates with septic
meningitis.

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 PREVENTION.

a) Good antenatal care.

b) Avoid prolonged membrane rupture by CS and labour induction.

c) Prevent nosocomial infection in nursery by practising barrier

nursing and frequent hand washing.

d) Isolation of infected neonates.

e) Intrapartum penicillin empiric prophylaxis for GBS in mothers at

risk (fever, preterm labour, previous infant with GBS infection,
amnionitis).

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Thank you!!!!!!!!!

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