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Emergency care of the patient with acute respiratory distress Part 1

Lesley King, MVB, Dipl. ACVECC, Dipl. ACVIM, Dipl. ECVIM (CA). Dana Clarke, VMD - 19/09/2015

Emergency care of the patient with acute respiratory distress - Part 1

Key Points

 

Introduction, initial assessment and stabilization

Respiratory distress in small animal patients is a true emergency which requires rapid stabilization, prompt recognition and treatment of the underlying problem, determination of diagnostic and therapeutic options, and an assessment of prognosis. The first steps in the management of the dyspneic patient include recognizing that the respiratory system is compromised, performing a physical examination, providing supplemental oxygen, and obtaining a brief but focused history from the owner.
 


Physical examination

Animals that present in respiratory distress must be handled carefully to minimize stress and struggling and the initial physical examination may be limited to assessment of mucous membranes, capillary refill, and thoracic auscultation. Commonly the clinician may note increased respiratory rate and/or effort, shallow chest excursions, excessive respiratory noise, extension of the head and neck, nostril flare, mouth breathing, elbow abduction, and an inability to lie down or be comfortable. Patients on the verge of respiratory arrest may have limited movement of the chest wall and a paradoxical respiratory pattern due to respiratory muscle fatigue (1-4).

 

It is imperative to assess airway patency at presentation by observing that the patient is able to move air during breathing; the animal should not be stressed by attempting to open the mouth. If complete airway obstruction is diagnosed, rapid sequence sedation, intubation and possibly positive pressure ventilation are indicated. Cyanosis is not a reliable indicator of hypoxemia, as it does not develop until the partial pressure of oxygen in arterial blood (PaO2) is <50 mmHg, and cannot be detected in severely anemic or hypoperfused patients. Therefore the presence of pink mucous membranes should not be perceived as an indication of adequate oxygenation (1,4). A brief period of thoracic auscultation at this time should include auscultation of the heart to detect arrhythmias or murmurs, auscultation of the lungs with particular attention to areas of dullness or abnormal lung sounds such as crackles or wheezes, and auscultation of the cervical trachea to detect loud sounds indicating a possible airway obstruction.

 

Many dyspneic patients, especially cats, are intolerant of handling. Therefore supplemental oxygen, regardless of the cause of respiratory distress, is imperative for all patients with respiratory compromise. If possible, a peripheral intravenous catheter should also be placed at presentation to provide vascular access.



Methods of oxygen supplementation

Methods of oxygen support include flow-by, mask, hood delivery, nasal oxygen catheters, oxygen cage, and positive pressure ventilation (3-7).


Flow-by oxygen is the provision of oxygen through a tube held in front of the patient’s face. Inexpensive and uncomplicated, it does require some patient restraint and someone to hold the line to the patient’s mouth and nose. It is most useful for short-term provision of supplemental oxygen during the initial assessment of the animal and during brief procedures such as radiographs and catheter placement (4-7) but may be insufficient for patients Figure 1that are panting or moving. Flow rates should be between 100-200 mL/kg/min, but high flow rates may not be well tolerated and are comparatively wasteful. The effectiveness of flow by oxygen can be improved via an oxygen mask: a plastic cone that attaches to the oxygen line. With similar flow rates to those given above, this technique provides higher percentages of inspired oxygen (especially with a well-fitted mask and a recumbent patient). Mobile patients will require restraint to keep the mask in place, and many distressed animals resist placement of the mask over their face. An oxygen hood can be fashioned from an Elizabethan collar partially covered with plastic wrap. An oxygen line is inserted inside the collar, with the plastic cover vented to allow expired heat and gases to escape. Commercially available hoods, with an adjustable collar and perforated holes for expired gas release, also exist. Hoods are generally well tolerated, can achieve high percentages of inspired oxygen and allow for patient monitoring and procedures without interrupting oxygen delivery. However, there is no control over the amount of inspired oxygen and some patients, especially those that are panting, may overheat. Humidification should be used for long term oxygen hood therapy (3-6). Nasal catheters can provide high percentages of inspired oxygen via an indwelling catheter (see Table 1) or human nasal oxygen prongs (which are less invasive and useful in quiet or recumbent patients - Figure 1), using flow rates of 0.5-3 L/min. This technique is useful in patients that are restless or panting, or too large or intolerant of an oxygen cage, and is less wasteful than other methods. It allows patient monitoring and further procedures without interruption of oxygen therapy, but given the time needed for catheter placement this method is usually reserved for more long-term treatment (rather than initial stabilization) and humidification should be added in this situation (3,4,6,7). Oxygen cages are extremely useful as they provide accurate and (if indicated) high concentrations of humidified oxygen, allowing patient observation without restraint. However cages are expensive and can be wasteful as oxygen concentration decreases rapidly when the door is open. If severe respiratory distress cannot be relieved using other techniques, intubation and positive pressure ventilation is the best way to control the airway, deliver oxygen or positive end-expiratory pressure, to relieve the patient’s anxiety and discomfort. Heavy sedation or light anesthesia, constant intensive monitoring, specialized equipment and training are required for this technique (4-7).

 

Regardless of the method of oxygen supplementation chosen, it is important to remember that prolonged periods (>24 hours) of high oxygen concentrations (>60%) should ideally be avoided to reduce the risk of oxygen toxicity due to free radical formation (4,6,7).

 Table 1


Obtaining a history

After the patient has been stabilized with supplemental oxygen, a preliminary history can be obtained from the owner. Important information includes the duration and nature of respiratory signs, the presence of coughing, gagging, or exercise intolerance, possibility of toxin or foreign body ingestion, voice changes, history of heart or pulmonary disease, use of heartworm preventative, and the presence of concurrent systemic illness, such as vomiting, anorexia, and endocrine diseases. A current medication list should also be obtained. Once a physical examination has helped determine the anatomic origin of the respiratory distress and the animal has been stabilized, a more complete history can be obtained and a definitive diagnostic and therapeutic plan reviewed with the owners.



Localization of respiratory compromise, diagnostics, and therapeutics

A more complete physical examination can be performed to localize the origin of respiratory distress. Based on this examination, the causes of respiratory distress can be assigned to one of five categories: airway obstruction, pulmonary parenchymal disease, pleural space disease, thoracic wall abnormalities, and “look-alikes”. Identification of the probable site of the problem, combined with the signalment and history, allows the determination of a list of likely differential diagnoses, necessary diagnostics and immediate therapeutic options.



Airway obstruction

These patients may have inspiratory and/or expiratory stridor or stertor, head and neck extension, heat and exercise intolerance, prolonged inspiration, cyanosis, a honking or dry cough, respiratory distress, retching, and collapse. Dogs may be hyperthermic and cats may have intermittent open mouth breathing. A prolonged inspiratory phase of respiration (because the upper airway is sucked closed on inspiration) may be noted and wheezes may be heard, particularly on expiration. Coughing is commonly seen in cats with asthma, and lower airway obstructive disease is associated with increased expiratory effort. Referred upper airway noise may be differentiated from pulmonary parenchymal sounds as the sound intensity and pitch is louder on auscultation of the larynx and trachea (1,2,4,8,9).

 

Common causes of airway obstruction in dogs include: brachycephalic airway syndrome, laryngeal paralysis, inflammation or edema of the pharynx or larynx, airway infections and/or abscessation, foreign body, coagulopathy induced hemorrhage, neoplasia, tracheal and mainstem bronchial collapse, and bronchitis (1,4,8,9). In cats, the most common causes of airway obstruction are feline asthma, nasopharyngeal polyps, pharyngeal and laryngeal neoplasia, inflammatory and granulomatous laryngeal disease, and viral nasal infections (2,4,8,9).

 

Since airway obstructions may impede oxygenation, ventilation, or both, useful diagnostics include pulse oximetry (Figure 2) and arterial or venous blood gas analysis. Hypoventilation is defined as arterial carbon dioxide partial pressure (PaCO2) >43 mmHg in dogs and >36 mmHg in cats, resulting in primary respiratory acidosis. PaCO2 >60 mmHg is consistent with significant hypoventilation and warrants definitive therapy to relieve the airway obstruction. When arterial blood gas sampling is not possible, venous carbon dioxide partial pressure (PvCO2) can be used. Hypoxemia is defined as arterial partial pressure of oxygen (PaO2)<80 mmHg and a value of PaO2 <60 mmHg (which corresponds to <90% pulse oximetry) is consistent with severe hypoxemia and requires therapeutic intervention.

 

In these patients initial stabilization should be aimed at provision of supplemental oxygen, establishing vascular access, and applying cooling measures. Sedative and/or anxiolytic therapies can relieve respiratory distress and decrease respiratory drive, thus decreasing the degree of airway collapse. Intravenous fluid therapy, wetting of the fur and the use of a fan will aid cooling. Anti-inflammatory doses of corticosteroid may also be considered; this can be life-saving in patients with severe airway edema or inflammation but should be used selectively as it may impede a definitive diagnosis of lymphoma (1,8). Cats with feline asthma may benefit from parenteral bronchodilators such as terbutaline if they have no evidence of heart disease. Inhaled drugs (e.g. albuterol, fluticasone) may be substituted if complicating systemic disease is present. In the majority of patients, sedation, cooling and head/neck positioning to optimize airway patency are sufficient for stabilization.

 Figure 2

For those with complete airway obstruction, or when cooling and sedative efforts are ineffective, induction of anesthesia and intubation is required. If endotracheal intubation cannot be achieved, an emergency tracheostomy must be performed.

 

The cause of an upper airway obstruction can usually be diagnosed by a sedated upper airway/ laryngeal examination, cervical and thoracic radiographs, fluoroscopy, rhinoscopy/laryngoscopy/ tracheoscopy/bronchoscopy, and/or computed tomography (CT). If a hematoma caused by a coagulopathy (e.g. secondary to rodenticide) is suspected, prothrombin time (PT) and partial thromboplastin time (PTT) should be performed. Transtracheal lavage, endotracheal lavage, or bronchoalveolar lavage should be considered in patients suspected to have lower airway (bronchial) or concurrent pulmonary parenchymal disease.

 

 

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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