///2012 Abstract Details
2012 Abstract Details2018-05-01T17:55:36+00:00

Emergent Cesarean Section for NRFHRT in the Setting of Maternal Fever of Unknown Origin

Abstract Number: F-56
Abstract Type: Case Report/Case Series

Christopher Sikorski M.D.1 ; Ted Yaghmour M.D.2

33 y/o G2P1 at 38 weeks with no significant PMH/PSH presented to L&D with a fever, sore throat, fetal tachycardia, reduced urine output (Cr=1.1), and low platelets (98) for fluid resuscitation and fever workup. Four hours later her baby developed profound bradycardia. She was emergently taken for C-section under general anesthesia, which was accomplished by RSI with propofol and succinylcholine, and maintained with sevoflurane and N2O. Empiric antibiotics were given. Oxytocin infusion was started after uncomplicated delivery. There was no visual evidence of chorioamnionitis. The rate of oxytocin was doubled due to uterine atony. The patient became progressively hypotensive, requiring intermittent boluses of phenylephrine. Final EBL was 1800mL, UOP was 150mL, and total IVF was 3L crystalloid and 1L colloid. At the end of surgery, 4.5mg neostigmine and 0.6mg glycopyrrolate were given for reversal. The patient regained 4/4 TOF but remained clinically weak with spontaneous but poor tidal volumes. After half an hour, an extra 1mg of neostigmine was given but did not yield any clinical improvement. Despite sustained tetanus, a poor inspiratory effort and an inability to follow commands persisted for an hour. Moreover, she remained febrile and hemodynamically tenuous. Thus, she was left intubated and transported to the ICU. There she abruptly went into pressor-dependent shock and multiorgan failure with severe ARDS, acute heart failure (EF 30% with global hypokinesis), anuric renal failure requiring CVVH, and DIC necessitating multiple blood products. Broad-spectrum antibiotics were started for presumed sepsis of unclear etiology. Serial blood, urine, stool, and respiratory cultures and viral panels were all negative. Placental pathology was consistent with maternal bacteremia. Eventually, uterine biopsy led to the diagnosis of Group A Streptococcal (GAS) Toxic Shock Syndrome. Antibiotics were appropriately adjusted. The patient was successfully extubated on POD 8, and her heart and kidney functions gradually recovered. She was discharged to a rehab institute and is doing relatively well, though she has suffered pressor-induced ischemic necrosis of her digits. (Her baby’s post-delivery course was uneventful.) This case illustrates that GAS infection should be considered in febrile parturients who present with a viral-like prodrome, as previously reported by Crum et al (Group A streptococcal toxic shock syndrome developing in the third trimester of pregnancy. Infect Dis Obstet Gynecol 2002;10:209–216). It also shows the potential for confounding factors when assessing recovery from neuromuscular blockade. Although in practice we sometimes feel confident extubating patients before they definitively follow commands and/or consistently generate appropriate tidal volumes, it is crucial to exert judgment comprehensive of the entire clinical picture. Otherwise, we may run the risk of prematurely extubating patients.

SOAP 2012