-POSTGRAD. MED. J. (I963), 39, 724

BLOOD VESSEL INJURY:FEATURES OF THE PATHOLOGYEDWARD A. EDWARDS, M.D. RICHARD V. FIDDIAN, M.Chir.*Department of Anatomy, Harvard Medical School, Boston I5, Massachusetts, U.S.A.

THE pathology of trauma to vessels may bediscussed under the heading of injuries withbreach of the vessel wall and the less commonocclusions of apparently intact vessels. Con-comitant injury, such as that of the nerves, willnot be considered.

In every series of vascular injuries, variousdegrees of division of vessels are commoner thanocclusions (Morris, Creech and DeBakey, 1957;Neely, Hardy and Artz, I96I). Th2 former givethe following frequency of lesions in their series:

Laceration-36, 3 with subintimal dissectionTransection-7I.Contusion-6, 4 with thrombosisSpasm-3.

Lacerations and TransectionsThe most common cause of penetrating vessel

injury in America is wounding by knife or gun-shot, less commonly by a fracture fragment, orby the surgeon's rongeur or curette (as whenoperating on a herniated intervertebral disc.)Blunt trauma may also rupture arteries or veins,especially in the abdomen or chest (McBurney andGegan, I962; Shuck and Trump, I96I). Specialinterest focuses on the rupture of the thoracicaorta in car accidents. The rupture occurs at thejunction of the arch and the descending part. Ithas been attributed to contusion of the aorta,downward acceleration of the heart and arch, orto forward acceleration of the descending aorta(Zehnder, 1956). With large tears, death isimmediate; smaller tears lead to aneurysm forma-tion. Surprisingly, these aneurysms may remainunruptured for years, as in five cases recentlyreported by Steinberg (I957). Primary operativeinjury to vessels needs no comment, but secondaryerosion of a major artery by infection is reportedby Brunschwig and Brockunier (I960) as thecause of iliac artery rupture in a group of patients

Based upon a postgraduate lecture given at theAnnual Congress of the American College of Surgeonsat Atlantic City, October I6, I962. These studies wereaided by grants from the American Medical ResearchFoundation and the Massachusetts Heart Association.

* In receipt of a Peel Travelling Fellowship.

after gynxecological procedures. Extensive dis-section for malignancy and previous irradiationwere additional factors in these patients.

Hammostasis after a vessel is opened dependsupon three mechanisms (Quick, 1942). Con-traction of the vessel is most significant in thecase of arteries, especially after complete tran-section. An incomplete laceration may continueto bleed because contraction of the arterial muscletends to open the lips of the wound. The othertwo mechanisms are those of cellular aggregation,especially platelets, and of fibrinous clot formation.All three processes become more effective afterhmmorrhage has caused some hypotension.Hamorrhage thus usually ceases spontaneously inwounds of even the largest veins, until operativemanipulation releases the pressure of the peri-vascular ha-matoma (Starzl, Kaupp, Beheler andFreeark, I962). It should be noted that airembolism into the jugular or subclavian veins isfavoured if the patient is placed in the sittingposition and the local venous pressure is thuslowered.

Aside from immediate haemorrhage, a significantresult of arterial laceration is the formation of ananeurysm or fistula. Trauma rarely produces a trueaneurysm, but it may cause rupture or thrombosis of anexisting one. This sequence is well known in poplitealarteriosclerotic aneurysms, following sharp knee flexion,as in squatting. False aneurysms or pulsating hmema-tomas are very common after incomplete arterialdivision. A systolic murmur is characteristic. Severehemorrhage is a constant threat and the lesion, whenrecognized, should be dealt with at once.A side-by-side injury of an artery and vein produces

an arteriovenous fistula. Usually the decompressionoffered by the low pressure of the vein obviates thedanger of h2emorrhage, although rarely an interveningdissecting hematoma may exist. Small arteriovenousfistule have closed spontaneously, generally by throm-bosis, in months or years (Takaro and Scott, i960),but as Schumacher (in Elkin and DeBakey, 1955)observes, this happens so infrequently as to make thisa factor of little significance in planning treatment.The tendency for arteriovenous fistule to induce

cardiac enlargement and failure depends upon the sizeof the communication and the proximity of the lesion tothe heart. Thus large fistulae between the abdominalaorta and inferior vena cava produce early heart failure(Hufnagel and Conrad, 1962). Janes and Jennings (i96i)have reported on a group of young patients in each of

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December I963 EDWARDS and FIDDIAN: Blood Vessel Injury: Features of the Pathology

whom a fistula, one half-inch in length, was producedin the femoral artery and vein, in order to stimulategrowth of a short limb. These fistulm did producesome cardiac enlargement, but no instances of heartfailure were observed over the several years betweenthe making and the surgical closure of the fistulhe.Occasionally, infection may be established on the interiorof the fistula with the production of a subacute bacterialendocarditis. As with the similar process in cases ofpatent ductus arteriosus, cure is usually effected afterexcision of the fistula, unless the heart valves are alsoinvolved (Parmley, Orbison, Hughes and Mattingley,'954).The degree of ischemia resulting from blood

vessel injury depends on many factors and willbe discussed later.

Non-Penetrating OcclusionsBlunt injury, such as fracture and dislocation

at the elbow or knee, is the commonest cause oftraumatic occlusion of apparently intact vessels(Hoover, 196I; Makins, I919). Vascular spasm,internal parietal dissection and thrombosis arethree of the important mechanisms of thisocclusion (Gryska, I962). More insidious injury,as by infection, irradiation (Wolbach, I909), orchemical irritation, causes both inflammation andintimal proliferation. The latter is also a stage inhealing after mechanical trauma (Valls-Serra,195I) as well, so that partial or total occlusionmay develop slowly in a vessel not occludedearly after injury. There is little opportunity forrecanalization of a -post-traumatic thrombosis,since injury also leads to fibrosis and contractionof the vessel.That local spasm of an injured vessel is myogenic

in origin and thus unrelieved by nerve block, butrelieved by the local application of papaverine, is welldocumented by Kinmonth, Hadfield, Connolly, Leeand Amaroso (I956). There may be added to this aspasm of the distal arterial tree, often highly significantin the upper extremity, which is under nervous controland amenable to nerve block. However, spasm aloneis rare in an artery, and experience dictates that a vesselin apparent spasm which cannot be adequately relievedshould be explored, since thrombosis is usually present(Gryska, I962; Hoover, I96I; Morris and others, 1957).More rarely, an intimal rupture, with subintimalhiematoma, may cause obstruction in the contusedvessel, as it may in vessels which have also been laceratedexternally.

Certain special situations deserve mention.Ballistic wounds produce blast effects over wideareas, and arteries thus contused may show longthrombi (Makins, I919). Fibrosis may laterdevelop far beyond an apparently localizedwound. Jahnke (1958), in a long-term sttidy ofrepaired war injuries of arteries, found a highincidence of late fibrosis and thrombosis, andwas of the opinion that the initial seeminglyadequate debridement should have been moreextensive.

FIG. i.-Post-amputation arteriogram after high tensionelectrical burn of the forearm in a boy of 14.The soft tissues of the forearm were extensivelydestroyed, with thrombosis of both the radial andulnar arteries. Thrombosis did not extend beyondthe wrist. The limit of this process is indicated forthe ulnar artery and its branches ('Thromb').Some of the arteriographic medium is extravasated('Extrav').

The intravascular injection of chemical irritantsmay produce thrombosis. This occurs frequentlyafter intravenous therapy and is usually harmless.Intra-arterial injection is more serious. Gangreneof a limb has occurred after intra-arterial trans-fusion and is frequent after inadvertent injectionof pentothal (Stone and Donnelly, 1961).

Burns of thermal or electrical origin causeextensive local thrombi. In the case of hightension contact, the current is said to pass forgreat distances along the main vessels, withresultant extensive thrombosis and gangrene(Muir, 1958). Fig. i, however, shows that the

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726 POSTGRADUATE MEDICAL JOURNAL December i963..........A.

VEOU ....E..URE.

duringaffthxprmet

gfenea artria pressure.1/

: ~~i11 0 i

FEMORAL ART-ERY. FLO-W

+ --hr,2MilFIG.2.-ffeto feoralvenus cclsio onfoVntecopno rey nadgVne

ne-mbuani tei.Teatnain(atn) fvnu rsuercrigwsmdfe

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general arterial pressure.

thrombosis need not extend to the very end of thevascular tree. Frostbite readily produces majorvenous or arterial thrombosis, especially in thepresence of pre-existing arterial disease.

Variations in Ischaemic EffectThe degree of ischwmia produced by occlusion

or division of an artery depends first of all uponthe degree to which the artery is normally endowed-with collaterals. Thus, injuries to the poplitealartery show a greater incidence of gangrene thando injuries to the femoral artery (Edwards, 1958).Concomitant injury to collaterals obviously addsto the ischbmia.

It is well appreciated that effective collateralsare lacking for the supply of most viscera. Thesame is true for some portions of skin, the nervesgnd the muscles of the limbs (Edwards, 1954).Some individual muscles are notoriously limitedin their supply and may become ischmmic ornecrotic, quite out of proportion to the state ofthe remainder of the limb (Edwards, 1953).

The rectus femoris, for example, may becomeentirely necrotic on interruption of its singlesupply from the lateral femoral circumflex artery.The gastrocnemius is vulnerable because of thesingle artery to each of its two heads. The bicepshumeri likewise may have but one artery supplyingit, although in most subjects it possesses up toeight arteries. Occlusion of the anterior tibialartery may cause necrosis of the entire contentsof the anterior tibial compartment.

Theoretically, collaterals may exist in sufficientnumber so as to re-establish the original flow, butas the accompanying Table i (taken from a workon plumbing engineering) illustrates, these smallvessels must be exceptionally numerous indeed toattain such a happy result.Flow is, of course, also directly related to

pressure, and inversely related to viscosity.Adequate restoration of blood volume and pressureis thus of great importance in restoring blood flow,while the judicious use of saline or low-molecularweight dextran may assist flow considerably.

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December I963 EDWARDS and FIDDIAN: Blood Vessel Injury: Features of the Pathology

TABLE i.-The number of i-inch pipes that willdischarge as much as a single pipe of other sizesfor the same pressure loss. (From Babbitt, H. E.,Plumbing. McGraw-Hill Book Company, New-York, I960).

Size of pipe, in. j I 2 4 8 io

Number of j-in.pipes withsame capacity I 6.2 37.8 I 89 _I,200 2,090

Subfascial aedema, alone or associated withhmmorrhage, can produce ischamic changes in alimb. This is not infrequently the dominantmechanism of ischmmia following injury such assupracondylar fracture of the humerus. Theocclusion is relieved in these cases by division ofthe deep fascia.

Muscle is very sensitive to ischaimia and atleast partial necrosis follows arterial occlusionlasting four hours or more (Edwards, I953).Indeed, contracture of muscle may be notedwithin an hour of ischlemia. This early con-tracture wears off completely if blood flow isquickly restored. If high grade ischaemia con-tinues, autolysis then produces a flail limb within24 hours. Lesser degrees of unrelieved ischaemiago on to the fibrotic contracture of Volkmann(Griffiths, I940).

Since World War I, there has been a good dealof conflicting testimony regarding the effect ofvenous ligation for concomitant arterial occlusion.Since flow is directly related to differentialpressure, any increase in resistance to the outflowof an in vitro system lowers flow, but even themore recent physiologic experiments, with thebetter instrumentation now available, do notalways show this result in the living animal. Thefactor operating to help maintain the flow is theincreased transmural pressure which producespassive vasodilatation of the vascular tree and aconsequent reduction in resistance to flow(McDonald, I960; Read, Kuida and Johnson,I958).. The results in the dog, as observed in ourlaboratory, have varied somewhat. An immediatediminution in arterial flow was constant, but thiscould be quite transient and succeeded by asubstantial rise, while the venous pressure,although diminishing, was still far above its initiallevel (Figs. 2 and 3). When the inflow arterialpressure was very low, no such secondary rise inarterial flow was observed throughout the houror two of duration of our experiments, and in onecase thrombosis of a narrowed arterial lumenresulted (Fig. 4). One clinical counterpart of theseexperiments is arteriosclerosis, where venousligation or thrombosis may diminish flow suffi-ciently to precipitate gangrene.

FEMORAL ARTERY FLOW

FIG. 3.-Effect of femoral venous occlusion on arterialflow in another dog. While the flow vacillatedsomewhat, there was a tendency to a considerableincrease during the venous occlusion.

ARTERIAL PRESSURE Neosynephrine20mg. 220

120 mm.Hg. 116 116

VENOUS PRESSURE

13 mm. Hg. 16 13 10

5- min.

> FEMORAL ARTERY FLOW Thrombosis ofIV with .67mm. lumen narrowed arterial

6E inserted in Fem. art. lumenVein released

7ml./min.| 4 1

FIG. 4.-Effect of femoral venous occlusion on arterialflow when stenosis is present in the artery. Flowfalls with the venous occlusion, and thrombosis ofthe stenotic lumen finally occurs.

To return to arterial injury, it would seem fromour own observations and the work of others thatthere is no adequate justification for adding venousinsult to arterial injury, especially as reconstructivesurgery is so well established that the new pointof discussion is whether to reconstruct the veinas well as the artery, when both are injured.

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728 POSTGRADUATE MEDICAL JOURNAL December I963

Summary and ConclusionsThe most common cause of penetrating vessel

injury is wounding by knife or gun-shot, althoughblunt trauma may also rupture major vessels.Spontaneous haemostasis more readily followscomplete, than incomplete, transection. Incom-plete laceration may be followed by dissectinghlmatoma, aneurysm or arteriovenous fistula.

Blunt injury, as in fractures, is the commonestcause of traumatic vascular occlusion, which mayalso follow repeated lesser trauma, irritation of avessel by infection, irradiation, or the accidentalinjection of chemical irritants. Electrical burnscause thrombosis which does not necessarilyextend to the acral arterial tree.

Variation in ischimic effect depends at theoutset upon the excellence of collateral endow-ment. Not only the viscera, but also other tissues,notably the muscles, may anatomically lackadequate collaterals, and may thus be subject tototal necrosis after relatively localized vascularinterruption.Experiment also demonstrates that local venous

obstruction produces a fall in arterial flow whichis transient unless a general or local arterialhypotension exists. In other instances the fall maybe followed by a moderate increase. This hasbeen ascribed to passive vasodilatation of thevascular tree and a consequent reduction ofperipheral resistance.

REFERENCESBRUNSCHWIG, A., and BROCKUNIER, A. (I960): Postoperative Rupture of Major Vessels After Radical Pelvic Operation,

Amer. J. Obstet. Gynec., 8o, 485.EDWARDS, E. A. (I953): The Anatomic Basis for Ischemia Localized to Certain Muscles of the Lower Limb, Surg.,

Gynec. Obstet., 97, 87.(I954): Localized Ischemia in the Lower Extremities, G.P. (Kansas), 9, 40.(1958): The Anatomy of Collateral Circulation, Surg., Gynec. Obstet., Io7, I83.

ELKIN, D. C., and DEBAKEY, M. E. (editors) (1955): 'Surgery in World War II: Vascular Surgery', Medical Department,U.S. Army, Washington.

FORRESTER, A. C., and SAUNDERS, R. E. 0. (1955): Intra-arterial Thiopentone, Brit..7. Ana&sth., 27, 594.GRIFFITHS, D. L. (I940): Volkmann's Ischmemic Contracture, Brit..7. Surg., 28, 239.GRYSKA, P. F. (I962): Major Vascular Injuries: Principles of Management in Selected Cases of Arterial and Venous

Injury, New Engl. J7. Med., 266, 38I.HOOVER, N. W. (I96I): Injuries of the Popliteal Artery Associated with Fractures and Dislocations, Surg. Clin. N. Amer.,

4I, 1099.HUFNAGEL, C. A., and CONRAD, P. (I962): Abdominal Arteriovenous Fistulas, Surg., Gynec. Obstet., II4, 470.JAHNKE, E. J. (1958): Late Structural and Functional Results of Arterial Injuries Primarily Repaired: Study of One

Hundred and Fifteen Cases, Surgery, 43, 175.JANEs, J. M., and JENNINGS, W. K. (196I): Effect of Induced Arteriovenous Fistula on Leg Length: io-year Observa-

tions, Proc. Mayo Clin., 36, i.KINMONTH, J. B., HADFIELD, G. J., CONNOLLY, J. E., LEE, R. H., and AMAmoso, E. C. (1956): Traumatic Arterial

Spasm: Its Relief in Man and Monkeys, Brit. 3. Surg., 44, i64.MAKINS, G. H. (I9I9): 'On Gunshot Injuries to the Blood Vessels'. New York: William Wood.McBURNEY, R. P., and GEGAN, E. (I962): Blunt Trauma to the Aorta and Major Arteries, 7. Amer. med. Ass., I80, 330.McDONALD, D. A. (I960): 'Blood Flow in Arteries'. Baltimore: Williams and Wilkins.MoRRis, G. C., CREECH, O., and DEBAKEY, M. E. (1957): Acute Arterial Injuries in Civilian Practice, Amer. 3. Surg.,

93, 565.MUIR, I. F. K. (1958): The Treatment of Electrical Burns, Brit. 7. plast. Surg., 10, 292.NEELY, W. A., HARDY, J. D., and ARTZ, C. P. (I96I): Arterial Injuries in Civilian Practice: A Current Reappraisal

with Analysis of 43 Cases, 3. Trauma, I, 424.PARMLEY, L. F., ORBISON, J. A., HUGHES, C. W., and MATTINGLY, T. W. (1954): Acquired Arteriovenous Fistulas

Complicated by Endarteritis, and Endocarditis Lenta due to Streptococcus fecalis, New Engl. J7. Med., 250, 305.QUICK, A. J. (1942): 'The Hemorrhagic Diseases and the Physiology of Hemostasis'. Springfield, Illinois: Charles C

Thomas.READ, R. C., KUIDA, H., and JOHNSON, J. A. (1958): Venous Pressure and Total Peripheral Resistance in the Dog,

Amer. 3. Physiol., I92, 609.SHUCK, J. M., and TRUMP, D. S. (I96I): Nonpenetrating Abdominal Trauma with Injury to Blood Vessels, Amer.

Surg., 27, 693.STARZL, T. E., KAUPP, H. A., BEHELER, E. M., and FREEARK, R. J. (I962): The Treatment of Penetrating Wounds of

the Inferior Vena Cava, Surgery, 5I, 204.STEINBERG, I. (1957): Chronic Traumatic Aneurysm of the Thoracic Aorta, New Engl. Y. Med., 257, 9I3.STONE, H. H., and DONNELLY, C. C. (I961): The Accidental Intra-arterial Injection of Thiopentol, Anesth., 22, 995.TAKARO, T., and SCOTT, S. M. (I960): Spontaneous Closure of a Traumatic Arteriovenous Fistula of Seven Years'

Duration, Arch. Surg., 8i, 965.VALLS-SERRA, J. (I951): Arteritis por Muletas: Trombosis Aguda Tratada por Arteriectoma Axilar, Angiologia, 3, 59.WOLBACH, S. B. (I909): The Pathological Histology of Chronic X-ray Dermatitis and Early X-ray Carcinoma, Y. med.

Res., x6, 415.ZEHNDER, M. A. (1956): Delayed Post-traumatic Rupture of the Aorta in Young Healthy Individual after Closed

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