Hemodynamic Disorders

Topics
Edema

Hyperemia and Congestion

Hemorrhage
Hemostasis and Thrombosis: normal
hemostasis, thrombosis, DIC
Embolism
Infarction (red and pale)
Shock

Edema

Fluid distribution
~60% of lean body weight is water
~ 2/3 is intracellular
~ 1/3 is extracellular (mostly interstitial
fluid)
~5% of total body water is in blood plasma.

 Fluid homeostasis is critical to orderly cellular

functioning.
Although mild edema may be simply annoying
it may signal underlying disease or may be
life-threatening (pulmonary or brain oedema).

Edema
Definition:
Increased fluid in interstitial tissue spaces and
serous cavities.

Pathogenesis
The major factors that govern movement of
fluid between vascular and interstitial spaces
are:
Hydrostatic pressure
Plasma colloid osmotic pressure

Pathogenesis
Increased Hydrostatic Pressure (Impaired
venous return)

Congestive heart failure

Liver cirrhosis
Venous obstruction
I.
Thrombosis
II.
Compression (mass)
III.
Stasis

Reduced Plasma Oncotic Pressure

Nephrotic syndrome (glomerular protein

leakage)
Liver cirrhosis (loss of plasma protein
synthesis)
Malnutrition

Lymphatic Obstruction (lymphedema)

Inflammation (filariasis)
Neoplasia
Surgery/irradiation

Sodium/Water Retention

Excessive intake + renal insufficiency

Renal hypoperfusion
Hyperaldosterone

Inflammation

Acute
Chronic

Types of edema by distribution

Localised limited to an organ or limb

Lymphatic oedema
Allergic oedema
Inflammatory oedema
Generalized (anasarca) systemic distribution,
noticeable in subcutaneous tissue
Renal oedema
Cardiac oedema
Nutritional oedema

Types of edema by fluid

composition
Transudate
Exudate

Transudate
Edema occurring in hydrodynamic
derangements
In cardiac, renal, hepatic diseases
Low protein content specific gravity <1.012)

Hydrostatic
pressure

Osmotic
pressur
e

Exudate
Edema occurring in inflammatory conditions
(inflammatory oedema)
Cause: Increased vascular permeability
High protein content specific gravity >1.020)

Hydrostat
ic
pressure

Osmotic
pressur
e

Diapedesis

 Fluid collection in body cavities may have

various designations:
Hydrothorax (pleural effusion)
Hydropericardium
Hydroperitoneum (usually called ascites)

Morphology
Macroscopy:
Tissue appears enlarged, soft, overweight, with
tensed tunica and tinged color.
Most commonly encountered in subcutaneous
tissues, the lungs, and the brain.
Microscopy:
Subtle cell swelling, with clearing and separation
of the extracellular matrix elements.

 Subcutaneous edema
Pulmonary edema
Brain edema

Subcutaneous edema
various distributions depending on etiology
diffuse distribution

renal dysfunction, nephrotic syndrome

affects all parts of the body equally
initially may be more obvious in tissue with loose
connective tissue matrix - eyelids (periorbital oedema)

more conspicuous in site of higher hydrostatic

pressure - dependent
prominent feature of congestive heart failure
(particularly right heart failure)
pitting oedema

Pulmonary edema
Typical in left heart failure
Renal failure
Acute respiratory distress syndrome
Pulmonary infections (pneumonia)
Hypersensitivity reactions
Fluid accumulation both in the tissue space AND
pulmonary alveoli
Causes: pulmonary hydrostatic presure OR
capillary permeability

Mechanisms
Elevation in pulmonary hydrostatic pressure
(Haemodynamic edema)

left heart failure

mitral stenosis
pulmonary vein obstruction
thyrotoxicosis
nephrotic syndrome
obstruction to the lymphatic outflow by tumour or inflammation

Increased vascular permeability (Irritant edema)

fulminant pulmmonary infection

toxic substances,
ARDS

Acute high altitude edema anoxic damage to the

pulmmonary vessels

Macroscopy
Heavy, moist and subcrepitant lungs
Lungs are 2 to 3 x normal weight
On sectioning: frothy, blood-tinged fluid
(mixture of air, oedema fluid, and
extravasated red blood cells)
Fluid accumulates more in the basal lung
region

Pulmonary oedema

Microscopy
The alveolar capillaries are congested.
Initially, excess fluid collects in the
interstitium interstitial oedema.
Later, fluid fills alveolar spaces alveolar
oedema.
Oedema fluid pink, granular, proteinaceous,
eosinophilic material, often admixed with RBCs,
inflammatory cells.

Pulmonary edema

engorged capillaries
intra-alveolar air
spaces filled with
pink-stained
transsudate

Cerebral edema
Localized
abscess or
neoplasm
Generalized: brain is grossly swollen, with narrowed
sulci and distended, flattened gyri
encephalitis
hypertensive crises
obstruction to venous outflow.
Trauma may cause either generalized or localized
oedema

Brain Edema
Loose "spongy" or
vacuolated white matter
could be either around
a tumor
an infarct
due to metabolic
disease

Brain Edema
Oedematous, spongy
white matter.
Vacuolization
(sponginess ) is
probably due to swelling
of astrocytic processes.

vesicule

Fovea

Edema

Chilous ascites

Hyperemia and Congestion

= increased volume and pressure of blood
within dilated vessels in a given tissue

Hyperemia
Active process
Dilatation of arteries, arterioles,
capillaries
augmented tissue inflow
Sympathetic neurogenic
mechanism or release of
vasoactive substances
Erythema
(tissue is redder because of the
engorgement of vessels with
oxygenated blood)

Hyperemia
Forms:
Physiological - Skeletal muscle during exercise
Pathological

Inflammation
Fever
Chemical injury
Physical injury

Hyperemia of colonic mucosa

Cystitis- bladder mucosa hyperemia

Congestion (passive hyperaemia)

Passive process
Dilatation of venous side
decreased outflow
Cyanosis
(accumulation of
deoxygenated
hemoglobin)
Hypoxia

Congestion
Causes:
Systemic: congestive heart failure
Local: thrombosis, obstruction

Deep venous thrombosis - legs

Pylethrombosis - portal congestion
Vena cava superioris syndrome

 Congestion and edema commonly occur together:

congestion of capillaries development of edema
Long-standing congestion (chronic passive
congestion more common than acute) stasis of
poorly oxygenated blood chronic hypoxia
Parenchymal cell degeneration, cell death,
microscopic scarring.
Capillary rupture small hemorrhagic foci;
Breakdown and phagocytosis of the red cell debris
small clusters of hemosiderin-laden macrophages.

Pulmonary congestion
Acute congestion
cut surface is hemorrhagic and wet
alveolar capillaries engorged with blood
alveolar septal oedema
focal intra-alveolar hemorrhage

CVC of lung

hronic venous
congestion
)
failure
reumathic
mitral stenosis
In left heart (C
Macro:
Heavy and firm consistency
Sectioned surface is rusty brown brown induration
of the lungs (due to pigmentation and fibrosis)
Micro:
Thickened and/or fibrotic septae
Hemosiderin-laden macrophages alveolar spaces
(heart failure cells).

Lung, chronic passive

hyperemia/
congestion

Acute congestion

Pulmonary edema/
acute congestion

Chronic passive congestion

Hemosiderin in heart failure cells

Hepatic CVC

(chronic vascular congestion)

Macro
Liver is enlarged and tender; capsule is tensed
Cut surface nutmeg appearance: red and yellow mottled
appearance
red - congested centre of lobules
yellow - fatty peripheral zone

Nutmeg liver

Hepatic CVC
(chronic vascular
congestion)

Micro:
Changes more prominent in centrilobular area due to
more severe hypoxia than in peripheral area
Hepatocyte degeneration in centrilobular zone
centrilobular haemorrhagic necrosis
Severe long-standing hepatic congestion hepatic
centrilobular fibrosis (cardiac cirrhosis)
Fatty change in peripheral zone hepatocytes
Centrilobular necrosis can appear whenever there is
reduced hepatic blood flow (including shock of any
cause) because is the last to receive blood.

Nutmeg liver

centrilobular necrosis

"cardiac cirrhosis"

Splenic CVC
Occurs in
right heart failure
portal hypertension from liver cirrhosis
Macro:
early stages spleen is slighty to moderate enlarged
(up to 250 g; normal 150 g)
long-standing progressive enlargement (up to 500
1000g
deeply congested, tense and cyanotic spleen
cut surface is gray tan

Congestive
splenomegaly
heavy and enlarged spleen
grey tan cut surface

Splenic CVC
Micro:
Red pulp
enlarged due to congestion
sinusoids may convert into capillaries (capillarisation of
sinusoids)
Hyperplasia of the reticuloendothelial cells
Fibrous thickening of capsule and trabeculae
Gamna-Gandy bodies (siderofibrotic nodules) some
haemmorrhages overlying fibrous tissue get deposits of
haemosiderin pigment and calcium salts
Firmness of spleen in advanced stage more commonly in
hepatic cirrhosis

CONGESTIVE SPLENOMEGALY
Very prominent red pulp at the expense of the white pulp

Gamna-Gandy body

Kidney CVC
Macro:
Kidneys slightly enlarged
Medulla is congested
Micro:
Mild changes
Tubules may show regenerative changes
cloudy swelling
fatty change
Glomeruli may show mesangial proliferation
Dilated capillaries, filled with RBC; sometimes
extravasated red blood cells.

Congestive kidney

Consequences of chronic congestion

Systemic

Skin: cyanosis, anasarca

Liver: nutmeg liver (hepar moschatum),centrilobular necrosis, cardiac
fibrosis (cardiac cirrhosis)
Kidneys: stellate veins accentuated, cortex widened, sharp separation of
medulla and cortex
Spleen: enlarged, livid, fibrosis with time (Induratio cyanotica lienis)
Lungs: heavy, firm, heart failure cells, (induratio brunea pulmonis)

Local

May occur in every organ

E.g. Budd-Chiari sy (hepatic vein thrombosis), extremities etc.

Stasis

Arterial supply maintained, venous outflow stopped

Consequence: necrosis ( role of collaterals!)
Eg. Volvulus, incarcerated hernia

Haemorrhage

Haemorrhage
Definition

Escape of blood from a blood vessel.

Types

Sudden (acute)
Small repeated bleeds may occur over a period of
time(chronic)
External
Internal

Types
Hematoma bleeding enclosed within tissue
Petechiae minute hemorrhage (1-2 mm) within skin,
mucus membranes, serosal surfaces (increased iv
pressure, low platelet count, defective platelet
function)
Purpura medium areas of hemorrhage as above (>2 3
mm): same conditions as petechiae, plus vasculitis,
vascular fragility amyloidosis
Ecchymoses large (> 1cm) areas of subcutaneous
bleeding (bruises); hemoglobin (red-blue), degraded by
macrophages bilirubin (blue-green) hemosiderin
(yellow-brown)

Types

By location
Epistaxis
Hematemesis
Melena
Hematochesia

Bleeding into body cavities

Hemothorax
Hemopericardium
Hemoperitoneum
Hemarthrosis

Petechiae- pericardium
(thrombocytopenia)

Petechiae- white matter ( fat embolism due to

trauma)

Petechial hemorrhages
colonic mucosa

Ecchymoses

Purpura

Hypopharyngeal haemorrhagic tumor

Subcapsular liver
haematoma

Hemopericardium- due
to aortic dissection

Thalamus -hemorrhagehypertension

Apoplexia cerebrihypertension

Subarachnoid hemorrhage

Etiology
Trauma to vessel wall
Penetrating wound
During labour
Spontaneous haemorrhage
Rupture of aneurysm
Septicaemia
Bleeding diathesis (purpura)
Acute laeukemias, pernicious anaemia
Scurvy

Etiology
Inflammatory lesions
Chronic peptic ulcer
Typhoid ulcers
Syphilitic involvement of aorta
Blood vessels traversing tuberculous cavity in lung
Neoplastic invasion
Vascular diseases - atherosclerosis
Elevated pressure within vessels
Retinal haemorrhage in systemic hypertension
Varicose veins in legs or oesophagus

Pathogenesis
Vascular defects
Rupture of vessel wall (haemorrhagia per
rhexim
Erosion of vessel wall (haemorrhagia per
arrosionem)
Vessel wall abnormalities: due to hypoxia,
infections, drugs, impaired collagen synthesis,
Henoch-Schnlein purpura, Hereditary
hemorrhagic teleangiectasia etc.

 Related to thrombocytes:
Thrombocytopenia (low platelet count)
Decreased production of platelets
Bone marrow diseases, bone marrow infiltration,
drug induced, infections (HIV associated!) etc
Decreased survival of platelets
Immune thrombocytopenic purpura ( ITP,
autoimmune)
Thrombotic microangiopathies (TTP: thrombotic
thrombocytopenic purpura, HUS: Hemolyticuremic syndrome)
Thrombasthenia (defective platelet function): primary,
secondary (aspirin!!!)

- Abnormalities in clotting factors

- Primary, or Secondary ( acquired eg. In hepatic
diseases!
- Von Willebrand disease
- Hemophilia A (factor VIII deficiency)
- Hemophilia B ( Factor IX deficiency- Christmas
disease)
- Hemophilia C (Factor XI deficiency)
Disseminated intravascular coagulation (DIC,
consumption coagulopathy)
Causes: obstetric complications,
infections, neoplasms, excessive tissue
injury
Hemorrhage and thrombosis

Clinical Impact
Dependent on
Site
Amount of bleeding
Speed of bleeding
Acute loss >20% of blood volume hemorrhagic
(hypovolemic) shock
Chronic loss iron deficiency anaemia

Shock

Shock
Definition
Clinical syndrome of cardiovascular collapse
characterised by
Hypotension
and
Hypoperfusion
due to either a reduction in blood volume or
cardiac output.

Types of shock
Cardiogenic: MI, arrhythmia, tamponade, outflow
obstruction

Hypovolemic: traumatic hemorrhage, severe burns, disease

induced hemorrhage.
Neurogenic: Cord transection (peripheral pooling)
Anaphylactic: IgE mediated vasodilation and edema
Septic: Systemic infection primarily gram-negative
(endotoxic). Cytokine mediated vasodilation,
myocardial injury, and DIC.

 Stages of Shock

Initial non progressive stage: tachycardia,

vasoconstriction, renal conservation of water.
Progressive stage: lactic acidosis, vasodilation,
hypoxia, organ failure.
Irreversible stage: Lysosome release, ischemic bowel
syndrome, acute tubular necrosis, death.

Clinical Course

Hypovolemic/Cardiogenic: hypotension, weak rapid

pulse, tachypnea, cool clammy cyanotic skin.
Septic shock: warm red skin.
80% with hypovolemic shock survive.
80% with cardiogenic or endotoxic shock die.

Model of septic shock

Haemostasis and Thrombosis

Haemostasis and Thrombosis

We are not composed of static pipes
that transmit blood, so we have to
understand how the normal vessel
constituents interact with blood
normally!!!!

Haemostasis is a natural process that

maintains blood fluidity while also
controlling vascular injury repair
producing a local haemostatic plug

PLUMBERS
TOOL

Haemostasis

Integrity of small blood vessels

Adequate numbers of platelets
Normal amounts of coagulation
factors
Normal amounts of coagulation
inhibitors
Adequate amounts of calcium
ions in the blood

Role of endothelium in haemostasis

Antiplatelet properties
physical barrier
Prostacyclin synthesis
Nitric oxide synthesis

Anticoagulant properties

Heparin-like molecules (+antithrombin III inactivate

thrombin)
Thrombomodulin (+thrombin activates Protein C that
digests factors V and VII)

Fibrinolytic properties
Synthesis of t-PA

Pro thrombotic properties

Synthesis of von Willebrand factor vWF

Cytokine (Il-1, TNF) stimulation causes release of tissue
factor which in turn activates extrinsic clotting factors
Synthesis of plasminogen activator inhibitors (PAIs)

Role of platelets in haemostasis

Note: Platelets contain 2 types of storage granules:

Alpha granules store fibrinogen, PDGF, coagulation factors V and

VIII.
Dense or delta granules contain ADP, ATP, ionized calcium, histamine,
serotonin, and epinephrine.

Platelet adhesion: reaction between

platelet surface receptors, vWF,
and collagen
Platelet secretion: release of granule secretory products
that promote platelet-plug formation
Platelet aggregation: ADP and thromboxane promote
primary haemostasis. Platelet contraction and fibrin

Role of coagulation cascade

Coagulation factor activation occurs on phospholipid
surfaces derived from endothelial cell injury. This
helps to localize the reaction.
Extrinsic vs. Intrinsic coagulation distinctions are not
clear in vivo.
Inhibition of coagulation activation is extremely
important and highly dependent on endothelial
integrity.

Sequence of events
Initial injury
Arteriolar vasoconstriction
Neurogenic reflexes
Local endothelin release (endothelium)

Exposure of subendothelial matrix (collagen) and platelet

activation (primary hemostasis)
Tissue factor release (phospholipids) stimulates the
coagulation cascade with net fibrin deposition (secondary
hemostasis)
Fibrin-platelet plug is formed. Plasmin activation helps limit

Downloaded from: Robbins & Cotran Pathologic Basis of Disease

Downloaded from: Robbins & Cotran Pathologic Basis of Disease

Downloaded from: Robbins & Cotran Pathologic Basis of Disease

Thrombosis

Thrombosis
Inappropriate activation of the haemostatic process in
uninjured vasculature or formation of thrombus in the
setting of relatively minimal vascular injury
Virchow's Triad predisposing factors

Downloaded from: Robbins & Cotran Pathologic Basis of Disease

Factors predisposing to
thrombosis
Hypercoagulability

Any alteration of the coagulation pathways that

predisposes to thrombosis
Primary (genetic): Factor V and prothrombin gene
mutations most frequent

Factor V becomes resistant to protein C inactivation

Prothrombin levels elevated

Secondary (acquired)

Bed rest immobilization, obesity, cancer, atrial

fibrillation, myocardial infarction, tissue damage (surgery,
burns)

 Abnormalities of blood flow

turbulence

Endothelial injury
Local areas of stasis
Disruption of laminar flow
Moves platelets from center of
flow to the vessel wall
Prevents dilution of activated
clotting factors by flowing blood
Slows down the inflow of clotting
factor inhibitors
Promotes endothelial cell
activation

Thrombus morphology
Arterial thrombus

Begin at points of injury or areas of turbulence.

Extend in a retrograde fashion
Mural thrombi form in heart or large vessels
Lines of Zahn are indicative of arterial thrombi (adherent
masses of blood that demonstrate areas of pale alternating
with areas of red)
Arterial thrombi may or may not be occlusive

Venous thrombus

Begin in areas of stasis

Extend in a antegrade fashion
Are almost always occlusive
Contain lots of RBCs
Long - forming a cast of vein with markings on them from
venous valves

Venous Thrombi: Clinical

Venous trombus

Arterial thrombus

Arterial Thrombi Morphology

Arterial trombus

Downloaded from: Robbins & Cotran Pathologic Basis of Disease

Cardiac thrombi
Thrombi may form in any chamber of the heart on the
valve cusps
More common in the atrial appendadages, especially
right atrium, and on mitral and aortic valves called
vegetations which may be seen in infective
endocarditis and non-bacterial endocarditis
Are mural (non-oclusive) as are the mural thrombi
encountered in the aorta in atherosclerosis and in
aneurysmal dilatations

Fate of a thrombus (venous or

arterial)
Propagation: continued growth
may obstruct critical vessel.
Embolization: dislodgement of
thrombus or parts of it may
cause obstruction downstream.
Dissolution: fibrinolysis may
dissolve clot.
Organization: thrombus
induced injury leads to
inflammation and fibrosis. Recanalization may re-establish
some vascular flow

Venous thrombi fates

Effects of thrombosis

Ischemia
Congestion
Heart valve disease
DIC
Embolism

Disseminated Intravascular
Coagulation

Definition
Sudden onset of fibrin thrombi in the microcirculation
with consumption of coagulation factors and formation of
fibrin degradation products
A potential complication of any disease state/process
associated with the widespread activation of thrombin
Not usually visible grossly
readily apparent microscopically
can cause diffuse circulatory insufficiency (particularly in
the brain, lungs, heart, and kidneys)
development of the multiple thrombi rapid concurrent
consumption of platelets and coagulation proteins
(synonym consumption coagulopathy);
at the same time, fibrinolytic mechanisms are activated
bleeding disorder.

DIC
Obstetrical complications

abruptio placentae, ritention of death fetus, septic abortion,

amniotic liquid embolism

Infections

gram negative, meningococc, aspergillosis, malaria

Neoplasms

pancreatic, prostate, lung, stomach carcinoma

Sanguine disorders
promielocytic leucemia

Tissue injuries

trauma, burn, surgery

Vasculitis and vascular malformations

haemangioma, aneurysm

Varia

intravascular hemolisis, hepatopaties

Pathophysiology of disseminated intravascular

coagulation.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease

DIC

Embolism
Embolism is the process of partial or
complete obstruction of some part of the
cardiovascular system by any mass carried
in the circulation.
90% of all emboli are derived from a thrombus

Types of emboli
A. Matter
Solid detached thrombi, atheromatous material,
tissue fragments, parasites, foreign bodies
Liquid fat globules, amniotic fluid, bone marrow
Gaseous air, other gases
B. Presence of infection
Bland, when sterile
Septic, when infected
C. Source
Cardiac emboli
Arterial emboli
Venous emboli
Lymphatic emboli

D. Blood flow
Paradoxical embolism : Persistent oval hole,
embolism from the venous system can pass from the
right to the left side of the heart systemic
circulation.
Retrograde embolism: circulating emboli in the
reverse sense of blood flow - e.g. metastatic
deposits in the spine from prostate carcinoma
(through intraspinal veins which carry tumour emboli
from large thoracic and abdominal veins veins due to
increased pressure in body cavities).
Direct or ortograde embolism: emboli from the left
heart and systemic circulation reach to cerebral,
renal or splenic arteries; embolism from leg veins
reach the lung

Paradoxical emboli

arise in venous system

pass through a hole in
interventricular septum of
the heart
end up in the arterial
system (possible stroke)

Sources of artherial and venous emboli

Consequences of embolism
Obstruction of a vessel ischemia
( stroke, gangrene, swelling of the brain)
Infarction of the organ or its affected part ischaemic necrosis
in the lower limbs, spleen, brain, intestine
Septicaemia (septic emboli)
Sudden death by

massive pulmonary embolism

coronary embolism
embolism in the middle cerebral artery

Arteritis or mycotic aneurysm formation from bacterial

endocarditis
Myocardial infarction

 Pulmonary Thromboembolism
10% of hospital patients die from this (50,000/yr)
95% originate in the deep veins of the legs above knee
Saddle embolus is one that lodges at the common iliac
bifurcation
Most are asymptomatic due to small size
>60% of pulmonary arterial system blocked patients
develop sudden cardiac death, cor pulmonale, or shock
Multiple emboli may result in pulmonary hypertension

Pulmonary embolism

Consequences of pulmonary embolism

Thromboembolus in a
large pulmonary artery

Thromboembolus in small
peripheral artery

Systemic Thromboembolism
Arterial emboli
80% arise in the heart (mural thrombi).
Major lodgment sites include

lower extremities (75%)

brain (10%)
intestine, kidneys, and spleen are also targets

Consequences dependent on

size of emboli
caliber of vessel
collateral circulation
tissue sensitivity to ischemia

Other types of emboli

Fat and Marrow Embolism

Air Embolism
Amniotic Fluid Embolism
Tumor embolism - metastasis

Fat embolism

Major source is long bone fracture (bone marrow

emboli)
They develop in 90% of severe fractures
Most are asymptomatic
Consequences of significant emboli
Pulmonary insufficiency
Stroke
Anemia
Thrombocytopenia (10% fatal)

Pulmonary fat embolism

Hyperaemia
Oedema
Petechial haemorrhages
Changes of adult respiratory distress syndrome (ARDS)
Pulmonary infarction usually not a feature of fat
embolism because of the small size of globules
Routine stains: fat globules in pulmonary arteries,
capillaries and alveolar spaces appear as vacuoles
Frozen section essential for confirmation by fat stains

Sudan dyes (Sudan black, Sudan III and IV),

Oil red O
Osmic acid

Fatty emboli

Bone marrow embolus in the pulmonary circulation

Downloaded from: Robbins & Cotran Pathologic Basis of Disease

Gas embolism
Types
Air embolism:
Chest wall injury
Obstetric procedures
Angiography

Decompression sickness (caissons disease, divers

palsy)
Acute: the bends (air emboli in joints, tendons, the chokes
(lung), cerebral effects (vertigo, coma)
Chronic (avascular necrosis of bones, lung, skin involvement)

100 cc or more of air is clinically significant

Gas embolism- symptoms

Symptoms of the Bends by Frequency

Local joint pain 89%

Leg 30%
Arm 70%
Dizziness 5,3%
Paralysis 2,3%
Shortness of breath 1,6%
Extreme fatigue and pain 1,3%
Collapse 0,5%

Time of onset of symptoms

50% occurred within 30 minutes

85% occurred within 1 hour
95% occurred within 3 hours
1% delayed more than 6 hours

Gas embolism

Amniotic fluid embolism

1/50,000 deliveries
Mortality rate: 80%
Causes:
placental tears
uterine vein rupture

Micro

haemorrhages
congestion
oedema
ARDS
dilatation of right heart
amniotic fluid contents within the pulmonary microcirculation
DIC due to thrombogenic factors from amniotic fluid

Septic embolism
Causes
IV drug use
right-sided infective
endocarditis
septic thrombophlebitis
symptoms and signs of
pneumonia or sepsis.

Foreign body embolism

Caused by introduction of particulate matter into the
pulmonary arterial system
IV injection of inorganic substances:
Talc by heroin users
Elemental mercury by patients with mental
disorders

Tumor embolism
Complication of
malignancy (usually
adenocarcinoma)
Neoplastic cells
systemic venous and
pulmonary arterial system
lodge, proliferate, and
obstruct flow

Atheroemboli
(Kidney)

Septic embolus

Infarction

Infarction
Definition
Ischemic necrosis of tissue distal to an area of arterial
occlusion or in an area of obstructed venous outflow
Most result from atherosclerosis major cause of MI
and stroke
Commonly seen in

Kidney
Spleen
Lung
Intestine
Heart
Brain

Usually located beneath the tunica of the organ

Types of infarcts
By colour (reflecting the amount of haemorrhage)
red (haemorrhagic)
white (anaemic)
By presence or absence of microbial infection
septic
bland
By age:
Recent or fresh
Old or healed

Influencing Factors

Nature of vascular supply: alternative blood supply is

most important (lung and liver)

Rate of development: collateral vessels development

limits infarction.

Tissue vulnerability: neurons (3 min), heart (25 min),

connective tissue (hours)

Blood oxygen content: patients with anaemia or those

cyanotic are more susceptible.

Red (haemorrhagic) infarcts

Occur :
with venous occlusions (ovarian torsion)
in loose tissues (lung), which allow blood to collect
in the infarcted zone
in tissues with dual circulations (e.g., lung and small
intestine), permitting flow of blood from the
unobstructed vessel into the necrotic zone
in tissues that were previously congested because
of sluggish venous outflow
when flow is re-established to a site of previous
arterial occlusion and necrosis (e.g., following
fragmentation of an occlusive embolus or
angioplasty of a thrombotic lesion)

White (anaemic) infarcts

occur with arterial occlusions in solid organs with endarterial circulation where the solidity of the tissue
limits the amount of haemorrhage
Heart
Spleen
Kidney

Shape of infarct

Wedge-shape: infarct of liver, spleen, kidney, lung

Map-like shape: myocardial infarct
Segmental shape: intestinal infarct

At early stage, all infarcts are poorly defined.

The margins of both types of infarcts tend to become
better defined with time by a narrow rim of hyperemia
and/or hemorrhage attributable to inflammation at the edge
of infarct

Histopathology
Coagulative necrosis: liver, spleen, kidney, myocardium,
lung
Liquefactive necrosis: brain, pancreas
pyknosis, karyorrhexis and karyolysis can be seen
outline of original tissue can be discerned despite cells
being dead
Anaemic infarct few RBC
Haemorrhagic infarct engorgement and hemorrhage;
Secondary to infarct: hyperemia, hemorrhage,
inflammation (initially neutrophils, then macrophages),
organization
Most infarcts are ultimately replaced by scar tissue

Red Infarct
(Hemorrhagic)

White Infarct
(Anaemic)

Lung infarct
Causes

Embolism of pulmonary arteries (not always

lungs are irrigated also through bronchial
arteries)
Inadequate circulation
Chronic lung disease
Congestive heart failure

Lung infarct
Macro

Wedge-shaped (base on pleura)

Haemorrhagic
Most often in lower lobes
Fibrinous pleuritis usually covers the area
Cut surface: dark purple, may see the
blocked vessel
Old infarcts: retracted fibrous scars

Lung infarct
Micro

Coagulative necrosis of alveolar wall

Initially
Neutrophil infiltration
Intense alveolar congestion

Later

Haemosiderin
Phagocytes
Granulation tissue

Mesenteric infarct
Causes main: acute arterial obstruction:

severe atherosclerosis (often prominent at the

origin of mesenteric vessels)
aortic aneurysm
hypercoagulable states
oral contraceptive use
embolization of cardiac vegetations or aortic
atheromas.

Mesenteric infarct
Other causes

cardiac failure, shock, dehydration, or

vasoconstrictive drugs
Systemic vasculitides (polyarteritis nodosum,
Henoch-Schnlein purpura, or Wegener
granulomatosis)
Mesenteric venous thrombosis (inherited or
acquired hypercoagulable states, invasive
neoplasms, cirrhosis, trauma, or abdominal masses
that compress the portal drainage

Mesenteric infarct
Macro

Mucosal to transmural infarction

more often segmental and patchy
mucosa is hemorrhagic and may be ulcerated and
dark red or purple
the wall becomes edematous, thickened, and
rubbery
perforation may occur
Serositis, with purulent exudates and fibrin
deposition, may be prominent

Mesenteric infarct
Micro

Atrophy or sloughing of surface epithelium

Inflammatory infiltrates initially absent in acute ischemia,
but neutrophils are recruited within hours of reperfusion
Chronic ischemia fibrous scarring of the lamina propria
and, uncommonly, stricture formation
In acute phases bacterial superinfection and enterotoxin
release may induce pseudomembrane formation that can
resemble Clostridium difficileassociated
pseudomembranous colitis
When severe, there is extensive haemorrhage and
coagulative necrosis

Intestinal infarction

Arterial thrombosis/
embolism

Venous thrombosis

Nonoclussive ischemia/
Miscellaneous
-radiation injury
-volvulus
-stricture
-herniation

Cerebral infarct
localised area of tissue necrosis caused by
local vascular occlusionarterial or venous

Clinically

the signs and symptoms depend on

region(focal neurologic deficit = stroke)
significant atherosclerotic cerebrovascular
disease may produce transient ischaemic
attacks (TIA).

Cerebral infarct
Causes

Occlusion of the cerebral arteries by either thrombi

or most common cause
atherosclerosis, rarely arteritis of cranial arteries.

Embolic arterial occlusion is commonly derived

from the heart

Mural thrombosis complicating myocardial infarction

Atrial fibrillation
Endocarditis

 Other causes

Venous occlusion neoplasms (increased

predisposition to thrombosis)
Non-occlusive causes
Compression of the cerebral arteries from
outside such as occurs during herniation
Hypoxic encephalopathy

Cerebral infarct
The extent of damage depends upon:

rate of reduction of blood flow

type of blood vessel involved
extent of collateral circulation

Cerebral infarct
Macro

anaemic infarct becomes evident 6-12 hours after its

occurrence

affected area is soft and swollen

blurring of junction between grey and white matter
Within 2-3 days,infarct undergoes softening and disintegration
central liquefaction with peripheral firm glial reaction and thickened
leptomeninges, forming a cystic infarct
haemorrhagic infarct

is red
superficially resembles a haematoma
usually the result of fragmentation of occlusive arterial emboli or
venous thrombosis

Cerebral infarct
Micro
Initially

eosinophilic neuronal necrosis

lipid vacuolisation (breakdown of myelin)
infarcted area is infiltrated by neutrophils

After 2-3 days

progressive invasion by macrophages astrocytic and vascular

proliferation

Weeks to months

Macrophages clear away the necrotic debris (phagocytosis) followed

by reactive astrocytosis, often with little fine fibrosis
A haemorrhagic infarct has some phagocytes containing haemosiderin.

Cerebral infarct
3-4 months

old cystic infarct

cyst traversed by small blood vessels and
peripheral fibrillary gliosis

Small cavitary infarcts = lacunar infarcts

complication of systemic hypertension

Cerebral infarct

Liver Infarct

Kidney infarct

Acute Myocardial Infarction

Acute Myocardial Infarction
interruption of blood supply to a part of the
heart, causing necrosis of heart muscle due to
ischemia
Mechanism
Subendocardial (prologend ischemia caused by
partial occlusion of a coronary)
Transmural (complete occlusion of a major
coronary)

Common locations and regions

involved

Heart infarction

Infarction
1 to 2 days in duration

contraction
band necrosis

Infarction
is about 3 to 4 days old

Infarction
of 1 to 2 weeks in age

Old infarction

Complications of myocardial
infarction

Arrrithmias
Congestive heart failure
Cardiogenic shock
Mural thrombosis and thrmboembolism
Rupture
Cardiac aneurysm
Pericarditis
Postmyocardial infarction syndrome

Aneurism of ventricle

Rupture
of the myocardium