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Updated: Feb 12, 2026

Demonstration of the Rat Ischemic Skin Wound Model
Published on: April 1, 2015
Wound haematoma: The first sign in a case of late postpartum HELLP syndrome
Natasha Louise Pritchard1,2, Jodi Leanne Keane1,2
1Obstetrics and Gynaecology, Monash Health, Clayton, Victoria, Australia.
HELLP syndrome, a severe manifestation of preeclampsia characterised by haemolysis, elevated liver enzymes, and thrombocytopaenia, occurs in 0.5-0.9% of pregnancies and is associated with significant maternal and fetal morbidity and mortality. We present the case of a 30 year old primigravida (RL) who developed a wound haematoma nearly 72 h after an emergency caesarean section for failure to progress, with no prior hypertension or proteinuria documented. Although RL remained completely asymptomatic, investigations for delayed bleeding revealed severe class I HELLP syndrome with a platelet count of < 50,000 μL, significant haemolysis (haptoglobin < 0.06, LDH 1585), acute renal failure (eGFR 64, creatinine 103), fulminant hepatic failure (AST 2539, ALT 3200) and significant autoanticoagulation (INR 3.2, activated prothrombin time 46, fibrinogen 3.0). Paracetamol had been administered for post-operative analgesia and a paracetamol level was in the toxic level. Multidisciplinary input was sought from anaesthetics, intensive care, toxicology, general medicine, haematology and gastroenterology, with care subsequently coordinated in an intensive care unit. Blood pressure was strictly controlled with a sodium nitroprusside infusion. In addition to supportive care, vitamin K, a N-acetyl cysteine infusion, lactulose and mechanical thromboprophylaxis were administered. Eight weeks postpartum there were no residual biochemical abnormalities, the patient was well, and had a normal blood pressure. Our case reinforces the importance of a high level of clinical suspicion for the HELLP syndrome in women, irrespective of blood pressure in the first 48 h postpartum.
HELLP syndrome, a severe manifestation of preeclampsia characterised by haemolysis, elevated liver enzymes, and thrombocytopaenia, occurs in 0.5-0.9% of pregnancies and is associated with significant maternal and fetal morbidity and mortality. We present the case of a 30 year old primigravida (RL) who developed a wound haematoma nearly 72 h after an emergency caesarean section for failure to progress, with no prior hypertension or proteinuria documented. Although RL remained completely asymptomatic, investigations for delayed bleeding revealed severe class I HELLP syndrome with a platelet count of < 50,000 μL, significant haemolysis (haptoglobin < 0.06, LDH 1585), acute renal failure (eGFR 64, creatinine 103), fulminant hepatic failure (AST 2539, ALT 3200) and significant autoanticoagulation (INR 3.2, activated prothrombin time 46, fibrinogen 3.0). Paracetamol had been administered for post-operative analgesia and a paracetamol level was in the toxic level. Multidisciplinary input was sought from anaesthetics, intensive care, toxicology, general medicine, haematology and gastroenterology, with care subsequently coordinated in an intensive care unit. Blood pressure was strictly controlled with a sodium nitroprusside infusion. In addition to supportive care, vitamin K, a N-acetyl cysteine infusion, lactulose and mechanical thromboprophylaxis were administered. Eight weeks postpartum there were no residual biochemical abnormalities, the patient was well, and had a normal blood pressure. Our case reinforces the importance of a high level of clinical suspicion for the HELLP syndrome in women, irrespective of blood pressure in the first 48 h postpartum.
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