Anaesthetics/Pre-Op Flashcards

1
Q

What are the positional manoeuvres which can be used to open airway?

A
  • Head tilt/chin lift
  • Jaw thrust (used when any concern of C spine injury)
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2
Q

What is the different airway adjuncts?

A
  • Nasopharyngeal airway (good for seizures but cannot be used if basal skull fracture suspicion)
  • Oropharyngeal airway (Guedel)
  • Laryngeal airway (iGel)
  • Endotracheal tube
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3
Q

What error can happen with Endotracheal tube insertion and what should be monitored to check this?

A

Oesophageal intubation - monitor end-tidal CO2 (capnography)

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4
Q

What are 2 types of inhaled anaesthetics?

A
  1. Volatile liquids e.g. isoflurane
  2. Nitrous oxide
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5
Q

What are the side effects of inhaled anaesthetics?

A
  1. Fluranes -> Malignant hyperthermia
  2. NO -> Avoid in pneumothorax as can cause increase in pressure in air compartments
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6
Q

What are the different IV anaesthetic options?

A

Propofol - commonly used - has anti-emetic properties so useful for high risk N+V patients
Thiopental - can cause laryngospasm but acts quickly on the brain as is fat-soluble
Ketamine - useful in trauma as does not cause drops in BP

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7
Q

What are the different local anaesthetic options?

A

Lidocaine
- Works by blocking sodium channels
- Can be toxic (treated with IV 20% lipid emulsion)

Other options include
- Bupivacaine
- Prilocaine
- Cocaine

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8
Q

What is malignant hyperthermia?

A
  • Autosomal dominant
  • Hyperpyrexia and muscle rigidity following anaesthetic agents, commonly suxamethonium
  • Caused by excessive release of Ca2+ from skeletal muscle
  • Bloods show raised CK
  • Manage with Dantrolene
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9
Q

What are the types of muscle relaxants?

A

Suxamethonium
- Depolarising neuromuscular blocker
- Fastest onset and shortest duration

Others include
- Atracurium
- Vecuronium

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10
Q

What are causes of post-op pyrexia?

A

Early
- Blood transfusion
- Cellulitis
- UTI

Late
- VTE
- Pneumonia
- Wound infection

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11
Q

What is postoperative ileus?

A
  • A common complication of bowel surgery
  • Reduced bowel peristalsis resulting in pseudo obstruction
  • Presents like obstruction
  • Check potassium, magnesium and phosphate as can be caused by deranged electrolytes
  • Managed conservatively with fluids, NG feeding
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12
Q

What are the rules regarding food and drink with surgery?

A
  • Clear fluids until 2 hours before
  • Food stopped 6 hours before
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13
Q

What complications are diabetic patients at higher risk of?

A
  • Wound and resp infections
  • Post-operative AKI
  • Length of hospital stay
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14
Q

How can patients on metformin be managed?

A
  • If taken 1 or 2 times a day, continue as normal
  • If taken 3 times a day, omit lunchtime dose if prolonged surgery
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15
Q

How can patients on gliclazide be managed?

A

Omit doses on day of surgery BEFORE/DURING the operation (i.e. for morning surgery, if taken twice a day, just omit morning dose but if afternoon surgery, omit both morning and afternoon)

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16
Q

How should patients on DPP/GLP be managed?

A

Take as normal

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17
Q

How should patients on SGLT-2 inhibitors be managed?

A

Omit on day of surgery

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18
Q

How should patients on insulin be managed?

A

Once daily regime: reduce dose by 20%
Twice daily regime: half morning dose, do not change evening dose
Basal-bolus: Omit morning and lunchtime short acting insulins, reduce long acting by 20%

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19
Q

What is the surgical safety checklist?

A
  1. Before induction
  2. Before incision
  3. Before patient leaves the room
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20
Q

What needs to be on and functioning before anaesthesia?

A

Pulse oximeter is on and functioning

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21
Q

When should COCP/HRT be stopped before surgery?

A

4 weeks

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22
Q

What is cricoid pressure used for?

A

Prevent gastric contents entering the pharynx

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23
Q

Dropping sats following intubation?

A

Think oesophageal intubation

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24
Q

How should TPN be administered?

A

Central line

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25
Q

What should not be prescribed whilst a patient is using an opioid PCA?

A

Oral opioids

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26
Q

pyrexia, tachycardia and fasciculations with FH of similar symptoms

A

Think malignant hyperthermia

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27
Q

Long term mechanical ventilation in trauma patients can lead to what?

A

Tracheo-oeseophageal fistula formation

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28
Q

Treatment of local anaesthetic toxicity?

A

IV 20% lipid emulsion

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29
Q

What approach is preferred with central line insertion?

A

Internal jugular to reduce risk of pneumothorax

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30
Q

Types of airway management?

A

Airway adjuncts and positional manoeuvres to open the airway

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31
Q

2 types of positional manoeuvres to open the airway?

A

head tilt / chin lift

jaw thrust: preferred if concern about cervical spine injury

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32
Q

Type of positional manoeuvres to open the airway that is preferred if concern about cervical spine injury?

A

jaw thrust

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33
Q

Name 5 airway adjuncts?

A
  • oropharyngeal airway (Guedel)
  • nasopharyngeal airway
  • laryngeal mask airway (LMA; i-gel)
  • Tracheostomy
  • Endotracheal tube
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34
Q

Oropharyngeal airway (Guedel)?

A

Easy to insert and use

No paralysis required

Ideal for very short
procedures

Most often used as a bridge
to more definitive airway

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35
Q

Oropharyngeal airway (Guedel) most often used as…

A

a bridge to more definitive airway

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36
Q

Laryngeal mask airway (LMA; i-gel)?

A

Widely used

Very easy to insert

Device sits in pharynx and aligns to cover the airway

Poor control against reflux of gastric contents

Paralysis is not usually required

Commonly used for wide range of anaesthetic uses, especially in day surgery

Not suitable for high-pressure ventilation (small amount of PEEP often possible)

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37
Q

Laryngeal mask airway (LMA; i-gel) not suitable for what?

A

Not suitable for high-pressure ventilation (small amount of PEEP often possible)

and poor control against reflux of gastric contents

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38
Q

Laryngeal mask airway (LMA; i-gel) commonly used for?

A

wide range of anaesthetic uses, especially in day surgery

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39
Q

Tracheostomy?

A

Reduces the work of breathing (and dead space)

May be useful in slow weaning

Percutaneous tracheostomy widely used in ITU

Dries secretions, humidified air usually required

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40
Q

Tracheostomy- what is usually required?

A

humidified air as it dries secretions

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41
Q

Endotracheal tube?

A

Provides optimal control of the airway once the cuff inflated

May be used for long or short-term ventilation

Errors in insertion may result in oesophageal intubation
- accounts for around 5% of major airway complications
therefore monitor end-tidal CO2 (capnography)

Paralysis often required

Higher ventilation pressures can be used

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42
Q

Endotracheal tube- may be used…?

A

for long or short-term ventilation

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43
Q

Endotracheal tube- errors in insertion may result in what?

A

oesophageal intubation

accounts for around 5% of major airway complications
therefore monitor end-tidal CO2 (capnography)

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44
Q

Endotracheal tube- why is it good?

A

Higher ventilation pressures can be used

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45
Q

American Society of Anaesthesiologists (ASA) classification - how many types?

A

6

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46
Q

American Society of Anaesthesiologists (ASA) classification= ASA I?

A

A normal healthy patient

Healthy, non-smoking, no or minimal alcohol use

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47
Q

American Society of Anaesthesiologists (ASA) classification= ASA II?

A

A patient with mild systemic disease

Mild diseases only without substantive functional limitations. Examples include (but not limited to): current smoker, social alcohol drinker, pregnancy, obesity (BMI 30 - 40), well-controlled DM/HTN, mild lung disease

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48
Q

American Society of Anaesthesiologists (ASA) classification= ASA III?

A

A patient with severe systemic disease

Substantive functional limitations; One or more moderate to severe diseases. Examples include (but not limited to): poorly controlled DM/HTN, COPD, morbid obesity (BMI > 40), active hepatitis, alcohol dependence or abuse, implanted pacemaker, moderate reduction of ejection fraction, End-Stage Renal Disease (ESRD) undergoing regularly scheduled dialysis, history (>3 months) of Myocardial infarction, Cerebrovascular accidents

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49
Q

American Society of Anaesthesiologists (ASA) classification= ASA IV?

A

A patient with severe systemic disease that is a constant threat to life

Examples include (but not limited to): recent (< 3 months) of Myocardial infarction, Cerebrovascular accidents, ongoing cardiac ischaemia or severe valve dysfunction, severe reduction of ejection fraction, sepsis, DIC, ARD or ESRD not undergoing regularly scheduled dialysis

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50
Q

American Society of Anaesthesiologists (ASA) classification= ASA V?

A

A moribund patient who is not expected to survive without the operation

Examples include (but not limited to): ruptured abdominal/thoracic aneurysm, massive trauma, intra-cranial bleed with mass effect, ischaemic bowel in the face of significant cardiac pathology or multiple organ/system dysfunction

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51
Q

American Society of Anaesthesiologists (ASA) classification= ASA VI?

A

A declared brain-dead patient whose organs are being removed for donor purposes

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52
Q

Name 4 common IV induction agents?

A
  • propofol
  • sodium thiopentone
  • ketamine
  • etomidate
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53
Q

IV induction agents= propofol: MOA?

A

GABA receptor agonist

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54
Q

IV induction agents= propofol?

A

Rapid onset of anaesthesia

Pain on IV injection

Rapidly metabolised with little accumulation of metabolites

Proven anti emetic properties

Moderate myocardial depression

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55
Q

IV induction agents= propofol is rapidly….

A

metabolised with little accumulation of metabolites

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56
Q

IV induction agents= propofol: uses?

A

Widely used especially for maintaining sedation on ITU, total IV anaesthesia and for daycase surgery

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57
Q

IV induction agents= propofol has proven… properties?

A

anti emetic

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58
Q

IV induction agents= sodium thiopentone?

A

Extremely rapid onset of action making it the agent of choice for rapid sequence of induction

Marked myocardial depression may occur

Metabolites build up quickly

Unsuitable for maintenance infusion

Little analgesic effects

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59
Q

IV induction agents= sodium thiopentone: unsuitable for?

A

maintenance infusion (slowly metabolised so metabolites build up quickl)

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60
Q

IV induction agents= sodium thiopentone: use?

A

Extremely rapid onset of action making it the agent of choice for rapid sequence of induction

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61
Q

IV induction agents= choice for rapid sequence of induction?

A

sodium thiopentone

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62
Q

IV induction agents= ketamine?

A

May be used for induction of anaesthesia

Has moderate to strong analgesic properties

Produces little myocardial depression making it a suitable agent for anaesthesia in those who are haemodynamically unstable

May induce state of dissociative anaesthesia resulting in nightmares

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63
Q

IV induction agents= sodium thiopentone: analgesic effects?

A

little

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64
Q

IV induction agents= ketamine: MOA?

A

NMDA receptor antagonist

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65
Q

IV induction agents= ketamine: used?

A

induction of anaesthesia

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66
Q

IV induction agents= ketamine: analgesic properties?

A

moderate to strong

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67
Q

IV induction agents= ketamine: myocardial depression?

A

Produces little myocardial depression making it a suitable agent for anaesthesia in those who are haemodynamically unstable

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68
Q

IV induction agents= sodium thiopentone: myocardial depression?

A

marked myocardial depression may occur

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69
Q

IV induction agents= propofol: myocardial depression?

A

moderate myocardial depression

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70
Q

IV induction agents= ketamine: may cause what?

A

may induce state of dissociative anaesthesia resulting in nightmares

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71
Q

IV induction agents= what is a suitable agent for anaesthesia in those who are haemodynamically unstable?

A

ketamine and etomidate

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72
Q

IV induction agents= etomidate?

A

Has favorable cardiac safety profile with very little haemodynamic instability

No analgesic properties

Unsuitable for maintaining sedation as prolonged (and even brief) use may result in adrenal suppression

Post operative vomiting is common

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73
Q

IV induction agents= etomidate: cardiac safety?

A

Has favorable cardiac safety profile with very little haemodynamic instability

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74
Q

IV induction agents= etomidate: analgesic properties?

A

none

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75
Q

IV induction agents= etomidate: what is common?

A

post op vomiting

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76
Q

IV induction agents= etomidate: unsuitable for what?

A

maintaining sedation as prolonged (and even brief) use may result in adrenal suppression

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77
Q

Blood loss in surgery= unlikely chance of infusion:
- example of action
- example of operations

A

group and save

Hysterectomy (simple), appendicectomy, thyroidectomy, elective lower segment caesarean section, laparoscopic cholecystectomy

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78
Q

Blood loss in surgery= likely chance of infusion:
- example of action
- example of operations

A

cross-match 2 units

Salpingectomy for ruptured ectopic pregnancy, total hip replacement

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79
Q

Blood loss in surgery= definite chance of infusion:
- example of action
- example of operations

A

Cross-match 4-6 units

Total gastrectomy, oophorectomy, oesophagectomy
Elective AAA repair, cystectomy, hepatectomy

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80
Q

Group and save vs crossmatch?

A

Group and save is where the lab checks the patient’s blood group and saves a blood sample to match blood if needed.

Crossmatch is where the lab allocates units of blood, tests that it is compatible, and keeps it ready in the fridge.

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81
Q

Types of general anaesthetics?

A

inhaled and IV

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82
Q

Name 2 types of inhaled general anaesthetics?

A

Volatile liquid anaesthetics
(isoflurane, desflurane, sevoflurane)

Nitrous oxide

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83
Q

Inhaled general anaesthetics= name examples of inhaled volatile liquid anaesthetics?

A

isoflurane, desflurane, sevoflurane

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84
Q

Inhaled general anaesthetics= Volatile liquid anaesthetics
(isoflurane, desflurane, sevoflurane):

MOA?

A

Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors

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85
Q

Inhaled general anaesthetics= Volatile liquid anaesthetics
(isoflurane, desflurane, sevoflurane):

Adverse effects?

A
  • Myocardial depression
  • Malignant hyperthermia
  • Halothane (not commonly used now) is hepatotoxic
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86
Q

Inhaled general anaesthetics= Volatile liquid anaesthetics
(isoflurane, desflurane, sevoflurane):

Used for?

A

Used for induction and maintenance of anaesthesia

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87
Q

Inhaled general anaesthetics= nitrous oxide:

MOA?

A

Exact mechanism of action unknown. May act via a combination of NDMA, nACh, 5-HT3, GABAA and glycine receptors

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88
Q

Inhaled general anaesthetics= nitrous oxide:

adverse effects?

A
  • May diffuse into gas-filled body compartments → increase in pressure. Should therefore be avoided in certain conditions e.g. pneumothorax
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89
Q

Inhaled general anaesthetics= nitrous oxide:

used for?

A

Used for maintenance of anaesthesia and analgesia (e.g. during labour)

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90
Q

Inhaled general anaesthetics= what May diffuse into gas-filled body compartments → increase in pressure. Should therefore be avoided in certain conditions e.g. pneumothorax?

A

nitrous oxide

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91
Q

IV general anaesthetics= propofol:

MOA?

A

Potentiates GABAA

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92
Q

IV general anaesthetics= propofol:

Adverse effects?

A
  • Pain on injection (due to activation of the pain receptor TRPA1)
  • Hypotension
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93
Q

IV general anaesthetics= propofol:

Used for?

A
  • Very common induction agent for general anaesthesia and also used extensively in intensive care for ventilated patients
  • Has some anti-emetic effects - useful for patients with a high risk of post-operative vomiting
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94
Q

IV general anaesthetics= thiopental:

MOA?

A

A type of barbiturate (potentiates GABAA)

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95
Q

IV general anaesthetics= thiopental:

adverse effects?

A

Laryngospasm

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96
Q

IV general anaesthetics= thiopental:

it is….. so quickly affects…..?

A
  • Highly lipid-soluble so quickly affects the brain
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97
Q

IV general anaesthetics= etomidate:

MOA?

A

Potentiates GABAA

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98
Q

IV general anaesthetics= etomidate:

adverse effects?

A
  • Primary adrenal suppression (secondary to reversibly inhibiting 11β-hydroxylase)
  • Myoclonus
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99
Q

IV general anaesthetics= etomidate:

advantage?

A

Causes less hypotension than propofol and thiopental during induction and is therefore often used in cases of haemodynamic instability

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100
Q

IV general anaesthetics= ketamine:

advantages?

A
  • Acts as a dissociative anaesthetic (relieves pain).
  • Doesn’t cause a drop in blood pressure so useful in trauma
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101
Q

IV general anaesthetics= ketamine:

MOA?

A

Blocks NMDA receptors

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102
Q

IV general anaesthetics= ketamine:

adverse effects?

A
  • Disorientation
  • Hallucinations
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103
Q

Types of IV access?

A
  • venous access
  • Peripheral venous cannula
  • Central lines
  • Intraosseous access
  • Tunneled lines
  • Peripherally inserted central cannula
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104
Q

IV access= venous access?

A

A number of routes for establishing venous access are available.

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105
Q

IV access= peripheral venous cannula?

A

Easy to insert with minimal morbidity. Wide lumen cannulae can provide rapid fluid infusions. When properly managed infections may be promptly identified and the cannula easily re sited. Problems relate to their peripheral sites and they are unsuitable for the administration of vaso active drugs, such as inotropes and irritant drugs such as TPN (except in the very short term setting).

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106
Q

IV access= Central lines?

A

Insertion is more difficult and most operators and NICE advocate the use of ultra sound. Coagulopathies may lead to haemorrhage following iatrogenic arterial injury. Femoral lines are easier to insert and iatrogenic injuries easier to manage in this site however they are prone to high infection rates. Internal jugular route is preferred. They have multiple lumens allowing for administration of multiple infusions. The lumens are relatively narrow and thus they do not allow particularly rapid rates of infusion.

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107
Q

IV access= Intraosseous access?

A

This is typically undertaken at the anteromedial aspect of the proximal tibia and provides access to the marrow cavity and circulatory system. Although traditionally preferred in paediatric practice they may be used in adults and a wide range of fluids can be infused using these devices.

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108
Q

IV access= Tunneled lines?

A

Tunnelled lines such as Groshong and Hickman lines are popular devices for patients with long term therapeutic requirements. These devices are usually inserted using ultrasound guidance into the internal jugular vein and then tunnelled under the skin. A cuff of woven material is sited near the end and helps to anchor the device into the tissues. These cuffs require formal dissection to allow the device to be removed. Tunnelled lines can be linked to injection ports that are located under the skin. These are especially popular in paediatric practice.

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109
Q

IV access= Peripherally inserted central cannula?

A

Referred to as PICC lines, these are popular methods for establishing central venous access. Because they are inserted peripherally they are less prone to major complications relating to device insertion than conventional central lines.

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110
Q

Name the colours and sizes of IV cannulas?

A

Orange 14g

Grey 16g

Green 18g

Pink 20g

Blue 22g

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111
Q

Size of orange cannula and flow rate?

A

14g

270ml/ml

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112
Q

Size of grey cannula and flow rate?

A

16g

180ml/min

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113
Q

Size of green cannula and flow rate?

A

18g

80ml/min

114
Q

Size of pink cannula and flow rate?

A

20g

54ml/min

115
Q

Size of blue cannula and flow rate?

A

22g

33ml/min

116
Q

Largest cannulas (highest flow rate)?

A

Orange 14g (fastest)

then grey 16g

then green 18g

then pink 20g

then blue 22g (slowest)

117
Q

Way to remember how good different cannulas are?

A

blue is bad, pink is poor, green is good, grey is great and orange is outstanding

118
Q

Cannular colour, size and maximal flow rates?

A

Orange 14g 270ml/min
Grey 16g 180ml/min
Green 18g 80ml/min
Pink 20g 54ml/min
Blue 22g 33ml/min

119
Q

Name 4 local anaesthetic agents?

A

Lidocaine (Lignocaine)
Bupivacaine
Prilocaine
Cocaine

120
Q

Local anaesthetics: lidocaine MOA?

A

an amide

Local anaesthetic and a less commonly used antiarrhythmic (affects Na channels in the axon)

121
Q

Local anaesthetics: lidocaine - metabolised and excreted?

A

hepatic metabolism, protein bound, renally excreted

122
Q

Local anaesthetics: lidocaine toxicity?

A

due to IV or excess administration. Increased risk if liver dysfunction or low protein states. Note acidosis causes lidocaine to detach from protein binding. Local anesthetic toxicity can be treated with IV 20% lipid emulsion

123
Q

Local anaesthetic toxicity can be treated with what?

A

IV 20% lipid emulsion

124
Q

Local anaesthetics: lidocaine drug interactions?

A

beta blockers, ciprofloxacin, pheytoin

125
Q

Local anaesthetics: lidocaine- features of toxicity?

A

Initial CNS over activity then depression as lidocaine initially blocks inhibitory pathways then blocks both inhibitory and activating pathways. Cardiac arrhythmias.

126
Q

Local anaesthetics: lidocaine- when may increased doses be used?

A

when combined with adrenaline to limit systemic absoption

127
Q

Local anaesthetics: cocaine?

A

Pure cocaine is a salt, usually cocaine hydrochloride. It is supplied for local anaesthetic purposes as a paste.

128
Q

Local anaesthetics: cocaine- how is it used?

A

supplied for clinical use in concentrations of 4 and 10%. It may be applied topically to the nasal mucosa.

It has a rapid onset of action and has the additional advantage of causing marked vasoconstriction.

129
Q

Local anaesthetics: cocaine- MOA?

A

It is lipophillic and will readily cross the blood brain barrier. Its systemic effects also include cardiac arrhythmias and tachycardia.

130
Q

Local anaesthetics: cocaine- how often is it used?

A

Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical practice.

131
Q

Local anaesthetics: Bupivacaine MOA?

A

Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells, which prevents depolarization.

132
Q

Local anaesthetics: Bupivacaine uses?

A

It has a much longer duration of action than lignocaine and this is of use in that it may be used for topical wound infiltration at the conclusion of surgical procedures with long duration analgesic effect.

133
Q

Local anaesthetics: Bupivacaine disadvantage and advantage?

A

It is cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet fails.

Levobupivicaine (Chirocaine) is less cardiotoxic and causes less vasodilation.

134
Q

Local anaesthetics: Bupivacaine contraindication?

A

It is cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet fails.

135
Q

Local anaesthetics: prilocaine?

A

Similar mechanism of action to other local anaesthetic agents. However, it is far less cardiotoxic and is therefore the agent of choice for intravenous regional anaesthesia e.g. Biers Block.

136
Q

All local anaesthetic agents….

A

dissociate in tissues and this contributes to their therapeutic effect. The dissociation constant shifts in tissues that are acidic e.g. where an abscess is present, and this reduces the efficacy.

137
Q

Local anaesthetics= lidocaine (lignocaine):

dose plain and dose with adrenaline?

A

3mg/Kg

7mg/Kg

138
Q

Local anaesthetics= bupivacaine:

dose plain and dose with adrenaline?

A

2mg/Kg

2mg/Kg

139
Q

Local anaesthetics= prilocaine:

dose plain and dose with adrenaline?

A

6mg/Kg

9mg/Kg

140
Q

Local anaesthetics= actual doses depend on what?

A

site of administration, tissue vascularity and co-morbidities.

141
Q

Maximum total local anaesthetic doses?

A

Lignocaine 1% plain - 3mg/ Kg - 200mg (20ml)

Lignocaine 1% with 1 in 200,000 adrenaline - 7mg/Kg - 500mg (50ml)

Bupivicaine 0.5% - 2mg/kg- 150mg (30ml)

Maximum doses are based on ideal body weight

142
Q

Local anaesthetics= max doses are based on what?

A

ideal body weight

143
Q

What may be added to local anaesthetic drugs?

A

adrenaline

144
Q

Effects of adrenaline when added to local anaesthetic drugs?

A

It prolongs the duration of action at the site of injection and permits usage of higher doses.

It is contra indicated in patients taking MAOI’s or tricyclic antidepressants.

The toxicity of bupivacaine is related to protein binding and addition of adrenaline to this drug does not permit increases in the total dose of bupivacaine, in contrast to the situation with lignocaine.

145
Q

Malignant hyperthermia?

A

condition often seen following administration of anaesthetic agents

characterised by hyperpyrexia and muscle rigidity

146
Q

Malignant hyperthermia= features?

A

hyperpyrexia and muscle rigidity following the administration of anaesthetic agents

147
Q

Malignant hyperthermia= pathophysiology?

A

cause by excessive release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

148
Q

Malignant hyperthermia= associated with?

A

associated with defects in a gene on chromosome 19 encoding the ryanodine receptor, which controls Ca2+ release from the sarcoplasmic reticulum

149
Q

Malignant hyperthermia= susceptibility is inherited in what fashion?

A

autosomal dominant

150
Q

Malignant hyperthermia= what may have a similar aetiology?

A

neuroleptic malignant syndrome

151
Q

Malignant hyperthermia= causative agents?

A

halothane

suxamethonium

other drugs: antipsychotics (neuroleptic malignant syndrome)

152
Q

Malignant hyperthermia= Ix?

A

CK raised

contracture tests with halothane and caffeine

153
Q

Malignant hyperthermia= Mx?

A

dantrolene

154
Q

How does dantrolene work in the Mx of malignant hyperthermia?

A

prevents Ca2+ release from the sarcoplasmic reticulum

155
Q

Name 4 muscle relaxants?

A

Suxamethonium

Atracurium

Vecuronium

Pancuronium

156
Q

Muscle relaxants= suxamethonium?

A

Depolarising neuromuscular blocker

Inhibits action of acetylcholine at the neuromuscular junction

Degraded by plasma cholinesterase and acetylcholinesterase

Fastest onset and shortest duration of action of all muscle relaxants

Produces generalised muscular contraction prior to paralysis

Adverse effects include hyperkalaemia, malignant hyperthermia and lack of acetylcholinesterase

157
Q

Muscle relaxants= atracurium?

A

Non depolarising neuromuscular blocking drug

Duration of action usually 30-45 minutes

Generalised histamine release on administration may produce facial flushing, tachycardia and hypotension

Not excreted by liver or kidney, broken down in tissues by hydrolysis

Reversed by neostigmine

158
Q

Muscle relaxants= vecuronium?

A

Non depolarising neuromuscular blocking drug

Duration of action approximately 30 - 40 minutes

Degraded by liver and kidney and effects prolonged in organ dysfunction

Effects may be reversed by neostigmine

159
Q

Muscle relaxants= pancuronium?

A

Non depolarising neuromuscular blocker

Onset of action
approximately 2-3 minutes

Duration of action up to 2 hours

Effects may be partially reversed with drugs such as neostigmine

160
Q

Muscle relaxants= suxamethonium MOA?

A

Depolarising neuromuscular blocker

Inhibits action of acetylcholine at the neuromuscular junction

Degraded by plasma cholinesterase and acetylcholinesterase

161
Q

Muscle relaxants= suxamethonium adverse effects?

A

Produces generalised muscular contraction prior to paralysis

Adverse effects include hyperkalaemia, malignant hyperthermia and lack of acetylcholinesterase

162
Q

Muscle relaxants= which has the fastest onset and shortest duration?

A

suxamethonium

163
Q

Muscle relaxants= atracurium MOA?

A

Non depolarising neuromuscular blocking drug

164
Q

Muscle relaxants= atracurium duration of action?

165
Q

Muscle relaxants= atracurium adverse effects?

A

Generalised histamine release on administration may produce facial flushing, tachycardia and hypotension

Not excreted by liver or kidney, broken down in tissues by hydrolysis

166
Q

Muscle relaxants= atracurium is reversed by what?

A

neostigmine

167
Q

Muscle relaxants= vecuronium MOA?

A

Non depolarising neuromuscular blocking drug

168
Q

Muscle relaxants= vecuronium duration of action?

A

approx 30-40mins

169
Q

Muscle relaxants= vecuronium adverse effects?

A

Degraded by liver and kidney and effects prolonged in organ dysfunction

170
Q

Muscle relaxants= vecuronium effects may be reversed by what?

A

neostigmine

171
Q

Muscle relaxants= pancuronium MOA?

A

Non depolarising neuromuscular blocker

172
Q

Muscle relaxants= pancuronium onet and duration of action?

A

onset approx 2-3mins

duration up to 2hrs

173
Q

Muscle relaxants= pancuronium effects may be partially reversed by?

A

neostigmine

174
Q

Muscle relaxants= MOA of all?

A

all are non depolarising neuromuscular blockers

EXCEPT SUXAMETHONIUM WHICH IS A DEPOLARISING NEUROMUSCULAR BLOCK

175
Q

Nasopharyngeal airway?

A

lubricated and inserted into the nostril to provide a patent airway in patients with decreased Glasgow coma score (GCS).

They are ideal for patients having seizures, as you may not be able to insert an oropharyngeal airway (OPA).

They come in a variety of sizes. They are well tolerated in patients with low GCS and are relatively contraindicated in base of skull fractures as they can cause further damage.

176
Q

Nasopharyngeal airways are well tolerated in pts with low GCS but are relatively contraindicated in who?

A

base of skull fractures as they can cause further damage

177
Q

Neuromuscular blocking drugs are mainly used in….

A

an adjunct to anaesthetic agents. They cause muscle paralysis which is necessary prerequisite for mechanical ventilation.

178
Q

Neuromuscular blocking drugs cause what?

A

paralysis which is necessary prerequisite for mechanical ventilation.

179
Q

Types of neuromuscular blocking drugs?

A

depolarising and non-depolarising

180
Q

Depolarising neuromuscular blocking drugs= MOA?

A

Binds to nicotinic acetylcholine receptors resulting in persistent depolarization of the motor end plate

181
Q

Depolarising neuromuscular blocking drugs= examples?

A

Succinylcholine (also known as suxamethonium)

182
Q

Depolarising neuromuscular blocking drugs= adverse effects?

A

Malignant hyperthermia
Hyperkalaemia (normally transient)

183
Q

Depolarising neuromuscular blocking drugs= reversal?

184
Q

Depolarising neuromuscular blocking drugs= may cause?

A

fasciculations

185
Q

Depolarising neuromuscular blocking drugs= use?

A

The muscle relaxant of choice for rapid sequence induction for intubation

186
Q

The muscle relaxant of choice for rapid sequence induction for intubation?

A

Depolarising neuromuscular blocking drugs eg. suxamethonium

187
Q

Depolarising neuromuscular blocking drugs= contraindications?

A

patients with penetrating eye injuries or acute narrow angle glaucoma, as suxamethonium increases intra-ocular pressure

188
Q

Non-depolarising neuromuscular blocking drugs= MOA?

A

Competitive antagonist of nicotinic acetylcholine receptors

189
Q

Non-depolarising neuromuscular blocking drugs= examples?

A

Tubcurarine, atracurium, vecuronium, pancuronium

190
Q

Non-depolarising neuromuscular blocking drugs= adverse effects?

A

hypotension

191
Q

Non-depolarising neuromuscular blocking drugs= reversal?

A

Acetylcholinesterase inhibitors (e.g. neostigmine)

192
Q

Name an acetylcholinesterase inhibitor?

A

neostigmine

193
Q

Nutrition options in surgical patients?

A
  • oral intake
  • naso gastric feeding
  • naso jejunal feeding
  • feeding jejunostomy
  • percutaneous endoscopic gastrostomy
  • total parenteral nutrition
194
Q

Nutrition options in surgical patients= oral intake?

A

Easiest option

May be supplemented by calorie rich dietary supplements

May contra indicated following certain procedures

195
Q

Nutrition options in surgical patients= naso gastric feeding?

A

Usually administered via fine bore naso gastric feeding tube

Complications relate to aspiration of feed or misplaced tube

May be safe to use in patients with impaired swallow

Often contra indicated following head injury due to risks associated with tube insertion

196
Q

Nutrition options in surgical patients= naso gastric feeding often contraindicated when?

A

following head injury due to risks associated with tube insertion

197
Q

Nutrition options in surgical patients= naso gastric feeding Cx?

A

relate to aspiration of feed or misplaced tube

198
Q

Nutrition options in surgical patients= naso gastric feeding usually administered how?

A

via fine bore naso gastric feeding tube

199
Q

Nutrition options in surgical patients= naso jejunal feeding?

A

Avoids problems of feed pooling in stomach (and risk of aspiration)

Insertion of feeding tube more technically complicated (easiest if done intra operatively)

Safe to use following oesophagogastric surgery

200
Q

Nutrition options in surgical patients= naso jejunal feeding is safe to use following what surgery?

A

oesophagogastric

201
Q

Nutrition options in surgical patients= naso jejunal feeding is good why?

A

avoids problems of feed polling in stomach (and risk of aspiration) unlike naso gastric

202
Q

Nutrition options in surgical patients= naso jejunal feeding insertion?

A

Insertion of feeding tube more technically complicated than naso gastric (easiest if done intra operatively)

203
Q

Nutrition options in surgical patients= Feeding jejunostomy (J-tube)?

A

Surgically sited feeding tube

May be used for long term feeding

Low risk of aspiration and thus safe for long term feeding following upper GI surgery

Main risks are those of tube displacement and peritubal leakage immediately following insertion, which carries a risk of peritonitis

204
Q

Nutrition options in surgical patients= Feeding jejunostomy uses?

A

surgically sited feeding tube that may be used for long term feeding

low risk of aspiration so safe for long term feeding following upper GI surgery

205
Q

Nutrition options in surgical patients= Feeding jejunostomy main risks?

A

Main risks are those of tube displacement and peritubal leakage immediately following insertion, which carries a risk of peritonitis

206
Q

Nutrition options in surgical patients= percutaneous endoscopic gastrostomy (PEG)?

A

Combined endoscopic and percutaneous tube insertion

May not be technically possible in those patients who cannot undergo successful endoscopy

Risks include aspiration and leakage at the insertion site

207
Q

Nutrition options in surgical patients= percutaneous endoscopic gastrostomy (PEG) insertion?

A

Combined endoscopic and percutaneous tube insertion

208
Q

Nutrition options in surgical patients= percutaneous endoscopic gastrostomy (PEG) may not be technically possible in who?

A

patients who cannot undergo successful endoscopy

209
Q

Nutrition options in surgical patients= percutaneous endoscopic gastrostomy (PEG) risks?

A

aspiration and leakage at the insertion site

210
Q

Nutrition options in surgical patients= total parenteral nutrition (TPN)?

A

The definitive option in those patients in whom enteral feeding is contra indicated

Individualised prescribing and monitoring needed

Should be administered via a central vein as it is strongly phlebitic

Long term use is associated with fatty liver and deranged LFT’s

211
Q

Nutrition options in surgical patients= total parenteral nutrition (TPN) administration?

A

Should be administered via a central vein as it is strongly phlebitic

212
Q

Nutrition options in surgical patients= total parenteral nutrition (TPN) long term use is associated with what?

A

fatty liver and deranged LFTs

213
Q

Nutrition options in surgical patients= The definitive option in those patients in whom enteral feeding is contra indicated?

A

total parenteral nutrition (TPN)- Individualised prescribing and monitoring needed

214
Q

Early causes of post-op pyrexia (0-5 days) include?

A

Blood transfusion

Cellulitis

Urinary tract infection

Physiological systemic inflammatory reaction (usually within a day following the operation)

Pulmonary atelectasis - this if often listed but the evidence base to support this link is limited

215
Q

Late causes of post-op pyrexia (>5 days) include:

A

Venous thromboembolism

Pneumonia

Wound infection

Anastomotic leak

216
Q

When considering causes of post-op pyrexia, it is helpful to consider the memory aid of?

A

‘the 4 W’s’ (wind, water, wound, what did we do? (iatrogenic).

217
Q

Postoperative ileus (paralytic ileus)?

A

a common complication after surgery involving the bowel, especially surgeries involving extensive handling of the bowel.

218
Q

Postoperative ileus (paralytic ileus) pathophysiology?

A

There is reduced bowel peristalsis resulting in pseudo-obstruction.

219
Q

Postoperative ileus (paralytic ileus) features?

A

abdominal distention/bloating

abdominal pain

nausea/vomiting

inability to pass flatus

inability to tolerate an oral diet

220
Q

Postoperative ileus (paralytic ileus) Ix?

A

Deranged electrolytes can contribute to the development of postoperative ileus, so it is important to check potassium, magnesium and phosphate.

221
Q

Postoperative ileus (paralytic ileus) cause?

A

common complication after surgery involving the bowel, especially surgeries involving extensive handling of the bowel.

222
Q

Postoperative ileus (paralytic ileus) Mx?

A

nil-by-mouth initially, may progress to small sips of clear fluids

nasogastric tube if vomiting

IV fluids to maintain normovolaemia

additives to correct any electrolyte disturbances

total parenteral nutrition
occasionally required for prolonged/severe cases

223
Q

Ix findings for Postoperative ileus (paralytic ileus)?

A

abdominal X-ray in POI shows generalised gaseous distension without a transition point, whereas obstruction demonstrates dilated proximal bowel with collapse distal to the blockage.

CT abdomen with contrast (UK guideline-recommended for suspected obstruction) may reveal a transition point, stricture, or mass.

Laboratory findings (e.g., raised lactate, leucocytosis) suggest ischaemia in obstruction.

224
Q

Mx of postoperative ileus vs bowel obstruction?

A

POI is managed supportively (hydration, mobilisation), while obstruction may require nasogastric decompression, surgery, or adhesiolysis. Thus, differentiation relies on clinical evaluation, imaging, and contextual history.

225
Q

Surgical safety checklist= The checklist identifies three phases of an operation….?

A

1) Before the induction of anaesthesia (sign in)

2) Before the incision of the skin (time out)

3) Before the patient leaves the operating room (sign out)

226
Q

Surgical safety checklist?

A

tool to reduce mistakes

227
Q

Surgical safety checklist= in each phase of the checklist what is done?

A

a checklist coordinator must confirm that the surgery team has completed the listed tasks before proceeding with the operation.

228
Q

Surgical safety checklist= before induction of anaesthesia what must be checked (7)?

A

Patient has confirmed: Site, identity, procedure, consent

Site is marked

Anaesthesia safety check completed

Pulse oximeter is on patient and functioning

Does the patient have a known allergy?

Is there a difficult airway/aspiration risk?

Is there a risk of > 500ml blood loss (7ml/kg in children)?

229
Q

Surgical site infections may occur following…

A

a breach in tissue surfaces and allow normal commensals and other pathogens to initiate infection

230
Q

Surgical site infections (SSI) comprise up to …% of all healthcare-associated infections and at least …% of patients undergoing surgery will develop an SSI as a result.

231
Q

Surgical site infection= In many cases, the organisms are derived from the patient’s own body. Measures that may increase the risk of SSI include?

A

Shaving the wound using a razor (disposable clipper preferred)

Using a non-iodine impregnated incise drape if one is deemed to be necessary

Tissue hypoxia

Delayed administration of prophylactic antibiotics in tourniquet surgery

232
Q

Surgical site infection= prevention postop?

A

Don’t remove body hair routinely

If hair needs removal, use electrical clippers with a single-use head (razors increase infection risk)

Antibiotic prophylaxis if:
- placement of prosthesis or valve
- clean-contaminated surgery
- contaminated surgery

Use local formulary
- Aim to give single-dose IV antibiotic on anaesthesia
- If a tourniquet is to be used, give prophylactic antibiotics earlier

233
Q

Surgical site infection= prevention postop- when to give Abx prophylaxis?

A
  • placement of prosthesis or valve
  • clean-contaminated surgery
  • contaminated surgery

Use local formulary
- Aim to give single-dose IV antibiotic on anaesthesia
- If a tourniquet is to be used, give prophylactic antibiotics earlier

234
Q

Surgical site infection= prevention intraoperatively?

A

1) Prepare the skin with alcoholic chlorhexidine (Lowest incidence of SSI)
2) Cover surgical site with dressing

A recent meta analysis has confirmed that administration of supplementary oxygen does not reduce the risk of wound infection. In contrast to previous individual RCTs
Wound edge protectors do not appear to confer benefit

235
Q

Surgical site infection= what for surgical wounds healing by secondary intention?

A

Tissue viability advice for management of surgical wounds healing by secondary intention

236
Q

Thermoregulation during the perioperative period involves?

A

managing the body temperature of patients from one hour before surgery to 24 hours after surgery ends.

Maintaining a normal body temperature (normothermia) is crucial, with special attention given to preventing hypothermia, which is defined as a temperature below 36.0ºC. This is vital because even small drops in body temperature can negatively impact surgical outcomes.

237
Q

Patients are prone to hypothermia under anaesthesia why?

A

they cannot respond to cold, often wear minimal clothing, and are exposed to the effects of anaesthetic drugs

238
Q

RFs for hypothermia in perioperative period?

A

A higher ASA grade (2 or above)

Major surgery

Low body weight

Large amounts of cold IV infusions and blood transfusions

239
Q

Managing body temp pre-op to prevent hypothermia?

A

Measure the patient’s temperature one hour before anaesthesia. If below 36.0ºC, start active warming immediately. If it’s 36.0ºC or higher, begin warming 30 minutes before anaesthesia.

Do not move patients to the operating theatre if their temperature is below 36.0ºC unless the surgery is urgent.

240
Q

Managing body temp intra-op to prevent hypothermia?

A

Measure core temperature
accurately (within 0.5ºC) using oesophageal probes during surgery.

Use forced air-warming devices from the start of anaesthesia for surgeries longer than 30 minutes or for high-risk patients.

Warm all fluids and blood products over 500ml before administration.

241
Q

Managing body temp post-op to prevent hypothermia?

A

Document the patient’s temperature initially and then every 15 minutes in the recovery room.

Do not transfer patients to the ward if their temperature is below 36.0ºC. Keep them warm according to their comfort once above 36.0ºC.

Monitor for signs of hyperthermia, typically due to inflammation or the elimination of anaesthetic drugs.

242
Q

Cx of perioperative hypothermia?

A

Coagulopathy: Hypothermia can impair blood clotting, leading to increased bleeding.

Prolonged Recovery from Anesthesia: Even minor drops in body temperature can extend the effects of anaesthesia significantly.

Impaired Wound Healing: Reduced blood flow to the skin from vasoconstriction can lower immune response and delay healing.

Increased Risk of Infection: Poor healing and reduced immune function at the wound site can elevate the risk of infection.

Shivering: This can increase the metabolic rate significantly, posing risks such as myocardial ischemia in vulnerable patients.

243
Q

Definition of hypothermia?

A

body temperature below 35.0ºC

244
Q

All patients admitted to hospital should be individually assessed to identify risk factors for?

A

VTE development and bleeding risk.

For medical and surgical patients the recommended risk proforma is the department of healths VTE risk assessment tool.

245
Q

What medical pts would be deemed at risk of developing a VTE?

A

significant reduction in mobility for 3 days or more (or anticipated to have significantly reduced mobility)

246
Q

What surgical/trauma pts would be deemed at risk of developing a VTE?

A

hip/knee replacement

hip fracture

general anaesthetic and a surgical duration of over 90 minutes

surgery of the pelvis or lower limb with a general anaesthetic and a surgical duration of over 60 minutes

acute surgical admission with an inflammatory/intra-abdominal condition

surgery with a significant reduction in mobility

247
Q

General RFs for VTE?

A

active cancer/chemotherapy

aged over 60

known blood clotting disorder (e.g. thrombophilia)

BMI over 35

dehydration

one or more significant medical comorbidities (e.g. heart disease; metabolic/endocrine pathologies; respiratory disease; acute infectious disease and inflammatory conditions)

critical care admission

use of hormone replacement therapy (HRT)

use of the combined oral contraceptive pill

varicose veins

pregnant or less than 6 weeks post-partum

248
Q

After a patients VTE risk has been assessed, this should be compared to what?

A

their risk of bleeding to decide whether VTE prophylaxis should be offered. If indicated VTE prophylaxis should be started as soon as possible.

249
Q

2 types of VTE prophylaxis?

A

mechanical and pharmacological

250
Q

Mechanical VTE prophylaxis?

A

Correctly fitted anti-embolism (aka compression) stockings (thigh or knee height)

An Intermittent pneumatic compression device

251
Q

Pharmacological VTE prophylaxis?

A

Fondaparinux sodium (SC injection)

Low molecular weight heparin (LMWH)=
e.g. enoxaparin; reduced doses should be used in patients with severe renal impairment

Unfractionated heparin (UFH)=
used as an alternative to LWMH in patients with chronic kidney disease

252
Q

General Mx for VTE prophylaxis in medical and surgically pts?

A

In general, all medical patients deemed at risk of VTE after individual assessment are started on pharmacological VTE prophylaxis. This is providing the risk of VTE outweighs the risk of bleeding (this is often a clinical judgement) and there are no contraindications. Those at very high risk may be offered anti-embolic stockings alongside the pharmacological methods.

For surgical patients at low risk of VTE first-line treatment is anti-embolism stockings. If a patient is at high risk these stockings are used in conjunction with pharmacological prophylaxis.

253
Q

VTE prophylaxis, advice for pts= pre-surgical interventions?

A

Advise women to stop taking their combined oral contraceptive pill/hormone replacement therapy 4 weeks before surgery

254
Q

Advise women to stop COCP/HRT how long before surgery?

255
Q

VTE prophylaxis, advice for pts= post-surgical interventions?

A

Try to mobilise patients as soon as possible after surgery

Ensure the patient is hydrated

256
Q

For certain surgical procedures (hip and knee replacements) pharmacological VTE prophylaxis is recommended for….

A

all patients to reduce the risk of a VTE developing post-surgery (regardless of risk)

257
Q

Recommended VTE prophylaxis for elective hip surgery?

A

LMWH for 10 days followed by aspirin (75 or 150 mg) for a further 28 days

or

LMWH for 28 days combined with anti-embolism stockings until discharge

or

Rivaroxaban

258
Q

Recommended VTE prophylaxis for elective knee surgery?

A

Aspirin (75 or 150 mg) for 14 days

or

LMWH for 14 days combined with anti-embolism stockings until discharge

or

Rivaroxaban

259
Q

Recommended VTE prophylaxis for fragility fractures of the pelvis, hip and proximal femur surgery?

A

Offer VTE prophylaxis for a month to people with fragility fractures of the pelvis, hip or proximal
femur if the risk of VTE outweighs the risk of bleeding. Choose either:

LMWH , starting 6-12 hours after surgery

or

fondaparinux sodium, starting 6 hours after surgery, providing there is low risk of bleeding.

260
Q

When are anti-embolic stockings contraindicated?

A

peripheral arterial disease or peripheral neuropathy

261
Q

1st line VTE prophylaxis in medical patients?

A

low molecular weight heparin as a first-line option, or fondaparinux sodium as an alternative, for a minimum of 7 days.

Patients with renal impairment should be given either a low molecular weight heparin or heparin (unfractionated) and the dose should be adjusted as necessary.

262
Q

Surgical wounds are either what?

A

incisional or excisional and either clean, clean contaminated or dirty

263
Q

Main 4 stages of wound healing?

A

1) Haemostasis
2) Inflammation
3) Regeneration
4) Remodeling

264
Q

Wound healing stages= stage 1- haemostasis?

A

Minutes to hours following injury

Vasospasm in adjacent vessels, platelet plug formation and generation of fibrin rich clot.

265
Q

Wound healing stages= stage 2- inflammation?

A

Typically days 1-5

Neutrophils migrate into wound (function impaired in diabetes).

Growth factors released, including basic fibroblast growth factor and vascular endothelial growth factor.

Fibroblasts replicate within the adjacent matrix and migrate into wound.

Macrophages and fibroblasts couple matrix regeneration and clot substitution.

266
Q

Wound healing stages= stage 3- regeneration?

A

Typically days 7 to 56

Platelet derived growth factor and transformation growth factors stimulate fibroblasts and epithelial cells.

Fibroblasts produce a collagen network.

Angiogenesis occurs and wound resembles granulation tissue.

267
Q

Wound healing stages= stage 4- remodeling?

A

From 6 weeks to 1 year

Longest phase of the healing process and may last up to one year (or longer).

During this phase fibroblasts become differentiated (myofibroblasts) and these facilitate wound contraction.

Collagen fibres are remodeled.

Microvessels regress leaving a pale scar.

268
Q

What may effect the healing process of a wound?

A

A number of diseases may distort this process. Neovascularisation is an important early process. Endothelial cells may proliferate in the wound bed and recanalise to form a vessel. Vascular disease, shock and sepsis can all compromise microvascular flow and impair healing.

Conditions such as jaundice will impair fibroblast synthetic function and immunity with a detrimental effect in most parts of the healing process.

269
Q

Hypertrophic scars?

A

Excessive amounts of collagen within a scar. Nodules may be present histologically containing randomly arranged fibrils within and parallel fibres on the surface. The tissue itself is confined to the extent of the wound itself and is usually the result of a full thickness dermal injury. They may go on to develop contractures.

270
Q

Keloid scars?

A

Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond the boundaries of the original injury. They do not contain nodules and may occur following even trivial injury. They do not regress over time and may recur following removal.

271
Q

Drugs which impair wound healing?

A

Non steroidal anti inflammatory drugs

Steroids

Immunosupressive agents

Anti neoplastic drugs

272
Q

Delayed primary vs secondary closure of a wound?

A

Delayed primary closure is the anatomically precise closure that is delayed for a few days but before granulation tissue becomes macroscopically evident.

Secondary closure refers to either spontaneous closure or to surgical closure after granulation tissue has formed.

273
Q

Resp distress vs failure vs arrest?

A

“Respiratory distress” refers to difficulty breathing with increased effort, often noticeable by signs like rapid breathing or flaring nostrils, while “respiratory failure” means the lungs are unable to adequately provide oxygen to the body, and “respiratory arrest” is the complete cessation of breathing, essentially the most severe stage where a person is not breathing at all; essentially, respiratory distress can progress to respiratory failure, which if left untreated, can lead to respiratory arrest.

274
Q

Obesity only increases perioperative risk significantly when BMI is…

A

≥40 kg m−2, or when associated with significant comorbidities.

  • Day-case surgery is usually appropriate if BMI is <50 kg m−2 and comorbidities are optimised.
275
Q

What are common high-risk conditions that influence the Mx of anaesthesia?

A

Obstructive sleep apnoea and obesity hypoventilation syndrome?

276
Q

Obesity hypoventilation syndrome (OHS) (Pickwickian syndrome)?

A

a complex respiratory disorder characterized by chronic hypoventilation, obesity, and sleep-disordered breathing, particularly obstructive sleep apnea (OSA). Can result in significant morbidity and mortality if left untreated.

277
Q

Obesity hypoventilation syndrome (OHS) results from a combination of factors related to obesity and its effects on the respiratory system. These factors include:

A

Impaired respiratory mechanics: Excessive adipose tissue, particularly in the chest and abdominal regions, can restrict lung expansion and limit diaphragmatic movement, resulting in decreased lung volumes and increased work of breathing.

Altered ventilatory control: OHS patients may have impaired central respiratory drive, leading to inadequate ventilation and subsequent hypoventilation, particularly during sleep.

Sleep-disordered breathing: OSA is highly prevalent in OHS patients, contributing to nocturnal hypoventilation, intermittent hypoxia, and hypercapnia.

Hormonal and metabolic factors: Obesity is associated with hormonal and metabolic abnormalities that can further exacerbate hypoventilation, such as leptin resistance and insulin resistance.

278
Q

Obesity hypoventilation syndrome (OHS) features?

A

Obesity: Body mass index (BMI) ≥30 kg/m2, often with central adiposity.

Daytime hypoventilation: Manifests as dyspnea, exercise intolerance, and fatigue.

Sleep-disordered breathing: Symptoms may include loud snoring, witnessed apneas, nocturnal choking or gasping, and excessive daytime sleepiness.

Morning headaches and cognitive dysfunction: These symptoms may result from chronic hypercapnia and hypoxemia.

Signs of right heart failure: Including peripheral edema, jugular venous distention, and hepatomegaly, due to chronic hypoxemia and pulmonary hypertension.

279
Q

Obesity hypoventilation syndrome (OHS) diagnosis?

A

he diagnosis of OHS is based on the following criteria:

Obesity: BMI ≥30 kg/m2.

Hypoventilation: Daytime arterial blood gas analysis demonstrating hypercapnia and hypoxemia in the absence of other causes.

Sleep-disordered breathing: Polysomnography demonstrating the presence of OSA or other sleep-related breathing disorders.

Additional diagnostic tests may include pulmonary function tests, chest radiography, electrocardiography, and echocardiography to evaluate lung function, rule out alternative diagnoses, and assess the severity of the condition.

280
Q

Obesity hypoventilation syndrome (OHS) Mx?

A

Weight loss: Encouraging lifestyle modifications, such as a balanced diet and regular physical activity, is crucial. Bariatric surgery may be considered in refractory cases or for patients with severe obesity.

Positive airway pressure therapy: Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) can be used to treat OSA and nocturnal hypoventilation.

Oxygen therapy: Supplemental oxygen may be required for patients with persistent hypoxemia despite positive airway pressure therapy.