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The development of a spontaneous pneumoperitoneum during artificial pneumothorax therapy
AND
DISEASES
OF
THE
CHEST
129
THE DEVELOPMENT OF A SPONTANEOUS PNEUMOPERITONEUM DURING ARTIFICIAL PNEUMOTHORAX THERAPY A. W . ANDERSON AND R. GRENVILLE-IV[ATHERS From the Harrow Chest Clinic, N.W. Metropolitan Regional Hospital Board
THE occurrence of a spontaneous pneumoperitoneum as a complication of artificial pneumothorax therapy is believed to be sufficiently uncommon to warrant placing on record the details of the following case. The patient, a male aged twenty-three, had pulmonary tuberculosis with cavitation involving the middle zone of the right lung. After two months' bed rest a right phrenic crush was performed followed b y induction of a pneumoperitoneum. T w o months later a right artificial pneumothorax was induced and, following pneumonolysis, the pneumoperitoneum was abandoned. Just before discharge from sanatorium a right phrenic avulsion was performed. The artificial pneumothorax was maintained without difficulty for the next six months, refills being done weekly through the third intercostal space in the anterior axillary line. O n e day, six months after the phrenic avulsion and about five hours after a refill, the patient experienced a sudden tearing sensation in the abdomen followed by the same vague feeling of discomfort which he had experienced during artificial pneumoperitoneum therapy. H e attended the clinic two days later, when examination failed to reveal any evidence of surgical emphysema, but screening showed a very shallow right artificial pneumothorax and air below the diaphragm. There was no fluid in the right pleural sac nor was there any evidence of mediastinal emphysema. The following are the weekly pressures and amounts of air given for the six refills up to an including the one followed by the development of the pneumoperitoneum. _Initial Pressu~
Amount o f A # m c.~
Final Pressure
- xo
-4
3° o
-8
-3
-
-4 -5
35o 600
-8 -8
-3 -2
- x6 - io - x5 - 9
6oo 5oo
-8 -4 - 8 -
-
50o
-6
xo x3
xo
-5
-3
It will be observed that at no time was the pressure in the~pleural sac above zero. The pneumoperitoneum absorbed steadily, while refills of the artificial pneumothorax were continued at weekly intervals. The artificial pneumothorax was eventually abandoned as ineffective, owing to the formation of extensive adhesions, when most of the air escaped into the peritoneal sac. The occurrence of a spontaneous pneumothorax, usually on the right side, as a complication of artificial pneumoperitoneum therapy, has been described
I30
T H E B R I T I S H J O U R N A L OF T U B E R C U L O S I S
several times (Banyai, i946; Simmonds, i946; Mellies, i939). This occurrence, when refills have been done through the anterior abdominal wall and not through the lower intercostal spaces, has been ascribed to: (x) Air entering the mediastinum from the abdomen and thence bursting into the pleural space (Simmonds, i946). (2) Defects in the peritoneal covering of the under surface of the diaphragm (Laird, I945). (3) The passage of air alongside one of the mediastinal structures passing through the diaphragm (Banyai, i946 ). (4) The abnormal persistence of a pleuro-peritoneal canal (Sita-Lumsden, ~949). In all these cases, and in the two cases already described of a pneumoperitoneum developing during artificial pneumothorax therapy (Banyai, 1943), the air contained in the original cavity has been at a positive pressure, whereas in the case here described the pressure was negative. Anatomically the diaphragm is a complex structure with a fourfold origin: (i) Its central portion from the septum transversum, (2) its lateral parts from the pleuro-peritoneal membranes, plus (3) derivatives from the body wall and (4) a median dorsal portion from the dorsal mesentery. Defects in this structure occur from imperfect development of the pleuro-peritoneal membrane and are usually found on the left side. The passage of air through such a defect would be facilitated by a phrenic avulsion with its consequent muscular atrophy, although why air should pass through such a defect on only one single occasion is not evident, since no pleural exudate developed which conld have sealed the opening. It is presumed that the defect did not become evident while the artificial pneumoperitoneum was originally present, owing t o some muscle tissue still remaining following the phrenic crush. After the phrenic avulsion had been performed the muscular tissue would atrophy completely (since it is questionable if the lower thoracic nerves have any share in the motor innervation of the diaphragm), and the rise in intra-pleural pressure which occurs during coughing could be sufficient to cause air to leave the pleural space and pass into the peritoneal sac.
Summary A case of spontaneous pneumoperitoneum occurring during artificial pneumothorax therapy is described. The cause of this is presumed to be a developmental defect in the diaphragm which only became evident following muscular atrophy occurring as a result of the operation of phrenic avulsion. REFERENCES
BANYAI,A. L. (I946): Pneumoperitoneum Treatment. St. Louis: C. V. Mosby and Co. BAZWVAXA. , L. (x943): Amer. 07. Med. S~i., 186, 5x3. LAIRD,R. (I945)" Tubercle, 26, I49. SXMMONDS,F. A. H. (x946): Lancet, 1, 53o. SXTA-LUMSDEN,E. G. (I949): Thorax, 4, I47.
DISEASES
OF
THE
CHEST
129
THE DEVELOPMENT OF A SPONTANEOUS PNEUMOPERITONEUM DURING ARTIFICIAL PNEUMOTHORAX THERAPY A. W . ANDERSON AND R. GRENVILLE-IV[ATHERS From the Harrow Chest Clinic, N.W. Metropolitan Regional Hospital Board
THE occurrence of a spontaneous pneumoperitoneum as a complication of artificial pneumothorax therapy is believed to be sufficiently uncommon to warrant placing on record the details of the following case. The patient, a male aged twenty-three, had pulmonary tuberculosis with cavitation involving the middle zone of the right lung. After two months' bed rest a right phrenic crush was performed followed b y induction of a pneumoperitoneum. T w o months later a right artificial pneumothorax was induced and, following pneumonolysis, the pneumoperitoneum was abandoned. Just before discharge from sanatorium a right phrenic avulsion was performed. The artificial pneumothorax was maintained without difficulty for the next six months, refills being done weekly through the third intercostal space in the anterior axillary line. O n e day, six months after the phrenic avulsion and about five hours after a refill, the patient experienced a sudden tearing sensation in the abdomen followed by the same vague feeling of discomfort which he had experienced during artificial pneumoperitoneum therapy. H e attended the clinic two days later, when examination failed to reveal any evidence of surgical emphysema, but screening showed a very shallow right artificial pneumothorax and air below the diaphragm. There was no fluid in the right pleural sac nor was there any evidence of mediastinal emphysema. The following are the weekly pressures and amounts of air given for the six refills up to an including the one followed by the development of the pneumoperitoneum. _Initial Pressu~
Amount o f A # m c.~
Final Pressure
- xo
-4
3° o
-8
-3
-
-4 -5
35o 600
-8 -8
-3 -2
- x6 - io - x5 - 9
6oo 5oo
-8 -4 - 8 -
-
50o
-6
xo x3
xo
-5
-3
It will be observed that at no time was the pressure in the~pleural sac above zero. The pneumoperitoneum absorbed steadily, while refills of the artificial pneumothorax were continued at weekly intervals. The artificial pneumothorax was eventually abandoned as ineffective, owing to the formation of extensive adhesions, when most of the air escaped into the peritoneal sac. The occurrence of a spontaneous pneumothorax, usually on the right side, as a complication of artificial pneumoperitoneum therapy, has been described
I30
T H E B R I T I S H J O U R N A L OF T U B E R C U L O S I S
several times (Banyai, i946; Simmonds, i946; Mellies, i939). This occurrence, when refills have been done through the anterior abdominal wall and not through the lower intercostal spaces, has been ascribed to: (x) Air entering the mediastinum from the abdomen and thence bursting into the pleural space (Simmonds, i946). (2) Defects in the peritoneal covering of the under surface of the diaphragm (Laird, I945). (3) The passage of air alongside one of the mediastinal structures passing through the diaphragm (Banyai, i946 ). (4) The abnormal persistence of a pleuro-peritoneal canal (Sita-Lumsden, ~949). In all these cases, and in the two cases already described of a pneumoperitoneum developing during artificial pneumothorax therapy (Banyai, 1943), the air contained in the original cavity has been at a positive pressure, whereas in the case here described the pressure was negative. Anatomically the diaphragm is a complex structure with a fourfold origin: (i) Its central portion from the septum transversum, (2) its lateral parts from the pleuro-peritoneal membranes, plus (3) derivatives from the body wall and (4) a median dorsal portion from the dorsal mesentery. Defects in this structure occur from imperfect development of the pleuro-peritoneal membrane and are usually found on the left side. The passage of air through such a defect would be facilitated by a phrenic avulsion with its consequent muscular atrophy, although why air should pass through such a defect on only one single occasion is not evident, since no pleural exudate developed which conld have sealed the opening. It is presumed that the defect did not become evident while the artificial pneumoperitoneum was originally present, owing t o some muscle tissue still remaining following the phrenic crush. After the phrenic avulsion had been performed the muscular tissue would atrophy completely (since it is questionable if the lower thoracic nerves have any share in the motor innervation of the diaphragm), and the rise in intra-pleural pressure which occurs during coughing could be sufficient to cause air to leave the pleural space and pass into the peritoneal sac.
Summary A case of spontaneous pneumoperitoneum occurring during artificial pneumothorax therapy is described. The cause of this is presumed to be a developmental defect in the diaphragm which only became evident following muscular atrophy occurring as a result of the operation of phrenic avulsion. REFERENCES
BANYAI,A. L. (I946): Pneumoperitoneum Treatment. St. Louis: C. V. Mosby and Co. BAZWVAXA. , L. (x943): Amer. 07. Med. S~i., 186, 5x3. LAIRD,R. (I945)" Tubercle, 26, I49. SXMMONDS,F. A. H. (x946): Lancet, 1, 53o. SXTA-LUMSDEN,E. G. (I949): Thorax, 4, I47.