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K Peter

Publications and source records attributed to K Peter.

At least 181 records · Page 10Linked to original sources
PubMed1993

Effects of benzodiazepines on mid-latency auditory evoked potentials.

Midlatency auditory evoked potentials (MLAEP) reflect primary cortical processing of auditory stimuli. The effects of benzodiazepines on MLAEP have not yet been studied. We examined the effects of intravenous induction of general anaesthesia using the benzodiazepines midazolam, diazepam and flunitrazepam on MLAEP in 30 patients scheduled for minor gynaecological procedures. Anaesthesia was induced with midazolam (0.2-0.3 mg.kg-1, Group I, n = 10), diazepam (0.3-0.4 mg.kg-1, Group II, n = 10) or flunitrazepam (0.03-0.04 mg.kg-1, Group III, n = 10). Auditory-evoked potentials were recorded before and five to ten minutes after induction of general anaesthesia. Latencies of the peak V, Na, Pa, Nb and Pl (ms) and amplitudes Na/Pa, Pa/Nb and Nb/P1 (microV) were measured. In the awake state, MLAEP had high peak to peak amplitudes and a periodic waveform. After induction of anaesthesia there was no or only a small increase in latencies of the peaks Na, Pa, Nb and P1, which was significant only for P1 in the midazolam group. Amplitudes Na/Pa, Pa/Nb and Nb/P1 decreased only slightly and which reached statistical significance only for Na/Pa in the flunitrazepam group. The MLAEPs do not change markedly in amplitude or latency during induction of general anaesthesia with benzodiazepines. Primary cortical processing of auditory stimuli seems to be preserved under benzodiazepines. This may be seen in connection with cases of intraoperative awareness and especially the perception of auditory stimuli during anaesthetic regimens where benzodiazepines are used to suppress consciousness.

Acoustic Stimulation↗
PubMed1993

Determination of plasma volume with indocyanine green in man.

We investigated the feasibility of using indocyanine green (ICG) for plasma volume (PV) determination in man. Duplicate PV measurements were carried out in 23 healthy subjects to test repeatability. ICG (0.25 mg/kg) was injected intravenously into one arm and venous blood was withdrawn from the opposite arm. Optical density of plasma samples from minute 3 to 9 was measured in a densitometer. ICG concentration at injection time was determined by monoexponential extrapolation. The mean (SD) difference (MD) was -23 ml (183) or -0.6% (5.7%). Linear regression revealed PV2 = 0.92.PV1 + 226 (r = 0.92). The PV values corresponded well with data from other studies. In 26 surgical patients PV was determined using two methods: 1) the same as in healthy subjects and 2) using a modification of this method in whole blood (PVB). For PVB measurement blood was drawn through a cuvette-densitometer from an arterial line. Calculations were the same as in PV determination except for the use of hematocrit to achieve plasma concentrations of ICG from whole blood. In patients MD were -53 ml (144) or -1.3% (4.3) for PV and -19 ml (161) or -0.3% (5.1) for PVB. Comparing PVB and PV revealed MD = -113 ml (149) or -3.3% (4.2). The whole blood method is easier to perform and reduces blood waste to almost zero. In conclusion, ICG is a suitable tracer for PV determination.

Adult↗
PubMed1993

[Mid-latency auditory evoked potentials during increasing doses of fentanyl].

OBJECTIVE: Intraoperative awareness, and especially the perception of auditory stimuli occur occasionally under general anaesthesia with high-dose opioids. Mid-latency auditory evoked potentials (MLAEP) reflect the primary cortical processing of auditory stimuli. Hence, we studied the effects of fentanyl on MLAEP. METHODS: Institutional approval and informed consent was obtained in 20 patients scheduled for cardiac surgery. Anaesthesia was induced with fentanyl (10 micrograms/kg every 7[ up to a total dosage of 50 micrograms/kg). Auditory evoked potentials were recorded before and 5[ after every fentanyl dose on vertex (positive) and mastoids on both sides (negative). Auditory clicks were presented binaurally at 70 dBnHL at a rate of 9.3 Hz. Using the electrodiagnostic system Pathfinder I (Nicolet), 1000 successive stimulus responses were averaged over a 100 ms post-stimulus interval and analysed off-line. Latencies of the peak V, Na, Pa, Nb P1 and amplitudes Na/Pa, Pa/Nb, Nb/P1 were measured. V belongs to the brainstem generated potentials, which demonstrates that auditory stimuli were correctly transduced. Na, Pa, Nb, P1 are generated in the primary auditory cortex of the temporal lobe and are the electrophysiological correlate of the primary cortical processing of the auditory stimuli. By means of a Fast-Fourier transformation power spectra of the AEP were calculated. RESULTS: In the awake state AEP peak latencies were in the normal range. Power spectra indicated high energy in the 30-40 Hz frequency range. During increasing dosages of fentanyl the brainstem response V was stable. P1 increased in latency and Nb/P1 decreased in amplitude after 10 micrograms/kg of fentanyl significantly. The primary cortical potentials Na, Pa, Nb changed only very slightly in latencies or amplitudes even under highest doses of fentanyl (50 micrograms/kg) and could be identified like in the awake patients. In the power spectra high energy persisted in the 30 Hz frequency range. CONCLUSION: MLAEP and especially the primary cortical potentials Na, Pa, Nb did not change markedly in amplitude or latency during high-dose fentanyl analgesia. There is no dose-dependent effect of fentanyl on MLAEP as it can be observed under volatile anaesthetics (isoflurane, enflurane). The primary cortical processing of auditory stimuli can be completely blocked by volatile anaesthetics, but is still preserved under highest doses of fentanyl. This may be seen in connection with cases of awareness and perception of auditory stimuli during high-dose fentanyl analgesia.

Aged↗
PubMed1993

Effects of increasing doses of alfentanil, fentanyl and morphine on mid-latency auditory evoked potentials.

We have studied dose-dependent effects of alfentanil, fentanyl and morphine on mid-latency auditory evoked potentials (MLAEP). Anaesthesia was induced with alfentanil 100 micrograms kg-1 every 5 min to a total dose of 500 micrograms kg-1 (group I, n = 10), fentanyl 10 micrograms kg-1 every 7 min to a total dose of 50 micrograms kg-1 (group II, n = 10) or morphine 1 mg kg-1 for induction and 0.5 mg kg-1 every 15 min to a total dose of 3 mg kg-1 (group III, n = 10). MLAEP were recorded before and 3-15 min after every opioid dose on vertex (positive) and mastoids on both sides (negative). Latencies of the peaks V, Na, Pa, Nb, P1 (ms) and amplitudes Na/Pa, Pa/Nb and Nb/P1 (microV) were measured. Fast-Fourier transformation was used to calculate power spectra of the AEP. In the awake state, MLAEP had high peak-to-peak amplitudes and a periodic waveform. Power spectra indicated high energy in the 30-40 Hz frequency range. During general anaesthesia with increasing doses of alfentanil, fentanyl and morphine, the brainstem response V was stable. There was a marked increase only in latency and decrease in amplitude of P1. In contrast, for the early cortical potentials Na and Pa, only small increases in latencies and decreases in amplitudes were observed. After the largest doses of alfentanil (500 micrograms kg-1), fentanyl (50 micrograms kg-1) and morphine (3 mg kg-1), Na, Pa and Nb showed a similar pattern as in awake patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Mid-latency auditory evoked potentials during ketamine anaesthesia in humans.

We studied mid-latency auditory evoked potentials (MLAEP) during induction of general anaesthesia with ketamine 2 mg kg-1. MLAEP were recorded before, during and after induction of general anaesthesia on the vertex (positive) and mastoid (negative) positions. Latencies of the peak V, Na, Pa, Nb, P1 and amplitudes Na/Pa, Pa/Nb and Nb/P1 were measured. Fast-Fourier transformation was used to calculate power spectra of the MLAEP. In the awake state, MLAEP had large peak-to-peak amplitudes and a periodic waveform. Peak latencies remained within the normal range. Power spectra indicated high energy in the 30-40 Hz frequency range. After induction of general anaesthesia with ketamine, there was no change in latency of peaks V, Na, Pa, Nb, P1 and no apparent reduction in amplitudes Na/Pa, Pa/Nb and Nb/P1. In the power spectra, frequencies in the range of 30-40 Hz retained high energy. Amplitudes and latencies of MLAEP did not change during induction of general anaesthesia with ketamine. Primary processing of auditory stimuli in the primary auditory cortex seemed to be preserved under ketamine. Suppression of sensory (auditory) information processing must take place at a higher cortical level in a dissociative manner.

Adult↗
PubMed1993

Anaesthesia for coronary artery bypass grafting: opioid-analgesia combined with either flunitrazepam, propofol or isoflurane.

This is a prospective, open, randomized study comparing three different anaesthetic regimens with respect to haemodynamic stability (cardiac index and pressure measurements), ischaemia (ECG), and loss of awareness (midlatency auditory evoked potentials in 58 patients undergoing coronary artery surgery. Anaesthesia was based on fentanyl 0.01 mg kg-1 bw for induction and 0.8-2.0 mg h-1 in combination with nitrous oxide for maintenance before cardiopulmonary bypass and 0.2-0.6 mg h-1 without nitrous oxide during and after cardiopulmonary bypass. Eighteen patients were anaesthetised with flunitrazepam 0.01 mg kg-1 bw for induction and received thereafter 1-2 mg h-1 for maintenance (group F). In 40 patients anaesthesia was induced with etomidate and maintained with either isoflurane 0.4-1.2 vol% (group I) or propofol 4-10 mg kg-1 bw h-1 (group P). Vasodilators and inotropes were used for haemodynamic control when needed. Haemodynamic variables and ECG were studied at five timepoints (awake; after induction before surgery; after sternotomy; before cardiopulmonary bypass; and 20 min after separation from bypass). During surgical stimulation, vasodilators were needed significantly more frequently in group F, than in groups I and P. Surgery and sternotomy caused an increase in SVI and APs/SV in all groups. Differences between the groups were only found for systemic pressures, which after sternotomy were lowest in group I and before cardiopulmonary bypass were highest in group F. After termination of bypass all groups showed an increase in HR and a decrease in SVI, SVR, and LVSWI compared to the awake state, while CI remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Heparin-protamine reactions in pigs: role of oxygen-derived free radicals.

We tested the hypothesis that pulmonary hypertension and thromboxane A2 release after heparin neutralization by protamine are mediated by oxygen free radicals. Forty-five pigs in five groups were studied during general anesthesia. Group I animals received 250 IU heparin followed by 100 mg protamine after 15 min. Group II and group III animals received dimethyl sulfoxide (DMSO) and dimethylthiourea (DMTU) 30 min before heparin infusion. Group IV animals were given superoxide dismutase (SOD) 5 min before protamine. Group V served for testing the pulmonary vascular reactivity in DMTU-treated animals to a thromboxane A2 analogue (U-46619). Generation of oxygen free radicals by polymorphonuclear granulocytes (PMNs) was measured in vitro by chemiluminescence. Severe pulmonary hypertension and thromboxane A2 release after protamine were not prevented by either DMSO or SOD. DMTU reduced pulmonary vasoconstriction to U-46619 and protamine but not to TxA2 release, indicating that DMTU had unspecific vascular effects in group III. Heparin-protamine released no oxygen free radicals from isolated PMNs. The results indicate that oxygen free radicals do not have a key role in mediating pulmonary vasoconstriction after protamine neutralization of heparin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Effects of isoflurane, fentanyl, or thiopental anesthesia on regional cerebral blood flow and brain surface PO2 in the presence of a focal lesion in rabbits.

These studies were conducted to determine the effect of anesthetic drugs on tissue perfusion and O2 supply in the brain with focal cerebral edema. Using an open cranium preparation, we studied the effects of isoflurane (I; 1 minimum alveolar anesthetic concentration), of fentanyl (F; 0.5-1 microgram.kg-1 x min-1), or of thiopental (T; 32.5 mg.kg-1 x h-1) on regional cerebral blood flow (rCBF) and regional brain tissue PO2 in albino rabbits (n = 6 per group) with a focal brain lesion (cold injury). The doses of anesthetics were sufficient to suppress nociception. rCBF (H2 clearance) and tissue PO2 (multiwire surface electrode) were studied adjacent to and distant from the lesion. Cerebral hyperemia developed immediately after trauma in all groups, although the flow increase did not attain statistical significance. rCBF was subsequently reduced by about 25% in the vicinity of the lesion. Distant from the trauma, a continuing hyperemia (+30%) was later observed in animals with isoflurane, whereas rCBF was decreased then by 10%-20% in animals with fentanyl, or was unchanged with thiopental. Brain tissue PO2 was increased with isoflurane in areas distant from the lesion, but decreased with fentanyl. However, with thiopental, the PO2 level had already been lowered before trauma with a subsequent tendency toward normalization. The heterogeneity of the tissue PO2 in fentanyl anesthesia, as well as the increased frequency of hypoxic PO2 values with thiopental, might have resulted from microcirculatory disturbances. Thus, although isoflurane seemed to facilitate hyperemia with an increased O2 supply to the brain, fentanyl tended to induce the opposite response. Although these properties suggest the potential to manipulate perfusion and O2 supply in cerebral ischemia or hyperemia after head injury, the effects of such measures on intracranial pressure, neurologic status, and outcome have yet to be proven.

Anesthetics↗
PubMed1993

A note on the identity of porcine liver carboxylesterase and prolyl-beta-naphthylamidase.

Prolyl-beta-naphthylamidase from porcine liver is compared with the two prevalent isoenzymes of pig liver carboxylesterase by isoelectrofocusing experiments and by inhibition studies with phenyl-methyl-sulfonyl fluoride. The results suggest that prolyl-beta-naphthylamidase is identical with the amide-cleaving isoenzyme of carboxylesterase, not with the usually predominant methyl butyrate-hydrolysing isoenzyme. It is questionable whether the recently published sequence of prolyl-beta-naphthylamidase does belong to this enzyme or to the predominant carboxylesterase without amidase activity. Surprisingly, the amide-cleaving carboxylesterase isoenzymes from rat liver have almost no activity with prolyl-beta-naphthylamide.

2-Naphthylamine↗
PubMed1993

[Pharmacodynamics and clinical adverse effects of mivacurium. The effect of oral premedication with H1/H2 antagonists].

Duration of neuromuscular block may be prolonged by H1/H2 antagonists. This study was designed to determine the influence of H1/H2 antagonist treatment on onset, duration and recovery after mivacurium chloride (MIV), a new nondepolarizing neuromuscular blocking agent with a relatively short duration of action, which is metabolized by human plasma cholinesterase (PChE). METHODS. After approval from the hospital ethical committee and written informed consent, 48 ASA I-II patients of either sex (ages 18-65 years, weight 45-100 kg) were included in this double blind study and randomly allocated to four groups of 12 each: group A, 0.105 mg/kg MIV (1.5 x ED95) and H1/H2 antagonist; group B, 0.105 mg/kg MIV and placebo; group C, 0.21 mg/kg MIV (3 x ED95) and H1/H2 antagonist; Group D 0.21 mg/kg MIV and placebo. Premedication consisted of 2 mg lormetazepam p.o., 300 mg ranitidine and 0.1 mg/kg dimetindene, or placebo p.o. Anaesthesia was induced with thiopentone (5-7 mg/kg) and maintained with N2O/O2 at a 65/35 ratio, enflurane (0.8-1.5%) and supplements of fentanyl. The ulnar nerve was stimulated with supramaximal 2 Hz train-of-four (TOF) every 10 s. Neuromuscular twitch response was recorded with EMG. Onset time (time from end of injection to maximal or total block), maximal block (%), T125 (time from end of injection to 25% recovery) were recorded after each dose, and recovery index (T1 from 25% to 75% recovery) and TOF70 (time from end of injection to TOF ratio of 70%), after the last dose. RESULTS. The four groups did not differ with respect to age, weight or height. There was no difference in the pharmacodynamics of mivacurium between the groups receiving H1/H2 antagonists and those receiving placebo. Following 1.5 x ED95 the onset was at 3.7 +/- 1.2 (H1/H2) and 3.8 +/- 0.9 min (placebo), respectively. Clinical duration (T125) was 13.1 +/- 3.4 and 12.8 +/- 3.4 min. 3 x ED95 led to a significant faster onset and longer duration (P < or = 0.05). Onset was at 1.9 +/- 0.7 (H1/H2) and 2.1 +/- 0.5 min (placebo), respectively, and clinical duration 19.1 +/- 6.1 and 19.3 +/- 3.8 min. Duration of repetitive doses (10.1 +/- 5.3 min), recovery index (6.8 +/- 2.9 min) and interval from last dose to spontaneous recovery (22.4 +/- 7.0 min) did not differ between groups. Three patients in group D (placebo and 0.21 mg/kg MIV) had haemodynamic changes of over 20% from baseline. Flush and erythema were significantly less pronounced after H1/H2 premedication than after placebo (4 vs 12 pts). CONCLUSIONS. Our results suggest that time of onset and clinical duration of effects of MIV are not altered by dimetindene and ranitidine. The duration depends more heavily on the dose of MIV. The recovery of neuromuscular function, once it has begun, is prolonged neither by MIV nor by H1/H2 antagonists. As MIV is mainly broken down by PChE, it is evident that its duration of action is more prolonged by atypical PChE activity than by interaction with other drugs. Oral H1/H2 premedication may diminish haemodynamic side-effects and clinical signs of histamine release.

Administration, Oral↗
PubMed1993

[Monitoring intraoperative processing of acoustic stimuli with auditory evoked potentials].

130 Patients undergoing elective intra-abdominal, gynaecological, urological or cardiac surgery were studied after institutional approval and informed consent. In all patients auditory-evoked potentials (AEP) were recorded in the awake state and during general anaesthesia. Latencies of the peaks V, Na, Pa, Nb and P1 were measured. V belongs to the brainstem-generated potentials, which demonstrates that auditory stimuli were correctly transduced. Na, Pa, Nb, P1 are generated in the primary auditory cortex of the temporal lobe. During anaesthesia with isoflurane, enflurane, thiopentone, etomidate and propofol the peak V remains unchanged, whereas the mid-latency auditory-evoked potentials (MLAEP) show marked increases in latencies and decreases in amplitudes or are even completely suppressed. This indicates a successful stimulus transmission up to the level of the brainstem and midbrain. However, stimulus processing in the primary auditory cortex is blocked. Under increasing end-expiratory concentrations of isoflurane MLAEP show a dose-dependent increase of latencies and decrease of amplitudes. Under surgical anaesthesia with 1.2 vol%, MLAEP are nearly completely suppressed. A different picture can be seen when MLAEP were recorded during anaesthesia with the receptor-specific anaesthetics midazolam, flunitrazepam, diazepam, fentanyl and ketamine. During anaesthesia with receptor-specific anaesthetics, the brainstem peak V as well as the mid-latency components remain nearly unchanged compared with AEP from awake patients. This indicates that auditory stimuli reach the primary auditory cortex and are processed at a primary cortical level. With increasing doses of fentanyl one can observe only a significant decrease of amplitudes for the late component P1.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1993

[Acoustic evoked potentials of medium latency. Anesthesia induction with S-(+)-ketamine versus ketamine racemate].

Mid-latency auditory evoked potentials (MLAEP) reflect the primary cortical processing of auditory stimuli. They are widely suppressed during general anaesthesia with volatile anaesthetics. Under ketamine, in contrast, they seem to be preserved, which has been interpreted as indicating insufficient suppression of consciousness during ketamine anaesthesia. Ketamine exists in two optical isomeres, S-(+)-ketamine und R-(-)-ketamine, which differ in their pharmacodynamic properties: S-(+)-ketamine has higher anaesthetic-hypnotic and analgesic potency than R-(-)-ketamine. It thus appears obvious to question whether S-(+)-ketamine has a different effect on the primary cortical processing of sensory, i.e., auditory stimuli. We therefore studied the effects of S-(+)-ketamine versus ketamine-racemate on MLAEP. PATIENTS AND METHODS. Institutional approval and informed consent were obtained for 40 patients scheduled for minor gynaecological procedures. The patients were assigned randomly to one of the two experimental groups. All experimental evaluations were conducted under double-blind conditions. Anaesthesia was induced with S-(+)-ketamine 1 mg/kg (group I, n = 20) or ketamine-racemat 2 mg/kg (group II, n = 20). MLAEP were recorded before, during, and after induction of general anaesthesia from the vertex (positive) and mastoids on both sides (negative). Auditory clicks were presented binaurally at 70 dBnHL at a rate of 9.3 Hz. Using the electrodiagnostic system Pathfinder I (Nicolet), 1000 successive stimulus responses were averaged over a 100-ms poststimulus interval and analysed off-line. Latencies of the peak V, Na, Pa, Nb, P1, N1, and amplitudes Na/Pa, Pa/Nb, and Nb/P1 were measured. V belongs to the brainstem-generated potentials, which demonstrates that auditory stimuli were correctly transduced. Na, Pa, Nb, P1, and N1 are generated in the primary auditory cortex of the temporal lobe and are the electrophysiological correlate of the primary cortical processing of the auditory stimuli. A Fast-Fourier transformation calculated powerspectra of the AEP. RESULTS. In the awake state, AEP peak latencies were in the normal range. MLAEP had high amplitudes and a periodic wave form. Powerspectra indicated high energy in the 30-40-Hz frequency range. After induction of general anaesthesia with (S+)-ketamine or ketamine-racemat, there was no increase in the latencies of the peaks V, Na, Pa, Nb, P1, and N1. No decrease in amplitudes Na/Pa, Pa/Nb, or Nb/P1 could be observed. In the power spectra, frequencies in the range of 30-40 Hz retained high energy. CONCLUSIONS. MLAEP do not change in amplitude or latency during induction of general anesthesia with S-(+)-ketamine or ketamine-racemat. Primary cortical processing of auditory stimuli seems to preserved under S-(+)-ketamine and ketamine-racemat. This must be viewed in connection with dreams and hallucinations and could be interpreted as inadequate suppression of auditory information processing during general anaesthesia with S-(+)-ketamine and ketamine-racemat.

Adult↗
PubMed1993

Preoperative systemic etoposide/ifosfamide/doxorubicin chemotherapy combined with regional hyperthermia in high-risk sarcoma: a pilot study.

From November 1990 to September 1991, 23 adults with high-risk, nonmetastatic sarcomas (20 soft-tissue sarcomas and 3 chondrosarcomas) were entered in a pilot protocol (RHT-91) involving regional hyperthermia combined with systemic chemotherapy followed by surgery. Of these patients, 12 had undergone previous surgery and/or radiation, 5 had received previous multidrug chemotherapy, and 6 were previously untreated. A tumor size of > 8 cm and/or an extracompartmental tumor location (11 patients) or local recurrence (12 patients) were defined as high-risk factors in addition to tumor grading (21 patients had grade 2 or 3 sarcomas). Regional hyperthermia was produced by an electromagnetic deep-regional-heating device. For systemic chemotherapy, all patients received etoposide/ifosfamide/doxorubicin (EIA) and mesna, with regional hyperthermia being given only on days 1 and 4 in repeated EIA/regional hyperthermia cycles every 3 weeks. Tumor temperatures (range, 40 degrees-44 degrees C) were measured by invasive thermometry in all patients during each regional hyperthermia treatment. A total of 181 regional hyperthermia treatments were applied within the pelvic region (11 patients) or extremities (12 patients) bearing relatively large tumors (mean volume, 848 cm3). By the cutoff date for this analysis (October 15, 1991), 13 patients had undergone surgery after receiving 2-6 (mean, 3.8) cycles of EIA chemotherapy combined with regional hyperthermia; all tumors except one were resected without disfiguration. In 22 evaluable patients (minimum, 2 EIA plus regional hyperthermia cycles), the clinical response rate was 27%, with 6 patients showing partial responses (PRs). In addition, a pathologic response to preoperative thermochemotherapy was evaluable in 13 patients, with 4 responders (31%) having > 50% histologic necrosis. In all, 3 of the responders (1 PR and 2 patients with > 50% histologic necrosis) relapsed within 3 months of surgical resection. The other 7 responding patients (5 PRs and 2 patients with > 50% histologic necrosis) showed stable disease with local tumor control. The study (RHT-91) is continuing as a multicenter phase II trial (opened on November 19, 1991) in patients with high-risk soft-tissue sarcomas to test the potential of preoperative thermochemotherapy in regard to local control and survival.

Adolescent↗
PubMed1993

[Enteral nutrition of critically ill patients].

OBJECTIVE: The purpose of this article is to review the facilities of early enteral nutrition in critically ill patients. DATA SOURCES: Review articles as well as original papers are the main sources for this contribution. SELECTION CRITERIA: Pathophysiologic conditions of intestinal substrate assimilation during hypermetabolism are described. The resulting consequences for enteral alimentation are discussed. Practical aspects such as classification and different indications of formulas, performance of enteral nutrition as well as management of tube feeding complications are further subjects of this review. RESULTS: Paying attention to tolerance, enteral nutrition can be started early in the postoperative or posttraumatic course. Jejunal substrate application, however, reveals to be a major issue for successful management. CONCLUSION: Clinical performance as well as efficiency of enteral nutrition seem to be essentially dependent on the intestinal blood flow. New methods for estimating intestinal blood flow, such as tonometry, will have to be evaluated especially in critically ill patients to improve the indications for enteral nutrition.

Contraindications↗
PubMed1993

[The non-energetic importance of enteral nutrition of critically ill patients].

OBJECTIVE: The aim of this review is to describe recently discussed nonenergetic effects of enteral nutrition. DATA SOURCES: Results of current animal and clinical studies are summarized and the place of enteral nutritional regimen in critically ill patients is discussed. SELECTION CRITERIA: The possible protective effect of early enteral nutrition in critically ill patients concerning stress ulcus prophylaxis, infections, and the pathogenesis of multiple organ failure is gaining particular attention in this review. RESULTS: The reduction of intestinal bacterial translocation and the decline of catabolism during enteral substrate application seems to be proven by animal experiments. CONCLUSION: The relevance of early enteral nutrition in critically ill patients, however, needs to be investigated in further clinical studies.

Animals↗