My hospitalized patient with pneumonia has now suffered an acute myocardial infarction (MI). Can acute infection and MI be related?

Yes! Ample epidemiological studies implicate infection as an important risk factor for MI.1 The increased risk of MI has been observed during the days, weeks, months or even years following an infection.

A 2018 paper reported a several-fold risk of MI during the week after laboratory-confirmed infection caused by a variety of respiratory pathogens such as influenza virus (6-fold), respiratory syncytial virus (4-fold), and other respiratory viruses (3-fold). 2 Among patients hospitalized for pneumococcal pneumonia, 7-8% may suffer an MI.3,4 One study found a 48-fold increase in the risk of MI during the first 15 days after hospitalization for acute bacterial pneumonia.5 Similarly, an increase in the short-term risk of MI has been observed in patients with urinary tract infection and bacteremia.6

The risk of MI appears to be the highest at the onset of infection and correlates with the severity of illness, with the risk being the highest in patients with pneumonia complicated by sepsis, followed by pneumonia and upper respiratory tract infection. Among patients with pneumonia, the risk exceeds the baseline risk for up to 10 years after the event, particularly with more severe infections.1

Potential mechanisms of MI following infections include release of inflammatory cytokines (eg, interleukins 1, 6, tumor necrosis factor alpha) causing activation of inflammatory cells in atherosclerotic plaques, in turn resulting in destabilization of the plaques. In addition, the thrombogenic state of acute infections, platelet and endothelial dysfunction may increase the risk of coronary thrombosis at sites of plaque disruption beyond clinical resolution of the acute infection. 1

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  1. Musher DM, Abers MS, Corrales-Medina VF. Acute infection and myocardial infarction. N Engl J Med 2019;380:171-6.
  2. Kwong JC, Schwartz KL, Campitelli MA, et al. Acute myocardial infarction after laboratory-confirmed influenza infection. N Engl J Med 2018;378:345-53.
  3. Musher DM, Alexandraki I, Graviss EA, et al. Bacteremic and nonbacteremic pneumococcal pneumonia: a prospective study. Medicine (Baltimore) 2000;79:210-21.
  4. Musher DM, Rueda Am, Kaka As, Mapara SM. The association between pneumococcal pneumonia and acute cardiac events. Clin Infect Dis 2007;45:158-65.
  5. Corrales-Medina VF, Serpa J, Rueda AM, et al. Acute bacterial pneumonia is associated with the occurrence of acute coronary syndromes. Medicine (Baltimore) 2009;88:154-9.
  6. Dalager-Pedersen M, Sogaard M, Schonheyder HC, et al. Risk for myocardial infarction and stroke after community-acquired bacteremia: a 20-year population-based cohort study. Circulation 2014;129:1387-96.


My hospitalized patient with pneumonia has now suffered an acute myocardial infarction (MI). Can acute infection and MI be related?

My patient with cirrhosis now has an upper gastrointestinal bleed (UGIB) with hepatic encephalopathy (HE). What’s the connection between UGIB and HE?

Hepatic encephalopathy (HE) may be precipitated by a variety of factors including infection, hypovolemia, electrolyte imbalance (eg, hyponatremia, hypokalemia), metabolic alkalosis, sedatives, and of course UGIB. 1-3

Ammonia is often considered to play a central role in the the pathogenesis of HE, particularly when associated with UGIB. The ammoniagenic potential of UGIB is primarily attributed to the presence of hemoglobin protein in the intestinal tract. One-half of the ammoniagenesis originates from amino acid metabolism (mainly glutamine) in the mucosa of the small bowel, while the other half is due to the splitting of urea by the resident bacteria in the colon (eg, Proteus spp., Enterobacteriaceae, and anerobes).1,2

A large protein load in the GI tract, as occurs in UGIB, may result in hyperammonemia in patients with cirrhosis due to the limited capacity of the liver to convert ammonia to urea through the urea cycle as well as by the shunting of blood around hepatic sinusoids. Recent studies, however, also implicate the kidneys as an important source of ammonia in this setting, further compounding HE.3

It’s important to stress that ammonia is not likely to be the only mediator of HE. Enhanced production of cytokines due to infection or other inflammatory states, neurosteroids, endogenous benzodiazepines, and other bacterial byproducts may also play an important role in precipitating HE.2,4-6  So stay tuned!

Bonus pearl: Did you know that proinflammatory cytokines tumor necrosis factor-alpha and inerleukin-6 increase ammonia permeability across central nervous system-derived endothelial cells? 7



  1. Olde Damink SWM, Jalan R, Deutz NEP, et al. The kidney plays a major role in the hyperammonemia seen after simulated or actual GI bleeding in patients with cirrhosis. Hepatology 2003;37:1277-85.
  2. Frederick RT. Current concepts in the pathophysiology and management of hepatic encephalopathy. Gastroenterol Hepatol 2011;7:222-233.
  3. Tapper EB, Jiang ZG, Patwardhan VR. Refining the ammonia hypothesis: a physiology-driven approach to the treatment of hepatic encephalopathy. Mayo Clin Proc 2015;90:646-58.
  4. Shawcross DL, Davies NA, Williams R, et al. Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis. J Hepatol 2004;40:247-254.
  5. Shawcross DL, Sharifi Y, Canavan JB, et al. Infection and systemic inflammation, not ammonia, are associated with grade ¾ hepatic encephalopathy, but not mortality in controls. J Hepatol 2011;54:640-49.
  6. Shawcross D, Jalan R. The pathophysiologic basis of hepatic encephalopathy: central role for ammonia and inflammation.Cell Mol Life Sci 2005;62:2295-2304.
  7. Duchini A, Govindarajan S, Santucci M, et al. Effects of tumor necrosis factor-alpha and interleukin-6 on fluid-phase permeability and ammonia diffusion in CNS-derived endothelial cells. J Investig Med 1996;44:474-82.

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My patient with cirrhosis now has an upper gastrointestinal bleed (UGIB) with hepatic encephalopathy (HE). What’s the connection between UGIB and HE?

My previously healthy patient is admitted with a multi-drug resistant E. coli urinary tract infection. Could her urinary tract infection (UTI) be foodborne?

Yes! Although foodborne infections are often thought to cause infections limited to the GI tract, an increasing number of studies have linked foodborne E.coli to extraintestinal infections in humans, including UTIs.1

Supportive data include frequent genetic similarly between antimicrobial-resistant E. coli from humans and poultry-associated E. coli. 2 In fact, antimicrobial-resistant E. coli isolates from humans may be  genetically more similar to poultry isolates than susceptible commensal E. coli strains in the human GI tract.3

A U.S. study found that 14% of chicken meat products were contaminated with E. coli strains capable of causing extraintestinal disease, 1/3 of which were mutli-drug resistant.4  Another study found that 94% of retail chicken meat samples contained E. coli with ESBL-genes,  of which nearly 40% contained isolates present in humans.5

Among women, UTI caused by antimicrobial-resistant extraintestinal pathogenic E. coli has been linked to high levels of self-reported chicken consumption.6

The plausibility of foodborne transmission of antimicrobial-resistant E. coli to humans is further supported by the finding that drug resistant E coli from chicken carcasses widely contaminate the kitchen during meal preparation and can appear in the intestinal tract of those who prepare such food.2

Bonus Pearl: Did you know that women with multi-drug resistant E. coli UTI are 3.7 times more likely to report frequent consumption of chicken? 6

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  1. Manges AR. Escherichia coli and urinary tract infections: the role of poultry-meat. Clin Microbiol Infect 2016;22:122-29.
  2. Manges AR, Johnson JR. Reservoirs of extraintestinal pathogenic Escherichia coli. Microbiol Spectrum 2012;3(5):UTI-0006-2012.
  3. Johnson JR, Menard M, Johsnton B, et al. Epidemic clonal groups of Escherichia coli as a cause of antimicrobial-resistant urinary tract infections in Canada, 2002 to 2004. Antimicrob Agents Chemother 53;2733-2739.
  4. Johnson JR, Porter SB, Johnston B, et al. Extraintestinal pathogenic and antimicrobial-resistant Escherichia coli, including sequence type 131 (ST131) from retail chicken breasts in the United States in 2013. Apppl Environ Microbiol 83:e02956-16.
  5. Leverstein-van Hall MA, Dierikx CM, Stuart JC, et al. Dutch patients, retail chicken meat and poultry share the same ESBL genes, plasmids and strains. Clin Microbiol Infect 2011;17:873-880.
  6. Manges AR, Smith SP, Lau BJ, et al. Retail meat consumption and the acquisition of antimicrobial resistant Escherichia coli causing urinary tract infections: a case-control study. Foodborne Path Dis 4:419-431.


My previously healthy patient is admitted with a multi-drug resistant E. coli urinary tract infection. Could her urinary tract infection (UTI) be foodborne?

Does erythrocyte sedimentation rate (ESR) have diagnostic utility in my patient with chronic renal failure?

Short answer: often not! This is because most studies have shown frequently high ESR’s in stable “uninflamed” patients with chronic renal failure (CRF) (including those on dialysis) at levels often associated with infection, connective tissue disease, or malignancy. 1-4  

In fact, in a study involving patients with CRF, 57% of patients had markedly elevated ESR (greater than 60 mm/h), with 20% having ESR greater than 100 mm/h; type or duration of dialysis had no significant effect on ESR levels.1 Another study reported a specificity for abnormal ESR of only 35% for commonly considered inflammatory conditions (eg, infections or malignancy) among patients with CRF. 2

But is it the chronic inflammation in diseased kidneys or the uremic environment that elevates ESR? A cool study compared ESR in CRF in patients who had undergone bilateral nephrectomies with those with retained kidneys and found no significant difference in the ESR between the 2 groups. 4  So it looks like it’s the uremic environment, not diseased kidneys themselves that result in elevated ESR in these patients.

The mechanism behind these observations seem to reside entirely within the patients’ plasma, not the erythrocytes. Within the plasma, fibrinogen (not gammaglobulins) seem to be the most likely factor explaining elevated ESR among patients with CRF. 1,2

Bonus pearl:  Did you know that ESR is nearly 100 years old, first described in 1921? 5


  1. Barthon J, Graves J, Jens P, et al. The erythrocyte sedimentation rate in end-stage renal failure. Am J Kidney Dis 1987;10: 34-40.
  2. Shusterman N, Morrison G, Singer I. The erythrocyte sedimentation rate and chronic renal failure. Ann Intern Med 1986;105:801.
  3. Arik N, Bedir A, Gunaydin M, et al. Do erythrocyte sedimentation rate and C-reactive protein levels have diagnostic usefulness in patients with renal failure? Nephron 2000;86:224.
  4. Warner DM, George CRP. Erythrocyte sedimentation rate and related factors in end-stage renal failure. Nephron 1991;57:248.
  5. Fahraeus R. The suspension stability of the blood. Acta Med Scan 1921;55:70-92.


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Does erythrocyte sedimentation rate (ESR) have diagnostic utility in my patient with chronic renal failure?

How is prealbumin related to albumin?

Aside from being synthesized in the liver and serving as a transport protein in the blood, prealbumin (PA) doesn’t really have much in common with albumin. More specifically, PA is not derived from albumin and, in fact, the two proteins are structurally distinct from each other!

So where does PA get its name? PA is the original name for transthyretin (TTR), a transport protein that primarily carries thyroxine (T4) and a protein bound to retinol (vitamin A). The name arose because TTR migrated faster than albumin on gel electrophoresis of human serum.1

Because of its much shorter serum half-life compared to that of albumin ( ~2 days vs ~20 days),2 PA is more sensitive to recent changes in protein synthesis and more accurately reflects recent dietary intake (not necessarily overall nutritional status) than albumin. 3

But, just like albumin, PA may represent a negative acute phase reactant, as its synthesis drops during inflammatory states in favor of acute phase reactants such as C-reactive protein. 4 So be cautious about interpreting low PA levels in patients with active infection, inflammation or trauma.



  1. Socolow EL, Woeber KA, Purdy RH, et al. Preparation of I-131-labeled human serum prealbumin and its metabolism in normal and sick patients. J. Clin Invest 1965; 44: 1600-1609.
  2. Oppenheimer JH, Surks MI, Bernstein G, and Smith JC. Metabolism of Iodine-131-labeled Thyroxine-Binding Prealbumin in Man. Science 1965; 149: 748-750.
  3. Ingenbleek Y, Young VR. Significance of prealbumin in protein metabolism. Clin Chem Lab Med 2002; 40: 1281-1291.
  4. Shenkin A. Serum prealbumin: is it a marker of nutritional status or of risk of malnutrition? Clin Chem 2006;52:2177 – 2179.

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Contributed by Colin Fadzen, Medical Student, Harvard Medical School, Boston, MA.



How is prealbumin related to albumin?

How accurate are peripheral thermometers for estimating body temperature in my patient with chills?

Though convenient, oral, tympanic membrane, axillary, and temporal artery thermometers (AKA “peripheral thermometers”) may not be highly accurate in measuring body temperature.

A 2015 systematic review and meta-analysis of the performance of peripheral thermometers involving 75 studies (mostly in adults) found that compared to central thermometers (eg, pulmonary artery, urinary bladder, rectal), peripheral thermometers had a low sensitivity (64%, 95% CI 55%-72%), but much better specificity (96%, 95% CI 93%-97%) for fever (most commonly defined as 37.8° C [100° F] or greater).1

In the same study, for oral electronic thermometers, sensitivity was 74% with a specificity of 86%. For temporal artery thermometers, sensitivities ranged from 26% to 91%, while specificities ranged from 67% to 100%. For tympanic membrane thermometers, sensitivities ranged from 23% to 87%, with a specificity of 57% to 99%.

A 2016 study involving adult emergency department patients reported the sensitivity of peripheral thermometers (vs rectal temperature 38 C [100.4] or higher) as follows: oral (37%), tympanic membrane (68%), and temporal artery (71%). Specificity for fever was >90% for all peripheral thermometers. 2

So, it looks like while we may be pretty comfortable with a diagnosis of “fever” when our patient with chills has a high temperature recorded by a peripheral thermometer, lack of fever alone by these devices should not veer us away from the possibility of systemic infection. When in doubt and if possible, check a rectal temperature.


  1. Niven DJ, Gaudet JE, Laupland KB. Accuracy of peripheral thermometers for estimating temperature: A systematic and meta-analysis. Ann Intern Med 2015;163:768-777.
  2. Bijur PE, Shah PD, Esses D. Temperature measurement in the adult emergency department: oral tympanic membrane and temporal artery temperatures versus rectal temperature. Emerg Med J 2016;33:843-7.


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How accurate are peripheral thermometers for estimating body temperature in my patient with chills?

My elderly nursing home patient is admitted with recent poor oral intake, falls and oral temperatures of 99.1°-99.3° F(37.3°-37.4°C). Is she considered febrile at these temperatures?

Yes! Even though we often think of temperatures of 100.4°F (38° C) or greater as fever, older people often fail to mount an appropriate febrile response despite having a serious infection. 1

Infectious Diseases Society of America (IDSA) guideline on evaluation of fever in older adult residents of long-term care facilities has defined fever in this population as:2

  • Single oral temperature >100° F (>37.8° C) OR
  • Repeated oral temperatures >99° F (>37.2° C) OR
  • Rectal temperatures >99.5° F (>37.5° C) OR
  • Increase in temperature of >2° F (>1.1° C) over the baseline temperature

Even at these lower than traditional thresholds for defining fever, remember that many infected elderly patients may still lack fever. In a study involving bacteremic patients, nearly 40% of those 80 years of age or older did not have fever (defined as maximum temperature over 24 hrs 100° F [37.8°C] or greater).3  

So our patient meets the criteria for fever as suggested by IDSA guidelines and, particularly in light of her recent poor intake and falls, may need evaluation for a systemic source of infection.

Now that’s interesting! Did you know that blunted febrile response of the aged to infections may be related to the inability of cytokines (eg, IL-1) to reach the central nervous system?1


  1. Norman DC. Fever in the elderly. Clin Infect Dis 2000;31:148-51.
  2. High KP, Bradley SF, Gravenstein S, et al. Clinical practice guidelines for the evaluation of fever and infection in older adult residents of long-term care facilities: 2008 update by the Infectious Disease Society of America. Clin Infect Dis 2009;48:149-71.
  3. Manian FA. Fever, abnormal white blood cell count, neutrophilia, and elevated serum C-reactive protein in adult hospitalized patients with bacteremia. South Med J 2012;105;474-78.
My elderly nursing home patient is admitted with recent poor oral intake, falls and oral temperatures of 99.1°-99.3° F(37.3°-37.4°C). Is she considered febrile at these temperatures?

Is iron therapy contraindicated in my patient with active infection?

In the absence of randomized-controlled trials of iron therapy in patients with active infection, the harmful effects of iron therapy (IT) in this setting remains more theoretical than proven. 1,2

Although many pathogens (eg, E. coli, Klebsiella, Salmonella, Yersinia, and Staphylococcus species) depend on iron for their growth2,3, and iron overload states (eg, hemochromatosis) predispose to a variety of infections, studies evaluating the risk of infection with iron therapy have reported conflicting results.1-4 A 2015 systematic review and meta-analysis of 103 trials comparing IV iron therapy  with several other approaches, including oral iron therapy or placebo, found no increased risk of infections with IV iron.5 In contrast, an earlier systematic review and meta-analysis involving fewer number of trials found an increased risk of infections with IV iron. 6

These varied results are perhaps not surprising since the effects of iron therapy on the risk of infection is likely to be context-specific, depending on the patient’s preexisting iron status, exposure to potential infections and co-infection and genetic background. 4 Of interest, mice with sepsis have worse outcomes when treated with IV iron.7

Perhaps the most prudent approach is to hold off on iron therapy until the active infection is controlled, unless the benefits of urgent iron therapy is thought to outweigh its theoretical harmful effects.


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  1. Daoud E, Nakhla E, Sharma R. Is iron therapy for anemia harmful in the setting of infection? Clev Clin J Med 2011;78:168-70.
  2. Hain D, Braun M. IV iron: to give or to hold in the presence of infection in adults undergoing hemodialysis. Nephrology Nursing Journal 2015;42:279-83.
  3. Jonker FAM, van Hensbroek MB. Anaemia, iron deficiency and susceptibility of infections. J Infect 204;69:523-27.
  4. Drakesmith H, Prentice AM. Hepcidin and the iron-infection axis. Science 2012;338:768-72.  
  5. Avni T, Bieber A, Grossman A, et al. The safety of intravenous iron preparations: systematic review and meta-analysis. Mayo Clin Proc 2015;90:12-23.
  6. Litton E, Xiao J, Ho KM. Safety and efficacy of intravenous iron therapy in reducing requirement for allogeneic blood transfusion: systematic review and meta-analysis of randomized clinical trials. BMJ 2013;347:f4822.
  7. Javadi P, Buchman TG, Stromberg PE, et al. High dose exogenous iron following cecal ligation and puncture increases mortality rate in mice and is associated with an increase in gut epithelial and splenic apoptosis. Crit Care Med 2004;32:1178-1185.
Is iron therapy contraindicated in my patient with active infection?

How exactly do urinary tract infections (UTIs) cause delirium in my elderly patients?

 UTIs are often considered in the differential diagnosis of causes of delirium in the elderly. Though largely speculative, 2 possible pathophysiologic basis for this association are suggested:1-3

  •  Direct brain insult (eg, in the setting of sepsis/hypotension)
  • Indirect aberrant stress response, involving cytokines/inflammatory pathways,  hypothalamic-pituitary-adrenal [HPA] axis and sympathetic nervous system (SNS). One or both pathways can interact with the neurotransmitter and intracellular signal transduction systems underlying delirium in the brain, which may already be impaired in the elderly due to age-related or other pathologic changes.

The indirect aberrant stress pathway suggests that not only pain and discomfort (eg from dysuria) can contribute to delirium but UTI-associated circulating cytokines may also cause delirium.  Indeed, a large study of older adults undergoing elective surgery found a significant association between delirium postoperatively (postop day 2) and serum proinflammatory cytokine levels such as IL-6. 4  

The corollary is that bacteriuria is unlikely to be associated with delirium in the absence of significant systemic inflammatory response, pain or discomfort.



1.Trzepacz P, van der Mast R. The neuropathophysiology of delirium. In Lindesay J,  Rockwood K, Macdonald A (Eds.). Delirium in old age, pp. 51–90. Oxford University Press, Oxford , 2002.

2.Flacker JM, Lipsitz LA. Neural mechanisms of delirium: current hypotheses and evolving concepts. J Gerontol A Biol Sci Med Sci. 1999; 54: B239–B246

3. Maclullich AM, Ferguson KJ, Miller T, de Rooij SE, Cunningham C. Unravelling the pathophysiology of delirium: a focus on the role of aberrant stress responses. J Psychosom Res. 2008;65:229–38.

4. Vasunilashom SM, Ngo L, Inouye SK, et al. Cytokines and postoperative delirium in older patients undergoing major elective surgery. J Gerontol A Biol Sci Med Sci 2015;70:1289-95.

Contributed by Henrietta Afari MD, Mass General Hospital, Boston, MA

How exactly do urinary tract infections (UTIs) cause delirium in my elderly patients?

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)____________________________________________________________________________________________________


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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  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.  
  2. Jacob JA. New Sepsis Diagnostic Guidelines Shift Focus to Organ Dysfunction. JAMA. 2016;213[8]:739-740.


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)?