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Anesthesia Case of the Month History A 2.6-kg (5.72-lb) 10-year-old neutered male Yorkshire Terrier with a 6-month history of tracheal collapse was evaluated at the University of Florida Small Animal Hospital. The dog had been previously treated by the referring veterinarian with theophylline and butorphanol, but had recently been reevaluated because of increased coughing and signs of respiratory distress, for which it received additional treatment with dexamethasone sodium phosphate (0.23 mg/kg [0.104 mg/lb], IM), acepromazine (0.038 mg/kg [0.017 mg/lb], IM), and oxygen therapy via an oxygen cage. Despite additional treatment, there was no noticeable change in the patient’s condition. Initial physical examination on referral revealed a grade 2 of 6 left systolic heart murmur, coughing, dyspnea, cyanosis, and a palpably enlarged liver. Results of a CBC and serum biochemical analysis were within reference limits. Thoracic radiography revealed extra- and intrathoracic tracheal collapse with collapse of the principal bronchi, mild right-sided cardiomegaly, and generalized hepatomegaly (Figure 1). Fluoroscopic examination of the thorax revealed severe, dynamic extra- and intrathoracic tracheal, principal bronchial, and caudal lobar bronchial collapse. The patient was placed in an oxygen cage set to deliver 40% oxygen in the intensive care unit overnight and received acepromazine (0.02 mg/kg [0.009 mg/lb], IV) and butorphanol (0.2 mg/kg [0.09 mg/lb], IV) every 2 hours or as needed. Food was withheld overnight, and the following morning, the patient was anesthetized for tracheal stent placement. The dog was premedicated with butorphanol (0.19 mg/kg [0.086 mg/lb], IV), and induction of anesthesia with propofol (6 mg/kg [2.7 mg/lb], IV, to effect) immediately followed. The patient was orotracheally intubated with a 6.0-mm (internal diameter) sterile endotracheal tube. Anesthesia was maintained with isoflurane in oxygen (3 L/min) delivered via a Bain (nonrebreathing) system. Lactated Ringer’s solution was administered IV during anesthesia (7 mL/kg/h [3.2 mL/lb/h]). A multiparameter monitor,a including a lead II ECG for heart rate and rhythm, was used, and oxygen saturation as measured by pulse oximetry, end-tidal PCO2, respiratory rate, and blood pressure (noninvasive Doppler method) were recorded. The patient breathed spontaneously, and all monitored physiologic parameters were determined by the attending anesthesiologist to be within acceptable limits throughout induction and prior to stent deployment. The patient was transported under general anesthesia to the diagnostic imaging suite where, prior to This report was submitted by Tiffany D. Granone, DVM; from the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610. Address correspondence to Dr. Granone ([email protected]). JAVMA, Vol 246, No. 2, January 15, 2015
stent placement, preoperative thoracic radiographs were acquired and the patient end of the endotracheal tube was withdrawn such that the tip was repositioned just beyond the level of the larynx. Once radiographic measurements were completed and the appropriate stent size was determined, the administration of isoflurane was discontinued, and the patient was disconnected from the anesthetic breathing circuit. Flow-by oxygen (4 L/min) was provided by placing the breathing circuit in close proximity to the machine end of the patient’s endotracheal tube. An 8 X 72-mm intraluminal nitinol tracheal stentb was placed by inserting the self-expanding stent in the delivery system within the lumen of the endotracheal tube. The stent extended from the midcervical through the cranial thoracic trachea. The duration of fluoroscopic-guided stent placement was approximately 10 minutes, and no apparent complications were associated with stent deployment. During this time, the patient’s plane of anesthesia became light and the patient became tachypneic and was administered a bolus dose of propofol (0.77 mg/kg [0.35 mg/lb], IV) and lidocaine (0.77 mg/kg, IV). After deployment of the stent and removal of the delivery system, the patient was extubated and a right lateral thoracic radiograph was obtained to confirm correct stent placement. After extubation, oxygen was delivered at 4 L/min via a small animal facemask. The patient
Figure 1—Preoperative lateral radiograph of the thorax and cervical vertebrae of a 2.6-kg (5.72-lb) 10-year-old neutered male Yorkshire Terrier with a 6-month history of tracheal collapse. Fluoroscopy indicated severe, dynamic extra- and intrathoracic tracheal, principal bronchial, and caudal lobar bronchial collapse. Notice that cardiomegaly is also evident in this image. Vet Med Today: Anesthesia Case of the Month
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began to emerge from anesthesia and was observed to have signs of tachypnea and increased respiratory effort and noise. Following completion of postoperative radiography (Figures 2 and 3), the patient was positioned in sternal recumbency and administration of supplemental oxygen was continued. The patient was allowed to fully recover from anesthesia and continued to have signs of
tachypnea and increased respiratory effort and noise. In the immediate postoperative period, the dog received butorphanol (0.19 mg/kg, IV), acepromazine (0.02 mg/ kg, IV), lidocaine (0.77 mg/kg, IV), and supplemental oxygen via facemask. The patient was then admitted to the intensive care unit and was placed in an oxygen cage set to deliver 40% oxygen. Question On the basis of results of the postoperative radiographs, what is the most likely cause of this patient’s increased respiratory rate, effort, and noise immediately after tracheal stent placement? Answer
Figure 2—Lateral radiograph of the thorax and cervical vertebrae of the patient in Figure 1 obtained 5 minutes after endotracheal placement of an 8 X 72-mm intraluminal nitinol tracheal stent.b Notice the moderate right-sided pneumothorax and pneumomediastinum.
The most likely cause of the patient’s increased respiratory rate, effort, and noise was iatrogenic pneumothorax that we believe occurred during stent placement by inadvertent puncture of the airway (trachea) with the tip of the stent delivery system (introducer). Right lateral and ventrodorsal radiographs obtained to confirm stent placement revealed moderate right-sided pneumothorax, progressing to mild bilateral pneumothorax over 15 minutes, in addition to mild pneumomediastinum and pneumoretroperitoneum (Figures 2 and 3). As the patient began to emerge from anesthesia, respiratory rate, effort, and noise continued to increase, as the dog began to develop signs of distress. The patient was administered antitussives and sedatives, including butorphanol (0.19 mg/kg, IV, q 2 h), acepromazine (0.02 mg/kg, IV, q 2 h as needed), and hydrocodonehomatropine (0.22 mg/kg [0.1 mg/lb], PO, q 8 h). Thoracocentesis was performed, and 17 and 3 mL of air were removed from the right and left sides of the thorax, respectively. The patient received inhaled albuterol following thoracocentesis and was allowed to recover in the oxygen cage set to deliver 40% oxygen. All postprocedure treatments were performed approximately 30 minutes after stent placement and admission of the patient to the intensive care unit. Twenty-four hours after stent placement, followup thoracic radiographs were again obtained, which revealed resolution of the pneumothorax. The patient was discharged from the hospital 2 days after the initial surgery, with a follow-up visit recommend in 6 months. Discussion
Figure 3—Postoperative ventrodorsal radiograph of the thorax of the patient in Figure 1 obtained 15 minutes after endotracheal stent placement of an 8 X 72-mm intraluminal nitinol tracheal stent.b Notice the mild bilateral pneumothorax and pneumomediastinum. 190
Vet Med Today: Anesthesia Case of the Month
Tracheal collapse is a common problem in toy and small-breed dogs, with Pomeranians, Yorkshire Terriers, Miniature Poodles, and Pugs being commonly affected.1,2 The condition is a structural disease of the trachea, causing airway obstruction with a dynamic component that can affect the intra- and extrathoracic portions of the trachea and mainstem bronchi.3 Tracheal collapse results from cartilaginous degeneration of the C-shaped tracheal rings that maintain normal patency. In affected dogs, the tracheal cartilages have decreased glycosaminoglycan content, fewer chondrocytes, and decreased calcium concentrations, compared with those of clinically normal dogs.4 During respiration and the generation of normal airway pressures, the turgidity of the diseased trachea causes ventrodorsal collapse of the cartilage JAVMA, Vol 246, No. 2, January 15, 2015
rings and subsequent mechanical obstruction, which perpetuates signs of chronic airway inflammation.4 A diagnosis of tracheal collapse is commonly made with a combination of imaging techniques, including radiography, fluoroscopy, tracheoscopy, and occasionally ultrasonography.4 Collapse can affect the entire trachea and include the mainstem bronchi.2,4 Dogs often have signs of respiratory distress and commonly have an associated cough described as sounding like a goose honk. Surgical management of tracheal collapse is considered a salvage procedure because 65% to 78% of dogs are reported to respond to medical treatment.1,5 Surgical procedures described for the treatment of tracheal collapse include tracheal ring chondrotomy, plication of the dorsal tracheal membrane, prosthetic mesh reconstruction, and intra- and extraluminal prosthetic supports.1,6 All surgical procedures are aimed at restoring airway patency and reducing airway resistance. The use of prosthetic supports is among the most commonly used treatments for tracheal collapse. Extraluminal prosthetic supports have been associated with several complications, such as infection, disruption of the innervation or blood supply to the trachea causing laryngeal paralysis, necrosis of the trachea, and chronic coughing.7,8 A study by Becker et al4 found that 21% of dogs that had extraluminal tracheal prosthetics placed required a second surgery for treatment of unresolved respiratory distress attributable to postoperative laryngeal paralysis. In addition, use of extraluminal prostheses is limited to treatment of tracheal collapse confined to the cervical portion of the trachea and thoracic inlet.4,6 Because of this limitation and the associated complications, use of intraluminal prostheses has gained attention. Use of intraluminal stents has gained popularity in human medicine, where the prosthesis is placed in patients with obstructive tracheal disorders secondary to neoplasia.2,3,9 Use of intraluminal tracheal stenting originated from application of stents designed for use within the biliary, vascular, gastrointestinal, and respiratory systems in people.10,11 Initially, balloon-expanding stents were used; however, these stents had a tendency for acute recoil after the balloon was deflated, leading to stent migration and loss of luminal diameter.12 Since then, the advent and use of self-expanding stents made of various materials (ie, stainless steel and nickel-titanium alloys) has proven successful for palliative treatment of tracheal collapse in dogs.12 Of the self-expanding stents, the Palmaz-Shatz stent has been associated with a high rate of complications, including development of pneumothorax, infection, mucous plugs resulting in tracheal obstruction, stent migration, and compression of the upper stent ends.6,10 Rauber et al13 reported the occurrences of pneumothorax in 2 rabbits caused during the time of stent placement. Placement of intraluminal prostheses is often accompanied by the use of a rigid bronchoscope inserted into the trachea of an anesthetized patient. The stent delivery system is then inserted into the trachea adjacent to the bronchoscope until the tip of the introducer can be seen. The bronchoscope is then partially retracted to allow for deployment of the stent. Once the stent is fully deployed, the bronchoscope is then carefully retracted, making sure to not disrupt stent placeJAVMA, Vol 246, No. 2, January 15, 2015
ment.1 Following deployment, thoracic radiographs are taken to verify accurate placement. Of the stents in use today, those composed of shape memory alloys, such as nickel and titanium (nitinol), have been found to be advantageous owing to their ability to accommodate substantial strain before reaching irreversible deformation.1 A nitinol stentb designed specifically for use in dogs and cats is made of a woven nitinol material, classified as a reconstrainable, foreshortening stent. In a study by Durant et al1 examining the use of nitinol stentsb for treatment of end-stage tracheal collapse in dogs, complications noted were stent dislodgement with retraction of the bronchoscope during partial stent deployment and pneumonia. No other complications were noted in the immediate postoperative period. In a study by Sura and Krahwinkel,12 no complications were recorded during the anesthetic recovery period when endoscopy was used to obtain stent measurements or during the separate anesthetic episode for stent placement. Although the placement of an intraluminal tracheal stent is a minimally invasive procedure, anesthetic patient management presents a challenge owing to the difficulty of maintaining a patent airway throughout the procedure. A few anesthetic techniques address the approach to general anesthesia for the placement of tracheal stents, including SC administration of glycopyrrolate, followed by anesthetic induction with thiopental and maintenance of anesthesia with isoflurane in oxygen in an intubated patient.6 Others describe a total IV anesthetic method of administering propofol for both induction and maintenance of anesthesia.12 Weisse14 describes a method for anesthetizing patients that is almost identical to the method used in our patient. One method of stent placement is to perform the procedure in a patient that is not intubated. Via this method and the insertion of a bronchoscope, oxygenation of the patient may be compromised if the narrowed tracheal lumen becomes obstructed by the bronchoscope itself. In patients in which intraluminal tracheal stenting is performed when nonintubated, a means by which to provide supplemental oxygen is necessary. Oxygen supplementation may be provided by several techniques (flow-by, nasal oxygen via cannula, and oxygen insufflation via transtracheal catheterization), with flow-by administration being the simplest method of providing supplemental oxygenation to spontaneously breathing patients. In the patient described in the present report, the placement of the nitinol stent was under fluoroscopic guidance and the stent and introducer were placed through the lumen of the endotracheal tube. This was done to alleviate the need for extubation of the patient during the procedure and to facilitate the administration of inhalation anesthetic in oxygen. A potential disadvantage of stent placement in intubated patients is limited visibility of the surgical site with a smalldiameter endotracheal tube, and the inability to insert the bronchoscope through the lumen of a narrow endotracheal tube. At our institution, tracheal stenting is commonly performed in intubated patients with the use of fluoroscopy rather than bronchoscopy to mainVet Med Today: Anesthesia Case of the Month
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tain an airway and provide a means of ventilation for the patient if necessary. To our knowledge, there are no published reports of pneumothorax following the deployment of this type of stent. It is suspected that during placement and deployment of the stent, the tip of the stent delivery system punctured the trachea, causing the pneumomediastinum and subsequent pneumothorax and pneumoretroperitoneum. Pneumomediastinum is the presence of free gas within the mediastinal space and can be caused by penetrating neck wounds, esophageal or tracheal rupture or tear, or venipuncture or can be seen as a sequela of transtracheal wash.15 In dogs, the mediastinum is incomplete and is a potential space between the right and left pleural cavities.16 Several structures lie within the mediastinum, including the heart, trachea, esophagus, great vessels, lymphatics, vagus nerves, and thymus.16 The mediastinum communicates with the cervical facial planes through the thoracic inlet cranially and with the retroperitoneal space through the aortic hiatus caudally.16 Pneumomediastinum can lead to pneumoretroperitoneum via air dissecting caudally through the retroperitoneal space via the aortic hiatus through the diaphragm.17 Pneumomediastinum may lead to pneumothorax, but pneumomediastinum will not result from pneumothorax because the air collapses the mediastinal space between the 2 pleural reflections.17 At the time the patient described in this report began to develop clinical signs of increased respiratory effort, extubation had already taken place. Treatment with supplemental oxygen, antitussives, and sedatives was elected to maintain oxygenation, keep the patient calm, and reduce coughing, which may have led to dislodgment of the newly placed stent and collapse of the affected trachea beyond the stent (bronchial collapse). Once the pneumothorax was treated (via thoracocentesis), considerable improvement in the patient’s clinical signs was evident as well as improved tracheal air flow through the stent. Overall, the use of intraluminal nitinol tracheal stents, such as the one used in this case, has been associated with a fair to good outcome in those patients requiring tracheal stenting.1 Compared with other types of intraluminal stents and extraluminal prostheses, postoperative morbidity and mortality rates associated with complications of tracheal stenting are lower with intraluminal nitinol stents.1 Stent delivery system–induced pneumothorax should be considered in any patient with immediate postoperative stent complications.
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a. b.
IntelliVue MP50, Philips Healthcare, Andover, Mass. Vet Stent-Trachea, Infiniti Medical, Menlo Park, Calif.
References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.
Durant AM, Sura P, Rohrbach B, et al. Use of nitinol stents for end-stage tracheal collapse in dogs. Vet Surg 2012;41:807–817. Sun F, Uson J, Ezquerra J, et al. Endotracheal stenting therapy in dogs with tracheal collapse. Vet J 2008;175:186–193. Gellasch KL, Da Costa Gomez T, McAnulty JF, et al. Use of intraluminal nitinol stents in the treatment of tracheal collapse in a dog. J Am Vet Med Assoc 2002;221:1719–1723. Becker WM, Beal M, Stanley BJ, et al. Survival after surgery for tracheal collapse and the effect of intrathoracic collapse on survival. Vet Surg 2012;41:501–506. Mittleman E, Weisse C, Mehler SJ, et al. Fracture of endoluminal nitinol stent used in the treatment of tracheal collapse in a dog. J Am Vet Med Assoc 2004;225:1217–1221. Radlinsky MG, Fossum TW, Walker MA, et al. Evaluation of the Palmaz stent in the trachea and mainstem bronchi of normal dogs. Vet Surg 1997;26:99–107. Woo HM, Kim MJ, Lee SG, et al. Intraluminal tracheal stent fracture in a Yorkshire Terrier. Can Vet J 2007;48:1063–1066. Ouellet M, Dunn ME, Lussier B, et al. Noninvasive correction of a fractured endoluminal nitinol tracheal stent in a dog. J Am Anim Hosp Assoc 2006;42:467–471. Zakalunzy SA, Lane JD, Mair EA. Complications of tracheobronchial airway stents. Otolaryng Head Neck Surg 2003; 4:478–488. Moritz A, Schneider M, Bauer N. Management of advanced tracheal collapse in dogs using intraluminal self-expanding biliary wallstents. J Vet Intern Med 2004;18:31–42. Ruegemer JL, Perkins JA, Azarow KS, et al. Effect of the Palmaz balloon-expandable metallic stent in the trachea of pigs. Otolaryngol Head Neck Surg 1999;121:92–97. Sura PA, Krahwinkel DJ. Self-expanding nitinol stents for the treatment of tracheal collapse in dogs: 12 cases (2001–2004). J Am Vet Med Assoc 2008;232:228–236. Rauber K, Sawar SA, Hofmann M, et al. Endotracheal placement of balloon-expanded stents: an experimental study in rabbits. Radiology 1997;202:281–283. Weisse CWC. Intraluminal stenting for tracheal collapse. In: Bonagura JD, Twedt DC, eds. Kirk’s current veterinary therapy XIV. St Louis: Saunders Elsevier, 2009;635–642 Tufts University OpenCourseWare. Diseases of the pleura and the mediastinum. Available at: ocw.tufts.edu/Content/27/lecturenotes/331282. Accessed Jan 3, 2014. Biller DS, Larson MM. Mediastinal disease. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. 7th ed. St Louis: Saunders Elsevier, 2010;1119–1125 Berry CR. Thoracic radiographic interpretation: The mediastinum. Available at: veterinarycalendar.dvm360.com/avhc/ Medicine/Thoracic-radiographic-interpretation-The-mediastin/ ArticleStandard/Article/detail/746706. Accessed Jan 3, 2014.
JAVMA, Vol 246, No. 2, January 15, 2015
Anesthesia Case of the Month History A 2.6-kg (5.72-lb) 10-year-old neutered male Yorkshire Terrier with a 6-month history of tracheal collapse was evaluated at the University of Florida Small Animal Hospital. The dog had been previously treated by the referring veterinarian with theophylline and butorphanol, but had recently been reevaluated because of increased coughing and signs of respiratory distress, for which it received additional treatment with dexamethasone sodium phosphate (0.23 mg/kg [0.104 mg/lb], IM), acepromazine (0.038 mg/kg [0.017 mg/lb], IM), and oxygen therapy via an oxygen cage. Despite additional treatment, there was no noticeable change in the patient’s condition. Initial physical examination on referral revealed a grade 2 of 6 left systolic heart murmur, coughing, dyspnea, cyanosis, and a palpably enlarged liver. Results of a CBC and serum biochemical analysis were within reference limits. Thoracic radiography revealed extra- and intrathoracic tracheal collapse with collapse of the principal bronchi, mild right-sided cardiomegaly, and generalized hepatomegaly (Figure 1). Fluoroscopic examination of the thorax revealed severe, dynamic extra- and intrathoracic tracheal, principal bronchial, and caudal lobar bronchial collapse. The patient was placed in an oxygen cage set to deliver 40% oxygen in the intensive care unit overnight and received acepromazine (0.02 mg/kg [0.009 mg/lb], IV) and butorphanol (0.2 mg/kg [0.09 mg/lb], IV) every 2 hours or as needed. Food was withheld overnight, and the following morning, the patient was anesthetized for tracheal stent placement. The dog was premedicated with butorphanol (0.19 mg/kg [0.086 mg/lb], IV), and induction of anesthesia with propofol (6 mg/kg [2.7 mg/lb], IV, to effect) immediately followed. The patient was orotracheally intubated with a 6.0-mm (internal diameter) sterile endotracheal tube. Anesthesia was maintained with isoflurane in oxygen (3 L/min) delivered via a Bain (nonrebreathing) system. Lactated Ringer’s solution was administered IV during anesthesia (7 mL/kg/h [3.2 mL/lb/h]). A multiparameter monitor,a including a lead II ECG for heart rate and rhythm, was used, and oxygen saturation as measured by pulse oximetry, end-tidal PCO2, respiratory rate, and blood pressure (noninvasive Doppler method) were recorded. The patient breathed spontaneously, and all monitored physiologic parameters were determined by the attending anesthesiologist to be within acceptable limits throughout induction and prior to stent deployment. The patient was transported under general anesthesia to the diagnostic imaging suite where, prior to This report was submitted by Tiffany D. Granone, DVM; from the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610. Address correspondence to Dr. Granone ([email protected]). JAVMA, Vol 246, No. 2, January 15, 2015
stent placement, preoperative thoracic radiographs were acquired and the patient end of the endotracheal tube was withdrawn such that the tip was repositioned just beyond the level of the larynx. Once radiographic measurements were completed and the appropriate stent size was determined, the administration of isoflurane was discontinued, and the patient was disconnected from the anesthetic breathing circuit. Flow-by oxygen (4 L/min) was provided by placing the breathing circuit in close proximity to the machine end of the patient’s endotracheal tube. An 8 X 72-mm intraluminal nitinol tracheal stentb was placed by inserting the self-expanding stent in the delivery system within the lumen of the endotracheal tube. The stent extended from the midcervical through the cranial thoracic trachea. The duration of fluoroscopic-guided stent placement was approximately 10 minutes, and no apparent complications were associated with stent deployment. During this time, the patient’s plane of anesthesia became light and the patient became tachypneic and was administered a bolus dose of propofol (0.77 mg/kg [0.35 mg/lb], IV) and lidocaine (0.77 mg/kg, IV). After deployment of the stent and removal of the delivery system, the patient was extubated and a right lateral thoracic radiograph was obtained to confirm correct stent placement. After extubation, oxygen was delivered at 4 L/min via a small animal facemask. The patient
Figure 1—Preoperative lateral radiograph of the thorax and cervical vertebrae of a 2.6-kg (5.72-lb) 10-year-old neutered male Yorkshire Terrier with a 6-month history of tracheal collapse. Fluoroscopy indicated severe, dynamic extra- and intrathoracic tracheal, principal bronchial, and caudal lobar bronchial collapse. Notice that cardiomegaly is also evident in this image. Vet Med Today: Anesthesia Case of the Month
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began to emerge from anesthesia and was observed to have signs of tachypnea and increased respiratory effort and noise. Following completion of postoperative radiography (Figures 2 and 3), the patient was positioned in sternal recumbency and administration of supplemental oxygen was continued. The patient was allowed to fully recover from anesthesia and continued to have signs of
tachypnea and increased respiratory effort and noise. In the immediate postoperative period, the dog received butorphanol (0.19 mg/kg, IV), acepromazine (0.02 mg/ kg, IV), lidocaine (0.77 mg/kg, IV), and supplemental oxygen via facemask. The patient was then admitted to the intensive care unit and was placed in an oxygen cage set to deliver 40% oxygen. Question On the basis of results of the postoperative radiographs, what is the most likely cause of this patient’s increased respiratory rate, effort, and noise immediately after tracheal stent placement? Answer
Figure 2—Lateral radiograph of the thorax and cervical vertebrae of the patient in Figure 1 obtained 5 minutes after endotracheal placement of an 8 X 72-mm intraluminal nitinol tracheal stent.b Notice the moderate right-sided pneumothorax and pneumomediastinum.
The most likely cause of the patient’s increased respiratory rate, effort, and noise was iatrogenic pneumothorax that we believe occurred during stent placement by inadvertent puncture of the airway (trachea) with the tip of the stent delivery system (introducer). Right lateral and ventrodorsal radiographs obtained to confirm stent placement revealed moderate right-sided pneumothorax, progressing to mild bilateral pneumothorax over 15 minutes, in addition to mild pneumomediastinum and pneumoretroperitoneum (Figures 2 and 3). As the patient began to emerge from anesthesia, respiratory rate, effort, and noise continued to increase, as the dog began to develop signs of distress. The patient was administered antitussives and sedatives, including butorphanol (0.19 mg/kg, IV, q 2 h), acepromazine (0.02 mg/kg, IV, q 2 h as needed), and hydrocodonehomatropine (0.22 mg/kg [0.1 mg/lb], PO, q 8 h). Thoracocentesis was performed, and 17 and 3 mL of air were removed from the right and left sides of the thorax, respectively. The patient received inhaled albuterol following thoracocentesis and was allowed to recover in the oxygen cage set to deliver 40% oxygen. All postprocedure treatments were performed approximately 30 minutes after stent placement and admission of the patient to the intensive care unit. Twenty-four hours after stent placement, followup thoracic radiographs were again obtained, which revealed resolution of the pneumothorax. The patient was discharged from the hospital 2 days after the initial surgery, with a follow-up visit recommend in 6 months. Discussion
Figure 3—Postoperative ventrodorsal radiograph of the thorax of the patient in Figure 1 obtained 15 minutes after endotracheal stent placement of an 8 X 72-mm intraluminal nitinol tracheal stent.b Notice the mild bilateral pneumothorax and pneumomediastinum. 190
Vet Med Today: Anesthesia Case of the Month
Tracheal collapse is a common problem in toy and small-breed dogs, with Pomeranians, Yorkshire Terriers, Miniature Poodles, and Pugs being commonly affected.1,2 The condition is a structural disease of the trachea, causing airway obstruction with a dynamic component that can affect the intra- and extrathoracic portions of the trachea and mainstem bronchi.3 Tracheal collapse results from cartilaginous degeneration of the C-shaped tracheal rings that maintain normal patency. In affected dogs, the tracheal cartilages have decreased glycosaminoglycan content, fewer chondrocytes, and decreased calcium concentrations, compared with those of clinically normal dogs.4 During respiration and the generation of normal airway pressures, the turgidity of the diseased trachea causes ventrodorsal collapse of the cartilage JAVMA, Vol 246, No. 2, January 15, 2015
rings and subsequent mechanical obstruction, which perpetuates signs of chronic airway inflammation.4 A diagnosis of tracheal collapse is commonly made with a combination of imaging techniques, including radiography, fluoroscopy, tracheoscopy, and occasionally ultrasonography.4 Collapse can affect the entire trachea and include the mainstem bronchi.2,4 Dogs often have signs of respiratory distress and commonly have an associated cough described as sounding like a goose honk. Surgical management of tracheal collapse is considered a salvage procedure because 65% to 78% of dogs are reported to respond to medical treatment.1,5 Surgical procedures described for the treatment of tracheal collapse include tracheal ring chondrotomy, plication of the dorsal tracheal membrane, prosthetic mesh reconstruction, and intra- and extraluminal prosthetic supports.1,6 All surgical procedures are aimed at restoring airway patency and reducing airway resistance. The use of prosthetic supports is among the most commonly used treatments for tracheal collapse. Extraluminal prosthetic supports have been associated with several complications, such as infection, disruption of the innervation or blood supply to the trachea causing laryngeal paralysis, necrosis of the trachea, and chronic coughing.7,8 A study by Becker et al4 found that 21% of dogs that had extraluminal tracheal prosthetics placed required a second surgery for treatment of unresolved respiratory distress attributable to postoperative laryngeal paralysis. In addition, use of extraluminal prostheses is limited to treatment of tracheal collapse confined to the cervical portion of the trachea and thoracic inlet.4,6 Because of this limitation and the associated complications, use of intraluminal prostheses has gained attention. Use of intraluminal stents has gained popularity in human medicine, where the prosthesis is placed in patients with obstructive tracheal disorders secondary to neoplasia.2,3,9 Use of intraluminal tracheal stenting originated from application of stents designed for use within the biliary, vascular, gastrointestinal, and respiratory systems in people.10,11 Initially, balloon-expanding stents were used; however, these stents had a tendency for acute recoil after the balloon was deflated, leading to stent migration and loss of luminal diameter.12 Since then, the advent and use of self-expanding stents made of various materials (ie, stainless steel and nickel-titanium alloys) has proven successful for palliative treatment of tracheal collapse in dogs.12 Of the self-expanding stents, the Palmaz-Shatz stent has been associated with a high rate of complications, including development of pneumothorax, infection, mucous plugs resulting in tracheal obstruction, stent migration, and compression of the upper stent ends.6,10 Rauber et al13 reported the occurrences of pneumothorax in 2 rabbits caused during the time of stent placement. Placement of intraluminal prostheses is often accompanied by the use of a rigid bronchoscope inserted into the trachea of an anesthetized patient. The stent delivery system is then inserted into the trachea adjacent to the bronchoscope until the tip of the introducer can be seen. The bronchoscope is then partially retracted to allow for deployment of the stent. Once the stent is fully deployed, the bronchoscope is then carefully retracted, making sure to not disrupt stent placeJAVMA, Vol 246, No. 2, January 15, 2015
ment.1 Following deployment, thoracic radiographs are taken to verify accurate placement. Of the stents in use today, those composed of shape memory alloys, such as nickel and titanium (nitinol), have been found to be advantageous owing to their ability to accommodate substantial strain before reaching irreversible deformation.1 A nitinol stentb designed specifically for use in dogs and cats is made of a woven nitinol material, classified as a reconstrainable, foreshortening stent. In a study by Durant et al1 examining the use of nitinol stentsb for treatment of end-stage tracheal collapse in dogs, complications noted were stent dislodgement with retraction of the bronchoscope during partial stent deployment and pneumonia. No other complications were noted in the immediate postoperative period. In a study by Sura and Krahwinkel,12 no complications were recorded during the anesthetic recovery period when endoscopy was used to obtain stent measurements or during the separate anesthetic episode for stent placement. Although the placement of an intraluminal tracheal stent is a minimally invasive procedure, anesthetic patient management presents a challenge owing to the difficulty of maintaining a patent airway throughout the procedure. A few anesthetic techniques address the approach to general anesthesia for the placement of tracheal stents, including SC administration of glycopyrrolate, followed by anesthetic induction with thiopental and maintenance of anesthesia with isoflurane in oxygen in an intubated patient.6 Others describe a total IV anesthetic method of administering propofol for both induction and maintenance of anesthesia.12 Weisse14 describes a method for anesthetizing patients that is almost identical to the method used in our patient. One method of stent placement is to perform the procedure in a patient that is not intubated. Via this method and the insertion of a bronchoscope, oxygenation of the patient may be compromised if the narrowed tracheal lumen becomes obstructed by the bronchoscope itself. In patients in which intraluminal tracheal stenting is performed when nonintubated, a means by which to provide supplemental oxygen is necessary. Oxygen supplementation may be provided by several techniques (flow-by, nasal oxygen via cannula, and oxygen insufflation via transtracheal catheterization), with flow-by administration being the simplest method of providing supplemental oxygenation to spontaneously breathing patients. In the patient described in the present report, the placement of the nitinol stent was under fluoroscopic guidance and the stent and introducer were placed through the lumen of the endotracheal tube. This was done to alleviate the need for extubation of the patient during the procedure and to facilitate the administration of inhalation anesthetic in oxygen. A potential disadvantage of stent placement in intubated patients is limited visibility of the surgical site with a smalldiameter endotracheal tube, and the inability to insert the bronchoscope through the lumen of a narrow endotracheal tube. At our institution, tracheal stenting is commonly performed in intubated patients with the use of fluoroscopy rather than bronchoscopy to mainVet Med Today: Anesthesia Case of the Month
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tain an airway and provide a means of ventilation for the patient if necessary. To our knowledge, there are no published reports of pneumothorax following the deployment of this type of stent. It is suspected that during placement and deployment of the stent, the tip of the stent delivery system punctured the trachea, causing the pneumomediastinum and subsequent pneumothorax and pneumoretroperitoneum. Pneumomediastinum is the presence of free gas within the mediastinal space and can be caused by penetrating neck wounds, esophageal or tracheal rupture or tear, or venipuncture or can be seen as a sequela of transtracheal wash.15 In dogs, the mediastinum is incomplete and is a potential space between the right and left pleural cavities.16 Several structures lie within the mediastinum, including the heart, trachea, esophagus, great vessels, lymphatics, vagus nerves, and thymus.16 The mediastinum communicates with the cervical facial planes through the thoracic inlet cranially and with the retroperitoneal space through the aortic hiatus caudally.16 Pneumomediastinum can lead to pneumoretroperitoneum via air dissecting caudally through the retroperitoneal space via the aortic hiatus through the diaphragm.17 Pneumomediastinum may lead to pneumothorax, but pneumomediastinum will not result from pneumothorax because the air collapses the mediastinal space between the 2 pleural reflections.17 At the time the patient described in this report began to develop clinical signs of increased respiratory effort, extubation had already taken place. Treatment with supplemental oxygen, antitussives, and sedatives was elected to maintain oxygenation, keep the patient calm, and reduce coughing, which may have led to dislodgment of the newly placed stent and collapse of the affected trachea beyond the stent (bronchial collapse). Once the pneumothorax was treated (via thoracocentesis), considerable improvement in the patient’s clinical signs was evident as well as improved tracheal air flow through the stent. Overall, the use of intraluminal nitinol tracheal stents, such as the one used in this case, has been associated with a fair to good outcome in those patients requiring tracheal stenting.1 Compared with other types of intraluminal stents and extraluminal prostheses, postoperative morbidity and mortality rates associated with complications of tracheal stenting are lower with intraluminal nitinol stents.1 Stent delivery system–induced pneumothorax should be considered in any patient with immediate postoperative stent complications.
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a. b.
IntelliVue MP50, Philips Healthcare, Andover, Mass. Vet Stent-Trachea, Infiniti Medical, Menlo Park, Calif.
References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.
Durant AM, Sura P, Rohrbach B, et al. Use of nitinol stents for end-stage tracheal collapse in dogs. Vet Surg 2012;41:807–817. Sun F, Uson J, Ezquerra J, et al. Endotracheal stenting therapy in dogs with tracheal collapse. Vet J 2008;175:186–193. Gellasch KL, Da Costa Gomez T, McAnulty JF, et al. Use of intraluminal nitinol stents in the treatment of tracheal collapse in a dog. J Am Vet Med Assoc 2002;221:1719–1723. Becker WM, Beal M, Stanley BJ, et al. Survival after surgery for tracheal collapse and the effect of intrathoracic collapse on survival. Vet Surg 2012;41:501–506. Mittleman E, Weisse C, Mehler SJ, et al. Fracture of endoluminal nitinol stent used in the treatment of tracheal collapse in a dog. J Am Vet Med Assoc 2004;225:1217–1221. Radlinsky MG, Fossum TW, Walker MA, et al. Evaluation of the Palmaz stent in the trachea and mainstem bronchi of normal dogs. Vet Surg 1997;26:99–107. Woo HM, Kim MJ, Lee SG, et al. Intraluminal tracheal stent fracture in a Yorkshire Terrier. Can Vet J 2007;48:1063–1066. Ouellet M, Dunn ME, Lussier B, et al. Noninvasive correction of a fractured endoluminal nitinol tracheal stent in a dog. J Am Anim Hosp Assoc 2006;42:467–471. Zakalunzy SA, Lane JD, Mair EA. Complications of tracheobronchial airway stents. Otolaryng Head Neck Surg 2003; 4:478–488. Moritz A, Schneider M, Bauer N. Management of advanced tracheal collapse in dogs using intraluminal self-expanding biliary wallstents. J Vet Intern Med 2004;18:31–42. Ruegemer JL, Perkins JA, Azarow KS, et al. Effect of the Palmaz balloon-expandable metallic stent in the trachea of pigs. Otolaryngol Head Neck Surg 1999;121:92–97. Sura PA, Krahwinkel DJ. Self-expanding nitinol stents for the treatment of tracheal collapse in dogs: 12 cases (2001–2004). J Am Vet Med Assoc 2008;232:228–236. Rauber K, Sawar SA, Hofmann M, et al. Endotracheal placement of balloon-expanded stents: an experimental study in rabbits. Radiology 1997;202:281–283. Weisse CWC. Intraluminal stenting for tracheal collapse. In: Bonagura JD, Twedt DC, eds. Kirk’s current veterinary therapy XIV. St Louis: Saunders Elsevier, 2009;635–642 Tufts University OpenCourseWare. Diseases of the pleura and the mediastinum. Available at: ocw.tufts.edu/Content/27/lecturenotes/331282. Accessed Jan 3, 2014. Biller DS, Larson MM. Mediastinal disease. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. 7th ed. St Louis: Saunders Elsevier, 2010;1119–1125 Berry CR. Thoracic radiographic interpretation: The mediastinum. Available at: veterinarycalendar.dvm360.com/avhc/ Medicine/Thoracic-radiographic-interpretation-The-mediastin/ ArticleStandard/Article/detail/746706. Accessed Jan 3, 2014.
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