Over a thousand patients in North America with blunt traumatic head injury and coma who did not have hypovolaemic shock were randomised to different fluids pre-hospital. 250 ml Hypertonic (7.5%) saline was compared with normal (0.9%) saline and hypertonic saline dextran (7.5% saline/6% dextran 70). There was no difference in 6-month neurologic outcome or survival.
Out-of-Hospital Hypertonic Resuscitation Following Severe Traumatic Brain Injury
JAMA. 2010;304(13):1455-1464.
Tag Archives: outcome
Pre-hospital cooling post arrest
An Australian randomised controlled trial assessed the effect of pre-hospital cooling (using 2 litres ice cold Hartmann’s) of post-cardiac arrest patients on functional status at hospital discharge. The intervention group were marginally cooler on arrival but did not have improved outcomes.
The authors conclude: In adults who have been resuscitated from out-of-hospital cardiac arrest with an initial cardiac rhythm of ventricular fibrillation, paramedic cooling with a rapid infusion of large-volume, ice-cold intravenous fluid decreased core temperature at hospital arrival but was not shown to improve outcome at hospital discharge compared with cooling commenced in the hospital.
Induction of Therapeutic Hypothermia by Paramedics After Resuscitation From Out-of-Hospital Ventricular Fibrillation Cardiac Arrest
Circulation. 2010 Aug 17;122(7):737-42 Free Full Text
One issue from this study was that relatively short urban pre-hospital transport times meant some patients did not get the full two litres, and some had already received room temperature fluids during the cardiac arrest resuscitation. The authors suggest further study should involved initiating cooling during the arrest. In fact a European study has done just that, using a device call a RhinoChill (a portable transnasal cooling device) to lower temperature during arrest in a randomised controlled trial. This trial showed pre-hospital intra-arrest transnasal cooling is safe and feasible and is associated with a significant improvement in the time intervals required to cool patients.
Intra-arrest transnasal evaporative cooling: a randomized, prehospital, multicenter study (PRINCE: Pre-ROSC IntraNasal Cooling Effectiveness)
Circulation. 2010 Aug 17;122(7):729-36
Inferior MI – check V1 too
Lead V1 directly faces the right ventricle and during an inferior AMI may exhibit ST elevation with concomitant right ventricular infarction. Lead V1 also faces the endocardial surface of the posterolateral left ventricle, and ST depression may reflect concomitant posterolateral infarction (as the “mirror image” of ST elevation involving posterolateral epicardial leads). In this situation, V3 also shows ST depression. In lead V1, however, ST elevation from right ventricular AMI may potentially cancel out the ST depression from posterolateral AMI to give an isoelectric ST level. Diagnosis of right ventricular infarction during an inferior AMI may therefore be aided by evaluating both V1 and V3 ST levels. Both right ventricular infarction and postero-lateral infarction worsen the prognosis of an inferior AMI.
In 7967 patients with acute inferior myocardial infarction in the Hirulog and Early Reperfusion or Occlusion-2 (HERO-2) trial, V1 ST levels were analyzed with adjustment for lead V3 ST level for predicting 30-day mortality.
V1 ST elevation at baseline, analyzed as a continuous variable, was associated with higher mortality. Unadjusted, each 0.5-mm-step increase in ST level above the isoelectric level was associated with ~25% increase in 30-day mortality; this was true whether V3 ST depression was present or not. The odds ratio for mortality was 1.21 (95% confidence interval, 1.07 to 1.37) after adjustment for inferolateral ST elevation and clinical factors and 1.24 (95% confidence interval, 1.09 to 1.40) if also adjusted for V3 ST level. In contrast, lead V1 ST depression was not associated with mortality after adjustment for V3 ST level. V1 ST elevation ≥1 mm, analyzed dichotomously in all patients, was associated with higher mortality. The odds ratio was 1.28 (95% confidence interval, 1.01 to 1.61) unadjusted, 1.51 (95% confidence interval, 1.19 to 1.92) adjusted for V3 ST level, and 1.35 (95% confidence interval, 1.04 to 1.76) adjusted for ECG and clinical factors. Persistence of V1 ST elevation ≥1 mm 60 minutes after fibrinolysis was associated with higher mortality (10.8% versus 5.5%, P<0.001).
The authors conclude that V1 ST elevation identifies patients with acute inferior myocardial infarction who are at higher risk, although because no myocardial imaging was performed, could only speculate that the mechanistic link between V1 elevation and increased mortality is due to the occurrence of right ventricular infarction.
This is important to know about in terms of prognostication, but is it useful in the diagnosis of right ventricular AMI? The authors acknowledge that the ECG diagnosis of right ventricular infarction is classically made by recording lead V4R. In an autopsy study of 43 patients, ST elevation in lead V4R had higher sensitivity and specificity than ST elevation in lead V1 in diagnosing right ventricular infarction. Similarly, ST elevation in leads V7 through V9 adds significantly to precordial ST depression in aiding the diagnosis of posterolateral AMI. The authors contend that recording leads V4R and V7 through V9 is an additional step in the performance of a standard 12-lead ECG and, although recommended, may not be routinely performed.
I will continue to do a V4R in all inferior AMIs, and a V7-8 at least in patients with ST depression in V1-3.
Prognostic Value of Lead V1 ST Elevation During Acute Inferior Myocardial Infarction
Circulation. 2010 Aug 3;122(5):463-9
Unilateral pulmonary oedema worse
A few years ago in the Emergency Department I managed a sick hypotensive, hypoxic 20-something year old with a unilateral lung white-out and air bronchograms as pneumonia/septic shock. He died subsequently of refractory pulmonary oedema on the ICU, where the diagnosis of acute pulmonary oedema due to severe aortic stenosis was delayed. Post mortem findings showed pulmonary oedema but no pneumonia. A kind radiologist told me the chest x-ray would certainly have fitted with pneumonia. After this case I learned to echo sick hypotensive patients in the ED.
Circulation reports 869 cardiogenic pulmonary oedema patients, of which 2.1% had unilateral pulmonary oedema (UPE). In patients with UPE, blood pressure was significantly lower (P<=0.01), whereas noninvasive or invasive ventilation and catecholamines were used more frequently (P=0.0004 and P<0.0001, respectively). The prevalence of severe mitral regurgitation in patients with bilateral pulmonary edema and UPE was 6% and 100%, respectively (P<0.0001). In patients with UPE, use of antibiotic therapy and delay in treatment were significantly higher (P<0.0001 and P=0.003, respectively). In-hospital mortality was 9%: 39% for UPE versus 8% for bilateral pulmonary edema (odds ratio, 6.9; 95% confidence interval, 2.6 to 18; P<0.001). In multivariate analysis, unilateral location of pulmonary edema was independently related to death.
Prevalence, Characteristics, and Outcomes of Patients Presenting With Cardiogenic Unilateral Pulmonary Edema
Circulation. 2010 Sep 14;122(11):1109-15
Pneumonia scores equivalent
Got a favourite assessment tool for classifying the severity of community acquired pneumonia? Two systematic reviews showed no significant differences in performance between Pneumonia Severity Index (PSI) and various versions of CURB (CURB, CURB-65, and CRB-65).
An accompanying editorial* opines that CRB-65 is the simplest tool and can easily be remembered. It also discusses some of the more subtle strengths and weaknesses of the tools.
Severity assessment tools for predicting mortality in hospitalised patients with community-acquired pneumonia. Systematic review and meta-analysis
Thorax. 2010 Oct;65(10):878-83
Value of severity scales in predicting mortality from community-acquired pneumonia: systematic review and meta-analysis
Thorax. 2010 Oct;65(10):884-90
*Severity scores for CAP. ‘Much workload for the next bias’
Thorax 2010 Oct;65:853-855
No benefit from pre-hospital trauma doctor in Holland
Being human, I suffer from confirmation bias: I’ve become aware that I’m always on the look out for studies that show benefit from physician-provided pre-hospital care and therefore it’s possible I miss the ones that show no benefit. Of course, no ‘level 1’ evidence is out there yet. This study isn’t hugely impressive, but worth adding to the list. After adjusting for injury severity, trauma patients treated on scene by Dutch physicians had no difference in mortality compared with those that received standard care. In the subgroup analysis for patients with severe traumatic brain injury, the mortality rate with physician involvement was lower than that without, but was not statistically significant. On scene times averaged 2.7 minutes longer in the physician group although factors that might have contributed to this, such as entrapment or on scene interventions, were not recorded.
A major limitation in study design is that patients who died while under care at the scene or during transport were excluded from the analysis. The on scene time in these patients could have been prolonged by medical interventions in the field possibly contributing to the adverse outcome.
Take home message? More evidence needed.
The Association of Mobile Medical Team Involvement on On-Scene Times and Mortality in Trauma Patients
J Trauma. 2010 Sep;69(3):589-94
Scene time not linked to outcome in large cohort
Okay – I admit to loving this paper, partly because it blows away the dogma of short scene times and ‘scoop & run’, and the oft-quoted but obnoxious assertion that the only pre-hospital fluid of benefit is gasoline.
A massive database of 3656 sick trauma patients (SBP < 90, 10>resp rate>29, GCS≤12, or advanced airway intervention), transported by 146 EMS agencies to 51 hospitals, was analysed to identify any association between mortality and emergency medical services (EMS) timings (activation, response, on-scene, transport, and total time). Overall mortality in this group was 22%.
There was no significant association between time and mortality for any EMS interval: activation (odds ratio [OR] 1.00; 95% confidence interval [CI] 0.95 to 1.05), response (OR 1.00; 95% CI 9.97 to 1.04), on-scene (OR 1.00; 95% CI 0.99 to 1.01), transport (OR 1.00; 95% CI 0.98 to 1.01), or total EMS time (OR 1.00; 95% CI 0.99 to 1.01).
The authors state: “In this study, we were unable to support the contention that shorter out-of-hospital times… improve survival among injured adults with field-based physiologic abnormality… Our findings are consistent with those of previous studies that similarly have failed to demonstrate a relationship between out-of-hospital time and outcome using different patient populations, trauma and EMS systems, regions, data sources, and confounders”
Emergency Medical Services Intervals and Survival in Trauma: Assessment of the “Golden Hour” in a North American Prospective Cohort
Ann Emerg Med. 2010 Mar;55(3):235-246
Increased mortality with non-trauma centre care
A trauma database was analysed to see if patients who were transported from the field to a non-trauma centre (NTC) and subsequently sent on to a trauma centre (TC) for definitive care fared worse than similar patients who were transferred directly to the TC.
There were 1,112 patients of whom 318 (29%) were initially triaged to a NTC. After adjusting for confounders, this was associated with an increase in prehospital crystalloids (4.2 L vs. 1.4 L, p < 0.05) and a 12-fold increase in blood transfusions (60% vs. 5%, p < 0.001). Age, injury severity score, Acute Physiology and Chronic Health Evaluation II score, and time from injury to TC arrival were independent predictors of mortality. The odds of death were 3.8 times greater (95% CI, 1.6–9.0) when patients were initially triaged to a nontrauma facility.
The authors conclude: triaging severely injured patients to hospitals that are incapable of providing definitive care is associated with increased mortality. Attempts at initial stabilization at an NTC may be harmful. These findings are consistent with a need for continued expansion of regional trauma systems.
Scoop and Run to the Trauma Center or Stay and Play at the Local Hospital: Hospital Transfer’s Effect on Mortality
Journal of Trauma-Injury Infection & Critical Care September 2010;69(3):595-601
Surviving avalanche burial
Avalanche burial has a high mortality and yet in some cases there have been some amazing saves despite prolonged cardiac arrest. An international working group undertook a systematic review to examine 4 critical prognostic factors for burial victims in cardiac arrest. You have a better chance of surviving a prolonged burial if you have a patent airway and a pocket of air (even a very small one), are hypothermic, and preferably not hyperkalaemic.
Prognostic factors in avalanche resuscitation: A systematic review
Resuscitation. 2010 Jun;81(6):645-52
Oxygen in AMI – no benefit, possible harm
A Cochrane review examined the evidence from randomised controlled trials to establish whether routine use of inhaled oxygen in acute myocardial infarction (AMI) improves patient-centred outcomes, the primary outcomes being death, pain and complications.
Three trials involving 387 patients were included and 14 deaths occurred. The pooled relative risk (RR) of death was 2.88 (95% CI 0.88 to 9.39) in an intention-to-treat analysis and 3.03 (95% CI 0.93 to 9.83) in patients with confirmed AMI. While suggestive of harm, the small number of deaths recorded meant that this could be a chance occurrence. Pain was measured by analgesic use. The pooled RR for the use of analgesics was 0.97 (95% CI 0.78 to 1.20).
There is therefore no conclusive evidence from randomised controlled trials to support the routine use of inhaled oxygen in patients with acute AMI. A definitive randomised controlled trial is required.
Oxygen therapy for acute myocardial infarction
Cochrane Review