Are two sets of blood cultures adequate for evaluation of bacteremia in my febrile patient?

For great majority of patients, more than 2 sets of blood culture obtained closely apart is not likely to significantly improve the yield of detecting bacteremia. 

Although a 2004 report suggested that 2 sets of blood cultures over 24 h period had a sensitivity of only 80% for bacteremia, several other studies have found much higher sensitivities, ranging from ~90%- 99% 2-3. When broken down by organism, sensitivity of 2 sets of blood cultures may be highest for Staphylococcus aureus (97%), followed by E. coli (91%), and Klebsiella pneumoniae (90%) 2.  The Clinical and Laboratory Standards Institute guidelines recommend paired blood culture sets (each set with 2 bottles, 10 ml of blood in each) to detect about 90-95% of patients with documented bacteremia, and 3 sets for 95-99% detection rate 4.

It seems prudent to strike a balance between drawing more than 2 sets of blood cultures—with its attendant risk of picking up contaminants— and what may be a definite but small incremental increase in the rate of detection of true bacteremia. 

If you are concerned about “continuous” bacteremia (eg, in endocarditis) or a common blood culture contaminant causing true disease (eg, Staphylococcus epidermidis prosthetic valve infection), you may consider a 3rd or 4th set of blood cultures drawn 4-6 hrs after the initial sets.

Whatever you do,  please don’t order only 1 set of blood cultures! Aside from its generally low yield, when positive it may be difficult to distinguish contaminants from true invaders.

 

References

  1. Cockerill FR, Reed GS, Hughes JG, et al. Clinical comparison of BACTEC 9240 Plus Aerobic/F resin bottles and the Isolator aerobic cultures. Clin Infect Dis 2004;38:1724-30. https://www.ncbi.nlm.nih.gov/pubmed/9163464
  2. Lee A, Mirrett S, Reller LB, et al. Detection of bloodstream infections in adults: how many cultures are needed? J Clin Microbiol 2007; 45:3546-48. http://jcm.asm.org/content/45/11/3546
  3. Towns ML, Jarvis WR, Hsueh PR. Guidelines on blood cultures. J Microbiol Immunol Infect 2010;43:347-49. https://www.ncbi.nlm.nih.gov/pubmed/20688297
  4. Weinstein MP, Reller LB, Murphy JR, et al. The clinical significance of positive blood cultures: a comprehensive analysis of 500 episodes of bacteremia and fungemia in adults. I. Laboratory and eipidemiologic observations. Rev Infect Dis 1982;5:35-53. https://www.ncbi.nlm.nih.gov/pubmed/6828811
Are two sets of blood cultures adequate for evaluation of bacteremia in my febrile patient?

In my critically ill patient with infection, is capillary refill time greater than 2 seconds indicative of septic shock?

The data on the performance of capillary refill time (CRT) in adults is quite limited and what’s available does not suggest that the commonly cited 2 seconds cutoff is useful in assessing peripheral perfusion in critically ill adults1,2.

For example, a large study involving 1000 healthy adults reported that 45% of participants had a CRT > 2 seconds3.  Age also affects CRT with its 95 percentile upper limits reaching 4.5 seconds among healthy adults >60 y old3

Among patients with septic shock, a baseline median CRT of 5 seconds has been reported.  Values <5.0 seconds within 6 hours of treatment of septic shock has also been highly associated with successful resuscitation even before normalization of lactate levels4.

For these reasons, if CRT is used as a measure of peripheral perfusion in critically ill adults, a cut off of 5 seconds, not 2 seconds, may be more appropriate. But just like many other diagnostic tests, CRT should never be interpreted in isolation from other clinical parameters. 

References

  1. Lima A, Bakker J. Clinical Assessment of peripheral circulation. Critical Care 2015:21: 226-31. https://www.ncbi.nlm.nih.gov/pubmed/25827585  
  2. Lewin J, Maconochie I. Capillary refill time in adults. Emerg Med J 2008;25:325-6. https://www.ncbi.nlm.nih.gov/pubmed/18499809
  3. Anderson B, Kelly AM, Kerr D, et al. Impact of patient and environmental factors on capillary refill time in adults. Am J Emerg Med 2008;26:62-65. https://www.ncbi.nlm.nih.gov/pubmed/18082783
  4. Hernandez G, Pedreros C, Veas E, et al. Evolution of peripheral vs metabolic perfusion parameters during septic shock resuscitation. A clinical-physiologic study. J Crit Care 2012;27:283-288.  https://www.ncbi.nlm.nih.gov/pubmed/21798706
In my critically ill patient with infection, is capillary refill time greater than 2 seconds indicative of septic shock?

Should male patients with suspected urinary tract infection routinely undergo a prostate exam?

Yes! That’s because any urinary tract infection (UTI) in men has the potential for prostatic involvement1 —-as high as 83% by one report. 2  

To make the matters more confusing, patients with acute bacterial prostatitis (ABP) often present with symptoms just like those of UTI,  such as urinary frequency, dysuria, malaise, fever, and myalgias. 3  In the elderly, atypical presentation is not uncommon (eg, confusion, incontinence, fall). 4  Under these circumstances, bacteriuria and pyuria may also be related to ABP and the prostate exam should be an important part of your evaluation.

Although the sensitivity of prostate tenderness on digital rectal exam varies widely for ABP (9%-100%), a painful exam should raise suspicion for ABP, and by itself may be an independent predictor for clinical and bacteriologic failure of therapy. 1 Along with tenderness, fluctuance of prostate, particularly in the setting of voiding difficulties and longer duration of symptoms, may also suggest the presence of prostatic abscess. 5,6 

But be gentle when performing a prostate exam and don’t massage it because you could potentially cause bacteremia and worsening of sepsis! 1,7

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References

  1. Etienne M, Chavanet P, Sibert L, et al. Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infectious Diseases 2008;8:12. https://bmcinfectdis.biomedcentral.com/track/pdf/10.1186/1471-2334-8-12?site=bmcinfectdis.biomedcentral.com
  2. Ulleryd P, Zackrisson B, Aus G, et al. Prostatic involvement in men with febrile urinary tract infection as measured by serum prostate-specific antigen and transrectal ultrasonography. BJU Int 1999;84:470-4. http://onlinelibrary.wiley.com/doi/10.1046/j.1464-410x.1999.00164.x/pdf
  3. Krieger JN, Nyberg L, Nickel JC. NIH consensus definition and classification. JAMA 1999;282:236-37. http://jamanetwork.com/journals/jama/article-abstract/1030245
  4. Harper M, Fowlis. Management of urinary tract infections in men. Trends in Urology Gynaecology & Sexual Health. January/February 2007. http://onlinelibrary.wiley.com/doi/10.1002/tre.8/pdf
  5. Lee DS, Choe HS, Kim HY, et al. Acute bacterial prostatitis and abscess formation. BMC Urology 2016;16:38. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936164/
  6. Oliveira P, Andrade JA, Porto HC, et al. Diagnosis and treatment of prostatic abscess. International Braz J Urol 2003;29: 30-34. http://www.scielo.br/pdf/ibju/v29n1/v29n1a06.pdf
  7. Lipsky BA, Byren I, Hoey CT. Treatment of bacterial prostatitis. Clin Infect Dis 2010; 50:1641-52. https://academic.oup.com/cid/article/50/12/1641/305217

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Should male patients with suspected urinary tract infection routinely undergo a prostate exam?

What is the mechanism of anemia of chronic disease in my patient with rheumatoid arthritis?

Anemia of chronic disease (ACD)—or more aptly “anemia of inflammation”— is the second most common cause of anemia after iron deficiency and is associated with numerous acute or chronic conditions (eg, infection, cancer, autoimmune diseases, chronic organ rejection, and chronic kidney disease)1.

The hallmark of ACD is disturbances in iron homeostasis which result in increased uptake and retention of iron within cells of the reticuloendothelial system, with its attendant diversion of iron from the circulation and reduced availability for erythropoiesis1. More specifically, pathogens, cancer cells, or even the body’s own immune system stimulate CD3+ T cells and macrophages to produce a variety of cytokines, (eg, interferon-ɤ, TNF-α, IL-1, IL-6, and IL-10) which in turn increase iron storage within macrophages through induction of expression of ferritin, transferrin and divalent metal transporter 1.

In addition to increased macrophage storage of iron, ACD is also associated with IL-6-induced synthesis of hepcidin, a peptide secreted by the liver that decreases iron absorption from the duodenum and its release from macrophages2. TNF-α and interferon-ɤ also contribute to ACD by inhibiting the production of erythropoietin by the kidney.  Finally, the life span of RBCs is adversely impacted in AKD due to their reduced deformability and increased adherence to the endothelium in inflammatory states3.

Of interest, it is often postulated that by limiting access to iron through inflammation, the body hinders the growth of pathogens by depriving them of this important mineral2.

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References

  1. Weiss, G and Goodnough, L. Anemia of chronic disease. N Engl J Med 2005; 352; 1011-23. http://www.med.unc.edu/medclerk/medselect/files/anemia2.pdf
  2. D’Angelo, G. Role of hepcidin in the pathophysiology and diagnosis of anemia. Blood Res 2013; 48(1): 10-15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3624997/pdf/br-48-10.pdf                                                                                                                                  
  3. Straat M, van Bruggen R, de Korte D, et al. Red blood cell clearance in inflammation. Transfus Med Hemother 2012;39:353-60. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3678279/pdf/tmh-0039-0353.pdf

 

Contributed by Amir Hossein Ameri, Medical Student, Harvard Medical School

                     

What is the mechanism of anemia of chronic disease in my patient with rheumatoid arthritis?

My patient with cirrhosis has been admitted to the hospital several times this year with bacterial infections. How does cirrhosis increase susceptibility to infections?

Bacterial infections are a common cause of morbidity and mortality in patients with cirrhosis, affecting about 30% of such patients either at admission or during their hospitalization, with an attendant risk of mortality that is twice that of individuals without cirrhosis1.

Two major mechanisms may account for the observed immune dysfunction in cirrhosis: 1. Compromise of the immune surveillance function of the liver itself through damage of the reticulo-endothelial system (RES) and reduced synthesis of innate immunity proteins and pattern recognition receptors (PRRs); and 2. Dysfunctions of circulating and intestinal population of immune cells2.

Damage to the RES in cirrhosis leads to portal-system shunting, loss/damage of Kupffer cells (specialized hepatic macrophages) and sinusoidal capillarization, all hindering blood-borne pathogen clearance. Cirrhosis is also associated with a defect in hepatic protein synthesis, including complement components, decreased PRRs and acute phase reactants (eg C-reactive protein), which may in turn lead to the impairment of the innate immunity and bacterial opsonization.

Cirrhosis can also cause reduction in the number and function of neutrophils (eg, decreased phagocytosis and chemotaxis), B, T, and NK lymphocytes, and decreased in bacterial phagocytosis by monocytes. In addition, damage to the gut-associated lymphoid tissue (eg Peyer’s patches and mesenteric lymph nodes) may facilitate bacterial translocation.

References

  1. Pieri G, Agarwal B, Burroughs AK. C-reactive protein and bacterial infections in cirrhosis. Ann Gastroenterol 2014;27:113-120. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982625/pdf/AnnGastroenterol-27-113.pdf
  2. Albillos A, Lario M, Alvarez-Mon M. Cirrhosis-associated immune dysfunction: distinctive features and clinical relevance. J Hepatol 2014;61:1385-1396. http://www.journal-of-hepatology.eu/article/S0168-8278(14)00549-2/pdf

 

My patient with cirrhosis has been admitted to the hospital several times this year with bacterial infections. How does cirrhosis increase susceptibility to infections?

My patient with cirrhosis and suspected infection has a normal serum C-reactive protein (CRP). Does cirrhosis affect CRP response to infection?

CRP is primarily synthesized by the liver mainly as a response to IL-6 production in inflammatory states1.  Lower CRP production may then be expected in cirrhotic patients with significant infections and several studies support this view2

In a particularly convincing study involving E. coli-infected patients with bacteremia, the median CRP level in cirrhotic patients was about 40% that of non-cirrhotic patients (62 mg/L vs 146 mg/L)3.  In another study involving bacteremic patients with or without liver dysfunction, median CRP level was about 60% that of  patients with preserved liver function (81 mg/L vs 139 mg/L)4

Some investigators have reported a cut-off CRP value of 9.2 mg/L as a possible screening test for bacterial infections in patients with cirrhosis with a sensitivity and specificity of 88% (AUROC 0.93)5.

Collectively, these data suggest that although CRP response may be diminished in patients with advanced liver disease and acute infection, its synthesis is still maintained.

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 References

  1. Pieri G, Agarwal B, Burroughs AK. C-reactive protein and bacterial infection in cirrhosis. Ann Gastroenterol 2014;27:113-20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982625/pdf/AnnGastroenterol-27-113.pdf
  2. Ha YE, Kang C-I, Joo E-J, et al. Usefulness of C-reactive protein for evaluating clinical outcomes in cirrhotic patients with bacteremia. Korean J Intern Med 2011;26:195-200. http://pubmedcentralcanada.ca/pmcc/articles/PMC3110852/pdf/kjim-26-195.pdf
  3. Park WB1, Lee KD, Lee CS et al. Production of C-reactive protein in Escherichia coli-infected patients with liver dysfunction due to liver cirrhosis. Diagn Microbiol Infect Dis. 2005 Apr;51(4):227-30. https://www.ncbi.nlm.nih.gov/pubmed/15808312
  4. Mackenzie I, Woodhouse J. C-reactive protein concentrations during bacteraemia: a comparison between patients with and without liver dysfunction. Intensive Care Med 2006;32:1344-51. https://www.ncbi.nlm.nih.gov/pubmed/16799774
  5. Papp M, Vitalis Z, Altorjay I, et al. Acute phase proteins in the diagnosis and prediction of cirrhosis associated bacterial infection. Liver Int 2011;603-11. https://www.ncbi.nlm.nih.gov/pubmed/22145664

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

My patient with cirrhosis and suspected infection has a normal serum C-reactive protein (CRP). Does cirrhosis affect CRP response to infection?

How is the pathophysiology of sepsis-associated acute kidney injury (SA-AKI) different than AKI due to non-septic conditions?

Sepsis accounts for up to one-half of AKI cases in developed countries1.  Although sepsis-mediated hypoperfusion causing tubular necrosis has traditionally been implicated as the primary basis for SA-AKI,  an increasing number of studies have suggested that SA-AKI is a distinct subset of AKI differentiated from other causes by unique hemodynamic and inflammatory/immune-related mechanisms.  

Many animal and limited human studies have found that renal blood flow is an inconsistent predictor of SA-AKI, possibly related to the redistribution of blood in the renal microvasculature to the detriment of the renal medulla in sepsis2.

Cytokine-mediated response in sepsis can also lead to tubular cellular injury without necessarily causing necrosis. Of interest, an autopsy study found histological features of acute tubular necrosis in only 22% of patients with clinical diagnosis of SA-AKI 3.  

Differences in its pathophysiology may at least in part explain why oliguria, renal function recovery, hemodialysis and death are more common among SA-AKI patients4.

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References

  1. Alobaidi R, Basu RK, Goldstein SL, Bagshaw SM. Sepsis-associated acute kidney failure. Semin Nephrol 2015;35:2-11.  https://www.ncbi.nlm.nih.gov/pubmed/25795495
  2. Maiden MJ, Otto S, Brealey JK, et al. Structure and function of the kidney in septic shock. Am J Resp Crit Care Med 2016;194:692-700. https://www.atsjournals.org/doi/abs/10.1164/rccm.201511-2285OC
  3. Langenberg C, Bagshaw SM, May CN, Bellomo R. The histopathology of septic acute kidney injury: a systemic review. Crit Care 2008;12:R38.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2447560/
  4. Cruz MG, de Oliveira Dantas JGA, Levi TM, et al. Septic versus non-septic acute kidney injury in critically ill patients: characteristics and clinical outcome. Rev Bras Ter Intensiva 2014;26:384-391. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304467/
How is the pathophysiology of sepsis-associated acute kidney injury (SA-AKI) different than AKI due to non-septic conditions?

What is the association between sepsis and jaundice in patients without biliary obstruction?

Up to 20% of cases of jaundice in community hospitals may be due to sepsis and bacterial infections, often occurring within a few days of onset of bacteremia or even before other clinical features of infection become apparent. 1 

Although biliary obstruction as the cause of jaundice is usually suspected, many patients lack extrahepatic cause for their jaundice. Gram-negative bacteria (eg, E. coli) are often the culprit with intraabdominal or urinary tract infection, pneumonia, endocarditis, and meningitis sources also often cited. Hyperbilirubinemia (often 2-10 mg/dl) is commonly associated with elevated alkaline phosphatase and mild aminotransferases elevations, and usually resolves with treatment of infection.1

Although factors such as increased bilirubin load from hemolysis, hepatocellular injury, and drugs (eg, penicillins and cephalosporins) may play a role, cholestasis—likely due to cytokines such as tumor necrosis factor (TNF)α— is the predominant cause. 1  

Interestingly, anti-TNF-α antibodies block reduction in bile flow and bile salt excretion in laboratory animals2

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References

  1. Chand N, Sanyal AJ. Sepsis-induced cholestasis. HEPATOLOGY 2007;45: 230-240. https://aasldpubs.onlinelibrary.wiley.com/doi/full/10.1002/hep.21480
  2. Whiting J, Green R, Rosenbluth A, Gollan J. Tumor necrosis factor-alpha decreases hepatocyte bile salt uptake and mediates endotoxin-induced cholestasis. HEPATOLOGY 1995;22:1273-1278. https://www.deepdyve.com/lp/wiley/tumor-necrosis-factor-alpha-decreases-hepatocyte-bile-salt-uptake-and-J9rdeMQBpF

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What is the association between sepsis and jaundice in patients without biliary obstruction?

My elderly patient with acute heart failure with preserved ejection fraction (HFpEF) has a low serum albumin. Can hypoalbuminemia be associated with HFpEF?

Absolutely! As early as 1959, Guyton and Lindsey demonstrated the importance of serum colloid osmotic pressure in the pathogenesis of pulmonary edema1.

Specifically, they found that in dogs with normal plasma protein concentrations fluid began to transudate into the lungs when the left atrial pressure rose above an average of 24 mm Hg vs only 11 mm Hg when plasma protein concentration was reduced by about 50%.

Fast forward to 2003, Arques et al studied serum albumin and pulmonary artery wedge pressures in 4 groups of patients: acute HFpEF, heart failure with reduced ejection fraction (HFrEF), acute dyspnea from pulmonary origin and normal controls2.   Patients with HFpEF were significantly more likely to have hypoalbuminemia , compared to those with HFrEF, pulmonary disease or normal controls.  The main cause of hypoalbuminemia in the HFpEF was malnutrition in 77% and/or sepsis in 41% of patients.   Hypoalbuminemia was inversely related to age and plasma C-reactive protein.

Perhaps, we should pay more attention the nutritional status of our patients with HFpEF!

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References

  1. Guyton AC, Lindsey AW. Effect of elevated left atrial pressure and decreased plasma protein concentration on the development of pulmonary edema. Circ Res 1959;7: 649-657.
  2. Arquès S, Ambrosi P, Gélisse R et al. Hypoalbuminemia in elderly patients with acute diastolic heart failure. J Am Coll Card 2003;42:712-16. http://www.onlinejacc.org/content/42/4/71                                                                                                    
My elderly patient with acute heart failure with preserved ejection fraction (HFpEF) has a low serum albumin. Can hypoalbuminemia be associated with HFpEF?

What are the major changes in the definition of “sepsis” under the 3rd International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)?

Under Sepsis-3 [1], sepsis is defined as a “life-threatening organ dysfunction caused by a dysregulated host response to infection (suspected or confirmed)”. Systemic inflammatory response syndrome (SIRS) is no longer defined as part of the sepsis spectrum, and its criteria have been replaced by the Sequential Organ Failure Assessment (SOFA) with a change in score ≥2 (Table) having >10% in-hospital mortality. Septic shock is defined as hypotension requiring vasopressors to maintain a MAP ≥65 mm Hg and a lactate >2 mmol/L (18 mg/dL) despite adequate volume (>40% in-hospital mortality).

A bedside clinical tool “quickSOFA” (qSOFA), not meant to substitute for SOFA, is also proposed to identify patients primarily outside of the ICU who may be at high risk of adverse outcomes, based on the following criteria: systolic blood pressure ≤100 mmHg, respiratory rate ≥22/min, and altered mental status. A qSOFA score ≥2 is associated with poorer outcomes [1,2].

So what do these new guidelines mean for clinicians? Under the new terminology, “sepsis” now refers only to what was previously considered severe sepsis with or without shock, and those who may need more aggressive therapy, closer monitoring and possible transfer to an ICU [1,2]. As the guidelines stress, however, failure to meet qSOFA or SOFA criteria should by no means lead to a deferral or delay in evaluation or treatment of infection deemed necessary by clinicians, and SIRS criteria may still be useful in identification of infection [1].

It remains to be seen whether limiting the definition of sepsis to only patients with associated organ dysfunction will translate into an overall earlier diagnosis and improved prognosis for this condition.

Using SIRS criteria (ie, 2 or more of the following, heart rate >90/min, respiratory rate >20/min  or PaC02 <32 mm Hg, temperature<36 C or >38 C, WBC <4,000 or >12,000 or bandemia >10%) in patients suspected of having a potentially serious infection still makes sense if the goal is to identify it “upstream” before organ dysfunction or shock sets in.  Stay tuned!

 

Table. Sequential (sepsis-related) organ failure assessment (SOFA) score (adapted from ref.1)____________________________________________________________________________________________________

                                                                                             Points

Parameter                                0                      1                      2                      3                      4

____________________________________________________________________________________________________

Pa02/Fi02                           ≥400                 <400                <300                 <200*          <100*

Platelets (no./mL)           >150,000         <150,000         <100,000         <50,000       <20,000

Bilirubin (mg/dL)            <1.2                  1.2-1.9              2.0-5.9             6.0-11.9       >12.0

MAP (mm Hg) or VP      MAP≥70         MAP<70          DPA≤5           DPA 5.1-15        DPA>15

Glascow Coma Scale       15                    13-14            10-12                    6-9                 3-6

Creatinine (mg/dL)        <1.2                 1.2-1.9           2.0-3.4                  3.5-4.9        >5.0

OR U.O.  (mL/dL)                                                                                              <500                <200

____________________________________________________________________________________________________

MAP= mean arterial pressure, VP=vasopressor (includes agents other than dopamine), DPA=dopamine (in mcg/kg/min for ≥1 hour);U.O.= urine output

*With respiratory support

 

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References:

  1. Singer MS, Deutschman CS, Seymour CW, et al; The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315[8]:801-810. https://jamanetwork.com/journals/jama/fullarticle/2492881  
  2. Jacob JA. New Sepsis Diagnostic Guidelines Shift Focus to Organ Dysfunction. JAMA. 2016;213[8]:739-740. https://www.ncbi.nlm.nih.gov/pubmed/26903319

 

Contributed by Erik Kelly MD, Mass General Hospital, Boston, MA

What are the major changes in the definition of “sepsis” under the 3rd International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)?