Pathophysiology
P-II-23. Circulatory shock, Case 2
循環性ショック 症例2
Case Presentation
A previously healthy 12-year-old boy is brought to the Emergency Department after being stung by a bee on his right arm. Following the insect bite, the child initially complained of localized pain and swelling, then, about 15 minutes later, shortness of breath developed. His parents noticed that he was wheezing. The child reported feeling dizzy and weak.
Examination on Admission
Vital signs:
- Blood pressure: 69/45 mmHg
- Respiratory rate: 39/min
- Heart rate: 120/min
- Temperature: 37.1°C
Findings:
- Drowsy and pale, but able to adequately answer questions
- Generalized urticaria present on his body
- Lips and tongue not swollen; voice sounds normal
- Respiratory exam: tachypnoea and mild wheezing, mild subcostal retractions
- Abdomen soft and palpable
- Capillary refill time prolonged
- Bee sting on the right forearm shows moderate swelling
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “stung by a bee … about 15 minutes later, shortness of breath developed” | Rapid-onset IgE-mediated (type I) hypersensitivity reaction → anaphylaxis |
| BP 69/45 mmHg | Marked hypotension from systemic vasodilation (loss of vascular tone) |
| HR 120/min, RR 39/min | Compensatory tachycardia and tachypnoea |
| “Generalized urticaria” | Mast-cell/basophil degranulation with histamine release |
| “tachypnoea and mild wheezing, mild subcostal retractions” | Bronchospasm and lower-airway obstruction → increased work of breathing |
| “Lips and tongue not swollen; voice sounds normal” | No significant laryngeal angioedema yet — upper airway currently patent (must be monitored closely) |
| “Capillary refill time prolonged” | Poor peripheral perfusion despite distributive mechanism |
Key Points
- Type of shock: Anaphylactic shock — a form of distributive shock.
- Trigger: Bee venom acting as an allergen in a sensitized child → IgE-mediated mast-cell degranulation.
- Pathophysiology: Massive histamine/mediator release → systemic vasodilation + increased capillary permeability → relative hypovolemia and hypotension, plus bronchospasm.
- Multi-system involvement: Skin (urticaria), respiratory (wheezing, retractions), cardiovascular (hypotension, tachycardia).
- Management priority: First-line treatment is intramuscular epinephrine; secure the airway and give fluids — risk of rapid progression to airway obstruction.
一問一答
▶What type of shock occurs after a bee sting with hypotension, urticaria, and wheezing?
Anaphylactic shock (a form of distributive shock).
▶What immunological mechanism underlies anaphylaxis?
An IgE-mediated (type I) hypersensitivity reaction causing mast-cell and basophil degranulation.
▶Which mediator is chiefly responsible for the vasodilation and increased permeability in anaphylaxis?
Histamine (with other mediators such as leukotrienes and prostaglandins).
▶Why is anaphylaxis classed as distributive shock?
Widespread vasodilation and capillary leak cause maldistribution of blood and relative hypovolaemia despite normal total volume.
▶Why is the blood pressure low (69/45) in anaphylactic shock?
Systemic vasodilation and capillary fluid leak reduce vascular tone and effective circulating volume.
▶What causes the wheezing and respiratory distress in anaphylaxis?
Mediator-induced bronchospasm and airway oedema obstruct the lower airways.
▶What is the first-line treatment for anaphylactic shock?
Intramuscular adrenaline (epinephrine).
▶How does adrenaline reverse the features of anaphylaxis?
Alpha-1 vasoconstriction raises BP, beta-2 effects bronchodilate, and it stabilizes mast cells to reduce mediator release.
▶Why must the airway be monitored closely even though lips and tongue are not yet swollen?
Laryngeal angioedema can develop rapidly and cause life-threatening upper airway obstruction.
▶Why does generalized urticaria appear in anaphylaxis?
Histamine release causes cutaneous vasodilation and increased permeability, producing widespread hives.
▶Why is prolonged capillary refill present despite a 'distributive' mechanism?
Profound hypotension and reduced effective circulating volume cause genuine tissue hypoperfusion.
▶Besides adrenaline, what adjunctive treatments are used in anaphylaxis?
IV fluids, high-flow oxygen, antihistamines, and corticosteroids (adjuncts, not first-line).
▶What is a biphasic anaphylactic reaction?
A recurrence of anaphylaxis hours after the initial episode without re-exposure, requiring observation.
▶Why does a type I hypersensitivity reaction require prior sensitization?
First exposure produces specific IgE that binds mast cells; subsequent exposure cross-links IgE to trigger degranulation.
▶Why does increased capillary permeability worsen hypotension in anaphylaxis?
Fluid shifts from the intravascular space into tissues, further reducing circulating volume.
▶What are the main categories of distributive shock?
Anaphylactic, septic, and neurogenic shock.
▶Why is intramuscular (not subcutaneous) adrenaline preferred in anaphylaxis?
IM injection (anterolateral thigh) gives faster, more reliable absorption than subcutaneous.
▶Why is tachycardia present in anaphylactic shock?
Reflex sympathetic activation compensates for hypotension and reduced cardiac filling.
▶What long-term measures help prevent future anaphylaxis after a sting?
Avoiding the allergen, carrying an adrenaline auto-injector, and considering venom immunotherapy.
▶Why is rapid recognition critical in anaphylaxis?
It can progress within minutes to airway obstruction and cardiovascular collapse, so early adrenaline is life-saving.