Morphological appearance of embolism

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Morphological Appearance of Embolism

An embolus is a detached intravascular solid, liquid, or gaseous mass carried by blood from its point of origin to a distant site, where it causes partial or complete vascular occlusion. The vast majority are dislodged thrombi (thromboembolism). Other types include fat, air/gas, amniotic fluid, cholesterol, tumor fragments, and bone marrow.

1. Pulmonary Thromboembolism

Gross morphology:

Most (>95%) arise from DVT of the deep leg veins proximal to the popliteal fossa
The embolus is a dark red-brown, coiled, serpentine mass conforming to the shape of the vein of origin
It lodges in a pulmonary artery branch where the lumen narrows; a large embolus can straddle the bifurcation of the right and left pulmonary arteries - this is called a "saddle embolus"
On cut section it appears as a coiled or elongated thrombus, distinguishable from post-mortem clot by its laminated (lines of Zahn), dry, granular, and adherent appearance

Gross image - Saddle embolus in pulmonary arteries (Robbins & Kumar):

Embolus from a lower extremity DVT lodged at a pulmonary artery branchpoint

Gross photograph showing a dark red-brown thromboembolus lodged at the pulmonary artery bifurcation. The surrounding lung parenchyma is visible.

Histological morphology:

The embolus consists of fibrin mesh enmeshing red cells, platelet aggregates, and leukocytes
Organized (older) emboli show ingrowth of fibroblasts and endothelial cells from the vessel wall
Complete organization incorporates the embolus into the vascular wall; incomplete organization may leave a delicate bridging fibrous web across the vessel lumen

Downstream effects:

60%-80% of small emboli are clinically silent and organize
Medium-sized emboli cause pulmonary hemorrhage (but not infarction, due to dual blood supply from bronchial arteries) - unless bronchial circulation is compromised (left heart failure)
Small end-arteriolar emboli often produce infarction with hemorrhage
Emboli obstructing >60% of pulmonary circulation cause cor pulmonale or sudden death

2. Systemic Thromboembolism

80% arise from intracardiac mural thrombi (two-thirds from left ventricular infarcts, one-fourth from dilated left atria in atrial fibrillation)
Remainder from aortic aneurysms, ulcerated atherosclerotic plaques, or valvular vegetations
Common sites: lower extremities (75%), brain (10%), intestines, kidneys, spleen
Gross appearance is identical to thromboemboli elsewhere: dark red-brown, friable, and adherent to the vessel wall at the point of arrest

3. Fat Embolism

Cause: Fractures of long bones or soft tissue crush injuries rupture vascular sinusoids, releasing fat globules and marrow elements into the circulation.

Histological morphology:

Microscopic fat globules (empty "ghost" vacuoles in paraffin sections, since lipid is dissolved by processing solvents) within pulmonary and cerebral microvasculature
Associated hematopoietic bone marrow elements (megakaryocytes, erythroid precursors) often accompany the fat globules
The embolus may have an early organizing thrombus attached to it
Special stains required: Oil Red O or Sudan stains on frozen sections (fat is dissolved in routine paraffin processing) confirm fat globules
Platelet aggregates and red cell aggregates surround fat microemboli in the microvasculature

Histological image - Bone marrow/fat embolus in pulmonary vessel:

Bone marrow embolus in the pulmonary circulation showing hematopoietic cells and cleared fat vacuoles

H&E section: The embolus occupies a pulmonary vessel lumen. Hematopoietic cells are visible on the left, cleared vacuoles represent dissolved marrow fat, and the relatively uniform pink area on the right is early organizing thrombus.

4. Air/Gas Embolism

Cause: Entry of air into the vasculature (neurosurgery, obstetric procedures, chest trauma, mechanical ventilation) or rapid decompression (decompression sickness/"the bends")

Morphological appearance:

Gas bubbles coalesce to form frothy masses that obstruct vascular flow
In pulmonary vessels: foamy appearance to blood; edema, hemorrhage, and focal atelectasis or emphysema in surrounding lung
In decompression sickness: gas bubbles in skeletal muscles, joints, and bones cause ischemic necrosis - caisson disease results in multiple foci of avascular necrosis at the femoral heads, tibia, and humeri
Bubbles in the CNS vasculature produce ischemic lesions
100 mL of air is needed for significant pulmonary effect; 300-500 mL over seconds can be fatal

5. Amniotic Fluid Embolism

Cause: Tear in placental membranes or rupture of uterine veins during labor allows amniotic fluid/fetal tissue into maternal circulation.

Classic histological findings (autopsy):

Pulmonary microvasculature packed with squamous cells shed from fetal skin - appear as laminated, whorled eosinophilic structures
Lanugo hair (fine fetal hair)
Fat globules from vernix caseosa
Mucin from fetal respiratory or gastrointestinal tract
Associated pulmonary edema and diffuse alveolar damage

Histological image - Amniotic fluid embolism:

Fat embolus (A) and amniotic fluid embolus (B) - pulmonary arterioles packed with laminated squamous cells

Panel A: A fat/bone marrow embolus filling a pulmonary arteriole (clear vacuoles = fat, pink cells = hematopoietic marrow elements). Panel B: Small pulmonary arterioles packed with laminated whorls of fetal squamous cells - the hallmark of amniotic fluid embolism. Surrounding lung shows edema.

Summary Table

Type	Gross Appearance	Histological Features	Special Stains
Thromboembolism	Dark red-brown, laminated, coiled mass; saddle embolus at bifurcation	Fibrin, RBCs, platelets, leukocytes; organizing fibrosis	None specific
Fat embolism	Not visible grossly	Empty vacuoles (fat dissolved), marrow elements, platelet aggregates	Oil Red O / Sudan on frozen sections
Air embolism	Frothy blood in vessels	No specific histology; foam in vessels, lung edema/hemorrhage	None
Amniotic fluid embolism	Not visible grossly	Squamous cells, lanugo hair, vernix fat, mucin in pulmonary microvessels	PAS for mucin
Systemic thromboembolism	Same as pulmonary TE; lodges in end arteries	Same as above; infarction in supplied territory	None specific

Sources: Robbins, Cotran & Kumar - Pathologic Basis of Disease, pp. 130-132 | Robbins & Kumar Basic Pathology, pp. 93-96

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