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syndrome of abnormal carbohydrate
metabolism that is characterized by
-type 1(IDDM) insulin-requiring
Absolute deficiency of insulin
May be autoimmune based
Management requires exogenous insulin
Patients are prone to ketosis
-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
-secondary:Pancreatic disease (decreased insulin production)
-Secondary to endocrinopathies such as
Cushing’s disease, acromegaly, pheochromocytoma
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
5. Haemoglobin A1c ≥6.5%
1- diabetic patients are at increased risk for hypertension,
coronary artery disease,congestive heart failure, diastolic
dysfunction, cereberovascular, renovascular and peripheral
2-these patient may have clinically silent myocardial
ischemia or infarction.
3- DM considered one of the risk factors when determining
preoperative cardiac testing
-avoid nephrotoxic drugs, maintain
normovolumia, control of hyperglycemia
and/or hypertension and preservation of renal
Peripheral and automonic
may blunt the compensatory cardiovascular
response to hypotension so predisposing to
May cause gastroparesis so presdisposing to
Non enzymatic glycosylation of proteins and
abnormal cross linking of collagen :
-leading to decreased joint mobility
-if affecting tempromandubilar joint and/or
cervical spine will cause difficult airway
Stiff joint syndrome
-A positive “prayer” sign (inability to approximate their fingers and palms
while pressing their hands together with the fingers extended)
and palm printing have been reported to
identify patients with stiff joint syndrome.
-Changes in airway anatomy will create difficulty for intubation in
approximately one third of patients with longterm type I diabetes undergoing
Acute effects ooff hhyyppeerrggllyyccaaeemmiiaa
Dehydration and electrolyte disturbances (due to osmotic
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
Hyperosmolar Non-ketotic coma (Type II diabetics)
-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.
:DKA characterized by
• high anion-gap metabolic acidosis
-precipitating causes for DKA as infection ,
surgical stress, trauma and /or lack of insulin.
-Clinical manifestations of DKA include
tachypnea (respiratory compensation for the
metabolic acidosis), abdominal pain, nausea and
vomiting, and changes in sensorium.
Treatment of DKA
Identifying and treating the precipitating factors
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.
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.
Guidelines for DKA management
1. Routine monitoring, arterial access, central venous
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
4. Supplementation of potassium, phosphrus and
magnesium as guided by serial plasma determination.
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.
: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
Hyperosmolality (frequently exceeding 360 mOsm/L)
induces dehydration of neurons, causing changes in
mental status and seizures.
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
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
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
Detection of hypoglycemia under anesthesia
requires high index of suspicion and frequent
determination of plasma glucose levels.
Diabetic patients are incompletely able to counter hypoglycemia
despite secreting glucagon or epinephrine (counterregulatory
Treatment Consists of :
-Correcting the precipitating causes
The treatment of hypoglycemia in anesthetized or critically ill
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
Stress response to surgery with catabolic hormone
Interruption of food intake, pre- and perhaps post-surgery
Altered consciousness, masking the symptoms of
Circulatory disturbance that may alter the uptake of s.c.
The altered physiological state resulting from end
-Preoperative evaluation should include a thorough history and physical
-Prior anesthetic records should be reviewed to determine whether
difficulties with intubation or perioperative diabetic complications were
-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.
(HbA1c) levels reflect the adequacy of glucose control over the
preceding 1–3 months.
-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.
Myocardial ischemia or old infarction may be evident on an
ECG despite a negative history.
cardiac enlargement,pulmonary vascular congestion, or
pleural effusion, but is not routinely indicated.
Premedication with a nonparticulate antacid and
metoclopramide is often used in an obese diabetic
patient with signs of cardiac autonomic
RReeggiimmeenn ddeeppeennddss oonn
• Type of diabetes and its usual treatment
• Extent of surgery
• The amount of surgical stress and the catabolic
response to that stress
• Beware major surgery and emergency surgery,
especially trauma or surgery related to infective
TTyyppee II ddiiaabbeetteess
Preoperative Insulin Traditional Approach
Give 1/4 to 1/2 the daily dose of intermediate-acting
Add 1/2 unit of intermediate-acting insulin for each
unit of insulin prescribed
Start IV glucose 5-10 g/h
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 80
• Provide sufficient glucose (5-10g/h) and potassium (2-4 mEq/h)
Type IIII ddiiaabbeetteess oonn ddiieett aalloonnee
If fasting blood glucose < 7.8 mmol/l or 140.4
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
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
Type II diabetes oonn oorraall hhyyppooggllyyccaaeemmiicc
• There are 4 groups of oral hypoglycaemic agents (OHA)
Enhanced secretion of insulin in response to glucose and increased
sensitivity at its peripheral actions
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
Suppress the breakdown of complex carbohydrates in the gut delaying the
rise of blood sugar postprandially
Stop tthhee OOHHAA bbeeffoorree ssuurrggeerryy??
• The long acting sulphonylureas should be stopped 3 days before
surgery and converted to shorter acting drugs, or insulin if coming for
• Metformin need not be stopped (recommendation used to be 2 days)
Risk of lactic acidosis extremely low
• Omit morning OHA dose
• 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
• 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.
the patient receives a fraction—usually half—of
the total morning insulin dose in the form of
To decrease the risk of hypoglycemia, insulin is
administered after intravenous access has been
established and the morning blood glucose level is
intraoperative hyperglycemia (>150–180 mg/dL) is treated
with intravenous regular Insulin according to a sliding
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,
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:
A general target for the intraoperative maintenance
of blood glucose is less than 180 mg/dL.
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 .
Keep glucose between 4.4 – 8.0 mmol/l
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
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
Factors Adversely Affecting Diabetic
Metabolic response to trauma
Diseases underlying need for surgery
Other drugs e.g. steroids
Metabolic Responses to Surgery
• Secretion of stress
• Growth Hormone
• Relative decrease in
• Peripheral insulin
• Protein breakdown
Metabolic Response to Surgery and
Glucagon, cortisol and adrenaline secretion as part of the
neuroendocrine response to trauma, combined with iatrogenic
insulin deficiency or glucose overadministration may result in
Causes osmotic diuresis, making volume status difficult to
determine and risking profound dehydration and organ
hypoperfusion, and increased risk of UTI
osmotic diuresis, delayed wound healing, exacerbation of brain,
spinal cord and renal damage by ischaemia
Results in hyperosmolality with hyperviscocity, thrombogenesis
and cerebral oedema
Frequently measure blood glucose and administer insulin
Metabolic Response to Surgery and
Any patient who is in a severe catabolic state and has an insulin
deficiency (absolute or relative) can decompensate into keto-acidosis
Most common in type 1 patients
Increased risk postoperatively, often precipitated by the stress
response, infection, MI, failure to continue insulin therapy.
characterised by hyperglycaemia, hyperosmolarity, dehydration
(may lead to shock and hypotension) and excess ketone body
production resulting in an anion gap metabolic acidosis.
Monitoring of blood sugar
The key to any management regimen is to monitor plasma glucose levels
Patients receiving insulin infusions intraoperatively may need to have their
Glucose measured hourly. Those with type 2 diabetes vary in their ability to
produce and respond to endogenous insulin, and measurement every 2 or 3
may be sufficient.
Likewise, insulin requirements vary with the extensiveness of the surgical
Bedside glucose meters are capable of determining the glucose
concentration in a drop of blood obtained from a finger stick (or withdrawn
from a central or arterial line) within a minute.
These devices measure the color conversion of a glucose oxidase–
Their accuracy depends, to a large extent,on adherence to the device’s
specific testing protocol.
Monitoring urine glucose is of value only for detecting glycosuria.
-No single anesthetic technique is proven to be
superior in diabetics.
-Blood glucose should be monitored frequently
intraoperatively regardless of the anesthetic
the usual adrenergic and neuroglycopenic symptoms of hypoglycemia are
diminished or absent.
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.
diabetic nerves seem to be more sensitive to local anesthetics and are more
susceptible to local anesthetic-induced nerve injury
: 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
Finally, normothermia is maintained, and
postoperative analgesia is provided to
limit excessive stress and resultant
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
A diabetic neuropathy presenting post-op may be
attributed to the regional blockade
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
May have difficult airway (“Stiff-joint syndrome”)
Full stomach due to gastroparesis
Controlled ventilation is needed as patients with
autonomic neuropathy may have impaired
Aggravated haemodynamic response to intubation
Anaesthesia masks the symptoms of hypoglycaemia
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.
Perioperatively, there are increased levels of counterregulatory hormones
(catecholamines, glucocorticoids, growth hormone, and glucagon) mediating the
stress response, resulting in relative insulin resistance and difficulty in controlling
blood glucose levels.
Hyperglycemia may impair wound healing, inhibit white blood cell (WBC)
chemotaxis and function (associated with an increased risk of infection), worsen
central nervous system (CNS) and spinal cord injury under ischemic conditions, and
result in hyperosmolarity leading to hyperviscosity and thrombogenesis.
The presence of hyperglycemia may also portend the development of DKA or a
nonketotic hyperosmolar state.
Blood glucose >180 mg/dl (10 mmol/L) exceeds the Tmax of the kidney and
results in glycosuria. Glucose-induced osmotic diuresis may lead to dehydration
and an increased risk of urinary tract infection.
Blood glucose levels should be frequently monitored and maintained
at <180 mg/dl (10 mmol/L) with appropriate administration of insulin.
One unit of regular insulin generally lowers the blood glucose by
Approximately25-30 mg/dl (1.5 mmol/L) in a 70-kg patient.
Intravenous shortacting regular insulin (Humulin R) should be used for
initial control of blood glucose.
The absorption and efficacy of SC insulin may be unpredictable in the
perioperative period because of unreliable cutaneous blood flow and should
be avoided initially.
Finally, it may be reasonable to maintain blood glucose at the upper end of
the normal range in postoperative patients to avoid hypoglycemia.
It is commonly defined as a blood glucose <50 mg/dl
(2.8mmol/L) in adults and <40 mg/dl (2.2 mmol/L) in children.
Hypoglycemia may develop perioperatively as a result of
residual effects of preoperativelong-acting oral hypoglycemic
agents or perioperative insulin administration and may be
exacerbated by perioperative fasting or insufficient glucose
Recognition of perioperative hypoglycemia may be delayed
because presenting symptoms may be altered or absent as a
result of the effects of drugs such as anesthetics, analgesics,
sedatives, and sympatholytic agents. In addition, diabetics with
autonomic neuropathy have blunting of the adrenergic
response associated with hypoglycemia.
Neuroglycopenic symptoms and symptoms of the
adrenergic response to hypoglycemia are the two
main manifestations of hypoglycemia.
Neuroglycopenic manifestations generally begin with
confusion, irritability, fatigue, headache, and
Prolonged, severe hypoglycemia may cause seizures
and even focal neurological deficits,coma, and death.
Hypoglycemia must be considered early in the differential diagnosis of any
new neurological symptoms in the postoperative period, because prolonged
hypoglycemia results in irreversible neurological deficits.
Adrenergic symptoms and signs, including anxiety, restlessness,
tachycardia,hypertension, arrhythmias, and angina are due to
catecholamines released in response to hypoglycemia.
Patients with symptomatic hypoglycemia generally respond promptlyto IV
dextrose unless there has been severe hypoglycemia of sufficient duration
cause permanent neurological damage.
After obtaining a sample to determine the blood glucose, initiate therapy in
an adult with 50 ml of 50% (25 gm) dextrose (D50). Each milliliter of D50
raises the blood glucose by about 2 mg/dl (0.11 mmol/L) in a 70-kg patient.
Additional boluses of D50 or an infusion of 5–10% dextrose may be needed
to treat severe hypoglycemia and to prevent recurrent hypoglycemia.
Therapy should not be delayed while awaiting
confirmation of hypoglycemia. Glucagon (1–2 mg),
diazoxide, and octreotide (50–200 μg) have been used
rarely to treat refractory, sulfonylurea-induced cases of
Blood glucose levels should be monitored frequently
during the treatment of hypoglycemia, and the underlying
cause of the hypoglycemia should be identified and
Sources of the lecture:
• Clinical anesthesiology 2013
• ASA refresher course 2002, 2012
• Perioperative Management of Diabetes
Mellitus Amir B. Channa FFARCS, D.A.
(Eng) KKUH - Riyadh