Abstract
Introduction: Case Report: Severe gram negative septic shock with TAMOF in pregnancy. Severe septic shock causes systemic endothelial injury that results in pro-thrombotic and anti-fibrinolytic cellular responses, which clinically manifest as thrombocytopenia, systemic thrombosis, and multi-organ failure. In critical illness, new onset thrombocytopenia associated multi-organ failure (TAMOF) precludes poor outcome. TAMOF is a spectrum of microangiopathic disorders that include disseminated intravascular coagulation (DIC). DIC is a consumptive syndrome that is described clinically as the constellation of thrombocytopenia, decreased factors V and X, decreased fibrinogen, and increased D-dimer. Clotting factor consumption paradoxically results in thrombosis due to significantly reduced levels of ADAMTS13, protein C, protein S, and antithrombin III. Plasma exchange (TPE) is a well established treatment that effectively reverses the coagulopathy of DIC and improves survival in patients with TAMOF. Maternal physiology changes significantly via the effects of progesterone and estrogen produced by the placenta. Total body water is increased secondary to renal sodium retention, resulting in plasma volume increases up to 45% and functional anemia. Peripheral vascular resistance decreases up to 20%, causing tissue edema and maternal hypotension and tachycardia. Pregnancy induces a hypercoagulable state due to increased platelet production, fibrinogen concentration, and clotting factors. Thromboembolic complications of pregnancy are associated with increased morbidity and mortality. Pregnancy induces an immunocompromised state due to the presence of a semiallogeneic fetus, and LPS endotoxin is causes a systemic proinflammatory response and preeclampsia-like symptoms. Coupling normal pregnancy physiology with the physiologic response and consequences of severe sepsis increases mortality of both mother and fetus. We present a 31yo 26 week G7P6 patient who developed severe sepsis with TAMOF secondary to gram negative bacteremia. She presented after incomplete treatment of UTI and was admitted to ICU for hemodynamic instability with fetal distress, anuria, and anasarca. On admission, patient received norepinephrine, hydrocortisone, vasopressin, and piperacillin-tazobactam. Admission procalcitonin 55ng/mL, ADAMTS13 39%, and leukocyte count 14k with 78% PMNs and 16% bands. Cultures grew Proteus mirabilis. She received 5 TPE treatments and CVVH. After TPE, platelet count trended from 6k to 114k, D-dimer trended from greater than 20µg/mL to 2.6µg/mL, prothrombin time trended from 16s to 14s, and activated partial thromboplastin time trended from 32s to 23s. She was discharged after 16day hospitalization with 12day ICU stay. She delivered a viable female infant at 30 weeks via cesarean section with Apgar scores 5 at one minute and 9 at five minutes. As there is limited clinical research on TPE in pregnancy for the treatment of TAMOF and the fetal effects of TPE, our case illustrates a mortality benefit in this population.