842 BRIT. J. SURG., 1967, Vol. 54, No. 10, OCTOBER

MICROVASCULAR SURGERY BY JOHN R. COBBETT, F.R.C.S.

SENIOR SURGICAL REGISTRAR, QUEEN VICTORIA HOSPITAL, EAST GRINSTEAD

THE technical difficulties associated with small blood- vessel surgery are those of size and accuracy. Inaccuracy may well lead to narrowing or irregularity of the suture line with subsequent thrombosis. The problem of size may be solved by optical magnifica- tion, and that of accuracy by the use of fine instru- ments and by various mechanical techniques.

Suture anastomosis of vessels down to about 0.7 mm. is possible using ophthalmic and jewellers’ instruments with fine monofilament nylon. Inter- rupted sutures following two eccentrically-placed stay sutures are best. Suture methods are reliable, but require practice and are slow.

Staplers are quick but complex; most have a lower size limit of 1.5 mm. although one is available with a bushing size of 1.0 mm.

Spiked rings as used by Nakayama are simpler than staplers and are quick, but have a lower size limit of 2.0 mm.

The Blakemore-Lord cuff ligature technique is quick and simple but may leave some ‘step’ in the vessel lumen, and certainly leaves a rigid tube around the vessel. These factors tend to produce thrombosis in vessels under 3.0 mm.

Adhesives and electrocoaption are promising but lack tensile strength. Adhesives also cause local tissue reaction.

In the Research Laboratory, organ transplantation in the small animal has been made possible by these

techniques. In particular, the immunology of kidney transplantation is being studied in various centres using inbred strains of rats. In the Blond Labora- tories at the Queen Victoria Hospital at East Grin- stead, kidney homotransplantation is being performed in the rat using end-to-end suture of renal artery and vein.

In the clinical field, transplantation of intestine to replace cervical oesophagus has been reported from many centres. Replantation of amputated digits has also been achieved.

CASE REPORT Eight weeks ago a boy of 2: years was admitted, having

injured his right ring finger in a gate. One flexor tendon, two digital nerves, and a small bridge of dorsal skin were intact. The epiphysis of the proximal phalanx had been separated and displaced dorsally out of the wound. All other structures, including the two digital arteries, had been divided. That part of the finger beyond the injury appeared totally ischaemic.

After bony fixation, the radial digital artery was trimmed and direct end to-end anastomosis done using IO/O nylon. On release of the vascular clamps, good colour return was seen. Venous return was troublesome for 48 hours though a digital pulse could be demonstrated at all times. After this period, however, venous drainage improved, the finger remained pink and healed well.

Low molecular weight dextran was given postoperatively but no systemic anticoagulants were used. The diameter of the digital artery was approximately 0.7 mm.

HOMOGRAFT REPLACEMENT OF THE AORTIC VALVE BY DONALD ROSS

GUY’S HOSPITAL AND THE NATIONAL HEART HOSPITAL

THE first subcoronary replacement of the aortic valve was done in Guy’s Hospital in 1962 and the longest surviving case is now just over 4 years since operation. Homograft valves appeal to us because they are biological tissues with perfect design characteristics and have a central flow pathway offering no obstruc- tion to the ejection of blood from the left ventricle (Fig. I). An important additional advantage which was not apparent when they were first inserted is the fact that there have been no known embolic compli- cations from these valves in spite of not using anti- coagulants. This is in marked contrast with the mechanical aortic valve prosthesis, where embolism is one of its main disadvantages. Recently the homo- graft valve has been found useful in the treatment of infected valves in cases dying with active bacterial endocarditis. In these, we would hesitate to use a foreign body in the presence of infection but have found it necessary to operate on some of these patients who were dying from the mechanical effects of the

valve regurgitation before the infection was brought under control. In 7 recent cases it has been possible to excise the affected valve and replace it with a

FIG. 1.-Diagram showing the central flow pathway for the blood offered by homograft replacement.

ROSS: HOMOGRAFT REPLACEMENT OF AORTIC VALVE 843

homograft under continued antibiotic treatment for the bacterial endocarditis.

Homograft valves have disadvantages in that there are the problems of procurement, sterilization, and storage of these valves. Also there are technical problems involved in their insertion in order to achieve a competent mechanism, but these can all be overcome with a minimum of organization and effort.

theatre for sizing of the valve orifice at operation. The grossly dissected valves are then immersed in an antibiotic solution, sterilized in ethylene oxide gas, and stored in sterile containers after freeze-drying (Longmore, Lockey, Ross, and Pickering, 1966; Pickering, 1966). Some people store these valves in a nutrient medium like Hank's solution, but there is no evidence thus far that there is any advantage in trying to maintain the valves in a semi-viable state. In fact we do not know if the living valve survives or is immuno- logically inactive, but do know that these dead freeze- dried valves excite no immunological reaction (Davies, Lessof, Roberts, and Ross, 1965). Betapropiolactone

A B

as a result of redissection of an aortic root. FIG. 2.-A, An aneurysmal dilatation of the ascending aorta in Marfan's disease. 6, An avulsed homograft commissure at 8 months

The valve is used electively in all cases of isolated aortic valve stenosis and regurgitation, but, where there is an aneurysmal aortic root, as in Marfan's disease with cystic medionecrosis (Fig. 2A), the ascending arch is usually resected, replacing it with a Dacron prosthesis, and at the same time the valve with a mechanical prosthesis. Indeed the only known late failure of a valve in this series was in a patient of this type in whom the valve was replaced with a homograft and the aneurysmal aorta was excised elliptically. A redissection occurred at 8 months with the onset of left ventricular failure. At reoperation one cusp was found to be avulsed and the valve had to be replaced with a mechanical prosthesis (Fig. 2B). Also in cases of mixed valve disease, where it has been necessary to put a mechanical prosthesis in the mitral orifice, a mechanical prosthesis is used in both valve areas in the interests of speed instead of a homografted aortic valve. But it is hoped that mitral homograft valves will he used more often in future (one successful case of combined aortic and mitral homograft valves is now 6 months postoperative).

COLLECTION AND PROCESSING Valves are collected under unsterile conditions, if

possible from young donors, and as soon as possible after death. They are selected on their gross macro- scopic appearance and in addition are tested for tear- out strength before being accepted. They are then graded according to size, with obturators of internal diameter, increasing by I-mm. increments (Fig. 3). An identical set of obturators is, of course, kept in the

has been advocated as a sterilizing medium but has not been used in this series and apart from the case mentioned above there have been no known cases of

FIG. 3.-A set of cylindrical obturators for sizing the aortic root and homograft valve.

rupture in these grafts, but both betapropiolactone and freeze-drying may have deleterious effects and pre- dispose to late valve failure (Smith, 1967).

At operation a suitable sized freeze-dried valve is selected and is reconstituted within 15-20 minutes by immersion in a penicillin saline solution kept at 40" C.

TECHNIQUE OF INSERTION This has evolved over the past 4 years (Ross, 1967)

from a single layer of continuous sutures to a double layer of sutures (Barrett Boyes, 1965), to our present method of multiple interrupted sutures. At present

844

all soft muscular tissue is cut away from the lower margin of the graft (Fig. 4) which is then accurately matched to the site of the original valve excision and

BRIT. J. SURG., 1967, Vol. 54, No. 10, OCTOBER

of about 80 per cent in our early technique (Duran and Gunning, 1962) to about 40 per cent by the sub- sequent technique (Barrett Boyes, 1965), to about 24

A B FIG. 4.-A, A reconstituted homograft being dissected at the time of operation. B, The excised muscle and mitral valve tissue

removed from the lower margin of the graft.

FIG. S.-Technique of insertion of the lower margin of the homograft with multiple interrupted 4-0 mersilene sutures.

FIG.

per cent by our present methods. Now the regurgita- tion is usually detectable by a diastolic murmur only and haemodynamic evidence of regurgitation is unusual.

RESULTS Just over 2-30 aortic homografts have now been

inserted for isolated aortic valve disease and also for multi-valve disease and the difficult combination of

FIG. 7.-Radiograph of a homograft removed at 3+ years. This shows scattered calcium in the donor aortic wall, but also a focus of calcium in the thickened and regurgitant cusp. The other cusps were thin and pliable.

fmed in dace with between do and 4 4 multide inter-

6.-Reconstruction of the pulmonary outflow of Fallot with pulmonary atresia.

tract in cases

ventricular septa1 defect associated with aortic regurgitation. A small number of cases of pulmonary atresia have had a new right ventricular outflow tract constructed with an aortic homograft together with a segment of ascending aorta (Ross and Somerville, 1966) (Fig. 6). There has been a steady decline both in the hospital mortality, reflecting our increasing experience, and in our late deaths, presumably as a result of the reduced incidence of regurgitation.

PATHOLOGY Our first case operated upon died approximately 2

months ago. 44 vears from the time of his orirrinal rupted 470 sutures (Fig. 5). Adrtic reg&gitati&, which - _ was a major problem, has fallen from an incidence operation. His valve had been regurgitant from the

CARRUTHERS AND PARSONS : VENOUS PRESSURE MONITORING 845

time of its insertion and he died finally in left ventri- cular failure, before a second operation was done. At autopsy the valve showed considerable calcification within the donor aortic wall of the homograft. Some of this was residual calcification incompletely removed at the first operation, but the great bulk of it was undoubtedly calcium deposition in the donor aortic wall. The cusps, however, appeared to be largely free from calcification. Two other cases (39 and z+ years postoperative) have also been operated upon recently, electively, for persistent aortic regurgitation. Again both of these cases show fairly heavy calcification in the donor aortic wall but not in the cusps, which remain pliable. However one valve showed striking changes in that the regurgitant cusp only was thickened and on closer examination, and radiographic examination, this thickened cusp showed a small centre of calcification (Fig. 7).

Table Z.-TOTAL NUMBER OF HOMOGRAFTS INSERTED AT GUY’S HOSPITAL AND NATIONAL HEART HOSPITAL

I NO. I HOSPITAL DEATHS LATE DEATHS

Aortic stenosis 115 Aortic regurgitation 5 2 Multiplevalvedisease 1 5; 1 V . S . D . and A.R. Fallot 1 3 1

9 4 5 - -

I1 I

I 4

- I=/ I S (7.8 per cent) j (7.2 cent)

Total mortality to date 35 ( 1 5 per cent)

Calcification in the donor aortic wall has been described by Duran, Manley, and Gunning (1965) and has been anticipated in the present series. I t is of interest that the cusps themselves appear to be rela- tively resistant to calcification although there is no evidence of living cells within their substance. I t is easy to speculate that calcification is a result of dead tissue and that it would be avoided if living homo- graft valves were inserted. On the other hand, it is well known that the most heavily calcified valves found at surgery are those occurring on the basis of living congenitally bicuspid valves, so that the presence of a living valve alone is no guarantee in preventing calcification. Also valves which have undergone

pericardial reconstruction procedures have a living pericardial tissue extension but are equally prone to calcification (Bjork and Hultquist, 1964).

I t has been of interest to note the focus of calcifica- tion occurring in the single regurgitant valve described above with the two pliable non-regurgitant cusps remaining calcium-free. Herein may lie a clue to some of the factors determining the laying down of calcification in the aortic area. I t may be that fully functional cusps, which are both non-regurgitant and non-obstructive, will remain pliable while ill- functioning cusps, whether immobile or causing turbulence, seem to predispose to calcification whether the tissue is living or dead.

The aortic outflow area is a position of high velocity flow so that any obstructive or abnormal flow pathway would be likely to give rise to considerable turbulence. In this respect it has been interesting that the study of failed mechanical prostheses has revealed that all cases of plastic and silastic ball failure has been confined to the aortic area, while the mitral valve area with its low pressure flows has remained immune (Starr, Pierie, Raible, Edwards, Siposs, and Hancock (1966). A great deal remains to be learnt about the factors

determining calcification here as in other areas of the body, but our best guarantee of continued function pliability in these homograft valve cusps is presumably to achieve a functionally perfect and competent valve without leaks or obstructive turbulence.

REFERENCES BARRETT BOYES, B. G. (1965), B r . J . Surg., 52, 847. BJORK, V. O., and HULTQVIST, G. (1964),J. thorac. cardio-

vasc. Surg., 47,693. DAVIES, H., LESSOF, M. H., ROBERTS, C. I., and Ross, D. N.

(1965), Lancet, I, 927. DURAN, C. G., and GUNNING, A. J. (1962), Zbid., 2,

488. -- MANLEY, G., and GUNNING, A. J. (1969, Br. J.

surg., 52, 547. LONGMORE, D. B., LOCKEY, E., ROSS, D. N., and

PICKERING, B. N. (1966),Lancet, 2,463. PICKERING, B. N. (1966), Guy’s Hosp. Rep., 115, 10s. Ross, D. N. (1967), B r . J . Surg., 54, 165. -- and SOMERVILLE, J. (1966), Lancet, 2, 1446. SMITH, J. C. (1967), Thorax, 22, 114. STARR, A., PIERIE, W. P., RAIBLE, D. A., EDWARDS, M. L.,

SIPOSS, G. G., and HANCOCK, W. D. (1966), Circulation, 33, Suppl. I, 11s.

THE VALUE OF CENTRAL VENOUS PRESSURE MONITORING IN THE TREATMENT OF ACUTE RENAL DYSFUNCTION

BY R. K. CARRUTHERS AND F. M. PARSONS RENAL RESEARCH UNIT, THE GENERAL INFIRMARY, LEEDS

AN episode of reduced renal blood-flow may lead to acute tubular necrosis. Under these circumstances the organic change in the renal tubules is preceded by a period of functional renal failure. This period is now referred to as ‘acute renal dysfunction’ and it is during this time that the progress to tubular necrosis may be arrested and reversed, provided the precipitating cause is diagnosed and corrected without delay.

The majority of cases of acute renal dysfunction are associated with one or more of the following aetiological factors :-

I . Colloid loss (as in haemorrhage and burns). 2. Crystalloid loss (as in vomiting, diarrhoea,

3. Heart failure (e.g. myocardial ischaemia and paralytic ileus, fistula, etc.).

myocarditis).