Aussieaid Posted November 5, 2009 Share Posted November 5, 2009 The more I learn the more I find inconsistencies in everything to do with medicine. I guess that is why it is rare to find two doctors, nurses, paramedics, emts etc who will agree on everything. I usually end up researching as much as I can and then go with what makes the most sense/logic to me. I just agree to disagree and as long as someone has a good rationale behind why they are doing something I don't try to change their opinion to agree with mine. I think part of the thinking behind the not suctioning the mouth if there is meconium staining present is, as someone said, that it actually stimulates the baby to breathe when you want to avoid that and intubate them before they start breathing if possible. The Cushing's Triad is more the widening pulse pressure being manifested by a sudden increase in the SBP along with the bradycardia and the irregular respirations leading to apnea. The interesting thing I have found in kids who are actively herniating is that they actually become suddenly tachycardic followed by bradycardia and they often like to code at the time of herniation. With a more gradual increase in ICP I see more of the bradycardia (usually a junctional rhythm). We had a baby who lived the first year of his life in the PICU and we had to do chest compressions on him at least once a shift for a while because of bradycardia. He would go bradycardic, you'd do a few compressions and he was fine again. Didn't even have to use epi or atropine every time. If I remember correctly they found out that he had a pulmonary artery sling around the trachea along with his 101 other congenital defects. He was totally FUBAR! I also think that compressions are more of a first line in peds with bradycardia because it is usually related to hypoxia or a more immediately reversible cause other than a cardiac arrhythmia or heart block like it is in adults. 2 Link to comment Share on other sites More sharing options...
Brandon Oto Posted November 5, 2009 Author Share Posted November 5, 2009 Here's a source for the Cushing's that sort of covers all the bases: "The triad refers to three signs caused by Cushing's reflex: 1. Bradycardia 2. Hypertension (with widened pulse pressure) 3. Bradypnea (often irregular)" (http://books.google.com/books?id=0nDvZP8qnigC&pg=PA26&lpg=PA26&dq=source=bl&ots=n2tsb2aoql&sig=91t0v__evYsM7hIuZevbcwotk-U&hl=en&ei=CvHySrPFD4bAlAfTkt22Aw&sa=X&oi=book_result&ct=result&resnum=6&ved=0CBMQ6AEwBTge#v=onepage&q=&f=false) Fair enough. To be honest, in my rough understanding of Cushing's reflex, it's not clear to me why a widened pulse pressure would become evident. Correct me if I'm wrong, but the hypertension here is mainly a product of peripheral vasoconstriction -- right? Surely it CAN'T be a product of increased cardiac output, because we know that one of the other signs is BRADYcardia! But HTN due to vasoconstriction would seem to imply a rise in both systolic and diastolic pressures, at least in my mind. Am I missing something? Link to comment Share on other sites More sharing options...
tniuqs Posted November 5, 2009 Share Posted November 5, 2009 'Aussieaid' The more I learn the more I find inconsistencies in everything to do with medicine. I guess that is why it is rare to find two doctors, nurses, paramedics, emts etc who will agree on everything. I usually end up researching as much as I can and then go with what makes the most sense/logic to me. I just agree to disagree and as long as someone has a good rationale behind why they are doing something I don't try to change their opinion to agree with mine. Bravo on the research part ... but more likely will never agree upon any thing j/k I think part of the thinking behind the not suctioning the mouth if there is meconium staining present is, as someone said, that it actually stimulates the baby to breathe when you want to avoid that and intubate them before they start breathing if possible. The changes in Cardiovascular Circulation second paragraph very informative hence I provide this link: http://www.merck.com/mmpe/sec19/ch271/ch271a.html Some conjecture here, the first 4 breaths when a child is delivered are some of the important in the life of the human being One can quote AHA and during my last Mandatory PALS course I use Duct Tape over my mouth with this now very dummied down newer versions and quote it up the ying yang but there is far better information out there in goggle land or the actual text books. A side bar if those would tolerate ... My biggest complaint is the use of Atropine pre intubation in RSI of the pediatric population because all EBM research I have read and experience in OR in induction with anesthesia, basically a MYTH perpetuated by AHA. For some interesting controversy on that subject, I recieved a negative in a previous post ? I suspect someone did not like my suggestion "hang them by the feet" use gravity as your friend I suspect but will never know as IF this really affects me personally.This reputation thing is a popularity contest IMHO, sometimes a carry over from other threads ... whatever I do have an ex wife too I will respond with information to that end, please PM or post your objection and most pleased to help anyone out,in the spirit of this website, so for your pleasure and enjoyment the basis for my rationale: http://www.lotusbirth.com/doc/FEB2003Lotusbirth-532.htm The Cushing's Triad is more the widening pulse pressure being manifested by a sudden increase in the SBP along with the bradycardia and the irregular respirations leading to apnea. The interesting thing I have found in kids who are actively herniating is that they actually become suddenly tachycardic followed by bradycardia and they often like to code at the time of herniation. With a more gradual increase in ICP I see more of the bradycardia (usually a junctional rhythm). Personally the definition is quite clear in the literature and Hyperventilation as a treatment is just something to do while you watch the CONING http://www.health.qld.gov.au/cchs/congenital/Coning.pdf and an OZ reference btw. Inter cranial bleeds at birth are a very different pathology described in the link provided to Merck. http://www.merck.com...271/ch271a.html We had a baby who lived the first year of his life in the PICU and we had to do chest compressions on him at least once a shift for a while because of bradycardia. He would go bradycardic, you'd do a few compressions and he was fine again. Didn't even have to use epi or atropine every time. If I remember correctly they found out that he had a pulmonary artery sling around the trachea along with his 101 other congenital defects. He was totally FUBAR From the information provided the difference between bradycardia at birth and complications of Coartication of Great Vessels may be more succinct, are quite different situation and after actually working in a 25 bed unit NICU with ECMO capability. Firstly (heck some gerbils) no offence intended just the gallows humour, well some have Apnea and Brad's at least 4 times per shift,we were doing trials with the use of : http://www.springerlink.com/content/v5w680423nk80136/ The accepted practice for Apnea/Brads in Nursing and Respiratory in NICU/PICU was, curiously the criteria was if a Premie was sent to floors, had an issue then was admitted to PICU ... most patients that were never a candidate for discharge from NICU were actually older confusing really... argh Hospital Politics ! 1- Stimulation although EBM studies do suggest that stimulation in the preemie can cause apnea and brads atypical of the full term infant. 2-CPAP manually, PEEP of up to 10 cms AND with a practiced hand and gauge in line with flow inflating or what we called Jackson Reese Bagger(not advised for vast majority of Paramedic unless very practiced. 4-Pharmacological and or compressions. I also think that compressions are more of a first line in peds with bradycardia because it is usually related to hypoxia or a more immediately reversible cause other than a cardiac arrhythmia or heart block like it is in adults. Agree to Disagree based on experience and research information provided. cheers Link to comment Share on other sites More sharing options...
Aussieaid Posted November 5, 2009 Share Posted November 5, 2009 Bravo on the research part ... but more likely will never agree upon any thing j/k The changes in Cardiovascular Circulation second paragraph very informative hence I provide this link: http://www.merck.com/mmpe/sec19/ch271/ch271a.html Some conjecture here, the first 4 breaths when a child is delivered are some of the important in the life of the human being One can quote AHA and during my last Mandatory PALS course I use Duct Tape over my mouth with this now very dummied down newer versions and quote it up the ying yang but there is far better information out there in goggle land or the actual text books. A side bar if those would tolerate ... My biggest complaint is the use of Atropine pre intubation in RSI of the pediatric population because all EBM research I have read and experience in OR in induction with anesthesia, basically a MYTH perpetuated by AHA. For some interesting controversy on that subject, I recieved a negative in a previous post ? I suspect someone did not like my suggestion "hang them by the feet" use gravity as your friend I suspect but will never know as IF this really affects me personally.This reputation thing is a popularity contest IMHO, sometimes a carry over from other threads ... whatever I do have an ex wife too I will respond with information to that end, please PM or post your objection and most pleased to help anyone out,in the spirit of this website, so for your pleasure and enjoyment the basis for my rationale: http://www.lotusbirth.com/doc/FEB2003Lotusbirth-532.htm Personally the definition is quite clear in the literature and Hyperventilation as a treatment is just something to do while you watch the CONING http://www.health.qld.gov.au/cchs/congenital/Coning.pdf and an OZ reference btw. Inter cranial bleeds at birth are a very different pathology described in the link provided to Merck. http://www.merck.com...271/ch271a.html From the information provided the difference between bradycardia at birth and complications of Coartication of Great Vessels may be more succinct, are quite different situation and after actually working in a 25 bed unit NICU with ECMO capability. Firstly (heck some gerbils) no offence intended just the gallows humour, well some have Apnea and Brad's at least 4 times per shift,we were doing trials with the use of : http://www.springerlink.com/content/v5w680423nk80136/ The accepted practice for Apnea/Brads in Nursing and Respiratory in NICU/PICU was, curiously the criteria was if a Premie was sent to floors, had an issue then was admitted to PICU ... most patients that were never a candidate for discharge from NICU were actually older confusing really... argh Hospital Politics ! Agree to Disagree based on experience and research information provided. cheers LOL. I had to sit and reread your post a few times to follow it! Still not sure if I understand exactly what you were trying to say so forgive me if I have misunderstood something. I think the reasoning behind giving atropine pre-RSI is that it is better to prevent the bradycardia than try and get a kid back from bradycardia although we never used it with our intubations in the PICU. We would have it ready on infants but I rarely ever gave it. In my flight program it is protocol to give it for under 6 years of age (and no I don't agree with it!) The increase in the SBP by widening the pulse pressure in herniation is an autoregulatory mechanism to increase cerebral perfusion pressure to a brain that has decreased blood flow due to increased ICP. The bradycardia and irregular and slowing respirations is from pressure on the brainstem with ensuing ischemia as the brain herniates downward through the foramen magnum. The brainstem is the where the vital cardiovascular and respiratory centers are. It's funny you bring up "coning" because when I first came to the States people had no idea what I was talking about when I would say someone is "coning". As a tidbit that term comes from the way the brain is pushed down through the foramen magnum like down an ice-cream cone. I was not referring to neonatal head bleeds when I talked about herniation in pediatrics. We used to see a lot of TBI, shaken baby syndrome, near-drowners and cerebral edema from any other variety of insults to the brain (including mismanaged DKAs). I have certainly seen my share of herniations and taken care of way too many pediatric organ donors. The child I was talking about was not a regular preemie with apnea/brady spells. This pt had multiple congenital heart defects (coarctation was not one of them) as well as a number of other defects and was on a rate on the ventilator. His episodes were related to the tracheal sling not necessarily hypoxia. We managed the plain old apnea/brady babies with stimulation, O2, bagging and usually caffeine or maybe stronger meds as needed. CPR was rarely needed on these infants as they usually respond before you get to that point. I am a little confused as to what you agree to disagree on and exactly what relevance to my post your links were (interesting though they were!) Have a great weekend and feel free to disagree or agree as much as you like. I am always open for good discussions and learning new things. I just reread your post and I think you misunderstood what I meant about compressions being first line treatment in peds versus adults. I am not talking about the apnea/brady spells in neonates where you don't do compressions first. I was responding to the OP's thoughts about compressions being used earlier for bradycardia in pediatrics in general (i.e. PALS guidelines) and more as a last resort in adults (per ACLS guidelines). Cheers!! 1 Link to comment Share on other sites More sharing options...
tniuqs Posted November 5, 2009 Share Posted November 5, 2009 (edited) I think the reasoning behind giving atropine pre-RSI is that it is better to prevent the bradycardia than try and get a kid back from bradycardia although we never used it with our intubations in the PICU. We would have it ready on infants but I rarely ever gave it. In my flight program it is protocol to give it for under 6 years of age (and no I don't agree with it! When I first started reading this thread I though it was the three little pigs LOL. WHAT ??? your not disagreeing with any of my Ramblings ? Dang I'm taking my ball and going home ... Hell sometimes even after I hit send, I don't know what my point was cheers Edited November 5, 2009 by tniuqs Link to comment Share on other sites More sharing options...
armymedic571 Posted November 6, 2009 Share Posted November 6, 2009 Brandon, One addition I think should be made about Cushings triad is this: The vital signs you are looking for (hypertension/bradycardia/irregular respirations) is not a singular event, but something that needs to be trended. A singular set of vital signs does not constitute as a positive Cushings. Hope this helps.... 2 Link to comment Share on other sites More sharing options...
chbare Posted November 6, 2009 Share Posted November 6, 2009 The increase in the SBP by widening the pulse pressure in herniation is an autoregulatory mechanism to increase cerebral perfusion pressure to a brain that has decreased blood flow due to increased ICP. The bradycardia and irregular and slowing respirations is from pressure on the brainstem with ensuing ischemia as the brain herniates downward through the foramen magnum. The brainstem is the where the vital cardiovascular and respiratory centers are. I often see people quote this classic foramen magnum herniation pattern. While it can occur, and you may hear the term tonsillar herniation to describe the effect of the cerebellar mass moving in a general downward direction causing the cerebellar tonsils to compress the brain stem and upper cord, this is far from the only thing that can occur. In fact, we are neglecting a major portion of mass effect pathophysiology as it relates to this often misunderstood concept of herniation. If you recall, an invagination of the meninges exists, known as the tentorium cerebelli. In essence, the tentorium separates the cerebellar area from the superior aspects of the brain. Therefore, if you develop a supratentorial mass effect (space occupying lesion) or edema above the tentorium resulting in herniation, the herniation will in fact occur through the tentorial area. Two basic types of supratentorial or transtentorial herniations can occur. 1) Central; when the temporal lobes of the cerebrum and parts of the temporal lobes push downward through the tentorial notch. 2) Uncal; often associated with a lateral mass on one side such as an epidural hematoma, where the uncus of the temporal lobs is pushed over the tentorial shelf. Each type can has associated signs and symptoms. In addition, the exact cause of Cushing's triad seems to have many causes when looking at the literature. I have seen reflex changes, to ischemic changes, to pressure on the vagus nerve used as explanations for some or all of the exact findings. I suspect, multiple types of pathophysiology lead to these changes and perhaps attempting to identify one clear culprit is a bit myopic IMHO. Take care, chbare. 2 Link to comment Share on other sites More sharing options...
Jwade Posted November 6, 2009 Share Posted November 6, 2009 Brandon, One addition I think should be made about Cushings triad is this: The vital signs you are looking for (hypertension/bradycardia/irregular respirations) is not a singular event, but something that needs to be trended. A singular set of vital signs does not constitute as a positive Cushings. Hope this helps.... Army, Good point, I had thought about stating this during my initial response, but I probably wrongly assumed that vital sign trending was obvious when deciding whether or not cushing's is involved. Respectfully, JW Link to comment Share on other sites More sharing options...
Aussieaid Posted November 6, 2009 Share Posted November 6, 2009 I apologize for oversimplifying the explanation. I was simply trying to answer the OP's original question about Cushing's Triad and instead of getting sidetracked into all the different types of herniation I mentioned the type I have seen most commonly. The Cushing's triad can occur in the late phases of both the Central and Uncal herniation syndromes as well as other types of herniation so the point is kind of moot. Sorry I am too tired to think clearly to explain my thought so will check back tomorrow! Good night and keep safe! Link to comment Share on other sites More sharing options...
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