Pregnancy and the Reef Aquarium

[Pro_builder]

Nick,
Thanks for the great info. That is a really good question that should always be considered.

[ScottT1980]

Hey Maxx, do you know if anaphalaxis also causes the release of glucocorticoids or prostaglandins (or any arachadonic acid derivatives)?

[SaltyQueen]

There is always a constant release of glucocorticoids (cortisol) by the body- whether in anaphylaxis or not. Anaphylaxis does, however, increase the amount of cortisol secreted (as does ANY type of physical or mental stress). Synthetic glucocorticoids can trigger anaphylaxis (prednisone, dexamethasone, hydrocortisone...) if someone is allergic to them. Here's the pathophysiology of anaphylaxis concerning arachidonic acid & prostaglandins...

Anaphylaxis (physical stress) causes an increase in the secretion of glucocorticoids. The glucocorticoids, in addition to having an anti-inflammatory effect, also activate enzymes called lipocortins. These enzymes slow or inhibit the action of phospholipase A2, an enzyme involved in the release of arachidonic acid (AA) from cell membranes, so the release of AA is inhibited, &, consequently, prostaglandin synthesis in the cell is also inhibited. SO, less prostaglandins = less inflammation. This natural process, however, isn't enought to stop anaphylaxis, which is why we need epinephrine.

Just curious- why did you want to know?

[SaltyQueen]

Craig- My husband and I read that book- it's excellent!

[ScottT1980]

Just curious- why did you want to know?

I am a reproductive physiologist, or at least that is what my Master's reasearch involves. My studies have been endocrinology intensive. I just couldn't remember if anaphalxis caused the release of PGF2a. Essentially, I am trying to determine what about anaphalaxis compromises the fetus. If glucocorticoids are released beyond basal levels, then this can most certainly induce the fetal compromise (in fact, as you well know, this can be used to induce parturition along with PGF2a and oxytocin). Of course, it could be completly independent of hormone release and can be due to eosinophil prolifertaion and histamine release, I am not sure (immunology is next semester, perhaps then I will have a better understanding of that pathway). Or perhaps the concern with anaphalaxis is just in its treatment with epinephrine...

Because my model of interest is the bovine and ovine, I can get a little confused by the human model (and we don't even want to discuss the equine model). I am just curious by nature...

Thanks for the info saltyqueen, any knowledge regarding what I proposed?

Take er easy
Scott T.

P.S. I just reread the post and I hate sounding so objective when talking about an unborn human fetus so I apologize for the tone. This is exactly why I could never go into human medicine as I would be pretty miserable...

[Craig Manoukian]

SQ I agree. Why didn't it come out sooner,eh?

Scott you are too much. Don't be so hard on yourself bud.

[mick77]

Great info Nick! Thanks for taking the time to research!

[SaltyQueen]

well, without looking it up, I'm thinking the greatest concern with pregnancy & anaphylaxis would be the interrupted oxygen supply to the fetus. A human fetus can only survive a very short time without oxygen (that's why a caesarian is done so quickly when cord compression is suspected), and even then the risk of brain damage is great. If I were pregnant & having an anaphylactic reaction, my number one concern would be getting more oxygen to the baby. The epinephrine treatment is also a concern, but you don't really have any other options. While the drug may be harmful to the fetus (I believe it's a pregnancy class C drug, so we're not too sure about its effects), it's a necessity because if the mother dies, the fetus will as well, so the benefits outweight the risk in this situation. I'm not sure about the effects of glucocorticoids on the fetus, whether or not it could induce premature labor or not- not sure if this has ever even been studied. Logic tells me that if the mother is under enough stress, that will always increase the risk of inducing premature labor or prematurely rupturing her membranes. Let me know if you find any literature on that, as it'd be interesting and helpful to know

[SaltyQueen]

WOO HOO that was my 200th post!!!

[Maxx]

Essentially, I am trying to determine what about anaphalaxis compromises the fetus.

Scott,
My understanding is that anaphalaxis causes the release of histamines which will cause the tissues swelling and that there is the vaso-constriction which is what we (EMS) are concerned w/ immediately. I could be wrong, and will dig thru my BTLS book just for clarification. Our teacher was pretty hardcore about the pathophys concerning disease and processes, so I know we covered this to the extent tht we needed to know it. Keep in mind that in the pre-hospital setting we arent as concerned about long term scenarios if it intereferes w/ the immediate stabilization of the patient. For example, for copd patients running on hypoxic drive, (Congestive Pulmonary Obstructive Disorder patients. In these patients oxygen saturation isnt the impetus to breathe like everyone else. Its Co2. A healthy person is told to breathe by the body when O2 levels drop to a certain level in the blood stream. The influx of O2 allows for gas exchange and life goes on. However for COPD patients the lungs arent able to exchange gas as well due to a variety of reasons, and the heart doesnt pump as well as it should...so the levels of Co2 rise in the bloodstream. The body compensates for this and switches over to whats known as hypoxic drive, meaning the body tries to keep Co2 levels relatively constant in an effort to maintain O2 levels in a different manner. The problem w/ this is that when O2 levels are pushed up beyond what the body is normally trying to keep it at thru Co2 monitoring, it decides that its got more than enough O2 and quits breathing, since the Co2 levels don't reach high enough to "trigger" the body to breathe. Sounds like fun huh? ) Back to the scenario...COPD patients w/ a SAO2 (O2 saturation levels in blood) thats lower than 95% we (EMS) are gonna hit w/ O2 to bring their oxygen levels up. The rationale behind this is: Patients die w/o oxygen, we get called because the patient is having difficulty breathing and oftentimes has had difficulty for the last week or two as their lungs slowly fill up w/ fluid. Oxygen is a necessity at this point, and the stress of not being able to breathe causes their heart to work harder, (which its not really capable of doing in the first place, and consequently using more oxygen, which is a bad thing since they arent getting enough anyway). We raise their SAO2 and transport them to the hospital. Typically transport times (aside from rural areas) are around 15 minutes or less so the patient wont have been on O2 long enough to quit breathing on us, at the hospital treatment changes, fluid from lungs is drained and they're removed from supplemental O2, to prevent apnea (stop breathing). Several nurses that don't work the ER on a regular basis yet find themselves working it on days when EMS brings in a COPD patient are horrified that we have put them O2...and they usually try and scold/ report us to Drs./ Hospital admin etc because our treatment is different than what the hospital does, and we do things they do not. If a patient quits breathing on us, we can intubate them, and continue to breathe for them. We'd rather not as it complicates things for us, but it can be done quite easily. So its not as mis-informed/bad patient care as it appears.
The purpose of this long boring example is just to explain that treatment in the field is designed to do one thing....bring a living person to the ER/OR to save thru methods we cant carry/do on the truck.
So Scott, what we were taught concerning the treatment of anaphalaxis may not be the same thing Drs and ER RN's are taught....but I'll have a look anyway.
I always liked the detective aspect of this....
Nick

[Maxx]

SQ, yes Epi is a class C drug....

[ScottT1980]

Cool, SQ and Maxx, I will try to find some literature although you are right in that I suppose the immediate concern is hypoxia (thats what happens when you concentrate so hard in one field, you can forget the obvious). There is a lag time as far as hormone secretion goes anyway so if there would be any effect, it would be perhaps 20 minutes (roughly) or more after the onset of anaphylaxis. Now I wonder what epinephrine does to the fetal environment. I haven't read much on the effects of epinephrine on pregnancy in the domestic animals, I might try to dig something up there as well.

Thanks again and very informative...Maxx, I am like you in that I love to get down every aspect of the process so I can trace it throughout the body systems...

Take er easy
Scott T.

[Dracunculus]

Just putting my 2 cents in from the pathologist's point of view.

I would have to agree with SaltyQueen.. the main danger to the fetus from anaphylaxis would be hypoxia. Anaphylxis is also termed anaphylactic shock. In shock states (due to loss of blood, sepsis, anaphylaxis, and a whole host of other causes) there is decreased flow of blood (including oxygen) to the organs. Because of this, there is damage to the tissues throughout the body, resulting in multi-system organ failure if untreated.

The shock state of anaphylaxis is due to the exaggerated immune response which causes mass release of histamines and other vasoactive substances, which casues widespread vasodilatation and "leakiness" of blood vessels throughout the body. This is what causes edema (swelling) in the tissues including the larynx. This fluid all comes from plasma, the liquid component of the blood, which is shunted from within the vessels to the surrounding tissues. The dilatation of blood vessels markedly reduces blood pressure, which contributes to the lower flow in the extremities (which is why patients in shock are cold and clammy) and to the organs. This type of reaction is a normal local physiologic response to damage, which is why you get swelling in areas of infection or trauma...the swelling helps inflammatory cells get to the area of damage and also allows for more efficient clearing of any foreign or dead material. In anaphylaxis, the whole system gets "turned on" and overrides the normal checks and balances, while exerting the adverse effects described above to the rest of the body.

In shock, the oxygen exchange across the placenta is reduced due to lower flow of blood.

Physiologically, glucocorticoid levels should be elevated in times of stress, but I don't think that they are what is exerting the pathologic effect on the fetus.

HTH

[SaltyQueen]

scott- I suppose if there is a lag time for hormone secretion, Mom & fetus would both be dead before the increased cortisol would even have any effect. I mean, if it would take up to 20 minutes for there to be a marked increase in cortisol, and Mom & baby were going without oxygen for that whole time, they'd both die before you could ever measure the effects of the hormone increase on the fetus- maybe that's why there's not any literature on it? Just a thought.

Thanks all for the info. When I do become pregnant, I'll definetly be passing the tank maintenance on to my husband for the 9 months!

[Maxx]

When I do become pregnant, I'll definetly be passing the tank maintenance on to my husband for the 9 months!

Yay for his side!!!! I'm sure he'll be thrilled that I told you to go that route......lol.....sorry man......Buddy's just my first name....
Nick