Category Archives: Resus

Life-saving medicine

All Updates, Resus, Trauma, Ultrasound

E-FAST for pneumothorax

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Some further evidence of the superiority of ultrasound over chest x-ray for the detection of pneumothorax (although it’s not perfect):

INTRODUCTION: Early identification of pneumothorax is crucial to reduce the mortality in critically injured patients. The objective of our study is to investigate the utility of surgeon performed extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax.
METHODS: We prospectively analysed 204 trauma patients in our level I trauma center over a period of 12 (06/2007-05/2008) months in whom EFAST was performed. The patients’ demographics, type of injury, clinical examination findings (decreased air entry), CXR, EFAST and CT scan findings were entered into the data base. Sensitivity, specificity, positive (PPV) and negative predictive values (NPV) were calculated.
RESULTS: Of 204 patients (mean age–43.01+/-19.5 years, sex–male 152, female 52) 21 (10.3%) patients had pneumothorax. Of 21 patients who had pneumothorax 12 were due to blunt trauma and 9 were due to penetrating trauma. The diagnosis of pneumothorax in 204 patients demonstrated the following: clinical examination was positive in 17 patients (true positive in 13/21, 62%; 4 were false positive and 8 were false negative), CXR was positive in 16 (true positive in 15/19, 79%; 1 false positive, 4 missed and 2 CXR not performed before chest tube) patients and EFAST was positive in 21 patients (20 were true positive [95.2%], 1 false positive and 1 false negative). In diagnosing pneumothorax EFAST has significantly higher sensitivity compared to the CXR (P=0.02).
CONCLUSIONS: Surgeon performed trauma room extended FAST is simple and has higher sensitivity compared to the chest X-ray and clinical examination in detecting pneumothorax.

Extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax: experience at a community based level I trauma center
Injury. 2011 May;42(5):511-4

Acute Med, All Updates, ICU, Resus

Verapamil vs adenosine for SVT

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Most people reach for the adenosine once vagotonic manouevres have failed in SVT, but some patients find the side effects – albeit short-lived – pretty unpleasant. For this reason I’ve heard Jerry Hoffman espouse the relative benefits of verapamil in patients without contra-indications. A recent meta-analysis suggests both verapamil and adenosine have about a 90% success rate. The study did not look at recurrence rates of SVT, which one might expect to be higher with the shorter-acting adenosine.
The authors conclude:
The choice between the agents should be made on a case by case basis with awareness of the respective adverse effect profiles, and should involve informed discussion with the patient where appropriate.

OBJECTIVE: Verapamil and adenosine are the most common agents used to treat paroxysmal supraventricular tachycardia (PSVT). We performed a systematic review and meta-analysis to determine the relative effectiveness of these drugs and to examine their respective adverse effect profiles.
METHODS: We searched MEDLINE, EMBASE, CINAHL, the Cochrane database, and international clinical trial registers for randomized controlled trials comparing adenosine (or adenosine compounds) with verapamil for the treatment of PSVT in stable adult patients. The primary outcome was rate of reversion to sinus rhythm. Secondary outcome was occurrence of pooled adverse events. Odds ratios and 95% confidence intervals (CIs) were calculated using a random effects model (RevMan v5).
RESULTS: Eight trials were appropriate and had the available data. The reversion rate for adenosine was 90.8% (95% CI: 87.3-93.4%) compared with 89.9% for verapamil (95% CI: 86.0-92.9%). The pooled odds ratio for successful reversion was 1.27 (95% CI: 0.63-2.57) favouring adenosine. This was not statistically significant. There was a higher rate of minor adverse effects described with adenosine (16.7-76%) compared with verapamil (0-9.9%). The rate of hypotension was lower with adenosine [0.6% (95% CI: 0.1-2.4%)] compared with verapamil [3.7% (95% CI: 1.9-6.9%)].
CONCLUSION: Adenosine and verapamil have similar efficacy in treating PSVT. Adenosine has a higher rate of minor adverse effects, and of overall adverse effects, whereas verapamil has a higher rate of causing hypotension. A decision between the two agents should be made on a case-by-case basis and ideally involve informed discussion with the patient where appropriate.

The relative efficacy of adenosine versus verapamil for the treatment of stable paroxysmal supraventricular tachycardia in adults: a meta-analysis
Eur J Emerg Med. 2011 Jun;18(3):148-52

All Updates, Resus

It's up to you….

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Sometimes you have nothing to lose by doing a procedure that you may never have done before, if the patient is going to die or deteriorate without it.
In today’s competency-based-training-and-accreditation climate (a good thing), how does one achieve competence in a procedure that may be too rare to have even been seen, let alone practiced under supervision and formally assessed?
I spend a lot of time and energy trying to convince colleagues and trainees that there are situations where the benefit-harm equation is in favour of acting, despite reservations they may have about inadequate experience or training. These situations often require ‘surgical’ procedures. What they have in common is that they are all relatively simple to perform, but may save a life, a limb, or sight which otherwise may almost certainly be lost.
How best to train for these procedures, some of which may be too rare even for ‘see one, do one, teach one’ in an entire residency program? Simulators? Animal labs? Cadavers?

Slide from 'Making Things Happen' Course

In my view, the answer is to use the most high fidelity simulator in the universe – the human brain. It is those professionals who mentally rehearse the scenario and visualise the procedure over and over who are most likely to act when the patient needs it most. Several colleagues of mine over the years can recount incidents in which the indications for a thoracotomy or hysterotomy were present but they failed to act, talking themselves out of doing the procedure with a range of excuses from ‘I hadn’t had enough training’ to ‘No-one in the room wanted to do it’. Don’t be one of those! Get simulating now – you have all the equipment you need!

Ten steps to making it happen – be prepared
1. Pick a procedure (eg. thoracotomy)
2. Be ABSOLUTELY CLEAR on the indications – this helps remove any doubt when the time comes
3. Learn how to do it (talk to colleagues, read a book)
4. Know where the required equipment is kept
5. Start practicing in your mind – visualise seeing the patient, what you will say to your staff, where you will locate your equipment, what you will do procedurally step-by-step
6. Visualise possible outcomes and what your next steps would be (tamponade plus cardiac wound in a beating heart, tamponade plus wound plus VF, return of spontaneous circulation with bleeding from internal mammary arteries)
7. Read more and talk to more colleagues based on questions arising from your ‘simulations’
8. Travel, go on a course, get access to animal or cadaver labs if that’s an option in your setting
9. Speak to people who have done it in YOUR context (eg. for a resus room thoracotomy, talk to emergency physicians who have done it there, rather than a cardiothoracic surgeon who has only ever done them in the operating room)
10. Find an excuse on shift to talk about it to colleagues and rehearse the steps, locate the equipment, and so on. Remember: REPETITION IS THE MOTHER OF SKILL!

What’s on your list of life/limb/sight-saving procedures that can’t wait for someone else to do? Did I miss any? Should skull trephination be there? Comments welcome!

All Updates, Kids, Resus

Prehospital resuscitative hysterotomy

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My colleagues and I describe a tragic case in this month’s European Journal of Emergency Medicine1. Our physican-paramedic team was called to the home of a collapsed 38-week pregnant female who was in asystolic cardiac arrest. A peri-mortem caesarean delivery was performed by the physician in the patient’s home and the delivered newborn required intubation and chest compressions for bradycardia before resuming good colour and heart rate. Sadly there was ultimately a fatal outcome for both patients, but this case reminds us of the indications for this intervention and for emergency and pre-hospital physicians to be prepared to do it. A literature search yielded only one other reported prehospital case in recent medical literature2.

1.Prehospital resuscitative hysterotomy
Eur J Emerg Med. 2011 Aug;18(4):241-2
2.Out-of-hospital perimortem cesarean section
Prehosp Emerg Care. 1998 Jul-Sep;2(3):206-8

All Updates, PHARM, Resus, Trauma

Effect of physician specialty on pre-hospital intubation success

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Researchers from the London Helicopter Emergency Medical Service describe the success of pre-hospital laryngoscopy according to the grade and specialty of the HEMS physician…

There is conflicting evidence concerning the role and safety of prehospital intubation, and which providers should deliver it. Success rates for physician-performed rapid sequence induction are reported to be 97-100%, with limited evidence of improved survival in some patient groups. However, there is also evidence that prehospital intubation and ventilation can do harm. Prospective data were recorded on the success of intubation, the quality of the laryngeal view obtained and the number of attempts at intubation. These data were then analysed by the grade of intubating doctor and whether the intubating doctor had a background in anaesthesia or emergency medicine. All groups had a similar success rate after two attempts at intubation. Doctors with a background in anaesthesia and consultant emergency physicians had a significantly better first-pass intubation rate than emergency medicine trainees. The quality of laryngeal view was significantly better in doctors with an anaesthetics background.

Success in physician prehospital rapid sequence intubation: what is the effect of base speciality and length of anaesthetic training?
Emerg Med J. 2011 Mar;28(3):225-9

All Updates, ICU, Resus

Crike rate 1 in 500 in Scottish ED

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A review of over 2500 intubation attempts in the emergency department1, (of which 1671 were rapid sequence intubation attempts) revealed five cricothyroidotomies, giving a crike rate of 0.2% which is much lower than in some other ED based registries. In four patients, predictors of difficult airway were identified before the endotracheal intubation attempt, and formal preparation for rescue surgical airway was performed. Three of the surgical airways were performed by emergency medicine trainees, one by an emergency medicine specialist and one by an ear, nose and throat specialist. There was a 100% success rate for placement of all surgical airways on the first attempt.

Four surgical airways were done in trauma patients: laryngeal fracture, facial burns, Le Fort II facial fracture and penetrating neck injury.
This study is of interest to UK emergency physicians who may be interested in Edinburgh Royal Infirmary’s collaborative approach to emergency airway management by the Departments of Emergency Medicine, Anaesthesia and Critical Care.
It is not possible to tell from this paper whether there were patients in whom surgical airway was indicated but not performed, and therefore in my view the ostensibly ‘good’ low rate of 0.2% should be viewed with interest rather than awe. Having said that, this figure is more in keeping with my own experience and expectation from UK/Australasian practice; it has been highlighted in the UK EM literature before2, including by myself3, that in our patient group good training and supervision should result in lower surgical airway rates than the ~1% often quoted.


OBJECTIVES: To determine the frequency of and primary indication for surgical airway during emergency department intubation.

METHODS: Prospectively collected data from all intubations performed in the emergency department from January 1999 to July 2007 were analysed to ascertain the frequency of surgical airway access. Original data were collected on a structured proforma, entered into a regional database and analysed. Patient records were then reviewed to determine the primary indication for a surgical airway.

RESULTS: Emergency department intubation was undertaken in 2524 patients. Of these, only five patients (0.2%) required a surgical airway. The most common indication for a surgical airway was trauma in four of the five patients. Two patients had attempted rapid sequence induction before surgical airway. Two patients had gaseous inductions and one patient received no drugs. In all five patients, surgical airway was performed secondary to failed endotracheal intubation attempt(s) and was never the primary technique used.

CONCLUSION: In our emergency department, surgical airway is an uncommon procedure. The rate of 0.2% is significantly lower than rates quoted in other studies. The most common indication for surgical airway was severe facial or neck trauma. Our emergency department has a joint protocol for emergency intubation agreed by the Departments of Emergency Medicine, Anaesthesia and Critical Care at the Edinburgh Royal Infirmary. We believe that the low surgical airway rate is secondary to this collaborative approach. The identified low rate of emergency department surgical airway has implications for training and maintenance of skills for emergency medicine trainees and physicians.

1. Surgical airway in emergency department intubation
Eur J Emerg Med. 2011 Jun;18(3):168-71
2. Rapid sequence induction in the emergency department: a strategy for failure.
Emerg Med J. 2002 Mar;19(2):109-13
3. RSI by non-anaesthetists in the UK – lower incidence of cricothyrotomy than in the US
EMJ e-letters 2002; 3 April

Acute Med, All Updates, ICU, PHARM, Resus

How much oxygen after ROSC?

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I reported a previous JAMA publication demonstrating an association between hyperoxia and mortality in patients resuscitated post-cardiac arrest. The same authors have published furthur data to better define the relationship between supranormal oxygen tension and outcome in postresuscitation patients. They hypothesised that a linear dose-dependent relationship would be present in the association between supranormal oxygen tension and in-hospital mortality.

Background– Laboratory and recent clinical data suggest that hyperoxemia after resuscitation from cardiac arrest is harmful; however, it remains unclear if the risk of adverse outcome is a threshold effect at a specific supranormal oxygen tension, or is a dose-dependent association. We aimed to define the relationship between supranormal oxygen tension and outcome in postresuscitation patients.

Methods and Results– This was a multicenter cohort study using the Project IMPACT database (intensive care units at 120 US hospitals). Inclusion criteria were age >17 years, nontrauma, cardiopulmonary resuscitation preceding intensive care unit arrival, and postresuscitation arterial blood gas obtained. We excluded patients with hypoxia or severe oxygenation impairment. We defined the exposure by the highest partial pressure of arterial oxygen (PaO(2)) over the first 24 hours in the ICU. The primary outcome measure was in-hospital mortality. We tested the association between PaO(2) (continuous variable) and mortality using multivariable logistic regression adjusted for patient-oriented covariates and potential hospital effects. Of 4459 patients, 54% died. The median postresuscitation PaO(2) was 231 (interquartile range 149 to 349) mm Hg. Over ascending ranges of oxygen tension, we found significant linear trends of increasing in-hospital mortality and decreasing survival as functionally independent. On multivariable analysis, a 100 mm Hg increase in PaO(2) was associated with a 24% increase in mortality risk (odds ratio 1.24 [95% confidence interval 1.18 to 1.31]. We observed no evidence supporting a single threshold for harm from supranormal oxygen tension.

Conclusion– In this large sample of postresuscitation patients, we found a dose-dependent association between supranormal oxygen tension and risk of in-hospital death.

Relationship Between Supranormal Oxygen Tension and Outcome After Resuscitation From Cardiac Arrest
Circulation. 2011 Jun 14;123(23):2717-2722
Australasian investigators provided the following critique of the original JAMA study:

Unfortunately, these investigators used only the first set of arterial blood gases in the ICU to assess oxygenation, excluded close to 30% of patients because of lack of arterial blood gas data and did not adjust for standard illness severity scores. Their conclusion that hyperoxia is a robust predictor of mortality in patients after resuscitation form cardiac arrest was therefore potentially affected by selection bias and by insufficient adjustment for major confounders. Thus, their results are of uncertain significance and require confirmation.
They undertook their own study of 12,108 patients:

INTRODUCTION: Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients.
METHODS: We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined ‘hyperoxia’ as PaO2 of 300 mmHg or greater, ‘hypoxia/poor O2 transfer’ as either PaO2 < 60 mmHg or ratio of PaO2 to fraction of inspired oxygen (FiO2 ) < 300, ‘normoxia’ as any value between hypoxia and hyperoxia and ‘isolated hypoxemia’ as PaO2 < 60 mmHg regardless of FiO2. Mortality at hospital discharge was the main outcome measure.

RESULTS: Of 12,108 total patients, 1,285 (10.6%) had hyperoxia, 8,904 (73.5%) had hypoxia/poor O2 transfer, 1,919 (15.9%) had normoxia and 1,168 (9.7%) had isolated hypoxemia (PaO2 < 60 mmHg). The hyperoxia group had higher mortality (754 (59%) of 1,285 patients; 95% confidence interval (95% CI), 56% to 61%) than the normoxia group (911 (47%) of 1,919 patients; 95% CI, 45% to 50%) with a proportional difference of 11% (95% CI, 8% to 15%), but not higher than the hypoxia group (5,303 (60%) of 8,904 patients; 95% CI, 59% to 61%). In a multivariable model controlling for some potential confounders, including illness severity, hyperoxia had an odds ratio for hospital death of 1.2 (95% CI, 1.1 to 1.6). However, once we applied Cox proportional hazards modelling of survival, sensitivity analyses using deciles of hypoxemia, time period matching and hyperoxia defined as PaO2 > 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21).

CONCLUSIONS: Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO2 in these patients.

Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest.
Crit Care. 2011 Mar 8;15(2):R90. [Epub ahead of print]
Open Access Full Text
What’s the best approach in the light of these differing results? My approach is to avoid hypoxia, since that’s probably bad, and to actively avoid overoxygenating as part of my general neuroprotection checklist in a post-cardiac arrest patient. It would seem prudent to follow the recommendations of ILCOR, summarised by the European Resuscitation Council guidelines as:

Recognition of the potential harm caused by hyperoxaemia after ROSC is achieved: once ROSC has been established and the oxygen saturation of arterial blood (SaO2) can be monitored reliably (by pulse oximetry and/or arterial blood gas analysis), inspired oxygen is titrated to achieve a SaO2 of 94–98%

Acute Med, All Updates, ICU, PHARM, Resus

Paeds BVM for adult resuscitation

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Three hand-ventilation systems were used in a simulated adult resuscitation to determine the delivered volumes. The mean minute ventilation delivered by each of the three devices investigated was significantly different, with the paediatric (500-ml) self-inflating bag producing the result most consistent with the guideline.

There is a discrepancy between resuscitation teaching and witnessed clinical practice. Furthermore, deleterious outcomes are associated with hyperventilation. We therefore conducted a manikin-based study of a simulated cardiac arrest to evaluate the ability of three ventilating devices to provide guideline-consistent ventilation. Mean (SD) minute ventilation was reduced with the paediatric self-inflating bag (7.0 (3.2) l.min(-1) ) compared with the Mapleson C system (9.8 (3.5) l.min(-1) ) and adult self-inflating bag (9.7 (4.2) l.min(-1) ; p = 0.003). Tidal volume was also lower with the paediatric self-inflating bag (391 (52) ml) compared with the others (582 (87) ml and 625 (103) ml, respectively; p < 0.001), as was peak airway pressure (14.5 (5.2) cmH(2) O vs 20.7 (9.0) cmH(2) O and 30.3 (11.4) cmH(2) O, respectively; p < 0.001). Participants hyperventilated patients' lungs in simulated cardiac arrest with all three devices. The paediatric self-inflating bag delivered the most guideline-consistent ventilation. Its use in adult cardiopulmonary resuscitation may ensure delivery of more guideline-consistent ventilation in patients with tracheal intubation.

Comparison of the Mapleson C system and adult and paediatric self-inflating bags for delivering guideline-consistent ventilation during simulated adult cardiopulmonary resuscitation
Anaesthesia. 2011 Jul;66(7):563-7

All Updates, Kids, PHARM, Resus

Normal heart and respiratory rates in children

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A large review has established normal ranges of heart rate and respiratory rate in children from birth to 18 years of age. Some of the results differed markedly from some existing ranges quoted, such as in the Advanced Paediatric Life Support Course.

BACKGROUND: Although heart rate and respiratory rate in children are measured routinely in acute settings, current reference ranges are not based on evidence. We aimed to derive new centile charts for these vital signs and to compare these centiles with existing international ranges.

METHODS: We searched Medline, Embase, CINAHL, and reference lists for studies that reported heart rate or respiratory rate of healthy children between birth and 18 years of age. We used non-parametric kernel regression to create centile charts for heart rate and respiratory rate in relation to age. We compared existing reference ranges with those derived from our centile charts.

FINDINGS: We identified 69 studies with heart rate data for 143,346 children and respiratory rate data for 3881 children. Our centile charts show decline in respiratory rate from birth to early adolescence, with the steepest fall apparent in infants under 2 years of age; decreasing from a median of 44 breaths per min at birth to 26 breaths per min at 2 years. Heart rate shows a small peak at age 1 month. Median heart rate increases from 127 beats per min at birth to a maximum of 145 beats per min at about 1 month, before decreasing to 113 beats per min by 2 years of age. Comparison of our centile charts with existing published reference ranges for heart rate and respiratory rate show striking disagreement, with limits from published ranges frequently exceeding the 99th and 1st centiles, or crossing the median.

INTERPRETATION: Our evidence-based centile charts for children from birth to 18 years should help clinicians to update clinical and resuscitation guidelines.

Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: a systematic review of observational studies
Lancet. 2011 Mar 19;377(9770):1011-8

All Updates, ICU, PHARM, Resus, Trauma

How about pre-hospital tranexamic acid?

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The CRASH 2 trial showed improved outcomes in trauma from the administration of the antifibrinolytic drug tranexamic acid. A further analysis of the data has shown that benefit was only seen in CRASH-2 when tranexamic acid was administered within 3 hours of injury1.
An accompanying editorial2 makes the following interesting points:

  • Acute traumatic coagulopathy is a hyperacute process in which systemic fibrinolysis releases D-dimers that are detectable within 30 min of injury.
  • Those severely injured patients who develop acute coagulopathy are much more likely to die and to die early.
  • Once fully activated, fibrinolysis has been shown to continue unabated until endogenous antifibrinolytic elements are restored.
  • The earlier that tranexamic acid is administered, the more likely it might be to prevent full activation of fibrinolysis.
  • Hospital massive transfusion protocols incorporate fresh frozen plasma that contains all the endogenous antifibrinolytic elements in plasma and so the place for tranexamic acid in high income countries with such protocols is unclear.
  • The best place for tranexamic acid in developed trauma systems might actually be in the prehospital environment, where trauma bypass policies have extended prehospital times and the administration of plasma is uncommon and often impractical.

BACKGROUND: The aim of the CRASH-2 trial was to assess the effects of early administration of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage. Tranexamic acid significantly reduced all-cause mortality. Because tranexamic acid is thought to exert its effect through inhibition of fibrinolysis, we undertook exploratory analyses of its effect on death due to bleeding.

METHODS: The CRASH-2 trial was undertaken in 274 hospitals in 40 countries. 20,211 adult trauma patients with, or at risk of, significant bleeding were randomly assigned within 8 h of injury to either tranexamic acid (loading dose 1 g over 10 min followed by infusion of 1 g over 8 h) or placebo. Patients were randomly assigned by selection of the lowest numbered treatment pack from a box containing eight numbered packs that were identical apart from the pack number. Both participants and study staff (site investigators and trial coordinating centre staff ) were masked to treatment allocation. We examined the effect of tranexamic acid on death due to bleeding according to time to treatment, severity of haemorrhage as assessed by systolic blood pressure, Glasgow coma score (GCS), and type of injury. All analyses were by intention to treat. The trial is registered as ISRCTN86750102, ClinicalTrials.gov NCT00375258, and South African Clinical Trial Register/Department of Health DOH-27-0607-1919.

FINDINGS: 10,096 patients were allocated to tranexamic acid and 10,115 to placebo, of whom 10,060 and 10,067, respectively, were analysed. 1063 deaths (35%) were due to bleeding. We recorded strong evidence that the effect of tranexamic acid on death due to bleeding varied according to the time from injury to treatment (test for interaction p<0.0001). Early treatment (≤1 h from injury) significantly reduced the risk of death due to bleeding (198/3747 [5.3%] events in tranexamic acid group vs 286/3704 [7.7%] in placebo group; relative risk [RR] 0.68, 95% CI 0.57-0.82; p<0.0001). Treatment given between 1 and 3 h also reduced the risk of death due to bleeding (147/3037 [4.8%] vs 184/2996 [6.1%]; RR 0.79, 0.64-0.97; p=0.03). Treatment given after 3 h seemed to increase the risk of death due to bleeding (144/3272 [4.4%] vs 103/3362 [3.1%]; RR 1.44, 1.12-1.84; p=0.004). We recorded no evidence that the effect of tranexamic acid on death due to bleeding varied by systolic blood pressure, Glasgow coma score, or type of injury.

INTERPRETATION: Tranexamic acid should be given as early as possible to bleeding trauma patients. For trauma patients admitted late after injury, tranexamic acid is less effective and could be harmful.

1. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial
Lancet. 2011 Mar 26;377(9771):1096-101
2. Tranexamic acid for trauma
Lancet. 2011 Mar 26;377(9771):1052-4