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Journal of Obstrectic Anaesthesia and Critical Care
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 Table of Contents  
CASE REPORT
Year : 2018  |  Volume : 8  |  Issue : 2  |  Page : 115-117

Amniotic fluid embolus in the absence of disseminated intravascular coagulation and respiratory failure: A diagnostic challenge


Department of Anaesthesia and Intensive Care, Royal United Hospital, Bath, UK

Date of Web Publication3-Oct-2018

Correspondence Address:
Dr. Fiona C Oglesby
Department of Anaesthesia, Royal United Hospital, Combe Park, Bath, Avon, BA1 3NG
UK
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/joacc.JOACC_33_18

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  Abstract 


Amniotic fluid embolism (AFE) is a potentially catastrophic complication unique to pregnancy, characterised by its poorly understood pathophysiology and diverse clinical manifestations. We present the case of a 37-year-old G1P1 mother, who developed sudden cardiovascular collapse in the immediate post-partum period. We detail the diagnostic uncertainty surrounding the condition and use this case to illustrate the clinical spectrum of AFE presentation.

Keywords: Amniotic, amniotic fluid embolism, embolus, maternal collapse


How to cite this article:
Oglesby FC, Cook SC, Kelly FE, Marsh C. Amniotic fluid embolus in the absence of disseminated intravascular coagulation and respiratory failure: A diagnostic challenge. J Obstet Anaesth Crit Care 2018;8:115-7

How to cite this URL:
Oglesby FC, Cook SC, Kelly FE, Marsh C. Amniotic fluid embolus in the absence of disseminated intravascular coagulation and respiratory failure: A diagnostic challenge. J Obstet Anaesth Crit Care [serial online] 2018 [cited 2018 Dec 16];8:115-7. Available from: http://www.joacc.com/text.asp?2018/8/2/115/242625




  Introduction Top


There are numerous cases of suspected amniotic fluid embolism (AFE) reported in the literature, despite it being an uncommon condition with a reported incidence of 1:8000 to 1:80000.[1],[2] These describe the diagnostic triad of respiratory distress, coagulopathy and haemodynamic instability, with particular emphasis on the former two.[3] We report a case of AFE with isolated cardiovascular collapse, the first such report to our knowledge, in the hope that others may consider a diagnosis of AFE in cases of maternal collapse without all three of the classical features.


  Case Report Top


A 37-year-old (G1P1) presented to the birthing centre in established labour at 40+5 weeks' gestation. She had a history of well-controlled hypothyroidism, and her pregnancy had been uncomplicated. She gave birth to a healthy baby with ventouse assistance. A second-degree tear, with an associated 400 ml estimated blood loss, required transfer to theatre for repair. Of note, the obstetrician observed a significant volume of liquor and a high-pressure expulsion of amniotic fluid at the time of delivery.

A low-dose spinal block with 1.7 ml of 0.5% Hyperbaric-bupivacaine solution and 300 mcg of Diamorphine was administered at L3/4 interspace without complication. This provided a bilateral sensory block to T10, which was well tolerated. Intravenous fluids and a phenylephrine infusion (100 mcg/ml at 15 ml/h) were commenced to assist haemodynamic stability.

Towards the end of the procedure the patient described feeling 'light-headed'. This coincided with profound hypotension (63/37 mmHg), sinus tachycardia (>140 bpm) and a drop in GCS to 13/15 (E3V4M6). Phenylephrine, ephedrine and metaraminol boluses were administered with minimal effect and an early decision was made to insert a femoral arterial line to monitor invasive arterial blood pressure and a central venous cannula.

The level of the block was re-evaluated with no rise since initial testing. The obstetrician reported no bleeding and an abdominal ultrasound demonstrated no evidence of concealed haemorrhage. Initial arterial blood gases revealed a profound, partially compensated, metabolic acidosis: pH 7.3, PaO241.0 (on 15L of oxygen via a non-rebreathe mask), Pa CO22.26, Base Excess-14.9, cHCO3-9 and lactate 9.5. A haemoglobin drop from 105 g/dL to 65g/dL (Haemocue) and 89.4 g/dL (subsequent laboratory result) prompted a two-unit blood transfusion in the absence of an alternate clear cause for the rapid deterioration. The patient reported central chest tightness, but examination was unremarkable and an ECG showed sinus tachycardia with no evidence of ischaemia. Once central venous access was achieved, a high dose noradrenaline infusion was started and cardiovascular stability achieved. Blood results demonstrated an acute kidney injury with creatinine of 113 mcmol/L and hyperkalaemia (6.5 mEq/L). Calcium gluconate and insulin/dextrose infusions were started.

Differential diagnoses that were considered included concealed haemorrhage, AFE, pulmonary embolus (PE), septic shock, anaphylaxis, aortic dissection, Addisonian crisis, and coronary artery dissection. Intravenous antibiotics and hydrocortisone were given, and a contrast CT (chest/abdomen/pelvis) and CT angiogram were performed, both of which were unremarkable. A bedside echocardiogram with limited views did not demonstrate any major abnormalities.

On admission to Critical Care, the patient remained self-ventilating but still required moderate vasopressor support overnight. The following morning, she was also noted to have complete paralysis of both legs, with brisk reflexes, the presence of clonus and up-going plantars bilaterally. There was no sensory involvement. MRI head and spine 12 h post-event was unremarkable, with no evidence of spinal cord ischaemia or compression. Neurology review provided no further explanation for features that gradually improved. The patient steadily improved from a cardiovascular perspective over the 12 h following admission, with reducing noradrenaline requirements and resolution of the metabolic acidosis. Troponin-T was elevated (80 ng/ml initially; 284 ng/ml at 24 h). A cardiology review ruled out a primary cardiac aetiology following a formal transthoracic study at 36 h, which showed no persistent right heart strain or left ventricular impairment. Serial mast-cell tryptases were insignificant (2.3 ng/ml, 2.6 ng/ml and 1.9 ng/ml at 0, 4 and 12 h) and endocrine investigations were unremarkable. No source of sepsis was identified, and the baby was well. Coagulation profiles were normal at all stages. The patient was discharged to the Maternity Unit on Day 2, and by Day 3 was mobilising with a frame. She was discharged home on Day 11 with a full neurological recovery.


  Discussion Top


The reported mortality from AFE is 13–48% with 85% of patients experiencing permanent neurological impairment.[1],[4] The exact pathogenesis of AFE is unclear but is likely to be an immune response to amniotic fluid, foetal cells or other debris within the maternal circulation.

Classifications of AFE emphasise respiratory distress, cardiac failure or coagulopathy as predominate symptoms and signs. Criteria for submission to national databases consistently include respiratory distress and coagulopathy.[5],[6] The majority of cases present in labour or during caesarean section with only 11% occurring during vaginal delivery.[1] Presentation is similar to septic or anaphylactic shock, both of which must be ruled out when considering a diagnosis.[3]

This case was characterised by profound, resistant hypotension in the absence of cardiac abnormalities. Potential risk factors for AFE relevant to our patient include age (>35 years), instrumental delivery and polyhydramnios.[7]

Post-partum haemorrhage (PPH), with compromise exacerbated by spinal anaesthesia, is common. However, the estimated blood loss was only 400 ml, there was no improvement with intravenous fluids and a sensory level of T10 following spinal anaesthesia suggested that PPH alone was insufficient to explain the profound cardiovascular collapse. AFE, aortic dissection, PE, anaphylaxis or sepsis were all considered: mast-cell tryptases were not consistent with anaphylaxis; there was no evidence of infection pre-delivery, no growth in blood cultures and no neonatal sepsis making maternal sepsis unlikely; CT imaging, serial ECGs and echocardiograms ruled out other cardiorespiratory causes, with raised troponins thought to reflect profound hypotension and secondary myocardial injury; an endocrine-related event (Addisonian crisis) was considered, but cortisol levels were normal and the patient improved without continuing steroid supplementation making this very unlikely as a cause.

AFE is a diagnosis of exclusion in surviving individuals. Having thoroughly explored the alternative causes, we are confident this was a case of AFE. We propose that this supports the notion that AFE is a diverse clinical entity and should be considered in all cases of sudden and severe maternal cardiovascular collapse with or without additional features.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Dedhia J, Mushambi M. Amniotic fluid embolism. Contin Educ Anaesth Crit Care Pain 2007;7:152-6.  Back to cited text no. 1
    
2.
Davies S. Amniotic fluid embolus: A review of the literature. Can J Anaesth 2001;48:88-98.  Back to cited text no. 2
    
3.
Clark SL. Amniotic fluid embolism. Obstet Gynecol 2014;123:337-48.  Back to cited text no. 3
    
4.
Frati P, Foldes-Papp Z, Zaami S, Busardo FP. Amniotic fluid embolism: What level of scientific evidence can be drawn? A systematic review. Curr Pharm Biotechnol 2014;14:1157-62.  Back to cited text no. 4
    
5.
Tuffnell DJ. United Kingdom amniotic fluid embolism register. BJOG 2005;112:1625-9.  Back to cited text no. 5
    
6.
UK Obstetric Surveillance System: Amniotic Fluid Embolism. National Perinatal Epidemiology Unit, Nuffield Department of Population Health, Oxford University. Available from: https://www.npeu.ox.ac.uk/ukoss/current-surveillance/amf. [Last updated on 2015 Mar 31; Last accessed on 2018 May 24].  Back to cited text no. 6
    
7.
Sadera G, Vasudevan B. Amniotic fluid embolism. J Obstet Anaesth Crit Care 2015;5:3-8.  Back to cited text no. 7
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