patoloji-ders-notlari

Title

Serdar Balcı

Embolism, Infarction and Shock

Serdar BALCI, MD

medicalschoolpathology.com

Embolus

• intravascular solid, liquid, or gaseous mass
• carried by the blood to a site distant from its point of origin
• emboli derive from a dislodged thrombus
  • thromboembolism
• fat droplets
• bubbles of air or nitrogen
• atherosclerotic debris (cholesterol emboli)
• tumor fragments
• bone marrow
• amniotic fluid

emboli lodge in vessels too small to permit further passage

partial or complete vascular occlusion

ischemic necrosis (infarction)

embolization in the pulmonary circulation leads to hypoxia, hypotension, and right-sided heart failure

Pulmonary Thromboembolism

Robbins Basic Pathology

• A major cause of hospital deaths

• Venous emboli

• Originate from thrombi within deep leg veins

  • proximal to the popliteal fossa
  • lower leg thrombi is uncommon

• Paradoxical embolism

• Fragmented thrombi from DVTs

• Pass through the right side of the heart

• Pulmonary vasculature

• Depending on size occlude

  • main pulmonary artery
  • bifurcation of the right and left pulmonary arteries (saddle embolus)
  • smaller, branching arterioles

Can be multiple

Sequentially

Multiple places at the same time

Patient has increased risk if had one PTE

60-80% are small and clinically silent

Undergo organization, incorporated into the vascular wall

In some cases, organization of thromboemboli, bridging fibrous webs

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

• Embolic obstruction of medium-sized arteries → subsequent rupture of capillaries → pulmonary hemorrhage
• Does not cause pulmonary infarction
• Intact bronchial circulation (dual circulation)
• A similar embolus in the setting of left-sided cardiac failure
  • lead to a pulmonary infarct

Embolism to small end-arteriolar pulmonary branches usually causes infarction

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

Systemic Thromboembolism

• 80% arise from intracardiac mural thrombi

• 2/3 associated with left ventricular infarcts

• 25% with dilated left atria (secondary to mitral valve disease)

• Remainder

  • aortic aneurysms
  • thrombi overlying ulcerated atherosclerotic plaques
  • fragmented valvular vegetations
  • venous system (paradoxical emboli)

• 10% to 15% of systemic emboli are of unknown origin

• Common arteriolar embolization sites

  • lower extremities (75%)
  • central nervous system
  • intestines
  • kidneys
  • spleen

• consequences depend on

  • caliber of the occluded vessel
  • collateral supply
  • affected tissue’s vulnerability to anoxia

Fat embolism

• Soft tissue crush injury
  • rupture of marrow vascular sinusoids (long bone fracture)
  • releases microscopic fat globules into the circulation
• Fat, marrow emboli are common after vigorous cardiopulmonary resuscitation
  • Little clinical consequence
  • Fat and marrow embolism occurs in some 90% of individuals with severe skeletal injuries
  • Less than 10% show any clinical findings

Fat embolism syndrome

• pulmonary insufficiency
• neurologic symptoms
• anemia
• thrombocytopenia
• diffuse petechial rash
• fatal in 10% of cases
• 1 to 3 days after injury sudden onset of
  • tachypnea
  • dyspnea
  • tachycardia
  • irritability
  • restlessness
  • delirium or coma
• Pathogenesis
• Fat microemboli occlude pulmonary and cerebral microvasculature
  • directly and by triggering platelet aggregation
• Fatty acid release from lipid globules
  • Local toxic endothelial injury
  • Platelet activation and granulocyte recruitment

Autopsy Pathology: A Manual and Atlas

Robbins Basic Pathology

Amniotic Fluid Embolism

• Uncommon

• Complication of labor

• Immediate postpartum period (1 in 40,000 deliveries)

• Mortality rate 80%

  • Most common cause of maternal death in the developed world

• 85% of survivors suffer some form of permanent neurologic deficit

• Underlying cause

• entry of amniotic fluid into the maternal circulation

  • via tears in the placental membranes

• uterine vein rupture

• Onset is sudden

  • severe dyspnea
  • cyanosis
  • hypotensive shock
  • seizures and coma

• If acute phase is survived

  • pulmonary edema
  • disseminated intravascular coagulation
    • secondary to release of thrombogenic substances from amniotic fluid

• Histologic analysis in the maternal pulmonary microcirculation

  • squamous cells shed from fetal skin
  • lanugo hair
  • fat from vernix caseosa
  • mucin derived from the fetal respiratory or gastrointestinal tracts

• Other findings

  • marked pulmonary edema
  • diffuse alveolar damage
  • systemic fibrin thrombi
    • disseminated intravascular coagulation

Robbins Basic Pathology

Air Embolism

• Gas bubbles obstruct vascular flow
• Cause distal ischemic injury
• Can occur during surgery
• Small venous gas emboli generally have no deleterious effects
• **Sufficient air can enter the pulmonary circulation **
  • during obstetric procedures
  • chest wall injury to cause hypoxia
• Very large venous emboli may arrest in the heart and cause death

Decompression sickness,

• Scuba divers, underwater construction workers, and persons in unpressurized aircraft who undergo rapid ascent
• Caisson disease
  • recurrent or persistent gas emboli in the bones lead to multifocal ischemic necrosis
• High-pressure chamber

INFARCTION

Infarction

• An area of ischemic necrosis
• Caused by occlusion of the vascular supply to the affected tissue
• A major cause of death
  • myocardial infarction
  • cerebral infarction
  • pulmonary infarction
  • bowel infarction
  • ischemic necrosis of distal extremities (gangrene)
    • diabetic patients

Causes of infarction

• Arterial thrombosis
• Arterial embolism
• Vasospasm
• Expansion of an atheroma secondary to intraplaque hemorrhage
• Extrinsic compression of a vessel
  • by tumor
• Dissecting aortic aneurysm
• Edema within a confined space
  • in anterior tibial compartment syndrome
• Vessel twisting
  • in testicular torsion or bowel volvulus
• Traumatic vascular rupture
• Entrapment in a hernia sac

Venous thrombosis can cause infarction too

But the more common outcome is simply congestion

Bypass channels rapidly open to provide arterial inflow

Infarcts caused by venous thrombosis occur only in organs with a single efferent vein (testis or ovary)

Infarcts

Red infarcts

White Infarcts

Septic infarcts

Bland Infarcts

Robbins Basic Pathology

Red infarcts

• Venous occlusions
  • ovarian torsion
• Loose tissues
  • Lung
  • blood can collect in infarcted zones
• Tissues with dual circulations
  • lung and small intestine
  • partial, inadequate perfusion by collateral arterial supplies
• Previously congested tissues
  • Slow venous outflow
• **Flow is reestablished after infarction has occurred **
  • angioplasty of an arterial obstruction

Robbins Basic Pathology

White infarcts

• Arterial occlusions in solid organs with end-arterial circulations
  • heart, spleen, and kidney
• tissue density limits the blood from adjoining patent vascular beds
• Wedge-shaped
  • Occluded vessel at the apex
  • Organ periphery forming the base
  • When the base is a serosal surface, there is often an overlying fibrinous exudate
  • Lateral margins may be irregular
    • Reflecting flow from adjacent vessels

Margins of acute infarcts typically are indistinct and slightly hemorrhagic

With time, the edges become better defined

Ischemic coagulative necrosis

• An inflammatory response develop at the margins of infarcts
  • Few hours, well defined within 1-2 days
• Repair
  • Beginning in the preserved margins
  • Parenchymal regeneration or scar
  • In CNS → liquefactive necrosis

Kidney infarct, replaced by a large fibrotic scar

Robbins Basic Pathology

Septic infarctions

Infected cardiac valve vegetations embolize

When microbes seed necrotic tissue, infarct is converted into an abscess

Factors That Influence Infarct Development

• The anatomy of the vascular supply
• The time over which the occlusion develops
  • Collateral circulation
• The intrinsic vulnerability of the affected tissue to ischemic injury
• The blood oxygen content

SHOCK

Shock

final common pathway for several potentially lethal events

extensive trauma or burns

myocardial infarction

pulmonary embolism

sepsis

Shock is characterized by systemic hypoperfusion of tissues

can be caused by diminished cardiac output

reduced effective circulating blood volume

impaired tissue perfusion and cellular hypoxia

initially is reversible, prolonged shock often fatal

The most common forms of shock

• Cardiogenic shock
  • Low cardiac output due to myocardial pump failure
• Hypovolemic shock
  • Loss of blood or plasma volume
• Septic shock

Septic Shock

• Gram-positive bacteria constitute the most common cause of septic shock, followed by gram-negative organisms and fungi
• Systemic inflammatory response syndrome (SIRS)
  • When there is no microorganism product
• Coagulation is also affected

• Metabolic abnormalities
• Immune suppression
• Organ dysfunction
  • Multiorgan failure
  • Acute respiratory distress syndrome (ARDS)
• Superantigens
  • Toxic Shock Syndrome

Stages of Shock

• Nonprogressive stage
  • Reflex compensatory mechanisms are activated
  • Vital organ perfusion is maintained
• Progressive stage
  • Tissue hypoperfusion
  • Worsening circulatory and metabolic state
  • Acidosis
• Irreversible stage
  • Survival is not possible