Carpal Tunnel Syndrome and Diabetes, A Challenging Problem

Approximately 20% of diabetic patients will develop carpal tunnel syndrome. Peripheral neuropathy makes the condition of the carpal tunnel worse. It is suggested that the never that already has established hypoxia caused by diabetes is more vulnerable to local compression. Other mechanisms and explanations are also involved, so it is a difficult diagnosis). Some people believe that patients with diabetic neuropathy will have a high prevalence of carpal tunnel syndrome.

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Electrodiagnostic testing (EMG and nerve studies) cannot distinguish patients with clinical carpal tunnel syndrome from patients with diabetic polyneuropathy. The decision to treat these patients should be made independently of the electrodiagnostic findings. When treating the patient, try to figure out the patient’s blood sugar level. There may be difficulty in determining if the blood sugar is under control.

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HBA1C (the glycosylated hemoglobin test) is an important blood test that shows how well the diabetes is being controlled. The test provides an average blood sugar control over the last 2-3 moths. The normal range of hemoglobin A1c is between 4% and 5.6%. When the level is 6.5% or higher, this indicated diabetes. The goal of treatment is to make sure that the patient with diabetes has hemoglobin A1c less than 7%. The higher the levels of Hemoglobin A1c, the higher the risk of developing complications. People should have the test done every three months to check and see that their blood sugar is under control. At least, the test should be done twice a year.

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The difficulty in carpal tunnel syndrome in diabetic patients is the difficulty of diagnosis, the difficulty in determining if the diabetes is being controlled or not, and if there will be surgery needed, will the patient have complications or not.

Patients who develop complications in orthopedics include: diabetics, obese patients, heavy smokers and patients taking blood thinners.

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If the condition is acute or an emergency, we have to do surgery. If the condition is elective, then surgery can wait. If the patient has poor glycemic control, then you probably don’t want to perform elective surgery on the patient such as carpal tunnel release. Remember, elective surgery can wait.

High blood sugar is linked to increased wound complications after surgery. Hemoglobin A1c is used to monitor the patient’s blood sugar level. The higher preoperative Hemoglobin A1c level, the more there is a risk factor for surgical site infection. Elective surgery can be delayed until HBA1c level becomes normal or better. Joint replacement surgery for example is delayed until HBA1c levels are less than 7%.

Since carpal tunnel syndrome is common in patients with diabetes, we need to take time to sort things out with these conditions. We need to know that the patient has better control of their diabetes. Carpal tunnel syndromes is a small surgery, but it can have catastrophic effect if we do not have a good control of the patient’s diabetes. Hemoglobin A1c will help us monitor the patient. Carpal tunnel surgery can cause complications and infection providing that high levels of HBA1c levels is a true risk factor for infection postoperatively.

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Osteoporosis

Osteoporosis is a decrease in bone strength. The strength of the bone depends on mineral density and bone quality. Osteoporotic bone is at risk of fracture at the hip, wrist and spine.

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If fracture of the vertebral spine occurs, the patient will have a fivefold increased risk for having a second vertebral fracture or hip fracture. A second vertebral fracture means you may have more compression fractures in the future.

With one hip fracture, there will be a tenfold increase of another hip fracture occurring. Men with hip fractures have a higher mortality rate than women.

Lifetime risk of fractures of the hip, spine and wrist is 40 %. The decrease of bone strength and bone mass clearly predicts fracture risk.

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Osteoporosis affects 45% of women aged 50 or older. There is some correlation between osteoporotic fracture and risk of death. This is logical since 25% of patients with hip fracture die within one year. The lifetime risk is high with senile osteoporosis. There are about million osteoporosis related fractures that occur per year.

Men and women both begin to start “spending” or losing bone at a certain point in their lives. Banking or building up of bone during youth has benefits during the later years. Most individuals obtain their peak bone mass between ages of 16 and 25 years. Men begin to lose bone mass after the age of 25 years at a rate of 0.3% per year. Women begin to lose bone at a rate of 0.5% per year. After menopause there is an accelerated rate of bone loss at the rate of 2-3% of total bone loss per year for about 10 years.

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Osteoporosis has bone mineralization but abnormal osteoclast function. There are two types of osteoporosis:

  1. Type I: postmenopausal which occurs 15-20 years after menopause. It has increased risk of vertebral and wrist fractures. It is due to estrogen deficiency.
  2. Type II: senile which occurs in men and women over the age of 70 years. Vertebral and hip fractures are a risk. It occurs more in females than males with a ratio 2:1. It is due to aging and long term calcium deficiency.

20-25% of elderly patients could die within one year suffering of a hip fracture.

osteoporosis4.pngRisk factors for osteoporosis include: thin, north European descent, people who live sedentary lifestyles, smoker and drinkers, and anti-seizure medications as phenytoin (Dilantin) and phenobarbital.

The bone mineral density is measured by T- score which is relative to normal age, young, matched control (25 year old women) and Z-score which is relative to similar aged patients.

How is osteoporosis measured? It is measured by DEXA scan at the hip through the T –score. DEXA scan is important in predicting fracture risk.osteoporosis5.png

Lab findings as albumin, calcium, phosphate, vitamin D, parathyroid hormone and bone specific alkaline phosphatase are usually normal.

Vitamin D levels are low in about 70 % of patients with fracture. Vitamin D absorbs calcium from the intestines. With aging, the stomach acidity decreases and the calcium absorption decreases and vitamin D requirements increase. Elderly need more vitamins D to absorb the same amount of calcium.

Treatment of osteoporosis include: bisphosphonates, Denosumab and calcitonin. Bone stimulation can be achieved by parathyroid hormone, calcium and vitamin D.

When to initiate therapy? If T-score is less than -2 with no risk factors, if T-score is less than -1.5 with at least one risk factor as prior vertebral fracture or hip fracture.

What decides if you develop osteoporosis or not? Your savings: you can control this by adding more bone when you are young before the age of 25 years. You begin spending your bone after 25 years.

Heat Illness in Athletes

As summer approaches, athletes, coaches and other individuals will need to be aware of heat-related illnesses. Heat illnesses include a spectrum of conditions ranging from heat syncope, heat cramps and heat exhaustion to the more severe heat stroke.

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Heat Syncope (fainting) is a form of orthostatic hypotension that is related to dehydration. It occurs due to inadequate cardiac output and hypotension. It also occurs with standing quickly after sitting or lying down for prolonged durations in the heat. Symptoms include fainting, dizziness and light-headedness. Treatment includes oral rehydration (water, juice or sports drinks) and placing the patient flat on the ground in a cool area with slight elevation of the legs to push the blood back to the vital organs such as the brain.

Heat Cramps are painful muscle cramps that occur due to decreased sodium heat2.pngconcentration in the blood. The patient’s core temperature is usually not elevated. Sodium may decrease when salts are lost in sweat or with excessive water intake that does not include electrolytes leading to a situation called dilutional hyponatremia. Symptoms include painful muscle cramps occurring commonly in the abdominal muscles, arms, legs and thighs. Treatment includes rest, cooling and IV fluids or oral rehydration with fluids rich in electrolytes (sports drinks and juices) to replenish the sodium stores. Prevention could be achieved by consumption of fluids high in electrolytes before strenuous activities.

heat3Heat Exhaustion is the most common heat illness. The body temperature becomes elevated but is less than 40°C. The core body temperature is best measured rectally. The signs and symptoms of heat exhaustion include profuse sweating, core body temperature lower than 40°C, weakness and fatigue, cramping, headaches, nausea and vomiting,  fainting, hypotension, increased heart rate, and fast shallow breathing. Treatment includes rest, IV fluids or oral rehydration and rapid cooling by whole-body immersion in an ice bath.

Heat Stroke is the most severe form of heat illness. It is a medical emergency that needs immediate attention. The patient should be transported to the hospital as soon as possible. Heat strokes occur due to failure of the body’s normal thermoregulatory mechanism. If treatment is not started promptly, end-organ failure and ultimately death may occur. Heat strokes have a high mortality rate and require quick reduction of the patient’s temperature. The three characteristic features of this condition are a lack of sweating, core body temperature above 40°C (best measured rectally) and an altered mental status. Additional signs and symptoms include hot, dry skin, disorientation, confusion and hallucinations, headache and slurred speech. This is a serious medical emergency that requires rapid core body temperature reduction. The patient should have close monitoring of airway, breathing and circulation. The physician should implement basic life support and ACLS protocols. Rapid cooling by whole-body immersion in an ice bath will be utilized as well as IV fluids.

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What is Rheumatoid Arthritis?

Rheumatoid arthritis involves the synovium of the joints. The condition of rheumatoid arthritis will result in deformities. Rheumatoid arthritis occurs in females more than males.

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There may be a hereditary component with rheumatoid arthritis. Rheumatoid arthritis has spontaneous remissions and exacerbations. The disease can have a systemic nature. Pain and stiffness of joints especially in the morning (morning stiffness). Rheumatoid arthritis is typically poly-articular, bilateral, and symmetrical and most commonly affects the hands and feet.

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X-rays show periarticular erosions at the time of diagnosis. Osteopenia and minimal osteophyte formation favors the diagnosis of rheumatoid arthritis.

Pathogenesis

Rheumatoid is an auto immune disease. The disease has two important components: immunological reactions and increased degradative enzymes. The IgM (rheumatoid factor) is produced by the plasma cell as an antibody to the native IgG, which is altered in RA. 70% of the patients with RA have rheumatoid factor positive. Leukocytes are attracted to the immune complex forming deposits over the inflammatory surface of the synovium. These leukocytes ingest fibrin and immune complex and is called the rheumatoid cells. The leukocytes release lysosomal enzymes that causes acute inflammatory response and tissue necrosis as well as inflammatory mediators (IL-1, IL-6, and TNFα). The chondrocytes respond to stimulation by TNFα, IL-1 and other inflammatory mediators causing cells to become activated and secrete more metalloproteinases which lead to cartilage damage. The synovium becomes hypertrophied (Pannus), showing intimal hyperplasis and infiltration by plasma cells and lymphocytes.

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Stages of Rheumatoid Arthritis

Early stages (acute) include hot, swollen, tender joints (synovitis), wrist swelling, MCP swelling and Flexor Sheath Synovitis. Complicated rheumatoid arthritis include digital vasculitis, ecchymosis, skin atrophy and nodules. Advanced rheumatoid arthritis includes swelling of the MCP joints, lateral slippage of extensor tendons and tendon ruptures and ulnar deviation of fingers. X-rays show destruction of MCP with subluxation, ulnar deviation and wrist destruction.

Finger deformities include mallet, boutonniere, and swan neck.

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The thumb is also involved. These changes occur due to proliferation, inflammation and hypertrophy of the synovium. Involvement of the distal radioulnar joint is usually associated with rupture of the extensor digiti minimi.

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Rheumatoid Nodules

25% of patients with RA will have subcutaneous nodules on extensor surfaces of elbow and forearm. Nodules are often multiple and seen along the ulnar margin of the forearm or pulp of the digits. Vasculitis is more common in patients with SC nodules, it is a strongly seropositive disease (aggressive) with a less than favorable prognosis.

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Treatment

If the patient has synovitis, it should be treated by a splint and medical treatment. If the patient has joint space narrowing, bone erosions and osteopenia the patient will need a synovectomy. If the patient has joint destruction/fixed deformity or loss of hand function, surgery is based on the conditions.

Before operating on RA patients, x-ray of the cervical spine is needed because the patient may have subluxation of C1-C2. Metacarpophalangeal joint arthroplasty of the fingers usually results in decreased extensor lag and improvement of the ulnar drift.