Critical Care Anesthesiologists' Weblog

CORTICUS versus VASST in the coliseum of septic shock

noreply@blogger.com (Michael Avidan) — Mon, 21 Apr 2008 19:03:00 +0000

Ruminations on Sepsis

“Except on a few occasions the patient appears to die from the body’s response to infection rather than from the infection itself.” William Osler, The Evolution of Modern Medicine, 1904.
Septic shock is difficult to diagnose and difficult to treat. One of the most daunting problems facing a clinician is a patient who is known to have good heart function, but who has refractory shock despite aggressive fluid resuscitation and the institution of vasopressor drugs, such as dopamine or norepinephrine. It is estimated that septic shock results in approximately 215,000 deaths per year in the United States, a number similar to the number of deaths from acute myocardial infarction.1

Steroids

Physiology of steroids (in illness)

Addison first noted the essential role of the adrenal for survival in 1855.2 An increase in corticosteroid levels during illness is an important protective response.3 Free cortisol, rather than the protein bound hormone, is thought to be responsible for its physiological effects.4 Corticosteroid release is regulated by the hypothalamic-pituitary axis in a pulsatile manner.2 Vasopressin also plays an important physiological role in adrenal stimulation.5 In sepsis, inflammatory mediators such as cytokines, promote and maintain a high production of corticosteroids.2 The hypothalamic-pituitary-adrenal axis is itself massively activated in septic shock.4 There are many causes for adrenal insufficiency, and certainly this can occur with diseases, bleeding into the adrenal and infections, such as HIV.3 The concept of relative or functional adrenal insufficiency is somewhat controversial and difficult to define.2, 6

Rationale for using steroids in septic shock

Cortisol is commonly referred to as a “stress hormone” because it has several functions in the body’s response to stress. The role of cortisol in sepsis is associated with two factors: (1) hemodynamics and (2) inflammation. Cortisol maintains vascular tone by increasing the number of both alpha and beta adrenergic receptor as well as prevention of receptor desensitization, thereby enhancing vascular tone and cardiac contractility. In addition, cortisol improves vascular tone by blocking nitric oxide synthesis. Cortisol also suppresses the pro-inflammatory process that occurs in sepsis.

- Rashmi Rathor

Critically ill patients at some stage may develop adrenal insufficiency. Glucocorticoid insufficiency may be related to adrenal insufficiency or to a reduced delivery of glucocorticoid to target tissues and cells.7 Resistance of target tissues to steroids may also occur.2 In an animal model of sepsis, bacteremia was induced in male Sprague-Dawley rats by a intravenous injection of Escherichia coli.8 Dexamethasone alone afforded significant protection against Gram-negative bacteremic shock up to eight hours after the bacterial challenge.8 Dexamethasone plus antibiotics improved outcome more than either intervention alone.8 In a monkey model of endotoxemia, dexamethasone was shown to prevent lactic acidosis and hypoglycemia.9

Early experience with steroids in septic shock

In 1976, Schumer published a study in the Annals of Surgery that showed benefit from a short course of high dose corticosteroids in the treatment of septic shock.10 In a double-blind and randomized study, 172 patients in septic shock admitted over an 8-year period were treated with either high-dose steroid or saline. In the saline-treated patients, the mortality rate was 38.4% (33/86); in the steroid-treated patients, it was 10.4% (9/86).10 This was an impressive reduction in mortality.

Negative studies with steroids in septic shock

In a subsequent randomized controlled trial (RCT), however, which enrolled 59 patients with septic shock, high-dose steroids (30 mg/kg methylprednisolone or 6 mg/kg dexamethasone) were shown to improve hemodynamics, but not outcome.11 The same investigators were also unable to show that steroid administration decreased the likelihood of acute respiratory distress syndrome (ARDS).12 A study by Schein showed that plasma cortisol concentrations are increased in patients with septic shock, but that the degree of increase is variable.13 They found that neither patients who reversed their shock nor those who survived to hospital discharge had significantly different plasma cortisol concentrations from those who did not.13 High dose steroids were actually found to increase mortality through infectious complications.14 Among some intensivists, steroids acquired the reputation of accompanying the administration of “last rites.”15 The prudent warning was issued that current evidence provides no support for the use of corticosteroids in patients with sepsis or septic shock, and suggests that their use may be harmful.14 The warning was sounded that recent trials underscored the need for methodologically rigorous trials evaluating new immune-modulating therapies in well-defined critically ill patients with overwhelming infection.14

The pendulum swings, again

In 1992 the Society of Critical Care Medicine began to stratify patient with sepsis into different categories according to the severity of their disease (severe sepsis, septic shock). Around this same time, the role of the adrenal glands in the pathophysiology of severe sepsis and septic shock was becoming more clear. Accordingly, clinical trials designed after this time tended to investigate the affects of low-dose, long term steroid supplementation rather than high-dose steroids. The landmark study of this period was the Annane trial, “Effect of Treatment with Low Doses of Hydrocortisone and Fludrocortisone on Mortality in Patients with Septic Shock.” The study was a placebo-controlled, randomized, double-blind multi-center trial that enrolled patients between 1995 and 1999. Interestingly, the study was the first to separate patients into “responders” and “nonresponders” based on their response to the corticotrophin test (“nonresponders” were those found to be adrenally insufficient). Accordingly, the primary end point was 28 day survival in nonresponders and the study was powered to detect a 20% reduction in mortality between the control and study groups of nonresponders. Treatment consisted of placebo in the control group and 50 mg IV hydrocortisone Q6 hrs x 7 days and 50 micrograms of PO fludrocortisone daily x 7 days in both responders and nonresponders. Outcomes showed a statistically significant reduction in 28-day mortality, ICU mortality and hospital mortality among the nonresponders treated with steroids while the responders showed no statistically significant differences in outcome. Of note, this study failed to demonstrate a statistically significant difference in 1-year mortality of nonresponders and actually showed an increased mortality in responders receiving steroids (albeit, not a statistically significant difference) calling into question the wisdom of a broad-based treatment approach.

- David McFarland

Experts suggested that the increased risk of infection with steroids was associated only with high dose steroids. It was argued that, based on the high proportion of patients who have relative adrenal insufficiency, the benefits of low doses of steroids (200-300 mg/day hydrocortisone) and the minimal risks, low dose steroids should be used to treat septic shock.16 The positive effects of steroids were thought to included reversal of shock, and trends toward decreased organ system dysfunction and decreased mortality.16 In effect a stalemate had been reached and experts were forced to concede that there was still equipoise in relation to the protracted steroid debate.17 In a seminal study published in JAMA, a 7-day treatment with low doses of hydrocortisone (50 mg every six hours) and fludrocortisone (50 mcg/day) reduced the risk of death in patients with septic shock and relative adrenal insufficiency without increasing adverse events.18 The experts agreed to compromise that low doses of corticosteroids are recommended in patients with septic shock requiring vasopressor support.19 In the retrospective CORTICUS study, patients with either baseline cortisol levels <15>

And again!

The Corticosteroid Therapy of Septic Shock (CORTICUS) trial was a multicenter, randomized, double-blind study that examined the use of hydrocortisone in patients with septic shock. 499 patients were randomly administered either a tapering dose of hydrocortisone (initial dose 50mg) or placebo q6hour for five days. The patients were also classified into two groups, those with or without adrenal reserve as defined by response to the high-dose ACTH stimulation test. Those with inadequate adrenal reserve had a maximum cortisol increase of less than/equal to 9 mcg/dL whereas those with adequate adrenal reserve had greater than 9 mcg/dL rise in serum cortisol levels. At 28 days, there was no significant difference in mortality between the two study groups (i.e., placebo vs. hydrocortisone) regardless of adrenal reserve. As such, it was determined that that hydrocortisone did not improve survival or reversal of shock in patients with septic shock. Hydrocortisone did, however, expedite the reversal of shock, which was defined as the “maintenance of a systolic blood pressure of at least 90 mm Hg without vasopressor support for at least 24 hours.” The group administered steroids also demonstrated that hydrocortisone was associated with more episodes of superinfection.

- Rashmi Rathor

Interestingly in the largest prospective clinical RCT, the CORTICUS trial, hydrocortisone did not improve survival or reversal of shock in patients with septic shock, either overall or in patients who did not have a response to corticotropin, although hydrocortisone hastened reversal of shock in patients in whom shock was reversed.21 This study did confirm the previous finding that adrenal insufficiency is associated with worse prognosis in septic shock, but checking adrenal response appears to be unhelpful.21 An important consideration is that measurement of total cortisol in critical illness may be misleading; during critical illness, glucocorticoid secretion markedly increases, but the increase is not discernible when only the serum total cortisol concentration is measured.4 Forty percent of critically ill patients with hypoproteinemia may have subnormal serum total cortisol concentrations, even though their adrenal function is normal.4 Measuring serum free cortisol concentrations, when this becomes available, in critically ill patients with hypoproteinemia may help prevent the unnecessary use of glucocorticoid therapy.4 The measurement of salivary cortisol may also prove useful.2 The CORTICUS study concluded with the sentiment, based on Annane’s earlier study18, that hydrocortisone may still have a role among patients who are treated early after the onset of septic shock who remain hypotensive despite the administration of high-dose vasopressors (vasopressor unresponsive).21 It is probable that we have misunderstood and possibly therefore abused adrenal stimulation tests to guide therapy in the past.2 Responses in critically ill subjects are higher than those of healthy volunteers.2 Therefore, the Cosyntropin-induced increment in serum total cortisol should probably not be used as a criterion for defining adrenal function in critically ill patients.2 The results of the CORTICUS study are such that it does not exclude the possibility of the same benefit found by Annane.18 In order to answer the question with more precision, an even larger study will be needed; to detect a 15% reduction in the risk of death, a 2600 patient study would probably be necessary.22 As a word of caution, The hydrocortisone dose 50 mg every six hours may mistakenly labeled as low-dose as it leads to excessive elevation in serum cortisol to values much greater than those in patients with normal adrenal function.2 Lower doses should perhaps be explored.

Steroids in Cardiac Surgery

Steroid administration in this setting is theoretically appealing because they can be given before a predictable potent inflammatory-inducing event, cardiopulmonary bypass. Recent evidence suggests that perioperative steroids may decrease atrial fibrillation without increasing the risk of infection.23 Other studies have not found this. In a study evaluating low dose dexamethasone (8 mg in divided doses), it was found to be beneficial in reducing emetic symptoms and improving appetite after cardiac surgery. However, this dose of the corticosteroids did not seem to prevent atrial fibrillation or to have analgesic-sparing properties.24 Steroids do appear to decrease the need for vasopressors after CPB, but whether this is important is debatable. Large RCTs with steroids in cardiac surgery would be interesting.

Vasopressin

Physiology of vasopressin

Vasopressin is a peptide hormone released from the posterior pituitary gland that has multiple physiological effects. It induces vasoconstriction by activating V1 receptors on vascular smooth muscle, a mechanism distinct from that of adrenergic vasoconstriction.1 The most potent stimuli to vasopressin release are increased plasma osmolality, hypotension and hypovolemia.5 It takes a couple of hours to synthesize new vasopressin; it may be depleted with sustained stimuli for release.5 Vasopressin is also responsible for volume and osmolity regulation through its action on V2 receptors.5 Interestingly, vasopressin may cause vasodilatation in some vascular beds through oxytocin receptor stimulation, which results in nitric oxide realease.5

Rationale for using vasopressin in septic shock

Shock is associated with an initial spike in plasma vasopressin levels followed by a sustained fall.5 The reasons for the deficiency are not well understood. The rationale for the use of vasopressin is its relative deficiency in patients with septic shock and the hypothesis that exogenously administered vasopressin can restore vascular tone and blood pressure, thereby decreasing the need for the use of catecholamines, such as dopamine, epinephrine and norepinephrine.5, 25

Early experience with vasopressin in septic shock

Vasopressin for the treatment of septic shock is a new tool in the critical care arsenal with significant interest developing only within the last 10 years. One of the first studies to examine the effects of low-dose vasopressin in patients with septic shock was published in Circulation in 1997. Landry and colleagues enrolled 19 patients meeting standardized criteria for either septic shock or cardiogenic shock in two separate ICUs. All patients received vasopressin. In the septic shock cohort, starting plasma levels of AVP averaged 3.1 pg/mL while the cardiogenic shock cohort’s starting levels averaged 22.7 pg/mL. This suggested a relatively low state of AVP existed in the septic cohort. This study also observed an increase in SBP from a mean of 92 to 146 in the septic shock cohort suggesting a powerful vasoconstrictive effect.

In 1999 Malay and colleagues performed the first RCT to assess the efficacy of vasopressin in septic shock. In all, 10 patients were enrolled in a single institution. They were diagnosed by standardized criteria for septic shock and randomized to receive either vasopressin (o.04 units / min) or placebo in combination with other vasopressors. The primary end point was a rise in systolic arterial blood pressure. They found that patients randomized to the vasopressin group had a mean increased systolic arterial pressure of 27 mmHg (98 +/- 5 to 125 +/- 8 mm Hg, p <>

Patel and colleagues published a study in 2002 examining vasopressin as an adjunct to spare the use of other vasopressors. In this study 24 patients were admitted to an ICU and randomized to either a 4-hour vasopressin or norepi gtt in a double-blinded fashion. Open label vasopressors were titrated to achieve an acceptable BP and physiologic endpoints (urine output, creatine clearance, gastric mucosal CO2 tension and ST segment analysis) were used to assess end-organ perfusion. At the end of the 4 hour infusions the group randomized to norepi decreased their infusion rate from 20 mcg/min to 17 mcg/min where the AVP group decreased their norepi rate from 25 to 5.3 mcg/min (p <>

- David McFarland

Low dose vasopressin (less than 0.1 unit/minute) has been shown to increase blood pressure in patients with septic shock.26 In a small study of septic shock where, in one group vasopressin was added to high dose norepinephrine, the results were compelling. Vasopressin was associated with a massive reduction in norepinephrine requirements, and, intriguingly, in increased urine output and creatinine clearance.26

Negative studies with vasopressin in septic shock

The VASST trial was a multi-center RCT that was conducted to determine whether vasopressin use was associated with decreased mortality in patients with septic shock, especially those who had most severe shock.25 Almost 800 patients with septic shock were randomized to receive vasopressin of escalating doses of norepinephrine. There was no statistically significant difference in mortality between the groups (35.4% vs. 39.3% respectively).25 Interestingly, the 95% confidence interval for absolute risk reduction includes a 10% reduction in mortality attributable to vasopressin.25 Curiously, in post hoc analysis, there was an unexpected finding that patients with less severe sepsis tended to do better with vasopressin. This hypothesis merits further study.25 Importantly, the VASST trial did not evaluate vasopressin in situations where shock is refractory to norepinephrine; it is possible that vasopressin specifically has a role in such circumstances.1 My interpretation of the VASST study is that it does not put the use of vasopressin to rest in sepsis. If anything, it pricks my curiosity further and eases concerns about the safety of vasopressin.

Vasopressin in cardiac surgery

There is limited evidence surrounding the use of vasopressin in cardiac surgery. Anecdotally, we use vasopressin, both during cardiopulmonary bypass and after, when patients have refractory shock. We have no idea what impact this intervention has on outcome. One small (unconvincing) study suggests that the addition of vasopressin is not associated with increased predicted mortality associated with cardiac surgery.27 Specifically, and with scant evidence, vasopressin has been advocated for refractory shock in this setting, especially when there is coexisting pulmonary hypertension.28 In early animal studies, vasopressin was shown to cause pulmonary vasodilation. However, in a well-conducted dog study, vasopressin was shown to cause pulmonary vascular constriction and to exert an important negative inotropic effect on the right ventricle.29 This was not the case when phenylephrine was used to augment systemic BP.29 It may be that at high doses vasopressin causes constriction, but at low doses causes nitric oxide mediated pulmonary vasodilatation.5 One interesting study showed that vasopressin started before CPB in a dose that did not affect BP was associated with decreased vasopressor requirements post-CPB and a shorter ICU stay.30 The results from studies in septic patients may not translate to the cardiac surgery setting. Well-conducted studies in these patients would be valuable.

Concluding Remarks

There are strong anti-vasopressor sentiments, with norepinephrine having been given the nickname “leave-‘em-dead.” There is a widely held view that vasopressor use causally increases the likelihood of organ dysfunction, such as gut and kidney.31 It was thought that if shock resolved and vasopressor dose decreased, outcome would improve. The VASST and CORTICUS trials suggest that shock and vasopressor requirements, as surrogate measures, may not sufficiently reflect severity of the underlying disease process and the association with mortality is not straightforward. It is important to insert the caveat that both of these trials were not sufficiently powered to detect a lesser reduction in mortality that remains clinically important.21, 25 We are, after all, talking about mortality! In concluding about steroids and vasopressin in sepsis, it is tempting to ask, as one article did32, whether steroids and vasopressin are even more effective than activated protein C for the treatment of sepsis. The answer to this question may be that treatments for sepsis are like red wines; they have good years and bad years.

References:

1. Parrillo JE. Septic shock--vasopressin, norepinephrine, and urgency. The New England journal of medicine 2008;358(9):954-6.
2. Arafah BM. Hypothalamic pituitary adrenal function during critical illness: limitations of current assessment methods. The Journal of clinical endocrinology and metabolism 2006;91(10):3725-45.
3. Cooper MS, Stewart PM. Corticosteroid insufficiency in acutely ill patients. The New England journal of medicine 2003;348(8):727-34.
4. Hamrahian AH, Oseni TS, Arafah BM. Measurements of serum free cortisol in critically ill patients. The New England journal of medicine 2004;350(16):1629-38.
5. Holmes CL, Patel BM, Russell JA, Walley KR. Physiology of vasopressin relevant to management of septic shock. Chest 2001;120(3):989-1002.
6. Burchard K. A review of the adrenal cortex and severe inflammation: quest of the "eucorticoid" state. The Journal of trauma 2001;51(4):800-14.
7. Gonzalez H, Nardi O, Annane D. Relative adrenal failure in the ICU: an identifiable problem requiring treatment. Critical care clinics 2006;22(1):105-18, vii.
8. Pitcairn M, Schuler J, Erve PR, Holtzman S, Schumer W. Glucocorticoid and antibiotic effect on experimental gram-negative bacteremic shock. Arch Surg 1975;110(8):1012-5.
9. Schuler JJ, Erve PR, Schumer W. Glucocorticoid effect on hepatic carbohydrate metabolism in the endotoxin-shocked monkey. Annals of surgery 1976;183(4):345-54.
10. Schumer W. Steroids in the treatment of clinical septic shock. Annals of surgery 1976;184(3):333-41.
11. Sprung CL, Caralis PV, Marcial EH, et al. The effects of high-dose corticosteroids in patients with septic shock. A prospective, controlled study. The New England journal of medicine 1984;311(18):1137-43.
12. Schein RM, Bergman R, Marcial EH, et al. Complement activation and corticosteroid therapy in the development of the adult respiratory distress syndrome. Chest 1987;91(6):850-4.
13. Schein RM, Sprung CL, Marcial E, Napolitano L, Chernow B. Plasma cortisol levels in patients with septic shock. Critical care medicine 1990;18(3):259-63.
14. Cronin L, Cook DJ, Carlet J, et al. Corticosteroid treatment for sepsis: a critical appraisal and meta-analysis of the literature. Critical care medicine 1995;23(8):1430-9.
15. Matot I, Sprung CL. Corticosteroids in septic shock: resurrection of the last rites? Critical care medicine 1998;26(4):627-30.
16. Goodman S, Sprung CL. The International Sepsis Forum's controversies in sepsis: corticosteroids should be used to treat septic shock. Critical care (London, England) 2002;6(5):381-3.
17. Annane D, Briegel J, Keh D, Moreno R, Singer M, Sprung CL. Clinical equipoise remains for issues of adrenocorticotropic hormone administration, cortisol testing, and therapeutic use of hydrocortisone. Critical care medicine 2003;31(8):2250-1; author reply 2-3.
18. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and f ludrocortisone on mortality in patients with septic shock. Jama 2002;288(7):862-71.
19. Keh D, Sprung CL. Use of corticosteroid therapy in patients with sepsis and septic shock: an evidence-based review. Critical care medicine 2004;32(11 Suppl):S527-33.
20. Lipiner-Friedman D, Sprung CL, Laterre PF, et al. Adrenal function in sepsis: the retrospective Corticus cohort study. Critical care medicine 2007;35(4):1012-8.
21. Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. The New England journal of medicine 2008;358(2):111-24.
22. Finfer S. Corticosteroids in septic shock. The New England journal of medicine 2008;358(2):188-90.
23. Halonen J, Halonen P, Jarvinen O, et al. Corticosteroids for the prevention of atrial fibrillation after cardiac surgery: a randomized controlled trial. Jama 2007;297(14):1562-7.
24. Halvorsen P, Raeder J, White PF, et al. The effect of dexamethasone on side effects after coronary revascularization procedures. Anesthesia and analgesia 2003;96(6):1578-83, table of contents.
25. Russell JA, Walley KR, Singer J, et al. Vasopressin versus norepinephrine infusion in patients with septic shock. The New England journal of medicine 2008;358(9):877-87.
26. Patel BM, Chittock DR, Russell JA, Walley KR. Beneficial effects of short-term vasopressin infusion during severe septic shock. Anesthesiology 2002;96(3):576-82.
27. Suojaranta-Ylinen RT, Vento AE, Patila T, Kukkonen SI. Vasopressin, when added to norepinephrine, was not associated with increased predicted mortality after cardiac surgery. Scand J Surg 2007;96(4):314-8.
28. Tayama E, Ueda T, Shojima T, et al. Arginine vasopressin is an ideal drug after cardiac surgery for the management of low systemic vascular resistant hypotension concomitant with pulmonary hypertension. Interactive cardiovascular and thoracic surgery 2007;6(6):715-9.
29. Leather HA, Segers P, Berends N, Vandermeersch E, Wouters PF. Effects of vasopressin on right ventricular function in an experimental model of acute pulmonary hypertension. Critical care medicine 2002;30(11):2548-52.
30. Morales DL, Garrido MJ, Madigan JD, et al. A double-blind randomized trial: prophylactic vasopressin reduces hypotension after cardiopulmonary bypass. The Annals of thoracic surgery 2003;75(3):926-30.
31. Bomzon L, Rosendorff C. Renovascular resistance and noradrenaline. The American journal of physiology 1975;229(6):1649-53.
32. Bradley C. Steroids in sepsis--more effective than activated protein C? Intensive Crit Care Nurs 2001;17(4):242-4.

Virulence+Prevalence+Resistance=CAMRSA

noreply@blogger.com (Michael Avidan) — Tue, 12 Feb 2008 03:19:00 +0000

Bacterial resistance is a major public health problem that threatens many of the advances that have been made in the last century in the ongoing and interminable war between humans and microbes. S. Aureus is a common and virulent bacterium that has repeatedly shown an ability to develop resistance to antibiotics and to cause fatal epidemics. It has recently become apparent that community acquired methicillin resistant S. Aureus (CAMRSA) is on the rise. The biggest threat from infectious disease occurs when virulence, resistance and prevalence are all features of the same microbe. CAMRSA threatens to be such an organism.

Panton-Valentine leukocidin (PVL)-secreting S. Aureus is a particularly virulent strain of S. Aureus that may cause life-threatening hemoptysis, pulmonary necrosis and septic shock.The pneumonia is often preceded by influenza-like symptoms and has a high lethality rate. Lancet Leukocidin/neutrophil interactions in the pulmonary vasculature specifically may cause severe hemoptysis. S. Aureus should be considered in the differential diagnosis when adults present from the community with massive hemoptysis and suspected pneumonia. ICM Airway bleeding, erythroderma, and leukopenia are associated with fatal outcome from PVL-positive S. aureus necrotizing pneumonia. CID It is concerning that there is a rise in PVL-positive CAMRSA that may be occurring through horizontal gene transfer.CMI JID

From 2001 through 2002, there were 1647 cases of CAMRSA infection reported in Baltimore, Atlanta and Minnesota communities, representing between eight and twenty percent of all MRSA isolates. NEJM CAMRSA resulted in a range of infections such as invasive infections, including bacteremia and osteomyelitis, skin and wound infections, and pneumonia. NEJM The pneumonia severity index is a useful tool for aiding clinical judgment, guiding appropriate management and for suggesting prognosis. PSICALC, AFP

Using the best evidence, address the questions relating to the following patient:

A 53-year-old man with chronic liver disease probably secondary to a strong ethanol history is brought in by his wife from home in Baltimore with confusion, hypotension (BP = 85/50), fever (Temperature = 38.3), tachypnea (RR = 35/min) and hemoptysis. On examination, the patient is distressed and diaphoretic, he is using accessory muscles of respiration, and his pulse is thready at a rate of 110/minute. There are crackles with bronchial breath sounds heard at the right lower zone. The hematocrit = 36%, white blood count is elevated (19,000), electrolytes are within normal limits, BUN is elevated (32 mg/dL), and the arterial blood gas off oxygens reveals pH=7.32, PO2=68 mmHg, PCO2=32 mmHg. The chest x-ray shows features consistent with a right middle and lower lobe pneumonia. (See Above and URL)

The ECG shows a sinus tachycardia, but is otherwise unremarkable. The patient is becoming more lethargic and the ICU team decides to proceed with tracheal intubation, to institute mechanical ventilation and to obtain bronchial washings. Sputum is thick and bloody. Specimens from the right lower and middle lobes are sent to the laboratory. On Gram-stain, Gram-positive organisms in clusters are seen.

Questions:

1) What is the differential diagnosis?

2) What further tests would you request?

3) What treatment would you initiate?

4) How would you ventilate this patient?

5) If the culture grows methicillin resistant S. Aureus (MRSA), what strains are likely in this context?

6) How, if at all, would you modify your treatment in the light of this new information?

7) What would you tell the wife about the patient's prognosis?

8) What are the treatment prospects for MRSA?

The Tenuous Transplant

noreply@blogger.com (Michael Avidan) — Mon, 14 Jan 2008 18:30:00 +0000

A 36-year old man with a history of cystic fibrosis has undergone a bilateral lung transplant and is on the ICU 3 days following the surgery.

History:

He has chronic colonization with Pseudomonas aeruginosa and Burkholderia cepacia. He received pancreatic enzyme replacement, but was not insulin requiring. He had mild pulmonary hypertension with right heart hypertrophy, but preserved function. He was losing weight prior to surgery, was becoming progressively short of breath and was quite debilitated at the time of surgery. He was CMV negative prior to transplant. Home medications include pancreatic supplementation, albuterol, and oxygen. No epidural was placed for fear of infection. The surgery proceeded with cardiopulmonary bypass as the pulmonary pressures escalated dramatically with clamping of a pulmonary artery. The estimated blood loss was 1.5 L and the patient received 3 L of crystalloid and 2 units of blood during the surgery.

Intra-operative TEE showed normal LV function with RV hypertrophy, mild TR and dilated pulmonary arteries. There was no PFO. The flow velocities in the four pulmonary veins were normal following transplantation. No clots were seen. There was mild RV dysfunction following cardiopulmonary bypass.

Examination:

He weighs 55 kg and is 1.7m tall. He is intubated on the ICU.

The PAP = 45/25 mmHg, the CVP is 13 mmHg, the HR is 115/min and irregularly irregular, the BP is 95/60 mmHg and the temperature is 37.9 degrees Celsius.

The ventilation mode is volume control ventilation; the respiratory rate is 12/min, the tidal volume = 500 ml, the I:E ratio is 1:2, the FiO2 is 0.8, and the PEEP is 5 cmH2O.

Cardiorespiratory examination reveals normal heart sounds with an irregularly irregular rate, bilateral breath sounds, faint crackles and diminished sounds in the lower zones.

Urine output has been 20 and 15 ml/hr for the last two hours.

Special Investigations:

Blood results reveal a hemoglobin of 8.2 g/dL, platelet count of 90 x 1000/mcL and white blood count of 18.3 x1000/mcL.

There are no electrolyte abnormalities, the BUN is 29 mg/dL, the creatinine is 1.6 mg/dL (Baseline BUN was 12 and creatinine was 0.8) and the blood glucose is 210 mg/dL.

The arterial blood gas shows a pH = 7.33, PO2 = 71 mmHg, a PCO2 = 58 mmHg, and bicarbonate = 29 mmol/L.

The CXR shows the tracheal tube and the PA catheter appropriately positioned. There are significant bilateral patchy opacifications, with the right side markedly more affected than the left.

The ECG shows atrial fibrillation, mild ST elevation in precordial and inferior leads, and troponin I is mildly elevated (1.1 mcg/L), but trending down from a postoperative peak of 2.1 mcg/L.

Medications:

Propofol and fentanyl for sedation and analgesia.
Dobutamine at 3 mcg/kg/min for right heart failure.
Norepinephrine at 0.04 mcg/kg/min for hypotension.
Inhaled prostacyclin for pulmonary hypertension.
Meropenem, vancomycin, inhaled tobramycin, and inhaled colistin to cover previous infection.
Ganciclovir and trimethoprim/sulfamethoxezole for prophylaxis.
Methylprednisolone, tacrolimus and azathioprine for immunosuppression.
Subsutaneous heparin for DVT prophylaxis.
Famotidine for ulcer prophylaxis.

Questions:

Based on the information presented and the most up to date evidence, decide on the following management conundrums for this particular patient, critically citing peer reviewed literature to support your decisions. When you cite evidence, comment on its validity, its importance, and its applicability to this patient.

1) Would you give a blood transfusion?

2) Would you give a fluid challenge?

3) Would you target a blood sugar range of 80-120 mg/dL?

4) Would you promote diuresis?

5) Would you continue dobutamine?

6) Would you add vasopressin?

7) Would you cardiovert for atrial fibrillation?

8) Would you anti-coagulate for atrial fibrillation?

9) Would you treat atrial fibrillation with amiodarone or beta blockers?

10) Would you alter mechanical ventilation?

11) Would you alter sedation?

12) Would you plan to do a tracheostomy?

13) Would you change antimicrobial therapy?

14) Would you change immunosuppressive therapy?

Posted by Alex Chen and Michael Avidan.

The Esophagectomy Tightrope

noreply@blogger.com (Michael Avidan) — Mon, 14 Jan 2008 04:21:00 +0000

A 68-year old man has undergone an esophagectomy for cancer and is on the ICU 4 hours following the surgery.

History:

He has a 30-pack year smoking history, drinks 2 beers a day, and a history of coronary artery disease with stable angina. He snores at night and falls asleep during the day; he probably has undiagnosed obstructive sleep apnea. His home medications include aspirin, metoprolol and simvastatin. He lost about a liter of blood during his surgery and received 5 liters of crystalloid.

Examination:

He weighs 95 kg and is 1.8m tall. He is intubated on the ICU and is receiving propofol for sedation and fentanyl for analgesia. The CVP is 9 mmHg, the HR is 95/min, the BP is 105/60 and the temperature is 37.4 degrees Celsius. The ventilation mode is volume control ventilation; the respiratory rate is 12/min, the tidal volume = 800 ml, the I:E ratio is 1:3, the FiO2 is 0.6, and the PEEP is 5 cmH2O. Cardiorespiratory examination reveals distant heart sounds, bilateral breath sounds, faint crackles in the lower zones with a soft wheeze. Urine output has been 50 and 45 ml/hr for the last two hours.

Special Investigations:

Blood results reveal a hemoglobin of 8.2 g/dL, platelet count of 210 x 1000/mcL and white blood count of 12.3 x1000/mcL. There are no electrolyte abnormalities, the BUN is 19 mg/dL, the creatinine is 1.3 mg/dL and the blood glucose is 170 mg/dL. The arterial blood gas shows a pH = 7.37, PO2 = 78 mmHg, a PCO2 = 38 mmHg, and bicarbonate = 23 mmol/L. The CXR shows the tracheal tube and the central line appropriately positioned. There are bilateral patchy opacifications. The ECG is unchanged compared with the preoperative ECG, and troponin I is not elevated.

Questions:

Based on the information presented and the most up to date evidence, decide on the following management conundrums for this particular patient, critically citing peer reviewed literature to support your decisions. When you cite evidence, comment on its validity, its importance, and its applicability to this patient.

1) Would you give a blood transfusion?

2) Would you give a fluid challenge?

3) Would you target a blood sugar range of 80-120 mg/dL?

4) Would you promote diuresis?

5) Would you start low dose dopamine or use another pressor, such as phenylephrine?

6) Would you give a beta-blocker?

7) Would you give aspirin and a statin, and via what route?

8) Would you alter mechanical ventilation?

9) What steps would you take to prevent pneumonia?

10) Would you sedate this patient?

11) Would you try to extubate this patient to a CPAP mask?

12) Would you plan to do a tracheostomy?

13) What thrombosis prophylaxis would you use?

Images in Clinical Medicine - Quiz

noreply@blogger.com (Michael Avidan) — Fri, 16 Nov 2007 14:29:00 +0000

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).

Are intensivists prognostic pessimists?

noreply@blogger.com (Michael Avidan) — Sun, 11 Nov 2007 05:18:00 +0000

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:

Sometimes withholding or withdrawing advanced life support is the most compassionate course.
Quality of life, not just survival, should be considered in making decisions.
It may be helpful to seek the opinion of a colleague who is not emotionally vested in the care of a patient.
We should ask ourselves whether our judgment might be clouded by prognostic pessimism.
Prognostic optimism may be a euphemism for fear of litigation or defensive medicine.
For an optimistic perspective, always consult a surgeon.
The right to a dignified death should be viewed as a fundamental human right, just as the right to a dignified life is.
Unwarranted prognostic pessimism may lead to patients being denied life-saving interventions.
Unwarranted prognostic optimism may lead to patients being denied a dignified death.
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

noreply@blogger.com (Long Nguyen) — Sat, 10 Nov 2007 22:58:00 +0000

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?

A reduction in troponin T levels starting at 6 hour.
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?

The skeptics will argue that we should do nothing until firm evidence emerges. In fact if firm evidence emerges, it is probably wrong!
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.
The intellectual enthusiasts may argue that we MUST do a raft of randomized controlled studies with RIPC on the ICU.
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

noreply@blogger.com (Michael Avidan) — Sun, 09 Sep 2007 21:19:00 +0000

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.

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?

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

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?

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

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?

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

Would you begin TPN?
Would you initiate an insulin drip?

See you in San Francisco!

Does Epo save lives?

noreply@blogger.com (Michael Avidan) — Sun, 09 Sep 2007 16:57:00 +0000

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±2.0g 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. (hazardratio, 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?

Administer epoetin alfa to all anemic critically ill patients unless it is specifically contra-indicated.
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).
Await the results of further studies.
Conduct further studies yourself.
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):

Groundbreaking News - Insight into the Mechanisms of Action of Antibiotics

noreply@blogger.com (Michael Avidan) — Sun, 09 Sep 2007 00:26:00 +0000

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

noreply@blogger.com (Michael Avidan) — Sat, 08 Sep 2007 23:48:00 +0000

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

noreply@blogger.com (Michael Avidan) — Sat, 08 Sep 2007 22:40:00 +0000

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

noreply@blogger.com (Michael Avidan) — Fri, 07 Sep 2007 21:25:00 +0000

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

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

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