Carpopedal spasm (CPS) is defined as the painful, involuntary contraction of the muscles specifically located in the hands and feet. This sudden muscle tightness is a manifestation of tetany, a state of increased neuromuscular excitability, rather than a disease in itself. The presence of these spasms serves as an important physical sign indicating an underlying disturbance in the body’s chemistry, often related to electrolyte balance or blood pH levels. Understanding this physiological imbalance is crucial for diagnosis and effective management.
The Physical Manifestation of the Spasm
The appearance of carpopedal spasm is distinct and highly recognizable, particularly in the hands, where it is sometimes called the “obstetrician’s hand” or main d’accoucheur. This term comes from the characteristic posturing that resembles the position of a hand during a historical method of delivering a baby. The carpal spasm involves the wrist and fingers moving into a specific, rigid position.
The hand contracts with the wrist and the metacarpophalangeal joints flexing, while the distal and proximal interphalangeal joints extend. The thumb is typically pulled across the palm in adduction, forming a cone shape. In the feet, the pedal spasm involves a similar involuntary contraction, often presenting as rigid plantar flexion of the foot and toes. While the contraction is temporary, it is usually accompanied by intense pain, cramping, and a tingling sensation known as paresthesia.
The Primary Physiological Triggers
The spontaneous firing of motor neurons that causes these painful contractions is directly linked to an increase in neuromuscular excitability, which can be caused by two main physiological triggers.
Hypocalcemia
The most common and medically significant trigger is a deficiency of ionized calcium in the blood, a condition known as hypocalcemia. Calcium is a crucial stabilizer for nerve cell membranes, and when its free, unbound level drops, the nerve membrane’s threshold potential is lowered. This lowered threshold means nerve cells require less stimulation than normal to generate an action potential, making them hypersensitive and prone to firing spontaneously. This uncontrolled electrical activity then leads to the sustained, involuntary muscle contraction characteristic of tetany and carpopedal spasm. Hypocalcemia can result from various conditions, including hypoparathyroidism or a severe deficiency in Vitamin D.
Respiratory Alkalosis
A second significant cause is respiratory alkalosis, which frequently occurs during episodes of hyperventilation. Rapid, deep breathing causes an excessive expulsion of carbon dioxide (\(CO_2\)) from the body, leading to a decrease in the blood’s \(CO_2\) level and an increase in blood pH. This shift toward a more alkaline state causes plasma proteins, particularly albumin, to bind more tightly to free calcium ions. Even if the total amount of calcium in the blood is normal, the increased binding reduces the concentration of ionized calcium, which is the physiologically active form available to the nerves. This relative lack of free calcium triggers the same increase in neuromuscular excitability seen in true hypocalcemia, resulting in the characteristic spasms. Anxiety or panic attacks are common scenarios that lead to the hyperventilation and subsequent respiratory alkalosis.
Clinical Tools for Confirmation
Medical professionals use specific physical examination maneuvers to confirm the presence of latent tetany and increased neuromuscular excitability, even when a patient is not actively spasming. These clinical tools are diagnostic signs that help point toward an underlying issue like hypocalcemia.
Trousseau’s Sign
One reliable sign is Trousseau’s sign of latent tetany, which directly elicits a carpopedal spasm. The procedure involves placing a blood pressure cuff on the patient’s arm and inflating it to a pressure above the systolic blood pressure for two to three minutes. The resulting temporary lack of blood flow (ischemia) to the nerves of the forearm, combined with the underlying hypocalcemia, triggers the characteristic carpal spasm. This sign is highly sensitive for detecting low calcium levels.
Chvostek’s Sign
Another test for neuromuscular excitability is Chvostek’s sign, which involves lightly tapping the facial nerve near the ear. A positive result is indicated by a brief, involuntary twitching of the facial muscles on the side of the tap. While it is a recognized indicator of increased excitability, Chvostek’s sign is considered less sensitive for hypocalcemia than Trousseau’s sign.
Immediate Intervention and Addressing the Root Cause
Managing an episode of carpopedal spasm requires a two-pronged approach: immediate intervention to stop the acute spasm and long-term treatment directed at the underlying cause.
If the spasm is triggered by hyperventilation and respiratory alkalosis, the immediate goal is to increase the body’s carbon dioxide level. This can often be achieved by instructing the individual to slow their breathing rate or to breathe into a paper bag, which helps them re-inhale exhaled \(CO_2\). If the cause is identified as acute hypocalcemia, the most direct intervention is the intravenous administration of calcium, such as calcium gluconate, to rapidly restore free ionized calcium levels. This quick replacement stabilizes the nerve membranes, resolving the tetany and stopping the spasm.
Long-term treatment is entirely dependent on diagnosing the specific origin of the chemical imbalance. For chronic hypocalcemia, a definitive plan typically involves long-term oral supplementation with calcium and Vitamin D, as Vitamin D is necessary for intestinal calcium absorption. If the hypocalcemia is a secondary effect of a disorder like hypoparathyroidism, managing that endocrine condition is the primary focus to prevent future episodes. For spasms linked to recurrent hyperventilation, treatment shifts to addressing underlying psychological factors, such as anxiety or panic disorder, often through therapy and controlled breathing exercises.