Total anomalous pulmonary venous drainage

J

THoRAc CARDIOVASC SURG

1989;97:886-92

Total anomalous pulmonary venous drainage Forty-four patients with total anomalous pulmonary venous drainage underwent repair between 1979 and 1987. The anomalous drainage was supracardiac in 16, cardiac in 12, and infracardiac in 16. Median age at repair was 15 days and median weight, 3.3 kg. In 22 patients (50 %) the venous drainage was obstructed. Emergency operation was necessary in 12 patients, and the condition of seven additional patients deteriorated while they were awaiting semiurgent operation. There was one hospital death (mortality rate 2.3 %), occurring in a 2-week-old premature neonate with infracardiac drainage. In 17 of 44 patients, mean pulmonary artery pressure equaled or exceeded systemic arterial pressure immediately after repair. Four patients have required reoperation and two of these have died as a result of peripheral extension of pulmonary vein sclerosis. In the review period of from 1 month to 7 years, aU survivors are well and receiving no medication.

S. Sano, MD, PhD, W. J. Brawn, FRCS, FRACS, and R. B. B. Mee, FRACS,

Melbourne, Australia

Ltal anomalous pulmonary venous drainage (TAPVD) was repaired successfully in 1951 by Muller.' Since then there has been progressive improvement in operative results. However, the surgical mortality varies from 8% to 20% in most series." The mortality rate is higher in the younger infants. The causes for the higher surgical mortality in this group may include pulmonary congestion, elevated pulmonary vascular resistance, and the critical condition of many infants at the time of operation. The rapid development of pulmonary arterial and venous medial hypertrophy has been reported especially in obstructive pulmonary venous drainage. 8, 9 Thus early accurate diagnosis, prompt surgical intervention, and careful preoperative and postoperative care are the keys to success. This report examines our experience with the surgical management ofTAPVD at the Royal Children's Hospi-

tal. Patients and methods Between January 1979 and October 1987, 44 consecutive patients with simple TAPVD admitted to this institution underwent surgical repair. There were 30 boys and 14 girls. Twenty-eight patients were less than I month of age (Table I). From the Departmentof Cardiac Surgery, RoyalChildren's Hospital, Melbourne, Australia. Received for publication March 10, 1988. Accepted for publication Nov. 2, 1988. Address for correspondence: Mr. R. B. B. Mee, Director, Victorian Paediatric Cardiac Surgical Unit, Royal Children's Hospital, Flemington Road, Parkville, Melbourne, Australia. 3052.

886

Table I. Hospital mortality according to age No. of patients

Age (rna)

>1 >3 >6 Total


28 7 7

2

Hospital deaths (No.)

I 0 0 0

44

The median weight was 3.3 kg (2.1 to 11.6 kg). The anomalous drainage was supracardiac in 16 patients, cardiac in 12 patients, and infracardiac in 16 patients (Table II). Four patients with complex TAPVD, associated with major additional cardiac anomalies, were excluded from this series. These included one with a large ventricular septal defect, one with double-outlet right ventricle and ventricular septal defect, one with transposition of the great arteries and ventricular septal defect, and one with hypoplastic left heart syndrome. There was one hospital death in this small group with complex anomalies. The first 14 patients were catheterized preoperatively, but of the last 30 patients, 26 have been evaluated by twodimensional Doppler echocardiography alone. Balloon atrial septostomy was performed in seven of the first 14 patients during diagnostic cardiac catheterization, but in only four of the last 30 patients. In no case did balloon atrial septostomy result in sufficient clinical improvement in critically iII patients to permit deferral of the operation. All patients with infracardiac TAPVD, except one in whom drainage was directly to the inferior vena cava, were considered to have an obstructive lesion and clinically behaved as such. Five patients of 16 with supracardiac TAPVD had a

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887

Table II. Hospital mortality according to anatomic types No. of patients Anatomic type

Obstructive

Supracardiac Cardiac Infracardiac

2 15 (I) [2)

Total

22 (I) [2)

Nonobstructive

Total

II

10 1*

16 (0) [0) 12 (0) [0) 16 (I) [2)

22

44 (I) [2]

5

Parentheses indicate hospital death and brackets, late death. 'Direct drainage to inferior vena cava within pericardium

narrow left vertical vein causing obstruction. Two patients of 12 with cardiac TAPVD had a restrictive coronary sinus ostium. The preoperative condition of all patients is shown in Table III, according to the New York Heart Association (NYHA) functional classification (I to V).lO Emergency operation was performed in 12 patients. Of note, the condition of seven patients deteriorated while they were awaiting semiurgent surgical treatment and necessitated an emergency operation. Preoperative ventilation or inotropic support, or both, was necessary in 17 of 44 patients (39%). Operative technique. Profound hypothermia ( < 18° C) and circulatory arrest with cold crystalloid cardioplegia (appendix I) was used in all patients except for the 3-year-old patient with drainage to the coronary sinus. For profound hypothermia and circulatory arrest the mean time spent on cardiopulmonary bypass was 45 minutes (27 to 74 minutes), mean aortic crossclamp time was 39 minutes (23 to 74 minutes), and mean circulatory arrest time was 32 minutes (19 to 53 minutes) at a nasopharyngeal temperature of 18° C or less. Periods of low flow during repair were not used. The mean cooling time was 12 minutes and the mean rewarming time to a nasopharyngeal temperature greater than 36° C was 22 minutes. The composition of the perfusate and the perfusion method is summarized in appendix II. In all cases of supracardiac and infracardiac TAPVD, the apex of the heart was elevated over to the right side and the anastomosis between the left atrium and common pulmonary vein was constructed according to the method of Williams, Richardson and campbell. II The anastomosis was made as large as possible; occasionally, the common vein incision was extended into a lobar branch and a contiguous portion of the vertical vein was used. An approach across the right atrium was used for repair of intracardiac TAPVD. Coronary sinus drainage was corrected by the method of Van Praagh and associates" in five patients and by excision of tissue between the patent foramen ovale and coronary sinus with pericardial patching in four patients. In the three patients in whom the drainage was to the right atrium, either directly or to the root of the junction of the superior vena cava (SVC) and right atrium, pericardial patching was used. In all patients, communicating veins were either ligated or divided and interatrial communications were either directly sutured or patched with pericardium. Enlargement of the left atrium by pericardial patching of the atrial septal defect was performed in six early patients but has not been regarded as necessary in the past 5 years. The ductus arteriosus (or

m. Clinical condition immediately before the operation

Table

Anatomic types

Supracardiac Cardiac Infracardiac Total

NYHA functional class II

IV

V

Total

0

IO

I 0

9

6 2

7

9

16 12 16

26

I7

44

ligamentum arteriosum) was routinely ligated during the cooling phase. In infracardiac and supracardiac TAPVD, the pulmonary venous-left atrial anastomosis was made with continuous 6-0 or 7-0 Prolene suture (Ethicon, Inc., Somerville, N.J.). Preoperatively, critically ill infants were resuscitated, paralyzed, and their lungs ventilated to allow the emergency operation to proceed under the best clinical condition, Acidbase balance was corrected promptly and inotropic support was used if necessary. Phenoxybenzamine was administered to all patients for a-adrenergic blockade either just before or just after cardiopulmonary bypass was begun. Left atrial pressure and pulmonary artery pressure were routinely monitored. The ascending aorta is usually small in patients with TAPVD, and in two patients the aortic cannula was observed to be obstructive immediately after bypass was discontinued. Its immediate removal was followed by hemodynamic improvement in both patients. Postoperatively, all patients were paralyzed and the lungs mechanically ventilated for at least 24 hours. Pulmonary hypertension was managed by a regimen of moderate hyperventilation (arterial oxygen tension maintained between 25 and 35 mm Hg, according to individual patient responses) and continuing a-adrenergic blockade with phenoxybenzamine. Additional vasodilators (prostaglandin E" nitroprusside, nitroglycerin, and occasionally tolazoline) were sometimes necessary for breakthrough pulmonary hypertensive crises.

Results There was one hospital death (hospital mortality rate 2.3%), which occurred in a 2-week-old critically ill patient with infracardiac TAPVD in 1980. The child died of right ventricular failure during a pulmonary

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The Journal of Thoracic and Cardiovascular Surgery

Sano, Brawn, Mee

Table IV. Patients with acute deterioration Age at operation

Anatomic type

2 rno 2 days 1 wk 1 day 1 wk 1 day 2 days

Supracardiac Supracardiac Cardiac Supracardiac Infracardiac Supracardiac Supracardiac

Obstructed drainage

+ + + + +

Admission status (NYHA)

Preop. status (NYHAj

V V V IV IV V IV

V V V V V V V

BAS

+ + +

BAS, Balloon atrial septostomy.

Table V. Data on four patients undergoing reoperation after repair of total anomalous pulmonary venous drainage Case No.

Age at operation

Anatomic type (obstructed drainage)

Reap. interval

3 wk

Infracardiac (+)

1 mo

2

1 wk

Infracardiac (+)

1 mo

3

2 mo

Cardiac (-)

2 mo

4

1 day

Supracardiac (+)

1 mo

Findings Sclerosis of four PVs; wide open anastomosis Sclerosis of four PVs; wide open anastomosis Stenosis at RA-SVC junction Localized stenosis at origin of left and right PVs

Results Four PVs repaired; HD Four PVs repaired; LD SVC repair; SSS; pacemaker; alive and well PVs ostia repaired; alive and well

PV, Pulmonary vein; RA, right atrium; SVC, superiorvena cava; HD, hospital death; LD, late death; SSS, sick sinus syndrome.

hypertensive crisis. This patient had suprasystemic pulmonary artery pressure after being weaned from cardiopulmonary bypass. Pulmonary venous obstruction was clinically apparent in 22 (50%) patients. Seven of these required resuscitation preoperatively and 12 underwent an emergency operation. The condition of seven patients deteriorated while they were awaiting a semiurgent operation, five with obstructive drainage and three with previous balloon atrial septostomy (Table IV). Four of these seven patients were in NYHA class V on admission and required intensive care support (ventilation, dopamine). Initial stabilization led to a decision not to operate until the following day. All four lapsed into progressive acidosis, leading to emergency operation. The other three were in NYHA class IV on admission, with the operation planned in the next day or two. However, the condition of these patients deteriorated in the interim and necessitated intensive care resuscitation and urgent operation. Systemic or suprasystemic pulmonary artery pressure occurred in 10 and 7 of the 44 patients, respectively, immediately after repair. Pulmonary artery pressure in three of the patients with suprasystemic pressure remained unstable in the intensive care unit for more

than 2 days, and one of these patients died during a pulmonary hypertensive crisis. Four of the remaining 27 patients whose pulmonary artery pressure was below systemic soon after repair had unstable pulmonary artery pressure later on. However, pulmonary artery pressure had finally fallen below systemic levels in all patients within 4 days. The 43 early survivors have been followed up clinically from 1 month to 7 years postoperatively (mean 34 months). There have been four reoperations, three for recurrent pulmonary venous obstruction and one for SVC stenosis, and there have been two late deaths in this group (Table V). Of the four reoperations, all were necessary within 2 months after the initial repair. Twoof these patients had had repair of obstructed infracardiac drainage and required reoperation for pulmonary venous obstruction resulting from diffuse fibrosis of all lobar veins. The actual anastomosis between the left atrium and pulmonary venous confluence was wide open in both. Dense fibrosis of the common vein was observedat initial repair. In both patients, reoperation involved plastic repair of all four lobar veins, producing dramatic early relief of pulmonary venous obstruction. However, the fibrotic process recurred early, with bilateral extension and obstruction more peripherally, and resulted in

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Fig. 1. Postoperative left pulmonary arteriogram of patient 2 (Table V) in left anterior oblique (LAO) view shows diffuse stenosis of the pulmonary veins, which were repaired by local angioplasty to all four pulmonary veins. Patient died 6 weeks after reoperation because of recurrent and more distal pulmonary vein stenosis.

death in both patients within 6 weeks of reoperation (Fig. I) . SVC stenosis developed in one patient with TAPVD to the right atrium at the entrance of the SVC (Fig. 2, A); this condition has been surgically relieved (Fig. 2, B) . In the fourth patient with supracardiac drainage, localized stenosis developed at the ostia of all pulmonary veins (Fig. 3) because of fibrosis and thickening, but these stenoses have been surgically relieved and Doppler echocardiogram 3 months after the reoperation showed the drainage to be satisfactory. All 41 currently surviving patients are well and receiving no medication . Follow-up rhythm status. We do not have follow-up Holter monitoring data on the 41 survivors. Only one patient has had symptomatic rhythm problems. This is the patient in whom early reoperation for relief of SVC obstruction resulted in a sick sinus syndrome dominated by bradycardia; the patient was treated by demand ventricular pacing. It is anticipated that later rhythm assessment may show that this series of patients with TAPVD is prone to atrial arrhythmias. Discussion Children with T APVD usually have no other abnormalities, either cardiac or noncardiac. The early mortality rate after repair is now low. Late deaths are

Fig. 2. A, Postoperative SVC angiogram of patient 3 (Table V) shows severe stenosis at the junction of right atrium and SVC with retrograde flow in azygos vein. SVC obstruction was relieved byenlargingthe SVC with a pedicle of right atrial free wall. B, SVC angiogram after reoperation shows improvement in SVC-right atrial junction. RAO. Right anterior oblique.

primarily caused by fibrotic obstruction of pulmonary veins, which occurs in about 5% of all cases of T APVD and about 10% of the infracardiac type. This complication is likely to appear within 6 months of repair. Asymptomatic survival beyond 6 months postoperatively offers excellent long-term results . The majority of patients with TAPVD have severe symptoms, with some in extremis, and only 20% of the

The Journal of

890 Sana. Brawn. Mee

Fig. 3. Postoperativeright pulmonary arteriogram of patient 4 (Table V) in anteroposterior (AP) viewshows stenosis at the

orificeof pulmonary veins, which were successfully openedout 1 month after the initial repair. Patient remains well.

patients survive the first year of life." Surgical repair offers survival, and over the years the hospital mortality rate has fallen from high levels to the order of 8% to 20%.2-7 However, the hospital mortality rate can still be high in neonates with pulmonary venous obstruction who are in poor preoperative condition." 13 In our series, 28 patients (64%) were operated on in the first month of life with one hospital death. Infracardiac TAPVD classically has a higher operative mortality rate than other types.2.5,13,14 In this type, evidence of pulmonary venous obstruction is nearly always present. However, infracardiac drainage produced no significant increase in hospital mortality rate in our patients, which contrasts with the reported series. The importance of the preoperative condition of patients with TAPVD is difficult to determine. Neonates in whom TAPVD is diagnosed tend to be critically ill before the operation. In our series, an emergency operation was required in 12 patients, all neonates with obstruction, 10 of whom had infracardiac T APVD. The condition of seven of 44 patients deteriorated acutely while they were awaiting surgical treatment, which was generally planned within 24 hours of diagnosis, Thus we would recommend that all patients with T APVD have urgent repair before acute deterioration can occur. Exceptions might be those children who are admitted at

Thoracic and Cardiovascular Surgery

an older age in a stable condition without evidence of recent clinical deterioration, or pulmonary venous obstruction. We routinely monitor pulmonary artery pressure after repair, and we note that 14 neonates (50%) had suprasystemic or systemic pulmonary artery pressures when being weaned from bypass; by contrast, of the 16 patients over 1 month of age, only three (19%) had suprasystemic or systemic pulmonary artery pressures. Although in most of the patients pulmonary artery pressure had fallen and was stable in the intensive care unit, seven patients (18%) had unstable pulmonary artery pressure in the intensive care unit, for which additional vasodilators -were required. Pulmonary venous hypertension results in structural changes in the pulmonary veins and in the pulmonary arteries.v? Intimal hypertrophy and fibrosis 'of the pulmonary vessels are a common finding in patients with T APVD, and these vessels are capable of further vasoconstriction in response to stimuli such as infection, hypoxia, hypercarbia, and acidosis. For these reasons, careful attention to postoperative acid-base balance and ventilatory support during paralysis is required. The posterior approach to the left atrium as described by Williams, Richardson, and Campbell 1I has provided excellent exposure, allowing creation of a wide anastomosis without any problems with orientation or twisting of the suture line. The interatrial septum can be closed by direct suture, without any need to open the right atrium, in patients with supracardiac or infracardiac T APVD. The small size of the left atrium and ventricle has been cited as a cause of postoperative failure of TAPVD repair.i":" and therefore left atrial enlargement has been advocated in this condition. However, there is still controversy about the need for this.v' and for the past 5 years enlargement of the left atrium has not been performed in our unit. Our results support the contention that it is rare for the left ventricle or atrium to be too small to support the systemic circulation. Likewise, controversy has existed about whether the draining vertical vein should be interrupted or not. Our data would suggest that ligation or division of the vein, or both, does not jeopardize the surgical outcome. Reoperation after repair of TAPVD is required in 5% to 20% of cases," 4 usually because of residual anomaly, anastomotic obstruction, or pulmonary venous stenosis, In the combined experience from Green Lane Hospital and the University of Alabama at Birmingham," five patients of 35 early survivors had postoperative pulmonary venous obstruction, in two patients because of an anastomotic stricture and in three because of stenosis of the pulmonary veins. In our series anastomotic stenosis

Volume 97 Number 6 June 1989

had not occurred. It is likely that a continuous suture technique is adequate for an unobstructed anastomosis even in neonates. Pulmonary venous stenosis resulting from thickening and hypertrophy of the endocardium at the pulmonary venous ostia or diffuse fibrosis in the lobar veins has been a problem in three patients, one with supracardiac drainage and two with infracardiac drainage. Diffuse pulmonary venous stenosis in patients with infracardiac drainage could not be permanently corrected, and both patients have died. Friedli," Fleming," and their colleagues reported similar cases in infants with infradiaphragmatic drainage. It seems that pulmonary venous stenosis can be part of the T APVD disease complex regardless of the type of drainage, and the mechanism for this stenosis is unclear. Finally, we believe, as do others, that noninvasive preoperative diagnosis in contrast to invasive diagnosis allows the patients to be in better condition for the operation. This must be of benefit to the final surgical outcome. Although anectodol, this supposition is unlikely to be challenged by a more rigorous scientific study.

Addendum From October 1987 to August 1988, five additional infants with simpleTAPVD (three supracardiac [two obstructed], one cardiac [obstructed], and one infracardiac [obstructed]) have undergone repair, with no deaths. Four patients were less than 3 days old (all obstructed TAPVD) and the patient with unobstructed TAPVD was 27 days old. In addition, two further patients with complex TAPVD (aged 2 and 3 years), with mildly obstructive TAPVD and atrial isomerism, underwent successful repair by Fontan modifications. We thank L. Clark for typing the manuscript.

I. 2.

3.

4.

5.

REFERENCES Muller WHo The surgical treatment of transposition of the pulmonary veins. Ann Surg 1951;134:683-99. Turley K, Tucker WY, Ullyot DJ, Ebert PA. Total anomalous pulmonary venous connection in infancy: influence of age and type of lesion. Am J Cardiol 1979; 45:92-7. Whight CM, Barratt-Boyes BG, Calder AL, Neutze JM, Brandt PW. Total anomalous pulmonary venous connection: long-term results following repair in infancy. J THORAC CARDIOVASC SURG 1977;75:52-63. Katz NM, Kirklin JW, Pacifico AD. Concepts and practices in surgery for total anomalous pulmonary venous connection. Ann Thorac Surg 1978;25:479-87. Hammon JW, Bender HW, Graham TP, Boucek RJ, Smith CW, Erath HG. Total anomalous pulmonary venousconnection in infancy: ten years' experience including studies of postoperative ventricular function. J THORAC CARDIOVASC SURG 1980;80:544-51.

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6. Hawkins JA, Clark EB, Doty DB. Total anomalous pulmonary venous connection. Ann Thorac Surg 1983; 36:548-60. 7. Galloway AC, Campbell DN, Clarke DR. The value of early repair for total anomalous pulmonary venous drainage. Pediatr Cardiol 1985;6:77-82. 8. Haworth SG, Reid L. Structural study of pulmonary circulation and of heart in total anomalous pulmonary venous return in early infancy. Br Heart J 1977;39:8092. 9. Newfe1d EA, Wilson A, Paul MH, Reisch JS. Pulmonary vascular disease in total anomalous pulmonary venous drainage. Circulation 1980;61:103-9. 10. Kirklin JK, Blackstone EH, Kirklin JW, McKay R, Pacifico AD, Bargeron LM. Intracardiac surgery in infants under age 3 months: incremental risk factors for hospital mortality. Am J Cardiol 1981;48:500-6. II. Williams GR, Richardson WR, Campbell GS. Repair of total anomalous pulmonary venous drainage in infancy. J THORAC CARDIOVASC SURG 1964;47:199-204. 12. Van Praagh R, Harken AH, Delisle G, Gross RE. Total anomalous pulmonary venous drainage to the coronary sinus: a revised procedure for its correction. J THORAC CARDIOVASC SURG 1972;64:132-5. 13. Mazzucco A, Rizzoli G, Fracasso A, et al. Experience with operation for total anomalous pulmonary venous connection in infancy. J THORAC CARDIOVASC SURG 1983;85:686-90. 14. Bove EL, de Leval MR, Taylor JFN, Macartney FJ, Szarnicki RJ, Stark J. Infradiaphragmatic total anomalous pulmonary venous drainage: surgical treatment and long term results. Ann Thorac Surg 1981;31:544-50. 15. Burroughs JT, Edwards JE. Total anomalous pulmonary venous connection. Am Heart J 1960;59:913-31. 16. Mattew R, Thilenius OG, Replogle RL, Arcilla RA. Cardiac function in total anomalous pulmonary venous return before and after surgery. Circulation 1977;55:36170. 17. Nakazawa M, Jarmakani JM, Gyepes MT, Prochazka JV, Yabek SM, Marks RA. Pre- and postoperative ventricular function in infants and children with right ventricular volume overload. Circulation 1977;55:47983. 18. Kirklin JW, Barratt-Boyes BG. Total anomalous pulmonary venous connection. In: Kirklin JW, Barratt-Boyes BG, eds. Cardiac surgery. New York: John Wiley & Sons, 1986:499-523. 19. Friedli B, Davignon A, Stanley P. Infradiaphragmatic anomalous pulmonary venous return: surgical correction in a newborn infant. J THORAC CARDIOVASC SURG 1971; 62:301-6. 20. Fleming WH, Clark EB, Dooley KJ, et al. Late complication following surgical repair of total anomalous pulmonary venous return below the diaphragm. Ann Thorac Surg 1979;27:435-9.

Appendixes I and II on page 892.

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Appendix I. Royal Children's Hospital cardioplegia routine for patients under 10 kg Composition A. One bag of base solution-385 mI Na+ (mrnol/L) 23 K+ (rnmol/L) 15 Ca '" (mmol/L) 0.35 ci- (rnmol/L) 39 Glucose (gm) 2.52 Mannitol (gm) 2.48 Total (mrnol/L) 106 B. 100 ml 25% human albumin

Composition-Cont'd C. 26 ml (I ampule) modified cardioplegic buffer solution Na,CO, (gm) 0.28 NaHCO, 0.81 Administration A. Initial dose 110 m1/m'/min for 2 to 4 min (depending on perfusate temperature at time of delivery) B. Subsequent doses 110 m1/m'/min for 2 min at approximately 2Q-min intervals C. Delivery temperature at aortic root 5° to 6° C

Appendix II. Royal Children's Hospital perfusate and perfusion routine for patients below 7 kg A. Perfusate: Composition as below Estimated blood volume of patients 100 ml/kg Q-6 mo 90 ml/kg 6-18 mo When pump prime and patient's blood is mixed, hemoglobin value should be 9 gm/dl Donor blood used: Fresh heparinized «24 hr old) Pump prime diluent Heparin 30 rng/L Bicarbonate 10 mrnol/L Plasma-Lyte 148 Injection* in water (less 30 mI being volume of heparin/dextrose in fresh donor unit blood pack) Steroids: Methylprednisolone, 20 mg/kg (body weight) B. Flow rate (basic): 150 ml/kg body weight C. Perfusion pressure I. Depends on patient size 2-3 kg 25-35 mm Hg 3-5 kg 35-45 mm Hg 5-10 kg 45-55 mm Hg 2. Most neonates and infants are treated with phenoxybenzamine, 1-2 mg/kg intravenously before or just as cardiopulmonary bypass is begun, to maintain the above pressure ranges. 3. Under these conditions, flow rates not uncommonly exceed 150 nil/kg (150-250 ml/kg), 4. High perfusion pressures are treated aggressively with vasodilators. D. CPB flow pattern 1. Low flow is not used except momentarily. 2. We either use full flow, greater than full flow, or circulatory arrest. E. Oxygenator From January 1987 we have changed from Shiley'[ and Bentley:j: bubble oxygenators to the COBE membrane oxygenator§ *Travenol Labs, Deerfield, Ill. tShiley Incorporated, Irvine, Calif. tBaxter Healthcare Corporation, Bentley Laboratories, Inc., Irvine, Calif. §Cobe Laboratories, Inc., Lakewood, Colo.