Complicated acute appendicitis presenting as a rapidly progressive soft tissue infection of the abdominal wall: a case report

A 58-year-old European woman with a medical history of hypertension, asthma, and depression presented to our emergency department with abdominal pain of 1 week’s duration. Over the preceding 3 days, the patient’s condition had declined rapidly with general weakness and severe escalating but rather superficial abdominal pain.

On admission, the patient complained of abdominal pain. Her temperature was 35.1°C, blood pressure was 63/46 mmHg, and heart rate was 88 beats/minute. She was not oriented to time and space. Her physical examination revealed truncal obesity (36.3 kg/m²) with an irregular patch of erythema and tenderness in the right lower quadrant, and crepitation on palpation. The skin in the area of the erythema was hypoesthesic.

Initial laboratory test results showed a C-reactive protein of 439 mg/L as well as a white blood cell count of 50 g/L with 48% neutrophils. Her serum creatinine was 239 μmol/L, sodium was 131 mmol/L, and potassium was 3.3 mmol/L. An immediate abdominal CT was performed. No venous contrast was used, owing to the patient’s increased creatinine and oliguria. CT showed extensive subcutaneous emphysema in the right and left lower quadrants with small pockets of air-fluid levels (Fig. 1). There was no intraabdominal free fluid, free air, or any sign of intraabdominal inflammation. However, a contiguity of the cecum to the abdominal wall and to the subcutaneous collection was noted.

The differential diagnosis included necrotizing fasciitis, a tumor of the appendix or the cecum with perforation into the abdominal wall, or acute perforated appendicitis. After stabilization of the patient’s septic shock with 3 L of normal saline, she was urgently taken to the operating theater. First, diagnostic laparoscopy using a midline supraumbilical open approach was performed to evaluate for a potentially intraabdominal origin of the abdominal wall infection. It revealed an ileocecal area adherent to the abdominal wall without any signs of intraabdominal infection (Fig. 2). However, after lateral mobilization of the cecum, an abscess cavity with perforation into the abdominal wall was found (Fig. 3). After horizontal incision and debridement of the subcutaneous tissue were performed, the defect in the muscular layers of the abdominal wall measured 7 × 7 cm (Fig. 4). Perforated appendicitis appeared to be the source of the infectious process. The stump of the appendix was closed by a suture ligation. At that point, an ileocolic resection with a diverted ileostomy was not considered necessary, owing to the lack of intraabdominal infection and the fact that it would have been complicated by the extensive defect and inflammation of the abdominal wall as well as by the obesity of the patient. The defect of the abdominal wall was covered using an omental patch. A dressing with Betadine (Purdue Products, Stamford, CT, USA)-soaked gauze was applied to the debrided wound from the outside.

Postoperatively, the patient was admitted to the intensive care unit in continuing septic shock with multiorgan dysfunction, including acute kidney and liver failure as well as septic encephalopathy. She remained on mechanical ventilation for 5 days. Bacteriological results from blood cultures as well as abscess and peritoneal fluids were positive for Escherichia coli. Intravenous antibiotic therapy with piperacillin/tazobactam 4.5 g three times daily was started immediately after surgery and continued for 20 days. After 24 h, a second surgical look of the abdominal wall was performed in the operating theater with additional debridement of necrotic subcutaneous tissue. Afterward, the wound was dressed with a vacuum-assisted closure (VAC) device (V.A.C.® GranuFoam^TM; Acelity, San Antonio, TX, USA) according to standard procedure in our clinic. On the sixth postoperative day (POD), the patient was taken to the operating theater for a change of the VAC dressing. Unfortunately, we discovered a leakage of feces through the abdominal defect caused by an insufficiency of the appendicular stump. This led us to decide to perform a cecal wedge resection because the cecum showed good blood circulation and no signs of infection. According to our opinion, an ileostomy was not necessary in this situation. Performing an ileostomy clearly would have been very demanding in this severely obese patient with a huge defect of the abdominal wall.

Because of the highly contaminated wound, we used a biological mesh (STRATTICE™ Reconstructive Tissue Matrix; LifeCell/Acelity, Branchburg, NJ, USA) to cover the defect with no further reconstruction of the abdominal wall. The cutaneous and subcutaneous defect was closed by an axial transposition flap (skin and subcutaneous tissue) from the right upper abdomen on POD 14.

Three days later, the wound had to be partially reopened because of necrosis of the transposition flap. Again, a wound dressing with a VAC device was applied. The dressing was changed regularly, first with the patient under general anesthesia in the operating theater, later at bedside.

The patient was transferred to the surgical ward on POD 10 and discharged on POD 42 to a rehabilitation unit in improved general condition (Fig. 5). The further changes of the VAC dressing were performed on an outpatient basis. Three months after primary admission, the skin defect was closed by mesh skin graft.

Six months after the closure of the abdominal wall defect with a biological mesh, the patient developed an incisional hernia. A retromuscular hernia repair was performed with a mesh that is manufactured from approximately equal parts of absorbable poliglecaprone 25 monofilament fiber and nonabsorbable polypropylene monofilament fiber (ULTRAPRO; Ethicon/Johnson & Johnson, Somerville, NJ, USA) because it is the standard mesh for incisional hernias in our hospital. The patient’s postoperative course was uneventful, and she fully recovered.