Tough Case: Beach Chair Position

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BLADEMDA

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A 74 year old attorney presents for Right Shoulder replacement. He was a civil trial lawyer but retired 6 years ago. HIs main concern is "stroke" from the anesthesia as he was informed by the surgeon his position will be beach chair for 2.5 hours.

PMH:
HTN
CAD
One Coronary stent placed 2 years ago; recent stress test from 6/2011 is fine.
MI 2004
Obesity
Dyslipidemia
Mild GERD
Gout
NIDDM (diagnosed in 2009)

PSH:
Appy at age 14
CABG X 3 in 2004
Lap Chole in 2008

Meds:

Enalapril
Metoprolol
HCTZ
Baby Asa
Effient (off 6 days)
Tricor
Nexium
Pepcid
Allopurinol
Metformin
Lipitor

Vitals: Wt= 127 Kg Ht: 6'0" HR= 61 BP= 148/89 T=98.5

Labs:

Hgb= 13.9 Plt-278,000 CR= 1.26 BUN-18 K=3.9 EF= 45% Pt/PTT-WNL HgA1c= 7.4 Glucose= 174

EKG- NSR, occ PVC Q's in leads II,III, AVF
CXR- Mild Cardiomegaly, No acute disease, sternal wires noted from CABG



Patient is non stop about his concern from the anesthesia. He asks about doing the case awake under block vs GA. His primary concern is STROKE.
 
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What is your plan for the case? Any precautions to avoid a stroke in this guy? What's his risk factors?

Will you do him awake? Why or why not?
 
One more thing if his BP was 180/99 would you cancel the case? If so, why?
What if his HgbA1c was 8.5 or 9.1? Would you cancel the case? Why?
 
How often have we asked ourselves: shall I go ahead and anaesthetize this patient with uncontrolled hypertension, or should I postpone surgery until the arterial pressure is controlled? Does the benefit of preoperative arterial pressure control justify the inconvenience and financial consequences of postponing surgery? Are patients with uncontrolled hypertension at an increased perioperative risk? Are there any data on which I can base my decision? These and many other questions are addressed in the comprehensive review by Howell, Sear and Foëx in this issue of the Journal.http://bja.oxfordjournals.org/conte...NDEX=0&minscore=5000&resourcetype=HWCIT#ref-1
 
Anesth Analg. 2012 Jun;114(6):1301-4. Epub 2011 Nov 3.
Case report: focal cerebral ischemia after surgery in the "beach chair" position: the role of a congenital variation of circle of willis anatomy.

Drummond JC, Lee RR, Howell JP Jr.
Source

FRCPC, VA Medical Center-125, 3350 La Jolla Village Dr., San Diego, CA 92161. [email protected].

Abstract

A 50-year-old man underwent shoulder surgery in the beach chair position. His mean arterial blood pressure at arm level was approximately 65 mm Hg. Postoperatively, there was delayed awakening and a right hemiparesis. Radiologic evaluation revealed a congenital asymmetry of the circle of Willis that resulted in limited collateral flow to the left anterior and middle cerebral artery distributions. Similar anatomical variations are relatively common in the general population and may render some patients relatively and unpredictably more vulnerable to hypotension.
 
For all you would be lawyers and medical experts out there let's discuss my case so we all know what the evidence is as of 2012 and what you are willing to stay under oath on the stand.
 
-Tell him-**** happens-lawyers can't guarantee outcome of a lawsuit- we can't guarantee outcome of surgery and that stroke is possible.
-Document up the a**. BP cuff position, head positioning, etc
-For this case, use of cerebral oximetry-(just to cover my ass) Aggressive treatment of BP with documentation of placement of NIBP cuff position, high Inspired oxygen with air as diluent (no N2O), no spontaneous ventilation, generous on the IV fluids.
Supraclavicular Block plus supplemental GA from a patient care standpoint is best IMO. Since my defensive medicine radar is up, under sell the block so he won't choose it. A straight general anesthetic is medicolegally a better getaway than a block with supplemental GA. Even if it MAY not be the best choice for the patient.
 
Risk factor wise this guy has age, HLD, HTN, known CAD s/p CABG and stents. Did he smoke? He's taking a statin, BB, and low-dose ASA. Keep the ASA going, don't let surgeon stop that stuff. He has schmutz in his coronaries, I'm sure he's got some all over his carotids and cerebral vessels.

I would perform a peripheral nerve block for post-op pain control, and induce general. Probably place A-line after induction and watch closely as we slowly assume beach chair position. Keep BP within reasonable range of preop.

I leave debate about what type of PNB for others.
 
Long time lurker here.
Yes I would do the case. I would like to know his normal home BPs and his exercise tolerance though. I would do a block, interscalene vs supraclav with superficial cervical block. LMA if no sx with his mild GERD on nexium and NIBP. If he was so concerned, I would be willing to place an aline, even preinduction, if it made him more comfortable, as I am assuming he has uncontolled HTN at this point, and can expect some lability. In this case I can zero the transducer at his head. If only using NIBP, I will factor in the difference in cerebral perfusion pressure difference from his arm pressure to keep his CPP closer to his baseline.
 
Did this recently. 89 R shoulder. PCI 2 yrs ago. Interscalene block. Awake a line. Transducer at head. Neo gtt to maintain map.
 
Where do you put your a line transducer?


On the iPhone

At his ear.

I'd also do the block postop and not preop. Easier to keep his BP adequate in the beach chair under GA if he has some surgical stimulation.
 
At his ear.

I'd also do the block postop and not preop. Easier to keep his BP adequate in the beach chair under GA if he has some surgical stimulation.

I would do it before. Proper placement of BP cuff will allow you accurate measure of cerebral perfusion pressure. The issue, that seems to be understood by many here but not specifically laid out, is sitting position with the BP cuff on the lower extremity giving a false sense of security with MAP. With it on the leg, the MAP will read higher than the real MAP the head is seeing, putting the patient at risk. As long as you are measuring MAP correctly, it should be easy to maintain adequate MAP with or without a block using a phenylephrine gtt. Therefore, to me, the issue could become post op pain--->tachycardia--->myocardial ischemia. Therefore, we usually put them in preop for better patient satisfaction and safety. It also allows you to run a bit of a lighter anesthetic. If it were me, I would prefer to wake up pain free rather than deal with pain until the block was in. We are a busy place, so if placed post op, it may be 30-45 min before we get to them since we are doing other cases and blocks.
 
What is your plan for the case? Any precautions to avoid a stroke in this guy? What's his risk factors?

Will you do him awake? Why or why not?

"Yes Mr. Attorney, you could have a stroke. You could have late stent thrombosis and have a heart attack. You are in poor health and are (probably) having an elective procedure that is non-trivial. There are many risks. One of them, yes, it is possible you will have a stroke. Not at all likely, but certainly possible. Would you like me to discuss all the bad things that can (but most likely will not) go wrong?"

Coincidentally John Drummond has a case report in today's A&A about a postop stroke in a patient who spent time in the beach chair for shoulder surgery. (I just hate the beach chair position after working with people that are well trained shoulder specialists that do cuff repairs lickety split lateral)

In same issue I just read there are 250 million anesthetics per year worldwide for major surgery and 5 million periop major cardiovascular events. So there are some numbers Mr. Lawyer, 5 in 250ish +/-

I'd let the surgeon decide if he/she is comfortable with a replacement operation with whatever blood sugar value is day of surgery.

Then ISC block, let patient get himself comfortable in beach chair position before induction, some vitals while awake to shoot for intraop, preox with a simple mask, make sure I have some pressor/antipressor available, GA then LMA if good fit. Consider Aline zeroed to head, cerebral NIRS if available, and thank you surgeon for this interesting consult.
 
I would do it before. Proper placement of BP cuff will allow you accurate measure of cerebral perfusion pressure. The issue, that seems to be understood by many here but not specifically laid out, is sitting position with the BP cuff on the lower extremity giving a false sense of security with MAP. With it on the leg, the MAP will read higher than the real MAP the head is seeing, putting the patient at risk. As long as you are measuring MAP correctly, it should be easy to maintain adequate MAP with or without a block using a phenylephrine gtt. Therefore, to me, the issue could become post op pain--->tachycardia--->myocardial ischemia. Therefore, we usually put them in preop for better patient satisfaction and safety. It also allows you to run a bit of a lighter anesthetic. If it were me, I would prefer to wake up pain free rather than deal with pain until the block was in. We are a busy place, so if placed post op, it may be 30-45 min before we get to them since we are doing other cases and blocks.

We are also a busy place, but I'm usually able to place the block within 2 minutes of the patient being awake enough to mention they are in pain. Or at least to respond appropriately to the question of "are you in pain?". I time my day around making sure I can get the block done promptly upon their arrival in PACU. The patients like that they get several hours of extra analgesia compared to having it placed preoperatively. Although I do offer them that option, most desire it done afterwards. 1-2 minutes of pain when you won't really remember it tends not to worry them.
 
-Tell him-**** happens-lawyers can't guarantee outcome of a lawsuit- we can't guarantee outcome of surgery and that stroke is possible.
-Document up the a**. BP cuff position, head positioning, etc
-For this case, use of cerebral oximetry-(just to cover my ass) Aggressive treatment of BP with documentation of placement of NIBP cuff position, high Inspired oxygen with air as diluent (no N2O), no spontaneous ventilation, generous on the IV fluids.
Supraclavicular Block plus supplemental GA from a patient care standpoint is best IMO. Since my defensive medicine radar is up, under sell the block so he won't choose it. A straight general anesthetic is medicolegally a better getaway than a block with supplemental GA. Even if it MAY not be the best choice for the patient.


1. Patient understands the risk of stroke but wants to know is there anything you can do to minimize his risk?
2. Will you agree to do the case on this patient awake or with light sedation? Is spontaneous ventilation helpful or harmful from a risk reduction standpoint?
3. If you won't do the case under sedation/propofol would you do it under an LMA/block combo?
4. Would you block this patient preop or postop? Does the risk of brachial plexus injury from the shoulder surgery influence your decision? Does the fact the patient stopped his Effient only 6 days ago alter your decision for an ISB/SCB?
5. Would you place an arterail line for this case preinduction or after induction or not at all?
6. Any evidence that the BIS or Brain Oximetry reduces risk of stroke?
7. Where would you keep his BP during the case? Why?
8. If you have a CRNA in the room what is the minimum BP before giving pressors?
9. Any evidence over which pressor to use in this case?

I want the real world approach and NOT just an Oral Board answer.
 
We are also a busy place, but I'm usually able to place the block within 2 minutes of the patient being awake enough to mention they are in pain. Or at least to respond appropriately to the question of "are you in pain?". I time my day around making sure I can get the block done promptly upon their arrival in PACU. The patients like that they get several hours of extra analgesia compared to having it placed preoperatively. Although I do offer them that option, most desire it done afterwards. 1-2 minutes of pain when you won't really remember it tends not to worry them.

We get most of ours pretty timely, but their are some that the timing just doesn't work.
 
Risk factor wise this guy has age, HLD, HTN, known CAD s/p CABG and stents. Did he smoke? He's taking a statin, BB, and low-dose ASA. Keep the ASA going, don't let surgeon stop that stuff. He has schmutz in his coronaries, I'm sure he's got some all over his carotids and cerebral vessels.

I would perform a peripheral nerve block for post-op pain control, and induce general. Probably place A-line after induction and watch closely as we slowly assume beach chair position. Keep BP within reasonable range of preop.

I leave debate about what type of PNB for others.

Review the case again. This is how the patient presents in the holding area for surgery.
He is a non-smoker. He quite smoking Cigars 20 years ago. He drinks once a day.


How does his BP and HgA1C look to you? Are both acceptable for the surgery/anesthesia?

What exactly is reasonable range of BP for this patient? Can you elaborate on that range? Will you use his SBP or DBP or mean BP as the variable to decide if pressors are needed?
 
Reg Anesth Pain Med. 2000 May-Jun;25(3):318-21.
Complete brachial plexus palsy after total shoulder arthroplasty done with interscalene block anesthesia.

Walton JS, Folk JW, Friedman RJ, Dorman BH.
Source

Department of Anesthesia & Perioperative Medicine, Medical University of South Carolina, Children's Hospital, Charleston 29455, USA.

Abstract

BACKGROUND AND OBJECTIVES:

This report illustrates that brachial plexus palsy can result from either interscalene block or total shoulder arthroplasty. It is often impossible to determine which procedure caused the deficit; therefore, we believe the focus should be placed on treatment of the neurologic deficit. This report provides a suggested algorithm for diagnosis and treatment of postprocedure brachial plexus palsy.
METHODS:

Interscalene block was used as the operative anesthetic for our patient's total shoulder arthroplasty. Complete brachial plexus palsy was diagnosed postoperatively.
RESULTS:

The patient's postoperative treatment and recovery are described.
CONCLUSIONS:

Proper diagnosis and treatment of postprocedure brachial plexus palsy may improve recovery of function. Several precautions may reduce the likelihood of brachial plexus palsy following interscalene block for total shoulder arthroplasty.
 
http://www.ncbi.nlm.nih.gov/pubmed/15845712?dopt=Abstract


ISB/SCB is a very safe procedure even on total shoulders. But, the sitting position for a total shoulder is believed to carry higher risk for injury to the brachial plexus. That said, with U/S and careful block placement the timing of the nerve block (preop or postop) is up to the Anesthesiologist.
 
Decreasing the Risk of Cerebral Deoxygenation during Shoulder Surgery

Avoiding general anesthesia may reduce risk of ischemic neurologic injury
Maureen Leahy
Using regional anesthesia and sedation, rather than general anesthesia, for patients undergoing shoulder surgery in the beach-chair position reduces the risk of cerebral deoxygenation, according to study results presented by Jason L. Koh, MD, of the NorthShore University Health System, during the American Shoulder and Elbow (ASES) Specialty Day. This suggests that avoiding the use of general anesthesia may reduce the risk of ischemic neurologic injury in this patient population.
The research, summarized in "Cerebral Oxygenation in the Beach Chair Position: A Prospective Study on the Effect of General Anesthesia Compared to Regional Anesthesia and Sedation," earned the 2012 ASES Charles S. Neer Award for Dr. Koh and his colleagues.
The seated beach-chair position is commonly used for arthroscopic and open shoulder surgeries and is associated with a low risk of complications. However, noted Dr. Koh, rare catastrophic neurologic events such as blindness, stroke, coma, and even death have been reported in patients operated on in the beach-chair position under general anesthesia.
According to Dr. Koh, patients who are in the seated position can experience a ‘waterfall effect,' causing decreased flow to the brain. Awake patients are able to compensate and are able to maintain cerebral perfusion. However, patients under general anesthesia are unable to fully activate their sympathetic response and are subject to the vasodilating effects of anesthetic medications and limited cerebral autoregulation, resulting in relative cerebral hypoperfusion.
"We hypothesized, therefore, that patients operated on in the beach-chair position would have better cerebral oxygenation with a regional block and sedation than with general anesthesia," he said.
Study materials, methods
The prospective study involved 60 patients undergoing elective shoulder surgery. After conferring with the surgeon and anesthesiologist, the patients were enrolled in the following groups:
  • interscalene block (ISB) anesthesia and sedation with spontaneous ventilation (AWAKE) (n = 30)
  • ISB with general anesthesia with mechanical ventilation (ASLEEP) (n = 30)
  • Patients were excluded from the study for the following reasons:
  • pre-existing cerebrovascular disease or orthostatic hypotension
  • age younger than 18 years
  • history of allergy to local anesthetics
  • pre-existing coagulation abnormalities
  • American Society of Anesthesiologists (ASA) class IV or V
  • failure of the ISB in the holding area
The researchers obtained baseline and intraoperative data on all patients. Baseline data were obtained in the operating room, with patients in the supine position and breathing room air. Patients in both cohorts were demographically similar with regard to age, sex, height, weight, pre-existing medical conditions, and ASA class; baseline hemodynamic and oxygenation parameters were also similar.
Intraoperatively, cerebral tissue oxygen saturation (SctO2) and hemodynamic parameters including mean arterial pressure (MAP), heart rate (HR), and arterial oxygen saturation (SpO2) were obtained and recorded every 3 minutes. To minimize the risk of cerebral desaturation events, MAP and SctO2 values less than 20 percent of baseline were treated according to prearranged intervention protocols.
Aldrete scores measuring consciousness, breathing, blood pressure, oxygenation, and motor function were collected on arrival and every 15 minutes in the recovery room.
Results
Anesthesia time was longer in the ASLEEP cohort by a mean of 18 minutes, which was likely related to induction and emergence from the general anesthesia, Dr. Koh noted. The researchers found no significant differences in HR and SpO2 between the two cohorts at any time; MAP was also similar at all time points but one. Intervention for decreases in MAP, however, occurred in 73 percent of ASLEEP patients, compared to 10 percent of AWAKE patients (P < 0.001).
The researchers also found that SctO2 values were lower in the ASLEEP group than in the AWAKE group throughout the intraoperative period (P > 0.0001). Intervention for decreases in SctO2 occurred in 43 percent of ASLEEP patients, compared to 0 percent in the AWAKE group (P < 0.001).
In addition, the incidence of cerebral deoxygenation events (CDEs) was 56.7 percent in the ASLEEP group, compared to 0 percent in the AWAKE group (P < 0.001); the mean number of CDEs per patient was 2.97 in the ASLEEP cohort and 0 in the AWAKE cohort (P < 0.001). The total number of CDEs was also significantly higher in the ASLEEP cohort versus the AWAKE cohort (89 and 1, respectively; P < 0.001)
"We found that more than half of the ASLEEP patients had CDEs where the oxygen supply to the brain was decreased, but that all AWAKE patients maintained their cerebral oxygenation," said Dr. Koh. "The ASLEEP patients also had lower Aldrete scores in the recovery room and a longer time to meet discharge criteria. No permanent neurologic impairment was seen in either group."
He added, "Use of a regional block and sedation compared to general anesthesia decreases the risk of cerebral deoxygenation for patients in the beach-chair position, which may reduce the risk of neurologic events. We recognize, however, that the regional block and sedation may not be appropriate at times, due to areas of the shoulder that are not anesthetized, the need for muscle relaxation, the risk of airway obstruction, or the prolonged nature of the case."
Dr. Koh's coauthors include Steven D. Levin, MD (no conflicts); Eric L. Chehab, MD (no conflicts); and Glenn Murphy, MD (CASMED). Dr. Koh reports ties to Aesculap/B.Braun; Aperion; and Arthrex, Inc.
Maureen Leahy is assistant managing editor of AAOS Now. She can be reached at [email protected]
 
There is much to discuss about this case. Despite the low incidence of stroke, complications, (see editorial from Anesthesia and Analgesia June 2012) if this happens to one of your patients then the case will be reviewed. What did you do or not do to avoid this complication? What was your reasoning/evidence behind those decisions?
 
food for thought:

http://www.apsf.org/newsletters/html/2008/winter/17_problems_of_posture.htm

This was a topic of frequent discussion in my residency (with the author of this paper). For the physiologically inclined, take a look at studies of MAP and CPP in giraffes.

Wait a minute slim. I appreciate the reference but Dr. Munis is NOT the only opinion here on this topic. Dr. Munis doesn't think we need to keep the transducer at the ear/tragus level while maintaining BP at baseline value because that would make the patient hypertensive. Instead, maintain BP at baseline value with the transducer at the cuff level.
Here is another quote from Dr. Munis:


Dr. James R. Munis, head of the Division of Neuroanesthesia at the Mayo Clinic, provided a brief physiologic review of the differences in cerebral perfusion pressure in a "siphon" or closed vascular system compared to a "waterfall" or open system. He believes that cerebral perfusion pressure should be maintained at or near awake levels by keeping the blood pressure (measured in the upper arm) at the baseline awake level. He does not believe that is it necessary to correct for the difference in height between the head and heart level. Dr. Munis believes that correcting for the height difference and maintaining awake MAP values at the head level would essentially make the patient hypertensive.
 
Another expert:


Dr. David Cullen, previous chair in the Department of Anesthesiology at Tufts Medical Center, reviewed his case series of 4 patients who developed severe and permanent brain or spinal cord infarcts after having anesthesia with deliberate hypotension in the beach chair position. He reported that he was aware of an additional 11 cases in which patients suffered severe brain damage under similar circumstances. Dr. Cullen believes that anesthesia care providers need to maintain blood pressure at or near baseline levels in the sitting position. He provided the following recommendations to avoid hypotension in the sitting position: 1) titration of anesthetics to avoid excessive depth of anesthesia; 2) minimizing sudden changes in position; 3) administration of intravenous fluids to offset the effects of NPO status and the sitting position on venous return; 4) use of vaspressors to maintain blood pressure, as needed; and 5) correction of blood pressure for the difference in height between the site of measurement and the brain (1 cm height = 0.77 mmHg or 1 mmHg = 1.25 cm height) .
 
Dr. John C. Drummond, professor and former chair of the Department of Anesthesiology at the University of California at San Diego, started his lecture by showing erroneous representations of the lower limit of autoregulation in neuroanesthesia chapters in textbooks of anesthesia—some of which he admittedly authored. He presented an overview of studies of autoregulation and showed the wide range in reported lower limits of autoregulation (30-110 mmHg, Anesthesiology 1997). Dr. Drummond believes that the available evidence favors a lower limit of 70 mmHg in the heathy and normotensive adult in the supine position, rather than the conventional or classic limit of 50 mmHg. Dr. Drummond commented that his most recent chapter in Miller has been modified to reflect this change in interpretation of available studies. He also emphasized that over 45% of the population has an incomplete circle of Willis, which may decrease the autoregulatory capacity.
 
Did this recently. 89 R shoulder. PCI 2 yrs ago. Interscalene block. Awake a line. Transducer at head. Neo gtt to maintain map.

May I suggest that your approach to the case is questionable based on all available evidence in 2012?

Transducer at the head? Why? what BP was used to determine NEO drip? Did you use DBP or mean BP? Why Neo over other pressors? Is Neo the best choice?



http://www.cairnsanaes.org/page11/files/Soeding.PDF
Go ahead and read this study.
 
Dr. Nigel E. Sharrock, staff anesthesiologist from the Hospital for Special Surgery in New York, reviewed his experience with the use of deliberate hypotension in elderly patients undergoing hip surgery. He and his colleagues have published multiple papers on the use of this technique for minimizing blood loss, and its safety in elderly patients. Their anesthetic technique includes lowering the MAP to 45 to 55 mmHg, epidural anesthesia, and an epinephrine infusion to augment the cardiac output. He noted that when his center initially started using deliberate hypotension to a MAP of 50 mmHg with epidural anesthesia (without epinephrine) for hip surgery to decrease blood loss, patients would complain of feeling light-headed. A variety of vasoactive agents were used to augment the cardiac output, and epinephrine proved most effective for eliminating the presyncopal symptoms. Dr. Sharrock’s studies have shown that the epinephrine infusion significantly raises the cardiac output under these conditions. He believes that is why these patients did not have any significant increase in complications compared with control patients who had their MAP maintained between 60 to 70 mmHg. Complications that were examined included stroke, myocardial infarction, and postoperative cognitive dysfunction. Dr. Sharrock has examined small subsets of patients including those with hypertension (n = 31) chronic renal dysfunction (n = 54), moderate to severe aortic stenosis (n = 22), or low ejection fraction (n = 29). He has found no significant increase in complications in any group utilizing deliberate hypotension compared to patients kept normotensive. He has also studied postoperative cognitive dysfunction (POCD) in patients receiving hypotensive anesthesia compared to those in a normotensive group. At 7 days and 4 months postoperatively, there was no significant increase in POCD in the hypotensive group compared to the normotensive group. It was noted that hip surgery is performed in the lateral decubitus or supine position where the heart is relatively equal with the head level and the lower body. In contrast, the beach chair position places the lower body dependent to the heart, thereby decreasing venous return and cardiac output. The satisfactory outcomes in Sharrock’s studies may be partially attributed to good venous return and augmented cardiac output associated with the use of low dose epinephrine.
 
Review the case again. This is how the patient presents in the holding area for surgery.
He is a non-smoker. He quite smoking Cigars 20 years ago. He drinks once a day.


How does his BP and HgA1C look to you? Are both acceptable for the surgery/anesthesia?

What exactly is reasonable range of BP for this patient? Can you elaborate on that range? Will you use his SBP or DBP or mean BP as the variable to decide if pressors are needed?

BP appears poorly controlled but he may just be nervous. Be prepared for big swing in BP with induction. I would use MAP to decide if pressors are used. I would aim for MAP above 70-75. Cerebral auto regulation curve is likely shifted to the right in this patient.

I would discuss with pt and surgeon the risk of infection with his poorly controlled BS. I would not cancel for that HgA1C. Surgeon may or maybe nervous nancy (patient).

One question I have is why is patient still on effient 2 years out? I'm now spooked for a suboptimally deployed stent.
 
Why does phenylephrine decrease frontal lobe oxygenation but increase cerebral blood flow velocity?

February 8, 2012Leave a commentGo to comments

Hypotension represents the most frequent side effect of anesthesia. Its correction is of importance to secure perfusion pressure of vital organs such as the brain. As discussed in a previous post, I have been interested in the impact of vasopressors on cerebral blood flow and oxygenation since my postdoc. We, and others, have reported that the utilization of vasopressors increasing mean arterial pressure by peripheral vasoconstriction was associated with a reduction in frontal lobe oxygenation. We observed such results in the laboratory in normotensive healthy subjects and in the operating room in hypotension patients undergoing elective surgery.
We need to better understand what explains a reduction in frontal lobe oxygenation following the utilization of vasopressors like phenylephrine or norepinephrine because 1) these agents are first-line agents used to correct mean arterial pressure in hypotensive states and 2) a reduction in cerebral oxygenation during surgeries such as a coronary artery bypass is associated with neurological impairments after the surgery and neurological outcomes seem to be improved when the reduction in cerebral oxygenation is prevented or corrected.
One intriguing observation reported by Ainslie's group as well as our research group was that bolus/infusion of phenylephrine, a selective alpha-adrenergic agent, was associated with a reduction in frontal lobe oxygenation, but also with an increase in cerebral blood flow velocity measured in the middle cerebral artery. This was intriguing because one could argue that a reduction in cerebral oxygenation is the consequence of a reduction in flow. One suggestion could be that phenylephrine induces (whether directly or indirectly via a reduction in cardiac output) vasoconstriction of the middle cerebral artery, leading to an increase in cerebral blood flow velocity (remember that we are not measuring blood flow but blood flow velocity with transcranial doppler) and a decrease in frontal lobe oxygenation.
Shigehiko Ogoh's research team investigated that issue by evaluating the influence of phenylephrine on frontal lobe oxygenation (by near-infrared spectroscopy) and middle cerebral artery flow velocity (transcranial doppler) and blood flow changes in the internal carotid artery and internal jugular vein (by duplex ultrasonography).
The main results are presented in the figure below:
As others did, this team observed reduced frontal lobe oxygenation (not in the figure) and increased middle cerebral artery blood flow (MCAVmean) with infusion of phenylephrine vs. saline. Interestingly, blood flow in the internal carotid artery (ICA BF) did not change and blood flow in the internal jugular vein (IJV BF) increased (due to an enlargement of internal carotid artery diameter). No change in arterial oxygen or carbon dioxide tensions was observed. However, phenylephrine did not decrease cardiac output.
What was the interpretation of the authors?
The results suggest that the decrease in frontal lobe oxygenation during phenylephrine infusion is caused by a smaller arterial and larger venous contribution to the NIRS signal as an elevated MCAVmean with constant ICA flow conforms to elevated arterial tone, while venous tone is reduced as indicated by an enlarged IJV diameter
So phenylephrine seems to constrict the middle cerebral artery while cerebral blood flow is maintained. Although further research is needed to support such findings and explain how this agent could directly constrict this artery without crossing an intact blood brain barrier, this study suggests that the utilization of phenylephrine don't interrupt delivery of oxygen to the brain despite the reduction observed in frontal lobe oxygenation.
The authors suggest that the reduction in frontal lobe oxygenation could be related to a shift in the arterial versus venous contribution to the near-infrared signal (used to measure frontal lobe oxygenation). Indeed, an increased blood flow from the vertebral arteries (with no change in internal carotid artery blood flow) could have contributed to the higher venous blood flow during the infusion of phenylephrine. In addition, the authors suggested that we cannot exclude the influence of skin blood flow on the near-infrared signal.
These results and interpretations are very interesting and definitely move the field forward. However, one needs to keep in mind that a reduction in cerebral oxygenation has been associated with neurological impairments following cardiac surgeries. I am not convinced that this could be explained by a redistribution of cerebral blood flow or a reduction in skin blood flow.
One final issue I would like to discuss is the absence of impact of phenylephrine on cardiac output. We and others have reported reduced cardiac output with the administration of phenylephrine. As discussed in other posts (here and here), the potential mechanisms underlying the modulation of cerebral oxygenation by cardiac output could be sympathetically mediated vasoconstriction induced by a lowering in cardiac output or it could also depend on the distribution of circulating blood volume. So, the results from Ogoh's group cannot be necessarily generalized to subjects experiencing a reduction in cardiac output with phenylephrine.
Further research is warranted to characterize the influence of vasopressors on cerebral perfusion/oxygenation and as Ogoh's team did, we need to measure blood flow/blood flow velocity in different arteries during infusion studies in order to have a more complete picture.
Reference:
Ogoh, S., Sato, K., Fisher, J. P., Seifert, T., Overgaard, M., & Secher, N. H. (2011). The effect of phenylephrine on arterial and venous cerebral blood flow in healthy subjects. Clinical physiology and functional imaging, 31(6), 445&#8211;451. doi:10.1111/j.1475-097X.2011.01040.x
 
In an accompanying editorial, Drs. Harrington and Califf from Duke university suggest that patients with DES should be kept on Plavix and aspirin more-or-less indefinitely if at all possible, at least until future studies demonstrate the safety of stopping these drugs.



Pfisterrer M, Brunner-La Rocca HP, Buser PT, Rickenbacher P, Hunziker P, Mueller C, Jeger R, Bader F, Osswald S, Kaiser C. Late clinical events after clopidogrel discontinuation may limit the benefits of drug-eluting stents. J Am Coll Cardiol 2006;48:2584. Harrington RA, Califf RM. Late ischemic events after clopidogrel cessation following drug-eluting stenting. Should we be worried? J Am Coll Cardiol 2006;48:2592.

http://www.dukehealth.org/health_library/news/9972

Read the above link.
 
What is my chance of staying alive with my drug-eluting stent in place?

93% after 4 year follow up (A)
94% after 4 year follow up (B)
94% after 3 years (C)
90% after 5 years (D)

A. Spaulding C, Daemen J, Boersma E, Cutlip DE, Serruys PW. A pooled analysis of data comparing Sirolimus-Eluting Stent with Bare-Metal Stents. N Engl J Med 2007;356:989-997.

B. Stone GW, Moses JW, Ellis SG, Schofer J, Dawkins KD, et.al. Safety and Efficacy of Sirolimus and Paclitaxel-Eluting Coronary Stents. N Engl J Med 2007;356:998-1008..

C. Lagerqvist B, James SK, Stenestrand U, Lindback J, Nilsson T, et. al. Long-term outcomes with drug-eluting stents versus bare-metal stents in Sweden. N Engl J Med 2007;356:1009-1019.

D. Kastrati A, Mehilli J, Pache J, Kaiser C, Valgimigli M, et. al. Analysis of 14 trials comparing sirolimus-eluting stents with bare-metal stents. N Engl J Med 2007;356:1030-1039.
 
Researchers at Toronto General Hospital used data from more than 61,000 patients to compare people who took ACE inhibitors with those who did not, and found that being on the blood pressure medication long-term leading up to noncardiac surgery was associated with lower 30-day mortality.
When they looked more closely at the ACE inhibitor group, they found that those who chose to stop taking the drugs a few days prior to surgery, and delayed restarting it, fared no better than those who took the drug up to the morning of the procedure, and resumed once they were stable.
"Maintaining ACE inhibitors prior to surgery might be of some benefit," said study author Jason Toppin, MD. "And they definitely do not cause any problem."
Dr. Toppin's group presented its findings at the 2011 annual meeting of the Society of Cardiovascular Anesthesiologists (abstract 64).
 
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1. Patient understands the risk of stroke but wants to know is there anything you can do to minimize his risk?
2. Will you agree to do the case on this patient awake or with light sedation? Is spontaneous ventilation helpful or harmful from a risk reduction standpoint?
3. If you won't do the case under sedation/propofol would you do it under an LMA/block combo?
4. Would you block this patient preop or postop? Does the risk of brachial plexus injury from the shoulder surgery influence your decision? Does the fact the patient stopped his Effient only 6 days ago alter your decision for an ISB/SCB?
5. Would you place an arterail line for this case preinduction or after induction or not at all?
6. Any evidence that the BIS or Brain Oximetry reduces risk of stroke?
7. Where would you keep his BP during the case? Why?
8. If you have a CRNA in the room what is the minimum BP before giving pressors?
9. Any evidence over which pressor to use in this case?

I want the real world approach and NOT just an Oral Board answer.

1. Oxygenate and perfuse 🙂
2. Will do the case asleep with positive pressure ventilation. IMO distant airway, long procedure, venous air embolism add up to bigger threat. Keeping the ventilator on.
3. See # 2
4. Medically the block plus GA is better for the patient IMO. Medicolegally a straight GA is more of a clean getaway.
5. +/- on the Aline. If I use a cuff - take into account where the BP cuff is placed. Some folks put in on the forearm which will be quite a bit lower than the head for this patient.
6. No evidence, but it might sound nice to a jury.
7. The answer to the question "what is the minimum safe blood pressure?" is unknown, but I am more aggressive than most for treating. I hate it when the CRNA or resident lets the BP dwindle during prep and says, he is just "waiting for incision and stimulation."
 
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1. Oxygenate and perfuse 🙂
2. Will do the case asleep with positive pressure ventilation. IMO distant airway, long procedure, venous air embolism add up to bigger threat. Keeping the ventilator on.
3. See # 2
4. Medically the block plus GA is better for the patient IMO. Medicolegally a straight GA is more of a clean getaway.
5. +/- on the Aline. If I use a cuff - take into account where the BP cuff is placed. Some folks put in on the forearm which will be quite a bit lower than the head for this patient.
6. No evidence, but it might sound nice to a jury.
7. The answer to the question "what is the minimum safe blood pressure?" is unknown, but I am more aggressive than most for treating. I hate it when the CRNA or resident lets the BP dwindle during prep and says, he is just "waiting for incision and stimulation."


May I suggest that if you use a ventilator then keeping the CO2 at 50 is possibly better for CBF than keeping it at 30? In fact, the data seems to suggest that the main advantage of an LMA or IV sedation is a higher CO2/better CBF than artificial ventilation. Perhaps, CO is maintained better with spont. respirations as well.
http://www.aaos.org/news/aaosnow/apr12/clinical5.asp
 
1. Oxygenate and perfuse 🙂
2. Will do the case asleep with positive pressure ventilation. IMO distant airway, long procedure, venous air embolism add up to bigger threat. Keeping the ventilator on.
3. See # 2
4. Medically the block plus GA is better for the patient IMO. Medicolegally a straight GA is more of a clean getaway.
5. +/- on the Aline. If I use a cuff - take into account where the BP cuff is placed. Some folks put in on the forearm which will be quite a bit lower than the head for this patient.
6. No evidence, but it might sound nice to a jury.
7. The answer to the question "what is the minimum safe blood pressure?" is unknown, but I am more aggressive than most for treating. I hate it when the CRNA or resident lets the BP dwindle during prep and says, he is just "waiting for incision and stimulation."


I believe you are partially incorrect on number7. Allowing the BP/Mean BP to drift below 65 (cuff on the arm) in high risk patients undergoing surgery in the beach chair position will definitely make a lawsuit more likely if a serious neurological complication occurs.

In high risk groups like the case presented here I now use 70.
 
The evidence linking a high HGA1c with postop total joints infections is weak. That said, most Orthopods would want a HgA1c of less than 7.0 if possible. Cancel a case for elevated sugars or HgA1C? I would do so only if the numbers were extremely outside the norm for diabetics.


http://www.ncbi.nlm.nih.gov/pubmed/22054905
Hemoglobin A1c levels are not reliable for predicting the risk of infection after TJA.
 
Anesth Analg. 2002 Mar;94(3):661-6; table of contents.
Cerebral blood volume and blood flow responses to hyperventilation in brain tumors during isoflurane or propofol anesthesia.

Cenic A, Craen RA, Lee TY, Gelb AW.
Source

Department of Radiology, St. Joseph's Health Centre, Imaging Research Laboratories, University of Western Ontario, London, Canada.

Abstract

Using computerized tomography, we measured absolute cerebral blood flow (CBF) and cerebral blood volume (CBV) in tumor, peri-tumor, and contralateral normal regions, at normocapnia and hypocapnia, in 16 rabbits with brain tumors (VX2 carcinoma), under isoflurane or propofol anesthesia. In both anesthetic groups, CBV and CBF were highest in the tumor region and lowest in the contralateral normal tissue. For isoflurane, a significant decrease in both CBV and CBF was observed in all tissue regions with hyperventilation (P < 0.05), but without accompanying changes in intracranial pressure. However, the percent reduction in regional CBF with hypocapnia was two times larger than that observed in the CBV response (P < 0.01). In contrast, there were no significant changes in CBV and CBF in the Propofol group with hyperventilation for all regions (P > 0.10). In addition, there were no differences between CBV values for isoflurane at hypocapnia when compared with CBV values for propofol at normo- or hypocapnia (P > 0.34 and P > 0.35, respectively, in the tumor regions). Our results indicate that propofol increases cerebral vascular tone in both neoplastic and normal tissue vessels compared with isoflurane. CBV and CBF during normocapnia were significantly greater in all regions (tumor, peri-tumor, and contralateral normal tissue) with isoflurane than with propofol. CBV and CBF remained responsive to hyperventilation only with isoflurane. IMPLICATIONS: In rabbits with brain tumors, brain blood flow and volume were significantly larger in all regions (tumor, peri-tumor, and contralateral normal tissue) with isoflurane than with propofol during normocapnia, and remained responsive to a reduction in PaCO(2). Consequently, during hypocapnia, brain blood flow and volume values with isoflurane were similar to values with propofol.
 
Dr. John C. Drummond, professor and former chair of the Department of Anesthesiology at the University of California at San Diego, started his lecture by showing erroneous representations of the lower limit of autoregulation in neuroanesthesia chapters in textbooks of anesthesia—some of which he admittedly authored. He presented an overview of studies of autoregulation and showed the wide range in reported lower limits of autoregulation (30-110 mmHg, Anesthesiology 1997). Dr. Drummond believes that the available evidence favors a lower limit of 70 mmHg in the heathy and normotensive adult in the supine position, rather than the conventional or classic limit of 50 mmHg. Dr. Drummond commented that his most recent chapter in Miller has been modified to reflect this change in interpretation of available studies. He also emphasized that over 45% of the population has an incomplete circle of Willis, which may decrease the autoregulatory capacity.

The evidence is pretty clear that if you decide to go with MAP lower than 70 you better have a darn good reason.
 
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