This topic was broached in another thread and I was asked to do a write up about it, so here it is.
First I must disclaim that I cannot possibly cover every detail in this thread. So I plan to condense it to what I think is important to this discussion, based on my knowledge, education and experience.
Here we go:
True Aortic Aneurysm: is defined as a permnant and irreversable widening of the blood vessel. In order to fit the criteria the dilation should be >50% of the diameter. (normal infrarenal values: 14-24mm in males, 12-21mm females) making any dialation 3cm or larger in a male or 2.6cm in a female an aneurysm.
The location of the abdominal aneurysm is often infrarenal, however it can be superior to or even involve the renal arteries. Also high as above the celiac artery. It often involves collateral circularing arteries such as the hypogastic, rarely inferior mesenteric, and 1 or 2 others, plus normal anatomical variations.
The thoracic aneurysm is often just at the level of the aortic valve (which has a directimpact on the valve function and well as coronary circulation.
The reason for the abd localization is still under investigation. The prominant thoeries are that it is a collagen metabolism/structure deficency as well as tissue apoptosis from lack of blood supply from the absence of the vaso vasorum at this level, nonenzymatic glycosylization, atherosclerotic changes and hypertension.
Like all things where there are competing theories, the truth probably involves some combination.
The most important distinction of an aneurysm is that it involves all layers of the muscular artery.
So what does that mean to EMS?
There are several clinical findings that can point towards a potential Aortic aneurysm.
Risk factors include: HTN, smoking, family hx, currently under observation of aneurysm and male sex. (9:1 m/f ratio)
The most common findings in the thorax is: no symptoms followed by: chest pain radiating to the back, aortic regurgitation (heart tone), or cardiac failure from acute aortic syndrome. (look it up)
In the abd. is abd pain again radiating to the back. Palpable mass which increases in size on systole. Usually found in the area of the umbilicus, but anywhere from the costal margin to the bifurcation of the illiac ateries (which may be included) at the level of the umbilicus.
Usually minimally palpable aneurysm is 3cm. Which requires immediate evaluation and treatment. Especially if the pt has been taking nsaids. The sensitivity is ~50%. However the sensitivity increases as the size does being almost 80% sensitive at 5cm. (which is considered a vascular surgical emergency) Basically if the mass is bigger than all 4 of your fingers palpating it, life is bad.
This can be found on skillful palpation, ultrasonography, CXR, or CT. You do not need the radiology, but it really helps in fat people, where palpation is often difficult at best.
Which brings us to: The ruptured aortic aneurysm.
-Sudden onset of CP or abd pain. (often radiating to the back/retroperitoneal space)
-Sudden collapse with transient hypotension/ALOC.
-History of aneurysm
-Rapid onset of pain/hypotension/sweating
-Unequal pulse or BP in upper extremities
-Absent/weak pulses or mottling/cyanosis in the lower exremities.
(for brevity, surgical treatment won't be described)
By the book, only 50% of rupture patients make it to the hospital alive.
75%-95% die prior to completion of surgery. The ones who make it out of surgery can see post op complications increasing the mortality as high as 99%
Common complications include in order of occurance:
-Death (multiple etiologies including brain ischemia and swelling from the acute event, surgery, and resuscitation attempts)
-Renal failure
-Lower limb embolization
-Iscemic gut or infarction
The recommendations in our surgical textbook (and consequently our hospitals) include:
-Immediate transfer to the OR without resuscitation attempts in the ED.
-2 large bore IVs but no fluid resuscitation therapy prior to the entire surgical team being ready at the patient's side
-High flow oxygen via NRB prior to intubation
-Modest doses of analgesia (5-10mg morphine or equivalent)
-Fluid resuscitation to begin during surgery starting with 8 units FFP and PRBCs (or whole blood which to my knowledge is only used by the military) and 8 units platelts.
(I intentionally left out discussion on pseudoaneurysm, cerebral aneurysm, and peripherial aneurysm or I would be typing for weeks.)
What this all means is:
A ruptured aneurysm is extremely difficult to treat and survive. EMS can easily make these efforts futile by initiating crystalloid resuscitation or transporting the pt to a facility without onstaff surgical capability.
Facilities, in my experience, without surgical staff who receive these patients immediately terminate efforts and resort to end of life procedures.
Some ALS treatments which support other organ function like RSI may be beneficial to these patients. However, this is one of the few time critical emergencies EMS will see, and as was pointed out in the other thread, a BLS response and mindset maybe more beneficial.
The intracranial swelling on a patient with no blood in their veins is moot.
Rasing a systolic or even measuring systolic BP is moot. The location of the hemorrhage and the leaking of the vessle wall will cause the patient to bleed out faster or cause total wall rupture.
Additionally, SBP does not correlate to CVP which means you are measuring blood (via pressure) going out, but not blood coming back. Since organs (firstly the heart) are perfused by oxygenated blood completing the circuit, a break in the circuit makes your pressure measurements completely useless. Particularly if you are measuring water pressure instead of blood pressure because you infused a crystalloid.
There was a study done, if I recall properly, by Dr. McSwaine that showed MAST can increase intraperitoneal pressure and pneumatically tamponade the aorta and control bleeding by reducing the space the bleed can go into specific to this pathology.
Likewise, I have postulated in traumatic blood loss a long spineboard can act to increase pressure and reduce the space in the same manner as a surgical retropritoneal pack technique.
I know most EMS providers will now be thinking "our protocol says..." and I will agree it probably does.
But it may have been written based on "internal hemorrhage" using thoery postulated in the 1960s, instead of specifically to "ruptured aortic aneurysm" with the knowledge of 2011.
While I always welcome the thoughts of the people here, I hope that serious consideration will be given to how you are treating the patient when you suspect this pathology.
Rather than simply following a protocol, there is always the option to contact medical control and have a chat about it. While tht may seem counter intuitive. Arguing against a treatment that is far more likely to harm the very small chance the patient has survive is not only patient advocacy, but better medicine that performing that treatment inspite of such knowledge.
First I must disclaim that I cannot possibly cover every detail in this thread. So I plan to condense it to what I think is important to this discussion, based on my knowledge, education and experience.
Here we go:
True Aortic Aneurysm: is defined as a permnant and irreversable widening of the blood vessel. In order to fit the criteria the dilation should be >50% of the diameter. (normal infrarenal values: 14-24mm in males, 12-21mm females) making any dialation 3cm or larger in a male or 2.6cm in a female an aneurysm.
The location of the abdominal aneurysm is often infrarenal, however it can be superior to or even involve the renal arteries. Also high as above the celiac artery. It often involves collateral circularing arteries such as the hypogastic, rarely inferior mesenteric, and 1 or 2 others, plus normal anatomical variations.
The thoracic aneurysm is often just at the level of the aortic valve (which has a directimpact on the valve function and well as coronary circulation.
The reason for the abd localization is still under investigation. The prominant thoeries are that it is a collagen metabolism/structure deficency as well as tissue apoptosis from lack of blood supply from the absence of the vaso vasorum at this level, nonenzymatic glycosylization, atherosclerotic changes and hypertension.
Like all things where there are competing theories, the truth probably involves some combination.
The most important distinction of an aneurysm is that it involves all layers of the muscular artery.
So what does that mean to EMS?
There are several clinical findings that can point towards a potential Aortic aneurysm.
Risk factors include: HTN, smoking, family hx, currently under observation of aneurysm and male sex. (9:1 m/f ratio)
The most common findings in the thorax is: no symptoms followed by: chest pain radiating to the back, aortic regurgitation (heart tone), or cardiac failure from acute aortic syndrome. (look it up)
In the abd. is abd pain again radiating to the back. Palpable mass which increases in size on systole. Usually found in the area of the umbilicus, but anywhere from the costal margin to the bifurcation of the illiac ateries (which may be included) at the level of the umbilicus.
Usually minimally palpable aneurysm is 3cm. Which requires immediate evaluation and treatment. Especially if the pt has been taking nsaids. The sensitivity is ~50%. However the sensitivity increases as the size does being almost 80% sensitive at 5cm. (which is considered a vascular surgical emergency) Basically if the mass is bigger than all 4 of your fingers palpating it, life is bad.
This can be found on skillful palpation, ultrasonography, CXR, or CT. You do not need the radiology, but it really helps in fat people, where palpation is often difficult at best.
Which brings us to: The ruptured aortic aneurysm.
-Sudden onset of CP or abd pain. (often radiating to the back/retroperitoneal space)
-Sudden collapse with transient hypotension/ALOC.
-History of aneurysm
-Rapid onset of pain/hypotension/sweating
-Unequal pulse or BP in upper extremities
-Absent/weak pulses or mottling/cyanosis in the lower exremities.
(for brevity, surgical treatment won't be described)
By the book, only 50% of rupture patients make it to the hospital alive.
75%-95% die prior to completion of surgery. The ones who make it out of surgery can see post op complications increasing the mortality as high as 99%
Common complications include in order of occurance:
-Death (multiple etiologies including brain ischemia and swelling from the acute event, surgery, and resuscitation attempts)
-Renal failure
-Lower limb embolization
-Iscemic gut or infarction
The recommendations in our surgical textbook (and consequently our hospitals) include:
-Immediate transfer to the OR without resuscitation attempts in the ED.
-2 large bore IVs but no fluid resuscitation therapy prior to the entire surgical team being ready at the patient's side
-High flow oxygen via NRB prior to intubation
-Modest doses of analgesia (5-10mg morphine or equivalent)
-Fluid resuscitation to begin during surgery starting with 8 units FFP and PRBCs (or whole blood which to my knowledge is only used by the military) and 8 units platelts.
(I intentionally left out discussion on pseudoaneurysm, cerebral aneurysm, and peripherial aneurysm or I would be typing for weeks.)
What this all means is:
A ruptured aneurysm is extremely difficult to treat and survive. EMS can easily make these efforts futile by initiating crystalloid resuscitation or transporting the pt to a facility without onstaff surgical capability.
Facilities, in my experience, without surgical staff who receive these patients immediately terminate efforts and resort to end of life procedures.
Some ALS treatments which support other organ function like RSI may be beneficial to these patients. However, this is one of the few time critical emergencies EMS will see, and as was pointed out in the other thread, a BLS response and mindset maybe more beneficial.
The intracranial swelling on a patient with no blood in their veins is moot.
Rasing a systolic or even measuring systolic BP is moot. The location of the hemorrhage and the leaking of the vessle wall will cause the patient to bleed out faster or cause total wall rupture.
Additionally, SBP does not correlate to CVP which means you are measuring blood (via pressure) going out, but not blood coming back. Since organs (firstly the heart) are perfused by oxygenated blood completing the circuit, a break in the circuit makes your pressure measurements completely useless. Particularly if you are measuring water pressure instead of blood pressure because you infused a crystalloid.
There was a study done, if I recall properly, by Dr. McSwaine that showed MAST can increase intraperitoneal pressure and pneumatically tamponade the aorta and control bleeding by reducing the space the bleed can go into specific to this pathology.
Likewise, I have postulated in traumatic blood loss a long spineboard can act to increase pressure and reduce the space in the same manner as a surgical retropritoneal pack technique.
I know most EMS providers will now be thinking "our protocol says..." and I will agree it probably does.
But it may have been written based on "internal hemorrhage" using thoery postulated in the 1960s, instead of specifically to "ruptured aortic aneurysm" with the knowledge of 2011.
While I always welcome the thoughts of the people here, I hope that serious consideration will be given to how you are treating the patient when you suspect this pathology.
Rather than simply following a protocol, there is always the option to contact medical control and have a chat about it. While tht may seem counter intuitive. Arguing against a treatment that is far more likely to harm the very small chance the patient has survive is not only patient advocacy, but better medicine that performing that treatment inspite of such knowledge.
Last edited by a moderator: