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Year : 2008  |  Volume : 52  |  Issue : 5  |  Page : 562 Table of Contents     

Extreme Haemodilution to Haemoglobin of 1.2 gm.dl-1 due to Severe Blood Loss in Liver Transplantation

1 Consultants, Department of Anaesthesiology, Jaslok Hospital and Research Centre, 15 G Deshmukh Marg, Mumbai - 400 026, India
2 DNB Registrars, Department of Anaesthesiology, Jaslok Hospital and Research Centre, 15 G Deshmukh Marg, Mumbai - 400 026, India

Date of Acceptance15-Jul-2008
Date of Web Publication19-Mar-2010

Correspondence Address:
Jyotsna Goswami
1401, B Phoenix Towers, S.B.Marg, Lower Parel, Mumbai -400 013
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Source of Support: None, Conflict of Interest: None

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We report a case of a 50-year-old man, a known case of hepatitis C virus cirrhosis, who was presented for cadaveric orthotopic liver transplantation. There was severe intraoperative haemorrhage requiring massive transfusion of blood and blood products. During anhepatic phase the supply of our blood bank got exhausted. So we had to replace the ongoing blood loss with volume-expanders for approximately one hour. Patient tolerated haemodilution intraoperatively to the extent of haemoglobin 1.2 g.dl. -1

Keywords: Orthotopic liver transplantation, Hemodilution, Blood loss

How to cite this article:
Goswami J, Gomes P, Jagirdar N, Baxi V, Jain A, Bartarya S. Extreme Haemodilution to Haemoglobin of 1.2 gm.dl-1 due to Severe Blood Loss in Liver Transplantation. Indian J Anaesth 2008;52:562

How to cite this URL:
Goswami J, Gomes P, Jagirdar N, Baxi V, Jain A, Bartarya S. Extreme Haemodilution to Haemoglobin of 1.2 gm.dl-1 due to Severe Blood Loss in Liver Transplantation. Indian J Anaesth [serial online] 2008 [cited 2020 Sep 24];52:562. Available from: http://www.ijaweb.org/text.asp?2008/52/5/562/60675

   Introduction Top

Orthotopic liver transplantation (OLT) in cir­rhotic patients may be associated with significant intraoperative haemorrhage. Improvement in surgi­cal and anaesthetic techniques have contributed largely to significant reduction in transfusion re­quirement during the last decade [1] . However blood loss remains highly variable.

   Case report Top

A 50-year-old 75-kg-man with pre-existing diabetes and hypertension presented for cadaveric OLT for hepatitis C virus (HCV) cirrhosis He had history of encephalopathy (grade III) and several episodes of severe oesophageal variceal bleeding for which he received repeated blood transfusion. On examination he had pallor, icterus, bilateral basal crepts and ascites. Preoperative haemoglobin (Hb) was 7.9 g.dl -1 , haematocrit (HCT) 24, crea­tinine 1.5 mg.dl -1 , international normalized ratio (INR) 1.9, prothrombin time (PT) 22 sec, albumin 2.1 g.dl -1 and liver enzymes raised. Induction of anaesthesia was uneventful. Infusions of calcium glu­conate, dopamine and insulin were started. Aprotinin 2000 000 units bolus followed by infusion @ 250 000 units.h -1 was administered. After induction of anaesthesia the left antecubital vein and left radial artery were cannulated. The right internal jugular vein was cannulated with 9 Fr. advanced venous access system through which swan-ganz pulmonary artery catheter (PAC) was floated. Besides stan­dard monitoring, central venous pressure (CVP), arterial blood pressure (ABP), pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), other derived parameters like cardiac index (CI), systemic venous resistance (SVR), pul­monary venous resistance, urine output and tem­perature were also monitored. Blood sampling was done hourly for haematological {Hb, HCT, platelet count, PT, PTT, INR, and fibrinogen} and bio­chemical monitoring (electrolytes, lactate, glucose, arterial blood gases). Preanhepaic phase began with drainage of 2L of ascitic fluid. There was continuous blood loss which was replaced by col­loids and crystalloids. Investigations reported Hb 6.8 g.dl -1 , platelet 65 000 c.mm -1 , INR 4.1 and platelet dysfunction in thromboelastogram (TEG) which was corrected with blood and blood prod­ucts. Frusemide 10 mg and mannitol 0.5g.kg -1 were administered as urine output was low. Blood loss and transfusion requirement in this phase are shown in [Table 1]. On test clamping of inferior vena cava and portal vein there was drop in C.I by 50% and mean arterial pressure (MAP) by 15%. As we did not have the provision of venovenous bypass (VVB), volume was replaced with blood and blood products using rapid transfusion system and increase in pharmacological support. After trans­fusion of 20 units of packed red blood cells (PRBC), our blood bank informed us about non­availability of PRBC which would be available after at least 30-45 min. Hence we continued infu­sion of plasma-expanders for volume resuscitation and also increased inspiratory O 2 concentration (FiO 2 ) from 45% to 100%. Blood samples which was sent for analysis could not detect Hb at that point of time. CVP was maintained 13-14 mmHg, MAP at 50-60 mmHg and heart rate at 110-120 beats.min -1 [Table 2]. Profound metabolic acidosis was apparent with base excess of -10 mM.l -1 and pH of 7.1 [Table 3]. Finally 45 minutes later 4 units of PRBC arrived which was transfused and thereafter next drawn sample could detect Hb as 1.2 g.dl -1 (HCT 3.9). INR was still not recordable, platelet count 37 000 c.mm -1 and fibrinogen 68 g.dl­ 1. Plasma, platelet and cryoprecipitate transfusion were continued. Hypocalcemia and acidosis were corrected. Total clamping time was 2 h 10 min. Blood loss, urine output and amount of transfusion in anhepatic phase are charted in [Table 1]. At the end of anhepatic phase there was significant reduc­tion in arterial blood pressure ( MAP 30 mmHg) as soon as clamps were removed. Pharmacological support with bolus of phenylephrine, epinephrine and norepinephrine was tried followed by infusion of both epinephrine (0.05 mcg.kg -1 min -1 ) and nore-pinephrine (0.2 mcg.kg -1 min -1 ) which resulted into brief increase in arterial pressure followed by hy­potension. Vasopressin 40 units bolus followed by multiple small boluses of 4-6 units was adminis­tered which was effective to maintain haemodynamic parameters. Vasopressin infusion was started @ 2.5 - 4 units.h -1 . Hyperkalemia was corrected by calcium gluconate and sodium bicarbonate. Surgical bleeding continued. Protamine 50 mg was tried without any effect. Finally we decided to use recombinant factor VIIa (rfVIIa) 4.8 mg slowly over 10 min following which bleeding was con­trolled and haemodynamic parameters became stable. There was no urine output in this phase. Frusemide 100 mg bolus was given followed by infusion @ 40 mg.h -1 . All inotropic supports were slowly tapered off except dopamine @ 3 mcg.kg­-1. min -1 . Haemodynamic parameters, arterial blood gas values and ventilatory data in all 3 phases of surgery are shown in [Table 2] and [Table 3]. Patient was shifted to intensive care unit (ICU) and electively ventilated. Total blood loss and transfusion in this phase are shown in [Table 1]. Continuous venous­venous haemodialysis (CVVHD) was started to support renal function. Next day morning he was conscious, fully alert and was extubated. His liver and renal function improved slowly. On the 11 th postoperative day, he had massive intracerebral haemorrhage and died.

   Discussion Top

Despite recent progress in anaesthetic and surgical technique, severe blood loss remains a problem during liver transplantation which is diffi­cult to measure intraoperatively. Different transfu­sion predictors in liver transplant have been de­scribed in literature recently [2] . We expected signifi­cant blood loss which would require massive trans­fusion. Inspite of using antifibrinolytic agent imme­diately after induction, preexisting coagulopathy worsened, which made us to transfuse continuously to maintain haemodynamic and hematological pa­rameters. Venovenous bypass (VVB) is useful to reduce systemic venous congestion and thereby intraoperative bleeding. It also maintains cardiac output and renal function during cross-clamping [3] though it has its own complications [4] . Nowadays popularity of the combination of piggyback tech­nique and portocaval shunt has taken over use of VVB [5] . However in our case VVB was not used and there was continuous loss of blood. We maintained normovolemia with infusion of colloids and crystalloids during the period of non-availability of blood. Zollinger et al [6] reported haemoglobin of 1.1 g.dl -1 due to acute blood loss in a case of debulking of metastatic renal cell tumor where they found ST segment depression (at heart rate of 111 beats.min -1 ), and metabolic acidosis. There was also low mean blood pressure (50-60 mmHg) inspite of dopamine infusion and maintaining CVP of 15 mmHg. In another similar report Koehntop et al [7] described that acute intraoperative blood loss was replaced by non-blood fluid administration for approximately 1 h due to non-availability of blood and they observed frequent premature ventricular contractions at lower arterial pressure. They also observed hypothermia (35-33.5° C). In our case Hb was probably less than 1.2 g.dl -1 (as it was 1.2 after transfusion of 4 units of PRBC) for the period of 1 hr. We did not have any ECG changes but we observed metabolic acidosis and low mean arterial pressure during low haemoglobin phase. We also observed hypothermia (35-33° C) inspite of using all warming devices.

As long as normovolaemia is maintained tissue oxygenation is preserved during acute dilutional anaemia until so called critical haemoglobin con­centration (Hb crit ) is reached. At Hb crit the compen­satory mechanism of the body to sustain tissue oxygen demand become exhausted [8],[9] . Further haemodilution causes oxygen supply-demand mis­match and thereby tissue hypoxia. Hyperoxic ven­tilation [HV] increases physically dissolved oxygen in plasma and thereby arterial oxygen content (CaO 2 ) [9] . Habler et al [10] in their animal study showed that plasma oxygen increases with HV in case of acute normovolemic haemodilution (47%when Hb [10] 7g.dl -1 and 74% when Hb [11] 3 g.dl -1 ). Pape A et al [12] commented that myocardial oxygenation (coronary perfusion pressure, lactate extraction) and periph­eral tissue oxygenation appeared more affected at Hb 1.5 g.dl -1 . Van Bommel et al [13] conducted a study on pig model and concluded that HV during extreme anaemia increases cerebral oxygen deliv­ery. Similarly Weiskopf et al [14] showed that HV not only sustains myocardial function but it also sustains cerebral tissue oxygenation and function during profound hemodilution. According to Meier et al, HV can be considered a rescue therapy in the presence of acute bleeding and life-threatening acute anaemia. It creates a margin of safety for tissue oxygenation, allowing for extreme hemodilu­tion without risk of tissue hypoxia and may bridge the time until the availability of erythrocytes [9] . In the present case with a nadir Hb of 1.2 g.dl -1 , 'critical haemoglobin value' was reached unintentionally. Our patient survived the duration of surgery without any sign of postoperative brain hypoxia and myocardial ischemia except worsening of preexisting renal dys­function. Use of catecholamines and HV were probably the savior in this particular case. We conclude by emphasizing that anaesthesiologists should be prepared for unexpected massive intra­operative haemorrhage in liver transplantation and in that case venovenous bypass could be helpful. Maintaining normovolemia, inotropic support and increase in inspiratory oxygen to 100% may be helpful in surviving extreme haemodilution.

   References Top

1.A Steib, G Freys, C Lehmann, C Meyer, G Mahoudeau. Intraoperative blood losses and transfusion requirements during liver transplantation remain difficult to predict. Canadian Journal of Anesthesia 2001; 48: 1075-1079.  Back to cited text no. 1      
2.Luc Massicotte, Marie-Pascale Sassine, Serge Lenis, Andre Roy. Transfusion predictors in liver transplant. Anesthesia and Analgesia 2004; 98: 1245-­1251.  Back to cited text no. 2      
3.Dominic A Cave, Barry A Finegan. Massive gas­trointestinal bleeding complicating portal cross clamp­ing during liver transplantation. Anesthesia and Analgesia 2004; 98: 935-936.  Back to cited text no. 3      
4.Chari RS, Gan TJ, Robertson KM, et al. Venovenous bypass in adult orthotopic liver transplantation: routine or selective use? Journal of American Col­lege of Surgery 1998; 186: 683- 90.  Back to cited text no. 4      
5.Lerut JP, Molle G, Donataccio M, et al. Cavocaval liver transplantation without venovenous bypass and without temporary portocaval shunting:the ideal technique for adult liver grafting? Transpant International 1997; 10: 171-9.  Back to cited text no. 5      
6.Zollinger Andreas, Hager Pablo, Singer Thomas, Friedl Hans P, Pasch Thomas, Spahn Donut R. Extreme hemodilution due to massive blood loss in tumor surgery. Anesthesiology 1997; 87:985-987.  Back to cited text no. 6      
7.Koehntop Douglas E, Belani Kumar G. Acute severe hemodilution to a hemoglobin of 1.3 g / dl tolerated in the presence of mild hypothermia. Anesthesiology 1999;90:1798-1799.  Back to cited text no. 7      
8.Habler O, Messmer K. The physiology of oxygen transport. Transfusion Science 1997; 18: 425-35.  Back to cited text no. 8      
9.Meier Jens, Kemming Gregor I, Kisch Wedel Hille, Wolkhammer Stefan, Habler Oliver P. Hyperoxic ventilation reduces 6-hour mortality at the critical hemo­globin concentration. Anesthesiology 2004;100:70-76.  Back to cited text no. 9      
10.Habler O, Kleen M, Hutter J, et al. Effects of hyperoxic ventilation on hemodilution- induced changes in anesthetized dogs. Transfusion 1998; 38: 135-44.  Back to cited text no. 10      
11.Habler O, Kleen M, Hutter J, et al. Hemodilution and intravenous perflubron emulsion as an alternative to blood transfusions: Effects on tissue oxygenation during profound hemodilution in anesthetized dogs. Transfusion 1998; 38: 145-55.  Back to cited text no. 11      
12.Pape A, Meier J, Kertscho H, et al. Hyperoxic ventilation increases the tolerance of acute normovolemic anemia in anesthetized pigs. Critical Care Medicine, 2006;34:1475-1482.  Back to cited text no. 12      
13.Van Bommel J, Trouwborst A, Schwarte L, Siegemund M, Ince C, Henny CP. Intestinal and cerebral oxygenation during severe isovolemic hemodilution and subsequent hyperoxic ventilation in a pig model. Anesthesiology 2002; 97: 660-70.  Back to cited text no. 13      
14.Weiskopf R, Feiner J, Hopf H, et al. Oxygen reverses deficits of cognitive function and heart rate induced by acute severe isovolemic anemia. Anesthesiology 2002; 96: 871-7.  Back to cited text no. 14      


  [Table 1], [Table 2], [Table 3]


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