by Dr Ben Land
A 34 year old female with a history of Congenital Lymphangiomatosis presented to the ED with progressive SOB on exertion over a few weeks. She had previously been walking to work and cycling at level 8 on an exercise bike, but now was SOB after walking only a few metres. She had generalised chest pain and subjective fevers. She then had a single episode of haemoptysis, and estimated around 100mls of frank blood. She became acutely SOB after this. On ambulance arrival she was distressed, pale and clammy with SATs of 50% on air, which improved with 15L 02 via a Hudson mask.
Background history of Lymphangiomatosis: a rare disease characterised by abnormal proliferation of the lymphatic system, leading to chylous effusions. She had a peritoneal venous shunt placed a few years ago. She had a history of recurrent PE’s, and was taking Apixaban. She also had a chronic right pleural effusion.
On ED arrival she appeared pale and unwell, with markedly increased work of breathing. She was only able to talk in interrupted sentences and had a RR of 38. Her pulse was 84, with BP 97/70 and temp was 37.7. Chest exam revealed dullness in the right base. Her ECG showed a right axis deviation.
Portable chest X-ray showing her known chronic right pleural effusion, and also left upper lobe opacities compatible with scarring. Her shunt is visible with the tip situated within the right atrium.
Here are some clips of her bedside echo:
Parasternal long axis showing reasonable LV function. At a glance you can see that the anterior leaflet of the mitral valve nearly touches the septum in systole, which is a marker of pretty good LV function. On this view the RV outflow tract is dilated. In this view RV should be 1:1:1 with aorta and LA.
Parasternal short axis view which again shows hyperdynamic LV function: also note the D shaped LV due to straightening of the IV septum. The right ventricle isn't seen perfectly here, but is moderately dilated (should be 0.6:1- RV:LV, but in this case appears at least 1:1 or more).
The subcostal views demonstrated a hypoechoic mass in the RA which is closely associated with the tip of her peritoneal venous shunt. The differential for this is thrombus or vegetation associated with the shunt or the tricuspid valve. However, atrial myxoma should also be considered.
Note the vigorous movement of the tricuspid valve annulus, which suggests preserved RV function despite dilatation. A TAPSE >16mm (A4C) would further define this as normal. The RV dilatation is likely acute in this case as the RV free wall is thin. Features of chronic RV dysfunction are thick RV free wall (subcostal >6mm), pronounced RV wall trabeculation, RVSP >60mmHg, PAT <90ms. Comparison with a previous echo would be helpful.
Here's an IVC view again demonstrating the right atrial thrombus:
You can also see the right sided pleural effusion containing some abnormal lung tissue with B-lines, it's in the bottom left part of the screen here. We could (and might) write a separate blog post about her lung US which also demonstrated some great signs!
From the bedside echo, we made a diagnosis of RA thrombus with likely acute pulmonary embolism causing acute RV dilatation.
This patient went on to have a CTPA which confirmed the presence of non-occlusive and occlusive segmental and subsegmental PE involving all lung segments. The finding of right atrial thrombus may increase the mortality in patients with PE(1), and is associated with increased haemodynamic instability. Treatment options are the same as any PE including anticoagulation or thrombolysis, but surgical thrombectomy may also be considered for large clots(2). Our patient was already taking Apixaban and after some initial treatment was stable in ED. Given her complex history she was transferred to her usual treating team for further management.
Many thanks to Amaali for providing expert insight and editorial review, and to Rachel who allowed me to do the ultrasound on her patient. Please send any questions, comments, suggestions or feedback to myself or Amaali.
1. Torbicki A, Galie N, Covezzoli A, Rossi E, De Rosa M, Goldhaber SZ, on behalf of the ICOPER Study Group Right heart thrombi in pulmonary embolism: Results from the International Coooperative Pulmonary Embolism Registry. J Am Coll Cardiol. 2003;41:2245–51.
2. Kinney EL, Wright RJ. Efficacy of treatment of patients with echocardiographically detected right-sided heart thrombi: a meta-analysis. Am Heart J. 1989;118(3):569–573.
3. Burns KE, McLaren A. Catheter-related right atrial thrombus and pulmonary embolism: a case report and systematic review of the literature. Can Respir J. 2009;16(5):163–165.
4. Ogren M, Bergqvist D, Eriksson H, Lindblad B, Sternby NH. Prevalence and risk of pulmonary embolism in patients with intracardiac thrombosis: a population-based study of 23 796 consecutive autopsies. Eur Heart J. 2005;26(11):1108–1114.
5. Obeid AI, Mudamgha A, Smulyan H. Diagnosis of right atrial mass lesions by transesophageal and transthoracic echocardiography. Chest. 1993;103(5):1447–1451.
6. Rose PS, Punjabi NM, Pearse DB. Treatment of right heart thromboemboli. Chest. 2002;121(3):806–814.
Scott saw a patient overnight who presented with severe chest and back pain and L arm weakness. She was hypotensive and bradycardic; in cardiogenic shock.
Classic for a dissection.
Scott had a look with the ultrasound:
Subxiphoid view showing a pericardial effusion and the aorta with a dissection flap in the lumen (annotated below).
Abdominal Aorta (trans) showing a dissection flap in the lumen of the aorta (annotated below).
Cardiothoracics met the patient in CT and they were taken to theatre from CT. 40 minutes from presentation to theatre. Not Bad!
I know from the story the patient had an obvious dissection.
I think what US does (as it does in most ED situations) is that it allows us to be sure of the diagnosis; rather than the diagnosis being the highest one in a differential: thereby allowing activation of the appropriate unit and theatre with confidence.
US is best in these situations as a rule in test. Remember that TTE is not sensitive enough to rule out dissection.
But seeing a dilated aortic root, a dissection flap or significant aortic regurgitation has sensitivities in the 70-80s for aortic dissection with specificities in the 90s (1,2,3). So if you see pathology you can be confident you've made the diagnosis.
Keep scanning everyone.
1.Fojtik, JP, Costantino, TG, and Dean AJ THE DIAGNOSIS OF AORTIC DISSECTION BY EMERGENCY MEDICINE ULTRASOUND. The Journal of Emergency Medicine, Vol. 32, No. 2, pp. 191–196, 2007.
2. Victor MF, Mintz GS, Kolter MN, Wilson AR, Segal BL. Two- dimensional echocardiographic diagnosis of aortic dissection. Am J Cardiol 1981;48:1155–9
3.Sullivan PR, Wolfson AB, Leckey RD, Burke JL. Diagnosis of acute thoracic aortic dissection in the emergency department. Am J Emerg Med 2000;18:46–50.
Alex saw a patient in June who presented following a syncopal episode associated with chest radiating to the back and neck. He had an initial SBP 70/ which responded to IVT, HR 90-100, sats 95%. He had no past medical history.
Bedside echo was done promptly for the cause of hypotension:
Zoomed in subcostal view shows 1-2cm of pericardial fluid, containing some hyper echoic strands (likely clot in this case) and invagination of the RA (annotated below). Thank you Lisa for saving the images.
Given the story and the echo findings, a prompt diagnosis of type A aortic dissection was made. Cardiothoracics and cardiology attended promptly and the patient transitted rapidly to theatre from CT. He spent 1:45 minutes in ED.
Features suggestive of aortic dissection on ED cardiac ultrasound are:
dilated aortic root >3cm
hyperechoic flap which undulates independent of aortic pulsations (most sensitive)
Signs of tamponade are (in the presence of a pericardial effusion - remember it is still a clinical diagnosis):
RA invagination in systole (seen best in subcostal and apical 4 chamber: A4C views)
RV invagination in diastole (sometimes RV may be so collpased, it is difficult to visualise): seen best in subcostal and parasternal long axis.
Alternating RA and RV collapse gives the seasaw sign seen in the subcostal view
MV doppler variations >25% insp to exp (A4C)
TV doppler variations >40% insp to exp (A4C)
Left image: not much variation; right image: 23% variation inspiration to expiration
Rv and LV interdependence: ie RV collapsed on expiration and LV collapsed on inspiration (seen best in A4C or subcostal four chamber).
If there were a delay to theatre, this patient may have been temporised with intravascular volume expansion and pericardiocentesis.
The easiest technique for US guided pericardiocentesis is left parasternal or apical, with a linear transducer. This is described well in the following article (thanks George P):
29yo female presented yesterday with epigastric pain of 2/7 and vomitting. Her only PMHx was intussusception as a child for which she had had surgery.
She had opened her bowels yesterday. She stated she hadn't passed flatus today.
OE she was tachycardic HR 100, but otherwise stable and afebrile. Her abdomen wasn't distended and she was tender epigastrically without guarding.
BHCG was negative.
High on the differential was SBO.
On US, her GB and pancreas were normal. Aorta was 2 cm, nil flap.
However she became very tender on examination of the pelvis:
RIF: dilated loop of SI (note place circulars in video below); free fluid around the loop. Loop is dilated (>3cm) and completely filled with fluid.
No peristalsis in this dilated loop of bowel
LIF showed further distended loops of bowel with faecalised (grainy and faeces like: ie has been in the bowel a while) content and significant free fluid.
two videos showing washing machine (to and fro) movement of content due to bowel obstruction
CT showing the same as the US.
Important to note in this case: the patient had been seen the previous evening with vomiting and epigastric pain. Her ED US was deemed normal due to a normal GB, normal CBD and lack of hydronephrosis. Remember to keep an open mind if the ED US is negative and go searching for other pathology with US or perform a different diagnostic test if concerned.
Signs of bowel obstruction on US:
dilated loops of SI: >2.5cm
ineffective to and fro movement of contents
features suggestive of bowel ischaemia:
hyper echoic gas within the bowel wall with reverberation artefact (dirty shadowing)
absence of peristalsis
thick bowel wall >3mm
In a case of bowel obstruction always check for herniae
hyperechoic gas in within thickened bowel wall
Incidentally we had an elderly patient last night with vomitting and distended abdomen. This was her AXR (I don't know why we do these anymore)
On ED US, she had dilated SI loops, washing machining and free fluid. I know many of you would go straight to CT in this patient, but if you want extra reassurance before calling EGS, ordering the CT and booking a bed: have a look with US: it's really EASY!
Yigal had a 70yo patient who was sent in by the GP with central abdominal pain and a pulsatile mass in the epigastrium.
ED US was performed upon arrival and revealed:
transverse view of the aorta with a dissection flap undulating in its lumen
Longitudinal view of the aorta
A dissection flap is hyper echoic and undulates independent of aortic pulse. There may also be hypo echoic thrombus in the false lumen.Seeing a flap in the aorta is highly specific and sensitive for dissection. However, sometimes slice thickness artefact can lead to flap like lines in the aortic lumen. Just remember that a flap will be thick and seen in trans and long. An artefact will usually be thin, disappear in a different angle or view and can be linked to an adjacent structure like the IVC.
40yo male came into ED with severe RUQ pain 2 hours duration. Similar previous episodes, nil US, but this time the pain had woken him from sleep.
RUQ tender, but no guarding.
He was afebrile with normal obs
WCC normal, normal LFTs and lipase.
ED US revealed: not dilated, a thick walled GB with a several mobile stones but one stone impacted in the neck of the GB
Gb long. hyper echoic stone near the neck. The GB wall is thick and has a hypo echoic middle layer which could be GB wall oedema.
On sitting the patient up, the larger stones fall to the funds, but the stones at the neck remain (impacted)
The patient also had a positive sonographic murphey's.
The patient was admitted to EGS and scanned by radiology in the morning. The subsequent scan showed a severely dilated GB with perforation.
Without US, this patient may have been dc home...
Ali and Sarah had a patient post cardiac arrest after hanging. She had 25 mins of CPR in the field. On arrival, she was tachycardic 110, BP 110/, sats 100% on FiO2 1. Jana did a quick lung and cardiac US. Cardiac US was unremarkable, but the lung US showed a pneumothorax on the R. Jana didn't save any images (!!!!). But it would have looked like this:
M mode of R anterior lung showing barcode or stratosphere sign
CXR done while preparing for R chest tube.
This was an excellent pick as the patient had sats of 100% and equal air entry clinically. US helped expedite chest tube insertion.
The patient deteriorated haemodynamically en route to CT. An inotropic infusion was started assuming cariogenic shock.
CT revealed a large liver laceration and intraperitoneal free fluid. (This and the tension pneumothorax likely secondary to rib fractures from CPR.)
Given the amount of free fluid: FAST exam would likely have been positive.
CT abdo showing FF fluid around the liver and spleen
We all use US in ED to answer a specific question: is there a pneumothorax, is there hydronephrosis etc. But when the answer is negative, sometimes we forget to look for an alternate cause.
I'll check for hydronephrosis in a renal colic patient and then forget to look at the aorta.
We are so sophisticated with US now, we can look at multiple organ systems and make pertinent diagnoses. US can help differentiate the undifferentiated patient.
FAST for free fluid is part of the RUSH exam for undifferentiated shock.
None of us would think to do a FAST on cardiac arrest patients with no trauma. However, remember this case the next time you have an undifferentiated shock and look at the pipes and the tank as well as the pump to determine the cause.
Emcit RUSH https://emcrit.org/rush-exam/
Nama saw a 55yo female who presented with CP. She was treated with aspirin and GTN by MAS. Her obs were stable and she looked well. She had undergone a stress MIBI 2 years previously: NAD.
On examination, she had no murmurs, a clear chest and normal ECG.
However, she had RUQ tenderness and a positive Murphey's sign.
Does she have cardiac CP or biliary colic?
trop came back normal.
but so did WCC and CRP <2
But this is why we have US.
Nama did a beautiful GB US
Benign looking GB with hyper echoic stone and shadowing
Another view of the GB shows a stone in the GB neck and pericholecystic fluid.
The patient was fasted and admitted under EGS. She had a cholecystectomy for acute cholecystitis the next day.
The presence of gall stones and a positive sonographic Murphey's are two of the key features to look for with suspected acute cholecystitis in ED.
Other supportive features are
1. dilated GB >5cm (trans) >10cm (long)
2. thickened GB wall >4mm, fluid in GB wall, gas in GB wall
3. pericholecystic fluid
4. dilated CBD >6mm (with this need to consider ascending cholangitis).
Gordon had an elderly patient who presented via MAS sats 70%, diaphoretic, altered conscious state, HR 90. He had a hx of COPD, HT and CCF. No further hx.
Listening to his chest he had a few scattered crackles only.
CXR was not very helpful (see below)
Gordon did a lung US and echo which clarified the diagnosis of APO, R sided pleural effusion and cardiomyopathy.
Multiple coalescing B lines (vertical) seen anteriorly R and L.
Normal lung with horizontal A lines for comparison
R pleural effusion with collapsed lung.
dilated CM on PLAx
The patient had prompt and appropriate management for APO and responded well.
Bilateral multiple B lines anteriorly in a hypoxic patient is typically due to APO. However, other differentials could be:
1. bilateral pneumonia (would also have thickened pleural line)
2. pulmonary fibrosis (PHx and thickened pleural line)
3. ARDs (patchy, there will be skip areas, abnormal pleural line)
Cardiac US can also help with differentiation.
Ilya saw a patient last week with ongoing headaches post MVA in January. Headaches were worst in the morning with nausea and vomitting.
Ilya did the following optic nerve US to confirm bilateral papilloedema.
Images of the optic nerve entering into the globe posterior of the left and right eyes (labelling!! Ilya!!) show optic nerve sheath diameter (ONSD) >5mm indicating elevated ICP. Note that Ilya appropriately measured the nerve diameter 3mm posterior to the retina.
Studies vary from 4.8-6.5mm in the cut off diameter for ONSD on US. This may be due to inconsistencies in insinuating angle and measurement, as well as individual variation. However, a diameter >5mm is usually used as the cut off suggestive of ICP >20mmHg. BMJ is currently conducting a systematic review on ONSD US for elevated ICP (1).
It can be tricky to find the optic nerve due to its oblique entry into the globe. Holding the probe transverse and moving the probe laterally and fanning superiorly and inferiorly usually helps. Shrestha et al showed that the learning curve for accurate measurement requires at least 20 scans(2).
Nevertheless, getting good at this beats having to look for papilloedema with the ophthalmoscope!!
Ilya's patient went on to have an LP: opening pressure >34cmH2O.
1. Koziarz A, Sne N, Kegel F et al Optic nerve sheath diameter sonography for the diagnosis of increased intracranial pressure: a systematic review and meta-analysis protocol.BMJ Open. 2017 Aug 11;7(8):e016194.
2. Shrestha GS, Upadhyay B, Shahi A et al Sonographic Measurement of Optic Nerve Sheath Diameter: How Steep is the Learning Curve for a Novice Operator? Indian J Crit Care Med. 2018 Sep;22(9):646-649.