HEMODYNAMIC
DISORDERS
THROMBOSIS
DEFINITION:
It is the process of formation of solid mass in the
circulation from the constituents of flowing blood.
It may...
COMPOSITION OF THROMBUS
Fibrin, Platelets, RBC's
(Hemostatic plug formation: endothelial injury, platelet aggregation, fib...
PATHOGENESIS OF THROMBOSIS
(Predisposing Factors)
Virchow’s Triad
– Endothelial injury
– Stasis or turbulence of blood flo...
Endothelial Injury
– Tissue Damage (Surgery, Fractures, Burns)
– Atherosclerosis
– Hypertension
– Toxic Products
Abnormal Blood Flow
• Turbulence of Blood Flow
– Swirls, Eddies and increased pressure are injurious
– These changes occur...
Hypercoagulability
Any alterations of the coagulation pathways that predispose to
Thrombosis
Primary (Genetic) or Secondar...
Hemostasis & Thrombosis
• Hemostasis is the normal, rapid formation of a
localized “plug” at the site of vascular injury
•...
Hypercoagulable States
Inherited
Abnormality Approximate Rate
Factor VLeiden - APCR (Caucasion) 15-30%
Prothrombin Gene Mu...
EFFECTS OF THROMBI
Stenosis or blockage of arterial lumen
ischemia, infarction
Venous occlusion
local congestion and edema...
MORPHOLOGY OF THROMBI
THROMBI DEVELOP
IN THE CARDIOVASCULAR SYSTEM
Lines of Zahn:
Alternating Pale Layers of Platelets & F...
Atheroma with Thrombosis:Atheroma with Thrombosis:
Thrombus
(Lines of Zahn)
Layering
(Lines of Zahn)
Cardiac Mural Thrombus
Mural Thrombi
In Ventricles (Left) and Aortic Aneurysm (Right)
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th...
Cardiac Mural Thrombi
Notice underlying endocardial fibrosis
Right
Left
Thrombotic Vegetations
Mitral Valve
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
CLINICAL SETTING FOR CARDIAC /ARTERIAL
THROMBUS FORMATION
Myocardial Infarction (MI)
Rheumatic Heart Disease
Atheroscleros...
VENOUS THROMBOSIS
Superficial Veins of the Lower Extremities
– Cause Pain, Swelling - Rarely Embolize
– Associated With Va...
• Phlebothrombosis
It is due to stasis of blood in un-inflamed veins,
particularly the calf veins.
• Thrombophlebitis
It i...
PHLEBOTHROMBOSIS THROMBOPHLEBITIS
Main cause Stasis Inflammation
Primary thrombus Small Larger-depends on extent
of phlebi...
CLINCAL SETTING FOR VENOUS
THROMBUS FORMATION
Cardiac Failure (CHF)
Trauma
Surgery
Burns
3rd Term Pregnancy and Postpartum...
Valvular Thrombi (vegetations)
Infective Endocarditis
Non-bacterial Thrombotic Endocarditis (NBTE)
-Seen in patients dying...
FATE OF THROMBOSIS
Resolution (Dissolution)
Recent thrombi can undergo total lysis by activation of fibrinolytic system (m...
Thrombus Propagated into the
Inferior Vena Cava
CLINICAL SIGNIFICANCE:
Obstruction of arteries or veins can cause
ischemia, infarction, or may embolize
Venous thrombi may...
DIAGNOSIS:
• Clinical signs are unreliable.
• Phlebography using a contrast medium.
• Radioactive iodine-labelled fibrinog...
EMBOLISM
EMBOLISM
It is the process of carrying an abnormal mass (embolus)
in the blood stream to a point distant from its origin.
...
TYPES OF EMBOLI
Gas
(air, nitrogen , other gases)
Liquid
(amniotic fluid, radiographic contrast material, fat after soft t...
• ORIGIN & SITES OF EMBOLIZATION:
• Venous: Systemic veins Pulmonary arteries
• Arterial: Heart or aorta Systemic circulat...
EFFECTS OF EMBOLISM
Ischemia
Infarction
Sepsis if infected
(example: pulmonary embolism with pulmonary infarction)
Thromboembolism
A detached thrombus or part of thrombus constitutes the most
common type of embolism
*Arterial (systemic) ...
Systemic Thromboembolism
• Emboli traveling within the arterial circulation
• 80% arise from intra-cardiac mural thrombi (...
Pulmonary Thromboembolism
Generally originate from deep leg veins (popliteal, femoral & iliac)
Usually pass through the ri...
Thromboembolism
Pulmonary
Embolus
Saddle
Pulmonary
Embolus
Embolization (Embolus)
Thromboembolism of Pulmonary Artery
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th
ed....
Fat embolism syndrome
Microscopic fat globules derived from long bone fractures (fatty marrow) or
rarely from soft tissue ...
Bone Marrow Embolus
In Pulmonary Vessel
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th
ed., Saunders, Philade...
Air embolism
Gas bubbles within the circulation can obstruct vascular flow to cause distal
ischemic injury
Air can enter t...
Amniotic Fluid Embolism
Torn placental membrane- amniotic fluid release
Rupture of uterine veins
Infusion of amniotic flui...
Disseminated Intravascular Coagulation (DIC)
• Sudden widespread fibrin deposition in microcirculation
• Rapid consumption...
Clinical Consequences of DIC
Tumor Embolism
Tumor Embolism
Lymphatics (Carcinoma)
Blood vesseles (Sarcoma)
Common sites
Liver (Carcinoma)
Lung (Carcino...
INFARCTION
INFARCTION
An infarct is a localized area of ischemic necrosis caused by
occlusion of either the arterial supply or venous...
TYPES OF INFARCTS:
•Bland vs. Septic
(assumed to be bland unless specified as “septic”)
•Arterial (usually white/pale) vs....
MORPHOLOGY OF INFARCTS
White/Pale:
Occur with arterial occlusion or in solid organs with single blood supply (ex: kidneys,...
FACTORS AFFECTING INFARCTS:
• Nature of the vascular supply (dual arterial supply)
• Collateral circulation
• Rate of deve...
Hemorrhagic Lung Infarct Pale Splenic Infarct
Myocardial Infarction
MYOCARDIAL INFARCTION
Myocardial Infarction
Regional Full-Thickness (Left); Circumferential Subendocardial (Right)
Photo: Stevens A, Lowe J. Sli...
Mural Thrombus
Over Myocardial Infarction
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
Myocardial Infarction
Rupture
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
VentricleVentricle
Myocardial Infarction
Chronological Appearance
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
Myocardial Infarction
Chronological Appearance
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
Myocardial Infarction
Chronological Appearance
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
Myocardial Infarction
Chronological Appearance
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
RENAL INFARCTION
Kidney Infarction
Replaced by Fibrotic Scar (Left)
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th
ed., Saunde...
Lung Infarct
Wedge Shape...
Infarcted Colon
OK Colon
CLINICAL SIGNIFICANCE OF INFARCTION
•Usually cause pain;
•May cause loss of function (example: myocardial infarct may
caus...
SHOCK
SHOCK
It is defined as systemic hypo-perfusion due to reduction either in
Cardiac Output or Effective Circulating Blood Vo...
TYPES OF SHOCK
Three Main Categories:
Cardiogenic,
Hypovolemic, and
Septic
Others:
Neurogenic Shock (anesthetic and spinal...
CARDIOGENIC SHOCK
Results From Severe Myocardial Failure Due to:
– Intrinsic myocardial damage (myocardial infarction, ven...
HYPOVOLEMIC SHOCK
Results From Loss of Blood or Plasma Volume:
- Hemorrhage
- Fluid Loss (severe burns, trauma, vomiting, ...
SEPTIC (ENDOTOXIC) SHOCK
• Most common cause of death in ICU’s in the US
• Dissemination of infection into the vasculature...
Pathogenesis Of Septic Shock
• Endotoxins are bacterial wall lipopolysaccharides (LPS) which
consists of a toxic fatty aci...
Effects of Shock on Tissues
• Brain -- ischemic encephalopathy --> confusion, obtundation;
• Heart -- subendocardial ische...
Morphology
of Shock
Clinical Course of Shock
• Hypotension
• Weak, rapid pulse, tachycardia
• Rapid shallow respiration
• Drowsiness, confusio...
Hyperemia & Congestion
Increased volume of blood in an area compared to normal
Hyperemia
Hyperemia is an active process re...
MORPHOLOGY OF HYPEREMIA &
CONGESTION
– Hyperemia: tissue is red or purple, engorged with oxygenated blood,
swollen, often ...
PULMONARY CONGESTION
– Acute Pulmonary Congestion: engorged alveolar capillaries, alveolar septal edema, focal
minute intr...
Hyperemia in PneumoniaHyperemia
Infection
(Pneumonia)
Liver - Chronic Passive Congestion
“Nutmeg” Liver
Cross Section of a Nutmeg“Nutmeg” Liver
Chronic Passive
SIGNIFICANCE OF CONGESTION
If diffuse, usually indicates Heart failure;
If local, usually indicates a blockage upstream to...
HEMORRHAGE
Extravasation of blood due to rupture of blood vessels
– Rupture of a large vessel: Trauma, Atherosclerosis, In...
CAUSES OF HEMORRHAGE
– Trauma
– Vascular diseases with rupture (atherosclerosis, arteritis,
aneurysms, etc.).
– Low platel...
MORPHOLOGY OF HEMORRHAGE
Acute –
Red or purple collection of blood in tissue
Chronic or old –
Brown or maroon pasty materi...
EFFECTS OF HEMORRHAGE
Effects of hemorrhage depends on following factors:
Location
Rate
Duration
Co-morbid diseases
(emphy...
Hemorrhage
Why do bruises change color
as they Resolve?
• The RBC’s in a hemorrhage are broken down:
– hemoglobin (red) → ...
Intracerebral Hemorrhage
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th
ed., Saunders, Philadelphia, 2003.
PurpuraPurpuraColonic PetechiaeColonic Petechiae
ThrombocytopeniaThrombocytopenia
Idiopathic Thrombocytopenic PurpuraIdiop...
Clinical Effects of Hemorrhage
• <20% blood loss, little health effect in otherwise healthy individuals
– That’s why donat...
Anemia from Blood Loss
• This may be the only hint of Occult Cancer
– Carcinoma of the Colon
– Gastric Carcinoma (less com...
EDEMA
EDEMA
Excess accumulation of fluid in the interstitial tissue spaces.
• A transudate (protein-poor fluid -specific gravity...
SPECIAL TYPES OF EDEMA
• Pleural effusion (hydro-thorax)
• Pericardial effusion (hydro-pericardium)
• Ascites (edema in pe...
Normal Microcirculation
Capillary Arterial Venous
Hydrostatic Pressure + 36 + 16
Osmotic Pressure - 26 - 26
Net filtration...
Homeostasis is maintained by the opposing effects of
vascular hydrostatic pressure and plasma colloid osmotic
Pathophysiologic Categories of Edema
I. Increased Hydrostatic Pressure
II. Reduced Plasma Osmotic Pressure
III. Lymphatic ...
Increased Hydrostatic Pressure
A. Congestive Heart Failure
B. Portal Hypertension
C. Venous Thrombosis
Congestive Heart Failure
Inability of Heart to Pump blood in systemic circulation
↓
Blood backing up into the lungs
↓
Bloo...
Congestive Heart Failure
Renin-Angiotensin-Aldosterone Axis
Renin Aldosterone
Renal Na
reabsorption
Renal retention of
Na ...
Congestive Heart Failure
Renal Vasoconstriction
Renal
Vasoconstriction
Glomerular Filtration
Rate (GFR)
Tubular
reabsorpti...
Congestive Heart Failure
Anti-Diuretic Hormone
Anti-Diuretic
Hormone (ADH)
Renal retention of
H2O
Plasma volume
Transudati...
Central
Venous
Pressure
Renal
Perfusion
Renin Renal
Vasoconstriction
ADH
Congestive Heart Failure
Events Leading to Systemic Edema
Secondary to Primary Heart Failure
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology...
Clinically initially cardiac edema can be demonstrated in legs or sacrum
Portal Hypertension
• Portal Hypertension is “Increased resistance to portal blood flow”
• The most common cause of Portal...
AscitesAscites
Portal Hypertension
Sinusoidal
Hypertension
Renal
Perfusion
Hepatic Lymph
Overwhelms
Thoracic Duct
Aldosterone
ASCITES
Cir...
Venous Thrombosis
• Impaired venous outflow increases hydrostatic pressure
Reduced Plasma Osmotic Pressure
• Albumin is the serum protein MOST responsible for the maintenance of
colloid osmotic pre...
Inflammation
• Both Acute and Chronic Inflammation are associated with Edema
• Generalized edema in systemic infections, p...
Angioedema
Lymphatic Obstruction
• Impaired lymphatic drainage with resultant lymphedema, usually localized
• Commonly due to inflamm...
Elephantiasi
s
Elephantiasis (filariasis)
“peau d’orange” appearance in breast cancer
Sodium & Water Retention
• Contributory factors in several forms of edema
• Salt retention may be primary cause of edema
P...
EDEMA
INCREASED
HYDROSTATIC
PRESSURE
Congestive Heart Failure
Portal hypertension
(Ascites)
Venous Obstruction
•HEART
•LIV...
GENERALIZED EDEMA
• HEART
• LIVER
• KIDNEY
Edema Morphology
• Edema of the Subcutaneous Tissue is most easily detected Grossly (not
microscopically)
• Push your fing...
Pitting
edema
Pulmonary Edema
• Pulmonary Edema is most frequently seen in Congestive Heart Failure (LVF)
– May also be present in Mitra...
Pulmonary Edema
Pulmonary EdemaNormal Lung
Pulmonary Congestion
and Edema
Edema of the Brain
• Localized: Abscess, Neoplasm
• Generalized: Encephalitis, Hypertensive crises, Obstruction of
venous ...
Brain edema
Clinical Correlation
• Subcutaneous Edema-Annoying but Points to Underlying Disease
– However, it can impair wound healing...
140
Hemodynamic disorders med- 2011, final ii
Hemodynamic disorders med- 2011, final ii
Hemodynamic disorders med- 2011, final ii
Hemodynamic disorders med- 2011, final ii
Hemodynamic disorders med- 2011, final ii
Hemodynamic disorders med- 2011, final ii
Hemodynamic disorders med- 2011, final ii
Upcoming SlideShare
Loading in …5
×

Hemodynamic disorders med- 2011, final ii

6,264
-1

Published on

Published in: Education, Health & Medicine
0 Comments
4 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
6,264
On Slideshare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
375
Comments
0
Likes
4
Embeds 0
No embeds

No notes for slide

Hemodynamic disorders med- 2011, final ii

  1. 1. HEMODYNAMIC DISORDERS
  2. 2. THROMBOSIS
  3. 3. DEFINITION: It is the process of formation of solid mass in the circulation from the constituents of flowing blood. It may be within a blood vessel or cardiac chamber, in a living organism. Always formed ante-mortem. The mass itself is called Thrombus.
  4. 4. COMPOSITION OF THROMBUS Fibrin, Platelets, RBC's (Hemostatic plug formation: endothelial injury, platelet aggregation, fibrin meshwork ) LOCATION OF THROMBI Arteries, veins, heart chambers, heart valves TYPES OF THROMBI Arterial vs. venous; bland vs. septic
  5. 5. PATHOGENESIS OF THROMBOSIS (Predisposing Factors) Virchow’s Triad – Endothelial injury – Stasis or turbulence of blood flow – Blood hypercoagulability
  6. 6. Endothelial Injury – Tissue Damage (Surgery, Fractures, Burns) – Atherosclerosis – Hypertension – Toxic Products
  7. 7. Abnormal Blood Flow • Turbulence of Blood Flow – Swirls, Eddies and increased pressure are injurious – These changes occur in arteries and the heart – Atherosclerosis, Aneurysms, Myocardial Infarction, Cardiac Valve Lesions – Hyperviscosity Syndromes e.g. Sickle Cell Anemia, Polycythemia • Stasis of Blood Flow – More commonly a problem on the venous side leading to Venous Thrombosis – Can occur in the heart (Atrial Fibrillation or Infarction) – Pregnancy, long plane ride, immobility after surgery • Turbulence and Stasis : – Disrupt normal laminar flow and bring platelets in contact with endothelium – Prevent dilution of activated clotting factors – Retard the inflow of clotting factor inhibitors and permit thrombi build-up – Promote endothelial cell activation
  8. 8. Hypercoagulability Any alterations of the coagulation pathways that predispose to Thrombosis Primary (Genetic) or Secondary (Acquired) Disorders • Factor V Leiden mutation is the most common inherited cause of hypercoagulability, it is resistant to the anti-coagulant effect of Activated Protein C • Lack of Protein S, Protein C and Antithrombin III, patients present with venous thrombosis and recurrent thromboembolism in adolescence and early adulthood • Lupus ‘Anticoagulant’ with Lupus Erythematosus is associated with arterial and venous thrombosis & recurrent abortion • Smoking, Obesity, Oral Contraceptives (BCP)
  9. 9. Hemostasis & Thrombosis • Hemostasis is the normal, rapid formation of a localized “plug” at the site of vascular injury • Thrombosis is the pathologic formation of a blood clot within the non-interrupted vascular system in a living person
  10. 10. Hypercoagulable States Inherited Abnormality Approximate Rate Factor VLeiden - APCR (Caucasion) 15-30% Prothrombin Gene Mutation 8-13% Protein C Deficiency 5-6% Protein S Deficiency 5 - 6% Antithriombin Deficiency < 1% Hyperhomocysteinemia 3 - 5% Rogers: Am J Hem 41: 113, 1992
  11. 11. EFFECTS OF THROMBI Stenosis or blockage of arterial lumen ischemia, infarction Venous occlusion local congestion and edema and/or pulmonary embolism (travels) Left heart valve & chamber thrombi systemic embolism
  12. 12. MORPHOLOGY OF THROMBI THROMBI DEVELOP IN THE CARDIOVASCULAR SYSTEM Lines of Zahn: Alternating Pale Layers of Platelets & Fibrin With Darker Layers of Rbc’s (seen in areas with active blood flow like heart, aorta & large arteries not in veins) *Postmortem clots are gelatinous with a dark red dependent portion & yellow “chicken fat” supernatant, usually not attached to the underlying wall *Thrombi in heart chamber/aortic lumen are applied to the underlying structure, mural thrombi (non-occlusive) • *Arterial thrombi are Occlusive/Non-occlusive, begin at site of endothelial injury and grow along flow of blood & typically are firmly adherent to the injured arterial wall (atherosclerotic plaque) • *Venous thrombi are almost always Occlusive- 85-90% of venous thrombi form in lower extremities
  13. 13. Atheroma with Thrombosis:Atheroma with Thrombosis:
  14. 14. Thrombus (Lines of Zahn)
  15. 15. Layering (Lines of Zahn)
  16. 16. Cardiac Mural Thrombus
  17. 17. Mural Thrombi In Ventricles (Left) and Aortic Aneurysm (Right) Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.
  18. 18. Cardiac Mural Thrombi Notice underlying endocardial fibrosis Right Left
  19. 19. Thrombotic Vegetations Mitral Valve Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
  20. 20. CLINICAL SETTING FOR CARDIAC /ARTERIAL THROMBUS FORMATION Myocardial Infarction (MI) Rheumatic Heart Disease Atherosclerosis Rare large round thrombus obstructing mitral valve is called “ ball-valve thrombus” Thrombi formed in ventricles just before death composed of mainly fibrin (Agonal thrombi)
  21. 21. VENOUS THROMBOSIS Superficial Veins of the Lower Extremities – Cause Pain, Swelling - Rarely Embolize – Associated With Varicosities Abnormally Dilated, Tortuous Veins – Increased Risk of Infections – Increased Risk of Varicose Ulcers Deep Veins of the Lower Extremities – Thrombi in Deep Veins (Popliteal, Femoral, Iliac Veins) More Likely to Embolize – About 50% Are Asymptomatic (Formation of Collaterals) – May Produce Edema, Pain and Tenderness
  22. 22. • Phlebothrombosis It is due to stasis of blood in un-inflamed veins, particularly the calf veins. • Thrombophlebitis It is related to inflammation of the vein walls.
  23. 23. PHLEBOTHROMBOSIS THROMBOPHLEBITIS Main cause Stasis Inflammation Primary thrombus Small Larger-depends on extent of phlebitis. Propagated clot Long/poorly anchored Usually none-if present short and well-anchored Emboli Common, may be massive Rare unless infective Sterile Site Usually calf veins Anywhere Clinical Often silent Pain Signs of inflammation
  24. 24. CLINCAL SETTING FOR VENOUS THROMBUS FORMATION Cardiac Failure (CHF) Trauma Surgery Burns 3rd Term Pregnancy and Postpartum Cancer (migratory thrombophlebitis-Trousseau’s Syndrome) Bed Rest Immobilization
  25. 25. Valvular Thrombi (vegetations) Infective Endocarditis Non-bacterial Thrombotic Endocarditis (NBTE) -Seen in patients dying of chronic debilitating diseases- advanced cancer (50% cases) & other end stage diseases (cachectic, marantic or terminal endocarditis) Atypical Verrucous Endocarditis (Libman-sacks) -Seen in 50% of acute SLE, Systemic sclerosis, Collagen diseases Capillary thrombi Minute thrombi composed mainly of packed red cells in vasculitis & DIC
  26. 26. FATE OF THROMBOSIS Resolution (Dissolution) Recent thrombi can undergo total lysis by activation of fibrinolytic system (mostly small venous thrombi). After the first 2-3 h, thrombi won’t undergo lysis. Organization and recanalization Replacement by granulation tissue followed by recanalaization or healing totally to leave only a small fibrous‘Lump’ as evidence of a previous thrombus Propagation Accumulation of more platelet & fibrin and obstruction Embolization Early & infected thrombi may detache from site of origin and may block distal vesseles Hyalinization & Calcification (Degraded thrombus with superadded bacterial infection may lead to mycotic aneurysm)
  27. 27. Thrombus Propagated into the Inferior Vena Cava
  28. 28. CLINICAL SIGNIFICANCE: Obstruction of arteries or veins can cause ischemia, infarction, or may embolize Venous thrombi may lead to congestion, poor wound healing, skin ulcers and painful thrombosed veins Microthrombi in microcirculation (capillaries) may cause DIC
  29. 29. DIAGNOSIS: • Clinical signs are unreliable. • Phlebography using a contrast medium. • Radioactive iodine-labelled fibrinogen test. • Doppler ultrasound.
  30. 30. EMBOLISM
  31. 31. EMBOLISM It is the process of carrying an abnormal mass (embolus) in the blood stream to a point distant from its origin. *An embolus is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
  32. 32. TYPES OF EMBOLI Gas (air, nitrogen , other gases) Liquid (amniotic fluid, radiographic contrast material, fat after soft tissue trauma / fracture, bone marrow ) Solid (thrombus-- most common, foreign body- bullet, catheter; also atheroematous material, tumor cell clumps, tissue fragments, parasites, bacterial clumps etc. 99% are dislodged thrombus Rarely: Bullets, Fat, Air, Atherosclerotic Fragments, Tumor Fragments, Bone Marrow Emboli can be Bland (sterile) or Septic (infected)
  33. 33. • ORIGIN & SITES OF EMBOLIZATION: • Venous: Systemic veins Pulmonary arteries • Arterial: Heart or aorta Systemic circulation • Paradoxic: Systemic veins (through septal defect in heart or AV shunts in heart) systemic circulation *Retrograde: Embolus traveling against the flow of blood (metastatic deposits in spine from carcinoma prostate due to retrograde embolism through intraspinal veins from large thoracic & abdominal veins due to increased pressure in body cavities: during coughing or straining)
  34. 34. EFFECTS OF EMBOLISM Ischemia Infarction Sepsis if infected (example: pulmonary embolism with pulmonary infarction)
  35. 35. Thromboembolism A detached thrombus or part of thrombus constitutes the most common type of embolism *Arterial (systemic) thromboembolism (from within heart & arteries) *Venous thromboembolism Pulmonary thromboembolism (from veins of lower legs & upper limbs, pelvic vein, cavernous sinus of brain, right side of heart)
  36. 36. Systemic Thromboembolism • Emboli traveling within the arterial circulation • 80% arise from intra-cardiac mural thrombi (myocardial infarction) • Vegetations on the heart valves (mitral/aortic) & prosthetic heart valves may embolize to the systemic circulation • Infective endocarditis, Cardiomyopathy & CHD may be cause • Emboli developing in relation to atherosclerotic plaques, aortic aneurysms, pulmonary veins and paradoxic emboli • Major site of embolization are lower extremities (75%), brain (10%), intestine, kidney & spleen • Leads to infarction of the affected organs, gangrene, arteritis & mycotic aneurysm, myocardial infarction and sudden death.
  37. 37. Pulmonary Thromboembolism Generally originate from deep leg veins (popliteal, femoral & iliac) Usually pass through the right heart Into pulmonary vasculature 60% Pulmonary Arterial obstruction usually leads to sudden death, RVF Most pulmonary emboli (60-80%) are clinically silent because of small size • May occlude main pulmonary artery, across the bifurcation (Saddle Embolus) or pass into the smaller branching arterioles • Embolic obstruction of medium-sized arteries may result in hemorrhage without infarction because of intact bronchial circulation. If bronchial circulation is compromised as in left heart failure it results in infarction • Emboli obstructing small end-arteriolar pulmonary branches usually result in associated infarction • Multiple pulmonary emboli over time may cause pulmonary hypertension and right heart failure
  38. 38. Thromboembolism
  39. 39. Pulmonary Embolus
  40. 40. Saddle Pulmonary Embolus
  41. 41. Embolization (Embolus) Thromboembolism of Pulmonary Artery Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003; . Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
  42. 42. Fat embolism syndrome Microscopic fat globules derived from long bone fractures (fatty marrow) or rarely from soft tissue trauma and burns 10% of cases show clinical findings Clinically characterized by Pulmonary insufficiency, neurologic symptoms, anemia & thrombocytopenia Symptoms appear 1-3 days after injury Pathogenesis Mechanical obstruction in pulmonary & cerebral microcirculation and chemical injury to endothelium by free fatty acids resulting in skin rash
  43. 43. Bone Marrow Embolus In Pulmonary Vessel Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.
  44. 44. Air embolism Gas bubbles within the circulation can obstruct vascular flow to cause distal ischemic injury Air can enter the circulation during Chest wall injury, Operation on neck & head, Obstetrical operation & trauma, Intravenous infusion, Sudden atmospheric pressure changes in scuba & deep sea divers, underwater construction workers and in individual in unpressurized aircraft in rapid ascent (Decompression sickness- Caisson disease) Clinically characterized by Bends due to rapid gas bubble formation within skeletal muscle & about joint Chokes due to respiratory distress caused by edema, hemorrhage, focal atelectasis, emphysema CNS & CV effects due to focal ischemia Multiple foci of ischemic necrosis specially in heads of femur, tibia, humerus etc Clinical effects observed with air in excess of 100 ml
  45. 45. Amniotic Fluid Embolism Torn placental membrane- amniotic fluid release Rupture of uterine veins Infusion of amniotic fluid into maternal venous circulation Morphologically characterized by Lungs show squamous cells, lanugo hair, mucin from GIT & RS pulmonary edema, diffuse alveolar damage, systemic fibrin thrombi Clinically characterized by Severe dyspnea, cyanosis, hypotensive shock, seizures, coma & DIC Mortality rate> 80%
  46. 46. Disseminated Intravascular Coagulation (DIC) • Sudden widespread fibrin deposition in microcirculation • Rapid consumption of platelets and coagulation proteins • Secondary massive fibrinolysis, all the little thrombi dissolve • Clotting Disorder Turns Into a Bleeding Disaster Sepsis is common cause of DIC (30-50% of patients with gram negative sepsis)
  47. 47. Clinical Consequences of DIC
  48. 48. Tumor Embolism Tumor Embolism Lymphatics (Carcinoma) Blood vesseles (Sarcoma) Common sites Liver (Carcinoma) Lung (Carcinoma & Sarcoma) Bone (Prostate, Thyroid, Breast, Kidney, Lung
  49. 49. INFARCTION
  50. 50. INFARCTION An infarct is a localized area of ischemic necrosis caused by occlusion of either the arterial supply or venous drainage in a particular tissue • 90-99% of all infarcts due to arterial thrombotic or embolic events Less common causes of infarction are vasospasm, hemorrhage in atheromatous plaque, twisting of vessel, extrinsic compression or traumatic rupture of blood supply • Coagulative necrosis is characteristic of hypoxic death in all tissues except CNS • All infarcts tend to be wedge-shaped, with the occluded vessel at the apex
  51. 51. TYPES OF INFARCTS: •Bland vs. Septic (assumed to be bland unless specified as “septic”) •Arterial (usually white/pale) vs. Venous (red/hemorrhagic); •Bland and arterial most common
  52. 52. MORPHOLOGY OF INFARCTS White/Pale: Occur with arterial occlusion or in solid organs with single blood supply (ex: kidneys, spleen) Red/Hemorrhagic: Occur with venous occlusion, in loose tissues, tissues with dual circulation. All infarcts are wedge shaped, poorly defined & hemorrhagic in initial stage, later margins are better defined revealing hyperemia, become pale & sharply defined in solid organs and firmer & browner in spongy organs Microscopic evidence is visible after (12-18) hours if patient survives Characterized by coagulative / liquefactive necrosis surrounded by inflammatory zone, later there is evidence of regeneration & repair. Most infarcts are ultimately replaced by scars tissue. Septic infarction results from embolization of infected vegetation from heart valve or if microbes seed area of necrosis →abscess →organization
  53. 53. FACTORS AFFECTING INFARCTS: • Nature of the vascular supply (dual arterial supply) • Collateral circulation • Rate of development of occlusion • Duration of occlusion • Metabolic needs of the tissue/organ • Vulnerability of the tissue to hypoxia Brain - < 3 minutes Heart – 0.5-2 hours Kidney – 2-3 hours Skin fibroblasts - < 24 hours • Oxygen content of blood
  54. 54. Hemorrhagic Lung Infarct Pale Splenic Infarct
  55. 55. Myocardial Infarction
  56. 56. MYOCARDIAL INFARCTION
  57. 57. Myocardial Infarction Regional Full-Thickness (Left); Circumferential Subendocardial (Right) Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995. Left VentricleLeft Ventricle
  58. 58. Mural Thrombus Over Myocardial Infarction Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
  59. 59. Myocardial Infarction Rupture Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995. VentricleVentricle
  60. 60. Myocardial Infarction Chronological Appearance Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
  61. 61. Myocardial Infarction Chronological Appearance Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
  62. 62. Myocardial Infarction Chronological Appearance Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
  63. 63. Myocardial Infarction Chronological Appearance Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.
  64. 64. RENAL INFARCTION
  65. 65. Kidney Infarction Replaced by Fibrotic Scar (Left) Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.
  66. 66. Lung Infarct Wedge Shape...
  67. 67. Infarcted Colon OK Colon
  68. 68. CLINICAL SIGNIFICANCE OF INFARCTION •Usually cause pain; •May cause loss of function (example: myocardial infarct may cause heart failure); •May cause hemorrhage or sepsis (examples: lung infarct causes hemoptysis, bowel infarct causes GI bleeding or sepsis).
  69. 69. SHOCK
  70. 70. SHOCK It is defined as systemic hypo-perfusion due to reduction either in Cardiac Output or Effective Circulating Blood Volume. The End Results are: • Hypotension, followed by • Impaired Tissue Perfusion and Cellular Hypoxia • Reversible Cellular Injury→ Irreversible Tissue Injury→ Death • Non-Progressive Stage, Progressive Stage, Irreversible Stage
  71. 71. TYPES OF SHOCK Three Main Categories: Cardiogenic, Hypovolemic, and Septic Others: Neurogenic Shock (anesthetic and spinal cord injury) & Anaphylactic Shock
  72. 72. CARDIOGENIC SHOCK Results From Severe Myocardial Failure Due to: – Intrinsic myocardial damage (myocardial infarction, ventricular rupture, arrhythmia) – Extrinsic Compression (cardiac tamponade) – Outflow Obstruction (pulmonary embolism)
  73. 73. HYPOVOLEMIC SHOCK Results From Loss of Blood or Plasma Volume: - Hemorrhage - Fluid Loss (severe burns, trauma, vomiting, diarrhea etc.)
  74. 74. SEPTIC (ENDOTOXIC) SHOCK • Most common cause of death in ICU’s in the US • Dissemination of infection into the vasculature • Caused by overwhelming systemic microbial infection, most often by Gram-negative infection (Endo-toxic Shock) but can also occur with Gram-positive and fungal infections • Spread & expansion of localized infection (abscess, peritonitis, pneumonia) into the blood stream.
  75. 75. Pathogenesis Of Septic Shock • Endotoxins are bacterial wall lipopolysaccharides (LPS) which consists of a toxic fatty acid (Lipid A) core and a complex polysaccharide coat (unique to each species). Gram-positive bacteria and fungi have analogus molecules. • High quantities of LPS → (TNF & IL-1→ IL6 & IL8) -Systemic vasodilation (hypotension), -Diminished cardiac contractility, -Widespread endothelial injury and activation (SLA, ARDS, DAD), -Activation of coagulation system (DIC) • Multi-organ system failure and death
  76. 76. Effects of Shock on Tissues • Brain -- ischemic encephalopathy --> confusion, obtundation; • Heart -- subendocardial ischemia, infarction; contraction band necrosis --> decreased output • Kidneys -- acute tubular necrosis --> oliguria, anuria and electrolyte disturbances • Lungs -- diffuse alveolar damage (DAD) --> Adult respiratory distress syndrome (ARDS) --> hypoxia • GI tract -- mucosal necrosis, hemorrhages • Liver -- central necrosis, fatty change • Coagulation system -- disseminated intravascular coagulation (DIC)
  77. 77. Morphology of Shock
  78. 78. Clinical Course of Shock • Hypotension • Weak, rapid pulse, tachycardia • Rapid shallow respiration • Drowsiness, confusion & irritability • Cool, clammy skin – In septic shock the skin is initially warm and flushed secondary to peripheral vasodilation • Multi-organ failure ensues if shock continues
  79. 79. Hyperemia & Congestion Increased volume of blood in an area compared to normal Hyperemia Hyperemia is an active process resulting from augmented tissue inflow due to arteriolar dilation (e.g. Acute inflammation, Exercising muscles, Blushing, Sexual arousal) Congestion Congestion is a passive process resulting from impaired outflows from a tissue (cardiac failure-systemic or venous obstruction-local) Both can be Local or Diffuse
  80. 80. MORPHOLOGY OF HYPEREMIA & CONGESTION – Hyperemia: tissue is red or purple, engorged with oxygenated blood, swollen, often edematous. Examples- Lungs. – Congestion: tissue is blue-red in color due to accumulation of deoxygenated hemoglobin in the affected tissues. Later on tissue becomes brownish (iron deposition) & indurated (fibrosis). Examples – Liver, Legs, Lungs
  81. 81. PULMONARY CONGESTION – Acute Pulmonary Congestion: engorged alveolar capillaries, alveolar septal edema, focal minute intra-alveolar hemorrhage – Chronic Pulmonary Congestion: thickened & fibrotic septa along with presence of numerous hemosidrin–laden macrophages (Heart Failure Cells) HEPATIC CONGESTION – Acute Hepatic Congestion: central vein and sinusoids are distended with blood, central hepatocytes may show degeneration & peripheral hepatocytes may develop fatty change – Chronic Passive Congestion of Liver: central regions of hepatic lobules are grossly red- brown, slightly depressed & surrounding uncongested zones reveal fatty change (nutmeg liver). Microscopically there is centrilobular necrosis with hepatocyte drop out and hemorrhage & hemosidrin containing macrophages. Hepatic fibrosis (cardiac cirrhosis) may be seen in heart failure.
  82. 82. Hyperemia in PneumoniaHyperemia Infection (Pneumonia)
  83. 83. Liver - Chronic Passive Congestion
  84. 84. “Nutmeg” Liver Cross Section of a Nutmeg“Nutmeg” Liver
  85. 85. Chronic Passive
  86. 86. SIGNIFICANCE OF CONGESTION If diffuse, usually indicates Heart failure; If local, usually indicates a blockage upstream toward the heart; Cirrhosis can cause Varices in esophagus
  87. 87. HEMORRHAGE Extravasation of blood due to rupture of blood vessels – Rupture of a large vessel: Trauma, Atherosclerosis, Inflammatory or Neoplastic Erosion – Rupture of small vessels: hemorrhagic diathesis Hematoma is blood enclosed within tissue (red-blue → blue-green → golden brown) Petechiae are minute (1-2 mm) hemorrhages into skin, mucous membranes or serosal surfaces Purpuras are larger (3-5 mm) hemorrhages Ecchymoses are larger (1-2 cm) subcutaneous hematomas (bruises) Hemothorax, Hemopericardium, Hemoperitonium and Hemoarthrosis are bleeding in one or other body cavities. Hematochezia- bright red blood per rectum, Melena - dark black blood per rectum Hematuria - blood, gross or microscopic in urine Hemoptysis - coughing up of blood , Hematemesis - vomiting up of blood
  88. 88. CAUSES OF HEMORRHAGE – Trauma – Vascular diseases with rupture (atherosclerosis, arteritis, aneurysms, etc.). – Low platelets (below 10-15,000/cu mm) – Coagulopathy (factors less than 10% activity) – Ulcers, tumors, coagulation factors, infarcts,
  89. 89. MORPHOLOGY OF HEMORRHAGE Acute – Red or purple collection of blood in tissue Chronic or old – Brown or maroon pasty material
  90. 90. EFFECTS OF HEMORRHAGE Effects of hemorrhage depends on following factors: Location Rate Duration Co-morbid diseases (emphysema, anemia, heart disease)
  91. 91. Hemorrhage Why do bruises change color as they Resolve? • The RBC’s in a hemorrhage are broken down: – hemoglobin (red) → bilirubin (blue-green) → hemosiderin (golden-brown)
  92. 92. Intracerebral Hemorrhage Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.
  93. 93. PurpuraPurpuraColonic PetechiaeColonic Petechiae ThrombocytopeniaThrombocytopenia Idiopathic Thrombocytopenic PurpuraIdiopathic Thrombocytopenic Purpura
  94. 94. Clinical Effects of Hemorrhage • <20% blood loss, little health effect in otherwise healthy individuals – That’s why donating blood is OK – But suppose you have heart or lung disease - mild blood loss could decrease critical oxygen carrying capacity and → ‘heart attack’ • >20% blood loss → hemorrhagic shock • Bleeding into the brain stem is fatal while same blood loss from a finger cut is trivial • Chronic recurrent bleeding can lead iron deficiency anemia!
  95. 95. Anemia from Blood Loss • This may be the only hint of Occult Cancer – Carcinoma of the Colon – Gastric Carcinoma (less common)
  96. 96. EDEMA
  97. 97. EDEMA Excess accumulation of fluid in the interstitial tissue spaces. • A transudate (protein-poor fluid -specific gravity <1.012) or • An exudate (protein-rich fluid -specific gravity >1.020)
  98. 98. SPECIAL TYPES OF EDEMA • Pleural effusion (hydro-thorax) • Pericardial effusion (hydro-pericardium) • Ascites (edema in peritoneal cavity) • Anasarca (widespread edema) • Cerebral edema (in brain, intra- and extracellular)
  99. 99. Normal Microcirculation Capillary Arterial Venous Hydrostatic Pressure + 36 + 16 Osmotic Pressure - 26 - 26 Net filtration Pressure + 10 mmHg - 9 mm Hg (leak-out) (Reabsorb)
  100. 100. Homeostasis is maintained by the opposing effects of vascular hydrostatic pressure and plasma colloid osmotic
  101. 101. Pathophysiologic Categories of Edema I. Increased Hydrostatic Pressure II. Reduced Plasma Osmotic Pressure III. Lymphatic Obstruction IV. Sodium Retention V. Inflammation
  102. 102. Increased Hydrostatic Pressure A. Congestive Heart Failure B. Portal Hypertension C. Venous Thrombosis
  103. 103. Congestive Heart Failure Inability of Heart to Pump blood in systemic circulation ↓ Blood backing up into the lungs ↓ Blood backing up into the venous circulation ↓ Increasing Central Venous Pressure (CVP) ↓ Increased capillary pressure (Hydrostatic Pressure) ↓ Edema ↓ ↓ Cardiac Output → Decreased Arterial blood volume → Decrease Renal perfusion ↓ Activates the Renal Defense Mechanisms Renin-Angiotensin-Aldosterone Axis, Renal Vasoconstriction, Increased ADH
  104. 104. Congestive Heart Failure Renin-Angiotensin-Aldosterone Axis Renin Aldosterone Renal Na reabsorption Renal retention of Na + H2O Plasma volume Transudation EDEMA Decreased Renal Perfusion
  105. 105. Congestive Heart Failure Renal Vasoconstriction Renal Vasoconstriction Glomerular Filtration Rate (GFR) Tubular reabsorption of Na + H2O Plasma volume Transudation EDEMA Decreased Renal Perfusion Renal retention of Na + H2O
  106. 106. Congestive Heart Failure Anti-Diuretic Hormone Anti-Diuretic Hormone (ADH) Renal retention of H2O Plasma volume Transudation EDEMA Decreased Renal Perfusion Renal retention of Na + H2O
  107. 107. Central Venous Pressure Renal Perfusion Renin Renal Vasoconstriction ADH Congestive Heart Failure
  108. 108. Events Leading to Systemic Edema Secondary to Primary Heart Failure Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.
  109. 109. Clinically initially cardiac edema can be demonstrated in legs or sacrum
  110. 110. Portal Hypertension • Portal Hypertension is “Increased resistance to portal blood flow” • The most common cause of Portal Hypertension is CIRRHOSIS • Results in Ascites • Pathogenesis of Ascites is complex – Increased Portal Pressure (hydrostatic pressure) leads to increased liver sinusoidal hypertension. Fluid moves into the Space of Disse then into lymphatics • The hepatic lymph percolates into the peritoneal cavity – Normal thoracic duct lymph = 1 Liter/d – In cirrhosis, hepatic lymph flow far exceeds Thoracic duct capacity Cirrhosis → hypoalbuminemia → decrease in plasma osmotic pressure → ascites → decrease in blood volume → decreased renal perfusion → secondary hyperaldosteronism (increased renin etc.)
  111. 111. AscitesAscites
  112. 112. Portal Hypertension Sinusoidal Hypertension Renal Perfusion Hepatic Lymph Overwhelms Thoracic Duct Aldosterone ASCITES Cirrhosis Serum Albumin
  113. 113. Venous Thrombosis • Impaired venous outflow increases hydrostatic pressure
  114. 114. Reduced Plasma Osmotic Pressure • Albumin is the serum protein MOST responsible for the maintenance of colloid osmotic pressure. • A decrease in osmotic pressure can result from increased protein loss or decreased protein synthesis • Increased albumin Loss: – Nephrotic Syndrome • Increased protein permeability of the glomerular basement membrane – Protein losing gastroentropathy • Reduced albumin synthesis – Cirrhosis – Protein malnutrition
  115. 115. Inflammation • Both Acute and Chronic Inflammation are associated with Edema • Generalized edema in systemic infections, poisoning, certain drugs & chemicals, anaphylactic reactions and anoxia • Localized edema in infections, allergic reactions, insect bite, irritant drugs & chemical and Angioneurotic edema* *It involves skin of face & trunk and may involve lips, larynx, pharynx, lung etc
  116. 116. Angioedema
  117. 117. Lymphatic Obstruction • Impaired lymphatic drainage with resultant lymphedema, usually localized • Commonly due to inflammation or neoplastic obstruction, may be post-surgical & post-radiation in patient undergoing treatment for Breast Cancer Both Acute and Chronic Inflammation are associated with EDEMA Filariasis: A parasitic infection causing massive lymphatic & lymph nodes fibrosis in inguinal region resulting in edema of external genetalia & lower limbs called elephantiasis Carcinoma of breast with obstruction of superficial lymphatics can lead to an unusual appearance of the breast- “peau d’orange” (orange peel) Resection and/or radiation to axillary lymphatics can lead to arm edema
  118. 118. Elephantiasi s
  119. 119. Elephantiasis (filariasis)
  120. 120. “peau d’orange” appearance in breast cancer
  121. 121. Sodium & Water Retention • Contributory factors in several forms of edema • Salt retention may be primary cause of edema Post-streptococcal glomerulonephritis & Acute Renal failure • Increased salt with accompanying water cause increase hydrostatic pressure and decreased vascular colloid osmotic pressure leading to edema
  122. 122. EDEMA INCREASED HYDROSTATIC PRESSURE Congestive Heart Failure Portal hypertension (Ascites) Venous Obstruction •HEART •LIVER •KIDNEY INFLAMMATION Increased permeability DECREASED ONCOTIC PRESSURE Nephrotic Syndrome Cirrhosis (Ascites) Protein Malnutrition LYMPHATIC OBSTRUCTION Inflammatory Neoplastic SALT & WATER RETENTION
  123. 123. GENERALIZED EDEMA • HEART • LIVER • KIDNEY
  124. 124. Edema Morphology • Edema of the Subcutaneous Tissue is most easily detected Grossly (not microscopically) • Push your finger into it and a depression remains (pitting) • Swelling and wetness of the tissues • Subtle cell swelling with clearing and separation of extracellular elements • Dependent Edema is a prominent feature of Congestive Heart Failure (legs in standing & sacrum in recumbent position) • Periorbital edema is often the initial manifestation of Nephrotic Syndrome, later affecting all parts of body
  125. 125. Pitting edema
  126. 126. Pulmonary Edema • Pulmonary Edema is most frequently seen in Congestive Heart Failure (LVF) – May also be present in Mitral Stenosis, Cardiac Surgery, Renal failure, Adult Respiratory Distress Syndrome (ARDS), Pulmonary Infections, Inhalation of toxic substances, Aspiration, Radiation injury, Shock, Uremia, High altitude edema and Hypersensitivity reactions. • The Lungs are typically 2-3 times normal weight • Cross sectioning causes an outpouring of frothy, sometimes blood-tinged fluid representing mixture of air, edema fluid & extravasated red cells • Microscopically alveolar capillaries are congested and there is collection of eosinophilic, granular and pink proteinaceous material (edematous fluid) in interstitial and alveolar spaces
  127. 127. Pulmonary Edema
  128. 128. Pulmonary EdemaNormal Lung
  129. 129. Pulmonary Congestion and Edema
  130. 130. Edema of the Brain • Localized: Abscess, Neoplasm • Generalized: Encephalitis, Hypertensive crises, Obstruction of venous outflow, Trauma • In Generalized edema brain is grossly swollen with narrowed sulci and distended gyri showing flattening against skull • Vasogenic & Cytotoxic edema
  131. 131. Brain edema
  132. 132. Clinical Correlation • Subcutaneous Edema-Annoying but Points to Underlying Disease – However, it can impair wound healing or clearance of Infection • Pulmonary Edema-May cause death by interfering with Oxygen and Carbon Dioxide exchange & Creates a favorable environment for infection • Edema of Brain-The big problem is: There is no place for the fluid to go! Herniation into the foramen magnum will kill or brain stem vascular supply can be compressed and damage vital centers
  133. 133. 140
  1. A particular slide catching your eye?

    Clipping is a handy way to collect important slides you want to go back to later.

×