CRUSH INJURY, COMPARTMENT SYNDROME,
AND OTHER ACUTE TRAUMATIC ISCHEMIAS

Rationale

Acute traumatic ischemia (ATI) occurs when an injury compromises the circulation to an extremity. This compromise may place portions of the extremity or the entire extremity at risk of necrosis or amputation. Secondary complications such as infection, nonhealing wounds, and ununited fractures frequently develop. Ischemia can result either from injury to the macrosized blood vessels, as in open fractures with interruption of major arteries, at the microcirculation level, as in severe crush injuries and skeletal muscle compartment syndromes, or from combinations of the two.

Whenever hyperbaric oxygen (HBO,) is used for an ATI, the injury should be classified by a Standard Classification Method such as the Gustilo Grading System (Table 1) or The Mangled Extremity Severe Score (MESS) (Table 2) (1,2). For skeletal muscle-compartment syndromes the use of HB02 should be based on clinical findings coupled, when available, with interstitial fluid pressure measurements of the compartment (Table 3). Tables 1-3 provide specific criteria for using HB02 with these grading systems.

The rationale for using HB02 in ATIs is based on the pathophysiology of these conditions and how the mechanisms of HBO, influence them. The immediate threat to the limb is whether perfusion is sufficient to maintain viability of the tissues. Posttraumatic edema which is associated with traumatic injuries and ischemia further reduce oxygen availability to tissues. When tissue oxygen tensions fall below 30 mmHg, the host responses to infection and ischemia are compromised (3). Specifically, white blood cell killing becomes defective or nonexistent and host repair processes such as fibroblast migration, fibroblast proliferation and fibroblast secretion of collagen are arrested (4-6). Without a collagen matrix in the wound, neovascularization and wound healing cannot occur. The primary rationale for using HBO2, is that it increases tissue oxygen tensions in hypoxic tissues to levels which make it possible for the host responses to become functional. With HB02 at 2 atmospheres absolute (ata) the blood oxygen content is increased by 25 % whereas plasma and tissue oxygen tensions increase tenfold (i.e., 1000 %) (79). The net effect is that oxygen diffusion through tissue fluids is increased by a threefold factor (10, 11). Sufficient oxygen becomes physically dissolved in plasma to keep tissues alive despite inadequate hemoglobin-borne oxygen (9).

Edema reduction secondary to vasoconstriction is another effect of oxygenation. This mechanism reduces blood flow by 20 % (8). The benefit of vasoconstriction is a concomitant (i.e. 20 %) reduction in posttraumatic vasogenic edema (12-16). HBO, maintains oxygen delivery while the blood flow that contributes to edema formation is reduced. Concomitantly, blood flow m the microcirculation is improved through the edema reducing effects of vasoconstriction. In summary, the immediate effects of HBO are threefold in acute traumatic ischemias: (a) Enhanced oxygen at the tissue level, (b) Increased oxygen delivery per unit of blood flow, and (c) Edema reduction.

Finally, HBO may mediate the effects of the reperfusion injury in ATI's especially in those injuries where tissue ischemia is severe and/or prolonged (e.g. revascularization, replantations, etc.) by preventing sequestration of neutrophils on the endothelial wall, lipid peroxidation of cell membranes, and depletion of radical scavengers at the reperfusion site (19-30). Please refer to Section 1 1, Skin Graft and Flaps, Compromised for further discussion of the benefits of HBO in the reperfusion injury.

Ninety-three cases using HBO, in crush injuries were reported in the English language literature (31-37). Although none were controlled studies, all showed benefits from HBO2, for traumatic ischemias. In addition, Strauss summarized the reports of 634 cases from the Eastern European literature (38). The benefits of HB02 in these cases included "positive effects on local reparatory processes," "reduction of tissue damage," "accelerated recovery of neutrophile phagocytic activity," "accelerated diminution in edema," and "healing without suppuration." Recently published articles by Bouachour, et. al., Radonic, et. al., Shupak, et al., and Strauss and Hart offer additional reports consistent with the above series (39-42).

 

Utilization Review

The recommended treatment schedule is three 1.5-hour treatments per day over the first 48 hours followed by two 1.5-hour treatments daily over the second period of 48 hours and one 1.5-hour treatment daily over the third period of 48 hours. By the sixth day, restored perfusion, edema reduction, and demarcation or recovery should be sufficient to discontinue HBO, therapy. If HBO, therapy is to be continued beyond this time, utilization review should be obtained. The early application of HB02 therapy, preferably within 4 to 6 hours of the injury, is essential for efficacy. If surgery is delayed, HBO, therapy should be started before surgery.

 

Cost Impact

Hyperbaric oxygen decreases the complication rates associated with crush injuries, compartment syndromes, and other ATI'S. Complication rates approaching 50 % are reported in the management of open fractures with concomitant soft tissue defects and/or interruptions to the limb's blood supply (1,43,44). Complications include infection, nonunion, and amputation. In a recent report, it was found that when HBO, was used, presumably to arrest the progression of a skeletal muscle compartment syndrome and to obviate the need for surgical decompression, the estimated cost of management was one-fourth that of patients who had their compartment syndromes surgically decompressed. The addition of HBO2, to the management of patients with ATI's adds considerably to each patient's medical expenses. This expense is only a small percentage of the cost dealing with the complications of ATI's that could be reduced or prevented by HBO2.

  

 Table 1: Use of HBO, for Open Fracture (Gustilo Classification), 1 Crush Injuries

Type

Mechanism

Expected Outcome

HBO Indications

I

Small (< 1 cm) laceration
from inside to outside

Usually no different from a closed fracture

None

II

Large laceration, but minimal soft tissue damage

Usually no different from a closed fracture

Compromised hosts such as diabetics, advanced peripheral vascular disease, collagen vascular diseases, etc., where concern is raised about primary healing of flaps

III

Crush tissue:
A. Sufficient soft tissue to close wound (primary and delayed)
B. Flaps or grafts required to obtain soft tissue coverage

C. Major (macrovascular) vessel injury


Infections and/or nonunion rates < 10 %
About 50% incidence of complications (infection, nonunion)
About 50% incidence of complications (infections, nonunion)



Same as for type II fractures

All injuries


All injuries

 

Table 2: Use of HBO, for Mangled Extremities (mess score), Johansen'

A. Skeletal/soft tissue injury
Low energy (stab, simple fracture; low velocity gun shot wound)
Medium energy (open or multiple fractures, dislocations)
High energy (close-range shot gun or high velocity GSW, crush injury)
Very high energy (above plus gross contamination, soft tissue avulsion)

B.
Limb ischemia
Pulse reduced or absent, but perfusion present
Pulselessness, paresthesias, diminished capillary refill 2*
Cool, paralyzed, insensate, numb 3*
*Double score if ischemia time > 6 hours

C. Shock
Systolic BP always > 90 mmHg
Hypotension transiently
Persistent hypotension


D. Age
< 30
30-50
> 50

Points
1
2
3
4


1*
2*
3*



0
1
2



0
1
2


Although Johansen et al. recommended primary amputation if MESS score is seven (7) or greater, HBO, should be used in the following situations:

Mess Score
7 (possibly 8)

5, 6

3, 4

HB02 Indications
Uncompromised host where age, hypotension, and mild-to-moderate ischemia significantly contribute to the score
Compromised hosts with diabetes, peripheral vascular disease, collagen vascular disease, etc.
Severely compromised hosts with advanced levels of the above conditions.

 


Table 3: Use of HBO, for the Skeletal Muscle Compartment Syndrome


 I. Clinical Findings:

1. Severe pain in muscle compartment
2. Marked increase in pain with passive stretch of muscles in the compartment
3. Marked swelling of the compartment
4. Marked tenseness of the muscle compartment
5. Neuropathy, myelopathy, and/or encephalopathy
II. Skeletal-Muscle compartment pressure measurements: 1. Greater than 40 mmHg in the uncomprotnised host
2. Rising serial compartment pressure measurements as values approach 35 mmHg
3. 30-40 mmHg in mildly compromised host (diabetic, peripheral vascular disease, collagen vascular disease, etc.)
4. 20-30 mmHg in hypotensive patients where systolic blood pressure is 33 to 50% lower than is expected.

HBO Indications: Either or both of the following exist:

A. 3 (or more) clinical findings (from Section I above).
B. Any one of the above permutations for skeletal-muscle compartment pressure measurements (from Section II above).


 

References

1 Gustilo RB, Williams DN. The use of antibiotics in the management of open fractures. Orthopaedics 1984; 7:1617-1619.

2. Johansen K, Daines M, Howey T, Helfet D, Hansen ST Jr. Objective criteria accurately predict amputation following lower extremity trauma. J Trauma 1990; 30:568-573.

3. Hunt TK, Zederfeldt B, Goldstick TK. Oxygen and healing. Am J Surg 1969; 118:521-525.

4. Hohn C. Oxygen and leukocyte microbial killing. In: Davis JC, Hunt TK, eds. Hyperbaric oxygen therapy. Bethesda, MD: Undersea and Hyperbaric Medical Society, 1977: 1 01 -1 1 0.

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6. Hunt TK, Pai MP. The effect of varying ambient oxygen tensions on wound metabolism and collagen synthesis. Surg Gynecol Obstet 1972; 135:561-567.

7. Bassett BE, Bennett PB. Introduction to the physical and physiological bases of hyperbaric therapy. In: Hunt TK, Davis JC, eds. Hyperbaric oxygen therapy. Bethesda, MD. Undersea and Hyperbaric Medical Society, 1977:11-24.

8 . Bird AD, Telfer AB. Effect of hyperbaric oxygen on limb circulation. Lancet 1965; 1 :355-356.

9. Boerema 1, Meijne NG, Bnmunelkamp WK, Bouoma S, Mensch MH, Kamermans F, Stem Hanf M, Van Aalderen W. Life without blood: A study of the influence of high atmospheric pressure and hypothermia on dilution of the blood. J Cardiovasc Surg 1960;1:133-146.

10. Krogh A. The number of distribution of capillaries in muscle with calculations of the oxygen pressure head necessary for supplying the tissue. J Physiol 1919; 52:409-415.

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 12. Nylander G, Lewis D, Nordstrom H, Larson J. Reduction of postischemic edema with hyperbaric oxygen. Plast Reconstr Surg 1985; 76-596-603.

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14. Strauss MB, Hargens AR, Gershuni DH, Greenberg DA, Crenshaw AG, Hart GB, Akeson WH. Reduction of skeletal muscle necrosis using intermittent hyperbaric oxygen in a model compartment syndrome. J Bone Jt Surg 1983; 65A:656-662.

15. Strauss MB, Hargens AR, Gershuni DH, Hart GB, Akeson WH. Delayed use of hyperbaric oxygen for treatment of a model anterior compartment syndrome. J Orthop Res 1986; 4:108-1 1 1.

16. Sukoff MH, Ragatz E. Hyperbaric oxygenation for the treatment of acute cerebral edema. Neurosurgery 1982; 10:29-38.

17. Wells CH, Goodpasture JE, Horrigan DJ, Hart GB. Tissue gas measurements during hyperbaric oxygen exposure. In: Smith G, ed. Proceedings of the sixth international congress on hyperbaric medicine. Scotland: Aberdeen University Press, 1977:118-124.

18. Sheffield PJ. Tissue oxygen measurements with respect to soft tissue wound healing with normobaric and hyperbaric oxygen. HBO Rev 1985; 6:18-46

19. Bolli R. Oxygen-derived free radicals and postischemic myocardial dysfunction ("stunned myocardium"). J Am Coll Cardiol 1988; 12:239-249.

20. Ferrari R, Ceconi C, Curello S, Guamier C, Caldarera CM, Albertiini A, Visiol 0. Oxygen-mediated damage during ischemia and reperfusion: role of the cellular defense against oxygen. J Mol Cell Cardiol 1985; 17:937-945.

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23. Thom SR. Functional inhibition of Leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. Toxicol Appl Pharmacol 1993; 123:248-256.

24. Thom SR. Dehydrogenase conversion to oxidase and lipid peroxidation in brain after CO poisoning. J Appl Physiol 1992; 73: 1584-1589.

25. Thom SR, Elbuken ME. Oxygen-dependent antagonism of lipid peroxidation. Free Radio Biol Med 1991; 10:413-426.

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27. Zamborfi WA, Roth AC, Bergman BA, Russell RC, Stephenson LL, Suchy H. Experimental evaluation of oxygen in the treatment of ischemic skeletal muscle. Undersea Biomedical Research 1992; 19:(suppl):56.

28. Zamboni WA, Roth AC, Russell RC, Graham B, Suchy H, Kucan JO. Morphological analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. Plast Reconstr Surg 1993; 91:1110-1123.

29. Zamboni WA, Roth AC, Russell RC, Nemiroff PM, Casas L, Smoot EC. The effect of acute hyperbaric oxygen therapy on axial pattern skin flap survival when administered during and after total ischemia. J Reconstr Microsurg 1989; 5:343-347.

30. Zamboni WA, Roth AC, Russell RC, Smoot EC. The effect of hyperbaric oxygen on reperfusion of ischemic axial skin flaps: a laser Doppler analysis. Ann Plast Surg 1992; 28:339-341.

31. Barthelemy L, Bellet M, Michaud A, Cabon P. The value of thermography in the appreciation of the effectiveness of hyperbaric oxygen therapy in the treatment of acute arteritis of the lower limbs. Bord Med 1976; 9: 1095-1 100.

32. Illingworth CF, Smith G, Lawson DD, Ledingham IM, Sharp GR, Griffiths JC. Surgical and physiological observations in an experimental pressure chamber. Br J Surg 1961; 49:222-227.

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34. Maudsley RH, Hopkinson WI, Williams KG: Vascular injury treated with high pressure oxygen in a mobile chamber. J Bone Joint Surg 1963; 4@):346-350.

35. Schramek A, Haslunonai M. Vascular injuries in the extremities in battle casualties. Br J Surg 1977; 64:644-648.

36. Slack WK, Thomas DA, DeJode LRJ. Hyperbaric oxygen in the treatment of trauma, ischemia disease of limbs, and varicose ulceration. In: Brown FW, Cox BG, eds. Proceedings of the third international conference on hyperbaric medicine, Washington, DC: National Academy of Sciences, National Research Council, 1966:621-624.

37. Szekely 0, Szanto G, Takats A. Hyperbaric oxygen therapy in injured subjects. Injury 1973; 4:294-300.

38. Strauss MB. Role of hyperbaric oxygen therapy in acute ischemias and crush injuries-an orthopedic perspective. HBO Rev 1981; 2:87-106.

39. Bonachour G, Cronier P, Gouello JP, Toulemonde JL, Talha A, Alquier pH. Results of a randomized prospective clinical trial of hyperbaric oxygen therapy (HBO) versus placebo in crush injuries: HBO improves wound healing and reduces the need for surgery. European Undersea Biomedical Society (Proceedings); 1994:172.

40. Rado@c V, Baric D, Petricevic A, Andric D, Radonic S. Military injuries to the popliteal vessels in Croatia. J Cardiovase Surg 1994; 35:27-32.

41. Shupak A, Gozal D, Ariel A, Melamed Y, Katz A. Hyperbaric oxygenation in acute peripheral posttraumatic ischemia. J Hyperbaric Medicine 1987; 2:7-14.

42. Strauss MB, Hart GB. Hyperbaric oxygen and the

skeletal-muscle compartment syndrome. Contemporary Orthopedics 1989; 18: 167-174.

43. Weiland AJ, Moore JR, Daniel RK. The efficacy of free tissue transfer in the treatment of osteomyelitis. J Bone Jt Surg 1984: 66A:181-193.

44. Wood MB, Cooney V,/P, Irons GB. Lower extremity salvage and reconstruction by free tissue transfer. Analysis of results. Clin Orthop 1985; 201:151-161.

 


 


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