67. A 33-year-old woman with shoulder pain
Session: Posters in the Park: Posters in the Park
Wednesday, October 3, 2018: 5:30 PM
Room: N Hall D Opening Reception and Posters in the Park Area
Posters
  • IDweek case.pdf (2.7 MB)
  • Brief history of the Present Illness:

    A 33-year-old female presented to the Emergency Department with right shoulder pain that began suddenly two days prior to admission and was associated with edema, erythema and weakness due to pain. She presented to an urgent care center and was prescribed clindamycin capsules but didn’t notice improvement. She had no fever or chills. She moved to Texas 6 weeks ago. She swam in the Gulf of Mexico 3 weeks prior to presentation. No oyster consumption. There was no history of trauma, injury, or insect bite. Last intravenous drug use was over a year ago. No new creams or medications.

    Past Medical History including allergies:

    Bipolar schizophrenia.

    Polysubstance abuse: heavy alcohol intake, cocaine and prior injection heroin.

    Hepatitis C infection.

    Key Medications:

    Quetiapine 100 mg tablet PO daily

    Epidemiological history:

    Smoker, 1 pack/day. Cocaine use. Alcohol abuse. She moved to Texas from Florida 6 weeks ago.

    Physical Examination:

    Physical examination revealed an afebrile female in acute distress due to pain. The blood pressure was 141/78 mm Hg, pulse 90 beats per minute, temperature 99.1 F, oxygen saturation 99%, and respirations 17 per minute. She had significant edema of her right shoulder extending to her right hand and right chest wall. On the lateral aspect of her right arm there was one bulla with clear fluid surrounded by ecchymosis (figure 1). The skin was indurated and exquisitely tender to palpation without crepitus. No axillary lymphadenopathy, or obvious skin wound was appreciable. Radial pulse was palpable.

    Studies:

    Laboratory findings were significant for white blood cell count of 21.08 x 109/L (4.22-10.33 x 109/L), 15.98 x 109/L absolute neutrophil count (1.98-6.59 x 109/), hemoglobin 14 g/d (13.2-16.9 g/dL), platelets 246 x 109/L (160-383 x 109/L), bicarbonate 23 mmol/L (22-31 mEq/L), creatinine 0.67 mg/dL (0.51-0.95 mg/dL), AST 152 Units/L (10-35 Units/L), ALT 153 Units/L (10-35 Units/L), alkaline phosphatase 82 Units/L (35-104 Units/L), total bilirubin 0.6 mg/dL (0.2-1.3 mg/dL), albumin 2.7 g/dL (3.5-5.2 g/dL), lactate 1.1 mmol/L (0.5-2.2 mmol/L), HIV was nonreactive, Hepatitis C antibody was reactive, C-reactive protein 13.2 mg/dL (0.0-0.5 mg/dL), sedimentation rate 11 mm/hr (0-15 mm/hr), creatinine kinase was 14592 Units/L (26-192 Units/L). A right shoulder MRI revealed diffuse soft tissue edema with patchy enhancement involving the muscles of the right lateral chest wall, shoulder, arm, and forearm (figure 2).

    Differential Diagnosis:

    1. Vibrio vulnificus
    2. Aeromonas hydrophila
    3. Group A Streptococcus
    4. Clostridium spp.

    Diagnostic Procedure(s) and Result(s):

    The patient developed an extensive necrotizing fasciitis of the right upper extremity and chest requiring emergent fasciotomy and extensive tissue debridement (figure 3).

    Anaerobic culture from the debrided tissue grew Clostridium sordellii.

    Treatment/Follow-up:

    She completed 14 days course of Piperacillin/Tazobactam and Vancomycin; and 7 days of Clindamycin. She had a prolonged hospitalization requiring multiple right upper extremity and chest debridements, right mastectomy and eventually underwent skin grafting.

    Brief Discussion of Differential/Major Teaching points of case:

    Clostridium sordellii is an anaerobic, gram-positive, spore-forming bacillus commonly found in soil and animal intestines. Infections due to Clostridium sordellii, caused by toxigenic strains, are rare and often fatal. Lethal and hemorrhagic toxins are responsible for local necrosis with increased vascular permeability (1). Aldape et alsummarized 43 reported cases of Clostridium sordellii infection from 1927 to 2006 (2). Common clinical scenarios in this case series included myonecrosis in injection drug users, endometritis in women undergoing medical abortions with mifepristone or normal childbirth, none of which were present in our patient. The signs and symptoms in our case are similar to those in previously described cases, characterized by an afebrile infection that can underestimate the underlying rapid progression to septic shock, a leukemoid reaction and increased hematocrit. As in other cases, the initial imaging study revealed diffuse tissue edema without gas formation. Emergent surgery is critical for source control, removal of necrotic tissue (which reduces toxin accumulation), and for diagnosis, by obtaining tissue specimens. Antibiotics are mainly used as adjunctive therapy for suppression of toxin synthesis for which clindamycin has been the most used and studied. Prognosis is poor and the overall mortality rate has been documented as high as 69%(2).

    Final Diagnosis:

    Clostridium sordellii necrotizing fasciitis

    References:

    1. Carter GP, Awad MM, Hao Y, Thelen T, Bergin IL, Howarth PM, Seemann T, Rood JI, Aronoff DM, Lyras D. TcsL is an essential virulence factor in Clostridium sordellii ATCC 9714. Infect Immun. 2011 Mar;79(3):1025-32. PMID: 21199912

    2. Aldape MJ, Bryant AE, Stevens DL. Clostridium sordellii infection: epidemiology, clinical findings, and current perspectives on diagnosis and treatment. Clin Infect Dis. 2006;43(11):1436-46. PMID: 17083018

    IMAGES:

    Figure #, location of image, type of image, legend

    1. Right arm.
    2. MRI right upper extremity. Diffuse soft tissue edema. Patchy enhancement involving the muscles of the right lateral wall, shoulder, arm and forearm.
    3. Right chest and upper extremity after surgical debridement.

    Figure 1 is the most representative image of the case

    Alfredo Puing Vera, MD, Department of Internal Medicine, Division of Infectious Diseases, University of Texas Southwestern Medical Center, Dallas, TX and Ank E Nijhawan, MD, MPH, MSCS, Department of Internal Medicine, Division of Infectious Diseases and Geographic Medicine, UT Southwestern Medical Center, Dallas, TX

    Disclosures:

    A. Puing Vera, None

    A. E. Nijhawan, None

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