Zusammenfassung
Rauch besteht aus einer Mischung von Erstickungs-, Reiz- und Giftgasen sowie aus Ruß.
Die Erstickungsgase erniedrigen den Sauerstoffpartialdruck in der Umgebungsluft. Die
Reizgase führen zum Bronchospasmus. Die Giftgase im Rauch sind die „giftigen Zwillinge”
Kohlenmonoxid und Blausäure, die zu einer Sauerstofftransport- bzw. Sauerstoffutilisationstörung
führen. Ruß reizt und verlegt die Atemwege und transportiert Chemikalien in den Bronchialbaum.
Die Behandlung besteht aus den üblichen Basismaßnahmen. Der Einsatz von 100 % O2 ist in diesem Zusammenhang eine gezielte Antidottherapie. Patienten, die bewusstlos
aufgefunden werden (GCS ≤ 9), müssen eine Therapie mit dem Zyanidantidot Hydroxocobalamin
vor Ort erhalten und in eine Klinik zur weiteren Beurteilung verbracht werden. Innerhalb
von 6 Stunden sollten sie einer HBO-Behandlung in einer Druckkammer zugeführt werden.
Patienten mit einer Bewusstseinstrübung (GCS = 10–13) oder nach einer Synkope sollten
ebenfalls mit HBO behandelt werden, wenn sie eine Kleinhirnsymptomatik oder ein COHB
> 25 % aufweisen. Patienten mit Bronchialspastik müssen im Krankenhaus behandelt werden
bis die Spastik beseitigt und der „peak flow” normalisiert ist. β2 -Adrenorezeptor-Agonisten, aber keine Glukokortikoide, können Anwendung finden. Bewusstseinsklare
Patienten ohne pulmonale Symptome benötigen keine stationäre Behandlung.
Abstract
Smoke is a mixture of asphyxiants, irritant and toxic (chemical asphyxiants) gases
as well as soot. The asphyxiants decrease the partial pressure of oxygen in the environment.
The irritants lead to bronchospasm. Chemical asphyxiants, the so called „toxic twins”
are carbon monoxide and cyanide which lead to a disturbance of oxygen transport and
utilisation. Soot may create mechanical obstruction and is transporting chemicals
intra-bronchially. Treatment consists of the usual basic measures. The application
of 100 % oxygen via mask or mechanical ventilation is an antidotal treatment under
such circumstances. The patients who are unconscious (GCS ≤ 9) must be treated with
the cyanide antidote hydroxocobalamin and be brought to a clinic for further assessment.
Within 6 hours after the incidence they have to undergo HBO-treatment. Patients with
clouding of consciousness (GCS 10–13) or following a syncope should also receive HBO
treatment if they are showing cerebellar symptoms or a COHb > 25 %. Patients who exhibit
bronchial spasm have to be admitted to hospital till symptoms disappear and peak-flow
is normal. β2 adrenoreceptor-agonists but no glucocorticoids can be used. Patients with a clear
consciousness without pulmonary symptoms do not require hospital admission.
Schlüsselwörter
Rauchgase - Kohlenmonoxid - Blausäure - Hydroxocobalamin - HBO
Keywords
smoke - carbon monoxide - cyanide - hydroxocobalamin - HBO
Literatur
1
Harwood B, Hall J R.
What kills in fires: Smoke inhalation or burns?.
Fire J.
1989;
84
29-34
2
Nelson G L.
Regulatory aspects of fire toxicology.
Toxicology.
1987;
47
181-199
3
Zikria B A, Ferrer J M, Floch H F.
The chemical factors contributing to pulmonary damage in „smoke poisoning”.
Surgery.
1972;
71
704-709
4
Herndon D N, Barrow R E, Linares H A. et al .
Inhalation injury in burned patients: Effects and treatment.
Burns Incl Therm Inj.
1988;
14
349-356
5
Teixidor H S, Rubin E, Novick G S. et al .
Smoke inhalation: Radiologic manifestations.
Radiology.
1983;
149
383-387
6
Basmer P, Zwick G.
Messung des Giftcocktails in Bränden.
FFZ.
2002;
3
176-185
7
Haldane J.
The action of carbonic oxide on man.
J Physiol.
1895;
18
430-462
8
Schönemann B, Soballa M.
Das Rauchgasinhalationstrauma. Zur Relevanz der präklinischen Kohlenmonoxidmessung
am Beispiel eines Personalwohnheimbrandes.
Notarzt.
2009;
25
151-154
9
Ben-Eli D, Peruggia J, McFarland J. et al .
Detecting CO-FDNY Prehospital Assessment of COHb.
JEMS.
2007;
10
36-37
10
Baud F J, Barriot P, Toffis V. et al .
Elevated blood cyanide concentrations in victims of smoke inhalation.
N Engl J Med.
1991;
325
1761-1766
11
Sylvester D M, Hayton W L, Morgan R L. et al .
Effects of thiosulfate on cyanide pharmacokinetics in dogs.
Toxicol Appl Pharmacol.
1983;
69
265
12 Ryan J G. Cyanide. Emergency Toxicology (P. Viccellio, ed), 2nd edition. Philadelphia;
Lippincott-Raven 1998: 969-978
13 Ellenhorn M J, Schonwald S, Ordog G. et al .Cyanide poisoning. In Ellenhorns Medical
Toxicology: Diagnosis and Treatment of Human Poisoning, 2nd ed. Baltimore, Maryland;
Williams and Wilkins 1997: 1476-1484
14
Piantadosi C A, Sylvia A L.
Cerebral cytochrome aa3 inhibition by Cyanide in bloodless rats.
Toxicology.
1984;
33
67-79
15
Birky M M, Clarke F B.
Inhalation of toxic products from fires.
Bull Ny Acad Med.
1981;
57
997-1013
16
Rorison D G, McPherson S J.
Acute toxic inhalations.
Emerg Med Clin North Am.
1992;
20
409-435
17
Horvath E P, DoPico G A, Barbee R A. et al .
Nitrogen dioxide-induced pulmonary disease.
J Occup Med.
1978;
20
103-110
18
Morgan W K.
The respiratory effects of particles, vapours, and fumes.
Am Ind Hyg Assoc J.
1986;
47
670-673
19
Charan N B, Meyers C G, Lakshminarayan S. et al .
Pulmonary injuries associated with acute sulfur dioxide inhalation.
Am Rev Respir Dis.
1979;
119
550-560
20
Stone J P, Hazlett R N, Johnson J E. et al .
The transport of hydrogen chloride by soot from burning polyvinyl chloride.
J Fire Flammabil.
1973;
4
42-51
21
Youn Y, Lalonde C, Demling R.
Oxidants and the pathophysiology of burn and smoke inhalation injury.
Free Radic Biol Med.
1992;
12
409-415
22
Brenner B E.
Bronchial asthma in adults: Presentation to the emergency department.
Am J Emerg Med.
1983;
3
306-333
23
Clark W R, Nieman G F.
Smoke inhalation.
Burns.
1988;
14
473-494
24
Nieman G F, Clark W R, Hakim T.
Methylprednisolone does not protect the lung from inhalation injury.
Burns.
1991;
17
384-390
25
Robinson N B, Hudson L D, Riem M. et al .
Steroid therapy following isolated smoke inhalation injury.
J Trauma.
1982;
22
876-879
26
Pace N, Stajman E, Walker E L.
Acceleration of carbon monoxide elimination in man by high pressure oxygen.
Science.
1950;
111
652-654
27
Sasaki T.
On half-clearance time of carbon monoxide haemoglobin in blood during hyperbaric oxygen
therapy (OHP).
Bull Tokyo Med Dent Univ.
1975;
22
63-77
28
Myers R A, Snyder S K, Linberg S. et al .
Value of hyperbaric oxygen in suspected carbon monoxide poisoning.
JAMA.
1981;
246
2478-2480
29
Ziser A, Shupak A, Halpern P. et al .
Delayed hyperbaric oxygen treatment for acute carbon monoxide poisoning.
Br Med J (Clin Res Ed).
1984;
289
960
30
Ilano A L, Raffin T A.
Management of carbon monoxide poisoning.
Chest.
1990;
7
165-169
31
Myers R A, Goldman B.
Planning an effective strategy for carbon monoxide poisoning.
Emerg Med Reports.
1987;
8
193-200
32
Weaver L K, Hopkins R O, Chan K J. et al .
Hyperbaric oxygen for acute carbon monoxide poisoning.
N Engl J Med.
2002;
347
1057-1067
33
Hampson N B, Zmaeff J L.
Outcome of patients experiencing cardiac arrest with carbon monoxide poisoning treatment
with hyperbaric oxygen.
Ann Emerg Med.
2001;
38
36-41
34
Jones J, McMullen J, Dougherty J.
Toxic smoke inhalation: Cyanide Poisoning in Fire Victims.
Am J Emerg Med.
1987;
5
317-321
35
Barillo D J, Goode R, Esch V.
Cyanide Poisoning in Victims of Fire: Analysis of 364 cases and review of the literature.
J of Burns & Rehabilitation.
1994;
15
46-57
36
Ballantyne B.
Changes in blood Cyanide as a function of storage time and temperature.
J For Sci Soc.
1976;
16
305-310
37
Fortin J L, Giocanti J P, Ruttimann M. et al .
Prehospital administration of hydroxocobalamin for smoke inhalation-associated cyanide
poisoning: 8 years of experience in the Paris fire brigade.
Clinical Toxicology.
2006;
44
37-44
38
Raphael J C, Elkharrat D, Jars-Guincestre M C. et al .
Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication.
Lancet.
1989;
2
414-419
39
Thom S R, Taber R L, Mendiguren I L. et al .
Delayed neuropsychologic sequelae after carbon monoxide poisoning: Prevention by treatment
with hyperbaric oxygen.
Ann Emerg Med.
1995;
25
474-480
40
Ducasse J L, Celsis P, Marc-Vergnes J P.
Non-comatose patients with acute carbon monoxide poisoning: Hyperbaric or normobaric
oxygenation?.
Undersea Hyperb Med.
1995;
22
9-15
41
Scheinkestel C D, Bailey M, Myles P S. et al .
Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: A randomised
controlled clinical trial.
Med J Aust.
1999;
170
203-210
42 Juurlink D N, Buckley N, Stanbrook M B. et al .Hyperbaric oxygen for carbon monoxide
poisoning. The Cochrane Collaboration, Cochrane Library 2009
1
43
Weaver L K, Valentine K J, Hopkins R O.
Carbon monoxide poisoning: risk for cognitive sequelae and the role of hyperbaric
oxygen.
Am J Respir Crit Care Med.
2007;
176
491-497
Prof. Dr. med. Thomas Zilker
Klinikum rechts der Isar II Medizinische Klinik und Poliklinik – Toxikologische Abteilung
Ismaninger Straße 22
81675 München
Telefon: 089/4140-2250
eMail: tox@lrz.tum.de