Early cellular brain damage and systemic inflammatory response after cardiopulmonary resuscitation or isolated severe head trauma: a comparative pilot study on common pathomechanisms
T. Mussack et al., Early cellular brain damage and systemic inflammatory response after cardiopulmonary resuscitation or isolated severe head trauma: a comparative pilot study on common pathomechanisms, RESUSCITAT, 49(2), 2001, pp. 193-199
Severe neurological deficits are common characteristics of patients survivi
ng cardiopulmonary resuscitation (CPR) or isolated severe head trauma (SHT)
. For comparative evaluation of underlying pathomechanisms, 22 patients wit
h out-of-hospital cardiac arrest and successful CPR as well as 10 patients
with SHT were included in our prospective study. Circulating S-100B was det
ermined as an indicator of cellular brain damage. Interleukin-8 (IL-8), sol
uble E-selectin (sE-selectin) and polymorphonuclear (PMN-) elastase were me
asured as markers of systemic inflammation following whole body ischaemia a
nd reperfusion injury. Venous blood samples were drawn on scene (median tim
e 11.0 min after starting basic life support) and in the intensive care uni
t (median time 12.5 h thereafter) in CPR patients and at admission to hospi
tal (median time 43.8 min after trauma) and approx. 12 h later in SHT patie
nts. Biochemical parameters in these samples were compared with specimens t
aken from 20 healthy volunteers. Initial median S-100B levels of the CPR an
d SHT patients were both significantly increased compared with the controls
. Twelve hours later, significant falls in S-100B revealed no differences b
etween the two patient groups, but did not reach control values. Median IL-
8 and sE-selectin levels entry to the study were elevated in both patient g
roups compared with controls and showed further rises within the following
12 h. Finally, increased initial median levels of PMN-elastase revealed sig
nificant differences between the patient groups and between patients and co
ntrols. Twelve hours later, median PMN-elastase values were equally elevate
d in the CPR and SHT subjects. Our preliminary data suggest similar pathome
chanisms occurring after both CPR and SHT. Both clinical entities seem to b
e associated with early transient cellular brain damage as shown by prolong
ed rapidly increasing and subsequent fall in S-100B serum levels. In contra
st, the prolonged elevation of circulating IL-8, sE-selectin and PMN-elasta
se may indicate a very similar systemic inflammatory response by endothelia
l cells and neutrophils initiated by ischaemia and reperfusion injury in bo
th conditions. Further studies should be carried out to determine the cause
and the prognostic value of these biochemical parameters in relation to lo
ng-term neurological outcome. (C) 2001 Elsevier Science Ireland Ltd. All ri
ghts reserved.