Hemodynamic disorders part 2

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NON INFLAMMATORY CAUSES OF  EDEMA:

1) Increased hydrostatic pressure:

Ø Local increase in the intravenous pressure can result from impaired venous return.

Ø Generalized increase in this pressure can occur in congestive heart failure

Ø Because secondary hyperaldosteronism (retention of sodium and water) is a common feature of generalized edema.

Ø salt restriction, diuretics, and aldosterone antagonists are also of value in managing generalized edema resulting from other causes.

2)Reduced plasma oncotic pressure:

Ø Under normal conditions plasma osmotic pressure is mainly formed by albumin as it forms about half of the plasma proteins.

Ø Therefore in such conditions in which the albumin is either lost from circulation or produced in an inadequate amount will lead to a decrease in the osmotic pressure.

Ø Just like congestive heart failure the nephritic syndrome can also cause the generalized edema

Ø In nephritic syndrome damaged glomerular capillaries become leaky, leading to the loss of albumin (and other plasma proteins) in the urine and the development of generalized edema

Ø Reduced albumin synthesis occurs in the setting of severe liver
disease(e.g., cirrhosis)

Ø Regardless of cause, low albumin levels lead in a stepwise fashion to edema like

·      Reduced intravascular volume (due to reduced oncotic pressure).

·      Renal hypo perfusion (low blood supply to the kidney) and

·      Secondary hyperaldosteronism (increased water and NA retention).

Ø That is why nephritic syndrome or decreased albumin level will not only correct the plasma deficit but also can promote edema

 

3) Lymphatic obstruction:

Ø Impaired lymphatic drainage and consequent lymphedema usually result from a localized obstruction caused by an inflammatory or neoplastic condition

Ø For example, the parasitic infection filariasis can cause massive edema of the lower extremity and external genitalia (so-called elephantiasis) by engendering inguinal lymphatic and lymph node fibrosis.

Ø Infiltration and obstruction of superficial lymphatics by breast cancer may cause edema of the overlying skin, the characteristic finely pitted appearance of the skin of the affected breast is called peau d’orange (orange peel).

Ø One relatively common setting for this clinical entity is in women with breast cancer who undergo axillary lymph node resection and/or irradiation, both of which can disrupt and obstruct lymphatic drainage, resulting in severe lymphedema of the arm.

4) sodium and water retention:

Ø Excessive retention of salt (and its obligate associated water) can lead to edema by increasing hydrostatic pressure (due to expansion of the intravascular volume) and reducing plasma osmotic pressure.

Ø excessive salt and water retention are seen in a wide variety of diseases that compromise renal function, including post-streptococcal glomerulonephritis and acute renal failure

·     Diseases that cause edema

Diseases	Edema
Renal failure/nephrotic syndrome	Generalized
Congestive heart diseases	Generalized
superficial lymphatics by breast	Pitted with an orange appearance on the skin
Axillary lymph node resection	severe lymphedema of the arm.
parasitic infection filariasis	Severe edema of the lower extremity and external genitalia (so-called elephantiasis)
glomerulonephritis and acute renal failure	Generalized

Morphology of edema:

Ø Although any tissue can be involved, edema most commonly is encountered in subcutaneous tissues, lungs, and brain

Ø Subcutaneous edema can be diffuse but usually accumulates preferentially in parts of the body positioned the most significant distance below the heart where hydrostatic pressures are highest.

Ø edema typically is most pronounced in the legs with standing and the sacrum with recumbency, a relationship termed dependent edema

Ø Edema due to renal dysfunction or nephrotic syndrome often manifests first in loose connective tissues (e.g., the eyelids, causing periorbital edema).

Ø pulmonary edema, the lungs often are two to three times their average weight, and sectioning reveals frothy, sometimes blood-tinged fluid consisting of a mixture of air, edema fluid, and extravasated red cells

Ø Brain edema
can be localized (e.g., due to abscess or tumor) or generalized, depending on the nature and extent of the pathologic process or injury. With generalized edema, the sulci are narrowed while the gyri are swollen and flattened against the skull.

Edema may be caused by

Ø increased hydrostatic pressure (e.g., heart failure)

Ø increased vascular permeability (e.g., inflammation)

Ø decreased colloid osmotic pressure, due to reduced
plasma albumin

·      decreased synthesis (e.g., liver disease, protein
malnutrition)

·      increased loss (e.g., nephrotic syndrome)

Ø lymphatic obstruction (e.g., inflammation or neoplasia)

Ø sodium retention (e.g., renal failure)

Hemorrhage

Ø Hemorrhage, defined as the extravasation of blood from vessels, occurs in a variety of conditions

Ø Hemorrhage may be manifested by different appearances and clinical consequences

Ø Hemorrhage may be external or accumulate within tissue as a hematoma, which ranges in significance from trivial (e.g., a bruise) to fatal (e.g., a massive retroperitoneal hematoma resulting from rupture of a dissecting aortic aneurysm)

Ø Large bleeds into body cavities are given various names according to location—hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis (in joints).

Ø Extensive hemorrhages can occasionally result in jaundice from the massive breakdown of red cells and hemoglobin.

Some types of hemorrhage:

1) Petechiae are minute (1 to 2 mm in diameter) hemorrhages

Ø Occurs in the skin, mucous membranes, or serosal surfaces

Ø causes include low platelet counts (thrombocytopenia), defective platelet function, and loss of vascular wall support, as in vitamin C deficiency

Ø they are red, pink, or purple

2) Purpura are slightly larger (3 to 5 mm) hemorrhages.

Ø Purpura can result from the same disorders that cause petechiae, as well as trauma, vascular inflammation (vasculitis), and increased vascular fragility.

Ø They are red-purple or brown in color.

 

3) Ecchymoses are larger (1 to 2 cm) subcutaneous hematomas (colloquially called bruises).

Ø Caused when Extravasated red cells are phagocytosed and degraded by macrophages.

Ø  the characteristic color changes of a bruise are due to the enzymatic conversion of hemoglobin (red­-blue color) to bilirubin (blue-green color) and eventually hemosiderin(golden-brown).

 

§  Dependency of hemorrhage on blood volume, rate, and site of hemorrhage

Ø The clinical significance of any particular hemorrhage
depends on the volume of blood loss and the rate of bleeding. Rapid loss of up to 20% of the blood volume, or slow losses of even larger amounts, may have little impact on healthy adults.

Ø greater losses, however, can cause hemorrhagic (hypovolemic) shock

Ø The site of hemorrhage also is important; bleeding that would be trivial in the subcutaneous tissues can cause death if located in the brain

Ø chronic or recurrent external
blood loss (e.g., due to peptic ulcer or menstrual bleeding)
frequently culminates in iron deficiency anemia as a consequence of loss of iron in hemoglobin

Ø iron is efficiently recycled from phagocytosed red cells, so internal bleeding (e.g., a hematoma) does not lead to iron
deficiency.

Embolism 

Ø An embolus is an intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

Ø The vast majority of emboli derive from a dislodged
thrombus—hence the term thromboembolism

Ø Less common types of emboli include fat droplets, bubbles of air or nitrogen, atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow, and  amniotic fluid

Ø depending on the site of origin, emboli can lodge anywhere in the vascular tree.

Ø The primary consequence of systemic embolization is ischemic necrosis (infarction) of downstream tissues, while embolization in the pulmonary circulation leads to hypoxia, hypotension, and right-sided heart failure.

 

Pulmonary thromboembolism:

Ø The incidence of pulmonary embolism is 2 to 4 per 1000 hospitalized patients.

Ø Although the rate of fatal pulmonary embolus (PE) has declined from 6% to 2% over the last quarter-century.

Ø  pulmonary embolism still causes about 200,000 deaths per year in the United States.

Ø In greater than 95% of cases, venous emboli originate from thrombi within deep leg veins proximal to the popliteal fossa; embolization from lower leg thrombi is uncommon.

Ø Fragmented thrombi from DVTs are carried through
progressively larger channels and usually pass through the
right side of the heart before arresting in the pulmonary vasculature.

Ø Depending on size, a PE can occlude the main pulmonary artery, lodge at the bifurcation of the right and left pulmonary arteries (saddle embolus), or pass into the smaller, branching arterioles

Ø Frequently, multiple emboli occur, either sequentially or as a shower of smaller emboli from a single large thrombus

Ø  a patient who has had one pulmonary embolus is at increased risk for having more.

Ø Rarely, does an embolus passes through an atrial or ventricular defect and enter the systemic circulation (paradoxical embolism).

Clinical and pathological features of PE:

Ø Most pulmonary emboli (60% to 80%) are small and clinically silent.

Ø a large embolus that blocks a major pulmonary artery can cause sudden death

Ø Embolic obstruction of medium-sized arteries and subsequent rupture of capillaries rendered anoxic can cause pulmonary hemorrhage

Ø Such embolization does not usually cause pulmonary infarction since the area also receives blood through an intact bronchial circulation (dual circulation).

Ø However, a similar embolus in the setting of left-sided cardiac failure (and diminished bronchial artery perfusion) can lead to a pulmonary infarct

Ø Embolism to small end-arteriolar pulmonary branches
usually causes infarction.

Ø Multiple emboli occurring over time can cause pulmonary hypertension and right ventricular failure (cor pulmonale)

 

Systemic thromboembolism:

Ø Most systemic emboli (80%) arise from intracardiac mural
thrombi; two-thirds are associated with left ventricular
infarcts and another 25% with dilated left atria (e.g.,
secondary to mitral valve disease). The remainder originate from aortic aneurysms, thrombi overlying ulcerated
atherosclerotic plaques, fragmented valvular vegetations
or the venous system (paradoxical emboli); 10% to 15% of systemic emboli are of unknown origin

Ø By contrast venous emboli, which lodge primarily
in the lung, arterial emboli can travel virtually anywhere;
their final resting place understandably depends on their
point of origin and the relative flow rates of blood to the
downstream tissues. Common arteriolar embolization sites include the lower extremities (75%) and central nervous system (10%) intestines, kidneys, and spleen are less common targets

Ø The consequences of embolization depend
on the

·      caliber of the occluded vessel

·      the collateral supply, and

·      the affected tissue’s vulnerability to anoxia

Ø arterial emboli often lodge in end arteries and cause infarction.

Fat emboli:

Ø Soft tissue crush injury or rupture of marrow vascular sinusoids (long bone fracture) releases microscopic fat globules into the circulation.

Ø Fat and marrow emboli are common incidental findings after vigorous cardiopulmonary resuscitation but probably are of little clinical consequence.

Ø although fat and marrow embolism occurs in some
90% of individuals with severe skeletal injuries, less than 10% show any clinical findings

Ø However, a minority of patients develop a symptomatic fat embolism syndrome characterized by pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, and a diffuse petechial rash, which is fatal in 10% of cases

Ø Clinical signs and symptoms appear 1 to 3 days after the injury as the sudden onset of tachypnea, dyspnea, tachycardia, irritability, and restlessness, which can progress rapidly to delirium or coma

 

Amniotic fluid embolism:

Ø Amniotic fluid embolism is an uncommon, grave complication of labor and the immediate postpartum period (1 in 40,000 deliveries).

Ø The mortality rate approaches 80%, making it the most common cause of maternal death in the developed world

Ø Onset is characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma if the patient stands with initial symptoms then it causes pulmonary edema

Ø The underlying cause is the entry of amniotic fluid (and its contents) into the maternal circulation via tears in the placental membranes and/or uterine vein rupture

Gas embolism:

Ø Gas bubbles within the circulation can coalesce and obstruct vascular flow and cause distal ischemic injury.

Ø Thus, a small volume of air trapped in a coronary artery during bypass surgery or introduced into the cerebral arterial circulation by neurosurgery performed in an upright “sitting position” can occlude flow.

Ø Small venous gas emboli generally have no deleterious effects, but sufficient air can enter the pulmonary circulation inadvertently during obstetric procedures or as a consequence of a chest wall injury to cause hypoxia, and very large venous emboli may arrest in the heart and cause death

Ø A particular form of gas embolism called decompression
sickness is caused by sudden changes in atmospheric pressure.

Ø Thus, scuba divers, underwater construction workers,
and persons in unpressurized aircraft who undergo rapid
ascent is at risk. When air is breathed at high pressure
(e.g., during a deep-sea dive), increased amounts of gas
(particularly nitrogen) become dissolved in the blood and
tissues. If the diver then ascends (depressurizes) too
rapidly, the nitrogen expands in the tissues, and bubbles
out of solution in the blood to form gas emboli, which
cause tissue ischemia.

Ø Gas bubbles in the pulmonary vasculature cause edema, hemorrhages, focal atelectasis, or emphysema, leading to respiratory distress, the so-called chokes.

Ø A more chronic form of decompression sickness is called caisson disease (named for pressurized underwater vessels used during bridge construction) in which recurrent or persistent gas emboli in the bones lead to multifocal ischemic necrosis; the heads of the femurs, tibiae, and humeri are most commonly affected.

 

Infarction:

Ø An infarct is an area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue; the process by which such lesions form is termed infarction

Ø Infarction extremely important cause of clinical illness

Ø Roughly 40% of all deaths in the United States are a consequence of cardiovascular disease, with most of these deaths stemming from myocardial or cerebral infarction.

Ø Pulmonary infarction is a common clinical complication, bowel infarction often is fatal, and ischemic necrosis of distal extremities
(gangrene) causes substantial morbidity in the diabetic
population.

 

Factors affecting the infraction:

1)Anatomy of the vascular supply

2)Rate of occlusion

3)Tissue vulnerability to ischemia

4)Hypoxemia.

 

Ø  Arterial blockage can cause the infarction but it depends if there is a dual blood supply then infarction cant be occurs like bronchial artery

Ø But if there is a single blood supply like a kidney then there is infarction occurs.

Ø Slowly developing occlusions are less likely to cause infarction because they allow time for the development of collateral blood supplies

Ø Less the time of occlusion less will be an infraction

Ø Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes. Myocardial cells, although hardier than neurons, still die after only 20 to 30 minutes of ischemia. By contrast, fibroblasts within the myocardium remain viable after many hours of ischemia.

Ø Understandably, abnormally low blood O2 content (regardless of cause) increases both the likelihood & extent of infarction