Haemodynamic Disorders: Edema

Haemodynamic Disorders

Edema

• Abnormal accumulation of fluid in interstitial tissue and serous membranes.
• Mechanisms include increased hydrostatic pressure, sodium/water retention, vascular permeability, reduced oncotic pressure, and lymphatic obstruction.
• Increased hydrostatic pressure can be localized due to venous obstruction, or generalized in cases of right-sided heart failure.
• Sodium and water retention is caused by aldosterone in right-sided heart failure.
• Increased vascular permeability is caused by endothelial injury from inflammation, chemical or physical agents, and endothelial contraction.
• Lymphatic obstruction can be congenital, inflammatory, fibrotic, caused by tumors, from compression, or surgical removal.
• Types of edema are classified by fluid distribution (generalized or localized) and fluid nature (water only or water + proteins).
• Generalized edema can be cardiac, renal, or nutritional.
• Localized edema can be inflammatory, venous obstruction, or lymphatic obstruction.
• Generalized renal edema is due to proteinuria while generalized cardiac edema is related to right-sided heart failure.
• Localized inflammatory edema fluids are called exudates.
• Localized obstructive edema is caused by thrombosis or embolism.
• Liver cirrhosis and fibrosis lead to edema in splanchnic areas and ascites.
• Nephrotic edema is due to proteinuria.
• Nephritic edema involves increased aldosterone production and inflammation in capillaries due to immune complex deposition.

Hemorrhage

• Escape of blood outside blood vessels and the heart
• Bleeding can be external or internal.
• External examples include epistaxis and hematuria.
• Internal examples include hemoperitoneum and haemopericardium (cardiac tamponade).
• Interstitial examples include ecchymosis, petechiae, and hematoma.
• Small hemorrhages have no effect.
• Small repeated hemorrhages lead to anemia.
• Large hemorrhages can result in shock.

Shock

• Inadequate tissue perfusion.
• Cardiogenic shock stems from ruptured valves, arrhythmias, or tamponade.
• Septic shock results from severe "ENDOTOXIC" infection.
• Hypovolemic shock is caused by hemorrhage, burns, or dehydration.
• Anaphylactic shock stems from immune-mediated and allergic reactions.
• Neurogenic shock involves loss of vascular tone.
• Hypovolemic shock involves a reduction in effective circulating blood volume.
• Reduced blood volume decreases venous return and cardiac output.
• Reduced cardiac output causes hypoxia.
• Hypoxia leads to vasodilatation then blood pools in peripheral circulation.
• Vasodilation is followed by venous return reduction.
• Septic shock involves the release of toxins.
• Toxins lead to vasodilatation, pooling of blood in peripheral circulation, and endothelial cell damage.
• Endothelial cell damage causes DIC (disseminated intravascular coagulopathy).
• Necrosis of vital organs occurs.

Thrombosis

• Formation of a thrombus (solid mass of blood elements) inside the cardiovascular system during life
• Is caused by Virchow's Triad: endothelial injury, abnormal blood flow, and hypercoagulability.
• Degenerative causes of endothelial injury are atherosclerosis, myocardial infarction, and aneurysm.
• Mechanical causes are trauma, ligature, and pressure.
• Inflammatory causes are Arteritis, phlepitis, and endocarditis
• Turbulence in blood flow results from aneurysms, varicose veins, atheroma, or compression.
• Stasis (slow blood flow) develops in leg veins due to heart failure, in the auricle in valve diseases, and in the portal area in liver cirrhosis.
• Turbulent blood flow disrupts laminar flow
• Stasis leads to activation of blood coagulation factors
• Hypercoagulability can be due to increased platelets, RBCs, WBCs, or fibrinogen.
• Primary hypercoagulable states are inherited and secondary states are acquired
• Examples of Thrombosis
  • Factor V Leiden
  • Prothrombin gene mutation
  • Protein C & S deficiency
  • Antithrombin III deficiency
• Examples of SECONDARY Hypercoagulable States:
  • Cancer
  • Smoking
  • Obesity
  • Pregnancy
  • Major trauma/surgery
  • Prolonged immobilization

Types of Thrombi

• Platelet thrombi are made only of platelets, are weak, and pale
• Platelet Thrombi can be washed away by blood flow
• Mixed thrombi are made of platelet, fibrin network, RBCs, and WBCs.
• Mixed Thrombi are larger and more stable
• Propagating thrombi spread inside the blood vessel until it reaches an area of normal blood flow where it stops
• Types of thrombi are classified by size, color, site and presence of infection
• Thrombi are located at 1- cardiac; 2-Arterial; 3- Venous; 4- Or Capillaries
• Venous thrombosis is classified as thrombophlebitis (inflamed vein) or phlebothrombosis (non-inflamed vein).
• Inflammation cause endothelial injury in thrombophlebitis
• Stasis and hypercoagulability are causes in phlebothrombosis
• Types (Sites)
  • Septic: in case of appendicitis
  • Aseptic: due to irradiation

Describing a Thrombus

• Consist of occluding the lumen by a mass of adherent to the vessel wall.
• Shows pale areas :fused platelets and fibrin perpendicular to wall of blood vessel (lines of Zahn)
• Alternating with dark red areas: entangled red blood cells and WBCs.

Fate of the Thrombi

• Aseptic thrombi can undergo fibrinolysis, fragmentation, resolution, embolization, organization, recanalization, incorporation into the vessel wall, or calcification.
• Septic thrombi undergo fragmentation, resulting in septic emboli and multiple pyemic abscesses in the circulation.
• Clotting is the transformation of fibrinogen into fibrin.
• Outside the CVS, clotting leads to hemorrhage.
• Inside the CVS, clotting occurs during life in thrombosis and propagating thrombus and after death.

Thrombus vs Clot

• Thrombus occurs during life inside the CVS, while a clot forms postmortem or outside the body.
• Thrombi develop in flowing blood, while clots form in stagnant blood.
• Thrombi are adherent to the vessel wall, while clots are not adherent.
• Thrombi are firm and friable, while clots are soft and gelatinous.
• Thrombi are pale or red with pale strands, while clots are red with no pale strands.

Embolism

• Is impaction of the embolus in a blood vessel .
• An embolus is a detached intravascular solid, liquid, or gaseous mass that circulates and becomes impacted in a blood vessel.
• Detached thrombi (thrombo-embolism)
• Types of emboli are:
  • Air
  • Parasite
  • Fat
  • Tumor
  • Amniotic fluid
• Fat emboli: The fat of the bone marrow reaches the circulation after fracture of bones.
• Air embolism: results from injury of neck & chest veins.
• Parasitic emboli: Examples are bilharzial worms and ova.
• Tumor emboli: groups of tumour cells penetrate the wall of blood vessels especially veins.
• Amniotic fluid embolism can happen during labor

Effects of Emboli:

• Depends on
• Collateral vascular supply of the affected tissue
• The vulnerability of the tissue to ischemia
• Calibre of occluded vessel
• Aseptic emboli leads to Good collaterals
• Septic emboli lead to multiple pyemic accesses

Ischemia

• Cut of arterial blood supply
• In Acute ischemia there is sudden and complete blood supply cut off
• In Chronic ischemia there is Gradual and incomplete blood supply cut off
• Acute Causes are:
  • Thrombus
  • Embolus
  • Surgical ligature
  • Ergot poisoning leading to arterial spasm (vasoconstriction)
  • Twisting of vessels as in ovary and testis.
  • Frost bite: occlusion of capillaries and arterioles in severe cold due to spasm
• Chronic causes
  • Atherosclerosis
  • Compression from outside by enlarged lymph node, gravid uterus or tumors.
• Ischemia effects depend on:
  • Type of ischemia: acute or chronic
  • Degree of organ vascularity regarding number of arterial blood supply and efficiency of collaterals
  • Vulnerability of tissue to hypoxia
• Effects on oxygen concentrarion in blood
• Good collaterals show Degeneration of tissue (small number of cells)
• Bad collaterals cause Necrosis.

Infarction

• Area of coagulative necrosis due to acute ischemia.
• Greish White Triangular shape
• CNS Infarction→ Liquefactive necrosis
• Pale infarction: Grayish white Triangular shape
• Red infarction: Red Areas & Hemorrhage
• Microscopic appearance:
  • Ghosts of cells and stroma
  • Preserved outlines and architecture
  • Pale pink tissue, absent nuclei
  • May seen hemorrhage

Gangrene

• Defined as massive tissue necrosis followed by putrefaction.
• Necrosis is caused by ischemia and toxins
• Putrefaction is caused by saprophytic bacteria.
• Putrifaction involves The breakdown of proteins of necrotic tissue by saprophytic organism
• Hydrogen sulphide
• Iron of Hb with iron sulphide causes Black colouration
• Gangrene types: DRY, WET & GAS.

DRY Gangrene

• Involves the gradual occlusion of arterial blood supply
• Occurs in exposed organs
• Tissue fluid drained via opened lymphatics & veins and evaporation So tissue appears dry and mummified
• Gangrene step by step process:
  • The affected part becomes pale, numb, cold & painful
  • Necrosis starts, it becomes red: RBCs hemolysis & blood pigment diffusion
  • Saprophytic bacteria start putrefaction of necrotic tissue
  • The gangrenous part irritates the living one with inflammation and endothelial cell injury
• The gangrene spreads until it reaches a zone of good collateral circulation with the endothelial cell
  • At the site of gangrene stoppage is an inflammatory zone between healthy & gangrenous part
  • The formation of granulation tissue forms from the healthy part to create Line of separation with a conical stump.

WET Gangrene

• Involves edema & congestion
• Arterial occlusion leads to necrosis followed by putrefaction of necrotic tissue by saprophytic bacteria
• Involves a Sudden arterial & venous occlusion in the internal organs
• In moistened gangrene the saprophytic bacteria begin to invade fast
• Gangrene here speeds rapidly causing demarcations and toxemia

INFECTIVE Gangrene

• It is a subtype of gangrene with bacteria cause tissue necrosis and putrefaction
• Affects bed sores and gas gangrene
• Is known as Clostridium caused by anaerobic bacteria
• In 𝑑𝑒𝑒𝑝 𝑤𝑜𝑢𝑛𝑑𝑠 with anaerobic spores.
• Ischemia promotes germination
• It has different gases as hydrogen sulphide, hydrogen & carbon dioxide