Hemoglobin is NOT Different from Hematocrit… Once and for All!

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It starts in medical school, regularly appears in your medical training, sneaks around nursing schools and is an impetus for discussions in the ICU: The great myths about Hemoglobin (Hb) and Hematocrit (Hct).

These two haematological lab-parameters are part of our daily life at work and are mostly measured together… as a package. Some clinicians look at haemoglobin levels, others prefer hematocrits levels… but then there is always someone making a great deal of differentiating between the two parameters and making all sort of diagnostic conclusions. ‘Hct is better to determine dilution of the patient’ or ‘Acute blood loss is better determined by Hb than Hct’… and so on.

So here’s the question: What actually is the difference between Hb and Hct? Do we need to measure both in clinical practice?
What’s the difference?

Hemoglobin levels are mostly measured by automated machines designed to perform different tests in blood. Within the machine, the red blood cells are broken down to get the haemoglobin into a solution. The concentration of haemoglobin is then measured by spectrophotometry using the methemoglobin cyanide method.

Hematocrit levels in contrast are actually calculated by an automated analyzer… It is actually not measured directly! The analyser multiplies the red blood cell count by their mean corpuscular volume.
What is Fact?

There is NO difference between Hemoglobin and Hematocrits by means of clinical information!
In fact, virtually all haemoglobin in our blood is contained within erythrocytes
Therefore, whether the amount of Hb per litre of blood is determined or the blood’s volume occupied by the Hb filled erythrocytes is determined, similar information is gained.
Nijboer at al. have brilliantly proven that Hb and Hct correlate in all ranges and all patients and also nicely show this in their figure 1 (see below)
The only rare exceptions are macrocytic and polycystic anaemia in which the Hct is defined by erythrocytes containing a normal mean corpuscular Hb concentration

Conclusion
Hemoglobin is NOT different from Hematocrit

Both parameters provided identical clinical information
Once and for all!
Both parameters provided identical clinical information
Once and for all!

JTrauma

New Guidelines on the Treatment of Idiopathic Pulmonary Fibrosis – Get Updated!

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Idiopathic pulmonary fibrosis is one of these frustrating diseases you repeatedly encounter in the ICU and that mostly leaves you sort of frustrated at the end. Despite all the efforts in research we are still left with very little we can do. This is one reason why also intensivists need to keep themselves updated on this topic.

As knowledge is growing the ATS, ERS, JRS and ALAT (… thoracic and respiratory societies) made the effort to look into the latest evidence by performing systematic reviews and where appropriate meta-analyses. The aim was to update the guidelines published in 2011. These guidelines are also dedicated to Mr. William Cunningham who actively participated in the development of these guidelines, suffered from idiopathic pulmonary fibrosis for many years and who was directly confronted with the issues related with this condition.

The main conclusions can be briefly summarised as follows:

An Official ATS/ERS/JRS/ALAT Clinical Practice Guideline: Treatment of Idiopathic Pulmonary Fibrosis. An Update of the 2011 Clinical Practice Guideline, American Journal of Respiratory and Critical Care Medicine, Vol. 192, No. 2 (2015), pp. e3-e19.

OPEN ACCESS: Executive Summary 2015

An Official ATS/ERS/JRS/ALAT Statement: Idiopathic Pulmonary Fibrosis: Evidence-based Guidelines for Diagnosis and Management, Am J Respir Crit Care Med Vol 183. pp 788–824, 2011 OPEN ACCESS

Don’t Throw Away your Cooling Devices!

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When performing a kidney transplantation nowadays up to 50% of recipients developed a delayed graft function which is defined as the need of dialysis within seven days. The authors of this recently published NEJM-article asked themselves whether mild hypothermia might influence outcome in this regard.

In order to answer this question the investigators assigned organ donors after declaration of death according to neurologic criteria into two groups. They were either treated with mild hypothermia (34 to 35°C) or with normothermia (36.5 to 37.5°C). The target temperature was maintained until the patients were transferred to theatre for transplantation.

Primary outcome of this trial was delayed graft function among recipients. Secondary outcomes included the rates of individual organs transplanted into each treatment group at the total number of organs transplanted from each donor.

This trial had to be stopped early as an interim analysis showed significant efficacy of mild hypothermia. Up to this point a total of 572 patients received a kidney transplant (285 in the hypothermia group and 287 in the normothermia group). 28% of recipients in the hypothemia group developed delayed graft function compared to 39% in the normothermia group.

The authors therefore conclude that mild hypothermia significantly reduces the rate of delayed graft functions among recipients.

This study suggests that potential organ donors after declaration of death according to neurologic criteria should be treated with mild hypothermia.

Intensive care units that continue to treat patients with mild hypothermia after cardiac arrest might have two rewarm their patients for the diagnosis of neurological death before re-cooling them for organ transplantation

Anyhow, it seems reasonable not to get rid of your cooling devices!

Read more about the controversies of hypothermia in the ICU:
The Targeted Temperature Management Trial: Nielsen N, et al. New Engl J Med. 2013 Dec;369(23):2197-206

The 2 trials that introduced therapeutic hypothermia into ICU practice:
The Hypothermia After Cardiac Arrest Study Group, Holzer at al. New Engl J Med. 2002 Feb;346(8):549-556

Bernard S.A. et al. New Engl J Med. 2002 Feb;346(8):557-563

Review article on therapeutic hypothermia for non-VF/VT cardiac arrest:
Sandroni S. et al. Crit Care Med; 2013;17:215

Pyrexia and neurological outcome:
Leary M. et al. Resuscitation. 2013 Aug;84(8):1056-61

BIJC post on: The Effect of Pre-Hospital Cooling: Rather Worrying Results

New British Guidelines for Haematological Management of Major Haemorrhage

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Beverley Hunt at al. have just published an excellent practical guideline for the haematological management of major haemorrhage which also serves a a great educational review on this topic… an excellent piece of work!

The authors look at this topic point for point and review current literature in an easy to understand sort of manor. They define major blood loss when it leads to a heart rte of >110/Min or a systolic blood pressure of less than 90mmHg, or simply said: when bleeding becomes haemodynamic relevant. In general it is recommended to have a major haemorrhage protocol at hand (1D) and all staff should be trained to recognise major blood loss early (1D).

Here’s a summary of the recommendations made by the British Committee for Standards in Haematology (BCSH):

In Major Haemorrhage….

Red Blood Cells RBC
– Hospitals must be prepared to provide emergency Group 0 red cells and group specific red cells (1C)
– Patients must have correctly labelled samples taken before administration of emergency Group 0 blood (1C)
– There is NO indication to request ‘fresh’ or ‘young’ red cells (under 7d of storage, 2B)
– Note: The optimum target haemoglobin concentration (Hb) in this clinical setting in general is NOT established. Current literature shows a tendency towards restriction towards 70-90g/L, but the BCSH makes no recommendations therefore (see blow)

Cell Salvage (e.g. cell saver)
– 24h access to cell salvage should be available in cardiac, obstetric, trauma and vascular centres (2b)

Haemostatic Monitoring
– Use haemostatic tests regularly during haemorrhage, every 30-60min, depending on severity of blood loss (1C)
– Measure platelet count, PT, aPTT (1C)
– Note: The BCSG does not recommend TEG and ROTEM at this stage

Fresh Frozen Plasma FFP
– Use FFP in a 1:2 ratio with RBC initially (2C)
– Once bleeding is under control administer FFP when PT and/or aPTT is >1.5 times normal (recommended dose 15-20ml/kg, 2C)
– The use of FFP should not delay fibrinogen supplementation if necessary (2C)

Fibrinogen
– Supplement fibrinogen when levels fall below 1.5g/L

Prothrombin Complex Concentrates PCC
– Do not use PCC

Platelets
– Keep the platelet count >50 x 10^9/L (1B)
– If bleeding persists give platelets if count falls below 100 x 10^9/L (2C)

Tranexamic Acid TA
– Give tranexamic acid as soon as possible to patients with, or at risk of major haemorrhage (Recommended dose: 1g IV over 10min, followed by 1g IV over 8h, 1A)
– Note: TA has no known adverse effects
– Note: Aprotinin is not recommended

Recombinant Activated Factor VIIa (Novo Seven)
– Do not use

Specific Clinical Situations

Obstetrics
– Fibrinogen levels increase during pregnancy to 4-6g/L
– In major obstetric haemorrhage fibrinogen should be given when levels are <2.0g/L (1B)

GI-Bleed
– Use restrictive strategy for RBC transfusion is recommended in most patients (1A)

Trauma
– Transfuse adult trauma patients empirically with a 1:1 ratio of FFP : RBC (1B)
– Consider early use of platelets (1B)
– Give tranexamic acid as soon as possible (Dose 1g over 10min and then 1g over 8h, 1A)

Prevention of Bleeding in High-Risk Surgery
– Use tranexamic acid (Dose 1g over 10min and then 1g over 8h, 1B)
Hunt B et al. British J Haemat, July 6 2015

Read more HERE:

Great Review on Transfusion, Thrombosis and Bleeding Management

Restricitve Transfusion Threshold in Sepsis, the TRISS Trial

Transfusion: Harmful for Patients Undergoing PCI?

Oxygen in Acute Myocardial Infarction: Challenging the Next Medical Automatism

Nebulizer

A number of things we do for patients in the ICU we simply do… because it has been always done. Maybe because it seems to make sense or because we were simply taught to do so. One of these treatments is the application of oxygen to patients suffering of myocardial infarction. But in fact the impact of this measure is not that well established and we know that high concentrations of oxygen can actually be harmful. Some previous studies suggest possible increase in myocardial injury.

Stub et al. therefore performed a multicenter, prospective, randomised controlled trial comparing oxygen (8 L/min) with no supplemental oxygen in patients with STEMI diagnosed on paramedic 12-lead electrocardiogram. They finally included 441 patients into their study.

Their primary endpoint was evaluation of infarction size assessed by the cardiac enzymes troponin (cTnI) and creatine kinase (CK). While troponin levels did not differ there was a significant difference in the mean peak CK levels, being higher in the group with oxygen applied. By looking at the secondary endpoints they also found an increase in the rate of recurrent myocardial infarctions and in the frequency of cardiac arrhythmia among the oxygen group. Finally at 6-months the oxygen group had an increase in myocardial infarct size on cardiac MRI.

They conclude that patients with myocardial infarction but without hypoxemia may actually not benefit of supplemental oxygen therapy.

Time to question our automatisms when treating patients.
Stub et al. Circulation. 2015 Jun 16;131(24):2143-50.

Not Everyone Qualifies as a Donor for Fecal Microbiota Transplantation

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In 2013 a small open label, randomised, controlled trial in the NEJM hit the headlines: Nood et al. were able to show that the enteral infusion of donor feces is a potential therapeutic strategy against recurrent C. difficile infections. This was important news as the efficacy of antibiotic therapy decreases with subsequent recurrences. The study suggested that the enteral infusion of donor feces, as compared with vancomycin therapy, results in much better treatment outcomes.

But as we all know, every treatment has its side effects. Nood et al. described diarrhoea, cramping and belching as observed adverse events, but all of this resolved quite quickly…

Alang et al. have now published a brief report of a woman with recurrent C. difficile infections despite treatments with Metronidazol and Vancomycin. Despite all efforts diarrhoea re-occured again and she finally underwent fecal microbiota transplantation. After the application of donor stool form her daughter through the colonoscope her symptoms resolved and no further C. difficile infection occurred.

16 months later the patient presented again with an unintentional weight gain of about 15kg. The authors mention that several factor might have contributed to her weight gain (e.g. concurrent treatment of existing H. pylori). In regards of the fact that the patient had never been obese before and the donor also experienced a significant weight gain raises the possibility that the fecal transplantation might have at least partially caused her obesity. And important to know: Animal models have shown, that an obese microbiota can be transmitted.

Looks like Newport Hospital in Rhode Island took the appropriate action: their policy now is to use non-obese donors only.
Along et al. Open Forum Infectious Diseases, Nov 2014 OPEN ACCESS

Nood et al. N Engl J Med 2013;368:407-15. OPEN ACCESS

New Guidelines: Diagnosis and Treatment of Biofilm Infections

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The European Society for Clinical Microbiology and Infectious Diseases has now released new guidelines on the diagnosis and treatment of biofilm infections. Written for clinical microbiologists and infectious disease specialists this paper is a MUST READ for anyone involved in treating critically ill patients.

These guidelines outline the nature and properties of biofilms and and their implications on mostly chronic infections caused. As biofilms are very common in critically ill patients it is important to know what specific problems you might encounter, how to proceed and perform a proper diagnosis and what are the essential bits and pieces in the prevention and treatment of biofilm infections.
The article is OPEN ACCESS: Clin Microbiol Infect. 2015 Jan 14. pii: S1198-743X(14)00090-1.