Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Diseases of the lungs
 Pulmonary congestion and edema
 Pulmonary congestion
is caused by an increase in the amount of blood in the lungs due to
engorgement of the pulmonary vascular bed. It is sometimes followed by
pulmonary edema when intravascular fluid escapes into the parenchyma
and alveoli. The various stages of the vascular disturbance are
characterized by respiratory compromise, the degree depending upon the
amount of alveolar air space which is lost.
 Primary pulmonary congestion
 Early stages of most cases of pneumonia
 Inhalation of smoke and fumes.
 Anaphylactic reactions.
 Race horses with acute severe exercise-induced pulmonary
hemorrhage.
 Secondary pulmonary congestion
 Congestive heart failure (cardiogenic pulmonary edema)
 Ruptured chordae tendineae of the mitral valve
 Left-sided heart failure.
 Pulmonary edema
Pulmonary edema as a sequel to pulmonary capillary hypertension or
pulmonary microvascular damage.
Causes:- The common proximate causes of pulmonary edema are: injury to the endothelium of the pulmonary capillary with
subsequent leakage of protein -rich fluid into the interstitial
spaces,
 Elevated blood pressure in the alveolar capillaries.
 Damage to pulmonary vascular endothelium can occur in
infectious diseases (e.g. African horse sickness) or intoxications
(endotoxemia) .
 Physical injury, including inhalation of excessively hot air or
smoke, can damage the alveolar epithelium with secondary
damage to capillary endothelium.
Pulmonary edema occurs in:
 Acute anaphylaxis
 Acute pneumonia – Pasteurella haemolytica produces
several virulence factors that induce direct or leukocytemediated pulmonary endothelial cell injury.
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Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 Congestive heart failure and acute heart failure, e.g. the
myocardial form of enzootic muscular dystrophy in inherited
myocardiopathy of Hereford calves; ruptured mitral valve or
chordae tendonae .
 Inhalation of smoke or manure gas.
 After general anesthesia in horses.
Pathogenesis:
In pulmonary congestion, ventilation is reduced and oxygenation of the
blood is impaired. Oxygenation is reduced by the decreased rate of blood
flow through the pulmonary vascular bed. Hypoxemic anoxia develops
and is the cause of most of the clinical signs that appear.
In pulmonary edema hypoxemia occurs because of ventilation/perfusion
abnormalities, diffusion abnormalities and hypoventilation caused by the
physical obstruction of airflow by fluid and foam in the airways. The
edema is caused by damage to the capillary walls by toxins or anoxia or
by transudation of fluid due to increased hydrostatic pressure in the
capillaries. Filling of the alveoli, and in severe cases the bronchi,
effectively prevents gaseous exchange.
Clinical finding
 The depth of respiration is increased to the point of extreme
dyspnea with the head extended.
 the nostrils flared and mouth-breathing.
 Breathing movements are greatly exaggerated and can be best
described as heaving; there is marked abdominal and thoracic
movement during inspiration and expiration.
 A typical stance is usually adopted, with the front legs spread
wide apart, the elbows abducted and the head hung low.
 The respiratory rate is increased and The heart rate is usually
elevated (up to 100/min) .
 The nasal mucosa is bright red or cyanotic in terminal cases.
 In acute pulmonary congestion there are harsh breath sounds but no
crackles are present on auscultation.
 In pulmonary edema develops, loud breath sounds and crackles are
audible over the ventral aspects of the lungs
 . Coughing is usually present but the cough is soft and moist and is
not painful.
 A slight to moderate serous nasal discharge occurs in the early
stage of congestion but in severe pulmonary edema this increases
to a voluminous, frothy nasal discharge, which is often pink
colored due to blood.
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Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 Death in cases of pulmonary edema is accompanied by asphyxia
respiratory failure.
 Atelectasis:
Is collapse of the alveoli due to failure of the alveoli to inflate or because
of compression of the alveoli. Atelectasis is classified as.
 Obstruction (resorption) atelectasis: occurs secondary to
obstruction of the airways, with subsequent resorption of alveolar
gases and collapse of the alveoli. This disease is usually caused by
obstruction of small bronchioles by fluid and exudate. It is
common in animals with pneumonia or aspiration of a foreign
body.
 Compression (contraction) atelectasis: occurs when intrathoracic
(intrapleural) pressure exceeds alveolar pressure, thereby deflating
alveoli. This occurs when there is excessive pleural fluid or the
animal has a pneumothorax. In large animals it also occurs in the
dependent lung or portions of lung in recumbent animals.
 Pulmonary hypertension
Is an increase in pulmonary arterial pressure above normal values due to
structural or functional changes in the pulmonary vasculature. Primary
pulmonary hypertension occurs in cattle with high-altitude disease.
Chronic pulmonary hypertension results in right-Side congestive heart
failure due to right ventricular hypertrophy or cor pulmonale.
 Exercise-induced
(EIPH,Bleeders):
pulmonary
hemorrhage
of
horse
Etiology:
Pulmonary hemorrhage during strenuous exercise. Or it is rupture of
alveolar capillary membranes with subsequent extravasation of blood into
interstitial and alveolar spaces.
Epidemiology:
Present in most (> 80%) Thoroughbred and Standardbred racehorses,
although clinical signs are less common. Occurs worldwide in any horse
that performs strenuous exercise. Rarely causes death
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Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Pathogenesis:
Probably associated with rupture of pulmonary capillaries by the high
pulmonary vascular pressures generated during exercise.
 During exercise, the absolute magnitudes of both pulmonary
capillary pressure and alveolar pressure increase, with a
consequent increase in transmural pressure. Strenuous exercise is
associated with marked increases in pulmonary artery pressure in
horses.
 Rupture of alveolar capillaries occurs secondary to an exerciseinduced increase in transmural pressure (pressure difference
between the inside of the capillary and the alveolar lumen) . If
the transmural stress exceeds the tensile strength of the capillary
wall, the capillary ruptures.
 Values for mean pulmonary arterial pressure at rest of 20-25
mmHg increase to more than 90 mmHg during intense exercise
because of the large cardiac output achieved by exercising
horses. The increases in pulmonary artery pressure, combined
with an increase in left atrial pressure during exercise, probably
result in an increase in pulmonary capillary pressure.
 Other theories of the pathogenesis of EIPH include: small-airway
disease, upper airway and lower airways obstruction, hemostatic
abnormalities, changes in blood viscosity and erythrocyte shape.
 There may be a contributory role for inflammation and
obstruction of small airways, and tissue damage caused by large
and rapid change in intrathoracic pressure.
Clinical finding:
- Epistaxis during or shortly after exercise and is usually first noticed
at the end of a race, particularly when the horse is returned to the
paddock or winner's circle and is allowed to lower its head.
- Affected horses may cough or suddenly slow during a race.
- Physical examination :Rectal temperature and heart and breathing
rates may be elevated as a consequence of exercise in horses
examined soon after exercise, but values of these variables in
horses with EIPH at rest are not noticeably different from horses
with no evidence of EIPH.
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Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
- Affected horses may swallow more frequently during recovery
from exercise than do unaffected horses result of blood in the
larynx and pharynx.
- Endoscopic examination of the trachea and bronchi reveals blood.
- Tracheobronchoscopy: Observation of blood in the trachea or large
bronchi of horses 30-120 minutes after racing or strenuous exercise
provides a definitive diagnosis of EIPH.
Clinical pathology:
- Examination of airway secretions or lavage fluid :The presence of
red cells or macrophages containing either effete red cells or the
breakdown products of hemoglobin (hemosiderophages) in tracheal
or bronchoalveolar lavage fluid provides evidence of EIPH.
- Tracheal aspirates may be obtained any time after exercise by
aspiration either during tracheobronchoscopic examination or
through a percutaneous intratracheal needle.
Treatment and Control :
None of demonstrated efficacy. Furosemide is used as prophylaxis. :
There are no specific control measures, however, prevention of
environmental and infectious respiratory disease may reduce the
incidence of the disease
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