Hemodynamic Disorders, Thromboembolic disease, and Shock

By Dr.Haftom G.(MD)

04/17/2024 1
HEMODYNAMIC DISORDERS, THROMBOSIS, & SHOCK

1. Edema
- Definition, causes, & morphology
2.Hyperemia & congestion
- Definition & morphology
3 Hemorrhage
- Definitions of terms like hematoma, petechiae, purpura,
hemothorax, etc…
- Clinical significance
4.Hemostasis & thrombosis
- Normal hemostasis
- Thrombosis- Pathogenesis, morphology of thrombi, fate of
thrombus, clinical significance
5. Disseminated intravascular coagulation
6. Embolism- Definition, pulmonary thromboembolism, systemic
thromboembolism. fat embolism, air embolism, & amniotic fluid embolism
7.Infarction- Definition, types of infarct, factors that influence the
development of an infarct
8. Shock- Types, Pathogenesis of septic shock, stages of shock,
morphology. clinical course.
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Edema

- Approximately 60% lean body weight is

water, 2/3 of which are intracellular with
remainder in extracellular compartment
(most in the interstitial space)

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- Increased fluid in interstitial tissue spaces
or fluid accumulation in the body cavities
in excessive amount is called edema

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Depending on the site, fluid accumulation
in body cavities can be variously
designated as:
a) Hydrothorax(pleural effusion) –pleural cavity
b) Hydropericardium –pericardial cavity
c) Hydroperitoneum (ascites) – peritoneal cavity
d) Ansarca – is a severe & generalized edema of
the body with profound subcutaneous swelling

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There are two types of edema
 Inflammatory edema / Exudate
 Non inflammatory edema /Transudate
- Inflammatory edema are largely related to
local increases in vascular permeability

- Non inflammatory causes of edema occur

in hydrodynamic derangements

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Noninflammatory edema
- There are four primary forces that
determine fluid movement across the
capillary membrane. Each of them
categorized under two basic categories,
the hydrostatic pressure & the oncotic
pressure.
- These four primary forces are known as
STARLING FORCES

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1. The capillary hydrostatic pressure (Pc)
Which tends to force fluid outward from
the intravascular space through the
capillary membrane to the interstitium.

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2. The interstitial fluid hydrostatic
pressure (Pif)
Which tends to force fluid outward from
the interstitial space to the intra vascular
space.

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3. The plasma colloid osmotic pressure
(Пp)
- Which tend to cause osmosis of fluid in
ward through the capillary membrane
from the interstitium.

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4. The interstitial fluid colloid osmotic
pressure(Пif) - Which tend to cause
osmosis of fluid outward through the
capillary membrane to the interstitium.

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- Normally the exist of fluid into the
interstitium from the arteriolar end of the
microcirculation is nearly balanced by
inflow at the venular end; a small
residuum of excess interstitial fluid is
typically drained by the lymphatics .

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Pathophysiologic categories of edema
1. Increased hydrostatic pressure
- Local increase in venous pressure may result
from impaired venous outflow eg deep venous
thrombosis in lower extremities

- Generalized increases in venous pressure

occur most commonly in congestive heart
failure affecting right ventricular cardiac
function.
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In congestive heart failure, reduced
cardiac output translates into reduced
renal perfusion.
Renal hypoperfusion in turn triggers the
renin-angiotensin-aldosterone axis,
inducing sodium and water retention by
the kidneys (secondary aldosteronism)

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Cirrhosis: Fibrous scarring of the liver
that impairs return of blood through the
portal vein, thereby increasing venous
pressure in portal vein tributaries and
causing fluid to leak into the peritoneal
cavity.

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2.Reduced plasma osmotic pressure
It can result from excessive loss or reduced
synthesis of albumin (serum protein most
responsible for maintaining colloid osmotic
pressure).
 Nephrotic syndrome

 Protein malnutrition

 Diffuse liver pathology (cirrhosis)

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 Decreased production of albumin by
the liver (e.g., in cirrhosis or other forms
of generalized liver damage)

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 Increased loss of protein by the kidney
(e.g., certain glomerular diseases) or in
the gut (e.g., protein-losing
gastroenteropathy)

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3. Lymphatic obstruction
- Impaired lymphatic drainage leads to localized
edema – lymphedema
- It can result from inflammatory or neoplastic
obstruction
 Filariasis causes massive lymphatic & lymph node
fibrosis in the inguinal region resulting in edema of
the external genitalia & lower limb – Elephantiasis
 Axillary Lymph node infiltrated by cancer
removed by surgery or irradiatd leads to edema of
upper extremity
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In carcinoma of breast , infiltration &
obstruction of superficial lymphatics can
cause edema of the overlying skin , giving
rise to the so called peau d’orange (orange
peel) appearance . It results from an
accentuation of depressions in the skin at
the site of hair follicles.

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4. Sodium & water retention
- Salt retention can be a primary cause of
edema.
- Increased salt , with obligate accompanying
water , causes both increased hydrostatic
pressure & diminished vascular colloid
osmotic pressure.
- Salt & water retention can occur with any
acute reduction of renal function including
glomerulonephritis & acute renal failure.
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Morphology of edema
- Edema is most easily recognized grossly
- Microscopically it manifests only as
subtle cells swelling with clearing &
separation of extracellular matrix.
- Edema is most commonly encountered in
subcutaneous tissues, the lungs & the
brain

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Subcutaneous edema
- It can be diffuse or can be more prominent
at sites of high hydrostatic pressures.
- Edema distribution typically influenced
by gravity is called dependent
- Dependent edema is a prominent feature
of congestive heart failure, particularly of
the right ventricle

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Edema as a result of renal dysfunction or
nephrotic syndrome is more severe &
affects all parts of the body equally.
Initially it may affect tissues with loose
connective tissue matrix (periorbital
edema).

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Finger pressure over edematous
subcutaneous tissue displaces the
interstitial fluid & leaves a finger-shaped
depression - pitting edema

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Pulmonary edema
- It is most typically seen in the setting of
left ventricular failure but it can also be
seen in renal failure, , acute respiratory
distress syndrome, pulmonary infections
& hypersensitivity reactions.

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Grossly, the lungs are two or three times
their normal weight
Microscopically , alveoli filled with
frothy, blood-tinged fluid

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Brain edema
- It can be localized or generalized
- Localized (eg abscess or neoplasm),
generalized (eg encephalitis or
hypertensive crisis)
- With generalized edema, the brain is
grossly swollen, with narrowed sulci &
distended gyri.

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Clinical correlation
- The site of edema determines the clinical
significance
- Subcutaneous tissue edema is important
primarily because it signals underlying
disease. When significant, it can impair
wound healing

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- Pulmonary edema can cause death by
interfering with normal ventilatory
function.
- Brain edema is serious because if severe
the brain can herniate.

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Hyperemia and Congestion
- Both indicate an increased volume of
blood in a particular tissue

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Hyperemia
- Is an active process resulting from an
increased or augmented tissue inflow
because of arteriolar vasodilation
- Affected tissues become red
- Occur in exercising skeletal muscle or
acute inflammation commonly

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Congestion
- is a passive process resulted from
impaired out flow from a tissue.
- Occur systemically as in cardiac failure or
locally in isolated venous obstruction
- Affected tissue appear blue - red
(cyanosis) due to accumulation of
deoxygenated blood

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- Congestion & edema commonly occur
together

- In long standing congestion, the stasis of

poorly oxygenated blood causes chronic
hypoxia, which can result in parenchymal
degeneration or death

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Capillary rupture at the sites of
congestion may also cause small foci of
hemorrhage; break down & phagocytosis
of the red cells can result in small clusters
of hemosiderin-laden macrophages.

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In severe long standing hepatic
congestion (most commonly associated
with heart failure), hepatic fibrosis may
develop (cardiac cirrhosis)

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Hemorrhage
Definition:
- Extravasations of blood outside the blood
vessel

- Hemorrhage from large vessel is due to

vascular injury including trauma,
atherosclerosis, or inflammatory or
neoplastic erosion of the vessel wall
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An increased tendency to hemorrhage
from usually insignificant injury is seen in
clinical disorders called hemorrhagic
diathesis
 Fragility of blood vessels
 Platelet deficiency or dysfunction
 Coagulation disorders

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Hemorrhage can manifest in variety of
patterns depending on size, extent &
location of the bleeding

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-Hemorrhage may be external or interanal
Hematoma- accumulation of blood within a
tissue . It can be trivial (bruise) or life
threatening (retroperitoneal hematoma)

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- Petechiae – Minute 1 to 2 mm
hemorrhages to skin , mucous membranes
or serosal surfaces
- usually due to low platelet count
(thrombocytopenia)

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- Purpura- larger hemorrhages (>3mm )
that may be associated with same causes
as petechiae or also may occur secondary
to trauma, vascular inflammation
(vasculitis).

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- Ecchymosis – larger (> 1 to 2 cm)
subcutaneous hematoma & are
characteristically seen after trauma

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- Large accumulation of blood can occur in
body cavities & are called hemothorax,
hemopericardium, hemopertonium or
hemarthrosis

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Clinical significance
- Volume of bleeding

Loss of 40% or more of blood volume, or (about

2000 mL) can result in hypovolumic shock.
- Rate of bleeding
- Site of bleeding

(For example, a cut in the skin that causes 250 mL

of blood loss is usually not clinically significant
(the average blood donation is about 450 mL), but
a 5-mL hemorrhage in the brainstem can be fatal).

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Chronic & recurrent external blood loss
(eg peptic ulcer) leads to loss of iron &
subsequent iron deficiency anemia

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Hemostasis & thrombosis
- Normal hemostasis is the result of a set of
well- regulated processes that accomplish
two important functions
They maintain blood in a fluid , clot-free state
in normal vessels
They induce a rapid & localized hemostatic
plug at a site of vascular injury

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- Thrombosis is inappropriate activation of
normal hemostatic processes such as
formation of a blood clot (thrombus) in
uninjured vasculature or after minor
injury.

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- Both hemostasis & thrombosis are
regulated by three components
◦ Vascular wall
◦ Platelets
◦ Coagulation cascade

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- Whenever a vessel is ruptured or severed,
hemostasis is achieved by several
mechanisms:
A. After initial injury, there is brief period of
vasoconstriction
B. Formation of platelet plug –primary
hemostatic plug
C. Formation blood clot as a result of blood
coagulation –secondary hemostatic plug
D. Eventual growth of fibrous tissue in to the
blood clot to close the hole in the vessel
permanently
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Thrombosis
Pathologic coagulation of blood resulting
in the formation of a solid mass within a
chamber of the heart or within a blood
vessel

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- Three primary factors predispose to
thrombus formation –Virchow triad

 Endothelial injury
 Stasis or turbulence of blood flow
 Blood hypercoagulability

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Endothelial injury
- It is particularly important for thrombus
formation occurring in heart or in arterial
circulation

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- Physical loss of endothelium will lead to
exposure of subendothelial ECM ,
adhesion of platelets, release of tissue
factor & local depletion of prostacyclin.

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- Eg thrombus formation following
endocardial injury due to myocardial
infarction , ulcerated atherosclerotic artery
or at sites of traumatic or inflammatory
vascular injury.

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- But dysfunctional endothelium also may
lead to thrombosis

- As in case of hemodynamic stresses of

hypertension or bacterial endotoxin ,
hypercholesterolemia, products of cigarette
smoke

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Alterations in normal blood flow
- Turbulence results in arterial & cardiac
thrombosis by causing endothelial injury
or dysfunction

- Stasis is major factor in development of

venous thrombosis

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- Normal blood flow is laminar, such that
platelets flow centrally in the vessel
lumen, separated from the endothelium by
a slower moving clear zone of plasma.

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- Stasis and turbulence therefore:
◦ Disrupt laminar flow and bring platelets into
contact with the endothelium
◦ Prevent dilution of activated clotting factors
by fresh-flowing blood
◦ Retard the inflow of clotting factor inhibitors
and permit the buildup of thrombi
◦ Promote endothelial cell activation, resulting
in local thrombosis, leukocyte adhesion, etc

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Eg –
- Atherosclerotic plaque
- Aortic or arterial aneurysms
- Myocardial infarction
- Mitral valve stenosis
- Hyperviscosity syndrome (polycythemia
vera )

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Hypercoagulability
- It is defined as any alteration of the
coagulation pathways that predisposes to
thrombosis
- The causes of hypercoagulabilty can be
primary (genetic) or secondary (acquired)

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Of inherited causes of
hypercoagulability , mutation in factor V
gene & prothrombin gene are the most
common causes

- A specific factor V mutation called Leiden

mutation makes the protein resistant to
protein C mediated inactivation
- In these patients, recurrent deep venous
thrombosis is common
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Prothrombin gene mutation: Causes an
elevated level of prothrombin. Patients
with the prothrombin gene mutation have
a threefold risk of having venous
thromboses. The incidence is 1–2% of the
general population.

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Inherited causes of hypercoagulabilty
must be considered in patients under the
age of 50 who present with thrombosis in
the absence of any acquired
predisposition.

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Secondary (acquired) causes
- Unlike the hereditary disorders, the
pathogenesis of acquired thrombotic
diatheses is frequently multifactorial and
is therefore more complicated

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High risk for thrombosis
- Prolonged bed rest or immobilization
- Myocardial infarction
- Atrial fibrillation
- Tissue damage (surgery, fracture, burns)
- Cancer
- Prosthetic cardiac valves
- Disseminated intravascular coagulation
- Antiphospholipid antibody syndrome
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Lower risk for thrombosis
- Cardiomyopathy
- Nephrotic syndrome
- Hyperestrogenic states (pregnancy)
- Oral contraceptive use
- Smoking

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Morphology of thrombi
- Thrombi may develop any where in the
cardiovascular system (e.g., in cardiac
chambers, on valves, or in arteries, veins, or
capillaries). .
- Thrombi are of variable size and shape
depending on their origin and cause

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Arterial or cardiac thrombi usually begin
at a site of endothelial injury (eg
atherosclerotic plaque) or turbulence
(vessel bifurcation)

Venous thrombi characteristically occur in

sites of stasis.

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Arterial thrombi Venous thrombi
Arise at the site of endothelial injury Arise at area of stasis
Grow in a retrograde fashion, against Grow in the direction of
blood flow from its site of attachment flow towards the heart
They are usually occlusive Almost invariably occlusive
Has firm attachment Has loose attachment i.e, why
propagating tail may
Undergo fragmentation.

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-The most common site of arterial thrombi
in descending order are:
o Coronary arteries
o Cerebral arteries
o Femoral arteries
- They are typically a friable meshwork of
platelets, fibrin, erythrocytes, and
degenerating leukocytes.

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- Venous thrombi most commonly affects
the veins of lower extremities (90% of
cases)

- Because these thrombi form in the

sluggish venous circulation, they also tend
to contain more enmeshed erythrocytes
and are therefore called red, or stasis,
thrombi
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Fate of Thrombus
- If a patient survives the initial thrombotic
vascular obstruction, in the ensuing days
or weeks thrombi undergo some
combination of the following four events:

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Propagation
- The thrombus may accumulate more
platelets and fibrin, propagating to cause
vessel obstruction

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Embolization
- Thrombi may dislodges and travel to
other sites in the vasculature

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 Dissolution
- Thrombi may be removed by fibrinolytic
activity
- Commonly occur in recent thrombi

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 Organization and recanalization
-Organization refers to the in-growth of
endothelial cells, smooth muscle cells, and
fibroblasts into fibrin rich thrombus

- Organization accompanied by the formation

of capillary channels across the thrombus,
re establishing lumen continuity to some
extent. This is known as recanalization

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Clinical correlations
Thrombi are significant clinically in that:
- They cause obstruction of arteries and
veins
- They are possible source of emboli

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Venous Thrombosis
(phlebothrombosis)
- Venous thrombosis affects veins of the
lower extremity in 90% of cases

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A) Superficial venous thrombosis
- Usually occur in saphenous system
particularly when there are varicosities
- cause local edema, pain, and tenderness,
become symptomatic but rarely embolize
- Local edema due to impaired venous
drainage , predispose the involved overlying
skin to infection after slight trauma
developing a condition known as varicose
ulcer.
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 B)Deep venous thrombosis
- Are more serious as they may embolize
- Usually start in the larger veins at or
above knee (e.g., popliteal, femoral, and
iliac veins).
- Asymptomatic in approximately 50% of
patients, since deep venous obstruction
rapidly offset or relieved by collateral
bypass channels.
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Conditions associated with DVT
- Trauma, surgery, burns result in

a: Reduced physical activity leading to

stasis
b: Injury to vessels
c: Release of procagulant substance from
the tissue
- Pregnancy & puerperal state increase
coagulation factors & reduced synthesis of
antithrombotics
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- Malnutrition, debilitating conditions and
wasting diseases such as cancer

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Arterial & cardiac thrombosis

- Atherosclerosis is major initiator of

thrombosis related to abnormal vascular
flow & loss of endothelial integrity
- Myocardial infarction is related to dyskinetic
contraction of the myocardium as well as
damage to the adjacent endocardium &
cardiac mural thrombi can arise.
- Rheumatic heart disease may result in atrial
mural thrombi due to mitral valve stenosis
followed by left atrial dilation
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- In addition to obstructive features, arterial
thrombi may embolize to any tissue, but
particularly common in the brain, kidney,
spleen because of their large volume of in
flow of blood.

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Disseminated intravascular coagulation (DIC)

- It is an acute or chronic
thrombohemorrhagic disorder occurring
as a result of progressive activation of
coagulation pathway beyond physiologic
set point secondary to a variety of
diseases resulting in failure of all
components of hemostasis, hence the
other term for DIC is consumption
coagulopathy.

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Etiology & pathogenesis
- DIC is not a primary disease but
coagulopathy that occurs in the course of
variety of clinical conditions .
- It may result from pathologic activation of
extrinsic and/or intrinsic pathways of
coagulation or impairment of clot
inhibiting influences

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Two mechanisms that trigger DIC
 Release of tissue factor or thromboplastin
 Widespread injury to the endothelial cells

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Major disorders associated with DIC
Acute
Obstetric complication
 Placental abruption
 Septic abortion
 Retained dead fetus
 Amniotic fluid embolism
 Toxemia/ preeclampsia

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Infections
- Gram negative sepsis
- Meningococcemia
- Malaria
Burn, accidental trauma
Chronic
- Neoplasms
- Chronic illness

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Clinical course
- The consequences of DIC are two fold.
- First, there is widespread deposition of
fibrin within the microcirculation . This
may lead to ischemia of more severely
affected or more vulnerable organs &
hemolytic anemia resulting from
fragmentation of red cells as they squeeze
through narrowed microvasculature
(microangiopathic hemolytic anemia)
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Second , hemorrhagic diathesis may
dominate the clinical picture because of
consumption of platelets & clotting
factors & increase in fibrinolysis

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clinical presentation varies with stage & severity of the syndrome.

• The onset may be fulminant as endotoxic

shock, amniotic fluid embolism
• Chronic in case of carcinomatosis or
retention of dead fetus
• So Overall 50% of patients with DIC are
obstetric patients & about 33% of patients
have carcinomatosis

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- Clinically they may present:

- hemorrhage from multiple sites, usually from surgical incision

, vein punctures or catheter sites

- Respiratory symptoms such as dyspnea, cyanosis may occur

- convulsion & coma in case of CNS bleeding

- acute renal failure with oligouria
- less often they may present with acrocyanosis, pre gangrenous
changes in the digits, genitalia & nose areas where blood flow
is markedly decreased
- Circulatory failure may appear suddenly & may be
progressing

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Laboratory manifestations include
-Thromobcytopenia secondary to platelets
aggregation in the thrombus,
-Schistocytes or fragmented RBCs,
- Prolonged PT, PTT
- Reduced fibrinogen from depleted
coagulation proteins & increased fibrin
degradation product (FDP) from intense
fibrinolysis.
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Embolism
Definition
- An embolism is a detached intravascular
solid, liquid or gaseous mass that is
carried by blood to sites distant from its
point of origin.

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- Thrombus is source of emboli in 99% of
cases

- Rare forms of emboli include fat

globules & bubbles of air, amniotic fluid,
infected foreign material, bits of bone
marrow, platelets aggregates, fragment of
material from ulcerating atheromatous
plaque or fragment of a tumor
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- Emboli lodge in vessels too small to
permit further passage , resulting in a
partial or complete vascular occlusion.
The potential consequence of this is the
ischemic necrosis of distal tissue known
as infarction

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Depending on site of origin, emboli may
lodge in the pulmonary or systemic
circulations.

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Pulmonary thrombembolism
- In more than 95% of instance venous
emboli originate from deep leg vein
thrombi
- The effect of pulmonary embolism
depends on the size of the embolus and on
the state of pulmonary circulation

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- A large thrombus may become detached
enmass & block the out flow tract of the right
ventricle, the main pulumonary trunk, i across
the bifurcation, also called saddle embolus or
both of its branches causing sudden death,
right side heart failure (cor pulmonale) or
cardiovascular collapse occur when 60% or
more of the pulmonary circulation is
obstructed with emboli.

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- Most pulmonary emboli i.e around 60-
80% are clinically silent because they are
very small.

- They eventually become organized and

become incorporated into the vascular
wall.

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- Embolic obstruction of medium sized
arteries manifest as pulmonary
hemorrhage but usually does not cause
infarction because dual blood inflow to
the area from bronchial circulation.

- But in the presence of left side heart

failure, infarction could occur.

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Embolic obstruction of small end-
arteriolar pulmonary branches usually
does result in associated infarction

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Systemic thromboembolism
- Emboli travelling within arterial circulation
- Most (80%) arise from intra cardiac mural
thrombi,
- two third of which are associated with left
ventricular wall infarcts
- quarter with dilated left atria secondary to
rheumatic valvular heart disease
- The remainder from aortic aneurysm,
thrombi on ulcerated athrosclerotic plaques
or fragmentation of valvular vegetation
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Unlike venous emboli, which tend to
lodge primarily in one vascular bed (the
lung), arterial emboli can travel to a wide
variety of sites

The major sites for arteriolar

embolization are the lower extremities
(75%) & the brain (10%), with the rest in
the intestines, kidney & spleen
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In general, arterial embolization causes
infarction of the affected tissues
downstream of the obstructed vessel.

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Crossed embolism
Crossed or paradoxical embolism occurs
in the presence of interatrial or
interventricular defect (eg ventricular
septal defect) when an embolus is
transferred from the right to the left side
of the heart, then to systemic circulation.

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Fat Embolism
- Usually follows fracture of long bones
and other type of tissue injury, globules of
fat frequently enter the circulation.

- Fat enters the circulation by rupture of the

marrow vascular sinusoids or rupture of
venules in injured tissues.

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- Fat embolism syndrome typically being 1
to 3 days after injury during which the
raised tissue pressure caused by swelling
of damaged tissue forces fat in to marrow
sinosoid & veins.

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- Clinical features includes
- sudden onset of dyspnea, blood stained
sputum, tachycardia, mental confusion with
neurologic symptoms including irritability &
restlessness, sometime progress to delirium &
coma

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Air embolism
- Gas bubbles within the circulation can
obstruct vascular flow and cause distal
ischemic injury almost as readily as
thrombotic masses

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Air may enter the circulation during:
• Obstetric procedures
• Chest wall injury
• In deep see divers & under water
construction workers
• Neck wounds penetrating the large veins
• Cardio thoracic surgery.
• Arterial catheterization & intra venous
infusion.
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Generally, in excesses of 100cc is
required to have a clinical effect and
300cc or more may be fatal

The bubbles act like a physical

obstructions and may coalesce to form
frothy mass sufficiently large to occlude
major vessels

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The commonest symptoms are muscle
cramps (bends)[ following formation of
gas bubbles in skeletal muscle],
Cough (chokes) and dysnea

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Amniotic fluid embolism
- It is a grave but uncommon,
unpredictable complication of labor which
may complicate vaginal, caesarean
delivery and abortions.
- It has mortality rate over 20%

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- The amniotic fluid containing fetal
material enters maternal circulation via
tear in the placental membranes or
ruptured uterine veins

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- The onset is characterized by sudden
severe dyspnea, cyanosis, shock followed
by seizure & coma of the laboring
mother.
- If patient survives the initial crisis
pulmonary edema typically develops & in
50% cases they will develop DIC due to
fetal material activation of the
coagulation cascade.
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The classic finding is or are the presence
of:
- Squamous epithelial cells in pulmonary
microcirculation shed from fetal skin.
- Lanugo hair
- Fat from vernix caseosa.

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Infarction
Definition
- An infract is an area of ischemic necrosis
caused by occlusion of either the arterial
supply or venous drainage in a particular
tissue

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- Nearly 99% of all infarcts result from
thrombotic or embolic events & almost all
result from arterial occlusion

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- Other mechanism include
• Local vasospasm
• Expansion of atheroma due to hemorrhage in
to athermotous plaque.
• External compression of the vessels. e.g
trauma
• Twisting of vessels as in sigmoid volvulus or
ovarian torsion
• Entrapment of vessels at hernial sacks etc
traumatic vessel rupture
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- Infarction caused by venous thrombosis
are more likely to occur in organs with
single venous outflow channels, such
testis & ovary.

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Types of infarcts
Infarcts are classified deepening on:
A) The basis of their color (reflecting the amount
hemorrhages)
1] Hemorrhagic (red)
2] white(anemic)
B) The presence or absence of microbial
infection
1] Septic
2] Bland
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Red infarcts
It occurs
1) Venous occlusions as in ovarian torsion
2) In loose tissues such as lung which allow blood to
collect in infarcts zone.
3) Tissues with dual circulations (eg. lung),permitting
flow of blood from unobstructed vessel in to
necrotic zone.
4) In tissues that were previously congested because
of sluggish out flow.
5) When flow is re established to a site of previous
arterial occlusion & necrosis
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B. White infarcts
- It occurs in arterial occlusion in solid
organs with end-arterial circulation such
as heart, spleen, kidney

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Morphology
Gross
- All infarcts tend to be wedge shaped, with
the occluded vessel at the apex and the
periphery of the organ forming the base.

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Inflammatory response begins to develop
within a few hours and is usually well
defined within 1 to 2 days.

Eventually the inflammatory response is

followed by a reparative response
beginning in the preserved margins.

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In stable or labile tissues, parenchymal
regeneration can occur at the periphery
However, most infarcts are ultimately
replaced by scar

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Microscopy
- The dominant histologic feature of
infarction is ischemic coagulative
necrosis. The brain is an exception to this
generalization, where liquifactive necrosis
is common

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- Septic infarctions occur when bacterial
vegetations from a heart valve embolize
or when microbes seed in area of necrotic
tissue

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Factors that determine the size &
development of an infract
A. The nature of vascular supply
- The presence of dual blood supply as it
occur in the lung, liver, hand & forearm
may offset the occurrence of infarction
rapidly unlike renal & splenic circulation,
which have end arterial supply.

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B: Rate of development occlusion: slowly
developing occlusions are less likely to
cause infraction since they provide time
for the development of collaterals.

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C: Vulnerability or susceptibility to
hypoxia
- The susceptibility of a tissue to hypoxia
influences the likelihood of infarction.
- Eg Neurons undergo irreversible damage
when deprived of their blood supply for only 3
to 4 minutes.
- Myocardial cells dieafter 20-30min of
ischemia
- Fibroblasts are more resistant
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D: Oxygen content of blood
- The partial pressure of oxygen in blood
determines the outcome of vascular
occlusion

- E.g Partial obstruction of the flow of

blood in an anemic or cyanotic patient

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Shock
-is a state in which diminished cardiac
output or reduced effective circulating
blood volume impairs tissue perfusion
and leads to cellular hypoxia

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 Reduced blood
Diminished CO volume

Decreased tissue
perfusion

Tissue hypoxia

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Shock can be grouped into
Cardiogenic shock
Hypovolumic shock
Shock associated with systemic inflammation

Neurogenic shock
Anaphylactic shock

Less common cause

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04/17/2024 157
Hypovolumic shock
Definition:
Reduction in circulating blood volume
which result in reduction in preload lead
to inadequate left ventricular filling
culminating in decreased cardiac output

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Causes of hypovolumic shock include
◦ hemorrhage
◦ fluid loss from burns
◦ severe diarrhea & vomiting

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Cardiogenic shock
- It results from myocardial pump failure
(severe depression of cardiac performance)

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Causes
Myopathic
a) Acute myocardial infraction
b) Mycocarditis
c) Dilated cardiomyopathy/hypertrophic
cardiomyopathy
d) Myocardial depression in septic shock

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Mechanical
i) Intra cardiac
a) Left ventricle outflow obstruction
eg. Aortic stenosis, hypertrophic
cardiomyopathy
b) Reduction in forward cardiac out put
e.g. Aortic regurgitation, MR
c) Arrhythmia

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ii, Extra cardiac
- It is an obstructive shock
a) Pericardial tamponade (gross fluid accumulation
in the pericardial space) results in a decreased
ventricular diastolic filling → ↓CO
b) Tension pneumothorax (gas accumulation in
pleural space)
- Decrease venous return by creating a positive
pressure.
c) Acute massive pulumonary embolism.
Occupying 50-60% of pulumonary vascular
bed.
d) Severe pulmonary hypertension
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Distributive shock
Definition:
- Refers to a group of shock sub types caused
by profound peripheral vasodilatation
despite normal or high cardiac output
Cause:
- Septic shock
- Anaphylactic shock
- Neurogenic shock

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Septic shock
Definition: a kind of shock caused by
systemic microbial infection, most
commonly by gram negative infection
(end toxic shock ) but can also occur with
gram positive or fungal infections.

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Or
Sepsis with
1] Hypotension, arterial blood pressure
less than 90mmHg
2] Organ dysfunction
3] Unresponsive to fluid administration

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Neurogenic shock
- Shock may occur in setting of anesthetic
accident or spinal cord injury due to loss
of vascular tone & peripheral pooling of
blood

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Anaphylactic shock
- It is initiated by a generalized Ig-E
mediated hypersensitivity response , is
associated with systemic vasodilation &
increased vascular permeability

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Clinical course of shock
• Patient may manifest with a weak and
rapid pulse, tachypenia & cool, clammy,
cyanotic skin. In septic shock, skin
initially be warm & flushed because of
peripheral vasodilation. The patient may
present with confusion, restlessness,
decrease in urine out put, coma and death.

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- The prognosis varies with the origin of
shock & its duration.
- 80-90% of young patients with
hypovolumic shock survive where as
cardiogenic shock & septic shock carry
mortality rate up to 75%

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