July 2017

Author: Andy Neill / Codes: / Published: 01/07/2017


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  • Dave McCreary, EM Trainee, Australia.
  • Andy Neill, EM Trainee, Ireland

Tweet: Are decision rules better than physician gestalt?

Codes: CC21, CC4, CC5

Clinical Question:

  • Do clinical decision tools add much beyond our clinical impression?

Title of Paper:


  • Annal of Emergency Medicine, 2017


  • Schriger


  • There are a lot of clinical decision tools to help us risk stratify patients for various reasons, anything from ankle x-rays to assessing risk of acute MI. Most seem to have some degree of accuracy but its difficult to know how they hold up against something as basic as asking an experienced clinician what do you think is the likelihood of this patient having condition X?

Study type

  • The authors looked through annals of EM for 20 years for any article looking at a clinical decision tool
  • They included studies that presented a comparison of the tool with unstructured clinical gestalt


  • 170 articles looking at aids for decision making, 41 of them looking at specific tools. 21 of the 171 had a comparison with physician judgments
  • In the ones that did compare with physician judgement
    • A third showed the physician judgment was better
    • 40% showed they were the similar
    • Only 10% did the clinical decision tool clearly outperform physician judgments

Bottom line

  • The title says it all and it’s more a call to included physician judgment in research than it is a call to abandon decision tools.

Further Reading

  • EM Lit of Note alerted me to this but I couldn’t find the review on the website…


  • Robert Lloyd, CT2, England
  • Andy Neill, EM Trainee, Ireland

Tweet: What’s the best way to improve your performance as an emergency physician

Codes: CC23

Robert Lloyd is currently a CT2 EM trainee in England. We talked about some of the learning points from the recent book Peak by Anders Ericsson and Robert Pool

The recently published RAGE podcast covers a lot of similar ideas without reference specifically to deliberate practice. It is 2 hrs 45 mins of 3 blokes talking about how they think about excellence, training, weakness and improving. Well worth a listen


  • Sam Thenabadu, EM Consultant, London
  • Andy Neill, EM Trainee, Ireland

Sam is a paeds and adult EM consultant working in London and this is part of an interview from the London CPD conference 2016


  • Rosa McNamara, EM Consultant
  • Andy Neill, EM Trainee, Ireland

Tweet: please stop saying collapse query cause

Codes: HAP13, CAP13, CAP32, HAP5

Rosa Mcnamara is an emergency physician trained in Ireland and the UK with a special interest in care of the older person in the ED.

Further reading/listening:


  • Craig Davison, EM Consultant, Edinburgh

Tweet: Who gives a schistocyte?

Codes: CAP19


Can be nonspecific and mimic sepsis. Important to have it in the back of your mind especially if there’s something else in the history which increases risk Hb/RBC abnormalities, heart valves, new drugs, tropical diseases.

Fatigue, tachycardia, pallor and shortness of breath suggest anaemia.

The association of new onset jaundice, dark coloured urine, fever, abdominal pain, back pain should raise alarm bells and implies more severe intravascular haemolysis.

Examination might reveal hepatosplenomegaly in extravascular haemolysis. Lymphadenopathy may suggest a lymphoproliferative cause. Petechiae or bruising may reflect underlying thrombocytopenia or microangiopathic haemolytic anaemia (MAHA).

This podcast focussed on how we could take forward and understand the investigations of suspected haemolytic anaemia in the ED.

Are they haemolysing?

Haemoglobin value at diagnosis was the most important predictor of outcome, correlating with risk of death and the requirement of multiple medical therapies[1]

Generally, RBC destruction rate is much higher in intravascular haemolysis. RBC destruction in extravascular haemolysis is 10-fold less.[2]

Bilirubin: The lab will sometimes withhold the result if they think the same has undergone in vitro haemolysis. You can call and chat to the lab to find out the underlying result and point of care gas machines will often still give you a reading.

85% of circulating bilirubin derives from Hb breakdown in the Reticuloendothelial system. Other sources include ineffective red cell production in the bone marrow. As such it is more of a marker of extra rather than intravascular haemolysis, although it goes up in both. Obviously unconjugated bilirubin is cleared by the liver, so levels can go up due to impaired hepatic clearance.

Reticulocytes: are non nucleated precursors of RBSs. They have a high MCV and usually represent about 1% of peripheral RBCs. Marker of marrow activity and usually increased in haemolysis, but also other physiological and pathological conditions.

The compensatory reticulocytosis may be inadequate or absent in the presence of concomitant marrow involvement, iron and vitamin deficiency, infections, or autoimmune reaction against bone marrow-precursors.

In Autoimmune Haemolytic Anaemia 39% of children[3] and 20% of adults[4],[5] don’t see a rise in reticulocytes. This is bad and represents a high transfusion need and poorer outcomes.

Haptoglobin is a glycoprotein, made in the liver. Scavenges for free serum circulating haemoglobin which is not good for kidneys. In haemolysis obviously free haemoglobin binds with haptoglobin and the whole complex is degraded so haptoglobin is used up. In theory a marker of intravascular haemolysis it also decreases in conditions associated with extravascular haemolysis conditions as in reality some RBS escape the liver or spleen and are destroyed in the circulation.[6]

We also see a decrease in haptoglobin with liver impairment and malnutrition. Levels go up with inflammatory disorders, in smokers and also in nephrotic syndrome.

Lactate Dehydrogenase is an enzyme that catalyzes the conversion of lactate into pyruvic acid, located in cytoplasm and distributed in various organs (e.g., heart, muscle, liver, and brain). LDH is raised where there is increased cellular turnover. 5 isoenzymes are present. In particular, LDH-1 and LDH-2 isoenzymes are expressed in RBC.

Slightly raised in extravascular but 4-5x upper limit of normal in intravascular haemolysis. In AIHA appears to correlate with clinical severity.

Quite non specific though as is present throughout the body. Any condition with cell necrosis and increased cell turnover could cause increased LDH: myocardial infarction, heart failure, hepatitis of all aetiologies, extreme muscular effort, and solid and hematologic tumors

Blood film:

Schistocytes are Fragmented RBCs caused by underlying microangiopathic haemolytic anaemia (MAHA).

Schistocytes derive from a mechanical fragmentation of RBC due to an obstacle within the vessels, such as fibrin clots, mechanical artificial heart valve, or any other intravascular devices. In healthy individuals, normal schistocyte count is below 0.5%.

MAHA is caused by a group of similar conditions for instance: DIC, TTP, HUS, HELLP

A count superior to 1% is typical of thrombotic thrombocytopenic purpura (TTP) with a common range of 310%, whereas a value between 0.5% and 1% is suggestive of disseminated intravascular coagulation (DIC).

When warm autoantibodies attach to red blood cell surface antigens, these IgG-coated red blood cells are partially ingested by the macrophages of the spleen, leaving microspherocytes, the characteristic cells of AIHA. These spherocytes, which have decreased deformability compared with normal red blood cells, are trapped in the splenic sinusoids and removed from circulation.

The direct antiglobulin test (DAT), also known as the direct Coombs’ test, demonstrates the presence of antibodies or complement on the surface of red blood cells and is the hallmark of autoimmune haemolysis. The patient’s red blood cells are mixed with rabbit or mouse antibodies against human IgG or C3. Agglutination of the patient’s antibody- or complement-coated red blood cells by anti-IgG or anti-C3 serum constitutes a positive test. Red blood cell agglutination with anti-IgG serum reflects warm AIHA, while a positive anti-C3 DAT occurs in cold AIHA.

Autoimmune Haemolysis

Subdivided into warm or cold agglutination. Can be chronic or acute and severe depending on the subtype.

Managed with Haematology and mainly revolves around immunosuppression and supportive care.

Although most cases of autoimmune haemolysis are idiopathic, other potential causes should always be sought. Lymphoproliferative disorders (e.g. chronic lymphocytic leukemia, non-Hodgkin’s lymphoma) may produce warm or cold auto-antibodies.

Prescribed drugs can induce production of both types of antibodies.

Warm AIHA also is associated with autoimmune diseases (e.g. SLE)

Cold AIHA may occur following infections, particularly infectious mononucleosis and Mycoplasma pneumoniae infection.

Human immunodeficiency virus infection can induce both warm and cold AIHA.


W. Barcellini and B. Fattizzo, Clinical Applications of Hemolytic Markers in the Differential Diagnosis and Management of Hemolytic Anemia, Disease Markers, vol. 2015, Article ID 635670, 7 pages, 2015. doi:10.1155/2015/635670 (Open Access)

Dhaliwal G, Cornett PA, Tierney LM., Jr Hemolytic anemia. Am Fam Physician. 2004;69:2599606. (Open Access)

UCSF Internal Medicine Chief Resident Blog
EM Docs

[1] W. Barcellini, B. Fattizzo, A. Zaninoni et al., Clinical hetero-geneity and predictors of outcome in primary autoimmune hemolytic anemia: a GIMEMA study of 308 patients, Blood, vol. 124, no. 19, pp. 29302936, 2014.

[2] L. D. Petz and G. Garratty, Immune Hemolytic Anemias, Churchill Livingstone, Philadelphia, Pa, USA, 2nd edition, 2004

[3] N. Aladjidi, G. Leverger, T. Leblanc et al., New insights into childhood autoimmune hemolytic anemia: a French national observational study of 265 children, Haematologica, vol. 96, no. 5, pp. 655663, 2011.

[4] W. Barcellini, B. Fattizzo, A. Zaninoni et al., Clinical heterogeneity and predictors of outcome in primary autoimmune hemolytic anemia: a GIMEMA study of 308 patients, Blood, vol. 124, no. 19, pp. 29302936, 2014.

[5] J. L. Liesveld, J. M. Rowe, and M. A. Lichtman, Variability of the erythropoietic response in autoimmune hemolytic anemia: analysis of 109 cases, Blood, vol. 69, no. 3, pp. 820826, 1987.

[6] G. F. Krmczi, M. D. Semann, C. Buchta et al., Influence of clinical factors on the haemolysis marker haptoglobin, European Journal of Clinical Investigation, vol. 36, no. 3, pp. 202209, 2006.


  • Becky Maxwell, EM Consultant, Bristol.
  • Chris Connolly, EM Consultant, Sheffield

Tweet: How should we use this oxygen thing again?

Codes: CAP6, HAP6,

This month we turn our eye on the recently published BTS oxygen guidelines from Dr Driscoll and colleagues. Its a 100 page epic. We’ve pulled out the bits that have interested us, and caused pause for thought.

As always there’s no substitute for reading and digesting the guidance yourselves but we hope this helps!

As with all things in Medicine we think it’s important to know your normals.

The guideline quotes a paper from 1999 by Crappo et al where they looked at healthy seated volunteers at sea level. 18-24 year old showed a mean pO2 of 13.4 compared with those >64 pO211.89 (9.02-14.76) (1)

Studies around sleep also piqued our interest and the guideline is great here too. A healthy cohort of sleepers have mean range of saturation from 84-96%, and the younger cohort spent 10% of the night with saturations of <94%. Fascinating stuff and certainly one to think about next time youre checking sats on someone whos sleeping it off.

So whats the difference between hypoxia and hypoxaemia?

Hypoxia is where the oxygen supply can’t meet the tissue compartment’s oxygen demand. This can be

  • Hypoxaemic Hypoxia: the oxygen content of the blood is low, examples could include being at altitude, a V/Q mismatch, a right to left shunt, alveolar hypoventilation and diffusion impairment. This has the potential to get better with delivery of oxygen.
  • Histo-toxic hypoxia: This is where the cells can’t use the oxygen that’s being delivered to the tissues. A good example of this would be in cyanide poisoning.
  • Anaemic hypoxia: aa genuinely low haemoglobin can reduce the oxygen carrying capacity and therefore the delivery of oxygen to the tissues.


  1. Crapo RO, Jensen RL, Hegewald M, et al. Arterial blood gas reference values for sea level and an altitude of 1,400 meters. Am J Respir Crit Care Med 1999;160 (Pt 1):152531.
  2. The Guideline


  • Dave McCreary, EM Trainee, Australia.
  • Andy Neill, EM Trainee, Ireland

Tweet: What tests do we need in SVT?

Codes: CC21, CAP25, HAP23

Clinical Question:

  • Do we over investigate paroxysmal SVT in the ED?

Title of paper:


  • Emergency Medicine Australasia 2017


  • Aadith Ashok


  • SVT is a common ED presentation
  • There is limited evidence based guidance as to the investigation of these patients in the ED.
  • As such many clinicians default to investigations normally expected in the work up of acute coronary syndrome.

Study type

  • Retrospective, observational study


  • Adult ED patients with discharge diagnosis of ‘Paroxysmal Supraventricular Tachycardia’
  • They excluded patients with any other arrhythmia

What they looked at:

  • Primary outcome was the nature of laboratory and radiological investigations undertaken in these patients
  • Secondary outcome was the proportion of investigations that were normal and the impact of the investigations on patient management


  • 633 patients
  • Investigations:
    • >80% had FBC and U&Es measured
    • Around half had calcium, magnesium and troponin measured
    • 18% had TFTs measured
    • had CxR
  • Investigation results:
    • >80% were normal
    • Only potassium and magnesium altered ED management (replacement for boarderline low levels)
    • CxR reported abnormal – none due to SVT, none had further management
  • Troponins:
    • More likely to be tested if patient reported associated symptoms
    • More likely to be adnormal if patient reported associated symptoms
  • 7 patients overall ultimately diagnosed with AMI
    • All had risk factors
    • 4 had known IHD
    • 3 had normal, 1 mildly elevated, and 3 moderately elevated troponin

Bottom Line

  • Paroxysmal SVT is over investigated
  • The vast majority are truly benign and dont require more than an ECG in the ED
  • The investigations aren’t changing management
  • Even the ones that do (potassium, magnesium) have little basis in evidence – they may be treating the clinician more than the patient
  • Role for troponin still not clear, but doesn’t look particularly helpful from this study.
  • Further investigation should perhaps be based on clinical judgement / suspicion rather than a shotgun approach with tests.

Further Reading:


  • Simon Laing, EM Consultant, Bristol

Tweet: Pearls on acute limb ischaemia

Codes: CAP20, HAP 19

Acute limb ischaemia is a presentation that is imperative to pick up. It carries a high morbidity and mortality but is responsive to treatment, especially if picked up early.

This month we run through the Refernece section on the website of Acute Limb Ischaemia, focussing on the presentation and Rutherford grading system.


  • Dave McCreary, EM Trainee, Australia.
  • Andy Neill, EM Trainee, Ireland

Tweet: Does thrombolysis of sub-massive PE improve long term morbidity outcome

Codes: CC21 HMP4

Clinical Question:

  • Does thrombolysis of sub-massive PE improve long term morbidity outcomes?

Title of Paper:


  • Journal of American College of Cardiology, 2017


  • Konstantinides


  • Teeny PEs probably only need anti-coagulation, massive, shocked ones probably benefit from lysis. What to do with the in between ones is unclear
  • The original PEITHO study tried to look at these people (a bit sick but not massive PEs) and did not find a clear benefit of lysis, this is long term follow up data at 2 years


  • PE with signs of RV dysfunction on echo/CT and signs of necrosis on troponins

What they did

  • The original trial randomised them to lytics or usual care
  • This trial looked at longer term outcomes like findings on a later echo or symptoms reported by the patient even development of the dreaded CTEPH.


  • No difference over about 3 years
  • Of note 20% were dead (it was 2-3% at 30 days in the original trial – this is really important for long term follow up.)

Bottom line

  • In addition to not saving lives in most sub massive PEs, lytics do not seem to improve long term outcomes.
  • Having said that the definition of submassive PE is effectively based on blood pressure which is a totally arbitrary and somewhat naive view of haemodynamics in PE including a vast spectrum of pathology.

Further reading

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