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Approach to the patient with respiratory distress
Vet Clin Small Anim 35 (2005) 307–317
Approach to the Patient with Respiratory Distress Elizabeth Rozanski, DVM*, Daniel L. Chan, DVM Section of Emergency and Critical Care, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, 200 Westboro Road, North Grafton, MA 01536, USA
Respiratory distress of any origin represents a true emergency requiring rapid identification of the underlying cause, immediate alleviation of the sensation of difficulty in breathing, and provision of diagnostic and therapeutic information for the owners of affected animals. Clearly, there are a variety of potential underlying reasons for the development of respiratory distress. For the clinician in emergency practice, successful management of patients in respiratory distress revolves around developing a knowledge base of the potential causes of respiratory distress and ‘‘pattern recognition’’ of common emergent problems affecting dogs and cats. Prompt recognition of the underlying condition and appropriate therapeutic interventions are essential in the management of respiratory emergencies. The goals of this article are to review the function of the respiratory system, to describe pathophysiologic causes for hypoxemia, to illustrate various methods for classifying respiratory distress, to highlight common emergency conditions resulting in respiratory distress, and to provide guidelines for emergent management. Gas exchange As a review, the primary goal of the respiratory system is to promote gas exchange. Air enters the upper respiratory system via the nose or the mouth. The air is warmed and humidified and then passes down the respiratory tree. Larger particles of debris are filtered out. The trachea branches into the successive generation of smaller and smaller airways. Gas exchange occurs at the level of the alveoli. Although the flow of air (ventilation, termed V) is * Corresponding author. E-mail address: [email protected] (E. Rozanski). 0195-5616/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.cvsm.2004.12.003 vetsmall.theclinics.com
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obviously essential, the other aspect of gas exchange involves the delivery of blood (perfusion, termed Q) to the level of the alveoli. Blood reaches the capillaries adjacent to the alveoli by way of the pulmonary vasculature. The blood exits the right heart via the pulmonary outflow tract and then flows through the pulmonary arteries. These arteries branch into smaller and smaller vessels until they reach the level of the capillary. Red cells traverse the capillaries in single file; during contact with the alveoli, the oxygen diffuses out of the alveoli and binds to the hemoglobin, because the carbon dioxide (CO2, waste gas) diffuses off the hemoglobin molecule into the alveoli for expiration. In normal animals, the capillary endothelium is impermeable to larger molecules, such as albumin. Causes of hypoxemia In animals that develop hypoxemia, there are five possible broad causes. Each disease observed clinically fits into one of more of the following categories. These causes include a low inspired oxygen concentration (FiO2), hypoventilation, shunt, ventilation-perfusion (V-Q) mismatch, and diffusion impairment [1]. Normal oxygen concentration in room air is approximately 21%, and low FiO2 is an uncommon cause of hypoxemia. This may occur at higher altitudes or because of anesthesia machine dysfunctioning, however [1]. Low FiO2 may be simply corrected by supplementing oxygen. Hypoventilation results from absent or ineffective (low) tidal volumes as a result of such causes as drug therapy side effects (eg, opioids, propofol) or loss of central respiratory drive [2]. Respiratory muscle fatigue in patients with prolonged and severe dyspnea can result in hypoventilation [3]. Hypoventilation is treated by mechanical ventilation or by reversing the cause that triggered the hypoventilation. It should be emphasized that hypoventilation may not be appreciated as respiratory compromise because respiratory attempts are limited or depressed. Shunt refers to the complete bypassing of ventilated areas of the lungs by deoxygenated blood and re-entry into the circulatory system [4]. The classic example of a shunt is the right-to-left shunt that accompanies the cardiac defect of the tetralogy of Fallot (right ventricular hypertrophy, ventricular septal defect [VSD], pulmonic stenosis, and overriding aorta). In affected animals, the severity of the pulmonic stenosis results in the shunting of deoxygenated blood through the VSD into the left ventricle. Because oxygen supplementation cannot affect shunted deoxygenated blood, pure shunts are described as nonresponsive to oxygen supplementation. In certain conditions, significant alveolar pathologic changes can contribute to shunting. Alveoli filled with inflammatory exudates, edema, or blood can reduce gas exchange efficiency. Because this is not a true shunt, however, oxygen supplementation can improve oxygenation. V-Q mismatch refers to the poor coordination of the areas of the lung that are adequately perfused versus those that are appropriately ventilated,
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resulting in impairment of gas exchange [4]. Normally, there is a good match between areas that are appropriately ventilated and those that are adequately perfused. In some cases, however, areas of the lungs can be perfused but are not well ventilated (low V/Q ratio), whereas in other conditions, well-ventilated areas are inadequately perfused (high V/Q ratio). Conditions associated with a low V/Q ratio include pneumonia, edema, hemorrhage, and inflammatory exudates. Pulmonary thromboembolism is an example of a condition resulting in a high V/Q ratio. This mismatching results in the development of hypoxemia but is not necessarily accompanied by hypercarbia. Diffusion of CO2 is many times more efficient than that of oxygen, explaining the discrepancy when gas exchange is compromised. As a result of physiologic responses by the lung, V-Q mismatch generally responds to oxygen supplementation. The final area that may result in hypoxemia is diffusion impairment. Typically, during the transition phase through the capillary bed, the oxygen diffuses within the first third of the length of the capillary. If the alveolarcapillary membrane is significantly thickened, however, there may be diffusion impairment and gas exchange can become compromised. Diseases resulting in diffusion impairment include pulmonary interstitial pathologic findings such as fibrosis, severe interstitial pneumonia, and interstitial hemorrhage. Oxygen supplementation can increase the oxygen tension within the alveoli sufficiently to overcome diffusion impairment and alleviate hypoxemia.
Oxygen therapy Although an understanding of the potential causes of respiratory distress is indispensable, the first steps in the clinical evaluation of a patient presented with respiratory distress are to provide a supplemental source of oxygen and to obtain a brief history from the client or owner. All emergency facilities should be equipped to provide a form of supplemental oxygen. Supplemental oxygen may be provided by means of a variety of options, including flow-by oxygen, a face mask, nasal oxygen, an Elizabethan collar and cellophane wrap (‘‘oxygen hood’’), an oxygen cage, and intubation with intermittent positive-pressure ventilation (IPPV). Flow-by oxygen is provided by holding oxygen tubing near the mouth and nostrils of the affected patient. The flow rate is usually set at 100 mL/kg/min or greater. Flow-by oxygen is an easy and rapid solution; however, the actual increase over room airÕs 21% oxygen content may be minimal, particularly with an anxious or uncooperative animal. Oxygen may also be provided with a face mask, with the oxygen tubing attached to a cone that is placed over the nose and mouth of the patient. The FiO2 with a face mask is also variable, although a high percentage may be reached in weak animals. Flow-by and face mask oxygen may require veterinary personnel to hold the pet and the oxygen supply.
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Nasal oxygen involves placement of a flexible catheter into the nasal passages and insufflation of humidified oxygen. Nasal oxygen is particularly useful in pets that are not panting or are demonstrating open-mouthed breathing. Nasal oxygen is commonly placed after patient stabilization rather than urgently in the emergency setting. An improvised oxygen hood may be created with an Elizabethan collar and cellophane wrap or may be commercially purchased (Jorgenson Laboratories, Loveland, CO). An oxygen cage is also frequently used to provide supplemental oxygen. Oxygen cages are commonly well tolerated by cats and dogs and are also capable of achieving a high concentration of oxygen; however, if the cage door is opened for patient manipulation, the FiO2 falls rapidly. Finally, intubation and IPPV represent the best option for providing high levels of supplemental oxygen, removing respiratory fatigue, and eliminating patient fear and anxiety.
Assessment During the initial stabilization of the pet, a history should be obtained from the owner. In some cases, the precipitating cause of the respiratory distress is straightforward, such as with traumatic injuries, whereas in other cases, the onset may be more insidious. Animals with preexisting medical conditions, such as cardiac disease, neoplasia, or megaesophagus, may also be predisposed to the development of respiratory distress. Owners should be questioned as to past medical conditions and history of routine veterinary care, including heartworm prophylaxis; finally, progression of the signs of respiratory distress should be described. Specifically, distress may be acute in onset or may be more progressive. Particularly in cats, the development of respiratory distress may be preceded by anorexia, lethargy, or abnormal behavior. Respiratory distress may be further characterized by the location of the lesion or the underlying pathophysiologic condition. Often, localization of the lesion can help to guide the clinician to the most likely cause. Specifically, respiratory distress may be localized to the upper airway, lower airway, parenchyma, or pleural space. Common pathophysiologic causes for respiratory distress include anatomic abnormalities, airway collapse, infection, inflammation, trauma, and pulmonary edema of cardiac and noncardiac causes. For the emergency clinician, the most appropriate first step is to localize the lesion and then to review specific differential diagnoses based on signalment, history, and other physical examination findings.
Diseases of the upper airway Upper airway diseases may be appreciated by loud stridulous breathing with an increased inspiratory time. Many dogs are hyperthermic on initial
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presentation because of a decreased ability to cool. The upper airways represent the primary source of resistance to airflow. Upper airway obstructions can be dynamic or fixed. Dynamic obstructions are characterized by the paradoxic movement of tissues into the lumen of airways during inspiration. Common dynamic obstructions include laryngeal paralysis and tracheal collapse, whereas fixed obstructions include extraluminal obstructions, such as neoplasia or cellulitis, and intraluminal obstructions, such as laryngeal tumors or nasopharyngeal polyps. Dynamic and fixed severe upper airway obstructions also result in the development of airway mucosal edema and possibly everted laryngeal saccules as a result of irritation from the increased air flow rates through a narrow lumen. Emergently, upper airway obstruction should be suspected in any dog with loud and noisy breathing. Therapy for a suspected dynamic obstruction should include sedation and supplemental oxygen. In case of dynamic obstruction, sedation is beneficial in reducing the anxiety associated with inspiration, because with increased inspiratory efforts, there is a resulting paradoxic decline in airway diameter. Low doses of acepromazine (0.03–0.05 mg/kg administered intravenously) alone or in combination with butorphanol (0.1 mg/kg administered intravenously) are often effective. Hyperthermia should be treated by active cooling with room temperature (not cold) intravenous fluids and by placing the dog in a cool area. Because of airway swelling and edema, a single dose of a short-acting antiinflammatory glucocorticoid is advisable. If the dog has not improved within 15 to 30 minutes or the distress is worsening, more aggressive therapy is warranted. The dog should be heavily sedated or anesthetized and intubated. The emergency clinician should be competent in evaluating airway function and anatomy and in performing a tracheostomy if necessary. Additionally, because many upper airway conditions require medical or surgical interventions, the emergency clinician should fully discuss longterm outcomes and expectations with clients. The most common causes of upper airway obstruction may vary depending on location; however, in our practice, they include laryngeal paralysis, tracheal collapse, brachycephalic airway syndrome, and severe cellulitis. A complete discussion on the management of these conditions is beyond the scope of this article; however, despite their similarities, differences among the underlying diseases do exist regarding optimal management of affected patients. Awareness of the different nuances of these conditions is critical in their successful management. Laryngeal paralysis primarily affects older large-breed dogs, particularly retrievers. Usually, the clinical signs of noisy breathing have been present for some length of time before a crisis. Crises often occur during the first hot and humid days of the spring or summer months and may be associated with exercise. Dogs typically respond well to sedation. Dogs that do not rapidly improve should be sedated, have their laryngeal function evaluated, and be intubated. If palliative surgery is not readily available, dogs may
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require a tracheostomy or may be kept sedated/intubated until normothermia and eupnea are restored. In our practice, we commonly anesthetize patients with propofol for 30 to 60 minutes. If a dog cannot be safely extubated after this time, a tracheostomy may be performed rather than keeping a patient intubated and thereby raising the risk of aspiration pneumonia. Conversely, in dogs with severe brachycephalic airway syndrome or tracheal collapse, avoidance of a tracheostomy is preferable as compared with dogs with laryngeal paralysis. The reason for this is that many of these dogs become permanently dependent on the tracheostomy tube once placed. If a tracheostomy is unavoidable, plans should be made for surgical correction of the obstruction as soon as feasible. Brachycephalic dogs may also develop laryngeal collapse, which is not amenable to laryngoplasty and may ultimately necessitate a permanent tracheostomy. In cats, upper airway obstructions are less common but may be caused by nasopharyngeal polyps or infiltrative laryngeal diseases (neoplastic or granulomatous diseases). Nasopharyngeal polyps are a condition of young cats. Occasionally, cats with severe pleural effusion have the appearance of severe inspiratory distress. If sedation for an oral examination of a cat with a suspected upper airway obstruction is planned, supplies should be collected ahead of time for an emergency tracheostomy. The laryngeal lumen of affected cats may be only 1 or 2 mm in diameter and may require an urgent tracheostomy. If biopsy of a laryngeal mass is performed in a cat, a tracheostomy is almost always required because of subsequent airway swelling. Cats may also have a permanent tracheostomy placed, although it is less well tolerated than in dogs.
Diseases of the lower airways Respiratory distress may also result from lower airway disease, parenchymal lung disease, or pleural space disease. Thoracic radiographs are essential to help clarify the degree of pulmonary or pleural space involvement. Nevertheless, it is important to recall that radiography can be stressful, particularly in cats that are experiencing respiratory distress. Lower airway diseases include chronic bronchitis and feline asthma. Chronic bronchitis rarely presents emergently, although flare-ups do occur in some patients. Chronic bronchitis is defined as the presence of a cough on most days for the preceding 2 months, without evidence of other underlying cause. Canine chronic bronchitis commonly affects small-breed dogs. On auscultation, a mitral murmur is commonly identified. Conversely, feline lower airway disease may present as an emergency. In cats, airway disease seems to represent a continuum, with some cats having primarily inflammatory airway disease with cough and excessive mucus production, whereas other cats are the more prototypical ‘‘asthmatics’’ with reversible
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bronchoconstriction. Cats with severe bronchoconstriction are often presented emergently. It is important to distinguish the airway disease from congestive heart failure (CHF). Cats with airway disease are typically normothermic and have had a history of cough. Heart failure and airway disease may be accompanied by crackles.
Diseases affecting the lungs Parenchymal lung disease is often responsible for respiratory distress. Common causes of parenchymal lung disease include pulmonary edema (cardiogenic and noncardiogenic), pulmonary contusion, pneumonia, and neoplasia. Heart failure commonly manifests as respiratory distress. Heart failure in cats is usually appreciated by hypothermia combined with an increased respiratory rate and effort. Jugular venous distention may be present. A gallop or a murmur may be ausculted. Cats with CHF commonly have slow heart rates (130–140 beats per minute [bpm]). Heart disease in dogs is usually chronic valvular disease or dilated cardiomyopathy. Animals with a history of trauma or possible trauma that are presented with respiratory distress can be assumed to have some component of pulmonary contusion (or pneumothorax). Therapy for respiratory distress associated with pulmonary infiltrates includes supplemental oxygen and therapeutic agents directed toward the presumptive underlying cause. The distribution of the pulmonary infiltrates may be useful to help determine the underlying problem. Cardiogenic pulmonary infiltrates most often surround the perihilar region in dogs, whereas the distribution of pulmonary edema may vary in cats. Bacterial pneumonias typically have a cranioventral distribution. Neoplasia usually results in a nodular pattern, although metastatic disease may appear variable. Animals with suspected cardiogenic pulmonary edema should be treated initially with diuretics (furosemide, administered intravenously or intramuscularly, either 4 mg/kg every 4–6 hours or 1–2 mg/kg every 1–2 hours), cage rest, and supplemental oxygen. If rapid improvement is not observed, additional therapy with vasodilators (nitroprusside titrated to effect) is warranted. In practice, despite published guidelines, measurement of blood pressure during infusion of nitroprusside is usually not performed so as to limit patient stress, loss of supplemental oxygen (by opening the cage door), and technical difficulties in obtaining repeatable and reliable measurements. Specifically, it may be challenging or impossible to place an arterial line for direct blood pressure determinations in an animal with CHF. Oscillometric techniques are commonly inaccurate with small dogs or cats, and Doppler techniques are time-consuming and require a patient with respiratory distress to be restrained. Dobutamine, given as a continuous rate infusion (CRI), is useful in increasing cardiac output in dogs with dilated cardiomyopathies. Intravenous fluids should not be administered to
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a patient with heart failure, although the patient should be permitted ad libitum access to water. Hemodynamically significant arrhythmias should be treated. Patients should be transitioned to long-term medications after stabilization. Although an echocardiogram is not considered an emergent procedure, emergency clinicians should have a basic knowledge of echocardiography, including assessment of left atrial size, contractility, and the presence or absence of pericardial effusion. Noncardiogenic pulmonary edema may occur for a variety of reasons. In the emergency room, head trauma, upper airway obstruction, seizures, and electric cord injury are common triggers for the development of noncardiogenic edema [5]. Noncardiogenic pulmonary edema is typically characterized by high protein; it occurs as a result of permeability shifts in the capillaries rather than hydrostatic forces, as is the case with cardiogenic edema. There is no specific therapy that has been proven beneficial for hastening recovery from noncardiogenic edema [5]. Treatment recommendations include cage rest and supplemental oxygen. More specific therapy with diuretics or colloids has been advocated by various clinicians, although no consensus statement exists. Most dogs with noncardiogenic pulmonary edema rapidly improve within 24 to 48 hours [5]. Pulmonary contusions are common after traumatic injury, particularly in dogs. Animals severely affected with pulmonary contusions are presented short of breath soon after the injury, although, radiographically, the infiltrates often worsen over the first 12 to 24 hours. Dogs with contusions commonly have small- to moderate-volume pneumothoraces as well. Contusions generally heal rapidly. One study in dogs was unable to support the use of prophylactic antibiotics or corticosteroids [6]. Diuretics are also not indicated for animals with pulmonary contusions. Dogs with pneumonia may be presented to the emergency room with respiratory distress. Bacterial pneumonia is rare in cats. Pneumonia can be subdivided into community-acquired and hospital-acquired forms. Examples of community-acquired pneumonia include severe bronchopneumonia (eg, infectious kennel cough complex) and aspiration pneumonia in a dog with laryngeal paralysis or megaesophagus. Any dog that develops pneumonia while hospitalized for treatment of another condition is considered to have hospital-acquired pneumonia. Therapy for pneumonia includes broad-spectrum antibiotics, physiotherapy, and intravenous fluids. Ideally, a bacterial culture is performed before the institution of antibiotics. Animals are infrequently presented on an emergent basis with dyspnea secondary to metastatic disease, although cough and lethargy are common. Spontaneous pneumothorax may occasionally develop in a patient with pulmonary neoplasia. Treatment of suspected neoplastic disease is directed at supportive care. Common metastatic tumors include hemangiosarcoma and mammary gland adenocarcinoma. Occasionally, further imaging is indicated to attempt to localize a primary tumor; however, this is generally futile. Pulmonary lymphoma may respond well to therapy. It is also
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important to exclude a recent travel history in dogs with a nodular pulmonary pattern, because the systemic mycoses can mimic metastatic disease. Other less common causes of pulmonary infiltrates include eosinophilic pneumonitis, smoke inhalation, and pulmonary fibrosis [7–10].
Diseases of the pleural space Pleural space disease commonly results in marked respiratory distress. Common causes are pleural effusion, pneumothorax, and diaphragmatic hernia. Pleural space disease may often be suspected clinically based on a restrictive (short and shallow) breathing pattern. Thoracic radiographs are useful in documenting the extent of the pleural space disease but may not be safely obtained in animals with severe respiratory distress. Therapeutic thoracocentesis can remove significant volumes of effusion and results in rapid improvement in respiratory rate and effort. Effusions may be classified based on fluid characteristics (transudate, modified transudate, or exudate) or based on the underlying cause. Most effusions are modified transudates. Common causes for the development of pleural effusion include CHF and neoplasia. Other less common causes include chylothorax and pyothorax. An aliquot of fluid should be analyzed, and bacterial culture should be submitted if there is suspicion of an infectious cause. Anticoagulant rodenticides commonly result in substantial intrapleural hemorrhage. Thus, in dogs at risk of anticoagulant rodenticide intoxication, a prothrombin time should be evaluated before thoracocentesis. Pleural effusion is best treated based on the underlying cause. Pyothorax generally requires chest tube placement for drainage [11]. In dogs, chest tubes are generally inadequate; therefore, exploratory thoracotomy is indicated. Animals with long-standing effusion recognized by history or radiographically by rounding of the lung lobes may develop severe iatrogenic pneumothorax after thoracocentesis. Some pulmonary neoplasms are sensitive to chemotherapy, and this mode of therapy can improve respiratory compromise. Diuretics and vasodilators are almost always effective in relieving signs of CHF. Pneumothorax may be classified as traumatic or spontaneous. Traumatic pneumothorax is more common. For animals with a known history of injury, needle thoracocentesis may be performed if there is clinical suspicion that pneumothorax may be the cause of dyspnea. Because of the high density of tissue thromboplastin, a previously healthy injured lung heals rapidly; thus, chest tubes are not commonly required in the trauma patient. A commonly cited guideline is that three or more thoracocenteses (‘‘threestrike rule’’) within 24 hours is sufficient justification for placement of the chest tube in the traumatic pneumothorax. It is exceedingly rare to have a patient with trauma require a thoracotomy for resection of the traumatized lung. Conversely, most cases of spontaneous pneumothorax require surgical resection of the affected lobe. Spontaneous pneumothorax is
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defined as pneumothorax occurring without trauma [12]. Common causes include bulla/blebs and neoplasia (primary or metastatic) [12]. Additionally, cats with lower airway disease may occasionally develop spontaneous pneumothoraces [13]. For affected dogs, rapid surgical exploration and resection have been associated with decreased morbidity and expense [12]. Diaphragmatic hernia should be corrected as soon as the patient is considered stable enough for surgery [14]. In traumatic injuries, concurrent pulmonary contusions may markedly worsen gas exchange; thus, anesthesia and surgery may be postponed until clinical improvement. If significant herniation exists, however, including the presence of the stomach within the intrathoracic cavity, surgical repair is urgent. Anesthesia may still be safely performed with pulmonary contusions, although in addition to the positivepressure ventilation required because of the loss of diaphragmatic integrity, a small amount of positive end-expiratory pressure (PEEP) may be beneficial to help recruit collapsed alveoli. In chronic hernias, re-expansion pulmonary edema may result in severe respiratory failure [15]; thus, correction of chronic hernias should be undertaken with care and gradual reinflation of the lung. Summary Respiratory emergencies are common presentations to emergency clinicians. Appropriate assessment and timely interventions may be crucial in the stabilization of dyspneic patients. The emergency clinician should be fully prepared and equipped to correctly ascertain and treat the most likely cause of respiratory compromise of a patient. Based on history, signalment, clinical presentation, and brief physical examination findings, the clinician should be able to formulate a plan of action to relieve respiratory distress and communicate with the owner about the diagnostic and therapeutic strategies and overall prognosis of the patient. Prompt recognition of the underlying respiratory disease and complete familiarity with emergency diagnostic and therapeutic procedures can lead to the successful management of many emergency respiratory patients. References [1] Lee JA, Drobatz KJ. Respiratory distress and cyanosis in dogs. In: King LG, editor. Textbook of respiratory disease in dogs and cats. St. Louis: Elsevier; 2004. p. 1–11. [2] Rose DK, Cohen MM, Wigglesworth DF, et al. Critical respiratory events in the postanesthesia care unit. Patient, surgical, and anesthetic factors. Anesthesiology 1994; 81(2):410–8. [3] Barton L. Respiratory muscle fatigue. Vet Clin N Am Small Anim Pract 2002;32(5):1059–71. [4] West JB. Ventilation-perfusion relationships. In: Coryell PA, editor. Respiratory physiology—the essentials. 5th edition. Baltimore: Williams & Wilkins; 1998. p. 51–69. [5] Drobatz KJ, Saunders HM, Pugh CR, et al. Noncardiogenic pulmonary edema in dogs and cats: 26 cases (1987–1993). J Am Vet Med Assoc 1995;206(11):1732–6.
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[6] Powell L, Rozanski EA, Tidwell A, et al. A retrospective analysis of pulmonary contusion secondary to motor vehicle accidents in 143 dogs: 1994–1997. J Vet Emerg Crit Care 1999;9: 127–36. [7] Drobatz KJ, Walker LM, Hendricks JC. Smoke exposure in cats: 22 cases (1986–1997). J Am Vet Med Assoc 1999;215(9):1312–6. [8] Drobatz KJ, Walker LM, Hendricks JC. Smoke exposure in dogs: 27 cases (1988–1997). J Am Vet Med Assoc 1999;215(9):1306–11. [9] Clercx C, Peeters D, Snaps F, et al. Eosinophilic bronchopneumopathy in dogs. J Vet Intern Med 2000;14(3):282–91. [10] Corcoran BM, Cobb M, Martin MW, et al. Chronic pulmonary disease in West Highland white terriers. Vet Rec 1999;144(22):611–6. [11] Waddell LS, Brady CA, Drobatz KJ. Risk factors, prognostic indicators, and outcome of pyothorax in cats: 80 cases (1986–1999). J Am Vet Med Assoc 2002;221(6):819–24. [12] Puerto DA, Brockman DJ, Lindquist C, et al. Surgical and nonsurgical management of and selected risk factors for spontaneous pneumothorax in dogs: 64 cases (1986–1999). J Am Vet Med Assoc 2002;220(11):1670–4. [13] White HL, Rozanski EA, Tidwell AS, et al. Spontaneous pneumothorax in two cats with small airway disease. J Am Vet Med Assoc 2003;222(11):1547, 1573–5. [14] Schmiedt CW, Tobias KM, Stevenson MA. Traumatic diaphragmatic hernia in cats: 34 cases (1991–2001). J Am Vet Med Assoc 2003;222(9):1237–40. [15] Stampley AR, Waldron DR. Reexpansion pulmonary edema after surgery to repair a diaphragmatic hernia in a cat. J Am Vet Med Assoc 1993;203(12):1699–701.
Approach to the Patient with Respiratory Distress Elizabeth Rozanski, DVM*, Daniel L. Chan, DVM Section of Emergency and Critical Care, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, 200 Westboro Road, North Grafton, MA 01536, USA
Respiratory distress of any origin represents a true emergency requiring rapid identification of the underlying cause, immediate alleviation of the sensation of difficulty in breathing, and provision of diagnostic and therapeutic information for the owners of affected animals. Clearly, there are a variety of potential underlying reasons for the development of respiratory distress. For the clinician in emergency practice, successful management of patients in respiratory distress revolves around developing a knowledge base of the potential causes of respiratory distress and ‘‘pattern recognition’’ of common emergent problems affecting dogs and cats. Prompt recognition of the underlying condition and appropriate therapeutic interventions are essential in the management of respiratory emergencies. The goals of this article are to review the function of the respiratory system, to describe pathophysiologic causes for hypoxemia, to illustrate various methods for classifying respiratory distress, to highlight common emergency conditions resulting in respiratory distress, and to provide guidelines for emergent management. Gas exchange As a review, the primary goal of the respiratory system is to promote gas exchange. Air enters the upper respiratory system via the nose or the mouth. The air is warmed and humidified and then passes down the respiratory tree. Larger particles of debris are filtered out. The trachea branches into the successive generation of smaller and smaller airways. Gas exchange occurs at the level of the alveoli. Although the flow of air (ventilation, termed V) is * Corresponding author. E-mail address: [email protected] (E. Rozanski). 0195-5616/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.cvsm.2004.12.003 vetsmall.theclinics.com
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obviously essential, the other aspect of gas exchange involves the delivery of blood (perfusion, termed Q) to the level of the alveoli. Blood reaches the capillaries adjacent to the alveoli by way of the pulmonary vasculature. The blood exits the right heart via the pulmonary outflow tract and then flows through the pulmonary arteries. These arteries branch into smaller and smaller vessels until they reach the level of the capillary. Red cells traverse the capillaries in single file; during contact with the alveoli, the oxygen diffuses out of the alveoli and binds to the hemoglobin, because the carbon dioxide (CO2, waste gas) diffuses off the hemoglobin molecule into the alveoli for expiration. In normal animals, the capillary endothelium is impermeable to larger molecules, such as albumin. Causes of hypoxemia In animals that develop hypoxemia, there are five possible broad causes. Each disease observed clinically fits into one of more of the following categories. These causes include a low inspired oxygen concentration (FiO2), hypoventilation, shunt, ventilation-perfusion (V-Q) mismatch, and diffusion impairment [1]. Normal oxygen concentration in room air is approximately 21%, and low FiO2 is an uncommon cause of hypoxemia. This may occur at higher altitudes or because of anesthesia machine dysfunctioning, however [1]. Low FiO2 may be simply corrected by supplementing oxygen. Hypoventilation results from absent or ineffective (low) tidal volumes as a result of such causes as drug therapy side effects (eg, opioids, propofol) or loss of central respiratory drive [2]. Respiratory muscle fatigue in patients with prolonged and severe dyspnea can result in hypoventilation [3]. Hypoventilation is treated by mechanical ventilation or by reversing the cause that triggered the hypoventilation. It should be emphasized that hypoventilation may not be appreciated as respiratory compromise because respiratory attempts are limited or depressed. Shunt refers to the complete bypassing of ventilated areas of the lungs by deoxygenated blood and re-entry into the circulatory system [4]. The classic example of a shunt is the right-to-left shunt that accompanies the cardiac defect of the tetralogy of Fallot (right ventricular hypertrophy, ventricular septal defect [VSD], pulmonic stenosis, and overriding aorta). In affected animals, the severity of the pulmonic stenosis results in the shunting of deoxygenated blood through the VSD into the left ventricle. Because oxygen supplementation cannot affect shunted deoxygenated blood, pure shunts are described as nonresponsive to oxygen supplementation. In certain conditions, significant alveolar pathologic changes can contribute to shunting. Alveoli filled with inflammatory exudates, edema, or blood can reduce gas exchange efficiency. Because this is not a true shunt, however, oxygen supplementation can improve oxygenation. V-Q mismatch refers to the poor coordination of the areas of the lung that are adequately perfused versus those that are appropriately ventilated,
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resulting in impairment of gas exchange [4]. Normally, there is a good match between areas that are appropriately ventilated and those that are adequately perfused. In some cases, however, areas of the lungs can be perfused but are not well ventilated (low V/Q ratio), whereas in other conditions, well-ventilated areas are inadequately perfused (high V/Q ratio). Conditions associated with a low V/Q ratio include pneumonia, edema, hemorrhage, and inflammatory exudates. Pulmonary thromboembolism is an example of a condition resulting in a high V/Q ratio. This mismatching results in the development of hypoxemia but is not necessarily accompanied by hypercarbia. Diffusion of CO2 is many times more efficient than that of oxygen, explaining the discrepancy when gas exchange is compromised. As a result of physiologic responses by the lung, V-Q mismatch generally responds to oxygen supplementation. The final area that may result in hypoxemia is diffusion impairment. Typically, during the transition phase through the capillary bed, the oxygen diffuses within the first third of the length of the capillary. If the alveolarcapillary membrane is significantly thickened, however, there may be diffusion impairment and gas exchange can become compromised. Diseases resulting in diffusion impairment include pulmonary interstitial pathologic findings such as fibrosis, severe interstitial pneumonia, and interstitial hemorrhage. Oxygen supplementation can increase the oxygen tension within the alveoli sufficiently to overcome diffusion impairment and alleviate hypoxemia.
Oxygen therapy Although an understanding of the potential causes of respiratory distress is indispensable, the first steps in the clinical evaluation of a patient presented with respiratory distress are to provide a supplemental source of oxygen and to obtain a brief history from the client or owner. All emergency facilities should be equipped to provide a form of supplemental oxygen. Supplemental oxygen may be provided by means of a variety of options, including flow-by oxygen, a face mask, nasal oxygen, an Elizabethan collar and cellophane wrap (‘‘oxygen hood’’), an oxygen cage, and intubation with intermittent positive-pressure ventilation (IPPV). Flow-by oxygen is provided by holding oxygen tubing near the mouth and nostrils of the affected patient. The flow rate is usually set at 100 mL/kg/min or greater. Flow-by oxygen is an easy and rapid solution; however, the actual increase over room airÕs 21% oxygen content may be minimal, particularly with an anxious or uncooperative animal. Oxygen may also be provided with a face mask, with the oxygen tubing attached to a cone that is placed over the nose and mouth of the patient. The FiO2 with a face mask is also variable, although a high percentage may be reached in weak animals. Flow-by and face mask oxygen may require veterinary personnel to hold the pet and the oxygen supply.
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Nasal oxygen involves placement of a flexible catheter into the nasal passages and insufflation of humidified oxygen. Nasal oxygen is particularly useful in pets that are not panting or are demonstrating open-mouthed breathing. Nasal oxygen is commonly placed after patient stabilization rather than urgently in the emergency setting. An improvised oxygen hood may be created with an Elizabethan collar and cellophane wrap or may be commercially purchased (Jorgenson Laboratories, Loveland, CO). An oxygen cage is also frequently used to provide supplemental oxygen. Oxygen cages are commonly well tolerated by cats and dogs and are also capable of achieving a high concentration of oxygen; however, if the cage door is opened for patient manipulation, the FiO2 falls rapidly. Finally, intubation and IPPV represent the best option for providing high levels of supplemental oxygen, removing respiratory fatigue, and eliminating patient fear and anxiety.
Assessment During the initial stabilization of the pet, a history should be obtained from the owner. In some cases, the precipitating cause of the respiratory distress is straightforward, such as with traumatic injuries, whereas in other cases, the onset may be more insidious. Animals with preexisting medical conditions, such as cardiac disease, neoplasia, or megaesophagus, may also be predisposed to the development of respiratory distress. Owners should be questioned as to past medical conditions and history of routine veterinary care, including heartworm prophylaxis; finally, progression of the signs of respiratory distress should be described. Specifically, distress may be acute in onset or may be more progressive. Particularly in cats, the development of respiratory distress may be preceded by anorexia, lethargy, or abnormal behavior. Respiratory distress may be further characterized by the location of the lesion or the underlying pathophysiologic condition. Often, localization of the lesion can help to guide the clinician to the most likely cause. Specifically, respiratory distress may be localized to the upper airway, lower airway, parenchyma, or pleural space. Common pathophysiologic causes for respiratory distress include anatomic abnormalities, airway collapse, infection, inflammation, trauma, and pulmonary edema of cardiac and noncardiac causes. For the emergency clinician, the most appropriate first step is to localize the lesion and then to review specific differential diagnoses based on signalment, history, and other physical examination findings.
Diseases of the upper airway Upper airway diseases may be appreciated by loud stridulous breathing with an increased inspiratory time. Many dogs are hyperthermic on initial
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presentation because of a decreased ability to cool. The upper airways represent the primary source of resistance to airflow. Upper airway obstructions can be dynamic or fixed. Dynamic obstructions are characterized by the paradoxic movement of tissues into the lumen of airways during inspiration. Common dynamic obstructions include laryngeal paralysis and tracheal collapse, whereas fixed obstructions include extraluminal obstructions, such as neoplasia or cellulitis, and intraluminal obstructions, such as laryngeal tumors or nasopharyngeal polyps. Dynamic and fixed severe upper airway obstructions also result in the development of airway mucosal edema and possibly everted laryngeal saccules as a result of irritation from the increased air flow rates through a narrow lumen. Emergently, upper airway obstruction should be suspected in any dog with loud and noisy breathing. Therapy for a suspected dynamic obstruction should include sedation and supplemental oxygen. In case of dynamic obstruction, sedation is beneficial in reducing the anxiety associated with inspiration, because with increased inspiratory efforts, there is a resulting paradoxic decline in airway diameter. Low doses of acepromazine (0.03–0.05 mg/kg administered intravenously) alone or in combination with butorphanol (0.1 mg/kg administered intravenously) are often effective. Hyperthermia should be treated by active cooling with room temperature (not cold) intravenous fluids and by placing the dog in a cool area. Because of airway swelling and edema, a single dose of a short-acting antiinflammatory glucocorticoid is advisable. If the dog has not improved within 15 to 30 minutes or the distress is worsening, more aggressive therapy is warranted. The dog should be heavily sedated or anesthetized and intubated. The emergency clinician should be competent in evaluating airway function and anatomy and in performing a tracheostomy if necessary. Additionally, because many upper airway conditions require medical or surgical interventions, the emergency clinician should fully discuss longterm outcomes and expectations with clients. The most common causes of upper airway obstruction may vary depending on location; however, in our practice, they include laryngeal paralysis, tracheal collapse, brachycephalic airway syndrome, and severe cellulitis. A complete discussion on the management of these conditions is beyond the scope of this article; however, despite their similarities, differences among the underlying diseases do exist regarding optimal management of affected patients. Awareness of the different nuances of these conditions is critical in their successful management. Laryngeal paralysis primarily affects older large-breed dogs, particularly retrievers. Usually, the clinical signs of noisy breathing have been present for some length of time before a crisis. Crises often occur during the first hot and humid days of the spring or summer months and may be associated with exercise. Dogs typically respond well to sedation. Dogs that do not rapidly improve should be sedated, have their laryngeal function evaluated, and be intubated. If palliative surgery is not readily available, dogs may
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require a tracheostomy or may be kept sedated/intubated until normothermia and eupnea are restored. In our practice, we commonly anesthetize patients with propofol for 30 to 60 minutes. If a dog cannot be safely extubated after this time, a tracheostomy may be performed rather than keeping a patient intubated and thereby raising the risk of aspiration pneumonia. Conversely, in dogs with severe brachycephalic airway syndrome or tracheal collapse, avoidance of a tracheostomy is preferable as compared with dogs with laryngeal paralysis. The reason for this is that many of these dogs become permanently dependent on the tracheostomy tube once placed. If a tracheostomy is unavoidable, plans should be made for surgical correction of the obstruction as soon as feasible. Brachycephalic dogs may also develop laryngeal collapse, which is not amenable to laryngoplasty and may ultimately necessitate a permanent tracheostomy. In cats, upper airway obstructions are less common but may be caused by nasopharyngeal polyps or infiltrative laryngeal diseases (neoplastic or granulomatous diseases). Nasopharyngeal polyps are a condition of young cats. Occasionally, cats with severe pleural effusion have the appearance of severe inspiratory distress. If sedation for an oral examination of a cat with a suspected upper airway obstruction is planned, supplies should be collected ahead of time for an emergency tracheostomy. The laryngeal lumen of affected cats may be only 1 or 2 mm in diameter and may require an urgent tracheostomy. If biopsy of a laryngeal mass is performed in a cat, a tracheostomy is almost always required because of subsequent airway swelling. Cats may also have a permanent tracheostomy placed, although it is less well tolerated than in dogs.
Diseases of the lower airways Respiratory distress may also result from lower airway disease, parenchymal lung disease, or pleural space disease. Thoracic radiographs are essential to help clarify the degree of pulmonary or pleural space involvement. Nevertheless, it is important to recall that radiography can be stressful, particularly in cats that are experiencing respiratory distress. Lower airway diseases include chronic bronchitis and feline asthma. Chronic bronchitis rarely presents emergently, although flare-ups do occur in some patients. Chronic bronchitis is defined as the presence of a cough on most days for the preceding 2 months, without evidence of other underlying cause. Canine chronic bronchitis commonly affects small-breed dogs. On auscultation, a mitral murmur is commonly identified. Conversely, feline lower airway disease may present as an emergency. In cats, airway disease seems to represent a continuum, with some cats having primarily inflammatory airway disease with cough and excessive mucus production, whereas other cats are the more prototypical ‘‘asthmatics’’ with reversible
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bronchoconstriction. Cats with severe bronchoconstriction are often presented emergently. It is important to distinguish the airway disease from congestive heart failure (CHF). Cats with airway disease are typically normothermic and have had a history of cough. Heart failure and airway disease may be accompanied by crackles.
Diseases affecting the lungs Parenchymal lung disease is often responsible for respiratory distress. Common causes of parenchymal lung disease include pulmonary edema (cardiogenic and noncardiogenic), pulmonary contusion, pneumonia, and neoplasia. Heart failure commonly manifests as respiratory distress. Heart failure in cats is usually appreciated by hypothermia combined with an increased respiratory rate and effort. Jugular venous distention may be present. A gallop or a murmur may be ausculted. Cats with CHF commonly have slow heart rates (130–140 beats per minute [bpm]). Heart disease in dogs is usually chronic valvular disease or dilated cardiomyopathy. Animals with a history of trauma or possible trauma that are presented with respiratory distress can be assumed to have some component of pulmonary contusion (or pneumothorax). Therapy for respiratory distress associated with pulmonary infiltrates includes supplemental oxygen and therapeutic agents directed toward the presumptive underlying cause. The distribution of the pulmonary infiltrates may be useful to help determine the underlying problem. Cardiogenic pulmonary infiltrates most often surround the perihilar region in dogs, whereas the distribution of pulmonary edema may vary in cats. Bacterial pneumonias typically have a cranioventral distribution. Neoplasia usually results in a nodular pattern, although metastatic disease may appear variable. Animals with suspected cardiogenic pulmonary edema should be treated initially with diuretics (furosemide, administered intravenously or intramuscularly, either 4 mg/kg every 4–6 hours or 1–2 mg/kg every 1–2 hours), cage rest, and supplemental oxygen. If rapid improvement is not observed, additional therapy with vasodilators (nitroprusside titrated to effect) is warranted. In practice, despite published guidelines, measurement of blood pressure during infusion of nitroprusside is usually not performed so as to limit patient stress, loss of supplemental oxygen (by opening the cage door), and technical difficulties in obtaining repeatable and reliable measurements. Specifically, it may be challenging or impossible to place an arterial line for direct blood pressure determinations in an animal with CHF. Oscillometric techniques are commonly inaccurate with small dogs or cats, and Doppler techniques are time-consuming and require a patient with respiratory distress to be restrained. Dobutamine, given as a continuous rate infusion (CRI), is useful in increasing cardiac output in dogs with dilated cardiomyopathies. Intravenous fluids should not be administered to
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a patient with heart failure, although the patient should be permitted ad libitum access to water. Hemodynamically significant arrhythmias should be treated. Patients should be transitioned to long-term medications after stabilization. Although an echocardiogram is not considered an emergent procedure, emergency clinicians should have a basic knowledge of echocardiography, including assessment of left atrial size, contractility, and the presence or absence of pericardial effusion. Noncardiogenic pulmonary edema may occur for a variety of reasons. In the emergency room, head trauma, upper airway obstruction, seizures, and electric cord injury are common triggers for the development of noncardiogenic edema [5]. Noncardiogenic pulmonary edema is typically characterized by high protein; it occurs as a result of permeability shifts in the capillaries rather than hydrostatic forces, as is the case with cardiogenic edema. There is no specific therapy that has been proven beneficial for hastening recovery from noncardiogenic edema [5]. Treatment recommendations include cage rest and supplemental oxygen. More specific therapy with diuretics or colloids has been advocated by various clinicians, although no consensus statement exists. Most dogs with noncardiogenic pulmonary edema rapidly improve within 24 to 48 hours [5]. Pulmonary contusions are common after traumatic injury, particularly in dogs. Animals severely affected with pulmonary contusions are presented short of breath soon after the injury, although, radiographically, the infiltrates often worsen over the first 12 to 24 hours. Dogs with contusions commonly have small- to moderate-volume pneumothoraces as well. Contusions generally heal rapidly. One study in dogs was unable to support the use of prophylactic antibiotics or corticosteroids [6]. Diuretics are also not indicated for animals with pulmonary contusions. Dogs with pneumonia may be presented to the emergency room with respiratory distress. Bacterial pneumonia is rare in cats. Pneumonia can be subdivided into community-acquired and hospital-acquired forms. Examples of community-acquired pneumonia include severe bronchopneumonia (eg, infectious kennel cough complex) and aspiration pneumonia in a dog with laryngeal paralysis or megaesophagus. Any dog that develops pneumonia while hospitalized for treatment of another condition is considered to have hospital-acquired pneumonia. Therapy for pneumonia includes broad-spectrum antibiotics, physiotherapy, and intravenous fluids. Ideally, a bacterial culture is performed before the institution of antibiotics. Animals are infrequently presented on an emergent basis with dyspnea secondary to metastatic disease, although cough and lethargy are common. Spontaneous pneumothorax may occasionally develop in a patient with pulmonary neoplasia. Treatment of suspected neoplastic disease is directed at supportive care. Common metastatic tumors include hemangiosarcoma and mammary gland adenocarcinoma. Occasionally, further imaging is indicated to attempt to localize a primary tumor; however, this is generally futile. Pulmonary lymphoma may respond well to therapy. It is also
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important to exclude a recent travel history in dogs with a nodular pulmonary pattern, because the systemic mycoses can mimic metastatic disease. Other less common causes of pulmonary infiltrates include eosinophilic pneumonitis, smoke inhalation, and pulmonary fibrosis [7–10].
Diseases of the pleural space Pleural space disease commonly results in marked respiratory distress. Common causes are pleural effusion, pneumothorax, and diaphragmatic hernia. Pleural space disease may often be suspected clinically based on a restrictive (short and shallow) breathing pattern. Thoracic radiographs are useful in documenting the extent of the pleural space disease but may not be safely obtained in animals with severe respiratory distress. Therapeutic thoracocentesis can remove significant volumes of effusion and results in rapid improvement in respiratory rate and effort. Effusions may be classified based on fluid characteristics (transudate, modified transudate, or exudate) or based on the underlying cause. Most effusions are modified transudates. Common causes for the development of pleural effusion include CHF and neoplasia. Other less common causes include chylothorax and pyothorax. An aliquot of fluid should be analyzed, and bacterial culture should be submitted if there is suspicion of an infectious cause. Anticoagulant rodenticides commonly result in substantial intrapleural hemorrhage. Thus, in dogs at risk of anticoagulant rodenticide intoxication, a prothrombin time should be evaluated before thoracocentesis. Pleural effusion is best treated based on the underlying cause. Pyothorax generally requires chest tube placement for drainage [11]. In dogs, chest tubes are generally inadequate; therefore, exploratory thoracotomy is indicated. Animals with long-standing effusion recognized by history or radiographically by rounding of the lung lobes may develop severe iatrogenic pneumothorax after thoracocentesis. Some pulmonary neoplasms are sensitive to chemotherapy, and this mode of therapy can improve respiratory compromise. Diuretics and vasodilators are almost always effective in relieving signs of CHF. Pneumothorax may be classified as traumatic or spontaneous. Traumatic pneumothorax is more common. For animals with a known history of injury, needle thoracocentesis may be performed if there is clinical suspicion that pneumothorax may be the cause of dyspnea. Because of the high density of tissue thromboplastin, a previously healthy injured lung heals rapidly; thus, chest tubes are not commonly required in the trauma patient. A commonly cited guideline is that three or more thoracocenteses (‘‘threestrike rule’’) within 24 hours is sufficient justification for placement of the chest tube in the traumatic pneumothorax. It is exceedingly rare to have a patient with trauma require a thoracotomy for resection of the traumatized lung. Conversely, most cases of spontaneous pneumothorax require surgical resection of the affected lobe. Spontaneous pneumothorax is
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defined as pneumothorax occurring without trauma [12]. Common causes include bulla/blebs and neoplasia (primary or metastatic) [12]. Additionally, cats with lower airway disease may occasionally develop spontaneous pneumothoraces [13]. For affected dogs, rapid surgical exploration and resection have been associated with decreased morbidity and expense [12]. Diaphragmatic hernia should be corrected as soon as the patient is considered stable enough for surgery [14]. In traumatic injuries, concurrent pulmonary contusions may markedly worsen gas exchange; thus, anesthesia and surgery may be postponed until clinical improvement. If significant herniation exists, however, including the presence of the stomach within the intrathoracic cavity, surgical repair is urgent. Anesthesia may still be safely performed with pulmonary contusions, although in addition to the positivepressure ventilation required because of the loss of diaphragmatic integrity, a small amount of positive end-expiratory pressure (PEEP) may be beneficial to help recruit collapsed alveoli. In chronic hernias, re-expansion pulmonary edema may result in severe respiratory failure [15]; thus, correction of chronic hernias should be undertaken with care and gradual reinflation of the lung. Summary Respiratory emergencies are common presentations to emergency clinicians. Appropriate assessment and timely interventions may be crucial in the stabilization of dyspneic patients. The emergency clinician should be fully prepared and equipped to correctly ascertain and treat the most likely cause of respiratory compromise of a patient. Based on history, signalment, clinical presentation, and brief physical examination findings, the clinician should be able to formulate a plan of action to relieve respiratory distress and communicate with the owner about the diagnostic and therapeutic strategies and overall prognosis of the patient. Prompt recognition of the underlying respiratory disease and complete familiarity with emergency diagnostic and therapeutic procedures can lead to the successful management of many emergency respiratory patients. References [1] Lee JA, Drobatz KJ. Respiratory distress and cyanosis in dogs. In: King LG, editor. Textbook of respiratory disease in dogs and cats. St. Louis: Elsevier; 2004. p. 1–11. [2] Rose DK, Cohen MM, Wigglesworth DF, et al. Critical respiratory events in the postanesthesia care unit. Patient, surgical, and anesthetic factors. Anesthesiology 1994; 81(2):410–8. [3] Barton L. Respiratory muscle fatigue. Vet Clin N Am Small Anim Pract 2002;32(5):1059–71. [4] West JB. Ventilation-perfusion relationships. In: Coryell PA, editor. Respiratory physiology—the essentials. 5th edition. Baltimore: Williams & Wilkins; 1998. p. 51–69. [5] Drobatz KJ, Saunders HM, Pugh CR, et al. Noncardiogenic pulmonary edema in dogs and cats: 26 cases (1987–1993). J Am Vet Med Assoc 1995;206(11):1732–6.
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[6] Powell L, Rozanski EA, Tidwell A, et al. A retrospective analysis of pulmonary contusion secondary to motor vehicle accidents in 143 dogs: 1994–1997. J Vet Emerg Crit Care 1999;9: 127–36. [7] Drobatz KJ, Walker LM, Hendricks JC. Smoke exposure in cats: 22 cases (1986–1997). J Am Vet Med Assoc 1999;215(9):1312–6. [8] Drobatz KJ, Walker LM, Hendricks JC. Smoke exposure in dogs: 27 cases (1988–1997). J Am Vet Med Assoc 1999;215(9):1306–11. [9] Clercx C, Peeters D, Snaps F, et al. Eosinophilic bronchopneumopathy in dogs. J Vet Intern Med 2000;14(3):282–91. [10] Corcoran BM, Cobb M, Martin MW, et al. Chronic pulmonary disease in West Highland white terriers. Vet Rec 1999;144(22):611–6. [11] Waddell LS, Brady CA, Drobatz KJ. Risk factors, prognostic indicators, and outcome of pyothorax in cats: 80 cases (1986–1999). J Am Vet Med Assoc 2002;221(6):819–24. [12] Puerto DA, Brockman DJ, Lindquist C, et al. Surgical and nonsurgical management of and selected risk factors for spontaneous pneumothorax in dogs: 64 cases (1986–1999). J Am Vet Med Assoc 2002;220(11):1670–4. [13] White HL, Rozanski EA, Tidwell AS, et al. Spontaneous pneumothorax in two cats with small airway disease. J Am Vet Med Assoc 2003;222(11):1547, 1573–5. [14] Schmiedt CW, Tobias KM, Stevenson MA. Traumatic diaphragmatic hernia in cats: 34 cases (1991–2001). J Am Vet Med Assoc 2003;222(9):1237–40. [15] Stampley AR, Waldron DR. Reexpansion pulmonary edema after surgery to repair a diaphragmatic hernia in a cat. J Am Vet Med Assoc 1993;203(12):1699–701.