Figure 1.3 (a) Peristomal leakage notable for dried crusted skin without surrounding erythema. (b) Peristomal cellulitis distinguished from simple leakage by the deeper erythematous skin extending from the G‐tube site. (c) Peristomal candidiasis distinguished from cellulitis by its satellite lesions.
Stomal Candidiasis
Stomal candidiasis is much less common than bacterial infections of the stoma. Patients with candidiasis should be well appearing and have typical satellite lesions around the stomal site (Figure 1.3c). Similar to other forms of candidiasis, treatment with topical antifungal agents alone (nystatin or clotrimazole) is sufficient.
Necrotizing Fasciitis
Necrotizing fasciitis of the stoma is an exceedingly rare but life‐threatening complication. The patient will have erythematous, edematous, and tender skin with bullae. The lesion will rapidly expand, and the patient will look toxic. Similar to all infections, those patients with poor wound healing, diabetes, and malnutrition are at greatest risk. Necrotizing fasciitis is a surgical emergency that requires immediate surgical evaluation, wound debridement, and intravenous antibiotic treatment.
Stomal Bleeding
Bleeding at the stomal site is one of three things: hypergranulation tissue, mucosal irritation with or without prolapse, and upper GI bleeding. Distinguishing between the three is important because, while, to the patient they may all be an emergency, the severity and treatment are dramatically different.
A granuloma is a well‐circumscribed, pearly piece of tissue adherent to the stoma (Figure 1.4a). It presents as chronic, low‐grade bleeding. Its cause is unknown, but it is thought to arise from repetitive trauma from the G‐tube rubbing against the stoma. Hypergranulation tissue is of low risk but causes significant distress among patients and caregivers. Treatment is largely topical, including 0.1% triamcinolone cream, commercially available granuloma‐reducing agents, and salt packing. These agents are not without risk; specifically, triamcinolone can cause skin thinning, systemic absorption, and may precipitate a fungal infection. Silver nitrate application, kenalog injections, electrocautery, and G‐tube site revision are used in more persistent cases.
Another cause of chronic mild stomal bleeding is mucosal irritation. This too is caused by repetitive movement of the tube within the stoma and can be quickly resolved with properly sizing the tube. In addition, gauze and tape can be used to better secure the tube in position.
Finally, acute stomal bleeding is either prolapsed stomal tissue or upper GI bleeding. Prolapsed gastric tissue has a deeper red color compared to the color of a granuloma, and it is acute not chronic (Figure 1.4b). This distinction is important because silver nitrate would injure the gastric mucosa and should not be used in the setting of gastric tissue prolapse. Prolapse can be treated with the application of salt or sugar to shrink the gastric tissue and then firm and steady pressure to direct the tissue back into the stomal site. If this is unsuccessful, general surgery should be consulted. Significant stomal site bleeding without prolapsed tissue, skin irritation, or granuloma development is upper GI bleeding, until proven otherwise, and should be evaluated by endoscopy.
Figure 1.4 (a) Granuloma notable for its pearly color and irregular shape. (b) Prolapse distinguished from granuloma by the deeper erythema and more uniform shape.
Clogged Tubing
A clogged feeding tube is one of the most common causes for enteric feeding device malfunction. Residue from medications and formula build up over time and ultimately can lead to complete occlusion of the tube lumen. Resins and bulking agents are contraindicated through any enteric feeding device as they both can lead to obstruction of the tubing. Likewise, all medications and formula administrations should be followed by a 20 ml flush to prevent blockage.
The management of a clogged feeding tube depends on the type of tubing. An NG or OG tube should simply be replaced. Likewise, a G‐tube in a well‐healed tract with no trauma should also be replaced if simple declogging measures do not remove the obstruction. Every effort should be made to release the obstruction for GJ and NJ tubes, as the placement of both of these requires fluoroscopic guidance.
Most feeding tube obstructions can be flushed with a 60 ml syringe. First, try pumping air into the tubing to break apart the clot. If that does not work, the best irrigant is warm water. Carbonated beverages and colas have been studied and are inferior. Finally, if warm water does not remove the obstruction, then a mixture of pancreatic enzymes dissolved in a bicarbonate solution can be used. The mixture is left in the feeding tubing for two to three minutes, and then flushed through with warm water. One option is to mix a pancrelipase tablet with 650 mg of bicarbonate in 10 ml of water. If neither of these treatments is successful, a contrast‐enhanced radiograph should be ordered to confirm tube placement, and alternative diagnoses such as buried bumper or G‐tube displacement should be considered.
Ulceration
Ulcerations from enteric feeding devices can be at the proximal and distal ends of the tubing. For both NG and G‐tubes, the pressure of the device against the nasal ala and abdominal wall, respectively, can lead to local superficial bleeding. Bleeding that comes directly from a tube aspirate is more indicative of GI tract bleeding. In the case of an NG tube, the tubing can irritate the lining of the esophagus and develop into esophageal ulceration. For a G‐tube, the pressure of the internal retention device against the stomach lining can form an ulcer. Superficial ulcerations can be treated with tube repositioning, but internal ulcerations require tube removal to allow for healing.
Peritonitis
Peritonitis in a patient with an enteric feeding device is caused by an improperly placed tube, until proven otherwise. In the case of NG tube placement, the tube perforates the bowel wall; and in the case of G‐tube placement, the tube can be improperly placed in the peritoneum. Patients may initially be asymptomatic but will progress to diffuse abdominal tenderness, rebound, and sepsis. All NG tubes should have radiographic confirmation of their placement. For G‐tubes, patients with immature tracts, trauma to the tract, or any difficulty placing the G‐tube should have a contrast‐enhanced radiograph to confirm tube placement. Some argue that if a patient is observed receiving a feeding without difficulty, the tube is likely properly positioned. However, patients with multiple comorbidities may not be able to show discomfort. One must have a heightened level of suspicion and err on the side of caution when confirming NG and G‐tube replacements because while complications are rare, they can be life‐threatening.
Gastric Outlet Obstruction
Gastric outlet obstruction is a significant complication, but the insightful physician will be able to identify the problem and treat it within moments. Obstruction is caused by the retention balloon blocking the pylorus either because the tube migrated to the pylorus in the case of a standard G‐tube or because the balloon is overfilled in the case of a low‐profile button. Patients will present with abdominal pain, nausea, feeding intolerance, and nonbilious emesis. A contrast‐enhanced radiographic study that shows dye filling the small intestine but sparing the stomach confirms the diagnosis (Figure 1.5). Treatment is