PROPPR transfusion, (PROMMTTly!)

Around a third of the mortality from trauma is due to exsanguination. Haemostatic resuscitation, together with permissive hypotension and damage control surgery, is key in severe trauma management and is now very much in focus.

Years of military observational studies (eg here, here, here and there) and expert opinion have suggested that whole blood provides superior resuscitation in the acidotic, hypothermic, coagulopathic trauma patient. In the prospective observational PROMMTT trial, higher ratios of plasma:cells were associated with less early death.

Last month JAMA published PROPPR, a pragmatic USA multisite (level 1 TCs) RCT, involved about 650 patients (with sensible exclusions) who were:

1. ‘highest level trauma activation

SBP <90 mmHg,

respiratory compromise,

already needing blood,

abdomen/neck/chest gunshot wounds,

GCS <8,

or otherwise considered severe!

2. taken directly directly from scene

3. received at least 1 unit of blood in the first hour

4. had an Assessment of Blood Consumption score of 2 or more:

1 point for:

penetrating injury,

positive FAST scan,

arrival SBP 90 mm Hg or less,

arrival HR > or = 120.

They were treated with either a 1:1:1 (plasma:platelet:RBC – theoretically equivalent to whole blood) or 1:1:2 transfusion strategy.

Mortality at 24hr and 30 days was not technicaPROPPR outcomelly different between the groups (except briefly at the 3 hour mark interestingly). Overall, the median RBC transfusion was less than 10 units in 24hr, one of the (useless?) definitions of massive transfusion.

Patients in the treatment arm received more platelets and plasma, achieved haemostasis quicker and died less of exsanguination. Cryoprecipitate was barely used at all in this study, and the juries out on how this product fits into haemostatic resuscitation.

 

 

One potential criticism is that the treatment arms received platelets immediately whereas the 1:1:2 group received 9 other units of product (3 plasma, 6 RBC) before any platelets. This may have been done to minimise survivor bias (re RBC ratio) but it’s hard to believe this is completely insignificant. Also worth noting that only two thirds got tranexamic acid (given according to elastograms LY-30 etc) but use was similar in each group.

PROPPR

  • If the study had been powered to detect a less than 10% difference the result might have been more decisive. Although, strictly speaking, this trial does not show statistical benefit of 1:1:1 over 1:1:2 the Kaplan Meier curve is impressive and with a p value of 0.12 I’m at least 88% sure I’d like to have been in the treatment arm. We can’t be sure 1:1:>2 isn’t safe or better but is seems unlikely and equipoise lack would prevent investigation.
  • Strikingly little crystalloid was used – consensus is mounting that blood should be replaced with blood products only.
  • If the trend to benefit of the ‘whole blood’ approach is real it probably, as you’d expect, occurs in the first few hours.
  • The definition of massive transfusion needs formalizing and time-frame reduced to eg 1-3 hours.
  • Could we be less prescriptive and decide dosing dynamically, and is thrombo-elastography ready for this role (because standard coag studies are not practical or useful)?

 


 

Some of the best comment:

Bottom Line review

RebelEM

EMNerd

EMCrit podcast and paper

St.Emlyn’s blog

EMLitofNote

Skeptics guide to EM

Steroids for pneumonia

Steroid treatment given for community acquired pneumonia (CAP) has been looked at a number of times in the last decade, often in subtly different groups of patients with varying regimens of drug and dose. Almost all have shown benefit (eg Lancet 2011) . The assumption is that they reduce lung inflammation (proven CRP and IL-6 reduction) without causing significantly detrimental immune suppression, bleeding, or hyperglycaemia.

2 more recent studies now broadly support this:

1. Torres et al performed an RCT in 3 Spanish hospitals over 8 years. 120 patients with ‘severe’ CAP (CRP > 150mg/l) were given intravenous bolus of 0.5 mg/kg per 12 hours of methylprednisolone or placebo for 5 days, started within 36 hours of hospital admission.Treatment failure was the primary outcome.

(Early treatment failure was development of shock, new need for mechanical ventilation , or death within 72 hours. Late treatment failure defined as worse CXR, persistence of severe respiratory failure, or any early treatment failure criteria between 72 hours and 120 hours.)

There was less treatment failure in the steroid group (13  v 31%). Looking more closely it was the late treatment failure that was more affected, particularly the occurrence of septic shock. No statistically significant difference in hyperglycaemia.

Only 120 patients in 8 years raises concerns about recruitment and consequently external validity. Also there was no mortality difference between the groups – although the study was never properly powered to detect this it seems strange the dramatic benefit in treatment failure didn’t translate to survival.

Could this result be entirely explained by the haemodynamic benefits of steroid in the septic patient? Difficult to comment much given such small numbers (8 v 18 patients had ‘treatment failure’. Beyond this, it at least appears that methylprednisolone doesn’t do harm in this group.

2. A bigger study by Blum et al (which was to be called the STEP trial) examined CAP all-comers at 7 hospitals in Switzerland. Nearly 800 got either prednisolone 50mg for a week, or placebo. Strikingly more than two thirds of those initially assessed were ineligible (dementia, steroids for other reasons, GI bleeds).

The primary outcome here was return to clinical stability – a normal set of observations for 24hr. Antibiotic therapy was fairly loosely protocolised.

With this approach the intervention group stabilised quicker (3 v 4.5 days). Half of these patients had severe pneumonia (PSI class 4 or 5) but  only around 5% were admitted to ICU again making it small numbers for us to extrapolate from. The treatment effect did appear stronger in those with sepsis.

Respiratory complications (intubation, empyema etc) were less common in the steroid group. However hyperglycaemia was again more prevalent in the steroid group though this association didn’t last beyond 30 days.


Steroids pneumonia

2 more encouraging studies that show a benefit of steroid in community acquired pneumonia. However, they used composite surrogate outcome measures – neither were powered for looking at mortality – and neither focused on the group that comes to the ICU. So for critical care per se there remains a hypothesis-generating signal that steroids might help. In addition a focused study would need to contend with the fact that many ICU cases get steroids for treating shock.

 

See also:

Rebel EM – prednisolone for CAP

ICMWK favourite 10ish studies from 2014

Prospective trials (no MA/SR/reviews). In random order:

1. High versus low positive end-expiratory pressure during general anaesthesia for open abdominal surgery (PROVHILO trial): a multicentre randomised controlledtrial.

Lancet. 2014 Aug 9;384(9942):495-503. doi: 10.1016/S0140-6736(14)60416-5.

PROVE Network Investigators for the Clinical Trial Network of the European Society of Anaesthesiology, Hemmes SN et al,

 

BACKGROUND: The role of positive end-expiratory pressure in mechanical ventilation during general anaesthesia for surgery remains uncertain. Levels of pressure higher than 0 cm H2O might protect against postoperative pulmonary complications but could also cause intraoperative circulatory depression and lung injury from overdistension. We tested the hypothesis that a high level of positive end-expiratory pressure with recruitment manoeuvres protects against postoperative pulmonary complications in patients at risk of complications who are receiving mechanical ventilation with low tidal volumes during general anaesthesia for open abdominal surgery.

INTERPRETATION: A strategy with a high level of positive end-expiratory pressure and recruitment manoeuvres during open abdominal surgery does not protect against postoperative pulmonary complications. An intraoperative protective ventilation strategy should include a low tidal volume and low positive end-expiratory pressure, without recruitment manoeuvres.

Applying slightly extreme settings to a large, random group. It would have been surprising if they found a positive difference. The whole point of a good ventilator strategy – or any medical treatment – is to have some guidelines, often set by big trials, and then individualise as you apply your clinical knowledge to each patient. Keeping a PEEP of 12 with circulatory effects in an otherwise healthy patient doesn’t make sense. Applying PEEP of 12 and recruitment maneuvers on indication in selected patients might well be a good strategy, even if applying these settings categorically to large, random groups of patients is a bad idea.

From Scancrit review


 

2. High-protein enteral nutrition enriched with immune-modulating nutrients vs standard high-protein enteral nutrition and nosocomial infections in the ICU: a randomized clinical trial.

JAMA. 2014 Aug 6;312(5):514-24. doi: 10.1001/jama.2014.7698

van Zanten AR et al. MetaPlus study.

IMPORTANCE: Enteral administration of immune-modulating nutrients (eg, glutamine, omega-3 fatty acids, selenium, and antioxidants) has been suggested to reduce infections and improve recovery from critical illness. However, controversy exists on the use of immune-modulating enteral nutrition, reflected by lack of consensus in guidelines. OBJECTIVE: To determine whether high-protein enteral nutrition enriched with immune-modulating nutrients (IMHP) reduces the incidence of infections compared with standard high-protein enteral nutrition (HP) in mechanically ventilated critically ill patients.

CONCLUSIONS AND RELEVANCE: Among adult patients breathing with the aid of mechanical ventilation in the ICU, IMHP compared with HP did not improve infectious complications or other clinical end points and may be harmful as suggested by increased adjusted mortality at 6 months. These findings do not support the use of IMHP nutrients in these patients

 

The MetaPlus trial results add to the possible harmful effects reported in at least 3 recent, large, multicenter trials on immunonutrition: the REDOXS, EDEN-OMEGA, and SIGNET trials, showing no benefit or possibly harmful effects. See also PulmCCM nutrition


 

3. High versus low blood-pressure target in patients with septic shock.

N Engl J Med. 2014 Apr 24;370(17):1583-93. doi: 10.1056/NEJMoa1312173.

Asfar P et al. SEPSISPAM Investigators.

BACKGROUND: The Surviving Sepsis Campaign recommends targeting a mean arterial pressure of at least 65 mm Hg during initial resuscitation of patients with septic shock. However, whether this blood-pressure target is more or less effective than a higher target is unknown.

CONCLUSIONS: Targeting a mean arterial pressure of 80 to 85 mm Hg, as compared with 65 to 70 mm Hg, in patients with septic shock undergoing resuscitation did not result in significant differences in mortality at either 28 or 90 days.

 

Due to a lower mortality than predicted the study was under-powered.

16.5% of patients in the high MAP group vs. 10.3% (P=0.01) in the low MAP group failed to achieve target BP because the attending clinician decided to limit the vasopressor infusion. Whilst this is an ethically important safety factor, this compliance bias will favour the null hypothesis.

For the majority of patients in septic shock a target MAP of 65-70 is a good starting point. However, in patients with chronic hypertension I will target a higher MAP. This is because, even though this did not improve mortality, it did reduce the need for renal replacement therapy with a NNT of 9.5.

From Wessex Bottom Line review


 

4. A randomized trial of protocol-based care for early septic shock.

N Engl J Med. 2014 May 1;370(18):1683-93. doi: 10.1056/NEJMoa1401602.

ProCESS Investigators. Yealy DM et al.

BACKGROUND: In a single-center study published more than a decade ago involving patients presenting to the emergency department with severe sepsis and septic shock, mortality was markedly lower among those who were treated according to a 6-hour protocol of early goal-directed therapy (EGDT), in which intravenous fluids, vasopressors, inotropes, and blood transfusions were adjusted to reach central hemodynamic targets, than among those receiving usual care. We conducted a trial to determine whether these findings were generalizable and whether all aspects of the protocol were necessary.

CONCLUSIONS: In a multicenter trial conducted in the tertiary care setting, protocol-based resuscitation of patients in whom septic shock was diagnosed in the emergency department did not improve outcomes.

 Mortality ~20% but initial power calculation based on 30–46%, therefore interim adjustment made and recruitment target reduced. Adherence to protocol was 88.1% in EGDT group and 95.6% in protocol-based standard therapy group. Although pragmatic, this is not perfect and may reduce between group differences.

So adults with sepsis in the ED have ~20% 60-day mortality and providing care by a dedicated team following either a strict or relaxed protocol makes no difference to this.

From The Bottom Line review


 

5. Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke.

N Engl J Med. 2014 Mar 20;370(12):1091-100. doi: 10.1056/NEJMoa1311367.

Jüttler E et al. DESTINY II Investigators.

BACKGROUND: Early decompressive hemicraniectomy reduces mortality without increasing the risk of very severe disability among patients 60 years of age or younger with complete or subtotal space-occupying middle-cerebral-artery infarction. Its benefit in older patients is uncertain.

CONCLUSIONS: Hemicraniectomy increased survival without severe disability among patients 61 years of age or older with a malignant middle-cerebral-artery infarction. The majority of survivors required assistance with most bodily needs.

Although a clear mortality benefit there remains a high level of disability in the majority of these survivors – more than 90% had a functional outcome of worse than moderate disability.

Review paper


6. Fibrinolysis for patients with intermediate-risk pulmonary embolism

N Engl J Med. 2014 Apr 10;370(15):1402-11. doi: 10.1056/NEJMoa1302097.

Meyer G et al. PEITHO Investigators.

BACKGROUND: The role of fibrinolytic therapy in patients with intermediate-risk pulmonary embolism is controversial.

CONCLUSIONS: In patients with intermediate-risk pulmonary embolism, fibrinolytic therapy prevented hemodynamic decompensation but increased the risk of major hemorrhage and stroke.

Composite outcome is problematic here. Surprisingly low incidence of haemodynamic support requirement. Not powered to determine mortality benefit. The inclusion criteria of up to 15 days for tenecteplase could outweigh benefits at this late stage

Tenecteplase for intermediate risk PE improved haemodynamics but resulted in 10 times the intracranial haemorrhage (2% vs. 0.2%) and 5 times the major haemorrhage (6.3% vs. 1.2%).

Also look at TOPCOAT, with great review by The Bottom Line.


 

7. Lower versus higher hemoglobin threshold for transfusion in septic shock.

N Engl J Med. 2014 Oct 9;371(15):1381-91. doi: 10.1056/NEJMoa1406617.

Holst LB et al. TRISS Trial Group; Scandinavian Critical Care Trials Group.

BACKGROUND: Blood transfusions are frequently given to patients with septic shock. However, the benefits and harms of different hemoglobin thresholds for transfusion have not been established.

CONCLUSIONS: Among patients with septic shock, mortality at 90 days and rates of ischemic events and use of life support were similar among those assigned to blood transfusion at a higher hemoglobin threshold and those assigned to blood transfusion at a lower threshold; the latter group received fewer transfusions.

Hb target of 7 equivalent to 9.

Protocol violations may have reduced power. 10% of patients in the low Hb threshold group got blood whilst above the threshold. Patients with bleeding or acute coronary syndromes excluded.

Now TRISS, ProCESS and ARISE agree on a target of 7.

Bottom line and PulmCCM reviews


 

8. Trial of the route of early nutritional support in critically ill adults.

N Engl J Med. 2014 Oct 30;371(18):1673-84. doi: 10.1056/NEJMoa1409860.

Harvey SE et al. CALORIES Trial Investigators.

BACKGROUND: Uncertainty exists about the most effective route for delivery of early nutritional support in critically ill adults. We hypothesized that delivery through the parenteral route is superior to that through the enteral route.

CONCLUSIONS: We found no significant difference in 30-day mortality associated with the route of delivery of early nutritional support in critically ill adults.

 Not blinded. Caloric targets were unmet in in both groups (<50%). Why not in the PN group?

“Early nutritional support through the parenteral route is neither more harmful nor more beneficial than through the enteral route. Enteral feeding does increase episodes of vomiting and hypoglycaemia but with no evidence of harm or nosocomial infection. “

Wessex Bottom line


 

9. Goal-directed resuscitation for patients with early septic shock.

N Engl J Med. 2014 Oct 16;371(16):1496-506. doi: 10.1056/NEJMoa1404380.

ARISE Investigators; ANZICS Clinical Trials Group, Peake SL et al.

BACKGROUND: Early goal-directed therapy (EGDT) has been endorsed in the guidelines of the Surviving Sepsis Campaign as a key strategy to decrease mortality among patients presenting to the emergency department with septic shock. However, its effectiveness is uncertain.

CONCLUSIONS: In critically ill patients presenting to the emergency department with early septic shock, EGDT did not reduce all-cause mortality at 90 days.

 

Less sick patients than ProCESS and Rivers. ‘Usual care’ is now quite different. Early identification, source control, antimicrobials and some fluid resuscitation seem to be what makes the real difference.

Wessex Bottom line review here


 

10. Early versus on-demand nasoenteric tube feeding in acute pancreatitis.

N Engl J Med. 2014 Nov 20;371(21):1983-93. doi: 10.1056/NEJMoa1404393.

Bakker OJ et al. Dutch Pancreatitis Study Group.

BACKGROUND: Early enteral feeding through a nasoenteric feeding tube is often used in patients with severe acute pancreatitis to prevent gut-derived infections, but evidence to support this strategy is limited. We conducted a multicentre, randomized trial comparing early nasoenteric tube feeding with an oral diet at 72 hours after presentation to the emergency department in patients with acute pancreatitis.

CONCLUSIONS: This trial did not show the superiority of early nasoenteric tube feeding, as compared with an oral diet after 72 hours, in reducing the rate of infection or death in patients with acute pancreatitis at high risk for complications.

 

This moderate-sized randomized trial won’t change the perceived standard of care, which remains early enteral nutrition in patients with severe acute pancreatitis. It also illustrates the overlap and gray area in differentiating “ordinary” acute pancreatitis (who are advised to get no nutrition) from “severe” (who are supposed to get early enteric tube feedings). PulmCCM

 


 

A sneaky extra, personal favourite.

11. Prevalence and impact of frailty on mortality in elderly ICU patients: a prospective, multicenter, observational study.

Intensive Care Med. 2014 May;40(5):674-82. doi: 10.1007/s00134-014-3253-4.

Le Maguet P et al.

PURPOSE: Frailty is a recent concept used for evaluating elderly individuals. Our study determined the prevalence of frailty in intensive care unit (ICU) patients and its impact on the rate of mortality.

CONCLUSIONS: Frailty is a frequent occurrence and is independently associated with increased ICU and 6-month mortalities. Notably, the CFS predicts outcomes more effectively than the commonly used ICU illness scores.

 Shrinking’, weak, slow, easily-tired, minimally active patients do worse than expected from disease severity scores. Not a surprise but this article usefully builds on previous definitions of frailty and emphasises that patients can look very similar on paper (severity scores etc) but frailty is always worth assessing.

European comprehensive acute echo guidelines

 A slightly adapted summary of the recommendations from:

Important!

The use of echocardiography in acute cardiovascular care: Recommendations of the European Association of Cardiovascular Imaging and the Acute Cardiovascular Care Association 2015.

The document is a great read for the accomplished echo practitioner, with good use of images and clips.

Indicative echo signs in acute conditions – tableEuroecho diagnosis table adapted


Consider this before interpreting findings:

Definition of ‘normal range’ in the critical care setting

(lack of accurate data, exclusion of many patients from studies/randomized controlled trials)

Your competency

Keep your scan focused if you’re doing a ‘focused assessment’

Qulaity of equipment
Respiratory issues

Mechanical circulatory support

Differential effects on right and left heart

O2 and CO2 levels

Extracorporeal respiratory support

Cardiovascular issues

Filling and inotropic status

Effects of sedation, metabolic status on myocardial function


Acute chest pain

Do echo:

  1. Echo during pain if suspected myocardial ischaemia (if non-diagnostic ECG and cardiac necrosis biomarkers).
  2. In underlying cardiac disease (valvular, pericardial or primary myocardial disease);
  3. If haemodynamic instability unresponsive to simple therapeutic measures;
  4. In suspected acute aortic syndromes, myocarditis, pericarditis or pulmonary embolism.

Don’t do:

  1. If non-cardiac aetiology is apparent;
  2. If confirmed diagnosis of myocardial ischaemia/infarction

Suspected pericardial disease

Do echo:

  1. In suspected effusion, constriction or effusive-constrictive process;
  2. If pericardial friction rubs develop in acute myocardial infarction accompanied by symptoms such as persistent pain, hypotension, and nausea;
  3. For suspected bleeding in the pericardial space (i.e. trauma, perforation);
  4. For guidance and follow-up of pericardiocentesis.

Acute dyspnoea

Do echo:

  1. For distinguishing cardiac vs. non-cardiac aetiology of dyspnoea;
  2. For assessment of LV size and function in suspected HF;
  3. For determining the cause of failure to wean from mechanical ventilation.

 


Emergency echocardiographic evaluation in patients with suspected cardiomyopathies

  • Calculate 2D LV ejection fraction and additional signs of LV systolic dysfunction (sphericity index, pulsed tissue Doppler derived s’ velocity of mitral annulus, indexed stroke volume).
  • Assess LV geometry and regional differences in wall thickness.
  • Estimate LV filling pressure (E–e′ ratio, AR – A duration difference, LA volume index, pulmonary arterial systolic pressure).
  • Assess reduction of GLS, even if normal ejection fraction.
  • Actively diagnose/exclude LVOT obstruction in patients with HCM/LV hypertrophy.
  • Take cardiorespiratory support into account.

Suspected/confirmed pulmonary embolism

Do echo:

  1. In shock or hypotension but CT is not immediately available;
  2. For cardiac vs. non-cardiac aetiology of dyspnoea when clinical and laboratory clues are ambiguous;
  3. For therapeutic options in patients with pulmonary embolism at intermediate risk.

Reasonable to do:

  1. To search for clots in the RA, RV or PAs;
  2. For risk-stratification.

Don’t:

  1. For elective diagnostic strategy in haemodynamically stable, normotensive patients with suspected pulmonary embolism.

Shock

Do echo:

  1. For differential diagnosis
  2. To choose and guide appropriate therapy, including surgical intervention when indicated.

Cardiac murmur

Do echo:

  1. If clinical heart failure, myocardial ischaemia/infarction, syncope, thromboembolism, infective endocarditis, or clinical evidence of structural heart disease;
  2. Where mitral regurgitation is suspected in a patient on positive pressure ventilation, stress echocardiography (volume and/or pressure loading) may be indicated;
  3. In patients with critical aortic stenosis and cardiogenic shock, to assess suitability for BAV;
  4. In severe mitral stenosis and cardiogenic shock or pulmonary oedema  
  5. In patients requiring extracorporeal mechanical circulatory support.

Acute traumatic aortic injuries

Do echo:

  1. In suspected acute traumatic aortic injury; TOE is first-line (with CT).
  2. Intraoperatively to guide surgical and anaesthesic decisions.

Don’t:

  1. If cervical spine fractures – relative contraindication.

Suspected acute traumatic cardiac injuries

Do echo:

  1. Focused assessment immediately in isolated chest trauma, hypotension and tachycardia to exclude pericardial tamponade or tension PTX.
  2. To diagnose and guide filling in isolated chest trauma, no cardiac tamponade or PTX but having persistent tachycardia or hypotension, signs of HF, abnormal auscultatory findings, abnormal ECG tracings or recurrent arrhythmias.
  3. TOE is superior to TTE.

Don’t:

  1. In patients with minor chest injuries and no tachycardia, hypotension, respiratory difficulty, chest pain or other concerning symptoms.
“Echocardiography has become the primary imaging tool for bedside diagnosis and monitoring of patients in acute cardiovascular condi-
tions. It is non-invasive, rapid and accurate assessment of cardiac morphology and haemodynamics under stressful situations is very useful in assisting therapeutic procedures. The fact that echocardiography can be repeated when required makes it highly useful in emergency/critical care circumstances”

ECCO2R for NIV failure – ready for a proper look

ECCO2R NIVWe rightly like to avoid intubation in COPD exacerbations. Extracorporeal CO2 removal or ‘pulmonary dialysis’  has been around for a while and many feel it is beneficial in COPD (eg this case) but who is it best used for?

In an Italian matched cohort study Del Sorbo and colleagues looked at 200 patients with an exacerbation of COPD treated with NIV (up to 90yrs old!).

 

 

 

They focused specifically on the subset of 89 patients at risk of NIV failure, defined as:

  • 2 hours of continuous NIV
  • arterial pH less < 7.30
  • Paco2 greater than 20% of baseline
  • respiratory rate >30 or use of accessory muscles or paradoxical abdominal/chest movement.

However only 25 of the 89 ‘at risk’ patients intended for ECCO2R actually ended up with it, largely due to refusal of consent. In these 25 femoral vein (14F double lumen) pumped VV ECCO2R (?a converted haemofilter!) was popped in and heparinization commenced. (ECCO2R v ECMO  diagram for the uninitiated)

If after 2 hours they had a pH <7.25, rising oxygen requirement, were haemodynamically unstable or comatose they would be intubated.

The NIV-only control group was taken from 2 previous studies and propensity matched for ‘at risk’ criteria as well as other sensible parameters (APACHE, prior respiratory function, age etc). 21 matched patients were found.

 Primary outcome measure was intubation by 28 days.

Results:

3 of the ECCO2R ‘v’ 7 of the standard NIV group were intubated, ie RRR of over 70% and an ARR of 21%. Of course this was not statistically significant.

The ECCO2R group had better pH, CO2, oxygenation and respiratory rate.

But half the patients had adverse events. These were mainly circuit issues but haemorrhage was a problem in 4 of the 25.

There was a striking trend towards mortality 8% for ECCO2R,  ‘v’ 35% for NIV alone. Fewer ICU days too.

So, potentially useful in 1 in 8 COPD exacerbations requiring NIV, ECCO2R is not without risk but may avoid intubation or even be life saving. This now needs a closer look. Equipoise was clearly an issue in this study, and now surely shouldn’t be? Parallel effort to improve prediction of NIV failure is probably also warranted. 

 

ICU echo myths! Mayo et al both enthuse and warn.

Echo myths MayoMayo et al outline the misinformation regarding echocardiography use in the ICU. Some additional comments have been added!

1. Every echo exam should be comprehensive – False

Focused assessments are valuable. We are gathering evidence about powerful but easily achieved echo findings.

But stick to the protocol you’re competent with.

2. Echo is not a monitoring tool – False

Intermittent serial quantitative or qualitative measurements are often adequate for assessing trends and guiding therapy.

Serial assessment can be powerful, but this does come at the cost of being relatively labour intensive.

3. Intensivists do not need cardiologists – False

The echo skill sets of ICU doctors and cardiologists is diverging and an experienced echo-intensivist may be more familiar with assessing heart-lung interaction but the cardiologist will always be vital for many diagnoses and cardiac disease management plans.

Ability to acquire images does not imply ability to interpret images.

4. Echo is less reliable than other haemodynamic tools – FALSE

Every monitoring device has its limitations but there are occasions when echo  may be the more accurate (eg in the very unstable patient, active haemorrhage or anatomical abnormalities).

In addition no other modality gives rapid qualitative assessment of the heart.

5. In refractory or complicated shock, echo should be replaced by an alternative device – FALSE

Echo is an excellent diagnostic device in complex instability. Shock aetiology, fluid responsiveness, LV and RV systolic and diastolic function, preload/afterload, RV-ventilator interaction can all be addressed.

The roles of traditional monitoring and echo overlap. Often information really is power.

6. Training in transoesophageal echo is an optional part of advanced echo training – FALSE

This statement may depend on your definition of ‘advanced’ but some questions are very difficult to answer with TTE. Great vessels, some valves and intracardiac shunt (or even PAC placement) for example are better assessed with TOE.

As an advanced practitioner sometimes you’ll be frustrated you don’t have a TOE probe.

7. It’s easy to achieve competence in echo – FALSE

Adequate training is vital. In training you’ll learn as many limitations as applications. Some will be competent to accurately answer simple questions after 50 scans. There must be structured training and a means to maintain competency.

Echo images must be interpreted as meticulously as possible, potential confounders must be appreciated, and the findings put in clinical context.

8. There is a strong evidence base that supports echo – FALSE
9. Echo is academically supported worldwide – FALSE

Echo has been taken up worldwide due to its ‘intuitive obvious utility’ but an outcome benefit is yet to be demonstrated. There is a relatively small group of experienced enthusiasts who publish the bulk of the work in this area. The rise of echo despite this may also prove problematic when looking for equipoise in designing a study.

Do we even know the normal echo dataset for a ventilated patient or the expected effects of inotropes on echo values? We need to gather observational data to begin to generate hypotheses. Get studying!

10. There is no risk of medico-legal issues – FALSE

Train, stay competent and know your limits when interpreting findings.

Documentation about your focused assessment should emphasise that it was asking a specific question so that it is not later assumed that the exam was comprehensive. The patient has had a focused cardiac examination and not a formal echo.

 The multiple qualifications/accreditations are converging quickly and national standards are beginning to appear. It’s not acceptable to ‘dabble’ in echo!

E-CPR for all – just a dream, or the future?

CHEER ecmo tableA new meta-analysis of ECMO in cardiogenic shock and arrest showed an impressive 30-day survival rate of over 30% but at the cost of significant levels of complications (neurological/infective/renal).

A couple of months ago CHEER trial team published their results with a protocol that reads like science-fiction for many of us:

A senior team leader, 2 crit care doctors ready with femoral cannulae, another manning the IVC ultrasound, an ECMO nurse to run the mechanical CPR device and initiate the V-A ECMO circuit, and someone else to start the iced-saline.

Autopulse mechanical chest-compressor and cold infusion en-route to hospital. On arrival compressions are briefly paused while femoral cannulae go in (guidewire visualized in the IVC). Chest X-ray, heparinization then ECMO initiation. Coronary occlusion or pulmonary embolism is then addressed by PCI or thrombectomy. Cool for 24 hours and wean the ECMO using echo.

In-hospital as well as out of hospital arrests were included in this Melbourne single hospital prospective observational study. 24 of the intended 26 patients actually got ECMO. The arrests were largely VF and the aetiology was mainly ischemic but cardiomyopathies/channelopathies, PE and respiratory causes also featured. Fairly standard mix!

14 of the 26 got out of hospital. Unsurprisingly more in-hospital than out-of-hospital arrests survived (9/15 v 5/11). None survived asystole despite E-CPR. From arrest to starting ECMO  40 mins (median) passed in survivors and 78 mins in non-survivors (seems to take 15-30 mins from arrival of team to ECMO initiaition).

A highly-staffed process gives good ROSC and survival rates. Refine it by restricting to non-asystole and those who can get cannulated asap.

Given this protocol will never be achievable in smaller hospitals, is it more evidence for centralizing arrest management, or does it really emphasize that the priorities are:

  • shortening the time from arrest to arrest team
  • prompt definitive management thereafter.

 

 

Feed, or wait and eat, in pancreatitis

pancreas nutition pythonAnother addition to this year’s flurry of nutrition work.

Tradition has us bypassing the stomach and duodenum for nutrition in pancreatitis – intuitively sensible. To challenge this the Dutch PYTHON trial group has recently published its findings.

Multicentredly, they randomized 200-ish patients with acute ‘high-risk’ pancreatitis (defined as mGlasgow of >/= 3, CRP >150, APACHE >/=8) to start naso-jejunal feeding (25Kcal/Kg/dy if on ICU) within 24 hours or to wait up to 3 days and then encourage (the ‘on-demand’ group). Powered to detect 5% difference in major infection (pancreas or other) OR death within 6 months. The protocol was pretty well-adhered-to.

There was no difference in primary outcome (~30%), major infection rate (~25%), death rate (~10%), necrosis (~60%), mechanical ventilation (~12%). 5-10% got parenteral nutrition. 

 

  • Importantly only a fifth needed ICU care. So of those predicted to get severe pancreatitis presumably many didn’t.
  • Target calorie delivery was rarely achieved until day 3 or 4 in the early fed group and 6 or 7 in the other.
  • Interestingly, more than 2 thirds of of the ‘on-demand’ group didn’t need tube feeding.

 

So early NJ feeding doesn’t appear superior to delaying addressing nutrition until day 4 and starting oral intake.

How useful is this result? Accurately predicting severe pancreatitis is clearly problematic and for studies like this mean that the sample ends up being very heterogeneous. Regarding study design, mixing timing and route may have limited the applicability of these results, and many are inherently suspicious of composite outcome measures. 

We need a way to better predict severe pancreatitis. And then perhaps a 2×2 look at timing and route?

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