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Diabetes Complication Lecture
Diabetes Complication Lecture
Diabetic retinopathy
Stroke
Diabetic nephropathy
Leading cause of end-stage renal disease2
1Fong
DS, et al. Diabetes Care 2003;26 (Suppl. 1):S99S102. 2Molitch ME, et al. Diabetes Care 2003;26 (Suppl. 1):S94S98. 3Kannel WB, et al. Am Heart J 1990;120:672676. 4Gray RP & Yudkin JS. In Textbook of Diabetes 1997. 5Mayfield JA, et al. Diabetes Care 2003;26 (Suppl. 1):S78S79.
Macroangiopathy Atherosclerosis Risk of cardiovascular death in type 1 diabetics vs. Nondiabetics : >5X higher in males, 7X higher in females
Diabetes Complications
Macro vascular Micro vascular Neuropathy Infections
Mechanisms
Genetic susceptibility
Hyperglycemia
Tissue damage
Macrovascular Complications(1)
Have a 2 to 6 times higher risk for development of these complications than the general population The major cardiovascular risk factors in the non-diabetic population (smoking, hypertension and hyperlipidemia) also operate in diabetes, but the risks are enhanced in the presence of diabetes. Overall life expectancy in diabetic patients is 7 to 10 years shorter than non-diabetic people.
Macrovascular Complications(2)
Once clinical macro-vascular disease develops poorer prognosis for survival than normoglycemic patients with macrovascular disease The protective effect females have for the development of vascular disease are lost in diabetic females Clinical manifestation :
Ischemic heart disease Cerebrovascular disease Peripheral vascular disease
UKPDS:
Prospective study Newly detected type 2 DM:
335 with CAD, 8 year follow-up
Risk of MI in Diabetes
UKPDS:
3867 patients with newly diagnosed type 2 DM Intensive vs. Conventional therapy 10 year follow-up Microvascular endpoints improved Trend only towards reduced incidence of MI ( p=0.052)
Effect of Hypertension
Mortality vs systolic blood pressure
70
60 50 40 30 20 10 0 110 120 130 140 150 160 Systolic Blood pressure (mmHg) Non-diabetic Diabetic
Type 2
Mostly present at diagnosis, affects at least 60% of patients Hyperinsulinemia, secondary to insulin resistance Activation of the sympathetic nervous system
Effect of Cholesterol
Serum cholesterol vs Mortality
Ten Year Mortality (per 1000)
70 60 50 40 30 20 10 0 4 5 6 7 s-Cholesterol (mmol/L)
Non-diabetic Diabetic
Dyslipidaemia in DM
Most common abnormality is s HDL and s Triglyserides A low HDL is the most constant predictor of CV disease in DM Target lipid values: LDL <2.6 mmol/l, HDL >1.15 mmol/l, TG < 2.5 mmol/l
Eye Complications
Retinopathy (stages)
Background Pre-proliferative Proliferative Advanced diabetic eye disease Maculopathy
Glaucoma Cataracts
Pre-Proliferative Retinopathy
Rapid increase in amount of micro aneurisms Multiple hemorrhages Cotton wool spots (>5) Venous beading, looping and duplication
Proliferative retinopathy
Proliferative Retinopathy
New vessels (on disc, elsewhere) Fibrous proliferation (on disc, elsewhere) Hemorrhages (preretinal, vitreous)
Panretinal photo-coagulation
Stages of DN
Stage I : glomerular filtration and kidney hypertrophy Stage II : u-albumin excretion < 30mg/24h Stage III : Microalbuminuria (30 300 mg/24h) Stage IV : Overt nephropathy (> 300mg/24h, positive u dipstick) Stage V : ESRD characterized by blood urea and creatinine levels, hyperkalaemia and fluid overload
Microalbuminuria with incipient nephropathy is diagnosed if 2 or more of the tests are within the microalbumin range
Microalbuminuria
Increased risk for overt nephropathy Increased cardiovascular mortality Increased risk of Retinopathy Increased all-cause mortality
Microalbuminuria is an indication for screening for possible vascular disease and aggressive intervention to reduce all cardiovascular risk factors
Normal
30
20
30
Microalbum inuria
Albuminuri a Overt
30 - 299
300
20 - 199
30 - 299
300
200
Management of Nephropathy
Improvement of glycemic control Treatment of hypertension Treatment with angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor antagonis (AIIRA) Restriction of dietary intake of protein Once persistent elevation in u-Albumin is found refer to a Internist or Nephrologist
Diabetic Neuropathy
Sensorimotor neuropathy (acute/chronic) Autonomic neuropathy Mononeuropathy
Spontaneous Entrapment External pressure palsies
Sensorimotor Neuropathy
Patients may be asymptomatic / complain of numbness, paresthesias, allodynia or pain Feet are mostly affected, hands are seldom affected In Diabetic patients sensory neuropathy usually predominates
Autonomic Neuropathy
Symptomatic Postural hypotension Gastroparesis Diabetic diarrhea Neuropathic bladder Erectile dysfunction Neuropathic edema Charcot arthropathy Gustatatory sweating Subclinical abnormalities Abnormal pupillary reflexes Esophageal dysfunction Abnormal cardiovascular reflexes Blunted counter-regulatory responses to hypoglycemia Increased peripheral blood flow
Entrapment Neuropathies
Carpal tunnel syndrome (median nerve) Ulnar compression syndrome Meralgia paresthetica (lat cut nerve to the thigh) Lat Popliteal nerve compression (drop foot) All the above are more common in diabetic patients
Mononeuropathies
Cranial nerve palsies (most common are n. IV,VI,VII)
Management of Neuropathy
Burning pain TADs / Capsaicin Lancinating pain Anticonvulsants / TAD / Capsaicin Painful cramps Quinidine sulphate Restless legs - Clonazepam
Infections
The association between diabetes and increased susceptibility to infection in general is not supported by strong evidence However, many specific infections are more common in diabetic patients and some occur almost exclusively in them Other infections occur with increased severity and are associated with an increased risk of complications
Infections (cont)
Several aspects of immunity are altered in patients with diabetes There is evidence that improving glycemic control patients improves immune function
Specific Infections
Community acquired pneumonia Acute bacterial cystitis Acute pyelonephritis Emphysematous pyelonephritis Perinephric abscess Fungal cystitis Necrotizing fasciitis Invasive otitis externa Rhinocerebral mucormycosis Emphysematous cholecystitis
44
Diabetic Keto-Acidosis
Diabetic Ketoacidosis Most serious complication in Type 1 diabetes Precipitating Causes
Not enough insulin Skipping insulin Stress, trauma Insulin resistance
Symptoms of DKA
Abdominal pain Anorexia Dehydration Fuity breath Kussmauls Change LOC Hypotension N&V
Polyuria Somnolence Tachycardia Thirst Visual disturbances Warm, dry skin Weakness Wt. loss
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Assessment DKA
Hyperglycemia Hyperosmolality Dehydration Electrolyte imbalances Metabolic acidosis Hypoglycemia Fluid overload Rehydrate Reverse shock Give Potassium Corret pH Give insulin
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Treatment principle
48
HHNK
Hyperglycemic Hyperosmolar Noketotic Syndrome
Most commonly occurs in older adults with Type II diabetes Always look for precipitating factors Factors Associated with HHNK : Drugs, procedures, chronic illness, acute illness
49
Treatment
Similar to DKA More agresive fluid replacement Find underlying cause
50
Hypoglycemia
Also known as insulin reaction or hypoglycemic reaction Risk Factors
Overdose of insulin Omitting a meal Overexertion Nausea and vomiting Alcohol intake
51
Symptoms of Hypoglycemia
Adrenergic
Shakiness Irritability Nervousness Tachycardia Tremor Hunger Diaphoresis Pallor Paresthesias
Neuroglycopenic
Headache Mental illness Inability to concentrate Slurred speech Blurred vision Confusion Irrational behavior Lethargy LOC, coma, seizure
52
Interventions
Mild
carbohydrate 10-15 gram
Moderate
20-30 gram of carbs Glucagon, 1 mg SC or IM
Severe
50% dextrose 25 g IV Glucagon 1 mg IM or IV
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Retinopathy microaneurysms cluster at macula->terminal vessels obstructed->ischemia->new vessel proliferation Nephropathy-leads to hypertension. Assoc with the highest mortality. Cardiovascular disease- silent ischemia Peripheral neuropathy- numbness and tingling progressing to total insensitivity Stiff joint syndrome- prayer sign and atlantooccipital joint involvement
Autonomic nervous system dysfunction -orthostatic hypotension, resting tachycardia, absent beat-to-beat variation -hypogylcemic unawareness -gastroparesis occurs in 20-30%
DKA
Insulin transfers glucose and amino acids into the cells. Hyperglycemia->osmotic diuresis>dehydration->acidosis. Also, a build up of amino acids in the blood->lipolysis->free fatty acids->converted to ketone bodies in the liver Results in a intravascular fluid volume deficit of 5-8 liters, potassium deficit of 200-400 mEq, and NaCl deficit of 350-600 mEq
Treatment of DKA
Intubate for CNS depression Regular insulin 10 units IVP followed by 5-10 units/hr IV Normal saline 5-10 ml/kg/hr IV Add 5% glucose when serum blood sugar<250 mg/dl Potassium 0.3-0.5 mEq/kg/hr IV Monitor blood sugar, potassium, arterial pH and urine ketones hourly Identify cause (sepsis, MI, compliance)
Conclusion
This is just an outline of the major diabetic complications, and doesn't aim to be comprehensive All complications are preventable with good glycaemic control The progression of most complications can be halted if detected early and appropriate therapy instituted