High Dependency Midwifery Care – A Case Study
Rachel was a primigravida, with a body mass index (BMI) of 40 and anaemic, she had a spontaneous vaginal delivery with a second-degree tear with no other complications and was discharged home the following day. Rachel was two days postnatal and readmitted from home with abnormal vital signs: pyrexia of 40.5 degrees centigrade, heart rate of 130-140 per minute, tachyapnoea and feeling generally unwell. She was transferred to the obstetric observation bay on delivery suite and received one to one care for suspected sepsis. On admission the midwife and senior house officer were unable to cannulate and therefore unable to give intravenous antibiotics promptly. The shift was extremely busy and consequently there was a delay in administering antibiotics. A diagnosis of sepsis was later confirmed via laboratory investigations. Sepsis is a complex condition therefore I will be focusing upon the importance of timing when treating sepsis. As sepsis is a time critical illness I have chosen to analyze this specific case. Pseudonyms have been used to maintain confidentiality (Nursing and Midwifery Council, NMC, 2015).
Sepsis is a life-threatening condition in which organ dysfunction occurs due to a dysregulated host response to infection (United Kingdom Sepsis Trust, 2017). The definition of sepsis has changed over the years and will continue to develop with further research. However, having a definition is essential to ensure effective communication between healthcare professionals, determining the severity of the illness and developing standardized evidenced based treatment (United Kingdom Sepsis Trust, 2017). Additionally, the need to have a lay definition that uses accessible language to describe and educate the public regarding sepsis. This is particularly important as a study found that 80% of incidents in the UK originated in the community and that patients delayed accessing healthcare (National Confidential Enquiry into Patient Outcome and Death, 2015).
Maternal mortality from sepsis is estimated to be 1.8 per 100,000 live births in the UK with severe morbidity being estimated to be 50 times this (Acosta et al, 2014). An increase in the incidence of genital tract sepsis led to sepsis being the leading cause of direct maternal deaths in the 2006-2008 triennium (Centre for Maternal and Child Enquiries, CMACE, 2011). The report identified that there were missed opportunities for early intervention in particular timelier diagnosis and prompt treatment. Issues surrounding antibiotic administration were common and this was relatable in Rachel’s case. Since the CMACE 2011 report and its recommendations for practice there has been a reduction in maternal mortality. This can be attributed to the implementation of policies such as the “Sepsis 6” bundle as well as raised awareness of the risks of sepsis.
Multiple risk factors for maternal sepsis have been identified such as diabetes, impaired immunity, prolonged rupture of membranes, urinary tract infection and women who required invasive procedures such as caesarean section or removal of retained products of conception (National Institute for Health and Care Excellence, NICE, 2017). Another recognized risk factor is the acquisition or carriage of the organism group A streptococcal (GAS). GAS with genital tract trauma was directly responsible for 13 of the 29 maternal deaths from sepsis in the UK from 2006-2008 (CMACE, 2011). Rachel had three known risk factors for sepsis; obesity, anaemia and perineal trauma therefore these will be explored in more depth.
Obesity causes a chronic low-grade inflammatory state. This is characterized by increased cytokine production by adipocytes and macrophages infiltrating the adipose tissue, elevated acute phase reactants and activation of inflammatory signaling pathways (Desruisseaux et al, 2007). These alterations in obese patients compromise the natural adaptive response to infection. Obesity also provides challenges with skin hygiene and can consequently cause skin breakdown. Skin is the largest organ and plays a vital role with the immune system protecting patients from infection. Therefore, destruction of the epidermis or dermis can leave the wound susceptible to infection (Dean, 2011). Additionally, obesity may cause patients to have physical difficulties which inhibit activities of daily living such as bathing and toileting therefore potentially causing poor personal hygiene.
Iron is a fundamental component of the immune system therefore anaemia has been linked to impaired immune response and increased susceptibility to infection. In particular anaemia is associated with compromised cell mediated immunity, reduced neutrophil function, impaired natural killer cell activity and reduced T-lymphocyte cells (Kumar and Choudhry, 2010). There is evidence, in vitro, that decreased lymphocytes diminish the production of cytokines which are essential for a specific response to infection as they are key to several immunological steps (Hassan et al, 2016).
Perineal trauma is a risk factor for infection and subsequently sepsis as one in ten who sustained a perineal tear that required suturing developed a wound infection (Johnson, Thakar and Sultan, 2012). This can be attributed to the fact that perineal trauma is situated in a warm and moist area that is potentially contaminated due to being near the vagina, anus and urethra.
Sepsis is a complex illness that arises when an abnormal response to infection occurs and triggers organ dysfunction. It can be caused by a variety of pathogens such as bacteria, virus or fungus. Sepsis is characterized by inflammation and is a collection of physiological responses to infection which involves the immune system and coagulation cascade. Inflammation is the body’s normal response to infection however in sepsis the initial physiological responses become disordered. Receptors in the endothelium detect pathogens and the immune response of inflammation is initiated. The first step is vasodilation to ensure neutrophils, monocytes, macrophages, platelets and fibrin are mobilized to the affected site. Marked capillary permeability also occurs to ensure that pathogens are not isolated within the blood vessels. Additionally so that cytokines and white blood cells are able to enter the interstitial tissues and form a targeted response. Cytokines also known as “mediator molecules” are released to amplify the immune response and have both pro-inflammatory and anti-inflammatory actions. However these initial responses are facilitated by molecules which are interrelated therefore the ability to regulate the process can become disturbed consequently resulting in sepsis.
A cellular component of the immune response to neutralize the pathogens is also required. Leukocytes are essential to this process and are mobilized to the affected site by cytokines. A variety of different types with differing roles exist such as neutrophils which contain enzymes to attack the pathogen, monocytes which engulf the pathogen and B cells which produce antibodies which then bind to and destruct pathogens.
Sepsis can be regarded as an excessively pro- inflammatory response resulting in widespread microvascular and cellular injury. These injuries are characterized by endothelial damage, redistribution of blood flow, intravascular pooling and oedema. These injuries are typical of sepsis and play a significant role in the multi-organ dysfunction. Sepsis is a time critical illness as it results in a disruption of the supply of oxygen and nutrients to the tissues and vital organs resulting in acidosis, multi-organ failure and potentially death. Acute kidney injury can occur and is common in sepsis due to the reduced cardiac output which in turn reduces renal blood flow.
Pregnancy causes several physiological adaptations to occur therefore potentially masking common early physiological signs and symptoms of sepsis. For instance tachycardia may be masked by the increased basal heart rate in pregnancy which is due to increased blood volume and cardiac output. Sepsis also presents as vasodilation resulting in a state of relative hypovolaemia however in pregnancy vasodilation already occurs due to the raised level of progesterone or use of epidural analgesia in labour and hypovolaemia may be present as a result of a postpartum haemorrhage.
Tachypnoea is often the first sign a septic patient is deteriorating as it is the body’s mechanism of trying to meet the oxygen demand of the organs and tissues. This occurs as fluid and proteins leak into the interstitial tissues in the lungs causing swelling and reduced oxygen and carbon dioxide transfer across the alveoli. Also tachypnoea may be a compensatory mechanism for a metabolic acidosis to try and increase the oxygen supply to tissues and blow off carbon dioxide. Therefore oxygen saturations may be low.
Blood pressure and heart rate will be affected due to the circulatory response of vasodilation and increased capillary permeability. As a consequence of vasodilation relative hypovolaemia occurs this is further compounded by capillary leakage which causes the circulatory blood volume to decrease. The direct effect of this is a drop in blood pressure. Blood pressure is determined by cardiac output (CO) and the systemic vascular resistance (SVR). In sepsis the SVR known as the “tone” of blood vessels drops also causing the blood pressure to fall. Cardiac output may also decrease as sepsis can cause the diastole to be affected and not fill sufficiently consequently reducing the blood flow to organs. Organs require a good blood flow and pressure to function effectively this accompanied by the hypoxia of sepsis significantly contributes to organ failure.
In response to low blood pressure a compensatory tachycardia arises. This is activated by baroreceptors which detect the fall in blood pressure and trigger the sympathetic nervous system to increase the heart rate.
Either a pyrexia above 38 degrees centigrade or hypothermia below 36 degrees centigrade may be a sign of sepsis. Pyrogens, typically produced by bacteria, disturb the functioning of the hypothalamus, the part of the brain responsible for regulating body temperature. This occurs as pyrogens bind to and inhibit heat sensing neurons subsequently causing the body temperature to increase. Recent evidence indicates that high temperatures might be a protective mechanism to sepsis. With explanations such as high temperatures stimulate the activity and multiplication of white blood cells and augment the production of antibodies as well as impeding the growth of certain bacteria and viruses.
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