Proceeding of the SEVC Southern European Veterinary Conference

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1 Close this window to return to IVIS Proceeding of the SEVC Southern European Veterinary Conference Oct. 2-4, 2009, Barcelona, Spain Next conference : October 1-3, Barcelona, Spain Reprinted in the IVIS website with the permission of the SEVC

2 Management of Upper Airway Obstruction: Why We Do What We Do Manuel Boller Dr. med. vet., DACVECC Introduction Upper airway obstruction (UAO), with varying degrees of severity, is often seen in veterinary practice. If it occurs chronically, as is classically the case in dogs with brachycephalic syndrome, the animals (as well as the owners) are well adapted to the disease and affected animals may not present until an acute worsening occurs. In cases in which the airway obstruction occurs suddenly however, its features are dramatic, the degree of respiratory distress considerable and the anxiety level of both the pet and owner may be very high. Etiologies, general clinical appearance and evaluation Basically any anatomic location that is part of the upper airways can be the origin of increased airway resistance, and thus create clinical signs (Table 1). However, if the lesion is within the nasal cavity, the choanes or the nasopharynx, the animal might be able to breath through the mouth and thus prevent occurrence of dyspnea. Cats, in contrast to dogs, often refuse to mouth breathe, even with severe respiratory distress. An obstruction of the nasal cavity always has to be considered in feline patients. If the clinician gently encourages the cat to breath through the oral cavity by opening its mouth and the respiratory obstruction improves or resolves the lesion likely is in the nasal cavity, choanes or nasopharynx. In other situations, history, signalment and clinical presentation can favor one differential diagnosis over another, for example: an older Golden Retriever with a history of voice change that went for a walk in hot-humid summer weather during which he began breathing very noisily is all suggestive of laryngeal paralysis.1 Nevertheless, there is a very limited spectrum of clinical signs associated with UAO. Thus while one can generally make a diagnosis of UAO based on physical exam, making a diagnostic conclusion as to what the underlying etiology is based on the clinical appearance alone should generally be avoided. Respiratory effort, especially during the inspiratory phase, is greatly increased while respiratory rate can be variable. This is partially due to a significant prolongation of the inspiratory phase of each breath. Abnormal respiratory noises are also typical for UAO, namely stertor and/or stridor. Stertor describes a more snoring, coarse noise and points towards a partial obstruction of the nasal passages, choanes or nasopharynx. Stridor is a rather high-pitched inspiratory sound suggesting partial obstruction of larynx or trachea. Since the negative airway pressure during inspiration can worsen the obstruction, noises typically dominate during inspiration. However, if the obstruction does not change size over the respiratory cycle, e.g. with laryngeal paralysis, inspiratory and expiratory, or biphasic, noises may be heard. Likewise, dominance of an expiratory stridor suggests partial obstruction of the intrathoracic trachea. Sudden disappearance of these noises can be indicative of complete airway obstruction, since a no-flow condition will seize air turbulence formation and thus noise creation. The breathing pattern associated with UAO is typically paradoxical, in that the slight abdominal extension normally paralleling inspiration is not seen, but rather the contrary can be observed: the abdominal wall moves in, while the chest wall widens. Severely affected dogs may be standing, abducting their elbows and extending their neck, while cats are sitting and extending their neck. Animals with severe UAO experience high levels of anxiety and may be very protective of their upper airways rendering visual inspection of the animal s oropharyngeal area dangerous for the patient and technically difficult for the examiner without sedation. Cyanosis can be present with severe hypoxemia. Inspection and palpation of the head and neck area may provide the clinician with further clues about the etiology of the UAO. Examples are nasal discharge, asymmetries of the nasal roof, diffuse edema of the entire head/neck region with cranial vena cava syndrome, soft trachea with tracheal collapse and more. Hyperthermia, not infrequently more than 105F, can occur as a consequence of the increased work of breathing, the inability to dissipate heat over the airways and for environmental reasons.2 Besides collection of a medical minimal data base, the diagnostic work up of an upper airway obstruction is a combination of the following: ventrodorsal and lateral radiographs of neck and chest; skull films under general anesthesia; laryngoscopy; inspection of the nasopharynx with a dental mirror; endoscopic evaluation of the nasal nasopharynx, choanes, nasal cavity trachea and bronchi; computer tomography for evaluation of masses; fluoroscopy for dynamic evaluation of tracheal collapse; cytology and/or histopathology of abnormal tissues; microbiological diagnostics. Increased upper airway resistance and its consequences Physical aspects: With narrowing of the air passages the resistance to airflow increases in an exponential fashion. In order to maintain tidal volume, much more respiratory work is necessary. This not only raises whole body oxygen consumption but also enhances heat production thus contributing to hyperthermia. The heightened inspiratory effort against a high upper airway resistance creates more negative airway and intrapleural pressures leading to (1) exacerbation of partial airway obstruction downstream to the original UAO (e.g. worsening of laryngeal collapse in dogs with stenotic nares and overlong soft palate), (2) the complication of negative-pressure pulmonary edema in acute cases of UAO like laryngeal paralysis or strangulation with leash and (3) increased incidence of regurgitation due to a combination of aerophagia, air-filled esophagus and stomach, hiatal hernia and gastroesophageal reflux altogether rising the risk of aspiration.

3 Blood gas and acid-base abnormalities: Increased resistance to breathing does not, in the vast majority of the cases, create any abnormalities in blood gases until it is severe or associated with other abnormalities. This is because the ability to increase the inspiratory muscle effort is very powerful and allows the patient to maintain alveolar ventilation within the normal range. Ventilatory failure, defined as a decrease in alveolar ventilation, is indicated by an increase in arterial partial pressure of carbon dioxide (PaCO2) and is proof of severe increases in airway resistance. If PaCO2 is rising acutely, impending respiratory arrest has to be feared and appropriate measures have to be taken (see below). Some animals with chronic upper airway obstruction allow their PaCO2 to increase to quiet remarkable levels, e.g. above PaCO2 > 60 mm Hg (reference values Table 2). The resulting respiratory acidosis in these chronic cases is metabolically compensated to the degree that the ph rarely drops below 7.3, unless the hypercapnia is very severe (e.g. PaCO2 > 70 mm Hg) or a mixed acid-base disorder (e.g. additional metabolic acidosis) is present. In contrast, acute hypercapnia (< 24 h) is much less compensated and can cause severe acidemia. The increased alveolar concentration of carbon dioxide that occurs with hypercapnia replaces alveolar oxygen and thus the arterial partial pressure of oxygen (PaO2) drops as PaCO2 increases. This relationship between PaO2 and PaCO2 is reflected in the alveolar gas equation: PAO2 = FiO2 x (PB PH2O) 1.2 x PaCO2, where PAO2 is the alveolar partial pressure of oxygen; FiO2 the inspiratory oxygen fraction (e.g for air); PB the barometric pressure; PH2O the water vapor pressure in the alveoli (47 mm Hg). For example, if the animal has a PaCO2 of 60 mm Hg and is breathing air on sea level, the predicted PAO2 will be 78 mm Hg. Since the difference between alveolar and arterial PO2 is less than 10 mm Hg in normal lungs, the PaO2 will be around 70 mm Hg. If it is measured to be significantly lower, a pathologic process that compromises gas exchange, in addition to pure hypercapnia, must be considered (e.g. pulmonary parenchymal disease, as in pneumonia). Post-obstructive pulmonary edema, which is a type of non-cardiogenic pulmonary edema, can also occur in animals with acute UAO and has to be considered as possible differential diagnosis.3 If the animal remains calm and quiet, severe partial airway obstruction can be tolerated. However, anxiety and struggling may precipitate occurrence of a vicious cycle: (1) raised oxygen consumption; (2) increased ventilatory demand; (3) increased work of breathing; (4) further increase in oxygen consumption that can not be met. Hyperthermia: The inability to dissipate heat over the airways, along with anxiety and increased work load of the respiratory muscles, almost always goes along with an increased body temperature in more severely affected animals. This is especially true in dogs and makes them exquisitely sensitive to high environmental temperatures. In selected cases, e.g. retriever with laryngeal paralysis, the hyperthermia and associated heat stroke become the dominant cause for morbidity (seizures and cerebral edema, shock, diarrhea/hematochezia, SIRS, hepatic injury, pancreatitis, renal failure, DIC) requiring considerable medical attention.2 Even when not severe enough to cause heatstroke, hyperthermia increases oxygen consumption and carbon dioxide production with the danger for the animal to enter the above described vicious cycle. Management Clinical differentiation of UAO from other etiologies of respiratory distress is critical in order to institute appropriate emergency treatment.4 Any stressful interventions, like neck radiographs, should be avoided until considered safe for the patient. Initial treatment in the animal with severe acute UAO or acute deterioration of chronic UAO is very uniform and in its basic pattern not dependent on the underlying disease process.5 Emergency treatment is aimed at resolving the dyspnea by: reducing the degree of airway resistance; administering oxygen; correcting the hyperthermia; providing sedation; and, in selected cases, administering medications such as glucocorticoids. Oxygen should be administered to all animals with UAO immediately. Flow by oxygen is acceptable while the patient is initially examined and while an intravenous catheter is placed. Placing the animal in an oxygen cage is the least stressful way to supplemental oxygen, while other methods (like oxygen tents or masks) may increase anxiety and thus worsen the UAO. In absence of additional lung disease, hypoxemia associated with UAO is extremely oxygen responsive as apparent when reconsidering the alveolar gas equation. An inspiratory oxygen concentration of 30% (FiO2 = 0.3) will maintain PaO2 above 80 mm Hg, even in the presence of a PaCO2 of 100 mm Hg, indicating very severe hypoventilation. However, since additional pulmonary pathology, e.g. negative pressure pulmonary edema, can not be excluded initially, higher oxygen concentrations should be chosen until more patient data is available. Sedation is an important supportive measure and can be highly effective in lessening the degree of respiratory distress. Acepromazine administered at low doses (IM 0.02 mg/kg; IV in mg/kg increments) reliably decreases anxiety and is the drug of choice for that purpose in a hemodynamically stable animal. Butorphanol (0.1 to 0.2 mg/kg IM or IV) is preferred in hypotensive animals, and generally creates reliable sedation in older animals. Due to its potent antitussive effects, it might also be helpful in cases where coughing is part of the pathogenesis, as it is the case in animals with tracheal collapse. High doses of sedatives causing marked sedation should be avoided to limit respiratory depression and excessive relaxation of the upper airway muscles (e.g. sternohyoid, geniohyoid,..), the latter potentially worsening the UAO especially in brachycephalic dogs. Sedation will also help with correction of the hyperthermia in addition to various cooling methods, like a fan pointed directly into the patient s mouth since ventilation is the primary means of liberating heat in the dogs. Other methods that are aimed at promoting evaporative and conductive cooling include surface wetting and intravenous fluid administration. Those are employed according to the degree of hyperthermia present and are discontinued early enough to prevent hypothermia and shivering, which could be harmful in that it increases tissue oxygen consumption and carbon dioxide production putting more strain on ventilation. If

4 edema or swelling of the upper airways, especially the larynx, is suspected, for example after extubation or with hypersensitivity reactions, steroid administration is indicated (e.g. dexamethasone 0.2 mg/kg IV). Endotracheal intubation or temporary tracheostomy as mean of establishing a patent airway is indicated if the animals presenting with severe and imminently life-threatening UAO or if the above listed medical measures are not successful in relieving the dyspnea within 15 to 30 minutes. Also in an animal with acute UAO and venous or arterial PCO2 in the range of mm Hg, impending respiratory arrest has to be feared and the animal s airway has to be secured. In animals with chronic UAO, the baseline PaCO2 levels will be increased thus the above values do not apply; however a worsening acidemia may be indicative of deterioration of the patient. No matter what the blood gas results are or how chronic the problem is, severe respiratory distress alone justifies steps to secure the patient s airway. Prior to intubation, an intravenous catheter has to be placed. Flow by oxygen should be administered and the animal should be handled with minimal restraint. Endotracheal tubes of various sizes with guide wires and a laryngoscope with a sufficiently long blade should be prepared and a dedicated surgeon and a tracheotomy kit should be close by in case oral intubation is not possible. If the situation allows, the ventral neck of the animal should be clipped prior to induction of anesthesia. The author favors administration of intravenous midazolam (0.2 mg/kg) and butorphanol (0.2 mg/kg) rapidly followed by propofol (1-4 mg/kg to effect) allowing fast intubation. Endotracheal intubation is possible in the majority of the cases with adjusting the size of the tube appropriately. At the very least, passage of a red rubber tube should be attempted, as oxygen can be provided through this tube until a tracheotomy is performed. Once intubated, diagnostic steps should be taken as listed above to investigate and remove the cause of the UAO. If immediate removal of the obstructive process is not possible, e.g. laryngeal mass, and the obstruction is located proximal to the glottis, temporary tracheotomy should be performed. For a temporary tracheostomy, the animal is placed in dorsal recumbency with a cushion under the neck to elevate the trachea. The surgical site is aseptically prepared and a cervical ventral midline incision is made from the cricoid cartilage caudally for 2 to 10 cm, depending on the size of the animal. The sternohyoid muscles are separated along their midline and retracted laterally. The peritracheal connective tissue is dissected while care is taken not to injure the recurrent laryngeal nerves, carotid arteries, jugular veins, thyroid vessels and the esophagus. A long monofilament stay suture is placed around a tracheal ring immediately rostral and caudal to the planned tracheal incision, avoiding including the endotracheal cuff. A horizontal incision through the annular ligament is made between the 3rd to 5th tracheal rings. The incision should not span more than 50% of the circumference of the trachea to avoid tracheal avulsion. Pulling on the stay sutures will elevate the trachea and allow for introduction of a suitable tracheostomy tube. Prior to this, the trachea should be suctioned and cleared of blood and secretions. A cuffed sterile tracheostomy or endotracheal tube is preferred to facilitate administration of inhalational anesthesia and mechanical ventilation. The sternohyoid muscles, the subcutaneous tissue and skin are adapted on both sides of the tracheotomy site, while allowing enough opening for drainage. The tube is then secured with umbilical tape around the neck. The stay sutures are marked (e.g. cranial and caudal) and left in place to facilitate future change of the tube. Adequate care of the patient with a tracheostomy tube in place is critical and requires close 24 hour surveillance. The major cause for fatality is sudden, complete obstruction of the tube that failed to be noticed by medical personnel. Cardiopulmonary arrest occurs within minutes. This complication is especially of concern in small animals, especially cats since they produce copious amounts of thick bronchial secretions and can only accommodate tracheostomy tubes with a narrow diameter. The owners have to be made aware of the possibility of such an event occurring. The ideal tube thus is equipped with an inner cannula that can be removed and cleaned every 2 to 6 hours, or in an emergency situation. Suctioning through the tracheostomy tube should be minimized since it further damages the trachea, stimulates airway secretions and may cause clinically significant hypoxemia. The air that the animal breathes through a tracheostomy tube is not moisturized and warmed by passage through the upper airways. This leads to impaired mucociliary clearance due to direct damage of the ciliary apparatus of the airway epithelium and due to thickening of airway secretions. Nebulization with humidified air every 4 hours for 30 minutes should therefore be instituted. Antitussive medications should be avoided. Analgesia, e.g. buprenorphine 10 mcg/kg IV q6, is important. Once upper airway patency is re-established the tube can be removed and the surgery site is allowed to heal as an open wound. References 1. Holt DE, Brockman D. Laryngeal Paralysis. In: King LG (ed) Textbook of Respiratory disease in dogs and cats. St. Louis, Saunders, 2004: Drobatz KJ. Heat stroke. In: Silverstein DC, Hopper K (eds) Small animal critical care medicine. St. Louis, Saunders, 2009: Drobatz KJ, Saunders M, Pugh CR, Hendricks JC. Noncardiogenic pulmonary edema in dogs and cats: 26 cases ( ). J Am Vet Med Assoc. 1995; 206: Rozanski E, Chan DL. Approach to the patient with respiratory distress. Veterinary Clinics of North America - Small Animal Practice. 2005; 35: Holt DE. Upper Airway Obstruction, Stertor, and Stridor. In: King LG (ed) Textbook of Respiratory disease in dogs and cats. St. Louis, Saunders, 2004: Tabla 1: Enfermedades descritas como causantes de signos de obstrucción de vías respiratorias altas

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