Few definitive options exist to manage acute respiratory disease


Most dogs with ARDS show little response to oxygen supplementation and remain dyspneic.

Q What are some pulmonary complications in dogs that I might see in my practice?

A Dr. Lesley G. King at the 2004 Western Veterinary Conference in Las Vegas gave a lecture on pulmonary complications of critical illness in dogs. Some relevant points in this lecture are provided below.

Canine acute respiratory distress syndrome

Canine acute respiratory distress syndrome (ARDS) is an acute, usually fatal, complication of a number of disease states. In sepsis, a diffuse inflammatory process is triggered by bacterial endo-toxin that results in activation of an avalanche of diverse inflammatory mediators, including a variety of cytokines, the complement and arachidonic acid cascades, and cells such as neutrophils and macrophages. This common pathway of inflammation can affect the function of any or all organ systems in the septic dog. Alternatively, ARDS can be triggered by local pulmonary catastrophes, such as severe aspiration pneumonia, pulmonary contusions or smoke inhalation. In either case, because the lung has only one way to respond to inflammatory damage, the clinical and histopathologic findings are very similar.

In dogs with ARDS, the initial stages of the syndrome begin as a diffuse exudative vascular leak syndrome with infiltration of neutrophils and macrophages into the lung. These changes are accompanied by effusion of protein-rich fluid into the alveoli and clinical evidence of progressive pulmonary edema. As ongoing inflammation is combined with early attempts at repair by the lung tissue, proliferation of type II pneumocytes, formation of hyaline membranes within alveoli due to organization of protein-rich fluid and cellular debris, deficiency of surfactant, and collapse and atelectasis of alveoli occur. Much later, these changes are followed by interstitial fibrosis as the lung attempts to repair the damaged parenchymal tissue. The inflammatory changes in the lung can vary in severity and are usually unevenly distributed, often affecting the ventral areas first. At times, the process is mild and then termed acute lung injury. In more severely affected dogs, the inflammation is profound, overwhelming and leads to severe hypoxia.

ARDS is recognized clinically by the development of pulmonary edema in an animal with a predisposing cause of an inflammatory response. Animals that have ARDS are in severe respiratory distress and are usually cyanotic. Auscultation reveals harsh lung sounds that rapidly progress to crackles. Dogs might expectorate pink foam, and if intubated, sanguineus fluid can drain out of the endotracheal tube. Arterial blood gases usually reveal hypoxia and hypocarbia, and metabolic acidosis can be present. These animals usually have diffuse bilateral pulmonary alveolar infiltrates throughout all lung fields on thoracic radiographs.

Most dogs with ARDS show little response to oxygen supplementation and remain severely dyspneic. If placed on a ventilator, the lungs are found to have very poor compliance, and high peak airway pressures can be seen even if the tidal volume is small. Positive end expiratory pressure usually is required to achieve adequate oxygenation.

Few options

Few options are available for definitive management of ARDS, and supportive care is primarily aimed at treating the underlying cause and supporting oxygenation. Because of the variety of inflammatory cascades and cells that mediate the inflammatory response in ARDS, specific anti-inflammatory drugs, such as corticosteroids, largely are ineffective for treatment and can cause immunosuppression that can exacerbate sepsis. Advances such as liquid ventilation, synthetic surfactant therapy and inhaled nitric oxide have yet to be evaluated in dogs with naturally occurring disease.

Bacterial pneumonia

Bacterial pneumonia is another common complication in dogs. The protective reflex of laryngeal closure to prevent tracheobronchial aspiration, and the normal cough reflex that forcefully expels material from the airway when tracheobronchial aspiration occurs are compromised by muscle/nerve weakness, sedation or intubation. In these situations, the pharynx rapidly becomes colonized with pathogenic gram-negative bacteria that can then easily invade the tracheobronchial airway. The cleansing action of the mucociliary blanket is compromised by intubation and inhalation of dry, cold air. Further, bronchus-associated lymphoid tissue and alveolar macrophages can have decreased function as a result of malnutrition and protein catabolism.

Aspiration of gastrointestinal tract contents is perhaps the most common means by which bacterial pneumonia occurs in these dogs. Initial chemical damage to the lung is rapidly followed by bacterial multiplication. Any vomiting or regurgitating dog is a candidate for aspiration pneumonia, especially if combined with laryngeal abnormalities. However, aspiration pneumonia is not always associated with episodes of overt vomiting or regurgitation. "Silent aspiration" can occur in weak or semi-conscious animals (for example, extubated dogs recovering from anesthesia). In these dogs, aspiration of gastrointestinal contents can occur without overt vomition and without obvious coughing or distress.

The typical clue to the presence of pneumonia is a moist, productive cough, which can often be elicited on tracheal palpation. Mucous membranes vary in color from normal pink and moist to cyanotic, depending on the degree of compromise of gas exchange. In the hyper-dynamic stage of sepsis, the mucosal membranes might be hyperemic. Rectal temperature may be elevated or low, but in many cases, it is normal. On auscultation, rales or crackles might be detectable, especially in the cranioventral lung fields, although lung sounds might appear deceptively normal, especially in large recumbent dogs. If coughing is present in a susceptible dog, then thoracic radio-graphs can rule out the presence of pneumonia even if auscultation is normal. On radiographs, bacterial pneumonia usually manifests as an alveolar pattern, which can be variable in location and severity. The type of pneumonia often can be inferred by the distribution of alveolar disease on the radiograph — aspiration pneumonia is usually cranioventral whereas septic emboli can appear to be nodular.

Cytologic exam key

The definitive diagnosis of bacterial pneumonia resides with cytologic examination and microbiologic culture of samples obtained by transtracheal wash or bronchoalveolar lavage. Cytology of these aspirates often reveals an acute to chronic suppurative process with excessive mucus and proteinaceous material, many neutrophils and some alveolar macrophages. Intracellular bacteria might be evident but are not always seen. Cultures commonly demonstrate gram-negative organisms, but gram-positive and anaerobic bacteria or Mycoplasma also can act as respiratory pathogens.

Therapy for bacterial infection includes antibiotics, which should be given parenterally rather than orally in the critically ill dog, particularly those that are vomiting or regurgitating. Drugs with high activity against gram-negative and gram-positive organisms and are well distributed to the pulmonary parenchyma should be considered. Good choices for intravenous administration in critically ill dogs with pneumonia include fluoroquinolones or ampicillin/aminoglycoside combinations. In severely compromised dogs with hypoxia, oxygen supplementation also is required.

In addition, measures that maximize the host immune response are just as important for elimination of the organism by allowing the animal to clear mucus and secretions from the airway more efficiently. Maximum clearance of secretions from the airway can be achieved when the secretions are maintained in a moist state, rather than allowing them to become thick and viscid. Close attention should be paid to the hydration status of the dog, and provide intravenous fluids if necessary.

Nebulization can help

Coughing is one of the most important airway clearance mechanisms and is to be encouraged. Nebulization with an ultrasonic nebulizer also can make a big difference to the dog's ability to clear secretions. The tiny water droplets produced by the nebulizer are inhaled into the lungs, where they shower-out moistening and loosening secretions. If saline nebulization is combined with thoracic wall coupage, bouts of productive coughing can be initiated, which can significantly improve the rate of recovery. Nebulization and coupage for 10 minutes to 15 minutes several times daily are warranted. Similarly, any physical activity, by allowing the mobilization of secretions and by promoting an increased tidal volume per breath, will help the dog to clear the pneumonia. Dogs that are recumbent or have weak cough reflexes are among the most difficult to treat.

Pulmonary thromboembolism

The incidence of diagnosed pulmonary thromboembolism has increased dramatically in the last few years. Thrombi can develop as a result of a combination of hypercoagulability, vascular endothelial damage and abnormal blood flow patterns or blood stasis. In sepsis, disseminated intravascular coagulation and other disease states, the dog's coagulation system can become excessively active or the action of the fibrinolytic system can become depressed and result in hypercoagulability. Hyper-coagulability also occurs in animals that have been exposed to high levels of endogenous or exogenous steroids. Some disorders, such as protein-losing nephropathy, can result in low blood levels of antithrombin III, a serine protease that modulates the coagulation system.

Diffuse vascular damage occurs frequently as a consequence of a variety of inflammatory disorders, such as sepsis, pancreatitis or immune-mediated diseases, including immune-mediated hemolytic anemia. In each of these situations, various inflammatory mediators are activated, and all of these mediators can contribute to endothelial damage. Once endothelial damage has occurred, activation of the coagulation cascade follows and contributes to the development of thrombi. Stasis of blood is a feature of many critical illnesses. Any condition that leads to poor perfusion or shock may predispose to pooling of blood in the periphery or in the splanchnic vasculature. Other disorders that can be accompanied by blood stasis include vascular obstructive diseases and heart failure.

The diagnosis of pulmonary thrombo-embolism is difficult. Many animals with minor pulmonary showering by emboli can be completely asymptomatic, while those with major thromboembolic disease can develop profound respiratory distress and die acutely. The clinical hallmark of the disease is the development of respiratory difficulty in an animal with a predisposing cause of hypercoagulability. Auscultation findings are variable, ranging from normal to harsh or even crackles.

Most affected animals have significant hypoxia, which can be determined by clinical parameters, or by arterial blood-gas analysis or pulse oximetry. Thoracic radiographs are variable and often reveal normal to hyperlucent lung fields. Alternatively some animals with thromboembolism might have areas of alveolar disease or pleural effusion. Acute pulmonary thromboembolism often is accompanied by a sudden decrease in platelet count, which presumably is caused by platelet consumption. Definitive diagnosis of pulmonary thromboembolism is made by selective angiography. The finding of abnormal perfusion on scintigraphic ventilation/perfusion scanning also is strongly suggestive of thromboembolic disease.

If pulmonary thromboembolism is suspected, several potential therapies can be attempted. Aggressive supportive care, attention to tissue perfusion, oxygen supplementation and treatment of the underlying disease remain priorities for its management. If the size of the embolus is not excessive, then the dog's own fibrinolytic system might be able to break it down eventually and recanalize obstructed vessels. The time required for resolution in critically ill dogs might vary from just a few days to two or three weeks. "Clot buster" drugs, such as tissue plasminogen activator, streptokinase, or urokinase, actively break down clots within the circulation. Such drugs are most effective if delivered within two hours of development of the clot and if delivered directly onto the surface of the clot. This can be difficult to achieve.

If thromboembolic disease is suspected, prophylactic therapy with heparin seems to be helpful to prevent formation of more thrombi, but it has no effect to break down of thrombi that already are present. Unfractionated heparin doses of 100-300 IU/kg subcutaneously qid or CRI 10-50 IU/kg hourly can be administered. Unfractionated heparin therapy should be monitored by daily measurement of PTT values. Prolongation of the PTT by 50 percent from the baseline is adequate heparin therapy. Heparin therapy should be weaned gradually as the clinical state improves because rebound hypercoagulability can occur if it is suddenly withdrawn.

Dr. Hoskins is owner of DocuTech Services. He is a diplomate of the American College of Veterinary Internal Medicine with specialities in small animal pediatrics. He can be reached at (225) 955-3252, fax: (214) 242-2200, or e-mail:johnny@docu-techservices.com.

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