8 THE NATIONAL MEDICAL JOURNAL OF INDIA VOL. 7, NO. I, 1994

Surgery in patients with congenital coagulation disordersV. BHUSHAN, M. CHANDY, U. KHANDURI, D. DENNISON,A. SRIVASTAVA, S. APTE

ABSTRACTBackground. Surgery is occasionally necessary in

patients with congenital coagulation disorders. Majorsurgery for patients with haemophilia was not being done inIndia until recently. This paper reports the experience of asingle referral centre.

Methods. The data of 52 patients who were operatedupon were collected from the hospital records retrospec-tively between 1984 and 1986 and prospectively thereafter.They included the surgical procedure performed, replace-ment therapy used and complications encountered.

Results. Fifty-nine procedures were performed of which26 were major, 30 minor and 3 were diagnostic angiograms.Blood components produced in the hospital blood bankwere commonly used for replacement and primaryhaemostasis was achieved in all patients. Delayed bleedingdue to inadequate factor levels occurred in 12 proceduresand was controlled by increasing the factor replacement.One patient died of suspected acute myocardial ischaemia.

Conclusion. In India surgical procedures can be safelyperformed in patients with congenital coagulation dis-orders.Natl Med J India 1994;7:8-12

INTRODUCTIONNormal haemostasis is altered in patients with haemophiliaor other congenital coagulation defects and any invasiveprocedure in these patients needs to be performed with greatcaution. Surgical intervention is required more often in themthan in the normal population because of complicationsrelated to the underlying haemostatic defect and the inter-vention may be delayed leading to an increased morbidityand mortality. However, surgery done in haste withoutadequate knowledge of the underlying coagulopathy and itsmanagement may lead to an undesirable outcome. Thispaper reports the experience of surgery in patients withhaemophilia or related disorders from a single tertiaryreferral centre.

Christian Medical College, Vellore 632004, Tamil Nadu, indiaV. BHUSHAN, M. CHANDY, D. DENNISON,A. SRIVASTAVA, S. APTEDepartment of HaematologyU. KHANDURI Department of Clinical Pathology

Correspondence to M. CHANDY

© The National Medical Journal of India 1994

PATIENTS AND METHODSFifty-two consecutive patients with congenital coagulationdefects who underwent a surgical procedure at the ChristianMedical College and Hospital (CMCH), Vellore betweenOctober 1984 and March 1993 were included in this study.Patients were either primary attenders at our HaematologyClinic or were referred for surgery by other establishmentsincluding the Haemophilia Federation of India. Threepatients were operated elsewhere and had been referred foruncontrolled bleeding.

A congenital coagulation defect was defined as theinherited deficiency of any of the recognized blood coagula-tion factors including von Willebrand's factor. Patients withplatelet function disorders and acquired coagulation defectswere not included. Surgical procedures included any dentalor non-dental surgical intervention or an invasive diagnostictest. Surgery was classified as major, minor or diagnostic andeither elective or emergency according to common usage.

Close coordination was maintained between the laboratory,blood bank, haematologist and surgeon. A diagnosis of theunderlying coagulation defect was made in all patients.Baseline screening tests included the bleeding time, pro-thrombin time, activated partial thromboplastin time andurea solubility test. Assay for the deficient factor was donewhenever possible by the one-stage method using factor-deficient plasma. 1 (Factor assay was not being done in thishospital on a regular basis before 1985.) For patientswithout a previously diagnosed coagulation defect who hadto undergo emergency surgery, the diagnosis was made bybaseline screening tests and correction studies. Factorinhibitor screening was done and where present, the titre wasexpressed in Bethesda units.? Tests for hepatitis B surfaceantigen and, after April 1988, human immunodeficiencyvirus (HIV) serology were done on all patients preoperatively.

Replacement therapy was planned in advance. The factorlevel required for the procedure and for maintenance wasdecided based on the type of surgical procedure and theunderlying coagulation defect. 3 For all major elective opera-tions, a preoperative factor assay was done on the day of thesurgery an hour after administration of the calculated factor.Postoperative assays were done on an individual basis todecide the amount of factor required or to check the factorlevel if the patient had bleeding in spite of adequate factorreplacement. At least one factor assay was done post-operatively in every patient to document that the trough levelwas being maintained (most patients had two to threeassays). If there was bleeding, the assay was repeated. Forpatients with von Willebrand's disease the bleeding time wasused as an indicator of normal haemostasis."

BHUSHAN et at. : SURGERY IN CONGENITAL COAGULATION DISORDERS

The preparation used for replacement was decided on thebasis of the underlying haemostatic defect and the avail-ability of products. Cryoprecipitate, fresh frozen plasma(FFP), plasma prepared in the hospital blood bank andimported factor concentrates were used. All blood productsincluding batches of factor concentrates were screened forhepatitis B surface antigen and, after April 1988, for HIVantibody. Antifibrinolytic therapy with epsilon amino-caproic acid (EACA) or tranexamic acid was used formucosal procedures in addition to factor replacement.>

The data on patients who had surgery prior to 1986 wascollected retrospectively from their inpatient records. From1987 onwards it was entered prospectively at the time ofsurgery and during subsequent follow up. The replacementtherapy used and its duration was recorded in all patients.Complications looked for included inadequate haemostasisat the time of surgery, late postoperative bleeding, woundhaematomas or infection, congestive cardiac failure relatedto factor replacement and thrombotic episodes. Assessmentof bleeding at the time of surgery was subjective and wasclassified to be either normal or excessive.

RESULTS

Coagulation disordersThe underlying coagulation defects in the 52 patients whounderwent surgical intervention are listed in Table I.Haemophilia A was the commonest diagnosis, followed byvon Wille brand's disease. Only one patient with vonWillebrand's disease was suspected to have an inhibitor.

EpidemiologyThe predominant patient population was male with a sexratio of 12: 1. Among the 4 female patients, 3 had vonWillebrand's disease and 1 had factor XI deficiency. Themedian age of the patients was 20 years (range 1~3 years).Forty-four patients were from the southern states of AndhraPradesh (5), Kamataka (3), Kerala (15) and Tamil Nadu (21).Of the remaining 8 there were 2 each from Delhi and Nepal,and 1 each from Bihar, Chandigarh, Rajasthan and WestBengal.

Surgical proceduresA total of 59 procedures were performed on the 52 patients(6 patients had two procedures at the same sitting and onehad surgery for correction of Volkmann's ischaemic contrac-ture performed in two stages). Twenty-six of the procedures

TABLE1. Diagnosis

Factor VIII deficiency (n=32)Severe « 1%)Moderate (1-5%)Mild (>5%)Not known

Factor IX deficiency (n=5)Severe (1%)

von Willebrand's disease

Factor V deficiency

Others

22424

5

6

4

5*

• includes 1 each of factors VII, X, XI, XIII and combined factor (VIII +IX)deficiency

9

TABLEII. Procedures (n=59)

Diagnostic angiography

Minor procedures

Major proceduresOrthopaedicGeneral surgeryCardiothoracic and vascularNeurosurgicalObstetric and gynecologicalPlastic surgical

3

30

261432232

were major (6 emergency), 30 were minor and 3 werediagnostic angiograms. The major surgical procedures arelisted in Table II. Of the 30 minor procedures, 14were dental(10 dental extractions, 2 extraction and epulis excision and2 dental scaling with curettage). The remaining minorprocedures were wound debridement (5), biopsies (4),circumcision (3), haematoma decompression (1), excision ofsplenic tumour (1), urethrotomy (1) and Hickman catheterinsertion (1).

Replacement therapyBlood components from the hospital blood bank were usedmost commonly. Among haemophilia A patients who hadmajor surgery, 5 received cryoprecipitate with or withoutFFP, 5 received factor concentrates in addition and 3 weremanaged with factor concentrates alone. Of those who hadminor surgical procedures, 16 received cryoprecipitate withor without FFP, 2 received factor concentrate in additionand 1 was administered factor concentrate alone. Amongthe 5 patients with haemophilia B, all of whom had a majorsurgical procedure, 3 were managed with prothrombincomplex concentrate, 1 received FFP and bank plasma inaddition and 1was managed with FFP alone.

All patients with von Willebrand's disease were managedprimarily with cryoprecipitate. One patient however,developed an allergic reaction and showed no improvementin his coagulation parameters. He was suspected to carryan inhibitor to the von Wille brand factor and his dentalprocedure was deferred. He subsequently had dental scalingand curettage using DDA VP. His baseline factor VIII assayincreased from 8% to 23% DDA VP. He was given tranexamicacid in addition and near normal haemostasis was achieved.Thus one patient with factor VII deficiency and the otherwith factor X deficiency were managed with prothrombinconcentrate complex (PCC). Patients with factors V, XI andXIII deficiency were managed with FFP. The amount ofdifferent forms of replacement therapy used for the patientsare listed in Table III.

Antifibrinolytic drugs were used in 16patients (tranexamicacid-13, EACA-3). This group included 12 patients whohad dental procedures, 2 who had procedures involvingmucosal surfaces and 1who had a craniotomy for evacuationof a subdural haematoma. Antifibrinolytic therapy was nevergiven with PCC or when there was haematuria.

Factor replacement was continued till complete healing ofthe wound occurred. The presence of wound infectiondelayed wound healing and was associated with an increasein the duration of factor replacement. For major surgicalprocedures without infection the duration of factor replace-ment was 4-26 days with a mean of 10 days. The 2 patients in

10

TABLEIII. Replacement therapy

Factor VIII concentrate

CryoprecipitateFactor VIII deficiencyyon Willebrand's disease

Fresh frozen plasmaFactor VIII deficiencyFactor IX deficiencyFactor V deficiencyFactor XI deficiencyFactor XII I deficiency

Prothrombin complex concentrateFactor IX deficiencyFactor X deficiencyFactor VII deficiency

162000 units

933 units'782151

268 unitst169374393

63600 unitstt3200 unitstt2800 unitstt

• each unit refers to one bag containing 125-150 units of factor VIIIt each unit refers to one bag containing about 200 ml of plasmatt refers to the respective number of units of the factor that the patient wasdeficient inFor patients with factor IX and factor XII deficiency the number also includes bankplasma

this category who received less than 1 week of therapy haduncomplicated Caesarean sections. The duration of replace-ment for 4 patients with severe wound infection was 35-85days with a mean of 7 days. For the 27 patients who hadminor procedures alone, the corresponding figures foruninfected and infected wounds were 1-11 days (mean5 days) and 7-35 (mean 21 days) respectively.

ComplicationsPrimary haemostasis was achieved in all patients. There wasno unusual blood loss during the surgical procedures. Onepatient had excessive haemorrhage from the surgical wound onpostoperative day 4 which was due to an arterial bleeder. Latebleeding occurred in 12 other patients (5 minor and 7 majorprocedures), 4 to 11 days after surgery. These were thoughtto be due to inadequate factor replacement and were allcontrolled by increasing the factor level. Two patientsdeveloped congestive cardiac failure as a result of the largevolume of FFP transfused. They responded well to diuretictherapy. One of these patients was a 63-year-old malewith underlying ischaemic heart disease who had had a'commando' operation for buccal carcinoma. He died of anacute ischaemic episode 4 days later. Two patients developedGram-negative septicaemia which responded to parenteralantibiotic therapy.

lIIustrative examplesPatient 1. In 1984, a 28-year-old male with haemophilia

was admitted with massive upper gastrointestinal bleeding.In spite of adequate factor replacement he went into shock.A coeliac angiogram showed an arteriovenous malformationin the jejunum. He underwent resection of the arteriovenousmalformation under cover of FFP which was prepared in thehospital blood bank from 60 voluntary donors. The bleedingstopped but on postoperative day 6 he developed a woundhaematoma followed by dehiscence. He also developed Gram-negative septicaemia and congestive cardiac failure possiblydue to the large volume of FFP infused. After a prolongedhospital stay of 35 days he was discharged.

This is an example of an emergency surgical proceduredone when the hospital was not fully equipped for surgery in

THE NATIONAL MEDICAL JOURNAL OF INDIA VOL. 7, NO.1, 1994

haemophiliacs. Adequate factor concentrates were not avail-able, cryoprecipitate was not being prepared in the hospitalblood bank and there were no facilities for factor assays. Thepatient developed complications because of inadequatehaemostasis and congestive cardiac failure because of thelarge volume of FFP that was used as replacement therapy. Italso illustrates the need to look for a local cause in ahaemophiliac who has recurrent gastrointestinal bleeding.

Patient 2. A 14-year-old male was referred to our hospitalin March 1990 with uncontrolled bleeding and infection,following an attempted aspiration of a swollen knee joint.The patient had extensive infection of the right lower limbwith necrosis extending up to the periosteum. He was foundto have haemophilia B and was also HIV positive. He under-went repeated debridement with factor replacement usingPCC in an attempt to salvage the limb. He finally had toundergo disarticulation at the right hip joint. PCC was againused as replacement and preoperative and postoperativefactor IX assays were done to ensure adequate factor levels.A total of 40 000 units of factor IX were used. No unusualbleeding or complications related to factor replacement wereencountered.

This example demonstrates how a relatively complicatedcondition was managed without complications because of theavailability of factor concentrates and adequate laboratoryfacilities.

Patient 3. In 1986 a 14-year-old boy with haemophilia Ahad an osteotomy of the femur performed under cryo-precipitate cover and there was no excessive bleedingduring the procedure. On postoperative day 3, he had severebleeding from the wound which continued in spite of theadministration of additional cryoprecipitate. A factor assaydone showed that its level was adequate. Therefore, he wasre-explored and a bleeding artery was ligated resulting inprompt cessation of haemorrhage.

This example illustrates the importance of a factor assayand the need to look for local causes of bleeding when anadequate level of the deficient factor has been achieved.

Patient 4. In 1992, a 24-year-old male with haemophilia Awas referred for management of uncontrolled haematuria. Acystoscopy showed bleeding from the right ureter. Anangiogram, done under cover of adequate factor VIIIconcentrate, showed an arteriovenous malformation in theright kidney which was embolized.

This example reveals the importance of investigating for alocal cause of bleeding in a haemophiliac with unusual bleed-ing from a particular site.

Patient 5. A 20-year-old male with haemophilia A wasreferred to our hospital in 1991 for management of bleedingfrom a surgical wound 12 days after an above-knee amputa-tion of the right lower limb for gangrene (under factorconcentrate cover). At the local hospital, factor VIIIconcentrate was administered to achieve a peak level of300% for two days during and after the surgery. Sub-sequently, peak and trough levels of 130% and 50%respectively were maintained for 10 days. The hospital thenran out of supplies of factor concentrates and the patientbegan to bleed from the surgical wound. A total of over70 000 units of factor VIII had been used. His examinationshowed an infected wound and the level of factor VIII onassay at admission was 25%. He was managed with antibio-tics, daily dressings and factor cover using cryoprecipitate,FFP and factor concentrates. Factor cover was continued till

BHUSHAN et al. : SURGERY IN CONGENITAL COAGULATION DISORDERS

the wound had healed completely. Peak and trough levels of20% to 40% and 5% respectively were maintained. A totalof28 000 units of factor VII I was used during a 40-day period.

This example illustrates the importance of planned factorreplacement for surgical procedures in patients withhaemophilia. A considerable amount of factor was wastedduring the surgical procedure and in the immediate post-operative period. For any elective surgery the desired factorlevels and the product to be used for replacement should bedecided in advance.

DISCUSSIONMost of the literature on surgery in patients with haemophiliais restricted to individual case reports and does not provide acomplete overview" of the problems encountered. Therehave been only two reports of surgery in a large series ofpatients with haernophilia.i-" But data from Indian centresare scarce and in fact till recently most patients who couldafford it were advised to have surgery abroad.

Surgery in patients with haemophilia was previously doneonly in desperate situations because of the high mortalityrelated to uncontrolled haemorrhage. With fresh bloodalone, the highest concentration of deficient factors thatcould be achieved was 10% to 15% and the procedure-related mortality was over 10%.9,10Safe surgical proceduresin haemophiliacs became feasible after the availability ofblood components. The first advance in the use of replace-ment therapy for haemophilia was in 1961 with the discoverythat the Cohn fraction I contained a high concentration offactor III. 11A few years later, the production of cryoprecipitatefurther improved the treatment of patients with haemophiliaA.12 Factor concentrates became available in the late sixtiesand early seventies. The development of inactivation pro-cedures to render blood products free of viruses ,13techniques to overcome the problem of inhibitors" and therecent availability of recombinant coagulation factors" willmake surgery in patients with haemophilia even safer.

Among the blood components used for replacementtherapy plasma, cryoprecipitate and cryosupernatant are theones used most frequently. FFP has all the coagulationfactors. Cryoprecipitate has factors VIII, fibrinogen, factorXIII and von Willebrand factor; cryosupernatant containsthe hepatic coagulation factors II, VII, IX and X. Theamount of factor replacement required depends on theunderlying haemostatic defect, the volume of distribution ofthe factor, its half-life and the level of the factor required fornormal haemostasis. In factor VIII deficiency, each unit offactor per kilogram body weight raises the factor level by 2%and the half-life is 8 to 12 hours. The level recommended formajor surgery is 80% (100% for neurosurgery) and troughlevels of over 30% should be maintained for 5 to 7 days andover 20% for another 7 to 10 days. However, in this serieswhile the levels for surgery were as recommended the post-operative trough levels of factor VIII were maintained at20% to 40% for a minimum of 10 days if the wounds werehealing normally. This was necessary to reduce cost andconserve the limited supplies of concentrate. Since theincidence of late haemorrhage in this series was similar tothat reported by Kasper et al. 7 the results of a controlled trialcomparing the efficacy of two levels given for differentdurations would be of considerable importance.

11

In factor IX deficiency each unit of factor IX per kilogramraises the factor level by 1% and its half-life is 18 to 24 hours.Fifty to eighty per cent is recommended for surgery andtrough levels should be maintained above 30% for 7 days andabove 15% to 20% for a further 7 to 10days. We maintainedfactor IX trough levels between 15% to 30% for 10 dayspostoperatively.

A closely knit team which includes a haematologist, asurgeon and laboratory personnel is important for a centrewhich undertakes surgery in patients with coagulationdefects. The laboratory should be able to diagnose thehaemostatic defect correctly and do factor assays. Thedecision to operate should be taken after careful evaluationby the haematologist and the surgeon. The haernatologistshould be fully conversant with the amount of replacementtherapy necessary and should calculate the desired factorlevels in advance. For any major surgery it is advisable toadminister the first dose of the factor and do an assay todocument the level before starting the operation.

Postoperative bleeding is a frequent problem encounteredin patients with haemophilia. It occurred in 24% of ourpatients which is similar to that reported elsewhere." Themost likely cause of this is inadequate factor replacement. Ifthe patient has a low factor assay in spite of apparentlyadequate replacement therapy, inhibitors may be present. Ifscreening for these is negative the product being used forreplacement should be checked for its factor content. On oneoccasion we found the level in a batch of factor concentratesto be much lower than the amount indicated. If the patient isbleeding in spite of adequate factor levels other causes forbleeding should be looked for. In most of our patients thebleeding was related to our attempts to manage with lowermaintenance levels. In none of our patients was factorinhibitor detected prior to surgery.

Factor concentrate is the ideal replacement therapy. It iseasy to administer and has a reliable bioavailability withoutthe added risks of congestive failure when the amount offactor to be replaced is high. The products now available arevirus-inactivated and negative for the hepatitis B virus andHIV. However, factor concentrates are expensive. Theinternational price of one unit of factor VIII is Rs 15 and offactor IX Rs 10, so a surgical procedure requiring 20 000 unitsof factor VIII will cost Rs 300 000 for replacement therapyalone. Our poor patients received their factor replacementfree or at subsidized rates. In those who required more thanone surgical procedure we attempted to do both at thesame time and all diagnostic angiograms were immediatelyfollowed by the therapeutic procedure to reduce costs.

We have demonstrated that in India surgical procedurescan be safely performed in patients with congenital coagula-tion disorders if they are undertaken with adequateknowledge of the underlying defect and proper replacementtherapy. Factor concentrates are probably the most con-venient though expensive form of replacement. We hopethat the National Plasma Fractionation Centre in Bombaywill soon be able to provide these at lower cost. However,most procedures, except those requiring a large amount ofreplacement therapy, can be performed under the cover ofblood products which can be easily prepared in hospitalblood banks.

12

ACKNOWLEDGEMENTSThis study was funded in part by the Indian Council of Medical Researchas part of the Collaborative Study on Haemophilia No BMS 46/2/85.Coagulation factor concentrates were received as gifts from Baxter(through Americares), Behring, AlMA and the Haemophilia Federa-tion of India.

REFERENCESBiggs R, Eveling J, Richards G. The assay of antihaemophilic globulin activity.Br 1HaemaloI1955;1:20--34.

2 Kasper C. A more uniform measurement of factor VIII inhibitors. ThrombosisDiathesis Haemorrh 1975;34:612.

3 Menitove JE. Preparation and clinical use of plasma and plasma fractions. In:Williams WJ, Beutler E, Erslev AJ, Litchman MA (eds). Hematology, NewYork:McGraw-Hill,I990:1659-73.

4 Borchgrevink CF, Egeberg 0, Godal HC, et al. The effect of plasma andCohn's fraction I on the Duke and Ivy bleeding times in von Willebrand'sdisease. ACla Med Scand 1963;173:235-42.Walsh PN, Rizza CR, Mathews JM, et al. Epsilon aminocaproic acid therapyfor dental extractions in haemophilia and Christmas disease: A double blindcontrolled trial. Brl HaemaroI1971;20:46~75.

6 Britten AFH, Salzman EW. Surgery in congenital disorders of blood coagula-tion. Surg Gynecol Obstet 1966;123:133~58.

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7 Kasper CK, Boylen AL, Ewing NP, Luck JV Jr, Dietrich SL. Hematologicmanagement of hemophilia A for surgery. lAMA 1985;253:1279-83.

8 Kitchens CS. Surgery in hemophilia and related disorders. A prospective studyof 100consecutive procedures. Medicine [Baltimore] 1986;65:34-45.

9 Davidson CS, Epstein RD, Miller GF, Taylor FHL. Haemophilia: A clinicalstudy of forty patients. Blood 1949;4:97-119.

10 Craddock CG Jr, Fenninger LD, Simmons B. Haemophilia: Problem of surgicalintervention for accompanying diseases: Review of the literature and report ofa case. Ann Surg 1948;128:888-903.

11 McMillan CW, Diamond LK, Surge nor OM. Treatment of classic hemophilia:The use of fibrinogen rich in factor VIII for hemorrhage and for surgery.N Eng/J Med 1961;265:277-83.

12 Pool JG, Shannon AE. Production of high-potency concentrates ofantihemophilic globulin in a closed-bag system. N Engl 1 Med 1965;273:144~7.

13 Schimpf K, Mannucci PM, Kreutz W, el al. Absence of hepatitis after treat-ment with a pasteurized factor VIII concentrate in patients with hemophiliaand no previous transfusions. N Engl 1 Med 1987;316:918-22.

14 Nilsson 1M, Berntrop E, Zettervall O. Induction of immune tolerance inpatients with hemophilia and antibodies to factor VIII by combined treatmentwith intravenous IgG, cyclophosphamide and factor VIII. N Engl 1 Med1988;318:947-50.

15 Schwartz RS, Abildgaard CF, Aledort LM. et al. Human recombinant D:-;A·derived antihemophilic factor (factor VIII) in the treatment of hemophilia A.Recombinant factor VIII study group. N Engl 1 Med 1990;323:I8r)(}.-5.

Costing of a salt iodine monitoring laboratory in Indiac. S. PANDAV, K. ANAND, M. G. KARMARKAR

ABSTRACTBackground. Iodine deficiency disorders (100) are

an important public health problem in India and can be pre-vented by fortifying common salt with iodine. For theiodation programme to be effective, it is necessary tomonitor the iodine content of salt. The National IodineDeficiency Disorders Control Programme recommends thatone salt iodine monitoring laboratory should be set up ineach district.We calculated the cost of setting up such a laboratory in

the year 1993.Methods. We estimated that approximately 6000

samples of salt would be sent annually by health workers tothe district laboratory as part of the routine report system.We calculated the capital cost of the laboratory to includeland, buildings and equipment. The recurrent costs includedsalaries, chemicals and reagents, and maintenance assum-ing a uniform discount of 10%.

All India Institute of Medical Sciences, Ansari Nagar,New Delhi 110029, India

C. S. PANDAV, K. ANAND Centre for Community MedicineM. G. KARMARKAR Department of Laboratory Medicine

Correspondence to C. S. PANDAV

© The National Medical Journal of India 1994

Results. A total of Rs 81 550 would be needed for onesuch laboratory annually, of which Rs 73500 (89%) wouldbe recurrent costs. This comes to Rs 13.60 per sampletested or 5 paise per head per year in a district with anaverage population of 1.7 million. If the building is alreadyavailable and the staff in position only need to be trained,then Rs 16040 per year (equipment, chemicals and operat-ing costs) would be required. This comes to 1 paise perhead per year.

Conclusions. Setting up a salt iodine monitoring laboratory,a vital component for the salt iodation programme, hasmodest cost implications, especially if the building and staffalready exist. This is likely to be the case in most of thedistricts.Natl Med J India 1994;7:12-14

INTRODUCTIONIodine deficiency disorders (100) constitute a major publichealth problem in almost all parts of India. It is estimatedthat 150 million people are at risk for 100 of which 54 millionhave goitre, 2.2 million are cretins and 6.6 million havemilder neurological deficits.' One of the proven methods forpreventing 100 is to supplement common salt with iodine.?It is recommended that the supplementation process should