الفهرس 
FLUID DISTRIBUTION IN NORMAL INDIOVIDUALSOnly 14 pages are availabe for public view
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Abstract
Liver transplantation has emerged as an increasingly successful treatment for patients with end-stage liver disease (ESLD). In 1963, Starzl and colleagues performed the first liver transplantation procedure. This patient, along with the next 4, died from bleeding.
As transfusion support remains an integral part of solid-organ transplantation, so a clear understanding of the distribution of fluids through the intravascular extracellular volumes is essential to provide safe care of the patient and fluid replacement of these volumes.
The content and distribution of water in the human body changes with age group: in premature infant 90%, newborn infant 70-80%, 12-14 months 64% and adult 60% of body weight.
The total body water (TBW) is distributed among three major compartments: the blood plasma, the interstitial fluid (ISF), and the intracellular fluid (ICF). In an average human adult weighing approximately 70 kg, the TBW makes up approximately 60% of body weight or about 40 L. The ICF compartment comprises about tow thirds of the total body water (40% BW, 25 L). The remaining third of the body water found in the ECF (20% BW, 15L) compartment is further subdivided into plasma and interstitial fluid. The plasma makes up about a fifth of the ECF volume (20% of ECF, 3L) and the ISF which represents the other four fifths of the ECF compartment (about 12 L).
Fluid exchange between the intracellular and interstitial spaces is governed by the osmotic forces created by differences in nondiffusible solute concentrations. Fluid exchange across capillaries differs from that across cell membranes in that it is governed by significant differences in hydrostatic pressures in addition to osmotic forces. The net balance of all of these pressures determines whether the fluid leaves (Filtration at arterial end) or moves into (Reabsorption at venous end) the capillaries.
The liver has a wider variety of functions than any other organ in the body. Two of the most important functions are albumin and coagulation factors production.Albumin contributes up to 80% of the normal of the colloid osmotic pressure (COP). Critical illness alters the distribution of albumin between the intravascular and extravascular compartments. Critically ill patients have a lowered serum COP. A lowered COP is associated with increased morbidity and mortality.
The vitamin K-dependent coagulation factors II, VII, IX, and X are synthesized in the liver, together with factors V, XI, XII, and XIII and fibrinogen, which are not dependent on vitamin K for synthesis. The half-lives of the coagulation factors are relatively short; thus, abnormalities in coagulation quickly become apparent in acute liver damage.
Cirrhosis, the final stage of liver injury, occurs when there is fibrosis and nodular regeneration within the liver tissue. Cirrhosis leads to dysfunction of hepatic cells, porto-systemic shunting of blood, and portal hypertension, decreased production of clotting factors which can lead to an increased risk of bleeding and a prolongation of both the prothrombin time (PT) and international normalized ratio (INR) and decreased production of albumin which can decrease the oncotic pressure within the vasculature. This can lead to the development of peripheral edema and ascites. Without liver transplantation, cirrhosis is usually fatal and patients with cirrhosis who are admitted to ICUs have a greater than 50% mortality rate.
The liver is a highly vascular organ and extensive bleeding should be anticipated especially in patients with portal hypertension due to ESLD. Contributing factors to blood loss during liver transplantation can be categorized into: Preoperative factors, intraoperative and postoperative factors.
Preoperatively, patients with acute or chronic liver failure do not synthesize normal amounts of clotting factors II (prothrombin), VII, IX, and X. Cholestasis leads to decreased synthesis of vitamin K–dependent clotting factors (II, VII, IX, and X), further contributing to abnormal clotting. Thrombocytopenia is another common problem in cirrhotic patients. The cause of thrombocytopenia is multifactorial. The liver is the primary site of thrombopoietin synthesis, and thrombopoietin deficiency due to cirrhosis leads to low platelet production. In addition splenomegaly leads to platelet sequestration and destruction.
The events in the intraoperative period can be broadly categorized into stage I (the preanhepatic phase), The stage II (anhepatic phase) and stage III (reperfusion and postreperfusion period). Blood loss in stage I occurs mainly from transection of the fragile collaterals that develop from the portal hypertension. In addition, extensive bleeding may occur from raw surface of the liver.
Postoperative bleeding is not common, but it can occur from leaks at vascular suture lines or bleeding from the cut surfaces at bowel anastomoses. Failure of the graft to function will contribute to postoperative bleeding, causing coagulopathy. Less commonly, thrombocytopenia following liver transplant-tation causes bleeding.
Liver transplantation is a surgical procedure that can lead to massive blood loss and consequently result in transfusion of blood products. Preoperative identification of patients at high risk of massive intraoperative hemorrhage is of great interest. The most reliable variables affecting transfusion requirements include the severity of disease or Child classification, preoperative PT, history of abdominal operations, and factor V levels. Other variables include the preoperative haematocrit value, use of the piggyback transplantation method. Some investigators detected a significant association between the model for end stage liver disease (MELD) and total number of transfusions in LT.
Several studies have shown that intraoperative blood loss and red blood cell (RBC) transfusion requirements have a negative impact on outcome after LT, so the Hb level at which RBC transfused according to the ASA guidelines is about 60- 100 g/L as followed in many centers. Advances in the surgical and anesthetic management of patients undergoing LT, as well as better understanding of risk factors for massive blood loss, have resulted in a steady decrease in intraoperative blood loss and transfusion requirements. Currently, several centers report the complete avoidance of RBC transfusions in up to 40% of their LT recipients.
Platelet concentrates are frequently administered during LT for the prevention or treatment of bleeding. However, there is no consensus regarding the appropriate threshold for platelet transfusion. Many centers give platelets according to ASA guidelines when its count falls below or equal to 50 x 109 /L as platelet count <50,000/mm3 is correlated with a risk of diffuse microvascular bleeding, and to maintain it around 100 x 109/L.
FFP is usually used in LT to prevent diffuse microvascular bleeding. FFP is not indicated solely for augmentation of plasma volume or albumin concentration. According to an updated report by the American Society of Anesthesiologists, fresh frozen plasma is indicated for correction of excessive microvascular bleeding (i.e., coagulopathy) in the presence of a PT greater than 1.5 times normal or INR greater than 2.0, or an aPTT greater than 2 times normal.
Massicotte et al think that plasma transfusion at the beginning of the procedure will result in hypervolemia with a raised CVP and increased blood losses, probably through venous congestion. In fact, patients who received no plasma during their liver transplantation had less bleeding and require less blood products. In this study, avoidance of plasma transfusion is the most linked variable to the liver transplantation without RBC transfusion, also have stated that it is not necessary to correct coagulation defects before the anhepatic phase.
Maintenance of a normal intravascular volume is highly desirable in the perioperative period. It is important to maintain body fluid equilibrium by controlling the volume of fluid infusion intraoperatively. Excessive fluid administration is the strongest risk factor for postoperative pulmonary complications and inhospital mortality. Intraoperative restrictive fluid management may be advantageous because it improves postoperative organ functions and recovery and reduces complications
Certain drugs (e.g. aprotinin and tranexamic acid) can minimize blood loss. Aprotinin use results in attenuation of the systemic inflammatory response, fibrinolysis and thombin generation. This serves to decrease platelet aggregation and increase both the aPTT and activated clotting time. In high risk patients (those with cirrhosis, portal hypertension, PT >18 or bacterial peritonitis) aprotinin infusion (10,000 units.ml-1): 5ml test dose is given, and if no anaphylactic signs after 15minutes, 2million units over 30 minutes, followed by 500,000 units per hour to end of surgery. Patients with Budd-Chiari syndrome or a history of DVT or other thrombotic tendency are excluded.
Tranexamic acid is another synthetic drug that inhibits fibrinolysis. Both high-and low-dose tranexamic acid has significantly reduced the use of intraoperative red cells in several studies. The prophylactic administration of tranexamic acid (TA) at 10 mg/ kg/ h from anesthetic induction until portal vein unclamping can reduce fibrinolysis and intraoperative RBC transfusion in patients undergoing LT.
Use of the cell-saver device is a safe and effective method of salvaging RBCs during LT. If the patient has a known malignant lesion or there is an intra-abdominal infection and if the bowel is perforated at any time, autotransfusion should not be used.