Managing Medical and Obstetric Emergencies and Trauma. Группа авторов

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СКАЧАТЬ Hepatic system Hepatic failure or abnormal transaminases Urinary system Oliguria or acute kidney injury Haematological system Thrombocytopenia or disseminated intravascular coagulation Endocrine system Adrenal dysfunction and increased insulin resistance

      Although people with sepsis may have an infection, fever is not always present. The signs and symptoms of sepsis can be non‐specific and can be missed if clinicians do not think ‘Could this be sepsis?’

      The key actions for the diagnosis and management of sepsis (Knight et al., 2014, 2017) are:

       Timely recognition

       Fast administration of antibiotics

       Quick involvement of experts – senior review is essential

7.2 Sepsis in pregnancy

       Pregnant women have increased susceptibility to some infectious diseases, e.g. Plasmodium falciparum and Listeria monoctogenes

       In advanced pregnancy there are immunological changes that decrease adaptive immunity such that increased severity of infection is seen where cell‐mediated immunity is important. Pregnant women are more severely affected by influenza virus, hepatitis E virus, herpes simplex virus and malaria parasites

       The physiological changes of pregnancy that reduce lung capacity and promote urinary stasis may promote more severe infection

The 2014 MBRRACE‐UK report highlighted a substantial number of women who died following infection with influenza and the recommendation was made for influenza vaccination in pregnancy. The 2017 MBRRACE‐UK report re‐emphasised that pregnant women with influenza were dying from a vaccine preventable disease and that the messages around vaccination and treatment of influenza needed to be embedded to prevent deaths and to prepare for a future pandemic. Staff should remain aware of the possibility of influenza infection especially during peak seasonal periods. The Covid‐19 pandemic has highlighted these messages once again.

Antepartum causes of sepsis are commonly non‐pelvic in origin. Intrapartum and postpartum sepsis is more likely to be pelvic in origin. The classification of maternal infection is given in Box 7.1.

Box 7.1 Classification of maternal infection aligned with the WHO classification of maternal death

      1 Pregnancy‐specific infections:ChorioamnionitisEndometritisLactational mastitisSite of perineal traumaSurgical site, e.g. caesarean

      2 Infections exacerbated by pregnancy, including:Urinary tract infectionInfluenzaListeriosisHepatitis EHerpes simplex virusMalaria

      3 Incidental infections, including:Lower respiratory tract infectionsAcute appendicitisAcute cholecystitisAcute pancreatitisNecrotising fasciitisTuberculosisSexually transmitted diseases

      Source: Turner MJ. Maternal sepsis is an evolving challenge. Int J Gynecol Obstet 2019: 146: 39–42. © 2019 John Wiley & Sons

7.3 Pathophysiology of sepsis

      Once an infective agent enters the body it binds to the surface of immune cells such as macrophages and monocytes and initiates the immune and coagulation cascades. This involves the release of both pro‐ and anti‐inflammatory cytokines along with pro‐coagulant mediators which activate the extrinsic coagulation pathway and inhibit fibrinolysis. Infection becomes sepsis when the balance of pro‐ and anti‐inflammatory mechanisms tips towards pro‐inflammation.

      The pro‐inflammatory cytokines cause endothelial dysfunction and leaky capillaries resulting in vasodilatation and maldistribution of fluid. Activation of the extrinsic coagulation cascade and inhibition of fibrinolysis results in the formation of thrombi in the microcirculation. These thrombi then compromise organ perfusion, resulting in impaired delivery of oxygen to tissues and organs. If unchecked, this can lead to multiorgan failure and ultimately death.

      Clinical manifestations of haemodynamic alterations

      There is a decrease in arteriolar and venous tone. This causes venous pooling of blood and a drop in vascular resistance, resulting in hypotension. In the initial stages of sepsis, there is hypotension with reduced cardiac output and low filling pressures. With fluid resuscitation, cardiac output increases, resulting in a hyperdynamic circulation, but there is not much change in blood pressure owing to a reduced vascular resistance. There is an increase in pulmonary vascular resistance, resulting in raised pulmonary arterial pressures. The changes in the vascular tone differ in different vascular beds, resulting in the maldistribution of blood volume and flow. There is evidence to suggest that the ability of tissues to extract oxygen is impaired owing to mitochondrial dysfunction. This encourages anaerobic metabolism in tissues, promoting lactic acidosis.

7.4 Microbiology

      A study of severe maternal sepsis in the UK (2011–2012) identified genital tract infection (31%) and the organisim Escherichia coli (21%) to be the most common causes, followed by group A Streptococcus, group B Streptococcus, other streptococci and Staphylococcus. Risk factors for severe sepsis were if the woman was black or of other ethnic minority, primiparous, had a pre‐existing medical problem, had a febrile illness or were taking antibiotics in the 2 weeks preceding presentation, operative vaginal delivery or caesarean. Median time between delivery and sepsis was 3 days. Multiple pregnancy and group A Streptococcus were associated with progression to septic shock. In the women with group A streptococcal infection the progression of sepsis was often rapid. For each maternal sepsis death, 50 women had life‐threatening morbidity from sepsis.

A study from Ireland (2005–2012) looking at maternal bacteraemia again found E. coli to be the predominant pathogen followed by group B Streptococcus. The source of infection was the genital tract in 61% of cases and the urinary tract in 25%; 17% of sepsis episodes occurred antenatally, 36% intrapartum and 47% postpartum. Sepsis was associated with preterm delivery and a high perinatal mortality rate. The most virulent organisms were group A streptococci associated with postpartum sepsis at term and E. coli sepsis preterm.

      Group A Streptococcus is a common skin or throat commensal, carried asymptomatically by up to 30% of the population. It is easily spread and is responsible for streptococcal sore throat, a very common childhood condition. Worldwide, however, group A Streptococcus is still the most common cause of postpartum maternal death and can kill pregnant and recently pregnant women with devastating speed. The initial presentation can be vague and non‐specific, thus delaying treatment. Primary symptoms include myalgia, fever, mild confusion, dizziness and abdominal pain.

      Transmission in pregnant women is thought to be either through the blood stream with the throat as a portal of entry, or via the perineal route with translocation from colonisation in the vagina, even in the presence of an intact membrane, as bacteria can cross this apparent barrier. Translocation from the vagina may occur from nosocomial СКАЧАТЬ