- Email: [email protected]
Gastric damage from ingested acid in children
Gastric Damage From Ingested Acid in Children By D.A. Gillis, Gayle Higgins, and Richard Kennedy Halifax, Nova Scotia, Canada 9 Acid ingestion occurs relatively rarely and produces a spectrum of injury that is markedly different from the more commonly encountered alkaline burns of the oropharynx and esophagus. Gastric damage results from pylorospasm with pooling of the ingested caustic in a dependent location. Symptoms may be delayed for days or weeks, Perforation and/or strictures may require extensive gastric surgery. Early fiberoptic endoscopy is essential. 9 1 9 8 5 by Grune & S t r a t t o n . Inc.
INDEX WORDS: Caustic ingestion; gastric perforation; gastric stricture; gastroscopy.
OME OF THE HAZARDS related to the inges-
S tion of caustics are not widely appreciated. There are striking differences in the mechanism of injury, the sites of maximum damage, and the clinical presentation between ingested acids and alkalies (Fig 1). Strong alkali causes immediate tissue injury and tends to produce maximum damage in the oropharynx and esophagus; significant effects in the stomach are distinctly uncommon. By contrast, the damage caused by the ingestion of strong acid is likely to be minimal in the pharynx and esophagus, maximal in the stomach, and often delayed in its clinical presentation. 1'2'3This is well demonstrated by our experience with the following patients. CASE REPORTS
eventful and the patient remains asymptomatic one year later. Gastric emptying is normal.
Case 2 A two year old boy ingested an unknown quantity of soldering paste. No oral injury was noted. Rigid esophagoscopy in a community hospital on the following day revealed only superficial mucosal damage. He was treated with prednisone and ampicillin in hospital for five days. Oral fluids were well tolerated and he seemed normal when he went home. Two days later he became febrile and vomited several times. He was re-admitted looking very ill--listless, pale, and hypotensive. His abdomen was distended and diffusely tender. X-rays disclosed a pneumoperitoneum. Laparotomy, shortly after admission, revealed extensive gastric necrosis with a huge posterior perforation. A total gastrectomy was performed, re-establishing G-I continuity by anastomosing the distal end of the esophagus in an end-to-end fashion to a Roux-Y segment of jejunum. Shortly thereafter, he was transferred to the Izaak Walton Killam Hospital for continuing care. His early recovery was uneventful and he was on total parenteral nutrition for several weeks. Oral alimentation was reasonably well tolerated initially, but slowly progressive dyspbagia ensued. A firm stricture developed at the esophago-jejunal anastomosis (Fig 3). Symptoms persisted, despite repeated dilatations. Accordingly, a second operation was carried out after several weeks; the stricture was excised and the esophagus was anastomosed to the convexity of the jejunal loop with the addition of a distal enteroenterostomy. Recovery was uncomplicated. The patient has continued to do well. His weight gain has been satisfactory to date and he is able to take a normal diet in the form of multiple small feedings. He is currently asymptomatic, 27 months following the second surgical procedure.
DISCUSSION
Case 1 A previously healthy seven year old male ingested an undetermined volume of liquid soldering Flux. Transient abdominal pain and occasional vomiting subsided. There was no evidence of oral injury and the patient was discharged from the Charles A. Janeway Hospital after an initial period of observation lasting three days. Repetitive vomiting lead to his readmission three weeks later. Esophagoscopy at that time was negative. Radiological studies revealed an irregular contracted antrum with poor peristalsis and delayed emptying (Fig 2). Laparotomy disclosed extensive mural damage of the distal third of the stomach. A localized resection and gastrostomy was carried out. Subsequent attempts to dilate the pyloric canal were unsuccessful and a second surgical procedure (pyloroplasty) was required for clinical relief. Recovery was un-
From the Departments of Surgery, Izaak Walton Killam Hospital for Children, Halifax, Nova Scotia, Canada; and the Charles A. Janeway Child Health Centre, St. John's, Newfoundland, Canada. Presented at the Annual Meeting of the Canadian Association of Paediatric Surgeons, September 10-11, 1984, Montreal, Quebec, Canada. Address reprint requests to Dr D.A. Gittis, lzaak Walton Kiltam Hospital for Children, 5850 University Ave, Halifax, Nova Scotia, Canada, B3J 3G9. 9 1985 by Grune & Stratton, Inc. 0022-3468/85/2005~9005803.00/0 494
These cases illustrate the common pattern of injury caused by the ingestion of strong acid. In contrast to alkalies, acid causes little damage in the mouth and pharynx, typically passes quickly through the esophagus, and causes maximum harm to the wall of the stomach. Strong acid reaching the stomach may cause early perforation if a large volume is involved and if the organ is empty at the time of the accident. Typically, however, it produces pylorospasm with delayed gastric emptying and pooling of the caustic in a dependent position. 2'4'5 Thus, the antrum and mid portion of the stomach are prone to be damaged while the fundus is commonly spared. Transmural damage proceeds at a ALKALI
ACID
OROPHARYNGEAL INJURY
COMMON
UNCOMMON
TRANSIT TIME TO STOMACH
SLOW
RAPID
ESOPHAGEAL INJURY
SEVERE
MILD
GASTRIC INJURY
MILD
SEVERE
Fig 1.
Major differences between ingested acid and alkali.
Journal of Pediatric Surgery, Vol 20, No 5 (October), 1985: pp 494-496
GASTRIC DAMAGE FROM INGESTED ACID IN CHILDREN
Fig 2.
495
Antral stricture, Case 1.
variable but generally slow rate, depending on the volume and strength of the acid. Efforts to neutralize ingested acid may be counterproductive. The administration of water and/or a weak base may cause an exothermic reaction with increased thermal damage. 3 Thus, the early administration of a weak base and/or gastric lavage are not recommended. In contrast to the experience with ingested alkalies, the use of steroids seems to offer little in the management of patients who have ingested acid: There is, likewise, little evidence to support the routine use of antibiotics in these patients. Others have noted the occurrence of perforation 6'7 usually early after the injury. Thus, it would appear essential to identify gastric mucosal injury as quickly as possible. Early fiberoptic endoscopy is the method of choice. 4"8-1~Unfortunately, this was not carried out in either of our patients. Had this been done, it would likely have had a significant effect in reducing morbidity. The identification of gastric injury should mandate continued hospitalization, avoidance of oral feedings
Fig 3.
Stricture at esophago-jejunal anaStOmQsis, Case 2.
until healing is progressing well, and repeat endoscopy at appropriate intervals. It might be pos'sible to carefully aspirate pooled liquid at the time of the initial gastroscopy) Delayed symptoms result from obstructive scarring, usually m a x i m u m in the antrum and pyloric canal. Others have reported the need for surgical intervention after intervals of weeks or months) '4 Conservative surgery, such as antral resection or pyloroplasty, will usually be adequate. In a few instances, such as our second case, total removal of the stomach may be the only reasonable alternative. 5'6
REFERENCES
1. Wright JE, Hennessy EJ: Pyloric obstruction due to ingestion of corrosives. Med J Aust 2:761-767, 1972 2. LoweJE, Graham DY, Boisaubin EV, et al: Corrosiveinjury to the stomach: The natural history and role of fiberoptic endoscopy. Am J Surg 137:803-806, 1979
3. Penner GE: Acid ingestion: Toxicologyand treatment. Ann Emerg Med 9:374-378, 1980 4. Chong GC, Beahrs OH, Payne WS: Management of corrosive gastritis due to ingested acid. Mayo Clin Proc 49:861-865, 1974 5. Maull KI, Scher LA, Greenfield LJ: Surgical implications of acid ingestion. SGO 148:895-898, 1979
496
6. Chodak G, Passaro E: Acid ingestion. JAMA 239:225-226, 1978 7. Knopp R: Caustic ingestions, JACEP 8:329-335, 1979 8. Sugawa C, Mullins R J, Lucas CE, et ah The value of early endoscopy following caustic ingestion. SGO 153:553-556, 1981
GILLIS ET AL
9. Welsh J J, Welsh LW: Endoscopic examination of corrosive injuries of the upper gastrointestinal tract. Laryngoscope 88:13001309, 1978 10. Chung RSK, Den Besten L: Fibreoptic endoscopy in treatment of corrosive injury of the stomach. Arch Surg 110:725-728, 1975
INDEX WORDS: Caustic ingestion; gastric perforation; gastric stricture; gastroscopy.
OME OF THE HAZARDS related to the inges-
S tion of caustics are not widely appreciated. There are striking differences in the mechanism of injury, the sites of maximum damage, and the clinical presentation between ingested acids and alkalies (Fig 1). Strong alkali causes immediate tissue injury and tends to produce maximum damage in the oropharynx and esophagus; significant effects in the stomach are distinctly uncommon. By contrast, the damage caused by the ingestion of strong acid is likely to be minimal in the pharynx and esophagus, maximal in the stomach, and often delayed in its clinical presentation. 1'2'3This is well demonstrated by our experience with the following patients. CASE REPORTS
eventful and the patient remains asymptomatic one year later. Gastric emptying is normal.
Case 2 A two year old boy ingested an unknown quantity of soldering paste. No oral injury was noted. Rigid esophagoscopy in a community hospital on the following day revealed only superficial mucosal damage. He was treated with prednisone and ampicillin in hospital for five days. Oral fluids were well tolerated and he seemed normal when he went home. Two days later he became febrile and vomited several times. He was re-admitted looking very ill--listless, pale, and hypotensive. His abdomen was distended and diffusely tender. X-rays disclosed a pneumoperitoneum. Laparotomy, shortly after admission, revealed extensive gastric necrosis with a huge posterior perforation. A total gastrectomy was performed, re-establishing G-I continuity by anastomosing the distal end of the esophagus in an end-to-end fashion to a Roux-Y segment of jejunum. Shortly thereafter, he was transferred to the Izaak Walton Killam Hospital for continuing care. His early recovery was uneventful and he was on total parenteral nutrition for several weeks. Oral alimentation was reasonably well tolerated initially, but slowly progressive dyspbagia ensued. A firm stricture developed at the esophago-jejunal anastomosis (Fig 3). Symptoms persisted, despite repeated dilatations. Accordingly, a second operation was carried out after several weeks; the stricture was excised and the esophagus was anastomosed to the convexity of the jejunal loop with the addition of a distal enteroenterostomy. Recovery was uncomplicated. The patient has continued to do well. His weight gain has been satisfactory to date and he is able to take a normal diet in the form of multiple small feedings. He is currently asymptomatic, 27 months following the second surgical procedure.
DISCUSSION
Case 1 A previously healthy seven year old male ingested an undetermined volume of liquid soldering Flux. Transient abdominal pain and occasional vomiting subsided. There was no evidence of oral injury and the patient was discharged from the Charles A. Janeway Hospital after an initial period of observation lasting three days. Repetitive vomiting lead to his readmission three weeks later. Esophagoscopy at that time was negative. Radiological studies revealed an irregular contracted antrum with poor peristalsis and delayed emptying (Fig 2). Laparotomy disclosed extensive mural damage of the distal third of the stomach. A localized resection and gastrostomy was carried out. Subsequent attempts to dilate the pyloric canal were unsuccessful and a second surgical procedure (pyloroplasty) was required for clinical relief. Recovery was un-
From the Departments of Surgery, Izaak Walton Killam Hospital for Children, Halifax, Nova Scotia, Canada; and the Charles A. Janeway Child Health Centre, St. John's, Newfoundland, Canada. Presented at the Annual Meeting of the Canadian Association of Paediatric Surgeons, September 10-11, 1984, Montreal, Quebec, Canada. Address reprint requests to Dr D.A. Gittis, lzaak Walton Kiltam Hospital for Children, 5850 University Ave, Halifax, Nova Scotia, Canada, B3J 3G9. 9 1985 by Grune & Stratton, Inc. 0022-3468/85/2005~9005803.00/0 494
These cases illustrate the common pattern of injury caused by the ingestion of strong acid. In contrast to alkalies, acid causes little damage in the mouth and pharynx, typically passes quickly through the esophagus, and causes maximum harm to the wall of the stomach. Strong acid reaching the stomach may cause early perforation if a large volume is involved and if the organ is empty at the time of the accident. Typically, however, it produces pylorospasm with delayed gastric emptying and pooling of the caustic in a dependent position. 2'4'5 Thus, the antrum and mid portion of the stomach are prone to be damaged while the fundus is commonly spared. Transmural damage proceeds at a ALKALI
ACID
OROPHARYNGEAL INJURY
COMMON
UNCOMMON
TRANSIT TIME TO STOMACH
SLOW
RAPID
ESOPHAGEAL INJURY
SEVERE
MILD
GASTRIC INJURY
MILD
SEVERE
Fig 1.
Major differences between ingested acid and alkali.
Journal of Pediatric Surgery, Vol 20, No 5 (October), 1985: pp 494-496
GASTRIC DAMAGE FROM INGESTED ACID IN CHILDREN
Fig 2.
495
Antral stricture, Case 1.
variable but generally slow rate, depending on the volume and strength of the acid. Efforts to neutralize ingested acid may be counterproductive. The administration of water and/or a weak base may cause an exothermic reaction with increased thermal damage. 3 Thus, the early administration of a weak base and/or gastric lavage are not recommended. In contrast to the experience with ingested alkalies, the use of steroids seems to offer little in the management of patients who have ingested acid: There is, likewise, little evidence to support the routine use of antibiotics in these patients. Others have noted the occurrence of perforation 6'7 usually early after the injury. Thus, it would appear essential to identify gastric mucosal injury as quickly as possible. Early fiberoptic endoscopy is the method of choice. 4"8-1~Unfortunately, this was not carried out in either of our patients. Had this been done, it would likely have had a significant effect in reducing morbidity. The identification of gastric injury should mandate continued hospitalization, avoidance of oral feedings
Fig 3.
Stricture at esophago-jejunal anaStOmQsis, Case 2.
until healing is progressing well, and repeat endoscopy at appropriate intervals. It might be pos'sible to carefully aspirate pooled liquid at the time of the initial gastroscopy) Delayed symptoms result from obstructive scarring, usually m a x i m u m in the antrum and pyloric canal. Others have reported the need for surgical intervention after intervals of weeks or months) '4 Conservative surgery, such as antral resection or pyloroplasty, will usually be adequate. In a few instances, such as our second case, total removal of the stomach may be the only reasonable alternative. 5'6
REFERENCES
1. Wright JE, Hennessy EJ: Pyloric obstruction due to ingestion of corrosives. Med J Aust 2:761-767, 1972 2. LoweJE, Graham DY, Boisaubin EV, et al: Corrosiveinjury to the stomach: The natural history and role of fiberoptic endoscopy. Am J Surg 137:803-806, 1979
3. Penner GE: Acid ingestion: Toxicologyand treatment. Ann Emerg Med 9:374-378, 1980 4. Chong GC, Beahrs OH, Payne WS: Management of corrosive gastritis due to ingested acid. Mayo Clin Proc 49:861-865, 1974 5. Maull KI, Scher LA, Greenfield LJ: Surgical implications of acid ingestion. SGO 148:895-898, 1979
496
6. Chodak G, Passaro E: Acid ingestion. JAMA 239:225-226, 1978 7. Knopp R: Caustic ingestions, JACEP 8:329-335, 1979 8. Sugawa C, Mullins R J, Lucas CE, et ah The value of early endoscopy following caustic ingestion. SGO 153:553-556, 1981
GILLIS ET AL
9. Welsh J J, Welsh LW: Endoscopic examination of corrosive injuries of the upper gastrointestinal tract. Laryngoscope 88:13001309, 1978 10. Chung RSK, Den Besten L: Fibreoptic endoscopy in treatment of corrosive injury of the stomach. Arch Surg 110:725-728, 1975