SAQ 2022.2 Flashcards

1
Q

[22B01] Evaluate the methods for detection of myocardial ischaemia in the anaesthetised patient. Pass rate 45.3%

A

Pass rate 45.3%
Candidates were required to evaluate the range of methods at their disposal in the operating theatre:
* Clinical (eg.haemodynamic instability, dysrhythmias, prolonged hypotension, diaphoresis, chest pain/SOB in a patient undergoing regional anaesthesia)
* ECG - changes and consideration of limitations of a 3 lead ECG
* Echocardiography (eg. regional wall motion abnormalities)
Candidates who considered all these methods and went on to appraise the value of each method scored well. A significant number of candidates failed to make any comment on clinical methods and so were unable to achieve a pass mark for the question.

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2
Q

[22B02] Discuss the intraoperative and postoperative pain management of a trauma patient who requires a semi-elective below knee amputation for an isolated injury. Pass rate 77.3%

A

This was a well answered question where the majority of candidates considered a range of options and techniques for such a patient. Better candidates discussed the use of tricyclics and antineuropathic agents within their management plan in an attempt to reduce the incidence/severity of phantom limb pain.

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3
Q

[22B03] Discuss the perioperative management of a patient requiring clot retrieval for an acute ischaemic stroke. Pass rate 33.3%

A

Perioperative management for acute ischaemic stroke clot retrieval focuses on time-critical intervention, haemodynamic optimisation, anaesthetic technique selection, and post-procedural monitoring.

Time-Critical Intervention
Minimise delays from symptom onset to revascularisation (“door-to-groin” time <90 minutes). Rapid neuroimaging (CT/MRI), exclusion of contraindications (e.g., intracranial haemorrhage), and immediate transfer to angiography suite are priorities[1].

Haemodynamic Management
- Pre- and intra-procedure: Maintain systolic BP within 10% of baseline (typically 140–180 mmHg) to preserve cerebral perfusion in the penumbra. Avoid hypotension (SBP <140 mmHg), which exacerbates ischaemia[1].
- Vasopressors (e.g., noradrenaline) may be required to achieve targets.

Anaesthetic Technique
| General Anaesthesia (GA) | Local Anaesthesia/Sedation |
|——————————|——————————–|
| Advantages: Immobility, airway control, reduced procedural delays. | Advantages: Real-time neurological monitoring, faster recovery. |
| Disadvantages: Hypotension risk, delayed awakening masking stroke assessment. | Disadvantages: Patient movement, aspiration risk, incomplete analgesia[1]. |
GA is preferred for uncooperative patients; sedation is reserved for cooperative cases with stable airways.

Post-Procedural Monitoring
- High-acuity setting: Intensive care or stroke unit for BP monitoring (target SBP <140–160 mmHg post-reperfusion) and neurological assessments hourly.
- Complications: Monitor for haemorrhagic transformation, reperfusion injury, or cerebral oedema. Avoid hyperglycaemia and hyperthermia[1].

Collaboration with the neurointerventional team is essential, but anaesthetists must independently manage haemodynamic goals. Avoid overemphasising remote-site airway challenges unless directly relevant to the patient’s condition.

Citations:
[1] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/f024ed12-e8e6-48ef-8ef7-0401bdd85af7/2022.1-Final-Exam-Chair-s-report-v2.pdf

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4
Q

[22B04] You are asked to review a 32-year-old G1P1 woman complaining of right leg weakness the day after an instrumental vaginal birth of a 4.2 kg baby under epidural analgesia. Describe your assessment of the patient and management of the likely differential diagnoses. Pass rate 80.7%

A

The patient presents with postpartum right leg weakness following instrumental vaginal delivery under epidural analgesia. Key considerations include distinguishing between epidural-related complications and obstetric nerve injuries, with management guided by urgent assessment and targeted interventions.

Assessment
History:
- Epidural details: Insertion level, procedural difficulty, bloody tap, or paresthesia during placement[1][2].
- Labor course: Duration of second stage, lithotomy positioning time, and forceps use (risk factors for femoral/lumbosacral plexus injury)[3][5].
- Neurological timeline: Onset/resolution of weakness, associated symptoms (back pain, bowel/bladder dysfunction)[2][4].

Examination:
- Motor function: Bromage score (e.g., inability to flex knees = Bromage 3)[1][2].
- Sensory testing: Dermatomal deficits (pinprick/cold) to identify unilateral vs bilateral involvement[2][4].
- Reflexes: Absent patellar reflex suggests femoral neuropathy[3][5].
- Back inspection: Signs of infection or hematoma[2][4].

Investigations:
- MRI spine: If motor weakness persists >4 hours after epidural cessation or if red flags (e.g., bowel/bladder dysfunction, intense back pain) are present[2][4].
- Blood tests: CRP/WCC if infection suspected[2].

Differential Diagnoses
| Epidural-Related | Obstetric-Related |
|——————————–|————————————–|
| Local anesthetic motor block | Femoral neuropathy (lithotomy position)[3][5] |
| Epidural hematoma/abscess[2][4] | Lumbosacral plexus injury (fetal/forceps compression)[4][5] |
| Catheter migration (intrathecal)| Obturator/sciatic nerve injury[4] |

Management
1. Epidural-related causes:
- Local anesthetic effect: Stop epidural infusion; reassess Bromage hourly. Expect resolution within 2–4 hours[1][2].
- Hematoma/abscess: Immediate MRI + neurosurgical referral if progressive weakness/red flags[2][4].

  1. Obstetric nerve injury:
    • Femoral neuropathy: Physical therapy, knee brace, and analgesia (acetaminophen/NSAIDs)[3][5][7].
    • Lumbosacral injury: Electromyography for confirmation; multidisciplinary follow-up[3][4].
  2. Documentation: Detail neurological findings, interventions, and patient counseling.
  3. Referrals:
    • Neurosurgery: For MRI-confirmed compressive lesions[2][4].
    • Neurology/Physiotherapy: Persistent weakness or functional impairment[3][5].

Key Considerations
- Epidural vs obstetric injury: Unilateral weakness favors obstetric injury; bilateral deficits or sensory level suggests epidural pathology[2][4].
- Urgency: Delayed MRI (>6–12 hours) risks permanent deficit in compressive lesions[2][4].

This approach prioritizes excluding epidural hematoma/abscess while addressing reversible causes and initiating rehabilitation for nerve injuries.

Citations:
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC4799605/
[2] https://doclibrary-rcht.cornwall.nhs.uk/DocumentsLibrary/RoyalCornwallHospitalsTrust/Clinical/Anaesthetics/ManagementOfLegWeaknessWithEpiduralAnalgesiaClinicalGuideline.pdf
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC6936406/
[4] https://www.jvsmedicscorner.com/Anaesth-Obstetrics_files/Postpartum%20Spinal%20Cord,%20Root,%20Plexus%20and%20Peripheral%20Nerve%20Injuries%20Involving%20the%20Lower%20Extremities%20Review%202014.pdf
[5] https://www.apsf.org/article/postpartum-peripheral-nerve-injuries-what-is-anesthesias-role/
[6] https://www.cerebralpalsyguide.com/birth-injury/forceps-delivery-complications/
[7] https://rapm.bmj.com/content/early/2024/06/13/rapm-2024-105478
[8] https://www.childbirthinjuries.com/birth-injury/epidural-injuries/

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5
Q

[22B05] A 56-year-old male with haemophilia A is scheduled to undergo a total knee replacement. Describe the pathogenesis of haemophilia A and its complications. (50%) Discuss how the presence of haemophilia A influences your perioperative management of this patient. (50%) Pass rate 60.0%

A

Hemophilia A is an X-linked recessive disorder caused by mutations in the F8 gene, leading to deficient/dysfunctional factor VIII (FVIII) and impaired intrinsic coagulation pathway activation[1][7]. This results in defective thrombin generation, causing spontaneous bleeding (especially into joints) and prolonged hemorrhage after trauma[1]. The knee is a common site for hemarthroses, leading to synovitis, cartilage destruction, and arthropathy[1][2]. Approximately 30% of severe cases develop FVIII inhibitors (IgG antibodies), complicating replacement therapy[1][3].

Perioperative management considerations:
Preoperative
- Confirm FVIII activity level and inhibitor status[1][5]
- Target FVIII levels: 80-100% preoperatively using recombinant FVIII or plasma-derived concentrates[5][6]
- Consider continuous FVIII infusion for level stability during prolonged procedures[2][8]
- Antifibrinolytic agents (tranexamic acid) reduce bleeding risk (OR 3.00 for non-use)[2][3]

Intraoperative
- Avoid regional anesthesia if FVIII < 50%[8]
- Meticulous hemostasis and drain placement to monitor bleeding[2][4]
- For inhibitor-positive patients: Use bypass agents (rFVIIa 90-120 μg/kg q2h)[1][2]

Postoperative
- Maintain FVIII levels:
- Days 1-3: 60-80%
- Days 4-6: 40-60%
- Days 7-14: 30-50%[5][6]
- Monitor hemoglobin and joint drainage; 25% require transfusion[2][3]
- Delay pharmacologic thromboprophylaxis; prioritize mechanical methods[5][8]
- Factor replacement continues for 7-14 days, coordinated with physical therapy[4][5]

Key risks include major bleeding (25% in TKA)[2], inhibitor anamnestic responses[5], and hemarthrosis recurrence. Multidisciplinary care with hematology input is essential[4][5][8].

Citations:
[1] https://emedicine.medscape.com/article/779322-overview
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC8940712/
[3] https://pubmed.ncbi.nlm.nih.gov/35080347/
[4] https://www.health.qld.gov.au/haemophilia/html/bleed_surgery
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC9820308/
[6] https://www.currentsurgery.org/index.php/jcs/article/view/455/452
[7] https://journals.sagepub.com/doi/10.1177/2040620721993686
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC5341657/

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6
Q

[22B06] Justify the ongoing clinical use of nitrous oxide and ENTONOX. (50%) Discuss how the environmental impact of their use can be minimised. (50%) Pass rate 55.3%

A

Nitrous oxide (N₂O) and ENTONOX (50% N₂O/50% O₂) remain clinically valuable due to their rapid onset/offset, analgesic/anxiolytic properties, and dose-sparing effects on more toxic agents[1][2][3][5]. Justification for ongoing use includes:
- Reduced opioid requirements (30-60% dose reduction), lowering risks of respiratory depression and hypotension[2][4]
- NMDA receptor antagonism decreasing chronic post-surgical pain incidence[1][3]
- Safe pediatric/obstetric use with minimal side effects and no metabolic accumulation[3][4][5]
- Procedural sedation efficacy in colonoscopy, fracture reduction, and emergency settings, with faster recovery than IV sedation[3][5]
- Cost-effectiveness and self-administration capability enhancing patient autonomy[3][5]

Environmental mitigation strategies focus on N₂O’s potent greenhouse gas effects (265x CO₂ potency)[1]:
- Scavenging systems to capture waste gas for catalytic conversion to N₂/O₂[1]
- Low-flow anesthesia with closed circuits to minimize fresh gas use[1]
- Selective use protocols reserving N₂O for cases with clear benefit over alternatives[1]
- Infrastructure audits to detect/pipeline leaks in medical gas systems[1]
- Alternatives promotion (e.g., IV lidocaine, regional techniques) where equivalent analgesia exists[1]

The 2022.2 examiners emphasized justifying use case-by-case while implementing environmental safeguards, rather than outright elimination[1].

Citations:
[1] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/3692bdce-93b2-4aee-9e97-df1f27aa2ca8/2022.2-FEx-Examination-Report.pdf
[2] https://clinicalview.gehealthcare.com/article/use-or-not-use-nitrous-oxide-anesthesia-providers-decision-when-nitrous-oxide-should-be
[3] https://www.boconline.co.uk/wcsstore/UK_BOC_Industrial_Ntl_Store/pdf/downloads/Entonox-essential-guide.pdf
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC1821130/
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC3954179/

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7
Q

SAQ Describe the anatomy relevant to performing an adductor canal block. (50%) Outline the indications

A

The adductor canal block (ACB) targets the saphenous nerve within the subsartorial (adductor) canal, providing sensory analgesia while preserving quadriceps motor function.

Anatomy (50%)
The adductor canal is an aponeurotic tunnel in the medial thigh, extending from the femoral triangle apex to the adductor hiatus. Key structures include:
- Boundaries:
- Anteromedial: Sartorius muscle.
- Anterolateral: Vastus medialis muscle.
- Posterior: Adductor longus/magnus.
- Contents:
- Femoral artery and vein.
- Saphenous nerve (sensory terminal branch of the femoral nerve).
- Nerve to vastus medialis (motor, typically outside the canal).
- Posterior branch of the obturator nerve (variable presence).
- Landmark: Mid-thigh level, deep to sartorius, lateral to the femoral artery[1][5][6].

Indications
1. Knee surgery:
- Low-volume block (5–10 mL):
- Knee arthroscopy, ACL reconstruction (infrapatellar nerve coverage)[2][4].
- High-volume block (15–20 mL):
- Total knee arthroplasty (spreads proximally for anterior knee analgesia)[3][5].
2. Lower leg/ankle surgery:
- Combined with a sciatic block for medial leg/foot procedures (e.g., ORIF of medial malleolus)[4][5].
3. Advantages over femoral nerve block:
- Preserves quadriceps strength, enabling earlier mobility[3][5].

Summary
The ACB’s anatomical focus on the saphenous nerve in the subsartorial canal allows targeted analgesia for anteromedial knee and lower limb procedures. Its motor-sparing nature makes it preferable for postoperative rehabilitation in knee surgeries[1][3][5].

Citations:
[1] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/3692bdce-93b2-4aee-9e97-df1f27aa2ca8/2022.2-FEx-Examination-Report.pdf
[2] https://resources.wfsahq.org/atotw/ultrasound-guided-adductor-canal-block-saphenous-nerve-block/
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC9410636/
[4] https://myblockbuddy.com/all-lessons/adductor-canal-block/
[5] https://pain.ucsf.edu/peripheral-nerve-blocks/adductor-canal-blockssaphenous-nerve-block
[6] https://www.euroespa.com/wp-content/uploads/2018/01/adductor-canal-block-1.pdf

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8
Q

[22B08]
A patient presenting for surgery has a DDDR pacemaker. a) Explain the NASPE/BPEG Generic (NBG) pacemaker classification system. b) Describe the assessment and preoperative management of this DDDR device. *NASPE/BPEG - North American Society of Pacing and Electrophysiology/British Pacing and
Electrophysiology Group. Pass rate 73.3%

A

The NASPE/BPEG Generic (NBG) pacemaker classification system uses a 5-letter code to describe device function[1][3][4]:
- Position I (Chamber paced): D = Dual (atria and ventricles)
- Position II (Chamber sensed): D = Dual (atria and ventricles)
- Position III (Response to sensing): D = Dual (inhibits pacing if native activity detected, triggers pacing if needed)
- Position IV (Rate modulation): R = Rate-adaptive (adjusts heart rate based on physiological sensors)
- Position V (Multisite pacing): Omitted in this case (no multisite pacing)[4].

For a DDDR pacemaker, preoperative management includes[5][7][8][10]:
1. Device interrogation (ideally within 6 months) to confirm battery life, pacing thresholds, and % pacing burden (≥40% indicates dependency)[7][10].
2. Deactivate rate-responsive mode (R function) to prevent inappropriate tachycardia from surgical stimuli[5][7].
3. Magnet application (if pacemaker-dependent) to switch to asynchronous mode (DOO) and avoid electrocautery-induced inhibition[7][8].
4. Electrocautery precautions:
- Use bipolar cautery when possible[5][9].
- Place monopolar grounding pad contralateral to the device[9].
- Limit cautery bursts to <1 second with 10-second intervals[5].
5. Emergency backup: Ensure temporary pacing and defibrillation equipment are immediately available[6][8].

Key considerations include verifying magnet response (varies by manufacturer) and consulting the cardiology team for complex reprogramming[8][9].

Citations:
[1] https://pubmed.ncbi.nlm.nih.gov/2441363/
[2] https://resources.wfsahq.org/atotw/pacemakers-implantable-cardioverter-defibrillators-icds-part-1-anaesthesia-tutorial-of-the-week-299/
[3] https://www.ncbi.nlm.nih.gov/sites/books/NBK556011/
[4] https://litfl.com/pacemaker-rhythms-normal-patterns/
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC1420917/
[6] https://www.hrsonline.org/documents/2004-asa-practice-advisory-perioperative-managementpdf/download
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC5613599/
[8] https://www.openanesthesia.org/keywords/cardiac-implantable-electronic-devices-pacemakers/
[9] https://www.ahajournals.org/doi/10.1161/CIR.0000000000001264
[10] https://pmc.ncbi.nlm.nih.gov/articles/PMC4613927/

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9
Q

SAQ Discuss the intraoperative considerations for a patient undergoing a pneumonectomy. Pass rate 34.7%

A
  1. Lung isolation technique
  2. Vent strategy x6
    - Vt = 5-6 IBW
    Ppeak < 35
    Pplat < 30
    Normal pCO2
    PEEP 5
    Avoid hyperoxia - sats 94-98%
  3. Fluid mx
    - restrict vs avoid hypovol + AKI
  4. Clamp PA
    - suitability
    - CV collapse
    - Excessive rise CVP
    - - test RV

  • lung isolation technique
  • ventilation strategy
  • haemodynamic management including clamping of the pulmonary artery
  • fluid management
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10
Q

[22B10] Discuss the use of ultrasound during the initial presentation of a patient with major trauma. Pass rate 62.7%

A

Ultrasound, particularly the FAST (Focused Assessment with Sonography for Trauma) and eFAST (Extended FAST) protocols, is a critical tool in the initial assessment of major trauma patients. It provides rapid, non-invasive evaluation for life-threatening injuries while prioritizing hemodynamic stability and guiding urgent interventions.

Abdominal Pathology
- Detection of free fluid: FAST assesses the perihepatic (Morison’s pouch), perisplenic, pelvic, and pericardial regions for hemoperitoneum. A positive FAST (free fluid) has high specificity (98–99%) for intra-abdominal bleeding, warranting emergent laparotomy in unstable patients[1][7][14].
- Limitations: Sensitivity is lower (28–76%), particularly for retroperitoneal injuries, hollow viscus injuries, or minor solid organ injuries without significant bleeding[10][13]. Negative FAST cannot exclude abdominal trauma, necessitating repeat exams or CT in stable patients[9][13].

Cardiac Pathology
- Pericardial effusion/tamponade: The subxiphoid or parasternal view identifies hemopericardium with sensitivity up to 92% and specificity ~99%, crucial in penetrating chest trauma[2][9][14].
- Hemodynamic assessment: Transthoracic/transesophageal echocardiography evaluates cardiac contractility, right ventricular strain, and aortic injury, guiding fluid resuscitation and inotropic support[2][4].

Lung Pathology (eFAST)
- Pneumothorax: Detected via absent lung sliding, B-lines, or lung point. Superior to CXR, with sensitivity >90% in supine trauma patients[3][9].
- Hemothorax: Identifies as little as 20 mL pleural fluid (vs. 200 mL on CXR), aiding rapid chest tube placement[3][9].

Technique: FAST/eFAST Views
1. Pericardial: Subxiphoid/parasternal long-axis for effusion.
2. Right upper quadrant: Hepatorenal recess (Morison’s pouch).
3. Left upper quadrant: Splenorenal interface.
4. Pelvic: Pouch of Douglas/rectovesical space.
5. eFAST additions: Bilateral lung zones for pneumothorax/hemothorax[5][6][7].

Pitfalls and Limitations
- Operator dependence: Skill and experience significantly impact accuracy[4][10].
- Low sensitivity in stable patients: Up to 49% false-negative rates for intra-abdominal injury[13][15].
- Limited retroperitoneal evaluation: Misses injuries to kidneys, pancreas, or duodenum[9][12].
- Obesity/technical factors: Poor acoustic windows reduce diagnostic yield[10].

Predictive Values
- High specificity (98–100%): Positive FAST reliably indicates injury requiring intervention[1][14].
- Low negative predictive value (NPV 64–89%): Negative FAST does not exclude injury, especially with high-risk mechanisms[13][15].
- Context-dependent accuracy: Sensitivity improves in hypotensive patients (49–92%)[13][14].

In summary, FAST/eFAST is invaluable for rapid triage in unstable trauma patients but requires integration with clinical findings and CT for comprehensive evaluation. Its role is diagnostic for positives and screening for negatives, emphasizing repeat assessments or adjunct imaging when clinical suspicion persists.

Citations:
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC6464800/
[2] https://pubmed.ncbi.nlm.nih.gov/27907878/
[3] https://pubmed.ncbi.nlm.nih.gov/35173781/
[4] https://www.ultrasoundleadershipacademy.com/wp-content/uploads/2013/12/SUSS_IT.pdf
[5] https://en.wikipedia.org/wiki/Focused_assessment_with_sonography_for_trauma
[6] https://litfl.com/pocus-made-easy-efast/
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC10413405/
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC7807983/
[9] https://www.acep.org/sonoguide/basic/fast
[10] https://journal.astes.org.al/AJTES/index.php/AJTES/article/view/390
[11] http://www.revistamedicinamilitara.ro/wp-content/uploads/2021/07/Evaluation-of-the-accuracy-of-E-FAST-ultrasound-in-blunt-trauma-patients-referred-to-the-Emergency-Department.pdf
[12] https://academicmed.org/Uploads/Volume5Issue1/58-50.-JAMP_Shaiji-P.S-280-285.pdf
[13] https://pmc.ncbi.nlm.nih.gov/articles/PMC9568351/
[14] https://pubmed.ncbi.nlm.nih.gov/31385566/
[15] https://pmc.ncbi.nlm.nih.gov/articles/PMC5832486/

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11
Q

[22B11] A 75-year-old man presents with an acute dissection of the descending thoracic aorta. His blood pressure measures 190/110 mmHg. Justify your plan for his preoperative blood pressure management. (30%)

Describe the potential complications of thoracic endovascular aortic repair (TEVAR) and how you would mitigate them. (70%)

Pass rate 37.3%

A

Preoperative Blood Pressure Management
In acute Type B aortic dissection, immediate blood pressure control aims to reduce aortic shear stress and prevent propagation. Initial targets are systolic BP 100–120 mmHg and heart rate - < 70 bpm using intravenous beta-blockers (e.g., esmolol, labetalol) as first-line therapy, supplemented by vasodilators (e.g., nicardipine) if needed123. This “anti-impulse” strategy balances minimizing aortic wall stress while maintaining end-organ perfusion, particularly in patients with baseline hypertension23.

  • CSF drainage for high-risk cases (e.g., long aortic coverage, prior AAA repair)15
    Maintain MAP >90–100 mmHg perioperatively[1][6]- Staged procedures to preserve collateral circulation[7] |
    | Stroke | - Revascularize left subclavian artery if coverage is necessary[1][5]- Embolic protection devices in atheromatous arches[4][7] |
    | Endoleaks | - Ensure adequate proximal/seal zones during graft deployment[4][7]- Regular imaging surveillance[7] |
    | Renal Failure | - Preoperative hydration, minimize contrast load[1]- Avoid nephrotoxic agents, consider renal artery perfusion[4] |
    | Access Site Injury | - Ultrasound-guided femoral access[4][7]- Use closure devices or surgical repair for large sheaths[7] |

Key Considerations
- Uncomplicated Type B dissections are managed medically initially; TEVAR is reserved for complications (malperfusion, rupture)[3][8].
- Post-TEVAR blood pressure goals shift to 120–140/80–90 mmHg long-term to prevent residual dissection progression[2][3].

Citations:
[1] https://www.annalscts.com/article/view/16874/html
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC5465133/
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC4128933/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC7644296/
[5] https://evtoday.com/articles/2014-nov/neurologic-protection-during-tevar
[6] https://pmc.ncbi.nlm.nih.gov/articles/PMC2763456/
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC10148752/
[8] https://tsaco.bmj.com/content/6/1/e000678
[9] https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/thoracic-endovascular-aortic-repair

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Mnemonics for TEVAR Complications
A concise mnemonic for TEVAR complications is “SCARED”:
- Spinal cord ischemia
- CVA (stroke)
- Access site injury
- Renal failure
- Endoleaks
- Device complications (graft collapse/migration)

Key Complications and Mitigation
1. Spinal cord ischemia:
- Prevent: CSF drainage for high-risk cases (e.g., long-segment coverage, prior AAA repair)[2][5].
- Maintain MAP >90–100 mmHg perioperatively[2][4].

  1. Stroke:
    • Avoid emboli: Revascularize left subclavian artery (LSA) if coverage is required[4][2].
    • Minimize aortic arch manipulation in atheromatous disease[2][4].
  2. Access site injury:
    • Prevent: Ultrasound-guided femoral access and closure devices[3].
  3. Renal failure:
    • Hydrate preoperatively and limit contrast use[2][3].
  4. Endoleaks:
    • Ensure adequate proximal/distal seal zones during deployment[2][3].
  5. Graft collapse/migration:
    • Avoid oversizing (>15–30% aortic diameter)[2][3].

Critical Insight
Neurological complications (stroke, spinal ischemia) account for up to 30% of fatal outcomes[4][5]. LSA coverage without revascularization doubles posterior circulation stroke risk[4].

Citations:
[1] https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/thoracic-endovascular-aortic-repair
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC7644296/
[3] https://www.upmc.com/services/heart-vascular/services/procedures/tevar
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC6325786/
[5] https://tsaco.bmj.com/content/6/1/e000678

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12
Q

SAQ Discuss the advantages and disadvantages of the use of neuromuscular blocking drugs in a patient admitted to the intensive care unit. Pass rate 48.0%

A

Pros
1. Improved O2
2. MV
3. Red ICP
4. Prev self injury
5. Improve surgical cond

Cons
1. Muscle weakness and atrophy - ICUAW
2. CIM
3. Masking neuro signs
4. Haemodynamic effects
5. Awareness
6. Pressure ulcer
7. Allergies

Neuromuscular blocking agents (NMBAs) in ICU patients offer specific benefits but require careful risk-benefit analysis due to significant complications. Their use is justified in select scenarios but demands vigilant monitoring and adherence to evidence-based protocols.

Advantages
1. Facilitates mechanical ventilation
- Reduces ventilator-patient asynchrony, improving oxygenation in ARDS (PaO₂/FiO₂ 48 hours) correlates with ICU-acquired weakness, particularly when combined with corticosteroids or sepsis[1][2][4]. Retrospective studies in asthma patients show a 30% myopathy rate with NMBA infusions[2].

2. Risk of awareness
- NMBAs lack sedative/analgesic properties; inadequate sedation exposes patients to paralysis without amnesia, risking psychological trauma[2][4].

3. Other complications
- Prolongs mechanical ventilation duration and ICU stay (13% of ventilated patients in a 5,183-patient study)[1][4].
- Increases pneumonia risk due to impaired cough reflex[2][4].
- Corneal abrasions, deep vein thrombosis, and anaphylaxis[2][4].

Monitoring & Mitigation
- Quantitative monitoring (e.g., train-of-four) is mandatory to avoid overdose and residual paralysis[3][4].
- Daily sedation holds and NMBA interruption assess ongoing necessity[2][4].
- Avoid concomitant corticosteroids when possible to reduce CIM risk[2][4].

Key omission in poor answers: Failure to address awareness prevention (via adequate sedation/analgesia) and CIM pathophysiology[1].

Citations:
[1] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/840e79c1-fa2c-4f44-87de-927f4020284f/2023.2-Final-Exam-Report.pdf
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC6645848/
[3] https://clinicalview.gehealthcare.com/white-paper/neuromuscular-blockade-intensive-care-unit
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC9528036/

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https://clinicalview.gehealthcare.com/white-paper/neuromuscular-blockade-intensive-care-unit

To memorize the key advantages and disadvantages of neuromuscular blocking agents (NMBAs) in ICU, use the PROS vs. CONS mnemonic:

PROS (Advantages)
PProne positioning in severe ARDS (e.g., ACURASYS trial: reduced mortality with cisatracurium)[3]
RReduces ventilator asynchrony (improves lung-protective ventilation)[3]
OOxygenation optimization (enhances chest wall compliance)[3]
SStabilizes critical states (controls ICP, intra-abdominal hypertension)[3]

CONS (Disadvantages)
CCritical illness myopathy (prolonged infusions + corticosteroids increase risk)[3]
OOxygen dependency (prolongs mechanical ventilation duration)[3]
NNo sedation/analgesia (risk of awareness without amnesia)[4][5]
SSide effects (pneumonia, DVT, corneal abrasions)[3][4]

Key Monitoring Points
- Quantitative TOF monitoring mandatory to avoid overdose[2][3].
- Always pair NMBAs with adequate sedation/analgesia[4].
- Daily NMBA interruption to reassess necessity[3].

This mnemonic highlights high-yield exam topics, emphasizing awareness prevention and CIM pathophysiology, which were common omissions in weaker answers.

Citations:
[1] https://www.youtube.com/watch?v=eTYxzLw6jeo
[2] https://elsevier.health/en-US/preview/neuromuscular-blocking-agents
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC9528036/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC6385733/
[5] https://www.ismp.org/sites/default/files/attachments/2018-03/20160616.pdf

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13
Q

[22B13] Compare the algorithms for advanced life support of adults and term newborns and explain the rationale for the differences. Pass rate 74.7%

A

Neonatal and adult advanced life support (ALS) algorithms differ significantly due to distinct etiologies of arrest and physiological adaptations. Newborn resuscitation prioritizes ventilation, while adult ALS focuses on circulatory support.

Algorithm Differences
|————————-|———————————————————————————–|—————————————————————————-|
| Primary Cause | Respiratory failure (hypoxia/apnoea)[4][8] | Cardiac origin (e.g., ventricular fibrillation, coronary ischemia)[9] |
| Initial Steps | Dry, warm, assess breathing. Begin ventilation if apnoeic/gasping[2][8] | Immediate chest compressions + early defibrillation[3][9] |
| Compression:Ventilation Ratio | 3:1 (3 compressions : 1 breath)[6] | 30:2 (30 compressions : 2 breaths)[3][6] |
| Compression Depth | 1/3 anterior-posterior chest depth[1][2] | ≥5 cm (adults)[3] |
| Adrenaline Dose | 10–30 mcg/kg IV/IO (umbilical vein preferred)[2] | 1 mg IV/IO every 3–5 minutes[9] |
| AED Use | Not recommended (manual defibrillator with paediatric pads if <1 year)[3][6] | Immediate application with standard pads[3][9] |
| Airway Management | Face mask/PEEP, with prolonged (2–3 sec) initial inflations[8] | Bag-mask ventilation, advanced airway early[9] |

Rationale for Differences
1. Etiology of Arrest
- Newborns: Arrest is respiratory-driven (e.g., failure to initiate breathing, placental insufficiency)[4][8]. Effective ventilation rapidly improves heart rate and oxygen delivery.
- Adults: Arrest is cardiac-driven (e.g., ventricular fibrillation), requiring immediate compressions to maintain coronary perfusion[9].

  1. Physiological Adaptations
    • Newborn myocardium relies on glucose and is hypoxia-tolerant for minutes via anaerobic metabolism, but requires adequate lung aeration to reverse acidosis[4][8].
    • Adults depend on aerobic metabolism; prolonged ischemia causes irreversible organ damage, necessitating rapid circulation[9].
  2. Ventilation Priorities
    • Newborns: Higher initial inspiratory pressures (20–30 cmH₂O) to clear lung fluid, with PEEP to establish functional residual capacity[8].
    • Adults: Lower tidal volumes (6–7 mL/kg) to avoid barotrauma[3].
  3. Drug Dosing
    • Neonatal adrenaline doses are weight-adjusted due to immature hepatic/kidney function and lower blood volume[2].

Examiner Note: Higher-scoring answers integrate physiological principles (e.g., transition from fetal circulation, myocardial resilience to hypoxia) and cite exact compression ratios/doses per ANZCOR guidelines[1][2][6].

Citations:
[1] https://www.resus.org.nz/assets/Uploads/ANZCOR-Guideline-13.8-April-2021.pdf
[2] https://www.resus.org.nz/assets/Uploads/Neonatal-Resuscitation-All-Guidelines.pdf
[3] https://www.mycprcertificationonline.com/important-cpr-difference-between-adult-child
[4] https://www.anzcor.org/home/neonatal-resuscitation/physiology-of-birth-asphyxia/
[5] https://www.avive.life/blog/what-are-the-common-causes-of-cardiac-arrest-in-infants-and-children
[6] https://ronlitman.substack.com/p/resuscitation-of-infants-can-different
[7] https://www.ahajournals.org/doi/10.1161/01.CIR.95.8.2185
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC8606598/
[9] https://www.msdmanuals.com/professional/critical-care-medicine/cardiac-arrest-and-cardiopulmonary-resuscitation-cpr/cardiac-arrest
[10] https://www.resus.org.uk/library/2021-resuscitation-guidelines/paediatric-advanced-life-support-guidelines
[11] https://brisbanefirstaidcourses.com.au/blog/what-is-the-difference-between-adult-and-infant-cpr/
[12] https://www.anzcor.org/assets/anzcor-guidelines/guideline-11-2-protocols-for-adult-advanced-life-support-237.pdf
[13] https://www.rch.org.au/trauma-service/manual/how-are-children-different/
[14] https://www.resus.org.nz/assets/Guidelines/ANZCOR-Guideline-12.2-Paediatric-Advanced-Life-Support-PALSNov-2021.pdf
[15] https://resus.com.au/paediatric-resuscitation-guideline/
[16] https://www.aed.com/blog/what-are-the-differences-between-infant-child-and-adult-cpr/
[17] https://www.anzcor.org/home/paediatric-advanced-life-support/guideline-12-1-paediatric-basic-life-support-pbls-for-health-professionals/downloadpdf
[18] https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines
[19] https://www.youtube.com/watch?v=JjtX3m7lLDQ
[20] https://www.ahajournals.org/doi/10.1161/CIR.0000000000000901
[21] https://www.avive.life/blog/differences-infant-child-adult-cpr
[22] https://www.childrens.health.qld.gov.au/__data/assets/pdf_file/0031/179725/how-children-are-different-anatomical-and-physiological-differences.pdf
[23] http://www.gcs16.com/uploads/1/7/9/2/17925143/18_-_als-paediatric-summary-of-changes.pdf
[24] https://pubmed.ncbi.nlm.nih.gov/22887927/
[25] https://www.anzcor.org/home/neonatal-resuscitation/guideline-13-1-introduction-to-resuscitation-of-the-newborn/downloadpdf
[26] https://defibsplus.com.au/important-differences-between-adult-child-and-infant-cpr/
[27] https://www.nhlbi.nih.gov/health/cardiac-arrest/causes
[28] https://www.resus.org.uk/print/pdf/node/11331
[29] https://thefirstaidnest.com.au/2024/01/05/newborns-to-school-age-the-differences-cpr/
[30] https://www.mayoclinic.org/diseases-conditions/sudden-cardiac-arrest/symptoms-causes/syc-20350634
[31] https://www.ncbi.nlm.nih.gov/books/NBK572069/
[32] https://www.anzcor.org/home/paediatric-advanced-life-support/guideline-12-2-paediatric-advanced-life-support-pals/downloadpdf
[33] https://www.anzcor.org/home/neonatal-resuscitation/guideline-13-3-assessment-of-the-newborn/downloadpdf
[34] https://www.ahajournals.org/doi/10.1161/CIR.0000000000000902
[35] https://www.ahajournals.org/doi/10.1161/circ.102.suppl_1.I-253
[36] https://www.healthychildren.org/English/health-issues/injuries-emergencies/sports-injuries/Pages/Sudden-Cardiac-Death.aspx

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Parameter | Term Newborns | Adults |

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14
Q

[22B14] A patient has undergone an eight-hour elective cervical spine fusion involving both anterior and posterior approaches. Outline your approach to the extubation of this patient. Pass rate 56.0%

A

The extubation plan for this patient involves a cautious, multidisciplinary approach due to the high risk of airway compromise from combined anterior-posterior cervical fusion. Key considerations include:

1. Timing of extubation
- Delay extubation for ≥24 hours postoperatively to allow airway swelling assessment[1][4]
- Use overnight intubation with continuous airway monitoring[3][5]

2. Airway swelling evaluation
- Perform quantitative cuff leak test (CLT) with threshold >110 mL[1][4]
- Assess for audible air leak and check prevertebral soft tissue swelling via X-ray (C2/C5 measurements)[2][3]

3. Preparation for difficult reintubation
- Maintain cervical immobilization during extubation[6]
- Have advanced airway equipment available:
- Fiberoptic bronchoscope[1][4]
- Airway exchange catheter[6]
- Surgical tracheostomy kit[1][6]

4. Safety protocol
- Require consensus between ICU, anesthesia, and neurosurgery teams[1][4]
- Extubate in controlled environment during daytime with full staff availability[1][5]
- Consider prophylactic tracheostomy if:
- Failed CLT by POD3[1]
- Massive intraoperative swelling[5]
- Prolonged surgery (>10h)[2][5]

This approach balances airway protection with timely extubation while maintaining contingency plans for emergent reintubation[1][4][6]. Post-extubation monitoring in ICU for ≥24 hours is essential given delayed swelling peaks at 48-72 hours[2][3].

Citations:
[1] https://www.e-neurospine.org/upload/pdf/ns-1938382-191.pdf
[2] https://jkms.org/DOIx.php?id=10.3346%2Fjkms.2018.33.e77
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC6853803/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC7538349/
[5] https://jss.amegroups.org/article/view/6570/html
[6] https://www.thieme-connect.com/products/ejournals/pdf/10.1055/s-0039-1700806.pdf

Answer from Perplexity: pplx.ai/share

In their approach to extubation of this patient candidates were required to demonstrate an understanding of
the importance of:
* an assessment for the timing of extubation
* the potential for airway swelling
* the potential for difficult re-intubation
* ultimately having a safe plan for extubation.
The pass rate reflects that in general candidates were able to outline the main points of concern and provide a safe extubation plan. However, a fairly high number of answers having made some good points were missing one of the key points, and therefore could not achieve the pass mark.

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15
Q

[22B15] The following is the venous blood gas (VBG) result of a five-week-old infant with pyloric stenosis.
Parameter Result Reference Range
pH 7.50 7.32-7.42
pCO2 50 38-52 mmHg
HCO3 38 19-25 mmol/l
Base excess +5 -3 − +3
Sodium 129 136-145 mmol/l
Potassium 3.6 4.0-6.2 mmol/l
Chloride 92 100-110 mmol/l
Interpret this VBG.
Describe your preoperative resuscitation and justify your criteria for proceeding to surgery. PR 70.7%

A

The venous blood gas reveals a hypochloraemic metabolic alkalosis (pH 7.50, HCO₃⁻ 38 mmol/L, Cl⁻ 92 mmol/L) with compensatory respiratory acidosis (pCO₂ 50 mmHg). Electrolyte disturbances include hyponatraemia (129 mmol/L), hypokalaemia (3.6 mmol/L), and hypochloraemia, consistent with prolonged vomiting in pyloric stenosis. Gastric acid loss depletes H⁺ and Cl⁻, prompting renal retention of HCO₃⁻ and paradoxical aciduria (K⁺/H⁺ excretion) to conserve Na⁺, exacerbating alkalosis and hypokalaemia[1][2].

Preoperative Resuscitation
1. Fluid replacement:
- 0.9% NaCl + KCl (20–40 mmol/L) at 1.5× maintenance (e.g., 150 mL/kg/day) to correct chloride deficit and dehydration.
- Bolus (10–20 mL/kg) if hypovolaemic (tachycardia, prolonged capillary refill).

  1. Electrolyte monitoring:
    • Target Cl⁻ >100 mmol/L, K⁺ >4.0 mmol/L, and HCO₃⁻ 1 mL/kg/hr and restored euvolaemia (normal heart rate, capillary refill).

Criteria for Proceeding to Surgery
- Biochemical:
- Chloride >100 mmol/L
- Bicarbonate <30 mmol/L
- Base excess normalised (±3).
- Clinical:
- Established urine output and normovolaemia.

Delaying surgery until resuscitation is complete reduces risks of apnoea, arrhythmias, and anaesthetic instability from electrolyte imbalances[1][2]. Over-resuscitation with excessive fluid delays intervention, while under-resuscitation increases perioperative morbidity.

Mechanism: Vomiting → gastric H⁺/Cl⁻ loss → metabolic alkalosis → renal HCO₃⁻ retention and K⁺/H⁺ excretion → worsening hypokalaemia and paradoxical aciduria.

Guidelines: RCH/QCH emphasise chloride-guided resuscitation to reverse alkalosis and ensure safe anaesthesia induction[1][2].

Citations:
[1] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/3692bdce-93b2-4aee-9e97-df1f27aa2ca8/2022.2-FEx-Examination-Report.pdf
[2] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/f02192b3-762f-400e-aed9-e105bd0c102e/2023.1-Final-Exam-Report.pdf
[3] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/3578987c-01c4-4d61-8f11-d3fc75733d49/2024.2-Final-Examination-Report.pdf
[4] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/840e79c1-fa2c-4f44-87de-927f4020284f/2023.2-Final-Exam-Report.pdf
[5] https://ppl-ai-file-upload.s3.amazonaws.com/web/direct-files/collection_65793a3a-12f3-4917-b8d9-24d50f295927/5bf7e650-12b2-433f-9d62-685af9ffa428/2024.1-Final-Exam-Report.pdf
[6] https://www.rch.org.au/clinicalguide/guideline_index/Pyloric_stenosis/
[7] https://teachmepaediatrics.com/surgery/abdominal/pyloric-stenosis/
[8] https://www.cahs.health.wa.gov.au/~/media/HSPs/CAHS/Documents/Health-Professionals/Neonatology-guidelines/Pyloric-Stenosis.pdf?thn=0

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