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Frostbite

Frostbite

Frostbite results from prolonged exposure to below zero temperature. The risk is increased in people with poor circulation or at high altitude due to decreased oxygen tension in the air.

Tissue freezing causes local disruption in circulation and vascular damage, further leading to swelling and blistering that is complicated with thrombosis. Soft tissue damage can cause compartment syndrome and damage of peripheral nerves and tissue necrosis (tissue death).

These events can take longer time, even weeks to evolve and hyperbaric oxygen therapy is essential in breaking the vicious circle of tissue deprivation by blood supply (ischemia) and oxygen (hypoxia), which leads to further tissue loss.

Oxygen’s role

Many clinical reports are showing that early oxygen intervention enhances healing and  and cell regeneration. Best time to apply  oxygen is during rewarming, when oxygen demands are greatest but ability to deliver oxygen is compromised. Oxygenated tissue is less prone to ischemia-reperfusion injury, swelling, infection and whole compartment syndrome, saving fingers and toes from amputation. Oxygen therapy improves the microcirculation  thru angiogenesis (new capillary growth), strengthens the immune system response and enables peripheral nerve regeneration for return of sensitivity and function to affected limb (see examples below).

Good results with oxygen can be achieved even weeks after injury if the circulation is not substantially damaged .

Early warning signs

Frostbite is a progressive injury where serious complications can arise days or even weeks after exposure. Superficial redness, burning tingling and  numbness are signs of compromised micro-circulation. Tissue oxygen status can be assessed with micro-vascular assessment. If micro-circulation is  reestablished tissue can be saved and amputation prevented.

Symptoms: burning, tingling and gradual numbness; initial redness turns into gray/blue appearance; blistering of the skin in the final stage turns into necrosis of the skin and underlying soft tissue.

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-*- WARNING -*-
GRAPHIC WOUND IMAGES
BELOW

Benefits of hyperbaric oxygen therapy in acute and delayed frostbite injury

  • Improves tissue oxygenation
  • Improves tissue micro-circulation by enhancing capillary growth
  • Reduces tissue swelling and progression of the compartment syndrome
  • Reduces pain
  • Reduces and prevents infection by
    • Inhibiting bacterial growth
    • Increasing activity of white blood cell to destroy bacteria
    • Improving body’s defense mechanism
  • Enables quick demarcation of the necrotic tissue from the viable, so that part of the involved tissue can be salvaged
  • Reduces the need for surgical intervention and amputation
  • Enhances wound healing
  • Reduces possibility of thrombosis by acting as natural anticoagulant
  • Enhances peripheral nerve regeneration and return of sensitivity

Case file #1:  Delayed treatment of frostbite injury

Source:
“Hyperbaric Oxygen Therapy for a Delayed Frostbite Injury”
Brian F. McCrary, DO, MPH; Timothy A. Hursh, MD, MPH
Wounds.  2005;17(12):327-331

Non smoker, 28 year old mountain climber was trapped in snow for three days before descending to acute facility. She was diagnosed with Grade III frostbites to the third and fourth fingers of the right hand and fourth finger of the left hand, but was not treated and discharged with a topical gel and pain medication.  Hyperbaric treatment was initiated 22 days after injury.

Treatment protocol

After 22 days delay hyperbaric oxygen therapy was initiated and 21 daily session of 90 minutes at pressures up to 2.5 ATA were given in combination with wound care. After three sessions clear demarcation was seen between the viable healthy tissue and necrotic tissue. Wound debridement with antibiotic ointments  that was debrided.

Treatment outcome

After receiving 21 hyperbaric and wound care treatments over a 5-week period complete recovery with only superficial sloughing at the fingertips was seen. Sensitivity returned in all fingers.


Before hyperbaric therapy: -*- WARNING -*- Graphic wound images -

 


After 21 hyperbaric sessions: -*- WARNING -*- Graphic wound images -

 

Photos reproduced with permission from author.  Original source link here 

Comments

Treatment of frostbite is not routinely covered by medical insurance and is still on the list of investigational conditions of the UHMS. Positive treatment results with hyperbaric oxygen can be expected if early intervention is applied. However, if circulation is not substantially damaged, excellent results can be achieved even weeks after injury.

Case file 2: Frostbite

Source:
“Hyperbaric oxygen treatment in deep frostbite of both hands in a boy.”
von Heimburg D, Noah EM, Sieckmann UP, Pallua N.
Burns. 2001;27(4):404–408

11-year-old boy who suffered deep frostbite on six fingers while he was working outdoor at temperatures of -32 degrees C over a 4 hour period.

Treatment protocol

Three days later he was for the first time seen by a physician, who planned to amputate the affected fingers, but the family transferred the boy to the University Hospital in Aachen, Germany to Dr. von Heimburg. He treated him with hyperbaric oxygen daily for 14 days at 2.4 ATA for 90 minutes.

Treatment outcome

A total recovery of the severe frostbite was observed after 14 days of oxygen treatment. Twenty-eight months after the injury the boy reports fully regained sensibility and no pain.

Conclusions

Because of the low risk associated with hyperbaric oxygen, and its potential therapeutic efficiency, hyperbaric oxygen should be recommended as adjunct therapy in the treatment of deep frostbite.

Further reading:
  1. Jain KK: Textbook of hyperbaric medicine: Ch 14: Hyperbaric Oxygen Therapy in wound healing, plastic surgery and dermatology, Hogrefe & Huber Publishers, Inc., 3rd Ed.22: 213–241, 1999.
  2. “Hyperbaric Oxygen Therapy for a Delayed Frostbite Injury”, McCrary BF, Hursh TA, Wounds. 2005;17(12):327-331
  3. “Hyperbaric oxygen treatment in deep frostbite of both hands in a boy”, von Heimburg D, Noah EM, Sieckmann UP, Pallua N., Burns. 2001;27(4):404–408

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