mv braimbridge, frcs surgical practice and the building up of his

SURGERY OF THE DESCENDING THORACIC AORTAHunterian Lecture delivered at the Royal College of Surgeons of England

on30th April 1963

by

M. V. Braimbridge, F.R.C.S.Surgical Unit, St. Thomas's Hospital;

Late Senior Registrar, Brompton Hospital

JOHN HUNTER RETURNED from the army in Portugal in 1763 to begin hissurgical practice and the building up of his museum. He then made threecontributions to knowledge that are still relevant to the subject of thislecture given two centuries later.The first was his repudiation of the metaphysical and theoretical

approach to surgery that had been prevalent for centuries and its sub-stitution by the precise experimental background it has to-day. In spiteof his introduction being through the dissecting room, he appreciatedthat surgical progress depended on physiological knowledge andexperiment.The second contribution followed long afternoons spent in RichmDnd

Park studying the growth and shedding of deers' antlers, when he notedthat the obliteration of a main artery resulted in its function being takenover by smaller side vessels. This appreciation of collateral circulationled him to his third relevant contribution, when in 1785 he ligated thefemoral artery of a coachman, in the canal which has since borne his name,for a popliteal aneurysm. Seven months later the sac was almost oblit-erated and the leg had suffered no tissue loss. It was the start of safearterial surgery which has progressed until there is now no aneurysmthat cannot be treated.

ANATOMY OF THE DESCENDING AORTAAnatomically the descending thoracic aorta is the continuation of the

arch at the lower border of the fourth thoracic vertebra, though forpractical surgical purposes it may be said to begin beyond the leftsubclavian artery and end at the diaphragm.When its lumen is narrowed, a pressure gradient is formed between

the subclavian artery and descending aorta and collateral circulationdevelops. The aortic intercostal arteries anastomose with branches ofthe axillary artery laterally, internal mammary in front and superiorintercostal artery above. Less important anastomoses are formed bylower branches of the internal mammary artery and by the thyrocervicaltrunk.The collateral pathway is shortest to the first few intercostal arteries,

which become large and tortuous from the mechanical effect of theretrograde flow and erode the adjacent ribs to form the characteristicnotching (Bramwell and Morgan Jones, 1941).

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SURGERY OF THE DESCENDING THORACIC AORTA

Intercostal arteries give off a posterior division from which spinalarteries arise. It is a common belief that blood reaches the spinal cordfrom branches of the vertebral vessels, the anterior and posterior spinalarteries, which form a large median vessel anteriorly and other longitudinalarteries posteriorly. Adamkiewicz had in fact shown in 1882 that thecord was supplied by an inconstant number of spinal branches of cervical,intercostal and lumbar vessels, which divided into small dorsal and largeventral arteries running along the nerve roots. The ventral branchessupplied the adjacent cord through the anterior midline vessel, but hadlittle communication with the areas supplied by other spinal arteries aboveand below. The largest branch, the great spinal artery, usually arose nearthe tenth thoracic vertebra, but could arise from either side at any levelfrom T8 to L3, and it was solely responsible for supplying the lumbar andlower thoracic cord. Kadyi extended this work in 1886 and showedthat the dorsal branches were usually 16-17 in number. The ventralbranches were fewer and larger and usually numbered 5-10 althoughsometimes there were as few as two. The number depended on the siteof origin of the great spinal artery. If it arose in the lower thoracic regionthe ventral branches were few and large, if in the lumbar region theywere more numerous but smaller.

The ventral branches are particularly important because they supplymost of the spinal cord, only the posterior horns and adjacent whitematter receiving blood from the dorsal branches.

The distending force of the blood pressure is usually described as beingresisted primarily by the elastic tissue of the media. The aortic wall has,however, been shown to rely for its strength on fibrous tissue which issituated mainly in the adventitia, where 60 per cent. of its tensile strengthlies, though the media contains some scattered collagen also (Krafka,1939). The normal aortic wall can withstand a pressure of 3,000 mm. Hg(Oppenheim, 1918). The smooth muscle and elastic tissue of the mediasupply elasticity alone (Benda, 1902).

PATHOLOGY

The diseases that affect the descending aorta are congenital, traumatic,inflammatory and degenerative.

The congenital lesion is coarctation, which is of two types, preductal orinfantile where the stenosis is proximal to a persistent ductus arteriosus,and postductal or adult where the coarctation is distal to the duct whichis commonly obliterated. Surgery of preductal coarctation is hazardousfor four reasons: long atretic segments, associated cardiac abnormalities,few collateral pathways and heart failure. Results are poor. Discussionhere will be confined to the commoner postductal or adult type.

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M. V. BRAIMIBRIDGE

The acquired lesions of the aorta are primarily trauma, syphilis,arteriosclerosis and cystic medial necrosis. The first three damage thefibrous tissue of the aorta, which dilates and becomes aneurysmal. Thepreponderance of syphilis as a cause of thoracic aneurysms has beenreduced by penicillin, the automobile and an ageing population, but it isstill responsible for a third of descending aortic aneurysms (DeBakey et al.,1958). Endarteritis of the vasa vasorum causes nutritional failure,collagen is laid down and the adventitia and media are replaced by toughscar tissue, which makes the healed syphilitic aorta stronger than normal(Forbus, 1943). Active disease allows necrosis to outstrip fibrous replace-ment in localized areas and the characteristic saccular aneurysm is formed.Extension of disease into, and pressure on, the vertebral bodies accountsfor the prominence of bone erosion (Forbus, 1943).

Arteriosclerosis or atheroma begins as a plaque in the intima, but thereis degeneration and lipoid deposition in the overlying layers. The aorticwall is more diffusely weakened than in syphilis and a fusiform aneurysmresults.

Indirect trauma to the aorta follows automobile and aeroplane accidents,when sudden deceleration makes the descending aorta act as a solid viscuscarried forward by its own momentum. Closure of the glottis at themoment of impact fixes the diaphragm and lung hilum and considerablestrain is therefore placed on the aorta, which ruptures at the level of theligamentum arteriosum by which it is fixed to the pulmonary artery (Hass,1944). Complete rupture of the aorta is not always immediately fatal asthe blood may be contained by the surrounding fascia forming a fusiformaneurysm (Gerbode et al., 1957). Rupture of one quadrant produces asaccular aneurysm, and a split in the intima may start a dissection.

Cystic medionecrosis is basically a degeneration of intercellular groundsubstance and the layers of the media appear histologically to be filledwith mucinous material which allows them to split like wet blotting paper.Its aetiology is unknown, but a genetic factor may be involved as it isparticularly common in Marfan's syndrome and coarctation. It isassociated with spontaneous dissecting aneurysms, the aortic lumencommunicating with the media through an intimal tear usually in theascending aorta (78 per cent.), less often in the descending aorta (22 percent.), and blood spreads between the middle and outer thirds of the mediafor varying distances down and around the aorta (Shennan, 1934). Aorticbranches are sheared off or occluded, and the dissection may rupture intopericardium, pleura or mediastinum. Cure is difficult because only 6 percent. are confined to the descending aorta, 60 per cent. of those involvingit being extensions from above and 34 per cent. continuing into theabdomen (Shennan, 1934).

Coarctations and aneurysms of the aorta are dangerous conditions.The average expectation of life of a patient with a coarctation is 33 years

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(Abbott, 1928). A quarter die of unrelated causes (Riefenstein et al.,1947), but a third of the remainder die from rupture of the aorta, usuallyfrom proximal dissection in a wall involved by cystic medial necrosis butsometimes from rupture of associated aneurysms. A third are killed bysubacute bacterial endocarditis. The remaining third die from leftventricular failure or subarachnoid haemorrhage.

A patient with a saccular aneurysm of the descending aorta will die lessthan two years from the onset of symptoms (Colt, 1927; Kampmeier,1938). Death is due to rupture of the sac or to pressure on neighbouringviscera, particularly the left main bronchus and oesophagus.

Dissecting aneurysms rupture within 24 hours in two-thirds of patients,and 92 per cent. are dead within a week (Shennan, 1934). Chronicaneurysms follow rupture of the dissection back into the lumen, when adouble-barrelled aorta may become lined with endothelium and heal.Death is then twice as likely to be due to heart failure as rupture.

Treatment of both coarctations and aneurysms is imperative. Thetechnical problems presented by these pathological processes are four:stenosis of the aortic lumen with good collateral circulation (coarctation),saccular aneurysms which may be excised without obstructing the aorticlumen (syphilis), fusiform aneurysms requiring excision of an aorticsegment (trauma and arteriosclerosis) and dissecting aneurysms where thelesion is seldom confined to the descending aorta.

PHYSIOLOGY OF AORTIC OCCLUSION

Obstructing the descending aorta causes a sharp increase in the proximalblood pressure and gross diminution of blood flow distally. After removalof the obstruction, the blood pressure falls abruptly and may be followedby surgical shock.

Proximal hypertensionThe mechanism of the proximal hypertension depends whether occlusion

has been sudden or gradual. Sudden occlusion follows the applicationof aortic clamps for an aneurysm, while obstruction has been present fromfoetal life in coarctation. The high blood pressure could have a mechanicalreflex or renal origin, that is, it may be due to the physical obstruction ofthe clamp, a reflex from the distal ischaemic areas or release of a hyper-tensive substance by the kidney.The hypertension of acute occlusion has been shown to be mechanical.

The normal blood pressure is a function of cardiac output, peripheralresistance, aortic elasticity and blood volume. After clamping the aortaat the left subclavian artery the cardiac output changes little initiallythough authorities differ as to whether it rises or falls (Barcroft, 1931;Hamilton and Remington, 1948). The peripheral resistance increases

347

M. V. BRAIMBRIDGE

sharply because two-thirds of the arterial bed is excluded from the circula-tion. Aortic elasticity smoothes out the intermittent flow from the leftventricle and this reservoir is also reduced by 60 per cent. The effectiveblood volume is increased slightly by collapse of the distal vasculature.The purely mechanical origin of the hypertension was shown by

Brotchner, who occluded the arteries of various organs whose blood flowwas known (Levy and Blalock, 1937). The blood pressure increased by aproportional amount independent of cerebral asphyxia, vagal or carotidsinus reflexes, or renal ischaemia (Brotchner, 1939).The mechanism of the hypertension of coarctation does not unfortun-

ately allow such analysis, and there are many opinions regarding itsaetiology. Evidence has been put forward in favour of a purely mechani-cal origin of the hypertension (Bing et al., 1948), of reflex tone (Prinzmetaland Wilson, 1936) and renal vasoconstriction (Scott and Bahnson, 1951).The explanation of this contradictory evidence may be that hypertension,whatever its origin, is fixed by some poorly understood mechanism whichdoes not stop on removal of the initiating agent and so may maintainhypertension after excision of the stenosis (Pickering, 1955).

Distal ischaemiaThe distal blood pressure falls sharply after aortic occlusion but sub-

sequently rises slightly. Some collateral circulation must have developed,but not sufficient to prevent critical ischaemia of the spinal cord, kidneys,liver and gastro-intestinal tract.

Chronic occlusion, as in coarctation, causes minimal deprivation ofblood to distal viscera as the collateral circulation is often adequate tokeep the distal mean pressure nearly normal, although the pulse pressure isdiminished (Bing et al., 1948).

Spinal ischaemia. Spinal cord damage during thoracic aortic surgerydepends upon five factors: the anatomical pattern of its blood supply, thesite of occlusion, the nature of the operation, the presence of collateralvessels and the duration of cross-clamping. The anatomical patterncannot be predicted in advance in the individual patient. Upper thoracicprocedures are more likely to cause neurological damage in the presenceof the more segmental pattern associated with a lumbar great spinalartery, while a thoracic great spinal artery is particularly vulnerable duringlower aortic operations.The site of the occluding clamps determines how much of the spinal

cord will be made temporarily ischaemic. A clamp at the left subclavianartery deprives all the spinal branches of the intercostal and lumbar vesselsof an adequate blood supply, whereas occlusion lower in the thorax leavessome at least unaffected. A second clamp prevents collateral flow thathas circumvented the first from reaching lower spinal branches and theincidence of paraplegia increases markedly (Pontius et al., 1954).

348


The nature of the operation determines how many intercostal arteriesneed to be divided with consequent permanent obliteration of associatedspinal branches.The presence of collateral vessels, as in coarctation, should make

temporary occlusion of the aorta safe. Paraplegia nevertheless occursif the circulation is poorly developed because of a mild stenosis or ananomalous subclavian artery arising below the stricture and acting as themain collateral channel, or if the circulation is compromised at operationby dividing too many intercostal arteries or by occluding the left sub-clavian artery which provides half the collateral supply (Adams and vanGeertruyden, 1956). If a further operation becomes necessary, as for ananeurysm at the suture line, the collateral circulation cannot be reliedupon because obliteration of the pressure gradient after excision of thestenosis makes the anastomoses functionless.The last factor, the duration of occlusion, is the one most under the

surgeon's control, and it is important to know for how long the aorta maybe safely clamped without fear of spinal cord damage. Experimentalevidence is voluminous and gives wide limits for the critical time, due tothe different species of animal used and the varying methods of producingischaemia (Tureen, 1936). It has been frequently shown that occlusionof the dog's descending aorta for an hour makes 30-40 per cent. of sur-viving animals paraplegic (Pontius et al., 1954; Beattie et al., 1953). Theaddition of another clamp at the diaphragm or division of aortic inter-costal arteries may treble the incidence. Simple occlusion for as shorta time as 10-15 minutes can cause paralysis (Carrel, 1910).

Clinical evidence is less precise, but two patients have suffered spinalcord damage following aortic occlusion for 13 and 18 minutes (Ellisonet al., 1960; Crafoord, 1952). It is clear that the spinal cord unprotectedby previously established collateral vessels cannot tolerate aortic occlusionfor more than 15 minutes without risk.

Renal ischaemia. Morris showed that experimental aortic occlusionfor two hours lowered the glomerular filtration rate and renal blood flowto 90 per cent. three days later. Renal artery occlusion alone caused a50 per cent. drop. When clamps were placed on both aorta and renalartery they fell to less than 10 per cent. (Morris e(t al., 1956).

This evidence runs roughly parallel with clinical experience (DeBakeyet al., 1955), but the kidneys may survive total anoxia for two or threehours on occasion (Ellis et al., 1955; Hume et al., 1955).

Total renal ischaemia is a particular problem during excision of thoraco-abdominal aneurysms, but fortunately occlusion of the thoracic aortaalone is the least harmful of the three procedures and it is clear that renaldamage is unlikely if the kidneys are normal. Arteriosclerosis anddissecting aneurysms, however, affect the renal arteries themselves whenaortic occlusion may have the effects of Morris's last experiment.

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M. V. BRAIMBRIDGE

Hepatic ischaemia. The liver receives oxygen from two sources,hepatic artery and portal vein, and the canine liver is liable to virulentautodigestion by anaerobic organisms which make experimental studiesdifficult to interpret.

Total hepatic ischaemia is tolerated experimentally for 20-75 minutes(Drapanas et al., 1955; Burch et al., 1953). Clinical evidence is scantyand equivocal (Burch et al., 1953; Shumway and Lewis, 1955) and thereis no evidence pertaining to liver function after aortic occlusion alonefrom which definite conclusions can be drawn, but liver failure has notbeen described as the sole sequel of aortic surgery.

Gastro-intestinal ischaemia. The gastro-intestinal tract is the otherimportant structure to be made anoxic. The high mortality of experi-mental ischaemia has been shown to be due to the size of the intestinalvascular bed and the facility with which the bowel can lose fluid ratherthan to any particular sensitivity to anoxia (Edwards et al., 1954).Post-occlusive shockWhen clamps are removed from the aorta, the peripheral resistance is

abruptly lowered and the elastic aortic reservoir is increased. The bloodpressure slumps and ventricular fibrillation may ensue as the previouslyoverworked ventricles are deprived of an adequate coronary perfusion.A syndrome of hypotension, haemoconcentration and bloody diarrhoeamay prove fatal some hours later.The mortality following experimental abdominal aortic occlusive

manoeuvres is directly proportional to the area of vascular bed that hasbeen made ischaemic (Edwards et al., 1954; Parkins et al., 1955). Thoracicaortic occlusion deprives all the abdominal viscera of oxygen so that bloodpools in the dilated vessels and the bowel leaks fluid into its lumen(Erlanger and Gasser, 1919). A low effective blood volume results whichis responsible for both types of postocclusive shock, potentiating ventri-cular fibrillation by aggravating the initial blood pressure fall and causingirreversible shock which manifests itself as hypotension, haemoconcentra-tion and death.

METHODS OF AVOIDING THE EFFECTS OF AORTICOCCLUSION

The length of time that the aorta can be safely occluded is limited, soaortic replacement must be accelerated to keep within this limit or moretime must be gained by some ancillary procedure.Rapid anastomotic methods

Standard anastomoses may be done quickly or special apparatus usedto hasten insertion of a graft. The first fusiform aneurysm to be success-fully excised was replaced without any ancillary measures by DeBakey andCooley in 1953, but it took even them 45 minutes and the patient was luckyto avoid paraplegia.

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Grafts were more quickly inserted by everting them over cuffs whichwere tied into the lumen of the aorta, the cuffs being removable afterthe everted edges of vessel and graft had been joined (Poth et al., 1949).The suture had to be inserted without accurate tension and some periodof aortic occlusion with all its attendant hazards was unavoidable, a periodthat might be critically prolonged if there was disproportion between aortaand graft. For these reasons the method did not become popular.

Hypothermia

Reduction of the temperature to 300 C. halves the oxygen requirementsof the body, which may then tolerate an ischaemic insult that would causepermanent damage at normal temperatures. The high incidence ofparaplegia following experimental aortic occlusion was virtually abolishedby hypothermia as can be seen from the combined result of 142 similar

COMBINED COMPLICATION RATE OF EXPERIMENTALPERCENTAGE COMPLICATION RATE USING BYPASSAORTIC OCCLUSION WITH HYPOTHERMIAPECNAEOMLATNRTEUIGBAS

40 1 1normothermtic 80 tcontrolhypothermia (b)Complca aehypothermicx ashnth

C 30 VZ K Ao60

120 140

10lo

20

0

nDEATH PARALYSIS DEATH IN 24 hrs. PARALYSIS

(a) (b)Fig. 1. (a) Combined complication rate of experimental aortic occlusion withhypothermia. (b) Complication rate of experimental aortic occlusion with by-pass.

operations in the literature (Gross and Hufnagel, 1945; Beattie et al.,1953; Pontius et al., 1954; Parkins et al., 1955). Only 3 per cent. ofsurviving hypothermic animals were made paraplegic compared with37 per cent. of normothermic controls, but the 32 per cent. control mortal-ity rose to 35 per cent. with hypothermia (Fig. la).

Hypothermia has three inherent disadvantages: increased ventricularirritability which is a handicap to a labouring left ventricle, metabolicacidosis which itself initiates a shock-like state, and a tendency to causebleeding which can be fatal after a long and bloody operation. Clinicalevidence of difficulties was not uncommon (Bahnson, 1953; DeBakey et al.,1955).

Reduction of proximal hypertension by ganglion blocking drugs hasbeen advocated in addition to hypothermia (Julian et al., 1955). Itis difficult, even with such drugs, to keep the proximal pressure from risingsignificantly, and fluctuations can cause cardiac arrest.

351

M. V. BRAIMBRIDGE

Hypothermia of 300 C. has not proved the boon it initially promisedto be. Profound hypothermia of 150 C., as developed in this country byDrew (Drew et al., 1959), has not found a place either in descending aorticsurgery for two reasons: it requires multiple cardiac cannulations whichare technically difficult with the patient in the lateral position, and theavailable time is limited to some 50 minutes.

ShuntsClearly descending aortic surgery would be safest if physiological

homoeostasis could be maintained throughout the procedure. Thesimplest method of achieving this was an intraluminal shunt. A tubeover which a graft had been threaded was tied into the two ends of thedivided aorta and slipped out as the second anastomosis was almost com-pleted (Hufnagel, 1949). It had the same objections as the cuffanastomosis, and paraplegia could follow its use (Lam and Aram, 1951;DeCamp et al., 1950).A detour around the occluded segment was an improvement. Such

shunts were developed along three lines: the proximal blood pressurealone driving blood through the by-pass; using the definitive graft as ashunt; and putting a mechanical pump into the circuit. The three typesmay be termed temporary, permanent and pump-assisted.Temporary shunts had the roughly constant pressure head of the

proximal blood pressure, and flow therefore varied as the fourth power ofthe diameter and inversely as the length (Poiseuille's law). To be effectivethey had to be short and wide, which laid a cumbersome sausage of tubingacross the operative field and entailed insertion into the adjacent aortaitself.The number of anastomoses was reduced if the definitive graft was used

also as the shunt. The blood flow was then permanently maintainedthrough the by-pass while the intervening aortic segment was excised andthe ends oversewn. It left stumps which could rupture or act as a nidusfor thrombosis and embolism, but the permanent by-pass graft has never-theless found a place in the treatment of thoraco-abdominal aneurysms.The insertion of a mechanical pump into the circuit eliminated many of

these disadvantages, as lengths of small bore tubing could be used toremove the shunt from the operative field, cannulation of small vesselsreplaced aortic anastomoses and low pressure areas like the atrium couldact as the proximal source of blood. Accurate control of hypertensionwas possible as the pump speed could be altered at will.The drawbacks of the technique were the necessity for heparin, extra

apparatus and technicians and the risk of mechanical breakdown and airembolism, but meticulous haemostasis and experience have made the useof heparin safe, assistants can be quickly trained to manage such a simplecircuit and air embolism is immaterial in the lower part of the body.

352


A shunt must be shown to be superior to hypothermia in the preventionof complications before it can be recommended for aortic surgery.Comparison of a similar though smaller series of experimental operationsfrom the literature using shunts to obviate comparable occlusive insults isshown in Figure lb (Schafer and Hardin, 1952; Izant et al., 1953; King andShumacker, 1957). Spinal paresis was virtually abolished by eithertechnique, being 3 per cent. with hypothermia and absent with by-pass,but the mortality was 35 per cent. with hypothermia and only 5 per cent.with by-pass (Fig. 2). A shunt will prevent both death and paralysis,while hypothermia can only be relied upon to avert the latter.

C+ hours I 2 hours

(a) (b)Fig. 2. Experimental by-pass series. (a) Control group. (b) Temporary brachio-

femoral by-pass.

EXPERIMENTAL THORACIC AORTIC BY-PASSWhile I was working with Dr. Frank Gerbode in San Francisco in 1957,

it became apparent that a shunt was desirable outside the immediateoperative field using cannulations only, as the large temporary shuntsin current use had been found to be too unwieldy. Two approaches weretried. The first was a simple shunt from axillary to femoral artery, andthe second joined left atrium to femoral artery through a pump. Thecontrol for these experiments was a series in which the aorta was occludedwithout any protective measures being taken.The occlusive insult was designed to be severe. Two clamps were

applied to the aorta for an hour and a half, one near the left sub,lavianartery and one at the diaphragm.The control series consisted of nine animals (Fig. 2a). A left thora-

cotomy was performed, manometers were inserted into the internalmammary and femoral arteries, heparin was given and the aorta occluded.After 90 minutes the two clamps were removed, protamine administeredand the chest closed.

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M. V. BRAIMBRIDGE

In the second group of five animals a polythene cannula was insertedin the axillary and femoral arteries (Fig. 2b). Blood was allowed to flowthrough the shunt and the aorta was clamped. The flow in the shuntwas subsequently calculated by forcing blood through the tubing at thepressure gradient and temperature pertaining in each experiment, whichwas necessarily an approximation as the flow was not pulsatile. Afterremoval of the clamps the shunt was discontinued and the chest closed.

The third group consisted of 10 animals (Fig. 3). Incisions were madeas in the control group and manometers connected. The pericardium wasopened, heparin given and a catheter inserted into the left atrial appendage.A length of polyvinyl tubing previously filled with citrated blood connected

; n . I n t-rn in l

Cothtetr in-Femnoi'l art. ( / 8Cathret-r in Fernoral art

EXTRACORPOREAL BYPASS OFDESCENDING THORACIC AORTA

Fig. 3. Experimental by-pass series-left atrio-femoral by-pass.

this catheter via a roller pump to a cannula in the femoral artery. Theleft atrial side of the pump was connected to a blood reservoir and a Tycosmanometer. Air was removed and a by-pass begun by slowly startingthe pump. The aortic clamps were applied and the proximal pressurekept within normal limits by regulating the speed of the pump. After90 minutes the proximal and distal aortic pressures were equalized andthe clamps removed. The left atrial and femoral cannulae were removed,protamine given and the chest closed.

Because of a shortage of assistants, both surgery and pump regulationwere conducted single-handed. Asepsis could not be maintained andlong term survival was recognized as being unlikely.

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Certain technical points were found to be of value in the maintenanceof a smooth by-pass. A watch had to be kept on the manometer in theinternal mammary artery as the proximal blood pressure tended tofluctuate considerably. The position and size of the left atrial catheterwere found to be important. As large a catheter as possible, with multipleside holes, was placed in the centre of the atrium and the connecting tubingallowed to hang freely over the edge of the wound, creating a slight dragthat prevented the catheter tip from becoming entangled in the mitralvalve. A pronounced negative swing on the manometer on the atrialside of the pump indicated an incorrect position of the catheter or adiminished blood volume allowing the atrial wall to occlude it.

PERCENTAGE COMPLICATION RATE.

80 a 0 controlFig.axillary arteryOtleft atrium

Ca 60-mp

i40Ca

20-

DEATH IN 24 hrs. PARALYSIS

Fig. 4. Complication rates.

There is a difference of opinion about the desirability of including areservoir for gravity drainage of the left atrium, some saying it is essentialfor smooth running and the maintenance of a high flow (Snyder et al.,1960; Connolly et al., 1962), while others claim it to cause extra hazards, ahigh priming volume and a lower peak flow (Austen and Shaw, 1960).At no time has the simpler and safer technique of direct drainage provedunsatisfactory in our experience either experimentally or clinically.

Results

The three series of experiments were compared by their incidence ofcomplications and the variations in proximal and distal blood pressures.The mortality was taken as that occurring within 48 hours because it wasfelt unjustifiable to keep a paraplegic animal alive longer, and the randomeffects of infection due to the unsterile technique began to appear afterthat time.

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M. V. BRAIMBRIDGE

In the controls, seven (78 per cent.) died within 24 hours (Fig. 4). Fourdied of shock within six hours and three were found dead next morningin the kennels with bloody diarrhoea and congested intestines and kidneys.None of the axillary to femoral artery group and only one of the 10 pump-assisted shunt group died within 48 hours. Two animals in the lattergroup died later from large empyemata and these have been excluded,making the mortality 1 of 8 (12 per cent.).

Both the surviving animals (22 per cent.) in the control group wereparalysed. There were no neurological sequelae in the other two groups.

The complication rate of the control group was 100 per cent., but wasonly 0 and 12 per cent. in the other two groups. The combined complica-tion rates and mortality rates alone are highly significant statistically

1. PROXIMAL BLOOD PRESSURES

mm.

+40 440Hg.

B.P.bfore -.

occlusion

mm.-40- -0

Hg.

occlusion occlusion occlusionCONTROLS AXILLARY LEFT

E CONTROLS ARTERY ATRIUM

Fig. 5. Proximal blood pressures.

(p=.020, .010, .024 and .004 for the two respective groups) but there wereso few survivors in the control group that the difference in the incidence ofparalysis was not significant.

Analysis of the mean blood pressure changes above and below theoccluded aorta suggests the reason for the differences between the com-plication rates. The proximal blood pressure rose similarly (40 and39 mm. Hg) in the control and axillary artery groups, showing the haemo-dynamic inadequacy of a small shunt (11 ml./kilo/min.). The larger bloodflow of the left atrial group (52 ml./kilo/min.) kept the mean proximalpressure from rising more than 13 mm. Hg (Fig. 5).

At the end of the occlusive period the blood pressures of the two shuntgroups were unchanged, having fallen only 3 and 2 mm. Hg respectively,but the control group pressure had fallen back to its pre-occlusive level, afall that was unlikely to be due to myocardial failure as the peripheral

356


resistance of the control and axillary artery groups must have been similarbecause their initial hypertension was identical. The cause could onlybe a lowered effective blood volume with pooling of blood and fluid in theischaemic distal viscera, direct evidence for which was the bloody diarrhoeaand congested abdominal organs with which many of the animals died.The distal blood pressures showed reciprocal changes (Fig. 6). Immedi-

ately before by-pass the highest average mean pressure was in the controlgroup where manipulation had been minimal. Application of the clampslowered the distal pressure from 109 to 8 mm. Hg. The axillary/femoralgroup's pressure fell from 87 to 12 mm. Hg, such a slight improvementbeing another index of the smallness of the shunt. The mean pressurein the left atrial group fell by only 9 mm. Hg, which showed the effective-ness of the larger shunt.

2. DISTAL BLOOD PRESSURES.120 120

mm. 90 90

H.60 60

B.P.

30 30

occlusion occlusion occlusionAXILLARY LEFTCONTROLS ARTE A RI UM

Fig. 6. Distal blood pressures.

The distal pressure tended to increase with time, rising 3 and 7 mm. Hgin the control and axillary/femoral groups. There was a small fall(3 mm. Hg) in the left atrial group due to the smaller flow (41 ml./kilo/min.)at the end of the occlusive period.Removal of the clamps resulted in a mean pressure in the control

group of 41 mm. Hg on average, while it was 83 and 74 mm. Hg in theaxillary and left atrial groups, differences which are statistically highlysignificant (p =.001) and show the value of even a small flow of oxygenatedblood to the abdominal viscera.

ConclusionThis series of experiments has shown that morbidity and mortality are

minimized if a shunt of any size is used to circumvent the occludedthoracic aorta. The larger the shunt the nearer is the approximation to

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M. V. BRAIMBRIDGE

physiological homoeostasis and consequently the safer the operationshould be. The mortality was in fact higher when the larger shunt wasused but involved a difference of one animal only, and the effects ofproximal hypertension with the small shunt would have become apparentin a larger series.

SURGERY OF COARCTATIONThe 119 operations for coarctation described here were performed

between 1950 and 1962 at the Brompton Hospital. Analysis of theirclinical presentation, operative management and post-operative complica-tions outlines the problems of diagnosis and treatment that may beencountered in the surgery of coarctation.The patients were aged 3 to 56 with an average of 22 years, and the ratio

of male to female was 2: 1.SymptomsSymptoms were directly attributable to the physiological disturbance

produced by the constriction-proximal hypertension, turbulence at theisthmus and a diminished distal flow. The extra burden on the leftventricle caused dyspnoea on exertion in 29 per cent., palpitations in10 per cent., angina in 7 per cent. and actual heart failure in 4 per cent.The raised intracranial pressure gave rise to headache in 17 per cent.,hypertensive encephalopathy in 9 per cent. and cerebrovascular accidentsin 4 per cent. Vegetations followed turbulence at a bicuspid aortic valveor coarctation and subacute bacterial endocarditis occurred in 4 per cent.Inadequate peripheral blood supply gave rise to cold feet, paraesthesiaeand intermittent claudication in 18 per cent.The commonest symptoms were therefore mild dyspnoea, headache

and evidence of poor blood flow in the legs, but 34 per cent. of the patientswere entirely asymptomatic on direct questioning and many more hadignored minor symptoms and the lesion had been diagnosed at a routineexamination. Aneurysms were, however, subsequently found in 13 percent. of the asymptomatic group.SignsThe diagnosis of coarctation was simple from the physical signs but

was sometimes missed because none of the symptoms had been specificenough to demand appropriate examination. The patients were oftenheavily muscled around the shoulders as a result of the increased bloodflow through palpable collateral vessels and had a marked pulsation visibleabove the clavicles. The pulse was regular (99 per cent.) and there washypertension in the arms, the average pressure in the right arm (172/98)being slightly higher than that in the left (167/98). The diagnosis couldbe made in 99 per cent. of cases by the combination of proximal hyper-tension and a diminished and delayed femoral pulse.On auscultation there was an aortic ejection click (60 per cent.) and

ejection murmur (87 per cent.), an accentuated aortic component of the

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second sound which behaved normally on respiration (78 per cent.) and amitral diastolic murmur at times (45 per cent.). A coarctation murmurwas present posteriorly in 92 per cent. The electrocardiogram showedleft ventricular hypertrophy (59 per cent.) and the chest radiograph leftventricular prominence (73 per cent.), rib notching (85 per cent.) and thecoarctation site indicated by an absent, small or double aortic knuckle(85 per cent.). Angiography (venous, aortic or trans-septal) was used todemonstrate the lesion in a third of the cases.

Congenital lesions are often multiple and other anomalies are commonlyassociated with coarctation, a bicuspid aortic valve being the commonest(Abbott, 1928). Associated anomalies in this series were Turner's syn-drome, pectus excavatum, mental retardation and spastic paralysis (1 each),ventricular septal defect (1) and persistent ductus arteriosus (6). Theincidence of bicuspid aortic valves was of course unknown, but 12 percent. had aortic stenosis or incompetence. Mitral valve lesions occurredin 9 per cent.

OperationThe incidence of S.B.E., heart failure and cerebrovascular accidents

(12 per cent.) and the presence of aneurysms in 13 per cent. of the asympto-matic group were premonitory signs of the lethal nature of the coarctation,and resection was essential if the patients were to be allowed a normallife expectancy. If a coarctation has a lumen 40 per cent. or more of thenormal size, minimal physiological obstruction occurs (Gupta andWiggers, 1951) and four patients were judged to be too mild for surgeryduring the period under review, but the lumen in this series varied from0 to 5 mm. with a mean of 2 mm.

Relief of obstruction involves excision of the narrowed segment andrestoration of a normal lumen, for which are required a good exposure,proximal and distal control and mobilization of the adjoining aorta toclose the gap produced by the excised segment. Wedge resection andturning down the left subclavian artery are mentioned only to be con-demned, as end-to-end anastomosis or insertion of a graft covers alleventualities and gives a good lumen without compromising the collateralcirculation.

Exposure was obtained by placing the patient in the lateral position andmaking an incision through the fourth intercostal space, at the posteriorend of which lay the coarctation. Management of the large collateralarteries during incision of the chest wall muscles was made easier bylowering the patient's blood pressure where necessary with hypotensivedrugs and having an assistant apply pressure to the edges of the wound.

Proximal and distal control was obtained and the aorta mobilized fromthe left common carotid artery to the third aortic intercostal. The largethin-walled intercostal vessels were treated with circumspection and dividedonly where necessary for adequate mobilization.

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M. V. BRAIMBRIDGE

The anastomotic technique mainly used in this series was a posteriormattress suture inserted loosely, the aortic ends approximated withhorizontally lying clamps and the suture pulled tight and continuedanteriorly with or without a second continuous suture of the everted edges.A simpler and quicker method was used in a few cases, whereby eachstitch could be inserted under accurate tension. Clamps were appliedvertically, a double-ended 30 suture inserted posteriorly and tied, and theclamps rotated from side to side while a continuous " over-and-over"stitch was run up each side and locked at the front. An end-to-endanastomosis was performed in 72 per cent. of this series.Two coarctations were at unusual sites, which is the usual reported

incidence (Schuster and Gross, 1962), one in the abdomen and one nearthe diaphragm. Four had anomalous subclavian arteries arising belowthe coarctation, which were sacrificed except in one patient where it wasreimplanted in the anastomosis. Subsequently a false aneurysm developedat the site.

Grafts were used in 21 (18 per cent.) to bridge large gaps, 11 caused bylong narrow segments, five by aneurysms, four by poor neighbouringtissue and one was a by-pass for the abdominal coarctation. The majoritywere used in patients over the age of 25 and before 1956, since when greaterexperience and better mobilization have lowered the incidence. Fourof the patients in whom grafts were inserted died, but only one as a directcomplication, an Ivalon prosthesis rupturing. Several grafts have calcifiedbut none as yet has given rise to any other complication. The majorityof the grafts were homografts but there were one Ivalon and three crimpedTeflon prostheses used.Aneurysms were present in 29 patients (23 per cent.) Twenty-two were

on intercostal arteries, two involved the proximal aorta and four thedistal aorta of which one was a saccular mycotic aneurysm.Results

Twelve patients died, a mortality of 10 per cent., which is more thandouble that of Gross but similar to the heterogeneous American collectionof 1,600 cases (Schuster and Gross, 1962; Bailey, 1957). Seven of thetwelve were operative deaths, from haemorrhage in two, renal failure inone and inaccurate control of hypotensive drugs in another. Threepatients developed false aneurysms and died following attempts at repair,one of whom demonstrated the inadequacy of collateral vessels at a secondoperation after resection of the stenosis by developing paraplegia and renaland hepatic necrosis.

There were five late deaths, which followed extracorporeal operationsfor valve defects in two, cerebral thrombosis in one and unexplainedcollapse in two. The average age of the patients who died was 32 years,compared with the overall figure of 22, and no patient under the age of15 died.

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Post-operative morbidity included haemorrhage, hypertensive crises,abdominal pain and infection of the suture line. Careful haemostasis didnot prevent five large post-operative haemorrhages, two of which werefatal. Hypertension of 180 mm. Hg or more occurred in 15 patients (14 percent.) and was treated initially by sedation and posture. Hypotensivedrugs such as rauwiloid or a slow intravenous infusion of " Arfonad"were sometimes necessary in addition.

Abdominal pain after relief of a coarctation may be due to necrotizingarteritis of the mesenteric vessels following the introduction of a highpulse pressure into the distal visceral bed. Pain occurred in four patientsbut resolved without intestinal gangrene or the necessity for operation, amuch lower incidence than the 20 per cent. reported by Trummer andMannix (1963). Infection of the anastomosis is a disaster that may beprevented by intensive chemotherapy in the immediate post-operativeperiod. Two false aneurysms were due to infection of the suture linewith a staphylococcus and a fungus, and one other case of S.B.E. was dueto a micrococcus. Other complications were chylothorax (2), bothresolving on a low fat diet, atelectasis (2), thrombophlebitis (1), woundinfection (2), cerebral symptoms (3) and nerve damage (Horner's, recurrentand radial nerves) (3).

Collateral circulation maintained an adequate flow to the distal tissuesthroughout the period of aortic occlusion, except in one patient whodied in renal failure for no obvious reason that could be elicited from therecords. There was no case of spinal damage except at a second operation.

The blood pressure does not always return to normal after relief of acoarctation for reasons which are not yet known. In this retrospectiveseries there were 77 patients whose blood pressures had been recorded inboth arms before operation, on discharge from hospital and at a follow-upexamination. The average pre-operative blood pressure in this group was172/98 mm. Hg in the right arm and 167/98 in the left. It had fallen atthe time of discharge 3-4 weeks later to 139/83 mm. Hg, a figure which wasidentical with the level at follow-up examination (139/82 mm. Hg), ata mean of 3.6 years later. This similarity differs from most Americanseries, where a further fall is noticed after discharge, but may reflect thelonger time that the British patient remains in hospital after operation.

The average figures are an indication of the effects of operation, butaccurate assessment is only possible if the blood pressures are plottedagainst the expected pressures for the age and sex of the patient. It wasthen apparent that few systolic or diastolic pressures fell to the averagelevel for the patient's age at follow-up although considerable overallreduction had occurred, and, interestingly enough, the older patient hadreacted comparably to the younger.

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M. V. BRAIMBRIDGE

SURGERY OF ANEURYSMSCollateral circulation is no help in surgery of aneurysms of the descend-

ing aorta, nine of which have been excised in this series.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~. :_...... ,_ F ...~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~....... .~: .. 1Reproduced by permission of The C. V. Mosby Company, St. Louis, -Vissouri.

Fig. 7. Pre-operative radiograph. (From Gerbode, Braimbridge, Hood and French(1957) Surgery 42, 975.)

Four of the aneurysms were traumatic in origin, one syphilitic, onearteriosclerotic, two dissecting and one of unknown aetiology, possiblydue to congenital weakness of the aortic wall. Six aneurysms werefusiform, involving the proximal aorta, and the arteriosclerotic one wassaccular in the lower half. One of the dissecting aneurysms was confinedto the thorax and the other extended into the abdomen. The predilection

362


of trauma for the region near the ligamentum, of syphilis for the moreproximal aorta and arteriosclerosis for the lower part is borne out, butthe saccular aneurysm was arteriosclerotic and the syphilitic one fusiform.

The patients were aged 18-63. Four were asymptomatic. Threecomplained of cough and dyspnoea due to pressure on the left mainbronchus, two of dysphagia in addition and characteristically the syphiliticaneurysm had eroded the vertebrae with pain as a prominent symptom.The dissecting aneurysms presented classically with sudden pain in thechest and back and paraesthesiae in the lower limbs a few days beforeadmission.

Electromannometer tomecsure proximal Blood for prinmingrXtrisli pressure , sujstem

Cc theter toleft atriumnMnmtr+

moosure suctionPressure

De Bakeg pump

Catheter in \Miaonamter to MeosureFemoral kt pumping pressure

I Bubble bleeder

Reproduced by permission of The C. V. Mosby Company, St. Louis, Missouri.

Fig. 8. Left atrial/femoral by-pass. (From Gerbode, Braimbridge, Hood andFrench (1957) Surgery 42, 975.)

Physical signs were few in the asymptomatic patients except for somedelay in the left arm and leg pulses with hypertension in the right armof one patient whose aneurysm involved the left subclavian artery (nocoarctation was subsequently found). The blood pressures of the twodissecting aneurysms were 240 and 210 mm. Hg systolic and 120 diastolic,but the others were within normal limits. Systolic murmurs were heardover the left chest in four patients.The three patients with bronchial compression had signs of sputum

retention in the lungs and the narrowing was confirmed by bronchoscopy.The diagnosis was made by plain radiography and tomography in all but

363

M. V. BRAIMBRIDGE

two cases (Fig. 7), one of whom was diagnosed at thoracotomy and theother treated initially as a carcinoma with radiotherapy. Angiographywas used to delineate the lesions in six of the patients, retrogradeaortography in four, venous angiography in one and selective pulmonaryarterial angiography in one.

Reproduced by permission of The C. V. Mosby Company, St. LoUis, Missouri.Fig. 9. Traumatic fusiform aneurysm. (From Gerbode, Braimbridge, Hood and

French (1957) Surgery 42, 975.)

Indications for surgical intervention in aortic aneurysms are the presenceof symptoms, continued enlargement or embolism. Symptoms werepresent in five patients, evidence of enlargement in one and embolismin none. The risks of operation were assessed in the cases of the asympto-matic arteriosclerotic and two traumatic aneurysms by reference to thefigures from DeBakey's unit (DeBakey et al., 1958). Seventy-three

364


fusiform and saccular aneurysms were excised with an overall mortality of40 per cent. The factors affecting it were the patient's age (45 per cent.over 60, 12 per cent. under 50), aetiology (35 per cent. for arteriosclerosis,17 per cent. for syphilis and 0 for trauma), hypertension (32 per cent.over 150 mm. Hg systolic, 15 per cent. under 150), and pre-existing heartdisease (43 per cent. with and 11 per cent. without it). The factors areinterrelated in that the older patient tends to have an atheroscleroticaneurysm, hypertension, and heart disease.

Recommendation of operation in the two young patients with traumaticaneurysms was not difficult because the mortality was minimal on allcounts. The atherosclerotic aneurysm occurred in a patient of 63 withevidence of coronary ischaemia, but his blood pressure was only 140/70and he had a " blow-out " on a dilated aorta, the risk of which rupturingwas judged to be greater than that of surgery.

In the case of dissecting aneurysms, DeBakey had found that the onlyimportant factor was the level of the blood pressure, the mortality being41 per cent. when the systolic pressure of the patient exceeded 150 mm. Hg,but 0 per cent. when it was below that figure. The systolic pressures of thetwo patients in this series were 240 and 210 mm. Hg, which placed themin the high risk group.

Left atrio-femoral bypass was used in each case during excision of theaneurysms. The patient's thorax was adjusted in the lateral position withthe hips rotated backwards. Incisions were made in the right wrist andgroin for the radial artery pressure catheter and femoral arterial by-passcannula. A left thoracotomy was performed, the intercostal space ofentry being regulated by the site of the lesion, the fourth space for upperaneurysms and the seventh or eighth for the lower lesions, and in oneof the dissecting aneurysms two intercostal incisions were made. Normalaorta above and below the aneurysm was mobilized and dissection carriedaround the aneurysm itself only where there was no danger of rupturing it.The pericardium was opened and a purse-string suture placed around theleft atrial appendage.

A shunt was prepared as described for experimental by-passes (Fig. 8).The pump was slowly started, the aorta was clamped, and the pump speedwas adjusted to keep the proximal blood pressure at its normal level,counteracting the fluctuations produced by blood loss or inadvertentretraction of the heart.

The aneurysmal sac (Fig. 9) was removed if it had been mobilized butotherwise it was opened, its unobliterated intercostal vessels sutured fromthe inside and the lining removed at leisure after the graft had been inserted.

Four homografts, three Teflon and two Dacron prostheses were used.In the case of the fusiform aneurysms the graft was anastomosed to the

365

M. V. BRAIMBRIDGE

upper end of the aorta, usually by the vertical clamp single suture tech-nique which is a method particularly suitable for aneurysmal surgerywhere speed is a consideration. The suture line was tested by injectingsaline under pressure, the graft cut with nice judgement of the length thatwould neither kink nor exert too much tension and the lower anastomosiscompleted (Fig. 10). The by-pass was adjusted to bring the proximal and

Reproduced by permission of The C. V. Mosby Company, St. Louis, Missouri.

Fig. 10. Homograft in position. (From Gerbode, Braimbridge, Hood and French(1957) Surgery 42, 975.)

distal pressures to a roughly equal level and the aortic clamps wereremoved.

Bleeding through the graft material in a heparinized patient can be amajor problem. The homografts and woven Teflon prostheses did notleak like Dacron, which required " pre-clotting " with blood and thrombin.In the long run Dacron may nevertheless be the material of choice because

366


fibroblasts grow into its meshes whereas homografts calcify and maysubsequently rupture and Teflon is so inert that it is never incorporatedinto the tissues.The saccular aneurysm was excised locally and a Teflon patch sutured

circumferentially to the edges, a technique which is an improvement on

Reproduced by permission of The C. V. Mosby Company, Si. Louis, Missouri.

Fig. 1. Post-operative radiograph. (From Gerbode, Braimbridge, Hood andFrench (1957) Surgery 42, 975.)

lateral aortorraphy with a clamp on the neck in this part of the aortabecause the edges can be cut back to good stitch-holding tissue.The dissecting aneurysm confined to the thorax was completely excised

and replaced by a Dacron graft. The one extending into the abdomenwas removed from its upper end near the subclavian artery down to the

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M. V. BRAIMBRIDGE

diaphragm, where the false lumen was obliterated by sewing the intimaback to the adventitia and a Teflon graft inserted.Aneurysms extending into the descending aorta from the arch cannot be

treated in this way, but acute ruptures may be effectively palliated bydividing the descending aorta with the protection of an atrio-femoralby-pass, oversewing each end to reconstitute a single lumen and re-anastomosing the divided ends after cutting a window in the proximal partbetween the two lumina (DeBakey et al., 1958). In this way a re-entryhole is established which may allow healing of the lesion, and furtherdissection distally is prevented (DeBakey, 1956). No such case wasencountered in this series.Two of the patients died of haemorrhage, one of the traumatic cases

apparently from divided adhesions because no bleeding point couldbe identified post mortem, and one patient with a dissecting aneurysm diedfrom uncontrollable bleeding through the Dacron prosthesis. Theremaining seven patients are alive and well (Fig. 11).No patient developed any spinal neurological defect, but one, the elderly

arteriosclerotic patient, had a temporary elevation of blood urea to 112 mg.per cent. on the second day although his urinary output was satisfactorythroughout.

CONCLUSION

In conclusion, surgery of the descending thoracic aorta has progressedfrom tentative and hazardous beginnings to a position to-day whereoperation can be advised with confidence.

Resection of coarctations carries a significant mortality and morbiditybut, compared with the risks of inaction which allows three-quarters of thepatients to die before the age of 40, the mortality is acceptable and isnegligible if the patient is aged 15 or less.The results of the small series of operations for aneurysms are not

statistically valuable, but a mortality of 22 per cent. does at least indicatethe safety of descending thoracic aortic occlusion if an adequate by-pass isused.The series of coarctations were patients of Dr. Paul Wood and Dr.

Gibson and operations were performed by Sir Russell Brock and Mr.Tubbs, Mr. Cleland and Mr. Paneth at the Brompton Hospital. Thosewith aneurysms were patients of Sir Russell Brock, Sir Thomas HolmesSellors, Dr. Frank Gerbode, Professor Kinmonth, Mr. Cleland and Mr.Paneth. I am greatly indebted to these surgeons for permission to reportso many of their cases. I would particularly like to acknowledge mygratitude to Dr. Frank Gerbode, who first stimulated my interest in thissubject and under whose guidance these experiments were conducted.I would also like to thank Dr. Hinson, Dr. Henry, Miss Coombs and Mrs.Standing of the Brompton Hospital for their help with pathological andphotographic material, and Miss Jean Waldron for her diagrams,

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mv braimbridge, frcs surgical practice and the building up of his

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