Management of DM and its complications

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Management of DM and its complications
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• Complications are either
• Acute---DKA
• ---hyperosmolor non ketotic coma
• ---hypoglycemia
• ---lactic acidosis
• Chronic ---macrovascular
• ---microvascular

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• Prevalance of complications at the time of
  diagnosis UKPDS

newly diagnosed diabetes
Complications Prevalance
Any complication 50
retinopathy 21
Abnormal ECG 18
Absent foot pulses 14
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Impaired reflexes vibration sense 7
MI / angina / claudication 2.8
stroke 2.8
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• Chronic complications
• Macrovascular
• microvascular

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• Macrovascular complication
• 40-50 of people with DM die from these
  complications
• Factors that contribute to the ? risk include
• 1-? prevalance of hypertension in diabetics
• 2--? lipid profile
• 3abnoramlity in clotting system
• 4effect of hyperglycemia on progression of
  atherosclerotic lesions

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• Macrovascular complications
• Stroke
• MI
• Peripheral vascular disease
• Foot problems

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• Microvascular complications
• Retinopathy
• Nephropathy
• Neuropathy
• Foot problems

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• Coronary artery disease
• Coronary artery disease accounts for the majority
  of diabetic deaths
• Certain features of CAD in diabetics include
• Adjusted for age MI is 2-5 times more frequent in
  patients with diabetes
• Pts with DM who have MI have a lower survival
  rate compared to pts without DM
• ? incidence of silent MI 40
• Silent MI may present as new onset of CCF
• Small vessel disease with relatively patent
  coronary arteries are more common

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• Peripheral vascular disease PVD
• Special characteristics of PVD
• Locationtibial popliteal arteries are
  common----aorta ,ileal, femoral rare
• Extendmulti segmental occlusion
• Progressionaccelerated progression compared to
  non diabetics
• Gangrene---risk ? more than non diabetics over 40
  yrs of age

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• Retinopathy
• Backgroundthis is the most common type of
  retinopathy
• --not usually seen untill after 10 yrs of DM
• ---may be found in 30 of pts with type 2 DM
• Proliferative
• maculopathy

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• Nephropathy
• Consists of the following clinical stages
• ? GFR gt 150 mls /min
• Microalbuminurea 30-300 mg /24 hrs
• Clinical albuminuria also called macroalbuminuria
  gt 300 mg/ 24 hrs
• Worsening of proteinuria , hypertension and ?GFR
• Kidney failure occurs when GFR ? to 10mls/min

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• Factors influencing renal function in DM
• Glomerular basement membrane damage ? diabetic
  nephropathy
• Renal artery stenosis and ischaemia due to
  atherosclerosis
• Ascending infection
• Renal papillary necrosis

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• Neuropathy
• Different clinical presentations
• Symmetrical sensory polyneuropathy
• Mononeuritis multilplex
• Autonomic neuropathy

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• Sensory neuropathy
• Insidious onset of loss of sensation in feet and
  handsgloves and stockings
• Loss of vibration sense and reduced or absent
  ankle or knee jerk
• Loss of peripheral nerve function results in
  wasting of small muscles of feet and hands

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• Mononeuritis multiplex
• Nerves commonly affected are 3rd and 6th
• Amyotrophic motor neuropathy characterized by
  unilateral or bilateral pain and weakness of the
  quadricepsthey often recover spontanously
• Median nerve palsy leeds to carpal tunnel
  syndrome
• Peroneal nerve palsy leeds to foot drop

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• Autonomic neuropathy
• CVSloss of vagal parasympathetic tone
  produces
• --resting tachycardia
• --loss of sinus rhythm change in heart rate with
  respiration---sinus arrythmia
• Loss of sympathetic activity in arterioles
  results in peripheral vasodilatation and postural
  hypotension
• Rxsupport stockings
• --fludrocortisone
• -alfa blockers

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• GIT
• Gastroparesis--Delayed gastric emptying results
  in early statiety or recurrent vomiting
• --treated with dopamine agonist
• metochlorpramide
• domperidone
• erythromycin
• Nocturnal diarrhea
• loperamide
• Constipation due to colonic atony
• laxatives

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• Autonomic bladder
• Loss of bladder smooth muscle tone results in
  incomplete emptying , stasis , and ? risk of
  infection
• In severe cases the bladder is persistantly
  distendedatonic which results in over flow
  incontinance
• sympathomimeticscarbachol
• antichilinesterase drugs

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• Gustatory sweating
• Eating cause excessive facial sweating
• Anticholinergic drugs--probantheline
• Erectile dysfunction
• impotence

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• Foot disease
• Neuropathic foot ulcer
• Ischaemic foot ulcer
• Charcots arthropathy

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• Can we prevent type 2 DM
• Before pts develop DM ,they almost always have
  pre diabetes
• Clinical trails have documented that dietary
  changes and regular exercise prevent or delay the
  development of overt DM in individuals at high
  risk

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• Risk factors for type 2 DM
• Age gt 45
• 1st degree relative with type 2 DM
• History of gestational diabetes or delivery of
  infant gt9 lbs
• PCO
• Abdominal obesity
• CVD, hypertension ,dyslipidemia ,other metabolic
  syndrome features

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• Prediabetes
• Defined as-
• IFGFBS 100 -125 mg/dl5.6 - 6.9 mmol / l
• Impaired glucose tolerance---plasma glucose level
  140 199 mg/dl 7,8 11.0 mmol / l, 2 hrs after
  75 gms of glucose

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• Evaluation and treatment
• FBG
• HbA1c
• Serum electrolytes
• Urine for protein and microalbuminuria
• ECG
• Fasting lipid profile

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• Treatment
• Diet
• Exercise
• Stop smoking
• Treat hyperlipidemia ---statin group
• Treat hypertensionmainly ACEI
• Prevent proteinuria by prescribing ACEI
• Start ASA as prophylaxis for IHD
• OHG
• Insulin

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• ADA Rx goals for glycemic control

glycemia normal goal Further action required
Average preprandial glucose mg / dl lt 110 80 - 120 gt 140
Average pp glucose lt 140 lt 160 gt 180
HbA1c lt 6 lt 7 gt 8
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• OHG
• Biguanides
• Suppress hepatic glucose production
• Decrease intestinal glucose absorption
• Improve insulin sensitivity
• metformin
• Sulphonylurea
• Increase pancreatic insulin secretion
• glimepiride
• ---glipizide
• ---glyburide
• ---chlorpropamide

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• Thiazolidinediones
• ? post prandial hyperglycemia
• ---Rosiglitazone
• ---poglitazone

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• Cont..
• Alfa glucosidase inhibitors
• ?post prandial hyperglycemia by decreasing GIT
  carbohydrate absorption
• arcabose
• Meglitinides---
• Increase pancreatic insulin secretion through
  different glucose binding sites than used by
  sulphonylureas
• repaglinide

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• Type 2 diabetes is a progressive disease
• Over time most pts will need insulin to control
  glucose

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• Insulin therapy in type 2 diabetes
• Don,t wait forever
• Don,t be afraid of hypoglycemia
• Consider combination therapy
• Don,t under insulinize
• Consider insulin pump therapy

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• DIABETIC KETOACIDOSIS
• Leading cause of death in pts with type 1
  diabetes under the age of 20 yrs

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• Risk factors for DKA
• Results from absolute or relative insulin
  deffeciency
• Missing the dose of insulin
• Infection
• Increase food intake
• Stress like MI or surgery

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• Diagnosis
• Triad of.
• Hyperglycemiaglucose more than 15mmol /l
• Metabolic acidosisPH lt 7.2
• ---HCO3 lt17 mmol
  /l
• Ketones in the urine

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• Principles of management
• Rehydration
• Insulin
• Correction of K
• Correction of acidosis
• / - antibiotics

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• Rehydration
• 1 litre NS over 30 min
• 1 litre over 1 hr
• 1 litre over 1 hr
• 1 litre over 2 hrs
• 1 litre over 4 hrs
• I litre over 6 hrs
• Change ½ saline once BS reaches 13 mmol / l

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• Insulin therapy
• 10 -20 units of RI is given IM stat
• 4 - 6 units / hr by IV infusion untill BS ? to 10
  15 mmol/l then ? to 1 - 4 units / hr
• Aim to ? BS 3 6 mmol / hr
• Change to SC once BS ?13 mmol / l

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• Potassium replacement
• 1st 30 min if K gt 5.5 mmol/l no K
• If 3.5 5.5 --give 20 meq in the 1st litre
• If lt 3.5 --give 40 meq in the 1st litre
• Continue K infusion 20 meq in each litre to
  maintain K at the level of 3.5 4. 5

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• Bicarbonte replacement
• Bicarbonate is replaced when the PH is between
  7.0 7.1
• Antibiotics
• These are used when there is strong suspicion of
  infection

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• HYPOGLYCEMIA
• Causes
• Missed delayed or inadequate meal
• Unaccustomed exercise
• Alcohol
• Increase dose of drugs ..insulin or OHG
• Gastroparesis
• Malabsorption
• factitious

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• NON KETOTIC HYPEROSMOLAR DIABETIC COMA
• Characterized by
• Severe hyperglycemia--gt 50 mmol / l
• No ketones in the urine
• Severe dehydration
• Occurs in the elderly
• Risk of thrombosis is high
• Mortality is high

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• Management
• Differs from DKA in the following
• Very sensitive to insulin so very small dose
  should be started
• Calculate osmolality and start either ½ or ¼
  saline
• Plasma osmolality 2Na 2K glu urea280 - 295

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• Cont..
• Prophylactic SC heparin
• Fluid replacement should be adjusted according to
  CVP

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