Estimated Blood Loss Based on Patient Presentation

Adapted from American College of Surgeons. Advanced trauma life support, student course manual. 7th ed. Chicago, IL: American College of Surgeons; 2004.

    b) A cursory neurologic examination should be performed, noting level of consciousness (Glasgow Coma Scale, Table 142-2), cervical spine tenderness, and lateralizing defects.

Table 142-2
Glasgow Coma Scale Criteria

Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974;2:81–84.

 

    c) Gastroparesis and the likelihood of a full stomach predisposing to pulmonary aspiration are assumed.

    d) Respiratory drive may be impaired due to head injury or intoxicants, and the mechanical aspects of ventilation may be compromised due to spinal cord, chest wall, or diaphragmatic injury, as well abdominal distention, pulmonary contusion, hemothorax, pneumothorax, etc.

  i) An attempt to oxygenate a hypoxic patient prior to establishing definitive airway control through endotracheal intubation is always advisable.

2) Airway management Establishing airway patency is an essential feature in early trauma care. The injured patient is at risk for a compromised airway for multiple reasons.

    a) The tongue is the most common cause of an obstructed airway and is readily treated by anterior displacement of the mandible with a jaw thrust and oral airway.

    b) Direct trauma to the face may distort or obstruct the airway through disruption of the supporting bony architecture. Bilateral fractures of the mandible are particularly likely to result in loss of airway patency. Blunt trauma to the anterior neck may fracture the larynx or trachea and precipitate subcutaneous emphysema and soft tissue swelling. Penetrating neck injuries may produce hematomas sufficient to obstruct airflow (3).

  i) Indications for definitive airway control include the need for airway protection, the need for ventilation and oxygenation, and as part of an ongoing massive resuscitation. These problems may be due to

(1) Loss of consciousness

(2) Severe brain injury (GCS < 8)

(3) Severe maxillofacial injury

(4) Airway obstruction

(5) Risk of pulmonary aspiration

(6) Apnea

(7) Chest trauma, including pneumothorax

(8) Severe brain injury

  ii) Hoarseness, stridor, use of accessory respiratory musculature, and paradoxical motions of the chest or abdominal wall suggest some degree of airway obstruction and impending total airway collapse.

  iii) Cyanosis, pallor, declining pulse oximetry values, and apnea are signs mandating immediate airway intervention.

    c) Cervical spine stabilization. All forms of airway control, including chin lift, jaw thrust, and oral and nasopharyngeal airway insertion, result in some cervical spine motion, though immobilization may mitigate this somewhat (4).

  i) Airway immobilization precautions include an appropriately sized Philadelphia collar, sand bags placed on each side of the head and neck, and the patient resting on a hard board with the forehead taped and secured to the board.

  ii) Direct laryngoscopy, even with in-line spine stabilization, results in cervical motion, especially at atlanto-occipital and atlantoaxial levels. Straight and curved laryngoscope blades do not differ substantially in the motion they produce, though the Bullard laryngoscope causes less head and cervical spine extension than conventional laryngoscopy (4).

    d) Difficult intubations require the use of such airway adjuncts as gum elastic bougies, light wands, LMA, and fiberoptic bronchoscopes.

    e) The Bullard laryngoscope facilitates intubation while maintaining the neck in a neutral position, and now there are laryngoscope handles that transmit the viewed image to an attached screen and reduce (but not eliminate) the amount of cervical motion associated with intubation (Glidescope, Saturn Biomedical, Burnaby, BC, Canada).

    f) The intubating LMA (Fastrach, LMA North America, San Diego, CA) has led to successful intubations in patients with maxillofacial injuries and where there is difficult tracheal intubation along with difficult mask ventilation.

    g) Fiberoptic bronchoscopy is considered by some to be the preferred method of securing the airway in patients with potential cervical spine injuries. However, the overall experience using a standard laryngoscope is satisfactory and no particular recommendation can be made based on outcome data.

    h) Failure to establish a definitive airway by intubation necessitates a surgical airway. Cricothyroid puncture with jet ventilation is a useful temporizing measure prior to cricothyrotomy. Often performing a cricothyrotomy will be a bridging maneuver before formal tracheostomy unless oral intubation can be achieved under less stressful circumstances.

1) Fluid Resuscitation

    a) Intravenous (IV) access. Numerous large-gauge IV lines should be inserted (14-and 16-gauge peripheral cannulae and 9 French central introducers are ideal). Placement of IV lines above and below the diaphragm is recommended if physical findings suggest major thoracic or upper extremity vascular injury.

    b) Laboratory evaluations. Blood should be drawn for type and cross-match, as well as hematology, chemistry (including lactate), ABG, and coagulation profiles (including thromboelastography)

    c) IV infusions should be warmed, isotonic, and compatible with blood products.

    d) Blood products are administered predicated upon hemodynamic indicators and serial laboratory examinations. Failure to respond to crystalloid indicates a need for blood.

  i) If cross-matched blood is unavailable, transfuse O-negative or type-specific red blood cells. If more than 10 units of O negative red bloods cells are given, consider continuing to administer O-negative blood.

4) Monitoring

    a) Depending on patient and surgical factors, invasive monitoring, such as intra-arterial and CVP monitoring, offer additional diagnostic information not provided by standard monitors. Patients with closed head injuries may require ICP monitoring. Urine output should also be followed.

    b) Capnography. Measuring expired CO₂ not only verifies endotracheal intubation but may assist in diagnosis of other important events.

    c) Trauma patients will have increased gradients between alveolar and end-tidal CO₂ due to increased dead space. This may be due to hypovolemia, atelectasis, pulmonary contusion, pulmonary aspiration, etc.

  i) Acute, exponential increases in the CO₂ gradient are ominous and may be due to air embolism or acute decreases in CO, such as might occur with myocardial ischemia, cardiac tamponade, or tension pneumothorax.

    d) Temperature monitoring. Trauma patients usually arrive to the OR hypothermic. The anesthetized state and the OR environment potentiates this problem. Core temperature monitoring is ideal and esophageal monitoring is the norm.

  i) Hypothermia impairs wound healing, increases the likelihood of sepsis, slows drug metabolism and impairs coagulation. The triad of hypothermia, coagulopathy and acidosis is a lethal combination.

  ii) The OR should be warmed, convective air warming devices employed, and all fluids should be warmed. Wrapping the head or extremities in plastic sheeting may also be helpful.

5) Anesthetic agents Anesthetic agents should be titrated to effect, expecting that lower than normal doses may suffice where the patient is hypovolemic.

    a) Induction agents: While some agents are preferred for trauma patients, any agent, improperly used, can be deleterious. Two induction agents are preferable in this set-ting-ketamine and etomidate.

  i) Etomidate has relatively less effect on decreasing CO and SVR, though it causes adrenal depression and the impact of even a single dose in a critically injured patient remains unclear.

(1) It is the preferred agent in a patient who may have an evolving head injury as it decreases cerebral metabolic activity and is a cerebral vasoconstrictor.

  ii) Ketamine stimulates the sympathetic nervous system and often used in the hypovolemic patient. It does have some direct myocardial depressant effects but these are noted mostly in catechol-depleted patients.

(1) Ketamine is a bronchodilator and a cerebral vasodilator and increases cerebral metabolic activity, contraindicating its use where head injury is suspected.

  iii) Intraoperative awareness: Trauma patients are at risk for intraoperative awareness. Benzodiazepines and scopolamine should be administered, recognizing the latter has less impact on BP.

  iv) Nitrous oxide: Is contraindicated in trauma patients as it can rapidly diffuse into closed gas spaces, increasing the risk of tension pneumothorax, and can also expand any pneumocephalus or air embolism.

  v) Opioids. Opioids are cardiostable though they may potentiate the hypotensive effects of induction agents, volatile anesthetics, and benzodiazepines.

  vi) Muscle relaxants: Succinylcholine is routinely used to facilitate intubation and intermediate or long-acting nondepolarizing relaxants maintain good surgical conditions. Many patients are not extubated at case conclusion.

6) Trauma-related concerns for specific body regions

    a) Brain injury

  i) Secondary CNS injury: Little can be done to reverse the primary, direct CNS effects of acute injury. However, it is absolutely clear that without attention to maintaining intravascular volume, cerebral perfusion pressure and oxygenation, CNS injuries can be worsened. Agents that decrease cerebral metabolic activity are preferred. In the short-term, hyperventilation decreases ICP but over time, secondary changes in CSF pH decrease its benefit. Elevation of the head when tolerated and perhaps loosening slightly a cervical collar (facilitating jugular venous drainage) are also useful techniques. At times changing from a volatile anesthetic to an IV anesthetic technique may decrease ICP as volatile anesthetics do have cerebral vasodilator effects. Once a neurologic exam has been performed (looking in particular for lateralizing defects or posturing), use of muscle relaxants is common.

   (a) Coagulopathy: Patients with brain injuries have a high risk of impaired hemostasis. Serial measures of coagulation function should be performed and defects treated appropriately.

    b) Spinal cord injury

  i) All injured patients should be considered to have cervical spine injuries until disproven definitively. Cervical cord injuries can impair the patient’s ventilation and result in hypotension due to the inability to produce distal vasoconstriction (neurogenic shock). Like CNS injuries, spinal cord injuries can be worsened by hypotension and hypoxemia. Many of these patients will also receive 24 hours of IV steroids, though this therapy is controversial.

    c) Thoracic injury

  i) Thoracic injuries may be penetrating or blunt in etiology, and include injuries to the heart and pericardium; lung, pleural space, or bronchus; diaphragm.

  ii) Blunt cardiac injury

(1) Also called myocardial contusion, blunt cardiac injury is a clinical diagnosis. Associated injuries include sternal fractures, rib fractures, and pulmonary contusion.

  iii) Dysrhythmias: Sinus tachycardia with nonspecific ST segment changes is most common. Conduction blocks and ventricular rhythms may also be observed.

  iv) Myocardial ischemia: Patients may sustain injury to valves or papillary muscles. Coronary artery thrombosis is possible and most commonly occurs in the right coronary artery (presenting with ischemic changes in inferior ECG leads). Pump failure is an ominous finding. Cardiac enzymes add little to the evaluation of a patient suspected of having a contusion. Echocardiography is very useful and may reveal segmental wall motion defects.

  v) Cardiac tamponade: May arise from either blunt or penetrating trauma.

(1) Signs and symptoms. Bleeding into the pericardial space increases pericardial pressures and impairs cardiac filling. Positive-pressure ventilation further decreases venous return and may greatly exacerbate the reduction in CO. Stroke volume decreases, and tachycardia compensates for a time to increase CO.

(2) The classic signs associated with cardiac tamponade (Beck’s triad) are: hypotension, distant heart sounds, and distended neck veins. Neck vein distention may not be observed because of hypovolemia.

(3) Electrical alternans, where the major ECG axis is constantly changing, may be noted. This is due to the heart floating freely in the expanded pericardium.

(4) A patient with tamponade is at risk for cardiovascular collapse with anesthetic induction. Consider draining the pericardium using local anesthesia at the operative site (a subxiphoid pericardial window) prior to general anesthetic induction.

  vi) Tension pneumothorax and hemothorax

(1) Patients may sustain a pneumothorax in association with rib fractures, stab wounds and central line placement. If the pleural cavity does not communicate with the ambient environment, air may accumulate between the chest wall and lung and expand quickly with positive-pressure ventilation. Eventually, a tension pneumothorax will decrease venous return to the thorax and cause torsion of mediastinal vessels, leading to cardiovascular collapse.

   (a) Signs and symptoms: The chest may rise unevenly with inspiration, breath sounds become unequal, the hemothorax is tympanitic to percussion, and the trachea may shift away from the affected side. Neck veins may become distended if the patient is normovolemic. Airway pressures rise.

     (i) Treatment: Tension pneumothorax is a clinical diagnosis; do not delay treatment for radiologic confirmation of this life-threatening condition. The immediate treatment is the placement of a large-bore needle through the chest wall in the second intercostal space in the midclavicular line. A rush of air confirms the diagnosis. The needle should be left in place until a tube thoracostomy is performed. Nitrous oxide should not be used in trauma patients because it quickly diffuses into any air-filled cavity, such as a pneumothorax.

  vii) Air embolism. Penetrating lung injuries may result in systemic air entrainment via bronchovenous or alveolocapillary fistulas.

(1) Signs and symptoms: Air embolism should be suspected whenever unexpected signs of CNS or myocardial ischemia and precipitous cardiovascular collapse occur in the appropriate clinical context. When treating patients at risk, minimize inspiratory airway pressure, avoid PEEP, and administer small tidal volumes.

  viii) Abdominal compartment syndrome (ACS). The ACS is regularly encountered and challenges the anesthesiologist.

(1) Signs and symptoms. A victim of polytrauma with hypotension, oliguria, and respiratory failure manifesting as increasing airway pressures and decreasing oxygenation may have ACS. Diagnosis is by clinical suspicion and confirmed by measuring bladder pressure (>25 cm H₂O is diagnostic).

(2) Prompt recognition is important as the treatment, surgical decompression, is usually straightforward. However, low CO may be associated with elevated pulmonary arterial occlusion pressure, somewhat similar to what might be seen in cardiac failure, calling into question optimal fluid management. A trial of volume expansion is usually indicated when a pathologic increase in abdominal pressure is suspected despite seemingly normal intravascular status as assessed by invasive hemodynamic monitors.

7) Damage control: Damage control is the principle of performing the minimum necessary interventions to save life and limb, leaving further procedures for a later time, after the patient has obtained hemodynamic stability. Abbreviating the initial procedure has the advantage decreasing the incidence of metabolic acidosis, hypothermia, and coagulopathy, a triad known to have a high incidence of mortality.

References

1. Bonatti H, Calland JF. Trauma. Emerg Med Clin N Am 2008;26:625–648.

2. Cereda M, Weiss YG, Deutschman CS. The critically ill injured patient. Anesthesiol Clin 2007;25:13–21.

3. Pierre EJ, McNeer RR, Shamir MY. Early management of the traumatized airway. Anesthesiol Clin 2007;25:1–11.

4. Crosby ET. Airway management in adults after cervical spine trauma. Anesthesiology 2006;104:1293–1318.

5. Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: Directly addressing the early coagulopathy of trauma. J Trauma 2007;62:307–310.

Liver and Kidney Transplantation

Sara Cheng, MD, PhD

1) Liver transplantation

    a) General considerations

  i) Intraoperative problems often include massive hemorrhage and severe hemodynamic derangements. Aggressive management of coagulopathy and hemodynamic instability is mandatory (1).

    b) Preoperative considerations

  i) Graft allocation

(1) MELD (Model for End-Stage Liver Disease)

   (a) The MELD is a scoring system originally developed for assessing perioperative risk in cirrhotic patients. It is a disease severity score that is used in the United States to prioritize patients for liver transplantation (2).

     (i) All liver transplant candidates aged 12 and older are prioritized by the MELD system

     (ii) Patients under age 12 are prioritized by the PELD system (Pediatric End-stage Liver Disease).

   (b) Liver grafts are allocated to patients in a geographic region with the highest MELD/PELD scores.

   (c) MELD score is calculated based on the serum bilirubin, INR, and creatinine.

   (d) A MELD calculator can be accessed at www.UNOS.org. This score should be calculated and recorded on the anesthetic record.

(2) Status 1

   (a) Patients with acute (sudden and severe onset) liver failure and a life expectancy of hours to days without transplant

   (b) Status 1 is the only priority exception to MELD

   (c) Comprises <1% of liver transplant candidates

  ii) Donor risk index

(1) Strong predictors of graft failure include donor age >40 years, donation after cardiac death, cold ischemia time >12 hours, and split/partial grafts. African-American donor race, less height, other causes of brain death, and prolonged ischemia time are also significantly associated (3).

(2) Liver grafts harvested from donors with a high-risk index (one or more risk factors) are termed extended criteria organs.

(3) Anesthesiologists should be aware of the donor risk index, as recipients receiving extended criteria grafts are at higher risk for poor immediate graft function and coagulopathic blood loss in the operating room.

    c) Preoperative evaluation of the patient

  i) Patients should have a complete set of laboratory studies available for review, including complete blood counts, electrolytes, coagulation indices, and EKG. Stress echocardiography and pulmonary function tests (PFTs) may also be indicated.

  ii) The patient should be carefully assessed for

(1) Severity of liver disease

   (a) Including the presence of encephalopathy, signs of portal hypertension (ascites, esophageal varices, thrombocytopenia), electrolyte abnormalities, and deficits in hepatic synthetic function (INR, albumin)

(2) Comorbidities

   (a) Hepatopulmonary syndrome, portopulmonary HTN, renal insufficiency, and cirrhotic cardiomyopathy may all be present.

   (b) Significant coronary artery disease, cardiac dysfunction, and moderate-to-severe pulmonary HTN are generally considered contraindications to liver transplantation.

   (c) Patients with moderate-to-severe renal insufficiency (hepatorenal syndrome or other renal disease) may require intraoperative hemodialysis.

(3) Bleeding risk

   (a) Patients with elevated INR, thrombocytopenia, portal HTN, uremia, history of upper abdominal surgery, and intra-abdominal infection are at increased risk of large-volume blood loss in the operating room.

   (b) The number of risk factors should dictate the number of blood products that are immediately available for transfusion in the operating room.

    d) Preoperative checklist for preparation of the operating room (Table 143-1)

Table 143-1
Perioperative Checklist for Liver Transplantation

  i) Blood product availability

(1) A predetermined number of blood products based on the patient’s bleeding risk should be immediately available in the operating room at the beginning of the surgical procedure.

  ii) Rapid laboratory analysis

(1) Frequent monitoring of arterial blood gases, hematocrit, coagulation parameters, electrolytes, and glucose must be easily accessible.

(2) Thromboelastography is often very helpful and should be used if available.

  iii) Resuscitation and transplant medications

(1) In addition to the standard drugs for induction and maintenance of anesthesia, the following drugs should be readily available

   (a) Epinephrine, calcium chloride, sodium bicarbonate, phenylephrine, atropine, amiodarone, nitroglycerine, furosemide, methylprednisolone, aminocaproic acid, and propranolol

  iv) Intraoperative dialysis may be necessary in the case of hepatorenal syndrome.

    e) Intraoperative considerations (Table 143-2)

Table 143-2
Surgical Stages of Orthotopic Liver Transplantation

  i) Surgical procedure overview

(1) Orthotopic liver transplantation

   (a) The majority of liver transplantations are performed in an orthotopic manner, in which a whole diseased liver is replaced with a healthy donor liver.

   (b) Whole liver grafts are obtained from cadaveric donors.

   (c) Split liver grafts are primarily used in the case of child recipients or living donors.

(2) Heterotopic liver transplantation

   (a) Donor liver is placed at a different location from the existing diseased liver.

   (b) Rare procedure used for bridging recipients to orthotopic transplantation

  ii) Anesthetic management of preanhepatic phase

(1) Infectious concerns

   (a) Due to the high prevalence of blood-borne pathogens in liver transplant recipients, especially hepatitis C, all medical personnel should use universal precautions.

   (b) Patients will require immunosuppression, so every effort must be made to avoid infectious complications.

     (i) Use of aseptic technique for all invasive line placement

     (ii) Administer appropriate perioperative antibiotics.

     (iii) If blood loss is massive or the procedure long, redosing of antibiotics should be considered.

(2) Monitoring

   (a) In addition to standard ASA monitors, an arterial catheter should be placed for serial laboratory measurements and real-time BP monitoring during times of rapid hemodynamic change.

   (b) A central venous catheter should be used for infusion of drugs into the central compartment and transduction of central venous pressure (CVP).

   (c) The use of pulmonary artery catheters and transesophageal echocardiography (TEE) during liver transplantation varies widely between institutions.

   (d) In general, the ability to monitor cardiac output should be available to aid in the differential diagnosis of refractory hypotension, especially in high MELD patients.

(3) Intravenous therapy

   (a) Infusions should be chosen with the intent of reducing portal HTN, maintaining normal cardiac contractility, and counteracting renal retention of sodium and water.

   (b) High MELD patients with cirrhotic cardiomyopathy may require the use of ionotropes (Table 143-3).

(4) Induction and maintenance

   (a) Preoxygenation with 100% oxygen is essential.

     (i) All liver failure patients are considered full stomachs, necessitating the use of a rapid-sequence induction.

   (b) Thiopental or propofol are appropriate induction agents if the patient has adequate BP; otherwise, etomidate can be used.

   (c) Succinylcholine is the preferred neuromuscular blocker if the patient is normokalemic.

     (i) Rocuronium is not recommended due to the heavy reliance of this drug on hepatic metabolism.

   (d) Anesthesia should be maintained with volatile anesthetics with low blood-gas partition coefficients (desflurane) to allow rapid changes in the anesthetic depth.

(5) Anesthetic goals

   (a) Maintenance of normothermia

     (i) Use of fluid warmers, bed warmers, forced heated air devices, and control of ambient temperature are all appropriate.

   (b) Electrolyte management of sodium, potassium, and calcium

     (i) Maintain at as close to normal levels as possible, because derangements can lead to more severe hemodynamic instability at graft reperfusion.

   (c) Monitor blood loss

     (i) Surgical dissection can cause brisk bleeding during this period. Indicators of volume status include BP, visible blood loss, CVP, and area under the arterial BP tracing.

   (d) Monitor coagulation

     (i) Consider partial correction of severe coagulopathy and thrombocytopenia prior to line placement.

     (ii) Impaired intraoperative hemostasis is usually multifactorial, resulting from a combination of dilutional coagulopathy, thrombocytopenia, platelet dysfunction, hyperfibrinolysis, and poor graft function.

   (e) Administer blood products if necessary

     (i) An intraoperative transfusion ratio close to 1:1 of PRBC:FFP should be considered to avoid dilutional coagulopathy.

     (ii) Reasonable goals for transfusion are a hematocrit of 30% to 35% and platelets >50,000/mL.

     (iii) Drugs such as α-aminocaproic acid, DDAVP (arginine vasopressin), and recombinant fVIIa are not given routinely but should be considered on a case-by-case basis.

  iii) Anesthetic management of anhepatic phase

(1) This phase begins with surgical occlusion of the hepatic artery, portal vein, and the inferior vena cava above and below the liver.

(2) In addition to continuing attention to the concerns associated with the preanhepatic phase, this phase has additional hemodynamic issues related to caval occlusion.

(3) Acute hypotension is common secondary to poor venous return above the cross clamp.

   (a) Venous congestion below the cross clamp can cause a decrease in renal blood flow, leading to oligouria or anuria.

(4) Arterial BP can be maintained with use of an arterial vasoconstrictor such as phenylephrine.

(5) Judicious use of volume during this phase is recommended, as overzealous resuscitation during this period can worsen venous congestion and the risk of subsequent volume overload after caval unclamping.

(6) Venovenous bypass

   (a) Used by some centers to maintain cardiac preload during the anhepatic phase

   (b) This may decrease hemodynamic instability.

   (c) When used, pump flow rates must be kept above 800 ml/min to avoid pump thrombosis.

   (d) A low threshold of suspicion should be maintained for complications including vascular injury from bypass catheters, catheter kinking, pump thrombosis, hypothermia, and venous air embolus.

(7) Electrolyte abnormalities

   (a) Common electrolyte abnormalities during the anhepatic stage include metabolic acidosis, hyperkalemia, and hypocalcemia.

   (b) Must be aggressively corrected since the anhepatic patient has no means of physiologic compensation

   (c) Serum potassium should be lowered to below 3.5 mEq/L to lessen the risk of reperfusion syndrome (see below).

   (d) ABG measurements should be conducted at least every 30 minutes.

(8) IV steroid should be administered prior to reperfusion as part of induction therapy (short-term immunosuppression given at the time of transplant).

   (a) Methylprednisolone 500 to 1,000 mg is commonly used, as this dose has been shown to cause lymphocyte apoptosis and decreased subsequent graft rejection.

  iv) Anesthetic management of neohepatic phase

(1) Starts with removal of vascular clamps, resulting in reperfusion of the donor graft. It encompasses surgical reconstruction of the biliary tree and the conclusion of the surgery.

(2) Caval unclamping

   (a) Typically results in marked increases in cardiac preload and BP.

     (i) Pressors should be turned off just prior to unclamping.

     (ii) Small doses of nitroglycerin (10 to 20 μg) may be used for extreme HTN (SBP > 180), although higher pressures are preferable in preparation for the next phase of portal vein unclamping.

   (b) Portal vein unclamping

     (i) Allows recipient blood to enter the donor graft.

     (ii) Reperfusion syndrome

             1. Hemodynamic instability manifesting within 1 to 5 minutes after portal vein unclamping

             2. Caused by characteristics of the graft effluent (cold, acidic, hyperkalemic, vasoactive mediators)

             3. Symptoms include severe bradyarrythmias, hypotension, decreased contractility, and vasodilation

             4. Severity of symptoms is related to the extent that patient parameters are normalized prior to reperfusion.

             5. Prompt and repeated administration of atropine, epinephrine, phenylephrine, calcium, and bicarbonate may be required.

     (iii) Hepatic artery unclamping

             1. Does not usually have any noticeable hemodynamic consequences.

     (iv) Assessment of graft function

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