Think about what you would do if faced with the following situation:
You sedate and paralyse a patient with severe injuries in order to intubate them. You are unable to intubate due to a poor view and massive orofacial haemorrhage. An iGel provides temporary oxygenation while you prepare for a surgical airway.
Your first surgical airway attempt fails due to insertion of the bougie through a false (too superficial) passage. You spot your mistake and re-do the procedure successfully with a deeper incision. The patient’s airway is secure and there is good oxygenation and ventilation.
You discover that a colleague has videoed the procedure on his iPhone. However he only captured the first, unsuccessful attempt. The patient is not identifiable in the close up video. It’s late at night and only he and you know of the existence of the video. He asks you what you want him to do with it.
Do you…
(a) Ask your colleague to delete the video?
(b) Watch the video with him and look for learning points, and then delete it?
(c) Ask him for a copy of it and request that he doesn’t show it to anyone else?
(d) Other course of action
Consider your course of action given this situation, and then click below to reveal what my colleague did recently in exactly the same scenario…
[EXPAND What did he do?]
(d) He did something else entirely: he got a copy of the video, burned it onto a CD, and left it on his boss’s desk!
It takes a certain kind of practitioner to risk embarrassment and criticism in the pursuit of the greater educational good.
He had already ascertained what he would need to do differently next time, so had nothing personal to gain from his chosen action.
Instead, he believed that sharing the video would help prevent his colleagues from repeating the same mistake, and help his supervisors review their cricothyroidotomy training in order to better prepare their team for the procedure. Ultimately, this gesture was directed towards the good of our patients.
His actions may have saved more than one life that evening.
A mini-chest tube with Heimlich valve was an alternative to needle aspiration in patients with spontaneous pneumothorax, with some apparently favourable outcomes in this small study. The authors do not specify what type of chest tube they used but report it was 12 Fr diameter. They highlight an interesting difference in guidelines for the treatment of spontaneous primary pneumothorax:
“Traditional preference has been for chest tube insertion and admission to the ward. British Thoracic Society recommends needle aspiration (NA) as the initial treatment of choice, but American College of Chest Physicians Consensus prefers insertion of small-bore catheters (≤14F) or chest tubes (16-22F).”
OBJECTIVES: The aim of this study was to compare outcomes and complications associated with needle aspiration (NA) and minichest tube (MCT) insertion with Heimlich valve attachment in the treatment of primary spontaneous pneumothorax at an emergency department (ED).
METHODS: Patients presenting with primary spontaneous pneumothorax were randomized to NA or MCT. They had repeat chest x-rays immediately after the procedure and 6 hours later. Patients who underwent NA were discharged if repeat x-rays showed less than 10% pneumothorax. Those who had MCT were discharged if repeat x-rays did not show worsening of pneumothorax. They were reviewed at the outpatient clinic within 3 days. The primary outcomes of interest were failure rate and admission rate. The secondary outcomes were complication rate, pain and satisfaction scores, length of hospital stay, and rate of full recovery during outpatient follow-up.
RESULTS: There were 48 patients whose mean age was 25 years. We found no difference in failure rate between the groups, except that there were more MCT (24%) than NA patients (4%) with complete expansion at first review (difference, -0.20; 95% confidence interval, -0.38 to -0.01). Thirty-five percent of NA group and 20% of MCT group needed another procedure at the ED. Fifty-two percent of NA patients and 28% of MCT patients were admitted from the ED to the inpatient ward. Nine percent and 12%, respectively, of patients who had NA and MCT were admitted from the review clinic. Both groups of patients had equivalent pain scores, satisfaction scores, and complication rates.
CONCLUSION: Both MCT and NA allowed safe management of primary spontaneous pneumothorax in the outpatient setting.
A randomized controlled trial comparing minichest tube and needle aspiration in outpatient management of primary spontaneous pneumothorax Am J Emerg Med. 2011 Nov;29(9):1152-7
Atrial fibrillation can occur in the setting of severe sepsis, and often presents a therapeutic conundrum for critical care physicians, in that it can be relatively resistant to treatment until the sepsis has resolved, and its prognostic significance is unclear. A new study on a massive dataset shows atrial fibrillation in the setting of severe sepsis is associated with an increased risk of stroke and increased hospital mortality. Patients with severe sepsis who developed new-onset AF had a greater risk of in-hospital stroke than patients with preexisting AF and individuals without a history of AF.
Context New-onset atrial fibrillation (AF) has been reported in 6% to 20% of patients with severe sepsis. Chronic AF is a known risk factor for stroke and death, but the clinical significance of new-onset AF in the setting of severe sepsis is uncertain.
Objective To determine the in-hospital stroke and in-hospital mortality risks associated with new-onset AF in patients with severe sepsis.
Design and Setting Retrospective population-based cohort of California State Inpatient Database administrative claims data from nonfederal acute care hospitals for January 1 through December 31, 2007.
Patients Data were available for 3 144 787 hospitalized adults. Severe sepsis (n = 49 082 [1.56%]) was defined by validated International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) code 995.92. New-onset AF was defined as AF that occurred during the hospital stay, after excluding AF cases present at admission.
Main Outcome Measures A priori outcome measures were in-hospital ischemic stroke (ICD-9-CM codes 433, 434, or 436) and mortality.
Results Patients with severe sepsis were a mean age of 69 (SD, 16) years and 48% were women. New-onset AF occurred in 5.9% of patients with severe sepsis vs 0.65% of patients without severe sepsis (multivariable-adjusted odds ratio [OR], 6.82; 95% CI, 6.54-7.11; P < .001). Severe sepsis was present in 14% of all new-onset AF in hospitalized adults. Compared with severe sepsis patients without new-onset AF, patients with new-onset AF during severe sepsis had greater risks of in-hospital stroke (75/2896 [2.6%] vs 306/46 186 [0.6%] strokes; adjusted OR, 2.70; 95% CI, 2.05-3.57; P < .001) and in-hospital mortality (1629 [56%] vs 18 027 [39%] deaths; adjusted relative risk, 1.07; 95% CI, 1.04-1.11; P < .001). Findings were robust across 2 definitions of severe sepsis, multiple methods of addressing confounding, and multiple sensitivity analyses.
Conclusion Among patients with severe sepsis, patients with new-onset AF were at increased risk of in-hospital stroke and death compared with patients with no AF and patients with preexisting AF.
Incident Stroke and Mortality Associated With New-Onset Atrial Fibrillation in Patients Hospitalized With Severe Sepsis JAMA. 2011 Nov 13. [Epub ahead of print]
An interesting finding: in patients with myocardial infarction, hospital mortality increased consistently as the number of risk factors declined. There was also an inverse relationship between age and the number of coronary heart disease risk factors.
The authors discuss the possibility that the some of the zero risk factor group may have had risk factors unknown to the patient or not reported in the history, or may have had other factors that influence the disease, for example insulin resistance, abdominal obesity, psychosocial factors, poor nutrition, or physical inactivity.
Context Few studies have examined the association between the number of coronary heart disease risk factors and outcomes of acute myocardial infarction in community practice.
Objective To determine the association between the number of coronary heart disease risk factors in patients with first myocardial infarction and hospital mortality.
Design Observational study from the National Registry of Myocardial Infarction, 1994-2006.
Patients We examined the presence and absence of 5 major traditional coronary heart disease risk factors (hypertension, smoking, dyslipidemia, diabetes, and family history of coronary heart disease) and hospital mortality among 542 008 patients with first myocardial infarction and without prior cardiovascular disease.
Main Outcome Measure All-cause in-hospital mortality.
Results A majority (85.6%) of patients who presented with initial myocardial infarction had at least 1 of the 5 coronary heart disease risk factors, and 14.4% had none of the 5 risk factors. Age varied inversely with the number of coronary heart disease risk factors, from a mean age of 71.5 years with 0 risk factors to 56.7 years with 5 risk factors (P for trend < .001). The total number of in-hospital deaths for all causes was 50 788. Unadjusted in-hospital mortality rates were 14.9%, 10.9%, 7.9%, 5.3%, 4.2%, and 3.6% for patients with 0, 1, 2, 3, 4, and 5 risk factors, respectively. After adjusting for age and other clinical factors, there was an inverse association between the number of coronary heart disease risk factors and hospital mortality adjusted odds ratio (1.54; 95% CI, 1.23-1.94) among individuals with 0 vs 5 risk factors. This association was consistent among several age strata and important patient subgroups.
Conclusion Among patients with incident acute myocardial infarction without prior cardiovascular disease, in-hospital mortality was inversely related to the number of coronary heart disease risk factors.
Number of Coronary Heart Disease Risk Factors and Mortality in Patients With First Myocardial Infarction JAMA. 2011;306(19):2158-2159
The British Thoracic Society / SIGN Guidelines on asthma have been updated for 2011. There don’t seem to be any modificiations to the sections on acute severe asthma which were updated in 2009 and blogged here, although the treatment algorithms seem to be presented in a slightly different format and therefore are reproduced here:
Management of acute severe asthma in adults in hospital
Management of acute asthma in children in hospital
This paper is an excellent review article citing the cogent relevant evidence for optimal preoxygenation prior to RSI in the critically ill patient. The evidence has been interpreted with pertinent recommendations by two of the world’s heavy hitters in emergency medicine – Scott Weingart and Rich Levitan. If you can get a full text copy of the paper, laminate Figure 3 (‘Sequence of Preoxygenation and Prevention of Desaturation‘) and stick it to the wall in your resus bay!
The points covered include:
Why preoxygenate? Preoxygenation extends the duration of safe apnoea and should be considered mandatory, even in the crashing patient.
Standard non-rebreather facemasks set to the highest flow rate of oxygen possible should be used.
Allow 8 vital capacity breaths for co-operative patients or 3 minutes for everyone else.
Increasing mean airway pressure by CPAP/NIV or PEEP valves improves preoxygenation. However caution should be used in hypovolaemic shocked patients (decreased venous return) and should be reserved for patients who cannot preoxygenate >93-95% with high FiO2.
20-degree head up or reverse Trendelenburg (in suspected trauma) improves pre oxygenation.
Apnoeic diffusion oxygenation can extend safe duration of apnoea after the RSI. Set nasal cannulae at 15L/min and leave on during intubation attempts. Ensure upper airway patency (ear to sternal notch and jaw thrust).
Active ventilation during onset of muscle relaxation should be assessed on a case by case basis and reserved for patients at high risk of desaturation (6-8 breaths per minute slowly, TV 6-7ml/kg).
If there is a high risk of desaturation rocuronium (1.2 mg/kg) may provide a longer duration of safe apnoea than suxamethonium with similar onset time.
Patients requiring emergency airway management are at great risk of hypoxemic hypoxia because of primary lung pathology, high metabolic demands, anemia, insufficient respiratory drive, and inability to protect their airway against aspiration. Tracheal intubation is often required before the complete information needed to assess the risk of periprocedural hypoxia is acquired, such as an arterial blood gas level, hemoglobin value, or even a chest radiograph. This article reviews preoxygenation and peri-intubation oxygenation techniques to minimize the risk of critical hypoxia and introduces a risk-stratification approach to emergency tracheal intubation. Techniques reviewed include positioning, preoxygenation and denitrogenation, positive end expiratory pressure devices, and passive apneic oxygenation.
Being female or having atypical pain is associated with delays to diagnosis of aortic dissection. This recent study also shows that arrival in a non-tertiary hospital is another factor associated with delayed diagnosis. Patients may present with fever, abdominal pain, or heart failure (due to acute aortic insufficiency) that lead the clinician down alternative diagnostic algorithms. The strongest factors associated with operative delay were prolonged time from presentation to diagnosis, race other than white, and history of coronary artery bypass surgery.
Worth remembering at this point that in 2010 the AHA published Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease
Background- In acute aortic dissection, delays exist between presentation and diagnosis and, once diagnosed, definitive treatment. This study aimed to define the variables associated with these delays.
Methods and Results- Acute aortic dissection patients enrolled in the International Registry of Acute Aortic Dissection (IRAD) between 1996 and January 2007 were evaluated for factors contributing to delays in presentation to diagnosis and in diagnosis to surgery. Multiple linear regression was performed to determine relative delay time ratios (DTRs) for individual correlates. The median time from arrival at the emergency department to diagnosis was 4.3 hours (quartile 1-3, 1.5-24 hours; n=894 patients) and from diagnosis to surgery was 4.3 hours (quartile 1-3, 2.4-24 hours; n=751). Delays in acute aortic dissection diagnosis occurred in female patients; those with atypical symptoms that were not abrupt or did not include chest, back, or any pain; patients with an absence of pulse deficit or hypotension; or those who initially presented to a nontertiary care hospital (all P<0.05). The largest relative DTRs were for fever (DTR=5.11; P<0.001) and transfer from nontertiary hospital (DTR=3.34; P<0.001). Delay in time from diagnosis to surgery was associated with a history of previous cardiac surgery, presentation without abrupt or any pain, and initial presentation to a nontertiary care hospital (all P<0.001). The strongest factors associated with operative delay were prolonged time from presentation to diagnosis (DTR=1.35; P<0.001), race other than white (DTR=2.25; P<0.001), and history of coronary artery bypass surgery (DTR=2.81; P<0.001).
Conclusions- Improved physician awareness of atypical presentations and prompt transport of acute aortic dissection patients could reduce crucial time variables.
Correlates of Delayed Recognition and Treatment of Acute Type A Aortic Dissection: The International Registry of Acute Aortic Dissection (IRAD) Circulation. 2011 Nov 1;124(18):1911-1918
Image from WikipediaI enjoyed a paper from Critical Care Medicine this month which relates to a major bugbear of mine: the prescription of 0.9% saline for critically ill patients and the consequent metabolic acidosis this causes. However it did produce some interesting findings that helped me review my own biases here.
In short, an ICU team decided to reduce and where possible eliminate the use of high chloride fluids including 0.9% saline and Gelofusine and replace with lower chloride fluids, mainly Ringer’s Lactate (Hartmann’s solution).
It is known that saline causes a metabolic acidosis by elevating chloride and reducing the strong ion difference. This results in a normal anion gap, hyperchloraemic acidosis. The clinical significance of this is uncertain, but the iatrogenic acidosis is often confused by clinicians as a sign of severe illness, especially those clinicians that don’t look at the chloride or anion gap.
Not surprisingly, changing the fluid policy resulted in less acidosis (and also less hypernatraemia). There was however an increase in severe alkalaemia. The study was not designed to look at patient oriented outcomes.
My observations are:
This is an important reminder that saline causes acidosis
Because of the possibility of worsening alkalosis, fluid therapy choice should be individualised for an ICU patient based on their known acid-base issues; in some cases, saline may be appropriate.
These patients were managed for several days on an ICU. Alkalaemia is common on the ICU for reasons that include hypoalbuminaemia, furosemide use, and iatrogenic hyperventilation. These factors are less relevant in the ED resuscitation population where such a degree of alkalaemia is rarely seen.
The authors point out that their results are “consistent with previous acute treatment studies, which were conducted in the perioperative or experimental setting” – isn’t it a shame that ED-based studies are not forthcoming?
The authors point to an additional finding:
Furthermore, our results suggest that routine use of lactate fluids such as Hartmann’s or Ringer’s lactate is associated with a detectable iatrogenic increase in lactate in the first 48 hrs after ICU admission, when, presumably, lactate clearance is less effective.
While this is interesting, the mean [SD] lactate values in the two groups were 1.79 [1.57] and 2.05 [1.61] so while statistically significant I suspect this is clinically irrelevant. And as we know, the cause of a raised lactate is more of a concern than the fact of a raised lactate
A significant benefit of the change in fluid policy was a signficant cost saving, largely due to the omission of Gelofusine.
For me, this study reassures me that my current practice of preferring Ringer’s Lactate to Saline in the resuscitation setting is likely to minimise iatrogenic acidosis without significantly elevating the lactate, in a population rarely afflicted by significant alkalaemia. The biochemical effects of restricting chloride-rich fluids in intensive care Crit Care Med. 2011 Nov;39(11):2419-2424
[EXPAND Abstract]
Objective: To determine the biochemical effects of restricting the use of chloride-rich intravenous fluids in critically ill patients.
Setting: University-affiliated intensive care unit.
Patients: A cohort of 828 consecutive patients admitted over 6 months from February 2008 and cohort of 816 consecutive patients admitted over 6 months from February 2009.
Interventions: We collected biochemical and fluid use data during standard practice without clinician awareness. After a 6-month period of education and preparation, we restricted the use of chloride-rich fluids (0.9% saline [Baxter, Sydney, Australia], Gelofusine [BBraun, Melsungen, Germany], and Albumex 4 [CSL Bioplasma, Melbourne, Australia]) in the intensive care unit and made them available only on specific intensive care unit specialist prescription.
Measurements and Main Results: Saline prescription decreased from 2411 L in the control group to 52 L in the intervention group (p < .001), Gelofusine from 538 to 0 L (p < .001), and Albumex 4 from 269 to 80 L (p < .001). As expected, Hartmann’s lactated solution prescription increased from 469 to 3205 L (p < .001), Plasma-Lyte from 65 to 160 L (p < .05), and chloride-poor Albumex 20 from 87 to 268 L (p < .001). After intervention, the incidence of severe metabolic acidosis (standard base excess5 mEq/L) and alkalemia (pH >7.5) with an increase from 25.4% to 32.8% and 10.5% to 14.7%, respectively (p < .001). The time-weighted mean chloride level decreased from 104.9 ± 4.9 to 102.5 ± 4.6 mmol/L (p < .001), whereas the time-weighted mean standard base excess increased from 0.5 ± 4.5 to 1.8 ± 4.7 mmol/L (p < .001), mean bicarbonate from 25.3 ± 4.0 to 26.4 ± 4.1 mmol/L (p < .001) and mean pH from 7.40 ± 0.06 to 7.42 ± 0.06 (p < .001). Overall fluid costs decreased from $15,077 (U.S.) to $3,915.
Conclusions: In a tertiary intensive care unit in Australia, restricting the use of chloride-rich fluids significantly affected electrolyte and acid-base status. The choice of fluids significantly modulates acid-base status in critically ill patients.
The painful dogma of “GCS ≤8 = intubate” is nicely challenged by the A&E Academic Unit at Prince of Wales Hospital in Hong Kong, who provide some further evidence that patients with a higher GCS may have absent airway protective reflexes, and patients with a lower GCS may have intact reflexes.
AIM: To describe the relationship of gag and cough reflexes to Glasgow coma score (GCS) in Chinese adults requiring critical care.
METHOD: Prospective observational study of adult patients requiring treatment in the trauma or resuscitation rooms of the Emergency Department, Prince of Wales Hospital, Hong Kong. A long cotton bud to stimulate the posterior pharyngeal wall (gag reflex) and a soft tracheal suction catheter were introduced through the mouth to stimulate the laryngopharynx and elicit the cough reflex. Reflexes were classified as normal, attenuated or absent.
RESULTS: A total of 208 patients were recruited. Reduced gag and cough reflexes were found to be significantly related to reduced GCS (p=0.014 and 0.002, respectively). Of 33 patients with a GCS≤8, 12 (36.4%) had normal gag reflexes and 8 (24.2%) had normal cough reflexes. 23/62 (37.1%) patients with a GCS of 9-14 had absent gag reflexes, and 27 (43.5%) had absent cough reflexes. In patients with a normal GCS, 22.1% (25/113) had absent gag reflexes and 25.7% (29) had absent cough reflexes.
CONCLUSIONS: Our study has shown that in a Chinese population with a wide range of critical illness (but little trauma or intoxication), reduced GCS is significantly related to gag and cough reflexes. However, a considerable proportion of patients with a GCS≤8 have intact airway reflexes and may be capable of maintaining their own airway, whilst many patients with a GCS>8 have impaired airway reflexes and may be at risk of aspiration. This has important implications for airway management decisions.
Patients with acute exacerbations of asthma randomised to receive high concentration oxygen therapy showed a greater rise in CO2 than those who received titrated oxygen to keep SpO2 > 93%.
This study has a few weaknesses but raises an interesting challenge to the dogma of high flow oxygen (and oxygen driven nebulisers) for all acute asthma exacerbations.
The suggested main mechanism for the elevation in CO2 is worsening ventilation/perfusion mismatching as a result of the release of hypoxic pulmonary vasoconstriction and a consequent increase in physiological dead space. The authors remind us that this has been demonstrated in other studies on asthma and acute COPD exacerbations. The authors infer that high concentration oxygen therapy may therefore potentially increase the PaCO2 across a range of respiratory conditions with abnormal gas exchange due to ventilation/perfusion mismatching
Some of the weaknesses include lack of blinding, recruiting fewer patients than planned, and changing their primary outcome variable after commencing the study (which the authors are honest about) from absolute CO2 to increase in CO2 (since it was apparent on preliminary analysis of the first few patients that presenting CO2 was the primary determinant of subsequent CO2). Furthermore, the CO2 was measured from a transcutaneous device as opposed to the true ‘gold standard’ of arterial blood gas analysis, although good reasons are given for this.
Despite some of these drawbacks this study provides us with a further reminder that oxygen is a drug with some unwanted effects and therefore its dose needs to be individualised for the patient.
Background The effect on Paco(2) of high concentration oxygen therapy when administered to patients with severe exacerbations of asthma is uncertain.
Methods 106 patients with severe exacerbations of asthma presenting to the Emergency Department were randomised to high concentration oxygen (8 l/min via medium concentration mask) or titrated oxygen (to achieve oxygen saturations between 93% and 95%) for 60 min. Patients with chronic obstructive pulmonary disease or disorders associated with hypercapnic respiratory failure were excluded. The transcutaneous partial pressure of carbon dioxide (Ptco(2)) was measured at 0, 20, 40 and 60 min. The primary outcome variable was the proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min.
Results The proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min was significantly higher in the high concentration oxygen group, 22/50 (44%) vs 10/53 (19%), RR 2.3 (95% CI 1.2 to 4.4, p<0.006). The high concentration group had a higher proportion of patients with a rise in Ptco(2) ≥8 mm Hg, 11/50 (22%) vs 3/53 (6%), RR 3.9 (95% CI 1.2 to 13.1, p=0.016). All 10 patients with a final Ptco(2) ≥45 mm Hg received high concentration oxygen therapy, and in five there was an increase in Ptco(2) ≥10 mm Hg.
Conclusion High concentration oxygen therapy causes a clinically significant increase in Ptco(2) in patients presenting with severe exacerbations of asthma. A titrated oxygen regime is recommended in the treatment of severe asthma, in which oxygen is administered only to patients with hypoxaemia, in a dose that relieves hypoxaemia without causing hyperoxaemia.
Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma Thorax. 2011 Nov;66(11):937-41
