Hemodynamic Disturbances: Hemorrhage

Hemodynamic Disturbances

• Disorders of blood flow within the circulatory system.
• Circulatory disturbances include hemorrhage, thrombosis, embolism, infarction, hyperemia, congestion, edema and shock.
• This will be covered in two lectures, the first focusing on hemorrhage, thrombosis, embolism, and infraction.

Hemorrhage

• The escape of blood outside blood vessels or cardiac chambers.
• Can be caused by traumatic injury or spontaneous events

Causes of Hemorrhage

• Traumatic hemorrhage (Rhexis) relates to the rupture or cutting of a blood vessel due to mechanical injury to the vascular wall, whether accidental or surgical.
• Spontaneous hemorrhage (Diapedesis) refers to the passage of blood cells through capillary walls into the tissues.

Types of Hemorrhage

• Diseases of the vascular wall (e.g. atheroma and aneurysm).
• Inflammatory injury to the vascular wall, as in phlebitis.
• Increased intravascular tension, e.g. chronic venous congestion and hypertension.
• Hemorrhagic blood diseases, such as hemophilia (impairs the body's ability to make blood clots) and purpura.
• Vitamin C and K deficiency.

Classification of Hemorrhage

External Hemorrhage

• Involves the escape of blood outside the body.

Manifestations of External Hemorrhage

• Epistaxis: Bleeding from the nose.
• Haemoptysis: Coughing of blood, originating from the lung/bronchi; the blood is red, frothy, and alkaline.
• Hematemesis: Vomiting of blood, originating from the esophagus, stomach, or duodenum; the blood is digested, brown, acidic and mixed with food particles.
• Melena: Presence of dark, digested blood in the stools.
• Hematuria: Blood in urine.

Internal Hemorrhage

• Escape of blood inside the body cavities.

Manifestations of Internal Hemorrhage

• Hemothorax: Hemorrhage into the pleura.
• Hemopericardium: Hemorrhage into the pericardium.
• Hemoperitoneum: Hemorrhage into the peritoneum.
• Hematocele: Hemorrhage into the tunica vaginalis.
• Hemoarthrosis: Hemorrhage into a joint cavity.

Interstitial Hemorrhage

• Escape of blood into the interstitial tissue spaces.

Interstitial Hemorrhage Classification

• Petechial hemorrhage: Small amount of blood described as "pinpoint".
• Ecchymosis: Moderate amount of blood.
• Suffusions: Diffuse flat irregular areas of bleeding.
• Hematoma: Large amount of blood causing a swelling.
• Hemorrhage may also be classified according to pathogenesis, source, size, and shape.

Microscopic Characteristics of Hemorrhage

• Presence of erythrocytes outside the blood vessels.
• In recent hemorrhage, erythrocytes are intact and stain sharply.
• Soon after hemorrhage, RBCs disintegrate due to enzymatic action, releasing hemoglobin.

Fate of Hemoglobin after hemorrhage

• Leads to the generation of Bilirubin (Haematoidin)
• Leads to the generation of Haemosiderin.
• Haemosiderin appears as golden yellow granules, irregular in size and shape
• Haemosiderin is insoluble and retained in macrophages
• Haemosiderin contains iron and stains blue with Prussian blue.

Microscopic observations of free red blood cells.

• Indication of recent hemorrhage with liberation of a golden-yellow to brown hemosiderin pigment.

Effect of Hemorrhage

Small Amount

• Has no significant effect.

Small Amount Repeatedly (Chronic Hemorrhage)

• Can lead to anemia.

Moderate Amount (Less than 750 cc.)

• Can be compensated by immediate aortic arch and carotid sinus reflexes

Compensatory Adjustments

• Immediate hypotension stimulates the aortic arch and carotid sinus reflexes, increasing heart rate.
• Proteins are added from the liver.
• Red and white cells are added by the hyperplastic bone marrow.

Massive Amount

• Can causes hemorrhagic shock.
• Results in decreased cardiac output and blood pressure, leading to death.
• The size and location of hemorrhage are significant.
• A small hemorrhage in the brain can be fatal, while the same in muscle or subcutaneous tissue may be of minor importance.

Repeated hemorrhage

• From skin, gastrointestinal tract, or female genital tract can cause blood and iron losses, leading to anemia.

Massive hemorrhages:

• Massive hemorrhage in body cavities leads to red clots (RBCs & fibrin)
• Later replaced by white jelly clot (mostly platelets)
• The white jelly clots get organized (angioblasts, fibroblasts), shrink, and adhere.

Thrombosis

• The formation of a compact mass composed of the elements of circulating blood inside a vessel (intravascular) or a heart cavity during life (intravital).

Causes of Thrombosis

• Involves vascular wall damage, changes in blood flow, and alterations in blood composition.

Damage to the Vascular Endothelium

• Mechanical injury (contusion, laceration, abrasion).
• Parasites (e.g., strongyles vulgaris).
• Bacterial colonies and toxins.
• Arteriosclerosis, providing endothelium injury.
• Tumors invading blood vessel walls.

Slowing of Blood Stream (Stasis)

• In normal flow, larger cells are in the axial stream.
• Platelets are carried outside the central column (peripheral zone).
• Sluggish blood flow is seen in varicose or swelling of blood vessels and can results in arterial, cardiac, and venous thrombosis.
• Sluggish blood flow brings platelets into contact with endothelium.
• Favors platelets and fibrin deposition.

Changes in Blood Composition (Hypercoagulability of blood)

• Platelets: Increase in number and become stickier after operations.
• Fibrinogen: Increases during pregnancy and in lobar pneumonia.
• Red cells: Increase in polycythemia.
• White blood cells: Increase in leukemia.
• Plasma: Decreased plasma volume as in dehydration.

Thrombus Formation

• Aggregation of platelets on damaged endothelium releases thromboplastin, which, in the presence of Ca+2, converts prothrombin to thrombin.
• Thrombin converts fibrinogen to fibrin
• Results in the formation of fibrin mesh to blood flow
• This is called Zhan line
• The fibrin mesh entraps platelets and RBCs, forming a mixed thrombus.

Types of Thrombi

Pale thrombus

• Initial thrombus is composed of platelets deposited at the site of endothelial damage.

Mixed thrombus

• Platelets deposit as laminae at right angles to blood stream.
• Between the laminae is complete blood stasis with fibrin deposited, entangling red and white blood cells.

Propagating thrombus:

• Occludes a vein completely, proximal to the occlusion, blood stagnates and clots.

Thrombus characteristics:

• Soft, red, and fixed to the original thrombus but not to the vascular wall

Classifications of Thrombi

Color

• Pale thrombus is composed mainly of platelets and fibrin, common in the heart and arterial side (rapid flow).
• Red thrombus is made up mainly of red cells and fibrin, common on the venous side.
• Mixed thrombus has pale and red components (rapid & stasis of blood flow).

Presence of Bacteria

• Infected thrombus contains bacteria and is called a septic thrombus if pyogenic.
• Non-infected (aseptic) thrombus contains no bacteria.

Sites of Formation:

Veins

• Thrombosis in veins is common because they have slow blood flow and a thin wall.

Arteries

• Thrombosis in arteries is less common than in veins due to the rapid blood flow.
• Thrombosis in Capillaries: Capillary thrombosis occurs in acute inflammation.

Heart

• Thrombosis in heart is common, particularly on the left side

Manifestations of Heart Thrombosis

• Mural thrombi occurs over infarcts, usually on the endocardial surface of the left ventricle near the apex.
• Vegetations are pale thrombi over the valves in rheumatic and bacterial endocarditis.
• Auricular thrombi are common in the left auricle in mitral stenosis
• Auricular thrombi commonly adhere to the wall and is called ball thrombus.
• Agonal thrombi: Red thrombi occurring in the ventricles, common on the right side at death.

Fate of Thrombus

Septic Thrombus

• Fragments are degraded by proteolytic enzymes, forming septic emboli that cause pyaemic abscesses.

Aseptic Thrombus:

• Elements disintegrate.
• If small, it dissolves by fibrinolysis.
• If large, organization, organization and canalization, dystrophic calcification, detachment, or propagating thrombosis.

Organization

• The thrombus is invaded by capillaries and fibroblasts from the vascular wall, changing into a fibrous mass.
• Causes permanent vascular occlusion.

Organization and Canalization:

• Capillaries dilate, allowing the passage of blood through the thrombus, or the fibrosed thrombus shrinks from the vascular wall, leaving a space that gets lined by endothelium.

Dystrophic calcification:

• May occur, leading to phlebolith formation.

Detachment:

• Forms aseptic emboli, causing infarcts.

Propagating thrombus:

• Occurs due to the spread of venous thrombosis.

Thrombus vs Clot

• A mass of blood elements formed in stagnant blood with a glistening smooth surface that is not adherent to the vessel wall.

Clot Types

• (1) Red or current jelly clot: Occurs with rapid blood clotting, consisting of a fibrin network entangling red and white blood cells.
• (2) Yellow or chicken fat clot: Occurs with slow blood clotting, allowing the sedimentation of cells.

Clot Sedimentation

• Red cells in the dependent part with plasma, fibrin, and white cells in anticoagulant therapy or with coagulation factor deficiencies (hemophilia).

Venous Thrombus

• More common due to slow blood flow and thin walls.

Venous Thrombus Forms

• 1. Thrombophlebitis occurs after (inflammation precedes thrombus)
• 2. Phlebothrombosis (clot in vein w/o inflammation)

Arterial Thrombus

• Less common than venous thrombosis because of high pressure

Risk Factors for Arterial Thrombosis

• Atherosclerosis
• Arteritis
• Aneurysms

Arterial Thrombus Consequences

• Ischemia -> Necrosis and Infarction

Embolism

• The process of impaction of an embolus in a blood vessel.

Embolus

• An insoluble solid mass circulating in the blood stream

Embolism Location

• Systemic arteries
• Systemic veins
• Systemic lymph vessels.

Types of Emboli

• Detached thrombi
• Tumor emboli
• Parasitic emboli
• Air emboli.
• Fat emboli.
• Clumps of bacteria.
• Amniotic fluid emboli.

Thromboembolism

• (Detached thrombi):

Thromboembolism Locations

• Pulmonary embolism: The embolus impacts pulmonary blood vessels.
• Portal embolism: The embolus comes from gastrointestinal organs and impacts in the portal veins.
• Systemic embolism: The embolus impacts any blood vessel in systemic circulation.

Paradoxical embolism

• The embolus comes through venous return to be impacted in lung instead pass from right side of the heart to left side through ventricular septal defect (VSD) and passes to systemic circulation.

Air Embolism

Air Embolism Causes

• Injury to the large neck veins.
• Air sucked by negative pressure in the thorax.
• During cardiothoracic surgery.
• In Criminal Abortions
• Caisson's disease (decompression sickness): High pressure increases gases dissolved if decompression is rapid, but nitrogen can embolize

Air Embolism Volume

• Small amount of air is harmless, but 50-100 cc interferes with cardiac contraction, causing fatal heart failure

Fat Embolism

Fat Embolism Causes

• Rare and caused by
• Bone fractures
• Crush limb injuries
• Cutaneous buns
• Inflammation of fatty tissues
• Severe fatty changes in the liver.

Amniotic Fluid Embolism

• Results from uterine contractions in the fetal membranes

Amniotic Fluid Embolism Consequences

• Causes fatal pulmonary embolism in the mother.

Emboli Effects

• Depends on size, nature and collateral

Aseptic Embolism

• Produces transient ischemia if circulation is good and infarction is poor

Septic Embolus

• Produces pyemic abscess at site of impaction

Emboli Significance

• Depends on Character, Number, and organ location.
• 1- Character of Emboli: Size: Larger causes full obstruction and no collateral
• Septic causes new site of bacteria, Neoplastic means new cells.

Emboli Locations

• Emboli in lung are less dangerous
• Kidneys are more dangerous and can lead to heart and spleen infarction.

Infarction

• Definition: Infarct is an area of coagulative necrosis (liquefactive in the brain) from sudden iscahemia of either arterial supply or venous drainage.

Rate of Occlusion

• 99% is arterial

At risk organs

• Testis and ovary

At risk vessels

• End artery: artery of poor collateral branches (Renal, retinal, cerebral, coronary....)

Symptoms and Location

Wedge Shaped:

• Shaped or pyramidal shape directed by arteries

Red infarcts include red heme:

• (hemorrhagic) occur in soft and vascular organs as lung, liver and intestine

Pale Infarcts

• More common and occur in firm and less vascular organs as kidney, heart and spleen

Liquefactive infarcts

• Spinal cord and brain

Under the Microscope of Infarction

• Early necrotic cells show post-necrotic changes. Second those details structural details are lost
• Lastly the neurotic tissue appears as granules in pink regions

Infarction Types

Kidney caused by

(a) Thrombosis (b) Emboli on left heart

Gross Kidney

• Pale kidney cortex and medulla

Microscope Kidney

• cells structural pink debris shows macrophage.

Lung tissue infarcts caused by either :

• pulmonary artery

Description

• Hemorrhagic is firm and dark red tissue that contains fibrin
• Red cells are contained in alveolar space

Brain Infarcts

Thrombrois of cerebral artery may result from embolism

• Causes a base in surface of brain tissues
• Liquefaction occurs as myelin from the tissue breaks down in 2-3 days.

###Microscopic description

• Microglia cells take up the debris, and are full of foamy structures

###Heart and Intestine

• caused by coronary branch emboli

Fate of Infarction

• Small necrotic tissues are removed
• Large Necrotic tissue forms is surrounded by a fibrous capsule and calcifies
• General reactions: fever is seen
• Transaminase indicates myocardial infarct.