"A Man can't make a mistake can't make anything"

Tuesday, 15 May 2012

SURGICAL ASPECT OF DIABETIC FOOT (diagnosis , sign, symptoms, and management ) / komplikasi diabetes melitus pada kaki dan penanganannya.


A. Definition

Diabetes Mellitus (DM) is a hereditary metabolic disease that mostly, demham signs of hyperglycemia and glucosuria, accompanied by clinical symptoms or absence of acute or chronic, as a result of the lack of effective insulin in the body, lies in the primary disorder of carbohydrate metabolism that is usually accompanied too fat and protein metabolism disorders. (Askandar, 2000).

Gangrene is the process or condition that is characterized by the presence of dead or necrotic tissue, but a microbiological process of necrosis is caused by infection. (Askandar, 2001).

B. Classification

A. Diabetes Mellitus

a. Type I diabetes mellitus (IDDM)

Patients are very dependent on insulin due to an autoimmune process that attacks the insulin. IDDM is the type of DM-derived (Inherited).

b. Type II diabetes mellitus (NIDDM)

Type of DM is influenced by both heredity and environmental factors. A person has a substantial risk of suffering from NIDDM if their parents are people with DM and adopt the wrong lifestyle.

c. Gestational DM

DM of this type tend to occur in pregnant women and the family members who are also suffering from DM. Risk factor is overweight or obese.

d. Secondary DM

DM is associated with other conditions or syndromes (pancreatitis, hormonal abnormalities, and drugs).

2. Diabetic Foot Gangrene

Wagner (1983) of diabetic foot gangrene divide into six levels: Grade 0: no open lesions, the skin is still intact with the possible

with foot deformities such as "claw, callus". Grade I: superficial ulcers confined to the skin.

Degree II: penetrating ulcer in the tendon and bone. Degree III: An abscess in, with or without osteomyelitis.

Degree IV: Gangrene of the distal toes or legs with or without cellulitis.

Degree V: gangrene whole leg or part of the leg.

Meanwhile, Brand (1986) and Ward (1987) divide the gangrenous leg into two groups:

A. Diabetic foot due to ischemia (KDI)

Caused by decreased blood flow to the leg as a result of makroangiopati (atherosclerosis) of the large blood vessels ditungkai, especially in the calf.

KDI clinical picture:

- The patient complains of pain when resting.

- In cold palpability.

- Pulsation of blood vessels is less strong.

- Obtained ulcer to gangrene.

2. Diabetic foot due to Neuropathy (KDN)

Damage to somatic and autonomic nerves, there is no disturbance of the circulation. Encountered clinically in the foot a dry, warm, tingling, numbness, leg edema, a palpable pulsation of blood vessels leg either.

C. Etiology

A. Diabetes Mellitus

DM has a heterogeneous etiology, with a variety of lesions can lead to insulin insufficiency, but the genetic determinants usually plays an important role in the majority of DM. Another factor that is considered as a possible etiology of DM are:

A. Abnormalities of pancreatic beta cells, ranging from the loss of beta cells to release insulin beta cell failure.

2. Environmental factors that alter the function of beta cells, such as agents that can cause infection, dietary intake of carbohydrates and sugars which are processed in excess, obesity and pregnancy.

3. Immune system disorders. This system can be done by the autoimmunity that accompanied the formation of antibodies antipankreatik cells and cause damage to cells - the cells penyekresi insulin, and increased sensitivity of beta cells by the virus.

4. Insulin abnormalities. In obese patients, an interruption tissue sensitivity to insulin due to a lack of insulin receptors present on cell membranes to insulin responsir.

2. Diabetic Foot Gangrene

Factors that influence the occurrence of diabetic foot gangrene is divided into endogenous and exogenous factors.

Endogenous factors: a. Genetic, metabolic

b. Diabetic angiopathy

c. Diabetic neuropathy

Exogenous factors: a. Trauma

b. Infection

c. Drug

D. Pathophysiological

A. Diabetes Mellitus

Most of the pathological picture of DM can be associated with one of the main effects due to the lack of insulin following:

A. Decreased use of glucose by the cells - the cells of the body that lead to higher blood glucose concentrations as high as 300 - 1200 mg / dl.

2. Increased mobilization of fat from the fat storage areas that cause abnormal lipid metabolism that is accompanied by cholesterol deposits on artery walls.

3. Reduced protein in the body tissues.

Patients who have insulin deficiency can not maintain fasting plasma glucose levels are normal or tolerance after meals. At yng severe hyperglycemia exceeding normal kidney (blood glucose concentration of 160-180 mg/100 ml), there will be glycosuria because the renal tubules, the tubules can not reabsorb all the glucose. Glucosuria this will result in osmotic diuresis that causes polyuria accompanied by loss of sodium, chloride, potassium, and phosphate. Presence of polyuria lead to dehydration and polidipsi arise. Glucose due to the exit with the urine of patients will experience a negative protein balance and body weight decreased and tended to occur polifagi. The other is due to asthenia or lack of energy so that the patient becomes tired and sleepy due to the reduction or loss of body protein and also reduced the use of carbohydrates for energy.

Hyperglycemia of time will lead to atherosclerosis, thickening of the basement membrane and changes in peripheral nerves. This will facilitate the occurrence of gangrene.

b. Diabetic Foot Gangrene

There are two main theories regarding the occurrence of chronic DM complications due to hyperglycemia, the sorbitol theory and the theory of glycosylation.

A. Sorbitol theory

Hyperglycemia will cause a buildup of glucose levels in certain cells and tissues and can transport glucose without insulin. This excess glucose will not normally termetabolisasi discharged through glycolysis, but most of the enzyme aldose reductase with the mediation will be converted into sorbitol. Sorbitol would accumulate in cells / tissues and cause damage and changes in function.

2. Theory of glycosylation

As a result of hyperglycemia will lead to glycosylation of the proteins, particularly lysine-containing compounds. The process of protein glycosylation in the basement membrane can explain all the complications of both macro and micro vascular.

The Diabetic Foot (KD) alone caused by factors - factors mentioned in the etiology. The main factor that the onset of KD is angiopathy, neuropathy, and infection. Neuropathy is an important factor for the occurrence of KD. The presence of peripheral neuropathy will lead to sensory or motor disturbances. Sensory disturbance will cause a loss or decrease in pain sensation in the feet, so it would have went unnoticed trauma that causes ulcers on the foot motor disorders will also result in leg muscle atrophy, and changes the fulcrum that causes ulsetrasi the patient's leg. Angiopathy will cause disruption of blood flow to the legs. If blood clots occur in the larger blood vessels then the patient will feel pain in his legs after he walked a certain distance. Manifestations of other vascular disorders can be: the end of cold feet, leg pain at night, the arterial pulse is lost, the feet become pale when raised. The existence angiopathy will cause a decrease in the intake of nutrients, oxygen (oxygen) as well as antibiotics, causing poor healing wounds (Levin, 1993). Infection is often a complication of KD due to accompanying reduction in blood flow or neuropathy, angiopathy factors and infections that affect terhdap cure or treatment of KD.

E. Examination Support

A. Diagnostic Examination

• increased blood glucose

• Free fatty acids increased

• increased serum osmolality

• Arterial blood gases: pH decreases, HCO3 decreased

• U / creatinine increased / normal
• Urine: glucose + acetone positive

• Electrolytes: Na, K, phosphorus

2. Control Ktiteria DM

Good Medium Poor
Fasting GD (mg / dL) 80-109 110-139 ≥ 140
GD 2 hour PP (mg / dL) 110-159 160-199 ≥ 200
Koleseterol Total (mg / dL) <200200-239> 240
LDL cholesterol (mg / dL) non CHD <130130-159> 160
With CHD <100100-129> 130
HDL cholesterol (mg / dL)> 45 35-45 <35
Triglycerides (mg / dL) without CHD <200200-149> 250
With CHD <150150-199> 200
BMI: 18.5 to 22.9 Women 23-25> 25 / <18,
Men from 20 to 24.9 25-27
> 27 / <20
140-160 /
Blood pressure (mmHg) <140/90> 160/95

F. Complication

Complications arise by the DM bias include:

A. Diabetic Foot Gangrene

2. Neurophaty

3. Retinophaty

4. Nephrophaty

5. Chronic Heart Disease

While complications from gangrene that is:

A. Osteomyelitis

2. Sepsis

3. death

G. Management

A. Diet

Management of nutrition in patients with DM is directed to achieve the following objectives:

a. Meet all the essential elements of food (eg vitamins and minerals)

b. Achieve and maintain weight (BMI) as appropriate. Calculation

BMI = weight (kg) / (TB (m)) 2

Normal BMI women = 18.5 to 22.9 kg/m2 BMI normal men = 20 to 24.9 kg/m2

c. Meet the energy needs

d. Prevent fluctuations in blood glucose levels every day by seeking near-normal blood glucose levels by means of a safe and practical

e. Lowers blood fat levels if these levels increase

2. Oalahraga

Sports or physical exercise is done as follows:

- 5-10 'heating

- 20-30 'aerobic exercise (75-80% maximum heart rate)

- 15-20 'cooling

However, the exercise should also pay attention to the following

- Do not do physical exercise if blood glucose> 250 mg / dL

- If blood glucose <100 mg / dLsebelum exercise, then you should eat a snack before
- Recommended practice for patients with complications adapted to the conditions
- Exercises performed 2 hours after eating

- On the client with diabetic foot gangrene, it is not advisable to do physical exercises that are too heavy

4. Treatment for gangrene

- Dry

o Rest in bed

o Control of blood sugar with diet, insulin or antidiabetic drugs

o Measures to prevent the spread of gangrene amputation, but with a very clear indication
o Improve the circulation in order to overcome angiopathy with anti-platelet drugs aggregation (aspirin, diprydamol, or pentoxyvilin)

- Wet

o Rest in bed

o Control of blood sugar with diet, insulin or antidiabetic drugs

o Debridement

o Compress with warm water, not hot or cold water

o Give "topical antibiotic"

o Give an appropriate antibiotic or culture with broad-spectrum antibiotic

o To provide neuropathy pyridoxine (vitamin B6) or other neurotrophic

o Improve the circulation in order to overcome angiopathy with anti-platelet drugs aggregation (aspirin, diprydamol, or pentoxyvilin)

- Surgery

o Amputation soon

o Debridement and drainage, after calm then action can be taken was amputations or skin / arterial graft
5. Drug

a. Oral Hypoglycemic drug (OHD)

b. Insulin, with the indication:

- Ketoacidosis, hyperosmolar coma, and lactic acidosis

- DM with rapid weight loss

- DM is experiencing severe stress (systemic infection, severe surgery, etc.)

- Gestational DM

- Type I diabetes

- Failure to use OHD

No comments:

Post a Comment