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Anjali Shinde, MD Department of Pathology Mount Sinai Hospital Chicago DIC Tubular necrosis in kidney Shock can occur in the setting of anesthetic accident or a ... – PowerPoint PPT presentation

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  • Anjali Shinde, MD
  • Department of Pathology
  • Mount Sinai Hospital
  • Chicago

Overview-focus on hemodynamics and hemostasis
  • Edema (increased fluid in the extracellular
  • Hyperemia (increased flow)
  • Congestion (increased backup)
  • Hemorrhage (extravasation)
  • Hemostasis (keeping blood as a fluid)
  • Thrombosis (clotting blood)
  • Embolism (downstream travel of a clot)
  • Infarction (death of tissues w/o blood)
  • Shock (circulatory failure/collapse)
  • Pages 111-115, 121-132 in Robbins Pathologic
    basis of disease, eight edition

A. Edema
  • Approx. 60 of lean body weight is water
  • 2/3 intracellular, 1/3 extracellular
  • Abnormal increase in interstitial fluid within
    tissues is edema
  • Fluid collection in different body cavities
  • Hydrothorax, hydropericardium, ascities, anascara

Any imbalance in the above mechanisms leads to
Pathophysiologic categories of edema 1.
Increased hydrostatic pressure
  • Impaired venous return due to
  • Constrictive pericarditis
  • Congestive heart failure
  • Ascites
  • Venous obstruction or compression by thrombosis,
    external pressure or lower extremity inactivity
  • Arteriolar dilatation
  • Heat
  • Neurohumoral dysregulation

Pathophysiologic categories of edema (contd) 2.
Reduced plasma oncotic pressure
  • Protein losing glomerulopathies-leaky capillaries
    cause loss of albumin
  • Liver cirrhosis- reduced albumin synthesis
  • Malnutrition
  • Protein losing gastroenteropathy

Reduced plasma oncotic pressure
Pathophysiologic categories of edema (contd) 3.
Lymphatic obstruction
  • Impaired lymphatic drainage leads to lymphedema
  • Inflammatory
  • Neoplastic
  • Postsurgical
  • Postirradiation
  • Lymphedema egs.
  • Filiariasis causing elephantiasis
  • irradiation of breast and axilla for
    treatment of breast cancer
  • causing upper limb edema

Pathophysiologic categories of edema (contd) 4.
Sodium and water retention
  • Excessive water intake with renal insufficiency
  • Increased tubular reabsorption of sodium due to
    renal hypoperfusion and increased oncotic
  • Increased salt retention-with obligate
    associated water-causes both increased
    hydrostatic pressure (due to intravascular fluid
    volume expansion) and diminished vascular colloid
    osmotic pressure (due to dilution).

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Clinical consequences of edema
  • Subcutaneous edema signals potential cardiac or
    renal disease
  • Pulmonary edema impedes oxygen diffusion mostly
    left ventricular failure, also renal failure,
    acute respiratory distress syndrome, pulmonary
  • Brain edema- herniation of brain
  • stem or impedes vascular
  • supply to brain stem

B. Hyperemia and Congestion
  • Hyperemia and congestion- locally increased blood
  • Hyperemia - active process of arteriolar dilation
    -increased blood flow-erythema due to
    engorgement of vessels with oxygenated blood.
  • Eg inflammation, muscle during exercise
  • Congestion - passive process-reduced outflow of
    blood from a tissue.
  • Eg. cardiac failure, venous obstruction-cyanosi
    s- due to red cell stasis and the accumulation of
    deoxygenated hemoglobin-edema

Chronic passive Congestion-lung
  • chronic passive congestion (lung) causes
  • lack of blood flow
  • chronic hypoxia
  • ischemic tissue injury and scarring
  • septa are thickened and fibrotic, alveoli
    contain hemosiderin-laden macrophages called
    heart failure cells.

Acute and passive congestion-Liver
  • Acute hepatic congestion
  • -central vein and sinusoids are
    distended -centrilobular hepatocytes are
    ischemic -periportal hepatocytes (better
    oxygenated because of proximity to hepatic
    arterioles)develop fatty change.

Chronic passive congestion-Liver
  • chronic passive hepatic congestion
  • -centrilobular regions are grossly red-brown
    and slightly depressed and accentuated
    against the surrounding zones of uncongested
    tan liver (nutmeg liver)
  • -Microscopically, there is centrilobular
    hemorrhage, hemosiderin-laden macrophages,
    degeneration of hepatocytes.

Centrilobular zone-area of least perfusion
Normal liver
Nutmeg liver
C. Hemorrhage
  • Hemorrhage- extravasation of blood into the
    extravascular space
  • Capillary bleeding can occur under conditions of
    chronic congestion
  • Increased tendency to hemorrhage (usually with
    insignificant injury) occurs in a variety of
    clinical disorders that are collectively called
    hemorrhagic diatheses.
  • Rupture of a large artery or vein results in
    severe hemorrhage and is almost always due to
    vascular injury, including trauma,
    atherosclerosis, or inflammatory or neoplastic
    erosion of the vessel wall.

  • Hemorrhage may be external or
  • contained within a tissue hematoma.
  • Minute 1- to 2-mm hemorrhages
  • into skin, mucous membranes,
  • or serosal surfaces are called petechiae,
  • most commonly associated with locally
  • increased intravascular pressure,
  • low platelet counts (thrombocytopenia),
  • or defective platelet function (as in uremia)
  • Slightly larger (3 mm) hemorrhages
  • are called purpura, associated with
  • many of the same disorders that cause petechiae
  • can be secondary to trauma, vascular
  • (vasculitis), or increased vascular fragility
  • (e.g., in amyloidosis).

  • Larger (gt1 to 2 cm) subcutaneous hematomas (i.e.,
    bruises) are called ecchymoses. The red cells in
    these lesions are degraded and phagocytized by
    macrophages the hemoglobin (red-blue color) is
    then enzymatically converted into bilirubin
    (blue-green color) and eventually into
    hemosiderin (gold-brown color), accounting for
    the characteristic color changes in a bruise.
  • Depending on the location, a large accumulation
  • blood in a body cavity is denoted as a
  • hemothorax, hemopericardium, hemoperitoneum,
  • or hemarthrosis (in joints).

  • Clinical significance of hemorrhage- depends on
    the volume and rate of bleeding.
  • -Rapid loss of up to 20 of blood volume/slow
    losses of even larger amounts- little impact in
    healthy adults
  • - greater losses-can cause hemorrhagic
    (hypovolemic) shock
  • Site of hemorrhage- Intracranial hemorrhage can
    result in an increase in pressure that is
    sufficient to compromise the blood supply or to
    cause the herniation of the brainstem
  • Chronic or recurrent external blood loss (e.g.,
    peptic ulcer or menstrual bleeding)- iron
    deficiency anemia.

D. Shock
  • Shock -characterized by systemic hypotension due
    either to reduced cardiac output or to reduced
    effective circulating blood volume.
  • Final common pathway for several potentially
    lethal clinical events, including severe
    hemorrhage, extensive trauma or burns, large
    myocardial infarction, massive pulmonary
    embolism, and microbial sepsis.
  • Consequences are impaired tissue perfusion and
    cellular hypoxia. Cellular injury is reversible
    in beginning prolonged shock eventually leads to
    irreversible tissue injury -fatal

Causes of Shock
  • Cardiogenic shock results from low cardiac output
    due to myocardial pump failure. This can be due
    to intrinsic myocardial damage (infarction),
    ventricular arrhythmias, extrinsic compression
    (cardiac tamponade), or outflow obstruction
    (e.g., pulmonary embolism)
  • Hypovolemic shock results from low cardiac output
    due to the loss of blood or plasma volume, such
    as can occur with massive hemorrhage or fluid
    loss from severe burns
  • Septic shock results from vasodilation and
    peripheral pooling of blood as part of a systemic
    immune reaction to bacterial or fungal infection

Septic shock
  • Septic shock is associated with severe
    hemodynamic and hemostatic derangements
  • Can have a mortality rate near 20
  • Septic shock ranks first among the causes of
    death in intensive care units
  • Its incidence is rising, ironically due to
    improvements in life support for critically ill
    patients and the growing population of
    immunocompromised hosts (due to chemotherapy,
    immunosuppression, or HIV infection)
  • Currently, septic shock is most frequently
    triggered by gram-positive bacterial infections,
    followed by gram-negative bacteria and fungi.

Septic shock
  • In septic shock, systemic vasodilation and
    pooling of blood in the periphery - tissue
    hypoperfusion - widespread endothelial cell
    activation and injury, often leading to a
    hypercoagulable state that can manifest as DIC
  • Septic shock is associated with changes in
    metabolism that directly suppress cellular
    function. The net effect of these abnormalities
    is hypoperfusion and dysfunction of multiple
    organs-culminating in morbidity and mortality
    associated with sepsis.

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Septic shock
  • Metabolic abnormalities.-
  • Septic patients have insulin resistance and
    hyperglycemia. Cytokines such as TNF and IL-1,
    stress-induced hormones (such as glucagon, growth
    hormone, and glucocorticoids), and catecholamines
    all drive gluconeogenesis.
  • Pro-inflammatory cytokines suppress insulin
    release while simultaneously promoting insulin
    resistance in the liver and other tissues, likely
    by impairing the surface expression of GLUT-4, a
    glucose transporter.
  • Hyperglycemia decreases neutrophil
    function-thereby suppressing bactericidal
    activity-and causes increased adhesion molecule
    expression on endothelial cells.
  • Initially there is an acute surge in
    glucocorticoid production, then there is adrenal
    insufficiency and a functional deficit of
    glucocorticoids. This may stem from depression of
    the synthetic capacity of intact adrenal glands
    or frank adrenal necrosis due to DIC
    (Waterhouse-Friderichsen syndrome)

  • Immune suppression.- Sepsis can activate
    counter-regulatory immunosuppressive mechanisms,
    possibly causing a shift from pro-inflammatory
    (TH1) to anti-inflammatory (TH2) cytokines
  • Organ dysfunction.- Systemic hypotension,
    interstitial edema, and small vessel thrombosis
    all decrease the delivery of oxygen and nutrients
    to the tissues. High levels of cytokines and
    secondary mediators may diminish myocardial
    contractility and cardiac output, and increased
    vascular permeability and endothelial injury can
    lead to the adult respiratory distress syndrome
  • This may lead to failure of multiple organs,
    particularly the kidneys, liver, lungs, and
    heart, culminating in death.

  • Severity and outcome of septic shock are
    dependent upon the extent and virulence of the
    infection, the immune status of the host the
    presence of other co-morbid conditions and the
    pattern and level of mediator production.
  • Standard of care remains treatment with
    appropriate antibiotics, intensive insulin
    therapy for hyperglycemia, fluid resuscitation to
    maintain systemic pressures and corticosteroids
    to correct relative adrenal insufficiency
  • An additional group of secreted bacterial
    proteins called superantigens also cause a
    syndrome similar to septic shock (e.g., toxic
    shock syndrome). Superantigens are polyclonal
    T-lymphocyte activators that induce the release
    of high levels of cytokines that result in a
    variety of clinical manifestations, ranging from
    a diffuse rash to vasodilation, hypotension, and

Stages of shock- non progressive phase
  • In the early nonprogressive phase of shock,
    neurohumoral mechanisms maintain cardiac output
    and blood pressure. eg baroreceptor reflexes,
    catecholamine release, activation of the
    renin-angiotensin axis, ADH release, and
    generalized sympathetic stimulation. The net
    effect is tachycardia, peripheral
    vasoconstriction, and renal conservation of
    fluid, cool skin If the underlying causes are not
    corrected, shock passes into progessive phase

Shock- progressive phase
  • Progressive phase- there is tissue hypoxia
  • If there is persistent oxygen deficit,
    intracellular aerobic respiration is replaced by
    anaerobic glycolysis with excessive production of
    lactic acid. The resultant metabolic lactic
    acidosis lowers the tissue pH and blunts the
    vasomotor response arterioles dilate, and blood
    begins to pool in the microcirculation.
  • Peripheral pooling worsens cardiac output, and
    can cause anoxic injury with subsequent DIC.
  • With widespread tissue hypoxia, vital organs are
    affected and begin to fail.

Stages of shock
  • Without intervention, the process eventually
    enters an irreversible stage.
  • Widespread cell injury is reflected in lysosomal
    enzyme leakage
  • Myocardial contractile function worsens in part
    because of nitric oxide synthesis.
  • If ischemic bowel allows intestinal flora to
    enter the circulation, bacteremic shock may be
  • There can be complete renal shutdown as a result
    of acute tubular necrosis
  • At this stage, there can be a downward clinical
    spiral which almost inevitably culminates in

Shock- Morphology
  • Changes of hypoxic injury brain, heart,
    lungs, kidneys, adrenals, and gastrointestinal
    tract most affected.
  • Adrenal changes in shock increased synthesis of
  • Kidney- acute tubular necrosis
  • lungs -are seldom affected in pure hypovolemic
    shock, because they are somewhat resistant to
    hypoxic injury. In bacterial sepsis or trauma,
    changes of diffuse alveolar damage are seen
  • In septic shock, the development of DIC-
    fibrin-rich microthrombi, particularly in the
    brain, heart, lungs, kidney, adrenal glands, and
    gastrointestinal tract.- consumption of platelets
    and coagulation factors also often leads to the
    appearance of petechial hemorrhages on serosal
    surface and the skin
  • Except neuronal and myocyte ischemic loss,
    virtually all of these tissues may revert to
    normal if the individual survives. Unfortunately,
    most patients with irreversible changes due to
    severe shock die before the tissues can recover

Tubular necrosis in kidney
Shock- less common types
  • Shock can occur in the setting of anesthetic
    accident or a spinal cord injury (neurogenic
    shock), as a result of loss of vascular tone and
    peripheral pooling of blood.
  • Anaphylactic shock- systemic vasodilation and
    increased vascular permeability caused by an
    IgE-mediated hypersensitivity reaction causing
    acute widespread vasodilation, tissue
    hypoperfusion and hypoxia.

Clinical consequences of shock
  • Clinical manifestations of shock depend on the
    precipitating insult. In hypovolemic and
    cardiogenic shock the patient presents with
    hypotension, a weak, tachypnea and cool, clammy,
    cyanotic skin. In septic shock the skin may
    initially be warm and flushed because of
    peripheral vasodilation. The initial threat to
    life stems from the underlying catastrophe that
    precipitated the shock (e.g., myocardial infarct,
    severe hemorrhage, or sepsis).
  • Rapidly, however, the cardiac, cerebral, and
    pulmonary changes secondary to shock worsen the
    problem. Eventually, electrolyte disturbances and
    metabolic acidosis also exacerbate the situation.
  • Individuals who survive the initial complications
    may enter a second phase dominated by renal
    insufficiency and marked by a progressive fall in
    urine output as well as severe fluid and
    electrolyte imbalances.

Clinical consequences of shock
  • Prognosis varies with the origin of shock and its
  • Greater than 90 of young, healthy patients with
    hypovolemic shock survive with appropriate
  • Septic shock or cardiogenic shock associated with
    extensive myocardial infarction, can have
    substantially worse mortality rates, even with
    optimal care.
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