2. Diabetes mellitus is a clinical syndrome
characterized by chronic hyperglycemia and
disturbance in carbohydrate metabolism
The disease may result from defect in insulin
secretion or an adequate tissue responce to insulin
This leads to increased circulating glucose levels
with eventual microvascular and macrovascular
complication
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3. Insulin is secreted by β cells in the islets of
langerhans of pancreas.
Insulin is polypeptide with 51 amino acid.
it has two amino acid chains called α and β chains
Adults normally secrete approximately 50 units of
insuline each day.
Rate of insulin secretion is primary determined by
the plasma glucose concentration
Insulin the most important anabolic hormones, has
multiple metabolic effects.
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4. Promotes glycogenesis
Increase synthesis of
Triglcerides, cholestrol
and VLDL3
Increase protein
Synthesis
Inhibits glycogenolysis
Inhibits ketogenesis
Inhibits gluconeogensis
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5. Incresae amino acid
transport
Increase protein
sythesis
Increase glucose
transport
Enhance activity of
glycogen synthetase
Inhibits activity of
glycogen
phosphorylase
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6. Promotes triglycerides storage
Induces lipoprotein lipase, making fatty acids
available for absorption into fat cells
Increase glucose transport into fat cells
Inhibits intracellular lipolysis
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7. Primary diabetes mellitus
Type 1 diabetes
Type 2 diabetes
Secondary diabetes mellitus
a) Endocrine disease
cushing’s syndrome
Thyrotoxicosis
Pheochromocytosis
Acromegaly
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9. d)Gastational diabetes
Diabetes of pregnency
e) Associated with genetic syndromes
Down’s syndrome
Turner’s syndrome
Myotonic dystrophy
Kilnefelter’s syndrome
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10. Also called insulin dependent diabetes mellitus
(IDDM) or Juvenile- onset diabetes
Between 5% and 10% of all cases of diabetes are
type 1
Type 1 diabetes result from autoimmune destuction
of the pancreatic islets β cell with absolute loss of
insulin secreation
Type 1 diabetes is commonly presents in childhood
and adolescence
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11. Type 1 diabetes is caused by T-cell mediated
autoimmune distruction of β-cell in the pancrease.
The exact cause is unkown,althoug
Genetic susceptibility
Inheritance
human leukocyte antigen (HLA) system
Viral infecton
Pancreatic pathology
Immunological factor
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12. Its include 90-95% of those with diabetes
Term used previously include non-insulin depended
diabetes and adult or maturity onset diabetes
These patients have insulin resistance and usually
have relative insulin defiency
Most do not need insulin treatment for their survival
Type 2 diabetes usually manifests above 30 years
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13. Exact cause unknown
Genetics
Environmental factor
life style: overeating especially when combine
with obesity probably act as a diabetogenic factor
Pancreatic pathology
Reduction of insulin secretion cells
Resistance to insulin action
Delayed insulin secretion in response to oral
glucose
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15. Pathophysiology of GDM:
In early pregnency maternal estrogen and
progesterone increase and promote pancreatic β-
cells and increased insulin release
Increase in peripheral glucose utilization and
glycogen storage
As pregnancy progress increased level of human
chorionic somatomammotropin (HCS), cortisol,
prolactin, progesterone, and estrogen and leads to
insulin resistance in peripheral tissues
The pancrease release 1.5-2.5 times more insulin
in order to respond to insulin resistance
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16. GDM result when there is delayed or insufficient
insulin secreation in the presence of increasing
peripheral resistance
Independed risk factor for gastational diabetes :
Body mass index above 30 kg/m
Previous gastational diabetes
Family history of diabetes
Previous macrosomic baby weight 4.5 kg or
above
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17. White classification, named after priscilla white who
pioneered research on the effects of diabetes types
on perinatal outcome is widely used to assess
maternal and fetal risk.
Gastational diabetes (diabetes which began during
pregnancy)
Pregastational diabetes (diabetes that existed prior
to pregnancy)
There are 2 subtype of gastational diabetes
Type A1:
Type A2
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19. 1. Macrovascular (coronary artery disease, peripheral
arterial disease and stroke)
Mechanism of injury
o Atherosclerosis
o increased coagulability and impaired fibrinolysis
2. Microvascular complicataion ( diabetic nephropathy,
neuropathy, and retinopathy)
Mechanism of injury
o osmotic stress from sorbirol accumulation
o formation of advanced glycosylated end products
o free redical production and O2 species formation
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20. Diabetes nephropathy
Approximately 30_40% of individuals with type 1
diabetes and 5_10% of those with type 2 diabetes
develop end-stage renal disrease
Mechanism of injury
Glomerular hyperfiltration
Increase in glomerular hydrostatic pressure causes
glomerular deamge and microalbuminuria
Impaired endothelium-depended vasodilation
Earliest sign is microalbuminuria
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21. Diabetic neuropathy
Chronic sensorimotor distal symmetric
polyneuropathy is the most common form
-most common symptoms are burning, tingling
and numbness
Mononeuropathies are sudden onset. Median, ulnar
and radial commonly affected
Diabetic neuropathy: severe pain and muscle
weakness and atrophy usually in thigh muscles
Diabetic autonomic neuropathy (due to local
ischemia tissue accumulation of sarbitol and
immunological demage)
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22. Diabetic retinopathy
Dot hemorrhage, hard exudate, microaneurysms,
retinal edema
Proliferative retinopathy and retinal detachment
Cardiac complication :
Increased risk of coronary artery disease(slient)
Hypertension
Peripheral arterial disease
Systolic and diastolic dysfunction (related to
hypertension, coronary artery disease, left
ventricular hypertroph,y autonomic neuropathy)
Heart rate variability
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23. Central nervous system:
Cerebral vascular disease related to
_Hypertension
_Dyslipidemia
_Accelerated atherosclerosis
_Abnormal endothelial proloferation
_Increased coagulabillity and impaired fibrinolysis
Gastrointestinal system:
Risk of aspiration is increased because of
autonomic neuropathy
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24. Respiratory system:
Decreased lung volume and lung diffusing capacity
Reduced hypoxic-induced ventilatory drive
Diabetics may prone to respiratory depression from
opioids and sedative agent
Airway difficulties
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25. The “stiff joint” or limited joint mobility (LJM) or
diabetic cheiroarthopathy
Jonit supporting airway rigidity. Neck extension and
laryngoscopy may be difficult
Cause: nonenzymatic glycosylation of proteins and
abnormal cross-linking of collagen in jionts and
other tissue
Test:
prayer sign”
palm print test:
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28. There are three life-threating acute complication of
diabetes
Diabetic ketoacidosis (DKA)
Hyperosmolar hyperglycemic state
Hypoglycemia
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29. Diabetic ketoacidosis (DKA) is a complication of
decompensated diabetes mllitus.
Seen in type 1 diabetes during the catabolic stress
of acute illness such as trauma, surgery, or
infection.
Clinical feature are:
Symptoms of hyperglycemia like polyuria and
polydipsia.
Symptoms of acidosis and dehydration such as
respiratory distres, drowsiness, coma and
abdominal pain
Other symptoms like vomiting, malaise, cramps
Signs: include tachycardia, dehydration, acidosis,
depressed consiousness
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30. Mechanism:
Increased gluconeogenesis and hepatic and renal
glucose production along with impaired glucose
utlization in peripheral tissue cause hyperglycemia
and hyperosmlality.
The increase counter regulatory hormones lead to
lipolysis and hepatic fatty acid oxidation to ketone
bodies (hydroxybutyrate, actone and acetoacetate
acid) with resulting metabolic acidosis.
Osmotic diuresis leads water loss and electrolyte
distrurbance.
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31. HHS is characterized by severe hyperglycemia,
hyperosmolarity and dehydration
seen in the type 2 diabetics, more commonly in
elderly people with co existing disease.
Caused by plasma insulin concentration that are
inadequate for glucose utilization but are adequate
to prevent lipolysis and ketogenesis
The hyperglycemia and volume deficit is more
severe then DKA.
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32. Hyperosmolar nonketotic coma or(HHS)
Clinical features:
polyuria, polydipsia,
Slow onset over days to weeks.
Symptoms of hyperglycemia.
Sign of dehydration.
Sign of hyper viscosity and thrombosis like delirium
, coma, seizures, sensory and motor deficits.
Abdominal pain is unusual. Vomiting may be
present.
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33. Principle of treatment of DKA and HHS
1) correction of dehydration, hyperglycemia, and
electrolyte imbalances
2) identification of comorbid precipitating events
3) freqent patient monitring
Fluid therapy:
15-20 mL/kg body weight of 0.9% NACL is infused
in the first hour.
Further fluid resuscitation is guided by assignment
of fluid status, urine output and electrolytes level.
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34. 0.5% or 0.9% NACL may be used.
Total fluid deficit is corrected over 24 hours with
constant monitoring to avoid overload.
Patients in hemodynamic shock need fluid and
vasopressor therapy with advanced hemodynamic
monitoring.
Patients with pre existing cardiac dysfunction need
cautious fluid boluses.
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35. Insulin therapy:
I/v bolus of regular insulin 0.1 unit/k body wt.
Followed by a continuous infusion at a dose of 0.1
unit/kg/hr should be administered with the aim to
decrease plasma glucose concentration at a rate of
50-75 mg % per hour.
If the drop is not adequate, insulin dose can be
doubled to achieve steady drop.
Potassium theraphy:
Serum potassium < 3.3 mEq/l supplement
potassium at 20-30mEq/h before starting insuln to
aviod arythmias, cardiac arrest or respiratory
muscle weakness.
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36. Bicarbonate:
Bicarbonate is usually reserved for severe metabolic
acidosis with pH < 7.0.
50 or100 mmoL bicarbonate can be given depending on
the severity of acidosis,
Bicarbonates should not be used in presence of
hypokalemia till serum potassium levels are corrected.
Phosphate:
Supplementation is advised only at serum phosphate
concentration < 1.0 mg/dl or in the presence of anemia,
cardiac dysfunction or respiratory muscle weakness. If
needed, 20-30 mEa/L potassium phosphate can be
given.
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37. Monitring:
2-4 hourly estimation of serum electrolytes,
glucose, blood urea nitrogen, creatinine, osmolality
and acid status.
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38. Hypoglycemia in the diabetic patient is the result of
an absolute or relative excess of insulin relative to
carbohydrate intake and exercise.
If hypoglycemia is not treated, mental status
changes can progress from anxity,
lightheadedness, or confusion and coma
The treatment of hypoglycemia in anesthetized or
critically ill patients consist of intravenous
administration of 50% glucose
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39. Timing
Fasting
IV fluid
Monitoring
Standard monitoring
Glycosylated hemoglobin (HbAc)
Sugar control
Glucose supplement
Insulin supplement
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40. History:
which oral hypoglycemic agents
If insulin type of insulin and dosing schedule
Disease history
Complication history
Physical examination
Cvs examination
Respiratory system examination
CNS examination
Airway examination
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41. Investigation
Hemoglobin: anemia is present with renal
dysfunction
CBC : look for infection
Urine routine for microalbuminuria
Serum creatnine: to detect renal function
Fasting blood sugar:
Glycosylated Hb:HbA1c of less then 7% implies
good sugar control
Serum electrolyte: to detect abnormalities in
patient with history of vomiting, diarrhea, poor oral
intake. Also in patient on insulin
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42. Investigation
ECG: To detect asymptomatic myocardial
infarction. DM patient have increased incidence of
ST-segment and T-wave segment changes on ECG
X-ray chest: tuberculosis is common is diabetic.
Cardiac enlargement, and pulmonary vascular
congestion, or plural effusion.
Morning of surgery investigation:
Serum electrolyte, FBS, urine ketones
Emergency surgery:
Need full clinical and biochemical assessment.
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43. Reflex dysfunction of the ANS may be increased by
old age, diabetes longer then 10 year’s duration,
coronary artery disesae
Delay gastric emptying time
Premedication with antacid and medclompramide is
often used.
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44. lnduction:
Choice of agent for general anesthesia depends on
severity of systemic diseases, such as coronary artery
disease, nephropathy, hypertension and autonomic
neuropathy.
Epidural analgesia may be instituted after due
consideration to autonomic neuropathy, IHD and
peripheral neuropathy.
It should be avoided in sick patients with sepsis.
Epidural analgesia may help to attenuate
neurohormonal response to stress and avoid systemic
analgesics like NSAIDs and opioids which may have
serious side effects in a diabetic patient.
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45. A rapid sequence induction should be performed for
patients with GI symptoms.
Awake fiberoptic bronchoscopy would be preferred
technique for an anticipated diffiCUIt airway.
A careful induction with Etomidate or high dose
Fentanyl (4-5 mcg/kg) with midazolam and/or
thiopentone should be performed (exaggerated
hypotension due to autonomic neuropathy)
Succinylcholine should be avioded
Rocuronium may be used in RSI
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46. Maintenance of anesthesia:
Isoflurane and sevoflurane can be used
Nitrous oxide should be avoided
Airway pressure should be monitered
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47. Induction agent:
Ketamine may cause significant hyperglycemia.
Etomidate blocks adrenal steroidogenesis and
hence gortisol synthesis and decreases the
hyperglycemlc response to surgery by
apptoximately 18 mg% in non-diabetic subjects
The effect of popofol on insulin secretion is not
known
Halothane, enflurane, isoflurane and sevoflurane in
in vitro studies inhibit the insulin response to
glucose in a reversible and dose-dependent
manner but their effect in clinical situations is not
certain
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48. Benzodiazepines decrease the secretion of ACTH
and the production of cortisol, when used in high
doses.
High-dose opiate anesthetic techniques produce
hemodynamic, hormonal and metabolic stability
Ganglion-blocking agents (used for hypotensive
anesthesia prviously) may block sympametically
mediated hepatic gluconeogenesis with resultant
hypoglycemia
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49. The goal of intraoperative blood glucose
management is to avoid hypoglycemia while
mantaning blood sugar blow 180 mg/dL
Hyperglycemia is has been associated with
hyperosmolarity, infection, poor wound healing and
increased mortilty
Loose control (<180 mg/dL)
Tight control (<150 mg/dL)
Control of blood glucose in pregnant diabetic
patients improves fetal outcome.
There are several common perioperative
management regmens for insulin-depended
diabetic patients
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50. In the most time-honored (but not terribly effective)
approach, the patient receives a fraction-usually
half-of the total morning insulin dose in the form of
intermediate-acting insulin
To decrease the risk of hypoglycemia. insulin is
administered after intravenous access has been
established and the morning blood glucose
An alternative method is to administer regular
insulin as a continuous infusion.
Regular insulin can be added to normal saline in a
concentration of 1 unit/mL and the infusion begun at
0.1 unit/kg/h.
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51. the regular insulin infusion can be adjusted up or down
as required.
The dose required may be approximated by the
following formula:
Unit per hour = Plasma glucose (mg/dL) /150
When administering an intravenous insulin infusion to
surgical patients, adding some (eg, 20 mEq) KCl to each
liter of fluid may be useful, as insulin causes an
intracellular potassium shift.
The key to any management regimen is to monitor
plasma glucose levels frequently.
Patients receiving insulin infusions intraoperatively may
need to have their glucose measured hourly.
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52. Patients who take NPH(neutral protamine
hagedorn) or other protamine containing insulin
preparations have an increased risk of allergies
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53. “tight sugar control” refers to maintaince of blood
sugar within narrow range, typically between 70-
110 mg%
Hypoglycemia is a significant risk in this approach
Significant in cardiac surgery, neuronal injury,
burns, transplant surgery, critically ill paitents and
pregnant women.
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54. Close monitoring of blood sugar
And multimodal analgesic technique
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