PERIOPERATIVE CARE OF THE DIABETIC PATIENT Philippe SCHERPEREEL TBILISI 2014 Clinique d’Anesthésie Réanimation Hôpital Claude Huriez CENTRE HOSPITALIER UNIVERSITAIRE 59037 LILLE FRANCE
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PERIOPERATIVE CARE OF
THE DIABETIC PATIENT
Philippe SCHERPEREEL
TBILISI 2014 Clinique d’Anesthésie Réanimation
Hôpital Claude Huriez CENTRE HOSPITALIER UNIVERSITAIRE
59037 LILLE FRANCE
CLASS PATHOGENESIS PREVALENCE
TYPE 1(Former juvenile
or IDDM)
Immune mediated idiopathic formsof beta cell dysfunction leading to
absolute deficiency
0.4 %M = F
USUALYYOUNG
TYPE 2(Former NIDDM)
Insulin resistance relative insulindeficiency or secretory defect
6.6 %ADULT ONSET
(8.0 % > 65 y)TYPE 3 Wide range of specific types of
diabetes. Genetic defects of betacellfunction. Genetic defect of insulin action. Diseases of exocrine pancreas
TYPE 4 Gestational diabetes(30 – 50 % Type 2 within 10
years)
4.0 % ofpregnancies
CLASSIFICATION, PHYSIOPATHOLOGY AND PREVALENCE
STABILITY OF TYPE 1 DIABETES : 0.4 % INCREASING FREQUENCY OF TYPE 2 DIABETES
Greater number of aged patient Earlier occurence in younger people Lower threshold proposed byW.H.O.
7 mmol/l instead of 7.8 mmol/l Absolute increase linked to :
– environmental factors obesity, diet, sedentarity... – Acting on polygenic predisposition
WHO : TYPE 2 DIABETES IN THE WORLD 150 M in 2000 (6.0 %) 213 M in 2010
EPIDEMIOLOGY
MECHANISMS ASSOCIATED WITH INSULIN-RESISTANCE
INSULIN RESISTANCE IS A MAJOR FACTOR IN THE PATHOGENESIS OF DIABETES Mutations in glucose transporters (GLUT) Effects in signaling pathways and consequent
mechanisms (translocation, docking, fusion) Impairment of insulin-stimulated glucose tranport
– Free fatty acids uptake of glucose – Glucose and glucosamine insulin secretion
insulin action – TNF α insulin signaling in isolated muscle and adipose tissue
FACTORS CONTRIBUTING TO INSULIN RESISTANCE AFTER SURGERY
STRESS INDUCED ENDOCRINE REACTION
INFLAMMATORY MEDIATORS : TNFα, CYTOKINES (IL1)...
HYPOCALORIC NUTRITION
BED REST
INCREASED : Hepatic glycogenolysis Triglycerides lipolysis Proteic catabolism
NEUROENDOCRINE STRESS RESPONSE AND BLOOD GLUCOSE REGULATION
INSULIN
HYPERGLYCAEMIA
CATHECHOLAMINE GLUCAGON CORTISOL GROWTH HORMONE
COUNTER REGULATORY HORMONES
THE PERIOPERATIVE RISK IN THE DIABETIC PATIENT
IS LINKED NOWADAYS LESS TO THE METABOLIC CONTROL
PROBLEM TECHNICALY SOLVED New insulins Bedside monitoring of glycaemia constant infusion techniques
IS TIGHT PERIOPERATIVE CONTROL OF
DIABETES WARRANTED ? Roizen MF THAN TO END ORGAN PATHOLOGY
Multiple organs lesions Often clinically silent
MAJOR INTEREST OF THE ANAESTHETIC CONSULTATION
MECHANIMS OF DIABETIC END ORGAN PATHOLOGY
CLASSICALY :
Macroangiopathy by atherosclerosis Micro vascular lesions, more specific Autonomic neuropathy Collagen abnormalities
NOWADAYS, UNICIST HYPOTHESIS IMPAIRED GLYCOSYLATION OF PROTEINS
PREOPERATIVE ASSESSMENT OF THE DIABETIC PATIENT
EVALUATION OF THE RISK
CARDIOVASCULAR NEUROLOGICAL RENAL RESPIRATORY DIFFICULT INTUBATION METABOLIC IMMUNE AND INFECTIOUS
CARDIOVASCULAR RISK ASSESSMENT
1.1. CORONARY ARTERY DISEASE (CAD) 1.2. ARTERIAL HYPERTENSION 1.3. DIABETIC CARDIOMYOPATHY 1.4. CARDIAC AUTONOMIC NEUROPATHY
(CAN)
1.1. CORONARY ARTERY DISEASE (CAD)
THE DIABETIC IS A HIGH RISK PATIENT FOR CARDIAC ISCHAEMIA
MYOCARDIAL INFARCTION IS :
Twice more frequent The most usual cause of death in the older diabetic
MYOCARDIAL ISCHAEMIA IS : Often clinically silent Revealed by exercice ECG, perfusion scintigraphy Present up to 60 % of diabetics without symptom of
CAD
REPORTED AMONG 29 TO 54 % OF THE PATIENTS WITH TYPE 1 AS WELL TYPE 2 DIABETES
PHYSIOPATHOLOGY Angiotensin II Impairment of glycosylation of collagen
LOSS OF ELASTICITY OF VESSELS WALL Glomerulosclerosis and diabetic nephropathy
TREATMENT Alpha blockers, calcium channel blockers
angiotensin converting enzyme inhibitors Rather than diuretics and beta blockers
1.2. ARTERIAL HYPERTENSION
1.3. DIABETIC CARDIOMYOPATHY A - Physiopathology
SPECIFIC CARDIOMYOPATHY WITHOUT ANY HYPERTENSIVE OR ISCHAEMIC
CARDIOPATHY PHASE 1 :
Redistribution of the isoenzyme content of myosin Modification of specific contractile proteins Impairments of calcium exchanges
– INCREASED TOTAL CALCIUM CONTENT – DECREASED CALCIUM UPTAKE BY THE
SARCOPLASMIC RETICULUM
PHASE 2 : Deposit of abormal glycoproteins and collagen
TECHNIQUES Doppler echocardiography +++ Thallium scintigraphy
RESULTS : DECREASED L.V. PERFORMANCE
Diastolique relaxation L.V. Filing +++
– CONTRACTILITY – AFTER LOAD
RELATIONSHIP WITH THE SEVERITY OF THE MICROANGIOPATHY (Retinopathy, Nephropathy...)
1.3. DIABETIC CARDIOMYOPATHY B - Evaluation of L.V. function
FREQUENCY 20 to 40 %
USUALY SILENT Painless myocardial ischaemia Abnormal cardiovascular response to stress and
exercice Loss of cardiovascular reflexes (baroreflex) Unexpected sudden death
MUST BE SYSTEMATICALLY INVESTIGATED
MAIN CAUSE OF HAEMODYNAMC INSTABILITY
(INDUCTION, REGIONAL ANAESTHESIA...) ESPECIALY IN CASE OF ASSOCIATED CARDIOPATHY
1.4. CARDIAC AUTONOMIC NEUROPATHY A - Overview
SINUS TACHYCARDIA AT REST NOT MODIFIED BY Deep breathing Valsalva’s manoeuvre Head up tilt
ORTHOSTATIC HYPOTENSION
> 30 mmHg systolic, > 50 mmHg diastolic Revealed by lipothymia, vertigo, nausea... Worsen by hypovolemia
vasodilatators, antihypertensive drugs neuroleptics
AUTONOMIC TESTING
1.4. CARDIAC AUTONOMIC NEUROPATHY B - CLinical assessment
PARASYMPATHETIC (VAGAL) FUNCTION R.R. INTERVALS
– RESPIRATORY SINUS ARRYTHMIA – VALSALVA’S MANOEUVRE
SYMPATHETIC FUNCTION
DIASTOLIC BLOOD PRESSURE RESPONSE TO
– VALSALVA’S MANOEUVRE – HEAD UP TILT – COLD PRESSOR TEST
AUTONOMIC TESTING
CARDIAC AUTONOMIC NEUROPATHY (CAN)
TESTS RESULTS SCORING
DROP OF SYSTOLIC BP INORTHOSTATISM (mmHg)
≤ 1011 – 29≥ 30
00.51
R-R INTERVALS RATIO INORTHOSTATISM
≥ 1.041.01 – 1.03≤ 1.00
00.51
INCREASE DIASTOLIC BP DURINGGRASPING TEST (mmHg)
≥ 1611 – 15≤ 10
00.51
RESPIRATORY ARRYTHMIA( HR b/min)
≥ 1511 –14≤ 10
00.51
VALSALVA RATIO ≥ 1.211.11 – .1.20
≤ 1.10
01*1
* Boarder line result must be considered abnormal
CARDIAC AUTONOMIC NEUROPATHY (CAN) SCORE
SCORE
NORMAL 0 - 0.5
EARLY ABNORMALITIES 1.0 - 1.5
DEFINITIVE ABNORMALITIES 2.0 - 3.5
SEVERE ABNORMALITIES 4.0 - 5.0
2. NEUROLOGICAL RISK A - Pathogenesis
NON ENZYMATIC GLYCOSYLATION SORBITOL MYOINOSITOL SODIUM - POTASSIUM ATPase ACTIVITY CELLULAR PERMEABILITY TO SODIUM
ENDONEURAL OEDEMA (MNR)
VASA NERVORUM COMPRESSION
NERVE ISCHAEMIA
DIABETIC MOTOR AND SENSITIVE POLYNEUROPATHY Risk of litigation in case of regional anaesthesia
DYSAUTOMIC NEUROPATHY
Heart (CAN) : Cardiac instability Bladder : dysuria, retention and infection Stomach : gastroplegia, gastric stasis
– RISK OF INHALATION DUE TO FULL STOMACH – Prolonged preoperative fasting – Succion tube – IV-Erythromycin (Motilin-like)
Pancreas : vagal neuropathy – SELF MAINTENANCE OF DIABETES BY DECREASED REACTIONNAL
INSULIN SECRETION
2. NEUROLOGICAL RISK B - Clinical features
3. RENAL RISK
PREVIOUS DIABETIC RENAL FAILURE :
Glomerulosclerosis Papillary necrosis
INCREASED RISK OF POSTOPERATIVE
COMPLICATIONS :
Haemodynamic abnormalities : RENAL BLOOD FLOW
Bladder dysautonomy URINARY STASIS
Immune depression URO SEPSIS
4. RESPIRATORY RISK
EARLY IMPAIRMENT OF PULMONARY FUNCTION : Forced vital capacity (FVC) Forced expiratory volume at 1 second (FEV1) Diffusion capacity for carbon monoxyde (DLCO) Single breath alveolar volume (SBVA)
RELATIONSHIP WITH LONG TERM GLYCOSYLATED
HEMOGLOBIN (HbA1c) PLASMA LEVEL
PROBABLY DUE TO CROSS-LINKING OF PULMONARY COLLAGEN
CONCERNS TYPE 1 AS WELL TYPE 2
AVOIDED BY TIGHT BLOOD GLUCOSE CONTROL
5. RISK OF DIFFICULT INTUBATION
COLLAGEN ABNORMALITIES STIFF JOINT SYNDROM
JUVENIL-ONSET DIABETES (33.2 %) NON FAMILIAL SHORT STATURE TIGHY WAXY SKIN LIMITED JOINT MOBILITY
Small joints of the digits and hands
– Prayer sign Atloido-axis fixation
– Endotracheal intubation difficult or impossible x 10 in young Type 1 diabetic
– Profile X Ray of the neck with hyperextension
6. METABOLIC RISK
DANGER OF HYPOGLYCAEMIA IN AN ANAESTHETIZED PATIENT HYPERGLYCAEMIA
OSMOTIC POLYURIA DEHYDRATATION
INTEREST OF EUGLYCAEMIA
BETTER METABOLIC CONTROL LESS POSTOPERATIVE PROTEIN CATABOLISM
Wound healing IMPROVED IMMUNE DEFENCES
Sepsis
IS TIGHT PERIOPERATIVE CONTROL OF DIABETES WARRANTED?
Roizen MF, Anaesthesiology 1992
FRENCH RECOMMENDATIONS ALFEDIAM - SFAR
BLOOD GLUCOSE LEVEL MAINTAINED BETWEEN 1.2 - 2.1 g.l-1 (6.6 - 11.1 mmol.l-1) DURING THE OPERATIVE PERIOD
TIGHTER CONTROL BETWEEN 1.0 - 1.2 g.l-1 (5.5 - 6.6 mmol.l-1) IN THREE CIRCUMSTANCES : AORTO-CORONARY BY-PASS
SURGERY WITH TRANSIENT INTERRUPTION OF
CEREBRAL BLOOD FLOW
OBSTETRICS
7. INFECTIOUS RISK
DIABETES IMBALANCE DEPRESSES IMMUNE DEFENCES
EVEN DURING SHORT PERIODS HYPERGLYCAEMIA MAY IMPAIR
PHAGOCYTOSIS CHEMOTACTISM ADHERENCE BACTERICIDAL POWER OF LEUCOCYTES
LYMPHOCYTES B AND PLASMOCYTES ANTIBODIES SECRETION PLASMIC MEMBRANE INSULIN RECEPTORS
RESULTING IN PROLIFERATION OF BACTERIA SEPSIS NOSOCOMIAL INFECTIONS FULMINATING PNEUMOPATHIES
DIABETES SURGERY
INSULIN CONTROLLED SHORT AND/ORMINOR
LONG AND/ORMAJOR
EMERGENCY
NO
YES
NO
Oral antidiabeticdrugs maintainedexcept biguanides
IV insulin atconstant flow rate
IV INSULIN
AT CONSTANT
Blood glucosemonitoring
IV insulin atconstant flow rate
YES
YES
NO
SC insulin atusual dose
IV insulin atconstant flow rate
FLOW RATE
IV insulin atconstant flow rate
IV insulinrehydrat. acid
base status alter
In all cases, associated to 5 p cent Dextrose IV at constant flow rate 1.2 - 2.4 mg.kg-1.min-1 (125 ml.h for an adult).
NEW INSULIN PREPARATIONS HUMAN INSULIN
ANALOGONSET DURATION IMPROVEMENTS
LISPRO. B28 – LYS. B 29 –PRO
FASTEST15 – 30 min
HIGHER PEAK
SHORTER1 – 2 h.
Better control. HbA1 C level. Insulin resistance
GLARGINE. A – GLY ASP
. B 30 - ARG
SLOW120 min
NO PEAK
LONGER24 h.
Stability ofconcentrations less
hypoglycaemia
•Lispro insulin may be useful for insulin pump therapy •But no special interest demonstrated, at that time, by IV route during the operative
period Adsorption profile in both syringes and bags similar to human regular insulin
higher product concentration, faster flow rate prewash of the infusion tubing •Lispro, and especially glargine, constitue a progress for long term treatment
CLASS AGENTS ACTION SIDEEFFECTS
SULFONYLUREAS
. 1 st Generation
. 2 nd Generation
TolbutamineChlorpropamide
GlimepirideGliclazideGliburideGlipizide
Increase pancreaticrelease
Of endogenous insulineand insulin receptor
function
Hypoglycaemia
BIGUANIDES Metformine Improve insulin receptorfunction ?
Lactic acidosis
GLITAZONES. 1 st Generation
. 2 nd Generation
Troglitazone
RosiglitazonePioglitazoneDarglitazone
Stimulation of ppar-Ugamma receptor
(pancreas) sensitization oftarget cells to insulin
(reduction insulinoresist)
Liverdysfunction
(transaminases)
GLINIDES RepaglinideNateglinide
Rapid insulin secretion(early peak without
interglycaemia)ALPHA-
GLUCOSIDASEINHIBITORS
Acarbose Decreases GI digestionand absorption of
disaccharides
Diarrheaabdominal pain
subocclusionORAL HYPOGLYCAEMIC AGENTS
CONCLUSIONS
IN A DIABETIC PATIENT ANAESTHESIA TECHNIQUES MUST BE CHJOSEN ACCORDING TO AN EVENTUAL END ORGAN PATHOLOGY RATHER THAN METABOLIC INSIGHTS :
MAJOR IMPORTANCE OF THE PREOPERATIVE CONSULTATION
BLOOD GLUCOSE LEVELS MUST BE CONTROLLED BY STANDARDIZED PROTOCOLS :
EXCEPT IN FEW CASES, A REASONABLE LEVEL IS PREFERABLE TO A TIGHT CONTROL
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