DIABETES MELLITUS AND THE SURGEON

PRESENTER : DR. VIKAS KUMAR (JR GENERAL SURGERY)

MODERATOR : DR. R.S. JHOBTA(ASSOC.PROFF.)IGMC, SHIMLA

INTRODUCTION

Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia.

Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production.

DM is the leading cause of end-stage renal disease (ESRD), nontraumatic lower extremity amputations, and adult blindness.

CRITERIA FOR THE DIAGNOSIS OF DIABETES MELLITUS

Symptoms of diabetes plus random blood glucose concentration >200 mg/dL (11.1 mmol/L ) or 

Fasting plasma glucose >126 mg/dL (7.0 mmol/L ) or 

HbA1C > 6.5% or 

Two-hour plasma glucose  >200 mg/dL (11.1 mmol/L ) during an oral glucose tolerance test 

ETIOLOGIC CLASSIFICATION OF DIABETES MELLITUS

I. Type 1 diabetes (beta cell destruction, usually leading to absolute insulin deficiency)    

A. Immune-mediated    

B. Idiopathic

II. Type 2 diabetes (may range from predominantly insulin resistance with relative

insulin deficiency to a predominantly insulin secretory defect with insulin resistance)

  

III. Other specific types of diabetes    -A. Genetic defects of beta cell function characterized by

mutations in:        1. Hepatocyte nuclear transcription factor (HNF) 4 (MODY

1)      2. Glucokinase (MODY 2)         3. HNF-1 (MODY 3)         4. Insulin promoter factor-1 (IPF-1; MODY 4)         5. HNF-1 (MODY 5)        6. NeuroD1 (MODY 6)        7. Mitochondrial DNA        8. Subunits of ATP-sensitive potassium channel         9. Proinsulin or insulin

 -B. Genetic defects in insulin action         1. Type A insulin resistance         2. Leprechaunism         3. Rabson-Mendenhall syndrome         4. Lipodystrophy syndromes  

-C. Diseases of the exocrine pancreas —pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, hemochromatosis

-D. Endocrinopathies—acromegaly, Cushing's syndrome,glucagonoma, pheochromocytoma, hyperthyroidism,

    

-E. Drug- or chemical-induced —glucocorticoids, beta-adrenergic agonists, thiazide, protease inhibitors, antipsychotics

   

- F. Infections—congenital rubella, cytomegalovirus, coxsackievirus

-G. Uncommon forms of immune-mediated diabetes— "stiff-person" syndrome, anti-insulin receptor antibodies

  -  H. Other genetic syndromes sometimes associated with diabetes— Wolfram's syndrome, Down's syndrome, Klinefelter's

syndrome, Turner's syndrome,

IV. Gestational diabetes mellitus (GDM)

TYPE 1 DM

Type 1 DM is the result of interactions of genetic, environmental, and immunologic factors that ultimately lead to the destruction of the pancreatic beta cells and insulin deficiency.

GENETIC CONSIDERATIONS Susceptibility to type 1 DM involves multiple genes.

The concordance of type 1 DM in identical twins ranges between 40 and 60%

The major susceptibility gene for type 1 DM is located in the HLA region on chromosome 6.

IMMUNOLOGIC MARKERS

Islet cell autoantibodies (ICAs) are a composite of several different antibodies directed at pancreatic islet molecules such as GAD, insulin, IA-2/ICA-512, and ZnT-8, and serve as a marker of the autoimmune process of type 1 DM.

Assays for autoantibodies to GAD-65 are commercially available.

ENVIRONMENTAL FACTORS

Numerous environmental events have been proposed to trigger the autoimmune process in genetically susceptible individuals

Putative environmental triggers include viruses (coxsackie, rubella, enteroviruses most prominently), bovine milk proteins,etc

TYPE 2 DM

Insulin resistance and abnormal insulin secretion are central to the development of type 2 DM

GENETIC CONSIDERATIONS Type 2 DM has a strong genetic component. The concordance of type 2 DM in identical

twins is between 70 and 90%.

The disease is polygenic and multifactorial. The genes that predispose to type 2 DM are incompletely identified.

ENVIRONMENTAL FACTORS obesity, nutrition, and physical activity

RISK FACTORS FOR TYPE 2 DIABETES MELLITUS Family history of diabetes (i.e., parent or sibling with type 2 diabetes)

Obesity (BMI > 25 kg/m2)

Physical inactivity

Race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander)

Previously identified with IFG, IGT, or an A1C of 5.7–6.4%

History of GDM or delivery of baby >4 kg (9 lb)

Hypertension (blood pressure 140/90 mmHg)

HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL (2.82 mmol/L)

Polycystic ovary syndrome or acanthosis nigricans

History of cardiovascular disease

COMPLICATIONS OF DM

I) ACUTE Diabetic ketoacidosis (DKA) and Hyperglycemic hyperosmolar state (HHS)

II) CHRONIC

A) Microvascular   Eye disease   

 Retinopathy (nonproliferative/proliferative)    Macular edema  

Neuropathy    Sensory and motor (mono- and polyneuropathy)    Autonomic  

Nephropathy

B) Macrovascular Coronary heart disease   Peripheral arterial disease   Cerebrovascular disease

C) Others Gastrointestinal (gastroparesis, diarrhea)   Genitourinary (uropathy/sexual dysfunction)   Dermatologic   Infectious   Cataracts   Glaucoma   Periodontal disease   Hearing loss

DM AND THE SURGEON

I) EMERGENCYEmphysematous infectionsDKA and HHS

II) ELECTIVEPerioperative mgmtDiabetic footSurgical treatment

APPROACH TO THE PATIENT

HISTORY

In a patient with established DM, the initial assessment should include : prior diabetes care, the type of therapy, prior A1C levels, self-monitoring blood glucose results, frequency of hypoglycemia, presence of DM-specific complications, and assessment of the patient's knowledge about diabetes, exercise,

and nutrition presence of DM-related comorbidities should be sought

(cardiovascular disease, hypertension, dyslipidemia )

PHYSICAL EXAMINATION

In addition to a complete physical examination, special attention should be given to DM-relevant aspects such as

Weight or BMI, Retinal examination, Orthostatic blood pressure, Foot examination, Peripheral pulses, Insulin injection sites Neurological examination Cardiovascular examination (Blood pressure >130/80 mmHg is

considered hypertension in individuals with diabetes) Teeth and gums

LABORATORY ASSESSMENT CHG FBS RFT/e LFT HbA1C URINE R/M and for microalbumin (30-300mg/24hr) LIPID PROFILE FUNDUS EXAM. THYROID FXN

IMAGING STUDIES CXR ECHO

EMERGENCY CONDITIONS

SPECIFIC EMERGENCIES : EMPHYSEMATOUS CHOLECYSTITIS EMPHYSEMATOUS PYELONEPHRITIS

AND CYSTITIS DIABETIC KETOACIDOSIS HYPEROSMOLAR HYPERGLYCEMIA

SYNDROME

I) EMPHYSEMATOUS CHOLECYSTITIS

Emphysematous cholecystitis is an uncommon condition characterized by infection of the gallbladder wall by gas-forming bacteria, particularly anaerobes.

Pt. presents as acute cholecytitis

Gangrene and perforation commonly complicate the course of emphysematous cholecystitis.

Pockets of gas are evident in the area of the gallbladder fossa on plain abdominal films, ultrasonography, and abdominal CT.

Emergency antibiotic therapy with anaerobic coverage and early cholecystectomy are warranted because the

risk of gallbladder perforation is high

II) EMPHYSEMATOUS PYELONEPHRITIS AND CYSTITIS

Emphysematous cystitis and pyelonephritis are acute necrotizing infections characterized by gas formation in the tissues.

Gas is localized to the bladder wall and lumen in cystitis and in and around the kidney in pyelonephritis.

Emphysematous pyelitis is a gas-forming infection restricted to the collecting system; the renal parenchyma is spared.

E. coli is most commonly identified. Klebsiella and Proteus are less common.

Almost all patients display the classic triad of fever, vomiting, and flank pain in pyelonephritis.

Pneumaturia and irritative lower tract voiding symptoms in cystitis.

The diagnosis is established radiographically.

Tissue gas that is distributed in the parenchyma may appear on abdominal radiographs as mottled gas shadows over the involved kidney

A crescentic collection of gas over the upper pole of the kidney is more distinctive.

CT is the imaging procedure of choice

Emphysematous pyelonephritis is a surgical emergency.

Currently, percutaneous drainage is the recommended initial approach because it is reported to be associated with lower mortality rates than is medical management alone or emergency nephrectomy

III) DIABETIC KETOACIDOSIS AND HYPEROSMOLAR HYPERGLYCEMIA SYNDROME

DKA results from relative or absolute insulin deficiency combined with counterregulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone).

Surgery should be delayed, whenever feasible, in patients with DKA, so that the underlying acid-base disorder can be corrected or, at least, ameliorated.

Patients with HHS are markedly dehydrated and should be restored quickly to good volume and improved metabolic status before surgery.

Precipitating events   Inadequate insulin administration  Infection Infarction Drugs (cocaine) Pregnancy

Symptoms Nausea/vomiting Thirst/polyuria Abdominal pain Shortness of breath

Physical Findings Tachycardia Dehydration/hypotension Tachypnea/Kussmaul respirations/respiratory distress Abdominal tenderness (may resemble acute pancreatitis or surgical

abdomen) Lethargy/obtundation/cerebral edema/possibly coma

DKA is characterized by hyperglycemia, ketosis, and metabolic acidosis (increased anion gap) along with a number of secondary metabolic derangements.

Management of Diabetic Ketoacidosis

1. Confirm diagnosis ( plasma glucose, positive serum ketones, metabolic acidosis).

2. Admit to hospital; intensive-care setting may be necessary for frequent monitoring or if pH <7.00 or unconscious.

3. Assess:     Serum electrolytes (K+, Na+, Mg2+, Cl–, bicarbonate, phosphate)     Acid-base status—pH, HCO3–, PCO2, -hydroxybutyrate     Renal function (creatinine, urine output)

4. Replace fluids: 2–3 L of 0.9% saline over first 1–3 h (15–20 mL/kg per hour); subsequently, 0.45% saline at 250–500 mL/h; change to 5% glucose and 0.45% saline at 150–250 mL/h when plasma glucose reaches 200 mg/dL (11.2 mmol/L).

5. Administer short-acting insulin: IV (0.1 units/kg), then 0.1 units/kg per hour by continuous IV infusion; increase two- to threefold if no response by 2–4 h.

6. If the initial serum potassium is <3.3 mmol/L (3.3 meq/L), do not administer insulin until the potassium is corrected. If the initial serum potassium is >5.2 mmol/L (5.2 meq/L), do not supplement K+ until the potassium is corrected.

7. Assess patient: What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG).

8. Measure capillary glucose every 1–2 h; measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h. 

9. Monitor blood pressure, pulse, respirations, mental status, fluid intake and output every 1–4 h.

10. Replace K+: 10 meq/h when plasma K+ < 5.0–5.2 meq/L (or 20–30 meq/L of infusion fluid), administer 40–80 meq/h when plasma K+ < 3.5 meq/L or if bicarbonate is given.  

11. Continue above until patient is stable, glucose goal is 150–250 mg/dL, and acidosis is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour.

12. Administer long-acting insulin as soon as patient is eating. Allow for overlap in insulin infusion and SC insulin injection.

ELECTIVE CONDITIONS

I) PERIOPERATIVE MGMT.

II) DIABETIC FOOT

III) SURGICAL TREATMENT

PERIOPERATIVE MGMT.

I) TYPE I DM

Insulin-treated patients undergoing major elective surgery should preferably be admitted 2–3 days before surgery.

For elective procedures, the basal insulin should be given at 80% to 100% of the usual dose the evening before surgery, with an insulin infusion initiated the morning of surgery.

Even with normal basal insulin the night before surgery, low dose IV insulin will be required, and it is usually begun when the blood glucose level rises above 130 mg/dL.

Intravenous infusion of insulin, glucose, and potassium is now standard therapy and has replaced subcutaneous insulin therapy for the perioperative management of diabetes.

Adequate fluids must be administered to maintain intravascular volume.

The preferred fluids are normal saline and dextrose in water.

Fluids containing lactate (i.e., Ringer’s lactate) cause exacerbation of hyperglycemia.

Insulin-Two main methods of insulin delivery

have been used: either combining insulin with glucose and potassium in the same bag (the GIK regimen) or giving insulin separately as an infusion.

-Various regimens have been proposed for insulin infusion.

-Regardless of whether separate or combined infusions are given, close monitoring is required during these infusion regimens.

Regimen for Separate Intravenous Insulin Infusion forPerioperative Diabetes Management

Prepare a 0.1 unit/ml solution by adding 25 units regular insulin to 250 ml normal saline.

Flush 50 ml of insulin solution through infusion tubing to saturate nonspecific binding sites.

Set initial infusion rate (generally, 0.5-1.0 unit/h [5-10 ml/h]

Adjust infusion rate according to bedside blood glucose measurement as follows:

Blood Glucose (mg/dl) Insulin Infusion Rate<80 Check glucose after 15 min

80–140 Decrease infusion by 0.4 unit/h(4ml/h) 141–180 No change 181–220 Increase infusion by 0.4 unit/h (4 ml/h) 221–250 Increase infusion by 0.6 unit/h (6 ml/h) 251–300 Increase infusion by 0.8 unit/h (8 ml/h) >300 Increase infusion by 1 unit/h (10 ml/h)

GlucoseAdequate glucose should be provided to

prevent catabolism, starvation ketosis, and insulin-induced hypoglycemia.

The physiological amount of glucose required to prevent catabolism in an average nondiabetic adult is ~120 g/day (or 5 g/h).

With preoperative fasting, surgical stress, and ongoing insulin therapy, the caloric requirement in most diabetic patients averages 5–10 g/h glucose.

This can be given as 5 or 10% dextrose. An infusion rate of 100 ml/h with 5% dextrose delivers 5 g/h glucose.

If fluid restriction is necessary, the more concentrated 10% dextrose can be used.

Many now prefer to give 10% dextrose at a starting rate of ~100 ml/h.

The usual range of perioperative blood glucose that clinicians are comfortable with is ~120–180 mg/dl.

The insulin and glucose infusion rates should be adjusted accordingly if blood glucose monitoring shows marked deviation from the acceptable range.

Potassium

The infusion of insulin and glucose induces an intracellular translocation of potassium, resulting in a risk for hypokalemia.

In patients with initially normal serum potassium, potassium chloride, 10 mEq, should be added routinely to each 500 ml of dextrose to maintain normokalemia if renal function is normal.

Hyperkalemia and renal insufficiency are contraindications to potassium infusion.

II) TYPE II DM

Patients Treated With Oral Antidiabetic Agents

Second-generation sulfonylureas should be discontinued 1 day before surgery, with the exception of chlopropramide, which should be stopped 2–3 days before surgery.

Other oral agents can be continued until the operative day.

These should be taken the evening before surgery and omitted on the morning of surgery.

Metformin should be withhold 1–2 days before surgery, especially in sick patients and those undergoing procedures that increase the risks for renal hypoperfusion, tissue hypoxia, and lactate accumulation.

At a minimum, blood glucose should be monitored before and immediately after surgery in all patients.

Those undergoing extensive procedures should have hourly glucose monitoring during and immediately following surgery.

Bedside capillary blood glucose meters are adequate for these monitoring requirements.

The recommended treatment for patients undergoing major surgery and for those with poorly controlled type 2 diabetes (i.e.>200 mg%) is intravenous insulin infusion with glucose.

INTRAOPERATIVE

Insulin infusion regimen is continued

Look for complications : Hypoglycemia Arrythmias Silent MI Hypotension Decrease urine output if nephropathy +

POSTOPERATIVE MANAGEMENT

The ideal time to transition from IV insulin to subcutaneous insulin depends on several factors: the presence of postoperative nausea and vomiting, a planned subcutaneous regimen, the meal schedule, and discharge considerations.

For patients receiving an insulin infusion who were previously well controlled on oral agents the oral medication can be administered and 1 hour later the insulin infusion can be discontinued.

Of note, metformin should not be restarted until 48 hours after the procedure and not until normal renal function has been confirmed

For patients receiving an insulin infusion who are not well controlled on oral agents prior to admission or who are requiring more than two to three units of insulin per hour, a transition to subcutaneous insulin postoperatively is recommended.

The total daily insulin requirement can be estimated by taking the infusion rate for the preceding 4 to 8 hours and extrapolating this dose to a 24-hour amount.

This should be reduced empirically by 40% to address the acute stress of surgery and thus avoid hypoglycemia.

If the plan is to use a long-acting analogue (eg. Glargine ) for basal insulin and a rapid-acting analogue (eg. Lispro,aspart) for meals, half of the total insulin requirement can be given as the long-acting analogue, the remaining half being divided and given as a rapid-acting analogue prior to each meal.

INSULIN BY SLIDING SCALE IS NOT RECOMMENDED

DIABETIC FOOT

INTRODUCTION

Of all the late complications of diabetes, foot problems are probably the most preventable.

Foot ulceration is common and occurs in both T1DM and T2DM.

Approximately 5% to 10% of diabetic patients have had past or present foot ulceration, and 1% have undergone amputation.

Diabetes is the most common cause of nontraumatic lower limb amputation.

Rates are 15 times greater than those in the nondiabetic population.

The lifetime risk for development of a foot ulcer in a diabetic patient is estimated to be as high as 25%.

RISK FACTORS

Diabetic Neuropathy Peripheral Vascular Disease Past Foot Ulceration or Foot Surgery Retinopathy and renal dysfunction Callus, Deformity, and High Foot Pressures

I) NEUROPATHY

Changes in the vasonervorum with resulting ischemia ? cause Increased sorbitol in feeding vessels block flow and causes nerve

ischemia Intraneural acculmulation of advanced products of glycosylation

Abnormalities of all three neurologic systems contribute to ulceration

A) Autonomic Neuropathy

Regulates sweating and perfusion to the limb Loss of autonomic control inhibits thermoregulatory

function and sweating

Result is dry, scaly and stiff skin that is prone to cracking and allows a portal of entry for bacteria

B) Motor Neuropathy Mostly affects forefoot ulceration

Intrinsic muscle wasting – claw toes Equinous contracture

C) SENSORY NEUROPATHY

Loss of protective sensationStarts distally and migrates proximally in

“stocking” distributionLarge fibre loss – light touch and

proprioceptionSmall fibre loss – pain and temperatureUsually a combination of the two

Two mechanisms of UlcerationUnacceptable stress few times

rock in shoe, glass, burn

Acceptable or moderate stress repeatedly Improper shoe ware deformity

II) VASCULAR DISEASE

30 times more prevalent in diabetics

Diabetics get arthrosclerosis obliterans or “lead pipe arteries”

Calcification of the media

Often increased blood flow with lack of elastic properties of the arterioles

Not considered to be a primary cause of foot ulcers

However, the common combination of vascular disease with minor trauma can lead to ulceration.

Minor injury and subsequent infection increase the demand for blood supply beyond the circulatory capacity, and ischemic ulceration and risk of amputation develop.

RECOMMENDED EVALUATION OF A DIABETIC FOOT

Describe the lesion (cellulitis, ulcer, etc.) and any drainage (serous,purulent, etc.).

Enumerate the presence or absence and degree of various signs of inflammation.

Define whether or not infection is present and attempt to determine probable cause.

Examine the soft tissue for evidence of crepitus, abscesses, sinus tracts, foreign bodies.

Probe any skin breaks with sterile metal probe to see whether bone is exposed or palpable.

Measure the wound (length * width; estimate depth); consider taking photograph.

Palpate and record pedal pulses; use Doppler instrument if necessary.

Evaluate neurological status: protective sensation, motor and autonomic function.

Cleanse and debride the wound; remove any foreign material, eschar, or callus.

Culture the cleansed wound (preferably by curettage, aspiration, rather than swab).

Order plain radiographs of the infected foot in most cases; consider other imaging as needed.

Consider which consultants might need to see the patient and how quickly.

CLASSIFICATION OF FOOT ULCERS

I) WAGNER DIABETIC FOOT ULCER CLASSIFICATION SYSTEM

Grade Description 0 No ulcer, but high-risk foot (e.g., deformity, callus, insensitivity) 1 Superficial full-thickness ulcer

2 Deeper ulcer, penetrating tendons, no bone involvement 3 Deeper ulcer with bone involvement, osteitis

4 Partial gangrene (e.g., toes, forefoot)

5 Gangrene of whole foo

II) UNIVERSITY OF TEXAS WOUND CLASSIFICATION SYSTEM

Stage Grade 0 Grade 1 Grade 2 Grade 3

A Preulcer or Superficial ulcer Deep ulcer Wound

Postulcer lesion; to tendon or penetrating no skin break capsule bone or joint

B + Infection + Infection + Infection +InfectionC + Ischemia + Ischemia + Ischemia +Ischemia

D + Infection and + Infection and +Infection and +Infection and ischemia ischemia ischemia ischemia

MANAGEMENT

ADA identified six interventions with demonstrated efficacy in diabetic foot wounds:

(1) off-loading,

(2) debridement,

(3) wound dressings,

(4) appropriate use of antibiotics,

(5) revascularization, and

(6) limited amputation.

(1) OFF-LOADING

The TCC has long been recognized as the gold standard for off-loading a foot wound.

TCCs are not usually recommended for management of neuroischemic ulcers.

Removable cast walker (RCW) resulted in slower healing than the TCC

Removable casts and pneumatic cast boots (Aircast) may be used in cases without infection.

2) DEBRIDEMENT

Almost all infected foot lesions (other than primary cellulitis)must be debrided

Debridement is aimed at removing any eschar (full-thickness dead skin), other necrotic tissue or foreign material, or surrounding callus.

Debridement is best done mechanically (i.e., with instruments) rather than with enzymatic or chemical agents.

Definitive debridement will often require more than one session or need to be repeated at follow-up visits.

The presence of pus in an enclosed space requires drainage.

Fulminant soft tissue infections, such as gas gangrene or necrotizing fasciitis, require urgent debridement of involved tissue.

Drain any areas of suspected infection, regardless of the patient’s circulatory status.

Patients with systemic toxicity will not improve until the wound has been adequately surgically debrided and thoroughly drained.

One form of debridement therapy that is used in some patients with diabetic foot wounds is so-called larval (or maggot) biotherapy.

This form of therapy is found to be safe and effective.

One study even demonstrated that fewer days of antibiotic therapy were required in patients who were treated with maggot debridement.

3) WOUND DRESSINGS

4) ANTIBIOTICS

Antibiotics should usually be given intravenously for patients who are systemically ill, have a severe infection, are unable to tolerate oral agents, or are known or suspected to have pathogens that are

not susceptible to available oral agents.

Suggested Antibiotic Regimens for Treating Diabetic Foot Infections

Severity of Infection Recommended Alternative

Mild/moderate Cephalexin (500 mg qid); or Levofloxacin (500 mg po qd) ± Amoxiclav (875/125 mg bid);or clindamycin(300 mg po tid);or

Clindamycin (300 mg tid) TMP/SMX (2 DS po bid)

Moderate/severe Ampicillin/sulbactam (2g qid); or Ertapenem (1gm qd); orClindamycin (450 mg po qid) + Linezolid (600 mg bid)

ciprofloxacin (750 mg bid) ±aztreonam (2 gm tid)

Life-threateningImipenem/cilastatin (500 mg qid) Vancomycin (15 mg/kg bid) +Clindamycin (900 IV mg tid) + ceftazidime(1 gm tid) +

tobramycin (5.1 mg/kg/day) + ampicillin metronidazole(7.5 mg/kg IV qid)(50 mg/kg IV qid)

The selected antibiotic regimen should almost always include an agent that is active against staphylococci and streptococci

For mild to moderate infections, a 1- to 2-week course while for more serious infections, treatment has usually been given for 2 to 4 weeks.

Treatment of osteomyelitis should usually be parenteral (at least initially) and prolonged for at least 6 weeks.

If all of the infected bone is removed, a shorter course of antibiotic therapy (e.g., 2 weeks) might be sufficient.

5) REVASCULARIZATION

Lower-limb vascular procedures, including angioplasty and bypass grafting, have been shown to be safe and effective for patients with diabetic foot infections.

Feet with critical ischemia that once required amputation can now often be saved with these techniques.

While initial debridement must be performed even in the face of poor arterial circulation, revascularization is generally postponed until sepsis is controlled.

Waiting for more than a few days in hopes of sterilizing the wound is inappropriate, however, and can result in further tissue loss.

Several studies suggest that early recognition and aggressive surgical drainage of pedal sepsis followed by surgical revascularization are critical to achieving maximal limb salvage.

Long-term follow-up studies have shown that the presence of diabetes does not influence late mortality, graft patency, or limb salvage rates after lower-limb arterial reconstruction

6) LIMITED AMPUTATION

Amputation may range from ray amputation of a toe to transfemoral amputation of a limb

A number of factors influence level selection: amputation must be done proximal to an irreparably damaged or gangrenous

body part.

Tissue oxygen perfusion

Patients with uncontrolled psychosis or a history of major noncompliance with foot care programs

Nicotine addiction and poor plasma glucose control.

FOOT CARE

1. Take care of diabetes.

2. Check feet every day

3. Wash your feet every day.

4. Keep the skin soft and smooth.

5. Smooth corns and calluses gently.

6. Trim toenails straight across and file the edges with nail file.

7. Wear shoes and socks at all times

8. Protect feet from hot and cold.

9. Don’t cross legs for long periods of time.

10.Don’t smoke.

SURGICAL TREATMENT

1) GASTRIC BYPASS AND BILIOPANCREATIC DIVERSION

2) PANCREATIC TRANSPLANTATION

3) ISLET CELL TRANSPLANTATION