Subtotal Gastrectomy
in Infancy for Perforating
By R. Bilik, N. Freud, T. Sheinfeld,
Y. Ben-Ari,
A. Rachmel,
Necrotizing
Gastritis
N. Ziv, and M. Zer
Pe tah- Tikva, Israel 0 Necrotizing gastritis is a rare pathology causing a high rate of morbidity and mortality in the infants. A 4-week-old baby, with right hypoplastic kidney and ectopic ureter, was admitted because of profound septic shock and “coffee ground” vomitus. Aggressive treatment was started and hemodynamic stabilization was achieved. On the fourth admission day, ascites was noted and on the eighth day in a plain abdominal x-ray, free air was shown. At urgent explorative laparotomy, double posterior gastric wall perforations with extensive gastric wall necrosis were found, which required subtotal gastrectomy. The etiology and pathophysiology of this rare process are discussed with an emphasis on the difficulty in diagnosis of posterior gastric perforation into the lesser sac. p 1990 by W.B. Saunders Company. INDEX WORDS:
Necrotizing
gastritis.
P
ERFORATION of stomach in infants and children is a rare abdominal catastrophe associated with high morbidity and mortality.’ A better understanding of the pathophysiology, early management, and postoperative intensive care may improve the outcome of these patients, CASE
REPORT
A 4-week-old white girl was admitted to the Beilinson Medical Center because of recurrent “coffee ground” vomitus and deterioration in her general condition. A hypoplastic right kidney with ectopic insertion of the ureter to the vagina was known to have been present since birth. At admission the patient was apathic, grayish, with diminished response to pain and weak peripheral pulses. Her abdomen was distended and high-output gastric secretion contained coffee ground residual with bile. Hypothermia was noted, with body temperature of 35”C, systolic blood pressure of 60 mm Hg, heart rate of 180 beats/min, respiratory rate of 60 breaths/min, hemoglobin of 16.1 g%, and white blood cell count of 21,200 with a shift to the left. Blood glucose was 178 mg%; plasma electrolytes were Na+ 134 mEq/L, K+ 5.6 mEq/L, blood urea nitrogen 14 mg%, aspartate aminotransferase 128 W/L, lactate dehydrogenase >600 IU/L, phosphate alkalase 86 W/L, total protein 4.9 g%, and albumin 2.7 g%. Blood gases were pH 7.308, PO2 133 mm Hg, PCO, 30 mm Hg, HCO, 15.2 mEq/L, base excess (-9 mEq/L), and lactic acid 2.8 mg%. These clinical and laboratory parameters indicated profound septic shock. Plain x-ray of the abdomen showed normal gas distribution and no free air was detected. Aggressive resuscitation, including fluids and broad spectrum antibiotics, were immediately
From the Departments of Pediatric Surgery, Pediatric Intensive Care, and Pediatric Radiology, Beiiinson MedicaI Center and Sackler School of Medicine. Petah-Tikva, Israel. Address reprint requests to M. Zer, MD, Department of Pediatric Surgery, Beilinson Medical Center, Petah-Tikva. Israel 49100. o 1990 by W.B. Saunders Company. 0022-3468/90/2512-0014%03.00/0
1244
started. On the second day of hospitalization, edema of the abdominal wall, rubor, and induration along the Teres ligament were noted. Repeat plain x-ray film of the abdomen showed enlarged bowel loops and no evidence of free air. Paralytic ileus due to sepsis was assumed. An improvement in the clinical status was observed; the inflammation of the abdominal wall subsided and spontaneous normal bowel movement appeared. On the fourth hospitalization day, distention of the abdomen with ascites was noted. A sample aspirated from the ascites was sterile. On her eighth hospitalization day routine plain abdominal x-ray showed free air in a limited epigastric region. Explorative laparotomy was performed urgently. Double perforation and transmural necrosis of the posterior wall of the stomach were found, with extensive circular sloughing of all the mucosa from the antrum and part of the gastric body. No intestinal damage was detected. Subtotal gastrectomy (70%) with gastroenterostomy was performed. Bacteriological culture from the abdominal fluid yielded Escherichia coli and appropriate antibiotic therapy was administered. Despite the antibiotic therapy, severe wound infection developed in the postoperative period and was treated locally. On her ninth postoperative day oral feeding was started. Difficulty in oral feeding (small amount, 60 mL) and repeated bile vomiting were major problems and necessitated periodical use of an enteral continuous feeding pump. Recurrent episodes of septic fever with purulent vaginal discharge due to the ectopic right ureter required reintervention. The patient underwent repeat surgery on the 72nd postoperative day and the atrophic right kidney was removed. The patient was discharged from the hospital 97 days after her first abdominal operation. After 6 months of follow-up the patient is well, gaining weight slowly, with gastric input still around 80 to 100 mL per meal.
Pathology Pathological examination of the stomach confirmed transmural necrosis. The mucosa near the perforation was superficially lacerated and the gastric glands were markedly dilated, creating cystic formation (Fig 1). There was significant thickening of the submucosa with congestion of blood, hemorrhages, crypt abscesses, and evidence of severe chronic and acute inflammation. In some histological slides near the perforation site, inflammation was found in the muscle layer as continuity from the submucosa. Fresh thrombi were detected in the gastric muscle layer. The serosal layer of the gastric specimen showed severe inflammation. In many slides no continuity was observed between the inflammation of the serosal layer and the inflammation in the muscle layer. DISCUSSION
The two most common causes for gastric perforation in infancy are (1) mechanical causes, due to excessive distention or instrumentation (including gastric tube insertion), and (2) local mechanical ischemic causes, such as volvulus of stomach or incarceration in diaphragmatic hernia. Systemic blood flow impairment (“low4ow state”) due to profound shock, sepsis, disseminated intravascular coagulation, etc, may cause ulcerogenic diathesis
Journal of Pediatric Surgerv, Vol 25, No 12 (December), 1990: pp 1244-1245
NECROTIZING GASTRITIS IN INFANCY
1245
Fig 1. Markedly dilated gastric glands creating cystic formation. The mucosa near the perforation is superficially lacerated.
and gastric perforation in adults.’ However, these are very rare in children and exceptional in the neonatal period and in infancy. In the present case there was no evidence of any traumatic instrumentation or gastric distention. Volvulus or incarceration of the stomach was not observed. We assume that profound sepsis was the main underlying cause for the gastric damage. An ascending infection through the ectopic ureter of the right kidney could have been the source of the sepsis, and the peritoneal culture of E co/i supported our assumption of sepsis. Kumar and Spitz’ found stress ulcer to be a predisposing factor for gastric perforation in 15% of
the pediatric patients they studied. The extensive missing gastric mucosa with severe submucosa inflammation, as was found in this patient, may be evidence of the propagation in the inflammation process, starting from disseminated gastric stress ulcers. These gastric stress ulcers were probably an addition factor causing the gastric perforation. Perforation of the stomach due to necrotizing gastritis, as described by Strauss et al’ and Wanek et aL3 is becoming an entity increasingly known by the pediatric surgeons. The etiology of this abdominal catastrophe is not well explained and a number of hypotheses have been suggested.3 In one of these hypotheses, acute synergistic bacterial necrotizing gastritis was proposed by Strauss et al in adults,’ but was not reported in the pediatric population. A pathophysiological mechanism using the Strauss hypothesis may explain the present case. Profound septic shock could cause a decrease in blood flow to the gastric wall and emboli to the mural blood vessels, followed by the extensive damage to the gastric mucosa, exposing the bare unprotected gastric wall to a corrosive agent such as gastric acid. This could eventually cause the extensive necrosis and perforation. Perforation of the posterior necrotic gastric wall, as was observed in this case, enhanced the septic state of the patient. Localization of the process to the lesser sac caused difficulty and delay in the diagnosis, especially because generalized peritonitis was not present and free air could not be demonstrated until very late. The physical or mental development of a child were found not to be affected after subtotal or even total gastrectomy in 113 children reported by Moore4 and Dunn et aL5 Bradley et al’ concluded from their experience that the small amount of enteral intake was the main reason for not gaining weight after gastrectomy, without correlation to the type of the surgical procedure. Continuous enteral feeding especially in the immediate postoperative period and small amount of oral feeding later may achieve good results in the development of the child.
REFERENCES I. Strauss RJ. Friedman M, Platt N, et al: Gangrene of the stomach: A case of acute necrotizing gastritis. Am J Surg 135:253257, 1978 2. Kumar D, Spitz L: Peptic ulceration in children. Surg Gynecol Obstet 159:63-66. 1984 3. Wanek E, Oldham KT, Polley TZ, et al: Idiopathic infarction in childhood. Pediatr Surg Int 3:184-186, 1988
gastric
4. Moore TC: Gastrectomy in infancy and childhood: of international survey. Ann Surg 162:91-92, 1965 5. Dunn S, Weber T, Grosfeld hood. Arch Surg 118:656-660,1983
JL: Acute
II. Results
peptic ulcer in child-
6. Bradley EL, Issacs J, Hersh T, et al: Nutritional of total gastrectomy. Ann Surg 182:4115-4129, 1975
consequence
in Infancy for Perforating
By R. Bilik, N. Freud, T. Sheinfeld,
Y. Ben-Ari,
A. Rachmel,
Necrotizing
Gastritis
N. Ziv, and M. Zer
Pe tah- Tikva, Israel 0 Necrotizing gastritis is a rare pathology causing a high rate of morbidity and mortality in the infants. A 4-week-old baby, with right hypoplastic kidney and ectopic ureter, was admitted because of profound septic shock and “coffee ground” vomitus. Aggressive treatment was started and hemodynamic stabilization was achieved. On the fourth admission day, ascites was noted and on the eighth day in a plain abdominal x-ray, free air was shown. At urgent explorative laparotomy, double posterior gastric wall perforations with extensive gastric wall necrosis were found, which required subtotal gastrectomy. The etiology and pathophysiology of this rare process are discussed with an emphasis on the difficulty in diagnosis of posterior gastric perforation into the lesser sac. p 1990 by W.B. Saunders Company. INDEX WORDS:
Necrotizing
gastritis.
P
ERFORATION of stomach in infants and children is a rare abdominal catastrophe associated with high morbidity and mortality.’ A better understanding of the pathophysiology, early management, and postoperative intensive care may improve the outcome of these patients, CASE
REPORT
A 4-week-old white girl was admitted to the Beilinson Medical Center because of recurrent “coffee ground” vomitus and deterioration in her general condition. A hypoplastic right kidney with ectopic insertion of the ureter to the vagina was known to have been present since birth. At admission the patient was apathic, grayish, with diminished response to pain and weak peripheral pulses. Her abdomen was distended and high-output gastric secretion contained coffee ground residual with bile. Hypothermia was noted, with body temperature of 35”C, systolic blood pressure of 60 mm Hg, heart rate of 180 beats/min, respiratory rate of 60 breaths/min, hemoglobin of 16.1 g%, and white blood cell count of 21,200 with a shift to the left. Blood glucose was 178 mg%; plasma electrolytes were Na+ 134 mEq/L, K+ 5.6 mEq/L, blood urea nitrogen 14 mg%, aspartate aminotransferase 128 W/L, lactate dehydrogenase >600 IU/L, phosphate alkalase 86 W/L, total protein 4.9 g%, and albumin 2.7 g%. Blood gases were pH 7.308, PO2 133 mm Hg, PCO, 30 mm Hg, HCO, 15.2 mEq/L, base excess (-9 mEq/L), and lactic acid 2.8 mg%. These clinical and laboratory parameters indicated profound septic shock. Plain x-ray of the abdomen showed normal gas distribution and no free air was detected. Aggressive resuscitation, including fluids and broad spectrum antibiotics, were immediately
From the Departments of Pediatric Surgery, Pediatric Intensive Care, and Pediatric Radiology, Beiiinson MedicaI Center and Sackler School of Medicine. Petah-Tikva, Israel. Address reprint requests to M. Zer, MD, Department of Pediatric Surgery, Beilinson Medical Center, Petah-Tikva. Israel 49100. o 1990 by W.B. Saunders Company. 0022-3468/90/2512-0014%03.00/0
1244
started. On the second day of hospitalization, edema of the abdominal wall, rubor, and induration along the Teres ligament were noted. Repeat plain x-ray film of the abdomen showed enlarged bowel loops and no evidence of free air. Paralytic ileus due to sepsis was assumed. An improvement in the clinical status was observed; the inflammation of the abdominal wall subsided and spontaneous normal bowel movement appeared. On the fourth hospitalization day, distention of the abdomen with ascites was noted. A sample aspirated from the ascites was sterile. On her eighth hospitalization day routine plain abdominal x-ray showed free air in a limited epigastric region. Explorative laparotomy was performed urgently. Double perforation and transmural necrosis of the posterior wall of the stomach were found, with extensive circular sloughing of all the mucosa from the antrum and part of the gastric body. No intestinal damage was detected. Subtotal gastrectomy (70%) with gastroenterostomy was performed. Bacteriological culture from the abdominal fluid yielded Escherichia coli and appropriate antibiotic therapy was administered. Despite the antibiotic therapy, severe wound infection developed in the postoperative period and was treated locally. On her ninth postoperative day oral feeding was started. Difficulty in oral feeding (small amount, 60 mL) and repeated bile vomiting were major problems and necessitated periodical use of an enteral continuous feeding pump. Recurrent episodes of septic fever with purulent vaginal discharge due to the ectopic right ureter required reintervention. The patient underwent repeat surgery on the 72nd postoperative day and the atrophic right kidney was removed. The patient was discharged from the hospital 97 days after her first abdominal operation. After 6 months of follow-up the patient is well, gaining weight slowly, with gastric input still around 80 to 100 mL per meal.
Pathology Pathological examination of the stomach confirmed transmural necrosis. The mucosa near the perforation was superficially lacerated and the gastric glands were markedly dilated, creating cystic formation (Fig 1). There was significant thickening of the submucosa with congestion of blood, hemorrhages, crypt abscesses, and evidence of severe chronic and acute inflammation. In some histological slides near the perforation site, inflammation was found in the muscle layer as continuity from the submucosa. Fresh thrombi were detected in the gastric muscle layer. The serosal layer of the gastric specimen showed severe inflammation. In many slides no continuity was observed between the inflammation of the serosal layer and the inflammation in the muscle layer. DISCUSSION
The two most common causes for gastric perforation in infancy are (1) mechanical causes, due to excessive distention or instrumentation (including gastric tube insertion), and (2) local mechanical ischemic causes, such as volvulus of stomach or incarceration in diaphragmatic hernia. Systemic blood flow impairment (“low4ow state”) due to profound shock, sepsis, disseminated intravascular coagulation, etc, may cause ulcerogenic diathesis
Journal of Pediatric Surgerv, Vol 25, No 12 (December), 1990: pp 1244-1245
NECROTIZING GASTRITIS IN INFANCY
1245
Fig 1. Markedly dilated gastric glands creating cystic formation. The mucosa near the perforation is superficially lacerated.
and gastric perforation in adults.’ However, these are very rare in children and exceptional in the neonatal period and in infancy. In the present case there was no evidence of any traumatic instrumentation or gastric distention. Volvulus or incarceration of the stomach was not observed. We assume that profound sepsis was the main underlying cause for the gastric damage. An ascending infection through the ectopic ureter of the right kidney could have been the source of the sepsis, and the peritoneal culture of E co/i supported our assumption of sepsis. Kumar and Spitz’ found stress ulcer to be a predisposing factor for gastric perforation in 15% of
the pediatric patients they studied. The extensive missing gastric mucosa with severe submucosa inflammation, as was found in this patient, may be evidence of the propagation in the inflammation process, starting from disseminated gastric stress ulcers. These gastric stress ulcers were probably an addition factor causing the gastric perforation. Perforation of the stomach due to necrotizing gastritis, as described by Strauss et al’ and Wanek et aL3 is becoming an entity increasingly known by the pediatric surgeons. The etiology of this abdominal catastrophe is not well explained and a number of hypotheses have been suggested.3 In one of these hypotheses, acute synergistic bacterial necrotizing gastritis was proposed by Strauss et al in adults,’ but was not reported in the pediatric population. A pathophysiological mechanism using the Strauss hypothesis may explain the present case. Profound septic shock could cause a decrease in blood flow to the gastric wall and emboli to the mural blood vessels, followed by the extensive damage to the gastric mucosa, exposing the bare unprotected gastric wall to a corrosive agent such as gastric acid. This could eventually cause the extensive necrosis and perforation. Perforation of the posterior necrotic gastric wall, as was observed in this case, enhanced the septic state of the patient. Localization of the process to the lesser sac caused difficulty and delay in the diagnosis, especially because generalized peritonitis was not present and free air could not be demonstrated until very late. The physical or mental development of a child were found not to be affected after subtotal or even total gastrectomy in 113 children reported by Moore4 and Dunn et aL5 Bradley et al’ concluded from their experience that the small amount of enteral intake was the main reason for not gaining weight after gastrectomy, without correlation to the type of the surgical procedure. Continuous enteral feeding especially in the immediate postoperative period and small amount of oral feeding later may achieve good results in the development of the child.
REFERENCES I. Strauss RJ. Friedman M, Platt N, et al: Gangrene of the stomach: A case of acute necrotizing gastritis. Am J Surg 135:253257, 1978 2. Kumar D, Spitz L: Peptic ulceration in children. Surg Gynecol Obstet 159:63-66. 1984 3. Wanek E, Oldham KT, Polley TZ, et al: Idiopathic infarction in childhood. Pediatr Surg Int 3:184-186, 1988
gastric
4. Moore TC: Gastrectomy in infancy and childhood: of international survey. Ann Surg 162:91-92, 1965 5. Dunn S, Weber T, Grosfeld hood. Arch Surg 118:656-660,1983
JL: Acute
II. Results
peptic ulcer in child-
6. Bradley EL, Issacs J, Hersh T, et al: Nutritional of total gastrectomy. Ann Surg 182:4115-4129, 1975
consequence
