ICU Fellowship Vivas – SAH, LA toxicity, Difficult Airway

Dr Swapnil Pawar August 20, 2021 245 3

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    ICU Fellowship Vivas – SAH, LA toxicity, Difficult Airway
    Dr Swapnil Pawar

Written by Dr Madhuri Anupindi

1. Previously well 55-year old female WFNS 1, Fisher 3 SAH from an Acom aneurysm which occurred yesterday. She has been stable in ICU with a GCS of 15, a BP of 120/80mmHg and no focal neurological deficit since her admission. She has just returned from an endovascular procedure to secure the aneurysm with GCS 14 (confused), HR 59, BP 140/80mmHg. How would you assess this patient?

I am concerned that she has had a deterioration in neurology which may be secondary to complications from the subarachnoid itself such as rebleed, complications from the intervention such as bleeding, thromboembolism or the anaesthetic, or secondary to another medical cause such as a metabolic disturbance. The assessment would involve a focused history, examination and further investigations.



  • SAH history: grade, previous CT, BP control,
  • Co-morbidities/allergies, previous anaesthetics, drug history, regular meds, anticoagulants
  • Intervention and anaesthetic details: any complications, imaging, BP control, recent blood tests, mannitol/other meds given, specific meds


  • Vitals, temp, sats
  • Full neuro assessment
  • Vascular access site


  • Bedside: BSL, ECG, ABG
  • Bloods: FBC, UEC, CMP, coags, LFT, G+H
  • CTB +/- CTA if ongoing concerns

Describe your initial management.

Initial management

  • Ensure stability: ABCs,
    • Optimise sats, BP 120 – 150mmHg or 100 – 140mmHg if concerns re re-bleed, IV access
  • Evaluate cause this may be just secondary to anaesthetic but want to exclude cerebral complication (as described earlier)
  • Notify relevant teams: INR/Neurosurg
  • Specific management
    • Depends on the findings of the assessment
  • Supportive management
    • Neuroprotective measures
    • Nimodipine
    • Keep NBM

What are the potential complications from aneurysmal SAH?


  • Delayed cerebral ischaemia
  • Rebleeding
  • Hydrocephalus
  • Parenchymal haematoma
  • Intracranial hypertension
  • Seizures


  • Takotsubo’s cardiomyopathy
  • Arrhythmias
  • Hypotension/hypertension


  • Neurogenic pulmonary oedema


  • Electrolyte imbalance: hypo/hypernatremia
  • Fever
  • Hypoglycaemia/hyperglycaemia
  • Liver dysfunction


  • AKI

From interventions

  • Complications from vascular access
  • Ventriculitis

From ICU stay

  • Infection
  • Complications from intubation/ventilation
  • Delirium
  • Critical illness polyneuropathy
  • Thromboembolic disease
  • Stress ulcers

What is the role of Nimodipine in the management of aneurysmal SAH?


  • Cerebral vasospasm can occur in up to 40% of SAH patients and has significant morbidity and mortality
  • Difficult to detect clinically and may cause damage once occurs should try to prevent the same.
  • Nimodipine is a dihydropyridine calcium channel blocker that is thought to preferentially dilate cerebral vessels compared to peripheral vessels
  • May prevent neuronal damage by preventing the influx of Ca but the exact mechanism of benefit in SAH is unknown


  • Can be given PO, IV or intra-arterially at angio
  • The usual route is orally 60mg q4h for 21 days


  • Easy to administer, multiple routes available
  • Cheap
  • Reasonably safe


  • Can cause hypotension – some patients require high doses of vasopressors to counteract same which increases their risk of adverse effects from the vasopressors as well as from the arterial line/CVC required
  • May cause nausea, flushing,


  • Class 1 level A recommendation by American Heart Association management of aneurysmal SAH
  • BRANT trial 1989
    • Multicentre RCT of 554 patients with aneurysmal SAH found nimodipine decreased cerebral infarction and morbidity but had no effect on mortality
  • Cochrane review in 2007 of over 3000 patients has found it decreases the risk of poor outcomes in patients with aneurysmal SAH

Nimodipine is part of the current standard of care in aneurysmal SAH.

What are the advantages and disadvantages of coiling compared to clipping of an aneurysm after SAH?


  • Technical
    • Minimally invasive – does not require a craniotomy
    • Decreased cost
    • Greater ability to access and treat posterior fossa aneurysms
  • Patient-related
    • Improved independent survival at 1 year
    • Less risk of cognitive decline or epilepsy


  • Technical
    • Requires skilled operator and INR facilities
    • Inability to deal with major complications: would require neurosurgery
    • Fewer aneurysms completely obliterated
    • Smaller aneurysms < 3mm are impossible to coil
  • Patient-related
    • Greater risk of rebleeding
    • Requires anticoagulation

2. You are caring for a previously well 60M after an MBA yesterday. He has isolated chest injuries (bilateral rib fractures and pulmonary contusions). He has been stable in the ICU overnight receiving HFNP with multimodal analgesia including PCA. The anaesthetic registrar has just left after inserting a thoracic epidural when the bedside nurse calls for assistance. The patient has become disoriented and agitated with HR 55 in SR, BP 78/39, sats 88% on 40% HFNP with poor trace. Explain the likely causes for the deterioration.

My primary differential is local anaesthetic toxicity. Other likely causes include

  • Complications from thoracic epidural
    • Pneumothorax
    • Respiratory depression (less likely this early)
    • Thoracic haematoma
  • Unrelated to insertion
    • Secondary to trauma unrecognised injury
    • Respiratory
      • Pulmonary embolism
      • Aspiration
      • Worsening hypoxic respiratory failure secondary to thoracic trauma
      • Pulmonary haemorrhage
    • Cardiovascular
      • Myocardial infarction
      • Left ventricular failure secondary to cardiac contusion

What factors increase the risk of local anaesthetic toxicity?

Drug-related factors

  • Assigned a cardiovascular collapse: CNS ratio (ratio of drug dose required to cause cardiac collapse to the drug required to cause seizures) those with higher ratio have a greater margin of safety (early CNS symptoms may allow intervention to prevent subsequent arrest)
    • Bupivacaine has the lowest CC: CNS ratio, lignocaine has the highest

Block factors

  • Injection into a highly vascular site
  • Blocks that require large volumes and doses of local anaesthetic e.g. epidural
  • Whether it was co-administered with a vasoconstrictor (increased max dose if with adrenaline)
  • Continuous infusions

Patient factors

  • Extremes of age
  • Obesity – as if the maximum safe dose is calculated using actual rather than ideal body weight
  • Low alpha 1 acid glycoprotein levels
  • Hyperdynamic circulation e.g. pregnancy
  • Pre-existing cardiovascular disease, low cardiac output state, hepatic or renal dysfunction
  • Concomitant use of

This patient is thought to have local anaesthetic toxicity. How would you manage them?


  • Stop local anaesthetic!
  • Resuscitation
    • A – intubate if required
    • B – 100% fio2, avoid acidosis – HCO3/hyperventilate prevent hypoxia and acidosis as they potentiate LAST
    • C – CPR if needed, IV access, monitoring, IVF, inotropes may require prolonged CPR
      • If arrhythmias give amiodarone not lignocaine or other sodium channel blockers
    • D – sedation, avoid seizures – midazolam
  • Specific
    • Lipid emulsion 20% intralipid 1.5ml/kg over 1 minute, can give a max of 2 repeat boluses at 5-minute intervals if not haemodynamically stable then start infusion 0.25ml/kg/min
      • Continue infusion until HD stability restored
      • Max total dose = 12ml/kg
  • Organisational
    • Check dose of local anaesthetic given and if correct dose/technique
    • Critical incident notification
    • Open disclosure

3. A previously well 33M (90kg 182cm tall) is admitted post handing attempt. The paramedics were only able to pass a standard size 6 ETT. This is secured at 24cm and shortened to a total length of 27cm (pre-hospital transport policy). What are the potential airway problems in a patient after a hanging attempt?

Airway problems

  • Traumatic oedema of the larynx and supraglottic tissues causing upper airway obstruction
  • Laryngeal, cricoid or hyoid bone fractures or contusions
    • Cricoid most serious as the only complete ring can lead to complete airway obstruction
  • Tracheal perforation/disruption or laryngotracheal separation
  • Injury to vasculature
    • Compression of carotid against transverse process of 4th – 6th vertebra haemorrhage can lead to haematoma, thrombosis or thromboembolism
  • Difficulties of intubation itself
    • Maintain inline stabilisation, difficulty intubating in sub-optimal conditions
    • Distortion of anatomy with cricothyroidotomy
    • Supra-glottic airways can be counterproductive
    • May have hypoxia from hanging, aspiration, neurogenic or post obstructive pulmonary oedema
    • May have a spinal injury with neurogenic shock

What problems might you encounter with a size 6 ETT in this patient?

Problems with size 6 ETT:

  • Increased resistance
    • Higher peak airway pressures
    • Increased work of breathing
    • Requires humidified circuit
  • Difficulties with width
    • Difficulties with suctioning
    • Difficulties placing bronchoscope down
    • May have increased leak once airway oedema improves
    • Increased risk of obstruction
  • Cut at 27cm
    • Progressing to tracheostomy will be difficult
    • May dislodge


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