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Blutalkohol 2005 - BADS (Bund gegen Alkohol und Drogen im ...

Blutalkohol 2005 - BADS (Bund gegen Alkohol und Drogen im ...

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Verner/Schneider/Gebel/Panning/Wiese/Tröger/Breitmeier,<br />

Blood ethanol concentrations and inebriation symptoms following percutaneous ethanol injection<br />

therapy (PEIT) carried out on patients suffering from hepatocellular carcinoma<br />

patients after percutaneous ethanol injection therapy and unexpectedly high peak BECs are<br />

probable with a high risk for unexpected iatrogenic intoxications. They still can explain<br />

our early clinical signs after clinical examination of systemic alcohol toxicity after PEI,<br />

such as drowsiness, euphoria, slurring and lalling speech, nausea, vomiting, smell of alcohol,<br />

and desorientation, because of the flooding effect while high amounts of ethanol flow<br />

off into the brain and <strong>im</strong>pairs the central nervous system. The variable release of ethanol<br />

from the tumor can be explained by changes of the vascularisation and sudden destruction<br />

of cell barriers. Apart from the experience of the responsible therapist, consistency, vascularisation,<br />

size of the tumour and the stage of liver cirrhosis, extratumoral alcohol distribution<br />

was also influenced by injection pressure and the proper position of the injection needle.<br />

Insofar apart from the injected amount of ethanol its distribution during and after PEI<br />

is of <strong>im</strong>portance. Even small amounts of ethanol injected wrongly and hence bypassing the<br />

tumour can through direct systemic diversion join the brain circulation and can subsequently<br />

produce significant ethanol concentrations and related deficiencies. As a result of<br />

our research, blood alcohol concentrations of more than 2.00 % which in this way were<br />

never expected by the therapists, and the clinical deficiencies, the therapists decided to<br />

drastically reduce the amount of ethanol injected per session. Regarding the proven blood<br />

alcohol concentration and the deficiencies chronic liver patients should be monitored in relation<br />

to possible risks of anaesthesia. Such a monitoring can be very reliable through measuring<br />

breath alcohol concentration during therapy as well as afterwards on the ward [35].<br />

The a<strong>im</strong> of a gentle anesthetic procedure in patients with hepatic insufficiency is the selection<br />

of an anesthetic procedure which does not interfere negatively with liver function<br />

and oxygen supply of the organ. The synthetic opiate fentanil influences neither liver circulation<br />

nor pharmacokinetics [36]. With propofol only a slight slowdown of metabolism<br />

can be observed. The half-t<strong>im</strong>e of propofol is between 34 and 64 minutes, the effectiveness<br />

4-6 minutes. Anesthesia was started with a max<strong>im</strong>um of 2.0 mg/kg body weight and maintained<br />

with 6mg/kg body weight. Fentanil has a half-t<strong>im</strong>e of 2-4 hours and an effectiveness<br />

of 10 minutes. Respiratory depression continues for about 60-90 minutes. Fentanil was<br />

used with a min<strong>im</strong>um dose of about 0.005 mg/kg body weight. For opt<strong>im</strong>al care of the<br />

patient only concentrations at the lowest possible level of normally used amounts were<br />

administered. As a result after PEI no patient <strong>und</strong>er the influence of short-acting narcotics<br />

suffered an unnecessary extension of anaesthesia. Without having made blood level measurements<br />

of anaesthetics it turned out that patients at the t<strong>im</strong>e of medical examination at<br />

least 2 hours after PEI suffered no effects of anesthesia anymore and therefore any recorded<br />

deficiencies can be seen as being solely the result of ethanol injection.<br />

According to NORBERG et al. [37] the rate-l<strong>im</strong>iting step in oxidation is conversion of<br />

ethanol into acetaldehyd by cytosolic alcohol dehydrogenase (ADH), which has a low<br />

Michaelis-Menten constant (Km) of 0.05–0.1 g/l. When a moderate dose is ingested,<br />

zero-order elemination operates for a large part of the blood-concentration t<strong>im</strong>e course.<br />

As can be seen in figure 1 the BECs do probably in some cases not follow a kinetic of<br />

zero or any other order if the tumour release ethanol into hepatic veins. In other cases a<br />

kinetic of zero order, after the max<strong>im</strong>um BEC an <strong>im</strong>mediate and straight decline was to<br />

be shown (Fig. 1). Futhermore in a few cases a steady state or rather a biphasic t<strong>im</strong>e<br />

course for elemination were seen. In our opinion it can be suggested, that at the t<strong>im</strong>e of<br />

steady state or biphasic t<strong>im</strong>e course after max<strong>im</strong>um of blood ethanol concentration there<br />

is an equilibrium after the end of injection and max<strong>im</strong>um of BEC between the t<strong>im</strong>e-in-<br />

BLUTALKOHOL VOL. 42/<strong>2005</strong>

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