User login
What is the best workup for hypocalcemia?
Unexplained hypocalcemia can usually be diagnosed by a limited number of serum tests when the cause isn’t obvious from the history (recent neck surgery or renal failure):
- calcium (corrected for serum albumin)
- creatinine
- phosphorus
- magnesium
- parathyroid hormone (PTH).
The most common causes, categorized according to the results of these tests, are (strength of recommendation: C, expert opinion, case series, and physiologic principles):
- high PTH, high phosphorus, and high creatinine: renal failure
- high PTH, low or normal phosphorus, and normal creatinine: vitamin D deficiency or pancreatitis
- low PTH, high phosphorus, and normal creatinine: inadequate parathyroid gland function or hypomagnesemia.
Important supporting tests—serum albumin, phosphorus, magnesium
Grant Hoekzema, MD
Mercy Family Medicine Residency, St. Louis, Mo
Serious abnormal laboratory results often are encountered in outpatient testing using multitest panels such as basic and comprehensive metabolic profiles. Hypocalcemia found on a basic metabolic panel is a good example of such a result.
Given the broad differential diagnosis outlined by the authors of this Clinical Inquiry, we must interpret abnormal results with the proper supporting tests. In this case, the most important is serum albumin, which can be a critical indicator of whether the patient truly has hypocalcemia. That is why I tend to order a comprehensive metabolic panel when disorders of calcium metabolism are part of the differential.
This Clinical Inquiry also highlights the important role of phosphorus and magnesium in calcium metabolism. It’s important to note that these tests are no longer a regular component of many multitest blood panels and must be ordered when hypocalcemia is found.
Evidence summary
Normal values for total or corrected serum calcium are 8.5-10.2 mg/dL and for ionized calcium, 4.4-5.4 mg/dL. Because total serum calcium is approximately 50% free (ionized) and 50% bound, primarily to albumin, the serum level must be “corrected” if hypoalbuminemia exists. Because serum calcium comprises less than 1% of body stores, severe total body deficiency of calcium can exist without hypocalcemia.1,2
Ionized calcium is under tight physiologic control, monitored by calcium-sensing proteins in the parathyroid gland; low ionized calcium augments PTH secretion, which in turn has 3 primary actions:
- decreased calcium excretion by the kidneys
- increased activity of osteoclasts, leading to calcium release from bone
- increased activity of renal 25-OH vitamin D hydroxylase, resulting in elevated serum levels of calcitriol, the active form of vitamin D; elevated calcitriol in turn augments gastrointestinal absorption of calcium.
An adequate supply of 25-OH vitamin D to the kidneys requires adequate gastrointestinal absorption or sun-induced skin production of vitamin D and sufficient liver function to carry out the first of the 2 hydroxylation steps.1,3
Common causes of hypocalcemia
We found no studies that established the frequency of various causes of hypocalcemia in the general population, but reviewers concurred that the most common specific causes, in order of frequency, are (TABLE):2,3
- renal failure
- vitamin D deficiency
- hypomagnesemia
- pancreatitis
- hypoparathyroidism.
It is not surprising that renal failure is a common cause of hypocalcemia, given the high prevalence of chronic kidney disease in adults—11.2% of the total United States population older than 20 years has at least a mildly reduced glomerular filtration rate (stage 2, chronic kidney disease, with glomerular filtration rate <90 cc/min).4 Despite elevated PTH, serum calcium may be slightly reduced (and osteomalacia present) even in mild chronic kidney disease.5,6 Only severe or end-stage chronic kidney disease (glomerular filtration rate <30 cc/min, 5.8% of population) is often associated with actual hypocalcemia.5,6 Likewise, the prevalence of vitamin D deficiency (<15 ng/mL of 25-OH vitamin D) is 35% to 55% in the general population,7,8 and 95% in institutionalized elderly patients.9
Chronic kidney disease (66%) and vitamin D deficiency (24%) were the most common causes of hypocalcemia in a study of 594 elderly general medicine inpatients.10 In a study of 62 hypocalcemic patients in a medical intensive care unit, the cause of the hypocalcemia could be determined in only 28 (45%); most of the cases were caused by hypomagnesemia (28%), renal insufficiency (8%), and pancreatitis (3%).11
TABLE
Causes of hypocalcemia by key test results
| TEST RESULTS | COMMON CAUSES | LESS COMMON CAUSES |
|---|---|---|
| High PTH, high phosphorus | Renal failure |
|
| High PTH, low phosphorus | Vitamin D deficiency (with low bone calcium) caused by:
|
|
| Low PTH, high phosphorus | Hypoparathyroidism and hypomagnesemia |
|
| PTH, parathyroid hormone. | ||
Serious causes of hypocalcemia
The usual cause of critically low serum calcium (<7 mg/dL “corrected” or <3.2 mg/dL ionized) is parathyroidectomy or acute renal failure. Hypocalcemia resulting from partial parathyroidectomy or thyroidectomy (with inadvertent parathyroidectomy) occurs in approximately 5% of these surgeries; 99.5% of cases resolve completely within a year.12
Recommendations
Several reviewers recommend a similar workup and differential diagnosis for hypocalcemia. Unfortunately, none cites quantitative data on the prevalence of hypocalcemia and its causes.2,13
Some authors recommend measuring 25-OH vitamin D in all hypocalcemia patients with elevated PTH without hyperphosphatemia to confirm vitamin D deficiency.1,2 Others emphasize the importance of measuring ionized calcium to detect hypocalcemia, especially in critically ill patients, in whom many acute variables can decrease ionized calcium (alkalosis can increase protein binding, for example).1,3,14
Although several reviewers present an algorithmic approach to determining the cause of hypocalcemia,3 we could find no data on the derivation or validation of the diagnostic effectiveness of these algorithms.
1. Fukugawa M, Kurokawa K. Calcium homeostasis and imbalance. Nephron. 2002;92(suppl 1):41-45.
2. Ruppe M. Hypocalcemia. In: American College of Physicians (ACP) Physician’s Information and Education Resource (PIER) database. Available at: http://pier.acponline.org/index.html. Accessed October 30, 2007.
3. Carlstedt F, Lind L. Hypocalcemic syndromes. Crit Care Clin. 2001;17:139, 53, vii-viii.
4. Centers for Disease Control and Prevention (CDC). Prevalence of chronic kidney disease and associated risk factors—United States, 1999-2004. MMWR Morb Mortal Wkly Rep. 2007;56:161-165.
5. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis. 2003;42(4 suppl 3):S1-S201.
6. Rix M, Andreassen H, Eskildsen P, Langdahl B, Olgaard K. Bone mineral density and biochemical markers of bone turnover in patients with predialysis chronic renal failure. Kidney Int. 1999;56:1084-1093.
7. Thomas MK, Lloyd-Jones DM, Thadhani RI, et al. Hypovitaminosis D in medical inpatients. N Engl J Med. 1998;338:777-783.
8. Tangpricha V, Pearce EN, Chen TC, Holick MF. Vitamin D insufficiency among free-living healthy young adults. Am J Med. 2002;112:659-662.
9. Fardellone P, Sebert JL, Garabedian M, et al. Prevalence and biological consequences of vitamin D deficiency in elderly institutionalized subjects. Rev Rhum Engl Ed. 1995;62:576-581.
10. Hodkinson HM. Serum calcium in a geriatric inpatient population. Age Ageing. 1973;2:157-162.
11. Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med. 1988;84:209-214.
12. Pattou F, Combemale F, Fabre S, et al. Hypocalcemia following thyroid surgery: incidence and prediction of outcome. World J Surg. 1998;22:718-724.
13. Guise TA, Mundy GR. Clinical review 69: evaluation of hypocalcemia in children and adults. J Clin Endocrinol Metab. 1995;80:1473-1478.
14. Hastbacka J, Pettila V. Prevalence and predictive value of ionized hypocalcemia among critically ill patients. Acta Anaesthesiol Scand. 2003;47:1264-1269.
Unexplained hypocalcemia can usually be diagnosed by a limited number of serum tests when the cause isn’t obvious from the history (recent neck surgery or renal failure):
- calcium (corrected for serum albumin)
- creatinine
- phosphorus
- magnesium
- parathyroid hormone (PTH).
The most common causes, categorized according to the results of these tests, are (strength of recommendation: C, expert opinion, case series, and physiologic principles):
- high PTH, high phosphorus, and high creatinine: renal failure
- high PTH, low or normal phosphorus, and normal creatinine: vitamin D deficiency or pancreatitis
- low PTH, high phosphorus, and normal creatinine: inadequate parathyroid gland function or hypomagnesemia.
Important supporting tests—serum albumin, phosphorus, magnesium
Grant Hoekzema, MD
Mercy Family Medicine Residency, St. Louis, Mo
Serious abnormal laboratory results often are encountered in outpatient testing using multitest panels such as basic and comprehensive metabolic profiles. Hypocalcemia found on a basic metabolic panel is a good example of such a result.
Given the broad differential diagnosis outlined by the authors of this Clinical Inquiry, we must interpret abnormal results with the proper supporting tests. In this case, the most important is serum albumin, which can be a critical indicator of whether the patient truly has hypocalcemia. That is why I tend to order a comprehensive metabolic panel when disorders of calcium metabolism are part of the differential.
This Clinical Inquiry also highlights the important role of phosphorus and magnesium in calcium metabolism. It’s important to note that these tests are no longer a regular component of many multitest blood panels and must be ordered when hypocalcemia is found.
Evidence summary
Normal values for total or corrected serum calcium are 8.5-10.2 mg/dL and for ionized calcium, 4.4-5.4 mg/dL. Because total serum calcium is approximately 50% free (ionized) and 50% bound, primarily to albumin, the serum level must be “corrected” if hypoalbuminemia exists. Because serum calcium comprises less than 1% of body stores, severe total body deficiency of calcium can exist without hypocalcemia.1,2
Ionized calcium is under tight physiologic control, monitored by calcium-sensing proteins in the parathyroid gland; low ionized calcium augments PTH secretion, which in turn has 3 primary actions:
- decreased calcium excretion by the kidneys
- increased activity of osteoclasts, leading to calcium release from bone
- increased activity of renal 25-OH vitamin D hydroxylase, resulting in elevated serum levels of calcitriol, the active form of vitamin D; elevated calcitriol in turn augments gastrointestinal absorption of calcium.
An adequate supply of 25-OH vitamin D to the kidneys requires adequate gastrointestinal absorption or sun-induced skin production of vitamin D and sufficient liver function to carry out the first of the 2 hydroxylation steps.1,3
Common causes of hypocalcemia
We found no studies that established the frequency of various causes of hypocalcemia in the general population, but reviewers concurred that the most common specific causes, in order of frequency, are (TABLE):2,3
- renal failure
- vitamin D deficiency
- hypomagnesemia
- pancreatitis
- hypoparathyroidism.
It is not surprising that renal failure is a common cause of hypocalcemia, given the high prevalence of chronic kidney disease in adults—11.2% of the total United States population older than 20 years has at least a mildly reduced glomerular filtration rate (stage 2, chronic kidney disease, with glomerular filtration rate <90 cc/min).4 Despite elevated PTH, serum calcium may be slightly reduced (and osteomalacia present) even in mild chronic kidney disease.5,6 Only severe or end-stage chronic kidney disease (glomerular filtration rate <30 cc/min, 5.8% of population) is often associated with actual hypocalcemia.5,6 Likewise, the prevalence of vitamin D deficiency (<15 ng/mL of 25-OH vitamin D) is 35% to 55% in the general population,7,8 and 95% in institutionalized elderly patients.9
Chronic kidney disease (66%) and vitamin D deficiency (24%) were the most common causes of hypocalcemia in a study of 594 elderly general medicine inpatients.10 In a study of 62 hypocalcemic patients in a medical intensive care unit, the cause of the hypocalcemia could be determined in only 28 (45%); most of the cases were caused by hypomagnesemia (28%), renal insufficiency (8%), and pancreatitis (3%).11
TABLE
Causes of hypocalcemia by key test results
| TEST RESULTS | COMMON CAUSES | LESS COMMON CAUSES |
|---|---|---|
| High PTH, high phosphorus | Renal failure |
|
| High PTH, low phosphorus | Vitamin D deficiency (with low bone calcium) caused by:
|
|
| Low PTH, high phosphorus | Hypoparathyroidism and hypomagnesemia |
|
| PTH, parathyroid hormone. | ||
Serious causes of hypocalcemia
The usual cause of critically low serum calcium (<7 mg/dL “corrected” or <3.2 mg/dL ionized) is parathyroidectomy or acute renal failure. Hypocalcemia resulting from partial parathyroidectomy or thyroidectomy (with inadvertent parathyroidectomy) occurs in approximately 5% of these surgeries; 99.5% of cases resolve completely within a year.12
Recommendations
Several reviewers recommend a similar workup and differential diagnosis for hypocalcemia. Unfortunately, none cites quantitative data on the prevalence of hypocalcemia and its causes.2,13
Some authors recommend measuring 25-OH vitamin D in all hypocalcemia patients with elevated PTH without hyperphosphatemia to confirm vitamin D deficiency.1,2 Others emphasize the importance of measuring ionized calcium to detect hypocalcemia, especially in critically ill patients, in whom many acute variables can decrease ionized calcium (alkalosis can increase protein binding, for example).1,3,14
Although several reviewers present an algorithmic approach to determining the cause of hypocalcemia,3 we could find no data on the derivation or validation of the diagnostic effectiveness of these algorithms.
Unexplained hypocalcemia can usually be diagnosed by a limited number of serum tests when the cause isn’t obvious from the history (recent neck surgery or renal failure):
- calcium (corrected for serum albumin)
- creatinine
- phosphorus
- magnesium
- parathyroid hormone (PTH).
The most common causes, categorized according to the results of these tests, are (strength of recommendation: C, expert opinion, case series, and physiologic principles):
- high PTH, high phosphorus, and high creatinine: renal failure
- high PTH, low or normal phosphorus, and normal creatinine: vitamin D deficiency or pancreatitis
- low PTH, high phosphorus, and normal creatinine: inadequate parathyroid gland function or hypomagnesemia.
Important supporting tests—serum albumin, phosphorus, magnesium
Grant Hoekzema, MD
Mercy Family Medicine Residency, St. Louis, Mo
Serious abnormal laboratory results often are encountered in outpatient testing using multitest panels such as basic and comprehensive metabolic profiles. Hypocalcemia found on a basic metabolic panel is a good example of such a result.
Given the broad differential diagnosis outlined by the authors of this Clinical Inquiry, we must interpret abnormal results with the proper supporting tests. In this case, the most important is serum albumin, which can be a critical indicator of whether the patient truly has hypocalcemia. That is why I tend to order a comprehensive metabolic panel when disorders of calcium metabolism are part of the differential.
This Clinical Inquiry also highlights the important role of phosphorus and magnesium in calcium metabolism. It’s important to note that these tests are no longer a regular component of many multitest blood panels and must be ordered when hypocalcemia is found.
Evidence summary
Normal values for total or corrected serum calcium are 8.5-10.2 mg/dL and for ionized calcium, 4.4-5.4 mg/dL. Because total serum calcium is approximately 50% free (ionized) and 50% bound, primarily to albumin, the serum level must be “corrected” if hypoalbuminemia exists. Because serum calcium comprises less than 1% of body stores, severe total body deficiency of calcium can exist without hypocalcemia.1,2
Ionized calcium is under tight physiologic control, monitored by calcium-sensing proteins in the parathyroid gland; low ionized calcium augments PTH secretion, which in turn has 3 primary actions:
- decreased calcium excretion by the kidneys
- increased activity of osteoclasts, leading to calcium release from bone
- increased activity of renal 25-OH vitamin D hydroxylase, resulting in elevated serum levels of calcitriol, the active form of vitamin D; elevated calcitriol in turn augments gastrointestinal absorption of calcium.
An adequate supply of 25-OH vitamin D to the kidneys requires adequate gastrointestinal absorption or sun-induced skin production of vitamin D and sufficient liver function to carry out the first of the 2 hydroxylation steps.1,3
Common causes of hypocalcemia
We found no studies that established the frequency of various causes of hypocalcemia in the general population, but reviewers concurred that the most common specific causes, in order of frequency, are (TABLE):2,3
- renal failure
- vitamin D deficiency
- hypomagnesemia
- pancreatitis
- hypoparathyroidism.
It is not surprising that renal failure is a common cause of hypocalcemia, given the high prevalence of chronic kidney disease in adults—11.2% of the total United States population older than 20 years has at least a mildly reduced glomerular filtration rate (stage 2, chronic kidney disease, with glomerular filtration rate <90 cc/min).4 Despite elevated PTH, serum calcium may be slightly reduced (and osteomalacia present) even in mild chronic kidney disease.5,6 Only severe or end-stage chronic kidney disease (glomerular filtration rate <30 cc/min, 5.8% of population) is often associated with actual hypocalcemia.5,6 Likewise, the prevalence of vitamin D deficiency (<15 ng/mL of 25-OH vitamin D) is 35% to 55% in the general population,7,8 and 95% in institutionalized elderly patients.9
Chronic kidney disease (66%) and vitamin D deficiency (24%) were the most common causes of hypocalcemia in a study of 594 elderly general medicine inpatients.10 In a study of 62 hypocalcemic patients in a medical intensive care unit, the cause of the hypocalcemia could be determined in only 28 (45%); most of the cases were caused by hypomagnesemia (28%), renal insufficiency (8%), and pancreatitis (3%).11
TABLE
Causes of hypocalcemia by key test results
| TEST RESULTS | COMMON CAUSES | LESS COMMON CAUSES |
|---|---|---|
| High PTH, high phosphorus | Renal failure |
|
| High PTH, low phosphorus | Vitamin D deficiency (with low bone calcium) caused by:
|
|
| Low PTH, high phosphorus | Hypoparathyroidism and hypomagnesemia |
|
| PTH, parathyroid hormone. | ||
Serious causes of hypocalcemia
The usual cause of critically low serum calcium (<7 mg/dL “corrected” or <3.2 mg/dL ionized) is parathyroidectomy or acute renal failure. Hypocalcemia resulting from partial parathyroidectomy or thyroidectomy (with inadvertent parathyroidectomy) occurs in approximately 5% of these surgeries; 99.5% of cases resolve completely within a year.12
Recommendations
Several reviewers recommend a similar workup and differential diagnosis for hypocalcemia. Unfortunately, none cites quantitative data on the prevalence of hypocalcemia and its causes.2,13
Some authors recommend measuring 25-OH vitamin D in all hypocalcemia patients with elevated PTH without hyperphosphatemia to confirm vitamin D deficiency.1,2 Others emphasize the importance of measuring ionized calcium to detect hypocalcemia, especially in critically ill patients, in whom many acute variables can decrease ionized calcium (alkalosis can increase protein binding, for example).1,3,14
Although several reviewers present an algorithmic approach to determining the cause of hypocalcemia,3 we could find no data on the derivation or validation of the diagnostic effectiveness of these algorithms.
1. Fukugawa M, Kurokawa K. Calcium homeostasis and imbalance. Nephron. 2002;92(suppl 1):41-45.
2. Ruppe M. Hypocalcemia. In: American College of Physicians (ACP) Physician’s Information and Education Resource (PIER) database. Available at: http://pier.acponline.org/index.html. Accessed October 30, 2007.
3. Carlstedt F, Lind L. Hypocalcemic syndromes. Crit Care Clin. 2001;17:139, 53, vii-viii.
4. Centers for Disease Control and Prevention (CDC). Prevalence of chronic kidney disease and associated risk factors—United States, 1999-2004. MMWR Morb Mortal Wkly Rep. 2007;56:161-165.
5. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis. 2003;42(4 suppl 3):S1-S201.
6. Rix M, Andreassen H, Eskildsen P, Langdahl B, Olgaard K. Bone mineral density and biochemical markers of bone turnover in patients with predialysis chronic renal failure. Kidney Int. 1999;56:1084-1093.
7. Thomas MK, Lloyd-Jones DM, Thadhani RI, et al. Hypovitaminosis D in medical inpatients. N Engl J Med. 1998;338:777-783.
8. Tangpricha V, Pearce EN, Chen TC, Holick MF. Vitamin D insufficiency among free-living healthy young adults. Am J Med. 2002;112:659-662.
9. Fardellone P, Sebert JL, Garabedian M, et al. Prevalence and biological consequences of vitamin D deficiency in elderly institutionalized subjects. Rev Rhum Engl Ed. 1995;62:576-581.
10. Hodkinson HM. Serum calcium in a geriatric inpatient population. Age Ageing. 1973;2:157-162.
11. Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med. 1988;84:209-214.
12. Pattou F, Combemale F, Fabre S, et al. Hypocalcemia following thyroid surgery: incidence and prediction of outcome. World J Surg. 1998;22:718-724.
13. Guise TA, Mundy GR. Clinical review 69: evaluation of hypocalcemia in children and adults. J Clin Endocrinol Metab. 1995;80:1473-1478.
14. Hastbacka J, Pettila V. Prevalence and predictive value of ionized hypocalcemia among critically ill patients. Acta Anaesthesiol Scand. 2003;47:1264-1269.
1. Fukugawa M, Kurokawa K. Calcium homeostasis and imbalance. Nephron. 2002;92(suppl 1):41-45.
2. Ruppe M. Hypocalcemia. In: American College of Physicians (ACP) Physician’s Information and Education Resource (PIER) database. Available at: http://pier.acponline.org/index.html. Accessed October 30, 2007.
3. Carlstedt F, Lind L. Hypocalcemic syndromes. Crit Care Clin. 2001;17:139, 53, vii-viii.
4. Centers for Disease Control and Prevention (CDC). Prevalence of chronic kidney disease and associated risk factors—United States, 1999-2004. MMWR Morb Mortal Wkly Rep. 2007;56:161-165.
5. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis. 2003;42(4 suppl 3):S1-S201.
6. Rix M, Andreassen H, Eskildsen P, Langdahl B, Olgaard K. Bone mineral density and biochemical markers of bone turnover in patients with predialysis chronic renal failure. Kidney Int. 1999;56:1084-1093.
7. Thomas MK, Lloyd-Jones DM, Thadhani RI, et al. Hypovitaminosis D in medical inpatients. N Engl J Med. 1998;338:777-783.
8. Tangpricha V, Pearce EN, Chen TC, Holick MF. Vitamin D insufficiency among free-living healthy young adults. Am J Med. 2002;112:659-662.
9. Fardellone P, Sebert JL, Garabedian M, et al. Prevalence and biological consequences of vitamin D deficiency in elderly institutionalized subjects. Rev Rhum Engl Ed. 1995;62:576-581.
10. Hodkinson HM. Serum calcium in a geriatric inpatient population. Age Ageing. 1973;2:157-162.
11. Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med. 1988;84:209-214.
12. Pattou F, Combemale F, Fabre S, et al. Hypocalcemia following thyroid surgery: incidence and prediction of outcome. World J Surg. 1998;22:718-724.
13. Guise TA, Mundy GR. Clinical review 69: evaluation of hypocalcemia in children and adults. J Clin Endocrinol Metab. 1995;80:1473-1478.
14. Hastbacka J, Pettila V. Prevalence and predictive value of ionized hypocalcemia among critically ill patients. Acta Anaesthesiol Scand. 2003;47:1264-1269.
Evidence-based answers from the Family Physicians Inquiries Network
Are steroid injections effective for tenosynovitis of the hand?
Yes. Steroid injections are an effective first-line therapy for flexor tenosynovitis of the hand, with a number needed to treat [NNT] of 2.3 for injection of steroids and lidocaine (strength of recommendation [SOR]: B, based on 1 prospective RCT and 2 low-quality studies). Injection into the tendon sheath may not be critical to a successful outcome (SOR: B, based on 1 prospective uncontrolled trial).
For de quervain’s tenosynovitis, steroid injections without splinting are more effective than injection plus splinting or splinting alone. The cure rates are 83% (steroid alone), 61% (steroid plus splinting), and 14% (splinting alone) (SOR: B, based on a systematic review of descriptive noncontrolled studies). Injecting into the tendon compartments was more effective than injecting into the surrounding soft tissues (SOR: B, based on 1 prospective controlled trial).
Steroids are helpful, especially for a quick return to function
Robert Gauer, MD
Fort Bragg, NC
I often see flexor and de Quervain’s tenosynovitis in my practice, particularly among patients whose occupations require repetitive hand use. Acute treatment for these conditions typically consists of immobilization with buddy taping or finger/thumb spica splinting. For those who do not improve in 4 weeks, or require a quick return to function, I’ve found that corticosteroid injection using a 25- to 30-gauge needle can be very effective.
De Quervain’s tenosynovitis must be injected into the sheath between the abductor longus and extensor pollicis brevis; flexor tenosynovitis is injected in the nodule. I typically have excellent results, with patients returning to function within 72 hours. Depigmentation and atrophy can occur with injections, especially in small-statured or dark-pigmented patients. surgical release is rarely required for either condition.
Infectious tenosynovitis must be recognized early; it is typically due to lacerations or puncture wounds. In these cases, I immediately refer to orthopedic surgery for further treatment and evaluation.
Evidence summary
Flexor tenosynovitis and de Quervain’s tenosynovitis are the 2 most common types of tenosynovitis of the hand. While the term “tenosynovitis” implies an inflammatory condition, pathoanatomically it is better described as a friction overuse injury, resulting in fibrosis of the surrounding tissue and subsequent narrowing of the synovium.1
“Trigger finger” due to tenosynovitis
Flexor tenosynovitis: Steroid injections provided relief
A prospective, double-blinded RCT2 published by an orthopedic group in 1995 compared 24 patients with primary flexor tenosynovitis. Patients were injected with either 1 cc of betamethasone (Celestone 6 mg) and 3 cc of 1% lidocaine, or 4 cc of 1% lidocaine alone. A successful outcome was defined as absence of triggering and pain, both subjectively and on examination. Follow-up examination was completed for all patients at 3 weeks and 4 months after injection.
The treatment group had success outcomes for 10 of 14 patients (71%) at 3 weeks and 9 of 14 patients (64%) at 4 months, compared with 2 of 10 (20%) at both 3 weeks and 4 months in the control group (NNT=2.3; P<.05 at 4 months). No significant side effects were noted. It is unclear how the study blinded the white, thick consistency of betamethasone compared with the clear nature of lidocaine alone.
Injection site may not matter. In another prospective, uncontrolled trial, 107 patients with flexor tenosynovitis were injected with 1 cc of betamethasone, 0.5 cc of 1% lidocaine, and 0.5 cc of radio opaque dye.3 Some patients got their injections in the tendon sheath at the A1 pulley site, others got their injections in the subcutaneous tissue surrounding the pulley, and a third group got injections in both sites. Patients graded their relief subjectively as either good (total alleviation of symptoms), fair (lasting improvement), or poor (only transient improvement or none at all).
Those who received an intrasheath injection reported good results 47% of the time at 2 weeks follow-up, compared with 70% and 50% for patients in the subcutaneous and mixed groups, respectively. There was no statistically significant difference between the groups, suggesting that the exact location of injection may not be important.
de Quervain’s tenosynovitis: Steroids better than splinting
A pooled quantitative literature search concerning the treatment of de Quervain’s tenosynovitis compared 7 studies (a total of 459 wrists) with identical diagnostic and success criteria.4 Average follow-up was 9.6 months (range, 1 week to 7 years). There were no control groups in the studies, and none of the studies were randomized. Of the 226 cases treated with steroid injection alone, 83% were cured, though 30 of these needed a second injection. Sixty-one percent of those treated with injection and splint were cured, while 14% treated with splint alone reported cure.
Steroids outperform splinting and NSAIDs. A retrospective study not included in the above review compared steroid injection with splinting and nonsteroidal anti-inflammatory drugs (NSAIDs).5 Researchers stratified subjects into minimal, mild, or moderate-to-severe, based on their severity of disease and limitation on their activities of daily living. Mean follow-up was 2.3 years.
Of those cases treated with splinting and NSAIDs, 15 of 17 in the minimal group had resolution of symptoms, but only 4 of 20 in the mild group and 2 of 8 in the moderate-to-severe group had symptoms resolve. The injection group obtained better results, with 100% of cases in the minimal and mild groups resolving and 76% of those in the more severe group resolving completely, with an additional 7% reporting improvement.
Injection site appears to matter with de Quervain’s tenosynovitis. In 1 small, controlled, prospective, double-blinded study, the authors attempted to correlate clinical relief of de Quervain’s tenosynovitis with accuracy of injection into the first dorsal compartment.6 The researchers enrolled 19 patients. The same hand surgeon injected 3 cc of 1% lidocaine, 1 cc betamethasone, and 1 cc Omnipaque 300 dye into the abductor pollicis longus sheath and then attempted, with ulnar deviation of the needle, to fill the extensor pollicis brevis sheath.
Patients were followed-up at 1 month and 3 months postinjection. Success—defined as a negative Finkelstein’s test, absence of pain, and normal activities of daily living—was noted in 11 of 19 patients at 3 months. In a radiographic check, 4 of 5 of the patients with dye in both compartments were asymptomatic, while the 3 who had no dye in either compartment remained symptomatic. This suggests that the location of injection may be important in de Quervain’s tenosynovitis.
Recommendations from others
The Brigham and Women’s Hospital guidelines for treatment of de Quervain’s tenosynovitis state that corticosteroid injections “may be very helpful,” and that they should be considered if symptoms persist beyond 6 weeks of conservative treatment.7DeLee and Drez’s Orthopedic Sports Medicine text recommends corticosteroid injection for de Quervain’s tenosynovitis after 2 weeks of conservative treatment have failed.8
UpToDate recommends steroid injection for de Quervain’s tenosynovitis if pain persists for more than 2 to 6 weeks despite splinting, icing, and NSAID therapy.9 For flexor tenosynovitis, UpToDate recommends local injection when symptoms persist for 4 to 6 weeks despite splinting.10
1. Zingas C, Failla JM, Van Holsbeeck M. Injection accuracy and clinical relief of de Quervain’s tendinitis. J Hand Surgery (Am) 1998;23:89-96.
2. Murphy D, Failla JM, Koniuch MP. Steroid versus placebo injection for trigger finger. J Hand Surg (Am) 1995;20:628-631.
3. Taras JS, Raphael JS, Pan WT, et al. Corticosteroid injections for trigger digits: is intrasheath injection necessary? J Hand Surg (Am) 1998;23:717-22.
4. Richie CA, 3rd, Briner WW, Jr. Corticosteroid injection for treatment of de Quervain’s tenosynovitis: a pooled quantitative literature evaluation. J Am Board Fam Prac 2003;16:102-106.
5. Lane LB, Boretz RS, Stuchin SA. Treatment of de Quervain’s disease: role of conservative management. J Hand Surgery (Br) 2001;26:258-260.
6. Zingas C, Failla JM, Van Holsbeeck M. Injection accuracy and clinical relief of de Quervain’s tendinitis. J Hand Surgery (Am) 1998;23:89-96.
7. Brigham and Women’s Hospital. Upper Extremity Musculoskeletal Disorders: A Guide to Prevention, Diagnosis and Treatment. Boston, Mass: Brigham and Women’s Hospital; 2003:9.
8. DeLee J, Drez D, Miller M. DeLee and Drez’s Orthopaedic Sports Medicine: Principles And Practice. 2nd ed. Philadelphia, Pa: Saunders; 2003.
9. Anderson BC, Sheon RP. de Quervain’s tenosynovitis. UpToDate [online database]. Updated May 7, 2004. Waltham, Mass: UpToDate; 2004.
10. Anderson BC. Trigger finger (flexor tenosynovitis). UpToDate [online database]. Updated December 26, 2000. Waltham, Mass: UpToDate; 2000.
Yes. Steroid injections are an effective first-line therapy for flexor tenosynovitis of the hand, with a number needed to treat [NNT] of 2.3 for injection of steroids and lidocaine (strength of recommendation [SOR]: B, based on 1 prospective RCT and 2 low-quality studies). Injection into the tendon sheath may not be critical to a successful outcome (SOR: B, based on 1 prospective uncontrolled trial).
For de quervain’s tenosynovitis, steroid injections without splinting are more effective than injection plus splinting or splinting alone. The cure rates are 83% (steroid alone), 61% (steroid plus splinting), and 14% (splinting alone) (SOR: B, based on a systematic review of descriptive noncontrolled studies). Injecting into the tendon compartments was more effective than injecting into the surrounding soft tissues (SOR: B, based on 1 prospective controlled trial).
Steroids are helpful, especially for a quick return to function
Robert Gauer, MD
Fort Bragg, NC
I often see flexor and de Quervain’s tenosynovitis in my practice, particularly among patients whose occupations require repetitive hand use. Acute treatment for these conditions typically consists of immobilization with buddy taping or finger/thumb spica splinting. For those who do not improve in 4 weeks, or require a quick return to function, I’ve found that corticosteroid injection using a 25- to 30-gauge needle can be very effective.
De Quervain’s tenosynovitis must be injected into the sheath between the abductor longus and extensor pollicis brevis; flexor tenosynovitis is injected in the nodule. I typically have excellent results, with patients returning to function within 72 hours. Depigmentation and atrophy can occur with injections, especially in small-statured or dark-pigmented patients. surgical release is rarely required for either condition.
Infectious tenosynovitis must be recognized early; it is typically due to lacerations or puncture wounds. In these cases, I immediately refer to orthopedic surgery for further treatment and evaluation.
Evidence summary
Flexor tenosynovitis and de Quervain’s tenosynovitis are the 2 most common types of tenosynovitis of the hand. While the term “tenosynovitis” implies an inflammatory condition, pathoanatomically it is better described as a friction overuse injury, resulting in fibrosis of the surrounding tissue and subsequent narrowing of the synovium.1
“Trigger finger” due to tenosynovitis
Flexor tenosynovitis: Steroid injections provided relief
A prospective, double-blinded RCT2 published by an orthopedic group in 1995 compared 24 patients with primary flexor tenosynovitis. Patients were injected with either 1 cc of betamethasone (Celestone 6 mg) and 3 cc of 1% lidocaine, or 4 cc of 1% lidocaine alone. A successful outcome was defined as absence of triggering and pain, both subjectively and on examination. Follow-up examination was completed for all patients at 3 weeks and 4 months after injection.
The treatment group had success outcomes for 10 of 14 patients (71%) at 3 weeks and 9 of 14 patients (64%) at 4 months, compared with 2 of 10 (20%) at both 3 weeks and 4 months in the control group (NNT=2.3; P<.05 at 4 months). No significant side effects were noted. It is unclear how the study blinded the white, thick consistency of betamethasone compared with the clear nature of lidocaine alone.
Injection site may not matter. In another prospective, uncontrolled trial, 107 patients with flexor tenosynovitis were injected with 1 cc of betamethasone, 0.5 cc of 1% lidocaine, and 0.5 cc of radio opaque dye.3 Some patients got their injections in the tendon sheath at the A1 pulley site, others got their injections in the subcutaneous tissue surrounding the pulley, and a third group got injections in both sites. Patients graded their relief subjectively as either good (total alleviation of symptoms), fair (lasting improvement), or poor (only transient improvement or none at all).
Those who received an intrasheath injection reported good results 47% of the time at 2 weeks follow-up, compared with 70% and 50% for patients in the subcutaneous and mixed groups, respectively. There was no statistically significant difference between the groups, suggesting that the exact location of injection may not be important.
de Quervain’s tenosynovitis: Steroids better than splinting
A pooled quantitative literature search concerning the treatment of de Quervain’s tenosynovitis compared 7 studies (a total of 459 wrists) with identical diagnostic and success criteria.4 Average follow-up was 9.6 months (range, 1 week to 7 years). There were no control groups in the studies, and none of the studies were randomized. Of the 226 cases treated with steroid injection alone, 83% were cured, though 30 of these needed a second injection. Sixty-one percent of those treated with injection and splint were cured, while 14% treated with splint alone reported cure.
Steroids outperform splinting and NSAIDs. A retrospective study not included in the above review compared steroid injection with splinting and nonsteroidal anti-inflammatory drugs (NSAIDs).5 Researchers stratified subjects into minimal, mild, or moderate-to-severe, based on their severity of disease and limitation on their activities of daily living. Mean follow-up was 2.3 years.
Of those cases treated with splinting and NSAIDs, 15 of 17 in the minimal group had resolution of symptoms, but only 4 of 20 in the mild group and 2 of 8 in the moderate-to-severe group had symptoms resolve. The injection group obtained better results, with 100% of cases in the minimal and mild groups resolving and 76% of those in the more severe group resolving completely, with an additional 7% reporting improvement.
Injection site appears to matter with de Quervain’s tenosynovitis. In 1 small, controlled, prospective, double-blinded study, the authors attempted to correlate clinical relief of de Quervain’s tenosynovitis with accuracy of injection into the first dorsal compartment.6 The researchers enrolled 19 patients. The same hand surgeon injected 3 cc of 1% lidocaine, 1 cc betamethasone, and 1 cc Omnipaque 300 dye into the abductor pollicis longus sheath and then attempted, with ulnar deviation of the needle, to fill the extensor pollicis brevis sheath.
Patients were followed-up at 1 month and 3 months postinjection. Success—defined as a negative Finkelstein’s test, absence of pain, and normal activities of daily living—was noted in 11 of 19 patients at 3 months. In a radiographic check, 4 of 5 of the patients with dye in both compartments were asymptomatic, while the 3 who had no dye in either compartment remained symptomatic. This suggests that the location of injection may be important in de Quervain’s tenosynovitis.
Recommendations from others
The Brigham and Women’s Hospital guidelines for treatment of de Quervain’s tenosynovitis state that corticosteroid injections “may be very helpful,” and that they should be considered if symptoms persist beyond 6 weeks of conservative treatment.7DeLee and Drez’s Orthopedic Sports Medicine text recommends corticosteroid injection for de Quervain’s tenosynovitis after 2 weeks of conservative treatment have failed.8
UpToDate recommends steroid injection for de Quervain’s tenosynovitis if pain persists for more than 2 to 6 weeks despite splinting, icing, and NSAID therapy.9 For flexor tenosynovitis, UpToDate recommends local injection when symptoms persist for 4 to 6 weeks despite splinting.10
Yes. Steroid injections are an effective first-line therapy for flexor tenosynovitis of the hand, with a number needed to treat [NNT] of 2.3 for injection of steroids and lidocaine (strength of recommendation [SOR]: B, based on 1 prospective RCT and 2 low-quality studies). Injection into the tendon sheath may not be critical to a successful outcome (SOR: B, based on 1 prospective uncontrolled trial).
For de quervain’s tenosynovitis, steroid injections without splinting are more effective than injection plus splinting or splinting alone. The cure rates are 83% (steroid alone), 61% (steroid plus splinting), and 14% (splinting alone) (SOR: B, based on a systematic review of descriptive noncontrolled studies). Injecting into the tendon compartments was more effective than injecting into the surrounding soft tissues (SOR: B, based on 1 prospective controlled trial).
Steroids are helpful, especially for a quick return to function
Robert Gauer, MD
Fort Bragg, NC
I often see flexor and de Quervain’s tenosynovitis in my practice, particularly among patients whose occupations require repetitive hand use. Acute treatment for these conditions typically consists of immobilization with buddy taping or finger/thumb spica splinting. For those who do not improve in 4 weeks, or require a quick return to function, I’ve found that corticosteroid injection using a 25- to 30-gauge needle can be very effective.
De Quervain’s tenosynovitis must be injected into the sheath between the abductor longus and extensor pollicis brevis; flexor tenosynovitis is injected in the nodule. I typically have excellent results, with patients returning to function within 72 hours. Depigmentation and atrophy can occur with injections, especially in small-statured or dark-pigmented patients. surgical release is rarely required for either condition.
Infectious tenosynovitis must be recognized early; it is typically due to lacerations or puncture wounds. In these cases, I immediately refer to orthopedic surgery for further treatment and evaluation.
Evidence summary
Flexor tenosynovitis and de Quervain’s tenosynovitis are the 2 most common types of tenosynovitis of the hand. While the term “tenosynovitis” implies an inflammatory condition, pathoanatomically it is better described as a friction overuse injury, resulting in fibrosis of the surrounding tissue and subsequent narrowing of the synovium.1
“Trigger finger” due to tenosynovitis
Flexor tenosynovitis: Steroid injections provided relief
A prospective, double-blinded RCT2 published by an orthopedic group in 1995 compared 24 patients with primary flexor tenosynovitis. Patients were injected with either 1 cc of betamethasone (Celestone 6 mg) and 3 cc of 1% lidocaine, or 4 cc of 1% lidocaine alone. A successful outcome was defined as absence of triggering and pain, both subjectively and on examination. Follow-up examination was completed for all patients at 3 weeks and 4 months after injection.
The treatment group had success outcomes for 10 of 14 patients (71%) at 3 weeks and 9 of 14 patients (64%) at 4 months, compared with 2 of 10 (20%) at both 3 weeks and 4 months in the control group (NNT=2.3; P<.05 at 4 months). No significant side effects were noted. It is unclear how the study blinded the white, thick consistency of betamethasone compared with the clear nature of lidocaine alone.
Injection site may not matter. In another prospective, uncontrolled trial, 107 patients with flexor tenosynovitis were injected with 1 cc of betamethasone, 0.5 cc of 1% lidocaine, and 0.5 cc of radio opaque dye.3 Some patients got their injections in the tendon sheath at the A1 pulley site, others got their injections in the subcutaneous tissue surrounding the pulley, and a third group got injections in both sites. Patients graded their relief subjectively as either good (total alleviation of symptoms), fair (lasting improvement), or poor (only transient improvement or none at all).
Those who received an intrasheath injection reported good results 47% of the time at 2 weeks follow-up, compared with 70% and 50% for patients in the subcutaneous and mixed groups, respectively. There was no statistically significant difference between the groups, suggesting that the exact location of injection may not be important.
de Quervain’s tenosynovitis: Steroids better than splinting
A pooled quantitative literature search concerning the treatment of de Quervain’s tenosynovitis compared 7 studies (a total of 459 wrists) with identical diagnostic and success criteria.4 Average follow-up was 9.6 months (range, 1 week to 7 years). There were no control groups in the studies, and none of the studies were randomized. Of the 226 cases treated with steroid injection alone, 83% were cured, though 30 of these needed a second injection. Sixty-one percent of those treated with injection and splint were cured, while 14% treated with splint alone reported cure.
Steroids outperform splinting and NSAIDs. A retrospective study not included in the above review compared steroid injection with splinting and nonsteroidal anti-inflammatory drugs (NSAIDs).5 Researchers stratified subjects into minimal, mild, or moderate-to-severe, based on their severity of disease and limitation on their activities of daily living. Mean follow-up was 2.3 years.
Of those cases treated with splinting and NSAIDs, 15 of 17 in the minimal group had resolution of symptoms, but only 4 of 20 in the mild group and 2 of 8 in the moderate-to-severe group had symptoms resolve. The injection group obtained better results, with 100% of cases in the minimal and mild groups resolving and 76% of those in the more severe group resolving completely, with an additional 7% reporting improvement.
Injection site appears to matter with de Quervain’s tenosynovitis. In 1 small, controlled, prospective, double-blinded study, the authors attempted to correlate clinical relief of de Quervain’s tenosynovitis with accuracy of injection into the first dorsal compartment.6 The researchers enrolled 19 patients. The same hand surgeon injected 3 cc of 1% lidocaine, 1 cc betamethasone, and 1 cc Omnipaque 300 dye into the abductor pollicis longus sheath and then attempted, with ulnar deviation of the needle, to fill the extensor pollicis brevis sheath.
Patients were followed-up at 1 month and 3 months postinjection. Success—defined as a negative Finkelstein’s test, absence of pain, and normal activities of daily living—was noted in 11 of 19 patients at 3 months. In a radiographic check, 4 of 5 of the patients with dye in both compartments were asymptomatic, while the 3 who had no dye in either compartment remained symptomatic. This suggests that the location of injection may be important in de Quervain’s tenosynovitis.
Recommendations from others
The Brigham and Women’s Hospital guidelines for treatment of de Quervain’s tenosynovitis state that corticosteroid injections “may be very helpful,” and that they should be considered if symptoms persist beyond 6 weeks of conservative treatment.7DeLee and Drez’s Orthopedic Sports Medicine text recommends corticosteroid injection for de Quervain’s tenosynovitis after 2 weeks of conservative treatment have failed.8
UpToDate recommends steroid injection for de Quervain’s tenosynovitis if pain persists for more than 2 to 6 weeks despite splinting, icing, and NSAID therapy.9 For flexor tenosynovitis, UpToDate recommends local injection when symptoms persist for 4 to 6 weeks despite splinting.10
1. Zingas C, Failla JM, Van Holsbeeck M. Injection accuracy and clinical relief of de Quervain’s tendinitis. J Hand Surgery (Am) 1998;23:89-96.
2. Murphy D, Failla JM, Koniuch MP. Steroid versus placebo injection for trigger finger. J Hand Surg (Am) 1995;20:628-631.
3. Taras JS, Raphael JS, Pan WT, et al. Corticosteroid injections for trigger digits: is intrasheath injection necessary? J Hand Surg (Am) 1998;23:717-22.
4. Richie CA, 3rd, Briner WW, Jr. Corticosteroid injection for treatment of de Quervain’s tenosynovitis: a pooled quantitative literature evaluation. J Am Board Fam Prac 2003;16:102-106.
5. Lane LB, Boretz RS, Stuchin SA. Treatment of de Quervain’s disease: role of conservative management. J Hand Surgery (Br) 2001;26:258-260.
6. Zingas C, Failla JM, Van Holsbeeck M. Injection accuracy and clinical relief of de Quervain’s tendinitis. J Hand Surgery (Am) 1998;23:89-96.
7. Brigham and Women’s Hospital. Upper Extremity Musculoskeletal Disorders: A Guide to Prevention, Diagnosis and Treatment. Boston, Mass: Brigham and Women’s Hospital; 2003:9.
8. DeLee J, Drez D, Miller M. DeLee and Drez’s Orthopaedic Sports Medicine: Principles And Practice. 2nd ed. Philadelphia, Pa: Saunders; 2003.
9. Anderson BC, Sheon RP. de Quervain’s tenosynovitis. UpToDate [online database]. Updated May 7, 2004. Waltham, Mass: UpToDate; 2004.
10. Anderson BC. Trigger finger (flexor tenosynovitis). UpToDate [online database]. Updated December 26, 2000. Waltham, Mass: UpToDate; 2000.
1. Zingas C, Failla JM, Van Holsbeeck M. Injection accuracy and clinical relief of de Quervain’s tendinitis. J Hand Surgery (Am) 1998;23:89-96.
2. Murphy D, Failla JM, Koniuch MP. Steroid versus placebo injection for trigger finger. J Hand Surg (Am) 1995;20:628-631.
3. Taras JS, Raphael JS, Pan WT, et al. Corticosteroid injections for trigger digits: is intrasheath injection necessary? J Hand Surg (Am) 1998;23:717-22.
4. Richie CA, 3rd, Briner WW, Jr. Corticosteroid injection for treatment of de Quervain’s tenosynovitis: a pooled quantitative literature evaluation. J Am Board Fam Prac 2003;16:102-106.
5. Lane LB, Boretz RS, Stuchin SA. Treatment of de Quervain’s disease: role of conservative management. J Hand Surgery (Br) 2001;26:258-260.
6. Zingas C, Failla JM, Van Holsbeeck M. Injection accuracy and clinical relief of de Quervain’s tendinitis. J Hand Surgery (Am) 1998;23:89-96.
7. Brigham and Women’s Hospital. Upper Extremity Musculoskeletal Disorders: A Guide to Prevention, Diagnosis and Treatment. Boston, Mass: Brigham and Women’s Hospital; 2003:9.
8. DeLee J, Drez D, Miller M. DeLee and Drez’s Orthopaedic Sports Medicine: Principles And Practice. 2nd ed. Philadelphia, Pa: Saunders; 2003.
9. Anderson BC, Sheon RP. de Quervain’s tenosynovitis. UpToDate [online database]. Updated May 7, 2004. Waltham, Mass: UpToDate; 2004.
10. Anderson BC. Trigger finger (flexor tenosynovitis). UpToDate [online database]. Updated December 26, 2000. Waltham, Mass: UpToDate; 2000.
Evidence-based answers from the Family Physicians Inquiries Network