Transcript diabetes mellitus

Anesthetic implications of
diabetes mellitus
Moderator Dr Dara Negi
Dr Avinash Goyal
Introduction
the prevalence of diabetes mellitus (DM) is rapidly increasing
throughout the world
physicians will be confronted with an increasing population of
diabetic patients undergoing anesthesia and surgery
A significant number with type 2 DM are unaware that they are
diabetic until the time of surgery.
 Diabetics have higher morbidity and mortality as surgical
patients.
End-organ effects of diabetes are more important to periop
outcome
Tighter the control of glucose desired, more frequently glucose
levels to be measured
PHYSIOLOGICAL IMPACT
 6th leading cause of death by disease
 Decreases life expectancy of middle-aged people by 5-10
years
 2-4 x greater risk of death d/t heart disease
 Leading cause of blindness in 25-74 year olds
 Leading cause of non-traumatic amputations
 Responsible for 25-30% of all new dialysis patients
Diabetes mellitus
results from an inadequate supply of insulin
and/or an inadequate tissue response to
insulin,
yielding increased circulating glucose levels
with eventual microvascular and macrovascular
complications.
DIAGNOSIS
As per American Diabetes association (ADA)
A normal fasting plasma glucose is 70 to 100 mg/dL.
A random plasma glucose concentration of 200 mg/dL or
higher, with classical signs and symptoms
(polyuria,polydyspia,unexplained weight loss)
or
A fasting (no calorie intake >8hrs)plasma glucose
concentration of 126 mg/dL or higher
or
An abnormal oral glucose tolerance test (OGTT), in which
the glucose concentration is 200 mg/dL or higher 2
hours after a standard carbohydrate load (75 gm of
glucose).
• Glucose
– whole blood values are 10-15% lower than
plasma/serum
– Venous blood values are 10% lower than
capillary/arterial.
– Venous blood - loss of 0.33 mmol/L per
hour
– There is no decrease within 24 h in the
presence of sodium fluoride
Impaired Fasting Glucose
• Any fasting glucose between 101 and 125
mg/dL
• Increased risk for DM
• Must educate regarding risks and need for
lifestyle modifications
IMPAIRED GTT
• Defined as a plasma blood glucose of >/= to 140 but <
200 after a 2 hour 75 gram glucose tolerance test
• 8-10% of population have this problem with a 25 % risk
of developing DM 2
• Compounding risk factors effect risk of developing Type 2
DM
–
–
–
–
Age
Activity
Comorbidities
Weight
• Increased risk for macrovascular diseases
• Must educate regarding risks and need for lifestyle
modifications
HEMOGLOBIN A1c
 provides a valuable assessment of long-term glycemic
control
 Erythrocyte hemoglobin is nonenzymatically
glycosylated by glucose
 HbA1c is stable glycosylated hemoglobin
 Its percentage concentration indicates average plasma
glucose
 concentration during the preceding 60 to 90 days.
 Performed 2 times a year.
 The normal range for Hb A1c is 4% to 6%.
 Increased risk of microvascular and macrovascular
disease begins at a Hb A1c of 6.5%.
 Lowering HbA1C Reduces Risk of Complications
Glucose physiology
• Glucose is a crucial fuel source
• insulin facilitates glucose movement into cells
• Red blood cells, healing wounds, the brain,
and the adrenal medulla require glucose
approximately @ 2 mg/kg/min.
• Daily requirement of glucose for 70 Kg man is
200gm/day(90-100g stored as glycogen)
Normal glucose homeostasis is tightly
regulated by three interrelated processes
(1) glucose production in the liver,
(2) glucose uptake and utilization by peripheral
tissues, chiefly skeletal muscle,
(3) actions of insulin and counter-regulatory
hormones (e.g., glucagon).
Metabolic problem
• Diabetes is generalised catabolic state
• Lipids are mobilized with release of fatty acids
• Ketogenesis leads to acidosis & loss of cellular
potassium
• Gulconeogenesis & glycogenolysis ,with
decreased peripheral glucose utilization causes
hyperglycemia
• Glycosuria causes osmotic polyuria & dehydration
• Plasma hyperosmolarity ,acidosis,hyperkalemia
results leading to coma & death
GLUCOTOXICITY: high levels of glucose
causes
 nonenzymatic glycosylation reactions that lead to the
formation of abnormal proteins which weaken endothelial
junctions and decrease elastance, which is responsible for the
stiff joint syndrome (and difficult intubation secondary to
fixation of the atlanto-occipital joint), as well as decrease
wound-healing tensile strength.
 increase macroglobulin production by the liver (which would
increase blood viscosity) and promote intracellular swelling
by favoring the production of nondiffusible, large molecules
(such as sorbitol).
 Glycemia also disrupts autoregulation. Glucose-induced
vasodilation prevents target organs from protecting against
increases in systemic BP.
DM TYPE I
 Constitutes 5-10% of DM diagnosed
 Mostly appears in children and young adults
 caused by a T cell–mediated autoimmune destruction of beta cells of the
pancreas.
 At least 80% to 90% of beta-cell function must be lost before hyperglycemia
occurs
 A long preclinical period (9–13 years)
 presentation of clinical disease is often sudden and severe , Patients demonstrate
hyperglycemia over several days to weeks
 associated with fatigue, weight loss, polyuria, polydipsia, blurring of vision, and
signs of intravascular volume depletion
 The diagnosis is based on
• : a random blood glucose greater than 200 mg/dL
• hemoglobin (Hb) A1c level greater than 7.0%.
• ketoacidosis indicates severe insulin deficiency and unrestrained lipolysis.
 Beta-cell destruction is complete within 3 years of diagnosis , with the process
being slower in adults.
 TREATMENT-INSULIN
t
DM TYPE II
 Most common form of diabetes
 Involves about 90-95% of people with DM
 most type 2 diabetics have had the disease for approximately 4 to 7
years before it is diagnosed
 Associated with:
 older age
 obesity
 family history of DM
 prior history of gestational diabetes
 physical inactivity
 Ethnicity
 Patient with type II DM usually makes enough insulin but the body
cannot use it effectively => insulin resistance
 Gradually insulin production decreases over the following years
 Symptoms are similar to type I but develop more gradually
 TREATMENT- diet control ( wt loss),exercise & medications (OHGs)
Gestational diabetes
 Hyperglycemia first diagnosed during pregnancy
 Occurs in 2-5% of pregnancies
 Occurs due to placental hormone changes that effect insulin function (greater
resistance)
 Screening usually occurs during the 24th-28th week in high risk patients
 Criteria for diagnosis is different than for Type 1 and Type 2
 Dietary changes are initial treatment and insulin is the only BG lowering agent used
 Better maternal glycemic control lowers the incidence of neonatal hypoglycemia and
hyper bilirubinemia
 Postpartum BG levels usually return to normal
 Women with a history of gestational diabetes have a 20-50% chance of getting type II
DM within 5-10 years
SECONDARY DM
• DM occurs as a result of another problem (primary)
– Medications
•
•
•
•
Thiazides
Diuretics
Beta blockers
Steroids
• Treatment of the primary cause may resolve the DM
but lifestyle modifications and medications may be
needed as well
DRUG THERAPY IN DM
• Oral Diabetic Medications
– Sulfonylureas-gliclazide,tolbutamide
increases insulin release
longer duration of action
– Biguanides-(Metformin)
potentiates insulin
causes lactic acidoses in dehydrated pts
– Alpha-Glucosidase (acarbose)
Inhibitors-decrease absorption of glucose
– Nonsulfonylurea Secretagogues
• Meglitinide
• D-phenylalanine derivatives
– Thiazolidinediones (TZDs)-rosiglitazone
• Insulins
– Short acting -
Soluble / Neutral insulin
Insulin aspart
Insulin lispro
– Intermediate acting - Isophane
– Long acting - Insulin Zinc suspension
new insulin analogue - Glargine
Detemir
– Biphasic- mixture of short and intermediate
Biphasic lispro
Biphasic Isophane
Types of insulin
Insulin
Lispro
Aspart
Neutral/
regular
Isophane
ultratard
Glargine
Onset
10-20′
30′
1h
4h
2-4h
Peak
1h
1-3h
4-6h
6-18h
peak less
Duration
3-5h
4-8h
8-14h
24h
20-24h
Complications of DM
 ACUTE
– Metabolic
• Diabetic
ketoacidosis(DKA)
• Hyperosmolar
Hyperglycemic Nonketotic
Syndrome(HHNS)
• Hypoglycemia
– Infections
 CHRONIC
– Microvascular
• Retinopathy
• Nephropathy
– Macrovascular
• CAD
• CVD
• PVD
– Neuropathies
– Diabetic Foot Disorders
– Psychosocial concerns
DIABETIC KETOACIDOSIS (DKA)
Signs and symptoms
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–
–
–
–
–
–
Hyperglycemia (>300mg/dl)
Elevated serum ketones
Acidosis as evidenced by pH of 6.8-7.3
HCO3 < 18
Osmolarity <320
Dehydration
Electrolyte depletion
GI distress (abdominal pain, N/V)
Respiratory distress (Kussmaul’s respirations and acetone breath odor)
TREATMENT OF DKA
Managing diabetic ketoacidosis (DKA) in an
intensive care unit during the first 24-48 hours
always is advisable.
• Correction of fluid loss with intravenous fluids
• Correction of hyperglycemia with insulin
• Correction of electrolyte disturbances,
particularly potassium loss
• Correction of acid-base balance
• Treatment of concurrent infection, if present
Correction of Fluid Loss
• Rehydration alone reduces plasma glucose by 30-50%
• Initial correction of fluid loss is either by isotonic sodium
chloride solution or by lactated Ringer solution. The
recommended schedule for restoring fluids is as follows:
• Administer 1-3 L during the first hour.(15-20ml/kg)
• Administer 1 L during the second hour.
• Administer 1 L during the following 2 hours
• Administer 1 L every 4 hours, depending on the degree of
dehydration and central venous pressure readings
• When blood sugar decreases to less than 250 mg/dL,
isotonic sodium chloride solution is replaced with 5-10%
dextrose with half isotonic sodium chloride solution.
Insulin therapy
• Loading dose of 0.1U/kg i.v. of regular insulin
• Followed by infusion of 0.1U/kg per hour
• Average decline of plasma glucose should be
75-100ml/hr with target values around
250ml/dl
Electrolyte Correction
• If the potassium level > 6 mEq/L, do not
administer potassium supplement.
• If the potassium level is 4.5-6 mEq/L,
administer 10 mEq/h of potassium chloride.
• If the potassium level is 3-4.5 mEq/L,
administer 20 mEq/h of potassium chloride.
• Monitor serum potassium levels hourly,
Correction of Acid-Base Balance
• Bicarbonate typically is not replaced as acidosis
will improve with the other treatments alone.
• Administration of bicarbonate has been
correlated with cerebral edema in children.
• Sodium bicarbonate is infused if decompensated
acidosis starts to threaten the patient's life(pH
<7.1)
• If sodium bicarbonate is indicated, 100-150 mL
of 1.4% concentration is infused initially. This may
be repeated every half hour if necessary.
• Treatment of Concurrent Infection
Hyperosmolar Hyperglycemic
Nonketotic Syndrome(HHNS)
• Four Clinical Features
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–
–
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Hyperglycemia (> 600-2000)
Mild or no ketosis
Hyperosmolality of plasma or serum (>340)
Profound dehydration
• 10-20% mortality rate with HHNS
• Risk factors include
– Elderly with Type 2
– Undiagnosed DM
– Prolonged hyperglycemia
• Signs and Symptoms
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–
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–
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Hypotension
Dehydration
Tachycardia
Decreased mentation
Neurologic abnormalities (focal)
Treatment
• If the plasma osmolarity > 320 mOsm/L,
large volumes (1000–1500 mL/hr) of 0.45%
normal saline should be administered until the
osmolarity is less than 320 mOsm/L,followed
by 0.9% normal saline
Insulin infusion @ 0.1U/kg hr
Electrolyte disturbances are less severe
compared to DKA
hypoglycemia
 plasma glucose level less than 50 mg/dL.
 May occur in all types of DM and is usually related to illness
 Causes
 Excessive exogenous insulin or oral diabetes medications that increase
insulin production
 Excessive alcohol consumption especially w/o adequate food intake
 Impaired hepatic or renal function
 Too little food
 Excessive exercise
 Signs and symptoms
adrenergic (sweating, tachycardia,palpitations, restlessness, pallor) and
neuroglycopenic (fatigue,confusion, headache, somnolence,
convulsions,coma).
TREATMENT OF HYPOGLYCEMIA
• Mild (40-60 gm/dl)
– Ingestion of 15 grams of Carbohydrate
– Monitor BG levels and treat until euglycemia
– Educate to prevent
• Moderate (20-40 gm/dl)
– Ingestion of 15-30 grams of CHO and follow with a meal or snack
containing protein
– Monitor BG levels and treat until euglycemia
– Educate to prevent
• Severe (<20 gm/dl)
– Ingestion not possible-must use IV glucose 0.5 g/kg IV or IM glucagon 0.5
to 1.0 mg preferably.
– May use glucose gel, honey, syrup, or jelly inside cheek
– Monitor BG levels and treat until euglycemia
– Educate to prevent
• Each ML of 50% glucose will raise BG by 2 mg/dl
WOUND HEALING & INFECTIONS
Wound healing is impaired in diabetic pts
Infections are the common cause of diabetic complications
– Alterations in leukocyte function– ↓ chemostasis
– Impaired phagocytic activity
– Reduced intracellular killing
• Commonly seen infections
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–
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–
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Cutaneous-furunculosis and carbuncles
Vulvovaginits
Cellulitis
UTI
Ear
• Must be treated aggressively
MICROVASCULAR COMPLICATIONS
• Microangiopathies affecting the capillaries and
arterioles of tissues
– Retina (retinopathy)
– Renal glomeruli (nephropathy)
• RETINOPTHY
– Development and progression largely depend on the duration
and severity of hyperglycemia
– Early detection and treatment can be beneficial in visual
restoration
– Uncontrolled HTN is an aggravating factor
– 3 categories
• Nonproliferative
• Preproliferative
• proliferative
NEPHROPATHY
•
•
•
•
•
20-40% chance of developing with a diagnosis of DM
Earlier occurrence in Type 2 than Type 1 DM
Glomerulosclerosis with glomerular basement membrane thickening
39-54% decrease in development with tight BG control (DCCT)
Signs and symptoms
– Microalbuminuria/proteinuria
– Elevated creatinine clearance
• Aggrevating conditions
– HTN
– Neurogenic bladder/UTI/Nephrotoxic drugs
• Treatment
– Improving BG control
– HTN management (ACE inhibitors)
– Protein restriction
– Dialysis/kidney transplant
– Educate to prevent
MACROVASCULAR COMPLICATIONS
• Responsible for 80% of deaths in people with DM
• Major vessels affected
– Coronary arteries
– Cerebral arteries
– Peripheral arteries
• CORONARY
– MI risk is 2x> in men and 3x> in women with DM
– Treatment-Aimed at reducing modifiable risk factors
• Smoking cessation
• BG, HTN, and lipid control
– Medications may include ACE or ARBs, statin drugs, and ASA
• Exercise (focus on wt reduction)
• CEREBRAL
– 2x> risk of CVD in patients with DM
• PERIPHERAL
– 2-3x> risk in patients with DM
– Signs and symptoms include IC, diminished peripheral pulses, lower extremity hair loss, and
nocturnal rest pain
– Major factor in the development of gangrene and amputations in patients with DM
– Treatment
•
•
•
Aimed at modifiable risk factors as listed with CAD
Medication
Rest during periods of exertion
Peripheral neuropathy
• 50% of diabetics develop peripheral neuropathy
after 25 years
• Distal symmetrical diffuse sensorimotor
polyneuropathy is most common(stocking glove
neuropathy)
• Foot ulcers develop due to loss of cutaneous
sensitivity to pain and temp and impaired
perfusion
• Treatment includes optimal glucose control
,NSAIDS,Antidepressants,anticonvulsants for pain
relief
Diabetic Autonomic Neuropathy
• affect any part of the autonomic nervous system.
• Autonomic disturbances can be subclinical or clinical
• Subclinical DAN can occur within a year or two after
diagnosis
• Cardiovascular autonomic neuropathy is a common type
of DAN
• A resting tachycardia and a loss of heart rate variability
(HRV)(<10 beats per min)during deep breathing are early
signs.
• in the advance stages, severe orthostatic hypotension (>30
mm Hg with standing) is present.
• Impaired respiratory reflexes and impaired ventilatory
responses to hypoxia and hypercapnia are also present
Gastrointestinal effects of DAN
• Affects 25% of diabetics
• impair gastric secretion and gastric motility,
causing gastroparesis diabeticorum
• nausea, vomiting, early satiety, bloating, and
epigastric pain.
• In DAN, the counterregulatory hormone
responses to hypoglycemia are impaired and the
warning signs eliminated, creating a dangerous
situation of hypoglycemia unawareness.
Diabetes and accelerated physiologic
ageing(“RealAge”)
(‘X’ yrs for each choronologic yr of disease)
Diabetes cause accelerated aging Thus, the risks involved
with diabetes are similar to those for someone much older,
someone who has a much higher physiologic age (or “RealAge”).
Poor control of glucose
levels
Tight control glucose levels
Type 1
1.75
1.25
Type 2
1.5
1.06
Acute hyperglycemia causes
• dehydration,
• impaired wound healing,
• an increased rate of infection,
• worsening central nervous system/spinal cord
injury with ischemia,
• hyperviscosity with thrombogenesis
Preop evaluation
• History & general physical exam
– MEASURE BLOOD PRESSURE AND PULSE RATE- BOTH WHEN
THE PATIENT IS LYING DOWN AND STANDING
– ASSESS THE PATIENT'S MUSCLE STRENGTH, DEEP TENDON
REFLEXES, AND SENSE OF TOUCH.
• HBA1c levels
• Pulmonary,Cardiovascular & renal assessment
• CXR-cardiac enlargement,pleural effusion,
pulmonary vascular congestion
• ECG
• TM & C-spine mobility
• No insulin ,no glucose for short procedures
Pre-op evaluation
Autonomic Neuropathy
• typical symptoms and signs of postural
hypotension, gastroparesis, gustatory sweating,
and nocturnal diarrhoea.
• It is worth assessing all diabetic patients for
autonomic neuropathy.
• The easiest way is to assess heart rate variability.
The normal heart rate should increase by over 15
beats/minute in response to deep breathing.
Neuropathy is likely is there is less than 10
beats/minute increase
Peripheral Neuropathy
• The commonest type of peripheral neuropathy is
the “glove and stocking” type.
• However diabetics are also prone to
mononeuritis multiplex and some particularly
painful sensory neuropathies.
• Poor patient positioning is likely to result in
pressure sores that are often slow to heal given
poor peripheral blood flow.
• Documentation of existing neuropathy is prudent,
especially if considering a regional technique.
• Cardiovascular
• Diabetics are more prone to ischaemic heart disease
(IHD), hypertension, peripheral vascular disease,
cerebrovascular disease, cardiomyopathy and
perioperative myocardial infarction.
• Ischaemia may be “silent” as a result of neuropathy.
Routine ECG should be performed and appropriate
stress testing if in doubt.
• Autonomic neuropathy can result in sudden
tachycardia, bradycardia, postural hypotension and
profound hypotension after central neuraxial blockade
Respiratory
• Diabetics, especially the obese and smokers
are more prone to respiratory infections and
also have abnormal spirometry.
• Chest physiotherapy, humidified oxygen and
bronchodilators should be considered
Gastrointestinal
• Gastroparesis is characterised by a delay in gastric
emptying without any gastric outlet obstruction.
Increased gastric contents increase the risk of
aspiration.
• Always ask about symptoms of reflux and
consider a rapid sequence induction with cricoid
pressure even in elective procedures.
• If available prescribe an H2 antagonist such as
ranitidine150mg plus metoclopramide 10mg, at
least 2 hours preoperatively.
Airway
• Glycosylation of collagen in the cervical and
temporo-mandibular joints can cause difficulty
in intubation.
Prayer sign Patient is asked to
bring both thepalms together
as ‘Namaste’ and sign is
categorized as–
Positive – When there is gap
between palms.
Negative – When there is no
gap between palms
Inability to approximate the
palmer surfaces of the
phalangeal joints despite
maximal effort, secondary to
diabetic stiff-joint syndrome
Palm print
The patient is made to sit;
Palm and fingers of right hand are painted with
blue ink,
patient then presses the hand firmly against a
white paper placed on a hard surface.
It is categorized as:
Grade 0 – All the phalangeal areas are visible.
Grade 1 – Deficiency in the interphalangeal areas
of the 4th and 5th digits.
Grade 2 – Deficiency in interphalangeal areas of
2nd to 5th digits.
Grade 3 – Only the tips of digits are seen
Renal
• Diabetes is one of the commonest causes of endstage renal failure.
• Check urea, creatinine and electrolytes.
Specifically check the potassium especially in
view of the possible need for suxamethonium as
a result of gastroparesis.
• If unavailable, proteinuria is likely to indicate
kidney damage.
• Ensure adequate hydration to reduce
postoperative renal dysfunction.
Immune system
• Diabetics are prone to all types of infection.
Indeed an infection might actually worsen
diabetic control.
• Tight glycaemic control will reduce the incidence
and severity of infections and is routine practice
in the management of sepsis and diabetic foot
infections.
• Perform all invasive procedures with full asepsis.
• Autonomic neuropathy predisposes to
hypothermia under anaesthesia
• Diabetics are prone to cataracts and
retinopathy. Prevent surges in blood pressure,
for example at induction, as this might cause
rupture of the new retinal vessels.
• Diabetes affects oxygen transport by causing
glucose to covalently bind to the hemoglobin
molecule, decreasing oxygen saturation and
red blood cell oxygen transport in diabetic
patients
Anesthetic agents and diabetes
mellitus
• etomidate inhibits adrenal steroid genesis and may induce
a decrease in the glycemic response to surgery.
• alpha 2 agonist, clonidine, reduces sympathetic tone and
the release of norepinephrine from nerve terminals.
clonidine decreased circulating catecholamines &
improved blood glucose control and decreased insulin
requirements
• High doses of opiates induce hemodynamic ,hormonal
and metabolic stability
• Avoid lactate containing solutions-cause hyperglycemia
• Diabetics less able to metabolise lipid emulsionsprolonged infusions of propofol should be avoided-can
lead to hyperglycemia
• volatile anesthetics, such as halothane, enflurane,and
isoflurane, inhibit insulin response to glucose
• Halothane or sevoflurane, produced greater negative
inotropic effects in myocardium of diabetic compared
with nondiabetic patients
• BZDs reduce the secretion of adrenocorticotrophic
hormone (ACTH) and consequently cortisol, and
stimulate basal secretion of growth hormone
• Minimal in usual sedative doses but significant in
continuous infusion to patients in intensive care units
Anaesthetic Management
General principals
• Avoid hypoglycaemia (under 4mmol/l) as this can cause irreversible cerebral
damage
• Avoid severe hyperglycaemia (over 14mmol/l) to minimise dehydration and
metabolic upset
• Type 1 diabetics need insulin to prevent ketogenesis
• • Aim for a blood glucose between 6 and 10mmol/l
• Accurate, easy-to-use glucose monitors, make the practice of “permissive
hyperglycaemia” unacceptable given the known outcome benefits of tight control
• Diabetic patients should be placed first on the operating list to shorten the
preoperative fast and potentially allow normal oral intake later that same day
• Tight metabolic control is important for both type 1 and type 2 patients.
• The best marker for recent control is the percentage of glycosylated haemoglobin
(HbA1C). If available, levels less than 7% indicate good control whilst levels over 9%
and particularly 12%, indicate poor control and likely associated electrolyte and
water loss.
• These patients should be admitted preoperatively for correction of these
abnormalities and stabilisation of blood sugar levels before the addition of surgical
stressors.
• Continue all diabetic medication until the day of surgery
except:
a.) Chlorpropamide (stop 3 days prior as long acting,
substitute with a shorter acting sulphonylurea)
b.) Metformin only if major surgery as risk of lactic acidosis
c.) Glitazones
c.) Long acting insulin – substitute with short/intermediate
acting
Measure blood sugar preoperatively – 4 hourly if on insulin,
8 hourly if not
If the patient is expected to eat within 4 hours of the
operation then treat this group as having “Minor” surgery.
Otherwise, surgery is “Major
Minor surgery, type 2 diabetes NOT
on insulin (diet/tablet controlled)
• 1st on list
• Preoperative blood sugar <180mg/dl Take normal
medication inc. evening dose
• Preoperative blood sugar >180mg/dl Treat as if
“Major” surgery
• Omit oral hypoglycaemic on morning of surgery
• Monitor blood glucose 1 hour preop; intraoperatively if
over 1 hour; and 4hourly postop until eating.
• Recommence oral hypoglycaemics with first meal
Minor surgery, type 2 diabetes ON
insulin/type 1 diabetes,
•
•
•
•
•
1st on list
Take normal medication on day prior*
Omit morning SC insulin if glucose < 126mg/dl
Give half normal insulin if glucose >126mg/dl
Monitor blood glucose 1 hour preop; intraoperatively
at least once; 2 hourly until eating and then 4 hourly.
• Recommence normal SC insulin with first meal
• *If taking a long acting insulin, either convert to
short/intermediate acting several days prior or ½ the
dose the day prior to surgery
Major surgery, all types of diabetes,
• 1st on list
• Normal medication on day prior (unless very poorly controlled, in which
case, establish sliding scale below 3 days prior)
• Day of surgery, omit oral hypoglycaemics/ normal SC insulin
• Check blood glucose 1 hour preop;
• hourly intraop until 4 hours
• postop; 2 hrly thereafter and
• 4 hourly once stabilised.
• Insulin is the key infusion. With close monitoring, and adjustment
according to a sliding scale, there is no absolute requirement for
concurrent dextrose containing solutions,
• However, commonly 5% or 10% dextrose solutions containing 20mmol/l of
potassium are infused at a steady rate of 100ml/hr to provide
carbohydrate substrate.
•
• Titrate the insulin infusion (through a dedicated line with one-way valve) as
below.
Blood glucose (mmol/l) Insulin infusion rate (unit/hr)
If poor
control*
(unit/hr)
<4
0
0
4.1 – 9
1
2
9.1-13
2
3
13.1-17
3
4
17.1-28
4
6
>28
6 (check infusion running) 8
• *If glucose not maintained <10mmol/l then increase the rates,
Classic “Non-tight Control” Regimen
• Aim-to prevent hypoglycemia,ketoacidosis and
hyperosmolar states
• protocol
– NPO after midnight
– 6AM –start i.v. dextrose 5% @ 125ml/hr/70 kgBW
– ⅟2 usual morning insulin dose s/c
– Cont 5D intra op
– Post op -monitor glucose and give insulin on
sliding scale
“Tight Control” Regimen 1
• Aim-to keep glucose levels b/w 79-120 mg/dl. it Improves
– wound healing & prevent wound infection
– Neurologic outcomeafter global or focal ischemic insults
– Weaning from CPB
• Protocol (evening before surgery)
–
–
–
–
Determine preprandial glucose levels
Begin i.v. infusion of 5%Dextrose @ 50ml/hr/70kgBW
Piggyback an infusion of regular insulin with infusion pump (50U in 250 ml NS)
Infusion rate (U/hr)= plasma glucose(mg/dl)/150
(100 if pt taking steroids or BMI >35)
– blood glucose monitoring 4 hrly
– At the start of surgery -determine blood glucose levels and then, every 1-2
hrly for 24 hrs
• Hypoglycemia(<50mg/dl) is treated with 15 ml of 50% dextrose
• Tight control regimen 2 requires “feedback mechanical pancreas”
Alberti GIK Regimen
• Initial solution: 500 ml 10% glucose+15U
insulin+10 mmol KCl
• Infusion rate @ 100 ml/ h( 3U/h)
• Check BG every 2 hr
BG (mmol/L)
action
<6.5
10U insulin in 500 ml (2U/h)
>6.4-<11.1
15U insulin in 500ml(3U/h)
>11
20U insulin in 500ml(4U/h)
• Adjust in 5-U steps
Regional techniques
• are not contraindicated in the diabetic patient
• offer some potential advantages such as the avoidance
of intubation, having an awake patient to warn of
impending hypoglycaemia, and an earlier return to
normal eating patterns.
• Document any existing motor/sensory neuropathies
prior to performing any blocks
• look for evidence of autonomic neuropathy. If present,
expect increased hypotension after neuraxial blocks.
• The chances of epidural abscess are also increased.
• high spinal anesthesia (dermatome level T2–
T6) induced a reduction in the acute insulin
response to glucose, whereas low spinal
anesthesia (dermatome level T9–T12) induced
no such reduction.
future
• Non-invasive BS testing
• Continuous BS monitor + insulin pump
• “Artificial Pancreas”
• Islet cell transplants
• Stem-cell research
• Energy homeostasis breakthroughs
thanks