fluid & hemodynamics

FLUID AND FLUID AND HEMODYNAMICHEMODYNAMIC

SSElla C. Lim, M.D., DPSPElla C. Lim, M.D., DPSP

EDEMAEDEMA

Definition: Extravasation of fluid from Definition: Extravasation of fluid from vessels into interstitial spaces or body vessels into interstitial spaces or body cavities; the fluid may be cavities; the fluid may be protein poor protein poor (TRANSUDATE)(TRANSUDATE) or may be or may be protein protein rich (EXUDATE)rich (EXUDATE)..

Hydrothorax, hydroperitoneum Hydrothorax, hydroperitoneum (ascites), hydropericardium, anasarca(ascites), hydropericardium, anasarca

EDEMAEDEMA

Causes: Causes: (table 4-1 Pathophysiologic categories of (table 4-1 Pathophysiologic categories of edema)edema)

INCREASED HYDROSTATIC INCREASED HYDROSTATIC PRESSUREPRESSURECaused by a reduction in venous return Caused by a reduction in venous return

(heart failure)(heart failure) DECREASED COLLOID OSMOTIC DECREASED COLLOID OSMOTIC

PRESSURE PRESSURE caused by reduced caused by reduced concentration of plasma albumin concentration of plasma albumin (decreased synthesis – liver disease (decreased synthesis – liver disease OR increased loss – kidney disease)OR increased loss – kidney disease)

EDEMAEDEMA

CausesCauses:: LYMPHATIC OBSTRUCTIONLYMPHATIC OBSTRUCTION

that impairs interstitial fluid that impairs interstitial fluid clearance (e.g., scarring, tumors- clearance (e.g., scarring, tumors- pMRM, infection - filariasis)pMRM, infection - filariasis)

PRIMARY RENAL SODIUM PRIMARY RENAL SODIUM RETENTION RETENTION (renal failure)(renal failure)

INCREASED VASCULAR INCREASED VASCULAR PERMEABILITY PERMEABILITY (inflammation)(inflammation)

Lymphatic obstruction from Lymphatic obstruction from filariasisfilariasis

Pitting edema of the legPitting edema of the leg

EdemaEdema

HYPEREMIA & CONGESTIONHYPEREMIA & CONGESTION

HyperemiaHyperemia – – active processactive process resulting from augmented tissue resulting from augmented tissue inflow because of arteriolar dilation inflow because of arteriolar dilation (e.g., exercise, inflammation); (e.g., exercise, inflammation); oxygenated bloodoxygenated blood - - erythemaerythema

CongestionCongestion – – passive processpassive process resulting from impaired outflow from resulting from impaired outflow from a tissue; a tissue; deoxygenateddeoxygenated bloodblood - - cyanosiscyanosis..

Lung, acute pulmonary congestion Lung, acute pulmonary congestion & edema – medium power& edema – medium power

Lung, acute pulmonary Lung, acute pulmonary congestion & edema – medium congestion & edema – medium

powerpower Identify:Identify:

Congested alveolar septaCongested alveolar septa Intra-alveolar transudateIntra-alveolar transudate

The alveolar septa are prominent, due The alveolar septa are prominent, due to marked congestion of the capillaries. to marked congestion of the capillaries.

The alveolar lumens contain pale-The alveolar lumens contain pale-staining edema fluid. Compare this form staining edema fluid. Compare this form of pulmonary congestion with chronic of pulmonary congestion with chronic passive congestion in the next image. passive congestion in the next image.

What is the pathogenesis of What is the pathogenesis of pulmonary edema?pulmonary edema?

Pathogenesis of Pulmonary Pathogenesis of Pulmonary EdemaEdema

MI – LVF (left ventricular failure) - MI – LVF (left ventricular failure) - pump failure - impaired blood flow pump failure - impaired blood flow from lung to LA (left atrium) – from lung to LA (left atrium) – Increased hydrostatic pressure in Increased hydrostatic pressure in pulmonary alveolar capillaries - pulmonary alveolar capillaries - transudation of fluid into alveoli. transudation of fluid into alveoli.

Pulmonary edema in other cases may Pulmonary edema in other cases may also result from also result from damage to alveolar damage to alveolar capillariescapillaries (eg, ARDS). (eg, ARDS).

How does this type of edema differ How does this type of edema differ from that seen in acute from that seen in acute inflammation? inflammation?

The fluid in The fluid in pulmonary edemapulmonary edema is a is a transudatetransudate (ie, it is protein poor, (ie, it is protein poor, has low specific gravity, and does has low specific gravity, and does not contain inflammatory cells). not contain inflammatory cells).

Edema in inflammationEdema in inflammation is an is an exudateexudate..

Lung, chronic passive venous Lung, chronic passive venous congestion – grosscongestion – gross


Identify:Identify: HilusHilus PleuraPleura Cut surfaceCut surface

This is caused by any chronic This is caused by any chronic condition that retards the outflow of condition that retards the outflow of pulmonary venous blood from the pulmonary venous blood from the lungs to the left side of the heart lungs to the left side of the heart (eg, chronic mitral valve stenosis). (eg, chronic mitral valve stenosis).


Pooling of blood in the lung capillaries Pooling of blood in the lung capillaries and associated microhemorrhages and associated microhemorrhages produce a dark brown discoloration, produce a dark brown discoloration, noted here. noted here.

In addition, septal fibrosis causes the In addition, septal fibrosis causes the lung to become stiff. The fibrosis lung to become stiff. The fibrosis causes the lung to feel firm to the causes the lung to feel firm to the touch; also, the fibrosis causes the cut touch; also, the fibrosis causes the cut edges to be raised or to stand up. edges to be raised or to stand up.

This gross appearance is also called This gross appearance is also called brown induration of the lung.brown induration of the lung.

Lung, Chronic Passive Lung, Chronic Passive CongestionCongestion

What is the brown pigment that is What is the brown pigment that is derived from hemoglobin?derived from hemoglobin?

What are heart failure cells?What are heart failure cells?


HemosiderinHemosiderin

Hemosiderin laden macrophagesHemosiderin laden macrophages

Lung, chronic passive venous Lung, chronic passive venous congestion – high powercongestion – high power

Lung, chronic passive venous Lung, chronic passive venous congestion – high powercongestion – high power

Identify:Identify:Alveolar septaAlveolar septaMacrophages with Macrophages with

hemosiderinhemosiderin

Are the alveolar septa normal in Are the alveolar septa normal in thickness?thickness?


They are thickened, due to edema They are thickened, due to edema and reactive fibrosis.and reactive fibrosis.

What effect would such a histologic What effect would such a histologic picture have on gaseous exchange in picture have on gaseous exchange in the lung?the lung?


It would be markedly impaired. It would be markedly impaired.

What might the symptoms be?What might the symptoms be?


DyspneaDyspnea OrthopneaOrthopnea Paroxysmal nocturnal Paroxysmal nocturnal

dyspneadyspnea CoughCough

Liver, chronic passive venous Liver, chronic passive venous congestion – gross, cut surfacecongestion – gross, cut surface


This condition is caused by resistance or This condition is caused by resistance or obstruction to the outflow of venous blood obstruction to the outflow of venous blood from the liver, as may occur in chronic right from the liver, as may occur in chronic right heart failure (congestive heart failure). heart failure (congestive heart failure).

The area surrounding the central veins The area surrounding the central veins (centrizonal) becomes intensely congested, (centrizonal) becomes intensely congested, and the hepatocytes in the central zone may and the hepatocytes in the central zone may even become necrotic due to hypoxia. even become necrotic due to hypoxia.

These centrilobular areas are seen as the These centrilobular areas are seen as the dark red spots on the cut surface. dark red spots on the cut surface.


The alternating pale areas represent the The alternating pale areas represent the periportal hepatocytes, which have periportal hepatocytes, which have sustained a lesser degree of hypoxia. sustained a lesser degree of hypoxia.

This gross appearance is also calledThis gross appearance is also called NUTMEG LIVERNUTMEG LIVER. .

Remember that in the hepatic lobules, Remember that in the hepatic lobules, blood flows from the periportal to the blood flows from the periportal to the central zones, and hence the central zones, and hence the centrilobular areas are more vulnerable centrilobular areas are more vulnerable to hypoxia than are the peripheral to hypoxia than are the peripheral hepatocytes. hepatocytes.

NUTMEG NUTMEG

NUTMEGNUTMEG

Liver, chronic passive venous Liver, chronic passive venous congestion – medium powercongestion – medium power

Liver, chronic passive venous Liver, chronic passive venous congestion – medium powercongestion – medium power

Identify:Identify: Portal triadsPortal triads CongestionCongestion

The congestion and accompanying The congestion and accompanying sinusoidal dilatation are maximum in sinusoidal dilatation are maximum in and around central veins and and around central veins and decrease progressively toward portal decrease progressively toward portal triads. This is due to back pressure triads. This is due to back pressure opposite to the direction of normal opposite to the direction of normal blood flow in the hepatic lobule. blood flow in the hepatic lobule.

HEMORRHAGEHEMORRHAGE

HemorrhageHemorrhage vs. Congestion – vs. Congestion – extravasation of blood due to extravasation of blood due to vessel vessel rupturerupture

Hematoma – accumulation of blood Hematoma – accumulation of blood w/in tissuew/in tissue

Petechiae (1-2 mm)Petechiae (1-2 mm) Purpura (3 mm)Purpura (3 mm) Ecchymoses (>1 to 2 cm)Ecchymoses (>1 to 2 cm) Hemothorax, hemopericardium, Hemothorax, hemopericardium,

hemoperitoneum, hemarthrosishemoperitoneum, hemarthrosis

HEMATOMAHEMATOMA

PETECHIAE & PURPURAPETECHIAE & PURPURA

ECCHYMOSESECCHYMOSES

HEMOSTASISHEMOSTASIS Endothelial InjuryEndothelial Injury VasoconstrictionVasoconstriction – Endothelin – Endothelin Primary HemostasisPrimary Hemostasis – Platelet adhesion – Platelet adhesion

(vWF) – shape change – granule release (vWF) – shape change – granule release (ADP, TXA(ADP, TXA22) - recruitment – aggregation (1º ) - recruitment – aggregation (1º hemostatic plug)hemostatic plug)

Secondary HemostasisSecondary Hemostasis – TF & – TF & phospholipids (coagulation cascade) – phospholipids (coagulation cascade) – thrombin activation – fibrin polymerization – thrombin activation – fibrin polymerization – 2º hemostatic plug2º hemostatic plug

Thrombus & Antithrombotic eventsThrombus & Antithrombotic events – tPA – tPA (fibrinolysis) & thrombomodulin (blocks (fibrinolysis) & thrombomodulin (blocks coagulation cascade)coagulation cascade)

COAGULATION CASCADECOAGULATION CASCADE

Coagulation CascadeCoagulation Cascade Intrinsic PathwayIntrinsic Pathway – – Factor XIIFactor XII

(Hageman factor)(Hageman factor) Extrinsic PathwayExtrinsic Pathway – – Tissue FactorTissue Factor Common PathwayCommon Pathway – – Factor IXFactor IX – –

Thrombin – FibrinThrombin – Fibrin

Fibrinolytic CascadeFibrinolytic Cascade Plasminogen - Plasminogen - PlasminPlasmin


Three natural anticoagulants: Three natural anticoagulants: (1) (1) Proteins C & SProteins C & S - generates active - generates active

protein C that inactivates cofactors Va and protein C that inactivates cofactors Va and VIIIa. Protein C itself is activated by VIIIa. Protein C itself is activated by thrombin after the latter binds to thrombin after the latter binds to thrombomodulin on the endothelium. thrombomodulin on the endothelium.

(2) (2) AntithrombinAntithrombin is activated by binding is activated by binding to heparin-like molecules on the to heparin-like molecules on the endothelium; activated antithrombin endothelium; activated antithrombin causes proteolysis of active factors IXa, Xa, causes proteolysis of active factors IXa, Xa, XIa, XIIa and thrombin.XIa, XIIa and thrombin.


(3) (3) Tissue factor pathway inhibitor Tissue factor pathway inhibitor (TFPI)(TFPI) – – a protein secreted by a protein secreted by endothelium (and other cell types), endothelium (and other cell types), complexes to factor Xa and to tissue complexes to factor Xa and to tissue factor VIIa and inactivates them to factor VIIa and inactivates them to rapidly limit coagulation. rapidly limit coagulation.

THROMBOSISTHROMBOSIS

Definition: A thrombus is an intravascular Definition: A thrombus is an intravascular mass attached to the vessel wall & is mass attached to the vessel wall & is composed of coagulation factors/fibrin, composed of coagulation factors/fibrin, RBCs, & platelets.RBCs, & platelets.

Thrombi may propagate, resolve, become Thrombi may propagate, resolve, become organized, or embolize.organized, or embolize.

Thrombosis causes tissue injury by local Thrombosis causes tissue injury by local vascular occlusion or by distal vascular occlusion or by distal embolization.embolization.

Heart, coronary atherosclerosis Heart, coronary atherosclerosis with thrombosis - grosswith thrombosis - gross

Heart, coronary artery thrombosis Heart, coronary artery thrombosis ––

low powerlow power

Heart, coronary artery Heart, coronary artery thrombosis –thrombosis –

low powerlow power Identify:Identify:

IntimaIntimaThrombusThrombusRecanalizaRecanaliza

tiontionMediaMediaAdventitiaAdventitia

Heart, coronary artery Heart, coronary artery thrombosisthrombosis

This cross section of the coronary artery in This cross section of the coronary artery in the previous image shows marked the previous image shows marked concentric thickening of the intima, due to concentric thickening of the intima, due to intimal damage and subsequent deposition intimal damage and subsequent deposition of fibrous tissue. of fibrous tissue.

On one side, a fresh thrombus is attached On one side, a fresh thrombus is attached to the damaged endothelium. In some parts to the damaged endothelium. In some parts of the thrombus, there is formation of new of the thrombus, there is formation of new capillary channels. This process, called capillary channels. This process, called recanalization, can restore blood flow. recanalization, can restore blood flow.

Note that the media is thinned, secondary Note that the media is thinned, secondary to compression by the thickened intima. to compression by the thickened intima.


Thrombus development depends on the relative Thrombus development depends on the relative contribution of the components of Virchow’s contribution of the components of Virchow’s triad:triad: ENDOTHELIAL INJURYENDOTHELIAL INJURY (toxins, hypertension, (toxins, hypertension,

inflammation, metabolic products)inflammation, metabolic products) ABNORMAL BLOOD FLOWABNORMAL BLOOD FLOW – stasis or – stasis or

turbulence (aneurysms, atherosclerotic plaques)turbulence (aneurysms, atherosclerotic plaques) HYPERCOAGULABILITYHYPERCOAGULABILITY – – either primary either primary

(factor V Leiden, increased prothrombin synthesis, (factor V Leiden, increased prothrombin synthesis, antithrombin III deficiency) or secondary (bedrest, antithrombin III deficiency) or secondary (bedrest, tissue damage, malignancy, OCP use) – table 4-2 tissue damage, malignancy, OCP use) – table 4-2 (hypercoagulable states)(hypercoagulable states)


Prevent Prevent venous thrombusvenous thrombus with with heparin/warfarinheparin/warfarin

Prevent Prevent arterial thrombusarterial thrombus with with aspirinaspirin

Postmortem clotPostmortem clot vs thrombus: vs thrombus: resembles resembles chicken fatchicken fat (gelatinous, (gelatinous, rubbery, dark red at the ends and rubbery, dark red at the ends and yellowish elsewhere) without entrapped yellowish elsewhere) without entrapped cells & is cells & is NOT attached to the vessel NOT attached to the vessel wallwall. .

Lines of ZahnLines of Zahn

Postmortem clotPostmortem clot


What causes arterial What causes arterial thrombosis? ...venous thrombosis? ...venous thrombosis? thrombosis?


Arterial thrombosis is caused by Arterial thrombosis is caused by ENDOTHELIALENDOTHELIAL DAMAGEDAMAGE (eg, (eg, atherosclerosis or vasculitis).atherosclerosis or vasculitis).

Venous thrombosis is caused by Venous thrombosis is caused by STASISSTASIS (sluggishness) of blood (sluggishness) of blood flow.flow.

Both types of vessels are affected in Both types of vessels are affected in HYPERCOAGULABLEHYPERCOAGULABLE STATESSTATES such such as as ANTITHROMBINANTITHROMBIN DEFICIENCYDEFICIENCY or or PROTEIN CPROTEIN C DEFICIENCYDEFICIENCY. .

Venous thrombi – gross, cross Venous thrombi – gross, cross sectionsection

Venous thrombi – gross, cross Venous thrombi – gross, cross sectionsection

The thrombi are red due to The thrombi are red due to entrapped erythrocytes and have entrapped erythrocytes and have a laminated appearance, a laminated appearance, reflecting varying composition of reflecting varying composition of the thrombus, which relates to the thrombus, which relates to the rate of blood flow at the time the rate of blood flow at the time the thrombus was forming. the thrombus was forming.


What are the various fates of What are the various fates of thrombi?thrombi?


PropagationPropagation EmbolizationEmbolization DissolutionDissolution Organization with Organization with

recanalizationrecanalization

EMBOLISMEMBOLISM

An embolus is any detached solid, liquid, An embolus is any detached solid, liquid, or gaseous mass carried by the blood to a or gaseous mass carried by the blood to a site distant from its origin; the vast site distant from its origin; the vast majority are part of a dislodged thrombus.majority are part of a dislodged thrombus.

Pulmonary emboliPulmonary emboli derive primarily from derive primarily from lower extremity deep vein thrombosislower extremity deep vein thrombosis; ; their effect (sudden death, right heart their effect (sudden death, right heart failure, pulmonary hemorrhage, or failure, pulmonary hemorrhage, or infarction) depends on the size of the infarction) depends on the size of the embolus.embolus.

EMBOLISMEMBOLISM

Systemic emboliSystemic emboli derive primarily derive primarily from from cardiac mural or valvular cardiac mural or valvular thrombi, valve vegetation, atrial thrombi, valve vegetation, atrial myxoma, aortic aneurysms, or myxoma, aortic aneurysms, or atherosclerotic plaqueatherosclerotic plaque; whether an ; whether an embolus causes tissue infarction embolus causes tissue infarction depends on the site of the depends on the site of the embolization and collateral embolization and collateral circulation.circulation.

Atrial fibrillation predisposes to atrial Atrial fibrillation predisposes to atrial clot formation and embolization.clot formation and embolization.

Heart, view of the tricuspid valve from Heart, view of the tricuspid valve from the right atrial side - grossthe right atrial side - gross

EMBOLISMEMBOLISM

Fat embolismFat embolism – from traumatic – from traumatic fracture of the long bones and pelvisfracture of the long bones and pelvis CNS damage – ischemia, hemorrhageCNS damage – ischemia, hemorrhage Respiratory failure – hypoxemiaRespiratory failure – hypoxemia Thrombocytopenia – platelet consumption Thrombocytopenia – platelet consumption

in thrombiin thrombi

Amniotic fluid embolismAmniotic fluid embolism sudden onset dyspnea, cyanosis, sudden onset dyspnea, cyanosis,

hypotensive shockhypotensive shock DICDIC maternal death maternal death

EMBOLISMEMBOLISM

Decompression sickness (Caisson Decompression sickness (Caisson disease)disease) Rapid ascent from diving forces nitrogen Rapid ascent from diving forces nitrogen

gas bubbles to develop in tissues and gas bubbles to develop in tissues and lumen of blood vesselslumen of blood vessels

Pain in joints, muscles, bonePain in joints, muscles, bone Hemiparesis, bladder & bowel dysfunctionHemiparesis, bladder & bowel dysfunction Pneumothorax – dyspnea & pleuritic chest Pneumothorax – dyspnea & pleuritic chest

pain from rupture of subpleural blebpain from rupture of subpleural bleb Pulmonary embolusPulmonary embolus Aseptic necrosis in bones from infarctionsAseptic necrosis in bones from infarctions

INFARCTIONINFARCTION

Infarcts are areas of ischemic, usually Infarcts are areas of ischemic, usually coagulative necrosis, caused by occlusion of coagulative necrosis, caused by occlusion of arterial supply or less commonly venous arterial supply or less commonly venous drainage.drainage.

Infarcts are most commonly caused by Infarcts are most commonly caused by formation of occlusive arterial thrombi, or formation of occlusive arterial thrombi, or embolization of arterial or venous thrombi.embolization of arterial or venous thrombi.

Infarcts caused by Infarcts caused by venous occlusionvenous occlusion, or in , or in loose tissues with dual blood supplyloose tissues with dual blood supply, are , are typically typically hemorrhagic (red)hemorrhagic (red) whereas those whereas those caused by caused by arterial occlusion in compact arterial occlusion in compact tissuestissues are are pale (white)pale (white) in color. in color.

Heart, myocardial infarct: acute Heart, myocardial infarct: acute vs. healed – gross, cross section vs. healed – gross, cross section

Heart, myocardial infarct: Heart, myocardial infarct: acute vs. healed – gross, cross acute vs. healed – gross, cross

sectionsection Identify:Identify:

Acute infarct: coagulative necrosisAcute infarct: coagulative necrosis

Acute infarct: hyperemiaAcute infarct: hyperemia

Heart, myocardial infarct: Heart, myocardial infarct: acute vs. healed – gross, cross acute vs. healed – gross, cross

sectionsection The well-defined pale area in the The well-defined pale area in the

acute myocardial infarct represents acute myocardial infarct represents coagulative necrosis. coagulative necrosis.

It is surrounded by a red area of It is surrounded by a red area of reactive hyperemia. reactive hyperemia.

(In contrast, the ill-defined pale area (In contrast, the ill-defined pale area in the old myocardial infarct in the old myocardial infarct represents a fibrous scar.) represents a fibrous scar.)

Brain, cerebral infarct: acute vs. Brain, cerebral infarct: acute vs. chronic – gross, coronal sectionchronic – gross, coronal section

Brain, cerebral infarct: acute Brain, cerebral infarct: acute vs. chronic – gross, coronal vs. chronic – gross, coronal

sectionsection Identify: Acute hemorrhagic infarctIdentify: Acute hemorrhagic infarct

The well-defined hemorrhagic area The well-defined hemorrhagic area in the acute cerebral infarct in the acute cerebral infarct represents hemorrhagic liquefactive represents hemorrhagic liquefactive necrosis.necrosis.


What are the major similarities What are the major similarities between a myocardial and a cerebral between a myocardial and a cerebral infarct? infarct?

INFARCTIONINFARCTION The major similarity is in the etiology. The major similarity is in the etiology. Both types of infarcts are commonly Both types of infarcts are commonly

caused by caused by THROMBOTIC OCCLUSIONTHROMBOTIC OCCLUSION of the arteries supplying them. of the arteries supplying them.

Thrombi usually form on the same Thrombi usually form on the same underlying disease process (ie, underlying disease process (ie, atherosclerotic arterial disease). atherosclerotic arterial disease).

Also, the early histologic reactions, such Also, the early histologic reactions, such as neutrophilic infiltration and as neutrophilic infiltration and granulation tissue formation, are common granulation tissue formation, are common to both.to both.


What are the major differences What are the major differences between a myocardial and a between a myocardial and a cerebral infarct?cerebral infarct?


A A MYOCARDIAL INFARCTMYOCARDIAL INFARCT typically typically features features COAGULATIVE NECROSISCOAGULATIVE NECROSIS, , which heals by fibrosis and leaves which heals by fibrosis and leaves behind a behind a FIBROUS SCARFIBROUS SCAR. .

In contrast, a In contrast, a CEREBRAL INFARCTCEREBRAL INFARCT is is typically typically LIQUEFACTIVE NECROSISLIQUEFACTIVE NECROSIS, , in which dead tissue is digested without in which dead tissue is digested without being replaced by fibrosis, leaving being replaced by fibrosis, leaving behind a behind a CYSTIC, CAVITARY LESIONCYSTIC, CAVITARY LESION..

Lung, pulmonary infarct – gross, Lung, pulmonary infarct – gross, cut surfacecut surface


Identify:Identify: InfarctInfarct PleuraPleura

This image shows a triangular, This image shows a triangular, peripheral, subpleural area that is peripheral, subpleural area that is solid and airless. This is the typical solid and airless. This is the typical appearance of a pulmonary infarct. appearance of a pulmonary infarct.

It represents an area of coagulative It represents an area of coagulative necrosis resulting from loss of oxygen. necrosis resulting from loss of oxygen.


The anoxia (ischemia) is most commonly The anoxia (ischemia) is most commonly due to a detached venous thrombus that due to a detached venous thrombus that is carried from the leg veins to the right is carried from the leg veins to the right side of the heart and ultimately occludes side of the heart and ultimately occludes a pulmonary arterial branch (pulmonary a pulmonary arterial branch (pulmonary thromboembolism). thromboembolism).

The infarct appears red because of The infarct appears red because of hemorrhage into the necrotic area. hemorrhage into the necrotic area. Hemorrhage is favored by the dual blood Hemorrhage is favored by the dual blood supply of the lung and the loose texture supply of the lung and the loose texture of the lung. of the lung.

Lung, infarct - medium powerLung, infarct - medium power

Lung, infarct - medium powerLung, infarct - medium power

On the left side, air spaces and alveolar On the left side, air spaces and alveolar septa can be seen; however, the right half septa can be seen; however, the right half looks solid and eosinophilic. looks solid and eosinophilic.

On careful examination, it is possible to see On careful examination, it is possible to see faint outlines of the alveoli, but otherwise faint outlines of the alveoli, but otherwise the tissue looks structureless. These the tissue looks structureless. These features are typical of features are typical of coagulative coagulative necrosisnecrosis, which in this case resulted from , which in this case resulted from occlusion of a pulmonary vessel by a occlusion of a pulmonary vessel by a thrombus that originated from the veins of thrombus that originated from the veins of the leg. This is called pulmonary the leg. This is called pulmonary thromboembolism. thromboembolism.

Lung, infarct – high powerLung, infarct – high power

Lung, infarct – high powerLung, infarct – high power

Note that the outlines of the pulmonary Note that the outlines of the pulmonary alveoli can be seen, but the structural alveoli can be seen, but the structural details have been obscured in this area of details have been obscured in this area of coagulative necrosis. coagulative necrosis.

There are no intact nuclei. The pulmonary There are no intact nuclei. The pulmonary airspaces seem filled with debris, derived airspaces seem filled with debris, derived in this case from remnants of red blood in this case from remnants of red blood cells (ie, there was hemorrhage in this cells (ie, there was hemorrhage in this area of necrosis). This appearance is area of necrosis). This appearance is typical of pulmonary infarcts. typical of pulmonary infarcts.

They appear red on gross inspection, They appear red on gross inspection, because there is hemorrhage into the because there is hemorrhage into the area of necrosis (red infarcts). area of necrosis (red infarcts).

SHOCKSHOCK

Definition: Shock is reduced perfusion of Definition: Shock is reduced perfusion of tissue, which results in impaired oxygenation tissue, which results in impaired oxygenation of tissue.of tissue.

Shock causes systemic hypoperfusion due to either Shock causes systemic hypoperfusion due to either reduced cardiac output or reduced circulating blood reduced cardiac output or reduced circulating blood volume.volume.

Most common causes/types:Most common causes/types: Cardiogenic (cardiac pump failure due to MI)Cardiogenic (cardiac pump failure due to MI) Hypovolemic (blood loss, >20% blood Hypovolemic (blood loss, >20% blood

volume)volume) Sepsis (infections – g(-) bacteria)Sepsis (infections – g(-) bacteria)

SHOCKSHOCK Septic shock results from the host innate Septic shock results from the host innate

immune response to bacterial or fungal immune response to bacterial or fungal cells molecules (endotoxin), with systemic cells molecules (endotoxin), with systemic production of cytokines (TNF, IL-1), that production of cytokines (TNF, IL-1), that affect endothelial & inflammatory cell affect endothelial & inflammatory cell activation.activation.

HypotensionHypotension, , DICDIC, and , and metabolic metabolic acidosisacidosis constitute the clinical triad of constitute the clinical triad of septic shock.septic shock.

Shock of any form causes pathology by Shock of any form causes pathology by inducing prolonged tissue hypoxic injury.inducing prolonged tissue hypoxic injury.

SHOCKSHOCK

Other complications:Other complications: Multi-organ dysfunction Multi-organ dysfunction – most – most

common CODcommon COD

Ischemic Acute Tubular NecrosisIschemic Acute Tubular Necrosis – coagulation necrosis of tubular – coagulation necrosis of tubular cells leading to renal failurecells leading to renal failure

Kidney, renal tubular necrosis due Kidney, renal tubular necrosis due to shock – gross, outer & cut to shock – gross, outer & cut

surfaces surfaces

Kidney, renal tubular necrosis due Kidney, renal tubular necrosis due to shock – gross, outer & cut to shock – gross, outer & cut

surfacessurfaces Identify:Identify:

CortexCortex MedullaMedulla CalycesCalyces

In this image, note that the cortex is In this image, note that the cortex is very pale and bloodless. very pale and bloodless.

By comparison, the medulla looks By comparison, the medulla looks darker red and congested. darker red and congested.

Kidney, acute tubular necrosis Kidney, acute tubular necrosis

due to shock – high powerdue to shock – high power

Kidney, acute tubular necrosis Kidney, acute tubular necrosis due to shock – high powerdue to shock – high power

Identify:Identify: GlomeruliGlomeruli Tubules with necrotic epitheliumTubules with necrotic epithelium Tubules with intact epitheliumTubules with intact epithelium

The glomeruli are normal. Note the The glomeruli are normal. Note the Bowman space and the nuclei of the Bowman space and the nuclei of the glomerular cells. Several of the glomerular cells. Several of the proximal tubules show necrosis of the proximal tubules show necrosis of the epithelium. epithelium.

Kidney, acute tubular necrosis Kidney, acute tubular necrosis due to shock – high powerdue to shock – high power

In these tubules, the normal cuboidal In these tubules, the normal cuboidal epithelium has been replaced by epithelium has been replaced by eosinophilic, structureless debris in eosinophilic, structureless debris in which cellular outlines as well as the which cellular outlines as well as the nuclei are obscured.nuclei are obscured.

These tubules may be compared with These tubules may be compared with

normal (uninjured) tubules. These have normal (uninjured) tubules. These have a well-preserved layer of epithelial a well-preserved layer of epithelial cells that show distinct nuclei.cells that show distinct nuclei.

What are the major morphologic What are the major morphologic changes in multiple organ changes in multiple organ failure in a patient who dies of failure in a patient who dies of shock?shock?

Major morphologic changes in Major morphologic changes in Multiple Organ Failure in a patient Multiple Organ Failure in a patient

who dies of Shockwho dies of Shock Kidneys: Acute tubular necrosis. Kidneys: Acute tubular necrosis. Brain: Laminar cortical necrosis. Brain: Laminar cortical necrosis. Lungs: Shock lung (diffuse alveolar Lungs: Shock lung (diffuse alveolar

damage) with hyaline membranes damage) with hyaline membranes (seen mainly in septic shock). (seen mainly in septic shock).

Heart: Foci of necrosis, hemorrhage, Heart: Foci of necrosis, hemorrhage, contraction band necrosis. contraction band necrosis.

GI: Hemorrhages. GI: Hemorrhages. Liver: Central hemorrhagic necrosis, Liver: Central hemorrhagic necrosis,

fatty change.fatty change.

Brain, cortical laminar necrosis – Brain, cortical laminar necrosis – gross, coronal sectiongross, coronal section

Brain, cortical laminar Brain, cortical laminar necrosis – necrosis –

gross, coronal sectiongross, coronal section Identify: Identify:

Normal cortexNormal cortex Cortex with laminar necrosisCortex with laminar necrosis

Compare the thinned and discolored Compare the thinned and discolored cerebral cortex on the left side to the cerebral cortex on the left side to the relatively preserved cortex on the right relatively preserved cortex on the right side. Neurons in different areas of the brain side. Neurons in different areas of the brain have different susceptibilities to global have different susceptibilities to global ischemic damage, such as may occur in ischemic damage, such as may occur in shock. shock.

Brain, cortical laminar Brain, cortical laminar necrosis – necrosis –

gross, coronal sectiongross, coronal section Most patients with shock who are Most patients with shock who are

diagnosed and treated early suffer no or diagnosed and treated early suffer no or only mild ischemic damage to the brain, only mild ischemic damage to the brain, which may result only in a confusional which may result only in a confusional state. state.

However, more severe, prolonged, and However, more severe, prolonged, and irreversible shock can lead to laminar irreversible shock can lead to laminar cortical necrosis.cortical necrosis.

How does this picture differ from a How does this picture differ from a thrombotic/embolic infarct?thrombotic/embolic infarct?

A A thrombotic/embolic infarctthrombotic/embolic infarct in the in the brain is a brain is a localized lesionlocalized lesion present in present in the area supplied by the occluded the area supplied by the occluded vessel. vessel.

In contrast, In contrast, laminar cortical laminar cortical necrosisnecrosis is due to is due to global hypoxic global hypoxic changechange as in shock, and hence affects as in shock, and hence affects a large part of the cortical ribbon.a large part of the cortical ribbon.

The ENDThe END

fluid & hemodynamics

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