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Miscellaneous Lung Diseases
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C h a p t e r
3 7
Miscellaneous Lung Diseases
III PERSISTENT FETAL PULMONARY CIRCULATION
III EXERCISE-INDUCED PULMONARY HEMORRHAGE
Before birth, pulmonary arterial hypertension is the norm, ensuring preferential blood flow away from the lung and into the systemic circulation via the foramen ovale and ductus arteriosus. Drummand as well as Cottrill and O’Conner reported a patent foramen ovale and persistent arterial duct in a 10-hour-old Thoroughbred foal with presumed functional pulmonary hypertension.1,2
The precise cause or causes of exercise-induced pulmonary hemorrhage in racehorses are not known. Etiologic speculation has long focused on preexisting lung disease, specifically that involving the terminal bronchioles and associated vasculature. However, this theory has not been uniformly accepted, as evidenced by new explanations regularly appearing in the literature. One such example of alternative thinking is the capillary-failure theory, which contends that some pulmonary capillaries are simply not strong enough to withstand the extremely high blood pressure that develops during racing, and under such stress, ruptures.4 Whatever the cause or causes of exercise-induced pulmonary hemorrhage, in its severest expression the disease can lead to death.5 Fatal pulmonary hemorrhage, unassociated with racing, was reported in a 3-year-old Thoroughbred filly after a swim.6 Exerciseinduced pulmonary hemorrhage has also been described in polo ponies.7 Martin and co-workers recommend that tracheal wash, to search for evidence of bleeding, be performed after exercise rather than before.8
III CONGENITAL BRONCHOPULMONARY DYSPLASIA Freeman and co-workers described bronchpulmonary dysplasia in a premature Anglo-Trakehner filly foal hospitalized because of profound weakness and respiratory distress.3 Widespread pulmonary consolidation, noted in films made on admission, was interpreted as consistent with pulmonary atelectasis secondary to surfactant deficiency. Progress films made 2 weeks later showed worsening of the previously identified lung consolidation. The foal was euthanized shortly thereafter. Necropsy findings were consistent with congenital bronchopulmonary dysplasia, including the following characteristic features: ∑ Atelectatic lobules ∑ Diffuse alveolar septal thickening ∑ Bronchioles and alveoli clogged with eosinophilic material ∑ Peribronchial infiltrates with secondary luminal narrowing ∑ Segmental fibrinoid degeneration of arteries and arterioles with medial and adventitial proliferation
Radiology O’Callaghan and Goulden described two distinct radiographic appearances associated with exerciseinduced pulmonary hemorrhage in horses, both appearing in the dorsocaudal aspect of the lung as seen in a lateral thoracic radiograph: (1) a small to mediumsized, horizontally oriented, oval-shaped opacity high in the caudal lung field (Figure 37-1) and (2) a vague increase in the density of the dorsocaudal aspect of the lung.9 Later, as a result of a radiologic-pathologic correlation, O’Callaghan and co-workers noted a significant correlation between (1) lesion density, (2) hemosiderin content, and (3) neovascularization of the regional bronchial arteries.10,11 499
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SECTION V III The Thorax
III HYALINE MEMBRANE DISEASE (RESPIRATORY DISTRESS SYNDROME) Hyaline membrane disease is, in nearly all instances, a disease of premature foals that have yet to develop pulmonary surfactant. Without this critical compound, it is impossible to maintain normal lung inflation, which results in hypoxia. The production of surfactant can sometimes be induced in premature foals or, alternatively, a foal can be kept in an oxygen tent. Positivepressure ventilation is needed in severe cases, but associated intensive care unit costs can be substantial, and there are many potentially fatal complications associated with such therapy. Murry theorized that a lack of surfactant in full-term foals may be due hypothyroidism.12
Radiology Regrettably, some of the published information about the radiology of hyaline membrane disease in foals is either misleading or incorrect. For example, in one review on neonatal intensive care, the authors state that “hyaline membrane disease is typically represented (my italics) by a diffuse ground glass appearance with prominent air bronchograms in the human infant: the same appears to be true in the horse.”13 Although this statement may be true sometimes, especially in severe disease, it is by no means typical or even representative. In another report, the authors state that in its initial stages respiratory distress syndrome (RDS) is “characterized radiographically by alveolar and granular interstitial patterns,” which is not true.14 RDS nearly always first appears as an extremely subtle, generalized increase in interstitial lung density and only later shows as obvious opacification resulting from atelectasis.
It may also be possible that reports of this nature, especially those reporting regional consolidation in foals,15 are actually describing a particularly severe form of pneumonia, causing a precipitous and uncontrollable fall in blood oxygen tension resembling that seen with surfactant deficiency. Based on observing radiologists working in the neonatal intensive care unit at Emory University in Atlanta, Georgia, and performing a dozen or more radiographic examinations on what subsequently proved to be hyaline membrane disease in premature foals, I offer the following personal observations: ∑ Most premature foals with hyaline membrane disease appear normal, or nearly normal, at the time they are initially radiographed. ∑ The most frequently observed disease pattern seen with hyaline membrane disease, which is only visible in the highest-quality films, is a subtle, uniform increase in lung density; there is rarely overt consolidation and accordingly no bronchograms. ∑ Most premature foals suspected of having hyaline membrane disease are radiographed while lying on their sides and often have been recumbent for some time before being imaged. This means that there will almost always be substantial postural atelectasis,16 which will cause the partially collapsed lung to falsely appear consolidated (opaque), complete with bronchograms. ∑ If the foal is in respiratory distress, its breathing rate will almost certainly be elevated, increasing the potential for motion unsharpness and creating the illusion of increased interstitial density. Overly light images may create the same effect. ∑ RDS in septicemic foals can create dramatically abnormal lung that may be mistaken for hyaline membrane disease.
A Figure 37-1 • Lateral (A) and close-up lateral (B) views of the caudodorsal lung field of an adult racehorse with exerciseinduced pulmonary hemorrhage show a characteristic narrow, oval-shaped density in the thoracodiaphragmatic angle.
B
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CHAPTER 37 III Miscellaneous Lung Diseases
III ADULT RESPIRATORY DISTRESS SYNDROME In a word, the difference between RDS in premature foals and in adult horses is surfactant; the former lack it, and the latter do not. How, then, does surfactant play a role in the adult form of the disease? It is actually quite simple. Certain diseases cause protein, usually fibrin, to leak from the alveolar capillaries into the alveolus. The fibrin eventually coats the alveoli, rendering the pulmonary surfactant ineffective, resulting in uneven lung inflation and hypoxemia. As with premature foals, adult horses can be put on positive pressure ventilators, but unfortunately the delivery and maintenance of positive end-expiratory pressure (PEEP) is not without its own set of serious problems, such as oxygen toxicity and pressure-induced lung injury (barotrauma). Most horses that develop adult respiratory disease syndrome (ARDS) eventually die of their illness or are euthanized.
III CHYLOTHORAX Chylothorax can be caused by a wide variety of diseases (Box 37-1). In the case of diaphragmatic injury, the right crus is most vulnerable because of its association with the thoracic duct as it emerges through the aortic opening in the diaphragm.17 Shumacher and co-workers reported an idiopathic chylothorax in a 7-month-old Arabian filly.18
III NEAR DROWNING I previously reported the radiographic appearance of near drowning in dogs and horses. Humber also reported a case of near drowning of a horse, in which thoracic radiographs revealed pneumothorax and pneumomediastinum, in addition to increased interstitial density.19 Nuclear scintigraphy showed a small
B o x
3 7 - 1
Causes of Chylothorax in the Horse as Related to the Integrity and Pressure of the Thoracic Duct Traumatic rupture (rib fracture, diaphragmatic hernia, or congenital malformation) Neoplastic erosion Nonneoplastic, inflammatory erosion, including pneumonia, pleuropneumonia, and pleuritis Accidental puncture during catheterization (iatrogenic wounding) Right heart failure Large cranial mediastinal mass such as lymphoma Congenital anomaly, including malformation, atresia, and abnormal drainage Undetermined cause (idiopathic)
501
area of ventilation-perfusion mismatching in one of the caudal lung lobes dorsally.20
III DISSEMINATED INTRAVASCULAR COAGULATION Disseminated intravascular coagulation (DIC) is a mammalian blood disorder that is apparently triggered by a variety of diseases that cause excessive thrombin formation, which in turn activates and then exhausts the proteins responsible for coagulation. The result is fibrinous thrombosis, which may be confined to a single organ or, alternatively, involve the entire body. Morris and Beech reported DIC in six horses. Unfortunately, not all the horses were radiographed, and those that were showed no consistent pulmonary disease pattern.21 Plants from the Senicio family occasionally lead to severe respiratory disease in addition to liver failure. The precise cause of the dyspnea is not known, but pharyngeal or laryngeal paralysis is suspected. Thoracic radiographs show increased lung density, which necropsy indicates is the result of lung consolidation caused by pulmonary edema.22
III PULMONARY OSTEOPATHY (MARIE’S DISEASE, HYPERTROPHIC PULMONARY OSTEOARTHROPATHY) Pulmonary osteoarthropathy is a secondary inflammatory bone disease that is usually triggered by a large lung mass, such as an abscess or tumor. Precisely how and why the characteristic bone lesions develop is not known, but removing the inciting lung lesion or cutting the vagus nerve leads to regression. Occasionally pulmonary osteopathy is initiated by mild lung disease, as reported by McClintock and Hutchins.23 An ovarian dysgerminoma was reported as the cause of pulmonary osteopathy in a mare without lung disease.24 Unlike pulmonary osteoarthropathy in dogs, which is associated with distinctive diaphyseal palisades of periosteal new bone, lesions in horses are much less well-defined and generally confined to the metaphyses and adjacent diaphyses.
References 1. Drummand WH: Neonatal pulmonary hypertension, Equine Vet J 19:169, 1987. 2. Cottrill CM, O’Conner WN: Persistence of fetal circulatory pathways in a newborn foal, Equine Vet J 19:252, 1987. 3. Freeman KP, Cline JM, et al: Recognition of bronchopulmonary dysplasia in a newborn foal, Equine Vet J 21:292, 1989. 4. West JB, Mathieu-Costello O: Stress failure of pulmonary capillaries as a mechanism for exercise induced
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502
5.
6. 7. 8.
9. 10.
11.
12.
SECTION V III The Thorax
pulmonary hemorrhage in the horse, Equine Vet J 26:441, 1994. Gunson DE, Sweeney CR, Soma LR: Sudden death attributable to exercise-induced pulmonary hemorrhage in racehorses: nine cases (1981-1983), J Am Vet Med Assoc 193:102, 1988. Qualls CW: Cleft soft palate, nasal septal deviation, and epiglottic entrapment in a Thoroughbred filly, J Am Vet Med Assoc 179:910, 1981. Voynick BT, Sweeney CR: Exercise-induced pulmonary hemorrhage in polo and racing horses, J Am Vet Med Assoc 188:301, 1986. Martin BB, Beech J, Parente EJ: Cytologic examination of specimens obtained by means of tracheal washes performed before and after high-speed treadmill exercise in horses with a history of poor performance, J Am Vet Med Assoc 214:673, 1999. O’Callaghan MW, Goulden BE: Radiographic changes in the lungs of horses with exercise-induced eoistaxis, N Z Vet J 30:117, 1982. O’Callaghan MW, Pascoe JR: Exercise-induced pulmonary hemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VI. Radiological/pathological correlations, Equine Vet J 19:419, 1987. O’Callaghan MW, Pascoe JR: Exercise-induced pulmonary hemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VIII. Radiological/pathological correlations, Equine Vet J 19:428, 1987. Murry MJ: Hypothyroidism and respiratory insuffi-
13. 14. 15. 16. 17. 18. 19. 20. 21. 22.
23. 24.
ciency in a neonatal foal, J Am Vet Med Assoc 197:1635, 1990. Koterba AM, Drummond WH, Kosch P: Intensive care of the neonatal foal, Vet Clin N Am Equine Pract 1:1985, 1985. Costa LRR, Mirza MH, Williams J: What is your diagnosis? J Am Vet Med Assoc 215:623, 1999. Lloyd KC, Kelly AB, Dunlop CI: Treatment of respiratory distress in a prematurely born foal, J Am Vet Med Assoc 193:560, 1988. Clabough DL: Diseases of the equine neonate, Equine Vet Sci 9:5, 1988. Mair TS, Pearson H, et al: Chylothorax associated with a congenital diaphragmatic defect in a foal, Equine Vet J 20:304, 1988. Schumacher J, Bruise R, Spano J: Chylothorax in an Arabian filly, Equine Vet J 21:132, 1989. Humber KA: Near drowning of a gelding, J Am Vet Med Assoc 192:377, 1988. Weaver MP: Pulmonary perfusion and ventilation: a mismatch? Equine Vet J 27:80, 1995. Morris DD, Beech J: Disseminated intravascular coagulation in six hours, J Am Vet Med Assoc 183:1067, 1983. Pearson EG: Liver failure attributable to pyrrolizidine alkaloid toxicosis and associated with inspiratory dyspnea in ponies: three cases (1982-1988), J Am Vet Med Assoc 198:1651, 1991. McClintock SA, Hutchins DR: Case report: Hypertrophic osteopathy in a stallion with minimal thoracic pathology, Aust Vet Pract 11:115, 1981. McClennan MW, Kelly WR: Hypertrophic osteopathy and dysgerminoma in a mare, Aust Vet J 53:144, 1977.
C h a p t e r
3 7
Miscellaneous Lung Diseases
III PERSISTENT FETAL PULMONARY CIRCULATION
III EXERCISE-INDUCED PULMONARY HEMORRHAGE
Before birth, pulmonary arterial hypertension is the norm, ensuring preferential blood flow away from the lung and into the systemic circulation via the foramen ovale and ductus arteriosus. Drummand as well as Cottrill and O’Conner reported a patent foramen ovale and persistent arterial duct in a 10-hour-old Thoroughbred foal with presumed functional pulmonary hypertension.1,2
The precise cause or causes of exercise-induced pulmonary hemorrhage in racehorses are not known. Etiologic speculation has long focused on preexisting lung disease, specifically that involving the terminal bronchioles and associated vasculature. However, this theory has not been uniformly accepted, as evidenced by new explanations regularly appearing in the literature. One such example of alternative thinking is the capillary-failure theory, which contends that some pulmonary capillaries are simply not strong enough to withstand the extremely high blood pressure that develops during racing, and under such stress, ruptures.4 Whatever the cause or causes of exercise-induced pulmonary hemorrhage, in its severest expression the disease can lead to death.5 Fatal pulmonary hemorrhage, unassociated with racing, was reported in a 3-year-old Thoroughbred filly after a swim.6 Exerciseinduced pulmonary hemorrhage has also been described in polo ponies.7 Martin and co-workers recommend that tracheal wash, to search for evidence of bleeding, be performed after exercise rather than before.8
III CONGENITAL BRONCHOPULMONARY DYSPLASIA Freeman and co-workers described bronchpulmonary dysplasia in a premature Anglo-Trakehner filly foal hospitalized because of profound weakness and respiratory distress.3 Widespread pulmonary consolidation, noted in films made on admission, was interpreted as consistent with pulmonary atelectasis secondary to surfactant deficiency. Progress films made 2 weeks later showed worsening of the previously identified lung consolidation. The foal was euthanized shortly thereafter. Necropsy findings were consistent with congenital bronchopulmonary dysplasia, including the following characteristic features: ∑ Atelectatic lobules ∑ Diffuse alveolar septal thickening ∑ Bronchioles and alveoli clogged with eosinophilic material ∑ Peribronchial infiltrates with secondary luminal narrowing ∑ Segmental fibrinoid degeneration of arteries and arterioles with medial and adventitial proliferation
Radiology O’Callaghan and Goulden described two distinct radiographic appearances associated with exerciseinduced pulmonary hemorrhage in horses, both appearing in the dorsocaudal aspect of the lung as seen in a lateral thoracic radiograph: (1) a small to mediumsized, horizontally oriented, oval-shaped opacity high in the caudal lung field (Figure 37-1) and (2) a vague increase in the density of the dorsocaudal aspect of the lung.9 Later, as a result of a radiologic-pathologic correlation, O’Callaghan and co-workers noted a significant correlation between (1) lesion density, (2) hemosiderin content, and (3) neovascularization of the regional bronchial arteries.10,11 499
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SECTION V III The Thorax
III HYALINE MEMBRANE DISEASE (RESPIRATORY DISTRESS SYNDROME) Hyaline membrane disease is, in nearly all instances, a disease of premature foals that have yet to develop pulmonary surfactant. Without this critical compound, it is impossible to maintain normal lung inflation, which results in hypoxia. The production of surfactant can sometimes be induced in premature foals or, alternatively, a foal can be kept in an oxygen tent. Positivepressure ventilation is needed in severe cases, but associated intensive care unit costs can be substantial, and there are many potentially fatal complications associated with such therapy. Murry theorized that a lack of surfactant in full-term foals may be due hypothyroidism.12
Radiology Regrettably, some of the published information about the radiology of hyaline membrane disease in foals is either misleading or incorrect. For example, in one review on neonatal intensive care, the authors state that “hyaline membrane disease is typically represented (my italics) by a diffuse ground glass appearance with prominent air bronchograms in the human infant: the same appears to be true in the horse.”13 Although this statement may be true sometimes, especially in severe disease, it is by no means typical or even representative. In another report, the authors state that in its initial stages respiratory distress syndrome (RDS) is “characterized radiographically by alveolar and granular interstitial patterns,” which is not true.14 RDS nearly always first appears as an extremely subtle, generalized increase in interstitial lung density and only later shows as obvious opacification resulting from atelectasis.
It may also be possible that reports of this nature, especially those reporting regional consolidation in foals,15 are actually describing a particularly severe form of pneumonia, causing a precipitous and uncontrollable fall in blood oxygen tension resembling that seen with surfactant deficiency. Based on observing radiologists working in the neonatal intensive care unit at Emory University in Atlanta, Georgia, and performing a dozen or more radiographic examinations on what subsequently proved to be hyaline membrane disease in premature foals, I offer the following personal observations: ∑ Most premature foals with hyaline membrane disease appear normal, or nearly normal, at the time they are initially radiographed. ∑ The most frequently observed disease pattern seen with hyaline membrane disease, which is only visible in the highest-quality films, is a subtle, uniform increase in lung density; there is rarely overt consolidation and accordingly no bronchograms. ∑ Most premature foals suspected of having hyaline membrane disease are radiographed while lying on their sides and often have been recumbent for some time before being imaged. This means that there will almost always be substantial postural atelectasis,16 which will cause the partially collapsed lung to falsely appear consolidated (opaque), complete with bronchograms. ∑ If the foal is in respiratory distress, its breathing rate will almost certainly be elevated, increasing the potential for motion unsharpness and creating the illusion of increased interstitial density. Overly light images may create the same effect. ∑ RDS in septicemic foals can create dramatically abnormal lung that may be mistaken for hyaline membrane disease.
A Figure 37-1 • Lateral (A) and close-up lateral (B) views of the caudodorsal lung field of an adult racehorse with exerciseinduced pulmonary hemorrhage show a characteristic narrow, oval-shaped density in the thoracodiaphragmatic angle.
B
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CHAPTER 37 III Miscellaneous Lung Diseases
III ADULT RESPIRATORY DISTRESS SYNDROME In a word, the difference between RDS in premature foals and in adult horses is surfactant; the former lack it, and the latter do not. How, then, does surfactant play a role in the adult form of the disease? It is actually quite simple. Certain diseases cause protein, usually fibrin, to leak from the alveolar capillaries into the alveolus. The fibrin eventually coats the alveoli, rendering the pulmonary surfactant ineffective, resulting in uneven lung inflation and hypoxemia. As with premature foals, adult horses can be put on positive pressure ventilators, but unfortunately the delivery and maintenance of positive end-expiratory pressure (PEEP) is not without its own set of serious problems, such as oxygen toxicity and pressure-induced lung injury (barotrauma). Most horses that develop adult respiratory disease syndrome (ARDS) eventually die of their illness or are euthanized.
III CHYLOTHORAX Chylothorax can be caused by a wide variety of diseases (Box 37-1). In the case of diaphragmatic injury, the right crus is most vulnerable because of its association with the thoracic duct as it emerges through the aortic opening in the diaphragm.17 Shumacher and co-workers reported an idiopathic chylothorax in a 7-month-old Arabian filly.18
III NEAR DROWNING I previously reported the radiographic appearance of near drowning in dogs and horses. Humber also reported a case of near drowning of a horse, in which thoracic radiographs revealed pneumothorax and pneumomediastinum, in addition to increased interstitial density.19 Nuclear scintigraphy showed a small
B o x
3 7 - 1
Causes of Chylothorax in the Horse as Related to the Integrity and Pressure of the Thoracic Duct Traumatic rupture (rib fracture, diaphragmatic hernia, or congenital malformation) Neoplastic erosion Nonneoplastic, inflammatory erosion, including pneumonia, pleuropneumonia, and pleuritis Accidental puncture during catheterization (iatrogenic wounding) Right heart failure Large cranial mediastinal mass such as lymphoma Congenital anomaly, including malformation, atresia, and abnormal drainage Undetermined cause (idiopathic)
501
area of ventilation-perfusion mismatching in one of the caudal lung lobes dorsally.20
III DISSEMINATED INTRAVASCULAR COAGULATION Disseminated intravascular coagulation (DIC) is a mammalian blood disorder that is apparently triggered by a variety of diseases that cause excessive thrombin formation, which in turn activates and then exhausts the proteins responsible for coagulation. The result is fibrinous thrombosis, which may be confined to a single organ or, alternatively, involve the entire body. Morris and Beech reported DIC in six horses. Unfortunately, not all the horses were radiographed, and those that were showed no consistent pulmonary disease pattern.21 Plants from the Senicio family occasionally lead to severe respiratory disease in addition to liver failure. The precise cause of the dyspnea is not known, but pharyngeal or laryngeal paralysis is suspected. Thoracic radiographs show increased lung density, which necropsy indicates is the result of lung consolidation caused by pulmonary edema.22
III PULMONARY OSTEOPATHY (MARIE’S DISEASE, HYPERTROPHIC PULMONARY OSTEOARTHROPATHY) Pulmonary osteoarthropathy is a secondary inflammatory bone disease that is usually triggered by a large lung mass, such as an abscess or tumor. Precisely how and why the characteristic bone lesions develop is not known, but removing the inciting lung lesion or cutting the vagus nerve leads to regression. Occasionally pulmonary osteopathy is initiated by mild lung disease, as reported by McClintock and Hutchins.23 An ovarian dysgerminoma was reported as the cause of pulmonary osteopathy in a mare without lung disease.24 Unlike pulmonary osteoarthropathy in dogs, which is associated with distinctive diaphyseal palisades of periosteal new bone, lesions in horses are much less well-defined and generally confined to the metaphyses and adjacent diaphyses.
References 1. Drummand WH: Neonatal pulmonary hypertension, Equine Vet J 19:169, 1987. 2. Cottrill CM, O’Conner WN: Persistence of fetal circulatory pathways in a newborn foal, Equine Vet J 19:252, 1987. 3. Freeman KP, Cline JM, et al: Recognition of bronchopulmonary dysplasia in a newborn foal, Equine Vet J 21:292, 1989. 4. West JB, Mathieu-Costello O: Stress failure of pulmonary capillaries as a mechanism for exercise induced
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502
5.
6. 7. 8.
9. 10.
11.
12.
SECTION V III The Thorax
pulmonary hemorrhage in the horse, Equine Vet J 26:441, 1994. Gunson DE, Sweeney CR, Soma LR: Sudden death attributable to exercise-induced pulmonary hemorrhage in racehorses: nine cases (1981-1983), J Am Vet Med Assoc 193:102, 1988. Qualls CW: Cleft soft palate, nasal septal deviation, and epiglottic entrapment in a Thoroughbred filly, J Am Vet Med Assoc 179:910, 1981. Voynick BT, Sweeney CR: Exercise-induced pulmonary hemorrhage in polo and racing horses, J Am Vet Med Assoc 188:301, 1986. Martin BB, Beech J, Parente EJ: Cytologic examination of specimens obtained by means of tracheal washes performed before and after high-speed treadmill exercise in horses with a history of poor performance, J Am Vet Med Assoc 214:673, 1999. O’Callaghan MW, Goulden BE: Radiographic changes in the lungs of horses with exercise-induced eoistaxis, N Z Vet J 30:117, 1982. O’Callaghan MW, Pascoe JR: Exercise-induced pulmonary hemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VI. Radiological/pathological correlations, Equine Vet J 19:419, 1987. O’Callaghan MW, Pascoe JR: Exercise-induced pulmonary hemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VIII. Radiological/pathological correlations, Equine Vet J 19:428, 1987. Murry MJ: Hypothyroidism and respiratory insuffi-
13. 14. 15. 16. 17. 18. 19. 20. 21. 22.
23. 24.
ciency in a neonatal foal, J Am Vet Med Assoc 197:1635, 1990. Koterba AM, Drummond WH, Kosch P: Intensive care of the neonatal foal, Vet Clin N Am Equine Pract 1:1985, 1985. Costa LRR, Mirza MH, Williams J: What is your diagnosis? J Am Vet Med Assoc 215:623, 1999. Lloyd KC, Kelly AB, Dunlop CI: Treatment of respiratory distress in a prematurely born foal, J Am Vet Med Assoc 193:560, 1988. Clabough DL: Diseases of the equine neonate, Equine Vet Sci 9:5, 1988. Mair TS, Pearson H, et al: Chylothorax associated with a congenital diaphragmatic defect in a foal, Equine Vet J 20:304, 1988. Schumacher J, Bruise R, Spano J: Chylothorax in an Arabian filly, Equine Vet J 21:132, 1989. Humber KA: Near drowning of a gelding, J Am Vet Med Assoc 192:377, 1988. Weaver MP: Pulmonary perfusion and ventilation: a mismatch? Equine Vet J 27:80, 1995. Morris DD, Beech J: Disseminated intravascular coagulation in six hours, J Am Vet Med Assoc 183:1067, 1983. Pearson EG: Liver failure attributable to pyrrolizidine alkaloid toxicosis and associated with inspiratory dyspnea in ponies: three cases (1982-1988), J Am Vet Med Assoc 198:1651, 1991. McClintock SA, Hutchins DR: Case report: Hypertrophic osteopathy in a stallion with minimal thoracic pathology, Aust Vet Pract 11:115, 1981. McClennan MW, Kelly WR: Hypertrophic osteopathy and dysgerminoma in a mare, Aust Vet J 53:144, 1977.