Abstract

There is no clear indication that regional anesthesia is preferable to general anesthesia for patients with chronic obstructive pulmonary disease (COPD). With respect to postoperative pulmonary complications, the opinions vary [1-4]. In addition, there is no information regarding the degree of pulmonary function abnormality at which the morbidity and mortality risks would outweigh the benefits of elective surgery. Schwaber [5] recommends that only life-saving surgery should be performed when the forced expiratory volume in 1 s (FEV1) is less than 0.5 L. In contrast, Milledge and Nunn [6] found that patients without hypercapnia could safely tolerate surgery even with a FEV1 value of 0.45 L. In a subsequent study, Nunn et al. [2] reconfirmed that the surgery is safe in patients with a FEV1 value of 0.3-1 L. We present a successful regional anesthetic in a patient with severe chronic respiratory insufficiency, a FEV1 value of 0.27 L, and a baseline PaCO2 value of 101 mm Hg. Regional anesthesia for an elective surgery in a patient with such a severe COPD has not been described previously. Case Report A 55-yr-old, oxygen-dependent (2 L/min) woman (153 cm height and 44 kg weight) with severe end-stage emphysema was scheduled for elective left femoral-popliteal bypass with synthetic graft. The patient's main complaint was 6 wk of progressive increase in left leg numbness and coldness and left toe pain. An angiogram revealed occlusion of the left superficial femoral artery with distal flow in the area supplied by the popliteal artery. Although the surgery was not urgent, the course of the vascular disease and the present level of patient's continuous discomfort required left lower extremity revascularization. She was orthopneic, used accessory respiratory muscles while breathing at rest, and stated that this represented more or less her baseline. Because of her severe chronic dyspnea, and now her left leg pain, she was mostly bedridden. Her pulmonary function tests before surgery were: FEV1 0.27 L (12% predicted), forced vital capacity (FVC) 1 L (35% predicted), FEV1/FVC 0.27, and forced expiratory flow after 25%-75% of vital capacity has been expelled 0.13 L/s (5% predicted). Preoperative arterial blood gas analysis showed: pHa 7.29, PaCO (2) 101 mm Hg, PaO2 154 mm Hg, base excess (BE) 22 mmol/L, HCO3 49 mmol/L, SaO2 99%, and hematocrit 31%. The patient's preoperative medications included prednisone 7.5 mg by mouth every day, triamcinolone two inhalations four times daily, albuterol two inhalations four times daily, atrovent two inhalations three times daily, pirbuterol two inhalations four times daily, and continuous oxygen 2 L/min. She took all medications on the day of surgery. In addition, she received 100 mg of hydrocortisone IV preoperatively. She became visibly distressed and dyspneic during assisted transfer from the stretcher to the operating room table. Our anesthetic plan included continuous spinal anesthesia, routine monitoring, and an arterial line placement. No sedation was given at any time. Throughout the surgery, oxygen was administered nasally at rate of 2 L/min. An epidural set was used to perform continuous spinal anesthesia (18-gauge Touhy needle, 20-gauge catheter). The catheter was threaded intrathecally at the L3-4 level with the patient in the sitting position. Central venous monitoring was not used because it seemed that even a brief head-down positioning for placement of central venous access would be difficult because of the patient's orthopnea while awake. Her blood pressure (BP) before the administration of the local anesthetic was 150/60 mm Hg, and her heart rate was 80 bpm. For surgery, a semisitting position was used. The initial anesthetic consisted of 7.5 mg of isobaric 0.5% bupivacaine followed by an additional 5-mg dose 15 min later. Her BP at that time was 150/75 mm Hg, and her heart rate was 75 bpm. A good sensory and motor block to the T10 level was achieved, but the patient still felt the placement of the Foley catheter; therefore, an additional 3 mg of 0.75% hyperbaric bupivacaine was given, after which her BP was 130/60 mm Hg and her heart rate was 80 bpm. The patient remained in the semisitting position, and arterial blood gas analysis showed: pHa 7.33, PaCO2 97 mm Hg, PaO2 92 mm Hg, BE 23 mmol/L, HCO3 48 mmol/L, and SaO2 96%. The patient did well for the first 3 h of surgery, until an additional 5 mg of isobaric (0.5%) bupivacaine was administered in response to inadequate anesthesia (leg movement). This was immediately followed by a decrease in BP to 65/35 mm Hg (heart rate 98 bpm), which coincided with acute respiratory distress, confusion, and air gasping. In response to several IV boluses of 100 [micro sign]g of phenylephrine and 5 mg of ephedrine, and a fast infusion of 1 L of crystalloid solution, the BP increased to 120/80 mm Hg, and the respiratory distress resolved. Arterial blood gas analysis revealed: pHa 7.22, PaCO2 109 mm Hg, PaO2 80 mm Hg, BE 17 mmol/L, HCO3 44 mmol/L, SaO2 92%, and hematocrit 23%. However, the BP continued to decrease, which was treated with additional fluids and boluses of ephedrine. The patient showed respiratory distress every time her systolic BP decreased to approximately 90 mm Hg (three events). Finally, the BP stabilized after sufficient IV fluids, including 3 U of packed red cells, were administered. At the end of surgery, the patient was transferred to the intensive care unit. Her BP was 120/70 mm Hg, heart rate was 55 bpm, pHa was 7.23, PaCO2 was 102 mm Hg, PaO2 was 109 mm Hg (on 2 L O2 by nasal cannula), SaO2 was 97%, and hematocrit was 39%. The estimated blood loss during the surgery was 0.8 L. Her intensive care unit course was unremarkable, and the breathing pattern was comparable to that preoperatively. Her postoperative pain was successfully treated with the continuous administration of 0.0625% bupivacaine at the rate of 0.75 mL/h through the intrathecal catheter (11.3 mg of bupivacaine over 24 h), which was removed on second postoperative day. She was transferred to a regular nursing unit on Postoperative Day 2 and discharged home on Postoperative Day 5. Discussion General anesthesia for patients with severe COPD has theoretical advantages because it ensures patient cooperation and control of the airway and permits suctioning of bronchial secretions. In contrast, regional anesthesia is characterized by the absence of airway manipulation, minimal alteration of blood gases, and maintenance of ventilatory control, all of which may be advantageous for patients with COPD. However, regional anesthesia is not suitable for all patients and cases. It was not recommended by Safar and Karpinski [7] for patients with COPD because excessive blockade may result in respiratory muscles weakness and impaired cough. Hedenstierna and Lofstrom [8] demonstrated slight hypoventilation in elderly patients undergoing spinal anesthesia compared with those undergoing general anesthesia, which might have contributed to impaired gas distribution and ventilation-perfusion mismatch during the postoperative period in those patients. In contrast, the study by Paskin et al. [9] indicated that a midthoracic level of spinal anesthesia in the emphysematous patients caused only slight, clinically insignificant impairment of forced expiratory muscle function and a moderate increase in physiologic dead space, but alveolar ventilation, blood gas tensions, and respiratory gas exchange were not impaired. It is unclear whether general or regional anesthesia is superior for the patient with severe respiratory dysfunction. Some anesthesiologists believe that pulmonary morbidity in patients with significant, preexisting pulmonary disease is lower in those receiving regional anesthesia, but the accuracy of this theory has never been documented. Ravin [4] demonstrated that spinal anesthesia had no advantage over general anesthesia for lower abdominal surgery in patients with chronic obstructive pulmonary disease. Similarly, Boutros and Weisel [3] did not find any difference in outcome between regional and general anesthesia in patients with severe obstructive pulmonary disease, with respect to postoperative blood gases, pulmonary function studies, and the clinical course. The incidence of mechanically assisted ventilation in the postoperative period in this study was related only to the preexisting degree of pulmonary dysfunction, not to the type of anesthetic [3]. Despite the absence of scientific evidence to support the contention that regional anesthesia provides superior anesthetic management for patients with COPD, Nunn et al. [2] suggested that regional rather than general anesthesia may be safer in patients with severe respiratory dysfunction, because no patient in their review required mechanical ventilation after neuraxial anesthesia. Tarhan et al. [1] reported no deaths in 121 surgical patients with "moderate to severe chronic pulmonary disease" who had spinal or epidural anesthesia; however, 33 of 464 patients who had general anesthesia died from respiratory failure. They did not comment on possible differences in preoperative morbidity between the two anesthetic management groups; patients who received regional anesthesia may have been less sick or undergone lesser surgery. However, they found that thoracic and upper abdominal surgeries, all performed under general anesthesia, were associated with higher mortality. Although there is no clear evidence in the literature that certain anesthetic techniques are superior to others for patients with end-stage COPD, our case shows that elective surgery may be successfully performed in a patient with severe respiratory dysfunction by titrating the local anesthetic during continuous spinal anesthesia, but only if adequate cardiac output and hemoglobin concentrations are preserved. Our case also demonstrates that in patients with limited respiratory reserve, failing to tightly control these variables may lead to acute respiratory distress. In our patient, hypotension occurred because the local anesthetic was readministered intrathecally when unrecognized hypovolemia was present. This decrease in BP resulted in pulmonary hypoperfusion and greater ventilation of physiologic dead space, consequently increasing the work of breathing. These effects in themselves may account for the sudden increase in dyspnea in our patient. In addition, an acute decrease in oxygen delivery resulting from the combined effects of decreased cardiac output (hypovolemia) and acute anemia are potent dyspneogenic stimuli [10] and may have contributed to our patient's respiratory distress. Changes in oxygen delivery are more seriously affected if they occur in the lower range of normal cardiac output and in the range of anemic hemoglobin concentrations [11]. Therefore, even a cardiac output and hemoglobin concentration only slightly below normal may be poorly tolerated in patients with end-stage pulmonary disease. This was obvious in our patient, as the blood transfusion and increase in cardiac output almost immediately resolved the respiratory distress and dyspnea. Therefore, closely monitoring and replacing blood loss, as well as immediately replacing all intravascular volume losses, is necessary to avoid hypotension-induced respiratory distress in these patients. There are few studies of the predictive value of pulmonary function tests in patients with COPD undergoing anesthesia and surgery, and it is still unknown which test is the best predictor of postoperative pulmonary complications. Stein and Cassara [12] found that maximal expiratory flow rate, which correlates best with FEV1, and hypercapnia best predict postoperative pulmonary complications. In their early study, Milledge and Nunn [6] found that only patients with preoperative hypercapnia required postoperative ventilatory support. In a later retrospective analysis, Nunn et al. [2] found that in patients with a FEV1 value less than 1 L, the best predictors of the need for postoperative ventilation were the degree of hypoxemia and whether the patient was dyspneic at rest. Although hypercapnia had no significant predictive value for postoperative ventilation in Nunn et al.'s [2] study, the highest PCO2 value was approximately 50 mm Hg. Our literature search of the English literature (MEDLINE 1966-1997) did not reveal a single study or case report that examined the effects of anesthesia in patients with hypercapnia as severe as that in the patient we describe. Various studies that examined operative risks in patients with COPD used different outcome end points: the need for postoperative mechanical ventilation [2], death [13], or postoperative pulmonary complications [14]. There is no study that suggests specific limits of function below which surgery should not be undertaken. In the study by Nunn et al. [2], all patients with severe COPD and a FEV1 value between 0.3 and 1.0 L undergoing elective surgeries had a relatively uneventful anesthetic and postoperative course; four patients who received postoperative mechanical ventilation had the lowest preoperative PaO2 and underwent surgery under general anesthesia, but it was not clear what criteria were used to determine the need for postoperative ventilation. Milledge and Nunn [6] suggested that low FEV1 and arterial hypoxemia in the absence of hypercapnia should not be barriers to elective surgery, and that only hypercarbia >50 mm Hg may indicate the need for prolonged postoperative ventilatory support. Wong et al. [15] recently found that composite scoring systems, such as the ASA physical status, were the best predictors of postoperative pulmonary complications, whereas pulmonary factors alone did not predict the likelihood of postoperative pulmonary complications in patients with severe COPD. Finally, in the absence of a study that shows otherwise, we agree with Gass and Olsen [16], who suggest that "no preoperative pulmonary function test exists which absolutely contraindicates elective surgery." In conclusion, despite severe dyspnea at rest, low spirometric values, and severe hypercapnia, elective peripheral vascular surgery can be accomplished with a carefully performed regional anesthetic technique, provided that hemodynamic stability and oxygen carrying capacity are maintained.

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