Anesthesia For Liver Transplantatin : Anesthesia For Liver Transplantatin DR CHANDRA SEKHAR BEHERA
PG FINAL YEAR
ANAESTHSIOLOGY AIMS AND OBJECTIVES : AIMS AND OBJECTIVES The indications and anesthetic management for hepatic transplantation will be reviewed.
The presentation will focus on preoperative assessment, intraoperative management, variations in practice, and new developments. INTRODUCTION : INTRODUCTION End-stage liver disease is the fourth leading cause of death in the United States for individuals aged 45-54, trailing only cancer, heart disease and unintentional injury.
The liver is the second most commonly transplanted organ, trailing only the kidney.
For the calendar year 2005, the annual number of liver transplants performed in the U.S. rose slightly from the prior year to reach 6000. The number rose again in 2006 to 6,650.
The number of living donor transplants peaked at 519 in 2001, since 2003 the number has been relatively constant at approximately 300 per year. Donation after cardiac death (DCD) transplants have increased from 0.3% of the annual total in 1996 (n=12) to 4.3% in 2005 (n=264), as the number of centers performing DCD liver transplants increased from 7 to 33 over this period.
The implications of this trend, and its effect on graft survival, will be discussed. INTRODUCTION : INTRODUCTION The primary diagnoses for deceased donor (DD) liver recipients, and their percent of total DD liver transplants performed in 2005 are non-cholestatic cirrhosis (62%, up 2% from 2004), cholestatic liver disease (7%, down 1% from 2004), acute hepatic necrosis (8%), biliary atresia (3%), metabolic disease (3%) and malignant neoplasms (8%, up 1% from 2004).
Other diagnoses account for the remaining 10% of transplants. Over the last decade there has been an increase in the proportion of recipients transplanted due to malignant neoplasms (due to elevated priority assigned in 2002 by the MELD scoring system) and the increase in frequency of hepatitis C (from 21% of recipients in 1993 to almost 40% in 2004).
The category of non-cholestatic disease includes chronic hepatitis C virus, chronic hepatitis B virus and alcoholic liver disease Slide 5: PATHOPHYSIOLOGY OF
END STAGE LIVER DISEASE CNS : Chronic liver failure is infrequently associated with cerebral edema; however, the encephalopathy found in chronic liver disease may represent a common underlying pathophysiology, with only the rate and degree of change accounting for the clinically observed differences.
The failure of hepatic clearance leads to the accumulation of toxins such as ammonia and manganese, and to alterations in endogenous transmitters and messengers, including g-aminobutyric acid (GABA), glutamate and nitric oxide. CNS CVS : CVS A hyperdynamic state, characterized by an elevated cardiac output and arteriolar vasodilatation, occurs in up to 70% of patients with end-stage liver disease. Vasoactive substances, bypassing normal hepatic metabolism, are most likely responsible.
The clinical improvement seen after total hepatectomy in patients with acute liver failure suggests that toxic substances released from the necrotic liver may be involved.
As the criteria for transplantation is expanded, upper age limits for recipients have been liberalized, making an evaluation for ischemic heart disease part of the routine preoperative assessment.
Dobutamine stress echocardiography (DSE) is used in many centers to risk stratify patients preoperatively. The advantages of DSE include the ability to diagnose pulmonary hypertension and valvular heart disease.
Several studies have shown a high negative predictive value of a negative DSE test, though one study did not support this finding. 7-9 These studies will be reviewed.
The hyperdynamic circulatory state may resolve after transplant, though it has persisted for several years. A recent study supports earlier work indicating that cardiovascular risk is significantly elevated post transplant PULMONARY SYSTEM : PULMONARY SYSTEM The pulmonary complications associated with liver disease include restrictive lung disease,
intrapulmonary shunts, ventilation-perfusion abnormalities and pulmonary hypertension.
The restrictive disease results from ascites and/or pleural effusions and frequently responds to fluid removal. Hypoxemia occurring in the absence of ascites or intrinsic lung disease is referred to as hepatopulmonary syndrome.
This syndrome has been ascribed to shunting, ventilation-perfusion mismatch and/or diffusion defects.
A contrast (bubble) echocardiograph is useful for defining the cause of room air hypoxemia. In the presence of intrapulmonary shunting, microbubbles appear five or six beats after injection, while in the presence of V/Q defects the bubbles are absorbed in the lung.
Pulmonary hypertension, defined as a mean pulmonary artery pressure > 25 mmHg or pulmonary vascular resistance > 120 dyne×s-1×cm-5, in the presence of a normal wedge pressure, occurs in up to 2% of patients with chronic liver disease. Mild (mean PAP 25-35 mmHg) or moderate (mean PAP 35-45 mmHg) pulmonary hypertension does not contraindicate transplantation, particularly in situations in which the pulmonary arterial pressures are responsive to a pharmacologic trial of vasodilators.
Successful transplantation has been performed in patients with severe pulmonary hypertension after long-term vasodilator therapy.Pulmonary hypertension has been reported to improve, persist and even develop following liver transplantation.
There are no patient variables that predict the outcome of pulmonary hypertension after successful transplant. RENAL SYSTEM : RENAL SYSTEM The identification of patients with advanced renal disease needing combined liver-kidney transplants (approx 5% of liver transplant recipients in 2004) is important preoperatively, as is the treatment of preexisting acidbase abnormalities and plasma volume defects, which might worsen less advanced renal disease in the perioperative period.
The predominant functional cause of renal failure in patients with hepatic failure is hepatorenal syndrome (HRS). The diagnosis requires the absence of primary renal disease, proteinuria, hypovolemia and hemodynamic causes of renal hypoperfusion. A urinary sodium < 10 mEq/L and/or a fractional excretion of sodium < 1% is typical.
The syndrome has been treated with success with vasoconstrictors, which improve splanchnic vasodilatation, decrease endogenous vasoconstrictor levels and improve renal blood flow.18-20 Caution should be used in patients with acute hepatic necrosis, as cerebral blood flow has been shown to be adversely effected by terlipressin.
Nephrotoxic antibiotics and contrast used for diagnostic studies should be avoided if possible.
Cyclosporine adversely affects renal function postoperatively, typically decreasing GFR by 30-50%. GASTROINTESTINAL SYSTEM : GASTROINTESTINAL SYSTEM Esophageal varices, portal hypertension and ascites are common. Sclerotherapy and/or portosystemic shunts may be required.
Gastric emptying is delayed
Drug metabolism is affected.
End-stage liver disease patients tend to be sensitive to drugs, though they may be resistant to some drugs (e.g., pancuronium) due to increased binding to globulin.
The action of many drugs (such as opioids, lidocaine and propranolol) is prolonged due to an increased volume of distribution and/or decreased metabolism HEMATOLOGICAL AND COAGULATION SYSTEM : HEMATOLOGICAL AND COAGULATION SYSTEM Anemia, due to chronic disease, malnutrition and/or bleeding, is common.
Coagulation defects result from the decreased synthesis of all clotting factors except fibrinogen and factor VIII.
Splenic sequestration of platelets reduces the number of circulating platelets, while a functional defect also occurs.
Ongoing fibrinolysis may occur due to low levels of antiplasmin and inadequate clearance of tissue plasminogen activators. COAGULATION DISORDERS : COAGULATION DISORDERS Levels of procoagulant factors (II, V, VII, IX, X) and anticoagulant factors (protein C and S, antithrombin III) are frequently decreased in patients with end-stage liver disease
Thrombocytopenia as a result of hypersplenism, qualitative platelet dysfunction, and disorders of the fibrinolytic system (reduced levels of plasminogen, α2 -antiplasmin, and factor XIII and increased plasma tissue-type plasminogen activator levels) is often encountered during the perioperative period SURGICAL PROCEDURS : SURGICAL PROCEDURS DISSECTION
REPERFUSION (NEOHEPATIC) Slide 14: Anesthetic Management ANESTHESIA MAMAGEMENT : ANESTHESIA MAMAGEMENT Manipulation of the liver can impede venous return and result in hypotension. Similarly, acute decompression of ascites early during the dissection phase can result in hypotension. During this phase, adequate fluid replacement is crucial, and colloids are frequently used.
Diuresis should be established early during the procedure to facilitate fluid management, and it may produce some renal protection in anticipation of relative renal ischemia during the anhepatic period PRE-ANESTHETIC EVALUATION : PRE-ANESTHETIC EVALUATION pre-operative evaluation differ for an OLT patient and a routine patient.
Pre-operative evaluation is performed in two stages. In the early first stage all OLT candidates are examined by anesthesiologists; the later, second-stage evaluation is performed immedi- ately before surgery.
preparation phase is organized by Use of resources is the prime consideration during preparation for LT. One should plan for an operating room time of 8 to 20 hours , with an average total time of 8.5 hours for anesthesia, 7 of which are devoted to surgery .
The minimum anesthesia staff should be a 3:2 ratio of physicians to certified registered nurse anesthetists or technicians to deal with simultaneous administration of anesthesia and operation of the rapid-infusion system device and the hromboelastograph [2±6].
A courier, responsible solely for the transport of specimens and blood products, is indispensable.
A brief second examination is performed immediately before surgery when a donor organ has been identified. PRE-ANESTHETIC EVALUATION : PRE-ANESTHETIC EVALUATION Acessing any neurologic deterioration since the initial first-stage evaluation is necessary, and signs of progressive metabolic acidosis,infection or sepsis should be sought. Cardiovascular instability,pulmonary infection and severe coagulopathy should be corrected and treated.
The internist should ensure that the patient is in the best condition for surgery. Ideally, ascites should be controlled and nutrition improved, with prothrombin time showing a return toward normal.
Coagulation status should be determined, and parenteral vitamin K should be given at least 3 days pre-operatively if possible, although it is not always possible to anticipate and schedule the operation (i.e., using cadaveric transplants). Vitamin K administration corrects coagulation defects within 24±36 hours, unless liver function is so poor that vitamin K-dependent proteins such as Factor V and prothrom- bin cannot be synthesized.
Albumin, fresh-frozen plasma, and cryoprecipitate can be given immediately before surgery;
platelets can be infused (if the count is < 50,000/mm3) immediately after induction even before cannulation.
Urine output and creatinine levels should be determined. If the recipient is cytomegalovirus immunoglobulin G negative, the status of the donor liver should be determined MEDICATION : MEDICATION Thiopental: 3 x 20 ml (25 mg/ml)
Succinylcholine: 2 x 10 ml (20 mg/ml)
Pancuronium: 20 ml (1 mg/ml)
Fentanyl: 20 ml or more (50 mg/ml)
Lidocaine: 5 ml (20 mg/ml)
Ephedrine: 10 ml (5 mg/ml)
Atropine: 3 ml (0.4 mg/ml)
Dopamine: 6 mg x kg wt, in 1,000 ml NS (10 ml/hr = 1
mg/kg/min (Use to improve renal perfusion. Note: The larger volume allows more accurate administration in adults.)
Phenylephrine: 10 mg/250 ml (mix if patient unstable)
Cephazolin*: 1 g (q 4 hr)
Clindamycin*: 900 mg
Gentamicin*: 2.5 mg/kg/dose q 8 hr
Methylprednisolone: 1 g x 2 (1 g when anhepatic, 2
mg/kg before leaving operating room)
Immuran: 2 mg/kg when anhepatic, 2 mg/kg before
leaving operating room
Calcium chloride (injection): 10 ml x 20 vials
Sodium bicarbonate: 50 ml amps x 15
Epinephrine: 3 or more of 1/10,000 injection (10 ml)
Insulin (regular or Humulin U-100): 10 ml
50% Dextrose: 50 ml (used if required to lower
potassium: 5 g glucose/unit insulin) OTHER DRUGS : OTHER DRUGS Aprotinin
Recombinant factor VIIa EQUIPMENT : EQUIPMENT Peep valves (5±20 cm)
Blood infusion equipment
Rapid infusion device (~40 kg or more)
Warming blanket and Bair Hugger for both lower and upper body (2 heating plants required)
Circuit humidifier/heater: Mandatory! (Note: Must be able to reach 458C, not 418C)
TEG: Stored in an operating room dedicated for OLT.
Do not set up unless you are trained
Reflective wraps (for heat and extremities), if available Blood collection tubes
2 Alton-Dean high pressure blood warmers MONITORS : MONITORS ECG
Arterial (radial, contralateral to VVB)
Femoral or second radial (When setting up for 2 radials: arm board, arrow guidewire kit)
Pulmonary artery (If needed) Note: Do not use heparinized saline as flush, use NS Be very careful that your lines are properly marked
Place BP cuff on right arm (opposite VVB side)
Esophageal stethoscope; nasogastric tube
Temperature (esophageal and intravascular)
PA catheter (with oximeter*)
TEE with 2D probe, sterile gel, and 2 sets of 8.5 size PREMEDICATION : PREMEDICATION Since coagulation may be abnormal pre-operatively, intramuscular premedication is not advised.
Hepatic encephalopathy is another contraindication [7,8]. If coagulation and level of consciousness are normal, standard medications are not contraindicated.
The dose is usually adjusted downward because of reduced hepatic function, including drug elimination. Premedication is frequently reduced or even omitted.
Pre- operative counseling often suffices for the patient's preparation and allows family interaction with an alert individual before surgery.
However, if a patient so desires, short-acting benzo- diazepines are often appropriate. ANESTHETIC INDUCTION : ANESTHETIC INDUCTION Rapid-sequence induction is performed because many of these patients have ascites and, perhaps, the equivalent of a full stomach.
Delayed gastric emptying often exists in patients taking cyclosporine orally.
Thiopental 4 mg/kg, ketamine 1±2 mg/kg, or etomidate 0.3±0.5 mg/kg, is used.
Succinylcholine 1±2 mg/kg is added to facilitate tracheal intubation while cricoid pressure is maintained.
The induction agents are protein bound, and the free drug fraction is increased in liver disease
when serum albumin is low, leading to an enhanced effect.
Thiopental and etomidate are metabolized in the liver but their activity is terminated by redistribution. Hence, their duration of action is normal unless the doses are large or repeated. ANESTHETIC MANAGEMENT : ANESTHETIC MANAGEMENT NARCOTICS
Anesthetic maintenance is largely similar to that in other major abdominal surgery. A narcotic can be successfully used in patients with hepatic disease despite the pharmacologic consequences of decreased clearance and prolonged half-life
Fentanyl, sufentanil and alfentanil are suitable opioid analgesic agents because they have short half-lives and inactive metabolites. Interestingly, fentanyl does not decrease hepatic oxygen and blood supply or prevent increases in demand when used in moderate doses (50 mg/ kg bolus and 0.5 mg/kg/min infusions)
Studies comparing fentanyl and morphine pharmacokinetics in adult patients with normal or abnormal liver function have not shown a different effect on disposition and elimination in adults, or of alfentanil in children ANESTHETIC MANAGEMENT : INHALATION AGENTS
Halothane is avoided in favor of isoflurane for LT.
Halothane,enflurane and isoflurane all reduce liver blood flow, but halothane reduces hepatic arterial flow to a greater extent .
The use of halothane is not advised because of its potenial to cause hepatic damage. Nitrous oxide has been used for manyyears without increased anesthesia-related postoperative hepatic complications.
However, it is often considered counterproductive because of its sympathomimetic effect and accumulation in the intestinal lumen, with the potent i a l for subsequent distension in protracted cases.
Another reason to avoid nitrous oxide is that potenial air emboli created during the vascular anastomosis may in- ANESTHETIC MANAGEMENT ABNORMALITIES IN ELECTROLYTE LEVELS : ABNORMALITIES IN ELECTROLYTE LEVELS Hyponatremia
Hypomagnesemia VITAL ORGAN : VITAL ORGAN Encephalopathy
Increased Intracranial Pressure (ICP)
Increased CO, HR
Alcoholic Cardiomyopathy Slide 28: The administration of fresh frozen plasma, red blood cells, platelets, and cryoprecipitate remains the mainstay of therapy for blood loss and coagulopathy during liver transplantation INTRAOPERATIVE MANAGEMENT, PREANHEPATIC STAGE : INTRAOPERATIVE MANAGEMENT, PREANHEPATIC STAGE This stage begins with surgical incision and ends with the occlusion of flow through the portal vein, inferior vena cava and hepatic artery.
This phase involves dissection and mobilization of the liver.
With abdominal incision and drainage of ascites, hypovolemia typically occurs. This should be treated with colloid containing fluid to minimize preload changes. In the presence of preexisting coagulopathy, fresh frozen plasma is indicated soon after incision.
Thromboelastography (TEG) or standard laboratory tests (prothrombin time, fibrinogen and platelet count) are used to guide the correction of coagulopathy.
Fibrinolysis is unusual during this phase of the surgery, so cryoprecipitate is rarely necessary at this point.
Hyponatremia should not be corrected rapidly. Perioperative rises in the serum sodium of 21-32 mEq/L are associated with central pontine myelinolysis in one report, while an increase of 16 mEq/L was not.
Citrate intoxication, ionized hypocalcemia resulting from the infusion of citrate-rich blood products in the absence of hepatic function, is avoided by the administration of calcium chloride.
Ionized hypomagnesemia also results from citrate infusion.
Aggressive treatment of hypokalemia is best avoided, particularly in preparation for reperfusion and the associated rise in potassium.
Supplemental glucose is usually not required, except in patients with severe disease or those in fulminant hepatic failure.
The maintenance of urine output is desirable; however, the use of lowdose dopamine for this reason is unproven.
Avoidance of hypothermia is important. Heated venovenous bypass during the anhepatic phase permits core temperature control. INTRAOPERATIVE MANAGEMENT, ANHEPATIC STAGE : INTRAOPERATIVE MANAGEMENT, ANHEPATIC STAGE This stage begins with the occlusion of vascular inflow to the liver and ends with graft reperfusion. Occlusion of the vena cava reduces venous return by as much as 50%.
Venovenous bypass, which diverts inferior vena cava and portal venous flow to the axillary vein, attenuates the decrease in preload, improves renal perfusion pressure, lessens splanchnic congestion and delays the development of metabolic acidosis. The use of venovenous bypass is not without risk.
Air embolism, thromboembolism and inadvertent decannulation may be fatal or result in significant morbidity. Venovenous bypass is not uniformly used at all centers.
Hepatectomy is followed by vascular anastomoses of the supra- and infra-hepatic IVC and the portal vein.
Fibrinolysis may begin during this stage due to an absence of liver produced plasminogen activator inhibitor resulting in the unopposed action of tissue plasminogen activator.
The use of antifibrinolytics varies among centers INTRAOPERATIVE MANAGEMENT, NEOHEPATIC STAGE : INTRAOPERATIVE MANAGEMENT, NEOHEPATIC STAGE The reperfusion of the graft begins the neohepatic stage. Reperfusion is typically via the portal vein, though the sequence of revascularization may have implications.
Reperfusion is associated with abrupt elevations in potassium and hydrogen ion concentrations, an increase in preload and a decrease in systemic vascular resistance and blood pressure.
Hypothermia, monitored via blood Temperature, is a marker for the presence of graft outflow into the central circulation.
Potentially life-threatening hyperkalemia requires calcium chloride and possibly bicarbonate administration. However, even in the absence of treatment, elevated potassium levels fall spontaneously within minutes due to redistribution. The presence of EKG changes suggestive of hyperkalemia requires prompt treatment.
Fibrinolysis is most severe after reperfusion. Antifibrinolytics and cryoprecipitate may be required.
The hepatic arterial anastomosis and biliary reconstruction are generally performed after venous reperfusion.
Signs of graft function that may be observed in the operating room include decreased calcium requirements, improvement in acidosis, increased urine output, a rising core temperature and bile output from the graft. Slide 32: . Characteristic intraoperative changes in physiologic variables
Neohepatic stage Pre-anhepaticstage Anhepatic stage Early Late
Cardiac output High Low High High
Heart rate High High Low High
Mean arterial pressure Normal Low Very low Normal
Filling pressure Normal Low High Normal
Vascular resistance Low High Very low Low
PaO2 Normal Normal Normal Normal
PCO2 Normal Low Normal Normal
Base deficit Normal High Very high Normal
Serum Na+ Low Normal Normal Normal
Serum K+ Low Normal Very high Low
Serum Ca2+ Normal Very low Low Normal
Serum citrate Normal High High Low
(From Kang YG, Freeman JA, Aggarwal S, et al. Hemodynamic instability during liver
transplantation. ) transplant Proc 1989;21:3489±492. # 1989. Reprinted by permission of Appleton & Lange, Inc.) PEDIATRIC TRANSPLANTATION : PEDIATRIC TRANSPLANTATION Biliary atresia is the most common primary diagnosis in pediatric liver transplant recipients, while metabolic liver disease represents the second largest group.
Patients with biliary atresia typically have undergone prior abdominal surgery (Kasai procedure), which complicates transplant surgery.
Bleeding may not be severe in these patients because synthetic function is usually preserved.
The risk of hepatic artery thrombosis in children leads to less vigorous correction of any clotting defects. Fresh frozen plasma is used sparingly and antifibrinolytics are typically avoided. Slide 34: What are the recent innovations in liver transplantation? LIVING DONOR TRANSPLANTATION : LIVING DONOR TRANSPLANTATION Initial reports about LDLT in the early twentieth century establishedthe technical feasibility of the procedure .
The donor hepatectomy can include left lobes, left lateral segments , or extended right lobe. LDLT has some advantages for the pediatric recipient and the transplant population as a whole.
These include increased graft availability and survival, and decreased morbidity, mortality, rejections, and cost.
Potential donor evaluation should include bedside ABO blood type compatibility with the recipient (the only need in a cadaveric
donor). Also necessary is the exclusion of acute, chronic or viral
illness, and liver/biliary system function and anatomy assess-
ment, as well as psychological assessment.
Although the procedure is relatively safe for the donor, over 10% of donors have presurgical complications . Surgical experience and technical modifications have resulted in significant reduction of
these complications. LIVING DONOR TRANSPLANTATION : The mortality risk of hepatic resection in non-cirrhotic individuals is extremely low when the operation is performed in an experienced center .
Emergency transplantation from living donors can increase OLT applicability from 10 to 37% with high (85%) survival rates . Thus, where cadaveric organ donation is scarce, emergency LDLT can be applied to high urgency patients. LIVING DONOR TRANSPLANTATION SPLIT CADAVERIC-DONOR GRAFT : SPLIT CADAVERIC-DONOR GRAFT . LT in small children has been limited by the shortage of suitable cadaveric donor organs.
The number of new transplant candidates under 5 years of age has increased by 5% annually since 1988, while the annual number of CD transplants performed in this age group has fallen
The split is done between the adult recipient, (using the extended right lobe), and the pediatric recipient (using the left lobe) of the CD graft.
Split CD graft was the obvious technical solution to this problem of pediatric graft availability.
However, in high urgency patients where emergency OLT was needed, and the technique of emergency living donor liver transplant could not be applied or was not yet developed (i.e., prior to 1999) , split CD transplantation of two grafts was the only solution. NEW IMMUNOSUPPRESSIVE DRUGS : NEW IMMUNOSUPPRESSIVE DRUGS Cyclosporin is the most commonly used maintenance immunosuppressive drug.
Steroids are almost invariably added .
Azathioprine may be used as a third agent to reduce the dose of cyclosporine and, in some cases, may replace cyclosporine altogether when the latter is contraindicated or can no longer be used because of adverse side effects.
Anti-lymphocyte globulin preparations, including the monoclonal antibody OKT-3 , have been given prophylactically and for specific indications to prevent rejection. OKT-3 reacts gainst all mature T lymphocytes.
Other new drugs have been developed and tested in multicenter trials in the last decade . The most prominent is tacrolimus (FK506), which became an established immuno-suppressant agent for primary and rescue therapy (when experiencing rejection or poor tolerability to cyclosporin) in patients with liver, kidney and pancreas transplants. FULMINANT HEPATIC FAILURE : FULMINANT HEPATIC FAILURE Fulminant hepatic failure is an uncommon entity with the potential for rapid progression to coma.Cerebral edema and elevated intracranial pressure occur in up to 80% of patients with acute liver failure.The combination of coagulopathy and altered mental status is ominous, particularly when associated with a decrease of previously elevated liver enzyme values.
In patients with stage III or IV coma, intracranial pressure monitoring should be considered. Fresh frozen plasma and platelet concentrates are indicated prior to ICP monitor placement when the INR is > 2 or the platelet count is < 50,000, or in the presence of clinically significant microvascular bleeding.
The cerebral perfusion pressure should be maintained above 50 mmHg.29 Administration of diuretics, elevation of the patient’s head 10-20 degrees, maintenance of the arterial pressure and treatment of agitation are important in maintaining cerebral perfusion pressure. OUTCOMES : OUTCOMES The one-year patient and graft survival rates reported in the 2006 UNOS Annual Report for primary deceased donor liver transplants were 88% and 83%, respectively. The three-year patient and graft survival rates were 80%and74%,respectively.
Repeat transplantation is associated with a decrease in patient survival compared to primary transplants. Similarly, decreased survival is also seen in patients transplanted from the ICU.
The implementation of the severity-based organ allocation system in 2002 has resulted in an increase in the percentage of “not hospitalized” recipients. This finding most likely results from an increase in the number of patients transplanted for hepatocellular carcinoma (an increased number of points are awarded for this diagnosis under the new system) and the decreasing use of the ICU to maintain medical urgency status of patients.
Patient survival after DCD transplant is decreased compared to donation after brain death (DBD) transplants, though the difference in survival between the two groups appears to be diminishing. AFTER TRANSPLANTATION : AFTER TRANSPLANTATION During the ICU stay, additional procedures may be needed to identify and treat sources of infection, bleeding, or graft failure.
Such procedures are perfomed in up to 50% of the post-LTpatients, and in 50% of these patients more than one procedure is needed . Because the procedures are relatively short and the patients are already intubated, major issues concerning anesthesia are few.
However, bleeding or hemodynamicinstability is always a concern. POSTSURGICAL PAIN CONTROL : POSTSURGICAL PAIN CONTROL Interestingly, several studies have demonstrated that analgesic requirements in liver transplant patients are significantly decreased when compared with other major abdominal surgery MY REFERENCES : MY REFERENCES 1. Web-based Injury Statistics Query and Reporting System. CDC and the National Center for Injury Prevention and Control, 2004.
(Accessed May 31, 2007, at http://www.cdc.gov/ncipc/wisqars/.)
2. Annual Report of the U.S. Organ Procurement and Transplantation Network and the Scientific Registry of Transplant Recipients: Transplant Data 1996-2005. In: Services USDoHaH, ed.: Rockville, MD: Health Resources and Services Administration, Healthcare Systems Bureau, Division of Transplantation.; 2006.
3. Annual Report of the U.S. Organ Procurement and Transplantation Network and the Scientific Registry of Transplant Recipients: Transplant Data 1994-2003. URREA and UNOS, 2004. (Accessed May 6, 2005, at http://www.optn.org/data/annualReport.asp.)
4. Colquhoun SD, Lipkin C, Connelly CA. The pathophysiology, diagnosis, and management of acute hepatic encephalopathy. Adv Intern Med 2001;46:155-76.
5. Glauser F. Systemic hemodynamic and cardiac function changes in patients undergoing orthotopic liver transplantation. Chest 1990;98(5):1210.
6. Harrison P, Wendon J, Williams R. Evidence of increased guanylate cyclase activation by acetylcysteine in fulminant hepatic failure. Hepatology 1996;23(5):1067-72.
Miller anasthesia 7th edition
Anaesthesia and coexisting diseases ,stoelting Slide 44: THANK YOU steve_jobs‑founder APPLE CORP
“As you may know, I had a liver transplant,” Jobs told the audience ...