Diabetes Mellitus

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DIABETES MELLITUS AND ANAESTHETIC IMPLICATIONS

Dr.J.Edward Johnson
https://anaesthesianews.wordpress.com
DIABETES MELLITUS AND ANAESTHETIC IMPLICATIONS
INTRODUCTION:
➢ The liver is the primary source of endogenous glucose production via glycogenolysis and
gluconeogenesis.
➢ Following a meal, plasma glucose level increases, which stimulates an increase in plasma
insulin secretion that promotes glucose utilization. Late in the postprandial period (2–4
hours after eating) when glucose utilization exceeds glucose production, a transition
from exogenous glucose delivery to endogenous production becomes necessary to
maintain a normal plasma glucose level.
➢ Approximately 70%–80% of glucose released by the liver is metabolized by insulin-
insensitive tissues such as the brain, gastrointestinal (GI) tract, and red blood cells.
➢ During this time, diminished insulin secretion is fundamental to maintenance of a
normal plasma glucose concentration.
➢ Hyperglycemia-producing hormones (glucagon, epinephrine, growth hormone, cortisol)
comprise the glucose counterregulatory system and support glucose production.
➢ Glucagon plays a primary role by stimulating glycogenolysis and gluconeogenesis and
inhibiting glycolysis.
➢ Diabetes mellitus results from an inadequate supply of insulin and/or an inadequate
tissue response to insulin.
CLASSIFICATION:
Diabetes can be classified into the following general categories: (Classification and Diagnosis of
Diabetes: Standards of Medical Care in Diabetes - 2018) ADA
1. A. Type 1a diabetes : It is caused by autoimmune destruction of beta cells within
pancreatic islets, resulting in complete absence or minimal circulating levels of
insulin.
B. Type 1b diabetes: It is a rare disease of absolute insulin deficiency that is not
immune mediated.
2. Type 2 diabetes also is not immune mediated and results from defects in insulin
receptors and postreceptor intracellular signaling pathways.
3. Gestational diabetes mellitus (GDM) diabetes diagnosed in the second or third
trimester of pregnancy that was not clearly overt diabetes prior to gestation.
4. Specific types of diabetes due to other causes,
✓ Monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset
diabetes of the young [MODY]),
✓ Diseases of the exocrine pancreas (such as cystic fibrosis and pancreatitis), and
✓ Drug- or chemical-induced diabetes (such as with glucocorticoid use, in the
treatment of HIV/AIDS, or after organ transplantation)
SIGNS AND SYMPTOMS:
Type 1 Diabetes:
• Between 5% and 10% of all cases of diabetes are type 1.

• Type 1 diabetes is caused by T cell–mediated autoimmune destruction of beta cells in
the pancreas.
• The exact cause is unknown, although environmental triggers such as viruses (especially
enteroviruses), dietary proteins, or drugs or chemicals may initiate the autoimmune
process in genetically susceptible hosts.
• At least 80%–90% of beta cell function must be lost before hyperglycemia occurs.
• 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 the presence of a random blood glucose level higher than 200
mg/dL and a hemoglobin (Hb)A1c level above 7.0%.
• The presence of ketoacidosis indicates severe insulin deficiency and unrestrained
lipolysis.
Type 2 Diabetes
• Type 2 diabetes is responsible for 90% of all cases of diabetes mellitus in the world.
• Patients with type 2 diabetes are typically in the middle to older age group and are
overweight
• Type 2 diabetes is characterized by relative beta cell insufficiency and insulin resistance.
In the initial stages of the disease, an insensitivity to insulin on the part of peripheral
tissues leads to an increase in pancreatic insulin secretion to maintain normal plasma
glucose levels. As the disease progresses and pancreatic cell function decreases, insulin
levels are unable to compensate and hyperglycemia occurs.
• Three important defects are seen in type 2 diabetes:
(1) an increased rate of hepatic glucose release,
(2) impaired basal and stimulated insulin secretion, and
(3) inefficient use of glucose by peripheral tissues (i.e., insulin resistance)
• Obese patients exhibit a compensatory hyperinsulinemia to maintain normoglycemia.
These increased insulin levels may desensitize target tissues, causing a reduced
response to insulin.
Metabolic syndrome, or insulin-resistance syndrome:
At least three of the following:
1. Fasting plasma glucose level ≥ 110 mg/dL
2. Abdominal obesity (waist girth > 40 inches in men, >35 inches in women)
3. Serum triglyceride level ≥ 150 mg/dL
4. Serum high-density lipoprotein cholesterol level < 40 mg/dL in men, <50 mg/dL in
women
5. Blood pressure ≥ 130/85 mm Hg
DIAGNOSIS:
The American Diabetes Association (ADA) has established diagnostic criteria for diabetes
mellitus:
❖ Categories of increased risk for diabetes (prediabetes)
✓ FPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) (IFG) OR
✓ 2-h PG during 75-g OGTT 140 mg/dL (7.8 mmol/L) to 199 mg/dL (11.0 mmol/L)
(IGT) OR
✓ A1C 5.7–6.4% (39–47 mmol/mol)
❖ Criteria for the diagnosis of diabetes
✓ FPG ≥ 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least
8 h. OR
✓ 2-h PG ≥ 200mg/dL (11.1mmol/L) during OGTT. The test should be performed as
described by the WHO, using a glucose load containing the equivalent of 75-g
anhydrous glucose dissolved in water. OR
✓ A1C ≥ 6.5% (48 mmol/mol). The test should be performed in a laboratory using a
method that is NGSP certified and standardized to the DCCT assay. OR
✓ In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a
random plasma glucose ≥ 200 mg/dL (11.1 mmol/L).
➢ The HbA1c test provides a valuable measure of long-term glycemic control.
➢ Hemoglobin is nonenzymatically glycosylated by glucose, which freely crosses red blood
cell membranes.
➢ The percentage of hemoglobin molecules participating in this reaction is proportional to
the average plasma glucose concentration during the preceding 60–90 days.
➢ The normal range for HbA1c is 4%–6%. Increased risk of microvascular and
macrovascular disease begins when the HbA1c proportion is 6.5% or higher.
TREATMENT:
The cornerstones of treatment for type 2 diabetes are dietary adjustments along with weight
loss, exercise therapy, and oral antidiabetic drugs.
Oral Antidiabetic Drugs:
❖ The four major classes of oral antidiabetic medications are
1. The secretagogues (sulfonylureas, meglitinides), which increase insulin availability;
2. The biguanides (metformin), which suppress excessive hepatic glucose release;
3. The thiazolidinediones or glitazones (rosiglitazone, pioglitazone), which improve insulin
sensitivity;
4. The α-glucosidase inhibitors (acarbose, miglitol), which delay GI glucose absorption
➢ These agents are used to maintain glucose control, which is defined as a
✓ Fasting glucose level of 90–130 mg/dL,
✓ Peak postprandial glucose level below 180 mg/dL, and
✓ HbA1c level below 7% in the initial stages of the disease.
1. The sulfonylureas are usually the initial pharmacologic treatment for type 2 diabetes
mellitus.
✓ They act by stimulating insulin secretion from pancreatic beta cells;
✓ They can also enhance insulin-stimulated peripheral tissue utilization of glucose.
✓ The second-generation agents (glyburide, glipizide, glimepiride) are more potent
and have fewer side effects than their predecessors.
Another class of insulin secretagogues act as GLP-1 (glucagon-like peptide 1) agonists
or enhance endogenous GLP-1 activity in the gut. Exenatide and liraglutide are
examples and have been approved for treatment for type 2 diabetes.
✓ These agents (incretins) increase glucose-stimulated insulin secretion
✓ Suppress glucagon, and
✓ Slow gastric emptying.
Dipeptidyl peptidase-4 inhibitors (saxagliptin, sitagliptin, vildagliptin) inhibit the
degradation of native GLP-1 and thus enhance glucose-stimulated insulin secretion.
2. The biguanides
✓ Decrease hepatic gluconeogenesis and to a lesser degree enhance utilization of
glucose by skeletal muscle and adipose tissue by increasing glucose transport
across cell membranes.
✓ In addition to lowering glucose levels, they decrease plasma levels of
triglycerides and low-density lipoprotein cholesterol and reduce postprandial
hyperlipidemia and plasma free fatty acids.
✓ The risk of hypoglycemia is less than that with the sulfonylureas.
✓ Lactic acidosis is a rare but serious side effect of the biguanides; the risk is
particularly high in patients with renal insufficiency. It is much less common with
metformin than with its predecessor phenformin.
3. The thiazolidinediones or glitazones are insulin sensitizers
✓ That decrease insulin resistance by binding to peroxisome proliferator–activated
receptors located in skeletal muscle, liver, and adipose tissue.
✓ These drugs influence the expression of genes encoding proteins for glucose and
lipid metabolism, endothelial function, and atherogenesis; as a result, they may
influence diabetic dyslipidemia in addition to hyperglycemia.
4. The α-glucosidase inhibitors
✓ inhibit α-glucosidase enzymes in the brush border of enterocytes in the
proximal small intestine, which results in a delay in intraluminal production and
subsequent absorption of glucose.
✓ They are administered before a main meal to ensure their presence at the site
of action.
In most patients, therapy is initiated with a sulfonylurea or biguanide and titrated to achieve
fasting and peak postprandial glucose levels recommended by the ADA.
ALGORITHM FOR TREATMENT OF TYPE 2 DIABETES. FDA, US FOOD AND DRUG
ADMINISTRATION;
INSULIN:
Insulin is necessary to manage all cases of type 1 diabetes and many cases of type 2 diabetes.
Basal insulins:
✓ Intermediate acting (NPH, Lente, lispro protamine, aspart protamine) and administered
twice daily
✓ Long acting: (Ultralente, glargine, detemir) and administered once daily;
✓ Short acting (regular)
✓ Rapid acting (lispro, aspart, glulisine), which provide glycemic control at mealtimes.
➢ Rapid-acting insulins are preferred over regular insulin for prandial coverage.
➢ Insulin glargine has a later onset of action, longer duration of action, a less pronounced
peak of action, and a lower incidence of hypoglycemia, especially at night.
➢ long-acting insulin is usually prescribed with a short acting insulin to mimic physiologic
insulin release with meals.
➢ In general, patients with type 1 diabetes require 0.5–1 U/kg/day divided into multiple
doses, with approximately 50% given as basal insulin.
➢ Regular insulin is preferred over insulin analogues for intravenous (IV) infusions because it is
less expensive and equally effective
➢ The hypoglycemic effect can be exacerbated by simultaneous administration of alcohol,
sulfonylureas, biguanides, thiazolidinediones, angiotensin converting enzyme (ACE)
inhibitors, monoamine oxidase inhibitors, and nonselective β-blockers.
HYPOGLYCEMIA UNAWARENESS: Repetitive episodes of hypoglycemia, especially at night, can
result in hypoglycemia unawareness, a condition in which the patient does not respond with
the appropriate autonomic warning symptoms before neuroglycopenia. The diagnosis in adults
requires a plasma glucose level below 50 mg/dL. Symptoms are
✓ Adrenergic (sweating, tachycardia, palpitations, restlessness, pallor) and
✓ neuroglycopenic (fatigue, confusion, headache, somnolence, convulsions, coma).
Treatment includes administration of sugar in the form of sugar cubes, glucose tablets, or soft
drinks if the patient is conscious; and glucose 0.5 g/kg IV or glucagon 0.5–1 mg IV,
intramuscularly, or subcutaneously if the patient is unconscious.
DAWN PHENOMENON:
✓ Occurs in Type 1 DM
✓ Due to increased requirement of insulin post midnight
✓ This is because of glucagon surge causing hyperglycemia
SOMAGYI PHENOMENON:
Compensatory hyperglycemia following hypoglycemia. Occurs at early morning.
COMPLICATIONS:
➢ Acute complications:
✓ Diabetic ketoacidosis (DKA)
✓ Hyperosmolar nonketotic coma (HONC)
✓ Hypoglycemia (Blood glucose ≤ 50 mg/dl).
➢ Chronic complications:
✓ Microvascular:
o Eye disease:
▪ Retinopathy
▪ Macular edema.
o Neuropathy:
▪ Sensory and motor neuropathy (“stocking-glove” distribution),
foot fractures (Charcot joint)
▪ Autonomic neuropathy.
o Nephropathy.
✓ Macrovascular:
o Coronary artery disease
o Cerebrovascular accidents
o Peripheral vascular disease.
Cardiac complications: The diabetic patient has an increased risk of:
 Coronary artery disease

✓ Diabetic patients > 65 years of age have significant symptomatic/asymptomatic
coronary artery disease. Silent ischemia may be present because of diabetic
autonomic neuropathy
 Hypertension
 Peripheral arterial disease
 Systolic and diastolic dysfunction, related to:
✓ Coronary artery disease
✓ Hypertension
✓ Left ventricular hypertrophy
✓ Endothelial dysfunction
✓ Obesity
✓ Autonomic neuropathy.
Others:
 Cataract, glaucoma
 Gastrointestinal:
✓ Gastroparesis, constipation
✓ Diarrhea.
 Genitourinary:
✓ Uropathy
✓ Erectile dysfunction.
 Dermatological
 Infection
HOW TO ASSESS FOR AUTONOMIC NEUROPATHY:
Overt signs and symptoms of autonomic disease are as follows:
 Cardiovascular
✓ Resting tachycardia
✓ Exercise intolerance
✓ Orthostatic hypotension
✓ Silent myocardial ischemia.
 GI
✓ Esophageal dysmotility (dysphagia)
✓ Gastroparesis
✓ Constipation
✓ Diarrhea
✓ Fecal incontinence.
 Genitourinary
✓ Neurogenic bladder (diabetic cystopathy)
✓ Erectile dysfunction
✓ Retrograde ejaculation
✓ Female sexual dysfunction (e.g. loss of vaginal lubrication).
 Metabolic
✓ Hypoglycemia unawareness
✓ Hypoglycemia-associated autonomic failure.
 Sudomotor
✓ Anhidrosis
✓ Heat intolerance
✓ Gustatory sweating
✓ Dry skin.
 Pupillary
✓ Pupillomotor function impairment (e.g. decreased diameter of dark adapted
pupil)
✓ Argyll-Robertson pupil.
TESTS FOR DIABETIC AUTONOMIC NEUROPATHY (DAN)
✓ Early stage: Abnormality of heart rate response during deep breathing alone
✓ Intermediate stage: An abnormality of Valsalva response
✓ Late stage: The presence of postural hypotension.
The tests for parasympathetic control
➢ Heart rate variability (HRV) in response to:
1. Deep breathing
2. Standing
3. Valsalva maneuver.
The tests for sympathetic control
➢ Blood pressure response to:
1. Standing or passive tilting
2. Sustained handgrip
3. Response to the Valsalva maneuver
Response to the Valsalva maneuver: In the standard Valsalva maneuver, the supine patient,
connected to an ECG monitor, forcibly exhales for 15 s against a fixed resistance (40 mmHg)
with an open glottis. This results in a sudden transient increase in intrathoracic and intra-
abdominal pressures, with a characteristic hemodynamic response.
a) Phase I: Transient rise in blood pressure and a fall in heart rate due to compression of
the aorta and propulsion of blood into the peripheral circulation. Hemodynamic
changes are due to mechanical factors.
b) Phase II: Initial fall in blood pressure followed by the recovery of blood pressure later in
the phase. The blood pressure changes are accompanied by an increase in heart rate.
There is a fall in cardiac output due to decreased venous return which causes reflex
tachycardia and increased peripheral resistance.
c) Phase III: Drop in blood pressure and rise in heart rate when expiration stopped.
d) Phase IV: Overshoot of blood pressure above the baseline value due to residual
vasoconstriction in a setting of a now normal venous return and cardiac output. There
is a reflex bradycardia.
The Valsalva ratio is calculated from the ECG waveform by dividing the longest R-R interval after
the maneuver (in phase IV) to the shortest R-R interval during the maneuver.
A Valsalva ratio < 1.2 is abnormal.
HRV (Heart Rate Variability):
➢ Respiratory sinus arrhythmia (RSA) is a normal phenomenon due to vagal input to sinus
node during expiration causing cardio deceleration.
➢ Autonomic neuropathy decreases the HRV (difference in between maximum and
minimum heart rate during the respiratory cycle).
➢ A clinical but less accurate method is to ask the patient to breathe quietly and deeply at
a rate of six breaths per minute (at this rate there is maximum variation in heart rate)
✓ Normal variability > 15 beats /min
✓ Abnormal result < 10 beats /min
➢ Aging is associated with decreased RSA due to decreased vagal tone and decreased beta
receptor responsiveness and the criteria may not apply to patients above 60 years of
age.
Response to standing up (30: 15 ratio):
➢ There is a rapid increase in heart rate in response to standing that is maximal at
approximately the 15th beat after standing.
➢ This is followed by a relative bradycardia that is maximal at approximately the 30th beat
after standing.
➢ The heart rate should increase by 10%. 30:15 ratio is measured as the longest R-R
interval during beats 20–40 divided by the shortest R-R interval during beats 5–25.
➢ In patients with DAN, there is only a gradual increase in heart rate.
A. 30:15 ratio >1.04 is normal
B. 1.01 – 1.03 is borderline
C. < 1.01 is abnormal
Orthostatic hypotension:
➢ It is defined as a fall in blood pressure > 30 mm Hg for systolic or >10 mm Hg for
diastolic blood pressure in response to postural change, from supine to standing.
➢ Normally, blood pressure is rapidly corrected by baroreflex-mediated peripheral
vasoconstriction and tachycardia and the fall in SBP is
✓ < 10 mm Hg- Normal.
✓ A drop by 11–29 mm Hg is borderline and
✓ A drop > 30 mm Hg is significant.
Response to tilting: It is a more precise stimulus and may be used instead of standing. The
response is similar.
Sustained hand grip:
➢ Sustained muscle contraction causes a rise in systolic and diastolic blood pressure and
heart rate.
➢ Exercising muscle stimulates a reflex arc resulting in increased cardiac output and heart
rate.
➢ As the peripheral vascular resistance is maintained the diastolic pressure rises by > 16
mm Hg.
➢ A response of < 10 mm Hg is considered abnormal.
Gastroparesis: The finding of retained food in the stomach after an 8–12 h fast in the absence
of obstruction is diagnostic of gastroparesis.
Management of DAN: Control of blood sugar levels, ACE inhibitors and b-blockers have been
tried for control of the condition.
GLYCEMIC REGIMENS:
1. Sliding Sale
❖ Advantage: Easy to calculate
❖ Disadvantages:
✓ Not used in major surgery
✓ Blood glucose not optimally controlled
MODIFIED SLIDING SCALE
2. Classic Non tight Control Regimen:

➢ NPO from 12 midnight with glass of orange juice kept by the side for emergency
➢ At 6 AM on the day of surgery, IV 5% dextrose at 125 ml/hr/70 kg body weight
➢ After starting IV infusion, half the usual morning dose of usual type of insulin given S/C
➢ Continue 5% dextrose intraoperatively at atleast 125 ml/hr/70 kgs
➢ Monitor blood glucose postoperatively and treat as per the sliding scale.
3. Tight Control Regimen

➢ Aim: To maintain blood sugar between 79 and 120 mg/dl.
➢ Indications for Tight Glycemic Control
✓ Type 1 DM (as they need insulin to avoid DKA)
✓ Pregnant diabetics
✓ Major surgery or bowel anastomosis
✓ Those requiring postprocedure ICU stay
✓ Diabetics undergoing CPB
✓ Those with global CNS ischemia (e.g. following cardiac arrest)
✓ Surgery in those with DKA
✓ Type II DM does not benefit from tight perioperative control unless ICU stay
is required according to current data.
REGIMEN I:
➢ Determine preprandial blood glucose on the evening before surgery
✓ IV infusion of 5% dextrose at 50 ml/hr/70 kg body weight
✓ Piggy back regular insulin:
▪ 50 IU added to 250 ml NS
▪ Flush infusion line with first 60 ml of infusate.
✓ Rate of infusion:
▪ (Blood glucose)/150 normally
▪ (Blood glucose)/100 if:
o Patient on steroids (except inhaled)
o Obese with BMI > 35
➢ Repeat blood glucose Q4H and adjust insulin to obtain blood glucose 100–200 mg/dl.
➢ On morning of surgery:
▪ Administer nondextrose-containing fluids
▪ Insulin started with insulin infusion rate (BG/150 or BG/100).
➢ Determine blood glucose at the start of surgery and Q2H for rest of 24-hour period
➢ Treat hypoglycemia (< 50 mg/dl) with 15 ml 50% dextrose with termination of infusion.
REGIMEN II:
➢ Obtain feedback mechanism pancreas and set controls for desired blood glucose levels.
➢ Start 2 IV lines.
Advantages:
✓ Improves CNS outcome after global/focal ischemic event
✓ Decreased incidence of polyneuropathy
✓ Improves weaning from CPB
✓ Decreased renal dysfunction and need for dialysis
✓ Reduced need for blood transfusion
✓ Reduces deaths in ICU and duration of ICU stay
✓ Improved oxygen transport
✓ Prevents wound infection
✓ Improves wound healing.
Disadvantages
✓ Increased incidence of hypoglycemia
✓ Lack of potassium supplementation.
4. GIK REGIMEN:
Combination of 10% dextrose and insulin is added to 500 ml fluid bag

✓ This provides 250 gms glucose and 50 U insulin in 24 hours
✓ Advantage: Prevents hypo/hyperglycemia
✓ Disadvantage: New bag of fluid is required every time glucose falls outside range
5. VELLORE REGIMEN:
✓ Advantages: Simple, safe and inexpensive
✓ Disadvantages: Potassium levels are not corrected.
6. ALBERTI REGIMEN:
✓ Initial insulin solution: 500 ml 10% dextrose with 10mmol KCl and 15 IU insulin
✓ Infuse at 100 ml/hr (i.e. 3 IU/hr)
✓ Check blood glucose second hourly
✓ Adjust infusion rate according to result:
7. WATT-HIRSCH REGIMEN:
✓ Also called variable rate insulin regimen
✓ Infuse glucose at 5 gm/hr, K+ at 2–4 mEq/hr and insulin at 0.5–1 IU/hr
✓ Measure blood glucose hourly
✓ Insulin is either piggy backed with glucose or given as separate infusion.
PREOPERATIVE EVALUATION:
• History:
➢ Central nervous system:
✓ Peripheral neuropathy (glove and stocking neuropathy)
✓ Headache, syncope
✓ TIA/stroke
➢ Cardiovascular:
✓ MI: Increased chances if erectile dysfunction present
✓ Silent MI: Increased chances if autonomic neuropathy
✓ Hypertension
✓ Congestive cardiac failure: Especially if poor glycemic control
✓ Dyspnea on exertion/reduced exercise tolerance
➢ Respiratory:
✓ Frequent infections
✓ Reduced VC, FVC, FEV, DLCO.
➢ Gastrointestinal:
✓ Gastroparesis due to ganglion cell damage
✓ Postprandial vomiting, early satiety
✓ Delayed gastric emptying.
➢ Genitourinary:
✓ Erectile dysfunction
✓ Renal failure especially if age > 55 years and diabetes and hypertension coexist.
➢ Medication history, history of anesthetic exposure
➢ Episodes of hypoglycemia/hyperglycemia.
• Examination:
➢ Document vitals, orthostatic vital signs and skin breakdown points
➢ Sensory examination
➢ Airway examination:
➢ Stiff joint syndrome:
✓ Seen in poorly controlled DM
✓ Reduced mobility of cervical, atlantoocciptal and TM joint occurs.
➢ Prayer sign: inability to approximate palmar surface of interphalangeal joints
➢ Palm print sign:
✓ Alteration in palm print when it is taken on paper
✓ Indicates interphalangeal joint stiffness.
➢ Fundoscopy for retinopathy
➢ Tests for autonomic dysfunction
➢ Back for edema and infection: Difficult to perform subarachnoid block.
INVESTIGATIONS
➢ Routine blood: Hb, TC, DC, ESR
➢ Renal function tests
➢ Preoperative FBS < 110 mg% in noncritically ill patients: ACE recommendations
➢ ECG, treadmill test for silent MI
➢ Chest X-ray: Cardiomegaly
➢ Pulmonary function tests
➢ Glycated hemoglobin:
◼ Called HbA1c
◼ Best evidence of glucose control over the last 1–2 months
◼ Level < 2% recommended by ADA
◼ Microalbuminuria 29 mg/day with HbA1c 8.1% predicts 80% risk of CRF
◼ HbA1c 8.5–9% predicts increased chances of retinopathy.
CHOICE OF ANESTHETIC TECHNIQUE:
Regional Anesthesia : Technique of choice where applicable:
➢ Advantages:
◼ Avoids aspiration
◼ Better if difficult airway
◼ Patient is awake: Easy to recognize hypoglycemia
◼ Reduced incidence of DVT
◼ Reduced stress response to surgery
◼ Good postoperative analgesia
◼ Reduced chances of pulmonary infection.
➢ Disadvantages:
◼ Exaggerated hypotension especially if autonomic neuropathy present
◼ Increased risk of epidural abscess
◼ Caution if pre-existing neuropathy
◼ Increased risk of nerve injury.
➢ Guidelines:
◼ Local anesthetic requirement is lower
◼ Combination of LA with adrenaline may increase risk of ischemic or edematous
nerve injury
◼ Bradycardia may be unresponsive to atropine
◼ Isoprenaline/1:10,000 adrenaline used in such cases
◼ Chart pre-existing nerve damage as increased chance of nerve injury
◼ Technique: May be difficult if edema is present.
➢ Contraindications:
◼ Autonomic neuropathy
◼ Infections.
General Anesthesia
➢ Advantages:
◼ Better cardiovascular stability
◼ Airway is protected from silent aspiration.
➢ Disadvantages:
◼ Difficult intubation
◼ Difficult to recognize hypoglycemia
◼ Altered elimination of drugs due to renal involvement
◼ Increased stress response.
PREOPERATIVE EVALUATION
➢ Preoperative evaluation should emphasize the cardiovascular, renal, neurologic, and
musculoskeletal systems.
➢ Silent ischemia is possible if autonomic neuropathy is present, and stress testing should
be considered in patients with multiple cardiac risk factors and poor or indeterminate
exercise tolerance.
➢ For renal disease, control of hypertension is important. Meticulous attention to
hydration status, avoidance of nephrotoxins, and preservation of renal blood flow are
also essential.
➢ The presence of autonomic neuropathy predisposes the patient to perioperative
dysrhythmias and intraoperative hypotension. In addition, loss of compensatory
sympathetic responses interferes with detection and treatment of hemodynamic insults.
➢ Preoperative evaluation of the musculoskeletal system should look for limited joint
mobility caused by nonenzymatic glycosylation of proteins and abnormal cross-linking of
collagen.
➢ Gastroparesis may increase the risk of aspiration, regardless of nothing-by-mouth
status.
➢ If a patient takes subcutaneous insulin each night at bedtime, two-thirds of this dose
(NPH and regular) should be administered the night before surgery, and one-half of the
usual morning NPH dose should be given on the day of surgery. The daily morning dose
of regular insulin should be held.
➢ If the patient uses an insulin pump, the overnight rate should be decreased by 30%. On
the morning of surgery, the pump can be kept infusing at the basal rate or discontinued
and replaced with a continuous insulin infusion at the same rate. Alternatively the
patient can be given subcutaneous glargine and the pump discontinued 60–90 minutes
after administration.
➢ If the patient uses glargine and lispro or aspart for daily glycemic control, he or she
should take two-thirds of the glargine dose and the entire lispro or aspart dose the night
before surgery and hold all morning dosing.
➢ Oral hypoglycemics should be discontinued 24–48 hours preoperatively.
➢ It is advised that sulfonylureas be avoided during the entire perioperative period
because they block the myocardial potassium adenosine triphosphate (ATP) channels
responsible for ischemia- and anesthetic-induced preconditioning.
INTRAOPERATIVE MANAGEMENT
Aggressive glycemic control is important intraoperatively.
➢ Ideally a continuous infusion of insulin should be initiated at least 2 hours before
surgery. Intraoperative serum glucose levels should be maintained between 120 and
180 mg/dL. Levels above 200 mg/dL are likely to cause glycosuria and dehydration and
to inhibit wound healing.
➢ Typically 1 unit of insulin lowers glucose approximately 25–30 mg/dL. The initial hourly
rate for a continuous insulin infusion is determined by dividing the total daily insulin
requirement by 24. A typical rate is 0.02 unit/kg/h, or 1.4 units/h in a 70-kg patient. An
insulin infusion can be prepared by mixing 100 units of regular insulin in 100 mL of
normal saline (1 unit/mL).
➢ Insulin infusion requirements are higher for patients undergoing coronary artery bypass
graft surgery, patients receiving steroids, patients with severe infection, and patients
receiving hyperalimentation or vasopressor infusions.
➢ An insulin infusion should be accompanied by an infusion of 5% dextrose in half-normal
saline with 20 mEq KCl at 100–150 mL/h to provide enough carbohydrate (at least 150
g/day) to inhibit hepatic glucose production and protein catabolism.
➢ Serum glucose levels should be monitored at least every hour and even every 30
minutes in patients undergoing coronary artery bypass surgery or patients with high
insulin requirements.
➢ Glucose determination is preferentially made using venous plasma or serum samples;
arterial and capillary blood yields glucose values approximately 7% higher than those for
venous blood, and whole-blood determinations are usually 15% lower than plasma or
serum values. Urine glucose monitoring is not reliable.
➢ Avoidance of hypoglycemia is especially critical, since recognition of hypoglycemia may
be delayed in patients receiving anesthetics, sedatives, analgesics, β-blockers, or
sympatholytics and in those with autonomic neuropathy. If hypoglycemia does occur,
treatment consists of administration of 50 mL of 50% dextrose in water, which typically
increases the glucose level 100 mg/dL or 2 mg/dL/mL.
POSTOPERATIVE CARE
➢ Postoperative management of diabetic patients requires meticulous monitoring of
insulin requirements.
➢ Hyperglycemia has been associated with poor outcomes in postoperative and critically
ill patients.
➢ The risks of hypoglycemia must also be considered.
➢ Currently the ADA recommends that glucose levels be maintained between 140 and 180
mg/dL in critically ill patients and that insulin treatment be initiated if serum glucose
levels exceed 180 mg/dL.
ANESTHETIC DRUGS AFFECT BLOOD SUGAR CONTROL:
➢ Ketamine: may cause significant hyperglycemia
➢ Etomidate: blocks adrenal steroidogenesis and hence cortisol synthesis and decreases
the hyperglycemic response to surgery.
➢ Propofol: The effect of propofol on insulin secretion is not known. Diabetic patients
show a reduced ability to clear lipids from the circulation.
➢ Halothane, enflurane, isoflurane and sevoflurane: in in vitro studies inhibit the insulin
response to glucose in a reversible and dose-dependent manner.
➢ Benzodiazepines: decrease the secretion of ACTH and the production of cortisol, when
used in high doses. They reduce sympathetic stimulation but stimulate growth hormone
secretion and result in a decrease in the glycemic response to surgery. These effects are
minimal when midazolam is given in usual sedative doses.
➢ Opioids: High-dose opiate anesthetic techniques produce hemodynamic, hormonal and
metabolic stability. However, midazolam and fentanyl may cause hyperglycemia by
reducing glucose clearance.
➢ Ganglion-blocking agents: (used for hypotensive anesthesia previously) may block
sympathetically mediated hepatic gluconeogenesis with resultant hypoglycemia.
➢ B-blockers: The use of b-blockers is associated with slower recovery from hypoglycemia.
DIABETIC KETOACIDOSIS
✓ Rapid recognition and treatment of DKA is critical.
✓ Ketonaemia ≥3.0 mmol litre−1 or significant ketonuria (more than 2+ on urine sticks.
✓ Blood glucose >11.0 mmol litre−1 or known diabetes mellitus
✓ Bicarbonate <15.0 mmol litre−1, venous pH <7.3, or both.
➢ DKA results from a relative or absolute insulin deficiency with a concomitant increase in
counter regulatory hormones such as glucagon, catecholamines, cortisol, and growth
hormone.
➢ Hyperglycaemia ensues because of increased gluconeogenesis, accelerated glycogenolysis,
and impaired glucose utilization by peripheral tissues.
➢ This is magnified by transient insulin resistance because of the hormone imbalance itself.
➢ The combination of insulin deficiency and increased counter regulatory hormones leads to
the release of free fatty acids and their unrestrained oxidation in the liver to ketones.
➢ These ketones include acetone, 3-beta-hydroxybutyrate, and acetoacetate. The
predominant ketone in DKA is 3-β-hydroxybutyrate.
➢ Hydrogen ions produced by the dissociation of the ketone bodies causes the metabolic
acidosis.
➢ Hyperglycemia causes osmotic fluid shifts from intracellular to extracellular compartments.
➢ The glucose load in the glomerular tubules exceeds the renal threshold leading to
glucosuria and an obligatory osmotic diuresis.
➢ This diuresis causes a loss of sodium, potassium, and phosphate along with water and
glucose
PATHOPHYSIOLOGY:
THE CLASSICAL TRIAD OF DKA IS HYPERGLYCEMIA, KETONEMIA, AND METABOLIC ACIDOSIS.
HYPEROSMOLAR HYPERGLYCEMIC STATE:
➢ HHS is seen in type 2 diabetics, more commonly in elderly people with co-existing
diseases.
➢ HHS may be caused by plasma insulin concentrations that are inadequate for glucose
utilization but are adequate to prevent lipolysis and ketogenesis.
➢ The hyperglycemia and volume deficit is more severe than DKA.
Clinical features are:

✓ Slow onset over days to weeks
✓ Symptoms of hyperglycemia
✓ Signs of dehydration
✓ Signs of hyperviscocity and thrombosis like delirium, coma, seizures, sensory and
motor deficits
✓ Abdominal pain is unusual. Vomiting may be present.
Investigations for diagnosis in both DKA and HHS include
✓ CBC
✓ ABG
✓ Serum glucose
✓ Urine analysis
✓ Electrolytes
✓ Renal and liver biochemistry
✓ ECG
✓ X-ray chest and
✓ Appropriate cultures.
INVESTIGATIONS:
Initial investigations fall into three categories: Ongoing investigations are then required to
monitor the effect of treatment, and to ensure successful and safe treatment.
1. Establish diagnosis of DKA
2. Baseline investigations
3. Identify cause.
Investigations to establish diagnosis of DKA:
As DKA is the triad of: The following investigations are mandatory.
i. Ketonaemia ≥ 3.0 mmol litre−1 or significant ketonuria (more than 2+ on urine sticks)
ii. Blood glucose >11.0 mmol litre−1 or known diabetes mellitus
iii. Bicarbonate <15.0 mmol litre−1, venous pH <7.3, or both.
• Capillary ketone levels/urinalysis for ketones
• Blood sugar
• Blood gas for pH, bicarbonate, or both
Ongoing investigations:
To assure safe response to treatment, the following should occur hourly till resolution of the
ketosis: To assure metabolic stability, the following should occur at a minimum of 2 hourly
intervals until resolution of the ketosis:
• CBG/arterial blood glucose (if arterial line sited)

• Capillary blood ketones.
• pH
• bicarbonate
• potassium
Initial management:
DKA is a life-threatening condition and resuscitation along with initial treatment must occur
simultaneously with clinical assessment. Appropriate history, examination, and investigations
should be undertaken to diagnose the condition, identify the severity, and identify the cause.
Initial management should focus on:
i. Airway protection, if required
ii. Fluid resuscitation
iii. Insulin administration
iv. Assessment of severity
v. Identification of cause
Resuscitation:
An airway, breathing, circulation, disability, exposure (ABCDE) approach will provide structure
to the initial resuscitation. Appropriate venous access must be obtained.
Fluid resuscitation:
➢ The most important initial therapeutic invention in DKA is fluid replacement followed by
insulin administration.
➢ It is now universally agreed that crystalloids with a sodium concentration in the range of
130–154 mmol litre−1 should be used as the resuscitation fluid.
➢ There is ongoing debate on which crystalloid is superior.
➢ There is evidence to suggest that the use of balanced crystalloid solutions are associated
with a faster resolution of the metabolic acidosis and less hyperchloraemic metabolic
acidosis
➢ A typical fluid replacement regimen for a previously well 70 kg adult. However, the exact
rate of infusion should be formulated after clinical assessment of the individual patient.
➢ If the patient is shocked, the patient should receive an initial bolus of 500 ml over <15
min, and further fluid boluses dependent on clinical re-assessment.
INSULIN ADMINISTRATION:
➢ Administration of i.v. human soluble insulin is mandatory.
➢ Classically the insulin has been titrated against the surrogate marker of the blood
glucose using a variable rate i.v. insulin infusion (VRIII).
➢ The term ‘variable rate i.v. insulin infusion’ has now replaced the ambiguous and
obsolete term ‘sliding scale’.
➢ It is now recognized that glucose levels are a poor surrogate marker for resolution of
ketosis, and using the blood glucose as a marker to guide insulin therapy may (and does)
lead to the erroneous action of reducing insulin whilst the patient is still highly ketotic.
➢ A fixed rate administration of i.v. insulin whilst the patient remains ketotic avoids this
risk.
➢ Thus, recent evidence and guidelines suggest that a weight-dependent fixed rate i.v.
insulin infusion (FRIII) should be administered, rather than the variable rate i.v. insulin
infusion (VRIII).
PREPARATION AND ADMINISTRATION OF THE FIXED RATE I.V. INSULIN INFUSION:
The FRIII is administered via an infusion pump. The FRIII is constituted by adding 50 units of
human soluble insulin (Actrapid®, Humulin S®) to 0.9% sodium chloride to make a final volume
of 50 ml (1U/ml). Ideally this should be provided as a ready-made infusion. The FRIII is then
administered at a fixed rate of 0.1 U/Kg/hr (i.e. 7 ml/hr if weight is 70 kg).
The FRIII will need to be increased in increments of 1U/hr until the targets are met. A maximum
rate of 15 U/hr is recommended.
Metabolic targets for the continuation of the current fixed rate insulin infusion are:
i. Reduction of blood ketone concentration by >0.5 mmol/L/hr
ii. If blood ketone measurement is not available, the venous bicarbonate should increase
by 3.0 mmol/L/hr
iii. Reduction in CBG by 3.0 mmol/L/hr
• Non-administration of the insulin for any reason (e.g. tissued cannula, pump not
running, anti-syphon valve not used, etc.).
• Ongoing co-morbidity that will need senior review
• Insufficient insulin
Safe cessation of the FRIII:
The FRIII should be continued until resolution of the ketosis.
Resolution of DKA is defined as: Before stopping the FRIII, it is necessary to administer insulin in
another form; otherwise, the patient will re-develop ketosis.
The patient can either be recommenced on their usual regimen (if they are eating and drinking)
or converted to a variable rate i.v. insulin infusion with concurrent administration of 5%
dextrose in 0.45% saline with 0.15% potassium chloride.
i. pH >7.3
ii. bicarbonate >15.0 mmol litre−1
iii. blood ketone level <0.6 mmol litre−1.
Critical care referral:
Patients should be considered for critical care referral if any of the following criteria are
present: It is often necessary to admit emergency surgical patients to a level 2 or 3 facility, both
pre- and post-surgery.
i. Glasgow Coma Score (GCS) <12 or abnormal AVPU (alert, voice, pain, unresponsive)
scale
ii. Blood ketones >6 mmol/l
iii. Bicarbonate level <5 mmol/l
iv. Venous/arterial pH <7.0
v. Hypokalaemia on admission (<3.5 mmol/l)
vi. Oxygen saturation <92% on air (assuming normal baseline respiratory function)
vii. Systolic BP below 90 mmHg
viii. Pulse over 100 or below 60 beats min
ix. Anion gap >16 [Anion gap = (Na+ + K+) – (Cl− + HCO3−) ]
References:
1. STOELTING’S ANESTHESIA AND CO-EXISTING DISEASE, SEVENTH EDITION.
2. AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF
ENDOCRINOLOGY – CLINICAL PRACTICE GUIDELINES FOR DEVELOPING A DIABETES MELLITUS
COMPREHENSIVE CARE PLAN – 2015.
3. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetesd2018.
4. Objective ANAESTHESIA Review. A Comprehensive Textbook for the Examinees. Third
Edition.
5. Anesthesia Review for DNB Students. Kaushik Jothinath.
6. A Hallett, A Modi, N Levy, Developments in the management of diabetic ketoacidosis in
adults: implications for anaesthetists, BJA Education, Volume 16, Issue 1, January 2016, Pages
8–14,

Diabetes Mellitus

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Anaesthesia and Me

DIABETES MELLITUS AND ANAESTHETIC IMPLICATIONS

• Between 5% and 10% of all cases of diabetes are type 1.

 Coronary artery disease

2. Classic Non tight Control Regimen:

3. Tight Control Regimen

Combination of 10% dextrose and insulin is added to 500 ml fluid bag

THE CLASSICAL TRIAD OF DKA IS HYPERGLYCEMIA, KETONEMIA, AND METABOLIC ACIDOSIS.

Clinical features are:

• CBG/arterial blood glucose (if arterial line sited)

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