Dyspnoea or respiratory distress is a common emergency problem characterized by an increased respiratory rate and effort. Animals are often uncomfortable and restless; they may extend their neck and have increased respiratory noise. The respiratory distress patient is one of the most challenging patients to manage as they often cannot tolerate diagnostic tests and can require treatment without knowledge of a definitive diagnosis.
Triage means 'to sort' and describes the process in which patients are prioritized in order of their disease severity so that the sickest animals are treated first. Any patient arriving at the veterinary hospital for an acute complaint should be immediately evaluated by the triage nurse. This evaluation is based on the 'ABCs' and includes assessment of the animals breathing rate and effort and the perfusion parameters (mucous membrane colour, capillary refill time, heart rate, pulse quality and extremity temperature). Patients with any abnormality of concern on this examination, active bleeding or seizures should be transported to the treatment area immediately for further assessment and treatment. The respiratory distress patient will be evident by increase respiratory rate, exaggerated respiratory effort and/or excessive respiratory noise. These patients should be transported to the treatment area immediately and oxygen therapy started.
2. Oxygen, Oxygen, Oxygen
There are few if any adverse affects associated with short term oxygen therapy and all respiratory distress patients should be given the benefit of supplemental oxygen until they are adequately stabilized. Initially a high fraction of inspired oxygen (FIO2) is given to maximise the benefit to the patient, this can be reduced once effective monitoring of an animal's ability to oxygenate is established. Oxygen therapy requires a source of oxygen, either a dedicated tank, an in wall system or via an anaesthetic machine.
The simplest way to administer oxygen is by directing oxygen gas flow towards the patient's mouth and nose (flow-by), either via a Bain's circuit or a face mask. A face mask may allow administration of higher FIO2 than simple flow-by but close fitting masks may prevent adequate loss of carbon dioxide (CO2) and heat. Flow-by oxygen requires flow rates of 100-200 ml/kg/min and may deliver anything from 30% to 60% FIO2.
An Elizabethan collar with an oxygen source taped inside and covered with plastic wrap (e.g., Glad wrap®) is a cheap, readily available method in which reasonably high levels of oxygen can be administered. It is important to make a window in the top of the plastic wrap to prevent accumulation of heat and CO2. It is difficult to control the FIO2 in this situation and some animals with respiratory distress will not tolerate the placement of the collar.
Nasal Oxygen Catheter
A nasal oxygen catheter is generally well accepted by most patients and will supply an FIO2 of ~ 40% with an oxygen flow rate of 100-200 ml/kg/min. It is advantageous in that patient assessment and management can be performed without interruption to the oxygen therapy. Disadvantages include nasal mucosal irritation and it is impossible to determine the actual FIO2 being given. In order to reduce nasal irritation the administered oxygen should first pass through a bubble humidifier and local anaesthetic should be administered as required.
An oxygen cage allows administration of a known FIO2 to patients in a low stress, non-invasive manner. It is an excellent way to provide oxygen therapy and is essential for many cats. It uses a lot of oxygen and the cages are expensive to purchase. Large dogs may quickly overheat in an oxygen cage and must be monitored closely. A temporary oxygen cage can be made by covering the front of a normal cage with plastic or placing an entire cat carrier inside a plastic bag. Accumulation of carbon dioxide and heat can easily occur in these situations so adequate ventilation and monitoring is essential. Second hand human neonatal humidicribs can often be purchased cheaply and can be excellent oxygen cages from cats and small dogs.
3. Patient Evaluation
Evaluation of the respiratory distress patient may be limited depending on the animal's tolerance to handling. A physical examination including auscultation of the chest is ideal when possible. Thoracic radiographs are often diagnostic in respiratory distress patients but frequently cannot be taken initially as holding a respiratory distress patient down for radiographs can have fatal consequences. Another diagnostic test considered in the emergency room is thoracocentesis--if fluid or air is aspirated from the pleural space it is diagnostic. The maximal volume of air or fluid should be removed from the pleural space in this situation making this both a diagnostic and therapeutic procedure. Often response to therapy is the only diagnostic tool available. Drugs such as diuretics for suspected congestive heart failure or bronchodilators for suspected asthma may be given and the patient's response is evaluated.
4. Possible Causes and 5. Specific Treatment
The causes of respiratory distress can be divided into eight broad categories. By evaluation of the history, clinical signs and limited diagnostic tests the most likely cause(s) of respiratory distress can be determined and the specific treatment can be provided.
Upper Airway Disease
Upper airway obstructions will cause increased respiratory noise and effort, usually associated with inspiration. Complete upper airway obstructions will be associated with an absence of respiratory noise and marked respiratory efforts which will quickly progress to respiratory arrest. Causes of obstruction include foreign bodies, neoplasia, laryngeal paralysis, laryngeal edema, inflammatory lesions, abscesses, tracheal collapse and brachycephalic syndrome. Diagnosis of an upper airway problem is based on the clinical signs and response to treatment.
Treatment is based on oxygen therapy and reducing the degree of respiratory effort. Patients with upper airway disease have fewer difficulties if they will breathe slow and shallow breaths. If the temperature is elevated the animal should be actively cooled with water and fans. Sedation with low doses of acepromazine and/or butorphanol is often beneficial. If the animal is in severe distress, cyanotic etc., rapid induction of anesthesia and securing the airway with orotracheal intubation is indicated. If intubation is unsuccessful an emergency tracheostomy will be required.
Lower Airway Disease
Lower airway disease causes wheezes and respiratory distress on exhalation. Lower airway disease is most commonly due to bronchoconstriction, often of an allergic nature such as feline asthma. The wheezing may be audible on initial evaluation or it may require auscultation. If the disease process is chronic there may be visible bronchial changes on radiographs but in acute disease radiographs may be normal. Treatment includes oxygen therapy and bronchodilators. If allergic disease is suspected corticosteroids are indicated.
Pulmonary Parenchymal Disease
Pulmonary parenchymal disease describes disease of the lung tissue itself and can be due to trauma (pulmonary contusions), hemorrhage, infection, oedema, neoplasia or inflammatory disease. All these diseases result in variable degrees of alveolar fluid accumulation and alveolar collapse. Clinically patients will have respiratory distress; auscultation may reveal increased breath sounds and moist crackles or may be normal. Diagnosis is confirmed with thoracic radiographs where pulmonary infiltrates will be present. Treatment is always oxygen therapy and specific therapy for the primary disease if there is any.
Pleural Space Disease
Accumulation of air, fluid or soft tissue in the pleural space prevents lung expansion, this reduces tidal volume and predisposes to atelectasis. Animals with pleural space disease may present with acute respiratory signs or they may have a history of chronic progressive respiratory disease. Auscultation may be abnormal, fluid and soft tissue accumulations will dampen lung sounds making them difficult to hear. When there is fluid accumulation the loss of lung sounds is most distinct ventrally. Thoracic radiographs are diagnostic but thoracocentesis can be both therapeutic and diagnostic and should be performed immediately in any patient with severe respiratory distress suspected of having pleural space disease. If thoracocentesis cannot fully empty the pleural space or repeated thoracocentesis is required, chest drains may need to be placed.
Chest Wall Disease
Chest wall defects are primarily the result of trauma and are clearly evident at the time of physical examination. These include open chest wounds, rib fractures and open chest wounds. Emergency therapy for these problems includes oxygen therapy, thoracocentesis to ensure the pleural space is empty, analgesia and in some cases surgical intervention.
Blood clots can lodge in the pulmonary blood vessels and cause acute respiratory distress. This is called pulmonary thromboembolism (PTE). Dyspnoea and hypoxemia in a patient with normal thoracic radiographs is suggestive of PTE. Definitive diagnosis is extremely challenging and it is commonly assumed but not proven. Diagnosis of PTE is only likely in patients which have an underlying disease that may make them prone to forming abnormal blood clots. Such diseases include immune mediated haemolytic anemia, heart disease, neoplasia and protein losing kidney disease. In mild to moderate cases oxygen therapy and anticoagulant treatment to prevent further blood clot formation is recommended. In cases of severe respiratory distress and/or cardiovascular compromise blood clot lysis with tissue plasminogen activator or streptokinase is indicated. This therapy is associated with a significant risk of hemorrhage.
Abdominal distension causes anterior displacement of the diaphragm leading to respiratory compromise. Common causes of severe abdominal distension include gastric dilation volvulus, heavy pregnancy, ascites and intra-abdominal masses. Significant abdominal distension in a patient with respiratory distress should be decompressed as far as possible. In cases of severe abdominal distension pulmonary atelectasis can occur.
There are several causes of increased respiratory rate and/or effort that are due to stimulation of the central respiratory center in animals with no primary respiratory tract disease. These patients will have normal oxygenation and no abnormalities on auscultation or thoracic radiographs. They require no treatment of their respiratory signs but may benefit from treatment of their primary disease process.
Many brain diseases can cause stimulation of the medullary respiratory center. Diseases such as neoplasia, inflammatory brain disease and trauma can all lead to respiratory changes. These patients usually have other signs of brain disease such as obtundation, cranial nerve defects and behavioral changes. They may also have abnormal respiratory patterns such as apneustic breathing and Cheyne Stokes breathing.
Hyperthermia is also a potent stimulus of respiratory rate and effort, especially in dogs. Hyperthermia is the consequence of high ambient temperatures and/or exertion and should be differentiated from fever. Fever describes an elevation in body temperature due to endogenous pyrogens and will not trigger increases in respiratory rate and effort. Measurement of body temperature in animals with respiratory distress is very important. Hyperthermia may be the primary cause or a contributor to increased respiratory rate and effort and cooling will tend to improve these clinical signs.
Drugs such as opioids will directly stimulate the central respiratory centre producing rapid panting. On examination these animals will have a normal or lower than normal body temperature and a normal or higher than normal PCO2.
Metabolic acidosis will also stimulate increases in respiratory rate and depth of breathing in an effort to lower PCO2 and return pH towards normal.
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