Anesthetic Management for Prolonged Incidental Surgery in Advanced Liver Disease.

In spite of advances in perioperative management, operative procedures in patients with chronic liver disease pose a significant challenge for the anesthesiologist due to multisystem involvement, high risk of postoperative hepatic decompensation, and mortality. We describe the anesthetic management of an elderly patient with advanced liver disease (model for end-stage liver disease 16) for prolonged abdominal surgery. The use of invasive hemodynamic monitoring, point-of-care biochemical, and hematological surveillance coupled with prompt correction of all abnormalities was responsible for good outcome. The patient's inguinal swellings turned out to be extensions of a large peritoneal mesothelioma, necessitating a large abdominal incision and blood loss. Analgesia was provided by bilateral transversus abdominis plane blocks, which helped to reduce opioid use and rapid extubation.

INTRODUCTION

Patients with chronic liver disease (CLD) are at increased risk for perioperative morbidity and mortality.[1] The outcome is influenced by the severity of liver disease, anemia, type of surgery and anesthesia.[23] The model for end-stage liver disease (MELD) score is currently used to stratify severity.[1] MELD <10, 10–14, >14 correspond to Child-Turcotte-Pugh (CTP) scores of A, B, and C.[1] Whereas MELD <10 (CTP A) are relatively safe risks for anesthesia, mortality with MELD 10–14 (CTP B) approaches 29%–33%. Elective surgery is contraindicated in MELD ≥14 by many authorities.[4] We describe the perioperative management of a MELD 16 patient for major abdominal surgery.

CASE REPORT

This 67-year-old female patient was diagnosed 3 years previously with CLD (CTP-B) and operated for strangulated inguinal hernia. There was history of altered sensorium (likely hepatic encephalopathy) in the immediate postoperative period. She was discharged on oral propranolol 40 mg, torsemide 20 mg, spironolactone 50 mg-furosemide 20 mg combination, calcium, rabeprazole 20 mg, and glimepiride (2 mg) for hepatogenous diabetes mellitus.

She presented with bilateral large (15 × 10), irreducible inguinal swellings causing intermittent severe pain and uterovaginal prolapse interfering with walking and sitting, for which she requested surgery.

Preoperatively she was cachectic and confined to bed. Clinical examination revealed heart rate 63 bpm, palmar erythema, elevated jugular venous pressure, ecchymotic patches on the limbs, bilateral pedal edema, systolic murmurs over the precordium, and abdominal distension. Ultrasound (US) abdomen revealed moderate ascites. Echocardiography revealed left ventricular ejection fraction of 50% with moderate mitral and tricuspid regurgitation; upper gastrointestinal endoscopy revealed Grade 2 varices. Laboratory investigations demonstrated coagulopathy (prothrombin time (PT): patient 18 s, control 13 s), international normalized ratio (INR) 1.8 (partial thromboplastin time: 38 s, control 22), and thrombocytopenia (40,000/mm3). She was graded as ASA III, with CTP-C/MELD score 16 [Table 1].

Table 1

Preoperative laboratory values

Preoperatively, she received Vitamin K injection for 3 days. Lab reports on the morning of surgery were: Hb 8.6 g/dl, platelets 60 × 103 μ/L, INR 1.5, PT 13/18, [Na+] 135, and [K+] 3.2 mEq/l, respectively. After oral premedication with rabeprazole 10 mg, the patient was transferred to the operating room, and standard ASA monitoring attached and large-bore intravenous access secured in both forearms under local anesthetic infiltration. The left radial artery and right internal jugular were cannulated with US guidance before anesthetic induction. A “Rapid Infuser” (Belmont Inc., Boston, MA, USA) was primed and setup. The baseline blood pressure was 126/76 mmHg. General anesthesia was induced with fentanyl 100 μg and propofol 60 mg. Following tracheal intubation facilitated with atracurium 35 mg, bilateral transversus abdominis plane (TAP) block was placed under US guidance, using 15 ml of 0.25% ropivacaine on either side. Anesthesia was maintained with O2, N2O and desflurane (through closed circuit), fentanyl, and atracurium. Noradrenaline infusion (3 μg/min) was initiated and titrated to maintain MAP above 65 mm Hg. Nasopharyngeal temperature was monitored and core temperature maintained with forced-air warming. Arterial blood gas analysis (ABGA) 1 h after induction revealed hypokalemic metabolic alkalosis [Table 1]. Neutralized dextrose (500 ml 5% dextrose saline with 6 units insulin) and 40 mEq potassium, at 50 ml/h was begun. Blood sugar remained between 140 and 180 mg% throughout the procedure. Fresh frozen plasma (FFP) and platelet-rich plasma (PRP) were transfused throughout, from the beginning of surgery. Intraoperative liver-protective strategies included 1 g N-acetylcysteine, avoiding hyperventilation and maximizing oxygenation using FiO20.6 (SpO294%, PaO272 mm Hg).

During surgical exploration both inguinal canals were seen to be filled by a gelatinous mass arising from the peritoneum. The small inguinal incisions of presumed hernia repair had to be extended into a wide transverse laparotomy, followed by debulking of the mass and omentectomy and then vaginal hysterectomy. Surgery proved difficult because of the invasive nature of the tissue and blood loss from portosystemic collaterals. Total operative time was 8.5 h, with estimated blood loss at 1.5–1.8 l. A total of 2.5 L Ringer's acetate, 1.5 L dextrose-saline, 100 ml of 20% albumin, 5 units each of packed red cells and PRP, and 9 units of FFP were transfused during the procedure. ABG, hematocrit, and thromboelastography (TEG) were estimated at regular intervals to assess oxygenation, coagulation, and guide transfusion requirements [Table 2].

Table 2

Intraoperative arterial blood gas values

Postoperatively, she was placed on pressure support ventilation (FiO240%, pressure support 15, positive end-expiratory pressure 5). She was weaned off inotropes and extubated after 12 h.

On the evening of postoperative day (POD) 1, she developed behavioral changes suggestive of imminent hepatic encephalopathy. Serum ammonia levels were elevated (73 μg/dl). Administration of oral lactulose and rifaximin (400 mg) resulted in significant improvement in orientation over the next 24 h. Blood biochemistry and hematology showed a gradual return to normal over the next 5 days. She was discharged from hospital on POD 10 [Table 3].

Table 3

Postoperative laboratory investigations and transfusion requirement

The abdominal mass was diagnosed to be a mesothelioma on histopathology.

DISCUSSION

Nearly 10% of patients with advanced liver disease need surgery in the past two decades of life.[15] Abdominal and hernia surgery are some of the common procedures. Preoperative risk stratification of patients with cirrhosis requiring abdominal surgery is challenging. For prognosticating outcome in these patients, the CTP score and the MELD score are used. There is fairly good correlation between both scores, and CTP C is equivalent to MELD >15.[467] The MELD score of the patient described in the present case report was >16. The mortality associated with MELD >15/CTP C has been reported variably as 76%–82%.[89] MELD score >14 and Hb <10 g/dL are independent and better predictors of poor outcomes than CTP-C, together with ASA status >III and age >70 years.[8] Prenner and Ganger report a high 64-day mortality along with increased incidence of infection in patients with high MELD scores undergoing hernia repair.[9] In spite of the documented high mortality and advice to forego surgery, the patient in the present case (67 years, anemic, ascites, ASA >III) insisted on surgery to improve her quality of life.

Preoperative optimization with Vitamin K was administered for 3 days, which has been advocated in cirrhotic patients.[910] Although cirrhosis is a ‘re’ balanced state, preoperative coagulopathy correction is recommended, with FFP and platelets, especially if Vitamin K fails to correct INR.[1112]

Patients with end-stage liver disease are extremely sensitive to benzodiazepines which are notorious for precipitating encephalopathy.[13] Sedative premedication was therefore avoided. The anesthetic agents used (propofol, fentanyl) have been well documented for safety in cirrhotic patients.[1415] Volatile anesthetic agents can cause vasodilation and further impairment of hepatic blood flow. Desflurane undergoes least hepatic metabolism, preserves hepatic arterial buffer response, maintains systemic vascular resistance and hemodynamic stability and is probably the best choice in cirrhotics.[161718] Fentanyl has no active metabolite and is excreted renally.[19] It was used perioperatively in titrated boluses to supplement analgesia. Atracurium was used to maintain muscle relaxation.

Pain management is challenging in these patients due to drug toxicity consequent to impaired hepatic metabolism, altered volume of distribution, and unpredictable drug levels due to hypoalbuminemia.[19] NSAIDs need to be avoided due to risk of precipitating acute renal failure and opioid use should be restricted in cirrhotic patients.[20] We therefore used the TAP block for analgesia. TAP block is a peripheral somatic block for the anterior abdominal wall. It has been used in patients with liver disease for postoperative analgesia, in liver transplant recipients and for CTP A patients undergoing hepatic resection and has been reported to significantly reduce opioid use and recommended in cirrhotic patients.[17182122]

Maintenance of adequate hepatic blood flow and oxygen delivery during anesthesia is crucial to avoid hepatic decompensation.[18] Ziser et al. report a high incidence of intraoperative hypotension in cirrhotics.[23] Therefore, a low-dose infusion of norepinephrine was started soon after induction of anesthesia to ensure avoidance of hypotension. Norepinephrine at 0.1 μg/kg/min has been seen to be useful in preventing ascitic fluid loss-induced hypotension during emergency laparotomy in cirrhotics.[24] The therapeutic benefit of albumin in cirrhosis is well documented in the prevention and treatment of hepatorenal syndrome. Modulation of systemic inflammatory response and intravenous volume expansion associated with the use of intravenous albumin may help role in limiting end organ dysfunction in cirrhotics.[25] An albumin infusion was begun intraoperatively to accommodate the large fluid shifts that occurred due to prolonged surgery and significant blood loss.

Finally, N-acetylcysteine was used in view of its purported antioxidant and renoprotective effect.[26]

Invasive monitoring of blood pressure and central venous pressure (CVP) is vital to vasopressor and fluid management. However, CVP has been found to be a poor predictor of fluid responsiveness and its absolute values may be unreliable due to preexisting tricuspid regurgitation.[27] Although pulse pressure variation is a good alternative, the Vigileo system has been seen to have an unacceptable degree of error and unreliability for recording CI in cirrhotic patients perioperatively.[28] Transesophageal Doppler and transesophageal echo (TEE) are extremely useful modalities to assess cardiovascular variables and volume status in these patients. However, interpretation of TEE images is user-dependent, and presence of varices may complicate placement of TEE probe.[29] This patient had Grade 2 varices on preoperative endoscopy and therefore we decided to avoid placement of the TEE probe unless absolutely necessary.

FFP and platelet concentrate were begun with the surgery. TEG, a point of care coagulation testing, is extensively used in liver transplant recipients and patients with liver disease undergoing major surgery,[30] and has been advocated in cirrhotics undergoing surgery.[31] We used TEG and serial hematocrit estimations for focused blood product transfusion.

The patient had hepatogenous diabetes mellitus, which is seen in 70%–80% of patients with advanced cirrhosis.[32] Neutralized 5% dextrose saline (6 units in 500 ml) with hourly blood sugar monitoring maintained glucose homeostasis. Serial ABG measurements were used to correct acidosis, prevent hyperventilation and metabolic alkalosis, and correct potassium and calcium abnormalities immediately.

Mental status changes, decreasing urinary output, and worsening ascites are ominous signs heralding hepatic decompensation postoperatively.[18] Increase in bilirubin levels is common due to significant blood transfusion and ischemic hepatitis. Prompt recognition of mental changes, confirmatory ammonia levels, immediate institution of lactulose, and rifaximin reversed early encephalopathy.

Finally, mesothelioma has been reported to present as inguinal hernia in the elderly.[33] Cirrhosis, due to ascites, favors development of hernias. In the present case, it led to unanticipated prolonged surgery (8.5 h) with blood loss. This is probably the first report of surgery for mesothelioma in a cirrhotic patient.

CONCLUSION

A recent survey of 100 cirrhotic patients undergoing nontransplant abdominal surgery showed a mortality of 12% for both CTP B and C patients and attributed the improvement to better intra- and post-operative management.[34] However, Neeff et al. noted that this was data from a specialist liver center and state that mortality continues to be high for MELD >16, especially for intra-abdominal procedures.[35] Liver cirrhosis is an important risk factor for morbidity and mortality for any type of surgical procedure. A distinct and individualized approach is required to consider all the physiological derangements in these patients, to avoid decompensation. We have attempted to highlight the importance of low threshold for the use of invasive hemodynamic monitoring, frequent surveillance focusing on coagulation, glycemic, metabolic and electrolyte status, aggressive and rapid correction of all abnormalities, provision of appropriate regional anesthesia to reduce opioid use and finally, vigilant postoperative monitoring for coagulopathy and encephalopathy in the management of major nontransplant surgery in advanced liver disease.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.