Images in Clinical Medicine - Quiz

A patient is transferred to the ICU for stabilization prior to surgery. The patient is complaining of back pain. The blood pressure is 180/110 and the heart rate is 95 per minute. The surgeon says that he wants the patient optimized and that the patient needs emergency surgery.

• Based on the CT scan slices that are shown, what does the patient have?
• Do you agree with the surgeon's decision, based on the limited CT views?
• What would you do to "optimize" this patient?
• What further information about this patient do you want?

This image and the clinical scenario were contributed by Daniel Zurcher (Washington University final year medical student).

More on this post to follow...

Are intensivists prognostic pessimists?

An article appeared in the British Medical Journal suggesting that ICU clinicians have unwarranted prognostic pessimism that results in some patients, who might otherwise survive, being denied admission to ICU. In this study, clinicians were asked to estimate the likelihood of survival of patients with COPD and asthma exacerbations who required admission to ICU. The study found out that clinicians underestimated six-month survival by 13%. Sixty two percent of patients survived compared with the clinicians’ prediction of 49%.

• To me this seems like pretty good prediction. But I’m, after all, just a lousy ICU clinician.
• I have worked in both the UK and the US medical systems. My impression is that, if there is a tendency to unwarranted prognostic pessimism in the UK, there may be a tendency to unwarranted prognostic optimism in the US.
  

Clinician pessimism, according to the article, was particularly marked for the patients with the poorest clinician prognosis. Clinicians predicted a 180-day survival of around 3%, whereas the actual survival was 36%.

• The most important question may not be whether the patients survived, but rather how they survived. If they survived with a good quality of life, then the poor prognostic prediction – prognostic pessimism - could have had dire consequences. If they survived with a miserable quality of life, choosing not to pursue ICU admission may have been appropriate.

• Why may ICU clinicians be prognostic pessimists? Is this true for all clinicians? My experience is that surgeons are prognostic optimists. When I have expressed pessimism about a patient’s prognosis, my surgical colleagues have often pointed out that my seeing patients at their sickest biases my perspective. When patients recover, they often recover dramatically. When we discharge patients from the ICU, they are usually still debilitated. So, perhaps, as intensivists, our perspective is skewed.

A major concern about prognostic pessimism is that we are not uniform in our assessments. Many clinicians focus on different information, and this may lead them to form different conclusions. All ICU clinicians do not reach the same conclusions about a patient’s prognosis even when they are privy to the same information. This has been used to support the implementation of “objective outcome prediction models”. Such models, however, are also error prone as they work for populations BUT not for individuals.


One of the most poignant opinion pieces I have read appeared recently in the journal, JAMA. An experienced ICU clinician was confronted with a dreaded situation; his father had metastatic cancer and was critically ill. His condition was complicated by renal failure. The father and the physician’s family looked to him for guidance. The clinician confessed that being emotionally vested complicated his decision-making and may have affected the clarity of his thinking. After much deliberation, his father and his family, with his sanction, decided not to initiate dialysis. The father died. The ICU physician may at times second-guess this tough decision in moments of emotional turmoil. But, this decision was undoubtedly motivated by love and compassion, and required tremendous strength of character from all parties. In such difficult circumstances, it is vitally important that efforts are made to ensure that all family members are like-minded and agree with the chosen course of action.

Decisions regarding the pursuit of aggressive therapy versus palliative care must be addressed with patients and their families by physicians who are competent and experienced in end-of-life care as this will have a profound impact on both the quality of care delivered and effective use of limited hospital resources. A major problem is that regional culture plays an important part in end of life decision-making. Such cultural differences not only affect patients and their families but also the health care workers who make and carry out such decisions. This can lead to tension if there are cultural differences between physicians and patients’ families or among health care workers themselves.



Perspectives from a biased ICU Clinician:

1. Sometimes withholding or withdrawing advanced life support is the most compassionate course.
2. Quality of life, not just survival, should be considered in making decisions.
3. It may be helpful to seek the opinion of a colleague who is not emotionally vested in the care of a patient.
4. We should ask ourselves whether our judgment might be clouded by prognostic pessimism.
5. Prognostic optimism may be a euphemism for fear of litigation or defensive medicine.
6. For an optimistic perspective, always consult a surgeon.
7. The right to a dignified death should be viewed as a fundamental human right, just as the right to a dignified life is.
8. Unwarranted prognostic pessimism may lead to patients being denied life-saving interventions.
9. Unwarranted prognostic optimism may lead to patients being denied a dignified death.
10. Even the most insightful clinician may misjudge a patient’s prognosis. It may be better to err on the side of optimism than that of pessimism.
    

A Little Squeeze Goes a Long Way

A recent paper published in the Lancet renewed our interest in preconditioning, specifically remote preconditioning (RIPC). 57 patients undergoing CABG were randomly assigned to receive three 5-min cycles of right upper arm ischemia, which was induced by an automated BP cuff with the idea that ischemia in one vascular bed will afford protection in another – in this case the heart. Troponin T levels were taken before surgery and at 6, 12, 24, 48, and 72 hours after surgery.

What did they find?

1. A reduction in troponin T levels starting at 6 hour.
2. 43% reduction in the area under the curve between control and treatment group.
   
   

Are the findings important?

• This study used a surrogate maker to try to predict clinical outcomes. Although, there is a reduction in the level of Troponin T in the treatment group does this translate to meaningful clinical outcomes (eg. Atrial fibrillation, length of stay, etc). The authors do not report these findings. Certainly, we are concerned about myocardial injury, but a difference between a Troponin of 0.4 vs 0.7 is that clinically significant?

Are there any concerns?

• The authors reported no ill outcome in the treatment group. However, there maybe ethical concerns with the study design. Numerous papers have demonstrated the cardioprotective effects of volatile anesthetic. In this study a total intravenous anesthetic technique was used to perhaps amplify the results.
  

What should the intensivist do?

1. The skeptics will argue that we should do nothing until firm evidence emerges. In fact if firm evidence emerges, it is probably wrong!
2. The zealots may argue that every ICU patient should have tourniquets applied to every limb, each of which (the tourniquets, not the limbs!) should be intermittently inflated. This may become a new market niche for MAST suits.
3. The intellectual enthusiasts may argue that we MUST do a raft of randomized controlled studies with RIPC on the ICU.
4. The pragmatists may argue that this is a benign intervention that should be used, unless there are specific contra-indications (eg. Vascular disease, fistula, etc.).

Clinical Conundrums in Critical Care

Here is a foretaste of topical debates you can expect at the 2007 Annual ASCCA meeting in San Francisco. We invite you to express your views as comments and to prepare for lively discussion!


Posted on behalf of Dr. Avery Tung

Clinical Conundrums:
A 59 yr F with metastatic ovarian cancer undergoes pelvic exenteration under GA.

Her past medical history includes COPD, CHF, OSA, HTN on an ACEI, obesity, and NIDDM. She has previously undergone radiation and chemotherapy (Mitoxantrone). She has no allergies, and was taking Enalapril, Lasix, Metoprolol, Metformin, inhaled Beclomethasone and Albuterol 2x/day preoperatively.

She has previously had uncomplicated GA for a knee arthroscopy. Her exercise tolerance is fair…she has to rest after climbing 1 flight of stairs…but can walk 3 blocks and work in the garden without become short of breath. She can lay flat. An echocardiogram done 6 months ago reveals EF=35%, mild MR

Her preoperative vital signs were: HR 79, BP 150/90, RR 20. SpO2 on RA was 93%. BMI = 30 (86kg, 5’5”) with mild ascites on CT scan. Hct 41%, Cr 1.2, HCO3 = 32 meq/dl, K = 3.5.

The case was 8 hours long. EBL was 500cc, 800cc ascites were drained, and U/O was 170cc. Total intake included 6.5L crystalloid, 3U PRBC, 2FFP.

Abg 1 hr prior to case end was 7.32/41/128 on 100% FiO2

The patient was left intubated and brought to the ICU postoperatively. On admission, she was sedated and unresponsive. BP 108/40, HR 105. Her lines include 2 18G IVs and a R radial arterial line. Abg: 7.30/45/82 on 50% with PIP = 42 cm H20. BE = -5, Hct = 28, HCO3 = 19.

1. Perioperative beta blockade in patients chronically on beta blockade is now a SCIP measure. This patient was on a beta blocker preoperatively. Would you restart beta blockers at this time?

• Poldermans D. N Engl J Med. 1999 Dec 9;341(24):1789-94.(FFT)
• Lindenauer PK. N Engl J Med. 2005 Jul 28;353(4):349-61. (FFT)
  
• Yang H. Am Heart J. 2006 Nov;152(5):983-90.
  
• Juul AB. BMJ. 2006 Jun 24;332(7556):1482. (FFT)
  
• Brady AR. J Vasc Surg. 2005 Apr;41(4):602-9.
  
• Kertai MD. Arch Intern Med. 2003 Oct 13;163(18):2230-5. (FFT)
  
• Poldermans D. J Am Coll Cardiol. 2006 Sep 5;48(5):964-9.
  
• De Backer D. Crit Care. 2005;9(6):645-6.
  
• Pearse R. Crit Care. 2005;9(6):R694-9. (FFT)
  

1. Would you implement lung protective ventilation in this patient (PIP <30)?

• Petrucci N. Anesth Analg. 2004 Jul;99(1):193-200. (FFT)
• Young MP. Crit Care Med. 2004 Jun;32(6):1260-5.
• Gajic O. Intensive Care Med. 2005 Jul;31(7):922-6.
  
• Schultz MJ. Anesthesiology. 2007 Jun;106(6):1226-31. (Review)
• Eichacker PQ. Am J Respir Crit Care Med. 2002 Dec 1;166(11):1510-4. (FFT - Meta-analysis)
• Weinert CR. Am J Respir Crit Care Med. 2003 May 15;167(10):1304-9. (FFT)
  

1. This patient has no central access. Would you place a central line?

Over next 4 hours U/O (cc per hour) is low: 15, 15, 10, 5 despite Lactated Ringers infusing at 150cc/hr IV. BP 105/60, HR 95, JP draining 100/hr serosanguinous fluid, Abg 7.28/45/85 on 60%.
The urine output is low. How would you react?:

a. Continue to observe
b. Crystalloid 500cc IV fluid bolus
c. Albumin 250cc IV fluid bolus
d. More information?

• Roberts I. Cochrane Database Syst Rev. 2004 Oct 18;(4):CD000567.
• Vincent JL. Crit Care Med. 2004 Oct;32(10):2029-38.
• Martin GS. Crit Care Med. 2005 Aug;33(8):1681-7.
  
  

You elect to seek more hemodynamic information:
Which hemodynamic monitor would you choose?

a. Echocardiogram
b. CVP
c. PA catheter

Which measure of circulatory function would you want?

a. SvO2 >65%
b. CVP >13
c. Lactate < >d. U/O >20 cc/hr

• Connors AF. JAMA. 1996 Sep 18;276(11):889-97.
• Wheeler AP. N Engl J Med. 2006 May 25;354(21):2213-24. (FFT)
• Friese RS. Crit Care Med. 2006 Jun;34(6):1597-601.
• Gan TJ. Anesthesiology. 2002 Oct;97(4):820-6.
• Nguyen HB. Crit Care Med. 2004 Aug;32(8):1637-42.
• Sandham JD. N Engl J Med. 2003 Jan 2;348(1):5-14.
• Rivers E. N Engl J Med. 2001 Nov 8;345(19):1368-77.
  

CXR now shows mild pulmonary edema. Abg now 7.26/52/60 on 60%. PIP = 36 and Hct = 26%. CVP = 14

Would you transfuse this patient?

• Corwin HL. N Engl J Med. 2007 Sep 6;357(10):965-76.
• Hebert PC. N Engl J Med. 1999 Feb 11;340(6):409-17.
• Wu WC. N Engl J Med. 2001 Oct 25;345(17):1230-6.
• Carson JL. Lancet 1996;348:1055-60.

The patient develops sepsis and ARDS. After 6 days, bowel function has not yet returned. Prealbumin = 11 and AM glucose = 196.

1. Would you begin TPN?
2. Would you initiate an insulin drip?

• Van den Berghe G. N Engl J Med. 2001 Nov 8;345(19):1359-67.
• Van den Berghe G. N Engl J Med. 2006 Feb 2;354(5):449-61.
• Gandhi GY. Ann Intern Med. 2007 Feb 20;146(4):233-43. (FFT)
  

See you in San Francisco!

Does Epo save lives?

Efficacy and Safety of Epoetin Alfa in Critically Ill Patients
Corwin et al. NEJM Volume 357:965-976. September 6, 2007.

A multicenter study was conducted whose primary objective was to demonstrate that the administration of epoetin alfa to critically ill subjects reduces the proportion of subjects requiring red blood cell (RBC) transfusion as compared with placebo. (ClinicalTrials reference)

Secondary outcomes included:
Cumulative number of units of red blood cell transfusions received from Study Day 1 through Study Day 42.
Change in hemoglobin from Study Day 1 through Study Day 29.
Mortality through Study Day 29.
Cumulative mortality through Study Day 140.

The study was a prospective, randomized, placebo-controlled trial, which enrolled 1460 medical, surgical, or trauma patients between 48 and 96 hours after admission to the intensive care unit. Epoetin alfa (40,000 U) or placebo was administered weekly, for a maximum of 3 weeks; patients were followed for 140 days.

What did they find?

1) No difference in red cells transfused.
2) Higher hemoglobin in the epoetin alfa group. (Hemoglobin increase = 1.6±2.0 g per deciliter vs. 1.2±1.8 g per deciliter, P<0.001)
3) A tendency towards decreased mortality in the epoetin alfa group, especially in the trauma subgroup. (adjusted hazard ratio for death at 140 days in the trauma subgroup, 0.40; 95% CI, 0.23 to 0.69)
4) Increased thrombotic events in the epoetin alfa group. (hazard ratio, 1.41; 95% CI, 1.06 to 1.86)

Are the findings important?

If epoetin alfa is associated with decreased mortality (independent of blood transfusion!), this is an important and new finding. The finding appeared to be most robust in the trauma patients. With any unexpected finding, it is necessary to ask whether this is merely a chance finding. Statistical significance alone is insufficient to justify a change in clinical practice. There has to be biological plausibility for a finding. The authors speculate that it may be the action of epoeitin alfa as a cytokine with antiapoptotic activity that leads to the reduction in mortality.(JAMA. 2005;293:90-95. Kidney International (2006) 70, 246–250. Critical Care 2004, 8:337-341.) {Link to a diagram showing possible cytoprotection with epoeitin alfa}

Are there safety concerns?

Absolutely. This study found an increased risk of thrombosis in the epoeitin alfa group. Previous studies in patients with renal failure and with cancer have shown that epoeitin alfa is associated with increased risk of thrombosis and even of increased mortality. (Lancet 2003; 362(9392): 1255-1260. J Clin Oncol 2005;23:5960-5972. J Natl Cancer Inst 2006;98:708-714. N Engl J Med 2006;355:2085-2098.)


Erythropoietin (Epo) binds its receptor (Epo R) on the surface of red blood cell progenitors in the bone marrow causing proliferation, maturation, and differentiation, thereby preventing or correcting anemia. Epo may also bind Epo R expressed on the surface of cancer cells and may elicit tumor growth via cell proliferation, protection from apoptosis, and/or angiogenesis. (See - Brower, V. (2003) Nat. Med. 9:1439.)

So what should the intensivist do?

1. Administer epoetin alfa to all anemic critically ill patients unless it is specifically contra-indicated.
2. Exercise clinical judgment (e.g. consider epoetin alfa in certain settings such as acute hemorrhage where patients are otherwise healthy and there is no known risk for thrombosis or cancer).
3. Await the results of further studies.
4. Conduct further studies yourself.
5. Be highly skeptical and take the view that this was an industry funded study of an expensive drug that showed questionable benefit and heightened known safety concerns.

Further Reading on Erythropoietin (Review articles with free full text):

• Arch Intern Med. 2004 Feb 9;164(3):262-76.
• Blood. 2000 Aug 1;96(3):823-33.
• Cancer. 2006 Jan 1;106(1):223-33.
• Chest. 2005 Nov;128(5 Suppl 2):576S-582S.
• Chest. 2005 Nov;128(5 Suppl 2):568S-575S.

Groundbreaking News - Insight into the Mechanisms of Action of Antibiotics

One of the major threats to global health today is antimicrobial resistance. An important finding was reported by Kohanski and others this month in the journal Cell. Researchers from Boston have discovered that there is a common mechanism of bacterial cell death induced by three different classes of bactericidal antibiotics. This common mechanism involves reactive oxygen intermediates or “oxygen free radicals.” This finding provides hope for finding new methods of combating infection. Scientists can focus on methods of amplifying the oxidative damage cellular death pathway or on inhibiting cellular repair mechanisms.


NADH oxidases located in the plasma membrane catalyze the formation of superoxide (O2-) anions. Superoxide is dismutated to hydrogen peroxide and molecular oxygen by superoxide dismutase (SOD). Catalase can convert hydrogen peroxide to water. A Fenton reaction can take place in the presence of peroxidases, leading to the formation of hydroxyl (OH-) radicals.

Here is the abstract to the intriguing article:
(From - Kohanski et al. Cell, Vol 130, 797-810, 07 September 2007)
Antibiotic mode-of-action classification is based upon drug-target interaction and whether the resultant inhibition of cellular function is lethal to bacteria. Here we show that the three major classes of bactericidal antibiotics, regardless of drug-target interaction, stimulate the production of highly deleterious hydroxyl radicals in Gram-negative and Gram-positive bacteria, which ultimately contribute to cell death. We also show, in contrast, that bacteriostatic drugs do not produce hydroxyl radicals. We demonstrate that the mechanism of hydroxyl radical formation induced by bactericidal antibiotics is the end product of an oxidative damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH, destabilization of iron-sulfur clusters, and stimulation of the Fenton reaction. Our results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.

Important Websites and Links

Here are some important websites. Please comment if you know of other sites that are of potential interest to critical care anesthesiologists.

• The American Society of Critical Care Anesthesiologists
• The American Society Anesthesiologists
• The Journal Anesthesiology
• The Journal Critical Care Medicine
  
• The Journal Intensive Care Medicine
  
• Society of Critical Care Medicine
  
• European Society of Intensive Care Medicine
  
• Anaesthesia UK (an educational site with an ICU component)
  
• The WorldWide Anaesthetist - Clinically relevant lectures on anaesthesia and intensive care
  
• British journal of Anaesthesia
  
• Canadian Journal of Anesthesia
  
• Critical Care (journal and forum)
  
• Chest (journal)
  
• American Journal of Respiratory and Critical Care Medicine
  
• Faculty of 1000 Medicine. Based on the recommendations of a selected faculty of nearly 2500 international researchers and clinicians, it systematically highlights and reviews the most pertinent papers in any field of medicine
  
• Critical Care Medicine Tutorials (University of Pennsylvania)
• Clinical Trials - see what trials are in progress and how they are designed
• ICU Delirium - a resource providing information about brain dysfunction on the ICU
  

Why Critical Care Medicine Is Important to the Future of Anesthesiology

Perspective of a Nonintensivist:
Why Critical Care Medicine Is Important to the Future of Our Specialty
Ronald D. Miller, M.D.
ASA April 2006 Newsletter (Extracts)

• The creation of critical care units and evolution of critical care medicine (CCM) as a specialty were originally brought about by anesthesiologists.
• In 2004 ASA President-Elect appointed a Task Force on the Future Paradigms of Anesthesia Practice to address the projected evolution of anesthesiologists’ clinical practices over the next 20 years.
• Based on a broad base of information, however, the task force concluded that tertiary care hospitals of the future will be increasingly dominated by seriously ill patients who require procedures (i.e., surgical, imaging, cardiovascular) and monitored and/or critical care beds.
• Many groups, most notably the Leapfrog Group, have strongly recommended that critical care be delivered by individuals especially trained and board-certified in CCM.
• Major changes are occurring in many specialties, including vascular surgery, cardiac surgery and others.
• While operating room anesthesia has dominated our specialty for many years, in planning for our future, we would be well served to diversify our value to medicine specifically and society overall.
• Encouraging additional training in CCM and also encouraging anesthesiology residents to take critical care fellowships would provide a sound basis for our specialty’s role in the future tertiary care hospital.
• Significant involvement with CCM is crucial for our specialty’s future and the welfare of CCM overall.
• The combined training of anesthesiology and CCM creates the knowledge and skills for the physician leaders of the future tertiary care hospital and potentially with different models of care, the leaders for inpatient care generally.
• The methods to accomplish this goal include incorporating more critical care experience in our residency programs, lengthening our residencies, encouraging incentive-based choices of our fellowships or even redesigning some of our residencies to provide a combined anesthesiology and CCM residency for board certification in both specialties.

Ronald D. Miller, M.D., is Professor and Chair, Department of Anesthesia and Perioperative Care, University of California-San Francisco, San Francisco, California.

The Aims of this Weblog

Welcome to the Critical Care Anesthesiologists' Weblog!
The aims of this Blog include:

1. To promote the specialty of Critical Care Anesthesiology in the US (and elsewhere).
2. To garner support for the ASA and the ASCCA.
3. To provide a forum for anesthesiology residents and anesthesiology intensivists.
4. To address controversies in critical care.
5. To stimulate academic curiosity and debate.
6. To provide news of events, meetings and courses relevant to critical care anesthesiologists.
7. To draw attention to groundbreaking news and research in critical care.
8. To direct people to relevant resources, such as websites, academic departments and journals.
9. To educate through quizzes, clinical cases and medical mysteries.

We look forward to your comments and contributions.
ICU Bloggers.