Auto-Anticoagulation of Cirrhosis? Patients with liver failure commonly present with elevated INRs and low platelet counts. Liver dysfunction alters synthesis and production of both the pro- and anti-coagulants produced by the liver. In addition, numerous other effects alter normal coagulation in the cirrhotic patient: low platelets, platelet dysfunction, altered endothelial function (including elevated levels of prothrombotic vWF and tFVIII), elevated levels of nitric oxide, etc. Further confusing things: liver failure can dramatically increase rates of fibrinolysis. What does it all mean?
In other words: Does a liver failure patient with an INR of 2.3 needs DVT prophylaxis?
It depends on who you ask. The recent medical literature suggests that cirrhosis offers little, or no protection. Now, in the first study of its kind, researchers at the University of Missouri looked at the relationship between pathologic INR elevations and DVT. They retrospectively evaluated 190 hospitalized patients with varying degrees of chronic liver disease and found rates of DVT of 6.3% overall (by comparison, rates of DVT in high risk surgical inpatients without prophylaxis is between 4 - 8%). Interestingly, higher elevations in INR were associated with greater DVT risk. Lastly, the study found that receiving DVT prophylaxis didn't protect against DVT, although the study was underpowered to detect a statistical difference and only 25% of liver failure patients received some kind of prophylaxis. Sadly, there is no data available for surgical patients.
What everyone can agree on is that current panel of test used to diagnosis coagulation abnormalities in liver failure (plt count, PT, aPTT) are worthless because the balance of pro/anticoagulant factors is not considered by these tests (which tend to measure simple deficiencies of anticoagulants). Abnormal hemostatic tests have never been shown to correlate to bleeding tendencies in liver failure. Further, it is clear from liver transplantation surgery that preemptive "correction" of the abnormal values does not reduce, and probably promotes, bleeding. With this shift in thinking, many centers are now reporting the ability to keep liver transplantation "bloodless" (no transfusions needed) greater than half the time. To accurately diagnosis whether a liver failure patient is pro- anti- or euthrombotic requires much more sensitive testing, such as TEG, which is not widely available.
So we're left where we started, which is were every good paper ends: more research is needed! Do liver patients needs SCDs/heparin? Anyone's guess. How can we even measure coagulation in liver failure? Not really possible. Does prophylaxis even work in the setting of liver failure? No one has a clue. Is working in an ICU awesome anyway? Yes, very!
Dabbagh, O, et al. Coagulopathy does not protect against venous thromboembolism in hospitalized patients with chronic liver disease. Chest 2010; 137:1145.
Lisman, T, Porte, RJ. Rebalanced hemostasis in patients with liver disease: evidence and clinical consequences. Blood 2010; 116:878.
Gulley D et Al. Deep vein thrombosis and pulmonary embolism in cirrhosis patients. Dig Dis Sci . 2008; 53( 11): 3012- 3017.
Northup PG, et al. Coagulopathy does not fully protect hospitalized cirrhosis patients from peripheral venous thromboembolism. Am J Gastroenterol 2006 ;101(7):1524-1528.
Gotta have more? Old Issues HERE.
Answers to common and uncommon questions that come up during the course of ICU rounds at the University of Virginia Medical Center. Curated and developed by Jordan Hackworth, M.D.
Thursday, December 16, 2010
Thursday, December 9, 2010
ICU Rounds Report - Dec 9th, 2010
Creatinine, an oldie but a goodie? Creatinine is a breakdown product of creatine kinase in skeletal muscle. First found in blood in 1896, it was noticed that levels go way up with chronic kidney disease in the 1910's. We've been fixated on it every since as the biomarker for kidney function. It's been routinely measured on hospital inpatients for at least 60 years. It's worth reviewing it strengths and weaknesses.
In the strength column, we can place that we have lots of experience with it. It's widely available, cheap to measure and tracks chronic disease quite nicely. Downsides? First, I've never liked saying it. It's a funny word. Second, the production of creatinine is highly variable, dependent on multiple factors including age, sex, race, muscle mass, nutritional state and others. Second, up to 40% of urinary creatinine is secreted by the tubules not filtered. In other words, it will never directly correlate with GFR as well as something that is not secreted at all, such as cysatinC (CysC). This leads to delays in the diagnosis of acute drops in GFR. Which brings us to the third major problem: It's slow. When the kidney filtering slows or stops, it takes days the serum creatinine to rise because basal production rates are so slow. Currently, we have to wait 2 days to learn the kidneys have been injured, beyond the time when interventions are thought to possibly improve outcomes. Its like trying to diagnosis an acute MI without troponins and just waiting to see how it will all settle out.
These limitations have lead to the intense development of serum and urinary biomarkers that better reflect GFR, give real time information about kidney injury and will, in all likelihood, make our old friend creatinine obsolete for ICU use with in 10 years . We've got several great candidates which work quicker, correlate better with disease severity and give more prognostic information coming down the pipeline, some of which are already being used in POC testing around the world (NGAL, KIM-1, L-FAB).
Rabinowitch IM. The prognostic value of the study of the blood creatinine in nephritis: based upon the study of fourteen cases with complete postmortem examination. Can Med Assoc J 1921; 11:320–322.
Moore, E, et al. Novel biomarkers of acute kidney injury: ready for clinical application? Current Opinion in Critical Care. Dec 2010 16(6): 523–525
Ultrasound for ICP. Occasionally, (meningitis, trauma, liver failure, strokes) we wonder what the pressure inside the head is. CTs of course, let us peek inside but only allow inferences. Sometimes, we wonder so much about ICP that we have the brain surgeons put an invasive monitor thru the skull. That's nice because it can also be therapeutic (in the case of EVDs). But is there a quicker way? Yes! Does it work? Maybe!
In 2010, when someone asks the question, 'is there a quicker way' the correct answer is either Epic or Ultrasound. Ultrasound? Sure. Recall that the optic nerve is sheathed within the dura. It appears that elevated pressures allow CSF buildup in this semi-compliant sheath and widen the diameter. (That's also the basis for blathering on about papilloedema). Multiple studies have measured the diameter of the optic sheath with ultrasound (at a standardized location, 3mm past the globe) and found a nice concordance with ICP. On study found a diameter greater than 5 (normal=3mm) was strongly predictive of an of ICP >20 mm Hg (sensitivity and specificity 94% and 76%, respectively).
Further work with MRI looking at the optic nerve sheath has shown that it is even more sensitive. With MRI, a cut-off value of 5.30 mm yields a sensitivity of 100% for diagnosis an ICP greater than 20.
Soldatos T. Optic nerve sonography: a new window for the non-invasive evaluation of intracranial pressure in brain injury. Emerg Med J 2009;26:630-634
Geeraerts T, et al. Use of T2-weighted magnetic resonance imaging of the optic nerve sheath to detect raised intracranial pressure. Crit Care 2008;12(5):R114. Epub 2008 Sep 11.
In the strength column, we can place that we have lots of experience with it. It's widely available, cheap to measure and tracks chronic disease quite nicely. Downsides? First, I've never liked saying it. It's a funny word. Second, the production of creatinine is highly variable, dependent on multiple factors including age, sex, race, muscle mass, nutritional state and others. Second, up to 40% of urinary creatinine is secreted by the tubules not filtered. In other words, it will never directly correlate with GFR as well as something that is not secreted at all, such as cysatinC (CysC). This leads to delays in the diagnosis of acute drops in GFR. Which brings us to the third major problem: It's slow. When the kidney filtering slows or stops, it takes days the serum creatinine to rise because basal production rates are so slow. Currently, we have to wait 2 days to learn the kidneys have been injured, beyond the time when interventions are thought to possibly improve outcomes. Its like trying to diagnosis an acute MI without troponins and just waiting to see how it will all settle out.
These limitations have lead to the intense development of serum and urinary biomarkers that better reflect GFR, give real time information about kidney injury and will, in all likelihood, make our old friend creatinine obsolete for ICU use with in 10 years . We've got several great candidates which work quicker, correlate better with disease severity and give more prognostic information coming down the pipeline, some of which are already being used in POC testing around the world (NGAL, KIM-1, L-FAB).
Rabinowitch IM. The prognostic value of the study of the blood creatinine in nephritis: based upon the study of fourteen cases with complete postmortem examination. Can Med Assoc J 1921; 11:320–322.
Moore, E, et al. Novel biomarkers of acute kidney injury: ready for clinical application? Current Opinion in Critical Care. Dec 2010 16(6): 523–525
Ultrasound for ICP. Occasionally, (meningitis, trauma, liver failure, strokes) we wonder what the pressure inside the head is. CTs of course, let us peek inside but only allow inferences. Sometimes, we wonder so much about ICP that we have the brain surgeons put an invasive monitor thru the skull. That's nice because it can also be therapeutic (in the case of EVDs). But is there a quicker way? Yes! Does it work? Maybe!
In 2010, when someone asks the question, 'is there a quicker way' the correct answer is either Epic or Ultrasound. Ultrasound? Sure. Recall that the optic nerve is sheathed within the dura. It appears that elevated pressures allow CSF buildup in this semi-compliant sheath and widen the diameter. (That's also the basis for blathering on about papilloedema). Multiple studies have measured the diameter of the optic sheath with ultrasound (at a standardized location, 3mm past the globe) and found a nice concordance with ICP. On study found a diameter greater than 5 (normal=3mm) was strongly predictive of an of ICP >20 mm Hg (sensitivity and specificity 94% and 76%, respectively).
Further work with MRI looking at the optic nerve sheath has shown that it is even more sensitive. With MRI, a cut-off value of 5.30 mm yields a sensitivity of 100% for diagnosis an ICP greater than 20.
Soldatos T. Optic nerve sonography: a new window for the non-invasive evaluation of intracranial pressure in brain injury. Emerg Med J 2009;26:630-634
Geeraerts T, et al. Use of T2-weighted magnetic resonance imaging of the optic nerve sheath to detect raised intracranial pressure. Crit Care 2008;12(5):R114. Epub 2008 Sep 11.
Tuesday, December 7, 2010
ICU Rounds Report - Dec 7th, 2010
It's so cold out there! Survival after out of hospital cardiac arrest with a good outcome is a rare event. Despite advances across other fronts in medicine, survival with an intact brain hadn't improved much in the last 50 years until someone tried post-arrest cooling. Previously, post-resuscitation efforts have been entirely supportive. Now, for comatose patients after vfib arrest, cooling the body to 34 degrees for 24 hours can nearly double the chance of recovery. Currently at UVa, we're cooling 3-4 patients a month (last month we did 7!).
But how do we cool patients? Everything has been tried. From ice bags, cold saline, irrigating bladder/stomach with cold fluids to cardiopulmonary bypass. All present technical and clinical challenges, not the least of which is that body vigorously defends its tightly regulated core temperature by increasing metabolic rate and shivering, usually requiring paralysis. Surface cooling is cumbersome and ineffective. Intravascular cooling (which we use) is expensive and risky. What if there was another way?
Researchers in toasty warm LA have published a trial using cannabanoid agonists in rats after resuscitation in vfib arrest. The results are very good news if you are a rat in a coma after vfib arrest: the drug appears to safely lower body temperature to ~34 degrees with no other major noted side effects. More importantly, the neurologic and functional outcome was significantly improved relative to controls. The idea may represent a new therapeutic class for a common and lethal problem for thousands of Americans.
Finally, a quote from recent editorial on the new findings by Samuel Tisherman, "From the campaign 20 yrs ago (showing a frying pan representing marijuana and an egg representing your brain), to current controversies regarding legal medical uses, marijuana has a long history of capturing our interest. Wouldn't it be cool if a derivative actually improves brain function rather than frying it?"
Sun S, Tang W, Song F, et al: Pharmacologically induced hypothermia with cannabinoid receptor agonist WIN55, 212-2 after cardiopulmonary resuscitation. Crit Care Med 2010; 38:2282–2286
Bernard SA, Gray TW, Buist MD, et al: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002; 346:557–563
But how do we cool patients? Everything has been tried. From ice bags, cold saline, irrigating bladder/stomach with cold fluids to cardiopulmonary bypass. All present technical and clinical challenges, not the least of which is that body vigorously defends its tightly regulated core temperature by increasing metabolic rate and shivering, usually requiring paralysis. Surface cooling is cumbersome and ineffective. Intravascular cooling (which we use) is expensive and risky. What if there was another way?
Researchers in toasty warm LA have published a trial using cannabanoid agonists in rats after resuscitation in vfib arrest. The results are very good news if you are a rat in a coma after vfib arrest: the drug appears to safely lower body temperature to ~34 degrees with no other major noted side effects. More importantly, the neurologic and functional outcome was significantly improved relative to controls. The idea may represent a new therapeutic class for a common and lethal problem for thousands of Americans.
Finally, a quote from recent editorial on the new findings by Samuel Tisherman, "From the campaign 20 yrs ago (showing a frying pan representing marijuana and an egg representing your brain), to current controversies regarding legal medical uses, marijuana has a long history of capturing our interest. Wouldn't it be cool if a derivative actually improves brain function rather than frying it?"
Sun S, Tang W, Song F, et al: Pharmacologically induced hypothermia with cannabinoid receptor agonist WIN55, 212-2 after cardiopulmonary resuscitation. Crit Care Med 2010; 38:2282–2286
Bernard SA, Gray TW, Buist MD, et al: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002; 346:557–563
Wednesday, November 24, 2010
ICU Rounds Report - November 24th, 2010
Metformin Acidosis - The ICU Yeti? You've probably heard someone call oxygen toxicity the sasquatch of the ICU - frequently talked about but never seen. Speaking of mythical creatures - how many of you have actually seen acidosis from metformin? In 1950, metformin's cousin phenformin was introduced and was widely used as an oral hypoglycemic. Twenty-five years and over 300 cases of frequently-fatal metabolic acidosis later, the FDA removed the drug. When metformin (Glucophage), a chemically similar biguanide drug, was introduced in in 1995 there was wide spread concern about metabolic acidosis. Merck, the maker, and the government sponsored multiple large trials which, in aggregate, evaluated over 36,000 patient-years without a single incidence of acidosis due to metformin.
By contrast, some case reports have shown up from time to time. The FDA reports that among the first one million treated with metformin, 47 cases (20 fatal) were reported. Forty three of these occurred in the setting of acute renal failure and the rest occurred during sepsis, overdose or heart failure. In other words, when used according to the label, there is zero chance (or close enough to zero as to be clinically irrelevant) of the drug causing acidosis.
Salpeter S, Greyber E, Pasternak G, Salpeter E: Risk of fatal and non-fatal lactic acidosis with metformin in type 2 diabetes. Cochrane Database Syst Rev 2:CD002967, 2003
Stades AME, Heikens JT, Erkelens DW, Holleman F, Hoekstra JBL: Metformin and lactic acidosis: cause or coincidence? A review of case reports. J Int Med 255:179–187, 2004
Neurogenic Pulmonary Edema. After major head injury (status, trauma, hemorrhage) the aveloli and interstitial spaces in the lungs will occasionally fill with fluid causing patients to cough blood, breath quickly and desaturate. On autopsy studies, up to half of patients with those diseases will have evidence of it. We're not quite sure how it happens, but based on animal studies it is likely related to large, sudden increases in sympathetic outflow which causes 1)pulmonary microvascular damage 2)intense pulmonary vasocontriction raising transcapillary pressures and/or 3) acute, transient RV/LV dysfunction. The effect can be blocked with phentolamine in animal models. No human trials have been done to see if alpha blockade is safe or reasonable.
Onset is typically quite rapid after the head insult. Diagnosis is one of exclusion. Treatment is supportive and should be directed at the cause and sequelea of the head injury. Like neurogenic heart dysfunction, the huge majority of cases are transient and improve with time making prognosis more dependent on the extent of the head injury. This disease is sometimes confused with ARDS and may look radiographically similar. The treatment and prognosis are very different, however. Unlike ARDS, high PEEP levels and permissive hypercapnia should be avoided because of their effect on ICP.
Baumann, A, Audibert, G, McDonnell, J, Mertes, PM. Neurogenic pulmonary edema. Acta Anaesthesiol Scand 2007; 51:447.
By contrast, some case reports have shown up from time to time. The FDA reports that among the first one million treated with metformin, 47 cases (20 fatal) were reported. Forty three of these occurred in the setting of acute renal failure and the rest occurred during sepsis, overdose or heart failure. In other words, when used according to the label, there is zero chance (or close enough to zero as to be clinically irrelevant) of the drug causing acidosis.
Salpeter S, Greyber E, Pasternak G, Salpeter E: Risk of fatal and non-fatal lactic acidosis with metformin in type 2 diabetes. Cochrane Database Syst Rev 2:CD002967, 2003
Stades AME, Heikens JT, Erkelens DW, Holleman F, Hoekstra JBL: Metformin and lactic acidosis: cause or coincidence? A review of case reports. J Int Med 255:179–187, 2004
Neurogenic Pulmonary Edema. After major head injury (status, trauma, hemorrhage) the aveloli and interstitial spaces in the lungs will occasionally fill with fluid causing patients to cough blood, breath quickly and desaturate. On autopsy studies, up to half of patients with those diseases will have evidence of it. We're not quite sure how it happens, but based on animal studies it is likely related to large, sudden increases in sympathetic outflow which causes 1)pulmonary microvascular damage 2)intense pulmonary vasocontriction raising transcapillary pressures and/or 3) acute, transient RV/LV dysfunction. The effect can be blocked with phentolamine in animal models. No human trials have been done to see if alpha blockade is safe or reasonable.
Onset is typically quite rapid after the head insult. Diagnosis is one of exclusion. Treatment is supportive and should be directed at the cause and sequelea of the head injury. Like neurogenic heart dysfunction, the huge majority of cases are transient and improve with time making prognosis more dependent on the extent of the head injury. This disease is sometimes confused with ARDS and may look radiographically similar. The treatment and prognosis are very different, however. Unlike ARDS, high PEEP levels and permissive hypercapnia should be avoided because of their effect on ICP.
Baumann, A, Audibert, G, McDonnell, J, Mertes, PM. Neurogenic pulmonary edema. Acta Anaesthesiol Scand 2007; 51:447.
Friday, November 19, 2010
ICU Rounds Report - November 19th, 2010
From Lis
How bad is my hemorrhage, Doctor? Drs. Hunt, Hess and Fisher are often employed to help. Since the 1930's physicians have attempted to compile an adequate grading scale for sub-arachnoid hemorrhage. Ideally this scale would guide management decisions affected by severity, provide a working prognosis, allow for treatment research among the various grades, and monitor changes in severity in an individual patient.
Hunt and Hess (used at UVa):
The Hunt and Hess scale is a 1968 modification of an older scale (Botterell, 1956). The scale was designed to assess surgical risk and if patient is a surgical candidate when is the ideal time to operate. Today it is used to evaluate clinical outcome, which according to one study Hunt and Hess was the strongest predictor of clinical outcome at 6 months when compared to GCS/WFNS (Aulmann, 1998). The scale is built on three axes:
a. Intensity of meningeal inflammation reaction
b. Severity of neurological deficit
c. Level of arousal
d. Presence of significant associated systemic disease à increases grade by one level
The benefit of Hunt and Hess lie in its easy administration. Disadvantages include the low inter-rater reliability (κ = 0.42), vague terminology, and requiring the clinician to evaluate all three axes on a single scale. This forces us to choose which axis is most important and contributes to lax category boundaries and relatively arbitrary grading assignments. Finally, data indicates that there are only differences in outcome associated with some of the grades - specifically Grade 2 and 3 and Grade 3 and 4.
1 Asymptomatic or mild headache and slight nuchal rigidity
2 Moderate to severe headache, nuchal rigidity, no neurologic deficit except cranial nerve palsy
3 Drowsy or confused, mild focal neurological deficit
4 Stuporous, moderate or severe hemiparesis, possible early decerebrate rigidity and vegetative disturbances
5 Coma, decerebrate rigidity, moribund appearance
Fisher:
The Fisher Scale is a 1980 scale designed to predict cerebral vasospasm based on the blood pattern seen on the first post bleed CT scan. The main advantage of the Fisher scale is the high level of inter- rater reliability (κ = 0.90). Since its development, clinicians have started using it as a clinical outcome predictor as well. However the newer scales are combining patient age, Hunt and Hess, and Fisher in order to improve the predictive strength of the scale. One example is the Olgilvy and Carter scale.
1 No blood detected
2 Diffuse deposition or thin layer with all vertical layers (in interhemispheric fissure, insular
cistern, ambient cistern) less than 1 mm thick.
3 Localized clot and/or vertical layers 1 mm or more in thickness
4 Intracerebral or intraventricular clot with diffuse or no subarachnoid blood
Aulmann C, Steudl WI, Feldmann U. [Validation of the prognostic accuracy of neurosurgical admission scales after rupture of
cerebral aneurysms]. Zentralbl Neurochir 1998;59:171–180.
Hunt W, Hess R. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968;
28:14.
Rosen DS, Macdonald RL. Subarachnoid hemorrhage grading scales: a systematic review. Neurocrit Care. 2005;2(2):110-8.
Review.
STATs note: Kappa scores are generally thought to be a more robust measure than simple percent agreement calculation since κ takes into account that the agreement may be occurring by chance. Recall that if the raters are in complete agreement then κ = 1. If there is no agreement among the raters (other than what would be expected by chance) then κ ≤ 0.
-
How bad is my hemorrhage, Doctor? Drs. Hunt, Hess and Fisher are often employed to help. Since the 1930's physicians have attempted to compile an adequate grading scale for sub-arachnoid hemorrhage. Ideally this scale would guide management decisions affected by severity, provide a working prognosis, allow for treatment research among the various grades, and monitor changes in severity in an individual patient.
Hunt and Hess (used at UVa):
The Hunt and Hess scale is a 1968 modification of an older scale (Botterell, 1956). The scale was designed to assess surgical risk and if patient is a surgical candidate when is the ideal time to operate. Today it is used to evaluate clinical outcome, which according to one study Hunt and Hess was the strongest predictor of clinical outcome at 6 months when compared to GCS/WFNS (Aulmann, 1998). The scale is built on three axes:
a. Intensity of meningeal inflammation reaction
b. Severity of neurological deficit
c. Level of arousal
d. Presence of significant associated systemic disease à increases grade by one level
The benefit of Hunt and Hess lie in its easy administration. Disadvantages include the low inter-rater reliability (κ = 0.42), vague terminology, and requiring the clinician to evaluate all three axes on a single scale. This forces us to choose which axis is most important and contributes to lax category boundaries and relatively arbitrary grading assignments. Finally, data indicates that there are only differences in outcome associated with some of the grades - specifically Grade 2 and 3 and Grade 3 and 4.
1 Asymptomatic or mild headache and slight nuchal rigidity
2 Moderate to severe headache, nuchal rigidity, no neurologic deficit except cranial nerve palsy
3 Drowsy or confused, mild focal neurological deficit
4 Stuporous, moderate or severe hemiparesis, possible early decerebrate rigidity and vegetative disturbances
5 Coma, decerebrate rigidity, moribund appearance
Fisher:
The Fisher Scale is a 1980 scale designed to predict cerebral vasospasm based on the blood pattern seen on the first post bleed CT scan. The main advantage of the Fisher scale is the high level of inter- rater reliability (κ = 0.90). Since its development, clinicians have started using it as a clinical outcome predictor as well. However the newer scales are combining patient age, Hunt and Hess, and Fisher in order to improve the predictive strength of the scale. One example is the Olgilvy and Carter scale.
1 No blood detected
2 Diffuse deposition or thin layer with all vertical layers (in interhemispheric fissure, insular
cistern, ambient cistern) less than 1 mm thick.
3 Localized clot and/or vertical layers 1 mm or more in thickness
4 Intracerebral or intraventricular clot with diffuse or no subarachnoid blood
Aulmann C, Steudl WI, Feldmann U. [Validation of the prognostic accuracy of neurosurgical admission scales after rupture of
cerebral aneurysms]. Zentralbl Neurochir 1998;59:171–180.
Hunt W, Hess R. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968;
28:14.
Rosen DS, Macdonald RL. Subarachnoid hemorrhage grading scales: a systematic review. Neurocrit Care. 2005;2(2):110-8.
Review.
STATs note: Kappa scores are generally thought to be a more robust measure than simple percent agreement calculation since κ takes into account that the agreement may be occurring by chance. Recall that if the raters are in complete agreement then κ = 1. If there is no agreement among the raters (other than what would be expected by chance) then κ ≤ 0.
κ | Interpretation |
< 0 | No agreement |
0.0 — 0.20 | Slight agreement |
0.21 — 0.40 | Fair agreement |
0.41 — 0.60 | Moderate agreement |
0.61 — 0.80 | Substantial agreement |
0.81 — 1.00 | Almost perfect agreement |
-
Thursday, November 18, 2010
ICU Rounds Report - November 18th 2010
Sticky Platelets. Back in the days when the only thing to do with an MI was to talk about it (i.e. the 60 and 70's), physicians noticed that heart attacks tended to happen most commonly in the morning. Same for strokes and TIAs. Why? Partly because platelets tend to have diurnal variation and aggregate more avidly in the AM, particularly when people first assume the upright position after lying recumbent all night. These events also to the corresponds to the typically highest blood pressures of the day.
The platelet part of this theory was confirmed in the 1980's in a series of studies that measured platelet function in healthy men around the clock. Reliably, platelets are more likely to aggregate between 6-10am. The implications of this are two: first, don't get out of bed unless you really have to. Second, if you're treating patients at risk for arterial thrombosis with anti-platelet agents, make sure you're covering the morning.
Tofler GH, Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death. N Engl J Med. 1987 Jun 11;316(24):1514-8.
Teachable Moments. Patients undergoing major surgery or trauma are significantly more likely to pay attention to healthful suggestions, like to drink less or stop smoking. Multiple randomized trials of smoking cessation prior to major surgery have shown big benefits, particularly with cardiac and wound complications. Other trials have shown that repeatedly reminding patients to stop smoking and drink less makes an real, measurable impact. This is especially true at stressful times (i.e. new cancer diagnosis, major surgery, trauma).
Alcohol abuse is common problem in our patients and of course a significant risk factor for trauma. Up to 50% of trauma patients will screen positive to alcohol abuse. To decrease the trauma burden, researcher at Harborview Medical Center randomized over 700 trauma patients who screened positive for abuse symptoms to a brief (30 minute) intervention from an addiction counselor or routine care. Patients were told they were in a study regarding trauma outcomes and were not aware that the addiction intervention was part of the study. The results were striking.
At one year, alcohol use was reduced (self-reported) by 22 drinks per week (P<0.03). There was a 47% reduction in injuries requiring either emergency department or trauma center admission (hazard ratio 0.53, 95% confidence interval 0.26 to 1.07, p = 0.07) and a 48% reduction in injuries requiring hospital admission (3 years follow-up).
Given the risks, benefits and costs of this intervention, it seems like alcohol counseling should be routinely given to at risk trauma patients. While that happens from an institutional stand point, it seems reasonable for all of us to take some time and address alcohol and smoking in our patients in these "teachable moments."
Warner, DO. Surgery as a Teachable Moment Lost Opportunities to Improve Public Health Arch Surg. 2009;144(12):1106-1107.
Shi, Y et Al. Surgery as a Teachable Moment for Smoking Cessation. Anesthesiology. 2010 112(1): 102-107
The platelet part of this theory was confirmed in the 1980's in a series of studies that measured platelet function in healthy men around the clock. Reliably, platelets are more likely to aggregate between 6-10am. The implications of this are two: first, don't get out of bed unless you really have to. Second, if you're treating patients at risk for arterial thrombosis with anti-platelet agents, make sure you're covering the morning.
Tofler GH, Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death. N Engl J Med. 1987 Jun 11;316(24):1514-8.
Teachable Moments. Patients undergoing major surgery or trauma are significantly more likely to pay attention to healthful suggestions, like to drink less or stop smoking. Multiple randomized trials of smoking cessation prior to major surgery have shown big benefits, particularly with cardiac and wound complications. Other trials have shown that repeatedly reminding patients to stop smoking and drink less makes an real, measurable impact. This is especially true at stressful times (i.e. new cancer diagnosis, major surgery, trauma).
Alcohol abuse is common problem in our patients and of course a significant risk factor for trauma. Up to 50% of trauma patients will screen positive to alcohol abuse. To decrease the trauma burden, researcher at Harborview Medical Center randomized over 700 trauma patients who screened positive for abuse symptoms to a brief (30 minute) intervention from an addiction counselor or routine care. Patients were told they were in a study regarding trauma outcomes and were not aware that the addiction intervention was part of the study. The results were striking.
At one year, alcohol use was reduced (self-reported) by 22 drinks per week (P<0.03). There was a 47% reduction in injuries requiring either emergency department or trauma center admission (hazard ratio 0.53, 95% confidence interval 0.26 to 1.07, p = 0.07) and a 48% reduction in injuries requiring hospital admission (3 years follow-up).
Given the risks, benefits and costs of this intervention, it seems like alcohol counseling should be routinely given to at risk trauma patients. While that happens from an institutional stand point, it seems reasonable for all of us to take some time and address alcohol and smoking in our patients in these "teachable moments."
Warner, DO. Surgery as a Teachable Moment Lost Opportunities to Improve Public Health Arch Surg. 2009;144(12):1106-1107.
Shi, Y et Al. Surgery as a Teachable Moment for Smoking Cessation. Anesthesiology. 2010 112(1): 102-107
Wednesday, November 17, 2010
ICU Rounds Report - November 17th 2010
The TRACS trial is here! More than 10 years after the publication of the TRICC trial, we're finally getting some more proper, randomized data about blood transfusion in critical care. JAMA last month published the long awaited results of a single center RCT in Brazil involving over 500 patients randomized to liberal (transfuse to >30% hematocrit) vs conservative (>24%) transfusion strategy in patients undergoing routine CABG and/or valve surgery requiring bypass. The intervention significantly reduced PRBCs transfusion (78% and 47% receiving, respectively). Morbidity and mortality was the same in both groups.
Unlike our practice at UVa, all the blood given was young (median age 3 days) and not leukodepleted. Older blood, as is frequently transfused here, has been associated with worse outcome while leukodepletion (standard here) appears to improve outcomes.
In the same issue of JAMA, researches using the STS database found transfusion practices among 700 US hospitals for 100,000 patients undergoing CBP showed wide variance in the rates of product transfusion (RBC (7.8%-92.8%), plasma (0%-97.5%), and platelet (0.4%-90.4%)). These differences persisted after adjusting for hospital and patients factors. Like the TRACS trial, there was no apparent difference in mortality or morbidity.
Taken together, these results point to a continued epidemic of costly, unnecessary and potentially dangerous over-utilization of blood products. Previously, this was, in part, due to a lack of RCT-based evidence in this patient group. Now, this is no longer true. We can say with assurance that transfusion of even a single PRBC unit has real risks that must be carefully balanced against benefits which, while real, are increasingly harder to find.
Hajjar LA, Vincent J-L, Galas FRBG; et al. Transfusion requirements after cardiac surgery: the TRACS randomized controlled trial. JAMA. 2010;304(14):1559-1567
Bennett-Guerrero E, Zhao Y, O'Brien SM; et al. Variation in use of blood transfusion in coronary artery bypass graft surgery. JAMA. 2010;304(14):1568-1575.
A FAST HUG Every 5.7 weeks on rounds, someone mentions the mnemonic developed by critical care god Jean Louis Vincent, FAST HUGS. Here it is written down so you have a nice reference to check in case you fancy yet forget it. You can add (although Jean Louis doesn't think you should) a BID, to emphasize this should be done at least twice a day.
F Feeding
A Analgesia
S Sedation
T Thromboembolic prophylaxis
H Head of bed elevation
U Ulcer (stress) prophylaxis
G Glycemic control
S Spontaneous breathing trial
B Bowel regimen
I Indwelling catheter removal
D De-escalation of antibiotics
Vincent JL: Give your patient a FAST HUG (at least) once a day. Crit Care Med 2005; 33:1225–1229
Unlike our practice at UVa, all the blood given was young (median age 3 days) and not leukodepleted. Older blood, as is frequently transfused here, has been associated with worse outcome while leukodepletion (standard here) appears to improve outcomes.
In the same issue of JAMA, researches using the STS database found transfusion practices among 700 US hospitals for 100,000 patients undergoing CBP showed wide variance in the rates of product transfusion (RBC (7.8%-92.8%), plasma (0%-97.5%), and platelet (0.4%-90.4%)). These differences persisted after adjusting for hospital and patients factors. Like the TRACS trial, there was no apparent difference in mortality or morbidity.
Taken together, these results point to a continued epidemic of costly, unnecessary and potentially dangerous over-utilization of blood products. Previously, this was, in part, due to a lack of RCT-based evidence in this patient group. Now, this is no longer true. We can say with assurance that transfusion of even a single PRBC unit has real risks that must be carefully balanced against benefits which, while real, are increasingly harder to find.
Hajjar LA, Vincent J-L, Galas FRBG; et al. Transfusion requirements after cardiac surgery: the TRACS randomized controlled trial. JAMA. 2010;304(14):1559-1567
Bennett-Guerrero E, Zhao Y, O'Brien SM; et al. Variation in use of blood transfusion in coronary artery bypass graft surgery. JAMA. 2010;304(14):1568-1575.
A FAST HUG Every 5.7 weeks on rounds, someone mentions the mnemonic developed by critical care god Jean Louis Vincent, FAST HUGS. Here it is written down so you have a nice reference to check in case you fancy yet forget it. You can add (although Jean Louis doesn't think you should) a BID, to emphasize this should be done at least twice a day.
F Feeding
A Analgesia
S Sedation
T Thromboembolic prophylaxis
H Head of bed elevation
U Ulcer (stress) prophylaxis
G Glycemic control
S Spontaneous breathing trial
B Bowel regimen
I Indwelling catheter removal
D De-escalation of antibiotics
Vincent JL: Give your patient a FAST HUG (at least) once a day. Crit Care Med 2005; 33:1225–1229
Friday, November 12, 2010
ICU Rounds Report - Nov 12th 2010
We're back! I've been in the TCV-PO, where there was neither time nor medical students to help with the report. Now, the 'break' is over. Thanks for reading!
Colchicine is commonly used for both acute treatment and the prevention of gouty arthiritis. We've recently had a patient inadvertently continued on their home dose, which is problematic for many reasons. But first some background, and an interesting aside about American drug policy. The FDA has made arrangements for companies to test drugs grandfathered into common usage prior to the approval process in exchange for a few years of market exclusivity. Ostensibly, this is because the FDA cannot afford to run the trials themselves. Colchicine, despite being used for centuries, was recently approved (2009) after a drug company paid for a large clinical trial that proved efficacy according to modern FDA standards. Accordingly, exclusive approval to market the drug was given to URL Pharma and they promptly raised the price per tablet from $0.08 to $4.85, a move expected to cost Medicare over $50,000,000 this year alone. So, where's the savings?
But I digress. How does it work? The drug has several effects, including decreasing urate cyrstal deposition, its primary therapuetic effect. Unfortunately, it also has potent anti-mitotic effects, poisoning the mitotic spindle in a dose-related manner. It's side effects are related mostly to this and are seen in sites with rapidly dividing cells: anemia, neutropenia, GI mucosal sloughing leading to upset, gastritis, etc. More severe overdosing looks like arsenic poisoning and causes renal failure, pulmonary hemorrhage, shock and death. Needless to say, the drug should routinely be held in critically ill patients. For the rare ICU patient dealing with acute gout, corticosteroids remain a much better choice.
Kesselheim AS, Solomon DH (June 2010). "Incentives for drug development--the curious case of colchicine". N. Engl. J. Med. 362 (22): 2045–7.
The Perfect PEEP? The ARDS net trial seems to have helped settle the question of what tidal volumes we should be using, but finding the best PEEP level has been a harder question to settle. Based on the ARDSnet recommendations, our current practice (basically whatever amount above 5 cm H2O that is needed to oxygenate) does not take into account individual characteristics such as chest wall and lung compliance that might have an impact. Three large trials comparing high to low PEEP (ALVEOLI, LOVS and EXPRESS studies) have been done and each showed some improvement in oxygenation with more PEEP, but have not shown a mortality benefit.
Now, a group at Harvard has published the results of a small, single ICU pilot trial using intraesophageal ballons measuring (hopefully!) transpulmonary pressure, allowing PEEP to be adjusted based on individual respiratory compliance curves. The results of the pilot are positive and show improvement in recruitment, compliance and oxygenation. Whether this will result in a clinically meaningful benefit can only be shown with a much bigger trial, but the idea is exciting. Maybe Stuart could combine this with a NAVA catheter and we'll have found the perfect ventilator strategy?
Talmor D, Sarge T, Malhotra A, O'Donnell CR, Ritz R, Lisbon A, Novack V, Loring SH: Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med 2008, 359:2095-2104
Beta Blockers for Respiratory Failure. A soon-to-be published paper in Critical Care Medicine reminds us once again that patients admitted on beta-blockers do much, much better when they are continued. This paper, using data from the BASEL II ICU trial, evaluates patients admitted to an ICU with respiratory failure, of any cause. In this mixed group of non-septic patients admitted with respiratory failure (pneumonia, heart failure, asthma, COPD and pulmonary embolism) those on beta-blockers at the time of admission had much lower 28 day and one year mortality (OR 0.32 [0.18 – 0.52] P<0.0001), regardless of the eitology of the respiratory failure. Further, discontinuing beta-blockers at admission was found to be quite hazardous in this group (one year mortality 82 vs 41%, P <0.000001). Patients who were not on beta-blockers at the time of admission but placed on them prior to discharge had their mortality rate reduced by a third (p<0.001).
These results are a retrospective look at prospective data from a trial evaluating something else (B-type natriuretic peptide -guided management strategy on short-term outcome). Causality isn't proven with these results and they don't therefore justify placing patients admitted with respiratory failure on beta-blockers. They do, however, add a another shovel to the growing mountain of evidence that patients on beta-blockers at the time of admission should, whenever possible, have the beta-blockers continued. They also raise the question of whether beta-blockers should be used routinely for respiratory failure. Prior to this paper, that suggestion seemed crazy (metoprolol for asthma? carvedilol for acute PE?!)That question needs further study.
Noveanu M, et al. Effect of oral beta-blocker on short and long-term mortality in patients with acute respiratory failure: results from the BASEL-II-ICU Study Critical Care 2010, [in press] 14:R198 doi:10.1186/cc9317
Noveanu M, et al. Use of B-Type Natriuretic Peptide in the Management of Hypoxemic Respiratory Failure. Eur J Heart Fail 2010:[in press].
Colchicine is commonly used for both acute treatment and the prevention of gouty arthiritis. We've recently had a patient inadvertently continued on their home dose, which is problematic for many reasons. But first some background, and an interesting aside about American drug policy. The FDA has made arrangements for companies to test drugs grandfathered into common usage prior to the approval process in exchange for a few years of market exclusivity. Ostensibly, this is because the FDA cannot afford to run the trials themselves. Colchicine, despite being used for centuries, was recently approved (2009) after a drug company paid for a large clinical trial that proved efficacy according to modern FDA standards. Accordingly, exclusive approval to market the drug was given to URL Pharma and they promptly raised the price per tablet from $0.08 to $4.85, a move expected to cost Medicare over $50,000,000 this year alone. So, where's the savings?
But I digress. How does it work? The drug has several effects, including decreasing urate cyrstal deposition, its primary therapuetic effect. Unfortunately, it also has potent anti-mitotic effects, poisoning the mitotic spindle in a dose-related manner. It's side effects are related mostly to this and are seen in sites with rapidly dividing cells: anemia, neutropenia, GI mucosal sloughing leading to upset, gastritis, etc. More severe overdosing looks like arsenic poisoning and causes renal failure, pulmonary hemorrhage, shock and death. Needless to say, the drug should routinely be held in critically ill patients. For the rare ICU patient dealing with acute gout, corticosteroids remain a much better choice.
Kesselheim AS, Solomon DH (June 2010). "Incentives for drug development--the curious case of colchicine". N. Engl. J. Med. 362 (22): 2045–7.
The Perfect PEEP? The ARDS net trial seems to have helped settle the question of what tidal volumes we should be using, but finding the best PEEP level has been a harder question to settle. Based on the ARDSnet recommendations, our current practice (basically whatever amount above 5 cm H2O that is needed to oxygenate) does not take into account individual characteristics such as chest wall and lung compliance that might have an impact. Three large trials comparing high to low PEEP (ALVEOLI, LOVS and EXPRESS studies) have been done and each showed some improvement in oxygenation with more PEEP, but have not shown a mortality benefit.
Now, a group at Harvard has published the results of a small, single ICU pilot trial using intraesophageal ballons measuring (hopefully!) transpulmonary pressure, allowing PEEP to be adjusted based on individual respiratory compliance curves. The results of the pilot are positive and show improvement in recruitment, compliance and oxygenation. Whether this will result in a clinically meaningful benefit can only be shown with a much bigger trial, but the idea is exciting. Maybe Stuart could combine this with a NAVA catheter and we'll have found the perfect ventilator strategy?
Talmor D, Sarge T, Malhotra A, O'Donnell CR, Ritz R, Lisbon A, Novack V, Loring SH: Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med 2008, 359:2095-2104
Beta Blockers for Respiratory Failure. A soon-to-be published paper in Critical Care Medicine reminds us once again that patients admitted on beta-blockers do much, much better when they are continued. This paper, using data from the BASEL II ICU trial, evaluates patients admitted to an ICU with respiratory failure, of any cause. In this mixed group of non-septic patients admitted with respiratory failure (pneumonia, heart failure, asthma, COPD and pulmonary embolism) those on beta-blockers at the time of admission had much lower 28 day and one year mortality (OR 0.32 [0.18 – 0.52] P<0.0001), regardless of the eitology of the respiratory failure. Further, discontinuing beta-blockers at admission was found to be quite hazardous in this group (one year mortality 82 vs 41%, P <0.000001). Patients who were not on beta-blockers at the time of admission but placed on them prior to discharge had their mortality rate reduced by a third (p<0.001).
These results are a retrospective look at prospective data from a trial evaluating something else (B-type natriuretic peptide -guided management strategy on short-term outcome). Causality isn't proven with these results and they don't therefore justify placing patients admitted with respiratory failure on beta-blockers. They do, however, add a another shovel to the growing mountain of evidence that patients on beta-blockers at the time of admission should, whenever possible, have the beta-blockers continued. They also raise the question of whether beta-blockers should be used routinely for respiratory failure. Prior to this paper, that suggestion seemed crazy (metoprolol for asthma? carvedilol for acute PE?!)That question needs further study.
Noveanu M, et al. Effect of oral beta-blocker on short and long-term mortality in patients with acute respiratory failure: results from the BASEL-II-ICU Study Critical Care 2010, [in press] 14:R198 doi:10.1186/cc9317
Noveanu M, et al. Use of B-Type Natriuretic Peptide in the Management of Hypoxemic Respiratory Failure. Eur J Heart Fail 2010:[in press].
Need More? Old issues are online!
Friday, October 1, 2010
ICU Rounds Report - Oct 1st, 2010
October 1st, 2010
Big Changes Coming! You may have overheard the residents talking about the new Accreditation Council for Graduate Medical Education (ACGME) work hours announced this week, which will dramatically change the way residents work in our ICUs (and floors!) next July, 2011. Nervous hospitals grappling with the dramatic changes are asking the deadline be extended until 2012, but that is unlikely because of fears within the ACGME that if they don't act now, the federal government (and OSHA in particular) might.
What's new? The changes are primarily focused on first year residents (interns), who will be able to work shifts of only 16 hours or less (down from 30). The 80-hour week, mandatory time off between shifts and 1 day off in 7 rules remains. Senior residents can continue to work longer overnight shifts, but they are now capped at 28 (rather than 30) hours. Finally, residents must work no more than 6 nights in a row after July.
Who's doing this and why? The ACGME, which is private, non-profit agency tasked with accrediting of residency programs makes these rules. While they are optional, residencies that don't comply lose accreditation and hence, government funding. Hospitals are paid over $100,000/yr per resident by Medicare, so it's essentially mandatory. Since 1989, the ACGME has been under increasing pressure from consumer advocacy groups, OSHA and CMS to reduce medical errors by improving resident working conditions. Much debate ensured over how to do this. Finally, in July 2003 the ACGME implemented the current work hour restrictions, based on a law enacted in New York state after a previously healthy 18 year old girl died under the care of sleep deprived intern caring for 40 patients at once. Unfortunately, since the implementation of the new work hour rules in 2003, research has not shown an affect on patient outcomes, positive or negative.
There is, however, a large body of evidence that shows sleep deprivation leads to more medical mistakes and harms residents in 4 ways: motor vehicle accidents, mental health, pregnancy (!?) and needle sticks. Critics of the new rules say that these largely unproven benefits are offset by increased errors due to more frequent hand-offs. There are also concerns that residents trained under the new rules will be inadequately prepared to enter practice, having not obtained the necessary hours of patient care to achieve competency.
In the midst of the on-going controversy, Congress commissioned a study from the Institute of Medicine to evaluate the effects of long work hours. This report, published in 2008, stated essentially that residents were working dangerously long hours with too little supervision and called for a drastic overall of the resident education, including reduced work hours, protected time for naps during long shifts and heightened supervision, including 24 hour in-house attending coverage. The new ACGME recommendations are derived partially from that report, with the notable absences of a nap requirement (though 'strategic napping' is encouraged) and specific supervision protocols. Whether these new hour requirements are sufficient to stop the calls for reform from external forces remains to be seen. What they will do to patient care and the quality of resident education are even bigger question marks. Either way, get ready for some big changes.
More history about the dead 18 year old and some interesting further reading here.
Committee on Optimizing Graduate Medical Trainee (Resident) Hours and Work Schedules to Improve Patient Safety. Resi- dent duty hours: enhancing sleep, supervi- sion, and safety. Washington, DC: National Academies Press, 2008.
Nasca TJ, Day SH, Amis ES Jr. The new recommendations on duty hours from the ACGME Task Force. N Engl J Med 2010; 363(2):e3 (Web only). (http://www.NEJM.org.)
Blum AB, Raiszadeh F, Shea S, et al. US public opinion regarding proposed limits on resident physician work hours. BioMed Central. (http://www.biomedcentral.com/ 1741-7015/8/33.)
PT/OT for the Intubated Patient? When should we start PT/OT? Can it make a difference? ICU patients are known to quickly decondition, lose lean muscle mass and have prolonged rehabilitation marked by significant functional impairment. In the first study of it kind, researchers randomized a mixed ICU group to daily PT/OT in intubated patients compared to usual care (starting PT/OT when the tube is out). Both groups received protocol driven mechanical ventilation, daily SBTs, sedation holidays and glycemic control.
How did it work? First of all, it appears to be safe. One serious adverse event, in almost 500 sessions, occurred - a brief desaturation to less than 80%. Other outcomes? Patients given early PT/OT were almost twice as likely to return to independent functional statues at discharge (59 vs 35%, p=0.02), had half the delirium (median duration 2 vs 4 days p=0.02) and spent less time on the ventilator (average 21 vs 24 days, p=0.05). Sweet!
This study is exciting, but not perfect. It wasn't (couldn't!) be blinded, which introduces bias. Next, only patients with independent functional status prior to admission were included in the trial. We don't know if patients with impaired pre-ICU functional status would benefit. Many of our patients come from that group, and they are clearly the highest risk for further losing function. Finally, overall these patients were less sick (average APACHE II scores were ~20 in both arms) than many of our patients.
Schweickert WD, et al. Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomized controlled trial. Lancet 2009
From Danielle
Vasopressin and Sepsis. Vasopressin is an anti-diuretic hormone analog originally approved for use during diabetes insipidus. Since then it has been tested for use as a vasoconstrictor. Vasopressin has been shown to be beneficial during septic shock. It has been noted that a relative deficiency of vasopressin occurs during sepsis. In some prospective case-controlled studies, vasopressin was noted to increase systemic vascular resistance, mean arterial pressure, and urine output. Doses are usually 0.01-0.04units/minute IV.
Landry, et. al. 1997. "Vasopressin deficiency contributes to the vasodilation of septic shock." Circulation. 95(5):1122-5.
Tsuneyoshi I. 2001. "Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock." Crit Care Med . 29(3):487-93.
Malay, et. al. 1999. "Low-dose vasopressin in the treatment of vasodilatory septic shock." J Trauma. 47(4):699-703.
Leave you wanting more? Old issues are online here.
--
Big Changes Coming! You may have overheard the residents talking about the new Accreditation Council for Graduate Medical Education (ACGME) work hours announced this week, which will dramatically change the way residents work in our ICUs (and floors!) next July, 2011. Nervous hospitals grappling with the dramatic changes are asking the deadline be extended until 2012, but that is unlikely because of fears within the ACGME that if they don't act now, the federal government (and OSHA in particular) might.
What's new? The changes are primarily focused on first year residents (interns), who will be able to work shifts of only 16 hours or less (down from 30). The 80-hour week, mandatory time off between shifts and 1 day off in 7 rules remains. Senior residents can continue to work longer overnight shifts, but they are now capped at 28 (rather than 30) hours. Finally, residents must work no more than 6 nights in a row after July.
Who's doing this and why? The ACGME, which is private, non-profit agency tasked with accrediting of residency programs makes these rules. While they are optional, residencies that don't comply lose accreditation and hence, government funding. Hospitals are paid over $100,000/yr per resident by Medicare, so it's essentially mandatory. Since 1989, the ACGME has been under increasing pressure from consumer advocacy groups, OSHA and CMS to reduce medical errors by improving resident working conditions. Much debate ensured over how to do this. Finally, in July 2003 the ACGME implemented the current work hour restrictions, based on a law enacted in New York state after a previously healthy 18 year old girl died under the care of sleep deprived intern caring for 40 patients at once. Unfortunately, since the implementation of the new work hour rules in 2003, research has not shown an affect on patient outcomes, positive or negative.
There is, however, a large body of evidence that shows sleep deprivation leads to more medical mistakes and harms residents in 4 ways: motor vehicle accidents, mental health, pregnancy (!?) and needle sticks. Critics of the new rules say that these largely unproven benefits are offset by increased errors due to more frequent hand-offs. There are also concerns that residents trained under the new rules will be inadequately prepared to enter practice, having not obtained the necessary hours of patient care to achieve competency.
In the midst of the on-going controversy, Congress commissioned a study from the Institute of Medicine to evaluate the effects of long work hours. This report, published in 2008, stated essentially that residents were working dangerously long hours with too little supervision and called for a drastic overall of the resident education, including reduced work hours, protected time for naps during long shifts and heightened supervision, including 24 hour in-house attending coverage. The new ACGME recommendations are derived partially from that report, with the notable absences of a nap requirement (though 'strategic napping' is encouraged) and specific supervision protocols. Whether these new hour requirements are sufficient to stop the calls for reform from external forces remains to be seen. What they will do to patient care and the quality of resident education are even bigger question marks. Either way, get ready for some big changes.
More history about the dead 18 year old and some interesting further reading here.
Committee on Optimizing Graduate Medical Trainee (Resident) Hours and Work Schedules to Improve Patient Safety. Resi- dent duty hours: enhancing sleep, supervi- sion, and safety. Washington, DC: National Academies Press, 2008.
Nasca TJ, Day SH, Amis ES Jr. The new recommendations on duty hours from the ACGME Task Force. N Engl J Med 2010; 363(2):e3 (Web only). (http://www.NEJM.org.)
Blum AB, Raiszadeh F, Shea S, et al. US public opinion regarding proposed limits on resident physician work hours. BioMed Central. (http://www.biomedcentral.com/ 1741-7015/8/33.)
PT/OT for the Intubated Patient? When should we start PT/OT? Can it make a difference? ICU patients are known to quickly decondition, lose lean muscle mass and have prolonged rehabilitation marked by significant functional impairment. In the first study of it kind, researchers randomized a mixed ICU group to daily PT/OT in intubated patients compared to usual care (starting PT/OT when the tube is out). Both groups received protocol driven mechanical ventilation, daily SBTs, sedation holidays and glycemic control.
How did it work? First of all, it appears to be safe. One serious adverse event, in almost 500 sessions, occurred - a brief desaturation to less than 80%. Other outcomes? Patients given early PT/OT were almost twice as likely to return to independent functional statues at discharge (59 vs 35%, p=0.02), had half the delirium (median duration 2 vs 4 days p=0.02) and spent less time on the ventilator (average 21 vs 24 days, p=0.05). Sweet!
This study is exciting, but not perfect. It wasn't (couldn't!) be blinded, which introduces bias. Next, only patients with independent functional status prior to admission were included in the trial. We don't know if patients with impaired pre-ICU functional status would benefit. Many of our patients come from that group, and they are clearly the highest risk for further losing function. Finally, overall these patients were less sick (average APACHE II scores were ~20 in both arms) than many of our patients.
Schweickert WD, et al. Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomized controlled trial. Lancet 2009
From Danielle
Vasopressin and Sepsis. Vasopressin is an anti-diuretic hormone analog originally approved for use during diabetes insipidus. Since then it has been tested for use as a vasoconstrictor. Vasopressin has been shown to be beneficial during septic shock. It has been noted that a relative deficiency of vasopressin occurs during sepsis. In some prospective case-controlled studies, vasopressin was noted to increase systemic vascular resistance, mean arterial pressure, and urine output. Doses are usually 0.01-0.04units/minute IV.
Landry, et. al. 1997. "Vasopressin deficiency contributes to the vasodilation of septic shock." Circulation. 95(5):1122-5.
Tsuneyoshi I. 2001. "Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock." Crit Care Med . 29(3):487-93.
Malay, et. al. 1999. "Low-dose vasopressin in the treatment of vasodilatory septic shock." J Trauma. 47(4):699-703.
Leave you wanting more? Old issues are online here.
--
Jordan Hackworth, M.D.
Fellow, Critical Care Medicine
Department of Anesthesiology
University of Virginia
Department of Anesthesiology
University of Virginia
Tuesday, September 28, 2010
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
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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