After reading this note you will be able to recognise, grade and initiate emergency management of anaphylaxis in the Kenyan clinical setting, while remembering to verify drug doses and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
A rapid, systemic, IgE‑mediated (or sometimes non‑IgE) hypersensitivity reaction that leads to airway compromise, circulatory collapse, or both, occurring minutes to hours after exposure to a trigger.
Anatomy and physiology you need
| Structure | Relevance to anaphylaxis |
|---|---|
| Mast cells & basophils | Release histamine, tryptase, leukotrienes on activation |
| Endothelium | Becomes leaky → plasma extravasation, edema |
| Bronchial smooth muscle | Contracts → bronchospasm |
| Upper airway mucosa | Swells → laryngeal edema, stridor |
| Cardiovascular system | Vasodilation & increased permeability → hypotension |
| Gastro‑intestinal tract | Smooth‑muscle spasm → abdominal pain, vomiting |
Causes and risk factors
| Category | Common triggers in Kenya | Specific risk factors |
|---|---|---|
| Drugs | Penicillins, cephalosporins, NSAIDs, neuromuscular blockers, contrast media | Prior drug allergy, HIV (immune dysregulation) |
| Foods | Peanuts, tree nuts, shellfish, milk, eggs | Atopic dermatitis, asthma |
| Insect stings | Hymenoptera (bees, wasps), ants | Rural exposure, occupational beekeeping |
| Latex | Surgical gloves, catheters | Repeated surgeries, healthcare workers |
| Infections / disease states | TB treatment (rifampicin), antiretrovirals, malaria prophylaxis, sickle‑cell disease (transfusion reactions) | HIV infection, active TB, malaria endemic areas, sickle‑cell disease, rheumatic fever (immune complex load) |
| Physical factors | Exercise, cold, heat, vibration | Athletes, outdoor workers |
Pathophysiology
Trigger exposure → IgE binds to mast‑cell FcεRI → cross‑linking → mast‑cell degranulation → release of mediators (histamine, tryptase, prostaglandins, leukotrienes) →
- Vasodilation & ↑ vascular permeability → plasma leak → hypotension, edema
- Bronchial smooth‑muscle contraction → bronchospasm, wheeze
- Upper‑airway mucosal edema → stridor, voice change
- Cardiac effects (negative inotropy, tachyarrhythmia) → shock
- Gastro‑intestinal smooth‑muscle spasm → pain, vomiting
Non‑IgE mechanisms (e.g., direct mast‑cell activation by radiocontrast) follow a similar mediator cascade without prior sensitisation.
Clinical features
History questions that matter
| Question | Why it matters |
|---|---|
| Onset of symptoms – how quickly after exposure? | Anaphylaxis classically begins within minutes (often <30 min). A rapid onset points to IgE‑mediated reaction; slower onset suggests other causes. |
| What was the trigger? (food, drug, insect sting, latex, contrast, herbal remedy, recent vaccination) | Identifying the allergen guides avoidance and informs risk of recurrence. In Kenya, common triggers include peanuts, shellfish, penicillins, sulfonamides, antimalarials, and hymenoptera stings. |
| Prior episodes of similar reactions or known allergy? | A previous anaphylactic episode dramatically raises the pre‑test probability and dictates that the current event is likely anaphylaxis rather than a new disease. |
| Concomitant illnesses (HIV, TB, malaria, sickle cell disease, rheumatic fever) or recent infections? | Underlying immune dysregulation (e.g., HIV) or chronic inflammation can modify mast‑cell reactivity and may predispose to severe reactions. |
| Medications taken in the last 24 h (especially β‑blockers, ACE‑inhibitors, NSAIDs, antiretrovirals)? | β‑blockers can blunt response to epinephrine; ACE‑inhibitors may worsen angio‑oedema. |
| Pregnancy status | Pregnancy alters cardiovascular reserve and may affect drug choices (e.g., epinephrine is still first‑line). |
| Presence of wheeze, throat tightness, abdominal pain, vomiting, diarrhoea, urticaria, or feeling faint? | These are the cardinal organ system manifestations that define anaphylaxis (skin‑mucosal, respiratory, cardiovascular, gastrointestinal). |
| Any recent exposure to latex (e.g., during surgery) or to new cosmetics/soaps? | Latex allergy is a notable cause of peri‑operative anaphylaxis, especially in patients with multiple surgeries. |
| Family history of severe allergy or anaphylaxis? | May suggest a hereditary predisposition (e.g., mast‑cell activation disorders). |
Examination findings and why they occur
| Finding | Pathophysiologic basis |
|---|---|
| Cutaneous: diffuse urticaria, erythema, flushing, angio‑edema of lips/eyelids | Histamine and other mediators cause vasodilation, increased vascular permeability, and dermal edema. |
| Respiratory: wheeze, stridor, bronchospasm, reduced breath sounds, tachypnoea, use of accessory muscles | Bronchial smooth‑muscle contraction and laryngeal edema narrow airways; increased secretions add to obstruction. |
| Cardiovascular: hypotension, tachycardia, weak peripheral pulses, capillary refill >2 s, cool clammy skin | Systemic vasodilation and plasma leakage reduce preload; compensatory tachycardia may be blunted by β‑blockers. |
| Gastro‑intestinal: abdominal pain, nausea, vomiting, diarrhoea | Smooth‑muscle contraction of gut and increased permeability cause cramping and fluid loss. |
| Neurological: anxiety, sense of impending doom, altered mental status, syncope | Cerebral hypoperfusion from hypotension; catecholamine surge can cause agitation. |
| Ocular: conjunctival injection, periorbital edema | Vascular leakage in conjunctival vessels. |
| Other: generalized oedema, laryngeal swelling visible on indirect laryngoscopy | Direct effect of mediators on upper airway mucosa. |
A systematic “ABCDE” assessment (Airway, Breathing, Circulation, Disability, Exposure) ensures that each organ system is evaluated promptly.
Differential diagnosis
| Condition | Points toward it | What separates it from anaphylaxis |
|---|---|---|
| Acute asthma exacerbation | Wheeze, dyspnoea, known asthma | No skin/mucosal involvement, usually no hypotension, triggers are often respiratory irritants rather than systemic allergen. |
| Acute coronary syndrome | Chest pain, diaphoresis, risk factors | ECG changes, cardiac enzymes, pain often pressure‑like, no urticaria or angio‑edema. |
| Septic shock | Fever, source of infection, gradual onset | Usually slower progression, warm extremities early, leukocytosis, positive cultures; skin changes are petechiae, not urticaria. |
| Vasovagal syncope | Prodrome of nausea, pallor, bradycardia | No respiratory or cutaneous signs, rapid recovery after lying flat, trigger is usually emotional or orthostatic. |
| Angio‑edema (non‑anaphylactic) | Isolated facial/lip swelling | Absence of urticaria, bronchospasm, or hypotension; often drug‑induced (ACE‑inhibitor) without systemic mediator release. |
| Toxic shock syndrome | Fever, rash, desquamation, multi‑organ failure | Rash is diffuse erythematous macular, not urticarial; source is usually a toxin‑producing organism, and hypotension is refractory to epinephrine alone. |
| Mast‑cell activation disorder (e.g., systemic mastocytosis) | Recurrent flushing, abdominal pain, anaphylaxis‑like episodes | Persistent baseline symptoms, abnormal serum tryptase between attacks, bone marrow findings. |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Serum tryptase (draw 30‑120 min after onset) | Mast‑cell degranulation | Elevated >11 µg/L supports anaphylaxis; normal does not exclude it. |
| Complete blood count | Infection, eosinophilia | Marked eosinophilia suggests parasitic or allergic cause; neutrophilia may point to sepsis. |
| Basic metabolic panel | Electrolytes, renal function | Helps guide fluid resuscitation; hyperkalaemia may result from cell lysis. |
| Arterial blood gas (if respiratory distress) | Oxygenation, acid‑base status | Hypoxaemia or respiratory acidosis indicates severe airway involvement. |
| ECG | Cardiac ischemia, arrhythmia | ST changes suggest ACS; tachyarrhythmias may be secondary to hypoxia. |
| Chest X‑ray (if dyspnoea) | Pulmonary oedema, pneumothorax | Helps rule out alternative causes of respiratory compromise. |
| Urine pregnancy test (women of child‑bearing age) | Pregnancy status | Influences monitoring and drug safety considerations. |
| Skin prick or specific IgE (after recovery) | Allergen identification | Positive test confirms IgE‑mediated sensitisation; used for future avoidance. |
Diagnosis and severity
Diagnostic criteria (clinical) – Anaphylaxis is diagnosed when any one of the following is present:
- Acute onset (minutes to hours) of skin‑mucosal involvement plus either respiratory compromise or circulatory collapse.
- Two or more of the following after a likely exposure:
- Skin‑mucosal signs (urticaria, angio‑edema)
- Respiratory signs (wheeze, stridor, hypoxia)
- Cardiovascular signs (hypotension, syncope)
- Gastro‑intestinal signs (vomiting, diarrhoea)
- Isolated hypotension after known allergen exposure (systolic <90 mm Hg or a drop >30 % from baseline).
Severity grading (practical for the Kenyan setting)
| Grade | Clinical picture | Management focus |
|---|---|---|
| Mild | Cutaneous signs only, stable vitals | Observe, antihistamine, consider oral corticosteroid; educate on avoidance. |
| Moderate | Skin + respiratory symptoms or mild hypotension (responsive to fluids) | Immediate intramuscular epinephrine, high‑flow oxygen, nebulised β‑agonist, IV crystalloids, monitor vitals. |
| Severe / life‑threatening | Respiratory failure, refractory hypotension, altered mental status, cardiac arrest | Immediate IM epinephrine (repeat every 5‑15 min if needed), secure airway (intubation), aggressive IV fluids, vasopressors if unresponsive, continuous cardiac monitoring, consider adjunctive IV glucocorticoids and antihistamines. |
Severity is reassessed every 5 minutes during the acute phase; escalation is driven by airway patency, oxygen saturation, blood pressure, and mental status. Prompt recognition of progression from moderate to severe is critical, as delayed epinephrine is the most common cause of mortality.
Management
Immediate stabilisation
| Step | Action | Rationale |
|---|---|---|
| 1 | Call for help, activate emergency response | Time‑critical; ensure airway, breathing, circulation (ABC) support |
| 2 | Position – supine with legs raised (unless respiratory distress) | Improves venous return and counteracts distributive shock |
| 3 | High‑flow oxygen (≥10 L/min) via non‑rebreather | Treats hypoxia from bronchospasm and shunting |
| 4 | Secure airway – early intubation if stridor, altered consciousness, or rapid deterioration | Prevents airway obstruction from edema or laryngeal spasm |
| 5 | Intramuscular adrenaline (epinephrine) in the mid‑outer thigh | First‑line drug; reverses vasodilation, bronchoconstriction, and mucosal edema |
| 6 | Intravenous crystalloid bolus (e.g., normal saline) | Restores intravascular volume in distributive shock |
| 7 | Place large‑bore IV, obtain blood for labs (see below) | Enables rapid drug administration and monitoring |
Definitive treatment
- Adrenaline – repeat IM dose every 5–15 min if symptoms persist; consider IV infusion for refractory cases under cardiac monitoring.
- Adjuncts –
- H1‑antihistamine (e.g., diphenhydramine) – reduces cutaneous symptoms; given IV/IM after adrenaline.
- H2‑antihistamine (e.g., ranitidine) – synergistic with H1 blocker for urticaria and angio‑edema.
- Systemic corticosteroid (e.g., hydrocortisone) – prevents biphasic or protracted reactions; onset delayed, so give early.
- Bronchodilator (e.g., salbutamol) – inhaled via metered‑dose inhaler or nebuliser for wheeze or bronchospasm.
- Observation – Minimum 4 h for mild reactions, 24 h for moderate/severe or if biphasic risk (e.g., delayed‐onset allergens, asthma).
Monitoring & safety
- Continuous ECG, pulse oximetry, blood pressure, and respiratory rate.
- Re‑assess airway patency every 5 min.
- Watch for adrenaline‑related arrhythmias, especially in patients with underlying cardiac disease.
- Document allergen exposure; arrange referral for allergology work‑up and prescribe an adrenaline auto‑injector with education on its use.
Contra‑indications / cautions
- No absolute contraindication to adrenaline in anaphylaxis; relative caution in uncontrolled hypertension, hyperthyroidism, or recent myocardial infarction – still give because benefit outweighs risk.
- Antihistamines may cause sedation; use with caution in children or the elderly.
- Corticosteroids are contraindicated in active, uncontrolled infection (e.g., disseminated TB) unless benefits clearly outweigh risks; monitor for worsening infection.
Complications and prognosis
- Biphasic reaction – recurrence of symptoms 1–72 h after initial resolution; more common with severe initial reaction, delayed adrenaline, or inadequate observation.
- Cardiovascular collapse – profound hypotension, arrhythmias, or cardiac arrest; early adrenaline reduces mortality.
- Respiratory failure – due to severe bronchospasm or laryngeal edema; may require mechanical ventilation.
- Neurologic sequelae – hypoxic brain injury if cardiac arrest is prolonged.
- Psychological impact – anxiety or PTSD after a life‑threatening event; counseling advisable.
Prognosis is excellent when adrenaline is administered promptly; mortality in well‑resourced settings is <1 %. Delayed treatment or lack of adrenaline markedly increases fatality risk.
High‑yield exam points
- Key differentiators: anaphylaxis vs. acute asthma attack (wheeze present in both, but anaphylaxis has urticaria, angio‑edema, hypotension).
- Most common mistake: giving antihistamine before adrenaline – examiner expects adrenaline first.
- Look‑alike conditions: serum sickness, acute urticaria, vasovagal syncope, septic shock.
- Examiner may ask:
- “What is the first drug you would give and why?”
- “How would you assess severity in a child who is crying and has a rash?”
- “Explain the rationale for leg‑raising in anaphylactic shock.”
- “What are the indications for an adrenaline auto‑injector on discharge?”
Clinical case
Case: A 28‑year‑old male farmer presents 10 minutes after being stung by a bee while harvesting maize. He reports sudden throat tightness, difficulty breathing, generalized itching, and feeling faint. On exam: BP 85/50 mmHg, HR 120 bpm, SpO₂ 88 % on room air, diffuse urticaria, lip swelling, audible wheeze, and stridor.
Questions
- What is the immediate next step?
Answer: Administer intramuscular adrenaline in the mid‑outer thigh immediately, then give high‑flow oxygen and position supine with legs raised.
- Why is epinephrine preferred over antihistamines in this scenario?
Answer: Epinephrine reverses the life‑threatening vasodilation, bronchoconstriction, and mucosal edema; antihistamines only address cutaneous symptoms and have a delayed onset.
- What follow‑up plan should be arranged before discharge?
Answer: Observe for at least 4 hours, prescribe an adrenaline auto‑injector, provide written and verbal education on its use, arrange referral to an allergy clinic for skin testing, and advise avoidance of known insect stings.
Practice questions
Question 1
A 5‑year‑old girl with known peanut allergy accidentally ingests a small amount of peanut butter. Within minutes she develops facial swelling, vomiting, and a rash. Her blood pressure is 70/40 mmHg, pulse 130 bpm, and she is wheezing. What is the most appropriate next action?
A. Give oral antihistamine
B. Administer intramuscular adrenaline
C. Start intravenous fluids only
D. Observe for 30 min
Answer: B. Administer intramuscular adrenaline
Explanation: In a child with hypotension, airway compromise, and bronchospasm, adrenaline is the first‑line life‑saving drug.
Question 2
A 62‑year‑old man on chronic beta‑blocker therapy for hypertension presents with anaphylaxis after a contrast study. Which statement is true regarding his management?
A. Beta‑blockers contraindicate adrenaline use
B. Give a higher dose of adrenaline than usual
C. Use glucagon if adrenaline response is inadequate
D. Avoid corticosteroids because of infection risk
Answer: C. Use glucagon if adrenaline response is inadequate
Explanation: Beta‑blockade can blunt adrenaline’s effect; glucagon bypasses β‑receptors and can restore cardiovascular response.
Question 3
Which feature most strongly suggests a biphasic anaphylactic reaction rather than a prolonged single phase?
A. Recurrence of symptoms after a symptom‑free interval of >1 hour
B. Persistent hypotension despite fluids
C. Development of urticaria after adrenaline administration
D. Presence of wheeze on initial presentation
Answer: A. Recurrence of symptoms after a symptom‑free interval of >1 hour
Explanation: A biphasic reaction is defined by a second phase after an asymptomatic period.
Question 4
A patient with severe malaria receives quinine and later develops sudden hypotension, generalized erythema, and bronchospasm. Which is the most likely cause?
A. Malaria‑associated sepsis
B. Quinidine‑induced anaphylaxis
C. Acute hemolytic transfusion reaction
D. Neurogenic shock
Answer: B. Quinidine‑induced anaphylaxis
Explanation: Quinidine (a quinine analogue) is a known trigger of IgE‑mediated anaphylaxis; the rapid onset after drug exposure fits.
Question 5
During an anaphylaxis code, a nurse prepares an IV infusion of adrenaline. Which precaution is essential?
A. Dilute adrenaline to 1 mg/mL before infusion
B. Administer via a peripheral line only
C. Use a cardiac monitor and have defibrillator ready
D. Give a bolus of 500 mL normal saline first
Answer: C. Use a cardiac monitor and have defibrillator ready
Explanation: IV adrenaline can precipitate arrhythmias; continuous cardiac monitoring is mandatory.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.