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A7051 - PEA Arrest Due to Massive Pulmonary Embolism (PE) with Ensuing Consumptive Coagulopathy: Human Physiology Gone Wrong!
Author Block: R. Mocerino1, T. M. McGarry2, V. Kaul3; 1Internal Medicine, Elmhurst Hospital Center, Queens, NY, United States, 2Elmhurst Hosp Ctr, Elmhurst, NY, United States, 3Pulmonary and Critical Care Medicine, Mount Sinai School of Medicine / Elmhurst Hospital Center, Elmhurst, NY, United States.
INTRODUCTION: We present a case of a young female who developed consumptive coagulopathy after undergoing PEA arrest from a massive PE s/p tPA. A review of literature discovers an evolving association that has yet to be fully explored or explained.
CASE: Our patient is a 42-year-old female with no significant history who was noted to be profoundly short of breath on exertion by the family. She was intubated in the field by EMS. In the ED, the tube was checked via DL since patient was hypoxic. She developed bradycardia to 30s ending in PEA arrest. Peri-code echo showed ballooning of right ventricle and hence the patient received tPA. ROSC was achieved after 3 minutes and patient’s ICU course was complicated by hematoma of the left upper extremity and scalp. Initial ultrasound of lower extremities was negative for a thrombus. CTA was delayed due instability and was negative after 12 hours. Platelet count trended down from 140 K/mcL on admission to 7 K/mcL on hospital day 6, fibrinogen 69 mg/dL, LDH 564 U/L, D dimer 13070 ng/mL. Patient required daily platelet transfusions with concerns for DICs. Patient was noted to have swelling of right lower extremity on day 12 and ultrasound was positive for DVT. An IVC filter was placed. On hospital day 14 patient became hypoxemic and a V/Q scan showed multiple perfusion defects with follow up CTA significant for PE in right main pulmonary artery. On Hospital day 15, the patient was found to have positive heparin induced platelet antibody and serotonin releasing assay confirming the diagnosis of HIT. The patient was placed on argatroban drip and transitioned to warfarin for discharge.
DISCUSSION: The above patient presented many challenges. We feel the initial CT scan was negative since it was delayed by more than 3 hours. Another interesting feature was the persistence of a DIC-like syndrome after resuscitation. The association of PE with ensueing DIC-like syndrome was first described in a case report from 1987 in the Journal of Critical Care Medicine. Interestingly a retrospective review article found that massive PE leading to CPR is often associated with laboratory findings suggesting overt DIC. They also found high DIC scores predict in-hospital and 1-year mortality in patients with massive PE-induced clot coagulopathy. Hence we should be aware of potential pitfalls in diagnosis as well as coagulopathic downstream effects of massive PE.