beach chair position may decrease cerebral perfusion...

NEWSLETTERVolume 22, No. 2, 25-40 Circulation 81,489 Summer 2007

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Inside: Review of Maternal Arrest Cases ........................................................................................Page 28

Cardiology Perspective on Stents ........................................................................................Page 32

Dear SIRS: Alarm Requires Selection of Heart Rate Source ........................................Page 34

Donor List ..................................................................................................................................Page 35

Case Report: Wrap Delays Detection of Disconnect ........................................................Page 36

Q&A: Pipeline Pressure Primer............................................................................................Page 38

by David J. Cullen, MD, and Robert R. Kirby, MD

Case PresentationA 47-year-old, healthy female underwent general

anesthesia for shoulder arthroscopy. Preoperativeblood pressure (BP) was 125/83 mmHg. After pre-medication with 50 mg of meperidine, 40 mg hydrox-yzine, and 0.2 mg glycopyrrolate intramuscularly,anesthesia was induced with 200 mg propofol, 100mg succinylcholine, and 30 mg lidocaine. Becauseshe was hypertensive, just prior to induction, 50 mgof labetalol was given intravenously. Anesthesia wasmaintained with 2% isoflurane, 60% nitrous oxide,and oxygen. The patient was placed in the “barber-shop” position for the surgery. Twenty minutes intothe case, blood pressure decreased to 100/60 mmHgand then remained in the 80-90 mmHg systolic rangefor the remainder of the case. Oxygen saturation was100% and end tidal CO2 values were in the 30sthroughout the case. Upon arrival in the post-anes-thesia care unit (PACU), her blood pressure was113/60 mmHg but she did not awaken. Naloxone0.1 mg was given intravenously, but she remainedunresponsive and did not move her extremities.Another 0.1 mg of naloxone was given 35 min afterarrival in the PACU followed by 3 more doses ofnaloxone and 2 doses of physostigmine. During thistime, her trachea remained intubated and she waswell oxygenated. Neurologic evaluation suggested adiencephalic syndrome, possibly brain infarction.She was unresponsive to voice commands or painfulstimuli, and reflexes were decreased bilaterally. Acomputer axial tomography (CAT) scan of the headwas normal initially, but 5 days later suggested brainswelling and obliteration of the cistern. Magnetic res-

resistance increase. Under nonanesthetized condi-tions, these effects are compensated for by an increasein systemic vascular resistance by up to 50-80%. How-ever, this autonomic response is blocked by vasodilat-ing anesthetics, which further exacerbate andcompromise cardiac output. Blood pressure remainsunchanged or increases slightly in nonanesthetizedpatients in the sitting position but decreases in theanesthetized state. Cerebral perfusion pressure (CPP)decreases by approximately 15% in the sitting positionin non-anesthetized patients and could furtherdecrease under anesthesia because of vasodilationand impaired venous return. Venous return from thecerebral circulation is usually increased by inspiratorysubatmospheric pressure during spontaneous venti-lation, but this mechanism is nullified by positivepressure ventilation. Obstruction of the internaljugular veins in the sitting position may also impedecerebral venous drainage, especially with unfavorablepositions of the head and neck, such as flexion of thehead. Pohl and Cullen reported a series of cases in2005 that documented blood pressure decreases rang-ing from 28-42%; consequently, hypotension wasthought to be a likely cause of ischemic brain injury.Given the potential for peripheral vasodilatation andmyocardial depression that can occur in patients whoare anesthetized with potent intravenous and inhala-tional drugs, the effects of the upright position andanesthesia synergize.

Cerebral autoregulation has been thought tomaintain cerebral blood flow (CBF) constantbetween MAP of 50-150 mmHg. However, it mustbe remembered that in poorly controlled hyperten-sive patients, autoregulation of CBF is shifted to theright, requiring higher CPP/MAP to ensure ade-quate cerebral perfusion. In recent years, Drummondand others have emphasized that the quoted value of50 mmHg for the lower limit of autoregulation (LLA)should be modified upward to reflect a range ofvalues from 70-93 mmHg with a mean value of 80 ± 8mmHg rather than the specific number of 50 mmHg.Some orthopedic surgeons request deliberatehypotension for shoulder surgery. With the acquies-cence of the anesthesiologist or the nurse anesthetist,deliberate hypotension to mean arterial pressures of50-60 mmHg eliminates any margin for error in caseblood pressure falls further. In addition, neither thesurgeon nor the anesthesiologist nor the CRNA typi-cally seems to consider the added effect of the beachchair position on cerebral perfusion.

See “Perfusion,” Page 27

onance imaging (MRI) 1 week later showed changesin both cerebral hemispheres suggesting corticalinfarcts, involvement of the anterior and medial tem-poral lobe bilaterally, no significant edema, and nosignificant herniation. At no time was there any evi-dence of an intracranial bleed. After 2 weeks, herGlasgow coma scale was 3; her fundi were clear andcrisp. She had corneal reflexes, a positive gag, andnegative doll’s eyes; she was hyperreflexive withincreased tone and was unresponsive to noxiousstimuli in all 4 extremities. She is expected to remainin a persistent vegetative state.

Considerations When Using theBeach Chair Position

The beach chair (barbershop) position wasdeveloped in the 1980s for orthopedic shoulderarthroscopy procedures. Patients are sat up atangles varying from 30-90° above the horizontalplane with appropriate padding and with the headsecured in a headrest. Injuries to the brachialplexus are reduced compared to the lateral decubi-tus position, and the surgeon has excellent access tothe shoulder. The position helps the surgeonbecause the weight of the arm distracts the shoul-der joint while avoiding distortion of the intra-articular anatomy.

However, significant changes can develop whenpatients are moved to the upright position. Mean arte-rial pressure (MAP), central venous pressure (CVP),pulmonary artery occlusion pressure (PAOP), strokevolume, cardiac output, and PaO2 all decrease whilethe alveolar-arterial oxygen gradient (PAO2-PaO2),pulmonary vascular resistance, and total peripheral

Beach Chair Position May Decrease Cerebral PerfusionCatastrophic Outcomes Have Occurred

APSF NEWSLETTER Summer 2007 PAGE 26

NEWSLETTERThe Official Journal of the Anesthesia Patient Safety Foundation

The Anesthesia Patient Safety FoundationNewsletter is the official publication of the nonprofitAnesthesia Patient Safety Foundation and is pub-lished quarterly at Wilmington, Delaware. Annualcontributor status: Individual–$100, Corporate–$500.This and any additional contributions to the Founda-tion are tax deductible. © Copyright, AnesthesiaPatient Safety Foundation, 2007.

The opinions expressed in this Newsletter are notnecessarily those of the Anesthesia Patient SafetyFoundation or its members or board of directors.Validity of opinions presented, drug dosages,accuracy, and completeness of content are notguaranteed by the APSF.

APSF Executive Committee:Robert K. Stoelting, MD, President; Jeffrey B.

Cooper, PhD, Executive Vice President; George A.Schapiro, Executive Vice President; Paul A. Baumgart,Vice President; David M. Gaba, MD, Secretary; CaseyD. Blitt, MD, Treasurer; Sorin J. Brull, MD; Robert A.Caplan, MD; Nassib G. Chamoun; Robert C. Morell,MD; Michael A. Olympio, MD; Richard C. Prielipp,MD; Matthew B. Weinger, MD. Consultants to theExecutive Committee: John H. Eichhorn, MD; Lorri A.Lee, MD; and Ann S. Lofsky, MD.Newsletter Editorial Board:Robert C. Morell, MD, Editor; Sorin J. Brull, MD; JoanChristie, MD; Jan Ehrenwerth, MD; John H. Eichhorn,MD; Lorri A. Lee, MD ; Rodney C. Lester, PhD, CRNA;Glenn S. Murphy, MD; Denise O’Brien, MSN, RN;Karen Posner, PhD; Andrew F. Smith, MRCP FRCA;Wilson Somerville, PhD; Jeffery Vender, MD.

Address all general, contributor, and subscriptioncorrespondence to:Administrator, Deanna WalkerAnesthesia Patient Safety FoundationBuilding One, Suite Two8007 South Meridian StreetIndianapolis, IN 46217-2922e-mail address: [email protected]: (317) 888-1482

Address Newsletter editorial comments, questions, letters, and suggestions to:Robert C. Morell, MDEditor, APSF Newsletterc/o Addie Larimore, Editorial AssistantDepartment of AnesthesiologyWake Forest University School of Medicine9th Floor CSBMedical Center BoulevardWinston-Salem, NC 27157-1009e-mail: [email protected]

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Dr. Lorri Lee and Dr. Ann Lofsky have recentlybeen appointed consultants to the APSF ExecutiveCommittee. Their experience and expertise willcertainly make them important additions to ourorganization.

Lorri A. Lee, MD, received her training in anes-thesiology at the University of Washington whereshe is currently an associate professor in the Depart-ments of Anesthesiology and Neurological Surgery(adjunct). As an investigator for the ASA ClosedClaims Project, her research is focused on evaluatingtrends and associated factors in anesthesia-relatedpatient injuries and medical liability. Dr. Lee isdirector of the ASA Postoperative Visual Loss Reg-

istry and served on the ASA Perioperative Blind-ness Advisory Task Force

Ann Lofsky, MD, completed both internal med-icine and anesthesiology residencies at UCLAbefore entering private practice in anesthesiology.She is currently a partner in the anesthesia group atSaint John's Hospital in Santa Monica. For 13 years,Dr. Lofsky served on the board of directors of TheDoctors Company, a physician-owned medicalmalpractice insurer. In that capacity, she has writtenand lectured extensively on risk management andpatient safety concerns for anesthesia providers.She is now a governor emeritus and anesthesia con-sultant for The Doctors Company.

Physicians Lee and Lofsky NamedConsultants to Executive Committee

Anesthesia Patient Safety Foundationis pleased to announce the

APSF/American Society of Anesthesiologists (ASA)Endowed Research Award

in full support ($150,000) of a grant tobe awarded in October 2007 for initiation in January 2008.

The funds for this named grant will be providedfrom the APSF Endowment Fund, which was made possible

by the generous contributions of ASA to APSF overthe last several years.

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Lorri Lee, MD (left), and Ann Lofsky, MD (right), with Dr. Robert Stoelting, president of the APSF.


pressure. If the beach chair position is combined withthe use of deliberate hypotension, cerebral perfusionwill be severely compromised. An even more exag-gerated occurrence may develop when the BP cuffmust be placed on the leg because the contralateralarm is not available for BP measurement, e.g., in apatient with prior lymph node dissection for breastcancer. In the beach chair position, the legs are consid-erably lower than the trunk, therefore the BP differ-ence between the BP cuff measured on the leg and theBP in the brain will be even greater than the gradientbetween the arm and the brain.

The following case illustrates this point. A 54-year-old woman underwent left shoulder replace-ment surgery in the beach chair position. The patienthad no history of hypertension or myocardial infarc-tion. Preoperative electrocardiogram, echocardio-gram, thallium scan, and exercise tolerance test werenormal. The patient received an interscalene blockwith 40 ml of 0.5% bupivacaine with epinephrine(1:200,000). Because of a previous mastectomy, a 20-gauge intravenous catheter was placed in the rightfoot and a noninvasive BP cuff was placed on the calf.There was no documentation that the calf BP was val-idated to the left arm BP before the patient was anes-thetized and the left arm became unavailable. Noarterial catheter was placed although deliberatehypotension was used. Anesthesia was induced with100 mg propofol, 250 mg sodium pentothal, 50 mgrocuronium, and 250 mcg fentanyl. Anesthesia wasmaintained with 3.5% sevoflurane and 67% nitrousoxide in oxygen. Nitroglycerin, 50 mcg times 3 doses,and labetalol, 5 mg times 4 doses, were used to pro-duce deliberate hypotension. One hour after induc-tion, her systolic BP was between 85-100 mmHg. Twohours later, her BP was 70/40 mmHg and thenremained around 90/60 mmHg for the next 40 min,when it decreased to 50/25 and was treated withphenylephrine. Electrocardiography showed sinusrhythm throughout, oxygen saturations were alwayshigh, and end-tidal CO2 was in the high 20s for most ofthe case. In the PACU, emergence was delayed, andshe did not breathe spontaneously. A radial arterycatheter was finally placed while she was in thePACU, and BPs were normal. Apnea persisted and herpupils were fixed and dilated. Blood gas analysis oncontrolled ventilation showed a PaO2 of 236 mmHg,PaCO2 of 35 mmHg, and pH of 7.4, with glucose of 92mg/dl. Neurologic evaluation revealed brain deathwith no CBF, flat electroencephalogram, no reflexes,no response to pain, and no lesions on the CAT scan.At autopsy the upper spinal cord and medulla wereinfarcted. The anesthesia equipment tested normal. Inthis case, not only was deliberate hypotension used tovery low values, but BP was measured in the leg whilethe patient was in the sitting position. One can onlyimagine how low the BP was in the brain when BP inthe leg was 70/40 or 90/60.

In addition to avoiding deliberate hypotension,one must be extremely vigilant and treat aggressivelythe unexpected hypotension that often occurs duringanesthesia in the beach chair position for the reasonsenumerated above. These treatments are well knownto all anesthesia providers and include careful controlof the inhalation anesthetic concentration, adequateand timely fluid administration, and vasopressor infu-

sion, as needed during the time of the procedure whenthe patient is upright and at risk.

Head position is also important because somedegree of head manipulation is required when posi-tioning the patient in the seated position. Most sur-geons use a headrest to immobilize the head. Severalstudies suggest that CBF can be compromised bymechanical obstruction and injury to major veins orarteries. Blood flow reduction in the vertebral arterycaused by extension and rotation or tilt of the headmay result in posterior brain circulation infarcts.

Finally, hypotension and generalized circulatoryinstability can result from gas embolism. This rarecomplication has been reported with both air andcarbon dioxide distension of the joint capsule fol-lowed by pressurized injection of irrigation fluid.Thus, anesthesiologists and CRNAs should keep thepossibility of venous gas embolism in mind duringshoulder arthroscopy in the sitting position if suddencardiovascular collapse occurs.

SummaryDespite its low incidence, intraoperative stroke

associated with shoulder surgery, particularly inhealthy patients at no risk for stroke, is a totally unex-pected and devastating complication. Patients in thebeach chair position are at risk for an intraoperativestroke if borderline low BPs, as measured in the arm,are used without appreciating the effect on CPP andCBF. Because of the specific physiologic changes asso-ciated with the sitting position, great care should beapplied when using and interpreting BP cuff mea-surements in the nonoperative arm or, even more so,if leg measurements of BP must be used. Blood pres-sure values <80% of preoperative resting valuesshould be treated aggressively to enhance the marginof safety. Deliberate hypotension must be avoided. Athorough understanding of the physiologic changesassociated with the upright position, and the physicaleffects of gravity on BP in the brain is crucial to pre-vent catastrophic neurologic outcome during shoul-der surgery in the sitting position.

Dr. Cullen is formerly Chair of the Department ofAnesthesia and Pain Medicine, Caritas St. Elizabeth’sMedical Center and former Professor of Anesthesiology atTufts University School of Medicine in Boston, MA.

Dr. Kirby is an Emeritus Professor of Anesthesiologyat the University of Florida College of Medicine inGainesville.

General References

1. Pohl A, Cullen DJ. Cerebral ischemia during shouldersurgery in the upright position: a case series. J Clin Anesth2005;17:463-469.

2. Drummond JC. The lower limit of autoregulation: time torevise our thinking? Anesthesiology 1997;86:1431-1433.

3. Drummond JC, Patel PM. Neurosurgical anesthesia. In:Miller RD, Cucchiara RF, Miller ED, Jr., et al., eds. Anes-thesia, 5th ed. Philadelphia: Churchill Livingstone,2000:1903-5.

4. Faure EA, Cook RI, Miles D. Air embolism duringanesthesia for shoulder arthroscopy. Anesthesiology1998;89:805-6.

In the upright position, MAP at the brain is verydifferent when compared to the site at which the BP isactually measured, usually the arm. Unfortunately thisdifference may be overlooked. In the supine position,BP measured in the arm and BP perfusing the brainare essentially the same. However, if the patient isupright in the beachchair position, BP will be less inthe brain than at the heart or arm. The BP differencewill be equal to the hydrostatic pressure gradientbetween the heart/arm and the brain. For example,suppose the BP at the heart/arm is 120/80 mmHg,(MAP 93 mmHg). If the height of the external auditorymeatus (representing the base of the brain) is 20 cmabove the heart, the difference in BP at the heart com-pared to the brain will be 15 mmHg. Thus, the BP atthe base of the brain will be 105/65 mmHg (MAP 78mmHg). Most patients undergoing relatively straight-forward procedures such as shoulder arthroscopy oreven open shoulder surgery do not have intra-arterialBP monitoring available. Therefore, they do not havea transducer placed at the level of the external auditorymeatus to monitor BP at the base of the brain. Instead,it is up to the anesthesiologist and/or nurse anesthetistto correct the BP readings at the arm to account for theheight of the brain above the arm. Even accounting forthe hydrostatic gradient between the external auditorymeatus (base of brain) and the arm does not take intoaccount the added distance from the base of the brain,at the Circle of Willis, to the most cephalic portion ofthe cerebral cortex, an additional distance of 10-12 cm(depending on the patient’s height), which representsa further gradient of about 9 mmHg.

The case presented at the beginning of this articlesuggests that the gradient between the arm and brainwas not appreciated. Blood pressure was measured atthe arm with a non-invasive cuff, but was notadjusted upward to maintain an adequate MAP at thelevel of the brain during the procedure. Systolic BPsof 80-100 mmHg probably corresponded to MAPs of50-80 mmHg, but in the beach chair or upright posi-tion, MAP at the base of the brain was probably 15-20 mmHg lower, and at the top of the cerebral cortex,another 9 mmHg lower. It is reasonable to estimate aMAP of 30-40 mmHg at the cerebral cortex and a littlehigher at the brainstem. CAT scan on the fifth postop-erative day showed brain swelling and obliteration ofthe cistern. MRI 1 week later showed cortical infarctsin both cerebral hemispheres and no intracranialbleed. The injury was consistent with the hypoperfu-sion that occurred intraoperatively.

Estimates of the MAP at the head can be made oncethe patient is in the beach chair position. The criticalvariable is the vertical distance between the externalauditory meatus and the BP cuff. Once that distance isknown, it should be converted to a hydrostatic pressuregradient that then must be incorporated into BP man-agement during the procedure.

To quantitate the hydrostatic gradient, there is a0.77 mmHg decrease for every centimeter gradient(1 mmHg for each 1.25 cm). In general, the approxi-mate distance between the brain and the site of the BPcuff on the arm in the seated position will be 10-30 cmdepending on the angle of the sitting position and theheight of the patient; hence the brain MAP will be 8-24mmHg lower than the measured mean brachial artery

Consider Correction for Cuff Location“Perfusion,” From Page 25


See “Arrest,” Next Page

by Ann S. Lofsky, MD

Anesthesia-related maternal arrest is a fearedcomplication that places the lives of both mother andbaby at risk. Literature reviews on the subject havebeen traditionally hampered by a lack of specificsregarding the care provided and the aging of data bythe time it could be collected and analyzed. Validconcerns about the privacy of stricken families, theconfidentiality of the healthcare providers involved,and liability risks have likely acted together to pre-vent the wider dissemination of case specifics in anopen forum.

Despite recent advances and changing practicepatterns in obstetrical anesthesia, malpractice claimreviews indicate that maternal arrest on labor anddelivery continues to result in major morbidity andmortality. The Doctors Company recently reviewed22 anesthesiology claims that were filed after mater-nal arrests on labor and delivery wards between 1998and 2006. Anesthesia care was analyzed at the time ofinitial medical record review from both Standard ofCare and patient safety viewpoints. Characteristics ofthese claims and expert reviewer comments regard-ing suggested practice changes that might possiblyhave avoided the arrests or improved the outcomesare presented here with an aim toward improvingmaternal safety.

Overall OutcomeThe mothers, aged 17 to 41, suffered the most

severe complications post-arrest. Ten out of the 22died, including 3 who were declared brain dead andremoved from ventilators. Eleven suffered degrees ofanoxic brain damage, ranging from minimal to severe,but with neurological deficits deemed to be perma-nent at the time of final claim resolution. Only 1mother out of the 22 had no apparent residuals post-arrest and was suing primarily for emotional distress.

Surprisingly, the infant outcome in these casesappeared quite different. In all cases where informa-tion was available, infants (or children) had been eval-uated as developmentally normal at the time of finalmedical records review. This was true even for thebabies born with low Apgar scores, and included notonly the 10 babies delivered prior to the maternalarrests, but also the 12 born after their mothers hadsustained significant periods of circulatory and/orrespiratory arrest.

This disparity suggests that the fetus may well bemore resistant to periods of hypoxia and hypoten-sion than is the parturient, and it reaffirms theimportance of the anesthesiologist’s primary focusbeing the welfare of the mother. This raises the ques-tion as to whether maternal resuscitation should everbe intentionally delayed in order to expedite deliv-ery of the fetus.

Respiratory Arrests afterRegional Anesthetics

The most common scenario in this series (13patients) was a respiratory arrest following epiduralor spinal block. Included in this group were 11patients who developed unintentionally high neurax-ial blockade with resultant apnea and 2 patients whoarrested after intravenous sedation was administeredpost-cesarean section delivery under spinal anesthe-sia. None of these patients were attached to a mater-nal monitor with audible alarms at the time of thearrest, making delay in response and resuscitation afrequent reviewer concern.

Labor EpiduralsThere were 8 patients in this series who arrested

in labor rooms following attempted insertion anddosing of epidural catheters to relieve labor pains. Ofthese, 7 had subsequent evidence of unintentionalsubarachnoid blocks, either by positive aspiration ofthe catheter for cerebrospinal fluid (CSF) (3 patients)or air in the ventricles on CT scanning (4 patients),presumably introduced into the CSF during injectionthrough the needle or catheter.

All 8 of these arrests occurred within the first 30minutes of initial catheter placement. In half of thecases, anesthesia providers were not in the room atthe time, and the arrest was noted first by otherhealthcare workers. Reasons given by anesthesiaproviders for leaving the room after catheter place-ment included wanting to chart at the nursing desk,being called away to place another labor epidural orto attend to another labor patient’s needs, or needingto locate drugs or airway equipment.

In the 1 case in which the mother recovered with-out obvious neurologic impairment, she was placedsupine immediately by the anesthesiologist on initialcomplaint of difficulty breathing and ventilated withoxygen by Ambu-bag as soon as respirationsappeared inadequate. The obstetrician accomplisheda crash cesarean section within minutes while still inthe labor room, with only a benzodiazepine providedbefore incision. Blood pressure was supported withIV fluid infusion.

The other 7 cases involved the transfer of a motherin respiratory and/or circulatory arrest from the laborroom to the operating room for STAT cesarean sectiondue to fetal distress. In 4 of these cases, there weredocumented delays in the ventilation of the motherfor reasons including initial failure to notice maternalarrest, desire to wait for more optimal intubating con-ditions in the OR, difficulty locating an Ambu-bag orairway device, or an anesthesia provider not being inattendance. The improved outcome in the 1 caseinvolving immediate resuscitation suggests that therapid establishment of adequate ventilation and bloodpressure support might be crucial factors after unin-tentionally high spinal blockade.

Cesarean Sections There were 5 cases of maternal respiratory arrest

following regional anesthesia administered for elec-tive cesarean-section delivery. These all involvedspinal anesthetics, possibly because this is a preferredanesthesia choice for purely elective cases. In 2instances, the mothers received an intravenous ben-zodiazepine or opioid after delivery; both had alsoreceived spinal opioids. Maternal respiratory arrestsoccurred after delivery in these cases, although therewere possible delays in recognition of the arrests.

In the other 3 cases, the mothers received nointravenous anesthetics. One mother arrested imme-diately after the spinal was placed, with suspectedpreeclampsia and volume depletion as contributingfactors. The other 2 cases involved apparent highspinals, with delay in recognition and/or resuscita-tion also potential problems.

Contributing Factors Morbid obesity, which is known to complicate

regional anesthesia, was documented in 3 out of the8 labor epidural cases and 1 out of the 5 cesareansections. These proportions would appear to behigher than those present in most labor and deliv-ery populations and suggest that morbid obesitymay be a significant relative risk factor for maternalarrest following regional blocks.

Three mothers in this series carried the diagno-sis of preeclampsia. Two arrested at the time ofinduction of anesthesia for cesarean section(1 spinal, 1 general anesthetic). Reviewers raisedthe possibility of relative hypovolemia in thesecases and questioned whether invasive monitoringmight have provided useful additional information.

Arrests after MaternalHemorrhage

There were 7 cases involving arrests in mothersafter massive postpartum hemorrhage—3 afternormal spontaneous vaginal deliveries and 4 aftercesarean section births. Predisposing diagnoses,when available, included placenta accreta, placentalabruption, and traumatic arterial laceration. Know-ing there had been a maternal arrest due to hemor-rhage, reviewers attempted to identify ways in whichthe treatment might have been optimized, althoughit was acknowledged that the size and facilities of theobstetric units involved were varied.

A frequent reviewer impression was that thehemorrhage was so excessive by the time it was diag-nosed, it was extremely difficult for the anesthesiaprovider to “catch up” with the continuing bloodloss. Postpartum hemorrhage was not always ini-tially apparent through vaginal bleeding, as it wasoften primarily internal. The initial presentation wasfrequently hypotension and/or tachycardia in the

Doctors Company Reviews Maternal Arrests Cases(Reprinted with permission from The Doctors Company)


mother, which was usually treated first with intra-venous crystalloid and pressors. It was not alwaysclear when continued bleeding should have beensuspected as the cause of the maternal vital signinstability.

In some instances, delays in transfusing motherswere related to problems obtaining or transportingblood products from the blood bank, or to an inabil-ity to run the blood products through available intra-venous lines more rapidly. Some cases involveddelays in waiting for crossmatched blood when pos-sibly O-negative or type-specific blood might havebeen available. Reviewers commented that severalpatients might have benefited from earlier consider-ation of additional blood components—includingfresh frozen plasma, platelets, or cryoprecipitate.Laboratory tests of serial hemoglobin and hemat-ocrits, coagulation panels, or disseminated intravas-cular coagulation (DIC) screens were not alwaysordered.

Better communication might have facilitatedtransfusion in some cases. On retrospective reviews,potentially improvable delays were identified ininforming blood banks of the need for products, incalling for additional medical assistance, or in noti-fying obstetricians that postpartum patients werehemorrhaging and that surgical intervention (such asexploration, uterine ligation, or hysterectomy) mightbe required. Potentially useful equipment, such ascentral line kits or rapid infusion devices, were some-times available in the facility, but labor and deliveryward personnel might not have known how orwhere to obtain them.

General AnesthesiaIncluded in these maternal arrest cases were 5

general anesthetics and 17 regional blocks. Thislikely reflects an overall shift toward the use ofregional anesthesia in obstetrics. In 3 of the generalanesthetics cases, the arrest followed severe post-partum hemorrhage. In those cases, the choice ofanesthesia did not likely affect the ultimate outcomesignificantly. General anesthesia was chosen in 2cases for postpartum hysterectomy for patients whowere already severely bleeding. Only 1 generalanesthetic involved a difficult intubation and loss ofthe airway—traditionally one of the more fearedcomplications of emergency cesarean sections.Interestingly, aspiration of gastric contents, tradi-tionally listed as a leading cause of death in obstet-ric anesthesia,1 was not seen in this series of arrests.

DiscussionThe physiological changes of pregnancy

undoubtedly contribute to the high incidence ofanoxic brain damage and death cases after maternalarrests. The size of the full-term uterus decreasesfunctional residual capacity (FRC) in the mother,

leading to a much more rapid development ofhypoxia during periods of apnea than would beexpected in the woman’s non-pregnant state. Theincreased oxygen demand of pregnancy furthershortens the interval of apnea tolerated before arter-ial desaturation results. Although a pre-oxygenated,non-pregnant woman may sustain a several-minuteperiod of apnea without desaturating, that samepatient at 9 months’ gestation breathing room airmight not.

Maternal circulation is compromised in thesupine position due to compression of the vena cavaand aorta by the uterus, decreasing venous returnand cardiac output. The necessity of placing analready unstable mother supine, to combat risingspinal levels, to transport her to the operating room,or to manage the airway, may further complicate suc-cessful resuscitation.

MonitoringSince all respiratory arrests after labor epidurals

in these cases occurred within the first 30 minutesafter catheter insertion, increased monitoring duringthis time period would seem a worthwhile consider-ation. This could be visual—with the anesthesiaprovider, nurse, or a designee in the room with thepatient—or through electronic monitoring of pulseoximetry, capnography, or ventilation, with an alarmaudible to responsible personnel. Some birthing facil-ities have labor and delivery rooms equipped withpulse oximeters that read continuously at the nursingstations, yet that is not currently standard. Many ofthe maternal arrests following labor epiduralsoccurred on wards in which only fetal monitoringwas transmitted continuously to nurses. The out-comes in those cases suggest that by the time hypoxiadue to apnea becomes apparent on a fetal tracing, itmight already be too late to prevent anoxic braindamage in the mother.

In 4 cases of planned labor epidurals, the anes-thesiologist or CRNA observed symptoms or signsconsistent with unintentional spinal blockade priorto the arrest (such as positive aspiration for CSF ormaternal complaints of sudden headache or diffi-culty breathing). Since most labor epidural patientsin this series arrested after unplanned subarachnoidblocks, patients for whom there are suspicions of“wet tap” may be at increased risk and might benefitfrom closer observation and/or monitoring.

Case reviews suggest that keeping pulse oxime-ter or end-tidal carbon dioxide monitor alarms in anaudible mode continuously during cesarean sectionsis advisable, even after delivery of the newborn. Asof October 2005, the American Society of Anesthesi-ologists (ASA) standards for basic anesthesia moni-toring include the statement that whenever pulseoximeters or capnometers are utilized, the lowthreshold alarms should be audible.2

VentilationRapid recognition of maternal respiratory arrest

and restoration of oxygenation and ventilationshould be key goals. Airway devices such as self-inflating bag/mask systems, oral and nasal airways,laryngeal mask airways (LMAs), and intubationequipment should be immediately available ifneeded in labor rooms, with all nurses and anesthe-sia providers acquainted with their location. Therecently revised ASA Practice Guidelines for Obstet-rical Anesthesia contain more complete lists of poten-tially useful equipment.3

Because an anesthesia provider may not alwaysbe the first to arrive on the scene, labor and deliverynurses should also be able to assess the adequacy ofventilation, establish an airway, and begin ventila-tion if necessary. Supplemental oxygen should beavailable in the labor room and immediately avail-able in portable tank form, should transportation ofan apneic patient become necessary. Since hypoxiawill likely develop rapidly in a full-term apneicpatient, adequate ventilation and oxygenation of themother should ideally be established before trans-porting her to another location.

CirculationAs with any resuscitation, maternal blood pres-

sure and circulation should be evaluated and sup-ported, if necessary, with fluids and pressors. CPRshould be started as soon as maternal circulationappears inadequate. Since aortocaval compressionand an elevated hemidiaphragm can complicatestandard CPR, the American Heart Association sug-gests displacing the uterus to the left by tilting thepatient, and performing chest compressions higheron the sternum (slightly above the center).4

TransfusionMassive hemorrhage on labor and delivery is a

rare occurrence, and as a result, many anesthesiaproviders have little or no experience managing it.Yet, the incidence of major hemorrhage in the obstet-ric population appears to be increasing over time.The increased rate of repeat cesarean sections, withthe associated rise in incidence of placenta previaand placenta accreta, may largely account for this.5One New York hospital, after experiencing 2 mater-nal hemorrhage-related deaths, created a multidisci-plinary patient safety team specifically designed tohandle labor and delivery patients experiencingmajor bleeding episodes.5

Their obstetric rapid response team includesmembers of the trauma team, as the individuals iden-tified in that hospital with the most experience inestablishing large-bore intravenous lines and mas-sive volume and blood replacement. Efforts weremade to identify high-risk patients, who wereadvised about auto-donation of blood and type and

Respiratory Arrests After Epidural Occurred Within 30 Minutes

See “Arrest,” Next Page

“Arrest,” From Preceding Page


screened in advance of delivery. A cell saver bloodscavenging device was used, when necessary, afterthe fetus was delivered and after peritoneal lavage.5

With these and other interventions, that hospitalwas able to significantly decrease the number ofmaternal deaths, despite an increase in the totalnumber of cases of major obstetrical hemorrhage.This suggests that having a pre-planned and coordi-nated multi-departmental approach to maternalhemorrhage may well advance patient safety.

Patient SafetyWhile maternal arrest is, fortunately, a very rare

complication, the above cases are a testament to thefact that it still can and does occur—even when cur-rently acceptable anesthesia practices are followed.Anesthesia providers and labor and delivery staffshould consider planning their own response to a“worst-case scenario” before it happens to them. Afew questions that those providing obstetrical anes-thesia may wish to consider:

• If most maternal arrests occur within 30 minutesof the placement of a regional block, how willyour patient be monitored during that timeperiod, and who will respond if required?

• If a patient were discovered apneic in a labor anddelivery room, where is all potentially necessaryairway equipment kept? Would you have accessto all the drugs that you might need?

• Are a portable oxygen tank and a bag/maskimmediately available for transferring laborpatients for crash cesarean sections? Would youneed a portable monitor?

• During cesarean sections: As you currently usethem, would a monitor alarm notify you if apatient developed apnea at any time?

• How would you and your facility handle an unex-pected massive hemorrhage on the labor anddelivery ward?

• Who is available to help you with a maternalarrest on labor and delivery, and how would theybe notified if needed?

Every case included here was devastating onmany levels to the patients, families, and healthcareproviders involved. While it is tempting to search for“mistakes” in each individual scenario, the majorissues identified were rarely unique. It is hoped thatthrough taking a “systems” approach and focusinginstead on the common factors that these cases share,similar occurrences might be prevented and mater-nal safety improved.

Ann Lofsky, MD is currently a partner in the anesthesiagroup at Saint John’s Hospital in Santa Monica, CA, anda governor emeritus and anesthesia consultant for TheDoctors Company.

Plan for Worst-Case ScenarioReferences

1. Hawkins JL. Anesthesia-related maternal mortality. ClinObstet Gynecol 2003;46:679-87.

2. Standards for basic anesthetic monitoring. Amended bythe ASA House of Delegates October 25, 2005. Availableonline at: http://www.asahq.org/publicationsAndSer-vices/standards/02.pdf. Accessed May 18, 2007.

3. American Society of Anesthesiologists Task Force onObstetric Anesthesia. Practice guidelines for obstetricanesthesia: an updated report by the American Society ofAnesthesiologists Task Force on Obstetric Anesthesia.Anesthesiology 2007;106:843-63. Available online at:http://www.asahq.org/publicationsAndServices/OBguide.pdf. Accessed May 18, 2007.

4. 2005 American Heart Association guidelines forcardiopulmonary resuscitation and emergencycardiovascular care. Available online at:http://circ.ahajournals.org/content/vol112/24_suppl/.Accessed May 18, 2007.

5. Skupski DW, Lowenwirt IP, Weinbaum FI, et al. Improv-ing hospital systems for the care of women with majorobstetric hemorrhage. Obstet Gynecol 2006;107:977-83.

“Arrest,” From Preceding Page

by Robert C. Morell, MD

The intravascular injection or excessive absorptionof bupivacaine can lead to cardiac depression, severearrhythmias, and/or cardiac arrest, from which resus-citation may be difficult, prolonged, and even impos-sible. A past issue of this Newsletter highlighted theperspective of a patient and her anesthesiologist fol-lowing a bupivacaine cardiac arrest after a poplitealnerve block.1 The only reason that the patient survivedto tell her story was the heroic and quick action of theanesthesiologist and the resuscitation team at utilizingan available cardiac operating room to institute car-diopulmonary bypass after conventional resuscita-tive measures were not successful. A new alternativetherapy appears to exist. This new and importanttherapy was emphasized by one of our readers, Dr.Baumgarten, in a Letter to the Editor in the fall 2006issue of this Newsletter. Several case reports (includ-ing recent personal communication) and researchdata consistently indicate that the intravenousadministration of intralipid may facilitate and permitsuccessful resuscitation from bupivacaine cardiotox-icity where conventional advanced cardiac life sup-port protocols may fail. Weinberg and colleaguesdemonstrated that lipid infusion shifted the doseresponse to bupivacaine-induced asystole in rats andimproved survival of dogs from bupivacaine cardiactoxicity.2,3 As Dr. Baumgarten noted, Dr. Rosenblattand colleagues published a case report of a successfulresuscitation using a 20% lipid emulsion (intralipid),after a bupivacaine-induced cardiac arrest.4

Readers should note that other lipid containingmedications have not demonstrated such efficacy, and

one should be particularly careful not to assume thatpropofol would be a safe or effective alternative.Propofol has negative inotropic properties that maycause additional cardiac depression in the setting ofbupivacaine-induced cardiac decompensation.5

Along with standard resuscitative drugs, it wouldseem wise to insure the rapid availability of intralipidwhere regional anesthesia is performed involving theadministration of significant quantities of bupivacaine.Certainly, further study is warranted to answer anumber of questions including the relationship ofintralipid to local anesthetic toxicity caused by agentsother than bupivacaine, the optimum dose of lipidemulsion, the potential advantages of lipid infusionsvs. bolus dosing, and the optimal interval for redosing.

References1. van Pelt FA, Kenney L. Patient and doctor reconcile for

greater good. APSF Newsletter 2006;21:9-10.

2. Weinberg G, et al. Pretreatment or resuscitation with alipid infusion shifts the dose-response to bupivacaine-induced asystole in rats. Anesthesiology 1998;88:1071-1075

3. Weinberg G, Ripper R, Feinstein D, Hoffman W. Lipidemulsion infusion rescues dogs from bupivacaine-induced cardiac toxicity. Reg Anesth Pain Med2003;28:198-202.

4. Rosenblatt MA, Abel M, Fischer GW, Itzkovich CJ,Eisenkraft JB. Successful use of a 20% lipid emulsion toresuscitate a patient after a presumed bupivacaine-related cardiac arrest. Anesthesiology 2006;105:217-8.

5. Groban L, Butterworth J. Lipid reversal of bupivacainetoxicity: has the silver bullet been identified? Reg AnesthPain Med 2003;28:167-9.

Intralipid Might Save Lives As aRescue from Bupivacaine Toxicity

VisionThe vision of the Anesthesia PatientSafety Foundation is to ensure that nopatient shall be harmed by anesthesia.

YUMission

The APSF’s Mission is to improve continually the safety of patients duringanesthesia care by encouraging and con-ducting• safety research and education• patient safety programs and

campaigns• national and international exchange

of information and ideas.


by Tricia A. Meyer, PharmD

On June 15, 2007, the FDA released a safety alertconcerning reports over the past few months of casesof fever, chills, and body aches in several clusters ofpatients shortly after the administration of propofol.These new cases involved patients undergoing proce-dures in gastrointestinal suites. The FDA noted thatthe symptoms were similar to those reported whenpropofol was first introduced in the US. The postop-erative infection in these early cases was attributed tolapses in aseptic technique with risk factors thatincluded “batch” preparation of propofol syringes foruse throughout the day, reuse of syringes or infusionpump lines on different patients, use of propofolsyringes prepared more than 24 hours in advance,transfer of prepared syringes between operatingrooms or facilities, failure to wear gloves during inser-tion of intravenous catheters, and failure to disinfectthe stoppers of the propofol vials. It was also notedthat 50-ml and 100-ml vials were used as multi-dosevials. The formulation at that time did not containpreservatives.

In the most recently reported cases, investigatorsalso found use of the single-use vials for multiplepatients. To date, tests performed on multiple units ofpropofol vials and lots by the FDA have not identifiedany units contaminated with bacteria or endotoxins.Testing of other possible sources such as the lidocainecoadminsitered with propofol and the instrumenta-tion sterilization systems have not identified anypotentially causative agents.

Propofol is marketed as Diprivan® and is alsoavailable as a generic disodium edetate. Sodiummetabisulfite or benzyl alcohol is added to the propo-fol to retard the rate of microbial growth. Even thoughthe product contains preservatives, microbial growthis still possible and it is not an antimicrobially pre-served product under USP standards. The emulsion iscapable of supporting microbial growth in the eventof contamination during administration due to thelevel of soybean oil and egg lecithin or egg yolk phos-pholipids contained in the product.

Recommendations and considerations by the FDA are:

• Both the vial and prefilled syringe formulationmust be used on only 1 patient.

• Administration must commence immediately afterthe vial or syringe has been opened.

• In general anesthesia or procedural sedation:administration from a single vial or syringe mustbe completed within 6 hours of opening.

• In ICU sedation: propofol administered directlyfrom a vial must be limited to only 1 patient,must commence immediately on opening the vial

and must be completed within 12 hrs of openingthe vial.

Package Insert Guidelines:• Strict aseptic technique must always be used

during handling, including hand washing prior touse.

• Propofol should be visually inspected prior to usefor:

– particulate matter

– discoloration

– evidence of separation of the phases of theemulsion.

• Do not use if contaminated.

• Prepare for use just prior to administration to eachpatient.

• The vial rubber stopper should be disinfected using70% isopropyl alcohol.

• Discard unused portions within the required timelimits.

The FDA urges individuals to report adverseevents to the MedWatch Adverse Event ReportingProgram.

Tricia A. Meyer, PharmD, MS, is Director of theDepartment of Pharmacy and Assistant Professor, Depart-ment of Anesthesiology, Scott and White Hospital, TexasA&M Health Science Center, Temple, TX.

General References

1. FDA alert/information for healthcare professionals:propofol (marketed as Diprivan and as generic products)Information. U.S. Food and Drug Administration, Centerfor Drug Evaluation and Research. Available at:http://www.fda.gov/cder/drug/infopage/propofol/default.htm. Accessed June 17, 2007.

2. Bennett SN, McNeil MM, Bland LA, et al. Postoperativeinfections traced to contamination of an intravenous anes-thetic, propofol. N Engl J Med 1995;333:147-54.

3. Infections linked to lax handling of propofol. Am J HealthSyst Pharm 1995;52:2061, 2066.

4. Propofol injection. Deerfield, Il., Baxter Healthcare Corpo-ration, Sept. 2004.

5. Propofol injection. Bedford, OH., Bedford Laboratories,July 2005.

6. Diprivan®. Wilmington, DE, AstraZeneca, 2005 (currentlyAbraxis).

Propofol Safety Review A N E S T H E S I A P A T I E N T

S A F E T Y F O U N D A T I O N

CORPORATE ADVISORY COUNCIL

George A. Schapiro, ChairAPSF Executive Vice PresidentElizabeth F. Holland ..................Abbott Laboratories

Sean Lynch ..................................Anesthesia Healthcare Partners

Cliff Rapp ....................................AnesthesiologistsProfessional InsuranceCompany

Rick Eagle ....................................Arrow International

Nassib G. Chamoun....................Aspect Medical System

Stanley Horton, PhD ..................Bayer Pharmaceuticals

Raul A. Trillo, MD ......................Baxter Healthcare

Michael S. Ferrara........................Becton Dickinson

Timothy W. Vanderveen, PharmD ....................................Cardinal Healthcare

Sarah Hopkins ............................Cerner Corporation

Roger S. Mecca, MD....................Covidien

Thomas W. Barford ....................Datascope Corporation

Robert Clark ................................Dräger Medical

Mike Gustafson............................Ethicon Endo-Surgery

Paul A. Baumgart ........................GE Healthcare

Steven Pregulman, MD ..............Hospira

Steven R. Block ............................LMA of North America

Dana Capocaccia ........................Luminetx

Joe Kiana ......................................Masimo

Nancy Stahulak ..........................Medical Protective

Anne Young ................................Merck & Co.

Bert de Jong, MD ........................Organon

Dominic Corsale ..........................Oridion

Walter Huehn ..............................Philips Medical Systems

Edward C. Mills ..........................Preferred PhysiciansMedical Risk RetentionGroup

Ron Richard ................................ResMed

Michael Stabile, MD....................Safer Sleep

Andrew Rose ..............................Smiths Medical

Joseph Davin................................Spacelabs

Ann S. Lofsky, MD......................The Doctors Company

Terry Wall ....................................Vital Signs

Abe Abramovich

Casey D. Blitt, MD

Robert K. Stoelting, MD


Cardiology Experts Share Perspective on StentsResponse to Letter to the Editor: Antiplatelet Therapy Should Not Be Stopped

at the studies done on comparing aspirin withwarfarin compared to aspirin with thienopyri-dine, the warfarin is a big loser. I mean, a 5-foldincreased risk of ST; so in my mind, I’ve extrap-olated other antithrombin agents to the war-farin situation . . . . I tend to lean more in thecamp of the antiplatelet agents. But again, Iwould rather just keep the patient on theaspirin and the clopidogrel because I’m veryconcerned about the abrupt stopping of theantiplatelet agent, and then at the same timeyou’re inciting an inflammatory and hyperco-agulable state by performing surgery.

Discontinuation of dual antiplatelet therapywith clopidogrel and aspirin does occurbecause of cost, perceived risk of bleeding,patients and physicians unaware of the bene-fits and time of therapy required, and the dis-continuation of these drugs by physicians,dentists, surgeons, or their staff before surgicalprocedures. We avoid elective surgery formore than 1 year after DES, more than 3months after bare metal stents (BMS), as therisk of ST in both stent types remains highduring the postoperative period. With moreurgent procedures, if any provider—a physi-cian, dentist, or surgeon—feels that stoppingthe antiplatelet medicines is absolutely neces-sary, then there should first be a consultationwith the patient’s cardiologist. We havechanged our practice to never allow the dis-continuation of aspirin within the first year ofa DES, and would probably extend that tolonger duration in stents at high-risk of throm-bosis. Importantly, clopidogrel should berestarted as soon as possible. In general, we seemore surgeons willing to operate on dualantiplatelet therapies, or at least aspirin. If dualantiplatelet therapy has been discontinued forwhatever reason, aspirin should be restartedimmediately. Non-enteric coated aspirin (4baby aspirins) may be given, and the patientshould have antiplatelet effects within 2 hours.

Drug-eluting stents prevent the tissue growththat causes restenosis and reduce the need forangioplasty or bypass surgery, but it should benoted that the reduced tissue growth means thestent is exposed to blood for a longer time; thisincreases the risk of clotting. Dual antiplatelettherapy is also important in patients receivingbare metal stents, but the risk of thrombosis inthese procedures remains high for only 1 to3 months. Consideration should be given tousing a bare metal stent if patients are noncom-pliant with medications, or cannot afford totake clopidogrel for the full year, or if theyabsolutely cannot postpone an elective surgery.

Following is a summary of additional com-mentary from Deepak Bhatt, MD, FACC, associatedirector at the Cleveland Clinic Foundation and A.Michael Lincoff, MD, FACC, vice chairman of Car-diovascular Medicine at the Cleveland ClinicFoundation.

Although there are no evidence-based data sup-porting the perioperative use of a short-actingglycoprotein (GP) IIb/IIIa platelet inhibitor(“bridging therapy”), there appears to be a rolefor this use. There are instances in which theonly option perioperatively is fast-acting par-enteral antiplatelet inhibition with a GP IIb/IIIaantagonist. There are patients for whom there isincreased risk of stent thrombosis (ST); forexample, a patient had a complex DES proce-dure a month ago, and then needed hip surgeryafter falling and breaking their hip, and the sur-geon just absolutely refused to operate. Thispatient was brought into the hospital andstarted on a short-acting intravenous IIb/IIIainhibitor. Though practically speaking it meansbringing these patients in hospital, there aremany patients for whom that extra 4-day hospi-talization is worth it. One has to balance therisks and look at the consequences of thrombo-sis. In those instances, go ahead and proceedwith bridging therapy.5 Another option is can-grelor, which is being tested in Phase III trials.An intravenous short-acting ADP receptorantagonist, cangrelor may conceptually be afuture option in the perioperative period.

We are in agreement with Grines et al.: proce-dures should only be performed on patients withDES in institutions where 24-hour interventional car-diology coverage is present in the event that imme-diate percutaneous coronary intervention (PCI) isneeded for perioperative ST.6 Almost all case reportsto date have cited ST occurring postoperatively, mostcommonly in the Post Anesthesia Care Unit, andmanifesting as a ST-elevation MI (STEMI). Thus, theimportance of having immediate access to a coronarycatheterization laboratory must be emphasized.McFadden et al. reported ST and STEMI occurringpreoperatively after premature discontinuation ofdual antiplatelet therapy, or aspirin, in cases wherethe patient had completed their prescribed course ofclopidogrel.7 Stent thrombosis and its sequelae occuracutely. Therefore, it would be unlikely that a patientwith ST would be asymptomatic. However, in allcases, the anesthesiologist (or a member of the anes-thesia care team) and surgeon should speak with thepatient’s cardiologist in order to reach a consensus asto what the safest course of treatment may be. Weagree with Dr. Kempen that all patients with coro-nary stents undergo preoperative screening a week

We thank Dr. Kempen for his letter highlightingthe challenges of caring for patients with coronarydrug-eluting stents (DES). We have discussed some ofhis questions and other issues related to perioperativemanagement of patients with coronary stents withnoted national experts in this area from cardiology.Below is a synopsis of the perspective of Cindy L.Grines, MD, FACC, and chair of the 2007AHA/ACC/SCAI/ACS/ADA Science Advisorycommittee report on stent management, with herpermission.

The purpose of the 2007 AHA/ACC/SCAI/ACS/ADA Science Advisory was to alert bothpatients and healthcare professionals that stentthrombosis (ST) is a serious medical issue.1 Theguidelines for dual antiplatelet therapy havebeen changed to say emphatically that patientsshould receive a minimum of 12 months of dualantiplatelet therapy—and the minimum means,in many cases—physicians may want to goeven further than that period of time. There areseveral patient subsets that would likely bene-fit much longer than 12 months. These includepatients with acute coronary syndromes, longstents, multiple stents, overlapping stents, dia-betes, renal failure, all of which are additionalrisk factors for stent thrombosis. In thesepatients, indefinite clopidogrel (Plavix®) usemay be recommended. The guidelines were co-written by the American Heart Association, theAmerican College of Cardiology, as well as theAmerican College of Physicians, Surgeons andDentistry. The Science Advisory was an attemptto avoid the premature discontinuation of dualantiplatelet therapy; providers must realizestopping antiplatelet therapy in patients withDES without discussing it with their cardiolo-gist could result in their patients having a fatalheart attack. The leading adverse event associ-ated with early discontinuation of antiplatelettherapy is ST. Stent thrombosis occurs in up to29% of patients who discontinue antiplatelettherapy early. The mortality rate in patientswith ST ranges from 20-45%.1,2 Premature dis-continuation of dual antiplatelet therapy is thegreatest predictor of ST. In a single-site study of652 patients treated with sirolumis DES, pre-mature discontinuation of clopidogrel wasassociated with a 30-fold greater risk of ST, with>25% of patients who discontinued clopidogreltherapy within the first month suffering ST.1,3 Ina study of 500 patients who received DES afteran acute myocardial infarction (MI), the deathrate over the next 11 months was 7.5% for thosewho stopped taking their thienopyridine med-ication compared with 0.7% in those who hadnot stopped therapy.1,4

With regard to antithrombin agents, if you look See “Stents,” Next Page


the American College of Physicians. Circulation2007;115:813-8.

2. Iakovou I, Schmidt T, Bonizzoni E, et al. Incidence,predictors, and outcome of thrombosis after successfulimplantation of drug-eluting stents. JAMA 2005;293:2126-30.

3. Jeremias A, Sylvia B, Bridges J, et al. Stent thrombosisafter successful sirolimus-eluting stent implantation.Circulation 2004;109:1930-2.

4. Spertus JA, Kettelkamp R, Vance C, et al. Prevalence, pre-dictors, and outcomes of premature discontinuation ofthienopyridine therapy after drug-eluting stent place-ment: results from the PREMIER registry. Circulation2006;113:2803-9.

5. Rabbat MG, Bavry AA, Bhatt DL, Ellis SG. Understand-ing and minimizing late thrombosis of drug-elutingstents. Cleve Clin J Med 2007;74:129-36.

6. Brilakis ES, Banerjee S, Berger PB. Perioperative manage-ment of patients with coronary stents. J Am Coll Cardiol2007;49:2145-50.

7. McFadden EP, Stabile E, Regar E, et al. Late thrombosisin drug-eluting coronary stents after discontinuation ofantiplatelet therapy. Lancet 2004;364:1519-21.

8. Patrono C. Aspirin as an antiplatelet drug. N Engl J Med1994;330:1287-94.

9. Neumann FJ, Ott I, Gawaz M, Puchner G, Schomig A.Neutrophil and platelet activation at balloon-injuredcoronary artery plaque in patients undergoing angio-plasty. J Am Coll Cardiol 1996;27:819-24.

10. Mangano DT. Perioperative cardiac morbidity. Anesthe-siology 1990;72:153-84.

11. Cohen MC, Aretz TH. Histological analysis of coronaryartery lesions in fatal postoperative myocardial infarc-tion. Cardiovasc Pathol 1999;8:133-9.

12. Dawood MM, Gutpa DK, Southern J, et al. Pathology offatal perioperative myocardial infarction: implicationsregarding pathophysiology and prevention. Int J Cardiol1996;57:37-44.

13. Poldermans D, Schouten O, Vidakovic R, et al. A clinicalrandomized trial to evaluate the safety of a noninvasiveapproach in high-risk patients undergoing major vascu-

phenomenon occurs as a consequence of sympatheticactivation and cytokine release.10,11 Inflammatoryactivation from endothelial damage, as in PCI andsurgery, exacerbates the prothrombotic state, makingthe patient highly susceptible for thromboembolicevents. Autopsy results have shown this mechanismis responsible for at least half of all perioperativeinfarctions.12,13 Theoretically, apheresis plateletsadministered to patients with stents who have serumlevels of clopidogrel and aspirin may not developantiplatelet effects to provide adequate protectionfrom ST for hours to days. Also, activation of thetransfused platelets may occur, further increasing therisk of ST, MI, and death. Direct and autologousdonation of any blood component is being discour-aged by blood banks at many institutions, includingour own, because of increased cost and no provensafety benefit over homologous donation.

The controversy and concern surrounding coro-nary artery stents, especially in the case of DES, illus-trate the importance of instituting a multidisciplinaryapproach in the care of these patients.

Lisa Newsome, MDRoger Royster, MDWinston-Salem, NC

Richard Prielipp, MDMinneapolis, MN

References

1. Grines CL, Bonow RO, Casey DE Jr; American HeartAssociation; American College of Cardiology; Society forCardiovascular Angiography and Interventions; Amer-ican College of Surgeons; American Dental Association;American College of Physicians. Prevention of prema-ture discontinuation of dual antiplatelet therapy inpatients with coronary artery stents: a science advisoryfrom the American Heart Association, American Collegeof Cardiology, Society for Cardiovascular Angiographyand Interventions, American College of Surgeons, andAmerican Dental Association, with representation from

before scheduled surgery to ensure that the appro-priate care has been coordinated, dual antiplatelettherapy has been appropriately managed, and allappropriate parties are involved in this very complexcare.

Ideally, patients who have clopidogrel andaspirin discontinued for more than 5 days prior to aprocedure who are asymptomatic should haveaspirin reinstituted for 3-5 days to achieve steady-state before proceeding with surgery. We have can-celled a number of cases over the past few monthsbecause of premature discontinuation of dualantiplatelet therapy. If aspirin has been discontinuedfor 3-5 days, we have given 325 mg of non-entericcoated aspirin, and proceeded with surgery laterthat day to allow platelet inhibition to take effect.Studies have shown that 160 mg of aspirin willinhibit platelet function.8 The same effect can beachieved with aspirin 75-81 mg over 3-5 days.

We also agree with Dr. Grines that aspirinshould never be discontinued in the perioperativeperiod. However, in cases where the surgeonabsolutely refuses to operate with the patient onaspirin, then it is imperative that communicationoccur between the patient’s cardiologist, surgeon,and anesthesia provider, and the risks of ST versusmajor bleeding be carefully weighed. Again, the riskof ST is 29%, and the mortality rate from ST rangesfrom 20-45%. The surgeon must be made acutelyaware of this when considering whether to operatewhile the patient remains on aspirin.

The use of platelet infusions intraoperativelyshould be avoided except in the instance where thereis life-threatening bleeding. There are certain states(acute MI, unstable angina, trauma, surgery), inwhich platelet aggregation and activity are enhancedeven without an increase in platelet counts.9 This

Stents Require a Multidisciplinary Approach“Stents,” From Preceding Page

The Anesthesia Patient Safety Foundation is pleased to announce the

BOARD OF DIRECTORS WORKSHOPTraining Before Using Advanced Medical Devices in the Operating Room—

Voluntary or Mandatory for the Anesthesia Professional?

Friday, October 12, 2007

1300-1700 (Parc Ballroom II/III)Parc Fifty Five Hotel, 55 Cyril Magnin Street, San Francisco, CA

If you are interested in attending this Workshop, please email [email protected] to reserve your place. Space is limited and attendance will be possible only by invitation or a limited number of advanced reservations.

www.apsf.org

®


Dear SIRS:

I am a CRNA with 13 years of experience. I neverhad a problem with a pulse oximeter until I encoun-tered the Datex-Ohmeda Cardiocap 5. I was accus-tomed to a pulse oximeter alarming loudly anytime itwas low or not on the patient. I have had 2 incidencesin the last 2 years where the ECG beeped when thepulse oximeter was off, such that one might havethought the pulse oximeter reading was OK when notfacing the monitor. While another patient was undermonitored anesthesia care, the pulse oximeter initiallywas working, but ceased to work 3 minutes into thecase. Once again the ECG beeped, but without theannoyingly loud alarm from the pulse oximeter; therewas a single, short beep about every minute. Theprobe was not illuminated and had to be switched.

I think it is very dangerous to allow a monitor notto alarm if it is not working. I have worked with manymonitors over the course of my career, and feel this istaking a step backward if the software cannot beadjusted. I appreciate any information. Thanks.

Kathleen Piotrowski, MSN, CRNACuyahoga Falls, Ohio

In Response:

Thank you for the opportunity to respond. I’vereviewed this with our design center in Helsinki, Fin-land, and have observed the monitor’s behavior inorder to provide the most thorough response. First, Iwould like to provide you with my name and contactinformation and assure you that you are welcome tocontact me directly at any time.

The Cardiocap/5 monitor is designed with a 3-tiered approach to alarm logic where advisory alarmsare displayed in white with a single beep, serious alarmsare in yellow and provide 3 beeps, and life-threateningalarms display in red and give 5 beeps.

In the situation you describe, I believe the monitorperformed according to the specifications. The Car-diocap/5 monitor, by default, sources the heart rateautomatically looking for ECG, Pleth, or InvasivePressure for an available heart rate. When the heartrate is sourced from the ECG, you will hear the beatsound also sourced from the ECG, and the heart ratewill be displayed in the same color as the ECG wave-form and numeric. If the heart rate is sourced from thePleth, the beat sound will be sourced from Pleth andwill provide an audible tone different from the ECGtone. The heart rate will be displayed in the samecolor as the Pleth waveform and numeric.

If the current source becomes unavailable, forexample the SpO2 probe falls off the patient’s finger,the monitor will automatically search for another heartrate source (either ECG or invasive pressure). Whenthe monitor switches to another source, ECG for exam-ple, the tone of the beat sound will change, thenumeric on the display will change to match the colorand value coming from the ECG, and a white advisoryalarm will be displayed noting “SpO2 probe off” or“No SpO2 pulse,” whichever is applicable. After sev-eral seconds, the white advisory alarm will escalate toa yellow serious alarm and provide 3 beeps. Theyellow alarm remains active until it is either acknowl-edged, or the alarm event is corrected (i.e., probereturned to the patient’s finger).

Based on the information we have available, Iwould speculate that the monitor is performingaccording to specifications. I would be more thanhappy to discuss this situation further and to engageour Field Service team to complete a more thoroughinvestigation of the monitor to test the performance.Please feel free to contact me at the telephone or emailaddress listed above.

Best regards,Gina PetryProduct Manager—PerioperativeGE Healthcare TechnologiesMadison, Wisconsin

Editor’s Question:

This sounds like the identical mechanism on ourDatex-Ohmeda S/5 monitoring system, and it hasfooled some of our own clinicians as well. One optionyour response did not include is to select the heartrate source manually, instead of automatically. Atleast in the S/5, this would stop the tone, and causethe clinician to look upwards. Is that possible in theCardiocap/5?

Michael A. Olympio, MD

In Response:

You are correct—it should be the same mecha-nism as your S/5 monitor. The logic is almost identi-cal throughout the Datex-Ohmeda family of monitors.You can set the heart rate source manually to Pleth,for example. This setting cannot be saved as a default,however. The loss of a pulse from Pleth will result inthe loss of the beat sound and a yellow alarm.

Gina Petry

Michael Olympio, MD, Chair of the APSF Committee on Technologyand Co-Founder of the Dear SIRS Initiative.

Dear SIRS refers to the Safety InformationResponse System. The purpose of this column is to

allow expeditious communication of technology-

related safety concerns raised by our readers, with

input and responses from manufacturers and indus-

try representatives. This process was developed by

Drs. Michael Olympio, Chair of the Committee on

Technology, and Robert Morell, Editor of this

newsletter. Dr. Olympio is overseeing the column

and coordinating the readers’ inquiries and the

responses from industry. Dear SIRS made its debut

in the Spring 2004 issue.

S AFETY

I NFORMATION

R ESPONSE

S YSTEM

Alarm Requires Selection of Heart Rate SourceDear SIRS

The information in this column is provided for safety-related educational purposes only, and does not constitute medical or legal advice. Individual or group responsesare only commentary, provided for purposes of education or discussion, and are neither statements of advice nor the opinions of APSF. It is not the intention of APSF toprovide specific medical or legal advice or to endorse any specific views or recommendations in response to the inquiries posted. In no event shall APSF be responsible orliable, directly or indirectly, for any damage or loss caused or alleged to be caused by or in connection with the reliance on any such information.


Anesthesia Patient Safety FoundationCorporate DonorsFounding Patron ($500,000 and higher)American Society of Anesthesiologists (asahq.org)

Grand Patron ($150,000 to $199,999)Anesthesia Healthcare Partners, Inc.

(AHP) (ahphealthcare.com)

Cardinal Health Foundation (cardinal.com)

Sustaining Patron ($100,000 to $149,999)Merck & Co. (merck.com)

Sponsoring Patron ($75,000 to $99,999)GE Healthcare (gemedical.com)

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Tyco Healthcare (tycohealthcare.com)

Community Donors (includes Anesthesia Groups, Individuals,

Specialty Organizations, and State Societies)Grand Sponsor ($5,000 and higher)Alabama State Society of AnesthesiologistsAmerican Academy of Anesthesiologist Assistants American Association of Nurse AnesthetistsAsheville Anesthesia AssociatesFlorida Society of AnesthesiologistsDr. and Mrs. Thomas R. HillIndiana Society of AnesthesiologistsIowa Society of AnesthesiologistsFrank B. Moya, MD, Charitable FoundationRobert K. Stoelting, MDSustaining Sponsor ($2,000 to $4,999)Academy of AnesthesiologyAnaesthesia Associates of MassachusettsAnesthesia Consultants Medical GroupAnesthesia Resources ManagementArizona Society of AnesthesiologistsNassib G. ChamounGeorgia Society of AnesthesiologistsMadison Anesthesiology ConsultantsMassachusetts Society of AnesthesiologistsMichigan Society of AnesthesiologistsMinnesota Society of AnesthesiologistsOhio Society of AnesthesiologistsOld Pueblo Anesthesia GroupPennsylvania Society of AnesthesiologistsSociety of Cardiovascular AnesthesiologistsTennessee Society of AnesthesiologistsContributing Sponsor ($750 to $1,999)Affiliated Anesthesiologists, Inc.American Association of Oral and Maxillofacial

SurgeonsAmerican Society of Critical Care AnesthesiologistsAmerican Society of PeriAnesthesia Nurses

(aspan.org)J. Jeffrey Andrews, MDAnesthesia Associates of Northwest Dayton, Inc.Associated Anesthesiologists of St. Paul, MNAssociation of Anesthesia Program DirectorsSorin J. Brull, MDFrederick W. Cheney, MD

Connecticut State Society of AnesthesiologistsJeffrey B. Cooper, PhDSteven F. Croy, MDMark T. Destache, MD (Associated Anesthesiologists)District of Columbia Society of AnesthesiologistsDavid M. Gaba, MDJohn H. Eichhorn, MDIllinois Society of AnesthesiologistsKentucky Society of AnesthesiologistsJohn W. Kinsinger, MDThomas J. Kunkel, MDRodney C. Lester, CRNAEdward R. Molina-Lamas, MDMadison Anesthesiology ConsultantsMaryland Society of AnesthesiologistsMichiana Anesthesia CareMissouri Society of AnesthesiologistsRobert C. Morell, MDNebraska Society of AnesthesiologistsJohn B. Neeld, MD; in honor of Orin F. Guidry, MDNorthwest Anesthesia PhysiciansNeshan Ohanian, MDNevada State Society of AnesthesiologistsNurse Anesthesia of MaineOklahoma Society of AnesthesiologistsOregon Society of AnesthesiologistsOregon Anesthesiology GroupPhysician Anesthesia ServicePittsburgh Anesthesia AssociatesSanta Fe Anesthesia Specialists Society of Academic Anesthesia ChairsSociety for Ambulatory Anesthesia Society of Neurosurgical Anesthesia and

Critical CareSociety for Pediatric AnesthesiaSouth Dakota Society of AnesthesiologistsStockham-Hill FoundationTexas Society of AnesthesiologistsDrs. Mary Ellen and Mark WarnerWashington State Society of AnesthesiologistsWisconsin Society of AnesthesiologistsSponsor ($100 to $749)Robert L. Barth, MDManuel E. BonillaCalifornia Society of AnesthesiologistsRobert A. Caplan, MD

Melvin A. Cohen, MDColorado Society of AnesthesiologistsKathleen A. Connor, MD David M. Clement, MDPaula A. Craigo, MDJ. Kenneth Davison, MDJohn DesMarteau, MDWalter C. Dunwiddie, MDNorig Ellison, MDJan Ehrenwerth, MDThomas R. Farrell, MDAnthony Frasca, MDB. L. Friedberg, MDThomas R. Farrell, MDJane C. K. Fitch, MD/Carol E. Rose, MDIan J. Gilmour, MDGregory E. Ginsburg, MDBarry M. Glazer, MDJames D. Grant, MDGriffin Anesthesia AssociatesWilliam D. Heady, CRNAAlexander A. Hannenberg, MDPeter L. Hendricks, MDJames S. Hicks, MDDr. and Mrs. Glen E. HolleyHoward E. Hudson, Jr., MDIndianapolis Society of AnesthesiologistsRobert. H. Intress, MDRobert E. Johnstone, MDTamos Kallos, MDDaniel J. Klemmedson, DDS, MDKansas Society of AnesthesiologistsBettyLou Koffel, MDMaine Society of AnesthesiologistsAlan P. Marco, MDMaryland Association of Nurse AnesthetistsJohn P. McGee, MDTom L. McKibban, CRNACora B. McKnight, CRNAMedical Anesthesiology Consultants CorporationMississippi Society of AnesthesiologistsA. J. Montes, MDRoger A. Moore, MDErvin Moss, MDNew Hampshire Society of AnesthesiologistsNew Jersey State Society of Anesthesiologists

New Mexico Society of AnesthesiologistsL. Charles Novak, MDDenise O’Brien, RNMichael A. Olympio, MDCarmelita S. Pablo, MDPennsylvania Association of Nurse AnesthetistsMukesh K. Patel, MDGaylon K. Peterson, MDPhysician Specialists in AnesthesiaRichard C. Prielipp, MDRhode Island Society of AnesthesiologistsGail I. Randel, MDHenry C. Safford, CRNAEduardo A. Salcedo, MD (Salmon Medical

Innovations)Drs. Chris and David SantamoreMuthia Shanmugham, MBEugene P. Sinclair, MDSociety for Obstetric Anesthesia and PerinatologySociety for Technology in AnesthesiaSouth County Anesthesia AssociationShepard and Marlene StoneSara L. Strom, AA-CThe Woodlands Anesthesia AssociatesUniversity of Maryland Anesthesiology AssociatesVermont Society of AnesthesiologistsVirginia Society of AnesthesiologistsMatthew B. Weinger, MDWest Virginia Association of Nurse AnesthetistsWest Virginia State Society of AnesthesiologistsAndrew S. Weisinger, MDDr. and Mrs. WetchlerWichita Anesthesiology, CharteredLawrence Wobbrock, JDBenjamin and Elizabeth Yoder

In MemoriamIn memory of Dr. Marc Balin (anonymous)In memory of Maurice Chait, MD

(Texas Society of Anesthesiologists)In memory of Oneita M. Hedgecock, MD

(Texas Society of Anesthesiologists)In memory of Laurie A. Noll, MD

(The Coursin family)In memory of Bonnie J. Slarsky

(Jeffrey B. Cooper, PhD)In memory of Rex E. Thomas, MD

(Texas Society of Anesthesiologists)

Note: Donations are always welcome. Send to APSF; c/o 520 N. Northwest Highway, Park Ridge, IL 60068-2573 (Donor list current through July 10, 2007)

Supporting Patron ($15,000 to $24,999)Baxter Anesthesia and Critical Care (baxter.com)Dräger Medical (draeger.com)Preferred Physicians Medical Risk Retention Group (ppmrrg.com)

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Sustaining Donor ($5,000 to $9,999)Anesthesiologists Professional Assurance Company

(apacinsurance.com)Arrow International (arrowintl.com)Bayer Healthcare (bayerhealthcare.com)

Becton Dickinson (bd.com)Cerner Corporation (cerner.com)Datascope Corporation (datascope.com)LMA of North America (lmana.com)Luminetx Corporation (luminetx.com)ResMed (resmed.com)Safer Sleep (safersleep.com)Smiths Medical (smiths-medical.com)Tensys Medical (tensysmedical.com)The Doctors Company (thedoctors.com)Medical Protective (medpro.com)Vance Wall FoundationVital Signs (vital-signs.com)

Sponsoring Donor ($1,000 to $4,999)Anesthesia Business Consultants (anesthesiallc.com)Allied Healthcare (alliedhpi.com)Armstrong Medical (armstrongmedical.net)

Cook Critical Care (cookgroup.com)Intersurgical, Inc. (intersurgicalinc.com)King Systems (kingsystems.com)Medical Education Technologies, Inc. (meti.com)Micropore, Inc. (extendair.com)Roche Laboratories (roche.com)TRIFID Medical Group LLC (trifidmedical.com)W.R. Grace (wrgrace.com)Corporate Level Donor ($500 to $999)Belmont Instrument Corporation (belmontinstrument.com)Lippincott Williams and WilkinsProMed Strategies, LLCParticipating AssociationsAmerican Association of Nurse Anesthetists (aana.com)Subscribing SocietiesAmerican Society of Anesthesia Technologists and Technicians (asatt.org)


gas flow from completely dissipating away from thepatient. There was no CO2 rebreathing under thedrapes as is often seen with disconnects in facialcases. The discontinuity did cause loss of measuredexpired volume and some pressure, which activatedan alarm. The capnograph alarm was not triggeredbecause the capnogram persisted.

Obviously it was necessary and desirable to replacethe 15 mm connector into the endotracheal tube, andthis was easily accomplished. The unusual placementof the circumferential plastic drape combined withspontaneous ventilation created a unique circumstancethat in one way reduced patient danger (fresh gasremained available), but in other ways increaseddanger in that the characteristic disappearance of thecapnogram did not occur with this disconnect.

Anesthesiologists and nurse anesthetists shouldhave heightened awareness of breathing systemcontinuity during major facial surgery and of thepotential unusual implications of encasing all theconnections in a wrap of sterile plastic drape.

Gregory Rose, MDJohn Eichhorn, MDLexington, KY

To the Editor:

Accidental disconnection of components of thebreathing system during general anesthesia with anendotracheal tube persists as an occasional problem.It seems more likely in face surgery where the tube isin the midst of an active surgical field and not accessi-ble by the anesthesiologist. While the potential forgreat danger during controlled ventilation or theentrainment of room air and/or rebreathing duringspontaneous ventilation still exists, modern electronicmonitoring will almost always sound alarms andconvey information that leads to rapid discovery andre-connection of the wayward breathing system com-ponents. We report an unusual case of breathingsystem disruption with a misleading presentation inthat the capnogram appeared normal and there wasno gas irregularity.

A 50-year-old female was undergoing a facelift.After routine anesthesia induction and intubationwith a standard 7.5 mm endotracheal tube, the oper-ating room (OR) table was turned 180°. The breathingcircuit elbow piece was removed and replaced with astraight connector between the tube adapter and thecircuit Y-piece. All connections were snugly pushedtogether. The patient’s face, neck, endotracheal tube,and distal breathing circuit were prepped into the

field. A clear plastic 45 × 60 cm Steri-Drape™ 1010(3M, Minneapolis, MN) was spirally wrappedaround the parts of the endotracheal tube, connector,sample tubing, and circuit that were in the surgicalfield (see photo).

After approximately 1 hour of surgery, with thepatient on controlled ventilation, desflurane at 1MAC in 1 L/min oxygen, the reservoir bag of theDräger Apollo anesthesia machine was noted to becompletely empty, and, at the same time, the “lowvolume” alarm of the machine sounded. The capno-gram showed a pattern characteristic of spontaneousbreathing, with the waveform returning to baselineduring each breath. There was no decrease in FiO2.Oxygen flow was increased from 1 L/min to10 L/min with no filling of the bag or change in thealarm. Careful inspection revealed that the 15 mmconnector had come out of the end of the endotra-cheal tube. The surgeon quickly grasped the enfold-ing plastic drape and pushed the enclosed connectorback into the endotracheal tube.

Of particular interest in this incident is the factthat the plastic drape wrapped around both the distalcircuit tubing and the endotracheal tube preventedsignificant entrainment of room air and kept the fresh

Case Report

Wrap Delays Detection of Disconnect

APSF ExecutiveCommittee Invites

CollaborationFrom time to time the AnesthesiaPatient Safety Foundation recon-firms its commitment of workingwith all who devote their energiesto making anesthesia as safe ashumanly possible. Thus, the Foun-dation invites collaboration fromall who administer anesthesia, andall who provide the settings inwhich anesthesia is practiced, allindividuals and all organizationswho, through their work, affect thesafety of patients receiving anes-thesia. All will find us eager to lis-ten to their suggestions and towork with them toward the com-mon goal of safe anesthesia for allpatients.

Photograph of extensive wrapping of tracheal tube and connection, which delayed detection of the disconnect.


An invited conference sponsored by CardinalHealth Center for Safety and Clinical Excellence washeld June 7-8 in San Diego, to review and summarizeexpert opinion on tight glycemic control (TGC) foracute hospitalized patients. Speakers included SimonFinfer, MBBS (Nice-SUGAR trial, Sydney, Australia)and Philippe Devos, MD (VISEP/Glucontrol trials,Belgium), with another 45 participants from across theUnited States and Canada. Thought leaders repre-sented the disciplines of anesthesiology, intensivecare, endocrinology, surgery, hospitalist medicine,medical genetics, nutrition, nursing, pharmacy, bio-statistics, and healthcare biotechnology.

The central question, which anchored the confer-ence, was whether ICU patients benefit most from“intensive” or “tight” glycemic control (usuallydefined as blood glucose in the range of 80-110 mg/dL)or “tighter” control (typically translated as bloodglucose in the range of 110-150 mg/dL).

In the meantime, conference presentationsyielded these highlights:

• Insulin is the most common drug reported as amedication error to the U.S. Pharmacopeia.Moreover, the error harm rate (categories E, F, H,I) = 9.3%.

• Data from hospitals using “smart” IV pumps doc-umented a high frequency of averted insulindosing errors in addition to high variability in con-centrations and mixed use of weight-based andnonweight-based dosing units.

• The landmark ICU study by Dr. Greet Van denBerghe, Catholic University of Leuven in Belgium,targeted blood glucose of 80-110 mg/dL in thetreatment group. She noted decreased mortalityand morbidity (less renal failure, surgical woundinfections, blood transfusions, ICU ventilator days,etc.) in surgical ICU patients.

• Two recent European glucose control studies—VISEP (488 patients in 17 German Centers) andGluControl (1,101 randomized patients across 21ICU units in 7 European countries)—were bothstopped due to unacceptably high rates of hypo-glycemia and lack of beneficial effect.

• The on-going NICE-Sugar open-label, randomizedstratified study in 25 Australian, 19 Canadian, and2 American hospitals has a planned enrollment of7,000 patients! This study will compare 2 targetranges for blood glucose (81-108 mg/dL vs.<180 mg/dL). Conference participants expect thisto be the pivotal outcome investigation—and onethat will likely define the target glucose for futureICU patients. The study is well on its way to 4,000enrolled patients.

• Current data are insufficient to mandate TGC forpatients in the operating room. A recent random-ized study in cardiac surgery patients (Ann Int Med2007;46:233) found no difference in ICU or hospitalLOS despite TGC throughout the operative period.

• It is important to note that perioperative hyper-glycemia occurring in “non-diabetics” may actu-ally indicate undiagnosed Type II diabetes.Providers should consider hemoglobin A1c deter-minations in these patients to direct optimal meta-bolic management.

Additional insights based on the collectiveexperience of participants included

• Prevalence of diabetes is increasing rapidly.

• TGC requires an interdisciplinary team approach,a culture of safety, and a focus on professional edu-cation. Moreover, benchmarks to evaluate effec-tiveness are needed.

• Current “paper” ICU protocols for TGC achievetarget glucose concentrations about 40% of the time.

• Published TGC protocols differ significantly ininsulin dosing recommendations.

• Computerized protocols improve the efficacy to60%, and have the additional benefit of decreasinghypoglycemic episodes.

• Bedside glucometers rely on a number of differentchemical reagents, and users should be aware ofpotential confounding variables—even includingparameters like hematocrit, PaO2, and so forth.Interfering substances can generate seriously erro-neous meter readings.

• Total nursing time for each point-of-care glucosedetermination varies from 3.5-9 min (mediantime = 4.7 min). The aggregate time and RN work-load of applying TGC is substantial.

• Current continuous glucose monitors (CGM)measure glucose in the interstitial fluid, which lagsbehind blood concentrations by 3-10 min. Nonethe-

less, CGM appears to facilitate smoother, timeliertitration of insulin infusions, and patients reachtarget glucose values more quickly. Coordinationof this technology with a computerized protocolminimizes the incidence of hypoglycemia.

• Clinical experience suggests minimal risk of asingle episode of hypoglycemia (FBS ≤ 40 mg/dL),if diagnosed and managed in a timely fashion.

• Transitions from ICUs to Medical/Surgical careunits and from IV to oral feedings are especiallyproblematic in maintaining TGC.

• Intensive insulin therapy and TGC is cost effective,but may be population and protocol sensitive.

The optimal glucose threshold for TGC in ICUpatients remains under investigation, and anesthesiaproviders debate how these principles should apply topatients in the operating room. More data are needed.An independent APSF poll regarding triggers for ini-tiation of insulin therapy is also presented below.

Richard C. Prielipp, MD, MBA, FCCMProfessor and Chair of Anesthesiology University of MinnesotaMinneapolis, MN

Carol S. Manchester, MSN, APRN, BC-ADM, CDEDiabetic Clinical Nurse SpecialistUMMC-FairviewMinneapolis, MN

Timothy W Vanderveen, PharmD, MSVice President Cardinal Health Center for Safety and Clinical ExcellenceSan Diego, CA

Report on the 7th Invited Conference by Cardinal Health

Intensive Insulin TherapyJune 7-8, 2007, Center for Safety and Clinical Excellence, San Diego, CA

110 mg/dl(6.1 mM)

140 mg/dl(7.8 mM)

180 mg/dl(10 mM)

200 mg/dl(11.1 mM)

240 and above(13.3 mM)

Acidotic

4.1%

19.7%

26.5%

32.7%

12.9%

4.1%

Upper limit of glucosethat triggers insulin therapy (Percent)

APSF Poll Question:During general anesthesia in the OR, what is your current upper limit of glucose that triggers

(intravenous bolus or infusion) insulin therapy?

Results of an independent APSF Poll regarding readers’ triggers for initiation of insulin therapy.


Numerous questions to the Committee on Technology are individually and quickly answered each quarter by knowledgeable committeemembers. Many of those responses would be of value to the general readership, but are not suitable for the Dear SIRS column. Therefore, wehave created this simple column to address the needs of our readership.

The information provided in this column is for safety-related educational purposes only, and does not constitute medical or legal advice. Individual or group responsesare only commentary, provided for purposes of education or discussion, and are neither statements of advice nor the opinions of APSF. It is not the intention of APSF toprovide specific medical or legal advice or to endorse any specific views or recommendations in response to the inquiries posted. In no event shall APSF be responsible orliable, directly or indirectly, for any damage or loss caused or alleged to be caused by or in connection with the reliance on any such information.

Dear Q&A,

I have always thought that, in a hospital centralgas supply system, the oxygen pipeline shouldoperate at a slightly higher pressure than the airand nitrous oxide lines in order to mitigate theeffects of a possible cross connection. I am work-ing at a new hospital and the pipeline person isasking for documentation. Is this just an informalsafety measure or is it mandated by code?Thanks for your help.Samuel Tirer, MD

Dear Dr. Tirer,

The National Fire Protection Association (NFPA)99 Standard for Health Care Facilities, 2005 Edi-tion, states, “Piping systems, with the exceptionof nitrogen systems, shall be capable of maintain-ing 50-55 psig (345-380 kPa gauge) to all outlets atthe maximum flow rate.” Reading the NFPA islike reading IRS 1040 instructions, so perhapsthere is a qualifier (regarding different oxygenpressure) somewhere else in the document that Imissed in my scan. But I have never heard of dif-ferent wall pressure for O2.

I believe there is not a standard driving this, buta local preference. I have heard of hospitals set-

ting oxygen at the top of the allowable range,such that if a check valve failed somewhere in thesystem, the oxygen would prevent potentiallyhypoxic scenarios.

Using the highest pressure for oxygen in apipeline system is a very old practice for 2 reasons:

1) It allows one to certify that day-to-day runningof a mixed pipeline system is “safe” withoutusing an oxygen analyzer on each outlet. Inmany parts of the world this is the routinesafety check. Where gas-mixing devices areused, as with nitrous/oxygen for analgesia, itcould be part of the basic design.

2) If there is any sort of link between 2 lines,better that oxygen dilutes the other. I thinkyou’ll find this rule originates in old Britishstandard safe practice that preceded peoplewriting specs.

The APSF Committee on Technology

Dear Dr. Tirer,

The pressure ranges listed in Table 5.1.11 fromNFPA 99-2005 for medical air, oxygen, nitrousoxide, helium, and carbon dioxide are the same(50-55 psi). I can find nothing that says oneshould be greater than the other to avoid cross

To the Editor:

I would like to respond to Dr. Weinger’s leadarticle, published in the 2006-2007 winter issue of theAPSF Newsletter, which discusses the dangers of post-operative opioids. My particular interest is in regardto postoperative pain control for the obstructive sleepapnea (OSA) population. It seems much of the datawe have related to this safety issue are based on theuse of parenteral opioids postoperatively. Specifi-cally, the article mentions Dr Lofsky’s report on theeffect opioids have on the neural efferent system,which is said to be responsible for depression of

connections. NFPA 99 also requires stringentinitial testing, and specifies testing that is nec-essary after working on the system.

There are 2 tests acceptable to NFPA to ini-tially verify that there are no cross connectionsin a system. One is called the Individual Pres-surization Test, whereby the system beingchecked shall be pressurized to 50 psi, while allother disconnected, atmospheric lines aresimultaneously checked to determine that testgas is being dispensed only from theoutlets/inlets of the piping system being tested.

What some of your contacts may be referring tois the other acceptable method, or Pressure Dif-ferential Test. This test does require that the oxygensystem and the medical air system (and others) bepressurized and maintained to different, specified psi(50 psi, 60 psi, respectively for oxygen andmedical air), after which a pressure test is madeat every outlet to check for cross-connections.

NFPA does NOT say that the system needs tobe operated during normal use with those pres-sures—rather only for the verification test.

Mike Mahan, PENorth Carolina Baptist HospitalEngineeringWinston-Salem, NC

Letters to the Editor

Are Patients With Obstructive Sleep Apnea Safer at Home?upper airway patency. The opioid delivery of refer-ence in this discussion was patient-controlled anal-gesia (PCA). My questions are 1) Has our specialtydetermined the safety of oral opioid-based analgesicsfor the ambulatory patient with OSA, and 2) What isthe impact of the provision of parenteral opioids aspart of the general anesthetic or immediate postop-erative pain relief in the OSA patient being dis-charged to home? I ask these questions in light of thefact that there is an alteration in perioperative sleepthat is pronounced in the OSA population andobserved in the 24-hour postoperative period. Thisalteration, which is partly due to the exposure to

anesthetics and analgesics, is worsened by the effectof rapid eye movement (REM) sleep rebound1 andcan create a tenuous postoperative period while thepatient is home unmonitored.

Drs. Weinger and Morell did provide their per-sonal suggestion that it is likely safer for OSApatients to be discharged home on oral analgesicsrather than be admitted and receive parenteral opi-oids. I can easily agree with this due to all of thepotential life-threatening risks of PCA or intermit-tently dosed opioids when monitoring is substan-

See “OSA,” Next Page

Pipeline Pressure Primer


Innovative Technology and Pharmaceuticals (ITP)This column is dedicated to providing our readers with information regarding new and innovative technological or phar-maceutical developments that may directly or indirectly impact patient safety. By virtue of the unique and long-standingrelationship between the APSF and industry, it is inevitable that we will, from time to time, discuss or review products,devices, or pharmaceuticals that may be manufacturered, sold, or distributed by corporations or entities that have or con-tinue to supply financial or in-kind support to the APSF. We will strive to disclose those relationships as appropriate.

by Joel Saltzman, MD

Establishing vascular access for administration ofmedications, or to obtain blood for laboratory tests, isstressful for the patient and can be stressful for the prac-titioner; limiting the number of sticks is beneficial toboth. While most practitioners are adept at venipunc-ture, patients with extremes in age, habitus, co-mor-bidities, and multiple punctures present a challenge toeven the most experienced. Not uncommonly, the anes-thesia team is called upon to obtain venous access aftermultiple attempts by others in the hospital. By this time,we may be presented with a patient who is stressed,potentially dehydrated, sore, and angry, and with con-cerned family members. A new technology has beenable to “shine a light” on this problem, a green light.

Experienced practitioners have long been able toaccess the vascular system provided they can see or feelthe vessel, or to attempt a blind stick based on anatomi-cal landmarks. Multiple technologies have tried to assistthe practitioner to visualize the target. Ultrasound hasassisted, but requires the use of gels and a significantlearning curve with specialized training. Transillumi-nation with high-intensity light involves direct patientcontact, elimination of ambient light, and may result inheating at the site. One infrared device, VeinViewer byLuminetx, uses near-infrared technology to allow thepractitioner to visualize the vessel without direct con-tact, gels, heat, or advanced training. This device pro-jects the image of the vasculature directly onto thepatient’s skin, focusing attention on the patient ratherthan the monitor, and allows both hands to be free toperform the procedure. The practitioner may also visu-alize arteries as pulsatile structures if they are within the6-8 mm imaging range of depth.

The near infrared light source is used to differenti-ate red blood cells from surrounding tissues. The lightis reflected back from the surface tissue, but not reflected

from the blood in thevessels. The infraredlight photons arereceived by a detectorlocated in the digitalvideo camera; a com-puter digitizes thesephotons, produces animage and projects itonto the patient’s skin.The image is displayedin real-time, and veinsappear as a black road map on a green field. The non-ion-izing energy emitted from the LED light sources is manymagnitudes under previously established safety limits.

Whenever a clinician or an institution considers newequipment, safety and cost must be part of the equation.Although the machine is somewhat large, it is self-con-tained, well-balanced, and relatively easy to move.

This device may help alleviate trips to the operatingroom for central venous access—offsetting costs andrisks that may be deferred by placement of a PICC lineor simple peripheral vascular access. Anesthesia, Emer-gency Room, Radiology, Critical Care, phlebotomists,PICC teams, and others can all utilize this technologythroughout the hospital. There is also the potential toupdate and advance the capabilities of the equipmentwith software updates imported into the machine viathe 2 USB ports. In sum, the VeinViewer can potentiallyimprove patient safety by facilitating intravenous accessas an alternative to central venous cannulation, whilealso reducing patient discomfort.

Dr. Saltzman is Chief of Anesthesiology at Le BonheurChildren’s Medical Center, Memphis, TN.

DISCLOSURES: Luminetx Corporation is a financialcontributor to the APSF. Dr. Saltzman has no financialrelationship to Luminetx.

Letters to the Editor, continued

To the Editor:

I read with amazement the article “Dangers ofPostoperative Opioids” (Vol 21, #4). The article states,“We advocate the use of continuous monitoring ofoxygenation (generally pulse oximetry) and of venti-lation in non-ventilated patients receiving PCA, neu-raxial opioids, or serial doses of parenteral opioids.”Basically the APSF is instituting a new standard ofcare. This would require billions of dollars of equip-ment that the article acknowledges as being “plaguedby false positive . . . and false negative . . . alarms” andthousands of new personnel to monitor the equip-ment and monitors.

To the Editor:In the 2006-07 winter issue of the APSF Newslet-

ter, the suggestion was made that pulse oximetrymight be an acceptable monitor to assess and avoidopioid overdose—providing patients breathe onlyroom air. We believe that all post-anesthesia careunit (PACU) patients and those given intravenousand neuraxial opioids should initially be given sup-plemental oxygen regardless of the monitor used.Hypoxia in the postoperative period is often multi-factorial in nature (residual anesthetics, splinting,atelectasis, obesity, fluid overload, opioid medica-tion). Patients can be in pain without significantrespiratory depression, yet still be hypoxic. Supple-mental oxygen can correct this hypoxia and possi-bly avoid a catastrophic event. To withhold painmedication from patients because their room airsaturations are low would only serve to increasecomplications relating to the stress response.Patients on oxygen receiving opioids will usuallyhave elevated pCO2s; however, mild degrees ofhypercarbia are well tolerated. It would be ideal toreliably monitor oxygen saturation and expiredCO2 in all patients, but until these monitors becomewidely available on the hospital wards, we mustcontinue to rely on healthcare providers who aretrained to recognize pending opioid toxicity.

Merlin D. Larson, MDAndrew Itkin, MDJohn W. Severinghaus, MDSan Francisco, CA

Post-Op HypoxiaMultifactorial andShould Be TreatedWith SupplementalOxygen

dard, but are there any objective data to substantiatethis anecdotal evidence? As a resident physician, Iam becoming increasingly aware of the growingambulatory surgery population as well as an increas-ing prevalence of OSA as the obesity epidemic con-tinues.2 I would like to know that as I care forpatients in the ambulatory setting, with either formalor presumptive clinical diagnosis of OSA, the provi-sion of perioperative opioids is not placing them athigher risk for incurring a life-threatening respira-tory event while recovering at home.

Michelle Lawrence, MDChicago, Illinois

References

1. Benumof JL. Obesity, sleep apnea, the airway and anes-thesia. ASA Refresher Courses in Anesthesiology2002;30:27-40.

2. Kaw R, Michota F, Jaffer A, et al. Unrecognized sleepapnea in the surgical patient: implications for the periop-erative setting. Chest 2006;129:198-205.

“OSA,” From Preceding Page Reader Has Low Tolerance for Zero ToleranceI am surprised that the article did not recommend

the abandonment of PCA, neuraxial opioids, or serialdoses of parenteral opioids until perfect monitorswere developed. This would go along with the desireof the authors to have “zero tolerance” for any respi-ratory morbidity associated with the use of opioids.

The only people this article helps are malpracticelawyers who can now ask us, “Doctor, are you notaware that your own safety foundation recommendsmonitoring for EVERY patient receiving opioids?”

Robert F. LaPorta, PhD, MDGlen Cove, NY

New Feature

Anesthesia Patient Safety FoundationBuilding One, Suite Two8007 South Meridian StreetIndianapolis, IN 46217-2922

NONPROFIT ORG.U.S. POSTAGE

PAIDWILMINGTON, DEPERMIT NO. 1387


Inside This Issue▲ More About Drug-Eluting Coronary Stents and

Late Thrombosis

▲ Perils of Hypotension in the Beach Chair Position

▲ Review of Maternal Arrests

▲ Case Report and Letters to the Editor

beach chair position may decrease cerebral perfusion...

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