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Pulmonary Edema, Noncardiogenic 837

○ Neurogenic DIAGNOSIS of hypoxemia. Identify and treat underlying
○ Reexpansion Diagnostic Overview disease whenever possible. Additional therapies,
VetBooks.ir HISTORY, CHIEF COMPLAINT Provide oxygen and minimize stress during the patient’s needs. Diseases and Disorders
such as IV fluid therapy, should be tailored to
○ Negative pressure
diagnostic investigation. History often provides
Acute General Treatment
• History might identify known risk factors
(e.g., smoke inhalation, near drowning, clues that NPE is likely, as does physical exam. • Oxygen supplementation (flow-by, face mask,
Imaging studies confirm pulmonary infiltrates.
choking episode) If the cause of NPE is not clear based on history or oxygen cage [p. 1146]); if head trauma
• Varying degrees of respiratory distress or exam, testing to determine a cause can begin recognized, avoid nasal cannulas to minimize
(p. 879) after the patient is stabilized. increases in intracranial pressure (ICP).
• A trial dose of furosemide 2 mg/kg IV or IM
PHYSICAL EXAM FINDINGS Differential Diagnosis may be used to assess response to therapy
• Acute respiratory distress and tachypnea • Cardiogenic PE (pp. 408 and 409) before additional doses are prescribed.
○ Often mixed inspiratory and expiratory • Primary respiratory disease Diuretics are seldom useful in NPE because
effort ○ Infectious pneumonia: bacterial (p. 795), increased hydrostatic pressure is absent or
○ Cyanosis, serous nasal discharge, and viral (pp. 987 and 545), verminous (p. 595) transient.
cough possible ○ Aspiration pneumonia (p. 793) • IV fluids should be administered judiciously
• Thoracic auscultation ○ Foreign body (p. 355) as gauged by the animal’s hydration and
○ Often harsh or loud bronchovesicular ○ Neoplasia (p. 134) volume status and to avoid dramatic increase
sounds ± fine crackles, especially in the ○ Pulmonary contusions (p. 835) in capillary hydrostatic pressure.
dorsocaudal lung fields ○ Interstitial lung disease (p. 553) • Whenever possible, address the underlying
○ Murmur, arrhythmia, or gallop increases ○ Lung lobe torsion (p. 593) cause of NPE.
suspicion for cardiogenic pulmonary • Heartworm disease (pp. 415 and 418) ○ Upper airway obstruction (pp. 1004 and
edema but do not rule out NPE. • Pleural space disease (p. 791) 1166)
• Other findings can reflect cause of NPE: ○ Control seizures that can precipitate NPE
○ Lingual ulceration due to electric cord Initial Database (p. 903)
electrocution • Thoracic radiographs: varies ○ Treat sepsis (p. 907), uremia (pp. 23 and
○ Stridor with laryngeal paralysis or ○ Mixed interstitial and alveolar (≈77%) > 169), or other systemic disease
obstruction interstitial (≈26%) pattern ○ Unfortunately, many causes of NPE cannot
○ Uremic breath and/or small kidneys with ○ Peripheral (≈90%) > central distribution be readily resolved (e.g., near drowning,
uremia ○ Focal or multifocal (≈77%) > diffuse smoke inhalation, severe pancreatitis).
○ Bilateral (≈77%) > unilateral Supportive care allows time for the injury/
Etiology and Pathophysiology ○ Dorsal (≈58%) > ventral illness to resolve.
• Increased permeability edema secondary to • CBC/serum biochemistry profile/urinalysis: • Mechanical ventilation (p. 1185) if patient
direct endothelial and/or alveolar epithelial may be unremarkable or reflect systemic has a sustained increase in work of breath-
injury, resulting in proteinaceous fluid disease (e.g., uremia, pancreatitis, sepsis) ing, SpO 2 < 90%, PaO 2 < 60 mm Hg,
accumulation in the alveoli • Pulse oximetry: depends on severity of NPE; or PaCO 2 > 55 mm Hg despite oxygen
○ Any cause of ARDS (p. 27) < 95% on room air suggests respiratory therapy.
○ Pulmonary thromboembolism (p. 842) impairment • Unless needed to treat the underlying cause
○ Toxins/drugs: petroleum distillates, of NPE, there is no indication for antibiotics,
paraquat, zinc phosphate, arsenic, smoke Advanced or Confirmatory Testing glucocorticoids, or nonsteroidal antiinflam-
inhalation, organophosphate/carbamate, • Point-of-care test for N-terminal pro-brain-type matory drugs.
calcium channel blockers, cisplatin (cats), natriuretic peptide (NT-pro-BNP) to rule out
cytarabine, oxygen toxicity (prolonged, a cardiac cause for respiratory distress in cats; Chronic Treatment
high FIO 2 ), others a positive test warrants an echocardiogram Depends on the underlying disease process
• Mixed PE: a combination of increased • Echocardiogram to rule out cardiogenic PE
permeability and increased hydrostatic (especially if cardiac exam abnormal) Possible Complications
pressure from increased sympathetic nervous • Cage-side lung ultrasound exam (veterinary • Mechanical ventilation: acute lung injury,
system (SNS) discharge, resulting in increased bedside lung ultrasound exam [Vet BLUE]) hypotension, pneumothorax, and pneumonia.
systemic and pulmonary capillary pressure can detect changes suggestive of pulmonary • Appropriate ventilator settings, analgesia,
○ Re-expansion PE: acute re-expansion of edema (i.e., B lines in the dorsocaudal lung fluid therapy, and nursing care can minimize
chronically atelectic lung lobes field) or alternative causes of distress (e.g., complications.
○ Neurogenic PE: head trauma, seizures, pleural effusion, left atrial enlargement).
electrocution, near drowning • Arterial blood gas is nonspecific for NPE Recommended Monitoring
○ Negative pressure PE: strangulation, but can reveal hypoxemia. • Frequent assessment of vital parameters with
choking, upper airway obstruction • Heartworm antigen (dog) or antigen and focus on respiratory rate and effort
• Arterial hypoxemia and respiratory distress antibody (cat) testing • Blood pressure (invasive, Doppler, oscil-
secondary to ventilation perfusion mis- • If pneumonia or other lung disease is sus- lometric)
matching and, to a lesser extent, diffusion pected, bronchoscopy with bronchoalveolar • Oxygenation: arterial blood gas (p. 1058)
impairment lavage (pp. 1073 and 1074) for infectious/ or pulse oximetry
• Edema fluid from noncardiogenic cause inflammatory disease; with NPE, protein- • Ventilation: blood gas analysis or ETCO 2
has protein content equal to plasma, and aceous alveolar fluid expected • Serial thoracic radiographs or CT if improve-
cardiogenic edema fluid has a low protein ment lacking or to assess resolution
content. TREATMENT
• Reduced oncotic pressure alone is unlikely PROGNOSIS & OUTCOME
to cause PE because of generous pulmonary Treatment Overview
lymphatics, but low colloid oncotic pressure Minimize stress and handling of patients in Prognosis depends on the cause, severity,
can worsen edema severity. respiratory distress, and focus on alleviation and duration of NPE and on comorbidities.

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