Acute lung injury/acute respiratory distress syndrome in 15 foals

REASONS FOR PERFORMING STUDY: Few reports exist in the veterinary medical literature describing clinical and pathological findings resembling conditions described as (ALI) and acute respiratory distress syndrome (ARDS) in man. OBJECTIVES: To document history, clinical, laboratory and diagnostic findings, treatment and outcome of foals age 1-12 months diagnosed with ALI/ARDS at a referral hospital. METHODS: Medical records, including radiographic, cytological, microbiological, serological and post mortem findings, were reviewed in a retrospective manner to identify foals with acute onset of respiratory distress, a partial pressure of arterial oxygen (PaO2) to fraction of oxygen in inspired gases (FiO2) ratio of < or = 300 mmHg, pulmonary infiltrates on thoracic radiographs or post mortem findings consistent with ALI/ARDS. RESULTS: Fifteen foals age 1.5-8 months were included in the study. Seven foals had previously been treated for respiratory disease, and all foals developed acute respiratory distress <48 h prior to presentation. Findings on presentation included tachycardia and tachypnoea in all foals, with fever recorded in 8 cases. Eight cases met the criteria for ALI and 7 for ARDS. Radiographic findings demonstrated diffuse bronchointerstitial pattern with focal to coalescing alveolar radiopacities. An aetiological agent was identified in foals ante mortem (n = 6) and post mortem (n = 4). All foals were treated with intranasal oxygen and antimicrobial drugs; 13 received corticosteroids. Nine patients survived, 4 died due to respiratory failure and 2 were subjected to euthanasia in a moribund state. Follow-up was available for 7 foals; all performed as well as age mates or siblings, and one was racing successfully. CONCLUSIONS: A condition closely meeting the human criteria for ALI/ARDS exists in foals age 1-12 months and may be identical to previously described acute bronchointerstitial pneumonia in young horses. POTENTIAL RELEVANCE: ALI/ARDS should be suspected in foals with acute severe respiratory distress and hypoxaemia that is minimally responsive to intranasal oxygen therapy. Treatment with systemic corticosteroids, intranasal oxygen and antimicrobials may be beneficial in foals with clinical signs compatible with ALI/ARDS.     

Suggested Strategies for Ventilatory Management of Veterinary Patients with Acute Respiratory Distress Syndrome

Objective: To review the current recommendations and guidelines for mechanical ventilation in humans and in animals with acute respiratory distress syndrome.
Human data synthesis: Acute respiratory distress syndrome (ARDS) in humans in defined as an acute onset of bilateral, diffuse infiltrates on thoracic radiographs that are not the result of heart disease and a significant oxygenation impairment. These patients require mechanical ventilation. Research has shown that further pulmonary damage can occur as a result of mechanical ventilation. Various alveolar recruitment maneuvers and a low tidal volume with increased positive end expiratory pressure (PEEP) have been associated with an increased survival.
Veterinary dat synthesis: Two veterinary reports have characterized ARDS in dogs using human criteria. There are no prospective veterinary studies using recruitment that ventilator-induced lung injury (VILI) occurs in dogs, sheep, and rats.
Conclusion: Recruitment maneuvers in conjunction with low tidal volumes and PEEP keep the alveoli open for gas exchange and decrease VILI. Prospective veterinary research in needed to determine if these maneuvers and recommendation can be applied to veterinary patients.     

Pulmonary Abnormalities in Dogs with Leptospirosis

Background: Leptospirosis in dogs is a multiorgan disease affecting mostly kidneys and liver. Objectives: The objective was to characterize prevalence, clinical, and radiological features and outcome of dogs with leptospirosis and pulmonary abnormalities. Animals: Fifty dogs with leptospirosis. Methods: Medical records of dogs diagnosed with leptospirosis at the Small Animal Clinic, Berlin, were reviewed. Diagnosis was based on microscopic agglutination test, blood or urine polymerase chain reaction, and histopathology. Based on clinical and/or radiological signs, patients were grouped into dogs with lung abnormalities (group 1) or without (group 2). Severity of respiratory distress was scored as mild to moderate (grade 1) or severe (grade 2). Thoracic radiographs were scored based on pulmonary changes and location as grade 1 (caudal interstitial pattern), 2 (generalized mild to moderate reticulonodular interstitial pattern), or 3 (generalized severe reticulonodular interstitial pattern with patchy alveolar consolidations). Results of CBC and biochemistry were compared between groups. Results: Thirty‐five dogs had radiological pulmonary changes (grade 1: 5; grade 2: 14; grade 3: 16); 31 of them had pulmonary distress (grade 1: 13, grade 2: 18). Sixty‐seven percent of the dogs with dyspnea grade 2 were mainly euthanized because of respiratory distress. Fifteen percent of the dogs with dyspnea grade 1 and 21% without clinical respiratory signs were euthanized because of acute renal failure or sepsis. Conclusions and Clinical Importance: In 70% of dogs with leptospirosis pulmonary changes were detected. Lung involvement represented a severe complication causing increased case fatality depending on the severity of respiratory distress.     

IMAGING DIAGNOSIS—PULMONARY ALVEOLAR PROTEINOSIS IN A DOG

A young dog was presented for cyanosis and right heart failure. Radiographic and CT characteristics included right heart/pulmonary artery enlargement, hepatomegaly, abdominal effusion, and severe, generalized air‐space filling. Focal increased opacities were present in the peripheral lung, as were multiple pulmonary blebs and bullae. Echocardiographic findings were consistent with cor pulmonale and pulmonary hypertension. Bronchoscopic findings were consistent with chronic inflammation. Pulmonary alveolar proteinosis (PAP) was confirmed at necropsy. Pulmonary alveolar proteinosis is an interstitial lung disease that results in accumulation of phospholipoproteinaceous material and should be included as a differential diagnosis for dogs with these clinical and imaging characteristics.     

IMAGING DIAGNOSIS: ACUTE LUNG INJURY FOLLOWING MASSIVE BEE ENVENOMATION IN A DOG

A 5-year-old neutered male mixed breed dog presented for increased respiratory effort after being stung by over 100 bees and developing anaphylactic shock. Given the history, clinical signs and thoracic radiographic findings of a mild bilateral interstitial pattern, acute lung injury/acute respiratory distress syndrome (ALI/ARDS) was suspected. Further testing was performed to support this diagnosis. On computed tomographic images, there was a diffuse bilateral opacification of the lungs, with preservation of bronchial and vascular margins. Pulmonary function testing indicated decreased pulmonary compliance, decreased diffusion capacity and decreased functional residual capacity. These results supported the diagnosis of ALI/ARDS secondary to bee sting envenomation and development of anaphylactic shock. After 8 days of treatment with oxygen, steroids, antibiotics, and bronchodilators the dog improved. This case demonstrates the usefulness of computed tomography and pulmonary function testing in the diagnosis of ALI/ARDS.     

Severe pulmonary disease due to multisystemic eosinophilic epitheliotropic disease in a horse

Multisystemic eosinophilic epitheliotropic disease was diagnosed histologically in a 17-year-old Quarter Horse intact mare that was presented with a chronic history of respiratory distress. At necropsy, the lungs were poorly collapsed and the pulmonary parenchyma contained innumerable, discrete, spherical nodules in a miliary pattern. A few similar nodules were scattered in the liver and the renal lymph nodes. Histologically, these nodules consisted of fibrosing eosinophilic granulomas. Based on histologic findings and the absence of an etiologic agent, a diagnosis of multisystemic eosinophilic epitheliotropic disease was made.     

Clinical, radiological and pathological features of 12 Irish setters with canine leucocyte adhesion deficiency

The clinical, radiological and pathological findings in 12 dogs with canine leucocyte adhesion deficiency (CLAD) from six litters are described. All the dogs were younger than 15 weeks at admission, all had been febrile and 11 had been treated with antibiotics. Seven had been treated for omphalophlebitis. At admission, all had gingivitis, lymph node enlargement and profound neutrophilia. Ten dogs were radiographed and showed various skeletal lesions compatible with metaphyseal osteopathy, craniomandibular osteopathy and osteomyelitis. Four dogs had clinical signs of respiratory distress and seven exhibited a mild interstitial pneumonia at necropsy. Six dogs had skin wounds, with strikingly few neutrophils seen on stained sections. All dogs were euthanased before six months of age due to severe and incurable infections. The clinical signs, radiological features and haematology were strongly suggestive of CLAD. The diagnosis was confirmed by granulocyte function tests and flow cytometry, which revealed impaired adhesion, impaired C3b-mediated phagocytosis and absence of adhesion proteins CD11b/CD18.     

Bronchointerstitial Pneumonia and Respiratory Distress in Young Horses: Clinical, Clinicopathologic, Radiographic, and Pathological Findings in 23 Cases (1984–1989)

Twenty-three foals, between 1 and 7 months old, with signs of acute respiratory distress, were examined at the Veterinary Medical Teaching Hospital (VMTH), University of California, Davis, between 1984 and 1989. Characteristic features included sudden onset of severe respiratory distress and tachypnea, cyanosis unresponsive to nasal oxygen, pyrexia, hypoxemia, hypercapneic respiratory acidosis, poor response to treatment, and histopathologic lesions of bronchiolitis and bronchointerstitial pneumonia. Seven of the 23 foals were normal before the onset of respiratory distress, 3 foals were found dead, aqd 13 foals were being treated for respiratory tract infections at the time of presentation. Laboratory data obtained for 13 horses showed increased plasma fibrinogen concentration (630.7 ±193 mg/dL), leukocy-tosis (18,607 ± 7,784/μL), and neutrophilia (13,737 ± 8,211/μL). Thoracic radiographs showed a diffuse increase in interstitial and bronchointerstitial pulmonary opacity and, in 5 foals, an alveolar pulmonary pattern of increased density was also seen. In 3 foals heavy interstitial infiltration proceeded to a coalescing nodular radiographic appearance. Microbiological culture of tracheobronchial aspirates (TBA) from 9 foals yielded bacterial growth, but no one bacterial species was consistently isolated. Microbiological culture of postmortem specimens of the lung from 6 foals yielded growth of bacteria that included Escherichia coli, Enterobacter spp., Proteus mirabilis, Klebsiella pneumonias, Rhodococcus equi, or β-hemolytic Streptococcus spp. Tracheobronchial aspirates from 4 foals and lung samples collected from a further 4 foals at necropsy yielded no bacterial growth. Cultures were not taken from two foals premortem or postmortem. Virologic examination of TBA, lung tissue, or pooled organ tissue from 12 foals was negative. Viral culture of TBA from 1 foal showed cytopathic effects and positive immunoflu-orescence for equine herpes virus type II (EHV-II). In addition to the 3 foals that were found dead, 11 foals died or were euthanatized. Pathologic lesions were limited to the lungs in 50% of the foals; the remainder also had bowel lesions suggestive of hypoxic injury. The predominant histopathologic pulmonary lesions included bronchiolitis, bronchiolar and alveolar epithelial hyperplasia, and necrosis. Many bronchioles were filled with mucoid and fibrinocellular exudate. The peribronchiolar interstitium and adjacent alveolar spaces were also infiltrated with inflammatory cells and contained proteinaceous edema fluid. Type II cell hyperplasia and hyaline membrane formation were observed in the majority of foals and in 2 foals alveolar multinucleate giant cells were also present. Nine of 13 foals (69%) on which treatment was attempted at the VMTH survived after aggressive medical care that included external thermoregulatory control, oxygen by nasal insufflation, antimicrobial drugs, bronchodilating agents, nonsteroidal anti-inflammatory drugs, and corticosteroids. Persistent radiographic evidence of increased interstitial density was noted up to 24 months after initial presentation, and one horse remained exercise intolerant for at least 15 months after discharge. The exact etiopathogenesis of this disorder and long-term sequalae in the survivors have yet to be fully determined. However, it is likely that a number of different insults rather than a single agent may initiate the pulmonary damage that leads to severe interstitial pneumonia and subsequent acute respiratory distress or apparent sudden death in foals. (Journal of Veterinary Internal Medicine 1993; 7:277–288. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

Diffuse alveolar damage in a young cat

A 10-month-old cat was diagnosed with congenital subvalvular aortic stenosis. To resolve its hypoxia, oxygen therapy was administered a couple of times a week during two months. The oxygen partial pressure in the chamber was maintained between 30 and 35%, and the time for one procedure was 12-24 hr. The animal died due to severe respiratory failure. At necropsy, the lungs were voluminous and had a rubbery texture. Histologically, large type II pneumocytes with occasional atypia had diffusely proliferated within the lungs. Interstitial fibrosis was not observed, although some alveolar septa were thickened along with fibrinous exudates and neutrophilic infiltration. The histology of these lesions was consistent with diffuse alveolar damage (DAD), which might have been partially due to oxygen toxicity.     

CHARACTERIZATION OF SEVERE SMALL AIRWAY DISEASE IN A PUPPY USING COMPUTED TOMOGRAPHY

A young Golden Retriever dog developed severe respiratory distress following an initial clinical diagnosis of infectious tracheobronchitis. Severe expiratory flow limitation, associated with exertional respiratory distress and hypoxemia was present. Thoracic images obtained with conventional radiography were characterized by hyperinflation and abnormal bronchial and alveolar patterns. Computed tomography was performed and in conjunction with pulmonary functional changes was diagnostic of small airway disease. The dog was treated with a variety of antibiotics, anti-inflammatory agents, and antitussives, but the clinical signs worsened and the puppy was euthanized. Pathologic examination confirmed severe small airway disease, with emphysema and bronchiolitis.     

Association of bovine respiratory syncytial virus with atypical interstitial pneumonia in feedlot cattle

Thirty-three cattle with fatal respiratory tract disease were examined for gross and histologic lesions and for the presence of viral and bacterial agents in the lungs. Fifteen cattle had lesions characteristic of atypical interstitial pneumonia (AIP), and 18 had other respiratory tract diseases, including infectious bovine rhinotracheitis, shipping fever pneumonia, bronchopneumonia, pulmonary abscess, and edema of the trachea. Gross necropsy findings in the cattle with AIP were uncollapsed and emphysematous lungs; histopathologic findings included interstitial edema, thickening of alveolar walls, hyaline membrane formation, and hyperplasia of type-II pneumonocytes. The infective agents found in the lungs of the 33 cattle included bovine respiratory syncytial virus, bovine herpesvirus type 1, Pasteurella sp, mycoplasmas, and Corynebacterium pyogenes. Bovine respiratory syncytial virus was detected by use of immunofluorescence and immunoperoxidase on lung tissue sections; bovine herpesvirus type 1 was detected by these techniques and by isolation of the virus. Bovine respiratory syncytial virus was significantly (P = 0.01) associated with lesions of AIP (11 of 15), compared with those of other respiratory tract diseases (5 of 18).     

Thoracic trauma and post operative lung injury in a neonatal foal

A 24‐hour‐old Standardbred filly was referred with an acute history of weakness, respiratory distress and subcutaneous emphysema. Radiographic evaluation revealed left sided rib fractures, unilateral pneumothorax and pneumomediastinum. Serial arterial blood gas measurements pre‐ and post rib repair showed pulmonary dysfunction. Post operative radiographs revealed the presence of air bronchograms and a bronchointerstitial pattern, suggestive of alveolar parenchymal pathology consistent with pulmonary contusion, pulmonary oedema or ALI/ARDS. The filly was treated with intranasal oxygen and an active chest draining unit and recovered uneventfully.     

Respiratory syncytial virus pneumonia in young calves: clinical and pathologic findings

Nine young calves given respiratory syncytial virus by a combined intranasal and intratracheal route developed a severe respiratory tract disease in which coughing, tachypnea, and hyperpnea were prominent clinical features. Calves were euthanatized on postinoculation (initial) days (PID) 1 to 13. At necropsy, large areas of consolidation were present in the cranial, middle, accessory, and cranial parts of the caudal lung lobes of calves killed between PID 4 and 13. Histopathologic examination revealed widespread and severe lesions in small bronchi, bronchioli, and alveoli. Multinucleate epithelial syncytia on bronchiolar and alveolar walls, many containing eosinophilic intracytoplasmic inclusion bodies, were present in the lungs of calves killed on PID 4, 5, and 6. Necrosis and epithelial loss, hyperplasia, and metaplasia were also observed in the epithelium of small bronchi and bronchioli. The lumina of these airways were occluded to varying degrees with exudate. Exudate was present within alveoli, and interalveolar septa were markedly thickened. Collapse of the thickened septa produced large areas where alveolar air spaces were totally obliterated. Repair was evident in the lungs of calves killed at PID 10 and 13 with reepithelialization of damaged bronchiolar mucosa, organization of bronchiolar exudate leading to bronchiolitis obliterans, and peribronchial and peribronchiolar fibrosis. Inoculation of 3 calves by an intranasal route alone produced a less severe clinical disease with only minimal lesions present at necropsy.     

Vaccination against canine bordetellosis: protection from contact challenge

Eight collie-cross pups, eight weeks old, were inoculated intramuscularly with an aluminum hydroxide adjuvanted preparation of killed Bordetella bronchiseptica; the inoculation was repeated after two weeks. Two weeks after the second inoculation, the vaccinated dogs and a control group of four unvaccinated animals were placed in contact with a group of five pups of similar age which had been experimentally infected with a pathogenic strain of B bronchiseptica by an aerosol method. All four unvaccinated control dogs as well as all five experimentally infected dogs developed a respiratory disease characterised by persistent coughing. Six of the vaccinated dogs remained free from clinical respiratory disease while disease was less severe and of shorter duration in the remaining two than in controls. Only slight changes were found in the lungs of vaccinated animals at necropsy while in the controls there was a severe tracheobronchitis. There was a marked reduction in the numbers of B bronchiseptica isolated from the respiratory tract of vaccinated animals when compared with controls. An aluminium hydroxide adjuvanted vaccine may be of value in controlling naturally occurring canine respiratory disease in which B bronchiseptica is involved.     

Fibrin/fibrinogen in lungs and respiratory secretions of horses with chronic pulmonary disease

The concentration of soluble fibrinogen derivatives (SFD) and protease and procoagulant activities were determined in cell-free supernatants of equine respiratory secretions obtained from horses with chronic pulmonary disease. The concentration of neutrophils was estimated from direct smears of the secretions. Lung specimens and smears of the secretions were evaluated for the presence of fibrin or fibrinogen by use of immunohistochemical methods. Thirty-five of 80 specimens tested contained SFD. Respiratory secretions from horses with moderate or severe chronic pulmonary disease contained SFD more frequently than did secretions from mildly affected horses (P less than 0.05). Respiratory secretions with vast numbers of neutrophils had significantly (P less than 0.05) higher SFD concentrations than respiratory secretions with fewer neutrophils. Protease and procoagulant activities in respiratory secretion specimens were positively correlated with neutrophil content, clinical diagnosis, and SFD concentration. Immunohistochemically, macrophages that stained for fibrin or fibrinogen were observed in direct smears of respiratory secretions from horses with moderate and severe chronic small airway disease, but not in smears from mildly affected horses. Fibrin or fibrinogen was detected in a few thickened alveolar septa from 10 horses with moderate or severe chronic small airway disease, but not in lungs from horses with mild or no evidence of chronic small airway disease. Fibrin or fibrinogen was detected in alveolar septa, granulomas, and on alveolar macrophages in lungs of all horses with chronic granulomatous and chronic bronchointerstitial pneumonia. The presence of SFD in equine respiratory secretions may be an indicator of pulmonary inflammation.     

Pulmonary Lymphomatoid Granulomatosis in Seven Dogs (1976–1987)

Seven dogs with pulmonary lymphomatoid granulomatosis were reviewed. The disease occurred in six large-breed and one small-breed dogs. The dogs were five to 14 years old (mean, 8.4; median, 7), and four of seven dogs were males. Three dogs had been previously treated with adulticide therapy for canine dirofilariasis. Clinical histories included a progressive respiratory disease characterized by varying degrees of cough, dyspnea, exercise intolerance, and weight loss. Thoracic radiographic features included hilar lymphadenopathy, pulmonary masses of varying sizes, and mixed pulmonary patterns of lobar consolidation with ill-defined interstitial and alveolar pulmonary infiltrates. Cardiovascular changes compatible with chronic dirofilariasis were present in three dogs. The clinical course was usually progressive and fatal. The survival time ranged from six days to four years (mean, 12.5 mos; median, 3 mos). Gross and histologic features included mass lesions with areas of necrosis that replaced normal pulmonary architecture. Cytologically, these lesions were characterized by infiltration with pleomorphic, angioinvasive mononuclear cells that often resulted in vascular obliteration. The infiltrating cells resembled large lymphoid cells that possessed large hyperchromatic nuclei and small amounts of cytoplasm. Systemic lymphoid neoplasia with peripheral lymphadenopathy was diagnosed in two dogs. In both cases, lymph-node cytology was similar to the cellular infiltrates found in the lungs and consistent with a diagnosis of lymphomatoid granulomatosis. These features are compared with previously reported cases of canine lymphomatoid granulomatosis and those features identified in a similar disease described in man.     

PNEUMOCOELOM ASSOCIATED WITH SERRATOSPICULUM AMACULATA IN A BALD EAGLE

Serratospiculum amaculata Nemutodes were identified radiographically in the air sacs of an eagle which developed acute respiratory distress several days after treatment for severe head trauma. The nematodes were found at necropsy within the air sacs and lungs. One of the nematodes was found protruding through a hole in the lung. Although this parasite was reported in a falcon which died post operatively this is the first report of death in an eagle related to the presence of this parasite and is also the first time the parasite itself has been observed in a raptor antemortem.     

Observations on outbreaks of respiratory disease in calves associated with parainfluenza type 3 virus and respiratory syncytial virus infection.

In four outbreaks of indoor calf pneumonia, dyspnoea was a prominent clinical finding. At necropsy it was associated with pneumonia involving the cranial lobes of the lung and severe pulmonary emphysema. Histological examination of lung tissue revealed bronchiolitis and alveolitis with alveolar epithelial cell hyperplasia and multinucleate syncytium formation. Intraalveolar haemorrhage, intra-alveolar oedema and hyaline membrane formation were also noted. In all cases parainfluenza type 3 (PI3) virus was isolated from the lungs. In each of the four outbreaks there was evidence of PI3 virus and respiratory syncitial virus (RSV) infection.     

Malignant histiocytosis in Bernese Mountain dogs

Malignant histiocytosis was diagnosed in 10 male and 1 female Bernese Mountain Dogs. Nine of these dogs were closely related. The disease was characterized by a rapidly progressive and inevitably fatal course. Clinical signs varied, but lethargy, anorexia, weight loss, and respiratory and CNS abnormalities predominated. The lungs were the primary site of tumor involvement in 10 dogs. The eleventh dog had lymphadenopathy and severe anemia. Metastatic lesions were detected in all dogs. Anaplastic pulmonary carcinoma was diagnosed originally in 6 of the 11 cases, but this diagnosis was changed to malignant histiocytosis after electron microscopic examination of tissues and immunohistochemical identification of histiocytic markers in the tumor cells.