Elevated Lactate: Significance and Challenges


Given the evolving definition of sepsis and the continual push to report sepsis measures to State Health Departments and CMS, I thought the time is ripe to revisit a popular topic: the significance of elevated lactate in the ED. After all, not all elevated lactate is sepsis, and we may be able to spare some diagnostic errors in the ED by examining this popular lab value more closely.

What Causes High Lactate?
Most healthy tissues use O2-dependent aerobic metabolism for energy. Under stressful conditions when aerobic metabolism is not possible (i.e., when O2 is low), tissues switch to anaerobic metabolism, which creates lactate as a byproduct. Lactate is therefore an indicator of cellular stress.

Lactate is classically associated with hypoxia or hypoxemia (poor O2 delivery to tissues), but is actually produced under a variety of stress conditions. It is therefore more useful to think of lactate as a general indicator of impaired cellular metabolism rather than solely as a byproduct of poor perfusion.

Other markers of cellular stress, such as the anion gap or pH, are not as good as lactate. They cannot act as substitutes for lactate testing.

Healthy tissues still use anaerobic metabolism to some degree at baseline. This lactate is cleared quickly by the liver (320 mmol/L/hr), such that basal lactate levels do not rise much above 1 mmol/L. The liver does this because too much lactate can result in acidosis, which compounds cellular stress.

Why Do I Care?
Prognostication: Lactate predicts badness and whether your treatment for badness is working.
Diagnosis: It is also sensitive for occult severe sepsis (can screen for patients with high mortality risk despite being normotensive with good mental status), but not specific (lots of conditions cause elevated lactate), or 100% reliable (some patients with severe sepsis can still have a normal lactate despite being hypotensive or altered).

How Should I Order a Lactate Sample?
Don’t leave the tourniquet on for too long (which can falsely elevate the result) and trust your venous sample (it’s just as accurate as arterial). Ideally, the sample should be put it on ice if you anticipate >15 min delay to processing.

How Do I Approach the Patient with High Lactate?
Broadly, you should split your differential into hypoxic/ischemic causes (there’s not enough oxygen to enter the aerobic pathway) versus other metabolic causes (there’s enough oxygen, but the aerobic pathway itself is impaired, inhibited, or overwhelmed). If there isn’t a clear suspected source of infection, and/or the patient has renal failure, hepatic dysfunction, diabetes, or other co-morbidities, don’t anchor on sepsis.  Broaden your differential:


Similarly, in patients without a clear source of infection who have high initial lactate, consider reversible conditions upfront, including external and environmental factors such as drugs or hyperthermia that can be removed or quickly addressed. Also consider high metabolic states including heavy exercise or seizure.

What is the Significance of the Initial Lactate?
In Septic Patient: Higher mortality if initial lactate is > 4 (meets severe sepsis criteria).
In Cardiac Arrest Patient: Higher mortality if initial lactate is > 10 (92% mortality rate).
In Trauma Patient: Higher mortality if initial lactate is > 4 (84% sensitivity and 86% specificity for death).
In DKA Patient: Elevated lactate does NOT predict higher mortality.
In Liver Patient: Tread carefully. The liver is the primary organ for metabolizing lactate, but elevated lactate could be due to a secondary process (sepsis, anemia, tox) that has nothing to do with the liver. It may be useful to compare the initial value to a baseline lactate, but in general the lactate level will not be as reliable.

What is the Significance of the Repeat Lactate?
For critically ill patients, trending is most important within the first 24 hours (the “silver day” following the “golden hour”).
In Septic Patient: Less risk for badness if lactate falls to < 2.5 within 24 hours.
In Post-Arrest Patient: More risk for badness if lactate clearance < 10% within 24 hours.
In PE Patient: More risk for badness if lactate > 2 for 24 hours.
In Seizure Patient: If lactate remains elevated 1-2 hours after the seizure, consider alternative etiology.

EMNerd-The Case of the Dysrhythmic Heart

Amiodarone has long held the position as the preferred antiarrhythmic medication in the patient presenting with hemodynamically wide-complex tachycardia. Its popularity so universal that other antiarrhythmic medications, like procainamide, have found themselves marginalized to a dusty corner in the medications we used last century closet. Despite its claims of superiority, which are often stated with […]

EMCrit by Rory Spiegel.

4-hour standards and staffing. Can we square the circle?


It’s been a turbulent and highly unpredictable few weeks in the UK. The Brexit vote to leave the EU, a new Prime Minister and the main opposition Labour party seemingly at war with itself have dominated the headlines. In amongst this we have seen the retention of Jeremy Hunt as Secretary of State for health  amidst a brutal cabinet reshuffle.  I think it’s fair to say that this was not a popular choice for many NHS workers, but perhaps it does mean that we have a degree of predictability and continuity.

Or do we?

Yesterday I gave a talk at our local trainee’s day about the future of emergency medicine. I suggested that financial pressures in the UK may lead to a change in the targets that currently dominate departments and the experience of those working in them. The 4-hour target (standard as it is formally known) requires emergency departments to admit or discharge 95% of patients within 4 hours. We’ve not been meeting it for some time (and in fact some hospitals have more bespoke targets but let’s not get picky here). Have a look at the graph below, it does not read well.

Perhaps this is a time to bury bad news and so it was that we heard about a revision/relaxation of the standards for hospitals already in crisis. Some will welcome this, but beware, those of us who remember a time before targets a very much aware that they have driven substantial investment in emergency services and in particular staff. Not enough I grant you, but it has had a significant influence.

Similarly concerns around safe staffing followed reports into patient safety events at Mid Staffs hospital leading to increases in staffing and the stretching of NHS budgets. Many hospitals recruited extra staff to meet safe levels following internal reviews or external reviews from organisations such as the CQC. A safe hospital is not a cheap hospital, and safety relies on trained, motivated and capable staff to look after our patients and each other. This is especially the case in emergency care where staffing is a large part of the budget.

You don’t need to read the entire Francis report on Mid Staffs, but it has been highly influential. The tweet below from Shaun Lintern (who is well worth following) rather sums up that report, essentially it raised the major concern that financial and admin targets can pervert the delivery of safe and effective care. Clearly we don’t want to repeat this.

The double whammy yesterday was the less well publicised report from NHS Improvement stating that many UK hospitals had over recruited and would thus have their budgets cut as a result. The report lists trusts who have allegedly overspent in line with increases in activity or inflation. The methodology has been questioned and the reaction from trusts has been fierce.  Click on the link in Shaun Lintern’s tweet to read the hospitals named. You may well recognise them. I certainly know many well and I can assure you that they are not awash with staff. Many are in significant difficulties facing the constraints of finance, targets amidst a desire to care for patients and keep them safe.

It is difficult to see how emergency care services will balance the financial requirements announced yesterday together with a need to maintain patient safety and deliver a quality service. It is even more difficult to see who will be blamed when the equation cannot be met. I suspect that the NHS senior management will be happy to devolve that to trusts and departments, but we shall see.

For now, for anyone celebrating the death of the 4-hour target, beware, it’s bound to be replaced by something else and that may be even less palatable.




The views expressed here are mine and do not represent the position of the EMJ or BMJ publishing.

Boot Camp: Phase 1

As we welcome a new class of interns this July, our Louisville Lectures team wanted to highlight some of our most-viewed lectures. Our Boot Camp series will cover high-yield, critical topics that are useful to starting interns. 

Phase One

Or, A Matter of the Heart

We are starting with some basic EKG concepts and arrhythmia emergencies. Dr. Martin Espinoza and Dr. Lorrell Brown deliver two highly-watched videos. 

EKG Basics

EKGs. Your Cardiology attending makes it look like it's something you should have mastered in pre-school, and when you ask your fellow to explain what a J-point is, it turns into an opportunity to "broaden your reading". In this lecture, Dr. Martin Espinosa discusses concepts in EKGs for the medical resident.  


In this lecture, Dr. Lorrel Brown distills the scary heart rhythms into easy to remember principles and helps ease the heart pains of house staff officers.


Click here to claim your CME credit after viewing the presentation.

Some items in this lecture may have come from the lecturer’s personal academic files or have been cited in-line or at the end of the lecture. For more information, see our citation page.

©2015 LouisvilleLectures.org

Marfan Syndrome

Marfan SyndromeVacation can be so blissful! But, sometimes, that “EM mind” just won’t turn off.  Have you, like a thirsty vampire, ever glanced at someone’s neck and admired the large external jugular veins?  Do you pack your extra supply of suture material along with your bathing suit, just in case?  When you drive by the vacation spot’s local hospital, do you wonder what their resources are?  Well, if these things seem normal to you, then you, like me, are… slightly disturbed… and totally wed to being an emergency provider. Recently, I while floating on the lazy river, I saw a child who had obvious Marfan Syndrome features and my mind quickly sorted through some of the emergent conditions I should prepare myself to consider … again, … just in case.  So let’s quickly review what my mind came up with for Marfan Syndrome.


Marfan Syndrome: Basics

  • Marfan Syndrome is a disorder of the connective tissue.
  • It is inherited in a AUTOSOMAL DOMINANT fashion.
    • Frequency is at least 1 in 5,000 in the USA.
    • ~ 1/4th of cases are due to spontaneous genetic mutation.
    • There is no gender or ethnic preference or distinction.
  • Effected protein = Fibrillin-1
    • Important to the structure of connective tissue.
    • Involved in connective tissue throughout the body.
    • Normal fibrillin thought to inhibit growth of long bones and elastic fibers.


Marfan Syndrome: Clinical Features

  • Variance in the expression of the condition exists.
    • Not all patients will be affected the same.
    • Features may be present at birth or develop later.
      • May be diagnosed in adulthood.
      • Patients diagnosed earlier appear to have better clinical courses than those diagnosed later in life. [Willis, 2009]
  • Some of the clinical features are: [Kaemmerer, 2005; Pediatrics, 1996; Marfan.org]
    • Skeletal
      • Pecuts excavatum or Pecuts carinatum
      • Arm span:Height ratio >1.05
      • Thumb sign
        • Able to extend thumb beyond ulnar border of the hand when hand is flexed.
      • Wrist sign
        • Able to overlap the distal tips of the thumb and index finger when wrapped around contralateral wrist.
      • Scoliosis >20 degrees
      • Reduced extension of the elbows (<170 degrees)
      • High arched palate with crowding of the teeth
    • Cardiovascular
      • Aortic aneurysm
        • ~50-83% of kids with Marfan syndrome have dilation of the aortic root. [van Karnebeek, 2001]
      • Mitral valve prolapse
        • Diagnosed at a mean age of 9.7 years. [van Karnebeek, 2001]
      • Dilation of the main pulmonary artery
      • Calcification of the mitral annulus in patients < 40 years of age
      • Neonatal Marfans Syndrome presents with rapidly progressive and potentially fatal cardiovascular complications.
    • Ocular
      • Severe nearsightedness
      • Early glaucoma / cataracts
      • Flat cornea
    • Pulmonary
      • Apical blebs
      • Asthma / reactive airway disease
    • Nervous
      • Lumbosacral dural ectasia
    • Gastrointestinal
      • May develop colonic diverticula at early age. [Santin, 2009]
    • Dermatologic
      • Stretch marks (striae)


Marfan Syndrome: The Emergencies

  • Aortic dissection
    • Obviously, this is the most feared and greatest concern!
    • Fibrillin-1 is primarily expressed in the ascending aorta.
    • Dissections typically in the second decade of life.
  • There are other conditions that may require emergent evaluation and treatment:
    • Pneumothorax
      • Occurs in ~5% of patients
    • Cor Pulmonale
      • May develop due to severe and progressive chest wall deformities and scoliosis leading to mechanical restrictions.
    • Dislocation of the lens of the eye
      • ~50-80% of cases have lens dislocation.
      • Often the ophthalmologist may be the first to make the diagnosis.
    • Retinal detachment
      • Occurs in ~16% of cases.

Moral of the Morsel

  • Marfan syndrome affects many organ systems (not just aorta and bones).
  • The patient with Marfan syndrome who is dyspneic may be sort of breath due to a variety of issues including reactive airway disease and mechanical issues, but don’t overlook pneumothorax!
  • When your on vacation… close your eyes… otherwise you may start quizzing yourself on medical facts related to passersby’s pathology. 🙂




Singh MN1, Lacro RV2. Recent Clinical Drug Trials Evidence in Marfan Syndrome and Clinical Implications. Can J Cardiol. 2016 Jan;32(1):66-77. PMID: 26724512. [PubMed] [Read by QxMD]

Ekhomu O1, Naheed ZJ. Aortic Involvement in Pediatric Marfan syndrome: A Review. Pediatr Cardiol. 2015 Jun;36(5):887-95. PMID: 25669767. [PubMed] [Read by QxMD]

Miraldi Utz V1, Coussa RG2, Traboulsi EI3. Surgical management of lens subluxation in Marfan syndrome. J AAPOS. 2014 Apr;18(2):140-6. PMID: 24698610. [PubMed] [Read by QxMD]

Hofmann LJ1, Hetz SP. Pediatric bilateral spontaneous pneumothoraces in monozygotic twins. Pediatr Surg Int. 2012 Jul;28(7):745-9. PMID: 22543473. [PubMed] [Read by QxMD]

Morales-Chávez MC1, Rodríguez-López MV. Dental treatment of Marfan syndrome. With regard to a case. Med Oral Patol Oral Cir Bucal. 2010 Nov 1;15(6):e859-62. PMID: 20711146. [PubMed] [Read by QxMD]

Willis L1, Roosevelt GE, Yetman AT. Comparison of clinical characteristics and frequency of adverse outcomes in patients with Marfan syndrome diagnosed in adulthood versus childhood. Pediatr Cardiol. 2009 Apr;30(3):289-92. PMID: 19184183. [PubMed] [Read by QxMD]

Santin BJ1, Prasad V, Caniano DA. Colonic diverticulitis in adolescents: an index case and associated syndromes. Pediatr Surg Int. 2009 Oct;25(10):901-5. PMID: 19711089. [PubMed] [Read by QxMD]

Kaemmerer H1, Oechslin E, Seidel H, Neuhann T, Neuhann IM, Mayer HM, Hess J. Marfan syndrome: what internists and pediatric or adult cardiologists need to know. Expert Rev Cardiovasc Ther. 2005 Sep;3(5):891-909. PMID: 16181034. [PubMed] [Read by QxMD]

van Karnebeek CD1, Naeff MS, Mulder BJ, Hennekam RC, Offringa M. Natural history of cardiovascular manifestations in Marfan syndrome. Arch Dis Child. 2001 Feb;84(2):129-37. PMID: 11159287. [PubMed] [Read by QxMD]

[No authors listed] Health supervision for children with Marfan syndrome. American Academy of Pediatrics Committee on Genetics. Pediatrics. 1996 Nov;98(5):978-82. PMID: 8909500. [PubMed] [Read by QxMD]

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