Difference between revisions of "Pulmonary embolism"

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==Microscopic (VTE)==
==Microscopic (VTE)==
Features:
Features:
*Layers consisting of platelets and fibrin alternating with layers of RBCs; ''Lines of Zahn''.<ref name=Ref_PBoD8_124>{{Ref PBoD8|124}}</ref>
*Layers consisting of platelets and fibrin alternating with layers of RBCs - known as ''Lines of Zahn''.<ref name=Ref_PBoD8_124>{{Ref PBoD8|124}}</ref>
 
Note:
*Multiple laminations (layers), in general, suggest that clot was formed in a dynamic environment, i.e. in the context of blood flow.


Images:  
Images:  

Revision as of 03:20, 17 October 2012

Pulmonary embolism, abbreviated PE, is often on the differential in autopsies, as it is not easy to diagnose clinically. Pulmonary embolism is a non-specific term; it may refer to a number of things, including:

  • Pulmonary venous thromboembolism.
  • Pulmonary fat embolism.
  • Pulmonary foreign body embolism.
  • Pulmonary septic embolism.
  • Pulmonary bone marrow embolism.

PE usually refers to pulmonary venous thromboembolism, abbreviated VTE, if not otherwise specified.

General

  • Relatively uncommon ~ 1 in 1000 adults per year.[1]
  • Diagnosis in life dependent on strong clinical suspicion and radiology.

Clinical

  • Shortness of breath (dyspnea) - classic symptom.
  • Tachycardia.
  • Chest pain.
  • Findings associated with deep vein thrombosis.
    • Leg pain.
    • Leg swelling.

Notes:

  • Venous thrombosis OR~=12 for PE.[2]

Mechanism

The classic factors are given by Virchow's triad:[3][1]

  1. Hypercoagulability.
  2. Endothelial dysfunction/injury.
  3. Stasis.

Note:

  • The triad has a limited practical use. Like many questions about mechanism, the greatest utility, as far as I can determine, is pimping medical students and residents.

Risks factors (VTE)

A general mnemonic for hypercoagulable states PIANO:[4]

  • Pregnancy.
  • Immobility.
  • Accidental injury.
  • Nephrotic syndrome.
  • Oral contraceptive pills.

Hypercoagulable states due to intrinsic causes (memory device CALM SHAPES):[5]

  • Protein C deficiency.
  • Antiphospholipid antibody syndrome (APLA).
  • Leiden factor V deficiency.
  • Malignancy.
  • Protein S deficiency.
  • Homocystinemia.
  • Antithrombin III deficiency.
  • Prothrombin G20210A.[6]
  • Excess factor VIII.
  • Sticky platelet syndrome.

Gross (VTE)

Features:

  • Intravascular spaghetti (multiple cylindrical clots - from smaller vessels) with cream sauce (gray fibrin).
  • Leg swelling.
  • Lines of Zahn.[7]
    • Pale layers consisting of platelets and fibrin alternating with layers of RBCs; components layer during blood flow.

Notes:

  • Post-mortem thrombi: one (superior) yellow portion (called "chicken fat") and one (dependent) red portion (RBCs); components layer due to gravity.

Pre- and post-mortem clots

Feature/time Pre-mortem Post-mortem
Shininess dull shiny
Adherent to wall yes no
Colour gray dark purple or
bilayered red/yellow
Pressurized yes; "ejects itself" from lumen no; needs to be pulled-out
Consistency
-elastic modulus (E)
-fracture toughness (K) 		firm (high E)
brittle (low K) 		jello (low E)
elastic (high K)
Image - gross thrombus (pathguy.com),
thrombus (thrombosisadviser.com) 		coronary thrombus (luc.edu)[8]
Image - micro. pre- & post-mortem (elsevier.es)[9] thrombus (oxfordjournals.org),
thrombi (ucsf.edu)

Microscopic (VTE)

Features:

  • Layers consisting of platelets and fibrin alternating with layers of RBCs - known as Lines of Zahn.[7]

Note:

  • Multiple laminations (layers), in general, suggest that clot was formed in a dynamic environment, i.e. in the context of blood flow.

Images:

Microscopic (fat embolism)

Features:

  • Fat in vessels.

Images:

See also

References

  1. ↑ 1.0 1.1 Meetoo, D.. "In too deep: understanding, detecting and managing DVT.". Br J Nurs 19 (16): 1021-7. PMID 20852464.
  2. ↑ Reissig A, Haase U, Schulze E, Lehmann T, Kroegel C (July 2010). "[Diagnosis and therapy of pulmonary embolism prior to death]" (in German). Dtsch. Med. Wochenschr. 135 (30): 1477–83. doi:10.1055/s-0030-1262435. PMID 20648405.
  3. ↑ Reitsma, PH.; Versteeg, HH.; Middeldorp, S. (Mar 2012). "Mechanistic view of risk factors for venous thromboembolism.". Arterioscler Thromb Vasc Biol 32 (3): 563-8. doi:10.1161/ATVBAHA.111.242818. PMID 22345594.
  4. ↑ URL: http://www.usmle-forums.com/usmle-step-1-mnemonics/252-causes-hypercoagulable-states.html. Accessed on: 8 December 2011.
  5. ↑ Thomas RH (November 2001). "Hypercoagulability syndromes". Arch. Intern. Med. 161 (20): 2433–9. PMID 11700155. http://archinte.highwire.org/cgi/content/full/161/20/2433.
  6. ↑ Online 'Mendelian Inheritance in Man' (OMIM) 176930
  7. ↑ 7.0 7.1 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 124. ISBN 978-1416031215.
  8. ↑ URL: http://www.meddean.luc.edu/lumen/meded/mech/cases/case1/list.htm. Accessed on 8 October 2010.
  9. ↑ URL: http://www.elsevier.es/cardio_eng/ctl_servlet?_f=40&ident=13142654. Accessed on: 8 October 2010.
  10. ↑ URL: http://library.med.utah.edu/WebPath/EXAM/IMGQUIZ/fofrm.html. Accessed on: 6 December 2010.
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