References

Aldridge P, O'Dwyer L. Techniques for Oxygen Supplementation. In: Aldridge P., O'Dwyer L. West Sussex, UK: Wiley-Blackwell; 2013

Armstrong PJ, Hardie EM. Percutaneous endoscopic gastrostomy. A retrospective study of 54 clinical cases in dogs and cats. J Vet Intern Med. 1990; 4:(4)202-6

Ayres DA. Pulse Oximetry and CO-Oximetry. In: Burkitt Creedon JM, Davis H : Chichester, UK; 2012

Balakrishnan A, Drobatz KJ, Silverstein DC. Retrospective evaluation of the prevalence, risk factors, management, outcome, and necropsy findings of acute lung injury and acute respiratory distress syndrome in dogs and cats: 29 cases (2011–2013). J Vet Emerg Crit Care (San Antonio). 2017; 27:(6)662-73 https://doi.org/10.1111/vec.12648

Barton L. Aspiration pneumonia. In: King LG St Louis: Elsevier; 2004

Cameron JL, Caldini P, Toung JK, Zuidema GD. Aspiration pneumonia: physiologic data following experimental aspiration. Surgery. 1972; 72:(2)238-45

Darcy H, Humm K, ter Haar G. Retrospective analysis of incidence, clinical features, potential risk factors, and prognostic indicators for aspiration pneumonia in 3 brachycephalic dog breeds. J Am Vet Med Assoc. 2018;

Gray S, Powell LL. Blood Gas Analysis. In: Creedon J. M. Burkitt, Davis H. Chichester, UK: John Wiley & Sons, Ltd; 2012 https://doi.org/10.1002/9781118997246.ch22

Haskey E. How to nurse the intensive care unit ventilator patient. The Veterinary Nurse. 2013; 4:(2)108-13

Kogan DA, Johnson LR, Sturges BK, Jandrey KE, Pollard RE. Etiology and clinical outcome in dogs with aspiration pneumonia: 88 cases (2004–2006). J Am Vet Med Assoc. 2008; 233:(11)1748-55 https://doi.org/10.2460/javma.233.11.1748

Kelmer E, Love LC, Declue AE Successful treatment of acute respiratory distress syndrome in 2 dogs. Can Vet J. 2012; 53:(2)167-73

Kennedy TP, Johnson KJ, Kunkel RG, Ward PA, Knight PR, Finch JS. Acute acid aspiration lung injury in the rat: biphasic pathogenesis. Anaesthesia and Analgesia. 1989; 69:(1)87-92

Knight PR, Rutter T, Tait AR, Coleman E, Johnson K. Pathogenesis of gastric particulate lung injury: a comparison and interaction with acidic pneumonitis. Anesthesia and Analgesia. 1993; 77:(4)754-60

ABCs of Blood Gas Evaluation. 2011. https://www.acvs.org/files/proceedings/2011/data/papers/170.pdf (accessed 27th February, 2018)

Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med. 2001; 344:(9)665-71

Mendelson Curtis L. The aspiration of stomach contents into the lungs during obstetric anesthesia. Obstetrical & Gynecological Survey. 1946; 1:(6)837-9

Meola SD, Mazzaferro EM, Wheeler JL, McKiernan B. Medical and surgical management of severe barium aspiration in a dog. Journal of Veterinary Emergency and Critical Care. 2008; 18:(6)639-45

Sherman R, Karagiannis M. Aspiration Pneumonia in the Dog: A Review. Topics in Companion Animal Medicine. 2017; 32:(1)1-7

Tart KM, Babski DM, Lee JA. Potential risks, prognostic indicators, and diagnostic and treatment modalities affecting survival in dogs with pre-sumptive aspiration pneumonia: 125 cases. J Vet Emerg Crit Care (San Antonio). 2010; 20:(3)319-29 https://doi.org/10.1111/j.1476-4431.2010.00542.x

Toung T, Rosenfeld B, Yoshiki A, Grayson R, Traystman R. Sucralfate does not reduce the risk of acid aspiration pneumonitis. Crit Care Med. 1993; 21:(9)1359-64

Wilson DV, Walshaw R. Postanesthetic esophageal dysfunction in 13 dogs. J Am Anim Hosp Assoc. 2004; 40:(6)455-60

The forgotten complication: aspiration pneumonia in the canine patient

02 April 2018
8 mins read
Volume 9 · Issue 3

Abstract

Aspiration pneumonia is a common complication, with many risk factors, seen in canine patients in referral centres and first opinion practices. Nurses play a vital role in recognising signs of aspiration pneumonia: cough, changes in breathing rate and effort, and abnormal thoracic auscultation. Treatment centres on supportive care, while providing antibiotic therapy for the bacterial infection. This article will focus on management of the canine aspiration pneumonia patient.

Aspiration pneumonia is a disease that can occur in both canine and feline patients, however it is far more common in canines. It is caused by the inhalation of foreign matter (such as gastric contents, hydrocarbons, chemicals or water) into the larynx and lower respiratory tract. Aspiration of contaminated material can cause aspiration pneumonitis, which is the pulmonary injury that occurs after an aspiration event. Aspiration of gastric acid is an aseptic injury, but this adversely affects the lung's defences against infection, predisposing the lung to secondary infection (Tart et al, 2010). Aspiration pneumonitis and aspiration of contaminated material can both lead to aspiration pneumonia, the term used to describe the presumed secondary infection (Tart et al, 2010).

Aspiration pneumonia is usually associated with an underlying disease and there are several predisposing risk factors:

  • Gastrointestinal disease (vomiting/regurgitation) (Tart et al, 2010)
  • Neurological patients (e.g. seizures) (Marik, 2001)
  • Recent anaesthesia (Wilson and Walshaw, 2004)
  • The use of feeding tubes (Armstrong and Hardie, 1990)
  • Certain breeds — a recent study (pending publication) found that brachycephalic breeds (e.g. French Bulldogs, Pugs, English Bulldogs) were three times more likely to develop aspiration pneumonia compared with non-brachycephalic breeds (Darcy et al, 2018).
  • Many of these risk factors occur in critically ill hospitalised patients, so regular monitoring for changes in respiratory function is paramount.

    It is difficult to differentiate between pneumonia and pneumonitis in veterinary patients, so pulmonary issues associated with aspiration usually receive a diagnosis of aspiration pneumonia.

    Aspiration pneumonia is a serious complication, which is regularly diagnosed in referral centres but may be overlooked in first opinion. Survival rates are 77–82% (Kogan et al, 2008, Tart et al, 2010) in mild cases, but when aspiration pneumonia develops into acute respiratory distress syndrome (ARDS), or the patient requires mechanical ventilation, survival rates decrease (Balakrishnan et al, 2017) (Box 1).

    Criteria for identification of ARDS (Kelmer et al, 2012)

  • Acute tachypnoea and increase in respiratory effort <72 hour duration.
  • Inefficient gas exchange; PaO2:FiO2 ratio less than 200, increased A-a gradient.
  • Evidence of pulmonary inflammation.
  • Risk factors (direct or secondary pulmonary injury).
  • Non-cardiogenic pulmonary capillary leak.
  • Pathophysiology

    Aspiration of contaminated material severely compromises respiratory function. The degree of severity is dependent on the material aspirated and the volume.

    Severe pulmonary tissue damage occurs after inhaling:

  • Gastric fluid with a pH of <2.5 (Cameron et al, 1972).
  • A volume greater than 0.3–0.4 ml/kg (Toung et al, 1993).
  • A large particulate matter (Knight et al, 1993).
  • Aspiration of gastric acid first has caustic effects on the bronchial and alveolar epithelium, and the pulmonary parenchyma. This results in bronchoconstriction, and increases vascular permeability resulting in intrapulmonary haemorrhage and vasodilation. This usually occurs within 1 to 2 hours of aspiration (Gray, 2012).

    Two to 6 hours after aspiration, protein extravasation occurs, which leads to pulmonary oedema, adversely affecting gas exchange and thus resulting in ventilation-perfusion (V/Q) mismatch and reduced lung compliance (Kennedy et al, 1989).

    Food particle aspiration does not cause pulmonary oedema, but does incite a neutrophilic response due to the increase in inflammatory mediators (Knight et al, 1993). It may also lead to airway obstruction or even respiratory arrest, if the particulate is large (Knight et al, 1993).

    In severe cases, aspiration pneumonia can lead to ARDS, which is caused by the systemic inflammation. Such cases require intensive nursing and aggressive management. Patients are at risk of developing multiple organ dysfunction syndrome (MODS) (Balakrishnan et al, 2017) where the body is in a state of global inflammation. These patients have a guarded prognosis and often, despite best efforts, require euthanasia or experience cardiac arrest.

    Diagnosis

    In veterinary patients, most aspiration events are not observed so therefore, the diagnosis of aspiration pneumonia is assumed when acute respiratory distress occurs a few hours after vomiting, regurgitation or anaesthesia. It is also assumed if gastric contents are found in the airway, or if aspiration is witnessed (Barton, 2004). A definitive diagnosis of the disorder is challenging.

    The registered veterinary nurse (RVN) plays an important role in the assessment of these patients. Nurses should be confident recognising subtle changes in a patient, signs of respiratory distress and any abnormalities on thoracic auscultation. In one study, 70–75% of patients with suspected aspiration pneumonia had abnormal findings on thoracic auscultation (Tart et al, 2010).

    History

  • Cough
  • Lethargy or collapse
  • One or more of the previously mentioned risk factors.
  • Clinical signs

  • Commonly in respiratory distress — oxygen therapy should be given immediately if these signs are observed. Aspiration causes bronchoconstriction of the airways, causing increased respiratory effort (Mendelson Curtis, 1946), which progresses to consolidation of the lung which is the source of most of the clinical signs (Meola et al, 2008).
  • Abnormalities on thoracic auscultation include, but are not limited to, crackles and harsh or loud lungs sounds.
  • Mucous membranes can be normal (salmon pink), but in some cases can be hyperaemic or cyanotic (Tart et al, 2010).
  • Signs of sepsis/systemic inflammatory response syndrome (SIRS) can be present, if severe, and the patient should be monitored for SIRS when hospitalised.
  • Bilateral nasal discharge.
  • Radiography/computed tomography (CT)

    Plain radiography is an excellent tool used to diagnose aspiration pneumonia (Figure 1). The typical radiological abnormality found with aspiration pneumonia is an alveolar lung pattern, caused when the air is displaced from the alveoli due to the accumulation of fluid. An interstitial pattern can also be seen (Kogan et al, 2008). Kogan et al (2008) also found that the right middle lung lobe was the most commonly affected lobe. CT can also be used, but it is expensive and often not necessary.

    Figure 1. Radiograph showing an alveolar lung pattern seen in this patient with aspiration pneumonia.

    Percutaneous trans-tracheal wash (TTW)

    This can be used to obtain a sterile airway sample. TTW is usually preferred in unstable animals that are not recommended to have a general anaesthetic and larger breeds of dog.

    Bronchoalveolar lavage (BAL)

    Bronchoalveolar lavage is a more invasive procedure and requires general anaesthesia (GA) and intubation. This can be blind or via bronchoscope which enables visualisation of the airway and affected areas. This method also enables sampling directly from affected areas.

    Oxygen status

    Patients with aspiration pneumonia usually present hypoxaemic (Tart et al, 2010), which can be checked with pulse oximetry or arterial blood gas sampling. Normal SpO2 reference 95–100%, but this is not always accurate and may give a false reading due to various factors (e.g. poor perfusion to tissues, oedema) (Ayres, 2012) (Box 2).

    Definitions

    Ventilation — exchange of O2 and CO2 through breathing

    FiO2 — fraction of inspired O2

    PaO2 — partial pressure of O2

    PaCO2 — partial pressure of CO2

    Hypoxaemia — O2 deficiency in arterial blood

    Hypoxia — decreased oxygenation of the tissues.

    Fluid accumulation or oedema seen with aspiration pneumonia can lead to airway narrowing, which affects ventilation-perfusion (V/Q) ratio that impairs ventilation. Intrapulmonary shunting (an extremely low V/Q situation) can also occur when the alveoli are collapsed or when they are not ventilated due to being filled with a substance (Gray, 2012).

    An arterial blood gas sample can also be used to assess pulmonary function, and is considered gold standard. Changes seen regularly on arterial blood gas measurement in aspiration pneumonia patients include hypoxaemia and hypocapnia.

    A method to determine the severity of the pulmonary damage is to calculate the alveolar-arterial (PAO2–PaO2) gradient (Box 3), which is usually increased in patients with aspiration pneumonia due to ventilation-perfusion mismatch (V/Q mismatch) (Gray, 2012).

    Alveolar–arterial gradient

    The following sum can be used to calculate the alveolar(A) – arterial(a) gradient: 150–1.1(PaCO2) – PaO2 (Koenig, 2011)

    Normal value — less than 15 mmHg

    An alternative equation can be used to assess oxygenation in the face of oxygen supplementation — PaO2:FiO2. Normal values are: 400–500 mmHg, values less than 300 mmHg indicate acute lung injury, and ARDS is indicated when the value is <200 mmHg (Aldridge and O'Dwyer, 2013).

    If arterial blood gas measurement is not available, response to oxygen supplementation can be assessed.

    Treatment and nursing considerations

    Supportive treatment in these patients should not be underestimated. It is important that hydration is maintained, and that adequate nutrition is provided, and that the patient is urinating and defecating normally. It is also vital that any underlying condition is identified and managed accordingly.

  • Antibiotics — antibiotic therapy is indicated in cases of aspiration pneumonia where infection is present and identified. Samples obtained via TTW or BAL should have culture and sensitivity testing performed. Broadspectrum antibiotic therapy (e.g. amoxicillin-clavulanic acid) can be initiated while awaiting results.
  • Airway management — patients with aspiration pneumonia decompensate quickly, and may require endotracheal intubation. Situations where this may be necessary are:
  • Unable to maintain their own patent airway
  • Oxygen levels not responding to oxygen therapy
  • Impending respiratory failure (Aldridge and O'Dwyer, 2013).
  • Oxygen therapy — this is important for patients demonstrating signs of respiratory distress (i.e. tachypnoea, dyspnoea and tachycardia) or documented hypoxaemia. Tart et al (2010) found that oxygen was not statistically significant in terms of survival, but should be supplemented in the hypoxaemic patient. Oxygen supplementation is indicated when SpO2 is less than 93% or PaO2 is less than 80 mmHg on room air. When the patient presents in respiratory distress, short-term oxygen therapy can be provided via flow-by or masked oxygen during initial assessment and stabilisation (Figure 2). Longer-term oxygen therapy methods should be implemented for the hospitalised patient. These should be used in conjunction with a humidifier, to avoid drying out the respiratory mucosa, which can lead to infection(Aldridge and O'Dwyer, 2013). These methods are:
  • Nasal prongs — these are useful in the recumbent, lethargic animal. They can become dislodged if the patient is restless or ambulatory. In addition, the patient very easily removes them.
  • Nasal cannulae — these deliver oxygen directly into the respiratory tract using nasal catheters. These are less easy to dislodge than nasal prongs and can be unilateral (FiO2 up to 40%) or bilateral (FiO2 up to 60%) (Figure 3) (Box 4) (Aldridge and O'Dwyer, 2013).
  • Commercial oxygen kennel — useful in cases where the patient needs some time to settle (Figure 4). These can adequately deliver a FiO2 of up to 80%, but can take some time to reach this level. This can also be a useful tool in providing oxygen therapy in the short term.
  • Mechanical ventilation — in severe cases of aspiration pneumonia, mechanical ventilation may be warranted. This process can deliver an FiO2 of up to 100%. This is a specialist process offered by specialist referral centres, which requires intensive 24 hour nursing (Figure 5) (Box 5) (Haskey, 2013).
  • Positioning — it is important to prevent further episodes of aspiration. If possible, the patient should be in sternal recumbency, to prevent atelectasis due to inadequate lung expansion when in lateral recumbency.
  • Respiratory physiotherapy — nebulisation can loosen the respiratory secretions, there are no studies to support the use of coupage.
  • Exercise — stable patients can be exercised to help mobilise respiratory secretions.
  • Intravenous fluid therapy — care should be taken with intravenous fluid therapy: over hydration can increase pulmonary hydrostatic pressure, which worsens fluid extravasation into the pulmonary parenchyma thus further compromising respiratory function (Sherman et al, 2017).
  • Gastrointestinal management — due to the risks associated with further vomiting/regurgitation, gastro-protectants (e.g. omeprazole), gastrointestinal prokinetics (e.g. metoclopramide) and anti-emetics (e.g. maropitant) can be administered.
  • Figure 2. Patient receiving flow by oxygen therapy.
    Figure 3. Patient receiving oxygen supplementation via bilateral nasal cannulae.
    Figure 4. Patient receiving oygen supplementation in a commercial oxygen kennel.
    Figure 5. Patient on mechanical ventilation.

    How to place nasal oxygen cannulae (Aldridge, O'Dwyer, 2013)

    Equipment needed:

  • 0.5% Proxymetacaine
  • Skin suture
  • Silicon feeding tube
  • Sterile lubricating jelly
  • Adhesive tape
  • Method of placement:

  • Measure the feeding tube from the nostril to the medial canthus, and mark the tube.
  • 10 minutes prior to placement, insert a few drops of the 0.5% proxymetacaine down the desired nostril. This helps prevent the patient sneezing and struggling.
  • The patient's head is positioned dorsally, and the lubricated tube is placed into the ventral meatus, aiming for the base of the opposite ear.
  • The tube is advanced gently, until it is in situ.
  • Butterfly wings of tape are then attached to the tube near the nostril, where it is sutured in place.
  • The catheter should then be looped dorsally between the eyes and sutured in place.
  • Indications for mechanical ventilation

  • Severe hypoxaemia (PaO2 <60 mmHg at sea level) which is failing to respond to oxygen therapy, or the patient requires a high FiO2 (>0.6) to maintain the PaO2 within an acceptable range.
  • Severe hypoventilation (PaCO2 >60 mmHg).
  • Impending respiratory fatigue.
  • Conclusion

    Aspiration pneumonia is a serious complication of multiple disease processes, which can be difficult to diagnose. These patients can become critically ill and the nurse's role in identifying a progressive or rapid decline in respiratory function is essential. Supportive treatment is paramount and nurses are vital to patient comfort and survival.

    KEY POINTS

  • Aspiration Pneumonia is a common complication in canine veterinary patients.
  • Aspiration Pneumonia is a complication usually associated with various underlying diseases.
  • Veterinary nurses and the supportive care they provide can make a difference to the outcome of these cases.