Table of contents
- 1. Common Questions
- 2. Risk Factors
- 3. Diagnostic Testing
- 3.1. Prediabetes (IGT/IFG)
- 3.2. Other Tests
- 4. Complications
- 4.1. Retinopathy
- 4.2. Nephropathy
- 4.3. Neuropathy
- 4.4. DKA/HONK
- 4.5. Skin
- 5. Management
- 6. Notable Trials
Reference: Canadian Journal of Diabetes "Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada"
Common Questions
- Eating too much sugar causes diabetes: No (but can Increase calorie intake creating risk of DM)
- Avoiding sweet foods manages DMII - No
- Avoiding carbohydrate managers T2DM - No
- There is a diabetes diet - No, diet no different than "healthy heart" diet.
- Everyone with T2DM is overweight: - No
Risk Factors
- Age >40y
- First degree relative
- Member of high risk population
- History of GDM/Macrosomic infant
- Hypertension
- Dyslipidemia
- Overweight/Abdominal obesity
- Polycystic ovarian syndrome
- Acanthosis Nigricans
- Schizophrenia
Diagnostic Testing
- If unclear Type I vs. Type II DM: (young patient with hyperglycemia)
- Islet Cell Antibodies (ICA)
- Glutamic Acid Decarboxyllase Antibody titres (GADA)
- (If both negative -> diagnose Type II)
- Must distinguish b/c treatments very different.
- Screening:
- Screen everyone >40yrs old every 3 years
- Screen more frequently (i.e. yearly) if risk factors)
- if fasting glucose >5.6, start to watch more carefully (i.e. OGTT)
Based on 2008 Guidelines of the American Diabetes Association
Pre-diabetes | Impaired Fasting Glucose (IFG) | Fasting Glucose 6.1-6.9 |
Impaired Glucose Tolerance (IGT) | 2hr post 75g glucose load (OGTT) 7.8-11.0 | |
| HbA1c 6.0-6.4 | |
Diabetes |
|
Prediabetes (IGT/IFG)
- Increased risk of diabetes progression
- Associated with CVD outcomes
- Primary Prevention (Diabetes Prevention Program - Finnish Diabetes Prevention Trial)
- Lifestyle & Diet: 60% relative risk reduction of progression to diabetes
- Exercise: Advise 30min of moderate intensity exercise 5x/week
- Dietary Counceling: Target weight loss: 5% body weight
- Stop smoking
- Metformin: 30% RRR
- (Can also use Acarbose [alpha-glucosidase inhibitor], or rosiglitazone [not used generally], Orlistat)
- Lifestyle & Diet: 60% relative risk reduction of progression to diabetes
Other Tests
Complications
Microvascular
-
Retinopathy
- 10-15% will have this at diagnosis of Type II DM
- Must have retinal evaluations (either opthalmoscope or high quality retinal photograph)
- Screening Guidelines:
-
Population Start Screening Screening Frequency Type I DM 5 years after dx Annual Retinal Exam Type II DM
At Diagnosis Annual Retinal Exam Pregnant (any DM)
(accelerates retinopathy - DCCT trial)
First Trimester Every trimester then annually Planning to Conceive At preconception Same as pregnant - (In pregnancy, lower glucose, lower
-
- Non-Proliferative Diabetic Retinopathy:
- Chronic hyperglycemia causes edema, hard exudates, tiny hemorrhages on the retina
- Microaneurysm in vessel walls + occlusions cause "soft exudates" (aka "cotton wool spots")
- Proliferative Diabetic Retinopathy (more extensive)
- Blood vessels fryable, rupture, cause more extensive intraocular bleeding
- Fibrosis, contraction, causing retinal detachment.
- Treatment:
- Laser Photocoagulation - to damage retina causing avascular scar
- Reducing retinal surface area by 1/3 - perfusion of remaining retina improves.
- Lose some peripheral vision (esp noticed at night) - preserves central vision
- NEW! Now can inject VEGF antagonists monthly
-
Nephropathy
-
Damage to glomerular basement membrane by glucose
-
Genetic predisposition: Some patients never get this, others do.
-
Diagnosis:
-
Urine Albumin Creatinine Ratio (creatinine adjusts for hydration)
-
24hr Urine Correction (no longer done)
-
VERY sensitivy tests: becomes positive during menses, UTI, fevers, vigorous exercise
-
-
Start releasing protein (microalbuminuria), worsens over time.
-
At 1-3 grams/day of protein loss, creatinine starts to rise, causing hypertension and progressive CKD
-
NOTE: Any patient with microalbuminuria has 4-8x risk of cardiovascular disease
-
Risk factor modification: i.e. smoking cessation
-
-
Screening:
-
Same as Retinopathy
-
-
- Treatment:
- ACE inhibitors & ARBs - Slows rate of progression
-
Neuropathy
- Nerve cells are long + thin, and vulnerable to damage from glucose
- Appear late in diabetes that is not controlled
- Acute distal neuropathy can occur after hyperglycemia (demyelination - stocking glove distribution)
- Symptoms:
- Sharp stabbing burning pain in toes, fingers and hands.
- Dysesthesia: Often discomfort when touched
- Heaviness/clumsiness in feet
- Noticed at night (distracted during day)
- Treatment:
- Topical: Capsaicin Cream
- Apply to painful areas + put clean socks on (so don't get removed by bed sheets)
- Re-apply in the night
- Drugs:
- TCAs, and SNRIs are mainstays of therapy
- Gabapentin/Pregabalin: not very effective
- Education: Tell patients if control their HBA1c < 7% - can get improvement
- Topical: Capsaicin Cream
- Types:
- Symmetric Polyneuropathy (MOST COMMON)
- Acute Mononeuropathy
- Microvascular occlusion or vasa vasorum.
- Usually resolve spontaneously in a few months.
- No Treatment
- Diabetic Amyotrophy
- Proximal leg pain + weakness
- Entrapment Neuropathy
- Carpal tunnel
- Meralgia paresthetica (Lateral cutaneous nerve of thigh under inguinal liagment)
- Ohers:
-
Autonomic Neuropathy (Gi, CV, bladder, erectile problems
-
Mononeuropathy (CNIII palsy, carpal tunnel)
-
Polyradiculopathy (Lumbar radiculopathy - Femoral Nerve Muscle W
-
-
Progression:
-
Anesthetic: Eventually lose complete sensation - high risk of ulceration, infection, amputation
-
Annual foot exam to detect sensory deficits, ulcers, deformities
-
Patients should examine their feet too
-
-
Most Severe:
-
Charcot's Foot (french): Anesthetic foot. Small muscles lose innervation, integrity of foot is lost. Painless collapse of midfoot deformities. VERY high risk of ulcers.
-
Skin
-
Condition Description Photo Eruptive Xanthoma Blisters on extensor
surfaces and buttock areas
- Occurs in uncontrolled
diabetics and high lipids
Necrobiosis
lipoidica
Red swollen hard patches
on legs
Acanthosis
Nigricans
Management
Outpatient CDA Targets
- Based on CDA Guidelines 2013
- Glycemic Control Outpatient Targets (CDA 2013)
- HbA1c: <7.0% (for Type I and Type II or even <6.0 if safe)
- Most <7%
- Young and healthy: ≤6.5%
- Frail Elderly <8.5%
- Fasting/Preprandial Capillary Glucose: 4.0-7.0
- 2hr Postprandial Capillary Glucose: 5.0-10.0 (5.0-8.0 IF A1c not at target)
Other Targets:
- Blood Pressure: <130/80
- Lipids (same as high-risk framingham targets)
- LDL <2.0 mmol/L
- TG <1.5 mmol/L
- TC/HDL <4.0 mmol/L
Measure yearly ACR in ALL Diabetes pts (start 5 yrs after dx for Type I DM)
- HbA1c: <7.0% (for Type I and Type II or even <6.0 if safe)
- Keep pre-hospital oral hypoglycemics and insulin therapy if possible
In Hospital CDA Targets
- Based on CDA Guidelines 2013
-
Non-Critically Ill (as long as can be safely achieved)
- Pre-prandial Target 5.0 - 8.0 mmol/L
- (if BG < 3.9 --> modify regimen, unless can be explained (skipped meal))
- Target random < 10.0 mmol/L
- Insulin is recommended to achieve control (scheduled basal, bolus and correction (supplemental) insulin is the preferred method. Sliding-scale insulin (SSI) is discouraged)
Critiaclly Ill
- Target 8.0 - 10.0 mmol/L
- Based on NICE-SUGAR study (intensive control --> hypoglycemia risk)
- Infusion protocols recommended
Perioperative Control
For CABG:
- Maintain 5.5 - 10.0 mmol/L
- Continuous IV insulin infusion should be used.
For Other Surgery
- Target 5.0 and 10.0 mmol/L Perioperative
- Use "appropriate protocol"
- Pre-prandial Target 5.0 - 8.0 mmol/L
Approach/Counselling
Management of Prediabetes (IGT/IFG)
Management of Diabetes
|
Approach to Drugs
- Type 1 DM:
- Mainstay is insulin therapy
- Once stable on insulin (know insulin requirements), can apply for an insulin pump, which improves glucose control.
- Government of Ontario supplies insulin pumps (>$7000 value) every 5 years to all Type I DM patients.
- Type 2 DM:
- Start with metformin
- Add another oral agent (see Oral Agents Section)
- Once control cannot be established through oral agents, add Insulin (see Insulin Section)
- Generally keep some oral agents to prevent side effects of insulin (hypoglycemia, and weight gain).
- I.e. often add GLP-1 agonists and SGLT-2 antagonists for their weight loss and cardiovascular benefits, and to decrease insulin requirements.
- Risk Factor Modification
- Quit Smoking
- Assess Cardiovascular Risk
- Check Lipids
- Yearly screening (see Complications of Diabetes)
Notable Trials
- DM Type II
- UKPDS 33 - intensive glucose congrol: reduced diabetes endpoints.
- UKPDS 35 - for each 1% drop in HbA1c - 37% reduction in microvascular complications.
- ACCORD (Action to Control CV Risk in Diabetes)
- Large randomized control trial ~10,000 pts. (3.5 years)
- intensive glycemic control vs. standard.
- No difference in CVD
- 20% higher risk of death for ever 1.0% increase in HbA1c below 6.0%
- ADVANCE (Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation).
- Large randomized control trial ~10,000pts (5years)
- Intensive vs. standard glycemic control.
- No difference in CVD
- VADT Trial: (Veterans)
- 1791pts
- CV risk depends on length of time pts have diabetes.
- Intensive control only helps for <15yrs diabetes.
- Conclusions:
- Target <7.0% is reasonable, but <6% increases mortality --> try to attain if pt has DMII of short duration, long life expectancy, or no significant CVD or hypoglycemia.
- Target >7.0% reasonable if limited life expectancy, severe hypoglycemia, established microvascular and macrovascular complications, other comorbidities, or if <7.0 is difficult to attain. (Skyler et al - 2009 - Intensive glycemic control and the prevention of CV events....)
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