1. Anesthetic implications of diabetes mellitus
Moderator Dr Dara Negi
Dr Avinash Goyal

2. 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

3. 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 year olds
Leading cause of non-traumatic amputations
Responsible for 25-30% of all new dialysis patients

4. 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.

5. 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
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).

6. 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

7. 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

8. 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

9. 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

10. 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 2 mg/kg/min.
Daily requirement of glucose for 70 Kg man is 200gm/day(90-100g stored as glycogen)

11. Normal glucose homeostasis is tightly regulated by three interrelated processes
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).

15. 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

16. 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.

17. 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-INSULINt

18. 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)

19. 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

20. 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

21. 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

22. new insulin analogue - Glargine Detemir Biphasic lispro
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

23. Types of insulin 30′ 1h 4h 2-4h 1-3h 4-6h 6-18h peak less 3-5h 4-8h
Lispro
Aspart
Neutral/
regular
Isophane
ultratard
Glargine
Onset
10-20′
30′ 1h 4h
2-4h
Peak
1-3h
4-6h
6-18h
peak less
Duration
3-5h
4-8h
8-14h
24h
20-24h

24. Complications of DM ACUTE CHRONIC Metabolic Infections Microvascular
Diabetic ketoacidosis(DKA)
Hyperosmolar Hyperglycemic Nonketotic Syndrome(HHNS)
Hypoglycemia
Infections
CHRONIC
Microvascular
Retinopathy
Nephropathy
Macrovascular
CAD
CVD
PVD
Neuropathies
Diabetic Foot Disorders
Psychosocial concerns

26. DIABETIC KETOACIDOSIS (DKA)
Signs and symptoms
Hyperglycemia (>300mg/dl)
Elevated serum ketones
Acidosis as evidenced by pH of
HCO3 < 18
Osmolarity <320
Dehydration
Electrolyte depletion
GI distress (abdominal pain, N/V)
Respiratory distress (Kussmaul’s respirations and acetone breath odor)

27. TREATMENT OF DKA
Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 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

28. 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.

29. 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 ml/hr with target values around 250ml/dl

30. Electrolyte Correction
If the potassium level > 6 mEq/L, do not administer potassium supplement.
If the potassium level is mEq/L, administer 10 mEq/h of potassium chloride.
If the potassium level is mEq/L, administer 20 mEq/h of potassium chloride.
Monitor serum potassium levels hourly,

31. 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, mL of 1.4% concentration is infused initially. This may be repeated every half hour if necessary.
Treatment of Concurrent Infection

32. Hyperosmolar Hyperglycemic Nonketotic Syndrome(HHNS)
Four Clinical Features
Hyperglycemia (> )
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
Hypotension
Dehydration
Tachycardia
Decreased mentation
Neurologic abnormalities (focal)

33. 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 0.1U/kg hr
Electrolyte disturbances are less severe compared to DKA

34. 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).

35. 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 grams of CHO and follow with a meal or snack containing protein
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
Each ML of 50% glucose will raise BG by 2 mg/dl

36. 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
Cutaneous-furunculosis and carbuncles
Vulvovaginits
Cellulitis
UTI
Ear
Must be treated aggressively

37. 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

38. 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

39. 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

40. 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

41. 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

42. 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.

43. 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

45. Acute hyperglycemia causes
dehydration,
impaired wound healing,
an increased rate of infection,
worsening central nervous system/spinal cord injury with ischemia,
hyperviscosity with thrombogenesis

46. Preop evaluation History & general physical exam HBA1c levels
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

47. 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

48. 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.

49. 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

50. 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

51. 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.

52. Airway
Glycosylation of collagen in the cervical and temporo-mandibular joints can cause difficulty in intubation.

53. 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

54. 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

55. Renal
Diabetes is one of the commonest causes of end-stage 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.

56. 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.

57. 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

58. 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 emulsions-prolonged infusions of propofol should be avoided-can lead to hyperglycemia

59. 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

60. 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.

61. 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

62. 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

63. 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

64. 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.

65. 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)
<
4.1 –
> (check infusion running) 8
*If glucose not maintained <10mmol/l then increase the rates,

66. Classic “Non-tight Control” Regimen
Aim-to prevent hypoglycemia,ketoacidosis and hyperosmolar states
protocol
NPO after midnight
6AM –start i.v. dextrose 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

67. “Tight Control” Regimen 1
Aim-to keep glucose levels b/w 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 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”

68. Alberti GIK Regimen
Initial solution: 500 ml 10% glucose+15U insulin+10 mmol KCl
Infusion 100 ml/ h( 3U/h)
Check BG every 2 hr
Adjust in 5-U steps
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)

69. 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.

70. 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.

71. future Non-invasive BS testing Continuous BS monitor + insulin pump
“Artificial Pancreas”
Islet cell transplants
Stem-cell research
Energy homeostasis breakthroughs

72. thanks