Purpose: Trauma has the potential to cause haemorrhage, tissue damage, pain, visceral manipulation and psychological distress. Each of these consequences of trauma can cause changes in autonomic outflow, which dictates a patient's vital signs. Patients who are hypotensive and bradycardic due to a vagally mediated parasympathetic response to pain, psychological distress and visceral manipulation may be confused with those who exhibit bradycardia and hypotension following significant blood volume loss.
Methods: This review summarises literature that describes specific stimuli, patterns of injury and patient characteristics that are associated with a non-haemorrhagic vagal response to trauma.
Results: Twenty-six records described predominantly parasympathetic responses to trauma (both blunt and penetrating) and surgery ("iatrogenic trauma"). Such a non-haemorrhagic vagal response occurs following a wide variety of injury patterns. Patient age and sex are poor predictors of the likelihood of a non-haemorrhagic vagal response. The development and resolution of a non-haemorrhagic vagal response occurs over a heterogenous time period. It is unclear whether speed of onset and resolution is linked to the pattern of injury or other factors causing a predominantly parasympathetic response following non-haemorrhagic trauma.
Conclusion: The pattern of injury, patient demographic and speed of onset / resolution associated with the non-haemorrhagic vagal response to trauma may is heterogenous. It is therefore challenging to clinically distinguish between the hypotensive bradycardia due to hypovolaemia secondary to haemorrhage, or a parasympathetic response to trauma in the absence of bleeding.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11599317 | PMC |
http://dx.doi.org/10.1007/s00068-024-02648-y | DOI Listing |
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