Topical Corticosteroid for the Treatment of Hypergranulation Tissue at the Gastrostomy Tube Insertion Site: A Case Study

Hypergranulation tissue formation around a gastrostomy tube insertion site is a common feeding tube-related complication that affects patients who receive long-term enteral nutrition. Some clinicians recommend use of a topical corticosteroid in patients with gastrostomy tube insertion site hypergranulation. However, documentation is scant regarding appropriate treatment for this condition. This case report describes a 67-year-old bedridden man with spinocerebellar degeneration who presented with hypergranulation at the site of the gastrostomy tube, inserted 1 week earlier. The tissue was raw and inflamed, with bleeding and exudation.The gastrostomy site was gently cleansed with gauze dampened with tap water, and topical 0.05% clobetasol propionate ointment was applied directly to the hypergranulation tissue twice daily. After 4 days of treatment, the hypergranulation tissue almost completely disappeared, redness markedly decreased, and bleeding and exudation ceased, with no recurrence observed during the 6 months of follow-up. This case study supports other reports that short-term corticosteroid treatment may be a safe, quick, noninvasive, and effective treatment for hypergranulation at the gastrostomy tube insertion site. Further studies are needed to evaluate the safety, effectiveness, appropriate dosage, and duration of topical corticosteroid for the treatment of hypergranulation tissue. 

Hypergranulation tissue, an excess of granulation tissue, can develop around gastrostomy tubes (G-tubes) in patients receiving long-term enteral nutrition.^1-8 Various prospective and/or descriptive studies^1,2,4-7 have shown hypergranulation is a complication affecting 25% to 68% of patients who receive long-term enteral nutrition by tube feeding. Although hypergranulation is not life-threatening, it affects the quality of life both of patients and their caregivers because it can be associated with persistent bleeding, exudation, discomfort, or pain and may require hospital admittance.^2,5-8 In caring for patients, the first priority is to minimize tube friction around the gastrostomy insertion site because continual external tube friction is the fundamental cause of topical inflammation and hypergranulation development. The G-tube should be adequately anchored, with the tube flush against the inner stomach wall and a gauze pad placed between the outer flap of the device and the abdomen, if necessary, for a snug fit.⁸ Additionally, if present, dressing fibers and other potential irritants should be removed by gently cleansing every day to prevent hypergranulation.^3,8,9

Mr. V is a 67-year-old man with a 12-year medical history of spinocerebellar degeneration resulting in akinetic mutism and confinement to bed. Completely dependent on home enteral nutrition via a G-tube, he had received regular visits from a primary care physician and a dedicated nurse for 10 years. Table 1 details his medical profile. 

Mr. V was admitted to the hospital because his primary caregiver noticed hemorrhagic hypergranulation tissue around the G-tube, inserted 1 week earlier. At admission, the insertion site measured approximately 1 cm in diameter and showed effusive moist, fragile, hemorrhagic hypergranulation (see Figure 1, Day 0), appearing raw and inflamed with an accumulation of dirt and excessive exudate with bleeding. Before admission, the primary caregiver provided no specific treatment of the hypergranulation tissue except daily cleansing.

A topical corticosteroid (clobetasol propionate, the highest potency corticosteroid) was chosen for treatment in accordance with a previous dermatological case report¹³ of hypergranulation, although not around a G-tube. First, the dirt and exudate that had accumulated around the G-tube insertion site were carefully washed and removed using a gauze dampened with tap water. Next, 0.05% clobetasol propionate ointment (approximately 0.2 g) was applied directly to the hypergranulation tissue, and the site was covered with gauze. Care was taken to minimize any friction between the hypergranulation tissue and the G-tube. This procedure was performed twice daily at 10:00 a.m. and 4:00 p.m.

Every day after the procedure at 16:00, a photograph of the hypergranulation was taken for assessment of size, color, bleeding, and exudate. On day 1, the hypergranulation had receded markedly and lost some of its redness, and bleeding decreased (see Figure 1, day 1). On day 2, the hypergranulation receded further, and the bleeding ceased completely (see Figure 1, day 2). On day 4, the hypergranulation had almost completely flattened (see Figure 1, day 4), with no redness, bleeding, or exudate. Treatment was stopped at the end of day 4. Only daily care was continued; caregivers cleansed the gastrostomy insertion site using gauze dampened with tap water. Recurrence of the hypergranulation was not observed in the short term (7 days’ hospitalization) nor within 6 months’ follow-up. No adverse events occurred.

Before the present case, 2 of the authors’ patients had been given the same treatment and had successful resolution within 5 days, with no immediate recurrence. They were all bedridden elderly patients receiving long-term enteral nutrition via percutaneous endoscopic gastrostomy (PEG) in their homes. Although detailed data (PEG type, underlying disease, and the like) on these patients were unavailable and no photos of the healing process were taken, anecdotally the effect of corticosteroid treatment was consistent with that described in the current case.

Although the definitive etiology of hypergranulation developing around a G-tube has not been clarified, previous review articles^8,9,16 have indicated the primary cause is a prolonged inflammatory response stimulated by friction from the external feeding tube. Inflammation as a result of a bacterial infection is also one of the suggested causes of hypergranulation.^9,17 However, this was considered unlikely in the present case because pus was not present. Prolonged inflammation induced by various cytokines and growth factors is known to cause excessive vasodilation, angiogenesis, and capillary permeability^18-20; it can result in persistent bleeding, edema, exudation, and a raw, inflamed appearance in effusive hypergranulation tissue. 

In the present case, short-term application of a topical corticosteroid to effusive hypergranulation tissue at the G-tube insertion site resulted in a rapid reduction in redness, cessation of bleeding and exudate, and a decrease in the depth of hypergranulation tissue. These beneficial outcomes can be explained by the known actions of corticosteroids, including anti-inflammatory effects, capillary vasoconstriction, and granulation growth inhibition.^10-12 

This case study, together with the findings of previous studies,^9,13-15 suggests a topical corticosteroid may be considered a valid treatment for G-tube insertion site hypergranulation. Other reported treatments for hypergranulation, such as silver nitrate and surgical resection,^1,3,5,8 may not be appropriate because they directly damage the tissue and are likely to prolong or worsen the inflammatory response. These directly destructive or invasive methods have traditionally been used for treatment, possibly because they were believed by physicians to be beneficial, even though they could be painful. 

Three (3) main issues regarding the use of topical corticosteroids for hypergranulation at the gastrostomy insertion site require attention: 1) the strength of the corticosteroid; 2) the duration of application; and 3) the use of an occlusive dressing. Clobetasol propionate, the highest potency corticosteroid, was used, with reference to a previous dermatological case report.¹³ However, documentation is lacking regarding the relationship between the corticosteroid potency and treatment outcomes (eg, healing time, frequency of side effects) even in dermatological studies. Therefore, it is possible a corticosteroid with a weaker potency also may be effective in the treatment of hypergranulation around the G-tube. Further studies are needed to address the level of potency needed in the treatment of this condition using corticosteroids.

The duration of application is also a topic of debate. Long-term use of a high-potency corticosteroid has been known to result in numerous cutaneous side effects, including atrophy, striae, and infection.^21-23 Therefore, a standard needs to be developed for determining when the application of corticosteroid should be stopped in the treatment of hypergranulation. Based on the authors’ previous experience and the current case, it appears corticosteroid application can be stopped when the topical inflammatory response has almost dissipated. Specifically, cessation of treatment should be based on 3 signs: 1) diminished redness, 2) absence of bleeding, and 3) absence of exudate. In the present case, based on these 3 signs, corticosteroid application was stopped after 4 days of treatment. Despite the short period of treatment, no immediate or long-term recurrence of the hypergranulation was observed. This indicates a short corticosteroid treatment course inhibited topical inflammation at the gastrostomy site, leading to quick resolution of hypergranulation with no adverse effects.

Another matter for discussion is whether occlusive dressings, such as hydrocolloids, should be used. A prospective, noncontrolled, observational study¹⁷ (N = 10) demonstrated a polyurethane foam dressing could reduce hypergranulation tissue. Similarly, in a previous case report,¹³ an occlusive dressing was used in the treatment of intractable hypergranulation, with no reported complications. However, it also has been hypothesized that the use of these dressings could be a cause of hypergranulation tissue because they enhance granulation growth factors under the dressings.⁹ A review of the literature²³ suggested a high-potency topical corticosteroid should not be used under an occlusive dressing because local cutaneous side effects may be enhanced. In the present report, gauze was used instead of an occlusive dressing on the hypergranulation site. The gauze was useful in the initial healing process because it absorbed excess exudate and blood. Gauze is a simple, low-cost, manageable material that is easily applied by patients and caregivers. Therefore, based on previous literature^9,23 and the experience of the effective use of gauze in the current case, an occlusive dressing may be unnecessary in the treatment of hypergranulation around the G-tube insertion site.

This case study has 2 major limitations. The primary limitation is the lack of a reference standard for topical corticosteroid use for hypergranulation tissue. The cited references address corticosteroid use in both adults and children; the present case involved an adult. Because few reports are available on corticosteroid treatment of hypergranulation, further studies are required to evaluate the appropriate potency and dose of topical corticosteroid. 

A second limitation is that a biopsy of the hypergranulation tissue was not performed in this case study. This study was descriptive and subjective, with no pathological investigation, such as the use of hematoxylin and eosin staining to determine the degree of inflammation in a biopsy. However, visual inspection clearly showed a marked improvement in this case.

This case report describes the successful treatment and rapid reduction of hypergranulation around a G-tube using a topical corticosteroid. The treatment was simple, noninvasive, and safe. After 4 days’ treatment, redness markedly decreased, and bleeding and exudate ceased, leading to discontinuation of treatment and no further hypergranulation during 6 months’ follow-up. Further prospective studies with a large number of patients are required to evaluate the potency and dose of topical corticosteroid for the treatment of G-tube insertion site hypergranulation.

The authors thank Jarred Tucker for language assistance. The authors also thank Dr. Mary Cant from Edanz Editing, who provided professional editing services.

Please address correspondence to: Ryusuke Ae, MD, PhD, Division of Public Health, Center for Community Medicine, Jichi Medical University, Yakushiji 3311-1, Shimotsuke, Tochigi 329-0498 Japan; email: shirouae@jichi.ac.jp.