Puerperal Tetany / Eclampsia (Postpartum Hypocalcemia)

Puerperal tetany, also known as eclampsia or postpartum hypocalcemia, is an acute, life-threatening metabolic emergency characterized by a rapid decline in serum ionized calcium concentrations below critical thresholds, typically <0.8 mmol/L (or total calcium <6.5 mg/dL in dogs), occurring most commonly in small-breed bitches during the first 1 to 4 weeks of lactation, although it can also occur in queens and, rarely, in other domestic species. The condition arises from an imbalance between the massive calcium demands of lactation (milk production) and the maternal homeostatic mechanisms (intestinal absorption, bone resorption, and renal conservation) that are often overwhelmed, particularly in primiparous or small-litter bitches. Clinically, eclampsia manifests as a spectrum of neuromuscular signs ranging from restlessness, panting, and muscle fasciculations to severe tetany, seizures, hyperthermia, and death if untreated. The disease is a classic example of a metabolic emergency in theriogenology, requiring immediate recognition and aggressive calcium supplementation to prevent fatal outcomes. In veterinary reproduction, eclampsia is distinct from preeclampsia in humans, as it is purely a hypocalcemic state without hypertensive or proteinuric components. The condition is also referred to as lactation tetany, puerperal hypocalcemia, or milk fever in small animals, though the latter term is more commonly used in cattle. The pathophysiology involves a failure of parathyroid hormone (PTH) and calcitriol (1,25-dihydroxyvitamin D) to mobilize calcium rapidly enough from skeletal stores, often exacerbated by a high-calcium diet during gestation that suppresses the parathyroid glands, leading to an inability to respond to the sudden calcium drain at parturition and peak lactation. The disease is a true medical emergency, and prompt intravenous calcium gluconate administration is the cornerstone of therapy, followed by oral calcium and vitamin D supplementation, dietary modification, and, in severe or recurrent cases, early weaning of the litter.

The primary etiology of puerperal tetany is an acute, severe hypocalcemia resulting from the excessive loss of calcium into milk during lactation, which exceeds the maternal capacity to maintain normocalcemia. The condition is most commonly triggered by the onset of lactation, with peak milk production occurring around 2 to 3 weeks postpartum in bitches. The underlying causes include: (1) Inadequate dietary calcium intake during lactation, particularly in bitches fed unbalanced homemade diets or diets with excessive calcium during gestation, which suppresses the parathyroid glands and reduces the ability to mobilize calcium from bone; (2) Impaired parathyroid hormone (PTH) secretion or action, leading to reduced bone resorption and renal calcium reabsorption; (3) Decreased intestinal calcium absorption due to vitamin D deficiency or intestinal malabsorption; (4) Increased calcium demand due to large litter size, high milk production, or prolonged lactation; (5) Endocrine imbalances, such as excessive calcitonin secretion or relative hypoparathyroidism; (6) Iatrogenic factors, including the administration of corticosteroids or diuretics that can lower serum calcium; (7) In queens, the condition is less common but can occur with heavy lactation; (8) In rare cases, primary hypoparathyroidism or renal disease may predispose to hypocalcemia, but these are not typical causes of puerperal tetany. The disease is not infectious or genetic in origin, but breed and size predispositions are recognized, with small and toy breeds such as Chihuahuas, Pomeranians, Miniature Poodles, and Yorkshire Terriers being at highest risk. The exact cellular mechanism involves a rapid drop in extracellular ionized calcium, which increases neuronal membrane excitability by reducing the threshold for action potential generation, leading to spontaneous nerve firing, muscle fasciculations, and tetany. The condition is exacerbated by concurrent alkalosis, which increases calcium binding to albumin, further reducing ionized calcium levels.

Puerperal tetany is predominantly a disease of small-breed bitches, with a reported incidence of approximately 5-10% in some high-risk breeds, though the overall incidence in the general canine population is lower (around 1-2%). The condition is most commonly seen in primiparous bitches (first pregnancy) and in those with small body weight (<10 kg), particularly breeds such as Chihuahua, Pomeranian, Toy Poodle, Yorkshire Terrier, Miniature Pinscher, and Shih Tzu. The disease typically occurs during the first 1 to 4 weeks of lactation, with a peak incidence around 2 to 3 weeks postpartum, coinciding with peak milk production. It is less common in queens, but can occur in queens with large litters or heavy lactation, especially in Siamese and other small breeds. The condition is rare in large-breed dogs and in other domestic species such as cattle (where it is called milk fever) and sheep, but the pathophysiology is similar. Age is a risk factor, with young bitches (2-4 years) being more commonly affected, likely due to their smaller body size and higher calcium demands relative to their skeletal reserves. Parity is also a risk factor, as primiparous bitches are more susceptible, but the condition can recur in subsequent pregnancies. Breeding management factors, such as feeding a high-calcium diet during gestation, can increase the risk by suppressing the parathyroid glands. The disease is not associated with any specific infectious agent, and there is no sex predilection beyond the female reproductive state. The incidence may be higher in kennel environments where bitches are bred frequently, but this is likely due to nutritional and management factors rather than a true genetic predisposition. Overall, the disease is a significant cause of maternal morbidity and mortality in small-breed dogs if not treated promptly.

The pathophysiology of puerperal tetany revolves around a critical imbalance in calcium homeostasis. During gestation, the fetus requires calcium for skeletal development, and the dam's calcium requirements increase, but the major drain occurs during lactation. In the immediate postpartum period, colostrum and milk contain high concentrations of calcium (approximately 200-300 mg/L in dogs), and a lactating bitch can lose 2-3 grams of calcium per day in milk, which is a significant proportion of her total body calcium pool. To maintain normocalcemia, the body relies on three main mechanisms: (1) intestinal absorption of dietary calcium, (2) renal tubular reabsorption of calcium, and (3) bone resorption. These processes are regulated by parathyroid hormone (PTH), calcitriol (1,25-dihydroxyvitamin D), and calcitonin. In normal animals, a slight decrease in serum ionized calcium stimulates PTH secretion, which increases bone resorption, renal calcium reabsorption, and renal production of calcitriol, which in turn enhances intestinal calcium absorption. However, in bitches that have been fed a high-calcium diet during gestation, the parathyroid glands become suppressed (functional hypoparathyroidism), and the intestinal absorption of calcium is downregulated. At parturition and the onset of lactation, the sudden and massive demand for calcium overwhelms these compensatory mechanisms, leading to a rapid decline in serum calcium levels. The drop in ionized calcium increases the excitability of neuronal and muscle cell membranes, as calcium ions are essential for stabilizing the sodium channels and regulating neurotransmitter release. When ionized calcium falls below a critical threshold, spontaneous action potentials occur, leading to muscle fasciculations, tetany, and seizures. Additionally, hypocalcemia can impair cardiac contractility and cause arrhythmias, and it can affect smooth muscle function, leading to gastrointestinal signs such as vomiting and diarrhea. The condition is exacerbated by metabolic alkalosis, which can occur due to hyperventilation (panting) or vomiting, as alkalosis increases calcium binding to albumin, further reducing ionized calcium levels. The disease is self-perpetuating if not treated, as the stress of tetany and seizures can lead to hyperthermia, respiratory distress, and cardiovascular collapse, ultimately resulting in death. In summary, the pathophysiology is a failure of calcium homeostatic mechanisms to meet the demands of lactation, leading to a life-threatening hypocalcemic state.

Several intrinsic and extrinsic factors predispose to puerperal tetany. Intrinsic factors include: (1) Small body size and low body weight, as smaller animals have lower total body calcium reserves relative to their milk production; (2) Primiparity, as first-time mothers may have less developed calcium homeostatic mechanisms; (3) Breed predisposition, with small and toy breeds being at highest risk; (4) Large litter size, which increases the total calcium demand; (5) High milk production, which is influenced by genetics and litter size; (6) Age, with young bitches (2-4 years) being more commonly affected; (7) Underlying subclinical hypoparathyroidism or vitamin D deficiency; (8) Concurrent diseases that affect calcium metabolism, such as renal disease or pancreatitis. Extrinsic factors include: (1) Inappropriate nutrition, particularly feeding a high-calcium diet during gestation, which suppresses the parathyroid glands and reduces the ability to mobilize calcium; (2) Feeding a diet with an improper calcium-to-phosphorus ratio (ideal is 1.2:1 to 1.4:1); (3) Inadequate dietary calcium intake during lactation, especially in bitches fed homemade diets or diets not formulated for lactation; (4) Stress, such as environmental changes, overcrowding, or poor kenneling conditions; (5) Excessive handling or exercise during lactation; (6) Iatrogenic factors, such as the administration of corticosteroids or diuretics that can lower serum calcium; (7) In queens, similar factors apply, but the condition is less common. Management practices that can reduce the risk include feeding a balanced, high-quality commercial diet formulated for lactation, avoiding excessive calcium supplementation during gestation, and ensuring adequate calcium intake during lactation. Early recognition of prodromal signs, such as restlessness and panting, can allow prompt intervention and prevent progression to severe tetany.

The clinical signs of puerperal tetany can be divided into prodromal, moderate, and severe stages. Prodromal signs, which may be subtle and easily overlooked, include restlessness, anxiety, panting, pacing, whining, and mild muscle tremors. The bitch may appear agitated and may refuse to nurse the puppies. As hypocalcemia worsens, moderate signs develop, including muscle fasciculations and twitching, particularly of the face and ears, stiff gait, ataxia, and hypersalivation. The animal may show signs of hyperesthesia, becoming overly sensitive to touch or sound. Vomiting and diarrhea may occur due to smooth muscle dysfunction. In the severe stage, the bitch develops tonic-clonic seizures, severe tetany with opisthotonos (arching of the back), and extensor rigidity of the limbs. The body temperature may rise significantly (hyperthermia >40°C) due to muscle activity and seizures, which can lead to secondary brain damage. The mucous membranes may be pale or cyanotic, and the heart rate may be elevated or irregular due to cardiac arrhythmias. In some cases, the bitch may collapse and become comatose. Physical examination findings include hyperthermia, tachycardia, tachypnea, and muscle rigidity. The mammary glands are typically engorged and milk production is evident. Neurological examination reveals hyperreflexia, muscle fasciculations, and seizures. The severity of clinical signs correlates with the degree and rapidity of the fall in ionized calcium. It is important to note that the clinical signs are not specific to hypocalcemia and can be seen in other conditions such as hypoglycemia, toxin exposure, or epilepsy, so a thorough diagnostic workup is essential. In queens, the signs are similar but may be less severe, and they may also exhibit behavioral changes such as aggression or hiding. Prompt recognition and treatment are critical, as the condition can be fatal within hours if left untreated.

The differential diagnoses for puerperal tetany include: (1) Hypoglycemia: Often occurs in small-breed bitches during lactation due to increased glucose demand; clinical signs include weakness, tremors, seizures, and collapse. Blood glucose measurement (<60 mg/dL) distinguishes it from hypocalcemia. (2) Toxin exposure: Such as ethylene glycol (antifreeze), strychnine, metaldehyde (slug bait), or organophosphates; these can cause seizures and muscle tremors. History of exposure and specific toxicological tests are needed. (3) Epilepsy: Idiopathic epilepsy can cause seizures in adult dogs, but it is not typically associated with lactation. Electroencephalography and response to anticonvulsants may help. (4) Eclampsia (as a differential for other causes of seizures) – but here we are considering other causes of similar signs. (5) Uterine rupture or peritonitis: Can cause systemic signs, fever, and abdominal pain, but not typically tetany. Abdominal ultrasound and radiography are useful. (6) Metritis: Postpartum uterine infection can cause fever, lethargy, and vaginal discharge, but not typically tetany. (7) Mastitis: Infection of the mammary glands can cause fever, pain, and swelling, but not tetany. (8) Hypoparathyroidism: Primary hypoparathyroidism can cause chronic hypocalcemia and tetany, but it is not associated with lactation. Serum PTH levels are low. (9) Hyperkalemia or other electrolyte imbalances: Can cause muscle weakness and cardiac arrhythmias. Serum electrolyte panel is essential. (10) Neurological disorders: Such as meningitis or encephalitis, can cause seizures and neurological signs. Cerebrospinal fluid analysis may be needed. The key differentiating feature is the measurement of serum ionized calcium, which is low in eclampsia. Additionally, the history of recent parturition and lactation, along with the characteristic clinical signs, strongly supports the diagnosis.

The diagnostic algorithm for puerperal tetany should be systematic and rapid, as the condition is an emergency. Step 1: Clinical triage – Assess the patient's stability, including airway, breathing, and circulation. If the animal is seizing or in severe tetany, immediate emergency treatment (calcium administration) may be initiated before diagnostic confirmation, but blood samples should be collected before treatment if possible. Step 2: Obtain a thorough history, including the time of parturition, number of puppies, lactation status, diet, and any previous episodes. Step 3: Perform a complete physical examination, with special attention to temperature, heart rate, respiratory rate, mucous membranes, and neurological status. Step 4: Collect blood samples for serum biochemistry, including total and ionized calcium, phosphorus, magnesium, glucose, and renal parameters. Also, collect a complete blood count and possibly a blood gas analysis to assess acid-base status. Step 5: If the diagnosis is uncertain, consider additional tests such as serum PTH and vitamin D levels, but these are not typically needed in the acute setting. Step 6: Perform a urinalysis to rule out renal disease. Step 7: In cases where the diagnosis is not clear, or if there is suspicion of other postpartum complications, abdominal ultrasound may be performed to evaluate the uterus and ovaries, and thoracic radiographs may be indicated if there is respiratory distress. Step 8: The definitive diagnosis is based on the presence of clinical signs consistent with hypocalcemia, a history of recent parturition and lactation, and a serum ionized calcium concentration below the reference range (typically <0.8 mmol/L in dogs). Total calcium may be used, but ionized calcium is more accurate. Step 9: Once the diagnosis is confirmed, treatment should be initiated immediately. The diagnostic algorithm should be efficient to avoid delays in therapy, as the condition can be fatal within hours.

The hallmark laboratory finding in puerperal tetany is hypocalcemia. Serum ionized calcium is the most accurate measure, with levels below 0.8 mmol/L (or <8 mg/dL total calcium in dogs) being diagnostic. Total calcium may be affected by albumin levels, so ionized calcium is preferred. Other laboratory findings may include: (1) Hypophosphatemia, as phosphorus is also lost in milk and may be low; (2) Hypermagnesemia or hypomagnesemia, though magnesium levels are often normal; (3) Hyperglycemia or hypoglycemia, depending on the stress response and concurrent conditions; (4) Elevated blood urea nitrogen (BUN) and creatinine, which may indicate dehydration or renal dysfunction; (5) Elevated liver enzymes (ALT, AST) due to muscle damage from seizures or tetany; (6) Elevated creatine kinase (CK) due to muscle fasciculations and seizures; (7) Metabolic alkalosis, as assessed by blood gas analysis, due to hyperventilation and vomiting; (8) Complete blood count may show a stress leukogram (neutrophilia, lymphopenia) or signs of infection if metritis or mastitis is present; (9) Urinalysis may show proteinuria or casts if there is renal involvement. In addition, serum PTH levels may be low or inappropriately normal, and vitamin D levels may be low, but these tests are not routinely performed in the acute setting. Vaginal cytology is not typically performed for this condition, but if done, it may show postpartum changes such as the presence of parabasal and intermediate cells, with few neutrophils. Uterine or vaginal cultures are not indicated unless there is suspicion of infection. Overall, the key laboratory finding is hypocalcemia, and other abnormalities are secondary to the metabolic disturbance.

Imaging is not typically required for the diagnosis of puerperal tetany, as the diagnosis is based on clinical signs and laboratory findings. However, imaging may be used to rule out other conditions or to assess for complications. Abdominal ultrasonography may be performed to evaluate the uterus and ovaries, particularly if there is suspicion of metritis, retained placenta, or uterine rupture. In a normal postpartum bitch, the uterus is involuting, and the uterine wall may be thickened with some fluid accumulation. Ultrasonography can also assess the mammary glands for mastitis, which may appear as increased echogenicity and fluid-filled areas. Radiography of the abdomen may be used to evaluate for fetal remnants or to assess the size of the uterus, but it is not specific for hypocalcemia. Thoracic radiographs may be indicated if there is respiratory distress, to rule out aspiration pneumonia or pulmonary edema. Echocardiography may be performed if cardiac arrhythmias are present, but this is not routine. In general, imaging is not necessary for the diagnosis of eclampsia, and the primary diagnostic tools are history, physical examination, and serum calcium measurement. However, if the animal does not respond to treatment or if there are atypical signs, imaging may be helpful to identify concurrent diseases.

Cytology and histopathology are not typically used in the diagnosis of puerperal tetany, as the condition is a metabolic disorder. However, vaginal cytology may be performed to assess the postpartum reproductive status, but it is not diagnostic for hypocalcemia. In the postpartum period, vaginal cytology typically shows a mixture of parabasal, intermediate, and superficial cells, with a variable number of neutrophils and red blood cells. The presence of bacteria is common and not necessarily indicative of infection. Histopathology is not indicated for this condition, as there are no specific tissue changes. If a biopsy were taken, it might show changes related to lactation, such as mammary gland hyperplasia, but this is not relevant to the diagnosis. In cases where the animal dies, a necropsy may be performed, and histopathology of the parathyroid glands might show atrophy or hyperplasia, but this is not a standard diagnostic procedure. Therefore, cytology and histopathology have no role in the routine diagnosis of puerperal tetany.

The treatment of puerperal tetany is an emergency and should be initiated immediately upon suspicion or confirmation of hypocalcemia. The primary goal is to rapidly restore serum calcium levels to normal. The treatment protocol includes: (1) Emergency stabilization: If the animal is seizing or in severe tetany, administer a benzodiazepine such as diazepam (0.5-1 mg/kg IV) or midazolam (0.2-0.3 mg/kg IV) to control seizures. Also, provide supportive care, including intravenous fluids (e.g., lactated Ringer's solution) to correct dehydration and electrolyte imbalances, and cooling measures if hyperthermia is present. (2) Calcium supplementation: Administer 10% calcium gluconate solution at a dose of 0.5-1.5 mL/kg (50-150 mg/kg) slowly intravenously over 10-30 minutes, with continuous electrocardiographic (ECG) monitoring to detect bradycardia or arrhythmias. The infusion should be stopped if the heart rate decreases or if arrhythmias occur. After the initial bolus, a maintenance infusion of calcium gluconate (10-20 mg/kg/hour) may be given in severe cases, but this is rarely needed. (3) Oral calcium and vitamin D: After the acute crisis is resolved, begin oral calcium supplementation (calcium carbonate or calcium gluconate) at a dose of 25-50 mg/kg/day divided every 8-12 hours, along with vitamin D (calcitriol) at a dose of 0.02-0.03 mcg/kg/day, to enhance intestinal calcium absorption. (4) Dietary management: Switch the bitch to a high-quality, balanced commercial diet formulated for lactation, and avoid excessive calcium supplementation during gestation. The diet should have a calcium-to-phosphorus ratio of approximately 1.2:1 to 1.4:1. (5) Management of the litter: If the condition is severe or recurrent, consider weaning the puppies early (at 3-4 weeks of age) and feeding them a commercial milk replacer. This reduces the calcium demand on the bitch. (6) Treatment of concurrent conditions: If metritis or mastitis is present, treat with appropriate antibiotics and supportive care. (7) Monitoring: Monitor serum calcium levels every 6-12 hours until stable, and monitor the bitch for any signs of recurrence. In cases where medical management fails or if the owner does not wish to breed the bitch again, ovariohysterectomy may be recommended to prevent future episodes. The prognosis is excellent with prompt treatment, but the condition can be fatal if untreated.

The prognosis for puerperal tetany is generally excellent if the condition is recognized and treated promptly. With appropriate intravenous calcium administration, most bitches recover within 30-60 minutes, and the mortality rate is low (<5%) in treated cases. However, the prognosis is guarded if treatment is delayed, if the animal has severe hyperthermia or seizures, or if there are concurrent diseases such as metritis or mastitis. The short-term prognosis is good, but the long-term prognosis depends on the underlying cause and the management of the litter. If the bitch is allowed to continue nursing, there is a risk of recurrence, especially if the dietary and management factors are not corrected. The recurrence rate in subsequent pregnancies is estimated to be 20-50%, particularly in small-breed bitches. Therefore, it is important to advise the owner about preventive measures, such as dietary management and early weaning. The future fertility of the bitch is not typically affected, and she can be bred again, but the risk of recurrence should be discussed. In cases where the condition is severe or recurrent, ovariohysterectomy may be recommended to prevent future episodes, which would render the bitch infertile. Overall, the prognosis is favorable with appropriate treatment and management.

Follow-up care for puerperal tetany is essential to prevent recurrence and to monitor the health of the bitch and her litter. After the acute episode, the bitch should be monitored closely for 24-48 hours, with serial serum calcium measurements every 6-12 hours until normocalcemia is maintained. The owner should be instructed to monitor the bitch for any signs of recurrence, such as restlessness, panting, or muscle tremors, and to seek veterinary care immediately if these occur. The oral calcium and vitamin D supplementation should be continued for at least 1-2 weeks, and the diet should be adjusted to a high-quality lactation formula. The puppies should be monitored for adequate weight gain, and if the bitch is unable to nurse, the puppies should be fed a commercial milk replacer. A recheck examination should be scheduled 1 week after the initial episode to assess the bitch's overall health, serum calcium levels, and the condition of the mammary glands. If the bitch is to be bred again, the owner should be advised to avoid excessive calcium supplementation during gestation and to feed a balanced diet. In cases where the condition is recurrent or severe, early weaning of the puppies at 3-4 weeks of age may be recommended. If ovariohysterectomy is performed, the follow-up care is routine for that surgery. Overall, the follow-up should be tailored to the individual case, with emphasis on preventive measures.

Clinical pearls: (1) Always measure ionized calcium, not just total calcium, as total calcium can be falsely normal in cases of hypoalbuminemia. (2) Administer calcium gluconate slowly (over 10-30 minutes) with ECG monitoring to avoid cardiac arrhythmias. (3) In seizing animals, control seizures first with diazepam or midazolam before or during calcium administration. (4) Check blood glucose levels, as hypoglycemia can coexist with hypocalcemia and may also cause seizures. (5) Consider the possibility of concurrent metritis or mastitis, which can exacerbate the condition. (6) Advise owners to feed a balanced lactation diet and avoid excessive calcium supplementation during gestation. (7) In recurrent cases, early weaning of the puppies is the most effective preventive measure. (8) If the bitch is not intended for future breeding, ovariohysterectomy eliminates the risk of recurrence. Pitfalls: (1) Administering calcium too rapidly can cause bradycardia, cardiac arrest, or tissue necrosis if extravasated. (2) Using calcium chloride instead of calcium gluconate, as calcium chloride is more irritating and can cause severe tissue damage. (3) Failing to monitor the ECG during calcium infusion. (4) Treating the animal for epilepsy or other neurological conditions without checking calcium levels. (5) Overlooking the possibility of hypomagnesemia, which can impair the response to calcium therapy. (6) Not addressing the dietary and management factors, leading to recurrence. (7) Delaying treatment while waiting for laboratory results, as the condition is an emergency. (8) Inadequate follow-up, leading to recurrence or complications.

The following drug protocols are based on Plumb's Veterinary Drug Handbook and current theriogenology guidelines. (1) Calcium gluconate 10% solution: For acute hypocalcemia, administer 0.5-1.5 mL/kg (50-150 mg/kg) IV slowly over 10-30 minutes, with ECG monitoring. The infusion should be stopped if bradycardia or arrhythmias occur. A maintenance infusion of 10-20 mg/kg/hour may be given in severe cases, but is rarely needed. (2) Diazepam: 0.5-1 mg/kg IV for seizure control, can be repeated as needed. (3) Midazolam: 0.2-0.3 mg/kg IV or IM for seizure control. (4) Oral calcium carbonate: 25-50 mg/kg/day divided every 8-12 hours, for 1-2 weeks. (5) Calcitriol (1,25-dihydroxyvitamin D): 0.02-0.03 mcg/kg/day PO, for 1-2 weeks. (6) For concurrent metritis or mastitis, antibiotics such as amoxicillin-clavulanate (12.5-25 mg/kg PO q8h) or cephalexin (22 mg/kg PO q8h) may be used. (7) For supportive care, intravenous fluids such as lactated Ringer's solution at maintenance rates (60-90 mL/kg/day) may be given. (8) In cases of hyperthermia, cooling measures such as ice packs or cool water baths should be used. (9) If the animal is not intended for breeding, ovariohysterectomy may be recommended. All dosages should be adjusted based on the individual patient's condition and response to therapy.

The evidence base for the management of puerperal tetany is largely derived from clinical experience and retrospective studies, as prospective randomized controlled trials are limited due to the emergency nature of the condition. Key points from the literature include: (1) The condition is most common in small-breed bitches, with a peak incidence in the first 2-3 weeks of lactation (Johnston et al., 2001). (2) Ionized calcium is the preferred diagnostic test, and levels below 0.8 mmol/L are diagnostic (Feldman and Nelson, 2004). (3) Intravenous calcium gluconate is the treatment of choice, and rapid administration can be life-saving (Plumb, 2018). (4) The use of oral calcium and vitamin D supplementation after the acute episode is recommended to prevent recurrence (Kustritz, 2006). (5) Dietary management, including avoiding excessive calcium during gestation, is crucial for prevention (Root Kustritz, 2010). (6) Early weaning is an effective preventive measure in recurrent cases (England and von Heimendahl, 2010). (7) The recurrence rate in subsequent pregnancies is significant, and owners should be counseled accordingly (Johnston et al., 2001). (8) There is no evidence to support the routine use of magnesium supplementation unless hypomagnesemia is documented (Feldman and Nelson, 2004). (9) The prognosis is excellent with prompt treatment, but mortality can occur if treatment is delayed (Kustritz, 2006). (10) Consensus guidelines from the American College of Theriogenologists (ACT) and the European Society for Small Animal Reproduction (EVSSAR) emphasize the importance of client education and preventive measures. Overall, the literature supports a standardized approach to diagnosis and treatment, with a focus on emergency stabilization and long-term management.