Clinical Trial Details
— Status: Recruiting
Administrative data
| NCT number |
NCT03192956 |
| Other study ID # |
EPN 552-16 |
| Secondary ID |
|
| Status |
Recruiting |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
May 1, 2017 |
| Est. completion date |
December 30, 2025 |
Study information
| Verified date |
December 2023 |
| Source |
Sahlgrenska University Hospital, Sweden |
| Contact |
Anders Rosén, PhD |
| Phone |
+46725088800 |
| Email |
bandersrosen[@]gmail.com |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
Research hypothesis
- There is a correlation between the quantity of fluid markers of CNS injury in blood and
DCS.
- There is a correlation between quantity and kind of fluid markers of CNS injury in blood
and both diving profile and severity of DCS.
- There is a correlation between the quantity of inflammatory markers in blood an DCS.
Objectives:
- Assess whether individuals suffering decompression sickness exhibit fluid markers of
central nervous system injury.
- Evaluate the correlation between quantity and kind of fluid marker of CNS injury and
clinical signs of neurological impairment.
- Evaluate the correlation between quantity and kind of fluid marker of CNS injury and
clinical outcome after 3-6 months.
- Assess whether individuals suffering decompression sickness exhibit inflammatory markers
in blood.
Description:
Decompression sickness (DCS) is a risk associated with diving. Common symptoms are joint and
limb pain, skin rash, ataxia, hemiplegia, visual disturbances, paresthesias, limb numbness,
nystagmus and vertigo. Treatment consists of recompression in a hyperbaric chamber, commonly
referred to as hyperbaric oxygen treatment (HBOT).
It has been thought since the last quarter of the 19th century that DCS is caused by bubble
formation in the tissues when dissolved inert gas comes out of solution. It was long thought
that decompression schedules that did not give rise to any gas bubbles in the body also
averted DCS. However, with the advent of ultrasound Doppler technology in the 1970s it was
found that intravascular gas bubbles could exist even after uneventful dives. Dives well
within limits established by military and sports authorities have been shown to generate
intravascular bubbles. Hence, additional pathophysiological factors have been sought.
There is evidence of endothelial dysfunction, coagulopathy and inflammatory activation after
diving. Though, their role in the pathophysiology of DCS remains to be determined.
Studies have shown that fluid markers of CNS injury can be found in blood samples obtained
from athletes practising ice-hockey, boxing and american football. There is reason to believe
that fluid markers of CNS injury will be present in blood samples obtained from divers with
DCS as well.
Study subjects will be recruited by the attending physician at the Hyperbaric chamber at
SU/Omrade 2 after the patient has been given a diagnosis of decompression sickness. Prior to
treatment in the hyperbaric chamber, 4 ml of blood will be drawn via a plastic intravenous
catheter that is placed in an arm vein as part of normal, established care of injured divers
in the Emergency Department (to provide intravenous fluid and medications). A second 4 ml
sample will be obtained from the same catheter after the patient has completed treatment (the
typical hyperbaric treatment for decompression sickness lasts ~5.5 hours). The study object
will also provide information regarding his/her general health and the completed dive. All
study data, including blood samples, will anonymized and provided with a study code.
When feasible, blood samples will be obtained 1 week and 3-6 months after HBOT. These samples
will be handled the same as the two obtained on the day of injury.
