Название | Small Animal Surgical Emergencies |
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Автор произведения | Группа авторов |
Жанр | Биология |
Серия | |
Издательство | Биология |
Год выпуска | 0 |
isbn | 9781119658627 |
Irrespective of the need for a formal veterinary triage system, a brief, but thorough physical exam remains the gold standard for recognizing critical patient status. The initial triage assessment includes visual examination and assessment of four key body systems: cardiovascular, respiratory, neurologic, and urinary [6, 7]. Information regarding the patient's mentation and responsiveness, as well as respiratory rate and effort, are obtained quickly on brief visual exam, often before performing any parts of a physical examination. Thoracic and cardiac auscultation with concurrent pulse palpation and a more thorough assessment of neurologic status, if indicated, follows visual examination. After cardiovascular, respiratory, and neurologic status is determined, if the patient is stable enough for further evaluation, urinary triage can be performed. Any significant pain must be addressed urgently to improve patient comfort and so that the effects of pain do not alter interpretation of cardiovascular and respiratory findings. Additionally, aggression should not be considered a sign of patient stability, as many scared and stressed patients will be aggressive in the face of severe shock.
Respiratory Assessment
Before any physical examination, all patients should have their respiratory rate, effort, noise, and pattern observed from afar. If a patient is showing any changes in respiratory pattern or effort, oxygen supplementation should be provided immediately. If there is any respiratory compromise, the patient should be presumed to be in hypoxemic shock until proven otherwise and oxygen supplementation should be provided. Further respiratory triage involves auscultation of the upper airway, trachea, and thorax. During abbreviated thoracic auscultation, emphasis should be placed on determining heart rate, rhythm, the presence of murmur(s) or arrhythmia(s), and lung sounds in all lung fields. Visual and auditory assessment of respiratory pattern and noise combined with thoracic auscultation should help localize the anatomic origin of the respiratory distress. The impact of pain, stress, and anxiety on respiratory rate and effort should not be underestimated (Figure 1.1).
If respiratory noise is localized to the upper airway, diseases associated with an upper airway obstruction, including laryngeal paralysis, laryngeal collapse, brachycephalic airway disease, tracheal collapse, the presence of a tracheal, laryngeal, or pharyngeal mass, and the presence of a foreign body should be ruled out. See Chapter 28 for stabilization of the patient with upper airway obstruction.
Figure 1.1 Cat with open mouth breathing secondary to the pain associated with an aortic thromboembolism.
If decreased lung sounds relative to respiratory effort are heard dorsally, pneumothorax should be suspected. However, if decreased lung sounds are heard ventrally, pleural effusion should be considered. Lung sounds may not be completely absent in the presence of pleural effusion or pneumothorax, they may be reduced relative to the other lung fields but still present. See Chapter 34 for stabilization of the patient with pleural space disease. Diseases of the chest wall such as masses, rib fractures, and flail segments may also result in abnormal auscultation of the pulmonary parenchyma. For more information on chest wall disease, see Chapter 41.
For patients in respiratory distress with a heart murmur, arrhythmia, pleural effusion, or pulmonary crackles present on auscultation, cardiogenic and hypoxemic shock should be considered as possible differentials. This is particularly important since fluid therapy is often contraindicated in most patients with cardiac dysfunction or failure and must be ruled out, to the best of the clinician's ability on triage, prior to administering intravenous (IV) fluid therapy.
Hypoxemic Shock
Hypoxemic shock occurs secondary to decreased arterial blood oxygen content. Common causes of hypoxemic shock include pulmonary parenchymal disease, such as pneumonia, severe anemia, and hypoventilation (Figure 1.2). Many veterinary patients in hypoxemic shock are at the limits of their physiologic reserves, and are intolerant of excessive handling, restraint, and manipulation; they should be handled carefully. Clinical signs include weakness, mental depression, pale mucous membranes, dyspnea, crackles or increased bronchovesicular lung sounds, or decreased lung sounds ventrally (pleural effusion) or dorsally (pneumothorax), and cyanosis. Patients with diaphragmatic hernia may have decreased lung sounds dorsally or ventrally. Cyanosis is only seen with severe hypoxemia (at least 5 g/dl of deoxygenated hemoglobin), and thus the absence of cyanosis absolutely does not rule out hypoxemia. In anemic animals, cyanosis is unlikely to be detected due to decreased hemoglobin concentration, and therefore should not be relied upon to diagnose hypoxemia [8].
Figure 1.2 Lateral thoracic radiograph showing cranioventral pulmonary infiltrates creating an alveolar pattern consistent with aspiration pneumonia.
In any patient with suspected hypoxemic shock, supplemental oxygen should be provided until the ability to adequately oxygenate is confirmed. Diagnostics that can be helpful for the patient in hypoxemic shock include pulse oximetry (peripheral capillary oxygen saturation, SpO2), arterial blood gas analysis, thoracic radiographs, thoracic/trauma computed tomography (CT), and thoracic ultrasound. SpO2 may be less effective with bright lighting, poor perfusion, high motion, and pigmentation