two in two days…

I have recently prepared a lecture on a current, yet still controversial topic for work following exposure to these two interesting cases. Here are the cases & their discussion as well as the slide-show attached… 

case one.

a 74 year old male presents to ED following a syncopal episode at home. He apparently collapsed without warning whilst taking the rubbish outside.

With the paramedics, he is alert & oriented but has a pulse of 120 per min and a systolic blood pressure of 70mmHg. His prehospital ECG demonstrates a right bundle branch block that resolves prior to ED arrival.

He arrives to ED in extremis. He is agitated, hypoxic [SaO2 92% on 15L NRB, RR 32, clear chest] & shocked [P 124, BP 72/50, cold & mottled]. Whilst his GCS is 13, he has no focal neurological signs. His blood glucose & temperature are normal.

Before you continue. Pause to consider the potential diagnoses. How are you going to differentiate these further ??

[DDET Case 1 – initial RESULTS…]

massive PE cxr

Venous blood gas - metabolic [lactic] acidosis
Venous blood gas – metabolic [lactic] acidosis with impaired renal function.



Initial resuscitation.

  • High-flow oxygen via non-rebreather mask
  • 2x large-bore IV-access
  • Empiric fluid bolus

Differential diagnoses.

  • Undifferentiated shock [cardiogenic vs septic vs obstructive…]
    • ?AMI
    • ?AAA
    • ?Aortic dissection
    • ?Haemorrhage
    • ??sepsis, others….

You take your ultrasound to the bedside…




Massively dilated right ventricle with visualisation of blood clot 'in transit' through the right atrium.
Massively dilated right ventricle with visualisation of blood clot ‘in transit’ through the right atrium.

These findings on the RUSH exam allowed us to make the provisional diagnosis of massive pulmonary embolism with obstructive shock !



Unfortunately, soon after the diagnosis is made the patient deteriorates and has a PEA arrest. The decision is made to threat with empiric thrombolysis with alteplase.

There is a protracted period of resuscitation with periods of spontaneous circulation interspersed  with short bursts of CPR. Despite an ongoing, escalating adrenaline requirement he was safely [eventually] transferred to Intensive Care.

Unfortunately, he has a further PEA arrest and subsequently asystole some 7 hours after arriving to ED and could not be resuscitated.




Here are the slides from my presentation looking at the evidence & potential roles for thrombolysis for pulmonary embolism.

[slideshare id=33205118&doc=thrombolyticsforpulmonaryembolism-140406223428-phpapp02] 


[DDET Case TWO…]

case two – precisely 24 hours later….

a 47 year old female is bought to ED following a pre-hospital notification regarding her ‘life-threatening asthma’.

She was found by paramedics to have significant respiratory distress & profound hypoxia, so administered intramuscular adrenaline [500mcg x2] plus continuous salbutamol whilst transporting her to ED.

Upon arrival she is alert with a patent airway, but profound tachypnoea & hypoxia [RR 44, SaO2 92% 15L NRB]. Surprisingly she has a clear chest with good air-entry. There are no wheezes or crackles. She is tachycardic but normotensive [P 124/min, BP 118/70], with warm peripheries.

You cannot help but notice she has a “Cam boot” on her right foot. She sustained an undisplaced Weber B fracture 3 weeks earlier, which has been managed conservatively.

Again, pause to consider the potential diagnoses. How are you going to differentiate these further ??


[DDET Case 2 – initial RESULTS…]



Submassive ABG#1
A-a gradient of ~580… 



Initial resuscitation.

  • BiPAP initiated for oxygen requirement & work of breathing.
  • IV access & empiric fluid bolus
  • Heparin bolus + infusion based on presence of cam-boot & potential for DVT/PE
  • Empiric IV ABx given; atypical presentation.

Differential diagnoses.

  • Pulmonary embolism
  • ?Asthma – less & less likely…
  • ?Infectious
  • ?Metabolic

You take your ultrasound to the bedside…




Our concerns…


With these findings, our predominate concern was for submassive pulmonary embolism.

It is acknowledged that further investigation (ie. CTPA) was impossible without intubation & mechanical ventilation due to profound oxygen requirement and inability to lay-flat.

A decision is made for RSI, which takes place without issue.

Here is her CTPA…


Now ask yourself….
Are you going to use thrombolysis on this patient ?!?!



It is decided given her oxygen requirement, age and clot-burden to proceed to thrombolysis. She receives 100mg of alteplase over two hours.

The following morning she is extubated without issue [ie. normal gas-exchange] & is discharged home on Day 5 !!

This is her discharge ECHO…




  • Consider massive & submassive PE as a cause for undifferentiated shock.
  • Have a low threshold to investigate these patients yourself with a bedside ECHO [ie. specifically, RUSH exam, extension of BLUE protocol].
    • Includes undifferentiated shock or unexplained dyspnoea/hypoxia.
  • ECHO specifics to examine include:
    • RV size [esp. RV:LV ratio]
    • RV contractility ?hypokinesis.
    • Paradoxical septal motion [ie. flattening or leftward bowing]
    • McConnell’s sign – right ventricular free wall hypokinesis with apical sparing.
    • Tricuspid regurgitation.
  • Consider thrombolysis in:
    • Massive PE
    • Presumed massive PE with PEA arrest/shock
    • Submassive PE:
      • Profound RV dysfunction [abnormal ECHO + positive troponin]
      • Severe hypoxaemia/oxygen requirement
      • Age < 75
  • Consider contraindications carefully

Contraindications to Thrombolysis

  • Remember there are other alternatives:
    • Interventional radiology
    • Cardiothoracic surgery


[DDET The full slideshow…]

[slideshare id=33204988&doc=2in2days-140406222753-phpapp01]


[DDET References.]


  • Goldhaber SZ, Visani L, De Rosa M, et al. for ICOPER. Acute pulmonary embolism; clinical outcomes in the International Cooperative Pulmonary Embolism Registry. Lancet 1999;353:1386-1389
  • Grifoni, S., Vanni, S., Magazzini, S., Olivotto, I., Conti, A., Zanobetti, M., et al. (2006). Association of persistent right ventricular dysfunction at hospital discharge after acute pulmonary embolism with recurrent thromboembolic events. Archives of internal medicine, 166(19), 2151–2156. doi:10.1001/archinte.166.19.2151
  • Kline, J. A. (2009). Prospective Evaluation of Right Ventricular Function and Functional Status 6 Months After Acute Submassive Pulmonary Embolism. Chest, 136(5), 1202. doi:10.1378/chest.08-2988
  • Frémont, B. (2008). Prognostic Value of Echocardiographic Right/Left Ventricular End-Diastolic Diameter Ratio in Patients With Acute Pulmonary Embolism *. Chest, 133(2), 358. doi:10.1378/chest.07-1231
  • Böttiger, B. W., et al. (2008). Thrombolysis during resuscitation for out-of-hospital cardiac arrest. The New England journal of medicine, 359(25), 2651–2662.
  • British Thoracic Society Standards of Care Committee Pulmonary Embolism Guideline Development Group. (2003, June). British Thoracic Society guidelines for the management of suspected acute pulmonary embolism. Thorax.
  • Jaff, M. R., Mcmurtry, M. S., Archer, S. L., Cushman, M., Goldenberg, N., Goldhaber, S. Z., et al. (2011). Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement From the American Heart Association. Circulation, 123(16), 1788–1830. doi:10.1161/CIR.0b013e318214914f
  • Konstantinides, S., et al. Management Strategies and Prognosis of Pulmonary Embolism-3 Trial Investigators. (2002). Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism. The New England journal of medicine, 347(15), 1143–1150.
  • MD, M. S., PhD, C. B., DO, L. S., MD, F. R., DMD, M. M., & Investigators, M. (2013). Moderate Pulmonary Embolism Treated With Thrombolysis (from the “MOPETT“” Trial). The American Journal of Cardiology, 111(2), 273–277.
  • Steering Committee. (2012). Single-bolus tenecteplase plus heparin compared with heparin alone for normotensive patients with acute pulmonary embolism who have evidence of right ventricular dysfunction and myocardial injury: rationale and design of the Pulmonary Embolism Thrombolysis (PEITHO) trial. American Heart Journal, 163(1), 33–38.e1.
  • Sharifi, M., Bay, C., Schwartz, F., & Skrocki, L. (2014). Safe-dose thrombolysis plus rivaroxaban for moderate and severe pulmonary embolism: drip, drug, and discharge. Clinical cardiology, 37(2), 78–82. doi:10.1002/clc.22216
  • PEITHO RESULTS (slideshow) via ClinicTrialResults.org
  • MD, S. D., RN, P. M., BA, L. R., RDMS, M. L. M., MPH, J. R.-S., MPH, S. B., et al. (2014). Right Ventricular Dilatation on Bedside Echocardiography Performed by Emergency Physicians Aids in the Diagnosis of Pulmonary Embolism. Annals of Emergency Medicine, 63(1), 16–24. doi:10.1016/j.annemergmed.2013.08.016

Social Media covering Thrombolysis for Pulmonary Embolism.


Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.