Asian Journal of Transfusion Science

: 2011  |  Volume : 5  |  Issue : 2  |  Page : 188--189

Massive pulmonary embolism and cardio-pulmonary resuscitation leading to disseminated intravascular coagulation

Madiha Fyyaz, Sachin Gupta, Amitkumar Mehta 
 Department of Internal Medicine, Providence Hospital, Washington, DC, USA

Correspondence Address:
Sachin Gupta
Department of Internal Medicine, Providence Hospital, 1150 Varnum Street, NE, Washington, DC- 20017

How to cite this article:
Fyyaz M, Gupta S, Mehta A. Massive pulmonary embolism and cardio-pulmonary resuscitation leading to disseminated intravascular coagulation.Asian J Transfus Sci 2011;5:188-189

How to cite this URL:
Fyyaz M, Gupta S, Mehta A. Massive pulmonary embolism and cardio-pulmonary resuscitation leading to disseminated intravascular coagulation. Asian J Transfus Sci [serial online] 2011 [cited 2023 Apr 1 ];5:188-189
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Full Text


One of the earliest case reports citing pulmonary embolism (PE) as an inciting factor of disseminated intravascular coagulation (DIC) was published in the 1980s, followed by a few more in the next two decades. [1],[2] We report a rare association and management challenge of massive PE leading to cardio-pulmonary resuscitation (CPR) complicated by DIC. The Case is interesting because of coexisting contradictory coagulopathic states for management-PE and DIC.

An 80-year-old African American male with past medical history of hypertension, stroke and prostate cancer was brought into the Emergency Room (ER) for sudden onset of shortness of breath. He was in severe respiratory distress and tachycardic. While examining, he lost his pulse and his blood pressure dropped. He was given CPR for 10 min before he regained his vitals. He was intubated and put on ionotropic support for optimum blood pressure control.

After stabilization, lower extremity venous sonogram and computed tomography (CT) angiogram [Figure 1] of chest confirmed our diagnosis of left leg deep vein thrombosis (DVT) and massive PE. Soon after he started oozing from intravenous line sites which prompted us to do complete coagulation workup which revealed prothrombin time (PTT) of 29.7 sec and international normalized ratio (INR) of 2.73, aPTT of 45.6 sec, fibrinogen of 143 mg/dl and platelet count of 91,000/dl. He was in frank disseminated intravascular coagulopathy with DIC score of 6. After detailed discussion with the hematologist, heparin drip was initiated with close monitoring of PTT and bleeding. His condition improved dramatically. Ionotropic support was discontinued in 18 h and he was extubated on the third day of admission. He was then discharged home on oral warfarin.{Figure 1}

In a recent retrospective study by Leitner et al., PE and in particular massive PE leading to cardiac arrest and thus necessitating CPR was associated with findings suggestive of DIC. [3] The underlying mechanism postulated to be responsible for this condition may be systemic depletion of coagulation factors and platelets as a result of massive local activation of coagulation and also the spread of activated coagulation factors into the systemic circulation thus leading to DIC. [2],[4] Similar mechanisms underlie the pathogenesis of DIC in aneurysms and vascular malformations. [5]

In our case the bleeding from the vene puncture sites provided the clinical evidence of coagulopathy and the DIC score of >5 based on low platelets, low fibrinogen levels and increase in PTT and D-Dimers very well supported that overt DIC was present. Though we were not able to identify any well-defined cause for DIC the sequence of events suggests that massive PE followed by CPR was the most likely underlying cause for it.

Leitner et al., reported a 100% in-hospital mortality for these patients. [3] There are no well-defined guidelines for the management of patients having concurrent massive PE and DIC. Massive PE leading to cardiopulmonary collapse becomes an indication for thrombolytic therapy but that was not considered in this case due to underlying coagulopathy; but the institution of IV heparin in a controlled setting led to dramatic improvement and proved to be lifesaving. We need further studies to explain the exact mechanisms leading to DIC in such patients and to guide appropriate therapy.


Shibli, Mohammad, MD, Director Critical Care Units, Providence Hospital, Washington, DC.


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