Necrotizing fasciitis following percutaneous endoscopic gastrostomy

Necrotizing fasciitis following percutaneous endoscopic gastrostomy

Ionic distension. Large bowel obstruction was initially suspected because of the colonic distension, but a Gastrografin enema was normal. Over the fir...

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Ionic distension. Large bowel obstruction was initially suspected because of the colonic distension, but a Gastrografin enema was normal. Over the first 24 hours of hospital admission, the volume of gastric contents drained from the gastrostomy tube exceeded 2 liters. A Gastrografin study via the gastrostomy tube demonstrated gastric outlet obstruction by the Foley balloon; withdrawing the Foley catheter approximately 15 cm so that the balloon again abutted the gastric wall resulted in a marked reduction in gastrostomy tube output. Upper gastrointestinal endoscopy the following day showed a 1.5-cm nonobstructing ulcer in the duodenal bulb. Tube feedings were immediately resumed and were well tolerated. To prevent recurrent migration, the tube was wrapped with tape in the manner described below. The patient received 6 weeks of treatment with ranitidine for his ulcer and had no further difficulties. Although gastric outlet obstruction due to percutaneous endoscopic gastrostomy tubes, conventional gastrostomy tubes, and gastrostomy tube substitutes such as Foley catheters has been reported, '-4 the frequency of tube migration may be underrecognized. Withdrawing the catheter so the bumper or balloon abuts against the stomach wall and retaping it to the skin of the abdominal wall temporarily corrects the problem. If the tube becomes impacted in the small bowel, more vigorous traction may be required to return it to its proper place.' In addition to obstruction, ulceration may result from pressure necrosis of duodenal mucosa as seen in this case and reported previously.' A variety of suture techniques to prevent gastrostomy tube migration have been described, but suturing may result in skin irritation or infection. The gastrostomy "button" is useful, but gastrostomy tube slippage can still occur; also replacement kits containing additional "buttons" are far more expensive than Foley catheters. Buttons for Foley catheters used as gastrostomy tubes are not currently available. We anchor gastrostomy tubes by circumferentially wrapping 20 to 30 layers of silk tape tightly around the gastrostomy tube to create a flange of approximately l-cm thickness. This flange is positioned at the skin line when a Foley catheter is used or just above the "button" when a percutaneous endoscopic gastrostomy tube is utilized. This method securely anchors the gastrostomy tube externally and prevents migration without traumatizing the skin and at negligible expense.

Necrotizing fasciitis following percutaneous endoscopic gastrostomy To the Editor: Percutaneous endoscopic gastrostomy (PEG) is a frequently performed procedure associated with few reported complications.,,2 We present a case of necrotizing fasciitis (NF) following PEG. Physician awareness of this complication is stressed, since early surgical intervention is mandatory to prevent mortality. A 71-year-old man was admitted to the hospital following an acute left pontine infarct manifested by ataxia and dysphagia. Other medical problems included hypertension and diabetes mellitus. Enteral alimentation was begun via a nasoenteric tube but 7 days later he aspirated gastric contents and required endotracheal intubation. He developed a temperature of 101°F rectally and a leukocytosis to 16,000/ mm 3 • A new left lower lobe infiltrate was noted on chest xray, and gram stain of the sputum demonstrated grampositive diplococci. Parenteral cefotaxime and gentamicin were initiated. The sputum culture subsequently grew Streptococcus pneumonia. On hospital day 11, a PEG tube was placed under local anesthesia at the bedside without difficulty. Water was administered by tube for the first 24 hours, after which dilute commercial feedings were begun. He was extubated on hospital day 13. The following day his temperature reached 104°F and he required reintubation due to aspiration of tube feedings. His antibiotics were changed to amikacin and ampicillin. He became obtunded thereafter with persistent fever to 101°F. On hospital day 16 a small area of erythema and induration was noted on the left flank 10 cm from the PEG site. A percutaneous aspirate of this area grew no organisms and an ultrasound failed to demonstrate an abscess. The presumptive diagnosis of cellulitis was made and vancomycin was added to his antibiotic regimen. The patient remained febrile and the area of flank erythema increased in size, but no crepitus was present. On hospital day 20 a CT scan demonstrated a collection of fluid and gas within the abdominal wall extending from the PEG

Jonathan B. Schreiber, MD Pamela L. Garjian, MD Division of Gastroenterology Department of Medicine University of Maryland School of Medicine Baltimore. Maryland

REFERENCES 1. Fisher LS, Bonello JC, Greenberg E. Gastrostomy tube migration and gastric outlet obstruction following percutaneous endoscopic gastrostomy. Gastrointest Endosc 1987;33:381-2. 2. Connar RG, Sealy WC. Gastrostomy and its complications. Ann Surg 1956;143:245-50. 3. Haws EB, Sieber WK, Kiesewetter WB. Complications of tube gastrostomy in infants and children. Ann Surg 1966;164:28490. 4. Holder TM, Leape LL, Ashcraft KW. Gastrostomy: its use and dangers in pediatric patients. N Engl J Med 1972;286:1345-7.

VOLUME 34. NO.6, 1988

Figure 1. CT scan obtained 20 days after PEG showing fluid and gas in tissue planes (black arrow) adjacent to the PEG site (white arrow). 487

ensues. Roentgenographic studies may be helpful if positive;,10 but the diagnosis is made on clinical grounds and requires a high index of suspicion. Treatment consists of prompt, aggressive surgical debridement of all devitalized tissue combined with broad spectrum antibiotics. Hyperbaric oxygen has been used as an adjunct by some authors with gratifying results,14 although its use is still controversial.]1i Despite improved surgical techniques and anitmicrobial therapy, the mean mortality rate in reported series remains 38%,6 being in excess of 70% even in some recent reports.? The most important factors influencing survival are early diagnosis and surgical debridement. David W. Haas, P. Dharmaraja, John G. Morrison, John R. Potts III,

Figure 2. Initial incisions marking the extent of surgical debridement. An area of skin necrosis overlying the central focus of necrotizing activity is noted in the midst of the skin bridge.

site into the left flank (Fig. 1). Surgical consultation was obtained, and the patient was taken to the operating room where exploration revealed extensive necrosis of the subcutaneous tissue, including an area of abdominal wall fascia. The PEG tube had not become displaced and there was no evidence of intraperitoneal sepsis. The tube was removed, extensive debridement was performed (Fig. 2), and the wound was packed open. Cultures of the necrotic material grew Escherichia coli and Staphylococcus epidermidis. Postoperatively he was treated with penicillin G, gentamycin, and clindamycin. After a period of local wound care he underwent a split-thickness skin graft to the wound. With gradual improvement he was transferred out of the surgical intensive care unit on hospital day 43 and subsequently discharged to home. Complications following PEG are uncommon and relatively minor, tending to be infectious in nature. Three patients who developed NF following PEG have recently been described, two of whom died. 3 - 1i Necrotizing fasciitis is a rare, rapidly progressive bacterial infection characterized by necrosis of subcutaneous tissue and fascia, usually accompanied by severe systemic toxicity. Myonecrosis is rare. The perineum, extremities, and abdominal wall are the most common sites of involvement.6-8 NF may follow traumatic or surgical wounds, particularly after emergency laparotomy.9 These infections frequently occur in compromised hosts, and mortality is greatly increased in such patients. 5 ,6,9 Risk factors include diabetes mellitus, atherosclerosis, alcoholism, malnutrition, immunosuppression, and old age. 6,7,10 Microbiologic findings are variable,6,7,Il,12 but hemolytic streptococcal species, Staphylococcus aureus, and Enterobacteriaceae are frequently present. A combination of facultative aerobic and anaerobic bacteria is often isolated, and a synergistic action between these two had been postulated to explain the often fulminant course of the disease. 13 The clinical presentation and physical findings of NF are often nonspecific, and this contributes to the delays in diagnosis and treatment which are frequently reported. Early symptoms consist of fever, malaise, and the development of edema, pain, and erythema of the skin at the involved site. A rapid deterioration in the clinical status 488

MD MD MD MD

Nashvffle, Tennessee REFERENCES 1. Ponsky JL, Gauderer MWL, Stellato T A. Percutaneous endoscopic gastrostomy. Review of 150 cases. Arch Surg 1983;118:913-4. 2. Russell TR, Brotman M, Norris F. Percutaneous gastrostomy. A new simplified and cost-effective technique. Am J Surg 1984;148:132-5. 3. Grief JM, Ragland JJ, Ochsner MG, Riding R. Fatal necrotizing fasciitis complicating percutaneous endoscopic gastrostomy. Gastrointest Endosc 1986;32:292-3. 4. Cave DR, Robinson WR, Brotschi EA. Necrotizing fasciitis following percutaneous endoscopic gastrostomy. Gastrointest Endosc 1986;32:294-6. 5. Person JL, Brower RA. Necrotizing fasciitis/myositis following percutaneous endoscopic gastrostomy. Gastrointest Endosc 1986;32:309. 6. Janevicius RV, Hann SE, Batt MD. Necrotizing fasciitis. Surg Gynecol Obstet 1982;154:97-102. 7. Rouse TM, Malangoni MA, Schulte WJ. Necrotizing fasciitis: a preventable disaster. Surgery 1982;92:765-71. 8. Rea WJ, Wyrick WJ. Necrotizing fasciitis. Ann Surg 1970;172:957-64. 9. Casali RE, Tucker WE, Petrino RA, Westbrook KC, Read RC. Postoperative necrotizing fasciitis of the abdominal wall. Am J Surg 1980;140:787-90. 10. Fisher JR, Conway MJ, Takeshita RT, Sandoval MR. Necrotizing fasciitis. Importance of roentgenographic studies for soft tissue gas. JAMA 1979;241:803-6. 11. Pessa ME, Howard RJ. Necrotizing fasciitis. Surg Gynecol Obstet 1985;161:357-61. 12. Giuliano A, Lewis F Jr, Hadley K, Blaisdell FW. Bacteriology of necrotizing fasciitis. Am J Surg 1977;134:52-7. 13. Roberts DS. Synergic mechanisms in certain mixed infections. J Infect Dis 1969;120:720-6. 14. Gozal D, Ziser A, Shupak A, Areial A, Melamed Y. Necrotizing fasciitis. Arch Surg 1986;121:233-5. 15. Kaiser RE, Cerra FB. Progressive necrotizing surgical infections-a unified approach. J Trauma 1981;21:349-55.

Chloroquine phosphate-induced gastroduodenitis To the Editor: Chloroquine phosphate is a widely used drug for the treatment of malaria. Abdominal pain, nausea, and vomiting are common after administration of chloroquine phosphate. We describe endoscopically detectable mucosal changes in GASTROINTESTINAL ENDOSCOPY