Massive obstetric haemorrhage and coagulopathy — structured SAQ (15 marks)

(a) Interpretation and diagnosis (4 marks)

One mark each, maximum four. Marks for naming the abnormality AND its significance. ^[9][3]

• Massive obstetric haemorrhage with consumptive coagulopathy — disseminated intravascular coagulation secondary to major placental abruption with intrauterine fetal death. Diffuse oozing from raw surfaces and cannula sites is the clinical signature; abruption is the obstetric cause with the most severe fibrinogen consumption.^[9][5]
• Critical hypofibrinogenaemia. A Clauss fibrinogen of 1.1 g/L is far below the 2 g/L threshold at which the positive predictive value for severe postpartum haemorrhage was 100% in the Charbit cohort, and a FIBTEM A5 of 5 mm confirms it at the bedside — approximately 12 mm corresponds to a fibrinogen of 2 g/L, and the treatment threshold in the published obstetric algorithm was below 7 mm.^[3][4][5]
• A discriminating pair of viscoelastic values. FIBTEM A5 of 5 mm with an EXTEM A5 of 28 mm tells you the deficit is predominantly fibrinogen rather than platelets. This is exactly the discrimination that formulaic packs cannot make.^[4][5]
• The lethal triad is established, with hypocalcaemia. Temperature 34.8 degrees Celsius, pH 7.21 with lactate 5.8 mmol/L, and ionised calcium 0.72 mmol/L. Ionised calcium below 0.8 mmol/L is severe hypocalcaemia and is an independent, concentration-dependent predictor of mortality in massive transfusion.^[7][8]

Also creditable: thrombocytopenia at 78 times 10 to the ninth per litre with ongoing bleeding; prothrombin time at 1.8 times reference; the ISTH criteria for overt DIC being met on platelet count, prolonged prothrombin time and low fibrinogen with an expected raised fibrin-related marker; and the caution that pregnancy-normal reference ranges conceal how far she has fallen. ^[10][9]

(b) Blood product and drug management, with targets (5 marks)

One mark each, maximum five. A mark is lost for "give FFP and platelets" without a target. ^[1][6]

• Fibrinogen replacement first and immediately — cryoprecipitate or fibrinogen concentrate, dosed to raise the fibrinogen, targeting at or above 2 g/L (higher while bleeding continues) and a FIBTEM A5 above 12 mm. Abruption predictably requires higher fibrinogen doses than other causes.^[4][5][6]
• Platelets, targeting a count above 50 times 10 to the ninth per litre with ongoing bleeding, guided by a low EXTEM A5 once FIBTEM has been corrected.^[1][5]
• Fresh frozen plasma for the prolonged prothrombin time, aiming for prothrombin and activated partial thromboplastin times under 1.5 times reference — while recognising that plasma is a major driver of citrate-induced hypocalcaemia.^[1][7]
• Calcium replacement now, not later: 10 mL of 10% calcium gluconate IV (or 10 mL of 10% calcium chloride via a central line), then re-measure the ionised calcium and repeat as transfusion continues, targeting a normal value.^[7][2]
• Red cells to maintain oxygen carriage during active bleeding, and a second dose of tranexamic acid 1 g IV since bleeding is continuing more than 30 minutes after the first dose.^[14][1]

A mark is available for stating that fibrinogen must be given early: in the French population-based analysis, administration more than 3 hours after red cell transfusion began carried more than double the risk of maternal near-miss or death compared with administration before or within 30 minutes (adjusted relative risk 2.07, 95% CI 1.10–3.89). ^[11]

A mark is also available for stating that you would stop the crystalloid, and that you would activate or continue the massive haemorrhage protocol while naming the surgical decision point — products do not close a bleeding vessel. ^[1][2]

(c) Three non-product interventions and why they work (3 marks)

One mark each, maximum three. Marks require the mechanism, not just the action. ^[8][7]

• Active rewarming — warmed fluids and products through a rapid infuser, forced-air warming, raised theatre temperature. Hypothermia impairs platelet function and slows every enzymatic step of coagulation; randomised surgical trials show hypothermia causes increased bleeding rather than merely accompanying it, and a temperature below 35 degrees Celsius is associated with mortality and morbidity in trauma cohorts. Target above 36 degrees Celsius.^[8]
• Correct the acidosis by restoring perfusion, not by giving bicarbonate. Acidosis reduces coagulation factor activity and was one of the two main risk factors for severe hypocalcaemia in the massive transfusion cohort.^[7][8]
• Stop the crystalloid and get surgical or mechanical control of the bleeding source. Continued clear-fluid resuscitation produces a dilutional coagulopathy on top of the consumptive one; and no transfusion strategy corrects a bleeding vessel. Re-ask the surgical question every few minutes.^[1][5]

Also creditable: emptying the uterus of retained products, treating the underlying driver (the abruption and fetal death are the tissue-factor source), positioning and pressure, and cell salvage where set up. ^[9][1]

(d) Three complications to look for over six months (3 marks)

One mark each, maximum three. The mark requires both the complication and its presentation. ^[13][12]

• Acute kidney injury. Presents in the first days with oliguria and a rising creatinine after hypoperfusion and massive transfusion. Antepartum and postpartum haemorrhage are recognised predisposing causes of pregnancy-related acute kidney injury, with a reported incidence of about 1.0 to 2.8% in high-income countries. Monitor urine output and creatinine, and avoid further nephrotoxic insults.^[13]
• Sheehan syndrome. Postpartum ischaemic necrosis of the pituitary, enlarged in pregnancy, after severe peripartum bleeding. Presents with failure of lactation and amenorrhoea, then features of hypothyroidism and hypocortisolism, fatigue, cold intolerance and hyponatraemia. Because the symptoms are non-specific, diagnosis and treatment are typically substantially delayed — so ask about lactation and periods at every review and test the anterior pituitary if in doubt.^[12]
• Post-traumatic stress disorder and birth trauma, compounded here by stillbirth. Presents with intrusive memories, avoidance of hospitals or health care, hyperarousal and impaired bonding with future pregnancies. Requires a structured debrief, bereavement support, and a named follow-up rather than an incidental conversation.^[1][2]

Also creditable: iron deficiency anaemia needing intravenous iron; venous thromboembolism once haemostasis is secure, with daily reassessment; transfusion-related alloimmunisation affecting future pregnancies; and Asherman syndrome after intrauterine instrumentation. ^[1][2]