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]

shrouded shock…

the case.

46 year old male is bought into your resuscitation bay by local ambulance following a three metre fall from a work platform onto a horizontal metal railing below.

He has slipped in wet weather whilst on a narrow platform & dropped onto a two inch railing which has struck him across the lower chest wall (right side worse than left). He subsequently fell to the ground on his left side. There was no associated head strike or loss of consciousness & the patient was able to mobilise at the scene to put out a call for help.

He is complaining of right sided chest pain & right upper quadrant pain with an associated truncal contusion.

His vital signs are:

  • Pulse: 95-130 per minute (irregular)
  • Blood pressure: 90 systolic
  • Respiratory rate: 26 per minute
  • Pulse oximetry: 96% (on room air)
  • GCS: 15

Prehospital treatment included: IV access, 5mg intravenous morphine & 250mL Hartmann’s solution. He has a cervical collar and pelvic binder in situ.

He is normally fit and well, has no significant past medical history & no known allergies.

A: patent + protected.

B: RR 24, SaO2 100%. No subcutaneous emphysema. Good air entry.

C: P 130-140 (irregular), BP 84 systolic. Warm & well perfused. No long bone #s or external haemorrhage. RUQ tenderness++ (without peritonism).

D: GCS 15. PEARL. Moving all 4.

E: Afebrile. Moderate contusion to lower chest wall (R>>L).

myocardial contusion

Mobile supine CXR

myocardial contusion

Pelvis xray

Following your teams initial assessment he remains hypotensive (SBP 82mmHg) and tachycardic (130-150bpm, in atrial fibrillation).

  • Obtain intravenous access.
    • Send off bloods including VBG, FBC, biochemistry & cross-match.
  • Optimise perfusion.
    • Consider a fluid bolus (crystalloid versus uncrossmatched blood, 10mL/kg & reassess)
  • Search for a potential haemorrhagic or obstructive cause for his haemodynamic instability.
    • eFAST scan
    • Consider advanced CT imaging
  • Titrated analgesia.
    • Intravenous fentanyl aliquots would be a reasonable initial choice
  • Obtain a 12-lead ECG.

Pleural scans.



Pelvic scans.

Pericardial view.

Negative study.
No pneumothorax, intraperitoneal free fluid or pericardial effusion.

myocardial contusion

12-lead ECG

  • Rate:
    • 93-150 bpm.
  • Rhythm.
    • Irregularly irregular (without obvious P waves).
  • Axis.
    • Normal [+41*].
  • Intervals.
    • PR ~ n/a.
    • QRS ~ 130msec [RBBB morphology].
    • QTc ~ 430msec.
  • Segments.
    • Isoelectric PR & ST segments.

Atrial fibrillation with rapid ventricular response & right bundle branch morphology.

myocardial contusion

No significant abnormality here that changes management or guides further investigation.

Despite a 500mL fluid challenge, your patient remains hypotensive & tachycardic (Pulse 120-150, SBP 88mmHg).

You repeat your eFAST scan & it is unchanged.

The trauma team decide to proceed with advanced imaging (CT scan) to further elucidate his injuries.

His CT report summary reads:

  • No acute intraabdominal traumatic pathology (no free fluid or intraperitoneal gas).
  • No intrathoracic traumatic sequelae.
  • No spinal fracture or displacement.
  • Incidental finding of a hepatic haemangioma (identified in his RUQ eFAST scan).

In the patient with tachycardia and persistent hypotension, the utilistion of focused bedside echocardiography can delineate the potential underlying causes of shock (hypovolaemic, obstructive, pump failure).

In this case, you take your trusty ultrasound to the bedside…


Hyperdynamic left ventricle. Mildly dilated RV.


No overt intraventricular septal deviation.


Hypokinetic right ventricular free wall.


IVC collapsibility throughout the respiratory cycle suggesting the patient may respond to a fluid challenge.


Hyperdynamic left heart with features of RV dilatation and reduced contractility.

In the patient with blunt thoracic trauma, hypotension, presumed new RBBB & a normal CT scan, the following diagnosis must  be considered….

Myocardial contusion.

Myocardial contusion injuries are a common complication of blunt thoracic trauma. They are caused by a deceleration force to the chest wall resulting in (1) direct pressure on the myocardium or (2) indirect effects of sudden, increased intrathoracic pressures (especially shearing forces). Of note, minimal force may actually be required to cause such a contusion.

Blunt cardiac injury encompasses a wide spectrum of clinical manifestations ranging from an asymptomatic myocardial bruise to cardiac rupture and death. They remain a poorly defined clinical entity without a gold standard of diagnosis. It is estimated that up to 20% of all deaths at motor vehicle accident deaths are due to blunt cardiac injury. It is also commonly associated with work-related and industrial accidents, especially falls. These fatalities are largely due to arrhythmias, ventricular free-wall rupture or coronary artery laceration (resulting in extra-cardiac haemorrhage).

NB. Myocardial contusions can result from chest compressions during cardiopulmonary resuscitation.

  • The right ventricle (RV) is most commonly injured due to its anterior position in the mediastinum.
    • Cardiac output can drop (up to 40%) as a result of RV failure and preload reduction. 
    • This can be compounded by a reduction in the compliance of the LV from a shift in the interventricular septum.
  • The higher pressures of the left heart also make the aortic and mitral valves susceptible to injury (compared to the pulmonary and tricuspid valves).
    • Preexisting valvular pathology makes this more likely.


Persistent hypotension with no clear traumatic cause is suspicious of myocardial injury. Haemorrhagic, spinal and obstructive shock MUST to be considered and excluded in these instances. This is especially true in cases with associated significant chest wall and pulmonary injury.

Clinically, severe right ventricular dysfunction from myocardial contusion may mimic cardiac tamponade.

The patient with myocardial contusion may present with the clinical sequelae of:

  • Arrhythmias (including ventricular tachycardia & fibrillation)
  • Ventricular dysfunction (including congestive cardiac failure)
  • Acute valvular regurgitation
  • Ventricular aneurysm with thrombus
  • Pericardial effusion ± tamponade
  • Intracardiac structural damage
  • Cardiac rupture

These complications may arise immediately or delayed (even up to years post-injury).

Commonly associated thoracic injuries include:

  • Rib fractures ± flail chest
  • Pulmonary contusions
  • Pneumothorax
  • Haemothorax
  • Sternal fractures
  • Great vessel injury

With the spectrum of complications arising from myocardial contusion as well as the possible concomitant traumatic injuries there is a wide range of clinical presentations and variable physiological consequences.

You must consider a valvular injury (or one to papillary muscles, chordae or septum) in patients’ with a new murmur or pulmonary oedema following blunt chest trauma.


The definitive diagnosis of myocardial contusion can only be made on gross or histological examination of the hear. There remains no sensitive diagnostic test to clearly identify myocardial contusion or to predict those patients with the potentially lethal complications.


In patients with myocardial contusion, 40–83% have abnormal ECGs. Arrhythmias are the most common abnormality observed, usually occurring in the first 24–48 hours. There is no correlation between the complexity of arrhythmias and the degree of cardiac contusion, however atrial fibrillation is associated with a poor outcome.

Right bundle branch block is common followed by first degree heart block, right bundle branch block with hemiblock and third degree heart block, respectively. Contusions to the left ventricle may manifest as ST-T wave abnormalities, diffuse ST changes as seen in pericarditis, or as pathological Q waves.

Several studies have demonstrated abnormal transoesophageal echoes in patients with blunt thoracic trauma and normal presenting ECGs (24-41%).


    • An admission electrocardiogram (ECG) should be performed on all patients in whom BCI is suspected.
    • If the admission ECG reveals a new abnormality, the patient should be admitted for telemetry.
    • ECG alone is not sufficient to definitively rule out BCI (NPV ~95%).

Creatinine Kinase.

CK-MB is specific for myocardial and skeletal muscle trauma, and is a particularly good marker of cellular injury because it increases and peaks in the first 24 hours and decreases to normal levels within 72 hours. However, CK-MB levels are usually elevated in trauma patients because of multiple injuries & the source of the enzyme may be due to non-myocardial sources, making CPK-MB a non-specific marker of cell injury. There are also conditions in which CK-MB may be falsely elevated.

Summary: do not use.


Serum cardiac troponin is highly specific for myocardial injury. Previously, Troponin I was able to detect cardiac injury in patients with blunt chest trauma accurately (Sn 100% & Sp 97%) in a group of 44 patients using echocardiography as a reference for the diagnosis. There is however ICU data demonstrating elevated troponin in intubated trauma patients without echocardiography or ECG changes, raising the possibility of either false positive elevations (or Type 2 rise) OR a subclinical contusion.

Recent studies show that ECG alone is not sufficient to definitively rule out BCI. This recommendation is based on data from four studies representing more than 500 prospectively studied patients.

One study has looked at the use of troponin I in the paediatric trauma population. It found that elevation correlated with higher injury severity and need for interventions but did not correlate with abnormalities on cardiac echo and was not useful in detecting cardiac injury.


    • The addition of troponin I to the workup for BCI increases the NPV to 100%.
    • Elevated troponin seems to be a formal indication for echocardiography.
    • Troponin may be elevated for other reasons in trauma patients.
    • Do not use in paediatric patients.


Echocardiography is a valuable tool in the assessment of cardiac function after BCI. Unfortunately, echocardiography has little utility as a screening test for clinically significant BCI in the haemodynamically stable patient.


TTE is useful in diagnosing myocardial contusion, assessing ventricular function & detecting pericardial effusion.

TTE has identified myocardial contusion in up to 26% of patients with blunt chest trauma & pericardial effusion in up to 15%.

It rapidly differentiates contusion from effusion in the overtly shocked patient with blunt thoracic trauma.

Potential limitation is the association with poor-quality images secondary to accompanying chest injuries.


TOE provides high-quality images when transthoracic windows are poor, but is semi-invasive and not always possible in the emergency department or resuscitation bay.

Summary: Echocardiography is not useful as a primary screening modality but rather as a diagnostic test for patients who have unexplained hypotension or arrhythmias.

Nuclear medicine.

Using radionucleotide imaging, concentrated areas of 99mTc- pyrophosphate or reduced areas of perfusion may indicate the presence and extent of myocardial damage. These scans do have high false negative rates.

Summary: Nuclear medicine studies add little when compared with echocardiography and should not be routinely performed.


In patients with a normal ECG result and normal troponin I level, BCI is ruled out. The optimal timing of these measurements, however, has yet to be determined.

Here are some suggested diagnostic algorithms’ for the investigation of potential blunt cardiac injury:

Taken from Schultz & Trunkey (2004).

Taken from Bansal et al (2005).


Five studies evaluated the relationship of sternal fracture to BCI. Four of those studies concluded that sternal fracture was not a marker for BCI.

The presence of a sternal fracture alone does not predict the presence of BCI and thus should not prompt monitoring in the setting of normal ECG result and troponin I level.


Cardiac contusion is typically associated with significant extra-cardiac trauma, therefore resuscitation and clinical management will largely be dictated by these concomitant injuries. The clinician should focus on maximising oxygenation & ventilation, optimising perfusion, arresting haemorrhage as well as the provision of sound neuroprotective measures.

Myocardial contusions with minor ECG or cardiac biomarker abnormalities rarely produce clinically significant sequelae. These minor abnormalities usually resolve without any intervention within 24 hours.

Myocardial contusion with shock requires a precise understanding of the preload and afterload characteristics of both ventricles. Invasive cardiovascular monitoring and echocardiography will guide this assessment. Haemodynamic support in the setting of confirmed or suspected myocardial contusion is centred around judicious fluid administration and careful inotropic support. Intraaortic balloon pump counterpulsation has been used in some patients with refractory cardiogenic shock.

Arrhythmias may be a result of direct myocardial injury, or can occur because of electrolyte or acid/base disturbances, hypoxia or intoxication. Each of these should be addressed when managing these patients. DC cardioversion should be avoided if possible.

Extreme associated cardiac injuries may require cardiothoracic surgery or interventional angiography.

With all potential significant traumatic causes for hypotension largely excluded by his advanced imaging the diagnosis of myocardial contusion was made & later confirmed by a formal transthoracic echo demonstrating a mildly dilated right ventricle with moderate systolic impairment. Of note, his left ventricular size and function was normal.

He did have a troponin elevation which peaked at 415







His hypotension was responsive to fluid boluses & he did not require inotropic support.

He was admitted to a high-dependency bed and was reviewed by Cardiology and Intensive Care, who decided to treat his atrial fibrillation with amiodarone. 24 hours into his admission he reverted back to sinus rhythm.

Serial echo demonstrated the interval development of a small pericardial effusion without features of tamponade. This was merely observed and did not require intervention.

He was discharged home on day 5.

For those wondering, here is his discharge ECG…

myocardial contusion

Note the resolution of the right bundle branch block.

  1. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
  2. Schultz, J. M., & Trunkey, D. D. (2004). Blunt cardiac injury. Critical Care Clinics, 20(1), 57–70. 
  3. Rosen, C. (1993). Significance of myocardial contusion following blunt chest trauma. Annals of Emergency Medicine, 22(7), 1243. 
  4. Feghali, N. T., & Prisant, L. M. (1995). Blunt Myocardial Injury. Chest, 108(6), 1673–1677. 
  5. Bansal, M. K., Maraj, S., Chewaproug, D., & Amanullah, A. (2005). Myocardial contusion injury: redefining the diagnostic algorithm. Emergency Medicine Journal, 22(7), 465–469. 
  6. Kaye, P., & O’Sullivan, I. (2002). Myocardial contusion: emergency investigation and diagnosis. Emergency Medicine Journal, 19(1), 8–10.
  7. Cane, R. D., & Buchanan, N. (1978). The electrocardiographic and clinical diagnosis of myocardial contusion. Intensive Care Medicine, 4(2), 99–102.
  8. Clancy, K., Velopulos, C., Bilaniuk, J. W., Collier, B., Crowley, W., Kurek, S., et al. (2012, November). Screening for blunt cardiac injury: an Eastern Association for the Surgery of Trauma practice management guideline. The Journal of Trauma and Acute Care Surgery. 
  9. Edouard, A. R., Benoist, J. F., Cosson, C., Mimoz, O., Legrand, A., & Samii, K. (1998). Circulating cardiac troponin I in trauma patients without cardiac contusion. Intensive Care Medicine, 24(6), 569–573.
  10. Goldberg, S. P., Karalis, D. G., & Ross, J. J. (1993). Severe right ventricular contusion mimicking cardiac tamponade: the value of transesophageal echocardiography in blunt chest trauma. Ymem, 22(4), 745–747.

another bubble of trouble…

the case.

43 year old female is brought into your resuscitation bay by the paramedics.  She has a 2 day history of vomiting and diarrhoea on the background of type 2 diabetes and alcohol abuse.  Her son is concerned that she has become increasingly confused despite drinking her usual amount of alcohol.

As she passes by you notice that she is agitated, appears clinically dry and has some black discolouration around her mouth which her son believes to be red wine.

Her vital signs are:

  • Pulse: 170 regular
  • BP: 136/70
  • SaO2: 100% (room air)
  • RR : 40
  • GCS : 14 (E4V5M6)
  • Temp : 40.0*C

There are no family or friends available to provide a collateral history, however the paramedics inform you that she has a history of chronic right upper quadrant pain for which she takes regular codeine.  She does not appear to currently be in pain, but complains of nausea.

She has multiple drug allergies including: penicillins, cephalosporins and metronidazole.  The severity of these allergic responses is unclear.

On examination:

  • agitated yet cooperative.
  • tachypnoeic with no other chest signs.
  • clinically dry.
  • normal heart sounds.
  • abdomen soft with RUQ tenderness.  no evidence of an peritonism.
  • no blood on PR.
  • mild pitting oedema to the ankles.
  • moving all four limbs with good strength – no obvious focal neurological deficit.

Ketones = 0.1 mmol/L

  • Severe metabolic acidosis
    • HCO3 9, BE -14 (pH 7.40)
    • Anion Gap:
      • = Na – (HCO3 + Cl)
      • = 124 – (9 + 88)
      • = 27
      • HAGMA (Multifactorial with urea 20.2 & lactate 5.1)
    • Expected pCO2:
      • = (1.5x HCO3) +8
      • = (1.5 x 9) + 8
      • = 21.5 (±2)
    • Actual pCO2 = 15, ∴ potential concomitant respiratory alkalosis 
      • DDx – fever, pain, salicylate toxicity, VQ mismatch etc..
  • Moderate hyperglycaemia
    • However, ketones normal.
  • Mild hyponatraemia
    • Corrected Na = 131
  • Severe renal impairment
    • Creatinine 333, Urea 20.2.
    • ?Acute, ?2* to sepsis/hypoperfusion/dehydration
  • Moderately elevated lactate
    • ?Sepsis driven
    • ?Metformin-related
  • Mild anaemia


Severe high-anion gap metabolic acidosis with a concomitant respiratory alkalosis and an associated hyperglycaemia, hyponatraemia and mild anaemia.

Likely secondary to sepsis and associated acute kidney injury.

  • Sepsis
    • Gastroenteritis
    • Biliary
    • UTI
    • Pyelonephritis
  • Gastrointestinal
    • Pancreatitis
    • GI bleed
  • Metabolic / Endocrine
    • Hyperglycaemic Hyperosmolar State
  • Toxins
    • Ethanol poisoning (or toxic alcohol)
      • or acute withdrawal state
    • Paracetamol poisoning
    • Iron overdose
    • Mixed overdose
    • Metformin-induced lactic acidosis

  • Non-specific, slight LFT derangement.
  • NB. Calculated osmolality = 296, ∴ no significant osmolar gap.

  • Again, mild anaemia noted.
    • Macrocytosis (MCV 105) suggestive of chronic alcohol excess, however consider B12 or folate deficiency.
  • Normal WCC with mild lymphopenia.

  • Elevated INR without anticoagulation therapy.
    • Suggestive of mild liver disease or early coagulopathy from sepsis.

  • Optimise perfusion.
    • IV access
    • Fluid resuscitation
      • 0.9% Saline, 500ml-1000ml boluses
    • Maintain SBP >100 mmHg (MAP >65 mmHg)
      • May require vasopressors to achieve this
    • Aim for lactate clearance (>10% per hour), improved skin perfusion & normalisation of pulse/blood pressure.
    • Strict fluid balance
    • Aim for urine output of 0.5-1 mL/kg/hr.
  • Treat underlying sepsis
    • Early administration of broad-spectrum antibiotics
    • Identification of source
    • Source control if possible
  • Manage hyperglycaemia
    • Observe response to fluid bolus
    • Further control with insulin infusion
    • Cease oral hypoglycaemic agents
  • Detect other underlying illness
    • Screen for toxins: ethanol, paracetamol + salicylate levels requested
    • Further imaging requested: CT Brain plus CT abdomen/pelvis.
  • Supportive care:
    • Antiemetics
    • Antipyretics
    • Analgesia if required
    • Temperature control
    • Gentle sedation if required
    • Update family
  • Referral for ICU bed.

An indwelling catheter is placed and a small amount of cloudy urine is collected. Urinalysis demonstrates moderate blood, moderate leukocyte esterase but negative nitrites.

After initial resuscitation, she remains haemodynamically stable and appears to be slightly less confused, however during the wait for further imaging her blood pressure drops to 70/51 which is no longer responsive to fluid administration.

Peripheral inotropes are started whilst central access is obtained under gentle sedation.

Eventually, you obtain an abdominal CT…

There is a markedly abnormal appearance of the right kidney. There are extensive bubbly and linear streaks of gas throughout the majority of the renal parenchyma. There is also significant right peri-renal and peri-ureteric stranding. No definite collections can be appreciated on this non-contrast scan. No definite renal calculi are seen.

Appearances are consistent with extensive right emphysematous pyelonephritis which is thought to be Type I due to the extensive parenchymal involvement.

emphysematous pyelonephritis

Right sided emphysematous pyelonephritis

Emphysematous Pyelonephritis

– sepsis + delirium
– significant metabolic acidosis with respiratory alkalosis
– acute kidney injury

Emphysematous pyelonephritis is a necrotising, gas-producing infection of the kidney.  The common instigators are E. coli, Klebsiella pneumoniae and Proteus mirabilis. The pathogenesis is poorly understood, but elevated tissue glucose levels are thought to promote a favourable environment for gas-forming microorganisms. 

Risk factors:

  • Diabetes mellitus
  • Female
  • Age >60
  • Urinary tract obstruction

Clinical features:

Clinical features resemble those of acute, severe pyelonephritis. 

Thrombocytopenia, acute kidney injury, disturbance of consciousness or septic shock are commonly seen.


CT is the most definitive modality for diagnosis.  Contrast-enhanced CT is preferable, but may not be possible due to renal impairment.

Prognostic classification:

Emphysematous pyelonephritis can be categorised via two radiological classification systems.


CT features of emphysematous pyelonephritis differentiates into two types:

  • Type 1
    • greater than one-third renal parenchymal destruction
    • streaky or mottled appearance of gas
    • intra- or extrarenal fluid collections are characteristically absent
    • it is usually more aggressive and lead to death shortly, if not intervened early
    • mortality 70%
  • Type 2
    • destruction of less than one-third of the parenchyma
    • renal or extrarenal collections associated with bubbly or loculated gas, or gas within pelvicalyceal system or ureter
    • mortality 20%

Secondly into four classes based on the Huang-Tseng CT classification);

emphysematous pyelonephritis

Huang-Tseng CT classification of emphysematous pyelonephritis

Acute kidney injury, altered mental status and severe hyponatraemia are all significantly associated with mortality.


Treatment is fast becoming increasingly conservative.  Systemic antibiotics are the mainstay of management, in addition to percutaneous catheter drainage (PCD) or stenting to relieve any urinary tract obstruction.

Patients who either have severe radiological disease (class 3A or 3B) or multiple organ dysfunction have been shown to have better outcomes with nephrectomy.  If PCD is unsuccessful, nephrectomy is indicated.

You call the urology team who take the patient to the theatre for an emergency right-sided nephrectomy.

Given her complex medication allergies, Infectious Diseases are consulted who advise clindamycin and ciprofloxacin for ongoing antimicrobial coverage. This is later changed to meropenem.

She remains in intensive care for 48 hours post-op for inotropic support, following which she makes a progressive & uneventful recovery.


  1. emphysematous urinary tract infections –

  2. gas-forming infectionsLife in the Fast Lane

  3. Emphysematous pyelonephritis –

  4. Huang JJ, Tseng CC. Emphysematous pyelonephritis : clinicoradiological classification, management, prognosis and pathogenesis. Arch Intern Med 2000 Mar 27;160(6): 797-80

  5. Sanford et al. Emphysematous pyelonephritis : the impact of urolithiasis on disease severity. Transl Androl Urol. 2016 Oct; 5(5): 774-779

  6. Saadi A et al. Results of conservative management of emphysematous pyelonephritis. Nephrol Ther 2016 Dec; 12(7): 508-515

  7. Sharma et al. Emphysematous pyelonephritis : Our experience with conservative management in 14 cases. Urology Annals 2013; 5(3): 157-162

Author: Ming-Li Hodder
Web editing + additional writing: Chris Partyka