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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Monitoring of the hepatosplanchnic region

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The hepatosplanchnic area plays a pivotal role for the development of multi organ failure and serves as a sentinel organ of impending trouble for the whole organism in the critically ill patient. This is partly due to the fact that hepatosplanchnic malperfusion and thus covert tissue hypoxia may even occur under sufficient global perfusion and oxygenation. Moreover, the gastrointestinal tract is a susceptible organ for local hypoxia as a consequence of the particular microvascular architecture characterized by a countercurrent blood flow of a central inflow vessel with a capillary network to the villus tip. Therefore, particular interest exists in monitoring hepatosplanchnic blood flow, oxygen availability and functional organ performance in order to avoid insufficient regional blood flow and to monitor the effects of therapeutic measures.

The specific vascular anatomy of multiple vessel influx and the simultaneous high and low pressure perfusion of the liver via hepatic artery and portal vein impedes direct access to blood flow measurement of the hepatosplanchnic region in the clinical setting. A number of approaches are available aiming either at the gastrointestinal tract (1) or the liver (1, 2). The majority of available methods, though, has still to be regarded as research tools, as there is pulsed Doppler ultrasound flowmetry, laser Doppler flowmetry, remission spectrophotometry, measurement of intestinal permeability and the use of stable isotopes tracer techniques for measurement of endogenous glucose synthesis or substrate oxidation. As the aim of this chapter is to focus on methods with applicability for routine clinical use, we discuss mucosal tonometry, lidocaine metabolism and dye extraction techniques. It has to be noted, however, that these diagnostic approaches provide only integrative measures of perfusion, oxygenation and functional performance, so that in general they do not allow to discriminate changes of blood flow, oxygen exchange and metabolic activity.

Measurement of splanchnic blood flow, oxygen transport

The steady state technique on the basis of the Fick principle is used for the infusion of indocyaninegreen (ICG) by means of a primed continuous infusion technique of the dye (3). After measurement of both arterial and hepatic venous ICG concentrations under steady state conditions one can calculate splanchnic blood flow as

Image ch113e1.jpg

with Qspl for splanchnic blood flow, IRICG for ICG infusion rate [mg/min], ICGart for arterial and ICGhv for hepatic venous ICG concentration, Hct for haematocrit.

It has to be noted, however, that this technique makes catheterization of the hepatic vein necessary. Despite some specific limitations of this technique in the case of reduced ICG extraction, hepatic venous catheterization may give additional information of hepatic venous blood gas analysis yielding insight about splanchnic O2 transport. In particular monitoring hepatic venous O2 saturation may be helpful in monitoring hepatosplanchnic O2 availability due to the fact that after transplantation, trauma and sepsis there is increased O2 demand of the liver as reflected by decreased hepatic venous O2 saturation. It has to be noted, that the response of the hepatic venous O2 saturation cannot be predicted by mixed venous O2 saturation and, thus, continuous monitoring of hepatic venous O2 saturation by use of a fiberoptic catheter may be a valuable information for evaluating hepatic O2 availability. Nevertheless, it has to be stated, that the particular metabolic activity of the liver in the splanchnic area is not necessarily linked to the observed O2 uptake/supply relationship. Thus, measuring only hepatic venous O2 saturation without any parameter of metabolism and energy balance may fail to detect the impact of therapeutic interventions on the hepatosplanchnic organs (4). If hepatic venous O2 saturation can be assessed, calculation of mixed-venous/hepatic-venous O2 saturation can be a useful tool, as gradients > 10% seem to be pathognomonic for a hepatosplanchnic pathological VO2/DO2 dependency (5).

Measurement of regional PCO2

Tonometry is based on the fact that there is an equilibrium of diffusible CO2 in the surrounding tissue and in the lumen of a hollow visceral organ. Gastric and sigmoid tonometers are sampling tubes with a semipermeable silicone balloon on the catheter tip. Technically, both saline as well as phosphate buffer can be used for filling the balloon and after a sufficient equilibration time a sample is analyzed for regional PrCO2. Using a modified Henderson-Hasselbalch equation intramucosal pHi can be calculated as:

Image ch113e2.jpg

with pHi and pHa standing for intramucosal and arterial pH, and PaCO2 and PrCO2 for arterial and regional PCO2, respectively. F represents a manufacturer provided constant.

Gastrointestinal tonometry is considered to represent a non-invasive, organ-specific, metabolically oriented monitor of the adequacy of gut perfusion, oxygenation and cellular energy balance (6). There may be several factors that influence regional PrCO2 and thus PCO2 gap other than just perfusion. Factors that may be associated with an increase in PrCO2 include a reduction in regional blood flow with an insufficient disposal of locally generated PCO2. A reduction in regional DO2 independent from regional blood flow may either be linked to an increase in PrCO2 as does an increase in local O2 consumption with a simultaneous enhanced CO2 production. Enteral feeding and low gastric pH, in particular with bicarbonate containing duodenal reflux resulting in CO2 formation. Finally, disturbances of cellular energy metabolism may lead to an increase in anaerobic energy metabolism with enhanced ATP hydrolysis and a subsequent yield of H which is buffered by intracellular HCO3- to form CO2.

In contrast, PrCO2 may be decreased with an increase in regional blood flow and DO2. Reducing local O2 consumption and, as a consequence, local CO2 production results in decreased PrCO2. And, finally, reduced regional DO2 below a critical threshold and a simultaneous disturbance of aerobic CO2 production has to be considered as a potential source of decreased PrCO2.

Methodological problems of tonometry may arise from use of different solutions, blood gas analyzer dependent and user dependent inaccuracies. There is an ongoing debate about the role of intraluminal gastric pH, which per se may influence the observed PrCO2. Therefore, routine use of H2 blockers is recommended by some authors.

Due to the fact that calculation of pHi assumes an equilibrium between arterial and intracellular levels of HCO3- on the one hand and that the absolute value of pHi is strongly dependent on the systemic arterial PCO2, the calculation of pHi has been abandoned in favor of giving the pH gap (difference between arterial and intramucosal pH) and even more applicable the PCO2 gap (difference between arterial and intramucosal PCO2) rather than absolute pHi. A PCO2 gap ranging between 5–10 mmHg is referred to as normal.

In order to overcome the technical pitfalls of the used solution and the blood gas analyzer as well as user-dependent sources of error, an automated recirculating air tonometry has been developed and is commercially available (Tonocap®, Datex). This device has proven to show good accuracy and reproducibility together with a short equilibration time and, thus, offers a method of almost online monitoring of changes in PrCO2. The Tonocap® system automatically analyses CO2 at preset intervals and reduces time interval for equilibration to 12 min in vitro. Moreover this system offers the possibility of displaying the trend of the measured PrCO2.

Although there is still a lack of a clear therapeutic management protocol of increased PCO2 gap, measuring PrCO2 offers a new promising method of monitoring the splanchnic area.

Measurement of hepatosplanchnic metabolism

Dye extraction techniques

Measuring the ICG plasma disappearance rate after an i.v. dye bolus (0.5 mg/kg) integrates both liver blood flow and parenchymal function due to the high excretion of the unmetabolised dye into the bile within a single liver passage. The commercial availability of fiberoptic monitoring systems (COLD®, Pulsion) allowing rapid repetitive bedside measurements (7, 8) make this technique a useful tool for routine patient care. A normal plasma disappearance rate of ICG is ranging between 20–30%.

Lidocaine metabolism

Lidocaine is de-ethylated in the perivenous region of the liver by cytochrome P450 3A and forms monoethylglycinexylidide (MEGX), which can be measured by a fluorescence polarisation immunoassay. Thus, for the MEGX test a subtherapeutic dose of lidocaine (1 mg/kg) is injected and the plasma concentrations of MEGX are measured before and precisely 15 min after the lidocaine bolus. In healthy controls MEGX concentration around 75–100 μg/ml are reported. Values below 25 μg/ml are strongly suggestive of severe liver dysfunction. Although this test seems to be a good indicator of liver dysfunction in sepsis (9, 10), it has to be kept in mind, that due to the fact of hepatic perivenous location of MEGX formation changes in hepatic periportal metabolism are not reflected by this approach (11).


The results of the mentioned monitoring techniques are often complementary. Given the availability, complexity and invasiveness of most of the other measurement approaches, therefore, combining mucosal tonometry, MEGX formation test and the ICG plasma disappearance rate is an appropriate compromise between organ system specificity on the one hand and feasibility for routine clinical use on the other hand for monitoring liver and gut in patients with sepsis and septic shock.


Brinkmann A, Calzia E, Träger K, Radermacher P. Monitoring the hepato-splanchnic region: measurement techniques and clinical relevance. Intensive Care Med. (1998);24:542–556. [PubMed: 9681775]
Roe P G. Liver function tests in the critically ill patient. Clin Intensive Care. (1993);4:174–182. [PubMed: 10146457]
Uusaro A, Ruokonen E, Takala J. Estimation of splanchnic blood flow by the Fick principle in man and problems in the use of indocyanine green. Cardiovasc Res. (1995);30:106–112. [PubMed: 7553712]
Reinelt H, Radermacher P, Fischer G, Geisser W, Wachter U, Wiedeck H, Georgieff M, Vogt J. Effects of a dobutamine-induced increase in splanchnic blood flow on hepatic metabolic activity in patients with septic shock. Anesthesiology. (1997);86:818–824. [PubMed: 9105226]
de Backer D, Creteur J, Noordally O, Smail N, Gulbis B, Vincent J L. Does hepato-splanchnic VO2/DO2 dependency exist in critically ill septic patients? Am J Respir Crit Care Med. (1998);157:1219–1225. [PubMed: 9563742]
Fiddian-Green R G. Gastric intramucosal pH, tissue oxygenation and acid-base balance. Br J Anaesth. (1995);74:591–606. [PubMed: 7772437]
Eichelbrönner O, Reinelt H, Wiedeck H, Mezödy M, Roissant R, Georgieff M, Radermacher P. Aerosolized prostacyclin and inhaled nitric oxide in septic shock - different effects on splanchnic oxygenation? Intensive Care Med. (1996);22:880–887. [PubMed: 8905421]
Devlin J, Ellis A E, McPeake J, Heaton N, Wendon J A, Williams R. N-acetylcystein improves indocyanine green extraction and oxygen transport during hepatic dysfunction. Crit Care Med. (1997);25:236–242. [PubMed: 9034257]
Maynard N D, Bihari D J, Dalton R A, Beale R, Smithies M N, Mason R C. Liver function and splanchnic ischemia in critically ill patients. Chest. (1997);111:180–187. [PubMed: 8996014]
Esen F, Erdem T, Cakar N, Quintel M, Telci L, Akpir K, van Ackern K. Monoethylglycinexylidide (MEGX) as an early predictor of liver dysfunction in severe sepsis. Clin Intensive Care. (1997);8:260–266.
Reinelt H, Radermacher P, Kiefer P, Fischer G, Wachter U, Vogt J, Georgieff M. Impact of exogenous β-adrenoceptor stimulation on hepato-splanchnic oxygen kinetics and metabolic activity in septic shock. Crit Care Med. (1999);27:325–331. [PubMed: 10075057]
Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6989


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