2. PERIOPERATIVE MANAGEMENT OF SURGICAL PATIEN
WITH DIABETIS MELLITUS
Moderated by Dr. G.K
Thapliyal
Presented by Dr. Nishant 2
Irl B.Hirsch, M.D., Janet B. McGill, M.D., Philip E. Cryer, M.D.,
White, Ph D., M.D.
3. CONTENT
LAYOUT
⪠INTRODUCTION
⪠METABOLIC EFFECTS OF SURGERY AND
ANESTHESIA
⪠TREATMENT GOALS OF THE DIABETIC
PATIENT
⪠INSULIN DEPENDENT DIABETES MELLITUS
⪠NON INSULIN DEPENDENT DIABETES
MELLITUS
⪠EMERGENCY SURGERY
⪠CONCLUSION
3
4. Introduction:
⪠Need to normalize blood glucose
concentrations.
⪠Longstanding diabetes leads to a
number of complications.
⪠Diabetic patients had a 50%
chance of undergoing surgery at
some time during their life.
4
5. Why to stabilize plasma glucose
concentration?
⪠Lead to ketosis and acidemia.
⪠Electrolyte abnormalities and volume depletion from
osmotic diuresis.
⪠Impaired wound strength and wound healing.
⪠Interference with leukocyte chemotaxis, opsonization, and
phagocytosis.
⪠Exacerbates ischemic brain damage.
5
6. Objective
âŞObjective of this article is to review the various
options available to the anaesthesiologist
caring for a patient with diabetes .
6
8. Metabolic Effects of Surgery and Anesthesia
⪠Insulin promotes glycogen formation by insulin-sensitive
tissues.
⪠Insulin stimulates fatty acid transport and triglyceride synthesis
in adipose tissue and amino acid transport and protein
synthesis in muscle.
⪠GH has anabolic effects directed at protein preservation. Like
insulin, cortisol causes glycogen deposition, and cortisol is
also anabolic with respect to fat metabolism.
⪠Besides stimulating glycogenolysis and gluconeogenesis,
glucagon stimulates hepatic ketogenesis.
⪠The catecholamines are not catabolic with regard to protein
breakdown.
8
9. Metabolic Effects of Surgery and Anesthe
9
⢠Insulin inhibits glycogenolysis, gluconeogenesis, and
ketogenesis in the liver; inhibits lipolysis in adipose
tissue; and inhibits protein catabolism in muscle.
⢠In the fasting state, the insulin level decreases and the
counterregulatory hormones are secreted at relatively
high rates to provide a continuous supply of glucose,
fatty acids, and ketone bodies.
A total loss of these anabolic and anticatabolic effects
and can eventually lead to diabetic ketoacidosis (DKA).
10. ď§Surgery produces a stress response that is a function of the
degree of trauma and can be modified by anesthesia.
ď§Hyperglycemia is common in nondiabetic patients
ď§The hormonal etiology of this hyperglycemic state includes
(relative) insulin hyposecretion and insulin resistance.
ď§Catecholamine increases are common during surgery.
ď§Adrenocorticotrophic hormone (ACTH) and cortisol levels
are also elevated
10
Metabolic Effects of Surgery and Anesth
11. ď§GH has been shown to be increased perioperatively.
ď§Glucagon levels have been the most variable of the counter
regulatory hormone in measurement
ď§one would expect the perioperative hormonal milieu to result in
protein and fat breakdown.
ď§However, glycerol and free fatty acid (FFA) concentrations are
lower in surgical patients than in subjects not under going
surgery and fasted for a similar period.
ď§ This relative impairment of lipolysis is most likely due to
increased insulin levels, a result of insulin resistance.
11
Metabolic Effects of Surgery and Anesth
12. ⢠These catabolic effects compound the state of absolute
insulin deficiency and can lead to metabolic
decompensation in the patient with IDDM.
⢠It is possible for a patient with IDDM to develop an acidemia
with a plasma glucose concentration that is only moderately
elevated. .
⢠This phenomenon is called â euglycemic DKA.â
12
Metabolic Effects of Surgery and Anesth
13. ⢠Although less marked in the patient with NIDDM, changes
in protein and fat metabolism can occur in more severely
affected patients as a result of the inability to increase
insulin secretion in response to the surgery induced
hyperglycemia.
⢠In both groups of patients, frequent monitoring of plasma
glucose and urinary ketones is required to avoid metabolic
deterioration.
⢠It appears that central neural blockade has only a limited
impact on metabolic function.
13
Metabolic Effects of Surgery and Anesth
14. ⢠No significant changes have been noted in blood
glucose, lactate, alanine, ffa, glycerol, and ketones during
epidural anaesthesia.
⢠Plasma epinephrine and norepinephrine concentrations
decrease in proportion to the level of sensory analgesia
during spinal anaesthesia with tetracaine.
⢠The insulin response to hyperglycemia appears to be
inhibited by a high thoracic (T2-T6) blockade, where as a
low blockade (T9-T12) has no effect on insulin secretion.
14
Metabolic Effects of Surgery and Anesth
15. Treatment Goals for the Diabetic Patient during th
Perioperative Period
⪠Mimic normal metabolism.
⪠Adequate insulin to counterbalance the catabolic response.
⪠Adequate glucose should be provided to meet the
increased requirements of the surgical stress in addition to
basal caloric requirements.
⪠Finally, a regimen that is simple and minimizes the
possibilities of error in administration must be devised.
15
17. ⢠There are several preoperative issues that need to be
considered before the patient is taken to surgery (table 2).
17
18. ⢠Earlier reviews suggested admitting patients with IDDM 48-
72 h before surgery to improve metabolic control and to
assess cardiovascular status.
⢠However, the high costs involved limit this option.
⢠With the widespread use and accessibility of home blood
glucose monitoring, it usually is possible to correct serious
hyperglycemia without hospital admission
18
19. Cause Of Perioperative Mortality
⪠Coronary artery disease
⪠Endstage renal disease from diabetic nephropathy will
develop in about 35% of patients with IDDM
⪠Autonomic neuropathy
19
20. The regimen for achieving optimal preadmission
glycemic control
20
⢠Is arbitrary.
⢠Two injections of intermediate-acting (nph or lente) and
short-acting (regular) insulin each day.
⢠Use of long-acting (ultralente) insulin
⢠Most patients with poorly controlled diabetes can be â
fine-tunedâ 12 h prior to elective surgery . Therefore,
preadmission should be considered only for those patients
with poorly controlled IDDM.
21. INSULIN
⪠Intravenous (iv) insulin infusion
is the most rational way to
manage a patient with IDDM.
⪠Intra-and intersubject variations
in insulin absorption after sc
insulin injection.
⪠Alberti and Thomas showed
clear improvements in plasma
glucose and ketone body
concentrations with a glucose-
insulin-potassium (GIK)
infusion compared to sc insulin. 21
22. ⢠Watts et al.showed a wide range of insulin requirements (0.5-
5.0 U /h ) during insulin infusion, based on an algorithm-
dependent program in a group of patients with IDDM and
NIDDM.
⢠Within 8 h, the mean blood glucose level was within the target
range of 6.7-10.0 mM (120-180 mg/dl),and it remained stable
for the remainder of the study period (24 h after surgery),
22
23. 23
⢠However, the standard treatment group who received either sc
sliding-scale or fixed-rate iv insulin infusion had a final glucose
concentration ranging from 1.7-17.0 mM (30-306 mg/dl) at 12-
24 h after surgery
⢠This demonstrates marked variability in plasma glucose
concentrations, ranging from dangerous hypoglycemia to
excessive hyperglycemia.
⢠In addition, control patients had higher mean plasma glucose
concentrations than did patients receiving the algorithm-based.
24. ⢠The safest method to administer insulin in the
perioperative period is by iv infusion.
⢠The evening dose should consist only of the regular
insulin (the supper NPH insulin should be withheld). The
patient who takes NPH and regular insulin before
breakfast, regular insulin before supper, and NPH insulin
at bedtime, should simply have the bedtime NPH
injection withheld.
⢠The insulin infusion should be started no later than 7:00
AM, even if the procedure is scheduled for later in the
day.
24
25. ⢠Patients using continuous sc insulin infusion (CSII) are actually
the simplest to prepare since they receive only regular insulin
from their pump.
⢠There currently are two accepted regimens for initiating iv insulin
infusions.
⢠The GIK infusion proposed by Alberti et al and a variable-rate
insulin infusion as described by Watts et al
25
26. ⢠It is possible that for some smaller hospitals the
variable rate insulin infusion may be too complex. In
this situation the GIK infusion is perhaps the better
alternative.
⢠Pre admit the poorly controlled patient to initiate an
insulin infusion, one can administer the usual dose of
regular insulin with supper and begin the insulin
infusion between 10:00 and 11:00 pm.
⢠A schedule of glucose checks every 1 h for the first 4
h after the insulin infusion is started, and then every 2
h until surgery, is recommended. In the operating
room, the blood glucose should be estimated every 126
27. Other clinically important points are:
1. A blood glucose meter, rather than visually read
capillary glucose estimation, should be used for
patients receiving an insulin infusion.
2. The nurse or physician using the meter should be
properly trained in its use.
3. At least one plasma glucose sample should be sent
to the laboratory for conformation of the meterâs
accuracy. This check sample should be drawn
simultaneously with the capillary meter test.
27
28. ⢠As a general guideline, patients receiving an insulin infusion
require 0.3-0.4 U of insulin per gram glucose per hour (U
/g/h).
⢠Higher insulin requirements and thus higher insulin infusion
rates are necessary for some patients with
⢠Liver disease 0.5-0.6 U /g/ h
⢠Obesity 0.4-0.6 U /g/ h
⢠Severe infections 0.6-0.8U /g/ h
⢠Steroid therapy 0.5-0.8U /g/ h
⢠Cardiopulmonary bypass 0.8-1.2 U /g/
h
28
29. ⢠Another controversial issue regarding iv insulin
administration concerns the practice of injecting large bolus
doses of iv insulin without an insulin drip,
⢠The half-life of iv insulin is 4-5 min and the biologic half-life
less than 20 min.
⢠Depending on initial plasma glucose levels, patients given iv
insulin injection may manifest very high (but short-lived)
insulin concentrations, which may cause hypoglycemia in
the 60-120-min period prior to the administration of the
second bolus of insulin.
⢠This â roller coasterâ approach to glucose regulation may
result in an even greater rate of lipolysis and ketogenesis.
29
30. GLUCOSE
⢠Minimum of 100-125 g (400-500 calories) of exogenous
glucose
⢠Although this quantity of glucose was considered adequate
to produce a 50% decrease in protein catabolism during
starvation
⢠In fasting normal volunteers, glucose infused at the rate of
1 mg/kg/min had no effect on the rate of appearance of
glycerol (glycerol ra) or FFA (FFA ra). However, at 4 mg
/kg/min(16.8 g/ h for a 70-kg man), both glycerol ra and
FFA ra were suppressed.
⢠The prevention of ketone body and FFA accumulation in all
surgical patients is theoretically important since elevated
levels of circulating FFA have been shown to increase
myocardial oxygen consumption and in some instances,30
31. ⢠Sufficient glucose to prevent hypoglycemia and to provide
the basal energy requirements should be administered
during surgery in the insulinopenic patients.
⢠Some authors recommend 10 g glucose per hour (2.4
mg/kg/min), whereas most infuse 5 g each hour (1.2
mg/kg/min).
⢠In diabetic pediatric patients 5.0 mg/ kg/min (300 mg/kg/ h)
of glucose with adequate insulin to achieve the desired blood
glucose control
31
32. POTASSIUM
Metabolic factors that will influence the serum potassium level
⢠Changes in insulin concentration
⢠small incremental changes in blood tonicity
⢠changes in acid-base balance
In the normokalemic diabetic patient with normal renal function,
20 meq of potassium chloride should be added to each liter of
fluid
In a poorly controlled patient, it is reasonable to check the
serum potassium level 6-8 h after the insulin infusion is started
32
33. FLUIDS
⢠Patient is receiving adequate insulin, glucose, and
potassium, any additional fluids given during surgery (e.g.,
To treat intraoperative blood loss) should be non-glucose
containing.
⢠Glucose is provided in a solution of 5 or 10% dextrose in
0.45% saline
⢠Infusion via a central venous catheter is recommended
because of the increased risk of peripheral venous
thrombosis with these solutions.
⢠Higher insulin doses may be required for diabetic patients
receiving lr during the perioperative period.
33
34. GENERAL RECOMMENDATIONS
⢠Operations on diabetic patients should be scheduled early
in the day.
⢠With a variable-rate iv insulin infusion or GIK infusion,
postoperative management is simple and flexible.
⢠The capillary glucose should be monitored at the bedside
every 1-2 h while insulin is being infused.
⢠Insulin infusion be continued through the first light meal
and discontinued immediately before the subsequent
meal.
34
35. AMBULATORY (OUTPATIENT) SURGERY
35
For brief outpatient surgical procedures, it is often advisable
to deviate from the iv insulin infusion regimen suggested
above.
The option not to begin an insulin infusion will depend on:
1. The outpatientâs current metabolic status.
2. Preoperative insulin regimen.
3. The diet.
4. The physicianâs ability to handle a metabolic crisis
related to protracted postoperative nausea and vomiting.
36. 36
⢠In the patient with IDDM receiving sc insulin, the inability
to eat after surgery might complicate the medical
management.
⢠A variable-rate iv insulin infusion or GIK infusion -
diminishes the metabolic risks
⢠Metoclopramide, a gastrokinetic agent that increases
gastric motility, can be an effective antiemetic in patients
with gastroparesis â˘
⢠The lower dose of NPH insulin will reduce the risk of
afternoon hypoglycemia if surgery is delayed or
postoperative vomiting develops.
⢠Blood glucose concentrationsabove 11.1 mm (200 mg/dl)
require treatment with supplemental regular insulin.
37. 37
Non-Insulin-dependent Diabetes Mellitus:
Elective Surgery
⢠Majority of diabetic patients undergoing surgery
have NIDDM as opposed to IDDM.
⢠Much higher prevalence of macrovascular disease.
⢠Taking insulin although they are not â insulin-
dependent.
⢠Should be treated in a likewise manner during
surgery.
⢠The age of onset has been shown to be bimodal.
⢠IDDM can present in patients with NIDDM who
have â pancreatic exhaustion *âand â conversion* *
to IDDM
38. 38
AMBULATORY (OUTPATIENT) SURGERY
⢠Perioperative insulin therapy should be considered when
blood glucose concentrations (fasting or random) exceed
11.1 mm (200mg/dl) and definitely should be initiated when
they are in excess of 13.9 mm (250 mg/dl).
⢠Fasting plasma glucose concentrations exceeding 11.1 mm
tend to manifest absolute deficiency with respect to insulin
secretion.
⢠Impaired wound healing and strength occurs when plasma
glucose levels exceed 11.1 mm.
⢠The decision to begin a variable-rate insulin infusion or GIK
infusion should be individualized according to the patient
and type of operative procedure
39. 39
NEUROLOGICAL, MAJOR INTRACAVITARY AND OPE
HEART SURGERY
⢠An insulin infusion should be initiated if the capillary glucose
rises above 11.1 mm (200 mg/dl) during the operation.
⢠Hyperglycemia has been shown to worsen neurologic
outcome for patients after ischemic stroke.
⢠Cardiopulmonary bypass surgery deserves special attention
since it is associated with potentially greater metabolic
derangements.
⢠Plasma glucose concentrations can Increase to even higher
values during this procedure because of the large amounts of
glucose that frequently are infused (â cardioplegic solutionâ ),
because of insulin resistance during hypothermia, and
hyperglycemic effects of the commonly used adrenergic
agents.
40. 40
⢠Hyperosmolar hyperglycemic nonketotic coma (HHNC)
has been reported as a postoperative complication in
patients with NIDDM.
⢠This syndrome is characterized by marked
hyperglycemia, plasma hyperosmolarity, profound
dehydration, absence of ketoacidosis, and variable
mental status changes.
⢠Due to the increased plasma glucose concentrations
and insulin resistance present during coronary artery
bypass operations in patients with NIDDM,
⢠HHNC is much more likely to occur in this patient
population
⢠Other factors precipitating HHNC include
hyperalimentation and dextrose infusions (without
41. 41
Emergency Surgery
⢠A priority for diabetic patients scheduled for emergency
surgery is a complete evaluation of the patientâs
metabolic status.
⢠Plasma glucose, electrolytes, and pH should be
measured and urine ketones estimated.
⢠A saline infusion should be started, and if clinically
indicated, a central venous catheter should be inserted.
⢠If DKA is confirmed, surgery should be delayed while
standard treatment for this metabolic emergency is
instituted with iv fluids, insulin, and potassium
42. 42
CROSS REFERENCES
⢠Hjortrup A, Rasmussen BF, Kehlet H: Morbidity in diabetic
and nondiabetic patients after major vascular surgery.
Br Med J 287:1107-1108, 1983
They carried out a study to investigate postoperative morbidity
in diabetics undergoing major vascular surgery and in non-
diabetic controls matched for type of surgery, age, sex, weight,
and complicating diseases.
43. 43
Patients, methods, and results
⢠They reviewed the records of 64 consecutive diabetic patients
who had undergone elective aortoiliac or femoral bypass (43
patients) or aortoiliac thromboendarterectomy (21) from January
1975 to July 1982.
⢠64 patients were selected at random without knowledge of
postoperative morbidity but matched to the diabetics for age
(means 60 years (diabetics) and 57 years (non-diabetics)), sex
(27 women and 37 men), and weight (mean 78 kg (diabetics)
and 79 kg (non-diabetics)).
⢠Similar numbers of diabetics and controls had heart failure (25
and 21 respectively), angina pectoris (12 and 11), and
hypertension (12 and 13). Twenty three diabetic patients
compared with 18 controls were treated with digoxin.
⢠Diuretics were used in 26 diabetics and 19 controls. Beta-
44. 44
⢠The average duration of diabetes was 10-8 years (range four to
18 years).
⢠Twenty three patients received insulin and 22 oral antidiabetic
agents, and 19 were treated by diet.
⢠Two patients had severe retinopathy, five nephropathy, and 17
polyneuropathy. Postoperative treatment of the diabetics was
based on results of four daily blood glucose tests.
⢠All patients in both groups received prophylactic anticoagulation
with phenprocoumon and antibiotics (penicillin and an
aminoglycoside).
45. 45
⢠There was no difference in the total number of complications
between the two groups.
⢠The mean difference in the incidence of complications was 1
5%.
⢠Of the diabetics with complications, five received insulin and
six oral antidiabetic agents, and three were treated by diet.
⢠There was no difference in postoperative blood glucose
concentrations between diabetic patients with and without
complications.
46. 46
⢠They found no difference in the incidence of complications
postoperatively between diabetic patients and matched
controls. No correlation was found between the types of
diabetes and the incidence of complications. Blood
glucose concentrations were almost identical in diabetic
patients with and without complications.
47. 47
McMurrayJF: Wound healing with diabetes mellitus:
Better glucose control for better healing in diabetes.Surg Clin
North Am 64:769-778 1984
CROSS REFERENCES
48. 48
⢠Their studies of experimental wounds in diabetic animals
reveal that simple epithelial repair is not hindered in
diabetes.
⢠However, the repair of deeper wounds that require
collagen formation is reduced in diabetes.
⢠The contribution of impaired granulocyte function both in
defense against bacterial contamination and in the
initiation of collagen formation seems well established.
⢠Though it is of great academic interest whether the defects
in wound healing are ascribed to insulin lack, the presence
of extracellular hyperglycemia, or a deficit of intracellular
glucose, the practical clinical treatment remains relatively
simple.
49. 49
⢠Insulin treatment of hyperglycemic diabetic patients will
supply the needed insulin, lower the extracellular
glucose, and increase intracellular glucose levels.
⢠Traditional blood glucose measurement remains an
obviously important guide to the effectiveness of insulin
administration.
⢠Some aspects of experimental wound healing improve
with insulin supplementation, while others require that
insulin be supplied in sufficient amounts to lower the
glucose to 250 mg per dl or less
50. 50
⢠A blood glucose goal of 250 mg per dl during operation
and normalization of blood glucose preoperatively and
postoperatively is recommended.
⢠Previous glucose control in the diabetic patient can be
assessed by measurement of the blood
glycohemoglobin concentration.
⢠It may be accomplished by an intravenous infusion of
10 units of regular insulin in 1 liter of 5 per cent
dextrose solution at a rate of 125 ml per hr.
⢠Occasional patients will require supplementation with
small doses of regular insulin.
⢠When the blood glycohemoglobin concentration is
greatly elevated (50 per cent above normal),
preoperative consultation with an endocrinologist is
51. 51
⢠The poorly controlled or labile diabetic patients
present more difficult management problems.
Postponement of surgery until better glucose control
and protein nutrition is achieved is advisable when
possible.
⢠The key to good glucose management in these
patients is frequent measurement of their blood
glucose level and readjustment of their insulin
dosage as necessary.
⢠The intraoperative measurement of blood glucose
by the Chemstrip bG finger-stick method is quite
convenient.
⢠Insulin can be supplied and altered quickly when it
52. 52
Conclusio
n⢠Although excessive hyperglycemia, lipolysis, ketogenesis,
and proteolysis may adversely affect surgical outcome in
patients with diabetes, the evidence to support this view is
only indirect.
⢠By understanding basic physiologic and endocrinologic
principles, however, the anesthesiologist can make rational
decisions regarding the metabolic care of diabetic patients.
⢠Preoperative evaluation should include assessment of
chronic complications of diabetes.
⢠The use of a carefully titrated variable-rate insulin infusion or
a GIK infusion can minimize the metabolic derangements
associated with surgical stress.
⢠Finally, the metabolic effects of other factors, such as drugs,
obesity, infection, and hypothermia need to be considered.
Type 1 is insulin dependent diabetes mellitus and type 2 is non insulin dependent diabetes mellitus
This phenomenon was first described by Munro et al. EDKA is defined as a triad comprising high anion gap metabolic acidosis with positive serum and urine ketones when serum glycemic levels are <250 mg/dL
1) changes in insulin concentration,
i.e.y changes in serum insulin levels, are capable of stimulating potassium uptake by muscle, liver, and adipose
tissue90; 2) small incremental changes in blood tonicity as
seen with dehydration or hyperglycemia can cause a shift
of water and potassium from the intracellular to the extracellular space91; and 3) changes in acid-base balance,
e.g.y acidosis, result in hyperkalemia as hydrogen ions are
exchanged with intracellular potassium.