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Diploma in Anaesthesia > Preoperative assessment: Obesity, DM, Renal , Coagulation > Flashcards

Preoperative assessment: Obesity, DM, Renal , Coagulation Flashcards

1
Q

Why is airway management difficult in obese patients

A

Increased upper thoracic soft tissue
Large tongue
Palatal/pharyngeal fat

BVM - usually very difficult due to above while laryngoscopy is surprisingly straightforward

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2
Q

How is induction modified in the obese patient?

A

Meticulous preoxygenation in the Fowler’s position (obese patient’s desaturate rapidly when apnoeic)

Some patients who are unable to lie in the fowlers position will require awake fibreoptic intubation

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3
Q

Why does oxygen desaturation occur more rapidly in obese patients?

A
  1. Decrease FRC (exponentially with increasing BMI)
    - -> closing capacity encroaches on FRC particularly when supine –> decreased O2 reserve and V/Q mismatch –> arterial hypoxaemia.
  2. Increased O2 consumption by increased tissue mass (adipose tissue)

Combined effect is increased rate of desaturation

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4
Q

How is FRC affected by BMI

A

FRC decreases exponentially with increasing BMI

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5
Q

How does chest wall compliance change in obesity and what effect does this have on the work of breathing

A

Chest wall compliance is reduced by up to 30%

This significantly increases the work of breathing - worse supine than upright

High peak pressures are seen with artificial ventilation.

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6
Q

What are the consequences of OSA (Obstructive Sleep Apnoea) as it is more common in obesity

A

Pharyngeal airway collapse –> OSA

Severe OSA –> persistent intermittent hypoxia at night –> chronic hypoxic pulmonary vasoconstriction –> remodelling and pulmonary hypertension –> RVH and cor pulmonale

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7
Q

How does Obesity affect the cardiovascular system

A

HEART FAILURE RISK
Strong association with hypertension –> LVH

ATHEROSCLEROSIS RISK
T2DM
Hypercholesterolaemia

VTE RISK
(Immobility, increased blood viscosity - polycythemia in OSA, decreased fibrinolysis)
DVT
PE

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8
Q

How does obesity affect the GIT

A

Hiatus hernia is common

Volume and acidity of gastric contents is increased

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9
Q

List the body systems and summarise how obesity negatively impacts these systems in an anaesthetic context

A 
AIRWAY
Difficult airway (Increased oropharyngeal and upper thoracic soft tissue)

RSP
Decreased FRC and CC encroaches FRC
Increased O2 consumption (excess adipose tissue)
Increased work of breathing (decreased chest wall compliance)
OSA is common (cor pulmonale)

CVS
HF (HPT associated with obesity)
ATHEROSCLEROSIS (CHOL and T2DM)
VTE (immobility, polycythaemia, decr. fibrinolysis, sluggish blood flow d/t HF)

GIT
Hiatus hernia common
Increased acidity and volume gastric contents
Fatty Liver Disease
Gall stones

ENDOCRINE
T2DM
Hypothyroidism
HyperCHOL

CNS
Atherosclerosis associated risks

MSK
Osteoarthritis
Chronic back pain

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10
Q

How does obesity affect technical process in anaesthesia?

A

IV access
Airway management
Regional anaesthesia
Abnormal physical signs may be masked by the size of the patient

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11
Q

Define TBW (total body weight), IBW (Ideal body weight) and LBM (Lean Body Mass)

A

TBW = actual body weight

IDEAL BODY WEIGHT (IBW)
IBW(kg) = height (cm) - x
Males: x = 100
Females: x = 105

LEAN BODY MASS (LBM)

Male LBM = 1.1 x weight - 128(weight/height)^2

Female LBM = 1.07 x weight - 148(weight/height)^2

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12
Q

When is LBM overestimated?

A

When TBW is above IBW (i.e. in obesity)

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13
Q

List the pharmacokinetic changes in obesity

A

Proportionately less total body water
Proportionately more adipose tissue
Relatively lower LBM (but 20% higher absolute LBM)
Increased blood volume and cardiac output
Increased renal clearance
Hepatic clearance unchanged

Increased Vd for highly lipophilic drugs
(Prlonged administration –> greater tissue accumulation and delayed recovery)

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14
Q

Compare the prevalence of T1DM to T2DM

A

T2DM is 4 times as prevalent

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15
Q

What is the difference between T1DM and T2DM

A

T1DM - Impaired pancreatic insulin production

T2DM - Peripheral insulin resistance

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16
Q

What are the basic functions of insulin

A
  1. Promotes entry of glucose into cells where it is stored as glycogen
  2. Promotes synthesis of fates and proteins
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17
Q

In DIABETES:

Give examples of microvascular complications

Give examples of macrovascular complications

A

Microvascular

  • Proliferative retinopathy
  • Diabetic nephropathy

Macrovascular

  • Accelerated atherosclerosis
  • Autonomic and peripheral neuropathies
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18
Q

Simplify and demonstrate control of blood sugar

A

Low sugar –> pancreatic alpha cells –> glucagon –> glucose released from the liver

High sugar –> pancreatic beta cells –> insulin –> glucose taken up by fat cells

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19
Q

When can elective surgery be carried out in diabetic patients

A

Hgt < 7.5%

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20
Q

What considerations should be made considering each organ system with regard to administering and anaesthetic in a diabetic patient

A

CVS (Painless MI)
Cardiomyopathy and perioperative MI/Stroke more likely
MI may be painless (neuropathy

NERVOUS SYSTEM (CVS instability)
Autonomic dysfunction in 40% 
- CVS instability and urinary retention
Peripheral neuropathy:
- Loss of sensation plus PVD --> ulceration (patient positioning requires care)

RENAL (maintain renal blood flow)
Microvacscular angiopathy –> glomerulosclerosis –> proteinuria –> oedema –> renal failure

GIT
Impaired gastric emptying (autonomic neuropathy)
GORD is common

IMMUNE
Intercurrent infection (urinary/vulva/skin/chest) is very common
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21
Q

What is the aim of perioperative management of diabetic patients?

A

Eliminate any chance of hypoglycaemia and maintain metabolic control

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22
Q

Describe perioperative blood glucose management for a T1DM

A

CHO Substrate
Dextrose 5% + KCl 20 mmol/L at 50 - 100 ml/hour

INSULIN infusion
Titrated to Hgt according to sliding scale
Dedicated line with a 1 way valve
Number of units injected per day will inform dosing schedule
Keep glucose readings between 6.1 to 10 mmol/L

HOURLY HGT TESTING

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23
Q

Describe the perioperative blood glucose management in T2DM

A 
MINOR SURGERY (expected to resume oral intake immediately after surgery)
 --> do not require insulin

MAJOR SURGERY
Glucose + Insulin regimen is recommended
Long acting hypoglycaemics (glibenclamide) should have been stopped 24 hours before surgery

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24
Q

What are the symptoms of hypoglycaemia

A

Profuse sweating, pallor, dizziness, tachycardia, confusion, convulsions, coma

SNS activation and then CNS dysfuntion

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25
Q

What happens to the symptoms of hypoglycaemia during anaesthesia

A

Masked by general anaesthesia – possible irreversible brain damage

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26
Q

What is the difference bewteen dextrose and glucose

A

Dextrose is D-glucose which is a d-isomer of L-glucose (enantiomer)

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27
Q

How frequently should Hgt be monitored in diabetic patients during surgery?

A

At least hourly

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28
Q

What is the intraoperative treatment for hypoglycaemia

A

10 to 15 grams dextrose
100 to 150 mL of a 10% solution and repeat BP measurement

Emergency medicine dose is 50 mL 50% dextrose which is 25 grams of glucose (equivalent to a can of coke)

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29
Q

Why is there an age related decline in GFR?

A

Normal adult kidneys contain about 1 million nephrons –> this number decreases with age –> Age related decline in GFR

30
Q

How can renal disease impact the respiratory system in the anaesthetic context

A

Pulmonary oedema if fluid overload develops

31
Q

How can renal disease affect the CVS system in an anaesthetic context

A

80% of cases have associated HPT (dysfunction RAAS)

HPT + Fluid overload –> LVH –> Heart Failure

Accelerated atherosclerosis (decreased plasma triglyceride clearance) –> perioperative MI

32
Q

How does renal disease impact the haematological system in an anaesthetic context

A

Normochromic anaemia (EPO deficiency)

Platelet dysfunction (inadequate vascular endothelial release of vWF/Factor 8 complex which binds to and activates platelets.

33
Q

How can platelet dysfunction be minimized in patients with renal failure in the perioperative period

A

Administration of arginine vasopressin (DDAVP) 0.3 g/kg

34
Q

How does renal disease impact the GIT in anaesthetic context

A

Anorexia, N, V –> malnutrition

Urea –> mucosal irritant and bleeding may occurfrom any part of the GIT

Gastric: lower pH and increased volume

35
Q

How much will succinylcholine increase plasma potassium?

A

0.5 mmol/L –> caution in renal patients with pre-existing hyperkalaemia

36
Q

How does renal disease impact the metabolic system in an anaesthetic context

A

Hyperkalaemia (exacerbated by many drugs - BB, K sparing diuretics, ACE I, ARBs, NSAIDS, aminoglycosides, ciclosporin)

Chronic acidosis (H+ clearance impaired + inability to regenerate HCO3-)

Hypocalcaemia
Reduced levels of 1,25 dihydroxy Vit D

Hyperphosphataemia (Impaired phosphate excretion) –> Calcium phosphate is deposited in the tissues depleting calcium even further –> 2º hyperPTH

37
Q

At what GFR does acute renal failure occur?

At what GFR is dialysis usually required?

A

Failure: < 35 ml/min

Dialysis: < 15 ml/min

38
Q

What are risk factors for the development of perioperative renal failure

A

Pre-existing renal disease
Hypovolaemia
Sepsis
NSAIDS

39
Q

What is renal blood flow autoregulation

A

Similar to this concept for cerebral and coronary blood flow autoregulation.

Renal autoregulation ensures that renal blood flow and GFR remains constant for a wide range of mean arterial pressures (70 - 160 mmHg)

40
Q

Should the initial or maintenance of a drug be adjusted in renal failure and why?

A

The initial dose can remain the same –> drug distributes.

Maintenance dosing should be altered by either reducing dose or increasing intervals.

41
Q

In renal failure (GFR < 35), under what circumstances should the initial dose be adjusted?

A

Renal failure can cause hypoalbuminaemia

Drugs with protein binding > 90% will require a reduced initial dose as absolute protein binding capacity will be decreased in hypoalbuminaemia

42
Q

Give examples of the names of two active metabolites for two commonly used anaesthetic drugs and why this is relevant in patients with renal failure

A

Morphine
–> Morphine - 6 - glucuronide

Midazolam
–> 1 - hydroxy - midazolam

Active metabolites are often excreted by the kidneys and accumulation will lead to unwanted effects

43
Q

Which prostaglandins play a role in regulation of renal blood flow? Which drug inhibits these and under what circumstances should this drug be omitted

A

I2 and E2

NSAIDS

Omit in acute renal failure and hypovolaemia

Can precipitate renal failure by catastrophically reducing renal blood flow in hypovolaemia

44
Q

Describe the proportions related to RBF including total renal blood flow and the proportion of blood flow received to the cortex versus the medulla.

A

20% of Cardiac output is received by the kidneys

80% of the RBF is received by the cortex
20% of the RBF is received by the Medulla

45
Q

What is the commonest cause of perioperative renal failure

A

The renal medulla receives only 20% of the renal blood flow but has a high OER. It is therefore susceptible to hypoxic injury –> ATN is the commonest cause of perioperative acute renal failure

46
Q

How does adequate hydration and adequate circulating volume reduce the risk of perioperative renal dysfunction?

A

Decreased requirement for reabsorption of salt and water and hence reduction in medullary O2 requirements

47
Q

Give examples of 4 agents commonly associated with perioperative renal failure

A

NSAIDS
ACE I / ARBs
Aminoglycosides
Radiological contrast media

48
Q

Name 5 functions of blood and highlight those of particular importance to the anaesthetist

A
  1. Oxygen carriage
  2. Coagulation
  3. Immunity
  4. Nutrition
  5. Acid-base homeostasis
49
Q

Why must CO increase in anaemia

A

To maintain DO2

50
Q

How do preoperative Hb requirements differ for the young and fit versus the old and CVS compromised

A

Young and fit: > 8 g/dl

Old and shit (IHD) > 10 g/dl

51
Q

Define Sickle Cell Disease

A

Sickle Cell Disease is an autosomal recessive disease caused by a single amino acid substitution at position 6 of the beta -Hb chain (valine for glutamine). Valine is lipid soluble and in the deoxygenated conformation the aberrant valine is exposed to adjacent Hb molecules and binding to these leading to precipitation of Hb within the cell and ‘sickling’. Two forms of the condition occur: Heterozygous and homozygous

52
Q

How is perioperative management of heterozygous sickle cell disease patients altered?

How is perioperative management of hoozygous sickle cell disease patients altered?

A

Heterozygous
Ensure maintenance of hydration and oxygenation.

Homozygous
Consult haematologist
Consider preoperative transfusion or exchange transfusion to reduce the percentage of Hbs to around 40%

53
Q

How many haem groups and how any globin chains are in a haemoglobin molecule

A

4 x haem groups

4 x globin chains (2 alpha + 2 beta)

54
Q

What is thalassaemia

A

Absent or deficient synthesis of alpha or beta globin chains of Hb.

Prevalent in : Mediterranean, African and asian descent

55
Q

Why should the preoperative assessment include assessment of major organ function in beta thalassaemia

A

These patients are transfusion dependent which leads to iron overload and deposition in the heart liver and pancreas

56
Q

How is perioperative management altered in thalassaemia

A

Depends on severity of condition

  1. Rx haemolytic anaemia (?transfusion)
  2. Beta-thalassaemia patients are transfusion dependent which leads to iron deposition in the heart, liver and pancreas –> Preoperative preparation should assess major organ impairment
  3. Hyperplastic bone marrow in thalasaemia major may cause overgrowth and deformity of facial bones making careful airway assessment important
57
Q

Name and describe three common inherited coagulopathies

A 
HAEMOPHILIAs
Haemophilia A (factor 8 deficiency)
Christmas disease (factor 9 deficiency)
  • can’t generate thrombin
  • therefore can’t convert fibrinogen to fibrin
  • fail to form stable clot at site of injury

vWF DISEASE
von Willebrand’s disease
- deficiency vWF - this is a protein produced by the endothelium which carries factor 8 in the plasma and mediates platelet adhesion
- autosomal dominant
- various forms (vWF deficient or aberrant)

58
Q

How is perioperative management of patient’s with inherited bleeding diatheses altered?

A

Consult hematologist

Mild haemophiliacs and type 1 vWD
Consider:
DDAVP (Arginine vasopressin)
Tranexamic acid

Severe cases
Inconsultation with haematology use recombinant factors
Recombinant clotting factors are made in a lab. They don’t come from blood. They are made with recombinant DNA technology.

59
Q

Below what platelet count does spontaneous bleeding occur?

A

< 20 x10^9/L

60
Q

What is the minimum platelet count acceptable for surgery

A

> 50 x 10^9/L

61
Q

How many units of blood are used to make a standard Adult Therapeutic Dose (ATD) of platelets?

A

SIX units of blood are used

62
Q

By how much does one adult therapeutic dose (ATD) of platelets increase the platelet count?

A

20 - 40 x 10^9/L

63
Q

At what temperature are platelets stored. Subsequently, what is their shelf life?

A

Room temperature
FIVE DAY shelf life
Always check for availability

64
Q

What is the mechanism of action of Warfarin

A

Inhibits Vitamin K epoxide reductase which is an essential enzyme for activating vitamin K available in the body. Reduction of active vitamin K by warfarin inhibits vitamin K dependent carboxylation of Factors 2, 7, 9, 10.

65
Q

How is the INR calculated

A

PT patient/PT control

66
Q

What is prothrombin time and what is normal prothrombin time

A

Prothrombin time (PT) is the time taken to form a clot via the extrinsic pathway. Normal: 11 -13.5 seconds

activated partial thromboplastin time (aPTT) measures the time taken to form a clot by the intrinsic pathway. Normal: 30 - 40 seconds

67
Q

What is the difference between the intrinsic and extrinsic coagulation pathways

A

Intrinsic pathway is activated by exposed endothelial collagen

Extrinsic pathway is activated through tissue factor released by endothelial cells after external damage

68
Q

Describe perioperative management of a patient on warfarin with low embolic risk (AF with no history of stroke)

A

Warfarin can be stopped 4 days before surgery to allow INR to decrease below 1.5

69
Q

Describe perioperative management of a patient on warfarin with high risk of embolism (e.g. mechanical mitral valve)

A

Stop warfarin
When INR< 2 –> commence continuous IV infusion of unfractionated heparin preoperatively adjust to maintain the APTR 1.5 - 2.5

Unfractionated heparin should be stopped 6 hours before surgery and restarted as soon as possible postoperatively to minimize the time of reduced anticoagulation

70
Q

What is the APTR

A

Activated Partial Thromboplastin Time Ratio
The result is given as a ratio of the patient test time/ mean normal control time

Reference Range
Non anticoagulated Adult 0.87 – 1.13

For unfractionated heparin therapy 1.5 – 2.5

The result is given as a ratio of the patient test time/ mean normal control time

71
Q

How long does Vitamin K take to reverse the effects of warfarin and what is the dose and route of administration in the emergency setting

A

6 hours

1 - 2 mg IV

72
Q

If quicker warfarin reversal is required, what can be used?

A

Fresh frozen plasma 15 ml/kg

Prothrombin complex concentrate (PCC)

Diploma in Anaesthesia (73 decks)

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