ANAESTHESIA FOR PATIENT WITH DIABETES MELLITUS

DR. SHASHIKANT SHARMA
RESIDENT, UPUMS, SAIFAI, ETAWAH (U.P.)
ANAESTHESIA FOR
PATIENTS WITH
DIABETES MELLITUS

Diabetes mellitus comprises a group of metabolic
disorders that share the common phenotype of
hyperglycemia.
Common presenting symptoms of DM include
polyuria, polydipsia, weight loss, fatigue,
weakness, blurred vision, frequent superficial
infections and poor wound healing.

Type 1 DM
 Between 5% and 10% of all cases of diabetes
 Characterized by insulin deficiency and a tendency to develop ketosis.
 Usually diagnosed before the age of 40.
 Caused by T cell–mediated autoimmune destruction of beta cells in the
pancreas. The exact cause is unknown, although environmental triggers
such as viruses, dietary proteins or chemicals may initiate the autoimmune
process in genetically susceptible hosts.
 At least 80%–90% of beta cell function must be lost before hyperglycemia
occurs.

Type 2 DM
 Responsible for 90 % of all cases of DM.
 In the initial stages, an insensitivity to insulin on the part of peripheral
tissues leads to an increase in pancreatic insulin secretion to
maintain normal plasma glucose levels. As the disease progresses and
pancreatic cell function decreases, insulin levels are unable to
compensate and hyperglycemia occurs.
 Three important defects are seen in type 2 diabetes:
1. An increased rate of hepatic glucose release
2. Impaired basal and stimulated insulin secretion
3. Insulin resistance

o Criteria for the diagnosis of DM include one of the
following:
1. Fasting plasma glucose ≥126 mg/dl
2. Symptoms of diabetes plus a RBS concentration ≥200 mg/dl.
3. 2-h plasma glucose ≥200 mg/dl during a 75-g OGTT
4. HbA1c > 6.5%
o Two intermediate categories have also been
designated:
1. Impaired fasting glucose for a fasting plasma glucose level of 100–
125 mg/dl.
2. Impaired glucose tolerance (IGT) for plasma glucose levels of 140–
199 mg/dl 2 h after a 75-g oral glucose load.

METABOLIC SYNDROME
At least three of the following:
1. Fasting plasma glucose ≥ 110 mg/dl
2. Abdominal obesity (waist girth > 40 inch [men], 35 inch
[women])
3. Serum triglycerides ≥ 150mg/dl
4. Serum HDL cholesterol < 40 mg/dl (men), <50 (women)
5. BP ≥ 130/85 mm Hg


MANAGEMENT OF DIABETES
MELLITUS

Type of drug Mechanism Examples Advantages Disadvantage Contraindication
Biguanides Decrease Hepatic
glucose
production & insulin
resistance,
Anorexia
Metformin
phenformin
Weight loss Lactic
acidosis,
diarrhea,
nausea
Serum
creatinine
>1.5
mg/dl,CHF,
acidosis
Alpha
Glucosidase
Inhibitors
Reduce
Glucose
absorption
Acarbose,
Miglitol
Reduce
postprandial
glycemia
flatulence,
Deranged
LFT
Renal/liver disease
Dipeptidyl
peptidaseIV
inhibitors
Prolong endogenous
GLP-1 action
Sitagliptin Reduce dose with
renal
disease
Insulin
Secretagogues—
Sulfonylureas
increase Insulin
secretion
1 & 2 nd
generation
Lower fasting
bloodglucose
Hypoglycemia
weight
gain
Renal/liver disease
Insulin
Secretagogues—
Nonsulfonylureas
increase Insulin
secretion
Repaglinide
Nateglinide
Short onsetof
action,
lowers
postprandial
glucose
Hypoglycemia Renal/liver disease
Thiazolidinedione increase glucose
sensitivity
Pioglitazone Lower insulin
requirements
Peripheral
edema, CHF,
weight gain,
Congestive heart
failure,
liver disease

INSULIN THERAPY
 A long-acting insulin is usually prescribed with a short acting insulin to
mimic physiologic insulin release with meals.
 In general, patients with type 1 diabetes require 0.5–1 U/kg/day divided
into multiple doses, with approximately 50% given as basal insulin.
 Regular insulin is preferred over insulin analogues for IV infusions
because it is less expensive and equally effective.
 Hypoglycemia is the most frequent and dangerous complication of insulin
therapy.
 Repetitive episodes of hypoglycemia, especially at night, can result in
hypoglycemia unawareness, a condition in which the patient does not
respond with the appropriate autonomic warning symptoms before
neuroglycopenia.

COMPLICATIONS OF DIABETES
MELLITUS

Diabetic Ketoacidosis
 DKA is characterized by hyperglycemia (blood glucose 250 to 600
mg/dl), high anion gap metabolic acidosis (arterial pH ≤7.3) and
ketosis along with dehydration and electrolyte abnormalities.
 Prominent presenting symptoms include nausea, vomiting, abdominal
pain, labored breathing (Kussmaul’s respirations) and polyuria.
PATHOGENESIS
 Absolute lack of insulin causes increase in counter regulatory hormones
(cortisol, GH, catecholamines & glucagon), which promote lipolysis in
adipose tissue and release of free fatty acids (FFAs). In the liver, the FFAs
are converted to ketones.
 These patients suffer from a metabolic acidosis as a result of these
circulating ketoacids.
 Ketone bodies and hyperglycemia contribute to the osmotic diuresis.
 Although initial laboratory values are normal, but total body sodium and
potassium are depleted.

Hyperosmolar Hyperglycemic State
 Characterized by hyperglycemia (BG 600 to 1200 mg/dl),
hyperosmolarity (320 to 380 mOsm/L), dehydration and neurologic
sequelae.
 Insidious onset typically over weeks, patients experiencing polyuria,
polydipsia, weight loss and neurologic changes, including fatigue,
confusion or coma.
 Even in the absence of exogenous insulin, there is typically enough
intrinsic insulin production by beta cells to suppress hepatic lipoprotein
lipase and ketoacid production. As a result, HHS lacks the metabolic
acidosis prominent in DKA.
 Hyperglycemia is more, resulting in greater diuresis than DKA.
Resulting dehydration impairs renal function, decreasing glucose
excretion and worsening hyperglycemia.

DIAGNOSIS CRITERIA DKA HHS
Plasmaglucose (mg/dl) >250 >600
ph <7.3 >7.3
HCO3(mEq/l) <15 >15
Urine ketone +++ Small/-
Serum ketone +++ Small/-
Serum osmolality Variable >320 mosm/kg
Anion Gap >15 <15
Mental Status Alert, drowsy, stupor/coma Stupor/coma
Water deficit (ml/kg) 100 100-200
Sodium deficit (meq/kg) 7-10 5-13

ELECTROLYTE & BICARBONATE
MANAGMENT

Chronic Complications
PATHOGENESIS
Chronic hyperglycemia is essential for development of these changes. The
endothelial cells lining the blood vessels take in more glucose than normal
because they do not depend on insulin. They then form more surface
glycoproteins than normal & cause the basement membrane to grow
thicker and weaker.
 Microvascular complications are:
1. Diabetic nephropathy
2. Neuropathy
3. Retinopathy
 Macrovascular complications are:
1. Coronary artery disease
2. Peripheral Vascular disease
3. Cerebrovascular stroke

Diabetic Nephropathy
 Approximately 30%–40% of individuals with type 1 diabetes and 5%–
10% of those with type 2 diabetes develop end-stage renal disease.
Mechanism of injury:
1. Glomerular hyperfiltration
2. Increase in glomerular hydrostatic pressure causes glomerular damage
and microalbuminuria.
3. Impaired endothelium-dependent vasodilatation.
 The earliest sign is microalbuminuria (<300 mg/day)
 ACE inhibitors are particularly beneficial in diabetic patients because
they retard the progression of proteinuria and the decrease in GFR.

PERIPHERAL NEUROPATHY
 Mechanisms include local ischemia, tissue accumulation of sorbitol,
altered function of neuronal Na+/K+ ATPase pump activity and
immunologically mediated damage.
 A distal symmetric diffuse sensorimotor polyneuropathy is the MC
form.
 Sensory deficits usually overshadow motor abnormalities and appear in
the toes or feet and progress proximally toward the chest in a “stocking-
glove” distribution.
 Loss of large sensory and motor fibers produces loss of light touch and
proprioception as well as muscle weakness.
 Loss of small fibers decreases the perception of pain and temperature.
 Foot ulcers develop from mechanical and traumatic injury as a result of

RETINOPATHY
 Diabetic retinopathy findings includes Dot hemorrhages, hard
exudates, microaneurysms, retinal edema, Proliferative
retinopathy and retinal detachment.
 Visual impairment can range from minor changes in color vision to total
blindness.
 Strict glycemic control and blood pressure control can reduce the
risk of development and progression of retinopathy.

Autonomic Neuropathy
o Cardiovascular signs of autonomic neuropathy include abnormalities in
heart rate control as well as BP.
o A heart rate that fails to respond to exercise is indicative of significant
autonomic neuropathy and is likely to result in reduced exercise
tolerance.
o Silent ischemia may be present because of diabetic autonomic
Neuropathy

TESTS FOR DIABETIC AUTONOMIC
NEUROPATHY
• Early stage: abnormality of HR response during deep breathing
• Intermediate stage: abnormality of Valsalva response
• Late stage: presence of postural hypotension
• The test are valid marker of DAN if following factors ruled out.
1. End organ failure
2. Concomitant illness
3. Drungs: Diuretics, vasodilators, sympathatic blockers, vagolytics.

TEST FOR AUTONOMIC
NEUROPATHY
Heart rate variability (HRV) in response to:
1. Deep breathing
2. Standing
3. Valsalva maneuver
BP response to:
1. Standing or passive tilting
2. Sustained hand grip
3. Valsalva maneuver

Response to Valsalva maneuver
 Supine patient, connected to an ECG monitor, forcibly exhales for 15 s
against a fixed resistance (40 mmHg) with an open glottis. This results in a
sudden transient increase in intrathoracic and intra-abdominal pressures,
with a characteristic hemodynamic response.
 Phase I: Transient rise in BP and a fall in HR due to compression of
aorta and propulsion of blood into peripheral circulation. (mechanical
factors)
 Phase II: Initial fall in BP followed by recovery of BP later in the phase.
BP changes are accompanied by an increase in HR. (compensatory
mechanism)
 Phase III: Drop in BP and rise in HR when expiration stopped.
 Phase IV: Overshoot of BP above baseline value with reflex
bradycardia
 Valsalva ratio is calculated from the ECG waveform by dividing the
longest R-R interval after the maneuver (in phase IV) to the shortest R-R
interval during the maneuver. A Valsalva ratio < 1.2 is abnormal.

Heart Rate Variability (HRV)
 Respiratory sinus arrhythmia (RSA) is a normal phenomenon due to
vagal input to sinus node during expiration causing decreased HR.
 Clinical method is to ask the patient to breathe quietly and deeply at a
rate of six breaths per minute.
1. Normal variability > 15 beats /min
2. Abnormal result < 10 beats /min
 Aging is associated with decreased RSA due to decreased vagal tone
and decreased beta receptor responsiveness.
 Response to standing up (30: 15 ratio): There is a rapid increase in
HR in response to standing that is maximal at approximately the 15th
beat after standing. This is followed by a relative bradycardia that is
maximal at approximately the 30th beat after standing. (longest R-R
interval/ shorter R-R interval).
1. 30:15 ratio >1.04 is normal
2. 1.01 – 1.03 is borderline
3. < 1.01 is abnormal

 Orthostatic hypotension: It is defined as a fall in BP > 30 mmHg SBP
or >10 mmHg for DBP in response to postural change, from supine to
standing.
 Normally, BP is rapidly corrected by baroreflex-mediated peripheral
vasoconstriction and tachycardia.
1. Fall in SBP is < 10 mm Hg: Normal
2. Fall in SBP 11–29 mm Hg: borderline
3. Fall in SBP > 30 mm Hg is significant.
 Response to tilting: It is a more precise stimulus and may be used
instead of standing. The response is similar.
 Sustained hand grip: Sustained muscle contraction causes a rise in
SBP, DBP & HR. Exercising muscle stimulates a reflex arc resulting in
increased CO & HR.
 As the peripheral vascular resistance is maintained the diastolic
pressure rises by > 16 mm Hg normally.
 A response of < 10 mm Hg is considered abnormal.

GASTROPARESIS DIABETICORUM
 Diabetic autonomic neuropathy may also impair gastric secretion and
gastric motility, eventually causing gastroparesis diabeticorum in
approximately 25% of diabetic patients.
 Although it is often clinically silent, symptomatic patients will have
nausea, vomiting, early satiety, bloating and epigastric pain.
 Treatment of gastroparesis includes strict blood glucose control,
consumption of multiple small meals, reduction of the fat content of
meals.
 Diarrhea & Constipation both are also common among diabetic
patients and may be related to diabetic autonomic neuropathy.

Respiratory system
The underlying mechanisms include:
1. Impaired lung elasticity
2. Pulmonary microangiopathy
3. Chronic systemic inflammation of diabetes
Some of the reported lung dysfunctions attributed to diabetes are:
1. Decreased lung volume and lung diffusing capacity
2. Reduced hypoxic-induced ventilatory drive
3. Prone to respiratory depression from opioids and sedative agents
due to impaired chemoreceptor activity

Macrovascular Complications
 Cardiovascular disease is a major cause of morbidity and the
leading cause of mortality in diabetic individuals.
 Patients with poorly controlled diabetes demonstrate elevated
triglyceride levels, low levels of high-density lipoprotein
cholesterol, and an abnormally small, dense, more
atherogenic low-density lipoprotein cholesterol.
 Measures to prevent coronary artery disease include
maintaining lipid levels, glucose level, and blood pressure
within normal limits.

Stiff joint or limited joint mobility syndrome
 Manifests with joint rigidity. Joints
supporting the airway such as TMJ, A-O
and cervical spine joints are most
commonly involved. Neck extension and
laryngoscopy may be difficult.
 Cause: Nonenzymatic glycosylation of
proteins and abnormal cross-linking of
collagen in joints and other tissues, which
results in decreased elastic strength of
tissue.
 Prayer sign: Ability to oppose the palms
and fingers as in prayer. Diabetic patients
with stiff joints have a positive test as they
are unable to do this.

 Palm print test: Stiffness of the 4th
and 5th inter-phalangeal joints
causes alteration in palm print. The
palm and fingers of the dominant
hand of the patient is painted with
ink, Then the hand is firmly pressed
on a white sheet of paper on a hard
surface.
 Grade 0—All phalangeal areas
visible
 Grade 1—Deficiency in
interphalangeal areas of 4th
and/or 5th digit
 Grade 2—Deficiency in
interphalangeal areas of 2nd to 5th
digit
 Grade 3—Only the tips of digits
seen.

ANAESTHESIA MANAGEMENT
FOR DIABETES MELLITUS

Metabolic Consequences of Surgical Stress and
Anesthesia
 The stress of surgery and anesthesia alters the finely regulated balance
between hepatic glucose production and glucose utilization in peripheral
tissues.
 Cortisol increases hepatic glucose production, stimulates protein
catabolism and promotes gluconeogenesis, resulting in elevated
blood glucose levels.
 Catecholamine increase glucagon secretion and inhibit insulin release by
pancreatic β-cells.
 An increase in the secretion of catecholamines, cortisol, glucagon
and growth hormone occurs, which causes excessive release of
inflammatory cytokines.
 Increase in stress hormones also leads to enhanced lipolysis and high
free fatty acid (FFA) concentrations. Increased FFAs have been shown

 These processes result in a relative state of insulin resistance which is
most pronounced on the first postop day and may persist for 9-21 days
following surgery.
 Surgeries involving the thorax and abdomen are associated with a more
pronounced and prolonged duration of hyperglycemia when compared to
peripheral procedures.
 Laparoscopic procedures demonstrate a decreased incidence of insulin
resistance and hyperglycemia as compare to open procedures.
 GA is more frequently associated with hyperglycemia and higher levels of
catecholamines, cortisol and glucagon than regional anesthesia.

PREOP INVESTIGATION
1. Hb: to rule out anemia secondary to renal dysfunction
2. TLC: to rule out acute infective pathology
3. Urine routine: for albumin
4. Serum creatinine: To detect renal dysfunction.
5. Fasting and postprandial blood sugar: To assess quality of control
6. Glycosylated Hb: HbA1c <7% implies good blood sugar control over
the preceeding 8–12 weeks.
7. Serum electrolytes: To detect abnormalities in patients with history of
vomiting, diarrhea, poor oral intake or tube feeding, intestinal
obstruction, etc. Also in patients on insulin, ACE inhibitors, diuretics and
with renal dysfunction
8. ECG: To detect asymptomatic myocardial ischemia
9. X-ray chest: Tuberculosis is common in diabetics due to impaired
immunity
10. Morning of surgery investigations: Serum electrolytes, FBS, urine
ketones

PREOP. ADVICE FOR PATIENTS ON
OHGs

Shift To Insulin
• No need to shift to insulin in case of well controlled type 2 DM on OHGs,
minor surgery.
Indications of shift to insulin preoperatively
1. Poorly controlled type 2 DM
2. Well controlled type 2 DM for major surgery
3. Type 1 DM having minor surgery or major surgery
• Diet controlled type 2 DM - treat as non-diabetic, Monitor blood sugar
during surgery (hourly), treat if increased.

PREOP. ADVICE FOR PATIENTS ON
INSULIN
 Patients who take both evening and morning doses of insulin should
take their usual dose of evening short-acting insulin, but reduce their
long acting dose by 20% the night before surgery.
 On the morning of surgery, they should omit their short-acting
insulin and reduce long-acting dose by 50% (take this only if the fasting
glucose is >120 mg/dl).
 Premixed insulin → reduce their evening dose prior surgery by
20% and hold insulin completely on the morning of procedure.

 Listing: Diabetic patients should be placed first on the operating list.
This shortens their preoperative fast and the risk of hypoglycemia and
ketosis.
 Fasting: Delayed gastric emptying due to gastroparesis diabeticorum.
Gastroparesis may prolong retention of food in the stomach thereby
increasing the risk of regurgitation & aspiration.
 IV fluids:
1. Ringer’s lactate: Lactate undergoes gluconeogenesis in the liver
and may complicate blood sugar control. Can be used safely with
with monitoring of blood sugar.
2. Normal saline infusions in large volumes increase risk of
hyperchloremic acidosis. Thus, there is no ideal solution and
either solution may be used judiciously.
 Frequent blood glucose measurement is essential in the anesthetized
patient as the requirements for glucose and insulin in this period are
unpredictable and hypoglycemia may go undetected.
 Standard monitoring instituted are ECG, SpO2, BP, ETCO2 and
temperature.

GENERAL ANAESTHESIA
ADVANTAGES
1. High dose opiate technique may be useful to block the entire
sympathetic nervous system and the hypothalamic pituitary axis.
2. Better control of blood pressure in patients with autonomic
neuropathy.
DISADVANTAGES
1. May have difficult airway. (“Stiff-joint syndrome”)
2. Full stomach due to gastroparesis.
3. Controlled ventilation is needed as patients with autonomic neuropathy
may have impaired ventilatory control.
4. Aggravated haemodynamic response to intubation.
5. It may masks the symptoms of hypoglycaemia.

REGIONAL ANAESTHESIA
ADVANTAGES
1. Regional anaesthesia blunts the increases in catecholamines,
cortisol, glucagon and glucose.
2. Metabolic effects of anaesthetic agents avoided
3. An awake patient – hypoglycaemia readily detectable.
4. Decreased chance of Aspiration, PONV.
5. Rapid return to diet and OHA
DISADVANTAGES
1. If autonomic neuropathy is present, profound hypotension may occur.
2. Infections and vascular complications may be increased.
3. Medicolegal concern of risk of nerve injuries and higher risk of
ischaemic injury due to use of adrenaline with LA

PHARMACOLOGY
1. Propofol: lipid loading lead to impaired metobolism in DM, decreased
lipid clearance. Its of more concern when given in infusion.
2. Etomidate: decreases adrenal steroidogenesis decreased glycaemic
response to surgery.
3. Ketamine: causes significant hyperglycemia due to sympathetic
stimulation
4. Midazolam: decreases ACTH & Cortisol, decreased sympathoadrenal
stimulation, decreased glycemic response to surgery.
5. Alpha-2 adrenergic agonist: decreases sympathetic outflow from
hypothalamus, decreases ACTH. improves glycemic control.
6. Opioids: offers haemodynamics & metabolic stability. Blocks sympathetic
nervous system & hypothalamo-pituitary axis.
7. Volatile agents (halothane, isoflurane): inhibit glucose stimulated insulin
secretion in a dose dependent manner
8. Dexamethasone: reduce PONV, but increases blood sugar
9. NSAIDs: Aggravate gastritis & renal dysfunction

INTRAOPERATIVE MANAGMENT
 GI-infusion should be initiated at least 2 hours before surgery, only after
taking sample for FBS.
 Intraoperative serum glucose levels should be maintained between 120
and 180 mg/dl.
 1 unit insulin lowers BG 25-30mg/dl. Insulin infusion prepared by mixing
100 U regular insulin in 100 ml NS (1 U/ml)
 Initial hourly rate for continuous insulin infusion by dividing the total daily
insulin requirement by 24. A typical rate is 0.02 unit/kg/h.
 An insulin infusion should be accompanied by an infusion of 5% dextrose
in half-normal saline with 20 mEq KCl at 100–150 ml/h to provide enough
carbohydrate to inhibit hepatic glucose production and protein catabolism.
 Serum glucose levels should be monitored at least every hour and even
every 30 minutes in patients with high insulin requirements.

Prof. A. K. Sethi’s
EORCAPS-2016
Adsorption of Insulin
 Significant amounts of insulin adsorbed on to giving sets: high‐volume,
low‐insulin conc regimen used
 Reducing initial rates of insulin delivery
 In solution with conc of insulin of ∼10 U/L, this effect is minimal
Strategies to minimize:
1. use low concentrated solutions
2. use smaller containers
3. use shorter tubings
4. prime tubing with insulinized sol
5. add whole blood/human albumin

Different insulin regimen use to control B. sugar
1. Variable rate intravenous insulin infusion (VRIII)
2. In patient insulin algorithm
3. Tight control regimen
4. Vellore regimen
5. Alberti’s regimen
6. Sliding scale

GUIDELINES FOR GLYCEMIC TARGETS
o Society for Ambulatory Anesthesia recommends intraoperative blood
glucose levels <180 mg/dl.
o American Diabetes Association (ADA) recommend target glucose levels
between 140 and 180 mg/dl in critically ill patients & in non-ICU settings,
recommended a target fasting glucose of <140 mg/dl and a RBS of <180
mg/dl for patients treated with insulin.
o Society of Critical Care Medicine (SCCM) advises treatment be triggered
at blood glucose levels ≥150 mg/dl with a goal to maintain blood glucose
below that level and absolutely below 180 mg/dl.
o Society of Thoracic Surgeons Practice Guidelines recommend
maintaining serum glucose levels ≤ 180 mg/dl for at least 24 hours after
cardiac surgery.
o American College of Physicians target blood glucose range is 140-200

Inpatient Insulin Algorithm
• Algorithm 2: Start if pt requires higher insulin or receiving >80 U/d insulin as
outpatient, Moving up: algorithm failure, defined as BG outside goal range for 2
hrs & level does not change by at least 60 mg/dl within 1 hr, Moving down:
When BG is < 70 mg/dl for two checks OR if BG decreases by > 100 mg/dl in
an hr. Pt monitoring: Check BG every hr until it is within goal range for 4 hr,
then every 2 hr for 4 hr, & if it remains at goal, may decrease to every 4 hr,

 Avoidance of hypoglycemia is especially critical, since
recognition of hypoglycemia may be delayed in patients
receiving anesthetics, sedatives, analgesics, β-blockers and in
those with autonomic neuropathy.
TREATMENT OF HYPOGLYCEMIA (BG < 60 mg/dl)
 Discontinue insulin drip and Give D50W IV
 Patient conscious: 25 ml
 Patient unconscious: 50 ml
 Recheck BG every 20 min and repeat 25 min of D50W IV if <60
mg/dl
 Restart drip once BG is >70 mg/dl for two checks. Restart drip
with lower algorithm

VARIABLE RATE INTRAVENOUS INSULIN
INFUSION(VRIII)
 Make up a 50 ml syringe with 50 units of human insulin in
49.5mls of 0.9% NS. This makes concentration of insulin 1 unit
per ml.
 The substrate solution to be used alongside the VRIII should be
selected from 0.45% saline with 5% glucose and 20 mEq KCl.
 The rate of fluid replacement must be set to deliver the
hourly fluid requirements of the Individual.
 Delivery of the substrate solution and the VRIII must be via a
single cannula with appropriate one-way and anti-siphon
valves .

RATE OF INSULIN INFUSION
Bedside capillary glucose (mmol/L) Initial rate of insulin infusion
(units/hour)
<4 (<72 mg/dl) 0.5
4.1-7 (73 – 126 mg/dl) 1
7.1-9.0 (127 – 162 mg/dl) 2
9.1-11.0 (163 – 198 mg/dl) 3
11.1-14.0 (199 – 252 mg/dl) 4
14.1-17.0 (253 – 306 mg/dl) 5
17.1-20 (307 – 360 mg/dl) 6
>20 (>361 mg/dl) Seek diabetes term of medical advice

Vellore Regimen
 On day of surgery, OHA & insulin omitted, all pts BG measured at 6
AM. Insulin 5 U in 500 ml 5%D started in ward at 8 AM using measured
volume set @100 ml/hr.
 Intraop BG control with 1 U of insulin for every 1–50 mg of BG value
>100 mg/dl added to 100 ml of 5% D in a measured volume set.
 Hourly monitoring of BG till pts leave PACU. Simple & effective method
, combines advantages of combined glucose insulin & variable rate
insulin infusion. Most operative pts can be maintained in 120-180 mg/dl
range with insulin infusion rate 1 - 2 U/h.
 S. potassium measured during major surgery, supplementation given if
level <3.5 mEq/l.

Prof. A. K. Sethi’s
EORCAPS-2016
Vellore Regimen

TIGHT CONTROL REGIMEN
 Target Blood Sugar is 80-110 mg/dl.
Indications: Pregnancy, Cardiothoracic surgery, Neurosurgery.
Advantages:
1. Improve wound Healing
2. Prevent wound infection
3. Improve neurological outcome.
 Dissolve 50 U of insulin in 250 ml of NS and start infusion.
 Insulin infusion rate is adjusted by BG/150 U/hr (BG/100 U/hr if
pt is obese or on steroid or in sepsis).
RISK:
1. Hypoglycemia
2. Difficult in ward settings
3. Meticulous frequent monitoring

Blood
Sugar
(mg/dl)
(D10
+insulin +
K)
≤90 10+5+10
90-180 10+10+10
180-360 10+15+10
≥360 10+20+10
ALBERTI’S OR GKI REGIMEN
• Omit morning dose of insulin
• Start GKI after checking BS & K level
@100-125 ml/hr on morning of
surgery.
• 2-3 hourly blood sugar level charting
Advantages: simple & safe
Disadvantages:
1. fixed insulin concentration
2. Necessary change bag each time
3. Water load
4. Hyponatremia
5. Hyperglycemia

SLIDING SCALE S/C
Glucose in mg/dl Regular Insulin S/C
150-200 2 unit
201-250 4 unit
251-300 6 unit
301-350 8 unit
≥350 10 unit

THE POST-OPERATIVE PERIOD
 GI infusions should be continued until the patients can resume an
adequate diet.
 Currently the ADA recommends that glucose levels be maintained
between 140 and 180 mg/dl in critically ill patients and that insulin
treatment be initiated if serum glucose levels exceed 180 mg/dl.
 GI infusions should ideally be stopped after breakfast and a dose of
subcutaneous insulin/OHGs is given.
 Hyperglycemia detected post-operatively in patients not previously
known to have diabetes should be managed as if diabetes was present,
and the diagnosis of diabetes reconsidered once the patient has
recovered from their surgery.
 Diabetes medication requirements may be increased in the post-
operative period, and frequent BG monitoring is therefore essential.

SURGERY
 Little time for stabilisation of patients, but if 2-3 hr available
1. correction of fluid and electrolyte imbalance .
2. Correct hyperglycemia. (start GI infusion if sugar > 180mg/dl)
3. Treat acidosis.
4. Avoid hypoglycemia.
 Surgery should not be delayed in an attempt to eliminate ketoacidosis
completely if the underlying condition will lead to further metabolic
deterioration.
 Insulin therapy is initiated with a 10-unit intravenous bolus of regular
insulin, followed by continuous insulin infusion.
 The rate of infusion is determined most easily if one divides the last
serum glucose value by 150 (or 100 if the patient is receiving steroids,
has an infection, or is having BMI ≥35).

 Initially, normal saline solution is infused at a rate of 250 to 1000
ml/hour, depending on the degree of intravascular volume depletion.
 During the first 1 to 2 hours of fluid resuscitation, glucose level may
decrease more precipitously. When serum glucose reaches 250 mg/dl,
IV fluid should include 5% dextrose.
 Acidosis with an increased anion gap (≥16 mEq/L) in an acutely ill
diabetic patient may be caused by ketones in ketoacidosis, lactic acid in
lactic acidosis, increased organic acids from renal insufficiency, or all
three disorders.
 Persistent ketosis with a serum bicarbonate level less than 20 mEq/L in
the presence of a normal glucose concentration is an indication of the
continued need for intracellular glucose & insulin for reversal of lipolysis.

DIABETES IN PREGNANCY
 Gestational diabetes mellitus (GDM) is defined as any
presence of glucose intolerance with onset or first
recognition during pregnancy.
 Diabetes mellitus (DM) is the most common medical
complication of pregnancy, 4-5% of pregnancies are
complicated by diabetes & In 90% of diabetic pregnancies
the cause is GDM.

Pathophysiology of GDM
 The physiological changes of pregnancy are aimed to provide adequate
nutrients to the growing fetus. In early pregnancy, maternal estrogen and
progesterone increase and promote pancreatic ß-cell hyperplasia &
increased insulin release.
 Increases in peripheral glucose utilization and glycogen storage with a
concomitant reduction in hepatic glucose production result in lower
maternal fasting glucose levels.
 As pregnancy progresses, increased levels of HCG, cortisol, prolactin,
progesterone & estrogen lead to insulin resistance in peripheral tissues.
Cortisol has the highest diabetogenic potency and has peak effect at 26
weeks gestation.
 The pancreas releases 1.5–2.5 times more insulin in order to respond to
insulin resistance. GDM results when there is delayed or insufficient
insulin secretion in the presence of increasing peripheral resistance

Diagnosis and Screening
Risk factors for gestational diabetes:
1. Body mass index above 30 kg/m2
2. Previous macrosomic baby weighing 4.5 kg or above
3. Previous gestational diabetes
4. Family history of diabetes
5. Ethnicity: South Asian, Middle Eastern
 Classic symptoms are polydipsia, polyuria, and weight loss. Clinical
signs include hyperglycemia, persistent glycosuria & ketoacidosis.
 Universal screening for GDM is standard for patient with history of DM,
clinical risk factors or clinical features.
 Testing is typically performed at 24 to 28 weeks, but if strong risk factors
such as obesity, family history, or a personal history of GDM are present,
screening can be performed at the first visit.

American Diabetes
Association criteria
 Test is Performed after NPO
of 8 hrs.
 100 gm oral glucose given
and then plasma glucose
measurement done at 1, 2 & 3
hrs.
TIME SINCE 100
GM GLUCOSE
LOAD (hr)
CARPENTER &
COUSTON SCALE
Plasma glucose
(mg/dl)
Fasting >95
1 >180
2 >156
3 >140

DIPSI criteria
“Diabetes in Pregnancy
Study Group India”
 single step procedure, applicable
in Indian scenario as Indian
women have an eleven fold
increased risk of developing
glucose intolerance during
pregnancy.
 Single step procedure
irrespective of the last meal.
Pregnant women attending the
antenatal OPD are given 75g
anhydrous glucose in 250-300ml
of water and plasma glucose will
be estimated after 2 hour.
CRITERIA IN
PREGNAN
CY
OUTSIDE
PREGNAN
CY
2 hrs > 200
mg/dl
Diabetes
mellitus
Diabetes
mellitus
2 hrs >140
mg/dl
GDM IGT
2 hrs > 120
mg/dl
DGGT

Maternal Complications of DM
1. Diabetic ketoacidosis (DKA) is a potentially life-threatening metabolic
emergency for both mother and fetus. In pregnant patients, DKA can
occur at lower blood glucose levels (i.e., <200 mg/dl) and more rapidly
than in nonpregnant diabetics. Antenatal steroids for fetal lung maturity
and beta adrenergic tocolytics can precipitate or exacerbate DKA in
pregestational diabetics.
2. Hypoglycemia that is serious enough to require hospitalization may
occur in up to 45% of mothers with type 1 DM.
3. Preeclampsia is two to four times more common in pregestational
diabetics.
4. Preterm labor and delivery may be three to four times higher in
patients with DM
5. Rapid progression of microvascular and atherosclerotic disease can
occur in pregnant diabetics.
6. Diabetic Nephropathy

Fetal Complications of DM
1. Spontaneous abortion
2. Polyhydramnios
3. Macrosomia
4. Shoulder dystocia
5. Neonatal hypocalcemia and hypomagnesemia
6. Increased chances of Diabetes in future
7. Congenital malformations

GDM Management
 Management for GDM initially consists of diet and exercise. Moderate
exercise can improve glycemic control in GDM. Patients are encouraged
to maintain a consistent level of activity throughout pregnancy provided
there are no complications.
 Women with newly diagnosed GDM are started on a diabetic diet of
1,800 to 2,400 kcal/day.
 Oral hypoglycemic agents are acceptable GDM management when
dietary efforts fail. Metformin & 2nd generation sulphonylureas can be
safely given.
 Insulin therapy can improve glycemic control for GDM.
 In preterm labor, steroids can be given for fetal lung maturation but the
insulin dose may need to be modified. Beta-mimetic drugs should be
avoided for tocolysis.

CARE OF BABY
 The major concern is hypoglycemia. Babies should be fed a soon as
possible within 30 minutes and at 2–3 hours interval thereafter.
 The prefeed blood sugar should be above 36 mg%. Babies with low
blood sugars or clinical signs of hypoglycemia should receive tube feeds
or IV dextrose.
 Blood glucose testing should be carried out at 2–4 hours after birth.
Babies should be kept in hospital for at least 24 hours to ensure
adequate feeding and absence of hypoglycemia.
 Blood tests for polycythemia, hyperbilirubinemia, hypocalcaemia and
hypomagnesaemia.

POST-PARTUM CARE
 Women with gestational diabetes should discontinue hypoglycemic
treatment immediately after birth. However, they need blood sugar
examination at 6 weeks and annually thereafter.
 Metformin and glibenclamide can be given to lactating women with
preexisting type 2 diabetes. First generation sulfonylurea are secreted in
milk and should be avoided.
 Insulin dose should be reduced and blood sugar monitored frequently to
achieve optimum control.
 Women are at risk of hypoglycemia postnatally especially during
breastfeeding and should be advised to have a meal or snack before or
during feeds.

ANAESTHESIA FOR PATIENT WITH DIABETES MELLITUS

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