twist and shout….

the case.

34 year old female presents to ED with a 2 day history of worsening left-sided pleuritic chest pain associated with shortness of breath. There has been no associated cough, fever or sputum production.

She is one week post-Caesarian section; an uncomplicated, elective procedure from which she has recovered well.


  • prior LCSC (5 years ago)
  • Splenomegaly (?cause)
  • No regular medications
  • Penicillin allergy

On examination.
Alert but distressed in pain, able to speak in full sentences.
P 102, BP 126/70, RR 22, SaO2 99% (on air).
Heart sounds dual without rub or murmur.
Chest: Clear without crackles/wheeze. No pleural rub. Non-tender chest wall without rashes or vesicles.
Abdomen: Soft & NT with palpable spleen. Appropriately healing Caesarian scar.
No unilateral calf swelling or pitting oedema.

  • Pulmonary embolism
  • Pneumonia
  • Pneumothorax
  • Pleural effusion ?cause
  • Subphrenic pathology (including post-operative collection)
  • ….other ??

  • Hb 108, WCC 11.2, PLT 460
  • EUC/LFTs normal
  • ECG: Sinus tachycardia without features of right heart strain or myocardial ischaemia

Her is her CXR…

Twisting & Turning CXR

PA CXR with clear lung fields & normal cardiac silhouette. Costophrenic recess is preserved

Given the high pretest probability for PE and the lack of an obvious alternate diagnosis, you elect to proceed straight to advanced imaging and send your patient for a CTPA.

Here is her scan…


  • Suboptimal study; however no pulmonary embolism is demonstrated.
  • There is mild dependent atelectasis, worse on left.
  • The spleen is enlarged and its hilum faces laterally with varices. It also appears to sit inferiorly to its normal position (under the stomach & liver, and does not contact the diaphragm). It does not demonstrate its normal mottled appearance on the arterial phase.

Following a period of observation and titrated analgesia our patient settled and her observations normalised.

She was soon keen to go home and keep her newborn out of hospital. She was subsequently discharged with return precautions and a plan to followup with her GP the next morning.

The consultant radiologist has reviewed the images and amended the report.

It now reads;
” The spleen is enlarged and it is also rotated. It does not enhance normally and there is mild surrounding stranding. The splenic artery cannot be followed completely to the hilum. These findings are suspicious for splenic torsion.”

The patient is called back to the department and the diagnosis explained. She is admitted under the care of the surgeons and she undergoes further advanced imaging….

Arterial phase, axial CT of the abdomen. Red arrow demonstrating the laterally displaced splenic hilum.

Arterial phase, axial CT of the abdomen. Red arrow demonstrating the laterally displaced splenic hilum.


There are multiple case reports of spontaneous splenic torsion, typically relating to “a wandering spleen“.

What is a wandering spleen?

It is a rare condition characterised by the abnormal location of the spleen in the lower abdomen or pelvis. This results from increased splenic mobility due to the absence or laxity of its suspensory ligaments.

Wandering spleen has been described in patients ranging from 3 months to 82 years of age. It has an incidence of <0.25% of all splenectomies.


The causes of wandering spleen can be both congenital and acquired, with acquired risk factors including pregnancy, trauma & splenomegaly.

It can occur in all age groups, but classically occurs in 20-40 year old females. There are multiple case reports of splenic infarction occurring in postpartum women.


A wandering spleen may present clinically as an acute surgical abdomen secondary to torsion of the spleen around its vascular pedicle. This subsequently leads to splenic capsular stretch, ischaemia and infarction.

Although wandering spleen may be found incidentally as a mass in the abdomen without causing any complaint, it may cause chronic, subacute or acute abdominal pain secondary to torsion of the splenic pedicle resulting in vascular inflow and outflow thrombosis.

They are often found incidentally at surgery for completely unrelated complaints.


  • Acute torsion of the splenic pedicle with splenic infarction (most common complication)
  • Acute pancreatitis (due to pancreatic tail obstruction)
  • Upper GIT haemorrhage (from gastric fundus varices)


Splenectomy vs Splenopexy.

  • Splenic infarction typically requires splenectomy
  • Spleen preserving strategies (splenopexy) are reserved for healthy & non-infarcted spleens that are of normal size and without signs of hypersplenism.
    • They are highly recommended in paediatric patients to minimise the risk of post-splenectomy septicaemia.

  • Over the next 4 days in hospital our patient is managed conservatively with analgesia.
  • During this time she developed thrombocytosis (PLT > 1100) and was commenced on aspirin.
  • Given the fact she is now functionally asplenic, she was immunised according to a splenectomy program and was also commenced on roxithromycin 150mg daily (for prophylaxis, given penicillin allergy).
  • She received strict instructions on urgent medical review with onset of fever.

  1. Magowska, A. (2013). Wandering spleen: a medical enigma, its natural history and rationalization. World Journal of Surgery, 37(3), 545–550. doi:10.1007/s00268-012-1880-x
  2. Alimoglu, O., Sahin, M., & Akdag, M. (2004). Torsion of a wandering spleen presenting with acute abdomen: a case report. Acta Chirurgica Belgica, 104(2), 221–223.
  3. Anyfantakis, D., et al. (2013). Acute torsion of a wandering spleen in a post-partum female: A case report. International journal of surgery case reports, 4(8), 675–677. doi:10.1016/j.ijscr.2013.05.002

Mind the gap #2…

the case.

a 43 year old male presents to your ED with a three day history of severe epigastric pain and recurrent vomiting. He has now become increasingly breathless and is complaining of severe retrosternal chest pain.

On examination, he is appears unwell and is obviously diaphoretic. He is tachycardic (pulse 130, sinus) with a blood pressure of 148/80. He has no cardiac murmurs or pericardial rub & his chest is surprisingly clear to auscultation despite his respiratory rate of 36 per minute (SaO2 100%, room air). His temperature is normal.

The distinct fruity odour of ketones wafts through the room.

PMHx significant only for moderate, daily alcohol intake.

This is his initial venous blood gas…


BSL 7.2 mmol/L, Ketones “Hi” !!

MTG2 Electrolytes

  • Mild alkalaemia + features consistent with a metabolic acidosis.
    • pH 7.48, HCO3 17, BE -6. pCO2 23.
  • Expected CO2.
    • [HCO3 x 1.5] +8  (±2) – Winter’s formula
    • [17.6 x 1.5] +8
    • 34.4 (±2)
    • Lower than expected pCO2 consistent with additional respiratory alkalosis
  • Alternatively; expected HCO3 (for pCO2 of 23) in acute respiratory alkalosis
    • 24 – [(40 – 23)/10] (x2)
    • 24 – (1.7)x2
    • 20.6
    • This supports the presence of a concomitant metabolic acidosis (w/ actual HCO3 of 17)
  • Anion gap.
    • Na – [Cl + HCO3]
    • 136 – [85 + 15]
    • 36 – ie. markedly elevated – HAGMA.
  • Delta ratio.
    • [AG – 12 / 24 – HCO3]
    • [ 36-12 / 24 – 15 ]
    • 24 / 9
    • 2.67 ~ HAGMA + superimposed Metabolic alkalosis or Respiratory acidosis.
  • Additional findings;
    • Mild hypokalaemia
    • Moderate hypochloraemia
    • Obstructive LFT picture [ALP 354, GGT 846, Bili 60]
      ?Cholangitis ?Cholecystitis ??other
    • Moderate hypomagnesaemia + hypophosphataemia

Interpretation – a triple acid-base disturbance.

  1. High anion-gap metabolic acidosis; likely 2* to starvation or alcoholic ketoacidosis
  2. Hypokalaemic, hypochloraemic metabolic alkalosis; 2* to excessive vomiting [cause to be identified, possible biliary obstruction/cholangitis]
  3. Respiratory alkalosis; ?2* to pain/anxiety

Before getting too deeply entrenched in this topic, attached are basic notes on blood-gas analysis including anion gap & other secondary calculations.


This is used in the presence of a high-anion gap metabolic acidosis [HAGMA] to determine if it is truly a ‘pure’ HAGMA or if there is a coexistence of a normal-anion gap metabolic acidosis [NAGMA] or metabolic alkalosis.

Basic principles & assumptions.

  • If one molecule of acid (HA) is added to extra-cellular fluid & dissociates, the one H+ released will react with one molecule of HCO3 (to produce CO2 + H2O).
  • For every unit increase in an unmeasured ion (ie. anion gap increases by 1) there is a decrease in the serum bicarbonate by 1.
  • The delta ratio quantifies the relationship between the changes in anion gap & bicarbonate. For example: if all acids were to be buffered by bicarbonate, then the increase in anion gap should equal the decrease in bicarbonateThe ratio between these two (known as the DELTA ratio) should be equal to ONE.

The formula & interpretation of results.

Delta Ratio graphic

Delta ratio formula & interpretation of results


Some more specifics.

A low ratio (<0.4):

  • Occurs with a hyperchloraemic (normal-anion gap) acidosis.
  • Chloride (a measured anion) contributes to metabolic acidosis (effectively HCl) creating a low strong-ion difference.
  • The anion gap does not alter, whilst the serum bicarbonate decreases.

A high ratio (>2):

  • Occurs when there is a pre-existing elevated bicarbonate prior to the development of metabolic acidosis.
  • This typically arises from a metabolic alkalosis or compensation for a respiratory acidosis.

Lactic acidosis:

  • Typical delta-ratio in pure lactic acidosis is ~ 1.6 !!
  • Result from intracellular buffering; causing the rise in anion-gap to exceed the fall in bicarbonate.


You should be treating the patient that is in front of you & not just using these numbers in isolation. The chemistry is not perfect & you should have clinical evidence to support your diagnoses.

His ECG demonstrates a sinus tachycardia without features of cardiac ischaemia. His troponin was normal.

Here is his CXR…..


  • Erect CXR demonstrating clear lung fields and normal cardiac silhouette.
  • Retrocardiac air-fluid level adjacent to thoracic spine ?hiatus hernia, however with recurrent vomiting & retrosternal chest pain the differential diagnosis of Boerhaave syndrome needs considering.

With ongoing severe chest pain & an abnormal CXR, the decision is made to proceed to CT to further delineate the pathology.

The chest component of his CT revealed a small hiatus hernia, but no features of Boerhaave syndrome or aortic pathology.

Below is a single axial slice of his arterial-phase contrast CT…


Peri-pancreatic stranding & inflammatory changes consistent with acute pancreatitis


In the short-term our patient was managed with:

  • Analgesia:
    • Titrated intravenous opiates & subsequent Fentanyl PCA
  • IV fluids (kept nil-by-mouth)
    • Maintenance fluids
    • Dextrose infusion (to reverse ketosis)
    • Urinary catheter to guide fluid balance & titration
  • Correction of electrolytes (including potassium, phosphate & magnesium)
  • Thiamine (given history of alcohol intake)

He was admitted to a high-dependency bed under the care of the General Surgeons. His ultrasound failed to show evidence of persistent gallstones or biliary dilatation.

His pancreatitis (?induced by alcohol) was managed conservatively & made a progressive, uneventful recovery of the next 8 days.

  1. Delta ratio - LifeInTheFastLane
  2. Delta ratio –

Here are some more case-base examples to work through.

a splitting headache…

the case.

39 year old female presents to your Emergency Department with a four day history of a gradually worsening headache. Whilst she has a past history of migraines, this headache is much more severe and of different character to any migraine she has had previously.

Her husband has bought her in with the concern that she isn’t as ‘alert’ as normal and she ‘isn’t behaving quite right’. The patient continually requests that you “take this splitting headache away!”

She takes regular triptans for her migraines & also has a contraceptive vaginal ring in situ. She has no known allergies.

On examination she is slightly drowsy, has difficulty following commands & is unable to form complete sentences. Her observations are as follows; P 110, BP 140/88, afebrile, SaO2 98% (RA). Cardiorespiratory examination is unremarkable. She has no focal neurological deficits, specifically unremarkable cranial nerves & full limb strength with intact reflexes and sensation. Her gait is not assessed because of her drowsiness.

  • Space occupying lesion [tumour, abscess, other…]
  • Meningoencephalitis [viral vs bacterial vs other…]
  • Subarachnoid haemorrhage or other intracranial haemorrhage [extradural, subdural, intraparenchymal…]
  • Primary headache
  • Carotid or vertebral artery dissection
  • Vasculitis
  • Endocrine or metabolic [less likely…]

Basic laboratory investigations are unremarkable.

– BSL 7.2 mmol/L
– FBC normal
– Na 142 / K 4.3 / Ur 8.4 / Creat 76.
– CRP 21

Given the atypical nature of her headache and her altered mental state, you decide that she needs CNS imaging & send her for a CT…

Non-contrast (axial) CT brain.

Non-contrast (coronal) CT brain.

Non-contrast CT-brain report

Non-contrast CT-brain report

Upon returning from the radiology department, our patient has had an obvious deterioration in her neurological state. She is now obtunded with fluctuating periods of agitation.

Within minutes she has a generalised tonic-clonic seizure !!

Despite several doses of midazolam she continues to have short-lived seizure activity and requires intubation for airway protection and optimisation of ventilation.

With her airway secure, she returns to CT for further advanced imaging…

CT-Venogram (axial).

CT-Venogram (coronal).

CT venogram report

CT venogram report


Thrombosis of the dural sinus and/or cerebral veins (CVT) is an uncommon form of stroke, usually affecting young individuals. Despite advances in the recognition of CVT in recent years, diagnosis and management can be difficult because of the diversity of underlying risk factors and the absence of a uniform treatment approach.

It represents ~0.5-1% of all strokes.

  • 78% occur in patients < 50 years
  • 34% will have an inherited or acquired prothrombotic condition
Cerebral venous anatomy & sites of thrombosis.

Cerebral venous anatomy & sites of thrombosis.


  • Thrombophilias
    • Antithrombin III, Protein C & S deficiencies
    • Antiphospholipid & anticardiolipin antibodies
    • Factor V Leiden
    • Hyperhomocysteinaemia
  • Pregnancy & post-partum period (~6-8 weeks)
  • Oral contraceptive use
  • Malignancy
    • Local affects
    • Hypercoagulable state
    • Medications (eg. Tamoxifen)
  • Infection
    • Para-meningeal infections (ear, sinuses, dental, head & neck)
  • Dehydration
  • Substance abuse especially ecstasy
  • Haematologic
    • Nephrotic syndrome, polycythaemia, thrombocytosis, Fe-deficiency
  • Mechanical
    • Head trauma
    • Neurosurgery
    • Lumbar puncture
  • Systemic diseases
    • SLE
    • Thyroid disease
    • Inflammatory bowel disease
    • Sarcoidosis


Two major categories of clinical findings resulting from;

  1. Increased intracranial pressure (2* to impaired venous drainage)
  2. Focal brain injury from venous ischaemia/infarction or haemorrhage.

Patients typically present with a combination of these features.

  1. Headache is the most common symptom in CVT (~90%).
    • Typically diffuse and progresses in severity over days to weeks
    • Can be sudden & severe (“thunderclap”) or migraine-like.
    • Isolated headache (without neurology or papilloedema) occurs in ~25% of cases.
  2. Altered consciousness
  3. Altered vision
    • 6th nerve palsy
    • Cavernous sinus involvement
  4. Nausea & vomiting
  5. Seizures (focal or generalised, ~40% of cases)

Clinical features are often dependent upon the location of the thrombus (see table below).

Sinus thrombosis location+symptoms



  • Routinely: FBC, biochemistry & baseline coagulation profile
  • Screening for potential prothrombotic conditions may have a role (but won’t help you acutely…)

Lumbar puncture:

  • There are no specific CSF abnormalities in CVT.
  • Opening pressure is elevated in >80% of cases.
  • Elevated cell count & protein is also often seen.


  • A normal D-dimer may be considered to help identify patients with low probability for CVT.
  • However, a normal D-dimer should not preclude further evaluation in patients with high-suspicion for CVT.
  • Evidence limited to small prospective data (~400 patients)



  • Non-contrast CT scans are abnormal in only ~30% of cases.
  • The primary abnormality on a non-contrast CTB is hyperdensity of a cortical vein or dural sinus.

Noncontrast CT showing spontaneous hyperdensity of the right transverse sinus – Case courtesy of Dr Andrew Dixon, From the case Dural sinus thrombosis and venous infarction

  • Thrombosis of the posterior part of the superior sagittal sinus may result in a dense (or filled) delta sign (see below).
Direct visualisation of a clot in the cerebral veins on a non enhanced CT scan is known as the dense clot sign. ** image courtesy of 'The Radiology Assistant' @

Direct visualisation of a clot in the cerebral veins on a non enhanced CT scan is known as the dense clot sign. ** image courtesy of ‘The Radiology Assistant’ @

  • An ischaemic lesion that crosses usual arterial boundaries (or within proximity to a venous sinus) is suggestive of sinus thrombosis.
  • Intracerebral haemorrhage occurs in up to 30-40% of patients with CVT. They often have prodromal headache or bilateral parenchymal abnormalities.

CT Venography:

  • This may demonstrate a filling defect within the cerebral veins or sinuses known as the empty delta sign (see below).
Empty Delta Sign - sinus thrombus creates filling defect on contrast-enhanced CT *image courtesy of MediNuggets

Empty Delta Sign – sinus thrombus creates filling defect on contrast-enhanced CT *image courtesy of MediNuggets

  • A rapid & reliable method of diagnosing CVT
  • More useful in subacute & chronic disease states.
  • Equivalent to MR-venography.

MRI + MR-Venography:

  • More sensitive than CT at each stage after thrombosis.
  • Findings are variable depending on the age of the thrombus.
Case courtesy of Dr Ahmed Abd Rabou, From the case Dural venous sinus thrombosis

Case courtesy of Dr Ahmed Abd Rabou, From the case Dural venous sinus thrombosis

CT vs MRI in the Diagnosis of CVT - adapted from Saposnik et al (2011).

CT vs MRI in the Diagnosis of CVT – adapted from Saposnik et al (2011).


(1) Admit to a Stroke Unit.

(2) Anticoagulation.

  • Aim: prevent thrombus extension, facilitate recanalisation & prevent DVT/PE.
  • Initially: 
    • Unfractionated heparin vs Low-molecular weight heparin
    • No data to support one over the other for Mx of CVT.
  • Longer term:
    • Vitamin-K antagonists
    • Aiming for INR 2.0 – 3.0 for 3-6 months in most cases.
  • For advanced interventions – see below.

(3) Seek + Treat Precipitating Causes.

  • This includes bacterial infection (mastoiditis, meningitis etc) with management focusing on antibiotic therapy & surgical drainage of purulent collections.
  • If hormonal therapy if thought to be the culprit; remove the source if able.
  • Thrombophilia screening.

(4) Detect + Correct Complications.

  • Raised intracranial pressure + Hydrocephalus:
    • Consider this with increasing visual symptoms (or deteriorating visual acuity)
    • Management may include medical therapy (eg. acetazolamide), lumbar puncture, optic nerve decompression or shunts.
    • Decompressive craniectomy may be required in the setting of neurological deterioration due to severe mass effect or intracranial haemorrhage refractory to medical therapy.
  • Seizures:
    • Occur in up to 37% of adults (& ~50% of children) with CVT.
    • Anti-epileptic drugs are recommended following a single seizure (without parenchymal lesions).

(5) Advanced Interventions.

  • Fibrinolytic therapy.
    • 9-13% of patients w/ CVT have poor outcomes despite anticoagulation.
    • Recanalisation rates may be higher with thrombolysis, however this is reserved for cases of ongoing deterioration despite anticoagulation (or with increasing ICPs).
  • Direct catheter thrombolysis.
    • One small systematic review (169 patients) showed possible benefit of localised thrombolysis in severe CVT.
    • Carries a higher rate (17%) of intracerebral haemorrhage.
  • Mechanical Thrombectomy/Thrombolysis.
    • Various devices available; evidence is largely anecdotal.
  • Decompressive craniectomy.
    • Reserved for cases of refractory intracranial hypertension.
Algorithm for Management of CVT ** from Saposnik et al. 2011.

Algorithm for Management of CVT ** from Saposnik et al. 2011.

With her CT demonstrating extensive sinus thrombosis, our patient is commenced on a heparin infusion before heading to Intensive Care for ongoing management.

Following extensive thrombophilia screening it is thought that her contraceptive ring was the culprit.

Despite having a rocky inpatient course she is eventually discharged home without neurological deficit with ongoing anticoagulation (warfarin) and levetiracetam for seizure control.

  1. Saposnik, G., et al. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011; 42: 1158-1192 doi:10.1161/STR.0b013e31820a8364
  2. Piazza, G. Cerebral venous thrombosis. Circulation, 125(13), 1704–1709. doi:10.1161/CIRCULATIONAHA.111.067835
  3. Dural venous sinus thrombosis –

a covert combination…

the case.

72 year old male presents to your Emergency Department with a 4-5 hour history of palpitations. He appears well and has no associated symptoms.

BP 146/88, SaO2 99% (RA), chest clear.


  • Atrial fibrillation
  • Automatic implantable cardioverter-defibrillator [AICD]
    • Sick sinus syndrome with inducible VT on electrophysiology study
  • Hypertension

Here is his initial 12-lead ECG… ECG#1

Standard rate & calibration.

  •  Rate:
    • 150 bpm.
  • Rhythm.
    • Regular without obvious P waves.
  • Axis.
    • Rightward axis [+129*].
  • Intervals.
    • PR ~ n/a.
    • QRS ~ 160 msec [RBBB morphology]
    • QTc ~ 580 msec.
  • Segments.
    • QRS:T wave discordance
  • Other.
    • Features suggesting VT.
      • Fusion beats seen below (red & blue circles)
      • Monomorphic R-wave in V1.


Broad complex tachycardia with RBBB appearance and features of AV dissociation, highly concerning for ventricular tachycardia.

DDx: Atrial flutter (2:1) + RBBB.

annotated rhythm strip

My approach to any dysrhythmia, fast or slow, is to detect and correct;

  • Ischaemia
  • Electrolytes
  • Medications…

Meanwhile, the patient stays connected to a monitor with defibrillator pads placed for good measure. He is advised to stay nil by mouth, pending the need for sedation. You also arrange for his AICD to be interrogated.

We top up his magnesium and obtain this second ECG….

Broad complex tachycardia at a rate of 136 per minute. RAD. Underlined complex (#5) concerning for AV dissociation.

Broad complex tachycardia at a rate of 136 per minute. RAD. Underlined complex (#5) concerning for AV dissociation.


For more information on VT versus SVT with aberrancy see;

  1. Broad, fast & regular… – the blunt dissection
  2. VT versus SVT with aberrancy via

A-lead demonstrating fibrillation at a rate of 175-375 bpm. V-lead sensing independent ventricular tachycardia at a rate of 136/min.  There is no associated between the atrial & ventricular rhythms.

A-lead demonstrating fibrillation at a rate of 175-375 bpm. V-lead sensing independent ventricular tachycardia at a rate of 136/min. There is no association between the atrial & ventricular rhythms.

Double Tachycardia

ie. ventricular tachycardia with co-existing atrial fibrillation !!

Double tachycardia is a relatively uncommon type of tachycardia. It is classically defined as the simultaneous occurrence of organised atrial and ventricular tachycardias, or junctional and ventricular tachycardias.

Reported causes include;

  • Digitalis toxicity
  • Left ventricular dysfunction
  • Exercise
  • Catecholamine abuse

They can be difficult to diagnose and often require electrophysiology studies for further assessment. Interestingly, the presence of dual-lead ICDs now allow for this non-invasively.

Atrial Fibrillation with AICDs.

Atrial fibrillation is a very common dysrhythmia in patients requiring an AICD.

  • ~20% have AF at time of implantation
  • >50% of patients develop AF during the lifespan of their device.

In the setting of an AICD, AF can result in inappropriate ventricular shocks, ventricular arrhythmia induction & thromboembolism (after ventricular shocks in the presence of unknown AF).

Dual chamber rate-responsive pacing may prevent AF by improving haemodynamics, optimising ventricular filling and preventing retrograde atrial conduction. New overdrive pacing algorithms have been introduced to add incremental anti-arrhythmic benefits to physiological pacing. The aim is that consistent atrial pacing acts to suppress atrial fibrillation.

The PR Logic dual-chamber detection algorithm is widely used in dual-chamber Medtronic ICDs. It discriminates SVTs from ventricular tachycardias using hierarchal rules & timing of atrial and ventricular events.

Double Tachycardia Rules

annotated interrogation

An amiodarone bolus was administered and an infusion commenced following the AICD interrogation. Interestingly, his AICD was programmed to intervene on VT only at a rate exceeding 170 beats per minute.

Approximately 45 minutes into his infusion, our patient dropped his blood pressure into the 70’s with associated clamminess and distress. He received some ketamine sedation and was cardioverted to sinus rhythm.

He was discharged home two days later.

  1. Washizuka, T., Niwano, S., Tsuchida, K., & Aizawa, Y. (1999). AV reentrant and idiopathic ventricular double tachycardias: complicated interactions between two tachycardias. Heart, 81(3), 318–320.
  2. Santini, M., & Ricci, R. (2001). Atrial fibrillation coexisting with ventricular tachycardia: a challenge for dual chamber defibrillators. Heart, 86(3), 253–254.
  3. Weng, K.-P., Chiou, C.-W., Kung, M.-H., Lin, C.-C., & Hsieh, K.-S. (2005). Radiofrequency catheter ablation of coexistent idiopathic left ventricular tachycardia and atrioventricular nodal reentrant tachycardia. Journal of the Chinese Medical Association : JCMA, 68(10), 479–483. doi:10.1016/S1726-4901(09)70078-4
  4. Chowdhry, I. H., Hariman, R. J., Gomes, J. A., & El-Sherif, N. (1983). Transient digitoxic double tachycardia. Chest, 83(4), 686–687.
  5. Brown, M. L., Christensen, J. L., & Gillberg, J. M. (2002). Improved discrimination of VT from SVT in dual-chamber ICDs by combined analysis of dual-chamber intervals and ventricular electrogram morphology, 117–120.
  6. Jason’s Blog: ECG Challenge of the Week for Feb. 24th – March 3rd – another example of a double tachycardia case !!

against better judgement…

the case.

a 62 year old female is bought into your ED following a high-speed MVA. She has driven her car into telegraph pole at ~ 80km/hr.

She is haemodynamically stable, with an unremarkable primary survey. Of note, she has an obvious seat-belt abrasion over her anterior chest with significant sternal tenderness on palpation.

This is her mobile CXR taken in the resus-bay….

mobile CXR

Clearly her chest x-ray is abnormal. Whilst it is a poor inspiratory film [& the patient is supine], there is an abnormal mediastinal contour which is markedly widened. The trachea is also deviated to the right side.

In the setting of a moderate deceleration mechanism, this raises the suspicion of a blunt aortic injury. She needs to get to CT quickly…

In the meantime;

  • Two large-bore IVs are sited
  • Fentanyl administered for analgesia
  • EFAST performed: difficult study 2* to habitus. Possible LUQ free fluid.

Within the next 10 minutes she is transported to radiology for a CT ‘pan scan’….


  • Small 16×6 mm focal traumatic aortic dissection of the inner curvature of the aorta ~1.5cm distal to the origin of the left subclavian artery.
    • No other intrathoracic injuries
  • Multiple (undisplaced) pelvic fractures.
    • Left sacral ala
    • Anterior column of left acetabulum
    • Left pubic bone
    • Left inferior pubic rami
  • No intraabdominal injuries.
  • CTB + C-spine reported as normal also.

So let’s have a closer look…

Dissection01    Dissection02

Marked Dissection

Marked dissection 2

… with a pulse rate of 66 per minute & a blood pressure of 172/98.

What are you going to do now ?!?

This is a trauma patient with a blunt aortic injury. Extrapolating from the non-traumatic aortic dissections, you recognise the importance of both heart rate and blood pressure control in this scenario however cannot help but question the role of β-blockers & vasodilators in a patient with pelvic fractures & an equivocal FAST scan.

Against better judgement you commence a sodium nitroprusside infusion…


Blunt aortic injury is the second most common cause of death from blunt trauma following head injury.

The classic teaching of traumatic aortic injury is that it carries a dismal prognosis; that is 90% die at the scene and of the remaining 10%, 50% die within 24 hour and 90% will be dead within 4 months !! It is  It is important to recognise that this data originates from the 1950′s and now with the advent of endoluminal repairs one would expect better survival rates…

Current numbers suggest;

  • 50% of aortic injuries will rupture within 24 hours (~80% within the 1st week)
  • Overall mortality for those surviving to hospital evaluation is ~31%.

The most common location of injury is the aortic isthmus, accounting for 75-95% of cases. Whilst the aorta can be injured directly, there are several theories of various indirect forces resulting in aortic injury;

  • During deceleration the mobile heart & ascending aorta swing forward and can result in intimal tearing at the isthmus, where the descending aorta is fixed to the posterior chest wall.
  • Sudden rise in intraabdominal pressure creates a water-hammer effect within the aorta.
  • Osseous pinch results in entrapment of the aorta between the anterior chest wall & the vertebral column.
Aortic Isthmus. *adapted from

Aortic Isthmus.
*adapted from

Osseous pinch theory for Blunt Aortic Injury *adapted from ""

Osseous pinch theory for Blunt Aortic Injury                                                                   *adapted from “”

For more information on Aortic Dissection, especially clinical features, diagnostic tools and management - check out thebluntdissection – chest pain and… !!



Blunt aortic injury most often occurs after sudden deceleration, typically motor vehicle accidents (72% from ‘head-on’ collisions). Other causes include;

  • motor cycle or aircraft crashes
    • especially unrestrained drivers or ejected passengers.
  • pedestrian vs car
  • falls (>10 feet, 3 meters)
  • crush or compression injury


  • Chest (± back) pain
  • Dyspnoea
  • Hoarseness
  • 1st & 2nd rib fractures or sternal fracture
  • Multiple rib fractures (or flail chest)
  • Posterior displaced clavicle fracture
  • Brachial plexus injury
  • Palpable supraclavicular mass
  • Unexplained chest haematoma
  • Blood pressure differentials or pulse deficit


  • Widened mediastinum (>8cm)
  • Mediastinal/chest width ratio > 0.38
  • Obscured aortic knob
  • Depressed left main bronchus
  • Large haemothorax
  • Opacification of aorto-pulmonary window
  • Widened paratracheal & paraspinous stripes
  • Left apical cap
  • NG tube deviation
  • Others;
    • 1st or 2nd rib fractures
    • Multiple rib fractures
    • Sternal fracture
    • Posteriorly displaced clavicle fracture


Once the diagnosis is made, treatment must be timed properly. Whilst immediate operative repair used to be the rule, several studies now support a delayed repair with tight haemodynamic control especially with coexisting traumatic injuries such as head injury, exsanguinating bleeding, pelvic injuries or lung injury. The following table highlights this decision process;

adapted from

adapted from

In the unstable patient, management focuses on concomitant resuscitation whilst detecting and correcting the underlying cause of haemorrhage. It is important however, to avoid over resuscitation.


Associated injuries


Careful, meticulous blood pressure control is mandatory until definitive surgical repair can be performed. If operative repair is delayed, then systolic blood pressure should be corrected to 100-120 mmHg.

Whilst there are many feasible ways of doing this (depending on available medications & local practices), the key is to avoid rebound tachycardia which can increase shear stress on the intimal flap (ie. lowering the dP/dT). Therefore beta-blockers are often utilised with the vasodilator agent (eg. esmolol + nitroprusside), aiming for a pulse rate of 60 per minute.


Open surgical repair is usually indicated for;

  • Haemodynamic instability
  • Large-volume haemorrhage from chest tubes
  • Contrast extravasation on CT (or rapidly expanding mediastinal haematoma)
  • Penetrating aortic injury

Endovascular repair has documented benefits such as reduced blood loss, minimally invasive approach, allowance for neuroprotective positioning and reduction in rates of paraplegia. A significant limitation at present is, if the aortic injury occurs adjacent to a sharp bend the graft may provide poor apposition and risks device collapse. Proximity to the left subclavian artery can also result in ischaemia and care must be taken in those with a dominant left vertebral circulation.

… with the nitroprusside infusion trickling in her blood pressure gradually drifts down to 120 mmHg systolic !! Interestingly her pulse rate does not budge & you wonder if she is pre-morbidly beta-blocked. This was not clarified at the time due to language barrier.

Behind the scenes, arrangements are made with Interventional Radiology and Vascular Surgery to proceed to the angiography suite.

Here are her images…

Angio01    Post stent

Following an uneventful procedure, she is transferred to Intensive Care for ongoing observation and tight blood pressure control.

Here is her CXR on day 2…

day 2 CXR

She continues to make a slow but steady recovery….

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  2. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
  3. Parmley, L. F., et al. (1958). Nonpenetrating traumatic injury of the aorta. Circulation, 17(6), 1086–1101. doi:10.1161/01.CIR.17.6.1086
  4. Dosios, T. J., Salemis, N., Angouras, D., & Nonas, E. (2000). Blunt and penetrating trauma of the thoracic aorta and aortic arch branches: an autopsy study. The Journal of Trauma: Injury, Infection, and Critical Care, 49(4), 696–703.
  5. Reed KC & Curtis LA. Aortic Emergencies – Part II: Abdominal Aneurysms And Aortic Trauma. Emergency Medicine Practice. 2006; Volume 8, Number 3.
  6. Nagy, K., Fabian, T., Rodman, G., Fulda, G., Rodriguez, A., & Mirvis, S. (2000, June). Guidelines for the diagnosis and management of blunt aortic injury: an EAST Practice Management Guidelines Work Group. The Journal of Trauma: Injury, Infection, and Critical Care48(6): 1128-43.
  7. Fabian TC, Davis KA, Gavant ML,et al. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg. 1998;227:666-76
  8. Traumatic Aortic Injury –