Etiology of late developing incisional hernias — the possible role of mechanical stress

Etiology of late developing incisional hernias — the possible role of mechanical stress

Medical Hypotheses (1988) 25. 31-34 ,&‘ Longman Group UK Ltd 1988 Etiology of Late Developing Incisiona! Hernias the Possible Role of Mechanical Stre...

386KB Sizes 0 Downloads 12 Views

Medical Hypotheses (1988) 25. 31-34 ,&‘ Longman Group UK Ltd 1988

Etiology of Late Developing Incisiona! Hernias the Possible Role of Mechanical Stress J. D. URSCHEL, P. G. SCOTT and H. T. G. WILLIAMS Department Canada

of Surgery,

W. C. Mackenzie

Health

Sciences

Center, University

of Alberta,

Edmonton,

Abstract - The etiology of incisional hernias that develop a year or more after laparotomy is not understood. This subset of incisional hernias is not associated with the etiologic factors usually implicated in incisional hernia formation. Mechanical stress is known to have a profound influence on the structure of both normal and wounded tissue. It is hypothesised that mechanical stress plays an important role in the development of late incisional hernias. Keywords:

incisional

hernia;

stress,

mechanical;

Introduction

wound

healing.

within the first post-operative year (6), there is evidence that a significant number develop a year or more after sound fascial healing has apparently taken place (4, 6-8). Although there is a relative paucity of literature dealing with the etiology of these late developing ‘hernias, the available evidence indicates that the causal factors usually implicated in incisional hernia formation are not involved (4, 7). Fascial incisions that partially separate in the early weeks of healing, to leave a wider than normal scar, appear to have an increased risk of developing a hernia in subsequent months or years (9). The ability of a fascial would, whether abnormally wide or not, to stretch into an incisional hernia a year or more after laparotomy is a puzzling problem.

An incisional hernia may be defined as a hernia that develops in the scar of a laparotomy incision. The diagnosis is established by demonstrating a fascial defect during physical examination (1). Recent prospective studies have documented the development of incisional hernia in 4.7 to 11% of laparotomies (l-3). Wound infection is recognised as the most important etiologic factor associated with the formation of incisional hernias (2-5). Postoperative mechanical stress, in the form of abdomial distention from ileus, and excessive coughing associated with respiratory complications, represents another important causal factor (1, 2, 5).. While the majority of incisional hernias occur 31

32

MEDICAL HYPOTHESES

It is the purpose of this paper to construct a hypothesis to explain the pathogenesis of late developing hernias. Evidence supporting the concept that mechanical stress plays a major role in the regulation of tissue and wound structure will be reviewed. The possible involvement of mechanical stress in late incisional hernia formation will be discussed. Alteration of Mechanical Environment Structural Adaptation in Tissues

Causes

A number of investigators have studied the effect of tensile mechanical stress on cells in vitro. Increasing mechanical stress causes an increase in cellular activity, the nature of which varies with the cells under study and the methodology used. Accelerated cell cycling (10) and DNA synthesis (11, 12) have been observed. Increased synthesis of non-collagenous proteins (12, 13), collagen (13, 14), metalloproteinases (15), and proteoglycans (14) have been reported in cell culture or organ explant systems subjected to tension. The concept that changes in mechanical environment influence tissue structure is well established for calcified tissue. Bone deprived of normal intermittent stresses, because of immobilisation (16), rigid internal fixation (17), or denervation (18)) becomes osteoporotic. In contrast, increased mechanical stimuli result in the deposition of additional bone (19). The hypertrophic response of skeletal muscle to increased functional loads in well known (20). Cardiac muscle responds in a similar fashion to the altered mechanical environment seen in aortic valve stenosis (21). In benign prostatic hyperplasia, bladder smooth muscle hypertrophies to overcome the obstructing forces placed upon it (22). Small bowel, when partially obstructed, demonstrates increased collagen synthesis and content (23). Structural changes in blood vessels occur with increases in wall tension. Arteries exposed to hypertension display increased collagen content (24). Similarly, venous autografts employed in arterial reconstruction develop intimal fibrosis when placed in their new environment (25). Clearly, mechanical stress has an important influence on tissue structure. Structural Adaptation to Changes in Mechanical Environment Has Limitations

Tissues have a limited ability to withstand mechanical forces. For all of the cases of struc-

tural adaptation discussed above, excessive stress results in a variable degree of cell death and tissue failure. Fatigue fracture (16), ventricular dilatation in mitral or aortic valve incompetence (26), and bladder diverticuli seen in obstructive conditions (22) are specific examples, of tissue failure under excessive mechanical stress. Although the pathogenesis of direct inguinal hernias is far from clear, abdominal straining, as occurs in benign prostatic hyperplasia (27) and obstructing colonic diseases (28), is thought to be an important contributing factor. Mechanical Stress Influences

Wound Healing

There is an abundance of evidence pointing to the beneficial effect of limited intermittent stress on fracture healing (29, 30). While experimental work in soft tissues is not as conclusive, there is suggestive evidence that modest distracting forces enhance the strength of tendon (31), skin (32-34), ligament (35), and fascial wounds (36). The support for a beneficial effect of stress on fascial healing, however, has recently been weakened (37). As is the case with non-wounded tissue, excessive mechanical stress can be detrimental to wound repair. Inadequate immobilisation is often a contributing factor in fracture non-union (38). Tendon repairs subjected to premature stress may dehisce or partially separate (39). Skin incisions closed under tension are notorious for stretching into a wide, unsightly, scar (40). The propensity of knee ligament repairs and reconstructions to lengthen when subjected to the mechanical rigors of ambulation is a troublesome problem (41, 42). Finally, the stretching of a sub-total cystectomy scar in response to intermittent bladder distention is one case where stress induced expansion of repairing tissue may be beneficial (43). Two characteristics of soft tissue wounds could conceivably accentuate their responsiveness to changes in their mechanical environment. Firstly, wounds of fascia (44), skin (45), and most other soft tissues, never attain the full tensile strength of normal tissue. Secondly, wound remodeling, a process characterised by simultaneous collagen breakdown and synthesis, gives scar tissue an ability to change structure in repsonse to mechanical stress. Although scars often seem to be inert after several months of healing, many soft tissue wounds are actively engaged in remodeling for periods well over one year. The breakdown of old scars in scurvy (46)

MECHANICAL STRESS IN LATE DEVELOPING INCISIONAL HERNIAS

and the finding of significant collagenase activity in mature wounds (47) supports this concept. If scar tissue is indeed more sensitive than normal tissue to mechanical stress, it would seem probable that an initially broad scar would have a greater potential for stretching than a narrower wound since the zone of active remodeling would be much wider.

9.

10. 11.

12.

Conclusion Mechanical Stress May Be Important in the Etiology of Late Developing Incisional Hernias

Clearly, the structure of wounded and normal tissues is subject to the influence of mechanical factors. Mechanical stress causes stretching of soft tissue scars in many diverse tissues. It is appealing to hypothesise that mechanical stresses could cause a fascial scar to expand into an incisional hernia. Incisions characterised by a wider than normal fascial scar in the early weeks of healing would be especially likely to stretch in response to mechanical stress. The raised intra-abdominal pressure and increased abdominal muscle tension associated with coughing (48), heavy physical exertion (48), or straining during defecation and voiding (49), represent significant mechanical forces. Patients subjected to these forces on a repetitive basis, as occurs in chronic and bronchitis, benign prostatic hyperplasia, chronic constipation, may be at risk for late incisional hernia formation. In order to substantiate or refute this hypotensis, extensive clinical and experimental investigation is required. Long term clinical studies, experimentation with a suitable animal model, and the quantification of stresses acting on fascial wounds are needed.

13.

14

15.

16

17

18

19

20.

21.

22.

23.

References

?(

‘q.

1. Pollock A V. Luparotomy. J R Sot Med 74: 480. 1981. 2. Bucknall T E, Cox P J, Ellis H. Burst abdomen and incisional hernia: a prospective study of 1129 major laparotomies. Br Med J 284: 931, 1982. 3. Irvin T T, Stoddard C J, Greavey M G, et al. Abdominal wound healing: a prospective clinical study. Br Med J ii: 351, 1977. Ellis H, Ga.lraj H, George C D. Incisional hernias: when do they occur? Br J Surg 70: 290, 1983. Fischer I D. Turner F W. Abdominal incisional hernias: a ten year review. Can J Surg 17: 202, 1974. Akman P C. A study of jive hundred incisional hernias. J Int Coil Surg 37: 125. 1962. Harding K G, Mudge M, Leinster S J, et al. Lute development of incisional hernia: an unrecognized problem. Br Med J 286: 519, 1983. 8. Mudge M, Hughes L E. Incisional hernia: a IO year

25.

26.

27.

28. 29.

33

prospective study of incidence and attitudes. Br J Surg 72: 70, 1985. Playforth M J, Sauven P D, Evans M, et al. The prediction of incisional hernias by radio-opaque markers. Ann R Coil Surg Engl 68: 82, 1986. Curtis A S-G, S&har G M. The control of cell division bv tension or diffusion. Nature 274: 52. 1978. Brunette D M:* Mechanical stretching increases the number of epithelial cells synthesizing DNA in culture. J Cell Sci 69: 35, 1984. Hasegawa S. Saito S S, Suzuki Y, et al. Mechanical stretching increases the number of cultured bone cells synthesin’ng DNA and alters their pattern of protein svnthesis. Calcif Tiss Int 37: 431, 1985. hiekle M C, Reynolds J J, Sellers A, et al. Rabbit cranial sutures in vitro: a new experimental model for studying the response of fibrous joints to mechanical stress. Calcif Tiss Int 28: 137, 1979. Leung D Y M, Glagov S, Mathews M B. Cyclic stretching stimulates synthesis of matrix components by arterial smooth muscle cells in vitro. Science 191: 475. 1976. Miekle M C, Sellers A, Reynolds J J. Effect of tensile mechanical stress on the synthesis of metal-loproteinases by rabbit coronal sutures in vitro Calcif Tiss Int 30: 77. 1980. Lanyon L E. Mechanical function and bone remodeling. In: Bone in Clinical Orthopaedics. (Sumner-Smith. eb) W B Saunders, Philadelohia, 1982. Tonino A J. Davidson C’L, Klopper P J. et al. Protection from stress in bone and it.seffects. J Bone Joint Surg 588: 107. 1976. Gillespie J A. The nature of bone changes associated with nerve injuries and disuse. J Bone Joint Surg 36B: 464, 1’354. Goodship A E. Lanyon L E, McFie H. Functional adaptution of bone to increased stress: an experimental study. J Bone Joint Surg 6lA: 539, 1979. Costill D L. Coyle E F, Fink W F. et al. Adaptations in skeletal muscle following strength truining. J Appl Physio 146: 96. 1979. Hood W P Jr, Rackley C E, Rolett E L. Wall stress in the normal and hypertrophied human left ventricle. Am J Cardiol 22: 550, 1968. Rohbins S L, Cotran R S, Kumar V. Bladder. In: Pathologic Basis of Disease. 3rd ed. W B Saunders. Philadelphia. 1984. Stromberg B V, Klein L. Collagen dynamics of partial small bowel obstruction. Am J Surg 148: 257. lY84. Wolinsky H. Response of the rut aortic media to hypertension - morphological and chemical studies. Circ Res 26: 507. 1Y70. Brody W R, Kosek J C. Angel1 W W. Changes in vein grafts following aortocoronar_v bypass induced by pressure und ischemia. J Thorac Cardiovasc Surg 64: X47, lY72. Dodge H T, Kennedy J W, Petersen J. Quantitative angio-cardiographic methods in the evaluation of valvulur heart disease. Prog Cardiovasc Dis 16: 1, 1973. Craighead C C, Cotlar A M, Moore K. Association disorders with acute incarcerated groin hernia. Ann Surg 159: Y87. 1064. Maxwell J W. Davis W C, Jackson F C. Colon carcinoma and inguinal hernia. Surg Clin North Am 45: 1165, 1965. Sarmiento A, Schaeffer J F, Beckerman L, et al. Fracture healing in rat femora as affected by functional weight bearing. J Bone Joint Surg 59A: 369. 1977.

MEDICAL HYPOTHESES

34 30. Kenwright J, Richardson J B, Goodship A E, et al. Effect of controlled axial micromovement on healing of tibia1 fractures. Lancet ii: 118.5. 1986. 31. Woo SL-Y. Gelberman R H. Cobb N G. et al. The importance of controlled passiv; mobilizatidn on flexor tendon healing. Acta Orthop Stand 52: 615, 1981. 32. Forrester J C, Zederfeldt B H, Hayes T L, et al. Wolffs law in relation to the healing skin wound. J Trauma

10: 770. 1970. 33. Brunius V, Ahren C. Healing of skin incisions during reduced tension of the wound area. Acta Chir Stand 135: 383. 1969. 34. van Royen B J, O’Driscoll S W, Dhert W J A, et al. A comparison of the effects of immobilizafion and continuous passive motion on surgical wound healing in mature rabbits. Plast Reconstr Surg 78: 360, 1986. 35. Frank C, Akeson W H. Woo SL-Y, et al. Physiology and therapeutic value of passive joint motion. Clin Orthop

185: 113. 1984.

evaluation of factors affecting the strength of tendon repairs. Plast Reconstr Surg 59: 708, 1977. 40. McGregor I A. Fundamental Techniques of Plastic

Surgery and Their Surgical Applications. Churchill Livingstone. Edinburgh, 1980. 41. Alexander H. Weiss A B. Editorial. Clin Orthop 196: 2, 1985. 42. Frank C, Amiel D, Woo SL-Y, et al. Normal ligament properties and ligament repair. Clin Orthop 196: 15. 1985. 43. Peacock E E. Heading repair of peritoneum and viscera. In: Wound Repair. W B Saunders, Philadelphia, 1984. 44. Douglas D. The healing of aponeurotic incisions. Br J Surg 40: 79. 1952. 45. Levenson S M, Geever E F, Crowley L, et al. The healing of rat skin wounds. Ann Surg 161: 293, 1965. 46. Cohen I, Keiser H. Disruption of healed scars in scurvy -

the result of a disequilibrium

in collagen metabolism.

Plast Reconstr Surg 57: 213. 1976.

S, Ferguson D J. Effect of tension on healing of aponeurotic wounds. Surgery 44: 619. 1958. 37. Sauter E, Thibodeaux K, Myers B. Effect of high tension and relaxing incisions on wound healing in rats. South

47. Riley W, Peacock E E. Identification. distribution, and

Med J 78: 1451, 1985. 38. Sevitt. Non-union of fractures. In: Bone Repair and Frac: ture Healing in Man. Churchill Livingstone, Edinburgh. 1981. 39. Ketchum L D, Martin N L, Kappel D A. Experimental

pressure measurements using a wireless radio pressure pill and two wire connected pressure transducers: a comparison. Stand J Rehab Med 16: 139, 1984. 49. Light H G, Routledge J A. Intra-abdominal pressure. Factor in hernia disease. Arch Surg 90: 115, 1965.

36. Thorngate

significance of a collagenolytic. enzyme in human tissue.

Proc Sot EXD Biol Med 124: 207. 1967. 48. Nordin M, iXlfstrom G, Dahlquist P. Intra-abdominal