2011 Asthma Guidelines

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

Preoxygenation and Prevention of Desaturation

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.

Preoxygenation and Prevention of Desaturation During Emergency Airway Management
Ann Emerg Med. 2011 Nov 1. [Epub ahead of print]


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.

Delayed diagnosis of aortic dissection

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

Fluids contribute to acid-base disturbance on ICU

Image from Wikipedia
I 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




Objective: To determine the biochemical effects of restricting the use of chloride-rich intravenous fluids in critically ill patients.


Design: Prospective, open-label, before-and-after study.


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.


咽反射是沒用的 – just as we thought

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.


What is the relationship between the Glasgow coma scale and airway protective reflexes in the Chinese population?
Resuscitation. 2011 Jul 23. [Epub ahead of print]

Related post: Do all comatose patients need intubation?