what?
I recently attended an isolated arm trauma where the patient, a 55yom with no previous medical history, caught his arm on and was a corrugated metal fence while 7' up on a ladder, and was thereby suspended fully for a few seconds.
The patient sustained an approximately 6" laceration across his left antecubital fossa (ACF), which evolved into a skin flap approximately 4" in length. Ligament, adipose tissue, and vasculature was exposed.
On examination, the patient's neurovascular supply was grossly intact -- bounding radial pulse, fast capillary refill, and intact range of motion and sensation. There was no evidence of catastrophic or even significant haemorrhage requiring compression -- he appeared to have missed every single important structure (of which there are many) in the ACF.
In discussing this case with a colleague, they brought up the concept of 'ateriospasm.' They said that due to vasospasm in response to trauma, initial examination could suggest that there was no arterial compromise, but after up to 30 minutes the spasm could elapse, causing a delayed catastrophic bleed -- possibly with a higher chance of being missed if the wound has already been bandaged.
They suggested, in a case of severe trauma to an area with arteries close to the surface (such as the ACF), leaving an untightened tourniquet in situ proximally from the wound.
I decided to consult the evidence base and guidance surrounding this concept.
so what?
Evidence describing the phenomenon of delayed bleeding due to vasospasm is rare. Some post-operative case studies report various types of delayed bleeding phenomena. One case study described a delayed arterial bleed multiple days onwards from a pubic rami fracture -- this was due to a slow forming pseudoanuerysm caused by initially minor vascular damage.1
I also reviewed guidelines on the general management of haemorrhage. 2
Both these sources stress the importance of combating trauma-induced coagulopathy, mentioning the 'lethal triad' of acidosis, hypothermia, and coagulopathy. Interestingly, one source3 made the distinction between dilutional coagulopathy (due to volume replacement with fluids not containing haemoglobin or clotting factors) and consumptive coagulopathy (consumption of endogenous clotting factors due to activation of the clotting cascade -- the body may require exogenous clotting factors to keep up with demand in the case of catastrophic haemorrhage).
Prehospital efforts to avoid the lethal triad represent an opportunity to improve patient outcomes in major or potential haemorrhage, beyond the immediate cessation of bleeding via direct pressure or tourniquet.
now what?
Although common teaching and the evidence base do not support the concept of delayed-onset bleeding from vasospasm, such a thing is conceivable, especially if coagulopathy has impaired the formation of a clot at the terminus of a damaged vessel.
Control of coagulopathic environmental factors (chiefly temperature) is a prudent measure to combat this, and in general. O2 therapy, if indicated, or even breath coaching if a patient is experiencing anxiety or hyperventilation, due to a significant wound that is traumatic in appearance, may also help to prevent respiratory acidosis. Wounds and vitals should also be periodically checked in case of the eruption of a delayed bleed.