What is Dr. Zubair Khalid's research focus?

Dr. Zubair Khalid specializes in molecular virology, mRNA vaccine development, and computational biology, with a focus on avian pathogens like IBDV and Avian Reovirus.

Where is Dr. Zubair Khalid currently working?

Dr. Zubair Khalid is a Postdoctoral Research Associate at the University of Maryland (UMD), specifically within the Department of Animal and Avian Sciences.

Tetany: Causes, Mechanism and Clinical Signs

Name: Tetany: Causes, Mechanism and Clinical Signs
Creator: Dr. Zubair Khalid

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-09-20

Tetany is a clinical syndrome of involuntary, sustained skeletal muscle contraction caused by excessive excitability of motor nerves and muscle fibers, most often triggered by a fall in ionized calcium in the extracellular fluid. It is a sign of an underlying disorder of mineral or acid-base homeostasis rather than a disease in its own right, and its severity ranges from subtle facial twitching to generalized spasm, recumbency, and death.

Tetany matters because it is one of the few veterinary emergencies where the underlying mechanism is fully understood and the clinical picture is reproducible across species. A cow that goes down after calving, a lactating bitch that paces and trembles, and a dog with a stiff gait after parathyroid surgery all share the same final common pathway: reduced ionized calcium destabilizes the voltage-gated sodium channels of nerve and muscle membranes, which fire spontaneously. Recognizing the syndrome early lets a clinician localize the problem to calcium, magnesium, or acid-base regulation and act before the patient deteriorates.

The Physiology of Neuromuscular Excitability

Ionized calcium is the active fraction

Calcium circulates in three forms. Roughly half is bound to albumin and other proteins, a small fraction is complexed with citrate, phosphate, and bicarbonate, and the remainder is free ionized calcium (iCa). Only the ionized fraction is biologically active at the neuromuscular junction. Total calcium, the value reported on most standard chemistry panels, includes the protein-bound portion and can therefore mislead. A hypoalbuminemic patient can have a normal total calcium with a dangerously low ionized calcium, and a patient with marked hyperalbuminemia can have a low total calcium with normal ionized calcium.

In dogs, the normal ionized calcium range is approximately 1.1 to 1.3 mmol/L. Values are reported in mmol/L on most veterinary blood gas and ion-selective analyzers, while total calcium is usually reported in mg/dL. The two are not interchangeable, and the clinician must know which value the laboratory is reporting. Ionized calcium is the measurement that correlates with clinical tetany.

How calcium stabilizes the membrane

Calcium ions bind to negatively charged phospholipid head groups and to the extracellular loops of voltage-gated sodium channels. This bound calcium raises the threshold at which the sodium channel opens. When extracellular calcium falls, the channel becomes easier to open, and small depolarizing stimuli that would normally be subthreshold now trigger action potentials. The result is spontaneous and repetitive firing of motor axons and muscle fibers, which the patient experiences as cramps, fasciculations, and sustained contraction.

The same principle applies at the neuromuscular junction. Low calcium increases the probability of acetylcholine release by making the presynaptic terminal more excitable. The combination of hyperexcitable nerve and hyperexcitable muscle produces the classic tetanic state.

The calcium regulation pathway

Calcium homeostasis depends on three organs (intestine, bone, kidney) and three hormones (parathyroid hormone, calcitriol, and calcitonin). Parathyroid hormone (PTH) is the primary defender of ionized calcium. When the calcium-sensing receptor on the parathyroid chief cell detects a fall in ionized calcium, PTH secretion rises. PTH then acts on the kidney to increase calcium reabsorption and to stimulate 1-alpha-hydroxylase, which converts 25-hydroxyvitamin D to calcitriol (1,25-dihydroxyvitamin D3). Calcitriol increases intestinal calcium absorption and, with PTH, mobilizes calcium from bone. Calcitonin, secreted by thyroid C cells when calcium is high, opposes these actions and protects the skeleton.

The following flowchart traces the pathway from a fall in ionized calcium to the clinical signs of tetany.

flowchart TD
    A[Fall in ionized calcium] --> B[Calcium sensing receptor detects low calcium]
    B --> C[Parathyroid hormone secretion rises]
    C --> D[Renal calcium reabsorption increases]
    C --> E[Calcitriol synthesis increases]
    E --> F[Intestinal calcium absorption increases]
    D --> G[Serum ionized calcium restored]
    F --> G
    C --> H[Bone calcium resorption increases]
    H --> G
    A --> I[Sodium channels destabilize]
    I --> J[Nerves and muscle fire spontaneously]
    J --> K[Fasciculations cramps and tetany]
    G --> L[Tetany resolves]

PTH and calcitriol act together but not identically. Genetic models show that PTH plays the dominant role in appositional bone growth, while calcitriol acts mainly on endochondral bone formation [1]. Mice lacking both PTH and 1-alpha-hydroxylase die of tetany with severe hypocalcemia by three weeks of age, demonstrating that the two hormones have distinct and synergistic roles in postnatal mineral homeostasis [1].

Pregnancy and the perinatal window

During pregnancy, the maternal principal adjustment is increased PTH secretion, which holds ionized calcium within its narrow physiologic limits despite an expanding extracellular fluid volume, increased urinary excretion, and calcium transfer to the fetus [2]. PTH also drives renal synthesis of calcitriol to meet gestational calcium demand [2]. The placenta actively transports calcium from mother to fetus, making the fetus relatively hypercalcemic. Because calcitropic hormones do not cross the placenta, fetal hypercalcemia suppresses fetal PTH and stimulates fetal calcitonin, creating an environment favorable to skeletal growth [2].

At birth, the transplacental calcium supply stops abruptly. Serum calcium declines for 24 to 48 hours, then stabilizes and rises slightly [2]. In some neonates the fall is sufficient to cause tetany or convulsions [3]. This perinatal trough is a normal physiologic event that becomes pathologic when the neonate cannot mount an adequate PTH response or when dietary phosphate load is excessive.

What Tetany Is and What It Is Not

Tetany is a sign, not a diagnosis. The table below separates true hypocalcemic tetany from the conditions it is most often confused with.

Condition	Primary mechanism	Ionized calcium	Key clinical clue
Hypocalcemic tetany	Low iCa destabilizes sodium channels	Low	Responds to calcium replacement
Hypomagnesemia	Low Mg impairs PTH secretion and action	Low or normal	Tetany persists until Mg is corrected
Alkalosis-induced tetany	Alkalosis increases calcium binding to albumin	Low or normal	Hyperventilation, no hypocalcemia on total calcium
Tetanus	Tetanospasmin blocks inhibitory neurons	Normal	Trismus, risus sardonicus, wound history
Hypokalemic tetany	Low K alters membrane potential	Normal	Weakness predominates over spasm

The distinction matters because the treatments differ. Calcium replacement helps hypocalcemic tetany but does not correct tetanus, and magnesium must be given before calcium will work in hypomagnesemic patients.

Causes of Tetany

Parathyroid causes

Primary hypoparathyroidism is the classic endocrine cause of tetany in dogs. A retrospective study of 17 dogs with primary hypoparathyroidism found that seizures, muscle tremors and fasciculations, stiff gait, tetany, muscle cramping, behavioral change, and hyperventilation were the most common clinical signs [4]. All dogs had marked hypocalcemia with normal or mildly increased serum albumin, and the mean duration of clinical signs before diagnosis was 33 days [4]. The delay reflects how easily the early signs (facial rubbing, intermittent stiffness) are mistaken for something else.

Iatrogenic hypoparathyroidism is a recognized complication of parathyroid surgery. In a study of ultrasound-guided chemical parathyroid ablation in eight dogs with primary hyperparathyroidism, transient hypocalcemia developed in four dogs during the first five days after treatment, and one required treatment for hypocalcemic tetany [5]. This is the expected consequence of suddenly removing the source of PTH from a patient whose remaining parathyroid tissue is suppressed.

The calcium-sensing receptor is the key controller of extracellular calcium homeostasis, and gain-of-function mutations cause autosomal-dominant hypocalcemia, a condition in which affected family members suffer severe muscle pain, arthralgia, tetany, abdominal pain, and fatigue [6]. This illustrates that the set point of the parathyroid gland, not just the absolute calcium level, determines whether tetany occurs.

Nutritional causes

Nutritional hypocalcemia and hypomagnesemia are major causes of tetany in production animals. In dairy cows, milk fever is characterized by hypocalcemia at parturition as a consequence of a sudden increase in calcium demand and an unavoidable delay in calcium metabolism adaptation [7]. Tetany in the same species is usually due to impaired magnesium absorption from the rumen that cannot be compensated by absorptive or excretory adaptation, resulting in a net nutritional shortage of magnesium and culminating in hypomagnesemia [7]. The distinction between the two is clinically important because a downer cow with milk fever may not show overt tetany, while a cow with grass tetany typically does.

The interactions among calcium, phosphorus, magnesium, PTH, calcitonin, and vitamin D are dynamic and complex, and they vary with age, sex, physiologic state, and diet [8]. Three major diseases of mineral metabolism in cattle (milk fever, grass tetany, and wheat pasture poisoning) are used as models to study these interactions because they illustrate how soil, plant, and animal factors combine to produce disease [8].

In broiler breeder hens, calcium tetany is a poorly defined disease that results from acute hypocalcemia and is characterized by impaired mobility, increased mortality, and absence of gross lesions that would explain the impaired mobility [9]. A study using a handheld clinical analyzer found significant hypocalcemia (average ionized calcium 1.14 mmol/L) in affected hens compared with normal hens (average 1.53 mmol/L) in only one of three flocks sampled weekly, and some mobility-impaired hens without hypocalcemia had hypernatremia [9]. The authors concluded that calcium tetany is one cause of impaired mobility in breeder hens but that mobility impairment without hypocalcemia can also occur, and that diagnosis should be confirmed by finding significantly decreased ionized calcium [9].

Periparturient causes (eclampsia)

Puerperal tetany, also called eclampsia, is a reproductive cause of hypocalcemia in the bitch and queen [10]. It typically occurs during peak lactation, when calcium loss into milk exceeds the ability of the intestine and bone to replace it. The same article notes that mild hypocalcemia can occur during whelping and that the consequences of hypocalcemia before and during whelping in dogs and cats require attention [10].

In cattle, the periparturient hypocalcemia of milk fever is the most economically important example. Milk fever affects 8 to 9 percent of dairy cows, and farmers spend millions of dollars annually on treatment of the primary disease and the secondary problems that result [11]. The primary cellular or molecular lesions responsible for failure of calcium homeostasis have not been fully identified, but the current understanding is that aging and nutrition reduce the ability of intestine, bone, and kidney to respond rapidly to hormone signals during rapid increases in mineral demand [11].

Renal causes

Acute renal failure and chronic kidney disease can cause hypocalcemia through several mechanisms, including decreased calcitriol synthesis, hyperphosphatemia, and loss of renal calcium reabsorption. Endocrine causes of calcium disorders include hyperparathyroidism, hypoparathyroidism, thyroid disorders, hyperadrenocorticism, hypoadrenocorticism, and less commonly pheochromocytoma and multiple endocrine neoplasias [12]. Hypocalcemia may be caused by puerperal tetany, pancreatitis, intestinal malabsorption, ethylene glycol intoxication, acute renal failure, hypoparathyroidism, hypovitaminosis D, hypomagnesemia, and low albumin [12].

Iatrogenic causes

Iatrogenic hypocalcemia follows parathyroidectomy, parathyroid ablation, and certain drug therapies. The ablation study described above is the clearest veterinary example [5]. In human medicine, postoperative tetany occurs in patients with Graves' disease who have secondary hyperparathyroidism caused by a deficiency in calcium and vitamin D concomitant with transient hypoparathyroidism after surgery, and the incidence varies with season because serum 25-hydroxyvitamin D concentrations vary with season [13]. This seasonal effect is a reminder that vitamin D status modifies the risk of tetany after any procedure that compromises parathyroid function.

Other causes

Severe hemorrhagic acute pancreatitis can be complicated by gross hypocalcemia presenting as tetany, and tetany in this setting is a grave prognostic indicator [14]. Falciparum malaria can present with carpopedal spasm and tetany, and the mechanisms involve dysregulation of calcium, phosphorus, and magnesium metabolism [15]. In neonatal medicine, hypocalcemia is probably the most common disturbance of calcium homeostasis in the neonate and can be subdivided into three main groups on the basis of etiological mechanism [3]. Late infantile tetany with secondary hyperparathyroidism has been reported in infants fed humanized cow milk formula, with elevated PTH levels persisting for weeks after normocalcemia was restored [16].

Species Differences in Clinical Presentation

Dogs and cats

Small animals with hypocalcemic tetany typically show facial rubbing or pruritus, a stiff gait, muscle tremors and fasciculations, carpopedal spasm, and in severe cases seizures and hyperventilation [4]. The facial rubbing is a distinctive early sign that owners often report as the dog trying to scratch its muzzle. Carpopedal spasm, the involuntary flexion of the carpus and tarsus, is the veterinary equivalent of the human Trousseau sign. Behavioral change and circling can also occur [4].

Hemilingual tetany, also called hemilingual spasm, is a rare focal disorder of involuntary unilateral tongue contraction. A case report describes a 5-year-old Border collie with resting unilateral contraction of the right side of the tongue, resulting in curvature of the tongue with intermittent incomplete relaxation, and electromyography revealed fasciculation potentials on the affected side [17]. The signs disappeared during premedication and induction of anesthesia, and imaging found no abnormality of the tongue musculature, brain, or hypoglossal nerves [17]. This case shows that tetany can be focal and benign as well as generalized and life-threatening.

Cattle

Cattle with milk fever often present recumbent without overt tetany. This is a critical species difference. The hypocalcemia of milk fever produces muscle weakness and recumbency more prominently than spasm, so a downer cow after calving should be evaluated for hypocalcemia even without twitching. By contrast, hypomagnesemic tetany in cattle produces the classic picture of muscle twitching, hyperesthesia, and convulsions. The two conditions can coexist, and the clinician must assess both calcium and magnesium.

Horses

Horses are less commonly affected by the classic hypocalcemic tetany syndromes of small animals and cattle, but hypocalcemia and hypomagnesemia can occur with transport, lactation, and certain gastrointestinal disorders. The clinical approach is the same: measure ionized calcium and magnesium, assess acid-base status, and correct the underlying cause.

Birds

Calcium tetany in broiler breeder hens presents as impaired mobility and increased mortality without gross lesions [9]. The absence of lesions means the diagnosis rests on blood ionized calcium measurement, and the study authors emphasize that clinical presentation and necropsy alone can be inaccurate [9].

Amphibians

A tetany-like syndrome has been described in Panamanian golden frogs, characterized by rigid or inappropriately positioned limbs and difficulty hopping, swimming, and righting [18]. A treatment trial found that a combination of calcium, magnesium, and vitamin B complex was significantly more effective than calcium gluconate, magnesium chloride, or supplemental feeding alone in eliminating clinical signs, though the underlying cause remains unknown [18]. This is a reminder that tetany syndromes occur across vertebrate classes and that mineral interactions are often multifactorial.

How Tetany Is Recognized and Tested

Physical examination

The clinician looks for facial twitching, stiff gait, carpopedal spasm, and hyperesthesia. In dogs, facial rubbing and pruritus are common early signs [4]. In cattle, the presence of recumbency without spasm suggests milk fever rather than grass tetany. In all species, the clinician should assess whether the patient can stand, whether the spasm is focal or generalized, and whether there is a history of recent parturition, lactation, surgery, or dietary change.

Provocative tests

The Chvostek sign and Trousseau sign are human clinical correlates that help students understand the mechanism. The Chvostek sign is facial muscle twitching elicited by tapping the facial nerve over the parotid gland. The Trousseau sign is carpal spasm elicited by inflating a blood pressure cuff above systolic pressure for several minutes, which induces ischemia and alkalosis in the forearm. Both signs reflect the same principle: when ionized calcium is low, nerves and muscles fire with minimal provocation. These tests are not routinely performed in veterinary patients, but they illustrate the physiology.

Laboratory testing

Ionized calcium is the definitive measurement. Total calcium, albumin, phosphorus, magnesium, and PTH should also be measured to identify the cause. In dogs with primary hypoparathyroidism, all had marked hypocalcemia with normal or mildly increased albumin, and mean phosphate concentrations were elevated [4]. In broiler breeder hens, affected hens had significantly lower ionized calcium than normal hens in one flock, but not all mobility-impaired hens were hypocalcemic [9]. The lesson is that a single normal total calcium does not exclude tetany, and ionized calcium should be measured whenever the clinical picture is consistent.

Electrocardiography

Hypocalcemia prolongs the QT interval and can cause arrhythmias. Electrocardiography is a useful adjunct in any patient with suspected hypocalcemia, particularly before anesthesia.

Clinical Relevance, Limitations and Common Mistakes

The most common mistake is relying on total calcium alone. Ionized calcium is the fraction that drives neuromuscular excitability, and total calcium can be normal in a patient with low ionized calcium if albumin is low. A second mistake is failing to measure magnesium. Hypomagnesemia impairs PTH secretion and action, so calcium replacement alone will not resolve tetany until magnesium is corrected. A third mistake is assuming that a downer cow has milk fever without checking magnesium, because hypomagnesemic tetany and milk fever can coexist and require different treatments.

A fourth mistake is confusing tetany with tetanus. Tetanus is caused by tetanospasmin from Clostridium tetani, which blocks inhibitory interneurons, and it produces trismus and risus sardonicus with normal ionized calcium. A fifth mistake is overlooking alkalosis as a cause of tetany. Hyperventilation and certain metabolic alkaloses increase calcium binding to albumin, lowering ionized calcium without changing total calcium.

This article is educational and is not a substitute for veterinary diagnosis or treatment. Individual cases require evaluation by a licensed veterinarian who can measure ionized calcium and magnesium, assess acid-base status, and treat the underlying cause.

Quick Review

Ionized calcium, not total calcium, drives neuromuscular excitability. Normal canine iCa is roughly 1.1 to 1.3 mmol/L.
Tetany is a sign of low ionized calcium, hypomagnesemia, alkalosis, or tetanus, not a disease in itself.
PTH and calcitriol are the main defenders of calcium homeostasis, and their actions are distinct but synergistic.
Small animals show facial rubbing, stiff gait, and carpopedal spasm. Cattle with milk fever often present recumbent without overt tetany.
Hypomagnesemia must be corrected before calcium replacement will work.
Tetanus has normal ionized calcium and a wound history. Do not confuse it with hypocalcemic tetany.
Measure ionized calcium and magnesium in any patient with unexplained muscle spasm or recumbency.

Frequently Asked Questions

What is tetany in veterinary medicine?

Tetany is a syndrome of involuntary sustained muscle contraction caused by excessive excitability of motor nerves and muscle fibers, most often due to low ionized calcium.

Is tetany the same as tetanus?

No. Tetany is a sign of metabolic or electrolyte disturbance, while tetanus is a specific infection caused by Clostridium tetani that blocks inhibitory neurons.

Why do cows with milk fever not always show tetany?

Milk fever hypocalcemia often produces muscle weakness and recumbency more prominently than spasm, so overt tetany may be absent.

What is the difference between total calcium and ionized calcium?

Total calcium includes protein-bound and complexed calcium, while ionized calcium is the free, biologically active fraction that determines neuromuscular excitability.

Can hypomagnesemia cause tetany without hypocalcemia?

Yes. Low magnesium impairs PTH secretion and action, and tetany can occur with low or normal ionized calcium until magnesium is corrected.

What are Chvostek and Trousseau signs?

They are human clinical tests for latent tetany. Chvostek is facial twitching from tapping the facial nerve, and Trousseau is carpal spasm from forearm ischemia.