Tuesday Morning, April 17, 1973

TUESDAY MORNING, APRIL 17, 1973

8:30 A.M. Scientific Session

Regency Ballroom

17. A New Technique of Treating Esophageal Varices

MITSUO SUG1URA* and SHUNJI FUTAGAWA,* Tokyo, Japan

Sponsored by John E. Connolly

The high incidence of encephalopathy and progressive hepatic failure following portosystemic shunts for esophageal varices led us to abandon this technique. From 1964 to 1967 26 patients underwent simple transection of the thoracic esophagus. Recurrence of variceal bleeding was noted in 4 and esophageal varices disappeared radiographically in only IS patients. The excision of coronary veins plus esophageal transection in 14 patients did not improve the late results.

Our current technique has evolved from these earlier experiences and consists of extensive paraesophageal devascularization up to the tracheal bifurcation, transection of the distal thoracic esophagus, splenectomy, devascularization of the abdominal esophagus and cardia, selective vagotomy and pyloroplasty. Thoracic and abdominal operations are performed through separate incisions and can be done in two stages in poor-risk patients. Since 1967, 74 patients have undergone this new procedure, 14 emergency, 48 elective, and 12 prophylactic. The causes of esophageal varices were: cirrhosis 41, fibrosis 22, extrahepatic portal vein occlusion 7, hepatoma 3, and carcinoma of the pancreas 1. Overall operative mortality was 5.4%. A five-year followup study revealed that six patients died of hepatoma, the esophageal varices disappeared in all cases, and all 60 survivors were free from encephalopathy.

Although a longer follow-up is necessary, our preliminary results are encouraging and warrant further trial.

*By invitation

18. Surgical Management of Scleroderma of the Esophagus

R. D. HENDERSON* and F. G. PEARSON, Toronto,

Ontario, Canada

Misconceptions persist concerning the origin, and treatment of dysphagia in patients with scleroderma. This report of current experience clarifies aspects of pathogenesis, and an approach to treatment is suggested.

In the past four years, we have studied 22 patients with scleroderma, 16 of whom had significant complaints of reflux and dysphagia. In 6 of the 16 symptomatic patients a diagnosis of scleroderma was first made following our clinical assessment and esophageal motility studies. Nine of 16 patients with dysphagia had typical peptic strictures.

Twelve patients were treated surgically: Gastroplasty and Belsey hernia repair-9, Belsey repair-2, Thai esophagogastroplasty-1. Cine barium studies were done in all patients before and after operation. Motility studies were done in all 12 patients pre-operatively, and in 7 patients post-operatively.

Good results were obtained in 10 patients: S are completely asymptomatic; 3 have slight pharyngoesophageal motor dysphagia; 1 has slight gastroesophageal mechanical dysphagia; and 1 patient has symptomatic reflux, but relief of dysphagia. One patient was unimproved. There was one operative death.

There is no evidence that scleroderma results in esophageal stricture, other than by predisposing to reflux. Correction of reflux with dilatation of strictures gives good symptomatic relief. No healing problems were noted.

*By invitation

19. Reappraisal of Adjuncts to Avoid Ischemia in the Treatment of Descending Thoracic Aortic Aneurysms

E. STANLEY CRAWFORD, Houston, Texas

Paraplegia is a dreaded complication associated with excisional therapy of aneurysms involving the descending thoracic aorta. Various methods or adjuncts have been devised to prevent this complication, including bypass shunts of various types and hypothermia. These procedures and improved surgical techniques have reduced this complication to a minimum and it is difficult to determine which is more important. This paper is concerned with a consecutive series of 80 patients in whom descending thoracic aortic aneurysm were removed. Bypass shunts were employed in the first 38 patients. The last 42 patients were treated without special protective mechanisms. Paraplegia was present after operation in 3 of the former and in one of the latter patients. Of the 36 patients undergoing operation electively without shunts, none developed paraplegia and 94.S per cent survived despite being over sixty years of age in most cases. This experience would tend to require reappraisal of need for shunts, and this paper will deal both with this and other parameters in the conduct of operation felt to be more important.

*By invitation

20. Patterns of Myocardial Metabolism During Cardiopul-monary Bypass (CPB)and Coronary Perfusion

O. WAYNE ISOM*, NEIL D. KUTIN*, EMILY A. FALK*

and FRANK C. SPENCER, New York, New York

Much uncertainty prevails about methods of coronary perfusion, tolerance for ischemia, and fibrillating vs beating heart. Therefore, in 35 patients undergoing CPU (30 C) myocardial metabolism was studied during operation and for up to 70 hrs. Paired samples of arterial and coronary sinus blood, obtained from indwelling catheters, were analyzed for PQ2> PCO2> PH, lactate, and enzymes - CPK, LDH, SCOT. In 15 pts undergoing aortic valve replacement, coronary flow rates and myocardial oxygen consumption were also measured. The data, statistically analyzed for over 20 variables, were as follows:

Coronary blood flow (CBF) was 200-300 ml/min, oxygen extraction (AA-V) 2.5-3.0 vol %; MVO2 6-8 ml/min, about 20 per cent of normal. The table shows little difference between fibrillating (F) and non-fibrillating (NF) hearts, except greater enzyme production in F hearts (p < 0.05). Lactate extraction occurred in about one-half of each group.

	#pts	MVO2 ml/min	A-VO2 vol %	E0₂	%pts ext. Lactate	CPK	LDH	SCOT
NF	9	7.96	3.05	25%	56	206	345	125
F	6	6.13	2.7	24%	44	339	644	127

Marked laclate production (AA-V 85 mg%) occurred with 15 min ischemic periods. Metabolic recovery from shorter ischemic periods occurred in 5-10 min, but longer periods caused permanent alterations of oxygen consumption. An "overperfusion" injury was identified, characterized by localized edema, normal lactate metabolism, and severe arrhythmias (1-3 hrs duration). Coronary perfusion exceeding 300 ml/min led to significantly greater enzyme production than did lower perfusion rates (CPK 344 vs 172, p < 0.01).

Limitations of metabolic studies were found in one patient with a short left main coronary who developed a fatal myocardial infarction. CPK production occurred (A-V CPK 125 units) but lactate metabolism was near normal. The relationship of these data to the pathogenesis of hemorrhagic subendocardial necrosis will be discussed.

*By invitation

21. Anoxic Cardiac Arrest: An Experimental and Clinical Study of its Effects

S. R. K. IYENGAR,* E. J. P. CHARRETTE* and

R. B. LYNN Kingston, Ontario, Canada

"It is important to know not only the survival but also the quality of life after anoxic cardiac arrest," commented Dr. Gerbode in the Thoracic Surgery Forum of the last meeting of the Association. We have been engaged in the study of this problem for the past two years. During phase I of the investigation a correlation between the incidence of subendocardial hemorrhagic necrosis in dogs and anoxic cardiac arrest was established. Simple flushing of the coronary bed during anoxic arrest of 60-75 minutes with a balanced electrolyte solution, designated as "Beks" solution in our laboratory prevented the subendocardial lesions and there was no intraoperative death from low output. Impressed by these results, we have been routinely flushing the coronary bed with the "Beks" solution during aortic valve replacement. The results are being assessed.

In patients with aortic valvular stenosis, it is believed that in addition to left ventricular hypertrophy, the coronary blood flow is interfered with. In the second phase of our programme a canine model in which sub-coronary aortic stenosis was produced to simulate the situation in humans was produced to study the effects of anoxic arrest. The hypertrophied left ventricle was much more vulnerable to anoxic arrest. Whereas the lesions were subendocardial in the normal canine heart, they were extensive and deep in the hypertrophied left ventricle. At present investigation is in progress to study and improve the quality of myocardial function after anoxic arrest in long term canine survivors.

Myocardial damage incidental to anoxic arrest during open heart surgery adversely affects the quality of life and diminishes the maximum benefit that could otherwise be expected. Pharmacologic manipulation and intermittent flushing of the coronary bed during anoxic arrest offers a simple technique which deserves more extensive clinical trial.

*By invitation

22. Profound Local Hypothermia for Myocardial Protection During Open Heart Surgery

RANDALL B. GRIEPP,* EDWARD B. STINSON* and

NORMAN E. SHUMWAY, Stanford, California

Between 7/71 and 6/72, 329 adults underwent cardiac valve replacement (153), or aortocoronary bypass grafting (133), or both (43). The aorta was crossclamped during valve replacement and during the performance of distal coronary artery anastomoses. Local profound hypothermia during aortic cross-clamping was provided by a continuous infusion of normal saline at 4°C. into the pericardial cavity. Coronary artery perfusion was not used. Cardiopulmonary bypass times ranged from 40 to 200 minutes (average 105 minutes), and aortic crossclamp times ranged from 30 to 140 minutes (average 62 minutes).

Twelve hospital deaths occurred, yielding an operative mortality of 3.6%. Six patients could not be weaned from Cardiopulmonary bypass; three died of low cardiac output postoperatively, and three died as the result of factors not related to myocardial function. Average stay in the intensive care unit was 2.5 days, and average hospital stay was 10 days. No correlation is evident between duration of aortic crossclamping and morbidity or mortality.

This experience suggests that profound local hypothermia during aortic crossclamping affords excellent protection of the myocardium during the performance of cardiac valve replacement and aortocoronary bypass grafting.

*By invitation

23. The Hazard of Ventricular Fibrillation in Hypertrophied Ventricles During Cardiopulmonary Bypass

CHRISTOF E. HOTTENROTT,* HENRY J. KURKJI,* JAMES V.

MALONEY and GERALD D. BUCKBERG,* Los Angeles, California

We previously reported left ventricular ischemic damage occurs in most patients dying after Cardiopulmonary bypass, and defined pre- and postoperative factors contributing to this injury. This study provides evidence that any form of ventricular fibrillation during bypass impairs coronary flow to the hypertrophied left ventricle and causes ischemia.

Seven dogs with left ventricular hypertrophy (aortic stenosis 3-5 months) were compared to fifteen normal dogs' to determine how spontaneous ventricular fibrillation (60 minutes) during Cardiopulmonary bypass affects: (I) myocardial function (Sarnoff curves), (2) regional coronary flow (radioactive microspheres), (3) cardiac biochemistry (pH, lactate, potassium) and (4) histochemistry (acid fuchsin).

In normal ventricles, spontaneous fibrillation raised left ventricular oxygen consumption and subendocardial flow and lowered vascular resistance (P < .01). It did not impair myocardial function and biochemistry nor cause histochemical damage. Conversely, when hypertrophied left ventricles fibrillated spontaneously, oxygen consumption failed to rise, vascular resistance progressively increased, and biochemical evidence of severe ischemia occurred (myocardial lactate production, decreased coronary sinus pH, and loss of intracellular potassium, P<.01). Post-bypass ventricular function was depressed and histochemical ischemia was demonstrated. Clinical studies during aortic valve replacement confirmed these experimental findings.

This study shows that while spontaneous fibrillation may be safe in normal hearts, it is hazardous in hypertrophied hearts.

*By invitation

24. Evaluation of Functional, Metabolic and Structural Alterations in the Myocardium During Aortic Cross-clamping

EDWARD A. STEMMER, PETER McCART,* WILLIAM E. STANTON,*

WILLIAM THIBAULT* and JOHN E. CONNOLLY, Irvine, California

Inability of the myocardium to support satisfactory circulation is the most frequent cause of death after open heart procedures. Knowledge of the interrelationships between metabolism, structure and function of the myocardium can prevent deterioration of myocardial function and refractory myocardial failure.

The ability to maintain normal myocardial metabolism, function and ultrastructure was evaluated in 70 dogs undergoing cardiopulmonary bypass with sustained fibrillation, ischemic arrest, topical hypothermia, intermittent coronary perfusion or continuous coronary perfusion. Survival, arterial pressure, central venous pressure, left ventricular pressure, cardiac output, dp/dt, urinary output, myocardial oxygen consumption, myocardial potassium loss, lactate utilization, pyruvate metabolism, light microscopy and electronmicroscopy were studied in each animal during a baseline period, two hour test period and two hour recovery period.

The best survival with the least impairment of myocardial function was observed with continuous hypothermic coronary perfusion. The poorest survival with the greatest impairment of function occurred after normothermic anoxic arrest for more than 60 minutes. Topical hypothermic arrest without coronary . perfusion produced good survival but significantly compromised myocardial function. Electronmicroscopy demonstrated that damage to the mitochondria was associated with poor survival, elevated coronary sinus lactate and poor recovery of rayocardial function. Anoxia aggravated these changes while coronary perfusion minimized them.

11:15 A.M. Address of Honored Speaker

Sir Thomas Holmes Sellers

President, Royal College of Surgeons

THE GENERALITY OF SURGERY

*By invitation