4. objectives
General objective: at the end of this lesson:-
students should be able to understand DM and manage
diabetic patient perioperatively.
Specific objective: students should be able to:-
Define and classify type of DM
Diagnose and treat DM
Identify complications and treat
Perform preoperative assessment
Manage the patient intraoperative as well as postoperatively
11/23/2018by emebet4
5. Introduction
Brain storming question
Discuss on the following points in group and reflect.
1, definition, classification and cause of DM
2, clinical presentation and treatment of DM
3, Complication of DM
11/23/2018by emebet5
6. Intr…
Endocrine disease are common comorbid conditions in
patient under going surgery under anaesthesia.
DM is most common comorbid conditions affecting 20%
of patients undergoing surgery with aesthesia.
Diabetes mellitus : is a multisystem disorder caused by a
relative or absolute lack of insulin
Prevalence:
Approximately 15% have type 1 diabetes
The majority (82%) have type 2 diabetes
And 3% is gestational diabetes
11/23/2018by emebet6
7. Anatomy and physiology of pancreas
Position in the upper abdomen, just under the stomach
The major part of the pancreas, called the exocrine
pancreas functions as an exocrine gland, secreting
digestive enzymes in to GIT i.e. pancreatic amylase and
pancreatic lipase.
The endocrine cells of the pancreas are contained in
spherical bodies called pancreatic islets or islets of
langerhans
The main cell types in the islets are alpha and beta cells
11/23/2018by emebet7
8. Alpha/A cells -secrete glucagons (increase blood glucose)
beta or B cells – secrete insulin(decrease blood glucose)
the pancreatic islets also contain two rare cell types
delta or D cells – secrete somatostatin (a hormone that
inhibits the secretion of glucagons and insulin by the near
by alpha and beta cells
F cells- secrete pancreatic polypeptide , a hormone that
may inhibit the exocrine activity of pancreas
11/23/2018by emebet8
9. The role of glucagon and insulin
Glucose is the body’s major source of energy. It is used to
form adenosine tri-phosphate.
Glucose is the only fuel that the brain can utilize, but it
cannot be stored in the brain.
Therefore, the body attempts to maintain normoglycaemia to
provide a constant supply of glucose between meals.
Glucose is stored in the liver and muscles in the form of
glycogen.
11/23/2018by emebet9
10. Insulin- is a protein produced by the ß cells of the pancreas.
Insulin is necessary:-
To maintain glucose homeostasis
To balance stress hormones (e.g. adrenaline, NA, cortisol..)
To activates Na-K ATPase in cells and cause k influx
11/23/2018by emebet10
11. Insulin has anabolic and anti catabolic effect.
Anabolic effects include
Promotes glycogenesis
Increase synthesis of triglycerides
Increase protein synthesis
Promotes glycolysis
Increase amino acid transport
Promotes triglyceride storage
11/23/2018by emebet11
12. Anti catabolic effects:-
Inhibit glycogenolysis
Inhibit ketogenesis
Inhibit gluconeogenesis
Increase glucose transport
Enhance activity of glycogen synthetase enzyme
Inhibit activity of glycogen phosphorylaze
11/23/2018by emebet12
13. Glucagon:- produced by the - cells of the pancreas
Its main action takes place in the liver:
Promotes glycogenolysis
In adipose tissue:
it stimulates fat breakdown and gluconeogensis
All actions of glucagon are aimed at raising blood sugar
levels.
-It helps to protect the body from hypoglycaemia.
11/23/2018by emebet13
14. Diabetes mellitus
Def- DM is characterized by impairment of carbohydrate
metabolism caused by deficiency/abcesnse of insulin
activity , which lead to hyperglycemia and glycosuria .
Types of DM:-
•Type I absolute insulin deficiency
secondary to immune –mediated disease.
• Type II adult onset secondary to
resistance /relative deficiency of insulin
• Gestational DM- if diagnosed during pregnancy and may
or may not persist in postpartum period.
11/23/2018by emebet14
15. І) IDDM ( type I)
• Onset: child, adolescence rarely in older age
• Absolute deficiency of insulin.
• Destruction of β-cell of the pancreas- autoimmune.
• Has abrupt onset of the disease.
• Requires insulin therapy.
• Difficult to maintain good glucose balance.
• More likely to become ketotic and to develop end-organ
complication.
11/23/2018by emebet15
16. ІІ) NIDDM ( type II)
• Prevalence: - increases with age (> 45yrs) now a days it can
happen in pediatrics.
• Has genetic predisposition.
• Has gradual onset of the disease.
• May have normal or even elevated level of insulin.
• Due to –gradual decline in β- cell function impaired secretion
(lack) of insulin may be adequate to prevent lipolysis and
ketoacidosis but inadequate to lower blood glucose by affecting
the transport of glucose in to fat cells.
11/23/2018by emebet16
17. • Increased peripheral insulin resistance in skeletal muscles and
adipose tissues stimulates liver to increase glucose production.
• Most (80%) patients are over weight- enhanced obesity.
Obesity :
Increases resistance to the action of insulin.
Impairs suppression of hepatic glucose production.
11/23/2018by emebet17
18. pathophysiology
Insulin has both excitatory and inhibitory effects.
The fasting hyperglycaemia of diabetes:
Due to predominated over production of glucose by the liver
Underutilisation of glucose by peripheral tissues
Insulin “keeps the brakes on”
- by glycolysis, glycogenesis and Prevents over-
secretion of the “anti-insulin” hormones.
- Stimulate uptake and synthesis of amino acid,
protein and fat.
11/23/2018by emebet18
19. In the absence of insulin, the “brake” is removed and a sort
of metabolic events such as gluconeogenesis,
glycogenolysis, lipolysis and proteolysis may happen and
cause hyperglycaemia.
The resulting hyperglycaemia leads to:
An osmotic diuresis
Dehydration with associated sodium and potassium loss
11/23/2018by emebet19
20. In the absence of insulin
There will be ketogenesis
There will be metabolic academia- a state of diabetic
ketoacidosis (DKA)
If there is some residual insulin activity:
It is enough to inhibit lipolysis and ketogenesis but not
gluconeogenesis,
A hyperosmolar non-ketotic (HONK) diabetic coma can
happen
11/23/2018by emebet20
22. Treatment
Treatment of DM:
1. Dietary treatment: avoidance of obesity and doing exercise for
NIDDM.
2. Oral hypoglycemic drugs ( OHAs):
If dietary management fails.
Functioning β-cell is required.
Mechanisms of action of OHAs:
o Increase insulin release;
o Increase insulin sensitivity;
o Decrease gluconeogenesis.
o Increase glucose utilization in peripheral tissues and,
o Increase removal of glucose.
11/23/2018by emebet22
23. OHAs:
The four major classes of oral antidiabetic medications are
1, The secretagogues
• Examples; sulfonylureas, meglitinides
• Which increase insulin realease;
2, The biguanides (metformin),
which suppress excessive hepatic glucose release;
3, The thiazolidinediones or glitazones
• Examples;rosiglitazone, pioglitazone
• Which improve insulin sensitivity; and
4, The α-glucosidase inhibitors
Examples;acarbose, miglitol
which delay gastrointestinal glucose absorption
11/23/2018by emebet23
25. Insuline:
Insulin is necessary to manage
All cases of type 1 diabetes and
Many cases of type 2 diabetes
The various forms of insulin include:
1, basal insulins, are intermediate acting
NPH(neutral protamine hagdom), Lente, lispro protamine,
aspart protamine
Administered twice daily
2, long-acting (Ultralente, glargine)
administered once daily
3, short acting
Regular or rapid acting (lispro, aspart),
Which provide glycemic control at meal times
11/23/2018by emebet25
28. Diabetic Ketoacidosis
• Is a life threatening medical emergency. It is characterised by
hyperglycaemia, dehydration, metabolic acidosis and
ketonuria.
The diagnostic criteria for DKA includes:
A blood sugar >14.0 mmol/l or= >250mg/dl
Presence of urinary or plasma ketones,
A pH< 7.3 and a serum bicarbonate of less than 18 mmol/l
Osmolarity <320mosm/l
The main differential diagnosis is:
The hyperosmolar hyperglycaemic syndrome:
Which differs in the extent of dehydration, acidosis and
ketosis
11/23/2018by emebet28
29. PATHOPHYSIOLOGY :
DKA is due to an insulin deficiency, together with an excess of
the counter-regulatory hormones which causes hyperglycemia,
Lipolysis – release fatty acids and this degraded in the liver to
KBS which utilized as body fuels; liver production increase
for peripheral utilization leading to increased blood level of
ketone bodies, decrease in PH and end up with DKA.
Hyperglycemia and metabolic acidosis - are the two major
metabolic abnormalities in DKA .
Severe hyperglycemia causes a factitious hyponatremia: each 100
mg/dL increase in plasma glucose lowers plasma sodium
concentration by 1.6 mEq/L.
11/23/2018by emebet29
30. Clinical presentation
Symptoms: Signs:
-Polyuria -Dehydration(osmotic diuresis)
-Wt loss -Hypotension
-Weakness -Tachypnea (kusmaul breathing)
-Nausea, vomiting -Fruity smell of breath (acetone
-Abdominal pain breath)
U/A : +ve for KBS -Confusion,drowsiness & coma
11/23/2018by emebet30
31. Treatment:
1.Supportive
AW maintenance, supplemental oxygen, & RX of shock.
2.Fluid administration
• Initially 15-20ml/kg 1LNS over 30min-1 hr.
• Continue with 1L of NS|hr for the first 2-3hrs with rate of 4-
14ml/kg/hr
• Then half NS at slower rate till the pt is well hydrated
• When the serum glucose level falls to 200mg|dl ,change the IV
fluid to 5%-10% DW to prevent hypoglycemia
• Carefully monitor UOP.
11/23/2018by emebet31
32. 3. Insulin Therapy
• To increase glucose use in the tissue and to inhibit ketogenesis
initialy give 0.1u/kg Iv bolus insulin
• An intravenous insulin infusion should be commenced (50 units
actrapid in 50 mls 0.9% saline) at 0.1units/kg/hour.
• Blood glucose should be checked every hr. The expected rate of
fall in serum glucose is 75-100mg|dl|hr.
• When blood glucose reaches a range of 250mg|dl,5% glucose
solution should be infused to prevent hypoglycemia.
11/23/2018by emebet32
33. • Insulin infusion should not be stopped until the ketenomia
clears.
• It is preferable to give 5% or 10% DW with insulin injection
,rather than stop the insulin, because insulin is still required to
clear the acidosis and ketotic state.
Perioperative aim of medication is to maintain RBS in range of
110-180 mg/dl, and 80-120 mg/dl in critically ill patient.
11/23/2018by emebet33
34. 4. K+ Supplementation
• Initially hyperkalemia (M-acidosis K+ outflex from
ICF→ECF) & later hypokalemia b|c of renal loss & movement
of potassium back in to ICF as insulin administered acidosis is
corrected.
• DKA pt expected to have 3-10meq/kg K+ deficit.
• Start supplementation as soon as the pt has adequate UOP
• KCL is infused at a rate of 20-40mEq|hr.
• Monitor serum K+ closely.
• Supplement NaHCO3 if PH< 7.1 and {HCO3
-} <10 meq|dl or .
11/23/2018by emebet34
35. 5. Continuing management
Location of care
Starting an insulin sliding scale and conversion to
subcutaneous insulin
Antibiotic therapy
Thromboprophylaxis
Nasogastric tube drainage
Urinary catheterisation
Continuous ECG monitoring,
Notes recording and Diabetes team follow up
11/23/2018by emebet35
36. 2, Hypoglycemia
• Blood glucose level < 80mg|dl.
• Symptoms are uncommon until level falls to 2-
3mmol/l(40-50mg/dl
• It is the main danger to diabetics perioperatively
Cause
• Fasting with OH or insulin therapy
• Pancratic tumors, beta blokers, pitutary gland disease
• Liver disease and sepsis exacerbate hypoglycaemia.
• Hypoglycaemia may also result inadvertently by poor
blood glucose monitoring or equipment failure
11/23/2018by emebet36
38. Treatment :
• Give 25 - 50ml of 50% glucose IV each ml of glucose will
raise RBS by 2mg/dl.
• Glucagon 1mg IM or IV is an alternative but slower strategy.
• If the patient is awake, try any sugary food/solution by
mouth/NG tube
11/23/2018by emebet38
39. 3, Hyperglycemic Hyperosmolar syndrome
• Triggered (in type II) by infection, trauma, surgery (stress
increase insulin resistance) with relative insulin deficiency.
• Such pts present with hx of several weeks of polyuria, wt
loss and decreased oral fluid intake.
Characterized by:
- Marked hyperglycemia (>600 mg|dl).
- Hyperosmolarity (>330mosmol|L).
- Normal PH (>7.3).
- Profound dehydration.
- Hypokalemia (osmotic diuresis).
- Altered mental status .
11/23/2018by emebet39
40. Treatment: same as DKA
Insulin administration,
Volume replacement,
Electrolyte replacement.
11/23/2018by emebet40
41. Chronic complications
Vascular and nonvascular
Vascular - microvascular and macrovascular
Microvascular complications
Proliferative retinopathy
Diabetic nephropathy
Neuropathic (autonomic and peripheral neuropathies)
11/23/2018by emebet41
42. Microvascular dysfunction is unique to diabetes
It is characterized by:
Damage to small blood vessels(weakness in capillaries,
vasodilation and increase vascular pressure)
Impaired autoregulation of blood flow and vascular tone
Hyperglycaemia is essential for the development of these
changes
Intense glycaemic control is beneficial to prevent this
complication
11/23/2018by emebet42
43. 1. Nephropathy
Approximately 30% to 40% with type 1
5% to 10% of those with type 2 diabetes develop ESRD
Is due to increase glomerular capillary flow result increase in
extracellular matrix production which result endothelial
damage lead to glomerular permeability to macromolecules
and result glomerular sclerosis.
Due to impaired autoregulation glycosylated hemoglobin
level of 8.1% is the threshold at which the risk for
microalbuminuria increases.
Microalbuminuria of greater than 29 mg/day has an 80%
chance of experiencing renal insufficiency.
glomerular sclerosis will result HTN
11/23/2018by emebet43
44. The clinical course is characterized by:
Hypertension, albuminuria,
Peripheral edema, and
A progressive decrease in GFR
• As creatnin clearance < 15-20 ml/min excretion of K+ and acid
impaired and Patients develop hyperkalaemia and metabolic
acidosis.
Treatment
Treatment of hypertension can markedly slow the progression
If ESRD develops, dialysis should be done
11/23/2018by emebet44
45. 2, Retinopathy
Results from a variety of microvascular changes,
blood vessel occlusion, dilation due to weakness in
capillary walls.
The threshold for retinopathy is a glycosylated
hemoglobin value of 8.5% to 9.0% (12.5 mmol/L or
225 mg/dL),
Strict glycemic and BP control can reduce the risk
11/23/2018by emebet45
46. 3. Peripheral Neuropathy
Associated with longer duration (>25yr) DM, more than
50% develop PN
The commonest type is:
A distal symmetric diffuse sensorimotor polyneuropathy
Clinical features:
Loss of light touch, proprioception, and muscle weakness
dysesthesia, paresthesia, and neuropathic pain
Foot ulcers
11/23/2018by emebet46
47. Significant morbidity results from:
recurrent infection,
foot fractures and
Subsequent amputations
Treatment
Optimal glucose control
Optimal pain control
11/23/2018by emebet47
48. 4. Autonomic Neuropathy
It is detectable in up to 40% of type 1 diabetics.
The pathogenesis is not completely understood
Only a few have the typical symptoms and signs
- early satiety, lack of sweating, impotence
Cardiovascular signs include:
Resting tachycardia
Loss of heart rate variability(for deep breath or if
bradycardic for medication)
Reduced ejection fraction.
Dysrhythmias
Postural hypotension
11/23/2018by emebet48
49. Evaluating autonomic neuropathy
Normal Abnormal
Sympathetic Measure BP in
supine & standing
< 10mmhg 30 mmhg
Parasympathetic Pulse response to
deep breath
Increase>15bpm Increase<5bpm
11/23/2018by emebet49
50. It may also impairs the GIT:
Diabetic gastroparesis (25%)
Nausea and vomiting
Bloating and epigastric pain
Diarrhoea and constipation
Respiratory effects:
Altered respiratory reflexes
Impaired ventilator responses
11/23/2018by emebet50
51. Macrovascular complications
Macrovasular complication : is due to damage to great
capillarys as cerebrovascular, coronary and peripheral art
Cardiovasculaar complication is the leading cause of mortality
An average blood glucose value threshold for cardiovascular
disease is 5.4 mmol/L (96 mg/dL).
Diabetics are more prone to:
ischaemic heart disease (IHD)
Hypertension
peripheral vascular disease
cerebrovascular disease
cardiomyopathy
perioperative myocardial infarction
11/23/2018by emebet51
53. Perioperative anesthetic concerns
RS (Respiratory System):
Diabetic patients with AN= have unexplained cardiac or
respiratory arrest and have increased risk of perioperative
sudden death.
They are more susceptible to the depressant effect of
anaesthetics.
AN= prognosis is poor.
Mortality > 50% in 5 yr period.
11/23/2018by emebet53
54. GIT :
Gastroparesis: early satiety,nausea, vomiting & bowel
distention.
- if they have reflux considered as increase perioperative
risk of aspiration.
GUS :
Bladder dysfunction and deterorated renal function so needs
cateterisation.
CNS :
Hypoglycemic unawareness. Strict monitoring needed
Stiff joint Syndrome (SJS)
Glycosylation of collagen in the cervical and temporo-
mandibular joints , diagnosed with limited neck movement
and prayers sign. 11/23/2018by emebet54
55. Anesthesia management
Goal :
Avoid hypoglycaemia (under 4mmol/l) or 72mg/dl
Avoid severe hyperglycaemia (over 14mmol/l)or 250mg/dl
Aim for a blood glucose between 6 and 10mmol/l or110-
180mg/dl
Prevent hypokalaemia, hypomagnesaemia, and
hypophosphataemia
Measure random sugar preoperatively
4 hourly for IDDM
8 hourly for NIDDM
Test urine 8 hourly for ketones and sugar
11/23/2018by emebet55
56. Preoperative assesment
The preoperative evaluation should emphasize on:
Acute and chronic complications
If there is DKA and HONK or RBS>400mg/dl with symptoms
in elective patient surgery should be postponed and patient
should be treated.
Cardiovascular:
The diabetic is prone to hypertension, ischaemic heart disease
(may be ‘silent’),
Cerebrovascular disease, myocardial infarction, and
cardiomyopathy
Autonomic neuropathy
Careful history and examination
Routine ECG should be performed
Appropriate stress testing if in doubt(exercise tolerance)
11/23/2018by emebet56
57. Renal:
Diabetes is one of the commonest causes of ESRD
Check urea, creatinine and electrolytes
Specifically check the potassium, protienurea
diabetics are at risk of ARF and bladder retention
postoperatively
Ensure adequate hydration
Respiratory:
Especially the obese and smokers are more prone to
respiratory infections
CXR, spirometry, and ABG are gold standard
Chest physiotherapy, humidified oxygen and
bronchodilators should be considered
11/23/2018by emebet57
58. Airway:
Thickening of soft tissues and joint ligaments(glycosylation)
occurs,
Intubation may be difficult, incidence is 30% in type I DM
Gastrointestinal :
Gastroparesis
Always ask about symptoms of reflux and be prepared for
RSI
Eyes
cataracts and retinopathy are common
Avoid increase in BP.
Diabetics are prone to infections.
• strict aseptic technique in airway mx and regional anaesthesia
11/23/2018by emebet58
59. Investigation
• Blood glucose.
• Test urine for ketones and glucose.
• Measure HbA1 c (glycosilated hemoglobin) ,
• Measure of recent glycaemic control (normal 3.8–6.4%).
• If HbA1c is 7.5–10%,
highlight suboptimal control .
Surgery may proceed with caution.
• A value >10% ;
suggests inadequate control.
Refer to diabetic team and only proceed if surgery is
urgent.
11/23/2018by emebet59
60. Preoperative management
Timing- diabetic patient should be the 1st in operation schedule
Hydration
Medication
Continue all diabetic medication until the day of surgery
except:
a.) Chlorpropamide (stop 3 days prior as long acting, substitute
with a shorter.
b.) Metformin only if major surgery as risk of lactic acidosis-
discontinue ideally 24hr and if there is renal failure it is C/I.
c.) Glitazones - ideally 24hr
d) Sulfunylurase for 48hr
e.) Long acting insulin – substitute with short/intermediate
actings
11/23/2018by emebet60
61. 11/23/2018by emebet61
For insulin dependent patients
Evening dose insulin of a day before surgery should be 2/3 of usual
insulin evening dose.
Or if controlled, Put the patient on sliding scale on the day of
surgery, if not controlled put on sliding scale a days before surgery.
Using sliding scale administer short acting subcutaneous insulin
follow glucose level/4hr. and on morning of surgery put on 500ml
of 5% dextrose with 10meq KCL run with 30drop/min.
Preoperative sliding scale:-
62. Intraop management
Decide :
Type of operative procedure- minor/major;
IDDM/NIDDM;
Poorly controlled or well controlled preoperatively.
11/23/2018by emebet62
67. Anaesthetic Technique:
Monitoring –V|S, ECG, capinography, glucometry
Watch for sweating
Check BG level
Catheterize and monitor urine output
GA - rapid sequence induction
Use cuffed tubes;
Empty stomach -NGT.
Aspiration profilaxisis(10mg metoc, 30 ml 0.3mol Na citrate
30 min before surgery, 50mg rantidine ).
Allow safe awakening.
11/23/2018by emebet67
68. • No Contraindication for standard anesthetics for induction and
inhalational agents.
Reduce the dose of induction agents, if AN
Steroids are contraindicated but if controlled DM single dose
of prophylactic dexamethasone for PONV has no significant
hyperglycemia.
Regional Technique :-Advantage :
Get over the problem of aspiration,
Difficulty intubation.
Preserve glucose tolerance.
No stress response.
• If peripheral neuropathy, document before anaesthesia.
• Chance of epidural abscess also increased
11/23/2018by emebet68
69. Postop management
• NIDDM - stop infusion and restart OH when eating or drinking.
• IDDM -stop infusion when patient resumes eating or drinking
and restart SC insulin
• Monitor the patient, manage PONV, pain and anxiety
• Continue fluid management to avoid DHN and hypoglycemia
• Start early ambulation
11/23/2018by emebet69
70. Summery
Brain storming??
1, what are complications of DM with their
perioperative concern?
2, what will be the management for all complications?
3, what will be the perioperative management
of controlled/uncontrolled IDDM/NIDDM in
minor and major surgery.
11/23/2018by emebet70
