Brodifacoum contamination of synthetic cannabinoid causing unexplained coagulopathy in multiple trauma: A case report

Abstract

An 18-year-old female presented to the emergency department after a motor vehicle collision. Initial imaging revealed a liver laceration. Subsequent labs showed significantly elevated prothrombin time, international normalized ratio, and activated partial thromboplastin time. Thromboelastography demonstrated a flatline tracing. The patient denied use of anticoagulation but admitted to synthetic cannabinoid use. It was believed the patient had taken synthetic cannabinoid contaminated by brodifacoum. She was therefore given prothrombin complex concentrate and vitamin K with blood products. The patient underwent sequential embolization, laparotomy, thoracotomy, and repair of the vena cava with a shunt. Thirty minutes postoperatively, her coagulation tests and thromboelastography were much improved. Two and a half hours postoperatively, it was determined she had sustained non-survivable injuries. The patient experienced brain death due to prolonged hypotension as a result of hemorrhagic shock with bleeding exacerbated by brodifacoum. To our knowledge, this is the first case reported of a trauma-induced coagulopathy exacerbated by brodifacoum-contaminated synthetic cannabinoid. Her coagulopathy was clearly not due to trauma alone and contributed greatly to the difficulty in controlling hemorrhage. The synthetic cannabinoid-associated coagulopathy rendered her otherwise potentially survivable injuries fatal. Given the frequency of multiple trauma and the recent increase in the prevalence of synthetic cannabinoid, it can be expected that the incidence of trauma complicated by synthetic cannabinoid-associated coagulopathy will increase in the near future. For patients that present with prolonged prothrombin time and/or activated partial thromboplastin time, it is important to inquire about recent synthetic cannabinoid use.

Keywords: Brodifacoum; Coagulopathy; Multiple trauma; Synthetic cannabinoids; Thromboelastography; Traffic accidents.

Fig. 1

Transverse (A) and coronal (B) views of the patient's liver laceration pre-embolization demonstrating hemoperitoneum.

Fig. 2

(A) Pre-resuscitation kaolin thromboelastography tracing is flatline. (B) Kaolin thromboelastography post operation reveals a much-improved tracing after administration of prothrombin complex concentrate, vitamin K, and fresh frozen plasma. (C) Thromboelastography functional fibrinogen post operation reveals a normal functional fibrinogen maximum amplitude.

Fig. 3

In a 1:1 mixing study, if the aPTT or PT prolongation corrects, the patient has a factor deficiency. If the prolongation does not correct, the patient has a factor inhibitor issue.