Zusammenfassung
Hintergrund: Ein Anstieg des intraabdominellen Drucks ist kürzlich als potenzieller Risikofaktor
für frühe Organdysfunktionen bei Patienten mit schwerer akuter Pankreatitis beschrieben
worden. Daher erscheint die Untersuchung eines möglichen Zusammenhangs zwischen einem
erhöhten intraabdominellen Druck und frühen Organdysfunktionen wichtig für die Optimierung
der Behandlungsstrategie.
Patienten und Methoden: 71 Patienten mit schwerer akuter Pankreatitis wurden in die prospektive Studie aufgenommen.
Hierbei wurden der klinische Status, der Organdysfunktions-Score (SOFA-Score) und
der intraabdominelle Druck bestimmt. Als kritischer Grenzwert wurde ein Druck von
25 cm H2 O festgelegt. Die Patienten wurden im Verlauf der Studie bei Überschreiten des kritischen
Drucks der Hochrisiko-Gruppe (n = 18) bzw. bei Unterschreiten des Wertes der Niedrigrisiko-Gruppe
(n = 53) zugeordnet.
Ergebnisse: Hochrisiko- und Niedrigrisiko-Gruppe unterschieden sich nicht signifikant hinsichtlich
des durchschnittlichen Lebensalters und der initialen Organdysfunktion. Eine Progression
der Organdysfunktion wurde bei 61 % der Hochrisiko- Gruppe und bei 32 % der Niedrigrisiko-Gruppe
beobachtet (p < 0,05). Die Organfunktion verbesserte sich nach einer 3-4- tägigen
Behandlung lediglich bei den Überlebenden. Der maximale intraabdominelle Druck war
in der Hochrisiko-Gruppe gegenüber der Niedrigrisiko-Gruppe erhöht (p < 0,01), allerdings
fiel der Druck unter einer 3-5-tägigen Behandlung bei allen Überlebenden ab, lediglich
bei den Verstorbenen blieb der intraabdominelle Druck erhöht. Eine operative Therapie
erfolgte bei 78 % der Hochrisiko-Patienten und bei 32 % der Niedrigrisiko-Patienten
(p < 0,05). Die Gesamtmortalität betrug 8,5 %. Während die Mortalität in der Niedrigrisiko-Gruppe
bei 2 % lag, betrug sie in der Hochrisiko-Gruppe 28 % (p < 0,01).
Schlussfolgerung: Ein erhöhter intraabdomineller Druck könnte ein wichtiger Risikofaktor für eine frühe
Organdysfunktion bei Patienten mit einer schweren akuten Pankreatitis sein. Ein kritischer
Anstieg des intraabdominellen Drucks und eine persistierende Organdysfunktion stellen
eine Indikation für eine erneute Überprüfung der Behandlungsstrategie dar.
Abstract
Background: Sustained increase of the intra- abdominal pressure is recently recognized as a potential
risk factor of early organ dysfunction in patients with severe acute pancreatitis.
Assessment of the possible mutual relevance between increased intra-abdominal pressure
and early organ dysfunction is important for optimisation of the treatment strategy
in this category of patients.
Patients and methods: 71 patients with severe acute pancreatitis were entered in this prospective study.
Clinical routine, sequential organ failure assessment score (SOFA), and intra-abdominal
pressure were registered, considering 25 cm H2 O a critical value for the grouping in high-risk (n = 18) and low-risk (n = 53) patients
according to whether they experienced the critical level during their treatment course.
Results: The age structure and the initial presentation of the organ dysfunction were similar
between both groups. Progression of the organ dysfunction was observed in 61 % of
the high-risk patients, compared to 32 % of low-risk patients, p < 0.05. Organ function
improved after three to four day treatment only in survivors. Peak intra-abdominal
pressure was greater in high-risk patients, p < 0.01, but declined after three to
five day treatment period in all survivors, remaining critical in nonsurvivors. 78
% of high-risk and 32 % of low-risk patients were operated, p < 0.05. The overall
mortality was 8.5 %, consisting of 2 % mortality in the low-risk group and 28 % mortality
in the high-risk group, p < 0.01.
Conclusion: Increased intra-abdominal pressure could be an important risk factor of early organ
dysfunction in patients with severe acute pancreatitis. Critical increase of the intra-abdominal
pressure and persisting organ dysfunction are an indication for reassessment of the
treatment strategy.
Schlüsselwörter
Intraabdomineller Druck - akute Pankreatitis - Behandlungsstrategie
Key words
Intra-abdominal pressure - acute pancreatitis - treatment strategy
Literatur
1
American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference
.
Definitions for sepsis and organ failure and guidelines for the use of innovative
therapies in sepsis.
Crit Care Med.
1992;
20
864-874
2
Baron T H, Morgan D E.
Acute necrotizing pancreatitis.
N Engl J Med.
1999;
340
1412-1417
3
Bone R C, Balk R A, Cerra F B, Dellinger R P, Fein A M, Knaus W A, Schein R M, Sibbald W J.
Definitions for sepsis and organ failure and guidelines for the use of innovative
therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College
of Chest Physicians/Society of Critical Care Medicine.
Chest.
1992;
101
1644-1655
4
Bradley E L.
A clinically based classification system for acute pancreatitis. Summary of the International
Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992.
Arch Surg.
1993;
128
586-590
5
Bradley E L.
Operative vs. Nonoperative therapy in necrotizing pancreatitis.
Digestion.
1999;
60 (Suppl 1)
19-21
6
Buchler M, Uhl W, Beger H G.
Acute pancreatitis: when and how to operate.
Dig Dis.
1992;
10
354-362
7
Burch J M, Moore E E, Moore F A, Franciose R.
The abdominal compartment syndrome.
Surg Clin North Am.
1996;
76
833-842
8
Iberti T J, Kelly K M, Gentili D R, Hirsch S, Benjamin E.
A simple technique to accurately determine intra- abdominal pressure.
Crit Care Med.
1987;
15
1140-1142
9
Isenmann R, Rau B, Beger H G.
Bacterial infection and extent of necrosis are determinants of organ failure in patients
with acute necrotizing pancreatitis.
Br J Surg.
1999;
86
1020-1024
10
Isenmann R, Rau B, Beger H G.
Early severe acute pancreatitis: characteristics of a new subgroup.
Pancreas.
2001;
22
274-278
11
Ivatury R R, Diebel L, Porter J M, Simon R J.
Intra-abdominal hypertension and the abdominal compartment syndrome.
Surg Clin North Am.
1997;
77
783-800
12
Ivatury R R, Porter J M, Simon R J, Islam S, John R, Stahl W M.
Intra-abdominal hypertension after life-threatening penetrating abdominal trauma:
prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal
compartment syndrome.
J Trauma.
1998;
44
1016-1021
13 Johnson C. Role of cytokines and their antagonists. In: Buchler MW, Uhl W, Friess
H, Malfertheiner P (eds). Acute pancreatitis. Novel concepts in biology and therapy.
Blackwell, Berlin, Vienna 1999; 71-75
14
Kaplan A A.
Extracorporeal blood purification in the treatment of acute renal failure with multiorgan
involvement.
Blood Purif.
1996;
14
86-93
15
Kopelman T, Harris C, Miller R, Arrillaga A.
Abdominal compartment syndrome in patients with isolated extraperitoneal injuries.
J Trauma.
2000;
49
744-747
16
Kron I L, Harman P K, Nolan S P.
The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration.
Ann Surg.
1984;
199
28-30
17
Mann D V, Hershman M J, Hittinger R, Glazer G.
Multicentre audit of death from acute pancreatitis.
Br J Surg.
1994;
81
890-893
18
Maxwell R A, Fabian T C, Croce M A, Davis K A.
Secondary abdominal compartment syndrome: an underappreciated manifestation of severe
hemorrhagic shock.
J Trauma.
1999;
47
995-999
19
Mayberry J C, Goldman R K, Mullins R J, Brand D M, Crass R A, Trunkey D D.
Surveyed opinion of American trauma surgeons on the prevention of the abdominal compartment
syndrome.
J Trauma.
1999;
47
509-513
20
McKay C J, Evans S, Sinclair M, Carter C R, Imrie C W.
High early mortality rate from acute pancreatitis in Scotland, 1984-1995.
Br J Surg.
1999;
86
1302-1305
21
Meisner M, Tschaikowsky K, Palmaers T, Schmidt J.
Comparison of procalcitonin (PCT) and C-reactive protein (CRP) plasma concentrations
at different SOFA scores during the course of sepsis and MODS.
Crit Care.
1999;
3
45-50
22
Pupelis G, Austrums E, Snippe K, Berzins M.
Clinical significance of increased intraabdominal pressure in severe acute pancreatitis.
Acta Chir Belg.
2002;
102
71-74
23
Rangel-Frausto M S, Pittet D, Costigan M, Hwang T, Davis C S, Wenzel R P.
The natural history of the systemic inflammatory response syndrome (SIRS). A prospective
study.
JAMA.
1995;
273
117-123
24 Runkel N, Eibl G. Pathogenesis of pancreatic infection. In: Buchler MW, Uhl W,
Friess H, Malfertheiner P (eds). Acute pancreatitis. Novel concepts in biology and
therapy. Blackwell, Berlin, Vienna 1999; 255-261
25
Russell J A, Singer J, Bernard G R, Wheeler A, Fulkerson W, Hudson L, Schein R, Summer W,
Wright P, Walley K R.
Changing pattern of organ dysfunction in early human sepsis is related to mortality.
Crit Care Med.
2000;
28
3405-3411
26
Saggi B H, Sugerman H J, Ivatury R R, Bloomfield G L.
Abdominal compartment syndrome.
J Trauma.
1998;
45
597-609
27
Schein M, Wittmann D H, Aprahamian C C, Condon R E.
The abdominal compartment syndrome: the physiological and clinical consequences of
elevated intra- abdominal pressure.
J Am Coll Surg.
1995;
180
745-753
28
Sigurdsson G.
Intensive care management of acute pancreatitis.
Dig Surg.
1994;
11
231-241
29
Soran A, Chelluri L, Lee K K, Tisherman S A.
Outcome and quality of life of patients with acute pancreatitis requiring intensive
care.
J Surg Res.
2000;
91
89-94
30
Storset P, Smith-Erichsen N, Vaagenes P.
Organ function during early acute renal failure does not predict survival in long-term
intensive care.
Intensive Care Med.
1995;
21
797-801
31
Sugerman H J, Bloomfield G L, Saggi B W.
Multisystem organ failure secondary to increased intraabdominal pressure.
Infection.
1999;
27
61-66
32
Toh S K, Phillips S, Johnson C D.
A prospective audit against national standards of the presentation and management
of acute pancreatitis in the South of England.
Gut.
2000;
46
239-243
33
Vincent J L, de Mendonca A, Cantraine F, Moreno R, Takala J, Suter P M, Sprung C L,
Colardyn F, Blecher S.
Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive
care units: results of a multicenter, prospective study. Working group on “sepsis-related
problems” of the European Society of Intensive Care Medicine.
Crit Care Med.
1998;
26
1793-1800
34
Watson R A, Howdieshell T R.
Abdominal compartment syndrome.
South Med J.
1998;
91
326-332
35
Windsor J A, Hammodat H.
Metabolic management of severe acute pancreatitis.
World J Surg.
2000;
24
664-672
36
Zauner C, Gendo A, Kramer L, Kranz L, Grimm G, Madl C.
Metabolic encephalopathy in critically ill patients suffering from septic or nonseptic
multiple organ failure.
Crit Care Med.
2000;
28
1310-1315
Guntars PupelisMD, Assistant Professor
Rigas Stradina University
Clinical Hospital
Department of Surgery
2 Hipokrata Street
LV-1038 Riga
Latvia
Email: pupelis@gailes.lv