The Journal of Family Practice

A 27-year-old man presented to the urgent care clinic with acute bilateral hand swelling, blisters, numbness, and pain. History taking revealed that these symptoms developed after he was locked outside of his apartment for 45 minutes in –22°C (–8°F) weather following a night of heavy drinking.

On physical examination, the patient had a temperature of 36.2°C (97.2°F) and a heart rate of 116 beats/min. He had edema, tenderness, decreased sensation, and distal cyanosis involving all of his fingers (FIGURE 1). He also had large, tense, clear bullae over the dorsal aspect of his fingers (FIGURE 2).

IMAGE COURTESY OF MORTEZA KHODAEE, MD, MPH

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Second-degree frostbite

Frostbite is the result of tissue freezing, which generally occurs after prolonged exposure to freezing temperatures (typically –4°C or below).^1,2 The majority (~90%) of frostbite injuries occur in the hands and feet; however, frostbite has also been observed in the face, perineum, buttocks, and male genitalia.³

Angiography should be performed on patients with third- or fourth-degree frostbite. In cases of vascular occlusion, tPA and heparin can be started to reduce the risk for amputation.

Frostbite is a clinical diagnosis based on a history of sustained exposure to freezing temperatures, paresthesia of affected areas, and typical skin changes. Evidence is lacking regarding the epidemiology of frostbite within the general population.²

Pathophysiology. Intra- and extracellular ice crystal formation causes fluid and electrolyte disturbances, cell dehydration, lipid denaturation, and subsequent cell death.¹ After thawing, progressive tissue ischemia can occur as a result of endothelial damage and dysfunction, intravascular sludging, increased inflammatory markers, an influx of free radicals, and microvascular thrombosis.¹

Classification. Traditionally, frostbite has been classified according to a 4-tiered system based on tissue appearance after rewarming.² First-degree frostbite is characterized by white plaques with surrounding erythema; second degree by edema and clear or cloudy vesicles; third degree by hemorrhagic bullae; and fourth degree by cold and hard tissue that eventually progresses to gangrene.²

A simpler scheme designates frostbite as either superficial (corresponding to first- or second-degree frostbite) or deep (corresponding to third- or fourth-degree frostbite) with presumed muscle and bone involvement.²

Continue to: Risk factors

Risk factors. Frostbite is often associated with risk factors such as alcohol or drug intoxication, vehicular failure or trauma, immobilizing trauma, psychiatric illness, homelessness, Raynaud phenomenon, peripheral vascular disease, diabetes, inadequate clothing, previous cold-weather injury, outdoor winter recreation, and the use of certain medications (eg, beta-blockers).^1-3 Apart from environmental exposure, frostbite can also occur by direct contact with freezing materials, such as ice packs or industrial refrigerants.³

Differential includes nonfreezing injuries

Frostnip, pernio, and trench foot are other cold-weather injuries distinguished by the absence of tissue freezing.⁴ Raynaud phenomenon is a condition that is triggered by either cold temperatures or emotional stress.⁵

Frostnip is characterized by pallor and paresthesia of exposed areas. It may precede frostbite, but it quickly resolves after rewarming.²

Pernio occurs when skin is exposed to damp, cold, nonfreezing environments.⁶ It results in edematous and inflammatory skin lesions that may be painful, pruritic, violaceous, or erythematous.⁶ These lesions are typically found over the fingers, toes, nose, ears, buttocks, or thighs.^4,6 Pernio may be classified as either primary or secondary disease.⁵ Primary pernio is considered idiopathic.⁶ Secondary pernio is thought to be either drug induced or due to underlying autoimmune diseases, such as hepatitis or cryopathy.⁶

Trench foot develops under similar conditions to pernio but requires exposure to a wet environment for at least 10 to 14 hours.⁷ It is characterized by foot pain, paresthesia, pruritus, edema, erythema, cyanosis, blisters, and even gangrene if left untreated.⁷

Continue to: Raynaud phenomenon

Raynaud phenomenon results from transient, acral vasocontraction and manifests as well-demarcated pallor, cyanosis, and then erythema as the affected body part reperfuses.⁵ Similar to pernio, it can be categorized as either primary or secondary.⁵ Primary phenomenon is idiopathic. Secondary phenomenon is thought to be a result of autoimmune disease, use of certain medications, occupational vibratory exposure, obstructive vascular disease, or infection.⁵

In the absence of a history of exposure to subfreezing temperatures, frostbite can be excluded from the differential diagnosis.

Treatment entails rewarming

The aim of frostbite treatment is to save injured cells and minimize tissue loss.¹ This is accomplished through rapid rewarming and—in severe cases—reperfusion techniques.

Tissue should be rewarmed in a 37°C to 39°C water bath with povidone iodine or chlorhexidine added for antiseptic effect.¹ All efforts should be made to avoid refreezing or trauma, as this could worsen the initial injury.² Oral or intravenous hydration may be offered to optimize fluid status.¹ Supplemental oxygen may be administered to maintain saturations above 90%.¹ Nonsteroidal anti-inflammatory drugs are helpful for analgesia and anti-­inflammatory effect, and opioids can be used for breakthrough pain.¹ It is recommended that blisters be drained in a sterile fashion and that all affected tissue be covered with topical aloe vera and a loose dressing.^1,2,4

Treatment of severe frostbite. Angiography should be performed on all patients with third- or fourth-degree frostbite.³ If imaging shows evidence of vascular occlusion, tissue plasminogen activator (tPA) and heparin can be initiated within 24 hours to reduce the risk for amputation.^8-10

Continue to: Iloprost is another...

Iloprost is another proposed treatment for severe frostbite. It is a prostacyclin analog that may lower the amputation rate in patients with at least third-degree frostbite.¹¹ Unlike tPA, iloprost may be given to trauma patients, and it can be used more than 24 hours after injury.²

In cases of fourth-degree frostbite that is not successfully reperfused, amputation is delayed until dry gangrene develops. This often takes weeks to months.¹²

Our patient underwent rewarming and was orally rehydrated. He was discharged home with ibuprofen, oxycodone-­acetaminophen, topical aloe vera, and loose dressings. His bullae enlarged the next day (FIGURE 3). One week later, his blisters were debrided and dressed with silver sulfadiazine at his plastic surgery follow-up. He experienced sensory deficits for a few months, but eventually made a full recovery after 6 months with no remaining sequelae.

IMAGE COURTESY OF MORTEZA KHODAEE, MD, MPH

ACKNOWLEDGEMENT
The authors thank Lisa Kim, MD, for her clinical care of this patient.

CORRESPONDENCE
Morteza Khodaee, MD, MPH, University of Colorado School of Medicine, Department of Family Medicine, AFW Clinic, 3055 Roslyn Street, Denver, CO 80238; morteza.khodaee@ cuanschutz.edu

A 27-year-old man presented to the urgent care clinic with acute bilateral hand swelling, blisters, numbness, and pain. History taking revealed that these symptoms developed after he was locked outside of his apartment for 45 minutes in –22°C (–8°F) weather following a night of heavy drinking.

On physical examination, the patient had a temperature of 36.2°C (97.2°F) and a heart rate of 116 beats/min. He had edema, tenderness, decreased sensation, and distal cyanosis involving all of his fingers (FIGURE 1). He also had large, tense, clear bullae over the dorsal aspect of his fingers (FIGURE 2).

IMAGE COURTESY OF MORTEZA KHODAEE, MD, MPH

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Second-degree frostbite

Frostbite is the result of tissue freezing, which generally occurs after prolonged exposure to freezing temperatures (typically –4°C or below).^1,2 The majority (~90%) of frostbite injuries occur in the hands and feet; however, frostbite has also been observed in the face, perineum, buttocks, and male genitalia.³

Angiography should be performed on patients with third- or fourth-degree frostbite. In cases of vascular occlusion, tPA and heparin can be started to reduce the risk for amputation.

Frostbite is a clinical diagnosis based on a history of sustained exposure to freezing temperatures, paresthesia of affected areas, and typical skin changes. Evidence is lacking regarding the epidemiology of frostbite within the general population.²

Pathophysiology. Intra- and extracellular ice crystal formation causes fluid and electrolyte disturbances, cell dehydration, lipid denaturation, and subsequent cell death.¹ After thawing, progressive tissue ischemia can occur as a result of endothelial damage and dysfunction, intravascular sludging, increased inflammatory markers, an influx of free radicals, and microvascular thrombosis.¹

Classification. Traditionally, frostbite has been classified according to a 4-tiered system based on tissue appearance after rewarming.² First-degree frostbite is characterized by white plaques with surrounding erythema; second degree by edema and clear or cloudy vesicles; third degree by hemorrhagic bullae; and fourth degree by cold and hard tissue that eventually progresses to gangrene.²

A simpler scheme designates frostbite as either superficial (corresponding to first- or second-degree frostbite) or deep (corresponding to third- or fourth-degree frostbite) with presumed muscle and bone involvement.²

Continue to: Risk factors

Risk factors. Frostbite is often associated with risk factors such as alcohol or drug intoxication, vehicular failure or trauma, immobilizing trauma, psychiatric illness, homelessness, Raynaud phenomenon, peripheral vascular disease, diabetes, inadequate clothing, previous cold-weather injury, outdoor winter recreation, and the use of certain medications (eg, beta-blockers).^1-3 Apart from environmental exposure, frostbite can also occur by direct contact with freezing materials, such as ice packs or industrial refrigerants.³

Differential includes nonfreezing injuries

Frostnip, pernio, and trench foot are other cold-weather injuries distinguished by the absence of tissue freezing.⁴ Raynaud phenomenon is a condition that is triggered by either cold temperatures or emotional stress.⁵

Frostnip is characterized by pallor and paresthesia of exposed areas. It may precede frostbite, but it quickly resolves after rewarming.²

Pernio occurs when skin is exposed to damp, cold, nonfreezing environments.⁶ It results in edematous and inflammatory skin lesions that may be painful, pruritic, violaceous, or erythematous.⁶ These lesions are typically found over the fingers, toes, nose, ears, buttocks, or thighs.^4,6 Pernio may be classified as either primary or secondary disease.⁵ Primary pernio is considered idiopathic.⁶ Secondary pernio is thought to be either drug induced or due to underlying autoimmune diseases, such as hepatitis or cryopathy.⁶

Trench foot develops under similar conditions to pernio but requires exposure to a wet environment for at least 10 to 14 hours.⁷ It is characterized by foot pain, paresthesia, pruritus, edema, erythema, cyanosis, blisters, and even gangrene if left untreated.⁷

Continue to: Raynaud phenomenon

Raynaud phenomenon results from transient, acral vasocontraction and manifests as well-demarcated pallor, cyanosis, and then erythema as the affected body part reperfuses.⁵ Similar to pernio, it can be categorized as either primary or secondary.⁵ Primary phenomenon is idiopathic. Secondary phenomenon is thought to be a result of autoimmune disease, use of certain medications, occupational vibratory exposure, obstructive vascular disease, or infection.⁵

In the absence of a history of exposure to subfreezing temperatures, frostbite can be excluded from the differential diagnosis.

Treatment entails rewarming

The aim of frostbite treatment is to save injured cells and minimize tissue loss.¹ This is accomplished through rapid rewarming and—in severe cases—reperfusion techniques.

Tissue should be rewarmed in a 37°C to 39°C water bath with povidone iodine or chlorhexidine added for antiseptic effect.¹ All efforts should be made to avoid refreezing or trauma, as this could worsen the initial injury.² Oral or intravenous hydration may be offered to optimize fluid status.¹ Supplemental oxygen may be administered to maintain saturations above 90%.¹ Nonsteroidal anti-inflammatory drugs are helpful for analgesia and anti-­inflammatory effect, and opioids can be used for breakthrough pain.¹ It is recommended that blisters be drained in a sterile fashion and that all affected tissue be covered with topical aloe vera and a loose dressing.^1,2,4

Treatment of severe frostbite. Angiography should be performed on all patients with third- or fourth-degree frostbite.³ If imaging shows evidence of vascular occlusion, tissue plasminogen activator (tPA) and heparin can be initiated within 24 hours to reduce the risk for amputation.^8-10

Continue to: Iloprost is another...

Iloprost is another proposed treatment for severe frostbite. It is a prostacyclin analog that may lower the amputation rate in patients with at least third-degree frostbite.¹¹ Unlike tPA, iloprost may be given to trauma patients, and it can be used more than 24 hours after injury.²

In cases of fourth-degree frostbite that is not successfully reperfused, amputation is delayed until dry gangrene develops. This often takes weeks to months.¹²

Our patient underwent rewarming and was orally rehydrated. He was discharged home with ibuprofen, oxycodone-­acetaminophen, topical aloe vera, and loose dressings. His bullae enlarged the next day (FIGURE 3). One week later, his blisters were debrided and dressed with silver sulfadiazine at his plastic surgery follow-up. He experienced sensory deficits for a few months, but eventually made a full recovery after 6 months with no remaining sequelae.

IMAGE COURTESY OF MORTEZA KHODAEE, MD, MPH

ACKNOWLEDGEMENT
The authors thank Lisa Kim, MD, for her clinical care of this patient.

CORRESPONDENCE
Morteza Khodaee, MD, MPH, University of Colorado School of Medicine, Department of Family Medicine, AFW Clinic, 3055 Roslyn Street, Denver, CO 80238; morteza.khodaee@ cuanschutz.edu

A 27-year-old man presented to the urgent care clinic with acute bilateral hand swelling, blisters, numbness, and pain. History taking revealed that these symptoms developed after he was locked outside of his apartment for 45 minutes in –22°C (–8°F) weather following a night of heavy drinking.

On physical examination, the patient had a temperature of 36.2°C (97.2°F) and a heart rate of 116 beats/min. He had edema, tenderness, decreased sensation, and distal cyanosis involving all of his fingers (FIGURE 1). He also had large, tense, clear bullae over the dorsal aspect of his fingers (FIGURE 2).

IMAGE COURTESY OF MORTEZA KHODAEE, MD, MPH

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Second-degree frostbite

Frostbite is the result of tissue freezing, which generally occurs after prolonged exposure to freezing temperatures (typically –4°C or below).^1,2 The majority (~90%) of frostbite injuries occur in the hands and feet; however, frostbite has also been observed in the face, perineum, buttocks, and male genitalia.³

Angiography should be performed on patients with third- or fourth-degree frostbite. In cases of vascular occlusion, tPA and heparin can be started to reduce the risk for amputation.

Frostbite is a clinical diagnosis based on a history of sustained exposure to freezing temperatures, paresthesia of affected areas, and typical skin changes. Evidence is lacking regarding the epidemiology of frostbite within the general population.²

Pathophysiology. Intra- and extracellular ice crystal formation causes fluid and electrolyte disturbances, cell dehydration, lipid denaturation, and subsequent cell death.¹ After thawing, progressive tissue ischemia can occur as a result of endothelial damage and dysfunction, intravascular sludging, increased inflammatory markers, an influx of free radicals, and microvascular thrombosis.¹

Classification. Traditionally, frostbite has been classified according to a 4-tiered system based on tissue appearance after rewarming.² First-degree frostbite is characterized by white plaques with surrounding erythema; second degree by edema and clear or cloudy vesicles; third degree by hemorrhagic bullae; and fourth degree by cold and hard tissue that eventually progresses to gangrene.²

A simpler scheme designates frostbite as either superficial (corresponding to first- or second-degree frostbite) or deep (corresponding to third- or fourth-degree frostbite) with presumed muscle and bone involvement.²

Continue to: Risk factors

Risk factors. Frostbite is often associated with risk factors such as alcohol or drug intoxication, vehicular failure or trauma, immobilizing trauma, psychiatric illness, homelessness, Raynaud phenomenon, peripheral vascular disease, diabetes, inadequate clothing, previous cold-weather injury, outdoor winter recreation, and the use of certain medications (eg, beta-blockers).^1-3 Apart from environmental exposure, frostbite can also occur by direct contact with freezing materials, such as ice packs or industrial refrigerants.³

Differential includes nonfreezing injuries

Frostnip, pernio, and trench foot are other cold-weather injuries distinguished by the absence of tissue freezing.⁴ Raynaud phenomenon is a condition that is triggered by either cold temperatures or emotional stress.⁵

Frostnip is characterized by pallor and paresthesia of exposed areas. It may precede frostbite, but it quickly resolves after rewarming.²

Pernio occurs when skin is exposed to damp, cold, nonfreezing environments.⁶ It results in edematous and inflammatory skin lesions that may be painful, pruritic, violaceous, or erythematous.⁶ These lesions are typically found over the fingers, toes, nose, ears, buttocks, or thighs.^4,6 Pernio may be classified as either primary or secondary disease.⁵ Primary pernio is considered idiopathic.⁶ Secondary pernio is thought to be either drug induced or due to underlying autoimmune diseases, such as hepatitis or cryopathy.⁶

Trench foot develops under similar conditions to pernio but requires exposure to a wet environment for at least 10 to 14 hours.⁷ It is characterized by foot pain, paresthesia, pruritus, edema, erythema, cyanosis, blisters, and even gangrene if left untreated.⁷

Continue to: Raynaud phenomenon

Raynaud phenomenon results from transient, acral vasocontraction and manifests as well-demarcated pallor, cyanosis, and then erythema as the affected body part reperfuses.⁵ Similar to pernio, it can be categorized as either primary or secondary.⁵ Primary phenomenon is idiopathic. Secondary phenomenon is thought to be a result of autoimmune disease, use of certain medications, occupational vibratory exposure, obstructive vascular disease, or infection.⁵

In the absence of a history of exposure to subfreezing temperatures, frostbite can be excluded from the differential diagnosis.

Treatment entails rewarming

The aim of frostbite treatment is to save injured cells and minimize tissue loss.¹ This is accomplished through rapid rewarming and—in severe cases—reperfusion techniques.

Tissue should be rewarmed in a 37°C to 39°C water bath with povidone iodine or chlorhexidine added for antiseptic effect.¹ All efforts should be made to avoid refreezing or trauma, as this could worsen the initial injury.² Oral or intravenous hydration may be offered to optimize fluid status.¹ Supplemental oxygen may be administered to maintain saturations above 90%.¹ Nonsteroidal anti-inflammatory drugs are helpful for analgesia and anti-­inflammatory effect, and opioids can be used for breakthrough pain.¹ It is recommended that blisters be drained in a sterile fashion and that all affected tissue be covered with topical aloe vera and a loose dressing.^1,2,4

Treatment of severe frostbite. Angiography should be performed on all patients with third- or fourth-degree frostbite.³ If imaging shows evidence of vascular occlusion, tissue plasminogen activator (tPA) and heparin can be initiated within 24 hours to reduce the risk for amputation.^8-10

Continue to: Iloprost is another...

Iloprost is another proposed treatment for severe frostbite. It is a prostacyclin analog that may lower the amputation rate in patients with at least third-degree frostbite.¹¹ Unlike tPA, iloprost may be given to trauma patients, and it can be used more than 24 hours after injury.²

In cases of fourth-degree frostbite that is not successfully reperfused, amputation is delayed until dry gangrene develops. This often takes weeks to months.¹²

Our patient underwent rewarming and was orally rehydrated. He was discharged home with ibuprofen, oxycodone-­acetaminophen, topical aloe vera, and loose dressings. His bullae enlarged the next day (FIGURE 3). One week later, his blisters were debrided and dressed with silver sulfadiazine at his plastic surgery follow-up. He experienced sensory deficits for a few months, but eventually made a full recovery after 6 months with no remaining sequelae.

IMAGE COURTESY OF MORTEZA KHODAEE, MD, MPH

ACKNOWLEDGEMENT
The authors thank Lisa Kim, MD, for her clinical care of this patient.

CORRESPONDENCE
Morteza Khodaee, MD, MPH, University of Colorado School of Medicine, Department of Family Medicine, AFW Clinic, 3055 Roslyn Street, Denver, CO 80238; morteza.khodaee@ cuanschutz.edu

ILLUSTRATIVE CASE

A 27-year-old G1P000 at term with an uncomplicated pregnancy has been laboring for 6 hours with an epidural in place and a reassuring fetal heart tracing. She is at –2 station with complete cervical dilation and effacement. Should she push now or delay pushing to allow for more descent?

More than 10,000 women give birth each day in the United States, yet few of our approaches to labor management are evidence based.² For example, there are no clear guidelines on whether immediate pushing or delayed pushing (waiting 1-2 hours) in the second stage of labor (the time from complete cervical dilation to delivery of the fetus) leads to better outcomes.

A recent Cochrane review, which included very low- to moderate-quality trials of nulliparous and multiparous women using epidural analgesia showed that delayed pushing resulted in more vaginal deliveries, longer duration of second stage of labor, and shorter duration of pushing.³ But many of the trials included in this Cochrane review were noted to have study design limitations and significant heterogeneity.

A recent retrospective study found that delayed pushing resulted in longer duration of pushing and increased risks for cesarean section, operative vaginal delivery, and postpartum hemorrhage in nulliparous patients with and without epidurals.⁴ The World Health Organization recommends delayed pushing in women with epidural analgesia if time and fetal monitoring resources are available.⁵

STUDY SUMMARY

Does the timing of second stage pushing efforts affect outcomes?

This multicenter randomized controlled trial (RCT) evaluated the effect on spontaneous vaginal delivery of delayed pushing vs immediate pushing in 2404 term nulliparous women using epidural analgesia.¹ Patients were ≥ 37 weeks’ gestation. Once patients achieved 10 cm of cervical dilation, they were randomized in a 1:1 ratio to either immediate pushing or to delayed (for 60 minutes) pushing (unless there was an irresistible urge to push or they were otherwise instructed by their provider).

Outcome and results. The primary outcome was spontaneous vaginal delivery without the use of any operative support. The mean time to pushing after complete cervical dilation was 19 minutes in the immediate pushing group and 60 minutes in the delayed group. There was no difference in the rate of spontaneous vaginal delivery between the immediate and delayed pushing groups (86% vs 87%, respectively; P = .67). The immediate pushing group had a shorter duration of second stage of labor (102 minutes vs 134 minutes; mean difference [MD] = –32 minutes; 95% confidence interval [CI], –37 to –27; P < .001) and a slightly longer duration of active pushing (84 minutes vs 75 minutes; MD = 9.2 minutes; 95% CI, 6-13; P < .001).

Delaying pushing once the cervix is completely dilated is not indicated, even for nulliparous women receiving epidural analgesia.

There was no significant difference in operative vaginal or cesarean deliveries. Postpartum hemorrhage was lower in the immediate pushing group (2.3% vs 4%; risk ratio [RR] = 0.6; 95% CI, 0.3-0.9; P = .03; number needed to treat [NNT] = 58), as was chorioamnionitis (6.7% vs 9.1%; RR = 0.7; 95% CI, 0.66-0.90; P = .005; NNT = 40). There was no significant difference in neonatal morbidity between groups. And in subgroup analysis, there was no significant difference in rates of vaginal delivery based on fetal position (occiput anterior, posterior, or transverse) or station (defined as high [< 2 cm] or low [≥ 2 cm]) between groups. Recruitment was stopped early at 75% because there was no difference in the primary outcome and there was concern regarding an increased risk of hemorrhage in the delayed pushing group.

Continue to: WHAT'S NEW

WHAT’S NEW

There’s no good reason to delay pushing

Delaying pushing once the cervix is completely dilated is not indicated, even for nulliparous women receiving epidural analgesia, as it does not decrease the rate of spontaneous vaginal delivery. It does, however, increase the length of second stage labor and the risk of postpartum hemorrhage and chorioamnionitis.

CAVEATS

Study was stopped early, and groups were unblinded

This study was stopped early, so it is not known if it was underpowered for some of the secondary outcomes. Also, it was not possible to blind the groups, so it is not clear if any bias in patient management or diagnosis resulted.

CHALLENGES TO IMPLEMENTATION

Will current practice and culture pose obstacles?

Although the overt challenges to enacting a policy of immediate pushing are minimal, the inertia of current practice and culture could affect the implementation of this strategy.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

A 27-year-old G1P000 at term with an uncomplicated pregnancy has been laboring for 6 hours with an epidural in place and a reassuring fetal heart tracing. She is at –2 station with complete cervical dilation and effacement. Should she push now or delay pushing to allow for more descent?

More than 10,000 women give birth each day in the United States, yet few of our approaches to labor management are evidence based.² For example, there are no clear guidelines on whether immediate pushing or delayed pushing (waiting 1-2 hours) in the second stage of labor (the time from complete cervical dilation to delivery of the fetus) leads to better outcomes.

A recent Cochrane review, which included very low- to moderate-quality trials of nulliparous and multiparous women using epidural analgesia showed that delayed pushing resulted in more vaginal deliveries, longer duration of second stage of labor, and shorter duration of pushing.³ But many of the trials included in this Cochrane review were noted to have study design limitations and significant heterogeneity.

A recent retrospective study found that delayed pushing resulted in longer duration of pushing and increased risks for cesarean section, operative vaginal delivery, and postpartum hemorrhage in nulliparous patients with and without epidurals.⁴ The World Health Organization recommends delayed pushing in women with epidural analgesia if time and fetal monitoring resources are available.⁵

STUDY SUMMARY

Does the timing of second stage pushing efforts affect outcomes?

This multicenter randomized controlled trial (RCT) evaluated the effect on spontaneous vaginal delivery of delayed pushing vs immediate pushing in 2404 term nulliparous women using epidural analgesia.¹ Patients were ≥ 37 weeks’ gestation. Once patients achieved 10 cm of cervical dilation, they were randomized in a 1:1 ratio to either immediate pushing or to delayed (for 60 minutes) pushing (unless there was an irresistible urge to push or they were otherwise instructed by their provider).

Outcome and results. The primary outcome was spontaneous vaginal delivery without the use of any operative support. The mean time to pushing after complete cervical dilation was 19 minutes in the immediate pushing group and 60 minutes in the delayed group. There was no difference in the rate of spontaneous vaginal delivery between the immediate and delayed pushing groups (86% vs 87%, respectively; P = .67). The immediate pushing group had a shorter duration of second stage of labor (102 minutes vs 134 minutes; mean difference [MD] = –32 minutes; 95% confidence interval [CI], –37 to –27; P < .001) and a slightly longer duration of active pushing (84 minutes vs 75 minutes; MD = 9.2 minutes; 95% CI, 6-13; P < .001).

Delaying pushing once the cervix is completely dilated is not indicated, even for nulliparous women receiving epidural analgesia.

There was no significant difference in operative vaginal or cesarean deliveries. Postpartum hemorrhage was lower in the immediate pushing group (2.3% vs 4%; risk ratio [RR] = 0.6; 95% CI, 0.3-0.9; P = .03; number needed to treat [NNT] = 58), as was chorioamnionitis (6.7% vs 9.1%; RR = 0.7; 95% CI, 0.66-0.90; P = .005; NNT = 40). There was no significant difference in neonatal morbidity between groups. And in subgroup analysis, there was no significant difference in rates of vaginal delivery based on fetal position (occiput anterior, posterior, or transverse) or station (defined as high [< 2 cm] or low [≥ 2 cm]) between groups. Recruitment was stopped early at 75% because there was no difference in the primary outcome and there was concern regarding an increased risk of hemorrhage in the delayed pushing group.

Continue to: WHAT'S NEW

WHAT’S NEW

There’s no good reason to delay pushing

Delaying pushing once the cervix is completely dilated is not indicated, even for nulliparous women receiving epidural analgesia, as it does not decrease the rate of spontaneous vaginal delivery. It does, however, increase the length of second stage labor and the risk of postpartum hemorrhage and chorioamnionitis.

CAVEATS

Study was stopped early, and groups were unblinded

This study was stopped early, so it is not known if it was underpowered for some of the secondary outcomes. Also, it was not possible to blind the groups, so it is not clear if any bias in patient management or diagnosis resulted.

CHALLENGES TO IMPLEMENTATION

Will current practice and culture pose obstacles?

Although the overt challenges to enacting a policy of immediate pushing are minimal, the inertia of current practice and culture could affect the implementation of this strategy.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

A 27-year-old G1P000 at term with an uncomplicated pregnancy has been laboring for 6 hours with an epidural in place and a reassuring fetal heart tracing. She is at –2 station with complete cervical dilation and effacement. Should she push now or delay pushing to allow for more descent?

More than 10,000 women give birth each day in the United States, yet few of our approaches to labor management are evidence based.² For example, there are no clear guidelines on whether immediate pushing or delayed pushing (waiting 1-2 hours) in the second stage of labor (the time from complete cervical dilation to delivery of the fetus) leads to better outcomes.

A recent Cochrane review, which included very low- to moderate-quality trials of nulliparous and multiparous women using epidural analgesia showed that delayed pushing resulted in more vaginal deliveries, longer duration of second stage of labor, and shorter duration of pushing.³ But many of the trials included in this Cochrane review were noted to have study design limitations and significant heterogeneity.

A recent retrospective study found that delayed pushing resulted in longer duration of pushing and increased risks for cesarean section, operative vaginal delivery, and postpartum hemorrhage in nulliparous patients with and without epidurals.⁴ The World Health Organization recommends delayed pushing in women with epidural analgesia if time and fetal monitoring resources are available.⁵

STUDY SUMMARY

Does the timing of second stage pushing efforts affect outcomes?

This multicenter randomized controlled trial (RCT) evaluated the effect on spontaneous vaginal delivery of delayed pushing vs immediate pushing in 2404 term nulliparous women using epidural analgesia.¹ Patients were ≥ 37 weeks’ gestation. Once patients achieved 10 cm of cervical dilation, they were randomized in a 1:1 ratio to either immediate pushing or to delayed (for 60 minutes) pushing (unless there was an irresistible urge to push or they were otherwise instructed by their provider).

Outcome and results. The primary outcome was spontaneous vaginal delivery without the use of any operative support. The mean time to pushing after complete cervical dilation was 19 minutes in the immediate pushing group and 60 minutes in the delayed group. There was no difference in the rate of spontaneous vaginal delivery between the immediate and delayed pushing groups (86% vs 87%, respectively; P = .67). The immediate pushing group had a shorter duration of second stage of labor (102 minutes vs 134 minutes; mean difference [MD] = –32 minutes; 95% confidence interval [CI], –37 to –27; P < .001) and a slightly longer duration of active pushing (84 minutes vs 75 minutes; MD = 9.2 minutes; 95% CI, 6-13; P < .001).

Delaying pushing once the cervix is completely dilated is not indicated, even for nulliparous women receiving epidural analgesia.

There was no significant difference in operative vaginal or cesarean deliveries. Postpartum hemorrhage was lower in the immediate pushing group (2.3% vs 4%; risk ratio [RR] = 0.6; 95% CI, 0.3-0.9; P = .03; number needed to treat [NNT] = 58), as was chorioamnionitis (6.7% vs 9.1%; RR = 0.7; 95% CI, 0.66-0.90; P = .005; NNT = 40). There was no significant difference in neonatal morbidity between groups. And in subgroup analysis, there was no significant difference in rates of vaginal delivery based on fetal position (occiput anterior, posterior, or transverse) or station (defined as high [< 2 cm] or low [≥ 2 cm]) between groups. Recruitment was stopped early at 75% because there was no difference in the primary outcome and there was concern regarding an increased risk of hemorrhage in the delayed pushing group.

Continue to: WHAT'S NEW

WHAT’S NEW

There’s no good reason to delay pushing

Delaying pushing once the cervix is completely dilated is not indicated, even for nulliparous women receiving epidural analgesia, as it does not decrease the rate of spontaneous vaginal delivery. It does, however, increase the length of second stage labor and the risk of postpartum hemorrhage and chorioamnionitis.

CAVEATS

Study was stopped early, and groups were unblinded

This study was stopped early, so it is not known if it was underpowered for some of the secondary outcomes. Also, it was not possible to blind the groups, so it is not clear if any bias in patient management or diagnosis resulted.

CHALLENGES TO IMPLEMENTATION

Will current practice and culture pose obstacles?

Although the overt challenges to enacting a policy of immediate pushing are minimal, the inertia of current practice and culture could affect the implementation of this strategy.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Too few patients are being screened for abdominal aortic aneurysm (AAA), resulting in severe morbidity and mortality. Many patients with AAA aren’t identified until they present with rupture, leading to mortality as high as 90%.¹ Early detection is critical.

Medicare offers one-time free screening to eligible individuals > 65 years of age, and several professional organizations promote screening with published guidelines, which we discuss later in this article.

So who is at risk, who should be screened, and what is the best way to screen your patients?

Risk factors and sex differences

AAA has a prevalence of between 1% and 5% in men > 65 years old,^2,3 and it is 4 to 6 times more common in men than women.⁴ Major risk factors include smoking, older age, family history, and genetic factors, while hypertension, history of coronary artery disease, hyperlipidemia, and peripheral arterial disease have weaker associations.^3,4 Exercise and diabetes seem to have protective effects.⁵

The incidence and mortality of AAA increased between the 1950s and the mid-1990s; however, both indicators have decreased in numerous countries in the 21st century.⁶ Although the prevalence is much lower in women, they have a higher risk of rupture than men at equivalent lesion diameters.³ The prevalence of AAA in women who smoke and are > 70 years of age is > 1%.³

Silent but deadly

Most patients with AAA are asymptomatic. Their lesions are often detected incidentally on magnetic resonance imaging of the spine obtained for back pain, on an abdominal ultrasound (US) for gallstones, or on a routine computed tomography (CT) scan for the evaluation of abdominal pain. Some patients will experience vague abdominal discomfort from rapid expansion of an aneurysm prior to rupture, necessitating urgent repair. Also, some large aneurysms can erode into the spine and cause chronic back pain prior to rupture. An infrarenal abdominal aortic diameter > 30 mm defines an aneurysm,⁷ and once the diameter reaches 55 mm, the threat of rupture often justifies operative repair. (See “The preferred approach to repair.”)

Ruptured aneurysms will classically manifest with severe abdominal and/or back pain. Often a ruptured aneurysm will be contained in the retroperitoneum, allowing the patient to remain hemodynamically stable for a period of time and thus providing a window of opportunity for emergent repair.

Continue to: What is the evidence that screening is effective?

 

 

What is the evidence that screening is effective?

In 1988, researchers in Chichester, England, randomized > 6000 men ages 65 to 80 years to either a control group or a group that was offered a one-time US screen for AAA. After 15 years of follow-up, no significant difference in AAA mortality was seen between the groups, although 26% of those invited for screening declined to participate and accounted for more than half of the AAA-related deaths in the group receiving an invitation for screening.⁸

The MASS Trial,⁹ another British study, began in 1997 and screened men ages 65 to 74. More than 67,000 men were randomized, with 1 group invited for AAA screening and the other serving as a control. The final report on this trial was published in 2012. After 13 years of follow-up, there was a 42% reduction in AAA-related deaths in the group invited for screening, a small reduction in all-cause mortality, and a significant reduction in risk of AAA rupture (hazard ratio = 0.57). The researchers noted that 216 patients would have to be invited for screening to prevent 1 death over 13 years. They also reported that 21% of the invited patients that had an AAA-related death had an initial scan that was negative for AAA (aortic diameter < 3 cm). However, despite this finding, screening still appeared to be beneficial.

Lindholdt et al¹⁰ randomized > 12,000 Danish men ages 64 to 73 to serve as controls or to be invited for US screening for AAA. After 13 years of follow-up, those invited for screening had a 66% relative risk reduction in AAA-related mortality, with screening considered cost effective. There were no differences between the groups in all-cause mortality. Conversely, the Western Australia Trial studied an older group of men, ages 64 to 83, but was unable to show a benefit of screening in lowering AAA-related mortality.¹¹

Tikagi et al⁶ performed a meta-analysis on the data from the 4 trials above and reported up to 15 years of follow-up. Patients who attended screening sessions had a reduction in all-cause mortality with an odds ratio (OR) of 0.6, and a marked reduction in AAA-­related mortality with an OR of 0.4. The favorable data on screening have prompted the United Kingdom and Sweden to offer screening to all men ≥ 65 years, based on the current estimate of a 1% prevalence of AAA, although screening is felt to remain cost effective down to a prevalence of 0.35%.¹²

Handheld ultrasound is a viable method to detect AAA in an outpatient primary care setting at a reasonable cost.

Massachusetts General Hospital also reported¹³ that the detection rate of AAA increased, with the diagnosis made at smaller aneurysm dimensions, following publication of the US Preventive Services Task Force recommendations (reviewed below).

Continue to: When to screen

When to screen

Several professional organizations, as well as Medicare, have published AAA screening recommendations. While there are notable differences among them, their shared message is crucial: screen. Consider adding applicable reminders to your practice’s electronic medical record system to increase screening rates for eligible patients.

US Preventive Services Task Force ¹⁴

• Recommend one-time AAA screening with ultrasonography for men ages 65 to 75 years who have ever smoked (B recommendation).
• Selectively offer AAA screening to men ages 65 to 75 years who have never smoked, rather than routinely screening all men in this group (C recommendation). Individual attributes that could favor screening include a family history of AAA, the presence of other arterial aneurysms, and the number of risk factors for cardiovascular disease.
• Do not routinely screen women for AAA if they have never smoked and have no family history of AAA (D recommendation). For women ages 65 to 75 years who have ever smoked or have a family history of AAA, current evidence is insufficient to assess the balance of benefits and harms of screening for AAA (I statement). (See the related Practice Alert.)

Canadian Task Force on Preventive Health Care⁴

• Recommend one-time screening for AAA with US for men 65 to 80 years of age (weak level of recommendation; moderate-quality evidence).
• Do not recommend screening for men older than 80 years of age (weak recommendation; low quality of evidence).
• Do not recommend screening for women (strong recommendation; very low quality of evidence).

Society for Vascular Surgery¹⁵

• Recommend one-time US screening for AAA for men or women 65 to 75 years of age with a history of tobacco use (strong recommendation with high-quality evidence).
• Recommend one-time screening if there is a history of smoking for men or women > 75 years of age who are in good health and have not previously been screened. (Weak recommendation with low-quality evidence).
• Recommend one-time screening of men or women 65 to 75 years of age who are first-degree relatives of someone with AAA, or in those older than age 75 and in good health (weak recommendation with low-quality evidence).

How to screen

Physical exam. The abdominal aorta is often palpable in the epigastric region, and a thorough abdominal exam should include an attempt to detect it. It is critical that the patient be supine during palpation, to allow compression of the aorta against the lumbar spine. Even with a well-performed exam, however, its sensitivity is just 76% in the detection of AAA ≥ 5 cm.¹⁶

Continue to: Imaging

Imaging. US is the preferred imaging procedure when screening for AAA, given its high sensitivity and specificity.¹⁷ If US yields poor image quality, noncontrast CT is suggested, with magnetic resonance angiography being another alternative.¹⁸ Handheld US has the potential to supplement the physical exam, and has been shown to be a viable method to detect AAA in an outpatient primary care setting at a reasonable cost.¹⁹ Typically, a formal aortic US requires a patient to go without food or liquids for 8 hours before the procedure to obtain the best image; however, a good estimate of aortic diameter can be obtained without this restriction.

Despite Medicare coverage and recs, few people are screened

In 2007, Medicare started the SAAVE Program (Screening Aortic Aneurysm Very Effectively), offering a one-time US screening for AAA for eligible patients, as part of the Welcome to Medicare Program. Eligible individuals are men between 65 and 75 years of age with a history of smoking at least 100 cigarettes in their lifetime, and men or women in the same age group with a family history of AAA.²

Despite these recommendations, few patients receive screening. Centers for Medicare & Medicaid Services data show that < 10% of eligible men were screened between 2004 and 2008,²⁰ and Olchanski et al²¹ report that < 1% of eligible patients were screened from 2005-2009. A simulation model estimates that 131 additional life years could be gained per 1000 patients screened if the utilization rate could be increased to 80%, a seemingly achievable goal.²¹ Moreover, expanding the screening program to include female smokers could increase 10-year life expectancy by 13%.²¹ Reasons for underutilization of this Medicare screening benefit may include lack of awareness by physicians and patients, costs of co-pays, and underutilization of the basic Welcome to Medicare exam.²¹

An additional consequence of low utilization of AAA screening is a high percentage of patients who are identified only late in the course of the disease. Mell et al²² report that 39% of patients undergoing AAA repair were identified < 6 months prior to surgery, a higher percentage than would be expected in a well-screened population. They also determined that slightly more than one-third of patients undergoing surgery for ruptured AAA had diagnostic imaging performed > 6 months prior to surgery, suggesting the possibility that these patients may not have been properly surveilled for aneurysm expansion, although the authors note that other potential explanations include delays in treatment due to comorbidities, and patient-related factors such as refusal of surgery or noncompliance with follow-up.

CORRESPONDENCE
Jeffrey S. Todd, MD, 127 McClanahan Street, Suite 300, Roanoke, VA 24014; [email protected].

Too few patients are being screened for abdominal aortic aneurysm (AAA), resulting in severe morbidity and mortality. Many patients with AAA aren’t identified until they present with rupture, leading to mortality as high as 90%.¹ Early detection is critical.

Medicare offers one-time free screening to eligible individuals > 65 years of age, and several professional organizations promote screening with published guidelines, which we discuss later in this article.

So who is at risk, who should be screened, and what is the best way to screen your patients?

Risk factors and sex differences

AAA has a prevalence of between 1% and 5% in men > 65 years old,^2,3 and it is 4 to 6 times more common in men than women.⁴ Major risk factors include smoking, older age, family history, and genetic factors, while hypertension, history of coronary artery disease, hyperlipidemia, and peripheral arterial disease have weaker associations.^3,4 Exercise and diabetes seem to have protective effects.⁵

The incidence and mortality of AAA increased between the 1950s and the mid-1990s; however, both indicators have decreased in numerous countries in the 21st century.⁶ Although the prevalence is much lower in women, they have a higher risk of rupture than men at equivalent lesion diameters.³ The prevalence of AAA in women who smoke and are > 70 years of age is > 1%.³

Silent but deadly

Most patients with AAA are asymptomatic. Their lesions are often detected incidentally on magnetic resonance imaging of the spine obtained for back pain, on an abdominal ultrasound (US) for gallstones, or on a routine computed tomography (CT) scan for the evaluation of abdominal pain. Some patients will experience vague abdominal discomfort from rapid expansion of an aneurysm prior to rupture, necessitating urgent repair. Also, some large aneurysms can erode into the spine and cause chronic back pain prior to rupture. An infrarenal abdominal aortic diameter > 30 mm defines an aneurysm,⁷ and once the diameter reaches 55 mm, the threat of rupture often justifies operative repair. (See “The preferred approach to repair.”)

Ruptured aneurysms will classically manifest with severe abdominal and/or back pain. Often a ruptured aneurysm will be contained in the retroperitoneum, allowing the patient to remain hemodynamically stable for a period of time and thus providing a window of opportunity for emergent repair.

Continue to: What is the evidence that screening is effective?

 

 

What is the evidence that screening is effective?

In 1988, researchers in Chichester, England, randomized > 6000 men ages 65 to 80 years to either a control group or a group that was offered a one-time US screen for AAA. After 15 years of follow-up, no significant difference in AAA mortality was seen between the groups, although 26% of those invited for screening declined to participate and accounted for more than half of the AAA-related deaths in the group receiving an invitation for screening.⁸

The MASS Trial,⁹ another British study, began in 1997 and screened men ages 65 to 74. More than 67,000 men were randomized, with 1 group invited for AAA screening and the other serving as a control. The final report on this trial was published in 2012. After 13 years of follow-up, there was a 42% reduction in AAA-related deaths in the group invited for screening, a small reduction in all-cause mortality, and a significant reduction in risk of AAA rupture (hazard ratio = 0.57). The researchers noted that 216 patients would have to be invited for screening to prevent 1 death over 13 years. They also reported that 21% of the invited patients that had an AAA-related death had an initial scan that was negative for AAA (aortic diameter < 3 cm). However, despite this finding, screening still appeared to be beneficial.

Lindholdt et al¹⁰ randomized > 12,000 Danish men ages 64 to 73 to serve as controls or to be invited for US screening for AAA. After 13 years of follow-up, those invited for screening had a 66% relative risk reduction in AAA-related mortality, with screening considered cost effective. There were no differences between the groups in all-cause mortality. Conversely, the Western Australia Trial studied an older group of men, ages 64 to 83, but was unable to show a benefit of screening in lowering AAA-related mortality.¹¹

Tikagi et al⁶ performed a meta-analysis on the data from the 4 trials above and reported up to 15 years of follow-up. Patients who attended screening sessions had a reduction in all-cause mortality with an odds ratio (OR) of 0.6, and a marked reduction in AAA-­related mortality with an OR of 0.4. The favorable data on screening have prompted the United Kingdom and Sweden to offer screening to all men ≥ 65 years, based on the current estimate of a 1% prevalence of AAA, although screening is felt to remain cost effective down to a prevalence of 0.35%.¹²

Handheld ultrasound is a viable method to detect AAA in an outpatient primary care setting at a reasonable cost.

Massachusetts General Hospital also reported¹³ that the detection rate of AAA increased, with the diagnosis made at smaller aneurysm dimensions, following publication of the US Preventive Services Task Force recommendations (reviewed below).

Continue to: When to screen

When to screen

Several professional organizations, as well as Medicare, have published AAA screening recommendations. While there are notable differences among them, their shared message is crucial: screen. Consider adding applicable reminders to your practice’s electronic medical record system to increase screening rates for eligible patients.

US Preventive Services Task Force ¹⁴

• Recommend one-time AAA screening with ultrasonography for men ages 65 to 75 years who have ever smoked (B recommendation).
• Selectively offer AAA screening to men ages 65 to 75 years who have never smoked, rather than routinely screening all men in this group (C recommendation). Individual attributes that could favor screening include a family history of AAA, the presence of other arterial aneurysms, and the number of risk factors for cardiovascular disease.
• Do not routinely screen women for AAA if they have never smoked and have no family history of AAA (D recommendation). For women ages 65 to 75 years who have ever smoked or have a family history of AAA, current evidence is insufficient to assess the balance of benefits and harms of screening for AAA (I statement). (See the related Practice Alert.)

Canadian Task Force on Preventive Health Care⁴

• Recommend one-time screening for AAA with US for men 65 to 80 years of age (weak level of recommendation; moderate-quality evidence).
• Do not recommend screening for men older than 80 years of age (weak recommendation; low quality of evidence).
• Do not recommend screening for women (strong recommendation; very low quality of evidence).

Society for Vascular Surgery¹⁵

• Recommend one-time US screening for AAA for men or women 65 to 75 years of age with a history of tobacco use (strong recommendation with high-quality evidence).
• Recommend one-time screening if there is a history of smoking for men or women > 75 years of age who are in good health and have not previously been screened. (Weak recommendation with low-quality evidence).
• Recommend one-time screening of men or women 65 to 75 years of age who are first-degree relatives of someone with AAA, or in those older than age 75 and in good health (weak recommendation with low-quality evidence).

How to screen

Physical exam. The abdominal aorta is often palpable in the epigastric region, and a thorough abdominal exam should include an attempt to detect it. It is critical that the patient be supine during palpation, to allow compression of the aorta against the lumbar spine. Even with a well-performed exam, however, its sensitivity is just 76% in the detection of AAA ≥ 5 cm.¹⁶

Continue to: Imaging

Imaging. US is the preferred imaging procedure when screening for AAA, given its high sensitivity and specificity.¹⁷ If US yields poor image quality, noncontrast CT is suggested, with magnetic resonance angiography being another alternative.¹⁸ Handheld US has the potential to supplement the physical exam, and has been shown to be a viable method to detect AAA in an outpatient primary care setting at a reasonable cost.¹⁹ Typically, a formal aortic US requires a patient to go without food or liquids for 8 hours before the procedure to obtain the best image; however, a good estimate of aortic diameter can be obtained without this restriction.

Despite Medicare coverage and recs, few people are screened

In 2007, Medicare started the SAAVE Program (Screening Aortic Aneurysm Very Effectively), offering a one-time US screening for AAA for eligible patients, as part of the Welcome to Medicare Program. Eligible individuals are men between 65 and 75 years of age with a history of smoking at least 100 cigarettes in their lifetime, and men or women in the same age group with a family history of AAA.²

Despite these recommendations, few patients receive screening. Centers for Medicare & Medicaid Services data show that < 10% of eligible men were screened between 2004 and 2008,²⁰ and Olchanski et al²¹ report that < 1% of eligible patients were screened from 2005-2009. A simulation model estimates that 131 additional life years could be gained per 1000 patients screened if the utilization rate could be increased to 80%, a seemingly achievable goal.²¹ Moreover, expanding the screening program to include female smokers could increase 10-year life expectancy by 13%.²¹ Reasons for underutilization of this Medicare screening benefit may include lack of awareness by physicians and patients, costs of co-pays, and underutilization of the basic Welcome to Medicare exam.²¹

An additional consequence of low utilization of AAA screening is a high percentage of patients who are identified only late in the course of the disease. Mell et al²² report that 39% of patients undergoing AAA repair were identified < 6 months prior to surgery, a higher percentage than would be expected in a well-screened population. They also determined that slightly more than one-third of patients undergoing surgery for ruptured AAA had diagnostic imaging performed > 6 months prior to surgery, suggesting the possibility that these patients may not have been properly surveilled for aneurysm expansion, although the authors note that other potential explanations include delays in treatment due to comorbidities, and patient-related factors such as refusal of surgery or noncompliance with follow-up.

CORRESPONDENCE
Jeffrey S. Todd, MD, 127 McClanahan Street, Suite 300, Roanoke, VA 24014; [email protected].

Too few patients are being screened for abdominal aortic aneurysm (AAA), resulting in severe morbidity and mortality. Many patients with AAA aren’t identified until they present with rupture, leading to mortality as high as 90%.¹ Early detection is critical.

Medicare offers one-time free screening to eligible individuals > 65 years of age, and several professional organizations promote screening with published guidelines, which we discuss later in this article.

So who is at risk, who should be screened, and what is the best way to screen your patients?

Risk factors and sex differences

AAA has a prevalence of between 1% and 5% in men > 65 years old,^2,3 and it is 4 to 6 times more common in men than women.⁴ Major risk factors include smoking, older age, family history, and genetic factors, while hypertension, history of coronary artery disease, hyperlipidemia, and peripheral arterial disease have weaker associations.^3,4 Exercise and diabetes seem to have protective effects.⁵

The incidence and mortality of AAA increased between the 1950s and the mid-1990s; however, both indicators have decreased in numerous countries in the 21st century.⁶ Although the prevalence is much lower in women, they have a higher risk of rupture than men at equivalent lesion diameters.³ The prevalence of AAA in women who smoke and are > 70 years of age is > 1%.³

Silent but deadly

Most patients with AAA are asymptomatic. Their lesions are often detected incidentally on magnetic resonance imaging of the spine obtained for back pain, on an abdominal ultrasound (US) for gallstones, or on a routine computed tomography (CT) scan for the evaluation of abdominal pain. Some patients will experience vague abdominal discomfort from rapid expansion of an aneurysm prior to rupture, necessitating urgent repair. Also, some large aneurysms can erode into the spine and cause chronic back pain prior to rupture. An infrarenal abdominal aortic diameter > 30 mm defines an aneurysm,⁷ and once the diameter reaches 55 mm, the threat of rupture often justifies operative repair. (See “The preferred approach to repair.”)

Ruptured aneurysms will classically manifest with severe abdominal and/or back pain. Often a ruptured aneurysm will be contained in the retroperitoneum, allowing the patient to remain hemodynamically stable for a period of time and thus providing a window of opportunity for emergent repair.

Continue to: What is the evidence that screening is effective?

 

 

What is the evidence that screening is effective?

In 1988, researchers in Chichester, England, randomized > 6000 men ages 65 to 80 years to either a control group or a group that was offered a one-time US screen for AAA. After 15 years of follow-up, no significant difference in AAA mortality was seen between the groups, although 26% of those invited for screening declined to participate and accounted for more than half of the AAA-related deaths in the group receiving an invitation for screening.⁸

The MASS Trial,⁹ another British study, began in 1997 and screened men ages 65 to 74. More than 67,000 men were randomized, with 1 group invited for AAA screening and the other serving as a control. The final report on this trial was published in 2012. After 13 years of follow-up, there was a 42% reduction in AAA-related deaths in the group invited for screening, a small reduction in all-cause mortality, and a significant reduction in risk of AAA rupture (hazard ratio = 0.57). The researchers noted that 216 patients would have to be invited for screening to prevent 1 death over 13 years. They also reported that 21% of the invited patients that had an AAA-related death had an initial scan that was negative for AAA (aortic diameter < 3 cm). However, despite this finding, screening still appeared to be beneficial.

Lindholdt et al¹⁰ randomized > 12,000 Danish men ages 64 to 73 to serve as controls or to be invited for US screening for AAA. After 13 years of follow-up, those invited for screening had a 66% relative risk reduction in AAA-related mortality, with screening considered cost effective. There were no differences between the groups in all-cause mortality. Conversely, the Western Australia Trial studied an older group of men, ages 64 to 83, but was unable to show a benefit of screening in lowering AAA-related mortality.¹¹

Tikagi et al⁶ performed a meta-analysis on the data from the 4 trials above and reported up to 15 years of follow-up. Patients who attended screening sessions had a reduction in all-cause mortality with an odds ratio (OR) of 0.6, and a marked reduction in AAA-­related mortality with an OR of 0.4. The favorable data on screening have prompted the United Kingdom and Sweden to offer screening to all men ≥ 65 years, based on the current estimate of a 1% prevalence of AAA, although screening is felt to remain cost effective down to a prevalence of 0.35%.¹²

Handheld ultrasound is a viable method to detect AAA in an outpatient primary care setting at a reasonable cost.

Massachusetts General Hospital also reported¹³ that the detection rate of AAA increased, with the diagnosis made at smaller aneurysm dimensions, following publication of the US Preventive Services Task Force recommendations (reviewed below).

Continue to: When to screen

When to screen

Several professional organizations, as well as Medicare, have published AAA screening recommendations. While there are notable differences among them, their shared message is crucial: screen. Consider adding applicable reminders to your practice’s electronic medical record system to increase screening rates for eligible patients.

US Preventive Services Task Force ¹⁴

• Recommend one-time AAA screening with ultrasonography for men ages 65 to 75 years who have ever smoked (B recommendation).
• Selectively offer AAA screening to men ages 65 to 75 years who have never smoked, rather than routinely screening all men in this group (C recommendation). Individual attributes that could favor screening include a family history of AAA, the presence of other arterial aneurysms, and the number of risk factors for cardiovascular disease.
• Do not routinely screen women for AAA if they have never smoked and have no family history of AAA (D recommendation). For women ages 65 to 75 years who have ever smoked or have a family history of AAA, current evidence is insufficient to assess the balance of benefits and harms of screening for AAA (I statement). (See the related Practice Alert.)

Canadian Task Force on Preventive Health Care⁴

• Recommend one-time screening for AAA with US for men 65 to 80 years of age (weak level of recommendation; moderate-quality evidence).
• Do not recommend screening for men older than 80 years of age (weak recommendation; low quality of evidence).
• Do not recommend screening for women (strong recommendation; very low quality of evidence).

Society for Vascular Surgery¹⁵

• Recommend one-time US screening for AAA for men or women 65 to 75 years of age with a history of tobacco use (strong recommendation with high-quality evidence).
• Recommend one-time screening if there is a history of smoking for men or women > 75 years of age who are in good health and have not previously been screened. (Weak recommendation with low-quality evidence).
• Recommend one-time screening of men or women 65 to 75 years of age who are first-degree relatives of someone with AAA, or in those older than age 75 and in good health (weak recommendation with low-quality evidence).

How to screen

Physical exam. The abdominal aorta is often palpable in the epigastric region, and a thorough abdominal exam should include an attempt to detect it. It is critical that the patient be supine during palpation, to allow compression of the aorta against the lumbar spine. Even with a well-performed exam, however, its sensitivity is just 76% in the detection of AAA ≥ 5 cm.¹⁶

Continue to: Imaging

Imaging. US is the preferred imaging procedure when screening for AAA, given its high sensitivity and specificity.¹⁷ If US yields poor image quality, noncontrast CT is suggested, with magnetic resonance angiography being another alternative.¹⁸ Handheld US has the potential to supplement the physical exam, and has been shown to be a viable method to detect AAA in an outpatient primary care setting at a reasonable cost.¹⁹ Typically, a formal aortic US requires a patient to go without food or liquids for 8 hours before the procedure to obtain the best image; however, a good estimate of aortic diameter can be obtained without this restriction.

Despite Medicare coverage and recs, few people are screened

In 2007, Medicare started the SAAVE Program (Screening Aortic Aneurysm Very Effectively), offering a one-time US screening for AAA for eligible patients, as part of the Welcome to Medicare Program. Eligible individuals are men between 65 and 75 years of age with a history of smoking at least 100 cigarettes in their lifetime, and men or women in the same age group with a family history of AAA.²

Despite these recommendations, few patients receive screening. Centers for Medicare & Medicaid Services data show that < 10% of eligible men were screened between 2004 and 2008,²⁰ and Olchanski et al²¹ report that < 1% of eligible patients were screened from 2005-2009. A simulation model estimates that 131 additional life years could be gained per 1000 patients screened if the utilization rate could be increased to 80%, a seemingly achievable goal.²¹ Moreover, expanding the screening program to include female smokers could increase 10-year life expectancy by 13%.²¹ Reasons for underutilization of this Medicare screening benefit may include lack of awareness by physicians and patients, costs of co-pays, and underutilization of the basic Welcome to Medicare exam.²¹

An additional consequence of low utilization of AAA screening is a high percentage of patients who are identified only late in the course of the disease. Mell et al²² report that 39% of patients undergoing AAA repair were identified < 6 months prior to surgery, a higher percentage than would be expected in a well-screened population. They also determined that slightly more than one-third of patients undergoing surgery for ruptured AAA had diagnostic imaging performed > 6 months prior to surgery, suggesting the possibility that these patients may not have been properly surveilled for aneurysm expansion, although the authors note that other potential explanations include delays in treatment due to comorbidities, and patient-related factors such as refusal of surgery or noncompliance with follow-up.

CORRESPONDENCE
Jeffrey S. Todd, MD, 127 McClanahan Street, Suite 300, Roanoke, VA 24014; [email protected].

EVIDENCE SUMMARY

A Cochrane systematic review of vitamin D for managing asthma performed meta-analyses on RCTs that evaluated several outcomes.¹ The review found improvement in the primary outcome of asthma exacerbations requiring systemic steroids, mainly in adult patients, and in the secondary outcomes of emergency department visits or hospitalization, in a mix of adults and children (TABLE^1-6).

Most participants had mild-to-moderate asthma; trials lasted 4 to 12 months. Vitamin D dosage regimens varied, with a median daily dose of 900 IU/d (range, 400-4000 IU/d). Six RCTs were rated high-quality, and 1 had unclear risk of bias.

Supplementation reduced exacerbations in patients with low vitamin D levels

A subsequent (2017) systematic review and meta-analysis evaluating the primary outcome of exacerbations requiring steroids⁷ included another study⁸ (in addition to the 6 RCTs in the Cochrane review).

When researchers reanalyzed individual participant data from the trials in the Cochrane review, plus the additional RCT, to include baseline vitamin D levels, they found that vitamin D supplementation reduced exacerbations overall (NNT = 7.7) and in patients with low baseline vitamin D levels (25[OH] vitamin D < 25 nmol/L; 92 participants in 3 RCTs; NNT = 4.3) but not in patients with higher baseline levels (764 participants in 6 RCTs). Vitamin D supplementation reduced the asthma exacerbation rate in patients with low baseline vitamin D levels (0.19 vs 0.42 events per participant-year; P = .046).

Smaller benefit found on ED visits and hospitalizations

The Cochrane review, with 2 RCTs with adults (n = 658)¹ and 5 RCTs with children (n = 305),^2-6 evaluated whether Vitamin D reduced the need for emergency department visits and hospitalization with asthma exacerbations; they found a smaller benefit (NNT = 26.3).

Effects on FEV₁, daily asthma symptoms, and serious adverse effects

Several RCTs included in the 2017 meta-analysis found no effect of vitamin D supplementation on FEV₁, daily asthma symptoms (evaluated with the standardized Asthma Control Test Score), or reported serious adverse events.^2-6,9,10 No deaths occurred in any trial.

Additional findings in children from lower-quality studies

A 2015 systematic review and meta-analysis of RCTs evaluating vitamin D supplementation for children with asthma found¹¹:

• moderate-quality evidence for decreased emergency department visits (1 RCT from India, 100 children ages 3 to 14 years, decrease not specified; P = .015);
• low-quality evidence for reduced exacerbations (6 RCTs [3 RCTs also in Cochrane review], 507 children ages 3 to 17 years; risk ratio = 0.41; 95% confidence interval, 0.27-0.63); and
• low-quality evidence for reduced standardized asthma symptom scores (6 RCTs [2 RCTs also in Cochrane review], 231 children ages 3 to 17 years; amount of reduction not listed; P = .01).

Continue to: RECOMMENDATIONS

 

 

RECOMMENDATIONS

No published guidelines discuss using vitamin D in managing asthma. An American Academy of Family Physicians (AAFP) summary of the Cochrane systematic review recommends that family physicians await further studies and updated guidelines before recommending vitamin D for patients with asthma.¹² The AAFP also points out that the Endocrine Society has recommended vitamin D supplementation for adults (1500-2000 IU/d) and children (at least 1000 IU/d) at risk for deficiency.

Editor's takeaway

In the meta-analyses highlighted here, researchers evaluated asthma patients with a wide range of ages, baseline vitamin D levels, and vitamin D supplementation protocols. Although vitamin D reduced asthma exacerbations requiring steroids overall, the effect was driven by 3 studies of patients with low baseline vitamin D levels. As a result, disentangling who might benefit the most remains a challenge. The conservative course for now is to manage asthma according to current guidelines and supplement vitamin D in patients at risk for, or with known, ­deficiency.

EVIDENCE SUMMARY

A Cochrane systematic review of vitamin D for managing asthma performed meta-analyses on RCTs that evaluated several outcomes.¹ The review found improvement in the primary outcome of asthma exacerbations requiring systemic steroids, mainly in adult patients, and in the secondary outcomes of emergency department visits or hospitalization, in a mix of adults and children (TABLE^1-6).

Most participants had mild-to-moderate asthma; trials lasted 4 to 12 months. Vitamin D dosage regimens varied, with a median daily dose of 900 IU/d (range, 400-4000 IU/d). Six RCTs were rated high-quality, and 1 had unclear risk of bias.

Supplementation reduced exacerbations in patients with low vitamin D levels

A subsequent (2017) systematic review and meta-analysis evaluating the primary outcome of exacerbations requiring steroids⁷ included another study⁸ (in addition to the 6 RCTs in the Cochrane review).

When researchers reanalyzed individual participant data from the trials in the Cochrane review, plus the additional RCT, to include baseline vitamin D levels, they found that vitamin D supplementation reduced exacerbations overall (NNT = 7.7) and in patients with low baseline vitamin D levels (25[OH] vitamin D < 25 nmol/L; 92 participants in 3 RCTs; NNT = 4.3) but not in patients with higher baseline levels (764 participants in 6 RCTs). Vitamin D supplementation reduced the asthma exacerbation rate in patients with low baseline vitamin D levels (0.19 vs 0.42 events per participant-year; P = .046).

Smaller benefit found on ED visits and hospitalizations

The Cochrane review, with 2 RCTs with adults (n = 658)¹ and 5 RCTs with children (n = 305),^2-6 evaluated whether Vitamin D reduced the need for emergency department visits and hospitalization with asthma exacerbations; they found a smaller benefit (NNT = 26.3).

Effects on FEV₁, daily asthma symptoms, and serious adverse effects

Several RCTs included in the 2017 meta-analysis found no effect of vitamin D supplementation on FEV₁, daily asthma symptoms (evaluated with the standardized Asthma Control Test Score), or reported serious adverse events.^2-6,9,10 No deaths occurred in any trial.

Additional findings in children from lower-quality studies

A 2015 systematic review and meta-analysis of RCTs evaluating vitamin D supplementation for children with asthma found¹¹:

• moderate-quality evidence for decreased emergency department visits (1 RCT from India, 100 children ages 3 to 14 years, decrease not specified; P = .015);
• low-quality evidence for reduced exacerbations (6 RCTs [3 RCTs also in Cochrane review], 507 children ages 3 to 17 years; risk ratio = 0.41; 95% confidence interval, 0.27-0.63); and
• low-quality evidence for reduced standardized asthma symptom scores (6 RCTs [2 RCTs also in Cochrane review], 231 children ages 3 to 17 years; amount of reduction not listed; P = .01).

Continue to: RECOMMENDATIONS

 

 

RECOMMENDATIONS

No published guidelines discuss using vitamin D in managing asthma. An American Academy of Family Physicians (AAFP) summary of the Cochrane systematic review recommends that family physicians await further studies and updated guidelines before recommending vitamin D for patients with asthma.¹² The AAFP also points out that the Endocrine Society has recommended vitamin D supplementation for adults (1500-2000 IU/d) and children (at least 1000 IU/d) at risk for deficiency.

Editor's takeaway

In the meta-analyses highlighted here, researchers evaluated asthma patients with a wide range of ages, baseline vitamin D levels, and vitamin D supplementation protocols. Although vitamin D reduced asthma exacerbations requiring steroids overall, the effect was driven by 3 studies of patients with low baseline vitamin D levels. As a result, disentangling who might benefit the most remains a challenge. The conservative course for now is to manage asthma according to current guidelines and supplement vitamin D in patients at risk for, or with known, ­deficiency.

EVIDENCE SUMMARY

A Cochrane systematic review of vitamin D for managing asthma performed meta-analyses on RCTs that evaluated several outcomes.¹ The review found improvement in the primary outcome of asthma exacerbations requiring systemic steroids, mainly in adult patients, and in the secondary outcomes of emergency department visits or hospitalization, in a mix of adults and children (TABLE^1-6).

Most participants had mild-to-moderate asthma; trials lasted 4 to 12 months. Vitamin D dosage regimens varied, with a median daily dose of 900 IU/d (range, 400-4000 IU/d). Six RCTs were rated high-quality, and 1 had unclear risk of bias.

Supplementation reduced exacerbations in patients with low vitamin D levels

A subsequent (2017) systematic review and meta-analysis evaluating the primary outcome of exacerbations requiring steroids⁷ included another study⁸ (in addition to the 6 RCTs in the Cochrane review).

When researchers reanalyzed individual participant data from the trials in the Cochrane review, plus the additional RCT, to include baseline vitamin D levels, they found that vitamin D supplementation reduced exacerbations overall (NNT = 7.7) and in patients with low baseline vitamin D levels (25[OH] vitamin D < 25 nmol/L; 92 participants in 3 RCTs; NNT = 4.3) but not in patients with higher baseline levels (764 participants in 6 RCTs). Vitamin D supplementation reduced the asthma exacerbation rate in patients with low baseline vitamin D levels (0.19 vs 0.42 events per participant-year; P = .046).

Smaller benefit found on ED visits and hospitalizations

The Cochrane review, with 2 RCTs with adults (n = 658)¹ and 5 RCTs with children (n = 305),^2-6 evaluated whether Vitamin D reduced the need for emergency department visits and hospitalization with asthma exacerbations; they found a smaller benefit (NNT = 26.3).

Effects on FEV₁, daily asthma symptoms, and serious adverse effects

Several RCTs included in the 2017 meta-analysis found no effect of vitamin D supplementation on FEV₁, daily asthma symptoms (evaluated with the standardized Asthma Control Test Score), or reported serious adverse events.^2-6,9,10 No deaths occurred in any trial.

Additional findings in children from lower-quality studies

A 2015 systematic review and meta-analysis of RCTs evaluating vitamin D supplementation for children with asthma found¹¹:

• moderate-quality evidence for decreased emergency department visits (1 RCT from India, 100 children ages 3 to 14 years, decrease not specified; P = .015);
• low-quality evidence for reduced exacerbations (6 RCTs [3 RCTs also in Cochrane review], 507 children ages 3 to 17 years; risk ratio = 0.41; 95% confidence interval, 0.27-0.63); and
• low-quality evidence for reduced standardized asthma symptom scores (6 RCTs [2 RCTs also in Cochrane review], 231 children ages 3 to 17 years; amount of reduction not listed; P = .01).

Continue to: RECOMMENDATIONS

 

 

RECOMMENDATIONS

No published guidelines discuss using vitamin D in managing asthma. An American Academy of Family Physicians (AAFP) summary of the Cochrane systematic review recommends that family physicians await further studies and updated guidelines before recommending vitamin D for patients with asthma.¹² The AAFP also points out that the Endocrine Society has recommended vitamin D supplementation for adults (1500-2000 IU/d) and children (at least 1000 IU/d) at risk for deficiency.

Editor's takeaway

In the meta-analyses highlighted here, researchers evaluated asthma patients with a wide range of ages, baseline vitamin D levels, and vitamin D supplementation protocols. Although vitamin D reduced asthma exacerbations requiring steroids overall, the effect was driven by 3 studies of patients with low baseline vitamin D levels. As a result, disentangling who might benefit the most remains a challenge. The conservative course for now is to manage asthma according to current guidelines and supplement vitamin D in patients at risk for, or with known, ­deficiency.

In-office procedures are increasingly emphasized as a way to reduce referrals, avoid treatment delay, and increase practice revenue. Local analgesia is administered before many in-office procedures such as biopsies, toenail removal, and laceration repair. Skin procedures are performed most commonly; nearly three-quarters (74%) of family physicians (FPs) provided these services in 2018.¹ Administration of local anesthetic is often the most feared and uncomfortable step in the entire process.²

Knowledge of strategies to reduce pain associated with anesthetic administration can make a huge difference in the patient experience. This article explores evidence-based techniques for administering a local anesthetic with minimal patient discomfort.

4 factors influence the painof local anesthetic administration

Pain is perceived during the administration of local anesthetic because of the insertion of the needle and the increased pressure from the injection of fluid. The needle causes sharp, pricking “first pain” via large diameter, myelinated A-delta fibers, and the fluid induces unmyelinated C-fiber activation via tissue distention resulting in dull, diffuse “second pain.”

Four factors influence the experience of pain during administration of local anesthetic: the pharmacologic properties of the anesthetic itself, the equipment used, the environment, and the injection technique. Optimizing all 4 factors limits patient discomfort.

Pharmacologic agents: Lidocaine is often the agent of choice

Local anesthetics differ in maximal dosing, onset of action, and duration of effect (TABLE³). Given its ubiquity in clinics and hospitals, 1% lidocaine is often the agent of choice. Onset of effect occurs within minutes and lasts up to 2 hours. Alternative agents, such as bupivacaine or ropivacaine, may be considered to prolong the anesthetic effect; however, limited evidence exists to support their use in office-based procedures. Additionally, bupivacaine and ropivacaine may be associated with greater pain on injection and parasthesias lasting longer than the duration of pain control.^4-6 In practice, maximal dosing is most important in the pediatric population, given the smaller size of the patients and their increased susceptibility to toxicity.

Calculating the maximum recommended dose. To calculate the maximum recommended dose of local anesthetic, you need to know the concentration of the anesthetic, the maximum allowable dose (mg/kg), and the weight of the patient.^7,8 The concentration of the local anesthetic is converted from percentage to weight per unit volume (eg, 1% = 10 mg/mL; 0.5% = 5 mg/mL). Multiply the patient's weight (kg) by the maximum dose of local anesthetic (mg/kg) and divide by the concentration of the local anesthetic (mg/mL) to get the maximum recommended dose in milliliters. Walsh et al⁹ described a simplified formula to calculate the maximum allowable volume of local anesthetics in milliliters:

(maximum allowable dose in mg/kg) × (weight in kg) × (1 divided by the concentration of anesthetic).

For delivery of lidocaine with epinephrine in a 50-lb (22.7-kg) child, the calculation would be (7 mg/kg) × (22.7 kg) × (1 divided by 10 mg/mL) = 15.9 mL.

Continue to: The advantages (and misconceptions) of epinephrine

 

 

The advantages (and misconceptions) of epinephrine

The advantage of adding epinephrine is that it prolongs the effect of the anesthesia and it decreases bleeding. Epinephrine is commonly available as a premixed solution with lidocaine or bupivacaine at a concentration of 1:100,000 and is generally differentiated from “plain” local anesthetic by a red label and cap. Although maximum vasoconstriction may occur as long as 30 minutes after injection,¹⁰ adequate vasoconstriction is achieved in 7 to 10 minutes for excision of skin lesions.¹¹

Traditional teaching recommends against using epinephrine in the “fingers, toes, penis, ears, or nose” because of potential arterial spasm, ischemia, and gangrene distal to the injection site.¹² These concerns were based on experiences with procaine and cocaine mixed with epinephrine. Studies suffered from multiple confounders, including tourniquets and nonstandardized epinephrine concentrations.^13-15

Add epinephrine to the anesthetic solution to prolong anesthesia and decrease bleeding.

No association of distal ischemia with epinephrine use was identified in a recent Cochrane Review or in another multicenter prospective study.^16,17 Phentolamine, a non-selective alpha-adrenergic receptor antagonist and vasodilator, can be administered to reverse vasoconstriction following inadvertent administration of high-dose epinephrine (1:1000) via anaphylaxis autoinjector kits.

Dosing of phentolamine is 1 mL of 1 mg/mL solution delivered subcutaneously to the affected area; reversal decreases the duration of vasoconstriction from 320 minutes to approximately 85 minutes.¹⁸ As always, when applying literature to clinical practice, one must keep in mind the risks and benefits of any intervention. As such, in patients with pre-existing vascular disease, vaso-occlusive or vasospastic disease, or compromised perfusion due to trauma, one must weigh the benefits of the hemostatic effect against potential ischemia of already susceptible tissues. In such instances, omitting epinephrine from the solution is reasonable.

The benefits of sodium bicarbonate

The acidity of the solution contributes to the level of pain associated with administration of local anesthesia. Previously opened containers become more acidic.¹⁹ Addition of 8.4% sodium bicarbonate, at a ratio of 1 mL per 10 mL of 1% lidocaine with 1:100,000 epinephrine, neutralizes the pH to 7.4.¹⁹ A Cochrane Review showed that correction of pH to physiologic levels results in a significant reduction in pain.²⁰

Continue to: This solution can be...

This solution can be easily prepared, as standard syringes hold an additional milliliter (ie, 10-mL syringes hold 11 mL) and, thus, can accommodate the additional volume of bicarbonate.²¹

Warming the solution helps, too

Warming the solution to body temperature prior to injection decreases pain on injection.²² This may be done in a variety of ways depending on available in-office equipment. Water baths, incubators, fluid warmers, heating pads, or specific syringe warmers may be used. Multiple studies have shown improvement in patient satisfaction with warming.²³ Moreover, warming and buffering solution provide a synergistic effect on pain reduction.²³

Equipment: Size matters

Smaller diameter needles. Reducing the outer diameter of the needle used for injection improves pain by reducing activation of nociceptors.^24-26 Reduced inner diameter restricts injection speed, which further reduces pain.²⁵ We recommend 27- to 30-gauge needles for subcutaneous injection and 25- to 27-gauge needles for intra-articular or tendon sheath injections.

Appropriate syringe size. Filling a syringe to capacity results in maximal deployment of the plunger. This requires greater handspan, which can lead to fatigue and loss of control during injection.^26,27 Using a syringe filled to approximately half its capacity results in improved dexterity. We recommend 10-mL syringes with 5 mL to 6 mL of local anesthetic for small procedures and 20-mL syringes filled with 10 mL to 12 mL for larger procedures.

Topical local anesthetics may be used either as an adjunct to decrease pain during injection or as the primary anesthetic.²⁸ A variety of agents are available for clinical use, including eutectic mixture of local anesthetics (EMLA), lidocaine-epinephrine-tetracaine (LET), lidocaine, benzocaine, and tetracaine. FPs should be familiar with their different pharmacokinetic profiles.

Continue to: EMLA is a mixture of...

EMLA is a mixture of 25 mg/mL of lidocaine and 25 mg/mL of prilocaine. It is indicated for topical anesthesia on intact, nonmucosal, uninjured skin (maximal dose 20 g/200 cm² of surface area). It is applied in a thick layer and covered with an occlusive dressing (eg, Tegaderm) to enhance dermal penetration. The depth of penetration increases with application time and may reach a maximum depth of 3 mm and 5 mm following 60-minute and 120-minute application times, respectively.²⁸ Duration of effect is 60 to 120 minutes.

LET, which is a mixture of 4% lidocaine, 0.1% epinephrine, and 0.5% tetracaine, may be used on nonintact, nonmucosal surfaces. Typically, 1 mL to 5 mL of gel is applied directly to the target area and is followed by application of direct pressure for 15 to 30 minutes. LET is not effective on intact skin and is contraindicated in children < 2 years of age.²⁸

Cooling sprays or ice. Topical skin refrigerants, or vapocoolants (eg, ethyl chloride spray), offer an option for short-term local anesthesia that is noninvasive and quick acting. Ethyl chloride is a gaseous substance that extracts heat as it evaporates from the skin, resulting in a transient local conduction block. Skin refrigerants are an option to consider for short procedures such as intra-articular injections, venipuncture, or skin tag excision, or as an adjunct prior to local anesthetic delivery.^29-32 Research has shown that topical ethyl chloride spray also possesses antiseptic properties.^29,33

Environment: Make a few simple changes

Direct observation of needle penetration is associated with increased pain; advising patients to avert their gaze will mitigate the perception of pain.³⁴ Additionally, research has shown that creating a low-anxiety environment improves patient-reported outcomes in both children and adults.³⁵ Music or audiovisual or multimedia aids, for example, decrease pain and anxiety, particularly among children, and can be readily accessed with smart devices.^36-39

Warming and buffering solution provide a synergistic effect on pain reduction.

We also recommend avoiding terms such as “pinch,” “bee sting,” or “stick” in order to reduce patient anxiety. Instead, we use language such as, “This is the medicine that will numb the area so you will be comfortable during the procedure.”⁴⁰

Continue to: Injection technique

 

 

Injection technique: Consider these helpful tips

Site of needle entry. Prior to injecting local anesthesia, assess the area where the procedure is planned (FIGURE 1). The initial injection site should be proximal along the path of innervation. If regional nerves are anesthetized proximally and infiltration of local anesthesia proceeds distally, the initial puncture will be painful; however, further injections will be through anesthetized skin. Additionally, consider and avoid regional vascular anatomy.^41,42

Counter-stimulation. Applying firm pressure, massaging, or stroking the site prior to or during the injection decreases pain.^43,44 This technique may be performed by firmly pinching the area of planned injection between the thumb and index fingers, inserting the needle into the pinched skin, and maintaining pressure on the area until the anesthetic effect is achieved.

Angle of needle insertion. Perpendicular entry of the needle into the skin appears to reduce injection site pain (FIGURE 1). Anecdotal reports are supported by a randomized, controlled crossover trial that demonstrated significantly reduced pain with perpendicular injection compared to delivery at 45°.⁴⁵

Depth of injection. Subcutaneous needle placement is associated with significantly less pain than injection into superficial dermis.^2,46 Dermal wheals cause distention of the dermis, increased intradermal pressure, and greater activation of pain afferents in comparison to injection in the subcutaneous space.⁴⁶ One important exception is the shave biopsy in which dermal distention is, in fact, desirable to ensure adequate specimen collection.

Other methods of pain reduction should still be employed. In the setting of traumatic wounds when a laceration is present, injection into the subcutaneous fat through the wound is easy and associated with less pain than injection through intact skin.⁴⁷

Continue to: Speed of injection

Speed of injection. Rapid injection of anesthesia is associated with worse injection site pain and decreased patient satisfaction.^48-50 Slowing the rate of injection causes less rapid distention of the dermis and subcutaneous space, resulting in decreased pain afferent activation and increased time for nerve blockade. Its importance is underscored by a prospective, randomized trial that compared rate of administration with buffering of local anesthetics and demonstrated that slow administration impacted patient-perceived pain more than buffering solution.⁵¹

Needle stabilization. Following perpendicular entry of the needle into the area of planned infiltration, deliver 0.5 mL of local anesthetic into the subcutaneous space without movement of the needle tip.⁵² With a stabilized needle tip, pain associated with initial needle entry is no longer perceived within 15 to 30 seconds.

Any reinsertion of the needle should be through previously anesthetized skin.

It is paramount to stabilize both the syringe and the area of infiltration to prevent patient movement from causing iatrogenic injury or the need for multiple needlesticks. This can be accomplished by maintaining the dominant hand in a position to inject (ie, thumb on the plunger).

Needle reinsertion. Once subcutaneous swelling of local anesthesia is obtained, the needle may be slowly advanced, maintaining a palpable subcutaneous wavefront of local anesthesia ahead of the needle tip as it moves proximally to distally.^2,52 Any reinsertion of the needle should be through previously anesthetized skin; this blockade is assessed by the presence of palpable tumescence and blanching (from the epinephrine effect).⁵³

An example of the application of these injection pearls is demonstrated in the ­administration of a digital nerve block in FIGURE 2.^54,55 With the use of the techniques outlined here, the patient ideally experiences only the initial needle entry and is comfortable for the remainder of the procedure.

PHOTO COURTESY OF BRENT DEGEORGE, MD, PhD, AND ROBERTO MARTINEZ, MD, THE UNIVERSITY OF VIRGINIA DEPARTMENT OF PLASTIC SURGERY

CORRESPONDENCE
Katharine C. DeGeorge, MD, MS, Department of Family Medicine, University of Virginia, 1215 Lee Street, Charlottesville, VA, 22903; [email protected].