STANDARDS of CARE. Pulmonary edema is defined as the effusion of serous fluid into the EMERGENCY AND CRITICAL CARE MEDICINE

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1 Visit us at AUGUST 2003 VOL 5.7 STANDARDS of CARE EMERGENCY AND CRITICAL CARE MEDICINE FROM THE PUBLISHER OF COMPENDIUM NONCARDIOGENIC PULMONARY EDEMA Sarah Haldane, BVSC, MACVSc Resident Steven L. Marks, BVSc, MRCVS, DACVIM Associate Professor Marc Raffe, DVM, MS, DACVECC, DACVA Professor College of Veterinary Medicine University of Illinois Urbana, Illinois Pulmonary edema is defined as the effusion of serous fluid into the extravascular tissue of the lung. It is usually categorized into two forms: cardiogenic and noncardiogenic. Cardiogenic pulmonary edema (CPE) is caused by an increase in hydrostatic pressure due to congestion and fluid overload in the venous system and typically results from heart failure. Increased intravascular hydrostatic pressure causes fluid to move out of the vascular space into the pulmonary parenchyma and, as pressure increases, into the alveoli. Noncardiogenic pulmonary edema (NPE) occurs secondary to injury of the vascular endothelium, and fluid extravasation into the interstitium occurs due to increased vascular permeability. NPE can be categorized by the mechanism of endothelial injury. Inflammatory mediators or toxins can cause chemical injury to the endothelium. Inflammatory mediators include histamine, prostanoids, and complement, which are released in conditions of severe systemic inflammation such as pancreatitis or sepsis. Acute anaphylaxis or hypersensitivity reactions may also lead to the release of significant concentrations of inflammatory mediators. Aspiration of gastric contents, smoke inhalation, uremic toxins, and prolonged administration of high concentrations of oxygen can cause chemical injury, initially to the alveolar epithelium and subsequently to the vascular endothelium. Endothelial injury may also occur due to increased microvascular pressure (hypertension). Supraphysiologic catecholamine release secondary to acute sympathetic nervous system overstimulation is thought to be the mechanism of injury in neurogenic pulmonary edema and electrical cord injury. Physical injury to the lung parenchyma from blunt thoracic trauma may lead to NPE. High altitude and upper airway obstruction may increase vascular permeability by the stretching of the vascular endothelium and widening of endothelial pores. DIAGNOSTIC CRITERIA Historical Information History is important in distinguishing between CPE and NPE. The time of onset and duration of clinical signs is important. Most animals with noncardiogenic lung injuries have a history of sudden onset of dyspnea or respiratory distress. Cardiac failure may be preceded by the gradual onset of exercise intolerance, weight loss, or coughing as well as the historical presence of a heart murmur. A history of head or chest trauma, upper airway obstruction, or involvement in a house fire may be noted in animals with NPE. Some animals with NPE also may have a history of forcible restraint, such as for vaccination. Questions pertaining to the environment in which the animal resides should include: Access to toxins, toxic fumes, or electrical cords. Access to a water source such as a swimming pool or pond (near-drowning can also lead to NPE). Inside this issue: Peer-Reviewed Articles on 1 Noncardiogenic Pulmonary Edema 6 Canine Acquired Myasthenia Gravis Questions? Comments? soc.vls@medimedia.com, fax , or post on the Feedback page at 1

2 History of neurologic signs, especially seizures. Any systemic illness that may lead to overwhelming inflammation. CPE and NPE occur concurrently in some patients. Physical Examination Findings A thorough physical examination of all organ systems must be performed to provide evidence of any underlying systemic disease, trauma, neurologic disease, neardrowning, or toxin exposure. It may be necessary to initially stabilize the patient prior to an extensive physical examination (see Initial Treatment). Look for signs of concurrent cardiac disease, such as arrhythmias, heart murmurs, jugular pulses, poor peripheral pulses, or a prolonged capillary refill time. Hypovolemic or septic shock may also be evident. Patients often present in acute respiratory distress with a rapid, shallow breathing pattern and increased respiratory effort. Harsh lung sounds or crackles may be auscultated, especially in the caudodorsal lung fields. Mucous membranes may be cyanotic. Circumscribed, pale burn lesions affecting the lips, tongue, gums, and hard palate are commonly seen in cases of electrical cord injury. Singed fur or whiskers may also be detected in the region of the burn. Animals may be found collapsed and unconscious or may exhibit weakness, transient muscle stiffness, or seizures. KEY TO COSTS $ indicates relative costs of any diagnostic and treatment regimens listed. $ costs under $250 $$ costs between $250 $500 $$$ costs between $500 $1000 $$$$ costs over $1000 Laboratory Findings The emergency database, including a packed cell volume (PCV) and total protein determination, provides important initial information for stabilization of these critical patients. A complete blood count (CBC), chemistry panel, and urinalysis should be evaluated in affected patients. Laboratory findings reflect the underlying disease process and should be used to evaluate disease in body systems other than the heart and lungs. Hypoproteinemia can occur due to rapid and profound protein loss into extravascular tissues in severe cases of NPE, especially with concurrent systemic inflammatory disease. Coagulation testing may be important because concurrent disseminated intravascular coagulation (DIC) may lead to thrombocytopenia and prolonged clotting times. Arterial blood gases may be used to determine the magnitude of pulmonary dysfunction. Although they are not diagnostic for pulmonary edema, they may be used to assess the severity of the disease and monitor response to therapy. Knowledge of the degree of hypoxemia, ventilation, and acid base status is also beneficial. Other Diagnostic Findings The most useful diagnostic tool is thoracic radiography. NPE can appear as diffuse or patchy lung patterns (Figures 1 and 2). Initially, an interstitial pattern can be present but as NPE intensifies, fluid moves into the alveoli and produces an alveolar pattern. Classically, the disease is most severe in the caudodorsal lung lobes. NPE may appear focal or bilaterally symmetrical depending on underlying cause. Occasionally, AUGUST 2003 VOL 5.7 STANDARDS of CARE EMERGENCY AND CRITICAL CARE MEDICINE Editorial Mission: To provide busy practitioners with concise, peer-reviewed recommendations on current treatment standards drawn from published veterinary medical literature. This publication acknowledges that standards may vary according to individual experience and practices or regional differences. The publisher is not responsible for author errors. Compendium s Standards of Care: Emergency and Critical Care Medicine is published 11 times yearly (January/February is a combined issue) by Veterinary Learning Systems, 780 Township Line Road, Yardley, PA The annual subscription rate is $69. For subscription information, call , fax , soc.vls@medimedia.com, or visit Copyright 2003, Veterinary Learning Systems. Executive Series Editor Richard B. Ford, DVM, MS Editor in Chief Beth Thompson, VMD Editorial Staff Lilliane Anstee, Editorial Director Cynthia Laufenberg, Managing Editor Chris Reilly, Editorial Assistant Creative Director Sue Wiedorn Art Studio Manager Bethany L. Wakeley Editorial Review Board Nishi Dhupa, DVM, DACVECC Cornell University Cynthia Otto, DVM, DACVECC University of Pennsylvania Mark Rubash, DVM, DACVECC Houston, Texas Gregory Grauer, DVM, MS, DACVIM (Internal Medicine) Kansas State University Thomas Schermerhorn, VMD, DACVIM (Internal Medicine) Kansas State University 2 A U G U S T V O L U M E 5. 7

3 the infiltrates are more severe in the right lung. Systemic (extrapulmonary) disease may lead to a symmetrical distribution, while inhalation of toxins or aspiration of gastric contents may cause a more focal appearance. Evidence of cardiac disease, such as an abnormal cardiac silhouette, distended pulmonary veins, or perihilar distribution of edema, may help in the differentiation of NPE and CPE. Further evaluation of the heart may be achieved by electrocardiography and/or echocardiography. Pulmonary capillary wedge pressure (PCWP), measured using a pulmonary artery catheter, is an indirect measure of left atrial pressure. Increases in left atrial pressure will accompany leftsided congestive heart failure (CHF). PCWP values of >10 mmhg are supportive of CHF. PCWP is expected to be normal in cases of NPE. Central venous pressure and PCWP do not correlate and may not be used interchangeably in critically ill animals. Summary of Diagnostic Criteria History Lack of evidence of heart disease. Evidence of: Trauma. Neurologic injury. Toxin exposure. Smoke inhalation. Electrical cord injury. Near-drowning. Choking (upper airway obstruction). Sudden onset of clinical signs. Physical Examination Evidence of respiratory disease, especially harsh lung sounds and/or crackles. Evidence of severe systemic disease, neurologic disease, or trauma. Lack of evidence of cardiac disease (murmur, gallop, arrhythmias). Thoracic Radiographs Interstitial infiltrates. Mixed interstitial-alveolar or alveolar lung patterns. Distribution of lesions (caudodorsal; bilateral or focal lesions). No visible abnormalities of the cardiac silhouette or concurrent specific signs of pulmonary or pleural disease. Laboratory Evaluation Evidence of systemic disease may or may not be present. Echocardiography and Invasive Cardiovascular Diagnostics Echocardiography is used to rule out the presence of primary heart disease. PCWPs are the most effective way to differentiate between CPE and NPE. In the absence of this measurement, a combination of history, physical examination, diagnostic tests, and response to treatment is required. Differential Diagnoses CPE is the most important differential diagnosis. Other pulmonary parenchymal diseases include: Pneumonia (bacterial, viral, fungal, aspiration): Rule out on the basis of history, clinical signs, radiographic findings, and presence or absence of organisms on cultures of tracheal wash, bronchoalveolar lavage, or lung aspirate. Neoplasia: Primary or metastatic lesions. Rule out on basis of history, clinical signs, radiographic appearance, and lung aspirate or biopsy. Hemorrhage: Trauma or primary coagulopathy. Rule out on basis of history, clinical signs, and coagulation testing. Pulmonary thromboembolism: Secondary to systemic illness or drug therapy. Rule out on basis of history, coagulation testing, serum antithrombin concentrations, and imaging findings. TREATMENT RECOMMENDATIONS Initial Treatment Initial stabilization of the patient in respiratory distress may be lifesaving. Supplemental oxygen can be delivered via oxygen cage, mask, canopy, intranasal, or, if more invasive intervention is required, via transtracheal catheter, tracheostomy, or endotracheal intubation. Physical examination and further diagnostics of dyspneic patients may have to be performed in stages TABLE 1 Causes of Noncardiogenic P ulmonary Edema Increased Capillary Permeability Trauma Toxins: Chlorine, paraquat, hydrocarbons Smoke inhalation Uremia Aspiration of gastric contents Acute respiratory disease syndrome (ARDS) High altitude Upper airway obstruction Infectious pneumonia Increased Microvascular Pressure Volume overload Lymphatic insufficiency Neurogenic Electrical cord injury Other Near-drowning Pulmonary thromboembolism Narcotic overdose STANDARDS of CARE: EMERGENCY AND CRITICAL CARE MEDICINE 3

4 so as not to overly stress the patient. An IV catheter should be placed as soon as possible to facilitate vascular access. Opiate analgesics may be administered to act as anxiolytics, mild vasodilators, and to ameliorate dyspnea. Pure opiate agonists, such as morphine (0.1 to 0.5 mg/kg IM q4 6h $) or hydromorphone (0.02 to 0.05 mg/kg IV, IM q4 6h $), or agonist antagonist opiates such as butorphanol (0.1 to 0.4 mg/kg IV, IM q1 4h $), may be administered for this purpose. Sedation with phenothiazine or benzodiazepines may be useful in the dyspneic, anxious patient, and these agents also provide some vasodilatory effects. However, there is the risk of oversedation, respiratory depression, and hypotension when using these drugs. $ Diazepam (0.1 to 0.5 mg/kg IV) or acepromazine (0.05 to 0.1 mg/kg IV, IM, SC) are the most commonly used sedatives. Treatment of the underlying cause, if apparent, is vital to prevent ongoing damage to the pulmonary vascular endothelium. Trauma cases should be fully evaluated for other injuries and treated appropriately. In cases of electrical cord injury, burn sites may be clipped and cleaned. For burns outside the oral cavity, a topical antibacterial agent can be applied. Mild injuries may not require surgical debridement, although owners should be warned that burned tissue is likely to slough. Larger areas of necrosis will require strict wound care, debridement, and eventual surgical closure. $$ Diuretics are used in cases of CPE to bring hydrostatic pressures back to within the normal range. Inappropriate use of these medications in NPE may cause decreased cardiac output and can lead to increased morbidity and mortality associated with decreased tissue perfusion. However, a single dose of furosemide may decrease hydrostatic pressure and provide mild pulmonary vasodilation in situations of acute respiratory distress. Furosemide is a loop diuretic that can be given as a bolus dose (1 to 2 mg/kg cats, 2 to 4 mg/kg dogs IV, IM q6 8h). $ Alternative/Optional Treatments/Therapy If hypoxemia is refractory to supplemental oxygen therapy, intubation and mechanical ventilation may be required. Mechanical ventilation allows the administration of high concentrations of oxygen to the patient and facilitates the opening of occluded small airways and alveoli. Positive end expiratory pressure (PEEP) may be used in conjunction with intermittent positive pressure ventilation to prevent further collapse of the alveoli. Mechanical ventilation is time consuming and expensive but may be the only way to support critical patients while the pulmonary endothelium heals and the edema resolves. $$$$ Supportive Treatment Maintaining an adequate level of hemoglobin optimizes oxygen delivery. Whole blood or packed red blood cell transfusions may be administered to reach a PCV of 30%. Raising the PCV above 30% causes an increase in blood viscosity, which counteracts any further increase in oxygenation. Increasing the cardiac output may optimize oxygen delivery to the tissues. Hypovolemia, depressed myocardial contractility, and vasoconstriction will decrease cardiac output. In situations where there is systemic hypotension in the face of adequate blood volumes, positive inotropic agents may be administered to improve myocardial contractility and prevent volume overload associated with excessive fluid therapy. Dopamine (as a constant-rate infusion of 5 to 20 FIGURE 1 FIGURE 2 Caudodorsal distribution of NPE. Lateral distribution of NPE. 4 A U G U S T V O L U M E 5. 7

5 RESOURCE LIST Morphine: mg/kg IM q4 6h. Hydromorphone: mg/kg IV or IM q4 6h. Butorphanol (Torbutrol, Torbugesic, Fort Dodge): mg/kg IV or IM q1 4h. Furosemide (Lasix, Aventis): Given as bolus 1 2 mg/kg (cats) or 2 4 mg/kg (dogs) IV or IM q6 8h. Dopamine: As a constant-rate infusion of 5 10 µg/kg/min. Dobutamine (Dobutrex, Eli Lilly): As a constant-rate infusion of 5 20 µg/kg/min. µg/kg/min) or dobutamine (5 to 20 µg/kg/min) can be used to increase cardiac output. $$ Fluid therapy is controversial in PE, and the choice of fluids (crystalloids or colloids) can be challenging. The goals of fluid therapy are to maximize venous return and subsequent cardiac output without causing fluid overload and increased hydrostatic pressure. Both crystalloids and colloids (including natural and synthetic colloids as well as hemoglobinbased oxygen carriers) may increase hydrostatic pressure, which can worsen pulmonary edema. Increased vascular permeability may allow colloids to extravasate into the lung parenchyma, thereby exerting oncotic effects and pulling more fluid into the interstitial space. Fresh blood, fresh plasma, or fresh frozen plasma may be required if there is evidence of a consumptive coagulopathy. Patient Monitoring Monitoring will involve serial physical examinations with particular emphasis on thoracic auscultation and respiratory rate/effect. Thoracic radiographs may be repeated at 2- to 3-day intervals to compare with initial views and assess efficacy of treatment. Radiographic improvement or deterioration may lag 24 to 48 hours behind clinical signs. Arterial blood gases should be monitored to evaluate hypoxemia, ventilation, and acid base status. In cases where arterial blood gas measurements are not available, pulse oximetry may be used to assess the saturation of circulating hemoglobin. An oxygen saturation (SPO 2 ) of 92% is equivalent to an oxygen partial pressure of 60 mmhg, below which further intervention is required. If available, PCWP measurements are useful to titrate fluid therapy. Arterial blood pressure or central venous pressure measurements may also be useful monitoring tools, especially if the animal is receiving positive inotropic support. Home Management Management at home will be affected by the presence of underlying or concurrent disease. In most cases, patients will require strict rest at home for 1 to 2 weeks, followed by 1 to 2 weeks of restricted exercise. Milestones/Recovery Time Frames NPE usually resolves within 2 to 4 days unless the underlying cause or concurrent disease has not been resolved. A proportion of cases with severe NPE may decompensate into acute respiratory distress syndrome (ARDS), especially if the animal has concurrent severe systemic inflammation. The prognosis for these animals is guarded. Treatment Contraindications Mannitol administration may be indicated in cases of neurologic injury or disease with evidence of cerebral edema. Mannitol is an osmotic diuretic with powerful oncotic pull. This medication is potentially contraindicated in NPE due to pulmonary endothelial damage. Aggressive fluid therapy is also contraindicated in NPE. PROGNOSIS Favorable Criteria Ambulatory on presentation, mild clinical signs, and mild disease on thoracic radiographs. No underlying disease or concurrent trauma. Resolution of initiating cause. Unfavorable Criteria Recumbent on presentation. Refractory dyspnea and/or hypoxemia. Severe underlying or concurrent disease. RECOMMENDED READING Drobatz KJ, Concannon K: Noncardiogenic pulmonary edema. Compend Contin Educ Pract Vet 16(3): , Drobatz KJ, Saunders M: Noncardiogenic pulmonary edema, in Bonagura JD (ed): Kirk s Current Veterinary Therapy XIII. Philadelphia, WB Saunders, 2000, pp Hughes D: Pulmonary edema, in Wingfield WE, Raffe MR (eds): The Veterinary ICU Book. Jackson, WY, Teton New Media, 2002, pp Kolata RJ, Burrows CF: The clinical features of injury by chewing electrical cords in dogs and cats. JAAHA 17: , CHECKPOINT NPE is a relatively uncommon diagnosis in veterinary medicine, although it may be seen more commonly in emergency practices. Expert opinions may diverge on the optimal use of IV fluid therapy and diuretic administration in these cases. STANDARDS of CARE: EMERGENCY AND CRITICAL CARE MEDICINE 5