Pathology Chapter 4
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Transcript Pathology Chapter 4
Pathology – Chapter 4
60% of lean body weight is water
Two thirds of the body's water is intracellular
Remainder is in extracellular compartments
About 5% of total body water is in blood plasma
Movement of water and low molecular
weight solutes (salts)
Between the intravascular and interstitial spaces
Controlled primarily by opposing effect of:
Vascular
hydrostatic pressure
Plasma colloid osmotic pressure
Increased interstitial fluid
Increased capillary pressure
Diminished colloid osmotic pressure
Fluid accumulation
Movement of water into tissues (or body cavities)
exceeds drainage
Abnormal increase in interstitial fluid within
tissues
Edema
Fluid collections in the different body cavities
Hydrothorax
Hydropericardium
Hydroperitoneum (ascites)
Anasarca
Severe and generalized edema
Widespread subcutaneous tissue swelling
Transudate
Edema caused by:
Increased
hydrostatic pressure
Reduced plasma protein
Typically a protein-poor fluid
Heart failure, renal failure, hepatic failure, and
certain forms of malnutrition
Inflammatory edema
Protein-rich exudate
Result of increased vascular permeability
Lymphedema
Impaired lymphatic drainage
Typically localized
Causes
Chronic
inflammation with fibrosis
Invasive malignant tumors
Physical disruption
Radiation damage
Certain infectious agents
Parasitic filariasis
Lymphatic
obstruction
• Extensive inguinal lymphatic and lymph node fibrosis
• Edema of the external genitalia and lower limbs
• Massive = elephantiasis
Severe edema of the upper extremity
Complicate surgical removal and/or irradiation
Breast
and associated axillary lymph nodes
• Breast cancer
Morphology
Edema is easily recognized grossly
Microscopic examination
Clearing
and separation of the extracellular matrix
Subtle cell swelling
Most commonly seen:
Subcutaneous tissues, lungs, and brain
Subcutaneous edema
Diffuse or more conspicuous in regions with high
hydrostatic pressures
Distribution is influenced by gravity
Dependent
edema
• Legs when standing, the sacrum when recumbent
Subcutaneous edema
Pitting edema
Finger pressure over substantially edematous
subcutaneous tissue
Displaces the interstitial fluid and leaves a depression
Edema secondary to renal dysfunction
Affect all parts of the body
Manifests in tissues with loose connective tissue
matrix (eyelids)
Periorbital
edema
• Characteristic finding in severe renal disease
Soft tissue edema
Important because it signals underlying cardiac or
renal disease
Impairs wound healing or the clearance of infection
Pulmonary edema
Lungs are often two to three times their normal
weight
Sectioning yields frothy, blood-tinged fluid
Mixture
of air, edema, and extravasated red cells
Common clinical problem
Most frequently seen with left ventricular failure
Pulmonary edema
Lungs are often two to three times their normal
weight
Sectioning yields frothy, blood-tinged fluid
Mixture
of air, edema, and extravasated red cells
Common clinical problem
Most frequently seen with left ventricular failure
Brain edema
Localized or generalized
Depending on the nature and extent of the
pathologic process or injury
Generalized edema
Brain
is grossly swollen with narrowed sulci
Distended gyri show evidence of compression
against the unyielding skull
Brain edema
Life-threatening
Severe edema
Brain
substance can herniate (extrude)
• Foramen magnum
Brain
stem vascular supply can be compressed
Either condition can injure the medullary centers
• Cause death
Stem from locally increased blood volumes
Hyperemia
Active process
Arteriolar dilation
Sites
of inflammation
Skeletal muscle during exercise
Hyperemia
Leads
to increased blood flow
Affected tissues turn red (erythema)
Engorgement
of vessels with oxygenated blood
Congestion
Passive process
Reduced outflow of blood from a tissue
Systemic
Cardiac
failure
Congestion
Local
Isolated
venous obstruction
Dusky reddish-blue color (cyanosis)
Red
cell stasis
Accumulation of deoxygenated hemoglobin
Long-standing chronic passive congestion
Lack of blood flow causes chronic hypoxia
Results
in ischemic tissue injury and scarring
Capillary rupture
Cause
small hemorrhagic foci
Subsequent catabolism of extravasated red cells
• Leave residual telltale clusters of hemosiderin-laden
macrophages
Morphology
Cut surfaces
Discolored
due to the presence of high levels of
poorly oxygenated blood
Microscopic examination
Acute
pulmonary congestion
• Engorged alveolar capillaries
• Alveolar septal edema
• Focal intra-alveolar hemorrhage
Morphology
Microscopic examination
Chronic
pulmonary congestion
• Septa are thickened and fibrotic
• Alveoli often contain numerous hemosiderin-laden
macrophages
Heart failure cells
Morphology
Acute hepatic congestion
Central
vein and sinusoids are distended
Centrilobular hepatocytes can be frankly ischemic
Chronic passive hepatic congestion
Centrilobular
regions are grossly red-brown
• Areas are accentuated against uncongested
parenchyma
• Nutmeg liver
Morphology
Microscopic examination
Centrilobular
hemorrhage
Hemosiderin-laden macrophages
Degeneration of hepatocytes
Extravasation of blood into the extravascular
space
Increased tendency to hemorrhage (usually
with insignificant injury)
Occurs in a variety of clinical disorders
Collectively called hemorrhagic diatheses
Distinct patterns of tissue hemorrhage
Hemorrhage may be external
Contained
within a tissue
Hematoma
Petechiae
Minute 1- to 2-mm hemorrhages into skin,
mucous membranes, or serosal surfaces
Most commonly associated:
Locally
increased intravascular pressure
Low platelet counts (thrombocytopenia)
Defective platelet function (as in uremia)
Purpura
Slightly larger (≥3 mm) hemorrhages
Associated with many of the same disorders that
cause petechiae
Secondary to trauma, vascular inflammation
(vasculitis), or increased vascular fragility
(amyloidosis)
Ecchymoses
Larger (>1 to 2 cm) subcutaneous hematomas
(bruises)
Red cells in these lesions are degraded and
phagocytized by macrophages
Hemoglobin
(red-blue color)
• Enzymatically converted into bilirubin (blue-green
color)
Hemosiderin (gold-brown color), accounting for the
characteristic color changes in a bruise
Large accumulation of blood in a body cavity
Hemothorax
Hemopericardium
Hemoperitoneum
Hemarthrosis (in joints)
Normal hemostasis
Consequence of tightly regulated processes
Maintain blood in a fluid state in normal vessels
Permit the rapid formation of a hemostatic clot at
the site of a vascular injury
Thrombosis
Pathologic counterpart of hemostasis
Involves blood clot (thrombus) formation
Both hemostasis and thrombosis involve
three components:
Vascular wall (particularly the endothelium)
Platelets
Coagulation cascade
Endothelial cells
Key players in the regulation of homeostasis
Exhibit antiplatelet, anticoagulant, and fibrinolytic
properties
After injury or activation
Acquire
numerous procoagulant activities
Activated by infectious agents, hemodynamic
forces, plasma mediators, and cytokines
Antiplatelet effects
Intact endothelium prevents platelets from
engaging the highly thrombogenic subendothelial
ECM
Nonactivated platelets
Do
not adhere to endothelial cells
• Even if platelets are activated, prostacyclin (PGI2) and
nitric oxide produced by the endothelial cells impede
platelet adhesion
Antiplatelet effects
Endothelial cells
Also
elaborate adenosine diphosphatase
• Degrades adenosine diphosphate (ADP)
• Further inhibits platelet aggregation
Anticoagulant effects
Mediated by endothelial membrane-associated
heparin-like molecules
Thrombomodulin
• Binds to thrombin
• Converts it from a procoagulant into an anticoagulant
Via its ability to activate protein C, which inhibits clotting
by inactivating factors Va and VIIIa
Anticoagulant effects
Mediated by endothelial membrane-associated
heparin-like molecules
Tissue
factor pathway inhibitor
• Cell surface protein
• Directly inhibits tissue factor-factor VIIa and factor Xa
activities
Anticoagulant effects
Heparin-like molecules
Act
indirectly
Cofactors that enhance the inactivation of thrombin
and several other coagulation factors
• Through the use of plasma protein antithrombin III
Fibrinolytic effects
Endothelial cells synthesize tissue-type
plasminogen activator (t-PA)
Protease
that cleaves plasminogen to form plasmin
• Plasmin cleaves fibrin to degrade thrombi
Platelet effects
Endothelial injury allows platelets to contact the
underlying extracellular matrix
Subsequent adhesion occurs through interactions
with von Willebrand factor (vWF)
Product of normal endothelial
cells and an essential
cofactor for platelet binding to matrix elements
Procoagulant effects
Response to cytokines (TNF or IL-1) or bacterial
endotoxin
Endothelial
cells synthesize tissue factor
• Major activator of the extrinsic clotting cascade
• Activated endothelial cells
Augment the catalytic function of activated coagulation
factors IXa and Xa
Antifibrinolytic effects
Endothelial cells secrete inhibitors of plasminogen
activator (PAIs)
Limit
fibrinolysis and tend to favor thrombosis
Intact, nonactivated endothelial cells inhibit
platelet adhesion and blood clotting
Endothelial injury or activation
Results in a procoagulant phenotype that
enhances thrombus formation
Disc-shaped
Anucleate cell fragments
Shed from megakaryocytes in the bone
marrow into the blood stream
Play a critical role in normal hemostasis
Forming the hemostatic plug that initially seals
vascular defects
Providing a surface that recruits and concentrates
activated coagulation factors
Function depends on several glycoprotein
receptors
Contractile cytoskeleton
Two types of cytoplasmic granules
α-Granules
• Adhesion molecule P-selectin on their membranes
• Contain fibrinogen, fibronectin, factors V and VIII,
platelet factor 4, platelet-derived growth factor
(PDGF), and transforming growth factor-β (TGF-β)
Function depends on several glycoprotein
receptors
Two types of cytoplasmic granules
Dense
(or δ) granules
• Contain ADP and ATP, ionized calcium, histamine,
serotonin, and epinephrine
Following vascular injury…
Platelets encounter ECM constituents
Collagen
and the adhesive glycoprotein vWF
On contact with these proteins, platelets
undergo:
Adhesion and shape change
Secretion (release reaction)
Aggregation
Mediated largely via interactions with vWF
Acts as a bridge between platelet surface
receptors (glycoprotein Ib) and exposed collagen
vWF-GpIb associations
Necessary
to overcome the high shear forces of
flowing blood
Mediated largely via interactions with vWF
Genetic
deficiencies of vWF or its receptor result in
bleeding disorders
• Von Willebrand Disease
• Bernard-Soulier syndrome
Occurs soon after adhesion
Various agonists can bind platelet surface
receptors
Initiate an intracellular protein phosphorylation
cascade
Leads
to degranulation
Various agonists can bind platelet surface
receptors
Release of the contents of dense-bodies
Important
Calcium
is required in the coagulation cascade
ADP is a potent activator of platelet aggregation
• Causes additional ADP release
Amplifies aggregation process
Platelet activation
Appearance of negatively charged phospholipids
(particularly phosphatidylserine) on their surfaces
Bind
calcium and serve as critical nucleation sites for
the assembly of complexes containing the various
coagulation factors
Follows adhesion and granule release
Vasoconstrictor thromboxane A2
Important platelet-derived stimulus
Amplifies platelet aggregation
Formation of the primary hemostatic plug
Initial wave of aggregation is reversible
Concurrent activation of the coagulation
cascade
Generates thrombin
Stabilizes the platelet plug via two mechanisms:
Thrombin
binds to a protease-activated receptor on
the platelet membrane
• In concert with ADP and TxA2 causes further platelet
aggregation
Stabilizes the platelet plug via two
mechanisms:
Thrombin binds to a protease-activated receptor
on the platelet membrane
Platelet
contraction
• Event that is dependent on the platelet cytoskeleton
• Creates an irreversibly fused mass of platelets
• Constitutes the definitive secondary hemostatic plug
Thrombin converts fibrinogen to fibrin in the
vicinity of the platelet plug
• Cements the platelets in place
Noncleaved fibrinogen
Important component of platelet aggregation
Platelet activation by ADP
Triggers a conformational change in the platelet
GpIIb-IIIa receptors
Induces binding to fibrinogen
Large
protein that forms bridging interactions
between platelets that promote platelet
aggregation
Part 2
Third arm of the hemostatic process
Amplifying series of enzymatic conversions
Each step proteolytically cleaves an inactive
proenzyme into an activated enzyme
Culminates
in thrombin formation
Thrombin is the most important coagulation
factor
Can act at numerous stages in the process
Conclusion of the proteolytic cascade
Thrombin converts the soluble plasma protein
fibrinogen into fibrin monomers that polymerize
into an insoluble gel
Fibrin
gel encases platelets and other circulating
cells in the definitive secondary hemostatic plug
Fibrin polymers are covalently cross-linked and
stabilized by factor XIIIa (which itself is activated
by thrombin)
Assess the function of the two arms of the
coagulation pathway
Two standard assays
Prothrombin time
(PT)
Partial thromboplastin time (PTT)
The PT assay
Assesses the function of the proteins in the
extrinsic pathway
Factors VII, X,
II, V, and fibrinogen
Accomplished by adding tissue factor and
phospholipids to citrated plasma (sodium citrate
chelates calcium and prevents spontaneous clotting)
Coagulation is initiated by the addition of
exogenous calcium and the time for a fibrin clot to
form is recorded
Partial thromboplastin time (PTT)
Screens for the function of the proteins in the
intrinsic pathway
Factors XII, XI, IX, VIII, X, V,
II, and fibrinogen
Clotting is initiated through the addition of negative
charged particles (ground glass)
• Activates factor XII (Hageman factor), phospholipids,
and calcium, and the time to fibrin clot formation is
recorded
Thrombin
Exerts a wide variety of proinflammatery effects
Most effects of thrombin occur through its
activation of a family of protease activated
receptors (PARs)
Belong
to the seven-transmembrane G proteincoupled receptor family
PARs are expressed on endothelium, monocytes,
dendritic cells, T lymphocytes, and other cell types
Coagulation cascade must be restricted to the
site of vascular injury
Prevent runaway clotting of the entire vascular tree
Three categories of endogenous anticoagulants
Antithrombins (antithrombin III)
Inhibit the activity of thrombin and other serine
proteases, including factors IXa, Xa, XIa, and XIIa
Antithrombin III is activated by binding to heparin-like
molecules on endothelial cells
• Clinical usefulness of administering heparin to minimize
thrombosis
Three categories of endogenous anticoagulants
Proteins C and S
Vitamin
K-dependent proteins
Act in a complex that proteolytically inactivates factors
Va and VIIIa
TFPI is a protein produced by endothelium
Inactivates
tissue factor-factor VIIa complexes
Fine-tune the coagulation/anticoagulation
balance
Releasing plasminogen activator inhibitor
(PAI)
Blocks fibrinolysis by inhibiting t-PA binding to
fibrin
Confers an overall procoagulant effect
Production is increased by thrombin as well as
certain cytokines
Three primary abnormalities that lead to
thrombus formation (called Virchow's triad):
Endothelial injury
Stasis or turbulent blood flow
Hypercoagulability of the blood
Particularly important for thrombus
formation in the heart or the arterial
circulation
Normally high flow rates might otherwise impede
clotting by preventing platelet adhesion and
washing out activated coagulation factors
Endothelial cell injury
Thrombus formation within cardiac chambers (i.e.
after endocardial injury due to myocardial
infarction)
Over ulcerated plaques in atherosclerotic arteries
Sites of traumatic or inflammatory vascular injury
(vasculitis)
Endothelium
Does not need to be denuded or physically
disrupted to contribute to the development of
thrombosis
Any perturbation in the dynamic balance of
the prothombotic and antithrombotic
activities of endothelium can influence local
clotting events
Endothelial dysfunction
Induced by a wide variety of insults, including
hypertension, turbulent blood flow, bacterial
endotoxins, radiation injury, metabolic
abnormalities such as homocystinemia or
hypercholesterolemia, and toxins absorbed from
cigarette smoke
Turbulence
Contributes to arterial and cardiac thrombosis by
causing endothelial injury or dysfunction
Forming countercurrents and local pockets of
stasis
Stasis
is a major contributor in the development of
venous thrombi
Normal blood flow is laminar
Platelets (and other blood cellular elements) flow
centrally in the vessel lumen, separated from
endothelium by a slower moving layer of plasma
Stasis and turbulence therefore:
Promote endothelial activation
Enhancing
pro-coagulant activity through flowinduced changes in endothelial cell gene expression
Disrupt laminar flow and bring platelets into
contact with the endothelium
Prevent washout and dilution of activated clotting
factors by fresh flowing blood and the inflow of
clotting factor inhibitors
AKA thrombophilia
Less frequent contributor to thrombotic
states
Any alteration of the coagulation pathways
that predisposes to thrombosis
Divided into primary (genetic)
Secondary (acquired) disorders
Of the inherited causes of hypercoagulability
Most common
Point
mutations in the factor V gene
Prothrombin gene
Elevated levels of homocysteine
Contribute to arterial and venous thrombosis
Prothrombotic effects of homocysteine
May be due to thioester linkages formed between
homocysteine metabolites and a variety of
proteins, including fibrinogen
Rare inherited causes of primary
hypercoagulability
Deficiencies of anticoagulants
Antithrombin
III, protein C, or protein S
Present with venous thrombosis and recurrent
thromboembolism beginning in adolescence or early
adulthood
Acquired thrombophilic states
Heparin-induced thrombocytopenia (HIT)
syndrome
Occurs following
the administration of
unfractionated heparin
• May induce the appearance of antibodies
Recognize complexes of heparin and platelet factor 4 on
the surface of platelets
Heparin-induced thrombocytopenia (HIT)
syndrome
Occurs following the administration of
unfractionated heparin
• Complexes of heparin-like molecules and platelet
factor 4-like proteins on endothelial cells
• Binding of these antibodies to platelets
Results in their activation, aggregation, and consumption
Prothrombotic
state, even in the face of heparin
administration and low platelet counts
AKA lupus anticoagulant syndrome
Clinical manifestations
Recurrent thromboses, repeated miscarriages,
cardiac valve vegetations, and thrombocytopenia
Pulmonary embolism, pulmonary hypertension,
stroke, bowel infarction, or renovascular
hypertension
Fetal loss
Autoantibodies induce a hypercoagulable
state
Cause endothelial injury by activating platelets
and complement directly
Primary and secondary forms
Secondary antiphospholipid syndrome
Individuals
with a well-defined autoimmune disease
Systemic lupus erythematosus
Primary and secondary forms
Primary antiphospholipid syndrome
Exhibit
only the manifestations of a hypercoagulable
state
Lack evidence of other autoimmune disorders
Association with certain drugs or infections
Can develop anywhere in the cardiovascular
system
Size and shape of thrombi
Depend on the site of origin and the cause
Arterial or cardiac thrombi
Begin
at sites of turbulence or endothelial injury
Venous thrombi
Occur at
sites of stasis
Focally attached to the underlying vascular
surface
Arterial thrombi tend to grow retrograde from the
point of attachment
Venous thrombi extend in the direction of blood
flow
Gross and microscopic laminations
Lines of Zahn
Represent
pale platelet and fibrin deposits
alternating with darker red cell-rich layers
Signify that a thrombus has formed in flowing blood
Presence can therefore distinguish antemortem
thrombosis from the bland nonlaminated clots that
occur postmortem
Thrombi occurring in heart chambers or in
the aortic lumen
Mural thrombi
Abnormal myocardial contraction
• Arrhythmias, dilated cardiomyopathy, or myocardial
infarction
• Endomyocardial injury (myocarditis or catheter
trauma)
Arterial thrombi
Frequently occlusive
Most common sites
Coronary, cerebral,
and femoral arteries
Consist of a friable meshwork of platelets, fibrin,
red cells, and degenerating leukocytes
Usually superimposed on a ruptured
atherosclerotic plaque
Venous thrombosis (phlebothrombosis)
Invariably occlusive
Thrombus forming a long cast of the lumen
Thrombi form in the sluggish venous circulation
Contain more enmeshed red cells
Red, or stasis,
thrombi
Veins of the lower extremities are most commonly
involved (90% of cases)
Postmortem clots
Mistaken for antemortem venous thrombi
Gelatinous with a dark red dependent portion
where red cells have settled by gravity and a
yellow "chicken fat" upper portion
Usually not attached to the underlying wall
Red thrombi
Firmer
Focally attached
Gross and/or microscopic lines of Zahn
Vegetations
Thrombi on heart valves
Blood-borne bacteria or fungi
Adhere
to previously damaged valves (rheumatic
heart disease)
Directly cause valve damage
Infective endocarditis
Vegetations
Sterile vegetations
Nonbacterial
thrombotic endocarditis
Sterile, verrucous endocarditis
Libman-Sacks
endocarditis
Survival of the initial thrombosis
Ensuing days to weeks thrombi undergo some
combination of the following four events:
Propagation
• Thrombi accumulate additional platelets and fibrin
Embolization
• Thrombi dislodge and travel to other sites in the vasculature
Dissolution
• Result of fibrinolysis, which can lead to the rapid shrinkage and
total disappearance of recent thrombi
Organization and recanalization
• Older thrombi become organized by the ingrowth of
endothelial cells, smooth muscle cells, and fibroblasts
Deep venous thrombosis (DVT)
Larger leg veins-at or above the knee
Thrombi more often embolize to the lungs and
give rise to pulmonary infarction
Venous obstructions from DVTs can be
rapidly offset by collateral channels
DVTs are asymptomatic in approximately 50% of
affected individuals
Recognized only in retrospect after embolization
Obstetric complications to advanced
malignancy
Sudden or insidious onset of widespread
fibrin thrombi in the microcirculation
Not grossly visible
Diffuse circulatory insufficiency, particularly
in the brain, lungs, heart, and kidneys
Widespread microvascular thrombosis results
in platelet and coagulation protein
consumption
Fibrinolytic mechanisms are activated
Initially thrombotic disorder
Evolve into a bleeding catastrophe
Embolus
Detached intravascular solid, liquid, or gaseous
mass that is carried by the blood to a site distant
from its point of origin
Thromboembolism
Rare forms of emboli include fat droplets,
nitrogen bubbles, atherosclerotic debris
(cholesterol emboli), tumor fragments, bone
marrow, or even foreign bodies
Unless otherwise specified, emboli should be
considered thrombotic in origin
Occlusions—embolic
95% from deep leg veins
Indwelling central venous lines
Right atrial thrombi
50,000 deaths/year in US
Origin of emboli
Leg or pelvic veins
Large emboli
Sudden death
Lodging
• Major branches of pulmonary arteries
• Saddle emboli
Acute
cor pulmonale
Small emboli
Minimal symptoms
Exception
Inadequate
bronchial circulation
• Symptoms
Causes of emboli
Immobilized individuals
Hypercoagulable state (primary vs. secondary)
Heart failure
Extent of pulmonary artery
obstruction
Size of occluded vessel
Pathophysiologic response
Clinical significance
Number of emboli
Status of the cardiovascular
system
Release of vasoactive factors
Pathophysiologic consequences
Respiratory compromise
Hemodynamic compromise
Adequate cardiovascular function
Bronchial artery compensation
Hemorrhage without
infarction
Infarction
Inadequate circulation
Rare in young
Clinical course
Cardiopulmonary resuscitation
Electromechanical
dissociation
• Electrocardiogram has a rhythm
• No pulses are palpated
Survival (post-sizable pulmonary embolus)
Mimics
myocardial infarction
Diagnosis
Spiral CT
Other diagnostic methods
Ventilation
perfusion scanning
Pulmonary angiography
Duplex ultrasonography
• Deep vein thrombosis
Prevention
Major clinical problem
Prophylactic therapy
Early
ambulation
Stockings
Anticoagulation
Filter
Treatment
Thrombolysis
Anticoagulation
Gross examination
Parenchyma
75%
of all infarcts affect the lower lobes
Greater than 50%--multiple lesions
Wedge shaped
Hemorrhagic
Fibrinous pleural exudate
Scar
Embolus
http://www.path.uiowa.edu/cgi-bin-pub/vs/fpx_gen.cgi?slide=714&viewer=java&lay=&jpg=493
Microscopic examination
Ischemic necrosis
Alveolar
walls, bronchioles, and vessels
Infected embolus
Intense
neutrophilic inflammatory reaction
Septic infarct
Microscopic fat globules-with or without
associated hematopoietic marrow elements
Fractures of long bones (which have fatty
marrow)
Soft tissue trauma and burns
Common incidental findings after vigorous
cardiopulmonary resuscitation
No clinical consequence
Gas bubbles within the circulation
Coalesce to form frothy masses that obstruct
vascular flow (and cause distal ischemic injury)
More than 100 cc of air are required to have a
clinical effect in the pulmonary circulation
Decompression sickness
Sudden
decreases in atmospheric pressure
Scuba and deep sea divers, underwater construction
workers, and individuals in unpressurized aircraft in
rapid ascent are all at risk
The bends
Rapid formation of gas bubbles within skeletal
muscles and supporting tissues in and about joints
The chokes
Gas bubbles in the vasculature cause edema,
hemorrhage, and focal atelectasis or emphysema,
leading to a form of respiratory distress
Caisson disease
Chronic form of decompression sickness is called
(named for the pressurized vessels used in the
bridge construction; workers in these vessels
suffered both acute and chronic forms of
decompression sickness)
Persistence of gas emboli in the skeletal system
leads to multiple foci of ischemic necrosis; the
more common sites are the femoral heads, tibia,
and humeri
Amniotic fluid embolism
Ominous complication of labor and the immediate
postpartum period
Sudden severe dyspnea, cyanosis, and shock
Followed
by neurologic impairment ranging from
headache to seizures and coma
If the patient survives the initial crisis, pulmonary
edema typically develops, along with (in half the
patients) DIC, as a result of release of thrombogenic
substances from the amniotic fluid
Underlying cause
Infusion of amniotic fluid or fetal tissue into the
maternal circulation via a tear in the placental
membranes or rupture of uterine veins
Classic findings
Presence of squamous cells shed from fetal skin,
lanugo hair, fat from vernix caseosa, and mucin
derived from the fetal respiratory or
gastrointestinal tract in the maternal pulmonary
microvasculature
Final common pathway for several potentially
lethal clinical events
Including severe hemorrhage, extensive trauma or
burns, large myocardial infarction, massive
pulmonary embolism, and microbial sepsis
Shock is characterized by systemic hypotension
due either to reduced cardiac output or to
reduced effective circulating blood volume
The consequences are impaired tissue
perfusion and cellular hypoxia
Three general categories
Cardiogenic shock
Hypovolemic shock
Septic shock
Depend on the precipitating insult
Hypovolemic and cardiogenic shock
Patient presents with hypotension
Weak,
rapid pulse; tachypnea; and cool, clammy,
cyanotic skin
Septic shock
Skin may initially be warm and flushed because of
peripheral vasodilation
Rapidly, however, the cardiac, cerebral, and
pulmonary changes secondary to shock
worsen the problem
Electrolyte disturbances and metabolic
acidosis