We offer this section
of AnesthesiaWeb in order to let members interact directly with our Advisory
Board and occasional guest experts. Questions, which should be submitted
using the form included, are welcomed on guideline issues and other topics
of interest to the medical community. When submitting a question, please
allow up to three weeks for an answer.
Unfortunately, Board members are unable to advise site visitors on specific
case questions as they do not have complete information on the patient's
medical history.
Read the most
recent exchanges between AnesthesiaWeb users and the Advisory Board:
Should ACE inhibitors be stopped in patients undergoing surgery under spinal
anesthesia? Is the hypotension of spinal anesthesia augmented with ACE
inhibitors?
—arfaan@hotmail.com
In general, continuing all cardiac medications the day of surgery makes
sense. While it may seem reasonable to withhold ACE inhibitors for the
spinal, what happens when the spinal wears off and there is neither
sympatholysis nor regular medication decreasing afterload? Therefore, most
practitioners would choose to continue the current medication regimen.
Epidural vs. general anesthesia: Is it true that epidural has clear advantages over general, and, if so, why is it so underutilized in the US as compared to Europe and, if so, what are the reasons?
—fciferri@earthlink.net
This is a complicated question with a simple answer. No one can show a real
difference. One of the best studies to date - Norris et al. Anesthesiology
2001, looked carefully at the benefits of regional supplemented general
anesthesia and epidural postoperative analgesia in one of the patient
populations reputed to derive the most benefit - patients undergoing AAA's.
That thorough blinded study demonstrated what every well conducted
controlled randomized study to date has demonstrated - ABSOLUTELY NO
BENEFIT. While we would like to believe we can impact outcomes with our
savvy choice of anesthetic, this latest study confirmed that pain control,
economic outcomes, length of stay, cardiopulmonary outcomes, or any other
outcome of interest to patients was not enhanced by regional
anesthesia/analgesia. Earlier extubation was achieved with epidural
postoperative analgesia compared to IV PCA, but did not affect the larger
outcomes noted above.
A patient developed seventh cranial nerve palsy following epidural given for labour pains. Could you please tell me if any such cases are reported in the literature?
—msakhan4@hotmail.com
Dr. Joy Steadman responds:
It would help if there were an actual picture or description of the palsy in question. Horner's syndrome, which results in ptosis on the affected side, has been reported numerous times with epidural anesthesia. 6th and 3rd cranial nerve palsies are also not uncommon. Bell's palsy, which happens not infrequently during pregnancy due to the depressed immune system, is the result of HSV of the ear affecting the 7th cranial nerve. If the palsy onset and resolution were temporally related precisely to the onset and offset of the epidural anesthetic/analgesia, then certainly it may be related. If the palsy did not resolve after the anesthetic wore off, I would suspect some other reason. Certainly, an ENT consult and possibly an MRI would help elucidate the problem. On the other hand, an isolated 7th cranial nerve palsy that came on with the epidural and resolved when the epidural wore off would make a nice case report...especially if a picture were to illustrate the event.
I would like to know about the indications and limits of the use of hypertonic saline.
—rramzy@hotmail.com
Patients with profound hyponatremia (sodium,115-120 meq/L) or neurologic symptoms may require hypertonic (3%) saline. In these cases, 3% saline may be administered at a rate of 1-2ml/kg/hr to increase plasma Na by 1-2 meq/l/hr. However, this treatment should not continue for more than a few hours. Inappropriately rapid, aggressive treatment may result in abrupt brain dehydration or permanent neurologic sequelae such as central pontine myelinolysis or the osmotic demyelination syndrome, cerebral hemorrhage, or congestive heart failure.
There are data suggesting that the addition of relatively small volumes of hypertonic saline may be beneficial in multiple trauma patients with head injury.
Or what isn't new? One truly new finding is that injecting blood or other fluid into the epidural space causes a reactive vasoconstriction in the brain (at least in swine), which explains why blood patches have an immediate effect. Another very recent study, total of 48 patients, in New Mexico showed that injecting 10cc of preservative free saline into the CSF immediately after dural puncture with a large bore needle decreased the incidence of post dural-puncture headache compared with patients who received no saline in the CSF. This group also injected saline through the catheter if they used an intrathecal catheter. Prophylactic blood patch is beginning to wane in popularity due to the rise in case reports of untoward events after blood patch (including prolonged radicular symptoms, cauda equina syndrome, subarachnoid bleed, etc.). Most studies looking at blood patch are either very small, retrospective, unblinded, or have other serious methodologic flaws. Recumbency after patching probably doesn't really matter, and the requisite amount of blood required for a patch is still a matter of discussion although 18cc+/- 5cc may be the right ballpark.
Caffeine still gives safe symptomatic relief, while ergotamines and 'triptans' frequently cause side effects without guaranteeing headache relief. The jury is still out on the timing of blood patch, with a possible edge toward waiting 1-4 days after it develops. Blood patches after small needle holes are more successful than after large needle holes. MRI follow-up of blood patches show that by 18-24 hours most of the patch is resorbed.
I would like to know the incidence and pathophysiology of pulmonary edema that can be seen in patients with acute airway obstruction i.e., laryngeal spasm post extubation.
—jpony99@aol.com
Negative pressure pulmonary edema has long been described in association with airway obstruction and in particular the sudden relief of airway obstruction. This obstruction may take the form of epiglottitis, croup, laryngospasm, tonsillar hypertrophy and others; I have seen it with a child biting on an endotracheal tube at the conclusion of anesthesia.1-6 The most common postulated mechanism is an extreme difference between intrapleural and atmospheric pressure (increased alveolar-capillary transmural pressure) followed by a flooding of the lungs with increased venous return after relief of the obstruction. There are no prospective studies defining the incidence in children. There is an adult study describing an incidence of 0.094% in one institution.7 The bottom line is that if a child has severe upper airway obstruction, then negative pressure pulmonary edema may occur. This may occur in patients of any age, even neonates. Generally supportive therapy is all that is required and all returns to normal within 24 hours.
Reference List
Lang SA, Duncan PG, Shephard DA, Ha HC. Pulmonary oedema associated with airway obstruction. Can J Anaesth. 1990; 37: 210-218.
Lee KW, Downes JJ. Pulmonary edema secondary to laryngospasm in children. Anesthesiology. 1983; 59: 347-349.
Oudjhane K, Bowen A, Oh KS, Young LW. Pulmonary edema complicating upper airway obstruction in infants and children. Can Assoc Radiol J. 1992; 43: 278-282.
Scherer R, Dreyer P, Jorch G. Pulmonary edema due to partial upper airway obstruction in a child. Intensive Care Med. 1988; 14: 661-662.
Thomas CL, Palmer TJ, Shipley P. Negative pressure pulmonary edema after a tonsillectomy and adenoidectomy in a pediatric patient: case report and review. AANA J. 1999; 67: 425-430.
Travis KW, Todres ID, Shannon DC. Pulmonary edema associated with croup and epiglottitis. Pediatrics. 1977; 59: 695-698.
Polio is an anterior horn disease at the level of the spinal cord. The major concern for anesthesiologists is the relative response to neuromuscular blocking agents and the severity of the residual muscle weakness. It is known that these patients are more sensitive to neuromuscular blocking agents and that this is a particular concern if the muscles of respiration are involved. It is for this reason that most practitioners start out with about one-half to one-third of the standard dose of muscle relaxant and quantitate the response. Regarding the response to succinylcholine, there are no published studies. One review article suggests the possibility of acute hyperkalemia in patients with idiopathic anterior horn cell disease but there is little guidance as to patients with long-term disease. In general, it appears that there is no association of a hyperkalemic response in these patients but they may exhibit a prolonged or exaggerated response following succinylcholine.[1,2]
Reference List
Azar I. The response of patients with neuromuscular disorders to muscle relaxants: a review. Anesthesiology. 1984; 61: 173-187.
Beach TP, Stone WA, Hamelberg W. Circulatory collapse following succinylcholine: report of a patient with diffuse lower motor neuron disease. Anesth Analg. 1971; 50: 431-437.
What is your opinion about using succinycholine in a patient with neuroleptic malignant syndrome antecedent to conduct electroconvulsive therapy?
—jlso@ono.com
Typical triggers for neuroleptic malignant syndrome include phenothiazines, haloperidol, or any of the newer potent antipsychotic agents. Sudden withdrawal of drugs used to treat Parkinson's disease may also trigger NMS. ECT with succinylcholine does not appear to trigger NMS.
Typical triggers for neuroleptic malignant syndrome include phenothiazines, haloperidol, or any of the newer potent antipsychotic agents. Sudden withdrawal of drugs used to treat Parkinson's disease may also trigger NMS. ECT with succinylcholine does not appear to trigger NMS.
Reference:
Addonizio G, Susman VL. ECT as a treatment alternative for patients with symptoms of NMS. J Clin Psych. 1987;48:102.
What is the incidence of choking on foreign bodies such as dentures during the perioperative period?
—sadybin@vsnl.com
This is not known. However, to avoid this problem, doctors usually ask that
all foreign bodies (dentures, tongue rings, etc.) be removed prior to
surgery. In my opinion, the probability would be very low. Leaving a foreign
body in a patient who could potentially have their airway obstructed by its
displacement while sedated and recovering from anesthesia seems foolhardy.
Do you know of any reason for a very long recovery from a diprivan infusion for an endoscopy with no other drugs given 8 hrs and counting lab ok, CT OK?
—crnapc@greene.xtn.net
Delayed awakening has many causes. Bready and Smith in their book on
differential diagnosis give a good complete run down. Propofol is not known
to cause delayed awakening even after prolonged infusions (hence its
preferred use in the ICU).
The first thing is to rule out hypoxia, hypoglycemia and hypotension, which
can be immediately life threatening. Then one has to assess other potential
drug, metabolic and neurologic causes. There are at least 50 total
causes - everything ranging from central anticholinergic syndrome from
atropine given as part of the procedure to severe acidosis and hypercapnia
from a prolonged infusion of a respiratory depressant such as propofol to a
stroke. I hope the patient is OK.
What are the advantages and disadvantages of using spinal anesthesia for a TURP on an otherwise healthy 78-year-old male as opposed to general anesthesia?
—trenklaw@aol.com
The advantages of spinal anesthesia for TURP are that it allows assessment of the effect
of fluid absorption during the TURP on respirations (fluid overload) and
early assessment of any CNS effect of hyponatremia. The disadvantages
include a more prolonged recovery for an outpatient procedure compared to a
propofol LMA technique.
1. Is there a reference book with anesthesia clinical scenarios available?
2. Need info on use of Precedex infusions during surgeries. Can you help?
—KNDMAGNUS@AOL.COM
1. There a couple of excellent tomes. Common problems in cardiac anesthesia
and common problems in pediatric anesthesia is part of a series of books
that present common clinical issues. Oral board preparation books (OK, I'm
partial) such as Board Stiff Too (by Lubarsky and Gallagher) provide the
latest and greatest clinical scenario presentations. However, other such
books such as Yao and Artusio's book offer some good clinical scenarios as
well. Finally, the problem-based learning discussions at the ASA and other
meetings are great sources for such material.
2. As you are well aware, I am sure, Precedex requires a little advance
planning to bolus and achieve good therapeutic levels (tens of minutes). It
is primarily a sedative via alpha 2 adrenergic agonist activity (causes
presynaptic feedback inhibition of catecholamines in the CNS). Precedex is
not usually used except at the end of the case to prepare for postoperative
sedation. Its use as a sole agent (given limited amnesia and analgesia
alone) makes it a mediocre choice. It failed as a sole agent during
endoscopies - not enough analgesia. However, I see excellent potential uses
as a complement to surgeries using local anesthesia, as part of a
multi-modal MAC anesthetic (especially on those with sleep apnea given its
lack of respiratory depression), for use in fiberoptic intubations, and
other non-painful conscious sedations where having the patient must remain
still (such as auditory testing in children, or MRIs). For further
information, I recommend you contact your local Abbott Labs representative,
as Abbott makes the product.
