TA Reviews

Fluid and Shock

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M2

Pathology

TA Reviews

Fluid Disturbances and Shock

Jill Conway, 8/28/00

Water is 50-60% of total body weight, about 42 L.  2/3 of this is intracellular, 1/3 extracellular.  Extracellular fluid remains mostly in interstitial fluid, with 3.5-4L of total plasma volume.  About 65% of total blood volume is in the venous system.

Normal Tissue

Fluid balances are maintained in the microcirculation via hydrostatic and colloid osmotic (oncotic) pressures.  In the arteriole, plasma osmotic pressure is greater than the interstitial space, but the difference in hydrostatic pressure is greater, leading to net outflow of fluid.  Capillary forces are balanced.  Venules have much higher osmotic forces than the interstitial space and also relatively smaller hydrostatic forces, so net flow of fluid goes into the venule.  Small net accumulation of fluid in the interstitium should be absorbed by the lymphatic system. 

Edema means accumulation of excess fluid in interstitial tissues.  Essentially only four possible mechanisms of cause:

  1. increased hydrostatic pressure in vessels
    • includes sodium and water retention
  2. increased vascular permeability
  3. decreased plasma osmotic pressure
  4. decreased lymphatic effectiveness

Edema has specific terms depending on which body cavity or process is involved:

Anasarca = severe generalized edema

Hydrothorax, hydropericardium refers to accumulations in those cavities.

Hydroperitoneum is usually called ascites.

Subcutaneous edema designates generalized accumulation of fluid in subcutaneous space, usually from increased hydrostatic pressure.

Pulmonary edema = accumulation of fluid in the alveoli, usually as a consequence of left heart failure.

Edema fluid can be a transudate or an exudate depending on the source and content.  Transudates occur mostly from increased hydrostatic pressure squeezing thin, watery fluid out of the vascular bed (SG <1.012).

Exudates result from inflammatory processes leading to increased permeability leading to protein rich fluid with a specific gravity of over 1.020.

Increased Hydrostatic Pressure: CHF is typical.  Reduced CO leads to reduced effective renal perfusion.  This activates both the renin-angiotensin system and leads to increased secretion of aldosterone.  Both of these encourage retention of sodium and water in the kidney.  Increased fluid retention further stresses an already failing heart which cannot handle the overload.  Fluid leaks into interstitial space as a transudate from increased vessel hydrostatic pressure. Note that Na+ and water retention (from any cause) results in both increased hydrostatic pressure and decreased colloid osmotic pressure.  Typical sign:  dependent edema, sacral on lying and lower extremity on standing.  Left sided heart failure leads to lung congestion and pulmonary edema.  Right sided heart failure leads to generalized subcutaneous edema, dependent edema.                                                                

Reduced Plasma Osmotic Pressure:  the main source of colloid pressure is albumin which is produced by the liver.  Decreased albumin comes from loss of liver function and decreased production or through loss due to kidney abnormalities leading to leaky glomeruli capillaries.  Reduced plasma pressure from proteins results in a net loss of fluid from the vasculature.  Tends to be all over the body and pitting.

Lymphatic obstruction:  failure of the lymph system to remove excess fluid from the interstitium may occur with impaired drainage, filariasis, lymph node removal.  Edema from lymphatic obstruction is called lymphedema.  Primary lymphedema stems from congenital defects, often hypoplasia.  Secondary lymphedema may be caused by infectious obstruction (filariasis) or trauma, surgical resection, malignant obstruction, etc.  Initially, lymphedema tends to be a transudate and cause pitting edema, but becomes more proteinaceous over time and usually fibrotic (brawny edema).  Superimposed infections are common.

Hyperemia = excess amount of blood in an organ.  Hyperemia usually refers to increased local blood volume from an active process such as dilation of vessels in response to demand.  Some texts equate congestion with “passive hyperemia.”  Active hyperemia occurs in inflammation, during use of skeltal muscles, and in the skin as blushing and/or increased dissipation of heat. Reactive hyperemia refers to restoration of blood flow after ischemia.

Congestion = increased local fluid from a passive process of failure of outflow from a tissue such as venous obstruction.  Acute passive congestion most often arises from LV failure and subsequent congestion in the lungs.  Other examples include local obstruction from venous blockage.   

Consequences of congestion in the lung include increased alveolar pressure which leads to:

  1. Hemorrhages of RBCs into the alveoli, where macrophages digest the hemoglobin into hemosiderin.  Hemosiderin laden macrophages are called “heart failure cells.”
  2. Increased pressure in the alveoli forms pulmonary edema that diminishes gas exchange.
  3. 3)  Increased lung pressure and other sequelae of heart failure stimulates fibrosis in the lung, sometimes called “brown induration.”
  4. 4)  Increased capillary pressure leads to increased arterial pressure in the lungs causing pulmonary hypertension.

The liver becomes dilated from increased venous pressure in the central veins and hemorrhage can occur.  The centrilobular areas are the most poorly perfused in the liver and if congestion compromises arterial flow, centrilobular necrosis may occur.  The liver appears as darker centrilobular areas mixed with lighter staining peripheral areas, termed “nutmeg liver.”  The spleen will enlarge and become engorged with blood if the liver becomes congested.

Congestion commonly occurs with dependent edema and potentially ascites as well.

HEMORRHAGE:  blood leaving blood vessels due to rupture of endothelium.  Small hemorrhages often stem from bleeding diatheses.  The capillary system has very fragile vessel walls which are disrupted following normal blood flow; this requires the coagulation system to be intact in order to avoid hemorrhage.  Failure of the coagulation system (factor VIII deficiency in hemophilia or many other disorders) can lead to spontaneous hemorrhages without any apparent cause.  Large vessel hemorrhage most often has a traumatic cause.

Hematoma = accumulation of hemorrhage within a tissue.  Outcome depends on the size and location of the hematoma.

Petechiae = 1-2 mm hemorrhage.  Pinpoint siaze, often on the skin or conjunctiva from rupture of capillary or arteriole.  Associated with vasculidities.

Purpura = >3 mm hemorrhages, usually in the skin.

Ecchymoses = >1 cm hemorrhages superficially located, i.e., a “bruise”

Clinical significance of hemorrhage depends on location, extent, and duration.  Small focal brain hemorrhages may be very significant.  Ongoing hemorrhage may lead to anemia.  Rapid losses of >20% of plasma volume may lead to hypovolemic shock.

Shock = reduction of perfusion to vital tissues systemically.  Shock arises from either reduced CO unable to meet demand or reduction in effective blood volume.

Whatever the initial source of dysfunction, final pathway involves hypotension, inadequate perfusion of tissues, and hypoxia in vital organs.  Patients present with pale, cool skin, weak and thready pulse, tachypnea.

Shock progresses unless treated and typically follows the patterns below:

Stage I: Nonprogressive stage = effective compensation via baroreceptors, renin-angiotensin system, and other responses which maintain perfusion of vital organs.  Patient may be tachypneic and have an elevated pulse, but major organs will have effective oxygenation.  Blood pressure may be low but will be essentially adequate.

Stage II:  Progressive stage = failure to maintain adequate perfusion and tissue hypoxia, blood pressure will be lower indicating perfusion failure.

Stage III:  Irreversible stage = restoration of adequate O2 will not be sufficient for survival.  Organ damage (especially to kidneys) has been too significant for repair and restoration of function.

Cardiogenic Shock = source of reduced CO is cardiac in origin from AMI, cardiac rupture, or cardiac tamponade, usually associated with an ejection fraction of <20%

Hypovolemic Shock = reduction in cirulating blood volume from fluid loss due to GI distress, hemorrhage, burns, trauma to major vessels

Septic Shock = Inflammation mediated shock typically caused by bacterial wall LPS and activation of systemic inflammation resulting in leaky blood vessels, vasodilation, immune mediated damage to enodthelial cells.  Most common causes are gram-negative rods, such as E. coli, Pseudomonas) or gram-positive cocci (Staph, Strep).  May also be mediated by other bacterial toxins such as toxic shock syndrome.  More common in the very young and very old, or in those who are immunocompromised due to disease or corticosteroid therapy.  Fatal in 50-75% of cases.

Anaphylactic Shock = systemic vasodilation and increased permeability of vessels due to systemic IgE mediated hypersensitivity reaction.  (Technically, this leads to a hypovolemic shock as total circulating volume becomes markedly reduced.)

Neurogenic Shock = loss of vascular tone and peripheral pooling of blood from spinal cord injury or psychogenic causes

MODS:  multiple organ dysfunction syndrome:  very common (1/3 of patients) with septic shock after survival of initial infection.  Occurs with trauma and burns as well.  Mortality rates are >50%.  MODS involves a massive systemic activation of the inflammatory response, independent of that caused by the initial infection (i.e., it occurs in hypovolemic shock as well).  Mediators includeTNF, IL-1 and IL-6 as well as many others.

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