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


bubble of trouble…

the case.

76 year old male presents to your Emergency Department via ambulance with right hip pain and a fever of 38.1*C.

He reports a week long history of worsening right hip and buttock pain which is now significantly reducing his ability to both mobilise and weight bear. His pain is exacerbated by sitting down. There has been associated night sweats for the past 48 hours and he has experienced rigors this morning. He has had no falls and no recent trauma.

The patient had seen his GP for this problem 3 days earlier. The subsequent physiotherapy session only seemed to worsening his symptoms.

He has bought in an outpatient ultrasound which suggests “tendonitis” or “bursitis” as the cause of his symptoms.

Past Medical History.

  • Benign prostatic hypertrophy
  • Rectal Cancer with resection (10 years ago)
  • Renal cell carcinoma with right-sided nephrectomy (12 years ago)
  • Appendicectomy

Medications include a beta-blocker and a PPI.

On examination.

Looks very well and is comfortable at rest lying on his left side. He is however febrile to 38.1*C.

  • A: patent & protected
  • B: Sat 95% RA, no resp distress. RR 16/min. Chest clear.
  • C: Warm & well perfused. P 124/min, BP 122/64, Heart sounds dual (without murmurs or rub), JVP not elevated, no peripheral oedema.
  • D: GCS 15, PEARL 5mm, moving all 4 limbs.
  • E: Febrile. BSL 8.1. Warm, tender & erythematous (likely cellulitic area) extending from the popliteal fossa proximally towards the gluteal region. Significantly reduced hip flexion & extension secondary to pain. Knee range-of-motion, unremarkable.

You pause & ask yourself…

  • Infectious/Sepsis:
    • Cellulitis
    • Septic arthritis
    • Osteomyelitis
    • Soft tissue abscess/collection
    • Retroperitoneal/psoas abscess
    • Spinal
  • Inflammatory:
    • Bursitis
    • Tendonitis
  • Myositis
  • Rhabdomyolysis
  • Malignancy
    • +/- pathological fracture/bony infiltrate
  • Radiculopathy (sciatica)
  • ?dual pathology…


Surprisingly unhelpful given the clinical context.

Are you reassured by the normal lactate?

nf-fbc nf-biochem nf-crp

Supportive of the clinical picture of sepsis.
– Elevated WCC, predominate neutrophilia & significantly elevated CRP.

Moderate renal impairment.
– Elevated creatinine & urea
– ?Acute versus chronic in a patient with single kidney & previous bladder outlet obstruction.

  • Take cultures
  • Empiric, early broad-spectrum antibiotic administration
    • Flucloxacillin 2g q4-6h
    • Gentamicin (5-7mg/kg of ideal body weight)
  • IV fluids
    • Guided by systemic perfusion, pulse-rate, blood pressure, capillary return & hourly urine output.
  • Strict fluid balance
  • Analgesia
  • Antipyretics

… this time you notice that there is marked subcutaneous emphysema beneath the previously mentioned area of painful erythema !!!

Whilst you organise an urgent portable xray of the affected area, you decide to use your ultrasound to scan his leg…

This scan reveals various areas of
(1) soft tissue cobblestoning consistent with cellulitis (subcutaneous oedema)
(2) subcutaneous/fascial hypoechoic fluid collection
(3) subcutaneous emphysema with scatter artefact

Subcutaneous gas concerning for necrotising soft tissue infection

Subcutaneous gas concerning for necrotising soft tissue infection

This is what normal soft tissue should look like…


Diffuse subcutaneous emphysema extending medially & laterally, above & below the knee joint.

  • Transfer to a higher acuity area (monitored bed, resuscitation bay)
  • Administration of targeted broad-spectrum antibiotics
    • Meropenum 1g IV q8h plus
    • Clindamycin 600mg IV q8h
  • Aggressive fluid resuscitation with targeted early-goal directed therapy of sepsis
  • Immediate surgical bedside review for emergency debridement & source control
  • Tetanus prophylaxis

With the history of rectal cancer, surgical anastomosis & an indolent, week-long presentation they request an urgent CT of this patients’ abdomen & leg.

Here is his CT…

  1. Contained perforation of the rectum around the site of anastomosis with associated collection of faeculent material in the pre-sacral space.
  2. Gas extending from the collection via the right ischioanal fossa to the right leg.
    Gas in the right leg is subcutaneous as well as intra-fascial.
  3. Sacral bony changes could be related to the previous radiation therapy or represent sacral osteomyelitis.

Necrotising Fasciitis

In this case, secondary to rectal perforation complicated by a pelvic abscess & sacral osteomyelitis.

Necrotising soft tissue infections are a spectrum of illnesses characterised by fulminant, extensive soft-tissue necrosis, systemic toxicity & a high mortality (25-30%). Incorporated into this group are Fournier gangrene, necrotising fasciitis & gas-gangrene.

Risk factors:

  • Advanced age
  • Diabetes
  • Alcoholism
  • Peripheral vascular disease
  • Immunosuppression
  • Heart disease
  • Renal failure
  • HIV
  • Malignancy
  • Aspirin & NSAID use
  • Decubitus ulcers
  • Chronic skin conditions
  • IV drug use

Note: ~ half of all known cases of streptococcal necrotising fasciitis occur in young, previously healthy individuals.

Classification (Microbiology).


Classification of Necrotising Soft Tissue Infections. Courtesy of Misiakos et al (2014).


  • Rapid necrotising process begins with direct invasion of subcutaneous tissue from external trauma (IVDU, surgical incision, abscess, insect bite) or from direct spread from a perforated viscous (usually colon, rectum or anus).
  • Spontaneous development is rare.
  • Bacteria proliferate & invade subcutaneous tissue and deep fascia leading to release of exotoxins that lead to tissue ischaemia, liquefaction necrosis and systemic toxicity.
  • Tissue ischaemia produced in all such infections impedes immune system destruction of bacteria & prevents adequate delivery of antibiotics. Antibiotics are therefore rarely effective and immediate surgical intervention remains the cornerstone of successful management

Clinical Features.

Classically, patients have tissue pain, fever & diaphoresis. They will often have a tachycardia out of proportion to their fever. Only ~10-40% of the time do patients report trauma or a break in the skin 48 hours prior to presentation.

Pain out of proportion to clinical findings is perhaps the most important feature to help make the diagnosis early. Not all patients have severe pain though…

Brawny oedema & crepitus may be present at the painful area.

Haemorrhagic bullae & malodorous “dirty dishwater” discharge may also be present.

Haemorrhagic bullae – Courtesy of Medscape (Group A Streptococcal Infections)


The diagnosis of necrotising fasciitis is a CLINICAL one.

X-ray may show subcutaneous gas but CT is more sensitive and can demonstrate fascial thickening and oedema with deep tissue collection and gas formation (no additional benefit with IV contrast). MRI has best sensitivity but usually relates to delay to diagnosis/treatment.

The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) incorporates six routine laboratory tests (haemoglobin, creatinine, glucose, sodium, CRP & white blood cell count) into a weighted 13-point score. This was a retrospectively derived scoring tool designed to aid in the bedside diagnosis of necrotising fasciitis. Using a cut-off of ≥6 points, the score was initially validated in a small cohort, yielding a sensitivity of 90% & specificity of 95%. There are no prospective studies evaluating LRINEC performance. Systematic reviews of mostly retrospective studies have concluded that clinical suspicion is superior to laboratory testing or the LRINEC score.


  • Aggressive fluid resuscitation & early goal-directed therapy of sepsis
  • Early IV Antibiotics.
    • The Therapeutic Guidelines here in Australia recommend;
      Meropenem 1g IV q8h plus either Clindamycin or Lincomycin 600mg IV q8h.
  • Immediate surgical review for emergent debridement (source control) in the operating theatre remains the gold standard.
  • Provide tetanus prophylaxis
  • Supportive care
  • Later wound management & reconstruction.
  • Therapeutic controversies:
    • Hyperbaric oxygen
    • IV Ig

Our patient is taken from ED to the operating theatre shortly after the CT scan was obtained. Here he undergoes an exploratory laparotomy, formation of a colostomy and pelvic washout with simultaneous debridement of the right leg.

He has a reasonably stable post-operative course in the ICU & later returns to theatre for incision & drainage of his presacral abscess.

He continues to make a slow but progressive recovery and is discharged home on long-term antibiotics under the guidance of Infectious Diseases.


  1. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
  2. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
  3. Machado NO. Necrotizing fasciitis: The importance of early diagnosis, prompt surgical debridement and adjuvant therapy. North Am J Med Sci 2011; 3: 107-118.
  4. Sadasivan J, Maroju NK, Balasubramaniam A. Necrotizing Fasciitis. Indian Journal of Plastic Surgery : Official Publication of the Association of Plastic Surgeons of India. 2013;46(3):472-478. doi:10.4103/0970-0358.121978. PubMed.
  5. Puvanendran R, Huey JCM, Pasupathy S. Necrotizing fasciitis. Canadian Family Physician. 2009;55(10):981-987. PubMed.
  6. Krieg A, Röhrborn A, Schulte am Esch J, et al. Necrotizing fasciitis: microbiological characteristics and predictors of postoperative outcome.European Journal of Medical Research. 2009;14(1):30-36. doi:10.1186/2047-783X-14-1-30. PubMed.
  7. Misiakos EP, Bagias G, Patapis P, Sotiropoulos D, Kanavidis P, Machairas A. Current Concepts in the Management of Necrotizing Fasciitis. Frontiers in Surgery. 2014;1:36. doi:10.3389/fsurg.2014.00036. PubMed.
  8. Cheng N-C, Tai H-C, Chang S-C, Chang C-H, Lai H-S. Necrotizing fasciitis in patients with diabetes mellitus: clinical characteristics and risk factors for mortality. BMC Infectious Diseases. 2015;15:417. doi:10.1186/s12879-015-1144-0. PubMed.
  9. Hakkarainen TW, Kopari NM, Pham TN, Evans HL. Necrotizing soft tissue infections: Review and current concepts in treatment, systems of care, and outcomes. Current problems in surgery. 2014;51(8):344-362. doi:10.1067/j.cpsurg.2014.06.001. PubMed.
  10. Jeng, K. Necrotizing Fasciitis via 2015.

Author: Julie Nguyen
Web editing + additional writing: Chris Partyka

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.