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Lung perforation during chest tube placement in the stiff lung syndrome
Lung Perforation During Chest Tube Placement in the Stiff Lung Syndrome By Arthur J. Wilson and Henry F. Krous
A
R E V I E W O F O U R R E C E N T pediatric necropsy population indicates t h a t the u t i l i z a t i o n o f the chest t u b e is o c c a s i o n a l l y a c c o m p a n i e d by serious side effects, the m o s t i m p o r t a n t of which is p e r f o r a t i o n of the l u n g with c r e a t i o n of a p n e u m o t h o r a x . Since 1970, we h a v e e n c o u n t e r e d three cases in 443 p o s t m o r t e m e x a m i n a t i o n s . A review o f the recent l i t e r a t u r e failed to u n cover m e n t i o n of this serious c o m p l i c a t i o n , ~-13 a l t h o u g h the possibility o f its o c c u r r e n c e h a d been suggested by A b r a m s . ~4 A l u n g surface d e n s e l y a d h e r e n t to the chest wall is the m o s t likely s u b s t r a t e for p e r f o r a t i o n , b u t it is n o t a p r e r e q u i s i t e in p a t i e n t s with a "stiff l u n g " s y n d r o m e as d e m o n s t r a t e d by the three case r e p o r t s herein. W e define "stiff l u n g " as o n e with an i n t r i n s i c p a r e n c h y m a l lesion which has lost its n o r m a l resilience s e c o n d a r y to atelectasis, p n e u m o n i t i s , a n d / o r h y a l i n e m e m b r a n e disease. T h e d i a g n o s i s s h o u l d be suspected w h e n a p n e u m o t h o r a x fails to resolve despite p l a c e m e n t o f a chest t u b e in an i n f a n t with r e a s o n to have a "stiff l u n g " s y n d r o m e . CASE REPORTS
Case 1 (No. 011 79-80) K.A.M. was a 3000-g premature white male infant of 37-wk gestation born to a 20-yr-old primagravida mother, and admitted to Children's Orthopedic Hospital and Medical Center (COH&MC) at age 6 hr for respiratory distress. Labor had been induced by amniotomy after adequate cervical dilatation. The Apgar scores were 7 at 1 min and 8 at 5 min. Grunting respirations were present after birth. Admission blood gases while breathing 50~ 02 were pH 7.27; Pco, 56.1 mm Hg and Po, 42 mm Hg. Over the next 36 hr the infant became increasingly hypoxemic and acidotic despite being placed on the Bird respirator and increasing the inspired 02 concentrations. On the morning of the third hospital day the patient had a cardiorespiratory arrest, but was revived. Since postresuscitation radiographs demonstrated a left pneumothorax along with changes consistent with severe idiopathic respiratory distress syndrome (IRDS), a tube was placed in the left chest with subsequent minor improvement in blood gas values. Later the infant was noted to be hypoventilating on the right side and a right pneumothorax was diagnosed leading to placement of a polyethylene feeding tube in the right pleural cavity. Subsequent radiographs showed adequate parenchymal expansion and "good positioning" of the chest tube. Over the next few hours the child continued to deteriorate, with slowing of the heart rate to 40/min and increasing respiratory insufficiency. He died early on the fourth hospital day. At autopsy the combined lung weight was 100 g (expected 64 • 24 g). They were collapsed, firm, purple, normally lobated, and not adherent to the chest wall. A chest tube had perforated the right upper lobe (Fig. 1A). Microscopically, hyaline membrane disease was accompanied by From the Department of Pathology, University of Washington and Children's Orthopedic Hospital and Medical Center, Seattle, Wash. Arthur J. Wilson, M.D.: Resident in Pathology, University of Washington School of Medicine, Seattle, Wash. Henry F. Krous, M.D.: Instructor, Department of Pathology, University of Washington School of Medicine; Assistant Pathologist, Children's Orthopedic Hospital and Medical Center, Seattle, Wash. Address for reprint requests: Dr. Henry F. Krous, Children's Orthopedic Hospital and Medical Center, 4800 Sand Point Way NE, Seattle, Wash. 98105 9 1974 by Grune & Stratton, Inc. Journal of Pediatric Surgery, Vol. 9, No. 2 (April), 1974
213
214
WILSON AND KROUS
Fig. 1. (A) Photograph from Case 1 showing polyethylene feeding tube (used as a chest tube) passing through the right upper lobe of the lung. (B) Photograph from (~ase 2 showing a red rubber tube perforating the left upper lobe of the lung. Note that an unobstructed tube orifice is in the pleural space and remains functional. multiple small arterial thromboemboli, congestion, diffuse atelectasis, and focal bronchopneumonia. Cerebral hemorrhage, arising from the choroid plexus, was the terminal event.
Case 2 (No. 014-00-39) K.W. was a 2300-g premature white infant of approximately 35 wk gestation born to a non insulin-dependent gestational diabetic gravida II, para I, aborta 0 26-yr-old woman. Apgar scores were 6 at 1 min and 9 at 5 min. Shortly after birth the infant was transferred to C O H & M C for respiratory distress and hypoglycemia (27 mg/100 ml). Because o f rapidly progressive respiratory insufficiency (blood gases on 38~ 02: pH 7.329; Peo~ 48 mm Hg: Po~ 22 mm Hg) the Bird respirator was initiated with an F l 0 2 of 54~o. She subsequently developed bilateral pneumothorax for which number 17 and number 16 Rochester tubes were inserted. The chest tubes were "in place" by radiographic examination. The right pneumothorax appeared to resolve, but the left persisted, hence the left chest catheter was replaced with a number 14 red rubber tube resulting in a transient reexpansion of the left lung. Bilateral pneumothorax recurred and persisted on three subsequent chest radiographs despite the chest tubes being "in place." On the third hospital day her hematocrit fell from 4 0 ~ to 16~, she had multiple seizures, and died later in the day. At postmortem the right lung weighed 57.8 g and the left lung 37.3 g (expected 47 • 17 g combined) and lobation was normal. The firm, pale, and hypoexpanded lungs manifested interstitial emphysema, but no pleural adhesions. The left upper lobe had been perforated by the chest tube (Fig. IB). Microscopically, the immature lungs manifested atelectasis, congestion, and severe hyaline membrane disease. A cerebral hemorrhage arising in the subependymal germinal matrix was the terminal event.
Case 3 (No. 014-52-61) B.J.W. was a 2135-g premature white male infant of 39 wk gestation born to a 27-yr-old gravida II, para I-II female after an uneventful pregnancy. The 7-hr labor was spontaneous, and membranes were ruptured artificially 1 hr before birth, at which time the obstetrician noted oligohydramnios. The Apgar scores were 5 at 1 min and 7 at 5 min. Because the infant was anuric, cyanotic, and having intercostal retractions with grunting, he was transferred to C O H & M C at 2 hr of age. On admission here the infant was noted to have Potter's facies, and questionably palpable kidneys. Admission arterial blood gases while on 4 0 ~ oxygen were pH 7.21, Po~ 53 and Pco~ 89. Chest radiographs revealed bilateral pneumothorax and pneumomediastinum. A red rubber chest tube was placed in each hemithorax. The left chest tube was replaced within 1 hr because it was thought to be wedged between the heart and anterior chest wall. Postplacement radiographs revealed some reexpansion bilaterally, but a 50~ left pneumothorax persisted. Over
LUNG PERFORATION
215
the next 12 hr a nasotracheal tube was placed and the oxygen concentration was raised to 85~ with transient falls in the Po2 to 13 16 mm. Because of persistent anuria and suspected Potter's facies, dysmorphology consultation was obtained. They confirmed the diagnosis of Potter's syndrome. Renal arteriograms revealed bilateral nonfunctioning renal arteries. Late on the second hospital day, the infant was found dead. At autopsy the lungs were hypoplastic, firm, atelectatic, and not adherent to the chest wall. A red rubber chest tube had perforated the left upper lobe. Pulmonary hyaline membranes and mild pneumonitis were present microscopically. In addition, bilateral Potter's type ll polycystic kidneys and associated malformations16 were noted, along with disseminated intravascular fibrin thrombi. Acute cerebral edema with cerebellar tonsillar herniation was considered the cause of death. DISCUSSION
Because of the resiliency of normal lung p a r e n c h y m a and compressibility of the gas within the alveoli, it is easily distorted and displaced by extrinsic pressure. Thus, the proper insertion of a chest tube rarely causes perforation in a normal lung. Adherence of the lung to the chest wall may result in lung perforation from chest tube insertion. The cases in this report demonstrate that a "stiff lung" due to p u l m o n a r y atelectasis, hyaline membrane disease, a n d / o r pneumonia which is not adherent to the chest wall is subject to perforation since the decrease in pliability will not allow it to be displaced. The perforation appears to occur because with partial or total collapse of alveoli or filling of alveoli with hyaline membranes or products of infection, the lung becomes a firm nonpliable tissue mass. The antemortem diagnosis was not made in any of these cases. It should be suspected in a patient with known cause for a "stiff lung" syndrome in whom a p n e u m o t h o r a x does not resolve normally. The surgeon should maintain a high index of suspicion while placing or removing the chest tube and be aware that any sudden "give" during placement may signal perforation in such a patient. The details of introduction of the tube were not recorded in any of these cases, hence relative safety of one method versus another cannot be commented upon. If some of the chest tube orifices remain unobstructed in the pleural space (Fig. 1B), the catheter will function, obscuring the fact that lung has been penetrated. Subsequent removal may bring about unexpected reestablishment of pneumothorax a n d / o r hemorrhage. Hence, frequent examinations are indicated in the postremoval interval. That insertion of a chest tube is not a totally innocuous procedure is further attested to by the report of a traumatic arteriovenous fistula between the chest wall and lung created by intercostal catheter placement) 6 With the establishment of many premature and neonatal intensive care units around the country, a large patient population with "stiff lung" syndrome will require drainage of p n e u m o t h o r a x by insertion of intercostal catheters. This complication should be kept in mind and if the diagnosis is made, then appropriate chest tube maneuvers should be instituted. SUMMARY
Three necropsy cases, two premature infants with idiopathic respiratory distress syndrome and one with Potter's syndrome with p u l m o n a r y hypoplasia, sustained lung perforation during insertion of a chest tube for pneumothorax.
216
WILSON AND KROUS
I n n o n e o f t h e c a s e s w a s t h e d i a g n o s i s m a d e d u r i n g life. P e r f o r a t i o n
should be
suspected when a pneumothorax fails t o r e s o l v e o r h e m o t h o r a x d e v e l o p s a f t e r p l a c e m e n t o f a c h e s t t u b e in a c h i l d w i t h r e a s o n t o h a v e a " s t i f f l u n g " s y n d r o m e .
REFERENCES 1. Bernard WF, Maleom JA, Berry RW: A study of the pathogenesis and management of spontaneous pneumothorax. Dis Chest 42:403 412, 1962 2. Borja, AR, Ransdell, HT: Treatment of penetrating gunshot wounds of the chest. Experience with 145 cases. Am J Surg 122:81-84, 1971 3. Hilty-Tammiuaara R, SegerstriSm A: Choice of therapy in spontaneous pneumothorax in relation to later cardiopulmonary function. Scand J Resp Dis 51:93-104, 1970 4. Harbord RP, Homi J: Respiratory failure from contralateral pneumothorax and atelectasis. JAMA: 1179 1181, 1970 5. Yancy WS, Spock A: Spontaneous neonatal pleural effusion. J Pediatr Surg 2:313-319, 1967 6. Weech AA: Lung puncture and aspiration. Am J Dis Child 122:277, 1971 7. Angevine JM: Pneumothorax and aspiration. Arch Pathol 91:288, 1971 8. Glotzer D J: Pseudopneumothorax with "underwater-seal" pleural drainage. N Engl J Med 284:1388, 1971
9. Seremetis G: The management of spontaneous pneumothorax. Chest 57:65 68, 1970 10. Van De Water JM: The treatment of pleural effusion complicating pneumonia. Chest 57:259-1262, 1970 11. Aslam PA, Eastridge CE, Hughes FA Jr: Insertion of the apical chest tube. Surg Gynecol Obstet 130:1097 1098, 1970 12. Trapnell DH, Thurston JG: Unilateral pulmonary oedema after pleura[ aspiration. Lancet 1:1967-1969, 1970 13. Childress ME, Moy G, Mottram M: Unilateral pulmonary edema resulting from treatment of spontaneous pneumothorax. Am Rev Resp Dis 104:119-121, 1971 14. Abrams LD: Chest injuries. Br J Surg 56: 722-723, 1969 15. Osathanondh V, Potter EL: Pathogenesis of polycystic kidneys: Type 2 due to inhibition of ampullary activity. Arch Pathol 77:474-484, 1964 16. Cox A, Keshishian JM, Blades BB: Traumatic arteriovenous fistula of the chest wall and lung. J Thorac Cardiovasc Surg 54:109112, 1967.
A
R E V I E W O F O U R R E C E N T pediatric necropsy population indicates t h a t the u t i l i z a t i o n o f the chest t u b e is o c c a s i o n a l l y a c c o m p a n i e d by serious side effects, the m o s t i m p o r t a n t of which is p e r f o r a t i o n of the l u n g with c r e a t i o n of a p n e u m o t h o r a x . Since 1970, we h a v e e n c o u n t e r e d three cases in 443 p o s t m o r t e m e x a m i n a t i o n s . A review o f the recent l i t e r a t u r e failed to u n cover m e n t i o n of this serious c o m p l i c a t i o n , ~-13 a l t h o u g h the possibility o f its o c c u r r e n c e h a d been suggested by A b r a m s . ~4 A l u n g surface d e n s e l y a d h e r e n t to the chest wall is the m o s t likely s u b s t r a t e for p e r f o r a t i o n , b u t it is n o t a p r e r e q u i s i t e in p a t i e n t s with a "stiff l u n g " s y n d r o m e as d e m o n s t r a t e d by the three case r e p o r t s herein. W e define "stiff l u n g " as o n e with an i n t r i n s i c p a r e n c h y m a l lesion which has lost its n o r m a l resilience s e c o n d a r y to atelectasis, p n e u m o n i t i s , a n d / o r h y a l i n e m e m b r a n e disease. T h e d i a g n o s i s s h o u l d be suspected w h e n a p n e u m o t h o r a x fails to resolve despite p l a c e m e n t o f a chest t u b e in an i n f a n t with r e a s o n to have a "stiff l u n g " s y n d r o m e . CASE REPORTS
Case 1 (No. 011 79-80) K.A.M. was a 3000-g premature white male infant of 37-wk gestation born to a 20-yr-old primagravida mother, and admitted to Children's Orthopedic Hospital and Medical Center (COH&MC) at age 6 hr for respiratory distress. Labor had been induced by amniotomy after adequate cervical dilatation. The Apgar scores were 7 at 1 min and 8 at 5 min. Grunting respirations were present after birth. Admission blood gases while breathing 50~ 02 were pH 7.27; Pco, 56.1 mm Hg and Po, 42 mm Hg. Over the next 36 hr the infant became increasingly hypoxemic and acidotic despite being placed on the Bird respirator and increasing the inspired 02 concentrations. On the morning of the third hospital day the patient had a cardiorespiratory arrest, but was revived. Since postresuscitation radiographs demonstrated a left pneumothorax along with changes consistent with severe idiopathic respiratory distress syndrome (IRDS), a tube was placed in the left chest with subsequent minor improvement in blood gas values. Later the infant was noted to be hypoventilating on the right side and a right pneumothorax was diagnosed leading to placement of a polyethylene feeding tube in the right pleural cavity. Subsequent radiographs showed adequate parenchymal expansion and "good positioning" of the chest tube. Over the next few hours the child continued to deteriorate, with slowing of the heart rate to 40/min and increasing respiratory insufficiency. He died early on the fourth hospital day. At autopsy the combined lung weight was 100 g (expected 64 • 24 g). They were collapsed, firm, purple, normally lobated, and not adherent to the chest wall. A chest tube had perforated the right upper lobe (Fig. 1A). Microscopically, hyaline membrane disease was accompanied by From the Department of Pathology, University of Washington and Children's Orthopedic Hospital and Medical Center, Seattle, Wash. Arthur J. Wilson, M.D.: Resident in Pathology, University of Washington School of Medicine, Seattle, Wash. Henry F. Krous, M.D.: Instructor, Department of Pathology, University of Washington School of Medicine; Assistant Pathologist, Children's Orthopedic Hospital and Medical Center, Seattle, Wash. Address for reprint requests: Dr. Henry F. Krous, Children's Orthopedic Hospital and Medical Center, 4800 Sand Point Way NE, Seattle, Wash. 98105 9 1974 by Grune & Stratton, Inc. Journal of Pediatric Surgery, Vol. 9, No. 2 (April), 1974
213
214
WILSON AND KROUS
Fig. 1. (A) Photograph from Case 1 showing polyethylene feeding tube (used as a chest tube) passing through the right upper lobe of the lung. (B) Photograph from (~ase 2 showing a red rubber tube perforating the left upper lobe of the lung. Note that an unobstructed tube orifice is in the pleural space and remains functional. multiple small arterial thromboemboli, congestion, diffuse atelectasis, and focal bronchopneumonia. Cerebral hemorrhage, arising from the choroid plexus, was the terminal event.
Case 2 (No. 014-00-39) K.W. was a 2300-g premature white infant of approximately 35 wk gestation born to a non insulin-dependent gestational diabetic gravida II, para I, aborta 0 26-yr-old woman. Apgar scores were 6 at 1 min and 9 at 5 min. Shortly after birth the infant was transferred to C O H & M C for respiratory distress and hypoglycemia (27 mg/100 ml). Because o f rapidly progressive respiratory insufficiency (blood gases on 38~ 02: pH 7.329; Peo~ 48 mm Hg: Po~ 22 mm Hg) the Bird respirator was initiated with an F l 0 2 of 54~o. She subsequently developed bilateral pneumothorax for which number 17 and number 16 Rochester tubes were inserted. The chest tubes were "in place" by radiographic examination. The right pneumothorax appeared to resolve, but the left persisted, hence the left chest catheter was replaced with a number 14 red rubber tube resulting in a transient reexpansion of the left lung. Bilateral pneumothorax recurred and persisted on three subsequent chest radiographs despite the chest tubes being "in place." On the third hospital day her hematocrit fell from 4 0 ~ to 16~, she had multiple seizures, and died later in the day. At postmortem the right lung weighed 57.8 g and the left lung 37.3 g (expected 47 • 17 g combined) and lobation was normal. The firm, pale, and hypoexpanded lungs manifested interstitial emphysema, but no pleural adhesions. The left upper lobe had been perforated by the chest tube (Fig. IB). Microscopically, the immature lungs manifested atelectasis, congestion, and severe hyaline membrane disease. A cerebral hemorrhage arising in the subependymal germinal matrix was the terminal event.
Case 3 (No. 014-52-61) B.J.W. was a 2135-g premature white male infant of 39 wk gestation born to a 27-yr-old gravida II, para I-II female after an uneventful pregnancy. The 7-hr labor was spontaneous, and membranes were ruptured artificially 1 hr before birth, at which time the obstetrician noted oligohydramnios. The Apgar scores were 5 at 1 min and 7 at 5 min. Because the infant was anuric, cyanotic, and having intercostal retractions with grunting, he was transferred to C O H & M C at 2 hr of age. On admission here the infant was noted to have Potter's facies, and questionably palpable kidneys. Admission arterial blood gases while on 4 0 ~ oxygen were pH 7.21, Po~ 53 and Pco~ 89. Chest radiographs revealed bilateral pneumothorax and pneumomediastinum. A red rubber chest tube was placed in each hemithorax. The left chest tube was replaced within 1 hr because it was thought to be wedged between the heart and anterior chest wall. Postplacement radiographs revealed some reexpansion bilaterally, but a 50~ left pneumothorax persisted. Over
LUNG PERFORATION
215
the next 12 hr a nasotracheal tube was placed and the oxygen concentration was raised to 85~ with transient falls in the Po2 to 13 16 mm. Because of persistent anuria and suspected Potter's facies, dysmorphology consultation was obtained. They confirmed the diagnosis of Potter's syndrome. Renal arteriograms revealed bilateral nonfunctioning renal arteries. Late on the second hospital day, the infant was found dead. At autopsy the lungs were hypoplastic, firm, atelectatic, and not adherent to the chest wall. A red rubber chest tube had perforated the left upper lobe. Pulmonary hyaline membranes and mild pneumonitis were present microscopically. In addition, bilateral Potter's type ll polycystic kidneys and associated malformations16 were noted, along with disseminated intravascular fibrin thrombi. Acute cerebral edema with cerebellar tonsillar herniation was considered the cause of death. DISCUSSION
Because of the resiliency of normal lung p a r e n c h y m a and compressibility of the gas within the alveoli, it is easily distorted and displaced by extrinsic pressure. Thus, the proper insertion of a chest tube rarely causes perforation in a normal lung. Adherence of the lung to the chest wall may result in lung perforation from chest tube insertion. The cases in this report demonstrate that a "stiff lung" due to p u l m o n a r y atelectasis, hyaline membrane disease, a n d / o r pneumonia which is not adherent to the chest wall is subject to perforation since the decrease in pliability will not allow it to be displaced. The perforation appears to occur because with partial or total collapse of alveoli or filling of alveoli with hyaline membranes or products of infection, the lung becomes a firm nonpliable tissue mass. The antemortem diagnosis was not made in any of these cases. It should be suspected in a patient with known cause for a "stiff lung" syndrome in whom a p n e u m o t h o r a x does not resolve normally. The surgeon should maintain a high index of suspicion while placing or removing the chest tube and be aware that any sudden "give" during placement may signal perforation in such a patient. The details of introduction of the tube were not recorded in any of these cases, hence relative safety of one method versus another cannot be commented upon. If some of the chest tube orifices remain unobstructed in the pleural space (Fig. 1B), the catheter will function, obscuring the fact that lung has been penetrated. Subsequent removal may bring about unexpected reestablishment of pneumothorax a n d / o r hemorrhage. Hence, frequent examinations are indicated in the postremoval interval. That insertion of a chest tube is not a totally innocuous procedure is further attested to by the report of a traumatic arteriovenous fistula between the chest wall and lung created by intercostal catheter placement) 6 With the establishment of many premature and neonatal intensive care units around the country, a large patient population with "stiff lung" syndrome will require drainage of p n e u m o t h o r a x by insertion of intercostal catheters. This complication should be kept in mind and if the diagnosis is made, then appropriate chest tube maneuvers should be instituted. SUMMARY
Three necropsy cases, two premature infants with idiopathic respiratory distress syndrome and one with Potter's syndrome with p u l m o n a r y hypoplasia, sustained lung perforation during insertion of a chest tube for pneumothorax.
216
WILSON AND KROUS
I n n o n e o f t h e c a s e s w a s t h e d i a g n o s i s m a d e d u r i n g life. P e r f o r a t i o n
should be
suspected when a pneumothorax fails t o r e s o l v e o r h e m o t h o r a x d e v e l o p s a f t e r p l a c e m e n t o f a c h e s t t u b e in a c h i l d w i t h r e a s o n t o h a v e a " s t i f f l u n g " s y n d r o m e .
REFERENCES 1. Bernard WF, Maleom JA, Berry RW: A study of the pathogenesis and management of spontaneous pneumothorax. Dis Chest 42:403 412, 1962 2. Borja, AR, Ransdell, HT: Treatment of penetrating gunshot wounds of the chest. Experience with 145 cases. Am J Surg 122:81-84, 1971 3. Hilty-Tammiuaara R, SegerstriSm A: Choice of therapy in spontaneous pneumothorax in relation to later cardiopulmonary function. Scand J Resp Dis 51:93-104, 1970 4. Harbord RP, Homi J: Respiratory failure from contralateral pneumothorax and atelectasis. JAMA: 1179 1181, 1970 5. Yancy WS, Spock A: Spontaneous neonatal pleural effusion. J Pediatr Surg 2:313-319, 1967 6. Weech AA: Lung puncture and aspiration. Am J Dis Child 122:277, 1971 7. Angevine JM: Pneumothorax and aspiration. Arch Pathol 91:288, 1971 8. Glotzer D J: Pseudopneumothorax with "underwater-seal" pleural drainage. N Engl J Med 284:1388, 1971
9. Seremetis G: The management of spontaneous pneumothorax. Chest 57:65 68, 1970 10. Van De Water JM: The treatment of pleural effusion complicating pneumonia. Chest 57:259-1262, 1970 11. Aslam PA, Eastridge CE, Hughes FA Jr: Insertion of the apical chest tube. Surg Gynecol Obstet 130:1097 1098, 1970 12. Trapnell DH, Thurston JG: Unilateral pulmonary oedema after pleura[ aspiration. Lancet 1:1967-1969, 1970 13. Childress ME, Moy G, Mottram M: Unilateral pulmonary edema resulting from treatment of spontaneous pneumothorax. Am Rev Resp Dis 104:119-121, 1971 14. Abrams LD: Chest injuries. Br J Surg 56: 722-723, 1969 15. Osathanondh V, Potter EL: Pathogenesis of polycystic kidneys: Type 2 due to inhibition of ampullary activity. Arch Pathol 77:474-484, 1964 16. Cox A, Keshishian JM, Blades BB: Traumatic arteriovenous fistula of the chest wall and lung. J Thorac Cardiovasc Surg 54:109112, 1967.