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HEMODYNAMIC DISORDERS (Oedema, Hyperemia, Congestion & Hemorrhage)

Approximately 60% of lean body weight is water Two-thirds of the body water is intracellular and the remainder one-third is extracellular Most of the extracellular fluid is in the interstitial space Only about 5% of total body water is in blood plasma The normal blood volume of an adult is about 5 litre

It is the abnormal (or excess) collection of fluid in the interstitial spaces or body cavities Hydrothorax, hydropericardium and hydroperitoneum are fluid collections in the pleural, pericardial and peritoneal cavities respectively. The last one is more commonly called ascites

Oedema or fluid accumulation in the subcutaneous tissue; it is called pitting oedema as pressure with the finger-tip in the skin and soft tissue produces depression

A friction- blister of the skin is an example of trivial oedema

Marked oedema associated with inflammation of the larynx narrowing the airways; a life-threatening condition

Bilateral pleural effusion, here the fluid is serosanguinous i.e., mixed with blood

Pericardial effusion; here the effusion fluid is a purulent exudate

According to distribution, it can be generalized or localized Anasarca means severe and generalized oedema with profound subcutaneous tissue swelling Pitting oedema: when finger pressure on an oedematous skin and soft tissue produces a pit or depression due to displacement of the interstitial fluid Oedema fluid may be transudative or exudative in nature

Mechanism of oedema
The major factors that govern movement of fluid between vascular and interstitial spaces are the opposing effects of vascular hydrostatic pressure and plasma colloid osmotic pressure (C.O.P) mostly exerted by serum albumin The vascular hydrostatic pressure (H.P) tends to push fluid out of the blood vessel whereas the plasma C.O.P keeps it inside

Mechanism of oedema
Normally the H.P at the arteriolar end of capillary bed is about 32 mm of Hg and at the venous end is about 12 mm of Hg and the average plasma COP is 25 mm of Hg So there is outflow of fluid into the interstitium at the arteriolar end that is balanced by the inflow at the venous end of the microcirculation A small leftover amount of interstitial fluid is usually removed by the lymphatics

Blood pressure and colloid osmotic forces in the normal microcirculation; red arrow indicates the blood pressure ( about 32 mm of Hg at the arterolar end and 12 mm of hg at the venous end) & green arrow the colloid osmotic force (average 25 mm of Hg in the capillary bed)

So, either increased capillary pressure or decreased colloid osmotic pressure can result in increased interstitial fluid i.e., oedema As the interstitial fluid pressure increases, tissue lymphatics remove much of the volume ultimately returning it to the circulation If the ability of the lymphatics to drain tissue is exceeded, persistent tissue oedema results

In inflammation increased vascular hydrostatic pressure and reduced plasma colloid osmotic pressure in the microcirculation results in oedema

Pathophysiologic categories of oedema

Increased Hydrostatic Pressure Impaired venous return Congestive heart failure Constrictive pericarditis Ascites in liver cirrhosis Venous obstruction or compression in * Thrombosis * External pressure (e.g., mass) * Lower extremity inactivity Arteriolar dilation Heat Neurohumoral dysregulation

Reduced Plasma Osmotic Pressure (Hypoproteinemia) Protein-losing glomerulopathies (Nephrotic syndrome) Liver cirrhosis (Ascites) Malnutrition (Kwashiorkor) Protein-losing gastroenteropathy Lymphatic Obstruction Inflammatory Neoplastic Postsurgical Postirradiation

Sodium Retention Excessive salt intake with renal insufficiency Increased tubular reabsorption of sodium in Renal hypoperfusion Increased renin-angiotensin-aldosterone secretion Inflammation Acute inflammation Chronic inflammation Angiogenesis

Increased hydrostatic pressure

Local increase in hydrostatic pressure may result from impaired venous outflow such as deep vein thrombosis in the leg leads to oedema restricted to the leg Generalized increase in venous pressure with systemic oedema occurs most commonly in congestive heart failure affecting the right ventricular function. The mechanism of oedema in heart failure is quite complex

Events leading to oedema in heart failure, or with qed plasma osmotic pressure, as in nephrotic syndrome. ADH, antidiuretic hormone; GFR, glomerular filtration rate

Oedema in heart failure

In congestive heart failure the cardiac output is reduced as the heart cannot pump effectively So blood supply to the kidney is reduced This renal hypoperfusion triggers the reninangiotensin-aldosterone axis inducing sodium and water retention by the kidneys ( secondary aldosteronism). This process is designed to raise the intravascular volume and thereby improve cardiac output

Oedema in heart failure

If the failing heart cannot o the output, the extra fluid load results only in oed venous pressure and eventually oedema If the cardiac output is not restored or the renal water retention is not reduced ( e.g., by salt restriction, diuretics or aldosterone antagonists), a cycle of renal fluid retention and worsening oedema results

Reduced Plasma Osmotic Pressure

Albumin is the serum protein most responsible for maintaining colloid osmotic pressure. Reduced plasma osmotic pressure can result from either excessive loss or reduced synthesis of albumin. Nephrotic syndrome is an important cause of albumin loss due to leaky glomerular capillary wall and produces generalized oedema Reduced albumin synthesis occurs in diffuse liver pathology (e.g., cirrhosis) or in protein energy malnutrition

Reduced Plasma Osmotic Pressure

Reduced plasma osmotic pressure leads to a net movement of fluid into the interstitial tissues and a plasma volume contraction With qed intravascular volume, renal hypoperfusion with secondary aldosteronism follows. With persistence of the primary defect of low serum proteins, the retained salt and water can not correct the plasma volume deficit So oedema precipitated by hypoproteinemia is exacerbated by secondary salt and fluid retention

Lymphatic Obstruction
Usually produces localized oedema Can result from inflammatory or neoplastic obstruction.The parasitic infection filariasis causes massive lymphatic and lymph node fibrosis of the inguinal region. The resulting extreme oedema of the external genitalia and the lower limbs is called elephantiasis Involvement of the axillary lymph nodes by breast cancer, or by scarring following their surgical removal or radiation therapy may cause severe oedema of the arm

Sodium and Water Retention

In addition to contributing in several forms of oedema, may also act as a primary cause Increased salt, with the obligate accompanying water, causes bothoed hydrostatic pressure and qed vascular colloid osmotic pressure leading to oedema Salt retention may occur with any acute reduction of renal function, including post streptococcal glomerulonephritis and acute renal failure

Morphology of oedema
Most easily recognized grossly Microscopically oedema fluid manifests as subtle cell swelling,with clearing and separation of the extracellular matrix elements Most commonly seen in subcutaneous tissues, affected area pits on pressure Subcutaneous oedema may be diffuse, or may be more prominent at the site of highest hydrostatic pressures typically influenced by the gravity and is called dependent oedema

Dependent oedema ( is evident in the legs when standing, over the sacrum when recumbent) is a prominent feature of congestive heart failure particularly of the right ventricle Oedema of renal cause is usually more severe than cardiac oedema and is generalized in distribution but initially may manifest in the face around the eyelids as periorbital oedema

Pulmonary oedema is commonly seen in left ventricular failure, also in renal failure, adult respiratory distress syndrome, pulmonary infections and hypersensitivity reactions. The lungs are heavy, 2 to 3 times their normal weight and sectioning reveals frothy blood-tinged fluid composed of air, oedema fluid and extravasated red blood cells

Oedema of the brain may be localized to sites of injury like in abscess, neoplasm or may be generalized as in encephalitis, hypertensive crisis, or obstruction to the brains venous outflow. Trauma may cause generalized or local oedema. With generalized oedema, the brain is grossly swollen with narrowed sulci and distended gyri showing signs of flattening against the unyielding skull

Clinical importance of oedema

Is variable Subcutaneous oedema in cardiac and renal failure is important primarily for the underlying disease; but when significant, it impairs wound healing Pulmonary oedema can cause death by interfering with normal ventilation. Not only the oedema fluid impedes oxygen diffusion, but also favours bacterial infection Brain oedema is serious and can be rapidly fatal; both herniation of the brain through the foramen magnum or compressed brain stem vascular supply can injure the medullary centers and cause death

Swelling of brain due to oedema

Tonsillar herniation of cerebellum due to oedema

A local increased volume of blood in a particular tissue It is an active process resulting from increased tissue inflow because of arteriolar dilation, as in skeletal muscle during exercise, or at sites of inflammation The affected tissue is redder because of engorgement with oxygenated blood Morphology: Cut surfaces of the hyperemic tissue are hemorrhagic and wet

A local increased volume of blood in a particular tissue Is a passive process resulting from impaired outflow from a tissue May be systemic, as in cardiac failure, or may be local, as in isolated venous obstruction The tissue has a blue-red color (cyanosis) due to accumulation of deoxygenated blood

Congestion of capillary beds is closely related to the development of oedema, so congestion and oedema commonly occur together In long-standing congestion, the tissue becomes hypoxic due to poorly oxygenated blood which can result in parenchymal cell degeneration or death Capillary rupture at these sites may cause small foci of hemorrhage; breakdown and phagocytosis of red cell debris may result in small clusters of hemosiderin laden macrophages ( heart failure cells)

Chronic pulmonary congestion is seen in long-standing heart failure Chronic passive congestion of liver is seen in right heart failure

It means extravasation of blood due to vessel rupture Rupture of a large vessel is due to trauma, atherosclerosis, inflammatory or neoplastic erosion of the vessel wall The hemorrhagic lesions are named as follows * Hematoma: collection of hemorrhagic fluid within a tissue. May be relatively insignificant (as in bruise) or fatal causing death ( e.g., a massive retroperitoneal hematoma from ruptured aortic aneurysm)

Petechiae: minute 1 to 2 mm hemorrhages into skin, mucous membranes or serosal surfaces. Are found in locally raised intravascular pressure, low platelet count, defective platelet function, or clotting factor deficit Purpura: slightly larger ( 3 mm) hemorrhages than petechiae, may have same pathology and also trauma, vasculitis, or oed vascular fragility

Ecchymoses: larger (> 1 to 2 cm) subcutaneous hematomas, typical after trauma; undergoes progressive color changes from red-blue (hemoglobin) to blue-green (bilirubin) to gold-brown (hemosiderin) Hemothorax, hemopericardium, hemoperitoneum and hemarthrosis: are large collections of blood in one or another of the body cavities

A hematoma under the nail of great toe

Petechial hemorrhage on the epicardium of heart

Blotchy hemorrhages in the skin (ecchymosis)

Clinical importance
It depends on the volume, rate and site of blood loss Volume: rapid removal of upto 20% of the blood volume or slow loss of even larger amount may have little impact; but greater losses may produce hypovolemic shock Site: bleeding that is trivial in subcutaneous tissue may cause death if located in brain Rate: chronic or recurrent external blood loss causes iron deficiency anemia whereas internal bleeding may give rise to jaundice


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