Normal Coronary Artery.

Muscular artery with a clear lumen(no atherosclerosis). Vascular wall composed of single-cell layer endothelium, subendothelium, media, and adventitia. Normal endothelium produces anti-coagulation factors, but can also produce pro-coagulation upon injury; that is, platelets are inhibited by the presence of the endothelium but activated by exposure to collagen in the subendothelium. Normal blood flow is laminar with Platelets flowing in the center (far from endothelium) and plasma flowing more exteriorly adjacent to endothelium. 

Hemorrhage of the Arm

Larger hemorrhages are typically more associated with trauma whereas smaller tend to be associated with coagulation changes, inflammation, and/or vascular integrity. Proximally – Multiple purpura (hemorrhage > 3 mm) can be identified. These may result from coagulation abnormalities, trauma, inflammation, and increase vascular fragility. Your history and selected blood tests (platelet count) would help your differential. Distally – a large ecchymosis (hemorrhage > 1-2 cm) which is often most associated with trauma. Resolution of these hemorrhages typically produces a staging of colors. First, the dark blue/purple stage of the erythrocytes (RBC) entering subcutaneous tissue, followed by a greenish stage where RBC are broken down into bilirubin. Lastly, a yellowish tint appears as macrophages digest hemoglobin to form hemosiderin (iron, what forms the tint) and porphyrin (heme). 

Ecchymoses are larger than petechia and can appear with coagulation disorders.

Petechiae Hemorrhage on Epicardium of the Heart

Small hemorrhages (1-2mm) that form pinpoint bleeds. They can be found in any type of mucosa, skin, tissue, etc. Typically form as a result of abnormal coagulation (inherited and/or acquired) that could involve a decrease number of platelets (thrombocytopenia)-most typical, platelet dysfunction, clotting factor abnormalities, or from ischemia/hypoxic event. 

Hemoparicardium

Large hemorrhages can fill body cavity spaces and compress organs. This can include the peritoneum, retroperitoneum, thorax, and the pericardium. These types of hemorrhages typically have an abrupt onset due to a blunt trauma or penetrating injury causing a rupture of myocardium and/or coronary arteries with bleeding into the pericardial cavity. Without aggressive management, hemoparicardium can compress the heart resulting in cardiac tamponade (tachycardia, jugular vein distension, falling BP (decrease stroke volume), and muffled heart sounds).  

Subarachnoid Hemorrhage, Middle Cerebral Artery

Diffuse subarachnoid hemorrhage extends from the base of the brain to the lateral surface of the frontal and temporal lobes. 

Dura mater can be seen reflected above brain and absent of blood between arachnoid and dura indicating this is a subarachnoid hemorrhage. This type of hemorrhage, typically caused by an aneurysm, presents as the “worst headache of life” and rapid loss on consciousness (LOC). An aneurysm is a weakening in the wall of the artery that causes distension in the form of a pouch. The most common in the brain is the Berry Aneurysms typically found within the Circle of Willis. Sub-dural hemorrhages may present as headache, and epidural have a more transient presentation. Epidural hemorrhages, commonly involving the middle meningeal artery, presents as LOC post-trauma followed by waking up and feeling fine, a dangerous event which influences the person to not seek medical evaluation. Then, the person my have a second LOC event, go to the hospital, but be too late for medical treatment as the brain may have herniated (due to increase intracranial pressure) and death (this is of course one of many possible outcomes). 

Intraparenchymal Hemorrhage

Hemorrhage in the basal ganglia (esp the putamen) typically caused by hypertension damaging the endothelium and weakening vascular vessels and small penetrating arteries; resulting in predisposition to rupture microaneurysms.

A mass effect with midline shift, often w/ secondary edema, may lead to herniation.

Intraventricular Hemorrhage of Premature Infant

Also called a “germinal matrix(subependymal) bleed.” b/c while the vasculature is still maturing in the premature infant, the germinal matrix remains sensitive to changing levels of Oxygen and is susceptible to lesions. Physiologic response to hypoxic events can cause vessel damage and rupture. This type of hemorrhage is common in the NICU when babies are premture (this one's at 28 weeks).

Thrombus in Coronary Artery

The dark red thrombus is a complication of atherosclerosis and seen in the anterior descending coronary artery.

A thrombus is composed of the platelets from the primary response (activated platelets causing vasoconstriction, von Willebrand Factor [vWF] in platelet adhesion and aggregation, activation of coagulation cascade) and fibrin from the secondary response (intrinsic and extrinsic, especially Tissue Factor from endothelium). RBC may also become trapped in the thrombus. Virchow’s Triad describes conditions that cause thrombus formation: abnormal blood flow, endothelium damage, and hypercoagulability. Abnormal blood flow can occur due to hypertension, necrotic tissue, atherosclerosis, etc. and results in turbulent flow, which can damage the endothelium, and/or stasis, which allows collections of platelets, factors, etc. Furthermore, without laminar flow, the platelets have an increased ability to interact with the endothelium. 

Higher Magnification of Thrombus in Coronary Artery

Thrombus occludes the lumen and produces ischemia and/or infarction of the myocardium.

The red thrombus can be identified from the smooth vascular walls. The vessel can be seen narrowing due to an atherosclerotic plaque filled with cholesterol. In response to the plaque, an inflammatory response attracts neutrophils & macrophages to site causing a subsequent activation of the coagulation cascade that forms the thrombus. 

Cross-Section of Coronary Artery

Thrombus (pink triangle) occluding the lumen. Just to the right are white streaks/spikes of accumulated cholesterol and thickening of the intima (purple area). The media (outer pink ring) demonstrates irregular smooth muscle organization while it is also narrowing and the walls thinning. 

Lines of Zahn, Microscopic view of a Thrombus

A laminated thrombus (typical of arterial sorts) that demonstrates alternating lines of platelets & fibrin (light pink) and RBC (dark pink). There are four outcomes to a thrombus: propagation, complete restoration, reorganization, and fraction into emboli. 

Pulmonary Embolism

The typical source for such thromboemboli is from large veins in the legs and pelvis.

The lungs are particularly vulnerable to thromboembolisms within the venous system. One of the more common locations for formation is in the deep veins of the legs. Deep vein thrombosis (DVT) occurs from immobilization, venous stasis from lack of leg contraction, and hypercoagulability. Predisposing factors are past and/or family history of hypercoagulability as indicated by previous DVT and/or pregnancy loss, oral contraceptives, smoking, and long periods of immobilization (e.g. plane rides, or lectures). The typical signs and symptoms are lower extremity edema, erythema, and warmth to the touch. 

Pulmonary Embolism

The pulmonary thromboembolus is occluding the main pulmonary artery. Patients who are immobilized for weeks are at greatest risk.

This embolism is pale (less red) and more solid. The signs and symptoms of a pulmonary embolism can vary depending on the size of the embolus, number, and where in the lung it is located. A patient can feel absolutely nothing, have chest pain, and/or shortness of breath. Death may occur within minutes.

Saddle Pulmonary Thromboembolus

This embolus, red and gel-like, straddles the bifurcation of the pulmonary artery (as if the embolus was wearing the pulmonary artery like pants) and prevents blood flow in either direction. These types of emboli are severe and highly fatal. 

Microscopic Image of Pulmonary Embolism

This embolus is in lung tissue as indicated by the surrounding alveolar tissue. It is not organized into laminar sheets due to slower, low-pressure nature of venous flow but there are organized sections of platelets & fibrin (light pink) and captured RBC (darker pink). 

Magnified view of Microscopic Image of Pulmonary Embolism

Embolus is adherent to the pulmonary arterial wall and if the patient survives, the thromboembolus will organize and for the most part be removed.

This embolus is in the lung as indicated by the surrounding alveolar tissue. It has started an inflammation response as indicated by the inflammation-mediator cells around the thrombus and angiogenesis (small darker areas). Emboli can have four outcomes: resolve, recanalize (reorganize/incorporate into vessels by forming new lumen), propagate (get bigger), or form even more emboli. 

Pulmonary Fat Emboli

These emboli are in lung tissue as indicated by the surrounding alveolar tissue. The round, white circles are fat globs occluding the small pulmonary artery. Fat emboli originate from bone marrow that has escape into circulation either through a traumatic long bone, pelvic, or sternum fracture, burn injuries, severe fatty liver, or orthopedic surgeries. Fat emboli are typically asymptomatic unless the patient develops Fat Embolism Syndrome. As fats travel in the vasculature, they can irritate the endothelium consequentially activating coagulation. Small fibrin clots then form throughout the body causing DIC follow by multi-organ involvement. 

Amniotic Fluid Embolism

As a random complication of delivery, a tear in the placental membranes and introduction of amniotic fluid into the maternal circulation can lead to amniotic fluid emboli. This embolus is in the lung as indicated by the surrounding lung tissues albeit congested and collapsed. The embolus itself is formed by feral squames(this one), vernix, mucin, and lanugo hair that irritates the maternal vasculature causing acute dyspnea, cyanosis, shock, DIC, followed by mass hemorrhaging due to used up platelets, and death (fifth leading cause in pregnant mothers). 

Infarction of the Heart

One complication of a transmural myocardial infarction is rupture of the myocardium, most likely to occur 3 to 5 days following the initial event when the myocardium it the softest. White arrow marks=point of rupture in an anterior-inferior myocardial infarction of the left ventricular free wall and septum. The dark red blood clot forms the hemopericardium, which can lead to tamponade.

Infarction of cardiac tissue causes problems with the propagation of the electrical signal and also with the structural integrity. Here an infarction in the heart causes a tearing of the ventricular wall resulting in mass hemorrhage into the pericardium. 

Red Pulmonary Infarct

Infarcts occur in a wedge shape representing the tributaries of the occluded vessel. While this infarct is small and may not been fatal, it can lead to some loss of function for the organ. Red infarcts occur with congestions/venous obstruction, dual circulation, and reperfusion. Pulmonary artery carrying most of the blood and oxygen is cut off, but the bronchial arteries from systemic circulation(supplying ~1% of blood to lungs) is not.

Large thromboemboli can cause death, medium ones produce a lesion like seen here(a hemorrhagic pulmonary infarction) because the patient survives. 

Red Pulmonary Infarct

Infarct of the lung in the characteristic wedge shape. The fading off this infarct indicates that is older and was in process of resolving before death.

There's a larger area of infarction produced  by a medium-sized thromboembolus and the infarct has begun to organize at the margins. It's possible to have multiple small pulmonary thromboemboli that don't cause sudden death and don't occlude a large enough branh of the pulmonary artery to cause infarction, but if there's lots of small emboli they may collectively block enough small arteries to produce pulmonary hypertension. 

White Acute Renal Infarct

White infarcts occur in end artery organs (where artery is sole supplier, more susceptible to blood pressure extremes, hypovolemia). In this infarct, hyperemia (increase blood flow) occurs in surrounding tissue. Notice that the outer most portion is not infarcted due to perfusion from arteries in the renal capsule, but the remaining cortex and medulla is congested. Potential causes could be: thrombus from an atherosclerotic plaque, embolism (ex. fragment of mural thrombus in heart), or a valvular problem (either septic from bacterial living of valve leaflet [infectious endocarditis, particularly in a IV drug user], or thromboembolitic). This is coagulative necrosis from loss of blood supply with reultant tissue ischemia that produces the pale infarct.

Cerebral Infarct

This infarction (currently undergoing liquefactive necrosis) results from a cerebrovascular occlusion. The most common causes of ischemic stroke are: stenosis of the carotids and/or arteries that compose the Circle of Willis via atherosclerosis eventually causing a thrombosis and/or fragmenting an emboli, and thromboembolism is the heart as a result of irregular heartbeats (esp. atrial fibrillation), irregular flow pattern from myocardial infarct, or abnormalities of the heart valves. 

This is an intermediate to remote infarct in the distribution of the middle cerebral artery.

Ischemic Bowel

Fibrin Clot during DIC

Clot, pink in color indicating large fibrin component, blocks a capillary in alveolar tissue.

Disseminated Intravascular Coagulabilty (DIC) – complication to many severe processes (amniotic emboli, fat emboli, OB emergencies, severe burn) that causes systemic wide activation of thrombosis and fibrinolysis, exhausts coagulation factors, results in decreased platelets, prolonged prothrombin time, elevated partial thromboplastin time, and elevated D-dimer. Consumption of coagulation factors occurs with generation of fibrin split products.

Fibrin Clots in Glomerulus of Kidney during DIC

These clots, pink in color indicating fibrin, found in the glomeruli indicates to a pathologist that DIC was the mechanism at play. This is a fibrin stain.