Dept Of Anesthesiology & Critical Care, University Of Pennsylvania School Of Medicine

Chapters Written, Books Written and Books Edited Calendar Year 2008

 

1.     Abend NS, Kessler SK, Helfaer MA, Licht DJ:  Evaluation of the Comatose Child.  In Rogers’ Textbook of Pediatric Intensive Care 4^th edition (Editor-in-Chief, DG Nichols).Wolters Kluwer/Lippincott; p 846-861, 2008

 

2.     Ackerman A, Hunt E, Nadkarni VM:  Professionalism, Simulation Training, and Leadership in Pediatric Critical Care. In Rogers’ Textbook of Pediatric Intensive Care 4^th edition (Editor-in-Chief, DG Nichols). Wolters Kluwer/Lippincott; p 36-45, 2008

 

3.     Augoustides JG, Szeto W, Kohl BA, Cowie D, Hoo A, Gambone AJ, Jobes DR: Prolonged mechanical ventilation after aortic arch repair requiring deep hypothermic circulatory arrest: incidence, effects on outcome, and clinical predictors.  Open Anesthesiology Journal 208;2:1-8

 

4.     Ballantyne JC. Psychiatric disease, chronic pain and substance abuse. In: Handbook of Preoperative Assessment and Management, 2^nd edition, (ed) BJ Sweitzer. Lippincott, Williams & Wilkins; p 283-303, 2008.

 

5.     Berg RA, Miyasaka K, Rodriguez-Nunez A, Hazinksi MF, Zideman D, Nadkarni VM. Cardiopulmonary Resuscitation. In Rogers’ Textbook of Pediatric Intensive Care 4^th edition (Editor-in-Chief, David G. Nichols). Wolters Kluwer/Lippincott; p 323-339, 2008.

 

6.     Berg RA, Nadkarni VM:  Cardiopulmonary Resuscitation.  In Pediatric Respiratory Medicine (eds) Taussig LM, Landau LI. Mosby Inc; Chapter 20, 2008

 

7.     Gaiser R.  The pregnant patient for nonobstetric surgery, In Preoperative Assessment and Management (ed) Sweitzer B. Lippincott, Williams & Wilkens; p 344-56, 2008

 

8.     Hanson CW, III: Procedures in Critical Care.  McGraw Hill, 176 pages, 2008

 

9.     Hanson CW, III:  The Edge of Medicine: The Technology That Will Change Our Lives. Palgrave-Macmillan, 256 pages, 2008

 

10.     Kohl BA, Augoustides JG, Cheung AT: Echocardiography of the thoracic aorta. In Aortic Arch Surgery: principles, strategies and outcomes (eds) Coselli JS, Lemaire SA. Wiley-Blackwell; p 73-90, 2008

 

11.     Kukafka JD, Fleisher LA: Anesthesia.  In General Surgery Review, 2nd Edition. Makery MA (ed). Ladner-Drysdale;  393-406, 2008 

 

12.     McCunn M, Sutcliffe A, Mauritz W in conjunction with ITAACS Critical Care Committee: Guidelines for Mechanical Ventilation in Patients Following Traumatic Injury.  In Trauma Anesthesia. Smith CE (ed). Cambridge University Press; p 465-470, 2008

 

13.     Muravchick S: The Vendor-Customer Relationship. In Anesthesia Informatics. Stonemetz J, Ruskin K (ed.). Springer; p 23-36, 2008

 

14.     Nishisaki A, Scrattish L, Boulet J, Kalsi M, Maltese M, Castner T, Donoghue A, Hales R, Tyler L, Brust P, Helfaer M, Nadkarni V:  Effect of recent refresher training on in situ simulated pediatric tracheal intubation psychomotor skill performance. In Advances in patient safety:  New directions and alternative approaches.  Vol. 3. Performance and Tools.  AHRQ Publication No. 08-0034-3 Rockville, MD:  Agency for Healthcare Research and Quality; August 2008. (http://www.ahrq.gov/downloads/pub/advances2/vol3/Advances-Nishisaki_44.pdf )

 

15.     Sinha AC: The Drug-Impaired Anesthesia Provider. In Audio-Digest Anesthesiology, 50(07), April 2008 ISSN 0271-1265

 

16.     Strum DP, Vargas LG, May JH, Spangler W, Stanicu A: Operating Room Scheduling and Capacity Planning. In Anesthesia Informatics. Stonemetz J, Ruskin K (eds). Springer Verlag; p 361-90, 2008 

 

17.     Vernick W, Fleisher L: Ischemic Heart Disease.  In Preoperative Assessment and Management 2^nd edition.  Sweitzer, BJ (eds). Lippincott Williams & Wilkins; p 51-80, 2008.

 

18.    Watson TA, Fleisher LA: Acute heart failure in the postoperative period. In Acute

   Heart Failure. Mebazaa A, Gheorghiade M, Zannad FM, Parrillo JE (eds).

   Springer; p 323-32, 2008

 

19.    Weiner DJ, Helfaer MA, Allen JL:  Respiratory Effects of Anesthesia and

   Sedation.  In Pediatric Respiratory Medicine 2^nd edition (eds ) LM Taussig,  Landau LI. Mosby/Elsevier;  p 347-357, 2008

A surgical safety check List may reduce mortality and morbidity

This preliminary study was published in New England Journal of Medicine (Haynes AB et al: A surgical safety check list to reduce morbidity and mortality in a global population. 2009;360:491-9, January 29).  The primary result was that the introduction of a 19 item surgical safety check list reduced death from 1.5% to 0.8% (a 47% reduction) and inpatient complications from 11% to 7% (a 36% reduction).  Specifically there were statistically significant reductions in surgical site infection, unplanned return to the operating room, death and “any” complication.  Pneumonia was not statistically significant.  The study was conducted in eight hospitals selected for a diversity of economic circumstances and patient populations.  The authors prospectively collected data on 3733 consecutive patients before the introduction of the check list and then on 3955 consecutive patients after the introduction of the check list.  The primary end point was rate of complications including death within the first 30 days after surgery.  Enrolled subjects had to be greater than 16 years of age.  Patients undergoing cardiac surgery were excluded.

  The check list contained the following elements:

  Sign in – Before induction of anesthesia, members of the team (at minimum the nurse and an anesthesia professional) orally confirm that:

1) The patient has verified his or her identity, the surgical site and procedure, and consent.

2) The surgical site is marked or site marking is not applicable

3) Anesthesia safety check is completed

4) The pulse oximeter is on the patient and functioning

5) All members of the team are aware of whether the patient has a known allergy

6) The patient’s airway and risk of aspiration have been evaluated and appropriate equipment and assistance are available.

7) If there is a risk of blood loss of at least 500 ml (or 7 ml/kg of body weight in children) appropriate access and fluids are available.  Appropriate access is defined at two peripheral intravenous catheters or a central line placed prior to incision

Time out – Before skin incision the entire team (nurses, anesthesia professionals, surgeons and any others participating in the care of the patient) orally:

1) Confirms that all team members have been introduced by name and role

2) Confirms the patient’s identity, surgical site and procedure

3) Reviews the anticipated critical events (surgeon reviews critical and unexpected steps, operative duration, and anticipated blood loss; anesthesia staff review concerns specific to the patient; nursing staff review confirmation of sterility, equipment availability, and any other concerns)

4) Confirms that prophylactic antibiotics have been administered less than 60 minutes before incision is made or that antibiotics are not indicated

5) Confirms that all essential imaging results for the correct patient are displayed in the operating room

Sign out – Before the patient leaves the operating room:

1) The nurse reviews the following items aloud with the team (name of the procedure as recorded; that the needle, sponge and instrument counts are complete or not applicable; that the specimen, if any, is correctly labeled, including the patient’s name; and whether there are any issues with equipment that need to be addressed)

2) The surgeon, nurse, and anesthesia professional review aloud the key concerns for recovery and care of the patient.

 

Check list training:  All participants underwent training in the use of the check list prior to its introduction.  This included lectures, written materials or direct guidance.

Complications examined:  The complications sought were the ones used in the American College of Surgeons’ national Surgical Quality Improvement Program: acute renal failure, bleeding requiring the transfusion of 4 or more units of red cells within the first 72 hours after surgery, cardiac arrest requiring cardiopulmonary resuscitation, coma of 24 hours duration or more, deep-vein thrombosis, myocardial infarction, unplanned intubation, ventilator use for 48 hours or more, pneumonia, pulmonary embolism, stroke, major disruption of the wound, infection of the surgical site, sepsis, septic shock, the systemic inflammatory response syndrome, unplanned returned to the operating room, vascular graft failure, and death.  Urinary tract infection was not considered a major complication.

Developing and adapting the WHO check list:  WHO recognized that local situations may require adaption of the check list.  They provide the following guidelines: the checklist should be concise, it should take no more than a minute to complete each of the three sections, each item on the checklist must be linked to a specific unambiguous action, it should be a verbal exercise, it should be collaborative, and it should be integrated with existing processes.

WHO Goals for the surgical check list:

1) The team will operate on the correct patient at the correct site.

2) The team will use methods known to prevent harm from anesthetic administration, while protecting the patient from pain.

3) The team will recognize and effectively prepare for life-threatening loss of airway or respiratory function

4) The team will recognize and effectively prepare for risk of high blood loss

5) The team will avoid inducing any allergic or adverse drug reaction known to be a significant risk for the patient

6) The team will consistently use methods known to minimize risk of surgical site infection

7) The team will prevent inadvertent retention of instruments or sponges in surgical wounds

8) The team will secure and accurately identify all surgical specimens

9) The team will effectively communicate and exchange critical patient information for the safe conduct of the operation

10)  Hospitals and public health systems will establish routine surveillance of surgical capacity, volume and results.

Comments:  In a June, 2008 press release (7 months before publication of this paper) the American Society of Anesthesiologists supported the WHO initiative for the “safe surgery check list”.  A number of letters to the editor appeared in the May 28, 2009 issue of the New England Journal on the article.  As might be expected the article created wide spread international media interest.   In the “perspectives” section of The Lancet (February 14, 2009) Jeremy Laurance (health editor of The Independent, a British newspaper) commented favorably on the results as discussed by the senior author, Atul Gawande, when he gave the James Reason Inaugural Annual Lecture at London’s Royal Society of Medicine.  However, Time Magazine (January 14, 2009) quotes concerns raised by Peter Pronovost who has done seminal work on the role of check lists in improving ICU outcome.  Dr. Pronovost noted that covering every item on the check list after its introduction was not high (54%).  He was also concerned that the decrease in complications and improved outcomes seemed too large for the interventions described.  Others have wondered why the follow-up period was so short and whether or not the reported improvements were sustained.  I find it interesting that the New England Journal published it as a “special article” and not as an “original article.”   Finally the article describes decreased complications and death after the introduction of a check list, however it does not show how the check list as a whole or which particular parts of the check list may have had this effect.  This article should be viewed as a start to an approach that may be of use in improving surgical outcomes, and not as the definitive statement on this important issue.  This article, along with others, suggests that check lists should be taken seriously and not just as a chore to be dispensed with as quickly as possible.

 

David S. Smith, M.D., Ph.D.

Using a device without training may have cost a young girl her life

The January 6, 2009 issue of the Daily Mail (a British newspaper) relates the story of a five year old girl with hereditary spherocytosis who presented for elective splenectomy.  Multiple family members had the disease and had undergone the procedure in the past without complication.  The plan was to remove the spleen laparoscopically.  According to the article the surgical team decided to use a device that had been designed to morselize the uterus to ease removal during laparoscopic hysterectomy.  Neither the surgeon nor the surgical resident had specific training in the use of the device.  In addition the device had never been used on a child.  Somehow during the procedure the aorta was cut in two places and the girl died of hemorrhage.  Because the operation took place in Great Britain, the settlement was only about $15,000 and this was based on the lack of informed consent related to the use of the new device.  The court did not find for the plaintiff despite the fact that the spleen, the disposable parts of the device, etc. were all “lost,” that the physicians present seemed to change their account of events as time progressed, and that the family was not given access to any of the OR nurses.  The case emphasizes the risk inherent in “trying” new procedures, devices or techniques without informing the patient, obtaining appropriate training or thoroughly considering the risks.

 

David S. Smith, M.D., Ph.D.

Failure to read an x-ray results in a 2.18 million dollar settlement

Josh Atkins, M.D., calls our attention to a recent article in the Philadelphia Daily News (May 14, 2009).  After a 10 day trial a Jury awarded the money to the widow of a 51 year old man who presented to the emergency department with chest, back and leg pains.  A chest x-ray that was ordered was never read by the emergency department physician who ordered the film (he went off duty), nor was it seen by his replacement (inadequate hand off).  The radiologist read the film the next morning, but by then the patient had died. (link to original article:  ( http://www.philly.com/philly/hp/news_update/44960862.html )

 

David S. Smith, M.D., Ph.D.

Cardiac Arrest – Torsades de pointes – not just droperidol – not just theoretical

Many antipsychotics have been associated with prolongation of the QT interval.  The package insert for olanzapine (Zyprexa), a popular antipsychotic marketed by Eli Lilly and Company, notes that “in pooled studies of adults … there were no significant differences between olanzapine and placebo in the proportion of patients experiencing potentially important changes in ECG parameters, including QT.”  However recently Morissette P et al. showed that, at higher blood concentrations such as may be seen in patients with renal or hepatic insufficiency or very high daily drug dosing, olanzapine has direct cardiac electrophysiologic effects that might lead to QT prolongation in patients (olanzapine prolongs cardiac repolarization by blocking the rapid component of the delayed rectifier potassium current.  J Psychopharmacol 2007;21:735-741).  Also note the black box warning that this drug should not be used in elderly patients with dementia-related psychosis because there are reports of increased mortality.

 

David S. Smith, M.D., Ph.D.

Refereed Publications -- Calendar Year 2008

DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE

UNIVERSITY OF PENNSYLVANIA, PHILADELPHIA PA

 

1.         Abend NS, Huh JW, Helfaer MA, Dlugos DJ: Anticonvulsant medications in the pediatric emergency room and intensive care unit. Pediatric Emergency Care, 2008; 24: 705-18; quiz 719-21

2.         American College of Cardiology/American Heart Association Task Force on Practice G,  American Society of E,  American Society of Nuclear C,  Heart Rhythm S,  Society of Cardiovascular A,  Society for Cardiovascular Angiography and I,  Society for Vascular Medicine and B,  Society for Vascular S,  Fleisher LA,  Beckman JA,  Brown KA,  Calkins H,  Chaikof E,  Fleischmann KE,  Freeman WK,  Froehlich JB,  Kasper EK,  Kersten JR,  Riegel B,  Robb JF,  Smith SC, Jr.,  Jacobs AK,  Adams CD,  Anderson JL,  Antman EM,  Buller CE,  Creager MA,  Ettinger SM,  Faxon DP,  Fuster V,  Halperin JL,  Hiratzka LF,  Hunt SA,  Lytle BW,  Nishimura R,  Ornato JP,  Page RL,  Riegel B,  Tarkington LG, Yancy CW: ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesthesia & Analgesia, 2008; 106: 685-712

3.         Andrejko KM, Raj NR, Kim PK,  Cereda M, Deutschman CS: IL-6 modulates sepsis-induced decreases in transcription of hepatic organic anion and bile acid transporters. Shock, 2008; 29: 490-6

4.         Armstead WM, Christine AJ, Higazi AA-R, Cines DB: Urokinase plasminogen activator impairs SNP and PGE2 cerebrovasodilation after brain injury through activation of LRP and ERK MAPK. Journal of Neurotrauma, 2008; 25: 1375-81

5.         Armstead WM, Cines DB, Bdeir K,  Kulikovskaya I, Stein SC, Higazi AA-R: uPA impairs cerebrovasodilation after hypoxia/ischemia through LRP and ERK MAPK. Brain Research, 2008; 1231: 121-31

6.         Aronson S, Dyke CM, Stierer KA, Levy JH, Cheung AT, Lumb PD, Kereiakes DJ, Newman MF: The ECLIPSE trials: comparative studies of clevidipine to nitroglycerin, sodium nitroprusside, and nicardipine for acute hypertension treatment in cardiac surgery patients. Anesthesia & Analgesia, 2008; 107: 1110-21

7.         Atkins JH, Mandel JE: Recent advances in patient-controlled sedation. Current Opinion in Anaesthesiology, 2008; 21: 759-65

8.         Augoustides JG: Perioperative safety of aprotinin in coronary artery bypass graft surgery: is there life after BART? Drug Safety, 2008; 31: 557-60

9.         Augoustides JG, Watcha SM, Pochettino A, Jobes DR: Early tracheal extubation in adults undergoing single-lung transplantation for chronic obstructive pulmonary disease: pilot evaluation of perioperative outcome. Interactive Cardiovascular & Thoracic Surgery, 2008; 7: 755-8

10.       Augoustides JGT, Fleisher LA: The future for B-type natriuretic peptide in preoperative assessment [comment]. Anesthesiology, 2008; 108: 332-3

11.       Augoustides JGT, Plappert T, Bavaria JE: Hemodynamic collapse during pulmonary embolectomy due to loss of venous return from acute occlusion of the cardiopulmonary venous cannula with thromboembolus. Interactive Cardiovascular & Thoracic Surgery, 2008; 7: 661-2

12.       Augoustides JGT, Pochettino A, Carpenter J: Surgical management of thoracoabdominal aortic aneurysm associated with systemic lupus erythematosus. Journal of Thoracic & Cardiovascular Surgery, 2008; 136: 215-6

13.       Augoustides JGT, Szeto WY: Unmasked diabetes insipidus after pericardial drainage and biopsy for pericardial effusion in association with Erdheim-Chester disease. Journal of Thoracic & Cardiovascular Surgery, 2008; 136: 217-8

14.       Bachiller PR, McDonough JM, Feldman JM: Do new anesthesia ventilators deliver small tidal volumes accurately during volume-controlled ventilation? Anesthesia & Analgesia, 2008; 106: 1392-400

15.       Berg MD, Nadkarni VM, Berg RA: CPR-why the new emphasis? Pediatric Clinics of North America, 2008; 55: 861-72

16.       Berg MD, Nadkarni VM, Berg RA: Cardiopulmonary resuscitation in children. Current Opinion in Critical Care, 2008; 14: 254-60

17.       Berg MD, Nadkarni VM, Zuercher M, Berg RA: In-hospital pediatric cardiac arrest. Pediatric Clinics of North America, 2008; 55: 589-604

18.       Bianchi SL, Tran T, Liu C, Lin S,  Li Y,  Keller JM,  Eckenhoff RG, Eckenhoff MF: Brain and behavior changes in 12-month-old Tg2576 and nontransgenic mice exposed to anesthetics. Neurobiology of Aging, 2008; 29: 1002-10

19.       Borasino S, Morrison W, Silberman J, Nelson RM, Feudtner C: Physicians' contact with families after the death of pediatric patients: a survey of pediatric critical care practitioners' beliefs and self-reported practices. Pediatrics, 2008; 122: e1174-8

20.       Brannigan G, Henin J, Law R,  Eckenhoff R, Klein ML: Embedded cholesterol in the nicotinic acetylcholine receptor. Proceedings of the National Academy of Sciences of the United States of America, 2008; 105: 14418-23

21.       Bromberg Z, Raj N, Goloubinoff P, Deutschman CS, Weiss YG: Enhanced expression of 70-kilodalton heat shock protein limits cell division in a sepsis-induced model of acute respiratory distress syndrome. Critical Care Medicine, 2008; 36: 246-55

22.       Chaves PHM,  Varadhan R,  Lipsitz LA,  Stein PK,  Windham BG,  Tian J,  Fleisher LA,  Guralnik JM, Fried LP: Physiological complexity underlying heart rate dynamics and frailty status in community-dwelling older women. Journal of the American Geriatrics Society, 2008; 56: 1698-703

23.       Cheung AT, Hobson RW, 2nd: Hypertension in vascular surgery: aortic dissection and carotid revascularization. Annals of Emergency Medicine, 2008; 51: S28-33

24.       Cucchiaro G, Xiao Y, Gonzalez-Sulser A, Kellar KJ: Analgesic effects of Sazetidine-A, a new nicotinic cholinergic drug. Anesthesiology, 2008; 109: 512-9

25.       Daumerie G, Fleisher LA: Perioperative beta-blocker and statin therapy. Current Opinion in Anaesthesiology, 2008; 21: 60-5

26.       De Hert SG, Longrois D, Yang H, Fleisher LA: Does the use of a volatile anesthetic regimen attenuate the incidence of cardiac events after vascular surgery? Acta Anaesthesiologica Belgica, 2008; 59: 19-25

27.       Dorfman AT,  Marino BS,  Wernovsky G,  Tabbutt S,  Ravishankar C,  Godinez RI,  Priestley M,  Dodds KM,  Rychik J,  Gruber PJ,  Gaynor JW,  Levy RJ,  Nicolson SC,  Montenegro LM,  Spray TL, Dominguez TE: Critical heart disease in the neonate: presentation and outcome at a tertiary care center. Pediatric Critical Care Medicine, 2008; 9: 193-202

28.       Eckenhoff R,  Zheng W, Kelz M: From anesthetic mechanisms research to drug discovery. Clinical Pharmacology & Therapeutics, 2008; 84: 144-8

29.       Eckenhoff RG: Why can all of biology be anesthetized? [comment]. Anesthesia & Analgesia, 2008; 107: 859-61

30.       Elkassabany NM, Bhatia J, Deogaonkar A, Barnett GH, Lotto M, Maurtua M, Ebrahim Z, Schubert A, Ference S, Farag E: Perioperative complications of blood brain barrier disruption under general anesthesia: a retrospective review. Journal of Neurosurgical Anesthesiology, 2008; 20: 45-8

31.       Feldman JM: It takes an entrepreneur. [comment]. Anesthesia & Analgesia, 2008; 107: 748

32.       Fleisher LA: Obstetric anesthesia. Foreword. Anesthesiology Clinics, 2008; 26: xi

33.       Fleisher LA: Implications of preoperative heart failure: the next frontier in perioperative medicine? [comment]. Anesthesiology, 2008; 108: 551-2

34.       Fleisher LA, Poldermans D: Perioperative beta blockade: where do we go from here? [comment]. Lancet, 2008; 371: 1813-4

35.       Fogel MA,  Weinberg PM,  Parave E,  Harris C,  Montenegro L,  Harris MA, Concepcion M: Deep sedation for cardiac magnetic resonance imaging: a comparison with cardiac anesthesia. Journal of Pediatrics, 2008; 152: 534-9

36.       Freeman SS, Udomphorn Y, Armstead WM, Fisk DM, Vavilala MS: Young age as a risk factor for impaired cerebral autoregulation after moderate to severe pediatric traumatic brain injury. Anesthesiology, 2008; 108: 588-95

37.       Friese CR, Lake ET, Aiken LH, Silber JH, Sochalski J: Hospital nurse practice environments and outcomes for surgical oncology patients. Health Services Research, 2008; 43: 1145-63

38.       Frogel J, Vodur S, Horak J: Transesophageal echocardiography diagnosis of extracardiac left ventricular assist device inflow cannula obstruction in a patient with thoratec intracorporeal ventricular assist device biventricular support. Journal of the American Society of Echocardiography, 2008; 21: 777.e5-6

39.       Ganesh A, Adzick NS, Foster T, Cucchiaro G: Efficacy of addition of fentanyl to epidural bupivacaine on postoperative analgesia after thoracotomy for lung resection in infants. Anesthesiology, 2008; 109: 890-4

40.       Ganesh A, Audu P: Hyperosmolar, increased-anion-gap metabolic acidosis and hyperglycemia after etomidate infusion. Journal of Clinical Anesthesia, 2008; 20: 290-3

41.       Ganesh A, Gonzalez-Sulser A, Chaijale N, Cucchiaro G: Electrophysiologic effects of systemic and locally infused epibatidine on locus coeruleus neurons. European Journal of Pharmacology, 2008; 584: 93-9

42.       Ganesh A, Jobes DR: Ultrasound-guided catheterization of the internal jugular vein. [comment]. Anesthesiology, 2008; 108: 1155-6; author reply 1156-7

43.       Ganesh A, Wells L, Ganley T,  Maxwell LG, Cucchiaro G: Interscalene brachial plexus block for post-operative analgesia following shoulder arthroscopy in children and adolescents. Acta Anaesthesiologica Scandinavica, 2008; 52: 162-3

44.       Gavrin JR, McMenamin EM: Pain management in palliative care oncology patients. Current Pain & Headache Reports, 2008; 12: 257-61

45.       Girard T, Litman RS: Molecular genetic testing to diagnose malignant hyperthermia susceptibility. Journal of Clinical Anesthesia, 2008; 20: 161-3

46.       Glatz AC,  Gaynor JW,  Rhodes LA,  Rychik J,  Tanel RE,  Vetter VL,  Kaltman JR,  Nicolson SC,  Montenegro L, Shah MJ: Outcome of high-risk neonates with congenital complete heart block paced in the first 24 hours after birth. Journal of Thoracic & Cardiovascular Surgery, 2008; 136: 767-73

47.       Gopalareddy V, He Z, Soundar S, Bolling L, Shah M, Penfil S,  McCloskey JJ, Mehta DI: Assessment of the prevalence of microaspiration by gastric pepsin in the airway of ventilated children. Acta Paediatrica, 2008; 97: 55-60

48.       Guite JW, Logan DE, McCue R, Sherry DD, Rose JB: Parental beliefs and worries regarding adolescent chronic pain. Clinical Journal of Pain, 2009; 25: 223-32

49.       Gurnaney H, Stricker P, Ganesh A: An ounce of prevention is worth a pound of cure: regional anesthesia in children. [comment]. Anesthesia & Analgesia, 2009; 108: 669

50.       Gutsche JT, Szeto W, Cheung AT: Endovascular stenting of thoracic aortic aneurysm. Anesthesiology Clinics, 2008; 26: 481-99

51.       Hauck ES, Zou S, Scarfo K, Nantz MH, Hecker JG: Whole animal in vivo imaging after transient, nonviral gene delivery to the rat central nervous system. Molecular Therapy: the Journal of the American Society of Gene Therapy, 2008; 16: 1857-64

52.       Hecker JG,  Sundram H,  Zou S,  Praestgaard A,  Bavaria JE,  Ramchandren S, McGarvey M: Heat shock proteins HSP70 and HSP27 in the cerebral spinal fluid of patients undergoing thoracic aneurysm repair correlate with the probability of postoperative paralysis. Cell Stress & Chaperones, 2008; 13: 435-46

53.       Hehir DA, Dominguez TE, Ballweg JA, Ravishankar C, Marino BS, Bird GL, Nicolson SC, Spray TL, Gaynor JW, Tabbutt S: Risk factors for interstage death after stage 1 reconstruction of hypoplastic left heart syndrome and variants. Journal of Thoracic & Cardiovascular Surgery, 2008; 136: 94-9

54.       Huh JW, Widing AG, Raghupathi R: Midline brain injury in the immature rat induces sustained cognitive deficits, bihemispheric axonal injury and neurodegeneration. Experimental Neurology, 2008; 213: 84-92

55.       Jobes DR: Comment on point: counterpoint. [comment]. Journal of Applied Physiology, 2008; 104: 1841

56.       Kamerling SN, Lawler LC, Lynch M, Schwartz AJ: Family-centered care in the pediatric post anesthesia care unit: changing practice to promote parental visitation. Journal of PeriAnesthesia Nursing, 2008; 23: 5-16

57.       Kelz MB, Eckenhoff RG: Does it add up? [comment]. Anesthesia & Analgesia, 2008; 107: 365-6

58.       Kelz MB,  Sun Y,  Chen J,  Cheng Meng Q,  Moore JT,  Veasey SC,  Dixon S,  Thornton M,  Funato H, Yanagisawa M: An essential role for orexins in emergence from general anesthesia. Proceedings of the National Academy of Sciences of the United States of America, 2008; 105: 1309-14

59.       Kleinman ME, Srinivasan V: Postresuscitation care. Pediatric Clinics of North America, 2008; 55: 943-67

60.       Krishnan J, Morrison W, Simone S, Ackerman A: Implications of thrombocytopenia and platelet course on pediatric intensive care unit outcomes. Pediatric Critical Care Medicine, 2008; 9: 502-5

61.       Liang BA, Tran KM: Trust but verify: cooperation cannot mean abdication in the operating room. Journal of Clinical Anesthesia, 2008; 20: 150-3

62.       Liang G, Wang Q, Li Y, Kang B, Eckenhoff MF, Eckenhoff RG, Wei H: A presenilin-1 mutation renders neurons vulnerable to isoflurane toxicity. Anesthesia & Analgesia, 2008; 106: 492-500

63.       Litman RS, Flood CD, Kaplan RF, Kim YL,Tobin JR: Postoperative malignant hyperthermia: an analysis of cases from the North American Malignant Hyperthermia Registry. Anesthesiology, 2008; 109: 825-9

64.       Lorch SA, Millman AM, Zhang X, Even-Shoshan O, Silber JH: Impact of admission-day crowding on the length of stay of pediatric hospitalizations. Pediatrics, 2008; 121: e718-30

65.       Lurie KG,  Yannopoulos D,  McKnite SH,  Herman ML,  Idris AH,  Nadkarni VM,  Tang W,  Gabrielli A,  Barnes TA, Metzger AK: Comparison of a 10-breaths-per-minute versus a 2-breaths-per-minute strategy during cardiopulmonary resuscitation in a porcine model of cardiac arrest. Respiratory Care, 2008; 53: 862-70

66.       Ma D, Tillman TS, Tang P, Meirovitch E, Eckenhoff R, Carnini A, Xu Y: NMR studies of a channel protein without membranes: structure and dynamics of water-solubilized KcsA. Proceedings of the National Academy of Sciences of the United States of America, 2008; 105: 16537-42

67.       Mandel JE, Tanner JW, Lichtenstein GR, Metz DC, Katzka DA, Ginsberg GG, Kochman ML: A randomized, controlled, double-blind trial of patient-controlled sedation with propofol/remifentanil versus midazolam/fentanyl for colonoscopy. Anesthesia & Analgesia, 2008; 106: 434-9

68.       Mandel JE, Weller GER, Chennupati SK, Mirza N: Transglottic high frequency jet ventilation for management of laryngeal fracture associated with air bag deployment injury. Journal of Clinical Anesthesia, 2008; 20: 369-71

69.       Marino BS,  Pasquali SK,  Wernovsky G,  Pudusseri A,  Rychik J,  Montenegro L,  Shera D,  Spray TL, Cohen MS: Accuracy of intraoperative transesophageal echocardiography in the prediction of future neo-aortic valve function after the Ross procedure in children and young adults.[erratum appears in Congenit Heart Dis. 2008 Mar;3(2):159]. Congenital Heart Disease, 2008; 3: 39-46

70.       Marino BS,  Shera D,  Wernovsky G,  Tomlinson RS,  Aguirre A,  Gallagher M,  Lee A,  Cho CJ,  Stern W,  Davis L,  Tong E,  Teitel D,  Mussatto K,  Ghanayem N,  Gleason M,  Gaynor JW,  Wray J,  Helfaer MA, Shea JA: The development of the pediatric cardiac quality of life inventory: a quality of life measure for children and adolescents with heart disease. Quality of Life Research, 2008; 17: 613-26

71.       Mendoza-Paredes A,  Liu H,  Schears G,  Yu Z,  Markowitz SD,  Schultz S,  Pastuszko P,  Greeley WJ,  Nadkarni V,  Kubin J,  Wilson DF, Pastuszko A: Resuscitation with 100%, compared with 21%, oxygen following brief, repeated periods of apnea can protect vulnerable neonatal brain regions from apoptotic injury. Resuscitation, 2008; 76: 261-70

72.       Messe SR,  Bavaria JE,  Mullen M,  Cheung AT,  Davis R,  Augoustides JG,  Gutsche J,  Woo EY,  Szeto WY,  Pochettino A,  Woo YJ,  Kasner SE, McGarvey M: Neurologic outcomes from high risk descending thoracic and thoracoabdominal aortic operations in the era of endovascular repair. Neurocritical Care, 2008; 9: 344-51

73.       Morrison W: Resuscitation decisions for premature newborns.[comment]. Pediatrics, 2008; 122: 679-80; author reply 680

74.       Morrison WE, Simone S, Conway D, Tumulty J, Johnson C, Cardarelli M: Levels of vasopressin in children undergoing cardiopulmonary bypass. Cardiology in the Young, 2008; 18: 135-40

75.       Mukundakrishnan K, Ayyaswamy PS, Eckmann DM: Finite-sized gas bubble motion in a blood vessel: non-Newtonian effects. Physical Review E Statistical, Nonlinear, & Soft Matter Physics, 2008; 78: 036303

76.       Muravchick S: Clinical implications of mitochondrial disease. Advanced Drug Delivery Reviews, 2008; 60: 1553-60

77.       Muravchick S: Aging, anesthesia, and antioxidants.[comment]. Journal of Clinical Anesthesia, 2008; 20: 409-10

78.       Muravchick S,  Caldwell JE,  Epstein RH,  Galati M,  Levy WJ,  O'Reilly M,  Plagenhoef JS,  Rehman M,  Reich DL, Vigoda MM: Anesthesia information management system implementation: a practical guide. Anesthesia & Analgesia, 2008; 107: 1598-608

79.       Naim MY, Hoehn KS, Hasz RD, White LS, Helfaer MA, Nelson RM: The Children's Hospital of Philadelphia's experience with donation after cardiac death. Critical Care Medicine, 2008; 36: 1729-33

80.       Nathan AT, Marino BS, Hanna B, Nicolson SC: Novel use of dexmedetomidine in a patient with pulmonary hypertension. Paediatric Anaesthesia, 2008; 18: 782-4

81.       Nishisaki A,  Scrattish L,  Boulet J,  Kalsi M,  Maltese M,  Castner T,  Donoghue A,  Hales R,  Tyler L,  Brust P,  Helfaer M, Nadkarni V: Effect of cervical spine immobilization technique on pediatric advanced airway management: a high-fidelity infant simulation model. Pediatric Emergency Care, 2008; 24: 749-56

82.       October TW, Schleien CL, Berg RA, Nadkarni VM, Morris MC, National Registry of Cardiopulmonary Resuscitation I: Increasing amiodarone use in cardiopulmonary resuscitation: an analysis of the National Registry of Cardiopulmonary Resuscitation. Critical Care Medicine, 2008; 36: 126-30

83.       Oddo M,  Frangos S,  Milby A,  Chen I,  Maloney-Wilensky E,  Murtrie E,  Stiefel M,  Kofke WA,  Le Roux P, Levine JM: Induced normothermia attenuates cerebral metabolic distress in patients with aneurysmal subarachnoid hemorrhage and refractory fever. Stroke, 2009; 40: 1913-6

84.       Oddo M,  Levine JM,  Frangos S,  Carrera E,  Maloney-Wilensky E,  Pascual J,  Kofke WA,  Mayer S, LeRoux P: Effect of mannitol and hypertonic saline on cerebral oxygenation in patients with severe traumatic brain injury and refractory intracranial hypertension. J Neurol Neurosurg Psychiatry, 2009; 80: 916-20

85.       Oddo M,  Milby A,  Chen I,  Frangos S,  MacMurtrie E,  Maloney-Wilensky E,  Stiefel M,  Kofke WA,  Levine JM, Le Roux P: Hemoglobin concentration and cerebral metabolism in patients with aneurysmal subarachnoid hemorrhage. Stroke, 2009; 40: 1275-81

86.       Otto CM,  Markstaller K,  Kajikawa O,  Karmrodt J,  Syring RS,  Pfeiffer B,  Good VP,  Frevert CW, Baumgardner JE: Spatial and temporal heterogeneity of ventilator-associated lung injury after surfactant depletion. Journal of Applied Physiology, 2008; 104: 1485-94

87.       Pan JZ, Xi J, Eckenhoff MF, Eckenhoff RG: Inhaled anesthetics elicit region-specific changes in protein expression in mammalian brain. Proteomics, 2008; 8: 2983-92

88.       Pasquali SK,  Marino BS,  Kaltman JR,  Schissler AJ,  Wernovsky G,  Cohen MS,  Spray TL, Tanel RE: Rhythm and conduction disturbances at midterm follow-up after the Ross procedure in infants, children, and young adults. Annals of Thoracic Surgery, 2008; 85: 2072-8

89.       Peberdy MA,  Ornato JP,  Larkin GL,  Braithwaite RS,  Kashner TM,  Carey SM,  Meaney PA,  Cen L,  Nadkarni VM,  Praestgaard AH,  Berg RA, National Registry of Cardiopulmonary Resuscitation I: Survival from in-hospital cardiac arrest during nights and weekends. JAMA, 2008; 299: 785-92

90.       Piel DA, Deutschman CS, Levy RJ: Exogenous cytochrome C restores myocardial cytochrome oxidase activity into the late phase of sepsis. Shock, 2008; 29: 612-6

91.       Ramakrishna R, Stiefel M, Udoteuk J, Spiotta A, Levine JM, Kofke WA, Zager E, Yang W, Leroux P: Brain oxygen tension and outcome in patients with aneurysmal subarachnoid hemorrhage. Journal of Neurosurgery, 2008; 109: 1075-82

92.       Reynolds WW, Nelson RM: Empirical data and the acceptability of research risk: a commentary on the charitable participation standard. [comment]. Archives of Pediatrics & Adolescent Medicine, 2008; 162: 88-90

93.       Rickenbacher E, Baez MA, Hale L, Leiser SC, Zderic SA, Valentino RJ: Impact of overactive bladder on the brain: central sequelae of a visceral pathology. Proceedings of the National Academy of Sciences of the United States of America, 2008; 105: 10589-94

94.       Robinson MA, Baumgardner JE, Good VP, Otto CM: Physiological and hypoxic O2 tensions rapidly regulate NO production by stimulated macrophages. American Journal of Physiology - Cell Physiology, 2008; 294: C1079-87

95.       Roginski RS, Goubaeva F, Mikami M, Fried-Cassorla E, Nair MR, Yang J: GRINL1A colocalizes with N-methyl D-aspartate receptor NR1 subunit and reduces N-methyl D-aspartate toxicity. Neuroreport, 2008; 19: 1721-6

96.       Srinivasan V,  Morris MC,  Helfaer MA,  Berg RA,  Nadkarni VM, American Heart Association National Registry of CPRI: Calcium use during in-hospital pediatric cardiopulmonary resuscitation: a report from the National Registry of Cardiopulmonary Resuscitation. Pediatrics, 2008; 121: e1144-51

97.       Stricker P, Fiadjoe JE, McGinnis S: Intubation of an infant with Pierre Robin sequence under dexmedetomidine sedation using the Shikani Optical Stylet. Acta Anaesthesiologica Scandinavica, 2008; 52: 866-7

98.       Stricker PA, Budac S, Fiadjoe JE, Rehman MA: Awake laryngeal mask insertion followed by induction of anesthesia in infants with the Pierre Robin sequence. Acta Anaesthesiologica Scandinavica, 2008; 52: 1307-8

99.       Stricker PA, Fiadjoe JE, Feldman JM: Tracheal tube positioning in infants and children using the Draeger Apollo ventilator. Paediatric Anaesthesia, 2008; 18: 1259-60

100.    Tabbutt S,  Nicolson SC,  Adamson PC,  Zhang X,  Hoffman ML,  Wells W,  Backer CL,  McGowan FX,  Tweddell JS,  Bokesch P, Schreiner M: The safety, efficacy, and pharmacokinetics of esmolol for blood pressure control immediately after repair of coarctation of the aorta in infants and children: a multicenter, double-blind, randomized trial. Journal of Thoracic & Cardiovascular Surgery, 2008; 136: 321-8

101.    Tabbutt S, Nicolson SC, Dominguez TE, Wells W, Backer CL, Tweddell JS, Bokesch P, Schreiner M: Perioperative course in 118 infants and children undergoing coarctation repair via a thoracotomy: a prospective, multicenter experience. Journal of Thoracic & Cardiovascular Surgery, 2008; 136: 1229-36

102.    Tabbutt S,  Nord AS,  Jarvik GP,  Bernbaum J,  Wernovsky G,  Gerdes M,  Zackai E,  Clancy RR,  Nicolson SC,  Spray TL, Gaynor JW: Neurodevelopmental outcomes after staged palliation for hypoplastic left heart syndrome. Pediatrics, 2008; 121: 476-83

103.    Thaler ER,  Huang D,  Giebeig L,  Palmer J,  Lee D,  Hanson CW, Cohen N: Use of an electronic nose for detection of biofilms. American Journal of Rhinology, 2008; 22: 29-33

104.    Topjian AA, Berg RA, Nadkarni VM: Pediatric cardiopulmonary resuscitation: advances in science, techniques, and outcomes. Pediatrics, 2008; 122: 1086-98

105.    Tran KM,  Flake AW,  Kalawadia NV,  Maxwell LG, Rehman MA: Emergent excision of a prenatally diagnosed sacrococcygeal teratoma.  Paediatric Anaesthesia, 2008; 18: 431-4

106.    Udomphorn Y, Armstead WM, Vavilala MS: Cerebral blood flow and autoregulation after pediatric traumatic brain injury. Pediatric Neurology, 2008; 38: 225-34

107.    Vavilala MS, Tontisirin N, Udomphorn Y, Armstead W, Zimmerman JJ, Chesnut R, Lam AM: Hemispheric differences in cerebral autoregulation in children with moderate and severe traumatic brain injury. Neurocritical Care, 2008; 9: 45-54

108.    Vernick W, Fleisher LA: Risk stratification. Best Practice & Research Clinical Anaesthesiology, 2008; 22: 1-21

109.    Wade KC, Lorch SA, Bakewell-Sachs S, Medoff-Cooper B, Silber JH, Escobar GJ: Pediatric care for preterm infants after NICU discharge: high number of office visits and prescription medications. Journal of Perinatology, 2008; 28: 696-701

110.    Wei H, Liang G, Yang H, Wang Q, Hawkins B, Madesh M, Wang S, Eckenhoff RG: The common inhalational anesthetic isoflurane induces apoptosis via activation of inositol 1,4,5-trisphosphate receptors. Anesthesiology, 2008; 108: 251-60

111.    Weil DP, Stearns JD, Watson T, Horak J: An unusual fatal reaction to a test dose of aprotinin before elective thoracoabdominal aortic aneurysm repair. European Journal of Anaesthesiology, 2008; 25: 346-8

112.    Weiss S,  Nyzio JB,  Cines D,  Detre J,  Milas BL,  Narula N, Floyd TF: Antiphospholipid syndrome: intraoperative and postoperative anticoagulation in cardiac surgery. Journal of Cardiothoracic & Vascular Anesthesia, 2008; 22: 735-9

113.    Wu CL, Demeester JS, Herbert R, Maine DN, Rowlingson AJ, Fleisher LA: Correlation of postoperative epidural analgesia with morbidity and mortality following total knee replacement in Medicare patients. American Journal of Orthopedics, 2008; 37: 524-7

114.    Wu W-C, Wang J, Detre JA, Ratcliffe SJ, Floyd TF: Transit delay and flow quantification in muscle with continuous arterial spin labeling perfusion-MRI. Journal of Magnetic Resonance Imaging, 2008; 28: 445-52

115.    Wu W-C, Wang J, Detre JA, Wehrli FW, Mohler E, 3rd, Ratcliffe SJ, Floyd TF: Hyperemic flow heterogeneity within the calf, foot, and forearm measured with continuous arterial spin labeling MRI. American Journal of Physiology - Heart & Circulatory Physiology, 2008; 294: H2129-36

116.    Yang H, Liang G, Hawkins BJ, Madesh M, Pierwola A, Wei H: Inhalational anesthetics induce cell damage by disruption of intracellular calcium homeostasis with different potencies. Anesthesiology, 2008; 109: 243-50

117.    Zeltser I,  Jarvik GP,  Bernbaum J,  Wernovsky G,  Nord AS,  Gerdes M,  Zackai E,  Clancy R,  Nicolson SC,  Spray TL, Gaynor JW: Genetic factors are important determinants of neurodevelopmental outcome after repair of tetralogy of Fallot. Journal of Thoracic & Cardiovascular Surgery, 2008; 135: 91-7

118.    Zempsky WT,  Bean-Lijewski J,  Kauffman RE,  Koh JL,  Malviya SV,  Rose JB,  Richards PT, Gennevois DJ: Needle-free powder lidocaine delivery system provides rapid effective analgesia for venipuncture or cannulation pain in children: randomized, double-blind Comparison of Venipuncture and Venous Cannulation Pain After Fast-Onset Needle-Free Powder Lidocaine or Placebo Treatment trial. Pediatrics, 2008; 121: 979-87

119.    Zuppa AF, Barrett JS: Pharmacokinetics and pharmacodynamics in the critically ill child. Pediatric Clinics of North America, 2008; 55: 735-55

Consensus Statement – First international workshop on anesthetics and Alzheimer’s disease

The workshop was held in May, 2008 at the University of Pennsylvania and the consensus document was recently published in Anesthesia and Analgesia.  The statement provides 8 conclusions: 1) The benefits of general anesthetics in allowing surgery and other painful procedures likely outweighs the potentially toxic effects that are currently known.  2) Evidence from animal models suggests that inhaled anesthetic exposure increases the pathologic changes normally associated with Alzheimer’s disease.  For example, in adult wild type rats and mice, isoflurane exposure alone produces decrements in learning and memory that persist for weeks or months.  There are also a number of other well described changes in various animals.  3) In vitro studies provide evidence that inhaled anesthetics interact with recognized pathways of neurodegeneration and produce effects consistent with increased cellular stress.  4) A number of potential mechanisms for the accelerated neuropathyology seen after general anesthetics have been identified.  However the group felt that there is a higher priority to determining the magnitude and presence of anesthetic-induced long term behavioral effects, preferably in humans.  5) The data on the probability of a particular anesthetic drug to cause changes is sparse.  More work is needed; particularly work that directly compares the various anesthetic drugs.  6) Hypothermia during or after anesthesia may be an independent risk factor.  7) The potential effects of anesthesia and surgery at young ages on long term learning and memory have not been examined in clinical studies.  In adults, post operative cognitive decline is well described.  However, the relationship of anesthetic drug to post operative cognitive decline is speculative at best when based on the currently available studies.  8) The long time- course of neurodegenerative diseases coupled with the relatively short period of normal post operative follow-up means that acceleration of Alzheimer’s disease after anesthesia may not have been recognized.  Given the available evidence, the potential for anesthetics to have long term cognitive effects needs serious attention and further study.  In their closing statement the group cautioned against premature, extrapolated conclusions with respect to anesthesia safety.  They felt that “physicians working and publishing in the area have a responsibility to be objective and candid about the limitations surrounding the clinical implications of their work, particularly with in vitro and animal models, as well as with small or retrospective clinical studies.”  The entire statement is only 2.5 pages.  It is clearly written.  I have abstracted only part, it is worth reading in its entirety of you have an interest or concern about these issues.  Baranov D et al: Consensus statement: First international workshop on anesthetics and Alzheimer’s disease.  Anesth Analg 2009;108:1627-30

David S. Smith, M.D., Ph.D.

 

A slight break; the entries will now resume

Those of you who are following this weblog directly may have noticed that there has been no entry since April 24 (nearly nine weeks).  The reason for this hiatus has been my involvement in a number of risk reduction initiatives at my institution that have occupied most of my available non patient care time.  These are some of the issues that I and several associates have been considering 1) How to get improved information to the bedside when an anesthesia team is called for airway management in a deteriorating patient.  2)  Organizing an approach to quickly get surgeons to the bedside who can create a surgical airway when supraglottic approaches have failed and ventilation is not possible or very difficult.  3) Are there safe, readily available and fast techniques that will allow an anesthesiologist to provide a route for tracheal oxygenation until secure surgical access can be obtained?  The need for these types of initiatives may depend on an institution’s patient population and size.  Regardless, they are worth thinking about; they are a step beyond the American Society of Anesthesiology Difficulty Airway Guidelines.

This blog was begun nearly two years ago (the first entry was July 25, 2007).  There are now 149 entries.  The readership is not high; about 50 - 60 page views per day, though on some days we have been over 100.  There on google searches in which a entry from this blog will show up on the first or second page.

The focus has been and will continue to be on patient safety, particularly as it relates to our actvities at the University of Pennsylvania.

David S. Smith, M.D., Ph.D.

 

Massive Transfusion after trauma

Dr. McCunn prepared this summary of the changing practice with respect to massive transfusion.  Several years ago, our management of intra-abdominal trauma changed from ‘definitive’ care to ‘damage control laparotomy’, which includes only source control of 1) hemorrhage and 2) gross fecal spillage. The patient undergoes abdominal or extremity wound packing, and is then taken to the ICU for warming and ongoing resuscitation.  Another concept in trauma resuscitation that has emerged over the last several years is damage control resuscitation (also known as “hemostatic” resuscitation). This concept, and recent data, approximates a 1:1:1 ratio transfusion of PRBC:FFP:platelets for patients with traumatic exsanguinating hemorrhage.

          After WWII it was recognized that hemorrhagic shock (HS) was optimally treated with whole blood replacement. However, in the mid-70’s, studies suggested that the optimal resuscitation of HS patients consisted of 1-2 liters of lactated ringers, accompanied by whole blood transfusion over the first 45 min after emergency department (ED) arrival. By the mid-80’s, plasma, platelets and cryoprecipitate had been removed from red cells, yet resuscitation strategies for patients in HS had not been changed to account for the new blood components. We continued to transfuse PRBC as if they were whole blood, and increasingly large amounts of crystalloid were used to maintain BP and oxygen delivery. In this situation severe coagulopathy develops, as does microvascular non-surgical bleeding and mortality from uncontrolled bleeding increases. Although commonly referred to as “DIC”, what actually occurs is minimal intravascular coagulation and the new term that has been proposed is “Acute Coagulopathy of Trauma” (ACoT).

          In 2003, two independent studies described the “coagulopathy of trauma” that is present in 25% of trauma patients arriving in the ED. The triad of coagulopathy, acidosis, and hypothermia is then exacerbated and perpetuated by infusion of fluids that dilute clotting factors. Massive transfusion, traditionally described as > 10U of PRBC w/i 24 hours (and not accounting for other blood component therapy), carries a mortality rate between 20-50%, with most patients dying within 6-12 hours of hospital arrival. Damage control resuscitation addresses the lethal triad immediately on admission by using thawed human plasma as the primary resuscitation fluid in a ratio of 1:1 or 1:2 ratio with PRBC. The fibrinogen content appears to be particularly important in achieving hemostasis, and cryoprecipitate is also recommended in severe cases.  As noted in the table many current component blood products are deficient in fibrinogen when compared to a unit of fresh whole blood.

 

Fibrinogen Content in Various Blood Products (mg)

• 1 10U bag cryoprecipitate           2,500mg in 150 mL
• 1U fresh whole blood                 1,000 mg
• 1 six-pack platelets*                    480mg in 300 mL (80mg per unit x 6U)
• 1U FFP                                         400mg  in 200-250 mL
• 1U apheresis platelets                   300mg in 200-250 mL
• 1U pRBCs                                  < 100 mg

Data on fibrinogen content provided by J Hess MD, Director Blood Bank U Maryland/Shock Trauma Center and C Simon MD, Pathologist, Brooke Army Medical Center   *at HUP pooled platelets are "4-pack" = 80mg x 4U = 320mg / 225mL

 

          The recent and ongoing military experience in Iraq and Afghanistan has generated multiple studies demonstrating a decrease in mortality with a 1:1 transfusion practice. A retrospective analysis of 252 patients receiving massive transfusions (> 10 U PRBC in 24 hrs) at two U.S. Army Combat Support Hospitals (mean Injury Severity Score 21) had an overall mortality of 30%. Patients were identified as having received a low fibrinogen-to-RBC (F:R) ratio (< 0.2g) or a high F:R ratio (> 0.2 g). The mean F:R ratios transfused for the low and high groups were 0.1 g/unit and 0.48g/unit respectively (p < 0.0001). Mortality was 52% in the low and 24% in the high F:R ratio group (p< 0.001). Although other variables were associated with survival (temperature, BP, Hgb, INR, base deficit, platelet concentration, and ISS) the F:R ratio was independently associated with mortality.

          Civilian guidelines for massive transfusion have typically recommended a 1:3 ratio of plasma:RBC. Records of 467 massive transfusion patients transported from the scene to 16 Level I trauma centers between July 2005-June 2006 were reviewed; survival varied from 41-74% by center. The plasma:RBC ratio ranged from 0-2.89 and the platelet:RBC ratio ranged from 0-2.5. Plasma and platelet to RBC ratios and ISS were predictors of death at 6 hours, 24 hours and 30 days. Thirty-day survival was increased in patients with high plasma: RBC and high platelet:RBC  ratios.  Each was associated with decreased truncal hemorrhage and increased ICU, ventilator and hospital-free days.

         

References

Borgman M et al: The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat surgical hospital. J Trauma 2007; 63; 805-813.

Holcomb JB et al: Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surgery 2008; 3: 447-457.

Spinella PC et al: 31^st Combat Support Hospital Research Working Group. Risks associated with fresh whole blood and red blood cell transfusions in a combat surgical hospital. Crit Care Med 2007; 35: 2576-2581.

Stinger HK et al: The ratio of fibrinogen to red cells transfused affects survival in casualties receiving massive transfusions at an Army combat surgical hospital. J Trauma 2008; 64: S79-85.

Wilson RF et al: Five years of experience with massive blood transfusion. JAMA 1965; 194:851-854.

 

Maureen McCunn, M.D., Assistant Professor of Anesthesiology and Critical Care at the Hospital of the University of Pennsylvania

A Failure of Scientific Integrity

Steven L. Shafer, MD (a former PENN anesthesia resident and current editor in chief of Anesthesia and Analgesia) had the sad task of preparing and distributing the attached February 20^th letter which starts as follows: “Baystate Medical Center (“BMC”) conducted an investigation pursuant to the Baystate Health Policy on Misconduct in Research and Scholarly Activities (the “Policy”). Dr. Reuben cooperated fully in this investigation. BMC’s investigation determined that Dr. Reuben fabricated data reported in the referenced articles, and that all fabricated data were created under the sole control of Dr. Reuben.”  Ten of the 21 to be withdrawn papers appeared in Anesthesia and Analgesia.  Others appeared in Anesthesiology, J Clin Anesth and other respected journals.  It is unfortunate; activities such as these lead to questioning the integrity of the research process.  Peer review (based on prior examples of this sort) has a difficult time detecting fraud and fabrication.  This does not mean that the peer review process is a failure but only that it has limits and the underpinning of the research process is an implicit trust that the investigators actually did the work they claimed to have done and have based their findings on actually collected data.  A career is ruined, patients might have been given invalid treatments based on the conclusions in these papers, and the advancement of knowledge has been set back.

 

David S. Smith, M.D., Ph.D.

Advanced Trauma Life Support Update

Maureen McCunn, M.D. provides a summary of some of the changes in the most recent edition of the Advanced Trauma Life Support Guidelines(ATLS):  The current 8^th Edition of ATLS has numerous important changes of interest to anesthesiologists, including a renewed focus on the airway and resuscitation endpoints.

v      The Difficult Airway is finally addressed, as the new ATLS guidelines recommend that Airway evaluation be performed prior to attempting rapid sequence intubation (RSI), and a new evaluation mnemonic has been suggested “LEMON”: Look, Evaluate, Mallampati, Observe, and Neck.  Confirmation of intubation using a CO2 detector is now required (capnography is preferred, but if not available, colorimetric techniques are acceptable). The roles of the laryngeal mask airway (LMA), laryngeal tube airway (LTA), and gum elastic bougie, are specifically recognized as important adjuncts during emergency airway management.  Drugs recommended for RSI are left more to local practice, rather than advocating a single "ATLS" cocktail for the whole world.

v      ATLS now includes a far more extensive discussion on the importance of balancing the concept of “limited resuscitation” with the reality of experience demonstrating that excessive early crystalloid administration may dilute blood, dislodge clot and increase hemorrhage; but, inadequate fluid resuscitation in hypotensive, bleeding patients will result in exsanguination following penetrating torso injury.  A more developed discussion is now offered on the equivalency of Ringers lactate and normal saline during the initial resuscitation for shock, and that hypertonic saline is at least equivalent, and perhaps superior, in patients with traumatic brain injury. There is increased emphasis on using multiple end-points for resuscitation.

v      Tourniquets are now endorsed for the first time for use in exsanguinating extremity injury during the prehospital phase.

v      A new pelvic fracture algorithm is offered that emphasizes the use of pelvic binders and angiography.

v      Blast injury is now specifically addressed, because of the recent military experience with improvised explosive devices.

v      There is increased emphasis on early recognition of blunt carotid injury.

v      Methylprednisolone is no longer advocated for the management of acute spinal cord injury.

 

Maureen McCunn, M.D., Assistant Professor of Anesthesiology and Critical Care at the Hospital of the University of Pennsylvania

Survival after ruptured AAA is improved with aggressive platelet and fresh frozen plasma therapy

Dr. Greenblatt calls our attention to Johansson PI et al: Proactive administration of platelets and plasma for patients with a ruptured abdominal aortic aneurysm: evaluating a change in transfusion practice (Transfusion 2007;47:593-8).  The authors compared outcome in two groups of patients with a ruptured abdominal aortic aneurysm.  One group of 50 patients received the following when a rupture of the aortic was first suspected and again 30 min before aortic unclamping: two pooled buffy coat platelet concentrates along with fresh frozen plasma administered in a 1:1 ratio with red blood cells.  Outcome in this group was compared to a retrospective group of 82 patients treated during the previous 24 months using a protocol that called for platelet administration when two blood volumes had been replaced or suspicion of microvascular bleeding or ongoing bleeding.  Patients who died in the OR were excluded from the analysis.  The group given the more aggressive platelet and fresh frozen plasma therapy required less blood post operatively and had a higher 30 day survival (66% compared to 44%).  The authors conclude that proactive administration of platelets and fresh frozen plasma improves coagulation competence, reduces post operative hemorrhage and increases survival in massively bleeding ruptured AAA patients.

 

Eric Greenblatt, M.D., Ph.D. is Associate Professor of Clinical Anesthesiology and Critical Care at the Hospital of the University of Pennsylvania, Philadelphia, PA

This patient remembers and still resents how she was treated by her anesthesiologist

Chicago Tribune

December 17, 2008

Giving birth and getting mad at a doctor

Judith Graham

            The thing I remember best about my second birth (excluding the baby who came into my life) is the anesthesiologist who stood at my side talking over my body to my husband as if I wasn’t there.  He was a schmoozer, the kind of guy who wanted everyone to know when he walked into a room that he was somebody.  The doctor soon found out my husband had gone to a prestigious college and started asking whether they had friends in common. The subtext was clear: “Hey, we’re pretty impressive guys, aren’t we?”  I remember gritting my teeth and thinking, “If only you’d shut up I could focus on something really important.” Which was having that baby I was trying to push out.

          Why didn’t I say something like: “It’s terribly rude of you to be talking this way, as if I were a piece of furniture like the hospital bed”? Why didn’t I cuss or hiss “you two, be quiet now!”?  I thought about this on Tuesday after reading Angela Rozas’ column about Catherine Skol, a former police officer who filed a lawsuit against a doctor who she claims berated her, denied her pain relief and talked on his cell phone while she was giving birth.  Skol and her husband were afraid to complain at the time because they needed the physician’s help and he’d scared them into thinking complications were likely, Rozas wrote.

          I remembered addressing the anesthesiologist in my mind, saying something along the lines of: “You have no idea what it’s like for a woman to be in this kind of situation, do you? You just don’t get it, do you?”  Eventually the doctor administered the epidural, he left the room, and I had the baby, a perfectly healthy little girl.  That wasn’t the end of the story.

          Four days later, after developing a high fever and staying in the hospital sick as a dog, I learned that I had a staph infection at the epidural site. I will never know how I got it.  Did that anesthesiologist practice less than optimal hygiene before he inserted the needle? Was he too busy schmoozing? Or was it simply bad luck?  Two weeks after I returned home, the chief of anesthesiology for the hospital called me at home to inquire about my recovery. “They’re worried,” I remember thinking. But I had a new baby and a 16-month-old, and a lawsuit was the last thing on my mind.

          To this day, I occasionally replay the scene in my head, that male chitchat between my husband and my doctor. “Enough already,” I imagine saying. “This is about my body, my baby, and you’re here to help me. So shape up and get to it!”  There’s not going to be a next time: I’m past my childbearing years. But still I’m rehearsing, mentally.  My husband remains mortified about his role in the interaction.  He wishes he’d cut it off but he didn’t know how back then.  His natural friendliness and sense of politeness ruled against rebuffing the doctor’s queries.

          I wonder how many of you have gone through something similar, if not during childbirth then during other medical encounters. If you’re willing to share your stories, I’d be happy to include them here.

 

This article is reprinted with permission of the author

Multidose vials of anesthetics appear to be the most likely factor in transmission of hepatitis C between patients undergoing arthroscopy and endoscopy

The authors investigated two episodes of hepatitis C transmission between patients who underwent diagnostic procedures.  In both events the common factor appeared to be open multidose vials that had been used for several patients.  “In the arthroscopy episode the anaesthetist re-used the drawing up needle left in the ampoule and syringe to withdraw additional medication.  In the endoscopy episode a new needle and syringe were used every time the ampoules were accessed.  However it is possible in the second case that an open multi-dose vial of fentanyl left adjacent to the sharps container might have become contaminated.”  The authors strongly suggest the use of single dose containers.  If multidose containers must be used they suggest that the drugs be drawn up into individual syringes prior to the commencement of patient care and that this be done in a “clean” area remote from where the anesthesia care will be provided.  Tallis GF et al: Evidence of patient-to-patient transmission of hepatitis C virus through contaminated intravenous anaesthetic ampoules.  J Viral Hep 2003;10:234-239

 

David S. Smith, M.D., Ph.D.

Health care provider practices infect patients in outpatient settings

Over a 10 year period (1998 – 2008) health care practices resulted in 33 episodes (448 persons) of transmitting hepatitis B and hepatitis C in non hospital health care settings including outpatient clinics (12 outbreaks), hemodialysis centers (6 outbreaks) and long term care facilities (15 outbreaks).  “In the outbreaks involving outpatient clinics and several hemodialysis centers, the purported mechanism of patient to patient transmission was primarily syringe reuse or other infection control lapses that resulted in contamination of injectable medications or flush solutions.  In several outbreaks, single use medication vials (for example propofol) and bags of saline solution were inappropriately used for multiple patients.  Anesthesia delivery was a common factor in 6 outbreaks.” Thompson ND et al: Nonhospital health care-associated hepatitis B and C virus transmission: United States, 1998 – 2008.  Ann Intern Med 2009;150:33-39.

 

David S. Smith, M.D., Ph.D.

Reversal of Neuromuscular Blockade - a personal approach

Stanley Muravchick, M.D., Ph.D. discusses his approach to the reversal of neuromuscular blockade: “Although neuromuscular blockade (NMB) is routine, many anesthesiologists are sufficiently unsure of their ability to assess adequate recovery that they “reverse” with neostigmine even when the patient has spontaneously recovered sustained tetanus. The two most common justifications for this practice are 1) there might be cholinoceptors still blocked, and 2) why not – it can’t hurt. A recent study confirms that this ambiguity has become a worldwide issue, with “a lack of clarity in guidelines with respect to monitoring of neuromuscular function” and “no consensus as to what are reliable clinical signs of recovery from neuromuscular blockade, …and lack of understanding of the limitations of some clinical signs used to determine recovery” (Grayling et al., Anaesthesia 2007;62: 806-9). In fact, the neuromuscular junction has a great excess of cholinoceptors, and only about one-third of them need to function in order for neuromuscular transmission to be maximally strong (Paton WDM, et al, J Physiol 1967;191: 59-90). Measurement of train-of-four (TOF) ratios are fraught with error, but demonstration of sustained tetanus at 50 Hz or the clinical equivalent, which is ability to lift and hold the head or an extremity against gravity, is adequate proof that neostigmine is not needed if there has been a reasonable interval (30-45 min) since the last dose of relaxant. As far as the second justification, in addition to issues such as nausea and bradycardia, recent evidence (Eikermann M. et al, Anesthesiology  2007;107:621-9) supports the long-suspected concern that excessive cholinergic activity can itself produce clinically significant muscle weakness: “neostigmine markedly impairs upper airway … and diaphragmatic function, and breathing when given after recovery from vecuronium-induced neuromuscular block.”  In effect, neostigmine can produce a “cholinergic crisis.” My take on all this is that every patient receiving NMB should be monitored with a nerve stimulator. If they have a few obvious twitches, they get the full dose (0.07mg/kg) of neostigmine; if they have all four twitches but cannot sustain tetanus, they get a half dose; if they spontaneously recover sustained tetanus, they do not get neostigmine.”

 

Stanley Muravchick M.D., Ph.D. is Professor of Anesthesia, Department of Anesthesiology and Critical Care, University of Pennsylvania

Wrong sided surgery continues

Even with “time outs” wrong sided surgery continues to occur as this summary abstracted from an article in the Providence Journal (9/22/08) indicates: A doctor at the XXX Hospital operated on the wrong knee of a patient undergoing elective surgery. The surgical team had apparently followed the key safety protocols, including marking the correct knee and pausing to verify the site before operating -- but somehow still made the error, according to the hospital president and chief executive officer.   The mistake was first noticed by the patient when she regained consciousness. The hospital then performed the surgery on the correct knee, and the patient is doing well the hospital president said.

 

According to the hospital president's account, the surgeon marked the correct knee with the word "yes." Even so, the wrong knee was mistakenly draped for surgery. Then, in the operating room, the team took a "time out" before surgery to verify that they were about to do the correct surgery on the correct site.  "That was done by six people," the hospital president said. "They all agreed that they had the proper side ready. ... They knew the surgery was supposed to be on the left side. Somehow the system didn't work the way it should."

 

David S. Smith, M.D., Ph.D.

Intubation and the professional singer

WA Kofke’s patient presents for complex back surgery.  The patient will be prone for many hours.  She also has asthma.  Vocal cord injury related to anesthetic management could derail her singing career.  What can be done to minimize the risk vocal cord injury during general anesthesia?  What symptoms require immediate post operative intervention?  The patient asked that Dr. Kofke contact her voice doctor (Robert T. Sataloff, M.D., D.M.A., F.A.C.S; Professor and Chairman, Department of Otolaryngology - Head and Neck Surgery and Senior Associate Dean for Clinical Academic Specialties; Drexel University College of Medicine) who commented as follows:  “Avoidance of vocal fold trauma in voice professionals is an important issue.  Sadly, there are few evidence-based data to support clinical practice.  Whenever possible, we try to use a 5 or 5.5 tracheal tube.  However, in an asthmatic facing prolong surgery in the prone position, that might be difficult.  A 6.0 tube would certainly be reasonable if it is necessary to manage her pulmonary condition.  In addition to a neutral position of the head, the smaller tube and steroids, there are a few other suggestions that you might consider.  First, documentation of the informed consent discussion should be meticulous.  It is important for the record to reflect that she has been warned that voice damage can occur and could leave her speaking voice hoarse, and impair her ability to sing permanently.  Although you and I both know that such problems are rare, this is just the kind of patient who could end up with an unexpected vocal fold trauma or cricoarytenoid joint injury.  The keystone of virtually every case I have reviewed from a medical legal standpoint has been in the area of informed consent, since virtually all the untoward events I have been consulted on have been from recognized complications.  Second, if possible, I would plan on deep extubation.  Finishing emergence with spontaneous respiration by mask would prevent her from coughing on the tracheal tube or coughing during extubation.  It is, of course, important for your resident or CRNA to be certain that the cuff is completely deflated during extubation (a common mechanism for posterior arytenoid dislocation).  Third, it is helpful during emergence to untape the tube before your patient starts swallowing.  This is especially important if you decide not to extubate her while she is deep.  Coughing and swallowing against a fixed plastic obstruction causes sheering forces that are more traumatic to the vocal folds than direct contact alone which is what occurs after untaping (allows the tracheal tube to move with the larynx).  A laryngeal mask airway instead of a regular mask during emergence is reasonable as long as the person you have placing it has a great deal of experience with laryngeal mask ventilation.  I have seen three cases of arytenoid dislocation caused by LMAs, and the problems seem to occur with people who don't use them very often.  Fourth, I would recommend making a definite effort to speak with the patient postoperatively.  If she is hoarse following extubation, an otolaryngology consult should be obtained immediately.  The second most common claim that I see following anesthesia (inadequate informed consent being first) is delay in diagnosis.  This usually results in action against the anesthesiologist and the surgeon; the anesthesiologist usually is held accountable unless the surgery was performed as an outpatient.  Even then, the issue has been problematic for anesthesiologists.  If the patient stays in the hospital even one night and is not assessed with documentation by a written note about the voice, defense is difficult if problems arise.  More importantly, immediate evaluation of post-extubation hoarseness by an otolaryngologist allows identification of problems that require immediate intervention.  These may range from trauma along the vibratory margin that may require voice rest, to arytenoid subluxation which may respond to prompt reduction.  Hopefully (and most likely), there will be no postoperative hoarseness.  However, if there is, immediate otolaryngologic management of this recognized complication minimizes the likelihood of long-term dysphonia and complies with a state-of-the-art standard of care.”

          I asked a vocal cord expert who I work with, Natasha Mirza, M.D., to review the above comments.  She replied that “Dr. Sataloff has captured the gist of what is needed most in these professional voice users which is a detailed informed consent.  For shorter cases an LMA may be better with less risk of vocal fold injuries.  If intubation is necessary then the smaller the tube the better. Also post op it is always a good idea to ask the surgeon to write for a week of proton pump inhibitors to help prevent granulomas as we know that even a few hours of intubation can lead to VF irritation. I and my team will obviously be available to assist you all in any way we can if there are any issues in the post op period.”

          DSS notes: There is very little in the anesthesia literature on the anesthetic management of the professional singer or other people such as actors or announcers whose voices are their source of income.  Many years ago, I offered an opera singer a spinal anesthetic instead of a general anesthetic for her lumbar laminectomy.  Her response was on the order of – I would rather not sing again than have a spinal.  Clear communication is key to successful care of these patients.

          A few references:

1.     Torrey MJ, Wong JH, Finley-Detweiler R: The vocal athlete and endotracheal intubation: A management protocol.  J Voice 1998;12:349

2.     Bullough A, Craig R: Anesthesia for the professional singer (letter). Eur J Anaesthesiol 2001:18:414

3.     Errando CL: Anaesthesia for the professional singer (letter). Eur J Anaesthesiol  2002;19:687

4.     Anon: Post-intubation granuloma (editorial). BMJ 1973; November10:313

5.     Loh KW, Irish JC: Traumatic complications of intubation and other airway management procedures.  Anesthesiology Clin N Am 2002;20:953

6.     Zimmert M et al: Effects on vocal cord function and incidence of laryngeal disorder when using a laryngeal mask airway in comparison with an endotracheal tube.  Eur J Anaesthesiol 1999;16:511

7.     Hamadan A-L et al: Immediate post-operative vocal cord changes in patients using laryngeal mask airways versus endotracheal tube.  J Laryngol Otol 2008;121:879

 

Dr. Mirza is Associate Professor of Otorhinlaryngology: Head and Neck Surgery at the Hospital of the University of Pennsylvania

 

David S. Smith, M.D., Ph.D.

Yet another awareness under anesthesia article

This article on awareness with recall during general anesthesia (AWR) by Errando et al (Br J Anaesth 2008;101:178-185) has a number of interesting observations.  First, it is from a country (Spain) other than the United States. Second, it is prospective with a calculated power to detect a 95% confidence interval of 0.09 – 0.37%.  Third, it covers a fairly long time in two separate data collection periods (April 1995 – April 1997 and then December 1998 – November 2001).  Interviews were done in the PACU immediately post op.  If there was evidence of awareness then the patients were interviewed again at 7 days and 30 days (in my opinion this is a design flaw compared to the current standard of interview regardless of initial response).   Patients going to the ICU were excluded, as were patients less than 15 years old and those having cardiac surgery.  Patients aware because erroneous administration of neuromuscular blocker prior to a hypnotic drug were classified as not having AWR.  The interviews were formally structured.  The interviewers did not know the anesthetic given.

          Data from 4001 patients cared for by 42 different anesthesiologists at one institution was reported.  The incidence of patients reporting AWR 7 days after elective surgery was 0.6% (22 of 3477 pts).  Of interest was a difference in awareness depending on anesthesia type.  Patients who received only nitrous oxide oxygen for maintenance had an AWR rate of 5% (4 of 79 pts), with total intravenous anesthesia the reported AWR was 1.1% (14/1239), but when halogenated anesthetic drugs were used the AWR was only 0.59% (9/1514).  Patients receiving a benzodiazepine pre medication (dose and type not provided) had significantly less recall than those who received an opioid pre medication.  Twenty two patients with AWR provided descriptions of the experience.  11 reported hearing noise; 18 reported hearing conversations.  Twelve patients tried to move and 14 tried to communicate but could not.  Eleven patients had pain; five reported being cut with a scalpel and five felt suturing.  Nine reported feeling the tracheal tube in their mouth.  Eleven felt panic at the time they were awake and two had a sensation of eminent death.  Few if any of the patients discussed the event with their anesthesiologist though 16 told their surgeon.  Six episodes occurred at the beginning of surgery, two during and seven at the end.  From an analysis of the anesthesia record, in only 2 patients was awareness suspected by those caring for the patient.  Three of the patients had difficult intubation.  In fifteen patients there were errors in hypnotic drug dose and in two there were equipment failures.  My observations – their numbers of aware patients may have been even higher if they had included the CT patients.  These are high numbers compared to many of the recent United States studies; however their data comes from an earlier period (1995 – 2001).  In any event awareness under anesthesia is not just a United States phenomenon.  Their data on anesthesia type having an effect, a potential role for benzodiazepine pre medication and their descriptions of what it is like to be aware during surgery makes this paper worth reading. 

David S. Smith, M.D., Ph.D.

The Joint Commission targets the disruptive health care professional

A July 9, 2008 Sentinel Event Alert discusses the problem of behaviors that undermine the “culture of safety.”  From a Joint Commission news release “Health care is a high stakes, pressure packed environment that can test the limits of civility in the workplace…rude language and hostile behavior among health care professionals goes beyond being unpleasant and poses a serious threat to patient safety and the overall quality of care.”  Toward reducing these behaviors which may include (for example) verbal outbursts, physical threats, unwillingness to answer questions or return phone calls the Joint Commission will be implementing (January, 2009) new leadership standards that will require health care organizations to develop codes of conduct that define acceptable compared to disruptive and inappropriate behaviors and to develop a process for managing disruptive and inappropriate behaviors.  The sentinel text can be found at http://www.jointcommission.org/SentinelEvents/SentinelEventAlert/sea_40.htm

 

David S. Smith, M.D., Ph.D.

 

Clearing the cervical spine in the unconscious patient

It is Saturday night and yet again there comes another trauma patient in a hard collar to the OR.  Is the c-spine cleared?  The discussion goes on but what does that phrase mean to “clear the c-spine”?  The article by Harrison and Cairns provides a succinct and up to date discussion of the issues relating to “clearing the c-spine.”  Key points include: 1) The incidence of c-spine injury is 5% in association with blunt polytrauma.  2) Factors that increase the risk include the presence of a focal neurologic deficit, concurrent head injury and a Glasgow coma score < 8.  3)  The inability to do a neurologic exam or obtain patient self report of pain greatly complicates the diagnosis of spinal cord injury; radiologic exam is not an “easy” substitute.  4) The success rate for obtaining adequate lateral x-rays of the c-spine may be as low as 50% and with an ET tube in place the sensitivity for detecting injury may be as low as 30%.  The authors do not consider plain films adequate for c-spine clearance.  5)  The authors suggest that helical CT scans with 1 mm slices especially with 3D reconstruction may be the best “first step” in radiologic diagnosis.  6) Finally the authors note that communication may be the largest contributor to failures in timely c-spine clearance and suggest local development of agreed upon “best practices” with “sign off” sheets may help prevent errors leading to miss-identification, failed identification and inappropriate management.  Ref:  Harrison P, Cairns C: Clearing the cervical spine in the unconscious patient.  Cont Edu Anaesth Crit Care & Pain. 2008;8:117-120.

 

David S. Smith, M.D., Ph.D.

Low baseline hemoglobin concentration is associated with poorer surgical outcome but transfusion of asymptomatic patients may not improve outcome

Wu and associates did a retrospective cohort study using the Veterans Administration National Surgical Quality Improvement Program database (NSQIP) to examine the relationship between pre operative hemoglobin and 30 day post operative death or cardiac events after non cardiac surgery in patients older than 65.  A total of 310,311 patients operated upon between 1997 and 2004 were studied.  In this predominately male population, normal hemoglobin was defined as a hematocrit between 39 – 53.9%, anemia was defined as a hematocrit less than 39%, and polycythemia was defined as a hemoglobin greater than 54%.  Examples of operations included were inguinal hernioraphy, prostatectomy, angioplasty, total knee replacement, and partial colectomy.  Additional procedures within 30 days of the first were excluded.  Some very low risk procedures such as eye or nasal surgery are not part of the NSQIP data base.  The overall 30 day mortality was 3.89%.  Thirty day mortality and cardiac event rates increased with either positive or negative deviations from normal hematocrit levels.  There was a 1.6% increase in 30 day postoperative mortality with every percentage point increase or decrease from the normal range.  In a separate study they noted similar results for cardiac surgery.  The authors concluded that in this population of patients greater than 65 years old, even mild degrees of pre operative anemia or polycythemia were associated with increased risk of mortality or a cardiac event.  What this paper does not help with is what to do with these findings.  As the authors state, “if anemia is a modifiable risk factor and not simply a marker of other conditions that confer increased risk, then preoperative transfusion might be considered.”  However neither this nor other similar papers provide that guidance.  Ref: Preoperative hematocrit levels and postoperative outcomes in older patients undergoing noncardiac surgery.  JAMA 2007;297:2481 – 2488 (attached).

          Karkouti et al examined the effects of acute anemia on adverse outcomes after cardiac surgery in 10,179 patients and found that the incidence of post operative complications as indicated by a composite outcome variable of in hospital death, stroke or kidney failure was related to the percent change in hemoglobin concentration from baseline and not the absolute value of that variable.  Regardless of starting hemoglobin or lowest recorded intraoperative hemoglobin a 50% decrease in hemoglobin was associated with markedly increased risk of death, stroke or kidney failure.  Dr. Augoustides opines that “this study is consistent with my clinical experience that the safely tolerated degree of acute anemia is a function of baseline hemoglobin concentration.  The findings suggest a new rationale to assist in perioperative red blood cell transfusion decision making in cardiac surgery.”   Ref: The influence of baseline hemoglobin concentration on tolerance of anemia in cardiac surgery.  Transfusion. 2008;48:666-672 (attached)

          DSS note -- Both of these papers challenge the current dogma concerning transfusion thresholds.  Though the accepted transfusion threshold of 6 - 7 g/dl may be acceptable for healthy patients, there are now two subgroups, the elderly and patients undergoing cardiac surgery for whom lower hemoglobin concentrations are associated with poorer outcomes.

          Feedback --   Dr. Sarani sent the following comment “In regards to the beneficial effects of transfusion in elderly or cardiac pts, I respectfully disagree. Study after study has shown that transfusion is associated with worse outcomes in patients with asymptomatic anemia. Please see a recently published article which shows that although anemia is harmful in traumatic brain injury patients, transfusing anemic pts is even more harmful! I think that anemia is an index of illness, not the cause of illness in non-hemorrhaging patients and fixing it does little overall, unless there is evidence of end-organ ischemia. This is akin to giving albumin to hypoalbuminemic patients.”  Doctor Sarani provided two papers which are attached: Rao SV et al: Relationship of blood transfusion and clinical outcomes in patients with acute coronary syndromes.  JAMA 2004;292:1555-1562.  Salim A et al: Role of anemia in traumatic brain injury.  J Am Coll Surg 2008;207:398-406.

          DSS note -- The first two papers abstracted examined the relationship between anemia and outcome in very different patient populations than those in the papers provided by Dr. Sarani.  Also the initial two papers did not examine the effect of transfusion.  Thus it is possible that anemia is a marker but transfusion will not improve outcome.

 

          Joni Augoustides M.D., FASE is Associate Professor of Anesthesiology and Critical Care at the                              Hospital of the University of Pennsylvania

          Barbak Sarani M.D. is Assistant Professor of Surgery, University of Pennsylvania School of                        Medicine

 

David S. Smith, M.D., Ph.D.

Renal failure after general anesthesia

Kheterpal et al identified a group of 15,102 patients out of a population of 65,043 cases who underwent major, non cardiac surgery and who had an estimated pre operative creatinine clearance greater than 80 ml/min.  Of this group 9,078 patients had a creatinine measured during the first seven post operative days and formed the basis of this study.  121 patients developed acute renal failure (0.8%, ARF)) defined as an estimated creatinine clearance of 50 ml/min or less.  Of this group 14 patients (0.1%) required renal replacement therapy such as dialysis.  A significant portion of the ARF group had undergone vascular or general surgery procedures.  Independent pre operative predictors of post operative ARF included age greater than or equal to 59, emergency surgery, liver disease, body mass index greater than or equal to 32, high risk surgery, peripheral vascular occlusive disease, and chronic obstructive pulmonary disease requiring bronchodilators.  The risk of post operative ARF increased from 0.3% to 4.3% as the number of preoperative risk factors increased from zero to 3 or more.  Intraoperative variables associated with post operative ARF included the use of vasopressors, furosemide, or mannitol.  Thirty day, sixty day and one year all cause mortality was significantly higher in the patients who developed post operative ARF.  For example at one year all cause mortality was 15% in the normal renal function group and 31% in the ARF group.  In their discussion the authors note that post operative ARF in cardiac surgery patients is considerably higher (17%).  Intraoperative oliguria (urine output less than 0.5 ml/kg/h) was not associated with ARF.  The mean urine output was 1.0 ml/kg/h in both normal and ARF groups.  Recognize that this was a retrospective study using clinically available data.  Also note that this study provides no information on how to prevent or decrease the incidence of ARF.  However this study does provide information on incidence, patients at risk and may thus stimulate prospective hypothesis testing that may lead to a better understanding of this problem.  Even though the incidence appears low, the consequences in increased hospital stay, increased costs of care and poorer survival are significant.  Finally this study could only be done because of the availability of an electronic anesthesia record and pre operative data collection instrument that allowed electronic searching.  Ref: Predictors of postoperative acute renal failure after noncardiac surgery in patients with previously normal renal function.  Anesthesiology. 2007;107:892-902.

 

David S. Smith, M.D., Ph.D.

Epidural Catheter intravenous mix up dangers

The Institute for Safe Medication Practices devoted their July 2008 Newsletter to Epidural – IV mix ups.  They emphasized the problem of bupivacaine solutions prepared for epidural infusion being given intravenously with subsequent cardiac arrest.  In one case a nurse intending to hang a bag of saline instead hung a virtually identical bag of bupivacaine.  Though the number of such mix ups is low, many occurred in young women.  The reverse also occurs and a case of vincristine injected into the epidural space with subsequent patient death was noted in the report.  Some of the approaches to reduce the incidence of these mix-ups include: 1) substitution of ropivacaine for bupivacaine when clinically appropriate, 2) specially colored epidural tubing with no injection ports, 3) epidural pumps that are distinct from pumps used for intravenous infusions, 4) clear labeling “epidural use only” on bags and syringes used for epidural injection.  Other suggestions include: 1) strict separation of solutions intended for i.v. use from those intended for epidural use, 2) tracing tubing from origin to destination before attaching medication or fluids, 3) hang bags and attach syringes in such a way that their labels are facing out and easily readable.  A final suggestion is manufacturing epidural syringes, bags and tubing with connectors that are not compatible with intravenous syringes, bags or tubing.  This is not just an anesthesia problem.  As noted above, deaths have occurred when vincristine, meant for i.v. use, was given intrathecally (apparently this results in ascending paralysis and severe pain prior to death).   Also, as noted above, there have been cases of epidural solutions of local anesthetics being given i.v.  There are also reports of many types of drugs being given epidurally in error.  The crowded surface of the operating room anesthesia workspace might easily allow the wrong drug to be selected when syringes of drugs for epidural use are left near syringes of drugs meant for intravenous use. For entire article follow this link: http://www.ismp.org/newsletters/acutecare/articles/20080703.asp

 

David Smith, M.D., Ph.D.

The syndrome of post anesthesia mumps

John Tanner, M.D., Ph.D. relates the following case:  A 50 year old African American woman opted for interventional radiologic treatment (embolization) of her uterine fibroids rather than surgery.  She had a history of mild asthma and GERD.  She underwent the procedure under general anesthesia (induced with fentanyl, propofol, and succinylcholine, and maintained with sevoflurane) with endotracheal intubation for airway protection.  The anesthetic was uneventful; one low blood pressure reading thought to be due to use of nitroglycerin by the radiologist was easily treated with 100 mcg phenylephrine IV.  The patient had copious secretions and was given glycopyrrolate toward the end of the procedure.  She coughed on the endotracheal tube prior to extubation.  The next day she noticed swelling under her chin when she looked in the mirror.  She had no pain or other problems.  The swelling was barely noticeable on the second day after the procedure and eventually resolved.

          Dr. Tanner provides some annotated references: 1) Reilly DJ, “Benign Transient Swelling of the Parotid Glands Following General Anesthesia:  ‘Anesthesia Mumps’”, Anesth Analg 49:560, 1970.

(Three patients with acute, transient salivary gland swellings have been seen in approximately 1500 patients undergoing general anesthesia over a 10-month period.  The factors which appear to play a role are belladonna drugs, succinylcholine, straining, coughing, and the Valsalva maneuver.)  2) Bahadur et al, “Salivary gland swelling developing after endoscopy:  ‘anesthesia mumps’”, Gastrointestinal Endoscopy 63:345, 2006.

(“Swelling of the salivary glands has previously been reported as a complication of GA and a rare complication after endoscopy… {it is} usually unilateral and painless, and … {the swellings} spontaneously resolve over a period of a few hours.  We report a similar swelling that developed in ERCP under GA … The patient was reassured, well hydrated, and observed, with a gradual disappearance of his swelling over 12 hours.  As per ENT, he was given 3 days of antibiotics.  The etiology is unclear…it seems to be related to retention of secretions causing a blockage of the salivary ducts.  Dehydration may play a role.  Parasympathetic stimulation has also been implicated.  This is a benign, spontaneously resolving, though impressive, finding, which is usually treated with adequate hydration and observation.  Warm compresses may be helpful.”)  3) Serin et al, “A case of anesthesia mumps”, Anesth Analg 104:1005, 2007.  (The swelling disappeared spontaneously after 48 h.  Swelling of the salivary glands after GA is a rare event.  No treatment other than reassurance is indicated.  Adequate hydration and warm compresses may be helpful for relieving symptoms.  Rapid subsidence of the swelling can be expected in 1-5 days.”)  4) Gilgen-Anner et al, “Iodide mumps after contrast media imaging:  a rare adverse effect to iodine,” Ann Allergy Asthma Immunol. 99:93, 2007.  (“Iodine from contrast media may rarely elicit noninflammatory edema of the salivary glands.  These swellings resolved within a few days.”)

 

John Tanner, M.D., Ph.D. is Assistant Professor of Clinical Anesthesiology and Critical Care at the University of Pennsylvania

Patient Safety Goals for FY2009

These patient safety goals were developed by the Joint Commission (the group that accredits a majority of the health care organizations in the United States).  Compliance with Joint Commission Goals is one of the requirements for accreditation, thus the Joint Commission is a powerful force in directing national patient safety efforts.  As is typical for Joint Commission communications, the goals tend to be expressed in very general terms, leaving interpretation and implementation up to the organization.  The bold, red font goals are those that I think are directly applicable to issues of direct concern to the practice of Anesthesia.  The bold underlined goals are new for FY09.  The complete set of goals can be found at http://www.jointcommission.org/PatientSafety/NationalPatientSafetyGoals/09_hap_npsgs.htm .  The ones here are the ones I think most relevant to anesthesia practice

Goal 1: Improve the accuracy of patient identification.

A.     Eliminate transfusion errors related to patient misidentification.

 

Goal 2: Improve the effectiveness of communication among caregivers.

          A.  For verbal or telephone orders or for telephone reporting of critical test results, the individual giving the order verifies the complete order or test result by having the person receiving the information record and “read-back” the complete order or test result.

          D.  The organization implements a standardized approach to hand off communications, including an opportunity to ask and respond to questions.

 

Goal 3:  Improve the safety of using medications.

A.     Label all medications, medication containers (for example, syringes, medicine cups, basins), or other solutions on and off the sterile field.

B.     Reduce the likelihood of patient harm associated with the use of anticoagulation therapy.

 

Goal 7:  Reduce the risk of healthcare associated infections.

A.     Implement evidence-based practices to prevent healthcare-associated infections due to multiple drug-resistant organisms in acute care hospitals.

B.      Implement best practices or evidence-based guidelines to prevent central line-associated bloodstream infections.

C.     Implement best practices for preventing surgical site infections.

Goal 9:  Reduce the risk of patient harm resulting from falls.  At first one might think I am wasting space listing this Goal in an Anesthesia Department e-letter, but every patient under our care in an ICU is a fall risk.  Patients on the labor floor have been known to fall after we provide epidural analgesia.  Consider also the large number of patients in our pain clinics all of whom have some risk of fall either because of the problem that brings them to the clinic or after many types of therapeutic blocks.  Finally patients standing for the first time after general anesthesia for short procedures or day surgery are at risk of falling. Notice that the goal states that there is a need to reduce the “risk of patient harm” not just reduce the risk of falls.  Is there a need to redesign patient waiting areas or rooms so that if a fall occurs the probability of injury is reduced?  If so what design elements need to be incorporated?

Why care about these goals?  1) The Joint Commission’s ability to withhold accreditation gives it the power to drive the safety agenda.  2)  One can expect considerable institutional resources to be devoted to meeting these goals.  3) One can expect projects, mandates and protocols to be developed and implemented as the institution attempts to come into compliance.  Thus these goals may have a direct effect on practice and policy within an institution.  The most important reason to care about these goals is that they do have a direct effect toward improving patient care and thus they are the right things to do for our patients.

 

David S. Smith, M.D., Ph.D.

Tocolytics in pre term labor

Preterm birth is one of the major health problems in the United States.  Approximately 11-12% of all births occur preterm (as defined as < 37 weeks gestation) and the rate has increased by approximately 19% since 1990 (1).  The concern with preterm labor and birth is its outcome; it accounts for approximately 70% of all neonatal deaths and 50% of the long-term neurological disabilities (2).  Tocolysis has been a prominent component of efforts to prevent preterm labor and delivery.  It is hoped that medications will reduce uterine contractions and allow more time in utero for the fetus.  The literature supports that only a minority of patients benefit from tocolytic agents.

          Beta-mimetic Agents:  The beta-mimetic agents, such as terbutaline and ritodrine (FDA approved), work by relaxing the myometrial smooth muscle by a reduction in intracellular calcium.  Maternal side effects include hypokalemia, hyperglycemia, tachycardia, decreased systemic vascular resistance, and increased risk of pulmonary edema.  Beta-mimetics have been linked to at least 25 maternal deaths from pulmonary edema (3).  In 2003, the American College of Obstetricians and Gynecologists concluded, “It would appear, on the basis of currently available evidence, very difficult to support the use of beta-mimetics, which have a high incidence of side effects.  Although these drugs do delay delivery in the short term, there is no demonstrable benefit for the newborn (4).”

          Magnesium:   The use of magnesium sulfate as a tocolytic varies by location.  It is rarely used in Europe but is widely used in the United States, where it continues to be used because of its high safety profile.  Magnesium sulfate results in blurry vision and maternal weakness.  It potentiates the nondepolarizing muscle relaxants, necessitating a major reduction in dose of these medications.  A 2004 review found no benefit of magnesium for short- or long-term delay in delivery (5). 

          Calcium Channel Blockers:  Calcium channel blockers relax the myometrium.  A study of 1024 patients found that calcium channel blockers were more effective than beta-mimetic agents in prolonging pregnancy for 7 days or longer, were much less likely to cause maternal side effects, and were associated with reduced neonatal morbidity(6).  The most commonly used drug of this class is nifedipine.  These drugs should not be used in women with cardiovascular disease or those who are hemodynamically unstable.

          Prostaglandin Synthetase Inhibitors:           The discovery that prostaglandins play a role in the initiation of labor led to the study of prostaglandin synthetase inhibitors as agents for treating preterm labor.  Studies suggest that indomethacin is more effective than placebo in prolonging pregnancy (7).  The concern with the use of indomethacin is its fetal effects.  Premature closure of the ductus arteriosus and oligohydramnios have been associated with maternal administration of indomethacin.

          Atosiban:  Oxytocin antagonists have been developed.  Labor is accompanied by an increase in oxytocin receptors.  Atosiban is the only oxytocin antagonist that has undergone extensive study.  Atosiban has several advantages in that it is a specific inhibitor of myometrial contractility with little transplacental passage.  A multicenter trial compared atosiban to placebo in 501 women with preterm labor.  No difference in length of labor or neonatal outcome was noted (8).

          Conclusion:  Multiple studies have failed to show a benefit to maintenance of tocolysis for preventing the recurrence of preterm labor.  Because of its high neonatal mortality, physicians feel obligated to do something when a parturient presents in preterm labor.  At present, most interventions fail to demonstrate benefits.  The safest agent currently used for tocolysis appears to be nifedipine, although the American College of Obstetricians and Gynecologists has not identified a tocolytic of choice.

1.      Martin JA, Hamilton BE, Sutton PD, et al.  Births: Final data for 2002: National Vital Statistics Reports, Vol 52, No 10, Hyattsville, MD: National Center for Health Statistics, 2003.

2.      Hack M, Fanaroff AA.  Outcomes of extremely immature infants: A perinatal dilemma.  NEJM 1993; 329: 1649.

3.      MIngemarrson I, Lamon RF.  An update on the controversies of tocolytic therapy for the prevention of preterm birth.  Acta Obstet Gynaecol Scand 2003; 82:1.

4.      ACOG Practice Bulletin No 43: Management of preterm labor.  Obstet Gynecol 2003;101:1039.

5.      Crowther CA, Hiller JE, Doyle WW.  Magnesium sulphate for preventing preterm birth in preterm labour.  The Cochrane Library 2004; Issue 3: Chichester, UK.  John Wiley & Sons, 2004.

6.      King TF, Flenady V, Papatsonsis D, et al.  Calcium channel blockers for inhibiting preterm labour: A systematic review of the evidence and a protocol for administration of nifedipine.  Aust N Z J Obstet Gynaecol 2003; 43: 192.

7.      Moise KJ.  The effect of advancing gestational age on the frequency of ductal constriction secondary to maternal indomethacin use.  Am J Obstet Gynecol 1993; 168: 1350.

8.      Romero R, Bibai BM, Sanchez-Ramos L, et al.  An oxytocin receptor antagonist (atosiban) in the treatment of preterm labor: A randomized, double-blind, placebo-controlled trial with tocolytic rescue.  Am J Obstet Gynecol 000; 182: 1173.

 

Robert R. Gaiser, M.D.

 

Robert Gaiser is Professor of Anesthesiology and Critical Care at the Hospital of the University of Pennsylvania

Anesthesia awareness -- successful defense

This article by Lax JA and Attorri MD (Anesthesia Awarenss:  There is room for skepticism, Respiratory Therapy 2008;3:12) is particularly interesting in that it was written by two lawyers who recently, successfully defended an anesthesiologist against the claim of awareness under anesthesia.  They provide insight from the point of view of those who need to defend physicians.  It is clear from their success in the courtroom and the clarity of their article that they have a good grasp of the key issues.  Of particular importance in deceloping their defense was a careful, detailed review of just what the patient claimed to have remembered and its possible relationship to external location and time.   It is unclear to me why this timely article was published in Respiratory Therapy (http://www.nkms.com/articles/jal.article.excerpt.pdf ).  At a brief three pages it is worth reading.

David S. Smith, M.D., Ph.D.

Maternal Mortality and Anesthesia

Lawsuits against physicians insured by the Doctor’s Company for anesthesia related maternal arrests associated with labor and delivery were recently reviewed Ann Lofsky, M.D.  The series included 22 cases that occurred between 1998 and 2006.  Ten out of the 22 died, including 3 who were declared brain dead and removed from ventilators.  Eleven suffered some degree of anoxic brain damage.  Only one had no apparent post arrest neurologic residual deficit.  Respiratory arrest after epidural or spinal block was the most common event (13 of the 22 of which 11 had a high neuraxial blockade and apnea and 2 had a caesarian section under spinal anesthesia with arrest after i.v. sedation).   Of note was the fact that none of the patients were attached to a maternal monitor with audible alarms at the time of the arrest which may have delayed recognition of a developing problem.  Epidural Catheters: Eight of these thirteen patients arrested in labor rooms following attempted insertion and dosing of epidural catheters to relieve labor pains.  Of these, 7 had subsequent evidence of unintentional subarachnoid blocks.  All eight arrests occurred within the first 30 min of initial catheter placement.  In four cases the anesthesiologist was not in the room at the time of the arrest.  Seven of the 8 cases involved transfer of a mother in respiratory or circulatory arrest from the labor room to the operating room for a STAT section due to fetal distress.  In four of these cases there were documented delays in ventilation of the mother for reasons including failure to notice maternal arrest, desire for more optimal intubating conditions present in OR, difficulty locating an Ambu-bag, or anesthesia provider not present.  In the one patient who did not have neurologic residual, the patient was placed supine in the delivery room by the anesthesiologist and was ventilated by bag and mask as soon as ventilation appeared inadequate.  Blood pressure was supported by i.v. fluids and the caesarian section was done in the delivery room.  Spinal Anesthesia:  Five cases occurred in patients for elective caesarean section.  In two cases intravenous benzodiazepine or opioid were given after delivery.  In one case there was an arrest immediately after the spinal was placed.  The arrest was thought to have been secondary to pre-eclampsia and volume depletion.  In two other cases there was an apparent high spinal with delay in recognition or resuscitation.  Maternal hemorrhage leading to arrest occurred in 7 cases.  Three occurred after normal spontaneous vaginal delivery and 4 after caesarean section.  Common problems included difficulty in recognizing the presence of hemorrhage, delays in obtaining blood, waiting for typed and crossed blood, inadequate venous access, and not getting help.  In this total series of arrests 17 pts had regional blocks and five had general anesthetics.  One of the general anesthetics involved a difficult intubation and loss of airway.  There was no evidence of aspiration of gastric contents in the series.  Conclusions: 1) Since all of the respiratory arrest after labor epidurals in this series occurred within 30 minutes after catheter insertion increased monitoring and/or the continuous presence of the anesthesiologist might have prevented or allowed earlier recognition of a developing problem.  2) Having audible alarms for pulse oximetry might have called attention to a problem earlier.  3) Airway equipment including oxygen needs to be present and immediately available in the room when regional anesthetics are placed.  4) Ventilation and oxygenation of the mother should be established before transporting the mother to another location.  5) Massive hemorrhage on labor and delivery is rare, but the incidence may be increasing given the increased rate of repeat Cesarean sections and an associated rise in placenta previa and acreta.  One New York hospital established an obstetric rapid response team and demonstrated a reduction in maternal death despite an increase in their cases of major obstetrical hemorrhage.  This is a link to the article as it appeared in the Anesthesia Patient Safety Foundation Newsletter of 2007

(http://www.apsf.org/resource_center/newsletter/2007/summer/02_maternal_arrest.htm ).

          The Doctors Company is a very large and respected physician owned company specializing in physician malpractice insurance.

          Dr Arkoosh comments on the above: 1) Isn't it remarkable how far we have come with decreasing the risks from management of the maternal airway.  This is due to heightened awareness of the problem and implemented strategies to prepare for and respond to challenging maternal airways.  We need to apply this same level of diligence to potential complications from neuraxial blocks.  2) It has been shown over and over that we underestimate the amount of maternal blood loss.  Data from the UK consistently finds that we under resuscitate this patient population.  I would point out that it is not always possible to observe all of the maternal blood loss and that we should generally error on the side of giving what we think might be "too much".

 

Valerie Arkoosh M.D., MPH is Professor of Clinical Anesthesiology and Critical Care and Professor of Clinical Obstetrics and Gynecology at the University of Pennyslvania.

 

David S. Smith, M.D., Ph.D.

Large doses of fentanyl do not behave the same as smaller doses

Stanley Muravchick, M.D., Ph.D. notes that “In 1978 I witnessed narcotic-induced ventilatory arrest in a patient who had received 25 mcg/kg of fentanyl for anesthetic induction 6 hours earlier. The patient had been awake and responsive at time of extubation. No other opiates had been given.  This patient responded dramatically to naloxone.”

          Dr Muravchick notes that this phenomenon of late or "second peak" fentanyl depression was eventually reported by others.   Caspi J et al. reported that high-dose fentanyl anesthesia is widely used in cardiac surgery. Its immediate side-effects are well known. However, its late adverse effect manifested by extreme truncal rigidity, decreased chest wall compliance, hypoventilation, respiratory acidosis and hemodynamic instability is not sufficiently appreciated. Of 380 patients who underwent aortocoronary artery bypass under high-dose (100 mcg/kg) fentanyl anesthesia, 29 (7.6%) developed the sudden onset of extreme thoracic and abdominal rigidity, leading to respiratory depression 2 to 6 h postoperatively, after an apparently normal recovery from the anesthesia. In 15 patients, a high plasma level of fentanyl (5.2 to 7.8 ng/ml) correlated with the clinical events.  Administration of naloxone or a muscle relaxant rapidly reversed this late complication of fentanyl, thought to be due to re-entry of fentanyl into plasma from deposits in adipose tissue, muscle and the GI tract, leading to a secondary peak in plasma fentanyl. It is more likely to be encountered when hypothermia, rewarming, and acidosis occur in the postoperative period.  Awareness of this life-threatening complication is critical in patients undergoing surgery with fentanyl anesthesia (Caspi J et al: Delayed respiratory depression following fentanyl anesthesia for cardiac surgery, Critical Care Medicine.  1988;16:238-40).

          Dr Muravchick explains that though these clinical observations were published in 1988 the pharmacokinetic explanation for these phenomena had actually been established many years before as noted by Stoeckel H et al who wrote that the pharmacokinetics of fentanyl are complicated by an additional increase in plasma concentration during the elimination phase of the drug. We have confirmed that fentanyl is excreted in the gastric juice and reabsorbed from the alkaline medium of the small intestine. In addition, the stomach wall in rats has an important storage capacity for fentanyl. A maximum of about 20% of the dose was found in the stomach wall after i.v. injection. In man the resected part of the stomach contained 16% of the dose, 10 min after injection. These observations could be important in explaining the occurrence of respiratory depression in the period after operation (Stoeckel H, et al:  Pharmacokinetics of fentanyl as a possible explanation for recurrence of respiratory depression. BJA  1979;51:741-5, 1979).

 

Stanley Muravchick M.D., Ph.D. is Professor of Anesthesiology and Critical Care at the Hospital of the University of Pennsylvania

 

David S. Smith, M.D., PhD.

Anesthesia record practices lead to CMS review & potential sanctions

The following headlines tell part of the story

September 29, 2008, The Mercury News – “UC Irvine hospital’s anesthesiology records probed”

September 25, 2008, The Orange County Register – “UCI doctors faked surgical records, report says”

September 26, 2008, Los Angeles Times – “UCI Medical Center put under state supervision”

September 16, 2008, Los Angeles Times – “UC Irvine anesthesiology section head to step down”

An August 15, 2008 letter from the Centers for Medicare and Medicaid Services (CMS) to the University of California Medical Center Irvine states that “effective the date of this letter we are removing your status as a provider.  The hospital … may be subject to termination of its Medicare provider agreement.  

          The major issue was related to a practice in which anesthesiologists filled out anesthesia records before the surgery commenced.  For example in one case a medical record for a patient was filled out three months before an endoscopy was performed.  In another the anesthesia record noted that the patient left the OR at 10:30, but this notation was made at 9:30 while surgery was still in progress.  There was no evidence that any patients were harmed but this practice is considered falsification of records.  Apparently the practice started as a result of pressure to decrease turn around and move patients out of the OR faster.  In a September 26th e-mail to medical center employees the Vice Chancellor stated that the behavior described above “is absolutely unacceptable, unallowable, and never should have happened… the individual physicians involved…have been referred to the Medical Executive Committee for review and appropriate sanctions.”  There were also issues related to documentation of anesthesia machine maintenance and the adequacy of after hour’s coverage.  The Orange County Register has the most complete coverage including a link to the CMS Statement of Deficiencies (a 30 plus page document outlining in the issues in detail).

          Why the fuss?  All admit that no harm was done to these patients.  First the CMS is the largest health care payer in the country.  Loss of Medicare provider status may mean bankruptcy for a hospital. Second, falsification of medical records is a crime at some level in all States.  Third, falsification of records may lead to issues of fraud with respect to billing since anesthesia services are billed on the basis of time as well as case difficulty.  The penalties for fraudulent Medicare billing are draconian.  It does not appear that any of the anesthesiologists personally benefited from this practice; the practice as far as I can tell from the newspaper articles was related to productivity pressures.  Trying to solve demands for faster turn arounds and increased productivity by using unorthodox short cuts may compromise one’s professional status.  As noted in prior posts of this nature, the material has been gathered from a variety of public sources and my interpretations may not be accurate, though they are made in good faith

 

David S. Smith, M.D., Ph.D.

Poorly maintained anesthesia machine associated with awareness under anesthesia

Four hospitals in California were recently fined $25,000 each for serious mistakes resulting in patient harm or death.  Among the incidents was the use of a malfunctioning anesthesia machine which resulted in three patients being partially awake during their surgery.   With respect to the anesthesia machine the California Health and Human services Statement of Deficiencies notes that on 3/28/08 an Anesthesiologist expressed some question about the functionality of the anesthesia machine during a surgical procedure.  The same anesthesia machine was used again on 3/31/08 for three more surgical procedures.”  Source: San Diego Union Tribune, August 16, 2008.  In at least one of the three cases of awareness there were hemodynamic signs suggesting that too little anesthetic drug was being given.  None of the articles commented on the availability of or use of agent analyzers.  Also unclear is why it took 3 cases of awareness on the same day in the same OR before the machine was taken out of service.  It is cases such as these that fuel the national call by some groups and individuals for mandatory use of brain electrical activity monitors during general anesthesia.  As I have noted in past posts, there is considerable difficulty in interpreting and abstracting newspaper articles that deal with legal or potental legal issues.  I may have erred in some of my interpretation.

 

David S. Smith, M.D., Ph.D. 

Poor office records leads to pain medicine doctor being sanctioned by medical board

    An anesthesiologist specializing in pain medicine has been disciplined by the Texas Medical Board for “non therapeutic prescribing.”  One of his patients was admitted to an emergency room for a prescription overdose.  The Board’s citation related to failing to recognize that the patient was a drug abuser and prescribing drugs despite a lack of symptom improvement.  In a second case the physician had no records of the narcotic prescriptions he gave to a patient.  In essence the physician's records did not explain why he was prescribing, what he was prescribing or how much.  For this he will be under supervision for two years with his office records monitored by another physician.  He is also required to take 10 hours of pain management courses each year.  Source: Weatherford Democrat. September 12, 2008.

    Attemping to decipher court cases or legal adminisrative actions from newspaper accounts can be difficult.  Despite the risk of misinterpretation newspaper accounts are often the only readily available source of informaton.

 

David S. Smith, M.D., Ph.D.

Inhalation anesthetics produce damage by disrupting intracellular calcium homeostasis

Huafeng Wei continues his investigations into inhaled agent toxicity.  Using chicken lymphocytes he demonstrated that isoflurane, desflurane and sevoflurane at 2 MAC for 24 hours produced cell damage by increasing cytosolic calcium.  The calcium came from the endoplasmic reticulum.  In IP3 deficient lymphocytes this damage calcium translocation and cell damage did not occur (IP3 is a calcium channel located on the endoplasmic reticulum).  Isoflurane had a much greater effect than did desflurane or sevoflurane.  The clinical significance of these findings are as yet not clear.  The doses and duration of exposure was high for all three agents.  However from a mechanistic viewpoint these findings add to our understanding of the effect of inhaled anesthetics on intracellular calcium control (Yang H et al: Inhalational anesthetics induce cell damage by disruption of intracellular calcium homeostasis with different potencies.  Anesthesiology 2008;109: 1 – 8).

 

David S. Smith, M.D., Ph.D.

Heart failure is a significant risk factor in patients undergoing non cardiac surgery

Hammill and colleagues (Anesthesiology 2008;108:599 – 67) compared operative mortality and 30 day readmission for 159,327 Medicare patients undergoing non cardiac procedures.  Heart failure (HF) patients constituted 18% of his group, 34% of the patients had coronary artery disease (CAD) and 47% had neither condition (N).  Overall mortality was 8% in the HF group compared to 3.1% in the CAD group and 2.4% in the N group.  Thirty day readmission rates were also significantly higher for the HF group (17.1%) compared to the other two groups (CAD 10.8% and N 8.1%).  Specifically the risk of operative mortality was 63% greater in HF patients than in patients without HF or CAD.  The authors note that most of the anesthesia guidelines for patients with heart disease focus on coronary artery disease, yet 20% of the elderly present for common surgical procedures had heart failure.  There findings for HF prevalence are at variance with prior studies suggesting that HF was present in about 5 – 12% of the general surgical population.  The authors felt that this may be due to the small sample size of many of these earlier studies.  This study has demonstrated that patients with HF have substantially greater risk of death and 30 day readmission and the authors call for more studies to develop optimal management for this group of patients.

 

David S. Smith, M.D., Ph.D.

The circulatory effects of beta type natriuretic peptides

Atrial Natriuretic Peptide: Atrial natriuretic peptide (ANP) is mainly secreted from atria in response to excessive stretch (volume expansion).  It is a 28 amino acid polypeptide.  It attaches to cell membrane receptors with subsequent activation of guanylyl cyclase.

          ANP is a direct vasodilator.  ANP increases water (diuresis) and sodium excretion (natriuresis) by the kidney due to effects both on the glomerulus and the tubule.  Hypervolemia triggers ANP secretion e.g. heart failure, renal failure.  Furthermore, ANP serum levels will return to normal with successful therapy of the hypervolemic state.

 

Brain Natriuretic Peptide: Brain natriuretic peptide (BNP) was initially identified in the brain but is also present in the heart, particularly the ventricles.  It is a 32 amino acid polypeptide secreted by the ventricles in response to excessive myocardial stretch.  The circulating concentration of BNP is less than 20 percent of that of ANP in normal subjects, but can equal or exceed that of ANP in patients with congestive heart failure.

          BNP is a vasodilator and thus decreases systemic vascular resistance.  BNP also increases salt excretion by the kidney (natriuresis).

          The effects of ANP and BNP are a fall in systemic blood pressure, an increase in cardiac output and a decrease in blood volume.  They also both inhibit the renin-angiotensin system as well as systemic and renal sympathetic activity.

          The release of both ANP and BNP is increased in heart failure due to the high filling pressures. The plasma concentrations of both hormones are high in asymptomatic and symptomatic left ventricular dysfunction, permitting their application not only in diagnosis but also prognosis of heart failure.

          BNP may have a therapeutic role in heart failure due to its hemodynamic effects.  The drug, nesiritide (recombinant human BNP), has been approved for the therapy of acute decompensated heart failure.  Its full application will not be discussed here.

 

JG Augoustides, M.D.

Associate Professor of Anesthesiology and Critical Care

University of Pennsylvania

Cost of potentially preventable complications in surgical patients

The cumulative additional cost of potentially preventable complications in surgical patients may be as high as 1.5 billion dollars a year.  Encinosa and Hellinger (Health Services Research, early view July 2008, DOI: 10.1111/j.1475-6773.2008.00882.x) examined 5.6 million enrollees in the 2001- 2002 MarketScan Commercial Claims and Encounters Database (a data base of medical care claims data for 45 very large employer-sponsored benefit plans) and identified 161,004 patients with a major surgery admission who did not have another admission for major surgery within the prior 90 days.  The authors examined 14 patient safety indicators (PSI) which were grouped into technical problems (anesthesia complications, accidental lacerations, foreign body left in, transfusion reaction and similar events), infections (related to medical care, sepsis), pulmonary and vascular problems (pulmonary embolism and DVT), acute respiratory failure, metabolic problems, wound problems (such as hematoma or dehiscence) and nursing sensitive events (post op hip fracture, decubitus ulcers for example).  They identified 4,140 pts with an identified PSI and matched them to patients without an identified PSI.  They found that 2.6% of the patients who underwent major surgery had at least one of the 14 PSIs.  About 5.6% of this group had more than one PSI.  Patients with PSIs had a 90 day death rate of 6.3% compared to 0.6 in those without a PSI.  The 90 day readmission rate was 15% compared to 5.5%.  The 90 day cost for surgery was $66,879 on the average in those with PSIs compared to $18,284 for those without.  Post operative acute respiratory failure was the most expensive of the PSI groups costing $106,370 over the 90 day period and it had the highest 90 day death rate (12%).  Infection however had the highest readmission rate.  This is one of the first papers to determine complication rates and their costs beyond the period of hospitalization.  Costs from PSI continue after discharge.  The database represents a non medicare population and includes 4% of the commercially insured individuals in the United States.  The 14 PSIs examined account for 11% of the 90 days deaths, 2% of 90 day readmissions, and 2% of all 90 day expenditures after major surgery.  Decreasing the incidence of these PSIs could greatly decrease medical costs and improve the “bottom” line of acute care institutions.

 

David S. Smith, M.D., Ph.D.

Dead after knee surgery, a story of apparent multiple little failures

A 76 year old male entered a hospital for elective knee surgery.  Roughly twenty four hours after the surgery he was dead.  If the article, which appeared in the News and Observer, Raleigh, N.C. (June 8, 2008) , is at all accurate, the patient died because his doctors and nurses did not communicate with each other and no one was willing to say “stop.”  The article describes a series of “little” failures the cumulative effect of which was a fatality.  Note the following:  1) the apparent failure of those in the pre operative area to investigate what appeared to be a marked change in the patient’s medical condition, 2) an anesthesiologist who initiated treatment for angina but who did not appear to have communicated either orally or in writing about his observations or therapy (no progress note), 3) there appeared to be no one who willing to “stop” the operation for additional clincical investigation, 4) surgeons who appeared to deny any responsibility for knowing the patient’s medical condition just prior to surgery, 5) there were apparently multiple failures at many levels to document clinical findings and therapy, 6) an apparent failure to inform those responsible for the patient’s care post operatively about the suspected CHF and angina, and 7) delays in obtaining laboratory results.  Whatever time was “saved” by staying on schedule was lost many times over in the time required to be present at the multiple investigations and answer many hours of questioning.  Does the problem of communication and documentation sound familiar? (link to article: http://www.newsobserver.com/news/story/1100507.html )

 

David S. Smith, M.D., Ph.D.

Factor VIIa

The current “love affair” with recombinant factor 7a (rFVIIa) is growing.  What started as a replacement therapy for factor 7 deficient patients has now become a near first line therapy for bleeding thought to be refractory.  However recognize that the approved indications listed in the package insert only involve patients with hemophilia A and B, acquired hemophilia, and congenital FVII deficiency.  The growing list of other uses is “off label.”

            Aldouri reviewed the use of rFVIIa for controlling surgical bleeding in non hemophiliac patients (1).  In one small open labeled study in post operative cardiac surgery patients, doses of 30 mcg/kg given every three hours for a maximum of four doses or until bleeding was controlled resulted in a marked decrease in blood loss despite prior failure of conventional measures.  There have been similar positive results in patients with non cardiac surgical bleeding and in some trauma patients.  The first reported use in a trauma patient was with doses of 60 mcg/kg given at hourly intervals.

            Bowman et al reported on the use of rFVIIa to control post operative hemorrhage after complex cardiovascular surgery.  They performed a retrospective chart review to identify 36 patients who received this drug.  The criteria for use included: exclusion of all surgical causes of bleeding, failure to reverse coagulopathy with adequate pharmacologic and blood product replacement, correction of core body temperature to normal, adequate heparin reversal with protamine and chest tube drainage grater than 3 ml/kg/h or more for 2 hours or more.  With the most commonly used dose of 90 mcg/kg, bleeding was controlled in 30 of the 36 patients.  In 27 patients one dose was sufficient to achieve control.

            The early positive experience in the use of rFVIIa led Martinwitz and collaborators (3) to develop dosing guidelines for its use in trauma patients.  They suggested a dose (130 mcg/kg) that was about 30% greater than recommended for hemophiliacs.  In an initial cohort of 36 patients cessation of bleeding was obtained in 26 (72%).  Nine of the ten patients who did not respond exsanguinated in less than 24 hours.  More recently Spinella and associates (4) suggested that early use of rFVIIa may decrease 24 hour mortality in combat casualties who required massive transfusion (> 10 units of red blood cells within 24 hours).  The rFVIIa protocol called for an initial dose of 120 mcg/kg after the initial 4 – 6 units of RBC in patients with life threatening hemorrhage.  The authors conducted a retrospective review of 124 patients 49 of whom received rFVIIa and 75 who did not.  Twenty four hour mortality was 14% in the group that received rFVIIa and 35% in those who did not.  Thirty day mortality was also significantly better in the treated group.  They emphasize that rFVIIa alone is not adequate.  They encourage aggressive correction of acidosis and hypocalcemia.  They also emphasize the importance of adequate concentrations of platelets, fibrinogen and coagulation factors.  Note that the results from combat casualties my not be directly applicable to trauma patients typically seen at HUP.  Except for the cardiac surgery literature there is little that I could find that would apply directly to our trauma patients or other patients with uncontrolled intraoperative bleeding.  Regardless of the findings in the studies just cited a local protocol calls for a dose of 90 mcg/kg (rounded to the nearest 1.2 mg) infused intravenously for ongoing, non surgical bleeding refractory to conventional therapy.  Patients need to meet  the following criteria: patients without known coronary artery disease or peripheral vascular disease; transfusion of greater than 10 units of red blood cells with an ongoing requirement and no evidence of surgical bleeding.   The dose can be repeated in two hours if bleeding persists.   However, Novo Nordisk has just stopped a phase 3 clinical trial of NovoSeven brand rFVIIa in blunt trauma patients.  The reason for stopping the trial was an interim analysis that suggested  the end point of improved 30 day mortality and morbidity could not be reached because of a much lower than expected mortality in the overall study groups.  535 patients out of a planned 1502 had been enrolled in a 24 country, randomized, double blind, placebo – controlled trial using three single doses of rFVIIa (200 mcg/kg followed by 100 and 100 mcg/kg).  A recent review of the use of rFVIIa for the control of bleeding assessed the results of 17 randomized controlled trials (5).  Some of the trials used rFVIIa in an attempt to reduce blood loss during surgery with high blood loss.  Others were designed to examine the effect of rFVIIa on gastrointestinal bleeding, trauma or intracranial hemorrhage.  The authors concluded that, at present, the benefits of rFVIIa to control bleeding have not been demonstrated and that the rate of thrombotic complication may be higher than many anticipated.  What is clear from this study are the relatively few well controlled trials that have been done and that enthusiasm may be exceeding evidence. 

            From the package insert (2008), the risk of thrombotic adverse events is thought to be low.  Patients with disseminated intravascular coagulation, advanced atherosclerotic disease, crush injury or septicemia may be at increased risk of developing thrombotic events.  The drug is intended for intravenous bolus administration only.  NovoSeven Coagulation Factor VIIa is supplied as a white, lyophilized powder.  It should be used within three hours after reconstitution.  It should be reconstituted using aseptic technique into the provided histidine diluent.  The 1 mg vial should be reconstituted in 1.1 ml, and the 5.0 mg vial into 5.2 ml so that the final concentrations are 1.0 mg/ml.  Do not inject the diluent directly onto the drug powder.  Aim the needle so that the diluent goes down the vial wall.  After adding the diluent, gently swirl the vial until all the material is dissolved.  The reconstituted solution is clear.  For surgery in hemophilia A or B patients the recommended dosing is 90 mcg/kg immediately before surgery and every 2 hours during surgery.  After surgery the suggested dosing depends on the type of surgery.  For minor procedures dose every 2 hours for 48 hours then every 2 - 6 hours; for major procedures dose every 2 hours for the first five days, then every 4 hours until healing has occurred.

            Thrombosis after rFVIIa is of growing concern.  O’Connell et al (6) reviewed the FDA adverse event file for the initial five years after drug licensure for US sales and found 431 submissions related to rFVIIa.  The reports (N=168) described 185 thromboembolic events.  Seventeen of the events occurred in patients with hemophilia while 151 occurred during unlabelled use, mostly for the treatment of active bleeding.  The adverse events included cerebrobvascular accidents (N=39), acute myocardial infarction (N=34), other arterial thrombosis (N=26), pulmonary embolism (N=32), other venous thrombosis including DVT (N=42) and clotted devices (N=10).  In 36 of 50 reported deaths, the probable cause of death was related to the thromboembolism.  There is greater concern about the potential of thrombosis after rFVIIa in patients with implanted devices.  Apostolidou et al (7) describes the acute formation of a left atrial thrombus (observed by TEE) within minutes after administration of rFVIIa (90 mcg/kg over 5 min) in a patient with a left ventricular assist device.  Dr. Augoustides relates his concern (personal communication) that the thrombotic risk associated with rFVIIa may be higher in patients exposed to ECHMO, LVADs, or other clinical situations in which blood is being exposed to a foreign material under nonphysiologic flow conditions.

            Ref 1) Aldouri M: The use of recombinant factor VIIa in controlling surgical bleeding in non-haemophiliac patients. Pathophysiol Haemost Thromb 2002;32(suppl 1):41-46. 2) Bowman LJ et al: Use of recombinant activated factor VII concentrate to control postoperative hemorrhage in complex cardiovascular surgery.  Ann Thorac Surg 2008;85:1669-77.  3) Martinowtiz U et al: Guidelines for the use of recombinant activated factor VII (rFVIIa) in uncontrolled bleeding: a report by the Israeli multidisciplinary rFVIIa task force.  J Thromb Haemost 2005;3:340-8.  4) Spinella PC et al: The effect of recombinant activated factor VII on mortality in combat-related casualties with severe trauma and massive transfusion.  J Trauma 2008;64:286-294.  5) Birchall J et al: Evidence for the use of recombinant factor VIIa in the prevention and treatment of bleeding in patients without hemophilia.  Transfusion Med Rev 2008;3:177-187.  6)  O’Connell KA et al: Thromboembolic adverse events after use of recombinant human coagulation factor VIIa.  JAMA 2006;295:293-298.  7)  Apostolidou I et al: Acute left atrial thrombus after recombinant factor VIIa administration during left ventricular assist device implantation in a patient with heparin-induced thrombocytopenia.  Anesth Analg 2008;106:404-8

David S. Smith, M.D., Ph.D.

Take away message with respect to HIT and Heparin Alternatives

1)      Determining the risk for heparin induced thrombocytopenia (HIT) should become part of the perioperative interview.  A patient may know if they had a severe prior reaction to heparin (thrombosis or thrombocytopenia).  However many Pts will probably not know that they have received heparin.  However, pts who have had cardiac bypass, vascular surgery, or an interventional cardiac procedure most likely had heparin exposure and are at risk of heparin related reactions if they received heparin within 90 days of the planned procedure.

2)      Be prepared to use alternative anticoagulation regimens for pts with a history of HIT or HITT.  In patients with renal failure or significant renal insufficiency argatroban will most likely be the drug of choice.  In patients at risk for liver failure or multi-organ failure lepirudin will most likely be used.  For cardiac bypass bivalirudin is becoming very popular.

3)      The direct thrombin inhibitors are dangerous drugs.  There is no reversal except metabolic elimination when given in excess.  They require careful monitoring of coagulation for safe titration.  In the operating room ACT is the most available monitor for level of anticoagulation.

4)      When rFVIIa is used in patients with implanted devices such a LVADS there may be an increased risk of significant thromboembolism.  Consider a reduced dose or slow administration to allow earlier recognition of complications.

 

David S. Smith, M.D., Ph.D.

Heparin Alternatives

Argatroban – This direct thrombin inhibitor is finding increasing use during vascular surgery and transplant surgery in patients in whom heparin is contraindicated.  It is also indicated for prophylaxis or treatment of thrombosis in patients with HITT or for patients undergoing percutaneous coronary intervention.  This drug (as are the two below) belongs to a group that interacts with free or clot-bound thrombin.  In so doing it inhibits the conversion of fibrinogen to fibrin.  There is no pharmacologic reversal in the case of drug overdose (this is true for all direct thrombin inhibiters).  This drug, as well as the other direct thrombin inhibitors, is difficult to titrate.  Changes in liver function can produce radical changes in drug requirement.  Argatroban is the drug of choice in patients with severely impaired renal function as it is eliminated mostly by the liver.  The half life is 30 – 51 minutes but this can increase to more than 3 hours in patients with hepatic impairment.  The major risk of this drug is hemorrhage.  Each 2.5 ml vial contains 250 mg of drug.  Mix with 250 ml saline for a final concentration of 1 mg/ml.  For heparin induced thrombocytopenia the initial infusion rate is 2 mcg/kg/min.  This should be adjusted so that the aPTT is 1.5 – 3.0 times the initial baseline value.  Infusions without a bolus reach steady state in 1 – 3 hours.  The dose should not exceed 10 mcg/kg/min.  For percutaneous coronary intervention the initial dose is 25 mcg/kg/min along with a bolus of 350 mcg/kg given over 5 minutes.  The ACT should be checked after 5 minutes and the procedure can start if the ACT is greater than 300 sec.  I could find no suggested dosing for vascular surgery or renal transplantation.  However Hallman et al described the use of argatroban during carotid endarterectomy.  They used a bolus of 150 mcg/kg followed by an infusion of 5 mcg/kg/min.  This dose regimen provided adequate anticoagulation (ACT > 200s) by 10 minutes after the bolus dose (the drug may have acted faster but this was the first post administration sample reported by Hallman et al).  Proper use of this drug in the operating room requires ACT testing before starting the drug and at appropriate intervals.  Considering the risk of this drug I would suggest having a second person confirm the correctness of each step of preparation and the infusion settings.  Do not use this drug based only on the information presented here, read package insert first.  I would also suggest consulting with someone experienced in this drug’s use.   Ref: Hallman SE et al: The use of argatroban for carotid endarterectomy in heparin-induced thrombocytopenia.  Anesth Analg 2005;100:946-8

 

Bivalirudin – This direct thrombin inhibitor is also seeing increased use when heparin is not an option.  It is being used during percutaneous transluminal coronary angioplasty (PTCA), percutaneous coronary intervention (PCI) and cardiopulmonary bypass when heparin is contraindicated.  In patients with renal impairment a reduced dose is required.  No dosage adjustment is required with hepatic impairment.  The elimination half life is 25 minutes in pts with normal renal function.  The elimination half life can increase to as much as 3.5 hours in dialysis dependent patients.  For patients undergoing PTCA or PCI the initial bolus is 0.75 mg/kg followed by an infusion of 1.75 mg/kg/h.  APTT or ACT should be used to titrate the dosage.  When used during bypass special precautions must be taken to prevent blood stagnation in the circuit.  The drug comes as a powder (250 mg).  It should be reconstituted into 5 ml of sterile water for injection; gently swirl to dissolve.  Dilute to 500 ml for a final concentration of 0.5 mg/ml.  Proper use of this drug in the operating room requires ACT testing before starting the drug and at appropriate intervals.  Considering the risk of this drug I would suggest having a second person confirm the correctness of each step of preparation and the infusion settings.  Do not use this drug based only on the information presented here, read the package insert first.  I would also suggest consulting with someone experienced in this drug’s use.

 

Lepirudin – The attending in the UPENN CTICU use this drug exclusively unless there is significant kidney dysfunction.  I am told that they use aPTT monitoring as often as q2 hours, particularly if they suspect worsening renal function.  A suggested initial infusion is 0.15 mg/kg/h for pts up to 110 kg.  The target is an aPTT range of 1.5 – 2.5 times normal.   This drug can also be used as an IV push and there is some data on SQ use.  The elimination half life is 1.3 hours and its route of elimination is via the kidney.  Antibodies may develop during lepirudin therapy and fatal anaphylactic reactions have been reported in patients re-exposed in a second or subsequent treatment course.  For infusion use a final concentration or 0.2 or 0.4 mg/ml.  Lepirudin can be diluted with 5% dextrose in water, or normal saline.  Reconstitut 2 vials (50 mg each) using 1 ml of sterile water for injection or 0.9% sodium chloride for injection for each vial.  The contents of both vials should then be transferred to either a 500 ml or 250 ml bag for infusion.  Proper use of this drug in the operating room requires ACT testing before starting the drug and at appropriate intervals.  Considering the risk of this drug I would suggest having a second person confirm the correctness of each step of preparation and the infusion settings.  Do not use this drug based only on the information presented here, read the package insert first.  I would also suggest consulting with someone experienced in this drug’s use.

Acknowledgements:  Yianni Augoustides and Jiri Horak from the UPENN Department of Anesthesiology and Critical Care and Gene Gibson from Pharmacy made critical contributions to this discussion of rFVIIa and heparin alternatives.  This section could not have been written without their help.  I also received helpful advice from Barbara Konkle, M.D., Professor of Medicine, Department of Hematology, Oncology Division and Brain Birmingham from the Pharmacy’s anticoagulation service. However I am responsible for any errors in this presentation.

David S. Smith, M.D., Ph.D.

Anticoagulation in patients with a history of adverse heparin reactions

Everywhere one looks there are seems to be patients who have had an adverse reaction to heparin.  These reactions can manifest themselves as a classic anaphylactic reaction (1), thrombocytopenia (HIT) or thrombocytopenia combined with thrombosis (HITT).  Considering the frequent exposure of patients to heparin in the medical environment even low rates of reactions to heparin can translate into fairly high numbers.  Think about all the places heparin is used, flush for portacatheters and other central lines, renal dialysis, anticoagulation for vascular surgery, open heart surgery, heparin coatings on implanted devices, and as part of the peripheral infusion of thymoglobulin in patients undergoing renal transplant.  The consequence may be significant.  The thrombosis after heparin exposure may be severe enough to cause limb loss or death, and bleeding may occur as a consequence of thrombocytopenia.  Do we need to start asking patients about heparin exposure history just as we do for latex?  Are there diagnostic groups of patients at higher risk?  Consider a patient with a history of unexplained thrombocytopenia during a previous hospitalization.  What further information is needed?  What studies?   If you suspect a prior adverse reaction to heparin how would you anticoagulate this patient for aortic valve replacement or for a lower extremity revascularization?  While in the hospital this patient develops DVTs in both calves.  How would you treat them?  If a patient is sensitive to unfractionated heparin, are they necessarily sensitive to low molecular weight heparin?

            Howell et al (2) obtained venous samples from 115 patients in an 80,000 visit per year inner city emergency department and found that 5% of the patients had heparin antibodies.  All of the patients in their study with heparin antibodies gave a history of hospitalization or medical procedure in the preceding 90 days.  Gluckman et al (3) examined the development of heparin antibodies in patients undergoing percutaneous coronary revascularization.  Of the 154 patients in their study, seven were positive for anti-platelet factor 4 heparin antibodies at baseline.  Of these patients 4 had received unfractionated heparin within the previous 6 months and 2 had received unfractionated heparin 3 days before the baseline blood sample.  Of the 94 patients negative for antibody baseline, 16 (17%) became positive after heparin exposure.  The quandary is that after CABG surgery 50% of patients may be positive for heparin/PF4 antibodies, yet less than 1% develops HIT.

            One of the more frustrating aspects of type 2 HIT and HITT is that there are, at present, no specific tests to identify patients at risk.  The presence of antibodies does not necessarily mean that the patient will develop a reaction.  Thus screening for anti-PF4 heparin antibodies is not a solution to the problem of which patients are at risk.  According to my hematology consultant prior exposure to heparin is not a reason to avoid heparin or to obtain antibody levels.  A prior history of a reaction to heparin provides a reason use heparin alternatives if anticoagulation is required.

            Ref: 1) Alonso MA et al: Thrombocytopenia and anaphylaxis secondary to heparin in a hemodialysis patient.  Clin Nephrol 2005;63:236-240). 2) Howell MD, Powers RD: Utility of thrombocytopenia as a marker for heparin allergy in adult ED patients.  Am J Emg Med 2006;24:268-270. 3) Gluckman TJ et al: Incidence of antiplatelet factor 4) Heparin antibody induction in patients undergoing percutaneous coronary revascularization.  Am j Cardiol 2005;95:744-747.

 

David S. Smith M.D., Ph.D.

Succinylcholine and urgent out of the OR intubations

Should succinylcholine continue to be the first line muscle relaxant for urgent out of the OR intubation?

Succinylcholine and rapid sequence intubation – Two different chapters written by different authors in Miller’s Anesthesia state that succinylcholine remains the muscle relaxant of choice for rapid sequence intubation (1,2).  However, they provide a huge list of clinical situations in which succinylcholine should not be used.  Stene and Grande challenge the conventional wisdom and with respect to trauma patients note that “many trauma patients present for anesthesia without a complete medical/anesthetic history … [so that] the side effects of succinylcholine must be taken seriously and balanced against the benefits of the drug (3).

Hyperkalemia and cardiac arrest after succinylcholine – There are many contraindications to the use of succinylcholine because of disease states that increase the risk of succinylcholine related hyperkalemia and cardiac arrest.  Many patients who require urgent out of the OR intubation may have one or more of the following:

•          Severe metabolic acidosis with hypovolemia

•          Severe abdominal infection – sepsis

•          Critical illness polyneuropathy

•          Prolonged immobilization (typically associated with prolonged neuromuscular blocking drug use)

•          Severe traumatic injury

•          Crush injury

•          Spinal cord injury

•          Stroke with hemiplegia or paraplegia

•          Closed head injury without peripheral paralysis

•          Muscular dystrophies

•          Guillian-Barre syndrome

•          Motor neuron diseases such as Amyotrophic lateral sclerosis

•          Severe burns

Difficulty in obtaining pertinent clinical information in acute situations – One of the key issues that might make succinylcholine an unacceptable risk in many of the out of the OR situations is the difficulty in obtaining the needed medical information.  The following are common:

1. The history provided and knowledge of the patient’s medical problems is often incomplete – regular nurse off floor, cover resident, etc
2. Those caring for the patient may not know the importance of certain clinical issues with respect to anesthesia care and safety and thus fail to provide key information.
3. The information provided may be wrong
4. The urgency of the clinical situation may preclude more than a cursory, if at all, chart review
5. The chart has no problem list
6. The chart is large, bulky and key information buried within it
7. The chart may have missing pages
8. There may be no standardized documentation of prior intubations
9. There may be no standardized chart location for airway or intubation information.

Risks of succinylcholine include myalgia, rhadomyolysis, prolonged paralysis, renal failure, and hyperkalemic cardiac arrest – One has to decide if the benefits of succinylcholine (rapid onset, usually rapid offset) outweigh the disadvantages in a given clinical situation.  With the ready availability of Laryngeal Mask Airways, the advantages of succinylcholine’s rapid offset in situations of “can’t ventilate” or difficult mask ventilation may be less important now than in the past.

Choice of muscle relaxant for urgent intubations in already hospitalized patients – Both vecuronium and rocuronium in high enough doses can provide reasonable intubating conditions in 60 seconds.  Neither drug produces hemodynamic changes at these high doses.   Both drugs are free of the risk of hyperkalemic cardiac arrest.  Rocuronium may have a slightly faster onset and offset then vecuronium.  Some assert that intubating conditions after high dose rocuronium are more uniform than after vecuronium.  The main disadvantage of either drug is that prolonged muscle relaxation creates the inability to do an immediate neurologic exam on the patient.  I would not think this is a critical issue in most situations.  However, if a non depolarizer is used provision must be made, after intubation, for anxiolysis, sedation, or amnesia as is appropriate for the particular patient; three or four hours of awake paralysis is not acceptable.

Dose of non depolarizing muscle relaxant for rapid sequence induction --

ROCURONIUM

–         Dose  1 – 1.2 mg/kg

–         Onset  60 s

–         Intubation conditions are good to excellent – 93%

–         Duration  50 min +

 

VECURONIUM

–         Dose    0.3 mg/kg

–         Onset  60 s

–         Intubation conditions are good to excellent – 96%

–         Duration  83 min +

Ease of use in urgent clinical situations – In a 100 kg patient (probably more typical than the traditional 70 kg norm), the 30 mg of vecuronium for a rapid sequence induction dose requires three 10 mg vials to be opened, diluent added, the container shaken and the dissolved drug then drawn up into three 10 ml syringes or one 50 ml syringe.  In contrast the 100 mg of rocuronium required is contained, already dissolved, in a single 10 ml vial.  From the point of view of ease of use, rocuronium is much better than vecuronium.

Conclusions and action plan – Because of the potential presence of many conditions that might lead to hyperkalemic cardiac arrest in the patient who requires urgent out of the OR intubation many feel that succinylcholine should no longer be the drug of first choice in this specific clinical situation.

When confronting the patient for a potential urgent out of the OR intubation ask yourself the following questions –

1)      Does the patient need intubation?

2)      Is direct laryngoscopy appropriate?

3)      Does the patient need an induction dose of a hypnotic drug?

4)      Does the patient need a neuromuscular blocking drug?

5)      Is a non depolarizing muscle relaxant suitable?

6)      If 5) is yes then decide on high dose vs. standard intubating dose

7)      Is there enough clinical information to determine the suitability of succinylcholine?

References –

            1)   Naguib M, Lien CA: Pharmacology of muscle relaxants and their antagonists in Miller RD (ed): Miller’s Anesthesia, Philadelphia, Elsevier, 2005, page 504.

            2)  Dutton RP, McCunn: Anesthesia for trauma in Longnecker DL et al (eds): Anesthesiology, New York, McGraw Hill Medical, 2008, page 2457.

            3)  Stene JK, Grande CM: Anesthesia for trauma patients in Longnecker DL et al (eds): Anesthesiology, New York, McGraw Hill Medical, 2008, page 1667.

            4)  For a very nice discussion of succinylcholine in ICU patients as it relates to cardiac arrest secondary to immobilization see Naguib M (ref 1) page 532.

 

David S. Smith, M.D., Ph.D.

Post operative mortality and morbidity

Investigators from the University of Pennsylvania using a retrospective analysis of 144,740 operations done within the VA system demonstrated that morbidity, but not mortality, increases when non emergent general and vascular cases are started after 4 p.m.  They concluded that when considering a nonemergent procedure, surgeons most bear in mind that cases starting after “routine business” hours may face an elevated risk of complications.  Kelz RR et al: Time of day is associated with postoperative morbidity: an analysis of the National Surgical Quality Improvement Program Data.  Ann Surg 2008;247:544-552

David S. Smith, M.D., Ph.D.

No payment for events deemed avoidable

In the push to force “medicine” to reduce or eliminate errors Medicare, some private insurance companies and many states are creating lists of events for which payment will not be made.  The lists of events for which payment will be denied varies between payers.  Here is the list recently published by the State of New York for Medicaid payments:

1. Surgery performed on the wrong body part;   
2. Surgery performed on the wrong patient;   
3. Wrong surgical procedure on a patient;   
4. Foreign object inadvertently left in patient after  surgery;   
5. Medication error;   
6. Air embolism;   
7. Blood incompatibility;   
8. Patient disability from electric shock;   
9. Patient disability from use of contaminated drugs;   
10. Patient disability from wrong function of a device;   
11. Incidents whereby a line designated for oxygen  intended for patient is wrong item or contaminated;   
12. Patient disability from burns;   
13. Patient disability from use of restraints or  bedrails; and   
14. Patient disability from failure to identify and treat hyperbilirubinemia (bilirubin in blood) in newborns.

David S. Smith, M.D., Ph.D.

The Frank Murphy Memorial Lecture 2008 - Fontan Physiology

This is a continuation of Dr. Cripes comments concerning adult congenital heart disease:

Fontan physiology represents a unique set of circumstances in cardiac performance.  This circulation is often associated with CHD, but may be seen in other cardiac pathology.  The primary situation occurring, regardless if it is a result of a congenital malformation of the heart or massive RV dysfunction, is the loss of a traditional right sided pumping mechanism.  The return of systemic venous blood is directed passively into the pulmonary circulation.  There is no RV to pump blood.  In Fontan physiology pulmonary blood flow and cardiac output are dependent on a transpulmonary gradient (TPG).  The TPG may be used as a guide to gage the forward flow of blood in the pulmonary circulation.  The TPG is estimated by taking the CVP minus the LVEDP (PCWP if using a Swan-Ganz catheter).  An ideal TPG is approximately 5-8 mmHg. 

            Goals in caring for patients with Fontan physiology may be broken down into pre-pulmonary/cardiac, pulmonary and cardiac.  The pre-pulmonary/cardiac goals in Fontan physiology include the presence of an unobstructed venous return to pulmonary circulation.  The importance of an adequate preload cannot be overemphasized.  These patients are exquisitely preload sensitive.  The patient needs widely patent anastomotic connections in the case of a surgically corrected CHD. 

            The pulmonary component may be thought of in terms of decreasing or increasing resistance to blood flow across the pulmonary vascular bed.  Patients need a low pulmonary vascular resistance, as well as unobstructed pulmonary arteries.  Normal lung parenchyma with no pulmonary vascular disease is typically a low resistance system (e.g. 1 Woods unit). Events that may raise PVR such as acidosis, hypercarbia and hypoxia will be harmful.  Ventilator settings should include low (<15-20 mm Hg) mean airway pressures and normal alveolar ventilation.   Overventilation with high airway pressures (e.g. Valsalva breaths) and the resultant decrease in venous return and increased PVR may be more harmful than hypoventilation, atelectasis and the resulting hypercarbia/acidosis.  High levels of PEEP will increase pulmonary vascular resistance and cause a decrease in pulmonary blood flow. 

            In terms of cardiac effects on Fontan physiology, the maintenance of NSR with normal systolic and diastolic function is important.  Ideally there will be no outflow obstruction and a competent valve system.

            In summary the most important objective when caring for patients with Fontan physiology include maintenance of adequate intravascular volume or preload.  An appropriate ventilation strategy which minimizes high mean airway pressures, while also preventing atelectasis, hypoxia and hypercarbia is important.  Cardiac function should be maintained as NSR with optimal performance.

Dr. Cripe has recently completed his training in Anesthesiology at the University of Pennsylvania

The Frank Murphy Memorial Lecture 2008 - Congenital Heart Diseases

Chad Cripe, M.D., gave the Frank Murphy Memorial Lecture for 2008 on the subject of the implications of congenital heart disease in adults (CHD).  His major points for CHD are as follows:

Congenital heart diseases (CHD) may encompass a number of different structural lesions in the fetal circulation that persist after birth.  Some may be life threatening, requiring immediate surgical correction.  Others may go unnoticed until symptoms of advanced disease present themselves.  A physiologic classification of CHD exists in order to allow grouping of similar lesions.  These classifications include shunts, mixing lesions, obstructive lesions and regurgitant lesions. 

Shunts are lesions that produce abnormal blood flow within the heart from left to right or right to left.  In left to right shunts, such as ASD, VSD and PDA, some of the blood in the left side of the heart is directed to the right side of the heart without being delivered to the peripheral circulation.  This creates an excess volume overload on the heart.  In the case of right to left shunts, such as in Tetralogy of Fallot, Pulmonary Atresia and Eisenmenger complex, blood is diverted to the left heart without picking up much needed oxygen in the lungs.  This creates problems of hypoxia for these patients. 

Mixing lesions, such as transposition of the great arteries, tricuspid atresia and univentricular heart, represent the most complex type of CHD.  As the term mixing lesion implies, there is often a mixing of oxygenated and deoxygenated blood occurring in these patients.  The degree of mixing is often represented by the Qp:Qs ratio.  Qp represents flow to the pulmonary system, whereas Qs represents flow to the systemic circulation.  In healthy individuals the Qp:Qs ratio is approximately 1:1 (there exists a small amount of blood that is diverted back to the right heart from the pulmonary/bronchial circulation and cardiac thesbian vessels without being oxygenated).  The degree of shunting is variable and may often change quickly depending on the patient’s clinical situation.  Factors that increase or decrease pulmonary vascular resistance (PVR) will directly affect the Qp:Qs ratio.  Patients often develop some degree of cyanosis.  Changes in vascular resistance can also affect patients with shunting lesions.  For example, in patients with Tetralogy of Fallot, an increase in systemic vascular resistance leads to increased pulmonary blood flow and improved oxygenation.  In contrast, systemic vasodilation often leads to increased right to left shunt, hypoxia and cyanosis.

Obstructive lesions include pulmonic stenosis, aortic stenosis, coarctation of the aorta, mitral stenosis and hypoplastic left heart syndrome.  In these situations the heart sees a pressure overload as a result of the obstruction.  Signs of pressure overload may develop such as an increase in systolic and diastolic BP and and an increase in LV wall thickness. 

Regurgitant lesions are rare in CHD, yet may be seen commonly in some adult settings.  Ebstein’s anomaly is a congenital downward displacement of the tricuspid valve which occurs rarely in newborns.  The tricuspid valve becomes regurgitant and signs of volume overload may occur, such as an increase in diastolic BP, wall thickness and radius of the ventricle.

Dr. Cripe has recently completed his training in Anesthesiology at the University of Pennsylvania

When to give muscle relaxants after anesthesia induction

A recent editorial and a letter to the editors of Anaesthesia challenge the usefulness, safety and validity of the teaching that one should “prove the ability to ventilate by mask before giving a muscle relaxant”.  Both authors claim that the opposite may occur; that the act of trying to ventilate a lightly anesthetized patient by mask may actually create the airway obstruction and that NMBs are probably a better rescue approach for not being able to ventilate than hoping the patient will resume spontaneous ventilation. Refs: Calder I: Could “safe practice” be compromising safe practice? Should anaesthetists have to demonstrate that face mask ventilation is possible before giving a neuromuscular blocker? Anaesthesia 2008;63:113-115; Priebe HJ: Could “safe practice” be compromising safe practice? Should anaesthetists have to demonstrate that face mask ventilation is possible before giving a neuromuscular blocker (letter)? Anaesthesia 2008;63:671-672.

Dr. Levy a senior faculty member at the University of Pennsylvania rebuts as follows: “the assumption by both the editorial and the letter to the editor  is that the inability to ventilate the patient will not result in a change in clinical approach and that, in most cases, the administration of a neuromuscular blocking drug will occur anyway. What the authors failed to consider is that, based on the ability (or inability) to ventilate, the selected neuromuscular blocking drug may change. For example, instead of giving vecuronium, one might opt to use succinylcholine for more rapid onset. Even if face mask ventilation were successful, one might elect a more rapidly acting agent if there were considerable difficulty in obtaining air exchange. Although this does not invalidate the arguments presented, it does suggest that more complete consideration of the process might lead to different conclusions than those presented.”

Warren Levy, M.D., is Associate Professor of Anesthesiology and Critical Care at the University of Pennsylvania

David S. Smith, M.D., Ph.D.

Nasotracheal and orotracheal intubation are both associated with a about a 12% incidence of bacteremia but this may not be clinically significant

Valdes et al did a prospective study of 110 patients undergoing surgery under general anesthesia.  Venous blood samples were obtained before and then 30 seconds after intubation.  Bacteremia after tracheal intubation was detected in 6 of 50 patients who had orotracheal intubation and 7 of 60 patients after nasotracheal intubation.  Seven of the isolates (54%) were resistant to oxicillin.  Two patients had positive pre intubation blood cultures.  The authors discuss the controversy concerning the need of antibiotic prophylaxis for tracheal intubation in patients at risk for bacterial endocarditis.  They suggest that antibiotic prophylaxis should be considered after both orotracheal and nasotracheal intubation.  Valdes C et al: The incidence of bacteraemia associated with tracheal intubation.  Anaesthesia 2008;63:588-592.

PJ Brennan, an infectious disease specialist at the University of Pennsylvania raises concerns about the potential conclusions of this article. “I just want to note that bacteremia after events involving disturbance of colonized mucosal surfaces results in transient bacteremia very frequently. Dental procedures are best known for such events but many other procedures including tooth brushing, endoscopy, bowel movements and child birth are all associated with the common occurrence of bacteremia – most of these are reported to be more common than the incidence reported here after intubation. I suspect that any interruption of a mucosal surface, however minor, can cause bacteremia. The key issue is the incidence of endovascular infection after such events. In all other settings bacteremia is transient and the establishment of an endovascular infection is rare. The factors in determining prophylaxis include not only the bacteremia, which is a given, but the cardiovascular risk as well. I would not want to see this become a practice we adopt given the frequency of the index event (intubation), the infrequent nature of the adverse event (endovascular infection), the tenuous cause and effect association and the hazard of antibiotics and drug resistance.”

PJ Brennan M.D. is Professor of Medicine, Division of Infectious Diseases and Chief Medical Officer for UPHS.

David S. Smith, M.D., Ph.D.

Bad news for tight intraoperative glucose control

Dr. Kofke calls our attention to this prospective randomized study of tight intraoperative glucose control using insulin infusion compared to “conventional” management with tight control in both groups during the post operative period.  Four hundred cardiac surgery patients were randomly assigned to tight glycemic control (blood glucose levels between 80 – 100 mg/dl) during surgery or conventional glucose control.    Patients who did not become hyperglycemic during surgery were not included in the analysis.  Pre operatively the glucose levels were similar in both groups.  At the conclusion of cardiopulmonary bypass the mean blood glucose level in the tight control group was significantly lower (123 mg/dl) compared to 148 mg/dl in the conventional glucose control group.  All patients in the intensive treatment group received insulin during surgery and 15% of the patients in the conventional therapy group received insulin.  At the end of 24 hours in the ICU the mean glucose levels were the same in both groups (about 106 mg/dl, mean).  The two groups did not differ in the primary composite endpoint of sternal infection, death, prolonged ventilation, cardiac arrhythmias, stroke or renal failure.  Nor did investigators find a direct benefit from intraoperative from intensive insulin therapy for and of the individual components of the composite end point.  In fact the reverse result was obtained.  The intensive treatment group had significantly more strokes (8 vs. 1) and deaths (4 vs. 0) than the conventional treatment group.  There was no treatment effect for length of stay in the ICU or hospital.  The authors note that this does not directly contradict prior findings of benefits from tight glucose control as the key studies involved tight control vs. conventional control during the entire period from OR through ICU.  It is possible that tight glucose control during the relatively brief period of surgery is not as important as tight glucose control during the longer post operative period.  Gandhi GY et al: Intensive intraoperative insulin therapy versus conventional glucose management during cardiac surgery.  Ann Intern Med 2007;146:233-243

Dr. WA Kofke is Professor of Anesthesiology at UPENN

David Smith, M.D., Ph.D.