 The discussion on the so-called lactic acidosis and its causes have become increasingly attractive over the last couple of years as several biochemical explanations are challenged. A significant confusion persists on the various relationships between lactate, lactic acid and metabolic acidosis. Most clinicians continue to refer to the traditional understanding of impaired tissue oxygenation causing increased lactate production, impaired lactate clearance and therefore resultant metabolic acidosis. Just recently we had a discussion on our ward round on this topic when a team member presented the most recent article of UpToDate online on the causes of lactic acidosis. The authors state that 'Lactic acidosis is the most common cause of metabolic acidosis in hospitalised patients' and that 'Lactic acidosis occurs when lactate production exceeds lactate clearance. The increase in lactate production is usually caused by impaired tissue oxygenation...'... finally suggesting that lactate is no good! These statements support the classical understanding that: - Hyperlactatemia is caused by tissue hypoxemia, and - This in turn then leads to a metabolic acidosis called lactic acidosis This biochemical understanding has persisted for decades, but there are some good reasons to vigorously challenge this traditional aspect on the 'bad' lactate. Lactate turns out to be by far more complex in its characteristics and functions, so I decided to try and make a short but comprehensive overview of this molecule. What is lactate? Lactate is a small organic molecule with the chemical formula CH3CH(OH)CO2H and structurally looks like on the image to the left. It is produced in the cytoplasm of human cells mainly by anaerobic glycolysis by the conversion of pyruvate to lactate by LDH. This chemical reaction results typically in a blood lactate to pyruvate ratio of about 10:1. And while lactate is produced, NAD+ also is incurred, and this actually can accept protons itself, so does not result in acidosis itself. Lactate arises from the production of energy by consuming glycogen and glucose. 
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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:
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
For further information on acute exacerbations of IPF we recommend this Review Article:
| Acute Exacerbations in Patients with IPF,Kim Respiratory Research 2013, 14:86 |
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?
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?
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.
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.
In December 2014 the AHA, ACC and HRA have released a new bunch of guidelines on the management of patients with atrial fibrillation (AFib). The paper itself is worth reading as it looks into the basic understanding of this condition, its clinical evaluation and finally the treatment options.
As these guidelines are open access it can be considered mandatory Free Open Access Meducation FOAMed. Below is a summary of the Recommendations according to specific patient groups.
It's interesting to notice that digoxin still plays a role in patients with heart failure, especially when looking at the findings of Turakhia et al. in JACC, Aug 19 2014.
J Am Coll Cardiol. 2014;64(21):2246-2280 OPEN ACCESS
BIJC post on dixogin in critical care
As these guidelines are open access it can be considered mandatory Free Open Access Meducation FOAMed. Below is a summary of the Recommendations according to specific patient groups.
It's interesting to notice that digoxin still plays a role in patients with heart failure, especially when looking at the findings of Turakhia et al. in JACC, Aug 19 2014.
J Am Coll Cardiol. 2014;64(21):2246-2280 OPEN ACCESS
BIJC post on dixogin in critical care
Developed in the early 70'ies tramadol has become a very popular drug for pain relief for various reasons. Among others it is often said that tramadol is safe to use and has non-addictive properties, making this an ideal opioid to use for in and out of hospital. The facts though point in the opposite direction.
In JAMA Internal Medicine Fournier et al. have just published a case control analysis to look at the fact that tramadol before has been associated with the occurrence of significant hypoglycemia. Their cohort included a total of 334'034 patients whereas each case of hospitalization for hypoglycemia was matched with up to 10 controls on age, sex, and duration of follow-up. Basically they compared similar patients which were either started on tramadol or codeine for pain treatment. They were able to show that compared with codeine, tramadol use was associated with an increased risk of hospitalization for hypoglycemia, particularly in the first 30 days of use. It has to be noted though, that the overall incidence is low with 7 per 10'000 per annum.
In the same issue's commentary Nelson and Juurlink take the opportunity to point out some other remarkable problems associated with Tramadol, again showing us that things are not a simple as we think they are.
- Tramadol itself has only a low affinity to opioid receptors and mainly works over one of its metabolites: O-Desmethyltramadol (M1), which then binds to µ opioid receptors
- The expression of the enzyme that metabolites tramadol to M1 is extremely variable, thus: giving a certain dose of tramadol leaves you with an unknown dose of acting opioid!
- Despite suggestions to the contrary, tramadol does pose a risk for addiction
- And there are increasing reports of deaths involving this drug
- Other documented adverse effects are: serotonin syndrome and seizures
Conclusion: Tramadol remains a non-ideal drug in the setting of an ICU.
Fournier et al. JAMA Intern Med. 2015;175(2):186-193.
Nelson and Juurlink JAMA Intern Med. 2015;175(2):194-195.
In JAMA Internal Medicine Fournier et al. have just published a case control analysis to look at the fact that tramadol before has been associated with the occurrence of significant hypoglycemia. Their cohort included a total of 334'034 patients whereas each case of hospitalization for hypoglycemia was matched with up to 10 controls on age, sex, and duration of follow-up. Basically they compared similar patients which were either started on tramadol or codeine for pain treatment. They were able to show that compared with codeine, tramadol use was associated with an increased risk of hospitalization for hypoglycemia, particularly in the first 30 days of use. It has to be noted though, that the overall incidence is low with 7 per 10'000 per annum.
In the same issue's commentary Nelson and Juurlink take the opportunity to point out some other remarkable problems associated with Tramadol, again showing us that things are not a simple as we think they are.
- Tramadol itself has only a low affinity to opioid receptors and mainly works over one of its metabolites: O-Desmethyltramadol (M1), which then binds to µ opioid receptors
- The expression of the enzyme that metabolites tramadol to M1 is extremely variable, thus: giving a certain dose of tramadol leaves you with an unknown dose of acting opioid!
- Despite suggestions to the contrary, tramadol does pose a risk for addiction
- And there are increasing reports of deaths involving this drug
- Other documented adverse effects are: serotonin syndrome and seizures
Conclusion: Tramadol remains a non-ideal drug in the setting of an ICU.
Fournier et al. JAMA Intern Med. 2015;175(2):186-193.
Nelson and Juurlink JAMA Intern Med. 2015;175(2):194-195.
Microbiologically confirmed ventilator-associated pneumonia (VAP) or ventilator-associated conditions (VAC, e.g. worsening oxygenation) in intubated patients remains a major concern in ICU's. VAP is defined as a hospital-acquired pneumonia which develops within 48-72 hours after endotracheal intubation.
To prevent this complication ICU's uniformly have adapted the VAP-bundle, a bunch of measures aiming to prevent ventilator-associated pneumonia. Unfortunately the evidence of the VAP-bundle is not as robust as one might think it is. Here's the evidence of some elements of the VAP bundle:
- Elevation of the head to bed 45° (low evidence)
- Daily sedation interruptions (the impact on reducing VAP has not been shown so far)
- Daily oral chlorhexidine rinses (low evidence)
... it's most likely the combination of measures that is of benefit to the patient... hopefully! But hold on, there is another intervention that finally brings quite some evidence with it!
Active suctioning of the subglottic area, where nasal-oral secretions gather and create a rich culture medium for all sorts of micro-organisms, also aims to reduce the incidence of VAP. In contrast to the classical VAP-bundle the evidence here is strongly in favour for these devices!
In 2005 four registrars in cardiothoracic surgery looked into this topic and summarised their efforts online on Best Evidence Topics, best bets.org. In this blog they review 13 relevant articles on the use of subglottic suctioning and conclude: subglottic suction significantly reduces the incidence of VAP in high risk patients - which means a NNT of 8 if ventilated for more than 3 days. They also mention that this measure is cost effective, despite the more expensive tubes.
In the same year Dezfulian et al. presented a systematic meta-analysis of randomized trials in the American Journal of Medicine. They ended up with 5 studies including 869 patients. They also came to the conclusion that subglottic secretion drainage is effective in preventing VAP in patients expected to be ventilated for more than 72 hours.
In 2011 Hallais et al. looked into the issue of cost-effectiveness with a cost-benefit analysis. Even when assuming the most pessimistic scenario of VAP incidence and costs the replacement of conventional ventilation with continuous subglottic suctioning would still be cost-effective.
In 2011 Muscedere et al. published an 'official' review article in Critical Care Medicine and also ended up with 13 randomised clinical trial, most of them the same 'BestBETs' had already identified 6 years before. It is therefore not surprising to see that they also found a highly significant reduction in VAP. They were also able to demonstrate a reduction in ICU length of stay and duration of mechanical ventilation, although the strength of this association was weakened by heterogeneity of study results.
We finally would like to mention the latest randomised controlled trial on this topic which was published in Critical Care Medicine this January 2015. Damas et al. randomly assigned 352 patients to either receive subglottic suctioning or not. Again sublottic suctioning significantly reduced VAP prevalence and therefore also antibiotic use.
At least we have identified one area in critical care where an impressive pile of evidence supporting the use of subglottic suctioning in long-term intubated patients is present... and even better: cost-effective analyses also come out in great favour for this measure!
Take-home message: Subglottic suctioning does prevent VAP in patients likely to be ventilated more than (48-) 72 hours and should be used in these situations.
Review BestBETs 2005
Dezfulian C et al. Am J Med. 2005 Jan;118(1):11-8
Hallais C. et al. Infect Control Hosp Epidemiol. 2011 Feb;32(2):131-5
Muscedere J et al. Crit Care Med. 2011 Vol. 39, No. 8
Damas P et al. Crit Care Med. 2015 Jan;43(1):22-30
To prevent this complication ICU's uniformly have adapted the VAP-bundle, a bunch of measures aiming to prevent ventilator-associated pneumonia. Unfortunately the evidence of the VAP-bundle is not as robust as one might think it is. Here's the evidence of some elements of the VAP bundle:
- Elevation of the head to bed 45° (low evidence)
- Daily sedation interruptions (the impact on reducing VAP has not been shown so far)
- Daily oral chlorhexidine rinses (low evidence)
... it's most likely the combination of measures that is of benefit to the patient... hopefully! But hold on, there is another intervention that finally brings quite some evidence with it!
Active suctioning of the subglottic area, where nasal-oral secretions gather and create a rich culture medium for all sorts of micro-organisms, also aims to reduce the incidence of VAP. In contrast to the classical VAP-bundle the evidence here is strongly in favour for these devices!
In 2005 four registrars in cardiothoracic surgery looked into this topic and summarised their efforts online on Best Evidence Topics, best bets.org. In this blog they review 13 relevant articles on the use of subglottic suctioning and conclude: subglottic suction significantly reduces the incidence of VAP in high risk patients - which means a NNT of 8 if ventilated for more than 3 days. They also mention that this measure is cost effective, despite the more expensive tubes.
In the same year Dezfulian et al. presented a systematic meta-analysis of randomized trials in the American Journal of Medicine. They ended up with 5 studies including 869 patients. They also came to the conclusion that subglottic secretion drainage is effective in preventing VAP in patients expected to be ventilated for more than 72 hours.
In 2011 Hallais et al. looked into the issue of cost-effectiveness with a cost-benefit analysis. Even when assuming the most pessimistic scenario of VAP incidence and costs the replacement of conventional ventilation with continuous subglottic suctioning would still be cost-effective.
In 2011 Muscedere et al. published an 'official' review article in Critical Care Medicine and also ended up with 13 randomised clinical trial, most of them the same 'BestBETs' had already identified 6 years before. It is therefore not surprising to see that they also found a highly significant reduction in VAP. They were also able to demonstrate a reduction in ICU length of stay and duration of mechanical ventilation, although the strength of this association was weakened by heterogeneity of study results.
We finally would like to mention the latest randomised controlled trial on this topic which was published in Critical Care Medicine this January 2015. Damas et al. randomly assigned 352 patients to either receive subglottic suctioning or not. Again sublottic suctioning significantly reduced VAP prevalence and therefore also antibiotic use.
At least we have identified one area in critical care where an impressive pile of evidence supporting the use of subglottic suctioning in long-term intubated patients is present... and even better: cost-effective analyses also come out in great favour for this measure!
Take-home message: Subglottic suctioning does prevent VAP in patients likely to be ventilated more than (48-) 72 hours and should be used in these situations.
Review BestBETs 2005
Dezfulian C et al. Am J Med. 2005 Jan;118(1):11-8
Hallais C. et al. Infect Control Hosp Epidemiol. 2011 Feb;32(2):131-5
Muscedere J et al. Crit Care Med. 2011 Vol. 39, No. 8
Damas P et al. Crit Care Med. 2015 Jan;43(1):22-30
Again we have picked a review article looking at fluid resuscitation in the ICU. This article by Lira et al. in the Annals of Intensive Care looks at all the new literature available in regards of fluid therapy during resuscitation. Also review current recommendations and recent clinical evidence. This results in an excellent systematic review that leaves us with following conclusions:
- Currently no indications exist for the routine use of colloids over crystalloids
- In regards of current evidence (including the Albios trial), the cost and limited shelf time the use of albumin as a resuscitation fluid is not recommended
- The use of hydroxy-ethyl-starch (HES) during resuscitation should be avoided
- In light of the lack of evidence, and the theoretical potential for adverse effect, the suggestion is to avoid gelatine or dextran
- The use of 0.9% normal saline is associated with the development of hyperchloremic metabolic acidosis and increased risk of AKI in susceptible patients. Therefore balanced crystalloid solutions should be considered/ preferred
- Current literature supports the use of balanced crystalloid solutions (e.g. Hartmann's solution, Ringer's lactate) whenever possible
This makes things quite simple actually... but of course opinions differ!
Lira and Pinsky, Annals of Intensive Care Dec 2014, 4:38 OPEN ACCESS
Read here: The Albios trial
- Currently no indications exist for the routine use of colloids over crystalloids
- In regards of current evidence (including the Albios trial), the cost and limited shelf time the use of albumin as a resuscitation fluid is not recommended
- The use of hydroxy-ethyl-starch (HES) during resuscitation should be avoided
- In light of the lack of evidence, and the theoretical potential for adverse effect, the suggestion is to avoid gelatine or dextran
- The use of 0.9% normal saline is associated with the development of hyperchloremic metabolic acidosis and increased risk of AKI in susceptible patients. Therefore balanced crystalloid solutions should be considered/ preferred
- Current literature supports the use of balanced crystalloid solutions (e.g. Hartmann's solution, Ringer's lactate) whenever possible
This makes things quite simple actually... but of course opinions differ!
Lira and Pinsky, Annals of Intensive Care Dec 2014, 4:38 OPEN ACCESS
Read here: The Albios trial
'Anaesthesia', the Journal of the Association of Anaesthetists of Great Britain and Ireland have published an Open Access Supplement on various aspects of Transfusion, Thrombosis and Bleeding Management. This is an excellent opportunity to update your knowledge in this field and actually compulsory for anyone involved actively in critical care.
The supplement consists of multiple review articles which are kept nice and short and are perfect for reading in between...
In Conclusion: Reading highly recommended!
On following website you can find a list of all articles including links to the full text:
Anaesthesia, Vol. 70, Issue Supplement s1, January 2015: Transfusion, Thrombosis and Bleeding Management
The supplement consists of multiple review articles which are kept nice and short and are perfect for reading in between...
In Conclusion: Reading highly recommended!
On following website you can find a list of all articles including links to the full text:
Anaesthesia, Vol. 70, Issue Supplement s1, January 2015: Transfusion, Thrombosis and Bleeding Management
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