Hypocalcemia in cattle, also known as “milk fever” or “parturient paresis,” is a metabolic disorder characterized by abnormally low levels of calcium in the blood. This condition primarily affects dairy cows around the time of calving, the peripartum or transition period. During this phase, the cow’s body faces an immense and sudden demand for calcium for colostrum and milk production. Hypocalcemia is a significant concern in cattle health and production due to its widespread occurrence and causing substantial health problems.
Understanding Calcium’s Role and Hypocalcemia’s Onset
Calcium is a fundamental mineral, playing diverse roles in physiological processes. It is involved in muscle function, nerve transmission, blood clotting, and skeletal integrity. Approximately 98% of the body’s calcium is stored in bones and teeth, with the remainder circulating in body fluids as ions.
The body maintains a stable calcium balance, known as calcium homeostasis, through a regulatory system involving hormones like parathyroid hormone (PTH) and vitamin D3. PTH increases blood calcium by promoting its absorption from the intestine, reabsorption in the kidneys, and mobilization from bone stores. Vitamin D also supports calcium absorption and bone storage.
The transition period, typically three weeks before and after calving, represents a demanding phase for dairy cows. During this time, the calcium requirement escalates dramatically, increasing by approximately 400% compared to the dry period. A cow producing 10 liters of colostrum can lose around 20 to 30 grams of calcium in a single day, an amount significantly exceeding her entire blood plasma calcium. While the cow’s body attempts to adapt by mobilizing calcium from bones and increasing intestinal absorption, these mechanisms often cannot meet the sudden, massive outflow into milk, leading to a drop in blood calcium.
Recognizing Hypocalcemia
Hypocalcemia manifests in two main forms: clinical and subclinical. Clinical hypocalcemia, also called “milk fever,” presents with observable signs. Subclinical hypocalcemia is common, affecting a large proportion of dairy cows, with estimates ranging from 25% to 50% in early-lactation multiparous cows, and potentially over 50% in all dairy cows at or near calving.
Clinical hypocalcemia progresses through three stages, with worsening symptoms. In Stage 1, cows may exhibit hypersensitivity and excitability, restlessness, fine tremors, ear twitching, and head bobbing, while remaining standing. If untreated, the condition can advance to Stage 2, where the cow is unable to stand but can maintain a sternal (chest down) position. Signs at this stage include anorexia, confusion, a dry muzzle, cold extremities, subnormal body temperature, and a weak heart rate. Smooth muscle paralysis can lead to gastrointestinal stasis, bloat, and inability to urinate or defecate; cows often tuck their heads into their flanks or display an S-shaped curve to the neck.
Stage 3 represents the severe form, characterized by a progressive loss of consciousness leading to a coma. The cow is unable to maintain sternal recumbency, experiencing muscle flaccidity and unresponsiveness. The heart rate may approach 120 beats per minute, with undetectable peripheral pulses. Without prompt intervention, cows in Stage 3 survive only a few hours. Diagnosis of subclinical hypocalcemia typically requires blood tests to measure calcium levels within the first one to two days after calving.
Managing and Preventing Hypocalcemia
Immediate treatment for clinical hypocalcemia often involves intravenous (IV) calcium administration. Commonly, 500 milliliters of 23% calcium gluconate is administered slowly into the jugular vein, with heart monitoring. If cardiac arrhythmias occur, calcium administration should be temporarily stopped, then resumed at a slower rate. Oral calcium gels or pastes (50-70 grams calcium per dose) can be used for milder cases or as follow-up after IV calcium. They are absorbed within 30 minutes, increasing blood calcium for four to six hours. Oral calcium is generally recommended for standing cows; IV calcium is the treatment of choice for recumbent animals.
Prevention strategies are important, often more effective and cost-efficient than treating active cases. Dietary management during the dry period is a primary focus. A widely adopted method involves feeding a negative Dietary Cation-Anion Difference (DCAD) diet for at least 21 days before calving. This diet induces a mild metabolic acidosis, enhancing the cow’s responsiveness to parathyroid hormone and improving calcium mobilization from bones and gut absorption in preparation for lactation. Anionic salts (e.g., magnesium sulfate, calcium chloride, or magnesium chloride) are added to the diet to achieve a negative DCAD. Target urine pH values for Holstein cows are typically between 6.2 and 6.8.
Calcium restriction in the dry period is another approach to stimulate the cow’s calcium regulatory system before calving. This involves limiting calcium intake to less than 100 grams per cow per day, often by selecting low-calcium forages (e.g., grain silages or grasses, 0.4-0.8% calcium) instead of high-calcium forages (e.g., alfalfa, over 2% calcium). Magnesium supplementation is also important, influencing calcium homeostasis. Vitamin D supplementation (typically 20,000-30,000 IU/day) also supports calcium absorption and bone reserves. However, very high doses (e.g., up to 10 million IU) given pre-calving can be effective but carry a toxicity risk.
Management practices around calving also contribute to prevention. Maintaining dry cows at an appropriate body condition score (3.0-3.5) and preventing excessive weight gain or loss during the dry period are beneficial. Minimizing calving stress and ensuring adequate water intake also support their metabolism. Providing oral calcium supplements immediately after calving, especially for high-producing or older cows, can minimize the risk of clinical milk fever.
Consequences of Hypocalcemia
Hypocalcemia can have far-reaching consequences for cow health and farm operations. It directly impacts milk production, often reducing milk yield and potentially milk quality. It can also impair feed intake and rumen function, further decreasing productivity. Studies show that cows with subclinical hypocalcemia may produce less milk in early lactation, with some studies indicating a 3.5-7 pound daily decrease in affected cows compared to healthy ones.
Beyond direct milk production losses, hypocalcemia is strongly linked to an increased incidence of other periparturient diseases. Impaired immune function and muscle contraction from low calcium make cows more susceptible to conditions like retained placenta, metritis (uterine infection), ketosis, and displaced abomasum. For instance, cows with subclinical hypocalcemia are 3.4 to 5.5 times more likely to experience retained placenta, ketosis, or metritis compared to cows with normal calcium levels.
The negative effects extend to reproductive performance; hypocalcemia contributes to delayed estrus (return to cycling), reduced conception rates, and longer calving intervals. Cows with chronic subclinical hypocalcemia may take longer to show active ovaries and have lower first-service pregnancy odds. These challenges result in significant economic losses for dairy farms, including veterinary costs, treatment expenses, reduced milk sales, increased culling rates, and diminished lifetime productivity.