A detailed stepwise approach for the perioperative management of diabetes mellitus. Sources taken from latest edition of Harrison, Millers, Stoeltings and ADA Guidelines. By a anaesthetist, for a anaesthesist

1. PERIOPERATIVE MANAGEMENT OF
DIABETES MELLITUS
PRESENTER – DR. SOURAV MONDAL
MODERATOR- DR. A.S. YADAV (MD) &
DR. H.R. BAGHEL (MD)
DEPT. OF ANAESTHESIOLOGY ,SSMC, REWA , MP

2. INTRODUCTION
• Diabetes mellitus is a metabolic disorder with an
increasing global incidence and prevalence.
• With an increasing incidence worldwide, DM will be
likely a leading cause of morbidity and mortality in
the future.
• Poor peri-operative glycaemic control increases the
risk of adverse outcomes.

3. • The effects of surgical stress and anaesthesia have
unique effects on blood glucose levels, which should
be taken into consideration to maintain optimum
glycaemic control.
• Through careful glycaemic management in
perioperative period, we may reduce morbidity and
mortality and improve surgical outcomes

4. DEFINITION (WHO)
“ A metabolic disorder of multiple etiology
characterised by chronic hyperglycaemia with
disturbances of carbohydrate, fat and protein
metabolism resulting from defect in insulin
secretion, insulin action or both.”

5. EPIDEMIOLOGY
• India is the “Diabetes Capital of the World.”
• About 77 million are considered to be pre-diabetic.
• Over 60 million, already diagnosed with diabetes.
• Projected to at least double by 2030.
• Smoking, poor physical activity and alcohol use are
some pertinent risk factors of diabetes in India

6. CLASSIFICATION
Type 1 diabetes
Type 2 diabetes
Gestational diabetes mellitus (GDM)
Specific types of diabetes due to other causes
Monogenic diabetes syndromes
Diseases of the exocrine pancreas
Drug- or chemical-induced diabetes

7. PATHOGENESIS
TYPE I TYPE II

8. RISK FACTORS , SIGNS AND
SYMPTOMS
• TYPE I
– Peak incidence between 10- 15 yrs
– Polyuria
– Polydipsia
– Polyphagia
– Weight loss
– Fatigue
– Insulin dependent

9. • TYPE II
– Average age > 50 yrs
– Sedentary lifestyle
– Familial tendency
– Obesity
– Easily fatigued
– Polyuria
– polydipsia

10. CRITERIA FOR TESTING FOR
DIABETES OR PREDIABETES IN
ASYMPTOMATIC ADULTS

11. • Testing should be considered in overweight or obese
(BMI ≥25 kg/m2 or ≥ 23 kg/m2 in Asian Americans)
adults who have 1 or more of the following risk
factors :
– First degree relative with diabetes
– History of CVD
– Hypertension

12. – HDL cholesterol < 35mg/dl and/or a triglyceride
level > 250 mg/dl
– PCOD
– Physical inactivity
– Other clinical conditions associated with insulin
resistance

13. • Prediabetics (HbA1C ≥ 5.7 %, IGT, IFG) should be
tested yearly
• Women with GDM should have lifelong testing every
3 yrs
• For all other pts, testing should begin at age of 45
yrs. If results are normal , testing should be repeated
at a min of 3 yrs.

14. SCREENING AND DIAGNOSIS
OF DIABETES

16. GDM-DIAGNOSIS

22. MANAGEMENT

24. INSULIN PREPARATIONS

26. ANTIDIABETIC MEDICATIONS

29. COMPLICATIONS OF DIABETES

30. IMPACT OF SURGERY ON DIABETES
 Metabolic effects of starvation:
Period of starvation induces a catabolic state.
It will stimulate secretion of counter-regulatory hormones.
 Metabolic effects of major surgery:
counter- regulatory hormones (epinephrine,
glucagon, cortisol and growth hormone)
inflammatory cytokines IL-6 and tumor necrosis
factor-alpha.
 Hypoglycemia: Exacerbate the catabolic effect of surgery

31.  Neuro-hormonal changes result in
 Increased insulin resistance.
 Decreased peripheral glucose utilization.
 Impaired insulin secretion.
 Increased lipolysis
 Protein catabolism, leading to HYPERGLYCEMIA and
even KETOSIS in some cases…

32. PRE-OPERATIVE EVALUATION

33. GENERAL PRINCIPLES
 Diabetes should be well controlled prior to elective
surgery.
 Avoid insulin deficiency and anticipate increased
insulin requirements.
 The patient’s diabetes care provider should be
involved in the management of their patient’s
diabetes peri-operatively.

34.  Patients with diabetes should be on the morning list,
preferably first on the list.
 Patients should be well hydrated before the
procedure.

35. GOALS
 Establishment of certain glycemic target levels, <180
mg/dL in critical patients and < 140 mg/dL in stable
patients.
 Avoidance of severe hyperglycemia or hypoglycemia.
 Prevention of ketoacidosis.
 Maintenance of physiological electrolyte and fluid
balance.
 Reduction of overall patient morbidity and mortality.

36. PRE-OPERATIVE EVALUATION
ToAssess History/Examination Investigation
1. Anaemia ,
leukocytosis
Basic investigation,
H/O frequent
infections
CBC
2. Blood Sugar Control
Hypo/
Hyperglycemic
episodes,
Hospitalization
BS- F & PP
HbA1C
3. Nephropathy
H/O- HTN, Swelling over
body, Recurrent
UTI.
Urine R/E and
M/E, RFT
4. Cardiac Status
H/O- Angina/ MI , Swelling
of feet,
Exercise intolerance
ECG, CXR, ECHO,TMT
5. PVD
H/O- Intermittent Claudication,
Blanching of feet,
Non healing ulcer
USG doppler

37. To Assess History/Examination Investigation
6. Retinopathy H/O - Visual disturbances Fundus Examination
7. ANS
Early satiety, abdominal distension,
Anhidrosis, Impotence, Orthostatic
Syncope
Postural change in BP, HR
variability with exercise,
tachycardia response to
atropine
8. Metabolic &
Electrolyte
H/O- Starvation, Infection
Sign of DKA,
ABG, Urinary Ketone,
Sr. Electrolyte
9. Airway
Scleredema diabeticorum,
Stiff Joint Syndrome
(Prayer sign, Palm Print test)
X-ray cervical spine
AP & Lateral

38. Prayer Sign
Patient is unable to
approximate the palmar
surface of phalangeal joints
despite of maximal effort.
Palm PrintTest:
Degree of inter-phalyngeal
joint involvement can also be
assessed by scoring the ink
impression made by the palm
of dominant hand.

39. CLINICAL SYMPTOMS & SIGNS OF
DIABETICAUTONOMIC NEUROPATHY
(DAN)
CARDIOVASCULAR:
 Resting Tachycardia
 Exercise intolerance
 Orthostatic hypotension
 Painless MI
GI:
 Esophageal dysmotility
 Gastroparesis
 Constipation
 Diarrhoea
 Faecal incontinence

40. GENITOURINARY:
 Neurogenic bladder
 Erectile dysfunction
 Retrograde ejaculation
 Female sexual
dysfunction
METABOLIC:
 Hypoglycaemic
unawareness
 Hypoglycaemia
associated autonomic
failure

41. SUDOMOTOR:
 Anhidrosis
 Heat intolerance
 Gustatory sweating
 Dry skin
PUPILLARY:
 Functional impairment
 ARP

42. TESTS FOR DIABETIC AUTONOMIC
NEUROPATHY
 Early stage: abnormality of HR response during deep breathing
 Intermediate stage: abnormality of Valsalva response
 Late stage: presence of postural hypotension
 The test are valid marker of DAN if following factors ruled out.
1. End organ failure
2. Concomitant illness
3. Drugs: antidepressents, antihistamines, diuretics, vasodilators,
sympathatic blockers, vagolytics.

43. TEST FOR PARASYMPATHETICCONTROL
Heart rate variability (HRV) in response to:
 DEEP BREATHING:
 Respiratory sinus arrhythmia is a normal phenomenon due
to vagal input to sinus node during expiration causing
cardiodeceleration
 The patient lies quietly and breathes deeply at a rate of 6
breaths/min (a rate that produces maximum variation in
heart rate) while a heart monitor records the difference
between the maximum and minimum heart rates.
 Normal variability: >15 beats/min
 Abnormal variability: <10 beats/min

44.  STANDING:
 This test evaluates the cardiovascular response elicited by a
change from a horizontal to a vertical position.
 In healthy subjects,
• Standing  rapid increase in heart rate that is maximal at
approximately the 15th beat  relative bradycardia that is
maximal at approximately the 30th beat after standing.
 The patient is connected to an ECG monitor while lying down and
then made to stand to a full upright position.
 ECG tracings are used to determine the 30:15 ratio, calculated as
the ratio of the longest R-R interval (found at about beat 30) to the
shortest R-R interval (found at about beat 15).

45.  The maximum and minimum R-R intervals may not always
occur at exactly the 15th or 30th beats afterstanding
 Ziegler et al. redefined the maximum/minimum 30:15 ratio as
the longest R-R interval during beats 20–40 divided by the
shortest R-R interval during beats 5–25.
 In patients with diabetes and autonomic neuropathy, there is
only a gradual increase in heart rate(30:15ratio):
>1.04 = normal
1.01-1.03 = borderline
< 1.01 = abnormal

46.  VALSALVA MANEUVER:
supine patient, connected to an ECG monitor
forcibly exhales into the mouthpiece of a manometer, exerting a
pressure of 40mm
of Hg, for 15 seconds with an open glottis.
sudden transient increase in intra-thoracic and intra-abdominal
pressures, with a characteristic hemodynamic response.

47. The response has four phases and inhealthy individuals can be
observed as follows:
 Phase I: Transient rise in BP and a fall in HR
 Phase II: Early fall in BP with a subsequent recovery of BP later
in the phase, accompanied by an increase in HR.
 Phase III: BP falls and heart rate increases with cessation
of expiration.
 Phase IV: BP increases above the baseline value (overshoot)

48.  The Valsalva Ratio is determined from the ECG tracings by
calculating the ratio of the longest R-R interval after the
maneuver (reflecting the bradycardic response to blood
pressure overshoot) to the shortest R-R interval during or
shortly after the maneuver (reflecting tachycardia as a result
of strain).
 Ratio < 1.2 is abnormal

49. TEST FOR SYMPATHETICCONTROL
BP response to:
 STANDING OR PASSIVE TILTING
 Orthostatic hypotension is defined as a decrease in SBP of 20
mm Hg or a decrease in DBP of 10 mm Hg within 3 minutes of
standing when compared with blood pressure from the sitting
or supineposition.
 Alternatively, the diagnosis can be made by head-up tilt-table
testing at an angle of at least 60 degrees.
 BP is rapidly corrected by baroreflex-mediated peripheral
vasoconstriction and tachycardia.
• A fall of SBP by more than 30 mm Hg is abnormal
• A fall of 11 to 29 mm Hg is borderline

50.  RESPONSE TO ISOMETRIC EXERCISE:
 Sustained muscle contractionas measured by a handgrip
dynamometer causes a rise in systolic and diastolic blood
pressure and heartrate.
 The dynamometer is first squeezed to isometric maximum,
then held at 30% of maximum for 5 min.
 This rise is caused by a reflex arc from the exercising muscles to
central command and back along efferent fibers. The efferent
fibers innervate the heart and muscle, resulting in increased
CO, BP andHR.
 ↑ of DBP >16 mm of Hg = normal; <10 mm of Hg = abnormal

51. RESPONSE TO VALSALVA MANEUVER :
as already described

52. PATIENTS WHO REQUIRE INSULIN
THERAPY
 For all pts, discontinue all short acting insulin on the day
of surgery.
 Pts with T2DM should take none , or up to ½ of their
dose of long-acting or combination insulin, on the day of
sx
 Pts with T1DM should take a small amount usually 1/3 of
their usual morning long-acting insulin dose on the day
of sx.
 Pts with an insulin pump should continue their basal rate
only

53. PATIENTS ONOHA (WITHOUT
INSULIN)
Omit OHA 24-48 hours before surgery.
Restart it when patients are able to resume normal meals
(except metformin and thiazolidinediones following cardiac
surgery).
Commence an I-G infusion if the BGL >180mg/dl, if surgery is
prolonged and or if the patient is usually treated with more
than one oral AHG agent.
Subcutaneous insulin may be required post-operatively

54. PAC ORDERS
 Consent
 NPO orders
 Anxiolytics
 Stop long acting insulin, biguanides, sulfonylureas,
thiazolidinediones, GLP-1 agonists, alpha
glucosidase inhibitors night before surgery.
 Stop OHA 24 to 48 hours before surgery

55.  Morning blood sugar and s. electrolytes to be done
 Morning IV fluid according to regimen
 Arrange Glucometer, dextro-strips, insulin etc.
 Careful transport of the patient
 To be taken as the first case

56. PREOP FASTING
 Atleast 6 hours for solid foods.
 Patients with gastroparesis, 12 hours may be
needed. Such patients are given H2 receptor blocker
(Ranitidine) and prokinetics(metoclopramide).
 When fasting exceeds 8-10 hours then insulin-
glucose infusion has to be started to prevent
catabolism.

57. PHARMACOLOGICAL EFFECTS OF
DRUGS

58. Benzodiazepines
 secretion of ACTH production of cortisol, when used
in high doses during surgery.
 sympathetic stimulation but, paradoxically, stimulate
GH secretion and result in a decrease in the glycaemic
response tosurgery.
 Effects are minimal when midazolam is given in usual
sedative doses, but may be relevant if the drug is given
by continuous i.v. infusion to patients.

59. High‐dose opioids:
 Produce haemodynamic, hormonal and metabolic
stability.
 effectively block the entire sympathetic nervous system
and the HPA axis, probably by a direct effect on the
hypothalamus and higher centres.
 seen in normal patients and may be of benefit in the
diabetic patient.

60.  Blocks adrenal steroidogenesis and hence cortisol
synthesis by its action on 11 β-hydroxylase and
cholesterol cleavage enzymes & consequently decreases
the hyperglycaemic response to surgery .
Propofol
 Diabetic patients show a reduced ability to clear lipids
from the circulation
Etomidate:

61. Ketamine:
 Ketamine has a dual effect on blood glucoselevel.
 Low dose produces hyperglycaemia, mediated viaα2-
adrenoceptors
 High doses produce hypoglycaemia mediated through opioid
receptors with some involvement of β-adrenoceptors that
becomes evident only after blockade of α2-adrenoceptors.
Inhalationals
 Halothane, enflurane and isoflurane, in vitro, inhibit the
insulin response to glucose in a reversible and
dose‐dependent manner.

62. Muscle Relaxants:
 Succinyl choline should be avoided in patients with
extensive peripheral neuropathy due to risk of increased
potassium release.
 Atracurium and mivacurium are preferred in presence
of renal dysfunction.
 Rocuronium may be used in rapid sequence induction.

63. INTRAOPERATIVE
MANAGEMENT

64. GENERAL ANAESTHESIA &DIABETES
ADVANTAGES
• High dose opiate technique may
be useful to block the entire
sympathetic nervous system
and the hypothalamic pituitary
axis.
• Better control of blood pressure
in patients with autonomic
neuropathy.
DISADVANTAGES
 May have difficult airway. (“Stiff-joint
syndrome”)
 Full stomach due to gastroparesis.
 Controlled ventilation is needed as
patients with autonomic neuropathy
may have impaired ventilatory control.
 Aggravated haemodynamic response
to intubation.
 It may masks the symptoms of
hypoglycaemia

65. REGIONAL ANAESTHESIA &DIABETES
ADVANTAGES
 Regional anaesthesia blunts the
increases in catecholamines,
cortisol, glucagon, and glucose.
 Metabolic effects of anaesthetic
agents avoided
 An awake patient – hypoglycaemia
readily detectable.
 Decreased chance of Aspiration,
PONV and Thromboembolism.
 Rapid return to diet and s/c
insulin/OHA
DISADVANTAGES
 If autonomic neuropathy is
present, profound hypotension
may occur.
 Infections may be increased
(epidural abscesses are more
common in diabetics)
 Medicolegal concern of risk of
nerve injuries and higher risk of
ischaemic injury due to use of
adrenaline with LA

66. REGIMENS OF INSULINTHERAPY

67. SLIDING SCALE REGIMEN (S/C)
Glucose in mg/dl Regular Insulin
150-200 2 unit
201-250 4 unit
251-300 6 unit
301-350 8 unit
≥350 10 unit
Limitations:
× Little flexibility
× Variable insulin absorption
× Little rational of their use except minor surgery under local
anesthesia

68. SLIDING SCALE REGIMEN (I.V.)
 Insulin sliding scale uses 50 U of soluble Insulin diluted up to
50 ml with normal saline and run at a rate according to the
patient’s blood glucose.
 Dextrose @100ml/hr and potassium 20meq/L is also needed
to be infused concurrently.
Regular Insulin(ml/hr)Glucose(mg/dl)
<120 Stop infusion
121-150 0.5
151-180 2
181-220 3
221-260 4
261-300 5
>300 6

69. The amount of
Insulin
administered can
be altered easily
without having to
make up a new
mixture.
DISADVANTAGE
Risk of a failure to
administer
dextrose due to
blockage,
disconnection or
backflow.
ADVANTAGE

70.  Glucose – Potassium – Insulin infusion
 Alberti and Thomas regimen (1979)
 Tocommence on the morning of surgery:
500ml 10% glucose
+ 10U Insulin + 10 mmol Kcl
@ 100ml / hr
Blood sugar every 2-3hrs
Blood sugar
<5mmol / L (90mg/dl)
Insulin ↓ to 5U
Blood sugar
>10mmol / L (180-
270mg/dl)
Insulin ↑ to 15U
ALBERTI’S OR GKI REGIMEN

71. Mechanism :
 Lowering circulating levels of free fatty acids and subsequent
myocardial uptake(which are toxic to ischemic myocardium)
 Increased myocardial energy production through exogenous
glucose;
 Stabilization of intracellular potassium, which may be depleted during
times of myocardial ischemia.

72. × Insulin could be
adsorbed in the iv
fluid bag and infusion
set – could be
avoided by flushing
solution through
infusion set
ADVANTAGE
 Simple
 Safe
 Reproducible
 Remove the
risk of
accidental
insulin infusion
without
dextrose.
DISADVANTAGE
× Need to change the
bag if dose of insulin
needs to be
changed.

73. MODIFIED ALBERTI REGIMEN
500ml of 10%dextrose +
10mmols of KCL +15 U
Insulin @ 100ml/hr
Cont. new GIK
solution at adjusted
conc.
Increase Insulin
by 5 U
Decrease Insulin
by 5 U
Measure
BG every 2
hrs
BG<120mg
/dl
BG >200mg/dl
BG 120-200mg
continue @ same
rate

74. HIRSCH REGIMEN

75. TIGHT CONTROLREGIMEN
 Target Blood Sugar is 80-110 mg/dl.
 Indications: Pregnancy, CPB, Neurosurgery.
 Advantages:
 Improve wound Healing,
 Prevent wound infection,
 Improve neurological outcome.

76.  Start 5% Dextrose @ 50 ml/hr.
 Dissolve 50 U of insulin in 250 ml of NS and start
piggy back infusion.
 Insulin infusion rate = BG/150 U/hr and BG/100 U/hr
if pt is obese(BMI > 35 kg/m2), on steroids or in
sepsis.
• RISK of HYPOGLYCEMIA

77. NON-TIGHT REGIMEN
 Aim is to prevent hypoglycaemia, ketoacidosis and
hyperosmolar states.
 Intravenous infusion of 5% dextrose @ 125ml/hr is
started at 6am on the day of surgery. ½ the morning dose
of insulin is given s/c.
 5% dextrose is continued throughout the sx.
 Postoperatively glucose is monitored and treated with
sliding scale.

78. VELLORE REGIMEN
Blood sugar (mg/dL) Treatment
<70 Stop insulin if on insulin. Rapid infusion of 100 mL of
D5W, measure blood glucose after 15 min
71-100 Stop insulin, infuse D5W at 100mL/h
101-150 1U of insulin + 100 mL of D5W/h
151-200 2U of insulin + 100 mL of D5W/h
201-250 3U of insulin + 100 mL of D5W/h
251-300 4U of insulin + 100 mL of D5W/h
>300 1U of insulin for every 50 mg more than 100 mg/dL +
100 ml of D5W/h
Regular insulin 5 U in 500 mL of 5% dextrose in water solution
(D5W) should be started in the ward @ 100 mL/hr until the time
of operation.

79. CHOICE OF FLUIDS
There is no ideal solution; either of RL or NS may be
used judiciously.
 Ringer’s lactate: lactate undergo gluconeogenesis in
the liver and may complicate blood sugar control
when given in large volumes.
 Normal saline: infusions in large volume increase risk
of hyperchloremic metabolic acidosis.

80. THE POST-OPERATIVEPERIOD

81.  Insulin-glucose infusions should be continued until
the patients can resume an adequate diet (or
atleast 24 hrs).
 I-G infusions should ideally be stopped after
breakfast,and a dose of subcutaneous insulin (or
oral AHG) is given before breakfast.
 Hyperglycemia detected post-operatively in patients
but not previously known to have diabetes, should
be managed as if diabetes was present, and the
diagnosis of diabetes reconsidered once the patient
has recovered from their surgery.

82.  Diabetes medication requirements may be increased
(or occasionally decreased) in the post-operative
period, and frequent BGL monitoring is therefore
essential.
 Endocrinologist must be available for the post-
operative management of glycaemic instability.

83. ANAESTHESIA , DM &
SPECIAL SITUATIONS

84. DM & EMERGENCYSURGERY
 Usually Infected
 Usually Uncontrolled
 Dehydrated
 Metabolic decompensated
 Increased resistance to insulin
 More chances of acute Hyperglycemic complication

85. EMERGENCY SURGERY
 Little time for stabilisation of patients ,but if 2-3 hr
available
• correction of fluid and electrolyte imbalance .
• Correct hyperglycemia.(start I-G infusion if sugar
> 180mg/dl)
• Treat acidosis.
• Avoid hypoglycemia.
 However, surgery should not be delayed in an attempt to treat
ketoacidosis completely, if the underlying condition has the
possibility of leading to further metabolic deterioration.

86.  Likelyhood of intra-op hypotension and arrhythmia is
more particularly if pt has pre-op acidosis or
hypokalemia.
 Intra-op sugar to be monitored more frequently.
 Atleast hourly.
 LSCS – every 30 min.

87. PREGNANCY
 Pregnancy is a diabetogenic state. As pregnancy advances
insulin resistance increases.
 Hyperglycemia during pregnancy has both maternal and fetal
complications & adverse outcome.
 Challenges –Altered maternal physiology & disease
associated with pregnancy.
Maternal hyperglycaemia :
 Increases the risk of neonatal jaundice.
 The risk of neonatal brain damage, and
 Fetal acidosis if the fetus becomes hypoxic

88.  Needs tighter control.
 More prone for hypoglycaemia /hyperglycaemia
 DKA – usually occurs during 2nd/ 3rd trimester, even
develops with low glucose value of 200mg/dl.

89. DIABETIC CRISIS
HYPOGLYCAEMIC:
HYPERGLYCAEMIC :
• DKA
• HYPEROSMOLAR NONKETOTIC COMA.


90. HYPOGLYCEMIA
 Blood sugar < 70 mg/dl.
 Symptoms due to adrenergic excess and
Neuroglycopenia.
 Sweating, tachycardia/bradycardia , tremors,
hypotension, dizziness, irritability, seizures, or coma.
 Stop insulin & give dextrose 20-30 ml 50% dextrose
 Dextrose infusion
 Glucagon (0.5-1.0 mg IM )
 Octreotide (antidote to sulphonylurea induced
hypoglycaemia)

91. LAB VALUES IN DKA & HHS
DKA HHS
Glucose mmol/l (mg/dl) 13.9-33.3 (250-600) 33.3-66.6 (600-1200)
Na meq/l 125-135 135-145
K meq/l N to ↑ N
Mg N N
Cl N N
PO4 N to ↓ N
Creatinine µmol/l (mg/dl) Slightly ↑ Moderately ↑
Osmolarity (mOsm/ml) 300-320 330-380
Plasma ketones ++++ ±
Serum HCOӡ meq/l <15 meq/l N to slightly ↓
Arterial pH 6.8-7.3 >7.3
Arterial PCO2 mmHg 20-30 N
Anion gap meq/l ↑ N to slightly ↑

92. DKA - MANAGEMENT
Insulin replacement-
0.1U/kg bolus followed by 0.1U/kg/hr and if BG does not
↓ by 10%-repeat the loading dose –if still no response –
double the infusion dose in every 2 hr.
Fluids:
0.9% NS-2-3 ltr over 1- 3 hr(10-20ml/kg/hr)
subsequently, 0.45% NS @ 200-500 ml/hr
 0.45% NS & 5%D @ 150- 250ml/hr- when the BG<
250 mg/dl .
Sod bicarb if blood pH< 7.1
Electrolyte:
20-30meq of K+/hr after 2 hr of t/t
Replace phosphate when, <1mg/dl

93. HHS MANAGEMENT
 If plasma osmolarity is >320 mOsm/L, 1000–1500
mL/h of hypotonic saline should be administered
until the osmolarity is <320 mOsm/L, at which time
1000–1500 mL/h of isotonic saline can be given.
 Insulin therapy is initiated with an IV bolus of 15
units of regular insulin followed by a 0.1 unit/kg/h
infusion. The insulin infusion ↓ 2–3 units/h when
the glucose level↓ approximately 250–300 mg/dL.
 Electrolyte deficits are significant but usually less
severe than in DKA.

94. TAKE HOME MESSAGES
 Ensure glycemic control.
 Proper preoperative assessment and preparation, check
for DAN.
 Avoid prolong fasting, start insulin-glucose
Infusion.(keep BG level <180 mg/dl)

95.  Careful perioperative glucose management can reduce
surgical complications as well as hyper- or hypoglycaemic
sequelae which ultimately improves morbidity and
mortality.
is more dangerous than Remember: Hypoglycemia
hyperglycemia.