下夜班~~
趁着丸子姐睡着了
分享一下今早的英文交班
时间有限 能力有限 还望老师批评指正
Good morning, everyone.
Today is September 2nd.
We did two emergency cases at yesterday’s shift,craniectomy and liver transplantation.
The liver transplantation patient was 51-years-old, male,has been diagnosed with hepatitis B for 20 years.
The patient was evaluated for ASA IV level and cardiac function I level.
After a standardized induction sequence, anesthesia was maintained by titrating sevoflurane and remifentanil infusion to maintain MAP and HR within 20% of baseline values.
The key point of anesthesia management in this case is coagulation profile, volume status and general hemodynamic state.
Intraoperative bleeding was 3200 ml, we injected 18 units of RBCs and 3000 ml of FFP, when the patient left the operating room ,his hemoglobin was 10 grams per liter.
The operation was successful and lasted for 14 and half hours and the patient was transferred to ICU at 2:30 am.
That’s all.
Thanks for your attention.
补充 uptodate
ANESTHETIC MANAGEMENT
Induction and intubation — Rapid sequence anesthetic induction and endotracheal intubation with appropriate additional precautions against aspiration is nearly always employed, particularly for patients with inadequate time for fasting and those with increased intra-abdominal pressure due to moderate or severe ascites. (See "Rapid sequence induction and intubation (RSII) for anesthesia".)
As noted above, adequate blood pressure (BP) is maintained by activation of the sympathetic system to increase cardiac output (CO), thereby compensating for low systemic vascular resistance in patients with end-stage liver disease. Since this sympathetic drive is decreased during induction of general anesthesia, severe hypotension may occur. Administration of vasopressors, sometimes at significant doses, is typically necessary during induction of anesthesia in order to maintain hemodynamic stability. (See 'Cardiovascular changes' above and 'Hemodynamic and vasopressor management' below.)
For these reasons, we insert the intra-arterial catheter before induction. (See 'Cardiovascular monitoring' above.)
Maintenance of anesthesia — Either inhalation or intravenous agents may be employed to maintain general anesthesia during liver transplantation. The minimum alveolar concentration of sevoflurane to prevent motor responses to initial skin incision is lower in patients with end-stage liver disease (approximately 1.3 percent), compared with patients with normal liver function during major abdominal surgery (approximately 1.7 percent) [83].
During the maintenance phase of anesthesia, the liver transplantation surgical procedure occurs in four main stages, each with specific challenges and goals (table 3) (see 'Specific considerations in each surgical phase' below). Management of fluids, transfusion of blood products, and hemodynamics differ in each stage, and are also adjusted to accommodate individual patient- and surgery-specific factors.
Antibiotic prophylaxis — Prophylactic antibiotics should be administered before the surgical incision. Selection is based on routines for abdominal/biliary surgery. (See "Antimicrobial prophylaxis for prevention of surgical site infection following gastrointestinal procedures in adults".)
Immunosuppression — Immunosuppressive drugs should be administered during transplant per institutional protocol. Often, steroids are administered during the anhepatic phase so that plasma concentrations are maximal during reperfusion of the donor graft. Calcineurin inhibitors such as tacrolimus are typically administered after surgery (eg, on postoperative day one). (See "Liver transplantation in adults: Overview of immunosuppression".)
Hemodynamic and vasopressor management — Most patients require vasopressor therapy during induction of anesthesia and throughout the dissection phase to maintain adequate BP due to the chronic vasodilatory state associated with end-stage liver disease (see 'Cardiovascular changes' above), and the superimposed vasodilatory effects of general anesthetic agents. We maintain a mean arterial pressure (MAP) ≥65 to 75 mmHg in patients without preexisting hypertension throughout all phases of liver transplant procedures.
There is no general consensus regarding choice of vasopressors (table 4) [84]. We routinely administer norepinephrine (typically 2 to 10 mcg/minute [0.03 to 0.15 mcg/kg per minute]), and add vasopressin (typically 0.01 to 0.04 units/minute) to compensate for endogenous vasopressin deficiency. Vasopressin also beneficially reduces portal hypertension by decreasing portal venous flow and pressure and increasing portal and hepatic arterial flow [24,85].
Dobutamine, dopamine, and/or epinephrine may be added to provide inotropic support when appropriate.
Blood and coagulation management
Intraoperative blood salvage — Intraoperative blood salvage using a cell saver system is typically employed to separate, wash, and concentrate salvaged red blood cells (RBCs) for reinfusion, thereby avoiding or minimizing allogeneic blood transfusion. (See "Surgical blood conservation: Blood salvage".)
Cell savage systems are used in a majority of liver transplant centers and are recommended in the absence of contraindications, such as the presence of cancer (hepatocellular carcinoma), localized infection, or otherwise contaminated surgical field [41,42]. Suctioning of ascites, bile, and intestinal contents is avoided. (See "Surgical blood conservation: Blood salvage", section on 'Contraindications'.)
Salvaged blood does not contain any significant amount of potassium and can therefore be used even when severe hyperkalemia is present. (See 'Management of hyperkalemia/metabolic abnormalities' below.)
However, there are no coagulation factors in cell saver blood because plasma is washed away and replaced with 0.9% saline. Thus, dilutional coagulopathy may occur. (See 'Management of coagulopathy' below.)
Transfusion of red blood cells — Transfusion of RBCs and other blood products is usually necessary during liver transplantation surgery, although surgery without transfusion has become more common [86]. In addition to intraoperative blood salvage (see 'Intraoperative blood salvage' above), and administration of antifibrinolytic therapy (see 'Administration of antifibrinolytic agents'below), we apply various blood management strategies to maintain adequate hemoglobin (Hgb) and coagulation status while avoiding unnecessary transfusion. (See "Perioperative blood management: Strategies to minimize transfusions".)
Decisions to transfuse salvaged or allogeneic blood are guided by balancing risks of transfusion with risks of anemia (see "Intraoperative transfusion of blood products in adults", section on 'Risks of severe anemia versus risks of RBC transfusion'). Such decisions also depend on the results of point-of-care (POC) laboratory tests and use of an institutional transfusion algorithm or guideline. (See "Intraoperative transfusion of blood products in adults", section on 'General principles for transfusion decisions'.)
The selected Hgb transfusion trigger is <7 to 8 g/dL for many surgical patients (see "Intraoperative transfusion of blood products in adults", section on 'Red blood cells'). However, factors that may necessitate a more liberal transfusion trigger (typically Hgb <9 g/dL) in patients undergoing liver transplantation include severity of ongoing and anticipated blood loss and current intravascular volume status. For example, severe bleeding often occurs in the pre-anhepatic phase during surgical dissection of the diseased liver, particularly if the patient has portal hypertension and coagulopathy. (See 'Dissection/pre-anhepatic phase' below.)
In fact, use of a rapid transfusion system is often necessary during liver transplantation surgery. A sufficient reserve of blood products should be immediately available in or near the operating room. Moderate (>5.5 mEq/L) or severe (>6.5 mEq/L) hyperkalemia may occur during large volume transfusion of RBCs; if so, further transfusion of allogeneic RBC units is stopped until treatment of hyperkalemia has been initiated and lower potassium levels have been confirmed [87]. Infusion of salvaged blood is preferred when available, since little potassium remains in salvaged blood after the washing process (see 'Intraoperative blood salvage' above). However, allogeneic RBCs from the blood bank do contain potassium; the potassium concentration increases with age of the RBCs and can be >50 mmol/L [88]. Also, transfusion of older RBCs stored for >14 days may increase the risk of postoperative acute kidney injury in liver transplant recipients, possibly due to accumulated proinflammatory substances [89].
In some patients, it may be necessary to "prewash" some units of RBCs from the blood bank in order to lower potassium content. These washed units are kept in reserve until severe bleeding with hyperkalemia occurs. (See 'Management of hyperkalemia/metabolic abnormalities' below.)
Management of coagulopathy — Preoperative coagulopathy is present in many patients with end-stage liver disease, and is typically corrected during the dissection phase of liver transplantation surgery [1,2] (see 'Dissection/pre-anhepatic phase' below). However, correction of coagulopathy and blood management are complicated by the complex derangements of the coagulation system that may also lead to hypercoagulability (see 'Hematologic changes' above). For example, thrombosis of a tenuous hepatic artery anastomosis may occur more readily if coagulopathy is aggressively corrected, especially if platelets are transfused. Conversely, marginal donor organ quality (for example with a donation after cardiac death donor) may be a reason for more vigorous transfusion of coagulation factors since delays in function of the new liver may affect resolution of coagulopathy in the neohepatic phase of the surgical procedure. (See 'Neohepatic phase' below.)
Management of coagulopathy with transfusion of blood components (table 5) is influenced by the stage of surgery, whether clinically significant bleeding is occurring, and results of coagulation testing (table 2). (See 'Coagulation tests' above.)
●Fresh frozen plasma – Severe preexisting coagulopathy should be corrected during the dissection phase, primarily with the coagulation factors contained in fresh frozen plasma (FFP). FFP contains factors I, II, V, VIII, IX, X, XI, XIII, as well as anticoagulant protein C, protein S, and antithrombin III. Thus, FFP is a component of massive transfusion protocols during periods of significant bleeding. However, FFP contains only a small amount of fibrinogen. (See "Intraoperative transfusion of blood products in adults", section on 'Plasma' and "Massive blood transfusion", section on 'Coagulation proteins'.)
FFP should not be transfused based on an elevated international normalized ratio in the absence of clinical bleeding. Viscoelastic testing can help guide transfusion of FFP (table 2) [2,80,82]. (See 'Coagulation tests' above.)
Risk of over-transfusion with high volumes of FFP include transfusion-associated acute lung injury (TRALI) and thrombotic complications. As noted below, other factor concentrates may be substituted when appropriate (eg, fibrinogen concentrate, cryoprecipitate, prothrombin complex concentrate [PCC]).
●Cryoprecipitate or fibrinogen concentrate – Fibrinogen concentrate or cryoprecipitate is used to treat hypofibrinogenemia during liver transplantation in a patient with clinically significant bleeding with measured low fibrinogen concentration (ie, <150 to 200 mg/dL [80,90]) or when fibrinogen cannot be measured in a timely fashion. Abnormally low concentrations of fibrinogen impair clot formation and increase bleeding. (See "Perioperative blood management: Strategies to minimize transfusions", section on 'Fibrinogen concentrate'.)
Cryoprecipitate contains FVIII, von Willebrand factor (vWF), FXIII, and fibrinogen. It is used for the same indications if fibrinogen concentrates are not available. Fibrinogen concentrates may have less risk of inducing hypercoagulability compared with cryoprecipitate as they do not contain FVIII, vWF, and FXIII [91]. (See "Intraoperative transfusion of blood products in adults", section on 'Cryoprecipitate'.)
Fibrinogen concentration is frequently decreased after reperfusion due to fibrinolysis since the ischemic liver graft releases tissue plasminogen activator (tPA) that is washed into the circulation during reperfusion [92] (see 'Reperfusion phase' below). Viscoelastic testing can help guide transfusion of cryoprecipitate or fibrinogen concentrate (table 2) [80,82]. (See 'Coagulation tests' above.)
●Prothrombin complex concentrates – A 4-factor PCC may also be administered, with selection of a product that contains FII, FVII, FIX, FX as procoagulant factors, as well as the anticoagulant factors protein C, protein S, antithrombin III, and a small amount of heparin, which will decrease risk for excessive thrombin generation (table 6). Advantages of PCCs over FFP include rapid administration of a small volume, with avoidance of volume overload and transfusion reactions [93-100]. (See "Perioperative blood management: Strategies to minimize transfusions", section on 'Prothrombin complex concentrate (PCC)' and "Plasma derivatives and recombinant DNA-produced coagulation factors", section on 'PCCs'.)
●Platelets – Administration of platelets can usually be avoided during the dissection phase of liver transplantation surgery, even in patients with severe thrombocytopenia. Platelet function may be normal even if platelet count is low in patients with liver failure. This is because vWF levels are high and ADAMTS-13 levels are low in these patients. Thus, vWF can bind to a smaller amount of activated platelets with a connection that is less likely to be cleaved by ADAMTS-13. Furthermore, platelets that are typically sequestered in the enlarged spleen of patients with portal hypertension can be mobilized during bleeding.
Notably, administration of platelets is an independent predictor of worse outcome after liver transplantation [101]. Thus, we typically hold platelet transfusion until the hepatic artery anastomosis has been completed. If the hepatic artery anastomosis is precarious, we try to avoid transfusion of platelets even if the count is low. However, in a bleeding patient with a low rotational thromboelastometry (ROTEM) maximal clot firmness, a high thromboelastogram (TEG) maximal amplitude functional fibrinogen, and/or a low TEG maximal amplitude, platelet transfusion is generally indicated (table 2) [80,82]. (See 'Coagulation tests' above.)
Administration of antifibrinolytic agents — There is no general consensus regarding the utility and safety of routine prophylactic administration of an antifibrinolytic agent (eg, aprotinin, tranexamic acid [TXA], epsilon-aminocaproic acid [EACA]) to treat chronic hyperfibrinolysis and the increased severity of hyperfibrinolysis that may occur during reperfusion of the donor liver (see 'Hematologic changes' above and 'Reperfusion phase' below). We typically administer either EACA or TXA in patients with diffuse microvascular bleeding if there is evidence of hyperfibrinolysis on TEG or ROTEM tests [102]. (See 'Coagulation tests' above and "Perioperative blood management: Strategies to minimize transfusions", section on 'Antifibrinolytic agents'.)
Before withdrawal of aprotinin from global markets, a 2007 meta-analysis had noted reduced transfusion requirements with administration of either aprotinin or TXA compared with placebo in patients undergoing liver transplantation, without increased risk of hepatic artery stenosis [103]. Subsequently, a 2017 propensity-matched study of patients who received TXA during liver transplantation noted reductions in transfusion of RBC and FFP in liver transplant patients compared with patients having no TXA exposure, with no difference in thromboembolic complications [104]. Similarly, a 2016 retrospective study noted that administration of EACA did not increase thromboembolic or other complications after liver transplantation [105].
Fluid management — Intraoperative fluid choices include crystalloid or colloid solutions:
●Crystalloid solutions – We routinely select Plasmalyte as the balanced electrolyte solution to use as maintenance fluid, rather than Ringer's lactate solution or 0.9% saline solution. However, there is no clear evidence that one type of balanced electrolyte crystalloid solution is superior for liver transplantation surgery.
Plasmalyte has magnesium rather than calcium (as in Ringer's lactate solution), and can therefore be mixed with blood products that contain citrate. Also, the buffers in Plasmalyte are acetate and gluconate rather than lactate (as in Ringer's lactate solution). Since lactate must undergo hepatic transformation to function as a buffer, lactate accumulation may occur if Ringer's lactate solution is used in patients with end-stage liver disease.
We generally avoid use of 0.9% saline due to concern for hyperchloremic acidosis (even in patients with hyperkalemia). Evidence in patients undergoing kidney transplantation and other major surgical procedures suggests that use of 0.9% saline, particularly in large volumes, is associated with hyperchloremia, metabolic acidosis, renal vasoconstriction, decreased glomerular filtration rate, and kidney injury [106-115]. (See "Anesthesia for kidney transplantation", section on 'Choosing fluids' and "Intraoperative fluid management", section on 'Crystalloid solutions'.)
●Colloid solution – We routinely replace known albumin losses with 5% albumin solution (eg, when a large volume of ascites fluid is drained upon entering the peritoneal cavity) [116]. Exceptions include with documented coagulopathy such that FFP is selected instead. Administration of albumin may also improve outcomes in patients with hepatorenal syndrome [117] or spontaneous bacterial peritonitis [118]. However, randomized trials and meta-analyses have not demonstrated benefits of albumin compared with crystalloid solutions in other settings [119,120] and data are scant in liver transplantation patients [121,122].
We typically target a low to normal central venous pressure (CVP), unless complete caval clamping is applied during the anhepatic phase. If complete caval clamping is used, then a higher CVP is required as a larger proportion of preload is lost compared with the piggy-back technique. We usually aim for a CVP >10 mmHg in these cases. Some centers maintain a low CVP (ie, 7 to 10 mmHg) during the dissection phase of liver transplantation (ie, prior to the anhepatic phase) in order to minimize blood loss and subsequent need for transfusion [75,123-125]. However, CVP is not a reliable indicator of intravascular volume status (see "Intraoperative fluid management", section on 'Static (traditional) parameters'). It is important to avoid hypoperfusion of end-organs if a low CVP/low volume technique is employed.
Management of hyperkalemia/metabolic abnormalities — Preoperative electrolyte abnormalities are common in patients with end-stage liver disease, and are typically corrected during the dissection phase of liver transplantation surgery.
●Hyperkalemia – Hyperkalemia carries a high risk during liver transplantation, accounting for a large percentage of intraoperative cardiac arrests and deaths (7.4 percent of all cardiac arrest in one series [126]). Hyperkalemia may be particularly severe during reperfusion, but must be aggressively treated at any stage of liver transplantation. Treatments include:
·Any potassium levels above 4.5 to 5.0 mEq/L should be treated with insulin (and dextrose depending on glucose levels), furosemide, and calcium. (See "Anesthesia for kidney transplantation", section on 'Management of hyperkalemia'.)
Calcium is typically generously administered in patients requiring massive transfusion to compensate for hypocalcemia caused by the citrate anticoagulant in FFP and RBC transfused units (see "Massive blood transfusion", section on 'Low ionized calcium level'and "Massive blood transfusion", section on 'Recommendations for calcium infusion'). Either calcium chloride or calcium gluconatemay be administered as they have similar pharmacokinetic profiles (even in the absence of liver function) [127]. Calcium chloride should be given through a central venous access to minimize the risk of tissue necrosis with extravasation.
·Washing RBCs as part of the blood salvage process removes potassium. (See 'Intraoperative blood salvage' above.)
·It is critically important to give the surgeon early notification if hyperkalemia is present. In such cases, he or she may elect to leave the caval anastomosis unfinished after completion of the portal anastomosis, so that the donor graft can be flushed by temporarily unclamping the portal vein and draining the blood into the field through the hole in the caval anastomosis. This reduces the risk of potentially catastrophic hyperkalemia during reperfusion. However, advance planning is necessary to carry out these maneuvers. (See 'Specific surgical techniques' below.)
·In rare cases, intraoperative continuous renal replacement therapy (CRRT) may be necessary to treat hyperkalemia. However, CRRT is a very slow and inefficient way to remove potassium. (See 'Use of continuous renal replacement therapy' below.)
●Hyponatremia – Hyponatremia is common in liver failure patients with ascites. However, rapid correction of hyponatremia is associated with risk for neurologic complications and pontine myelinolysis. Too rapid correction may occur in the following circumstances:
·FFP administered in high volumes, since FFP contains a high concentration of sodium.
·Sodium bicarbonate administration. Alternative buffers that do not contain sodium (eg, trometamol, tris-hydroxymethyl aminomethane [THAM]) are no longer available in the United States.
·Use of CRRT. In rare cases, it may be necessary to add dextrose to the dialysate fluid to lower its sodium concentration. (See 'Use of continuous renal replacement therapy' below.)
●Hyperglycemia or hypoglycemia – Hyperglycemia is common during liver transplantation due to administration of steroids for immunosuppression and the use of catecholamine vasoactive agents (see 'Immunosuppression' above and 'Hemodynamic and vasopressor management' above). While precise cut-off values have not been established, we typically treat any hyperglycemia with a continuous infusion of regular insulin if blood glucose is >180 mg/dL. (See "Perioperative management of blood glucose in adults with diabetes mellitus", section on 'IV insulin'.)
Hypoglycemia is rare during liver transplantation, even though it is considered a late sign of severe acute liver failure [128]. Hypoglycemia is readily treated with intravenous dextrose if it does occur. (See "Perioperative management of blood glucose in adults with diabetes mellitus", section on 'Hypoglycemia'.)
Planning for extubation — Intraoperative or early extubation a few hours after surgery has become more common, rather than planning for prolonged intubation and controlled ventilation [129]. In some centers, such early extubation is accomplished for approximately two-thirds of liver transplant patients [130]. Most complications after early extubation are minor issues such as transient hypoxemia or surgical complications such as need for re-exploration within 36 hours. Nevertheless, early extubation is not suitable for all liver transplant recipients (eg, those with severe preoperative comorbidities, or intraoperative complications or concerns regarding poor graft quality). (See 'Liver pathophysiology: Anesthetic implications' above and 'Management of complications' below.)
Postoperative analgesia — Postoperative pain management is necessary, as in any major abdominal surgical procedure. The right subcostal incision is often most painful. We typically administer systemic opioids with a patient-controlled analgesia (PCA) technique. Other centers may use subcostal transversus abdominis plane (TAP) block [131], or thoracic epidural analgesia (TEA) in patients without severe coagulopathy [132].
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