Hyperbaric Management Of Frostbite

All HBO2 treatments must be directly supervised by a physician trained in hyperbaric medicine. Physicians that have the minimum required 40-hour introductory course training should be precepted by physician Board Certified in UHM or have a certificate of additional training (CAQ) in UHM. Support personnel includes nursing staff, preferably a certified hyperbaric nurse (CHRN), and certified hyperbaric technicians (CHTs).  For a multiple chamber treatment, one accompanies the patient as an inside attendant with one chamber "driver" and one outside observer. For monoplane chambers, one CHT can monitor two monoplane chambers.

Patients must be dressed in clothing that has a low potential for static discharge. Cotton/polyester fabric blends up to 60/40 are acceptable. To further reduce fire risk patients are screened for no oil or petroleum products in hair or skin, makeup, nail polish, or deodorants. All electronic devices, telephones, watches hearing aids, etc. are left out of the chamber. No chemical or gas heating devices are allowed in a chamber. Transdermal patches should be avoided or, at least, checked and covered. Diabetics should have glucose checks before and after treatment, following approved guidelines for treatment according to levels.

There is no specific treatment protocol identified but a used regimen according to submitted case studies is 2.0  to 2.5 ATA for 90 to 110 minutes, with or without an air break, twice a day for the first eight to 12 treatments and continued daily until the maximum medical benefit is determined. This typically occurs within 12 to 20 treatments.

The most commonly reported complications are related to barotrauma of the ears and/or more rarely the sinuses. There is a concern for oxygen toxicity which is reported very rarely, and no cases of recurrence or resulting sequelae have been reported. Another rare possible complication is barotrauma to parenchymal lung tissue from blebs or emphysematous bullae resulting in pneumothorax, but this also is a very rarely reported complication. One review of complications in 782 patients involving 11,376 HBO2 treatments showed 17% had experienced some ear pain or discomfort, but the barotraumatic injury was verified in only 3.8%of all patients. No barotrauma or teeth or sinuses were identified. Four patients experienced oxygen seizures, but none of these had recurrences or sequelae. Other known complications include a possible worsening of existing cataracts and a temporary change in refractory vision usually a self-limited increase in myopia resolving over several weeks post-treatment. Patients with confinement anxiety (claustrophobia) may require anxiolytic therapy.

The pathophysiologic evidence indicates the primary mechanism of tissue damage in slow onset frostbite is due to a multifactorial vascular response. The final stage of intracellular ice crystal formation may seal the necrotic fate of the tissue, at that point preventing a chance for tissue regeneration. There is a recoverable phase if rewarming occurs before the final tissue destruction, but endothelial reperfusion injury can occur again within 4 to 8 hours post-rewarming. All treatment options are focused at restoration and maintenance of microvascular flow post-rewarming and reduction of inflammation, specifically aimed at endovascular inflammatory effects and prevention of reperfusion injury. Treatment options are then divided into three phases: (1) prethaw field care, (2) immediate rewarming phase, which is preferable in the hospital, and (3) postthaw phase, which may continue for several weeks to months.[15]

In the majority of cases, however, the postthaw phase treatment is delayed until the physical evidence of tissue damage is manifest when the wounds are staged and assessed, typically more than 24 to 48 hours post-rewarming. This is due to a lack of early recognition protocols and inability to identify true frostbite in the earliest stages.[16][17][16] This diagnostic dilemma sometimes leads to further loss of tissues that are hovering between stages of reversible to irreversible damage, either from effects of reperfusion injury or further vascular insult due to due persistent or progressive effects of inflammation.[18][19][18] In tissue damage by direct high thermal injury (burns), there is a penumbral area surrounding the immediately damaged tissue (central zone of coagulation) known as the zone of stasis where tissues are viable but prone to injury through vasoconstriction, vascular thrombosis, and endothelial fibrin deposition. Since observed tissue damage in frostbite is similar and the mechanism of destruction is related, low thermal injury, the treatment goal of reducing further penumbral tissue loss in phase 3, is time sensitive and prevention of further loss dependent on early intervention. Cauchy advocates early diagnosis and intervention through a new classification system used within the first 24 hours based on the topography of the presenting lesions, augmented by isotopic bone scans (99mTc-HMDP).[20]

Current treatment options are plagued by lack of high-level evidence provided by well-designed randomized control trials (RCTs), but all therapeutic strategies are aimed at inhibition of endovascular inflammation and early reperfusion. Vasodilators such as nitroglycerine or papaverine have been useful, but studies are not graded with use alone but when combined with thrombolytic agents such as tissue plasminogen activator (rTPA) or streptokinase in a stepwise approach it receives a 1B-C recommendation by ACCP classification criteria.  Iloprost, a prostacyclin analogue with vasodilatory properties, also has received a 1B recommendation, but currently, the drug is not available in the United States.

Hyperbaric oxygen sustains the metabolic needs for injured tissue with the immediate reversal of hypoxia and reduces the endothelial inflammation and inhibition of reperfusion injury by reducing leukocyte adhesion. No randomized control trials have been performed to assess this theory, and it has not received an ACCP recommendation, but multiple case series have been presented with hyperbaric oxygen treatment initiated during various time intervals following rewarming. All conclude that some level of tissue recovery occurred with decreased levels of amputation, but these results have not been matched to controls. Cases that initiate hyperbaric oxygen treatment earlier tend to have better results than delayed treatment, most likely from sustaining penumbral areas of injury. Several studies have combined hyperbaric treatment with vasodilating, anticoagulation or hemorrheologic agents such as pentoxifylline with reported success.[21]

Adjuvant therapy with hyperbaric oxygen for the treatment of frostbite is reasonable, well tolerated and safe but the evidence supporting treatment is limited to level 4 evidence at best, primarily from case series with no better than historical outcomes to match.  Nurses and clinicians involved in wound care should be aware of hyperbaric oxygen as a therapeutic option.