Third-Trimester Thrombocytopenia With Haemolysis and Hypertension
A 32-year-old woman, G2P1, attends her 35-week antenatal visit with a two-day history of frontal headache and right upper-quadrant discomfort. Blood pressure is 152/98 mmHg on two readings. Her platelet count is 84 × 10^9/L, down from 210 × 10^9/L at 28 weeks; haemoglobin is 10.8 g/dL, MCV 88 fL, and WBC 11.2 × 10^9/L. The EDTA blood film shows 2–3 schistocytes per high-power field and no platelet clumps. Chemistry results are AST 96 U/L, ALT 88 U/L, LDH 520 U/L, haptoglobin 18 mg/dL, uric acid 7.8 mg/dL, and creatinine 0.9 mg/dL. The urine protein-to-creatinine ratio is 0.45 g/g. PT is 11.8 s, aPTT 29 s, fibrinogen 180 mg/dL (her 28-week value was 420 mg/dL), and D-dimer 3.4 µg/mL FEU. A citrate tube was drawn after the EDTA tube but has not been analysed. The obstetric team asks whether this is gestational thrombocytopenia and whether outpatient monitoring is safe.
1. How should the laboratory interpret the platelet count and film, and what must be done before excluding pseudothrombocytopenia?
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The platelet count of 84 × 10^9/L is a true drop of more than half from the 28-week value and is below the usual threshold for gestational thrombocytopenia, which is generally mild and above 70 × 10^9/L. Before accepting true thrombocytopenia, pseudothrombocytopenia must be excluded. The EDTA film shows no platelet clumps, which makes EDTA-dependent agglutination unlikely, but it does not exclude it completely. The available citrate tube should be analysed with a corrected count, because citrate dilutes plasma and the result must be adjusted for the anticoagulant volume. A manual phase-contrast count can confirm the automated count and detect large platelets or platelet satellitism. The presence of schistocytes is important: pseudothrombocytopenia does not cause red-cell fragmentation, whereas this film suggests a microangiopathic process. Therefore the working interpretation is true thrombocytopenia with microangiopathic haemolysis, not a spurious EDTA effect. The citrate result should be reported alongside the EDTA result, with a comment that the film was reviewed. The laboratory should not simply repeat the EDTA count and delay communication; the clinical picture and film already require urgent obstetric review.
2. Explain how the haemolysis, liver enzyme, and coagulation results fit together. Which diagnoses must be considered, and which is most likely?
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The combination of thrombocytopenia, schistocytes, high LDH, low haptoglobin, and raised AST and ALT points to microangiopathic haemolysis with hepatic involvement. In pregnancy this is the classic pattern of HELLP syndrome (haemolysis, elevated liver enzymes, low platelets). The fibrinogen of 180 mg/dL is particularly informative: fibrinogen normally rises in pregnancy, often to 300–600 mg/dL, so 180 mg/dL represents relative hypofibrinogenaemia and suggests consumption. The raised D-dimer supports activation of coagulation, even though PT and aPTT are still normal; normal screening clotting times do not exclude early disseminated intravascular coagulation. The differential includes pre-eclampsia with haemolysis, acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura, and other causes of disseminated intravascular coagulation such as sepsis or abruption. Acute fatty liver usually produces more profound liver failure, hypoglycaemia, and coagulopathy. Thrombotic thrombocytopenic purpura typically causes severe microangiopathy with neurological or renal features and only modest liver enzyme elevation, and ADAMTS13 would be markedly reduced. The overall pattern, hypertension, right upper-quadrant pain, and proteinuria make HELLP syndrome the most likely diagnosis.
3. What should the laboratory report and communicate now, and what additional testing would you recommend?
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The laboratory should telephone the obstetric team immediately and report the platelet count, LDH, AST, and fibrinogen as urgent abnormal results. The platelet count is falling rapidly and the film shows schistocytes; these findings should not wait for the citrate count. The citrate sample should still be analysed and a manual count performed, but the call must not be delayed. The laboratory should issue a comment describing the schistocytes and the haemolytic pattern, and should recommend urgent clinical review rather than outpatient monitoring. Additional useful tests include glucose, ammonia, renal function, coagulation profile with fibrinogen and D-dimer, and a repeat blood count and film. If the diagnosis remains uncertain or neurological or renal features dominate, ADAMTS13 testing should be discussed, but treatment for HELLP should not be delayed while waiting for it. The laboratory should document who was called, the time, the results read back, and the advice given. This is a critical-value communication with a significant risk of maternal and fetal morbidity.