Chest 10/2014; 146(4_MeetingAbstracts):931A. DOI:10.1378/chest.1994664 · 7.13 Impact Factor
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ABSTRACT: Infectious Disease Cases ISESSION TYPE: Affiliate Case Report SlidePRESENTED ON: Sunday, October 27, 2013 at 07:30 AM - 08:30 AMINTRODUCTION: Necrotizing fasciitis is characterized by fulminant soft-tissue destruction, systemic toxicity, and high mortality. Infections are classically caused by beta-hemolytic Streptococcal species or anaerobic organisms. Group C Streptococcal species are endogenous to humans and domestic animals but are infrequently reported to cause infections in humans. To date, animal exposure has not been documented as a direct cause of systemic infection with Group C subspecies. Guinea pigs are known to be carriers of Streptococcus equi and we present a case of necrotizing fasciitis and septic shock caused by Group C Streptococcal bacteremia following guinea pig exposure.CASE PRESENTATION: A 44 year old Caucasian male with a past medical history significant for asthma presented to an urgent care center with headache, myalgias, and bilateral thigh pain. Rapid flu swab was negative and he was sent home with a prescription for Tamiflu. Two days later he presents to the emergency department with extensive erythema and swelling of bilateral lower extremities. Crepitus and blistering were observed in bilateral thighs and he was taken promptly for fasciotomies and debridement. He then went on to develop septic shock requiring vasopressor support and blood cultures were positive on two successive days for Streptococcus equi. Despite appropriate antibiotic therapy he developed progressive lower extremity and abdominal wall necrosis requiring further surgical debridement. Subsequent questioning revealed that our patient had received two guinea pigs from a pet store in addition to two others he already owned one week prior to the onset of symptoms. Cultures of all four guinea pigs performed by the CDC were positive for Streptococcus equi.DISCUSSION: This case illustrates a rapidly progressive, necrotizing soft tissue infection caused by a Group C Streptococcal species directly related to guinea pig exposure. Previous case reports have not shown a link to animal exposure or the severity of symptoms observed in this previously health patient. Early diagnosis and aggressive surgical debridement along with hemodynamic support and broad antibiotic coverage remain the mainstays of treatment. Despite prompt initiation of treatment the mortality remains as high as 34%.CONCLUSIONS: Necrotozing fasciitis and septic shock are not well-documented complications of Group C Stretococcal infection. Our case illustrates direct animal to human transmission resulting in multi-system organ failure in a previously immunocompetent host. Better screening of domestic animals available for purchase as pets may be needed to prevent similar outbreaks in the future.Reference #1: Broyles LN, Van Beneden C, Beall B, et al. Population-based study of invasive disease due to beta-hemolytic streptococci or groups other than A and B. Clin Infect Dis 2009; 48:706DISCLOSURE: The following authors have nothing to disclose: Daniel Fitelson, Charles Read, Megan FlynnNo Product/Research Disclosure Information.
Chest 10/2013; 144(4_MeetingAbstracts):195A. DOI:10.1378/chest.1704391 · 7.13 Impact Factor
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ABSTRACT: Atypical Presentations in the ICUSESSION TYPE: Affiliate Case Report SlidePRESENTED ON: Wednesday, October 30, 2013 at 11:30 AM - 12:30 PMINTRODUCTION: Influenza is known to induce rhabdomyolysis. This is a case of a young man with influenza A complicated with severe rhabdomyolysis with the highest associated creatine kinase reported in the literature of over 4 million.CASE PRESENTATION: 30 year old male with a past medical history of asthma presented with 5 day history of progressively worsening myalgias particularly of his bilateral lower extremities, subjective fevers, productive cough, and 1 day of dark colored urine. His creatine kinase (CK) on admission was 67,997, urine toxicology screen was negative, influenza A positive for which he completed a course of ostelamivir. Over the next 48 hours he had progressive acute kidney injury (AKI) with his creatine increasing from 1.6 to 2.99 despite some initial improvement with aggressive intravenous fluids (IVF) and intravenous sodium bicarbonate. His CK peaked to 4,312,211 U/L on the second day of admission with a subsequent CK of over 1 million on day three with a myoglobin of 35,964 ng/ml. MRI of his lower extremities at this time showed diffuse muscle edema of bilateral thigh musculature without of muscle atrophy Hemodialysis (HD) was initiated for up trending CK, worsening AKI (his creatine peaking at 8.09), and progression to anuria. His 31 day hospital course was further complicated with a superimposed Streptococcus pneumoniae pneumonia, hypoxic respiratory failure requiring mechanical ventilation, and subsequent acute respiratory distress syndrome (ARDS) necessitating airway pressure release ventilation (APRV) and nitric oxide. With worsening hypoxia, his hospital course ended with a (pulseless electrical activity) PEA arrest. His CK had declined to 734 and creatine 1.98.DISCUSSION: Our patient had a complicated course of influenza A with rhabdomyolysis resulting in CKs above 4 million, which is the highest level documented in the literature to date. A CK of over 1 million was reported in an exercise induced rhabdomyolysis for which the patient was treated with IVF with resolution of his AKI without requiring HD. Review of the literature of influenza induced rhabdomyolysis revealed varying CK levels (200-500k) that did not correlate with AKI progression requiring HD. The 2009 H1N1 strain was associated with increased rates of rhabdomyolysis, and those requiring HD had higher mortality.CONCLUSIONS: Rhabdomyolysis is a relatively uncommon complication of Influenza A. The CK level itself does not predict need HD. Rhabdomyolysis induced by influenza A requiring HD itself is a poor prognostic indicator associated with an increased mortality.Reference #1: Ayala E, Kangawa F, Wener J. Rhabdomyolysis associated with 2009 influenza A (H1N1). JAMA 2009; 302(17):1863-1864.Reference #2: Berry L, Braude S. Influenza A infection with rhabdomyolysis and acute renal failure a potentially fatal complication. Postgrad Med J 1991;67:389-390.Reference #3: Casares P, Marull J. Over a million Creatine Kinase due to a heavy work-out: A case report. Cases J 2008; 1(1):173-176.DISCLOSURE: The following authors have nothing to disclose: Rupinder Kullar, Daniel Fitelson, Sharon O'BrienNo Product/Research Disclosure Information.
Chest 10/2013; 144(4_MeetingAbstracts):273A. DOI:10.1378/chest.1704774 · 7.13 Impact Factor