Escolar Documentos
Profissional Documentos
Cultura Documentos
140 The Journal of Lancaster General Hospital • Winter 2007/2008 • Vol. 2 – No. 4
hyperbaric oxygen therapy
promote wound healing, limit edema, and destroy certain Sensory neuropathy diminishes perceptions of pain
anaerobic bacteria. HBO therapy is currently approved and pressure and predisposes to worsening of the initial
for a variety of tissue healing and other applications injury and exacerbation of the inflammatory process.
(Table 1). Autonomic system deficits contribute to chronic wound
formation via inhibition of normal sweat and oil pro-
PATHOPHYSIOLOGY duction, leaving the skin dry and nonelastic. Motor
Peripheral neuropathy, a key factor in the development neuropathy may cause atrophy of intrinsic muscles and
of diabetic foot ulcers,10,11 is already present in up to 10% fibrosis resulting in unfavorable weight distribution
of patients at the time their diabetes is diagnosed, and and gait patterns, and increased risk of pressure-related
in nearly half of patients who have diabetes for 7 years ulceration.
or more. It is characterized by neuronal demyelination
and atrophy, with a combination of sensory, motor, and Diabetes may also compromise healing of chronic wounds13
autonomic deficits.12 by causing abnormal cellular and inflammatory pathways,
vascular disease, and tissue hypoxia. Chronic hyperglyce-
Diabetic foot ulcers commonly begin as a minor wound, mia may be toxic to macrophages and fibroblasts, and the
often caused by ill fitting shoes, foreign bodies, improper accumulation of advanced glycosylation end products may
nail trimming, or burns from hot bath water. The high- adversely affect cytokine function, growth factor produc-
est incidence of diabetic foot ulcers occurs at sites of tion, and extracellular matrix formation.
previous ulceration. Ulceration may also result from
moderate repetitive stress associated with walking or Oxygen and Wound Healing
day-to-day activity, and is often preceded by a callus at The role of oxygen in wound healing is well established.14
the site of injury. Molecular oxygen serves as a nutrient to support the
increased energy demand of regenerating tissues and is
needed for replication of fibroblasts, mobility of macro-
phages, ingrowth of granulation tissue, and other key
elements of wound healing. Oxygen administered under
TABLE 1. CURRENT APPROVED INDICATIONS
increased ambient pressure enhances in vitro phagocytosis
FOR HBO THERAPY.
in regions of limited perfusion by increasing local oxy-
• Air or gas embolism
gen tension to levels consistent with normal phagocytic
• Carbon monoxide poisoning and carbon
function.15 In addition, derivatives of oxygen commonly
monoxide poisoning complicated by cyanide
referred to as reactive oxygen species (ROS) appear to
poisoning
promote wound repair. Enzymes that convert oxygen to
• Clostridial myositis and myonecrosis
ROS are found in nearly every cell type in the wound
(gas gangrene)
microenvironment. At low concentrations, ROS may
• Crush injury, compartment syndrome and other
serve as cellular messengers that regulate a variety of
acute traumatic ischemias
events closely linked to wound repair including cell
• Decompression sickness
proliferation, angiogenesis, and synthesis of extracel-
• Enhancement of healing in selected problem
lular matrix.
wounds
• Exceptional blood loss (anemia)
Since oxygen is so important to wound healing, hypox-
• Intracranial abscess
emia due to peripheral vascular disease (PVD) may be
• Necrotizing soft tissue infections
a contributing factor to the initial formation of diabetic
• Osteomyelitis (refractory)
foot ulcers. About 8% of patients with diabetes have
• Delayed radiation injury (soft tissue and bony
PVD at the time of initial diagnosis, and its prevalence
necrosis)
increases to 45% after 20 years. Impaired circulation may
• Skin grafts and flaps (compromised)
also inhibit delivery of leukocytes and antibiotics to the
• Thermal burns
wound, and promote the growth of anaerobic organ-
Source: Undersea and Hyperbaric Medical Society
isms. In addition, aminoglycosides and other antibiotics
depend on oxygen to function.
The Journal of Lancaster General Hospital • Winter 2007/2008 • Vol. 2 – No. 4 141
hyperbaric oxygen therapy
A B
D E
Limb salvage in two diabetic patients was accomplished by utilizing multiple modalities including a course of hyperbaric oxygen. Plates A-C
display progressive healing of an exposed Achilles tendon, and Plates D & E display healing of an infected foot.
OVERVIEW OF HBO THERAPY enough to sustain life without any contribution from
Administration of 100% oxygen at ambient pressure oxygen bound to hemoglobin.16
causes a 5-fold increase in the amount of dissolved oxy-
gen in blood. HBO therapy – administration of 100% Hyperbaric chambers are classified by the National Fire
oxygen at 2 to 3 ATM – increases the dissolved oxygen Protection Association as Class A (multi-occupant) or
in blood and tissues up to 20-fold, a level that is high Class B (single occupant). Both generally use compressed
142 The Journal of Lancaster General Hospital • Winter 2007/2008 • Vol. 2 – No. 4
hyperbaric oxygen therapy
The Journal of Lancaster General Hospital • Winter 2007/2008 • Vol. 2 – No. 4 143
hyperbaric oxygen therapy
A group of 28 patients with diabetes whose foot ulcers did should stop the use of tobacco in any form until therapy
not improve after 3 months of standard treatment were is complete.
randomized to HBO therapy or a control group.19 HBO
therapy was administered twice daily, 5 days per week for Patients generally experience no negative effects fol-
2 weeks, and each session lasted 90 minutes at 2.5 ATM. lowing HBO therapy. Some patients report a “cracking”
After completion of HBO therapy, the mean decrease in sensation in their ears between treatments as oxygen
ulcer size was 41.8% in the study group and 21.7% in the behind the eardrums is absorbed into the circulation.
control group (P = .037). The difference in healing rates This sensation can be relieved in the same manner as
between the groups was no longer significant at 4 weeks clearing the ears during compression and decompression.
after the completion of HBO therapy. Other patients report feeling light headed immediately
following a HBO therapy session, but this sensation is
HBO therapy enhanced the healing of ischemic, non- usually brief and self-limiting.
healing diabetic leg ulcers in a study of 18 patients ran-
domized to receive 30 sessions of HBO therapy (100% HBO therapy has historically been the focus of substan-
oxygen at 2.4 ATM for 90 minutes daily) or a control tial political maneuvering among providers, insurers,
group.20 Healing with complete epithelialization was and pharmaceutical companies, due in part to the fact
achieved in 5 of 8 ulcers in the treatment group and 1 that oxygen is not patentable and does not benefit from
of 8 ulcers in the control group. The median decrease of the political advocacy used to promote other therapies.
the wound area was 100% in the treatment group and Systemic HBO therapy is expensive, with a session cost-
52% in the control group (P = .027). ing anywhere from $200 to $400 in private clinics to over
$2,000 in U.S. hospitals. Even at that, given the high
Transcutaneous oximetry, performed either during HBO costs of amputation and rehabilitation, HBO therapy may
therapy or with the patient breathing 100% oxygen at be a cost-effective modality in select patients.22 In 2003,
ambient pressure, can help identify patients who are Medicare and Medicaid extended coverage for HBO
likely to benefit from HBO therapy.21 Clinical factors therapy to ulcers that had failed standard wound care
that affect the response to HBO therapy include renal therapy and were classified as Wagner grade 3 or higher
failure, smoking history, number of HBO treatments, and (i.e. a wound that is no longer superficial, but probes to
interruption of the HBO treatment regimen. bone and may be ischemic and/or infected.).
144 The Journal of Lancaster General Hospital • Winter 2007/2008 • Vol. 2 – No. 4
hyperbaric oxygen therapy
REFERENCES
1. Rathur HM, Boulton AJ. The diabetic foot. Clin Dermatol 13. Brem H, Tomic-Canic M. Cellular and molecular basis of wound
2007;25:109-120. healing in diabetes. J Clin Invest 2007;117:1219-1222.
2. Boulton AJ, Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The 14. Gordillo GM, Sen CK. Revisiting the essential role of oxygen in
global burden of diabetic foot disease. Lancet 2005;366:1719-1724. wound healing. Am J Surg 2003;186:259-263.
3. Boyko EJ, Ahroni JH, Stensel V, et al. A prospective study of risk 15. Mader JT, Brown GL, Guckian JC, Wells CH, Reinarz JA.
factors for diabetic foot ulcer. The Seattle Diabetic Foot Study. Diabetes A mechanism for the amelioration by hyperbaric oxygen of experimental
Care 1999;7:1036-1042. staphylococcal osteomyelitis in rabbits. J Infect Dis 1980;142:915-922.
4. Armstrong DG, Lavery LA, Vela SA, Quebedeaux TL, Fleischli JG. 16. Tibbles PM, Edelsberg JS. Hyperbaric-oxygen therapy. New Engl J
Choosing a practical screening instrument to identify patients at risk for Med 1996;334:1642-1648.
diabetic foot ulceration. Arch Intern Med 1998;158:289-292.
17. Wunderlich RP, Peters EJ, Lavery LA. Systemic hyperbaric oxygen
5. Singh N, Armstrong DG, Lipsky Ba. Preventing foot ulcers in patients therapy: lower-extremity wound healing and the diabetic foot. Diabetes
with diabetes. JAMA 2005;293:217-228. Care 2000;23:1551-1555.
6. Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders. 18. Faglia E, Favales F, Aldeghi A, et al. Adjunctive systemic hyperbaric
A clinical practice guideline (2006 revision). J Foot Ankle Surg 2006;45(5 oxygen therapy in treatment of severe prevalently ischemic diabetic foot
Suppl):S1-66. ulcer. A randomized study. Diabetes Care 1996;19:1338-1343.
7. Frykberg RG. Diabetic foot ulcerations: management and adjunctive 19. Kessler L, Bilbault P, Ortaga F, et al. Hyperbaric oxygenation accel-
therapy. Clin Podiatr Med Surg 2003;20:709-728. erates the healing rate of nonischemic chronic foot ulcers: a prospective
randomized study. Diabetes Care 2003;26:2378-2382.
8. Bakker DJ. Hyperbaric oxygen therapy and the diabetic foot. Diabetes
Metab Res Rev 2000;19(Suppl 1):S55-58. 20. Abidia A, Laden G, Kuhan G, et al. The role of hyperbaric oxygen
therapy in ischemic diabetic lower extremity ulcers: a double-blind ran-
9. Strauss MB. Hyperbaric oxygen as an intervention for managing domised-controlled trial. Eur J Vasc Endovasc Surg 2003;25:513-518.
wound hypoxia: its role and usefulness in diabetic foot wounds. Foot Ankle
Int 2005;26:15-18. 21. Fife CE, Buyukcakir C, Otto GH, et al. The predictive value of
transcutaneous oxygen tention measurement in diabetic lower extremity
10. Rathur HM, Boulton AJ. The neuropathic diabetic foot. Nat Clin ulcers treated with hypernabir oxygen therapy: a retrospective analysis of
Pract Endocrinol Metab 2007;3:14-25. 1144 patients. Wound Repair Regen 2002;10:198-207.
11. Murray HJ, Boulton AJ. The pathophysiology of diabetic foot ulcer- 22. Guo S, Counte MA, Gillespie KN, Schmitz H. Cost-effectiveness
ation. Clin Podiatr Med Surg 1995;12:1-17. of adjunctive hyperbaric oxygen in the treatment of diabetic foot ulcers.
Int J Technol Assess Health Care 2003;19:731-737.
12. Bansal V, Kalita J, Misra UK. Diabetic neuropathy. Postgrad Med J
2006;82:95-100.
The Journal of Lancaster General Hospital • Winter 2007/2008 • Vol. 2 – No. 4 145