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Fluid and Hemodynamic

Disorders
Dr. Dexter MD FRC Path
Undercover Professor
Department of Pathology
SGU SOM, Grenada
OBJECTIVES
Hemostasis Recanalization
Coagulation
Clot
Thrombosis
Thrombus
Thrombocytopenia
Embolism Hemorrhage
Embolus Occult bleeding
Lines of Zahn Hemosiderin
Organization Hematemesis
Petechia Hemoptysis
Ecchymoses Melena
Purpura Hemarthrosis
Hematoma
Infarct
- pale
- red
- bland
- septic
OBJECTIVES
Hematuria Shock
Hemothorax Hyperemia
Hemopericardium Congestion
Fibrinolysis Congestive heart failure
Thrombolysis edema
Factor V leiden Lymphedema
D-dimer Anasarca
Hypercoagulable state Effusion
Virchow's triad Ascites
Stasis Transudate
Trousseau syndrome Exudate
EDEMA
Recapitulate the factors that govern the fluid exchange
(at the arteriolar and venular ends of the capillaries)
between vascular and extravascular space.
Trace the pathway of fluid from the tissue space to the
heart (lymphatics, thoracic duct, left subclavian vein,
superior vena cava)
Define edema as an abnormal accumulation of fluid in
interstitial space and serous cavities (hydrothorax,
hydropericardium, hydroperitoneum ascites)
Define anasarca as severe edema that affects the
body in a generalized fashion.
Distinguish localized edema from generalized edema
and list the common causes for each.
EDEMA
Explain the pathogenetic mechanism of edema based
on capillary hydrostatic pressure and colloid osmotic
pressure in capillaries and tissues.
Distinguish the properties of exudates from those of
transudate.
Explain the mechanism of edema in venous blockage,
congestive heart failure, lymphatic obstruction, renal
disease, liver disease and protein malnutrition.
Describe the morphology of edema clinically and
microscopically.
Distinguish pitting edema from non-pitting edema
Explain the effects of edema in subcutaneous tissue,
lungs, and brain.
Derive the main lines of management of edema based
on the knowledge of pathology.
Normal Circulation
Heart
Aorta & Arteries
Microcirculation
Arterioles
Capillaries
Venules
Veins & Venules
Lymphatics
Normal capillary filtration
Hydrostatic pressure = 32 mm of Hg
Oncotic pressure = 26 mm of Hg
Colloid osmotic pressure in tissues
Hydrostatic pressure in tissues = 3 mm of Hg Lymphatics Thoracic duct Left Subclavian Vein
Superior Vena Cava Heart
EDEMA - Definition
Edema is an abnormal excess
accumulation of fluid in the intercellular
spaces or body cavities
Occurs most commonly in - Subcutaneous
tissues, lungs and the brain.
EDEMA IS GIVEN DIFFERENT NAMES IN
DIFFERENT LOCATIONS:
Pleural space pleural effusion
(hydrothorax)
Pericardium pericardial effusion
(hydropericardium)
Peritoneum ascites (hydroperitoneum)
Anasarca severe generalized edema
Classification of Edema
Based on mechanism
Increased hydrostatic pressure
Decreased plasma oncotic pressure
Lymphatic obstruction
Sodium retention
Altered membrane permeability
Based on distribution
Localized
Generalized
Based on content of accumulation
Transudate
Exudate
Clinocopathological
Congestive Heart Failure
Pulmonary Edema
Cirrhosis Of The Liver
Renal Disease
Increased hydrostatic pressure
Impaired venous
return
Congestive heart
failure
Venous obstruction
or compression
Thrombosis
External pressure
(e.g. tumor)
Hypervolemia
Sodium retention
(renal failure)
Usually
generalized
Reduced plasma oncotic pressure
- hypoproteinemia
Reduced albumin
synthesis
malnutrition, liver
disease
Increased albumin
loss renal
disease
Reduced albumin
absorption
protein losing
enteropathy
Usually
generalized
Lymphatic obstruction
Inflammatory
Neoplastic
Post
surgical/radiation
Usually
localized
Altered membrane permeability
Inflammation
Acute
chronic
Angiogenesis
Burns
Congestive heart failure
Right heart failure
Increased hydrostatic pressure edema
Dependent edema (legs, sacrum)
Left heart failure
Reduced GFR, sodium retention, renin-angiotensin-
aldosterone axis
Pulmonary edema
Management
Salt restriction, Diuretics
Aldosterone antagonists
Renal disease
Damages basement membrane
Excess albumin loss hypoalbuminemia (Nephrotic
Syndrome)
Decreased plasma oncotic pressure - edema
Glomerulonephritis
inflammatory damage with clogging of glomerular
capillaries reduced GFR
Secondary hyperaldosteronism sodium and water
retention
Generalized edema initially periorbital edema
Liver disease
Cirrhosis of liver
Portal hypertension increased hydrostatic
pressure in splanchnic circulation- ascites
Decreased albumin synthesis reduced
plasma oncotic pressure
Malnutrition
Reduced serum albumin
Decreased plasma oncotic pressure
Decrease in effective plasma volume
Secondary hyperaldosteronism
Sodium and water retention
Edema
Features Transudate Exudate
Process Passive (increased
pressure)
Active
(inflammation)
Vascular
permeability
normal Increased
Plasma protein leak Absent Present
Protein content of
fluid
Low S.G.<1012
Protein<1.5g/dl
High S.G >1020
Proteins> 1.5 g/dl
Fibrin absent Present
Inflammatory cells absent present
Morphology of edema
Skin
M/E cell swelling,
clearing and separation
of the extracellular
matrix
Pitting or non pitting
edema (myxedema)
Impaired wound healing
Thickening
Susceptible to infection
Pulmonary edema Morphology
Interstitial early phase
Alveolar - frothy fluid in alveolar lumen
M/E - severely congested alveolar
capillaries and alveoli filled with
homogenous pink-staining fluid
Clinical features
Cough, dyspnea
Severe cases frothy sputum, cyanosis
Cerebral edema
2 Categories
Vasogenic edema
disruption of blood brain barrier interstitial edema
Infections, trauma, neoplasms
Cytotoxic edema (Gray matter)
Intracellular edema due to cell injury
Hypoxic-ischemic insult
Headache, papilledema
Motor/ sensory abnormalities
Treat by intravenous mannitol and steroids
Morphology
Gross
Flattened gyri
and narrowed
sulci
Compression of
ventricular
cavities
Herniation
Transtentorial (Uncal) displacement of the
temporal lobe
presses on III cranial nerve and parasympathetic
fibers impaired ocular movements, pupillary dilation
Posterior cerebral artery compression damage to
visual cortex
Tonsillar herniation -Tonsillar herniation through
the foramen magnum
Brain stem compression respiratory centers in
medulla oblongata
Brain stem herniation Duret hemorrhages in
midbrain and pons
Death due to cardio-respiratory arrest
Herniation
Subfalcine herniation displacement of
cingulate gyrus under the falx cerebri
Compression of branches of anterior cerebral
artery
Ischemic injury of primary motor and /or
sensory cortex
Weakness and /or sensory abnormalities in
leg
Hyperemia and Hemorrhage
OBJECTIVES
Distinguish hyperemia as an active process caused by
arteriolar dilation from congestion as a passive
phenomenon caused by impaired outflow from veins.
Elucidate the causes of acute and chronic congestion of
lungs, liver and describe the morphological changes.
Define hemorrhage as extravasation of blood and due to
rupture of blood vessels.
Identify the common causes of hemorrhage (trauma,
atherosclerosis, vasculitis, aneurysm, bleeding diathesis)
Define the different varieties of hemorrhage viz.
petechiae, purpura, ecchymosis, hematoma,
hemothorax, hemopericardium, hemoperitoneum,
hemarthrosis.
Explain the chronological changes that take place in the
extravasated blood in the tissues.
Recognize that severe blood loss can lead to shock.
Definition
Hyperemia active increase in the volume of
blood in tissues (red)
Caused by arteriolar dilation
Physiological - blushing, skeletal muscle during
exercise
Pathological - inflammation
Congestion passive increase in the volume of
blood in tissues (blue-red color); usually also
accompanied by edema
Impaired venous flow from tissues e.g. cardiac failure,
venous obstruction
Always pathological
Morphology
Lung
Acute pulmonary congestion (left ventricular
failure)
Alveolar capillaries engorged
Alveolar septal edema
Chronic pulmonary congestion (brown
induration)
Thickened fibrous septa
Heart failure cells (hemosiderin laden
macrophages)
Morphology
Liver
Acute passive venous congestion (right heart failure,
Budd-Chiari syndrome)
Central vein and sinusoids distended with blood
Degeneration of central hepatocytes
Chronic congestion NUTMEG LIVER
Central region of hepatic lobule is reddish brown and are
accentuated against the surrounding zones of uncongested
tan liver
M/E
centrilobular necrosis
Hemorrhage
Hemosiderin laden macrophages
Long standing cases fibrosis (cardiac cirrhosis)
Hemorrhage
Extravasation of blood to the exterior of
the body or into nonvascular body space
due to rupture of blood vessels
Trauma, atherosclerosis, aneurysms,
bleeding disorders
HEMORRHAGE IS GIVEN DIFFERENT
NAMES IN DIFFERENT LOCATIONS:
Hemothorax, Hemopericardium,
Hemoperitoneum, Hemarthrosis
Soft tissues hematoma
Petechiae a pin point hemorrhage in skin
or conjunctiva; represents rupture of
capillary or arteriole
Purpura diffuse superficial hemorrhage in
the skin up to 1 cm in diameter
Ecchymosis a larger superficial
hemorrhage
Chronological changes that occur
to extravasated blood
Hb (red-blue)
Bilirubin (blue, green)
Hemosiderin (brown)
Clinical features of hemorrhage
Hemoptysis coughing blood
Hemetemesis vomiting blood
Malena passing blood in stool
Minor petechiae harmless
If recurrent iron deficiency anemia
If severe hypovolemic shock
Brain stem hemorrhage sudden death
Disseminated intravascular
coagulation (DIC)
OBJECTIVES
Define DIC as a serious and often fatal complication of many
illnesses that involves widespread small thrombi in
microcirculation and bleeding through out the body. Recognize
that it can occur in acute, subacute and chronic forms. Recognize
the need to diagnose it early and treat.
Explain the main mechanism of diffuse endothelial injury that
leads to DIC, with examples
(Gram negative septicemia, immune mediated type II and III
hypersensitivity, release of thromboplastic substances into
circulation- amniotic fluid, snake bite, acute promyelocytic
leukemia, extensive tissue necrosis, proteolytic enzymes and
mucin released by carcinomas).
Recognize that concurrent fibrinolysis proceeds hand in hand with
widespread microthrombi.
Explain the development of lactic acidosis and microinfarcts in
DIC.
OBJECTIVES
Explain the pathogenesis of bleeding in DIC based on
consumptive coagulopathy and fibrin degradation
products (FDPs) acting as anticoagulants (inhibit
thrombin, platelet aggregation and fibrin
polymerization).
Elucidate the clinical features of shock and bleeding in
DIC.
Explain the basis of investigations that can be
performed to confirm the diagnosis of DIC (FDPs, D-
dimers, coagulation tests)
Based on the understanding of the pathogenesis of
DIC, indicate broad lines of its management (heparin
to prevent formation of thrombi, replacement of
platelets and plasma)
Disseminated intravascular
coagulation (DIC)
Widespread small thrombi in the
microcirculation throughout the body
accompanied by simultaneous bleeding
Acute, subacute, chronic
Serious and often fatal
Not primary but an end point of other
diseases
Recognize early and treat
Causes
Idiopathic
Diffuse endothelial injury
Gram negative sepsis (endotoxic)
Viral, ricketssiae
Immunologic injury (type II, III, SLE)
Release of thromboplastic agents in circulation
activation of coagulation
Amniotic fluid embolism
snake bite
Promyelocytic leukemia
Extensive tissue necrosis, burns
Mucin, proteolytic enzymes from carcinoma
PATHOGENESIS OF DIC
TISSUE INJURY ENDOTHELIAL CELL INJURY
EXTRINSIC INTRINSIC
Intravascular Coagulation
Plasmin
Bleeding
Thromboplastins
Contact Activation
Platelet Aggregation
Thromboplastins
Microangiopathic Hemolytic
anemia and ischemic
tissue injury
Consumption of Va, VIIIa,
Fibrinogen and Platelets
Fibrin Microthrombi
Microvascular occlusion
Cleaves Va, VIIIa, Fibrinogen
and Platelet receptors
Fibrinogen and
Fibrin split products
Inhibit:
Platelet aggregation
Fibrin polymerization
Thrombin
Endotoxins and D.I.C
Activate monocytes
Activated monocytes release IL-1, TNF
IL-1 and TNF act on endothelial cell
surface and increase the expression of
tissue factor and reduce the expression of
thrombomodulin
Injured endothelial cells induce platelet
aggregation and activation of intrinsic
pathway by exposure of collagen
Effects of D.I.C
Decreased tissue perfusion shock, lactic
acidosis, microinfarcts
Bleeding consumptive coagulopathy
Diagnosis
FDPs
D-dimers
Management of DIC
Heparin to prevent formation of thrombi
Replace platelets and plasma
SHOCK
OBJECTIVES
Define shock; recognize the importance of shock in
clinical practice.
Explain the common causes of cardiogenic,
hypovolemic, septic, and distributive varieties of shock
and highlight the pathogenesis of shock in each type.
Identify theoretically the three stages of shock (non
progressive, progressive and irreversible) and explain
the pathophysiological changes and clinical features at
each stage. Distinguish septic shock from hypovolemic
shock based on clinical features. Define the lesions
that lead to a fatal outcome.
Describe the morphological changes produced by
hypoxic injury in the following organs brain, heart,
kidney, lungs, adrenals, GIT, liver.
Shock
Is a clinical state characterized by a
generalized decrease in perfusion of
tissues associated with reduction in
effective cardiac output
Causes
Cardiogenic- results from myocardial pump failure.
intrinsic myocardial damage (infarction), ventricular arrhythmias
extrinsic compression (cardiac tamponade)
outflow obstruction (pulmonary embolism).
Hypovolemic - results from loss of blood or plasma
volume.
Hemorrhage
Fluid loss from severe burns or trauma.
Vomiting, diarrhea
Septic - caused by systemic microbial infection.
Most commonly, gram-negative infections (endotoxic shock)
Gram-positive and fungal infections.
Causes
Distributive - imbalance between compartments
Neurogenic
Simple fainting peripheral pooling of blood. Fall down self
correct due to recumbent position increased venous return
restores cardiac output.
Anesthetic loss of vascular tone, peripheral pooling
Spinal cord injury
Anaphylactic generalized IgE mediated response
Systemic vasodilation, increased permeability
Reduced tissue perfusion
Septic shock
Endotoxins are lipopolysaccharides from the
walls of gram negative bacteria
They are released when walls are degraded by
inflammatory response
LPS has a toxic fatty acid (Lipid A) core and a
coat of complex polysaccharides including O Ag.
Similar molecule in walls of gram positive
bacteria, fungi and super antigen of bacterial
walls
LPS plays the dominant role in shock
Septic shock
LPS in low doses
activates monocytes, macrophages, and neutrophils.
The mononuclear phagocytes respond to LPS by producing TNF, which
in turn induces IL-1 synthesis.
Both TNF and IL-1 act on endothelial cells (and other cell types) to
produce further cytokines (e.g., IL-6 and IL-8) and induce adhesion
molecules.
local acute inflammatory response - improves clearance of the infection
LPS in moderate dose
Release of NO and PAF - vasodilation
systemic effects of TNF and IL-1 - including fever, increased synthesis
of acute-phase reactants, and increased production of circulating
neutrophils
LPS at higher doses septic shock syndrome characterized by
Systemic vasodilation (hypotension)
Diminished myocardial contractility
Widespread endothelial injury and activation
Activation of the coagulation system, culminating in DIC
Effects
Hypotension- due to peripheral pooling
secondary to vasodilation
Impaired tissue perfusion
Cellular hypoxia
Cell injury
Cell death
Stages of shock
Initial non-progressive
Progressive
Irreversible
Non-progressive stage
Stage of compensation - Compensated by reflex
mechanisms
Baroreceptors release of catecholamines,
renin, angiotensin, ADH
Generalized sympathetic stimulation
tachycardia, peripheral vasoconstriction, renal
conservation of fluid
Cutaneous vasoconstriction cool, pale skin
Septic shock peripheral vasodilation, flushed and
warm
Coronary, cerebral vessels less sensitive to
sympathetic response so maintain blood flow
and oxygen delivery
Progressive stage
Stage of impaired tissue perfusion
Imbalance between circulation and metabolic needs
Intracellular aerobic respiration replaced by anaerobic
glycolysis
Excess lactic acid production low pH
Sludging of RBCs
Blunting of vasomotor response
Arterioles dilate and blood pools into microcirculation
Reduced cardiac output, anoxic endothelial injury,
DIC
Patient confused, urine output decreases
Irreversible shock
Stage of decompensation
Severe widespread cell and tissue injury
Leakage of lysosomal enzymes (aggravate shock)
Perfusion of brain and myocardium at critical level
ATN, ARF (renal uremia)
Failure of multiple organ systems
Survival difficult even if hemodynamics are
corrected
Morphological changes
Mainly due to hypoxic injury
Brain, heart, kidney, lungs, adrenals, gut,
liver, pancreas,
Brain
Ischemic encephalopathy
Edema, mottled discoloration in gray matter
Watershed infarcts
Laminar cortical necrosis
Pyramidal cells of hippocampus, purkinje cells
of cerebellum
Gray white junction blurred
Neuronal necrosis
Hemorrhages
Heart
Focal and widespread
necrosis
Contraction band
necrosis
kidney
Acute tubular
necrosis
Lungs
Adult respiratory
distress syndrome
(ARDS)
Gut
Hemorrhagic
enteropathy
Gastric stress ulcers
Adrenal hemorrhage Liver
Fatty change
Central hemorrhagic
necrosis
Pancreas
Necrosis
Pancreatitis
All organs can recover except for neurons
and myocytes
Clinical features
Weak rapid pulse
Tachypnea
Cool clammy cyanotic skin
Septic shock (warm, flushed skin)
Gradual loss of function cardiac, cerebral,
pulmonary
Electrolyte disturbances, metabolic acidosis
Renal failure
Life threatening : MI, bleeding. sepsis
THROMBOSIS, EMBOLISM, AND
INFARCTION
OBJECTIVES
Recapitulate the normal process of coagulation,
fibrinolysis and the factors involved.
Recapitulate the role of endothelial cells in hemostasis.
Define thrombosis, distinguish it from clotting.
Recognize the normal and abnormal situations for
thrombosis to occur.
Enlist the important causes of endothelial cell injury,
loss of laminar blood flow and hypercoagulability of
blood which are the main factors that predispose to
thrombosis.
Explain the fate of thrombus 9dissolution, organization
and recanalization, propagation, embolization)
OBJECTIVES
Distinguish a postmortem clot from thrombus based on gross and
microscopic features.
Differentiate the sites, predisposing factors and clinical effects of
venous versus arterial thrombosis.
Define and classify embolism (thrombo, fat, air, bone marrow,
tumor, amniotic fluid, atherosclerotic, foreign body, infective) and
derive the clinical scenarios.
Enlist the common situations of arterial and pulmonary
thromboemboli.
Discuss the effects of minor, major and massive pulmonary
thromboemboli.
Explain the role played by cardiac, pulmonary status and
collateral circulation in determining the outcome of emboli.
OBJECTIVES
Explain how paradoxical emboli develop.
Define infarction, distinguish arterial and venous infarcts and list
common sites.
Identify the main causes of infarction in a given clinical situation
(obstruction by thrombosis, embolism, hemorrhage into
atherosclerotic plaque, torsion of blood vessels, hypo perfusion,
vasculitis)
Explain the difference between the pathogenesis of red and pale
infarcts
Analyze clinical vignettes of commonly occurring ischemic
pathologies (as discussed in the lectures) due to thrombosis and
embolism to identify mechanisms, pathogenesis, relevant
investigations and predict usual outcomes (Pulmonary embolism,
stroke, myocardial infarction, gangrene legs, intestinal infarction,
pulmonary embolism.
Hemostasis
Well-regulated processes that maintain
blood in a fluid, clot-free state in normal
vessels
Dependent on three general components:
Vascular wall
Platelets
Coagulation cascade
Thrombosis
Inappropriate activation of normal
hemostatic process, such as formation of
thrombus in an uninjured vessel or
thrombotic occlusion of a vessel after
relatively minor injury.
Endothelial cell injury
Stress induced by hypertension
Bacterial toxins in shock
Hypercholesterolemia
Homocystinuria
Cigarette smoking (CO?)
All predispose to thrombus formation at
the site of endothelial injury
Loss of laminar flow
Stasis
Endothelial cell hypoxia/ damage
Allows platelets to come in contact with
endothelium
Allows local activation of coagulation factors
Allows buildup of platelets/fibrin
Prevents dilution of activated clotting factors
Reduces flow of clotting inhibitors
Stasis in aneurysms, in leg veins
Turbulence
Turbulence occurs where there is
structural damage to vasculature
Atherosclerotic plaques, aneurysms
Platelets come in contact with damaged
endothelium
Hypercoagulability of blood
Hereditary and Acquired
Hereditary lack of natural anticoagulants
Factor V mutation (Leiden) commonest
Anti-thrombin III deficiency
Protein C deficiency
Protein S deficiency
Acquired syndromes
Terminal cancer
Thrombogenic substances released from
necrotic tumor cells (Trousseau syndrome)
Cardiac failure
Anoxic damage to tissues, release of
Thrombogenic substances
Severe trauma, burns
Oral contraceptives increased
production of clotting factors
Morphology of thrombi
Gross
Dark gray friable mass
Arterial thrombi - pale
Venous thrombi red
Microscopy - lines of Zahn
Alternate pale and dark lines
Light platelet and fibrin
Dark - RBCs
Thrombus versus Clot
Clot Thrombus
Platelets not involved Platelets involved
Occurs outside vessel (test
tube, hematoma) or inside
(Postmortem)
Occurs only inside vessel
Red Red (venous), Pale (arterial)
Gelatinous Firm
Not attached to the vessel
wall
Attached to the vessel wall
Sites of thrombosis arterial
Heart (mural)
Aorta (on
atherosclerotic
plaque)
Aneurysm (mural)
In other arteries
(occlusive)
Coronaries
Carotids, cerebral
Femoral
Mesenteric
Venous thrombosis
Takes the shape of vessels in which it
forms
Redder than arterial thrombus
Superficial veins of legs (varicosities)
Deep veins of legs (90%)
Deep calf veins- (at or above the knee)
femoral, popliteal, iliac
Deep leg veins - Edema of ankle and foot,
pain, tenderness.
Asymptomatic in 50%- due to collaterals .
High risk of embolization
Trousseau's Syndrome - Unexplained
thrombophlebitis, recurrent -look for
underlying abdominal malignancy like
pancreatic cancer ( release of
procoagulants)
Effect of thrombi on organs
Venous thrombus
Edema, congestion
Rarely- the pressure of
edema leads to secondary
block of the artery leading
to infarction
Embolization to lungs
Arterial thrombus
Acute - Infarct
Slow - atrophy,
fibrosis
Heart - systemic
emboli
Embolism
Occlusion of a part of vascular tree by a
mass (solid, liquid, gas) that is carried by
the blood to a site distant from its point of
origin
Classification
99% of Emboli represent part of dislodged
thrombus Thromboembolism
Others
Fat
Air/gas bubbles
Bone marrow
Tumor cells
Amniotic fluid
Atherosclerotic plaque debris
Foreign body
Pulmonary Thromboembolism
Incidence 65% of all autopsies
Mostly asymptomatic
The commonest origin is from the deep leg
veins and reaches the lungs but most of
these are clinically silent
Major contributor to death in 15% of the
hospitalized patients
Usually occurs the first time they get out of the
bed
Classification
Massive
Sudden obstruction of 60% of pulmonary vasculature;
sudden death, no time to develop infarction
Major
Multiple medium sized vessels occluded dyspnea,
pain
Infarction only in 10% because of collateral circulation
by bronchial arteries
Minor
Small vessels obstructed, get lysed, remain
asymptomatic
Systemic Thromboembolism
Thrombi that travel in arterial circulation
Sites of origin
Heart : mural thrombus (80%)
Aorta : ulcerated atherosclerotic plaques
Venous circulation : paradoxical through ASD,
VSD
Effect : embolize to the lower extremities
(75%) and brain (10%)
they block an end artery leading to infarction
Fat embolism
Trauma to bone, subcutaneous tissue, burns
Fat globules enter the circulation by rupture of
the marrow vascular sinusoids or rupture of
venules
Pathogenesis
Mechanical blockage - Globules enlarge in circulation,
platelets adhere
Biochemical injury Free fatty acids are released
from adipose tissue in the circulation and are toxic to
endothelial cells DIC, clogged pulmonary and
systemic capillaries
Fat embolism
Fat embolism syndrome
characterized by pulmonary insufficiency, neurologic
symptoms, anemia, and thrombocytopenia and is
fatal in about 10% of cases.
Typically, the symptoms appear 1 to 3 days after
injury, with sudden onset of tachypnea, dyspnea, and
tachycardia.
Neurologic symptoms include irritability and
restlessness, with progression to delirium or coma.
Fat embolism
Diagnosis : fat globules in sputum, urine
Postmortem : frozen section of tissues
since routine processing through alcohol
will dissolve the fat
Air embolism
Air may be introduced into the venous circulation
through neck wounds, thoracocentesis, Cut in
internal jugular vein, and hemodialysis
Child birth, abortion
150 ml of air causes death
Air bubbles tend to coalesce and physically
obstruct the flow of blood in the right ventricle,
lungs, and the brain
Frothy mixture in right ventricle ineffective
ejection, may occlude large vessels
Nitrogen embolism
(The bends, Caissons disease)
Deep sea diving without using Caissons chamber
(exposed to high pressure)
Scuba diving (deeper than 10 meters)
O2, N2 dissolve in high amounts in blood and tissues due
to high pressure
Sudden resurfacing releases N2, O2
O2 reabsorbed, N2 bubbles out ruptures tissues and in
vessels it forms emboli
Platelets adhere to N2 form secondary thrombi and
aggravate the ischemia
Brain (death), muscles, joints (bends), lungs edema,
hemorrhage (chokes)
Caissons disease more chronic form
with persistent gas emboli in bones
Necrosis in femur, tibia, humerus
Treatment
Pressure chamber slow decompression
Bone marrow embolism
Seen in small
pulmonary vessels
after vigorous cardiac
resuscitation
Incidental finding at
autopsy
Not a cause of death
Amniotic fluid embolism
1 in 50,000 deliveries
Sudden event after
labor
Squames, hair,
meconium in
pulmonary vessels
Usually fatal DIC,
pulmonary edema,
diffuse alveolar
damage
Atherosclerotic emboli
Usually an incidental
finding at autopsy
Involves small
dislodged fragments
of atherosclerosis
from main renal artery
in to smaller intrarenal
branches producing
small infarcts
No clinical symptoms
Infarction
Definition an area of ischemic necrosis
caused by occlusion of either the arterial
supply or the venous drainage in a
particular tissue
99% of infarcts result from thrombotic or
embolic events
Other causes of infarction
Hemorrhage in atherosclerotic plaque
Torsion of blood vessels
Venous or arterial or both
Hypoperfusion
Secondary to MI
Severe hemorrhage
Septic shock
Vasculitis
Rupture
thrombosis
Types of infarcts
White infarcts (pale)
Little bleeding into the organ affected
Solid organs like kidney, spleen, heart
Arterial occlusion
Red infarcts
Large amount of bleeding into the organ
Soft organs with tissue spaces - lungs
Tissues with dual blood supply (lungs and small
intestine)
Venous infarcts (congestion followed by infarction)
When flow is reestablished after arterial occlusion and
necrosis
Morphology of infarcts
Gross :
wedge shaped, with the occluded vessel at the apex
and the periphery of the organ forming the base
Initially congested and ill defined margins
Well defined, rim of hyperemia
Later brown due to hemosiderin
Micro
Ischemic coagulation necrosis
Septic
Abscess formation
Factors that influence the
development of infarction
Nature of the vascular supply
Rate of development of occlusion
Sudden is dangerous and leads to infarction,
slow occlusion leads to ischemia, fibrosis
Tissue vulnerability to hypoxia
Brain versus skeletal muscle, bone
Oxygen carrying capacity of blood
Nature of the blood supply
Dual blood supply less chances of
infarction
Lungs, liver
Circle of Willis
Hand (ulnar and radial arteries)
Collateral circulation
Enlargement of anastomoses in the coronary
circulation reduces the risk of infarction
Evolution of infarct
Polymorphs, macrophages
Granulation tissue, lymphocytes, plasma
cells
Scar contraction
Cerebral infarction initially coagulation
necrosis later liquefactive necrosis
followed by reactive astrocytosis
Importance of age of infarct medico legal
Pulmonary infarction - etiology
Pulmonary thromboemboli of medium size
+
Compromised bronchial circulation or
cardiac failure
Medium sized emboli in the presence of
good bronchial circulation only
hemorrhage no infarction
Morphology
Wedge shaped red infarct with base
towards the pleura
Fibrinous exudate on pleura usually in
lower lobes (75%)
Cerebral infarcts
Most are located in the vertebro-basilar
artery territory and are caused by
atherosclerosis with superimposed
thrombosis
Thromboembolism is a less common
cause of cerebral infarction and is seen
mostly in the internal carotid artery territory
Evolution of cerebral infarcts
12 hours
Starts as coagulation necrosis
Softening, color changes
May have hemorrhage due to reperfusion
48 hours
Edema of the infarcted region, acts like a
intracerebral mass causing raised intracranial
pressure
Microglia engulf necrotic material, Gitter cells
Later evolution of cerebral infarcts
Further breakdown of the tissue
constituents, softening
Liquefaction necrosis
Cyst formation
Overlying meninges thickened
Surrounding regions of gliosis
Myocardial infarction
Coronary atherosclerosis with
superimposed thrombosis
Left anterior descending is the commonest
involved
Coagulation necrosis
Initially blotchy, later pale scar tissue
Cardiac enzymes raised in serum
Presents with severe chest pain (angina)