Presentation 2

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FLUID TRANSFUSION

IN LIVER

TRANSPLANTATION

Fluid regulation is essential to homeostasis.

Disturbances in water or electrolyte levels→body functions fail to proceed.

The content of water in the human body changes with age.

Age GroupApproximate Water

Content in Body

Premature infant90%

Newborn infant70-80%

12-24 months64%

Adult60%

TBW is distributed among 3 major compartments.

ICF and ECF which are separated by cell membranes.

ECF divided into plasma and ISF, they are separated by capillary walls.

Fluid exchange between the intracellular and interstitial spaces is governed by the osmotic forces.

changes in osmolality between the IC and IS compartments result in a net water movement from the hypoosmolar to the hyperosmolar compartment.

Fluid exchange across capillaries is governed by differences in hydrostatic pressures and osmotic forces.

BHP tends to push the fluids out of the capillaries.

IFHP tends to push fluid back into the capillaries.

BCOP tends to pull fluids into the capillaries. IFOP tends to move fluid out of the

capillaries into the interstitial compartment.

Capillary fluid exchange

• The net balance of all of these pressures determines whether the fluid leaves (Filtration) or moves into (Reabsorption) the capillaries.

Both ICF and ECF osmolalities are regulated to maintain normal water content in tissues.

Plasma osmolality is regulated by osmoreceptors in the hypothalamus.

↑ECF osmolality →shrink of osmorecptor

cells and release ADH → water reabsorption in renal-collecting tubules → reduce plasma osmolality to normal again.

↓Extracellular osmolality →swelling of osmoreceptors → suppress the release of ADH→ water diuresis →↑osmolality to normal.

Activation of osmoreceptors by increases in ECF osmolality induces thirst and causes the individual to drink water.

• Extracellular fluid volume is directly proportionate to total body Na+ content.

• A positive sodium balance increases ECF volume, whereas a negative sodium balance decreases ECF volume.

• This regulation is achieved via sensors that detect changes in the intravascular volume.

• The baroreceptors at the carotid sinus and afferent renal arterioles and stretch receptors in both atria function as sensors of intravascular volume.

1. Renin–Angiotensin–Aldosterone.2. Atrial Natriuretic Peptide (ANP).3. Brain Natriuretic Peptide (BNP).4. Pressure Natriuresis.5. Sympathetic Nervous System Activity.6. GFR and Plasma Sodium Concentration.7. Tubuloglomerular Balance. 

Cirrhosis, the final stage of liver injury, occurs

when there is fibrosis and nodular regeneration

within the liver tissue.

Cirrhosis → dysfunction of hepatic cells,

portosystemic shunting of blood, and portal

hypertension.

↓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.

↓production of albumin → ↓blood oncotic

pressure → development of peripheral edema

and ascites.

Normal portal pressures are between 5 - 10 mmHg.

When liver becomes nodular and fibrotic, blood backs into the portal vein.

When portal pressures > 10 mmHg→ development of varices in the esophagus, stomach, and rectum.

As the pressure continues to increase,

patients are at greater risk of variceal

rupture and life-threatening hemorrhage.

Portal hypertension is associated with a

marked increase in the escape of the

intravascular fluid to the interstitial space.

Impaired renal ability to excrete Na+ is the earliest renal dysfunction in cirrhosis.

peripheral arterial VD → underfilling of circulatory volume → activation of (RAAS), (SNS) and release of ADH to restore circulatory integrity.

The result is sodium and water retention, there is fluid retention and ascites, as the liver disease progresses.

Patients with cirrhosis may develop a specific acute renal failure called hepatorenal syndrome (HRS).

Diagnosis is made when s. creatinine is over 1.5 mg/dL and there is no data suggesting other etiologies of RF.

The hallmarks of HRS are reversible renal constriction and mild systemic hypotension.

Pathogenesis may involve both ↑ vasoconstrictor and

↓ vasodilator factors → renal VC, hypoperfusion and

↓ GFR → ↓ renal synthesis of VDs and ↑ intrarenal

synthesis of VCs (angiotensin-II, adenosine), thus leading

to a vicious circle that perpetuates the renal failure.

Two patterns of HRS are observed in clinical practice: type 1 and type 2.

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.

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.

HPS is a progressive, debilitating complication of ESLD that occurs in 4 to 25% of LT candidates.

Diagnosis rests on the triad of cirrhosis, hypoxemia, and intrapulmonary vascular dilation.

Pulmonary features include digital clubbing, cyanosis, dyspnea, and orthodeoxia.

HPS appears to resolve after LT.

PPH refers to the development of pulmonary arterial hypertension in the setting of portal hypertension with or without liver disease.

It is defined as mean pulmonary artery pressure (PAP) more than 25 mm Hg, with a normal pulmonary capillary wedge pressure.

Patients with a mean PAP of 50 mm Hg or greater have a cardiopulmonary mortality rate of 100%.

It is the accumulation of fluid in the pleural space as a consequence of liver disease.

The most common symptom is dyspnea without chest pain.

Right-sided pleural effusion is seen in 66% of the patients with hepatic hydrothorax.

The management options include medical management of ascites, and therapeutic thoracocentesis for the control of shortness of breath.

Without liver transplantation, cirrhosis is usually fatal.

Patients with cirrhosis who are admitted to ICUs have a greater than 50% mortality rate.

Transfusion support remains an integral part of solid-organ transplantation.

The liver is a highly vascular organ and extensive bleeding should be anticipated especially with PH.

Preoperative Factors: include liver failure, cirrhosis, cholestasis, and splenomegaly.

Intraoperative Period: Intraoperative events can be broadly

categorized into: stage I (the preanhepatic phase), 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.

extensive bleeding may occur from raw surface of the liver.

This can get compounded by the preexisting coagulopathy.

Post-Operative Factors: 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 transplantation may cause bleeding.

Liver transplantation is a surgical procedure that can lead to massive blood loss and consequently result in transfusion of blood products.

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.

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.

There is a significant association between MELD and total number of transfusions in LT.

On average, an increase of 3 points in MELD score was associated with one additional blood component treatment.

The NMELD equation offers higher sensitivity, specificity, predictive values and accuracy than the current MELD score in predicting short-term patient outcome.

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).

Two factors influence blood loss: a

mechanical or vascular component and a biochemical one.

The biochemical is evaluated from the INR and the platelet count.

The mechanical factor, controlled by the surgeon, seems to be the more important of the factors influencing the transfusion rate.

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.

Many cirrhotic patients have a low platelet count due to hypersplenism, increased platelet consumption, bone marrow depression, and reduced thrombopoietin levels.

The ASA does not recommend prophylactic administration of platelets in patients undergoing surgery.

Platelet count <50,000/mm3 is correlated with a risk of diffuse microvascular bleeding.

According to ASA guidelines, many centers give platelets when its count falls below or equal to 50,000 /mm3 and to maintain it around 100,000/mm3 .

Multiorgan failure.

Stroke.

Patient and graft survival were significantly reduced

in patients who received platelet transfusions.

Infection.

vasopressor use.

respiratory medication. Use.

FFP is usually used in LT to prevent diffuse microvascular bleeding.

FFP is not indicated solely for augmentation of plasma volume or albumin concentration.

plasma transfusion at the beginning of the procedure will result in hypervolemia with a raised CVP and increased blood losses.

It is not necessary to correct coagulation defects before the anhepatic phase.

FFP is indicated for:

1.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.

2.Correction of excessive microvascular bleeding secondary to coagulation factor deficiency in patients transfused with more than one blood volume.

Fibrinogen concentration should be obtained before the administration of cryoprecipitate in a bleeding patient if possible.

Transfusion of cryoprecipitate is rarely indicated if fibrinogen concentration is > 150 mg/dl.

Transfusion of cryoprecipitate is usually indicated when the fibrinogen concentration < than 80–100 mg/dl in the presence of excessive microvascular bleeding.

Postoperative fluid overload is a risk factor for postoperative pulmonary complications after liver transplantation.

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.

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/mm3 and a

fibrinogen level >100 mg /dL is satisfactory.

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.

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