Management of DM and its complications

Complications are either… Acute---DKA

---hyperosmolor non ketotic coma

---hypoglycemia

---lactic acidosis Chronic ---macrovascular

---microvascular

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 %

Impaired reflexes +vibration sense

7%

MI / angina / claudication

2.8 %

stroke 2.8 %

Chronic complications

Macrovascular microvascular

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

3—abnoramlity in clotting system

4—effect of hyperglycemia on progression of atherosclerotic lesions

Macrovascular complications

Stroke MI Peripheral vascular disease Foot problems

Microvascular complications

Retinopathy Nephropathy Neuropathy Foot problems

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

Peripheral vascular disease {PVD}Special characteristics of PVDLocation—tibial + popliteal arteries are

common----aorta ,ileal, femoral –rareExtend—multi segmental occlusionProgression—accelerated progression

compared to non diabeticsGangrene---risk ↑ more than non diabetics

over 40 yrs of age

Retinopathy Background—this 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

NephropathyConsists of the following clinical stages: ↑ GFR > 150 mls /min Microalbuminurea 30-300 mg /24 hrs Clinical albuminuria also called

macroalbuminuria > 300 mg/ 24 hrs Worsening of proteinuria , hypertension and

↓GFR Kidney failure occurs when GFR ↓ to ≤

10mls/min

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

Neuropathy

Different clinical presentations Symmetrical sensory polyneuropathy Mononeuritis multilplex Autonomic neuropathy

Sensory neuropathy Insidious onset of loss of sensation in feet

and hands—gloves 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

Mononeuritis multiplex Nerves commonly affected are 3rd and 6th Amyotrophic motor neuropathy

characterized by unilateral or bilateral pain and weakness of the quadriceps—they often recover spontanously

Median nerve palsy leeds to carpal tunnel syndrome

Peroneal nerve palsy leeds to foot drop

Autonomic neuropathy CVS—loss 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 Rx—support stockings --fludrocortisone -alfa blockers

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

Autonomic bladder Loss of bladder smooth muscle tone

results in incomplete emptying , stasis , and ↑ risk of infection

In severe cases the bladder is persistantly distended—atonic which results in over flow incontinance

sympathomimetics—carbachol antichilinesterase drugs

Gustatory sweating Eating cause excessive facial sweatingAnticholinergic drugs--probantheline

Erectile dysfunction impotence

Foot disease

Neuropathic foot ulcer Ischaemic foot ulcer Charcots arthropathy

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

Risk factors for type 2 DM Age > 45 1st degree relative with type 2 DM History of gestational diabetes or delivery of

infant >9 lbs PCO Abdominal obesity CVD, hypertension ,dyslipidemia ,other

metabolic syndrome features

Prediabetes

Defined as- IFG—FBS =100 -125 mg/dl…5.6 - 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

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

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

ADA Rx goals for glycemic control

glycemia normal goal Further action required

Average preprandial glucose mg / dl

< 110 80 - 120 > 140

Average pp glucose < 140 < 160 > 180

HbA1c < 6 < 7 > 8

OHG Biguanides— Suppress hepatic glucose production Decrease intestinal glucose absorption Improve insulin sensitivity metformin Sulphonylurea Increase pancreatic insulin secretion —glimepiride ---glipizide ---glyburide ---chlorpropamide

Thiazolidinediones—

↓ post prandial hyperglycemia

---Rosiglitazone---poglitazone

Cont..Alfa glucosidase inhibitors— ↓post prandial hyperglycemia by decreasing GIT

carbohydrate absorption arcaboseMeglitinides--- Increase pancreatic insulin secretion through

different glucose binding sites than used by sulphonylureas

repaglinide

Type 2 diabetes is a progressive disease

Over time most pts will need insulin to control glucose

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

DIABETIC KETOACIDOSIS

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

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

Diagnosis

Triad of. Hyperglycemia—glucose more than

15mmol /l Metabolic acidosis—PH < 7.2

---HCO3 <17 mmol /l Ketones in the urine

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

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

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

Potassium replacement 1st 30 min if K+ > 5.5 mmol/l– no K+ If 3.5 5.5 --give 20 meq in the 1st litre If < 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

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

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

NON KETOTIC HYPEROSMOLAR DIABETIC COMA

Characterized by Severe hyperglycemia--> 50 mmol / l No ketones in the urine Severe dehydration Occurs in the elderly Risk of thrombosis is high Mortality is high

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 + urea=280 - 295

Cont.. Prophylactic SC heparin Fluid replacement should be adjusted

according to CVP