Multi-drug resistant Acinetobacter (MDRA) is not normally considered a pathogen for postoperative necrotizing fasciitis. Changing epidemiological factors may contribute to increased recognition of this pathogen in nosocomial infections.
Following a routine colonoscopy, a 69-year old male with hypertension and peripheral vascular disease presented to an outside hospital with pleuritic chest pain and shortness of breath following several episodes of nausea and vomiting. A Chest CT scan showed a left sided pleural effusion. A chest tube was placed, and the patient was transferred to a tertiary care hospital with a diagnosis of an esophageal perforation. Upon arrival, he was emergently taken to the OR. He underwent a bronchoscopy, left sided thoracotomy with primary repair of a distal esophageal perforation with intercostal muscle flap, and a pericardial window. Postoperatively, the patient was intubated, maintained on vasopressors, and given broad-spectrum antibiotics. Within the next 16 hrs, the patient developed severe sepsis, manifested by renal failure and worsening hemodynamics. He developed multisystem organ failure. His serum creatinine kinase (CK) levels increased to 3,924, (baseline 259). Over the next 10 days, the BUN gradually increased to 99 (baseline 21), and his creatinine increased to 4.9. CK levels progressively increased and peaked at 143,000 (Fig. 1). He developed right lower extremity compartment syndrome, requiring bedside fasciotomies and right above knee amputation. Following the amputation, he developed frank cellulitis of his right stump, buttock and flank. At this point, the family decided against any more aggressive treatment. The patient died on POD11. The muscle biopsy showed multi-drug resistant Acinetobacter Calcoaceticus-Baumanii complex, with intermediate sensitivity to Amikacin, Imipenem, Colistin, and Tobramycin. The only other positive culture was a sputum culture growing the same organism on POD8.
Necrotizing fasciitis (NF) is a rapidly progressive infection of the subcutaneous tissues that leads to destruction of fascia and fat, characterized by fascial necrosis with thrombosis of the subcutaneous blood vessels, leading to cutaneous gangrene. Type I NF is a polymicrobial process, often seen in the postoperative setting and associated with gas formation. Type II NF is usually due to infection with group A beta-hemolytic streptococci and occasionally in conjunction with Staph Aureus. Other reported organisms implicated in the pathogenesis include pseudomonas, Clostridia, Streptococcus pneumoniae, serratia, aeromonas, and vibrio. Acinetobacter is a free-living gram-negative bacterium, commonly found in water and soil. It is an inhabitant of the human skin. Acinetobacter baumannii is resistant to all available antibacterials except sublactum1. It has been identified as a difficult to eradicate nosocomial pathogen with a potential to cause opportunistic infections, leading to fatal disease in intensive care units. In the world’s literature, there are only three cases reporting soft tissue infections caused by multi-drug resistant Acinetobacter1. Acinetobacter baumanni has been found to be an increasingly important cause of nosocomial infections, particularly in ICUs during the period between 1963-2003. This species has intrinsic resistance to certain antimicrobial agents, has acquired resistance, and has been reported to cause blood stream infections in patients at military medical facilities treating service members injured in Afganistan, Iraq, and Kuwait1. Since MDRA poses therapeutic difficulties, spread of infection could be very hazardous.
Acinetobacter is an opportunistic pathogen in patients with severe co-morbidities. Although uncommon as a skin pathogen, acinetobacter may become a menacing agent in patients with necrotizing fasciitis. Given the potential of this multi-drug resistant organism to cause deadly outbreaks, the appropriately compromised host in the infectious cauldron of an ICU provides the setting for the perfect storm.
Namrata Patil, None.