Clinical Image of the Month: Lambl’s Excrescence

Welcome back to another Clinical Image of the Month from the case files of the Brown EM Residency.



A 77 y.o. female with PMHx significant for liver cirrhosis, COPD on 2L O2, fibromyalgia, depression, and GERD who presents to the ED for evaluation of abdominal and RLE pain after a mechanical fall. Patient denies head trauma and LOC and is not on blood thinners. Patient does report moderate ETOH use. Her mobility is quite limited by both her fibromyalgia as well as her underlying dyspnea which has previously been attributed to her COPD. She reports having episodes of diaphoresis for at least one to two years, which occur on a daily basis. She denies any clear fevers. She additionally denies any clear exertional chest pain or other associated complaints.

Vital signs are stable. Patient had a right hip XR which revealed a displaced and mildly angulated femoral neck fracture with moderate override and no other acute osseous or articular abnormality. An incidental finding was seen on the CT abdomen and pelvis, partially shown below:




Lower chest: Cardiomegaly. Arteriosclerosis of the aorta and coronary arteries. There is left ventricular apical bulbous morphology suggesting old MI. A 21 x 11 mm thrombus is seen in the LV apex. Moderate bilateral pleural effusions with associated relaxation atelectasis. Large hiatal hernia.

Cardiology was consulted for the LV thrombus. In the Emergency Department, an echocardiogram which showed severely reduced LV function (EF25%), moderately reduced RV function and redemonstrated the LV apical thrombus. Additionally, a mobile mass on the aortic valve was noted.


Echocardiogram 2D Complete

  • Left ventricle is mildly dilated and global systolic function is severely reduced

  • There is a fixed non-mobile 10mm X 15mm thrombus at the LV apex

  • Right ventricle is dilated with moderately reduced systolic function

  • Inadequate coaptation of the mitral leaflets resulting in moderate-to-severe mitral insufficiency

  • There is a thin 8mm-long mobile echodensity on the aortic side of the aortic valve of unclear etiology, unusual appearance for endocarditis or thrombus.

  • Sclerodegenerative valve disease with mild aortic insufficiency

  • Mild pulmonary hypertension

  • Biatrial enlargement

Cardiology suspected that her cardiomyopathy was secondary to alcohol abuse, but due to the mobile mass on the aortic valve, there was suspicion for endocarditis. Blood cultures were drawn, patient was started on IV antibiotics, and a heparin drip.

Throughout her inpatient stay, the patient remained afebrile and blood cultures were negative. What’s the diagnosis?



Lambl’s excrescences (LE) are thin, filiform strands of connective tissue found on the closure lines of valves.  Minor endothelial damage promotes thrombus formation and deposition of layers of mucopolysaccharide matrix. They are often seen as an incidental finding on transesophageal echocardiogram and are more commonly observed on the mitral valve than the aortic valve.

In one prospective review of healthy volunteers undergoing TEE, there were similar rates of cardioembolic disease between groups with LEs and those without. Additionally, they observed that aspirin and warfarin use did not alter prevalence or cardioembolic risk of LEs. In another study, LE were seen in up to 39% of elderly patients undergoing TEE for suspected cardiogenic embolic stroke. While they are typically small (1x10mm) they have the potential of embolization, with case reports attributing larger LEs to stroke or MI.

In the absence of clear evidence that they cause cardioembolic disease, Lambl’s excrescences as an isolated, incidental finding do not warrant prophylactic antithrombic therapy. More research is needed to determine the clinical significance of LEs.


Case Conclusion

The patient received a TEE two days later to further evaluate this and it was determined to be Lambl's excrescence, not endocarditis. Further ischemic workup was recommended by cardiology with nuclear stress test and medical optimization as an outpatient.


Faculty Reviewer: Dr. Alyson McGregor



  1. Chu A, Aung TT, Sahalon H, Choksi V, Feiz H. Lambl’s Excrescence Associated with Cryptogenic Stroke: A Case Report and Literature Review. Am J Case Rep. 2015; 16:876-81.

  2. Nakahira J, Sawai T, Kutsumata T, Imanaka H Minami T. Lambl’s excrescence on aortic valve detected by transesophageal echocardiography. Anesth Analg. 2008 June;106(6):1639-40.

  3. Roldan CA, Schevchuck O, Tolstrun K, Roldan PC, Macias L, Qualls CR, Greene ER, Hayek R, Charlton GA, Sibbitt WL Jr. Lambl’s Excrescences: Association with Cerebrovascular Disease and Pathogenesis. Cerebrovasc Dis. 2015;40(1-2): 18-27.

Fibrinolytic Therapy for STEMI


You are on a swing shift at a remote, island-based community hospital when a 58 year-old male presents with sudden onset chest pain. The pain started at rest, radiates to his jaw, and is associated with diaphoresis and nausea. He has a history of coronary artery disease (CAD), and during his last cardiac catheterization in 2008, a stent was placed in his proximal left anterior descending coronary artery. His past medical history is also significant for diabetes, chronic obstructive pulmonary disease, hyperlipidemia, and hypertension.  He is an active smoker.

On exam, he is not only diaphoretic and clenching his chest, but also describes the pain as “an elephant sitting on my chest.” Initial vital signs are P 110, BP 175/100, RR 20, PO2 98% on RA, T 98.9 F. You give him aspirin 324 mg and nitroglycerin sublingual 0.4 mg, and his chest pain improves from a 10/10 to 8/10. His initial electrocardiogram (EKG) is below.

Figure 1: The patient’s presenting EKG.

Figure 1: The patient’s presenting EKG.


ST elevation myocardial infarction (STEMI)

Management Options

You call the critical care transport ambulance, as well as the nearest cardiac catheterization team to alert them of your patient.   Unfortunately, it is a stormy evening in the middle of winter and all bridges off the island are closed; helicopters are grounded due to the storm.  There are no transfer options available to your patient at this time. What else can you do?

Indications for Fibrinolytic Therapy

According to the American Heart Association, there are several considerations when it comes to fibrinolytic therapy in myocardial infarction:

Class I recommendations:

  1. STEMI

  2. Symptom onset in the last 12 hours

  3. Percutaneous Cardiac Intervention (PCI) cannot be performed within 120 minutes of arrival to the Emergency Department

  4. Absence of any contraindications (see below)

Class II recommendations:

  1. Evidence of ongoing ischemia 12-24 hours after symptom onset

  2. Large area of myocardium affected

  3. Hemodynamic instability

Absolute contraindications:

  1. Any prior intracranial hemorrhage

  2. Known structural cerebral vascular lesion

  3. Ischemic stroke <3 months

  4. Suspected aortic dissection

  5. Known intracranial malignancy

  6. Active bleeding or bleeding diathesis

  7. Significant closed head trauma <3 months

  8. Intracranial/intraspinal surgery <2 months

  9. Severe uncontrolled HTN (>175/110)

  10. Oral anticoagulants

Relative contraindications:

  1. Significant HTN on arrival (pressure > 180 mmHg)

  2. Ischemic stroke >3 months

  3. Dementia

  4. Other intracranial pathology

  5. Traumatic CPR >10 min

  6. Major surgery <3 weeks

  7. Internal bleeding <3 weeks

  8. Non-compressible vascular punctures

  9. Pregnancy

  10. Active peptic ulcer disease

PCI versus Systemic Fibrinolytic Therapy

If you are able to transfer the patient to a hospital with PCI capability within 1 hour of presentation or they have contraindications to fibrinolytic therapy, it is recommended that you transfer the patient as soon as possible. Otherwise, the goal is fibrinolytic infusion within 30 minutes of arrival to the ER. In either case, concurrently initiate maximal medical management including full-dose aspirin, Plavix or Brilinta, and anticoagulation (unfractionated heparin or lovenox). Tenecteplase is generally the preferred fibrin-specific agent, given its ease of use and lower rates of non-cerebral bleeding compared to other agents.

Reassess After Fibrinolysis

If your patient has resolution of chest pain and >70% reduction of ST elevation, or ST elevation resolves within 60-90 minutes, you have likely restored flow. If you see <50% decrease in STE and no reperfusion arrhythmias (see below) at 2 hours after fibrinolytic dosing, you have partially improved flow but not completely restored it.

Criteria for Transfer after fibrinolytic therapy

  1. Immediate transfer: acute heart failure or cardiogenic shock

  2. Urgent transfer: failed reperfusion or reocclusion

  3. 3-24 hours: hemodynamically stable, successful reperfusion

Reperfusion Arrhythmias 

You plan for ICU admission because you are unable to transfer the patient to a PCI center when the nurse hands you the following EKG:

Figure 2: Accelerated idioventricular rhythm.

Figure 2: Accelerated idioventricular rhythm.

This is an example of accelerated idioventricular rhythm. This is a normal sign of reperfusion after STEMI and does not require treatment.   In fact, such a rhythm is generally viewed as a positive response to fibrinolytic therapy as indicates reperfusion. 


  1. Regular rhythm

  2. Rate 50-110bpm (slower is ventricular escape, faster is VT)

  3. Three or more ventricular complexes

  4. Fusion (F) and capture (C) beats (see below)

Figure 3: Fusion and capture beats after successful reperfusion.

Figure 3: Fusion and capture beats after successful reperfusion.

General goals of care after fibrinolytic therapy should be to transfer for diagnostic angiography and percutaneous coronary evaluation which is promptly accomplished for your patient the following day after the storm resolves.

Faculty reviewer: Dr. Kristina McAteer


  1. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:529.

  2. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:e362.

  3. White HD. Thrombolytic therapy in the elderly. Lancet 2000; 356:2028.

  4. Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med 2013; 368:1379.

  5. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Lancet 1986; 1:397.

  6. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet 1988; 2:349.
    Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Lancet 1994; 343:311.

  7. Labinaz M, Sketch MH Jr, Ellis SG, et al. Outcome of acute ST-segment elevation myocardial infarction in patients with prior coronary artery bypass surgery receiving thrombolytic therapy. Am Heart J 2001; 141:469.

  8. Peterson LR, Chandra NC, French WJ, et al. Reperfusion therapy in patients with acute myocardial infarction and prior coronary artery bypass graft surgery (National Registry of Myocardial Infarction-2). Am J Cardiol 1999; 84:1287.

  9. Karnash SL, Granger CB, White HD, et al. Treating menstruating women with thrombolytic therapy: insights from the global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries (GUSTO-I) trial. J Am Coll Cardiol 1995; 26:1651.

  10. Woodfield SL, Lundergan CF, Reiner JS, et al. Angiographic findings and outcome in diabetic patients treated with thrombolytic therapy for acute myocardial infarction: the GUSTO-I experience. J Am Coll Cardiol 1996; 28:1661.

  11. Mak KH, Moliterno DJ, Granger CB, et al. Influence of diabetes mellitus on clinical outcome in the thrombolytic era of acute myocardial infarction. GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol 1997; 30:171.

Ultrasound Case of the Month: August 2018

The Case

This is an 82 year-old male who presented to the ED with acute chest pain and palpitations. He had a known history of AAA s/p repair. Patient denied abdominal, back, or flank pain. There was no loss of consciousness. An EKG was performed and was consistent with SVT with aberrancy. A bedside abdominal ultrasound was performed and the following images were obtained:

Figure 1: Proximal axial abdominal aortic ultrasound

Figure 1: Proximal axial abdominal aortic ultrasound

Figure 2: Longitudinal abdominal aorta ultrasound

Figure 2: Longitudinal abdominal aorta ultrasound

Figure 3: Distal axial abdominal aorta ultrasound

Figure 3: Distal axial abdominal aorta ultrasound


Known AAA s/p repair (also SVT with aberrancy)

Case Follow-up

The patient remained HDS and adenosine was given with good effect. He was admitted to medicine, and had no further episodes of SVT. He was discharged home with cardiology follow up.


The images were acquired using the curvilinear probe. The probe was placed on the abdomen just superior of the umbilicus and just left of midline. Both longitudinal and axial views were acquired.

Ultrasound is the initial test of choice for suspected AAA in the ED. It has sensitivity of 94-99%, and has been shown to decrease mortality in AAA patients by 20-50% compared to CT--likely due to decreased time to diagnosis.

A normal abdominal aorta is typically < 3cm in diameter. A complete AAA ultrasound should evaluate the aorta from the xiphoid process past the aortic bifurcation. US may be considered positive if the aorta is >3 cm in a patient with clinical concern for AAA,  or > 5 cm without clinical concern.

Faculty Reviewer: Dr. Kristin Dwyer

For an in-depth tutorial on the abdominal aorta ultrasound, check out this video from EM:RAP HD:

Additional Resources