Difference between revisions of "Pulmonary embolism"

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*Pulmonary bone marrow embolism.
*Pulmonary bone marrow embolism.
*Pulmonary tumour embolism.
*Pulmonary tumour embolism.
*Pulmonary amniotic fluid embolism.


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

Revision as of 07:32, 17 November 2014

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.
  • Pulmonary tumour embolism.
  • Pulmonary amniotic fluid 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 venous thromboembolism

A general mnemonic for hypercoagulable states PIANO:[4]

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:

Microscopic (amniotic fluid)

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.