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FLUID & HAEMODYNAMIC
DISORDERS
 Body water- Salt water
Life from ocean
Milieu interior or Internal
environment
Interstitial fluid bathing cells to
maintain morphology & function
Homeostasis : Exchange of
fluids,electrolytes,metabolites,etc
across Body fluid compartments &
membranes to maintain constant
Milieu interior
 Body fluid comprtments
 ECF 27%{Plasma 5% Interstitial fluid 12%others 10%}
 ICF 33%
 Mineral, fat, proteins 40%
 Composition – Water 50 – 70%
 Electrolytes:Cations + ve charge ICF:KMg ECF: Na
 Anions - ve charge ICF : Phosphates Proteins ECF
: Chloride Bicarbonate
WATER & ELECTROLYTE BALANCE
 Water Input : Bowel absorption,parentral 2.8 L
 output : kidney 1.5 L skin 800 ml lungs 400 ml
 Electrolytes : ICF : K PO4 ECF : Na Cl
Endothelial cell wall permeable Cell
membrane poor permeabilty
 Sodium pump maintains equilibrium by pushing
out Na , water follows
ACID BASE BALANCE
 Acid : Molecule /ion can give H+ ion (Donor)
 Base : “ “ “ “ can take H+ ION (Acceptor)
 Acids during normal metabolic activity -- Carbonic ( aerobic activty ) Lactic,
Sulfuric, Keto
 But Ph maintained at 7.4 +/ - 0.5 by Buffer system ( bicarbonate, Hb,
Carbonic anhydrase), Pulmonary ( CO 2 removal) and Renal mechanism (H+
ions with phosphates, NH4 ions , bicarbonate)
FLUID EXCHANGE
 Water /Crystalloids (electro) – free interchange
 Colloids ( plasma proteins) -- minimal
 Hydrostatic pressure -- Capillary blood pressure
32mm Hg arteriolar 12 mm Hg Venular end
 Osmotic pressure : Crystalloid - electrolytes
Colloid ( oncotic ) --plasma proteins
 Arteriolar end – fluid goes out – Hydrostatic pr
 Venular end - fluid comes in – Oncotic pr
DISTURBANCES IN BODY FLUIDS
 Main derangements are :
 Oedema : Free fluid in Interstitial tissue &
serous cavities
 Dehydration : pure deprivation of water
– Na retention - Hypernatremia
 Overhydration : increased ECF due to pure
water excess or water intoxication
OEDEMA
 Greek – swelling
 Abnormal & excessive accumulation of
free fluid in Interstitial tissue spaces &
serous cavities
 Body cavities – ascites, pleural &
pericardial effusions
 Interstitial spaces – pitting & non pitting
 Localised or generalised
PATHOGENESIS OF OEDEMA
 Decreased plasma oncotic pressure hypoprotenimeia –N S,
Glomerulonephritis, protein losing enteropathies, Cirrhosis
 Increased capillary hydrostatic pressure – Cardiac : CCF,
Constrictive pericarditis , Ascites, Mechanical obstn :
Thrombus,Varicosities, tumors, pregnancy
 Lympatic obstruction – Ca breast surgery, Filariasis, Tumor
pressure on thoracic duct
PATHOGENESIS OF OEDEMA
 Tissue factors – oncotic pressure in Interstitial
space , Tissue tension
 Incresed capillary permeability – damage to
endothelium by drugs, toxins,anoxia, infections,
anaphylaxis, inflammation, allergy
 Sodium & water retention - Na 80 %reabsorbed
due to Renal / extra renal mechanisms
Water retention due to release of ADH
MECHANISM OF SODIUM RETENTION
 Renal mechanism : Hypovolemia - stimulation of Baroreceptors
(carotid sinus/ aortic arch ) – Vasomotor centre in brain –
Sympathetic outflow – Renal ischemia -- decrased GFR –
decrased Sodium excretion – Sodium retention
 Extra renal mechanism : Decreased Na in tubules – Renin from
Juxta glomerular apparatus – Angotensinogen –Adrenal cortex
– Aldosterone – Incresed Na reabsorption in tubules -
MECHANISM OF WATER RETENTION
 ADH ( Vasopressin) – stored in post.
Pitutary
 Hypovolemia & increased Na in in plasma
– release of ADH – concentration of urine -
-- water retention
 Examples of oedema due to Na & water
retention : CCF, NS, Glomerulonephritis
and Ascites due to Cirrhosis
PULMONARY OEDEMA
 Local but functional impairment due to fluid in alveoli
affecting gas exchange
 Increased pulmonary hydrostatic pressure as in left heart
failure , MS, Pulmn vein obstruction, cardiac surgery.
Pressure by tumor/ inflamn.
 Increased pressure in capillaries over rides plasma oncotic
pressure -fluid in septa/ intstm- prolonged – damage to
cells – leakage of proteins & fluid into alveoli
PULMONARY OEDEMA
 Increased permeabilty ( Irritant oedema) ;
damage to endothelium & alveolar lining cells –
increased permeabilty --leakage of proteins &
fluid eg aspiration,inhalation of toxins , ARDS,
Shock, Uremia, Drug reactions
 Acute High Altitude oedema – sudden ascent to
> 2500 mts without acclimatisation – congestion –
haemorrages & fluid in lungs
PULMONARY OEDEMA
 Basal accumulation of fluid
 Gross : heavy, moist , sub crepitant
 C/S ; exudes frothy fluid
 Microscopy : pink,granular,
proteinaceous fluid in alveoli &
interstitium, congestion of capillaries.
Bright eosinophilic lines on margins –
alveolar membranes
PULMONARY OEDEMA
PULMONARY OEDEMA
RENAL OEDEMA
 NS : heavy proteinuria – hypoalbumeniemia - decreased
plasma oncotic pressure –decrea plasma volume – Renin/
Angiotensinogen / Aldosterone mech – Na & water retention
severe, generalised oedema
 Glomerulonephritis : Renin/ Agnts / Aldstrn Mild, Loose tissue
of face, genitilia , ankle
 Acute tubular injury :Loss of reabsorption and concentrating
abilities
RENAL OEDEMA
CARDIAC OEDEMA
 Heart failure : decreased cardiac output – hypovolemia –
renal & extra renal mechanisms, ADH secretion - Na &
water retention
 Increased Central venous press – transmitted backwards –
increased caplillary pressure
 Chronic hypoxia – damage to endothelium - increased
permeabilty
 Left failure – Pulmonary Right - Systemic
CARDIAC OEDEMA ( DEPENDANT OEDEMA)
CEREBRAL OEDEMA
 Life threatening due to space constraints
 Vasogenic : increased pressure & also capillary
permeabilty eg. Contusions,infarcts abscess,
 Cytotoxic : intracellular accumulation due to acute
hypoxia, toxic chemicals, metabolic derangements
 Interstitial : excessive fluid crossing Ependymal lining of
ventricles eg. N C Hydrocephalus
CEREBRAL OEDEMA
 Gross : White matter swollen, Gyri
flattened, Sulci narrowed
 C/S : Soft, gelatinous
 Microscopy : separation of tissue
elements, astrocyte swelling, widening of
perivascular spaces, halo around blood
vessels
CEREBRAL OEDEMA
HEPATIC OEDEMA
 Cirrhosis with Portal hypertension
 Portal hypertension – increased
hydrostatic pressure
 Hypoproteinemia - decreased oncotic
pressure
 Sodium & water retention
 Ascites : Fluid collection in peritoneal
cavity
ASCITES
NUTRITIONAL OEDEMA
 Protein deficiency : Kwashiokor, famine,
starvation, chronic alcoholism
 Vitamin deficiency : Vit B1 (beri beri)
 Mechanism – Hypoproteinemia
Sodium & water retention
NUTRITIONAL OEDEMA
PITTING OEDEMA
NON PITTING OEDEMA
 Pre tibial Myxedema : accumulation of
mucopolysaccharides
 Lymphatic obstruction due to
inflammation & fibrosis eg. Filariasis
PRE TIBIAL MYXEDEMA
FILARIASIS
INTERSTITIAL OEDEMA
DEHYDRATION
 Loss of water but not Na - hypernatremia
 Intense thirst,oliguria,fever, mental confusion
 GIT : Cholera, diarrhoea, severe vomitting
 Renal : ARF diuretic phase, D. Insipidius, Addison’s disease, excessive use of diuretics
 Blood/plasma loss: injuries, child birth,burns
 Skin : Hyperthermia, excessive sweating
 Accmln : Intstnl obstn , sudden ascites
DEHYDRATION
 Organs dark & shrunken
 Haemoconcentration, raised PCV & Hb
 Increased blood urea & sodium
 Renal shutdown
 Shock
OVERHYDRATION
 Increased ECF volume : pure water excess
, water intoxication
 Nausea, vomitting, headache, confusion
 Convulsions, coma, death
 Excessive IV infusions : N. saline, Ringer
lactate
 Renal Na/water retention : CCF, Acute GN,
CRF, Cirrhosis, Cushing’s syndrome
OVERHYDRATION
 Sudden weight gain
 Reduced plasma electrolytes
 Reduced plasma proteins
 Reduced PCV
HEMODYNAMIC DERANGEMENTS
DISTURBANCES IN VOLUME
 Active Hyperemia
 Passive Hyperemia or Venous congestion
 Haemorrage
 Acute or Chronic
ACTIVE HYPEREMIA
 Active Hyperemia : increased volume due
to Arteirolar dilatation
 Sympathetic mechn, Vasoactive substn
 Redness( Erythema), Incr temperature
 Blushing, Inflammation,menopausal
flush,goitre, A-V malformations, exercise
BLUSHING
PASSIVE HYPEREMIA ( CONGESTION)
 Venous congestion due to impaired
drainage , usually chronic ( CVC)
 Local : Obstn to venous flow eg, portal
vein in cirrhosis, bandage, plaster, hernia
tumors, pregnancy, thrombus
 Systemic : Heart failure, emphysema,
Pulmonary fibrosis
 Left heart failure– pulmn Right - systemic
CVC LUNG
 Right heart failure , Rheumatic mitral
stenosis – high pulmn venous pressure
 Gross ; heavy, firm, dark, rusty brown
induration of lung(fibrosis & pigmentation)
 Microscopy: widened alveolar septa
(dilated capillaries & oedema), Fibrosis,
haemorrages & hemosiderin laden
macrophages ( heart failure cells)
CVC – BROWN INDURATION LUNG
CVC LUNG
CVC LIVER
 Right heart failure or occlusion of Inferior
Venacava
 Gross : enlarged, tender, tense capsule
 C/S : Nutmeg appearance (red & yellow
mottled)
 Microscopy : Central vein & sinusoids
congested Periphery fatty change
 Later Centrilobular necrosis – Fibrosis &
regeneration - Cardiac cirrhosis
CVC LIVER – NUTMEG APPEARENCE
CVC LIVER
C V C SPLEEN
 Right heart failure, Portal hypertension
 Gross : Mod enlarged, cyanotic ,tense
 C/S : grey tan
 Microscopy : Red pulp : enlarged, sinusoidal
dilatation, haemorrage, increased splenic
macrpohages, fibrosis of capsule/ trabeculae
 Gamna gandy bodies : Siderofibrotic nodules
haemorrage, fibrosis & hemosiderin/ Ca depn
C V C SPLEEN
C V C SPLEEN
C V C KIDNEY
 Gross : enlarged , congested medulla
 Microscopy : mild changes
glomeruli – mesangial proliferation
tubules -- cloudy swelling, fatty change

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Oedema B( Dr. MURALI BM)

  • 1.
  • 2. FLUID & HAEMODYNAMIC DISORDERS  Body water- Salt water Life from ocean Milieu interior or Internal environment Interstitial fluid bathing cells to maintain morphology & function Homeostasis : Exchange of fluids,electrolytes,metabolites,etc across Body fluid compartments & membranes to maintain constant Milieu interior
  • 3.  Body fluid comprtments  ECF 27%{Plasma 5% Interstitial fluid 12%others 10%}  ICF 33%  Mineral, fat, proteins 40%  Composition – Water 50 – 70%  Electrolytes:Cations + ve charge ICF:KMg ECF: Na  Anions - ve charge ICF : Phosphates Proteins ECF : Chloride Bicarbonate
  • 4. WATER & ELECTROLYTE BALANCE  Water Input : Bowel absorption,parentral 2.8 L  output : kidney 1.5 L skin 800 ml lungs 400 ml  Electrolytes : ICF : K PO4 ECF : Na Cl Endothelial cell wall permeable Cell membrane poor permeabilty  Sodium pump maintains equilibrium by pushing out Na , water follows
  • 5. ACID BASE BALANCE  Acid : Molecule /ion can give H+ ion (Donor)  Base : “ “ “ “ can take H+ ION (Acceptor)  Acids during normal metabolic activity -- Carbonic ( aerobic activty ) Lactic, Sulfuric, Keto  But Ph maintained at 7.4 +/ - 0.5 by Buffer system ( bicarbonate, Hb, Carbonic anhydrase), Pulmonary ( CO 2 removal) and Renal mechanism (H+ ions with phosphates, NH4 ions , bicarbonate)
  • 6. FLUID EXCHANGE  Water /Crystalloids (electro) – free interchange  Colloids ( plasma proteins) -- minimal  Hydrostatic pressure -- Capillary blood pressure 32mm Hg arteriolar 12 mm Hg Venular end  Osmotic pressure : Crystalloid - electrolytes Colloid ( oncotic ) --plasma proteins  Arteriolar end – fluid goes out – Hydrostatic pr  Venular end - fluid comes in – Oncotic pr
  • 7. DISTURBANCES IN BODY FLUIDS  Main derangements are :  Oedema : Free fluid in Interstitial tissue & serous cavities  Dehydration : pure deprivation of water – Na retention - Hypernatremia  Overhydration : increased ECF due to pure water excess or water intoxication
  • 8. OEDEMA  Greek – swelling  Abnormal & excessive accumulation of free fluid in Interstitial tissue spaces & serous cavities  Body cavities – ascites, pleural & pericardial effusions  Interstitial spaces – pitting & non pitting  Localised or generalised
  • 9. PATHOGENESIS OF OEDEMA  Decreased plasma oncotic pressure hypoprotenimeia –N S, Glomerulonephritis, protein losing enteropathies, Cirrhosis  Increased capillary hydrostatic pressure – Cardiac : CCF, Constrictive pericarditis , Ascites, Mechanical obstn : Thrombus,Varicosities, tumors, pregnancy  Lympatic obstruction – Ca breast surgery, Filariasis, Tumor pressure on thoracic duct
  • 10. PATHOGENESIS OF OEDEMA  Tissue factors – oncotic pressure in Interstitial space , Tissue tension  Incresed capillary permeability – damage to endothelium by drugs, toxins,anoxia, infections, anaphylaxis, inflammation, allergy  Sodium & water retention - Na 80 %reabsorbed due to Renal / extra renal mechanisms Water retention due to release of ADH
  • 11. MECHANISM OF SODIUM RETENTION  Renal mechanism : Hypovolemia - stimulation of Baroreceptors (carotid sinus/ aortic arch ) – Vasomotor centre in brain – Sympathetic outflow – Renal ischemia -- decrased GFR – decrased Sodium excretion – Sodium retention  Extra renal mechanism : Decreased Na in tubules – Renin from Juxta glomerular apparatus – Angotensinogen –Adrenal cortex – Aldosterone – Incresed Na reabsorption in tubules -
  • 12. MECHANISM OF WATER RETENTION  ADH ( Vasopressin) – stored in post. Pitutary  Hypovolemia & increased Na in in plasma – release of ADH – concentration of urine - -- water retention  Examples of oedema due to Na & water retention : CCF, NS, Glomerulonephritis and Ascites due to Cirrhosis
  • 13. PULMONARY OEDEMA  Local but functional impairment due to fluid in alveoli affecting gas exchange  Increased pulmonary hydrostatic pressure as in left heart failure , MS, Pulmn vein obstruction, cardiac surgery. Pressure by tumor/ inflamn.  Increased pressure in capillaries over rides plasma oncotic pressure -fluid in septa/ intstm- prolonged – damage to cells – leakage of proteins & fluid into alveoli
  • 14. PULMONARY OEDEMA  Increased permeabilty ( Irritant oedema) ; damage to endothelium & alveolar lining cells – increased permeabilty --leakage of proteins & fluid eg aspiration,inhalation of toxins , ARDS, Shock, Uremia, Drug reactions  Acute High Altitude oedema – sudden ascent to > 2500 mts without acclimatisation – congestion – haemorrages & fluid in lungs
  • 15. PULMONARY OEDEMA  Basal accumulation of fluid  Gross : heavy, moist , sub crepitant  C/S ; exudes frothy fluid  Microscopy : pink,granular, proteinaceous fluid in alveoli & interstitium, congestion of capillaries. Bright eosinophilic lines on margins – alveolar membranes
  • 18. RENAL OEDEMA  NS : heavy proteinuria – hypoalbumeniemia - decreased plasma oncotic pressure –decrea plasma volume – Renin/ Angiotensinogen / Aldosterone mech – Na & water retention severe, generalised oedema  Glomerulonephritis : Renin/ Agnts / Aldstrn Mild, Loose tissue of face, genitilia , ankle  Acute tubular injury :Loss of reabsorption and concentrating abilities
  • 20. CARDIAC OEDEMA  Heart failure : decreased cardiac output – hypovolemia – renal & extra renal mechanisms, ADH secretion - Na & water retention  Increased Central venous press – transmitted backwards – increased caplillary pressure  Chronic hypoxia – damage to endothelium - increased permeabilty  Left failure – Pulmonary Right - Systemic
  • 21. CARDIAC OEDEMA ( DEPENDANT OEDEMA)
  • 22. CEREBRAL OEDEMA  Life threatening due to space constraints  Vasogenic : increased pressure & also capillary permeabilty eg. Contusions,infarcts abscess,  Cytotoxic : intracellular accumulation due to acute hypoxia, toxic chemicals, metabolic derangements  Interstitial : excessive fluid crossing Ependymal lining of ventricles eg. N C Hydrocephalus
  • 23. CEREBRAL OEDEMA  Gross : White matter swollen, Gyri flattened, Sulci narrowed  C/S : Soft, gelatinous  Microscopy : separation of tissue elements, astrocyte swelling, widening of perivascular spaces, halo around blood vessels
  • 25. HEPATIC OEDEMA  Cirrhosis with Portal hypertension  Portal hypertension – increased hydrostatic pressure  Hypoproteinemia - decreased oncotic pressure  Sodium & water retention  Ascites : Fluid collection in peritoneal cavity
  • 27. NUTRITIONAL OEDEMA  Protein deficiency : Kwashiokor, famine, starvation, chronic alcoholism  Vitamin deficiency : Vit B1 (beri beri)  Mechanism – Hypoproteinemia Sodium & water retention
  • 30. NON PITTING OEDEMA  Pre tibial Myxedema : accumulation of mucopolysaccharides  Lymphatic obstruction due to inflammation & fibrosis eg. Filariasis
  • 34. DEHYDRATION  Loss of water but not Na - hypernatremia  Intense thirst,oliguria,fever, mental confusion  GIT : Cholera, diarrhoea, severe vomitting  Renal : ARF diuretic phase, D. Insipidius, Addison’s disease, excessive use of diuretics  Blood/plasma loss: injuries, child birth,burns  Skin : Hyperthermia, excessive sweating  Accmln : Intstnl obstn , sudden ascites
  • 35. DEHYDRATION  Organs dark & shrunken  Haemoconcentration, raised PCV & Hb  Increased blood urea & sodium  Renal shutdown  Shock
  • 36. OVERHYDRATION  Increased ECF volume : pure water excess , water intoxication  Nausea, vomitting, headache, confusion  Convulsions, coma, death  Excessive IV infusions : N. saline, Ringer lactate  Renal Na/water retention : CCF, Acute GN, CRF, Cirrhosis, Cushing’s syndrome
  • 37. OVERHYDRATION  Sudden weight gain  Reduced plasma electrolytes  Reduced plasma proteins  Reduced PCV
  • 38. HEMODYNAMIC DERANGEMENTS DISTURBANCES IN VOLUME  Active Hyperemia  Passive Hyperemia or Venous congestion  Haemorrage  Acute or Chronic
  • 39. ACTIVE HYPEREMIA  Active Hyperemia : increased volume due to Arteirolar dilatation  Sympathetic mechn, Vasoactive substn  Redness( Erythema), Incr temperature  Blushing, Inflammation,menopausal flush,goitre, A-V malformations, exercise
  • 41. PASSIVE HYPEREMIA ( CONGESTION)  Venous congestion due to impaired drainage , usually chronic ( CVC)  Local : Obstn to venous flow eg, portal vein in cirrhosis, bandage, plaster, hernia tumors, pregnancy, thrombus  Systemic : Heart failure, emphysema, Pulmonary fibrosis  Left heart failure– pulmn Right - systemic
  • 42. CVC LUNG  Right heart failure , Rheumatic mitral stenosis – high pulmn venous pressure  Gross ; heavy, firm, dark, rusty brown induration of lung(fibrosis & pigmentation)  Microscopy: widened alveolar septa (dilated capillaries & oedema), Fibrosis, haemorrages & hemosiderin laden macrophages ( heart failure cells)
  • 43. CVC – BROWN INDURATION LUNG
  • 45. CVC LIVER  Right heart failure or occlusion of Inferior Venacava  Gross : enlarged, tender, tense capsule  C/S : Nutmeg appearance (red & yellow mottled)  Microscopy : Central vein & sinusoids congested Periphery fatty change  Later Centrilobular necrosis – Fibrosis & regeneration - Cardiac cirrhosis
  • 46. CVC LIVER – NUTMEG APPEARENCE
  • 48. C V C SPLEEN  Right heart failure, Portal hypertension  Gross : Mod enlarged, cyanotic ,tense  C/S : grey tan  Microscopy : Red pulp : enlarged, sinusoidal dilatation, haemorrage, increased splenic macrpohages, fibrosis of capsule/ trabeculae  Gamna gandy bodies : Siderofibrotic nodules haemorrage, fibrosis & hemosiderin/ Ca depn
  • 49. C V C SPLEEN
  • 50. C V C SPLEEN
  • 51. C V C KIDNEY  Gross : enlarged , congested medulla  Microscopy : mild changes glomeruli – mesangial proliferation tubules -- cloudy swelling, fatty change