A 64-year-old man is transferred to the ICU for acute onset of confusion, septic shock, acute renal failure and disseminated intravascular coagulation. He was admitted to the general medical ward 4 h prior with a soft tissue infection of the hand, noted after removing a large splinter from the area 2 days prior. Immediate surgical exploration and debridement of the deep soft tissue infection demonstrated gram-positive cocci in chains. He was placed on both clindamycin and penicillin G.
What additional therapy should be considered?
See the Answer
IV immune globulin
Case report: A 64-year-old man presents to the ED with 2 days of increasing right hand pain, fever, chills, nausea, and vomiting. While woodworking 2 days prior, he removed a large splinter from his right hand with pliers. Past medical history is significant for alcoholism.
On physical examination, temperature is 39.1°C, pulse rate is 108/min, respiratory rate is 18/min and blood pressure is 136/66 mm Hg. Neurologic, cardiopulmonary, and abdominal examinations are not revealing. The palmar aspect of the right hand is tender. Local edema, erythema, ecchymoses, and sloughing of the skin are noted.
Laboratory examination demonstrates WBC count of 22,500/μL, with 98% polymorphonuclear leukocytes, a hemoglobin of 12.6 g/dL, and a platelet count of 340,000/μL. Blood urea nitrogen, serum creatinine, and serum electrolyte levels are normal. Serum glucose level is 210 mg/dL.
Urgent surgical exploration and debridement of the wound reveals no foreign body. Gram stain of the deep tissue shows gram-positive cocci in chains. The patient is placed on both clindamycin and penicillin G and admitted to the general medical ward. Four hours after hospitalization, he develops confusion and hypotension (systolic blood pressure of 60 mm Hg). He is transferred to the ICU where IV fluid resuscitation and vasopressors are instituted. Laboratory studies now indicate acute renal failure and disseminated intravascular coagulation. Over the next 24 h, the patient develops ARDS, requiring low tidal volume mechanical ventilation support.
Discussion: The patient has streptococcal toxic shock syndrome.1 Virtually all patients become hypotensive within 4 to 8 h of presentation, but roughly half have a normal blood pressure on initial evaluation. The vast majority has findings consistent with a soft tissue infection, such as edema, and erythema, followed by bruising and sloughing of skin. Necrotizing fasciitis and myositis indicate advanced infection. Diagnosis of streptococcal toxic shock syndrome requires isolation of group A streptococcus from a normally sterile area and hypotension, plus two or more of the following: renal impairment, coagulopathy, liver injury, ARDS, erythematous macular rash, and soft tissue infection.
Early surgical exploration and debridement of deep soft tissue group A streptococcus infection is mandatory. Clindamycin is a cornerstone of treatment. Compared with lactam antibiotics, clindamycin reduces mortality, presumably due to suppression of bacterial toxin production in addition to its antibacterial properties. Penicillin G is necessary in case of clindamycin resistance, which is rare in the United States.
Although controversial, the use of IV immune globulin in streptococcal toxic shock syndrome is supported by case reports and retrospective series. A double blind, randomized controlled trial2 comparing IV immune globulin with placebo in 21 patients demonstrated a mortality rate of 10% (1 in 10) in the intervention group compared with 36% (4 of 11) in the placebo group. Although statistical significance was not reached in this study in which all patients received clindamycin and penicillin, this could be accounted for by the small sample size.
References
1. The Working Group on Severe Streptococcal Infections. Defining the group A streptococcal toxic shock syndrome: rationale and consensus definition. JAMA. 1993;269(3):390-391.Clin Infect Dis. 2003;37(3):333-340.
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