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Post Operative ICU Management of Orthotopic Liver Transplant Patients

Post Operative ICU Management of Orthotopic Liver Transplant Patients







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    Post Operative ICU Management of Orthotopic Liver Transplant Patients Post Operative ICU Management of Orthotopic Liver Transplant Patients Presentation Transcript

    • Post Operative ICU Management of Orthotopic Liver Transplant Patients S/P Chronic Hepatic Failure Dr. Ahmad Kharrouby PGY2, Surgery Surgical Intensive Care Unit
    • Introduction
      • The immediate postoperative care for liver recipients involves:
        • (1) stabilizing the major organ systems (e.g., cardiovascular, pulmonary, and renal);
        • (2) evaluating graft function and achieving adequate immunosuppression
        • (3) monitoring and treating complications directly and indirectly related to the transplant
    • Introduction
      • This initial care should generally be performed in an intensive care unit (ICU) setting because recipients usually require mechanical ventilatory support for the first 12 to 24 hours
      • The goal is to maintain:
        • adequate oxygen saturation
        • acid-base equilibrium
        • stable hemodynamics
    • Introduction
      • Continuous hemodynamic monitoring is important to ensure adequate perfusion of the graft and vital organs
      • Hemodynamic instability occurring early posttransplant is usually due to fluid imbalance, but the presence of ongoing bleeding must first be excluded
    • Introduction
      • Hemodynamic instability also may be secondary to the myocardial dysfunction that is often seen early in the reperfusion phase, but which may persist into the early postoperative period
      • The usual treatment is to optimize preload and afterload, and to use inotropic agents such as dopamine or dobutamine if necessary
    • Introduction
      • Fluid management, electrolyte status, and kidney function require frequent evaluation
      • Serum transaminase levels will usually
        • Rise during the first 48 to 72 hours post-transplant secondary to preservation injury
        • Then should fall rapidly over the next 24 to 48 hours
        • Normalize in 1 week
    • Introduction
      • Platelet counts usually decrease in the first week after LT and recover during the second week
      • This may be caused by platelet sequestration in the liver and spleen due to preservation injury &/or hypersplenism
      • Once the liver has recovered, as manifested by the return of bilirubin to normal levels, the platelet count increases
    • Outline
      • Hemodynamic
      • Pulmonary
      • Hepatic allograft function
        • Primary nonfunction and initial poor function
        • Rejection
        • Technical Complications
          • Hepatic artery thrombosis
          • Portal vein thrombosis
          • Bile duct obstruction
        • Recurrent infection and neoplasm
      • Electrolytes, glucose, and lactate
      • GI Tract
      • Nutrition
      • Infection Surveillance
      • Post transplantation Immunossuppression
      • Kidney dysfunction
      • Abdominal compartment syndrome
    • A-Hemodynamic
    • A-Hemodynamic
      • Intravascular volume resuscitation usually is required in the immediate postoperative period secondary to:
        • Third-space losses
        • Increased body temperature
        • Vasodilatation
      • Adequate perfusion is assessed by:
        • Left and right heart filling pressures
        • Cardiac output
        • Urine output
        • Absence of metabolic acidosis
        • Sequential Hemoglobin levels
    • A-Hemodynamic
      • Avoid Lactated Ringer, & use NSS and other colloid solutions instead, because lactate that is metabolised in the liver will be already elevated
    • A-Hemodynamic
      • Hepatic edema might ensue secondary to aggressive resuscitation & increased intravascular volume, so aim to CVP 6-10 to minimize increased hepatic vein pressures & sinusoidal congestion that impair graft perfusion & exacerbate reperfusion injury
    • A-Hemodynamic
      • Hypertension is common and should be aggressively treated using nitroprusside
      • Diuretics may be required to remove excess fluid acquired intraoperatively, but they may result in hypokalemia
      • Serial hematocrits and transfuse accordinglly
      • Correction of bleeding parameters using FFPs, platelet transfusions, and even Desmopressin and factor 7 infusions to be done accordingly
    • B-Pulmonary
    • B-Pulmonary
      • Ventilatory support is required postoperatively until the patient
        • Is awake and alert
        • Is able to follow commands and protect the airway
        • Is able to maintain adequate oxygenation and ventilation
      • Infectious and noninfectious pulmonary complications can occur in up to 75% of liver recipients
      • TRALI is common in these patients
    • C-Hepatic allograft function
    • C-Hepatic allograft function
      • Monitoring of hepatic allograft function begins intraoperatively after revascularization
    • C-Hepatic allograft function
      • Reassessinent of hepatic allograft function continues postoperatively
      • initially occurring every 6 hours
    • C-Hepatic allograft function
      • Satisfactory hepatic allograft function is indicated by an:
        • Improving coagulation profile
        • Decreasing transaminase levels
        • Normal blood glucose
        • Hemodynamic stability
        • Adequate urine output
        • Bile production
        • Clearance of anesthesia
    • C-Hepatic allograft function
      • Early elevations of bilirubin and transaminase levels may be indicators of preservation injury
      • The peak levels of SGOT and SGPT usually are less than 2,000 units/L and should decrease rapidly over the first 24 to 48 hours postop.
    • C-Hepatic allograft function
      • After the patient leaves the intensive care unit
        • LFTs are obtained daily
        • Bile is inspected daily
        • A T-tube cholangiogram may be obtained to ensure adequate biliary drainage and to rule out extravasation
      • It is important to correctly diagnose the cause of liver dysfunction, because each cause has its own unique treatment
    • C-Hepatic allograft function
        • Common Causes:
        • Primary nonfunction and initial poor function
        • Rejection
        • Technical Complications
          • Hepatic artery thrombosis
          • Portal vein thrombosis
          • Bile duct obstruction
        • Recurrent infection and neoplasm
      • The most common causes of early graft loss include primary nonfunction and hepatic artery thrombosis
    • 1-Primary nonfunction and initial poor function
      • The use of UW solution for organ preservation has decreased the incidence of primary nonfunction
      • For poorly understood reasons, however, 1% to 9% of transplanted livers fail immediately after the surgery
    • 1-Primary nonfunction and initial poor function
      • Primary nonfunction is characterized by:
        • Hemodynamic instability
        • Poor quantity and quality of bile
        • Renal dysfunction
        • Failure to regain consciousness
        • Increasing coagulopathy
        • Persistent hypothermia
        • Lactic acidosis in the face of patent vascular anastomosis (as demonstrated by Doppler ultrasonography)
      • Without re-transplantation, death ensue
    • 2-Rejection
      • Acute rejection is relatively common after liver transplantation, with 60% of recipients experiencing at least one cell-mediated or acute rejection episode
      • However, rejection is an extremely uncommon cause of graft loss because it can be treated by increasing immunosuppression (increase corticostroids dose)
    • 3-Technical complications
      • A variety of technical problems can lead to liver allograft dysfunction, including:
        • Hepatic artery stenosis or thrombosis
        • Portal vein stenosis or thrombosis
        • Biliary tract obstruction
        • Bile duct leak
        • Hepatic vein or vena caval thrombosis
      • Hepatic artery thrombosis
      • Incidence of about 3 to 5% in adults and about 5 to 10% in children
      • May occur in the early post transplantation period and may lead to:
        • Fever
        • Hemodynamic instability
        • Rapid deterioration of the patient,
        • Marked elevation of the transaminases
        • Associated bile leak soon after liver transplantation due to the loss of the bile ducts' main vascular supply
      • Hepatic artery thrombosis
      • Acute hepatic artery thrombosis may be treated by attempted thrombectomy
      • If this is unsuccessful, retransplantation is needed,
      • Hepatic artery thrombosis that occurs long after liver transplantation may produce intra- and extrahepatic bile duct strictures and may be an indication for elective retransplantation
      • Occasionally, hepatic artery thrombosis is completely asymptomatic
    • hepatic artery thrombosis, particularly early after transplantation when the allograft is devoid of arterial collaterals, results in selective necrosis of the Biliary tree and surrounding connective tissue
    • Typical appearance of a liver allograft that failed because of hepatic artery thrombosis leakage of bile
      • Portal vein stenosis or thrombosis
      • Portal vein stenosis or thrombosis is rare
      • When it occurs, the patient's condition may deteriorate rapidly, with:
        • Profound hepatic dysfunction
        • Massive ascites
        • Renal failure
        • Hemodynamic instability
      • Although surgical thrombectomy may be successful, urgent re-transplantation is often necessary
      • Late portal vein thrombosis may allow normal liver function but usually results in variceal bleeding and ascites
      • Bile duct obstruction
      • Bile duct obstruction is diagnosed by cholangiography
      • A single short bile duct stricture may be treated by either percutaneous or retrograde balloon dilation
      • A long stricture, ampullary dysfunction, or failed dilation necessitates revision of the biliary tract anastomosis
      • Fever and abdominal pain in the early post transplantation period should raise the possibility of biliary anastomotic disruption, which requires urgent surgical revision
    • 4-Recurrent Infection and neoplasm
      • CMV can cause hepatic allograft dysfunction and usually occurs within 8 weeks of transplantation
        • Diagnosis is made by liver biopsy, with CMV inclusion bodies being found with light microscopy or by PCR in peripheral blood
        • Treatment consists of decreasing baseline immunosuppression and administering ganciclovir (5 mg/kg every 12 hours via central venous access for 3 weeks)
    • 4-Recurrent Infection and neoplasm
      • Viral hepatitis and malignancy (e.g" hepatoma, cholangiocarcinoma, neuroendoc:rine tumors) can recur in the hepatic allograft but are uncommon in the early post-transplantation period
        • The clinical presentation includes elevations on liver function tests
        • The diagnosis is made by liver biopsy
        • Imaging studies (e.g., CT scan, liver ultrasonography) are important for following patients transplanted for neoplasms
    • D-Electrolytes, glucose, and lactate
    • D-Electrolytes, glucose, and lactate
      • The use of diuretics may result in hypokalemia
      • Whereas cyclosporine or tacrolimus toxicity may cause hyperkalemia
      • Transfusion of citrate rich blood products results in decreased serum magnesium & calcium
      • Magnesium levels are maintained above 2 mg/dL (0,82 mmol/L) because the seizure threshold is lowered bv the combination of hypomagnesemia and cyclosporine or tacrolimus
    • D-Electrolytes, glucose, and lactate
      • Calcium should be measured as free ionized calcium and kept above 4.4 mg/dL, Transfusion of citrate rich blood products results in decreased serum magnesium & calcium
      • Phosphorus levels should be maintained above 2.5 mg/dL to avoid respiratory muscle weakness and altered oxygen hemoglobin dissociation
    • D-Electrolytes, glucose, and lactate
      • Central pontine myelinolysis, which may result from marked fluctuations in serum sodium levels and osmolality, is an uncommon cause of a patient not regaining consciousness posttransplant
    • D-Electrolytes, glucose, and lactate
      • Glucose homeostasis is necessary because steroid administration may result in hyperglycemia, which is best managed with intravenous insulin because it is short acting and easily absorbed
      • Cyclosporine and tacrolimus are diabetogenic immunosuppressants and may alter glucose homeostasis
      • Hypoglycemia is a complication of liver failure, and in the presence of liver dysfunction, glucose administration may be necessary
    • D-Electrolytes, glucose, and lactate
      • Lactate
        • Patients with pre-op fulminant hepatic failure/necrosis should have lactate levels that trend towards normal after transplantation providing their fluid status is adequate
        • Elevated lactate levels also are seen in:
          • Hypoperfusion states
          • Late sepsis
          • Primary non-function
    • E-GI tract
    • E-GI tract
      • H2 blockade, proton pump inhibition, and/or antacids are used to prevent stress ulcers
      • Endoscopy is performed liberally for any GI bleeding to determine the etiology
      • Nystatin and GI tract decontamination solution containing gentamicin and polymyxin B are used in the perioperative period to prevent esophageal candidiasis and translocation of bacterial pathogens
    • F-Nutrition
    • F-Nutrition
      • Patients who are severely malnourished should be placed on nutritional supplementation as soon as stable fluid and electrolyte status and adequate graft function have been reached
    • F-Nutrition
      • Patients with adequate preoperative nutrition can be maintained on routine intravenous fluids until GI tract function returns (usually 3 to 5 days)
      • Enteral nutrition is used as soon as the postoperative ileus resolves, Total parenteral nutrition (TPN) is indicated when the Gl tract is nonfunctional
    • G-Infection surveillance
    • G-Infection surveillance
      • Sepsis is a major cause of early mortality
      • The most common causes of bacterial infection after liver transplantation include
        • Line sepsis
        • Urinary tract infection
        • Infected ascites
        • Cholangitis
        • Pneumonia
        • Biliary anastomotic leak
        • Intra­abdominal abscess
    • G-Infection surveillance
      • Prophylactic antibiotics covering biliary pathogens are administered for the first 48 hours after liver transplantation
    • G-Infection surveillance
      • If a fever develops in the liver transplant recipient, a thorough examination should be performed:
        • Chest x-ray
        • Cultures of blood, urine, indwelling lines, and bile also are necessary
        • A T-tube cholangiogram and Doppler ultrasonography of the liver can be performed to rule out perihepatic fluid collection and to evaluate hepatic vasculature
    • G-Infection surveillance
      • Hepatitis B or C recurs in the liver allograft following transplantation
    • G-Infection surveillance
      • Hepatitis B:
        • protocols are currently under investigation using different combinations of hepatitis B Ig, hepatitis B vaccines, lamivudine, retroviral agents, and monoclonal antibodies
        • The diagnosis is suspected if the level of liver transaminases increases, and it is confirmed by biopsy
        • Recurrent disease may be severe enough to lead to life-threatening hepatitis and cirrhosis
        • Strategies to prevent hepatitis B recurrence include:
          • The use of lamivudine before transplant to arrest viral replication
          • And high-dose hepatitis B Ig and lamivudine after transplant
    • G-Infection surveillance
      • Hepatitis C:
        • Recurrence after transplant, although it is ubiquitous, does not commonly lead to significant problems for many years and is associated with mild transaminitis
        • Occasionally, hepatitis C recurrence can be early, aggressive, and severe
        • Antiviral therapy has been used to treat hepatitis C recurrence but with very limited success
    • H-Posttransplantation Immunosuppression
    • H-Posttransplantation Immunosuppression
      • Currently, the immunosuppressive agents used to prevent rejection include corticosteroids and cyclosporine or tacrolimus
      • Occasionally, azathioprine or mycophenolate mofetil may be added to reduce cyclosporine or tacrolimus doses in patients with renal disease or autoimmune liver disease
    • I-Kidney dysfunction
    • I-Kidney dysfunction
      • Some degree of kidney dysfunction is very common post-transplant, affecting almost all liver recipients
      • About 10% develop kidney failure severe enough to require dialysis
      • Postoperative kidney problems that may have been present pretransplant are most commonly due to HRS or ATN
    • I-Kidney dysfunction
      • Usually, such problems will improve posttransplant, but recipients with severe pretransplant kidney dysfunction are at greater risk for persistent kidney impairment posttransplant
      • Some patients will require renal tranplantation
      • Other causes of postoperative renal dysfunction include:
        • Systemic hypovolemia
        • Drug nephrotoxicity
        • Pre-existing kidney disease
    • J-Abdominal Compartment Syndrome
    • J-Abdominal Compartment Syndrome
      • Relatively common
      • Incidence (pressure >25mmHg) ? 31%
      • Major effects on organ function (renal, respiratory, cardiovascular, liver & gut)
      • Multi-factorial etiology
      • Measure routinely (bladder, gastric pressure)
      • Laparostomy, only Skin closure
    • Main References
        • The Washigton Manual of Surgery
        • Schwartz’s Principles of surgery
        • emedicine website
        • Presentations for:
          • Dr. Derek Manas
          • Dr. Geoffrey Schultz
          • Dr Elizabeth Sizer
        • And other articles
      • Thanks for all above mentioned references, for their valuable information, & contribution in improving the health care of liver transplant patients
    • Thank You