Juniper Publishers: Spontaneous Bacterial Peritonitis during Pregnancy: A Rare Occurrence
JUNIPER PUBLISHERS- JOURNAL OF GYNECOLOGY AND WOMEN’S
HEALTH
Journal of Gynecology and Women’s Health-Juniper
Publishers
Authored by Yogita Dogra*
Abstract
Acute abdomen during pregnancy is not an uncommon
emergency in obstetrical practice. But dilemma occurs when no cause is
found despite thorough workup and investigations, even on laparotomy.
Peritonitis though may occur during pregnancy following tubal rupture in
ectopic pregnancy or other intra abdominal conditions but spontaneous
bacterial peritonitis is rarest of rare occurrence during pregnancy and
that too with staphylococci. Only 2-4% cases of spontaneous bacterial
peritonitis with staphylococcus aureus have been mentioned in
literature. In a rare case we came across, a primigravidae who presented
with pain abdomen, fever and ascites which later on diagnosed to be a
case of spontaneous bacterial peritonitis and the microorganism isolated
was found to be staphylococcus aureus. We are reporting this case
because of rare occurrence of this entity in pregnancy and the paucity
of literature.
Introduction
Microbial contamination of the peritoneal cavity is
termed as peritonitis or intra-abdominal infection, and is classified
according to etiology [1].
Peritonitis has been categorized as primary, secondary, or (more
recently) tertiary. Peritonitis complicating peritoneal dialysis can be
considered as an additional category [2]. Acute peritonitis may be classified as primary (spontaneous), where an infection has arisen de novo
within the peritoneum, or secondary, where the inflammatory process
involving the peritoneum is the result of an identifiable primary
process [3].
Bacterial peritonitis is usually polymicrobial, both aerobic and
anaerobic organisms being present. The exception is primary peritonitis
(‘spontaneous’ peritonitis), in which a pure infection with
streptococcal, pneumococcal or Haemophilus bacteria occurs.
Infecting organisms may reach the peritoneal cavity via a number of
routes viz gastrointestinal perforation e.g. perforated ulcer,
diverticular perforation; exogenous contamination e.g. drains, open
surgery, trauma; transmural bacterial translocation (no perforation)
e.g. inflammatory bowel disease, appendicitis, ischaemic bowel; female
genital tract infection e.g. pelvic inflammatory disease; haematogenous
spread (rare) e.g. septicaemia [4].
Although the route of infection in primary peritonitis is usually not
apparent it is thought to be hematogenous, lymphogenous, transmural
migration through an intact gut wall from the intestinal lumen or, in
women, from the vagina or via the fallopian tubes [5]
and rarely require surgical intervention while the effective therapy
for secondary peritonitis requires source control to resect or repair
the diseased organ; debridement of necrotic, infected tissue and debris;
and administration of antimicrobial agents directed against aerobes and
anaerobes [1].
We are presenting here a rarest of rare case of spontaneous bacterial
peritonitis with staphylococcal infection in a primigravida at 26 weeks
with successful pregnancy outcome.
Case Report
A 21 years old primigravida reported to labour room
at Kamla Nehru Hospital, Shimla at 26+6 weeks with complaints of pain
abdomen and fever for 3-4 days. She was admitted for similar complaints
at local practitioner where USG abdomen and pelvis revealed as cites with
thick septations for which she was referred to our hospital. There was
no significant past and family history. On examination, vitals were
stable. Height of uterus corresponded to 26 weeks with tense and
distended abdomen. Fetal heart sound could not be localised. Laboratory
investigations revealed hemoglobin 9.5g/dl, total lymphocyte count
6800/uL with differential lymphocyte count N79L20M0E0,
ESR-65mm, renal and liver function tests were within normal limits;
total serum proteins were 6.9 g/dl with serum albumin 3.2g/dl and blood
sugar was normal. USG abdomen and pelvis showed normal liver and gall
bladder, moderate maternal ascites with thick septations, single live
fetus with gestational age 26+4 weeks with severe oligohydramnios. She
was started on antibiotics, received two doses betamethasone and
nifidipine tocolysis. USG guided diagnostic ascitic tap was done at 27+2
weeks. Microscopic examination revealed field full of pus cells and
gram staining showed predominant polymorphonuclear cells with gram
positive cocci (Staphylococci) in groups and clusters. Culture
was sterile. Glucose-1mg/dl, proteins-4.9g/dl (exudate),
LDH->20000U/l, ADA-323u/l, mycobacterium tuberculosis PCR negative.
Repeat USG at 27+6 weeks suggested massive multiloculated septated
collection in abdomen occupying whole of bilateral lumbar regions and
epigastric region. Decision for exploratory laparotomy was taken.
Intraoperatively, 1.5-2 litres multiseptated collection of thick non
foul smelling pus was drained. The uterus was 28 weeks size. Bilateral
ovaries could not be visualised. Pouch of douglas was completely
obliterated. Peritoneal toileting was done after breaking all loculi.
Abdomen was inspected carefully but primary source of peritonitis could
not be identified. The post operative period was uneventful. She
received antibiotics and tocolysis. Pus culture was sterile. She went
into preterm labour at 30 weeks and had preterm vaginal delivery of a
female child 1.25kg. Both mother and baby were discharged under
satisfactory conditions.
Discussion
Idiopathic peritonitis is un common, constituting
about 1 per cent of all cases of peritonitis and occurs when no obvious
source for the peritoneal infection can be demonstrated. It is a
diagnosis by exclusion and is confirmed in retrospect when the results
of blood cultures or peritoneal swabs become available. Formerly,
pneumococci were implicated, but in recent years haemolytic streptococci, Escherichia coli, and Klebsiella spp.
are more frequently cultured. It was classically described in young
girls where the port of entry was presumed to be through the fallopian
tubes. Adult primary peritonitis arises via haematogenous spread or
translocation of bacteria through the bowel wall, especially in the
presence of exogenous (e.g. steroid therapy) or endogenous (intercurrent
disease) immunosuppresssion [3].
Spontaneous bacterial peritonitis (SBP) is a known complication of
ascites due to cirrhosis; it has also been reported in some
non-cirrhotic conditions with ascites [6].
Spontaneous bacterial peritonitis is thought to occur as a result of
prolonged bacteraemia due to impaired host-defense mechanisms and
decreased bactericidal activity in the ascitic fluid. Bactericidal
activity parallels the total protein concentration in the fluid [7]. Spontaneous bacterial peritonitis can vary in its presentation from being clinically dramatic to totally asymptomatic [3]. Fever of about 38°C (100 °F) is the most common presenting feature and occurs in 50 to 80 per cent of patients [2,3,5].
Abdominal pain, usually diffuse, occurs in 25 to 72 per cent of
patients; rebound tenderness is elicited in over 50 per cent of
patients. However it can occur in the absence of abdominal pain or fever
[3]. A diagnostic abdominal paracentesis essential [3,8]. Ascitic fluid absolute white blood cell count lower than 250 polymorphonuclear cells/mm3 usually denotes uninfected ascites, while counts above this suggest infection, but a count above 500/mm3 establishes with more than 80 per cent certainty the diagnosis of spontaneous bacterial peritonitis [3].
Pelvic infection via the fallopian tubes is responsible for a high
proportion of ‘nongastrointestinal’ causes of peritonitis. Idiopathic
streptococcal and staphylococcal peritonitis in adults is fortunately
rare. In streptococcal peritonitis, the peritoneal exudate is odourless
and thin, contains some flecks of fibrin and may be blood-stained [4]. Staphylococcus aureus is an unusual cause of primary peritonitis, accounting for only 2-4% of cases [5]. The use of intravaginal tampons has led to an increased incidence of Staphylococcus aureus infections: these can be associated with ‘toxic shock syndrome’ and disseminated intravascular coagulopathy [4].
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