Trousseau’s sign is a classic clinical finding used to detect heightened nerve and muscle irritability, which results from an underlying electrolyte imbalance. Recognizing this sign is important because it often indicates a serious, though correctable, metabolic issue. The following sections explore the procedure for observing the sign, the science behind its occurrence, the medical conditions it indicates, and the standard approach to treatment.
Eliciting Trousseau’s Sign
Trousseau’s sign is elicited using a non-invasive procedure that temporarily restricts blood flow to the arm. A standard blood pressure cuff is placed on the upper arm and inflated to approximately 20 mmHg above the patient’s systolic blood pressure.
The pressure must be maintained for two to three minutes to occlude the brachial artery and induce temporary ischemia. A positive result is the onset of a carpopedal spasm, an involuntary contraction of the muscles in the hand and wrist.
The hand adopts a characteristic posture: the wrist and the joints at the base of the fingers flex, while the joints of the fingers and thumb extend. This distinct hand shape is sometimes referred to as main d’accoucheur, or “hand of the obstetrician.” The development of this spasm is a localized manifestation of latent tetany caused by the underlying electrolyte abnormality.
The Mechanism of Neuromuscular Excitability
The physiological basis for a positive Trousseau’s sign is the role of calcium ions in stabilizing nerve cell membranes. Calcium ions bind to specific sites on voltage-gated sodium channels, maintaining the electrical charge across the membrane. This stabilizing effect keeps the nerve’s depolarization threshold normal, preventing spontaneous firing.
When blood calcium concentration drops, this stabilization is reduced, making the nerve membrane more permeable to sodium ions. The lowered threshold causes nerves to become hyper-excitable, requiring less stimulation to fire an action potential. This increased irritability leads to spontaneous firing of motor neurons, resulting in muscle spasms and tetany.
The temporary ischemia induced by the inflated cuff further reduces the local threshold for nerve firing, triggering the carpal spasm. Lack of blood flow and localized accumulation of metabolic byproducts exacerbates the heightened excitability of the peripheral nerves. This combination produces the involuntary muscle contraction seen in the hand.
Underlying Conditions Indicated
Trousseau’s sign primarily indicates severe hypocalcemia, a condition marked by abnormally low levels of calcium in the blood. Hypocalcemia is associated with systemic diseases that disrupt calcium balance. The most common causes involve a deficiency or failure of the hormones and nutrients that regulate calcium.
Primary hypoparathyroidism is a frequent cause, resulting from decreased production of parathyroid hormone (PTH), which raises blood calcium levels. Damage to the parathyroid glands, often following thyroid surgery, commonly leads to this deficiency. Vitamin D deficiency or malabsorption is another common etiology, as Vitamin D is required for the gut to absorb calcium effectively.
Chronic kidney disease can also lead to hypocalcemia by impairing the kidneys’ ability to convert Vitamin D to its active form and by causing phosphate retention. Acute pancreatitis is another cause, where fatty acids bind to calcium in the abdominal cavity, removing it from circulation. Trousseau’s sign mandates immediate investigation to find and treat the root cause.
Treatment for Severe Hypocalcemia
A positive Trousseau’s sign, especially when accompanied by other symptoms of tetany, signals a medical emergency requiring immediate intervention. Acute management for severe, symptomatic hypocalcemia begins with the intravenous (IV) administration of calcium. Calcium gluconate is the preferred agent, often administered as a 10% solution over five to ten minutes to rapidly restore serum calcium concentrations.
Continuous electrocardiographic (ECG) monitoring is required during this rapid infusion because a sudden influx of calcium can affect heart rhythm. Following the initial bolus, a continuous IV infusion of calcium is started to maintain stable levels while the underlying cause is determined. The goal of acute therapy is to resolve neuromuscular excitability and raise serum calcium to a safe range.
Once the patient is stable, long-term management focuses on treating the specific disease that caused the deficiency. This often involves oral calcium and active Vitamin D supplements, which do not require processing by the kidneys. Patients with permanent hypoparathyroidism may also require synthetic parathyroid hormone replacement therapy to achieve normal calcium balance and prevent recurrence.