Suspension Trauma / HHS treatment recommendations

[cavedoc]

The report that Dwight posted (I haven't read it all) mentions a thing call 'Rescue Death' in other words it there have been several people recorded who have been pulled off rope in otherwise perfect health and no serious injuries as the result of the fall but they have died within hours or days of being taken off rope, autopsies have then been done to find the cause(s) of thier deaths. I won't try to explain these but generally consistant with blood pooling and the build up of blood toxins <snip>

Incidently the report Dwight posted seems to make a lot of the same recomendations as the website however it does have references which is useful.

Yeah. When I couldn't open the original I dug around on the web site and found a pdf of Joe Ivy's summary. Now I've skimmed the report Dwight recommended. The web site and the report do parallel each other pretty well. I will try to pull some of those references. Some things do strike me having read it now--some of the cited references recommended lying flat while others recommended the keeping upright, but the final conclusion is to maintain upright. Yet the articles that actually addressed what they did when when people felt ill or fell unconscious was to lay them down flat, and they all felt better.

The "rescue death" issue is a mixed bag. Death a few days later is from end organ damage from the shock. The concerning ones are those who died a few minutes after rescue. Several hypothesize that this is a right sided heart failure from acute volume overload. Interesting hypothesis. Interesting too that they then recommend giving more fluid. I haven't managed to sort that one out in my head yet.

The volume overload issue might be why there is no problem in the OR with tourniquets since volume is not trapped in the limb in that situation.

Interesting discussion here. I'll try to pull some of those references from Dwight's/Seddon's summary. And if any of you pick me off a rope unconscious, you can lay me flat until I get those references.

[kmstill]

Sorry for the late comment, just found the thread and adding in my $0.02 concerning animal models. Length is a bit long, so feel free to stop reading now.

My understanding of harness hang is that it's primarily an ischemic-reperfusion event (compartment syndrome, crush injury...). There is actually a significant body of work concerning ischemia-reperfusion injuries in animals. Common clinical scenarios include the feline saddle thrombus (clot blocking lower aorta), canine GDV (twisted stomach blocking off blood flow), and myelitis secondary to prolonged or surgical recumbency in large animals (surgery, downer cow, slinging). Add to this the tome of animal model research studies, mostly focused on myocardial or spinal ischemia (obvious animal model for human benefit).

Without getting into the biochem physiology too heavily, the nutshell of the current understanding is that 1) we don't know enough and 2):
Lack of oxygen to tissue cells eventually depletes ATP and negatively impacts ATP-driven cellular functions. This (jump a bunch of steps) ultimately results in production of Reactive Oxygen Species (ROS) and a marked change in intra-vs-extracellular electrolyte balance. These free-radical ROSs alter cell membranes, affect electrolyte balances, and damage/kill cells. Organs especially sensitive to this damage include the heart, lungs, kidney, liver, and intestine; ultimately (given enough time), multiple organs crash and burn (multi-organ dysfunction syndrome, MODS) leading to death.

Significant electrolyte changes include increased potassium (released from damaged tissue and compounded by acidosis secondary to lactate release from damaged tissue) and decreased calcium (secondary to increased cellular influx due to ROS damage and to hypophospotemia from kidney compromise) as well as others. Both of these electrolytes play a significant role on heart contractility and rhythm and alone can lead to fatal arrhythmias. Already stressed/ sensitized hearts are affected more by changes in these electrolytes than are healthy hearts.

Numerous other factors also play a role, and the immune system itself has become implicated as a major player in reperfusion injuries (tissue damage, cytokines, inflammation....). It's worth a brief comment that reperfusion mechanisms (e.g. non-septic systemic inflammation) share many elements with infectious/septic systemic inflammation. Those of you on the human medicine side are well aware of the cardiac sensitives of septic patients; vets know well how sensitive a cow with toxic mastitis is to calcium administration.

As for tourniquet vs. harness hang - even the most basic of tourniquet events will have measurable (if not clinical) reperfusion effects (this has been well demonstrated on mice). In my understanding though, it seems to be a factor of time x tissue (muscle) mass to create a dose-dependent clinical effect, all of course moderated by the underlying condition of the individual animal/patient. I've personally used tourniquets in surgery on cows, horses, cats, and dogs with no clinical negative effects - though my applications are usually on distal extremities (low muscle mass) and for short (<20 min) periods. Compare that to harness hang, where the majority percent of the body's large muscle masses are affected and the patient is classically unconscious, minimizing any muscular contribution to blood flow. Similarly, in the vet world, muscle perfusion/ myositis as a direct injury is of greatest concern when anesthetizing large animals (e.g. horse, cow) due to their weight and mass. It's my expectation (though not fact - any info out there on this?) that the relatively short time frame necessary to develop harness hang must be offset by significant muscle tissue involvement and ROS generation. Another comment is that prior (short) ischemia-reperfusion events are actually protective in future ischemia-perfusion injuries. Perhaps the typical harness hang individual is actually set up by general health and lack of preceding incidents?

Treatment wise - I'd be interested in hearing more about what the current "best practices" are from the human docs. We're hitting the animals with a variety of drugs (dependent of course on underlying cause), many with questionable efficacy and lack of great alternatives. One new direction is in antileukocyte therapy. One mainstay has become lidocain tx. What/ what else are you all doing?

Sorry for the monologue.
Kelly :)