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724 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E
Preventing complications salvage and in practice, there has been no confirmed case
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Strategies to prevent the following complications should of AFE following use of cell salvage infusion. Regard-
be implemented: less, it is common practice to use a different suction
device from the time of amniotic membrane rupture until
l Complications of major blood transfusion: these are after delivery (which is not re-used) with blood aspirated
similar in the obstetric patient as the non-obstetric from the surgical field collected by the cell salvage
patient and include: acid–base disturbance, trans- device. A leukocyte depletion filter should always be
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fusion related acute lung injury (TRALI), hypocal- used during the re-infusion of salvaged maternal blood
caemia, hyperkalaemia and hypothermia. Standard to filter any remaining foreign proteins. None of the
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monitoring and treatment of these complications currently available cell saver equipment is able to discern
should be used. fetal from adult red blood cells and any present fetal cells
l Increased risk of thrombosis: particularly in the early are transfused to the woman. It is important for Rhesus-
postpartum period as the risk is exacerbated by lengthy negative women to have a post-infusion Kleihauer-Betke
theatre procedures, bed rest associated with ICU test to quantify the amount of fetal red cells in the
admission and following major haemorrhage with an maternal circulation to ensure that an adequate dose of
associated massive blood transfusion. Suitable throm- anti-D immunoglobulin can be given to prevent
boprophylaxis should be considered as soon as fea- isoimmunisation.
sible and thromboembolic stockings and/or sequential
compression devices should be applied.
l Acute renal failure: irreversible renal failure has been AMNIOTIC FLUID EMBOLISM
reported as a sequela of acute renal failure following Amniotic fluid embolism (AFE) is a rare and incom-
severe postpartum haemorrhage. Routine monitor- pletely understood obstetric emergency that usually
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ing and management of renal impairment is required, occurs during labour or pregnancy termination, or shortly
keeping in mind that a pregnant patient has a lower after delivery. Traditional understanding of the condition
urea and creatinine level than non-pregnant patients. was based around the notion that amniotic fluid entered
Careful titration of fluid for renal purposes is needed the maternal blood stream via the endocervical veins or
due to the increased propensity for pulmonary placental bed, with amniotic fluid, fetal cells, hair, or
oedema. other fetal debris functioning as an embolus, and result-
l Rh isoimmunisation: the potential to develop Rh ing in the dramatic cardiorespiratory collapse seen with
isoimmunisation in Rh-negative women who have the condition. However, not all women diagnosed with
experienced antepartum haemorrhage should be con- AFE have evidence of fetal squames/amniotic fluid sub-
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sidered. A Kleihauer-Betke test should be done to stances in the pulmonary vasculature and many women
quantify the amount of fetal cells in the maternal who do not develop AFE have fetal cells found in the
circulation and determine the dose of anti-D immu- maternal circulation. 112
noglobulin required.
l Sheehan’s syndrome: necrosis of the pituitary gland is More recently, improved understanding of the mechanics
a very rare complication of severe obstetric haemor- of labour and the interaction of amniotic fluid and mater-
rhage. The anterior lobe is most often affected due to nal blood, as well as the striking similarities between
physiological changes that occur during pregnancy. clinical and haemodynamic findings in AFE and both
Whilst the syndrome may go undetected for many anaphylaxis and septic shock, have led to a belief that a
years, one of the earliest symptoms is a failure to common pathophysiological mechanism is likely to be
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establish lactation, due to the absence of prolactin responsible for all these conditions. As AFE resembles
secretion. Sheehan’s syndrome can be prevented by an anaphylactic reaction to fetal material rather than an
maintaining adequate circulating volume, oxygen- embolic event, the term ‘anaphylactoid syndrome of
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ation and perfusion. pregnancy’, instead of AFE, has been proposed. AFE has
also been likened to systemic inflammatory response syn-
drome, with the related inappropriate release of endog-
Use of Intra-operative Cell Salvage for enous inflammatory mediators. The trigger for AFE is
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Obstetric Haemorrhage not well understood, although it is thought to be a fetal
The introduction of cell salvage in obstetrics has been antigen (which may arise from amniotic fluid). It is pos-
sible that all labouring women are exposed to the fetal
delayed compared to other surgeries for two key reasons: antigen, with those affected by AFE exhibiting a rare and
the theoretical risk of amniotic fluid embolism (AFE) and abnormal maternal immune response. One of the dif-
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the risk of rhesus isoimmunisation. New technologies, ficulties blocking improved understanding of AFE is the
combined with an increasing obstetric haemorrhage rate, lack of a diagnostic test.
has seen cell salvage being introduced since the mid-
1990s, now becoming common practice. 109,110 Historical Regardless of the level of understanding, the abnormal
understanding of amniotic fluid embolism argued against mediator release gives rise to acute lung injury, resulting
the risk of infusing blood that potentially contained in acute dyspnoea and hypoxia and often the develop-
amniotic fluid. The more recent understanding that AFE ment of acute respiratory distress syndrome. Within 30
is more aligned with an anaphylactic reaction has less- minutes of the antigen insult, there is evidence of severe
ened these concerns as a woman has already been exposed pulmonary hypertension with acute right ventricular
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to the contents of the fluid that are infused following cell failure. It is thought that inflammatory mediators are a

