Tag Archives: critical care

Airway lessons relearned


A UK study examined all out-of-operating room intubations over a one month period in nine hospitals1.
Patients whose indication for tracheal intubation was cardiac arrest and who were intubated without the use of drugs were excluded from analysis, as were neonatal intubations.
Disappointing – but not surprising – findings were the lack of universally applied capnography and the use of propofol as the most commonly used induction agent. However more senior intubators were less likely to use propofol than more junior ones (who used it in 93% of intubations!), and the seniors were also more likely to use non-depolarising neuromuscular blocking drugs (NMBDs) than juniors.
The authors report that in seven (4%) patients, pre-oxygenation “was felt to be impossible“. I find it hard to imagine this situation unless RSI is being done on combative patients without prior sedation, which if this is the case makes me shudder.
The authors express their understandable concern over the absence of an alternative airway such as a laryngeal mask in 12% of cases.
Although the adverse event rate seems high, they point out that they used the term ‘adverse events’ rather than ‘complications’ as the events may not be directly attributable to the intubation. In other words, some patients may have been hypoxaemic or hypotensive to start with due to their underlying clinical problem.
I find this study interesting because the results are similar to those reported in a study I and my colleagues conducted a decade ago2, in which ICU intubations were shown to be more hazardous that ED intubations. This can be explained by the higher proportion of patients on ICU with shock and/or respiratory failure. On the other hand, ED patients more commonly required intubation for neurological presentations, with relatively stable cardiorespiratory physiology.
Take a look at the breakdown of cases in the recent study:

and compare this with our findings:

…this is why I have to argue when I hear it occasionally stated that ‘all ED airways are difficult airways’ – some are actually easy, in patients with long stable apnoea times who make great teaching cases.
The authors “speculate that the low rate of hypoxaemia and airway complications may be related to the high proportion of intubations undertaken by those with anaesthesia as a base speciality, and to the almost universal use of NMBDs.” They do not provide strong data to support the first half of their statement. The supplementary data available online indeed show that the majority of intubators were anaesthesia-based, but how their adverse event rates compare with those of the emergency physicians and paediatricians who also undertook intubations is not available.
I don’t want to detract from the important message Dr Bowles and colleagues are conveying: that the lessons from the 4th National Audit Project on major complications of airway management in the UK still need to be applied.
This paper is one aspect of the potentially life-saving work done by this team, which includes the intubation checklist they created.


BACKGROUND: Tracheal intubation is commonly performed outside the operating theatre and is associated with higher risk than intubation in theatre. Recent guidelines and publications including the 4th National Audit Project of the Royal College of Anaesthetists have sought to improve the safety of out-of-theatre intubations.

METHODS: We performed a prospective observational study examining all tracheal intubations occurring outside the operating theatre in nine hospitals over a 1 month period. Data were collected on speciality and grade of intubator, presence of essential safety equipment and monitoring, and adverse events.

RESULTS: One hundred and sixty-four out-of-theatre intubations were identified (excluding those where intubation occurred as part of the management of cardiac arrest). The most common indication for intubation was respiratory failure [74 cases (45%)]. Doctors with at least 6 month’s experience in anaesthesia performed 136 intubations (83%); consultants were present for 68 cases (41%), and overall a second intubator was present for 94 procedures (57%). Propofol was the most common induction agent [124 cases (76%)] and 157 patients (96%) received neuromuscular blocking agents. An airway rescue device was available in 139 cases (87%). Capnography was not used in 52 cases (32%). Sixty-four patients suffered at least one adverse event (39%) around the time of tracheal intubation.

CONCLUSIONS: Out-of-theatre intubation frequently occurs in the absence of essential safety equipment, despite the existing guidelines. The associated adverse event rate is high.

1. Out-of-theatre tracheal intubation: prospective multicentre study of clinical practice and adverse events
Br J Anaesth. 2011 Nov;107(5):687-92


BACKGROUND: Emergency rapid sequence intubation (RSI) performed outside the operating room on emergency patients is the cornerstone of emergency airway management. Complication rates are unknown for this procedure in the United Kingdom and the factors contributing to immediate complications have not been identified.

AIMS: To quantify the immediate complications of RSI and to assess the contribution made by environmental, patient, and physician factors to overall complication rates.

METHODS: Prospective observational study of 208 consecutive adult and paediatric patients undergoing RSI over a six month period.

RESULTS: Patients were successfully intubated by RSI in all cases. There were no deaths during the procedure and no patient required a surgical airway. Patient diagnostic groups requiring RSI are described. Immediate complications were hypoxaemia 19.2%, hypotension 17.8%, and arrhythmia 3.4%. Hypoxaemia was more common in patients with pre-existing respiratory or cardiovascular conditions than in patients with other diagnoses (p<0.01). Emergency department intubations were associated with a significantly lower complication rate than other locations (16.9%; p = 0.004). This can be explained by the difference in diagnostic case mix. Intubating teams comprised anaesthetists, non-anaesthetists, or both. There were no significant differences in complication rates between these groups.
CONCLUSIONS: RSI has a significant immediate complication rate, although the clinical significance of transient events is unknown. The likelihood of immediate complications depends on the patient’s underlying condition, and relevant diagnoses should be emphasised in airway management training. Complication rates are comparable between anaesthetists and non-anaesthetists. The significantly lower complication rates in emergency department RSI can be explained by a larger proportion of patients with comparatively stable cardiorespiratory function.

2. The who, where, and what of rapid sequence intubation: prospective observational study of emergency RSI outside the operating theatre
Emerg Med J. 2004 May;21(3):296-301 Free Full Text

Training in prehospital and retrieval medicine

I’ve been too busy to blog literature updates for a couple of weeks since I and my colleagues have been flat out running a two week training course in prehospital and retrieval medicine.
Our Helicopter Emergency Medical Service physicians and paramedics care for a wide range of adult and paediatric trauma and critical care patients in some challenging environments. We therefore need to provide a fairly comprehensive induction course for new recruits.
The new guys did us proud. They just need to stay this awesome.

β-2 agonists could worsen ARDS outcome

Image: Wikipedia. I really fancy a curry now.

A previous study (BALTI-1) suggested β-2 agonists may help in ARDS by reducing extravascular lung water. A randomised trial in the UK aimed to recruit 1334 patients to compare intravenous salbutamol infused for seven days with placebo (0.9% saline). However the Data Monitoring and Ethics Committee recommended that the study stop after the second interim analysis of 273 patients because of a significant increase in mortality. It is unclear why salbutamol is harmful, and could be due to lung, cardiovascular, or other metabolic effects, such as activation of the renin-angiotensin aldosterone system affecting fluid balance.


BACKGROUND:In a previous randomised controlled phase 2 trial, intravenous infusion of salbutamol for up to 7 days in patients with acute respiratory distress syndrome (ARDS) reduced extravascular lung water and plateau airway pressure. We assessed the effects of this intervention on mortality in patients with ARDS.

METHODS:We did a multicentre, placebo-controlled, parallel-group, randomised trial at 46 UK intensive-care units between December, 2006, and March, 2010. Intubated and mechanically ventilated patients (aged ≥16 years) within 72 h of ARDS onset were randomly assigned to receive either salbutamol (15 μg/kg ideal bodyweight per h) or placebo for up to 7 days. Randomisation was done by a central telephone or web-based randomisation service with minimisation by centre, pressure of arterial oxygen to fractional inspired oxygen concentration (PaO2/FiO2) ratio, and age. All participants, caregivers, and investigators were masked to group allocation. The primary outcome was death within 28 days of randomisation. Analysis was by intention-to-treat. This trial is registered, ISRCTN38366450 and EudraCT number 2006-002647-86.

FINDINGS:We randomly assigned 162 patients to the salbutamol group and 164 to the placebo group. One patient in each group withdrew consent. Recruitment was stopped after the second interim analysis because of safety concerns. Salbutamol increased 28-day mortality (55 [34%] of 161 patients died in the salbutamol group vs 38 (23%) of 163 in the placebo group; risk ratio [RR] 1·47, 95% CI 1·03-2·08).

INTERPRETATION:Treatment with intravenous salbutamol early in the course of ARDS was poorly tolerated. Treatment is unlikely to be beneficial, and could worsen outcomes. Routine use of β-2 agonist treatment in ventilated patients with this disorder cannot be recommended.

FUNDING:UK Medical Research Council, UK Department of Health, UK Intensive Care Foundation.

Effect of intravenous β-2 agonist treatment on clinical outcomes in acute respiratory distress syndrome (BALTI-2): a multicentre, randomised controlled trial
Lancet 379(9812, 21–27 January 2012, Pages 229–235

FIRST: Fluids in Resuscitation of Severe Trauma

This is the first randomized, controlled, double-blind study comparing crystalloids with isotonic colloids in trauma. 0.9% saline was compared with hydroxyethyl starch, HES 130/0.4, as a resuscitation fluid in pre-defined subgroups of penetrating and blunt trauma. While a primary outcome measure of gastrointestinal recovery might not seem an obvious choice to some of us, previous research has indicated this to be an issue with crystalloid and the authors clearly defined this as a predefined outcome when registering the trial here.

I don't have any pictures of colloids. Here's where I work.

Colloids tend to require smaller volumes than crystalloid to achieve the same degree of plasma expansion. An interesting finding in this study is that the volume of saline administered was 1.5 times that of hydroxyethyl starch – a very similar ratio to that seen in the SAFE study which compared saline with 4% albumin in intensive care patients.
The authors assert: “..the better lactate clearance in the P-HES group indicated superior tissue resuscitation with the colloid.” There are a number of reasons why this might be a bit of stretch, including the use of epinephrine in some patients which is known to be a cause of hyperlactataemia.
This is a small study whose conclusions should be treated with caution, but which provides an important contribution to the pool of fluid resuscitation literature. If you have full text access to the British Journal of Anaesthesia, the letters pages provide excellent critiques and responses regarding potential flaws in this paper. Nevertheless, it’s one to know about – I’m sure the FIRST trial is going to be quoted for some time to come, including, I suspect, by the manufacturers of certain colloids.


Background The role of fluids in trauma resuscitation is controversial. We compared resuscitation with 0.9% saline vs hydroxyethyl starch, HES 130/0.4, in severe trauma with respect to resuscitation, fluid volume, gastrointestinal recovery, renal function, and blood product requirements.

Methods Randomized, controlled, double-blind study of severely injured patients requiring>3 litres of fluid resuscitation. Blunt and penetrating trauma were randomized separately. Patients were followed up for 30 days.

Results A total of 115 patients were randomized; of which, 109 were studied. For patients with penetrating trauma (n=67), the mean (sd) fluid requirements were 5.1 (2.7) litres in the HES group and 7.4 (4.3) litres in the saline group (P<0.001). In blunt trauma (n=42), there was no difference in study fluid requirements, but the HES group required significantly more blood products [packed red blood cell volumes 2943 (1628) vs 1473 (1071) ml, P=0.005] and was more severely injured than the saline group (median injury severity score 29.5 vs 18; P=0.01). Haemodynamic data were similar, but, in the penetrating group, plasma lactate concentrations were lower over the first 4 h (P=0.029) and on day 1 with HES than with saline [2.1 (1.4) vs 3.2 (2.2) mmol litre−1; P=0.017]. There was no difference between any groups in time to recovery of bowel function or mortality. In penetrating trauma, renal injury occurred more frequently in the saline group than the HES group (16% vs 0%; P=0.018). In penetrating trauma, maximum sequential organ function scores were lower with HES than with saline (median 2.4 vs 4.5, P=0.012). No differences were seen in safety measures in the blunt trauma patients.
Conclusions In penetrating trauma, HES provided significantly better lactate clearance and less renal injury than saline. No firm conclusions could be drawn for blunt trauma.

Resuscitation with hydroxyethyl starch improves renal function and lactate clearance in penetrating trauma in a randomized controlled study: the FIRST trial (Fluids in Resuscitation of Severe Trauma)

Br J Anaesth. 2011 Nov;107(5):693-702

Adjacent haemofiltration catheters can remove CVC drugs

An important consideration when siting your lines in your critical care patients who require renal replacement therapy…


Dual-lumen haemodiafiltration catheters enable continuous renal replacement therapy in the critically ill and are often co-located with central venous catheters used to infuse drugs. The extent to which infusions are immediately aspirated by an adjacent haemodiafiltration catheter remains unknown. A bench model was constructed to evaluate this effect. A central venous catheter and a haemodiafiltration catheter were inserted into a simulated central vein and flow generated using centrifugal pumps within the simulated vein and haemodiafiltration circuit. Ink was used as a visual tracer and creatinine solution as a quantifiable tracer. Tracers were completely aspirated by the haemodiafiltration catheter unless the infusion was at least 1 cm downstream to the arterial port. No tracer was aspirated from catheters infusing at least 2 cm downstream. Orientation of side ports did not affect tracer elimination. Co-location of central venous and haemodiafiltration catheters may lead to complete aspiration of infusions into the haemodiafilter with resultant drug under-dosing.

Adjacent central venous catheters can result in immediate aspiration of infused drugs during renal replacement therapy
Anaesthesia. 2012 Feb;67(2):115-121

Vasopressin – what it does and doesn't do

The current Surviving Sepsis campaign guidelines recommend that vasopressin should not be administered as the initial vasopressor in septic shock, and that vasopressin at constant dosage of 0.03 units/min may be added to norepinephrine with anticipation of an effect equivalent to that of norepinephrine alone. European intensivists conducted a systematic review to determine vasopressin’s risks and benefits in vasodilatory shock. There was no demonstrated survival benefit but its use is associated with a significant reduction in norepinephrine requirement.
Interestingly, the authors point out: ‘Low-dose vasopressin may help to restore blood pressure in patients with hypotension refractory to catecholamines, and may favor pulmonary vasodilation and increase glomerular filtration rate and plasma cortisol levels’.
My take home: consider its use if an apparent vasodilatory shock state is refractory to catecholamines, but don’t stress if you don’t have access to it (or it will complicate practical aspects of organising resuscitation and transfer), since there’s still no clear evidence for outcome benefit.


OBJECTIVE:
To examine the benefits and risks of vasopressin or its analog terlipressin for patients with vasodilatory shock.

DATA SOURCE:
We searched the CENTRAL, MEDLINE, EMBASE, and LILACS databases (up to March 2011) as well as reference lists of articles and proceedings of major meetings; we also contacted trial authors. We considered randomized and quasirandomized trials of vasopressin or terlipressin versus placebo or supportive treatment in adult and pediatric patients with vasodilatory shock. The primary outcome for this review was short-term all-cause mortality.

STUDY SELECTION:
We identified 10 randomized trials (1,134 patients). Six studies were considered for the main analysis on mortality in adults.

DATA EXTRACTION AND SYNTHESIS:
The crude short-term mortality was 206 of 512 (40.2%) in vasopressin/terlipressin-treated patients and 198 of 461 (42.9%) in controls [six trials, risk ratio (RR) = 0.91; 95% confidence interval (CI) 0.79-1.05; P = 0.21; I (2) = 0%]. There were 49 of 463 (10.6%) patients with serious adverse events in the vasopressin/terlipressin arm and 51 of 431 (11.8%) in the control arm (four trials, RR = 0.90; 95% CI 0.49-1.67; P = 0.75; I (2) = 26%). Metaregression analysis showed negative correlation between vasopressin dose and norepinephrine dose (P = 0.03).

CONCLUSIONS:
Overall, use of vasopressin or terlipressin did not produce any survival benefit in the short term in patients with vasodilatory shock. Physicians may value the sparing effects of vasopressin/terlipressin on norepinephrine requirement given its apparent safe profile.

Vasopressin for treatment of vasodilatory shock: an ESICM systematic review and meta-analysis
Intensive Care Med. 2012 Jan;38(1):9-19

A big brain saves a little one

Something I’ve been teaching for years – but never actually done – has been described in a case report from Oman.
A 2 year old child suffered a respiratory arrest due to an inhaled foreign body, which led to a bradyasystolic cardiac arrest. She was intubated by the resuscitation team who could not achieve any ventilation through the tube. The tube was removed and reinserted by an ‘expert’ (there is no mention of capnometry, for what it’s worth) and the same problem persisted.
The life-saving manouevre was to insert the tracheal tube further down into the right main bronchus and then withdraw to the trachea. This forced the obstructing object distally so that one-lung ventilation was then possible, resulting in return of spontaneous circulation and oxygen saturations in the mid-80’s. The object – a broken piece of plastic – was removed bronchoscopically and happily the child made an uneventful recovery.
Is this technique in your list of life-saving tricks? Hopefully, it is now.
A child is alive because a doctor was able to ‘think outside the guidelines’ in an incredibly high pressure situation. Rigid adherence to ACLS procedures here would have been futile. The guidelines save lives, but a few more can be saved when care can be individualised to the clinical situation by a thinking clinician.
Well done Dr Mishra and colleagues.

Sudden near-fatal tracheal aspiration of an undiagnosed nasal foreign body in a small child

Emerg Med Australas. 2011 Dec;23(6):776-8
[And here’s something else to consider if you have no airway equipment with you and your basic choking algorithm isn’t working]

Steroid replacement after etomidate: no benefit

More fuel for the etomidate debate…
In essence:

  • Etomidate has been a useful induction agent for RSI for many years due to its greater haemodynamic stability compared with thiopentone or propofol
  • It is widely used in the USA
  • It inhibits the 11β-hydroxylase enzyme that converts 11β-deoxycortisol into cortisol in the adrenal gland
  • A single dose of etomidate has been demonstrated to inhibit cortisol production for up to 48 hrs
  • This has led to concerns about its use in the critically ill, particular in patients with severe sepsis / septic shock
  • This small study randomised patients receiving etomidate to hydrocortisone or placebo, with no significant difference in these patient-oriented outcomes: duration of mechanical ventilation, intensive care unit length of stay, or 28-day mortality
  • This study suggests that replacement doses of hydrocortisone are not required after a single dose of etomidate
  • No randomised study has conclusively demonstrated increased mortality due to etomidate; however while controversy and the possibility of harm remain, I personally see no reason not to use ketamine for RSI in haemodynamically compromised patients.
  • Ketamine was compared with etomidate in a previous controlled trial


OBJECTIVE: To investigate the effects of moderate-dose hydrocortisone on hemodynamic status in critically ill patients throughout the period of etomidate-related adrenal insufficiency.

DESIGN: Randomized, controlled, double-blind trial (NCT00862381).

SETTING: University hospital emergency department and three intensive care units.

INTERVENTIONS: After single-dose etomidate (H0) for facilitating endotracheal intubation, patients without septic shock were randomly allocated at H6 to receive a 42-hr continuous infusion of either hydrocortisone at 200 mg/day (HC group; n = 49) or saline serum (control group; n = 50).

MEASUREMENTS AND MAIN RESULTS: After completion of a corticotrophin stimulation test, serum cortisol and 11β-deoxycortisol concentrations were subsequently assayed at H6, H12, H24, and H48. Forty-eight patients were analyzed in the HC group and 49 patients in the control group. Before treatment, the diagnostic criteria for etomidate-related adrenal insufficiency were fulfilled in 41 of 45 (91%) and 38 of 45 (84%) patients in the HC and control groups, respectively. The proportion of patients with a cardiovascular Sequential Organ Failure Assessment score of 3 or 4 declined comparably over time in both HC and control groups: 65% vs. 67% at H6, 65% vs. 69% at H12, 44% vs. 54% at H24, and 34% vs. 45% at H48, respectively. Required doses of norepinephrine decreased at a significantly higher rate in the HC group compared with the control group in patients treated with norepinephrine at H6. No intergroup differences were found regarding the duration of mechanical ventilation, intensive care unit length of stay, or 28-day mortality.

CONCLUSION: These findings suggest that critically ill patients without septic shock do not benefit from moderate-dose hydrocortisone administered to overcome etomidate-related adrenal insufficiency.

Corticosteroid after etomidate in critically ill patients: A randomized controlled trial
Crit Care Med. 2012 Jan;40(1):29-35

Emergency percutaneous airway

An excellent thorough review of emergency needle and surgical cricothyroidotomy – collectively described as ’emergency percutaneous airway’ – reveals a number of pearls.
Regarding anatomy:

  • The cricothyroid menbrane has an average height of 10 mm and a width of 11 mm
  • Transverse incision in the lower half of the cricothyroid membrane is recommended to avoid the cricothyroid arteries and the vocal cords

Regarding oxygenation / ventilation via a cricothyroid needle:

  • High pressure source ventilation via a needle (eg. by Sanders injector or Manujet) may cause laryngospasm, so a neuromuscular blocking agent should be considered
  • Barotrauma may result from an obstructed upper airway, so efforts should be made to maintain upper airway patency where possible (eg. with a supraglottic airway)
  • A device has been manufactured that provides suction-generated expiratory ventilation assistance (using oxygen flow and the Bernoulli principle) – the Ventrain
  • The Fourth National Audit Project reported a much lower success rate and described several complications of attempted re-oxygenation via a narrow-bore cricothyroidotomy
  • Where there is no kink-resistant cannula or suitable high-pressure source ventilation device readily available, it is probably safer to perform a wide-bore cannula puncture or surgical cricothyroidotomy.

Wide-bore cannula-over trocar devices:

  • Include the Quicktrach II and Portex cricothyroidotomy kit
  • Sometimes require considerable force to push the device through the cricothyroid membrane, risking compression of the airway and damage or perforation of the posterior tracheal wall.

Seldinger cricothyroidotomy kits:

  • Separate the puncture and dilatation steps, minimising the risk of trauma
  • Include the Melker emergency cricothyroidotomy set, available in sizes 3.0–6.0 mm ID
  • Tend to be preferred by anaesthetists over the surgical and wide-bore cannula-over-trocar techniques
  • Seldinger technique in human cadavers and manikin studies by those well trained, inexperienced operators have low success rates and a long performance time

What about after?

  • High-pressure source ventilation may aid subsequent intubation by direct laryngoscopy as bubbles may be seen emerging from the glottis.
  • The Seldinger technique has been recommended to convert a narrow-bore cannula into a cuffed wide-bore cricothyroidotomy
  • While conversion of cricothyroidotomy to tracheostomy within 72 h has been advocated because of the increased risk of developing subglottic stenosis with prolonged intubation through the cricothyroid membrane, this risk may be much lower than previously believed
  • The risk of conversion, although less well examined, may also be appreciable

Which technique is best?

  • The recent NAP4 audit reported a success rate of only 37% for narrow-bore cannula-over-needle cricothyroidotomy, 57% for wide-bore cannula techniques and 100% for surgical cricothyroidotomy
  • Simulation studies show conflicting results about whether seldinger or surgical technique is faster.
  • Reported success rates of the different techniques (in simulations) also vary widely and range for surgical cricothyroidotomy from 55% to 100%, for wide-bore cannula-over-trocar from 30% to 100%, and for Seldinger technique from 60% to 100%.

The one area of some consensus is that conventional (low-pressure source) ventilation should not be used with a narrow-bore cannula; a high-pressure oxygen source and a secure pathway for the egress of gas are both mandatory to achieve adequate ventilation.
Complications may be related to technique:

  • Complications of narrow-bore cannula techniques are ventilation-related and include barotrauma, subcutaneous emphysema, pneumothorax, pneumomediastinum and circulatory arrest due to impaired venous return; Cannula obstruction due to kinking also occurs.
  • Seldinger technique may be complicated by kinking of the guidewire, which increases the risk of tube misplacement
  • Bleeding and laryngeal fracture may complicate the surgical method, and long-term complications include subglottic stenosis, scarring and voice changes.

Equipment and strategies for emergency tracheal access in the adult patient
Anaesthesia. 2011 Dec;66 Suppl 2:65-80

Two new anaphylaxis guidelines

Many local and national guidelines for the management of anaphylaxis exist, but did you know there was a World Allergy Organization, and it has a very detailed guideline on this important life threatening condition?

Some interesting snippets from the guideline are included here

Anaphylaxis and cardiac disease

  • Anaphylaxis can precipitate acute myocardial infarction in susceptible individuals: in patients with ischemic heart disease, the number and density of cardiac mast cells is increased, including in the atherosclerotic plaques. Mediators released during anaphylaxis contribute to vasoconstriction and coronary artery spasm.
  • Epinephrine is not contraindicated in the treatment of anaphylaxis in patients with known or suspected cardiovascular disease, or in middle-aged or elderly patients without any history of coronary artery disease who are at increased risk of ACS only because of their age. Through its beta-1 adrenergic effects, epinephrine actually increases coronary artery blood flow because of an increase in myocardial contractility and in the duration of diastole relative to systole.
  • Glucagon has noncatecholamine-dependent inotropic and chronotropic cardiac effects, and is sometimes needed in patients taking a beta-adrenergic blocker who have hypotension and bradycardia and who do not respond optimally to epinephrine.
  • Anticholinergic agents are sometimes needed in beta-blocked patients, for example, atropine in those with persistent bradycardia or ipratropium in those with epinephrine-resistant bronchospasm.

How quickly can untreated anaphylaxis kill you?

Studies show median times to cardiorespiratory arrest after exposure to the offending stimulus were 5 minutes after administration of contrast media or drugs, 15 minutes after an insect sting, and 30 minutes after food ingestion.

What about confirming the diagnosis with serum tryptase measurements?

  • Blood samples for measurement of tryptase levels are optimally obtained 15 minutes to 3 hours after symptom onset.
  • Blood samples for measurement of histamine levels are optimally obtained 15–60 minutes after symptom onset. These tests are not specific for anaphylaxis.
  • Increased serum tryptase levels are often found in patients with anaphylaxis from insect stings or injected medications, and in those who are hypotensive
  • However, levels are often within normal limits in patients with anaphylaxis triggered by food and in those who are normotensive
  • Serial measurement of tryptase levels during an anaphylactic episode, and measurement of a baseline level after recovery are reported to be more useful than measurement at only one point in time.
  • Normal levels of either tryptase or histamine do not rule out the clinical diagnosis of anaphylaxis


How does epinephrine help?

  • Epinephrine is life-saving because of its alpha-1 adrenergic vasoconstrictor effects in most body organ systems (skeletal muscle is an important exception) and its ability to prevent and relieve airway obstruction caused by mucosal edema, and to prevent and relieve hypotension and shock.
  • Other relevant properties in anaphylaxis include its beta-1 adrenergic agonist inotropic and chronotropic properties leading to an increase in the force and rate of cardiac contractions, and its beta-2 adrenergic agonist properties such as decreased mediator release, bronchodilation and relief of urticaria
  • Epinephrine in a dose of 0.01 mg/kg of a 1:1,000 (1 mg/mL) solution injected promptly by the intramuscular route is effective and safe in the initial treatment of anaphylaxis. In other anaphylaxis scenarios, this low first-aid dose is unlikely to be effective. For example, if shock is imminent or has already developed, epinephrine needs to be given by slow intravenous infusion, ideally with the dose titrated according to noninvasive continuous cardiac monitoring.

What is the empty ventricle syndrome?

  • Patients with anaphylaxis should not suddenly sit, stand, or be placed in the upright position.
  • Instead, they should be placed on the back with their lower extremities elevated or, if they are experiencing respiratory distress or vomiting, they should be placed in a position of comfort with their lower extremities elevated.
  • This accomplishes 2 therapeutic goals: 1) preservation of fluid in the circulation (the central vascular compartment), an important step in managing distributive shock; and 2) prevention of the empty vena cava/empty ventricle syndrome, which can occur within seconds when patients with anaphylaxis suddenly assume or are placed in an upright position.
  • Patients with this syndrome are at high risk for sudden death. They are unlikely to respond to epinephrine regardless of route of administration, because it does not reach the heart and therefore cannot be circulated throughout the body

Should we give antihistamines, beta 2 agonists, and steroids?

The evidence base for use of these second line medications in the initial management of anaphylaxis, is extrapolated mainly from their use in treatment of other diseases such as urticaria (antihistamines) or acute asthma (beta-2 adrenergic agonists and glucocorticoids). Concerns have been raised that administering one or more second-line medications potentially delays prompt injection of epinephrine, the first-line treatment


Is ‘biphasic anaphylaxis’ a real phenomenon we should be concerned about?

  • Biphasic anaphylaxis occurs when symptoms recur within 1–72 hours (usually within 8–10 hours) after the initial symptoms have resolved, despite no further exposure to the trigger.
  • It occurs in up to 23% of adults and up to 11% of children.
  • After apparent resolution of symptoms, duration of monitoring in a medically supervised setting should be individualized. For example, patients with moderate respiratory or cardiovascular compromise should be monitored for at least 4 hours, and if indicated, for 8–10 hours or longer.
  • Protracted uniphasic anaphylaxis is uncommon, but can last for days.

World Allergy Organization Guidelines for the Assessment and Management of Anaphylaxis
World Allergy Organization Journal 2011;4(2):13-37 Full Text
[EXPAND click for abstract]

The illustrated World Allergy Organization (WAO) Anaphylaxis Guidelines were created in response to absence of global guidelines for anaphylaxis. Uniquely, before they were developed, lack of worldwide availability of essentials for the diagnosis and treatment of anaphylaxis was documented. They incorporate contributions from more than 100 allergy/immunology specialists on 6 continents. Recommendations are based on the best evidence available, supported by references published to the end of December 2010. The Guidelines review patient risk factors for severe or fatal anaphylaxis, co-factors that amplify anaphylaxis, and anaphylaxis in vulnerable patients, including pregnant women, infants, the elderly, and those with cardiovascular disease. They focus on the supreme importance of making a prompt clinical diagnosis and on the basic initial treatment that is urgently needed and should be possible even in a low resource environment. This involves having a written emergency protocol and rehearsing it regularly; then, as soon as anaphylaxis is diagnosed, promptly and simultaneously calling for help, injecting epinephrine (adrenaline) intramuscularly, and placing the patient on the back or in a position of comfort with the lower extremities elevated. When indicated, additional critically important steps include administering supplemental oxygen and maintaining the airway, establishing intravenous access and giving fluid resuscitation, and initiating cardiopulmonary resuscitation with continuous chest compressions. Vital signs and cardiorespiratory status should be monitored frequently and regularly (preferably, continuously). The Guidelines briefly review management of anaphylaxis refractory to basic initial treatment. They also emphasize preparation of the patient for self-treatment of anaphylaxis recurrences in the community, confirmation of anaphylaxis triggers, and prevention of recurrences through trigger avoidance and immunomodulation. Novel strategies for dissemination and implementation are summarized. A global agenda for anaphylaxis research is proposed.

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This month has also seen the publication guidelines from the UK’s National Institute for Health & Clinical Excellence, entitled ‘Anaphylaxis: assessment to confirm an anaphylactic episode and the decision to refer after emergency treatment for a suspected anaphylactic episode’
Their guideline summary is as follows:

After a suspected anaphylactic reaction in adults or young people aged 16 years or older, take timed blood samples for mast cell tryptase testing as follows:

  • a sample as soon as possible after emergency treatment has started
  • a second sample ideally within 1–2 hours (but no later than 4 hours) from the onset of symptoms.

After a suspected anaphylactic reaction in children younger than 16 years, consider taking blood samples for mast cell tryptase testing as follows if the cause is thought to be venom-related, drug-related or idiopathic:

  • a sample as soon as possible after emergency treatment has started
  • a second sample ideally within 1–2 hours (but no later than 4 hours) from the onset of symptoms.

Patients who have had emergency treatment for suspected anaphylaxis should be observed for 6–12 hours from the onset of symptoms, depending on their response to emergency treatment
After emergency treatment for suspected anaphylaxis, offer people a referral to a specialist allergy service (age-appropriate where possible) consisting of healthcare professionals with the skills and competencies necessary to accurately investigate, diagnose, monitor and provide ongoing management of, and patient education about, suspected anaphylaxis.
After emergency treatment for suspected anaphylaxis, offer people (or, as appropriate, their parent and/or carer) an appropriate adrenaline injector as an interim measure before the specialist allergy service appointment.
Before discharge a healthcare professional with the appropriate skills and competencies should offer people (or, as appropriate, their parent and/or carer) the following:

  • information about anaphylaxis, including the signs and symptoms of an anaphylactic reaction
  • information about the risk of a biphasic reaction
  • information on what to do if an anaphylactic reaction occurs (use the adrenaline injector and call emergency services)

Anaphylaxis: assessment to confirm an anaphylactic episode and the decision to refer after emergency treatment for a suspected anaphylactic episode
CG134 Anaphylaxis: NICE guideline