Fat embolism syndrome pathophysiology

Jump to navigation Jump to search

Fat embolism syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Fat embolism syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Fat embolism syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Fat embolism syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Fat embolism syndrome pathophysiology

CDC on Fat embolism syndrome pathophysiology

Fat embolism syndrome pathophysiology in the news

Blogs on Fat embolism syndrome pathophysiology

Directions to Hospitals Treating Fat embolism syndrome

Risk calculators and risk factors for Fat embolism syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

Overview

Fat embolism syndrome (FES) is the presence of fat globules in the circulation post traumatic insult which can lodge into the small sized capillaries in the lung, brain and skin leading to devastating clinical manifestations. The two widely accepted theories which explain the pathophysiology of FES are mechanical and biochemical theory.

Pathophysiology

Two major theories have been described to explain the pathophysiology of fat embolism syndrome(FES):[1][2]

  • Mechanical theory
  • Biochemical theory

Mechanical theory

The theory proposes that there is mechanical obstruction by fat cells from the bone marrow in the end-capillaries after trauma.

  • Post traumatic insult, the fat cells travel via venous sinusoids to the capillaries.
  • These cells have potent prothrombotic and proinflammatory potential.
  • They trigger rapid aggregation of platelets and accelerated fibrin generation as they travel through the venous system, eventually lodging in the pulmonary arterial circulation.
  • Pulmonary capillary obstruction leads to interstitial hemorrhage and edema, alveolar collapse, and reactive hypoxemic vasoconstriction.
  • Massive fat emboli may also lead to macrovascular obstruction and shock.
  • Fat cells may also enter the arterial circulation via a patent foramen ovale or directly through the pulmonary capillary bed, causing the characteristic neurological and dermatologic findings of FES

Biochemical theory

This theory attributes the clinical manifestations of FES to the pro inflammatory effect of fat emboli.[3][4][5]

  • Tissue lipases break down the fat in the bone marrow, forming high levels of the following toxic intermediaries;
    • Free fatty acids:

Free fatty acids are released into the circulation after hydrolysis and deposit into the end capillaries of the lung, manifesting as acute respiratory distress syndrome.

    • Cytokines:

Patients with FES are also found to have high levels of certain cytokines such as tumor necrosis factor alpha, Phospholipase A2, interleukin 1 and 6.

    • C-reactive proteins:

The elevation is c-reactive proteins is responsible for lipid agglutintion in FES which results in microvasculature obstruction and stagnant blood flow.

  • Eventually, these intermediate products lead to end-organ dysfunction.
  • In the lung, toxic injury to pneumocytes and pulmonary endothelial cells causes vasogenic and cytotoxic edema as well as hemorrhage.
  • Acute lung injury or acute respiratory distress syndrome results from damaged pulmonary endothelium that triggers a proinflammatory cytokine cascade.

Video

{{#ev:youtube|eeAQ2akVjL8}}

Genetics

  • There is no genetic association of FES.

Gross pathology

Microscopic pathology

Hematoxylin and eosin staining shows the following changes in the lungs, kidneys and brain:[6]

Lung:

Immunohistochemical staining shows the following changes:

Kidney:

  • Hematoxylin and eosin staining shows fat deposits in the glomeruli.

Brain:

References

  1. Parisi DM, Koval K, Egol K (2002). "Fat embolism syndrome". Am J Orthop (Belle Mead NJ). 31 (9): 507–12. PMID 12650535.
  2. Robert JH, Hoffmeyer P, Broquet PE, Cerutti P, Vasey H (1993). "Fat embolism syndrome". Orthop Rev. 22 (5): 567–71. PMID 8316420.
  3. Husebye EE, Lyberg T, Røise O (2006). "Bone marrow fat in the circulation: clinical entities and pathophysiological mechanisms". Injury. 37 Suppl 4: S8–18. doi:10.1016/j.injury.2006.08.036. PMID 16990064.
  4. Estèbe JP (1997). "[From fat emboli to fat embolism syndrome]". Ann Fr Anesth Reanim. 16 (2): 138–51. PMID 9686075.
  5. Hofmann S, Huemer G, Kratochwill C, Koller-Strametz J, Hopf R, Schlag G; et al. (1995). "[Pathophysiology of fat embolisms in orthopedics and traumatology]". Orthopade. 24 (2): 84–93. PMID 7753543.
  6. . doi:10.1042/CS2007001. Missing or empty |title= (help)