Intensive Care Doctor-Community

The study included 134 patients with advanced CKD and low bicarbonate levels, also called metabolic acidosis. One group received a small daily dose of sodium bicarbonate in tablet form, in addition to their usual care. For this group, the rate of decline in kidney function was greatly reduced—about two-thirds slower than in patients. "In fact, in patients taking sodium bicarbonate, the rate of decline in kidney function was similar to the normal age-related decline," says Yaqoob.

Rapid progression of kidney disease occurred in just nine percent of patients taking sodium bicarbonate, compared to 45 percent of the other group. Patients taking sodium bicarbonate were also less likely to develop end-stage renal disease (ESRD) requiring dialysis.

Patients taking sodium bicarbonate also had improvement in several measures of nutrition. Although their sodium levels went up, this didn't lead to any problems with increased blood pressure.

Low bicarbonate levels are common in patients with CKD and can lead to a wide range of other problems. "This is the first randomized controlled study of its kind," says Yaqoob. "A simple remedy like sodium bicarbonate (baking soda), when used appropriately, can be very effective."

The researchers note some important limitations of their study—there was no placebo group and the researchers were aware of which patients were receiving sodium bicarbonate. "Our results will need validation in a multicenter study," says Yaqoob.

Other authors were Ione de Brito-Ashurst, RD, Mira Varaganum, PhD, and Martin J. Raftery, MD (William Harvey Research Institute and Barts and the London NHS Trust, London). The authors reported no financial disclosures.

Journal reference:

1. Ione de Brito-Ashurst , Mira Varagunam , Martin J. Raftery , and Muhammad M. Yaqoob. Bicarbonate Supplementation Slows Progression of CKD and Improves Nutritional Status. Journal of the American Society of Nephrology, 2009; DOI: 10.1681/ASN.2008111205

"Hypoglycemia is associated with adverse outcomes in mixed populations of patients in intensive care units," write Michael E. Matheny, MD, MS, MPH, from the Brigham and Women's Hospital in Boston, Massachusetts, and colleagues. "It is not known whether the same risks exist for diabetic patients who are less severely ill. In this study, we aimed to determine whether hypoglycemic episodes are associated with higher mortality in diabetic patients hospitalized in the general ward."

Between January 2003 and August 2004, a total of 2582 patients with diabetes had a total of 4368 admissions to the general ward of a teaching hospital. Using multivariable analysis, the investigators examined associations between the number and severity of hypoglycemic episodes and inpatient mortality, LOS, and mortality within 1 year after hospital discharge.

Hypoglycemia, defined as a blood glucose level of 50 mg/dL or less, occurred in 7.7% of admissions. For every additional day with hypoglycemia, there was an increase in LOS by 2.5 days (P < .0001), in the odds of inpatient death by 85.3% (P = .009), and in the odds of death within 1 year from discharge by 65.8% (P = .0003). For every 10-mg/dL decrease in the lowest blood glucose level recorded during hospitalization, the odds of death during hospitalization were increased 3-fold (P = .0058).

"Hypoglycemia is common in diabetic patients hospitalized in the general ward," the study authors write. "Patients with hypoglycemia have increased LOS and higher mortality both during and after admission. Measures should be undertaken to decrease the frequency of hypoglycemia in this high-risk patient population."

Limitations of this study include retrospective analysis, precluding determination of causality; inclusion only of patients admitted to a single academic hospital in Boston; and inability to distinguish type 1 from type 2 diabetes. Other limitations include lack of nutrition information for individual patients, lack of data regarding immediate clinical sequelae, and use of point-of-care blood glucose levels.

"Extra care should be taken to prevent hypoglycemic events in this population already at high risk for adverse events, with particular attention being paid to matching the antihyperglycemic regimen to the nutritional intake," the study authors conclude. "At the same time, hypoglycemia among diabetic patients in the general ward could be interpreted as a warning sign of an impending clinical deterioration. It could therefore serve as a useful indicator for the necessity of increased monitoring, more aggressive treatment of infections, transitioning to a more intensive care setting, and case management."

This study was supported in part by grants from the Diabetes Action Research and Education Foundation and the National Library of Medicine. The study authors have disclosed no relevant financial relationships.

Diabetes Care. 2009;32:1153-1157.

"Dietary factors are important and probably causative risk factors for obesity, insulin resistance, and diabetes, which are the most important, known risk factors for hepatic steatosis," write George N. Ioannou, MD, MS, from the Division of Gastroenterology, Department of Medicine and Research Enhancement Award Program, Veterans Affairs Puget Sound Health Care System and University of Washington in Seattle, and colleagues. In addition, "It is possible that the quantity and composition of dietary lipid can either promote or protect against the development or progression of hepatic steatosis."

The authors write that if dietary composition affects the development or progression of hepatic steatosis, it is likely to play a part in the natural history of the 3 most important liver conditions in the United States: nonalcoholic fatty liver disease, hepatitis C virus (HCV) infection, and alcoholic liver disease.

Previous research has shown that a high-cholesterol diet in rabbits and mice induced profound steatosis, inflammation, and cetrilobular fibrosis, whereas a diet low in animal protein for hepatitis B virus transgenic mice was associated with decreased liver injury and decreased incidence of hepatocellular carcinoma.

In this study, the investigators sought to determine whether dietary intake was associated with the subsequent development of cirrhosis-related or liver cancer–related death or hospitalization in the US population.

They examined data from the first National Health and Nutrition Examination Survey (NHANES I), a cross-sectional study of 14,407 participants conducted between 1971 and 1975 by the National Center for Health Statistics. It ascertained dietary intake at baseline using a 24-hour dietary recall questionnaire and then used a Nutrient Composition Data Bank to calculate grams of protein, carbohydrate, and fat consumed. The NHANES I Epidemiologic Follow-up Study then collected data on specific health conditions that developed in the intervening years, through personal interviews, hospitalization records, and death certificates.

For this study, Dr. Ioannou and his team evaluated a cohort of 9221 adults (aged 25 – 74 years, 82.9% white) from the NHANES I Epidemiologic Follow-up Study who were without evidence of cirrhosis at entry into the original study.

Potential confounders identified included daily consumption of protein, carbohydrate, fat, tea or coffee, and alcohol; sex; race; age; educational attainment; geographical region; diabetes; body mass index; and subscapular-to-triceps skin fold ratio. In addition, as hepatitis B and HCV RNA testing was not available when the NHANES I participants were recruited, the investigators used data from NHANES III, a cross-sectional study from 1988 to 1994 that included measurements of viral hepatitis serologies.

During an average follow-up of 13.3 years, the investigative team found that 118 of the 9221 participants had a new diagnosis of cirrhosis and 5 had a new diagnosis of liver cancer.

After adjusting for the potential confounders, the investigators found that patients who reported a diet high in protein were at higher risk for hospitalization or death because of cirrhosis or liver cancer (P = .0001), whereas those reporting a diet high in carbohydrates were at a significantly lower risk (P = .003).

In addition, cholesterol consumption was associated with a higher risk for cirrhosis or liver cancer (P = .007), whereas total number of calories, total quantity of fat consumed, and serum cholesterol level were not. The authors write that because cholesterol has never before been linked to human liver disease, this strong association "is potentially our study's most important finding."

Using the NHANES III data, the investigators found no association between any dietary composition and HCV infection. They write that this lack of association "strongly suggests that the presence of underlying liver disease does not cause a change in dietary intake and instead makes it more plausible that differences in dietary intake of proteins, carbohydrates, cholesterol, and perhaps other lipid components contribute to the development of cirrhosis or liver cancer."

Study limitations include the 24-hour dietary recall, which may not accurately reflect long-term dietary intake, and the absence of data on HCV infection, a major cause of cirrhosis and liver cancer in the United States. However, the authors explain that because of the NHANES III study data, "HCV infection is unlikely to be an important source of uncontrolled confounding."

They conclude, "Our study raises the possibility that dietary factors may be important, modifiable, and hitherto unrecognized determinants of liver disease progression."

This study was supported by the American Liver Foundation and American Association for the Study of Liver Diseases Jan Albrecht Award. The authors have disclosed no relevant financial relationships.

Hepatology. 2009;50:175–184.

The discovery, reported in this week’s Science by a team led by scientists from Oxford University and Ludwig-Maximilians-University, Munich, opens up a new area of molecular research into conditions such as heart disease and cancer.

‘Previous work from Oxford has shown that some of these enzymes, called oxygenases, affect which genes are expressed in response to low levels of oxygen. What we have now found is that they also regulate the specific form this expression takes – to give the different proteins that make up everything from heart cells to tumours,’ said Professor Chris Schofield of Oxford University’s Department of Chemistry, one of the authors of the paper.

Genes, stored in the form of DNA, are converted into proteins by a ‘middleman molecule’ called Messenger Ribonucleic Acid – or ‘mRNA’.

Individual genes can often give rise to many different proteins because of a process known as mRNA splicing which enables the cutting and pasting of the mRNA that is produced from DNA. The proteins that the new oxygenase, termed Jmjd6, acts on are involved in regulating the 'cutting and pasting' process.

Angelika Böttger, who led the Munich group, said: ‘The discovery of a role for an oxygenase in mRNA splicing reveals that it is very likely that oxygen levels are involved in regulating almost all steps in the process of gene expression. The challenge now is to determine how the pattern of genes changes in different environments when oxygen is in short supply, enabling us to tackle important questions such as "why do tumour cells respond differently to low oxygen levels than normal cells?"'

Results of a retrospective review of 25,587 patients 50 years and older who were hospitalized with sepsis between 1999 and 2004 were presented by Ahmed I. Shah, MD, from the Department of Cardiology at Kaiser Permanente Los Angeles Medical Center, in California. The group was approximately half men and half women, and the mean age was 72 years.

Dr. Shah's team divided patients into 3 groups, according to statin use: current users, who were taking a statin before and on the day of hospitalization; remote users, who had taken a statin 2 or more months before hospitalization, but not afterward; and never users, who had not taken a statin for at least 1 year before admission.

Current users were divided into a low-dose group and a high-dose group. Low dose was defined as lovastatin 40 mg or less daily, simvastatin 10 mg or less daily, and atorvastatin 10 mg or less daily.

Of the cohort, 70% were never users, 11% were remote users, and 19% were current users. Of the current users, approximately half were on low doses and half were on moderate to high doses. Current users were more severely ill and had more comorbidities than never users.

Patients were followed for up to 12 months after admission or until death. Twelve-month mortality rates were calculated.

The adjusted hazard ratios for all-cause mortality were:

• 0.83 (0.76–0.91; P < .0001) for current users vs never users;
  
  
• 0.76 (0.72–0.81; P < .0001) for current users vs remote users;
  
  
• 0.87 (0.79–0.96; P < .009) for low-dose users vs never users;
  
  
• 0.79 (0.72–0.88; P < .0001) for high-dose users vs never users; and
  
  
• 0.90 (0.83–0.99; P < .03) for high-dose vs low-dose users.

"In hospitalized septic patients, current high-dose statin use is associated with a statistically significantly lower rate of 1-year mortality," Dr. Shah told meeting attendees. However, he emphasized that this was a retrospective review and not a prospective interventional study.

"This has become a very hot area for research over the past 5 to 6 years, but most of the data are like this," Robert Duncan Hite, MD, FCCP, associate professor of medicine and director of the Medical Intensive Care and Critical Care Research Section on Pulmonary, Critical Care, Allergy and Immunologic Disease at Wake Forest University School of Medicine, in Winston-Salem, North Carolina, told Medscape Critical Care in an interview after Dr. Shah's presentation.

These are "retrospective analyses of large databases in which the use of statins is examined but cannot be controlled for other important variables that might explain differences in outcomes," Dr. Hite said.

"There are several prospective, randomized, blinded trials currently ongoing around the world. Even once those [results] are available, and assuming they prove to be successful, we will still not know whether all statins [are] of equal benefit and what the optimal dose is," he pointed out. "Since statins are not without toxicity and little is known about the metabolism of statins in sepsis, dosing will have to be considered carefully."

Dr. Hite concluded: "For now, I would not recommend that statins be initiated in a septic patient, but it is reasonable to continue statins in a septic patient previously taking astatin. This is a change that I and many others have made in their practice over the past few years as a result of data similar to the data provided by this study.

The review, published in the July 7, 2009, issue of the Journal of the American College of Cardiology, was written by a group led by Dr David Holmes (Mayo Clinic, Rochester, MN).

They explain that dual antiplatelet therapy (aspirin plus clopidogrel [Plavix, Sanofi-Aventis/Bristol-Myers Squibb]) is given routinely in the treatment of ACS and after coronary stent deployment, and anticoagulant therapy might be indicated for stroke prevention in a variety of conditions that include atrial fibrillation and profound left ventricular dysfunction as well as after mechanical prosthetic heart valve replacement. Triple antithrombotic therapy may be needed when a patient has multiple diseases, the most common situations being patients with AF and or mechanical prosthetic heart valves who also have coronary artery disease and require a stent.

Coauthor Dr Dean Kereiakes (Christ Hospital, Cincinnati, OH) commented to heartwire : "This is a growing problem in the context of the aging population. Both atrial fibrillation and the need for prosthetic heart valves rise with age, and so does the risk of falling, which further increases bleeding risk. ACS is very common, and given the increasingly widespread use of drug-eluting stents (for which dual antiplatelet therapy is recommended for at least one year), the significant bleeding hazards associated with triple antithrombotic therapy is a real issue, which will become worse in the future."

The authors note that before committing a patient to triple therapy for an indefinite period, the physician should carefully consider alternative approaches. For example, in patients who require long-term oral anticoagulation who are undergoing stenting, serious consideration should be given to the use of bare-metal stents, for which dual antiplatelet treatment is recommended for a shorter time. And for AF patients, thought should be given to left atrial appendage occlusion devices or pulmonary vein ablation that could avoid the need for long-term warfarin.

Kereiakes added that for patients needing a heart valve, the new On-X valve (On-X Life Technologies, Austin, TX) should be considered; it has lower warfarin requirements than other valves. "New valve technology such as this will help immensely to reduce levels of anticoagulation needed," he said.

Balancing the Need for Treatment With Bleeding Risk

Holmes et al say that patients who are treated with triple therapy present significant clinical challenges because of the imperative to balance bleeding risks against the risk of stopping one of the therapies. They point out that there is very limited published information regarding use of triple antithrombotic therapy, so concrete recommendations are difficult.

Data that are available suggest that up to 21% of patients receiving triple antithrombotic therapy need a transfusion (a figure that might increase with longer treatment durations), and the relative risk of major bleeding is three- to fivefold higher than in patients receiving dual antiplatelet therapy alone. But this is confounded by the fact that patients receiving triple therapy are typically older and have multiple comorbidities, which might increase bleeding potential. Short-term use of triple therapy (for one month) is associated with at least a twofold lower risk of major bleeding compared with prolonged use (more than six months). But patients receiving dual antiplatelet therapy only after PCI (prolonged warfarin interruption) have a threefold increase in stroke or thromboembolic events, compared with patients receiving triple therapy or warfarin plus a single antiplatelet agent.

Keep Aspirin Dose and INR Low

Holmes et al advise that for patients receiving triple therapy, the dose of aspirin should be kept as low as possible (75 to 81 mg), clopidogrel should be given at its standard dose of 75 mg/day, and warfarin should be administered under tight control to achieve a slightly lower target international normalized ratio (INR) of 2.0 to 2.5. They also suggest that proton-pump inhibitors (PPIs) should be considered as prophylaxis against gastric bleeds.

The issue of using PPIs with clopidogrel has been fraught with controversy as it is thought that there may be an interaction between these agents. But Kereiakes commented to heartwire : "The latest consensus of experts is that there is no good evidence events are increased when PPIs are given with clopidogrel. The studies suggesting increased events are confounded. I do give PPIs as prophylaxis to patients on triple antithrombotic therapy, but I tend to use pantoprazole and esomeprazole, which have the least incriminating data regarding an interaction with clopidogrel."

PCI in Patients Taking Warfarin

In patients on warfarin who need PCI, the authors suggest that it may be better to choose a bare-metal stent and commit the patient to a short course of clopidogrel, rather than to an extended course of triple therapy. They suggest that bare-metal stents should be considered for use in target vessels less likely to benefit from drug-eluting stents (eg, vessels >3 mm in diameter, short lesions <15>

One alternative they mention is to use a drug-eluting stent for very high-risk lesions and accept the increased risk of bleeding. For patients with high bleeding risk treated with a drug-eluting stent, they advise that triple therapy may be limited to three to six months, with warfarin plus clopidogrel and a prophylactic PPI continued thereafter.

How to Cope With Bleeding

The authors note that bleeding on triple therapy is a particularly difficult problem. Severe or life-threatening bleeding usually requires reversal of warfarin therapy and, in some cases, platelet transfusions to counteract clopidogrel therapy. If dual antiplatelet therapy requires urgent discontinuation, the patient should be closely monitored for the risk of stent thrombosis. In patients with mild or moderate bleeding, every effort should be made to maintain the INR as close to 2.0 as possible, and the aspirin dose should be kept at <100>

If bleeding persists, they advise that aspirin be discontinued first, as clopidogrel seems to be more important than aspirin in preventing stent thrombosis after PCI.

New Drugs and Stent Designs

Holmes et al point out that all these uncertainties will be further compounded by the imminent arrival on the market of new anticoagulant and antiplatelet drugs and new stent designs. The factor Xa antagonists rivaroxaban (Xarelto, Johnson & Johnson) and apixaban (Bristol-Myers Squibb), which might replace warfarin, also dramatically increase bleeding risk when combined with aspirin plus clopidogrel and so may not much help patients requiring triple therapy. The new antiplatelet drug prasugrel (Lilly/Daiichi Sankyo) is more potent than clopidogrel and associated with higher bleeding rates and so is not likely to be suitable for use in combination with warfarin, but the AstraZeneca compound AZD 6140 is shorter acting and reversible, which might be advantageous when used in patients who also require warfarin, they note.

The new protease-activated receptor 1 (PAR-1) antagonist SCH 530348 (Schering-Plough) has shown promising results in preliminary trials, with no increase in bleeding yet seen, and the authors suggest that if this drug becomes clinically available, it may replace clopidogrel in patients who require warfarin, giving a modified triple combination that might have an improved safety profile.

Finally, the cyclooxygenase inhibitor triflusal (Uriach Pharma) is potentially associated with lower bleeding risk and has been demonstrated as safe and effective in combination with warfarin in patients with AF and so could prove useful in patients requiring oral anticoagulation and undergoing PCI, but randomized studies are needed, they add.

In addition, new stents are being introduced with thinner struts and polymer coatings, which are thought to be associated with better endothelialization and less vascular inflammation than previous drug-eluting stents. And another new generation of stents that employ bioabsorbable polymers or are designed to capture circulating endothelial precursor cells to promote vascular healing are in development, and the hope is that these stents could be less subject to late thrombosis and might require shorter durations of dual antiplatelet therapy.

Kereiakes has received grant and/or research support from Amylin Pharmaceuticals and Daiichi Sankyo and consulting fees from Lilly. Another coauthor has served as a consultant to Schering-Plough and Portola Pharmaceuticals.

High troponin levels "may represent secondary cardiac injury in medical patients," which could, in turn, increase mortality. Treatment of patients with very high levels of troponin may decrease the risk for mortality, investigators announced here at the Society of Critical Care Medicine 38th Critical Care Congress.

Vipin Koshal, MD, Chief Cardiology Fellow at the University of Cincinnati, Ohio, presented his team's findings from a database of 43,415 ICU patients hospitalized in 116 Veterans Administration hospitals between 2005 and 2006 with recorded troponin levels.

Patients were divided into 3 groups: those with negative or undetectable levels of troponin; those with intermediate levels, or below 10% of the coefficient variance; and those with high levels, at or above 10% of the coefficient variance. Cases were then stratified into quintiles according to predicted mortality.

In all, 45% of cases were negative for troponin, 35% had intermediate levels, and 20% had high levels.

The odds ratio (OR) for mortality was not significantly increased in patients with intermediate levels of troponin, with an OR = 1.071 (95% confidence interval [CI], 1.004 – 1.143).

But mortality was increased significantly in patients with high troponin levels, with an OR = 1.464 (95% CI, 1.364 – 1.572).

The proportion of patients with high troponin levels increased with severity of illness. Among those with a predicted mortality below 2.5%, 11% had high troponin levels. Among those with a greater than 30% chance of mortality, 34% had high troponin levels.

Approximately 45% of patients with intermediate or high troponin levels were treated with beta-blockers, Dr. Koshal reported.

Nontreatment among those with high levels increased the OR for mortality by 40% (OR, 1.140; 95% CI, 1.025 – 1.268). Nontreatment did not increase mortality risk in those with intermediate troponin levels (OR, 1.066; 95% CI, 0.972 – 1.169).

"There appears to be a protection of myocardium in patients with high troponin levels that does not happen in patients with intermediate levels," Dr. Koshal told Medscape Critical Care.

"It's important to keep in mind that these are noncardiac patients," he added. "We don't know how this happens. There may be a small leak in troponin. Even the high levels [in these patients] were lower than in cardiac patents. This is not the same scenario as in cardiac patients, who would probably already be on beta-blockers."

"The clinical message is that in the absence of contraindications, such as hypotension, beta-blockers could be beneficial for the noncardiac patient with high troponin levels," Dr. Koshal said in an interview with Medscape Critical Care after his presentation.

"A main limitation of these findings is that many noncardiac patients with elevated troponins have hemodynamic compromise, in particular low blood pressure, and are therefore not treated" and are not candidates for treatment, Robert Duncan Hite, MD, FCCP, associate professor and director of medical intensive care and critical care research at Wake Forest University School of Medicine in Winston-Salem, North Carolina, told Medscape Critical Care.

Dr. Hite commented that the retrospective design of Dr. Koshal's study is a major limitation. "A finding that those who are not treated vs those who are treated in this retrospective manner may simply identify those who were sicker. It is unlikely that this study will change practice."

Dr. Hite said that "a potentially more important question for this clinical scenario is whether these patients should have more formal studies of their cardiac disease, such as stress tests or cardiac catheterization, after they recover from their acute illness. That is not the current standard in practice."

Randomized studies of noncardiac ICU patients with high troponin levels randomized to beta-blockers or placebo are needed, he said.

Dr. Hite and Koshal have disclosed no relevant financial relationships.

Society of Critical Care Medicine (SCCM) 38th Critical Care Congress: Abstract 226. Presented February 3, 2009.

The Twenty-First Century has thrust health care into an era of modernization, precipitated by advances in medical technology and computerization of everything in sight. We have made fantastic strides in the diagnosis and treatment of many serious illnesses. Patients are living longer and more productive lives as a result of these wonderful advances.

However, concomitant with these changes, we have experienced the indisputable depersonalization of patient care. Patients are often treated as diseases or numbers. We often hear medical personnel referring to a patient as “the gallbladder in room 232” or “the COPDer in 476”. We order test after test instead of taking a history because if we don’t “prove” our diagnosis with a test, we may be subjected to a lawsuit later if something goes wrong.

Health care costs have spun out of control. Forty-three million people in the US can no longer afford health insurance. Access to care has deteriorated. Prenatal care and birth rates are suffering. Doctors’ salaries are restricted by insurance companies. Busy primary care physicians have to see 30-40 patients a day to make enough income to pay off their own expenses beginning with a $250,000 debt for medical training.

There is no time to spend 20 minutes with an 80 year-old patient with diabetes, arthritis, heart failure, and hypertension out of control who has just developed shortness of breath recently, and who needs 6 prescriptions rewritten. Other patients in the waiting room are feeling ignored.

These are very difficult challenges. Unfortunately, in the middle of it all, we often lose site of the fact that our patients are people – in many cases, very ill people - who are looking to us for support and guidance as well as medical care. There is an art to providing this support and to personalizing care for each and every patient in the midst of an imperfect environment.

Anyone who works in the health care profession knows there is a right way and a wrong way to approach patient care. They also know this is somewhat different for every patient they encounter due to multiple variables – type of illness, gender, age, background, etc. This is an art that we learn mostly by experience – both by our own personal experience and by observing the experiences of others. How well we assimilate the information from these experiences and how well we use that knowledge determines a very large part of how we interact with patients and how we are perceived as medical professionals.

The key word here is the art of patient care. For the purposes of this site, the reference is not so much on the science of medicine per se, but rather on how medical personnel can interact with patients to improve the healing process, rather than dismantle it.

This is not to say that science is unimportant; but rather that concern for the humanity of the patient should not be so overwhelmed by science as to be nonexistent at the bedside. Indeed, true clinical competence is a blend of knowledgeable application of medical science along with the recognition and understanding of the human condition. The art of this blend, the integration of these two disciplines, and how well it is done, is what determines the quality of patient care that we provide. One without the other is not sufficient.

This can be a science unto itself. One of the influences that this site will hopefully promote is more discussion and ultimately more research on how to practice this art in a more meaningful and fulfilling way for both ourselves and our patients alike. In addition, the more formal exploration and inclusion of these concepts into medical training programs would have a huge effect on the future of medicine in this country.

Some people say you have to be born with this talent. I don’t think so. I do think it comes easier to some than others; but, whatever the genetics and background of the individual, patient care is an art that can be learned and practiced and improved upon, just as drawing or painting a thoughtful picture can be learned and practiced to the point where it can be greatly appreciated by others.

So what kind of doctor or nurse or care partner do you want to be?

What is your approach to patient care?

How do patients perceive your approach to them and your overall competence?

If you long to be one of those caring, well-respected and revered medical professionals that patients (and even other professionals) admire and tell their friends and neighbors about, you’ve found the right place.

Read and study the pages on this site. You will become a much more people-oriented professional, knowledgeable about how to approach all kinds of patients and challenging situations, and who will at the very least be perceived as someone who cares and is concerned about his or her patients.

If you practice what you learn here, you may find yourself actually rediscovering virtues you didn’t know you had. If you already have the nurturing gene, these pages will help you hone that talent into something very special; and your patients will benefit from it in ways you never thought possible.

"Among a large array of laboratory variables, procalcitonin has emerged as the leading one to indicate systemic infections with high accuracy," senior author Dr. Stefan Schroeder, from West Coast Hospital, Heide, Germany, told Reuters Health.

"There is extensive clinical evidence that procalcitonin allows reliable differentiation between systemic inflammatory response syndrome and bacterial or fungal sepsis and closely correlates with the systemic severity of infections in various diseases and medical disciplines," he added. "Moreover, some recent clinical studies have also shown that procalcitonin is a reliable means to guide antibiotic therapy in community acquired pneumonia and sepsis."

The goal of the present study was to determine if a procalcitonin-based algorithm could be used to guide antibiotic therapy in intensive care patients. Included in the investigation were 110 surgical intensive care patients who were receiving antibiotic therapy for confirmed or suspected high-grade bacterial infections. All of the subjects met at least two standard criteria for a systemic inflammatory response syndrome.

The subjects were randomized to receive antibiotic therapy for 8 consecutive days or as dictated by procalcitonin levels. In the procalcitonin group, if a patient had clinical improvements in signs and symptoms and if the procalcitonin level fell below 1 ng/mL or dropped by 25% to 35% from the initial value over 3 days, then antibiotic therapy could be discontinued.

The duration of antibiotic therapy was reduced by 2 days, on average, in the procalcitonin group compared to controls: 5.9 vs. 7.9 days (p <>

"Beyond a reduction of the length of antibiotic treatment, procalcitonin-guidance also had a favorable effect on the length of the intensive care stay," Dr. Schroeder said. The average length of stay was 15.5 days in the procalcitonin group compared with 17.7 days in the control group (p = 0.046).

The results clearly show that a procalcitonin-guided algorithm is a helpful approach to reduce the length of antibiotic therapy without negatively influencing the outcome of surgical intensive care patients, Dr. Schroeder said.

"Monitoring of procalcitonin is a valuable tool for therapeutic decision-making concerning the length of antibiotic treatment," he added. "However, adequate interpretation of procalcitonin concentrations always requires the background of clinical course and symptoms. This concept contributes to less extensive antibiotic treatment with positive effects on economical factors and the development of drug-resistances in intensive care medicine."

Regarding future research, Dr. Schroeder said that "our procalcitonin-based algorithm is certainly practicable and simple. However, procalcitonin cut-off points for antibiotic termination have not uniquely defined. Thus, procalcitonin-controlled antibiotic therapy must still be tested in heterogenous groups of patients, particularly the safety."

Crit Care. 2009;13:R83.

Clinical Context

Study Highlights

• Participants for study enrollment were all admitted to 1 surgical intensive care unit in Germany. All participants required antibiotic therapy based on confirmed or highly suspected bacterial infection along with at least 2 criteria for systemic inflammatory response syndrome.
• Participants were randomly assigned in the open-treatment study to receive either 8 days of antibiotics or a varying course of antibiotics based on procalcitonin levels. Antibiotics were discontinued among subjects in the procalcitonin-guided therapy group when the procalcitonin level decreased to less than 1, or when this value decreased by 25% to 35% of the initial value during 3 days.
• The type of antibiotic chosen was left to the discretion of the treating physician.
• The main outcomes of the study were the duration of antibiotic use, the duration of stay in the intensive care unit, and participants' clinical outcomes of hospitalization.
• 57 patients were assigned to the procalcitonin-guided therapy group, and 53 comprised the control group. The mean age of participants was 67 years old, and peritonitis and pneumonia accounted for the vast majority of admissions. The severity of illness between groups at baseline was similar.
• The most popular antibiotic choices for all patients were acylaminopenicillin plus a beta-lactamase inhibitor or nitroimidazole.
• Procalcitonin-guided therapy was associated with a significantly shorter duration of antibiotic treatment vs standard therapy (5.9 days vs 7.9 days, respectively).
• Procalcitonin-guided therapy was also associated with a shorter stay in the intensive care unit vs standard therapy (15.5 days vs 17.7 days, respectively).
• Disease severity scores remained similar between groups during the study, as did leukocyte counts and C-reactive protein concentrations.
• 14 participants in the control group died during hospitalization vs 15 subjects in the procalcitonin-guided therapy group. This difference between groups was not significant.

Clinical Implications

• Sepsis can be difficult to diagnose among critically ill patients, as common signs of sepsis are nonspecific in the setting of severe illness, and traditional laboratory tests may lag behind progression of infection.
• In the current study, antibiotic treatment guided by procalcitonin levels reduced the durations of antibiotic therapy and intensive care unit stay among critically ill surgical patients. Procalcitonin-guided therapy did not harm clinical outcomes vs standard therapy.