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Critical bleeding protocol for infants used for a catastrophic subgaleal haemorrhage

A male baby was born by emergency caesarean section at 39 weeks of gestation to a 30-year-old gravida 2, para 1 mother. The pregnancy was uncomplicated. The birth weight was 3509 g (40th percentile). Birth was complicated by obstructed labour, occiput posterior fetal position and prolonged fetal bradycardia leading to an emergency section. The fetal head was impacted and, despite the use of a fetal pillow (Safe Obstetric Systems, Essex, UK), the head was difficult to extract from the pelvis. Neither forceps nor vacuum devices were used to facilitate delivery. At birth, the baby was apnoeic, pale and bradycardic. The baby was intubated and had good chest expansion. Cardiac compressions were administered and the baby received intravenous adrenaline. Spontaneous respirations and cardiac output were established at 10 min of life. The baby was admitted to the neonatal intensive care unit for ongoing care and for therapeutic hypothermia. Truncal petechiae were noted at 20 min of age. The platelet count was 145 10/L (200–500 10/L) and Hb 175 g/dL (135–215 g/dL). Coagulation studies were abnormal with an international normalised ratio of 3.5 (critically high >6.0), prothrombin time of 45 and activated partial thromboplastin time of 133 (critically high >120). In response, the baby was administered 1 mg intramuscular vitamin K and 20 mL/kg of fresh frozen plasma in an effort to correct the coagulopathy prior to commencement of cooling. His neurological status and tone improved, he became agitated and required sedation. At 4 h of life, whilst applying amplitude integrated electroencephalogram electrodes, we noted a diffuse occipital swelling and bogginess over both mastoid processes and an increase in head circumference of 4 cm. Haemoglobin measured at that time was 168 g/dL and his mean arterial blood pressure was low between 22 and 28 mmHg. The baby was now pale and hypotonic. Volume resuscitation included 20 mL/kg of normal saline and 20 mL/kg of cross-matched packed red cells. Hypotension responded to dopamine and dobutamine. The plan to cool was abandoned due to ongoing bleeding and existing evidence of worsening coagulopathy in cooled infants. The head circumference continued to increase and he developed coagulopathy, disseminated intravascular coagulation (DIC) and thrombocytopenia. The coagulation studies at 7 h of life were: international normalised ratio of 3.2, activated partial thromboplastin time 76 s, prothrombin time 40.3 s, D-dimer >10 mg/L (<2 mg/L) and fibrinogen level of 1.1 g/L (2–4.3 g/L). His clotting factor analysis at that time was normal for a neonate with values between 37 and 80%. He developed severe metabolic acidosis. Over the following 24 h, the baby received a total of 230 mL/kg of blood products, including 110 mL/kg packed red blood cells, 80 mL/kg fresh frozen plasma, 30 mL/kg platelets and 20 mL/kg cryoprecipitate. He also received 4 mmol/kg sodium bicarbonate to correct metabolic acidosis. In view of ongoing bleeding and critical illness, treatment with tranexamic acid (TXA) was trialled. We commenced TXA with a 15 mg/kg loading dose, followed by 2 mg/kg/h maintenance for 12 h. The TXA dose, transfusions and intensive care management were guided by the National Blood Authority Australia critical bleeding protocol for infants and children (Fig. 1). TXA was associated with improving clinical condition, stabilisation of head circumference, a reduced amount of blood products used in the following 24 h and resolution of acidosis. He developed focal seizures and was treated with phenobarbitone and levetiracetam. Table 1 illustrates the blood results and products given over the first 24 h. On day 3 of life, a magnetic resonance imaging (MRI) assessed intracranial injury after the traumatic birth and critical illness during the early post-natal period. The MRI showed a large subgaleal haemorrhage and multiple intracranial mostly early subacute haemorrhages (parenchymal, subarachnoid, epidural, subdural and intraventricular) but no hypoxic injury. Figures 2 Key Points 1 Vacuum delivery is the main risk factor for subgaleal haemorrhage; however, there is a significant incidence of subgaleal haemorrhages in neonates without instrumental delivery. 2 The National Blood Authority Australia has published a ‘Critical bleeding protocol for infants and children’ in lieu of a massive transfusion protocol for this age group. 3 Tranexamic acid can be used in neonates with significant bleeding. It is a drug that is easy to give and potentially lifesaving. The dosing for neonates is described in this article.