ICU Fellowship Vivas – Can’t Intubate, Can’t Ventilate & C-Spine Injury

Dr Swapnil Pawar December 24, 2021 376

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    ICU Fellowship Vivas – Can’t Intubate, Can’t Ventilate & C-Spine Injury
    Dr Swapnil Pawar


Written by – Dr Madhuri Anupindi

  1. Urgent review of 72M with a BMI of 40 who was recently admitted to ICU following an apparently uneventful elective R carotid endarterectomy. He is complaining of SOB and is refusing to lie flat. He has the following observations: sats 93% on 15L o2, stridor and RR of 40/min, HR 120, BP 200/110mmHg. Describe your immediate management priorities.

This is a life-threatening situation as this patient has signs of acute airway obstruction with a high risk of complete loss of his airway. My priorities are to urgently secure this gentleman’s airway, ensure adequate oxygenation and haemodynamic optimisation, and simultaneous assessment and management of the cause of his obstruction. My main concern would be an expanding haematoma causing external airway compression but other causes could be anaphylaxis, residual neuromuscular blockade, post-extubation stridor, or less likely recurrent laryngeal nerve injury.


  • I would initially call for urgent further assistance from ICU staff and both anaesthetics and ENT as this gentleman is likely to have a very difficult airway with a high likelihood of requiring a surgical airway. I would also notify the admitting surgical team.
  • While the ideal environment for securing his airway would be in OT, unlikely to be safe for transfer to OT and more likely to have to do this in ICU
  • Allocate airway person x 2, assistant, drugs, front of neck, scribe and runner, team leader

Airway management

  • Assess airway
    • Keep sitting up and quick information about previous airway grade (although likely to have changed)
    • BVM difficulties
    • Neck anatomy
  • Assess for the cause of obstruction:
    • neck haematoma ? expanding à remove sutures to decompress haematoma
    • rash, urticaria, signs of anaphylaxis à adrenaline (although very hypertensive)
  • Prepare and plan for intubation
    • Pre-oxygenate HFNP +++, apnoeac oxygenation and all monitoring in situ, all equipment present and checked airway adjuncts – NPA/guedels, suction, etoc2, ETT, LMA, bougie/stylet, bronchoscope, front of neck access
    • Prepare patient: inform of the plan, keep calm
    • Have concrete intubation plan including a plan if failure and ensure the whole team is aware of the plan
      • Most experienced operator (will likely be challenging due to significant oedema and loss of anatomical landmarks and patient’s obesity)
      • All staff aware of the plan including failure/emergency plans for example:
      • Plan A CMAC D blade with stylet, ramping, RSI as unlikely to tolerate awake intubation and more familiarity
      • Plan B: BVM with adjuncts with the urgent front of neck access (LMA unlikely to be suitable in airway obstruction)
        • Prepared for surgical airway: difficult landmarks, horizontal incision with blunt dissection for anatomy, ENT scrubbed
      • Ventilator set up to minimise apnoea time, ETCO2 attached to BVM

Optimise haemodynamics

  • IV access large-bore x 2 at least, arrest trolley, resus drugs
  • Control BP to minimise bleeding: boluses hydralazine

Outline three techniques that could be considered to secure this gentleman’s airway and their advantages and disadvantages?

There are several techniques available to secure this gentleman’s airway, choice of which will depend on equipment, staff availability, experience and personal preference.

Rapid sequence induction with video laryngoscope and high dose of paralysis:

  • Advantages: staff familiarity, facilitates rapid airway access, the patient can remain sitting up until post-induction, can use normal laryngoscope if required (e.g. if a lot of bleeding in the airway), can have the second operator with ETT loaded on the bronchoscope
  • Disadvantages: can lose airway control, may be difficult to position patient post-induction

Awake intubation

  • Advantages: maintains patients own respiratory effort and avoids paralysis
  • Disadvantages: may not obtain an optimal view, may cause patient distress and discomfort if inadequate local anaesthetic/sedation used, less familiarity amongst staff, not possible if the patient is in extremis, positioning can be difficult

Awake fibreoptic intubation

  • Advantages: maintains patients own respiratory effort and avoids paralysis, the patient can remain sitting up
  • Disadvantages: scope can obstruct the airway inlet in the stridulous awake patient, requires expertise, the view can be obstructed by blood/secretions


This patient undergoes an RSI and is unable to be intubated by the anaesthetist despite optimisation strategies. He is unable to be effectively oxygenated using supraglottic devices or a bag valve mask. You decide to perform a cricothyroidotomy. How is this performed?

This is a life-threatening situation and a can’t intubate can’t oxygenate emergency situation should be declared. 100% Oxygen should be still administered via the upper airway and the patient should be appropriately anaesthetised and paralysed. They should be positioned with the neck extended and all monitoring in situ and necessary equipment available including emergency drugs and the arrest trolley.

Equipment required for the cricothyroidotomy is a scalpel, bougie, cuffed size 6 ETT, lubricant, 10ml syringe, tube ties, end-tidal co2. The technique used depends on whether the cricothyroid membrane is palpable or not (it may not be in this gentleman due to his obesity).

If cricothyroid membrane palpable:

  • Transverse stab incision through a membrane with the scalpel
  • Turn scalpel 90 degrees (sharp edge caudally)
  • Slide tip of bougie along with the scalpel and into the trachea
  • Railroad a lubricated size 6 ETT over the bougie and into the trachea
  • Remove bougie
  • Inflate the cuff, attach etoco2 and confirm the position with capnography
  • Secure ETT

Impalpable cricothyroid membrane

  • Make an 8 – 10cm vertical skin incision caudad to cephalad
  • Use blunt dissection with fingers of both hands to separate the tissues
  • Identify and stabilise the larynx
  • Proceed with the technique for palpable cricothyroid membrane as outlined earlier

Post cricothyroidotomy care:

  • Ensure patient is well sedated, ETT is secure, they are ventilating/oxygenating well on appropriate ventilator settings and that their haemodynamics are stable
  • ENT contacted and plan in place for formal tracheostomy
  • The initial cause of upper airway obstruction was identified and treated
  • Team/staff aware of difficult airway and that there are signs and education of staff about what to do if the airway becomes obstructed/lost
  • Documentation
  • Update family
  • Quality assurance: review about the process and how to improve in the future
  1. 66M in ED who fell from a height and complaining of neck pain and weakness in all four limbs. He was intubated shortly after admission for rapid shallow breathing and hypoxia. His current BP is 75/40mmHg. Describe your management.

This gentleman has had a significant trauma with a likely cervical spinal cord injury. He requires initial resuscitation and management as per ATLS guidelines including a primary survey, secondary survey, definitive management and supportive management.

Airway and C spine:

  • Confirm ETT in appropriate position with normal ETCO2
  • Full spinal precautions need to be maintained

Breathing and ventilation

  • Lung protective ventilation 6 – 8ml/kg, assess for air entry and signs of chest trauma
  • Aim sats > 92%
  • Evaluate for pneumo/tension pneumothorax à decompress chest if present
  • CXR confirm ETT position and look for injury


  • Adequate IV access, full BP/HR monitoring
  • Has significant hypotension which in this setting of trauma can be due to multiple causes including bleeding from an injury, obstructive shock from tension pneumothorax or tamponade, distributive shock from spinal cord injury, anaphylaxis or secondary to induction agents.
  • Assess for signs of significant bleeding and aim control same
  • Bloods for FBC, UEC, LFT, CMP, coags, fibrinogen, ABG, G+H, consider etoh level
  • Fast scan
  • IV fluid bolus, blood products if signs of bleeding
  • Likely to require CVC and vasopressor support: can start peripheral if good IV access à BP targets hard to know, need to exclude bleeding as may have permissive hypotension initially
    • If bleeding excluded and thought to be purely neurogenic then hypertense for cord perfusion


  • Difficult to assess now intubated but see if neurology including anal tone recorded earlier
  • Check for priapism/reflexes if paralysis worn off


  • Log roll, look at back for other injuries
  • Temp: keep normothermia
  • BSL
  • IDC
  • CT pan scan including C spine given mechanism and findings
    • Potentially MRI depending on stability

Secondary survey

Definitive management of injuries

  • OT/interventional radiology
  • Will require ICU admission

Supportive management

  • PPI
  • Update family
  • DVT prophylaxis: mechanical initially

How would you clinically assess this patient’s level of injury?

The patient’s level of spinal injury is assessed using the American Spinal Injury Association (ASIA) Impairment Scale. This involves a standardised examination consisting of a myotomal based motor exam, dermatomal based sensory exam and an anorectal exam. The findings of these exams then determine the injury grade and level. This assessment is often done later during the admission as it requires resolution of any neurogenic shock, the absence of distracting injuries, and for the patient to be alert, co-operative and able to communicate, respond and follow commands.

ASIA Classification

  1. Determine sensory level for right and left side
    1. Sensory level is most caudal intact dermatome for both pin prick and light touch sensation
  2. Determine motor level for right and left side
    1. Defined by lowest key muscle function that has a grade of at least 3/5, providing the key muscle functions represented by the segments above that level are intact (5/5)
    2. In regions where there is no myotome to test, the motor level is presumed to be the same as the sensory level if testable motor function above that level is also normal
  3. Determine the neurological level of injury
    1. Most caudal segment of the cord with intact sensation and antigravity (3 or more) muscle function strength, provided that there is normal sensory and motor function rostrally
  4. Determine whether injury is complete or incomplete
    1. No voluntary anal contraction AND S4-5 sensory scores = 0 AND deep anal pressure = No then injury is complete
    2. Otherwise injury is incomplete
  5. Determine ASIA impairment scale grade
    1. Injury complete = AIS A
    2. Injury sensory incomplete = AIS B
      1. Sensory but not motor function is preserved below the neurological level and includes the sacral segment S4-5 AND no motor function is preserved more than three levels below the motor level on either side of body
    3. Injury motor incomplete = AIS C
      1. Motor function is preserved at most caudal sacral segments for voluntary anal contraction OR
      2. Sensory incomplete and has some sparing of motor function more than three levels below the ipsilateral motor level on either side of the body (< ½ of key or non-key muscles below level of injury graded ³ 3 more)
    4. Injury motor incomplete = AIS D
      1. AIS C BUT with ³ ½ of key muscle functions below the single neurological level of injury having a muscle grade of ³ 3
    5. Normal
      1. Sensation and motor function normal in all segments (follow up testing only once recovered)

What are the characteristic features of a cord transection versus central cord syndrome?

Cord transection:

  • Bilateral loss of motor and sensory function below the level of the lesion
  • Initially flaccid areflexia followed by hyperreflexia and spasticity
  • Sacral sensation absent in complete injuries

Central cord syndrome

  • Generally from a hyperextension injury
  • Bilateral motor impairment affecting the upper limbs more than the lower limbs and the distal muscles more than the proximal muscles
  • Variable sensory impairment and bladder dysfunction
    • Most common sensory deficit: cape like distribution of pain and temperature loss across upper back and down the back of the upper limbs
    • There can be dissociated sensory loss: loss of pain and temperature at the level of the lesion or loss of pain and temperature on one or both sides over a number of dermatomes with normal sensation above and below that level
    • Touch and proprioception often preserved
  • Sacral sensation preserved
  • Motor loss is usually greater than sensory loss
  • May be areflexic in upper limbs

What are the physiological  consequences of a cervical spinal cord injury?


Initially tone decreased à eventually this will increase and UMN signs develop

Anal tone lax in complete lesion

Weakness and sensory loss will depend on level of injury

Reflexes initially absent but will increase with time

Upgoing plantar reflex



Decreased maximum tidal volume

  • Damage above T1 à paralysis of intercostal and chest wall muscles à decreased chest wall expansion and diaphragm now solely responsible for respiratory effort à decreased maximum tidal volume and restrictive pattern on spirometry
  • Total lung capacity decreased, vital capacity decreased to 50 – 80%, tidal volume and expiratory reserve volume decreased

Rapid respiratory fatigue

  • Diaphragm cannot generate a sustained respiratory effort à capacity to compensate for acidosis is limited

Increased vital capacity in supine position

  • Greater stretch of diaphragm when supine
  • When upright abdominal contents move downward but this means diaphragm also moves downward and has less ability to descend further à less expansion of intrathoracic volume

Respiratory failure

  • Lesions above C3 à respiratory arrest
  • Lesions above C5 à respiratory failure
  • Increased likelihood with VC < 15ml/kg

Poor cough and difficulty with clearance secretions


Decreased peripheral vascular resistance

  • Descending sympathetic control lost and tonic contraction of muscles also lost à decreased afterload à decreased resting SBP

Decreased preload

  • Pooling of blood in venous capacitance vessels

Increased alpha-adrenoceptor responsiveness

  • Alpha adrenoreceptors increase in number and respond more vigorously
  • This effect takes weeks – months (not present in recently paralysed patient)

Autonomic dysreflexia

  • Loss of sympathetic control + hyperproliferation of adrenoreceptors à vagal reflex amplified and sympathetic stimulation below transection level can lead to exaggerated reflex sympathetic response à hypertension
  • Examples of stimuli include noxious stimuli, bladder distension, constipation

Loss of postural homeostatic reflexes

  • Loss of efferent limb of baroreceptor reflex arc à orthostatic hypotension


  • Sympathetic innervation of heart lost à unopposed vagal control à bradycardia
  • Stimulation of autonomic nervous system e.g. suctioning à unopposed vagal response rather than balanced sympathetic-parasympathetic response à asystolic arrest

Fixed cardiac output

  • Cardiac output cannot increase in response to stress or exercise as sympathetic input abolished
  • Tendency to cardiac failure with overvigorous fluid management

DVT and PE

  • 4 – 10% without prophylaxis


Decreased gastric transit, acute gastric dilatation

  • Severity correlates with level of spinal cord injury
  • Loss of sympathetic control à impaired gastric emptying à oesophageal distension leads to over-relaxation of stomach à gastric dilatation à can increase risk of aspiration

Acute gastric dilatation due to body cast syndrome

Paralytic ileus

  • Intestinal oedema + Loss of bowel control à slow stool propulsion à ileus

Stress ulceration

  • Common potentially due to unopposed vagal influence à stimulation of parietal cells à increased HCL production
  • Greatest risk is between day 4 – 10 after injury, risk reverts to normal with chronic injury



  • Posterior pituitary secretes vasopressin due to vasodilated state à renal water retention and hyponatremia
  • Diurnal secretion of vasopressin lost


  • Exaggerated action of RAAS system due to loss of sympathetic inhibition à may have hypokalaemia and hyponatremia

Insulin resistance

  • Inactivity + muscle wasting à insulin resistance
  • Reactive hypoglycaemia post meals à normal sympathetic response abolished

Suxamethonium sensitivity

  • Muscles proliferate acetylcholine receptors à can cause hyperkalaemia
  • Try avoid suxamethonium

Hypercalcaemia, osteoporosis and renal calculi

  • Disuse of bones à wasting à increased ALP, calcium and phosphate à hypercalciuria and renal calculi

Disordered thermoregulation  à hypothermia

  • Loss of sympathetic control à body temperature reflects environment

Nitrogen wasting

  • Muscle wasting and increased protein catabolism


Bladder denervation

  • Urinary retention and increased risk of UTI

Pressure areas

  • Loss of mobility and sensation

May have priapism immediately after injury

Briefly outline the role of early decompression in spinal cord injury.

Early surgical decompression in spinal cord injury is usually defined as within 24 hours of injury and may reduce the length of ICU stay and post-injury complications. The rationale behind it is that decompression may relieve pressure within the cord parenchyma which may partially restore microvascular blood flow, reduce ischaemia, and remove mechanical compression of the neuroglial cell membranes. Spinal surgery can also facilitate restabilisation of the spine.

  • STASCIS trial in 2012 showed decompression of cervical spine injuries within 24 hours led to improved neurologic recovery (greater proportion of patients demonstrated a 2 or more grade improvement in AIS at 6 months) and no difference in the complication rate
    • Multicentre, non randomised prospective cohort study of 313 adults with cervical spinal cord injury
  • There have been smaller studies since then that show that an even shorter time from injury to decompression may be associated with improved neurological outcomes

Early stabilisation also helps to facilitate easier nursing care and positioning.

The optimal timing of decompression in spinal cord injury is unknown but evidence favours earlier decompression.


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