Nitrous Oxide During Surgery

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  • 8/13/2019 Nitrous Oxide During Surgery


    Ventilation with Nitrous Oxide During OpenCholecystectomy Increases the Incidence ofPostoperative HypoxemiaMohammad Maroof, FFARCS, Rashid M. Khan, MD, and Mahmood Siddique, M DDepartment of Anesthesiology, King Fahad National Guard Hospital, Kingdom of Saudi Arabia

    The effect of intraoperative use of air versus nitrousoxide (N,O) on postoperative oxygen 0,) aturation inblood was evaluated in 40 ASA Class I and I1 patientsundergoing elective, open cholecystectomy. Patientswere allocated randomly to two groups on the basis of

    saturation did not differ significantly P > 0.05) be-tween the groups Over the first24 h postoperatively, twas significantly higher p< 0.05) in Group A as corn-pared to Group 48 ki postoperatively.ncidence Ofhypoxemia 0, aturation

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    Table 1. Demographic CharacteristicsSexWeight Hemoglobin Ma1e:Female(No. patients)AgeGroup yr) (kg) gm )

    A, air 37.8 * 9.15 73.5 * 15.15 13.0 1.02 4:16B, N 2 0 38.55 * 8.73 71.75 8.31 12.90 * 0.91 6:14Results are expressed as mean SD, except in last column.

    (5 L/min) for 30-45 min after having recorded the ini-tial O2saturation while breathing room air.Postoperative pain was relieved with a combinationof meperidine (1mg/kg) and promethazine (0.25 mg/kg) administered intramuscularly as required. Postop-erativeO2saturation was monitored by pulse oximetry(OHMEDA BIOX 3700) and recorded by an anesthesi-ologist blind to the group assignment. The same oxime-ter and probe were used in all patients at all time in-tervals during the study period to avoid errors betweendifferent pulse oximeters.O2saturation 0.05). The dose of intraoperative fentanyl was signifi-cantly larger in Group A as compared to Group B, butthere was no significant difference in the dose of post-operative meperidine administered during 48 h to pa-tients of either group (Table2). The incidence of post-operative hypoxemia was nearly similar between thegroups on arrival in the ward from postanesthetic careunit. However, by the end of 48 h there were 40%hy-poxic patients in Group B as compared to none inGroup A (Table 3). Similarly, there was a statisticallyinsignificant P > 0.05) difference in the mean O sat-uration between the groups during the first 24 h, but amarked improvement was observed at the end of 48 hin Group A. By contrast, in Group B patients, mean 0 2saturation continued to deteriorate for the first 48 h.The difference in mean O2 saturation between thegroups was significant P < 0.05) at 48 h (Table 4).

    Table 2. Duration of Surgery and Perioperative Use ofNarcoticsDuration of Intraoperative Postoperativesurgery fentanyl meperidineGroup (min) (I ) (mg)

    A, air 104.20* 19.68 154.50 * 52.51* 325.17 * 25.20B, N 2 0 112.20 * 23.79 117.25* 28.16 330.35 41.07Results are expressed as mean * SD.* P < 0.05.

    DiscussionSeveral factors have been considered responsible forthe pathogenesis of postoperative hypoxemia. Earlypostoperative hypoxemia is caused by a combinationof reduced functional residual capacity resulting fromanesthesia and surgery, development of atelectasis (71,and the respiratory depressant effect of anesthesia andopioid analgesia (2).Similarly, many factors may con-tribute to late hypoxemia, such as an increase inalveolar-arterialPo2difference secondary to persistentreduction in functional residual capacity (8) and alter-ation in the relationship of closing volume to functionalresidual capacity 9). Additional factors, such as im-paired diaphragm function(lo),splinting of ventilationby abdominal distension, and pain (11) leading to ag-gravation in peripheral atelectasis, may add substan-tially to postoperative hypoxemia. By specially design-ing this study, we were able to keep all of the abovevariables plus the duration of surgery and postopera-tive narcotics near constant in the two groups. This en-abled us to show a direct cause-and-effect relationshipbetween the use of N 2 0 or air and postoperative O2saturation.Our study demonstrated that the intraoperative useof N 2 0 for cholecystectomy was associated with ahigher incidence of postoperative hypoxemia (40%). ycontrast, the use of air in place of N 2 0 led to betterpreservation of postoperative O2 saturation as indi-cated by the fact that there was only a 10 and 0incidence of hypoxemia in this group at 24 and 48 h,respectively. Furthermore, the degree of postoperativeO2saturation continued to improve for the first 48 hin patients receiving air intraoperatively. This was de-spite the use of a significantly higher dose of intra-operative fentanyl in Group A to provide satisfactoryanalgesia in lieu of N 2 0 . In contrast, patients receiving

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    Table 3. Incidence of Postoperative Hypoxemia in Two Groups at Different Time Interval


    Postoperative Hypoxemia 0, saturation ~ 9 0 )At arrival in End of first End of firstthe ward, 24 h 48 h

    No.patients No.patients No.PatientsA, air 2 (10) 2* (10) 0 0 )B, N 2 0 3 (15) 8* (40) 8* (40)

    < 0.05.Table 4. Mean O 2 Saturation Characteristics Within First 48 H after Anesthesia

    Postoperative O2 saturation ( )PreoperativeO2 saturation At arrival in End of first End of firstGroup ( ) the ward 24 h 48 h97.15 1.46 93.30 3.76* 93.95 k 3.12* 95.10 k 1.7797.00 1.68 92.35 2.27* 92.05 4.22 91.35 k 4.68*t

    Results are expressed as mean ? SD.P < 0.05 within group paired 1-test).t P < 0.05 compared in between the group unp aired 1-test).

    intraoperative N 2 0 showed gradual deterioration inpostoperative O2saturation during the study period.The difference in the mean O2saturation between thetwo groups was most marked at the end of the first 48h. None of the patients in our series developed clinicalevidence of frank atelectasis or pneumonia that wouldnecessitate chest radiograph or magnetic resonanceimaging postoperatively.That there is no significant difference in the 2 sat-uration between the groups of patients on arrival in theward probably reflects the predominant action of theresidual anesthetics. However, the role of absorptionatelectasis in Group B patients may be observed, evenat this time interval, as a lower mean O2 saturation,although insignificant when compared to Group Apatients.Lampe et al. (6) have reported near identical inci-dence of hypoxemia 02 aturation 4 6 )within thefirst 24 h after anesthesia in patients receiving intra-operative N 2 0 or 100 02. owever, the same groupof workers covering >2 postoperative days of O2sat-uration monitoring have documented a higher inci-dence of hypoxemia in patients receiving intraopera-tive N 2 0 when compared to those receiving 100 0 2(21 versus 15 ,respectively). The findings of thisstudy show a higher incidence of hypoxemia in theN 2 0 group reported by Eger I1 et al. (12) although thedifference remains statistically insignificant. The find-ings of our study are not in total agreement with thoseof Lampe et al. (6) or Eger I et al. (12) mainly becausein their study patients undergoing nonabdominal sur-gery (and hence less prone to hypoxemia) were selectedand 100 O2was used in the control group as opposed

    to air used in our study. We believe that nitrogen or airprovides greater protection against absorption atelecta-sis than does 100 O2and thereby lessens hypoxemia.Furthermore, Lampe et al. (6)and Eger I et al. (12)havedefined hypoxemia asO2saturation

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    short-acting narcotics for maintenance of anesthesiamay be more appropriate in reducing the degree andduration of postoperative hypoxemia in patients un-dergoing open cholecystectomy.We are most grateful to Miss Nerissa Monte Nico for secretarial helpin this manuscript.


    6. Lampe GH, Wauk LZ, Whitendale P, et al. Postoperative hypox-emia after nonabdominal surgery. A frequent event not causedby nitrous oxide. Anesth Analg 1990;71:597-601.7. Hedenstiema G. Gas exchange during anaesthesia. Br Anaesth8. Meyers JR, Lembeck L, OKane H, Baue AE. Changes in func-tional residual capacity of the lung after operation. Arch Surg1975;110:576-83.9. Alexander JI, SpenceAA, Parikh RK, Stuart B. The role of airwayclosure in postoperative hypoxaemia. Br Anaesth 1973;45:36-60.

    10. Ford GT, Whitelaw WA, Rosenal TW, et al. Diaphragm function


    1 .



    after upper abdominal surgery in humans. Am Rev Resp Dis1983;127:431-6.11. Atkinsons ushman GB,L~~ A.Accidents,comp~icationsndsequelae of anaesthesia. In: A synopsis of anaesthesia. Bombay:KM Varghese Company, 1987321-2.12. Eger 11EL L a m p GH, Wauk LZ, et al. Clinical pharmacology ofnitrous oxide: an argument for its continued use. Anesth Analg13. Forbes AR, Horrigan RW. Mucociliary flow in the trachea duringanesthesia with enflurane, ether, nitrous oxide and morphine.14. Smith WDA. Pharmacology of nitrous oxide. Int Anesthesiol

    Knudsen J. Duration of hypoxaemia after uncomplicated upperabdominal and thoracoabdominal operations. Anaesthesia 1970;Jones JG, Sapsford DJ, Wheatley RG. Postoperative hypoxaemia:mechanisms and time course. Anaesthesia 1990;45:566-73.Reeder MK, Goldman MD, Loh L, et al, ~~~~~~~~~~i~~y-poxaemia after major abdominal vascular surgery. Br Anaesth1992;68:23-6. 1990;71:575-85.cawleyH, Dundee JW, Attempts to reduce respiratoryplications following upper abdominal operations. Br Anaesth1981;531073-8. Anesthesiology 1977;46:319-21.Web SJS, Nunn JF. A comparison between the effect of nitrousoxide and nitrogen on arterial Po*.Anaesthesia 1967;22:69-80.


    Clin 1971;9:91-123.