Case

A 2-year-old boy and his mother were referred to the ED by the child’s pediatrician after a routine venous blood lead level (BLL) taken at the boy’s recent well visit revealed an elevated lead level of 52 mcg/dL (normal range, <5 mcg/dL). The child’s mother reported that although her son had always been a picky eater, he had recently been complaining of abdominal pain.

The patient’s well-child visits had been normal until his recent 2-year checkup, at which time his pediatrician noticed some speech delay. On further history taking, the emergency physician (EP) learned the patient and his mother resided in an older home (built in the 1950s) that was in disrepair. The mother asked the EP if the elevation in the child’s BLL could be due to the drinking water in their town.

What are the most likely sources of environmental lead exposure?

In 2016, the topic of lead poisoning grabbed national attention when a pediatrician in Flint, Michigan detected an abrupt doubling of the number of children with elevated lead levels in her practice.¹ Upon further investigation, it was discovered that these kids had one thing in common: the source of their drinking water. The City of Flint had recently switched the source of its potable water from Lake Huron to the Flint River. The lower quality water, which was not properly treated with an anticorrosive agent such as orthophosphate, led to widespread pipe corrosion and lead contamination. This finding resulted in a cascade of water testing by other municipalities and school systems, many of which identified lead concentrations above the currently accepted drinking water standard of 15 parts per billion (ppb).

Thousands of children each year are identified to have elevated BLLs, based on the Centers for Disease Control and Prevention definition of a “level of concern” as more than 5 mcg/dL.² The majority of these exposures stem from environmental exposure to lead paint dust in the home, but drinking water normally contributes as a low-level, constant, “basal” exposure. While lead-contaminated drinking water is not acceptable, it is unlikely to generate many ED visits. However, there are a variety of other lead sources that may prompt children to present to the ED with acute or subacute lead poisoning.

Lead is a heavy metal whose physical properties indicate its common uses. It provides durability and opacity to pigments, which is why it is found in oil paint, house paint used before 1976, and on paint for large outdoor structures, where it is still used. Lead is also found in the pigments used in cosmetics, stained glass, and painted pottery, and as an adulterant in highly colored foodstuffs such as imported turmeric.³

The physicochemical characteristics of lead make it an ideal component of solder. Many plumbing pipes in use today are not lead, but join one another using lead solder at the joints, sites that are vulnerable to corrosion. The heavy molecular weight of lead makes it a useful component of bullets and munitions.

Tetraethyl lead was used as an “anti-knock” agent to smooth out the combustion of heterogenous compounds in automotive fuel before it was removed in the mid-1970s.⁴ Prior to its removal, leaded gasoline was the largest source of air, soil, and groundwater contamination leading to environmental exposures.⁴ At present, the most common source of environmental lead exposure among young children is through peeling paint in deteriorating residential buildings. Hazardous occupational lead exposures arise from work involving munitions, reclamation and salvage, painting, welding, and numerous other settings—particularly sites where industrial hygiene is suboptimal. Lead from these sites can be inadvertently transported home on clothing or shoes, raising the exposure risk for children in the household.⁴

What are the health effects of lead exposure?

Like most heavy metals, lead is toxic to many organ systems in the body. The signs and symptoms of lead poisoning vary depending on the patient’s BLL and age (Table 1).⁵ The most common clinical effect of lead in the adult population is hypertension.⁶ Additional renal effects include a Fanconi-type syndrome with glycosuria and proteinuria. Lead can cause a peripheral neuropathy that is predominantly motor, classically causing foot or wrist drop. Abdominal pain from lead exposure is sometimes termed “lead colic” due to its intermittent and often severe nature. Abnormalities in urate metabolism cause a gouty arthritis referred to as “saturnine gout.” ⁶

The young pediatric central nervous system (CNS) is much more vulnerable to the effects of lead than the adult CNS. Even low-level lead exposure to the developing brain causes deficits in intelligence quotient, attention, impulse control, and other neurocognitive functions that are largely irreversible.⁷

Children with an elevated BLL may also develop constipation, anorexia, pallor, and pica.⁸ The development of geophagia (subtype of pica in which one craves and ingests nonfood clay or soil-like materials), represents a “chicken-or-egg” phenomena as it both causes and results from lead poisoning.

Lead impairs multiple steps of the heme synthesis pathway, causing microcytic anemia with basophilic stippling. Lead-induced anemia exacerbates pica as anemic patients are more likely to eat leaded paint chips and other lead-containing materials such as pottery.⁸ Of note, leaded white paint is reported to have a pleasant taste due to the sweet-tasting lead acetate used as a pigment.

The most dramatic and consequential manifestation of lead poisoning is lead encephalopathy. This can occur at any age, but manifests in children at much lower BLLs than in adults. Patients can be altered or obtunded, have convulsive activity, and may develop cerebral edema. Encephalopathy is a life-threatening emergency and must be recognized and treated immediately. Lead encephalopathy should be suspected in any young child with hand-to-mouth behavior who has any of the above environmental risk factors.⁴ The findings of anemia or the other diagnostic signs described below are too unreliable and take too long to be truly helpful in making the diagnosis.

How is the diagnosis of lead poisoning made?

The gold standard for the diagnosis of lead poisoning is the measurement of BLL. However, the turnaround time for this test is usually at least 24 hours, but may take up to several days. As such, adjunctive testing can accelerate obtaining a diagnosis. A complete blood count (CBC) to evaluate for microcytic anemia may demonstrate a characteristic pattern of basophilic stippling.⁹ A protoporphyrin level—either a free erythrocyte protoporphyrin (FEP) or a zinc protoporphyrin level—will be elevated, a result of heme synthesis disruption.⁹ Urinalysis may demonstrate glycosuria or proteinuria.⁶ Hypertension is often present, even in pediatric patients.

An abdominal radiograph is essential in children to determine whether a lead foreign body, such as a paint chip, is present in the intestinal lumen. Long bone films may demonstrate “lead lines” at the metaphysis, which in fact do not reflect lead itself but abnormal calcium deposition in growing bone due to lead’s interference with bone remodeling. A computed tomography (CT) scan of the brain in patients with encephalopathy will often demonstrate cerebral edema.⁶

Of note, capillary BLLs taken via finger-stick can be falsely elevated due contamination during collection (eg, the presence of lead dust on the skin). However, this screening method is often used by clinicians in the pediatric primary care setting because of its feasibility. Elevated BLLs from capillary testing should always be followed by a BLL obtained by venipuncture.²

Case Continuation

The patient’s mother was counseled on sources of lead contamination. She was informed that although drinking water may contribute some amount to an elevated BLL, the most likely source of contamination is still lead paint found in older homes such as the one in which she and her son resided.

Diagnostic studies to support the diagnosis of lead poisoning were performed. A CBC revealed a hemoglobin of 9.8 g/dL with a mean corpuscular volume of 68 fL. A microscopic smear of blood demonstrated basophilic stippling of red blood cells. An FEP level was 386 mcg/dL. An abdominal radiograph demonstrated small radiopacities throughout the large intestine, without obstruction, which was suggestive of ingested lead paint chips.

What is the best management approach to patients with suspected lead poisoning?

The first-line treatment for patients with lead poisoning is removal from the exposure source, which first and foremost requires identification of the hazard through careful history taking and scene investigation by the local health department. This will avoid recurrent visits following successful chelation for repeat exposure to an unidentified source. Relocation to another dwelling will often be required for patients with presumed exposure until the hazard can be identified and abated.

Patients who have ingested or have embedded leaded foreign bodies will require removal via whole bowel irrigation or surgical means.

Following decontamination, chelation is required for children with a BLL more than 45 mcg/dL, and adults with CNS symptomatology and a BLL more than 70 mcg/dL. Table 2 provides guidelines for chelation therapy based on BLL.⁵

Work-up and Management in the ED

The patient with lead poisoning, while an unusual presentation in the ED, requires specialized management to minimize sequelae of exposure. Careful attention to history is vital. When in doubt, the EP should consult with her or his regional poison control center (800-222-1222) or with a medical toxicologist or other expert.

There are several scenarios in which a patient may present to the ED with lead toxicity. The following scenarios, along with their respective clinical approach strategies, represent three of the most common presentations.

Scenario 1: The Pediatric Patient With Elevated Venous Blood Lead Levels

The EP should employ the following clinical approach when evaluating and managing the pediatric patient with normal mental status whose routine screening reveals a BLL sufficiently elevated to warrant evaluation or admission—perhaps to discontinue exposure or initiate chelation therapy.

• Obtain a history, including possible lead sources; perform a complete physical examination; and obtain a repeat BLL, CBC with microscopic examination, and renal function test.
• Obtain an abdominal film to look for radiopacities, including paint chips or larger ingested foreign bodies.
• If radiopaque foreign bodies are present on abdominal radiograph, whole bowel irrigation with polyethylene glycol solution given via a nasogastric tube at 250 to 500 cc/h for a pediatric patient (1 to 2 L/h for adult patients) should be given until no residual foreign bodies remain.
• Obtain a radiograph of the long bone, which may demonstrate metaphyseal enhancement in the pediatric patient, suggesting long-term exposure.
• Ensure local or state health departments are contacted to arrange for environmental inspection of the home. This is essential prior to discharge to the home environment.
• Begin chelation therapy according to the BLL (Table 2).

Scenario 2: Adult Patients Presenting With Signs and Symptoms of Lead Toxicity

The adult patient who presents to the ED with complaints suggestive of lead poisoning and whose history is indicative of lead exposure should be evaluated and managed as follows:

• Obtain a thorough history, including the occupation and hobbies of the patient and all family members.
• Obtain vital signs to evaluate for hypertension; repeat BLL, CBC with smear, and serum creatinine test. Perform a physical examination to evaluate for lead lines.
• Obtain radiographic images, which may demonstrate a leaded foreign body, such as in the patient with prior history of gunshot wounds.
• If the BLL is sufficiently elevated or clinical findings are sufficiently severe, admit for chelation.

Scenario 3: The Pediatric or Adult Patient Presenting With Altered Mental Status

The patient presenting with altered mental status of unclear etiology—regardless of age—and in whom lead encephalopathy is a possible cause, should be worked-up and managed as follows:

• Obtain BLL, CBC, FEP levels. Consider radiographic imaging to assess for ingested or embedded foreign bodies.
• If abnormalities in the above laboratory studies are consistent with lead poisoning, initiate chelation immediately—prior to receiving repeat BLL result.
• Obtain a CT scan of the head to assess for cerebral edema.
• Provide supportive care for encephalopathy, including airway control and management of increased intracranial pressure.

Case Conclusion

The patient was admitted to the hospital for whole bowel irrigation and chelation therapy with succimer. The local health department conducted an investigation of the home and found multiple areas of peeling lead paint and lead dust, and ordered remediation of the property before it could be re-occupied by the family. A test of the home’s drinking water found no elevation above the 15 ppb standard.

The patient was discharged from the hospital in the care of his mother. They were relocated to a lead-free home, with follow-up by the pediatrician for ongoing monitoring of the BLL and developmental milestones.

Case

A 2-year-old boy and his mother were referred to the ED by the child’s pediatrician after a routine venous blood lead level (BLL) taken at the boy’s recent well visit revealed an elevated lead level of 52 mcg/dL (normal range, <5 mcg/dL). The child’s mother reported that although her son had always been a picky eater, he had recently been complaining of abdominal pain.

The patient’s well-child visits had been normal until his recent 2-year checkup, at which time his pediatrician noticed some speech delay. On further history taking, the emergency physician (EP) learned the patient and his mother resided in an older home (built in the 1950s) that was in disrepair. The mother asked the EP if the elevation in the child’s BLL could be due to the drinking water in their town.

What are the most likely sources of environmental lead exposure?

In 2016, the topic of lead poisoning grabbed national attention when a pediatrician in Flint, Michigan detected an abrupt doubling of the number of children with elevated lead levels in her practice.¹ Upon further investigation, it was discovered that these kids had one thing in common: the source of their drinking water. The City of Flint had recently switched the source of its potable water from Lake Huron to the Flint River. The lower quality water, which was not properly treated with an anticorrosive agent such as orthophosphate, led to widespread pipe corrosion and lead contamination. This finding resulted in a cascade of water testing by other municipalities and school systems, many of which identified lead concentrations above the currently accepted drinking water standard of 15 parts per billion (ppb).

Thousands of children each year are identified to have elevated BLLs, based on the Centers for Disease Control and Prevention definition of a “level of concern” as more than 5 mcg/dL.² The majority of these exposures stem from environmental exposure to lead paint dust in the home, but drinking water normally contributes as a low-level, constant, “basal” exposure. While lead-contaminated drinking water is not acceptable, it is unlikely to generate many ED visits. However, there are a variety of other lead sources that may prompt children to present to the ED with acute or subacute lead poisoning.

Lead is a heavy metal whose physical properties indicate its common uses. It provides durability and opacity to pigments, which is why it is found in oil paint, house paint used before 1976, and on paint for large outdoor structures, where it is still used. Lead is also found in the pigments used in cosmetics, stained glass, and painted pottery, and as an adulterant in highly colored foodstuffs such as imported turmeric.³

The physicochemical characteristics of lead make it an ideal component of solder. Many plumbing pipes in use today are not lead, but join one another using lead solder at the joints, sites that are vulnerable to corrosion. The heavy molecular weight of lead makes it a useful component of bullets and munitions.

Tetraethyl lead was used as an “anti-knock” agent to smooth out the combustion of heterogenous compounds in automotive fuel before it was removed in the mid-1970s.⁴ Prior to its removal, leaded gasoline was the largest source of air, soil, and groundwater contamination leading to environmental exposures.⁴ At present, the most common source of environmental lead exposure among young children is through peeling paint in deteriorating residential buildings. Hazardous occupational lead exposures arise from work involving munitions, reclamation and salvage, painting, welding, and numerous other settings—particularly sites where industrial hygiene is suboptimal. Lead from these sites can be inadvertently transported home on clothing or shoes, raising the exposure risk for children in the household.⁴

What are the health effects of lead exposure?

Like most heavy metals, lead is toxic to many organ systems in the body. The signs and symptoms of lead poisoning vary depending on the patient’s BLL and age (Table 1).⁵ The most common clinical effect of lead in the adult population is hypertension.⁶ Additional renal effects include a Fanconi-type syndrome with glycosuria and proteinuria. Lead can cause a peripheral neuropathy that is predominantly motor, classically causing foot or wrist drop. Abdominal pain from lead exposure is sometimes termed “lead colic” due to its intermittent and often severe nature. Abnormalities in urate metabolism cause a gouty arthritis referred to as “saturnine gout.” ⁶

The young pediatric central nervous system (CNS) is much more vulnerable to the effects of lead than the adult CNS. Even low-level lead exposure to the developing brain causes deficits in intelligence quotient, attention, impulse control, and other neurocognitive functions that are largely irreversible.⁷

Children with an elevated BLL may also develop constipation, anorexia, pallor, and pica.⁸ The development of geophagia (subtype of pica in which one craves and ingests nonfood clay or soil-like materials), represents a “chicken-or-egg” phenomena as it both causes and results from lead poisoning.

Lead impairs multiple steps of the heme synthesis pathway, causing microcytic anemia with basophilic stippling. Lead-induced anemia exacerbates pica as anemic patients are more likely to eat leaded paint chips and other lead-containing materials such as pottery.⁸ Of note, leaded white paint is reported to have a pleasant taste due to the sweet-tasting lead acetate used as a pigment.

The most dramatic and consequential manifestation of lead poisoning is lead encephalopathy. This can occur at any age, but manifests in children at much lower BLLs than in adults. Patients can be altered or obtunded, have convulsive activity, and may develop cerebral edema. Encephalopathy is a life-threatening emergency and must be recognized and treated immediately. Lead encephalopathy should be suspected in any young child with hand-to-mouth behavior who has any of the above environmental risk factors.⁴ The findings of anemia or the other diagnostic signs described below are too unreliable and take too long to be truly helpful in making the diagnosis.

How is the diagnosis of lead poisoning made?

The gold standard for the diagnosis of lead poisoning is the measurement of BLL. However, the turnaround time for this test is usually at least 24 hours, but may take up to several days. As such, adjunctive testing can accelerate obtaining a diagnosis. A complete blood count (CBC) to evaluate for microcytic anemia may demonstrate a characteristic pattern of basophilic stippling.⁹ A protoporphyrin level—either a free erythrocyte protoporphyrin (FEP) or a zinc protoporphyrin level—will be elevated, a result of heme synthesis disruption.⁹ Urinalysis may demonstrate glycosuria or proteinuria.⁶ Hypertension is often present, even in pediatric patients.

An abdominal radiograph is essential in children to determine whether a lead foreign body, such as a paint chip, is present in the intestinal lumen. Long bone films may demonstrate “lead lines” at the metaphysis, which in fact do not reflect lead itself but abnormal calcium deposition in growing bone due to lead’s interference with bone remodeling. A computed tomography (CT) scan of the brain in patients with encephalopathy will often demonstrate cerebral edema.⁶

Of note, capillary BLLs taken via finger-stick can be falsely elevated due contamination during collection (eg, the presence of lead dust on the skin). However, this screening method is often used by clinicians in the pediatric primary care setting because of its feasibility. Elevated BLLs from capillary testing should always be followed by a BLL obtained by venipuncture.²

Case Continuation

The patient’s mother was counseled on sources of lead contamination. She was informed that although drinking water may contribute some amount to an elevated BLL, the most likely source of contamination is still lead paint found in older homes such as the one in which she and her son resided.

Diagnostic studies to support the diagnosis of lead poisoning were performed. A CBC revealed a hemoglobin of 9.8 g/dL with a mean corpuscular volume of 68 fL. A microscopic smear of blood demonstrated basophilic stippling of red blood cells. An FEP level was 386 mcg/dL. An abdominal radiograph demonstrated small radiopacities throughout the large intestine, without obstruction, which was suggestive of ingested lead paint chips.

What is the best management approach to patients with suspected lead poisoning?

The first-line treatment for patients with lead poisoning is removal from the exposure source, which first and foremost requires identification of the hazard through careful history taking and scene investigation by the local health department. This will avoid recurrent visits following successful chelation for repeat exposure to an unidentified source. Relocation to another dwelling will often be required for patients with presumed exposure until the hazard can be identified and abated.

Patients who have ingested or have embedded leaded foreign bodies will require removal via whole bowel irrigation or surgical means.

Following decontamination, chelation is required for children with a BLL more than 45 mcg/dL, and adults with CNS symptomatology and a BLL more than 70 mcg/dL. Table 2 provides guidelines for chelation therapy based on BLL.⁵

Work-up and Management in the ED

The patient with lead poisoning, while an unusual presentation in the ED, requires specialized management to minimize sequelae of exposure. Careful attention to history is vital. When in doubt, the EP should consult with her or his regional poison control center (800-222-1222) or with a medical toxicologist or other expert.

There are several scenarios in which a patient may present to the ED with lead toxicity. The following scenarios, along with their respective clinical approach strategies, represent three of the most common presentations.

Scenario 1: The Pediatric Patient With Elevated Venous Blood Lead Levels

The EP should employ the following clinical approach when evaluating and managing the pediatric patient with normal mental status whose routine screening reveals a BLL sufficiently elevated to warrant evaluation or admission—perhaps to discontinue exposure or initiate chelation therapy.

• Obtain a history, including possible lead sources; perform a complete physical examination; and obtain a repeat BLL, CBC with microscopic examination, and renal function test.
• Obtain an abdominal film to look for radiopacities, including paint chips or larger ingested foreign bodies.
• If radiopaque foreign bodies are present on abdominal radiograph, whole bowel irrigation with polyethylene glycol solution given via a nasogastric tube at 250 to 500 cc/h for a pediatric patient (1 to 2 L/h for adult patients) should be given until no residual foreign bodies remain.
• Obtain a radiograph of the long bone, which may demonstrate metaphyseal enhancement in the pediatric patient, suggesting long-term exposure.
• Ensure local or state health departments are contacted to arrange for environmental inspection of the home. This is essential prior to discharge to the home environment.
• Begin chelation therapy according to the BLL (Table 2).

Scenario 2: Adult Patients Presenting With Signs and Symptoms of Lead Toxicity

The adult patient who presents to the ED with complaints suggestive of lead poisoning and whose history is indicative of lead exposure should be evaluated and managed as follows:

• Obtain a thorough history, including the occupation and hobbies of the patient and all family members.
• Obtain vital signs to evaluate for hypertension; repeat BLL, CBC with smear, and serum creatinine test. Perform a physical examination to evaluate for lead lines.
• Obtain radiographic images, which may demonstrate a leaded foreign body, such as in the patient with prior history of gunshot wounds.
• If the BLL is sufficiently elevated or clinical findings are sufficiently severe, admit for chelation.

Scenario 3: The Pediatric or Adult Patient Presenting With Altered Mental Status

The patient presenting with altered mental status of unclear etiology—regardless of age—and in whom lead encephalopathy is a possible cause, should be worked-up and managed as follows:

• Obtain BLL, CBC, FEP levels. Consider radiographic imaging to assess for ingested or embedded foreign bodies.
• If abnormalities in the above laboratory studies are consistent with lead poisoning, initiate chelation immediately—prior to receiving repeat BLL result.
• Obtain a CT scan of the head to assess for cerebral edema.
• Provide supportive care for encephalopathy, including airway control and management of increased intracranial pressure.

Case Conclusion

The patient was admitted to the hospital for whole bowel irrigation and chelation therapy with succimer. The local health department conducted an investigation of the home and found multiple areas of peeling lead paint and lead dust, and ordered remediation of the property before it could be re-occupied by the family. A test of the home’s drinking water found no elevation above the 15 ppb standard.

The patient was discharged from the hospital in the care of his mother. They were relocated to a lead-free home, with follow-up by the pediatrician for ongoing monitoring of the BLL and developmental milestones.

Case

A 2-year-old boy and his mother were referred to the ED by the child’s pediatrician after a routine venous blood lead level (BLL) taken at the boy’s recent well visit revealed an elevated lead level of 52 mcg/dL (normal range, <5 mcg/dL). The child’s mother reported that although her son had always been a picky eater, he had recently been complaining of abdominal pain.

The patient’s well-child visits had been normal until his recent 2-year checkup, at which time his pediatrician noticed some speech delay. On further history taking, the emergency physician (EP) learned the patient and his mother resided in an older home (built in the 1950s) that was in disrepair. The mother asked the EP if the elevation in the child’s BLL could be due to the drinking water in their town.

What are the most likely sources of environmental lead exposure?

In 2016, the topic of lead poisoning grabbed national attention when a pediatrician in Flint, Michigan detected an abrupt doubling of the number of children with elevated lead levels in her practice.¹ Upon further investigation, it was discovered that these kids had one thing in common: the source of their drinking water. The City of Flint had recently switched the source of its potable water from Lake Huron to the Flint River. The lower quality water, which was not properly treated with an anticorrosive agent such as orthophosphate, led to widespread pipe corrosion and lead contamination. This finding resulted in a cascade of water testing by other municipalities and school systems, many of which identified lead concentrations above the currently accepted drinking water standard of 15 parts per billion (ppb).

Thousands of children each year are identified to have elevated BLLs, based on the Centers for Disease Control and Prevention definition of a “level of concern” as more than 5 mcg/dL.² The majority of these exposures stem from environmental exposure to lead paint dust in the home, but drinking water normally contributes as a low-level, constant, “basal” exposure. While lead-contaminated drinking water is not acceptable, it is unlikely to generate many ED visits. However, there are a variety of other lead sources that may prompt children to present to the ED with acute or subacute lead poisoning.

Lead is a heavy metal whose physical properties indicate its common uses. It provides durability and opacity to pigments, which is why it is found in oil paint, house paint used before 1976, and on paint for large outdoor structures, where it is still used. Lead is also found in the pigments used in cosmetics, stained glass, and painted pottery, and as an adulterant in highly colored foodstuffs such as imported turmeric.³

The physicochemical characteristics of lead make it an ideal component of solder. Many plumbing pipes in use today are not lead, but join one another using lead solder at the joints, sites that are vulnerable to corrosion. The heavy molecular weight of lead makes it a useful component of bullets and munitions.

Tetraethyl lead was used as an “anti-knock” agent to smooth out the combustion of heterogenous compounds in automotive fuel before it was removed in the mid-1970s.⁴ Prior to its removal, leaded gasoline was the largest source of air, soil, and groundwater contamination leading to environmental exposures.⁴ At present, the most common source of environmental lead exposure among young children is through peeling paint in deteriorating residential buildings. Hazardous occupational lead exposures arise from work involving munitions, reclamation and salvage, painting, welding, and numerous other settings—particularly sites where industrial hygiene is suboptimal. Lead from these sites can be inadvertently transported home on clothing or shoes, raising the exposure risk for children in the household.⁴

What are the health effects of lead exposure?

Like most heavy metals, lead is toxic to many organ systems in the body. The signs and symptoms of lead poisoning vary depending on the patient’s BLL and age (Table 1).⁵ The most common clinical effect of lead in the adult population is hypertension.⁶ Additional renal effects include a Fanconi-type syndrome with glycosuria and proteinuria. Lead can cause a peripheral neuropathy that is predominantly motor, classically causing foot or wrist drop. Abdominal pain from lead exposure is sometimes termed “lead colic” due to its intermittent and often severe nature. Abnormalities in urate metabolism cause a gouty arthritis referred to as “saturnine gout.” ⁶

The young pediatric central nervous system (CNS) is much more vulnerable to the effects of lead than the adult CNS. Even low-level lead exposure to the developing brain causes deficits in intelligence quotient, attention, impulse control, and other neurocognitive functions that are largely irreversible.⁷

Children with an elevated BLL may also develop constipation, anorexia, pallor, and pica.⁸ The development of geophagia (subtype of pica in which one craves and ingests nonfood clay or soil-like materials), represents a “chicken-or-egg” phenomena as it both causes and results from lead poisoning.

Lead impairs multiple steps of the heme synthesis pathway, causing microcytic anemia with basophilic stippling. Lead-induced anemia exacerbates pica as anemic patients are more likely to eat leaded paint chips and other lead-containing materials such as pottery.⁸ Of note, leaded white paint is reported to have a pleasant taste due to the sweet-tasting lead acetate used as a pigment.

The most dramatic and consequential manifestation of lead poisoning is lead encephalopathy. This can occur at any age, but manifests in children at much lower BLLs than in adults. Patients can be altered or obtunded, have convulsive activity, and may develop cerebral edema. Encephalopathy is a life-threatening emergency and must be recognized and treated immediately. Lead encephalopathy should be suspected in any young child with hand-to-mouth behavior who has any of the above environmental risk factors.⁴ The findings of anemia or the other diagnostic signs described below are too unreliable and take too long to be truly helpful in making the diagnosis.

How is the diagnosis of lead poisoning made?

The gold standard for the diagnosis of lead poisoning is the measurement of BLL. However, the turnaround time for this test is usually at least 24 hours, but may take up to several days. As such, adjunctive testing can accelerate obtaining a diagnosis. A complete blood count (CBC) to evaluate for microcytic anemia may demonstrate a characteristic pattern of basophilic stippling.⁹ A protoporphyrin level—either a free erythrocyte protoporphyrin (FEP) or a zinc protoporphyrin level—will be elevated, a result of heme synthesis disruption.⁹ Urinalysis may demonstrate glycosuria or proteinuria.⁶ Hypertension is often present, even in pediatric patients.

An abdominal radiograph is essential in children to determine whether a lead foreign body, such as a paint chip, is present in the intestinal lumen. Long bone films may demonstrate “lead lines” at the metaphysis, which in fact do not reflect lead itself but abnormal calcium deposition in growing bone due to lead’s interference with bone remodeling. A computed tomography (CT) scan of the brain in patients with encephalopathy will often demonstrate cerebral edema.⁶

Of note, capillary BLLs taken via finger-stick can be falsely elevated due contamination during collection (eg, the presence of lead dust on the skin). However, this screening method is often used by clinicians in the pediatric primary care setting because of its feasibility. Elevated BLLs from capillary testing should always be followed by a BLL obtained by venipuncture.²

Case Continuation

The patient’s mother was counseled on sources of lead contamination. She was informed that although drinking water may contribute some amount to an elevated BLL, the most likely source of contamination is still lead paint found in older homes such as the one in which she and her son resided.

Diagnostic studies to support the diagnosis of lead poisoning were performed. A CBC revealed a hemoglobin of 9.8 g/dL with a mean corpuscular volume of 68 fL. A microscopic smear of blood demonstrated basophilic stippling of red blood cells. An FEP level was 386 mcg/dL. An abdominal radiograph demonstrated small radiopacities throughout the large intestine, without obstruction, which was suggestive of ingested lead paint chips.

What is the best management approach to patients with suspected lead poisoning?

The first-line treatment for patients with lead poisoning is removal from the exposure source, which first and foremost requires identification of the hazard through careful history taking and scene investigation by the local health department. This will avoid recurrent visits following successful chelation for repeat exposure to an unidentified source. Relocation to another dwelling will often be required for patients with presumed exposure until the hazard can be identified and abated.

Patients who have ingested or have embedded leaded foreign bodies will require removal via whole bowel irrigation or surgical means.

Following decontamination, chelation is required for children with a BLL more than 45 mcg/dL, and adults with CNS symptomatology and a BLL more than 70 mcg/dL. Table 2 provides guidelines for chelation therapy based on BLL.⁵

Work-up and Management in the ED

The patient with lead poisoning, while an unusual presentation in the ED, requires specialized management to minimize sequelae of exposure. Careful attention to history is vital. When in doubt, the EP should consult with her or his regional poison control center (800-222-1222) or with a medical toxicologist or other expert.

There are several scenarios in which a patient may present to the ED with lead toxicity. The following scenarios, along with their respective clinical approach strategies, represent three of the most common presentations.

Scenario 1: The Pediatric Patient With Elevated Venous Blood Lead Levels

The EP should employ the following clinical approach when evaluating and managing the pediatric patient with normal mental status whose routine screening reveals a BLL sufficiently elevated to warrant evaluation or admission—perhaps to discontinue exposure or initiate chelation therapy.

• Obtain a history, including possible lead sources; perform a complete physical examination; and obtain a repeat BLL, CBC with microscopic examination, and renal function test.
• Obtain an abdominal film to look for radiopacities, including paint chips or larger ingested foreign bodies.
• If radiopaque foreign bodies are present on abdominal radiograph, whole bowel irrigation with polyethylene glycol solution given via a nasogastric tube at 250 to 500 cc/h for a pediatric patient (1 to 2 L/h for adult patients) should be given until no residual foreign bodies remain.
• Obtain a radiograph of the long bone, which may demonstrate metaphyseal enhancement in the pediatric patient, suggesting long-term exposure.
• Ensure local or state health departments are contacted to arrange for environmental inspection of the home. This is essential prior to discharge to the home environment.
• Begin chelation therapy according to the BLL (Table 2).

Scenario 2: Adult Patients Presenting With Signs and Symptoms of Lead Toxicity

The adult patient who presents to the ED with complaints suggestive of lead poisoning and whose history is indicative of lead exposure should be evaluated and managed as follows:

• Obtain a thorough history, including the occupation and hobbies of the patient and all family members.
• Obtain vital signs to evaluate for hypertension; repeat BLL, CBC with smear, and serum creatinine test. Perform a physical examination to evaluate for lead lines.
• Obtain radiographic images, which may demonstrate a leaded foreign body, such as in the patient with prior history of gunshot wounds.
• If the BLL is sufficiently elevated or clinical findings are sufficiently severe, admit for chelation.

Scenario 3: The Pediatric or Adult Patient Presenting With Altered Mental Status

The patient presenting with altered mental status of unclear etiology—regardless of age—and in whom lead encephalopathy is a possible cause, should be worked-up and managed as follows:

• Obtain BLL, CBC, FEP levels. Consider radiographic imaging to assess for ingested or embedded foreign bodies.
• If abnormalities in the above laboratory studies are consistent with lead poisoning, initiate chelation immediately—prior to receiving repeat BLL result.
• Obtain a CT scan of the head to assess for cerebral edema.
• Provide supportive care for encephalopathy, including airway control and management of increased intracranial pressure.

Case Conclusion

The patient was admitted to the hospital for whole bowel irrigation and chelation therapy with succimer. The local health department conducted an investigation of the home and found multiple areas of peeling lead paint and lead dust, and ordered remediation of the property before it could be re-occupied by the family. A test of the home’s drinking water found no elevation above the 15 ppb standard.

The patient was discharged from the hospital in the care of his mother. They were relocated to a lead-free home, with follow-up by the pediatrician for ongoing monitoring of the BLL and developmental milestones.

Case

A 21-year-old woman presented to the ED with pain and swelling on the right side of her neck. She stated the pain started earlier that morning and worsened when she ate or swallowed. The patient denied a recent or remote history of drooling, voice changes, or neck swelling. She reported no fevers, chills, or any other complaints, and had no pertinent medical history—specifically, no history of recent dental work. Her surgical history included tonsillectomy and cholecystectomy. There was no family history of diabetes, thyroid disease, autoimmune disease, or any other diseases. The patient stated that she was not on any prescription or over-the-counter medications. Regarding her social history, she denied past or cu

Vital signs at presentation were: blood pressure, 124/63 mm Hg (sitting); heart rate, 73 beats/min; respiratory rate, 15 breaths/min; and temperature, 98°F. Oxygen saturation was 99% on room air. On clinical examination, pain was noted in the patient’s right submandibular area and was tender to palpation. The swelling extended to the angle of the mandible posteriorly (Figure 1a and 1b). There was no erythema or increased surface temperature to suggest overlying cellulitis. The oral examination showed no evidence of dental infection, angioedema, or Ludwig angina. The pharynx was normal in appearance. The otological examination was unremarkable, and there was no evidence of mastoiditis.

Laboratory evaluation included a complete blood count (CBC), basic metabolic profile (BMP), and rapid streptococcal test (RST). The results of the patient’s CBC revealed a white blood cell count (WBC) of 11.1 x 10⁹/L; the BMP was unremarkable; and the RST was negative.

A soft tissue neck computed tomography (CT) scan with contrast was obtained, which revealed mild right submandibular gland enlargement with abnormal enhancement (Figure 2). Stranding was also noted in the right submandibular space along with thickening of the right platysma muscle, and few surrounding lymph nodes were prominent (Figure 3). The findings were consistent with acute submandibular sialadenitis.

Discussion

Comparatively little has been published on acute submandibular sialadenitis over the past three decades, and much of that which is cited in the literature comes from a rather small pool of case reports.¹ In a literature review, Raad et al¹ noted, “Pertinent literature on [this] subject includes case reports but no studies describing the microbial and clinical characteristics of this disease.” Further, many of the published case reports describe neonatal presentations of submandibular sialadenitis, the incidence of which is rare in this patient population.^2-4

Submandibular and Parotid Glands

The submandibular gland is the second largest salivary gland, the parotid gland being the largest. The duct of the salivary gland, the Wharton’s duct, opens under the tongue in the area of the lingual frenulum. Ductal obstruction is more frequently seen with the submandibular gland than with the parotid gland.¹ The reason for this is unclear, but may be related to several factors. One factor may be that, unlike the Stenson’s duct of the parotid gland, the Wharton’s duct does not pass through a muscle; thus, there is no muscular massage supporting the movement of secretion, as there is with buccinator muscle massage of Stenson’s duct. In addition, submandibular saliva is more viscous than parotid saliva due to its higher protein content and higher concentration of calcium phosphate.¹

Etiology

Submandibular gland obstruction can occur in the absence of infection. Noninfectious cases typically present with pain upon eating and swallowing. A bacterial infectious etiology is associated with odynophagia, but also includes persistent pain and tenderness. This presents as pain associated with eating. Bacterial infection of the submandibular gland adds the element of persistent pain, associated with such features as tenderness. In addition, purulent discharge from the Wharton’s duct may be present in infectious cases, and accompanied by fever, chills, and an elevated WBC.¹

Several bacteria have been isolated in infectious submandibular sialadenitis, the most common pathogens being Staphylococcus aureus. However, streptococci, Pseudomonas aeruginosa, Moraxella catarrhalis, and Escherichia coli bacteria have also been identified in cases of infectious submandibular sialadenitis.⁵

Viral etiologies of sialadenitis, such as mumps, are generally bilateral and nonsuppurative. The human immunodeficiency virus can also cause bilateral nonsuppurative salivary gland infections.⁶

Imaging Studies

As illustrated in our case, CT imaging can assist in confirming the diagnosis of acute submandibular sialadenitis by defining the anatomic involvement and identifying the presence of an abscess. Ultrasound can also be used and has been described as a first-line imaging procedure.^7,8

Treatment

Surgical Intervention. Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics.⁵ If ductal obstruction is identified, removal of the calculus may be needed. This may involve ductal dilation, sialolithectomy, or even ductoplasty if a stricture is identified.¹

Antibiotic Therapy. With respect to antibiotic selection, Chandak et al⁵ recommend oral amoxicillin-clavulanic acid. Other antistaphylococcal coverage recommendations have been made in the literature. Gland massage may be helpful after the tenderness has resolved,⁵ and sialogogues (eg, lemon drops, vitamin C lozenges) can also provide some relief.⁶ In addition, to avoid disease recurrence and prevent dental complications, Chandak et al⁵ emphasize the crucial role of hydration and excellent oral hygiene.

Conclusion

We suspected acute submandibular sialadenitis in our patient based on clinical findings, which were confirmed on CT imaging. Patients with acute submandibular sialadenitis may present with submandibular gland obstruction in the absence of bacterial infection. Noninfectious obstruction typically presents as pain associated with eating and swallowing, whereas infectious cases include constant pain and tenderness in the affected area. In addition, patients with infectious etiology may also have purulent discharge from Wharton’s duct, fever, chills, and an elevated WBC. Several bacteria have been isolated, the most common being S aureus. However, streptococci, P aeruginosa, M catarrhalis and E coli have also been identified. Computed tomography studies are helpful in confirming the diagnosis, defining anatomical involvement, and in identifying abscess formation.

Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics. Antibiotic selection involves antistaphylococcal coverage, such as amoxicillin-clavulanic acid. Glandular massage may be helpful after the tenderness has resolved. In addition, the literature emphasizes the crucial role of hydration and excellent oral hygiene in disease recurrence and to prevent dental complications.

Case

A 21-year-old woman presented to the ED with pain and swelling on the right side of her neck. She stated the pain started earlier that morning and worsened when she ate or swallowed. The patient denied a recent or remote history of drooling, voice changes, or neck swelling. She reported no fevers, chills, or any other complaints, and had no pertinent medical history—specifically, no history of recent dental work. Her surgical history included tonsillectomy and cholecystectomy. There was no family history of diabetes, thyroid disease, autoimmune disease, or any other diseases. The patient stated that she was not on any prescription or over-the-counter medications. Regarding her social history, she denied past or cu

Vital signs at presentation were: blood pressure, 124/63 mm Hg (sitting); heart rate, 73 beats/min; respiratory rate, 15 breaths/min; and temperature, 98°F. Oxygen saturation was 99% on room air. On clinical examination, pain was noted in the patient’s right submandibular area and was tender to palpation. The swelling extended to the angle of the mandible posteriorly (Figure 1a and 1b). There was no erythema or increased surface temperature to suggest overlying cellulitis. The oral examination showed no evidence of dental infection, angioedema, or Ludwig angina. The pharynx was normal in appearance. The otological examination was unremarkable, and there was no evidence of mastoiditis.

Laboratory evaluation included a complete blood count (CBC), basic metabolic profile (BMP), and rapid streptococcal test (RST). The results of the patient’s CBC revealed a white blood cell count (WBC) of 11.1 x 10⁹/L; the BMP was unremarkable; and the RST was negative.

A soft tissue neck computed tomography (CT) scan with contrast was obtained, which revealed mild right submandibular gland enlargement with abnormal enhancement (Figure 2). Stranding was also noted in the right submandibular space along with thickening of the right platysma muscle, and few surrounding lymph nodes were prominent (Figure 3). The findings were consistent with acute submandibular sialadenitis.

Discussion

Comparatively little has been published on acute submandibular sialadenitis over the past three decades, and much of that which is cited in the literature comes from a rather small pool of case reports.¹ In a literature review, Raad et al¹ noted, “Pertinent literature on [this] subject includes case reports but no studies describing the microbial and clinical characteristics of this disease.” Further, many of the published case reports describe neonatal presentations of submandibular sialadenitis, the incidence of which is rare in this patient population.^2-4

Submandibular and Parotid Glands

The submandibular gland is the second largest salivary gland, the parotid gland being the largest. The duct of the salivary gland, the Wharton’s duct, opens under the tongue in the area of the lingual frenulum. Ductal obstruction is more frequently seen with the submandibular gland than with the parotid gland.¹ The reason for this is unclear, but may be related to several factors. One factor may be that, unlike the Stenson’s duct of the parotid gland, the Wharton’s duct does not pass through a muscle; thus, there is no muscular massage supporting the movement of secretion, as there is with buccinator muscle massage of Stenson’s duct. In addition, submandibular saliva is more viscous than parotid saliva due to its higher protein content and higher concentration of calcium phosphate.¹

Etiology

Submandibular gland obstruction can occur in the absence of infection. Noninfectious cases typically present with pain upon eating and swallowing. A bacterial infectious etiology is associated with odynophagia, but also includes persistent pain and tenderness. This presents as pain associated with eating. Bacterial infection of the submandibular gland adds the element of persistent pain, associated with such features as tenderness. In addition, purulent discharge from the Wharton’s duct may be present in infectious cases, and accompanied by fever, chills, and an elevated WBC.¹

Several bacteria have been isolated in infectious submandibular sialadenitis, the most common pathogens being Staphylococcus aureus. However, streptococci, Pseudomonas aeruginosa, Moraxella catarrhalis, and Escherichia coli bacteria have also been identified in cases of infectious submandibular sialadenitis.⁵

Viral etiologies of sialadenitis, such as mumps, are generally bilateral and nonsuppurative. The human immunodeficiency virus can also cause bilateral nonsuppurative salivary gland infections.⁶

Imaging Studies

As illustrated in our case, CT imaging can assist in confirming the diagnosis of acute submandibular sialadenitis by defining the anatomic involvement and identifying the presence of an abscess. Ultrasound can also be used and has been described as a first-line imaging procedure.^7,8

Treatment

Surgical Intervention. Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics.⁵ If ductal obstruction is identified, removal of the calculus may be needed. This may involve ductal dilation, sialolithectomy, or even ductoplasty if a stricture is identified.¹

Antibiotic Therapy. With respect to antibiotic selection, Chandak et al⁵ recommend oral amoxicillin-clavulanic acid. Other antistaphylococcal coverage recommendations have been made in the literature. Gland massage may be helpful after the tenderness has resolved,⁵ and sialogogues (eg, lemon drops, vitamin C lozenges) can also provide some relief.⁶ In addition, to avoid disease recurrence and prevent dental complications, Chandak et al⁵ emphasize the crucial role of hydration and excellent oral hygiene.

Conclusion

We suspected acute submandibular sialadenitis in our patient based on clinical findings, which were confirmed on CT imaging. Patients with acute submandibular sialadenitis may present with submandibular gland obstruction in the absence of bacterial infection. Noninfectious obstruction typically presents as pain associated with eating and swallowing, whereas infectious cases include constant pain and tenderness in the affected area. In addition, patients with infectious etiology may also have purulent discharge from Wharton’s duct, fever, chills, and an elevated WBC. Several bacteria have been isolated, the most common being S aureus. However, streptococci, P aeruginosa, M catarrhalis and E coli have also been identified. Computed tomography studies are helpful in confirming the diagnosis, defining anatomical involvement, and in identifying abscess formation.

Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics. Antibiotic selection involves antistaphylococcal coverage, such as amoxicillin-clavulanic acid. Glandular massage may be helpful after the tenderness has resolved. In addition, the literature emphasizes the crucial role of hydration and excellent oral hygiene in disease recurrence and to prevent dental complications.

Case

A 21-year-old woman presented to the ED with pain and swelling on the right side of her neck. She stated the pain started earlier that morning and worsened when she ate or swallowed. The patient denied a recent or remote history of drooling, voice changes, or neck swelling. She reported no fevers, chills, or any other complaints, and had no pertinent medical history—specifically, no history of recent dental work. Her surgical history included tonsillectomy and cholecystectomy. There was no family history of diabetes, thyroid disease, autoimmune disease, or any other diseases. The patient stated that she was not on any prescription or over-the-counter medications. Regarding her social history, she denied past or cu

Vital signs at presentation were: blood pressure, 124/63 mm Hg (sitting); heart rate, 73 beats/min; respiratory rate, 15 breaths/min; and temperature, 98°F. Oxygen saturation was 99% on room air. On clinical examination, pain was noted in the patient’s right submandibular area and was tender to palpation. The swelling extended to the angle of the mandible posteriorly (Figure 1a and 1b). There was no erythema or increased surface temperature to suggest overlying cellulitis. The oral examination showed no evidence of dental infection, angioedema, or Ludwig angina. The pharynx was normal in appearance. The otological examination was unremarkable, and there was no evidence of mastoiditis.

Laboratory evaluation included a complete blood count (CBC), basic metabolic profile (BMP), and rapid streptococcal test (RST). The results of the patient’s CBC revealed a white blood cell count (WBC) of 11.1 x 10⁹/L; the BMP was unremarkable; and the RST was negative.

A soft tissue neck computed tomography (CT) scan with contrast was obtained, which revealed mild right submandibular gland enlargement with abnormal enhancement (Figure 2). Stranding was also noted in the right submandibular space along with thickening of the right platysma muscle, and few surrounding lymph nodes were prominent (Figure 3). The findings were consistent with acute submandibular sialadenitis.

Discussion

Comparatively little has been published on acute submandibular sialadenitis over the past three decades, and much of that which is cited in the literature comes from a rather small pool of case reports.¹ In a literature review, Raad et al¹ noted, “Pertinent literature on [this] subject includes case reports but no studies describing the microbial and clinical characteristics of this disease.” Further, many of the published case reports describe neonatal presentations of submandibular sialadenitis, the incidence of which is rare in this patient population.^2-4

Submandibular and Parotid Glands

The submandibular gland is the second largest salivary gland, the parotid gland being the largest. The duct of the salivary gland, the Wharton’s duct, opens under the tongue in the area of the lingual frenulum. Ductal obstruction is more frequently seen with the submandibular gland than with the parotid gland.¹ The reason for this is unclear, but may be related to several factors. One factor may be that, unlike the Stenson’s duct of the parotid gland, the Wharton’s duct does not pass through a muscle; thus, there is no muscular massage supporting the movement of secretion, as there is with buccinator muscle massage of Stenson’s duct. In addition, submandibular saliva is more viscous than parotid saliva due to its higher protein content and higher concentration of calcium phosphate.¹

Etiology

Submandibular gland obstruction can occur in the absence of infection. Noninfectious cases typically present with pain upon eating and swallowing. A bacterial infectious etiology is associated with odynophagia, but also includes persistent pain and tenderness. This presents as pain associated with eating. Bacterial infection of the submandibular gland adds the element of persistent pain, associated with such features as tenderness. In addition, purulent discharge from the Wharton’s duct may be present in infectious cases, and accompanied by fever, chills, and an elevated WBC.¹

Several bacteria have been isolated in infectious submandibular sialadenitis, the most common pathogens being Staphylococcus aureus. However, streptococci, Pseudomonas aeruginosa, Moraxella catarrhalis, and Escherichia coli bacteria have also been identified in cases of infectious submandibular sialadenitis.⁵

Viral etiologies of sialadenitis, such as mumps, are generally bilateral and nonsuppurative. The human immunodeficiency virus can also cause bilateral nonsuppurative salivary gland infections.⁶

Imaging Studies

As illustrated in our case, CT imaging can assist in confirming the diagnosis of acute submandibular sialadenitis by defining the anatomic involvement and identifying the presence of an abscess. Ultrasound can also be used and has been described as a first-line imaging procedure.^7,8

Treatment

Surgical Intervention. Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics.⁵ If ductal obstruction is identified, removal of the calculus may be needed. This may involve ductal dilation, sialolithectomy, or even ductoplasty if a stricture is identified.¹

Antibiotic Therapy. With respect to antibiotic selection, Chandak et al⁵ recommend oral amoxicillin-clavulanic acid. Other antistaphylococcal coverage recommendations have been made in the literature. Gland massage may be helpful after the tenderness has resolved,⁵ and sialogogues (eg, lemon drops, vitamin C lozenges) can also provide some relief.⁶ In addition, to avoid disease recurrence and prevent dental complications, Chandak et al⁵ emphasize the crucial role of hydration and excellent oral hygiene.

Conclusion

We suspected acute submandibular sialadenitis in our patient based on clinical findings, which were confirmed on CT imaging. Patients with acute submandibular sialadenitis may present with submandibular gland obstruction in the absence of bacterial infection. Noninfectious obstruction typically presents as pain associated with eating and swallowing, whereas infectious cases include constant pain and tenderness in the affected area. In addition, patients with infectious etiology may also have purulent discharge from Wharton’s duct, fever, chills, and an elevated WBC. Several bacteria have been isolated, the most common being S aureus. However, streptococci, P aeruginosa, M catarrhalis and E coli have also been identified. Computed tomography studies are helpful in confirming the diagnosis, defining anatomical involvement, and in identifying abscess formation.

Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics. Antibiotic selection involves antistaphylococcal coverage, such as amoxicillin-clavulanic acid. Glandular massage may be helpful after the tenderness has resolved. In addition, the literature emphasizes the crucial role of hydration and excellent oral hygiene in disease recurrence and to prevent dental complications.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

BY JEFF BAUER

A large retrospective analysis found a wide variation in opioid prescribing among emergency physicians (EPs) working within the same ED. The study also found that Medicare patients treated by EPs who wrote the most prescriptions for opioids were more likely to use opioids for 6 months after their ED visit than were those treated by EPs who wrote fewer opioid prescriptions.

Researchers evaluated initial visits to an ED by approximately 378,000 Medicare beneficiaries (average age: 68 years) from 2008 through 2011. None of these patients had received a prescription for an opioid in the 6 months before the ED visit, and none of the visits resulted in a hospital admission. Prescriptions for opioids (excluding methadone) were identified by the national drug code in the Medicare Part D database. An opioid prescription was attributed to the treating EP if the patient filled the prescription within 3 days after the ED visit.

Investigators categorized the treating EPs in this study as “high-intensity” or “low-intensity” opioid prescribers by calculating the proportion of all ED visits that resulted in an opioid prescription being filled. They then grouped the EPs into quartiles of opioid prescribing within each hospital. High-intensity prescribers were those in the top quartile of opioid prescribing rates, and low-intensity prescribers were those in the bottom quartile.

The primary outcome was long-term opioid use, defined as 6 months or more of opioids supplied in the 12 months after the initial ED visit. This did not include prescriptions filled within 30 days of the initial visit.

Overall, approximately 215,700 patients were treated by low-intensity prescribers and 162,000 by high-intensity prescribers. In general, the patient characteristics and diagnoses were similar in both groups. The rate of opioid prescribing of high-intensity prescribers was approximately triple the rate of low-intensity prescribers. High-intensity prescribers provided an opioid prescription for 21.4% of ED visits, compared to 7.3% among low-intensity prescribers.

Long-term opioid use at 12 months was significantly higher among patients who had been initially treated by high-intensity prescribers compared to those who had been treated by low-intensity prescribers (1.51% vs 1.16%; unadjusted odds ratio [OR], 1.31). There was minimal change in this difference after the results were adjusted for the patients’ age, race, sex, disability status, and presence of chronic conditions (OR, 1.30). The number needed to harm was calculated as 49, meaning theoretically, for every 49 patients who received a new opioid prescription in the ED, one would become a long-term user. The authors noted, however, that “…prescriptions provided by other physicians in the months after an [ED] visit are necessary for long-term opioid use to take hold.”

Researchers pointed out several limitations to their study. Because the study was observational, it could not establish causality. Researchers were not able to directly attribute opioid prescriptions to the treating EPs, but instead used prescriptions filled within 3 days of an ED visits as a surrogate; some opioid prescriptions could have been written by another clinician, such as the patient’s primary care physician during a follow-up visit. Because the study focused on Medicare patients, the results may not be applicable to younger patients. Based on their analysis, researchers could not determine whether an opioid prescription was appropriate, and therefore they could not quantify the extent of opioid overprescribing.

For more on EPs and opioid prescribing, see “The New Opioid Epidemic and the Law of Unintended Consequences” by Emergency Medicine Editor in Chief Neal Flomenbaum, MD (Emergency Medicine. 2017;49[2]:52) and “The New Opioid Epidemic: Prescriptions, Synthetics, and Street Drugs” by Rama B. Rao, MD and Emergency Medicine Associate Editor, Toxicology Lewis S. Nelson, MD (Emergency Medicine. 2017;49[2]:64-70).

Barnett ML, Olenski AR, Jena AB. Opioid-prescribing patterns of emergency physicians and risk of long-term use. N Engl J Med. 2017;376(7):663-673. doi:10.1056/NEJMsa1610524.

Lower Admission Rates, Other Factors Tied to High Rate of Death Soon After ED Discharge Among Older Adults

BY JEFF BAUER

Each year, approximately 10,000 older adult patients die within 7 days of discharge from an ED in the United States, despite having no obvious life-threatening illness, according to a large retrospective study. Emergency departments with lower rates of inpatient admission from the ED, lower patient volumes, and lower charges had significantly higher rates of death after discharge.

Researchers evaluated Medicare claims data related to slightly more than 10 million ED visits from 2007 to 2012. Because the goal was to study generally healthy patients, the following patients were excluded: individuals who were age 90 years and older; were receiving palliative or hospice care; or had received a life-limiting diagnosis, such as a myocardial infarction (MI) or a malignancy, either in the ED or in the year prior to the ED visit. The primary outcome was death within 7 days after discharge from an ED. The cause of death was determined by linking claims to death certificates; this information was available only for a subset of patients who visited an ED in 2007 or 2008.

Overall, during the 6-year study, 0.12% of discharged patients died within 7 days of discharge; this translates to more than 10,000 early deaths per year nationally. The leading causes of death were atherosclerotic heart disease (13.6%), MI (10.3%), and chronic obstructive pulmonary disease (9.6%).

Emergency departments ranked in the lowest fifth for admission rates admitted 15% of patients, compared to 56% of patients at EDs with the highest admission rates. The early death rate of patients treated at EDs with the lowest rates of inpatient admissions from the ED was 3.4 times higher than the death rate seen in EDs with the highest inpatient admission rates (0.27% vs 0.08%, respectively). This was true despite the fact that EDs with low-admission rates treated healthier patients, as evidenced by the overall 7-day mortality rate of all patients treated in the ED, whether they were admitted or discharged. Emergency departments that saw higher volumes of patients and had higher charges for visits had significantly fewer deaths.

Obermeyer Z, Cohn B, Wilson M, Jena AB, Cutler DM. Early death after discharge from emergency departments: analysis of national US insurance claims data. BMJ. 2017;356:j239. doi:10.1136/bmj.j239.

Tertiary Center Repeat Computed Tomography Scans Find Additional Injuries

MICHELE G. SULLIVAN

FRONTLINE MEDICAL NEWS

Imaging obtained at nontertiary trauma centers (NTCs) probably does not tell the whole story of a trauma patient’s injuries, according to a new retrospective study.

Repeat scans done at a Level 1 trauma center identified new injuries in 76% of patients who were transferred, Morgan Bonds, MD, reported at the annual scientific assembly of the Eastern Association for the Surgery of Trauma. About half of these previously unobserved injuries were considered clinically significant, said Dr Bonds, a surgical resident at the University of Oklahoma, Oklahoma City.

Her study examined imaging and clinical assessment of 203 trauma patients who were initially worked up at an NTC, and then transferred to the Level 1 University of Oklahoma tertiary trauma center (TTC). The facility’s primary radiologist reviewed all of the initial computed tomography (CT) scans while blinded to the NTC interpretation. The initial scans and interpretations were then compared with those done at the TTC.

The team split imaging and interpretation disconnects into four categories:

• Type A errors: A missed injury on the NTC scan. “This represents the expertise and experience of our primary radiologist,” Dr Bonds said.
• Type B errors: Missed injuries on scans where NTC radiologists saw other injuries that the TTC radiologist did not confirm. “This represents the experience of our radiologist and also the inexperience and overreaction of the NTC radiologists.”
• Type C errors: New injuries seen on additional TTC imaging of the same body area. “This represents the quality of the image.”
• Type D errors: New injuries found upon any new imaging, whether of a previously scanned or newly scanned body area. “This represents quality of work-up—the decision of the trauma team to more fully investigate the patient’s injuries, as well as the quality of the CT tech performing the scan.”

During the study period, 203 patients presented at the TTC with prior scans conducted at an NTC.

The mean age of the patients was 43 years; most (67%) were men. The mean Injury Severity Score was 16; 97% had experienced blunt trauma. Shock was present in 3% and a traumatic brain injury in 8%. Repeat scans were most common for neck and cervical spine injuries (54%) and thoracic/lumbar spine injuries (53%), and least common for chest injuries (32%).

An inadequate NTC work-up as judged by the TTC attending was the most common reason for obtaining new images (76%). Poor image quality was the next most common reason (31%).

Among the 203 patients, 99 (49%) had a type A error. Of these injuries missed on the initial scan, 90% were considered to be clinically significant.

Type B errors occurred in 15% of patients. Type C errors (new injuries in different body area) occurred in 54% of patients and, of these, 76% were considered clinically significant. Type D errors (new injuries seen in any imaging of any area) occurred in 73% of patients.

“This study confirms that images are often repeated or completed after having images done at NTCs,” Dr Bonds said. “Relying on NTC image interpretation can lead to undertreating our patients. One potential solution to this issue could be image sharing between NTCs and TTCs. This might reduce both the rate of missed injuries and the need for repeat scans.”

Cutaneous Eruption Reported in Pregnant Woman With Locally Acquired Zika Virus

M. ALEXANDER OTTO

FRONTLINE MEDICAL NEWS

Zika presented in a young, pregnant Florida woman as erythematous follicular macules and papules on the trunk and arms, scattered tender pink papules on the palms, and a few petechiae on the hard palate, according to a report in the New England Journal of Medicine.

The report advises how Zika virus may present during pregnancy. “Medical providers on the front line should be aware of the constellation of symptoms in patients reporting travel to endemic areas, including areas in Southern Florida, where other non-travel-associated cases have been confirmed,” wrote investigators led by Lucy Chen, MD, of the University of Miami.

The 23-year-old woman presented on July 7, 2016 at 23 weeks and 3 days’ gestation with a 3-day history of fever, widespread pruritic rash, and sore throat, which were followed by myalgias and joint pain 2 days later. The cutaneous eruption was noted on physical examination; neither conjunctivitis nor lymphadenopathy was present. The patient and her partner said they had not traveled outside the United States for 2 years.

Zika virus RNA was detected in the woman’s urine and serum specimens with the use of reverse-transcriptase polymerase chain reaction and persisted for 2 weeks in urine samples and for 6 weeks in serum samples. On histopathology, skin lesions revealed a mild perivascular lymphocytic infiltration in the upper dermis, admixed with some neutrophils. Liver and renal functions were normal.

Fetal ultrasonography performed on the day of presentation showed an estimated fetal weight of 644 g (53rd percentile), an estimated head circumference of 221 mm (63rd percentile), and normal intracranial anatomy. Fevers and rash subsided after 3 days of supportive care. Screening for measles, varicella, rubella, syphilis, Epstein-Barr virus, influenza, hepatitis B, hepatitis C, mumps, and dengue was negative.

An initial immunoglobulin M test on July 7 was negative; seroconversion occurred 1 week after presentation and remained positive through delivery.

A full-term infant weighing 2,990 g was delivered vaginally. Neonatal ultrasonography and magnetic resonance imaging of the head showed a normal head size and intracranial anatomy, with no calcifications. Placental tissue was negative for Zika virus, and neonatal laboratory testing revealed no evidence of infection.

The case was confirmed by the Miami-Dade County Department of Health as the first non-travel-associated Zika infection in the United States.

Chen L, Hafeez F, Curry CL, Elgart G. Cutaneous eruption in a U.S. woman with locally acquired Zika virus infection. N Engl J Med. 2017;376(4):400-401. doi:10.1056/NEJMc1610614.

Lab Values Poor Surrogate for Detecting Pediatric Rocky Mountain Spotted Fever in Children

WHITNEY MCKNIGHT

FRONTLINE MEDICAL NEWS

Three fatalities observed in a retrospective analysis of six cases of Rocky Mountain spotted fever (RMSF) in children were associated with either a delayed diagnosis pending laboratory findings or delayed anti-rickettsia treatment, researchers said.

“The fact that all fatal cases died before the convalescent period emphasizes that diagnosis should be based on clinical findings instead of RMSF serologic and histologic testing,” wrote the authors of a study published online in Pediatric Dermatology.

Rechelle Tull of the department of dermatology, Wake Forest University, Winston-Salem, NC, and her colleagues conducted a retrospective review of 3,912 inpatient dermatology consultations over a period of 10 years at a tertiary care center, and identified six patients aged 22 months to 2 years (mean, 5.1 years) diagnosed with RMSF. The patients were evaluated in the months of April, May, and June, and three of the six patients infected with the vector-borne obligate intracellular bacterium, Rickettsia rickettsii, had died within 4 days of hospitalization, according to the authors.

Two of the fatal cases involved delayed anti-rickettsial therapy after the patients were misdiagnosed with group A Streptococcus. None of the six children were initially evaluated for R rickettsii; they averaged three encounters with their clinician before being admitted for acute inpatient care, where they received intravenous doxycycline after nearly a week of symptoms.

“All fatal cases were complicated by neurologic manifestations, including seizures, obtundation, and uncal herniation,” a finding that is consistent with the literature, the authors said.

Although the high-fatality rate might be the result of the small study size, Ms Tull and her coinvestigators concluded that the disease should be considered in all differential diagnoses for children who present with a fever and rash during the summer months in endemic areas, particularly since pediatric cases of the disease are associated with poorer outcomes than adult cases.

Given that RMSF often remains subclinical in its early stages, and typically presents with nonspecific symptoms of fever, rash, headache, and abdominal pain when it does emerge, physicians might be tempted to defer treatment until after serological and histological results are in, as is the standard method. Concerns over doxycycline’s tendency to stain teeth and cause enamel hypoplasia are also common. However, empirical administration could mean the difference between life and death, since treatment within the first 5 days following infection is associated with better outcomes—an algorithm complicated by the fact that symptoms caused by R rickettsii have been known to take as long as 21 days to appear.

In the study, Ms Tull and her colleagues found that the average time between exposure to the tick and the onset of symptoms was 6.6 days (range, 1-21 days).

Currently, there are no diagnostic tests “that reliably diagnose RMSF during the first 7 days of illness,” and most patients “do not develop detectable antibodies until the second week of illness,” the investigators reported. Even then, sensitivity of indirect fluorescent antibody serum testing after the second week of illness is only between 86% and 94%, they noted. Further, the sensitivity of immunohistochemical (IHC) tissue staining has been reported at 70%, and false-negative IHC results are common in acute disease when antibody response is harder to detect.

Ms Tull and her colleagues found that five of the six patients in their study had negative IHC testing; two of the six had positive serum antibody titers. For this reason, they concluded that RMSF diagnosis should be based on “clinical history, examination, and laboratory abnormalities” rather than laboratory testing, and urged that “prompt treatment should be instituted empirically.”

Tull R, Ahn C, Daniel A, Yosipovitch G, Strowd LC. Retrospective study of Rocky Mountain spotted fever in children. Pediatr Dermatol. 2016 Dec 19. doi:10.1111/pde.13053. [Epub ahead of print]

BY JEFF BAUER

A large retrospective analysis found a wide variation in opioid prescribing among emergency physicians (EPs) working within the same ED. The study also found that Medicare patients treated by EPs who wrote the most prescriptions for opioids were more likely to use opioids for 6 months after their ED visit than were those treated by EPs who wrote fewer opioid prescriptions.

Researchers evaluated initial visits to an ED by approximately 378,000 Medicare beneficiaries (average age: 68 years) from 2008 through 2011. None of these patients had received a prescription for an opioid in the 6 months before the ED visit, and none of the visits resulted in a hospital admission. Prescriptions for opioids (excluding methadone) were identified by the national drug code in the Medicare Part D database. An opioid prescription was attributed to the treating EP if the patient filled the prescription within 3 days after the ED visit.

Investigators categorized the treating EPs in this study as “high-intensity” or “low-intensity” opioid prescribers by calculating the proportion of all ED visits that resulted in an opioid prescription being filled. They then grouped the EPs into quartiles of opioid prescribing within each hospital. High-intensity prescribers were those in the top quartile of opioid prescribing rates, and low-intensity prescribers were those in the bottom quartile.

The primary outcome was long-term opioid use, defined as 6 months or more of opioids supplied in the 12 months after the initial ED visit. This did not include prescriptions filled within 30 days of the initial visit.

Overall, approximately 215,700 patients were treated by low-intensity prescribers and 162,000 by high-intensity prescribers. In general, the patient characteristics and diagnoses were similar in both groups. The rate of opioid prescribing of high-intensity prescribers was approximately triple the rate of low-intensity prescribers. High-intensity prescribers provided an opioid prescription for 21.4% of ED visits, compared to 7.3% among low-intensity prescribers.

Long-term opioid use at 12 months was significantly higher among patients who had been initially treated by high-intensity prescribers compared to those who had been treated by low-intensity prescribers (1.51% vs 1.16%; unadjusted odds ratio [OR], 1.31). There was minimal change in this difference after the results were adjusted for the patients’ age, race, sex, disability status, and presence of chronic conditions (OR, 1.30). The number needed to harm was calculated as 49, meaning theoretically, for every 49 patients who received a new opioid prescription in the ED, one would become a long-term user. The authors noted, however, that “…prescriptions provided by other physicians in the months after an [ED] visit are necessary for long-term opioid use to take hold.”

Researchers pointed out several limitations to their study. Because the study was observational, it could not establish causality. Researchers were not able to directly attribute opioid prescriptions to the treating EPs, but instead used prescriptions filled within 3 days of an ED visits as a surrogate; some opioid prescriptions could have been written by another clinician, such as the patient’s primary care physician during a follow-up visit. Because the study focused on Medicare patients, the results may not be applicable to younger patients. Based on their analysis, researchers could not determine whether an opioid prescription was appropriate, and therefore they could not quantify the extent of opioid overprescribing.

For more on EPs and opioid prescribing, see “The New Opioid Epidemic and the Law of Unintended Consequences” by Emergency Medicine Editor in Chief Neal Flomenbaum, MD (Emergency Medicine. 2017;49[2]:52) and “The New Opioid Epidemic: Prescriptions, Synthetics, and Street Drugs” by Rama B. Rao, MD and Emergency Medicine Associate Editor, Toxicology Lewis S. Nelson, MD (Emergency Medicine. 2017;49[2]:64-70).

Barnett ML, Olenski AR, Jena AB. Opioid-prescribing patterns of emergency physicians and risk of long-term use. N Engl J Med. 2017;376(7):663-673. doi:10.1056/NEJMsa1610524.

Lower Admission Rates, Other Factors Tied to High Rate of Death Soon After ED Discharge Among Older Adults

BY JEFF BAUER

Each year, approximately 10,000 older adult patients die within 7 days of discharge from an ED in the United States, despite having no obvious life-threatening illness, according to a large retrospective study. Emergency departments with lower rates of inpatient admission from the ED, lower patient volumes, and lower charges had significantly higher rates of death after discharge.

Researchers evaluated Medicare claims data related to slightly more than 10 million ED visits from 2007 to 2012. Because the goal was to study generally healthy patients, the following patients were excluded: individuals who were age 90 years and older; were receiving palliative or hospice care; or had received a life-limiting diagnosis, such as a myocardial infarction (MI) or a malignancy, either in the ED or in the year prior to the ED visit. The primary outcome was death within 7 days after discharge from an ED. The cause of death was determined by linking claims to death certificates; this information was available only for a subset of patients who visited an ED in 2007 or 2008.

Overall, during the 6-year study, 0.12% of discharged patients died within 7 days of discharge; this translates to more than 10,000 early deaths per year nationally. The leading causes of death were atherosclerotic heart disease (13.6%), MI (10.3%), and chronic obstructive pulmonary disease (9.6%).

Emergency departments ranked in the lowest fifth for admission rates admitted 15% of patients, compared to 56% of patients at EDs with the highest admission rates. The early death rate of patients treated at EDs with the lowest rates of inpatient admissions from the ED was 3.4 times higher than the death rate seen in EDs with the highest inpatient admission rates (0.27% vs 0.08%, respectively). This was true despite the fact that EDs with low-admission rates treated healthier patients, as evidenced by the overall 7-day mortality rate of all patients treated in the ED, whether they were admitted or discharged. Emergency departments that saw higher volumes of patients and had higher charges for visits had significantly fewer deaths.

Obermeyer Z, Cohn B, Wilson M, Jena AB, Cutler DM. Early death after discharge from emergency departments: analysis of national US insurance claims data. BMJ. 2017;356:j239. doi:10.1136/bmj.j239.

Tertiary Center Repeat Computed Tomography Scans Find Additional Injuries

MICHELE G. SULLIVAN

FRONTLINE MEDICAL NEWS

Imaging obtained at nontertiary trauma centers (NTCs) probably does not tell the whole story of a trauma patient’s injuries, according to a new retrospective study.

Repeat scans done at a Level 1 trauma center identified new injuries in 76% of patients who were transferred, Morgan Bonds, MD, reported at the annual scientific assembly of the Eastern Association for the Surgery of Trauma. About half of these previously unobserved injuries were considered clinically significant, said Dr Bonds, a surgical resident at the University of Oklahoma, Oklahoma City.

Her study examined imaging and clinical assessment of 203 trauma patients who were initially worked up at an NTC, and then transferred to the Level 1 University of Oklahoma tertiary trauma center (TTC). The facility’s primary radiologist reviewed all of the initial computed tomography (CT) scans while blinded to the NTC interpretation. The initial scans and interpretations were then compared with those done at the TTC.

The team split imaging and interpretation disconnects into four categories:

• Type A errors: A missed injury on the NTC scan. “This represents the expertise and experience of our primary radiologist,” Dr Bonds said.
• Type B errors: Missed injuries on scans where NTC radiologists saw other injuries that the TTC radiologist did not confirm. “This represents the experience of our radiologist and also the inexperience and overreaction of the NTC radiologists.”
• Type C errors: New injuries seen on additional TTC imaging of the same body area. “This represents the quality of the image.”
• Type D errors: New injuries found upon any new imaging, whether of a previously scanned or newly scanned body area. “This represents quality of work-up—the decision of the trauma team to more fully investigate the patient’s injuries, as well as the quality of the CT tech performing the scan.”

During the study period, 203 patients presented at the TTC with prior scans conducted at an NTC.

The mean age of the patients was 43 years; most (67%) were men. The mean Injury Severity Score was 16; 97% had experienced blunt trauma. Shock was present in 3% and a traumatic brain injury in 8%. Repeat scans were most common for neck and cervical spine injuries (54%) and thoracic/lumbar spine injuries (53%), and least common for chest injuries (32%).

An inadequate NTC work-up as judged by the TTC attending was the most common reason for obtaining new images (76%). Poor image quality was the next most common reason (31%).

Among the 203 patients, 99 (49%) had a type A error. Of these injuries missed on the initial scan, 90% were considered to be clinically significant.

Type B errors occurred in 15% of patients. Type C errors (new injuries in different body area) occurred in 54% of patients and, of these, 76% were considered clinically significant. Type D errors (new injuries seen in any imaging of any area) occurred in 73% of patients.

“This study confirms that images are often repeated or completed after having images done at NTCs,” Dr Bonds said. “Relying on NTC image interpretation can lead to undertreating our patients. One potential solution to this issue could be image sharing between NTCs and TTCs. This might reduce both the rate of missed injuries and the need for repeat scans.”

Cutaneous Eruption Reported in Pregnant Woman With Locally Acquired Zika Virus

M. ALEXANDER OTTO

FRONTLINE MEDICAL NEWS

Zika presented in a young, pregnant Florida woman as erythematous follicular macules and papules on the trunk and arms, scattered tender pink papules on the palms, and a few petechiae on the hard palate, according to a report in the New England Journal of Medicine.

The report advises how Zika virus may present during pregnancy. “Medical providers on the front line should be aware of the constellation of symptoms in patients reporting travel to endemic areas, including areas in Southern Florida, where other non-travel-associated cases have been confirmed,” wrote investigators led by Lucy Chen, MD, of the University of Miami.

The 23-year-old woman presented on July 7, 2016 at 23 weeks and 3 days’ gestation with a 3-day history of fever, widespread pruritic rash, and sore throat, which were followed by myalgias and joint pain 2 days later. The cutaneous eruption was noted on physical examination; neither conjunctivitis nor lymphadenopathy was present. The patient and her partner said they had not traveled outside the United States for 2 years.

Zika virus RNA was detected in the woman’s urine and serum specimens with the use of reverse-transcriptase polymerase chain reaction and persisted for 2 weeks in urine samples and for 6 weeks in serum samples. On histopathology, skin lesions revealed a mild perivascular lymphocytic infiltration in the upper dermis, admixed with some neutrophils. Liver and renal functions were normal.

Fetal ultrasonography performed on the day of presentation showed an estimated fetal weight of 644 g (53rd percentile), an estimated head circumference of 221 mm (63rd percentile), and normal intracranial anatomy. Fevers and rash subsided after 3 days of supportive care. Screening for measles, varicella, rubella, syphilis, Epstein-Barr virus, influenza, hepatitis B, hepatitis C, mumps, and dengue was negative.

An initial immunoglobulin M test on July 7 was negative; seroconversion occurred 1 week after presentation and remained positive through delivery.

A full-term infant weighing 2,990 g was delivered vaginally. Neonatal ultrasonography and magnetic resonance imaging of the head showed a normal head size and intracranial anatomy, with no calcifications. Placental tissue was negative for Zika virus, and neonatal laboratory testing revealed no evidence of infection.

The case was confirmed by the Miami-Dade County Department of Health as the first non-travel-associated Zika infection in the United States.

Chen L, Hafeez F, Curry CL, Elgart G. Cutaneous eruption in a U.S. woman with locally acquired Zika virus infection. N Engl J Med. 2017;376(4):400-401. doi:10.1056/NEJMc1610614.

Lab Values Poor Surrogate for Detecting Pediatric Rocky Mountain Spotted Fever in Children

WHITNEY MCKNIGHT

FRONTLINE MEDICAL NEWS

Three fatalities observed in a retrospective analysis of six cases of Rocky Mountain spotted fever (RMSF) in children were associated with either a delayed diagnosis pending laboratory findings or delayed anti-rickettsia treatment, researchers said.

“The fact that all fatal cases died before the convalescent period emphasizes that diagnosis should be based on clinical findings instead of RMSF serologic and histologic testing,” wrote the authors of a study published online in Pediatric Dermatology.

Rechelle Tull of the department of dermatology, Wake Forest University, Winston-Salem, NC, and her colleagues conducted a retrospective review of 3,912 inpatient dermatology consultations over a period of 10 years at a tertiary care center, and identified six patients aged 22 months to 2 years (mean, 5.1 years) diagnosed with RMSF. The patients were evaluated in the months of April, May, and June, and three of the six patients infected with the vector-borne obligate intracellular bacterium, Rickettsia rickettsii, had died within 4 days of hospitalization, according to the authors.

Two of the fatal cases involved delayed anti-rickettsial therapy after the patients were misdiagnosed with group A Streptococcus. None of the six children were initially evaluated for R rickettsii; they averaged three encounters with their clinician before being admitted for acute inpatient care, where they received intravenous doxycycline after nearly a week of symptoms.

“All fatal cases were complicated by neurologic manifestations, including seizures, obtundation, and uncal herniation,” a finding that is consistent with the literature, the authors said.

Although the high-fatality rate might be the result of the small study size, Ms Tull and her coinvestigators concluded that the disease should be considered in all differential diagnoses for children who present with a fever and rash during the summer months in endemic areas, particularly since pediatric cases of the disease are associated with poorer outcomes than adult cases.

Given that RMSF often remains subclinical in its early stages, and typically presents with nonspecific symptoms of fever, rash, headache, and abdominal pain when it does emerge, physicians might be tempted to defer treatment until after serological and histological results are in, as is the standard method. Concerns over doxycycline’s tendency to stain teeth and cause enamel hypoplasia are also common. However, empirical administration could mean the difference between life and death, since treatment within the first 5 days following infection is associated with better outcomes—an algorithm complicated by the fact that symptoms caused by R rickettsii have been known to take as long as 21 days to appear.

In the study, Ms Tull and her colleagues found that the average time between exposure to the tick and the onset of symptoms was 6.6 days (range, 1-21 days).

Currently, there are no diagnostic tests “that reliably diagnose RMSF during the first 7 days of illness,” and most patients “do not develop detectable antibodies until the second week of illness,” the investigators reported. Even then, sensitivity of indirect fluorescent antibody serum testing after the second week of illness is only between 86% and 94%, they noted. Further, the sensitivity of immunohistochemical (IHC) tissue staining has been reported at 70%, and false-negative IHC results are common in acute disease when antibody response is harder to detect.

Ms Tull and her colleagues found that five of the six patients in their study had negative IHC testing; two of the six had positive serum antibody titers. For this reason, they concluded that RMSF diagnosis should be based on “clinical history, examination, and laboratory abnormalities” rather than laboratory testing, and urged that “prompt treatment should be instituted empirically.”

Tull R, Ahn C, Daniel A, Yosipovitch G, Strowd LC. Retrospective study of Rocky Mountain spotted fever in children. Pediatr Dermatol. 2016 Dec 19. doi:10.1111/pde.13053. [Epub ahead of print]

BY JEFF BAUER

A large retrospective analysis found a wide variation in opioid prescribing among emergency physicians (EPs) working within the same ED. The study also found that Medicare patients treated by EPs who wrote the most prescriptions for opioids were more likely to use opioids for 6 months after their ED visit than were those treated by EPs who wrote fewer opioid prescriptions.

Researchers evaluated initial visits to an ED by approximately 378,000 Medicare beneficiaries (average age: 68 years) from 2008 through 2011. None of these patients had received a prescription for an opioid in the 6 months before the ED visit, and none of the visits resulted in a hospital admission. Prescriptions for opioids (excluding methadone) were identified by the national drug code in the Medicare Part D database. An opioid prescription was attributed to the treating EP if the patient filled the prescription within 3 days after the ED visit.

Investigators categorized the treating EPs in this study as “high-intensity” or “low-intensity” opioid prescribers by calculating the proportion of all ED visits that resulted in an opioid prescription being filled. They then grouped the EPs into quartiles of opioid prescribing within each hospital. High-intensity prescribers were those in the top quartile of opioid prescribing rates, and low-intensity prescribers were those in the bottom quartile.

The primary outcome was long-term opioid use, defined as 6 months or more of opioids supplied in the 12 months after the initial ED visit. This did not include prescriptions filled within 30 days of the initial visit.

Overall, approximately 215,700 patients were treated by low-intensity prescribers and 162,000 by high-intensity prescribers. In general, the patient characteristics and diagnoses were similar in both groups. The rate of opioid prescribing of high-intensity prescribers was approximately triple the rate of low-intensity prescribers. High-intensity prescribers provided an opioid prescription for 21.4% of ED visits, compared to 7.3% among low-intensity prescribers.

Long-term opioid use at 12 months was significantly higher among patients who had been initially treated by high-intensity prescribers compared to those who had been treated by low-intensity prescribers (1.51% vs 1.16%; unadjusted odds ratio [OR], 1.31). There was minimal change in this difference after the results were adjusted for the patients’ age, race, sex, disability status, and presence of chronic conditions (OR, 1.30). The number needed to harm was calculated as 49, meaning theoretically, for every 49 patients who received a new opioid prescription in the ED, one would become a long-term user. The authors noted, however, that “…prescriptions provided by other physicians in the months after an [ED] visit are necessary for long-term opioid use to take hold.”

Researchers pointed out several limitations to their study. Because the study was observational, it could not establish causality. Researchers were not able to directly attribute opioid prescriptions to the treating EPs, but instead used prescriptions filled within 3 days of an ED visits as a surrogate; some opioid prescriptions could have been written by another clinician, such as the patient’s primary care physician during a follow-up visit. Because the study focused on Medicare patients, the results may not be applicable to younger patients. Based on their analysis, researchers could not determine whether an opioid prescription was appropriate, and therefore they could not quantify the extent of opioid overprescribing.

For more on EPs and opioid prescribing, see “The New Opioid Epidemic and the Law of Unintended Consequences” by Emergency Medicine Editor in Chief Neal Flomenbaum, MD (Emergency Medicine. 2017;49[2]:52) and “The New Opioid Epidemic: Prescriptions, Synthetics, and Street Drugs” by Rama B. Rao, MD and Emergency Medicine Associate Editor, Toxicology Lewis S. Nelson, MD (Emergency Medicine. 2017;49[2]:64-70).

Barnett ML, Olenski AR, Jena AB. Opioid-prescribing patterns of emergency physicians and risk of long-term use. N Engl J Med. 2017;376(7):663-673. doi:10.1056/NEJMsa1610524.

Lower Admission Rates, Other Factors Tied to High Rate of Death Soon After ED Discharge Among Older Adults

BY JEFF BAUER

Each year, approximately 10,000 older adult patients die within 7 days of discharge from an ED in the United States, despite having no obvious life-threatening illness, according to a large retrospective study. Emergency departments with lower rates of inpatient admission from the ED, lower patient volumes, and lower charges had significantly higher rates of death after discharge.

Researchers evaluated Medicare claims data related to slightly more than 10 million ED visits from 2007 to 2012. Because the goal was to study generally healthy patients, the following patients were excluded: individuals who were age 90 years and older; were receiving palliative or hospice care; or had received a life-limiting diagnosis, such as a myocardial infarction (MI) or a malignancy, either in the ED or in the year prior to the ED visit. The primary outcome was death within 7 days after discharge from an ED. The cause of death was determined by linking claims to death certificates; this information was available only for a subset of patients who visited an ED in 2007 or 2008.

Overall, during the 6-year study, 0.12% of discharged patients died within 7 days of discharge; this translates to more than 10,000 early deaths per year nationally. The leading causes of death were atherosclerotic heart disease (13.6%), MI (10.3%), and chronic obstructive pulmonary disease (9.6%).

Emergency departments ranked in the lowest fifth for admission rates admitted 15% of patients, compared to 56% of patients at EDs with the highest admission rates. The early death rate of patients treated at EDs with the lowest rates of inpatient admissions from the ED was 3.4 times higher than the death rate seen in EDs with the highest inpatient admission rates (0.27% vs 0.08%, respectively). This was true despite the fact that EDs with low-admission rates treated healthier patients, as evidenced by the overall 7-day mortality rate of all patients treated in the ED, whether they were admitted or discharged. Emergency departments that saw higher volumes of patients and had higher charges for visits had significantly fewer deaths.

Obermeyer Z, Cohn B, Wilson M, Jena AB, Cutler DM. Early death after discharge from emergency departments: analysis of national US insurance claims data. BMJ. 2017;356:j239. doi:10.1136/bmj.j239.

Tertiary Center Repeat Computed Tomography Scans Find Additional Injuries

MICHELE G. SULLIVAN

FRONTLINE MEDICAL NEWS

Imaging obtained at nontertiary trauma centers (NTCs) probably does not tell the whole story of a trauma patient’s injuries, according to a new retrospective study.

Repeat scans done at a Level 1 trauma center identified new injuries in 76% of patients who were transferred, Morgan Bonds, MD, reported at the annual scientific assembly of the Eastern Association for the Surgery of Trauma. About half of these previously unobserved injuries were considered clinically significant, said Dr Bonds, a surgical resident at the University of Oklahoma, Oklahoma City.

Her study examined imaging and clinical assessment of 203 trauma patients who were initially worked up at an NTC, and then transferred to the Level 1 University of Oklahoma tertiary trauma center (TTC). The facility’s primary radiologist reviewed all of the initial computed tomography (CT) scans while blinded to the NTC interpretation. The initial scans and interpretations were then compared with those done at the TTC.

The team split imaging and interpretation disconnects into four categories:

• Type A errors: A missed injury on the NTC scan. “This represents the expertise and experience of our primary radiologist,” Dr Bonds said.
• Type B errors: Missed injuries on scans where NTC radiologists saw other injuries that the TTC radiologist did not confirm. “This represents the experience of our radiologist and also the inexperience and overreaction of the NTC radiologists.”
• Type C errors: New injuries seen on additional TTC imaging of the same body area. “This represents the quality of the image.”
• Type D errors: New injuries found upon any new imaging, whether of a previously scanned or newly scanned body area. “This represents quality of work-up—the decision of the trauma team to more fully investigate the patient’s injuries, as well as the quality of the CT tech performing the scan.”

During the study period, 203 patients presented at the TTC with prior scans conducted at an NTC.

The mean age of the patients was 43 years; most (67%) were men. The mean Injury Severity Score was 16; 97% had experienced blunt trauma. Shock was present in 3% and a traumatic brain injury in 8%. Repeat scans were most common for neck and cervical spine injuries (54%) and thoracic/lumbar spine injuries (53%), and least common for chest injuries (32%).

An inadequate NTC work-up as judged by the TTC attending was the most common reason for obtaining new images (76%). Poor image quality was the next most common reason (31%).

Among the 203 patients, 99 (49%) had a type A error. Of these injuries missed on the initial scan, 90% were considered to be clinically significant.

Type B errors occurred in 15% of patients. Type C errors (new injuries in different body area) occurred in 54% of patients and, of these, 76% were considered clinically significant. Type D errors (new injuries seen in any imaging of any area) occurred in 73% of patients.

“This study confirms that images are often repeated or completed after having images done at NTCs,” Dr Bonds said. “Relying on NTC image interpretation can lead to undertreating our patients. One potential solution to this issue could be image sharing between NTCs and TTCs. This might reduce both the rate of missed injuries and the need for repeat scans.”

Cutaneous Eruption Reported in Pregnant Woman With Locally Acquired Zika Virus

M. ALEXANDER OTTO

FRONTLINE MEDICAL NEWS

Zika presented in a young, pregnant Florida woman as erythematous follicular macules and papules on the trunk and arms, scattered tender pink papules on the palms, and a few petechiae on the hard palate, according to a report in the New England Journal of Medicine.

The report advises how Zika virus may present during pregnancy. “Medical providers on the front line should be aware of the constellation of symptoms in patients reporting travel to endemic areas, including areas in Southern Florida, where other non-travel-associated cases have been confirmed,” wrote investigators led by Lucy Chen, MD, of the University of Miami.

The 23-year-old woman presented on July 7, 2016 at 23 weeks and 3 days’ gestation with a 3-day history of fever, widespread pruritic rash, and sore throat, which were followed by myalgias and joint pain 2 days later. The cutaneous eruption was noted on physical examination; neither conjunctivitis nor lymphadenopathy was present. The patient and her partner said they had not traveled outside the United States for 2 years.

Zika virus RNA was detected in the woman’s urine and serum specimens with the use of reverse-transcriptase polymerase chain reaction and persisted for 2 weeks in urine samples and for 6 weeks in serum samples. On histopathology, skin lesions revealed a mild perivascular lymphocytic infiltration in the upper dermis, admixed with some neutrophils. Liver and renal functions were normal.

Fetal ultrasonography performed on the day of presentation showed an estimated fetal weight of 644 g (53rd percentile), an estimated head circumference of 221 mm (63rd percentile), and normal intracranial anatomy. Fevers and rash subsided after 3 days of supportive care. Screening for measles, varicella, rubella, syphilis, Epstein-Barr virus, influenza, hepatitis B, hepatitis C, mumps, and dengue was negative.

An initial immunoglobulin M test on July 7 was negative; seroconversion occurred 1 week after presentation and remained positive through delivery.

A full-term infant weighing 2,990 g was delivered vaginally. Neonatal ultrasonography and magnetic resonance imaging of the head showed a normal head size and intracranial anatomy, with no calcifications. Placental tissue was negative for Zika virus, and neonatal laboratory testing revealed no evidence of infection.

The case was confirmed by the Miami-Dade County Department of Health as the first non-travel-associated Zika infection in the United States.

Chen L, Hafeez F, Curry CL, Elgart G. Cutaneous eruption in a U.S. woman with locally acquired Zika virus infection. N Engl J Med. 2017;376(4):400-401. doi:10.1056/NEJMc1610614.

Lab Values Poor Surrogate for Detecting Pediatric Rocky Mountain Spotted Fever in Children

WHITNEY MCKNIGHT

FRONTLINE MEDICAL NEWS

Three fatalities observed in a retrospective analysis of six cases of Rocky Mountain spotted fever (RMSF) in children were associated with either a delayed diagnosis pending laboratory findings or delayed anti-rickettsia treatment, researchers said.

“The fact that all fatal cases died before the convalescent period emphasizes that diagnosis should be based on clinical findings instead of RMSF serologic and histologic testing,” wrote the authors of a study published online in Pediatric Dermatology.

Rechelle Tull of the department of dermatology, Wake Forest University, Winston-Salem, NC, and her colleagues conducted a retrospective review of 3,912 inpatient dermatology consultations over a period of 10 years at a tertiary care center, and identified six patients aged 22 months to 2 years (mean, 5.1 years) diagnosed with RMSF. The patients were evaluated in the months of April, May, and June, and three of the six patients infected with the vector-borne obligate intracellular bacterium, Rickettsia rickettsii, had died within 4 days of hospitalization, according to the authors.

Two of the fatal cases involved delayed anti-rickettsial therapy after the patients were misdiagnosed with group A Streptococcus. None of the six children were initially evaluated for R rickettsii; they averaged three encounters with their clinician before being admitted for acute inpatient care, where they received intravenous doxycycline after nearly a week of symptoms.

“All fatal cases were complicated by neurologic manifestations, including seizures, obtundation, and uncal herniation,” a finding that is consistent with the literature, the authors said.

Although the high-fatality rate might be the result of the small study size, Ms Tull and her coinvestigators concluded that the disease should be considered in all differential diagnoses for children who present with a fever and rash during the summer months in endemic areas, particularly since pediatric cases of the disease are associated with poorer outcomes than adult cases.

Given that RMSF often remains subclinical in its early stages, and typically presents with nonspecific symptoms of fever, rash, headache, and abdominal pain when it does emerge, physicians might be tempted to defer treatment until after serological and histological results are in, as is the standard method. Concerns over doxycycline’s tendency to stain teeth and cause enamel hypoplasia are also common. However, empirical administration could mean the difference between life and death, since treatment within the first 5 days following infection is associated with better outcomes—an algorithm complicated by the fact that symptoms caused by R rickettsii have been known to take as long as 21 days to appear.

In the study, Ms Tull and her colleagues found that the average time between exposure to the tick and the onset of symptoms was 6.6 days (range, 1-21 days).

Currently, there are no diagnostic tests “that reliably diagnose RMSF during the first 7 days of illness,” and most patients “do not develop detectable antibodies until the second week of illness,” the investigators reported. Even then, sensitivity of indirect fluorescent antibody serum testing after the second week of illness is only between 86% and 94%, they noted. Further, the sensitivity of immunohistochemical (IHC) tissue staining has been reported at 70%, and false-negative IHC results are common in acute disease when antibody response is harder to detect.

Ms Tull and her colleagues found that five of the six patients in their study had negative IHC testing; two of the six had positive serum antibody titers. For this reason, they concluded that RMSF diagnosis should be based on “clinical history, examination, and laboratory abnormalities” rather than laboratory testing, and urged that “prompt treatment should be instituted empirically.”

Tull R, Ahn C, Daniel A, Yosipovitch G, Strowd LC. Retrospective study of Rocky Mountain spotted fever in children. Pediatr Dermatol. 2016 Dec 19. doi:10.1111/pde.13053. [Epub ahead of print]

HOUSTON – Stroke patients with arm weakness had a clinically significant boost in arm function after about 19 weeks on a rehabilitation program that combined vagus nerve stimulation with rehabilitation training sessions in a multicenter, randomized, and sham-controlled proof-of-concept study with 17 patients.

This promising result follows a prior 21-patient study with a similar design and results (Stroke. 2016 Jan;47[1]:143-50), making the next step a pivotal trial with about 120 randomized patients that should start in 2017, Jesse Dawson, MD, said at the International Stroke Conference sponsored by the American Heart Association.

Mitchel L. Zoler/Frontline Medical News

[email protected]
On Twitter @mitchelzoler

HOUSTON – Stroke patients with arm weakness had a clinically significant boost in arm function after about 19 weeks on a rehabilitation program that combined vagus nerve stimulation with rehabilitation training sessions in a multicenter, randomized, and sham-controlled proof-of-concept study with 17 patients.

This promising result follows a prior 21-patient study with a similar design and results (Stroke. 2016 Jan;47[1]:143-50), making the next step a pivotal trial with about 120 randomized patients that should start in 2017, Jesse Dawson, MD, said at the International Stroke Conference sponsored by the American Heart Association.

Mitchel L. Zoler/Frontline Medical News

[email protected]
On Twitter @mitchelzoler

HOUSTON – Stroke patients with arm weakness had a clinically significant boost in arm function after about 19 weeks on a rehabilitation program that combined vagus nerve stimulation with rehabilitation training sessions in a multicenter, randomized, and sham-controlled proof-of-concept study with 17 patients.

This promising result follows a prior 21-patient study with a similar design and results (Stroke. 2016 Jan;47[1]:143-50), making the next step a pivotal trial with about 120 randomized patients that should start in 2017, Jesse Dawson, MD, said at the International Stroke Conference sponsored by the American Heart Association.

Mitchel L. Zoler/Frontline Medical News

[email protected]
On Twitter @mitchelzoler

A reporting system for lung cancer screening with low-dose computed tomography may underemphasize important abnormal findings other than nodules, researchers say, potentially leading to missed malignancies.

The American College of Radiology Lung Imaging Reporting and Data System, or Lung-RADS, was introduced in 2014 to standardize reporting for low-dose CT findings and also to reduce false-positive rates, by applying tighter criteria that was used in the National Lung Screening Trial.

Lung-RADS does not have specific reporting categories for patients with isolated hilar and mediastinal adenopathy or pleural effusion in the absence of lung nodules, even though these can indicate malignancy. It does allow for the inclusion of what is called an “S” code to indicate clinically significant findings other than nodules.

In the March 2017 issue of CHEST, Hiren Mehta, MD, and his colleagues at the University of Florida in Gainesville, report on four cases from their center in which patients with these pathologies had their scans read as Lung-RADS category 1, indicating a less than 1% likelihood of malignancy. No S codes were added to their reports. Subsequent testing in these patients revealed cancers (CHEST. 2017 March;151[3]:525-26).

The four cases were:

• A 56-year-old male with hilar and mediastinal adenopathy who was recommended for repeat screening at 12 months. The patient presented 6 months later with pneumonia; biopsy revealed large cell lung cancer.
• A 76-year-old male with paratracheal lymph nodes and a solitary subcarinal lymph node. A subsequent biopsy revealed adenocarcinoma.
• A 67-year-old male whose scan showed bulky hilar and mediastinal adenopathy. Subsequent testing revealed Hodgkin’s lymphoma.
• A 75-year-old female whose scan showed a small pleural effusion and no nodules. Repeat scanning at 1 year showed enlargement of the effusion and lung adenocarcinoma.

Dr. Mehta and colleagues noted in their analysis that Lung-RADS has not been studied prospectively in real practice settings and that the four cases – two of which involved delayed diagnosis – reveal “a significant limitation” of Lung-RADS.

“Based on our experience, we believe that particular caution should be exercised in reporting Lung-RADS 1 category for patients with adenopathy/pleural effusion with no lung nodules, as a majority of the lung cancer screening scans will be ordered by [primary care providers] ... [As] with any new system, an ongoing evaluation of the performance of Lung-RADS should be conducted so that the sensitivity and mortality benefit seen in the [National Lung Screening Trial] is not compromised.”

We strongly believe, based on our experience with these 4 cases that the new version of Lung-RADS 2.0 should [account for shortcomings of the current Lung-RADS] and have a separate category for findings that are highly suspicious for malignancy but do not have an accompanying lung nodule,” they wrote.

The investigators did not disclose outside funding or conflicts of interest related to their findings.

*This story was updated March 16, 2017, with the correct journal source.

A reporting system for lung cancer screening with low-dose computed tomography may underemphasize important abnormal findings other than nodules, researchers say, potentially leading to missed malignancies.

The American College of Radiology Lung Imaging Reporting and Data System, or Lung-RADS, was introduced in 2014 to standardize reporting for low-dose CT findings and also to reduce false-positive rates, by applying tighter criteria that was used in the National Lung Screening Trial.

Lung-RADS does not have specific reporting categories for patients with isolated hilar and mediastinal adenopathy or pleural effusion in the absence of lung nodules, even though these can indicate malignancy. It does allow for the inclusion of what is called an “S” code to indicate clinically significant findings other than nodules.

In the March 2017 issue of CHEST, Hiren Mehta, MD, and his colleagues at the University of Florida in Gainesville, report on four cases from their center in which patients with these pathologies had their scans read as Lung-RADS category 1, indicating a less than 1% likelihood of malignancy. No S codes were added to their reports. Subsequent testing in these patients revealed cancers (CHEST. 2017 March;151[3]:525-26).

The four cases were:

• A 56-year-old male with hilar and mediastinal adenopathy who was recommended for repeat screening at 12 months. The patient presented 6 months later with pneumonia; biopsy revealed large cell lung cancer.
• A 76-year-old male with paratracheal lymph nodes and a solitary subcarinal lymph node. A subsequent biopsy revealed adenocarcinoma.
• A 67-year-old male whose scan showed bulky hilar and mediastinal adenopathy. Subsequent testing revealed Hodgkin’s lymphoma.
• A 75-year-old female whose scan showed a small pleural effusion and no nodules. Repeat scanning at 1 year showed enlargement of the effusion and lung adenocarcinoma.

Dr. Mehta and colleagues noted in their analysis that Lung-RADS has not been studied prospectively in real practice settings and that the four cases – two of which involved delayed diagnosis – reveal “a significant limitation” of Lung-RADS.

“Based on our experience, we believe that particular caution should be exercised in reporting Lung-RADS 1 category for patients with adenopathy/pleural effusion with no lung nodules, as a majority of the lung cancer screening scans will be ordered by [primary care providers] ... [As] with any new system, an ongoing evaluation of the performance of Lung-RADS should be conducted so that the sensitivity and mortality benefit seen in the [National Lung Screening Trial] is not compromised.”

We strongly believe, based on our experience with these 4 cases that the new version of Lung-RADS 2.0 should [account for shortcomings of the current Lung-RADS] and have a separate category for findings that are highly suspicious for malignancy but do not have an accompanying lung nodule,” they wrote.

The investigators did not disclose outside funding or conflicts of interest related to their findings.

*This story was updated March 16, 2017, with the correct journal source.

A reporting system for lung cancer screening with low-dose computed tomography may underemphasize important abnormal findings other than nodules, researchers say, potentially leading to missed malignancies.

The American College of Radiology Lung Imaging Reporting and Data System, or Lung-RADS, was introduced in 2014 to standardize reporting for low-dose CT findings and also to reduce false-positive rates, by applying tighter criteria that was used in the National Lung Screening Trial.

Lung-RADS does not have specific reporting categories for patients with isolated hilar and mediastinal adenopathy or pleural effusion in the absence of lung nodules, even though these can indicate malignancy. It does allow for the inclusion of what is called an “S” code to indicate clinically significant findings other than nodules.

In the March 2017 issue of CHEST, Hiren Mehta, MD, and his colleagues at the University of Florida in Gainesville, report on four cases from their center in which patients with these pathologies had their scans read as Lung-RADS category 1, indicating a less than 1% likelihood of malignancy. No S codes were added to their reports. Subsequent testing in these patients revealed cancers (CHEST. 2017 March;151[3]:525-26).

The four cases were:

• A 56-year-old male with hilar and mediastinal adenopathy who was recommended for repeat screening at 12 months. The patient presented 6 months later with pneumonia; biopsy revealed large cell lung cancer.
• A 76-year-old male with paratracheal lymph nodes and a solitary subcarinal lymph node. A subsequent biopsy revealed adenocarcinoma.
• A 67-year-old male whose scan showed bulky hilar and mediastinal adenopathy. Subsequent testing revealed Hodgkin’s lymphoma.
• A 75-year-old female whose scan showed a small pleural effusion and no nodules. Repeat scanning at 1 year showed enlargement of the effusion and lung adenocarcinoma.

Dr. Mehta and colleagues noted in their analysis that Lung-RADS has not been studied prospectively in real practice settings and that the four cases – two of which involved delayed diagnosis – reveal “a significant limitation” of Lung-RADS.

“Based on our experience, we believe that particular caution should be exercised in reporting Lung-RADS 1 category for patients with adenopathy/pleural effusion with no lung nodules, as a majority of the lung cancer screening scans will be ordered by [primary care providers] ... [As] with any new system, an ongoing evaluation of the performance of Lung-RADS should be conducted so that the sensitivity and mortality benefit seen in the [National Lung Screening Trial] is not compromised.”

We strongly believe, based on our experience with these 4 cases that the new version of Lung-RADS 2.0 should [account for shortcomings of the current Lung-RADS] and have a separate category for findings that are highly suspicious for malignancy but do not have an accompanying lung nodule,” they wrote.

The investigators did not disclose outside funding or conflicts of interest related to their findings.

*This story was updated March 16, 2017, with the correct journal source.

LAS VEGAS – Certain cervicovaginal microbiota predispose women to spontaneous preterm birth, according to a new study, while other microbiota were found to be protective against preterm delivery.

The findings stand in contrast to previous clinical trials that “targeted uterine activity and/or uterine infection,” said Michal Elovitz, MD, the first author of a study presented at the annual Pregnancy Meeting sponsored by the Society for Maternal-Fetal Medicine.

[email protected]

On Twitter @karioakes

LAS VEGAS – Certain cervicovaginal microbiota predispose women to spontaneous preterm birth, according to a new study, while other microbiota were found to be protective against preterm delivery.

The findings stand in contrast to previous clinical trials that “targeted uterine activity and/or uterine infection,” said Michal Elovitz, MD, the first author of a study presented at the annual Pregnancy Meeting sponsored by the Society for Maternal-Fetal Medicine.

[email protected]

On Twitter @karioakes

LAS VEGAS – Certain cervicovaginal microbiota predispose women to spontaneous preterm birth, according to a new study, while other microbiota were found to be protective against preterm delivery.

The findings stand in contrast to previous clinical trials that “targeted uterine activity and/or uterine infection,” said Michal Elovitz, MD, the first author of a study presented at the annual Pregnancy Meeting sponsored by the Society for Maternal-Fetal Medicine.

[email protected]

On Twitter @karioakes

Mefloquine is an antimalarial drug that is associated with a significant risk of chronic neuropsychiatric adverse effects (AEs). The drug was licensed by the FDA in 1989 after development by scientists affiliated with Walter Reed Army Institute of Research (WRAIR). By the early 1990s, mefloquine had become the U.S. military’s drug of choice both for treatment of uncomplicated malaria and for antimalarial prophylaxis and was administered as a convenient weekly dose. Mefloquine was prescribed widely to U.S. military personnel beginning with operations in Somalia in 1992 and over the next 2 decades during certain deployments to Iraq and Afghanistan and to other malaria-endemic areas.¹

In 2013, following a decline of U.S. military use, the FDA added a boxed warning to the mefloquine product documentation to caution that neuropsychiatric AEs from the drug could last years after use and even be permanent. The U.S. military subsequently deemed mefloquine to be a prophylactic “drug of last resort.”² Recently, researchers at WRAIR have acknowledged that chronic neuropsychiatric AEs attributable to mefloquine, including nightmares, insomnia, anxiety, irritability, and cognitive dysfunction, may confound the diagnosis of posttraumatic stress disorder (PTSD).³ The VA has awarded at least 1 disability claim for service-connected psychiatric conditions that it attributed to mefloquine exposure, and it is likely that in the coming years such claims will increase.²

Susceptibility to Chronic Neuropsychiatric AEs

Why mefloquine seems to cause chronic neuropsychiatric AEs in only certain individuals is unclear, although genetic susceptibility to drug-induced toxic encephalopathy and neurotoxicity are suspected.¹ There is no screening test for susceptibility to AEs before mefloquine use, so the current U.S. product documentation cautiously warns that when used for prophylaxis, mefloquine should be discontinued at the onset of any neurologic or psychiatric symptom, many of which are considered prodromal to more serious AEs that may occur with continued dosing.⁴

Although chronic neuropsychiatric AEs have been reported to develop after only a single weekly dose, most clinically significant chronic AEs seem to occur among those who developed at least 1 prodromal neuropsychiatric symptom during early use but who continued weekly use despite these symptoms in a manner contrary to current product documentation guidance.⁴ In contrast, when mefloquine is administered for the treatment of malaria, typically at 5 times the weekly prophylactic dose and commonly in split doses over 8 to 12 hours, dosing is often complete by the time prodromal symptoms develop. Consequently, when mefloquine is used for treatment of malaria, the risks of more serious AEs are significantly higher than when the drug is used as directed in prophylaxis.⁵

Screening for Symptomatic Mefloquine Exposure

As the boxed warning indicates, certain psychiatric symptoms that occur with mefloquine use may become chronic and may confound psychiatric diagnosis. Particularly among veterans, these symptoms risk being misattributed, potentially affecting treatment decisions.⁶ Clinicians caring for veterans with persistent psychiatric symptoms should therefore screen for prior symptomatic mefloquine exposure and consider the possible AEs of the drug when formulating a differential diagnosis and treatment plan.

For example, a veteran with a history of symptomatic mefloquine exposure who later is diagnosed with PTSD may experience 1 or more symptoms, such as insomnia or cognitive dysfunction, which may be primarily attributable to the chronic AEs of the drug. The origins of the symptoms may be distinct from exposure to trauma and may not respond as effectively to certain conventional therapies for PTSD, requiring consideration of alternate therapies.³ The confounding role of psychiatric symptoms attributable to mefloquine exposure may explain failed response to medications and psychotherapy. Multidisciplinary evaluation and management may be appropriate for such patients.

If symptomatic mefloquine exposure is suspected, a clinician must establish evidence of exposure to the drug and the veteran’s development of neuropsychiatric symptoms associated with such exposure. The following sections provide guidance to aid in screening both for exposure to the drug and for the development of specific neuropsychiatric symptoms during prophylaxis or following the treatment of malaria.

Mefloquine Exposure

Mefloquine was licensed in the U.S. as a branded medication (Lariam) from 1989 to 2011, and the drug also has been available in a variety of generic equivalents from 2003 to the present. All versions of mefloquine approved in the U.S. have been formulated as a white/slightly-off-white, smaller than dime-sized round tablet, containing 250 mg of mefloquine hydrochloride.

When used for prophylaxis in military settings, the drug was often dispensed informally without documentation, sometimes including directly observed therapy under command direction.^1,2 Therefore, even in the absence of prescribing documentation, a veteran who endorses a consistent history of malaria prophylaxis with mefloquine should be considered as having evidence of exposure.²

Exposure to mefloquine is unlikely if the veteran reports taking a daily antimalarial medication—more likely it was doxycycline or atovaquone/proguanil (marketed as Malarone). In rare cases, the drug may have been erroneously prescribed or been mistakenly taken daily for prophylaxis or, in more common cases, a prophylactic “loading dose” (typically 1 tablet daily for 3 days prior to weekly dosing) was used.^7,8

Exposure also was unlikely if the veteran reports taking an antimalarial that was dosed weekly with a tablet that was not of the appropriate color, shape, and size. More likely that drug was chloroquine. Although most prophylactic use of mefloquine among U.S. veterans followed its licensing by the FDA in 1989, the drug is known to have been administered to a small number of U.S. military personnel prior to its licensing during clinical trials, including personnel deployed on certain operations during the 1980s.¹

For treatment of malaria, mefloquine was used widely until better-tolerated drugs became available, beginning in the early 2000s, although some use of mefloquine in the military continues to this day. In most cases, clinicians should rely on records of hospitalization to identify whether mefloquine was administered. In rare cases where documentation is unavailable, exposure should be assumed if the veteran reports a reliable history of taking about 5 tablets (corresponding to the usual treatment dose of 1,250 mg) of appropriate color, shape, and size in response to confirmed or suspected malaria infection, either in 1 dose, or in split doses over 8 to 12 hours.

Symptoms During Prophylaxis

If prophylactic exposure to the drug has been established, the clinician should confirm the presence of neuropsychiatric symptoms during the exposure. Particularly among veterans deploying to malaria-endemic combat areas, such symptoms may have occurred during a period of heightened stress coincident with their initial deployment, and the veterans may have misattributed these symptoms to nonmefloquine factors. The clinician should therefore take a careful history to identify specific symptoms listed in the mefloquine product documentation. Many AEs will commonly manifest following the first 3 doses, and the clinician may find that focusing on this period is useful.⁹

When mefloquine is used for prophylaxis, anxiety and depression each affect between 1% and 10% of users. Other AEs that may develop include panic attacks; severe mood swings; behavioral AEs, including agitation, aggression, restlessness, and mania; symptoms of psychosis, including paranoia, delusions, and hallucinations; dissociative symptoms, including depersonalization; suicidal ideation; and cognitive AEs, including confusion.

The common symptoms of insomnia and abnormal dreaming affect > 10% of users. Particularly if multiple symptoms occur or if any of these symptoms occur following or coincident with symptoms of disturbed sleep, these should be considered strong evidence of symptomatic exposure.⁴ Veterans who report a history of continued mefloquine use despite the onset of such symptoms may be at particularly increased risk of chronic AEs.

The clinician should consider as evidence of symptomatic exposure information provided by others, including reports of obvious signs of nightmares or psychosis affecting the veteran. Clinicians should be aware that confusion and other psychiatric AEs caused by mefloquine during prophylactic use may limit the validity of self-reported history. Similarly, a history of seizure with mefloquine use or of the development of specific neurologic symptoms, particularly visual disturbances, dizziness, vertigo, disequilibrium, and paresthesias, also should be considered strong evidence of symptomatic exposure and indication of an increased risk of chronic psychiatric AEs.⁴

Posttreatment Adverse Effects

Although chronic psychiatric AEs following malaria infection have long been attributed to cerebral involvement, recognition that mefloquine may independently cause chronic neuropsychiatric AEs may require that individual cases be reexamined to properly assign causation.¹⁰ Particularly in uncomplicated cases of malaria, neuropsychiatric symptoms that develop only after treatment with mefloquine should be considered plausibly to be due to the drug and as evidence of symptomatic exposure.

As with use of mefloquine in prophylaxis, these neuropsychiatric symptoms may evolve in the weeks to months following exposure. They also may contribute to lasting and significant changes in personality, mood, cognition, thought, sleep, and behavior.⁶

Conclusion

Chronic AEs from mefloquine may provide a parsimonious explanation for the onset and persistence of a veteran’s psychiatric symptoms, particularly in cases where these may have failed to respond to treatment. Clinicians evaluating veterans who are seeking care for lasting psychiatric symptoms should ensure that they screen for prior symptomatic mefloquine exposure. As recognition grows of the drug’s chronic AEs, symptomatic mefloquine exposure is likely to emerge as a significant known confounder in the diagnosis of psychiatric disorders, including PTSD, among the current generation of U.S. veterans.

Mefloquine is an antimalarial drug that is associated with a significant risk of chronic neuropsychiatric adverse effects (AEs). The drug was licensed by the FDA in 1989 after development by scientists affiliated with Walter Reed Army Institute of Research (WRAIR). By the early 1990s, mefloquine had become the U.S. military’s drug of choice both for treatment of uncomplicated malaria and for antimalarial prophylaxis and was administered as a convenient weekly dose. Mefloquine was prescribed widely to U.S. military personnel beginning with operations in Somalia in 1992 and over the next 2 decades during certain deployments to Iraq and Afghanistan and to other malaria-endemic areas.¹

In 2013, following a decline of U.S. military use, the FDA added a boxed warning to the mefloquine product documentation to caution that neuropsychiatric AEs from the drug could last years after use and even be permanent. The U.S. military subsequently deemed mefloquine to be a prophylactic “drug of last resort.”² Recently, researchers at WRAIR have acknowledged that chronic neuropsychiatric AEs attributable to mefloquine, including nightmares, insomnia, anxiety, irritability, and cognitive dysfunction, may confound the diagnosis of posttraumatic stress disorder (PTSD).³ The VA has awarded at least 1 disability claim for service-connected psychiatric conditions that it attributed to mefloquine exposure, and it is likely that in the coming years such claims will increase.²

Susceptibility to Chronic Neuropsychiatric AEs

Why mefloquine seems to cause chronic neuropsychiatric AEs in only certain individuals is unclear, although genetic susceptibility to drug-induced toxic encephalopathy and neurotoxicity are suspected.¹ There is no screening test for susceptibility to AEs before mefloquine use, so the current U.S. product documentation cautiously warns that when used for prophylaxis, mefloquine should be discontinued at the onset of any neurologic or psychiatric symptom, many of which are considered prodromal to more serious AEs that may occur with continued dosing.⁴

Although chronic neuropsychiatric AEs have been reported to develop after only a single weekly dose, most clinically significant chronic AEs seem to occur among those who developed at least 1 prodromal neuropsychiatric symptom during early use but who continued weekly use despite these symptoms in a manner contrary to current product documentation guidance.⁴ In contrast, when mefloquine is administered for the treatment of malaria, typically at 5 times the weekly prophylactic dose and commonly in split doses over 8 to 12 hours, dosing is often complete by the time prodromal symptoms develop. Consequently, when mefloquine is used for treatment of malaria, the risks of more serious AEs are significantly higher than when the drug is used as directed in prophylaxis.⁵

Screening for Symptomatic Mefloquine Exposure

As the boxed warning indicates, certain psychiatric symptoms that occur with mefloquine use may become chronic and may confound psychiatric diagnosis. Particularly among veterans, these symptoms risk being misattributed, potentially affecting treatment decisions.⁶ Clinicians caring for veterans with persistent psychiatric symptoms should therefore screen for prior symptomatic mefloquine exposure and consider the possible AEs of the drug when formulating a differential diagnosis and treatment plan.

For example, a veteran with a history of symptomatic mefloquine exposure who later is diagnosed with PTSD may experience 1 or more symptoms, such as insomnia or cognitive dysfunction, which may be primarily attributable to the chronic AEs of the drug. The origins of the symptoms may be distinct from exposure to trauma and may not respond as effectively to certain conventional therapies for PTSD, requiring consideration of alternate therapies.³ The confounding role of psychiatric symptoms attributable to mefloquine exposure may explain failed response to medications and psychotherapy. Multidisciplinary evaluation and management may be appropriate for such patients.

If symptomatic mefloquine exposure is suspected, a clinician must establish evidence of exposure to the drug and the veteran’s development of neuropsychiatric symptoms associated with such exposure. The following sections provide guidance to aid in screening both for exposure to the drug and for the development of specific neuropsychiatric symptoms during prophylaxis or following the treatment of malaria.

Mefloquine Exposure

Mefloquine was licensed in the U.S. as a branded medication (Lariam) from 1989 to 2011, and the drug also has been available in a variety of generic equivalents from 2003 to the present. All versions of mefloquine approved in the U.S. have been formulated as a white/slightly-off-white, smaller than dime-sized round tablet, containing 250 mg of mefloquine hydrochloride.

When used for prophylaxis in military settings, the drug was often dispensed informally without documentation, sometimes including directly observed therapy under command direction.^1,2 Therefore, even in the absence of prescribing documentation, a veteran who endorses a consistent history of malaria prophylaxis with mefloquine should be considered as having evidence of exposure.²

Exposure to mefloquine is unlikely if the veteran reports taking a daily antimalarial medication—more likely it was doxycycline or atovaquone/proguanil (marketed as Malarone). In rare cases, the drug may have been erroneously prescribed or been mistakenly taken daily for prophylaxis or, in more common cases, a prophylactic “loading dose” (typically 1 tablet daily for 3 days prior to weekly dosing) was used.^7,8

Exposure also was unlikely if the veteran reports taking an antimalarial that was dosed weekly with a tablet that was not of the appropriate color, shape, and size. More likely that drug was chloroquine. Although most prophylactic use of mefloquine among U.S. veterans followed its licensing by the FDA in 1989, the drug is known to have been administered to a small number of U.S. military personnel prior to its licensing during clinical trials, including personnel deployed on certain operations during the 1980s.¹

For treatment of malaria, mefloquine was used widely until better-tolerated drugs became available, beginning in the early 2000s, although some use of mefloquine in the military continues to this day. In most cases, clinicians should rely on records of hospitalization to identify whether mefloquine was administered. In rare cases where documentation is unavailable, exposure should be assumed if the veteran reports a reliable history of taking about 5 tablets (corresponding to the usual treatment dose of 1,250 mg) of appropriate color, shape, and size in response to confirmed or suspected malaria infection, either in 1 dose, or in split doses over 8 to 12 hours.

Symptoms During Prophylaxis

If prophylactic exposure to the drug has been established, the clinician should confirm the presence of neuropsychiatric symptoms during the exposure. Particularly among veterans deploying to malaria-endemic combat areas, such symptoms may have occurred during a period of heightened stress coincident with their initial deployment, and the veterans may have misattributed these symptoms to nonmefloquine factors. The clinician should therefore take a careful history to identify specific symptoms listed in the mefloquine product documentation. Many AEs will commonly manifest following the first 3 doses, and the clinician may find that focusing on this period is useful.⁹

When mefloquine is used for prophylaxis, anxiety and depression each affect between 1% and 10% of users. Other AEs that may develop include panic attacks; severe mood swings; behavioral AEs, including agitation, aggression, restlessness, and mania; symptoms of psychosis, including paranoia, delusions, and hallucinations; dissociative symptoms, including depersonalization; suicidal ideation; and cognitive AEs, including confusion.

The common symptoms of insomnia and abnormal dreaming affect > 10% of users. Particularly if multiple symptoms occur or if any of these symptoms occur following or coincident with symptoms of disturbed sleep, these should be considered strong evidence of symptomatic exposure.⁴ Veterans who report a history of continued mefloquine use despite the onset of such symptoms may be at particularly increased risk of chronic AEs.

The clinician should consider as evidence of symptomatic exposure information provided by others, including reports of obvious signs of nightmares or psychosis affecting the veteran. Clinicians should be aware that confusion and other psychiatric AEs caused by mefloquine during prophylactic use may limit the validity of self-reported history. Similarly, a history of seizure with mefloquine use or of the development of specific neurologic symptoms, particularly visual disturbances, dizziness, vertigo, disequilibrium, and paresthesias, also should be considered strong evidence of symptomatic exposure and indication of an increased risk of chronic psychiatric AEs.⁴

Posttreatment Adverse Effects

Although chronic psychiatric AEs following malaria infection have long been attributed to cerebral involvement, recognition that mefloquine may independently cause chronic neuropsychiatric AEs may require that individual cases be reexamined to properly assign causation.¹⁰ Particularly in uncomplicated cases of malaria, neuropsychiatric symptoms that develop only after treatment with mefloquine should be considered plausibly to be due to the drug and as evidence of symptomatic exposure.

As with use of mefloquine in prophylaxis, these neuropsychiatric symptoms may evolve in the weeks to months following exposure. They also may contribute to lasting and significant changes in personality, mood, cognition, thought, sleep, and behavior.⁶

Conclusion

Chronic AEs from mefloquine may provide a parsimonious explanation for the onset and persistence of a veteran’s psychiatric symptoms, particularly in cases where these may have failed to respond to treatment. Clinicians evaluating veterans who are seeking care for lasting psychiatric symptoms should ensure that they screen for prior symptomatic mefloquine exposure. As recognition grows of the drug’s chronic AEs, symptomatic mefloquine exposure is likely to emerge as a significant known confounder in the diagnosis of psychiatric disorders, including PTSD, among the current generation of U.S. veterans.

Mefloquine is an antimalarial drug that is associated with a significant risk of chronic neuropsychiatric adverse effects (AEs). The drug was licensed by the FDA in 1989 after development by scientists affiliated with Walter Reed Army Institute of Research (WRAIR). By the early 1990s, mefloquine had become the U.S. military’s drug of choice both for treatment of uncomplicated malaria and for antimalarial prophylaxis and was administered as a convenient weekly dose. Mefloquine was prescribed widely to U.S. military personnel beginning with operations in Somalia in 1992 and over the next 2 decades during certain deployments to Iraq and Afghanistan and to other malaria-endemic areas.¹

In 2013, following a decline of U.S. military use, the FDA added a boxed warning to the mefloquine product documentation to caution that neuropsychiatric AEs from the drug could last years after use and even be permanent. The U.S. military subsequently deemed mefloquine to be a prophylactic “drug of last resort.”² Recently, researchers at WRAIR have acknowledged that chronic neuropsychiatric AEs attributable to mefloquine, including nightmares, insomnia, anxiety, irritability, and cognitive dysfunction, may confound the diagnosis of posttraumatic stress disorder (PTSD).³ The VA has awarded at least 1 disability claim for service-connected psychiatric conditions that it attributed to mefloquine exposure, and it is likely that in the coming years such claims will increase.²

Susceptibility to Chronic Neuropsychiatric AEs

Why mefloquine seems to cause chronic neuropsychiatric AEs in only certain individuals is unclear, although genetic susceptibility to drug-induced toxic encephalopathy and neurotoxicity are suspected.¹ There is no screening test for susceptibility to AEs before mefloquine use, so the current U.S. product documentation cautiously warns that when used for prophylaxis, mefloquine should be discontinued at the onset of any neurologic or psychiatric symptom, many of which are considered prodromal to more serious AEs that may occur with continued dosing.⁴

Although chronic neuropsychiatric AEs have been reported to develop after only a single weekly dose, most clinically significant chronic AEs seem to occur among those who developed at least 1 prodromal neuropsychiatric symptom during early use but who continued weekly use despite these symptoms in a manner contrary to current product documentation guidance.⁴ In contrast, when mefloquine is administered for the treatment of malaria, typically at 5 times the weekly prophylactic dose and commonly in split doses over 8 to 12 hours, dosing is often complete by the time prodromal symptoms develop. Consequently, when mefloquine is used for treatment of malaria, the risks of more serious AEs are significantly higher than when the drug is used as directed in prophylaxis.⁵

Screening for Symptomatic Mefloquine Exposure

As the boxed warning indicates, certain psychiatric symptoms that occur with mefloquine use may become chronic and may confound psychiatric diagnosis. Particularly among veterans, these symptoms risk being misattributed, potentially affecting treatment decisions.⁶ Clinicians caring for veterans with persistent psychiatric symptoms should therefore screen for prior symptomatic mefloquine exposure and consider the possible AEs of the drug when formulating a differential diagnosis and treatment plan.

For example, a veteran with a history of symptomatic mefloquine exposure who later is diagnosed with PTSD may experience 1 or more symptoms, such as insomnia or cognitive dysfunction, which may be primarily attributable to the chronic AEs of the drug. The origins of the symptoms may be distinct from exposure to trauma and may not respond as effectively to certain conventional therapies for PTSD, requiring consideration of alternate therapies.³ The confounding role of psychiatric symptoms attributable to mefloquine exposure may explain failed response to medications and psychotherapy. Multidisciplinary evaluation and management may be appropriate for such patients.

If symptomatic mefloquine exposure is suspected, a clinician must establish evidence of exposure to the drug and the veteran’s development of neuropsychiatric symptoms associated with such exposure. The following sections provide guidance to aid in screening both for exposure to the drug and for the development of specific neuropsychiatric symptoms during prophylaxis or following the treatment of malaria.

Mefloquine Exposure

Mefloquine was licensed in the U.S. as a branded medication (Lariam) from 1989 to 2011, and the drug also has been available in a variety of generic equivalents from 2003 to the present. All versions of mefloquine approved in the U.S. have been formulated as a white/slightly-off-white, smaller than dime-sized round tablet, containing 250 mg of mefloquine hydrochloride.

When used for prophylaxis in military settings, the drug was often dispensed informally without documentation, sometimes including directly observed therapy under command direction.^1,2 Therefore, even in the absence of prescribing documentation, a veteran who endorses a consistent history of malaria prophylaxis with mefloquine should be considered as having evidence of exposure.²

Exposure to mefloquine is unlikely if the veteran reports taking a daily antimalarial medication—more likely it was doxycycline or atovaquone/proguanil (marketed as Malarone). In rare cases, the drug may have been erroneously prescribed or been mistakenly taken daily for prophylaxis or, in more common cases, a prophylactic “loading dose” (typically 1 tablet daily for 3 days prior to weekly dosing) was used.^7,8

Exposure also was unlikely if the veteran reports taking an antimalarial that was dosed weekly with a tablet that was not of the appropriate color, shape, and size. More likely that drug was chloroquine. Although most prophylactic use of mefloquine among U.S. veterans followed its licensing by the FDA in 1989, the drug is known to have been administered to a small number of U.S. military personnel prior to its licensing during clinical trials, including personnel deployed on certain operations during the 1980s.¹

For treatment of malaria, mefloquine was used widely until better-tolerated drugs became available, beginning in the early 2000s, although some use of mefloquine in the military continues to this day. In most cases, clinicians should rely on records of hospitalization to identify whether mefloquine was administered. In rare cases where documentation is unavailable, exposure should be assumed if the veteran reports a reliable history of taking about 5 tablets (corresponding to the usual treatment dose of 1,250 mg) of appropriate color, shape, and size in response to confirmed or suspected malaria infection, either in 1 dose, or in split doses over 8 to 12 hours.

Symptoms During Prophylaxis

If prophylactic exposure to the drug has been established, the clinician should confirm the presence of neuropsychiatric symptoms during the exposure. Particularly among veterans deploying to malaria-endemic combat areas, such symptoms may have occurred during a period of heightened stress coincident with their initial deployment, and the veterans may have misattributed these symptoms to nonmefloquine factors. The clinician should therefore take a careful history to identify specific symptoms listed in the mefloquine product documentation. Many AEs will commonly manifest following the first 3 doses, and the clinician may find that focusing on this period is useful.⁹

When mefloquine is used for prophylaxis, anxiety and depression each affect between 1% and 10% of users. Other AEs that may develop include panic attacks; severe mood swings; behavioral AEs, including agitation, aggression, restlessness, and mania; symptoms of psychosis, including paranoia, delusions, and hallucinations; dissociative symptoms, including depersonalization; suicidal ideation; and cognitive AEs, including confusion.

The common symptoms of insomnia and abnormal dreaming affect > 10% of users. Particularly if multiple symptoms occur or if any of these symptoms occur following or coincident with symptoms of disturbed sleep, these should be considered strong evidence of symptomatic exposure.⁴ Veterans who report a history of continued mefloquine use despite the onset of such symptoms may be at particularly increased risk of chronic AEs.

The clinician should consider as evidence of symptomatic exposure information provided by others, including reports of obvious signs of nightmares or psychosis affecting the veteran. Clinicians should be aware that confusion and other psychiatric AEs caused by mefloquine during prophylactic use may limit the validity of self-reported history. Similarly, a history of seizure with mefloquine use or of the development of specific neurologic symptoms, particularly visual disturbances, dizziness, vertigo, disequilibrium, and paresthesias, also should be considered strong evidence of symptomatic exposure and indication of an increased risk of chronic psychiatric AEs.⁴

Posttreatment Adverse Effects

Although chronic psychiatric AEs following malaria infection have long been attributed to cerebral involvement, recognition that mefloquine may independently cause chronic neuropsychiatric AEs may require that individual cases be reexamined to properly assign causation.¹⁰ Particularly in uncomplicated cases of malaria, neuropsychiatric symptoms that develop only after treatment with mefloquine should be considered plausibly to be due to the drug and as evidence of symptomatic exposure.

As with use of mefloquine in prophylaxis, these neuropsychiatric symptoms may evolve in the weeks to months following exposure. They also may contribute to lasting and significant changes in personality, mood, cognition, thought, sleep, and behavior.⁶

Conclusion

Chronic AEs from mefloquine may provide a parsimonious explanation for the onset and persistence of a veteran’s psychiatric symptoms, particularly in cases where these may have failed to respond to treatment. Clinicians evaluating veterans who are seeking care for lasting psychiatric symptoms should ensure that they screen for prior symptomatic mefloquine exposure. As recognition grows of the drug’s chronic AEs, symptomatic mefloquine exposure is likely to emerge as a significant known confounder in the diagnosis of psychiatric disorders, including PTSD, among the current generation of U.S. veterans.

Researchers from the University of Toronto had found in earlier studies that low-density lipoprotein (LDL) levels are elevated in up to 75% of patients with chronic lymphocytic leukemia (CLL). They also found that statins delayed the need for chemotherapy in those patients by nearly 3 years. They furthered their research using data on 2,124 patients with CLL and 7,935 controls in a population-based, case-control study. The researchers found a significantly higher incidence of hypercholesterolemia before CLL was diagnosed and a survival benefit of 3.7 years for patients taking statins.

In a new study to understand why hypercholesterolemia is apparently a tumor promoter for CLL, researchers first used an in vitro model of the “microenvironments” called pseudofollicles, where CLL cells proliferate. The researchers purified CLL cells from patients and activated them in lipid-poor conditions with interleukin-2 and resiquimod to represent stimulatory signals in pseudofollicles.

Related: New Treatments for Chronic Lymphocytic Leukemia

Adding LDLs increased viable cell numbers and signal transduction in molecules that mediate growth and proliferation of CLL cells.

To determine whether the effects were unique to CLL, the researchers conducted a similar experiment using peripheral blood mononuclear cells from donors without CLL. Their results suggested that normal blood cells handled cholesterol from LDLs in a different way than did CLL cells.

In another experiment, the researchers used circulating CLL cells from an additional cohort of 30 patients, including 11 who had been taking statins for at least 6 months. Cholesterol content of circulating CLL cells correlated directly with blood LDL levels, suggesting that LDLs may enhance proliferative responses of CLL cells to inflammatory signals. Statin use was associated with lower cholesterol in CLL cells, fewer circulating leukemia cells, and longer doubling times in vivo.

Related: Pneumatic Tube-Induced Reverse Pseudohyperkalemia in a Patient With Chronic Lymphocytic Leukemia

Researchers from the University of Toronto had found in earlier studies that low-density lipoprotein (LDL) levels are elevated in up to 75% of patients with chronic lymphocytic leukemia (CLL). They also found that statins delayed the need for chemotherapy in those patients by nearly 3 years. They furthered their research using data on 2,124 patients with CLL and 7,935 controls in a population-based, case-control study. The researchers found a significantly higher incidence of hypercholesterolemia before CLL was diagnosed and a survival benefit of 3.7 years for patients taking statins.

In a new study to understand why hypercholesterolemia is apparently a tumor promoter for CLL, researchers first used an in vitro model of the “microenvironments” called pseudofollicles, where CLL cells proliferate. The researchers purified CLL cells from patients and activated them in lipid-poor conditions with interleukin-2 and resiquimod to represent stimulatory signals in pseudofollicles.

Related: New Treatments for Chronic Lymphocytic Leukemia

Adding LDLs increased viable cell numbers and signal transduction in molecules that mediate growth and proliferation of CLL cells.

To determine whether the effects were unique to CLL, the researchers conducted a similar experiment using peripheral blood mononuclear cells from donors without CLL. Their results suggested that normal blood cells handled cholesterol from LDLs in a different way than did CLL cells.

In another experiment, the researchers used circulating CLL cells from an additional cohort of 30 patients, including 11 who had been taking statins for at least 6 months. Cholesterol content of circulating CLL cells correlated directly with blood LDL levels, suggesting that LDLs may enhance proliferative responses of CLL cells to inflammatory signals. Statin use was associated with lower cholesterol in CLL cells, fewer circulating leukemia cells, and longer doubling times in vivo.

Related: Pneumatic Tube-Induced Reverse Pseudohyperkalemia in a Patient With Chronic Lymphocytic Leukemia

Researchers from the University of Toronto had found in earlier studies that low-density lipoprotein (LDL) levels are elevated in up to 75% of patients with chronic lymphocytic leukemia (CLL). They also found that statins delayed the need for chemotherapy in those patients by nearly 3 years. They furthered their research using data on 2,124 patients with CLL and 7,935 controls in a population-based, case-control study. The researchers found a significantly higher incidence of hypercholesterolemia before CLL was diagnosed and a survival benefit of 3.7 years for patients taking statins.

In a new study to understand why hypercholesterolemia is apparently a tumor promoter for CLL, researchers first used an in vitro model of the “microenvironments” called pseudofollicles, where CLL cells proliferate. The researchers purified CLL cells from patients and activated them in lipid-poor conditions with interleukin-2 and resiquimod to represent stimulatory signals in pseudofollicles.

Related: New Treatments for Chronic Lymphocytic Leukemia

Adding LDLs increased viable cell numbers and signal transduction in molecules that mediate growth and proliferation of CLL cells.

To determine whether the effects were unique to CLL, the researchers conducted a similar experiment using peripheral blood mononuclear cells from donors without CLL. Their results suggested that normal blood cells handled cholesterol from LDLs in a different way than did CLL cells.

In another experiment, the researchers used circulating CLL cells from an additional cohort of 30 patients, including 11 who had been taking statins for at least 6 months. Cholesterol content of circulating CLL cells correlated directly with blood LDL levels, suggesting that LDLs may enhance proliferative responses of CLL cells to inflammatory signals. Statin use was associated with lower cholesterol in CLL cells, fewer circulating leukemia cells, and longer doubling times in vivo.

Related: Pneumatic Tube-Induced Reverse Pseudohyperkalemia in a Patient With Chronic Lymphocytic Leukemia

Improving health care safety is one of the top priorities of the U.S. health care system. A key element for health care safety is the elimination of sentinel events—unexpected occurrences involving death or serious physical or psychological injury, such as loss of limb or function—or even the risk.¹ Problems in communication, continuity of care, and planning have been identified as the root cause in more than 80% of documented sentinel events.² As a direct result, The Joint Commission (JC) added National Patient Safety Goal 2E, which instructs each organization to implement a standardized approach to patient handoff.¹ According to the JC, the objective of a handoff is to “provide accurate information about a patient’s care, treatment, and services, current condition, and any recent or anticipated changesand must include open communication and opportunities for questions.”^1,3 The JC identified the patient handoff from anesthesia providers to the Surgical Intensive Care Unit (SICU) and Postanesthesia Care Unit (PACU) an opportunity for an improvement.^1,3

At the Memphis VAMC in Tennessee, there was no established protocol for patient handoff from anesthesia providers to the SICU and PACU. The Anesthesia and SICU staffs were frustrated by inconsistent and incomplete postsurgical handoffs. Issues identified by the anesthesia team included difficulty contacting SICU staff to give a report and inconsistent availability of staff on first arrival to SICU. The SICU staff felt communication was rushed and there were inconsistencies in length and quality of the reports, resulting in incomplete postsurgical handoffs.

A baseline survey showed only 75% of staff felt the handoff report was thorough, and 67% “felt like a team.” In response, a multidisciplinary safe patient handoff committee (SPHOC) was formed by representatives from the involved units to discuss issues and offer solutions. The SPHOC efforts were aided by the VA National Center for Patient Safety (NCPS).

This quality improvement project was implemented as part of the U.S. Army Graduate Program in Anesthesia Nursing (USAGPAN) and the Northeastern University doctorate of nursing practice curriculum. The goal was to develop a simple, reliable, easily trainable handoff protocol for implemententation. This goal aligned with the priorites of the Memphis VAMC, USAGPAN, and VA to establish a culture based on patient safety and continuity of care.⁴

Methods

Standardization of handoffs began with JC National Patient Safety Goal 2E. There has been a wealth of medical literature on the need for standardization of handoffs and the implementation of specific handoff protocols in the postoperative setting. The SPHOC completed a review of the literature supporting standardization of handoff protocols. After completion, a second literature search was completed to identify the concepts for the implementation phase of the project. A critical appraisal of the evidence was completed using the method described by Melnyk and Fineout-Overholt.⁵ Literature from January 2005 through March 2015 was obtained via the Cumulative Index to Nursing and Allied Health Literature (CINAHL) and Google Scholar. The search methods included the keywords handover, handoff, transfer, and safety combined with anesthesia, PACU, surgery, operating room, and intensive care. Articles about handoffs not originating in the operating room (OR) were excluded.

The 13 articles found in the literature review established an overall need for standardization of handoffs outside the OR. Four articles identified a correlation between adverse events and poor or incomplete handoffs.^3,6-8 Multiple articles discussed the need to develop a standardized handoff protocol in order to increase team work and quality of care.^3,6,7,9,10 Petrovic and colleagues reported a 10% decrease in missed information and a boost in staff satisfaction from 61% to 81% with a standardized handoff.⁹ Additionally, a decrease in handoff time by > 1 minute was noted.⁸ Two articles identified an increase in quality of care after the implementation of a standardized handoff protocol.^8,10

The second phase of the literature review examined relevant handoff information, best practices for participation in the handoff, and established staff buy-in for the process. Segall and colleagues created a table with handoff strategies consistently identified in the literature.¹⁰ The most relevant of these were using a structured written checklist to guide communication, using protocols to standardize the process, and providing formal team training.¹⁰

Six articles identified a written checklist and standardized handoff process as successful strategies used to improve patient safety.^11-16 Zavalkoff and colleagues discussed the use of a template sheet filled out by the anesthesia provider prior to the handoff for consistency and accuracy of report.¹⁶ Catchpole and colleagues drew correlations between a Formula 1 pit stop and anesthesia handoffs and discussed the teamwork portion of the handoff protocol relating to staff buy-in.¹⁴ After delegating roles and making a set protocol for the handoff process, the study group was able to meet their objectives of efficient and safe handoff.¹⁴

With the information provided from the literature review, the SPHOC established a standardized handoff for the postsurgical patient. The committee created a handoff sheet for the anesthesia provider to use for report. This also included standardizing the handoff process and delineating specific roles for each provider.

After completing a NCPS training workshop, goals were identified at a SPHOC meeting. The SPHOC discussed current barriers to safe patient transfer and suggestions to overcome the barriers. Initial interventions planned by SPHOC focused on the problems of unsafe handoffs and delays in transfer. First, SICU identified the best phone number to call, which was distributed to the anesthesia and OR staffs. Additionally, the committee began tracking the number of attempted calls to reach SICU and availability of the nurse to take the report.

Implementation

A standardized handoff form was created by SPHOC, and anesthesia providers began to call time-out after the patient was deemed stable. After time-out was called, the SICU nurse provided his or her undivided attention and received the report. When SPHOC deemed the process successful, it was implemented in PACU as well. The entire OR, PACU, and anesthesia staffs were updated regarding the progress of the SPHOC on a monthly basis.

The implementation phase involved SPHOC tracking compliance of handoff sheets and time-outs. Compliance was tracked by counting the number of handoff sheets collected at the end of the day vs the total number of cases on the OR schedule. Tracking compliance with SICU transfers was monitored by the SICU members of the SPHOC through a tracking form. Initially a high level of SICU weekly compliance (93%) was noted.

Building on this success, SPHOC extended use of the handoff sheets and time-out to the PACU. Student registered nurse anesthetists (SRNAs) were tasked with education of the anesthesia and PACU staffs. Education continued via individual teaching, presentation at staff meetings, and e-mail reminders. To prevent confusion, no additional changes were made to the handoff sheet for an extended trial.

Despite these interventions, PACU compliance began to lag, averaging 33% over 3 weeks. Encouraging staff buy-in and a change in culture were identified as strategies to improve compliance. The third month of the trial started with 71% compliance. Interventions regarding staff buy-in emphasized individual accountability. Names were attached to handoff sheets, and those found with < 80% of sheets completed were provided with additional education. Those participants with ≥ 80% compliance were praised for their efforts.

Fostering a culture change proved to be more challenging. Interviews and discussions with anesthesia staff identified forgetting to fill out the sheet as the most common reason for noncompliance. Laminated copies of the handoff sheet were affixed to all anesthesia machines as a visual reminder. A sign denoting where to place the completed handoff sheets was placed in the PACU as a visual cue. The SPHOC stocked each anesthesia machine with handoff sheets on a daily basis.

To strengthen the culture of change, the PACU and SICU RNs were encouraged to ask for a time-out from the anesthesia provider. Handoff sheets were printed on yellow card stock to encourage anesthesia staff to “slow down for patient safety.” With these interventions, compliance increased to 98% by the end of the month.

Survey

An anonymous and voluntary survey was created and distributed to all staff involved in the handoff process. The 5-question survey was based on a 5-point Likert scale from 1 for strongly disagree to 5 for strongly disagree. The survey included the following questions: The new surgery report is very thorough; I feel more comfortable when assuming care of the postoperative patient; staff is more attentive when listening to the surgery report when a time-out is called; I feel the new surgery report is more effective and efficient; I feel I am more of a team with the OR with our changes in handoff of care process.

The survey was used as a baseline and to evaluate further changes in the process. Medical literature has shown that improper handoff communication was the leading cause of adverse events in the postsurgical patient.^3,6

Results

Surgery to SICU transfers using the Handoff card increased from 33% in the first month to an average of 98% after interventions. In the 10-month intervention period, time-outs in SICU increased from 29% to 99%. The SICU staff present at patient arrival increased from 83% to 97%. Anesthesia handoff report for PACU patient transfers increased from 79% to 99%. The time-outs in PACU increased from 39% to 99% after interventions.

After compliance initially increased, SPHOC focused on the more complex aspects of the handoff process—staff satisfaction, which was chosen based on an area of weakness identified in the initial survey results. Overall, staff was satisfied with the handoff sheets; however, only 67% of SICU staff reported that they felt part of the team with the OR as a result of the handoff of care process.

To address this issue, the team delineated roles for providers when a new surgical patient arrived in the SICU. This was dubbed the ABCs of safe handoff with roles for the anesthesia provider or respiratory therapist, the circulating nurse and SICU nurse, and the anesthesia provider. A graphic representation explains the mnemonic, the roles created, and laminated copies were distributed throughout the OR and SICU (Figure). Subsequent surveys showed 80% of staff felt more like a team with the new process.

Conclusion

The overall impact of the project has been to further promote a culture of patient safety at the Memphis VAMC and establish continuity of care as an institutional priority. The existing handoff sheet, time-out, and cross-check have been adapted to all hospital-wide transfers. With the SPHOC guidance and expertise, PACU began using a handoff sheet and time-out when transferring patients to the medical/surgical floors. The handoff sheet has also been adapted to fit the needs of transfers from the emergency department to the medical/surgical floors.

The framework of a standardized handoff is adaptable for other units to customize and has been adopted hospital-wide. The project is sustainable as it requires almost no money to create and sustain. The primary weakness of the process is the requirement of sustained staff participation and buy-in. Each unit and hospital invariably comes with a different culture and priorities; therefore, the process developed at Memphis VAMC may not meet the needs of other facilities. ˜

Acknowledgments
Special thanks to Susan Baldwin, RN; Bianca Mathews, MSN, RN; Wendy Regel, RN; Armance White, CRNA; Reginald Witt, MD; Odie Powell, RN; Alma Farris, RN; Clarisa Reed, RN; Susan Baily, RN; Linda Sueing, RN; Teresa Nguyen, RN; and John Craig, DNP, CRNA.

Improving health care safety is one of the top priorities of the U.S. health care system. A key element for health care safety is the elimination of sentinel events—unexpected occurrences involving death or serious physical or psychological injury, such as loss of limb or function—or even the risk.¹ Problems in communication, continuity of care, and planning have been identified as the root cause in more than 80% of documented sentinel events.² As a direct result, The Joint Commission (JC) added National Patient Safety Goal 2E, which instructs each organization to implement a standardized approach to patient handoff.¹ According to the JC, the objective of a handoff is to “provide accurate information about a patient’s care, treatment, and services, current condition, and any recent or anticipated changesand must include open communication and opportunities for questions.”^1,3 The JC identified the patient handoff from anesthesia providers to the Surgical Intensive Care Unit (SICU) and Postanesthesia Care Unit (PACU) an opportunity for an improvement.^1,3

At the Memphis VAMC in Tennessee, there was no established protocol for patient handoff from anesthesia providers to the SICU and PACU. The Anesthesia and SICU staffs were frustrated by inconsistent and incomplete postsurgical handoffs. Issues identified by the anesthesia team included difficulty contacting SICU staff to give a report and inconsistent availability of staff on first arrival to SICU. The SICU staff felt communication was rushed and there were inconsistencies in length and quality of the reports, resulting in incomplete postsurgical handoffs.

A baseline survey showed only 75% of staff felt the handoff report was thorough, and 67% “felt like a team.” In response, a multidisciplinary safe patient handoff committee (SPHOC) was formed by representatives from the involved units to discuss issues and offer solutions. The SPHOC efforts were aided by the VA National Center for Patient Safety (NCPS).

This quality improvement project was implemented as part of the U.S. Army Graduate Program in Anesthesia Nursing (USAGPAN) and the Northeastern University doctorate of nursing practice curriculum. The goal was to develop a simple, reliable, easily trainable handoff protocol for implemententation. This goal aligned with the priorites of the Memphis VAMC, USAGPAN, and VA to establish a culture based on patient safety and continuity of care.⁴

Methods

Standardization of handoffs began with JC National Patient Safety Goal 2E. There has been a wealth of medical literature on the need for standardization of handoffs and the implementation of specific handoff protocols in the postoperative setting. The SPHOC completed a review of the literature supporting standardization of handoff protocols. After completion, a second literature search was completed to identify the concepts for the implementation phase of the project. A critical appraisal of the evidence was completed using the method described by Melnyk and Fineout-Overholt.⁵ Literature from January 2005 through March 2015 was obtained via the Cumulative Index to Nursing and Allied Health Literature (CINAHL) and Google Scholar. The search methods included the keywords handover, handoff, transfer, and safety combined with anesthesia, PACU, surgery, operating room, and intensive care. Articles about handoffs not originating in the operating room (OR) were excluded.

The 13 articles found in the literature review established an overall need for standardization of handoffs outside the OR. Four articles identified a correlation between adverse events and poor or incomplete handoffs.^3,6-8 Multiple articles discussed the need to develop a standardized handoff protocol in order to increase team work and quality of care.^3,6,7,9,10 Petrovic and colleagues reported a 10% decrease in missed information and a boost in staff satisfaction from 61% to 81% with a standardized handoff.⁹ Additionally, a decrease in handoff time by > 1 minute was noted.⁸ Two articles identified an increase in quality of care after the implementation of a standardized handoff protocol.^8,10

The second phase of the literature review examined relevant handoff information, best practices for participation in the handoff, and established staff buy-in for the process. Segall and colleagues created a table with handoff strategies consistently identified in the literature.¹⁰ The most relevant of these were using a structured written checklist to guide communication, using protocols to standardize the process, and providing formal team training.¹⁰

Six articles identified a written checklist and standardized handoff process as successful strategies used to improve patient safety.^11-16 Zavalkoff and colleagues discussed the use of a template sheet filled out by the anesthesia provider prior to the handoff for consistency and accuracy of report.¹⁶ Catchpole and colleagues drew correlations between a Formula 1 pit stop and anesthesia handoffs and discussed the teamwork portion of the handoff protocol relating to staff buy-in.¹⁴ After delegating roles and making a set protocol for the handoff process, the study group was able to meet their objectives of efficient and safe handoff.¹⁴

With the information provided from the literature review, the SPHOC established a standardized handoff for the postsurgical patient. The committee created a handoff sheet for the anesthesia provider to use for report. This also included standardizing the handoff process and delineating specific roles for each provider.

After completing a NCPS training workshop, goals were identified at a SPHOC meeting. The SPHOC discussed current barriers to safe patient transfer and suggestions to overcome the barriers. Initial interventions planned by SPHOC focused on the problems of unsafe handoffs and delays in transfer. First, SICU identified the best phone number to call, which was distributed to the anesthesia and OR staffs. Additionally, the committee began tracking the number of attempted calls to reach SICU and availability of the nurse to take the report.

Implementation

A standardized handoff form was created by SPHOC, and anesthesia providers began to call time-out after the patient was deemed stable. After time-out was called, the SICU nurse provided his or her undivided attention and received the report. When SPHOC deemed the process successful, it was implemented in PACU as well. The entire OR, PACU, and anesthesia staffs were updated regarding the progress of the SPHOC on a monthly basis.

The implementation phase involved SPHOC tracking compliance of handoff sheets and time-outs. Compliance was tracked by counting the number of handoff sheets collected at the end of the day vs the total number of cases on the OR schedule. Tracking compliance with SICU transfers was monitored by the SICU members of the SPHOC through a tracking form. Initially a high level of SICU weekly compliance (93%) was noted.

Building on this success, SPHOC extended use of the handoff sheets and time-out to the PACU. Student registered nurse anesthetists (SRNAs) were tasked with education of the anesthesia and PACU staffs. Education continued via individual teaching, presentation at staff meetings, and e-mail reminders. To prevent confusion, no additional changes were made to the handoff sheet for an extended trial.

Despite these interventions, PACU compliance began to lag, averaging 33% over 3 weeks. Encouraging staff buy-in and a change in culture were identified as strategies to improve compliance. The third month of the trial started with 71% compliance. Interventions regarding staff buy-in emphasized individual accountability. Names were attached to handoff sheets, and those found with < 80% of sheets completed were provided with additional education. Those participants with ≥ 80% compliance were praised for their efforts.

Fostering a culture change proved to be more challenging. Interviews and discussions with anesthesia staff identified forgetting to fill out the sheet as the most common reason for noncompliance. Laminated copies of the handoff sheet were affixed to all anesthesia machines as a visual reminder. A sign denoting where to place the completed handoff sheets was placed in the PACU as a visual cue. The SPHOC stocked each anesthesia machine with handoff sheets on a daily basis.

To strengthen the culture of change, the PACU and SICU RNs were encouraged to ask for a time-out from the anesthesia provider. Handoff sheets were printed on yellow card stock to encourage anesthesia staff to “slow down for patient safety.” With these interventions, compliance increased to 98% by the end of the month.

Survey

An anonymous and voluntary survey was created and distributed to all staff involved in the handoff process. The 5-question survey was based on a 5-point Likert scale from 1 for strongly disagree to 5 for strongly disagree. The survey included the following questions: The new surgery report is very thorough; I feel more comfortable when assuming care of the postoperative patient; staff is more attentive when listening to the surgery report when a time-out is called; I feel the new surgery report is more effective and efficient; I feel I am more of a team with the OR with our changes in handoff of care process.

The survey was used as a baseline and to evaluate further changes in the process. Medical literature has shown that improper handoff communication was the leading cause of adverse events in the postsurgical patient.^3,6

Results

Surgery to SICU transfers using the Handoff card increased from 33% in the first month to an average of 98% after interventions. In the 10-month intervention period, time-outs in SICU increased from 29% to 99%. The SICU staff present at patient arrival increased from 83% to 97%. Anesthesia handoff report for PACU patient transfers increased from 79% to 99%. The time-outs in PACU increased from 39% to 99% after interventions.

After compliance initially increased, SPHOC focused on the more complex aspects of the handoff process—staff satisfaction, which was chosen based on an area of weakness identified in the initial survey results. Overall, staff was satisfied with the handoff sheets; however, only 67% of SICU staff reported that they felt part of the team with the OR as a result of the handoff of care process.

To address this issue, the team delineated roles for providers when a new surgical patient arrived in the SICU. This was dubbed the ABCs of safe handoff with roles for the anesthesia provider or respiratory therapist, the circulating nurse and SICU nurse, and the anesthesia provider. A graphic representation explains the mnemonic, the roles created, and laminated copies were distributed throughout the OR and SICU (Figure). Subsequent surveys showed 80% of staff felt more like a team with the new process.

Conclusion

The overall impact of the project has been to further promote a culture of patient safety at the Memphis VAMC and establish continuity of care as an institutional priority. The existing handoff sheet, time-out, and cross-check have been adapted to all hospital-wide transfers. With the SPHOC guidance and expertise, PACU began using a handoff sheet and time-out when transferring patients to the medical/surgical floors. The handoff sheet has also been adapted to fit the needs of transfers from the emergency department to the medical/surgical floors.

The framework of a standardized handoff is adaptable for other units to customize and has been adopted hospital-wide. The project is sustainable as it requires almost no money to create and sustain. The primary weakness of the process is the requirement of sustained staff participation and buy-in. Each unit and hospital invariably comes with a different culture and priorities; therefore, the process developed at Memphis VAMC may not meet the needs of other facilities. ˜

Acknowledgments
Special thanks to Susan Baldwin, RN; Bianca Mathews, MSN, RN; Wendy Regel, RN; Armance White, CRNA; Reginald Witt, MD; Odie Powell, RN; Alma Farris, RN; Clarisa Reed, RN; Susan Baily, RN; Linda Sueing, RN; Teresa Nguyen, RN; and John Craig, DNP, CRNA.

Improving health care safety is one of the top priorities of the U.S. health care system. A key element for health care safety is the elimination of sentinel events—unexpected occurrences involving death or serious physical or psychological injury, such as loss of limb or function—or even the risk.¹ Problems in communication, continuity of care, and planning have been identified as the root cause in more than 80% of documented sentinel events.² As a direct result, The Joint Commission (JC) added National Patient Safety Goal 2E, which instructs each organization to implement a standardized approach to patient handoff.¹ According to the JC, the objective of a handoff is to “provide accurate information about a patient’s care, treatment, and services, current condition, and any recent or anticipated changesand must include open communication and opportunities for questions.”^1,3 The JC identified the patient handoff from anesthesia providers to the Surgical Intensive Care Unit (SICU) and Postanesthesia Care Unit (PACU) an opportunity for an improvement.^1,3

At the Memphis VAMC in Tennessee, there was no established protocol for patient handoff from anesthesia providers to the SICU and PACU. The Anesthesia and SICU staffs were frustrated by inconsistent and incomplete postsurgical handoffs. Issues identified by the anesthesia team included difficulty contacting SICU staff to give a report and inconsistent availability of staff on first arrival to SICU. The SICU staff felt communication was rushed and there were inconsistencies in length and quality of the reports, resulting in incomplete postsurgical handoffs.

A baseline survey showed only 75% of staff felt the handoff report was thorough, and 67% “felt like a team.” In response, a multidisciplinary safe patient handoff committee (SPHOC) was formed by representatives from the involved units to discuss issues and offer solutions. The SPHOC efforts were aided by the VA National Center for Patient Safety (NCPS).

This quality improvement project was implemented as part of the U.S. Army Graduate Program in Anesthesia Nursing (USAGPAN) and the Northeastern University doctorate of nursing practice curriculum. The goal was to develop a simple, reliable, easily trainable handoff protocol for implemententation. This goal aligned with the priorites of the Memphis VAMC, USAGPAN, and VA to establish a culture based on patient safety and continuity of care.⁴

Methods

Standardization of handoffs began with JC National Patient Safety Goal 2E. There has been a wealth of medical literature on the need for standardization of handoffs and the implementation of specific handoff protocols in the postoperative setting. The SPHOC completed a review of the literature supporting standardization of handoff protocols. After completion, a second literature search was completed to identify the concepts for the implementation phase of the project. A critical appraisal of the evidence was completed using the method described by Melnyk and Fineout-Overholt.⁵ Literature from January 2005 through March 2015 was obtained via the Cumulative Index to Nursing and Allied Health Literature (CINAHL) and Google Scholar. The search methods included the keywords handover, handoff, transfer, and safety combined with anesthesia, PACU, surgery, operating room, and intensive care. Articles about handoffs not originating in the operating room (OR) were excluded.

The 13 articles found in the literature review established an overall need for standardization of handoffs outside the OR. Four articles identified a correlation between adverse events and poor or incomplete handoffs.^3,6-8 Multiple articles discussed the need to develop a standardized handoff protocol in order to increase team work and quality of care.^3,6,7,9,10 Petrovic and colleagues reported a 10% decrease in missed information and a boost in staff satisfaction from 61% to 81% with a standardized handoff.⁹ Additionally, a decrease in handoff time by > 1 minute was noted.⁸ Two articles identified an increase in quality of care after the implementation of a standardized handoff protocol.^8,10

The second phase of the literature review examined relevant handoff information, best practices for participation in the handoff, and established staff buy-in for the process. Segall and colleagues created a table with handoff strategies consistently identified in the literature.¹⁰ The most relevant of these were using a structured written checklist to guide communication, using protocols to standardize the process, and providing formal team training.¹⁰

Six articles identified a written checklist and standardized handoff process as successful strategies used to improve patient safety.^11-16 Zavalkoff and colleagues discussed the use of a template sheet filled out by the anesthesia provider prior to the handoff for consistency and accuracy of report.¹⁶ Catchpole and colleagues drew correlations between a Formula 1 pit stop and anesthesia handoffs and discussed the teamwork portion of the handoff protocol relating to staff buy-in.¹⁴ After delegating roles and making a set protocol for the handoff process, the study group was able to meet their objectives of efficient and safe handoff.¹⁴

With the information provided from the literature review, the SPHOC established a standardized handoff for the postsurgical patient. The committee created a handoff sheet for the anesthesia provider to use for report. This also included standardizing the handoff process and delineating specific roles for each provider.

After completing a NCPS training workshop, goals were identified at a SPHOC meeting. The SPHOC discussed current barriers to safe patient transfer and suggestions to overcome the barriers. Initial interventions planned by SPHOC focused on the problems of unsafe handoffs and delays in transfer. First, SICU identified the best phone number to call, which was distributed to the anesthesia and OR staffs. Additionally, the committee began tracking the number of attempted calls to reach SICU and availability of the nurse to take the report.

Implementation

A standardized handoff form was created by SPHOC, and anesthesia providers began to call time-out after the patient was deemed stable. After time-out was called, the SICU nurse provided his or her undivided attention and received the report. When SPHOC deemed the process successful, it was implemented in PACU as well. The entire OR, PACU, and anesthesia staffs were updated regarding the progress of the SPHOC on a monthly basis.

The implementation phase involved SPHOC tracking compliance of handoff sheets and time-outs. Compliance was tracked by counting the number of handoff sheets collected at the end of the day vs the total number of cases on the OR schedule. Tracking compliance with SICU transfers was monitored by the SICU members of the SPHOC through a tracking form. Initially a high level of SICU weekly compliance (93%) was noted.

Building on this success, SPHOC extended use of the handoff sheets and time-out to the PACU. Student registered nurse anesthetists (SRNAs) were tasked with education of the anesthesia and PACU staffs. Education continued via individual teaching, presentation at staff meetings, and e-mail reminders. To prevent confusion, no additional changes were made to the handoff sheet for an extended trial.

Despite these interventions, PACU compliance began to lag, averaging 33% over 3 weeks. Encouraging staff buy-in and a change in culture were identified as strategies to improve compliance. The third month of the trial started with 71% compliance. Interventions regarding staff buy-in emphasized individual accountability. Names were attached to handoff sheets, and those found with < 80% of sheets completed were provided with additional education. Those participants with ≥ 80% compliance were praised for their efforts.

Fostering a culture change proved to be more challenging. Interviews and discussions with anesthesia staff identified forgetting to fill out the sheet as the most common reason for noncompliance. Laminated copies of the handoff sheet were affixed to all anesthesia machines as a visual reminder. A sign denoting where to place the completed handoff sheets was placed in the PACU as a visual cue. The SPHOC stocked each anesthesia machine with handoff sheets on a daily basis.

To strengthen the culture of change, the PACU and SICU RNs were encouraged to ask for a time-out from the anesthesia provider. Handoff sheets were printed on yellow card stock to encourage anesthesia staff to “slow down for patient safety.” With these interventions, compliance increased to 98% by the end of the month.

Survey

An anonymous and voluntary survey was created and distributed to all staff involved in the handoff process. The 5-question survey was based on a 5-point Likert scale from 1 for strongly disagree to 5 for strongly disagree. The survey included the following questions: The new surgery report is very thorough; I feel more comfortable when assuming care of the postoperative patient; staff is more attentive when listening to the surgery report when a time-out is called; I feel the new surgery report is more effective and efficient; I feel I am more of a team with the OR with our changes in handoff of care process.

The survey was used as a baseline and to evaluate further changes in the process. Medical literature has shown that improper handoff communication was the leading cause of adverse events in the postsurgical patient.^3,6

Results

Surgery to SICU transfers using the Handoff card increased from 33% in the first month to an average of 98% after interventions. In the 10-month intervention period, time-outs in SICU increased from 29% to 99%. The SICU staff present at patient arrival increased from 83% to 97%. Anesthesia handoff report for PACU patient transfers increased from 79% to 99%. The time-outs in PACU increased from 39% to 99% after interventions.

After compliance initially increased, SPHOC focused on the more complex aspects of the handoff process—staff satisfaction, which was chosen based on an area of weakness identified in the initial survey results. Overall, staff was satisfied with the handoff sheets; however, only 67% of SICU staff reported that they felt part of the team with the OR as a result of the handoff of care process.

To address this issue, the team delineated roles for providers when a new surgical patient arrived in the SICU. This was dubbed the ABCs of safe handoff with roles for the anesthesia provider or respiratory therapist, the circulating nurse and SICU nurse, and the anesthesia provider. A graphic representation explains the mnemonic, the roles created, and laminated copies were distributed throughout the OR and SICU (Figure). Subsequent surveys showed 80% of staff felt more like a team with the new process.

Conclusion

The overall impact of the project has been to further promote a culture of patient safety at the Memphis VAMC and establish continuity of care as an institutional priority. The existing handoff sheet, time-out, and cross-check have been adapted to all hospital-wide transfers. With the SPHOC guidance and expertise, PACU began using a handoff sheet and time-out when transferring patients to the medical/surgical floors. The handoff sheet has also been adapted to fit the needs of transfers from the emergency department to the medical/surgical floors.

The framework of a standardized handoff is adaptable for other units to customize and has been adopted hospital-wide. The project is sustainable as it requires almost no money to create and sustain. The primary weakness of the process is the requirement of sustained staff participation and buy-in. Each unit and hospital invariably comes with a different culture and priorities; therefore, the process developed at Memphis VAMC may not meet the needs of other facilities. ˜

Acknowledgments
Special thanks to Susan Baldwin, RN; Bianca Mathews, MSN, RN; Wendy Regel, RN; Armance White, CRNA; Reginald Witt, MD; Odie Powell, RN; Alma Farris, RN; Clarisa Reed, RN; Susan Baily, RN; Linda Sueing, RN; Teresa Nguyen, RN; and John Craig, DNP, CRNA.