canary in the mine…

the case.

16 year old female presents to your Emergency Department after falling from her mountain bike on a nearby track. As she fell to the ground, she reports landing on the handlebars which struck her upper abdomen.

She describes navigating a difficult section of a familiar track when her front wheel impacted a large tree root causing a loss of balance and the subsequent accident. A handlebar from her bike impacted her upper abdomen causing immediate pain and a moderate sized contusion. She has vomited once since the injury.

She otherwise appears to be ok.
– Was wearing a helmet at the time, did not lose consciousness and recalls all events.
– Has no dyspnoea, painful breathing or chest pain.
– Has no extremity pain, swelling or deformity.

She has no significant past medical history, takes no regular medications and has no known allergies.

On examination, she looks well but is in moderate pain.

  • A. patent & protected.
  • B. No chest wall crepitus, tenderness or emphysema. Respiratory rate 18/min. SaO2 98% (room air) Clear lung fields.
  • C. Warm and well perfused. Pulse rate 92 per minute. Blood pressure 110/68. No active external haemorrhage or long bone fractures.
  • D. GCS 15. Moving all 4 limbs. Pupils 5mm and reactive to light.
  • E. Well circumscribed abdominal wall contusion (~3 cm diameter) in the epigastrium, just left of the midline. She has moderate tenderness on deep palpation with voluntary guarding, but no rebound or percussion tenderness.

Your colleagues place a cannula and administer some analgesia.
During that time you grab your ultrasound …

The remainder of her images are normal.

Free fluid at the caudal liver edge & the splenorenal interface.

In the unstable patient with blunt abdominal trauma, the test characteristics of the FAST scan are impressive (Sn 73-88%, Sp 98-100%). However, in patients with penetrating trauma & in those with stable haemodynamics, this sensitivity falls away to 50% or less. This brings into question whether or not the FAST scan still has a role in the bedside assessment of these patients, where advanced imaging with contrast CT provides a greater level of diagnostic accuracy.

Here is a talk that I gave at the 2017 SWAN Trauma Conference on the role of the FAST scan in stable blunt trauma patients…

& here are the accompanying slides…

Despite her normal haemodynamics, this positive FAST scan signifies that she is carrying a significant intraabdominal injury & a high likelihood of clinical deterioration.

You notify your surgical colleagues & arrange an urgent abdominal CT…

  • Grade III splenic laceration (predominant grade II anterior laceration with other small subcapsular lacerations).
  • Intra parenchymal vascular injury is noted.
  • Small volume of free fluid.

Whilst your patient remains stable, with normal vital signs, the decision is made to proceed to interventional radiology. Here she undergoes selective angio-embolisation of a branch of the splenic artery.

She is admitted to the High Dependency Unit for overnight observation, where her haemodynamics and haemoglobin remain stable. Her recovery is uneventful and is discharged well 5 days later.

  1. Natarajan B, Gupta PK, Cemaj S, Sorensen M, Hatzoudis GI, Forse RA. FAST scan: is it worth doing in hemodynamically stable blunt trauma patients? Surgery. 2010; 148(4):695-700; discussion 700-1. [pubmed]
  2. Dammers D, El Moumni M, Hoogland I, Veeger N, ter Avest E. Should we perform a FAST exam in haemodynamically stable patients presenting after blunt abdominal injury: a retrospective cohort study Scand J Trauma Resusc Emerg Med. 2017; 25(1). [pubmed]
  3. Lee BC, Ormsby EL, McGahan JP, Melendres GM, Richards JR. The utility of sonography for the triage of blunt abdominal trauma patients to exploratory laparotomy. AJR. American journal of roentgenology. 2007; 188(2):415-21. [pubmed]
  4. Liu K. FAST Scan: Is it Worth Doing in Hemodynamically Stable Blunt Trauma Patients? The Journal of Emergency Medicine. 2011; 40(5):607-608. [link]
  5. Cho Y, Judson R, Gumm K, Cho Y, Santos R, Walsh M, et al. Blunt Abdominal Trauma. Trauma Service Guidelines: The Royal Melbourne Hospital; 2012. [link]
  6. Fleming S, Bird R, Ratnasingham K, Sarker S, Walsh M, Patel B. Accuracy of FAST scan in blunt abdominal trauma in a major London trauma centre International Journal of Surgery. 2012; 10(9):470-474. [link]
  7. Hsu JM, Joseph AP, Tarlinton LJ, Macken L, Blome S. The accuracy of focused assessment with sonography in trauma (FAST) in blunt trauma patients: Experience of an Australian major trauma service Injury. 2007; 38(1):71-75. [link]
  8. Bowra J, Forrest-Horder S, Caldwell E, Cox M, D’Amours SK. Validation of nurse-performed FAST ultrasound. Injury. 2010; 41(5):484-7. [pubmed]
  9. Behboodi F, Mohtasham-Amiri Z, Masjedi N, Shojaie R, Sadri P. Outcome of Blunt Abdominal Traumas with Stable Hemodynamic and Positive FAST Findings. Emergency (Tehran, Iran). 2016; 4(3):136-9. [pubmed]
  10. Matsushima K, Frankel HL. Beyond focused assessment with sonography for trauma: ultrasound creep in the trauma resuscitation area and beyond. Current opinion in critical care. 2011; 17(6):606-12. [pubmed]
  11. Richards JR, McGahan JP. Focused Assessment with Sonography in Trauma (FAST) in 2017: What Radiologists Can Learn Radiology. 2017; 283(1):30-48. [link]
  12. The Use of FAST Scan by Paramedics in Mass-casualty Incidents: A Simulation Study Prehosp. Disaster med.. 2014; 29(06):576-579. [link]

cracking under pressure…

the case.

a 44 year old male presents to your Emergency Department with severe, crushing retrosternal chest pain. He reports that the pain started suddenly approximately one hour ago whilst at rest.

It is described as a retrosternal pressure or tightness which radiates up to his neck, through to the back & down towards his umbilicus.

The pain is associated with severe palpitations. There is no associated dyspnoea, cough or haemoptysis. There have been no syncopal or near-syncopal episodes and he has no neurological symptoms. He has never had pain like this before.

Past Medical History:

  • Hypertension
  • Hypercholesterolaemia


  • Simvastatin
  • Ezetimibe

No significant social history.

On examination. 
He looks unwell. He is profoundly clammy and diaphoretic.

  • A: Patent & protected.
  • B: Tachypnoeic (28 breaths per minute), minimal work of breathing. SaO2 95% (RA). Chest clear to auscultation.
  • C: Pulse rate 135 per minute, Blood pressure 190/110 (no differential between left & right arms). Good peripheral pulses without pulse deficit. Heart sounds dual without murmurs or rub.
  • D: GCS 15. Equal and reactive pupils (4mm). Moving all 4 limbs. No focal motor or sensory changes.
  • E: Temperature 37.7*C. Blood glucose 8.2 mmol/L.

You can’t help but notice that he has a new dressing over his left deltoid. When you enquire about this, he tells you that earlier that day he underwent an elective resection of a skin lesion under general anaesthetic at a nearby hospital. This was apparently an uneventful procedure & recovery and he was discharged home only a few hours ago.

  • Narrow complex (sinus) tachycardia at a rate of ~140 beats per minute.
  • Normal axis.
  • ~1mm of ST segment elevation in aVR with diffuse, widespread ST segment depression (V3-6, I & aVL)
  • PR & QRS intervals normal.
  • Prolonged QT interval.

Differential diagnoses include;
(1) left main coronary artery occlusion
(2) proximal LAD occlusion
(3) severe triple vessel disease
(4) diffuse sub-endocardial ischaemia (myocardial O2 supply/demand mismatch)

  1. Severe metabolic acidosis:
    • HCO3 13, BE -15.
    • Uncompensated with a pH 7.17
    • Exp pCO2 = (1.5×13) + 8 = 20 + 8 = 28.
    • Actual = 37, therefore a contributing relative respiratory acidosis.
  2. High anion gap (Cl = 102)
    • 141 – (102+13) = 26
  3. Severely elevated lactate: 15mmol/L !!
    • DDx: sepsis, hyperadrenergic state, ingestion, malperfusion/ischaemia, MH
  4. Severe hyperglycaemia: 28 mmol/L
    • ?new onset diabetes ?stress response
    • Are there ketones contributing to the acidosis?? In this case, they were normal.
  5. Mild hypokalaemia:
    • K 3.8mmol/L, however when corrected for acidosis is more likely <3!
  6. Mildly elevated serum creatinine.
    • ?acute vs chronic
    • ?contributory vs incidental finding
  7. Hb 170
    • ?haemoconcentration 

  • Normal cardiomediastinal contour.
  • Clear lung fields without collapse or consolidation.
  • No pleural effusions.

  • Acute coronary syndrome
  • Aortic dissection
  • Hypertensive crisis – but why?
    • Cardiovascular
    • Renal
    • Endocrine
    • Haematologic
    • Intoxication/ingestion
  • Malignant hyperthermia (cases of delayed onset MH have been reported)
  • Sepsis
  • Thyroid storm
  • Intoxication/ingestion
    • Sympathomimetic toxidrome
    • Anticholinergic toxidrome
    • Serotonin syndrome
    • Neuroleptic malignant syndrome
    • Salicylate toxicity
    • Methylxanthine toxicity

  • IV access
  • Analgesia
    • Titrated intravenous opiates is suitable (eg. Fentanyl 50mcg IV q5-10mins)
  • Nitrates:
    • Easier (& quicker) to start with a sublingual tablet followed by infusion for blood pressure control & reduction of ongoing ischaemic chest pain
  • Detect and correct electrolyte derangement especially potassium

With a strong clinical suspicion for aortic dissection, antiplatelet therapy & anticoagulation are withheld and a CT Aortogram is arranged urgently…

Did you see it? Did you see it?

Upon return from radiology, he continues to complain of severe retrosternal pain…

His pulse remains 136 per minute with a blood pressure of 196/118 mmHg despite your GTN infusion now running at 250 micrograms per minute.

The nurse looks at you and asks, “What are we going to do now??


Phaeochromocytoma is a catecholamine-secreting neuroendocrine tumour (a paraganglioma), most frequently arise from the chromaffin cells of the adrenal medulla.


  • Incidence is very low ~2 people/million/year.
  • Most common between ages of 20 and 50 years.
    • 50% of cases are diagnosed only at post-mortem examination.
  • “10% rule”
    • Bilateral in 10% of cases
    • 10% are extra-adrenal
    • 10% are malignant
    • ~10% are found in children
    • ~10% are familial
  • Phaeochromocytomas are the secondary cause of hypertension in 0.1% of hypertensive patients.
  • A proportion of patients are diagnosed at the time of incidental surgery when induction of anaesthesia may precipitate a hypertensive crisis.
    • Mortality in this instance is close to 80%.

Clinical presentation.

Classically, phaeochromocytoma manifests as spells with the following 3 characteristics…

These spells may or may not be associated with severe hypertension.

Typical patterns of the spells are as follows:

  • Frequency may vary from monthly to several times per day
  • Duration may vary from seconds to hours
  • Over time, spells tend to occur more frequently and become more severe as the tumour grows.

The typical features of phaeochromocytoma are predominantly cardiovascular:

    • Paroxysmal (~45%)
    • Sustained (50%)
    • NB. ~5% are normotensive
  • Palpitations and tachycardia
  • Headaches
  • Tremor
  • Sweating
  • Anxiety
  • Chest pain (± myocardial infarction)
  • Cardiac failure (± acute pulmonary oedema)

Other symptoms include;

  • Nausea
  • Weakness
  • Anxiety or a sense of doom
  • Epigastric pain
  • Flank pain
  • Constipation


Clinical suspicion remains the single most important factor in
the identification of phaeochromocytoma.

Phaeochromocytomas can present as a component of familial syndromes (esp. thyroid cancers). It is important to be aware of this association.

Image courtesy of Alderazi et al.

Measurements of urinary catecholamines and their metabolites, metanephrines, over 24 hours have been the mainstay of biochemical diagnosis of phaeochromocytoma for many years (Sn 88%, Sp 99%).

Tests for catecholamines and their metabolites

  • Urinary catecholamines
  • Plasma catecholamines
  • Urinary fractionated metanephrines
  • Plasma free metanephrines (these appear to be the best single investigation)
  • Urinary vanillylmandelic acid

Clonidine suppression test
In patients with phaeochromocytoma, serum catecholamine levels will not decrease in response to clonidine (they are independent of neurogenic control).


  • CT scan (including dedicated adrenal study with washout)
  • MRI
  • Nuclear medicine (esp.I-123 MIBG)
  • PET scan

Check for alternate diagnoses:

  • Thyroid function (TSH, T4)
  • Plasma renin activity
  • Cortisol levels (plasma & urine)


Phaeochromocytoma is known for life-threatening acute hypertensive emergencies, as well as clinical consequences of long-lasting hypertension.

Spells or crises can result from a variety of precipitants including;

  • Postural changes, physical exertion, emotion
  • Certain foods or beverages (especially those with tyramine eg. cheese, beer, wine)
  • Direct tumour stimulation (abdominal pressure or injury)
  • Drugs/medication:
    • histamine, ACTH, metoclopramide, phenothiazine, TCAs or anaesthetic agents.

Organ-Specific Hypertensive Complications

  • Cardiac
    • Acute coronary syndromes (including myocardial infarction)
    • Cardiomyopathies (incl. Takotsubo)
    • Myocarditis
    • Heart failure including pulmonary oedema and cardiogenic shock
    • Dysrhythmias
  • Cerebrovascular
    • Stroke
    • Hypertensive encephalopathy
  • Vascular
    • Shock
    • Postural hypotension
    • Aortic dissection
    • Organ ischaemia
    • Limb ischaemia
  • Renal
    • Acute renal failure
    • Haematuria
  • Gastrointestinal
    • Intestinal ischaemia (necrosis or peritonitis)
  • Ocular
    • Acute blindness
    • Retinopathy
  • Multisystem failure
    This complication consists of multiple organ system failure

    • Fever over 40°C
    • Encephalopathy
    • Severe hypertension and/or hypotension
    • Pulmonary oedema
    • Anuric acute renal failure
    • DIC


Management of phaeochromocytoma-related emergencies depends on the symptoms; however, it should always include pharmacologic treatment to block the effects of high levels of circulating catecholamines and prevent life-threatening catecholamine-induced complications.

This review will not cover the pre-operative management of these patients.

  • Control of hypertension.
    • Rapidly acting α-1 antagonist:
      • Phentolamine: 0.5-1mg per minute in aliquots or via infusion.
    • Slowly acting non-competitive α-1 antagonist:
      • Phenoxybenzamine reserved for post-crisis care & pre-op optimisation
      • Prazosin 
    • Others:
      • GTN
      • Sodium nitroprusside
      • β-blockers (only after adequate α-blockade) – eg. atenolol or propranolol
      • Calcium channel blockers
  • Maintenance of circulating volume in the face of vasodilation.
    • IV fluid replacement
  • Control of atrial fibrillation.
    • Verapamil, diltiazem or amiodarone
  • Assessment of myocardial damage.
    • ECG
    • Echocardiography
    • Troponins
  • Seek and treat precipitating cause
  • Admit for further workup & operative planning

Definitive treatment is surgical removal and if complete resection is achieved, without metastases, then surgery is curative  in >90% of cases. Following this, hypertension usually resolves.

Following confirmation of the adrenal lesion, the patients blood pressure is managed acutely with a high-dose GTN infusion and aliquots of phentolamine. He is subsequently admitted to the Intensive Care Unit for ongoing short-term care.

Over the following 48 hours he is transitioned onto oral antihypertensives, in this case, prazosin.

His 24-hour urinary collection demonstrated;

Normal metanephrine < 0.40, Normal normetanephrine < 0.90.

A subsequent dedicated adrenal CT demonstrated an absolute washout of 79%.

Here is his I-123 MIBG scan…

The scan appearances in the right adrenal gland are most in keeping with a MIBG avid pheochromocytoma. There is no scan evidence of MIBG avid disease elsewhere in this study.

After 5 days in hospital, he was discharged home with ongoing specialist input. He later underwent a successful, elective surgical resection of his phaeochromocytoma & is doing well…

  1. Alderazi Y, Yeh MW, Robinson BG. Phaeochromocytoma: current concepts. The Medical journal of Australia. 2005; 183(4):201-4. [pubmed]
  2. Zuber SM, Kantorovich V, Pacak K. Hypertension in pheochromocytoma: characteristics and treatment. Endocrinology and metabolism clinics of North America. 2011; 40(2):295-311, vii. [pubmed]
  3. Myklejord DJ. Undiagnosed Pheochromocytoma: The Anesthesiologist Nightmare Clinical Medicine & Research. 2004; 2(1):59-62. [pubmed]
  4. Pacak K, Eisenhofer G, Ahlman H. Pheochromocytoma: recommendations for clinical practice from the First International Symposium. October 2005. Nature clinical practice. Endocrinology & metabolism. 2007; 3(2):92-102. [pubmed]
  5. Frederick MJ, Colwell AS. Acute hypertensive crisis secondary to pheochromocytoma during elective cosmetic surgery. Plastic and reconstructive surgery. 2015; 135(1):238e-9e. [pubmed]
  6. Bensghir M, Elwali A, Lalaoui S et al. Management of undiagnosed pheochromocytoma with acute appendicitis World J Emerg Surg. 2009; 4(1):35. [pubmed]
  7. Raut M, Kar S, Maheshwari A et al. Rare postoperative delayed malignant hyperthermia after off-pump coronary bypass surgery and brief review of literature Ann Card Anaesth. 2016; 19(2):357-362. [pubmed]

an abominable airway…

the case.

a 28 year old male presents to your Emergency Department with a 2-3 week history of increasing neck swelling. He is now spitting out frank purulent discharge from his mouth and reports fevers and night sweats.

He reports a rapid increase in neck swelling which is now preventing him from eating a normal diet. His purulent secretions started about 10 days ago & also appear to be getting worse. He has had no associated cough, chest pain, haemoptysis, vomiting, headaches or photophobia.


  • Squamous cell carcinoma of the tongue.
    • Diagnosis made ~4 months ago.
    • Declined initial treatment (both chemotherapy & local radiation therapy were recommended)

He currently takes no regular medications & has no known drug allergies.
He is a non-drinker & smokes ~15 cigarettes per day.

On examination:

A. Interesting & intimidating. Expectorating purulent secretions +++. Limiting mouth opening (~1.5cm). Significant bilateral submandibular neck swelling (L>>R) with mild overlying erythema.

B. Respiratory rate 22/min. SaO2 96% on room air. Clear chest on auscultation.

C. Tachycardic to 130/min. BP 126/70. Capillary refill <2 seconds. Dual heart sounds.

D. GCS 15. No focal deficits.

E. Febrile to 39*C. No rashes. Blood glucose 8.2 mmol/L.

primary surgical airway

  • Metabolic alkalosis
    • HCO3 41, BE 14.
    • Compensated pH 7.44, pCO2 61primary surgical airway
    • Expected pCO2:
      • = (0.7 x 41) + 20
      • = 28.7 + 20
      • = 48.7
    • Actual pCO2 = 61, ∴ likely concomitant respiratory acidosis.
  • Moderate hypokalaemia
  • Markedly elevated iCa: 1.81
  • Lactate 1.7 (?sepsis driven)

primary surgical airway   

  • Hypokalaemic, hypochloraemic metabolic alkalosis
    • ?secondary to vomiting, malignancy, endocrinopathy.
  • Life threatening hypercalcaemia
    • Likely a paraneoplastic process (PTH-related protein or ectopic Vitamin D production)
    • Alternatively, from metastatic osteolysis
    • Other differential diagnoses include:
      • Primary hyperparathyroidism
      • Medications (thiazides, lithium, oestrogens)
      • Granulomatous diseases (sarcoidosis, tuberculosis, histoplasmosis)
      • Milk-alkali syndrome
  • Non-specific LFT derangement
  • Elevated WCC with predominate neutrophilia 
    • Not unexpected given the presence of sepsis.

  • Intravenous access & volume replacement
    • 0.9% Saline or Hartmann’s solution, empiric 500-1000mL
    • Reassess pulse rate, blood pressure, capillary refill & urine output
  • Empiric antibiotic therapy
    • Clindamycin 600mg IV or Benzylpenicillin 2.4g IV
    • ± Metronidazole 500mg
  • Steroids
    • 10mg IV dexamethasone
  • Correction of electrolytes:
    • Potassium:
      • 10-20mmol KCl per hour & reassess
    • Calcium:
      • Restore intravascular volume (IV fluids)
      • Maintain urine output ~ 100-150mL/hr
      • Bisphosphonates (palmidronate or zolidronic acid)
  • Analgesia
  • Antipyretics
  • Supportive care

You feel that he is able to maintain his own airway at present & he is capable of lying flat.

Here is his CT neck:

As your patient arrives back from radiology you notice he now looks unwell !!

He is in obvious respiratory distress with tachypnoea (respiratory rate of 34/minute) and moderate work of breathing. His room air oxygen saturations are now 68% !!

He is clammy & tachycardic but normotensive.

He is confused, but cooperative.

  • Transfer to a resuscitation bay
    • Full cardiorespiratory monitoring.
    • Advanced airway equipment (including difficult airway trolley) moved to the bedside.
  • Call for help.
    • This will be dependent upon your facility & the experience of your available staff at hand.
    • Anaesthetics & ENT surgery would be great allies in this scenario, especially if he doesn’t rapidly improve.
    • Asking for an operating theatre to be on stand-by with fibre-optic equipment ready would also be a good idea.
  • Maximise oxygenation.
    • High-flow oxygen via non-rebreather mask ± high-flow nasal oxygen.
    • Non-invasive ventilation may also be worth trying.
  • Assess & treat reversible pathology.
    • Trial of nebulised adrenaline (5mg).
    • Consider a further dose of intravenous steroid acknowledging this takes time for effect.

  • The ENT surgeon is “on their way“…
  • Anaesthetics come to the bedside & quickly make a plan for an attempt at an awake fibre optic intubation in their theatre, with surgical backup.
  • The patient improves somewhat. His oxygen saturations climb to 99% on oxygen & his work of breathing settles.

5 minutes later, he rapidly deteriorates!!!

He continues to desaturate (to 80%) despite high-flow supplemental oxygenation and he develops significant increased work of breathing. He is now clammy, diaphoretic and very agitated. He is ripping off his oxygen mask, pulling off monitoring and tugging on his IV lines.

  • Get control.
    • How? What agent(s)?
    • We used Ketamine IV aliquots (10-20mg) & titrated cautiously to effect (wanting to maintain spontaneously respirations).
  • Abort the plan to transfer to theatre.
  • Prepare for a definitive airway.
    • Difficult airway trolley at the bedside.
    • Surgical airway kit opened. 
    • Cricothyroid membrane identified and marked (± infiltration to the site with local anaesthetic).
  • Prepare the team.
    • Role designation.
    • Brief team (& patient) on likely sequence of events.
    • Cognitive rehearsal.

Unlike other ‘blunt dissections’, this discussion has been designed to encourage reflection and promote critical thinking about your preferred method of surgical airway. It is written as a stark reminder that these cases can present with little-to-no warning. The onus is on us, as critical care clinicians, to constantly revisit our practice, procedures and undertake cognitive rehearsal to allow for peak performance during intimidating and challenging scenarios.

Primary surgical airway


  • Restricted mouth opening (burns, facial trauma).
  • Distorted anatomy (facial trauma, laryngeal injury, haemorrhage).
  • Limited access to the upper airway due to entrapment in the prehospital environment.

NB – Surgical airways are indicated & the final step in a “cannot intubate, cannot oxygenate” (CICO) scenario.


  • ability to secure an airway via less invasive means
  • airway trauma that renders access via the cricothyroid membrane futile
    • e.g. laryngeal fracture, tracheal transection
      Tracheostomy should be performed in these instances, or access can be achieved via the traumatic airway opening.
  • Children < 10 years of age
    • young children are prone to laryngeal trauma and they have a higher incidence of postoperative complications
    • needle cricothyroidotomy is generally advised, however life-saving surgical cricothyroidotomy has been successfully performed in children

The equipment.

What’s available?

There is a wide array of proprietary surgical airway sets available for use. These are typically made for insertion via the modified Seldinger technique and have a variety of needles, dilators, tracheal hooks, tubes, cannulae and wires (see below).

It is crucial that you know (1) what your facility has stocked & available & (2) what your preferred piece of equipment is prior to identifying a patient requiring its use.

primary surgical airway

What I prefer…

primary surgical airway

Image credit: Dr Tor Ercleve (2014)

The theory.

A demonstration.

A real scenario.

This video demonstrates the method on a live patient (courtesy of

…and now it’s up to you!!

You must now decide:

  • What equipment you will use?
  • How will you position the patient? Do you extend the neck?
    Who will do this when the decision is made?
  • What steps you will take in the procedure?
  • What side of the bed you will perform this task?
  • How you will coordinate your teams movement once the decision is made?

Once decided, incorporate them into your Difficult Airway Plan & announce it your team !!

The team decides that a transfer to the operating theatre is unsafe. With his CT scan being interpreted as an ‘unintubatable’ oral airway, the decision is made to proceed with a primary surgical airway in the Emergency Department.

The patient receives 10-20mg aliquots of intravenous ketamine resulting in behavioural control and allows the team to commence an aggressive re-oxygenation (& preoxygenation) strategy.

Your anaesthetic colleagues take the head of the bed, providing two-handed bag-valve mask and intermittent positive pressure ventilation with the additional of 10 cmH2O of PEEP, two nasopharyngeal airways and an oropharyngeal airway. This results in an improvement in oxygen saturations back to 98%.

At this stage, you find out that your surgical colleagues are not onsite & are over 45 minutes away…

This procedure is yours.

The cricothyroid membrane is identified and marked. It is subsequently anaesthetised with subcutaneous lignocaine (+ adrenaline).

An open surgical cricothyroidotomy is performed…

Scalpel. Finger. Bougie. Size 6 endotracheal tube. End-tidal CO2.

Once the tube placement is confirmed & secured, the patient is muscle relaxed & his sedation is increased.

primary surgical airway

Now what do you do about that gastric bubble?

Following a night in the Intensive Care Unit he is taken to the Operating Theatre for a formal surgical tracheostomy. Whilst in theatre it is confirmed that his airway was truely unintubatable via both direct and fibreoptic means…

  • Surgical Cricothyroidotomy – LITFL Critical Care Compendium
  • Surgical Airway –
  • Greater Sydney Area HEMS. PREHOSPITAL EMERGENCY ANAESTHESIA MANUAL Version 2.2, January 2016.
  • Hamaekers AE, Henderson JJ. Equipment and strategies for emergency tracheal access in the adult patient. Anaesthesia. 66 Suppl 2:65-80. 2011. [pubmed]
  • Paix BR, Griggs WM. Emergency surgical cricothyroidotomy: 24 successful cases leading to a simple ‘scalpel-finger-tube’ method. Emergency medicine Australasia : EMA. 24(1):23-30. 2012. [pubmed]