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Diabetes Mellitus - A Comprehensive Overview

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1. DEFINITION

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2. CLASSIFICATION OF DIABETES MELLITUS

Type 1 DM (T1DM)

• Pathogenesis: Autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency
• Autoantibodies: Islet cell antibodies (ICA), anti-GAD65, anti-insulin, anti-IA-2, anti-ZnT8
• Onset: Usually childhood/adolescence but can occur at any age
• Risk of DKA: High - the hallmark acute complication
• Treatment: Insulin is mandatory; no alternative
• Subtypes: Immune-mediated (1A) and idiopathic (1B)

Type 2 DM (T2DM)

• Pathogenesis: Insulin resistance + progressive beta-cell dysfunction (relative insulin deficiency)
• Risk factors: Obesity (especially central), physical inactivity, family history, older age, ethnicity
• Onset: Usually after age 40, but rising in youth due to obesity epidemic
• Long asymptomatic period - many have complications at diagnosis
• Treatment: Lifestyle modification, oral agents, eventually insulin in many

Gestational DM (GDM)

• Any degree of glucose intolerance with onset or first recognition during pregnancy
• Risk of developing T2DM later (~50% within 10 years)

Other Specific Types

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3. DIAGNOSTIC CRITERIA

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4. PATHOPHYSIOLOGY IN BRIEF

• T1DM: Autoimmune T-cell mediated destruction of beta cells → zero insulin → unopposed glucagon → hyperglycemia + ketosis
• T2DM: Insulin resistance in muscle/liver/fat → compensatory hyperinsulinemia → eventual beta-cell exhaustion → progressive hyperglycemia
• Chronic hyperglycemia activates four damaging pathways:
  1. Polyol pathway (sorbitol accumulation)
  2. Advanced glycation end-products (AGEs)
  3. Protein kinase C activation
  4. Hexosamine pathway
• These pathways damage the microvasculature (basement membrane thickening, pericyte loss) and accelerate atherosclerosis

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5. COMPLICATIONS OF DIABETES MELLITUS

A. ACUTE COMPLICATIONS

Diabetic Ketoacidosis (DKA)

• Primarily T1DM; absolute insulin deficiency
• Triad: hyperglycemia + ketonemia + metabolic acidosis
• Glucose typically >250 mg/dL, pH <7.3, bicarbonate <15 mEq/L, ketones elevated
• Precipitants: infection, missed insulin, new onset T1DM
• Management: IV fluids, insulin infusion (0.1 units/kg/hr), potassium replacement, treat precipitant

Hyperosmolar Hyperglycemic State (HHS)

• Primarily T2DM; enough residual insulin to prevent ketosis
• Glucose >600 mg/dL, plasma osmolality >320 mOsm/kg, profound dehydration, altered sensorium
• Management: Aggressive fluid replacement (main priority), insulin, electrolyte correction

Hypoglycemia

• Most common acute complication of insulin/sulfonylurea therapy
• Glucose <70 mg/dL; symptoms: sweating, tremor, tachycardia, confusion
• Treatment: 15-20g fast-acting carbs (conscious); IM glucagon or IV dextrose (unconscious)

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B. CHRONIC COMPLICATIONS

Microvascular Complications

• Leading cause of new blindness in adults
• Progression: Non-proliferative (NPDR) → Proliferative (PDR) → macular edema
• NPDR features: microaneurysms, dot-blot hemorrhages, hard exudates, soft exudates (cotton-wool spots)
• PDR features: neovascularization (NVD/NVE), vitreous hemorrhage, traction retinal detachment
• Treatment: Glycemic + BP control; laser photocoagulation; anti-VEGF injections for macular edema; vitrectomy

• Most common cause of end-stage renal disease (ESRD)
• Progression: hyperfiltration → microalbuminuria (30-300 mg/day) → macroalbuminuria → declining GFR → ESRD
• Treatment:
  • Glycemic control (HbA1c <7%)
  • BP target <130/80 mmHg
  • ACE inhibitor or ARB (first-line, renoprotective)
  • SGLT-2 inhibitors (reduce CKD progression - e.g., empagliflozin, dapagliflozin)
  • Finerenone (mineralocorticoid receptor antagonist)

• Most common complication overall; affects >50% of long-standing diabetics
• Types:
  • Distal symmetric polyneuropathy (DSPN): "stocking-glove" distribution; loss of sensation, pain, numbness; most common type
  • Autonomic neuropathy: Gastroparesis, orthostatic hypotension, resting tachycardia, neurogenic bladder, erectile dysfunction, Charcot foot
  • Painful neuropathy: Burning, electric-shock like pain, worse at night
  • Mononeuropathy: CN III, VI palsy; carpal tunnel
  • Amyotrophy (Bruns-Garland): Proximal asymmetric lower limb weakness and pain
• Treatment: Glycemic control; pregabalin/gabapentin; duloxetine/amitriptyline; topical capsaicin; SNRIs

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Macrovascular Complications

• 2-4x increased risk of MI, stroke, and cardiovascular death
• DM accelerates atherosclerosis via dyslipidemia, hypertension, endothelial dysfunction
• Management: Statins (all T2DM patients with ASCVD), aspirin, GLP-1 RA or SGLT-2 inhibitors with proven CV benefit

• Accelerated atherosclerosis of lower limb arteries; DM is a major risk factor
• Often presents as claudication or critical limb-threatening ischemia (CLTI)
• Contributes critically to diabetic foot

• Increased risk of ischemic stroke

• Diabetic cardiomyopathy independent of CAD
• SGLT-2 inhibitors reduce hospitalizations for heart failure

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Other Complications

• Gastrointestinal: gastroparesis (delayed emptying), diarrhea
• Genitourinary: neurogenic bladder, erectile dysfunction
• Infections: increased susceptibility (impaired neutrophil function)
• Dermatologic: necrobiosis lipoidica, acanthosis nigricans, diabetic dermopathy
• Cheiroarthropathy (limited joint mobility), periodontal disease, hearing loss

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6. THE DIABETIC FOOT

Epidemiology & Pathophysiology

• ~1 in 4 diabetic patients will develop a foot complication during their lifetime
• 15-20% of diabetic foot ulcers (DFUs) result in lower extremity amputation (LEA)
• 85% of all amputations are preceded by DFU
• Annual incidence of foot complications: 1-2% per year

1. Peripheral neuropathy (sensorimotor + autonomic) - loss of protective sensation, altered gait, dry/cracked skin
2. Peripheral arterial disease (ischemia) - impaired wound healing and tissue survival
3. Infection - immune defects, hyperglycemia impair bacterial killing; infection spreads rapidly to deep structures

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CLASSIFICATION OF DIABETIC FOOT ULCERS

Wagner Classification (Simple, widely used)

University of Texas Classification (UT)

• Two axes: Depth (0-3) and Stage (A=clean, B=infected, C=ischemic, D=infected+ischemic)

SINBAD Classification

• Six variables: Site, Ischemia, Neuropathy, Bacterial infection, Area, Depth
• Each scores 0-1, total 0-6; simple for audit/communication

WiFi Classification (Society for Vascular Surgery - most comprehensive)

• W = Wound (depth/extent: 0=no wound, 1=superficial, 2=deep into tendon/joint, 3=to bone/full thickness)
• I = Ischemia (ankle-brachial index/toe pressures: 0=no ischemia, 1-2=moderate, 3=severe)
• f = foot Infection (0=none, 1=local <2 cm, 2=local >2 cm/abscess/osteomyelitis, 3=SIRS)

• Risk of major LEA at 1 year (Clinical Stage 1-4)
• Likelihood of benefit from revascularization

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EXAMINATION OF THE DIABETIC FOOT

1. General and Vascular Assessment

• Pulses: Femoral, popliteal, posterior tibial, dorsalis pedis - absent/diminished suggests PAD
• Capillary refill time (normal <2 seconds)
• Ankle-Brachial Index (ABI): <0.9 = PAD; <0.4 = critical ischemia; >1.3 = calcified vessels (unreliable)
• Buerger's test: Pallor on elevation, dependent rubor on lowering = significant ischemia
• Toe pressures / TBI (toe-brachial index): more reliable in calcified vessels; <0.7 abnormal
• Skin temperature: Cool/cold = ischemia; warm = infection or Charcot
• Hair loss, skin atrophy, dystrophic nails = chronic ischemia signs

2. Neurological Assessment

• 10-g Semmes-Weinstein monofilament (key test): apply to 10 sites on plantar surface; inability to feel = loss of protective sensation (LOPS)
• Vibration: 128 Hz tuning fork at hallux; loss = early large-fiber neuropathy
• Temperature discrimination: warm/cool rods
• Pinprick sensation
• Proprioception (joint position sense)
• Ankle reflexes: absent in advanced neuropathy
• Motor exam: Intrinsic muscle wasting, toe deformities (claw toe, hammer toe), Charcot deformity

3. Wound Assessment

• Location: Neuropathic ulcers = plantar surface/pressure points; ischemic ulcers = toe tips/margins
• Callus debridement first - overriding callus hides wound extent
• Probe-to-bone test: Insert sterile probe into wound; if bone is felt = osteomyelitis until proven otherwise (PPV ~89%)
• Wound depth and undermining
• Signs of infection: Odor, purulent drainage, erythema >2 cm, warmth, swelling, fluctuance
• Maceration: Suggests infection or fluid overload
• Necrosis/gangrene: Dry (black, demarcated) vs. wet (spreading infection, odor, systemic upset)
• Sinus tracts - probe gently to determine depth

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INVESTIGATIONS

Laboratory

Imaging

Microbiology

• Superficial swabs are unreliable for determining deep infection organisms
• Deep tissue biopsy or bone biopsy is the gold standard for osteomyelitis culture
• Common organisms: S. aureus, beta-haemolytic streptococci, aerobic Gram-negative bacilli
• Pseudomonas is over-represented; anaerobes present in necrotic/abscess tissue

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MANAGEMENT OF THE DIABETIC FOOT

1. Glycemic Control

• Poor glycemic control impairs wound healing and immune function
• HbA1c every 3 months; target <7-7.5%; insulin often required during admission
• Involve endocrinology team proactively

2. Wound Care

• Debridement: Sharp debridement of devitalized tissue (clinic or operative)
• Dressing selection (by wound type):
  • Healthy wound = collagen dressing
  • Fibrinous tissue = enzymatic (e.g., collagenase/Santyl, MediHoney)
  • Deep healthy wound = VAC (negative pressure wound therapy / NPWT)
  • Locally infected = iodine-based (Iodosorb) or topical mupirocin
  • Macerated wound = silver alginate or absorptive foam
• Edema management: Multilayer compression; address systemic cause

3. Offloading

• Neuropathic ulcers are caused/perpetuated by pressure
• Total contact cast (TCC): Gold standard for offloading; redistributes plantar pressure; requires weekly change and clean wound
• DH walking boot, wedge shoes, heel-off shoes = alternatives
• Patients with PAD: caution with compression

4. Infection Management

• Mild/local infection: Oral antibiotics (e.g., co-amoxiclav, flucloxacillin) + wound care
• Moderate/severe infection: IV antibiotics; empirical cover for S. aureus, streptococci, Gram-negatives, Pseudomonas (e.g., piperacillin-tazobactam) and anaerobes (metronidazole)
• Surgical debridement: Mandatory for collections, necrosis, abscess, or extensive osteomyelitis
• Osteomyelitis treatment:
  • Conservative: 6-12 weeks antibiotics if no extensive bone involvement
  • Surgical: excision of infected bone (ray amputation / sequestrectomy) + antibiotics
• Refer urgently if: spreading cellulitis, systemic SIRS, critical ischemia, wet gangrene

5. Revascularization for Ischemia

• If ABI <0.6 or non-healing wound + confirmed PAD → revascularization assessment
• Options:
  • Endovascular (angioplasty ± stenting): Preferred for limited disease, elderly, comorbid patients
  • Open bypass surgery (femoro-popliteal/distal bypass): For extensive occlusive disease
  • Hybrid procedures: Combination
• Target: restore inline pulsatile flow to the foot
• Revascularization significantly improves amputation-free survival

6. Amputation

• Performed when limb not salvageable, non-revascularizable ischemia, life-threatening infection
• Levels (distal to proximal):
  • Toe amputation
  • Ray amputation (toe + metatarsal)
  • Transmetatarsal amputation (TMA)
  • Syme's (ankle disarticulation)
  • Below-knee amputation (BKA)
  • Above-knee amputation (AKA)
• Goal: most distal level with adequate tissue perfusion for healing

7. Prevention

• Annual foot examination for all diabetic patients
• Education on daily foot inspection, foot hygiene, appropriate footwear
• Custom therapeutic footwear (redistributes pressure)
• Regular podiatry review
• Aggressive glycemic, BP, and lipid control
• Smoking cessation

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7. QUICK SUMMARY TABLE: NEUROPATHIC vs. ISCHEMIC FOOT

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• Harrison's Principles of Internal Medicine 22E (2025), Chapters 415, 416, 417
• Bailey and Love's Short Practice of Surgery 28E, Chapter 43
• Current Surgical Therapy 14E (Kavousi, Hicks, Abularrage - Diabetic Foot chapter)

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Treatment Guidelines for Diabetes Mellitus & Diabetic Foot

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PART 1: TREATMENT GUIDELINES FOR DIABETES MELLITUS

GLYCEMIC TARGETS (ADA 2024)

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A. LIFESTYLE + NON-PHARMACOLOGIC TREATMENT

Medical Nutrition Therapy (MNT)

• High-quality, nutrient-dense foods; limit processed carbohydrates
• Mediterranean-style diet (rich in monounsaturated/polyunsaturated fats) preferred
• Carbohydrate monitoring for postprandial control; use glycemic index
• Avoid fructose/sucrose beverages
• Sodium < 2300 mg/day
• No routine vitamin/antioxidant supplements (except Vit D/calcium for bone health)
• Weight loss target: 5-10% of body weight in T2DM significantly improves glycemic control

Physical Activity

• ≥ 150 minutes/week of moderate-intensity aerobic exercise (or 75 min vigorous)
• Resistance training 2-3 times/week
• Reduce prolonged sitting; break sedentary time every 30 minutes

Psychosocial Care

• Screen for depression, anxiety, "diabetes distress" at every visit
• Involve diabetes educator, dietitian, psychologist as needed

Monitoring

• CGM (Continuous Glucose Monitoring): Preferred; provides glucose trend, TIR, time below range, hypoglycemia alerts
• HbA1c: Every 3 months (unstable) or every 6 months (stable, at target)
• Self-monitoring blood glucose (SMBG): Fingerstick, if CGM not available

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B. PHARMACOLOGIC TREATMENT - TYPE 1 DM

Insulin Preparations (Harrison's 22E)

Insulin Regimen Strategies for T1DM

• Basal insulin (glargine or degludec) once daily = suppresses fasting hepatic glucose
• Bolus insulin (rapid-acting) with each meal = carbohydrate coverage + correction
• Insulin-to-carbohydrate ratio + correction factor individualised

• Delivers variable basal rate + manual bolus at meals
• More physiologic than MDI

• CSII + CGM; algorithm suspends insulin when glucose falls or predicted to fall

• CGM + pump + algorithm adjusts basal rate in real time
• Closest to physiologic insulin replacement currently available

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C. PHARMACOLOGIC TREATMENT - TYPE 2 DM

Step-by-Step Algorithm (ADA/EASD 2024)

Does the patient have:
- Established ASCVD or high CV risk?  → Prioritize GLP-1 RA or SGLT-2 inhibitor
- Heart failure?                       → Prioritize SGLT-2 inhibitor
- CKD (eGFR ≥20)?                     → Prioritize SGLT-2 inhibitor
- Obesity / weight loss needed?        → Prioritize GLP-1 RA or GLP-1/GIP dual agonist
- Hypoglycemia risk?                   → Avoid sulfonylureas/insulin if possible

• First-line in all T2DM without contraindications
• Contraindicated: eGFR < 30 mL/min, active liver disease, significant alcohol use, risk of lactic acidosis, IV contrast procedures

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Drug Classes for T2DM - Detailed

• Mechanism: Activates AMP kinase → reduces hepatic gluconeogenesis, improves insulin sensitivity in muscle/liver
• HbA1c reduction: 1.0 - 2.0%
• Benefits: Weight neutral/modest loss, no hypoglycemia, CV-neutral, inexpensive
• Side effects: GI (nausea, diarrhea, metallic taste - take with food); B12 deficiency with long-term use; lactic acidosis (rare)
• Dose: Start 500 mg daily with food; titrate to 1000 mg BD (max 2550 mg/day)

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• Mechanism: Block SGLT-2 in proximal renal tubule → block glucose reabsorption → glucosuria → glucose lowering (insulin-independent)
• Drugs: Empagliflozin, Dapagliflozin, Canagliflozin
• HbA1c reduction: 0.5 - 1.0%
• Additional benefits:
  • Weight loss (3-5 kg)
  • BP reduction (3-6 mmHg systolic)
  • Reduces ASCVD events and CV mortality (empagliflozin, canagliflozin)
  • Reduces heart failure hospitalizations
  • Slows CKD progression (empagliflozin, canagliflozin, dapagliflozin)
• Side effects: Genital mycotic infections (both sexes), UTIs, polyuria, DKA risk (euglycemic DKA - especially if insulin omitted during illness), increased fracture risk (canagliflozin), lower limb amputation risk (canagliflozin)
• Contraindication: eGFR < 20 mL/min (not effective); T1DM
• Do not initiate if: eGFR < 30 (CKD Stage 3b), but can continue if eGFR falls during treatment

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• Mechanism: Mimic GLP-1 incretin hormone → glucose-dependent insulin secretion, suppress glucagon, slow gastric emptying, central appetite suppression
• Drugs:
  • Injectable: Semaglutide (weekly, Ozempic), Liraglutide (daily, Victoza), Dulaglutide (weekly), Exenatide
  • Oral: Semaglutide (Rybelsus, daily)
• HbA1c reduction: 1.0 - 1.8%
• Additional benefits:
  • Significant weight loss (5-15 kg)
  • Reduces ASCVD events (liraglutide, semaglutide) - mortality benefit in T2DM with CVD
  • Reduces CKD progression (semaglutide - FLOW trial 2024)
  • Reduces BP
• Side effects: Nausea, vomiting, diarrhea (dose-dependent, transient); pancreatitis risk; Black box warning: thyroid C-cell tumors (contraindicated in personal/family history of medullary thyroid cancer or MEN2); slows gastric emptying (affects oral drug absorption)
• No hypoglycemia when used as monotherapy

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• Drug: Tirzepatide (Mounjaro) - weekly SC injection
• Mechanism: Dual agonism at GIP + GLP-1 receptors → greater weight loss than GLP-1 RA alone
• HbA1c reduction: 1.9 - 2.6% (dose-dependent)
• Weight loss: 6 - 13 kg on average (superior to all other agents)
• Doses: 2.5 mg/week → titrate every 4 weeks to max 15 mg/week
• Beneficial effects on lipids, BP, fatty liver
• Side effects same as GLP-1 RAs; slightly higher pancreatitis rate

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• Mechanism: Inhibit DPP-4 enzyme → prolong action of native GLP-1 and GIP → enhanced glucose-dependent insulin secretion
• Drugs: Sitagliptin (100 mg OD), Vildagliptin, Saxagliptin, Linagliptin, Alogliptin
• HbA1c reduction: 0.5 - 1.0%
• Benefits: Weight neutral; no hypoglycemia; oral dosing; generally well tolerated
• Side effects: Nasopharyngitis; rare - pancreatitis, severe joint pain, angioedema; Saxagliptin increases heart failure risk (avoid in HF patients)
• Renal dose adjustment: Sitagliptin (50 mg if eGFR 30-50; 25 mg if < 30); Linagliptin - no adjustment needed (biliary excretion)

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• Mechanism: Bind sulfonylurea receptor → close ATP-K+ channel → depolarize beta cell → calcium influx → insulin release (glucose-independent)
• Drugs: Glipizide, Glibenclamide (glyburide), Gliclazide, Glimepiride
• HbA1c reduction: 1.0 - 2.0%
• Side effects: Hypoglycemia (most significant - especially glyburide); weight gain (2-4 kg)
• Avoid in: Elderly (hypoglycemia risk), renal failure, irregular meals
• Note: Older agents but inexpensive; avoid if hypoglycemia is a concern

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• Mechanism: PPARγ agonists → improve insulin sensitivity in adipose/muscle/liver
• Drug: Pioglitazone (Actos)
• HbA1c reduction: 0.5 - 1.4%
• Benefits: No hypoglycemia; reduces TG, raises HDL; may reduce NASH
• Side effects: Fluid retention / edema; weight gain (2-4 kg); heart failure exacerbation (contraindicated in NYHA class III/IV HF); bone fractures; possible bladder cancer (controversial for pioglitazone)

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• Mechanism: Rapid-acting insulin secretagogues (same receptor as SU but shorter acting)
• Drugs: Repaglinide, Nateglinide
• Use: Post-meal glucose spikes; useful in irregular meal patterns; dose with each meal
• Side effects: Hypoglycemia (less than SUs); weight gain

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• Mechanism: Inhibit brush border enzymes → delay intestinal carbohydrate absorption → reduce post-meal glucose
• Drug: Acarbose, Miglitol
• HbA1c reduction: 0.5 - 0.8%
• Side effects: Flatulence, diarrhea, abdominal pain (limits use)

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• Added when oral agents + injectables fail to maintain target HbA1c
• Starting regimen: Basal insulin at night (glargine or degludec, 10 units or 0.1-0.2 units/kg) + continue oral agents (except sulfonylureas may need dose reduction)
• Escalation: Add prandial insulin for persistent post-meal hyperglycemia
• Combination: Basal insulin + GLP-1 RA (very effective; reduces insulin dose required and weight gain)

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Summary: Drug Choice by Comorbidity (ADA 2024 / ESC/EASD Guidelines)

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D. TREATMENT OF ACUTE COMPLICATIONS

DKA Treatment Protocol (Harrison's 22E)

• 1-2 L 0.9% NaCl over first hour
• Then 250-500 mL/hr 0.9% NaCl (or 0.45% if Na > 135 meq/L)
• Switch to D5 0.45% saline when glucose drops to 11.1-13.9 mmol/L (200-250 mg/dL)

• IV regular insulin bolus 0.1 units/kg IV, then 0.1 units/kg/hr infusion
• If glucose not falling by 10% in first hour: double infusion rate
• Reduce insulin to 0.02-0.1 units/kg/hr when glucose reaches 200-250 mg/dL
• Do NOT stop insulin until anion gap closes and patient eating

• If K+ < 3.5 mEq/L: hold insulin, give 20-40 mEq/hr KCl first
• If K+ 3.5-5.0 mEq/L: add 20-30 mEq K+ to each liter of IV fluid
• If K+ > 5.0 mEq/L: hold K+, monitor hourly

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HHS Treatment

• Fluid deficit often 9-10 L (more profound than DKA); replace over 1-2 days
• 1-3 L 0.9% NaCl first 2-3 hours, then 0.45% saline
• Insulin: 0.1 units/kg IV bolus → 0.1 units/kg/hr infusion
• Potassium replacement as in DKA
• Mortality up to 15% - aggressive monitoring required

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E. CARDIOVASCULAR RISK REDUCTION IN DM

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PART 2: TREATMENT GUIDELINES FOR THE DIABETIC FOOT

OVERALL PRINCIPLE: MULTIDISCIPLINARY TEAM

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STEP 1 - GLYCEMIC OPTIMIZATION

• HbA1c checked every 3 months; target < 7-7.5%
• Tight inpatient glycemic control (IV insulin infusion if needed) as hyperglycemia impairs:
  • Neutrophil chemotaxis and phagocytosis
  • Wound healing
  • Tissue oxygenation
• Involve endocrinology for all inpatient DFU admissions

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STEP 2 - WOUND CARE

• Remove all devitalized, necrotic, and callus tissue
• Conservative mindset: preserve viable tissue, excise dead tissue
• Hydroresection / jet lavage for deep spaces
• Aggressive debridement before revascularization should be avoided

• Multilayer compression bandaging (if no critical ischemia)
• Treat underlying cause (venous HTN, lymphedema, cardiac failure)

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STEP 3 - PRESSURE OFFLOADING

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STEP 4 - INFECTION MANAGEMENT

Antibiotic Selection by Severity

• Surface swabs are unreliable - do NOT rely on them
• Obtain deep tissue biopsy or bone biopsy for microbiology
• Blood cultures for systemic sepsis

Surgical Debridement Indications

• Collections / abscess
• Wet gangrene / necrotizing fasciitis (surgical emergency)
• Necrotic tissue not responding to conservative management
• Extensive osteomyelitis
• Devitalized tissue that prevents wound healing

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STEP 5 - MANAGEMENT OF ISCHEMIA (PAD)

Vascular Assessment Thresholds

• ABI < 0.6 or ankle pressure < 60 mmHg = significant ischemia; consider revascularization
• Toe pressure < 30 mmHg = inadequate for wound healing (< 40 mmHg in diabetics)
• TcPO2 < 20 mmHg = healing failure very likely; > 60 mmHg = adequate healing

TASC Classification of Arterial Lesions (for revascularization planning)

Endovascular Options

• Balloon angioplasty ± stenting: Iliac arteries - durable; femoro-popliteal - less durable
• Drug-eluting stents / drug-coated balloons: Improved 1-year patency for femoropopliteal
• Subintimal dissection + reentry: For long occlusions
• Atherectomy: Plaque excision to restore lumen

Open Bypass Surgery

• Femoro-popliteal bypass (above or below knee)
• Femoro-distal bypass (tibial or pedal vessels) for isolated distal disease
• Conduit: Autologous saphenous vein preferred > synthetic (PTFE/Dacron)
• Assess cardiac risk before open bypass (diabetes + PAD = high CAD prevalence)

ICG Fluorescence Angiography (SPY System)

• Newer technique using indocyanine green + laser camera
• Objectively assesses tissue perfusion to guide amputation level and flap viability

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STEP 6 - OSTEOMYELITIS MANAGEMENT

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STEP 7 - AMPUTATION (When Limb Not Salvageable)

• Non-revascularizable critical ischemia
• Life-threatening wet gangrene / necrotizing fasciitis
• Extensive osteomyelitis not amenable to conservative surgery
• Intractable pain with no reconstructive option
• Patient preference or unacceptably poor functional prognosis

• Nutritional optimization before surgery
• Prevent bedsores, UTIs, falls
• Physiotherapy for rehabilitation
• Enhanced recovery protocols

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STEP 8 - PREVENTION AND FOOT CARE

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DIABETIC FOOT - DECISION ALGORITHM SUMMARY

DFU Identified
     │
     ├─ Assess Wound (Probe, Debride, X-ray)
     ├─ Assess Ischemia (ABI, toe pressure, duplex)
     └─ Assess Infection (cultures, WBC, CRP, MRI if needed)
            │
            ▼
     WIfI Classification (Grade Wound / Ischemia / Infection 0-3)
            │
     ┌──────┴──────┐
  No ischemia    Ischemia present
  (ABI ≥ 0.9)   (ABI < 0.6 or toe pressure < 30-40 mmHg)
     │                   │
  Offload            Vascular referral
  Wound care         Duplex / CTA / MRA
  Antibiotics        Revascularisation (endovascular or bypass)
     │                   │
     └─────────┬──────────┘
               │
          Infection present?
          ┌────┴────┐
         Yes        No
          │          │
    IV antibiotics  Local wound care
    Surgical debridement  Offloading
    Bone Bx if osteomyelitis  Regular review
          │
    Not healing / gangrene?
          │
     Amputation planning
     (most distal viable level)

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• Harrison's Principles of Internal Medicine 22E (2025), Chapters 416, 417
• Katzung's Basic & Clinical Pharmacology 16E, Chapter 41
• Current Surgical Therapy 14E - Diabetic Foot chapter (Kavousi, Hicks, Abularrage)
• Bailey & Love's Short Practice of Surgery 28E, Chapter 43
• Fuster & Hurst's The Heart 15E, Chapter 7 (ESC/EASD/ACC/AHA Guidelines for DM and CVD)