On ausculta- tion of the left side of the thorax increased breath sounds were heard. On the right, respiratory sounds were decreased in intensity. Percussion of.
ISSN 0008-5286
THE CANADIAN VETERINARY JOURNAL Volume 23
LA REVUE VtTERINAIRE CANADIENNE October-octobre
No.10
CASE REPORT
Recurrent Pneumothorax Associated with a Pulmonary Emphysematous Bulla in a Dog: Surgical Correction and Proposed Pathogenesis L. STOGDALE, C.D. O'CONNOR, M.C. WILLIAMS AND M.M.S. SMUTS
Department of Medicine (Stogdale), Department of Pathology (Williams), Department of Anatomy (Smuts), Faculty of Veterinary Science, University of Pretoria, Onderstepoort, Republic of South Africa and 101 Valley View Avenue, Morningside, Durban, Republic of South Africa (O'Connor) Summary A three year old dog was affected with recurrent dyspnea for two months, due to a recurrent pneumothorax. This followed an episode of mild blunt trauma to the .thorax and transient strangulation. Conservative therapy of aspiration of air by repeated thoracentesis gave only temporary relief. Thoracic radiographs indicated the presence of a bulla in the right middle lung lobe. An exploratory thoracotomy confirmed the diagnosis, and a lobectomy was successfully performed. The pathogenesis of acquired pulmonary bullae is postulated. Reasons for the predisposition of the right middle lung lobe are outlined. These are related to the anatomy of the right middle bronchus, and include its position between the right pulmonary artery and vein, its oval shape, and the absence of cartilagenous support at its origin.
une dyspnee recurrente, imputable a un pneumothorax recurrent. La condition resultait d'un leger traumatisme du thorax, avec un objet mousse, et d'une strangulation passagere. La therapie conservatrice d'aspiration d'air, par des thoracenteses repetees, ne procura qu'un soulagement temporaire. Des radiographies du thorax revelerent la presence d'une bulle d'air dans le lobe pulmonaire moyen droit. Une thoracotomie exploratrice permit de confirmer cette constatation et on proceda avec succ's a l'excision du lobe emphysemateux. Les auteurs presentent leur conception de la pathogenese des bulles d'air pulmonaires acquises. Selon eux, la predisposition du lobe pulmonaire moyen droit resulterait du fait que la bronche moyenne droite passe entre l'artere et la veine pulmonaires droites, qu'elle est de forme ovale et que son point d'origine est depourvu d'un support cartilagineux.
or acquired. Congenital pulmonary cysts are of bronchial origin, and are therefore lined with respiratory epithelium. Acquired bullae and blebs result from alveolar wall rupture, frequently in association with a check valve (oneway) obstruction in the air passage. Cysts, or pneumatoceles, are also associated with pneumonia, bronchiectasis, abscesses, or tumors (2,3). Closed pneumothorax occurs when the integrity of the visceral pleura is disrupted. This may be caused by blunt trauma, infection, neoplasia, or by rupture of cystic or emphysematous lung tissue. The clinical findings, course, radiographic appearance and treatment of a dog affected with a recurrent pneumothorax caused by a bulla in the right middle lung lobe are described in this report. The etiology of pulmonary bullae, pathogenesis, and the reasons for the predisposition of the right middle lobe to this lesion, are discussed.
Resume' Pneumothorax recurrent, d8 a une bulle emphysemateuse pulmonaire, chez une chienne; sa correction chirurgicale et une conception de sa pathogenese Pendant deux mois, une chienne castree et agee de trois ans manifesta
Introduction Pulmonic cystic lesions occasionally occur in the dog. Such lesions do not cause signs unless they are so extensive as to cause respiratory embarrassment, or rupture resulting in a pneumothorax (1). Cysts may be congenital
History A three year old neutered female mixed breed Terrier, weighing 5.0 kg, was presented to a veterinarian because of breathing difficulties. The patient had been normal prior to a minor traumatic incident nine days
Present address of Dr. Stogdale: Department of Veterinary Internal Medicine, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N OWO.
Can. vet. J. 23: 281-287 (October 1982)
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previously. The little dog had been tied to a chair and in pulling it over onto herself had become entangled in her leash. She had collapsed, presumably due to strangulation, but had appeared to recover when she was released. Veterinary examination revealed severe dyspnea, cyanosis, and an increase in resonance on percussion of the right thorax. Air was removed by thoracentesis. This resulted in a significant improvement in the patient's condition. The signs recurred six weeks later, and a severe pneumothorax was seen on thoracic radiographs obtained at this time. Thoracentesis was repeated to remove the air, and the dog was referred to the Faculty of Veterinary Science for further investigation.
Clinical and Radiographic Findings On admission, the dog's habitus and general condition were good. She was willing to walk but dyspneic. The respiratory rate was 100/ min with forced abdominal expiration. On auscultation of the left side of the thorax increased breath sounds were heard. On the right, respiratory sounds were decreased in intensity. Percussion of the left thorax was normal ventrally, but slightly resonant dorsally. On the right side, markedly increased resonance was evident over the entire lung field. The mucus membranes were slightly congested, and the capillary refill time was delayed to 35s. The heart rate was 180/min. The heart sounds could be heard normally on the left side, while on the right, they sounded resonant. There was no pulse deficit, and its character was normal. No other significant physical findings were evident. The hematology results showed an absolute polycythemia. The leukon, blood urea nitrogen, total serum protein, serum liver enzyme levels, urinalysis and fecal analysis were all normal. Survey radiographs were obtained, with care being taken not to stress the dog. The lateral radiograph, taken at full inspiration, showed a fairly severe, bilateral pneumothorax, with secondary collapse of the lungs, and a flattening of the diaphragmatic curvature (Figure 1). A large, thin-walled radiolucent structure approximately 6.0 cm long and 3.0 cm across at its widest 282
FIGURE 1. Lateral radiograph of the thorax, taken at full inspiration. There is a severe, bilateral pneumothorax, and lung collapse. A large radiolucent bulla (arrows) extends from ventral to the tracheal bifurcation to the cranial surface of the diaphragm.
part, extended from 2.5 cm ventral to the tracheal bifurcation in a caudal direction. It was roughly pear-shaped, with the apex located cranially, and the wide rounded base, caudally. This structure extended well beyond the periphery of the collapsed lung. Two smaller spherical radiolucent structures, of a similar appearance, were located between the apex of the large bullous lesion, and the tracheal bifurcation. Their walls were only partly visible. The radiolucent appearance of
all these structures indicated that they contained air, and not fluid. A diffuse density, stretching from the tracheal bifurcation in a caudal direction, dorsal to the bullous lesions, and measuring 5.0 cm by 1.5 cm, suggested the possibility of pulmonary atelactasis of a middle lung lobe. The dorsoventral radiograph confirmed the bilateral pneumothorax, and the bullous lesion in the middle lobe of the right lung (Figure 2). The long axis of the bulla stretched in a
04,40'.
FIGURE 2. Dorsoventral radiograph of the thorax, taken at full inspiration. There is severe, bilateral pneumothorax. The bulla in the right middle lobe (arrows) occupies most of the caudal half of the right hemithorax. Dextrocranial to the right atrium is a density suggestive of lung atelectasis surrounding the main right lobe bronchus.
caudolateral direction for 6.5 cm. Septae were visible within the bulla, but the smaller bullae, seen on the lateral radiograph, were not visible. The apex of the lesion was associated with a well demarcated oval shaped tissue density, 2.5 cm long and 1.0 cm wide. This density was located dextrocranial to the right atrium. An air-filled tube was evident centrally, in the caudal half of the density, suggesting the possibility of pulmonary atelectasis around the main right middle lobe bronchus. Rib abnormalities were not evident. The radiographic diagnosis was a bullous lesion of the right middle lung lobe, complicated by atelectasis of the lobe, and pneumothorax. Thoracentesis was performed using an 18 gauge needle. Approximately 1.0 L of air was removed from the right pleural space, and 0.1 L was aspirated from the left side. An immediate decrease in the severity of the dyspnea was noted, and the respiratory rate decreased to 70/ min. The radiographic examination was repeated. Considerable pneumothorax was still present. The smaller bullous lesions were no longer evident, but the large bulla appeared to have increased in size, and was now seen to extend to the thoracic wall, on the dorsoventral radiograph (Figure 3). The pulmonary density, at the apex of the bulla, had assumed a more rounded shape. Additional, poorly demarcated densities were present in the right hilar area, and were obscuring part of the right cardiac outline. Based on the history, and the physical, clinicopathological and radiographic findings, a diagnosis of pulmonary bulla or cyst, with recurrent pneumothorax, was made. Surgical intervention was considered to be necessary, as the problem had not been resolved by means of conservative therapy. Treatment During the two days prior to surgery procaine penicillin,' 20 000 IU/kg/d was injected subcutaneously, and
FIGURE3. Dorsoventral radiograph ofthe thorax, taken at full inspiration, after 1.0 L ofair had been removed from the pleural cavity by thoracentesis. Pneumothorax is still present. The bulla in the right middle lobe (arrows) has enlarged, now extending to the thoracic wall. A number ofdensities in the right middle lobe are partially obscuring the right cardiac outline.
0.4 L of air was aspirated from the pleural cavity. On the day of surgery, a 14 gauge through-the-needle catheter2 was inserted into the right pleural cavity, and connected to a water-trap, hydrostatic siphon suction system (4,5). After 0.6 L of air was removed, the catheter was left connected to the suction apparatus to maintain negative intrapleural pressure, and thus minimize the anesthetic risk. Into the right jugular vein, a 14 gauge throughthe-needle catheter2 was inserted, and a continuous slow infusion of isotonic electrolyte solution3 was commenced (2 mL/ min). A central venous pressure (CVP) was connected: the dog's CVP was normal, namely, 5 cm H20. The dog's bladder was catheterized, and the urine output was monitored (4,5). Ampicillin sodium,4 50 mg/ kg was injected intravenously, and atropine sulphate, 0.04 mg/kg, was given subcutaneously. General anesthesia was induced using 5 mg/kg thiopentone sodium5 intravenously, as a 2.5% solution. The
dog was rapidly intubated, and anesthesia was maintained with 0.5-1.0% halothane6 in oxygen, delivered by means of a semiclosed system. A thoractomy was performed, incising through the fifth intercostal space on the right side. When the chest was opened, positive pressure respiration was instituted at a rate of 10/ min. At this time, the CVP decreased to -2 cm H20, and the urine output ceased. To counteract the hypotension, the rate of fluid therapy was increased to 15 mL/min and 100 mg prednisolone sodium succinate7 was given intravenously. The middle lobe of the right lung was grossly enlarged, due to a single large bulla (6 x 4 x 4 cm) (Figure 4). This was surrounded by a thin rim of lung tissue which appeared to be emphysematous. No other gross pathology was evident within the right hemothorax. A lobectomy was performed, and the entire lobe was placed in a 10% formaldehyde solution. The thoracic incision was sutured routinely. The residual air was
'Novocillin, Novo Industries, Johannesburg, South Africa. 2Venecath, Abbott Laboratories S.A. (Pty.) Ltd., Johannesburg, South Africa. 3Lactated Ringer's Injection, U.S.P., Baxter Travenol Laboratories, Inc., Deerfield, Illinois, U.S.A. 4Penbritin, Beecham Research Laboratories, Johannesburg, South Africa. 5lntraval Sodium, Maybaker (S.A.) (Pty.) Ltd., Port Elizabeth, South Africa. 6Fluothane, I.C.I. South Africa (Pharmaceuticals) Limited, Johannesburg, South Africa. 7Solu-Delta-Cortef, The Upjohn Company, Kalamazoo, Michigan, U.S.A.
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FIGURE 4. The middle lobe of the right lung, prior to its removal. The air-filled bulla occupies most of the lobe cranially (to the right). It is surrounded by emphysematous lung tissue.
removed by the siphon pump, via the catheter which was replaced in the right pleural cavity. Positive pressure respiration was then stopped, spontaneous respiration resumed, and the dog was taken off the anesthetic machine. She was immediately placed in an intensive care cage which contained oxygen-rich air. The CVP was 1 cm H20, the capillary refill time was slightly delayed, and the urine output was 0.5 mL/ kg/ h. The isotonic electrolyte solution was replaced by 5% dextrose8 in order to stimulate urine production. The rate of fluid administration was maintained at approximately 14 mL/ min. Postoperatively, tilidine hydrochloride drops,9 1 mg/ kg were given orally for pain, and ampicillin sodium,'0 50 mg/ kg, was injected intravenously. Within half an hour of the completion of surgery, the CVP had risen to 4 cm H20, and the urine output was 2 mL/kg/h. At this time, the patient had recovered from anesthesia, and was lying quietly. Her respiratory rate was 48/min, and normal in character. The heart rate was 120/min, and the pulse quality and capillary refill time were normal. The rate of fluid adminis-
tration was slowed to 2 mL/ min. The patient's recovery proceeded satisfactorily: she was breathing room air, her cardinal signs were stable, and she was ambulatory five hours after the completion of surgery. Isotonic electrolyte solution" was given at maintenance rate, 60 mL/kg/d, for another day, and ampicillin sodium'2 was continued for two more days. The following day, the patient was alert and active. Her respiratory rate was 44/ min, her heart rate was 116/min, and the pulse was strong. The dog was walked, and coughing was elicited in order to stimulate the removal of any blood or mucus present in the respiratory tract. Two days after the surgery, the patient was fully recovered. On the third postoperative day, follow-up urinalysis, hematology, and thoracic radiographs were obtained. The urine and hematology were normal. The thoracic radiographs showed the presence of a small amount of pleural effusion, as evidenced by the fissure lines separating the lung lobes, both dorsal and ventral to the tracheal bifurcation (Figure 5). The lung lobes were now fully inflated,
Pathological Findings The right middle lobe bronchus opened into a single large bulla, which occupied the whole lobe except for a peripheral rim of lung tissue (Figure 4). This peripheral zone was 0.5-1.0 cm in width, and had alveolar emphysema. Within the bulla, septa of connective tissue stretched radially from the bronchus to the inner surface of the bulla. Microscopically, the bronchiolar walls were thickened as a result of peribronchiolar fibroplasia, and there was dystrophic calcification in a number of areas (Figure 6). Severe emphysema was present in the peripheral rim of lung tissue, resulting in the formation of large pseudoalveoli. The walls of the pseudoalveoli were markedly thickened as a result of fibroplasia and smooth muscle hyper-
FIGURE5. Lateral radiograph of the thorax, taken at full inspiration, three days postoperatively. The fissure lines between the lung lobes (arrows) indicate the presence of a small amount of pleural effusion. The lungs are fully inflated, and no localized lesions are visible.
85% Dextrose, Baxter Travenol Laboratories, Inc., Deerfield, Illinois, U.S.A. 9Valoron, Warner Pharmaceuticals (Pty.) Ltd., Millbrow, South Africa. '°Penbritin, Beecham Research Laboratories, Johannesburg, South Africa. "Lactated Ringer's Injection, U.S.P., Baxter Travenol Laboratories, Inc., Deerfield, Illinois, U.S.A. '2Penbritin, Beecham Research Laboratories, Johannesburg, South Africa.
284
and no localized radiolucent or radiodense lesions were evident. Based on these results, the dog was discharged. A month later, the patient was clinically normal, and has shown no evidence of recurrence of a respiratory problem.
FIGURE 7. Photomicrograph of the affected lung lobe, showing the severe emphysema. Smooth muscle hyperplasia is present in some alveolar walls, and around the bronchiole (upper left). H & E.
tured, and the inherent elasticity of the lung parenchyma recoils, resulting in an air-filled cavity of several centimetres in diameter. Thus, their walls are not lined by an epithelium, such as is present in congenital cysts of bronchial origin. By definition, bullae are located within the lung tissue, while blebs lie between the visceral pleura and the pulmonary parenchyma (1,2,3). The lesion present in the subject of this report was a bulla, surrounded by alveolar emphysema. There are four theories as to the cause of pulmonary bullae. Undoubtedly bullae in different animals have differing etiologies, although most are diagnosed following blunt thoracic trauma, when respiratory distress occurs, and thoracic radiographs are taken. Some bullae may be congenital (7). Fagan (10) has described acquired pulmonary bullae in three humans following trauma; previous chest radiographs being normal. He has postulated the pathogenesis to be a sudden compression of an area of lung tissue, resulting in collapse of a portion of the bronchial tree. This would cause a sudden increase in the intra-alveolar pressure with consequent rupture of the lung lobule supplied by the occluded bronchus. Alternative theories are that either direct physical force could rupture alveolar septa (11); or that blunt chest trauma could cause a concussion wave, which would create shearing stresses of sufficient strength to tear alveolar walls (12). Thus, bullae may arise when alveolar walls are damaged by congenital malformation, bursting (increased air pressure), rupture (direct physical force), or shearing (disparate tissue stresses). In the dog described in this report, we postulate that the cause of the pulmonary bulla was mild trauma (a chair falling over on the small dog), together with transient closure of the glottis (temporary strangulation by her leash). Thus, the sudden increase in intra-alveolar air pressure could not be dissipated, causing bursting of the alveolar walls. The pathogenesis of bulla maintenance, enlargement, and rupture resulting in pneumothorax, has not yet been elucidated in either humans or dogs. However, the most likely cause is a valvular or partial obstruction of an
X1OO.
airway which causes air trapping
FIGURE 6. Photomicrograph of the right middle lobe main bronchus showing marked thickening of the bronchial wall as a result of peribronchial fibroplasia. H & E. XIOO.
plasia of the terminal bronchioles and alveolar ducts (Figure 7). Scattered foci of interstitial round cell infiltration, mainly lymphocytes and macrophages, as well as a few neutrophils, were observed. The final diagnosis was an acquired bulla of the right middle lung lobe, resulting in a recurrent pneumothorax. Discussion The occurrence of cavity pulmonary lesions in animals has been reviewed
(2), and the definitions of these various lesions have been fully described (2,3). Bullae are only rarely diagnosed in dogs as they usually do not cause clinical signs (1,2). Their presence only becomes apparent when they rupture, resulting in a spontaneous pneumothorax or pneumomediastinum (1,2, 3,6,7,8,17) or when they become very large, causing a space-occupying lesion within the thoracic cavity (9). Bullae or emphysematous bullae are formed when alveolar walls are rup-
285
TABLE I THE REPORTED LOCATION OF PULMONARY BULLAE IN DOGS
Lung Lobe Multiple lobes Right cranial lobe Right middle lobe Right caudal lobe Left cranial lobe Left caudal lobe Total
Reference 2, 3, 6 2 1, 2, 7, 8, 13 this report 1, 2, 9 2 2
Number of Bullae (congenital and acquired), (%) 7 (33.3%) 2 ( 9.5%) 7 (33.3%) 3 (14.3%) 1 ( 4.8%) 1 ( 4.8%) 21 (100%)
Number of (suspected) Acquired
Bullae, (%) 7 (53.8%) 0 5 (38.5%) 1 ( 7.7%) 0 0 13 (100%)
bronchi, has virtually no cartilagenous support at its origin, and so it collapses and closes with very little external pressure. These three factors, the position between the right pulmonary artery and vein, the oval shape, and the abscence of cartilagenous support, predispose this bronchus to collapse. In the dog described in this report, it appears that a minor traumatic incident damaged the lung parenchyma, and due to the inherent predisposition of the right middle lobe bronchus to collapse, a check valve was formed. This resulted in the maintenance and enlargement of the bulla, and a buildup of intralobar pressure, until finally the visceral pleura was ruptured. A slow leakage of air into the pleural cavity continued, as a result of the valvular action of the bronchial opening. Thus, in this case, a total lobectomy was necessary to remove the cause of the pneumothorax, and so
(2,13). The air becomes trapped when bronchus lies between the pulmonary either bronchial damage results in a artery dorsally, and the pulmonary check (one-way) valve, or when collat- vein ventrally (16). eral ventilation, through the pores of Upon examination of a number of Kohn, permits air to enter the area canine cadavers, we observed that the during inspiration, but prevents it right middle bronchus, at its origin, is from escaping during expiration (1). oval in shape. The narrowest diameter From the gross and histopathological is in the dorsoventral plane, and the findings in our patient's right middle widest diameter is in the craniocaudal lung lobe, it appears that a check valve direction (Figure 9). In addition, this was present in the lobar bronchus. bronchus, in contrast to all the other Collapse of a bronchus at expiration can be caused by damage to the supportive tissues in the bronchial wall, or may be due to a constitutional weakness (13). From a review of the literature describing pulmonary bullae in dogs (Table I), it is evident that the most common distribution of bullae in dogs is in multiple lobes, associated with moderate to severe trauma, and pulmonary contusion (2,3,6). However, the right middle lobe is obviously predisposed to the formation of this lesion: 38.5% of suspected acquired single bullae occurred in this lobe (1,2,7,8,13). Interestingly, this lobe is also more susceptible than the other lobes to collapse and pneumonia (14), and to torsion (15). The right middle lobe bronchus branches from the principal bronchus just caudal to the base of the heart (Figure 8). The right pulmonary artery, after supplying branches to the cranial lobe, runs in a caudal direction, across the dorsal surface of the origin of the middle bronchus. It then enters the caudal lobe. The artery to the middle lobe courses along the dorsocranial surface of the bronchus. The vein from this lobe lies along the cranioventral FIGURE8. The lungs and heart from a normal dog, viewed from the cranio-lateral aspect, on the right aspect of the bronchus, and joins the side. The right cranial lobe, and the cranial half of the middle lobe have been removed. The right pulmonary vien ventrally to the pulmonary blood vessels have been dissected out. The right pulmonary artery (PA) can be seen origin of the middle lobe bronchus. crossing dorsally over the origin of the middle bronchus (MB). Alongside the right middle bronchus, Thus, the origin of the right middle the middle lobar artery (MLA) lies craniodorsally, and the vein (MLS) lies cranioventrally. 286
6.
7.
CrB
8. 9.
MB
10.
11. 12.
13.
FIGURE9. The bronchial origins of the right lung of a normal dog, viewed from the dorsal aspect. The dorsum of the right bronchus and trachea have been removed. The cranial bronchus (CrB), and the caudal bronchus (CdB) are round in shape, while the middle bronchus (MB) is oval at its origin.
equipment utilization. In: Sattler FP, Knowles RP, Whittick WG, eds. Veterinary critical care. Philadelphia: Lea & Febiger, 1981: 97-100. BARBER DL, HILL BL. Traumatically induced bullous lung lesions in the dog: a radiographic report of three cases. J Am Vet Med Assoc 1976; 169: 1085-1089. TEUNISSEN GHB. Spontaneous pneumothorax. Kleintier-Praxis, 1972; 17: 61-65. ELWOOD GS. What is your diagnosis? J Am Vet Med Assoc 1958; 133: 37-38. BRUGA RD, RATHFON BL. What is your diagnosis? J Am Vet Med Assoc 1970; 156: 366-368. FAGAN ci. Traumatic lung cyst. Am J Roentgerol Radium Ther Nucl Med 1966; 96: 186-194. JOYNT GHC, JAFFE F. Solitary pulmonary hematoma. J Thorac Cardiovasc Surg 1962; 43: 291-302. WILLIAMS JR, BONTE FJ. Plumonary damage in nonpenetrating chest injuries. Radiol Clin North Am 1963; 1: 439-448. SUTER FP, ETTINGER SJ. Chronic respiratory disorders. In: Ettinger SJ ed. Textbook of veterinary internal medicine: diseases of the dog and cat. Philadelphia: WB Saunders, 1975: 724-753.
14. LORD PF, SUTER PF, CHAN KF, APPLEFORD M,
effect a cure ( 17). However, it must be pointed out that the majority of bullae which occur as a result of trauma resolve spontaneously in both man (10) and dogs (2,6). References 1. SUTER PF, ETTINGER SJ. Miscellaneous dis-
eases of the thorax. In: Textbook of veterinary internal medicine: diseases of the dog and cat. Ettinger SJ ed. Philadelphia: WB Saunders, 1975: 807-822.
2. SILVERMAN S, POULOS PW, SUTER PF. Cavitary pulmonary lesions in animals. J Am Vet Rad 1974; XVII: 134-146. 3. BERZON JL, RENDANO VT, HOFFER RE. Recurrent pneumothorax secondary to ruptured plumonary blebs: a case report. J Am Anim Hosp Assoc 1979; 15: 707-711. 4. KIRK, RW, BISTNER si. Handbook of veterinary procedures and emergency treatment. 3rd ed. Philadelphia: WB Saunders, 1981: 515-516. 5. HASKINS SC. Standards and techniques of
ROOT CR. Pleural, extrapleural and pulmonary lesions in small animals: a radiographic approach to differential diagnosis. J Am Vet Rad Soc 1972; XII: 4-17. 15. LORD PF, GREINER TP, GREENE RW, DEHOFF
WD. Lung lobe torsion in the dog. J Am Anim Hosp Assoc 1973; 9: 473-482. 16. MILLER ME, CHRISTENSEN GC, EVANS HE.
Anatomy of the dog. Philadelphia: WB Saunders, 1964: 728-739. 17. YOSHIOKA MM. Management of spontaneous pneumothorax in twelve dogs. J Am Anim Hosp Assoc 1982; 18: 57-62.
RESEARCH GRANT APPLICATIONS INVITED Applications are invited for grants in aid of research on animal diseases in Canada. The deadline for receiving applications is November 30. For further information and application forms contact: The Secretary Canadian Veterinary Research Trust Fund 339 Booth Street Ottawa, Ontario Ki R 7K1 287
