Prodromal Phase of Infection Associated with Hypocoagulability, Acute Phase with Hypercoagulability based on Thromboelastography and Platelet Mapping

Authors:
Aseal Liqa, Conor Dillon, Hassan Nadeem, Meredith Essandoh, Monica Patten, Robert Sawyer, Tjasa Hranjec

Body of Abstract:
Background: Infected patients are considered to be hypercoagulable.  We hypothesized that coagulopathy associated with infection would be measurable by Thromboelastography with Platelet Mapping (TEG-PM).  

Methods:  A single center, chart review identified adult, trauma patients, admitted to our Trauma Intensive Care Unit (ICU) with hospital length of stay (LOS) ≥7 days, diagnosis of anemia of critical illness and evaluation of coagulopathy via TEG-PM before (prodrome phase – prior to diagnosis) and after (acute phase – following institution of treatment) the infectious work-up, over a 12-month period. Patients on continuous reno-renal replacement and full anticoagulation were excluded.  Univariate analysis was used to evaluate change in coagulation parameters between prodromal and acute phase of infection based on paired sample testing.    

Results: A total of 20 patients underwent coagulopathy evaluation via TEG-PM in the setting of anemia of critical illness.   Patients were mostly male (65%), with mean age 43±4 years, mean length of stay of 29.1±3.3 days, all with diagnosis of infection.  Thromboprophylaxis was initiated in 80% of the patients, with mean anti-Xa 0.19±0.1; due to progressive anemia, enoxaparin was held in 20% of the patients.  TEG-PM was collected in 20 patients during the prodromal phase, mean 0±0.5 days surrounding the infectious work-up; 16 received evaluation of coagulopathy during the acute phase with mean 3.9±0.7 days surrounding the infectious work-up.  Acute phase was associated with hypercoagulable TEG parameters (Table 1).  During the prodromal phase, however, R parameter displayed significant hypocoagulability.  Platelet activity, specifically MA-AA, and fibrinogen (CFF) increased during the prodromal phase, but MA remained within normal limits.  Lysis was non-contributory. Patients received a total of 150 red blood cell (RBC) transfusions, mean 6.6±1.6 units per patient, range 1-30.  Forty percent of the patients had an identifiable bleeding source (gastrointestinal, retroperitoneal, hemoptysis) at the time of the prodromal phrase, requiring extensive diagnostic and therapeutic interventions and active resuscitation.  Three patients developed deep venous thrombosis (DVT), diagnosed 4.3±1.3 days after infectious work-up (acute phase).  

Conclusion: Acute phase of infection is associated with hypercoagulable state, as diagnosed by TEG-PM, and may lead to DVT formation.  Surprisingly, prodromal phase, when signs and symptoms of infection may be overlooked and attributed to other causes, TEG-PM shows hypocoagulability, that may lead to significant bleeding necessitating active resuscitation and transfusion.  TEG-PM may be a useful adjunct in infectious diagnosis during the prodromal phase.