This document discusses obstetric sepsis. It begins by defining sepsis and its spectrum from SIRS to septic shock. Common causes of obstetric sepsis include septic abortion, PROM, chorioamnionitis, and postpartum endometritis. Common organisms include E. coli, Klebsiella, streptococci, and staphylococci. Sepsis causes a systemic inflammatory response and release of inflammatory mediators that can lead to endothelial dysfunction, organ damage, and septic shock. Management involves controlling infection with antibiotics, removing the infection source, and providing supportive care like fluid resuscitation and vasopressors. Specific treatments depend on the type and severity of infection.

1. Obstetrics
Sepsis
Dr.
Kawita
Bapat

2.
What
is
sepsis?
Bone RC, et al. Chest 1992;101:1644
Opal SM, et al. Crit Care Med 2000;28:S81; Levy M et al. Crit Care Med 31:2003
A spectrum of body response & changes
Sepsis
SIRS
Infection/
Inflammation
Severe
Sepsis
Septic
Shock
Clinical response arising from
a nonspecific insult, including
≥ 2 of the following:
• Temperature ≥38oC or ≤36oC
• HR ≥90 beats/min
• Respirations ≥20/min, PCO2< 32
• WBC count ≥12,000/mm3 or
≤4,000/mm3 or >10% immature
neutrophils (Band Forms) SIRS = Systemic Inflammatory Response Syndrome
SIRS with a
presumed or
confirmed
Infectious
process
Sepsis with
≥1 sign of organ failure
v Cardiovascular
v Renal
v Respiratory
v Hepatic
v Hematologic / DIC
v CNS
v Metabolic acidosis
Severe
sepsis
with
persistent
refractory
hypo-
tension

3. Etiology of Obstetric Sepsis
• Septic abortion
• PROM / PPROM
• Chorioamnionitis
• Postpartum endometritis
• Wound sepsis
• Respiratory infection / Pneumonia
• Pyelonephritis / Urinary Tract Infection
• Necrotising fasciitis
• Acute appendicitis/ pancreatitis/ cholecystitis

4. Pathophysiology
Common
organisms
are
:
§ E.
Coli
§ Klebsiella
§ Group
A
β
haemoly@c
streptococcous
§ Group
B
Streptococcus
(GBS).
§ Staphylococcus
§ Bacteroids
§ N.
Gonorrhoea
§ C.
Trachoma@s
§ Cl.
Welchii
§ Mycoplasma
hominis
§ H.
influenzae

5. Pathophysiology
§ TNF - α
§ IL – 1 β and I L – 6
§ Arachidonic acid metabolites
(Leukotrienes, PG, Tx)
§ complement system
§ coagulation cascade
§ Fibrinolytic system
§ Prekallikrein
§ Bradykinin
§ Histamine
§ β- endorphine / Encephalin
§ Mycocardial depressant factors.
Inflammatory
mediators are :

6. Mechanism
These
inflammatory
mediators
cause
:
§ Endothelial
dysfunc@on
§ Increased
vascular
permeability
§ Myocardial
suppression
§ Ac@va@on
of
coagula@on
cascade
leading
to
DIC.

7.
Evolu@on
of
Sepsis
In
Early
Stage
of
sepsis
Released
Vasoac@ve
Mediators
cause
§ Vasodila@on
§ Platelet
aggrega@on
§ Capillary
plugging
§ Endothelial
damage
Resul@ng
in
§ Cellular
hypoxia
§ lac@c
acidosis
§ Worsening
of
@ssue
perfusion
In Late Stage of sepsis
Poor tissue perfusion causes :
v Decreased vascular resistance
v Decreased Cardiac output
v Vasoconstriction
v Further decrease in tissue
perfusion
v End organ damage.
Many cytokines cause global
myocardial dysfunction , which
results in septic shock.

8. Investigations
§ CBC, ESR, BIood grouping and Rh typing
§ Serum β HCG
§ Urine – Routine, Microscopic culture and
sensitivity.
§ Blood culture
§ Blood Gas Analysis
§ Blood Glucose, electrolytes, BUN,
creatinine
§ Coagulation Profile
§ Liver function test

9. Special
Inves@ga@ons
§ Endocervical and high vaginal swab culture must
be taken prior to internal examination.
§ The material is sent for
§ Gram staining
§ Culture both in aerobic and anaerobic medium
§ Sensitivity test
§ USG
§ Supine and upright x-ray of abdomen – Air, FB
§ CT, MRI – special cases to see for myometrial
necrosis.

10. Management
§ Hospitalisation and isolation if possible.
§ Overall assessment of case and Patient is put
in accordance to clinical grading
§ Aim of treatment:
v Control of sepsis
v Removal of source of infection
v Supportive therapy
v Assessment of response to treatment

11. Management
GENERAL
MANAGEMENT
:
1. Control
by
administering
Broad-­‐spectrum
an@micirobial
therapy.
Mul@ple
drugs
are
preferable
as
it
is
commonly
a
mixed
infec@on.
2. Prophylac@c
TIG
along
with
Tetanus
Toxoid.
3. Maintenance
of
haemodynamic
status
Early
Goal
directed
therapy
(EGDT)
v Rapid
crystalloid
infusion.
MAP
should
be
maintained
at
65
mm
Hg
and
urine
output
should
be
30
ml/hr
v Blood
transfusion.
v Inser@on
of
CVC,
PAC.
CVP
is
ideally
maintained
at
8-­‐12
mm
Hg
v Administra@on
of
ionotropes
like
Dopamine,
Norepinephrine
or
Dobutamine

12. General Management…contd
4. Tissue oxygenation
v Supplemental oxygenation maintaining oxygen
saturation > 70%
v B.T if haematocrit < 30%
v Mechanical ventilation in ARDS
5. Treatment of acute renal failure, DIC etc as indicated.
6. Use of anti – inflammatory agents like Hydrocortisone or
Dexamethasone.
7. Human recombinant activated Protein C (HRAPC)
8. Supportive measures:
v GI haemorrhage prophylaxis by H2 receptor blockers
v Maintainance of nutrition: Enteral nutrition is preferable
but total parenteral nutrition may be required.
v DVT prophylaxis by Prophylactic heparin
v Skin care

13. Specific
Management
-­‐
Sep@c
Abor@on
SPECIFIC MANAGEMENT :
Grade – I :
§ Evacuation should be performed after 24 hrs of antibiotic therapy unless
haemorrhage is profuse.
§ Gentle approach avoiding vigorous curettage.
Grade – II :
1. Evacuation of uterus.
2. Posterior colpotomy.
Grade – III :
Patients with septic shock are to be managed by both critical care physician and
gynaecolgists.
After the patient is stabilised after active resuscitation and critical care, surgery is
to be undertaken.

14. Specific
Management
-­‐
Sep@c
Abor@on
Indica@ons
for
laparotomy
are
:
1.
Injury
to
the
uterus
/
gut
2.
Presence
of
FB
3.
Unresponsive
peritoni@s
sugges@ve
of
collec@on
of
pus
in
abdominal
cavity.
4.
Uterus
too
big
to
be
safely
evacuated
per
vagina.

15. ON
LAPAROTOMY
:
Ø Explora@ve
laparotomy
by
senior
gynaec
and
skilled
anaesthesist.
When
gut
injury
is
suspected
general
surgeon
should
be
consulted.
Ø Removal
of
uterus
irrespec@ve
of
parity
if
it
is
gangrenous.
Ø If
perfora@on
is
small
and
uterus
is
healthy
debridement
and
repair.
Uterus
can
be
evacuated
through
the
perfora@on
site.
Ø Adnexa
to
be
removed
or
preserved
according
to
pathology.
It
should
be
removed
in
Cl.
Welchii
infec@on.
Ø Thorough
inspec@on
of
gut
and
omentum.
Exteriorisa@on
of
gut
is
ideal
in
shock.
Ø If
nothing
is
found
simple
drainage
of
pus
is
effec@ve.

16. Specific Management : Role of
Antibiotics
General
consensus
• Women
<
37
weeks
will
benefit
from
an@bio@cs
– Oracle
study
2001
– Mercer
et
al
1997
– Lewis
et
al
1996
Controversial
issues
• Which
an@bio@cs?
• Dura@on
of
course
PROM
/
PPROM

17. An@bio@cs
in
PROM
/
PPROM
• Erythromycin in PROM had beneficial effects on
the occurrence of major neonatal disease,
• Administration of co-amoxiclav was associated
with a significant increase in the occurrence of
neonatal necrotizing enterocolitis.
• No difference in rates of Preterm birth, Low Birth
Weight, neonatal death, chronic lung disease,
abnormal cerebral USG, or composite neonatal
outcome between any antibiotic & placebo.
• Neither beta-lactam nor macrolide antibiotic in
women with spontaneous preterm labour
prolonged pregnancy or improved neonatal
health.

18. Preven@ng
Preterm
Birth
• Erythromycin – most studied and well accepted
• Co-amoxyclav and Ampicillin have drawbacks
• 2nd/3rd generation cephalosporins may be used
• New evidence emerging with Clindamycin
• Oral 300mg BD X 5 days or intravaginal 2%
crème X 3 days
– Low risk women detected to have abnormal genital flora
early in 2nd trimester (12-22 wk)
– 60% reduction in preterm labour and NICU admission.
– Reduces late miscarriage rate.

19. Specific Management
Antibiotics in Chorioamnionitis
• Gilstrap
Bawdon
&
Burris
measured
Levels
of
5
an@bio@cs
in
maternal
blood,
cord
blood
&
placental
membranes
• Ampicillin
provided
highest
ra@o
of
placental
to
maternal
blood:
3.97
• Hence
Ampicillin
-­‐
Gentamycin
coverage
is
appropriate
although
addi@onal
anaerobic
coverage
may
be
needed
Gilstrap
Bawdon
&
Burris
1988

20. Factors Influencing Outcome
• Immune response of the host
• Virulence of the micro organism
• Burden of infection
• Presence of super antigen and other
virulence factors
• Resistance to opsonization and
phagocytosis
• Antibiotic resistance

21. Scope
of
Surgery
• Caesarean section for obstetric indications
Chorioamnionitis and PROM are not
indications of C-section as such.
• Drainage of abscess
• Wound debridement and secondary suture
• Dilatation & Evacuation
• Exploration of uterus
• Hysterectomy

22. Activated Protein C
• Anticoagulant / Anti-inflammatory agent
• No study on pregnant mothers.
• 24 µg / kg / min for 4 days.
• M/A : Stimulates fibrinolysis.
• Decreases thrombin formation by
– Inhibiting platelet activation
– Inhibiting neutrophil recruitment
– Inhibiting mast cell degranulation
Liaw PC et al. Blood 104:2003.
• Trials like ADDRESS trial or PROWESS trial have not shown any
benefit. Also, there is increased chance of haemorrhage. (Bernard GR
et al. NEJM 344:2001.)
• Contraindications are Recent trauma or surgery, Active
hemorrhage, Concurrent anti-coagulant use, thrombocytopenia or
recent stroke

23. GBS- the fact file
§ It is a gram positive group B streptococcus.
§ It is normally present in vagina and lower intestinal
tract of healthy women in 15-40% (India 12-27%).
§ A pregnant carrier who tests positive for GBS and
receives antibiotics during labour has only 1 in 4000
chance of delivering a baby with disease.
§ If she does not receive antibiotics – the risk is 1 in
200 i.e. 20 times higher.
§ Most of the deaths due to GBS occur during the
period between onset of labour and 72 hours.

24. Burden of invasive GBS

25. GBS during pregnancy and
postpartum
v ? Still birth and late miscarriage.
v ? Preterm labour.
v ? Pre labour rupture of membranes.
v Chorioamnitis
v Post partum endometritis
v Post partum septicemia
v UTI

26. Risk of GBS Infection in Neonate
v 1
in
1000
when
the
woman
is
not
known
to
be
a
carrier
v 1
in
400
when
she
is
carrying
GBS
infec@on
during
pregnancy
(1
in
8000
a0er
receiving
IV
an7bio7c)
v 1
in
300
when
she
is
carrying
GBS
infec@on
at
delivery.
(1
in
6000
a0er
receiving
IV
an7bio7c)
v 1
in
100
when
she
had
previous
baby
infected
with
GBS.
(1
in
2000
a0er
receiving
IV
an7bio7cs)

27. Recent recommendations on GBS
All
pregnant
women
should
be
screened
for
GBS
at
35-­‐37
weeks
of
gesta@on.
Pregnant
women
who
are
colonized
with
GBS
should
be
treated
with
IV
penicillin.
Two
condi@ons
warrant
chemoprophylaxis
regardless
of
coloniza@on:-­‐
1) Women
with
risk
factors
such
as
PROM,
intrapartum
fever,
prolonged
ROM
>
18
hours.
2) Women
with
history
of
GBS
disease
such
as
prior
episode
of
GBS
bacteriuria
or
a
previous
new
born
with
invasive
disease
Joint
recommenda@ons
by
CDC,
ACOG
&
AAP

28. Conclusion
Essence of sepsis management:
• Early goal directed therapy (EGDT)
• Maintenance of Lung perfusion
• Antibiotics
• Activated protein C (APRC) in select cases
• Judicious use of corticosteroid, vasopressin
and Dobutamine
• Support organ function
• Prevention of nosocomial infection.

29. That’s all for now!
Thank you !