Subscribe to RSS
DOI: 10.1055/s-2000-13006
Outcome-Faktoren des schweren Schädel-Hirn-Traumas
Eine retrospektive Analyse von 228 (161) Patienten Factors for Outcome in Severe Head Injury.Publication History
Publication Date:
31 December 2000 (online)
![](https://www.thieme-connect.de/media/ains/200002/lookinside/thumbnails/10.1055-s-2000-13006-1.jpg)
Zusammenfassung.
Ziel der Studie: Outcome-Analyse nach schwerem Schädel-Hirn-Trauma (initiale GCS ≤ 8) mit Identifikation von Ergebnis-relevanten Faktoren der Prähospital- und Intensivmedizinischen Phase. Vergleich mit früheren Behandlungsergebnissen aus der eigenen Klinik. Methodik: Retrospektive Erhebung des Glasgow Outcome Scale (GOS)-Score von 228 Patienten mit schwerem Schädel-Hirn-Trauma (1988 - 95) am Ende der Intensivbehandlung und von 161 Patienten 6 Monate nach dem Trauma. Korrelation mit Alter, GCS, präklinischer Hypotonie und Hypoxie, ICP, CPP, Trometamol- und Thiopental-Therapie. Erfassung der Infektionsrate. Ergebnisse: Outcome (n = 228) am Ende der intensivmedizinischen Behandlungsphase (Median 9, Min-Max 2 - 77 Tage): GOS 1: 20 %, GOS 2 + 3 : 79 %, GOS 4: 1 %. Outcome (n = 161) 6 Monate nach Trauma: GOS 1: 35,4 %, GOS 2+3: 17,4 %, GOS 4+5: 47,2 %. Höheres Lebensalter ist mit einem schlechteren Ergebnis verbunden. In der Prähospitalphase sind der GCS, Hypotonie und/oder Hypoxie signifikant mit dem Outcome korreliert. GOS von 30 Patienten mit Hypotonie und Hypoxie: GOS 1:53 %, GOS 2+3: 27 %, GOS 4+5: 20 %. GOS von 40 Patienten ohne Hypotonie und Hypoxie: GOS 1: 25 %, GOS 2+3: 10 %, GOS 4+5: 65 %. Während der intensivmedizinischen Phase sind Höhe des CPP (ICP nicht signifikant!) und hirndrucksenkende Therapie mit Trometamol und/oder Thiopental signifikant mit dem Ergebnis korreliert. Letalität für CPP unter 50 mmHg (n = 32): GOS 1: 69 %, bei CPP-Werten über 50 mmHg (n = 29) GOS 1: 20 %. Die Patientengruppe (n = 32) mit therapieresistenter Hirndrucksteigerung wies, trotz maximaler Intensivtherapie inklusive Trometamol und Thiopental, die schlechtesten Outcome-Zahlen auf: GOS 1: 66 %, GOS 2+3: 6 %, GOS 4+5: 28 %. Das beste Ergebnis war dagegen in der Gruppe (n = 71) zu verzeichnen, die weder Trometamol noch Thiopental benötigten: GOS 1: 27 %, GOS2+3: 18 %, GOS 4+5: 55 %. Die Behandlung mit Thiopental ging nicht mit einer erhöhten Rate pulmonaler und anderer Infektionen einher. Im Vergleich zur Studie von 1980 - 88 konnte trotz Therapiemodifikationen keine Verbesserung des Ergebnisses festgestellt werden. Schlußfolgerung: Präklinische Hypotonie und Hypoxie sind maßgeblich an der hohen Morbidität und Letalität des schweren SHT beteiligt. Für die dadurch verursachte sekundäre Hirnschädigung existieren zur Zeit nur unzureichende therapeutische Konzepte. Die Vermeidung bzw. aggressive Therapie von Hypotonie und Hypoxie in der frühen posttraumatischen Phase scheint im Augenblick der wichtigste Ansatz zur Verbesserung des Outcomes nach schwerem SHT zu sein.
Objective: To study outcome from severe head injury (SHI: GCS ≤ 8) and to investigate impact of prehospital factors and clinical intensive care parameters on outcome. To compare with former study results (1980 - 88) of our clinical setting. Methods: Retrospectively, the history of 228 patients with SHI treated between 1988 and 1995 was looked into. The outcome was measured with the Glasgow Outcome Scale (GOS) post intensive care (median 9, min-max 2 - 77 days) and 6 months after trauma by a questionnaire. The GOS was related to age, Glasgow Coma Scale (GCS on the scene), prehospital hypotension and hypoxia (HH), intracranial pressure (ICP), cerebral perfusion pressure (CPP), intensive therapy including Tromethamine and/or Thiopentone. The rate of infections was determined. Results: Increasing age influences outcome negatively. Prehospital GCS and HH were significantly correlated with outcome. GOS of 30 patients with HH: GOS 1: 53 %, GOS 2+3: 27 %, GOS 4+5: 20 %. GOS of 40 patients without HH: GOS 1: 25 %, GOS 2+3: 10 %, GOS 4+5: 65 %. During intensive care the level of CPP (not ICP) as well as tromethamine and/or thiopentone treatment for control of elevated ICP were significantly correlated with outcome. Mortality rate in 32 patients with CPP < 50 mmHg was 69 %, in 29 patients with CPP > 50 mmHg only 20 %. Patients treated additionally with Tromethamine and Thiopentone because of uncontrollable intracranial hypertension showed a significantly worse outcome: GOS 1: 66 %, GOS 2+3: 6 %, GOS 4+5: 28 %, compared to those who needed neither Tromethamine nor Thiopentone: GOS 1: 27 %, GOS 2+3: 18 %, GOS 4+5: 55 %. Thiopentone treatment was not associated with an increased rate of pulmonary and other infections. In comparison to our former outcome study, covering the years 1980 - 88, we have not seen any improvements in outcome, despite modifications in intensive care protocols. Conclusions: Prehospital hypotension and hypoxia have a significant negative impact on outcome by causing secondary brain damage. Despite various modifications in intensive care therapy an unchanged portion of secondary brain damage will not prove treatable. Therefore, prevention or early aggressive treatment of hypotension and hypoxia is the most promising way of improving outcome after severe head injury at the moment.
Schlüsselwörter:
Schädel-Hirn-Trauma - Outcome - Hypotonie - Hypoxie - lntensivtherapie
Key words:
Severe head injury - outcome - hypotension - hypoxia - intensive care
Literatur
- 1 Alexandre A, Colombo F, Nertempi P, Benedetti A. Cognitive outcome and early indices of severity of head injury. J Neurosurg. 1983; 59 751-761
- 2 Chesnut R M, Marshall L F, Klauber M R, Blunt B A, Baldwin N, Eisenberg H M, Jane J A, Marmarou A, Foulkes M A. The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993; 34 216-222
- 3 Chesnut R M. Medical management of severe head injury: present and future. New Horizons. 1995; 3 581-593
- 4 Choi S C, Muizelaar J P, Barnes T Y, Marmarou A, Brooks D M, Young H F. Prediction tree for severely head injured patients. J Neurosurg. 1991; 75 251-255
- 5 Choi S C, Barnes T Y, Bullock R, Germanson T A, Marmarou A, Young H F. Temporal profile of outcomes in severe head injury. J Neurosurg. 1994; 81 169-173
- 6 Clifton G L, Hayes T Y, Levin H S, Michel M E, Choi S C. Outcome measures for clinical trials involving traumatically brain injured patients: report of a conference. J Neurosurg. 1992; 31 975-978
- 7 Cunitz G. Die Erstversorgung des Schädel-Hirn-Trauma-Patienten. Anaesthesist. 1995; 44 369-391
- 8 Dearden N M, Gibson J S, Gibson R M, Cameron M M. Effect of high-dose dexamethasone on outcome from severe head injury. J Neurosurg. 1986; 64 81-88
- 9 Gaab M R, Seegers K, Smedema R J, Heissler H E, Goetz C. A comparative analysis of THAM (Trometamol-buffer) in traumatic brain oedema. Acta Neurochir (Suppl.). 1990; 51 320-323
- 10 Gennarelli T A, Spielman G M, Langfitt T W, Gildenberg P L, Harrington T, Jane J A, Marshall L F, Miller D, Pitts L H. Influence of the type of intracranial lesion on outcome from severe head injury. J Neurosurg. 1982; 56 26-32
-
11 Jantzen J- PAH.
Anästhesie bei Patienten mit Schädel-Hirn-Trauma. In: Aktuelles Wissen für Anästhesisten: Refresher Course. Deutsche Akademie für Anästhesiologische Fortbildung (Hrsg). Nr.22. Springer, Berlin Heidelberg 1996 - 12 Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet. 1975; 1 480-484
- 13 Jennett B, Teasdale G, Braakman R, Minderhoud J, Heiden J, Kurze T. Prognosis of patients with severe head injury. J Neurosurg. 1979; 4 283-289
- 14 Jennett B, Teasdale G, Galbraith S, Pickard J, Grant H, Braakman R, Avezaat C, Maas A, Minderhoud J, Vecht C J, Heiden J, Small R, Caton W, Kurze T. Severe head injuries in three countries. J Neurol Neurosurg Psychiat. 1977; 40 291-298
- 15 Jennett B. Diagnosis and management of head trauma. J Neurosurg. 1991; (Suppl.) 1 15-19
- 16 Katz D I, Alexander M P. Traumatic brain injury. Arch Neurol. 1994; 51 661-670
- 17 Langfitt T W. Measuring the outcome from head injuries. J Neurosurg. 1978; 48 673-678
- 18 Langfitt T W, Gennarelli T A. Can the outcome from head injury be improved?. J Neurosurg. 1982; 56 19-25
- 19 Lobato R D, Cordobes F, Rivas J J, de la Fuente M, Montero A, Barcena A, Perez C, Cabrera A, Lamas E. Outcome from severe head injury related to the type of intracranial lesion. J Neurosurg. 1983; 59 762-774
- 20 Marshall L F, Gautille T, Klauber M R, Eisenberg H M, Jane J A, Luerssen T G, Marmarou A, Foulkes M A. The outcome of severe closed head injury. J Neurosurg. 1991; (Suppl.)75 28-36
- 21 Marshall L F, Marshall S B, Klauber M R, van Berkum Clark M, Eisenberg H M, Jane J A, Luerssen T G, Marmarou A, Foulkes M A. A new classification of head injury based on computerized tomography. J Neurosurg. 1991; (Suppl.)75 14-20
- 22 Muizelaar J P, Marmarou A, Ward J D, Kontos H A, Choi S C, Becker D P, Gruemer H, Young H F. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. 1991; 75 731-739
- 23 Neusser M. Behandlungsergebnisse von schweren Schädelhirntraumen unter besonderer Berücksichtigung der Intensivtherapie. Dissertationsschrift 1989; Univ. Ulm
- 24 Pitts L H. Neurotrauma and trauma systems. New Horizon. 1995; 3 546-548
- 25 Prough D S, DeWitt D S. Head trauma and brain resuscitation. Current Opinion in Anesthesiology. 1996; 9 188-193
- 26 Rosner M J, Coley I B. Cerebral perfusion pressure, intracranial pressure and head elevation. J Neurosurg. 1986; 65 636-641
- 27 Rosner M J, Daughton S. Cerebral perfusion pressure management in head injury. J Trauma. 1990; 30 933-941
- 28 Rosner M J, Rosner S D, Johnson A H. Cerebral perfusion pressure: management protocol and clinical results. J Neurosurg. 1995; 83 949-962
- 29 Schalén W, Messeter K, Nordström C H. Complications and side effects during thiopentone therapy in patients with severe head injuries. Acta Anaesthesiol Scand. 1992; 36 369-377
- 30 Schüttler J, Schmitz B, Bartsch A C, Fischer M. Untersuchungen zur Effizienz der notärztlichen Therapie bei Patienten mit Schädel-Hirn- bzw. Polytrauma. Anaesthesist. 1995; 44 850-858
- 31 Singbartl G, Cunitz G. Pathophysiologische Grundlagen, notfallmedizinische Aspekte und anaesthesiologische Maßnahmen beim schweren Schädel-Hirn-Trauma. Anaesthesist. 1987; 36 321-332
- 32 Singbartl G. Die Bedeutung der präklinischen Notfallversorgung für die Prognose von Patienten mit schwerem Schädel-Hirn-Trauma. Anästh Intensivther Notfallmed. 1985; 20 251-260
- 33 Stocchetti N, Furlan A, Volta F. Hypoxemia and arterial hypotension at the accident scene in head injury. J Trauma. 1996; 40 764-767
- 34 Strebel S. Therapie des Hirndrucks. Anaesthesist. 1994; 43 405-420
- 35 Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974; 2 81-84
- 36 Vollmer D G, Torner J C, Jane J A, Sadovnic B, Charlebois D, Eisenberg H M, Foulkes M A, Marmarou A, Marshall L F. Age and outcome following traumatic coma: Why do older patients fare worse?. J Neurosurg. 1991; (Suppl.)75 37-49
- 37 Wilberger J E, Cantella A. High-dose barbiturates for intracranial pressure control. New Horizons. 1995; 3 469-473
- 38 Wolf A L, Levi L, Marmarou A, Ward J D, Muizelaar P J, Choi S, Young H, Rigamonti D, Robinson W L. Effect of THAM upon outcome in severe head injury: a randomized prospective clinical trial. J Neurosurg. 1993; 78 54-59
Dr. Oberstarzt Alfred Thomas
Bundeswehrzentralkrankenhaus
Abt. X, Anästhesie, Intensivmedizin, Notfallmedizin, Schmerztherapie
Röbenacher Straße 170
56072 Koblenz
Email: alfred.thomas@t-online.de