Post‐anesthetic pulmonary edema in two horses

Case 1 A two‐year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO₂: 3.7 kPa [28 mmHg]) and hypocapnia (PaCO₂: 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra‐nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. Case 2 An 11‐year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4‐hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO₂: 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood‐gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.     

Suspected air embolism associated with post-anesthetic pulmonary edema and neurologic sequelae in a horse

A 523 kg Quarter Horse was anesthetized for unilateral eye enucleation. The anesthetic period was unremarkable. During anesthetic recovery the cap on the jugular venous catheter became dislodged. Clinical signs of pulmonary edema associated with moderate arterial hypoxemia subsequently developed. Although pulmonary edema resolved with medical therapy, the day following anesthetic recovery, clinical signs of vestibular disease and blindness developed. Treatment included nasal oxygen insufflation, flunixin meglumine, furosemide, dexamethasone, thiamine, dimethylsulfoxide, antimicrobials, and phenylbutazone. The horse recovered and was discharged from the hospital after 7 days of treatment and was neurologically normal at 6 weeks. While venous air embolism was not confirmed in this case, the catheter cap complication followed by signs of pulmonary edema and neurologic sequelae support the presumptive pathogenesis of this horse's complications. Diagnostic confirmation of air embolism in horses with compatible acute clinical signs should be documented with echocardiography.     

Pulmonary edema and emphysema in cattle after intraruminal and intravenous administration of 3-methylindole.

Intraruminal and intravenous administration of 3-methylindole (3MI; skatole) caused interstitial pulmonary edema and emphysema in cattle. In 3 adult heifers given the intraruminal dose of 0.2 g of 3 MI per kilogram of body weight, clinical signs of respiratory disease appeared between 6 and 12 hours after dosing, and death due to pulmonary edema and emphysema occurred at 33, 69, and 72 hours. The mean plasma concentration of 3MI became maximal (18.5 mug/ml) at 3 hours and then decreased to low concentrations by 48 hours. In 2 heifers given an intraruminal dose of 0.1 g of 3MI/kg, clinical signs developed, but they did not die during the 96-hour experiment. The mean plasma concentration of 3 MI became maximal (16.8 mug/ml) at 3 hours and decreased to 1.6 and 0.4 mug/ml at 12 and 36 hours, respectively. At necropsy of the heifers, the lung were large, firm, dark red, and heavier than normal. Diffuse pulmonary edema was the predominant change in cattle which died early, and interstitial emphysema was more severe at later stages of the disease. During the early stages, alveoli were overdistended, and a few more ruptured. Most alveolar spaces were filled with proteinaceous residue, but the alveolar septums were smooth and of normal thickness. At later stages, proliferation of alveolar cells was observed, and alveolar septums were thickened. In 3 cows given 0.06 g of 3MI/kg by jugular infusion, clinical signs appeared in all cows, and 1 cow died of pulmonary edema and emphysema 56 hours after the infusion was started. Severe pulmonary lesions seen in all of the cows given a 3MI infusion were similar to those in the cows given an intraruminal dose of 3MI. The mean plasma concentration of 3MI increased to 10.7 mug/ml at 9 hours after starting the infusion and decreased to 0.5 mug/ml at 18 hours. The results indicate that 3MI, a product of ruminal tryptophan fermentation, can cause pulmonary edema and interstitial emphysema in cattle and support the hypothesis that 3MI is the causative agent in tryptophan-induced pulmonary disease.     

Safety and efficacy of a technique for thoracoscopically guided pulmonary wedge resection in horses

OBJECTIVE: To evaluate the safety and efficacy of thoracoscopically guided pulmonary wedge resection in horses. ANIMALS: 10 horses (5 control horses and 5 horses affected with recurrent airway obstruction [ie, heaves]). PROCEDURE: Each horse underwent a thoracoscopically guided pulmonary wedge resection. Before, during, and after surgery, heart rate, respiratory rate, arterial blood gases, and systemic and pulmonary arterial pressures were measured. Physical examination, CBC, and thoracic radiography and ultrasonography were performed 24 hours before and 2 and 48 hours after surgery. Pulmonary specimens were assessed by histologic examination. A second thoracoscopic procedure 14 days later was used to evaluate the resection site. RESULTS: The technique provided excellent specimens for histologic evaluation of the lung. Heart and respiratory rates decreased significantly after horses were administered sedatives. A significant transient decrease in Pao2 was detected immediately after pulmonary wedge resection, but we did not detect significant effects on arterial pH, Paco2, or mean arterial and pulmonary arterial pressures. All horses except 1 were clinically normal after thoracoscopic surgery; that horse developed hemothorax attributable to iatrogenic injury to the diaphragm. The second thoracoscopy revealed minimal inflammation, and there were no adhesions. CONCLUSIONS AND CLINICAL RELEVANCE: Thoracoscopically guided pulmonary wedge resection provides a minimally invasive method for use in obtaining specimens of lung tissues from healthy horses and those with lung disease. This technique may be useful for the diagnosis of diseases of the lungs and thoracic cavity.     

Complications of Balloon Catheterization Associated With Aberrant Cerebral Arterial Anatomy in a Horse With Guttural Pouch Mycosis

A 3-year-old Quarter Horse gelding was treated for left guttural pouch mycosis by ligation and balloon catheterization of the left internal carotid artery. Catheter advancement was shorter (10 cm) than the normally reported distance (13–15 cm), but was observed endoscopically during placement as it coursed within the internal carotid artery through the guttural pouch. The horse developed a persistently abnormal respiratory pattern after catheter placement, failed to gain consciousness, developed pulmonary edema, and died 5.5 hours postoperatively. Postmortem examination revelaed an aberrant left internal carotid arterial course with location of the embolectomy catheter at the junction of the basilar and caudal cerebellar arteries. Brainstem neuronal necrosis and alveolar and interstitial pulmonary edema were identified on histological examination. Angiography may be used to identify aberrant branching patterns. Failure to identify and occlude aberrant branches may result in fatal epistaxis and Brainstem lesions.     

Black walnut toxicosis in ten horses

Black walnut toxicosis was diagnosed in 10 horses at one stable. The time from exposure to shavings to development of clinical signs was 8 to 12 hours. Most common clinical signs were moderate to severe laminitis (Obel grade 2 or 3), pitting edema of the distal portion of the limbs, and rapid respiratory rate. Two horses had clinical signs of colic and 2 other horses had anorexia and lethargy. All 10 horses recovered without complications.     

Ruminal and plasma concentrations of 3-methylindole associated with tryptophan-induced pulmonary edema and emphysema in cattle.

Five Hereford cows were given an intraruminal dose of L-tryptophan (0.35 g/kg of body weight), and 2 cows were used as controls. Of the 5 treated cows, 3 developed clinical signs of interstitial pul monary edema, and emphysema and severe pulmonary lesions were seen at necropsy after 96 hours. Another cow developed moderate clinical signs and pulmonary lesions, and the remaining cow had few clinical signs and mild pulmonary lesions. The severity of clinical signs in each cow was related to the severity of pulmonary lesions at necropsy. The 3-methylindole (3MI) was present in ruminal fluid and plasma within 6 hours after administration of tryptophan, and the concentrations increased to 3.0 and 9.0 mug/ml within 12 to 24 hours. Severity of pulmonary lesions was related to maximal concentration and duration of 3MI in the plasma. At necropsy, gross lesions were characterized by diffuse, pulmonary edema and interstital emphysema; and the lungs were dark red, firm, and heavier than normal. Predominant microscopic changes included accumulation of proteinaceous residue, hypertrophy and hyperplasia of alveolar lining epithelium, thickening of alveolar septums, and emphysematous thickening of interstitial tissues. These changes were similar to previously reported 3MI-induced pulmonary lesions. The presence of 3MI in ruminal fluid and plasma after administration of tryptophan and the relationship between concentration of 3MI and severity of clinical signs indicate that 3MI is the principal metabolite of ruminal fermentation which leads to the development of acute pulmonary edema and emphysema in cattle given tryptophan.     

Treatment of granular cell tumor via complete right lung resection in a horse

A 7-year-old warmblood mare was referred because of a respiratory tract disorder; pulmonary granular cell tumor was diagnosed. Pulmonary granular cell tumor is a locally invasive but rare type of tumor with low metastatic potential. The entire right lung was resected to ensure removal of all neoplastic tissue. The horse recovered well and has minimal difficulties functioning with one lung. Most of these tumors are diagnosed during postmortem examination. To our knowledge, this is the first report of pulmonary granular cell tumor treated by complete lung resection in a horse.     

Lung ring-down artifact as a sign of pulmonary alveolar-interstitial disease

Three dogs with presumptive cardiogenic pulmonary edema underwent a thoracic ultrasonographic examination. Multiple ring-down artifacts involving both sides of the thorax emanating from the pleural-lung interface were detected. When clinical and radiographic signs of pulmonary edema were resolved, ring-down artifacts were not observed. The ring-down artifact may be a useful diagnostic sign for screening the lung of animals with acute respiratory distress where radiographs are not feasible.     

Atelectasis causes gas exchange impairment in the anaesthetised horse

The anatomical basis of gas exchange impairment in the anaesthetised horse was studied by computerised tomography (CT; three shetland ponies) and morphological analysis (one pony and three horses). By means of CT, densities were seen in dependent lung regions early during anaesthesia, both with spontaneous breathing and with mechanical ventilation. The densities remained for some time where they had initially been created when the animal was turned from dorsal to sternal recumbency. Deep insufflation of the lungs reduced the dense area. Gas exchange was impaired roughly in proportion to the dense area. On histological analysis, the densities were atelectatic and congested with blood. Gravimetry showed no more extravascular water per unit lung tissue in the atelectatic than in the 'normal' regions, and the blood content was increased only slightly. It is concluded that the horse develops atelectasis in dependent lung regions early during anaesthesia in dorsal recumbency, and that atelectasis is the most likely explanation for the large shunt and impaired arterial oxygenation regularly seen during anaesthesia.     

The pathology of peracute experimental Clostridium perfringens type D enterotoxemia in sheep.

The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased respiratory efforts, recumbency, paddling, bleating, convulsions, blindness, and opisthotonus. Diarrhea was not observed in any of the animals. The time lapse between the beginning of intraduodenal infusion and onset of clinical signs varied between 30 minutes and 26 hours, and the clinical course varied between 1 and 9 hours. Gross postmortem changes were observed in these 12 animals and included pulmonary edema; excess pericardial, peritoneal, or pleural fluid with or without strands of fibrin; liquid small intestinal contents; leptomeningeal edema; cerebellar coning; and subcapsular petechiae on kidneys. Histological changes consisted of severe edema of pleura and interlobular septa and around blood vessels and airways and acidophilic, homogeneous, proteinaceous perivascular edema in the brain. Five of 12 animals (42%) with clinical signs consistent with enterotoxemia lacked specific histological lesions in the brain. None of the intoxicated or control animals developed nephrosis. Glucose was detected in the urine of 3 of 6 animals that were tested for this analyte. These results stress the importance of the use of histological examination of the brain, coupled with epsilon toxin detection, for a definitive diagnosis of C. perfringens type D enterotoxemia in sheep.     

Erysipelothrix rhusiopathiae bacteremia in a horse

Erysipelothrix rhusiopathiae serotype 5 was isolated from blood obtained antemortem from a horse with presenting problems of laminitis, uveitis, acute blindness, localized ventral edema and depression. The patient failed to respond to therapy and died 96 hours after the onset of clinical signs. Cultures of the lung postmortem yielded Erysipelothrix rhusiopathiae serotype 5, Beta-hemolytic Streptococcus sp., Escherichia coli, Proteus sp., and Klebsiella sp.     

Pathophysiologic study of 3-methylindole-induced pulmonary toxicosis in immature cattle

In 5 Friesian calves given 3-methylindole (3-MI) (100 mg/kg once a week for 8 weeks, except calf 4, given a 50 mg/kg dose on weeks 3 to 8), pulmonary function (PF) values and arterial blood gas tensions (PaO2 and PaCO2) were measured 24 hours after dosing was done and were correlated with clinical, biochemical, and pathologic changes. Three of the calves (No. 1, 2, and 3) showed acute respiratory distress syndrome 24 hours after the first 3-MI treatment, with a large increase in respiratory frequency, minute viscous work, and PaCO2 and a large decrease in tidal volume, dynamic lung compliance, and PaCO2. They died 36, 38, and 84 hours after dosing. Pulmonary function changes were compatible with the severe pulmonary edema and alveolar damage observed at necropsy. The 2 other calves, after they were given the 1st dose, showed only subacute respiratory distress syndrome with less severe changes in PF values recorded at 24 hours. Furthermore, they became progressively more tolerant to the 2nd, 3rd, and 4th weekly treatments, and showed base-line PF values after the 5th weekly treatment. Pathologic changes were not observed in lung biopsy material from these 2 animals at 2 and at 12 weeks after the 8th (or last) 3-MI treatment.     

Lymphosarcoma and associated immune-mediated hemolytic anemia and thrombocytopenia in horses

Three horses with equine lymphosarcoma were examined because of clinical signs including chronic weight loss, respiratory distress, peripheral edema, and chronic colic. Clinicopathologic findings included evidence of an immune-mediated hemolytic anemia. Immune-mediated thrombocytopenia also was diagnosed in 1 of the horses and suspected in another. One horse died in spite of treatment, 1 died 5 hours after surgical removal of a tumor encircling the jejunum, and 1 was euthanatized because of deteriorating condition. Necropsy of each horse revealed extensive neoplastic infiltration of peripheral lymph nodes and abdominal or thoracic viscera with neoplastic lymphocytes.     

Pulmonary edema at recovery after colic operation with in-situ nasogastric tube in a horse

After an uneventful general anesthesia, in a horse negative pressure pulmonary edema developed due to acute upper airway obstruction during the anesthetic recovery phase after colic surgery. No pathologic alteration of respiration was observed until the horse stood up and began suffocating. The horse had recovered with the nasogastric tube in situ. This, together with the postmortem diagnosis of laryngeal hemiplegia resulted in impairment of airflow through the larynx and development of pulmonary edema. Our objective is to alert clinicians about the possible hazard of recovery with an in-situ nasogastric tube.     

Pathophysiologic studies of calves given 3-methylindole intraruminally

Intraruminal administration of 0.25 g of 3-methylindole (3MI; skatole/kg of body weight) to seven young calves generally caused mild respiratory signs and lesions, accompanied by only slight changes in cardiopulmonary function. Moderate depression, trembling, and irregular respiratory rate were observed between postadministration hours (PAH) 6 and 12. By PAH 24 at this dosage, abnormal clinical signs were not present. Statistically significant (P less than or equal to 0.05) changes observed in blood gas data from the seven calves were a decrease in aortic oxygen tension at PAH 12, increases in free-flowing venous oxygen tension in the intervals between PAH 6 and 12 and between PAH 6 and 24, and an increase in occluded venous oxygen tension at PAH 24. All calves had increases (although generally not statistically significant) in heart rate, cardiac output, cardiac index, stroke volume, and stroke index after 3MI administration. Mean aortic and pulmonary arterial pressure changes were generally small and variable. At necropsy, the lungs of the calves did not collapse when the thorax was opened. Patchy areas of consolidation (0.5 cm in diameter) were scattered throughout the parenchyma. Pulmonary edema or emphysema was not observed grossly. Microscopically, the alveolar septae were irregularly thickened because of edema, infiltration by polymorphonuclear and mononuclear cells, and vascular congestion. Interstitial lesions were patchy in distribution and severity and corresponded to the areas of consolidation observed grossly. Alveolar epithelial hypertrophy and hyperplasia were present, and an occasional focus of alevoli contained fluid of edema. Degeneration of individual hepatocytes was observed in scattered areas of the liver, especially in the periportal areas. It was concluded that differences in 3MI dosage response may exist between young calves and adult cattle in which calves are more resistant to the pulmonary cytotoxicity of 3MI.     

Primary malignant pulmonary neoplasia in two horses

Although primary malignant pulmonary neoplasia of horses is rarely encountered, this diagnosis was confirmed in 2 horses on the basis of necropsy and histopathologic findings. One horse, with cystic mucinous adenocarcinoma, had respiratory tract and neurologic signs directly attributable to the neoplasm, and a tentative antemortem diagnosis of pulmonary neoplasia was made. The other horse, with anaplastic bronchogenic carcinoma, did not have clinical signs of pulmonary neoplasia.     

Pulmonary aspergillosis in horses: 29 cases (1974-1997)

OBJECTIVE: To analyze medical records and identify factors that veterinarians can use to prevent pulmonary aspergillosis in horses or that would enable them to diagnose it as early as possible. DESIGN: Retrospective study. ANIMALS: 29 horses. PROCEDURE: Medical records were reviewed for horses with pulmonary aspergillosis diagnosed on the basis of characteristic postmortem findings. Information on history, clinical signs, disease progression, and postmortem findings was obtained. RESULTS: 25 of 29 (86.2%) horses had primary (n = 20) or secondary (5) disease compatible with loss of integrity of the gastrointestinal (GI) tract. The remaining 4 horses had a non-GI tract disorder; only 1 of these 4 had clinical signs associated with the respiratory tract (i.e., pleuropneumonia). Although 22 (75.9%) horses had various signs of respiratory tract disorders, an antemortem diagnosis of Aspergillus pneumonia was made in only 1 horse and was suspected in only 1 other. Fungal organisms were seen histologically in tissues other than the lung in 12 (41.4%) horses. CLINICAL IMPLICATIONS: Horses with enteritis, colitis, typhlitis, or other diseases of the GI tract that result in mucosal compromise, and horses with clinical signs of respiratory tract disease, particularly if the horse's condition is unresponsive to treatment with antimicrobial agents; should be considered at high risk of having pulmonary aspergillosis. Immunosuppression from debilitating disease may also predispose horses to aspergillosis. Because invasive pulmonary aspergillosis can be difficult to diagnose, clinicians should be aware of clinical and epidemiologic settings in which this disease would develop.     

African Horse Sickness Fever in Vaccinated Horses: Short Communication

Our investigation has shown that multiple vaccinations with inactivated African horse sickness (AHS) vaccines containing all 9 serotypes and produced at the Central Veterinary Research Laboratory in Dubai, UAE, protect horses from AHS. However, the immunization did not prevent African horse sickness fever (AHSF) in approximately 10% of the vaccinated horses despite high enzyme-linked immunosorbent assay and virus neutralizing antibodies. African horse sickness fever is a very mild form of AHS with similar clinical signs. From all 6 horses which had developed AHSF, no virus was isolated from EDTA blood withdrawn during the acute phase of infection. Despite high neutralizing antibodies, serotype 9 was detected by polymerase chain reaction in 4 of them. All 6 horses recovered within 72 hours, after they developed mild clinical signs of AHS.