OR story from today

[castiron]

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I’m a MSIII on my OBGYN rotation right now. Had a CRAZY experience in the OR today:

42 yo AAF with PMH of DVE 9/11 and Popliteal artery embolism 10/11 admitted for having exploratory surgery for a right sided ovarian mass measuring 20x17x19 cm (about the size of a basketball!). She had been admitted the night before and had been pre-opped both by our team and the anesthesiologist.

Pt was wheeled into the OR and was O2 sats around 96-97% with BP 130/75, HR 80s. Anesthesiologist intubated the patient and left the room with the CRNA stating clearly he will be in the next room and to call him if anything happens at all. While we were scrubbing in, the patient’s sats started to drop to low 90’s. Our resident says:

“Is everything ok, do we need to call staff?” – PGY3 OBGYN

“Yea, yea, its ok, I think she is just having some trouble breathing with the meds we gave her. This happens sometimes. ” – CRNA

Resident nods and just continues to wait. Staff OBGYN is not in room yet.

About 30 seconds later, sats went down to 86-88%. BP has decreased to 105/60s and HR began to go up to 110s.

“What is going on, do you want me to get Dr. XXX in here???”- PGY3 OBGYN

“ No, its ok. I know what I’m doing.” – CRNA with an extra dose of attitude. Honestly, she said this.

Another 30 seconds, sats at 75-80%. BP has dropped to 70-80/40-50 and patient is tacchy at 170-180.

“……….” – CRNA ,

“What the #*$ is happening? Are you doing anything besides fluids?? I’m getting XXX!!!” – PGY# OBGYN

“It’s ok, I’m giving her crystalloid fluids, she’ll come out of it!” – CRNA

Dr. XXX walks in and yells:

“Why the FXXX didn’t you get me earlier Gawd damn it!!! ”

At this point, Dr.XXX first went up beside of her and pushed the patient over onto her right side while looking at the med students and explaining the hemodynamics of venous return on the heart/lungs . He then told the nurse to hold that position and watch the BP. BP started to creep up a small bit, around 80-90 systolic now. He then started pushing Dopamine, dexamethasone, phenylephrine, etc (not sure what else)

Sats went up to about 83%, BP was around 90-100/50-60 when the anesthesiologist finally called it.

He then came over to the med students and explained that she threw a PE more than likely.

As it turned out, she did throw a PE.


I was completely amazed at how this unfolded before my eyes. This was the first time a case had been cancelled after patient had already been intubated and the team was within minutes of cutting. I could not get over the ARROGANCE of the CRNA and how she refused to call the MD even after the patient was deteriorating before our eyes!

This further confirmed my decision to become an anesthesiologist.

When the **** hits the fan, you can see the difference.

Note: I understand this may be just a “small” complication to most of you but it was my first I had ever seen, so cut me some slack!


Also, I did change certain elements to protect patients identity. The conversations however, were all accurate.

 

[Noyac]

Nice case and good job describing the actions.

 

[Random Anesthesiologist]

Would the size of the mass impede circulation if the pt was turned on her left?

And OMG!

 

[castiron]

Sorry, I mistyped, he pushed the mass that was on her right side, from the right to the left, Lateral chaise position.

 

[pgg]

Would the size of the mass impede circulation if the pt was turned on her left?

Sure, same reason we don't put pregnant women flat on their back, especially after a spinal or epidural. Big gravid uterus compresses the IVC and reduces venous return to the heart, hypotension, puking mom, fetal bradycardia ...

An ovarian basketball could do the same.

She may well have thrown a PE too, but I bet the mass compressing her IVC was a big part of her symptoms (especially since the position change helped - you wouldn't really expect it to help much with a non-air embolism).

Thanks for posting the case.

 

[Random Anesthesiologist]

Sure, same reason we don't put pregnant women flat on their back, especially after a spinal or epidural. Big gravid uterus compresses the IVC and reduces venous return to the heart, hypotension, puking mom, fetal bradycardia ...

An ovarian basketball could do the same.

She may well have thrown a PE too, but I bet the mass compressing her IVC was a big part of her symptoms (especially since the position change helped - you wouldn't really expect it to help much with a non-air embolism).

Thanks for posting the case.

This is what I was thinking as I was reading the case. What a doozy.

 

[castiron]

After the case was canceled, pt was wheeled to SICU and critical care team took over. Pt was extubated today, ~4-5 hours after case cancellation I believe, and is doing well without any complications. She is supposed to get an IVC filter by IR soon, and medicine will follow up on her Fragmin dosing and medical risk assessment for future surgeries. We plan to see her back in clinic next week to pre-op again to give it another go.

 

[proman]

I'm assuming you guys got a CT-PA?

 

[fakin' the funk]

She may well have thrown a PE too, but I bet the mass compressing her IVC was a big part of her symptoms (especially since the position change helped - you wouldn't really expect it to help much with a non-air embolism).

I don't really like the story of just venous compression causing profound hypoxemia. I think there has to be an intrathoracic process also.

Maybe the mass compressing veins managed to dislodge some localized clot.

 

[fakin' the funk]

About 30 seconds later, sats went down to 86-88%. BP has decreased to 105/60s and HR began to go up to 110s.

Another 30 seconds, sats at 75-80%. BP has dropped to 70-80/40-50 and patient is tacchy at 170-180.

You gotta have anaphylaxis on the differential also, what with the timing (post-induction) and this constellation of signs/symptoms.

In any case, it's time to reach for the epi.

 

[castiron]

Offical CT Angio this morning showed showed that she had a small right lower lobe embolism, but also had a large right pleural effusion.

It was interesting because after the MD had pushed the mass over to the left thus decompressing the IVC, her BP started to go up minimally, but then it started to trend down? Very slowly, not rapid. The position change seemed to help things at first, but in the sustained position, it seemed as time went by she continued to deteriorate.

Anesthesia's post op note indicated that only Dopamine, Phenylephrine, and fluids were given once he entered the room. No Epi.

 

[cincincyreds]

I’m a MSIII on my OBGYN rotation right now. Had a CRAZY experience in the OR today:

42 yo AAF with PMH of DVE 9/11 and Popliteal artery embolism 10/11 admitted for having exploratory surgery for a right sided ovarian mass measuring 20x17x19 cm (about the size of a basketball!). She had been admitted the night before and had been pre-opped both by our team and the anesthesiologist.

Pt was wheeled into the OR and was O2 sats around 96-97% with BP 130/75, HR 80s. Anesthesiologist intubated the patient and left the room with the CRNA stating clearly he will be in the next room and to call him if anything happens at all. While we were scrubbing in, the patient’s sats started to drop to low 90’s. Our resident says:

“Is everything ok, do we need to call staff?” – PGY3 OBGYN

“Yea, yea, its ok, I think she is just having some trouble breathing with the meds we gave her. This happens sometimes. ” – CRNA

Resident nods and just continues to wait. Staff OBGYN is not in room yet.

About 30 seconds later, sats went down to 86-88%. BP has decreased to 105/60s and HR began to go up to 110s.

“What is going on, do you want me to get Dr. XXX in here???”- PGY3 OBGYN

“ No, its ok. I know what I’m doing.” – CRNA with an extra dose of attitude. Honestly, she said this.

Another 30 seconds, sats at 75-80%. BP has dropped to 70-80/40-50 and patient is tacchy at 170-180.

“……….” – CRNA ,

“What the #*$ is happening? Are you doing anything besides fluids?? I’m getting XXX!!!” – PGY# OBGYN

“It’s ok, I’m giving her crystalloid fluids, she’ll come out of it!” – CRNA

Dr. XXX walks in and yells:

“Why the FXXX didn’t you get me earlier Gawd damn it!!! ”

At this point, Dr.XXX first went up beside of her and pushed the patient over onto her right side while looking at the med students and explaining the hemodynamics of venous return on the heart/lungs . He then told the nurse to hold that position and watch the BP. BP started to creep up a small bit, around 80-90 systolic now. He then started pushing Dopamine, dexamethasone, phenylephrine, etc (not sure what else)

Sats went up to about 83%, BP was around 90-100/50-60 when the anesthesiologist finally called it.

He then came over to the med students and explained that she threw a PE more than likely.

As it turned out, she did throw a PE.


I was completely amazed at how this unfolded before my eyes. This was the first time a case had been cancelled after patient had already been intubated and the team was within minutes of cutting. I could not get over the ARROGANCE of the CRNA and how she refused to call the MD even after the patient was deteriorating before our eyes!

This further confirmed my decision to become an anesthesiologist.

When the **** hits the fan, you can see the difference.

Note: I understand this may be just a “small” complication to most of you but it was my first I had ever seen, so cut me some slack!


Also, I did change certain elements to protect patients identity. The conversations however, were all accurate.

What test confirmed the PE? This case does sound like IVC compression. I helped someone out with something similar a few years ago and got the BP back by pushing the patient on her side to get the mass off of the IVC.

Anyway, I work in a hospital with no CRNAs because the first time one of them would do something stupid like this I would end up punching them in the face and I would be the one losing the license. It is important to know when to ask for help.

 

[RemyMcswain]

Offical CT Angio this morning showed showed that she had a small right lower lobe embolism, but also had a large right pleural effusion.

It was interesting because after the MD had pushed the mass over to the left thus decompressing the IVC, her BP started to go up minimally, but then it started to trend down? Very slowly, not rapid. The position change seemed to help things at first, but in the sustained position, it seemed as time went by she continued to deteriorate.

Anesthesia's post op note indicated that only Dopamine, Phenylephrine, and fluids were given once he entered the room. No Epi.

It's my understanding that the size of the PE isn't critical to causing symptoms. Lung tissue is very inflammatory and it's possible that she had a severe inflammatory reaction to the embolus. Sever enough that she lost hypoxic vasoconstriction regulation in her lung (leading to v/q mismatch and hypoxemia) as well as generalized pulmonary vasoconstriction causing rv strain (decreased preload leading to hypotension) and tachycardia secondary to the catecholamines. Pleural effusion also prob secondary to PE inflammatory reaction and not the cause of hypoxemia.

In addition to the ct I would have ordered a BNP to see if there was an element of ventricular strain. Did she get central line in sicu? What was her cvp? Did her hypoxemia respond to increaed fi02?

 

[Idiopathic]

this is multifactorial, and those cases are rarely very satisfying (inciting event possible, but never any "aha!" diagnosis)

ultimately, hypoxia and hypotension 2/2 altered CO and/or systemic vasoplegia and bronchospasm. you could see this with PE, anaphylaxis, MI, hypovolemia (volume status, hemorrhage, IVC compressions). Dopamine is probably the wrong drug, given the scenario you describe.

My differential has anaphylaxis as #1, 2 and 3, and hypovolemia/IVC compression as #4, post-induction PE is way down the list (regardless of what the CT showed - its infinitely more likely that this patient had a chronic PE).

 

[castiron]

We spoke with the staff radiologist today about the CT angiogram. He said that there was NO evidence of acute pulmonary embolism. The preliminary reading was done over the phone by an house officer, PGY?. Staff radiologist stated that though the CT was of inferior quality, there was no evidence that supported a recurrent PE. Pulmonary vascular markings were unchanged from previous CT scan 28 days earlier. Pleural effusion was noted however and could possible be due to some sort of CP process.

BNP was not order after being transferred to the SICU. Central line was not placed. Pt was weaned off the ventilator shortly after being transferred. 1L O2 NC was placed with sats in 97-100%. Now she is breathing RA and holding same sats.

CBC, BMP, Mg, and Phos were only tests ordered in SICU. All WNL for her.

 

[RemyMcswain]

How soon after induction would one see anaphylaxis? Is the reaction 2/2 the induction agent, inhalational agent, paralytic?

 

[Gern Blansten]

How soon after induction would one see anaphylaxis? Is the reaction 2/2 the induction agent, inhalational agent, paralytic?

I believe the most common offenders that we deal with are NMB's and Antibiotics.

Dopamine would not have been on my radar screen for this scenario and we would have had to scramble to find some if it was since it is not a commonly used drug in our OR's.

For the original poster, when you used the term "called it," that usually implies that the patient died, not that the case was cancelled. That is why I think a few of us were confused. You read some vitals that were concerning, but consistent with life and said the staff anesthesiologist "called it." I thought you meant the patient died. Thankfully, as I read on further, I saw that the patient was ok. Thanks for the story. Certainly important issues to consider.

 

[Gern Blansten]

How soon after induction would one see anaphylaxis? Is the reaction 2/2 the induction agent, inhalational agent, paralytic?

Forgot to answer one part:

In my experience, the onset of anaphylaxis is pretty sudden, as in within 5 minutes, and pretty profound.

 

[PreciousDex]

😕 Quick question for those more experienced/knowledgeable than me:

I'm a little confused about how IVC compression/low preload could cause this scenario by itself. I understand that the decreased venous return and cardiac output could cause the hypotension, but what would be the physiologic reason for the profound hypoxemia? There would obviously be less blood circulating, but I would think the blood that is circulating would be adequately oxygenated (and so SpO2 wouldn't change much assuming you still have enough pulsation to get a good waveform) since there wouldn't be anything wrong with the lungs or pulmonary circulation...

 

[Idiopathic]

😕 Quick question for those more experienced/knowledgeable than me:

I'm a little confused about how IVC compression/low preload could cause this scenario by itself. I understand that the decreased venous return and cardiac output could cause the hypotension, but what would be the physiologic reason for the profound hypoxemia? There would obviously be less blood circulating, but I would think the blood that is circulating would be adequately oxygenated (and so SpO2 wouldn't change much assuming you still have enough pulsation to get a good waveform) since there wouldn't be anything wrong with the lungs or pulmonary circulation...

alterations in cardiac output coupled with atalectasis/bronchoconstriction could certainly do this. remember, rarely is it one thing in isolation. Also, hypoxemia tends to reinforce itself in compromised situations, as SVO2 decreases with SAO2 and if any intrapulmonary shunt exists, oxygenation may get worse before it gets better. A small amount of atalectasis may be much worse in this situation.

Venous admixture/physiologic shunt plays a role, but Im not sure exactly how to describe that

 

[Idiopathic]

How soon after induction would one see anaphylaxis? Is the reaction 2/2 the induction agent, inhalational agent, paralytic?

rarely (never?) the inhalational agent. i have never seen even a case report of anaphylaxis with volatile anesthetic. for board purposes, you need to consider common offenders (nmb/abx/latex are 1/2/3, i think). usually you would see anaphylaxis this extreme happen quickly (<5 min), and its probably the antibiotic in this case. epinephrine is the drug of choice, along with recognition and stopping the offending agent. maintain preload and may need epi drip to maintain contractility while the antigen is cleared.

this case is pretty much textbook for anaphylaxis.

 

[doctor712]

A little legwork for my friends here...pasted several paragraphs from abstract here...
D712


Anaphylaxis During the Perioperative Period
David L. Hepner, MD* and Mariana C. Castells, MD PhD&#8224;
+ Author Affiliations

*Department of Anesthesiology, Perioperative and Pain Medicine, and
&#8224;Allergy and Clinical Immunology Training Program, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
Address correspondence and reprint requests to David L. Hepner, MD, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis St., Boston, MA 02115. Address e-mail to [email protected]

Anaphylaxis is generally an unanticipated severe allergic reaction, often explosive in onset, that can occur perioperatively, especially during a surgical procedure when multiple drugs are administered during the conduction of an anesthetic. Because patients are under drapes and mostly unconscious or sedated, the early cutaneous signs of anaphylaxis are often unrecognized, leaving bronchospasm and cardiovascular collapse as the first recognized signs of anaphylaxis. A survey of anaphylaxis during anesthesia demonstrated that cardiovascular symptoms (73.6%), cutaneous symptoms (69.6%), and bronchospasm (44.2%) were the most common clinical features (5).

The incidence of anaphylaxis and anaphylactoid reactions during anesthesia is very difficult to estimate but has been calculated to range from 1 in 3,500 to 1 in 13,000 cases (6,7). Another report from Australia estimated the incidence to be between 1 in 10,000 and 1 in 20,000 (8), whereas the most recent report, from Norway, estimated the incidence to be 1 in 6,000 (9). Muscle relaxants are associated with the most frequent incidence of anaphylaxis, and over the last two decades, natural rubber latex (NRL, or cis-1,4-polyisoprene) has emerged as the second most common cause of anaphylaxis (5,10). However, one report (5) found that the incidence of cases of latex anaphylaxis is decreasing as a result of identification of at-risk patients and preventive measures. Antibiotics and anesthesia induction drugs account for the next group of drugs more likely to lead to an anaphylactic reaction

Induction Drugs Barbiturates.
The incidence of anaphylaxis to thiopental is estimated to be 1 in 30,000 administrations, and previous exposure and female sex are associated with an increased incidence (68). Although IgE-mediated hypersensitivity reactions to thiopental, a thiobarbiturate, have been described, no reports of IgE-mediated hypersensitivity reactions to methohexital, an oxybarbiturate, have been described (16). Diagnosis is via the detection of thiopentone-reactive IgE antibodies by the RAST method (6,69,70). Alternative diagnosis is via skinprick or intradermal tests to thiopental with a dilution of 1:1000 to 1:10 of 2.5% thiopental (16)

Inhaled Anesthetics
There are no reports of anaphylaxis related to volatile anesthetics. However, these drugs have been associated with hepatic injury due to an immune-mediated toxicity (84). Patients generate an antibody response (IgG antibodies) toward a covalently bound metabolite (trifluoroacetyl metabolite) of halothane, as detected by an enzyme-linked immunosorbent assay (ELISA) (85), and can present with a rash, fever, arthralgia, eosinophilia, and increased liver enzymes (86). Prior administration of halothane increases the incidence and severity of hepatitis. Although volatile anesthetic immune-induced hepatitis is much more common with halothane, other volatile anesthetics with trifluoroacetyl metabolites can induce immune hepatitis (87). Enflurane and isoflurane have been associated with an immune-mediated hepatic injury without prior exposure to halothane (84,88). Two reports support desflurane-induced hepatotoxicity (89,90), but because of its decreased metabolism, desflurane is less likely to cause immune-mediated hepatitis. Sevoflurane is not metabolized to trifluoroacetyl metabolites and does not cause immune-mediated hepatitis.


Further,

Barash's Clinical Anesthesia (pg 62) discusses Halothane Anaphylaxis and lists a chart but I don't think I can post from a Copyrighted Book that I found on web.

And then, though I cannot tell if the induction was inhalational or IV (unless I pay for paper and read in full)...I'm not at hospital at moment.

J Pak Med Assoc. 2007 Sep;57(9):463-6.
Severe anaphylactic reaction at induction of anaesthesia.
Ahmed A, Kumar A.
Source
Department of Anaesthesia, Aga Khan University, Karachi.
Abstract
Anaphylaxis is an IgE mediated severe allergic reaction causing release of vasoactive substances from mast cells and basophils after re-exposure to an antigen. Signs and symptoms include flushing, urticaria, hypotension, tachycardia, bronchospasm, cardio-respiratory arrest etc. It can occur at induction of anaesthesia when multiple drugs are being administered, but prompt diagnosis with correct management is the key to a successful outcome. This case report describes a patient who developed severe bronchospasm with difficulty in inflating the lungs and dropping oxygen saturations, alongwith hypotension, tachycardia and widespread flushing, at induction of anaesthesia for elective breast surgery. She was promptly managed and her hypotension was corrected, but the bronchospasm was more resistant to treatment. The patient also developed ST segment elevation, which was successfully managed with intravenous glyceryltrinitrate. The bronchospasm responded slowly to salbutamol and aminophylline. The patient underwent surgery and was discharged home on the third postoperative day.
PMID: 18072642 [PubMed - indexed for MEDLINE]

D712

 

[doctor712]

Also found 9 OB Anesthesia case presentations from a talk by

Tom Archer, MD, MBA
Director, Obstetric Anesthesia
UCSD
September 14, 2011

The last case was Anaphylaxis and here is the TEXT FROM THE PDF:

Case 9– anaphylaxis
to cefazolin (Added: again, ABX, but I thought I'd post because you guys are talking about learning point of Anaphylaxis...)

• Rapid administration of epinephrine (40
mcg x 3 doses, vasopressin total of 4
units, IV volume increased BP.
• Arterial line started initial ABG shows
BE of -7.
• Wheezing and hives abate. Intubation not
needed. Baby delivered OK.

Patient recovered in OB PACU. Received
a few more small doses of epinephrine
(5-10 mcg).
• Observed in ICU for one day.
• I am not aware of any further problems.

Anaphylaxis learning points
• Vigilance and recognition.
• Rapid use of epinephrine when usual
measures for spinal hypotension not
effective. Adjunctive use of vasopressin?
• Abundant IV volume administration.
• Be ready to intubate, but not needed here

Measures of secondary importance–
steroids, H1 (diphenhydramine) and H2
blockers (famotidine).

D712

 

[RemyMcswain]

Thanks for the input Idiopathic. Good case.

Im just an intern, so I have minimal experience in the OR, but this sounds like if she was having an anaphylactic reaction, it was a serious one. In that case, would the bronchospasm be bad enough that her peak airway pressures shoot up? Did that happen in the OR?

Also, what did her CXR look like in SICU? If someone had a severe anaphylactic reaction, that resolved with epi or spontaneously, would one expect an opacified CXR after symptoms resolved?

Thanks

 

[castiron]

I believe the most common offenders that we deal with are NMB's and Antibiotics.

For the original poster, when you used the term "called it," that usually implies that the patient died, not that the case was cancelled. That is why I think a few of us were confused. You read some vitals that were concerning, but consistent with life and said the staff anesthesiologist "called it." I thought you meant the patient died. Thankfully, as I read on further, I saw that the patient was ok. Thanks for the story. Certainly important issues to consider.

That was a poor use of words, sorry about that. The anesthesiologist canceled the case

Thanks for the input Idiopathic. Good case.

Also, what did her CXR look like in SICU? If someone had a severe anaphylactic reaction, that resolved with epi or spontaneously, would one expect an opacified CXR after symptoms resolved?

Thanks

No CXR was done in the SICU.

Great posts too, thanks for all the information! wow!

 

[PreciousDex]

alterations in cardiac output coupled with atalectasis/bronchoconstriction could certainly do this. remember, rarely is it one thing in isolation. Also, hypoxemia tends to reinforce itself in compromised situations, as SVO2 decreases with SAO2 and if any intrapulmonary shunt exists, oxygenation may get worse before it gets better. A small amount of atalectasis may be much worse in this situation.

Venous admixture/physiologic shunt plays a role, but Im not sure exactly how to describe that

thanks! i think that makes sense...

so would it be accurate (although perhaps over-simplified 🙂 ) to say that the effects of any preexisting shunt (from atelectasis, etc.) are amplified in the low perfusion state?

and i was doing some reading about venous admixture after reading your post -- is the role of venous admixture that, because of the decreased CO and resulting decreased mixed venous O2 content, the decrease in PaO2 produced by venous admixture is worsened?

 

[urge]

I’m a MSIII on my OBGYN rotation right now. Had a CRAZY experience in the OR today:

42 yo AAF with PMH of DVE 9/11 and Popliteal artery embolism 10/11 admitted for having exploratory surgery for a right sided ovarian mass measuring 20x17x19 cm (about the size of a basketball!). She had been admitted the night before and had been pre-opped both by our team and the anesthesiologist.

Pt was wheeled into the OR and was O2 sats around 96-97% with BP 130/75, HR 80s. Anesthesiologist intubated the patient and left the room with the CRNA stating clearly he will be in the next room and to call him if anything happens at all. While we were scrubbing in, the patient’s sats started to drop to low 90’s. Our resident says:

“Is everything ok, do we need to call staff?” – PGY3 OBGYN

“Yea, yea, its ok, I think she is just having some trouble breathing with the meds we gave her. This happens sometimes. ” – CRNA

Resident nods and just continues to wait. Staff OBGYN is not in room yet.

About 30 seconds later, sats went down to 86-88%. BP has decreased to 105/60s and HR began to go up to 110s.

“What is going on, do you want me to get Dr. XXX in here???”- PGY3 OBGYN

“ No, its ok. I know what I’m doing.” – CRNA with an extra dose of attitude. Honestly, she said this.

Another 30 seconds, sats at 75-80%. BP has dropped to 70-80/40-50 and patient is tacchy at 170-180.

“……….” – CRNA ,

“What the #*$ is happening? Are you doing anything besides fluids?? I’m getting XXX!!!” – PGY# OBGYN

“It’s ok, I’m giving her crystalloid fluids, she’ll come out of it!” – CRNA

Dr. XXX walks in and yells:

“Why the FXXX didn’t you get me earlier Gawd damn it!!! ”

At this point, Dr.XXX first went up beside of her and pushed the patient over onto her right side while looking at the med students and explaining the hemodynamics of venous return on the heart/lungs . He then told the nurse to hold that position and watch the BP. BP started to creep up a small bit, around 80-90 systolic now. He then started pushing Dopamine, dexamethasone, phenylephrine, etc (not sure what else)

Sats went up to about 83%, BP was around 90-100/50-60 when the anesthesiologist finally called it.

He then came over to the med students and explained that she threw a PE more than likely.

As it turned out, she did throw a PE.


I was completely amazed at how this unfolded before my eyes. This was the first time a case had been cancelled after patient had already been intubated and the team was within minutes of cutting. I could not get over the ARROGANCE of the CRNA and how she refused to call the MD even after the patient was deteriorating before our eyes!

This further confirmed my decision to become an anesthesiologist.

When the **** hits the fan, you can see the difference.

Note: I understand this may be just a “small” complication to most of you but it was my first I had ever seen, so cut me some slack!


Also, I did change certain elements to protect patients identity. The conversations however, were all accurate.

I thought the tube was main stemmed. Plus a bunch of ephedrine to fix the hypotension.

It doesn't smell like anaphylaxis to me.

Who knows...

 

[Idiopathic]

Thanks for the input Idiopathic. Good case.

Im just an intern, so I have minimal experience in the OR, but this sounds like if she was having an anaphylactic reaction, it was a serious one. In that case, would the bronchospasm be bad enough that her peak airway pressures shoot up? Did that happen in the OR?

Also, what did her CXR look like in SICU? If someone had a severe anaphylactic reaction, that resolved with epi or spontaneously, would one expect an opacified CXR after symptoms resolved?

Thanks

not sure what you mean by this. you could certainly see pulmonary edema if there were significant enough capillary leak from an inflammatory response, but with something resolving this quickly i wouldnt expect to see it.

also an argument that should be made for volume control ventilation as opposed to pressure control, especially near induction. you may not get alarms with your PC mode if you have severe bronchospasm (at least not until your minute ventilation falls below crisis values) but with volume control your vent will let you know when your peaks are too high.

 

[Idiopathic]

I thought the tube was main stemmed.

should be able to tolerate some one lung ventilation i would think. even the sickest lungers usually can handle it for a little while. but it certainly would do this also

 

[AnesNavy]

Anyway, I work in a hospital with no CRNAs because the first time one of them would do something stupid like this I would end up punching them in the face and I would be the one losing the license. It is important to know when to ask for help.

👍

 

[fakin' the funk]

I thought the tube was main stemmed. Plus a bunch of ephedrine to fix the hypotension.

HR of 170-180 from mainstem?!

 

[fakin' the funk]

I'm a little confused about how IVC compression/low preload could cause this scenario by itself. I understand that the decreased venous return and cardiac output could cause the hypotension, but what would be the physiologic reason for the profound hypoxemia?

Low CO in and of itself cannot cause arterial desaturation.

But low CO in the presence of either shunt (low V/Q, aka venous admixture) or anemia can indeed cause arterial desaturation, via venous desaturation followed by inadequate oxygenation of pulmonary capillary blood at the alveoli.

Keep in mind that at best we all have 3-5% right-to-left "physiologic" shunt at baseline due to bronchial circulation etc.

Add in the fact that during anesthesia, patient tend to have atelectasis/effusions/pneumonia/mainstem ("pathologic" shunt) and low CO.

So while low CO can "cause" hypoxemia, it also indicates that you have another problem on your hands...a problem which, as Idiopathic pointed out, is on a positive-feedback loop.

I refer y'all to the ICU Book which has an excellent section on all the various kinds of hypoxemia.

 

[PreciousDex]

Low CO in and of itself cannot cause arterial desaturation.

But low CO in the presence of either shunt (low V/Q, aka venous admixture) or anemia can indeed cause arterial desaturation, via venous desaturation followed by inadequate oxygenation of pulmonary capillary blood at the alveoli.

Keep in mind that at best we all have 3-5% right-to-left "physiologic" shunt at baseline due to bronchial circulation etc.

Add in the fact that during anesthesia, patient tend to have atelectasis/effusions/pneumonia/mainstem ("pathologic" shunt) and low CO.

So while low CO can "cause" hypoxemia, it also indicates that you have another problem on your hands...a problem which, as Idiopathic pointed out, is on a positive-feedback loop.

I refer y'all to the ICU Book which has an excellent section on all the various kinds of hypoxemia.

👍 Awesome explanation! Thanks.

Great case... Thanks for posting, castiron.