Diabetes – Anaesthetic Management

7/29/2019 Diabetes Anaesthetic Management

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Diabetes Anaesthetic Management

Complications, Diabetic Ketoacidosis

Co-ordinator Dr. Gurjeet Khurana

Presented by Dr. S. D. Arya


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Diabetes Mellitus


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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


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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 after75 gm glucose load


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GTT Glucose conc

whole blood plasma

venous capillary venous capillary

(mg/dl)

DiabetesFasting 126 110 126 110

2 hrs after 200 180 220 200

Impaired glucose toleranceFasting < 126 < 110 < 126 < 110

2 hrs after 140-200 120-180 160-220 140-200


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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 ratelimiting step


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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


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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


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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


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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)


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Comparative C/F of Type 1 & 2 DM

Type 1 Type 2

Age onset < 40 yrs > 40 yrs

Duration of symptoms weeks monthsyrs

Body wt N or low obeseKetonuria yes no

Autoantibodies yes no

Family history uncommon commonOther autoimmune d common uncommon

Compl at diagnosis no 25%

Death without insulin yes no


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S/S of hyperglycemia

Thirst Dry mouth

Polyuria Polydipsia

Tiredness, fatigue Headache

Recent change in wt

Blurring of vision

Nausea

Mood change, irritability


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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 loss12-15% - verge of DKA

Urine sugar & ketones


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Insulin & oral hypoglycemics


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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


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Disadv/problems with insulin

i.v. bolus

Very short half life (6-8 mins)

Unphysiological

ed chances of hypoglycemias.c.route

Marked individual variations in absorption

Altered cutaneous blood flow fluid shifts &haemodynamic changes

Delayed onset

Immediate titration not possible


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Anaesthetic Management


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Anaesthetic Management Goals

To maintain glycaemic control

To avoid further deterioration of pre existing endorgan disease

To shift patient soon on pre operative glycaemic

control drugs


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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 controlwith short drugs

Assessment for cardioresp fn., IHD, CVD, renal

dysfn, peripheral neuropathy, joint mobility,retinopathy

Limit hospital stay & cost

Quantification of risk


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PAC

Assessment History/exam Invsg

BS control hypo/hyper gly BS-F & PP

episodes Hb A1 C

hospitalizationmedical t/t

Nephropathy H/O HT R/M urine

H/O recurrent UTI microalb

oedema KFT


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Assessment History/exam Invsg

Cardiac status H/O angina, MI ECG

exercise tolerance ECHOdyspnea, swelling chest x-ray

PVD H/O intermittent

claudication, non

healing ulcersRetinopathy H/O visual disturbance fundus

ing lens power exam

Stiff jt syndrome X ray

cervical spine (lat)

Metabolic & ABG

electrolytes S electrolytes

ANS


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Autonomic Nervous System Neuropathy

Hypoglycemic unawareness

Deconditioning

Greater in presence of systemic hypertension

renal failureperipheral sensory neuropathy


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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 vagaldenervation

HR response to drugs viz atropine, propranololblunted

Shortening of QT interval dysrhymias Prevent angina, cause sudden MI

Unexplained hypotension may be due topainless MI


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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 Hbmol & altering allosteric intetactions b/w chains


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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


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Stiff joint syndrome

Limited joint mobility

Prayers sign, Palm print testAtlanto 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


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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


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PAC Orders

Consent NPO Orders

Anxiolytics Aspiration prophylaxis

Stop long acting insulin night before Sx

Morning sample of BS & serum electrolytesMorning i.v. fluids according to regimen

Arrange for dextrose, insulin etc.

Careful transfer of patient

To be taken as first case in morning


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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


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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


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No insulin, no glucose

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


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Sliding Scale


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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


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contd.

B sugar Infusion< 90 mg/dl 10% D + 5 U + 10 K+

90 180 10 + 10 + 10

180 360 10 + 15 + 10

> 360 10 + 20 + 10


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contd.

Post op GKI @ 100 125 ml/hr, check B sugar4 hrly, till pt starts orally

Stop GKI, give regular insulin

Dose 20% extra, if steroids intake or infection

No lactate containing fluids


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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 Sxstop all biguanides

stop long acting sulfonylureas 3-4

days prior, shift to tolbutamide

no OHA on day of Sx


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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 GKIregular insulin once pt starts orally


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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 ofhypoglycemia, difficult in ward settings,

meticulous monitoring


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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


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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


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DM with renal failure

Alberti regimen not suitable fluid overloadadditional K+

For major Sx H.A.@ 1 unit/ml, adjusted20% D @ 40 ml/hr,10% or 5% in stressful condsliding 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, omittedfrom overnight bags


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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)


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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


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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


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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


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Clonidine glycaemic control improved due to

ed sympathoadrenal activity.

inhibits ACTH release withstimulation of GH release


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Regional Anaesthesia

Advantages

Disadvantages


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Complications of DM


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Acute complications

Diabetic ketoacidosisDiabetic nonketotic hyperosmolar coma

Hypoglycemia

Lactic acidosis


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Chronic complications

Microvascular retinopathy

nephropathyneuropathy

Macrovascular cerebrovascular

cardiovascular

peripheral vascular disease


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Diabetic Ketoacidosis

Ketoacidosis is a state of of uncontrolled catabolism a/winsulin deficiency.

Glucose Ketones

Hyperglycemia Acidosis

Glycosuria

Vomiting

Osmotic diuresisFluid & eletrolyte depletion

Renal hypoperfusion impaired excretion of

ketones & Hydrogen ions


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Pathogenesis of DKA

Insulin deficiency

Increased counter regulatory hormones -

glucagon, cortisol, GH, catecholamines

Dehydration -osmotic diuresis of hyperglycemia

fluid deprivation due to GIT disturbancehydration reduces hyperglycemia

without altering acid-base balance


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Insulin deficiency

Activated lipolysis

ed plasma FFA conc

ed hepatic fatty acids

ketogenesisactivation of Carnitine

Acyltransferase

ed hepatic carnitineed Malonyl CoA content

Glucagon excess


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Causes -

previously undiagnosed diabetes

interruption of insulin therapy

stress of intercurrent illness, MIinfection

emotional disturbance


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Clinical features

Symptoms - Signs -

Nausea, vomiting Tachycardia

Thirst, polyuria Dry mucus memb

Abdominal pain ed skin turgor

Altered mental function Tachypnea

Sluggish/extreme tiredness Kussmaul resp

Fruity smell in breath FeverShortness of breath Lethargy, coma


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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 6.8-7.3arterial pCO2 20-30 mmHg

s. bicarbonate - < 15 mEq/l


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Fluid & electrolytes :

5-8 lt fluid deficit (100 ml/kg)

Na 125-135 mEq/l (deficit 350-600 mEq)

K normal ored (deficit 200-400 mEq)

Mg, Cl - normal

Phosphate - ed

Creatinineslightly ed

Osmolality : 320 340 mOsm/llowest osmolality a/w stupor or coma in

DKA is 320 mOsm/l


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Management :

Invg electrolytes, BG, arterial blood gases,

TLC, ketone stick tests, chest x-ray, bloodculture

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


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Insulin

s.c., i.m. route

i.v. route

0.4 u/kg: bolus half i.v.

0.15 u/kg bolus half s.c.or i.m.

0.1 u/kg as infusion

0.1 u/kg/hr sc or imif BG does not fall by 50-70 mg/dl in first hr

double insulin infusion hrly iv bolus(10 u )

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


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K+ supplementation

if initial S.K < 3.3 mEq/l hold insulin, give 40mEq/hr K until S.K 3.3 mEq/l

if initial S.K 5 mEq/l do not give K, check S.Kevery 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


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Bicarbonate

pH < 6.9 6.9-7.0 > 7.0

NaHCO3 (100 mmol) 50 mmol no bicarb

in 400 ml fluid in 200 ml

@ 200 ml/hr @ 200 ml/hr

repeat HCO3 every 2 hr until pH 7.0


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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


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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


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DKA HONK

Glucose 250-600 600-1200

Osmolality 320-340 330-380

pH 6.8-7.3 > 7.3

Potassium N, or N or

Bicarbonates < 15 N to slightly Sodium 125-135 135-145

pCO2 20-30 N

Anion gap N to slightly

Ketones ++++ +/-Creatinine slightly moderately

Mg, Cl N N


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Hypoglycemia

More common than DKA in IDDM pts

Min 36-54 mg/dl glucose necessary for CNS fn

Sym NS activated diaphoresis, tachycardia,

neuroglycopenia, impairedcognition, 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


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Counter regulatory hormones secreted, stimulatehepatic glucose release

Hypoglycemia during stress, exercise, sleep or in

alcohol ingestion may not result in recognizedsymptoms

IDDM pts on insulin therapy manifest loweredglucose threshold for glucagon release (35mg/dl)

T/t rapidly absorbed carbohydrate orally, 15 gm,180 ml orange juice25 ml of 50% glucose i.v.Glucagon 1 mg i.m./i.v.

Repetitive episodes of severe hypoglycemia resultin cognitive deficits


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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 absentplasma HCO3 & pH ed pH < 7.2

H+ > 63 mmol/lanion gap

lactic acid > 5 mmol/l

T/t NaHCO3 + insulin & glucosesod dichloroacetate


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Retinopathy

Related to degree & duration of hyperglycemia

Pregnancy is a risk factor

Microaneurysms near maculla responsible forcentral vision & visual acuity

Terminal capillaries obstructed, retina ischaemic

Proliferation of new vessels

T/t photo coagulation of leaking vessels with

argon laser


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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 dialysisrenal transplantation


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Yrs after DM Clinical course

0 enlarged kidney, microalbuminuria

2 glm basement thickening, in

mesangial matrix

10-15 microalbuminuria

10-20 persistent proteinuria, in glm fn

azotemic period

20 uremic period, diabetic

retinopathy, hypertension,

nephrotic syndrome


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Cardiovascular Disease

Risk factors in NIDDM obesity, hypertension,

dyslipidemia (high LDL)

hyperglycemiawith nephropathy a/w high IHD

Combination of peripheral neuropathy &

peripheral vascular disease results in higher risk

of amputation


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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


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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/wpositioning during anaesthesia & Sx -

exacerbates


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Pancreas Transplant Recipients

Restores normal glucose metabolism

Do not require insulin to compensate for stress

response to Sx

Catecholamine response to hypoglycemia notdocumented

Chronic dysuria due to amylase in urine

Loss of HCO3 & water dehydration &

metabolic acidosis


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New treatments for DM

Implanted (like a pacemaker) glucose analyzerwith 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


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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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Diabetes – Anaesthetic Management