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Emergency care of the patient with acute respiratory distress Part 2

Lesley King, MVB, Dipl. ACVECC, Dipl. ACVIM, Dipl. ECVIM (CA). Dana Clarke, VMD - 28/09/2015

Emergency care of the patient with acute respiratory distress - Part 2


Pulmonary parenchymal disease

Dogs with pulmonary parenchymal disease are often depressed; signs may include: panting or breathing open-mouthed, with nostril flare, coughing, head and neck extension, and anxiety. Cats only breathe through an open mouth when they have severe respiratory compromise and (in contrast to dogs) rarely cough. Physical examination findings may include weakness, tachypnea, tachycardia, fever, mucopurulent nasal discharge, harsh lung sounds, and/or crackles. A heart murmur and/or arrhythmias are usually heard in dogs that have respiratory signs due to congestive heart failure. The same is not always true of cats with congestive heart failure, when cardiac auscultation may be normal. Pulse quality may be diminished whilst cyanosis may be seen in severely hypoxemic patients although hypoperfusion may produce pallor of the mucous membranes (1,2,4).

 

Figure 3Common causes of pulmonary parenchymal disease include parasitic or bacterial pneumonia, pulmonary edema (cardiogenic or non-cardiogenic), pulmonary contusions, smoke inhalation, pneumonitis (chemical and uremic), aspiration pneumonia, fungal or viral infection, pulmonary thromboembolism, neoplasia, pulmonary fibrosis, and acute respiratory distress syndrome (ARDS). Cardiogenic edema occurs frequently in cats, whereas aspiration pneumonia is uncommon in this species (1-4,10).

 

Thoracic radiographs are particularly important in this situation. For example, classic radiographic changes associated with pneumonia include a cranio-ventral alveolar pattern (Figure 3), whereas cardiogenic pulmonary edema in dogs is generally associated with a heavy perihilar interstitial to alveolar pattern (Figure 4). In contrast, noncardiogenic pulmonary edema is associated with a caudo-dorsal interstitial to alveolar pattern (Figure 5).

 

Pulmonary parenchymal disease causes hypoxemia primarily by mismatch of ventilation and perfusion, but also due to diffusion impairment and intrapulmonary shunt. Pulse oximetry and blood gas analysis are important in determining the severity of disease, and hematology and biochemistry may assist diagnosis. Lower respiratory tract sampling via transtracheal, endotracheal, or bronchoalveolar lavage can be important diagnostics to determine the origin of pulmonary parenchymal disease, especially in patients with atypical radiographic changes or when multiple disease processes are suspected, and cytology, bacterial culture and sensitivity, and fungal culture are usually indicated. Emergency therapy for patients with pulmonary parenchymal disease depends on the clinician’s educated guess about the most likely etiology.



Pleural space diseaseFigure 4 and 5

Clinical signs in these patients may include a short, shallow restrictive breathing pattern, increased respiratory rate, nostril flaring, orthopnea, an abdominal component to respiration, and a reluctance to lie down. Cats may have open mouth breathing. The degree of respiratory distress depends on the rate of development of the pleural space-occupying lesion, especially pleural effusion. Paradoxical respiration may be noted in patients with a diaphragmatic hernia. Thoracic auscultation may reveal decreased or dull lung sounds ventrally (pleural effusion) or dorsally (pneumothorax), an auscultable fluid line, muffled cardiac sounds, or borborygmi if stomach or intestines are in the chest. Thoracic auscultation changes may be unilateral or bilateral and are not always equal. Cats with a mediastinal mass have decreased chest wall compressibility (1,2,4,11,12).

 

Common causes of pleural space disease include pneumothorax and pleural effusions. Pleural effusions may be pure or modified transudates due to congestive heart failure, vasculitis, and lung lobe torsion; pyothorax, chylothorax, hemothorax, feline infectious peritonitis, and neoplastic effusions are also common. Diaphragmatic hernia and pleural space masses also occur (1,2,4,11,12).

 

If pleural disease is suspected, it is imperative to evacuate the pleural space as quickly as possible (Table 2). Oxygen supplementation and vascular access is established if it can be done without stress. Thoracocentesis is both therapeutic and diagnostic, and any fluid obtained submitted for cytology and culture. Thoracocentesis is not indicated for patients with pleural space masses, diaphragmatic hernias, or hemothorax secondary to coagulopathy that is not causing significant respiratory compromise. Other diagnostics (e.g. radiography or ultrasound) should be delayed until after the animal has been stabilized by thoracocentesis, allowing the pulmonary parenchyma to be visualized effectively.

 

Normally blood aspirated during thoracocentesis should clot quickly, unless a coagulopathy or a hemorrhagic effusion (e.g. due to neoplasia or lung lobe torsion) is present; if this occurs further testing to confirm these suspicions should be performed. If unexpected air is aspirated, the collection system should be checked for leaks. If no leaks are present, thoracoentesis should be temporarily aborted as long as the animal is still stable, because an iatragenic pneumothorax may have been created (3,4,12,13). If negative pressure is not achieved during thoracocentesis, if the patient re-accumulates a significant amount of air within a short period requiring multiple thoracocentesis events, or for the medical management of certain pleural effusions such as pyothorax, thoracostomy tubes (unilateral or bilateral) may be needed and are best placed using general anesthesia (1,3,4,14).


 

Thoracic wall abnormalities

Abnormalities of thoracic wall function may occur because of dysfunction at several levels. In some cases, respiratory distress may be secondary to thoracic wall injuries or trauma. Those patients often demonstrate pain on manipulation or palpation of the thorax, and may have a flail chest with paradoxical motion of a segment of chest wall. Lacerations, bruising or concurrent pulmonary contusions may occur. Alternatively, abnormal thoracic wall and diaphragmatic function may result from defective neuromuscular control of breathing, which may be caused by disease in the brain, spinal cord, peripheral nerves or neuro-muscular junctions. Such patients typically lack diaphragmatic and abdominal muscle movement, and have clinical evidence of hypoventilation with elevated PaCO2 levels on blood gas analysis (1,3,15).

 

Table 2

 

Common causes of thoracic wall dysfunction include traumatic injuries, anesthetics and central respiratory depressants, severe hypokalemia, myasthenia gravis, botulism, tick paralysis, polyradiculoneuritis, congenital abnormalities, some snake envenomation, thoracic wall neoplasia, and spinal cord or phrenic nerve disease (1,3,15).

 

Diagnostics for these patients include blood gas analysis, pulse oximetry, capnography, and thoracic radiographs. Neurologic examination findings consistent with cervical spinal cord or brainstem dysfunction may support a neurologic origin. Measurement of acetylcholine receptor antibody titers, edrophonium response testing, and electromyelography (EMG) can aid in the diagnosis of myasthenia gravis. EMG and the confirmation of botulism toxin in serum, feces, or vomited material can support a diagnosis of botulism. There are no specific diagnostic tests for tick paralysis, polyradiculoneuritis, and snake venoms, though geographic location, signalment, and history may support a diagnosis (15).

 


“Look-alikes”

Whilst rare, some non-respiratory conditions can mimic respiratory disease. Examples include hyperthermia, compensation for metabolic acidosis, anemia, pain, stress, anxiety, hypovolemia, abdominal distension (cranial organomegaly and abdominal effusion), hyperadrenocorticism or corticosteroid therapy, and certain opioid medications (16). History, physical examination, thoracic radiographs, blood gas analysis and serum chemistry can be helpful to distinguish these conditions from real respiratory disease.



Conclusion

Respiratory distress is a common and serious emergency encountered by veterinarians. An understanding of the need for careful patient handling and the provision of supplemental oxygen is vital. Veterinarians should recognize the signalment, history, and physical examination findings seen with common respiratory diseases. An understanding of respiratory disease pathophysiology and localization as well as the diagnostic and therapeutic techniques essential for management of each category of dysfunction is crucial for successful treatment.


This article was kindly provided by Royal Canin, makers of a range of veterinary diets for dogs and cats. For the full range please visit www.RoyalCanin.co.uk or speak to your Veterinary Business Manager:

 

 



 

REFERENCES

1. Lee JA, Drobatz KJ. Respiratory distress and cyanosis in dogs. In: King LG. Textbook of respiratory disease in dogs and cats. Philadelphia: WB Saunders 2004; 1-12.

2. Mandell DC. Respiratory distress in cats. In: King LG. Textbook of respiratory disease in dogs and cats. Philadelphia: WB Saunders 2004; 12-17.

3. Tseng LW, Waddell LS. Approach to the patient in respiratory distress. Clin Tech Small Anim Pract 2000; 15: 53-62.

4. Macintire DK, Drobatz KJ, Haskins SC, et al. Manual of small animal emergency and critical care medicine. Philadelphia: Lippencott, Williams and Wilkins, 2005; 115-159.

5. Rozanski E, Chan DL. Approach to the patient with respiratory distress. Vet Clin Small Anim Pract 2005; 35: 307-317.

6. Tseng LW, Drobatz KJ. Oxygen supplementation and humidification. In: King LG. Textbook of respiratory disease in dogs and cats. Philadelphia: WB Saunders 2004; 205-213.

7. Mazzaferro EM. Oxygen therapy. In: Silverstein DC, Hopper K. Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009; 78-81.

8. Costello MF. Upper airway disease. In: Silverstein DC, Hopper K. Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009; 67-72.

9. Holt DE. Upper airway obstruction, stertor, and stridor. In: King LG. Textbook of respiratory disease in dogs and cats. Philadelphia: WB Saunders 2004; 35-42.

10. De Clue AE, Cohn LA. Acute respiratory distress syndrome in dogs and cats: a review of clinical findings and pathophysiology. J Vet Emerg Crit Care 2007; 17: 340-347.

11. Suave V. Pleural space disease. In: Silverstein DC, Hopper K. Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009; 125-130.

12. Silverstein DC. Pleural space disease. In: King LG. Textbook of respiratory disease in dogs and cats. Philadelphia: WB Saunders 2004; 49-52.

13. Sigrist NE. Thoracocentesis. In: Silverstein DC, Hopper K. Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009; 131-133.

14. Sigrist NE. Thoracostomy tube placement and drainage. In: Silverstein DC, Hopper K. Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009; 134-137.

15. Donahue S. Chest wall disease. In: Silverstein DC, Hopper K. Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009; 138-140.

16. Hall K, Lee JA. Nonrespiratory look-alikes. In: Silverstein DC, Hopper K. Small Animal Critical Care Medicine. Philadelphia: WB Saunders 2009; 141-144.

This article was previously published in 2012.

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