Il m

Hypoxia

Figure 2.2.6-3. Effect of oedema on oxygenation of cells

In situation with severe oedema oxygen supply is maintained only by physically dissolved oxygen in plasma. Usually this fraction of oxygen under normobaric conditions is insufficient for tissue needs. HBO allows oxygenation of cells only by high levels of physically dissolved oxygen in plasma even when the red cell blood flow is disturbed

Crush injuries are characterized by a vicious circle of ischemia, hypoxia, oedema, disturbed microcirculation, and secondary ischemia in the border area of the tissue affected by primary trauma. Hypoxia plays a central role in this vicious circle. Is it possible to interrupt this circle, partially viable tissue may recover; otherwise there will be a loss of function due to cell death.

Primary

Direct effect of the injury...

• Tissue destruction by high energy transfer to tissues

Interruption of blood vessels

Secondary

Delayed loss of tissue...

■ Stasis ill microcirculation ReperTusiiin injury Infection

Figure 2.2.6-4. Causes of tissue destruction in crush injury. Self perpetuating circle where hypoxia plays the main role

In the initial phase of tissue repair and infection control the metabolic needs of tissues increase by a factor of twenty or more5. The host responses to infection and ischemia are compromised when tissue oxygen tension falls below 30 mmHg. Specifically white blood cell killing becomes defective or nonexistent and host repair processes such as fibroblast secretion of collagen are arrested6. Without a collagen matrix in the wound, neovascularization and wound healing cannot occur. Thus hypoxic tissues lose the ability to resist infections and their self-healing possibilities.

2.2.1 Classification of crush injuries

The most widely used classification system for crush injuries is Gustilo's7 classification of open fractures (see Table 2.2.6-1). It should be used as a reference comparing treatment interventions with the severity of injury and to give prognostic indications. In the most severe grades III B and III C the complication rates reach 50% with standard surgical interventions as described below.

In 1996 the 3rd Consensus Conference of the European Committee for Hyperbaric Medicine in Milano8 recommended a combination of Gustilo's classification with a host scoring (Strauss9, see table 2.2.6-2) as objective criteria for using HBO as an adjunct in the treatment of crush injuries. For the uncompromised host, HBO is recommended for all Gustilo Grade III B

Hypoxia / Ischemia A

Oedema and III C fractures. In the compromised host the indication for using adjunctive HBO should start at Grade II (see Table 2.2.6-1.).

Table 2.2.6-1. Gustilo Classification and HBO Indication for Crush Injuries

Type

Mechanism

Expected outcome

Infection rate

Amputation rate

Large laceration, but minimal soft tissue damage Crush injuries:

Usually not different from a closed fracture Usually not different from a closed fracture

minimal

3%

A

Sufficient soft tissue to close wound ( primary or delayed)

Complication rate < 10%

4%

0%

B

Flaps or grafts required to cover bone

> 50% incidence of complications

52%

16%

C

Major vessel injury

About 50% incidence of complications

42%

42%

These recommendations correspond to the UHMS committee report1 which states that when ever HBO is used for acute traumatic ischemia the injury should be classified by a Standard Classification Method such as the Gustilo Grading System or the Mangled Extremity Severety Score (MESS).

Table 2.2.6-2. Criteria for using HBO as an adjunct in the treatment of crush injuries_

Type_HBO Indication_

I None

II Only in compromised hosts, such as diabetics, advanced peripheral vascular disease, collagen vascular disease, etc., concern about

_primary healing of flaps_

III A See Type II fractures

III B All injuries

III C All injuries

Table 2.2.6-3. Evaluation of host status (Strauss10)

Factors

Scoring criteria

2

1

0

Points

Point

Point

Age

< 40 years

40-60 years

> 60 years

Ambulation

Community

Household

None

Smoking/Steroid Medication

None

> 5 years ago

Current

Cardial/Renal

Normal

Compensated with

Decompensated

medication

even under

medication

Neuropathy/Deformity

None

Mild to moderate

Severe

Comments 1. Use V points when severity of involvement is between two scoring criteria

2. For ambulation scoring criteria subtract V point if walking aids are required

3. When two factors are listed, use the scoring criteria which reflects the more severe involvement

Comments 1. Use V points when severity of involvement is between two scoring criteria

2. For ambulation scoring criteria subtract V point if walking aids are required

3. When two factors are listed, use the scoring criteria which reflects the more severe involvement

Score

Severity of compromise

8-10

Normal host

4-7

Impaired host

3 or less

Severely compromised host

The mangled extremity severity score (MESS) is an other classification system originally used to select which severely injured extremity should undergo primary amputation. It can offer objective criteria for the use of HBO as adjunct treatment in crush injuries11.

2.2.2 Treatment

Crush injuries must be diagnosed without delay and treated aggressively to prevent or minimize irreversible damage not only to the injured tissue. Multidisciplinary treatment by emergency physicians and surgeons as well as intensivists is mandatory. Even under best conditions the risk of complications is high with a need of reoperation in more than 50% of severe injuries. Many of those patients end up with poor outcome.

In the treatment of crush injuries, priority should be given to the restoration of circulation. In limb trauma with large vessel damage, vascular reconstructive surgery has to be considered immediately. The survival of the limb may depend on anatomical reconstruction of damaged vessels and on the time period between injury and repair. Sufficient blood supply to traumatized tissues is mandatory to avoid secondary complications. Ischemia is the primary cause of tissue hypoxia in acute traumatic ischemias.

Haemodynamics must be stabilized mainly by correcting hypovolaemia and blood loss.

Primary surgical treatment of crush injuries consists of meticulous cleansing to the depths of the open wounds. Debridement of all nonviable tissue and foreign material is mandatory, but marginally viable tissue should be retained and protected. Debridement to clean-bleeding, normal-appearing bone, eliminating foreign material regardless of the skeletal defect created is important.

Bacterial colonisation is common especially in open fractures. Hypoxia favourites bacterial grow in two ways:

• The reduction of local oxygen partial pressure in wounds reduces the neutrophil phagocytic activity. The rate of free radical production and hence the oxidative bacteria killing depends mainly on local oxygen tension.

• Anaerobic bacterial grow is increased in hypoxic tissue.

Calculated antibiotic treatment in open fractures therefore has to be carried out immediately. HBO has a direct bactericidal effect mainly to anaerobic bacteria. A bacteriostatic effect on Escherichia coli, Staphylococcus and Pseudomonas species is reported with even synergistic effects when combined with certain antibiotics12.

The next therapeutic step is the reestablishment of skeletal stability, by external fixation. Plate fixation or nail fixation is usually postponed to second step interventions. Temporary physiologic resurfacing by an allograft (artificial skin) or a vacuum sealing may be helpful, particularly with large, contaminated defects. Primary tendon or nerve repairs are contraindicated in the majority of crush injuries. At one- to three-day intervals, dressings are changed and, if open treatment was used initially, redebridement of the wound is carried out until only viable healthy tissue remains

HBO should be considered as an important adjunct in this early management of severe crush injuries to reduce oedema formation and increase tissue oxygen tensions in hypoxic tissues to levels which make it possible for the host responses to become functional.

The recommended treatment schedule is three treatments at a pressure of 240 kPa for 90 minutes of oxygen therapy at pressure within the first 24 hours of treatment, followed by twice daily HBO for three days (i.e. a total of 7 treatments). After the acute phase of the first three days therapy should be continued for at least five days or longer if clinical judgement suggests that HBO treatment should continue (for instance because of infection, delayed wound healing or ischemic complications of flap repair surgery).

Figure 2.2.6-5. Typical crush injury after primary surgical debridement and stabilisation with fixateur externe

Figure 2.2.6-5. Typical crush injury after primary surgical debridement and stabilisation with fixateur externe

Bone reconstruction is undertaken only after oedema has subsided. Ideally, delayed primary wound closure or resurfacing by split-thickness skin graft is performed four days to one week after initial treatment if the wound remains clean and shows no evidence of contamination, infection or further necrosis. HBO can help to shorten this time interval.

2.3 Reperfusion injury

Restarting blood flow after more than about ten minutes of ischemia (depending on the kind of tissue) is typically more damaging than the ischemia itself because the ischemia sets the stage for oxygen to generate free-radicals rather than contribute to cellular energy production. Membrane damage is the most important consequence.

For reperfusion, the focus of membrane damage is more on endothelial cells as well as platelets, leucocytes and other cells in the blood stream. Where as ischemic damage is focused more on organ tissue. Even if the physicochemical causes of ischemia reperfusion are still under investigation it seems that Eicosanoids generated by arachidonic acid (especially leukotrienes) greatly increase the adhesion of leukocytes & platelets to capillary walls, plugging them up. Superoxide also increases the adhesion of leucocytes to vessel walls. Eicosanoids and associated oxygen free-radicals make capillary walls more "leaky", causing oedema with the consequence of a vicious circle of hypoxia and oedema. In reperfusion these effects quickly become pronounced enough to block capillaries entirely resulting in the no reflow phenomenon (see chapter 1.7)

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