2022-7-25✓

Aid
1st a
✓
Pathom

Embolism and Infarction

Dr. Marwa Ali Abdulnabi

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 ‫إنسداد وعاء دموي‬

EMBOLISM
‫منفصل‬

• An embolus is a detached intravascular solid,

liquid, or gaseous 0mass that is carried by the
blood to a site distant from its point of origin.

• About 99% of all emboli represent some part

of a dislodged thrombus, hence the term
thromboembolism.
• Depending on the site of origin, emboli may
lodge anywhere in the vascular tree

5-
• The clinical outcomes are best understood
from the standpoint of whether emboli lodge
in the pulmonary or systemic circulations.
1- Pulmonary Thromboembolism

• In more than 95% of cases, venous emboli

originate from deep leg vein thrombi above
we-
=

the level of the knee. ↓

it is'm
•
Ii
It jɵssHÑÉ thrombus
into
TIMM
-

• They are carried through progressively larger

HIM # Ew
channels and pass through the right side of
=
the heart before entering the pulmonary
=
vasculature.
Embolism → occlusion → infarction
#• Depending on the
‫تحبس‬
-0
A
size of the embolus, it may
occlude the main pulmonary artery, or pass
B-
out into the smaller, branching arterioles.

#• Patient who has had one pulmonary embolus

is at high risk of having more.
-
-

not thrombus

anymore cz

It 's moving
• Most pulmonary emboli (60% to 80%) are
clinically silent because they are small.
-
.

(&w a)
• They eventually become organized and
become incorporated into the vascular wall.
 • Sudden death and0 right ventricular failure
(corpulmonale), or cardiovascular collapse
occurs when 60% or more of the pulmonary
circulation is obstructed with emboli.
99% of emboli are dislodged
thrombi
•

qg% of pulmonary
thromboemolism are a venous thrombus originating
•

from the deep

veins of the leg .

• 60-70 % of pulmonary emboli are silent cz they're small .

2- Systemic Thromboembolism
• Systemic thromboembolism refers to emboli
in the arterial circulation.

• The major sites for arteriolar embolization are

the lower extremities (75%) and the
brain(10%), the intestines, kidneys& spleen
affected to a lesser extent.
 fat
3- Fat embolism → mass

in the blood

• Microscopic fat globules can be found in the

1
circulation after fractures of long bones or
2

after soft-tissue trauma.

3- Nontraumatic disease e.g. D.M., pancreatitis
 of heart !
to the right side
• Fat embolism syndrome is characterized by
②
① pulmonary insufficiency, neurologic
③ ④
symptoms, anemia, and thrombocytopenia; it
⑤ decrease in the number of platelets in the blood

is fatal in about 10% of cases.

irritability, Restlessness, with progression to delirium or coma.

⑥
Typically, the symptoms appear 1 to 3 days after injury, with
sudden onset of tachypnea, dyspnea, and tachycardia.
rapid breathing shortness of breath
 .MN →

-:Pathogenesis
☆

• The pathogenesis of fat emboli syndrome

involves Mechanical obstruction &
Biochemical injury.
00
• Fat microemboli occlude pulmonary and
cerebral microvasculature; this occlusion is
‫ﯾﺘﻔﺎﻗﻢ‬

aggravated by platelet and erythrocyte

aggregation.
 4- Air Embolism
mass
• Gas
- bubbles within the circulation can
obstruct vascular flow (and cause distal
ischemic injury) almost as readily as
thrombotic masses can.
Air embolism
• When bubbles of air or gas within circulation obstruct vascular flow
• But how?
• 1- During labor when air forced into ruptured uterine venous sinuses.
• 2-During injury to the lung or chest wall a large vein opened & permit
entrance of air during the (–)ve pressure phase of inspiration
• A particular form of
Caisson disease
gas embolism, called
decompression sickness, occurs when

T individuals are exposed to sudden changes in

atmospheric pressure.
• Deep-sea divers and underwater construction
Workers are at risk.
NITROGEN BUBBLES
• When air is breathed at high pressure (e.
g.,during a deep-sea dive), increased amounts
of gas (particularly nitrogen) become
‫ ﯾﺬاب‬/‫ﯾﺘﺤﻠﻞ‬
dissolved in the blood and tissues.
• If the diver then ascends too rapidly, the
‫صعد‬

nitrogen expands in the tissues and bubbles

out of solution in the blood to form gas emboli
‫ُبْؤِرّي‬

that can induce focal ischemia in a number of

tissues, including00
brain and heart.
.
5-Amniotic fluid Embolism
• Grave complication of labor occur in1 in 500000 deliveries
I

• Pathogenesis:- tear in placental membrane & uterine

MMM veins with
①
infusion of amniotic fluid into the uterine vein.

If the patient survives the initial crisis, pulmonary edema typically

develops, along with (in half the patients) disseminated intravascular
coagulation (DIC), due to release of thrombogenic substances from
.amniotic fluid

https://youtu.be/JElAfDhLjTs
Pathophsiology
• 1- Embolization to the pulmonary microcirculation%a debris

¥p;
in amniotic fluid
• 2-Release of -vasoconstrictor agents e.g. PG→ reduce
pulmonary blood flow
• 3- blockage of pulmonary circulation by micro thrombi
 Clinically
I insufficiency
• Respiratory difficulties. .cyanosis
2 • vascular collapse. ↳
3 4
• may progress to convulsion, coma & death
 INFARCTION

☒⇔iñ
\ Coagulative
I
• An infarct is an area of ischemic necrosis
caused by occlusion of either the arterial
supply or the venous drainage in a particular
tissue.
TRAE
Causes of vascular obstruction
• 1- thrombus or emboli(97%-99%)
• 2- Expansile tumor,
• 3- Arterial spasm
• 4- Trapping of a viscus in a hernial sac
• 5- =
Twisting of mobile viscus
• Although venous thrombosis can cause
infarction, it more often merely induces
_
‫احتقان‬

venous obstruction and congestion.

‫مجرى جانبى‬

• Usually, bypass channels open rapidly after

the occlusion forms, providing some outflow
from the area that, in turn, improves the
arterial inflow
• Infarcts caused by venous thrombosis ‘are
more likely in organs with a single venous
outflow channel (e. g.,00
testis and ovary).
 Morphology
• Infarcts are classified on the basis of their
color (reflecting the amount of hemorrhage)
and the presence or absence of microbial

#
infection.
• Infarcts may be red (hemorrhagic) or white
(anemic) and may be either septic or bland.
‫مسبب عفنا‬
‫مصاب بفقر الدم‬ ‫رقيق‬
 ‫مسدودة‬

‫جوزة الطيب الكبد‬

sprinkle,
spray; pour;
drip
 so does

iskemiccanmg.tk
%
necrosis .

9 B
• All infarcts tend to be wedge shaped, with the
‫محتبسة‬

occluded vessel at the apex and the periphery

of the organ forming the base.

• The dominant histologic characteristic of

infarction is-_
ischemic coagulative necrosis.
^^
A infarct Iad
,
↳ G-
• 1- White infarction occur
with arterial occlusion, or
in solid organs like kidney,
spleen, heart
 • 2- Red infarction occur
I • ►With venous occlusion like
ovarian torsion
2 • ►in loose tissue e.g. lung

3 • ►Tissue with double or

anastomotic circulation e.g.
small intestine
4 • ►Congested tissue because
of sluggish venous outflow
when flow is re-established to a site of
previous arterial occlusion and necrosis (e.g.,
fragmentation of an occlusive embolus or
.angioplasty of a thrombotic lesion)
 f. A

←
Red
infants
Lung
• 3- Septic infarction occur when microbes seed an area
of necrotic tissue with abscess formation.
Histological features
• The dominant feature of infarction is ischemic coagulative necrosis (with
exception to brain)
spread
• ►The first 12-18 hours post infarction show hemorrhagic suffusion.
• ►With in 1-2 days inflammatory response develop along the margins of
infarction
• ►Gradual degradation of necrotic tissue with phagocytosis to the tissue debris
by inflammatory cells
• ►Then reparative response beginning in preserved margins (scar formation)
Liquefactive necrosis (brain)
• This is liquefactive necrosis in the brain
in a patient who suffered a "stroke"
with focal loss of blood supply to a
portion of cerebrum. This type of
infarction is marked by loss of neurons
and neuroglial cells and the formation
of a clear space at the center left
Coagulative necrosis (kidney)
• Microscopically, the renal cortex has undergone
anoxic injury at the left so that the cells appear
pale and ghost-like. There is a hemorrhagic
zone in the middle where the cells are dying or
have not quite died, and then normal renal
parenchyma at the far right. This is an example
of coagulative necrosis
Coagulative necrosis (kidney)
• Microscopically, the renal cortex has undergone
anoxic injury at the left so that the cells appear
pale and ghost-like. There is a hemorrhagic
zone in the middle where the cells are dying or
have not quite died, and then normal renal
parenchyma at the far right. This is an example
of coagulative necrosis
Coagulative necrosis (kidney)
• lMicroscopically, the renal cortex has undergone
anoxic injury at the left so that the cells appear
pale and ghost-like. There is a hemorrhagic
zone in the middle where the cells are dying or
have not quite died, and then normal renal
parenchyma at the far right. This is an example
of coagulative necrosis
2

SHOCK
3
SHOCK
4
SHOCK
2022-7-25
F. A
Pathom a

SHOCK
Dr. Marwa Ali Abdulnabi
 Shock is the final common pathway for a number of
potentially lethal clinical events.
i?£
8 *÷
1. Severe hemorrhage →
2. Extensive trauma or burns
shock
‫واسع‬

②
3. Large myocardial infarction
LMES 4. Massive pulmonary embolism
5. Microbial sepsis
‫ خمج الدم‬,‫تعفن الدم‬
 ‫ب الَّدم‬ ِ ‫ص اْن‬
ِ ‫سيا‬ ُ ‫َنْق‬

•Shock gives rise to systemic hypoperfusion, it can be caused

i¥i⇔
either by reduced cardiac output or by reduced effective
- now

circulating blood volume, and the end results are

msn.perfus.im, ③
hypotension, impaired tissue perfusion, and cellular hypoxia.
( Blood ) ( tissue
] ( cell]

head •Persistence of shock eventually causes irreversible tissue ☆

to
)
ginecrosis
!

injury and death of the patient.

b-
MORPHOLOGY of shocks

• Shock is multiorgan system failure

• brain → ischemic encephalopathy
• heart →Focal & widespread coagulative necrosis, subendocardial hemorrhage
• Kidneys→Acute tubular necrosis
• lungs→ septic shock the lungs show diffuse alveolar damage (shock lung)
• Adrenal→cortical cell lipid depletion
• GIT→ patchy mucosal hemorrhage & necrosis (hemorrhagic enteropathy)
• Liver → Fatty change, central hemorrhagic necrosis
 Types
1
• Cardiogenic result from myocardial pump failure
2 • Hypovolemic result from loss of blood or plasma

34
• Septic (endotoxic shock) cause by systemic microbial infection
• Neurogenic occur following spinal cord injury due to loss of vascular tone
5. Anaphylactic initiated by a generalized IgE mediated hypersensitivity reaction associated with
systemic vasodilatation & increase vascular permeability
 Pathogenesis of septic shock
Cardiogenic shock results from failure of the cardiac pump. This may be caused by
myocardial damage (infarction), ventricular arrhythmias, extrinsic compression
(cardiac tamponade,), or outflow obstruction (e.g., pulmonary embolism)

Hypovolemic shock results from loss of blood or plasma volume. This may be caused by.
hemorrhage, fluid loss from severe burns, or trauma

Septic shock is caused by microbial infection. Most commonly this occurs in the setting
of gram-negative infections (endotoxic shock), but it can also occur with gram-positive
and fungal infections. Notably, there need not be systemic bacteremia to induce septic
.shock; host inflammatory responses to local extravascular infections may be sufficient
 Pathogenesis of septic shock
Less commonly, shock may occur in the setting of an anesthetic accident or a spinal cord injury
(neurogenic shock), as a result of loss of vascular tone and peripheral pooling of blood

Anaphylactic shock represents systemic vasodilation and increased vascular

permeability caused by an immunoglobulin E hypersensitivity reaction . In these
situations, acute severe widespread vasodilation results in tissue hypoperfusion and
-
.cellular anoxia
-
 pdf‫هي بس هاي املذكورة بالـ‬
‫محمد القرطاس‬.‫مال د‬

Stages of shock:
①
1. Non progressive stage: during which reflex compensatory
② my

mechanisms are activated and perfusion of vital organs is

maintained.
1g It'd
← 6&-Ñ! -2

①
2. A progressive stage characterized by tissue hypo perfusion and jÑM
⇔ia⇔
-
'
.

② onset of worsening circulatory and metabolic imbalances.

①
3. An irreversible stage that sets in after the body incurred cellular and
②

.ueorosis&deatÑsI&Hs-M¥
tissue injury so severe that even if the hemodynamic defects are injury slip -1

corrected, survival is not possible.

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>
defects
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 Pathogenesis of septic shock
• Most cases of septic shock (about 70%) are caused by endotoxin-producing
gram-negative bacilli hence the term endotoxic shock .

winkers
• Endotoxines are bacterial wall lipopolysaccharids (LPS) consisting of a toxic
fatty acid (lipid A ) core common to all gram negative bacteria, and a
complex polysaccharide coat (including O antigen) unique for each species.
(analogous molecules in the walls of gram-positive bacteria and fungi can
also elicit septic shock). ②

0
③

(toxic
inner &
outer

②
①
 • Free LPS attaches to a circulating LPS- binding protein, and the complex
then binds to a specific receptor (CD14) on monocytes, macrophages, and
neutrophils.

• Engagement of CD14 resulting in profound activation of mononuclear cells

and production of potent cytokines such as IL-1 and TNF.

• These cytokines act on endothelial cells and have a variety of effects

①
including reduced synthesis of anticoagulation factors .
②producing additional cytokines (IL-6 and IL-8) that enhances the local
②_ clearance of the infection.
acute inflammatory response and improves
• At low doses , LPS predominantly activates monocytes, macrophages,
and neutrophils, it can also activate complement thereby contributing
to local eradication of bacteria.
• With moderately severe infections, and with higher levels of LPS,
( mediators ) NO
cytokine-induced secondary effectors (e.g.,Nitric oxide and
PAF of
zndary mediators
platelet-activating factor) become significant. bacterial infection are :

NO PAF

• In addition, systemic effects of TNF and IL-1 may begin to be seen,

including fever and increased production of circulating neutrophils.

- bacterial infection

test Clinical effects ofseptics-t-r-okstit.egai.tn

 11-1,TNf, 1L -618 NO PAF
• At higher levels of LPS, the same cytokine and secondary mediators, but at
high levels result in septic shock which characterized by:
I
-

1. Systemic vasodilation (hypotension).

3 - -

2. Diminished myocardial contractility

⇒ 3. widespread endothelial injury and activation, causing systemic leukocyte

÷ 4.
adhesion
(DAD)

diffuse alveolar capillary damage in the lung.

i3
,
i} ,
• The hypoperfusion resulting from the combined effects of
£-7
widespread vasodilation, myocardial pump failure, and DIC causes
multiorgan system failure that affects many organs in the body
mainly the liver, kidneys and central nervous system.
• Unless the underlying infection is rapidly brought under control, the
patient usually dies.