diabetic and anesthesia

1. DIABETES MELLITUS AND
ANAESTHETIC IMPLICATIONS
DR RIZWAN ANSARI
FCPS
DEPARTMENT OF ANESTHESIOLOGY
CRITICAL CARE & PAIN MANAGEMENT BMC

2. TOPIC TO BE COVERED
1. INTRODUCTION
2. TYPES OF DIBETES MILLITUS
3. DIAGNOSTIC CRITERIA OF DM
4. PATHPHYSIOLOGY OF DM
5. COMPLICATIONS OF DIABETES MELLITUS
6. TREATMENT REGIMENS
7. PERIOPERATIVE MANAGEMENT OF DIABETES

3.  According to the International Diabetes
Federation, in 2022, 26.7% of adults in Pakistan
are affected by diabetes
 Studies have found that presence of
diabetes in surgical patients is associated
with a 50% increase in mortality and a
100% increase in the incidence of surgical
infections, MI and AKI.
INTRODUCTION

4. Diabetes mellitus is characterized
by hyperglycemia and glycosuria
arising from impairment of
carbohydrate metabolism due to
an absolute or relative deficiency
of insulin or of insulin
responsiveness.
DEFINATION

5.  Type 1 diabetes, the cause is an
absolute deficiency of insulin
secretion
 Type 2 diabetes, the cause is a
combination of resistance to insulin
action and an inadequate
compensatory insulin secretory
response.
TYPES OF DIABETES MILLITUS

6. DIAGNOSTIC CRITERIA
The diagnostic criteria for Type2 DM
ADA American Diabetic association: -
HbA1C value of 6.5% or higher. -
 A fasting plasma glucose level of 126 mg/dL (7.0
mmol/L) or higher. Fasting means no caloric intake for
at least 8 hours.
Oral Glucose Tolerance Test (OGTT): A 2-hour plasma
glucose level of 200 mg/dL (11.1 mmol/L) or higher
during a 75-g oral glucose tolerance test

7. WHO Diagnostic Criteria: -
Fasting Plasma Glucose level of 126
mg/dL (7.0 mmol/L) or higher.
 Random Plasma Glucose: A random
plasma glucose level of 200 mg/dL (11.1
mmol/L) or higher in the presence of
diabetes-related symptoms (polyuria,
polydipsia, weight loss)
Glycated haemoglobin (HbA1c) is a measure of long-
term glycaemic control, reflecting the level of
exposure of haemoglobin to plasma glucose in the
preceding 3–4 months.

8. Adults normally secrete approximately
50 units of insulin each day from the β
cells of the islets of Langerhans in the
pancreas
PATHOPHYSIOLOGY
The plasma half-life after endogenous
secretion from cells is about 4-6
minutes.
 INSULIN

9. INSULIN, THE MOST IMPORTANT ANABOLIC HORMONE AND ANTI CATBOLOIC
HARMONE
ACTION OF INSULIN

10. PATHOPHYSIOLOGY

11. COMPLICATIONS OF DIABETES
 ACUTE
 Diabetic ketoacidosis (DKA)/metabolic consequen
 Hypoglycaemia, the clinical signs of which
may be masked completely by anaesthesia
 Hyperosmolar COMA

12. CHRONIC COMPLICATION OF DIABETES MALLITIS

13. TYPES OF NEUROPATHY IN DM
Chronic sensory peripheral neuropathies
 Mononeuropathies
 Acute motor neuropathies
Diabetic Autonomic neuropathy
 Care in positioning patients in the operating theatre is
important.
Local anaesthetic nerve or plexus blocks should be
used with caution in patients with an acute
neuropathy, as neurological deficits may occur to the
local anaesthetic solution

15. TREATMENT REGIMENS
 NON-INSULIN GLUCOSE-LOWERING DRUGS
1. Sulphonylureas (e.g. glibenclamidean d gliclazide)
 insulin secretagogues relying on adequate β-cell function in the
pancreas. With a long half-life and partial renal excretion, they should
be avoided in the elderly and patients with inspired renal function.
2. Meglitinides (e.g. nateglinide)
 short-acting insulin secretagogues, similar to sulphonylureas. They
are rarely used because of frequent dosing requirements.
3. Intestinal α-glucosidase inhibitors (e.g. acarbose)
 inhibit monosaccharide absorption in the gut. Their use is limited by
GI adverse effects.

16. 5. Biguanides (e.g. metformin)
 Recommended by most guidelines as first-line treatment for type 2
diabetes.
 They act by a combination of decreasing gluconeogenesis, increasing
insulin sensitivity and reducing intestinal absorption of glucose.
 Metformin may be associated with the development of lactic acidosis,
though this is rare. Dosage should be reviewed in patients with reduced
renal function.
 Previous guidelines advised discontinuing metformin up to 48 h before
surgery. Current guidelines support its continued use in patients with
short fasting times and who are at low risk of AKI.

17. 6. Thiazolidinediones (e.g. pioglitazone)
 Increase cellular sensitivity to naturally released insulin. Their use is
reducing because of the associated risks of heart failure, bladder
cancer and bone fracture.
7. Glucagon-like peptide-1 (GLP-1)
 Analogues (e.g. dulaglutide) act to mimic the effect of incretin
hormones such as GLP-1.
 Incretin hormones are released by the upper GI tract in response to
glucose in the gut lumen increasing glucose-dependent insulin
secretion, reducing glucagon secretion and reducing gastric emptying.
They can be given as a weekly s.c. injection
8. Diepptidyl peptidase-4 (DPP-4) inhibitors (e.g. alogliptin
and linagliptin)
 Act by inhibiting the enzyme DPP-4 responsible for the inactivation of GLP-1.

19. INSULIN
Insulins in current use can be classified by:
Pharmakokinetic profile:
 speed of onset and duration of action (e.g. NovoRapid, 10-min
onset, or Levemir, 24-h duration of action);
Insulin type:
 human analogue, bovine or porcine
Formulation:
 single type or mixture, also described as biphasic (e.g. NovoMix).

20.  Once daily: used in patients with type 2 diabetes to supplement
their oral medication.
 Twice daily: a biphasic formulation injected at breakfast and
evening meal, commonly used in both type 1 and type 2
diabetes.
 Basal bolus: typically a long-acting insulin given at night with a
rapid-acting insulin given three times a day with meals.
 Continuous s.c. insulin infusion (CSII): a pump delivers an hourly
basal rate of a very rapid insulin analogue. The rate can be
adjusted in response to oral intake or CBG concentrations.
Further classification may be used when
considering the type of insulin administration
regime:

22. ANESTHETIC CONCERNS

23. PREOPERATIVE ASSESSMENT
CVS
 IHD (sometimes asymptomatic), cerebrovascular disease, MI and cardiomyopathy
are all associated with DM.
Autonomic neuropathy
 can lead to tachy- or bradycardia and postural hypotension.
Renal
 40% of diabetics develop microalbuminuria, which is associated with
hypertension, IHD and retinopathy. This may be reduced by treatment with ACE
inhibitors.
Respiratory
 Perioperative chest infections are more common, especially if other risk factors
such as smoking and obesity.
Airway
 Thickening of soft tissues (glycosylation) occurs, especially in ligaments around
joints, leading to limited joint mobility syndrome. Intubation may be difficult if
the neck is affected or there is insufficient mouth opening.
GI
50% of patients have delayed gastric emptying ± reflux.
Peripheral neuropathy is common; document any existing sensory loss if regional
technique planned

24.  Measure glycosylated Hb (HbA1c), a measure of recent glycaemic
control (normal 20–48mmol/mol, 4–6.5%).

 If capillary blood ketones are >3mmol/L or urinary ketones > +++,
cancel surgery.
 A preoperative chest radiograph is not routinely indicated in diabetic
patients.
 Diabetic patients have an increased incidence of ST-segment and T
segment abnormalities on preoperative electrocardiograms (ECGs).
Myocardial ischemia or old infarction may be evident on an ECG
despite a negative history.
INVESTIGATION
If blood glucose is >12mmol/L check
capillary blood ketones or urinary ketones.

25. INTRAOPERATIVE MANAGEMENT
For elective surgery, the aim should be
 Same-day admission
 Minimal fasting period
 Normoglycaemia (CBG 6–10mmol L –1 ) (110-180mg/dl)
 Minimal change to the patient's normal routine.
 For both type 1 and type 2 diabetic patients undergoing surgery
who are stable and expected to miss one meal only, glycaemic
control can be achieved by simple manipulation of their usual
medications

26.  Individuals with type 1 diabetes should NEVER go without insulin,
as they are at risk of diabetic ketoacidosis.
 Patients with a planned short starvation period (no more than
one missed meal in total) should be managed by modification of
their usual diabetes regime
 Patients expected to miss >1 meal should have a VRIII
 Consider an RSI if gastric stasis is suspected.
 Regional techniques may be useful for extremity surgery and to
reduce the risk of undetected hypoglycaemia.
 Autonomic dysfunction may exacerbate the hypotensive effect of
spinals and epidurals

27. For well-controlled patients Type 1
diabetes
Give SC rapid-acting insulin analogue.
Assume that 1 unit will drop blood glucose by
3mmol/L
 Recheck blood glucose hourly.
Type 2 diabetes:
Give 0.1 units/kg of SC rapid-acting insulin analogue,

30. Patients undergoing surgery with a long starvation period
(i.e. two or more missed meals)
 A number of glucose, K+ and insulin regimes have been described in the
past (e.g. Alberti regime
 But the VRIII is widely used and should be commenced on admission.
 If the patient is already on a long-acting insulin analogue, this should be
continued at 80% the usual dose, even if planning to use a VRIII through
the perioperative period.

31.  The term variable-rate intravenous insulin infusion (VRIII) is now used
to replace the previously used term sliding scale.
 There is increasing recognition of the iatrogenic complications
associated with the incorrect management of a VRIII in the
perioperative period.
 These include significant hypoglycaemia, hyperglycaemia,
hyponatraemia and hypokalaemia.
VARIABLE-RATE INTRAVENOUS INSULIN INFUSION
 The recommended 1st-choice solution for VRIII is 0.45% sodium
chloride with 5% glucose, and either 0.15% or 0.3% potassium
chloride (KCl)
 Glucose/insulin infusions should be administered through the
same cannula to prevent accidental administration of insulin
without glucose

33. Hypoglycaemia
 Blood glucose <4mmol/L is the main danger to diabetics perioperatively.
 Fasting, recent alcohol consumption, liver failure and septicaemia commonly exacerbate
this.
 Characteristic signs are tachycardia, light-headedness, sweating and pallor. This may
progress to confusion, restlessness, incomprehensible speech, double vision,
convulsions and coma. If untreated, permanent brain damage will occur, made worse by
hypotension and hypoxia.
 Anaesthetised patients may not show any of these signs. Monitor blood sugar
preoperatively and then hourly if stable, and suspect hypoglycaemia with unexplained
changes in the patient’s condition.
 If hypoglycaemia occurs, give 75mL of 20% glucose over 15min or 150mL of 10%
glucose, and repeat blood glucose after 15min.
 Alternatively, give 1mg of glucagon (IM or IV); 10–20g (2–4 teaspoons)
of sugar by mouth or an NGT is an alternative.

34.  Insulin-glucose infusion should be
continued till at least 2 hours after
the first meal. Blood sugar should
be monitored every 2 hourly and
normal insulin regime or oral
hypoglycemic agents can be started
with the first meal
POST-OPERATIVE PERIOD

35. DIABETIC KETOACIDOSIS
The diagnosis is based on
Presence of ketosis (ketonaemia
>3.0mmol L –1
 Ketonuria >2+ on urine testing sticks
CBG greater than 11.0mmol L –1 and
Acidaemia PH <7.3

36. The most common causes are
 Infection
 Missed insulin treatment
 First presentation of diabetes
 Surgical stress
 Prolong starvation

37. PATHOPHYSIOLOY OF DIABETIC KETOACIDOSIS
Due to the lack of insulin, glucose cannot
enter into cells, and the carbohydrate-based
metabolism is changed over to fat oxidation.
This is an extension of normal physiological
mechanisms that compensate for starvation.
Free fatty acids are produced in fat cells and
transported to the liver. In the liver, they are
broken down into acetate, then to ketoacids
(acetoacetate and beta-hydroxybutyrate).
The ketoacids are then exported from the
liver to peripheral tissues (notably brain and
muscle) where they can be oxidised.

38. MANAGEMENT OF A PATIENT WITH DKA
 FLUID REPLACEMENT AND INSULIN ADMINISTRATION
 0.9% saline with added potassium is used,
 Initially 1000ml given at 1000ml/h
 2000ml given at 500mlh reducing to 250mlh thereafter.
 Mandatory reassessment of cardiovascular status at 12 hours
 once blood glucose is less than 14 mmol/L, then 10% dextrose should be
commenced at 125 mL/hr and ran with the normal saline

39.  The latest guidelines for the management of DKA no longer
recommend the use of a sliding scale insulin
 A fixed rate insulin infusion is made by drawing up 50 units
of human soluble insulin (e.g. actrapid) and making it up to
50 mL with 0.9% sodium chloride. This is then run at 0.1
units/kg/hr until the ketone level is less than 0.6 mmol/
Goal
 Aim is to reduce blood ketones and suppress ketogenesis
Achieve a fall of ketones of at least 0.5 mmol/L/hr ° Get
resolution within 12–24 hours

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