erwise be necessary. The use of astraight-line, depreciation fundingsystem for capital equipment in hos-pitals not owned by the provincialgovernment cannot help but, duringthese inflationary times, lead institu-tions into obsolescence as a result ofinability to replace worn equipmentand acquire new technology.

For anyone who might think oth-erwise, let me assure you that thefrustration felt by the medicalprofession regarding the funding ofhospitals in Canada is shared equal-ly, if not to a greater degree, byhospital administrators. Attemptingto cope with an increasing numberof legitimate demands with dimin-ishing resources causes one to devel-op an appreciation for the plight ofham in a sandwich.

R. SCOTT ROWANDActing executive director

St. Paul's HospitalSaskatoon, Sask.

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She was admitted to our hospital,where acute emphysematous pye-lonephritis was diagnosed, and 6hours later the right kidney wasremoved.

For these two patients the startinginsulin infusion rate was set at 8 and20 ml/h (1.6 and 4.0 U/h) respec-tively. The rate was adjusted lateraccording to the blood glucose levels(Fig. 1). Within 4 hours after thestart of the infusion the blood glu-cose levels of both patients markedlydecreased, and the levels were main-

tamed in a safe range (4.5 to 14.0mmol/l [80 to 250 mg/dl]) through-out the acute stage of their illnesses.Before the infusion was stopped,when the blood glucose level waslower than 10.9 mmol/l (200 mg/dl),subcutaneous administration of in-sulin was resumed to prevent re-bound hyperglycemia.The treatment I have described

prevented the wide fluctuations inthe blood glucose level so oftenobserved with intermittent insulinadministration or a constant rate of

Modulated intravenousinfusion of insulinTo the editor: Since 1973 severalmethods of continuously infusing in-sulin intravenously have been suc-cessfully used to manage diabeticketoacidosis or nonketotic hyperos-molarity.'7 I treated two critically illpatients with diabetes mellitus byinfusing modulated low doses of in-sulin intravenously.The insulin solution was prepared

by adding 0.25 ml (20 U) of regularinsulin to 100 ml of 0.9% sodiumchloride solution, for a final concen-tration of 0.2 U/ml. The insulin waspumped through the mainline intra-venous tubing at a rate modulatedaccording to the glucose level in adrop of blood obtained by finger-prick. The level was instantly readfrom a reflectance meter (AmesCompany, Elkhart, Indiana) and therate of insulin infusion adjusted bymeans of the sliding scale shown inTable I.The first patient was a

38-year-old man with poorly con-trolled insulin-dependent diabetes.He was admitted to the intensivecare unit with a blood pressure of250/170 mm Hg and acute pulmo-nary edema. The other patient, a42-year-old obese woman, hadnewly diagnosed untreated diabetes.

Insulin infusion Insulin infusionstops

0EE

0U Insulin infusionstops

15

10

*

5

I0 2 4 5 12 16 20 24 28 32

Hours

FIG. 1-Blood glucose levels of two critically ill patients with diabetes mellitus whoreceived a continuous intravenous infusion of regular insulin at a rate modulated bythe blood glucose level, as determined by a bedside reflectance meter (solid line) or alaboratory analyser (broken line). Once the level was below 10.9 mmol/l subcutaneousadministration of regular insulin was resumed (asterisk).

1168 CMA JOURNAL/DECEMBER 15, 1982/VOL. 127

insulin infusion. This approachmight be extended to the manage-ment of most acute diabetic condi-tions, including diabetic coma andpre- and postoperative care of thediabetic patient. It might prove par-ticularly useful in nonspecializedcentres.

ANTOINE GATTEREAU. MD

H6tel-Dieu de MontrealMontreal, PQ

References1. GENUTH SM: Constant intravenous insulin infusion in

diabetic ketoacidosis. J,-IMA 1973: 223: 348-13512. Ktoso.s W. CASEY J. KRAEGEN E, LAZARUS L:

Treatment of severe diabetes mellitus by insulin infusion.Br MedJ 1974:2: 69t-694

3. PAGE MM. ALBERTt KGMM. GREENWOOD R. GUMAAKA. HOCKADAY TOR. LowY C. NABARRO JON, PYKEDA, SONKSEN PH, WATKtNS PJ. WEST TET: Treat-ment of diabetic coma with continuous low-dose infusionof insulin. bid: 687-690

4. KELLER U. BERGER W, RITZ R, TRUOG P: Course andprognosis of 86 episodes of diabetic coma. A five yearexperience with a unifortvr schedule of treatment. Diabe-rologia 1975: II: 93-100

5. SOLER NG, FtTZGERALD MG. WRIGHT AD. MALINSJM: Comparative study of different insulin regimens inmanagement of diabetic ketoacidosis. Lancer 1975; 2:122 1-1224

6. WEST TET, LowY C: Control of blood glucose duringlabour in diabetic women with combined glucose andlow-dose insulin infusion. Br MedJ 1977; 1:1252-1254

7. HAtGH S. TEVAARWERK G3M. HARDING PEG. HURSTC: A method for maintaining normoglycemia duringlabour and delivery in insulin-dependent diabetic women.(art Med Asroc 1 1982: 26: 487-490

Sex rQle ideologyTo the editor. Drs. Leichner andHarper are to be commended fortackling an extremely importantissue in their article "Sex role ideol-ogy among physicians" (Can MedAssoc J 1982; 121: 380-383).

I believe that it is important forall physicians to accept the, premisethat a strongly traditional sex roleideology is not desirable in caringfor women patients. However, Iquestion whether Leichner andHarper's results truly show that"overall, physicians' sex role ideolo-gy is appropriately nontraditional".

I question the validity of conclu-sions based on a 35.6% return ratefor a questionnaire mailed to approx-imately three quarters of the totalnumber of practising physicians inManitoba. With this small returnrate the results cannot reflect thebeliefs of the majority of the sample.The authors point out that the pro-portion of women in the sample isapproximately double that in thetotal physician population and thatin each subgroup, except for psychi-atry, the response rate is significant-ly higher among women than it is

DIARRHEA... RECURRENTABDOMINAL PAIN...huquent cmnplmints heardin the d.*r's oliceDisadeharide malabsorption must be a major considerationin the differential diagnosis. The disaccharide, lactose, isnormally digested by theenzyme, lactase, in the healthy smallintestine. Inadequ4te endogenous lactase results in a gastricresponse to milk. Lactase deficiency has been demonstratedin a numlwr of disorders and can be transient or permanentIt can be of genetic origin and is frequently encounteredin older persons.Prior to LactAid if your patient demonstrated a lactasedeficiency you had only two alternatives:a) Remove milk from the diet6) Prescribe a canned nondactose milk analogNow you have a third alternative: Keep the patient on regularmilk-treated with LactAid luctaise enzyme. The patientadds LactAid to milk to convert the lactose into its digestiblesugars. The level of conversion is easily controlled by theamount of LactAid used, essentially 100% lactose. removalis attained if desired. LactAid lactase enzyme is sold in drugand specialty food stores.LactAid easily and economically modifies fresh, canned orreconstituted milk. LactAid will in fact successfully modifyalmost any fluid dairy product, including infant formulasand tube feedings.LactAid is a yeast-derived Beta-galactosidase i. a carrierof glycerol and water. Please request sample, literature andpatient information/order pad.

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