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Diabetic Foot Problem - Charcot Joint Disease

A Serious Diabetic Foot Problem

Charcot Joint Disease

Charcot Foot is the degeneration of a weight bearing joint in the foot. It is a process of bone destruction, bone resorption and eventual deformity.

If it is left unchecked it could lead to ulceration, superinfection, loss of function of the foot , possible amputation and death.

Diabetes mellitus neuropathy (the most common in the U.S. today, resulting in destruction of foot and ankle joints), with Charcot joints in 1/600-700 diabetics. The neuropathy is related to long-term poor glucose control.

One mechanism is the loss of peripheral sensations where you can't sense touching on the ankle surface. This can lead to minute further damage to the joint called microtrauma.

The damage to the ankle is unnoticed by a diabetic. This results in inflammatory resorption of traumatized bone that causes weakness in the effected weight-bearing joint that, in turn, makes the joint susceptible to further trauma. It is a vicious cycle.

It results, from the decline in fine motor control of the joint and unnatural pressure on some joints. This leads to more microtrauma. Desensitized nerves in the ankle joint cause an increase in the blood flow to the joint. This leads to hyperimia which leads to further resorption of bone tissue. The bone resorption along with mechanical stress will cause destruction of the ankle.

If untreated or unrecognized the final result may be amputation. In the serious states infection could set in and result in death.

Please continue to consult with a Diabetologist and ask questions if you suspect numbness in the foot and ankle could lead to complications.

Pituitary Gland and Diabetes Insipidus

Diabetes Insipidus

When the Pituitary Gland is involved there are three types of diabetes insipidus: 

Central Diabetes Insipidus a deficiency of the hormone ADH (Anti-Diuretic Hormone) in the Posterior Pituitary Gland. The urine is very dilute but without the sugar taste of the urine associated with diabetes mellitus.

Neurogenic Diabetes Insipidus is an insensitivity of the kidneys to ADH that controls excretion of body fluid. The urine is very diluted sense the inability of the hormone ADH to restrict water loss. Again, like in Central Diabetes Insipidus, no glucose is present in the urine.

Iatrogenic Diabetes Insipidus - an artifact of medical drug use that causes the kidneys to excrete large amounts of urine. There is no glucose in the urine.

Diabetes Insipidus is characterized by excessive thirst and the excretion of large amounts of severely diluted urine, that, with a reduction of fluid intake, that has no effect on the concentration of the urine. This means the patient needs to continually take fluids into their body to prevent dehydration from the fluid loss excreted from the body. You need reserve water if you are exposed to conditions where excess water is lost normally.

Diabetes Mellitus and Diabetes Insipidus are two entirely separate conditions with unrelated mechanisms. Both cause the production of large amounts of urine (Polyuria). Diabetes Mellitus causes polyuria by a process called osmotic diuresis due to high blood sugar leaking into the urine and  carrying excess water with it. 

Osmosis is the process where water moves through a selectively permeable membrane from an area of low solute concentration to an area of high solute concentration. When leakage of blood glucose from the blood capillaries into the tubular ducts takes place it increases the solute concentration in the tube above that in the blood capillaries. Water, therefore, flows into the tubule by osmosis. Since this causes diuresis excretion from the kidneys along with the sugar the taste of urine in diabetes mellitus is sweet to the taste.

Diabetic Retinopathy

Diabetic Retinopathy

It is damage to the retina coat of the eye caused by complications from diabetes. It can lead to blindness. It affects approximately 80% of diabetics with a history of diabetes for at least ten years.

The necessity for an early eye examination schedule by an ophthalmologist is essential. The earlier the detection, in a diabetic patient, the possibility to reduce the effects of diabetic retinopathy increases.

The detection of diabetic retinopathy is difficult. A diabetic experiences no early warning signs. The presence of blood capillaries in the eye are especially sensitive to poor blood glucose control. High blood  glucose damages the capillaries in the retina of the eye. This is the beginning of the non-proliferative  diabetic retinopathy. Detection of this stage of the disease is one reason for the very early schedule of visits to an ophthalmologist. You can't detect the early changes. Early changes, that are reversible, and do not threaten central vision is called background retinopathy.

If you didn't see an ophthalmologist and schedule a series of  examinations to detect the early start of the disease you may detect vision changes. Blurring vision makes driving and reading difficult. Blurred vision is minor the first time you experience it. The blood capillaries, in the retina, begin to leak. This is called ocular hemorrhage and blurs vision. Proliferative diabetic retinopathy is the proliferation of new blood capillaries at the back of the eye that leak. A second, more severe leaking of blood from the capillaries, begins soon after. The onset may occur in several days to several weeks later.

Your eye has the ability to reabsorb the few red blood cells that leak the first time from the capillaries. The next phase a much greater amount of blood leaks. The reabsorption of the blood may take  from only a few days to as much as years to clear. These hemorrhages usually take place at night during sleep. The blurring of the vision deepens. Your activities that require clear vision decline.

The elevation of blood glucose that causes the blood capillaries to leak also cause a swelling of the crystalline lens of your eyes. Edema, or swelling, is the result of sugar alcohol accumulating in the lens. You experience the thickening of the lens as blurred distance  vision. Your near vision is not affected or the changes are slight.

Hyperglycemia causes the death and thickening of the basement membranes of the capillary cells. The capillary begins to leak. Holes begin to open that allow the contents of the capillary spill into the chamber of the eye that contains the retina. Some diabetics develop macular edema. When fluid from the capillary moves into the macula your vision blurs even more. The macular portion of the retina is responsible for the detailed portion of our vision.

As the proliferative diabetic retinopathy progresses severe non-proliferative diabetic retinopathy enters an advanced, or proliferative stage when blood vessels grow. Without treatment these new capillaries can bleed, cloud vision and destroy the retina.

Glaucoma can result as the capillaries grow and prevent the proper reabsorption of the fluid in the eye. The build up of pressure can damage the optic nerve. The blindness is now permanent.