collective crises…

the case.

a 28 year old female is brought into your resuscitation bay by paramedic crews following a two day history of nausea and vomiting. As she rolls past, you notice that she is distressed with pain, looks clinically very dry and is quite drowsy.

Her vital signs are:

  • Pulse: 156
  • BP – unrecordable
  • SaO2 – 82%
  • RR – 32
  • GCS – 13 (E3V4M6)
  • Temp – 38.2*C

As you commence your primary survey her sister enters the room and informs you that she has had nausea and vomiting for “a few days” and that she has developed “a strange bruise around the belly button”.

On examination:

  • Distressed with pain.
  • Tachypnoeic without obvious accessory muscle use. 
  • Cold hands & feet. Warm centrally.
  • Chest clear to auscultation.
  • HS dual. No murmurs, rubs or gallop.
  • Abdomen: generalised tenderness with periumbical swelling, tenderness and surrounding ecchymoses. No organomegaly. No prior surgical scars.
  • No peripheral oedema.
  • No focal neurological deficit.

You pause for a moment and think…

  • Sepsis:
    • Pneumonia
    • Meningoencephalitis
    • Intra-abdominal (biliary, appendicitis, colitis, etc…)
    • + others…
  • Gastrointestinal:
    • Pancreatitis ?Cullen’s sign
    • Mesenteric ischaemia
    • Bowel obstruction
    • Malignancy (+gastric outlet obstruction)
  • Cardiogenic:
    • Dysrhythmia
    • Valvular heart disease
    • Myo-pericarditis
  • Metabolic/Endocrine:
    • Diabetic ketoacidosis
    • Adrenal insufficiency
  • Ectopic pregnancy


  • Mixed acid-base disturbance
    • Features of metabolic acidosis:
      • Lactate >8, Urea 26 – contributing to a HAGMA
    • Features of respiratory acidosis:
      • Elevated pCO2 (56 mmHg)
    • Likely concomitant metabolic alkalosis:
      • Despite above findings, pH is only 7.32.
      • Hx of vomiting predicts volume-contracted metabolic alkalosis
  • Severe hyperlactataemia
  • Life threatening hyperkalaemia requiring immediate correction
  • Moderate hyponatraemia
  • Elevated serum urea & creatinine
    • Acute kidney injury ?2* hypovolaemia/hypotension/sepsis
  • Elevated haematocrit
    • Supportive of volume depletion


Mixed acid-base disturbance with markedly elevated lactate, acute kidney injury and life-threatening hyperkalaemia plus evidence of hypovolaemia.

This could be explained by septic shock, gut ischaemia or toxic ingestion (toxic alcohol, metformin or iron overdose, etc).
The combination of hyperkalaemia, hyponatraemia & elevated lactate raises suspicion for adrenal insufficiency.

The patients’ sister wants to give you more details that she thinks is important…

  • She tells you that the patient has a history of Arthritis as well as Adult-onset Still’s disease
  • She takes 25mg of Prednisone daily
  • She has not opened her bowels or passed flatus for the past 2 days.

You are now convinced her umbilical swelling is an incarcerated hernia

  1. Maximise oxygenation.
    • High flow oxygen via non-rebreather mask
  2. Optimise perfusion
    • IV access
    • 20mL/kg 0.9% Saline bolus (~500-1000mL), repeat x2
    • Aim: SBP >100 (MAP >65), cap refill <2 sec, lactate clearance (>10% per hour), urine output >0.5 mL/kg/hr.
  3. Correct life-threatening hyperkalaemia
    • Calcium (QRS >100msec)
      • 20mL of 10% gluconate solution
    • Salbutamol
      • 10mg via nebuliser
    • Insulin + dextrose
  4. Steroid replacement
    • IV Hydrocortisone 4mg/kg (~200mg)
    • Continue 50-100mg q6h IV
  5. Treat potential underlying sepsis
    • Fever at triage, plus elevated lactate & abdominal pain.
    • Empiric antibiotics (Ampicillin, Metronidazole, Gentamicin)
  6. Detect & correct underlying precipitating illness
    • Urgent surgical bedside review
    • Strict fluid balance
    • Nasogastric tube
  7. Supportive care
    • Analgesia
      • Simple (paracetamol)
      • Titrated intravenous opiates
    • Urinary catheter
    • Control temperature
    • DVT prophylaxis
    • Update family

Adrenal Crisis

Adrenal crisis refers to acute adrenal insufficiency, which is the clinical manifestation of deficient production or action of glucocorticoids, with or without deficiency also in mineralocorticoids and adrenal androgens. It is a disorder that can result from primary adrenal failure or secondary adrenal disease due to impairment of the hypothalamic–pituitary axis.

Adrenal cortex refresher.

The adrenal cortex has three distinct zones, which secrete the various hormones under the direct control of well understood feedback mechanisms.

The Adrenal Glands. Three cortical layers with different hormone production & function. Courtesy of BC Open Textbooks

The Adrenal Glands. Three cortical layers with different hormone production & function. Courtesy of BC Open Textbooks

The basics.

Adrenal crisis is most common in patients with primary adrenal insufficiency, but may also occur in those with secondary or tertiary adrenal insufficiency (eg. from acute illness or stressor in patients with chronic adrenal insufficiency who are not adequately replaced). It is a life-threatening emergency that requires immediate diagnosis and management.

Depending on the underlying mechanism, adrenal insufficiency is classified as primary, secondary, or tertiary.

Primary adrenal insufficiency.

  • Mineralocorticoid deficiency
  • Results from disease intrinsic to the adrenal cortex.
  • Causes:
    • Autoimmune adrenalitis (eg. Addison’s)
      • Isolated vs Polyendocrinopathy
    • Infectious adrenalitis (eg. TB, HIV, syphilis)
    • Bilateral adrenal haemorrhage (Waterhouse-Friderichsen syndrome)
    • Bilateral adrenal metastases/infiltration
    • Genetic disorders
  • Major clinical features: volume depletion & hypotension

Secondary & tertiary adrenal insufficiency.

  • aka. central adrenal insufficiency
  • Isolated glucocorticoid deficiency
  • Causes:
    • Pituitary tumours
    • Post-pituitary surgery/radiation
    • Pituitary infiltration/infection
    • Pituitary apoplexy (including Sheehan’s syndrome)
    • Genetic disorders
    • Drug-induced adrenal insufficiency – as in this case, is the most common cause of tertiary adrenal insufficiency.
  • Major clinical features: hypotension (from decreased vascular tone)
    • Volume depletion tends not to occur

Clinical features.

Primary adrenal insufficiency.

This clinical picture results from deficiency of all adrenocortical hormones (aldosterone, cortisol, androgens); they can also include signs of other concurrent autoimmune conditions. Most of the symptoms are non-specific (fatigue, anorexia, weight loss, nausea & vomiting). Hypoglycaemia can be the presenting sign in children.

A specific sign of chronic (but not acute) primary adrenal insufficiency is hyperpigmentation. This predominantly affects areas of skin subjected to pressure (elbows, knuckles, palmar creases, lips, buccal mucosa). It is caused by stimulation of the melanocortin-1 receptor in the skin by the high circulating corticotropin concentrations.

Central adrenal insufficiency.

The clinical manifestations of secondary or tertiary adrenal insufficiency result from glucocorticoid deficiency only (secretion of aldosterone and adrenal androgens is preserved). They may also herald signs of the primary underlying disorder as well.


A life-threatening adrenal crisis can be the first presentation of adrenal insufficiency. The acute presentation can be precipitated by a physiological stress, such as surgery, trauma, or an intercurrent infection.

Clinical features include vomiting, fever, confusion, abdominal pain, myalgia, joint pains, severe hypotension and hypovolaemic shock.

Investigations typically reveal hypoglycaemia, hyponatraemia (with hypoosmolarity), hyperkalaemia & elevated urea and creatinine.

The diagnosis is made clinically, or by (1) plasma cortisol level < 80 mmol/L or (2) a short synacthen test of 250mcg (normal response = cortisol > 525mmol/L).


Treatment of acute adrenal crisis consists of immediate administration of hydrocortisone (100mg IV q6h) and volume replacement. Hypoglycaemia should be immediately reversed and electrolyte derangements should be corrected as required (especially hyperkalaemia).

NB. The use of hydrocortisone will complicate further assessment of adrenal function. An alternative, which does not interfere with measurement of cortisol and ACTH stimulation testing, is the administration of dexamethasone 4 to 6 mg every 12 h given intravenously or intramuscularly.

Mineralocorticoid replacement (oral fludrocortisone 0.1mg Q6 hrly) may be required beyond the acute resuscitation phase, however is often not required in patients with secondary adrenal insufficiency or in those with primary adrenal insufficiency receiving more than 50mg hydrocortisone daily, given its potent mineralocorticoid activity at high doses.

The underlying precipitating cause should be sought and addressed also.

Stress dose steroids in patients with chronic adrenal insufficiency.

Recommendations regarding glucocorticoid coverage during non-surgical illnesses are largely based on expert consensus. Traditionally patients have been advised to double or triple their daily dose of glucocorticoid therapy during a febrile illness until recovery.

Here is her CXR…


Clear lung fields. Visible dilated loops of small-bowel in upper abdomen.

The Surgical Registrar arrives at the patients’ bedside. He announces that he will take the patient to theatre now if you can prove that they have a bowel obstruction…

Dilated small bowel loops (>3.4cm) with oedematous wall.

Dilated small bowel loops (>3.4cm) with oedematous wall.

The patient leaves your resus bay for the operating theatre within 90 minutes of arriving to hospital.

She undergoes a laparotomy, small bowel resection (~8cm) with an end-to-end anastomosis and umbilical hernia repair. Following this, she makes an uneventful recovery with stress-dose steroid coverage under the guidance of the Endocrinologists.


  1. Charmandari, E., Nicolaides, N. C., & Chrousos, G. P. (2014). Adrenal insufficiency. The Lancet, 383(9935), 2152–2167.

  2. Jung, C., & Inder, W. J. (2008). Management of adrenal insufficiency during the stress of medical illness and surgery. The Medical Journal of Australia, 188(7), 409–413.

  3. Shenker, Y., & Skatrud, J. B. (2001). Adrenal insufficiency in critically ill patients. American Journal of Respiratory and Critical Care Medicine, 163(7), 1520–1523.

  4. Clinical manifestations of adrenal insufficiency in adults –

  5. Treatment of adrenal insufficiency in adults –

  6. Adrenal insufficiency – Life in the Fast Lane

Similar cases via #FOAM.

UOTW #44 via Ultrasound of the Week

Clinical Case 064: Um-bil-obstruction via Broome Docs

Author: Andi Rauch
Web editing + additional writing: Chris Partyka

an insidious intruder…

the case.

28 year old male presents to your tertiary emergency department with chest pain, exertional dyspnoea and left calf pain.

He describes a six week history of progressive exertional dyspnoea that has become especially worse over the past 48 hours. He presents to hospital today (via his family doctor) as he is now only able to walk ~5 metres before succumbing to dyspnoea and left leg pain. His GP found him to be a little ‘wheezy’ prior to the transfer, so he was given two doses of nebulised salbutamol. This had little effect.

He has no significant past medical history and he takes no regular medications.

On review of systems; he reports mild cigarette use (no illicit drug use), no recent overseas travel or sick contacts, no recent surgery, no haemoptysis and no prior history (or family history) of thromboembolic disease.

On examination:

  • Alert & oriented but with moderate respiratory distress & increased work of breathing.
  • RR 30, SaO2 94% (4L via NP). Reduced air entry bibasally (no added sounds).
  • Pulse 130/min and regular. HS dual without murmurs or rub. Distended JVP.
  • Abdomen soft & non-tender.
  • Mild calf tenderness bilaterally (L>R) but no pitting oedema or overlying erythema.

  • Acute coronary syndrome
  • Pulmonary embolism
  • Cardiomyopathy
  • Valvular heart disease
  • Acute pericarditis/myocarditis
    • ± pericardial effusion
  • Pneumonia (atypical)
  • Thyroid disease
  • Autoimmune (SLE, RA etc)
  • Toxins (amphetamines/cocaine)

LV thrombus ECG, Left ventricular thrombus

12-lead ECG.

  • Sinus tachycardia (rate ~126/min).
  • Left axis deviation.
  • Poor R-wave progression.
  • LVH with repolarisation abnormality.
  • Inferior T-wave flattening.

Young DCM ABG, Left ventricular thrombus

  • 1* Respiratory alkalosis
    • pH 7.50, pCO2 21
  • Expected HCO3
    • Expect pCO220mmol/L
    • Actual = 16 ∴ concomitant metabolic acidosis
  • Concomitant metabolic acidosis.
    • Anion Gap = 138 – (99+20)
    • = 138-119
    • = 19 (∴ HAGMA 2* hyperlactataemia)
  • A-a gradient:
    • PAO2 = PiO2 – (PaCO2 x 1.25)
    • = 0.28 x(760-47) – (21×1.25)
    • = 200-25
    • =175
    • PaO2 = 80
    • A-a gradient = ~95mmHg (markedly elevated).


  1. Primary respiratory alkalosis with  a markedly elevated A-a gradient.
    • DDx include pulmonary embolism, congestive cardiac failure, pneumonia, collapse/consolidation or interstitial lung disease.
  2. Concomitant high-anion gap (hyperlactataemic) metabolic acidosis.
    • Suggestive of hypoperfusion state ?sepsis  ?cardiac failure ??other…

NB. It is important to note that a chronic alkalaemia can also lead to an elevated lactate (Ref 9.)

Young DCM CXR, Left ventricular thrombus

Cardiomegaly with mild pulmonary vascular congestion (correlate clinically).

and then his lungs…

  • Globally poor LV ejection fraction consistent with a dilated cardiomyopathy.
  • Diffuse, symmetrical B-lines on lung ultrasound confirmatory of interstitial pulmonary oedema.
Young DCM EPSS, DCM with Left ventricular thrombus

Dilated cardiomyopathy with markedly reduced LVEF demonstrated by an EPSS >35mm.  Ref. McKaigney, C. et al (2014)

Left Ventricular Thrombus

Left ventricular thrombus is a frequent complication in patients with acute anterior myocardial infarction and in those with dilated cardiomyopathy. The clinical importance of left ventricular thrombus lies in the potential for systemic embolisation, particularly stroke.

Echocardiographic studies from the pre-thrombolytic era demonstrated that left ventricular thrombus developed in a third (& up to 56%) of patients with anterior Q wave MIs, primarily when apical akinesis or dyskinesis is present, but were infrequent in those with non-anterior and non-transmural MI (<5%). In the modern era where PCI is so readily available, these rates have fallen to approximately 5 to 15%.

Left ventricular thrombus is also a common finding in patients with congestive heart failure (incidence is approximately 10-30%) as a result of severe left ventricular systolic dysfunction (especially those with dilated cardiomyopathy).


The genesis of left ventricular thrombus (LVT) is dependent upon Virchow’s Triad of (1) stasis, (2) hypercoagulable state and (3) endothelial injury. The most common clinical settings complicated by left ventricular thrombus are acute myocardial infarction and dilated cardiomyopathy.

LV Thrombus post-AMI.

  • All pathophysiologic prerequisites are present:
    • Regional & global LV dysfunction leading to stasis
    • Endothelial injury
    • Hypercoagulable state.
  • Apical stasis associated with specific abnormal flow patterns is predictive of subsequent thrombus formation.
  • Thrombus primarily develops in the first week following MI.

LV Thrombus + Dilated Cardiomyopathy.

  • Left ventricular thrombi that complicate dilated cardiomyopathy also are located more commonly at the apex, perhaps reflecting the propensity for left ventricular stasis to be located furthest from the inflow and outflow tracts.
  • Hypercoagulability and endothelial dysfunction also are associated with dilated cardiomyopathy, fulfilling Virchow’s triad.
  • Coexisting right ventricular thrombus (resulting in biventricular thrombus) has been recorded as high as 15.2% in subjects with dilated cardiomyopathy and left ventricular thrombus.
  • Unlike in AMI, the formation of LV thrombus in these patients is not marked by a distinct clinical event, therefore are more likely to be ‘an occult’ clinical discovery.


  • Embolisation of an LV thrombus post-AMI typically occurs in the second week (or beyond).
    • Increased occurrence in patients with improved LV function (either spontaneously, or as a result of reperfusion strategies).
  • In patients’ with dilated cardiomyopathy, the natural history is less clear.
    • Those who do present with embolisation typically have larger ventricles and more impaired systolic function.
    • Echo features of the thrombi such as protrusion, mobility & central echolucency appear to predict embolisation risk more accurately than serial ejection fraction assessment.

Making the diagnosis.

Transthoracic echocardiography (TTE) is the cornerstone imaging modality for the diagnosis of left ventricular thrombi; influenced by its availability, safety and convenience. It has been demonstrated to have sensitivity of 90–95% and specificity of 85–90% in a setting with adequate imaging.

Given the propensity for thrombi to form at the apex of the LV, the best imaging planes to visualise LVT are the apical views, where the transducer is closest to the region of interest.

Echocardiographic criteria for LVT include:

  • A distinct echogenic mass within the LV cavity that is contiguous with, but acoustically distinct from the underlying endocardial surface.
    • It is seen throughout the cardiac cycle and visualised on at least 2 orthogonal views.
    • May be sessile/layered or protruding/mobile.
  • An associated underlying region of severe wall motion abnormality.
    • This is usually severe hypokinesis, akinesis, dyskinesis, or aneurysmal dilatation.
  • Additionally; spontaneous echo contrast  is commonly seen within the LV of patients with intracardiac thrombi. This is believed to be due to the interaction of red cells and plasma proteins in situations of low, stagnant flow.
    • The presence of spontaneous echo contrast in association with marked wall motion abnormalities should warrant a high suspicion for the presence of LVT.

Examples of LVT on echo.

Multiple LVT with central lucency and LV spontaneous echo contrast in DCM - Image from

Multiple LVT with central lucency and LV spontaneous echo contrast in DCM – Image from Talle et al (2014).

An apical mural thrombus (T) - Image from Stokman et al (2001).

An apical mural thrombus (T) – Image from Stokman et al (2001).

Pedunculated apical thrombus (arrows) at high risk for embolization, seen protruding into the LV cavity, with mobility throughout the cardiac cycle - Image from Billingsley (2005)

Pedunculated apical thrombus (arrows)
at high risk for embolization, seen
protruding into the LV cavity, with
mobility throughout the cardiac cycle – Image from Billingsley (2005)

Despite the advances in ultrasound imaging technologies and higher-frequency transducers, approximately 10-30% of 2D TTE examinations remain inadequate. The use of contrast echocardiography with intravenous ultrasound contrast agents has provided incremental value in the structural assessment of the LV.

Transoesophageal echocardiography plays a less important clinical role in the diagnosis of LVT, but may be helpful for patients with very poor transthoracic acoustic windows or small thrombi.

Newer imaging techniques such as cardiac CT and MRI have produced promising results for detection of LVT, especially in patients with poor acoustic windows and smaller thrombi.


The goal of treatment is to prevent systemic embolus, especially stroke. In the SOLVD study prevention and treatment cohorts, the annual incidence of stroke, PE and peripheral emboli in patients with heart failure (LVEF 35%) in sinus rhythm was 2.4% and 1.8% in women and men, respectively.

No data exists for the primary prevention of LVT in patients with dilated cardiomyopathy.

Prevention of systemic thromboembolism, in particular stroke, has been proposed with warfarin (target INR 2-3) indefinitely, but there are no randomised trials to verified the efficacy of this strategy. There appears to be clinical equipoise with regard to the use of anticoagulation over antiplatelet therapy (WASH & WATCH trials).

The treatment of LVT should be directed by the clinical risk for systemic embolism.

    • Features: recent MI, recent systemic embolus and/or thrombus protrusion or mobility on echo.
    • TREATMENT = Anticoagulation (Heparin + Warfarin)
    • Features: remote MI, absence of clinical evidence of systemic embolus and/or mural or sessile thrombus without mobility on echo.
    • TREATMENT = Warfarin (INR 2-3) for 3 months with repeat imaging for ?resolution.
    • Features: mural LVT without protrusion or mobility located within a left ventricular aneurysm
    • TREATMENT: May not be required…

Finally; intravenous thrombolytics have been used to lyse left ventricular thrombi but carry the risk of precipitating embolic events and are not routinely recommended.

Your colleagues in Cardiology quickly review the patient after your initial referral & agree with the findings of your point-of-care ultrasound.

They arrange for a CT Aortogram with arterial run-off with a clinical concern of systemic embolisation from this LV thrombus with unilateral leg pain and an elevated lactate.

Here are the scans…

Young DCM CT report

Young DCM CT Runoff Tibial art, Left ventricular thrombus

Following review of the above images our patient is admitted to the Coronary Care Unit after being commenced on a heparin infusion…

  • Vascular surgery were consulted regarding his popliteal artery occlusion. They managed this conservatively.
  • He was commenced on various medications for his cardiomyopathy including bisoprolol, perindopril and ivabradine plus frusemide for diuresis.

Unfortunately, this young man was lost to follow-up & to date a precipitating cause for his cardiomyopathy has not been identified…

  1. Stokman, P. J., Nandra, C. S., & Asinger, R. W. (2001). Left Ventricular Thrombus. Current Treatment Options in Cardiovascular Medicine, 3(6), 515–521.

  2. Greaves, S. C., Zhi, G., Lee, R. T., Solomon, S. D., MacFadyen, J., Rapaport, E., et al. (1997). Incidence and natural history of left ventricular thrombus following anterior wall acute myocardial infarction. The American Journal of Cardiology, 80(4), 442–448.

  3. Talle, M. A., Buba, F., & Anjorin, C. O. (2014). Prevalence and Aetiology of Left Ventricular Thrombus in Patients Undergoing Transthoracic Echocardiography at the University of Maiduguri Teaching Hospital. Advances in Medicine, 2014, 731936.

  4. Stratton, J. R., & Resnick, A. D. (1987). Increased embolic risk in patients with left ventricular thrombi. Circulation, 75(5), 1004–1011.

  5. Stratton, J. R., Nemanich, J. W., Johannessen, K. A., & Resnick, A. D. (1988). Fate of left ventricular thrombi in patients with remote myocardial infarction or idiopathic cardiomyopathy. Circulation, 78(6), 1388–1393.

  6. Abdelmoneim, S. S., Pellikka, P. A., & Mulvagh, S. L. (2014). Contrast echocardiography for assessment of left ventricular thrombi. Journal of Ultrasound in Medicine, 33(8), 1337–1344.

  7. Billingsley, I. M., & Leong-Poi, H. (2005). Left Ventricular Thrombus: Diagnosis, Prevention, and Management. Cardiology Rounds. (St Michael’s Hospital, University of Toronto). via

  8. Bettari, L., Fiuzat, M., Becker, R., Felker, G. M., Metra, M., & O’Connor, C. M. (2011). Thromboembolism and antithrombotic therapy in patients with heart failure in sinus rhythm: current status and future directions. Circulation: Heart Failure, 4(3), 361–368.

  9. Hall, A. M., & Bending, M. R. (2009). Severe hyperlactaemia in the setting of alkalaemia. Clinical Kidney Journal, 2(5), 408–411.

  10. McKaigney, C. et al (2014). E-point septal separation: a bedside tool for emergency physician assessment of left ventricular ejection fraction. The American Journal of Emergency Medicine, 32(6), 493–497.

Author: Ruta Zaliunaite
Web editing + additional writing: Chris Partyka

a perplexing paradox…

The case.

a 70 year old female is bought to your ED at 10pm via ambulance with a dense left-sided hemiparesis following a witnessed collapse at home only 30 minutes earlier.

She had apparently been well during the day and was seen to collapse to the ground whilst taking the rubbish outside after dinner. Her next-door neighbour states that the patient was alert but unable to communicate immediately after the event.

Her past medical history is significant for:

  • T2DM (on insulin)
  • HTN
  • Heavy smoker

Upon arrival to the department the patient looks unwell. She is pale and incredibly diaphoretic… 

On examination:

  • P 104/min (sinus), BP 70 systolic, SaO2 70% (15L NRB mask), RR 34, Temp 36.4*C
  • Chest clear to auscultation
  • HS dual. No murmurs, rubs or gallop.
  • Abdomen soft & non-tender without palpable pulsatile masses.
  • GCS 10/15 (E4, V1, M5) with obvious left-sided facial droop & dense (0/5) hemiparesis.
  • No peripheral oedema. Peripheral pulses present. No limb swelling.

You pause for a moment and think…

Collapse & hemiparesis 

  • ? Ischaemic stroke
  • ? Intracranial haemorrhage (including SAH, AVM)
  • ? Seizure with Todds paresis

But she’s terribly diaphoretic!!

  • ? Hypoglycaemia (can cause focal neurology and is considered a stroke mimic)

But how do you explain the hypoxia or the shock??

  • ? Myocardial infarction
  • ? Aortic dissection
  • ? Dysrhythmia
  • ? Acute valvular pathology / AAA rupture

But her chest is clear!!

  • ? Pulmonary embolism

With such a diverse list of potential diagnoses, you commence resuscitation and continue your investigations…..

  • BSL 8.4mmol/L
  • ECG: no STEMI or evidence of ischaemia
  • CXR:

Perplexing paradox CXR

During the first 15 minutes in the Emergency Department her treatment includes;

  • 2x IV access
  • Fluid bolus – 1L 0.9% Saline
  • Arterial line is placed
  • Peripheral adrenaline infusion commenced & rapidly titrated to 20mcg/min
  • Pre-oxygenation whilst the team set up for rapid-sequence intubation

  • No pericardial effusion
  • No PTx or intraperitoneal fluid.
  • No AAA
  • A large right ventricle is noted
  • Her IVC is distended and non-collapsing

Following an uneventful RSI, she remains hypoxic and shocked.

Her observations are now…

  • Pulse 110
  • BP 76/50 – now on 30mcg/min of adrenaline
  • SaO2 94% on FiO2 1.0 & PEEP 8cmH2O

This is her blood gas…

Perplexing paradox ABG

Severe hypoxaemia with an Aa gradient >500

You are now faced with a challenging scenario…

This critically ill lady has features of a simultaneous acute stroke plus massive pulmonary embolism !!

She is too sick to move from your resuscitation bay and you do not consider it safe to transfer her to radiology for advanced imaging.

Given this challenging clinical snookering you decide to administer empiric intravenous thrombolysis (alteplase) based on the likelihood that this is most likely a thrombotic aetiology.

Within 10 minutes of your bolus dose her haemodynamics normalise and you are able to wean the vasopressor infusion back to 5 mcg/min. Her oxygen requirement also subsequently falls…

CT Brain.

There is a hyperdense left MCA (at M1/M2 junction) consistent with acute thrombosis. There is acute infarct involving the insular cortex and frontal operculum.

Perplexing Paradox CTB


Multiple segmental and subsegmental pulmonary emboli demonstrated bilaterally. There is minor reflux of contrast into the IVC and the right ventricle is prominent in keeping with a degree of right heart strain.

Perplexing Paradox CTPA

Paradoxical Embolism

The basics.

Paradoxical embolism refers to the clinical phenomenon of thromboembolism originating in the venous vasculature which traverses through an intracardiac or pulmonary shunt into the systemic circulation.

Paradoxical embolisms have been documented in medical literature as far back as 1877. These result from a venous thromboembolism that transits from the right- to the left-sided cardiac chambers. They may occur via interventricular or interatrial defects, or via pulmonary arteriovenous malformations.

Of the 500,000+ strokes per annum in the United States, a cause remains unidentified or unproven in 40-45% of cases despite comprehensive diagnostic workups. These strokes are known as cryptogenic strokes. The most common cause of cryptogenic stroke is probably paradoxical embolism due to a patent foramen ovale (PFO).

Patent foramen ovale.

Normal foetal circulation is dependent on the foramen ovale, which provides a communication for oxygenated blood flow between the right atrial and left atrial during lung maturation. At birth, decreased pulmonary vascular resistance and increased left atrial pressure promote closure of the foramen ovale.

Patent Foramen Ovale. Image courtesy of

Patent Foramen Ovale.
Image courtesy of

Whilst PFO’s are found in ~27% of the general population, their incidence is much higher (OR 2.9) in patients with cryptogenic stroke. The annual risk of cryptogenic and recurrent stroke in PFO populations is 0.1% and 1%, respectively.


The precise mechanism of stroke in patients with a PFO is unresolved. Under physiological conditions, a pressure gradient is maintained between the left and right atrium, which results in passive closure of the PFO. In the case of increased right atrial pressure exceeding left atrial pressure (as observed at the end of Valsalva manoeuvres such as coughing, sneezing or squatting) a transient right-to-left shunt may occur carrying particulate matter such as thrombi into the systemic circulation. A permanent increase in right-sided cardiac pressures, as observed after pulmonary embolism or other causes of pulmonary arterial hypertension, results in a significant and possibly permanent right-to-left interatrial shunt, thereby increasing the risk for paradoxical embolism.

Clinical features.

The clinical diagnosis of paradoxical embolism requires a venous source of embolism, an intracardiac defect or a pulmonary fistula and evidence of arterial embolism.

Depending on the site of embolisation, paradoxical embolism may result in neurological deficits related to ischaemic stroke, chest pain and ECG changes indicative of myocardial infarction, acute abdominal pain from mesenteric ischaemia, back pain and haematuria as a result of renal infarction, or cold and pulseless extremities secondary to peripheral arterial occlusion.

Paradoxical Embolism: Pathophysiology, Diagnostic Tools, and Prevention Image courtesy of J Am Coll Cardiol. 2014;64(4):403-415.

Making the diagnosis.

The formal diagnostic evaluation required in patients with cryptogenic stroke will far exceed any Emergency Department length of stay. However, in patients with cryptogenic embolism and a coexisting intracardiac communication at the atrial level, the presumptive diagnosis of paradoxical embolism should be seriously entertained.


Transthoracic or transoesophageal echocardiography are the diagnostic method of choice for the noninvasive detection of intracardiac shunts and a patent ductus arteriosus. It also allows clinicians to assess the size of a defect and provides information on shunt quantity and direction.

The “bubble study”.
Accurate PFO detection requires peripheral injection of agitated saline or echocardiographic contrast medium at the end of a sustained and rigorous Valsalva manoeuver. The echo criteria for PFO diagnosis include the early detection of contrast microbubbles in the left atrium within 3 cardiac cycles after opacification of the right atrium (see below).

Transthoracic echocardiography showing contrast medium passing through the patent foramen ovale. Courtesy of Rev Esp Cardiol. 2011;64:133-9.

Transthoracic echocardiography showing contrast medium passing through the patent foramen ovale.
Image courtesy of Rev Esp Cardiol. 2011;64:133-9.

Transoesophageal echo (TOE) is considered to be the “gold standard” technique for the diagnosis of right-to-left shunts, however the use of sedation to facilitate the study often reduces the performance of Valsalva manoeuver. Keep in mind however that the sensitivity of transthoracic echo (TTE) may be as low as 63%.
Other imaging techniques.

These include transcranial doppler sonography, computed tomography and cardiac MRI.



Antiplatelet therapy (aspirin, clopidogrel or a dipyridamole) is first-line in the secondary prevention of systemic paradoxical embolism. Further anticoagulation with heparin, LMWH, warfarin or rivaroxaban etc is indicated for cardioembolic disease and in the presence of concomitant pulmonary embolism.


Percutaneous closure of cardiac septal defects is frequently performed however evidence supporting this practice is inconclusive when compared to medical therapy alone.

The patient is transferred to the intensive care unit on minimal vasopressor support.

24 hours into her admission she has a formal transthoracic echo (whilst still intubated and sedated) which demonstrates normal LV and RV size and systolic function. Her pulmonary pressures are normal and there is no evidence of intracardiac shunt on a bubble study.

A cause was never found for her paradoxical embolism, but one is left to ponder whether the acute pulmonary hypertension caused by a massive pulmonary embolism was enough to drive a transient right-to-left shunt resulting in her subsequent ischaemic stroke.

  1. Windecker, S., Stortecky, S., & Meier, B. (2014). Paradoxical embolism. Journal of the American College of Cardiology, 64(4), 403–415.
  2. Maron, B. A., Shekar, P. S., & Goldhaber, S. Z. (2010). Paradoxical embolism. Circulation, 122(19), 1968–1972.
  3. Poole-Wilson, P. A., May, A. R., & Taube, D. (1976). Paradoxical embolism complicating massive pulmonary embolus. Thorax, 31(3), 354–355.
  4. Pinto, F. J. (2005). When and how to diagnose patent foramen ovale. Heart, 91(4), 438–440.
  5. Naidoo, P., & Hift, R. (2011). Massive pulmonary thromboembolism and stroke. Case Reports in Medicine, 2011, 398571.
  6. d’audiffret, A., Pillai, L., & Dryjski, M. (1999). Paradoxical emboli: the relationship between patent foramen ovale, deep vein thrombosis and ischaemic stroke. European Journal of Vascular and Endovascular Surgery : the Official Journal of the European Society for Vascular Surgery, 17(6), 468–471.

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.