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* From the Departments of Anesthesiology and Critical Care Medicine, and
Thoracic and Hyperbaric Surgery, University Medical School of Graz, Graz, Austria.
Beatrice Ratzenhofer-Komenda MD, Department of Anesthesiology and Critical Care Medicine, University Hospital, LKH - Universitätskliniken Graz, Auenbrugger Platz 29, A-8036 Graz, Austria. Phone: +43-316-385-3359; Fax: +43-316-385-3847; E-mail: beatrice.ratzenhofer{at}kfunigraz.ac.at
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Abstract |
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 TOP Abstract IntroductionClinical featuresAnesthesia and ventilationDiscussionReferences |
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Clinical features: An 8 cm postintubation tracheal tear was repaired in a 66-yr-old woman with acute myocardial reinfarction, mediastinal and subcutaneous emphysema, cardiac failure and unrecognized lymphoma. Intraoperative monitoring included dual oximetry: arterial (SaO2) and mixed venous saturations (SvO2). Maintenance of free surgical access and a series of life-threatening events like dislocation of the jet catheter required many ventilation modes. An episode of supraventricular tachycardia was interrupted by cardioversion. Differential lung ventilation with a combination of conventional and high-frequency jet ventilation (HFJV) modes preserved oxygenation (PO2 139.2 mmHg, PCO2 42.4 mmHg, FiO2 1.0) until acute tube obstruction and decrease of saturation values (SaO2 58%, SvO2 45%) required emergency HBO: immediate cardiac and respiratory stabilization was provided by double-lung HFJV and apneic oxygenation under hyperbaric conditions at 2.5 atmospheres absolute for 35 min (SaO2 100%).
The patient recovered from surgery but died of non-Hodgkin lymphoma.
Conclusion: The combination of different ventilation modes including HFJV and the additional use of HBO resulted in sufficient oxygenation during tracheal repair.
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Introduction |
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TOPAbstractIntroductionClinical featuresAnesthesia and ventilationDiscussionReferences |
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Clinical features |
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TOPAbstractIntroductionClinical featuresAnesthesia and ventilationDiscussionReferences |
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On admission to the cardiac care unit, the ECG showed a sinus rhythm of 68 bpm, left axis deviation, elevated ST segments and a negative T, in leads II, III, aVF and V6 as well as descending ST segments in V4 and V5. A diagnosis of recurrent myocardial infarction was made. After a short period of hemodynamic stabilization the patient developed ventricular tachycardia of 193 bpm and dyspnea and the trachea was easily intubated under emergency conditions. Three cardioversion attempts failed and subsequent cardiopulmonary resuscitation was successful. To prevent left ventricular failure she was sedated and ventilation was maintained with synchronized intermittent ventilation. The initial ventilator setting that maintained peripheral arterial saturation between 97% and 100% was: FiO2 0.3, respiration rate 12 bpm, VT 0.65 L, I:E ratio 1:2, positive end-expiratory pressure (PEEP) 6.90 kPa. She was anticoagulated with a continuous infusion of heparin (1000 IU
hr–1). Heart rate was controlled by continuous infusion of 0.013 mgkg–1min–1 lidocaine. Approximately six hours after intubation the patient developed subcutaneous emphysema of the neck and chest. The subcutaneous emphysema was thought to be the result of a minor tracheal injury or from a small alveolar leak due to low-grade emphysema. Over the next few hours the patient's hemodynamic condition deteriorated. The subcutaneous emphysema expanded to the lower abdomen. Computed tomography of the neck and thorax showed a subglottic lesion of the anterior tracheal wall with emphysema of the adjacent tissue and mediastinum. The heart was dilated and a 1 cm pericardial effusion was visible. Both lungs contained multiple emphysematous and atelectatic areas. There was a small pleural effusion on the right side. The air-filled areas of the subcutaneous emphysema spread into the retroperitoneal space. Ventilation was continued with assisted spontaneous breathing at an inspiratory pressure of 14.71 kPa and a PEEP of 4.91 kPa at FiO2 of 0.3. Arterial blood gas analysis showed pH 7.40, PaCO2 42.1 mmHg, PaO2 66.2 mmHg, base excess 1.0 mEqL–1, serum bicarbonate 25.8 mEqL–1, SaO2 95.1%. Over the next few hours the trachea was extubated and the patient was given oxygen ( 4 Lmin–1) via a face mask providing arterial saturation values between 96 and 98%.
Over the next 48 hr the patient became increasingly hemodynamically unstable due to mediastinal compression: three further episodes of ventricular tachycardia occurred. One episode stopped without intervention. With the next episode, the trachea was reintubated without difficulty to give anesthesia and ventilation for the cardioversion procedure. Cardioversion was successfully performed twice and a continuous infusion of 0.01 mgkg–1hr–1 amiodarone was applied in addition to the current medication.
Physical examination showed an extensive subcutaneous emphysema. Bronchoscopy showed an 8-cm tear in the membraneous part of the trachea extending from the first tracheal cartilage to the beginning of the right mainstem bronchus. Blood pressure was 115/52 mmHg with a heart rate of 78 bpm. Hemoglobin and electrolyte concentrations were normal. Serum tests were consistent with myocardial infarction (creatine kinase (CK) 90 UL–1; CK-MB 22 UL–1; Lactate dehydrogenase 342 UL–1, ASAT 36 UL–1; Troponin I 3 ngmL–1 (upper limit: 2 ngmL–1). Transesophageal echocardiography showed left-ventricular dilatation, aneurysm of the anterior wall and the apex, akinesia of the posterior wall and hypokinesia of the rest of the myocardium. The ejection fraction was 25%. The right atrium and the right ventricle were normal in diameter. Arterial blood gas analysis showed pH 7.30, PaCO2 60.1 mmHg, PaO2 56.9 mmHg, base excess 1.7 mEqL–1, serum bicarbonate 28.7 mEqL–1, SaO2 85.9%. The blood sample was drawn at the ventilator setting as follows: synchronized intermittent ventilation mode (SIMV): FiO2 0.7, respiration rate 12 bpm, tidal volume (VT) 0.65 L; minute volume 7.6 L, I:E ratio 1:1.5, positive end-expiratory pressure (PEEP) 6.90 kPa.
Emergency surgery was planned for the hyperbaric chamber of the Department of Thoracic and Hyperbaric Surgery, which is equipped and used routinely as an operating room for thoracic surgery.2
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Anesthesia and ventilation |
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kg–1min–1 lidocaine iv, 6 µgkg–1min–1 dobutamine and 3 µgkg–1min–1 dopamine. Anesthesia was induced with 0.04 mgkg–1 midazolam, 0.2 mgkg–1 etomidate and 1.27 µgkg–1 fentanyl. Total intravenous anesthesia was maintained with continuous infusion of 0.03 mgkg–1hr–1 midazolam and 4 µgkg–1hr–1 fentanyl. Muscle relaxation was obtained with 0.08 mgkg–1hr–1 vecuronium bromide. After induction, a pulmonary artery catheter was inserted for continuous monitoring of mixed venous saturation (SvO2). Dual oximetry values (SaO2 and SvO2) were recorded (Explorer, Edwards Critical Care, Baxter Immuno Corp., Vienna, Austria).
Ventilation modes
STEP 1: DEPENDENT LUNG CONTROLLED MECHANICAL VENTILATION (CMV)
Because airway leakage impaired adequate ventilation the original 7.5-mm tube (inner diameter) was replaced with a reinforced 7.0-mm tracheal tube to pass the leak. The unaffected left main stem bronchus was intubated bronchoscopically and one-lung ventilation was begun (Figure 1a
) with controlled mechanical ventilation (CMV), tidal volume VT 0.6 L, respiration rate 14 bpm, PEEP 2.90 kPa, FiO2 0.7-1.0. Oxygenation was adequate with the patient supine but dual oximetry values decreased when she was turned to the left lateral decubitus position to perform a right lateral thoracotomy (Figure 2).
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). Additional non-dependent lung ventilation was performed through a sterile ventilation hose that crossed the surgical field and was connected to a second ventilator. Laceration of the tracheal tissue was visible at that time. Identification and dissection of the anatomical structures was difficult. The lymph nodes were enlarged and biopsies were taken for histology. Differential lung ventilation resulted in an improvement of arterial and mixed venous oxygen saturations. Differential lung ventilation settings were as follows: dependent lung: CMV: VT 0.6 L, respiration rate 14 bpm, PEEP 3.90 kPa, FiO2 1.0; non-dependent lung: CMV: VT 0.5 L, respiration rate 12 bpm, PEEP 3.90 kPa, FiO2 1.0 to 0.7. The non-dependent lung tube interfered with tracheal reconstruction and had to be removed.
STEP 3: DEPENDENT-LUNG CMV AND NON-DEPENDENT LUNG HIGH-FREQUENCY JET VENTILATION (HFJV) THROUGH A JET CATHETER VIA THE SURGICAL FIELD
The non-dependent lung, single-lumen endobronchial tube was replaced with a 14-French suction catheter via the surgical field and HFJV was begun through this catheter (Figure 1c) at the following settings: dependent lung: CMV: VT 0.6 L, respiration rate 14 bpm, PEEP 3.90 kPa, FiO2 1.0; non-dependent lung: HFJV: 150 bpm, outlet pressure 600.05 mmHg, FiO2 0.7. The pressure within the bronchial system distal to the tip of the catheter did not exceed 110.26 mmHg; alarm limits interrupting the jet stream delivery were preset at 147.80 mmHg (VDR – Bronchotron-1, Percussionaire Corp., Idaho, U.S.A).
Oxygenation remained adequate until the jet catheter escaped from the forceps. Repositioning the catheter was unsuccessful and oxygen saturation decreased rapidly. Overall, the dependent lung endobronchial tube laid over the surgical field made surgical access difficult and impeded the reconstruction.
STEP 4: EMERGENCY DEPENDENT-LUNG CMV OVER THE SURGICAL FIELD AND PRECARINAL HFJV THROUGH THE ENDOTRACHEAL TUBE
Because of hypoxia the left main stem bronchus was intubated urgently with a reinforced 6.0-Charriere endotracheal tube. A double-lumen nasogastric tube was inserted into the tracheal tube to provide HFJV through the larger port and optionally a continuous flow of oxygen through the smaller port (Figure 1d). The differential lung ventilation settings were as follows: Emergency dependent lung CMV: VT 0.6 L, respiration rate 14 bpm, PEEP 3.90 kPa, FiO2 1.0; non-dependent lung: precarinal HFJV 150 bpm, outlet pressure 1.0 bar, FiO2 1.0. This provided sufficient oxygenation but precluded surgical reconstruction. Blood gas analysis showed pH 7.38, PCO2 41.4 mmHg, PO2 139.2 mmHg, serum bicarbonate 24.2 mEqL–1.
Before the positions of the tubes could be changed to obtain better surgical access, the patient developed a sudden episode of supraventricular tachycardia that required cardioversion. Shortly after the hemodynamic status and heart rhythm were restored, the left endobronchial tube became acutely obstructed due to herniation of the cuff. Attempts to deflate the cuff were unsuccessful. With low mixed venous and arterial saturation values, it was decided to continue surgery under hyperbaric conditions (Figure 2).
STEP 5: DOUBLE-LUNG HYPERBARIC HFJV AND APNEIC HYPERBARIC OXYGENATION (HBO)
Compression was begun at a rate of 0.4 atmospheres per minute. In the interest of time, paracentesis for pressure equilibration was not performed.
Only high-frequency tidal volumes were applied via the jet catheter inserted through the endotracheal tube (Figure 1e). The high-frequency ventilation mode remained unchanged except for the reduction of outlet pressure in the beginning of the HBO session.
Ambient pressure was kept at 2.5 ATA (atmospheres absolute). Arterial saturation returned to normal so that additional CMV support via the endotracheal tube was unnecessary. Because dissection and adaptation of the fragile tissue required a calm surgical field, HFJV was replaced by hyperbaric apneic oxygenation for five minutes without a decrease in SaO2. Elevated ambient pressure was maintained at 2.5 ATA for 35 min (isopression phase) until reconstruction of the trachea was completed. Hemodynamic variables and peripheral arterial saturation stabilized under hyperbaric conditions and the heart rate remained rhythmic. Mixed venous saturation values were not displayed in the hyperbaric environment.
When the trachea was closed, HFJV was stopped and CMV installed with monitoring of the airway pressures (Hyperlog, Dräger Corp., Lübeck, Germany). Decompression was started at a rate of 0.3 atmospheres per minute with a three-minute safety stop at 0.3 ATA. The hyperbaric protocol followed the guidelines of the U.S. Navy diving manual.3
After decompression, the respiratory regimen was guided with pressure-controlled ventilation (PCV) to avoid high airway pressures. The tube was positioned fibreoptically next to the carina to bypass most of the sutures. The chest was closed under normobaric conditions. Hemodynamic and ventilation parameters remained stable until the end of surgery (Figure 2).
Postoperative course
The trachea was extubated on the fourth postoperative day in a stable respiratory and hemodynamic state. However, over the next eight hours the patient developed dyspnea and the trachea was reintubated. Bronchoscopy showed external compression of the trachea, most likely by the enlarged lymph nodes. Histology of tissue samples obtained at surgery revealed a non-Hodgkin-lymphoma. Insertion of an endotracheal stent was impeded by the fragile tissue prone to local bleeding. The patient recovered from surgery and from myocardial reinfarction with her ejection fraction increasing from 20 to 50 percent but the trachea remained intubated with CPAP. She died of her underlying malignancy three months later after three cycles of chemotherapy.
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Discussion |
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TOPAbstractIntroductionClinical featuresAnesthesia and ventilationDiscussionReferences |
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Our patient required emergency surgery to close the trachea despite a recent myocardial infarction. During the operation, differential lung ventilation by conventional and high-frequency ventilation (HFV) modes11,12 were successful initially. When an episode of supraventricular tachycardia suggesting cardiac compromise was followed by obstruction of the endobronchial tube, respiratory and cardiac function had to be restored immediately. The life-threatening situation did not permit transporting the patient to the OR where the device for extracorporeal membrane oxygenation was installed, nor was a portable device available. Emergency hyperbaric oxygenation was begun as a last-ditch effort to increase oxygen delivery. A higher amount of oxygen dissolved in the plasma can provide sufficient tissue oxygenation during periods of low oxygen supply and prolong tolerance to hypoxia.2 There are reports that HBO may be useful as an adjunct in the management of cardiogenic shock.13 Outcome evaluations of patients undergoing HBO therapy after acute myocardial infarction suggest a beneficial effect of hyperbaric oxygen.14 HBO may have benefitted our patient.
High-frequency ventilation is often used with major conducting airway surgery but has not been applied under hyperbaric conditions.15 High-frequency ventilation during open airway surgery is advantageous over conventional ventilation modes as it provides an unobstructed and immobile surgical field and adequate gas exchange. Magnusson and coworkers16 report on modest hypercarbia without hypoxaemia in a series of 10 pediatric and seven adult patients undergoing tracheal resection. The major drawback is the risk of barotrauma which is minimized by monitoring airway pressure and qualified surgical assistance to avoid airway obstruction by debris or dislocation of the jet catheter. The pressure valves in the HFV device used in our patient are vented to the atmosphere providing an equilibrium with the ambient pressure which may explain why the device did not fail when it was accidentally exposed to the hyperbaric environment.
Care of the critically ill and surgery in the hyperbaric environment require special considerations:17 The cuff of the endotracheal tube is filled with water in order to save its seal during compression and to avoid distension during decompression. Glass bottles are replaced by plastic infusion bags to avoid iv infusion of bubbles generated during decompression within the liquid and because of the danger of fracture. Myringotomy is performed in the intubated patient unable to achieve pressure equilibration actively. Myringotomy was impeded in our patient by severe impending hypoxemia. Elevation of pressure did not cause damage to the eardrum, possibly because compression was performed at a moderate rate. Prevention of fire hazard in the hyperbaric environment is crucial. A fire extinguishing system operational from inside and outside of the chamber must be provided.
All equipment and circuits within the hyperbaric facility must be pressure tested, spark proof and explosion proof. Flammable materials must be removed from the patient and no flammable or volatile liquid is allowed inside the chamber. Fire is less of a hazard in the multiplace chamber when oxygen concentration is kept < 23%. At a volume of 75,500 L, the hyperbaric chamber where our patient was treated was flooded at a rate of 100000 Lmin–1. Breathing air during the isopression phase, the medical personnel is potentially at risk for developing decompression sickness. Therefore, pure oxygen is inhaled to wash out nitrogen and reduce bubble formation during the decompression period.
The staff working in hyperbaric facilities has to be well trained and familiar with the pathophysiology of hyperbarism for patient and personal safety.
Accepted for publication November 14, 1999.
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References |
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2 Friehs G, Klepp G, Gollmann K, Rader W, Stolze A. Hyperbare oxygenation in der klinik, erste erfahrungen. Zbl Chir 1975; 100: 321–31.
3 US Navy Diving Manual (1995), Navsea 0094-LP-001-9010. Navy Department Washington, D.C. 20362. Best Publishing Co., 23005/2 South Avalon Boulevard, Carson, California 90745, U.S.A.
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Marty-Ané C-H, Picard E, Jonquet O, Mary H. Membranous tracheal rupture after endotracheal intubation. Ann Thorac Surg 1995; 60: 1367–71.
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Kaloud H, Smolle-Jüttner F-M, Prause G, List WF. Iatrogenic ruptures of the tracheobronchial tree. Chest 1997; 112: 774–8.
11 Benumof JL. High-frequency and high-flow apneic ventilation during thoracic surgery. In: Benumof JL (Ed.). Anesthesia for Thoracic Surgery. WB Saunders Company, Harcourt Brace Jovanovich Inc., 1987: 288–96.
12 Rouby J-J, Viars P. Clinical use of high frequency ventilation. Acta Anaesthesiol Scand 1989; 33(Suppl 90): 134–9.
13 Jain KK. Hyperbaric oxygen therapy in cardiovascular diseases. In: Jain KK (Ed.). Textbook of Hyperbaric Medicine, 3rd ed. Seattle: Hogrefe & Hogrefe Publishers, 1999: 393–419.
14 Shandling AH, Ellestad MH, Hart GB, et al. Hyperbaric oxygen and thrombolysis in myocardial infarction: the "HOT MI" pilot study. Am Heart J 1997; 134: 544–50.[Medline]
15
Perera ER, Vidic DM, Zivot J. Carinal resection with two high-frequency jet ventilation delivery systems. Can J Anaesth 1993; 40: 59–63.
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Magnusson L, Lang FJW, Monnier P, Ravussin P. Anaesthesia for tracheal resection: report of 17 cases. Can J Anaesth 1997; 44: 1282–85.
17 Kindwall EP. The multiplace chamber. In: Kindwall EP (Ed.). Hyperbaric Medicine Practice, 2nd ed. Flagstaff, Arizona: Best Publishing Company, 1995: 83–94.
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