Treatment including addressing the cause, such as improving the diet, treating diarrhea, or stopping an offending medication. People without a significant source of potassium loss and who show no symptoms of hypokalemia may not require treatment.

Mild hypokalemia (>3.0 meq/l) may be treated with oral potassium chloride supplements (Klor-Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as leafy green vegetables, avocados, tomatoes, coconut water, citrus fruits, oranges, or bananas. Both dietary and pharmaceutical supplements are used for people taking diuretic medications.

Severe hypokalemia (<3.0 meq/l) may require intravenous supplementation. Typically, a saline solution is used, with 20–40 meq/l KCl per liter over 3–4 hours. Giving IV potassium at faster rates (20–25 meq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A generally safe rate is 10 meq/hr. Even in severe hypokalemia, oral supplementation is preferred given its safety profile. Sustained-release formulations should be avoided in acute settings.

Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic, such as amiloride, triamterene, spironolactone, or eplerenone. Concomitant hypomagnesemia will inhibit potassium replacement, as magnesium is a cofactor for potassium uptake.

When replacing potassium intravenously, infusion by a central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral infusion, or the rare occurrence of damage to the vein. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of KCl per 50 ml of fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors.

Treatment of HSH involves administration of high doses of magnesium salts. These salts may be taken orally or otherwise (e.g. subcutaneously). This treatment works by increasing magnesium absorption through the non-TRPM6 mediated paracellular uptake pathways. This treatment must be continued throughout life.

Management of this condition includes|:

- Intravenous calcium gluconate 10% can be administered, or if the hypocalcaemia is severe, calcium chloride is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac electrical instability, and associated symptoms are then not cured or relieved by prompt administration of corrective doses of calcium, but rather exacerbated. Such rapid administration of calcium would result in effective over correction – symptoms of hypercalcemia would follow.

- However, in either circumstance, maintenance doses of both calcium and vitamin-D (often as 1,25-(OH)-D, i.e. calcitriol) are often necessary to prevent further decline

Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium supplementation is often sufficient. In more severe cases the following treatments are used:

- Intravenous calcium gluconate, because the actions of magnesium in neuromuscular and cardiac function are antagonized by calcium.

Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:

- Intravenous diuretics, in the presence of normal kidney function

- Dialysis, when kidney function is impaired and the patient is symptomatic from hypermagnesemia

High phosphate levels can be avoided with phosphate binders and dietary restriction of phosphate. If the kidneys are operating normally, a saline diuresis can be induced to renally eliminate the excess phosphate. In extreme cases, the blood can be filtered in a process called hemodialysis, removing the excess phosphate.

Treatment includes spironolactone, a potassium-sparing diuretic that works by acting as an aldosterone antagonist.

Proper dietary management will prevent most cases of milk fever. This generally involves close attention to mineral and fiber levels in the diet prior to calving, as well as improving cow comfort to eliminate other problems that may interfere with appetite and so trigger hypocalcemia.

Oral administration of a dose of a calcium salt in a gel has been advised by some veterinarians.

An orally administered bolus containing a much higher concentration of calcium than the injectable solutions can also be given so long as the cow is standing or sitting up. If the cow is lying 'flat out' then immediate intravenous therapy is required to avoid death.

Risk factors of early neonatal hypocalcemia

- Prematurity

- Perinatal asphyxia

- Diabetes mellitus in the mother

- Maternal hyperparathyroidism

- Intrauterine growth retardation (IUGR)

- Iatrogenic

Risk factors of late neonatal hypocalcemia

- Exogenous phosphate load

- Use of gentamicin

- Gender and ethnic: late neonatal hypocalcemia occurred more often in male infants and Hispanic infants

- Others

Treatment consists of vitamin K supplementation. This is often given prophylactically to newborns shortly after birth.

Treatment generally involves calcium injection by intravenous, intramuscular or subcutaneous routes. Before calcium injection was employed, treatment comprised inflation of the udder using a pneumatic pump. Inflation of the udder worked because the increased pressure created in the udder pushed the calcium in the udder back into the bloodstream of the cow.

Intravenous calcium, though indicated in many cases, is potentially fatal through "heart blockade", or transient high calcium levels stopping the heart, so should be administered with care.

Cows are to be fed jaggery along with the lime water mixture.

In unclear cases of downer cows, intravenous calcium injection can lead to diagnosis. The typical reaction will be a generalized tremor of the skeletal muscles, and sometimes cardiac arrhythmia. Defecation, urination and eructation are frequent during the treatment, due to pharmacological effect of calcium on the smooth muscles.

Neonatal hypocalcemia is an abnormal clinical and laboratory hypocalcemia condition that is frequently observed in infants.[1]

Healthy term infants go through a physiological nadir of serum calcium levels at 7.5 - 8.5 mg/dL by day 2 of life. Hypocalcemia is a low blood calcium level. A total serum calcium of less than 8 mg/dL (2mmol/L) or ionized calcium less than 1.2 mmol/L in term neonates is defined as hypocalcemia. In preterm infants, it is defined as less than 7mg/dL (1.75 mmol/L) total serum calcium or less than 4mg/dL (1 mmol/L) ionized calcium. [2]

Both early onset hypocalcemia (presents within 72h of birth) and late onset hypocalcemia (presents in 3-7 days after birth) require calcium supplementation treatment.

Bed rest has not been found to improve outcomes and therefore is not typically recommended.

Mothers whose fetus is diagnosed with intrauterine growth restriction by ultrasound can use management strategies based on monitoring and delivery methods. One of these monitoring techniques is an umbilical artery Doppler. This method has been shown to decrease risk of morbidity and mortality before and after parturition among IUGR patients.

Time of delivery is also a management strategy and is based on parameters collected from the umbilical artery doppler. Some of these include: pulsatility index, resistance index, and end-diastolic velocities, which are measurements of the fetal circulation.

The affected animal should be left in the pasture, and not forced to come back to stall because excitation can darken the prognosis, even after adequate treatment.

Intravenous mixed calcium and magnesium injection are used. Subcutaneous injection of magnesium sulfate (200 ml of 50% solution) is also recommended.

Magnesium supplements are used to prevent the disease when ruminants, for obvious economic reasons, must have access to dangerous pastures.

X-linked recessive hypoparathyroidism is treated like other forms of the disease, using calcium and vitamin D supplementation. Supplementation with parathyroid hormone is another treatment option.

Homeopathy, acupuncture, and traditional Chinese medicine should not be used.

In people with secondary hyperparathyroidism, the high PTH levels are an appropriate response to low calcium and treatment must be directed at the underlying cause of this (usually vitamin D deficiency or chronic kidney failure). If this is successful PTH levels should naturally return to normal levels unless PTH secretion has become autonomous (tertiary hyperparathyroidism)

The goal of newborn screening programs is to detect and start treatment within the first 1–2 weeks of life. Treatment consists of a daily dose of thyroxine, available as a small tablet. The generic name is levothyroxine, and several brands are available. The tablet is crushed and given to the baby with a small amount of water or milk. The most commonly recommended dose range is 10-15 μg/kg daily, typically 12.5 to 37.5 or 44 μg.

Within a few weeks, the T and TSH levels are rechecked to confirm that they are being normalized by treatment. As the child grows up, these levels are checked regularly to maintain the right dose. The dose increases as the child grows.

If the underlying cause of the hypocalcemia can be addressed, the hyperparathyroidism will resolve. In people with chronic renal failure, treatment consists of dietary restriction of phosphorus, supplements with an active form of vitamin D such as calcitriol, doxercalciferol, paricalcitol, etc. and phosphate binders which can be divided into calcium-based and non-calcium based.

Extended Release Calcifediol was recently approved by the FDA as a treatment for secondary hyperparathyroidism (SHPT) in adults with stage 3 or 4 chronic �kidney disease (CKD) and low vitamin D blood levels (25-hydroxyvitamin D less than 30 ng/mL). It can help treat SHPT by increasing Vitamin D levels and lowering parathyroid hormone or PTH. It is �not for patients with stage 5 CKD or on dialysis.

In the treatment of secondary hyperparathyroidism due to chronic kidney disease on dialysis calcimimetics do not appear to affect the risk of early death. It does decrease the need for a parathyroidectomy but caused more issues with low blood calcium levels and vomiting.

Most people with hyperparathyroidism secondary to chronic kidney disease will improve after renal transplantation, but many will continue to have a degree of residual hyperparathyroidism (tertiary hyperparathyroidism) post-transplant with associated risk of bone loss, etc.

The clinician must protect the patient against hypotension, renal failure, acidosis, hyperkalemia and hypocalcemia. Admission to an intensive care unit, preferably one experienced in trauma medicine, may be appropriate; even well-seeming patients need observation. Treat open wounds as surgically appropriate, with debridement, antibiotics and tetanus toxoid; apply ice to injured areas.

Intravenous hydration of up to 1.5 L/hour should continue to prevent hypotension. A urinary output of at least 300 ml/hour should be maintained with IV fluids and mannitol, and hemodialysis considered if this amount of diuresis is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys.

To prevent hyperkalemia/hypocalcemia, consider the following adult doses:

- calcium gluconate 10% 10ml or calcium chloride 10% 5 ml IV over 2 minutes

- sodium bicarbonate 1 meq/kg IV slow push

- regular insulin 5–10 U

- 50% glucose 1–2 ampules IV bolus

- kayexalate 25–50 g with sorbitol 20% 100 ml by mouth or rectum.

Even so, cardiac arrhythmias may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly.

Treatment depends entirely on the type of hyperparathyroidism encountered.

Treatment consists of maintaining normal levels of calcium, phosphorus, and Vitamin D. Phosphate binders, supplementary Calcium and Vitamin D will be used as required.

Much like with phototherapy the level at which exchange transfusion should occur depends on the health status and age of the newborn. It should however be used for any newborn with a total serum bilirubin of greater than 428 μmol/l ( 25 mg/dL ).

Note that, in neonates, sepsis is difficult to diagnose clinically. They may be relatively asymptomatic until hemodynamic and respiratory collapse is imminent, so, if there is even a remote suspicion of sepsis, they are frequently treated with antibiotics empirically until cultures are sufficiently proven to be negative. In addition to fluid resuscitation and supportive care, a common antibiotic regimen in infants with suspected sepsis is a beta-lactam antibiotic (usually ampicillin) in combination with an aminoglycoside (usually gentamicin) or a third-generation cephalosporin (usually cefotaxime—ceftriaxone is generally avoided in neonates due to the theoretical risk of kernicterus.) The organisms which are targeted are species that predominate in the female genitourinary tract and to which neonates are especially vulnerable to, specifically Group B Streptococcus, "Escherichia coli", and "Listeria monocytogenes" (This is the main rationale for using ampicillin versus other beta-lactams.) Of course, neonates are also vulnerable to other common pathogens that can cause meningitis and bacteremia such as "Streptococcus pneumoniae" and "Neisseria meningitidis". Although uncommon, if anaerobic species are suspected (such as in cases where necrotizing enterocolitis or intestinal perforation is a concern, clindamycin is often added.

Granulocyte-macrophage colony stimulating factor (GM-CSF) is sometimes used in neonatal sepsis. However, a 2009 study found that GM-CSF corrects neutropenia if present but it has no effect on reducing sepsis or improving survival.

Trials of probiotics for prevention of neonatal sepsis have generally been too small and statistically underpowered to detect any benefit, but a randomized controlled trial that enrolled 4,556 neonates in India reported that probiotics significantly reduced the risk of developing sepsis. The probiotic used in the trial was "Lactobacillus plantarum".

A very large meta-analysis investigated the effect of probiotics on preventing late-onset sepsis (LOS) in neonates. Probiotics were found to reduce the risk of LOS, but only in babies who were fed human milk exclusively. It is difficult to distinguish if the prevention was a result of the probiotic supplementation or if it was a result of the properties of human milk. It is also still unclear if probiotic administration reduces LOS risk in extremely low birth weight infants due to the limited number of studies that investigated it. Out of the 37 studies included in this systematic review, none indicated any safety problems related to the probiotics. It would be beneficial to clarify the relationship between probiotic supplementation and human milk for future studies in order to prevent late onset sepsis in neonates.

Medication is used to relieve fever, seizures, and weight loss or dehydration. When medication is use for opiate withdrawal in newborn babies is deemed necessary, opiates are the treatment of choice; they are slowly tapered down to wean the baby off opiates. Phenobarbital is sometimes used as an alternative but is less effective in suppressing seizures; however, phenobarbital is superior to diazepam for neonatal opiate withdrawal symptoms. In the case of sedative-hypnotic neonatal withdrawal, phenobarbital is the treatment of choice. Clonidine is an emerging add-on therapy.

Opioids such as neonatal morphine solution and methadone are commonly used to treat clinical symptoms of opiate withdrawal, but may prolong neonatal drug exposure and duration of hospitalization. A study demonstrated a shorter wean duration in infants treated with methadone compared to those treated with diluted tincture of opium. When compared to morphine, methadone has a longer half-life in children, which allows for less frequent dosing intervals and steady serum concentrations to prevent neonatal withdrawal symptoms.