Doctors spot early nerve damage in ICU patients within hours of admission
Critically ill patients show signs of nerve dysfunction within 24 hours of intensive care admission, according to new research. The finding could help hospitals identify which patients face higher risk of long-term paralysis and muscle wasting, potentially changing treatment priorities and improving outcomes for ICU survivors.
Originaltitel: Changes of motor nerve membrane excitability during the acute phase of critical illness.
Nervexcitabilitetstestning kan bli ett tidigare diagnostiskt verktyg för att skilja muskelskada från nervskadering på intensivvården. Studie från Bern University Hospital visar att alla 26 kritiskt sjuka patienter uppvisade nervhypoexcitabilitet redan inom 24 timmar efter intubation, vilket bestod till dag 10. Endast patienter med akut njursvikt (AKI) utvecklade ytterligare nervmembrandepolarisering. Vid dag 10 hade 15,4 procent av patienterna kritisk sjukdomspolyneuropati, medan 23,1 procent visade myosinförlust förenlig med kritisk sjukdomsmyopati. Forskare från Uppsala universitet deltog i analysen av muskelprover. Resultaten förändrar förståelsen för svaghet vid intensivvård — myosinförlust, inte nervskadering, verkar vara huvudorsaken. För inköpschefer och chefsläkare betyder det att standardiserad nervexcitabilitetstestning kan möjliggöra snabbare differentiering och optimerad rehabplanering på IVA.
OBJECTIVE: To investigate early alterations in motor nerve membrane properties during critical illness using nerve excitability testing. METHODS: Adult critically ill patients admitted to the intensive care unit were examined within 24 h of intubation (day 1) and on days 2, 5 and 10. Examinations included neurological examination, nerve excitability testing, laboratory analyses and review of medication records; and on day 10 conventional nerve conduction studies, electromyography and a fine needle muscle biopsy. RESULTS: All critically ill patients (N = 26) showed nerve hypoexcitability within 24 h compared to healthy subjects, which persisted up to day 10. Additional nerve membrane depolarisation was only observed in critically ill patients with acute kidney injury (AKI) (n = 13). Four patients fulfilled the diagnostic criteria for critical illness polyneuropathy (CIP) at day 10 (15.4%), and six (23.1%) had a reduced myosin:actin ratio indicative of myosin loss consistent with critical illness myopathy. CONCLUSIONS: Nerve hypoexcitability appears to be a key feature of the early phase of critical illness, whereas additional nerve membrane depolarisation is associated with AKI, which may be linked to changes in serum potassium levels. SIGNIFICANCE: The findings do not support CIP as predominant explanation for nerve membrane depolarisation and muscle weakness seems to be associated with myosin loss.