Diabetes Mellitus | Medical Science Optional Notes for UPSC PDF Download

Diabetes Mellitus - Complications

Diabetic Ketoacidosis (DKA)

Key Abnormalities in DKA

• Insulin deficiency leads to hyperglycemia, hyperosmolality, osmotic diuresis, and electrolyte loss, resulting in hypovolemia.
• Insulin deficiency triggers lipolysis, generating free fatty acids, hepatic ketone production (ketogenesis), and ketosis.
• Bicarbonate consumption occurs as a buffer, causing anion gap metabolic acidosis.
• Insulin deficiency induces hyperosmolality, leading to K+ shift out of cells, coupled with a lack of insulin to promote intracellular K+ uptake, depleting total body K+ despite normal or elevated serum K+.

Management of DKA

• Administer an IV bolus of regular insulin (0.1 units/kg).
• Correct potassium levels before using insulin if below 3.3 meq/L.
• Provide an IV bolus of normal saline until vitals stabilize.
• Titrate IV insulin infusion based on the drop in serum glucose.
• Once vitals stabilize, transition to half normal saline to prevent hyperchloremia from large volumes of normal saline.
• Introduce 5% dextrose when serum glucose reaches 250 mg/dl to prevent cerebral edema from rapid changes in plasma osmolality.
• Address underlying conditions (e.g., infection) precipitating DKA.
• Replace potassium loss and administer bicarbonate if severe acidosis is present (pH < 7).
• Shift to a subcutaneous long-acting plus short-acting insulin regimen and gradually wean off IV insulin once the patient resumes eating.

Diabetic Nephropathy

• Significance: Diabetic nephropathy stands as the primary cause of chronic kidney disease, leading to end-stage renal disease and necessitating renal replacement therapy.
• Definition: Diabetic kidney disease involves albuminuria and a reduced glomerular filtration rate (GFR) (<60 mL/min/1.73 m2).
• Risk Factors: Factors contributing to the risk include race (African Americans, Native Americans), a family history of diabetic nephropathy, and smoking, which accelerates the decline in renal function.
• Pathogenesis:
  • Chronic Hyperglycemia: A key factor in the development of diabetic nephropathy.
  • Soluble Factors: Including growth factors, angiotensin II, endothelin, and advanced glycation end products.
  • Hemodynamic Alterations: Affecting renal microcirculation, leading to glomerular hyperfiltration, increased capillary pressure, and structural changes.
  • Glomerular Changes: Thickening of the capillary basement membrane, diffuse mesangial sclerosis, nodular glomerulosclerosis (Kimmelstiel-Wilson lesion), and nephrosclerosis.
• Clinical Features:
  • Increased Glomerular Capillary Pressure: Associated with albuminuria despite basement membrane thickening due to leaky diabetic capillaries.
  • Nodular Glomerulosclerosis: Characterized by ball-like deposits (nodules) of laminated matrix in the glomerular periphery, pathognomonic for diabetes.
• Investigations:
  • Estimated GFR: A key measure, with values below 60 mL/min/1.73 m2 indicating reduced kidney function.
  • Urinary Albumin to Creatinine Ratio: Elevated levels (>30 mg/g Cr) signify albuminuria.
• Irreversible Changes: Once marked albuminuria and reduced GFR are evident, the pathological alterations are likely irreversible.
• Screening Recommendations: Initiate screening for albuminuria five years after the onset of type 1 diabetes mellitus and at the time of type 2 diabetes mellitus diagnosis.

Screening for albuminuria

Conditions Leading to Albuminuria:

• Urinary Tract Infection
• Hematuria
• Heart Failure
• Febrile Illness
• Severe Hyperglycemia
• Severe Hypertension
• Vigorous Exercise

If two out of three albuminuria tests are positive, treatment should be initiated.

Treatment Strategies:

• Improved Glycemic Control: Focus on optimizing blood glucose levels.
• Strict Blood Pressure Control: Aim for a blood pressure goal below 140/90 mmHg.
• Administration of ACE Inhibitor or ARB: Implement the use of an ACE inhibitor or angiotensin II receptor blocker (ARB).
• Treatment of Dyslipidemia: Address abnormal lipid levels.
• Protein Intake Management: ADA recommends a protein intake of 0.8 mg/kg of body weight per day for individuals with diabetic kidney disease.
• Renal Replacement Therapy:
  • Consider referral for transplant evaluation when the GFR approaches 20 mL/min per 1.743 m².
  • Preemptive renal transplantation from a living kidney donor may be a preferred therapy.

Diabetic Foot 

Differential Diagnosis

• Buerger's Disease
• Raynaud's Disease
• Embolism
• Scleroderma
• Physical Agents (Trauma, Radiation, Electric Burns, Pressure Necrosis)
• Varicose Veins

Examination

• Capillary Refill Time:
  • Normal: 2-3 seconds
  • Prolonged in severe ischemia (>10 seconds)
• Arterial Pulses Examination:
  • Evaluate femoral, popliteal, posterior tibial, and dorsalis pedis arteries.
  • Check for aortic aneurysms and renal artery bruit.
  • Listen for arterial bruit over pulses.

General Investigations (Surgical Fitness)

• Complete Blood Picture (CBP) to rule out polycythemia.
• Random Blood Sugar (RBS) for diabetics.
• Serum Creatinine and Blood Urea.
• Lipid Profile for concomitant coronary disease.
• ECG/2D ECHO for cardiovascular assessment.
• Arterial Blood Gas (ABG)/Pulmonary Function Tests (PFT) for COPD evaluation.

Special Investigations

• Handheld Doppler Ultrasound for blood flow detection.
  • Normal artery shows triphasic signal; abnormal if biphasic or monophasic.
• Ankle Brachial Pressure Index (ABPI):
  • Normal ABPI: 0.9 to 1.3
  • Claudication: <0.9
  • Rest Pain: <0.5
  • Imminent Necrosis: <0.3
• Duplex Scanning, Digital Subtraction Percutaneous Angiography (DSA), CT Angiography, and MR Angiography (newer techniques).

Definitive Investigations for Ulcer

• Obtain cultures from the debrided ulcer base or purulent drainage.
• Determine wound depth through inspection and probing.
• Perform plain radiographs for chronic ulcers to assess osteomyelitis possibility.
• Magnetic Resonance Imaging (MRI) for specific evaluation.

Management

• Off-loading: Complete avoidance of weight bearing on the ulcer to enhance wound healing.
• Debridement: Surgical removal of necrotic tissue is important and effective.
• Wound Dressings: Use dressings like hydrocolloid to create a moist environment and control exudate.
• Appropriate Antibiotics:
  • Topical antibiotics have limited value.
  • Oral antibiotics for mild infections; IV antibiotics for severe cases.
• Revascularization:
  • Consider vascular insufficiency in all patients.
  • Peripheral arterial bypass procedures can promote wound healing.
• Limited Amputation:
  • Emphasize patient education on proper footwear selection and foot care.
  • Daily foot inspection for early signs of issues.
  • Avoid self-treatment and seek prompt medical consultation for abnormalities.
• Risk Factor Modification:
  • Include orthotic shoes, callus management, nail care, and prophylactic measures.
  • Address other vascular disease risk factors (smoking, dyslipidemia, hypertension) and improve glycemic control.