Hyperbaric Treatment of Diabetic Foot Ulcer

Etiology

DFUs occur due to changes in the biomechanics of the bony and soft tissue architecture of the foot, peripheral neuropathy, and atherosclerotic peripheral arterial disease, all of which occur at a higher frequency in patients with DM. Nonenzymatic glycation predisposes ligaments to stiffness. Diabetic neuropathy causes loss of protective sensation. Both of these contribute to loss of proprioception, poor balance, and lack of awareness of pain in the feet and lower limbs of patients with DM. Ulcers usually begin as small areas of pressure or irritation or from a minor trauma that is not perceived by the insensate neuropathic patient.[1][2]

Epidemiology

Type II DM is a public health epidemic in the United States. The rate of obesity and DM, even in young people, is increasing at an alarming rate. With this increased incidence is an increase in the number of serious DFUs and infection. Diabetes is the leading cause of nontraumatic amputations in the United States. A patient who undergoes an amputation of a lower limb for a diabetic foot infection has a greater than 50% chance of losing the contralateral limb in the next year. There is a 70% mortality at five years in a patient who has undergone an amputation and has diabetes and a 74 % mortality rate at two years in a patient with DM who is on renal replacement therapy.[3][4]

There are several Grading Systems for DFUs, with the Classic Wagner Grading system being the most commonly used; it consists of 5 grades based on anatomy and presence of infection and gangrene, from Grade 0 to Grade 5. The most superficial ulcer is a Wagner grade 1, the deepest, most serious, infected, and gangrenous is a Wagner 4. Most patients being treated at Wound Centers for DFUs present with Wagner 2 through 4 ulcers.

Wagner Scale

• Grade 0: no open lesions, may have healed lesions
• Grade 1: superficial ulcer, no penetration in deeper layers 
• Grade 2: deeper ulcer reaching tendon, bone, or joint 
• Grade 3: deeper tissues are involved, with abscess, osteomyelitis, or tendonitis
• Grade 4: gangrene of some part of the foot
• Grade 5: gangrene of the whole foot or enough of the foot that limb amputation is indicated

Pathophysiology

DFUs are most common in patients who have diabetic peripheral neuropathy and angiopathy as well as a foot deformity, such as Charcot foot. The combination of an insensate foot and structural and biomechanical alterations present a perfect composition for a small scrape or cut or an area of prolonged pressure to develop into an ulcer in a fairly short period in a patient with DM and poor glycemic control. The classic Charcot or "rocker bottom" foot that is seen in longstanding patients with DM places the patient at even greater risk for developing ulcers on parts of the foot that are not designed to be major weight-bearing surfaces. Most patients with DFUs have poor glycemic control and do not regularly inspect their feet or receive routine podiatric care as primary prevention. Prolonged hyperglycemia impairs leukocyte function and makes these wounds prone to infection with both gram-positive and gram-negative organisms.

History and Physical

Patients presenting with DFUs should be queried as to how long the wound has been present and what treatment, if any, has been tried. Many neuropathic patients are unaware that a wound is present until drainage begins or tissue becomes necrotic and malodorous. This is the classic "fetid foot" presentation. Patients with DM are immunocompromised and often do not mount a fever or elevated white blood cell count in the face of significant infection. 

The patient should have both feet examined at every visit. The toes should be manually separated and interdigital tissue assessed for cracks, fissures, or signs of fungal infection. The patient should be asked about glycemic control and informed that for DFUs to heal the blood sugar must be consistently 150 mg/dL or less. A Semmes-Weinstein 10-gram monofilament test to assess for loss of protective sensation should be performed and result documented. Dorsalis pedis and posterior tibial pulses should be assessed. If these are not palpable, Doppler signals should be assessed and documented. It is recommended that all patients over 50 years of age should undergo a baseline arterial ultrasound with Ankle-Brachial and Toe-Brachial indices and Pulse Volume Recordings. Any abnormality in peripheral circulation warrants referral to a vascular surgeon.

The patient's footwear and gait should be assessed and documented. Many DFUs are caused by inappropriate footwear which causes friction and pressure on the deformed diabetic foot.

The wound is the last thing that should be assessed. The length, width, and depth should be documented in centimeters. Any tunneling or undermining should be noted. The wound bed should be assessed to determine if the wound extends to or probes to the bone. The periwound tissues should be assessed for fluctuance, induration, or maceration from moisture associated with wound drainage. Odor, color, and quality of wound drainage should be noted and documented.

Evaluation

Once the DFU is assessed and staged, it is helpful to obtain certain laboratory and radiographic data.

Baseline CBC with differential count, chemistry with BUN and creatinine, sedimentation rate, and C-reactive protein to assess for osteomyelitis, as well as a glycosylated hemoglobin level are all helpful. If bone involvement is suspected, plain film radiograph followed by MRI or a 3-phase bone scan may be necessary. 

Wounds that are staged as a Wagner 3 or higher that have failed conventional wound care for 30 days should be referred for hyperbaric medicine consultation. Chronic wounds are oxygen starved as are the periwound tissues. The only way to increase oxygen delivery to these hypoxic tissues is with hyperbaric oxygen treatments. Hyperbaric oxygen increases oxygen concentration to the wound, stimulates angiogenesis in and around the wound, facilitates delivery of certain antibiotics to the tissues, stimulates fibroblasts, and encourages migration of growth factors to the wound bed.

Hyperbaric oxygen is, simply, 100% oxygen delivered under supra-atmospheric pressure. The patient is treated in either a multiplace or monoplace pressure vessel for human occupancy or a chamber. Treatments usually are conducted at 2 to 2.4 atmospheres absolute. This pressure is equivalent to 33 feet and 42 feet of sea water. Patients usually are treated for approximately 60 to 90 minutes every day for 30 to 60 treatments. Patients at risk of oxygen toxicity at these hyperoxic levels are given 5-minute air breaks every 30 minutes throughout the treatment, during which time they breathe 21% oxygen from a face mask or handheld mouthpiece. This decreases the risk of seizures from oxygen toxicity to approximately 1:10,000 treatments. 

Treatment / Management

The mainstay of treatment for DFUs is offloading. DFUs will not heal until they are adequately offloaded and have no sustained pressure on the wound bed. Multiple modalities exist for offloading including custom molded shoe inserts and neuropathic walker boots. Total contact casting is the gold standard to offload DFUs on the weight-bearing surface of the heel. 

Clinical practice guidelines recommending the use of hyperbaric oxygen therapy in the treatment of DFU suggest adding hyperbaric oxygen treatment (HBOT) to patients with Wagner 3 or higher DFU who have recently had a surgical debridement of an infected foot. HBOT delivered acutely in the postoperative period will reduce the risk of major amputation and incomplete reepithelialization. Further recommendations suggest adding HBOT to the standard of care treatment in patients with Wagner 3 or higher DFU that have not shown significant improvement after 30 days of treatment to reduce the risk of major amputation and incomplete reepithelialization. Recommendations also suggest against the use of HBOT in patients with Wagner 2 or lower DFU. [13]

Studies have demonstrated that patients who received hyperbaric oxygen (HBO2) treatment for DFUs healed faster and remained healed at one year, more than their cohorts who were not treated with HBO2.  

Differential Diagnosis

• Anaemia

• Arthritis

• Atherosclerosis

• Autonomic neuropathy

• Chronic venous insufficiency

• Diabetic foot infections

• Muscle pain

• Metabolic neuropathies

• Myxedema

• Radicular pain