A 61-year-old male sustained a 1.75% TBSA mixed-depth flame burn to the left lower calf. He had a past medical history of chronic lower leg ulceration, due to chronic venous hypertension and recurrent deep vein thromboses, for which he took rivaroxaban. He also suffered from a depressive illness and excessive alcohol intake.
The patient attended the emergency department approximately 12 hours post-injury. On examination, the burn was assessed to be deep-dermal in depth and suitable for Nexobrid . The last dose of rivaroxaban had been taken 32 hours prior to treatment and it was felt safe to proceed with enzymatic debridement. Blood clotting times on admission were normal.
A popliteal sciatic nerve block was performed in theatre and Nexobrid  (2 grams) was applied to the burn. Approximately 30 minutes following his return to the ward, the patient suffered a peri-arrest event, with obvious haemorrhage at the site of debridement. The blood pressure (measured non-invasively) fell to 50/40 mmHg and the heart rate was 110 beats per minute (BPM). Cardiovascular stabilisation was achieved quickly, with administration of intravenous fluids, 2 units of packed red cells and TXA (1 gram). The Nexobrid  was completely removed, the limb was elevated and calcium alginate and a compressive crepe dressing were applied. Estimated blood loss was up to two litres. No bleeding point could be determined at the time of emergency management.
Following initial stabilisation, the patient suffered a second major haemorrhage from the site and a cardiac arrest occurred, which was corrected following two cycles of cardiopulmonary resuscitation (CPR) and intravenous adrenaline. Once stabilised and when it was clear that no further bleeding was taking place, a careful visual wound inspection was carried out. A single discrete breach of a venous varicosity within the Nexobrid -treated area was observed. The remaining vein tissue appeared normal. Ligation of the vessel was undertaken prior to transfer to intensive care for post-arrest ventilatory support and invasive monitoring. It was noted during his admission to intensive care that the patient had developed a new left-sided hemiparesis. Computed tomography (CT) scanning demonstrated a posterior cerebral artery (PCA) infarct (Figure 2).