Deborah C. Skolnik, MLS

Evidence summary

Postherpetic neuralgia (PHN) is defined as pain lasting 1 to 3 months after resolution of acute herpes zoster (shingles) rash. It occurs in approximately 10% to 15% of patients and can cause significant morbidity.

Tricyclic antidepressants provide effective pain relief

Five systematic reviews have concluded that tricyclic antidepressants (TCAs) are effective treatments for PHN.^1-5 Amitriptyline, the best studied TCA, provides at least moderate pain relief in two-thirds of patients with a pooled number needed to treat (NNT) for TCAs of 2.64 (95% confidence interval [CI], 2.1-3.54)⁵ (TABLE).

Selective serotonin reuptake inhibitors—including fluoxetine, paroxetine, citalopram, and sertraline—have been studied in a variety of neuropathic pain syndromes, but not for treating PHN.¹

TABLE
What’s the NNT for drugs used to treat postherpetic neuralgia?

Anticonvulsants help, too

Five systematic reviews found gabapentin to be effective, with a range of NNT from 2.8 to 5.3 for as much as 50% pain reduction based on the visual analog score (VAS).^2-6 Pregabalin is also effective, with an NNT of 4.93 (95% CI, 3.34-6.07) for up to 50% pain reduction.^7,8 Limited data are available concerning the effectiveness of valproate.⁵

A look at the role of narcotics

Four systematic reviews found that controlled-release oxycodone reduced pain by 50%, based on the VAS.^2-5 Another systematic review reported only limited evidence of effectiveness.⁶ In pooled results from systematic reviews, opioids decreased pain by 50% on the VAS (NNT=2.67; 95% CI, 2.10-3.77).⁶

An RCT of 76 patients demonstrated that morphine, with methadone as backup, both reduced the intensity of pain and relieved pain more than placebo.⁹

Tramadol, a selective opioid agonist, showed moderate effectiveness in a small RCT (N=125), with an NNT of 4.76 (95% CI, 2.61-26.97).^3,5,6 The mean pain intensity, degree of pain relief, and amount of rescue medication required were all better in the tramadol group than the placebo group.

Evidence for topical therapy is limited

The anesthetic lidocaine patch 5% has shown efficacy in PHN with allodynia based on 3 RCTs of lower quality (short duration, recruitment of patients who had improved on lidocaine previously, no report of baseline levels of pain); the NNT was 2 (95% CI, 1.4-3.3).¹⁰ A systematic review of these 3 RCTs concluded that evidence is insufficient to recommend the lidocaine patch as treatment for PHN.¹⁰

Capsaicin, a topical counterirritant, reduced pain in fewer than 20% of patients in 2 RCTs reported in systematic reviews, with an NNT of 3.26 (95% CI, 2.26-5.85).^2-6 Blinding was limited in these studies because of the stinging associated with treatment.

Recommendations

A 2004 practice parameter of the American Academy of Neurology recommends TCAs (amitriptyline, nortriptyline, desipramine, and maprotiline), gabapentin, pregabalin, opioids, topical lidocaine, and capsaicin to treat PHN (level of evidence: A), but notes that amitriptyline has significant cardiac effects in the elderly compared with nortriptyline and desipramine.³

In 2006, the European Federation of Neurological Societies determined that TCAs, gabapentin, pregabalin, and opioids had established efficacy (level of evidence: A), but recommended opioids as second-line therapy because of potential adverse events with long-term use.⁴ The federation’s guidelines designate capsaicin, tramadol, topical lidocaine, and valproate as drugs with lower efficacy or limited strength of evidence (level of evidence: B). Nevertheless, they recommend considering topical lidocaine for elderly patients with allodynia and small areas of pain.⁴

Evidence summary

Postherpetic neuralgia (PHN) is defined as pain lasting 1 to 3 months after resolution of acute herpes zoster (shingles) rash. It occurs in approximately 10% to 15% of patients and can cause significant morbidity.

Tricyclic antidepressants provide effective pain relief

Five systematic reviews have concluded that tricyclic antidepressants (TCAs) are effective treatments for PHN.^1-5 Amitriptyline, the best studied TCA, provides at least moderate pain relief in two-thirds of patients with a pooled number needed to treat (NNT) for TCAs of 2.64 (95% confidence interval [CI], 2.1-3.54)⁵ (TABLE).

Selective serotonin reuptake inhibitors—including fluoxetine, paroxetine, citalopram, and sertraline—have been studied in a variety of neuropathic pain syndromes, but not for treating PHN.¹

TABLE
What’s the NNT for drugs used to treat postherpetic neuralgia?

Anticonvulsants help, too

Five systematic reviews found gabapentin to be effective, with a range of NNT from 2.8 to 5.3 for as much as 50% pain reduction based on the visual analog score (VAS).^2-6 Pregabalin is also effective, with an NNT of 4.93 (95% CI, 3.34-6.07) for up to 50% pain reduction.^7,8 Limited data are available concerning the effectiveness of valproate.⁵

A look at the role of narcotics

Four systematic reviews found that controlled-release oxycodone reduced pain by 50%, based on the VAS.^2-5 Another systematic review reported only limited evidence of effectiveness.⁶ In pooled results from systematic reviews, opioids decreased pain by 50% on the VAS (NNT=2.67; 95% CI, 2.10-3.77).⁶

An RCT of 76 patients demonstrated that morphine, with methadone as backup, both reduced the intensity of pain and relieved pain more than placebo.⁹

Tramadol, a selective opioid agonist, showed moderate effectiveness in a small RCT (N=125), with an NNT of 4.76 (95% CI, 2.61-26.97).^3,5,6 The mean pain intensity, degree of pain relief, and amount of rescue medication required were all better in the tramadol group than the placebo group.

Evidence for topical therapy is limited

The anesthetic lidocaine patch 5% has shown efficacy in PHN with allodynia based on 3 RCTs of lower quality (short duration, recruitment of patients who had improved on lidocaine previously, no report of baseline levels of pain); the NNT was 2 (95% CI, 1.4-3.3).¹⁰ A systematic review of these 3 RCTs concluded that evidence is insufficient to recommend the lidocaine patch as treatment for PHN.¹⁰

Capsaicin, a topical counterirritant, reduced pain in fewer than 20% of patients in 2 RCTs reported in systematic reviews, with an NNT of 3.26 (95% CI, 2.26-5.85).^2-6 Blinding was limited in these studies because of the stinging associated with treatment.

Recommendations

A 2004 practice parameter of the American Academy of Neurology recommends TCAs (amitriptyline, nortriptyline, desipramine, and maprotiline), gabapentin, pregabalin, opioids, topical lidocaine, and capsaicin to treat PHN (level of evidence: A), but notes that amitriptyline has significant cardiac effects in the elderly compared with nortriptyline and desipramine.³

In 2006, the European Federation of Neurological Societies determined that TCAs, gabapentin, pregabalin, and opioids had established efficacy (level of evidence: A), but recommended opioids as second-line therapy because of potential adverse events with long-term use.⁴ The federation’s guidelines designate capsaicin, tramadol, topical lidocaine, and valproate as drugs with lower efficacy or limited strength of evidence (level of evidence: B). Nevertheless, they recommend considering topical lidocaine for elderly patients with allodynia and small areas of pain.⁴

Evidence summary

Postherpetic neuralgia (PHN) is defined as pain lasting 1 to 3 months after resolution of acute herpes zoster (shingles) rash. It occurs in approximately 10% to 15% of patients and can cause significant morbidity.

Tricyclic antidepressants provide effective pain relief

Five systematic reviews have concluded that tricyclic antidepressants (TCAs) are effective treatments for PHN.^1-5 Amitriptyline, the best studied TCA, provides at least moderate pain relief in two-thirds of patients with a pooled number needed to treat (NNT) for TCAs of 2.64 (95% confidence interval [CI], 2.1-3.54)⁵ (TABLE).

Selective serotonin reuptake inhibitors—including fluoxetine, paroxetine, citalopram, and sertraline—have been studied in a variety of neuropathic pain syndromes, but not for treating PHN.¹

TABLE
What’s the NNT for drugs used to treat postherpetic neuralgia?

Anticonvulsants help, too

Five systematic reviews found gabapentin to be effective, with a range of NNT from 2.8 to 5.3 for as much as 50% pain reduction based on the visual analog score (VAS).^2-6 Pregabalin is also effective, with an NNT of 4.93 (95% CI, 3.34-6.07) for up to 50% pain reduction.^7,8 Limited data are available concerning the effectiveness of valproate.⁵

A look at the role of narcotics

Four systematic reviews found that controlled-release oxycodone reduced pain by 50%, based on the VAS.^2-5 Another systematic review reported only limited evidence of effectiveness.⁶ In pooled results from systematic reviews, opioids decreased pain by 50% on the VAS (NNT=2.67; 95% CI, 2.10-3.77).⁶

An RCT of 76 patients demonstrated that morphine, with methadone as backup, both reduced the intensity of pain and relieved pain more than placebo.⁹

Tramadol, a selective opioid agonist, showed moderate effectiveness in a small RCT (N=125), with an NNT of 4.76 (95% CI, 2.61-26.97).^3,5,6 The mean pain intensity, degree of pain relief, and amount of rescue medication required were all better in the tramadol group than the placebo group.

Evidence for topical therapy is limited

The anesthetic lidocaine patch 5% has shown efficacy in PHN with allodynia based on 3 RCTs of lower quality (short duration, recruitment of patients who had improved on lidocaine previously, no report of baseline levels of pain); the NNT was 2 (95% CI, 1.4-3.3).¹⁰ A systematic review of these 3 RCTs concluded that evidence is insufficient to recommend the lidocaine patch as treatment for PHN.¹⁰

Capsaicin, a topical counterirritant, reduced pain in fewer than 20% of patients in 2 RCTs reported in systematic reviews, with an NNT of 3.26 (95% CI, 2.26-5.85).^2-6 Blinding was limited in these studies because of the stinging associated with treatment.

Recommendations

A 2004 practice parameter of the American Academy of Neurology recommends TCAs (amitriptyline, nortriptyline, desipramine, and maprotiline), gabapentin, pregabalin, opioids, topical lidocaine, and capsaicin to treat PHN (level of evidence: A), but notes that amitriptyline has significant cardiac effects in the elderly compared with nortriptyline and desipramine.³

In 2006, the European Federation of Neurological Societies determined that TCAs, gabapentin, pregabalin, and opioids had established efficacy (level of evidence: A), but recommended opioids as second-line therapy because of potential adverse events with long-term use.⁴ The federation’s guidelines designate capsaicin, tramadol, topical lidocaine, and valproate as drugs with lower efficacy or limited strength of evidence (level of evidence: B). Nevertheless, they recommend considering topical lidocaine for elderly patients with allodynia and small areas of pain.⁴

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

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.

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

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.

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

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.

Evidence summary

Sebaceous cysts—more correctly referred to as epidermal inclusion cysts—are benign lesions of the skin. They rarely require intervention out of medical necessity, but are removed for cosmetic reasons. If the cysts become inflamed, secondary to internal discharge of the cysts’ contents, or grow so large that they interfere with the patient’s functioning, they may need to be removed.¹

Traditional wide excision—involving dissection and removal of the cyst completely from the surrounding tissue through an elliptical incision—is considered the gold standard of treatment. This time-consuming endeavor frequently leads to significant scarring in comparison with minimal excision or punch biopsy, but has almost no recurrence when the cyst wall is entirely removed.²

Minimal excision and punch biopsy techniques are purported to produce minimal bleeding, have faster healing times, and produce less scarring.² Though both techniques offer a shorter procedural time, they appear to have a slightly higher rates of recurrence.

The minimal incision technique involves kneading the lesion following injection of anesthetic and expressing the cyst contents through a 2- to 3-mm incision. Following expulsion of the cyst contents, the loosened capsule is delivered through the small opening. Closure with suture is optional.³

Punch biopsy excision is similar to the minimal excision technique except that the incision is made using a single-use disposable dermal punch following injection of lidocaine. Expulsion of the cyst contents, with cyst wall, via lateral pressure is performed and occasionally followed by closure with one suture.²

The majority of authors agree that inflamed cysts should be allowed to convalesce prior to attempted removal, though one group (Kitamura et al⁴) suggests primary resection, wound lavage, and primary suture without drainage for infected epidermal cysts. Rarely are these cysts truly infected. The inflammation is secondary to sebaceous cyst wall rupture with leakage of cyst contents, which elicits the inflammatory response.⁵

A small study points to cosmetic benefits of punch biopsy

To date, no randomized controlled trials have been published that compare the 3 most common techniques for treatment of sebaceous cysts. Only 1 small (n=60) randomized study compared traditional wide excision with punch biopsy.⁶ They found punch biopsy to be less time-consuming and to offer superior cosmetic results. However, cysts larger than 2 cm took longer with the punch biopsy technique.

Only a single dermatologist performed all of the surgeries, which could introduce bias. There was no mention of blinding of the researcher that subsequently measured the wounds. Of the 31 patients randomized to the punch biopsy technique, there was 1 recurrence in the 16 months of follow-up compared with none in the wide excision arm. This study excluded patients with infected, inflamed, or recurrent cysts.

Recommendations from others

UpToDate does not recommend excision of an inflamed cyst, suggesting that the inflamed cyst wall is more friable and, therefore, more difficult to remove completely.⁷ This may lead to a higher rate of recurrence.

Lookingbill and Marks in Principles of Dermatology⁸ suggest that, frequently, no therapy is indicated for these lesions. If removal is desired or indicated, every effort should be made to remove the entire cyst lining in order to prevent recurrence of the cyst. They recommend removal of the cyst via the traditional wide excision technique. If the cyst ruptures accidentally during the procedure they suggest removing the remaining contents and wall with a curette.

Evidence summary

Sebaceous cysts—more correctly referred to as epidermal inclusion cysts—are benign lesions of the skin. They rarely require intervention out of medical necessity, but are removed for cosmetic reasons. If the cysts become inflamed, secondary to internal discharge of the cysts’ contents, or grow so large that they interfere with the patient’s functioning, they may need to be removed.¹

Traditional wide excision—involving dissection and removal of the cyst completely from the surrounding tissue through an elliptical incision—is considered the gold standard of treatment. This time-consuming endeavor frequently leads to significant scarring in comparison with minimal excision or punch biopsy, but has almost no recurrence when the cyst wall is entirely removed.²

Minimal excision and punch biopsy techniques are purported to produce minimal bleeding, have faster healing times, and produce less scarring.² Though both techniques offer a shorter procedural time, they appear to have a slightly higher rates of recurrence.

The minimal incision technique involves kneading the lesion following injection of anesthetic and expressing the cyst contents through a 2- to 3-mm incision. Following expulsion of the cyst contents, the loosened capsule is delivered through the small opening. Closure with suture is optional.³

Punch biopsy excision is similar to the minimal excision technique except that the incision is made using a single-use disposable dermal punch following injection of lidocaine. Expulsion of the cyst contents, with cyst wall, via lateral pressure is performed and occasionally followed by closure with one suture.²

The majority of authors agree that inflamed cysts should be allowed to convalesce prior to attempted removal, though one group (Kitamura et al⁴) suggests primary resection, wound lavage, and primary suture without drainage for infected epidermal cysts. Rarely are these cysts truly infected. The inflammation is secondary to sebaceous cyst wall rupture with leakage of cyst contents, which elicits the inflammatory response.⁵

A small study points to cosmetic benefits of punch biopsy

To date, no randomized controlled trials have been published that compare the 3 most common techniques for treatment of sebaceous cysts. Only 1 small (n=60) randomized study compared traditional wide excision with punch biopsy.⁶ They found punch biopsy to be less time-consuming and to offer superior cosmetic results. However, cysts larger than 2 cm took longer with the punch biopsy technique.

Only a single dermatologist performed all of the surgeries, which could introduce bias. There was no mention of blinding of the researcher that subsequently measured the wounds. Of the 31 patients randomized to the punch biopsy technique, there was 1 recurrence in the 16 months of follow-up compared with none in the wide excision arm. This study excluded patients with infected, inflamed, or recurrent cysts.

Recommendations from others

UpToDate does not recommend excision of an inflamed cyst, suggesting that the inflamed cyst wall is more friable and, therefore, more difficult to remove completely.⁷ This may lead to a higher rate of recurrence.

Lookingbill and Marks in Principles of Dermatology⁸ suggest that, frequently, no therapy is indicated for these lesions. If removal is desired or indicated, every effort should be made to remove the entire cyst lining in order to prevent recurrence of the cyst. They recommend removal of the cyst via the traditional wide excision technique. If the cyst ruptures accidentally during the procedure they suggest removing the remaining contents and wall with a curette.

Evidence summary

Sebaceous cysts—more correctly referred to as epidermal inclusion cysts—are benign lesions of the skin. They rarely require intervention out of medical necessity, but are removed for cosmetic reasons. If the cysts become inflamed, secondary to internal discharge of the cysts’ contents, or grow so large that they interfere with the patient’s functioning, they may need to be removed.¹

Traditional wide excision—involving dissection and removal of the cyst completely from the surrounding tissue through an elliptical incision—is considered the gold standard of treatment. This time-consuming endeavor frequently leads to significant scarring in comparison with minimal excision or punch biopsy, but has almost no recurrence when the cyst wall is entirely removed.²

Minimal excision and punch biopsy techniques are purported to produce minimal bleeding, have faster healing times, and produce less scarring.² Though both techniques offer a shorter procedural time, they appear to have a slightly higher rates of recurrence.

The minimal incision technique involves kneading the lesion following injection of anesthetic and expressing the cyst contents through a 2- to 3-mm incision. Following expulsion of the cyst contents, the loosened capsule is delivered through the small opening. Closure with suture is optional.³

Punch biopsy excision is similar to the minimal excision technique except that the incision is made using a single-use disposable dermal punch following injection of lidocaine. Expulsion of the cyst contents, with cyst wall, via lateral pressure is performed and occasionally followed by closure with one suture.²

The majority of authors agree that inflamed cysts should be allowed to convalesce prior to attempted removal, though one group (Kitamura et al⁴) suggests primary resection, wound lavage, and primary suture without drainage for infected epidermal cysts. Rarely are these cysts truly infected. The inflammation is secondary to sebaceous cyst wall rupture with leakage of cyst contents, which elicits the inflammatory response.⁵

A small study points to cosmetic benefits of punch biopsy

To date, no randomized controlled trials have been published that compare the 3 most common techniques for treatment of sebaceous cysts. Only 1 small (n=60) randomized study compared traditional wide excision with punch biopsy.⁶ They found punch biopsy to be less time-consuming and to offer superior cosmetic results. However, cysts larger than 2 cm took longer with the punch biopsy technique.

Only a single dermatologist performed all of the surgeries, which could introduce bias. There was no mention of blinding of the researcher that subsequently measured the wounds. Of the 31 patients randomized to the punch biopsy technique, there was 1 recurrence in the 16 months of follow-up compared with none in the wide excision arm. This study excluded patients with infected, inflamed, or recurrent cysts.

Recommendations from others

UpToDate does not recommend excision of an inflamed cyst, suggesting that the inflamed cyst wall is more friable and, therefore, more difficult to remove completely.⁷ This may lead to a higher rate of recurrence.

Lookingbill and Marks in Principles of Dermatology⁸ suggest that, frequently, no therapy is indicated for these lesions. If removal is desired or indicated, every effort should be made to remove the entire cyst lining in order to prevent recurrence of the cyst. They recommend removal of the cyst via the traditional wide excision technique. If the cyst ruptures accidentally during the procedure they suggest removing the remaining contents and wall with a curette.