DrBaboon
11-26-05, 00:46
I'm still jumping around in Austere Medicine, so I have both an incomplete view of the book, and might have some other ideas in the future.
Thought I'd toss out a couple topics to consider when revising - they are somewhat related.
Bed Sores is a topic in the book. I'd like to suggest working on it a bit more.
Risk assessment for Pressure Ulcers as published isn't bad, but can be updated. Geriatric Medicine has used Braden Scales for risk assessment for almost 20 years, and it's a useful tool. In many ways, it recapitulates what's in the book already, but this is a handy way to get it done and get people thinking about risk. It's also user-friendly, and can be part of a simple chart. Of my 2 hospitals, both took forever to adopt the use of Braden Scales.
Here's the catch - while the Braden Scale was a landmark tool in the mid-1980's, it's been surpassed. It's just that people are even less familiar with the "better" tools than the Braden Scale.
The Braden Scale assumes that its risk factors are equal to each other in terms of impact, and that they are additive. It's also possible to have people with higher Braden scores who are really not going to get pressure ulcers - so that you spend a lot of poorly triaged time working with people who don't need time spent on them that way. For example - the ambulatory patient with crummy skin and poor nutrition. The key thing is that they are ambulatory - so that will outweigh their other identified risks.
The newer epidemiology on Pressure Ulcer development is that the root is someone who does not reposition themself, and then the other risks stack onto that immobility. The risks do not add up as they stack on top of immobility, they multiply - so additional risks are worse than what the Braden Scale predicts.
http://www.bradenscale.com/bradenscale.htm
All in all - my suggestion is to incorporate mention of the Braden Scale - it's simply so widespread as to be "the coin of the realm" inspite of having been surpassed in some ways. We can easily add text to the book to make the spirit of that information available.
I'll also make a pitch for understanding the mechanism of injury in pressure ulcers. It's ischemia. There is sufficient application of pressure to occlude blood flow. The time frame to develop a pressure ulcer is as short a time as it takes for tissue to die from being deprived of blood flow. The depth and territory of the pressure ulcer is going to depend on the territory of the ischemia. Pressure tends to distribute in tissue as a "truncated cone." Sort of like bullets in a .40S&W round. The smaller area - the actual truncated part of the cone - is at the skin surface. The wider part of the cone is deep in the tissue. That's where undermining and other wound geometry comes into play in pressure ulcer development.
Our collegues in anesthesia are probably even more sensitive to this topic than those of us in geriatrics. Immobile patients under anesthesia for prolonged surgeries have high risks for peripheral nerve injuries, as well as pressure ulcer development.
Here's an extreme example, and one that's certainly not an everyday need.
Imagine a patient with a temporal-parietal aneurysm who is going to a craniotomy in a lateral position. It turns into a 12 hour surgery, possibly including a hypotensive anesthesia technique.
They show up in the recovery room with a swollen, necrotic ear on the contralateral side.
Ischemia.
The other suggestion is that I think the section on wound debridement could be broadened.
There is sharp instrument/surgical debriding, which is what is discussed in the book.
There is also auto-lytic debriding - which occurs naturally, and can be hastened by some of the debriding agents we apply. There are indications for either approach.
The maggot discussion is pretty helpful, and has elements of both surgical and auto-lytic debriding. I've had a little experience with maggots - it's often been a major upset to the staff, whether it's been used intentionally or unintentionally. The 2 key things in my experience are getting "sterile" maggots, and having a reasonable dressing constructed to keep the maggots captive. There's good information on the subject in the book already, but some mention of some other materials for dressings are merited.
Some/many of those types of supplies are applicable in other aspects of chronic wound care, including pressure ulcers.
I'd propose a simple rationale for changing dressings, and selecting dressing material.
Something like: The junkier the wound, the more often you change the dressing, and the more you want the dressing to stick to the wound. The cleaner the wound (and the more the wound is trying to heal), you want to change the dressing as infrequently as possible, and you want dressing materials which don't stick to the wound.
Inevitably, dressing materials stick to any wound, to some extent. Changing a dressing is a debriding method - whether you intend for it to be debriding or not.
The "brick wall" that you hit, is that sooner or later you start removing healthy tissue that is part of the wound's attempt to heal, and you delay or prevent wound healing.
Gauze is a mainstay of dressings which we all use. It is, however, an instrument of debriding wounds. There is no such thing as not having it stick to a wound, and the wound base gets caught in the weave of the gauze. It sticks less when we apply saline, but it still debrides. If the wound is junky and needs debriding, that's desireable - for now. It's probably not nearly so desireable a few days or a week into the care of that wound.
The use of gauze also means changing the dressing more often. Even if we apply saline, it will evaporate in however many hours, leaving a dried wound base, and in all likeklyhood, killing more tissue in the wound. If we change the dressing before it dries out, we are changing the wound too often, but if we change it once or twice a day, we're letting the wound dry out (and we're still possibly changing it too often if it no longer needs debriding). So these requirements are in conflict with each other, and they each cause further damage to the wound.
This probably means having at least some more modern dressing materials available (or figuring out a way to improvise or approximate what they offer), which optimize the extent of wound hydration, have a semi-permeable barrier over the wound, and are sticky enough to remain in place but are not so sticky to remove much granulation tissue from the wound bed if it no longer needs debriding. The alginate dressing materials, hydrocolloids, and other materials fit that bill.
FWIW - hydrocolloids are also good top dressings to keep maggots in captivity.
Thought I'd toss out a couple topics to consider when revising - they are somewhat related.
Bed Sores is a topic in the book. I'd like to suggest working on it a bit more.
Risk assessment for Pressure Ulcers as published isn't bad, but can be updated. Geriatric Medicine has used Braden Scales for risk assessment for almost 20 years, and it's a useful tool. In many ways, it recapitulates what's in the book already, but this is a handy way to get it done and get people thinking about risk. It's also user-friendly, and can be part of a simple chart. Of my 2 hospitals, both took forever to adopt the use of Braden Scales.
Here's the catch - while the Braden Scale was a landmark tool in the mid-1980's, it's been surpassed. It's just that people are even less familiar with the "better" tools than the Braden Scale.
The Braden Scale assumes that its risk factors are equal to each other in terms of impact, and that they are additive. It's also possible to have people with higher Braden scores who are really not going to get pressure ulcers - so that you spend a lot of poorly triaged time working with people who don't need time spent on them that way. For example - the ambulatory patient with crummy skin and poor nutrition. The key thing is that they are ambulatory - so that will outweigh their other identified risks.
The newer epidemiology on Pressure Ulcer development is that the root is someone who does not reposition themself, and then the other risks stack onto that immobility. The risks do not add up as they stack on top of immobility, they multiply - so additional risks are worse than what the Braden Scale predicts.
http://www.bradenscale.com/bradenscale.htm
All in all - my suggestion is to incorporate mention of the Braden Scale - it's simply so widespread as to be "the coin of the realm" inspite of having been surpassed in some ways. We can easily add text to the book to make the spirit of that information available.
I'll also make a pitch for understanding the mechanism of injury in pressure ulcers. It's ischemia. There is sufficient application of pressure to occlude blood flow. The time frame to develop a pressure ulcer is as short a time as it takes for tissue to die from being deprived of blood flow. The depth and territory of the pressure ulcer is going to depend on the territory of the ischemia. Pressure tends to distribute in tissue as a "truncated cone." Sort of like bullets in a .40S&W round. The smaller area - the actual truncated part of the cone - is at the skin surface. The wider part of the cone is deep in the tissue. That's where undermining and other wound geometry comes into play in pressure ulcer development.
Our collegues in anesthesia are probably even more sensitive to this topic than those of us in geriatrics. Immobile patients under anesthesia for prolonged surgeries have high risks for peripheral nerve injuries, as well as pressure ulcer development.
Here's an extreme example, and one that's certainly not an everyday need.
Imagine a patient with a temporal-parietal aneurysm who is going to a craniotomy in a lateral position. It turns into a 12 hour surgery, possibly including a hypotensive anesthesia technique.
They show up in the recovery room with a swollen, necrotic ear on the contralateral side.
Ischemia.
The other suggestion is that I think the section on wound debridement could be broadened.
There is sharp instrument/surgical debriding, which is what is discussed in the book.
There is also auto-lytic debriding - which occurs naturally, and can be hastened by some of the debriding agents we apply. There are indications for either approach.
The maggot discussion is pretty helpful, and has elements of both surgical and auto-lytic debriding. I've had a little experience with maggots - it's often been a major upset to the staff, whether it's been used intentionally or unintentionally. The 2 key things in my experience are getting "sterile" maggots, and having a reasonable dressing constructed to keep the maggots captive. There's good information on the subject in the book already, but some mention of some other materials for dressings are merited.
Some/many of those types of supplies are applicable in other aspects of chronic wound care, including pressure ulcers.
I'd propose a simple rationale for changing dressings, and selecting dressing material.
Something like: The junkier the wound, the more often you change the dressing, and the more you want the dressing to stick to the wound. The cleaner the wound (and the more the wound is trying to heal), you want to change the dressing as infrequently as possible, and you want dressing materials which don't stick to the wound.
Inevitably, dressing materials stick to any wound, to some extent. Changing a dressing is a debriding method - whether you intend for it to be debriding or not.
The "brick wall" that you hit, is that sooner or later you start removing healthy tissue that is part of the wound's attempt to heal, and you delay or prevent wound healing.
Gauze is a mainstay of dressings which we all use. It is, however, an instrument of debriding wounds. There is no such thing as not having it stick to a wound, and the wound base gets caught in the weave of the gauze. It sticks less when we apply saline, but it still debrides. If the wound is junky and needs debriding, that's desireable - for now. It's probably not nearly so desireable a few days or a week into the care of that wound.
The use of gauze also means changing the dressing more often. Even if we apply saline, it will evaporate in however many hours, leaving a dried wound base, and in all likeklyhood, killing more tissue in the wound. If we change the dressing before it dries out, we are changing the wound too often, but if we change it once or twice a day, we're letting the wound dry out (and we're still possibly changing it too often if it no longer needs debriding). So these requirements are in conflict with each other, and they each cause further damage to the wound.
This probably means having at least some more modern dressing materials available (or figuring out a way to improvise or approximate what they offer), which optimize the extent of wound hydration, have a semi-permeable barrier over the wound, and are sticky enough to remain in place but are not so sticky to remove much granulation tissue from the wound bed if it no longer needs debriding. The alginate dressing materials, hydrocolloids, and other materials fit that bill.
FWIW - hydrocolloids are also good top dressings to keep maggots in captivity.