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From the Department of Anesthesiology, Program in Critical Care, London Health Sciences Centre, 339 Windermere Road, London, Ontario N6A 5A5 Canada.
Address correspondence to: Lorne Porayko MD. Phone: 519-663-3363; Fax: 519-663-3079; E-mail: lporayko{at}yahoo.com
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Abstract |
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Clinical Features: A 63-yr-old man underwent reduction pneumoplasty for bullous emphysema. Postoperatively, ventilation was inadequate, secondary to bilateral high output bronchopleural fistulae. High frequency jet ventilation was initiated and achieved adequate ventilation (pH>7.2). Over the following 24 hr, progressive hypoxemia (Sa02 < 86%) developed along with the acute respiratory distress syndrome. Nitric oxide was delivered by continuous flow at the patient Y-connector during combined high frequency jet and conventional ventilation (two conventional low volume breaths/minute). Substantial improvement in oxygenation (FiO2 0.8 0.5, SaO2 > 92%) was noted initially and was sustained over 72 hr. Subsequently, the patient was weaned to conventional ventilation without difficulty. Mechanical ventilation was discontinued on postoperative day sixteen.
Conclusion: The simultaneous use of nitric oxide and high-frequency jet ventilation was used safely and effectively in this patient as a method of support for acute respiratory distress syndrome with co-existing large bilateral bronchopleural fistulae.
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Introduction |
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Case report |
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. Preoperative arterial blood gases were pH 7.41, PO2 66 mmHg, PCO2 44 mmHg, HCO3- 28 meq•L-1, and oxygen saturation (SaO2) 93% while breathing room air. Computed tomography (CT) scan of the chest revealed extensive bullous disease. After assessment, he was discharged home for six weeks of rehabilitation prior to a planned reduction pneumoplasty procedure. On the day of the procedure a thoracic epidural (T7–8) and radial arterial catheter were inserted. General anesthesia was induced with 100 µg fentanyl, 100 mg propofol and muscle relaxation with 50 mg rocuronium. A #37 French double-lumen endotracheal tube was placed and its position confirmed by bronchoscopy. Anesthesia was maintained with isoflurane (0.2-0.5%), propofol infusion (10-50 µg•kg–1•min–1), and intermittent doses of rocuronium. Bilateral bullectomy was performed, through a median sternotomy incision, using sequential one-lung ventilation. Two chest tubes were placed in each hemithorax. The double lumen endotracheal tube was exchanged for a standard size #8.0 endotracheal tube at the end of the procedure. The intra-operative course was complicated by persistent episodes of hypotension and desaturation (SaO2 < 80%); therefore, he was brought to the intensive care unit (ICU) postoperatively. On arrival, the blood pressure was 76/56 mmHg with a pulse rate of 108 per minute. A pulmonary artery catheter was inserted which revealed a cardiac index of 2.01 L•min–1•m–2, central venous pressure (CVP) 11 mmHg, pulmonary capillary wedge pressure (PCWP) 12 mmHg, and systemic vascular resistance index of 2023 dynes•sec•cm–5m–2. Volume resuscitation and inotropic support were initiated. A 12-lead electrocardiogram showed widespread ST-segment elevation (1-2 mm), which was interpreted as pericardial reaction to surgery. On postoperative day one (POD#1) a mild elevation of troponin I = 4.1 (µg•L–1) was noted suggesting a small subendocardial myocardial infarction had occurred. An echocardiogram revealed no pericardial fluid and normal ventricular function. However, the patient continued to require inotropic support to maintain blood pressure and cardiac index. He was initially administered 100 mg hydrocortisone iv q8h steroids until postoperative day six; thereafter, high dose methylprednisolone was initiated as per the Meduri2 protocol for treatment of ARDS.
On arrival in the ICU, pressure control ventilation was initiated with a peak inspiratory pressure (PIP) of 26 cm H2O, respiratory rate 15 min–1, positive end expiratory pressure (PEEP) of 5 cm H2O, and FiO2 of 1.0. Initial blood gas analysis in the ICU revealed a pH of 7.28, PO2 47, PCO2 57, HCO3- 26, and SaO2 80% (Table II). A chest x-ray revealed collapse of the right upper lobe, which re-expanded after bronchoscopy and lavage. High output air leaks were evident, severely impairing effective ventilation: delivered tidal volumes were 600 ml and expired volumes of only 100 ml were measured. Ventilation continued to be compromised.
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On POD #2 ventilation was provided by combined high frequency jet ventilation (CHFV)3 in an effort to reduce the leak via the bronchopleural fistulae. Deep sedation (5-15 mg•hr–1 morphine and 2-4 mg•hr–1 midazolam) and intermittent paralysis with 10 mg vecuronium were required. A jet rate of 100 min–1, with a conventional intermittent mandatory ventilation rate of two low tidal volume (300 ml) breaths per minute, and driving pressure of 25 cm H2O were initiated. The bilateral chest tube leak lessened and blood gases improved substantially: pH 7.41, PO2 70 mmHg, PCO2 42 mmHg, HCO3- 26 meq•L-1, and SaO2 94% with FiO2 of 0.8. The driving pressure was reduced in an attempt to further decrease the bronchopleural leak.
On POD#3 ventilation deteriorated again and chest x-rays revealed development of bilateral airspace disease consistent with ARDS (PCWP=12). Blood gases continued to deteriorate and on POD #7 they were pH 7.14, PCO2 93 mmHg, PO2 93 mmHg, HCO3- 30 meq•L-1, SaO2 94% with FIO2 of 0.8 and PEEP of 5 cm H2O. Whenever the PEEP was increased, the output from the bilateral bronchopleural fistulae also increased dramatically. The concern of oxygen toxicity with ongoing persistently high FiO2 requirements and deteriorating respiratory acidosis prompted the idea of delivering inhaled nitric oxide while continuing with the HFJV. The experimental nature of the proposed ventilation technique was discussed with the patient's family. There was no English literature available for technical guidance. Other tertiary care teaching hospitals throughout the area were contacted for advice, but none had attempted the simultaneous use of NO and HFJV. The integrated CHFJV-NO injection system we assembled is described below (Figure).
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The Monaghan 225 was used to provide a low level of PEEP (5 cm H20), a ventilation rate of 2-4 per minute, and a continuous entrainment flow for the jet breaths. Gas from this ventilator was humidified by a Fisher-Paykel MR 450 Servo Humidifier (G). The FiO2 was titrated by Bird Oxygen Blenders on each ventilator (J). Proximal airway pressures were monitored with a Novametrix Pneumoguard Model 1200 (H).
Nitric Oxide (1000 ppm) (K) was delivered by a constant flow (3 lpm) to the Jet line (F). The inhaled nitric oxide (NO) and nitrogen dioxide (NO2) were initially measured at two points: at the patient "Y" connection (L) and distal to the exhalation valve (I). The measured values of inhaled NO were nominal (1-2 ppm) compared to the expired concentrations (10-20 ppm). Changes in ventilation and NO flow resulted in insignificant changes in the measured values at the patient "Y" connector, whereas expected changes were noted in the measured levels in the expired side. We assumed this was due to insufficient mixing time of the gases on the inspiratory side. The inspired measurements were therefore discontinued after approximately 24 hr.
The inspired gas concentrations were measured by the NO and NO2 monitoring system of the Siemens 300 Nitric Oxide Ventilator (M). The exhaled gases were analyzed for NO and NO2 with Micro Medical Microgas electrochemical analyzers (N). Exhaled gases and all escaping gases from the chest tube drainage system were scavenged by an active suction system (O).
With the addition of NO at 20 ppm, both oxygenation and ventilation improved so that 12 hr after the initiation of NO, FiO2 was reduced to 50% with blood gas analysis revealing pH 7.35, PO2 64 mmHg, PCO2 49 mmHg, HCO3- 27 meq•L-1on the same ventilation parameters. On POD#10 blood gases had improved substantially and the NO was gradually weaned over the course of 24 hr. The air leak from the chest tubes had also decreased substantially and pressure control ventilation was resumed. On POD#12 sedation was reduced and the patient was placed on pressure support ventilation of 10, PEEP of 7, FiO2 of 0.5 with resultant minute ventilation of 8.1 litres. Blood gases revealed pH 7.41, PO2 78 mmHg, PCO2 51 mmHg, HCO3- 32 meq•L-1and SaO2 of 95%. With sedation reduced, a right-sided motor deficit was detected and CT scan of the head revealed a left parietal temporal infarct. On POD#15 a tracheostomy was performed. On POD#16 tracheostomy mask trials of spontaneous breathing were started and on POD#19 the patient was able to sustain spontaneous breathing. The patient was eventually discharged to a peripheral hospital for continued rehabilitation.
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Discussion |
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Combining these two therapies led to a number of concerns. One problem was the ability to measure the dynamic levels of NO and NO2 accurately in the inspired and expired gases, as well as in the ambient atmosphere. The administration of NO at high levels (i.e. > 40 ppm) is associated with lung injury and thus close monitoring is essential.6 The ability to monitor respiratory gases accurately while using HFJV is problematic. Rapid response chemiluminescence analysis was not available but would be preferable, particularly during jet ventilation, in which wide swings in inspiratory flow may entrain dangerously high peak NO levels. The biological long-term effects of the possibly large regional swings in NO concentrations during HFJV require further study before they are implemented into routine practice. The large chest tube leaks led to concern regarding adequate scavenging of NO to protect bedside staff. The system as outlined above was developed and implemented. Another problem, specific to the use of HFJV, was providing adequate humidification. Adding saline to the jet line has been known to cause mucosal dessication as saline droplets are propelled into the airways. There were also concerns that the measurement of airway pressures at the jet connector were not a true reflection of intrapulmonary pressures. Despite these known deficiencies, the results were encouraging with a rapid improvement in oxygenation. Eventually, discontinuation of mechanical ventilatory support was accomplished.
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Conclusion |
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The primary concern with delivering this therapy was with safety of the patient and bedside staff. The difficulty in establishing predictable NO levels while using jet ventilation is a severe limitation of this technique. Neither HFJV for treatment of bronchopleural fistulae nor nitric oxide therapy for ARDS has been shown to improve patient outcome. Nevertheless, when faced with deteriorating blood gases using conventional therapy, an alternative strategy is often implemented. The use of this combined therapy, with its known deficiencies, must be cautiously approached until randomized outcome studies are available.
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Acknowledgments |
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Accepted for publication September 24, 1999.
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References |
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2
Meduri GU, Headley AS, Golden E, et al. Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome. A randomized controlled trial. JAMA 1998; 280: 159–65.
3 Ip-Yam PC, Allsop E, Murphy J. Combined high-frequency ventilation (CHFV) in the treatment of acute lung injury – a case report. Ann Acad Med Singapore 1998; 27: 437–41.[Medline]
4
Baumann MH, Sahn SA. Medical management and therapy of bronchopleural fistulas in the mechanically ventilated patient. Chest 1990; 97: 721–8.
5 Marini JJ. A lung protective approach to ventilating ARDS. Respiratory Clinics of North America 1998; 4: 633–63.
6
Troncy E, Francoeur M, Blaise G. Inhaled nitric oxide: clinical applications, indications, and toxicology. Can J Anaesth 1997; 44:973–88.
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