34.2 Anaphylaxis and Acute Coronary Syndrome
Key Takeaways
- Anaphylaxis is recognised by sudden onset of airway, breathing or circulation problems, usually with skin or mucosal changes.
- Adrenaline is given intramuscularly into the anterolateral thigh and repeated at five-minute intervals if there is no response.
- Patients in anaphylaxis must be laid flat with legs elevated; sudden sitting or standing can cause empty ventricle cardiac arrest.
- In suspected acute coronary syndrome give GTN 400 to 800 micrograms sublingually and 300 mg dispersible aspirin to chew unless contraindicated.
- Oxygen in acute coronary syndrome is given only if oxygen saturation is below 94%.
Detailed Emergency Protocols
1. Anaphylaxis
- Pathophysiology: A severe, life-threatening, systemic Type I IgE-mediated hypersensitivity reaction. Exposure to an offending allergen (e.g., latex, chlorhexidine, penicillin, local anaesthetic preservatives) cross-links membrane-bound IgE on sensitized mast cells and basophils. This triggers explosive degranulation and the release of histamine, leukotrienes ($LTC_4, LTD_4$), and platelet-activating factor (PAF). These mediators cause systemic arterial vasodilation, profound capillary endothelial hyperpermeability (plasma extravasation), and bronchial smooth muscle spasm.
- Clinical Presentation:
- Airway (Life-Threatening): Pharyngeal/laryngeal oedema, hoarseness, inspiratory stridor, sensation of throat swelling.
- Breathing (Life-Threatening): Severe expiratory wheeze, tachypnoea, dyspnoea, hypoxaemia ($SpO_2 <92%$).
- Circulation (Life-Threatening): Profound hypotension, thready tachycardia, dizziness, cardiovascular collapse.
- Cutaneous (Common but Non-Life-Threatening): Erythema, generalized urticarial wheals, facial angioedema (lips, eyelids, tongue).
Emergency Protocol: Anaphylaxis
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CHAIRSIDE POSITIONING IMMEDIATE PHARMACOTHERAPY
- Lay patient STRICTLY FLAT - Intramuscular (IM) Adrenaline 1:1000
- Elevate lower extremities Adult: 500 mcg (0.5 mL) into
- CRITICAL: DO NOT SIT OR STAND UP! anterolateral mid-thigh (vastus lateralis)
(Prevents catastrophic "Empty Heart" PEA) - Repeat at 5-minute intervals if no response
- If dyspnoeic with no collapse, partial incline permitted - High-flow Oxygen: 15 L/min non-rebreather
- If pregnant: Left lateral tilt - Call 999: State "Anaphylaxis"
- Adrenaline Dosing Schedule (IM 1:1000 / 1 mg/mL into vastus lateralis):
- Adults and children $>12$ years: 500 micrograms (0.5 mL)
- Children 6 to 12 years: 300 micrograms (0.3 mL)
- Children 6 months to 6 years: 150 micrograms (0.15 mL)
- Pharmacodynamics: Intramuscular adrenaline acts rapidly: $\alpha_1$-adrenergic stimulation drives arteriolar constriction, reversing peripheral vasodilation and reducing laryngeal oedema; $\beta_1$ stimulation increases cardiac inotropy and chronotropy, restoring perfusion; $\beta_2$ stimulation produces bronchial smooth muscle dilation and halts further mediator release from mast cells.
2. Acute Coronary Syndrome (ACS) & Myocardial Infarction
- Pathophysiology: Atherosclerotic plaque rupture in a coronary artery triggers platelet aggregation, occlusive thrombosis, and acute myocardial ischaemia or transmural infarction.
- Clinical Presentation: Crushing, heavy, vice-like retrosternal chest pain radiating to the left arm, neck, mandible, or epigastrium, lasting $>15$ minutes and not relieved by rest or GTN. Accompanied by pallor, diaphoresis (cold sweats), nausea, vomiting, dyspnoea, and a sense of impending doom.
- Chairside Management:
- Positioning: Sit the patient upright or in a comfortable semi-recumbent position. This lowers systemic venous return, reducing myocardial preload and oxygen consumption.
- Glyceryl Trinitrate (GTN): Administer 400 to 800 micrograms (1 to 2 puffs) sublingually. Causes systemic venodilation and coronary artery vasodilation. Caution: Withhold if systolic blood pressure is $<90\text{ mmHg}$.
- Dispersible Aspirin: Administer 300 mg dispersible aspirin; instruct the patient to chew the tablet before swallowing to ensure rapid buccal and gastric absorption. Irreversibly acetylates platelet COX-1, halting thromboxane $A_2$ synthesis and preventing further coronary thrombus propagation.
- Oxygen Caution: Administer oxygen ONLY if $SpO_2 <94%$ (or $<88%$ in hypercapnic respiratory disease). Routine hyperoxia induces paradoxical coronary artery vasoconstriction and generates reactive oxygen species, exacerbating myocardial reperfusion injury.
- Emergency Call: Call 999 immediately, requesting an emergency ambulance for suspected acute myocardial infarction.
Differentiating Anaphylaxis From Its Mimics
The most examinable diagnostic skill is separating anaphylaxis from the conditions that resemble it, because the treatment differs sharply. A vasovagal faint produces pallor, sweating, nausea, a slow pulse and hypotension, with rapid recovery once the patient is laid flat and the legs are raised — there is no rash, no wheeze and no airway swelling. A panic attack or hyperventilation produces tachypnoea, paraesthesia of the fingers and around the mouth, carpopedal spasm and light-headedness with a normal blood pressure and normal saturations. An adrenaline reaction after an intravascular local anaesthetic injection produces palpitations, tremor, anxiety and pallor lasting a few minutes with no urticaria. Acute asthma produces wheeze and respiratory distress without hypotension or skin changes.
Anaphylaxis is distinguished by its sudden onset and rapid progression, by life-threatening airway, breathing or circulation problems, and usually — though not always — by skin or mucosal changes. Skin changes alone, without airway, breathing or circulation involvement, are not anaphylaxis and do not require adrenaline. Conversely, the absence of a rash does not exclude anaphylaxis, and delaying adrenaline while waiting for one is a recognised cause of death.
After the Adrenaline
Treatment does not stop with the first injection. The patient is given high-flow oxygen, and repeated doses of intramuscular adrenaline are given at five-minute intervals if there is no improvement. An ambulance is called at once, stating "anaphylaxis". Everyone who has had anaphylaxis is transferred to hospital for observation, because biphasic reactions can occur hours after apparent recovery, and because they require specialist follow-up, allergy referral and provision of adrenaline auto-injectors. Chlorphenamine and hydrocortisone are no longer recommended as part of the initial emergency management of anaphylaxis in current Resuscitation Council UK guidance; adrenaline, oxygen and fluid are the priorities, and offering an antihistamine as the first-line answer in an SBA is wrong.
The trigger must be recorded, reported to the MHRA through the Yellow Card scheme where a medicine is implicated, and clearly flagged in the patient's record. The commonest dental triggers are latex, chlorhexidine — which is present in many mouthwashes, skin preparations and some dressings and is a frequently overlooked cause — and antibiotics, particularly penicillins.
A 34-year-old patient undergoes an extraction of an impacted third molar. Three minutes after the administration of local anaesthetic containing chlorhexidine skin prep, the patient becomes acutely restless, develops severe periorbital and labial angioedema, audible inspiratory stridor, widespread urticaria, and a profound blood pressure drop to 68/42 mmHg. What is the immediate first-line pharmacological therapy and correct patient positioning?