Health Dictionary

Overview

There are no specific physical exam findings for non-bacterial thrombotic endocarditis. Patients with NBTE may show signs of systemic thromboembolism, cardiac dysfunction, and underlying diseases.

Physical Examination

There are no specific findings for non-bacterial thrombotic endocarditis. Patients with NBTE may show signs of systemic thromboembolism, cardiac dysfunction, and underlying diseases.

General appearance

Patients with NBTE usually appear non-toxic. Patients may present with acute signs of cerebral or systemic embolisms of signs or cardiac dysfunction.

Vital Signs

Fever (if due to malignancy or complicated by secondary infectious endocarditis
Hypotension (if severe left ventricular dysfunction is present)
Tachycardia
Tachypnea
Orthopnea

Skin

Raynaud’s phenomenon (incase of peripheral embolism)
Malar rash (in patients with SLE)

HEENT

HEENT examination of patients with NBTE is usually normal.

Neck

Jugular venous distension may be noted secondary to heart failure due to valvular dysfunction
Lymphadenopathy (in the case of malignancy)

Lungs

lung fields may be dull on percussion in the presence of secondary infection, or pleural effusion due to malignancy

Heart

Left ventricular hypertrophy due to aortic or mitral valve disease can present as any of the following:

- Displacement of apex beat
- Enlarged and sustained apical impulse
- S4
- S2 (due to aortic root dilatation)

Abdomen

Abdominal distension
Abdominal pain/tenderness in the left upper quadrant due to splenic embolism
Flank pain
Ascites may be observed in cases of heart failure and fluid overload

Genitourinary

Genitourinary examination of patients with NBTE is usually normal

Extremities

Clubbing may be seen in patients with malignancies
Cyanosis due to peripheral embolism
Pedal edema may be observed if heart failure is present
Polyarthralgia and arthritis may be observed

Some physical examination findings in patients with Nonbacterial thrombotic endocarditis
Pathology	Physical examination finding
Left ventricular hypertrophy^[1]^[2]^[3]^[4]^[5]^[6]	LVH can present as any of the following: Displacement of apex beat Enlarged and sustained apical impulse S₄ S₂ (due to aortic root dilatation) ECG findings of LVH include: Increased QRS voltage Increased QRS duration (widened QRS associated with complete or incomplete LBBB) Left axis deviation (horizontal/frankly leftward (≥-30º) QRS axis in the frontal plane leads or normal/vertical axis) Right axis deviation Repolarization abnormalities such as ST depressions and T wave inversions in leads with relatively tall R waves (referred to as LV “strain” pattern or “LVH with associated ST–T wave abnormalities“) Prominent positive T waves in the lateral chest leads Left atrial abnormality has the following two important major presentations: Increased duration of P waves (≥120 milliseconds) in the limb leads Biphasic P waves with a prominent negative (terminal) component (≥40 milliseconds in duration and/or ≥1 mV in depth) in V1
Congestive heart failure	Physical examination findings of CHF include: Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Peripheral edema Lethargy Rales on lung examination
Secondary infective endocarditis (IE)^[7]^[8]^[9]^[10]	IE can present as: Fever Rigors Night sweats Headache Myalgias Anorexia Malaise Shortness of breath Cough Joint pains Presence of a new or changing heart murmur in 80% to 85% of patients (due to aortic insufficiency, tricuspid regurgitation or mitral regurgitation) Widened pulse pressure (due to aortic insufficiency) Petechiae (10% to 40% of patients) Osler’s nodes (7% to 10% of patients) Janeway lesions (6% to 10% of patients) Splinter hemorrhages (5% to 15% of patients) Evidence of embolization Conjunctival hemorrhage Roth’s spots in retina Poor oral hygiene Teeth might have periodontitis, plaque or calculus Gingivitis Splenomegaly (15% to 30% patients) Left upper quadrant pain (due to splenic infarct from embolization) Flank pain (due to embolus to the kidney) Stroke and focal neurologic findings (due to septic emboli) Seizures Intracranial hemorrhage Signs of a brain abscess Gangrene of fingers Back pain (due to vertebral osteomyelitis)
Mitral valve disease^[11]	High-pitched “blowing” holosystolic murmur of mitral regurgitation (more common) which is best heard at the apex of the heart with the patient in left lateral decubitus position. Mid-diastolic, rumbling murmur of mitral stenosis (with or without an Austin Flint murmur).
Aortic valve disease	Early diastolic murmur of aortic regurgitation Widened pulse pressure due to aortic insufficiency Bobbing of the uvula (new-onset aortic regurgitation)
Tricuspid valve disease	Holosystolic murmur of tricuspid regurgitation

References

↑ https://www.medscape.com/answers/241381-7641/what-are-signs-of-left-ventricular-hypertrophy-lvh-in-cardiac-exam-of-hypertension-high-blood-pressure
↑ Okin PM, Devereux RB, Nieminen MS, Jern S, Oikarinen L, Viitasalo M; et al. (2001). “Relationship of the electrocardiographic strain pattern to left ventricular structure and function in hypertensive patients: the LIFE study. Losartan Intervention For End point”. J Am Coll Cardiol. 38 (2): 514–20. doi:10.1016/s0735-1097(01)01378-x. PMID 11499746.
↑ Pinto IJ, Nanda NC, Biswas AK, Parulkar VG (1967). “Tall upright T waves in the precordial leads”. Circulation. 36 (5): 708–16. doi:10.1161/01.cir.36.5.708. PMID 4227953.
↑ Okin PM, Devereux RB, Fabsitz RR, Lee ET, Galloway JM, Howard BV; et al. (2002). “Quantitative assessment of electrocardiographic strain predicts increased left ventricular mass: the Strong Heart Study”. J Am Coll Cardiol. 40 (8): 1395–400. doi:10.1016/s0735-1097(02)02171-x. PMID 12392827.
↑ Shah AS, Chin CW, Vassiliou V, Cowell SJ, Doris M, Kwok TC; et al. (2014). “Left ventricular hypertrophy with strain and aortic stenosis”. Circulation. 130 (18): 1607–16. doi:10.1161/CIRCULATIONAHA.114.011085. PMID 25170097.
↑ Mehta A, Jain AC, Mehta MC, Billie M (2000). “Usefulness of left atrial abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block”. Am J Cardiol. 85 (3): 354–9. doi:10.1016/s0002-9149(99)00746-8. PMID 11078306.
↑ https://emedicine.medscape.com/article/216650-clinical
↑ Jingushi N, Iwata M, Terasawa T (2017). “Clinical features of patients with infective endocarditis presenting to the emergency department: a retrospective case series”. Nagoya J Med Sci. 79 (4): 467–476. doi:10.18999/nagjms.79.4.467. PMC 5719206. PMID 29238103.
↑ Hoen B, Duval X (2013). “Clinical practice. Infective endocarditis”. N Engl J Med. 368 (15): 1425–33. doi:10.1056/NEJMcp1206782. PMID 23574121.
↑ Cahill TJ, Prendergast BD (2016). “Infective endocarditis”. Lancet. 387 (10021): 882–93. doi:10.1016/S0140-6736(15)00067-7. PMID 26341945.
↑ Hojnik, Maja; George, Jacob; Ziporen, Lea; Shoenfeld, Yehuda (1996). “Heart Valve Involvement (Libman-Sacks Endocarditis) in the Antiphospholipid Syndrome”. Circulation. 93 (8): 1579–1587. doi:10.1161/01.CIR.93.8.1579. ISSN 0009-7322.

[1] ttps://www.medscape.com/answers/241381-7641/what-are-signs-of-left-ventricular-hypertrophy-lvh-in-cardiac-exam-of-hypertension-high-blood-pressure

[pmid11499746-2] Okin PM, Devereux RB, Nieminen MS, Jern S, Oikarinen L, Viitasalo M; et al. (2001). “Relationship of the electrocardiographic strain pattern to left ventricular structure and function in hypertensive patients: the LIFE study. Losartan Intervention For End point”. J Am Coll Cardiol. 38 (2): 514–20. doi:10.1016/s0735-1097(01)01378-x. PMID 11499746.

[pmid4227953-3] Pinto IJ, Nanda NC, Biswas AK, Parulkar VG (1967). “Tall upright T waves in the precordial leads”. Circulation. 36 (5): 708–16. doi:10.1161/01.cir.36.5.708. PMID 4227953.

[pmid12392827-4] Okin PM, Devereux RB, Fabsitz RR, Lee ET, Galloway JM, Howard BV; et al. (2002). “Quantitative assessment of electrocardiographic strain predicts increased left ventricular mass: the Strong Heart Study”. J Am Coll Cardiol. 40 (8): 1395–400. doi:10.1016/s0735-1097(02)02171-x. PMID 12392827.

[pmid25170097-5] Shah AS, Chin CW, Vassiliou V, Cowell SJ, Doris M, Kwok TC; et al. (2014). “Left ventricular hypertrophy with strain and aortic stenosis”. Circulation. 130 (18): 1607–16. doi:10.1161/CIRCULATIONAHA.114.011085. PMID 25170097.

[pmid11078306-6] Mehta A, Jain AC, Mehta MC, Billie M (2000). “Usefulness of left atrial abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block”. Am J Cardiol. 85 (3): 354–9. doi:10.1016/s0002-9149(99)00746-8. PMID 11078306.

[7] ttps://emedicine.medscape.com/article/216650-clinical

[pmid29238103-8] Jingushi N, Iwata M, Terasawa T (2017). “Clinical features of patients with infective endocarditis presenting to the emergency department: a retrospective case series”. Nagoya J Med Sci. 79 (4): 467–476. doi:10.18999/nagjms.79.4.467. PMC 5719206. PMID 29238103.

[pmid23574121-9] Hoen B, Duval X (2013). “Clinical practice. Infective endocarditis”. N Engl J Med. 368 (15): 1425–33. doi:10.1056/NEJMcp1206782. PMID 23574121.

[pmid26341945-10] Cahill TJ, Prendergast BD (2016). “Infective endocarditis”. Lancet. 387 (10021): 882–93. doi:10.1016/S0140-6736(15)00067-7. PMID 26341945.

[HojnikGeorge1996-11] Hojnik, Maja; George, Jacob; Ziporen, Lea; Shoenfeld, Yehuda (1996). “Heart Valve Involvement (Libman-Sacks Endocarditis) in the Antiphospholipid Syndrome”. Circulation. 93 (8): 1579–1587. doi:10.1161/01.CIR.93.8.1579. ISSN 0009-7322.

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