All about lower airway disease
Lower airway disease patients are some of my favourites to care for. We get to flex our ECC muscles and perform fun diagnostics, as well as promote patient-friendly, stress-free techniques. There are a lot of practical skills we can perform in these patients too, from diagnostic imaging and bronchoscopy to nasal oxygen cannula placement and arterial blood gas sampling.
In order to plan effective nursing care for the lower airway patient, we need to understand the type of lower airway disease present, and how each is treated and diagnosed. Today we’re talking all about the most common lower airway diseases we see in practice, and how to nurse these patients.
Let’s recap...
The lower airway includes the trachea, bronchi, bronchioles and alveoli. The trachea bifurcates at the carina into the left and right principal bronchi; these principal bronchi divide into lobar bronchi, which each supply a lung lobe.
Lobar bronchi branch into smaller and smaller segmental and subsegmental bronchi, before ending in a terminal bronchus which has an attached alveolar sac.
At each alveolar sac, gaseous exchange (the uptake of oxygen and inhalant anaesthesia, and release of carbon dioxide and other waste gases) occurs.
The trachea and bronchial structure (rings of cartilage and smooth muscle) serve to keep the structures open, allowing the passage of air through them; goblet cells produce mucous to moisten inhaled air and trap inhaled particles, and ciliated epithelial cells move the mucous layer towards the pharynx where it is coughed out or swallowed.
A number of lower airway diseases are commonly seen in practice, including tracheal collapse, canine chronic and infectious tracheobronchitis, feline “asthma”, pulmonary parenchymal diseases such as pneumonia or pulmonary oedema.
Tracheal Collapse
Pathophysiology
Tracheal collapse is a syndrome characterised by a flattening of the tracheal rings, and laxity of the dorsal tracheal membrane. Progressive degeneration of the tracheal rings and softening of the cartilage is seen, resulting in airway collapse during respiration. This collapse can occur at the level of the cervical trachea, intrathoracic trachea, mainstem bronchi or bronchioles, and can affect multiple areas.
Risk Factors and Clinical Signs
Genetics are thought to play a role in this condition, with toy and small breeds predisposed.
Dogs typically present with a history of chronic, loud coughing with a unique ‘goose honking’ sound. This cough is triggered by the mechanical collapse of the trachea, or by chemical stimulation.
Diagnostics
The condition is diagnosed by a combination of clinical history, physical examination and imaging such as radiography, fluoroscopy and endoscopy. Endoscopy allows direct visualisation of the collapsed area and grading of the collapse. A bronchoalveolar lavage should also be performed at the time of endoscopy and sent for culture, to determine the presence of secondary bacterial infection.
Treatment and Nursing Care
Management includes treatment with antitussives to control the signs and interrupt the self-perpetuating cough cycle. Bronchodilators are sometimes used but their use in tracheal collapse cases is controversial. Secondary airway inflammation may be treated with short courses of steroids (inhaled or oral), and concurrent bacterial infections should be treated with appropriate antibiotics.
Weight management in overweight patients is also recommended; weight control and inhaler training for inhaled medications are key areas for nurse involvement and owner education.
For patients not improving on medical management, correction with tracheal stent placement is indicated. This is placed under endoscopic or fluoroscopic guidance.
Canine Infectious Tracheobronchitis
Pathophysiology
Infectious tracheobronchitis, or Kennel Cough, is a severely contagious infectious disease with several infectious agents identified as causative agents, including canine adenovirus 2, parainfluenza virus, and Bordetella bronchiseptica. Concurrent infection with multiple agents is common in this condition. These patients often have a history of exposure to other dogs, e.g. after a period in boarding kennels, or a rescue centre.
Clinical Signs
Clinical signs include acute onset, severe cough which is persistent and exacerbated by exercise or excitement and can be elicited by putting pressure on the cervical trachea (‘tracheal pinch’). The cough may be productive or non-productive and may end in a terminal retch.
Diagnostics and Treatment
The condition is normally diagnosed presumptively, based on clinical history and examination. Often bloodwork and thoracic radiographs are unremarkable. It is usually a self-limiting condition treated with supportive care and symptomatic treatment. Antitussives may be used to control coughing (provided secondary pneumonia is not present), and the patient should be rested for approximately 7 days. If secondary bacterial infection is suspected or pneumonia is present, antibiotics are indicated; otherwise, routine administration of antibiotics is not recommended. Steroids should be avoided in these patients due to the infectious nature of the disease.
Chronic Bronchitis
Canine chronic bronchitis is a non-infectious disease defined by the presence of a daily cough for at least 2 months, lacking an identifiable specific cause. It is diagnosed by exclusion, following imaging to rule out other causes of cough (e.g. radiography/CT, bronchoscopy and BAL). Bronchial inflammation is confirmed on cytology (e.g. on BAL and bronchoscopy) to diagnose the condition.
In this condition, chronic inflammation of the airways results in a cycle of injury and repair, which repeats. Often, secondary airway collapse is seen.
The condition is treated with anti-inflammatory agents (typically steroids). These may be administered systemically, or locally by use of a metered-dose inhaler and AeroDawg chamber device. Inhalers should be introduced gradually, over a period of time, with reward-based training, to ensure patient compliance and wellbeing during therapy.
Bronchodilators may be indicated, but their use in this condition is controversial. Antitussive agents may also be used if the cough is non-productive and persists despite treatment of airway inflammation.
Environmental/other considerations include weight management and minimising exposure to airway irritants such as smoke, dust and aerosol sprays. These patients are at risk of respiratory distress, and so care should also be taken during hot or humid conditions, or with overexertion.
Feline “Asthma”
Pathophysiology & Clinical Signs
Feline bronchial disease (or feline lower airway disease, or feline “asthma”) is a syndrome of bronchoconstriction and airway inflammation. It is characterised by recurring episodes of wheezing, coughing and respiratory distress. Allergic and genetic predispositions to developing the condition are suspected. Cats usually present with respiratory distress, or due to coughing.
Diagnosis
Diagnosis is usually reached after finding evidence or airway injury and inflammation on radiographs/CT and bronchoscopy/BAL (on BAL cytology, (usually eosinophilic) inflammation is seen) and by excluding other causes of respiratory distress/cough (e.g. cardiac disease, upper airway disease, neoplasia or pneumonia). On radiographs, an interstitial or bronchial pattern may be seen. Bronchoscopy may show inflammation and narrowing of the airways, mucous plugs and areas of airway collapse.
Treatment & Nursing Care
Management of the respiratory distress patient involves minimising stress, providing oxygen therapy, and relieving any bronchoconstriction with bronchodilator agents. Sedative agents (e.g. butorphanol) may also help reduce stress and facilitate handling. Dyspnoeic cats particularly are on a knife-edge, balancing an increased oxygen demand due to stress with a reduced oxygen supply due to underlying disease. Minimal handling and supportive oxygen therapy in a quiet environment, to allow time for stabilisation, prior to other treatments or investigations is recommended.
Treatment of the condition involves administration of corticosteroids and bronchodilators; this is often achieved with inhalant therapy using an AeroKat chamber device and metered dose inhalers.
Pulmonary Parenchymal Diseases
Pathophysiology
Pulmonary diseases affect the alveolar-capillary membrane in the alveoli, compromising gaseous exchange. This can result in reduced O2 diffusion into the bloodstream and hypoxia and hypoxaemia can rapidly result. CO2 levels are often normal even in the case of hypoxaemia, because CO2 is able to diffuse more readily into the bloodstream than O2. If respiratory fatigue develops from long-term tachypnoea or dyspnoea, CO2 levels may increase; this can also be the case in patients with reduced respiratory drive (e.g. unconscious patients) or those with airway obstructions.
There are various types of pulmonary parenchymal disease including pneumonia (bacterial, viral, fungal or protozoal), pulmonary oedema, pulmonary contusions, pulmonary fibrosis, eosinophilic bronchopneumopathy, acute respiratory distress syndrome and pulmonary neoplasia.
Clinical Signs
Clinical signs of pulmonary disease include tachypnoea or dyspnoea +/- cyanotic mucous membranes; orthopnoea may also be present (with the head/neck extended and shoulders abducted to ease ventilation). Cough may be seen if the disease extends into the airways. Other signs are fairly non-specific and include lethargy, pyrexia, weight loss or anorexia, exercise intolerance, and generalised lymphadenopathy.
Cardiac arrhythmias may be noted secondary to hypoxia, and harsh crackles may be detected on lung auscultation. In areas of lung consolidation, dull or reduced heart and lung sounds may be heard.
Initial Stabilisation
Stabilisation with oxygen therapy and a ‘hands-off’ approach should be used in all respiratory patients, especially those with pulmonary disease or pleural space disease; diagnostic tests should be delayed until the patient’s condition has stabilised.
Diagnostics
Diagnostic tests performed in pulmonary diseases include thoracic radiographs or CT (interstitial or alveolar patterns are typically seen on radiographs) and bronchoscopy with bronchoalveolar lavage for cytology and bacterial/fungal culture.
Other (first-line) tests include pulse oximetry as a quick and simple method of evaluating oxygen saturation and determining hypoxaemia, and arterial blood gas analysis.
If available, arterial blood gases are the most accurate way of determining respiratory function, as they measure PO2, PCO2, sO2 and TCO2. A heparinised syringe must be used for sample collection and the dorsal pedal artery is typically used for sampling. When collecting the sample, it is important not to introduce any room air into the syringe, as this could affect results. The sample should be immediately processed using a point of care analyser. Normally, the PO2 should be >85-100mmHg whilst the patient is breathing room air (21% oxygen content); this is multiplied by 5 for a patient receiving 100% oxygen (e.g. via an ET tube), or by 3 for a patient receiving around 60% oxygen, etc. The chart below provides an overview of the inspired oxygen concentration achieved with each method of oxygen supplementation.
Treatment and Nursing Care
Supportive care of these patients typically involves oxygen administration, fluid therapy, sedation/anxiolysis to relieve stress which can exacerbate dyspnoea, nebulisation and respiratory physiotherapy. Care should be taken with coupage if performed; many ECC specialists are moving away from the use of coupage and replacing it with regular mobilisation (e.g. walking the patient if able to, immediately after nebulisation) to loosen airway secretions. The patient should be kept in a calm, dark, quiet area of the hospital but still in view of the nurse in the ward at all times. Oxygen supplementation should be provided by the most suitable method based on the individual patient – considering their tolerance levels (e.g. many do not tolerate nasal prongs), degree of hypoxaemia and disease process.
So that’s an overview of some of the most common airway diseases we see in practice. As you can see there is a lot of potential for us to do more with these patients, and we can make a huge difference just with oxygen, and a calm, hands-off environment! Want to know more about nursing the respiratory patient? Join me over on instagram for more respiratory nursing chatter!
References
Kirby, R. and Linklater, A. 2016. Monitoring and intervention for the critically ill small animal: the rule of 20. Wiley-Blackwell.
Merrill, L. 2012. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell.
