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44. Postpartum Sepsis
44.1 Introduction
Maternal sepsis contributes to nearly 10–15% of maternal morbidity and 8–10% of maternal mortality. It is still responsible for poor general health of women in developing countries [1]. The maternal sepsis is seen in 0.1–0.6 per 1000 deliveries in developed countries resulting in high mortality rate of 10% [2]. In developing world, the incidence of sepsis varies from 0.03% to 0.7% contributing to almost one third of all maternal deaths [3]. As per WHO fact sheet 2010 [4], sepsis results in maternal mortality in 8%. In India it is still a direct cause of death in 13% as per report of ICMR [5]. There are many reasons for it, one being late recognition of severe sepsis and late arrival at the referral site, despite intensive planning in policy making and interventions adopted during policy implementation. A decline in number of total maternal mortality by 4.5% annually has been observed due to improved maternal healthcare in the last few years, although proposed decline of 5.5% has not been achieved to meet WHO-defined millennium development goal 5 (MDG-5).
44.2 Definition
Postpartum sepsis is defined as any genital tract infection which occurs within 28 days of miscarriage, induced abortions and childbirth. Any maternal fever more than 38 °C on 2 successive days in the first 10 postpartum days excluding the first 24 h indicates puerperal infection. Although institutional deliveries are being encouraged where aseptic norms for childbirth are observed rigidly now, incidence of sepsis after delivery is significantly high. The number of illegal abortions has also declined due to strict observance of norms of MTP Act and PC-PNDT Act.
44.3 Sepsis
Sepsis is broadly defined as infection leading to systemic inflammatory response syndrome in various intensities from mild to severe. It is mild when there is initial inflammatory response represented by pyrexia and pain. It is called severe sepsis when it has either induced tissue hypoperfusion recognizable as systolic blood pressure being <90 mmHg, MAP <70 mmHg, SBP fall by >40 mmHg or SBP being <2SD below normal for patient’s age after excluding other causes of hypotension, increased lactate levels and oliguria. Septic shock is defined as severe hypotension as a result of severe sepsis which becomes refractory to fluid resuscitation, further progressing to multiorgan dysfunction syndrome (MODS).
44.4 Sepsis and Pregnancy Physiology
Pregnancy is a special situation where maternal physiological changes are significantly altered with a little reserve for compensation in case of sepsis. The cardiovascular system undergoes hyperdynamic circulatory changes with increased blood volume, increased cardiac output and reduced systemic vascular resistance. There is decrease in albumen levels predisposing to pulmonary oedema due to hyperpermeability of capillaries and increased minute ventilation leading to fluid shift to third space. The respiratory system changes bring mild respiratory alkalosis with mild metabolic acidosis with little compensatory reserve in sepsis. All the more the interpretation of physiological limits is individually variable and ill defined.
44.5 Sepsis Microbiology
The causative organisms are a spectrum of aerobic Gram-positive as well as Gram-negative bacteria besides anaerobic infections.
The common aerobic Gram-positive bacteria are beta-haemolytic streptococci—groups A, B and D, Streptococcus faecalis, Staphylococcus aureus and enterococci. The Gram-negative intestinal bacilli are Escherichia coli, Proteus mirabilis and Klebsiella pneumoniae. The Gram variable organism is Gardnerella vaginalis. The anaerobic group includes commonly Peptococcus, Peptostreptococcus, anaerobic streptococci, Bacteroides fragilis, Bovis and fusobacteria. Some uncommon infections of Clostridia group as Cl. welchii and Cl. tetani and others from Mobiluncus species and Prevotella species may occur. Some specific organisms in obstetrical practice are Chlamydia trachomatis, Mycoplasma hominis and Neisseria gonorrhoeae.
44.6 Sepsis Pathology
The normal flora inhabiting the lower genital tract or neighbouring urinary or anal tract acts as an inoculum on the devitalized, traumatized mucosal surface or raw placental site, which promotes bacterial proliferation and spreads into the bloodstream to manifest as clinical infection.
Puerperal infection is usually multimicrobial causing endometritis/endomyometritis originating from sloughed out infected decidua, placental site and underlying myometrium. It spreads out via the bloodstream and lymphatics and by contiguity. There occurs inflammation of pelvic cellular tissues as well as exudation and pus formation presenting as infected adnexal masses. The resultant parametritis may spread as pelvic cellulitis and peritonitis and form pelvic abscess with a collection in the pouch of Douglas, trying to spread into generalized peritoneal cavity as well as subhepatic region under the diaphragm. The salpingitis whether perisalpingitis, interstitial salpingitis or sometimes endosalpingitis may form tubo-ovarian abscess and rupture. The broad ligament abscess may point towards inguinal ligament. The severe form of infection may exhibit as septicaemia and septicaemic endotoxic shock. The exotoxins of Staphylococcus aureus in puerperium may cause toxic shock syndrome. At times, necrotizing fasciitis may occur due to Group B haemolytic streptococci or due to polymicrobial infection.
44.7 Pathogenesis
It is related to interaction of host factors with infecting organisms and type of procedural interference. The mechanism is a host response initiation leading to hyperinflammation as systemic inflammatory response syndrome (SIRS) stimulating resultant compensatory anti-inflammatory response of complement system and coagulation cascade. This provokes acute phase reaction with leucocyte recruitment and oxidative stress. There occurs leukocyte apoptosis with microcirculatory dysfunction and metabolic alterations of the autonomic nervous system causing neuroendocrinal reaction and multiorgan dysfunction or failure.
The host factors are local tissue factors which are related to tissue necrosis or haematoma resulting in local hypoperfusion and resultant loss of tissue integrity. Various cellular energy processes are disturbed resulting in damage of local endothelial, parenchymal or immune competent cells, thus affecting membrane permeability; cellular electrolyte transfer involving Na, K and calcium; as well as release of neurotransmitters or hormones. This activates various cytokines, lipid peroxidation and release of free radicals and enzymes like phospholipases, proteases and endonucleases resulting in membrane disintegration and DNA damage. This causes apoptosis and necrosis of local endothelial, parenchymal and immune cells. The systemic factors are related to severity of tissue insult, haemorrhagic shock as well as insufficient lactate clearance. The injury factor depends on site of injury like abdominal or vaginal, so type of mutilation, extent of tears, lacerations and operative interventions are important factors. The therapeutic factors include any delay in recognizing injury, delayed institution of antibiotics and delay in doing reparative procedures. The other issues are need of ventilation, prolonged ICU stay, massive blood transfusions or occurrence of resistant nosocomial infections. The individual patient factors are also related to genetic predisposition to exaggerated inflammatory response and coagulation cascade due to gene polymorphisms of TNF β2/β2 and heat shock protein 70-2A/A genotypes resulting in increased mortality of septic patients. The patient may be diabetic, may be alcohol and drug user or may be suffering from chronic renal insufficiency or chronic obstructive airway disease besides having immunosuppression.
The infective organisms are usually from the perineum and vagina, and the invasion is due to inadequate levels of asepsis observed or improper tissue handling during surgical procedures where tissue devitalization has occurred due to prolonged operative time or where it has already been a handled case from domiciliary settings.
44.8 Risk Factors
They are many antenatal factors like miscarriage, prolonged rupture of membrane, chorioamnionitis, preterm labour, poor economic status, malnutrition, obesity, anaemia, diabetes, upper respiratory tract infection in the subject and her close associates, winter season, previous history of pelvic infection, genital tuberculosis, drug abuse and immunosuppression. Some intrapartum factors are prolonged labour with ruptured membranes, repeated per vaginum examinations, difficult instrumental delivery, emergency caesarean section, postpartum haemorrhage, manual removal of placenta, exploration for retained products of conception, unhygienic conditions at birth place and lack of aseptic precautions. Many a times the risk factors are more than one, so risk of developing severe sepsis is compounded, e.g. with diabetes and obesity requiring emergency caesarean—the risk of developing severe sepsis is more than the nondiabetic subject. Some social and demographic factors prevalent in developing countries in low-resource settings are traditional birth attendant practices, unclean domiciliary childbirth, delayed recognition of sepsis, poor accessibility to healthcare, lack of awareness and social taboos.
44.9 Clinical Symptomatology
Clinical features reflect the severity of underlying pathology. The subject complains of low-grade fever, pain in the lower abdomen and associated uterine tenderness in endometritis. With endomyometritis, the fever may be high grade with rigors with significant tachycardia where per vaginum examination reveals subinvoluted tender uterus with foul smelling lochia. This with parametrial tenderness may represent parametritis where per vaginum examination reveals posterior fornix tenderness, induration and nodularity explaining uterosacral ligament involvement justifying abdominal and pelvic pain both. The excitation pain on cervical motion is indicative of parametritis and pelvic peritonitis. The toxic look of patient with all of the above symptoms and presence of loose stools may suggest pelvic abscess formation which on P/V and P/R examination is seen as a bulge in posterior fornix due to collection in the pouch of Douglas. The most severe presentation is in situation of surgical complications due to injury of the bowel or bladder, septicaemic shock with multiple organ failure resulting in renal and hepatic impairment and coagulation failure as terminal end disease.
44.10 Septic Shock
It is due to toxins liberated in the bloodstream leading to septicaemia. The first stage is reversible and has two phases. The initial phase is warm phase due to vasodilatation where hypotension is associated with fever 101–105 °F with rigors, tachycardia, tachypnoea and flushed skin. The patient is usually alert. Oliguria may ensue. Leucopenia exists. The latter phase is that of vasoconstriction where the patient has cold clammy skin, subnormal temperature, bradycardia, cyanosis, occasional jaundice, disseminated intravascular coagulopathy (DIC) and oliguria. Leucocytosis exists.
The second stage is irreversible due to prolonged cellular hypoxia resulting in metabolic acidosis, acute renal failure, cardiovascular failure, pulmonary oedema, adrenal failure exhibited as multiorgan dysfunction syndrome (MODS) and finally death.
This needs differentiation from amniotic fluid embolism, pulmonary embolism, adult respiratory distress syndrome and myocardial infarction.
Grade I—when sepsis is limited to the uterus only
Grade II—when it is beyond the uterus but limited to the pelvis
Grade III—when it is beyond the pelvis presenting as generalized peritonitis, endotoxic shock, acute renal failure and jaundice
44.11 Diagnosis
History of exact chronology of the events leading to sepsis is very important and all details questioned from the subject or the relatives. The type of childbirth process, settings in which it was done and also if any complication occurred for which any added intervention was performed are enquired. The information related to urinary and bowel function is recorded. The associated obstetrical complication with preexisting medical or surgical comorbidity should be considered while planning further management. If the patient has been received from outside, the referral notes should be thoroughly checked to note antibiotics given, record of any drug allergy and blood transfusions in view of existing clinical status.
Examination—Thorough general physical examination is performed and vitals are monitored. The urine output and proper bowel function are ascertained. Per abdomen as well as per vaginum examination is done to know pelvic findings related to the vagina, cervix, uterus and adnexa. Per rectum examination is done for any additional information. The derangement of clinical parameters is proportionate to the severity of sepsis and organ damage.
The additional findings of middle ear infection or sinusitis potentiating CNS involvement, rectal or vaginal pain or discharge indicating genital tract infections, upper respiratory tract infections or respiratory symptoms indicating group A streptococcus or influenza are important.
The following “red flag” signs and symptoms should be considered important for early diagnosis and assessment for underlying sepsis as per Centre for Maternal and Child Enquiries (CMACE) UK report 2011 [6]. If the woman looks anxious and sick and presents with persistent vaginal bleeding and pain in the lower abdomen in the postpartum period, sepsis should be ruled out first.
Hyperthermia >38 °C or unexplained hypothermia
Persistent tachycardia >100/min
Dyspnoea particularly a respiratory rate >20/min
Pain abdomen or chest pain
Vomiting and/or diarrhoea
Pain and tenderness in renal angle
Significant vaginal discharge/foul smelling infected lochia
Uterine tenderness
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