{ قالوا سبحانك لا علم لنا إلا ما علمتنا إنك أنت العليم الحكيم } البقرة  (32)
FLUID TRANSFUSION  IN  LIVER TRANSPLANTATION
<ul><li>Fluid regulation is essential to homeostasis. </li></ul><ul><li>Disturbances in water or electrolyte levels->body ...
<ul><li>TBW is distributed among 3 major compartments. </li></ul><ul><li>ICF and ECF which are separated by cell membranes...
<ul><li>Fluid exchange between the intracellular and interstitial spaces is governed by the osmotic forces. </li></ul><ul>...
<ul><li>Fluid exchange across capillaries is governed by differences in hydrostatic pressures and osmotic forces. </li></u...
Capillary fluid exchange <ul><li>The net balance of all of these pressures determines  whether the fluid leaves (Filtratio...
<ul><li>Both ICF and ECF osmolalities are regulated  </li></ul><ul><li>to maintain normal water content in tissues. </li><...
<ul><li>↓ Extracellular osmolality ->swelling of osmoreceptors -> suppress the release of ADH-> water diuresis ->↑osmolali...
<ul><li>Extracellular fluid volume is directly proportionate to total body Na +  content .  </li></ul><ul><li>A positive s...
<ul><li>Renin–Angiotensin–Aldosterone. </li></ul><ul><li>Atrial Natriuretic Peptide (ANP). </li></ul><ul><li>Brain Natriur...
<ul><li>Cirrhosis, the final stage of liver injury, occurs when there is fibrosis and nodular regeneration within the live...
<ul><li>↓ bile production  -> ↓vit K  absorption ->↓  production  of  vitamin K-dependant clotting factors II, VII, IX, an...
<ul><li>Normal portal pressures are between 5 - 10 mmHg.  </li></ul><ul><li>When liver becomes nodular and fibrotic, blood...
<ul><li>As the pressure continues to increase, patients are at greater risk of variceal rupture and life-threatening hemor...
<ul><li>Impaired  renal ability to excrete Na +  is the earliest renal dysfunction in cirrhosis. </li></ul><ul><li>periphe...
<ul><li>Patients with cirrhosis may develop a specific acute renal failure called hepatorenal syndrome (HRS). </li></ul><u...
<ul><li>Pathogenesis may involve both  ↑  vasoconstrictor and </li></ul><ul><li>↓   vasodilator factors  ->  renal VC, hyp...
<ul><li>Two patterns of HRS are observed in clinical practice: type 1 and type 2. </li></ul><ul><li>Type 1 HRS is an acute...
<ul><li>HPS is a progressive, debilitating complication of  ESLD that occurs in 4 to 25% of LT candidates. </li></ul><ul><...
<ul><li>PPH refers to the development of pulmonary arterial hypertension in the setting of portal hypertension with or wit...
<ul><li>It is the accumulation of fluid in the pleural space as a consequence of liver disease. </li></ul><ul><li>The most...
<ul><li>Without liver transplantation, cirrhosis is usually fatal. </li></ul><ul><li>Patients with cirrhosis who are admit...
<ul><li>Preoperative Factors :   include liver failure, cirrhosis, cholestasis, and splenomegaly.  </li></ul><ul><li>Intra...
<ul><li>Blood loss in stage I occurs mainly from transection of the fragile collaterals that develop from the portal hyper...
<ul><li>Post-Operative Factors: </li></ul><ul><li>Postoperative bleeding is not common, but it can occur from leaks at vas...
<ul><li>Liver transplantation is a surgical procedure that can lead to massive blood loss and consequently result in trans...
<ul><ul><li>The most reliable variables affecting transfusion requirements include the severity of disease or Child classi...
<ul><li>There is a significant association between MELD and total number of transfusions in LT.  </li></ul><ul><li>On aver...
<ul><li>Using a lower HB value as the threshold for transfusing seems to be attributable to small transfusion  (ASA guidel...
<ul><li>The mechanical factor, controlled by the surgeon, seems to be the more important of the factors influencing the tr...
<ul><li>Many cirrhotic patients have a low platelet count due to hypersplenism, increased platelet consumption, bone marro...
<ul><li>Platelet count <50,000/mm 3  is correlated with a risk of diffuse microvascular bleeding. </li></ul><ul><li>Accord...
<ul><li>Multiorgan failure. </li></ul><ul><li>Stroke. </li></ul><ul><li>Patient and graft survival were significantly redu...
<ul><li>FFP is usually used in LT to prevent diffuse microvascular bleeding. </li></ul><ul><li>FFP is not indicated solely...
<ul><li>FFP is indicated for: </li></ul><ul><li>Correction of excessive microvascular bleeding ( i.e. , coagulopathy) in t...
<ul><li>Fibrinogen concentration should be obtained before the administration of cryoprecipitate in a bleeding patient if ...
<ul><li>Postoperative fluid overload is a risk factor for postoperative pulmonary complications after liver transplantatio...
<ul><li>Replacement of blood products is necessitated in the presence of active bleeding or any planned intervention. Othe...
<ul><li>At the end, improvements in the care for liver transplant patients should not be limited to surgical and anestheti...
<ul><ul><li>THANK YOU </li></ul></ul>
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    1. 1. { قالوا سبحانك لا علم لنا إلا ما علمتنا إنك أنت العليم الحكيم } البقرة (32)
    2. 2. FLUID TRANSFUSION IN LIVER TRANSPLANTATION
    3. 3. <ul><li>Fluid regulation is essential to homeostasis. </li></ul><ul><li>Disturbances in water or electrolyte levels->body functions fail to proceed. </li></ul><ul><li>The content of water in the human body changes with age. </li></ul>Approximate Water Content in Body Age Group 90 % Premature infant 70-80 % Newborn infant 64 % 12-24 months 60 % Adult
    4. 4. <ul><li>TBW is distributed among 3 major compartments. </li></ul><ul><li>ICF and ECF which are separated by cell membranes. </li></ul><ul><li>ECF divided into plasma and ISF, they are separated by capillary walls. </li></ul>
    5. 5. <ul><li>Fluid exchange between the intracellular and interstitial spaces is governed by the osmotic forces. </li></ul><ul><li>changes in osmolality between the IC and IS compartments result in a net water movement from the hypoosmolar to the hyperosmolar compartment. </li></ul>
    6. 6. <ul><li>Fluid exchange across capillaries is governed by differences in hydrostatic pressures and osmotic forces. </li></ul><ul><li>BHP tends to push the fluids out of the capillaries. </li></ul><ul><li>IFHP tends to push fluid back into the capillaries. </li></ul><ul><li>BCOP tends to pull fluids into the capillaries. </li></ul><ul><li>IFOP tends to move fluid out of the capillaries into the interstitial compartment. </li></ul>
    7. 7. Capillary fluid exchange <ul><li>The net balance of all of these pressures determines whether the fluid leaves (Filtration) or moves into (Reabsorption) the capillaries. </li></ul>
    8. 8. <ul><li>Both ICF and ECF osmolalities are regulated </li></ul><ul><li>to maintain normal water content in tissues. </li></ul><ul><li>Plasma osmolality is regulated by osmoreceptors in the hypothalamus. </li></ul><ul><li>↑ ECF osmolality ->shrink of osmorecptor cells and release ADH -> water reabsorption in renal-collecting tubules -> reduce plasma osmolality to normal again. </li></ul>
    9. 9. <ul><li>↓ Extracellular osmolality ->swelling of osmoreceptors -> suppress the release of ADH-> water diuresis ->↑osmolality to normal. </li></ul><ul><li>Activation of osmoreceptors by increases in ECF osmolality induces thirst and causes the individual to drink water. </li></ul>
    10. 10. <ul><li>Extracellular fluid volume is directly proportionate to total body Na + content . </li></ul><ul><li>A positive sodium balance increases ECF volume, whereas a negative sodium balance decreases ECF volume. </li></ul><ul><li>This regulation is achieved via sensors that detect changes in the intravascular volume. </li></ul><ul><li>The baroreceptors at the carotid sinus and afferent renal arterioles and stretch receptors in both atria function as sensors of intravascular volume. </li></ul>
    11. 11. <ul><li>Renin–Angiotensin–Aldosterone. </li></ul><ul><li>Atrial Natriuretic Peptide (ANP). </li></ul><ul><li>Brain Natriuretic Peptide (BNP). </li></ul><ul><li>Pressure Natriuresis. </li></ul><ul><li>Sympathetic Nervous System Activity. </li></ul><ul><li>GFR and Plasma Sodium Concentration. </li></ul><ul><li>Tubuloglomerular Balance.  </li></ul>
    12. 12. <ul><li>Cirrhosis, the final stage of liver injury, occurs when there is fibrosis and nodular regeneration within the liver tissue. </li></ul><ul><li>Cirrhosis -> dysfunction of hepatic cells, portosystemic shunting of blood, and portal hypertension. </li></ul>
    13. 13. <ul><li>↓ bile production -> ↓vit K absorption ->↓ production of vitamin K-dependant clotting factors II, VII, IX, and X -> ↑ risk of bleeding and a prolongation of both the PT and INR. </li></ul><ul><li>↓ production of albumin -> ↓blood oncotic pressure -> development of peripheral edema and ascites. </li></ul>
    14. 14. <ul><li>Normal portal pressures are between 5 - 10 mmHg. </li></ul><ul><li>When liver becomes nodular and fibrotic, blood backs into the portal vein. </li></ul><ul><li>When portal pressures > 10 mmHg -> development of varices in the esophagus, stomach, and rectum. </li></ul>
    15. 15. <ul><li>As the pressure continues to increase, patients are at greater risk of variceal rupture and life-threatening hemorrhage. </li></ul><ul><li>Portal hypertension is associated with a marked increase in the escape of the intravascular fluid to the interstitial space. </li></ul>
    16. 16. <ul><li>Impaired renal ability to excrete Na + is the earliest renal dysfunction in cirrhosis. </li></ul><ul><li>peripheral arterial VD -> underfilling of circulatory volume -> activation of (RAAS), (SNS) and release of ADH to restore circulatory integrity. </li></ul><ul><li>The result is sodium and water retention, there is fluid retention and ascites, as the liver disease progresses. </li></ul>
    17. 17. <ul><li>Patients with cirrhosis may develop a specific acute renal failure called hepatorenal syndrome (HRS). </li></ul><ul><li>Diagnosis is made when s. creatinine is over 1.5 mg/dL and there is no data suggesting other etiologies of RF. </li></ul><ul><li>The hallmarks of HRS are reversible renal constriction and mild systemic hypotension. </li></ul>
    18. 18. <ul><li>Pathogenesis may involve both ↑ vasoconstrictor and </li></ul><ul><li>↓ vasodilator factors -> renal VC, hypoperfusion and </li></ul><ul><li>↓ GFR -> ↓ renal synthesis of VD s and ↑ intrarenal </li></ul><ul><li>synthesis of VC s (angiotensin-II, adenosine), thus leading </li></ul><ul><li>to a vicious circle that perpetuates the renal failure. </li></ul>
    19. 19. <ul><li>Two patterns of HRS are observed in clinical practice: type 1 and type 2. </li></ul><ul><li>Type 1 HRS is an acute form in severe liver disease and is progressive. It is associated with poor prognosis with 80% mortality at 2 weeks. </li></ul><ul><li>Type 2 HRS occurs in patients with diuretic-resistant ascites. The course of renal failure is slow. The survival time is longer than that of patients with type 1 HRS. </li></ul>
    20. 20. <ul><li>HPS is a progressive, debilitating complication of ESLD that occurs in 4 to 25% of LT candidates. </li></ul><ul><li>Diagnosis rests on the triad of cirrhosis, hypoxemia, and intrapulmonary vascular dilation. </li></ul><ul><li>Pulmonary features include digital clubbing, cyanosis, dyspnea, and orthodeoxia. </li></ul><ul><li>HPS appears to resolve after LT. </li></ul>
    21. 21. <ul><li>PPH refers to the development of pulmonary arterial hypertension in the setting of portal hypertension with or without liver disease. </li></ul><ul><li>It is defined as mean pulmonary artery pressure (PAP) more than 25 mm Hg, with a normal pulmonary capillary wedge pressure. </li></ul><ul><li>Patients with a mean PAP of 50 mm Hg or greater have a cardiopulmonary mortality rate of 100%. </li></ul>
    22. 22. <ul><li>It is the accumulation of fluid in the pleural space as a consequence of liver disease. </li></ul><ul><li>The most common symptom is dyspnea without chest pain. </li></ul><ul><li>Right-sided pleural effusion is seen in 66% of the patients with hepatic hydrothorax. </li></ul><ul><li>The management options include medical management of ascites, and therapeutic thoracocentesis for the control of shortness of breath. </li></ul>
    23. 23. <ul><li>Without liver transplantation, cirrhosis is usually fatal. </li></ul><ul><li>Patients with cirrhosis who are admitted to ICUs have a greater than 50% mortality rate. </li></ul><ul><li>Transfusion support remains an integral part of solid-organ transplantation. </li></ul><ul><li>The liver is a highly vascular organ and extensive bleeding should be anticipated especially with PH. </li></ul>
    24. 24. <ul><li>Preoperative Factors : include liver failure, cirrhosis, cholestasis, and splenomegaly. </li></ul><ul><li>Intraoperative Period: </li></ul><ul><li>Intraoperative events can be broadly categorized into: stage I (the preanhepatic phase), stage II (anhepatic phase) and stage III (reperfusion and postreperfusion period). </li></ul>
    25. 25. <ul><li>Blood loss in stage I occurs mainly from transection of the fragile collaterals that develop from the portal hypertension. </li></ul><ul><li>extensive bleeding may occur from raw surface of the liver. </li></ul><ul><li>This can get compounded by the preexisting coagulopathy. </li></ul>
    26. 26. <ul><li>Post-Operative Factors: </li></ul><ul><li>Postoperative bleeding is not common, but it can occur from leaks at vascular suture lines or bleeding from the cut surfaces at bowel anastomoses. </li></ul><ul><li>Failure of the graft to function will contribute to postoperative bleeding, causing coagulopathy. </li></ul><ul><li>Less commonly, thrombocytopenia following liver transplantation may cause bleeding. </li></ul>
    27. 27. <ul><li>Liver transplantation is a surgical procedure that can lead to massive blood loss and consequently result in transfusion of blood products. </li></ul><ul><li>As the quantity of blood products required contributes to higher mortality and morbidity, preoperative identification of patients at high risk of massive intraoperative hemorrhage is of great interest. </li></ul>
    28. 28. <ul><ul><li>The most reliable variables affecting transfusion requirements include the severity of disease or Child classification, preoperative PT, history of abdominal operations, factor V levels, preoperative haematocrit value, operative time and use of the piggyback transplantation method. </li></ul></ul>
    29. 29. <ul><li>There is a significant association between MELD and total number of transfusions in LT. </li></ul><ul><li>On average, an increase of 3 points in MELD score was associated with one additional blood component treatment. </li></ul><ul><li>The NMELD equation offers higher sensitivity, specificity, predictive values and accuracy than the current MELD score in predicting short-term patient outcome. </li></ul>
    30. 30. <ul><li>Using a lower HB value as the threshold for transfusing seems to be attributable to small transfusion (ASA guidelines; threshold for RBC transfusion: 60-100 g/L) . </li></ul><ul><li>Two factors influence blood loss: a mechanical or vascular component and a biochemical one. </li></ul><ul><li>The biochemical is evaluated from the INR and the platelet count. </li></ul>
    31. 31. <ul><li>The mechanical factor, controlled by the surgeon, seems to be the more important of the factors influencing the transfusion rate. </li></ul><ul><li>The anesthesiologist’s and the surgeon’s experience and attitude seem to be more important than the correction of any biochemical variables during the liver transplant. </li></ul>
    32. 32. <ul><li>Many cirrhotic patients have a low platelet count due to hypersplenism, increased platelet consumption, bone marrow depression, and reduced thrombopoietin levels. </li></ul><ul><li>The ASA does not recommend prophylactic administration of platelets in patients undergoing surgery . </li></ul>
    33. 33. <ul><li>Platelet count <50,000/mm 3 is correlated with a risk of diffuse microvascular bleeding. </li></ul><ul><li>According to ASA guidelines, many centers give platelets when its count falls below or equal to 50,000 /mm 3 and to maintain it around 100,000/mm 3 . </li></ul>
    34. 34. <ul><li>Multiorgan failure. </li></ul><ul><li>Stroke. </li></ul><ul><li>Patient and graft survival were significantly reduced in patients who received platelet transfusions. </li></ul><ul><li>Infection. </li></ul><ul><li>vasopressor use. </li></ul><ul><li>respiratory medication. Use. </li></ul>
    35. 35. <ul><li>FFP is usually used in LT to prevent diffuse microvascular bleeding. </li></ul><ul><li>FFP is not indicated solely for augmentation of plasma volume or albumin concentration. </li></ul><ul><li>plasma transfusion at the beginning of the procedure will result in hypervolemia with a raised CVP and increased blood losses. </li></ul><ul><li>It is not necessary to correct coagulation defects before the anhepatic phase. </li></ul>
    36. 36. <ul><li>FFP is indicated for: </li></ul><ul><li>Correction of excessive microvascular bleeding ( i.e. , coagulopathy) in the presence of a PT > 1.5 times normal or INR >2.0, or an aPTT >2 times normal. </li></ul><ul><li>Correction of excessive microvascular bleeding secondary to coagulation factor deficiency in patients transfused with more than one blood volume. </li></ul>
    37. 37. <ul><li>Fibrinogen concentration should be obtained before the administration of cryoprecipitate in a bleeding patient if possible. </li></ul><ul><li>Transfusion of cryoprecipitate is rarely indicated if fibrinogen concentration is > 150 mg/dl. </li></ul><ul><li>Transfusion of cryoprecipitate is usually indicated when the fibrinogen concentration < than 80–100 mg/dl in the presence of excessive microvascular bleeding. </li></ul>
    38. 38. <ul><li>Postoperative fluid overload is a risk factor for postoperative pulmonary complications after liver transplantation. </li></ul><ul><li>The recipient is generally kept in an euvolemic or slightly hypovolemic state in the posttransplant period, with minimal intravenous infusions, to optimize graft function and avoid pulmonary edema. </li></ul>
    39. 39. <ul><li>Replacement of blood products is necessitated in the presence of active bleeding or any planned intervention. Otherwise, maintenance of an INR between 1.5-2, a platelet count > 50,000/mm 3 and a fibrinogen level >100 mg /dL is satisfactory. </li></ul>
    40. 40. <ul><li>At the end, improvements in the care for liver transplant patients should not be limited to surgical and anesthetic measures to minimize intraoperative blood loss, but also include a conservative and more targeted use of blood products, weighing in each individual patient the short-term benefits versus increased postoperative risk for adverse events. </li></ul>
    41. 41. <ul><ul><li>THANK YOU </li></ul></ul>
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