S208
P359
INTENSIVE CARE MANAGEMENT OF A DIFFICULT CASE OF STATUS EPILEPTICUS
M.Gemma, M.Bricchi, S.Franceschetti, F.Fiaechino.
We describe the case of a 10-ys-old boy with very prolonged status
epilepticus (S.E.), which was unresponsive to pharmacological therapy and
exhibited EEC and clinical polymorphism.
The patient was been affected for 7 years by post-measles generalized
epilepsla without impairment of mental status. In 1599 he was admitted in
the Intensive Care (ICU) of our Hospital for subcontinous tonic seizures.
In a few hours S.E. prompted i.e. infusion of Sodium Thiopentone, which
was prolonged for 11 days (total dose 34 g). After 12 barbiturate-free
days Sodium Thiopentone was newly required for 5 days (total dose 25 g).
The patient required ICU for a 3 months period, during the first 60 days
of which he was ventilated with IPPV. Subcontinous EEG monitoring was
applied every day. A suppression-burst EEG pattern was often needed to
control seizures with Thiopentone infusion. Many enteral and parenteral
antiepileptic drugs, variably associated, were used in order to control
seizures during these 3 months; ACTH, Sodium Valproate, Clonazepam,
Carbamazepine, Phenitoine, Diazepam, Lidocaine, Nimodipine, Magnesium
Sulfate, Chlormethiazole. These drugs were given untill either a know,,.
plasmatic therapeutic range or the recommended daily dose was achieved,
but none proved efficacious. S.E. stopped after 45 days, but seizures
remained subcontinous for another.15 days.
At admission CT scan showed light cortical atrophia. Twenty-five days
later MR imaging reveiled transverse and sigmoid sinus thrombosis. After
45 days from admission a CT scan and a MRI showed wide parieto-occipital,
frontal and basilar lesions, which were interpreted as ischemic damage.
Inc month later these were consistently reduced (CT scan) and were
virtually no more present at a further MRI control 6 months later. Hence
such lesions are best interpreted as neuronal damage due to seizure
tct ivity.
In 1991 three other hospitalizations were required because of S.E. Now,
as during the periods between hospitalizations, the patient returned to a
relatively normal life standard without rilevant intellectual impairment.
ibis case strongly indicate the need of prolonged supportive therapy for
S.E.. Moreover caution should be applied in interpreting
ieuroradiological imaging in patients affected by S.E..
Div. Neuroanestesia e Rianimazione -.Ist. Neurologico "C.Besta"
V i-e delarie ii - 20133 tff3ane halte - - - - - - Yis eelvria I1 2093 ftano Tta-lt
Metabolism
P361
24h VARIATION IN METABOLIC RATE IN ICU
PATIENTS
L Lind.
In the healthy subject a decreased metabolic rate is
seen during the night when compared to daytime.
The variations in metabolic rate over 24h-periods were
determined by indirect calorimetry (Deltatrac,Datex) in
mechanically ventilated ICU patients.Energy expenditure
(EE),Oxygen consumption (V02) and CO2-production(VCO2)
were continously recorded during 105 24h-periods.
The mean 24h variation in V02 was 94ml/min,129ml/min
for VCO2 and 832 kcal for EE.
A normal 24h variation in V02,VCO2 and EE was only seen
in 40% of the patients but also in those the peak V02,
VCO2 and EE were randomely distributed during daytime.
V02,VCO2 and EE co-varied (r>0.70) with temparature. in
20%,with blood pressure in 30% and with heart rate in
40% of the patients.
In conclution,less than half of the patients showed a
normal 24h variation in metabolic rate suggesting a
disturbed metabolism in the critically ill patient
Department of Anesthesiology,Gavle Hospital,S-801 87,
SWEDEN
P360
INTENSIVE CARE MANAGEMENT. IN A NEUROSURGICAL PATIENT WITH
VON WILLEBRAND DISEASE
M. Bricchi, M. Gemma, C. Arian, P. Fiacchino.
Perioperative parenteral desmopressin has been recently accepted as
standard therapy of the bleeding diathesis in patients with von,
Willebrand disease (VWD) undergoing surgery. We suggest that a.
controindication to this choice could be neurosurgery. Cutaneous,
splancnic and coronary vasoconstriction, hyponatremia and alterations of
central neural circulatory control are side effects of desmopressin,
which are prominent and notoriously dangerous in neurosurgical patients,
particularly at the dosage requiered in this context (0.3 ug/Kg or even
more).
A 40-yr-old woman suffering for glossopharyngeal neuralgia was scheduled
for microsurgical vascular decompression of the nerve in the
supracerebellar space of the cerebellopontine angle. The patient, born in
an area with A high prevalence of vWD, was known to be affected by vWD.
Such a disease was diagnosed eight years before at the occurrence of a
serious postoperative hematoma 15 days after mastectomy and was
responsible of a number of late postoperative hemorrhagic events during
patient's life. Although desmopressin proved efficacious in this patient
in other settings, we chose a perioperative therapy with i.v. infusion of
cryoprecipitate, in order to avoid the above-mentioned side effects. At
the admission to our hospital bleeding time, prothrombin time and partial
thromboplastin time were normal; Factor VIII activity (FVIII Act) was
69%, Ristocetin-cofactor activity (vWFRCo) was 35%. Twelve hours
preoperatively 1500 I.C. of cryoprecipitate were administered i.v..
During the first six postoperative days the patient was treated in the
Intensive Care Unit with 900 I.U. l.v. every day, in order to keep vWFRCo
at 75% and FVIII Act at 100%. Tranexanie, acid was administered also (3
g/day i.v for the first 6 days, 1.5 g/day during the second postoperative
seek).
No hemorrhagic complication, either systemic or related to s -.irgery,
ensued. A CT scan performed 5 days after surgery was entirely negative.
We suggest cryoprecipitate as an efficacious perioperative therapy for
riD, which seems safer than the more widely accepted desmopressin therapy
in neurosurgical patients.
Div. Neuroanestesia e Rianimazione - Ist. Neurologico "C.Besta"
P362
EFFECT OF INCREASED COPPER & ZINC INTAKES
ON TRACE ELEMENT STATUS, LEUCOCYTES, SKIN
GRAFTING AND RECOVERY IN MAJOR BURNS.
MM. Berger. C. Cavadini' S. Guinchard" S. Krupp H. Dirren"
To determine if greatly increased trace element (TE) intakes can
influence recovery after major burns, 10 patients aged 34 6
years (meaniSO),, and burnt 40 7 % of total body surface, were
studied from the first postinjury day (D1) until 025.
METHODS Group 1 (n=5) received standard TE intakes (G 1: 5 mg
Zn, 0.7 mg Cu /24H), and Group 2 (n=5) increased intakes (G2:
30 mg Zn, 3.3 mg Cu /24H) from Dito D7 by intravenous
infusion. Energy and protein intakes were similar. Samples: serum
and urine from D1-7, and D10, 015, D20, D25; cutaneous
exudate D1-7. Cu & Zn were analysed by FAAS. Recovery was
assessed by infectious complications, leucocytosis (neutrophils
N, lymphocytes a LY), skin grafting requirements and hospital stay.
RESULTS Serum: mean TE levels were below normal in both
groups, but reverted earlier to normal in G2. Urine: after 03, Cu &
Zn excretions were increased in G2. Exudate: total mean
cutaneous losses in 7 days were Cu 24 mg and Zn 115 mg
(G1>G2: not significant). Leucocytes: after 02, total leucocyte
count increased significantly more in G2, was maximal between
D4 and D15, the N increase being larger than the LY increase
IN count 1.3to1.9 times larger in G2). Recovery: G1 required more
grafting than G2 (better adhesion in G2). Hospital stay was
shorter in G2 (57 in G 1 versus 45 days in G2): hospital stay per
%burnt area was 1.6 days in G 1 versus 1.1 day in G2 (p <0.04).
COticWsION The larger TE intakes in G2 were partly retained,
resulting in significantly higher serum TE levels, associated with
better skin graft adhesion and shortened hospital stay in G2.
These results may indicate that major burns are a state of greatly
increased TE requirements due to the large exudative losses.
Anestheslologle - Centre des Br01es, & Nestle Research Centre",
Centre Hospitalier Universitaire Vaudois, CH - 1011 Lausanne, Switzerland.
 S209

P363
DUODENOJFJUNAL MOTILITY DURING CONTINUOUS ENTERAL
FEEDING: MANOMETRIC STUDY IN CRITICALLY ILL PATIENTS.
A. Dive, M. Monlait, Ph. Jonart, J. Jamart, P. Mahieu.
Fasting intestinal motility is characterized by a succession of motor complexes
migrating from the stomach down to the terminal ileum. These Migrating Motor
Complexes (MMC) are composed of 3 phases; a period of highly propulsive
contractile activity (Phase 3 or "activity front" (A.F)), proceeded by a period of
irregular contractions (Phase 2) and followed by a period of quiescence (Phase 1).
After a meal, this fasting activity is normally interrupted and replaced by irregular.
contractions ("feeding pattern') which facilitate nutrient absorption. As intolerance
to enteral feeding frequently occurs in critically iN (CI) patients, we interested on
the pattern of motility before and during continuous feeding in 7 mechanically
ventilated C.I. patients admitted for neurological or respiratory failure.
Mgfhsd : Duodenal and jejunal contractions were simultaneously recorded during 2
successive periods of fasting (4 hours) and feeding (4 hours) with a liquid diet
(Nuttisrt A, 1kcalml) administered via a naso-gastric tube (10oml/hour).
Manometry was performed by means of a mtiltilumen tube (perfused catheter
technique). MMC were identified on each tracing (multichannel paper chart
recorder) by, detection of their A.F. (bursts of high frequency (> 9/min) regular
contractions, propagating aborally). Cycle period of the MMC was defined as the
time interval between 2 successive A.F.
P364
VARIATIONS OF PLASNI ANINOICIDS ALINING AND GLITANINB IN SEPTIC PATIENTS SUBJBCTBD
TO PANNNTBRAL NUTRITION (PN) NITO A NIGH PN0P01TION OF gN/NCBBD CHAIN ANINOACIDS
(BCAA).
JisAnes Jilenez J,Ortia Leyba C,Barros Perez N,Garnacho Nostero J,Porras Lopes
F,Goasales Neoemdet F.
The aaaust of glutaaise in the free amino acid pool can be increased directly by
the infusion of glutasine or indirectly by the infusion of BCAI.The objective of
this research was the study of differences ja the plasma Nino acids ^lanine(ALA)
and Glutaaise(GLD) of septic patients subjected to differences types of PN.
NATENIAL IN NBTBODS:
A prospetive study ras performed over 40 patients all of then with sepsis of
abdominal origin divided into to groups of 20 patients each,Group I sas give a
solution with 22,5% of BCIA,Croup II a solution with 45% of BCAA.Nittoges intake
was 1,4+0,4gr IA/kg/d with a constant calories /gr of nitrogen ratio of 150:1(60%
carbobydrates,40% long chain tryglicerides).The plasma aainogras was determined
through high resolution liquid chronatography.Al,data were seasured,before
starting PN( basal),? and 15 days after the start of P11.
RESULTS
11000 IG8010 II

basal 7 days p 15 days basal 7 days- p 15days p

- A normal fasting motor activity was present during the fasting period in 6 patients
(16 MMC identified; mean 2,66/patient). ALA 227174 276!88 .005 31396 .003 2701123 36901 .003 411!129 .001
- During continuous feeding, the usual feeding pattern of motility was not observed psol/1 _
in any of these 6 patients, as MMC were still present (17 MMC; 2,83/patient).
A patient failed to exhibit any MMC during both fasting and feeding. CLU 303!82 31899 as 402!145 .0001 318!119 425!151 .0001 483!130 .0001
- MMC were morphologically similar during fasting and feeding (peristaltic peal/l
propagation of A.F.; cycle period comparable : 62' 23' vs 51' 13' (no); duration
of A.F. similar: 352" 107" vs 349" 114" (n. ^) (Wilcoxon signed rank test)). CONCLUSIONS: I) The plasma concentrations of ALA and`CLU in septic patiens achieve
Conclusion: high levels when high BCAA solutions are used. 2) The BC/A could be used to
- Continuous enteral feeding does not interrupt fasting motor activity in syotheaite ALA and CLU in muscle and that this was the source of these two amino
mechanically ventilated C.I.patients; acids.
- Abnormal persistance of a highly propulsive contractile activity (A.F. of the
MMC) in the intestine during feeding could contribute to the high incidence of Intensive Care Usit,gospital Virgen del Nocio.Sevilla,Spain.
diarrhea observed in these patients.

Intensive Care Department; St-Luc Univ. Hospital - 1200 Brussels, BELGIUM.

P365 P366
METABOLISM AND PARENTERAL NUTRITION OF CRITICALLY ALCOHOLIC KETOACIDOSIS (AKA): CLINICAL AND BIOLOGICAL
ILL PATIENTS IN INTERNAL MEDICINE APPROACH. - F. Statkowsky. B. Guidet. T. Vassal. G. Offenstadt. P. Amstutz.
T.HiAller, A.Mill1er, H.Lange AKA is an unrecognized syndrom in Europe, whereas in USA it is involved in 20 %
Parenteral nutrition in intensive care medicine is of ketoacidosis (KA). We report 6 cases gathered in a 2 years period.
still a matter of discussion. Almost all Methods : all clinical and biological data were prospectively investigated in pa-
recommendations concerning amount and composition tients suspected of AKA . All results are expressed as mean DS.
of nutritients are based on studies in surgical Results: 3 women and 2 men (age 42.8 10.5 years) have been studied during 6
patients. Therefore the metabolic effects of episodes of AKA. A patient had 2 AKA. The SAPS was 9 4. At admission, the
different caloric regimens in internal medicine most commun symptoms were : vomiting (n = 5), asthenia (n = 4), anorexia (n = 4),
ICU-patients were tested during the initial phase abdominal pains (n = 3), weight loss (n = 3), thirst (n = 3) and lipothymia (n = 2).
of multi-organ failure. Intestinal disorders were present since Ito 4 days. Physical examination found: res -
20 patients were monitored for 1514 hrs. Each pirations 28 t 7/mn, pulse 110 8/mn, temperature 36,9 0,5C, extracellular de-
patient received a hypocaloric (14 kcal/kg body
weight(bw)/day), Ysoceloric (28 kcal/kg bw/d) and shydratation was always present and requiered colloids infusion to treat shock in 2
hypercaloric (56 kcal/kg bw/d) nutrition. In the cases, abdomen disconfort (n = 3) with hepatomegaly (n = 4). Glasgow coma score
was 14.t 1. Laboratory data were in blood: sodium 133 4 mmol/l, potassium.4,2
first caloric regimen amino acids (AA) and
carbohydrates (CH) were given in a fixed ratio of t I mmol/l. chloride 95 6 mmol/I, urea nitrogen 4 1 mmol/l, creatinine 264
1,6, in the second regimen fat was added either as 163 umol/l, protein 81 5 g/I (N = 55-75 g/I), hematocrit 40 3 %, ASAT 93 35
a NCT/LCT or as LCT solution. Metabolism was U1/l (N < 30 UI/I), ALAT 33 t 16 UI/I (N < 35 UVI),'tGT 742 t 589 UIQ (N < 49
monitored by indirect calorimetry, body temp., UI/I), LDH 381 68 UI/I (N < 330 UI/q, amylase 73 29 UI/I (N <60 UI/q; MCV
lactate-level and N-balance. was constantly higher than 100 3 (104 4 3), haemostasis and haemogram were
Hypercaloric nutrition with CH+Protein increased normal. Glycemia was 8 4,8 mmol/l, hypoglycaemia was present in I case and by-
energy expenditure (EE)(+2,2 kcal/kg bw/d),' perglycaemia in 3. Only I patient had a-positive alcoholemia (0,6 g/l). In urines,
temperature (+0,4eC), and lactate-level (+1,0 sodium level was always < 20 mmol/I.
mmol/1). Isocaloric nutrition with HCT/LCT and LCT pH Pa02 PaCO2 HCO3_ AG Lactates pyruvates OH-B K/G u
solutions increased EE (+0,7/ +0,1 kcal/kg bw/day),
temp.(+0,01/ +0,1*C) and lactate levels (+0,04/ Ia 7,14 133 12 4,6 37,4 4,4 - - 3/0
+0,1 mmol/l), whereas Cl + protein hypocaloric 2 7,30 126 17 6 35 1,3 81,9 0,76 3/1
nutrition decreased these parameters (-0,4 kcal/kg lb 7,03 137 10 2,5 36.5 1,4 - - 3/3
bw/d, -0,1'C, -0,2 mmol/1 reap.). The different. 4 7,30 91 27 14 26 - - - 3/0
caloric regimens did not alter protein catabolism, 5 7,30 78 30 15 25 2,3 30 7,65 4/0
apart from an increase in urea production under 6 7,21 85 13 5 27 3,06 8 4/0
hypercaloric nutrition. AG: union gap = Na" - (CI + HCO3 ). Lactates 0,3-1,6 mmol/I. Pyruvates 45-80 mol/t.
-

In summary, hypercaloric nutrition had an
detrimental effect on. all metabolic parameters (EE,
temp., lactate levels); In addition, no benificial
effect was seen for protein catabolism. Therefore,
a hypocaloric nutrition is recommended during the
initial phase of multi-organ failure in ICU
patients of internal medicine.
Department of Nephrology, Centre of Int. Med.
Philipps-University DW-3550 Marburg FRG
OH - B = - hydroxybutyrate 0,02 - 0,21 mmol/l.. K/G u = ketonuria and glycosuria in +.
Evolution has been favourable after rehydratation with pH correction in 102 hours
and plasmatic bicarbonates in 24 10 48 hours. Insuline infusion was never necessary.
Conclusion: AKA is often unrecognized and could be very misleading. Clinicians
must be aware that besides diabetic KA, AKA is another cause of KA with some
peculiar signs : no or slight increase of glycemia, past history of alcohol abuse, re-
cent digestive disorders and alcoholic abstinence, alcoholic hepatitis, increased
MCV . AKA is important to diagnose since insuline is not indicated.
ICU, Saint Antoine Hospital, 75571 Paris cedex 12 France
5210
P367
ALCOHOLIC KETOACIDOSIS (AKA) : PROSPECTIVE STUDY
OF ACTH, CORTISOL, INSULIN AND GLUCAGON SERIC
LEVELS. F. Staikowsky, B. Guidet, T. Vassal, G. Offenstadt, P. Amstutz
Physiopathology of AKA is still obscur. A relative deficiency in insulin and an in-
crease of glucagon have been suggested. However the dosage of these hormones has
never been studied together. The aim of this study was to clarify the hormonal pro-
me of AKA before treament.
Methodes: cortisolaemia, ACTH, insulineamia and glucagoneamia has been asse-
sed by radiolmmunoassays; glycemia was mesured at the same time. Blood sampling
was done at admission in ICU. The results are expressed as mean OS.
Results: 3 women and 2 men (age 42,8 10.5 years. SAPS 9 4. ) have been
included during 6 episodes of AKA. All patients cured after rehydratation with pH
correction in 10 2 hours and plasma bicarbonates in 24 to 48 hours. Insuline infu-
sion was never necessuv,
ACTH Cortisol Insulin Glucagon Glycemia
(9-52 DI!/l) 1(220-610 nmol/l (5-15 mUm (60-200'01!1l] <3,9-6.1\
Ia 10,3 - 5 654 6,1
2 0 1712 18 406 15,9
Ib 0 - 5 335 II
3 0 772 225 2,2
4 3,3 810 7 489 5,6
5 22 1257 8 274 7,2
Comments. our results confirm an increase of glucagoneamia (397 157 pg/l) and
a non-adapted insulin concentration (8,6 5,6 mUll). Other ketogenetic factors were
present in these patients: recent alcoholic weaning, starvation and hypovolemia. The
extracellular fluid volume contraction related to the conjugated action of vomiting
and decrease of oral intake could stimulate the sympathetic system and the "stress"
hormones secretion (cortisol, glucagon, GH). Cortisolaemia was always high (1138
442 nmol/l). These hormones activate the adipocyte lipase inducing an excessive
release of free fatly acids and glycerol into the circulation. The increase of gluca-
gon/insulin ratio in the portal circulation together with an excessive flow of free
fatty acids to liver are important factors for ketone bodies production in man. ACTH
was variable. but it was very low in 4 cases. Although. there was no cirrhosis, the
alteration of liver functions in these heavy drinkers, could alter the normal course of
different metabolic pathways and favour ketogenesis in the liver.
Conclusion: hormonal profile of AKA is unremarkable. Nevertheless it is pos-
sible that starvation. diminution of alcoholic intoxication and alcoholic hepatitis in-
duce a deviation of liver metabolism in favour of ketogenesis.
leu, Saint Antoine Hospital. 75571 Paris cedex 12 France
P369
OXYGEN CONSUMPTION IN CRfI1CAlLY IlL PATIENTS: 'IHE
INFLUENCE OF BARBl1URAlES DURING 1HE ACUTE PHASE
P.Guglia, HSteltzer, W.Petricek, ABalassa, P.Germann, AF.Hammerle
In critically ill patients alterations of oxygen consumption (V02) are held to be an
important determinant parameter of multi-organ failure and post-operativ
survival. In patients with severe head injury (SHI), increased energy turnover has
been found, a certain role in the management of V02 being played by barbiturate
therapy. Little has sofar been published with regard to continuous V02 measure-
ment, barbiturate therapy and the survival of intensive care patients' during the
acute phase, which is why we studied what influence barbiturate therapy might
have on oxygen consumption (V02), C02-production (VC02) and the survival of
the intensive care patient during the 1st 48 hours after admission to the ICU.
We studied 19 patients under controlled ventilation. The 1st group consisted of 10
patients with severe head injury (SHI), the 2nd group of9 patients, suffering from
acute respiratory insufficiency (ARI) post-operatively. Measurement of the
metabolic parameters and calculation of energy requirements was undertaken by
continuous, indirect calorimetries from the moment of admission until 48 h after.
After subdivision 'into 6 measurement phases, values were averaged arithmetically
and processed statistically by multivariate analysis for repetitive measurements.
All patients received a standardized sedation bypass of 3.3 mcglkglh Sufentanil
and 0.3 mglkglh Midazolam. Group 1 (SHI) received 5 mglkglh Thiopental
additionally. For both groups caloric supply amounted to 1100 kcal/die, When
compared with SHI-patients, ARI-patients demonstrated significantly higher
values for V02 and VC02. In each of the 6 measurement intervals surviving ARI-
patients demonstrated significantly higher .values for V02 and VC02 in
comparison to those, who died. With regard to V02 and VC02 SHI-patients did
not demonstrate any significant difference hetween survivors and deceased.
In our study we found a clearly reduced respiratory quotient in the SHI-group.
This may be explained by the wellknown cytoprotective effect of Thiopental.
Apart from this the group of surviving SHl-paticnts demonstrated clearly, that in
critically ill patients the level of the V02-valuc is not necessarily relevant to' a
higher survival rate. From the study reported on, it can not yet be derived,
whether an initial oxygen deficit during the phase of early shock cduld bc avoided
or respectively reduced by early b~rbitur:tle administration.
P368
WEIGHT CHANGES IN CRmCAllV ILL PATIENTS EVALUATED
BYTETRAPOLARIMPEDANCE
AN Roos, RGJ Westendorp, M FrOlich, AE Meinders.
Weight changes are Important Information In the dally clinical
management of criticany ill patients. These rapid weight changes are
merely due to changes In total body water. COnical impression, fluid
balances, either corrected for the Insensible loss or not, are unreliable.
Exact weight measurements are generally time consuming, laborious and
cumbersome. _
Tetrapolar Impedance measurements (BIA 101 RJL SyStems, Detroit,
USA) Is a simple, noninvasive, rapid method to measure body resistance
which correlates to total body water. This method Is valktated In healthy
volunteers.
We hypothesized that In criticaJIy m patients changes In resistance
correlates with weight changes and Is a simple method during admission
In the MICU.
452 paired measurements of weight (Sling-Scale 2001, illinOiS, USA) and
resistance were analyzed .In 31 patients. The mean admission to. the
MICU was 18.5 days (range 4 - 52), The average number of
simultaneous measurements was 14.5 (range 3 - 44). The mean weight
on admission was 73.1 16.3 kg. If the weight changed /UOre than 2.5
kg (26 patients) a significant correlation was found in 24 patients; weight
changes less than 2.5 kg (n=5) showed no correlation. The sensitivity to
detect weight changes more than 2.5 kg was 920/...
Day to day changes in resistance correlated to weight changes
(P<0.OO01, r2..0,34; n=415), The day to day fluid balance corrected for
insensible losses correlated to day to day weight changes in only 7
patients,
We conclude that dally impedance measurements can simply detect
weight changes in critically ill patients and Is more sensitive than a daily
fluid balance.
Department of General Intemal Medicine, Medical intensive Care Unit,
University Hospital, P,O. Box 9600, 2300 RC Leiden, The Netherlands.
P370
HYPERPROTEIC VS NORMOPROTEIC ENTERAL DIET IN STRESSED PA-
TIENTS:EFFECT IN NITROGEN BALANCE AND PROTEIN LEVELS:
Celaya S,Luque P,HomsC,Lopez J,Gual1art A,Pardo F,NavarroM,
Benefits of early tube feedinh in ICU patients are well d~
cumented,but ideal composition of formulas remain contro-
versia1.This study was performed to know the effect in
visceral protein levels and nitrogen(N) equilibrium from
hyperproteic vs normoproteic isoca10tic diets in acute str~
ssed patients.METHODS:27 ICU patients were randomly assig-
ned to receive 2 different comercial diets:A)-48% HC,30%fat
and 22% protein. B)-51%HC,34%fat and 15%protein with simi-
lar composition. Were excluded all patients:-dead before 10
days;-delay tube feeding(>3days);-Gastrointestinal into1e-
rance(>24h).19 patients were availaible for the study.No
difference in APACHE score,mortality,age and sex were found
between groups.Caloric needs were based in Harris-Benedict
X 1.3.We compared daily N ba1ance.blood glucose, caloric and
N intake.Albumin, transferrin,prealbumin,cho1esterol ,trig ly-
cerides,Cu,Zn ,Fe plasma levels were determinated the day
0,52 and102.The "u" Man-Whitney was the statistical method.
RESULTS:Diet. tolerance was similar in both groups. No diffe-
r ence in caloric requeriments(2128+353 vs 2245+457 Kc1) and
caloric intake were found.Cumu1ative N balance in group A
was -30.7+14.5 vs -53+22.4 in B(n.s.).Cumulative urea N ex
cretionwas 244 gr in A
vs 214 gr in B(p<O,05).No differen--
ce in plasma protein leve1s,cho1esterol,triglycerides were
found between groups.A1though net N balance was negative m
decrease in serum protein levels was found,Cu,Zn,Fe levels
were similar in both groups.CONCLUSIONS:l)-Hyperproteic
diet improve N equilibrium in acute stressed patients but
not statistical difference were found vs normoproteic.2)-
High N intake increase urinary N loss. 3)-P1asma protein
levels were no afected for protein enteral diet proportion.
4) We failed to demonstrate any benefits from 22% protein
diet in these patients.
UCI,University C.Hospita1;San Juan Bosco 15;50009 ZARAGOZA
SPAIN
 8211

P371 P372
ALT!lU nSfS O~ 1NnoiD rUNcTloN IN ICU FArr!NTS' SiCK !UTNr'OID
SYHDROn! IS!!!l ".,.OTHY'OIDI5" AND HyrIIY"HY'Olo,slf. RIYIIiTY BLOOD LACTATE LEVELS ARE BETTER PROGNOSTIC INDICATORS THAN
ANALYStS ANI) 'ft~1(1) rA'~"!T!19 POI CLI!UCAL SUSPICION 0' S!S.
JC SARnlfHTO, .. SOLII. JJ' OVAI,DIOLA. .1. TO""S. P. VELA9CO, TNF OR IL-6 LEVELS IN PATIENTS WITH SEVERE SEPSIS
!SOU lRaL, l TO~~iU ' G. Marecaux, M.R. Pinsky", E. Dupont, J.L. Vincent
---i;ji;;;n-- 3C;--"'; ;~r-70 --i- -;; j---ho.,ii ii'i i ie. -'-,at i;;;i;--.;; or
.It,rltlopt' . t" th,rOld I_net Ion te.t,. ru-tloe.lad, I.elt" ----------~--------------------------- --------------------
th,.fOld ""dt-a.,. (9fS). Se".flt".,r _~.J1r.,.to .. 01 th,fOI.
Several experimental and clinical studies have directly
hor.0"8"n " ..... eorr"la.e' 11 _Ith fl8.",tt, of t,he crltlca' related the magnitude of the blood cytokines response to
I1hes s . 13 1I1Il11~ hlls 'n'tllll, ... ftd 'n .Gr" e.er. CII
.rop .. T4 "~e'. ,_ 'I"n. V. rroa,ectl"ely ,tud ... 13. T4, 'T4 the severity of sepsis and the likelihood' of death. As
In' ISH , .,.1. ,,, t:l30 Jlillt'l"tlll edeltted t o . rol "t leu Ind blood lactate levels have been shown to represent reliable
tried to l"l!ttt" "h'eh .~"oet.tlo" 0' ,ar terl e te , ,.Iat
to eeeee c.,.tttorC", It. ",.rtor -ne It" th.t of APACM2-II. v. prognostic indicators in various forms of acute circula-

211' ratle"t. '34.4I.

aha tried! t.o .Idle"tll, . the rar' .et.rl Ctt A",. th.t eo.l rU
,Iplclon 11liOdt a,s 1ft crUlcal ",.,t.nt, adUtt to .tt ICU .

could I"alytleall, .U,n08ed 01 h.vl",

h.d.. 9!9. ."Ile 20 ,1':1.,,,tl '3.2

"nl, tltO ot thell .... ellnle,.1 ..... lclon.... I""';1I "a. ,r."loa.l,
I.
'''',poth,re''''. lift
tory failure, we compared the time course of arterial
blood levels Of tumor necrosis factor (TNF). interleukin-6
(IL-6) and lactate concentrations in 38 patients with sep-
. , M ~ ,hed ,,11 'Ive .houed el8.at I on a I horlo"l. eo.,' t Ittll tic shock as defined by arterial hypotension in the pre-
ulth h,,.ert).yr" I Uhr ", tt, u"der clinical .... 'tclon sence of fever, leukocytosis and either positive blood
"orullt, a.""8 r.tI.~'1 11th lOll thyroid hor.one le.ell Cltoth
S!9 ai",,11 h'rttth.,roid' "ltI."UI "Ill' .18ftllleAntl, hllher H'9 cultures or a suspected source of infection. These were
And 75 _ . . . . . toectl"'.I,. thl" 0" p.tllntl!' alt" "or.,1 ot' ele"ated
hor .."",5 113 .lld ..0 I r.arectlv.,I,t. T3 .... " .111 of pltle"tl
the lung (N-12). the abdomen (10). an infected catheter
"ho delllc4 , I""'.r thlln that 01 lur.,vor. 10.41 'f .. O. 12 "1/11 v, (3), others, (10) or unknown (3). A total of 23 patients
.. 12 ! 0.22 Itt: I . It.. ArACh!-1I ,ho ... d II." IIi cln t ' II I "ere"c.,
het ... tln pltte"tt IlIilt" Ind "lthout 9!9 157 . 14" 01 th_ were treated with adrenergic agents; '20 patients (53%)
1I.lple had an i\rACH!:-ll .all.l. ) IS. t . I , . ' . died. TNF, IL-6 (ELISA) and lactate (enzymatic technique)
Alhr _\II t '''.r .... analyill', the hotao". with the .olt
"redlctt..,.., .'VIIIII." "Ill' T3. A 1011ltle Aod.1 hl.ed on ,It. l.v.I,. levels were determined at the onset of shock, 24 hours and
the JI.,stooll-e ""rlt 01 the Ielt .e"trlcle a"d 09' ."o"ed. 48 hours later. At the onset of shock. TNF and IL-6 levels
800dn"s o( ."of
'1 t
outeo . . I,.tter tIIA" AtACH!-II.
~oC eurv.I ,.rlor.,nc. .Ith t"'"lct to
were greater in 'non-survivors than in survivors (mean
On th. oth.r ".ltd ".rlor d . . . lIltlvllr t. anlll,ll. oyer S.D. 204392 vs 129l95 pgjmL and 965619851 vs
97 dllf.re"t ell"lcll Ind "loIOllc.1 ""r. t.r Iecti"
.ost ,relll.ett",e ,.rl.t\8rl 01 9l9 aftd h,pothyrOldl, Jlf'"Othro.bln 69222248804 UjmL, respect~vely). Lactate levels were
.etlvlt}' ( 7 0 ' to.fd. r.tlo ..... 7'. "ltr 11 < 139 ol~1 fo.r.~ ,strikingly greater in the non-survivors (6.14.8 vs
2.9'. h,.,oeal-e, ( 21.~ .10' ...1 to.r 8' hyrorroteu . . . . ( 60
1/1 Io.r.~ 4.91. -SI < M Y8Arl' fo.r 2). 'lch,cArdla ) 100 3. 52. 0 mEqjL). For the, first 48 hours. lactate levels
h.p .. 'o ..... ~ 'n. tech,.,r".1 ) 25 e,.p.. fo.r.!!! 4.1). and remain?d,h~gher in the non-survivors (p<0.05); they were
hypoouolal.tt, ~290 .101/1 lo.r ..... 51.
Co"cI\ulo~'IIIS~g _,ltd hypothyroldllll hlllv. ,. hisher-thliln more d1scr1minant than TNF or IL-6 levels.
eXJ"",eteti Inct,J""c. In erltlcltl '&-ll,,"tll Aftd Itre a!"OcIAted "tth
hl~h lortlto.lt,12IT"" IO~,' "redlctlv. teltt "Ithre~r.et to OU'~O.II
In' conclusiot)., blood lactate levels represent a better
III T3. The .'IIII('C tlol'l 01 T3. LV". I"d os, ""rlorll b"it"' .. thllln p~ognosti:, indicator than cytokine levels in patients
~rAC"~- '" 3'" "'18h IUltr'elon Ind 01 91!S ca" lo. ,Uta".I,h.d
In III y"'lI"I r.tI4l"t. vlth. lonl' rrothro."ln tile. h,rona,r 18. w1th sept1c shock. The clinical val~e of cytokines deter-
~:~~;;~~:~u. hYJ"l'Iorroteln . . . . . hy,ool.ohllty. tachyCArdia and minations was limited.
bl':rAn"P:NT 0' IMT~gIV! C""I! "!OleIN!. MCTir. IlADALOHA.Sr,UN
Dr:rARTHl':HT 01' IMTl!pf9IV! CARl! Hl':DICINI.MOSF.JOAN23.TAIIACONA.9'AIN Dept of Intensive Care, Erasme University Hospital, Route
de Lennik 808, 1070 Brussels, Belgium .
Dept of Anesthesiology, University of Pittsburgh, USA.

P373 P374
ENTERAL NUTRITION WITH SOY-POLYSACCHARIDE FIBER
(SPF) FEEDS IN ICU PATIENTS.IS IT PREFERABLE ? THE MAGNESIUM DISORDERS IN ICU PATIENTS
P.Botsis, M Eforakopoulou,G.Stamatiou, H.loannidou S. Tragaras, Ch.auianou, H,Ioannidou

In a randomized study the effect of tube-feeding with SPF The purpose of the study was to assess:1 )The frequency of
containing feeds vs without SPF on nutritional status and the magnesium disorders in ICUpatients.2)The causative
incidence of diarrhea,was compared in 20 ICU patientsIhey factors.3)Their clinical importance.
met the following criteria before enterinft the study. 1) Se- A prospective study was done on 150 ICU patients who had a.r1
rum albumin)3gm!dl 2)APACHE II score{10 3)no abdominal o~ average daily intake of 1. 5mFq!L Mg++ ,and no specific Mg++
peration.Patients were randomly assigned to receive eithel correction. Serum electrolytes (K,Na) ,were assessed daily.
SPF-containing formula or SPF-free formula for ten conti- Magnesium,phosphorous,calcium,and serum albumin were mea-
nu ous days.Energy requirements were estimated with Harris sured twice a week.We tried to correlate the magnesium dis-
Benedict equations.Daily measurements of lymphocytes court orders to' clinical signs.The clinical examination invol-
and serum glucose were done,whereas transferrin,serum al- ved' tetany tests (neuromuscular irritability,nystagmus,
bumin,triglyceride,cholesterol,and urinary urea nitrogen Chvost.ec I s and Trousseau's signs) as well as cardiovascular
were determined twice during the study. Stool frequency disordElrs.Results were statistically analyzed with x' test
and weight were also examined daily. Statistical analysis and Yates correction. Hypomagnesemia (Mg less than 1.4mFq!L
was done using wilcoxon unpaired and student t.tests . was found in 38 of the 150 patients (27%).It was correla-
Results SPF-plus SPF-free Significanre ted with the type of nutrition(Hypomagnesemia 36% in TPN
vs 14% in enteral nutrition p 0.01.The duration of the ICU
lymphocyte count(nun')846+ 202 1131+ 425 p{0.01 stay (39% for more than 15 days stay vs 17% fot less p(OD1.
albumin (gm!cU) 3.24+ 0.44 2.89+-0:36 NS The daily amount of fluid therapy (38% for more than 41"&';)!
transferrin (mg!dl) 188+-26 388.4+80.5 p\0.OO1 vs 18% for, less ~0.05,and severe sepsis which was accom~
triglyceride(mg!dl) 154~8+ 38 201.9+75 NS nied with a 41% incidence of hypomagnesemia vs 11% without
cholesterole(mg!dl) 188.4+ 42 247.9+ 29 P(0.05 sepsis p(0.01.Amphotericin B administration was followed
glucose (mg!dl) 108.3+19 124.342)0 p{O,05 by severe hypomagnesemia.No statistical correlation was
urine N (g!24h) 7.5+r 9.05+4.3 NS found in diarrheas p)O,1 ,and administration of diuretics
stool freq.!24h ,1.7+ 0.4 ,1.5+ 0.15 NS p~.1 ,Tetany was found in 5 patients(3.3%) with serum Mg
stool weight(g/24h)250+-45280+-48 NS 0.8mFq!L,arid cardiac arrhythmias in 4 patients (2.6%) with
Conclusions:a)In ICU patients SPF containing feeds do not Mg 0.6mEq!L) .Hypermagnesemia was always due to iatrogenic
influence the bowel'function,wheras SPF free formula sig~ causes.
nificantly improves nutritional parameters.b)The statist~ Conclusions:Hypomagnesemia is often seen in ICU patients~
cally significant decrease of glucose andcholesterole 'rPN,long stay in ICU,large amoUnt of fluid administration
observed in the, patients while using SPF-feeds suggests and sepsis are related to hypomagnesemia.wheras diarrheas
the'use of them in diabetic and hyperlipidemic subjects. and diuretics are not. Complications rarely occUr and. only
in excessive hypomagnesemias, but are easily preventable
with regular assessment of the serum Mg levels and easil~'
Department of ICU,KAT GENERAL HOSPITAL,2 Nikis str 14561 treated.
Athens ,Greece
Department of Intensive Care Unit,KAT Hospital,Athens: GR
S212
P375
INANSES 2. NIT.RCDEN Ni EXCRETION INDUCED BY GLUCOSE AND INSULIN INFUSION IN
TRAUNATIIEC PATIEN'S
D. Radr.z:ani, 1. Savioli, D. Codazzi, 6. Ronzoni, S. lapichino.
Aim of this scud. as to investigate the variation of N excretion induced by the
infusion of gl,,ccse and insulin. Six patients (pts) tage (8-67, weight 40-87
admitted to our .CU for lajor accidental or surgical trauma were studied, all
pts were ventilated because of respiratory insufficiency and/or flail chest.
After a 24 bra periao of siniaal nutritional intake (less than 350 kcal as '
glucose), pte received parenteral glucose (1956 3 197 kcal/day( about 972 of
their resting energy expenditure as measured in the last hr of the basal period,
the infusion was maintained for the following 24 hrs. Urine were collected in a
bag, a sample was taken every 4 hrs starting at 21th hr of the basal period and
ending at 24th hr after the end of the glucose infusion, for a tdtal of 13
samples. Samples were frozen at -70 degrees and then analyzed for total N (N
Analyzer-Carlo Erbat and urea content, both N and urea elimination during the
four hrs period were computed from the concentration time the urine volume.
Blood urea was measured every 24 hrs and did not change. During the whole study
period pts did not receive amino acids. Pts resulted to be severely catabolic as
assessed by the N excretion during the basal period. N excretion begin to
significantly decrease only from the 13th hr of glucose infusion, values
remained lower than basal ones for 12 hrs after the stop of glucose infusion,
reaching A minimum of 0.67 tiles the basal value, and than rose progressively
(see table). Urea excretion fairly followed N losses, being about 80X of tcta;
N.
i a
In conclusion glucose plus insulin infusion is able to reduce N losses Oct)
lag time of about 12 hrs, this action is reversible and takes other 12 hrs to
vanish. This delay could depend upon the N transit tute and an the time
necessary for c .lete activationr cf metabolic pathways.
BASIL ------------ SLUCCHE --------------I-------- STP GLUCOSE -----------
t ae _. ? 5 9 13 1 2:
7 1 5 9 13 " difference in distribution space of ions H+ and anions.
N 2.01 2. 1.62 1.76 1.50* 1.77 1.390 1.40# 1.354 1.48+ 1.64 1.63 1.64
as C.2C,33 0.25 0.23 2.24 3,32 0.24 0.25 5.23 0.23 0.28 6.25 0.32
3.17 3.1: 3.3; 2.75 2,463 2. 9 2.3502.23* 2.42 2.69 2.71 2.92 2,95
es 3.41 ,,
u
3.40 0,37 303 0.53 0.42 0.42 0.41 0.41 3.57 0.45 0.49
p . 2.05 t, p 3.01 f, p . 2.:, 01 d is basal..
N = !lit c_en ;;4h U = Urea gi4h
.:C E. 'lacla, IE'CS Csoeiale.1agg ore, !ilana, Italy
P377
GLUCOSE AND LIPID METABOLISM IN A MODEL OF
ACUTE TRAUMA: THE POSTSURGICAL STATE.
L.S. Brandi, D. Santoro, F. Altomonte, A. Natali, G.,Buzzigoli and E.
Ferrannini
Aim of the present study was to quantitate whole body and muscle
glucose and lipid metabolisms in a model of trauma-induced insulin
resistance, the postsurgical state. We studied 9 nondiabetic, non obese
patients (age 48 5 yrs; BMI 23 I kg/mz) 6-8 hours after major,
abdominal uncomplicated surgery (S), and 8 matched healthy subjects
as controls (C). A 3-step euglycemic insulin clamp (.5, 1.0, and 5 mU
min Ikg -1 ) was combined with continuous indirect calorimetry with
- om required respiratory support. IGF1 and IGF-BP1 levels
canopy and the forearm technique to study muscle metabolism. Plasma
glucose and insulin levels were simlar in the two groups at the baseline
and throught the study. In the fasting state, S showed significantly (p <
.05 or less) higher arterial concentrations of lactate (1.43 .10 vs .74
.09 mM), FFA (.94 .07 vs .36 .05 mM), butyrate (1841 .734 vs
216 47 jiM), and glycerol (79 7 vs 36 4 NM) than C. Whole body
lipid and protein oxidation (4.9 .6 and 5.3 .6 jamol min'kg') and
energy expenditure (5.0 .2 kJ min') were significantly elevated in S
as compared to C (2.4 .4 and 4.3 .6 mol min-'kg-', and 4.4 .2 kJ ian 28.4 ng/ml, interquartile range 13.2-52.2 ng/ml). In 2
min-', respectively), while carbohydrate oxidation was lower (4.6 1.4
vs 11.1 1.8 jumol min-'kg-'). Basal hepatic glucose production
(measured by 3 H-6-glucose) was higher (p < .002) in S (16.4 .8 mot
min-'kg') than in C (2.4 .7 pumol mitr'kg 1), and significantly less
suppressed by insulin. During hyperinsulinemia, glucose uptake,
oxidation, and non oxidative disposal were all markedly impaired in S
at each insulin dose, while lipid oxidation was less suppressed and
energy expenditure failed to rise. At baseline, forearm muscle glucose
uptake was reduced, and release of FFA, lactate, pyruvate, alanine, and
glycerol was increased in S vs C. Since glucose production, oxidation,
and storage, lipolysis, protein degradation, and thermogenesis all were
resistant to insulin in S, we conclude that the insulin resistance of this
model of trauma. is: 1) severe, 2) metabolically complete, 3) located
both in the liver and peripheral tissues; and 4) not corrected by high
insulin levels.
Department of Anesthesiology and Intensive Care University of Pisa,
and Institute of Clinical Physiology, Via Roma 67, 56100 Pisa, Italy
P376
1IYPERCHLOREMIC ACIDOSIS (HCIA) : AN IMMEDIATE
PHYSIOLOGICAL RESPONSE TO GRAND -MAL
SEIZURES LACTIC ACIDOSIS ?
F. Brivet*, M. Bernardin*, P. Chdrin*, J. Chatas**, P.
Galanaud*. J. Dormont*
In principle, anion gap Increment (D AG) of anion
retention metabolic acidosis is equal to bicarbonate
deficit (D TCO2). Mechanisms of HCIA associated to
lactic acidosis (LA), recently reported, are unclear.
Patients (pts) with grand -mal seizures (GMS) may serve
as unique model of LA and help to clarify the
pathogenesis of HCIA.
METHODS : 35 GMS were retrospectively studied. HCIA
component was defined by a ratio D AG / D TCO2 <_ 0.8.
D AG = [Na+ - (Cl + TCO2)] - 12 ; D TCO2 = 26 - arterial
-
TCO2. Difference in distribution space of H+ and anions
was studied by the ratio Na +/Ci .
-
RESULTS : Pts studied : Age (mean SD) : 51.7 21.3
years, SAPS : 14.7 t 6.6, ICU mortality rate : 21 %.
Biological data after seizures : pH : 7.22 0.17 ; PaCO2
4.6k 1.6 KPa, TCO2 : 14.6 5.3 mmol/I ; D AG : 11.8
7.2 mEq/I ; lactates : 14.6 6.9 mmol/l. HCIA prevalence
31.4 % versus 73 %, 60 to 120 min after recovery.
On admission :- D AG / D TCO2 ratios were unrelated with
creatinine, PaCO2 ; but dependent of the ratio Na+/CI :
-
r= 0.803, p < 0.001. D AG / D TCO2 = 6.5 (Na +/CI ) - 8.1.
-
DISCUSSION : The role of chloride Infusion and renal
excretion Is excluded. HCIA may be mediated by a
CONCL"SIQN, : HCIA may be 1/ associated to LA after
selzurt 2/ secondary to lactate antiport, 3/ an
immediate physiological response to acute metabolic
acidosis, 4/ be overshawoded by the classical concept
of pure anion gap acidosis.
* Medical Intensive Care Unit, ** Laboratory of Chemistry,
HSpital Antoine BAclere - 92140 CLAMART - France
P378
CIRCULATING LEVELS OF INSULIN-LIKE GROWTH FACTOR 1 [IGF)
AND INSULIN-LIKE GROWTH FACTOR BINDING PROTEIN 1 (IGF-BP1)
IN CRITICAL ILLNESS. A.C. Timmins, A.M. Cotterill, J.M.P.
Holly, C.J. Hinds.
The catabolic response to critical illness can occur desp-
ite nutritional support and may have a deterimental effect
on outcome. IGF1 mediates somatic growth, has both mitoge-
nic and insulin like activity and circulates bound to spe-
cific proteins (IGF-BP 1-6). Circulating levels of IGF1
and IGF-BP1 were measured in a heterogeneous group of 14
critically ill patients, (median age 67.5 years [range 35-
77]; median APACHE II score 14.5 [range 4-39]), all of wh-
were measured daily until discharge or death from intensi-
ve care using an established radioimmune assay. In all ex-
cept one survivor IGF1 levels remained depressed through-
out (median 45.5 ng/ml, interquartile range 38.5-60.7 ng/
ml). There were no significant differences between surviv-
ors (S) and non-survivors INS) during the first 5 days fo-
llowing admission. IGF-BP1 levels were elevated to within
the range found in fasting subjects in both S and NS (med-
patients who remained on intensive care for a much longer
period ( 35 days) IGF1 levels increased slowly and prog-
ressively in a S, whereas in a NS levels remained low. In
two acutely injured neurosurgical patients IGF1 levels we-
re well within the normal range on admission but subseque-
ntly fell. Reduced IGF levels may represent an adaptive
response which allows the catabolic rather than the anabo-
lic effects of high circulating growth hormone levels to
predominate (Ross R et al Clin Endocrinol 35: 47-54 1991).
Although this may be beneficial in the fasted patient it
may prevent utilization of substrates in critically ill
patients receiving nutritional support. The administration
of exogenous IGF1 might reduce catabolism and improve nut-
ritional status in critically ill patients.
Department of Intensive Care and Endocrinology, St. Barth-
olomew's Hospital, West Smithfield, London EC1A 7BE,
England
 S213

P379 P380
111E > CF ICf MD K r- icr U il'AIl M FAT 941SM (N I1WW FIICI3f X18
ENERGY EXPENDITURE IN CRITICALLY ILL PATIENTS
G. VignaLi,A.GUadagnucci,A. Baretta,G. Rogato,G.TUI Ii*,F. Leonardi. AM, UN; PHIW S IN )HIW(iC+UX VEKMJI ED 1(11 PATIFNIS
A.R.hbral,A.Turhen,B.Ersz,F.Giigin
Determination of Energy Expenditure (EE) utilizing the thernodi Lution
pulmonary artery - catheter is easy and not expensive in critically ill 4he effects of Intralipid (ILT 106) and Lipofundin (ICI' S^.+h{P Si) an
patients. 4e performed 258 measurements, in 44 patients in intensive care, to
evaluate resting metabolicexpenditure and its evolution during spontaneous arterial blood gas analysis and lung nochanics v.e e canpared.
or pharmacological changes of patients status. 22 mechanically ventilated,nonseptic,enterally notwished ICU patients
EE was calculated. as EE(kcal/24h)=V02A0.00486* 1 440 (RQ=0.86) where without renal,hepatic or netabolic,dysfunctions were investigated.
V02(ol/min)=COA(Ca02-CvO2)*10. our aim was also to examine the possibility of
calculating the CO2 production and the respiratory quotient by Eq.:
11 patients(group I)were given Intralipid 1 g/Icg for a duration of 5 h.
VCO2=CO*(CtvCO2-CteCO2)*22.41; RQ=VtO2/VO2. Mean values of EE measured with and to another 11 patients (group II) Lipofundin (1(I1V) wes arini iict irated
theroodilution are about 26 kcal/Kg/24h;. the Harris-Benedict's equation during the sane interval,the dosage not being altered.Before the
underestimates the Energy Expenditure of the patients, the introduction of a Initiation of (0),at the and of infusion (1) and 3,5,8 and 12 h.after the
correction factor overestimates it. termination of infusion (2,3,4,5) arterial blood pas analysis and some
Tab. Measured and theorical Energy Expenditure%
other estimations were carried.The results obtained, related the 1,3 and
vo2*o.00486*1440 = 1737 sd=442.8 5 the intervals are presented in table I.
(V02*0.0039WCO2*0.0011)* 1440 - .1966 sd=584.1
BEE (Harris.Benedict)*1440 = 1368 sd=226.6
= 2394 sd=3%.5
Table I: Avared values of the measured parameters
RME (BEE*1.75)
0 1 3 5
Physiological and mathematical problems do not permit the evaluation of C.02 1a02 Gr,I 106.31+10.49 101.33 11.00 89.71.46 94.30T10.90
production that is overestimated, with this technique, as the value of Mn Hg Gr.II 85.11+5.07 92.45+6.66 85.25+4.25 83.63+3.90
respiratory quotient shows (ROF1.4 SD=0.85). The CO2 content is given by
equation tCO2-O.230*pCO2+HCO3 where HCO3=0.230ApCO2*antiLog(pH -pKp) and
1'a002 Gr.I 40.52+2.47 39.59+2.14 42.19+2.44 43.58+2.53
pKp=6.125-log(1+antilog(pH-8. 7 )). In our study the venous-arterial difference ram Hg Gr.II 35.6111.10 34.97+1.68 36.94+1.69 40.04+1.95
of HCO3 is 1.67 aniol/l (S0=1.33). Small errors, amplified by Logarithmic Camp. Gr.I 42.7314.59 42.73+4.12 41.27+3.85 41.55+4.17
scale,in the measured pCO2 or pH could,easily, determine this difference. A 1/cid-E 3 Gr.II 55.(70T6.79 55.275.% 53.18.27 54.75i6.32
2 mmHg error in measured pCO2, at cdnstant pH, generates a 1.22 mmol (2.73
Eff.Vent. Gr.I 10.14 .73 9.97 .68 10.0610.70 10.07T0.71
voL%) error in tCO2 content.
Conclusion: determination of EE utilizing the thermodilution pulmonary artery 1/grin. Gr.11- 13.22+1.46 13.0311.47 13.371.56 13.05+1.55
catheter is simple and not expensive in suitable patients. The thernodilution Peak P. Cr.I 26.5512.27 24.64+1.83 26.55+1.73 25.91+1.54
does not permit the evaluation of VCO2 and of RO.The calculated EE could be tin El23 Gr.II 26.09+1.24 25.55+1.43 26.18+0.95 27.5511.54
inaccurate during change of respiratory quotient. Wait' Cr.I 9.010.98 8.29+1.03 8.590.91 8.851.09
Departments of Anaesthesiology and Intensive Care,SS Giacomo e Cristoforo (m.F12D Gr.ii 8.650.66 8.43111.70 8.64}0.67 8.84+0.74
Hospital, Massa; * Departments of Anaesthesiology and Intensive Care, All of the values are nonsignificant in comparison with the baseline
Torregalli Hospital, Florence, Italy. values.

We conclude that both LCF and PCF+I.CF containing fat ermilsions have
no significant effects on lung functions.Therefore these solutions can be
safely used in.IQJ patients.

Department of Anesthesiology and Bioche m istry

Aegean llnivercity Hospital,Iss rIIURKTYE

P381
PLASMA ALUMINIUM CONCENTRATION AND URINARY
EXCRETION IN LONG-TERM VENTILATED PATIENTS DU-
RING STRESS ULCER PROPHYLAXIS WITH SUCRALFATE
Tryba M, Kurz- Mller K, Thole H, Wilhelm M'
Sucralfate has become a standard therapy for stress ulcer prophylaxis in many ICU's.
The recommended dosage regimen of 6 g sucralfate daily contains 1020 mg
aluminium. A twofold increase of plasma-aluminium levels and a three-fold increase
of urinary aluminium excretion has been observed three weeks after the treatment
with 4 g sucralfate daily in dyspeptic patients. Encephalopathy due to toxic plasma
aluminium levels has been observed in patients with compromised renal function.
However, up to now no investigations of aluminium resorption and excretion during
long-term treatment with sucralfate have been performed in severely ill ICU-patients.
Methods: 11 long-term ventilated patients were included in the study. All patients
received 6 x 1 g sucralfate suspension intragastrally. Plasma-aluminium
concentration was determined 3 h after the morning dose of sucralfale. Results:
Seven of the patients were male. The mean age of the patients were 57.2 10.8 y.
(19-83 y) and the mean duration of treatment was 11.34.2 days (4-17 days).
Renal function was compromised in eight patients ( max. plasma creatinine levels
2.7 mg / dl, normal values < 1.4 mg / dl).
dayplate aluminium fun / I) 24 h urinary excretion (up / lt
0 10.05.7
2 13.1 9.3 50.8 47.1
4 21.1 7.1 40.650.7
13.6 8.6 35.533.7
6
10 7.332.8 32.832.8
14 7.47.4 31.629.0
Analysis of the patient's data showed that the observed increase of the plasma
aluminium levels correlated with the infusion of fresh frozen plasma.
Discussion: In contrast to antacids (].) the administration of 6 g sucralfate did not
lead t9 an increase of plasma aluminium in critically ill patients. Sucralfate can be
safely administered even in critically ill patients with compromised renal function at
least for a period of two weeks.
Reference: 1. Rauch H at al. Intens Care Med 1989; 15:84
P382
STRESS ULCER PROPHYLAXIS : WHAT IS THE ROLE OF CONVENTIONAL THERAPY ?
F.Bobbio Pallavicini,G.Verde,N.Bonizzoni*,G.Bichisao,F.Cassini
While gastric alkalinization in ICUs became popular,extensive experimen-
tal and clinical studies focuses on the gastric mucosal acidosis,but not
gastric acidity,as the primary cause of stress induced gastric oucosal in
jury.Noreover,there is increasingly attention on the mucous protective of
feet of enteral nutrition(EN) in ICU pts.In this study we compared the of
fectiveness of H2-receptor-antagonists(H2a) and of EN for stress ulcer
bleeding prophylaxis.Altoghether 3360 pts were analyzed,from january 1980
to december 1990.The study was performed retrospectively between 1980 3d
1988(period A=2280pts) and perspectively during 1989-90(period 8=580pts)
All pts underwent a common metabolic-nutritional and stress ulcer prophy
laxis prograo:parenteral nutrition(PN) until the enteral route was not a
vailable;start of EN early how possible in small amounts and growing pro
gressively;gastric alkalinization(antacids or H2a) during PN until EN ex-
ceeding 800Kcal/day;only EN in pts with uninjured gastro-intestinal tract
stop of gastric alkalinization when EN> 80OKcal/day.Because the study was
retrospective to some extend,the episodes of stress-related gastro-intes t
final haesorrage(6IH) with macroscopic appearance were recorded only.Allt
ogether,51 episodes of GI8 in 47 pts were observed.
Groups GIH According to the literature,the GIN rate in
a) Antacids 6 (1.74%) our series was low:1.53Z(44) during period
b) H2a 33 (1.57%) A,1.20%(7) during period B.The impact of
c) EN 7 (0.31%) H2a vs antacids was not significant.EN it
d) EN + H2a 5 (0.38X) i appears to be effectivenes for stress ulc-
er prophylaxis,compared to antacids and H2a
p<O.OI: c,d vs a,b
Servizio di Anastasia e Rianimazione I /II;,Policlinico San Natteo IRCCS
Pie C.Golgi , 27100 Pavia Italia

Department of Anesthesiology, Intensive Care Medicine and Pain Therapy,

University Hospital Bergmannsheil, Gilsingstr. 14, D-4630 Bochum, Germany
. Institute of Toxicology, University of Dsseldorf, Germany