IVC and Iliac Thrombosis

So this is something I think is easy to do but often not taught during education of clinicians who wish to investigate for DVT at the bedside. There is a lot of discussion and literature and controversy over the use of an abbreviated 2 point technique (the femoral vein from saphenofemoral junction to bifurcation, and popliteal vein through trifurcation) vs. a "3 point" technqiue (entire femoral and superficial femoral vein as well as the popliteal vein).

One thing that is not often talked about however is checking for phasicity in the common femoral vein as a marker of proximal venous thrombosis. The idea is that diaphragmatic movement results in changes in intra-thoracic and proximal IVC pressure and will result in increases and decreases in femoral vein flow over the course of the respiratory cycle. The absence of these changes implies that something is blocking the transmission of these pressure changes to the proximal femoral vein. If bilateral femoral veins lack phasicity, thrombus or ocmpression of the IVC is most likely. If unilateral phasicity is absent, iliac thrombosis or compression is most likely on that side.

I've checked for this hundreds of times in patients with leg swelling, but just recently saw my first case of iliac vein thrombosis (where femoral and popliteal exams were completely normal aside from the lack of phasicity). The image above demonstrates normal phasic respiratory flow (on the left side of the pulse wave Doppler tracing), and a flow response to deep breathing (on the right side of the pulse wave Doppler tracing.)

The image above demonstrates absent phasic respiratory flow in the proximal femoral vein on the ipsilateral side of the iliac vein thrombosis. Remember that absent phasicity suggests occlusion of the vein (iliac or IVC) and that this can be due to thrombus or any number of causes of external compression.

References:

Lin EP, Bhatt S, Rubens D, Dogra VS.The importance of monophasic Doppler waveforms in the common femoral vein: a retrospective study. J Ultrasound Med. 2007 Jul;26(7):885-91

Selis JE, Kadakia S. Venous Doppler sonography of the extremities: a window to pathology of the thorax, abdomen, and pelvis. AJR Am J Roentgenol. 2009 Nov;193(5):1446-51.

Willeput R, Rondeux C, De Troyer A. Breathing affects venous return from legs in humans. J Appl Physiol. 1984 Oct;57(4):971-6.

Right Heart Strain

Diagnosis of right heart strain can be of great clinical utility in patients with dyspnea, tachypnea, hypoxemia and/or hemodynamic instability as it significantly reorganizes the differential diagnosis to focus on entities such as massive pulmonary embolism and cor pulmonale of any etiology. Transthoracic echocardiography can be used to identify right heart strain, and the clinician's first goal is to demonstrate an increase in right ventricular diameter. This is one of the core 3 questions clinicians should ask while evaluating the heart during clinical ultrasound examinations (is there a pericardial effusion?, what is the left ventricular function?, and is there evidence of right heart strain?). In patients in cardiac arrest or with severe hemodynamic instability, the finding of right heart strain in the appropriate clinical setting may prompt clinicians to consider the administration of tissue plasminogen activator or other thrombolytic agents.

The normal right ventricular to left ventricular ratio (in size) is 0.6:1.0 (the right ventricle is approximately two thirds the size of the left ventricle). A right ventricle equal or greater in size as compared to the left ventricle strongly suggests right heart strain. Flattening of the interventricular septum resulting in a "D-shaped" left ventricle on the parasternal short axis view occurs with right ventricular pressure overload (where the septum remains flat throughout the cardiac cycle) or right ventricular volume overload (where the septum resumes a normal shape during systole).

Of note, measurement of the velocity of triscuspid regurgitation, often associated with right ventricular pressure and/or volume overload (aka strain), can be used to estimate the degree of pulmonary hypertension present.

Also of note is McConnell's sign, where apical right ventricular systolic function is preserved in the setting of global right ventricular dyskinesis. This was felt to strongly suggest pulmonary embolism as the etiology of right heart strain, but has been called into question recently (see references).

Clinicians should remember, however, that while some features suggest chronic right heart strain (increased trabeculations, hypertrophy of free and septal walls) and some features suggest acute right heart strain (normal wall thickness), it can be difficult to determine if right heart strain is acute or chronic, and by no means does the finding of an enlarged right ventricle confirm the diagnosis of pulmonary embolism.

Thanks to Drs. Chilstrom and Secko for the McConnell's and Triscuspid Regurgitation clips. Be sure to cycle through the clips by clicking on the left or right arrows in the video player.



References:
McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996 Aug 15;78(4):469-73.

Casazza F, Bongarzoni A, Capozi A, Agostoni O. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction. Eur J Echocardiogr. 2005 Jan;6(1):11-4.

Lodato JA, Ward RP, Lang RM. Echocardiographic predictors of pulmonary embolism in patients referred for helical CT. Echocardiography. 2008 Jul;25(6):584-90.

Pediatric Lung Sonography

Ever been in the middle of a pediatric resuscitation and wanted to know if the endotracheal tube was in the mainstem bronchus or the trachea or the esophagus? Or if the barotrauma of positive pressure had caused a pneumothorax? There's a lot out there on diaphragm excursion vs. lung sliding vs. visualization of the endotracheal tube at the neck and it's worth checking out though there is still a need for additional research in this potentially high-yield application (see references). Video below is from a 3 day old infant with poor breath sounds after pre-hospital intubation. Notice that a linear transducer shows you more than 5 interspaces and is a great way to get a global view of the hemithorax in a neonate. In this case there are A-lines (A vs B vs C vs E vs W vs Z coming in a future post) with no visible pleural sliding on the right side of the screen (towards the patient's feet), and normal sliding on the left side of the screen (towards the patient's head) with B-lines and a small pleural effusion present (likely a result of barotrauma with subsequent atelectasis of the right lung and reactive effusion vs. small hemothorax).

Thanks to Jen Chao for setting up the ultrasound course in El Salvador this past spring where this clip was obtained.



References

Kerrey BT, Geis GL, Quinn AM, Hornung RW, Ruddy RM. A prospective comparison of diaphragmatic ultrasound and chest radiography to determine endotracheal tube position in a pediatric emergency department. Pediatrics. 2009 Jun;123(6):e1039-44. Epub 2009 May 4.

Blaivas M, Tsung JW. Point-of-care sonographic detection of left endobronchial main stem intubation and obstruction versus endotracheal intubation. J Ultrasound Med. 2008 May;27(5):785-9.

Galicinao J, Bush AJ, Godambe SA. Use of bedside ultrasonography for endotracheal tube placement in pediatric patients: a feasibility study. Pediatrics. 2007 Dec;120(6):1297-303.

Hsieh KS, Lee CL, Lin CC, Huang TC, Weng KP, Lu WH. Secondary confirmation of endotracheal tube position by ultrasound image. Crit Care Med. 2004 Sep;32(9 Suppl):S374-7.