Problem 50 A collapsed, breathless woman
You are working in an emergency department overnight and you receive an urgent call from the ambulance service. A paramedic crew is en route to your hospital with a 50-year-old woman who collapsed at home shortly after taking her first dose of antibiotic. Vital signs are: HR 110 bpm, BP 80 mmHg palpable at the radial pulse, oxygen saturation of 92% on room air improving to 98% on high-glow oxygen, Glasgow Coma Scale score (GCS) 14 with some confusion. Facial swelling and wheeze is noted. Nebulized salbutamol and intravenous fluid are being given. Estimated time to arrival is approximately 10 minutes.
The patient arrives on an ambulance stretcher and is wheeled straight into the resuscitation bay.
You note the following on a rapid focused examination of the patient:
Airway: mild stridor and hoarse, soft voice. There is swelling of the face and tongue. There are no airway adjuncts being used.
Breathing: respiratory rate 32 with use of accessory muscles. She can speak in short phrases. There is no tracheal tug. Air entry is moderate, with widespread expiratory wheeze. She continues to saturate between 96 and 98% on 15 L oxygen via a Hudson mask.
Circulation: pulse is thready, tachycardic and regular. She has poor capillary refill of >5 seconds and is cold, sweaty and pale. Her HR is 130 bpm (post salbutamol) and BP is 80/40 mmHg. She has one 18G IV cannula in situ and has received approximately 750 mL of normal saline thus far.
Answers
Airway. Is it patent, or fully or partly occluded? Is there stridor, or snoring if the patient is unconscious? Do they have obvious swelling or rash of their perioral region, mouth, lips, tongue or neck?
Breathing. Respiratory rate? Effort of breathing including use of accessory muscles? What is the volume of speech they are able to produce? Is it full sentences, phrases or words? What does their chest sound like – is there equal air entry and are there added sounds, e.g. wheeze, or is it silent? (Silent is a bad sign.) Oxygen saturations, noting the oxygen flow rate and delivery method? Arterial blood gas?
Circulation. Palpable pulse? Rhythm (on monitor)? Blood pressure? Are they peripherally shut down, as often assessed by capillary refill time, and colour and temperature of peripheries? What is the blood pressure? What does cardiac monitoring and a 12-lead ECG show? What intravenous access do they have? How much of what fluid has been given so far?
A Glasgow Coma Scale score estimation is also performed as a guide of cerebral function.
Airway. Intubation may be required before the obstruction worsens and intubation becomes impossible. Facial and tongue oedema may make endotracheal intubation extremely difficult. Alert the staff (and yourself) that the patient may require a cricothyroidotomy or emergency tracheostomy.
Breathing. Continue high-flow oxygen via a non-rebreather mask (i.e. aiming for as close as possible to 100% FiO2). Continuous nebulized beta agonists in the form of salbutamol or adrenaline (epinephrine) to treat the bronchoconstriction. Adrenaline is particularly useful in this setting because it treats both bronchoconstriction and hypotension via beta-1 and -2 adrenergic effects (see Table 50.1). Note that pulse oximeters are prone to falsely low readings from inadequate application to the patient’s finger and peripheral shutdown. In this case application of a special earlobe probe may be beneficial.
Circulation. Ensure the patient has sufficient IV access – this usually consists of two large-bore (18G or larger) IV cannulae. Your patient only has one cannula so a second should be inserted. Crystalloid (e.g. normal saline) solutions are generally preferred over colloid (e.g. albumin or hetastarch) because of similar efficacy and low cost. Normal saline is preferred over dextrose (because of rapid tissue uptake) or compound sodium lactate (a.k.a. Hartmann’s solution) or lactated Ringer’s solution; the lactate contained in both may contribute to the metabolic acidosis which occurs in anaphylaxis.
Removal of allergen (e.g. removal of the venom sac from bee or wasp stings or cessation of the medication infusion or blood product). Do not induce emesis even if the causative agent (e.g. medication or food) is in the gut. Provoking emesis increases the risk of aspiration.
Adrenaline – the Silver Bullet in Anaphylaxis
• 500 µg of adrenaline (0.5 mL of 1 : 1000 adrenaline) intramuscularly is recommended, although smaller doses intravenously and titrated to effect can be used, as can endotracheal and subcutaneous routes.
• Patients at risk of anaphylaxis should wear an identifying MedicAlert® (or similar) bracelet, which will increase the likelihood that adrenaline will be administered in an emergency.
• Patients in whom episodes are unpredictable, who are allergic to foods that are extremely difficult to avoid, or when the cause cannot be identified should carry injectable adrenaline and be trained in its use, and should always carry a mobile telephone.
• Patients should consider notifying family, friends and work colleagues or school teachers about their allergy and if they carry an adrenaline pen inform them of its location and provide instructions on adrenaline use. Carrying a pocket/wallet card describing an anaphylaxis action plan (Figure 50.1), such as that supplied by the Australasian Society of Clinical Immunology and Allergy (ASCIA – see further information at the end of the chapter) which contains all this information is recommended.
• In some circumstances it may be possible to reduce the severity of allergy by specific immunotherapy.
Dunn R, Dilley S, Brookes J, et al, editors. The emergency medicine manual. Australia: Venom Publishing, Tennyson, 2003. Textbook with comprehensive notes on the pathophysiology of anaphylaxis
www www.allergy.org.au. Australasian Society of Clinical Immunology and Allergy (ASCIA): an excellent resource for both doctors and patients on the many issues involved in anaphylaxis including a number of action plans that can be printed off and used by patients
