Pre-operative evaluation and preparation of a patient of Diabetes Mellitus

1. PREOPERATIVE EVALUATION AND
PREPATION OF A PATIENT WITH
DIABETES MELLITUS

2. PRE OPERATIVE EVALUATION
• Determine the type of diabetes and its management.
• Quality of DM control- episodes of hypo or
hyperglycemia
• Review of medications.
• Ensure that the patient is capable of managing their
diabetes after discharge from hospital.
• Consider the presence of complications of diabetes
that might be adversely affected by or that might
adversely impact upon the outcome of the proposed
procedure.
• Identify high-risk patients requiring critical care
management.

3. • Q. What are the macrovascular events?
• Coronary artery disease
• Cerebrovascular disease
• Peripheral vascular disease.
• Q. What are microvascular events?
• Retinopathy
• Nephropathy.
• Neuropathy
MOA- Atherosclerosis
increased coagulability
MOA- Sorbital, advanced glycosylated end products,
ROS

4. CARDIAC COMPLICATION---
• CAD
• Hypertension
• Peripheral arterial disease
• Systolic and diastolic dysfunction
CENTRAL NERVOUS SYSTEM-
• Cerebral vascular disease
RENAL DYSFUNCTION- d/t HTN, dyslipedemia, anemia
GIT- risk of aspiration
Respiratory system-
• Reduced hypoxic induced ventilatory drive(in DAN)
• Respiratory depression from opiods& sedatives d/t impaired
chemoreceptor
• Airway difficulties

5. AIRWAY DIFFICULTIES-
An intubation is called difficult if a conventionally trained
anaesthesiologist needs more than three attempts or more
than ten minutes for a successful endotracheal intubation
The reported incidence of difficult laryngoscopy in diabetic
patients approximate 27-31%
•Joint rigidity- TMJ, atlanto-occipital joint, cervical joints
•Neck extension and laryngoscope difficult
•Cause- non enzymatic glycosylation of proteins and abnormal
cross-linking of collagen in joints and other tissues

6. • This is due to the non-enzymatic glycosylation of collagen and its
deposition in the joints resulting in ‘limited joint mobility’ (LJM)
syndrome, which occurs in 25-45% of patients with long standing
diabetes.
• The atlanto-occipital joint involvement limits adequate extension of
head and neck during laryngoscopy leading to intubation difficulties
• CAUSES- tissue glycosylation associated with chronic
hyperglycaemia seen in diabetic patients.
• Diabetic patients have an abnormality of collagen metabolism and
increased cross-link formation as a result of which collagen fibrils
are abnormally stable, relatively insoluble and resistant to the
enzymatic degradation. These changes are potentially reversible

7. . What tests are done to predict airway difficulty?
Prayer Sign:
Patient is unable to approximate
the palmar surface of phalangeal
joints despite of maximal effort.
Palm Print Test:
Degree of inter-phalyngeal joint
involvement can also be assessed
by scoring the ink impression
made by the palm of dominant
hand.

8. • Grade 0: all phalangeal area visible
• Grade 1: def in the inter phalangeal areas of 4th and/or 5th digit.
• Grade 2: def in the inter phalangeal area of 2nd to 5th digit.
• Grade 3: only tips of digits are seen.
• Higher grade~ higher chance of difficult intubation.

9. • Palm print sign was the most significant,
sensitive (76.9%) and most specific (89.3%)
index in predicting difficult laryngoscopy.
• The prayer sign was the next most sensitive
(61.5%), but not statistically significant.

10. • Diabetes accelerates the progression of atherosclerosis, so
it is not surprising that diabetics have a higher incidence of
CAD than non diabetics.
• Diabetes is considered a CAD equivalent,and it is a risk
factor for perioperative cardiac complications on a par with
previous MI
• There is a high incidence of both silent MI and myocardial
ischemia.
• Autonomic neuropathy and erectile dysfunction are strong
predictors of silent ischemia in these patients.
SOME FACTS ABOUT DIABETES!!!

11. • The majority of diabetics develop secondary disease in
one or more organ systems, which must be identified
preoperatively so that an appropriate plan can be
developed for perioperative management.
• Poorly controlled blood glucose concentrations and
longer duration of disease also correlate with cardiac
risk.
• Heart failure is twice as common in men and five times
as common in women with diabetes as in persons
without diabetes.

12. • They also state that most diabetic patients >65 years of age
have significant CAD, with the incidence of silent ischemia
increased due to associated diabetic autonomic
neuropathy.
• Diabetics are also more likely than the general population
to have cerebral vascular, peripheral vascular, and renal
vascular disease.
• Diabetes mellitus is the leading cause of renal failure
requiring dialysis.-- serum creatinine and eGFR
• Peripheral neuropathies and vascular disease make
these patients more susceptible to positioning injuries
during surgery as well as postoperatively

13. • Diabetes and Accelerated Physiologic Aging
• a patient with type 1 diabetes who has poor control of
blood glucose ages approximately 1.75 years
physiologically for every chronologic year of the
disease and 1.25 years if blood glucose has been
controlled tightly.
• A patient with type 2 diabetes ages approximately 1.5
years for every chronologic year of the disease and
approximately 1.06 years with tight control of blood
glucose and blood pressure

14. Why autonomic neuropathy is most dangerous complication of
diabetes mellitus?
• Autonomic neuropathy may predispose the patient to hemodynamic instability
during anesthesia and theoretically increase the risk of pulmonary aspiration
because of the associated gastroparesis.
• Diabetic patients with significant autonomic neuropathy
may have impaired respiratory responses to hypoxia and
are particularly susceptible to the action of drugs that have
depressant effects.
• Patients with ANS dysfunction are at increased risk of aspiration during induction
and are very prone to develop intraoperative cardiovascular lability.
• Stiff joint syndrome due to glycosylation of protein and abnormal collagen cross-
linking may signiicantly affect the temporomandibular, atlantooccipital, and
cervical spine joints in patients with long-standing type 1 diabetes, resulting in
dificulty with intubation.

15. Manifestations of autonomic neuropathy
• Resting tachycardia
• Orthostatic hypotension
• Absent beat-to-beat variation in heart rate
with deep breathing
• Cardiac dysarrhythmias (QT abnormalities)
• Sudden death syndrome
• Gastroparesis (vomiting, diarrhea, abdominal
distension)—chances of aspiration during
induction.

16. • early satiety,
• lack of sweating,
• lack of pulse rate change with inspiration or orthostatic
maneuvers, and
• impotence,
• have a very frequent incidence of painless myocardial
ischemia
• nocturnal diarrhea, and
• dense peripheral neuropathy.

17. • What are the ophthalmic changes in
autonomic neuropathy?
• Decreased pupil size
• Resistance to mydiatrics
• Decreased or absent reflexes to light.

18. • Q. How assessment of autonomic nervous system
done?
• Parasympathetic nervous system
• – Heart rate response to standing
• – Heart rate response to deep breathing
• --Heart rate responses to valsalva
• Sympathetic nervous system
• – Blood pressure response to standing
• – Blood pressure response to sustained

19. • ASSESSMENT
Parasympathetic nervous system
• – Heart rate response to standing-HR is measured as the patient changes
from supine to standing position (increases maximum around 15th beat
after standing ----- relative bradycardia ---max around 30th beat). Normal
value: Ratio 30:15- >1.04.) less than 1.04-abnormal.
• – Heart rate response to deep breathing-RESPIRATORY SINUS ARRYTHMIA
• Patient takes 6 deep breaths in 1 minute. The maximum and minimum HR
during each cycle are measured and the mean of the differences
(maximum HR – minimum HR) during three successive cycles is taken as
the maximum – minimum HR.
• Normal value—mean difference >15 bpm. Abnormal- < 10 bpm
• 5 beats/minute or less in all patients who subsequently sustain
cardiorespiratory arrest.

20. – Heart rate responses to valsalva--Patient blows into a mouth
piece maintaining a pressure of 40 mm Hg for 15 seconds. The
valsalva ratio is the ratio of the longest R-R interval on the ECG
immediately after release, to the shortest R-R interval during
the maneuver. Normal value—Ratio >1.21.
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.

21. 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.

22. Sympathetic nervous system
– Blood pressure response to standing--Patients with autonomic dysfunction (or
hypovolemia) have more than a 20-mm Hg decrease in systolic BP, or more than a 10-
mm Hg decrease in diastolic BP when changing from a supine to standing position.
– Blood pressure response to sustained--Patient maintains a handgrip
of 30% of maximum squeeze for up to 5 minutes.
EARLY STAGE-abnormality of HR during deep breathing only
INTERMEDIATE STAGE- abnormality of Valsalva response
LATE STAGE- postural hypotensio

25. Assessment of Albuminuria and
Estimated Glomerular Filtration Rate

31. Investigation of a diabetic patient for surgery
• Hemoglobin—anemia present with renal dysfunction. Baseline
guide forintraoperative blood transfusion
• CBC—suggestive for infections
• Urine for microalbuminuria—nephropathy
• Serum creatinine , eGFR—to detect renal dysfunction
• Fasting and postprandial blood glucose
• Glycosylated Hb: HbA1c of <7% implies good sugar control
• Serum electrolytes: Serum potassium level in patients on insulin

32. • ECG: To detect asymptomatic myocardial ischemia.
The 2002 American College of Cardiology/AHA guidelines
on perioperative cardiac assessment of patients
undergoing non cardiac surgery place diabetics, especially
those receiving insulin, at a minimum of intermediate risk.
• X-ray chest: Tuberculosis is common in diabetics.
• Investigation on morning of surgery—serum electrolytes,
fasting blood sugar, urine ketones.

36. • What are the principles of anesthetic management in a patient
with diabetes mellitus?
• TIMING- Diabetic patients should be placed first on the operation
list. This shortens the preoperative fast and the risk of
hypoglycemia and ketosis.
• FASTING -Delayed gastric emptying due to diabetic autonomic
neuropathy is found in these patients. Undiagnosed gastroparesis
prolongs retention of food in the stomach and increases the risk of
regurgitation and aspiration.
• A 12 hour fasting may be beneficial.
• Agents which can gastric volume < 25 mL and pH > 2.5)
• Administration of metoclopramide, 10 mg preoperatively to
facilitate gastric emptying

37. • MONITORING- Frequent, rapid and accurate blood
glucose measurement is essential in anesthetized
patients as the requirements of glucose and insulin in
this period are unpredictable and hypoglycemia may go
undetected.
Standard monitoring: ECG, SpO2, BP, EtCO2 and
temperature should be instituted.
• HbA1c measurement has no value in intraoperative or
postoperative period but is a valuable guide to long-
term glycemic control during preoperative evaluation.

38. MANAGEMENT OF DRUG THERAPY

40. • Emergency Surgery
• Many diabetic patients requiring emergency surgery for trauma or
infection have significant metabolic decompensation, including
ketoacidosis .
• Even a few hours may be sufficient for correction of any fluid and
electrolyte disturbances that are potentially life-threatening.
• It is futile to delay surgery in an attempt to eliminate ketoacidosis
completely if the underlying surgical condition will lead to further
metabolic deterioration.
• The likelihood of intraoperative cardiac arrhythmiasand hypotension
resulting from ketoacidosis will be reduced if intravascular volume
depletion and hypokalemia are at least partially treated.

43. Although there currently exists no consensus target range, in general
the literature suggests keeping glucose levels between 150
and 200 mg/dL (8 to 11mmol/L) during surgery
Moreover, a study discovered that intraoperative hyperglycemia
(glucose greater than 200mg/dL) as well as relative
normoglycemia (glucose less than 140mg/dL) was found to
be associated with significant morbidity and mortality.
Glucose levels ranging from 140 to 170mg/dL had the lowest risk of adverse
outcomes
World Health Organization (WHO) surgical safety target, which establishes that the ideal
in-hospital glucose range for non-critically ill diabetic patients should be 108---180
mg.dL−1(6---10 mmol.L−1in the USA, with the lower limit of 100 mg.dL−1or 5.6
mmol.L−1).

44. J. B. Marks, “Perioperative management of
diabetes,” American
Family Physician, vol. 67, no. 1, pp. 93–100,
2003.

45. When subcutaneous insulin is used in the preoperative period or operating room to treat
hyperglycemia, BG testing should occur at least every 2 h.
Correctional insulin is defined as the supplemental insulin provided for BG greater than
180 mg/dl (10 mM) after BG testing.
Correctional dosing with a rapid-acting insulin can be calculated with the following formula:
measured glucose minus 100/insulin sensitivity factor.
Insulin sensitivity factor is equal to 1,800 divided by the patient’s total daily dose (TDD) of
insulin.

46. The TDD is equivalent to the patient’s daily amount of basal, prandial, and correctional
insulin.
Should TDD not be available or if a patient is using only oral medications at home, a
sensitivity factor (denominator) of 40 provides a safe calculation for a correctional insulin
dose.

47. Data comparing subcutaneous insulin to
IV insulin infusion in the operative setting are lacking.
The short duration of action of rapid-acting insulin analogs limits the risk of “insulin
stacking” with repeat dosing.
However, limiting the number of intraoperative subcutaneous insulin
doses to two, within the 4-h operative time, may reduce the
risk hypoglycemia.
Rapid-acting insulin should not be dosed more frequently than every 2 h to minimize
the risk of insulin stacking.

48. An IV insulin infusion is recommended in patients undergoing procedures with anticipated
hemodynamic changes, significant fluid shifts,
Algorithms are available that recommend subcutaneous insulin dosing regimens to treat
intraoperative hyperglycemia.
Duggan EW, Klopman MA, Berry AJ, Umpierrez G: The Emory
University Perioperative Algorithm for the Management of
Hyperglycemia and Diabetes in Non-cardiac Surgery Patients.
Curr Diab Rep 2016; 16:34

49. Standard GIK solution:
500 ml 10% dextrose solution + 15 units short-acting insulin + 10 mmol KCl.
Infuse over 5 hours (100 mL/h)
5 % dextrose solutions are used by some instead of 10% D.
Short acting insulin is added at 0.32 units/gram of dextrose.
Potassium is avoided in patients with renal dysfunction and those with hyperkalemia.

50. Intraoperative management of glucose
• Vellore regimen
Insulin rate = Blood sugar in mg% divided by 150 in patients Insulin rate = Blood
sugar in mg% divided by 100 in patients on steroids, with infection, BMI > 35.
disadvantage of the above fixed dose regimen based on spot blood sugar levels is
that they do not account for variations in insulin receptor sensitivity in individual
patients and can lead to fluctuations in blood sugar levels.

51. When to postpone surgery?In general, surgery should be postponed in patients
with significant complications of hyperglycemia, such as dehy-dration, ketoacidosis
or HHS.
However, surgery may beindicated for patients with preoperative
hyperglycemia,provided that the patient has adequate glycemic control in recent
months.
Depending on individual circumstances,an upper limit of HbA1c between 8% and
9% is acceptable.
The latest British guidelines recommend that surgery shouldbe postponed in the
presence of HbA1c above 8.5% (meanof 200 mg.dL−1) in order to improve glycemic
control andreduce complications.
For the Australian Society of Dia-betes, HbA1c value should be above 9% (mean
blood glucoseof 215 mg.dL−1) for postponing surgery.

52. • In young adults, the ‘resting’ brain consumes approximately
110 g of glucose per day, i.e. 5.5 mg glucose per 100 g of
brain tissue per minute.
• The glucose level at which cognitive function declines is
subject to substantial variation; in some people cognitive
dysfunction already occurs at plasma glucose levels
between 3.0 and 4.0 mmol/L, whereas others continue to
function well at levels below 2.5 mmol/L

53. • The glycemic threshold for decreased insulin secretion is approximately 4.5 mmol/l
(81 mg/dl).
• Increments in pancreatic β cell glucagon and adrenomedullary epinephrine
secretion normally occur as glucose levels fall just below the physiological range -
approximately 3.8 mmol/l [68 mg/dl]).
• If these defenses fail to abort the hypoglycemic episode, lower glucose levels
trigger a more intense sympathoadrenal response that causes neurogenic (or
autonomic) symptoms; neuroglycopenic symptoms occur at about the same
glucose level (threshold equal to approximately 3.0 mmol/l (54 mg/dl).
• If all of these defenses fail, lower glucose levels cause overt functional brain failure
that can progress from measurable cognitive impairments (threshold equal to
approximately 2.8 mmol/l [50 mg/dl]) to aberrant behaviors, seizure, and coma.
Coma can occur at glucose levels in the range of 2.3–2.7 mmol/l (41–49 mg/dl) as
well as at lower glucose levels

54. • Profound, prolonged hypoglycemia can cause brain
death. In studies of insulin-induced hypoglycemia in
monkeys, 5–6 hours of blood glucose concentrations of
less than 1.1 mmol/l (20 mg/dl) were required for the
regular production of neurological damage ; the
average blood glucose level was 0.7 mmol/l (13 mg/dl).
• In the in vivo studies, blood glucose concentrations
averaged 0.4 mmol/l (7 mg/dl), causing an isoelectric
EEG, during hypoglycemia .

55. THE END