Description
Case Study 2: Helen is a 32-year-old P1 who was driven to your maternity unit by her partner Sam. She is semiconscious and has had a notable diuresis. She is 36/40 and has been a type 1 diabetic form the age of 12. Sam informs you that Helen has been nauseated and vomiting for two days and hasn’t checked her blood sugar since yesterday morning when it was 9.5mmols/l. Critically discuss Hope’s case with reference to the guidelines above.
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A SAMPLE CASE STUDY ON SEPSIS
Word Count 2,741
Introduction
For the purpose of this case study I will examine the clinical presentation, treatment
and outcome of a postnatal woman presenting with sepsis. Sepsis itself will be
explored alongside the pathophysiology underpinning her symptoms. The clinical
pathway undertaken to treat and manage her symptoms and prevent deterioration of
her condition will be explored. Janes* past medical and surgical history, a summary
of her labour and postnatal care are included in appendix 1.
Pregnancy is a normal physiologic process defined by the presence of the utero
placental complex. Physiologic changes associated with pregnancy may result in
strain on organ systems with limited reserve and result in deterioration of pre existing
medical conditions (Neligan and Laffey 2011). Severe illness in pregnancy is
relatively rare with the normal physiological changes often masking the early warning
signs normally seen in a deteriorating patient (PROMPT 2017). The Royal College of
Obstetricians and Gynaecologist (RCOG (2012) highlight how the symptoms of
sepsis can often be less distinctive than in the non pregnant population and not all
symptoms may be present therefore a high index of suspicion is vital. Nurses are in
the ideal position to identify sepsis early and ensure timely treatment (Casey 2016).
Nurses and midwives must be equipped with the knowledge and skills to recognise
the signs of sepsis and take swift and appropriate action to treat it without delay.
The Surviving Sepsis Campaign (SSC) was launched in 2012 and has a 7-point
agenda: building awareness of sepsis, improving diagnosis and recognition,
increasing the use of appropriate treatment, educating health care professionals,
improving post–intensive care unit care, developing guidelines of care and
implementing a performance improvement programme (Dellinger et al. 2013). The
fourth revision occurred in January 2017 providing 93 recommendations on early
management of sepsis and septic shock generated from 55 international experts
from 25 global organisations. This demonstrates the commitment to tackle and
address this global problem (DeBacker and Dorman 2017). Dellinger et al (2013)
categorise sepsis as follows; systemic inflammatory response syndrome (SIRS),
Sepsis, Severe Sepsis and septic shock.
SIRS is defined as the presence of 2 or more of the following features
•
Temperature >38c or 100bpm
•
Respiratory Rate >20 bpm
•
White Cell Count >12 or 7.7 mmol/L (in absence of diabetes)
•
Acutely altered mental status
Sepsis is defined as signs of systemic inflammation (SIRS) with proven or presumed
infection
Severe Sepsis is sepsis accompanied with life threatening organ dysfunction
Septic Shock is sepsis induced hypotension despite adequate fluid resuscitation.
(Dellinger et al. 2013)
Pathophysiology
Sepsis is an intricate process that involves interaction between the body’s
inflammatory and anti inflammatory activities. It is the body’s systemic inflammatory
response to bacterial infection (Jones 2017). Sepsis causes complex dysfunction in
the body’s inflammatory and coagulopathy pathways, leading to vasodilatation,
vessel leakage and increased metabolic demands. This increases oxygen demand
which, combined with intravascular losses, causes hypoperfusion and ischaemia at
cellular levels and organ dysfunction (Porth, 2005; Abraham and Singer 2007).
Daniels and Nutbeam (2010) identify how understanding the classification of sepsis
helps in comprehending the underlying pathophysiology, in determining the severity
of the condition and in practicing evidenced based care. Sepsis can affect every
system in the body. Early recognition of critical illness, prompt involvement of senior
clinical staff and multi-disciplinary team working remain the key factors in providing
high quality care to sick pregnant and postpartum women (MBRRACE 2016).
Sepsis – A Case Study
Jane presented feeling generally unwell and experiencing lower abdominal pain at
her Lower Segment Caesarean Section (LSCS) scar site. She appeared pale. Her
vital signs were immediately recorded on the Irish Maternity Early Warning System
(IMEWS). The IMEWS is a standardised system that provides guidance and
processes for the early detection of life threatening illness in pregnancy and up to 42
days postpartum. It was published in 2013 in response to the HIQA Galway report
(National Clinical Effectiveness Committee (NCEC) 2014a). Among pregnant women
with proven bacteraemia, introduction of IMEWS has been associated with an
improvement in the recording of vital signs, particularly respiratory rate (Maguire et
al. 2015). Vital signs are a fundamental part of identifying if someone has sepsis or
displays potential to developing illness as regular monitoring can help identify a
deteriorating patient (Lister and Dougherty 2015). As I recorded Jane’s IMEWS I was
acutely aware of the significance and underlying pathophysiology of each parameter
on the IMEWS chart. This aids comprehension in understanding why a patient’s
condition is deteriorating and in delivering treatment.
Jane’s respirations were 22 (I yellow trigger). PROMPT (2017), identify respirations
as the single most important parameter for early detection of a deteriorating woman.
Jane’s increased respiratory rate could indicate an inadequate oxygen delivery to the
tissues with the cells reducing to anaerobic metabolism increasing lactate production
resulting in tachypnoea as a compensatory measure. In sepsis as blood flow
remains deregulated due to nitric acid and lactic acid this leads to a lack of oxygen
delivery to the tissues (Casey 2017). This is reflected in 02 saturations Jane’s
recorded normal at 97%. While it was reassuring that Jane’s temperature was within
normal limits (37.1’c) this does not outrule sepsis as temperature is not a sensitive
marker of deterioration (PROMPT 2017). Hypothermia can indicate severe infection
and a fluctuating pyrexia coupled with failure to respond to antibiotics can indicate a
persistent focus of infection or abscess (PROMPT 2017). Jane was tachycardic with
a heart rate of 114bpm (I yellow trigger), often the only sign of a deteriorating patient
at any early stage and a woman presenting with tachycardia should be considered
hypovolaemic until proven otherwise (PROMPT 2017). In septic shock the volume of
fluid in the body is diverted away from the essential organs to the skin, skeletal
muscle and fat and into the tissues. This triggers arterial and venous vasodilation
with the body initially compensating by increasing heart rate (Casey 2017).
Hypotension is a late sign of deterioration as it signifies decompensation. Jane was
hypotensive with a Blood Pressure of 98/48mmhg (2 yellow triggers). Low blood
pressure and dehydration are commonly seen in patients with sepsis but generally
respond to fluid replacement (McClelland and Moxon 2014). Decreased urinary
output can indicate end organ damage. As Jane was unable to void urine coupled
with her hypotension concern was mounting (she hadn’t drank much overnight).
Jane’s AVPU indicated that she was alert and orientated. Jane scored her pain as
5/10. Pain score aids midwives in administrating analgesia. Pain can elevate blood
pressure and heart rate. Jane was complaining of lower abdominal pain, which can
be indicative of pelvic sepsis with severe lower abdominal pains indicative of
bacterial toxins on the bowel wall (PROMPT 2017). I held administrating analgesia
until review by a registrar as analgesia can mask a temperature particularly
paracetamol. Jane was also asked about her bowel movements as diarrhoea can be
an indicator for pelvic sepsis. Jane had no history of vomiting another indicator for
sepsis (PROMPT 2017). Jane’s skin was examined for signs of a rash with her skin
feeling warm yet clammy to touch.
Jane appeared haemodynamically unstable with her IMEWS scoring 4 yellow
triggers and complaining of lower abdominal pain. As per the escalation guideline the
plan is to call the obstetrician, request immediate review repeating a full set of
observation within 15 minutes or monitor continuously (NCEC 2014a). Considering
maternal sepsis Jane had 2 SIRS criteria prompting initiation of the sepsis 6 care
bundle (Appendix 2). Its goal is to prevent severe sepsis and septic shock (Dellinger
et al. 2013). A random blood glucose was then taken as part of the SIRS criteria and
was recorded as 7.4mmols. In obstetric care there are 4 levels of care depending on
a woman’s condition level 0 – level 3 (Appendix 3). Jane required level 1, a higher
level of observation. Jane was immediately moved to the labour ward located within
our maternity department for closer one to one monitoring. If it was further away
Jane would have been stabilised on the postnatal ward first. As the shift was only
starting I opted to stay with Jane and one of the labour ward midwives went to the
ward for the shift.
The management of the septic patient in the first hour is a time critical emergency
and requires a team based approach involving all relevant healthcare staff members
(NCEC 2014b). This patient was reviewed immediately by the Registrar with the
SHO called to attend. The CMM 2 was aware of Jane’s condition. Within that first
one hour prompt and efficient treatment was instigated as organ failure and mortality
are directly linked to ongoing untreated hypotension and shock (Dellinger et al.
2013). Oxygen was prescribed on the drug kardex and administered via a face mask
and reservoir bag at 15l/min titrating o2 saturations between 94-98%. In sepsis as
blood flow remains deregulated due to nitric acid and lactic acid there is a lack of
blood flow there lack of oxygen to the tissues (Casey 2017). By administrating
Oxygen I was increasing its delivery to the tissues. Patients with sepsis need highflow oxygen until there is clear evidence that no hypoperfusion exists (McClelland
and Moxon 2014).
The SHO sited 2 large grey size 16 cannula’s under aseptic technique. Bloods were
obtained first; FBC, CRP, U&E, Clotting and LFTs. The lab was phoned and
informed regarding the urgency of these bloods. Where sepsis affects the
cardiovascular system there is inadequate oxygen and tissue perfusion and
anaerobic metabolism occurs. This leads to an accumulation of serum lactic level
known as sepsis with hypofusion (Abraham and Singer 2007). A serum lactate was
also obtained within minutes via a blood gas located on the labour ward. It is
important to obtain it within the first hour and repeated to ensure resuscitation is
improving perfusion as high lactate level is indicative of inadequate end organ
perfusion. The result was 2.4mmols this is only a slight rise so provided some
reassurance. A lactate of >2mmols/L indicates severe sepsis and >4mmols/L
indicates septic shock . A raised lactate, though not specific to sepsis, provides clear
evidence of metabolic compromise and development of severe sepsis (McClelland
and Moxon 2014).
Volume resuscitation is crucial for the effective treatment of sepsis particularity in
combating hypotension improving cardiac function and in tissue perfusion
(McClelland and Moxon 2014). An initial bolus of 500 mls isotonic crystalloid
(Hartmans) was administered over 15 minutes. The SSC currently recommends
30ml/kg of crystalloids for patients with hypotension or raised lactate (>4mmol)
(Dellinger et al, 2013). Jane was continuously monitored for signs of hypovolaemia,
normovolaemia and fluid overload. A strict fluid intake and output chart was
maintained. Fluid balance is a good indicator of circulating volume and renal
function, and therefore essential for good sepsis management and the prevention of
acute kidney injury (McClelland and Moxon 2014). Aerobic and anaerobic blood
cultures were obtained by the SHO under aseptic technique prior to the
commencement of I.V. antibiotics. The healthcare assistant on duty hand delivered
these bloods to the lab as the cant be sent in the pod system.
A urinary catheter was inserted to allow for accurate measurement of urine via an
hourly urometer. Prior to inserting the size 12 urinary catheter a low vaginal swab
was obtained and after insertion a CSU was taken for microbiology testing, both
required as part of the Sepsis 6 care bundle. Initially when placed it failed to drain
any urine which was concerning however within 15 minutes it began draining well
above the recommended amount of 38mls/hr, Jane’s target urinary output. A target
urinary output > 0.5mls/kg per hour was aimed for. Kidneys require 20% cardiac
output to maintain glomerular filtration rate. This again signifies the importance of
fluid resuscitation as cardiac output improves so does renal perfusion improves.
Catheter insertion can introduce another source for infection but strict aseptic
technique was adhered to, catheter care was observed and the plan was to remove
it as soon as possible. The administration of broad spectrum antibiotics within one
hour of suspicion of sepsis with or without septic shock is recommended as for every
hour delay starting antibiotics the risk of death increases 7.6 % (Dellinger et al.
2013). Intravenous vancomycin and clindamycin were administered as a LSCS
wound site infection was suspected as it appeared quite red and hot to touch. A
LSCS wound swab was obtained. LSCS is the leading risk factor for puerpural
sepsis (Jones 2017). There are other possible causes of infection in the postpartum
period that we remained mindful of so as not to impede treatment or additional
investigations. These include retained products of conception, episiotomy and
prolonged rupture of the amniotic membranes, breast abscess, haematoma, mastitis,
urinary tract infection (NCEC 2014b; Neligan and Laffey 2011). A diagnosis of
severe sepsis was made.
Janes IMEWS was continuously repeated. Her temperature rose to 37.5 scoring 1
yellow trigger. She remained tachycardiac, tachypnoea and hypotensive for an hour
but they didn’t worsen. Her blood pressure improved first to within normal
parameters followed by an improvement in respiration and heart rate. Myself and the
registrar worked closely together with all communication within the MDT done
through use of the ISBAR (Identification, Situation, Background, Assessment and
Recommendation) tool. This tool allows for the optimisation of critical information an
essential component of patient care safety and risk management (Health Service
Executive 2014).
Her bloods returned as HB 9.0 hgb (normal 12-16) Platelets 180 (normal 150-400),
White cell count 21.0 (normal 4.00-11.00). CRP 11.0 (normal 7.0/dl for adequate 02 delivery and a raised WCC and CRP are indicative of
infection. A high platelet count coupled with arising CRP and fluctuating pyrexia can
indicate a collection of pus or infected haematoma (NCEC 2014). Jane attended for
a CT abdomen that day which was normal indicating only a small amount of free fluid
in the pelvic cavity. Her lactate had fallen to 1.4 mmols when repeated. Critically ill
women require monitoring and multi disciplinary team management (MDT) under the
leadership of one named consultant, a senior obstetrician, a microbiologist or
infectious disease clinician (RCOG 2012). Jane’s was discussed at the 0900 daily
labour ward handover to gather input from the MDT. Jane’s obstetric consultant was
present but he had been informed of Jane’s condition prior to this. It is apparent that
swift implementation of the sepsis 6 care bundle prevented Jane’s condition from
deteriorating and she stabilised within 2 hours. While the anaesthetist was available
for consultation we didn’t require his input. Antibiotic therapy should be reviewed
daily to reduce toxicity, risk of resistance and cost (Dellinger et al. 2013).
Breastfeeding can limit the use of some antimicrobials this further strengthens the
need for consultation with the microbiologist (NCEC 2014b). The microbiologist was
involved and no change was made to her antibiotic regime. No growth was shown on
her swabs. The five moment of hand hygiene were strictly adhered to by all
individuals caring for Jane.
Over the day Jane was monitored closely her observations were recorded as per the
IMEWS escalation guideline and all care was carried out as per local guidelines.
Accurate record keeping was maintained. Jane was continuously reassured with
consent obtained for any tests and procedures. Her husband had been phoned to
attend when her condition deteriorated. Her baby was brought from SCBU when
ever Jane requested. A full debriefing was provided to Jane and her husband the
following day with ample opportunities for questioning. RCOG (2014) recommends
educating all pregnancy woman about the signs and symptoms of genital tract
infection and its prevention prior to discharge. Jane’s PHN and GP we informed to
allow for follow up at discharge. Jane was transferred back to the postnatal ward
before the shift ended following removal of her catheter. An informal staff debriefing
took place with all staff involved in Jane’s care.
Conclusion
As midwives we are in a privileged position of sharing the special journey into
parenthood with a woman. This places us in an ideal position to identify a
deterioration in a woman’s condition. The introduction of the IMEWS coupled with
the SSC have been instrumental in improving outcomes for pregnant and postnatal
women. A MDT approach is pivotal in continuing to provide evidenced based care
that has the women at the centre. Continuous staff education relating to sepsis, its
recognition and treatment will continue to ensure safe, effective high quality care is
delivered to women attending our maternity departments.
*Jane not her real name
Reference List
Abraham, E. and Singer, M. (2007). Mechanisms of sepsis induced organ
dysfunction. Critical Care medicine, 35(10), pp. 2408-2616.
Casey G. (2016). Could this be sepsis? Kai Tiaki Nursing New Zealand, 22(7), pp.
20-24.
Daniels R. and Nutbeam T. (2010). The ABC of sepsis. Journal of Tropical
Paediatrics, 50(4), p. 287.
Dellinger R.P., Levy M.M., Rhodes A., Bion J. Annane, D. and Gerlach, H. (2013).
Surviving Sepsis Campaign: International guidelines for management of severe
sepsis and septic shock: 2012. Critical Care Medicine, 41 (2), pp. 580–637.
DeBacker, D. and Dorman, T. (2017). Surviving Sepsis Guidelines A Continuous
Move Toward Better Care of Patients With Sepsis [online], Available from:
https://jamanetwork.com/journals/jama/article-abstract/2598893
JAMA.
2017;317(8):807-808. doi:10.1001/jama.2017.0059 [accessed 12 November 2017].
Health Service Executive (2014). Guidelines for the Critically Ill Woman in Obstetrics
& Gynaecology, Anaesthetic and Critical Programmes Clinical Strategy &
Programmes Division. Version 1.1 Dublin: Stationary Office.
Jones J. (2017). Managing sepsis effectively with national early warning scores and
screening tools. British Journal of Community Nursing, 22 (6), pp. 278-281.
Lister S. and Dougherty L. (2015). The Royal Marsden Manual of Clinical Nursing
Procedures. 9th ed. Oxford: Wiley-Blackwell.
Maguire P.J., O’Higgins A.C., Power K.A., Daly N. McKeating A. and Turner M.J.
(2015). Maternal bacteraemia and the Irish maternity early warning system.
International Journal of Gynaecology and Obstetrics. May 129(2), pp.142-145.
McClelland H. and Moxon A. (2014). Early identification and treatment of sepsis.
Nursing Times,110 (4), pp. 14-17.
MBRRACE (2016). Marian Knight, Manisha Nair, Derek Tuffnell, Sara Kenyon, Judy
Shakespeare, Peter Brocklehurst, Jennifer J Kurinczuk (Eds.) Saving Lives,
Improving Mothers’ Care Surveillance of maternal deaths in the UK 2012–14 and
lessons learned to inform maternity care from the UK and Ireland Confidential
Enquiries into Maternal Deaths and Morbidity 2009–14 [online], Available from:
https://www.npeu.ox.ac.uk/downloads/files/mbrrace-uk/reports/MBRRACEUK%20Maternal%20Report%202016%20-%20website.pdf [Accessed 12 November
2017].
National Clinical Effectiveness Committee (NCEC)(2014a). The Irish Maternity Early
Warning System (IMEWS) National Clinical Guideline No. 4 Dublin: Department of
Health.
National Clinical Effectiveness Committee (NCEC) (2014b). Sepsis Management
National Clinical Guideline No. 6 Dublin: Department of Health.
Neligan P.J. and Laffey J.G. (2011). Clinical review: Special populations- critical
illness and pregnancy. Critical Care, 15(4), pp. 227 -237.
Royal College of Obstetricians and Gynaecologist (RCOG) (2012). Bacterial Sepsis
following Pregnancy. Green-Top Guideline No. 64b. United Kingdom: RCOG.
Porth M.C. (2005). Pathophysiology: Concepts
Philadelphia: Lippincott Williams and Wilkins.
of
Altered
Health
States.
Practical Obstetric Multi-Professional Training (PROMPT) (2017). Care of the
critically ill pregnant woman. PROMPT- CiPP Course Participant Handbook. United
Kingdom: CiPP Editorial Team.
Appendix 1
Case Study
Background
Jane a 32 year old P1 presented in established labour. She had an emergency
Lower Segment Caesarean Section (LSCS) for failure to advance. There were no
complications at the LSCS. Jane was low risk throughout her pregnancy, labour and
postnatal period.
Social History
Irish married lady living with her husband and 2 year old daughter. She was a non
smoker.
Past Medical History
Nil of note
Labour and postnatal Summary
Jane had an uncomplicated postnatal recovery. On day 4 postpartum Jane
complained of mild pain in her LSCS site. Her notes indicated it was “mildly red and
SHO was asked to review”. Her bloods had been taken day 2 post LSCS and were
normal. Owing to this no further action was taken Jane was not commenced on oral
antibiotics. Plan as per SHO was to “monitor wound”. On day 5 Jane’s wound was
documented as ‘healing well’. There was no reference to redness at the wound site
or Jane complaining of pain.
Normally women post LSCS are discharged Day 4 postpartum Jane remained in
hospital for social reasons. Her baby was under the care of SCBU for jaundice and
was receiving phototherapy. The maternity department was quiet and as she was
breastfeeding and lived an hour from the hospital she was allowed to remain as an in
patient.
On the morning of Day 6 postpartum at approximately 0700 when asked at morning
round Jane complained of pain at her LSCS scar site. On inspection her wound was
documented as ‘mild redness noted’. She identified her pain score as 2-3/10.
Analgesia was given and the SHO was phoned to review. Before the SHO had
reviewed her at 0810 during morning handover Jane rang the call bell complaining of
severe lower abdominal pain at her LSCS scar pain. She felt generally unwell.
Appendix 2
Sepsis 6 care bundle
Complete within one hour
Take 3
Give 3
Appropriate Cultures
Maintain 02 (94-98%)
FBC +/- lactate
Consider I.V. fluid bolus
Start urine output chart
I.V.antibiotics
Appendix 3
Levels of Care
Level 0 Patients whose needs can be met through normal ward care.
Level 1 Patients at risk of their condition deteriorating and needing a higher level of
observation or those recently relocated from higher levels of care.
Level 2 Patients requiring invasive monitoring/intervention that include support for a
single failing organ system (excluding advanced respiratory support).
Level 3 Patients requiring advanced respiratory support (mechanical ventilation)
alone or basic respiratory support along with support of at least one additional organ.
(HSE 2014)
A SAMPLE CASE STUDY ON POSTPARTUM
HAEMORRHAGE
Word Count: 2,749
1
Introduction
In this case study the subject I intend to explore is Postpartum haemorrhage (PPH)
and its impact on maternal wellbeing. I will examine the clinical presentation,
management, treatment, and outcome of a postnatal woman presenting with a PPH.
Obstetric haemorrhage remains one of the leading causes of maternal morbidity and
mortality worldwide. It was the second leading cause of direct maternal death in the
United Kingdom from 2013 to 2015 (Knight et al. 2017). Primary PPH is a prominent
cause of a major obstetric haemorrhage (Mavrides et al. 2016) In fact one of Ireland’s
maternity units seen an increase in the incidence of Primary PPH of 11.3% in 20082014 (Sheehan et al.2014)
The case I have chosen involves both Primary and Secondary PPH which resulted in
re-admission to hospital requiring surgical intervention and level 2 Critical Care. Due
to the complications surrounding the case and word limitations I will only discuss
Secondary PPH. The primary aim of this case study is to demonstrate an
understanding of the pathophysiology of PPH with accurate and reliable diagnostic
skills and emphasising the importance of early clinical intervention. A high proportion
of morbidity can be prevented through early recognition with adequate intervention
and proper choices of therapies (Woiski et al. 2016). The woman involved in this
case study will be known as Mary to protect her identity. Mary’s past medical and
surgical history along with a summary of her labour and delivery are included in
Appendix 1.
There are many definitions to describe PPH. Kasap et al. (2016) defines it as
bleeding of 500ml or more following a vaginal birth,1000 ml or more after a
caesarean section, classifying it as primary if occurring within 24 hours and
secondary from 24hours to 12 weeks. While Mavrides et al. (2016) further divides
primary into two categories minor 500-1000ml in the absence of adverse effects and
major more than 1000ml, but does not state a blood volume for Secondary PPH.
PRactical Obstetric Multi-Professional Training (PROMPT) defines secondary PPH
as a blood loss of 500ml or more occurring from 24 hours to 12 weeks postpartum
(Winter et al. 2017). While Carroll et al. (2016) suggests a definition for Secondary
PPH “any blood loss from the genital tract in excess of normal lochia at any time
period after 24 h post birth to 6 weeks postpartum” (Carroll et al. 2016, p10).
Although Secondary PPH may occur anytime between 24hours and 12 weeks
2
following the birth, it is most commonly between day 7 and day 14 (Chandraharan et
al. 2017)
There are many risk factors associated with PPH both antenatal and intrapartum,
though it can occur without any risk factors. Nevertheless a history of severe PPH
increases the risks by nine-fold in future pregnancies (Nyfløt et al., 2017)
Pathophysiology
In pregnancy blood volume, coagulation, and clotting factors are increased as a
normal physiological process which allows the body to compensate well in the early
stages of haemorrhage. The blood volume in pregnancy is increased by as much as
30ml/kg giving a total volume of 6-7litres at term (Winter et al. 2017). Mousa et al.
(2014) states a blood loss of up to 500ml at delivery is physiological which brings the
blood parameters to their normal non pregnant level. Yet the signs of hypovolaemic
shock can be masked because of the increased circulating volume (Mavrides et al.
2016). Hypovolaemia will lead to insufficient blood to the heart for normal function,
affecting oxygen transportation which will result in hypoperfusion of vital organs. If
not corrected hypoperfusion can cause the release of endothelial tissue factor and
activation of coagulation cascade resulting in disseminated intravascular coagulation
(Hossain et al. 2013)
Following delivery, the uterus contracts and this causes the placenta to separate
from the uterine wall, exposing blood vessels that were in contact with the placenta
surface. Haemostasis is achieved when the uterus contracts compressing the blood
vessels and by transient activation of the coagulation system (Chireau et al. 2015). If
the uterus fails to contract then PPH will occur. The most common cause of primary
PPH is atonic uterus. PROMPT defines the causes of PPH by using 4 T’s, Tone,
(uterine tone) Tissue, (retained products) Trauma (genital tract tears) and Thrombin
(coagulopathy) (Winter et al. 2017). However Secondary PPH can be caused by
retained products of conception, endometritis and subinvolution of the placenta site.
(Mavrides at al. 2016)
3
Postpartum Haemorrhage- Case Study
Mary presented on day 11 postnatal, complaining of feeling unwell and giving a
history of passing clots at home and having intermittent lower abdominal crampy
pains. She felt faint and dizzy and appeared pale and anxious. Having a low
Haemoglobin (HB) further bleeding regardless of blood volume could have an
adverse effect on her wellbeing (WHO 2012)
I immediately put Mary lying flat on the bed with her legs elevated and administered
high flow oxygen 15litres per minute via a facial oxygen mask (Winter et al. 2017).
The RCOG also recommends giving a high concentration of oxygen regardless of
maternal oxygen concentration (Mavrides et al. 2016). I checked and recorded
Mary’s vital signs on the Irish Maternity Early Warning System (Appendix 2). The
IMEWS is a bedside tool designed to give an early warning score when the vital
signs deviate from the normal parameters thus prompting early recognition and
intervention. The aim is to improve the management of a deteriorating woman, during
pregnancy and up to 42 days postnatal (HSE 2014a) I found Mary’s temperature to
be 37.0C, her Pulse 100 beats per minute (BPM) and Respirations 20, Blood
pressure 60/30 and oxygen Sp02 97%. These findings gave an early warning score
of 2 yellow and 2 pink triggers on the IMEWS chart therefore alerting a prompt
intervention and the need to continuously monitor the vital signs. Indeed changes in
respiratory rate can be an early indicator of deterioration in wellbeing (HSE 2014a). If
the Systolic blood pressure falls below 100mmHg the blood loss could be as much as
25% of the maternal blood volume (Winter et al. 2017). As a result hypotension is a
late sign of deterioration and indicates decompensation (HSE 2014a). Although
Mary’s temperature was within normal limits (36-37.4 degree centigrade) I used a
Mistral –air blanket to keep her warm. According to the Mavrides et al. (2016)
hypothermia could exacerbate acidosis.
I called for assistance requesting the appropriate obstetric staff including the
Obstetrician for an instant review. The management of PPH contains four
components which must be undertaken simultaneously, Communication,
Resuscitation, Monitoring and Investigation (HSE 2012). In order that clear concise
information was given I used the Identification-situation-background-assessmentrecommendation (ISBAR) tool. This structured communication tool was developed to
enhance communication within the team to benefit patient care management (HSE
4
2014a).However the management of a major PPH can be frightening for the woman
and her partner as the room quickly becomes crowded and numerous simultaneous
activities are taking place. Therefore it was important that Mary and her partner were
kept informed on events from the onset. (Mavrides et al. 2016)
As part of my extended role as a midwife and being aware of the need for urgent fluid
replacement, I inserted a size 16 gauge intravenous cannula in Mary’s left hand. An
Intravenous infusion (IV) of Hartmann solution which is a crystalloid solution was
commenced to help restore fluid volume so to improve cardiac output and perfusion.
PROMPT recommends an IV infusion of warmed crystalloid fluids as cold fluids can
cause cardiac arrhythmias and the fluids should be infused rapidly until the systolic
blood pressure is restored within normal limits (Winter et al. 2017). Therefore I
applied a pressure bag to aid the infusion rate. In the same way the WHO (2012)
recommends isotonic crystalloid fluids in preference to colloids fluids. According to
Mauvrides et al. (2016) the bases of resuscitation in a PPH is to restore the blood
volume and the oxygen capacity. Likewise the Mothers and Babies: Reducing Risk
through Audits and Confidential Enquiries across the UK (Knight et al. 2017) states
that the key management of Obstetric haemorrhage is to assess the blood loss and
identify the need and replace the fluids and blood products.
In the meantime the Senior House Officer (SHO) inserted a second 16 -gauge
intravenous cannula in Mary’s right arm and obtained blood samples for, Full blood
Count, coagulation screen, Urea and electrolytes, Liver function test , C-Reactive
protein and group and cross- match of 6 units. I contacted the Laboratory Specialists
to inform them, that urgent bloods for Mary were being sent and required urgent
processing. The HSE (2012) clearly state that involving the Laboratory specialists in
the early stages is crucial in the management of PPH. Mary received 2 litres of
intravenous Hartmann Solution prior to commencement of a blood transfusion (1 unit
of Red Blood Cells) It is essential to commence a blood transfusion of Red Blood Cell
as soon as possible on the basi
