Pathogenesis and local manifestations
Traumatic toxemia develops based on three pathogenetic factors: severe pain irritation, traumatic toxemia (massive absorption of tissue breakdown products), and plasma loss along with blood.
Immediately after release, the limb appears pale, covered with abrasions and bruises. The main initial symptom is pain (dolor). It is significant, especially with a concomitant periosteal contusion. The pain dynamics is specific: initially severe, then subsiding somewhat, but sharply increasing 1–3 hours later due to progressive traumatic edema and blood imbibition of the tissues.
Loss of function (functio laesa) does not occur instantly. Unlike fractures or dislocations, movements may initially be preserved, but as the hematoma grows (especially in hemarthrosis), they become impossible.
Over the course of several hours, the edema rapidly increases. The skin acquires a patchy purplish-cyanotic hue, and blisters with serous or hemorrhagic contents form. The tissues become «woody» — no pitting remains upon palpation. Pulsation in the distal arteries disappears, and all types of sensation are completely lost.
Periods of the disease
The disease proceeds in three stages, each with its own clinical and laboratory presentation.
- Period I (1–3 days). Characterized by increasing edema and vascular insufficiency. Immediately after release, the condition may appear satisfactory: pallor, mild tachycardia, normal blood pressure. However, clinical signs of shock develop rapidly: the pulse accelerates, blood pressure drops, body temperature rises, and anxiety increases.
There is a sharp drop in diuresis (sometimes immediately) — down to 50–70 mL per day. The urine becomes lacquer-red, and then dark brown. It contains a huge amount of protein (600–1200 mg/L), erythrocytes, and myoglobin casts of the tubules. Hemoconcentration is noted in the blood (hematocrit, hemoglobin, and erythrocyte counts rise) and azotemia progresses.
- Period II (from day 3 to days 9–12). Acute renal failure (ARF) comes to the foreground. Circulation is restored, and blood pressure returns to normal. The patient is bothered by moderate tachycardia and low-grade fever (37.3–37.5 °C), and pain in the limb subsides. Meanwhile, oliguria transitions to anuria, and blood biochemistry shows sky-high urea and creatinine levels. In extensive lesions and treatment failure, uremia develops, which can lead to a fatal outcome on days 5–7.
- Period III (recovery). Occurs in a favorable course. The condition improves, polyuria appears, and azotemia decreases (urine clears of erythrocytes and casts). Locally, severe burning pain occurs, edema subsides, and sensation returns. Extensive skin necrosis is exposed at the injury sites. Dull gray, dead muscle tissue can protrude into the wound and slough off in pieces. Joint stiffness and muscle atrophy are typical outcomes.
Management tactics
At the prehospital stage, assistance is provided immediately after release. Narcotic analgesics (morphine, trimeperidine) are administered. The damaged limb is tightly bandaged (with an elastic or regular bandage) and a transport splint is applied for immobilization and compression. For signs of impending cardiovascular insufficiency, norepinephrine or ephedrine is used, and infusion of plasma substitutes (medium-molecular-weight dextran 50,000–70,000) is initiated.
In the hospital, treatment tactics strictly depend on the disease period:
- In Period I, anti-shock and detoxification therapy is initiated immediately. The total infusion volume is 3,000–4,000 mL/day (strictly accounting for diuresis). Anti-shock plasma substitutes, albumin, plasma, and sodium bicarbonate solutions are infused (to correct acidosis and prevent renal tubular blockade).
Locally, circular procaine blockade and hypothermia are used (applying ice packs for 2–3 days following a schedule: 3–5 hours of cooling, then a 1.5–2 hour break). Broad-spectrum antibiotics are prescribed. If diuresis continues to drop despite intensive therapy, extensive fascial incision — fasciotomy — is indicated.
- In Period II, after the patient emerges from shock, the main goal is combating ARF. Hardware hemodialysis («artificial kidney») is used.
- In Period III, local complications are treated: necrosis is excised, and purulent wounds are managed according to general surgical rules.
An extreme radical measure for extensive lesions and a life-threatening condition for the patient is amputation of the crushed limb.
Briefly: answers to topical questions
What specific toxic substances are absorbed into the blood and cause traumatic toxemia in crush syndrome?
In crush syndrome, tissue breakdown products and necrosis are absorbed into the blood, causing traumatic toxemia. Tissue destruction also results in the release of intracellular potassium and its redistribution into the bloodstream.
What are the surgical indications for limb amputation in crush syndrome?
The surgical indication for limb amputation in crush syndrome is a threat to the patient's life in severe cases of the disease. Amputation is also indicated upon the development of local complications such as limb gangrene. The operation is a radical measure and is performed on vital indications to save the patient's life.
What are the indications for performing a wide fasciotomy in crush syndrome?
Wide fasciotomy in crush syndrome is performed when renal failure increases and diuresis decreases during the first period of the disease. In modern practice, this operation is used as an exception, because any wound under such conditions inevitably suppurates. Fasciotomy is performed as the «lesser of two evils» only when timely evacuation of the victim to a specialized hospital is impossible.
Which blood biochemical parameters change in the second period of crush syndrome?
In the second period of crush syndrome, which corresponds to the period of acute renal failure, progressive azotemia is noted in the blood: urea and creatinine levels increase.
Three factors of crush syndrome pathogenesis: BTP. Pain (severe pain irritation), Toxemia (absorption of tissue breakdown products), Plasmaloss (fluid portion of blood shifting into edema).
Class and exam questions
Why is limb pain undulating in nature?
Immediately after compression, pain is caused by direct tissue damage (especially the periosteum), after which it may subside slightly. 1–3 hours later, the pain resumes or sharply intensifies due to tissue distension from progressive traumatic edema and hematoma.
What are the characteristics of urine in traumatic toxemia?
Diuresis drops catastrophically (down to 50–70 mL/day). Urine acquires a lacquer-red and then dark brown color due to myoglobin. The sediment contains a colossal amount of protein (600–1200 mg/L), myoglobin casts of the tubules, and numerous erythrocytes.
In what cases are fasciotomy or amputation resorted to?
Fasciotomy is indicated in the first period if renal failure progresses and diuresis decreases. Amputation of the crushed limb is an extreme radical measure used in severe conditions and a direct threat to the patient's life.
What else to study on this topic
- The mechanism of myoglobin cast formation in renal tubules
- Differential diagnosis of crush syndrome and compartment syndrome
- Rationale for sodium bicarbonate use in tissue ischemia
- Indications for hemodialysis in acute renal failure of traumatic origin
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