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GASTROJEJUNOSTOMY; AN EFFECTIVE SURGICAL OPTION TO MANAGE CORROSIVE INDUCED GASTRIC OUTLET OBSTRUCTION
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Accidental corrosive ingestion is a common occurrence in developing nations. In most of the cases these agents damage the oesophagus and stomach. Isolated injury of pylorus of stomach has a relatively low incidence. We report such a case of accidental ingestion of corrosive acid, which resulted in isolated stenosis of the pyloric antrum. The diagnosis was confirmed by Barium meal and endoscopy. The patient underwent gastro jejunostomy and recovered well after the surgery. A brief discussion of mechanism of corrosive injury, clinical features, investigations and management follows.
Ingested corrosive agents produce oropharyngeal and gastroesophageal injuries ranging from minor burns to severe necrosis, depending on the agent amount, concentration, and duration of exposure. The aim of this study was to present our patients with corrosive ingestion retrospectively. Four hundred seventy-three children younger than 16 years of age (mean age, 3.7+/-0.1 years) who were admitted to our hospital for suspected corrosive ingestion between the years 1995 and 2003 were studied. Two hundred eighty-six (60.5%) of 473 patients were males. Household bleaches (36.6%) and oven cleaners (23%) were the most frequently encountered corrosive agents. During endoscopy, lesions in the esophagus were recorded in 379 children. Eighty-one of the cases had gastric lesions. During the follow-up, esophageal stricture, esophageal perforation, and gastric outlet obstruction (GOO) developed in 11 cases, 1 case, and 2 cases, respectively. Caustic ingestion of alkali substances such as oven cleaner seem to cause more severe injuries. Early admission to the hospital with clinical and endoscopic evaluation and early surgery when required may reduce morbidity and mortality.
Two cases of primary squamous-cell carcinoma arising in a stomach damaged by corrosive acid burns are reported. Thirty-three previously reported cases of pure squamous carcinoma of the stomach are tabulated and their pathogenesis is discussed. A plea is made for treating corrosive acid burns of the stomach by some form of resection of the entire area involved rather than by more conservative methods, such as gastrojejunostomy, which have been used in the past.
Compared with the ingestion of corrosive substances in children, this problem tends to be more serious, in adults, because its intent is often suicidal, rather than accidental. The severity and extent of damage produced to the gastrointestinal tract depends on the morphological form of the caustic agent. In the acute stage, perforation and necrosis may occur. Long-term complications include esophageal stricture, antral stenosis, and the development of esophageal carcinoma. X-rays of the abdomen and chest should be done initially to detect any evidence of perforation. Endoscopy should be performed as soon as possible in all cases to evaluate the extent and severity of damage, unless there is evidence of perforation. A complete examination is feasible in most cases. Stricture formation is more common in patients with second- and third-degree burns. Measures to prevent stricture formation, including the use of steroids, have not been successful. Esophageal carcinoma usually occurs 40 yr after the time of injury.
A survey of US poison control centers was conducted by the American Association of Poison Control Centers to characterize the current status of poison control centers and to prepare an accurate list of centers. Data from 36 AAPCC certified regional centers and from 63 non-regional centers is presented.
More than 5,000 caustic ingestions are estimated to occur each year. Liquid lye is associated with the greatest morbidity. Endoscopy is the only method for evaluating the extent of the injury; clinical signs and symptoms (e.g., vomiting, dysphagia, abdominal pain, oral burns, leukocytosis) are not reliable. In less severe burns (involving only mucosal irritation or ulceration), current therapy with antibiotics and steroids results in a very favorable prognosis. Circumferential or very deep burns have a much poorer outcome, with a greatly increased risk of stricture formation and/or perforation. The risk of developing esophageal carcinoma may be 1,000 times greater for individuals who have had a lye burn than in the general population. It cannot be overemphasized that prevention is still the key to decreasing this morbidity.
Ingestion of acid often causes severe damage to the stomach. Ingestion of alkali, however, usually injures the esophagus and spares the stomach. Early complications of acid ingestion, e.g., massive gastric hemorrhage or perforation, are unusual. The absence of severe symptoms in most patients soon after ingestion of acid is often misleading. Gastric outlet obstruction is a common late result and may develop following an asymptomatic interval. The authors' experience with three patients with severe complications following ingestion of acid is presented. The initial treatment, as well as the surgical management, are discussed.
Two hundred eighty-five children with possible caustic burns of the esophagus have been managed at two university hospitals using similar protocols. Of these, 235 (82%) had immediate esophagoscopy and 69 (29%) had demonstrated esophageal burns. They were treated with steroids and antibiotics. Eight (12%) with proven burns developed strictures that responded to prolonged dilatations and none have required esophageal replacement. The remainder are free of swallowing symptoms. By contrast, eight patients from other hospitals who were not treated by this protocol were referred for esophageal replacement6 and prolonged dilatation.2 Our strong impression is that immediate steroid-antibiotic therapy greatly decreases the incidence of esophageal stricture but does not completely eliminate it. Those children who develop strictures on this treatment regimen seem to have milder esophageal scarring, which usually responds to dilatation rather than requiring esophageal replacement.
Gastric cicatrization is a well recognized late sequela of corrosive gastric injury, but the optimum timing and type of surgery for this complication are still unclear. Over a 7-year period (1988-1994) 34 patients underwent elective surgery for gastric lesions secondary to corrosive ingestion. A total of 18 (53%) patients had an associated esophageal stricture and presented with dysphagia, 15 (44%) patients had features of gastric outlet obstruction, 6 (18%) had diffuse gastric injury, and 28 (82%) had a segmental lesion. A tube jejunostomy was done in 23 (68%) patients to improve nutrition and resulted in a significant increase in weight and in the serum protein level after 8 weeks of tube feeding. Elective surgery was performed 3 to 24 months (average 7 months) after ingestion of the corrosive substance. Gastric resection was done in 20 (59%) patients and gastrojejunostomy (without vagotomy) in 11 (32%); at follow-up the latter group did not exhibit development of a stomal ulcer. In patients with an associated esophageal stricture, endoscopic dilatation was successful in 89% patients and simplified the surgical approach. In conclusion, the success of surgery for corrosive-induced gastric injury depends on selecting the right procedure and intervening at the appropriate time.
Deep circumferencial burns of the esophagus always result in stricture formation and obstruction of the lumen. The usual treatment of caustic esophageal strictures is long-term esophageal dilatations. A new method of treatment, long-term stenting of the strictured esophagus gave superior results when compared with the classic dilatation therapy (healing rates, 68% v 33%; P < .01). Although success in the stent group was very satisfactory, the 32% failure rate requires explanation. In the years between 1991 and 1993, 53 stent-treated patients were screened for gastroesophageal reflux (GER). All patients were investigated with 24-hour ambulatory distal esophageal pHmetry. In 18 patients reflux index (RI) was found to be below 4. In 14 patients RI was between 4.1 and 19. In the final group of 21 patients RI was over 20 (minimum, 21.8; maximum, 72.8). When these data were compared with the healing rates of the patients, it was found that none of the 21 patients with RI over 20 responded to the described therapy. We conclude that the esophagus, after a serious caustic insult, not only narrows but also shortens thus altering the lower esophageal sphincter function leading to serious GER. Therefore all caustic esophageal burn patients should be screened for GER periodically during the dilatation or stent therapy programs, and GER should be controlled before RI approaches 20.
To present our long-term results of the treatment of caustic-induced prepyloric obstruction, and to set out guidelines for the management of such patients.
Retrospective study.
General hospital (medical centre), Taiwan.
30 patients (8 male and 22 female, mean age 34 years, range 13-62) who developed prepyloric obstruction out of 271 treated for caustic injuries of the upper gastrointestinal tract.
Gastrojejunostomy (n = 24), antrectomy and Billroth I reconstruction (n = 4), and antrectomy and Billroth II reconstruction (n = 2). Four patients required second operations: oesophageal reconstruction for stricture (n = 3), and gastrojejunostomy for restenosis of Billroth I anastomosis (n = 1).
Morbidity and mortality.
No patient died postoperatively, and there were three complications--wound infection, internal bleeding, and stenosis of the Billroth I anastomosis. 21 patients were able to enjoy their normal diet postoperatively, 5 required periodic dilatation of oesophageal strictures, and 4 required further operations.
Gastrojejunostomy gives good long term results as long as there is no oesophageal stricturing, and morbidity and mortality are low. The long term outcome is dependent on the degree of oesophageal involvement.
Diagnosis and treatment of caustic ingestion injuries remain controversial. Based on experience with a wide spectrum of upper gastrointestinal tract injuries from caustic ingestion, prospectively observed in 58 adult patients treated in a teaching hospital in Milan, the authors suggest an early staging of the lesions by endoscopy, followed by resective surgery for high-degree esophagogastric lesions. Ingestion of a large amount of corrosive agent results in a life-threatening condition that requires a much more aggressive diagnostic and therapeutic approach than was formerly recommended. Early surgery plays a fundamental role in the prevention of acute hemorrhagic and perforative complications as well as of development of scar tissue and neoplastic stricture over time. The multidisciplinary approach to the management of these patients is underlined, stressing the need of close cooperation between a number of different specialists.
A retrospective clinical study was performed to determine the incidence, management, and outcome of gastric outlet obstruction (GOO) caused by caustic ingestion in children. Of 220 patients who sustained caustic substance ingestion and were treated at our unit between 1976 and 1996, 168 ingested alkaline substances; of these, 9 children (5.3%) developed GOO in addition to esophageal strictures. The remaining 52 patients ingested acid agents, and 2 of them (3.8%) presented with GOO without esophageal strictures. The overall incidence of corrosive GOO was 5% (n = 11). The mean age of the patients with GOO was 5.7 +/- 2.8 years (range 2-14) with a female:male ratio of 6:5. Sodium hydroxide (n = 6), potassium hydroxide (n = 3), and hydrochloric acid (n = 2) were the ingested caustic agents. The patients were subdivided into two groups according to serial endoscopic and radiologic findings: group I: moderate (dense superficial and spotty ulcerations with intact mucosa) mucosal injury with partial pyloric obstruction; and group II: severe (deep ulcerations, extreme hemorrhagic erosions, eschar formation with white plaques) mucosal injury with complete pyloric obstruction. Group I consisted of 5 patients who ingested alkali agents while group II included 6 who presented with ingestion of alkaline (n = 4) and acid (n = 2) agents. Surgical treatment included Billroth I (n = 6) operations performed in group II and Finney (n = 3) and Heineke-Mikulicz (n = 2) pyloroplasty procedures done in group I. All patients are alive without any complaints. Fiberoptic endoscopy should be the preferred method of evaluating a patient with ingestion of a corrosive agent. It determines the presence of injury and assesses the extent of damage, establishing the diagnosis and allowing therapy to be instituted immediately. Our experience revealed that substantial damage has occurred early after ingestion, and early surgical intervention has decreased the morbidity and mortality. The extent of the mucosal injury and status of the pylorus and antrum determined the type of surgical treatment. A Billroth I procedure recommended for severely injured mucosa with complete pyloric obstruction, and pyloroplasty for moderate mucosal injury associated with partially obstructed but still viable pylorus. In contrast to the current belief, alkali ingestion also has a high risk of corrosive gastric injury causing GOO, which should be considered during assessment of the injury. We emphasize that a detailed evaluation of radiologic and especially endoscopic findings is very important for determining the timing, necessity, and type of appropriate surgical treatment.
To review the initial signs, symptoms, and endoscopic findings in children admitted to the hospital for ingestion of caustic hair relaxer.
Retrospective medical chart review of all children admitted to the hospital with a diagnosis of caustic ingestion from January 1, 1992, to June 30, 1997. Demographics, admission signs and symptoms, and operative findings were recorded from the medical records.
An urban tertiary care children's hospital.
Fifty-nine children (<3 years old) admitted to the hospital for ingestion of hair relaxers.
Two hundred nine patients were evaluated for possible caustic ingestion. Only 163 medical charts were available for review. Of these, 59 (36.2%) ingested hair relaxers. Initial signs and symptoms ranged from none to drooling and vomiting and second-degree oral cavity bums. Fifty-six patients (95%) underwent endoscopy, which revealed normal esophageal mucosa in 53 of them, mild erythema of the distal esophagus in 2, and mild esophagitis in 1.
In our experience, hair relaxer ingestion makes up a significant proportion of all children admitted to the hospital for caustic ingestion. No significant esophageal injury was associated with hair relaxer ingestion, suggesting that endoscopy may not be necessary in these patients. Alternative management is suggested. We believe that patients who ingest hair relaxer should be admitted to the hospital for observation if parents are thought to be unreliable, and should undergo endoscopy if they cannot tolerate oral intake. Asymptomatic patients may be cared for as outpatients if they demonstrate adequate oral intake.
Methods:
During the last 5 years, 61 children were admitted to the authors' hospital because of corrosive substance ingestion, and among them 6 patients were seen with gastric outlet obstruction. Two of them had ingested acid substances, and the other 4 had ingested alkali corrosives. The mean age was 2.9 years (range, 1.5 to 3). Their common complaint was postprandial vomiting, which had begun 3 weeks after the event (range, 1 week to 10 weeks). Endoscopic evaluation and barium contrast radiographies were performed at admission. Four patients had a pyloric stricture, 1 had an antral stricture, and another had an antropyloric stricture. Balloon dilatation of the pylorus (in 1 patient), pyloroplasty (in 3 patients), and Billroth I procedures (in 2 patients) were performed. The mean follow-up period was 22 months (range, 6 weeks to 48 months). One patient, who had undergone a Billroth I procedure, underwent reoperation because of intestinal obstruction 3 months later. On follow-up they are all free of symptoms.
Conclusions:
The treatment of gastric outlet obstruction caused by corrosive ingestion should be treated surgically. Although endoscopic and radiologic evaluation helps to determine the time and necessity, once the diagnosis is confirmed, early definitive surgical intervention should be performed, and the type of the surgery depends mostly on the findings of the surgeon at laparotomy. Endoscopic balloon dilatation of the pylorus maybe attempted in suitable cases. Special care should be given to prevent children from accidental corrosive ingestion.
An experimental study was performed to modify the healing response in caustic esophageal burns to prevent stricture development. Two different agents with different modes of actions, caffeic acid phenethyl ester (CAPE) and epidermal growth factor (EGF), were studied. CAPE has antiinflammatory, immunomodulatory, antioxidant, and antimitotic properties. EGF has known properties in supporting wound healing and in protecting esophagus from injuries.
The model described by Gehanno and its modification by Liu was used to create standard esophageal burns with 50% NaOH. The study was performed with 76 rats in 4 main groups (sham, CAPE, EGF, and control) and 2 subgroups in each for 5 and 28 days of observation. Efficacy of treatment was assessed in 28-day subgroups by measuring weight gain, contrast esophagograms on day 27, histologic evaluation by measuring stenosis index (wall thickness/lumen diameter), and collagen deposition, and biochemically by determining tissue hydroxy proline (OHP) content.
In the end of the study, increase rates of mean body weights of the animals in the 28-day subgroups were as follows: sham, 30%; CAPE, 23%; EGF, 22%; and control, 14%. Although all the animals in subgroups significantly gained weight, the mean weight gain was significantly low in controls when compared with sham, CAPE, and EGF groups (P <.05). Contrast esophagograms on day 27 showed no stenosis in the sham, mild stenosis in CAPE and EGF, and severe stenosis with proximal dilatation in controls. Stenosis indices of the subgroups were as follows: sham, 0.29; CAPE, 0.41; EGF, 0.41; control, 0.84. Index was significantly higher in controls (P <.05). Collagen accumulation scores in the esophageal wall were as follows: Sham, 0.0; CAPE, 0.87; EGF, 0.30; control, 2.70. Scores also were significantly higher in controls (P <.05). Tissue (OHP) levels were as follows (mg/g dry tissue): Sham, 1.48; CAPE, 1.53; EGF, 1.90; control, 4.01. Production of OHP was significantly higher in controls.
The results of the parameters in the study indicate that administration of CAPE and EGF has beneficial effects in the prevention of caustic esophageal strictures. Those effects of CAPE may occur through its antiinflammatory, immunomodulatory, and antioxidant properties, and EGF may occur through its induced proliferative properties on the esophagus.
There has been an increase in the number of patients admitted to our hospital with caustic esophageal injuries during the last five years. The aim of this study was to analyze the complications and results of the treatment of corrosive esophagogastric injury. Between 1990 and 2000, 120 caustic ingestion accidents were admitted to our unit. The mean age was 4 years, with a 2 : 1 male to female ratio. The average time between the caustic ingestion and admission to hospital was 14.9 days. The ingested substances were alkali in 80.9 % and acid in 19.1 % of the cases. Stenosis of the esophagus developed in 31 (25.8 %) and gastric outlet obstruction (GOO) in 6 (5 %) patients. Management of the esophageal stricture consisted of dilatation in 28 patients. Three children underwent colonic interposition without a dilatation attempt. Six children were lost to follow-up; 4 patients were successfully treated; 13 patients were still in the dilatation program at the time of writing with 6 improving and 2 patients waiting for interposition surgery; 4 patients underwent colonic interposition and 1 patient underwent resection of the stenotic part of the esophagus. Among the patients in the dilation program, we observed 4 esophageal perforations. Three of them were treated medically and further dilatations were carried out, while one was managed by colonic interposition. The treatment modalities for GOO cases consisted of pyloroplasty in 3, Billroth I in 2 and balloon dilation of the pylorus in 1 child. Although balloon dilatation of the esophagus carries the risk of perforation, it should be the first line of treatment in suitable cases. GOO cases may require surgical therapy following a detailed endoscopic evaluation.
To analyze the feasibility and safety of transhiatal approach for resection of corrosively scarred esophagus. BACKGROUND SUMMARY DATA: The unrelenting corrosive strictures of esophagus merit esophageal substitution. Because of the risk of complications in the retained esophagus, such as malignancy, mucocele, gastroesophageal reflux, and bleeding, esophageal resection is deemed necessary. Transthoracic approach for esophageal resection is considered safe. The safety and feasibility of transhiatal resection of the esophagus is not established in corrosive injury of the esophagus.
Transhiatal approach was used for resection of the scarred esophagus for all patients between January 1986 and December 2001. The intraoperative complications, indications for adding thoracotomy, and postoperative outcome were studied in 51 patients. Follow-up period varied from minimum of 6 months to 15 years.
Esophageal resection was achieved in 49 of 51 patients whereas thoracotomy was added in 2 patients. In 1 of the patients tracheal injury occurred whereas in other patient there were dense adhesions between tracheal membrane and esophagus. Gastric tube was used for esophageal substitution in 40 (78.4%) patients whereas colon was transplanted in 11 (21.6%) patients. Colon was used only when stomach was not available. One patient (1.9%) had tracheal membrane injury whereas 4 patients (7.8%) had recurrent laryngeal nerve palsy. One patient each had thoracic duct injury and intrathoracic gastric tube leak. There was no operative mortality. Anastomotic complications like leak were present in 19.6% and stricture in 58.8% patients. All the patients were able to resume their normal duties and swallow normal food within 6 months of the surgery.
One-stage transhiatal esophageal resection and reconstruction could be safely used for the extirpation of scarred esophagus. Use of gastric conduit was technically simple, quicker, and offered good functional outcome. Postoperative anastomotic stricture amenable to dilatations was the commonest complication.
Gastric outlet obstruction (GOO) is a well-known complication of acid ingestion. However, most reports deal with adults. In this report, the authors present their experience with the treatment of acid-induced GOO in children.
The records of patients admitted for unintentional ingestion of corrosive agents between 1980 and 2002 were reviewed retrospectively. Data concerning age at ingestion, type of ingested substance, time between ingestion and the first signs of GOO, weight loss, treatment, complications, duration of hospital stay, and long-term follow-up were reviewed.
GOO was not observed in any of the children admitted for alkaline ingestion, whereas GOO developed in 8 of 98 children (8.2%) in a mean period of 26.7 +/- 10 days after the ingestion of acid substances. Presenting symptoms were frequent nonbilious vomiting and marked weight loss. All had pyloric obstructions in the upper gastrointestinal series and required surgical intervention. Gastrojejunostomy was the operation of choice for all patients. Oral feedings were started on the third postoperative day. The complications were wound infection in 1 and upper gastrointestinal bleeding in another in the early postoperative period. Mean follow-up is 8.33 +/- 4.45 (4.8-18.7) years. No late complications such as marginal ulcus or stricture at the anastomosis site were observed in the series.
Treatment of GOO with gastrojejunostomy gives good long-term results in children. This procedure is safe and causes minimal morbidity particularly in patients without extensive gastric damage.
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