Sepsis in obese pregnant women (concise version)


Introduction

The terms “overweight” and “obesity” are defined by the World Health Organisation (WHO) as an abnormal or excessive fat accumulation that presents a risk to health. Obesity is further classified into three categories: Class 1 (BMI 30.0–34.9 kg/m 2 ), Class 2 (BMI 35–39.9 kg/m 2 ) and Class 3 or morbid obesity (BMI >40.0 kg/m 2 ). Animal, epidemiological and limited human studies have reported that obesity increases susceptibility to both bacterial and viral infections. There is increasing evidence of the increased risk of sepsis in association with obesity in pregnancy.

Obesity is now one of the most frequently occurring obstetric comorbidities with 21.3% of the UK antenatal population obese at booking. Maternal sepsis is defined by the WHO as a “life threatening condition defined as organ dysfunction resulting from infection during pregnancy, childbirth, postabortion, or postpartum period.” The most recent Mothers and Babies: Reducing Risk through Audit and Confidential Enquiries Across the UK (MBRRACE-UK) Report (November 2018) highlights that more than a third of maternal deaths occurred in women classified as obese. Obesity has been recognised as an independent risk factor for both infection and sepsis in pregnancy and this chapter will discuss the epidemiology, immunology, infection sites, management and specific intra and postpartum care of obese pregnant woman with infection.

Epidemiology of obesity and sepsis

Obesity is a global epidemic affecting both developed and developing countries. The rate of obesity worldwide has tripled since 1975 and the United Kingdom has one of the highest obesity rates in the world at 27%.

Risk factors for obesity include social deprivation, age >35 years, ethnic minorities, regional location and diabetes mellitus.

Obesity in pregnancy : 21.3% are obese at booking with one in two overweight and one in 20 having BMI >35.

The higher a woman’s booking BMI, the greater the risk of adverse perinatal outcomes, including the risk of ICU admission and death.

Table 42.1 summarises MBRRACE-UK, UK Obstetric Surveillance System (UKOSS) and Confidential Enquiry into Maternal and Child Health (CEMACH) reported findings regarding the epidemiology of sepsis in obese patients.

Table 42.1
Compilation of data regarding obesity and sepsis in pregnant women taken from CEMACH, MBRRACE-UK and UKOSS reports.
Report Findings
MBBRACE-UK (2017)
  • Sepsis remains a key theme.

  • At examination of all direct and indirect causes of death 34% of women were obese.

  • Decreasing numbers of maternal deaths from genital tract sepsis and influenza.

  • Same pattern not observed in cases of indirect sepsis (such as pneumonias).

  • In 47% of cases improvements in care that would have altered the outcomes could have been made.

CEMACH (2003–05)
  • Obesity a risk factor for maternal death.

  • 33% of those with sepsis were obese.

  • Regarding deaths of pregnant women in this report, 28% were obese (compared to a background of 16%–19%).

  • Substandard care of sepsis identified in 71% of deaths.

UKOSS (2014)
  • 365 cases of severe maternal sepsis to 757 controls.

  • Interestingly did not associate obesity with development of severe sepsis.

MBRARACE-UK (2018)
  • Decrease in deaths related to indirect sepsis and improved care for these women.

  • Worrying increase in the number dying from direct causes.

CEMACH (2006–08) Substandard care reduced only slightly to being a factor in 69% of sepsis deaths compared with the previous 71%.

Potential for improvements in care leading to better outcomes and avoidable harm is emphasised by these reports: clinical guidelines, care bundles and annually audited skills and drills sessions have been employed in the hope to improve care. Multidisciplinary care is crucial.

Immunology

Adipose tissue is known to have both endocrine, steroidogenesis and immunological function. Mechanism of dysregulation of the immune system in obesity is yet to be established but there is clear evidence that adipose tissue causes immunosuppression. Mechanisms include suppressed function of both CD4 and CD8 T cells, T cell diversity, impaired NK cells, decreased cytokine production, disrupted lymphoid tissue architecture , alterations in leucocyte coordination and function , failure to coordinate innate and adaptive immune responses , dysfunction of thymus and spleen and inhibited effectiveness of vaccines.

Table 42.2 summarises these effects,

Table 42.2
Effects and results of obesity on the immune system.
Immune system effect Result
Lower levels of NK and CD8 cells (responsible for apoptosis of infected cells—particularly viruses) Increased morbidity/mortality to viruses—seen in obese pregnant women in H1N1 influenza pandemic
Higher baseline levels of cytokines/monocytes Chronic inflammatory state—desensitising the immune system to acute infection
Increased systemic inflammation and oxidative stress Increases B cell proliferation at the expense of T cells
Change to memory T cell response Increased risk of repeat infections, even from previously exposed pathogens

Specific infections

There are numerous associated risk factors that put an obese woman at risk of an infection , including anaemia, diabetes mellitus, operative deliveries, cervical cerclage, amniocentesis, Group B streptococcus (GBS) carriage, manual removal of placenta, black or ethnic minorities, young age, multiparity, preterm birth, induction of labour, immunosuppression and ruptured membranes.

Genital tract

Signs and Symptoms : offensive, green vaginal discharge, preterm labour, foetal distress (may be a sign of chorioamnionitis and foetal infection), meconium stained liquor, premature rupture of membranes, stillbirth.

Investigations: Microbiology swab of vagina, placenta and baby for culture and sensitivities (if CS include uterine cavity swab), continuous CTG if maternal temperature >38°C once or >37.5°C twice, foetal scalp electrode good practice in obese patients, placenta to histopathology.

Management: 10 days oral erythromycin if preterm premature rupture of membranes (higher incidence in obese patients due to subclinical infection ), prophylactic antibiotics against GBS to all women in preterm labour, inform neonatal team at delivery if chorioamnionitis suspected.

Postnatal:

  • 1.

    Consider endometritis if postnatal vaginal discharge, heavy lochia and/or delayed uterus inversion are present. Commonly associated with streptococcal and Gram-negative anaerobes. Endometritis more common in obese women.

  • 2.

    Perineum should be inspected as a site of infection postnatally

Breast

Breast pain can be a symptom of: breast abscess, necrotising fasciitis and toxic shock syndrome.

Causative organisms : Staphylococcus , Streptococcus , methicillin-resistant Staphylococcus aureus (MRSA).

Hospital review if no response to first line antibiotics within 48 hours, recurrence of symptoms or signs of sepsis.

Surgical site infection

Obese women are twice as likely to develop a surgical site infection following caesarean section.

Causative organisms : polymicrobial (24%) . Staphylococcus aureus , anaerobes (23.2%), MRSA (17%), Enterobacteriaceae (13.3%), Streptococci (7.4%).

Signs and symptoms : wound exudate, swelling, high dose of opiate pain relief required.

Necrotising fasciitis signs and symptoms : no visible skin changes in deep infection, severe pain, eventual skin blistering and necrosis.

Investigations : MRI to diagnose deep soft tissue infection.

Management: swabs of exudate/infected tissue, antibiotics to cover likely causative organisms and then directed at any pathogens from swabs, surgical drainage or debridement in cases where worsening or no improvement, involvement of plastic surgeons early if necrotising fasciitis suspected.

Infection at regional anaesthesia sites is rare but should be considered. Resiting of epidural cannulas is more common in the obese patient; multiple attempts at resiting can predispose to an infection. Urgent neurology review if suspected.

Hospital acquired infections

Obesity increases susceptibility to nosocomial infections: MRSA, carbapenemase producing enteroabacteiaceae (CPE) and Clostridium difficile ( C. diff ). . See Table 42.3 .

Table 42.3
Summary of nosocomial infections.
Description/symptoms Associated with Risk factors Investigations Management
MRSA Staphylococcus aureus strains with resistance to β-lactam antibiotics
  • Mastitis

  • Cellulitis

  • Breast abscess

  • Pelvic thrombophlebitis

  • Pneumonia

  • Wound infection

  • UTI

  • Sepsis

  • Previous MRSA colonisation/infection

  • Multiparity

  • Whole genome sequencing

  • Surveillance swabs in outbreaks on wards

  • Discuss with microbiology

  • Isolation until negative proven, barrier nursing, good hand hygiene

  • Vancomycin, teicoplanin

CPE
  • Part of normal bowel flora but are highly resistant to most antibiotics.

  • Increasingly common in Europe

  • UTI

  • Intra-abdominal infections

  • Sepsis

Hospital stay abroad in last 12 months
  • Rectal swab or

  • Faecal culture

Isolation until negative result returned
C. diff Diarrhoea, Abdominal distension, abdominal pain, fever, vomiting Foetal loss, ICU admission, colectomy, septic shock, death Inflammatory bowel disease, recent/current antibiotic use, long term antibiotic therapy Stool sample
  • Oral metronidazole or vancomycin

  • Frequent hand hygiene (alcohol hand sanitisers do not eradicate C. diff spores)

  • Avoidance of unnecessary antibiotics

Urinary tract infection

Source of sepsis in just over a third of women who died of pregnancy-related sepsis in the 2013–15 triennium.

Causative organisms : Gram-negative bacteria, these may produce β-lactamases making them resistant to many antibiotics (approx. 12% of coliform infections ).

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