Circulatory Disturbances

(Disturbances of Blood and Body Fluids)

by
Dr. Irtaza Hussain Sahu
Lecturer Pathology, F.V.S

Pictures Demonstration
• Hyperaemia & Congestion
•Hemorrhage
•Thrombosis & Embolism
•Infarction & Edema
 Circulatory Disturbances
(Disturbances of Blood and Body Fluids)
Normal Fluid Homeostasis Circulatory Disturbances
Vessel wall integrity (Thrombosis or hge& shock)

Blood pressure (Congestion, oedema or shock)

Blood volume (Congestion, oedema or shock)
Protein content (Oedema)
Blood as liquid (Thrombosis, embolism,
ischaemia, infarction , gangrene
or haemorrhage & shock )
 Hyperaemia and Congestion
Definition: Each can be defined as an increase in blood
volume in a particular tissue.
Hyperaemia is an increase in blood flow in an organ or tissue due to
dilatation of arteries or arterioles i.e. active hyperaemia,
hyperaemia while congestion is
passive hyperaemia due to engorgement of veins and venules by blood.

Active Hyperaemia
Physiological Condition Pathological Condition
e.g. in skeletal &cardiac
muscles in muscular e.g. in acute inflammation
(dilatation of arteries
exercise, in splanchnic area &arterioles)
after eating.
The affected tissue is redder because of engorgement with
oxygenated blood.
 Circulatory Disturbances
(Disturbances of Blood and Body Fluids)
Normal capillaries

arteriole venule

Hyperaemia erythema

Increased inflow
e.g. exercise
&inflammation

Congestion cyanosis & hypoxia Local obstruction

(inside or outside),
congestive H F
Congestion and Hyperemia
CONGESTION AND HYPEREMIA
 Systemic Venous Congestion (Chronic
Venous Congestion)
Clinical Features of congestive heart
failure or Rt side heart failure :
1. Cyanosis (bluish discolouration) in lips and nails
due to the presence of reduced blood
(deoxygenated blood).
2. Congested pulsating neck veins due to increased
venous pressure.
3. Oedema of lower limbs due to increased venous
pressure.
4. Enlarged tender liver.
liver
 Pathological Features of Chronic Venous
Congestion in Various Organs (Liver)
1.Liver
Gross Picture: The
liver is enlarged , firm
and the cut surface
shows alternating dark
areas of congestion
with pale areas of fatty
change, giving the
Nutmeg cut surface of the liver (dark areas of
liver the nutmeg congestion alternating with pale areas of fatty
appearance. change)
Figure: Liver with chronic passive congestion and hemorrhagic necrosis. A, Central areas are red and slightly depressed
compared with the surrounding tan viable parenchyma, forming a "nutmeg liver" pattern (so called because it resembles
the alternating pattern of light and dark seen when a whole nutmeg is cut). B, Centrilobular necrosis with degenerating
hepatocytes and hemorrhage.
Nutmeg liver
 Pathological Features of Chronic Venous Congestion in
Various Organs (Liver)

Microscopic Picture of Liver in

Chronic Venous Congestion
1.The central vein in hepatic lobule
is congested as well as the
hepatic sinusoids in the central
area.
2.The central hepatocytes will
show atrophy and necrosis.
3.The mid zonal
hepatocytes may show fatty
change due to relative hypoxia.
4.The
Early CVC of liver (congestion of
peripheral hepatocytes are central vein &central hepatic
normal. sinusoids)
 Pathological Features of Chronic Venous
Congestion in Various Organs (Liver)
Hepatic Lobule

Congested central
vein & hepatic
sinusoids
Fatty change in midzonal
hepatocytes (due to relative
hypoxia)

Atrophied central hepatocytes

(due to pressure necrosis,
hypoxia & anoxia)
Normal peripheral
hepatocytes (better
nourished as they are near
the portal v &hepatic a)
Microscopically, the nutmeg pattern results from congestion
around the central veins, as seen here.
This is usually due to a "right sided" heart failure .
• Liver is divided histologically into lobules.

• The center of the lobule is the central vein.

• At the periphery of the lobule are portal triads.

• Functionally, the liver can be divided into three
zones, based upon oxygen supply.

• Zone 1 encircles the portal tracts where the

oxygenated blood from hepatic arteries enters.
•
• Zone 3 is located around central veins, where
oxygenation is poor. Zone 2 is located in between.
 Pathological Features of Chronic Venous Congestion in
Various Organs (Spleen)

A cirrhotic liver
Chronic venous congestion can cause a form of
splenic enlargement referred to as congestive
splenomegaly.
Causes of Splenic Venous Congestion:
1.Systemic or central venous congestion is
encountered in right side heart failure. It
produces moderate enlargement of the spleen
that rarely exceeds 500gms.
2.Intrahepatic causes that retard portal venous
drainage as in various forms of cirrhosis or in
bilharzial periportal fibrosis.
fibrosis These cause
striking congestive splenomegaly. The weight
of the spleen can reach to 5000gms.
3.Extrahepatic disorders that obstruct the
portal or splenic veins.
Congested and Enlarged Spleen
 Pathological Features of Chronic Venous Congestion in Various
Organs (Spleen)

2.Spleen Gross Picture: It is moderately to markedly enlarged, firm

with deep red to grey red cut surface (depending on the degree of fibrosis).
The capsule is thickened.
Microscopic Picture: The sinusoids of red pulp are dilated and engorged
with blood &their walls are thickened by fibrous tissue. Haemorrhage may
occur that will result in liberation of haemosiderin granules from haemolysed
RBCs that will undergo fibrosis with formation of fibrosiderotic nodules called
Gamma-Gandy nodules.
nodules The white pulp (lymphoid follicles) is first hyperplastic
then later becomes atrophied due to pressure by areas of hge & fibrosis.
 Pathological Features of Chronic Venous Congestion in Various
Organs (Lung)

3.Lung Gross Picture: The lungs are enlarged, heavy, firm and deep red in
colour (brown induration). Frothy blood oozes from the cut surface on squeezing.
Microscopic Exam.: The alveolar septa are thickened by congested dilated
capillaries and oedema fluid followed later by fibrosis. As a result of
microhaemorrhages, the alveoli contain oedema fluid, RBCs either intact or
haemolysed and haemosiderin laden macrophage (heart failure cells).

Congested alveolar wall

Thickened alveolar heart failure cells

septa (fibrosis)
Congested Lungs
Acute Pulmonary Congestion
Heart Failure Cells” in Alveoli“
Chronic Pulmonary Congestion
 Pathological Features of Chronic Venous Congestion in Various
Organs (Kidney)

4.Kidney
Gross Picture: The kidneys are
slightly enlarged, firm with
congested cut surface.
Microscopic Picture: the
convoluted tubule cells show cloudy
change or fatty change due to
hypoxia.

5. Other organs as brain,

adrenals stomach and intestines
also show congestion.
Hemorrhage
 Classification of Hemorrhages based on Size

• Petechiae: measure less than 3 mm. Tiny and

punctate (minute, pinpoint) 

• Purpura: measure 3-5 mm.

• Ecchymoses: greater than 1 cm to 2 cm. large

& blotchy
• Here are petechial
hemorrhages seen on
the epicardium of the
heart.
• Petechiae (pinpoint
hemorrhages)
represent bleeding
from small vessels
and are classically
found when a
coagulopathy is due
to a low platelet
count.
• They can also appear
following sudden
hypoxia.
• The blotchy areas of hemorrhage in the skin are called
ecchymoses (singular ecchymosis), or also as areas of
purpura.
• Ecchymoses are larger than petechiae.
• They can appear with coagulation disorders.
Figure: A, Punctate petechial hemorrhages of the colonic mucosa, a consequence of
thrombocytopenia. B, Fatal intracerebral hemorrhage. Even relatively inconsequential volumes
of hemorrhage in a critical location, or into a closed space (such as the cranium), can have
.fatal outcomes
Intracerebral Hemorrhage
Pericardial Hemorrhage
 Thrombosis
Definition Thrombosis: Formation of a solid or a semisolid mass
from the constituents of the blood within the vascular system within life.
Thrombus: an aggregation of blood factors primarily platelets & fibrin
with entrapment of cellular elements, frequently causing vascular
obstruction at the point of its formation
Types of Thrombi

1.Pale Thrombus 2. Red Thrombus 3.Mixed Thrombus

•In a flowing blood as in
cardiac chambers or in
arteries
•Formed mainly of platelets
•Firm pale reddish grey
•In a stagnant blood adjacent
to complete vascular
occlusion
•Formed of fibrin entrapping
RBCs, leucocytes& platelets.
•The red color is due to R.B.C
trapped in the fibrin network.
•Soft dark red and gelatinous
•In a slowly flowing blood
usually in veins & arteries
•Formed of alternating
layers of platelets and
fibrin entrapping RBCs
and leucocytes.
•Alternating red &pale
layers
 Thrombosis
Pathogenesis (Causes= Predisposing Factors)
Three primary influences predispose to thrombus formation called Virchow’s triad
Myocardial infarction or
Endothelial Injury valvulitis (cardiac chambers),
atherosclerosis, vasculitis,
hypertension, smoking,
radiation, chemical irritation
(arteries), prolonged recumbency &
inflammation (veins)
Thrombosis

Abnormal Blood Flow Hypercoagulability

Turbulence (arteries) Stasis (veins)
&(cardiac Primary causes (Genetic)
chambers) Secondary Causes (Acquired):
Atherosclerosis, aneurysm, High Risk Causes & Low Risk
dilated atria, atrial fibrillation, Causes
venous stasis, varicose veins
Figure: Normal hemostasis. A, After vascular injury, local neurohumoral factors induce a transient vasoconstriction. B,
Platelets adhere (via GpIb receptors) to exposed extracellular matrix (ECM) by binding to von Willebrand factor (vWF)
and are activated, undergoing a shape change and granule release. Released adenosine diphosphate (ADP) and
thromboxane A2 (TXA2) lead to further platelet aggregation (via binding of fibrinogen to platelet GpIIb-IIIa receptors), to
form the primary hemostatic plug. C, Local activation of the coagulation cascade (involving tissue factor and platelet
phospholipids) results in fibrin polymerization, "cementing" the platelets into a definitive secondary hemostatic plug. D,
Counter-regulatory mechanisms, such as release of t-PA (tissue plasminogen activator, a fibrinolytic product) and
thrombomodulin (interfering with the coagulation cascade), limit the hemostatic process to the site of injury.
Excessive adhesion of platelets - Blockage
Thrombosis Embolism
 Arterial Thrombi

Occlusive thrombus in wall of atherosclerotic coronary artery

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Pathogenesis of Thrombosis

2.Abnormal Blood Flow

(Turbulence & Stasis)

Iliac artery aneurysm with laminated Left atrial mural thrombus in a case of
thrombus rheumatic mitral stenosis
Venous Thrombosis
Due to stasis, hypercoagulability
&endothelial injury
 Venous Thrombosis
3.Hypercoagulability: It is any alteration of the coagulation
pathways that predispose to thrombosis.

Swollen, painful, dusky

red left lower limb

A case of deep venous thrombosis

(DVT) in a patient suffering from
systemic lupus erythematosus
 At Autopsy, post mortem clots may be
confused for venous thrombi:

Post Mortem Clots Red Thrombi

Gelatinous; red cells More enmeshed

settled by gravity
Not attached to the
underlying wall
erythrocytes, under
transection reveal vague
strands of pale gray fibrin
Firmer, almost always
have a point of
attachment

Thrombosis Embolism
Thrombotic Vegetations
Mitral Valve

Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.

Abdominal Aortic Aneurysm Thrombus
Deep Vein Thrombosis (DVT)
Plaque with Recent Thrombus
 Thrombosis
Sites of Thrombosis
in heart (atria , ventricles & on valves); in arteries ; in veins ; and in
capillaries.

Large mural thrombus on top Left atrial mural thrombus in a

of myocardial infarction case of rheumatic mitral stenosis
Sites of Thrombosis
Aortic Valve
Thrombi=vegetation
Sites of Thrombosis

Multiple thrombi on
atheromatous patches in
aorta
 The Microscopic Picture of a Thrombus
Apparent laminations called lines of Zahn are seen
formed of pale layers of platelets and fibrin that alternate
with darker layers containing more red cells.

RBCs Platelets & fibrin Platelets & fibrin RBCs

 Fate of the Thrombus
If the patient survives the
immediate effects of a
thrombotic vascular obstruction,
thrombi undergo some
combination of the following
four events
1.Propagation: the
thrombus may accumulate
more platelets and fibrin
eventually obstructing other
critical vessel.
2.Dissolution: Thrombi may 3.Embolization:
be removed by the fibrinolytic Thrombi may dislodge as
activity. thrombotic emboli.
 Fate of the Thrombus

4.Organization and Recanalization:

Thrombi may induce inflammation
and fibrosis (organization) and may
eventually recanalize.

Organization &Recanalization
(multiple capillary channels)
 Thrombosis
Outcomes

Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7 th ed., Saunders, Philadelphia, 2003.
 Consequences of Thrombosis

Acute myocardial infarct secondary to coronary artery thrombosis

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Early Organizing Thrombus
►
Thrombosis
Thrombus: an aggregation of
blood factors primarily
platelets & fibrin with
entrapment of cellular
elements, frequently causing
vascular obstruction at the
point of its formation

► Thrombosis : Formation of a
solid or a semisolid mass from
the constituents of the blood
within the vascular system
within life.

Thrombosis Embolism
 Pulmonary Thromboembolism

Embolus migrates from deep leg veins through venous system to

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pulmonary circulation
 Figure: Embolus derived from a lower extremity deep venous thrombosis and now impacted in a
pulmonary artery branch.

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 Pulmonary Thromboembolism

Saddle embolus in branching main pulmonary artery

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 Pulmonary Thromboembolism

Small pulmonary embolus in branch of pulmonary artery

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 Systemic Thromboembolism

Renal infarct secondary to systemic thromboembolism

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 Other Forms of Embolism

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Fat emboli in the lung
 Other Forms of Embolism

Kidney showing cholesterol embolism from an atherosclerotic plaque

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 Figure: Bone marrow embolus in the pulmonary circulation. The cellular elements on the left side of the embolus are hematopoietic
precursors, while the cleared vacuoles represent marrow fat. The relatively uniform red area on the right of the embolus is an early
organizing thrombus.

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 Infarction: Infarcts are areas of ischemic,
usually coagulative, necrosis caused by
occlusion of arterial supply or less
commonly venous drainage.Infarcts are
most commonly caused by formation of
occlusive arterial thrombi, or embolization of
arterial or venous thrombi.Infarcts caused by
venous occlusion, or in loose tissues with
dual blood supply, are typically hemorrhagic
(red) whereas those caused by arterial
occlusion in compact tissues are pale
(white) in color.

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 Infarction (Infarct)
Lung (Left); Spleen (Right)
Figure: Red and white infarcts. A, Hemorrhagic, roughly wedge-shaped pulmonary infarct (red infarct). B, Sharply
demarcated pale infarct in the spleen (white infarct).

Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7 th ed., Saunders, Philadelphia, 2003.
.Figure: Remote kidney infarct, now replaced by a large fibrotic scar
Pulmonary Infarction
Small Intestine Infarction
 Kidney Infarction
Replaced by Fibrotic Scar (Left)
Pale Infarct (Wedge) of Spleen
 EDEMA
• Edema = the abnormal (excess) accumulation
of fluid in interstitial tissue spaces or in body
cavities.
• Edema fluid is outside both the vascular fluid
and cellular fluid compartments (i.e. within
interstitium).
 EDEMA
• Gross appearance;
• Pale (Color is less intense)
• Watery appearance (Incision results flow of
edematous fluid from the cut surface)
• Subcut. tissue jelly like appearance.
• Pits on pressure
• Fibrosis
• Microscopic appearance;
• Enlarged intracellular spaces, faint pink staining
fluid.
• Atrophy.
Figure 4-1 Variables affecting fluid transit across capillary walls. Capillary hydrostatic and osmotic forces are normally balanced so
that there is no net loss or gain of fluid across the capillary bed. However, increased hydrostatic pressure or diminished plasma
osmotic pressure leads to a net accumulation of extravascular fluid (edema). As the interstitial fluid pressure increases, tissue
lymphatics remove much of the excess volume, eventually returning it to the circulation via the thoracic duct. If the ability of the
lymphatics to drain tissue fluid is exceeded, persistent tissue edema results.
Figure: Pathways leading to systemic edema due to primary heart failure, primary renal failure, or reduced plasma osmotic
pressure (e.g., from malnutrition, diminished hepatic synthesis, or protein loss due to the nephrotic syndrome). ADH,
antidiuretic hormone; GFR, glomerular filtration rate.
Edema
Normal alveoli
 Pulmonary Edema

This is the alveolar spaces filled with extravasated fluid from the congested blood vessels. This is typically seen in
the setting of left ventricular failure where blood is not efficiently pumped out of the heart and therefore is gets
.backed up in the lungs. The lungs fill with this fluid and will be 2-3 times their weight
 Fluid in Trachea/Bronchi

When this becomes overwhelming for the small alveolar spaces we see fluid coalesce into froth in the airways. The
froth is a mixture of air, edema fluid and sometimes can have extravasated rbcs so the froth can sometimes be pink.
 Abdominal Ascites

Again we see large amounts of accumulated fluid into the abdomen and we can see these large engorged
blood vessels that have an enormous amount of hydrostatic pressure in the abdomen. Called caput medusa
as most of these patients have blood vessels coalescing around the navel giving it a snake head appearance.
 Edematous Brain

When the edema of the brain is generalized either due to infection like encephalitis, trauma,
obstruction to normal venous blood outflow we see the brain becomes grossly swollen with
narrowed sulci and distended gyri. The brain takes on a flattened appearance as it presses
against the unyielding skull.
 Normal Brain

This is a normal brain with normal ridges called gyri and distinct depressions called sulci
Shock: Shock causes systemic hypoperfusion due to •
either reduced cardiac output or reduced circulating
blood volume.The most common causes of shock are
cardiogenic (cardiac pump failure due, for example, to
myocardial infarction), hypovolemic (due, for example, to
blood loss), and sepsis (due to infections).Septic shock
results from the host innate immune response to
bacterial or fungal cell molecules (most commonly
endotoxin), with systemic production of cytokines, such
as TNF and IL-1, that affect endothelial and inflammatory
cell activation.Hypotension, DIC, and metabolic
disturbances constitute the clinical triad of septic
shock.Shock of any form causes pathology by inducing
.prolonged tissue hypoxic injury