ICU Rounds Report - Sept 28th 2010

September 28th, 2010

Is this A-line infected? We spend a lot of time worrying about central lines and wonder often, is this line the cause of something bad? Should we worry about the a-line too? Increasingly, the wide-spread belief that arterial lines don't cause infection is being questioned. Despite lore to the contrary, multiple well conducted randomized clinical controlled trials and one large review have shown the arterial lines are just as likely as central lines be colonized and cause CR-BSI. The misconception likely comes from huge, retrospective papers assessing the safety of arterial lines that report very low rates of line-associated sepsis, even though those studies were not designed to look at CR-BSI.  Finally, remember the large biopatch trial that caused biopatches to suddenly appear overnight in hospitals around the country looked at both arterial and venous lines, finding a clear benefit for placing them on both.

Although it defies common practice at UVa, I believe a preponderance of evidence argues for using a more careful sterile technique and biopatches for lines that could possibly be in place for more than 48 hours. I challenge the defenders of the lazy, dirty technique to find meaningful evidence that a careful sterile technique is not justified.
Lucet JC, Timsit JF Infectious risk associated with arterial catheters compared with central venous catheters Crit Care Med. 2010 Apr;38(4):1030-5.
Timsit, JF. Chlorhexidine-Impregnated Sponges and Less Frequent Dressing Changes for Prevention of Catheter-Related Infections in Critically Ill Adults: A Randomized Controlled Trial. JAMA. 2009;301(12):1231-1241.    
Traore O, Liotier J, Souweine B:  Prospective study of arterial and central venous catheter colonization and of arterial- and central venous catheter-related bacteremia in intensive care units.   Crit Care Med 33. 1276-1280.2005;
Koh DB, Gowardman JR, Rickard CM, et al:  Prospective study of peripheral arterial catheter infection and comparison with concurrently sited central venous catheters.   Crit Care Med 36. 397-402.2008;
Khalifa R, Dahyot-Fizelier C, Laksiri L, et al:  Indwelling time and risk of colonization of peripheral arterial catheters in critically ill patients.   Intensive Care Med 34. 1820-1826.2008;
Maki DG, Kluger DM, Crnich CJ:  The risk of bloodstream infection in adults with different intravascular devices: A systematic review of 200 published prospective studies.   Mayo Clin Proc 81. 1159-1171.2006;

BIS Monitors. The BiSpectral Index was developed in the early 1990's as a measure of consciousness. The machine monitors EEG information and processes it using a propriety algorithm into a single number, 0 - 100. One hundred implies full consciousness, where 0 represents no EEG activity ('burst suppression'). General anesthesia is 40-60. Conscious sedation is 65-80. I don't know what 61-64 is. Someplace magical, I suppose. Originally validated for patients undergoing OR anesthesia with propofol, its use has expanded to anesthetics with other agents and monitoring sedation in the ICU. Numbers below 60 are associated with a very low risk of recall and are the usual OR target. For the ICU, I think below 70 is an appropriate target.

How well does it work? The original, industry funded trial done in over 2400 patients in Australia in patients under general anesthesia with volatile anesthetics, found that the BIS could reduce awareness by 80%, with a estimated cost of $2200 to prevent one case of awareness. Four years later, a similar trial done with private funding here in the US found no benefit to using the BIS. Nevertheless, it still is commonly used and likely has an evolving role in monitoring sedatives and anesthetics.

For ICU monitoring, many small trials have been done which show mixed results. Overall, commonly used sedation scales (such as RASS) appear to be better when they can be used. For paralyzed patients, BIS is often the only practical monitor available and is therefore recommend by many authors, despite the mixed results. It appears that in paralyzed patients use of the BIS can limit drug accumulation and may reduce ICU length of stay. Several recent software updates have been made, reportedly to address ICU concerns.
Avidan MS. Anesthesia awareness and the bispectral index. N Engl J Med. 2008 Mar 13;358(11):1097-108.
Myles PS. Bispectral index monitoring to prevent awareness during anaesthesia: the B-Aware randomised controlled trial. Lancet. 2004 May 29;363(9423):1757-63.
S.A. Nasraway, The bispectral index: expanded performance for everyday use in the intensive care unit?, Critical Care Medicine 33 (2005), pp. 685–687.

From Danielle:
Alvimopan. Postoperative ileus (POI) after abdominal surgery (e.g. bowel resection) causes significant patient discomfort, morbidity, and prolongs length of stay in the hospital.  One contributing factor to POI is the use of narcotics for post-operative pain. Opiods bind to mu-receptors in the GI tract and may exacerbate POI. Alvimopan (Entereg, Adolor) is a oral, peripherally acting mu-receptor antagonist approved for accelerating GI recovery after abdominal surgery. It was approved in May 2008.

To date, four randomized, double-blind, placebo-controlled, parallel-group, phase 3 trials conducted in the U.S. and Canada and a single phase 3 trial conducted in Europe have shown some benefit to the use of Alvimopan post-operatively. Delaney et. al, 2005, found that in patients undergoing total abdominal hysterectomy and partial colectomy with primary anastomosis time to stool or tolerance of solid foods was reduced. Wolff et. al,2004,  in a similar study population, found similar results with mean time difference to be 15-22 hours. Most trials as of now have differing results regarding whether or not patient length of stay in the hospital is changed or if there is benefit to patient outcomes beyond time to GI recovery.
Delaney et. al. 2005. "Phase III Trial of Alvimopan, a Novel, Peripherally Acting, Mu Opioid Antagonist, for Postoperative Ileus After Major Abdominal Surgery."Diseases of the Colon and Rectum. 1114-1130.
Wolff, et. al. 2004. "Results of a Multicenter, Randomized, Double-Blind, Placebo-Controlled, Phase III Trial of Major Abdominal Surgery and Postoperative Ileus." Ann Surg. 240:728-735

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ICU Rounds Report - Sept 23rd 2010

September 23rd, 2010

Routine Use of NG Tubes. Who needs an NGTube? When can we pull them out in non-obstructed patients? Cochrane has compiled the results of 37 randomized studies comparing routine NGT use to none (or immediate post-operative removal) in over 5700 patients undergoing open abdominal surgery of any type (gyn, emergency, onc, upper GI, lower GI, etc). The results strongly suggest that NGTs, used 'prophylactically' cause, or at least worsen, ileus. Patients without routine tubes had less ileus (p<0.00001!), less pulmonary complication (p=0.01) and shorter length of stay. There was no significant difference in any other outcome (leaks, hernias, or infections).

The bottom line is best summed up by the typically non-committal folks at Cochrane, "Routine nasogastric decompression does not accomplish any of its intended goals and so should be abandoned in favour of selective use of the nasogastric tube."
Verma R, Nelson RL. Prophylactic nasogastric decompression after abdominal surgery. Cochrane Database of Systematic Reviews 2007, Issue 3. Art. No.: CD004929



From Cara
Troponin Leaks. Cardiac enzymes, troponins in particular, have become the gold standard for evaluating and establishing a diagnosis of Acute Coronary Syndrome.  However, numerous studies have shown that troponins are elevated in some patients without any clinical signs or symptoms of acute coronary syndrome, prompting the recognition of the "troponin leak" phenomenon. Conditions associated with elevated troponins in the absence of ACS include (get ready, this list is LONG!): tachy- or bradyarrhythmias, or heart block, critically ill patients, especially with diabetes, respiratory failure or sepsis, hypertrophic cardiomyopathy, coronary vasospasm, acute neurological disease, including stroke or subarachnoid hemorrhage, cardiac contusion or other trauma including surgery, ablation, pacing, implantable cardioverter-defibrillator shocks, cardioversion, endomyocardial biopsy, cardiac surgery, following interventional closure of atrial septal defects, rhabdomyolysis with cardiac injury, congestive heart failure-acute and chronic, pulmonary embolism, severe pulmonary hypertension, renal failure, aortic dissection, aortic valve disease, apical ballooning syndrome – Takotsubo, cardiomyopathy, infiltrative diseases (ie, amyloidosis, hemochromatosis, sarcoidosis, and scleroderma), inflammatory diseases (ie, myocarditis or myocardial extension of endo-/pericarditis, Kawasaki disease), drug toxicity or toxins (ie, adriamycin, 5-flurouracil, herceptin, snake venom), burns, especially if affecting >25 percent of body surface area, extreme exertion, transplant vasculopathy.

One rather common condition encountered in the ICU setting associated with troponin leak is sepsis or SIRS.  It is thought that these conditions cause the release of myocardial depressive factors that induce the degradation of troponin into low molecular weight particles.  Sepsis also increases membrane permeability, allowing these troponin particulars to be released into the circulation for detection on assays.  Increased myocardial oxygen demand coupled with decreased oxygen supply in sepsis or SIRS likely contributes to the troponin leak in these patients as well.

In a particularly eloquent study, Ammann et al. studied 20 patients with either SIRS, sepsis, or septic shock.  They found that 17 out of the 20 patients had elevated troponins.  Interestingly, coronary angiography, autopsy, and stress echo demonstrated that 10 of the 17 did not have significant coronary artery disease. It will be interesting to see whether future studies will address whether cardiac interventions could improve outcomes in these patients.
Ammann, P, Fehr, T, Minder, EI, et al. Elevation of troponin I in sepsis and septic shock. Intensive Care Med 2001; 27:965.
UptoDate.org - article entitled "Elevated Cardiac Troponin Concentration in the Absence of an Acute Coronary Syndrome"


From Danielle
Delirium: Pharmaceutical Prevention. Delirium affects patients' consciousness and increases the morbidity and mortality of ICU patients. Patients are at increased risk of self-extubation if ventilated, staying longer in the hospital, and subsequently suffering from more hospitalized infections, etc. This increases the healthcare costs. Pharmaceutical management of delirium has primarily focused on treatment and not prevention.
The MIND trial was a double blind, randomized, placebo controlled trial that assessed whether scheduled antipsychotics would improve the number of days alive without coma and delirium in 6 tertiary MICU/SICUs across the country. The randomized 101 mechanically ventilated patients to receive scheduled haloperidol, ziprasidone or placebo q6h. Outcomes measured included number of days alive without delirium or coma, ventilator free days, length of hospital stay, and mortality. Study concluded that there was no significant difference between the three trial groups regarding outcomes or safety profile.

By contrast, another double blind, prospective randomized placebo controlled pilot trial (mentioned previously in the rounds report) assessed whether scheduled quetiapine (q12h) in addition to as needed haloperidol would reduce length of stay, length of delirious episode, agitation, mortality, need for prn haloperidol in critically ill patients. This trial found that scheduled quetiapine was associated with faster resolution of delirium, less agitation, and fewer doses of prn haloperidol. There was no significant reduction in length of stay or mortality. Between the two groups there was no difference in incidence of QT prolongation or extrapyramidal signs. However, quetiapine was associated with increased somnolence. Thus the debate continues regarding the benefit of scheduled anti-psychotics. Additional studies to assess safety and efficacy are needed.
Girard, et. al. 2010. "Feasibility, efficacy, and safety of antipsychotics for intensive care unit delirium: The MIND randomized, placebo-controlled trial." Crit. Care. Med. 38(2):428-438.
Delvin, et. al. 2010. "Efficacy and safety of quetiapine in critically ill patients with delirium: A prospective, multicenter, randomized, double-blind, placebo-controlled pilot study." Crit. Care. Med. 38(2): 419-418.

Need more Rounds Reports? Old Issues are archived at UVARounds.blogspot.com

--

Jordan Hackworth, M.D.

Fellow, Critical Care Medicine
Department of Anesthesiology
University of Virginia

ICU Rounds Report - Sept 22nd 2010

From Cara
Contraction Alkalosis.  Contraction alkalosis is a form of metabolic alkalosis – an increase in pH due to an increase in HCO3.  What differentiates contraction alkalosis from other types of metabolic alkalosis is that the extracellular amount of bicarbonate remains the same whereas the bicarbonate concentration artificially increases due to loss of extracellular fluid that is relatively bicarbonate free.

This was first described by Cannon et al.'s 1965 study of contraction alkalosis in patients with congestive heart failure following diuresis with ethacrynic acid (a seldom used ototoxic non-sulfonamide loop diuretic).  They found that diuresis was accompanied by increase in bicarbonate, rise in pH, and increase in arterial carbon dioxide pressure.  Further, the fluid lost in the process of diuresis had virtually no bicarbonate, demonstrating that the extracellular fluid "contracted" around a stable amount of bicarbonate.

Administration of intravenous loop diuretics in an edematous patient is the most common cause of contraction alkalosis.  Other causes include states wherein a high chloride, low-bicarbonate solution is lost, such as sweat losses in cystic fibrosis, gastric secretion losses in patients with achlorhydria, and congenital chloride diarrhea.  
CANNON PJ, "CONTRACTION" ALKALOSIS AFTER DIURESIS OF EDEMATOUS PATIENTS WITH ETHACRYNIC ACID. Ann Intern Med. 1965 May;62:979-90.

Timing of ICU admission. With increasing talk of 24 hour ICU staffing around the county (and here!) comes an interesting meta-analysis published by a group at Jefferson Medical College that complies the results of 10 studies evaluating the link between admission time and mortality. The good news: being admitted at night didn't seem to affect mortality overall (odds ratio [OR], 1.0 [95% CI, 0.87-1.17]; P = .956). Bad news? Coming in over the weekend increased your risk of dying by almost 10% (OR, 1.08 [95% CI, 1.04-1.13]; P < .001). No one knows why this is, but the researchers posit that decreased staff-to-patient ratios, unavailability of board-certified intensivists, physician fatigue, lack of ancillary staff, and difficulty in obtaining complex diagnostic tests or therapies may be the cause.

This follows previous studies that found patients with acute, severe medical illness (aortic aneurysm, ICH, etc) are more likely to die when admitted through the ED on a weekend. Finally, remember that trauma patients presenting between midnight and 6 am are more likely to be sick and much more likely to die.  Overall, more evidence suggesting that more intensive staffing (including 24 hour in-house intensivists) may be coming...
Cavallazzi R, Marik PE, Hirani A, Pachinburavan M, Vasu TS, Leiby BE. Association between time of admission to the intensive care unit and mortality: A systematic review and meta-analysis. Chest 2010;138:68–75
Bell CM. Mortality among patients admitted to hospitals on weekends as compared with weekdays. N Engl J Med 2001 345(9):663–668
Vaziri K.  Optimizing physician staffing and resource allocation: sine-wave variation in hourly trauma admission volume. J Trauma 2007 62(3):610–614.

Does Quetiapine Work? Seems to calm patients down a bit, but what are the data? Sarah Gruber (thanks Sarah!) points to a well-done, multicenter, placebo controlled RTC published this year in CCM that randomized 36 mixed ICU patients to either placebo or 50 mg every 12 hrs of quetiapine. The results were positive.

Quetiapine was associated with a shorter time to first resolution of delirium (1.0  vs. 4.5 days, p =.001) and a reduced duration of delirium (36  vs. 120 hrs; p =.006). There was a trend towards reduced mortality and decreased hospital LOS, but they were not significant in this small trial. Side effects, including rates of QTc prolongation and extrapyramidal symptons were similar in both groups.

Among the atypical antipyschotics, the authors point out that quetiapine has several favorable characteristics that make it a good choice in the ICU:  a short half-life that facilitates dose titration, lower propensity to alter the QTc interval, and very rare reports of extrapyramidal symptom effects.
Devlin JW. Efficacy and safety of quetiapine in critically ill patients with delirium: a prospective, multicenter, randomized, double-blind, placebo-controlled pilot study. Crit Care Med. 2010 Feb;38(2):419-27.

--

Jordan Hackworth, M.D.

Fellow, Critical Care Medicine
Department of Anesthesiology
University of Virginia

ICU Rounds Report - Sept 21st 2010

September 21st, 2010

Fever. What's your definition of fever? The IDSA (Infectious Disease Society of America) and ACCCM (American College of Critical Care Medicine) say in the ICU it is anything greater than 38.3 (high fever is >39.5). Obviously that doesn't apply to immunocompromised patients. In a mixed ICU group, nearly halve of admissions will get a fever. For our surgical patients, it appears the number is about 75%. All new fevers need a workup and about half of all fevers are eventually found to be non-infectious. Surprisingly, in a series of over 24,000 ICU admissions, fever appears to not affect mortality (because it was so common?). There is a mortality difference among those with high (>39.5) fever and normal or no fever, however (20 vs 12%, P<0.05).

Apart from chasing and managing the etiology, should we treat the fever per se? Probably not, except for head injured patients or those with severe fevers >41C. The biggest trial to date on the issue randomized 86 non-head injured trauma ICU patients from 3 ICUs to Tylenol/cooling blankets vs allowing fevers to run (and treat only if they got to > 40 C). The trial was stopped early because of a trend towards death in the group being treated. (7 deaths vs one in the non-treatment group, p = 0.06) and suggests that treatment of fever may be detrimental in trauma ICU patients. A similar but smaller trial in surgical ICU patients found no difference in outcome. My bias? Let it ride...

O'Grady, NP, Barie, PS, Bartlett, JG, et al. Guidelines for evaluation of new fever in critically ill adult patients: 2008 update from the American College of Critical Care Medicine and the Infectious Diseases Society of America. Crit Care Med 2008; 36:1330.
Laupland, KB, Shahpori, R, Kirkpatrick, AW, et al. Occurrence and outcome of fever in critically ill adults. Crit Care Med 2008; 36:1531.
Gozzoli, V, Schottker, P, Suter, PM, Ricou, B. Is it worth treating fever in intensive care unit patients? Preliminary results from a randomized trial of the effect of external cooling. Arch Intern Med 2001; 161:121.
Schulman, CI, Namias, N, Doherty, J, et al. The effect of antipyretic therapy upon outcomes in critically ill patients: a randomized, prospective study. Surg Infect (Larchmt) 2005; 6:369.

Testing for HITT. Heparin induced thrombocytopenia and thrombosis (type 2, the clinically relevant type) remains a challenge to diagnosis. There are 3 tests used clinically, all are sendouts at UVa. Up to 3% of patients treated with heparin will go on to develop HITT.

1) Serotonin Release Assay. The gold standard. Normal platelets are radiolabeled with serotonin then mixed with patient serum and heparin in different concentrations. Basically if, in the presence of heparin, the serum's antibodies causes the normal platelets to leak serotonin the test is positive. Advantages: This is the only test with good specificity (95%) and sensitivity (95%). Downsides: this test is expensive, tough to perform (takes a week) and is a send out.

2) Heparin induced platelet aggregation. Again healthy donor platelets are mixed with patient serum in the presence of heparin. To have HITT, patients must cause aggregation of the donor platelets in the presence of clinically relevant heparin concentrations. This test is specific (<90%) but not sensitive. It is a slow and a sendout.

3) ELISA Immunoassay. (Called Platelet AB, Heparin-induced at UVa) For many hospitals (not this one) it is done in house. Unlike the top two, this is not a functional assay but simply a look to see if the patient antibodies are present. This is done by mixing patient serum with known heparin antigens and running an ELISA. It is highly sensitive - so it's good at ruling out. Since most of our patients have low pretest probability, this is a good first choice. It's not specific, though so if it comes back positive, it is worth considering a confirmatory test (either of the above). It is a the quickest test to come back (usually 2-3 business days).

Arepally, GM, Ortel, TL. Clinical practice. Heparin-induced thrombocytopenia. N Engl J Med 2006; 355:809.

Continuous Renal Replacement Therapy and Thrombocytopenia. It seems like patients on continuous renal replacement therapies (CRRTs) often have low platelet counts. Coincidence? Nope. Many trials have found that platelet counts and platelet functional ability both drop with CRRT. Concominant HITT? Maybe, but extremely unlikely. A retrospective study published in 2008 showed that one third of patients who received CRRT with concurrent heparin had a greater than 50% decrease in platelet count from baseline and a platelet count less than 100,000/mm3. Almost all these patients were not judged to have HITT.

Holmes et al. The clinical diagnosis of heparin-induced thrombocytopenia in patients receiving continuous renal replacement therapy. Journal of Thrombosis and Thrombolysis. 2008. Volume 27, Number 4, 406-412
Boldt J. Continuous hemofiltration and platelet function in critically ill patients. Crit Care Med. 1994 Jul;22(7):1155-60.

From Danielle

Autonomic Dysreflexia (AD). An uncontrolled sympathetic responses in patients with spinal cord injuries (SCI), is suspected to affect around 50-70% SCI patients with T6 or higher lesions. The primary component is a severe elevation in blood pressure, but other signs and symptoms include headache, flushing, and blotching of skin above the level of the lesion. Most likely, signs and symptoms of AD are due to an imbalance between the parasympathetic pathways above the spinal cord lesion and sympathetic pathway below the spinal cord lesion. Any number of events can trigger AD. They include surgery, anesthesia, bladder distention, urinary tract infections, genital stimulation, GU or GI manipulation, constipation, fractures, skin ulcerations, pregnancy and labor.

Many non-randomized studies have looked at ways to prevent AD. Most studies have focused on preventing the occurrence or autonomic nervous system's detection of GU triggers that cause AD. For example, botulinum toxin maybe be injected into the detrusor muscle to provide relief from bladder distention. Perhaps more importantly, it might be effective to do epidural or nerve blocks during procedures to reduce the occurrence of AD during urological procedures or labor.

Treatment of AD involves managing the triggers that cause episodes and when necessary, pharmaceutical management of elevated blood pressure. Studies have not been done to see which anti-hypertensive medications are most effective. The body of evidence is primarily based on case reports and extrapolation of hypertensive crisis management in patients without spinal cord injuries. In general, there is a consensus to use short acting, rapid onset, anti-hypertensives such as nifedipine which has been reported numerous times to lower blood pressure and control AD episodes. Alpha blockers have had mixed results when used, but sildenafil and captopril have been effective in some case reports.

Krassioukov, et. al. (2009). "A Systematic Review of the Management of Autonomic Dysreflexia After Spinal Cord Injury." Arch. Phys. Med. Rehabil. 90:682-696.

SICU Rounds Report - Sept 16th 2010

From Brent (PharmD Student)

Acetazolamide use and outcomes in the ICU.  Acetazolamide (Diamox) reversibly inhibits carbonic anhydrase which results in a decrease in hydrogen ion secretion at the renal tubule and increased renal excretion of sodium, potassium, bicarbonate, and water.  This action can help correct alkalosis and fluid overload.

In a placebo-controlled study of intubated COPD patients on mechanical ventilation in the ICU, one dose of Diamox 500mg was shown to reverse metabolic alkalosis, but did not have a benefit from weaning patients from the ventilator or improving PaCO2.  The PaCO2/FiO2 ratio was increased, but no other respiratory markers were improved.

Diamox does significantly decrease serum bicarbonate and blood pH.  There is some concern with overcorrecting metabolic alkalosis with multiple doses, but side effects are uncommon with conventional dosing.  Of note, a trial comparing one dose of 500mg to multiple doses of 250mg of Diamox showed similar efficacy in reversing nonchloride responsive metabolic alkaloses in MICU patients.  Using the single 500mg dose would further reduce risk of side effects from use.  Also, avoiding repeat dosing for 3 to 5 days is recommended to reduce pH overcorrection and risk of hyperchloremic, hypokalemic metabolic acidosis

Currently, there is not enough data to state that the time to vent wean is decreased by using acetazolamide, but risk of poor outcomes from acetazolamide use are relatively rare when dosed in moderation.

Faisy, Christophe, et al. "Effectiveness of acetazolamide for reversal of metabolic alkalosis in weaning COPD patients from mechanical ventilation." Intensive care medicine 36.5 (2010):859-863.

Lexicomp

Mazur, J. E., et al. "Single versus multiple doses of acetazolamide for metabolic alkalosis in critically ill medical patients: a randomized, double-blind trial." Critical care medicine 27.7 (1999):1257-1261.

From Patrick

AIVR.   Accelerated Idioventricular Rhythm (AIVR) is in the middle of the spectrum of ventricular rhythms that includes on one end of the spectrum the normal intrinsic ventricular escape rhythm (<40bpm) and on the other end ventricular tachycardia (>100-120bpm).  However, rate alone is not sufficient to differentiate AIVR (40bpm - 120bpm) from vtach (> 100-120bpm), because some slow vtach's can have overlapping rates with AIVR.

AIVR is generally transient and rarely causes hemodynamic instability or requires treatment.  In fact, AIVR has been extensively studied in STEMI patients and has been shown to be a marker of reperfusion or of reopening of occluded coronary arteries.  The underlying mechanism of AIVR appears to be enhanced automaticity (due to ischemia, reperfusion, hypoxia, drugs, or  electrolyte abnormalities, all of which accelerate phase 4 action potential depolarization rates leading to faster spontaneous cell depolarization enhanced automaticity) of the His-Purkinje fibers or the myocardium itself.

Diagnosing AIVR.  Pts typically have a history of myocardial ischemia with recent reperfusion through drugs or coronary artery interventions, hx of cardomyopathy or myocarditis, and occasionally pts will have a history of digoxin use, anesthetic agents, or even cocaine.  AIVR rarely occurs in pts without apparent heart disease or triggers.  Again, the most common cause of AIVR is myocardial ischemia - reperfusion.  Other common causes are digoxin toxicity (a possibility in our SIMU patient), cocaine toxicity, various anesthesia agents (desflurane and

halothane), cardiomyopathies, electrolyte abnormalities, and postresuscitation.  Other arrhythmias to consider on the differential are slow ventricular tachycardia, complete heart block, SVT with aberrancy, or junctional rhythm with aberrancy.  Characteristics that distinguish

AIVR from the others is that AIVR starts off gradually, with the ectopic ventricular focus firing gradually and gradually faster until it surpasses the rate of the sinus node; as a result, it is not

uncommon to see ventricular fusion beats (partial ventricular capture from two different rhythms) as a result of the sinus rhythm and ectropic ventricular rhythm overlapping in rate.  Similarly, AIVR usually ends gradually as a result of the AIVR rate decreasing or sinus rate increasing.  In contrast, ventricular tachycardia has a sudden onset and termination.  AIVR is different from SVT or junctional rhythms with aberrancy in that it is a wide QRS complex arrhythmia, whereas arrhythmias from above the SA node are normally narrow complex.

Work-up. Tests to perform in pts with suspected AIVR include Troponins (or CK / CK-MB), BUN and creatinine (to assess renal function in pts with suspected dig toxicity), digoxin levels, electrolytes, and echo / nuclear perfusion scan / coronary angiogram to assess cardiac disease

/ ischemia.  EKG is the most important test to obtain because it can be used to distinguish AIVR from other malignant arrhythmias such as Vtach or complete heart block.

Treatment.  Rarely requires treatment because it is usually self-limited and hemodynamically tolerated.  If treatment is performed, it is usually aimed at the underlying cause of the AIVR (treating ischemia, digoxin toxicity, electrolyte abnormalities, etc.).  Rarely, AIVR may lead to

intolerated rapid ventricular rate or even degenerate into vtach / vfib, in which case atropine can be used to increase the sinus rate and inhibit AIVR.

Pezeshkian NG, Yang Y.  Accelerated Idioventricular Rhythm.  Emedicine cardiology site - http://emedicine.medscape.com/article/150074-overview.  Updated Apr 2010.

Hohnloser SH, Zabel M, Kasper W, Meinertz T, Just H. Assessment of coronary artery patency after thrombolytic therapy: accurate prediction utilizing the combined analysis of three noninvasive markers. J Am Coll Cardiol. Jul 1991;18(1):44-9.

Erkelsen CJ, Sørensen JT, Kaltoft AK, Nielsen SS, Thuesen L, Bøtker HE, et al. Prevalence and significance of accelerated idioventricular rhythm in patients with ST-elevation myocardial infarction treated with primary percutaneous coronary intervention. Am J Cardiol. Dec 15 2009;104(12):1641-6.

From Max

"Orthopedic" Bowel Regimen for Opioid-related Constipation.  Almost universally, if you are on an opioid you will have constipation. Defined: Fewer than 3 bowel movements per week, along with symptoms such as small or hard stools, abdominal bloating or pain, straining, need for digital manipulation, and nausea. ICU patients of course have limited mobility, which makes things worse. According to Max, some of these patients may also suffer from depression which, apparently, is a strong risk factor for constipation. Also, decrease in oral intake, especially fluid and fiber, furthers the problem. So here's how we attack it:

Bulking Agents. Psyllium, calcium polycarbophil, methylcellulose. Work by retaining water in the stool. However, psyllium has been associated with anaphylactic reactions and bloating is noted in patients receiving large quantities. Mechanical obstruction of the esophagus and colon has also been reported with the use of bulking agents.

Osmotic Laxatives. Polyethylene glycol, lactulose, and milk of magnesia. These agents contain poorly absorbed ions or molecules, which create an osmotic gradient and lead to water retention within the intestinal lumen. Adverse effects with osmotic laxatives may include electrolyte abnormalities, hypovolemia, and diarrhea.

Stool Softeners. Docusate sodium and docusate calcium. Soap like compounds that allow more interaction between water and solid stool to form "softened" stool. Safe with minimal side effects.

Stimulant Laxatives. These are the most exciting. Senna or bisacodyl-containing laxatives. They stimulate colon mucosal sensory nerve endings on contact and to inhibit water absorption via epithelial transport alteration. Adverse effects include abdominal discomfort, electrolyte imbalances, allergic reactions, hepatotoxicity, cathartic colon, and melanosis coli.

Maintain a high index of suspicion for the possibility of bowel obstruction or fecal impaction. If things are bad, Max believes rectal disimpaction must occur before treating constipation with an oral laxative regimen.

If a patient has not been on a bowel regimen, the STEP 1 regimen should be started. If there is no response in 24 hours, move to the next step. At any given time, if there has been no bowel movement in 3 or more days, a sodium phosphate or mineral oil enema should be administered. If this is not effective, a high colonic tap water enema should be administered.

• Step 1 à Docusate 100 mg PO bid and Senna 1 tab po qd to bid
• Step 2 à Docusate 100 mg PO bid and Senna 2 tabs po bid and Bisacodyl rectal suppository 1-2 after breakfast
• Step 3 à Docusate 100 mg PO bid and Senna 3 tabs po bid and Bisacodyl rectal suppository 3-4 after breakfast
• Step 4 à Docusate 100 mg PO bid and Senna 4 tabs po bid and Lactulose or Sorbitol 15 ml po bid and Bisacodyl rectal suppository 3-4 after breakfast
• Step 5 à Indicated for no Bowel Movement in 4 days. Sodium phosphate enema or oil retention enema or high-colonic tap water enema. Continue until adequate results.
• Step 6 à Docusate 100 mg PO bid and Senna 4 tabs po bid and Lactulose or Sorbitol 30 ml po bid and Bisacodyl rectal suppository 3-4 after breakfast
• Step 7 à Docusate 100 mg PO bid and Senna 4 tabs po bid and Lactulose or Sorbitol 30 ml po qid and Bisacodyl rectal suppository 3-4 after breakfast.

Morrison S. et al. A Novel Interdisciplinary Analgesic Program Reduces Pain and Improves Function in Older Adults After Orthopedic Surgery. J Am Geriatr Soc. 2009;57(1):1-10

Ho J. et al. Update on Treatment Options for Constipation. ORTHOSuperSite. 2008

Bowel Regimen in Chronic Narcotic Use. Family Practice Notebook.com. Web access on sept 14th, 2010.

SICU Rounds Report - Sept 15th 2010

The TRICC Trial. Almost every day we're asked to transfuse someone when they dip below the '10/30' mark. This dated recommendation came from a paper in 1942 and still haunts even the most storied of medical centers. Sadly, except for highly selected patient group (active MI, sepsis with low SVO2, etc.) there is not a bit of evidence, retrospective or otherwise, that says it is beneficial. In fact, volumes of retrospective papers have found that number to be too high and transfusing to meet it leads to prolonged hospital stay, increased infections rates and worsening mortality.  Goal directed therapy (i.e. optimizing perfusion) is a better target than arbitrary numbers. To do that well, we need way more data. Sadly, the only major, well-conducted study on the issue in adults has been the TRICC trial. (There are several small RTCs with varying results, but in most of those the restrictive group was similar to the liberal strategy of the TRICC trial!) Two others major trials are apparently due out in the next 12 months.

What is the TRICC trial? Transfusion Requirements in Critical Care trial was run by a consortium of Canadian ICU's. The trial looked at a big, mixed group (over 800 patients w/ARDS, trauma, head injury, GI, heart disease, sepsis, etc) of anemic ICU patients and randomized them to a liberal (transfuse when hbg < 9) or conservative strategy (transfuse when hbg <7). In hospital mortality was cut by a 20% in the conservative group (p<0.05). In those that were less sick and in those under 55, conservative strategies cut the mortality rate by half (p<0.02)!

What about coronary artery disease? Retrospective analysis have found that anemic patients with active, unstable myocardial ischemia do worse, and the TRICC trial did not have enough patients in this group to make any statements one way or another. However, it did say, "there were no significant differences in 30-day mortality between treatment groups in the subgroup of patients with a primary or secondary diagnosis of cardiac disease (20.5 percent in the restrictive-strategy group and 22.9 percent in the liberal-strategy group; 95 percent confidence interval for the difference, ¡6.7 to 11.3 percent; P=0.69)." This suggest that, unless the patient has active ischemia, patients with a history of stable coronary artery disease can be safely treated like those without CAD.

Note the same group basically repeated the TRICC trial in kids - it showed about the same thing - that a conservative transfusion strategy is at least as good.
Adams RC, Lundy JS: Anesthesia in cases of poor surgical risk. Some suggestions for decreasing the risk. Surg Gynecol Obstet 1942, 74:1011-1019.
Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. N Engl J Med 1999;340:409-417[Erratum, N Engl J Med 1999;340:1056.]
Lacroix, J, Hebert, PC, Hutchison, JS, et al Transfusion strategies for patients in pediatric intensive care units. Pediatric Acute Lung Injury and Sepsis Investigators Network. N Engl J Med 2007;356,1609-1619

From Scott:
ACE Inhibitors in Acute Decompensated Heart Failure. There is question whether or not ACEI have a place in acute decompensation in heart failure.  This is complicated by the fact that these drugs are a mainstay of chronic systolic heart failure therapy.  

The use of ACEI in ADHF depends largely on whether or not the patient is already taking ACEI chronically.  For patients that are already taking ACEI, they should be cautiously continued in the setting of ADHF in the absence of hemodynamic instability or contraindications.  They should be DISCONTINUED in the following settings:  Hypotension, Acute Renal Failure and Hyperkalemia.
Currently, using ACEI and ARBs in the acute setting of ADHF is not recommended. While there are some studies advocating the use of these, the recommendations I found opted against their use for several reasons:

• Many patients with ADHF develop hypotension and/or worsening renal function>  Determining the etiology of these can be complicated by recent addition of a new ACEI.  Hypotension may also be prolonged with the addition of these long-acting drugs.
• Enalaprilat in particular (an IV ACEI) can have deleterious effects during acute MI, especially during HF or aggressive diuresis.  Thus, this drug should be avoided in all pts with MI, and likely those with other causes of HF.
• Aggressive diuretic therapy (frequently used in pts with acute pulmonary edema) can also increase the body's response to ACEI therapy, which may increase the risks of hypotension and renal dysfuntion.

ACEI are great drugs in chronic heart failure, preventing many long term physiologic changes in the myocardium, but are not great drugs in ADHF.  The evidence I found recommends sticking to mainstays of therapy: Supplemental O2, Diuresis with a loop diuretic, Vasodilator therapy in patients without hypotension, and potential ionotrope therapy.
Colucci, WS.  Gottlieb, SS, et al.  Treatment of Acute Decompensated Heart Failure: Components of Therapy.  UpToDate.com, Updated May 30, 2010.  Copyright 2010 UpToDate.
Heart Failure Society of America.  Evaluation and management of patients with acute decompensated heart failure.  J Card Fail 2006; 12:e86.

From Patrick:
Basic measurements from a Swan-Ganz and what they mean.  
Cardiac output is derived from PAC thermodilution method (10ml cold H2O @ a known temp is injected through a proximal thermistor port and temp is measured again at the distal port 6-10cm downstream).  Faster temperature change = high CO, slower temperature change = low CO.
There are multiple methods to calculate CO, each with its own advantages / disadvantages, including: Fick principle, Finapres methodology, Dilution method, Ultrasound dilution method, Doppler ultrasound method, Pulse pressure method, MRI.

Cardiac Index = CO / BSA = (SV * HR) / BSA. Cardiac index is basically the cardiac output (CO) in relation to the body surface area (BSA), thus normalizing cardiac output to the size of the individual.  Normal  values are 2.6-4.2 L/min/m2.  CI below 1.8L/min/m2 is indicative of cardiogenic shock. (BSA is derived from various formulas that are available, the most commonly used being the formula of DuBois and DuBois: BSA = (W^0.425 x H^0.725) x 0.007184.)

PA Pressure is directly measured through the catheter.  Normal PA pressure is about 25-systolic / 10-diastolic with a mean of 15mmHg.  Higher PA pressures of course indicate pulmonary hypertension.

SvO2 or mixed venous oxygen saturation should be measured in the pulmonary artery, where IVC, SVC and coronary sinus blood have mixed. This can be sampled from blood asiparated from a PA catherter or fiber-optic based probes allow for direct measurement of oxygen
saturation of the ventricular tissues.  SvO2 = SaO2 - [VO2 / (1.36 x Hb x CO)].  If SaO2, oxygen consumption (VO2) and Hb remain stable, the SvO2 can be used as an indirect indicator of cardiac output.  Otherwise, an increase in oxygen consumption, decrease in Hb, CO and
arterial oxygenation (SaO2) will result in a decreased SvO2.

Controversy surrounds the use of PAC and the outcomes of critically ill patients undergoing PAC monitoring.  Some studies have shown reduction in mortality, while others have shown an  increase in mortality.  A large RCT suggested that addition of a pulmonary artery catheter (Swan-Ganz) in 433 CHF patients did not affect overall mortality and hospitalization in comparison to careful clinical assessment (ESCAPE trial).  Similar neutrality of harm/benefit with PAC use was seen in critically ill patients (3).  More prospective RCT are recommended to define the role of PAC in the critically ill, although it continues to be an established way of monitoring the hemodynamics in such patients (4). See attached article for more information.
Du Bois & Du Bois,Arch Intern Med 1916, 17:863
The ESCAPE Investigators and ESCAPE Study Coordinators. Evaluation Study of Congestive Heart Failure and Pulmonary Artery
Catheterization Effectiveness. JAMA. 2005;294:1625-1633.
Shah MR, Hasselblad V, Stevenson LW, Binanay C, O'Connor CM, Sopko G, Califf, RM.  Impact of the Pulmonary Artery Catheter in Critically Ill Patients. JAMA. 2005;294:1664-1670
Mathews L, Singh RKK.  Swan-Ganz Catheter in Hemodynamic Monitoring.  J Anaesth Clin Pharmacol 2006; 22(4) : 335-345.

From Chris:
The APACHE II Scoring System. The Acute Physiology and Chronic Health Evaluation Scoring System (APACHE) was the first scoring system of its kind to be commonly used in ICUs.  The initial system was very, very complicated.  It used 34 physiologic variables and a chronic health evaluation.  But, it also required a lot of time to both gather the data and do the actual calculations (no useful computers way back in the 80's).  The APACHE II system is a simplification of the original formula that was published in 1985.  It uses 12 physiologic markers, patient age, and a chronic health evaluation.  It give you a number between 0 and 71.  The idea is that you can use the same calculation to determine the "seriousness" of their illness.  Additional studies have shown that it often correlates very well with patient morbidity and mortality and the number is used in a lot of other clinical calculations.  A 1 point increase theoretically equates to approximately a 1% increase in mortality risk.  Importantly , though it was designed as a standard measure, it does not take into account the patient's actual diagnosis.  This means that, strictly speaking, you can't use the APACHE II score to compare patients across different diseases.  A person with CAP and an APACHE II score of 25 has a very different mortality risk than a patient admitted for sepsis and DIC with the same APACHE score.

The original article says that, in order to be of prognostic value, the score must be combined with "an accurate description of disease."

The score can be used for prognosis, and to classify patients for research.

The 12 Physiologic parameters: Rectal temp; MAP; HR; RR, O2 delivery (ml/min) Po2; pH; NA; K; Cr; Hct; WBC.  You get 0-4 points for each 1 of these based on how far you are from the normal values.  Then, you add, points for age and a chronic health index score.  You use a chart, or an iPhone, to do the calculations.
Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985 Oct;13(10):818-29.
Miller RD Ed. Miller's Anesthesia, 7th ed.  2009