Correspondence
Anesthesiology
N Engl J Med 1998; 338:684-687March 5, 1998
- Article
To the Editor:
In an otherwise excellent and long-overdue review of anesthesiology, Wiklund and Rosenbaum (Oct. 16 and 23 issues)1 have included several errors. Their discussion of halothane, in the section on inhalational anesthetics in part 1, states, “Hepatotoxicity has not been reported in children.” In fact, halothane hepatitis has been reported in children, although it is generally agreed that the incidence in children is lower than that in adults.2 The authors also state, “Desflurane is highly fluorinated, nearly as insoluble as nitrous oxide, and as potent as isoflurane.” One of the minor disadvantages of desflurane is that it is the least potent of any of our modern anesthetics, with a minimal anesthetic concentration (expressed as a percentage of 1 atmosphere) of 7.2 percent in young adults as compared with 1.19 percent with isoflurane.3
In part 2 of their review, the authors note, “Toxic effects in the central nervous system and cardiovascular system occur at the same blood level of bupivacaine.” In fact, as with all local anesthetics, central nervous system toxic effects with bupivacaine (seizures and coma) occur at lower doses and blood levels than cardiac toxic effects, although the difference with bupivacaine is definitely smaller than that with lidocaine.4
4 ReferencesRobert G. Merin, M.D.
Jerry L. Brown, D.O.
Medical College of Georgia, Augusta, GA 30912-27001
Wiklund RA ,Rosenbaum SH . Anesthesiology. N Engl J Med 1997;337:1132-41, 1215
Full Text | Web of Science | Medline2
Stock JG ,Strunin L . Unexplained hepatitis following halothane. Anesthesiology 1985;63:424-439
CrossRef | Web of Science | Medline3
Eger EI II . New inhaled anesthetics. Anesthesiology 1994;80:906-922
CrossRef | Web of Science | Medline4
Feldman HS ,Arthur GR ,Covino BG . Comparative systemic toxicity of convulsant and supraconvulsant doses of intravenous ropivacaine, bupivacaine, and lidocaine in the conscious dog. Anesth Analg 1989;69:794-801
Web of Science | Medline
To the Editor:
Drs. Wiklund and Rosenbaum neglect to inform the reader of the important role of the anesthesiologist in monitoring the patient's body temperature and maintaining normothermia (37°C). In cardiac surgery and neurosurgery, temperature fluctuations are accepted and are often an integral part of the technique. In these cases, the patient's temperature is closely monitored and may be actively returned to normal postoperatively. In other situations, the patient's perioperative temperature is allowed to fall for little scientific or medical reason. One method to prevent infection is to maintain normothermia during surgical procedures. Mild perioperative hypothermia is common during major surgery and may promote surgical-wound infection and dehiscence. Hypothermia impairs immune function and, by triggering thermoregulatory vasoconstriction, decreases subcutaneous oxygen tension. Reduced levels of oxygen in tissues impair oxidative killing through secondary effects on granulocyte chemotaxis.1 There are the additional, well-appreciated risks of increased blood loss, hemodynamic instability, and myocardial ischemia, especially in elderly patients.2 Kurz and colleagues showed that the maintenance of normothermia in patients undergoing colorectal surgery significantly reduced wound-infection rates from 19 percent to 6 percent. This allowed earlier removal of sutures, establishment of oral intake, and a reduction in the hospital stay of 2.6 days.3
Methods to prevent perioperative heat loss and consequent heat debt include the control of the patient's thermal environment throughout the hospital stay. In addition, warming of all intravenous fluids, use of heat and moisture exchangers, insulation, and convective warming mattresses ensure that unintentional heat loss is prevented.
3 ReferencesDavid Watson, F.R.C.A.
Edinburgh Royal Infirmary, Edinburgh EH3 9YW, United KingdomIan F. Laurenson, M.R.C.P.
University of Edinburgh Medical School, Edinburgh EH8 9AG, United KingdomAlastair F. Nimmo, F.R.C.A.
Edinburgh Royal Infirmary, Edinburgh EH3 9YW, United Kingdom1
Salo M . Hypothermia and infection. Acta Anaesthesiol Scand 1994;38:199-200
CrossRef | Web of Science | Medline2
Bush HL Jr ,Hydo LJ ,Fischer E ,Fantini GA ,Silane MF ,Barie PS . Hypothermia during elective abdominal aortic aneurysm repair: the high price of avoidable morbidity. J Vasc Surg 1995;21:392-402
CrossRef | Web of Science | Medline3
Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization.N Engl J Med 1996;334:1209-15.
To the Editor:
Wiklund and Rosenbaum briefly discuss preoperative cardiac-risk stratification. The authors state that resting ventricular function provides an accurate indication of cardiac risk in patients with congestive heart failure and that “an ejection fraction of less than 35 percent in patients undergoing abdominal aortic surgery is known to be associated with the greatest risk of postoperative cardiac decompensation, myocardial infarction, or cardiac death from cardiac causes.” These statements contradict the literature on the relation between the ejection fraction and adverse postoperative cardiac events. Studies have shown that patients with ejection fractions of less than 35 percent can undergo major vascular surgery with an acceptable rate of 30-day mortality.1 Other studies have shown no correlation between the ejection fraction and the incidence of postoperative myocardial infarction or death.2 In a prospective study comparing the use of the ejection fraction with that of dipyridamole–thallium imaging before aortic operations, the ejection fraction was an inferior predictor of postoperative cardiac events.3 A recent report examined the use of echocardiography to assess cardiac risk before noncardiac surgery. An ejection fraction of less than 40 percent did not add significantly to predictive models containing clinical risk factors.4
The ejection fraction should not be used as the primary tool to identify high-risk patients before noncardiac surgery, as Wiklund and Rosenbaum imply. The ejection fraction may, on occasion, supplement the history and physical examination in the preoperative assessment. The physiologic state of the patient — that is, how well compensated the congestive heart failure is at the time of surgery — is a better determinant of the postoperative outcome than the ejection fraction alone.
4 ReferencesDaryl Potyk, M.D.
Internal Medicine Spokane, Spokane, WA 99220-25551
Kazmers A ,Cerqueira MD ,Zierler RE . Perioperative and late outcome in patients with left ventricular ejection fraction of 35% or less who require major vascular surgery. J Vasc Surg 1988;8:307-315
CrossRef | Web of Science | Medline2
McCann RL ,Wolfe WG . Resection of abdominal aortic aneurysm in patients with low ejection fractions. J Vasc Surg 1989;10:240-244
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McPhail NV ,Ruddy TD ,Calvin JE , et al. Comparison of left ventricular function and myocardial perfusion for evaluating perioperative cardiac risk of abdominal aortic surgery. Can J Surg 1990;33:224-228
Web of Science | Medline4
Halm EA ,Browner WS ,Tubau JF ,Tateo IM ,Mangano DT . Echocardiography for assessing cardiac risk in patients having noncardiac surgery. Ann Intern Med 1996;125:433-441[Erratum, Ann Intern Med 1997;126:494.]
Web of Science | Medline
To the Editor:
In their review, Wiklund and Rosenbaum describe the use of nonsteroidal antiinflammatory drugs (NSAIDs) as part of the multimodal approach to pain relief. The authors recommend ketorolac and piroxicam as the NSAIDs of choice for the treatment of postoperative pain. This recommendation is surprising, because these drugs are among the NSAIDs with the worst risk–benefit ratios. Piroxicam is one of the leading NSAIDs implicated in gastrointestinal ulceration, perforation, and bleeding and is also a long-acting inhibitor of platelet aggregation.1,2 Furthermore, its long half-life is a disadvantage in short-term treatment. Thus, piroxicam should not be used for the treatment of postoperative pain. Ketorolac has proved analgesic efficacy but carries a high risk of severe gastrointestinal damage and deterioration of renal function.3 Because of the high incidence of severe adverse effects, ketorolac in oral and parenteral formulations was withdrawn from the markets in many countries. Thus, ketorolac should be used very cautiously as a second-choice NSAID in the multimodal approach to pain relief.
On the basis of the risk–benefit profiles of the currently available NSAIDs, ibuprofen at a dose of up to 1500 mg per day is favorable for the treatment of postoperative pain, if an NSAID is needed. Ibuprofen at this dosage is effective for analgesia, but seldom causes gastrointestinal ulceration, renal failure, or bleeding.1,4
4 ReferencesDirk O. Stichtenoth, M.D.
Jürgen C. Frölich, M.D.
Hannover Medical School, 30623 Hannover, Germany1
Bateman DN . NSAIDs: time to re-evaluate gut toxicity. Lancet 1994;343:1051-1052
CrossRef | Web of Science | Medline2
Koytchev R ,Alken R-G ,Gromnica-Ihle E . Serum concentration of piroxicam and inhibition of platelet aggregation in patients with rheumatoid arthritis and M. Bechterew. Agents Actions 1994;43:48-52
CrossRef | Medline3
Reynolds JEF. Martindale: the extra pharmacopoeia (electronic version). Englewood, Colo.: Micromedex, 1997.
4
Frolich JC . A classification of NSAIDs according to the relative inhibition of cyclooxygenase isoenzymes. Trends Pharmacol Sci 1997;18:30-34
CrossRef | Web of Science | Medline
To the Editor:
Wiklund and Rosenbaum claim that autologous blood transfusion is waning in popularity because of “limited improvement in outcome” and “markedly increased cost.” They cite a cost of $4,783 per unit for autologous transfusion and $68 per unit for allogeneic transfusion. A more reasonable figure for autologous transfusion would be about $25 to $50 more per unit than the cost per unit of allogeneic blood.1 Because about half of all autologous units from donors are discarded, the cost per unit actually transfused may be about $50 to $100 for two units collected. The base-line cost of collecting and processing the discarded autologous unit (perhaps another $60 to $100) might be added, for a maximal total cost of $110 to $200 more than that of a single allogeneic unit.
The reference provided for the marginal clinical utility of autologous blood, and its alleged cost ineffectiveness, is an article published in 1995 in the Journal.2 The authors of that report neglected to incorporate into the costs of perioperative allogeneic transfusion the complications of transfusion-associated immunomodulation, including the prolonged hospital stays and increases in postoperative infections among patients receiving allogeneic blood. These previously controversial complications are now supported by abundant data from animal models and clinical studies, including randomized trials.3 The total costs of allogeneic transfusions are strikingly increased by the acute, postoperative, nonviral infectious complications that often follow, amounting to approximately $1,000 to $2,000 in expenditures per unit transfused.1,4 Unlike Wiklund and Rosenbaum, I suggest that for patients requiring perioperative transfusions, the outcomes will be better and the costs will be lower if the patients are treated with some combination of autologous transfusions, preoperative hemodilution, intraoperative blood salvage, preoperative erythropoietin, and leukocyte-reduced allogeneic transfusions — topics largely unaddressed in the authors' review.
4 ReferencesNeil Blumberg, M.D.
University of Rochester Medical Center, Rochester, NY 146421
Blumberg N ,Kirkley SA ,Heal JM . A cost analysis of autologous and allogeneic transfusions in hip-replacement surgery. Am J Surg 1996;171:324-330
CrossRef | Web of Science | Medline2
Etchason J ,Petz L ,Keeler E , et al. The cost effectiveness of preoperative autologous blood donations. N Engl J Med 1995;332:719-724
Full Text | Web of Science | Medline3
Blumberg N ,Heal JM . Immunomodulation by blood transfusion: an evolving scientific and clinical challenge. Am J Med 1996;101:299-308
CrossRef | Web of Science | Medline4
Jensen LS ,Grunnet N ,Hanberg-Sorensen F ,Jorgensen J . Cost-effectiveness of blood transfusion and white cell reduction in elective colorectal surgery. Transfusion 1995;35:719-722
CrossRef | Web of Science | Medline
To the Editor:
Wiklund and Rosenbaum do not mention the risk of peripheral-tissue necrosis in pressure areas in the preoperative assessment of patients, monitoring during anesthesia, or postoperative complications, despite their comment that the number of patients over 65 years old undergoing noncardiac surgery is likely to double over the next three decades.
Pressure sores are common in elderly patients, and the incidence of intraoperative pressure sores is increasing. Versluysen1 showed that in a group of 100 patients with femoral-neck fractures, sores developed in 66, and in 20 percent of these patients, the sores occurred on the day of the operation. In a prospective study of 125 surgical patients (mean age, 58 years; range, 23 to 84), Kemp et al.2 found that 15 patients (12 percent) had a total of 23 sores, 70 percent of which were first observed when the patients were being transferred from the operating table to the stretcher. Discriminant-function analysis showed that age, time on the operating table (two to more than eight hours), and extracorporeal circulation (including prolonged hypotensive episodes) were significantly associated with the development of sores. Patients undergoing long cardiovascular operations are particularly vulnerable.
2 ReferencesMary R. Bliss, M.B., B.S.
Homerton Hospital, London E9 6SR, United Kingdom1
Versluysen M . How elderly patients with femoral fracture develop pressure sores in hospital. BMJ 1986;292:1311-1313
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Kemp MG ,Keithley JK ,Smith DW ,Morreale B . Factors that contribute to pressure sores in surgical patients. Res Nurs Health 1990;13:293-301
CrossRef | Web of Science | Medline
Author/Editor Response
The authors reply:
To the Editor: The comments of Drs. Merin and Brown are appreciated. Their first point concerns halothane hepatitis in children. The review they cite clearly states that halothane has very little potential for liver damage in children, even with repeated exposure. The citation disputes the diagnosis in the few published reports and questions the presence in children of the metabolic pathways suspected in halothane hepatitis. It cannot be proved that hepatic necrosis has never occurred in a child exposed to halothane; the point we make is that hepatic necrosis is not a major issue in children as compared with adults.
Second, desflurane is one of several anesthetics with potencies of the same order of magnitude — that is, the minimal anesthetic concentration as a percentage of 1 atmosphere is between 1 percent and 10 percent. This range of values provides an acceptable compromise between potency and speed of induction and recovery, as compared with halothane (minimal anesthetic concentration, 0.7 percent) and nitrous oxide (minimal anesthetic concentration, 100 percent).
Finally, we believe our statement that cardiovascular and central nervous system toxicity occurs at bupivacaine blood levels of 3 to 5 μg per milliliter is correct. In the study cited by Drs. Merin and Brown, the administration of bupivacaine at twice the dose required to produce seizures caused death in four of six dogs, as compared with two of six with lidocaine and one of six with ropivacaine. In sheep, cardiovascular collapse occurs at plasma levels of bupivacaine that are only 1.6 times the level associated with the onset of seizures.1 These end points, however, are not clinically comparable, because central nervous system toxicity is usually self-limited and reversible, whereas cardiovascular collapse, especially with bupivacaine, is not. Clinically, the margin of safety is much greater with other local anesthetics.
Watson et al. raise an important issue: control of hypothermia in the operating room. Similarly, Dr. Bliss reminds us of the importance of preventing pressure necrosis. These and many other issues were beyond the scope of our review.
Dr. Potyk is incorrect. We do not recommend use of the ejection fraction “as the primary tool” for preoperative cardiac evaluation. We recommend use of the American College of Cardiology and American Heart Association guidelines to stratify risk.2
Drs. Stichtenoth and Frölich misrepresent our statement about ketorolac and piroxicam. We do not recommend them as NSAIDs of choice. We simply state that these agents provide excellent pain relief after certain procedures, such as laparoscopy, arthroscopy, and even hip arthroplasty.
Dr. Blumberg takes issue with the cost accounting used in an article published in the Journal. Perhaps his comments should be directed to the authors of that article. The direct costs of autologous and directed blood donation are high, and it is not cost effective for the procedures we cited, hysterectomy and transurethral prostatectomy. We agree that autologous donation may be cost effective for some procedures, such as joint replacement, for which autologous donation may eliminate the need for allogeneic transfusion.
2 ReferencesRichard A. Wiklund, M.D.
Stanley H. Rosenbaum, M.D.
Yale University School of Medicine, New Haven, CT 06520-80511
Morishima HO ,Pedersen H ,Finster M , et al. Bupivacaine toxicity in pregnant and nonpregnant ewes. Anesthesiology 1985;63:134-139
CrossRef | Web of Science | Medline2
Guidelines for perioperative cardiovascular evaluation for noncardiac surgery: report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
Web of Science | Medline
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