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From the Department of Anesthesiology, American University of Beirut-Medical Center, Beirut, Lebanon.
Address correspondence to: Dr. Anis Baraka, American University of Beirut, Department of Anesthesiology, P.O. Box 11 0236, Beirut, Lebanon. Phone: 961-1-350000; Fax: 961-1-744464; E-mail: abaraka{at}aub.edu.lb
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Clinical features: A 27-yr-old female, ex-smoker presented with productive cough and dyspnea of 18-month duration. The chest x-ray revealed diffuse abnormalities involving both lungs consisting of interstitial emphysema with irregular shadowing. Preoperative PaO2 was 88 mmHg and pulmonary function tests showed moderate obstructive disease. The patient underwent right open lung biopsy. After induction of anesthesia, a left double lumen tube was inserted and its position verified with auscultation and fibreoptic bronchoscopy. Upon initiation of OLV, the patient developed severe hypoxemia and the PaO2 dropped from 500 mmHg during two-lung ventilation (TLV) to 50 mmHg. Hypoxemia was readily corrected by resuming TLV.
Conclusion: The severe hypoxemia during OLV in this patient with RB-ILD may be attributed to impaired hypoxic pulmonary vasoconstriction. Other causes were not excluded. Caution is warranted when initiating OLV in these patients.
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An extensive search through Medline, Embase, Cochrane and other databases failed to reveal any report on the use of one-lung ventilation (OLV) in patients with RB-ILD. This report presents a young female with RB-ILD who underwent open lung biopsy and developed severe hypoxemia during OLV.
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Case report |
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The chest x-ray revealed diffuse interstitial infiltrates with honey combing. Diffuse abnormalities involving both lungs and all lobes were present on the computed tomography scan of the chest. These were more extensive in the upper and mid zones and consisted of interstitial emphysema with irregular interstitial shadowing. No lymph node enlargement in the hila or mediastinum nor any evidence of bronchiectasis were seen.
Arterial blood gases on room air showed a PaO2 of 88 mmHg, a SpO2 of 97%, a PaCO2 of 38 mmHg and a pH of 7.45. Moderate obstructive disease with a 15–20% decrease in obstruction with bronchodilators was documented by pulmonary function tests (PFT) with a carbon monoxide diffusion capacity predicted of 22.45 mL•min-1•mmHg-1 and pre-bronchodilators of 18 mL•min-1•mmHg-1.
The preoperative differential diagnosis included alpha-1-antitrypsin deficiency, histiocytosis and sarcoidosis. The patient was scheduled for right thoracotomy for an open lung biopsy and possible lobectomy. She was premedicated with diazepam 5 mg po and glycopyrrolate 0.2 mg im. An 18-gauge peripheral angiocatheter was inserted for iv access, and a total of 700 mL of lactated Ringer’s solution was given. The patient was monitored intraoperatively with electrocardiography, an arterial line, end-tidal capnography and pulse oximetry. After preoxygenation with 100% O2, anesthesia was induced with lidocaine 75 mg, propofol 100 mg, cisatracurium 8 mg, sufentanil 20 µg and midazolam 2 mg. A left 35-French double-lumen tube (DLT) was used; correct placement of the tube was verified by chest auscultation and by fibreoptic bronchoscopy (FOB). Position of the DLT was rechecked after positioning of the patient in the left lateral decubitus at an angle of around 45° to the plane of the operating table. Anesthesia was maintained with isoflurane 0.4–1.8% in 100% O2 and the lungs were ventilated with a tidal volume of 10 mL•kg-1 at a respiratory rate of 12 breaths•min-1 and an I/E ratio of 1:2. Intraoperatively the blood pressure ranged between 105/65–140/80 mmHg, and the heart rate ranged between 90 and 110 beats•min-1.
During two-lung ventilation (TLV), results of arterial blood gas analysis were: PaO2 500 mmHg; SO2 100%; PaCO2 36 mmHg; and pH 7.42. One minute following initiation of OLV the SpO2 started to drop, and the patient developed severe hypoxemia with an SpO2 dropping down to 85% at the end of the procedure which lasted ten minutes and was limited to lung biopsy; the results of arterial blood gas analysis at that time were: PaO2 50 mmHg; SO2 85%; PaCO2 44 mmHg; and pH 7.38. Proper positioning of the DLT and adequate ventilation of the dependent lung were confirmed. Following lung biopsies from the right upper lobe and the right lower lobe, TLV was resumed, and the SpO2 increased to 100%. Arterial blood gas analysis were: PaO2 420 mmHg; SO2 100%; PaCO2 39 mmHg; and pH 7.40.
At the end of surgery, neuromuscular blockade was reversed with neostigmine 2.5 mg and glycopyrrolate 0.5 mg, and the patient was extubated. Histopathology showed patchy interstitial lung disease consistent with RB-ILD.
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Discussion |
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Our patient developed severe hypoxemia upon initiation of OLV. Hypoxemia during OLV may be attributed to several factors including preoperative lung disease, preoperative medications, and hemophilus influenza infection, in addition to malpositioning of the DLT, inadequate ventilation of the dependent lung, as well as the intraoperative use of isoflurane anesthesia. The moderate preoperative abnormalities of PFT and PaO2 cannot explain the severe hypoxemia that developed upon initiation of OLV. Also, the patient was not receiving any preoperative medications, and the culture of hemophilus influenza organism was positive for only 20.000•mL-1. The appropriate positioning of the DLT was confirmed by FOB, and ventilation of the dependent lung was adequate as evidenced by chest auscultation and by a normal PaCO2 during OLV. Isoflurane anesthesia inhibits HPV in the nondependent lung by approximately 21% and only increases nondependent blood flow from 21 up to 24% of the total blood flow.12 This 4% increase in the shunt does not explain the occurrence of severe hypoxemia during OLV.
Identifying patients at risk of developing severe hypoxemia during OLV is difficult. A recent report suggests that PaO2 during TLV may be the only intraoperative variable that can predict PaO2 during OLV; a positive relationship exists between these two variables.13 However, the PaO2 in our patient with RB-ILD decreased from 500 mmHg during TLV down to 50 mmHg upon initiation of OLV, despite adequate ventilation of the dependent lung with 100% O2. This hypoxemia may be attributed to excessive shunting in the non-ventilated lung. The shunt would amount to 50% according to the iso-shunt lines.14 Hypoxemia was immediately corrected upon resuming TLV without alternative plans such as continuous positive airway pressure or positive end-expiratory pressure, since the time needed to obtain the lung biopsies was short.
There is evidence that HPV is decreased in certain types of lung diseases including pneumococcal pneumonia, granulomatous pulmonary disease and chronic obstructive pulmonary disease (COPD).15–17 Patients with COPD have a decrease in the total cross-sectional area of the pulmonary vascular bed due to anatomic changes from chronic constriction of smooth muscles in response to alveolar hypoxia.18 Benumof and Wahrenbrock have shown that these patients have blunted pulmonary vasoconstrictive reflexes.19 We speculate that patients with RB-ILD, similar to COPD patients, may have an impaired HPV response. As a result, transpulmonary shunting may persist in the non-ventilated lung. This might be attributed to the presence of bronchial wall thickening and prominent peribronchovascular interstitium, resulting in a pulmonary vasculature incapable of HPV.
In conclusion, this report presents the case of a patient with RB-ILD who developed severe hypoxemia during OLV. This may have resulted from impaired HPV secondary to the changes in the bronchial wall and the peribronchovascular interstitium associated with RB-ILD. We advise clinicians to be extremely cautious when administering anesthesia to patients with RB-ILD.
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Footnotes |
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Revision received January 8, 2003. Accepted for publication October 28, 2002.
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2 Sadikot RT, Johnson J, Loyd JE, Christman JW. Respiratory bronchiolitis associated with severe dyspnea, exertional hypoxemia, and clubbing. Chest 2000; 117: 282–5.
3 Myers JL, Veal CF Jr, Shin MS, Katzenstein ALA. Respiratory bronchiolitis causing interstitial lung disease. A clinicopathologic study of six cases. Am Rev Respir Dis 1987; 135: 880–4.[Medline]
4 Yousem SA, Colby TV, Gaensler EA. Respiratory bronchiolitis-associated interstitial lung disease and its relationship to desquamative interstitial pneumonia. Mayo Clin Proc 1989; 64: 1373–80.[Medline]
5 King TE. Respiratory bronchiolitis-associated interstitial lung disease. Clin chest med 1993; 14: 693–8.[Medline]
6 Colby TV. Bronchiolitis. Pathologic considerations. Am J Clin Pathol 1998; 109: 101–9.[Medline]
7 Niewoehner DE, Kleinerman J, Rice DB. Pathologic changes in the peripheral airways of young cigarette smokers. N Engl J Med 1974; 291: 755–8.
8 Benumof JL. Special physiology of the lateral decubitus position, the open chest, and one-lung ventilation. In: Benumof JL (Ed.). Anesthesia for Thoracic Surgery, 1st ed. Philadelphia: WB Saunders, Inc.; 1987: 104–24.
9 Benumof JL. General respiratory physiology and respiratory function during anesthesia. In: Benumof JL (Ed.). Anesthesia for Thoracic Surgery, 1st ed. Philadelphia: WB Saunders, Inc.; 1987: 39–103.
10 Sykes MK, Arnot RN, Jastrzebski J, Gibbs JM, Obdrzalek J, Hurtig JB. Reduction of hypoxic pulmonary vasoconstiction during trichloroethylene anesthesia. J Appl Physiol 1975; 39: 103–8.
11 Benumof JL, Alfery DD. Anesthesia for thoracic surgery. In: Miller RD (Ed.). Anesthesia, 5th ed. Philadelphia: Churchill Livingstone Inc.; 2000: 1665–752.
12 Benumof JL. Choice of anesthetic drugs and techniques. In: Benumof JL (Ed.). Anesthesia for Thoracic Surgery, 1st ed. Philadelphia: WB Saunders, Inc.; 1987: 202–22.
13 Guenoun T, Journois D, Silleran-Chassany J, et al. Prediction of arterial oxygen tension during one-lung ventilation: analysis of preoperative and intraoperative variables. J Cardiothorac Vasc Anesth 2002; 16: 199–203.[Medline]
14 Benatar SR, Hewlett AM, Nunn JF. The use of iso-shunt lines for control of oxygen therapy. Br J Anaesth 1973; 45: 711.
15 Light RB, Mink SN, Wood LD. Pathophysiology of gas exchange and pulmonary perfusion in pneumococcal lobar pneumonia in dogs. J Appl Physiol 1981; 50: 524–30.
16 Irwin RS, Martinez-Gonzalez-Rio J, Thomas HM III, Fritts HW Jr. The effect of granulomatous pulmonary disease in dogs on the response of the pulmonary circulation to hypoxia. J Clin Invest 1977; 60: 1258–65.
17 Benumof JL. Hypoxic pulmonary vasoconstriction and infusion of sodium nitroprusside (Editorial). Anesthesiology 1979; 50: 481–3.[Medline]
18 Casthely PA, Lear S, Cottrell JE, Lear E. Intrapulmonary shunting during induced hypotension. Anesth Analg 1982; 61: 231–5.
19 Benumof JL, Wahrenbrock E. Blunted hypoxic pulmonary vasoconstriction by increased lung vascular pressures. J Appl Physiol 1975; 38: 846–50.
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