Diabetes Anaesthetic Management Complications, Diabetic Ketoacidosis

Co-ordinator Dr. Gurjeet Khurana

Presented by Dr. S. D. Arya

Diabetes Mellitus

WHO definition

Symptoms + plasma glucose conc > 11.1 mmol/l

Two fasting glucose conc > 7 mmol/l Two random glucose conc > 11.1 mmol/l, if pt is asymptomatic

WHO criteria for oral GTT

Unrestricted carbohydrate diet for 3 days Fasted overnight ( for at least 8 hrs) Rest before test (30 mins) Plasma glucose measured before & 2 hrs after 75 gm glucose load

GTT

Glucose conc whole blood plasma venous capillary venous capillary (mg/dl)

Diabetes Fasting 126 110 2 hrs after 200 180 Impaired glucose tolerance Fasting < 126 < 110 2 hrs after 140-200 120-180

126 220 < 126 160-220

110 200 < 110 140-200

Insulin Secretion
86 AA precursor polypeptide preproinsulin proteolysis proinsulin insulin Glucose > 70 mg/dl insulin synthesis Insulin secretion begins with its transport into cells by GLUT 2 glucose transporter Glucose phosphorylation by glucokinase rate limiting step

Effects of Insulin
On liver promotes glycogenesis, es synthesis of triglycerides, cholesterol, VLDL es glycogenolysis, ketogenesis, gluconeogenesis On muscle promotes protein synthesis promotes glycogen synthesis On fat promotes triglyceride storage es glucose transport into fat cells es intracellular lipolysis

Blood Glucose Regulation

Liver blood glucose buffer system Insulin & glucagon feedback control system Hypothalamus epinephrine Growth hormone, cortisol

Importance: brain, retina, germinal epth of gonads uses glucose as the only energy source

Excess glucose ECF fluid extra cellular hyperosmolality cellular dehydration Glycosuria Osmotic diuresis polyuria, polydipsia depletion of fluid & electrolytes Lipolysis - ed serum fatty acid conc ed protein synthesis

Diabetes Risk Factors

Family history of type 2 DM Overweight (BMI > 25 kg/sqm) Habitual sedentary physical activity High risk ethnic groups H/O gestational diabetes H/O large babies (birth wt > 9 lbs) Hypertension Hyperlipidemia ( high triglycerides, low HDL)

Comparative C/F of Type 1 & 2 DM

Type 1 Age onset < 40 yrs Duration of symptoms weeks Body wt N or low Ketonuria yes Autoantibodies yes Family history uncommon Other autoimmune d common Compl at diagnosis no Death without insulin yes Type 2 > 40 yrs months yrs obese no no common uncommon 25% no

S/S of hyperglycemia

Thirst Polyuria Tiredness, fatigue Recent change in wt Blurring of vision Nausea Mood change, irritability

Dry mouth Polydipsia Headache

Investigations

Blood glucose Glycosylated Hb Hb A1c over 60 days of 1% Hb A1c means of 2 mmol/l BG non diabetic range < 6.05% goal in IDDM < 7.5% > 9% - osm diuresis, water & electrolyte loss 12-15% - verge of DKA Urine sugar & ketones

Insulin & oral hypoglycemics

Prevention of insulin adsorption on tubing & glass bottles

Add albumin/polygelline Add pts own blood Flushing with 50 ml saturates binding sites Use conc insulin small vol

Disadv/problems with insulin

i.v. bolus Very short half life (6-8 mins) Unphysiological ed chances of hypoglycemia s.c.route Marked individual variations in absorption Altered cutaneous blood flow fluid shifts & haemodynamic changes Delayed onset Immediate titration not possible

Anaesthetic Management

Anaesthetic Management Goals

To maintain glycaemic control To avoid further deterioration of pre existing end organ disease To shift patient soon on pre operative glycaemic control drugs

Pre operative assessment - Aims

Type of DM, its duration & t/t Evaluation & t/t of end organ damage: responsible for 5 fold in peri operative mortality Assessment of BS control & to obtain control with short drugs Assessment for cardioresp fn., IHD, CVD, renal dysfn, peripheral neuropathy, joint mobility, retinopathy Limit hospital stay & cost Quantification of risk

PAC
Assessment BS control History/exam hypo/hyper gly episodes hospitalization medical t/t H/O HT H/O recurrent UTI oedema Invsg BS-F & PP Hb A1 C

Nephropathy

R/M urine microalb KFT

Assessment Cardiac status

History/exam Invsg H/O angina, MI ECG exercise tolerance ECHO dyspnea, swelling chest x-ray PVD H/O intermittent claudication, non healing ulcers Retinopathy H/O visual disturbance fundus ing lens power exam Stiff jt syndrome X ray cervical spine (lat) Metabolic & ABG electrolytes S electrolytes ANS

Autonomic Nervous System Neuropathy

Hypoglycemic unawareness
Deconditioning Greater in presence of systemic hypertension renal failure peripheral sensory neuropathy

Cadiovascular manifestations Resting tachycardia lack of vasoconstriction due to sympath NS stimulation Orthostatic hypotension norep es less in standing position ed or absent beat to beat variability of HR in response to deep breathing cardiac vagal denervation HR response to drugs viz atropine, propranolol blunted Shortening of QT interval dysrhymias Prevent angina, cause sudden MI Unexplained hypotension may be due to painless MI

Resp system

ed vent response to PaCO2 & PaO2 ed susceptibility to vent depressant drugs FVC & FEV ed 2,3,DPG More chances to resp tract infection DM affects O2 transport glucose binding to Hb mol & altering allosteric intetactions b/w chains

Sudden death syndrome May manifest as sudden death syndrome ed incidence of post op cardio resp arrest Sudden unexpected profound bradycardia responsive only to epinephrine Gastroparesis Delayed gastric emptying Nausea, vomiting, diarrhoea, abd distension Metoclopramide

Stiff joint syndrome Limited joint mobility Prayers sign, Palm print test Atlanto occipital jt Non familial short stature, tight waxy skin Glycosylation of tissue proteins responsible

Diabetic scleredema Thickening & hardening of skin Induration non pitting & symmetrical Ant spinal artery syndrome

Others ed A-V shunting ed skin capillary blood flow ed sweating neuropathic foot Greater intra op core body temp es delayed onset of thermoregulatory vasoconstriction

PAC Orders
Consent NPO Orders Anxiolytics Aspiration prophylaxis Stop long acting insulin night before Sx Morning sample of BS & serum electrolytes Morning i.v. fluids according to regimen Arrange for dextrose, insulin etc. Careful transfer of patient To be taken as first case in morning

Classification of surgeries

Minor - < 30 mins; unlikely to interfere with t/t

Intermediate 30 min - 2 hrs; might interfere on day of Sx Major - > 2 hrs; likely to interfere with Mx & diet

Peri operative glucose/insulin therapy - Goals

Provide adequate carbohydrate normal obligatory requirement 180 gm/day rate of infusion 5-10 gm/hr (1.2-2.4 mg/kg/d) 5% D i.v. @ 125 ml/hr Mimic physiologic condition 1-2 unit insulin/hr Simple practical & error free regimen Correction of acid/base electrolyte imbalance Maintain BS @ 120 - 180 mg/dl

No insulin, no glucose

Partial morning dose insulin (s.c.) with dextrose

Sliding Scale

Albertis Regimen

(Type 1 DM)

Stabilize BG 2-3 days prior to Sx Shift to short acting insulin on day before Sx Omit morning dose of insulin Start GKI (10, 10, 10) after checking BG & K+ @ 100 125 ml/min 2 3 hrly B sugar level charting

contd. B sugar < 90 mg/dl 90 180 180 360

Infusion 10% D + 5 U + 10 K+ 10 + 10 + 10 10 + 15 + 10

> 360

10 + 20 + 10

contd.

Post op GKI @ 100 125 ml/hr, check B sugar 4 hrly, till pt starts orally Stop GKI, give regular insulin
Dose 20% extra, if steroids intake or infection No lactate containing fluids

Albertis Regimen

(Type 2 DM)

Diet controlled treat as normal pt., check BS On OHA uncontrolled insulin controlled OHA to continue 1 day prior to Sx stop all biguanides stop long acting sulfonylureas 3-4 days prior, shift to tolbutamide no OHA on day of Sx

contd.
Minor Sx manage as non diabetic, if BS control Major Sx start GKI infusion

Post operatively Minor Sx OHA, dose with first meal full dose next day Major Sx continue GKI regular insulin once pt starts orally

Tight Control Regimen

To keep BS in 99-120 mg/dl Indicated in pregnancy, CPB, neurological & cardiac Sx Adv. improves wound healing, prevents wound infection, improves neurological outcome, improves weaning from CPB Disadv. no monitoring of K+ , more chances of hypoglycemia, difficult in ward settings, meticulous monitoring

contd. Pre-prandial G, night before Sx Start 5% D @ 50 ml/hr Piggy back insulin, 50 U in 250 ml NS Flush initial 60 ml to saturate insulin binding sites Infusion rate @ BS/150 ml/hr (100, if pt on steroid, sepsis, obesity) 4 hrly BS monitoring Intraop 1-2 hrly monitoring If BS < 50, give 15 ml of 50% D

Post op complications

Hypoglycemia Hyperglycemia Infection Delayed wound healing Peri op ed MI risk : watch for 72 hrs Problems due to autonomic neuropathy PONV Pain Restoration of routine OHR

DM with renal failure

Alberti regimen not suitable fluid overload additional K+ For major Sx H.A.@ 1 unit/ml, adjusted 20% D @ 40 ml/hr, 10% or 5% in stressful cond sliding scale or s.c. in post-op For minor Sx morning dose omitted, 5% D @ 40 ml/hr Pt on dialysis insulin in dialysis bags, omitted from overnight bags

DM & Obesity

ed risk of post op resp failure, atrial & vent arrhythmias, renal insufficiency, leg wound infection
Metabolic syndrome hyperglycemia with insulin resistance, hypertension, central visceral obesity, dyslipidemia (high TG & low HDL)

DM & Emergency Sx

Usually infected, uncontrolled, dehydrated Metabolic decompensation Resistance to insulin Little time for stabilization but 2-3 hrs sufficient to correct fluid & electrolyte imbalance If Sx lead to further metabolic deterioration, correct ketoacidosis first

Propofol infusion in Diabetic pts

Lipid load resulting from propofol infusion may lead to impairment of metabolism, in ICU set up

Unlikely to be relevant during induction

Etomidate & Midazolam in DM

Etomidate : inhibitory effect on adrenal steroid genesis & glycaemic response to Sx

Midazolam - ACTH & cortical secretion sympathoadrenal activity, stimulates GH secretion. Net effect is ed glycaemic response to Sx

Clonidine glycaemic control improved due to ed sympathoadrenal activity. inhibits ACTH release with stimulation of GH release

Regional Anaesthesia

Advantages

Disadvantages

Complications of DM

Acute complications
Diabetic ketoacidosis Diabetic nonketotic hyperosmolar coma Hypoglycemia Lactic acidosis

Chronic complications Microvascular retinopathy nephropathy neuropathy Macrovascular cerebrovascular cardiovascular peripheral vascular disease

Diabetic Ketoacidosis
Ketoacidosis is a state of of uncontrolled catabolism a/w insulin deficiency. Glucose Ketones

Hyperglycemia Glycosuria
Osmotic diuresis

Acidosis Vomiting

Fluid & eletrolyte depletion Renal hypoperfusion impaired excretion of ketones & Hydrogen ions

Pathogenesis of DKA

Insulin deficiency Increased counter regulatory hormones glucagon, cortisol, GH, catecholamines Dehydration osmotic diuresis of hyperglycemia fluid deprivation due to GIT disturbance hydration reduces hyperglycemia without altering acid-base balance

Insulin deficiency Activated lipolysis

ed plasma FFA conc ed hepatic fatty acids ketogenesis activation of Carnitine Acyltransferase

ed hepatic carnitine ed Malonyl CoA content

Glucagon excess

Causes previously undiagnosed diabetes interruption of insulin therapy stress of intercurrent illness, MI infection emotional disturbance

Clinical features
Symptoms Nausea, vomiting Thirst, polyuria Abdominal pain Altered mental function Sluggish/extreme tiredness Fruity smell in breath Shortness of breath Signs Tachycardia Dry mucus memb ed skin turgor Tachypnea Kussmaul resp Fever Lethargy, coma

Laboratory findings :

BG 300 600 mg/dl Eugenic DKA BG < 350 mg/dl in alcoholic, pregnancy, young pts Acid Base abnormality: bicarbonate level ed ed anion gap pH 6.8-7.3 arterial pCO2 20-30 mmHg s. bicarbonate - < 15 mEq/l

Fluid & electrolytes : 5-8 lt fluid deficit (100 ml/kg) Na 125-135 mEq/l (deficit 350-600 mEq) K normal or ed (deficit 200-400 mEq) Mg, Cl - normal Phosphate - ed Creatinine slightly ed Osmolality : 320 340 mOsm/l lowest osmolality a/w stupor or coma in DKA is 320 mOsm/l

Management : Invg electrolytes, BG, arterial blood gases, TLC, ketone stick tests, chest x-ray, blood culture Oxygen, NG tube, urinary catheter, CVP, ECG Antibiotics Fluid therapy 0.9% NS 1 lt in 30 mins 1 lt hourly for 2 hrs 1 lt 2 hrly 1 lt 2-4 hrly change to 5%D when BG 180-270 mg/dl

Insulin
s.c., i.m. route
0.4 u/kg: bolus half i.v. half s.c.or i.m. 0.1 u/kg/hr sc or im if BG does not fall by 50-70 mg/dl in first hr double insulin infusion hrly iv bolus(10 u ) i.v. route 0.15 u/kg bolus 0.1 u/kg as infusion when BG reaches 250 mg/dl change to 5%D + 0.45% NaCl 150-200 ml/hr +insulin(0.05-0.1 u/kg/hr i.v.) or 5-10 u s.c. every 2 hr

K+ supplementation if initial S.K < 3.3 mEq/l hold insulin, give 40 mEq/hr K until S.K 3.3 mEq/l if initial S.K 5 mEq/l do not give K, check S.K every 2 hr if initial S.K b/w 3.3-5 mEq/l give 20-30 mEq K in each lt fluid Keep S.K b/w 4 - 5 mEq/l

Bicarbonate

pH < 6.9 NaHCO3 (100 mmol) in 400 ml fluid @ 200 ml/hr

6.9-7.0 > 7.0 50 mmol no bicarb in 200 ml @ 200 ml/hr

repeat HCO3 every 2 hr until pH 7.0

Hyperosmolar Hyperglycemic Non Ketotic Coma

Severe hyperglycemia - > 600 mg/dl Vol depletion ~ 25% of total body water Hyperosmolarity - > 350 mosm/kg Normal pH, absence of symptoms Osmotic diuresis dehydration, somnolence, coma Ppt factors advanced age, sepsis, hyperalimentation using conc carbohydrate soln

contd. Pathophysiology relative insulin def & inadequate fluid intake

Each 100 mg/dl in BG es plasma Na+ by 1.6 mEq/l T/t hypotonic saline low dose i.v. insulin K+ supplementation

DKA Glucose Osmolality pH Potassium Bicarbonates Sodium pCO2 Anion gap Ketones Creatinine Mg, Cl 250-600 320-340 6.8-7.3 N, or < 15 125-135 20-30 ++++ slightly N

HONK 600-1200 330-380 > 7.3 N or N to slightly 135-145 N N to slightly +/moderately N

Hypoglycemia

More common than DKA in IDDM pts Min 36-54 mg/dl glucose necessary for CNS fn Sym NS activated diaphoresis, tachycardia, neuroglycopenia, impaired cognition, confusion, headache, irritability, retrograde amnesia, seizures, unconsciousness Symptoms appear when BG falls to 40 mg/dl or abrupt from 300 mg/dl to 100 mg/dl

Counter regulatory hormones secreted, stimulate hepatic glucose release Hypoglycemia during stress, exercise, sleep or in alcohol ingestion may not result in recognized symptoms IDDM pts on insulin therapy manifest lowered glucose threshold for glucagon release (35mg/dl) T/t rapidly absorbed carbohydrate orally, 15 gm, 180 ml orange juice 25 ml of 50% glucose i.v. Glucagon 1 mg i.m./i.v. Repetitive episodes of severe hypoglycemia result in cognitive deficits

Lactic Acidosis

Type B lactic acidosis Usually in pts on Metformin Pt very ill, over breathing, severely dehydrated, breath does not smell of acetone, ketonuria mild or absent plasma HCO3 & pH ed pH < 7.2 H+ > 63 mmol/l anion gap lactic acid > 5 mmol/l T/t NaHCO3 + insulin & glucose sod dichloroacetate

Retinopathy

Related to degree & duration of hyperglycemia Pregnancy is a risk factor Microaneurysms near maculla responsible for central vision & visual acuity Terminal capillaries obstructed, retina ischaemic Proliferation of new vessels T/t photo coagulation of leaking vessels with argon laser

Nephropathy

Micro albuminuria Macro albuminuria Hypertension nephrotic syndrome - GFR end stage renal disease Controlling B.P., low protein diets - progress ACE inhibitors delay onset & slow progress T/t dialysis renal transplantation

Yrs after DM

Clinical course

0 2 10-15 10-20 20

enlarged kidney, microalbuminuria glm basement thickening, in mesangial matrix microalbuminuria persistent proteinuria, in glm fn azotemic period uremic period, diabetic retinopathy, hypertension, nephrotic syndrome

Cardiovascular Disease

Risk factors in NIDDM obesity, hypertension, dyslipidemia (high LDL) hyperglycemia with nephropathy a/w high IHD Combination of peripheral neuropathy & peripheral vascular disease results in higher risk of amputation

Peripheral Neuropathy

Symmetrical sensorimotor neuropathy: numbness, tingling in toes, feet Depend on duration of NIDDM Hypoesthesia, parasthesia, dysthesia, anaesthesia Insensitive foot vulnerable to trauma, neuropathic foot ulcers gangrene amputation Acute hyperglycemia es nerve fn & chronic hyperglycemia a/w axonal degeneration, loss of myelinated & unmyelinated nerve fibers

cotnd. Mononeuropathies asymmetrical, affect cranial or peripheral nerves. Is sec to vascular occlusion leading to nerve infarcts. Radial N, common peroneal N Entrapment syndrome ulnar N at cubital tunnel median N at carpal tunnel Unavoidable pressure on extremities a/w positioning during anaesthesia & Sx exacerbates

Pancreas Transplant Recipients

Restores normal glucose metabolism Do not require insulin to compensate for stress response to Sx Catecholamine response to hypoglycemia not documented Chronic dysuria due to amylase in urine Loss of HCO3 & water dehydration & metabolic acidosis

New treatments for DM

Implanted (like a pacemaker) glucose analyzer with electric transmission to a surface (watch) monitor Glucagon like peptide receptor antagonist: GIP-1 New islet implantation medication that makes islet cells transplants more successful & rejection medication less hazardous Medications viz INGAP peptide: regrowth of normally functioning islet cells

Inhaled insulin - Exubera

Fast acting, dry powder formulation, orally inhaled before meals Loss during pulm inhalation 5 unit exubera = 1 unit of injected form Lung disease caution PFTs checked before starting, & checked every 6-12 months

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