I0

TIME No. OF SINCE CASES

FRACTURE --I_---- ~-

z years 7

3 years 8 ___-

T H E B R I T I S H J O U R N A L O F S U R G E R Y

PERCENTAGE CORRECTION

OF DEFORMITY

66

75

slowly, and this has been our experience as well as that of Blount and others (1942). Irrespective of age, angulation at this level should be accepted with the greatest caution. Case 7 (Table IZr), with fracture of the mid-shaft of the radius, had 61 per cent correction

Table ZV.-THE AVERAGE RATES OF CORRECTION OF ANGULAR DEFORMITIES IN THE DISTAL THIRD OF FOREARM

(Based on 26 Cases from Table Z Z Z )

of 26’ angulation in 5 years (Fig. 13), whereas in the same period Cases 1-6 had almost complete correction of the deformities following fractures of the distal third. Similarly, Case 17, with a fracture of the mid-shaft of the radius and ulna, had 51 per cent correction of the deformity while the average correc- tion for the deformities of the distal third was 75 per cent in the same period.

FACTORS CONTRIBUTING TO ANGULAR DEFORMITY

An analysis of the factors contributing to the angular deformity in these 36 cases revealed the following causes in order of frequency:-

I. Failure of the parents to follow the detailed instructions, e.g., to report for a check radiograph I week after reduction or when the plaster had become soft or disintegrated.

2. Immobilization in mid-pronation for fractures of the distal third of the forearm.

3. Either deliberate acceptance of or failure to appreciate a commencing tilt in a check radiograph I week following reduction.

4. Acceptance of a position of incomplete reduction with consequent deterioration in angulation.

5 . Established malunion at the first visit to hospital because the fracture had been unnoticed and/or untreated.

SUlMlMARY The 1767 consecutive fractures of the forearm in

children under 12 years are reviewed. The results of follow-up of 36 cases with considerable residual angulation at the fracture site are discussed and the causes contributing to this assessed.

I t is evident that :- I. Angular deformity of the distal third of the

forearm usually corrects fully with growth of the bone within 5 years, provided that the lower radial epiphysis does not fuse in the meantime. There is therefore very little, if any, indication for repeated closed manipula- tions or for open reduction in patients below the age of 10 years. As fusion of the lower radial epiphysis may occur as early as 15 years, correction should be considered in patients showing angular deformity in consequence of an injury sustained after the age of 10 years.

2. Angular deformity of the mid-shaft of the forearm bones corrects relatively poorly and results in limitation of pronation and/or supination. There is therefore more justification for repeated attempts to correct the displacement in fractures at this level.

REFERENCES AITKEN, A. P. (1935a),J. BoneJt Surg., 17, 302. -- (1935b), Zbid., 17, 922. BLOUNT, W. P. (I955), Pediat. Clin. N. Amer., 1097. -- SCHAFFER, A. A., and JOHNSON, J. H. (I942), J .

Amer. med. Ass., 120, 1x1. BOSWORTH, B. M. (1941), Surg. Gynec. Obstet., 72, 667. CAFFEY, J. (1956), Pediatric X-ray Diagnosis, 3rd ed., 691.

Chicago: The Year Book Publishers. GIBERSON, R. G., and IVINS, J. C . (I952), Minnesota

Medicine, 35, 744. WATSON-JONES, R. (I955), Fractures and Joint Injuries,

4th ed. Edinburgh and London: E. & S. Livingstone, Ltd.

THE AETIOLOGY OF POST-OPERATIVE ABDOMINAL ADHESIONS*

AN EXPERIMENTAL STUDY

BY HAROLD ELLIS PROFESSOR OF SURGERY, WESTMINSTER MEDICAL SCHOOL, LONDON

INTRODUCTION LIKE so many other common phenomena in surgery, little is known about the fundamental aetiology of the fibrous adhesions which may follow abdominal operations. We do know that injury to, or inflamma- tion of, the abdominal viscera results in an outpouring of fibrin which can cause these structures to adhere to

* This paper represents the substance of a thesis accepted for the degree of D.M. (Oxon.).

their neighbours within as little as three hours (Trompke and Siegner, 1956). The majority of these fibrinous adhesions are transient and become absorbed within a few days (Jackson, 1958). Some, however, become organized by the ingrowth of fibroblasts and blood capillaries to become established fibrous adhesions.

The crucial point is thus the factor which determines whether fibrin is absorbed or is converted into fibrous tissue. The generally accepted view

P O S T - O P E R A T I V E A B D O M I N A L A D H E S I O N S

OF ADHESIONS

I1

GANGRENE OF

(Connolly and Smith, 1960) is that this depends on post-operative adhesions, and that these adhesions the integrity of the peritoneal endothelium; if this is represent not scar tissue but vascular grafts from intact the fibrin disappears, if it is damaged adhesions adjacent healthy organs into a devascularized develop. It is as if these fibrous adhesions represent substrate. the scar tissue which forms in the healing of the destroyed serosa. Following on from this supposition, it is widely taught that damage to the peritoneum must be avoided and serosal defects meticulously

OBSERVATIONS All the experiments here described were performed

on male albino rats weighing between 250 and 300 g.

A B FIG. ~q.--Increasing bulk of adhesion formation with increasing lengths of mesenteric division. A, z's-cm. mesentery divided; rat

killed after 14 days. The only adhesion present is.a,strand fFom the fat fringe of the left testis to the centre of the devascularized bowel. Note its vascular nature. 6, 4-cm. mesentery divided; animal killed 14 days later. The affected segment of bowel IS buried in a mass of adhesions made up of small intestine, testicular fat fringe, and parietal peritoneal wall. Again note the vascularity of these adhesions.

Table Z.-EXTENT OF ADHESIONS FOLLOWING INCREASING LENGTHS OF MESENTERIC DIVISION

LENGTH OF

DIVIDED ADHESIONS ADHESION (in cm.)

MESENTERY 1 N"gER N O SINGLE

5 1 8 1 - 1 4

6 7

7

9

Total I 65 I 3 I 33

- I -

4 7 I I i 7 1 7

7 7

29

repaired if persistent post-operative adhesions are to be prevented. I t is interesting, therefore, that many years ago von Dembowski (1888) and Franz (1902) both showed experimentally that parietal peritoneal defects would heal without adhesion formation; findings that were later confirmed by Robbins, Brunschwig, and Foote (1949) and by Williams (1955).

In this paper we put forward an hypothesis that it is not serosal integrity but tissue ischzemia which is the important factor in the aetiology of fibrous

I. Mesenteric Division Experiments.-In 65 rats the small intestine mesentery was divided close against the bowel wall for distances of from 0.5 to 9 crn. When no major arcade vessels were divided (3 animals) the intestine remained a normal colour ; when one or more arcades were divided, immediate blanching of the affected segment was noted. Fourteen rats died of peritonitis or intestinal obstruction, the remainder were sacrificed 24 hours to 7 weeks post-operatively. All were submitted to

I2 T H E B R I T I S H J O U R N A L O F S U R G E R Y

autopsy, at which three observations were of mesentery-deprived intestine was striking and led to particular interest :- the question of what the fate of such devascularized

a. Adhesion formation had occurred in 62 of the bowel would be if these adhesions were prevented 65 animals and (apart from adhesions to the abdominal from forming to it. To investigate this, a sheet of incision) was confined entirely to the segment of thin, sterile polythene film was loosely wrapped

A

C

devascularized bowel : this localization was seen even in animals with general peritonitis. The exceptions were the 3 rats who had had short mesenteric divisions without damaging the vascular arcades, in none of whom did adhesions develop.

b. The bulk of adhesion formation was roughly proportional to the extent of the mesenteric division. With divisions of up to 3 cm. a single adhesion was usually found, either to adjacent intestine, or across the divided mesentery to the omentum or to a testicular fat fringe. With longer mesenteric divisions, a mass of adhesions would develop in close association with the affected segment of intestine (Table Z and Fig. 14).

c. The adhesions were invariably vascular; vessels could be seen streaming from them into the under- lying devascularized bowel, and they would ooze blood on attempted separation.

Gangrene was not seen in the mesenteric divisions of up to 4 cm. in length. Two of 8 animals with 5-cm. divisions developed gangrene of the affected segment, and this occurred in 15 out of the 16 rats subjected to divisions of between 6 and 9 cm. The exception was I rat with a 7-cm. division which had developed a highly vascular adhesion to the omentum (Table I).

2. Polythene-wrap Experiments.-The appar- ently vascular nature of the adhesions to the

B FIG. I 5.-Gangrene following prevention of adhesion forma-

tion to mesentery-deprived intestine. A, 2.S-cm. mesentery divided, intestine wrapped loosely in polythene film to prevent adhesions from reaching the devascularized segment. 24 hours later the bowel is gangrenous. B, Control experiment. kolythene film sutured around intestine with mesentery intact; 24 hours later the bowel remains viable. C, The contrast when adhesions are allowed to form. 2.5-cm. mesentery divided; 24 hours later the affected segment of intestine is edematous and there is azone of patchy discoloration 3 mm. wide, but the bowel is histo- logically viable. Adhesions have formed across the divided mesentery and also from the testicular fat fringe.

around segments of intestine whose mesentery had been severed for a length of 2.5 cm. This was performed in 10 rats and in every case gangrene of the segment took place by 24 hours (Fig. 15 A). The intestine of 6 control animals, in which the polythene was sutured around the intact bowel, remained perfectly healthy (Fig. 15 B). This invariable gangrene was in marked contrast to the viable appearance of similar segments of devascularized intestine, inspected at 24 hours, in which adhesions had been allowed to develop (Fig. 15 C).

A segment of intestine receives its blood from two sources, the adjacent mesentery and the collateral channels in the bowel wall. When the mesenteric blood-supply is cut off, the intramural collateral vessels are alone unable to maintain the viability of a 2.5-cm. length of intestine, hence the gangrene which invariably follows wrapping such segments in polythene. In contrast, when adhesions are allowed to form to the ischiEmic bowel, lengths of mesentery- deprived intestine of 2.5 cm. invariably, up to 5 cm. usually, and even up to 7 cm. rarely, are vascularized from these adhesions and remain viable (Table I).

3. Omental Graft Experiments.-In order to study the vascular ingrowth from adhesions into the ischasmic bowel, segments of mesentery-deprived intestine from 2.5 to 5 cm. in length were wrapped in a pedicle of omentum (Fig. 16 A). This procedure was performed in 71 rats. Nine animals died 4-20 days post-operatively, the remainder were sacrificed 1-48 weeks after operation. In all cases the omentum had become firmly adherent to the underlying intestine.

At autopsy, it could readily be shown that new vessels had grown in from the omentum to link up with the blood-vessels in the wall of the devascularized

I3

bowel. This was done by isolating the affected ischaemic tissue, with frank necrosis of the underlying intestine so that it remained attached only by its bowel. pedicle of omentum (Fig. 16 B). Micropaque was These investigations suggested that adhesions then injected into the aorta and could be seen, both at had developed in response to the stimulation of

P O S T - O P E R A T I V E A B D O M I N A L A D H E S I O N S

/ u 2 5 cms.

B

C D FIG. 16.-The vascular nature of pedicled omental grafts. A, A pedicled raft of omentum is sutured around the segment of intestine

whose mesentery has been divided.. B, At subsequent autopsy the segment ofintestine 1:s divided from all its attachments apart from the now adherent omentum. C, Injection of micropaque intra-arterially demonstrates radiographically a free communication between the vessels in the omentun and in the originally ischemic segment of bowel wall. D, This is a sketch made of a dissection carried out under a x 5 magnifying lens. Micropaque-filled vessels are seen streaming from the omental adhesions into the underlying devascularized intestine and there link up with vessels in the bowel wall. (The omental graft had been performed 3 weeks previously in this case.)

dissection and radiographically, to flow across vessels in the adherent omentum into the underlying bowel (Fig. 16 C and D).

Similar pedicled grafts of omentum sutured around the intact intestine merely pulled away, leaving only a fine strand of omentum adherent at the points of suture; thus without the stimulus of underlying ischaemic intestine, there was no tendency for adhesions to develop. In contrast, free grafts of omentum, completely deprived of their blood-supply, wrapped around the devascularized intestine, provoked an intense mass of adhesions to develop to the

ischaemic intestine and that these adhesions were vascular ingrowths from adjacent viable structures.

Farther experiments, performed on the parietal peritoneum, appeared to support this hypo- thesis.

4. Adhesion Formation in Relation to the Parietal Peritoneum.-A total of 58 defects, measuring from I cm. square to z cm. x 3 cm., were excised by sharp dissection from the parietal peritoneum. The rats were sacrificed 1-13 weeks later. In 53 cases the defects were found to have healed without adhesion formation. A striking

14 T H E B R I T I S H J O U R N A L O F S U R G E R Y

feature was the rapidity of peritoneal healing: application of free grafts, in an area of anoxic tissue within 7 days these large raw areas would be covered on the parietal wall, adhesions formed in 39 instances. with a shining membrane, often quite indistinguish- Careful naked-eye examination of these adhesions able from the adjacent intact peritoneum or else revealed fine vessels which bridged across from the apparent only as a slight haze. adhesion to the body wall. This was confirmed by

In contrast, 19 such windows were repaired by first isolating the segment of abdominal wall com- meticulous suture with fine black silk; 16 of these pletely from the body apart from its adhesion

FIG. I ~ . - A I-cm. square segment of peritoneum was crushed with arterv forceos on the rieht oarietal wall. On the left side a s&%r area was -gxcised-bybysKarp’ dissection. At autopsy I week later the left side has healed smoothly and completely; the omentum has become adherent to the crushed area on the right.

developed adhesions. Repair of such defects could only be achieved by dragging adjacent peritoneum together under tension, with the inevitable con- sequence of the production of patches of ischaemic tissue in the sutured area. This tissue, we suggest, provided the stimulus for adhesions to develop. This phenomenon was not merely a foreign-body response to the presence of the silk, since similar lengths of black silk sutured loosely into the parietal peritoneum in 6 instances did not result in local adhesion formation.

Three further experiments were performed, in each of which a zone of ischzmic tissue was produced on the parietal wall.

a. In 6 animals an area of parietal peritoneum I cm. square, together with the immediately subjacent abdominal wall, was crushed by artery forceps applied for 5 minutes. In 5 instances adhesions developed, although not to control areas of the same size excised by sharp dissection from the opposite abdominal wall (Fig. 17).

b. In 16 instances a small hillock of parietal peritoneum was lifted up by artery forceps and firmly ligated with black silk at its base, thus strangu- lating a button of peritoneum about 2-3 mm. in diameter. Adhesions developed to 13 of these 16 ischaemic nodules.

c. In 6 animals, I-cm. square ‘windows’ were cut away from the parietal peritoneum on each flank. On one side this ischaemic tissue was grafted back on to the defect using fine silk sutures: the other side was left raw. Two weeks later the animals were killed. Adhesions had developed to 5 of the grafts, yet all the ungrafted areas had healed smoothly and without adhesions having formed to them.

To summarize, then, of a total of 58 peritoneal defects left raw, adhesions developed in only 5 cases. However, in a total of 47 operations which resulted, whether from ligation, crush injury, suturing, or the

L. . . _ . .

FIG. IS.-A silk ligature had been applied to a button of parietal peritoneum 4 weeks previously. At autopsy the omentum was found adherent to this spot. The abdominal wall surrounding this area was excised from its surroundings apart from its omental adhesion and micropa ue was then injected into the aorta. This drawing, made unjer the x 5 dissection microscope, shows a tortuous new vessel connecting the artery in the omental adhesion to one in the abdominal wall.

attachment and then injecting micropaque into the aorta. The injection material was then seen to flow along vessels in the adhesion, through the newly formed linking vessels, to connect up with arteries in the abdominal wall (Fig. IS).

Adhesions to the Laparotorny Scar.-A total of 206 animals used in these experiments survived for more than I week after operation. At autopsy, adhesions to the midline laparotomy scar (which had been sutured in all cases with two layers of continuous thread) had developed in 33 cases (16 per cent). This occurred independently of the presence of peritonitis, intestinal obstruction, or infection of the laparotomy wound.

DISCUSSION The Role of Ischemic Tissue in the Aetiology

of Adhesions.-We can sum up our experimental findings by stating that fibrous adhesions developed in relation to areas of ischzmia induced either in the small intestine or on the parietal peritoneal wall of the rat. These adhesions appeared to be vascular ‘grafts’ from adjacent viable structures and could provide a sufficient blood-supply to their host tissues to main- tain viability.

Our findings at least suggest that tissue ischaemia is a potent stimulus to adhesion formation.

There are many other examples in experimental surgery of adhesions developing to tissues deprived of their blood-supply; not only, as in our own experi- ments, to intestine (Poth and McClure, 1950; Rabinovici and Fine, 1952) and peritoneum (GirgolafF, 1906; Springer, 1906; Verne and Perel, 1952), but also to the spleen (de Renzi and Boeri, 1903), the gall-bladder and kidney (Rubin, I~II), and to ischaemic omentum (Springer, 1910).

In man, instances are widespread where the presence of adhesions can be explained by this hypothesis. Thus pelvic tumours which have undergone avascular degeneration or torsion may become wrapped in dense adhesions to neighbouring

15 P O S T - O P E R A T I V E A B D O M I N A L A D H E S I O N S

structures (Hertzler, 1935; Strassmann, 1914)~ and fragments from a ruptured spleen, which have become completely deprived of their blood-supply, may adhere to adjacent tissues and survive (Zeifer, Juncker, and Fox, 1960). The adhesions which form to the line of a bowel anastomosis or a laparotomy scar can be explained by the strangulating effect of sutures in these situations. The adhesions encoun- tered between the sac and the contents of an irreducible hernia may represent the response to the anoxia of the strangulated tissues.

It is well known that laparotomy performed some time after an episode of general peritonitis usually reveals very little in the way of widespread persistent adhesions-there is no evidence that the peritonitis itself results in fibrous adhesions-yet the strands that are present are localized to those areas where intense tissue anoxia can be assumed to have occurred, for example, to the appendix, after an attack of appendicitis which has been treated conservatively, or to the gall-bladder, after an episode of acute cholecystitis.

Intraperitoneal adhesions may be encountered after irradiation of the abdomen (Saltzstein, 1945; Warren and Friedman, 1942; and White, 1940). This phenomenon, we suggest, is due to the pro- gressive endarteritis affecting the blood-vessels of the bowel wall following its exposure to radiation (Aldridge, 1942; Cade, 1948; Friedman, 1942).

Against this theory might be argued the clinical observation that, although fresh adhesions bleed when divided, long-standing adhesions are usually avascular along their line of attachment. Here the observations of North (1957) are of great interest. He found that the collateral vessels which develop in the rabbit’s ear after vascular interruption resorb once the main arterial channel has recanalized. We postulate that a similar phenomenon occurs in many human intra-abdominal adhesions. Initially these are vascular; subsequently, if the blood-supply is restored through normal channels, the vessels within the adhesion absorb leaving only fibrous strands as relics of the past.

The nature of the stimulus which provokes adhesions to form to ischaemic tissue remains a subject for speculation. It is possible that it is a chemotactic phenomenon in response to some substance produced by anoxic cells, resembling the polypeptides isolated from inflammatory exudate by Menkin (1947)~ which reproduce the local and general manifestations of the inflammatory process.

To Reperitonealize or Not ?-We have already quoted our own and other experimental evidence that defects of the parietal peritoneum, if left alone, heal speedily and usually without adhesions. The rapid rate of healing is not by a process of encroachment from the edges of the defect, but appears to be the differentiation of a new mesothelium from the underlying connective tissue (Williams, 1955 ; our own unpublished observations). That extensive parietal defects in man behave in a similar fashion is suggested by the absence of intestinal obstruction due to adhesions when large areas of pelvic floor are left denuded of peritoneum in radical pelvic eviscerative operations (Robbins and others, 1949).

Turning to serosal defects of the bowel, we find considerable diversity in experimental results. Some

authors (Craig and Bianchi, 1956; Gustavsson, Blomback, Blomback, and Wallen, 195s; Gellhorn, 1909; Hubay, Weckesser, and Holden, 1953) reported almost invariable adhesion formation after experi- mental excision of the peritoneal wall of the intestine. This was denied by Adams (1913) and inconstant results were reported by Cone (1959)~ Straus (1916)~ and Trusler (1931). These conflicting findings are resolved if the ischaemic theory of adhesion formation is invoked. We suggest that a serosal defect without underlying vascular injury will fail to provoke the necessary stimulus to adhesion proliferation and will heal rapidly by differentiation of a new mesothelium from the subjacent connective tissue. More severe serosal injury can only be achieved by some degree of damage to the local blood-supply, and we postulate that it is this ischaemic tissue which precipitates adhesions to form. This concept is supported by the work of Donaldson (1938)~ who found that adhesions failed to develop when the serosa of cats and rabbits was rubbed vigorously, although more violent injuries did cause adhesions to develop.

In this context, the work of Thomas, Greene, and Rhoads (1950) is of interest. They found that peritoneal defects fashioned on the intestinal wall of guinea-pigs and rats precipitated adhesions in 3 I per cent of cases. When such defects were sutured, however, adhesions occurred in 79 per cent of the animals. Such repairs can only be achieved at the expense of some damage to local blood-supply and this seems the probable explanation for the high incidence of adhesions in the second group of cases. These results are similar to our own findings that adhesions develop to the majority of sutured defects of the parietal peritoneum.

There is nothing to indicate, either from our own experimental work of from reviewing many other reports on this subject (Boys, 1942; Connolly and Smith, 1960)~ that reperitonealization prevents the development of post-operative adhesions. We suggest that when adhesions develop to raw areas they do so because of the associated vascular injury and not because of the peritoneal defect itself. The teaching that raw surfaces within the abdominal cavity must be avoided wherever possible results from a faulty concept based on a false comparison with the healing of similar lesions of cutaneous surfaces, which inevitably result in formation of scar tissue. Peri- toneum, a mesodermal derivative, is quite different in its behaviour, and a gap in it heals, not by scar tissue, but by differentiation of a new mesothelium from underlying connective tissue cells.

The Concept of Adhesions as Vascular Growths to Ischaemic Tissues.-The rapid growth of blood-vessels from adjacent viable organs into anoxic tissues via adhesions appears to offer an easily applied method of supplying an adjuvant blood-supply to potentially ischaemic intestine. Naturally the surgeon tries not to leave bowel of doubtful viability within the abdominal cavity; circumstances may arise, however, when this aim cannot be achieved. Where possible in such cases the intact omentum should be tacked around the damaged bowel, thus facilitating capillary invasion. Detached, ‘free’ grafts of omentum should be avoided; they will merely prevent vascular ingrowth into the underlying bowel. In our experi- ments such grafts invariably precipitated intense

16 T H E B R I T I S H J O U R N A L O F S U R G E R Y

adhesion formation to themselves, together with necrosis of the underlying devascularized segments of intestine.

SUMMARY The production of ischaemic areas of small

intestine or abdominal wall in the rat is followed by the formation of adhesions which can be shown by injection studies to be in the nature of vascular grafts to the devascularized tissues. It is postulated that tissue ischaemia, and not serosal damage, is the important factor in the aetiology of post-operative adhesions.

Acknowledgements.-This study was begun in the Nuffield Department of Surgery, Oxford, and was completed in the experimental surgery laboratory at Westminster Medical School. Valuable help was provided by Dr. G. N. Ardran and Mr. M. Tuckey, of the Nuffield Institute of Medical Research, Oxford; by Dr. Ian Dawson; and by Dr. Peter Hansel1 and the Department of Medical Photography at Westminster Hospital.

~~

REFERENCES ADAMS, J. E. (1913), Lancet, I, 663. ALDRIDGE, A. H. (1942), Amer.3. Obstet. Gynec., 44, 833. BOYS, F. (1942), Surgery, I I, 118. CADE, S. (1948), Malignant Disease and its Treatment by

CONE, D. F. (1959),Johns Hopk. Hosp. Bull., 105, 8 . CONNOLLY, J. E., and SMITH, J. W. (1960), Znt. Abstr.

CRAIG, R. L., and BIANCHI, R. G. (1956), Amer. J . Surg.,

VON DEMBOWSKI, T. (1888), Arch. klin. Chir., 37,745. DONALDSON, J. K. (1938), Arch. Surg., Chicago, 36,20.

Radium, 2nd ed., vol. I. Bristol: Wright.

Surg., 110, 417.

91, 369.

FRANZ, K. (1902)~ Z . Geburtsh. Gynak., 47,64. FRIEDMAN, N. B. (1942), Arch. Path. Lab. Med., 34, 749. GELLHORN, G. (1909), Surg. Gynec. Obstet., 8, 505. GIRGOLAFF, S. S. (1906), Zbl. Chir., 33,1212. GUSTAVSSON, E., BLOMBACK, B., BLOMBACK, M., and

HERTZLER, A. E. (1935), Surgical Pathology of the

HUBAY, C. A., WECKESSER, E. C., and HOLDEN, W. D.

JACKSON, B. B. (1958), Surgery, 44, 507. MENKIN, V. (1947), Lancet, I, 660. NORTH, K. A. K. (1957), “Factors Involved in the

Establishment of a Collateral Circulation.” D.Phi1. (Oxon.) Thesis.

POTH, E. J., and MCCLURE, J. N. ( I~so) , Ann. Surg., 131, 159.

RABINOVICI, N., and FINE, J. (1952), Zbid., 135,344. DE RENZI, E., and BOERI, G. (1903), Berl. klin. Wschr., 40,

ROBBINS, G. F., BRUNSCHWIG, A., and FOOTE, F. W., jun.

RUBIN, I. C. ( I ~ I I ) , Surg. Gynec. Obstet., 12, 117. SALTZSTEIN, H. C. (I945), Surgery, 18, 556. SPRINGER, C. (1906), Zbl. Chir., 33, 1297. -- ( I ~ I O ) , Beitr. klin. Chir., 67, 17. STRASSMANN, P. (1914), Surg. Gynec. Obstet., 19, 53. STRAUS, D. C. (1916), Zbid., 22,602. THOMAS, J. W., GREENE, J. W., and RHOADS, J. E. ( I ~ s o ) ,

TROMPKE, R., and SIEGNER, K. (1956), Arch. klin. Chir.,

TRUSLER, H. M. (I93I), Arch. Surg., Chicago, 22, 983. VERNE, J. M., and PEREL, L. (1952), Pr. mid., 60,619. WARREN, S. , and FRIEDMAN, N. B. (I942), Amer. J. Path.,

WHITE, W. C. (1940), Ann. Surg., I 12,769. WILLIAMS, D. C. (I955), Brit. J. Surg., 42, 401. ZEIPER, H. D., JUNCKER, A., and Fox, R. A. (1960),

WALLEN, P. (1955), Acta chir. scand., 109, 327.

Peritoneum. Philadelphia : Lippincott.

(1953), Surg. Gynec. Obstet., 96, 65.

773.

(1949), Ann. surg., 130, 466.

Surg. Forum, 125.

281, 323.

18,499.

Amer.3. Surg., 100,693.

SURGICAL REPAIR OF ATRAUMATIC LACERATION OF THE EXTRAPERICARDIAL SUPERIOR VENA CAVA WITH SURVIVAL

BY W. BURNETT AND H. D. BAILLIE FROM THE DEPARTMENT OF SURGERY, WESTERN INFIRMARY, GLASGOW

PENETRATING wounds of the chest complicated by laceration of the superior vena cava are usually quickly fatal. Only 4 cases have been reported as having survived this injury (Bigger, 1933 ; Hudson, 1952; Elkan, 1958; Ochsner, Crawford, and de Bakey, 1961). In z of these cases the vena cava was injured in its intrapericardial part (Bigger and Elkan). In the other 2 cases the wound was extrapericardial, Hudson’s case being complicated by division of the right phrenic nerve. In all 4 cases the entrance wound was on the anterior chest wall.

We describe here a case of laceration of the superior vena cava which resulted from a penetrating injury of the chest due to the explosion of a home- made bomb.

CASE REPORT A 13-year-old boy was admitted as an emergency to

the Western Infirmary, Glasgow, having been injured half an hour earlier by the explosion of a bomb which he

had made by packing a mixture of sugar and sodium chlorate into a copper tube. He was conscious, and complained only of thirst and of difficulty in breathing. He appeared pale and restless, the pulse was thready, the rate being 90 per minute; the systolic blood-pressure was 82 mm. Hg. There was a ragged wound 2 in. long over the second right interspace close to the sternum, the only other external injury being a minor cut on the dorsum of the left hand. The right side of the chest showed greatly diminished air entry, and was dull to percussion with a shift of the mediastinum to the left. A large haemothorax was assumed to be present. Although shocked, the patient showed no signs of further deterioration whilst under observation; it was thought, therefore, that the intrathoracic hzmorrhage had ceased.

Following an admission-room radiograph, an irregular fragment of metal was seen to be lodged high in the right side of the chest near the great vessels (Fig. 19). Preliminary blood transfusion was carried out through a polythene cannula inserted into the long saphenous vein at the right ankle. The systolic blood-pressure rose to normal level after 14 pints of blood had been given and