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Emergency And Acute Medicine: Hypoparathyroidism
Basics
Description Hypoparathyroidism results from deficiency of parathyroid hormone (PTH), whereas pseudohypoparathyroidism is due to end-organ resistance to PTH. PTH reduces urinary calcium loss, increases urinary phosphate loss, stimulates renal conversion of vitamin D to its active form, and mobilizes calcium and phosphate from bone. Hypocalcemia is the primary metabolic abnormality. Calcitonin promotes deposition of calcium and phosphate into bone. Magnesium is required for both PTH production and peripheral PTH action. Primary hypoparathyroidism reflects intrinsic gland failure, while pseudohypoparathyroidism features elevated PTH with tissue resistance and is often associated with hypothyroidism and hypogonadism. Genetic associations include congenital absence (DiGeorge syndrome), autoimmune polyglandular syndrome type I, Wilson disease, and Albright hereditary osteodystrophy.
Etiology
Failure of parathyroid function due to autoimmune destruction, surgical removal or vascular disruption, radiation injury, or severe hypomagnesemia. Pseudohypoparathyroidism is caused by end-organ resistance to PTH.
Diagnosis
Signs And Symptoms The most common symptomatic presentation occurs postoperatively after parathyroid or thyroid surgery. Neonates may have transient disease with neurodevelopmental consequences proportional to hypocalcemia duration. Symptoms relate to hypocalcemia severity and acuity. Neuromuscular findings include circumoral and distal paresthesias, carpopedal spasm, tetany, positive Chvostek and Trousseau signs, laryngospasm, bronchospasm, muscle cramps, and seizures. Cardiovascular manifestations include prolonged QT interval, heart block, heart failure, ventricular arrhythmias, and vasoconstriction. Neuropsychiatric features include confusion, hallucinations, memory impairment, dementia, extrapyramidal symptoms, and raised intracranial pressure with papilledema. Dermatologic findings include brittle hair and nails, psoriasis, hyperpigmentation, and lenticular cataracts.
Essential Workup
In asymptomatic hypocalcemia, check albumin and correct total calcium. If symptomatic with normal total calcium, evaluate for alkalosis and obtain ionized calcium. Symptomatic low ionized calcium warrants PTH measurement.
Diagnosis Tests And Interpretation
Lab Corrected calcium = measured calcium + 0.8(4 − albumin). Obtain ionized calcium if symptomatic. Check electrolytes, BUN, creatinine, glucose, magnesium, phosphorus, and ABG if alkalosis suspected. Ionized calcium decreases by 3–8% for every 0.1 pH unit increase. Phosphate is typically elevated except in vitamin D deficiency.
Diagnostic Procedures ECG shows QT prolongation due to ST-segment lengthening.
Differential Diagnosis
Pseudohypocalcemia from hypoalbuminemia, alkalosis-related reduction in ionized calcium, hypomagnesemia, congenital PTH resistance, vitamin D deficiency, renal failure, sepsis, pancreatitis, rhabdomyolysis, acute hyperphosphatemia, and chelation from citrate or toxins.
Treatment
Prehospital Consider calcium administration for refractory ventricular fibrillation or status epilepticus in known or suspected hypocalcemia.
Initial Stabilization/Therapy Secure airway if laryngospasm is present. Initiate cardiac monitoring and seizure precautions. Administer IV calcium for unstable rhythms or tetany.
Emergency Department Treatment/Procedures Life-threatening hypocalcemia requires IV calcium chloride or calcium gluconate. Non–life-threatening cases should receive slow calcium infusion with frequent monitoring. Avoid rapid correction unless unstable. Replace magnesium if deficient. Maintain calcium at the lowest asymptomatic level, then transition to oral therapy. Bind phosphate when elevated and supplement vitamin D, preferably with calcitriol. Avoid high-phosphate beverages and evaluate for associated endocrinopathies.
Medication
First Line Calcium gluconate IV for most cases; calcium chloride reserved for life-threatening instability. Magnesium sulfate IV if deficient.
Second Line Oral calcium salts (carbonate or acetate), phosphate binders (sevelamer), magnesium oxide, vitamin D or calcitriol, and thiazide diuretics to reduce urinary calcium loss.
Follow-Up And Disposition
Admission Criteria Symptomatic hypocalcemia, ECG abnormalities, inability to tolerate oral therapy, or markedly low corrected calcium.
Discharge Criteria Asymptomatic patients without admission criteria.
Follow-Up Recommendations Repeat calcium, phosphorus, and magnesium levels within 1–2 days for patients requiring treatment.
Key Points And Cautions
Postoperative hypocalcemia is the most common symptomatic presentation. Symptoms are often mistaken for anxiety or hyperventilation. Exclude sepsis or rhabdomyolysis in nonoperative cases. Except in life-threatening situations, avoid rapid IV calcium administration to prevent complications.
Basics
Description Hypoparathyroidism results from deficiency of parathyroid hormone (PTH), whereas pseudohypoparathyroidism is due to end-organ resistance to PTH. PTH reduces urinary calcium loss, increases urinary phosphate loss, stimulates renal conversion of vitamin D to its active form, and mobilizes calcium and phosphate from bone. Hypocalcemia is the primary metabolic abnormality. Calcitonin promotes deposition of calcium and phosphate into bone. Magnesium is required for both PTH production and peripheral PTH action. Primary hypoparathyroidism reflects intrinsic gland failure, while pseudohypoparathyroidism features elevated PTH with tissue resistance and is often associated with hypothyroidism and hypogonadism. Genetic associations include congenital absence (DiGeorge syndrome), autoimmune polyglandular syndrome type I, Wilson disease, and Albright hereditary osteodystrophy.
Etiology
Failure of parathyroid function due to autoimmune destruction, surgical removal or vascular disruption, radiation injury, or severe hypomagnesemia. Pseudohypoparathyroidism is caused by end-organ resistance to PTH.
Diagnosis
Signs And Symptoms The most common symptomatic presentation occurs postoperatively after parathyroid or thyroid surgery. Neonates may have transient disease with neurodevelopmental consequences proportional to hypocalcemia duration. Symptoms relate to hypocalcemia severity and acuity. Neuromuscular findings include circumoral and distal paresthesias, carpopedal spasm, tetany, positive Chvostek and Trousseau signs, laryngospasm, bronchospasm, muscle cramps, and seizures. Cardiovascular manifestations include prolonged QT interval, heart block, heart failure, ventricular arrhythmias, and vasoconstriction. Neuropsychiatric features include confusion, hallucinations, memory impairment, dementia, extrapyramidal symptoms, and raised intracranial pressure with papilledema. Dermatologic findings include brittle hair and nails, psoriasis, hyperpigmentation, and lenticular cataracts.
Essential Workup
In asymptomatic hypocalcemia, check albumin and correct total calcium. If symptomatic with normal total calcium, evaluate for alkalosis and obtain ionized calcium. Symptomatic low ionized calcium warrants PTH measurement.
Diagnosis Tests And Interpretation
Lab Corrected calcium = measured calcium + 0.8(4 − albumin). Obtain ionized calcium if symptomatic. Check electrolytes, BUN, creatinine, glucose, magnesium, phosphorus, and ABG if alkalosis suspected. Ionized calcium decreases by 3–8% for every 0.1 pH unit increase. Phosphate is typically elevated except in vitamin D deficiency.
Diagnostic Procedures ECG shows QT prolongation due to ST-segment lengthening.
Differential Diagnosis
Pseudohypocalcemia from hypoalbuminemia, alkalosis-related reduction in ionized calcium, hypomagnesemia, congenital PTH resistance, vitamin D deficiency, renal failure, sepsis, pancreatitis, rhabdomyolysis, acute hyperphosphatemia, and chelation from citrate or toxins.
Treatment
Prehospital Consider calcium administration for refractory ventricular fibrillation or status epilepticus in known or suspected hypocalcemia.
Initial Stabilization/Therapy Secure airway if laryngospasm is present. Initiate cardiac monitoring and seizure precautions. Administer IV calcium for unstable rhythms or tetany.
Emergency Department Treatment/Procedures Life-threatening hypocalcemia requires IV calcium chloride or calcium gluconate. Non–life-threatening cases should receive slow calcium infusion with frequent monitoring. Avoid rapid correction unless unstable. Replace magnesium if deficient. Maintain calcium at the lowest asymptomatic level, then transition to oral therapy. Bind phosphate when elevated and supplement vitamin D, preferably with calcitriol. Avoid high-phosphate beverages and evaluate for associated endocrinopathies.
Medication
First Line Calcium gluconate IV for most cases; calcium chloride reserved for life-threatening instability. Magnesium sulfate IV if deficient.
Second Line Oral calcium salts (carbonate or acetate), phosphate binders (sevelamer), magnesium oxide, vitamin D or calcitriol, and thiazide diuretics to reduce urinary calcium loss.
Follow-Up And Disposition
Admission Criteria Symptomatic hypocalcemia, ECG abnormalities, inability to tolerate oral therapy, or markedly low corrected calcium.
Discharge Criteria Asymptomatic patients without admission criteria.
Follow-Up Recommendations Repeat calcium, phosphorus, and magnesium levels within 1–2 days for patients requiring treatment.
Key Points And Cautions
Postoperative hypocalcemia is the most common symptomatic presentation. Symptoms are often mistaken for anxiety or hyperventilation. Exclude sepsis or rhabdomyolysis in nonoperative cases. Except in life-threatening situations, avoid rapid IV calcium administration to prevent complications.
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