Pathophysiology
P-II-25. Circulatory shock, Case 4
循環性ショック 症例4
Case Presentation
A 47-year-old man injures his thumb while repairing a lawnmower. The following day his thumb is painful and the skin around the wound is red. Since he is rather busy, he does not take care of his injured thumb.
By the evening hours, when he arrives home, his thumb becomes swollen, it is pulsating, and his wound is leaking yellowish-whitish pus. He also notices two red streaks on the inner side of his forearm. Suddenly, he becomes nauseous, and he starts shivering. His wife takes him to the nearest hospital, which takes around 35 minutes due to heavy traffic.
Examination on Arrival
- Temperature: 39.7°C
- Face is flushed; he is in poor condition
- Petechiae and oedema observed all around his body
- Pulse rate: 125/min
- Blood pressure: 90/60 mmHg
- Respiratory rate: 30/min
- No further significant changes detected on physical examination
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “injures his thumb … does not take care of his injured thumb” | Untreated contaminated wound → portal of entry for infection |
| “wound is leaking yellowish-whitish pus” | Established local bacterial infection (abscess formation) |
| “two red streaks on the inner side of his forearm” | Lymphangitis — infection spreading along lymphatic channels |
| “nauseous … starts shivering”; Temp 39.7°C | Systemic inflammatory response / bacteremia with high fever and rigors |
| “Face is flushed” | Vasodilation → warm shock typical of early septic/distributive shock |
| “Petechiae and oedema … all around his body” | Increased capillary permeability and possible disseminated intravascular coagulation (DIC) |
| Pulse 125/min, BP 90/60 mmHg, RR 30/min | Tachycardia, hypotension, and tachypnoea — meets systemic inflammatory response / sepsis criteria |
Key Points
- Type of shock: Septic shock — a form of distributive shock.
- Source: A neglected, contaminated thumb wound → local infection → lymphangitis → bacteremia.
- Pathophysiology: Microbial products trigger systemic inflammatory mediators → widespread vasodilation + increased capillary permeability → ↓SVR and relative hypovolemia → hypotension.
- Clinical signature: Warm, flushed skin and bounding pulse early on (contrast with cold hypovolemic shock); petechiae suggest DIC.
- Management priority: Early broad-spectrum antibiotics, fluid resuscitation, and source control (drainage/debridement).
一問一答
▶What type of shock develops from a neglected infected thumb wound with high fever and hypotension?
Septic shock, a form of distributive shock.
▶How does warm, flushed skin in septic shock differ from hypovolaemic shock?
Septic shock has low SVR with warm vasodilated skin early on, whereas hypovolaemic shock has high SVR with cold, clammy skin.
▶What do two red streaks running up the inner forearm from an infected wound indicate?
Lymphangitis — infection spreading along the lymphatic channels.
▶Why is the skin warm and flushed in early septic shock?
Widespread vasodilation increases skin blood flow, producing 'warm shock' (contrasting with cold hypovolaemic shock).
▶What is the pathophysiology of septic shock?
Microbial products trigger systemic inflammatory mediators causing widespread vasodilation and increased capillary permeability, lowering SVR and producing relative hypovolaemia and hypotension.
▶What do petechiae appearing all over the body in sepsis suggest?
Increased capillary permeability and possible disseminated intravascular coagulation (DIC).
▶What is disseminated intravascular coagulation (DIC) in sepsis?
Widespread activation of coagulation consuming clotting factors and platelets, causing both microthrombi and bleeding (e.g. petechiae).
▶Why does pus form at the wound site?
It is an established local bacterial infection with neutrophil accumulation and tissue breakdown (abscess formation).
▶Why does the patient develop a high fever (39.7°C) and rigors?
Bacteraemia triggers a systemic inflammatory response with pyrogen release, causing high fever and shivering.
▶What is the portal of entry for infection in this case?
A neglected, contaminated thumb wound that allowed bacteria to enter.
▶Why are tachycardia (125/min) and tachypnoea (30/min) present in sepsis?
They are compensatory responses to hypotension and the systemic inflammatory state (part of SIRS/sepsis criteria).
▶What are the three priorities in managing septic shock?
Early broad-spectrum antibiotics, fluid resuscitation, and source control (drainage/debridement of the infection).
▶Why is 'source control' essential in septic shock?
Eliminating the infection focus (e.g. draining the abscess) stops ongoing release of microbes and toxins driving the shock.
▶Why is septic shock classified as distributive shock?
The primary defect is maldistribution of blood from low vascular tone and capillary leak, not loss of blood volume or pump failure.
▶Why does fluid resuscitation help in septic shock despite normal total blood volume?
Vasodilation and capillary leak create relative hypovolaemia, so fluids restore effective circulating volume and venous return.
▶Why does increased capillary permeability cause generalized oedema in sepsis?
Fluid and protein leak from the intravascular space into the interstitium, producing tissue oedema.
▶How does a localized infection progress to bacteraemia and shock?
Untreated local infection spreads via lymphatics and bloodstream, releasing microbes/toxins that trigger a systemic inflammatory response.
▶If untreated, what may septic shock progress to?
Multi-organ dysfunction syndrome (MODS) and death from refractory hypotension and tissue hypoperfusion.
▶What is added if hypotension persists despite adequate fluid resuscitation in septic shock?
Vasopressors (e.g. noradrenaline) to restore vascular tone and blood pressure.
▶Why is early treatment critical in septic shock?
Delays increase mortality; prompt antibiotics, fluids, and source control markedly improve survival.