Spontaneous Gastric Rupture in the Newborn
M. Bayatpour, MD, FAAP,” Nashville, Tennessee L.
Bernard, MD, FACS,t Nashville, Tennessee
F. McCune, MD,* Nashville, Tennessee W. Barbel, MD,+ Nashville, Tennessee
Spontaneous rupture of the stomach during the neonatal period is the most common type of nonobstructive perforation that requires emergency surgical intervention [I]. The number of reported cases in the literature is up to 200 so far [2]. The fatality rate is still very high, ranging from 27 to 83 per cent [I-3]. The success of therapy depends on early diagnosis and immediate surgical treatment. A case of spontaneous gastric rupture during the neonatal period which was treated successfully by surgical repair is reported herein. Case Report
A 5 pound 3 ounce (2,360 gm) premature male infant was born on June 21,1977 at 11:13 AM to a twenty year old black female, gravida 2, para 1. Her last menstrual period occurred October 3, 1976, and the expected date of confinement was July 10, 1977. No known significant complications developed during pregnancy. The patient denied use of drugs or tobacco, but drank beer occasionally. The membranes ruptured a few hours before the baby was born vaginally in vertex presentation. The baby’s Apgar scores were 6 and 8 at 1 and 5 minutes, respectively. Initial physical examination in premature nursery revealed a normal premature male infant of low birth weight. The infant had an apneic episode for 1 minute and became cyanotic, requiring resuscitation at 6:30 PM on June 21, 1977. A nasogastric tube was inserted during resuscitation and thick mucous secretion removed. Chest x-ray films were negative. The remainder of the physical examination was noncontributory. The infant was kept under close supervision for respiratory distress. He received oral feedings and tolerated the formula well.
From the Departments of Pediatrics* and Surgeryt. Mehany Medical College, Nashville. Tennessee. Reprint requests should be addressed to M. Bayatpour, MD, Department of Pediatrics, Meharty Medical College, Nashville, Tennessee 37208.
Volume 137, February 1979
On June 23,1977 at 4:30 AM, the nurses noted that the baby’s abdomen was quite distended. He was also jaundiced, and there was a mild degree of inflammatory change present around the umbilicus. The total bilirubin was 8.00 mg/lOO ml with 0.5 mg direct. An x-ray film of the chest showed free air under the diaphragm, and an upright film of the abdomen showed massive pneumoperitoneum. (Figure 1.) The patient was given nothing by mouth and began receiving intravenous fluids, intravenous penicillin 100 mg/kg/24 hours, and gentamicin 6 mg intramuscularly every 12 hours. Blood, nasopharyngeal, ear, and umbilical specimens were collected and sent to the microbiology laboratory for culture and sensitivity studies. A surgical consultation was obtained, and he was taken to the operating room at 11:00 AM on the same day. Surgical Procedure Under endotracheal anesthesia, the patient’s abdomen was prepped with Betadinb, and appropriate sterile linens were applied. The abdomen was entered via a vertical incision extending from the tip of the xiphoid process to a point approximately 2 cm below the umbilicus. On entering the abdomen, a considerable quantity of intragastric contents was noted in the left upper quadrant of the abdomen, having extruded through a large rent along the greater curvature of the stomach. The rent in the stomach extended from near the cardia to a point about midway along the body of the stomach. The margins of the rent appeared cyanotic for a distance of 2 to 3 mm on either side of the opening. A nasogastric tube extruding through the rent was removed by way of the nostril. The gastric contents were suctioned and lavaged using normal saline. The rent in the gastric wall was closed in two layers, the initial layer being a continuous through-and-through suture of 4-O chromic catgut. This was reinforced with Lembert’s sutures of 5-O silk. On conclusion of the gastric repair, exploration of the remainder of the gastrointestinal tract was carried out to assure that no perforations were missed. No other areas of perforation or of apparent circulatory em-
267
Bayatpour et al
removed, dehiscence of the abdominal wound developed and was surgically corrected on the same day. Oral feeding was restarted on July 121977. Thereafter, he continued to do well without any problems. He was discharged from the hospital on August 3,1977, his weight 6 pounds 7 ounces (2,950 gm).
He is being followed in the Pediatric Clinic. At three months of age he weighed 13 pounds 8 ounces (6,146 gml.
Comments
Figure 1. Upright film of the abdomen showing massive pneumoperitonium.
barassment being evident, Stamm gastrostomy was performed in the antrum of the stomach. A # 12 Foley catheter was inserted and fixed in place with a purse string suture of 4-O chromic catgut. The catheter was brought out through aseparate left upper quadrant stab wound, and the gastric wall was fixed to the parietal peritoneum at the point of exit of the tube with the same suture as used for the purse string. The patient’s abdomen was then closed in a single layer with interrupted figure eight sutures of 3-O black silk. The patient tolerated the procedure well and was returned to the Pediatric Intensive Care Unit in satisfactory condition. Intravenous fluids and antibiotics continued to be administered after surgery. Intravenous hyperalimentation was begun on June 25,1977. Liver function studies, complete blood count, differentials, and electrolyte levels were studied twice weekly. After surgery his total bilirubin level increased as high as 15.00 mg/lOO ml, and he was treated with phototherapy for two days. He continued to respond to therapy, and on June 30,1977, a small amount of oral feeding was started. July On 1,1977, when his sutures were
266
The clinical presentation of neonatal gastric rupture is not exclusive. The features include 13-61 vomiting, abdominal distension, respiratory distress, and if not treated, evidence of shock, including cold and clammy extremities and cyanosis. The most common feature is severe abdominal distension, but this is not pathognomonic for gastric rupture. Diagnosis of the gastric rupture is based on the x-ray film of the abdomen. The upright film will show the “saddle” or “football” sign due to massive pneumoperitoneum [5]. It is more common among premature, low birth weight, black male infants. Furthermore, there is usually a history of respiratory distress [6]. The most common time for the rupture is within the first week of life. The case presented herein is a so-called classic one. The patient was a premature, low birth weight, black male with mild respiratory distress. The cause and pathogenesis of neonatal gastric rupture is not known. There are different hypotheses and speculations, such as birth trauma [ 71, mechanical injury [8], idiopathic [9], congenital absence of the muscle [10,11], hypoxia [6], and more recently, increased intraluminal pressure [12]. Brody [lo] in 1940 reported the possible role of congenital absence of muscle fiber within the greater curvature of the stomach. However, Shaw, Blanc, and Santulli [13], following their experimental work in 1965, reported that the absence of the muscle fiber was in fact due to retraction of the fibers from the edges. Touloukian, Posch, and Spencer [14], in their experimental studies on newborn piglets, demonstrated that during asphyxia, the risk of gastric necrosis is high. During the period of asphyxia, there is a redistribution of the blood supply within different organs. More blood flows to the vital organs, such as the heart and brain, and much less to the less vital gastrointestinal tract. This theory was also supported by Scholander [15] in his work on seals. Touloukian, Posch, and Spencer [14] reported six cases of neonatal gastric rupture from Yale-New Haven and reviewed eighty-seven cases in the liter-
The American Journal of Surgery
Neonatal Spontaneous Gastric Rupture
ature. Respiratory distress and perinatal complications were reported among 69 per cent of the patients. We reviewed 203 premature, low birth weight babies who were born in Hubbard Hospital from July 1976 to October 1977. There were forty-six babies (28 males and 18 females) who suffered from mild to severe respiratory distress and perinatal complications. The case reported herein is the only one of gastric rupture. Therefore, it seems unlikely that hypoxia is the primary etiologic factor in neonatal gastric rupture. Shaker et al [12] in 1973 reported increased intraluminal pressure as a possible cause of gastric rupture. Such pressure causes mucosal hypoxia, necrosis, and rupture. Experimental work by James et al [2] in 1976 showed that air-fluid trapped within the esophagogastric junction could cause rupture of the stomach. According to James et al, all babies swallow 360 ml air/hour. This amount is enough to cause rupture if entrapped at the cardia. Regardless of the pathogenesis and cause, the mortality is still high. Shashikumar et al [I] reported nineteen cases of neonatal gastric rupture for a period from 1963 to 1974. Overall mortaIity was 45 per cent. However, they indicated that the mortality was 62 per cent for patients seen before 1970 and 27 per cent for those operated on since 1970. Hara and Crump [3] reported on six patients-with neonatal gastric rupture, five of whom (83 per cent) died with or without surgery. Success in treatment depends on early diagnosis and prompt surgical intervention. Exploration of the entire gastrointestinal tract is mandatory to rule out necrotizing enterocolitis with perforations of the small and/or large bowel. Summary
Spontaneous rupture of the stomach during the neonatal period is the most common type of nonob-
Volume 137, February 1979
structive perforation. The clinical manifestations include severe abdominal distension, vomiting, and respiratory distress. However, diagnosis is based on an upright x-ray film of the abdomen which shows the “saddle” or “football” sign due to massive pneumoperitoneum. The fatality rate is still quite high. Success in treatment depends on early diagnosis and immediate surgical intervention. References 1. Shashikurnar VL, Bassuk A, Pilling GP, Cresson SL: Spontaneous gastric perforation in the newborn: a clinical review of nineteen cases. Ann Surg 182: 22, 1975. 2. James AE, Hellef RM. White JI, Schaffer JA, Shaker IJ, Hailer JA, Dorst JP: Spontaneous rupture of the stomach in the newborn: clinical and experimental evaluation. Pediatrfks 10: 79. 1976. 3. Hara S, &ump EP: Spontaneous rupture of the stomach in the newborn. JAMA 54: 689, 1962. 4. lnouya WY, Evans G: Neonatal gastric perforation-a report of six cases and a review of 143 cases. Arch Surg 88: 47 1, 1962. 5. Graivier L, Steinberg JB, Doerr JL: Spontaneous gastric perforation in the neonate: case report. Am Surg 32: 275, 1965. 6. Touloukian RI: Gastric ischemia: the primary factor in neonate perforation. C/in Padiafr 12: 219, 1973. 7. Pendergrass EP, Booth RE: Report of a case of rupture of the stomach in an infant three days old. Am J Roenfgenoi 56: 590, 1946. 8. Stein FE, Wright LT: Rupture of hollow and solic vicera in newborn. Hasp Bull 6: 32, 1953. 9. Castleton KE, Hatch FF: Idiopathic perforation of stomach in newborn. Arch Surg 76: 874, 1958. 10. Brody H: Ruptured diverticulum of the stomach in a newborn infant associated with congenital occluding duodenum. Arch Pathcl29: 125, 1940. 11. Herbut PA: Congenital defect in musculature of the stomach with rupture in the newborn infant. Arch Pafhol 36: 91, 1943. 12. Shaker IJ, Schaffer JA, James AE, White JJ: Acrophagia. a mechanism for spontaneous rupture of the stomach in the newborn. Am Surg 39: 619, 1973. 13. Shaw A, Blanc WA. Santulli TV: Soontaneous rupture of the stomach in the newborn: a clinical and experimental study. Surgwy 58: 561, 1965. 14. Touloukian RJ, Posch JN, Spencer R: The pathogenesis of ischemic gastroenterocolitis of asphyxiated neonatal piglets. J Padiafr Surg 7: 194, 1977. 15. Scholander PF: Master switch of life. Sci Am 209: 92, 1963.
269
M. Bayatpour, MD, FAAP,” Nashville, Tennessee L.
Bernard, MD, FACS,t Nashville, Tennessee
F. McCune, MD,* Nashville, Tennessee W. Barbel, MD,+ Nashville, Tennessee
Spontaneous rupture of the stomach during the neonatal period is the most common type of nonobstructive perforation that requires emergency surgical intervention [I]. The number of reported cases in the literature is up to 200 so far [2]. The fatality rate is still very high, ranging from 27 to 83 per cent [I-3]. The success of therapy depends on early diagnosis and immediate surgical treatment. A case of spontaneous gastric rupture during the neonatal period which was treated successfully by surgical repair is reported herein. Case Report
A 5 pound 3 ounce (2,360 gm) premature male infant was born on June 21,1977 at 11:13 AM to a twenty year old black female, gravida 2, para 1. Her last menstrual period occurred October 3, 1976, and the expected date of confinement was July 10, 1977. No known significant complications developed during pregnancy. The patient denied use of drugs or tobacco, but drank beer occasionally. The membranes ruptured a few hours before the baby was born vaginally in vertex presentation. The baby’s Apgar scores were 6 and 8 at 1 and 5 minutes, respectively. Initial physical examination in premature nursery revealed a normal premature male infant of low birth weight. The infant had an apneic episode for 1 minute and became cyanotic, requiring resuscitation at 6:30 PM on June 21, 1977. A nasogastric tube was inserted during resuscitation and thick mucous secretion removed. Chest x-ray films were negative. The remainder of the physical examination was noncontributory. The infant was kept under close supervision for respiratory distress. He received oral feedings and tolerated the formula well.
From the Departments of Pediatrics* and Surgeryt. Mehany Medical College, Nashville. Tennessee. Reprint requests should be addressed to M. Bayatpour, MD, Department of Pediatrics, Meharty Medical College, Nashville, Tennessee 37208.
Volume 137, February 1979
On June 23,1977 at 4:30 AM, the nurses noted that the baby’s abdomen was quite distended. He was also jaundiced, and there was a mild degree of inflammatory change present around the umbilicus. The total bilirubin was 8.00 mg/lOO ml with 0.5 mg direct. An x-ray film of the chest showed free air under the diaphragm, and an upright film of the abdomen showed massive pneumoperitoneum. (Figure 1.) The patient was given nothing by mouth and began receiving intravenous fluids, intravenous penicillin 100 mg/kg/24 hours, and gentamicin 6 mg intramuscularly every 12 hours. Blood, nasopharyngeal, ear, and umbilical specimens were collected and sent to the microbiology laboratory for culture and sensitivity studies. A surgical consultation was obtained, and he was taken to the operating room at 11:00 AM on the same day. Surgical Procedure Under endotracheal anesthesia, the patient’s abdomen was prepped with Betadinb, and appropriate sterile linens were applied. The abdomen was entered via a vertical incision extending from the tip of the xiphoid process to a point approximately 2 cm below the umbilicus. On entering the abdomen, a considerable quantity of intragastric contents was noted in the left upper quadrant of the abdomen, having extruded through a large rent along the greater curvature of the stomach. The rent in the stomach extended from near the cardia to a point about midway along the body of the stomach. The margins of the rent appeared cyanotic for a distance of 2 to 3 mm on either side of the opening. A nasogastric tube extruding through the rent was removed by way of the nostril. The gastric contents were suctioned and lavaged using normal saline. The rent in the gastric wall was closed in two layers, the initial layer being a continuous through-and-through suture of 4-O chromic catgut. This was reinforced with Lembert’s sutures of 5-O silk. On conclusion of the gastric repair, exploration of the remainder of the gastrointestinal tract was carried out to assure that no perforations were missed. No other areas of perforation or of apparent circulatory em-
267
Bayatpour et al
removed, dehiscence of the abdominal wound developed and was surgically corrected on the same day. Oral feeding was restarted on July 121977. Thereafter, he continued to do well without any problems. He was discharged from the hospital on August 3,1977, his weight 6 pounds 7 ounces (2,950 gm).
He is being followed in the Pediatric Clinic. At three months of age he weighed 13 pounds 8 ounces (6,146 gml.
Comments
Figure 1. Upright film of the abdomen showing massive pneumoperitonium.
barassment being evident, Stamm gastrostomy was performed in the antrum of the stomach. A # 12 Foley catheter was inserted and fixed in place with a purse string suture of 4-O chromic catgut. The catheter was brought out through aseparate left upper quadrant stab wound, and the gastric wall was fixed to the parietal peritoneum at the point of exit of the tube with the same suture as used for the purse string. The patient’s abdomen was then closed in a single layer with interrupted figure eight sutures of 3-O black silk. The patient tolerated the procedure well and was returned to the Pediatric Intensive Care Unit in satisfactory condition. Intravenous fluids and antibiotics continued to be administered after surgery. Intravenous hyperalimentation was begun on June 25,1977. Liver function studies, complete blood count, differentials, and electrolyte levels were studied twice weekly. After surgery his total bilirubin level increased as high as 15.00 mg/lOO ml, and he was treated with phototherapy for two days. He continued to respond to therapy, and on June 30,1977, a small amount of oral feeding was started. July On 1,1977, when his sutures were
266
The clinical presentation of neonatal gastric rupture is not exclusive. The features include 13-61 vomiting, abdominal distension, respiratory distress, and if not treated, evidence of shock, including cold and clammy extremities and cyanosis. The most common feature is severe abdominal distension, but this is not pathognomonic for gastric rupture. Diagnosis of the gastric rupture is based on the x-ray film of the abdomen. The upright film will show the “saddle” or “football” sign due to massive pneumoperitoneum [5]. It is more common among premature, low birth weight, black male infants. Furthermore, there is usually a history of respiratory distress [6]. The most common time for the rupture is within the first week of life. The case presented herein is a so-called classic one. The patient was a premature, low birth weight, black male with mild respiratory distress. The cause and pathogenesis of neonatal gastric rupture is not known. There are different hypotheses and speculations, such as birth trauma [ 71, mechanical injury [8], idiopathic [9], congenital absence of the muscle [10,11], hypoxia [6], and more recently, increased intraluminal pressure [12]. Brody [lo] in 1940 reported the possible role of congenital absence of muscle fiber within the greater curvature of the stomach. However, Shaw, Blanc, and Santulli [13], following their experimental work in 1965, reported that the absence of the muscle fiber was in fact due to retraction of the fibers from the edges. Touloukian, Posch, and Spencer [14], in their experimental studies on newborn piglets, demonstrated that during asphyxia, the risk of gastric necrosis is high. During the period of asphyxia, there is a redistribution of the blood supply within different organs. More blood flows to the vital organs, such as the heart and brain, and much less to the less vital gastrointestinal tract. This theory was also supported by Scholander [15] in his work on seals. Touloukian, Posch, and Spencer [14] reported six cases of neonatal gastric rupture from Yale-New Haven and reviewed eighty-seven cases in the liter-
The American Journal of Surgery
Neonatal Spontaneous Gastric Rupture
ature. Respiratory distress and perinatal complications were reported among 69 per cent of the patients. We reviewed 203 premature, low birth weight babies who were born in Hubbard Hospital from July 1976 to October 1977. There were forty-six babies (28 males and 18 females) who suffered from mild to severe respiratory distress and perinatal complications. The case reported herein is the only one of gastric rupture. Therefore, it seems unlikely that hypoxia is the primary etiologic factor in neonatal gastric rupture. Shaker et al [12] in 1973 reported increased intraluminal pressure as a possible cause of gastric rupture. Such pressure causes mucosal hypoxia, necrosis, and rupture. Experimental work by James et al [2] in 1976 showed that air-fluid trapped within the esophagogastric junction could cause rupture of the stomach. According to James et al, all babies swallow 360 ml air/hour. This amount is enough to cause rupture if entrapped at the cardia. Regardless of the pathogenesis and cause, the mortality is still high. Shashikumar et al [I] reported nineteen cases of neonatal gastric rupture for a period from 1963 to 1974. Overall mortaIity was 45 per cent. However, they indicated that the mortality was 62 per cent for patients seen before 1970 and 27 per cent for those operated on since 1970. Hara and Crump [3] reported on six patients-with neonatal gastric rupture, five of whom (83 per cent) died with or without surgery. Success in treatment depends on early diagnosis and prompt surgical intervention. Exploration of the entire gastrointestinal tract is mandatory to rule out necrotizing enterocolitis with perforations of the small and/or large bowel. Summary
Spontaneous rupture of the stomach during the neonatal period is the most common type of nonob-
Volume 137, February 1979
structive perforation. The clinical manifestations include severe abdominal distension, vomiting, and respiratory distress. However, diagnosis is based on an upright x-ray film of the abdomen which shows the “saddle” or “football” sign due to massive pneumoperitoneum. The fatality rate is still quite high. Success in treatment depends on early diagnosis and immediate surgical intervention. References 1. Shashikurnar VL, Bassuk A, Pilling GP, Cresson SL: Spontaneous gastric perforation in the newborn: a clinical review of nineteen cases. Ann Surg 182: 22, 1975. 2. James AE, Hellef RM. White JI, Schaffer JA, Shaker IJ, Hailer JA, Dorst JP: Spontaneous rupture of the stomach in the newborn: clinical and experimental evaluation. Pediatrfks 10: 79. 1976. 3. Hara S, &ump EP: Spontaneous rupture of the stomach in the newborn. JAMA 54: 689, 1962. 4. lnouya WY, Evans G: Neonatal gastric perforation-a report of six cases and a review of 143 cases. Arch Surg 88: 47 1, 1962. 5. Graivier L, Steinberg JB, Doerr JL: Spontaneous gastric perforation in the neonate: case report. Am Surg 32: 275, 1965. 6. Touloukian RI: Gastric ischemia: the primary factor in neonate perforation. C/in Padiafr 12: 219, 1973. 7. Pendergrass EP, Booth RE: Report of a case of rupture of the stomach in an infant three days old. Am J Roenfgenoi 56: 590, 1946. 8. Stein FE, Wright LT: Rupture of hollow and solic vicera in newborn. Hasp Bull 6: 32, 1953. 9. Castleton KE, Hatch FF: Idiopathic perforation of stomach in newborn. Arch Surg 76: 874, 1958. 10. Brody H: Ruptured diverticulum of the stomach in a newborn infant associated with congenital occluding duodenum. Arch Pathcl29: 125, 1940. 11. Herbut PA: Congenital defect in musculature of the stomach with rupture in the newborn infant. Arch Pafhol 36: 91, 1943. 12. Shaker IJ, Schaffer JA, James AE, White JJ: Acrophagia. a mechanism for spontaneous rupture of the stomach in the newborn. Am Surg 39: 619, 1973. 13. Shaw A, Blanc WA. Santulli TV: Soontaneous rupture of the stomach in the newborn: a clinical and experimental study. Surgwy 58: 561, 1965. 14. Touloukian RJ, Posch JN, Spencer R: The pathogenesis of ischemic gastroenterocolitis of asphyxiated neonatal piglets. J Padiafr Surg 7: 194, 1977. 15. Scholander PF: Master switch of life. Sci Am 209: 92, 1963.
269
