- Email: [email protected]
Primal scream therapy: A new cause of Mallory-Weiss tear
1
1 BRIEF CLINICAL OBSERVATIONS
PRIMAL SCREAM THERAPY: A NEW CAUSE OF MALLORY-WEISS TEAR Although mucosal lacerations at the esophagogastric junction were first recognized by Mallory and Weiss [l] in 1929, these tears were not commonly diagnosed until the advent of fiberoptic endoscopy. Most studies now conclude that Mallory-Weiss tears cause 10% to 15% of cases of upper gastrointestinal bleeding requiring hospitalization [2,3]. There are many reports of various precipitating factors predisposing to tears, such as coughing, trauma, hiccuping, gastroscopy, heavy lifting, and Valsalva maneuvers [4-71. We report a patient who developed acute gastrointestinal bleeding from a Mallory-Weiss tear as a result of screaming during primal and confrontational therapy for alcohol rehabilitation. The association of Mallory-Weiss tear and screaming has not been previously reported. A 55-year-old man was admitted to the Palo Alto Veterans Administration Medical Center on June 29, 1988, because of upper gastrointestinal bleeding. He had been well until half an hour after a 25minute forceful screaming session during primal and confrontational therapy for alcohol rehabilitation. He developed nausea, and 3.5 hours later vomited his lunch and about 500 mL of coffee-ground material. Prior to the current episode of hematemesis the patient had no nausea, vomiting, diarrhea, fever, chills, sweats, or malaise. Past medical history was significant for a 30-year history of binge drinking. The patient denied any alcohol use in the last 5 years except for a 4-day binge that started 2 weeks before his admission. The patient denied taking aspirin or nonsteroidal antiinflammatory agents. Physical examination on presentation revealed a well-nourished man in no distress. His temperature was 36.5’C, blood pressure 130/82 mm Hg supine and standing, and pulse BO/minute supine and 96lminute standing. Respiratory rate was 16/ minute. Breath sounds were nor-
mal; no murmurs, SB,or Sq was noted. The abdomen was soft and nontender; normal bowel sounds were present. No hepatosplenomegaly was noted. Rectal examination revealed no masses, but stool was guaiac-positive and brown. No spider angiomas or palmar erythema was noted. The hematocrit was 40% and decreased to 35% with hydration. The leukocyte count was 17.5 thousandlpl, but decreased to 9.8 thousandlpl within the same day. The mean corpuscular volume was 92 fL, and the red blood cell distribution width was 13.2%. A nasogastric tube was placed and clear bilious gastric fluid was obtained. There was no evidence of acute bleeding during the hospitalization. An esophagogastroduodenoscopy performed 16 hours after the bleeding episode revealed a 2-cm nonbleeding Mallory-Weiss tear covered with exudate, mild distal esophagitis, and a 3-cm hiatal hernia. The patient had no further episodes of bleeding during the hospital admission and no evidence of bleeding 2 months after the initial episode. This case demonstrates a previously unreported cause of a Mallory-Weiss tear. With the advent of fiberoptic esophagogastroduodenoscopy, visual examination of the upper gastrointestinal tract is being increasingly performed, and Mallory-Weiss tears are more commonly diagnosed [B]. Although many authors emphasize the history as a major determinant of the appropriate degree of suspicion for tears, recent studies suggest that many patients with Mallory-Weiss tears do not have a classic history of retching or vomiting before hematemesis. Knauer [B] reported that 43 of 58 patients (75%) had symptoms of emesis or retching preceding actual upper gastrointestinal bleeding. Graham and Schwartz [2] found that the classic history is not a sensitive indicator for tears. They reported that only 29% of patients gave a classic history of pre-hematemesis retching, vomiting, or coughing. Thus, the absence of a classic history does not exclude the diagnosis. Previous case reports have implicated
July 1990
The American
coughing, trauma, or even no apparent precipitating factor in Mallory-Weiss tears. A mucosal tear can theoretically occur during a forceful scream or yell. During such activity, pleural pressures increase in order to effect a rapid exhalation of air. As pleural pressures increase, intraesophageal pressures also increase. Pleural and esophageal pressures are closely related, and a rapid rise in esophageal pressures from a sudden scream or yell can result in an esonhageal mucosal laceration [9,lb]. The association of hiatal hernia with Mallory-Weiss tears has been reported, with an incidence of 35% to 100%. Knauer [B] reported a frequency of 72% in his series of 75 patients. Of the 15 cases studied by Watts [6], hiatal hernia was diagnosed in 14. The presence of a hiatal hernia in our patient may have increased his risk of developing a Mallory-Weiss tear. JONATHAN~RITIKIN,M.D. ROSENDOBALLIN HARVEY YOUNG,M.D. Palo Alto
Veterans
Administration Medical Center Palo Alto, California and Stanford University M;c$diiE Stanford,
California
1. Mallory GK. Weiss S: Hemorrhages from lacerations of the cardiac orifice of the stomach due to vomiting. Am J Med Sci 1929; 178: 506-515. 2. Graham DY. Schwartz JT: The spectrum of the Mallory-Weiss tear. Medicine 1978; 57: 307318. 3. St. John DJB, Masterson JP, Yeomans ND, Dudley HAF: The Mallory-Weiss syndrome. Br Med J 1974; 1: 140-143. 4. Atkinson M, Bottrill MB, Edwards AT, Mitchell WM. Peet BG. Williams RE: Mucosal tears of the esophagogastric juncbon. Gut 1961; 2: l-11. 5. Holmes KD: Mallory-Weiss syndrome: review of 20 cases and literature review. Ann Surg 1966; 164: 810-820. 6. Watts HD: Mallory-Weiss syndrome occurring as a complrcabon of endoscopy. Gastrointest Endosc 1976; 22: 171-172. 7. Weaver DH. Maxwell KB, Casleton JG: MalloryWeiss syndrome. Am J Surg 1969; 118: 887-892. 8. Knauer CM: Mallory-Weiss syndrome. Gastroenterology 1976; 71: 5-8. 9. Fishman AP. ed: Pulmonary diseases and disorders, ed 2. New York: McGraw-Hill, 1988; 2118. lO.Fenn WO. Rahn H. section eds. Handbook of physiology, section 3, vol 1. Washrngton: American Physrology Society, 1964; 309-376. Submitted October
Journal
25, 1989, and accepted
of Medicine
Volume
89
April 4. 1990
121
1 BRIEF CLINICAL OBSERVATIONS
PRIMAL SCREAM THERAPY: A NEW CAUSE OF MALLORY-WEISS TEAR Although mucosal lacerations at the esophagogastric junction were first recognized by Mallory and Weiss [l] in 1929, these tears were not commonly diagnosed until the advent of fiberoptic endoscopy. Most studies now conclude that Mallory-Weiss tears cause 10% to 15% of cases of upper gastrointestinal bleeding requiring hospitalization [2,3]. There are many reports of various precipitating factors predisposing to tears, such as coughing, trauma, hiccuping, gastroscopy, heavy lifting, and Valsalva maneuvers [4-71. We report a patient who developed acute gastrointestinal bleeding from a Mallory-Weiss tear as a result of screaming during primal and confrontational therapy for alcohol rehabilitation. The association of Mallory-Weiss tear and screaming has not been previously reported. A 55-year-old man was admitted to the Palo Alto Veterans Administration Medical Center on June 29, 1988, because of upper gastrointestinal bleeding. He had been well until half an hour after a 25minute forceful screaming session during primal and confrontational therapy for alcohol rehabilitation. He developed nausea, and 3.5 hours later vomited his lunch and about 500 mL of coffee-ground material. Prior to the current episode of hematemesis the patient had no nausea, vomiting, diarrhea, fever, chills, sweats, or malaise. Past medical history was significant for a 30-year history of binge drinking. The patient denied any alcohol use in the last 5 years except for a 4-day binge that started 2 weeks before his admission. The patient denied taking aspirin or nonsteroidal antiinflammatory agents. Physical examination on presentation revealed a well-nourished man in no distress. His temperature was 36.5’C, blood pressure 130/82 mm Hg supine and standing, and pulse BO/minute supine and 96lminute standing. Respiratory rate was 16/ minute. Breath sounds were nor-
mal; no murmurs, SB,or Sq was noted. The abdomen was soft and nontender; normal bowel sounds were present. No hepatosplenomegaly was noted. Rectal examination revealed no masses, but stool was guaiac-positive and brown. No spider angiomas or palmar erythema was noted. The hematocrit was 40% and decreased to 35% with hydration. The leukocyte count was 17.5 thousandlpl, but decreased to 9.8 thousandlpl within the same day. The mean corpuscular volume was 92 fL, and the red blood cell distribution width was 13.2%. A nasogastric tube was placed and clear bilious gastric fluid was obtained. There was no evidence of acute bleeding during the hospitalization. An esophagogastroduodenoscopy performed 16 hours after the bleeding episode revealed a 2-cm nonbleeding Mallory-Weiss tear covered with exudate, mild distal esophagitis, and a 3-cm hiatal hernia. The patient had no further episodes of bleeding during the hospital admission and no evidence of bleeding 2 months after the initial episode. This case demonstrates a previously unreported cause of a Mallory-Weiss tear. With the advent of fiberoptic esophagogastroduodenoscopy, visual examination of the upper gastrointestinal tract is being increasingly performed, and Mallory-Weiss tears are more commonly diagnosed [B]. Although many authors emphasize the history as a major determinant of the appropriate degree of suspicion for tears, recent studies suggest that many patients with Mallory-Weiss tears do not have a classic history of retching or vomiting before hematemesis. Knauer [B] reported that 43 of 58 patients (75%) had symptoms of emesis or retching preceding actual upper gastrointestinal bleeding. Graham and Schwartz [2] found that the classic history is not a sensitive indicator for tears. They reported that only 29% of patients gave a classic history of pre-hematemesis retching, vomiting, or coughing. Thus, the absence of a classic history does not exclude the diagnosis. Previous case reports have implicated
July 1990
The American
coughing, trauma, or even no apparent precipitating factor in Mallory-Weiss tears. A mucosal tear can theoretically occur during a forceful scream or yell. During such activity, pleural pressures increase in order to effect a rapid exhalation of air. As pleural pressures increase, intraesophageal pressures also increase. Pleural and esophageal pressures are closely related, and a rapid rise in esophageal pressures from a sudden scream or yell can result in an esonhageal mucosal laceration [9,lb]. The association of hiatal hernia with Mallory-Weiss tears has been reported, with an incidence of 35% to 100%. Knauer [B] reported a frequency of 72% in his series of 75 patients. Of the 15 cases studied by Watts [6], hiatal hernia was diagnosed in 14. The presence of a hiatal hernia in our patient may have increased his risk of developing a Mallory-Weiss tear. JONATHAN~RITIKIN,M.D. ROSENDOBALLIN HARVEY YOUNG,M.D. Palo Alto
Veterans
Administration Medical Center Palo Alto, California and Stanford University M;c$diiE Stanford,
California
1. Mallory GK. Weiss S: Hemorrhages from lacerations of the cardiac orifice of the stomach due to vomiting. Am J Med Sci 1929; 178: 506-515. 2. Graham DY. Schwartz JT: The spectrum of the Mallory-Weiss tear. Medicine 1978; 57: 307318. 3. St. John DJB, Masterson JP, Yeomans ND, Dudley HAF: The Mallory-Weiss syndrome. Br Med J 1974; 1: 140-143. 4. Atkinson M, Bottrill MB, Edwards AT, Mitchell WM. Peet BG. Williams RE: Mucosal tears of the esophagogastric juncbon. Gut 1961; 2: l-11. 5. Holmes KD: Mallory-Weiss syndrome: review of 20 cases and literature review. Ann Surg 1966; 164: 810-820. 6. Watts HD: Mallory-Weiss syndrome occurring as a complrcabon of endoscopy. Gastrointest Endosc 1976; 22: 171-172. 7. Weaver DH. Maxwell KB, Casleton JG: MalloryWeiss syndrome. Am J Surg 1969; 118: 887-892. 8. Knauer CM: Mallory-Weiss syndrome. Gastroenterology 1976; 71: 5-8. 9. Fishman AP. ed: Pulmonary diseases and disorders, ed 2. New York: McGraw-Hill, 1988; 2118. lO.Fenn WO. Rahn H. section eds. Handbook of physiology, section 3, vol 1. Washrngton: American Physrology Society, 1964; 309-376. Submitted October
Journal
25, 1989, and accepted
of Medicine
Volume
89
April 4. 1990
121