Letters to the Editor:
Perioperative Beta-Blockade Requires Further Study—Not Standard of Care
AHRQ Responds: Promotes Beta-Blockade, Encourages Further Study
Ultrasound Guidance Should Not Be Standard of Care
Policies & Procedures Needed For Sleep Apnea Patients
OSA Protocol Promotes Safer Care
Beware of All Sedatives in Patients With Sleep Apnea
Concentrated Solutions Cause Concern
Perioperative Beta-Blockade Requires Further Study—Not Standard of Care
To the Editor:
I would like to respond to Dr. Royster’s lead article published in the Summer 2002 APSF Newsletter, touting the potential benefit of perioperative beta-blockade.1 I agree that “. . . it seems logical that beta-blockade might be beneficial during the stressful surgical period.”1 However, interventions that seem logical, rational, and, therefore, beneficial, sometimes surprise us, and ultimately turn out, not only not helpful, but indeed harmful. Witness the “rational” treatment of arrhythmias during myocardial infarction with antiarrhythmic drug therapy. That was ultimately proven harmful by the CAST trial.2 More recently, we all thought that hormone replacement therapy was a logical and beneficial treatment for women undergoing menopause, until recently proven otherwise by a large, randomized controlled trial.3
If we look closely at the outcome data for the use of beta-blockade in the perioperative period, we see there are only 3 studies (to the best of my knowledge) that directly addressed the question of whether beta-blockade affects perioperative outcome. Ischemia is not an outcome, myocardial infarction and death are. As such, Mangano showed no difference in in-hospital mortality between those receiving perioperative beta-blockade versus those not receiving beta-blockade.4 The two groups in that study showed different outcomes months to years after surgery, in a mere 200 patients. Clearly, a much larger study is needed. Poldermans did show a remarkable reduction in in-hospital adverse outcomes between the beta-blockade treated group versus the “standard” treatment group.5 However, one of the controversial aspects of his study was the fact that the “standard-treatment” group had 17% adverse outcomes; an adverse event rate much higher than most of us would expect.5 Could Poldermans’ findings be due to an idiosyncratic high event rate in the control group (standard treatment) and not an efficacious effect of beta-blockade in the experimental group? We do not know the answer. Urban (in an underpowered study involving a “low risk” group of patients) found no difference in primary outcomes (myocardial infarction and death) between patients treated postoperatively with beta-blockers versus those who were not.6 In addition, several recent observational studies have shown no protective effect of perioperative beta-blockade. In a subgroup of patients with extensive dobutamine-induced wall motion abnormalities, cardiac complications occurred in 36% of patients receiving perioperative beta-blockers and in 33% of those who were not receiving beta-blockers.7 In a re-evaluation of the incidence of myocardial infarction after noncardiac surgery, Badner, showed that perioperative beta-blockade was not protective.8 Finally, Lee in a prospective analysis of over 2500 patients showed no difference in cardiac complications between those receiving preoperative beta-blockade and those patients who were not.9 Clearly what we have here is the need for a large randomized controlled trial—trials for which the Veterans Affairs Cooperative Studies program are world famous. In the meantime, I would hold off labeling perioperative beta-blockade therapy with the emotionally laden medical legal term: “standard of care.” Yes, there is reasonable evidence supporting the use of perioperative beta-blockade. I believe, however, for the reasons I cited above, that competent and equally good practitioners can still differ. One can still believe that perioperative beta-blockade is not indicated in moderate to high-risk patients presenting for noncardiac surgery.
Bruce Kleinman, MD
Hines, Illinois
AHRQ Responds: Promotes Beta-Blockade, Encourages Further Study
To the Editor:
The AHRQ Patient Safety Practices report, developed by the UCSF-Stanford Evidence-based Practice Center, found that the perioperative beta-blockade in appropriate patients was strongly supported by published evidence demonstrating reduced perioperative morbidity and mortality.1 Dr. Royster’s lead article in the Summer 2002 APSF Newsletter summarized this evidence and supported our report’s conclusion. In response to Dr. Royster's prediction that this practice may evolve into a standard of care, Dr. Kleinman argues that, while existing evidence supports use of perioperative beta-blockade, sufficient questions remain to warrant a larger trial.
Perioperative beta-blockade ranked in the top category of the 70-plus patient safety practices reviewed in the AHRQ Report because evidence indicating that this practice reduces adverse events from medical care (our operational definition of patient safety practices) is much better than that of most of the other candidate safety practices reviewed. Thus, this high ranking results just as much from the paucity of evidence supporting other practices as it does from the strong, but not ironclad, evidence supporting perioperative beta blockade.
Many of Dr. Kleinman’s concerns regarding strength of evidence apply equally well to other prominent patient safety practices. For example, the major clinical trial to examine the impact of computerized order entry showed only a non-significant reduction in adverse drug events.2 Thus, the mandate that hospitals across the country adopt this multi-million dollar technology3 rests largely on one study showing an impact on a surrogate safety outcome—medications errors, rather than on compelling evidence about the clinical outcome of interest—adverse events. Similarly, fatigue’s impact on clinical performance has been on errors and other surrogate endpoints in simulated scenarios.4 Nonetheless, work hour restrictions are being vigorously pursued5 despite little hard evidence in favor of their benefit and some evidence for possible harm (e.g., due to increased handoffs).6
In the end, we agree with Dr. Kleinman that the evidence supporting perioperative beta-blockers is strong, but not as firm as one would like for a clinical practice potentially affecting millions of patients. As with all probabilistic decisions, the conclusion one draws on the basis of existing evidence depends on whether we would rather risk adopting an ineffective (or even harmful) safety practice or risk missing the opportunity to adopt an effective one. In this case, the editors of the AHRQ report and the investigators who reviewed this specific practice7 interpreted the available evidence as favoring use of perioperative beta-blockade. We did not intend to imply that this or any other practice reviewed in the report yet has sufficient supporting evidence to warrant the label standard of care. In fact, we highlighted perioperative beta-blockade as a practice for which further research would be highly beneficial.1 The balancing act facing all of us—as clinicians and advocates of patient safety—is how to promote practices that will improve safety without demanding overly stringent standards of evidence. In this case, in our judgment a reasonable compromise would be to promote use of perioperative beta-blockade (without necessarily labeling it as standard of care) but to follow-up such promotion with well-designed outcomes analyses.
Kaveh G. Shojania, MD
Robert M. Wachter, MD
Department of Medicine, University of California San Francisco
Kathryn M. McDonald, MM
Center for Primary Care and Outcomes Research, Stanford University
Ultrasound Guidance Should Not Be Standard of Care
To the Editor:
The “opinion” of Webster and Blitt in a recent APSF Newsletter mandating routine use of ultrasound (US) in guiding central venous access (CVA) was very disturbing.1 Recently, a drug with an excellent safety profile and many years of effective use was “black boxed” by the FDA. The FDA’s case was supported by weak data and a flawed argument that has since been easily rebuked in our literature.2 Now I am told that the thousands of central access procedures my colleagues and I perform yearly without significant complications (a check of the Medical University of South Carolina Anesthesia QA Database [2001] revealed the following: 2,036 central axis placements, 3 adverse events, and 0 adverse outcomes) should be performed exclusively under US guidance? What is next? All general anesthesia cases require BIS? All endotracheal tube placements should be confirmed fiberoptically?
The Institute of Medicine report is being used to indiscriminately mandate the use of technology or protocols to increase “safety.” Fortunately, the Agency for Healthcare Research and Quality report did not jump on this bandwagon and recommended that experienced anesthesiologists continue obtaining CVA without US guidance. Closer examination of Blitt and Webster’s bibliography in support of their “strong disagreement” with this position show it is only of limited relevance, and in instances contradicts their position. Two references involve access in chronic hemodialysis patients, which are more likely to involve difficult CVA than our typical population. Other references suggest that landmark-based cannulation is successful 95% of the time, and that the internal jugular may lie behind or even medial to the carotid artery, but this occurs less than 6% of the time. So the need for US guiding on every CVA procedure is not supported for routine cases. To assume US guided placement will lead to fewer lawsuits is absurd as most litigation occurs in the absence of a deviation from the standard of care.3 Furthermore, most of the complications of CVA are inadvertent arterial puncture or cannulation, neither of which have serious sequela and the latter of which can be avoided by transducing the access. Serious complications are rare and involve retained guide wires or torn vessels, neither of which will be reduced by US guidance. Webster and Blitt backpedal halfway through their opinion suggesting practitioners “have a look” with US, and not use it for “complete guidance,” whatever that means. Certainly US guided CVA has merit, particularly in children and in patient populations with known difficult access. But recommending routine use on the basis of legal scare mongering or without scientific evidence should not occur in the newsletter of the APSF, the respected authority on patient safety, even as an opinion.
Frank J. Overdyk, MSEE, MD
Charleston, SC
To the Editor:
We disagree with the opinion article "Portable ultrasound facilitates central vascular access: a case for routine use."1 Thousands of central vascular access devices (CVAD) are safely placed in patients daily without the use of ultrasound. To state that “portable ultrasound should be routinely used in all elective vascular access procedures even when performed by experienced anesthesiologists” is to call for the use of such devices as a standard of care.
One might as well contend that all intubations should be conducted using fiberoptic bronchoscopes to confirm endotracheal tube placement. To state that ultrasound be done on all patients routinely is unfortunate and will only result in more litigation.
Robert F. LaPorta, PhD, MD
David B. Berger, MD
Glen Cove, NY
Policies & Procedures Needed For Sleep Apnea Patients
To the Editor:
Recent articles in the Anesthesia Patient Safety Foundation Newsletter strongly indicate that, at present, disastrous respiratory outcomes during the perioperative management of patients with obstructive sleep apnea (OSA) are a major problem for the anesthesia community.1,2 A recent review of the literature indicates that the disastrous outcomes are due to either intubation failure, respiratory obstruction soon after extubation, or respiratory arrest after narcotic and sedative medication (both preoperatively and postoperatively).3 In order to diminish the frequency and severity of these negative outcomes there are many problems that must be (urgently) solved. The most major and urgent problem areas are a failure to recognize the disease preoperatively, uncertainties regarding perioperative airway management, and the scheduling and management of OSA patients for outpatient surgery.
First, although general physician (primary care doctors, surgeons, anesthesiologists) recognition of OSA is rapidly growing,4,5 the preoperative management system must still deal with the fact that 80-95% of the approximately 18 million Americans believed to have OSA presently come to anesthesia and surgery without a diagnosis of OSA.6,7 Consequently, the anesthesiologist remains the last physician who has a chance to make a presumptive clinical diagnosis of OSA prior to surgery for most patients who actually have OSA. Nevertheless, even if the anesthesiologist does have a high degree of suspicion or does make a presumptive clinical diagnosis of OSA based on abnormal breathing during sleep (apnea and/or snoring), frequent arousals (periodic extremity twitching, vocalization, turning, snorting) and daytime somnolence, the degree of severity of the OSA, as quantified by a sleep study apnea hypopnea index (AHI), is still missing. Postoperative pain control and mechanical ventilation decisions are likely to be different for patients with an AHI of 14 vs. 64 (i.e., high mild vs. very severe). Furthermore, the prudent anesthesiologist will also want to know the cardiovascular ravages of OSA such as dual circulation hypertension, biventricular failure, the lowest SpO2 and presence of arrhythmias during sleep. Finally, since 60-90% of OSA patients are obese (BMI >29 kg/m2),3,8 preoperative baseline PaCO2 is necessary to diagnosis the presence of the Obesity Hypoventilation Syndrome (OHS). Postoperative pain control and mechanical ventilation decisions are also likely to be different for patients with a preoperative PaCO2 of 42 mmHg (no OHS) vs. 58 mmHg (definite OHS). Often none of the above information, essential for making intelligent, objective perioperative management decisions, is available preoperatively (especially in outpatient settings). We need an entire new preoperative management system to properly evaluate OSA patients.
Second, anesthesiologists need to prove or disprove the validity of current airway management techniques. We need to know when an awake intubation is required. The second iteration of the American Society of Anesthesiologists’ Difficult Airway Algorithm (approved by the House of Delegates 10/02) will contain an eleven-step difficult tracheal intubation evaluation scheme. Assuming that recognition of difficult intubation results in awake intubation as per the original American Society of Anesthesiologists’ Difficult Airway Algorithm,9-11 does strict adherence to the new scheme decrease/eliminate intubation failures? Is mask ventilation with the use of bilateral jaw thrust and mask seal (which requires a two-person effort) with an in situ oropharyngeal airway more efficacious than unilateral jaw thrust and mask seal (as is classically delivered by a single practitioner)? We need to know who requires an unquestionable awake extubation. Many other important questions remain to be answered. What is a really good endpoint for an awake extubation (i.e., how do we know the pharyngeal muscles have enough tone to hold the airway open spontaneously?), and how do we achieve that endpoint? Is that endpoint a rational oriented patient who responds to commands in a clear, crisp, and unambiguous manner, or is it something less definite than that? Is the risk:benefit analysis for extubation different for OSA patients awakening from postnasal surgery, or for OSA patients with severe coronary artery disease, or severe asthma, who may have an increased risk of nasal bleeding, myocardial infarction, and bronchospasm, respectively, if they were to undergo an awake extubation? Who should receive postoperative CPAP? If the patient was on nocturnal CPAP preoperatively, should the patient always be on CPAP postoperatively (including the time period before the patient goes into a deep natural sleep)? Finally, postoperative pain management represents a huge problem. We need to know who can/should go to an ICU, vs. a step-down unit, vs. an isolated room on a ward, vs. home. For those patients without continuous visual surveillance, will remote pager oximetry monitoring systems allow a caregiver to be more consistently in touch with the patient?
Lastly, and most importantly, managing the OSA patient in the outpatient setting is an enormous problem. It is absurd to think that we can manage a 5' 8'', 440 lb, BMI = 69, morbidly obese patient with a history consistent with severe OSA for an outpatient knee arthroscopy in the same manner as we do for a non-OSA, normal weight patient. Nevertheless, this difficult problem is currently being presented to many anesthesiologists daily. Anesthesiologists in outpatient facilities are being presented with these difficult situations because the primary care doctors and surgeons do not recognize and work up the disease. There is a desperate need for all same day surgery/ambulatory/outpatient surgery facilities (meaning the anesthesiologist, surgeons, and nurses who work there) to write policies and procedures for acceptable outpatient surgery candidates that take into consideration the special problems and risks of OSA patients. Writing down the acceptable boundaries will necessarily increase medical awareness of the disease and help to decrease the administration of anesthetics to risky patients in risky environments.
The frequency and severity of adverse outcomes in OSA patients undergoing anesthesia and surgery will likely not decrease until these preoperative evaluation deficiencies, intraoperative airway, postoperative pain management, and outpatient scheduling problems are solved. It is hoped that this letter will at least cause the thoughtful reader, whether it be an anesthesiologist, surgeon, perioperative nurse, hospital administrator, or third party payer administrator, to try to help solve these problems.
Jonathan L. Benumof, MD
San Diego, California
OSA Protocol Promotes Safer Care
To the Editor:
Sleep apnea can be a complicating factor in the administration of anesthesia, and in the provision of pain relief perioperatively. This document is designed to outline an approach to the perioperative management of surgical patients diagnosed or suspected of having sleep apnea. Signs and symptoms of sleep apnea are outlined in Table 1.
Table 1. Clinical Features of Obstructive Sleep Apnea
| Symptoms | Signs |
| Nocturnal Events | |
| Witnessed loud snoring and apnea | Short sleep latency |
| Restless sleep with frequent movements | Obesity (BMI >30) |
| Sudden awakenings with choking or shortness of breath | Hypertension |
| Nocturnal awakenings and insomnia | Upper airway abnormalities |
| Nocturnal enuresis or frequent nocturia | Pulmonary hypertension, RV hypertrophy on ECG, cardiomegaly |
| Nocturnal sweating | Polycythemia |
| Diurnal History | |
| Excessive daytime sleepiness | |
| Poor memory or concentration | |
| Morning headaches | |
| Morning dry throat |
The recommendations in this document are not intended to be absolute. Management of individual cases must be subject to the clinical judgment of the professionals involved in the care of the patient, and management may deviate from these guidelines if clinical circumstances warrant.
It is also recognized that this document will evolve. As our experience with these patients increases it is expected that these guidelines should change.
Perioperative Management
Patients presenting for elective surgery will usually have been seen in the preanesthetic clinic. There will be two major types of sleep apnea patients encountered in the clinic:
A. Patients previously diagnosed with sleep apnea syndrome (SAS)
B. Patients with suspected SAS
Postoperative Management of Previously Diagnosed and Suspected SAS
The principles of patient disposition take into account both the severity of SAS, the effects of the surgical procedure, and the postoperative analgesic regimen.
Procedures can be described as high, intermediate, and low risk. High risk procedures include all cases entering body cavities, all large joint replacements, upper airway cases, and/or cases requiring parenteral or long-acting neuraxial opioids. Intermediate risk procedures are those not included in the high-risk category that require parenteral or long-acting neuraxial opioids. Low risk procedures are the same as intermediate risk but for which postoperative pain can be managed with oral medications, codeine being the most potent. The Acute Pain Service should be consulted for all SAS patients having high and intermediate risk procedures.
Options for postoperative disposition are monitored area (M), standard ward bed (W), or home (H). The proposed disposition would be as in Table 2.
Table 2. Sleep Apnea Scale
| Surgical Risk |
Severe
|
Moderate
|
Mild
|
| High |
M
|
M
|
M/W*
|
| Intermediate |
M
|
M/W*
|
W
|
| Low |
W
|
W/H*
|
W/H*
|
| *Cases where there is an option should be dealt with on an individual basis, and there should be agreement among the involved consultants. | |||
|
M=monitored area |
The physicians involved in the patient's care should ensure that an appropriate postoperative disposition is arranged prior to beginning the case.
Patients having low risk procedures performed under local or regional anesthesia with little or no sedation and no neuraxial opioids can be discharged home the same day.
After an overnight stay in a monitored area, if no respiratory interventions relating to SAS are required and the patient is otherwise stable, the patient can be transferred to a lower intensity nursing care unit.
R. Deutscher, MD
D. Bell, MD
S. Sharma, MD
St. Boniface Hospital
Winnipeg, Manitoba
Beware of All Sedatives in Patients With Sleep Apnea
To the Editor:
We commend Dr. Lofsky on her article in the Summer 2002 APSF Newsletter regarding sleep apnea.1 As noted very appropriately, the sleep apnea syndrome patient’s problems do not end in the operating room, and the postoperative period may be an equally high-risk time for these patients. We would like to further comment on several aspects of the postoperative care of these patients.
First, the propensity for all sedatives to exacerbate the sleep-related apneic episodes in patients with obstructive sleep apnea syndrome (OSAS) cannot be overemphasized. The title of the article is misleading, as it suggests that opioids are the only offenders. Since sleep is synonymous with apneas in these patients, apneic episodes will occur with the administration of all sedatives as a direct extension of their pharmacologic action. As well, OSAS patients are in a state of chronic sleep deprivation, since their sleep is continually disturbed by arousals which occur when the episodes of apnea result in hypoxemia. Consequently, these patients are often extremely sensitive to the sedating effects of even very small doses of these drugs. Furthermore, benzodiazepines and barbiturates preferentially decrease neural input to the upper airway dilating muscles, thereby directly promoting upper airway obstruction.2,3
Although, it is ideal to avoid all sedatives in OSAS patients, many will require opioid analgesics in the postoperative period. The lowest effective dose should be used, and an antagonist such as naloxone should be immediately available. Dr. Lofsky cites a case report of a patient who became comatose after receiving meperidine, which was not satisfactorily reversed with naloxone.4 Review of this case report, however, shows that the patient also received 25 mg promethazine intramuscularly with the meperidine, and reversal was attempted with both naloxone and physostigmine. It is quite possible that the noloxone was an effective opioid-antagonist agent, but the persistent obtundation was due to promethazine, which is not reliably reversed by physostigmine. We are unaware of any other reports of OSAS patients who have failed to respond to naloxone.
We fully agree that patients with OSAS require additional monitoring in the postoperative period. Dr. Lofsky recommends audible pulse oximetry on the ward, but from a practical point of view this is problematic. Certainly a bedside pulse oximeter emitting an audible tone with every pulse would not be tolerated by either the patient or anyone else on the ward. If only the alarms are audible, the situation may be no better, as these patients may have hundreds of episodes of apnea and hypoxemia per night. A centralized pulse oximetry monitoring station may be less distracting to the patient, but the staff on the ward must be prepared to respond frequently and appropriately to any abnormalities detected. Many wards are ill-equipped to do this. Therefore, the PACU or ICU is usually the most appropriate place for OSAS patients to be monitored postoperatively. This should be maintained for at least the first postoperative night, and consideration should be given to continuing it until all opioid or sedative medications are discontinued.
M. Denise Daley, MD, FRCPC
Peter H. Normal, MD, FRCPC
Houston, TX
Concentrated Solutions Cause Concern
To the Editor:
An area of error prevention that might be addressed by the Anesthesia Patient Safety Foundation concerns the accidental administration of concentrated and dangerous medications.
The most widely cited example of this is the accidental intravenous administration of concentrated potassium chloride. Patients are killed or severely injured when concentrated solutions of KCl (intended for dilution prior to administration) are injected as if already diluted. In fact, JACHO’s first Sentinel Event Alert (Issue 1-February 27, 1998) highlighted this very topic. JACHO reviewed 10 incidents of patient death resulting from accidental administration of KCl, 8 of which resulted from the direct infusion of concentrated KCl. In all cases, a contributing factor was the availability of concentrated KCl on the nursing unit. In 6 of the 8 cases, the KCl was mistaken for some other medication, primarily due to similarities in packaging and labeling. Most often, KCl was mistaken for sodium chloride, heparin, or furosemide (Lasix®). In light of this experience, the Joint Commission suggested that health care organizations not make concentrated KCl available outside of the pharmacy unless appropriate specific safeguards are in place.
Anesthesiologists have a situation analogous to the KCl scenario. It is the availability of concentrated solutions of epinephrine, phenylephrine, and ephedrine. Epinephrine (1 mg/ml, 1:1000) and phenylephrine (10 mg/ml, 1%) are added to local anesthetic solutions to prolong spinal anesthesia and (or) to minimize systemic toxicity from regional anesthesia by decreasing vascular absorption. Phenylephrine and ephedrine (50 mg/ml) are used also as vasopressors when spinal or epidural anesthesia causes hypotension. Except when epinephrine is added to a spinal anesthetic agent, these 3 drugs are diluted. For example, epinephrine is diluted to 5 µg/ml when used in nerve blocks or epidural anesthesia, and when used as a vasopressor, phenylephrine is diluted to 40-50 µg/ml and ephedrine to 5-10 mg/ml.
Dilution Requires Extra Care
Each dilution is an opportunity for overdose secondary to an error in calculation, and the similar appearance of epinephrine and ephedrine ampoules makes accidental injections of the wrong drug too easy. In the course of treating hypotension during a spinal anesthetic I personally picked up the epinephrine ampoule that came in the spinal kit and diluted it, thinking that I had picked up an ampoule of ephedrine. I’ve heard of another anesthesiologist who accidentally injected 2 mg of phenylephrine (2 ml of 1:10 dilution of 1% phenylephrine). Accidentally injecting 2 ml of a 1:10 dilution of epinephrine or phenylephrine instead of a 1:10 dilution of ephedrine can be devastating, particularly if given to a patient with coronary or cerebrovascular disease.
Eliminating these concentrated solutions from anesthesia carts can prevent the dilutional errors and minimize the likelihood of injecting the wrong drug. A safer alternative would be to provide anesthesiologists with 10 ml vials or syringes of dilute ephedrine 5 mg/ml) or phenylephrine (50 µg/ml for bolus administration) or 100 ml bags of phenylephrine (20-40 µg/ml) for infusion. Keeping concentrated KCl out of the hands of nurses and physicians has minimized (if not eliminated) accidental injections of concentrated KCl.
Epinephrine poses a more challenging problem, as anesthesiologists have grown accustomed to using the concentrated solution to prolong spinal anesthesia or to limit the systemic toxicity when large amounts of local anesthetics are used for major nerve blocks. For example, 0.2-0.3 ml of 1:1000 epinephrine is added to 2-3 ml of spinal anesthetic and 0.1-0.2 ml of 1:1000 epinephrine is added to 20-40 ml of local anesthetic used for major nerve blocks. I no longer use epinephrine in my spinal anesthetics, as it does not prolong lidocaine or bupivacaine spinal anesthesia. Epinephrine does prolong tetracaine spinal anesthesia, but I have stopped using tetracaine, substituting bupivacaine in its place. In any case, the proposed mechanism by which epinephrine prolongs spinal anesthesia is the decreased vascular absorption of the local anesthetic, which maintains the local anesthetic in the CSF for a longer period of time, I simply add more local anesthetic if I want a longer acting spinal. Therefore, there is really no need for epinephrine in a spinal kit, and its absence would eliminate the possibility of confusing the spinal kit epinephrine with an ampoule of ephedrine used to treat spinal hypotension. For anesthesiologists who insist on keeping epinephrine in the spinal kit, I propose that unused epinephrine ampoules be discarded with other waste after the induction of spinal anesthesia to prevent them from being confused with ephedrine ampoules.
Major nerve blocks require large amounts of local anesthetic, and epinephrine is added to these solutions in order to minimize systemic toxicity and to prolong the block’s duration. The local anesthetics manufactured with epinephrine have a low pH to prevent the degradation of the epinephrine. Because of the low pH, these solutions have slow onset. Adding fresh epinephrine to plain local anesthetic solutions that have a higher pH produces a solution with a faster onset and longer duration. Consequently, I like to add fresh epinephrine to plain local anesthetic solutions because they act faster. However, if eliminating concentrated epinephrine solutions from the anesthesia cart will prevent adverse reactions, then I would change my practice and increase the pH by adding sodium bicarbonate to local anesthetics that come premixed with epinephine. The result would be the same as that produced by adding concentrated epinephrine to a plain local anesthetic, and there would be no need to have concentrated solutions of epinephrine in the anesthetizing locations, where they could accidentally cause harm if injected full strength.
System Changes May Reduce Errors
The New England Journal of Medicine is beginning a series on patient safety.1 The central message of the recently released Institute of Medicine (IOM) report “To Err Is Human” was that errors are caused more by faulty systems than individual carelessness. The IOM report made four major points: the problem of accidental injury is serious, the cause is not careless people but faulty systems, we need to redesign our systems, and patient safety must become a national priority.
The concept that errors result largely from the failures of systems, not from individual carelessness or inadequacy, is fundamental to the new effort to address safety and runs counter to the traditional focus of medical training on individual performance. However, the concept is based on a wealth of studies in cognitive psychology and human-factors engineering, as well as substantial experience in other industries, showing that achieving safety requires more than a reliance on individual carefulness.
Changes based on this concept were first introduced into health care in the 1980s by anesthesiologists. Mortality related to anesthesia was dramatically reduced by the use of critical-incident analysis, standardization, and checklists, as well as changes in training and supervision and the nearly universal implementation of new monitoring techniques.
The IOM believes that introducing “system changes” is more likely to have an impact on patient safety than telling practitioners not to make mistakes. To be sure, anesthesiologists need to be knowledgeable concerning the drugs that they administer and they need to be careful in their practice. However, the changes that I am recommending are “system changes” that will make it less likely that patients will be harmed by even the most careful and conscientious anesthesiologist.
Surely the changes that I am proposing will meet resistance. Change always does. However, I believe they are easily implemented and in the best interests the patient.
Donald H. Lambert, PhD, MD
St. Johnsbury, VT
1. Leape L, Epstein AM, Hamel MB. A series on patient safety. N Engl J Med 2002;347:1272-1274.