Anesthesia consideration for diabetes mellitus

1. DIABETES MELLITUS
Dr. Ibrahim Elkathiri

2. THE PANCREAS
 Adults normally secrete approximately 50
units of insulin each day from the β cells
 facilitating glucose and potassium entry into
adipose and muscle cells;
 Increasing glycogen, protein, and fatty acid
synthesis;
 decreasing glycogenolysis, gluconeogenesis,
ketogenesis, lipolysis, and protein
catabolism.

3. EFFECTS ON LIVER
 Anabolic
 Promotes glycogenesis
 Increases synthesis of triglycerides, cholesterol,
and VLDL1
 Increases protein synthesis
 Promotes glycolysis
 Anticatabolic
 Inhibits glycogenolysis
 Inhibits ketogenesis
 Inhibits gluconeogenesis

4. EFFECTS ON MUSCLE
 Anabolic
 Increases amino acid transport
 Increases protein synthesis
 Anticatabolic
 Increases glucose transport
 Enhances activity of glycogen synthetase
 Inhibits activity of glycogen phosphorylase

5. EFFECTS ON FAT
 Promotes triglyceride storage
 Induces lipoprotein lipase, making fatty acids
available for absorption into fat cells
 Increases glucose transport into fat cells,
thus increasing availability of α-glycerol
phosphate for triglyceride synthesis
 Inhibits intracellular lipolysis

6. DIABETES MELLITUS

7. DEFINITION
 syndrome of abnormal carbohydrate
metabolism that is characterized by
hyperglycemia and glycosuria

8. CLASSIFICATION
 type 1(IDDM) insulin-requiring
 Absolute deficiency of insulin
 May be autoimmune based
 Management requires exogenous insulin
 Patients are prone to ketosis

9.  type 2 (NIDDM) insulin resistant:
 Relative deficiency of insulin/peripheral
resistance to insulin/excessive hepatic glucose
release
 Generally seen in obese adults
 Patients produce adequate amounts of insulin to
prevent ketosis but are at risk for hyperosmolar
state
 Initially managed with diet control, weight loss,
and oral hypoglycemic agents

10.  gestetional
 secondary: Pancreatic disease (decreased
insulin production)
 Drug induced
 Secondary to endocrinopathies such as
Cushing’s disease, acromegaly,
pheochromocytoma

11. DIAGNOSIS
 According to American Diabetes
Association:
1. Fasting (8hr) plasma glucose value 126
mg/dl
2. Symptoms of D.M :polydipsia, polyuria and
unexplained weight loss.
3. Random blood glucose value 200mg/dl
4. 2hr post oral glucose challenge value
200mg/dl

12. COMPLICATIONS
 There are three life-threatening acute
complications of diabetes and its treatment
 diabetic ketoacidosis (DKA),
 hyperosmolar nonketotic coma,
 and hypoglycemia

13. CHRONIC EFFECTS OF HYPERGLYCAEMIA
 Microvascular Proliferative retinopathy Diabetic nephropathy (close
association with hypertension, which is found in 30-60% of diabetics)
 Macrovascular
1. Atherosclerosis
2. Coronary heart disease (beware silent ischaemia, cardiomyopathy)
3. Cerebrovascular disease
4. Peripheral vascular disease
 Neuropathic
1. Peripheral : Motor (Mononeuropathies, pressure palsies). Sensory
polyneuropathy
2. Autonomic:
 Diarrhea / Urinary incontinence / Postural hypotension / Cardiac
denervation / Impaired ventilatory control – risk of resp arrest with
anaesthesia/ Gastroparesis
 “Stiff joint syndrome” (airway)
 Increased incidence of infections

15. ACUTE EFFECTS OF HYPERGLYCAEMIA
 Dehydration and electrolyte disturbances (due
to osmotic diuresis)
 Acidaemia (accumulation of lactic + ketoacids)
 Fatigue, weight loss and muscle wasting
(lipolysis and proteolysis in absolute insulin
deficiency)
 Poor wound healing and impaired wound
strength
 Diabetic ketoacidotic coma (Type I diabetics due
to absolute insulin deficiency)
 Hyperosmolar Non-ketotic coma (Type II

16. DIABETIC KETOACIDOSIS
 Mainly in type 1 IDDM
 Decreased insulin activity allows the
catabolism of free fatty acids into ketone
bodies (acetoacetate and β-
hydroxybutyrate), some of which are weak
acids .
 Accumulation of these organic acids results
in DKA and an anion-gap metabolic acidosis.

17. DKA characterized by
• hyperglycemia
• dehydration
• hyperosmolarity
• high anion-gap metabolic acidosis

18. TREATMENT OF DKA
 Identifying and treating the precipitating
factors
 Fluid resuscitation
 Glycometabolic control
 Electrolyte replacement

19. The goal for decreasing blood glucose in
Ketoacidosis should be 75–100 mg/dL/h or
10%/h.
Therapy generally begins with an intravenous
insulin infusion at 0.1 units/kg/h.
Several liters of 0.9% saline (1–2 L the first
hour,
followed by 200–500 mL/h) may be required to
correct dehydration in adult patients.

20. When plasma glucose decreases to 250 mg/dL, an infusion of D 5
W
should be added to the insulin infusion to decrease the possibility of
hypoglycemia and to provide a continuous source of glucose (with
the
infused insulin) for eventual normalization of intracellular
metabolism.
Patients may benefit from precise monitoring of urinary output during
initial treatment of DKA.
Bicarbonate is rarely needed to correct severe acidosis (pH < 7.1)
as the acidosis corrects with volume expansion and with
normalization of the plasma glucose concentration.

21. GUIDELINES FOR DKA MANAGEMENT
1. Routine monitoring, arterial access, central venous
line
2. Aggressive crystalloid replacement 1-3 L in the first
hour, with 0.9 saline.
3. Intravenous insulin titrated by serial plasma glucose
determinations adding dextrose infusion as glucose
values 200mg/dl
4. Supplementation of potassium, phosphrus and
magnesium as guided by serial plasma determination.

22. HYPEROSMOLAR NONKETOTIC STATE
-Occur predominantly in type 2 DM
-Comparing with DKA ,NKHS patients are
typically more dehydrated, hyperosmolar and
hyperglycemic.
-Ketoacidosis is not a feature of hyperosmolar
nonketotic coma possibly because enough
insulin is available to prevent ketone body
formation.

23. NKHS CHARACTERIZED BY
 Neurologic alterations : may include confusion ,
coma ,
seizures and/or focal neurological deficits.
 Severe dehydration with significant hypotension
leading to lactic acidosis
(NKHS patients lack acidemia due to ketone bodies)
 Thrombotic events due to hypovolumia, hypotension
and hyperviscosity.
 Hyperosmolality (frequently exceeding 360 mOsm/L)
induces dehydration of neurons, causing changes in
mental status and seizures.

24. NKHS MANAGEMENT
 Fluid resuscitation is the mainstay of
treatment (0.9 saline)
 Due to greater hyperglycemia and
hyperosmolarity in NKHS, these pateints are
at increased risk of developing cerebral
edema
 so more gradual (>24hr) correction of
hyperglycemia and hyperosmolarity is
recommended along with frequent neurologic
evaluations.

25. HYPOGLYCEMIA
 hypoglycemia is present when plasma glucose
is less than 50 mg/dL.
Hypoglycemia in the diabetic patient is the result
of an absolute or relative excess of insulin
relative to carbohydrate intake and exercise.
Causes of hypoglycemia:
-residual effects of long acting drugs
-overaggressive antidiabetic treatment
-decreased caloric intake

26. DIAGNOSIS OF HYPOGLYCEMIA
 Two major ways to detect hypoglycemia:
-altered mental status up to coma and death.
-physiologic responses to increased
catecholamines
But the ability to recognize these manifestions
during perioperative period and under
anesthesia , is compromized
 Detection of hypoglycemia under anesthesia
requires high index of suspicion and frequent
determination of plasma glucose levels.

27. TREATMENT
Diabetic patients are incompletely able to counter hypoglycemia
despite secreting glucagon or epinephrine (counterregulatory
failure).
Treatment Consists of :
-Dextrose adminstration
-Correcting the precipitating causes
The treatment of hypoglycemia in anesthetized or critically ill
patients
Intravenous administration of 50% glucose (each milliliter
of 50% glucose will raise the blood glucose of a 70-kg patient by
approximately 2 mg/dL).
Awake patients can be treated orally with fluids containing glucose
or sucrose.

28. ANESTHETIC MANAGEMENT
Anesthetic management should include:
-preoperative
-intraoperative
-postoperative
-Perioperative hyperglycemia
-Perioperative hypoglycemia

29. PERI-OPERATIVE GOAL
maintaining blood glucose values below 180
mg/dl during the perioperative period while
reducing blood glucose variability and
avoiding hypoglycemia.

30. PERI-OP PROBLEMS
 Stress response to surgery with catabolic hormone
secretion
 Interruption of food intake, pre- and perhaps
postsurgery (also PONV)
 Altered consciousness, masking the symptoms of
hypoglycaemia
 Circulatory disturbance that may alter the uptake of
s.c. insulin
 The altered physiological state resulting from end
organ pathology

31. PREOPERATIVE MANAGEMENT
-Preoperative evaluation should include a thorough history
and physical exam .
-Prior anesthetic records should be reviewed to determine
whether difficulties with intubation or perioperative
diabetic complications were documented previously.
-Laboratory investigations should include determination of
blood
glucose, potassium, blood urea nitrogen (BUN), and
creatinine in
addition to a urinalysis for glucose, ketones, and protein.
-Glycosylated hemoglobin (HbA1c) levels reflect the
adequacy of glucose control over the preceding 1–3
months.

32. -Hemoglobin A 1c
Abnormally elevated hemoglobin A 1c
concentrations identify patients who have
maintained poor control of blood glucose over
time. These patients may be at greater risk for
perioperative hyperglycemia, perioperative
complications, and adverse outcomes.
-The perioperative morbidity of diabetic patients is
related to their preexisting end-organ damage.

33. -ECG
Myocardial ischemia or old infarction may be
evident on an ECG despite a negative
history.
-chest radiograph
cardiac enlargement,pulmonary vascular
congestion, or pleural effusion, but is not
routinely indicated.

34. Premedication with a nonparticulate antacid
and metoclopramide is often used in an
obese diabetic patient with signs of cardiac
autonomic dysfunction.

35. TYPE I DIABETES
Preoperative Insulin Traditional Approach
 Give 1/4 to 1/2 the daily dose of intermediate
acting insulin subcutaneously
 Add 1/2 unit of intermediate-acting insulin for
each unit of insulin prescribed
 Start IV glucose 5-10 g/h
not recommend because it is not terribly effective

36. PREOPERATIVE INSULIN CONTINUOUS IV
INFUSION
• These patients should all be treated on I.v. insulin infusion
before, during and after surgery.
• This is true for major surgery, although there are some
alternatives in minor surgery
• Place 50 U. Regular Insulin in 1000 ml NS.
• Give 10 ml/h
• Measure blood glucose q.h.
• Adjust infusion rate to keep glucose level at 120-180 mg/dl
• Turn infusion off for 30 min if glucose level falls below 100
mg/dl
• Provide sufficient glucose (5-10g/h) and potassium (2-4
mEq/h)

38. NEW INSULIN DELIVERY MODES
1. Continuous subcutaneous infusions
2. Continuous intra-peritoneal infusions

39. TYPE II DIABETES ON DIET ALONE
 If fasting blood glucose < 7.8 mmol/l or
140.4
mg/dl
 Close observation including hourly dextrose
measurement (glucometer in theatre)
 Conversion to a GIK regime if the glucose
rises
>8.0 mmol/l or 144 mg/dl

40. If the patient is taking an oral hypoglycemic agent
preoperatively rather than insulin, the drug can be
continued until the day of surgery.
Sulfonylureas and metformin have long halflives and
many clinicians will discontinue them 24–48 h before
surgery. They can be started postoperatively when the
patient resumes oral intake.
Metformin is restarted if renal and hepatic function
remain adequate.

41. TYPE II DIABETES ON ORAL HYPOGLYCAEMIC
There are 4 groups of oral hypoglycaemic agents (OHA)
• Sulphonylureas
Enhanced secretion of insulin in response to glucose and increased
sensitivity at its peripheral actions
• Biguanides
Promote glucose utilization and reduce hepatic glucose production
• Thiazolidinediones (Rosiglitazone)
Enhance insulin action in the periphery
Inhibit hepatic gluconeogenesis
Enhances glucose uptake into tissues via GLUT-4 glucose transporter
Preserves the β-cells of the pancreas
• Modifiers of glucose absorption e.g.. Ά-glucosidase inhibitor acarbose
Suppress the breakdown of complex carbohydrates in the gut delaying the
rise of blood sugar postprandially

42. STOP THE OHA BEFORE SURGERY?
o The long acting sulphonylureas should be
stopped 3 days before surgery and converted to
shorter acting drugs, or insulin if coming for
major surgery
o Metformin need not be stopped
(recommendation used to be 2 days) Risk of
lactic acidosis extremely low
o Canagliflozin, dapagliflozin, and empagliflozin
should be stopped at least 3 days in advance of
scheduled surgery,
o ertugliflozin should be stopped at least 4 days
before scheduled surgery.

43. o Omit morning OHA dose
o If the patient is for minor surgery the OHA is
omitted on the day of surgery and they can then
be treated without insulin, with close
observation and conversion to GIK if the
glucose rises above 8.0 mmol/l or 144 mg/dl
o If the patient is for major surgery the patient
should be established on insulin pre-op, even if
well controlled. There is good evidence that
continuous I.v insulin infusions are superior to
intermittent s.c. boluses and also to I.v. boluses.

44. INTRAOPERATIVE MANAGEMENT
the patient receives a fraction (usually half) of
the total morning insulin dose in the form of
intermediate-acting insulin.
To decrease the risk of hypoglycemia, insulin is
administered after intravenous access has
been established and the morning blood
glucose level is checked.

45. intraoperative hyperglycemia (>150–180
mg/dL) is treated with intravenous regular
Insulin according to a sliding scale.
One unit of regular insulin given to an adult
usually lowers plasma glucose by 25–30
mg/dL.
It must be stressed that these doses are
approximations and do not apply to patients
in catabolic states (eg, sepsis, hyperthermia).

46. Regular insulin can be added to normal saline in a
concentration of 1 unit/mL and the infusion begun at 0.1
unit/kg/h.
As blood glucose fluctuates, the regular insulin infusion can be
adjusted up or down as required.
The dose required may be approximated by the following
formula:
Unit per hour= Plasma glucose (mg/dl) / 150
A general target for the intraoperative maintenance of blood
glucose is less than 180 mg/dL.

47. When administering an intravenous insulin
infusion to surgical patients, adding some
(eg, 20 mEq) KCl to each liter of fluid may be
useful, as insulin causes an intracellular
potassium shift .

48. MINOR SURGERY
 If patient is expected to resume oral intake
quickly after surgery, a reduced approach may
be acceptable
 These patients will be given ½ their
intermediate acting insulin, and a 5% dextrose
solution at 100-150 ml/hour to prevent
hypoglycaemia.
 Intra-op and recovery room blood sugar
monitoring is essential.
 It is suggested that the blood sugar is
measured every 30 mins to hourly.

49. MINOR SURGERY
 Keep glucose between 80-140 mg/dl.
 Both I.v insulin infusions and I.v glucose
may be needed to achieve control.
 Once the patient has had their first meal
post-op they can be given the rest of their
insulin dose depending on the measured
blood glucose

50. MAJOR SURGERY
 Places a much larger catabolic stress on
patients
 A glucose, Potassium and insulin (GIK) infusion
is a simple reliable way of controlling the
patient’s blood sugar in the perioperative period
 Ideally it should be started in the preoperative
period especially in those patients that are not
well controlled
 It is essential that there are frequent, accurate
measurements of the blood sugar made
throughout the perioperative period

51. INTRAOPERATIVE MANAGEMENT
-No single anesthetic technique is proven to be
superior in diabetics.
-Blood glucose should be monitored frequently
intraoperatively regardless of the anesthetic
technique chosen.

52.  General anesthesia
the usual adrenergic and neuroglycopenic symptoms of
hypoglycemia are diminished or absent.
 Regional anesthesia
allow the patient to notify the anesthesiologist of
complications such as hypoglycemia or myocardial
ischemia, although this is less reliable in patients with
significant autonomic neuropathy.
 Local anesthesia
diabetic nerves seem to be more sensitive to local
anesthetics and are more susceptible to local
anesthetic-induced nerve injury

53. INTRAOPERATIVE FLUIDS
 Non-dextrose-containing fluid should be
used to replace blood loss, urine output, and
third-space or insensible deficits.
 Dextrose is infused only as needed to avoid
hypoglycemia and limit protein catabolism.
 Finally, normothermia is maintained, and
postoperative analgesia is provided to limit
excessive stress and resultant antiinsulin
effect.

54. A FEW ANAESTHETIC CONSIDERATIONS
 First case in the morning to minimize the
starvation period
 No anaesthetic technique is indicated or
contraindicated in diabetics, and the stress
imposed by the anaesthetic is usually minor
compared to the stress of the surgery.
 The challenge is to give the most stable
anaesthetic possible and limit the
hyperglycaemic reaction to surgical stress

55. REGIONAL ANAESTHESIA
 Pro:
 Regional anaesthesia blunts the increases in
coritcol, glucagon, and glucose.
 Spinal or epidural may modulate the
catecolamine secretion, preventing high glucose
and ketosis. This effect could continue in the
post operative period, if the block is continued
 An awake patient is a good monitor to prevent
hypoglycaemia
 A swifter return to normal eating

56. REGIONAL ANAESTHESIA
 Con:
 If autonomic neuropathy is present, profound
hypotension may occur. This could be
disastrous in a patient with cardiac
complications
 Infections and vascular complications may be
increased (epidural abscesses are more
common in diabetics)
 A diabetic neuropathy presenting post-op may
be attributed to the regional blockade

57. GENERAL ANAESTHESIA
 Pro:
 High dose opiate technique may be useful to
block the entire sympathetic nervous system
and the hypothalamic pituitary axis
 Better control of blood pressure in patients
with autonomic neuropathy

58. GENERAL ANAESTHESIA
 Con
 May have difficult airway (“Stiff-joint syndrome”)
 Full stomach due to gastroparesis
 Controlled ventilation is needed as patients with
autonomic neuropathy may have impaired
ventilatory control
 Aggravated haemodynamic response to
intubation
 Anaesthesia masks the symptoms of
hypoglycaemia

59. POSTOPERATIVE
Close monitoring of blood glucose must continue
postoperatively.
There is considerable patient-to patient variation in
onset and duration of action of insulin preparations .
For example, the onset of action of subcutaneous
regular insulin is less than 1 h, but in rare patients its
duration of action may continue for 6 h.
NPH insulin typically has an onset of action within 2 h,
but the action can last longer than 24 h.
Another reason for close monitoring is the progression
of stress hyperglycemia in the recovery period.