Drug release in a cancer cell

Image courtesy of PNAS

A diabetes medication and an antihypertensive drug may prove effective in the treatment of hematologic malignancies and other cancers, according to preclinical research published in Science Advances.

Past research has shown that metformin, a drug used to treat type 2 diabetes, has anticancer properties.

However, the usual therapeutic dose is too low to effectively fight cancer, and higher doses of metformin could be too toxic.

With the current study, researchers found that the antihypertensive drug syrosingopine enhances the anticancer efficacy of metformin without harming normal blood cells.

The team screened over a thousand drugs to find one that could boost metformin’s efficacy against cancers.

They identified syrosingopine and tested it in combination with metformin—at concentrations substantially below the drugs’ therapeutic thresholds—on a range of cancer cell lines and in mouse models of liver cancer.

Thirty-five of the 43 cell lines tested were susceptible to both syrosingopine and metformin. This included leukemia, lymphoma, and multiple myeloma cell lines.

In addition, the mice given a short course of syrosingopine and metformin experienced a reduction in the number of visible liver tumors.

The researchers also tested syrosingopine and metformin in peripheral blasts from 12 patients with acute myeloid leukemia and a patient with blast crisis chronic myeloid leukemia. All 13 samples responded to the treatment.

On the other hand, syrosingopine and metformin did not affect peripheral blood cells from healthy subjects.

“[A]lmost all tumor cells were killed by this cocktail and at doses that are actually not toxic to normal cells,” said study author Don Benjamin, of the University of Basel in Switzerland.

“And the effect was exclusively confined to cancer cells, as the blood cells from healthy donors were insensitive to the treatment.”

The researchers believe metformin functions by lowering blood glucose levels for cancer cells, starving them of essential nutrients needed for their survival. However, it is not clear how syrosingopine works in conjunction with metformin.

The team emphasized the need for more research evaluating the drugs in combination.

“We have been able to show that the 2 known drugs lead to more profound effects on cancer cell proliferation than each drug alone,” Dr Benjamin said. “The data from this study support the development of combination approaches for the treatment of cancer patients.”

Drug release in a cancer cell

Image courtesy of PNAS

A diabetes medication and an antihypertensive drug may prove effective in the treatment of hematologic malignancies and other cancers, according to preclinical research published in Science Advances.

Past research has shown that metformin, a drug used to treat type 2 diabetes, has anticancer properties.

However, the usual therapeutic dose is too low to effectively fight cancer, and higher doses of metformin could be too toxic.

With the current study, researchers found that the antihypertensive drug syrosingopine enhances the anticancer efficacy of metformin without harming normal blood cells.

The team screened over a thousand drugs to find one that could boost metformin’s efficacy against cancers.

They identified syrosingopine and tested it in combination with metformin—at concentrations substantially below the drugs’ therapeutic thresholds—on a range of cancer cell lines and in mouse models of liver cancer.

Thirty-five of the 43 cell lines tested were susceptible to both syrosingopine and metformin. This included leukemia, lymphoma, and multiple myeloma cell lines.

In addition, the mice given a short course of syrosingopine and metformin experienced a reduction in the number of visible liver tumors.

The researchers also tested syrosingopine and metformin in peripheral blasts from 12 patients with acute myeloid leukemia and a patient with blast crisis chronic myeloid leukemia. All 13 samples responded to the treatment.

On the other hand, syrosingopine and metformin did not affect peripheral blood cells from healthy subjects.

“[A]lmost all tumor cells were killed by this cocktail and at doses that are actually not toxic to normal cells,” said study author Don Benjamin, of the University of Basel in Switzerland.

“And the effect was exclusively confined to cancer cells, as the blood cells from healthy donors were insensitive to the treatment.”

The researchers believe metformin functions by lowering blood glucose levels for cancer cells, starving them of essential nutrients needed for their survival. However, it is not clear how syrosingopine works in conjunction with metformin.

The team emphasized the need for more research evaluating the drugs in combination.

“We have been able to show that the 2 known drugs lead to more profound effects on cancer cell proliferation than each drug alone,” Dr Benjamin said. “The data from this study support the development of combination approaches for the treatment of cancer patients.”

Drug release in a cancer cell

Image courtesy of PNAS

A diabetes medication and an antihypertensive drug may prove effective in the treatment of hematologic malignancies and other cancers, according to preclinical research published in Science Advances.

Past research has shown that metformin, a drug used to treat type 2 diabetes, has anticancer properties.

However, the usual therapeutic dose is too low to effectively fight cancer, and higher doses of metformin could be too toxic.

With the current study, researchers found that the antihypertensive drug syrosingopine enhances the anticancer efficacy of metformin without harming normal blood cells.

The team screened over a thousand drugs to find one that could boost metformin’s efficacy against cancers.

They identified syrosingopine and tested it in combination with metformin—at concentrations substantially below the drugs’ therapeutic thresholds—on a range of cancer cell lines and in mouse models of liver cancer.

Thirty-five of the 43 cell lines tested were susceptible to both syrosingopine and metformin. This included leukemia, lymphoma, and multiple myeloma cell lines.

In addition, the mice given a short course of syrosingopine and metformin experienced a reduction in the number of visible liver tumors.

The researchers also tested syrosingopine and metformin in peripheral blasts from 12 patients with acute myeloid leukemia and a patient with blast crisis chronic myeloid leukemia. All 13 samples responded to the treatment.

On the other hand, syrosingopine and metformin did not affect peripheral blood cells from healthy subjects.

“[A]lmost all tumor cells were killed by this cocktail and at doses that are actually not toxic to normal cells,” said study author Don Benjamin, of the University of Basel in Switzerland.

“And the effect was exclusively confined to cancer cells, as the blood cells from healthy donors were insensitive to the treatment.”

The researchers believe metformin functions by lowering blood glucose levels for cancer cells, starving them of essential nutrients needed for their survival. However, it is not clear how syrosingopine works in conjunction with metformin.

The team emphasized the need for more research evaluating the drugs in combination.

“We have been able to show that the 2 known drugs lead to more profound effects on cancer cell proliferation than each drug alone,” Dr Benjamin said. “The data from this study support the development of combination approaches for the treatment of cancer patients.”

IN THIS ARTICLE

• Types of shoulder dislocations
• Schematics of the shoulder with three types of dislocations
• Association with seizures

CASE  A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.

An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).

The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations). 

The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.¹ While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.¹ For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.²

The three types of shoulder dislocations include anterior, posterior, and inferior.

ANTERIOR

Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.³ They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).

A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed. 

Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.⁴ The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.⁵ The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.⁴

Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.⁶ Both can be seen on plain films, although Bankart lesions are best seen on CT.⁴

The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.⁷

POSTERIOR 

Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.² They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures). 

Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).⁸ This position is sometimes misdiagnosed as a “frozen shoulder.”²

INFERIOR

Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall. 

Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction:  a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.⁹

ASSOCIATION WITH SEIZURES

Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.¹⁰

Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.¹¹

Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.¹²

In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).¹⁰

The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.^10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.⁸

After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon. 

CONCLUSION

This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.

IN THIS ARTICLE

• Types of shoulder dislocations
• Schematics of the shoulder with three types of dislocations
• Association with seizures

CASE  A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.

An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).

The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations). 

The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.¹ While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.¹ For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.²

The three types of shoulder dislocations include anterior, posterior, and inferior.

ANTERIOR

Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.³ They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).

A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed. 

Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.⁴ The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.⁵ The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.⁴

Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.⁶ Both can be seen on plain films, although Bankart lesions are best seen on CT.⁴

The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.⁷

POSTERIOR 

Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.² They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures). 

Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).⁸ This position is sometimes misdiagnosed as a “frozen shoulder.”²

INFERIOR

Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall. 

Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction:  a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.⁹

ASSOCIATION WITH SEIZURES

Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.¹⁰

Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.¹¹

Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.¹²

In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).¹⁰

The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.^10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.⁸

After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon. 

CONCLUSION

This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.

IN THIS ARTICLE

• Types of shoulder dislocations
• Schematics of the shoulder with three types of dislocations
• Association with seizures

CASE  A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.

An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).

The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations). 

The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.¹ While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.¹ For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.²

The three types of shoulder dislocations include anterior, posterior, and inferior.

ANTERIOR

Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.³ They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).

A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed. 

Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.⁴ The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.⁵ The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.⁴

Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.⁶ Both can be seen on plain films, although Bankart lesions are best seen on CT.⁴

The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.⁷

POSTERIOR 

Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.² They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures). 

Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).⁸ This position is sometimes misdiagnosed as a “frozen shoulder.”²

INFERIOR

Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall. 

Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction:  a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.⁹

ASSOCIATION WITH SEIZURES

Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.¹⁰

Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.¹¹

Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.¹²

In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).¹⁰

The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.^10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.⁸

After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon. 

CONCLUSION

This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.

Clinical question: Does pulse variability on plethysmography, or the Pleth Variability Index (PVI), correlate with disease severity in obstructive airway disease in children?

Background: Asthma is the most common reason for hospitalization in the United S. for children 3-12 years old. Asthma accounts for a quarter of ED visits for children aged 1-9 years old.¹ Although systems have been developed to assess asthma exacerbation severity and the need for hospitalization, many of these depend on reassessments over time or have been proven to be invalid in larger studies.^2,3,4 Pulsus paradoxus (PP), which is defined as a drop in systolic blood pressure greater than 10 mm Hg, correlates with the severity of obstruction in asthma exacerbations, but it is not practical in the children being evaluated in the ED or hospital.^5,6 PP measurement using plethysmography has been found to correlate with measurement by sphygmomanometry.⁷ Furthermore, PVI, which is derived from amplitude variability in the pulse oximeter waveform, has been found to correlate with fluid responsiveness in mechanically ventilated patients. To this date, no study has assessed the correlation between PVI and exacerbation severity in asthma.

A printout of the first ED pulse oximetry reading was used to obtain the PImax and PImin as below:

Researchers followed patients after the initial evaluation to determine disposition from the ED, which included either discharge to home, admission to a general pediatrics floor, or admission to the PICU. The hospital utilized specific criteria for disposition from the ED (see Table 1).

References

1. Care of children and adolescents in U.S. hospitals. Agency for Healthcare Research and Quality website. Available at: https://archive.ahrq.gov/data/hcup/factbk4/factbk4.htm. Accessed Nov. 18, 2016.

2. Kelly AM, Kerr D, Powell C. Is severity assessment after one hour of treatment better for predicting the need for admission in acute asthma? Respir Med. 2004;98(8):777-781.

3. Keogh KA, Macarthur C, Parkin PC, et al. Predictors of hospitalization in children with acute asthma. J Pediatr. 2001;139(2):273-277.

4. Keahey L, Bulloch B, Becker AB, et al. Initial oxygen saturation as a predictor of admission in children presenting to the emergency department with acute asthma. Ann Emerg Med. 2002;40(3):300-307.

5. Guntheroth WG, Morgan BC, Mullins GL. Effect of respiration on venous return and stroke volume in cardiac tamponade. Mechanism of pulsus paradoxus. Circ Res. 1967;20(4):381-390.

6. Frey B, Freezer N. Diagnostic value and pathophysiologic basis of pulsus paradoxus in infants and children with respiratory disease. Pediatr Pulmonol. 2001;31(2):138-143.

7. Clark JA, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004;158(1):48-51.
 

Clinical question: Does pulse variability on plethysmography, or the Pleth Variability Index (PVI), correlate with disease severity in obstructive airway disease in children?

Background: Asthma is the most common reason for hospitalization in the United S. for children 3-12 years old. Asthma accounts for a quarter of ED visits for children aged 1-9 years old.¹ Although systems have been developed to assess asthma exacerbation severity and the need for hospitalization, many of these depend on reassessments over time or have been proven to be invalid in larger studies.^2,3,4 Pulsus paradoxus (PP), which is defined as a drop in systolic blood pressure greater than 10 mm Hg, correlates with the severity of obstruction in asthma exacerbations, but it is not practical in the children being evaluated in the ED or hospital.^5,6 PP measurement using plethysmography has been found to correlate with measurement by sphygmomanometry.⁷ Furthermore, PVI, which is derived from amplitude variability in the pulse oximeter waveform, has been found to correlate with fluid responsiveness in mechanically ventilated patients. To this date, no study has assessed the correlation between PVI and exacerbation severity in asthma.

A printout of the first ED pulse oximetry reading was used to obtain the PImax and PImin as below:

Researchers followed patients after the initial evaluation to determine disposition from the ED, which included either discharge to home, admission to a general pediatrics floor, or admission to the PICU. The hospital utilized specific criteria for disposition from the ED (see Table 1).

References

1. Care of children and adolescents in U.S. hospitals. Agency for Healthcare Research and Quality website. Available at: https://archive.ahrq.gov/data/hcup/factbk4/factbk4.htm. Accessed Nov. 18, 2016.

2. Kelly AM, Kerr D, Powell C. Is severity assessment after one hour of treatment better for predicting the need for admission in acute asthma? Respir Med. 2004;98(8):777-781.

3. Keogh KA, Macarthur C, Parkin PC, et al. Predictors of hospitalization in children with acute asthma. J Pediatr. 2001;139(2):273-277.

4. Keahey L, Bulloch B, Becker AB, et al. Initial oxygen saturation as a predictor of admission in children presenting to the emergency department with acute asthma. Ann Emerg Med. 2002;40(3):300-307.

5. Guntheroth WG, Morgan BC, Mullins GL. Effect of respiration on venous return and stroke volume in cardiac tamponade. Mechanism of pulsus paradoxus. Circ Res. 1967;20(4):381-390.

6. Frey B, Freezer N. Diagnostic value and pathophysiologic basis of pulsus paradoxus in infants and children with respiratory disease. Pediatr Pulmonol. 2001;31(2):138-143.

7. Clark JA, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004;158(1):48-51.
 

Clinical question: Does pulse variability on plethysmography, or the Pleth Variability Index (PVI), correlate with disease severity in obstructive airway disease in children?

Background: Asthma is the most common reason for hospitalization in the United S. for children 3-12 years old. Asthma accounts for a quarter of ED visits for children aged 1-9 years old.¹ Although systems have been developed to assess asthma exacerbation severity and the need for hospitalization, many of these depend on reassessments over time or have been proven to be invalid in larger studies.^2,3,4 Pulsus paradoxus (PP), which is defined as a drop in systolic blood pressure greater than 10 mm Hg, correlates with the severity of obstruction in asthma exacerbations, but it is not practical in the children being evaluated in the ED or hospital.^5,6 PP measurement using plethysmography has been found to correlate with measurement by sphygmomanometry.⁷ Furthermore, PVI, which is derived from amplitude variability in the pulse oximeter waveform, has been found to correlate with fluid responsiveness in mechanically ventilated patients. To this date, no study has assessed the correlation between PVI and exacerbation severity in asthma.

A printout of the first ED pulse oximetry reading was used to obtain the PImax and PImin as below:

Researchers followed patients after the initial evaluation to determine disposition from the ED, which included either discharge to home, admission to a general pediatrics floor, or admission to the PICU. The hospital utilized specific criteria for disposition from the ED (see Table 1).

References

1. Care of children and adolescents in U.S. hospitals. Agency for Healthcare Research and Quality website. Available at: https://archive.ahrq.gov/data/hcup/factbk4/factbk4.htm. Accessed Nov. 18, 2016.

2. Kelly AM, Kerr D, Powell C. Is severity assessment after one hour of treatment better for predicting the need for admission in acute asthma? Respir Med. 2004;98(8):777-781.

3. Keogh KA, Macarthur C, Parkin PC, et al. Predictors of hospitalization in children with acute asthma. J Pediatr. 2001;139(2):273-277.

4. Keahey L, Bulloch B, Becker AB, et al. Initial oxygen saturation as a predictor of admission in children presenting to the emergency department with acute asthma. Ann Emerg Med. 2002;40(3):300-307.

5. Guntheroth WG, Morgan BC, Mullins GL. Effect of respiration on venous return and stroke volume in cardiac tamponade. Mechanism of pulsus paradoxus. Circ Res. 1967;20(4):381-390.

6. Frey B, Freezer N. Diagnostic value and pathophysiologic basis of pulsus paradoxus in infants and children with respiratory disease. Pediatr Pulmonol. 2001;31(2):138-143.

7. Clark JA, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004;158(1):48-51.
 

We work in complex environments and in a flawed and rapidly changing health care system. Caregivers, patients, and communities will be led through this complexity by those who embrace change. Last October, I had the privilege of attending and facilitating the SHM Leadership Academy in Orlando, which allowed me the opportunity to meet a group of people who embrace change, including the benefits and challenges that often accompany it.

SHM board member Jeff Glasheen, MD, SFHM, taught one of the first lessons at Leadership Academy, focusing on the importance of meaningful, difficult change. With comparisons to companies that have embraced change, like Apple, and some that have not, like Sears, Jeff summed up how complacency with “good” and a reluctance to tackle the difficulty of change keeps organizations – and people – from becoming great.

“Good is the enemy of great,” Jeff preached.

He largely focused on hospitalists leading organizational change, but the concepts can apply to personal change, too. He explained that “people generally want things to be different, but they don’t want to change.”

Leaders in training

Ten emerging hospitalist leaders sat at my table, soaking in the message. Several of them, like me 8 years ago, had the responsibilities of leadership unexpectedly thrust upon them. Some carried with them the heavy expectations of their colleagues or hospital administration (or both) that by being elevated into a role such as medical director, they would abruptly be able to make improvements in patient care and hospital operations. They had accepted the challenge to change – to move out of purely clinical roles and take on new ones in leadership despite having little or no experience. Doing so, they gingerly but willingly were following in the footsteps of leaders before them, growing their skills, improving their hospitals, and laying a path for future leaders to follow.

A few weeks prior, I had taken a new leadership position myself. The Cleveland Clinic recently acquired a hospital and health system in Akron, Ohio, about 40 miles away from the city. I assumed the role of president of this acquisition, embracing the complex challenge of leading the process of integrating two health systems. After 3 years overseeing a different hospital in the health system, I finally felt I had developed the people, processes, and culture that I had been striving to build. But like the young leaders at Leadership Academy, I had the opportunity to change, grow, develop, take on new risk, and become a stronger leader in this new role. A significant part of the experience of the Leadership Academy involves table exercises. For the first few exercises, the group was quiet, uncertain, tentative. I was struck both by how early these individuals were in their development and by how so much of what is happening today in hospitals and health care is dependent upon the development and success of individuals like these who are enthusiastic and talented but young and overwhelmed.

I believe that successful hospitalists are, through experience, training, and nature, rapid assimilators into their environments. By the third day, the dynamic at my table had gone from tentative and uncertain to much more confident and assertive. To experience this transformation in person at SHM’s Leadership Academy, we welcome you to Scottsdale, Ariz., later this year. Learn more about the program at www.shmleadershipacademy.org.

At Leadership Academy and beyond, I implore hospitalists to look for opportunities to change during this time of New Year’s resolutions and to take the opposite posture and want to change – change how we think, act, and respond; change our roles to take on new, uncomfortable responsibilities; and change how we view change itself.

We will be better for it both personally and professionally, and we will stand out as role models for our colleagues, coworkers, and hospitalists who follow in our footsteps.

Dr. Harte is a practicing hospitalist, president of the Society of Hospital Medicine, and president of Hillcrest Hospital in Mayfield Heights, Ohio, part of the Cleveland Clinic Health System. He is associate professor of medicine at the Cleveland Clinic, Lerner College of Medicine in Cleveland.

We work in complex environments and in a flawed and rapidly changing health care system. Caregivers, patients, and communities will be led through this complexity by those who embrace change. Last October, I had the privilege of attending and facilitating the SHM Leadership Academy in Orlando, which allowed me the opportunity to meet a group of people who embrace change, including the benefits and challenges that often accompany it.

SHM board member Jeff Glasheen, MD, SFHM, taught one of the first lessons at Leadership Academy, focusing on the importance of meaningful, difficult change. With comparisons to companies that have embraced change, like Apple, and some that have not, like Sears, Jeff summed up how complacency with “good” and a reluctance to tackle the difficulty of change keeps organizations – and people – from becoming great.

“Good is the enemy of great,” Jeff preached.

He largely focused on hospitalists leading organizational change, but the concepts can apply to personal change, too. He explained that “people generally want things to be different, but they don’t want to change.”

Leaders in training

Ten emerging hospitalist leaders sat at my table, soaking in the message. Several of them, like me 8 years ago, had the responsibilities of leadership unexpectedly thrust upon them. Some carried with them the heavy expectations of their colleagues or hospital administration (or both) that by being elevated into a role such as medical director, they would abruptly be able to make improvements in patient care and hospital operations. They had accepted the challenge to change – to move out of purely clinical roles and take on new ones in leadership despite having little or no experience. Doing so, they gingerly but willingly were following in the footsteps of leaders before them, growing their skills, improving their hospitals, and laying a path for future leaders to follow.

A few weeks prior, I had taken a new leadership position myself. The Cleveland Clinic recently acquired a hospital and health system in Akron, Ohio, about 40 miles away from the city. I assumed the role of president of this acquisition, embracing the complex challenge of leading the process of integrating two health systems. After 3 years overseeing a different hospital in the health system, I finally felt I had developed the people, processes, and culture that I had been striving to build. But like the young leaders at Leadership Academy, I had the opportunity to change, grow, develop, take on new risk, and become a stronger leader in this new role. A significant part of the experience of the Leadership Academy involves table exercises. For the first few exercises, the group was quiet, uncertain, tentative. I was struck both by how early these individuals were in their development and by how so much of what is happening today in hospitals and health care is dependent upon the development and success of individuals like these who are enthusiastic and talented but young and overwhelmed.

I believe that successful hospitalists are, through experience, training, and nature, rapid assimilators into their environments. By the third day, the dynamic at my table had gone from tentative and uncertain to much more confident and assertive. To experience this transformation in person at SHM’s Leadership Academy, we welcome you to Scottsdale, Ariz., later this year. Learn more about the program at www.shmleadershipacademy.org.

At Leadership Academy and beyond, I implore hospitalists to look for opportunities to change during this time of New Year’s resolutions and to take the opposite posture and want to change – change how we think, act, and respond; change our roles to take on new, uncomfortable responsibilities; and change how we view change itself.

We will be better for it both personally and professionally, and we will stand out as role models for our colleagues, coworkers, and hospitalists who follow in our footsteps.

Dr. Harte is a practicing hospitalist, president of the Society of Hospital Medicine, and president of Hillcrest Hospital in Mayfield Heights, Ohio, part of the Cleveland Clinic Health System. He is associate professor of medicine at the Cleveland Clinic, Lerner College of Medicine in Cleveland.

We work in complex environments and in a flawed and rapidly changing health care system. Caregivers, patients, and communities will be led through this complexity by those who embrace change. Last October, I had the privilege of attending and facilitating the SHM Leadership Academy in Orlando, which allowed me the opportunity to meet a group of people who embrace change, including the benefits and challenges that often accompany it.

SHM board member Jeff Glasheen, MD, SFHM, taught one of the first lessons at Leadership Academy, focusing on the importance of meaningful, difficult change. With comparisons to companies that have embraced change, like Apple, and some that have not, like Sears, Jeff summed up how complacency with “good” and a reluctance to tackle the difficulty of change keeps organizations – and people – from becoming great.

“Good is the enemy of great,” Jeff preached.

He largely focused on hospitalists leading organizational change, but the concepts can apply to personal change, too. He explained that “people generally want things to be different, but they don’t want to change.”

Leaders in training

Ten emerging hospitalist leaders sat at my table, soaking in the message. Several of them, like me 8 years ago, had the responsibilities of leadership unexpectedly thrust upon them. Some carried with them the heavy expectations of their colleagues or hospital administration (or both) that by being elevated into a role such as medical director, they would abruptly be able to make improvements in patient care and hospital operations. They had accepted the challenge to change – to move out of purely clinical roles and take on new ones in leadership despite having little or no experience. Doing so, they gingerly but willingly were following in the footsteps of leaders before them, growing their skills, improving their hospitals, and laying a path for future leaders to follow.

A few weeks prior, I had taken a new leadership position myself. The Cleveland Clinic recently acquired a hospital and health system in Akron, Ohio, about 40 miles away from the city. I assumed the role of president of this acquisition, embracing the complex challenge of leading the process of integrating two health systems. After 3 years overseeing a different hospital in the health system, I finally felt I had developed the people, processes, and culture that I had been striving to build. But like the young leaders at Leadership Academy, I had the opportunity to change, grow, develop, take on new risk, and become a stronger leader in this new role. A significant part of the experience of the Leadership Academy involves table exercises. For the first few exercises, the group was quiet, uncertain, tentative. I was struck both by how early these individuals were in their development and by how so much of what is happening today in hospitals and health care is dependent upon the development and success of individuals like these who are enthusiastic and talented but young and overwhelmed.

I believe that successful hospitalists are, through experience, training, and nature, rapid assimilators into their environments. By the third day, the dynamic at my table had gone from tentative and uncertain to much more confident and assertive. To experience this transformation in person at SHM’s Leadership Academy, we welcome you to Scottsdale, Ariz., later this year. Learn more about the program at www.shmleadershipacademy.org.

At Leadership Academy and beyond, I implore hospitalists to look for opportunities to change during this time of New Year’s resolutions and to take the opposite posture and want to change – change how we think, act, and respond; change our roles to take on new, uncomfortable responsibilities; and change how we view change itself.

We will be better for it both personally and professionally, and we will stand out as role models for our colleagues, coworkers, and hospitalists who follow in our footsteps.

Dr. Harte is a practicing hospitalist, president of the Society of Hospital Medicine, and president of Hillcrest Hospital in Mayfield Heights, Ohio, part of the Cleveland Clinic Health System. He is associate professor of medicine at the Cleveland Clinic, Lerner College of Medicine in Cleveland.

Unveiling the hospitalist specialty code

The Centers for Medicare & Medicaid Services announced in November the official implementation date for the Medicare physician specialty code for hospitalists. On April 3, “hospitalist” will be an official specialty designation under Medicare; the code will be C6. Starting on that date, hospitalists can change their specialty designation on the Medicare enrollment application (Form CMS-855I) or through CMS’ online portal (Provider Enrollment, Chain, and Ownership System, or PECOS).

Appropriate use of specialty codes helps distinguish differences among providers and improves the quality of utilization data. SHM applied for a specialty code for hospitalists nearly 3 years ago, and CMS approved the application in February 2016.

Stand with your fellow hospitalists and make sure to declare, “I’m a C6.”
 

Develop curricula to educate, engage medical students and residents

The ACGME requirements for training in quality and safety are changing – it is no longer an elective. As sponsoring institutions’ residency and fellowship programs mobilize to meet these requirements, leaders may find few faculty members are comfortable enough with the material to teach and create educational content for trainees. These faculty need further development.

Sponsored by SHM, the Quality and Safety Educators Academy (QSEA) responds to that demand by providing medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. The 2017 meeting is Feb. 26-28 at the Tempe Mission Palms Hotel in Arizona.

This 2½ day meeting aims to fill the current gaps for faculty by offering basic concepts and educational tools in quality improvement and patient safety. Material is presented in an interactive way, providing guidance on career and curriculum development and establishing a national network of quality and safety educators.

For more information and to register, visit www.shmqsea.org.
 

EHRs: blessing or curse?

SHM’s Health Information Technology (HIT) Committee invited you to participate in a brief survey to inform your experiences with inpatient electronic health record (EHR) systems. The results will serve as a foundation for a white paper to be written by the HIT Committee addressing hospitalists’ attitudes toward EHR systems. It will be released next month, so stay tuned then to view the final paper.

SHM chapters: Your connection to local education, networking, leadership opportunities

SHM offers various opportunities to grow professionally, expand your CV, and engage with other hospitalists. With more than 50 chapters across the country, you can network, learn, teach, and continue to improve patient care at a local level. Find a chapter in your area or start a chapter today by visiting www.hospitalmedicine.org/chapters.

Enhance opioid safety for inpatients

SHM enrolled 10 hospitals into a second mentored implementation cohort around Reducing Adverse Drug Events Related to Opioids (RADEO). The program is now in its second month as the sites work with their mentors to enhance safety for patients in the hospital who are prescribed opioid medications by:

• Developing a needs assessment.
• Putting in place formal selections of data collection measures.
• Beginning to take outcomes and process data collection on intervention units.
• Starting to design and implement key interventions.

Even if you’re not in this mentored implementation cohort, visit www.hospitalmedicine.org/RADEO and view the online toolkit or download the implementation guide.
 

Earn recognition for your research with SHM’s Junior Investigator Award

The SHM Junior Investigator Award was created for junior/early-stage investigators, defined as faculty in the first 5 years of their most recent position/appointment. Applicants must be a hospitalist or clinician-investigators whose research interests focus on the care of hospitalized patients, the organization of hospitals, or the practice of hospitalists. Applicants must be members of SHM in good standing. Nominations from mentors and self-nominations are both welcome.

The winner will be invited to receive the award during SHM’s annual meeting, HM17, May 1-4, at Mandalay Bay Resort and Casino in Las Vegas. The winner will receive complimentary registration for this meeting as well as a complimentary 1-year membership to SHM.

For more information on the application process, visit www.hospitalmedicine.org/juniorinvestigator.
 

Unveiling the hospitalist specialty code

The Centers for Medicare & Medicaid Services announced in November the official implementation date for the Medicare physician specialty code for hospitalists. On April 3, “hospitalist” will be an official specialty designation under Medicare; the code will be C6. Starting on that date, hospitalists can change their specialty designation on the Medicare enrollment application (Form CMS-855I) or through CMS’ online portal (Provider Enrollment, Chain, and Ownership System, or PECOS).

Appropriate use of specialty codes helps distinguish differences among providers and improves the quality of utilization data. SHM applied for a specialty code for hospitalists nearly 3 years ago, and CMS approved the application in February 2016.

Stand with your fellow hospitalists and make sure to declare, “I’m a C6.”
 

Develop curricula to educate, engage medical students and residents

The ACGME requirements for training in quality and safety are changing – it is no longer an elective. As sponsoring institutions’ residency and fellowship programs mobilize to meet these requirements, leaders may find few faculty members are comfortable enough with the material to teach and create educational content for trainees. These faculty need further development.

Sponsored by SHM, the Quality and Safety Educators Academy (QSEA) responds to that demand by providing medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. The 2017 meeting is Feb. 26-28 at the Tempe Mission Palms Hotel in Arizona.

This 2½ day meeting aims to fill the current gaps for faculty by offering basic concepts and educational tools in quality improvement and patient safety. Material is presented in an interactive way, providing guidance on career and curriculum development and establishing a national network of quality and safety educators.

For more information and to register, visit www.shmqsea.org.
 

EHRs: blessing or curse?

SHM’s Health Information Technology (HIT) Committee invited you to participate in a brief survey to inform your experiences with inpatient electronic health record (EHR) systems. The results will serve as a foundation for a white paper to be written by the HIT Committee addressing hospitalists’ attitudes toward EHR systems. It will be released next month, so stay tuned then to view the final paper.

SHM chapters: Your connection to local education, networking, leadership opportunities

SHM offers various opportunities to grow professionally, expand your CV, and engage with other hospitalists. With more than 50 chapters across the country, you can network, learn, teach, and continue to improve patient care at a local level. Find a chapter in your area or start a chapter today by visiting www.hospitalmedicine.org/chapters.

Enhance opioid safety for inpatients

SHM enrolled 10 hospitals into a second mentored implementation cohort around Reducing Adverse Drug Events Related to Opioids (RADEO). The program is now in its second month as the sites work with their mentors to enhance safety for patients in the hospital who are prescribed opioid medications by:

• Developing a needs assessment.
• Putting in place formal selections of data collection measures.
• Beginning to take outcomes and process data collection on intervention units.
• Starting to design and implement key interventions.

Even if you’re not in this mentored implementation cohort, visit www.hospitalmedicine.org/RADEO and view the online toolkit or download the implementation guide.
 

Earn recognition for your research with SHM’s Junior Investigator Award

The SHM Junior Investigator Award was created for junior/early-stage investigators, defined as faculty in the first 5 years of their most recent position/appointment. Applicants must be a hospitalist or clinician-investigators whose research interests focus on the care of hospitalized patients, the organization of hospitals, or the practice of hospitalists. Applicants must be members of SHM in good standing. Nominations from mentors and self-nominations are both welcome.

The winner will be invited to receive the award during SHM’s annual meeting, HM17, May 1-4, at Mandalay Bay Resort and Casino in Las Vegas. The winner will receive complimentary registration for this meeting as well as a complimentary 1-year membership to SHM.

For more information on the application process, visit www.hospitalmedicine.org/juniorinvestigator.
 

Unveiling the hospitalist specialty code

The Centers for Medicare & Medicaid Services announced in November the official implementation date for the Medicare physician specialty code for hospitalists. On April 3, “hospitalist” will be an official specialty designation under Medicare; the code will be C6. Starting on that date, hospitalists can change their specialty designation on the Medicare enrollment application (Form CMS-855I) or through CMS’ online portal (Provider Enrollment, Chain, and Ownership System, or PECOS).

Appropriate use of specialty codes helps distinguish differences among providers and improves the quality of utilization data. SHM applied for a specialty code for hospitalists nearly 3 years ago, and CMS approved the application in February 2016.

Stand with your fellow hospitalists and make sure to declare, “I’m a C6.”
 

Develop curricula to educate, engage medical students and residents

The ACGME requirements for training in quality and safety are changing – it is no longer an elective. As sponsoring institutions’ residency and fellowship programs mobilize to meet these requirements, leaders may find few faculty members are comfortable enough with the material to teach and create educational content for trainees. These faculty need further development.

Sponsored by SHM, the Quality and Safety Educators Academy (QSEA) responds to that demand by providing medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. The 2017 meeting is Feb. 26-28 at the Tempe Mission Palms Hotel in Arizona.

This 2½ day meeting aims to fill the current gaps for faculty by offering basic concepts and educational tools in quality improvement and patient safety. Material is presented in an interactive way, providing guidance on career and curriculum development and establishing a national network of quality and safety educators.

For more information and to register, visit www.shmqsea.org.
 

EHRs: blessing or curse?

SHM’s Health Information Technology (HIT) Committee invited you to participate in a brief survey to inform your experiences with inpatient electronic health record (EHR) systems. The results will serve as a foundation for a white paper to be written by the HIT Committee addressing hospitalists’ attitudes toward EHR systems. It will be released next month, so stay tuned then to view the final paper.

SHM chapters: Your connection to local education, networking, leadership opportunities

SHM offers various opportunities to grow professionally, expand your CV, and engage with other hospitalists. With more than 50 chapters across the country, you can network, learn, teach, and continue to improve patient care at a local level. Find a chapter in your area or start a chapter today by visiting www.hospitalmedicine.org/chapters.

Enhance opioid safety for inpatients

SHM enrolled 10 hospitals into a second mentored implementation cohort around Reducing Adverse Drug Events Related to Opioids (RADEO). The program is now in its second month as the sites work with their mentors to enhance safety for patients in the hospital who are prescribed opioid medications by:

• Developing a needs assessment.
• Putting in place formal selections of data collection measures.
• Beginning to take outcomes and process data collection on intervention units.
• Starting to design and implement key interventions.

Even if you’re not in this mentored implementation cohort, visit www.hospitalmedicine.org/RADEO and view the online toolkit or download the implementation guide.
 

Earn recognition for your research with SHM’s Junior Investigator Award

The SHM Junior Investigator Award was created for junior/early-stage investigators, defined as faculty in the first 5 years of their most recent position/appointment. Applicants must be a hospitalist or clinician-investigators whose research interests focus on the care of hospitalized patients, the organization of hospitals, or the practice of hospitalists. Applicants must be members of SHM in good standing. Nominations from mentors and self-nominations are both welcome.

The winner will be invited to receive the award during SHM’s annual meeting, HM17, May 1-4, at Mandalay Bay Resort and Casino in Las Vegas. The winner will receive complimentary registration for this meeting as well as a complimentary 1-year membership to SHM.

For more information on the application process, visit www.hospitalmedicine.org/juniorinvestigator.
 

Here are 5 articles in the January issue of Clinician Reviews (individual articles are valid for one year from date of publication—expiration dates below):

1. Gluten-free Adherence Triples While Celiac Disease Prevalence Remains Stable

To take the posttest, go to: http://bit.ly/2h2LFDu
Expires September 6, 2017

2. Fluoxetine Appears Safer  for Bone Health in At-risk Older Patients

To take the posttest, go to: http://bit.ly/2he1FTD
Expires September 15, 2017

3. High Free T4 Levels Linked to Sudden Cardiac Death

To take the posttest, go to: http://bit.ly/2gMJqUz
Expires September 16, 2017

4. Morning Sickness Linked to Lower Risk for Pregnancy Loss

To take the posttest, go to: http://bit.ly/2uaWMkH
Expires September 26, 2017

5. Anxiety, Depression May Precede Parkinson's by 25 Years

To take the posttest, go to: http://bit.ly/2gMFQtr
Expires September 27, 2017

Here are 5 articles in the January issue of Clinician Reviews (individual articles are valid for one year from date of publication—expiration dates below):

1. Gluten-free Adherence Triples While Celiac Disease Prevalence Remains Stable

To take the posttest, go to: http://bit.ly/2h2LFDu
Expires September 6, 2017

2. Fluoxetine Appears Safer  for Bone Health in At-risk Older Patients

To take the posttest, go to: http://bit.ly/2he1FTD
Expires September 15, 2017

3. High Free T4 Levels Linked to Sudden Cardiac Death

To take the posttest, go to: http://bit.ly/2gMJqUz
Expires September 16, 2017

4. Morning Sickness Linked to Lower Risk for Pregnancy Loss

To take the posttest, go to: http://bit.ly/2uaWMkH
Expires September 26, 2017

5. Anxiety, Depression May Precede Parkinson's by 25 Years

To take the posttest, go to: http://bit.ly/2gMFQtr
Expires September 27, 2017

Here are 5 articles in the January issue of Clinician Reviews (individual articles are valid for one year from date of publication—expiration dates below):

1. Gluten-free Adherence Triples While Celiac Disease Prevalence Remains Stable

To take the posttest, go to: http://bit.ly/2h2LFDu
Expires September 6, 2017

2. Fluoxetine Appears Safer  for Bone Health in At-risk Older Patients

To take the posttest, go to: http://bit.ly/2he1FTD
Expires September 15, 2017

3. High Free T4 Levels Linked to Sudden Cardiac Death

To take the posttest, go to: http://bit.ly/2gMJqUz
Expires September 16, 2017

4. Morning Sickness Linked to Lower Risk for Pregnancy Loss

To take the posttest, go to: http://bit.ly/2uaWMkH
Expires September 26, 2017

5. Anxiety, Depression May Precede Parkinson's by 25 Years

To take the posttest, go to: http://bit.ly/2gMFQtr
Expires September 27, 2017

Did mother’s allergic reaction cause fetal injury?

When a mother was admitted to the labor and delivery unit, she had strep throat; ampicillin was administered. She experienced anaphylactic symptoms that were attended to. The baby, delivered vaginally 3 hours later, was severely distressed and showed signs of asphyxia. He was found to have a permanent brain injury.

PARENTS’ CLAIM:

The ObGyn and hospital nurses failed to properly manage the mother’s anaphylactic reaction to ampicillin. Fetal heart-rate tracings indicated fetal distress. Standard of care required prompt intervention with epinephrine and/or emergency cesarean delivery. Brain injury occurred because these procedures were not performed.

DEFENDANTS’ DEFENSE:

The nurses denied fault and explained that they appropriately and immediately responded to mild anaphylactic symptoms in the mother. They could not administer epinephrine because the ObGyn did not order it.

The ObGyn denied violating the standard of care that included minimizing the mother’s allergic reaction. Because the mother didn’t have a rash, it was not necessary to order epinephrine. The baby sustained an unknown injury earlier in the pregnancy that was unrelated to labor.

VERDICT:

A Tennessee defense verdict was returned.

Resident blamed for shoulder dystocia

A mother presented to a federally funded health center in labor. A first-year resident managed labor and delivery under the supervision of the attending physician. Shoulder dystocia was encountered and the baby suffered a permanent brachial plexus injury.

PARENTS’ CLAIM:

Negligence occurred when the resident used excessive force by pulling on the infant’s neck during delivery. The resident, who had just received his medical license, was poorly supervised by the attending physician.

DEFENDANTS’ DEFENSE:

Suit was brought against the resident, the attending physician, the federal government, and the hospital’s residency program. The resident denied using excessive force. As soon as delivery became complex, the attending physician completed the delivery. The baby’s injuries were unpredictable and unavoidable.

VERDICT:

A $290,000 settlement with the federal government was reached before trial. A Pennsylvania defense verdict was returned for the other parties.

Related Article:
Tackle the challenging shoulder dystocia emergency by practicing delivery of the posterior arm

What caused brachial plexus injury?

An experienced midwife delivered a baby who sustained a brachial plexus injury resulting in flail arm syndrome.

PARENTS’ CLAIM:

The midwife mismanaged the delivery causing permanent injury. The child has gained little improvement with surgery and physical therapy.

DEFENDANTS’ DEFENSE:

The injury was caused by the natural forces of labor. The midwife used appropriate techniques during the birth.

VERDICT:

A Washington defense verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Did mother’s allergic reaction cause fetal injury?

When a mother was admitted to the labor and delivery unit, she had strep throat; ampicillin was administered. She experienced anaphylactic symptoms that were attended to. The baby, delivered vaginally 3 hours later, was severely distressed and showed signs of asphyxia. He was found to have a permanent brain injury.

PARENTS’ CLAIM:

The ObGyn and hospital nurses failed to properly manage the mother’s anaphylactic reaction to ampicillin. Fetal heart-rate tracings indicated fetal distress. Standard of care required prompt intervention with epinephrine and/or emergency cesarean delivery. Brain injury occurred because these procedures were not performed.

DEFENDANTS’ DEFENSE:

The nurses denied fault and explained that they appropriately and immediately responded to mild anaphylactic symptoms in the mother. They could not administer epinephrine because the ObGyn did not order it.

The ObGyn denied violating the standard of care that included minimizing the mother’s allergic reaction. Because the mother didn’t have a rash, it was not necessary to order epinephrine. The baby sustained an unknown injury earlier in the pregnancy that was unrelated to labor.

VERDICT:

A Tennessee defense verdict was returned.

Resident blamed for shoulder dystocia

A mother presented to a federally funded health center in labor. A first-year resident managed labor and delivery under the supervision of the attending physician. Shoulder dystocia was encountered and the baby suffered a permanent brachial plexus injury.

PARENTS’ CLAIM:

Negligence occurred when the resident used excessive force by pulling on the infant’s neck during delivery. The resident, who had just received his medical license, was poorly supervised by the attending physician.

DEFENDANTS’ DEFENSE:

Suit was brought against the resident, the attending physician, the federal government, and the hospital’s residency program. The resident denied using excessive force. As soon as delivery became complex, the attending physician completed the delivery. The baby’s injuries were unpredictable and unavoidable.

VERDICT:

A $290,000 settlement with the federal government was reached before trial. A Pennsylvania defense verdict was returned for the other parties.

Related Article:
Tackle the challenging shoulder dystocia emergency by practicing delivery of the posterior arm

What caused brachial plexus injury?

An experienced midwife delivered a baby who sustained a brachial plexus injury resulting in flail arm syndrome.

PARENTS’ CLAIM:

The midwife mismanaged the delivery causing permanent injury. The child has gained little improvement with surgery and physical therapy.

DEFENDANTS’ DEFENSE:

The injury was caused by the natural forces of labor. The midwife used appropriate techniques during the birth.

VERDICT:

A Washington defense verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Did mother’s allergic reaction cause fetal injury?

When a mother was admitted to the labor and delivery unit, she had strep throat; ampicillin was administered. She experienced anaphylactic symptoms that were attended to. The baby, delivered vaginally 3 hours later, was severely distressed and showed signs of asphyxia. He was found to have a permanent brain injury.

PARENTS’ CLAIM:

The ObGyn and hospital nurses failed to properly manage the mother’s anaphylactic reaction to ampicillin. Fetal heart-rate tracings indicated fetal distress. Standard of care required prompt intervention with epinephrine and/or emergency cesarean delivery. Brain injury occurred because these procedures were not performed.

DEFENDANTS’ DEFENSE:

The nurses denied fault and explained that they appropriately and immediately responded to mild anaphylactic symptoms in the mother. They could not administer epinephrine because the ObGyn did not order it.

The ObGyn denied violating the standard of care that included minimizing the mother’s allergic reaction. Because the mother didn’t have a rash, it was not necessary to order epinephrine. The baby sustained an unknown injury earlier in the pregnancy that was unrelated to labor.

VERDICT:

A Tennessee defense verdict was returned.

Resident blamed for shoulder dystocia

A mother presented to a federally funded health center in labor. A first-year resident managed labor and delivery under the supervision of the attending physician. Shoulder dystocia was encountered and the baby suffered a permanent brachial plexus injury.

PARENTS’ CLAIM:

Negligence occurred when the resident used excessive force by pulling on the infant’s neck during delivery. The resident, who had just received his medical license, was poorly supervised by the attending physician.

DEFENDANTS’ DEFENSE:

Suit was brought against the resident, the attending physician, the federal government, and the hospital’s residency program. The resident denied using excessive force. As soon as delivery became complex, the attending physician completed the delivery. The baby’s injuries were unpredictable and unavoidable.

VERDICT:

A $290,000 settlement with the federal government was reached before trial. A Pennsylvania defense verdict was returned for the other parties.

Related Article:
Tackle the challenging shoulder dystocia emergency by practicing delivery of the posterior arm

What caused brachial plexus injury?

An experienced midwife delivered a baby who sustained a brachial plexus injury resulting in flail arm syndrome.

PARENTS’ CLAIM:

The midwife mismanaged the delivery causing permanent injury. The child has gained little improvement with surgery and physical therapy.

DEFENDANTS’ DEFENSE:

The injury was caused by the natural forces of labor. The midwife used appropriate techniques during the birth.

VERDICT:

A Washington defense verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Removal of wrong ovary?

Several years earlier, a patient had undergone a hysterectomy but retained her ovaries and fallopian tubes. She reported recurrent pelvic pain, especially on the left side, to a gynecologic surgeon. Ultrasonography (US) results showed a small follicular cyst on the right ovary and a simple cyst on the left ovary. The patient consented to diagnostic laparoscopy with possible left salpingo-oophorectomy. During the procedure, the surgeon removed the right fallopian tube and ovary. After recovery, the patient continued to have left-sided pelvic pain. When she saw another surgeon a year later, US results showed that the left ovary and tube were still intact. The patient underwent left salpingo-oophorectomy.

PATIENT’S CLAIM:

The surgeon removed the wrong ovary and tube, a breach of the standard of care, and didn’t adequately explain his surgical actions.

DEFENDANTS’ DEFENSE:

Standard of care was maintained. During surgery, the surgeon encountered severe adhesions on the patient’s left side and was unable to visualize her left ovary. He decided that what had appeared to be an ovary on US most likely was a fluid collection, and that the patient’s left ovary must have been removed at hysterectomy. The surgeon concluded that the hemorrhagic cyst on the right ovary and adhesions were causing the patient’s pain, and removed them. The patient had given him permission to perform laparoscopic surgery, but he did not have her consent to convert to laparotomy, which would have been necessary to confirm the absence of her left ovary.

VERDICT:

An Alabama defense verdict was returned.

Related Article:
Medical errors: Meeting ethical obligations and reducing liability with proper communication

Was wrong hysterectomy procedure chosen?

After being treated by her ObGyn for postmenopausal bleeding with medication and dilation and curettage, a 50-year-old woman underwent total abdominal hysterectomy (TAH). At an office visit 3 weeks postsurgery, she reported uncontrollable urination. The patient was admitted to a hospital, where cystogram results showed a vesico-vaginal fistula (VVF). She was treated with catheter drainage and referred to a urologist. The patient underwent 2 unsuccessful repair operations. A third repair, performed 10 months after the TAH, was successful.

PATIENT’S CLAIM:

The ObGyn should have performed laparoscopic supracervical hysterectomy (LSH) instead of TAH because the patient’s cervix would have remained intact and VVF would not have developed. Medical bills totaled $194,000.

PHYSICIAN’S DEFENSE:

The standard of care did not require LSH. Had the ObGyn left the cervix intact, the patient could have continued bleeding with increased risk of cervical cancer. A bladder injury is a known complication of hysterectomy.

VERDICT:

A Mississippi defense verdict was returned.

Woman dies after uterine fibroid removal

A 39-year-old woman with a history of hypertension, diabetes, moderate obesity, and end-stage renal disease underwent myomectomy. A first-year resident assisted the attending anesthesiologist during the procedure. While the patient was under general anesthesia, her blood pressure (BP) dropped rapidly and remained at an abnormally low level for 45 minutes. Then the patient’s heart rate dropped to around 30 bpm and remained at that level for 15 minutes before her BP and heart rate were finally restored. The patient never regained consciousness and remained in an irreversible coma until she died 6 days later.

ESTATE’S CLAIM:

The anesthesiologist and resident negligently allowed the patient’s BP and heart rate to fall to dangerously low levels. Because the patient had hypertension, diabetes, and obesity, she required a higher BP to maintain adequate cerebral perfusion. The physicians precipitated the patient’s hypotension by giving her an excessive dose of morphine and bupivacaine via epidural catheter prior to induction of general anesthesia, and then failed to give her sufficient doses of vasopressors to increase her BP to safe levels. They failed to properly treat the condition in a timely manner, causing brain damage, and ultimately, death.

DEFENDANTS’ DEFENSE:

The case was settled during mediation.

VERDICT:

A $900,000 Massachusetts settlement was reached.

Related Article:
Total abdominal hysterectomy the Mayo Clinic way

Ureter injured during hysterectomy

A 47-year-old woman’s right ureter was damaged during laparoscopic hysterectomy. During surgery, the gynecologist called in a urologist to repair the injury. The patient reported postsurgical complications including renal function impairment. A computed tomography scan showed a right ureter obstruction. When surgery confirmed complete obstruction of the ureter, she had a temporary nephrostomy drain placed. After 4 weeks, the patient returned to the operating room to have the right ureter implanted into the bladder. The patient reported occasional painful urination with increased urinary frequency and decreased right kidney size.

PATIENT’S CLAIM:

The gynecologist lacerated the ureter because he did not adequately identify and protect the ureter; this error represented a departure from the standard of care. The urologist failed to properly repair the injury. The patient sought recovery of $990,000 for past and future pain and suffering.

DEFENDANTS’ CLAIM:

The suit against the urologist and hospital was dropped, but continued against the gynecologist. The gynecologist claimed that the patient’s injury was a thermal burn, and is a known complication of the procedure.

VERDICT:

A $500,000 New York verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Removal of wrong ovary?

Several years earlier, a patient had undergone a hysterectomy but retained her ovaries and fallopian tubes. She reported recurrent pelvic pain, especially on the left side, to a gynecologic surgeon. Ultrasonography (US) results showed a small follicular cyst on the right ovary and a simple cyst on the left ovary. The patient consented to diagnostic laparoscopy with possible left salpingo-oophorectomy. During the procedure, the surgeon removed the right fallopian tube and ovary. After recovery, the patient continued to have left-sided pelvic pain. When she saw another surgeon a year later, US results showed that the left ovary and tube were still intact. The patient underwent left salpingo-oophorectomy.

PATIENT’S CLAIM:

The surgeon removed the wrong ovary and tube, a breach of the standard of care, and didn’t adequately explain his surgical actions.

DEFENDANTS’ DEFENSE:

Standard of care was maintained. During surgery, the surgeon encountered severe adhesions on the patient’s left side and was unable to visualize her left ovary. He decided that what had appeared to be an ovary on US most likely was a fluid collection, and that the patient’s left ovary must have been removed at hysterectomy. The surgeon concluded that the hemorrhagic cyst on the right ovary and adhesions were causing the patient’s pain, and removed them. The patient had given him permission to perform laparoscopic surgery, but he did not have her consent to convert to laparotomy, which would have been necessary to confirm the absence of her left ovary.

VERDICT:

An Alabama defense verdict was returned.

Related Article:
Medical errors: Meeting ethical obligations and reducing liability with proper communication

Was wrong hysterectomy procedure chosen?

After being treated by her ObGyn for postmenopausal bleeding with medication and dilation and curettage, a 50-year-old woman underwent total abdominal hysterectomy (TAH). At an office visit 3 weeks postsurgery, she reported uncontrollable urination. The patient was admitted to a hospital, where cystogram results showed a vesico-vaginal fistula (VVF). She was treated with catheter drainage and referred to a urologist. The patient underwent 2 unsuccessful repair operations. A third repair, performed 10 months after the TAH, was successful.

PATIENT’S CLAIM:

The ObGyn should have performed laparoscopic supracervical hysterectomy (LSH) instead of TAH because the patient’s cervix would have remained intact and VVF would not have developed. Medical bills totaled $194,000.

PHYSICIAN’S DEFENSE:

The standard of care did not require LSH. Had the ObGyn left the cervix intact, the patient could have continued bleeding with increased risk of cervical cancer. A bladder injury is a known complication of hysterectomy.

VERDICT:

A Mississippi defense verdict was returned.

Woman dies after uterine fibroid removal

A 39-year-old woman with a history of hypertension, diabetes, moderate obesity, and end-stage renal disease underwent myomectomy. A first-year resident assisted the attending anesthesiologist during the procedure. While the patient was under general anesthesia, her blood pressure (BP) dropped rapidly and remained at an abnormally low level for 45 minutes. Then the patient’s heart rate dropped to around 30 bpm and remained at that level for 15 minutes before her BP and heart rate were finally restored. The patient never regained consciousness and remained in an irreversible coma until she died 6 days later.

ESTATE’S CLAIM:

The anesthesiologist and resident negligently allowed the patient’s BP and heart rate to fall to dangerously low levels. Because the patient had hypertension, diabetes, and obesity, she required a higher BP to maintain adequate cerebral perfusion. The physicians precipitated the patient’s hypotension by giving her an excessive dose of morphine and bupivacaine via epidural catheter prior to induction of general anesthesia, and then failed to give her sufficient doses of vasopressors to increase her BP to safe levels. They failed to properly treat the condition in a timely manner, causing brain damage, and ultimately, death.

DEFENDANTS’ DEFENSE:

The case was settled during mediation.

VERDICT:

A $900,000 Massachusetts settlement was reached.

Related Article:
Total abdominal hysterectomy the Mayo Clinic way

Ureter injured during hysterectomy

A 47-year-old woman’s right ureter was damaged during laparoscopic hysterectomy. During surgery, the gynecologist called in a urologist to repair the injury. The patient reported postsurgical complications including renal function impairment. A computed tomography scan showed a right ureter obstruction. When surgery confirmed complete obstruction of the ureter, she had a temporary nephrostomy drain placed. After 4 weeks, the patient returned to the operating room to have the right ureter implanted into the bladder. The patient reported occasional painful urination with increased urinary frequency and decreased right kidney size.

PATIENT’S CLAIM:

The gynecologist lacerated the ureter because he did not adequately identify and protect the ureter; this error represented a departure from the standard of care. The urologist failed to properly repair the injury. The patient sought recovery of $990,000 for past and future pain and suffering.

DEFENDANTS’ CLAIM:

The suit against the urologist and hospital was dropped, but continued against the gynecologist. The gynecologist claimed that the patient’s injury was a thermal burn, and is a known complication of the procedure.

VERDICT:

A $500,000 New York verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Removal of wrong ovary?

Several years earlier, a patient had undergone a hysterectomy but retained her ovaries and fallopian tubes. She reported recurrent pelvic pain, especially on the left side, to a gynecologic surgeon. Ultrasonography (US) results showed a small follicular cyst on the right ovary and a simple cyst on the left ovary. The patient consented to diagnostic laparoscopy with possible left salpingo-oophorectomy. During the procedure, the surgeon removed the right fallopian tube and ovary. After recovery, the patient continued to have left-sided pelvic pain. When she saw another surgeon a year later, US results showed that the left ovary and tube were still intact. The patient underwent left salpingo-oophorectomy.

PATIENT’S CLAIM:

The surgeon removed the wrong ovary and tube, a breach of the standard of care, and didn’t adequately explain his surgical actions.

DEFENDANTS’ DEFENSE:

Standard of care was maintained. During surgery, the surgeon encountered severe adhesions on the patient’s left side and was unable to visualize her left ovary. He decided that what had appeared to be an ovary on US most likely was a fluid collection, and that the patient’s left ovary must have been removed at hysterectomy. The surgeon concluded that the hemorrhagic cyst on the right ovary and adhesions were causing the patient’s pain, and removed them. The patient had given him permission to perform laparoscopic surgery, but he did not have her consent to convert to laparotomy, which would have been necessary to confirm the absence of her left ovary.

VERDICT:

An Alabama defense verdict was returned.

Related Article:
Medical errors: Meeting ethical obligations and reducing liability with proper communication

Was wrong hysterectomy procedure chosen?

After being treated by her ObGyn for postmenopausal bleeding with medication and dilation and curettage, a 50-year-old woman underwent total abdominal hysterectomy (TAH). At an office visit 3 weeks postsurgery, she reported uncontrollable urination. The patient was admitted to a hospital, where cystogram results showed a vesico-vaginal fistula (VVF). She was treated with catheter drainage and referred to a urologist. The patient underwent 2 unsuccessful repair operations. A third repair, performed 10 months after the TAH, was successful.

PATIENT’S CLAIM:

The ObGyn should have performed laparoscopic supracervical hysterectomy (LSH) instead of TAH because the patient’s cervix would have remained intact and VVF would not have developed. Medical bills totaled $194,000.

PHYSICIAN’S DEFENSE:

The standard of care did not require LSH. Had the ObGyn left the cervix intact, the patient could have continued bleeding with increased risk of cervical cancer. A bladder injury is a known complication of hysterectomy.

VERDICT:

A Mississippi defense verdict was returned.

Woman dies after uterine fibroid removal

A 39-year-old woman with a history of hypertension, diabetes, moderate obesity, and end-stage renal disease underwent myomectomy. A first-year resident assisted the attending anesthesiologist during the procedure. While the patient was under general anesthesia, her blood pressure (BP) dropped rapidly and remained at an abnormally low level for 45 minutes. Then the patient’s heart rate dropped to around 30 bpm and remained at that level for 15 minutes before her BP and heart rate were finally restored. The patient never regained consciousness and remained in an irreversible coma until she died 6 days later.

ESTATE’S CLAIM:

The anesthesiologist and resident negligently allowed the patient’s BP and heart rate to fall to dangerously low levels. Because the patient had hypertension, diabetes, and obesity, she required a higher BP to maintain adequate cerebral perfusion. The physicians precipitated the patient’s hypotension by giving her an excessive dose of morphine and bupivacaine via epidural catheter prior to induction of general anesthesia, and then failed to give her sufficient doses of vasopressors to increase her BP to safe levels. They failed to properly treat the condition in a timely manner, causing brain damage, and ultimately, death.

DEFENDANTS’ DEFENSE:

The case was settled during mediation.

VERDICT:

A $900,000 Massachusetts settlement was reached.

Related Article:
Total abdominal hysterectomy the Mayo Clinic way

Ureter injured during hysterectomy

A 47-year-old woman’s right ureter was damaged during laparoscopic hysterectomy. During surgery, the gynecologist called in a urologist to repair the injury. The patient reported postsurgical complications including renal function impairment. A computed tomography scan showed a right ureter obstruction. When surgery confirmed complete obstruction of the ureter, she had a temporary nephrostomy drain placed. After 4 weeks, the patient returned to the operating room to have the right ureter implanted into the bladder. The patient reported occasional painful urination with increased urinary frequency and decreased right kidney size.

PATIENT’S CLAIM:

The gynecologist lacerated the ureter because he did not adequately identify and protect the ureter; this error represented a departure from the standard of care. The urologist failed to properly repair the injury. The patient sought recovery of $990,000 for past and future pain and suffering.

DEFENDANTS’ CLAIM:

The suit against the urologist and hospital was dropped, but continued against the gynecologist. The gynecologist claimed that the patient’s injury was a thermal burn, and is a known complication of the procedure.

VERDICT:

A $500,000 New York verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

The article by Hagerty and Rich in this issue of the Cleveland Clinic Journal of Medicine¹ covers an important topic—whether elderly patients with atrial fibrillation should receive anticoagulant therapy for it, or whether the risk of bleeding with this therapy outweighs the benefit of preventing stroke.

See related article

BETTER RISK PREDICTORS ARE NEEDED

Prediction tools are available for estimating the risk of stroke in patients with atrial fibrillation without anticoagulation^2,3 and to estimate bleeding risk from anticoagulation^4–7 (Table 1). Both tools have limitations, but as Hagerty and Rich point out, the stroke risk scales are likely better than the bleeding risk scales.

For example, Fang et al⁸ note that the risk of intracranial hemorrhage increases significantly after age 85. The bleeding risk scales use lower age cutoffs than this, perhaps increasing their sensitivity but decreasing their specificity.

Although HAS-BLED^5,6 includes antiplatelet drugs such as nonsteroidal anti-inflammatory drugs and aspirin as risk factors for bleeding, ATRIA⁴ and HEMORR₂HAGES⁷ do not.

Other drugs such as macrolides, quinolones, and high-dose corticosteroids raise the international normalized ratio (INR). These are typically used short-term, but can cause major fluctuations in the INR that may not be detected by monthly INR checks. Incorporating the short-term use of such drugs into bleeding risk scales would be difficult if not impossible a priori. Yet clinicians should be aware that these drugs can affect bleeding risk.

As Hagerty and Rich note,¹ the bleeding risk scores were developed for warfarin, and their applicability to patients treated with novel oral anticoagulants is uncertain.

All three of the available bleeding risk scales consider prior bleeding as a risk factor, but the severity of the prior bleeding varies. Although it is understandable to include major bleeding as a risk factor since it carries an increased risk of death, minor bleeding can affect morbidity and quality of life. Only the ATRIA score⁴ considers both major and minor bleeding, while HEMORR₂HAGES⁷ does not specify bleeding severity, and HAS-BLED^5,6 considers only major bleeding. Clearly, there is a need to update these existing bleeding risk scores so that they can apply to novel oral anticoagulants and consider both major and minor bleeding.

As the authors note, for predicting the risk of stroke, the CHA₂DS₂-VASc score³ provides more precision than the CHADS₂ score² at the lower end of the benefit spectrum. Unfortunately, there is no similar screening tool to predict bleeding risk from anticoagulation with greater precision in the middle to lower part of the risk spectrum.

THE PATIENT’S PREFERENCES MATTER

The patient’s life expectancy and personal preferences are important independent factors that affect the decision of whether to anticoagulate or not. It is the responsibility of clinicians who care for older adults to make sure that these two important considerations are included in any anticoagulation decision-making for this group of patients.

The article by Hagerty and Rich in this issue of the Cleveland Clinic Journal of Medicine¹ covers an important topic—whether elderly patients with atrial fibrillation should receive anticoagulant therapy for it, or whether the risk of bleeding with this therapy outweighs the benefit of preventing stroke.

See related article

BETTER RISK PREDICTORS ARE NEEDED

Prediction tools are available for estimating the risk of stroke in patients with atrial fibrillation without anticoagulation^2,3 and to estimate bleeding risk from anticoagulation^4–7 (Table 1). Both tools have limitations, but as Hagerty and Rich point out, the stroke risk scales are likely better than the bleeding risk scales.

For example, Fang et al⁸ note that the risk of intracranial hemorrhage increases significantly after age 85. The bleeding risk scales use lower age cutoffs than this, perhaps increasing their sensitivity but decreasing their specificity.

Although HAS-BLED^5,6 includes antiplatelet drugs such as nonsteroidal anti-inflammatory drugs and aspirin as risk factors for bleeding, ATRIA⁴ and HEMORR₂HAGES⁷ do not.

Other drugs such as macrolides, quinolones, and high-dose corticosteroids raise the international normalized ratio (INR). These are typically used short-term, but can cause major fluctuations in the INR that may not be detected by monthly INR checks. Incorporating the short-term use of such drugs into bleeding risk scales would be difficult if not impossible a priori. Yet clinicians should be aware that these drugs can affect bleeding risk.

As Hagerty and Rich note,¹ the bleeding risk scores were developed for warfarin, and their applicability to patients treated with novel oral anticoagulants is uncertain.

All three of the available bleeding risk scales consider prior bleeding as a risk factor, but the severity of the prior bleeding varies. Although it is understandable to include major bleeding as a risk factor since it carries an increased risk of death, minor bleeding can affect morbidity and quality of life. Only the ATRIA score⁴ considers both major and minor bleeding, while HEMORR₂HAGES⁷ does not specify bleeding severity, and HAS-BLED^5,6 considers only major bleeding. Clearly, there is a need to update these existing bleeding risk scores so that they can apply to novel oral anticoagulants and consider both major and minor bleeding.

As the authors note, for predicting the risk of stroke, the CHA₂DS₂-VASc score³ provides more precision than the CHADS₂ score² at the lower end of the benefit spectrum. Unfortunately, there is no similar screening tool to predict bleeding risk from anticoagulation with greater precision in the middle to lower part of the risk spectrum.

THE PATIENT’S PREFERENCES MATTER

The patient’s life expectancy and personal preferences are important independent factors that affect the decision of whether to anticoagulate or not. It is the responsibility of clinicians who care for older adults to make sure that these two important considerations are included in any anticoagulation decision-making for this group of patients.

The article by Hagerty and Rich in this issue of the Cleveland Clinic Journal of Medicine¹ covers an important topic—whether elderly patients with atrial fibrillation should receive anticoagulant therapy for it, or whether the risk of bleeding with this therapy outweighs the benefit of preventing stroke.

See related article

BETTER RISK PREDICTORS ARE NEEDED

Prediction tools are available for estimating the risk of stroke in patients with atrial fibrillation without anticoagulation^2,3 and to estimate bleeding risk from anticoagulation^4–7 (Table 1). Both tools have limitations, but as Hagerty and Rich point out, the stroke risk scales are likely better than the bleeding risk scales.

For example, Fang et al⁸ note that the risk of intracranial hemorrhage increases significantly after age 85. The bleeding risk scales use lower age cutoffs than this, perhaps increasing their sensitivity but decreasing their specificity.

Although HAS-BLED^5,6 includes antiplatelet drugs such as nonsteroidal anti-inflammatory drugs and aspirin as risk factors for bleeding, ATRIA⁴ and HEMORR₂HAGES⁷ do not.

Other drugs such as macrolides, quinolones, and high-dose corticosteroids raise the international normalized ratio (INR). These are typically used short-term, but can cause major fluctuations in the INR that may not be detected by monthly INR checks. Incorporating the short-term use of such drugs into bleeding risk scales would be difficult if not impossible a priori. Yet clinicians should be aware that these drugs can affect bleeding risk.

As Hagerty and Rich note,¹ the bleeding risk scores were developed for warfarin, and their applicability to patients treated with novel oral anticoagulants is uncertain.

All three of the available bleeding risk scales consider prior bleeding as a risk factor, but the severity of the prior bleeding varies. Although it is understandable to include major bleeding as a risk factor since it carries an increased risk of death, minor bleeding can affect morbidity and quality of life. Only the ATRIA score⁴ considers both major and minor bleeding, while HEMORR₂HAGES⁷ does not specify bleeding severity, and HAS-BLED^5,6 considers only major bleeding. Clearly, there is a need to update these existing bleeding risk scores so that they can apply to novel oral anticoagulants and consider both major and minor bleeding.

As the authors note, for predicting the risk of stroke, the CHA₂DS₂-VASc score³ provides more precision than the CHADS₂ score² at the lower end of the benefit spectrum. Unfortunately, there is no similar screening tool to predict bleeding risk from anticoagulation with greater precision in the middle to lower part of the risk spectrum.

THE PATIENT’S PREFERENCES MATTER

The patient’s life expectancy and personal preferences are important independent factors that affect the decision of whether to anticoagulate or not. It is the responsibility of clinicians who care for older adults to make sure that these two important considerations are included in any anticoagulation decision-making for this group of patients.

People who have been exposed to an infectious disease should be evaluated promptly and systematically, whether they are healthcare professionals at work,¹ patients, or contacts of patients. The primary goals are to prevent acquisition and transmission of the infection, allay the exposed person’s anxiety, and avoid unnecessary interventions and loss of work days.^1,2 Some may need postexposure prophylaxis.

ESSENTIAL ELEMENTS OF POSTEXPOSURE MANAGEMENT

Because postexposure management can be challenging, an experienced clinician or expert consultant (eg, infectious disease specialist, infection control provider, or public health officer) should be involved. Institution-specific policies and procedures for postexposure prophylaxis and testing should be followed.^1,2

Postexposure management should include the following elements:

• Immediate care of the wound or other site of exposure in cases of blood-borne exposures and tetanus- and rabies-prone injuries. This includes thoroughly washing with soap and water or cleansing with an antiseptic agent, flushing affected mucous membranes with water, and debridement of devitalized tissue.^1–6
• Deciding whether postexposure prophylaxis is indicated and, if so, the type, dose, route, and duration.
• Initiating prophylaxis as soon as possible.
• Determining an appropriate baseline assessment and follow-up plan for the exposed individual.
• Counseling exposed women who are pregnant or breast-feeding about the risks and benefits of postexposure prophylaxis to mother, fetus, and infant.
• Identifying required infection control precautions, including work and school restriction, for exposed and source individuals.
• Counseling and psychological support for exposed individuals, who need to know about the risks of acquiring the infection and transmitting it to others, infection control precautions, benefits, and adverse effects of postexposure prophylaxis, the importance of adhering to the regimen, and the follow-up plan. They must understand that this treatment may not completely prevent the infection, and they should seek medical attention if they develop fever or any symptoms or signs of the infection of concern.^1,2

IS POSTEXPOSURE PROPHYLAXIS INDICATED?

Postexposure management begins with an assessment to determine whether the exposure is likely to result in infection; whether the exposed individual is susceptible to the infection of concern or is at greater risk of complications from it than the general population; and whether postexposure prophylaxis is needed. This involves a complete focused history, physical examination, and laboratory testing of the potentially exposed individual and of the source, if possible.^1,2

Postexposure prophylaxis should begin as soon as possible to maximize its effects while awaiting the results of further diagnostic tests. However, if the exposed individual seeks care after the recommended period, prophylactic therapy can still be effective for certain infections that have a long incubation period, such as tetanus and rabies.^5,6 The choice of regimen should be guided by efficacy, safety, cost, toxicity, ease of adherence, drug interactions, and antimicrobial resistance.^1,2

HOW GREAT IS THE RISK OF INFECTION?

Exposed individuals are not all at the same risk of acquiring a given infection. The risk depends on:

• Type and extent of exposure (see below)
• Characteristics of the infectious agent (eg, virulence, infectious dose)
• Status of the infectious source (eg, whether the disease is in its infectious period or is being treated); effective treatment can shorten the duration of microbial shedding and subsequently reduce risk of transmission of certain infections such as tuberculosis, meningococcal infection, invasive group A streptococcal infection, and pertussis^7–10
• Immune status of the exposed individual (eg, prior infection or vaccination), since people who are immune to the infection of concern usually do not need postexposure prophylaxis²
• Adherence to infection prevention and control principles; postexposure prophylaxis may not be required if the potentially exposed individual was wearing appropriate personal protective equipment such as a surgical mask, gown, and gloves and was following standard precautions.¹

WHO SHOULD BE RESTRICTED FROM WORK OR SCHOOL?

Most people without symptoms who were exposed to most types of infections do not need to stay home from work or school. However, susceptible people, particularly healthcare providers exposed to measles, mumps, rubella, and varicella, should be excluded from work while they are capable of transmitting these diseases, even if they have no symptoms.^11,12 Moreover, people with symptoms with infections primarily transmitted via the airborne, droplet, or contact route should be restricted from work until no longer infectious.^1,2,7,9–15

Most healthcare institutions have clear protocols for managing occupational exposures to infectious diseases, in particular for blood-borne pathogens such as human immunodeficiency virus (HIV). The protocol should include appropriate evaluation and laboratory testing of the source patient and exposed healthcare provider, as well as procedures for counseling the exposed provider, identifying and procuring an initial prophylactic regimen for timely administration, a mechanism for formal expert consultation (eg, with an in-house infectious diseases consultant), and a plan for outpatient follow-up.

The next section reviews postexposure management of common infections categorized by mode of transmission, including the risk of transmission, initial and follow-up evaluation, and considerations for postexposure prophylaxis.

BLOOD-BORNE INFECTIONS

Blood-borne pathogens can be transmitted by accidental needlesticks or cuts or by exposure of the eyes, mucous membranes, or nonintact skin to blood, tissue, or other potentially infectious body fluids—cerebrospinal, pericardial, pleural, peritoneal, synovial, and amniotic fluid, semen, and vaginal secretions. (Feces, nasal secretions, saliva, sputum, sweat, tears, urine, and vomitus are considered noninfectious for blood-borne pathogens unless they contain blood.¹⁶)

Healthcare professionals are commonly exposed to blood-borne pathogens as a result of needlestick injuries, and these exposures tend to be underreported.¹⁷

When someone has been exposed to blood or other infectious body fluids, the source individual and the exposed individual should be assessed for risk factors for hepatitis B virus, hepatitis C virus, HIV, and other blood-borne pathogens.^3,4,16,18 If the disease status for these viruses is unknown, the source and exposed individual should be tested in accordance with institutional policies regarding consent to testing. Testing of needles or sharp instruments implicated in an exposure is not recommended.^3,4,16,18

Determining the need for prophylaxis after exposure to an unknown source such as a disposed needle can be challenging. Assessment should be made on a case-by-case basis, depending on the known prevalence of the infection of concern in the local community. The risk of transmission in most source-unknown exposures is negligible.^3,4,18 However, hepatitis B vaccine and hepatitis B immunoglobulin should be used liberally as postexposure prophylaxis for previously unvaccinated healthcare providers exposed to an unknown source.^3,4,16,18

Hepatitis B

Hepatitis B virus (Table 1) is the most infectious of the common blood-borne viruses. The risk of transmission after percutaneous exposure to hepatitis B-infected blood ranges from 1% to 30% based on hepatitis Be antigen status and viral load (based on hepatitis B viral DNA).^1,2,4,16

Hepatitis B vaccine or immunoglobulin, or both, are recommended for postexposure prophylaxis in pregnant women, based on evidence that perinatal transmission was reduced by 70% to 90% when these were given within 12 to 24 hours of exposure.^4,16,19

Hepatitis C

The risk of infection after percutaneous exposure to hepatitis C virus-infected blood is estimated to be 1.8% per exposure.¹⁶ The risk is lower with exposure of a mucous membrane or nonintact skin to blood, fluids, or tissues from hepatitis C-infected patients.^16,18

Since there is no effective postexposure prophylactic regimen, the goal of postexposure assessment of hepatitis C is early identification of infection (by monitoring the patient to see if he or she seroconverts) and, if infection is present, referral to an experienced clinician for further evaluation (Table 1). However, data supporting the utility of direct-acting anti-hepatitis C antiviral drugs as postexposure prophylaxis after occupational exposure to hepatitis C are lacking.

Human immunodeficiency virus

The estimated risk of HIV transmission from a known infected source after percutaneous exposure is 0.3%, and after mucosal exposures it is 0.09%.²⁰

If postexposure prophylaxis is indicated, it should be a three-drug regimen (Table 1).^3,18 The recommended antiretroviral therapies have been proven effective in clinical trials of HIV treatment, not for postexposure prophylaxis per se, but they are recommended because they are effective, safe, tolerable, and associated with high adherence rates.^3,16,18,21 If the source individual is known to have HIV infection, information about his or her stage of infection, CD4+ T-cell count, results of viral load testing, current and previous antiretroviral therapy, and results of any genotypic viral resistance testing will guide the choice of postexposure prophylactic regimen.^3,18

The clinician should give the exposed patient a starter pack of 5 to 7 days of medication, give the first dose then and there, and arrange follow-up with an experienced clinician within a few days of the exposure to determine whether a complete 30-day course is needed.^3,16,18

SEXUALLY TRANSMITTED INFECTIONS

In the case of sexually transmitted infections, “exposure” means unprotected sexual contact with someone who has a sexually transmitted infection.²² People with sexually transmitted infections often have no symptoms but can still transmit the infection. Thus, people at risk should be identified and screened for all suspected sexually transmitted infections.^23–25

Patients with sexually transmitted infections should be instructed to refer their sex partners for evaluation and treatment to prevent further transmission and reinfection. Assessment of exposed partners includes a medical history, physical examination, microbiologic testing for all potential sexually transmitted infections, and eligibility for hepatitis A virus, hepatitis B virus, and human papillomavirus vaccines.²² Ideally, exposed partners should be reassessed within 1 to 2 weeks to follow up testing results and to monitor for side effects of and adherence to postexposure prophylaxis, if applicable.

Public health departments should be notified of sexually transmitted infections such as gonorrhea, chlamydia, chancroid, and syphilis.²²

Expedited partner therapy, in which index patients deliver the medication or a prescription for it directly to their partners, is an alternative for partner management where legally allowed by state and local health departments (see www.cdc.gov/std/ept/legal/).²²

Recommended postexposure prophylactic regimens for sexually transmitted infections (Table 2) are based on their efficacy in the treatment of these infections.^22,26–28 The regimen for HIV prophylaxis is the same as in Table 1.^3,18,26

Chlamydia

Chlamydia is the most commonly reported communicable disease in the United States. The risk of transmission after sexual intercourse with a person who has an active infection is approximately 65% and increases with the number of exposures.^22,29

Gonorrhea

Infection with Neisseria gonorrhoeae is the second most commonly reported communicable disease in the United States. The transmission rate of gonorrhea after sex with someone who has it ranges from 50% to 93%.²² When prescribing postexposure prophylaxis for gonorrhea, it is essential to consider the risk of antimicrobial resistance and local susceptibility data.²²

Human immunodeficiency virus

Risk of HIV transmission through sexual contact varies depending on the nature of the exposure, ranging from 0.05% to 0.5%.³⁰

Syphilis

The risk of transmission of syphilis in its early stages (primary and secondary) after sexual exposure is approximately 30%. Transmission requires open lesions such as chancres in primary syphilis and mucocutaneous lesions (mucous patches, condyloma lata) in secondary syphilis.²²

After sexual assault

In cases of sexual assault, the risk of sexually transmitted infections may be increased due to trauma and bleeding. Testing for all sexually transmitted infections, including HIV, should be considered on a case-by-case basis.²²

Survivors of sexual assault have been shown to be poorly compliant with follow-up visits, and thus provision of postexposure prophylaxis at the time of initial assessment is preferable to deferred treatment.²² The recommended regimen should cover chlamydia, gonorrhea, and trichomoniasis (a single dose of intramuscular ceftriaxone 250 mg, oral azithromycin 1 g, and either oral metronidazole 2 g or tinidazole 2 g), in addition to HIV if the victim presents within 72 hours of exposure (Table 2).^22,26

Hepatitis B virus vaccine, not immunoglobulin, should be given if the hepatitis status of the assailant is unknown and the survivor has not been previously vaccinated. Both hepatitis B vaccine and immunoglobulin should be given to unvaccinated survivors if the assailant is known to be hepatitis B surface antigen-positive.²²

Human papillomavirus vaccination is recommended for female survivors ages 9 to 26 and male survivors ages 9 to 21.

Emergency contraception should be given if there is a risk of pregnancy.^22,26

In many jurisdictions, sexual assault centers provide trained examiners through Sexual Assault Nurse Examiners to perform evidence collection and to provide initial contact with the aftercare resources of the center. 

Advice on medical management of sexual assault can be obtained by calling National PEPline (888–448–4911).

INFECTIONS TRANSMITTED BY THE AIRBORNE ROUTE

Airborne transmission of infections occurs by inhalation of droplet nuclei (diameter ≤ 5 μm) generated by coughing and sneezing. Certain procedures (eg, administration of nebulized medication, sputum induction, bronchoscopy) also generate droplets and aerosols, which can transmit organisms.¹

Measles

Measles (Table 3) is highly contagious; up to 90% of susceptible individuals develop measles after exposure. The virus is transmitted by direct contact with infectious droplets and by the airborne route. It remains infectious in the air and on surfaces for up to 2 hours; therefore, any type of exposure, even transient, is an indication for postexposure prophylaxis in susceptible individuals.¹¹

Both the measles, mumps, rubella (MMR) vaccine and immune globulin may prevent or modify disease severity in susceptible exposed individuals if given within 3 days of exposure (for the vaccine) or within 6 days of exposure (for immune globulin).^31,32

Tuberculosis

Mycobacterium tuberculosis is transmitted from patients with pulmonary or laryngeal tuberculosis, particularly if patients cough and are sputum-positive for acid-fast bacilli. Patients with extrapulmonary tuberculosis or latent tuberculosis infection are not infectious.^1,7

Postexposure management of tuberculosis occurs through contact investigation of a newly diagnosed index case of tuberculosis disease. Contacts are categorized as household contacts, close nonhousehold contacts (those having regular, extensive contact with the index case), casual contacts, and transient community contacts. The highest priority for contact investigations should be household contacts, close nonhousehold or casual contacts at high risk of progressing to tuberculosis disease (eg, those with HIV, those on dialysis, or transplant recipients), and unprotected healthcare providers exposed during aerosol-generating procedures.^7,33

Postexposure management includes screening exposed individuals for tuberculosis symptoms and performing tuberculin skin testing or interferon-gamma release assay (blood testing) for those who had previously negative results (Table 3). Chest radiography is recommended for exposed immunocompromised individuals, due to high risk of tuberculosis disease and low sensitivity of skin or blood testing, and for those with a documented history of tuberculosis or previous positive skin or blood test.^7,33,34

A positive tuberculin skin test for persons with recent contact with tuberculosis is defined as a wheal 5 mm or larger on baseline or follow-up screening. Prior bacillus Calmette-Guérin vaccination status should not be used in the interpretation of tuberculin skin testing in the setting of contact investigation.^7,33

All exposed asymptomatic people with a positive result on testing should be treated for latent tuberculosis infection, since treatment reduces the risk of progression to tuberculosis disease by 60% to 90% .^7,33,35–37

Varicella and disseminated herpes zoster

Varicella zoster virus is transmitted by direct contact with vesicular fluid of skin lesions and inhalation of aerosols from vesicular fluid or respiratory tract secretions. Varicella (chickenpox) is highly contagious, with a secondary attack rate in susceptible household contacts of 85%.¹² Herpes zoster is less contagious than varicella.³⁸

Postexposure prophylaxis against varicella is recommended for susceptible individuals who had household exposure, had face-to-face contact with an infectious patient while indoors, or shared the same hospital room with the patient.¹²

Postexposure prophylactic options for varicella and herpes zoster include varicella vaccine (not zoster vaccine) and varicella zoster immune globulin (Table 3).^12,38–40

Varicella vaccine is approximately 90% effective if given within 3 days of exposure, and 70% effective if given within 5 days.^12,39

Antiviral agents should be given if the exposed individual develops manifestations of varicella or herpes zoster.^12,38

INFECTIONS TRANSMITTED BY THE DROPLET ROUTE

Droplet transmission occurs when respiratory droplets carrying infectious agents travel directly across short distances (3–6 feet) from the respiratory tract of the infected to mucosal surfaces of the susceptible exposed individual. Droplets are generated during coughing, sneezing, talking, and aerosol-generating procedures. Indirect contact with droplets can also transmit infection.¹

Group A streptococcal infection

Although group A streptococcal infection (Table 4) may spread to close contacts of the index case and in closed populations (eg, military recruit camps, schools, institutions), secondary cases of invasive group A streptococcal infection rarely occur in family and institutional contacts.^9,41,42

Postexposure prophylaxis for contacts of people with invasive group A streptococcal infection is debated, because it is unknown if antibiotic therapy will decrease the risk of acquiring the infection. It is generally agreed that it should not be routinely given to all contacts. The decision should be based on the clinician’s assessment of each individual’s risk and guidance from the local institution. If indicated, postexposure prophylaxis should be given to household and close contacts, particularly in high-risk groups (eg, Native Americans  and those with risk factors such as old age, HIV infection, diabetes mellitus, heart disease, chickenpox, cancer, systemic corticosteroid therapy, other immunosuppressive medications, intravenous drug use, recent surgery or childbirth).^9,41,42

Influenza

Influenza (Table 4) causes a significant burden in healthcare settings, given its prevalence and potential to cause outbreaks of severe respiratory illness in hospitalized patients and residents of long-term-care facilities.^13,43

Neuraminidase inhibitors are effective as prophylaxis after unprotected exposure to influenza, particularly in outbreak situations. However, their use is not widely recommended, since overuse could lead to antiviral resistance. In selected cases, postexposure prophylaxis may be indicated for close contacts who are at high risk of complications of influenza (eg, age 65 or older, in third trimester of pregnancy or 2 weeks postpartum, morbid obesity, chronic comorbid conditions such as a cardiopulmonary and renal disorder, immunocompromising condition) or who are in close contact with persons at high risk of influenza-related complications.^13,44,45

Meningococcal disease

N meningitidis is transmitted from individuals with meningococcal disease or from asymptomatic carriers.⁸

Postexposure prophylaxis is effective in eradicating N meningiditis and is recommended for all close contacts of patients with invasive meningococcal disease (Table 4).⁴⁶­ Close contacts include household contacts, childcare and preschool contacts, contacts exposed in dormitories or military training centers, those who had direct contact with the index case’s respiratory secretions (eg, intimate kissing, mouth-to-mouth resuscitation, unprotected contact during endotracheal intubation or endotracheal tube management), and passengers seated directly next to an index case on airplane flights of longer than 8 hours.

Postexposure prophylaxis is not indicated for those who had brief contact, those who had contact that did not involve exposure to oral or respiratory secretions, or for close contacts of patients with N meningitidis isolated in nonsterile sites only (eg, oropharynyx, trachea, conjunctiva).^8,46

Pertussis

Pertussis is highly contagious, with a secondary attack rate of approximately 80% in susceptible individuals. Approximately one-third of susceptible household contacts develop pertussis after exposure.¹⁰

Postexposure prophylaxis for pertussis should be given to all household and close contacts (Table 4).^10,47

Rubella

Transmission occurs through droplets or direct contact with nasopharyngeal secretions of an infectious case. Neither MMR vaccine nor immunoglobulin has been shown to prevent rubella in exposed contacts, and they are not recommended.¹¹

INFECTIONS TRANSMITTED BY DIRECT CONTACT

Direct contact transmission includes infectious agents transmitted from an infected or colonized individual to another, whereas indirect contact transmission involves a contaminated intermediate object or person (eg, hands of healthcare providers, electronic thermometers, surgical instruments).¹

There are no available postexposure prophylactic regimens for the organisms most commonly transmitted by this route (eg, methicillin-resistant Staphylococcus aureus, Clostridium difficile), but transmission can be prevented with adherence to standard precautions, including hand hygiene.¹

Hepatitis A

Person-to-person transmission of hepatitis A virus occurs via the fecal-oral route. Common-source outbreaks and sporadic cases can occur from exposure to food or water contaminated with feces.^1,15

Postexposure prophylaxis is indicated only for nonimmune close contacts (eg, household and sexual contacts) (Table 5). Without this treatment, secondary attack rates of 15% to 30% have been reported among households.^15,48 Both hepatitis A vaccine and immune globulin are effective in preventing and ameliorating symptomatic hepatitis A infection. Advantages of vaccination include induction of longer-lasting immunity (at least 2 years), greater ease of administration, and lower cost than immune globulin.^15,48

Scabies

Scabies is an infestation of the skin by the mite Sarcoptes scabiei var hominis. Person-to-person transmission typically occurs through direct, prolonged skin-to-skin contact with an infested person (eg, household and sexual contacts). However, crusted scabies can be transmitted after brief skin-to-skin contact or by exposure to bedding, clothing, or furniture used by the infested person.

All potentially infested persons should be treated concomitantly (Table 5).^14,49

INFECTIONS TRANSMITTED BY MAMMAL BITES AND INJURIES

Bites and injury wounds account for approximately 1% of all visits to emergency departments.⁵⁰ Human bites are associated with a risk of infection by blood-borne pathogens, herpes simplex infection, and bacterial infections (eg, skin and soft-tissue infections, bacteremia). Animal bites are associated with a risk of bacterial infections, rabies, tetanus, hepatitis B virus, and monkeypox.⁵⁰

Rabies

Human rabies (Table 5) is almost always fatal. Essential factors in determining the need for postexposure prophylaxis include knowledge of the epidemiology of animal rabies in the area where the contact occurred and the species of animal involved, availability of the animal for observation or rabies testing, health status of the biting animal, and vaccination history of both the animal and exposed individual.⁶ Clinicians should seek assistance from public health officials for evaluating exposures and determining the need for postexposure prophylaxis in situations that are not routine.⁵¹

High-risk wild animals associated with rabies in North America include bats, raccoons, skunks, foxes, coyotes, bobcats, and woodchucks. Bats are the most common source of human rabies infections in the United States, and transmission can occur from minor, sometimes unnoticed, bites. The types of exposures that require postexposure prophylaxis include bites, abrasions, scratches, and contamination of mucous membranes or open wound with saliva or neural tissue of a suspected rabid animal.

Human-to-human transmission of rabies can rarely occur through exposure of mucous membrane or nonintact skin to an infectious material (saliva, tears, neural tissue), in addition to organ transplantation.⁶

Animal capture and testing is a strategy for excluding rabies risk and reducing the need for postexposure prophylaxis. A dog, cat, or ferret that bites a person should be confined and observed for 10 days without administering postexposure prophylaxis for rabies, unless the bite or exposure is on the face or neck, in which case this treatment should be given immediately.⁶ If the observed biting animal lives and remains healthy, postexposure prophylaxis is not recommended. However, if signs suggestive of rabies develop, postexposure prophylaxis should be given and the animal should be euthanized, with testing of brain tissue for rabies virus. Postexposure prophylaxis should be discontinued if rabies testing is negative.

The combination of rabies vaccine and human rabies immunoglobulin is nearly 100% effective in preventing rabies if administered in a timely and accurate fashion after exposure (Table 5).⁶

Tetanus

Tetanus transmission can occur through injuries ranging from small cuts to severe trauma and through contact with contaminated objects (eg, bites, nails, needles, splinters, neonates whose umbilical cord is cut with contaminated surgical instruments, and during circumcision or piercing with contaminated instruments).⁵

Tetanus is almost completely preventable with vaccination, and timely administration of postexposure prophylaxis (tetanus toxoid-containing vaccine, tetanus immune globulin) decreases disease severity (Table 5).^2,5,52

People who have been exposed to an infectious disease should be evaluated promptly and systematically, whether they are healthcare professionals at work,¹ patients, or contacts of patients. The primary goals are to prevent acquisition and transmission of the infection, allay the exposed person’s anxiety, and avoid unnecessary interventions and loss of work days.^1,2 Some may need postexposure prophylaxis.

ESSENTIAL ELEMENTS OF POSTEXPOSURE MANAGEMENT

Because postexposure management can be challenging, an experienced clinician or expert consultant (eg, infectious disease specialist, infection control provider, or public health officer) should be involved. Institution-specific policies and procedures for postexposure prophylaxis and testing should be followed.^1,2

Postexposure management should include the following elements:

• Immediate care of the wound or other site of exposure in cases of blood-borne exposures and tetanus- and rabies-prone injuries. This includes thoroughly washing with soap and water or cleansing with an antiseptic agent, flushing affected mucous membranes with water, and debridement of devitalized tissue.^1–6
• Deciding whether postexposure prophylaxis is indicated and, if so, the type, dose, route, and duration.
• Initiating prophylaxis as soon as possible.
• Determining an appropriate baseline assessment and follow-up plan for the exposed individual.
• Counseling exposed women who are pregnant or breast-feeding about the risks and benefits of postexposure prophylaxis to mother, fetus, and infant.
• Identifying required infection control precautions, including work and school restriction, for exposed and source individuals.
• Counseling and psychological support for exposed individuals, who need to know about the risks of acquiring the infection and transmitting it to others, infection control precautions, benefits, and adverse effects of postexposure prophylaxis, the importance of adhering to the regimen, and the follow-up plan. They must understand that this treatment may not completely prevent the infection, and they should seek medical attention if they develop fever or any symptoms or signs of the infection of concern.^1,2

IS POSTEXPOSURE PROPHYLAXIS INDICATED?

Postexposure management begins with an assessment to determine whether the exposure is likely to result in infection; whether the exposed individual is susceptible to the infection of concern or is at greater risk of complications from it than the general population; and whether postexposure prophylaxis is needed. This involves a complete focused history, physical examination, and laboratory testing of the potentially exposed individual and of the source, if possible.^1,2

Postexposure prophylaxis should begin as soon as possible to maximize its effects while awaiting the results of further diagnostic tests. However, if the exposed individual seeks care after the recommended period, prophylactic therapy can still be effective for certain infections that have a long incubation period, such as tetanus and rabies.^5,6 The choice of regimen should be guided by efficacy, safety, cost, toxicity, ease of adherence, drug interactions, and antimicrobial resistance.^1,2

HOW GREAT IS THE RISK OF INFECTION?

Exposed individuals are not all at the same risk of acquiring a given infection. The risk depends on:

• Type and extent of exposure (see below)
• Characteristics of the infectious agent (eg, virulence, infectious dose)
• Status of the infectious source (eg, whether the disease is in its infectious period or is being treated); effective treatment can shorten the duration of microbial shedding and subsequently reduce risk of transmission of certain infections such as tuberculosis, meningococcal infection, invasive group A streptococcal infection, and pertussis^7–10
• Immune status of the exposed individual (eg, prior infection or vaccination), since people who are immune to the infection of concern usually do not need postexposure prophylaxis²
• Adherence to infection prevention and control principles; postexposure prophylaxis may not be required if the potentially exposed individual was wearing appropriate personal protective equipment such as a surgical mask, gown, and gloves and was following standard precautions.¹

WHO SHOULD BE RESTRICTED FROM WORK OR SCHOOL?

Most people without symptoms who were exposed to most types of infections do not need to stay home from work or school. However, susceptible people, particularly healthcare providers exposed to measles, mumps, rubella, and varicella, should be excluded from work while they are capable of transmitting these diseases, even if they have no symptoms.^11,12 Moreover, people with symptoms with infections primarily transmitted via the airborne, droplet, or contact route should be restricted from work until no longer infectious.^1,2,7,9–15

Most healthcare institutions have clear protocols for managing occupational exposures to infectious diseases, in particular for blood-borne pathogens such as human immunodeficiency virus (HIV). The protocol should include appropriate evaluation and laboratory testing of the source patient and exposed healthcare provider, as well as procedures for counseling the exposed provider, identifying and procuring an initial prophylactic regimen for timely administration, a mechanism for formal expert consultation (eg, with an in-house infectious diseases consultant), and a plan for outpatient follow-up.

The next section reviews postexposure management of common infections categorized by mode of transmission, including the risk of transmission, initial and follow-up evaluation, and considerations for postexposure prophylaxis.

BLOOD-BORNE INFECTIONS

Blood-borne pathogens can be transmitted by accidental needlesticks or cuts or by exposure of the eyes, mucous membranes, or nonintact skin to blood, tissue, or other potentially infectious body fluids—cerebrospinal, pericardial, pleural, peritoneal, synovial, and amniotic fluid, semen, and vaginal secretions. (Feces, nasal secretions, saliva, sputum, sweat, tears, urine, and vomitus are considered noninfectious for blood-borne pathogens unless they contain blood.¹⁶)

Healthcare professionals are commonly exposed to blood-borne pathogens as a result of needlestick injuries, and these exposures tend to be underreported.¹⁷

When someone has been exposed to blood or other infectious body fluids, the source individual and the exposed individual should be assessed for risk factors for hepatitis B virus, hepatitis C virus, HIV, and other blood-borne pathogens.^3,4,16,18 If the disease status for these viruses is unknown, the source and exposed individual should be tested in accordance with institutional policies regarding consent to testing. Testing of needles or sharp instruments implicated in an exposure is not recommended.^3,4,16,18

Determining the need for prophylaxis after exposure to an unknown source such as a disposed needle can be challenging. Assessment should be made on a case-by-case basis, depending on the known prevalence of the infection of concern in the local community. The risk of transmission in most source-unknown exposures is negligible.^3,4,18 However, hepatitis B vaccine and hepatitis B immunoglobulin should be used liberally as postexposure prophylaxis for previously unvaccinated healthcare providers exposed to an unknown source.^3,4,16,18

Hepatitis B

Hepatitis B virus (Table 1) is the most infectious of the common blood-borne viruses. The risk of transmission after percutaneous exposure to hepatitis B-infected blood ranges from 1% to 30% based on hepatitis Be antigen status and viral load (based on hepatitis B viral DNA).^1,2,4,16

Hepatitis B vaccine or immunoglobulin, or both, are recommended for postexposure prophylaxis in pregnant women, based on evidence that perinatal transmission was reduced by 70% to 90% when these were given within 12 to 24 hours of exposure.^4,16,19

Hepatitis C

The risk of infection after percutaneous exposure to hepatitis C virus-infected blood is estimated to be 1.8% per exposure.¹⁶ The risk is lower with exposure of a mucous membrane or nonintact skin to blood, fluids, or tissues from hepatitis C-infected patients.^16,18

Since there is no effective postexposure prophylactic regimen, the goal of postexposure assessment of hepatitis C is early identification of infection (by monitoring the patient to see if he or she seroconverts) and, if infection is present, referral to an experienced clinician for further evaluation (Table 1). However, data supporting the utility of direct-acting anti-hepatitis C antiviral drugs as postexposure prophylaxis after occupational exposure to hepatitis C are lacking.

Human immunodeficiency virus

The estimated risk of HIV transmission from a known infected source after percutaneous exposure is 0.3%, and after mucosal exposures it is 0.09%.²⁰

If postexposure prophylaxis is indicated, it should be a three-drug regimen (Table 1).^3,18 The recommended antiretroviral therapies have been proven effective in clinical trials of HIV treatment, not for postexposure prophylaxis per se, but they are recommended because they are effective, safe, tolerable, and associated with high adherence rates.^3,16,18,21 If the source individual is known to have HIV infection, information about his or her stage of infection, CD4+ T-cell count, results of viral load testing, current and previous antiretroviral therapy, and results of any genotypic viral resistance testing will guide the choice of postexposure prophylactic regimen.^3,18

The clinician should give the exposed patient a starter pack of 5 to 7 days of medication, give the first dose then and there, and arrange follow-up with an experienced clinician within a few days of the exposure to determine whether a complete 30-day course is needed.^3,16,18

SEXUALLY TRANSMITTED INFECTIONS

In the case of sexually transmitted infections, “exposure” means unprotected sexual contact with someone who has a sexually transmitted infection.²² People with sexually transmitted infections often have no symptoms but can still transmit the infection. Thus, people at risk should be identified and screened for all suspected sexually transmitted infections.^23–25

Patients with sexually transmitted infections should be instructed to refer their sex partners for evaluation and treatment to prevent further transmission and reinfection. Assessment of exposed partners includes a medical history, physical examination, microbiologic testing for all potential sexually transmitted infections, and eligibility for hepatitis A virus, hepatitis B virus, and human papillomavirus vaccines.²² Ideally, exposed partners should be reassessed within 1 to 2 weeks to follow up testing results and to monitor for side effects of and adherence to postexposure prophylaxis, if applicable.

Public health departments should be notified of sexually transmitted infections such as gonorrhea, chlamydia, chancroid, and syphilis.²²

Expedited partner therapy, in which index patients deliver the medication or a prescription for it directly to their partners, is an alternative for partner management where legally allowed by state and local health departments (see www.cdc.gov/std/ept/legal/).²²

Recommended postexposure prophylactic regimens for sexually transmitted infections (Table 2) are based on their efficacy in the treatment of these infections.^22,26–28 The regimen for HIV prophylaxis is the same as in Table 1.^3,18,26

Chlamydia

Chlamydia is the most commonly reported communicable disease in the United States. The risk of transmission after sexual intercourse with a person who has an active infection is approximately 65% and increases with the number of exposures.^22,29

Gonorrhea

Infection with Neisseria gonorrhoeae is the second most commonly reported communicable disease in the United States. The transmission rate of gonorrhea after sex with someone who has it ranges from 50% to 93%.²² When prescribing postexposure prophylaxis for gonorrhea, it is essential to consider the risk of antimicrobial resistance and local susceptibility data.²²

Human immunodeficiency virus

Risk of HIV transmission through sexual contact varies depending on the nature of the exposure, ranging from 0.05% to 0.5%.³⁰

Syphilis

The risk of transmission of syphilis in its early stages (primary and secondary) after sexual exposure is approximately 30%. Transmission requires open lesions such as chancres in primary syphilis and mucocutaneous lesions (mucous patches, condyloma lata) in secondary syphilis.²²

After sexual assault

In cases of sexual assault, the risk of sexually transmitted infections may be increased due to trauma and bleeding. Testing for all sexually transmitted infections, including HIV, should be considered on a case-by-case basis.²²

Survivors of sexual assault have been shown to be poorly compliant with follow-up visits, and thus provision of postexposure prophylaxis at the time of initial assessment is preferable to deferred treatment.²² The recommended regimen should cover chlamydia, gonorrhea, and trichomoniasis (a single dose of intramuscular ceftriaxone 250 mg, oral azithromycin 1 g, and either oral metronidazole 2 g or tinidazole 2 g), in addition to HIV if the victim presents within 72 hours of exposure (Table 2).^22,26

Hepatitis B virus vaccine, not immunoglobulin, should be given if the hepatitis status of the assailant is unknown and the survivor has not been previously vaccinated. Both hepatitis B vaccine and immunoglobulin should be given to unvaccinated survivors if the assailant is known to be hepatitis B surface antigen-positive.²²

Human papillomavirus vaccination is recommended for female survivors ages 9 to 26 and male survivors ages 9 to 21.

Emergency contraception should be given if there is a risk of pregnancy.^22,26

In many jurisdictions, sexual assault centers provide trained examiners through Sexual Assault Nurse Examiners to perform evidence collection and to provide initial contact with the aftercare resources of the center. 

Advice on medical management of sexual assault can be obtained by calling National PEPline (888–448–4911).

INFECTIONS TRANSMITTED BY THE AIRBORNE ROUTE

Airborne transmission of infections occurs by inhalation of droplet nuclei (diameter ≤ 5 μm) generated by coughing and sneezing. Certain procedures (eg, administration of nebulized medication, sputum induction, bronchoscopy) also generate droplets and aerosols, which can transmit organisms.¹

Measles

Measles (Table 3) is highly contagious; up to 90% of susceptible individuals develop measles after exposure. The virus is transmitted by direct contact with infectious droplets and by the airborne route. It remains infectious in the air and on surfaces for up to 2 hours; therefore, any type of exposure, even transient, is an indication for postexposure prophylaxis in susceptible individuals.¹¹

Both the measles, mumps, rubella (MMR) vaccine and immune globulin may prevent or modify disease severity in susceptible exposed individuals if given within 3 days of exposure (for the vaccine) or within 6 days of exposure (for immune globulin).^31,32

Tuberculosis

Mycobacterium tuberculosis is transmitted from patients with pulmonary or laryngeal tuberculosis, particularly if patients cough and are sputum-positive for acid-fast bacilli. Patients with extrapulmonary tuberculosis or latent tuberculosis infection are not infectious.^1,7

Postexposure management of tuberculosis occurs through contact investigation of a newly diagnosed index case of tuberculosis disease. Contacts are categorized as household contacts, close nonhousehold contacts (those having regular, extensive contact with the index case), casual contacts, and transient community contacts. The highest priority for contact investigations should be household contacts, close nonhousehold or casual contacts at high risk of progressing to tuberculosis disease (eg, those with HIV, those on dialysis, or transplant recipients), and unprotected healthcare providers exposed during aerosol-generating procedures.^7,33

Postexposure management includes screening exposed individuals for tuberculosis symptoms and performing tuberculin skin testing or interferon-gamma release assay (blood testing) for those who had previously negative results (Table 3). Chest radiography is recommended for exposed immunocompromised individuals, due to high risk of tuberculosis disease and low sensitivity of skin or blood testing, and for those with a documented history of tuberculosis or previous positive skin or blood test.^7,33,34

A positive tuberculin skin test for persons with recent contact with tuberculosis is defined as a wheal 5 mm or larger on baseline or follow-up screening. Prior bacillus Calmette-Guérin vaccination status should not be used in the interpretation of tuberculin skin testing in the setting of contact investigation.^7,33

All exposed asymptomatic people with a positive result on testing should be treated for latent tuberculosis infection, since treatment reduces the risk of progression to tuberculosis disease by 60% to 90% .^7,33,35–37

Varicella and disseminated herpes zoster

Varicella zoster virus is transmitted by direct contact with vesicular fluid of skin lesions and inhalation of aerosols from vesicular fluid or respiratory tract secretions. Varicella (chickenpox) is highly contagious, with a secondary attack rate in susceptible household contacts of 85%.¹² Herpes zoster is less contagious than varicella.³⁸

Postexposure prophylaxis against varicella is recommended for susceptible individuals who had household exposure, had face-to-face contact with an infectious patient while indoors, or shared the same hospital room with the patient.¹²

Postexposure prophylactic options for varicella and herpes zoster include varicella vaccine (not zoster vaccine) and varicella zoster immune globulin (Table 3).^12,38–40

Varicella vaccine is approximately 90% effective if given within 3 days of exposure, and 70% effective if given within 5 days.^12,39

Antiviral agents should be given if the exposed individual develops manifestations of varicella or herpes zoster.^12,38

INFECTIONS TRANSMITTED BY THE DROPLET ROUTE

Droplet transmission occurs when respiratory droplets carrying infectious agents travel directly across short distances (3–6 feet) from the respiratory tract of the infected to mucosal surfaces of the susceptible exposed individual. Droplets are generated during coughing, sneezing, talking, and aerosol-generating procedures. Indirect contact with droplets can also transmit infection.¹

Group A streptococcal infection

Although group A streptococcal infection (Table 4) may spread to close contacts of the index case and in closed populations (eg, military recruit camps, schools, institutions), secondary cases of invasive group A streptococcal infection rarely occur in family and institutional contacts.^9,41,42

Postexposure prophylaxis for contacts of people with invasive group A streptococcal infection is debated, because it is unknown if antibiotic therapy will decrease the risk of acquiring the infection. It is generally agreed that it should not be routinely given to all contacts. The decision should be based on the clinician’s assessment of each individual’s risk and guidance from the local institution. If indicated, postexposure prophylaxis should be given to household and close contacts, particularly in high-risk groups (eg, Native Americans  and those with risk factors such as old age, HIV infection, diabetes mellitus, heart disease, chickenpox, cancer, systemic corticosteroid therapy, other immunosuppressive medications, intravenous drug use, recent surgery or childbirth).^9,41,42

Influenza

Influenza (Table 4) causes a significant burden in healthcare settings, given its prevalence and potential to cause outbreaks of severe respiratory illness in hospitalized patients and residents of long-term-care facilities.^13,43

Neuraminidase inhibitors are effective as prophylaxis after unprotected exposure to influenza, particularly in outbreak situations. However, their use is not widely recommended, since overuse could lead to antiviral resistance. In selected cases, postexposure prophylaxis may be indicated for close contacts who are at high risk of complications of influenza (eg, age 65 or older, in third trimester of pregnancy or 2 weeks postpartum, morbid obesity, chronic comorbid conditions such as a cardiopulmonary and renal disorder, immunocompromising condition) or who are in close contact with persons at high risk of influenza-related complications.^13,44,45

Meningococcal disease

N meningitidis is transmitted from individuals with meningococcal disease or from asymptomatic carriers.⁸

Postexposure prophylaxis is effective in eradicating N meningiditis and is recommended for all close contacts of patients with invasive meningococcal disease (Table 4).⁴⁶­ Close contacts include household contacts, childcare and preschool contacts, contacts exposed in dormitories or military training centers, those who had direct contact with the index case’s respiratory secretions (eg, intimate kissing, mouth-to-mouth resuscitation, unprotected contact during endotracheal intubation or endotracheal tube management), and passengers seated directly next to an index case on airplane flights of longer than 8 hours.

Postexposure prophylaxis is not indicated for those who had brief contact, those who had contact that did not involve exposure to oral or respiratory secretions, or for close contacts of patients with N meningitidis isolated in nonsterile sites only (eg, oropharynyx, trachea, conjunctiva).^8,46

Pertussis

Pertussis is highly contagious, with a secondary attack rate of approximately 80% in susceptible individuals. Approximately one-third of susceptible household contacts develop pertussis after exposure.¹⁰

Postexposure prophylaxis for pertussis should be given to all household and close contacts (Table 4).^10,47

Rubella

Transmission occurs through droplets or direct contact with nasopharyngeal secretions of an infectious case. Neither MMR vaccine nor immunoglobulin has been shown to prevent rubella in exposed contacts, and they are not recommended.¹¹

INFECTIONS TRANSMITTED BY DIRECT CONTACT

Direct contact transmission includes infectious agents transmitted from an infected or colonized individual to another, whereas indirect contact transmission involves a contaminated intermediate object or person (eg, hands of healthcare providers, electronic thermometers, surgical instruments).¹

There are no available postexposure prophylactic regimens for the organisms most commonly transmitted by this route (eg, methicillin-resistant Staphylococcus aureus, Clostridium difficile), but transmission can be prevented with adherence to standard precautions, including hand hygiene.¹

Hepatitis A

Person-to-person transmission of hepatitis A virus occurs via the fecal-oral route. Common-source outbreaks and sporadic cases can occur from exposure to food or water contaminated with feces.^1,15

Postexposure prophylaxis is indicated only for nonimmune close contacts (eg, household and sexual contacts) (Table 5). Without this treatment, secondary attack rates of 15% to 30% have been reported among households.^15,48 Both hepatitis A vaccine and immune globulin are effective in preventing and ameliorating symptomatic hepatitis A infection. Advantages of vaccination include induction of longer-lasting immunity (at least 2 years), greater ease of administration, and lower cost than immune globulin.^15,48

Scabies

Scabies is an infestation of the skin by the mite Sarcoptes scabiei var hominis. Person-to-person transmission typically occurs through direct, prolonged skin-to-skin contact with an infested person (eg, household and sexual contacts). However, crusted scabies can be transmitted after brief skin-to-skin contact or by exposure to bedding, clothing, or furniture used by the infested person.

All potentially infested persons should be treated concomitantly (Table 5).^14,49

INFECTIONS TRANSMITTED BY MAMMAL BITES AND INJURIES

Bites and injury wounds account for approximately 1% of all visits to emergency departments.⁵⁰ Human bites are associated with a risk of infection by blood-borne pathogens, herpes simplex infection, and bacterial infections (eg, skin and soft-tissue infections, bacteremia). Animal bites are associated with a risk of bacterial infections, rabies, tetanus, hepatitis B virus, and monkeypox.⁵⁰

Rabies

Human rabies (Table 5) is almost always fatal. Essential factors in determining the need for postexposure prophylaxis include knowledge of the epidemiology of animal rabies in the area where the contact occurred and the species of animal involved, availability of the animal for observation or rabies testing, health status of the biting animal, and vaccination history of both the animal and exposed individual.⁶ Clinicians should seek assistance from public health officials for evaluating exposures and determining the need for postexposure prophylaxis in situations that are not routine.⁵¹

High-risk wild animals associated with rabies in North America include bats, raccoons, skunks, foxes, coyotes, bobcats, and woodchucks. Bats are the most common source of human rabies infections in the United States, and transmission can occur from minor, sometimes unnoticed, bites. The types of exposures that require postexposure prophylaxis include bites, abrasions, scratches, and contamination of mucous membranes or open wound with saliva or neural tissue of a suspected rabid animal.

Human-to-human transmission of rabies can rarely occur through exposure of mucous membrane or nonintact skin to an infectious material (saliva, tears, neural tissue), in addition to organ transplantation.⁶

Animal capture and testing is a strategy for excluding rabies risk and reducing the need for postexposure prophylaxis. A dog, cat, or ferret that bites a person should be confined and observed for 10 days without administering postexposure prophylaxis for rabies, unless the bite or exposure is on the face or neck, in which case this treatment should be given immediately.⁶ If the observed biting animal lives and remains healthy, postexposure prophylaxis is not recommended. However, if signs suggestive of rabies develop, postexposure prophylaxis should be given and the animal should be euthanized, with testing of brain tissue for rabies virus. Postexposure prophylaxis should be discontinued if rabies testing is negative.

The combination of rabies vaccine and human rabies immunoglobulin is nearly 100% effective in preventing rabies if administered in a timely and accurate fashion after exposure (Table 5).⁶

Tetanus

Tetanus transmission can occur through injuries ranging from small cuts to severe trauma and through contact with contaminated objects (eg, bites, nails, needles, splinters, neonates whose umbilical cord is cut with contaminated surgical instruments, and during circumcision or piercing with contaminated instruments).⁵

Tetanus is almost completely preventable with vaccination, and timely administration of postexposure prophylaxis (tetanus toxoid-containing vaccine, tetanus immune globulin) decreases disease severity (Table 5).^2,5,52

People who have been exposed to an infectious disease should be evaluated promptly and systematically, whether they are healthcare professionals at work,¹ patients, or contacts of patients. The primary goals are to prevent acquisition and transmission of the infection, allay the exposed person’s anxiety, and avoid unnecessary interventions and loss of work days.^1,2 Some may need postexposure prophylaxis.

ESSENTIAL ELEMENTS OF POSTEXPOSURE MANAGEMENT

Because postexposure management can be challenging, an experienced clinician or expert consultant (eg, infectious disease specialist, infection control provider, or public health officer) should be involved. Institution-specific policies and procedures for postexposure prophylaxis and testing should be followed.^1,2

Postexposure management should include the following elements:

• Immediate care of the wound or other site of exposure in cases of blood-borne exposures and tetanus- and rabies-prone injuries. This includes thoroughly washing with soap and water or cleansing with an antiseptic agent, flushing affected mucous membranes with water, and debridement of devitalized tissue.^1–6
• Deciding whether postexposure prophylaxis is indicated and, if so, the type, dose, route, and duration.
• Initiating prophylaxis as soon as possible.
• Determining an appropriate baseline assessment and follow-up plan for the exposed individual.
• Counseling exposed women who are pregnant or breast-feeding about the risks and benefits of postexposure prophylaxis to mother, fetus, and infant.
• Identifying required infection control precautions, including work and school restriction, for exposed and source individuals.
• Counseling and psychological support for exposed individuals, who need to know about the risks of acquiring the infection and transmitting it to others, infection control precautions, benefits, and adverse effects of postexposure prophylaxis, the importance of adhering to the regimen, and the follow-up plan. They must understand that this treatment may not completely prevent the infection, and they should seek medical attention if they develop fever or any symptoms or signs of the infection of concern.^1,2

IS POSTEXPOSURE PROPHYLAXIS INDICATED?

Postexposure management begins with an assessment to determine whether the exposure is likely to result in infection; whether the exposed individual is susceptible to the infection of concern or is at greater risk of complications from it than the general population; and whether postexposure prophylaxis is needed. This involves a complete focused history, physical examination, and laboratory testing of the potentially exposed individual and of the source, if possible.^1,2

Postexposure prophylaxis should begin as soon as possible to maximize its effects while awaiting the results of further diagnostic tests. However, if the exposed individual seeks care after the recommended period, prophylactic therapy can still be effective for certain infections that have a long incubation period, such as tetanus and rabies.^5,6 The choice of regimen should be guided by efficacy, safety, cost, toxicity, ease of adherence, drug interactions, and antimicrobial resistance.^1,2

HOW GREAT IS THE RISK OF INFECTION?

Exposed individuals are not all at the same risk of acquiring a given infection. The risk depends on:

• Type and extent of exposure (see below)
• Characteristics of the infectious agent (eg, virulence, infectious dose)
• Status of the infectious source (eg, whether the disease is in its infectious period or is being treated); effective treatment can shorten the duration of microbial shedding and subsequently reduce risk of transmission of certain infections such as tuberculosis, meningococcal infection, invasive group A streptococcal infection, and pertussis^7–10
• Immune status of the exposed individual (eg, prior infection or vaccination), since people who are immune to the infection of concern usually do not need postexposure prophylaxis²
• Adherence to infection prevention and control principles; postexposure prophylaxis may not be required if the potentially exposed individual was wearing appropriate personal protective equipment such as a surgical mask, gown, and gloves and was following standard precautions.¹

WHO SHOULD BE RESTRICTED FROM WORK OR SCHOOL?

Most people without symptoms who were exposed to most types of infections do not need to stay home from work or school. However, susceptible people, particularly healthcare providers exposed to measles, mumps, rubella, and varicella, should be excluded from work while they are capable of transmitting these diseases, even if they have no symptoms.^11,12 Moreover, people with symptoms with infections primarily transmitted via the airborne, droplet, or contact route should be restricted from work until no longer infectious.^1,2,7,9–15

Most healthcare institutions have clear protocols for managing occupational exposures to infectious diseases, in particular for blood-borne pathogens such as human immunodeficiency virus (HIV). The protocol should include appropriate evaluation and laboratory testing of the source patient and exposed healthcare provider, as well as procedures for counseling the exposed provider, identifying and procuring an initial prophylactic regimen for timely administration, a mechanism for formal expert consultation (eg, with an in-house infectious diseases consultant), and a plan for outpatient follow-up.

The next section reviews postexposure management of common infections categorized by mode of transmission, including the risk of transmission, initial and follow-up evaluation, and considerations for postexposure prophylaxis.

BLOOD-BORNE INFECTIONS

Blood-borne pathogens can be transmitted by accidental needlesticks or cuts or by exposure of the eyes, mucous membranes, or nonintact skin to blood, tissue, or other potentially infectious body fluids—cerebrospinal, pericardial, pleural, peritoneal, synovial, and amniotic fluid, semen, and vaginal secretions. (Feces, nasal secretions, saliva, sputum, sweat, tears, urine, and vomitus are considered noninfectious for blood-borne pathogens unless they contain blood.¹⁶)

Healthcare professionals are commonly exposed to blood-borne pathogens as a result of needlestick injuries, and these exposures tend to be underreported.¹⁷

When someone has been exposed to blood or other infectious body fluids, the source individual and the exposed individual should be assessed for risk factors for hepatitis B virus, hepatitis C virus, HIV, and other blood-borne pathogens.^3,4,16,18 If the disease status for these viruses is unknown, the source and exposed individual should be tested in accordance with institutional policies regarding consent to testing. Testing of needles or sharp instruments implicated in an exposure is not recommended.^3,4,16,18

Determining the need for prophylaxis after exposure to an unknown source such as a disposed needle can be challenging. Assessment should be made on a case-by-case basis, depending on the known prevalence of the infection of concern in the local community. The risk of transmission in most source-unknown exposures is negligible.^3,4,18 However, hepatitis B vaccine and hepatitis B immunoglobulin should be used liberally as postexposure prophylaxis for previously unvaccinated healthcare providers exposed to an unknown source.^3,4,16,18

Hepatitis B

Hepatitis B virus (Table 1) is the most infectious of the common blood-borne viruses. The risk of transmission after percutaneous exposure to hepatitis B-infected blood ranges from 1% to 30% based on hepatitis Be antigen status and viral load (based on hepatitis B viral DNA).^1,2,4,16

Hepatitis B vaccine or immunoglobulin, or both, are recommended for postexposure prophylaxis in pregnant women, based on evidence that perinatal transmission was reduced by 70% to 90% when these were given within 12 to 24 hours of exposure.^4,16,19

Hepatitis C

The risk of infection after percutaneous exposure to hepatitis C virus-infected blood is estimated to be 1.8% per exposure.¹⁶ The risk is lower with exposure of a mucous membrane or nonintact skin to blood, fluids, or tissues from hepatitis C-infected patients.^16,18

Since there is no effective postexposure prophylactic regimen, the goal of postexposure assessment of hepatitis C is early identification of infection (by monitoring the patient to see if he or she seroconverts) and, if infection is present, referral to an experienced clinician for further evaluation (Table 1). However, data supporting the utility of direct-acting anti-hepatitis C antiviral drugs as postexposure prophylaxis after occupational exposure to hepatitis C are lacking.

Human immunodeficiency virus

The estimated risk of HIV transmission from a known infected source after percutaneous exposure is 0.3%, and after mucosal exposures it is 0.09%.²⁰

If postexposure prophylaxis is indicated, it should be a three-drug regimen (Table 1).^3,18 The recommended antiretroviral therapies have been proven effective in clinical trials of HIV treatment, not for postexposure prophylaxis per se, but they are recommended because they are effective, safe, tolerable, and associated with high adherence rates.^3,16,18,21 If the source individual is known to have HIV infection, information about his or her stage of infection, CD4+ T-cell count, results of viral load testing, current and previous antiretroviral therapy, and results of any genotypic viral resistance testing will guide the choice of postexposure prophylactic regimen.^3,18

The clinician should give the exposed patient a starter pack of 5 to 7 days of medication, give the first dose then and there, and arrange follow-up with an experienced clinician within a few days of the exposure to determine whether a complete 30-day course is needed.^3,16,18

SEXUALLY TRANSMITTED INFECTIONS

In the case of sexually transmitted infections, “exposure” means unprotected sexual contact with someone who has a sexually transmitted infection.²² People with sexually transmitted infections often have no symptoms but can still transmit the infection. Thus, people at risk should be identified and screened for all suspected sexually transmitted infections.^23–25

Patients with sexually transmitted infections should be instructed to refer their sex partners for evaluation and treatment to prevent further transmission and reinfection. Assessment of exposed partners includes a medical history, physical examination, microbiologic testing for all potential sexually transmitted infections, and eligibility for hepatitis A virus, hepatitis B virus, and human papillomavirus vaccines.²² Ideally, exposed partners should be reassessed within 1 to 2 weeks to follow up testing results and to monitor for side effects of and adherence to postexposure prophylaxis, if applicable.

Public health departments should be notified of sexually transmitted infections such as gonorrhea, chlamydia, chancroid, and syphilis.²²

Expedited partner therapy, in which index patients deliver the medication or a prescription for it directly to their partners, is an alternative for partner management where legally allowed by state and local health departments (see www.cdc.gov/std/ept/legal/).²²

Recommended postexposure prophylactic regimens for sexually transmitted infections (Table 2) are based on their efficacy in the treatment of these infections.^22,26–28 The regimen for HIV prophylaxis is the same as in Table 1.^3,18,26

Chlamydia

Chlamydia is the most commonly reported communicable disease in the United States. The risk of transmission after sexual intercourse with a person who has an active infection is approximately 65% and increases with the number of exposures.^22,29

Gonorrhea

Infection with Neisseria gonorrhoeae is the second most commonly reported communicable disease in the United States. The transmission rate of gonorrhea after sex with someone who has it ranges from 50% to 93%.²² When prescribing postexposure prophylaxis for gonorrhea, it is essential to consider the risk of antimicrobial resistance and local susceptibility data.²²

Human immunodeficiency virus

Risk of HIV transmission through sexual contact varies depending on the nature of the exposure, ranging from 0.05% to 0.5%.³⁰

Syphilis

The risk of transmission of syphilis in its early stages (primary and secondary) after sexual exposure is approximately 30%. Transmission requires open lesions such as chancres in primary syphilis and mucocutaneous lesions (mucous patches, condyloma lata) in secondary syphilis.²²

After sexual assault

In cases of sexual assault, the risk of sexually transmitted infections may be increased due to trauma and bleeding. Testing for all sexually transmitted infections, including HIV, should be considered on a case-by-case basis.²²

Survivors of sexual assault have been shown to be poorly compliant with follow-up visits, and thus provision of postexposure prophylaxis at the time of initial assessment is preferable to deferred treatment.²² The recommended regimen should cover chlamydia, gonorrhea, and trichomoniasis (a single dose of intramuscular ceftriaxone 250 mg, oral azithromycin 1 g, and either oral metronidazole 2 g or tinidazole 2 g), in addition to HIV if the victim presents within 72 hours of exposure (Table 2).^22,26

Hepatitis B virus vaccine, not immunoglobulin, should be given if the hepatitis status of the assailant is unknown and the survivor has not been previously vaccinated. Both hepatitis B vaccine and immunoglobulin should be given to unvaccinated survivors if the assailant is known to be hepatitis B surface antigen-positive.²²

Human papillomavirus vaccination is recommended for female survivors ages 9 to 26 and male survivors ages 9 to 21.

Emergency contraception should be given if there is a risk of pregnancy.^22,26

In many jurisdictions, sexual assault centers provide trained examiners through Sexual Assault Nurse Examiners to perform evidence collection and to provide initial contact with the aftercare resources of the center. 

Advice on medical management of sexual assault can be obtained by calling National PEPline (888–448–4911).

INFECTIONS TRANSMITTED BY THE AIRBORNE ROUTE

Airborne transmission of infections occurs by inhalation of droplet nuclei (diameter ≤ 5 μm) generated by coughing and sneezing. Certain procedures (eg, administration of nebulized medication, sputum induction, bronchoscopy) also generate droplets and aerosols, which can transmit organisms.¹

Measles

Measles (Table 3) is highly contagious; up to 90% of susceptible individuals develop measles after exposure. The virus is transmitted by direct contact with infectious droplets and by the airborne route. It remains infectious in the air and on surfaces for up to 2 hours; therefore, any type of exposure, even transient, is an indication for postexposure prophylaxis in susceptible individuals.¹¹

Both the measles, mumps, rubella (MMR) vaccine and immune globulin may prevent or modify disease severity in susceptible exposed individuals if given within 3 days of exposure (for the vaccine) or within 6 days of exposure (for immune globulin).^31,32

Tuberculosis

Mycobacterium tuberculosis is transmitted from patients with pulmonary or laryngeal tuberculosis, particularly if patients cough and are sputum-positive for acid-fast bacilli. Patients with extrapulmonary tuberculosis or latent tuberculosis infection are not infectious.^1,7

Postexposure management of tuberculosis occurs through contact investigation of a newly diagnosed index case of tuberculosis disease. Contacts are categorized as household contacts, close nonhousehold contacts (those having regular, extensive contact with the index case), casual contacts, and transient community contacts. The highest priority for contact investigations should be household contacts, close nonhousehold or casual contacts at high risk of progressing to tuberculosis disease (eg, those with HIV, those on dialysis, or transplant recipients), and unprotected healthcare providers exposed during aerosol-generating procedures.^7,33

Postexposure management includes screening exposed individuals for tuberculosis symptoms and performing tuberculin skin testing or interferon-gamma release assay (blood testing) for those who had previously negative results (Table 3). Chest radiography is recommended for exposed immunocompromised individuals, due to high risk of tuberculosis disease and low sensitivity of skin or blood testing, and for those with a documented history of tuberculosis or previous positive skin or blood test.^7,33,34

A positive tuberculin skin test for persons with recent contact with tuberculosis is defined as a wheal 5 mm or larger on baseline or follow-up screening. Prior bacillus Calmette-Guérin vaccination status should not be used in the interpretation of tuberculin skin testing in the setting of contact investigation.^7,33

All exposed asymptomatic people with a positive result on testing should be treated for latent tuberculosis infection, since treatment reduces the risk of progression to tuberculosis disease by 60% to 90% .^7,33,35–37

Varicella and disseminated herpes zoster

Varicella zoster virus is transmitted by direct contact with vesicular fluid of skin lesions and inhalation of aerosols from vesicular fluid or respiratory tract secretions. Varicella (chickenpox) is highly contagious, with a secondary attack rate in susceptible household contacts of 85%.¹² Herpes zoster is less contagious than varicella.³⁸

Postexposure prophylaxis against varicella is recommended for susceptible individuals who had household exposure, had face-to-face contact with an infectious patient while indoors, or shared the same hospital room with the patient.¹²

Postexposure prophylactic options for varicella and herpes zoster include varicella vaccine (not zoster vaccine) and varicella zoster immune globulin (Table 3).^12,38–40

Varicella vaccine is approximately 90% effective if given within 3 days of exposure, and 70% effective if given within 5 days.^12,39

Antiviral agents should be given if the exposed individual develops manifestations of varicella or herpes zoster.^12,38

INFECTIONS TRANSMITTED BY THE DROPLET ROUTE

Droplet transmission occurs when respiratory droplets carrying infectious agents travel directly across short distances (3–6 feet) from the respiratory tract of the infected to mucosal surfaces of the susceptible exposed individual. Droplets are generated during coughing, sneezing, talking, and aerosol-generating procedures. Indirect contact with droplets can also transmit infection.¹

Group A streptococcal infection

Although group A streptococcal infection (Table 4) may spread to close contacts of the index case and in closed populations (eg, military recruit camps, schools, institutions), secondary cases of invasive group A streptococcal infection rarely occur in family and institutional contacts.^9,41,42

Postexposure prophylaxis for contacts of people with invasive group A streptococcal infection is debated, because it is unknown if antibiotic therapy will decrease the risk of acquiring the infection. It is generally agreed that it should not be routinely given to all contacts. The decision should be based on the clinician’s assessment of each individual’s risk and guidance from the local institution. If indicated, postexposure prophylaxis should be given to household and close contacts, particularly in high-risk groups (eg, Native Americans  and those with risk factors such as old age, HIV infection, diabetes mellitus, heart disease, chickenpox, cancer, systemic corticosteroid therapy, other immunosuppressive medications, intravenous drug use, recent surgery or childbirth).^9,41,42

Influenza

Influenza (Table 4) causes a significant burden in healthcare settings, given its prevalence and potential to cause outbreaks of severe respiratory illness in hospitalized patients and residents of long-term-care facilities.^13,43

Neuraminidase inhibitors are effective as prophylaxis after unprotected exposure to influenza, particularly in outbreak situations. However, their use is not widely recommended, since overuse could lead to antiviral resistance. In selected cases, postexposure prophylaxis may be indicated for close contacts who are at high risk of complications of influenza (eg, age 65 or older, in third trimester of pregnancy or 2 weeks postpartum, morbid obesity, chronic comorbid conditions such as a cardiopulmonary and renal disorder, immunocompromising condition) or who are in close contact with persons at high risk of influenza-related complications.^13,44,45

Meningococcal disease

N meningitidis is transmitted from individuals with meningococcal disease or from asymptomatic carriers.⁸

Postexposure prophylaxis is effective in eradicating N meningiditis and is recommended for all close contacts of patients with invasive meningococcal disease (Table 4).⁴⁶­ Close contacts include household contacts, childcare and preschool contacts, contacts exposed in dormitories or military training centers, those who had direct contact with the index case’s respiratory secretions (eg, intimate kissing, mouth-to-mouth resuscitation, unprotected contact during endotracheal intubation or endotracheal tube management), and passengers seated directly next to an index case on airplane flights of longer than 8 hours.

Postexposure prophylaxis is not indicated for those who had brief contact, those who had contact that did not involve exposure to oral or respiratory secretions, or for close contacts of patients with N meningitidis isolated in nonsterile sites only (eg, oropharynyx, trachea, conjunctiva).^8,46

Pertussis

Pertussis is highly contagious, with a secondary attack rate of approximately 80% in susceptible individuals. Approximately one-third of susceptible household contacts develop pertussis after exposure.¹⁰

Postexposure prophylaxis for pertussis should be given to all household and close contacts (Table 4).^10,47

Rubella

Transmission occurs through droplets or direct contact with nasopharyngeal secretions of an infectious case. Neither MMR vaccine nor immunoglobulin has been shown to prevent rubella in exposed contacts, and they are not recommended.¹¹

INFECTIONS TRANSMITTED BY DIRECT CONTACT

Direct contact transmission includes infectious agents transmitted from an infected or colonized individual to another, whereas indirect contact transmission involves a contaminated intermediate object or person (eg, hands of healthcare providers, electronic thermometers, surgical instruments).¹

There are no available postexposure prophylactic regimens for the organisms most commonly transmitted by this route (eg, methicillin-resistant Staphylococcus aureus, Clostridium difficile), but transmission can be prevented with adherence to standard precautions, including hand hygiene.¹

Hepatitis A

Person-to-person transmission of hepatitis A virus occurs via the fecal-oral route. Common-source outbreaks and sporadic cases can occur from exposure to food or water contaminated with feces.^1,15

Postexposure prophylaxis is indicated only for nonimmune close contacts (eg, household and sexual contacts) (Table 5). Without this treatment, secondary attack rates of 15% to 30% have been reported among households.^15,48 Both hepatitis A vaccine and immune globulin are effective in preventing and ameliorating symptomatic hepatitis A infection. Advantages of vaccination include induction of longer-lasting immunity (at least 2 years), greater ease of administration, and lower cost than immune globulin.^15,48

Scabies

Scabies is an infestation of the skin by the mite Sarcoptes scabiei var hominis. Person-to-person transmission typically occurs through direct, prolonged skin-to-skin contact with an infested person (eg, household and sexual contacts). However, crusted scabies can be transmitted after brief skin-to-skin contact or by exposure to bedding, clothing, or furniture used by the infested person.

All potentially infested persons should be treated concomitantly (Table 5).^14,49

INFECTIONS TRANSMITTED BY MAMMAL BITES AND INJURIES

Bites and injury wounds account for approximately 1% of all visits to emergency departments.⁵⁰ Human bites are associated with a risk of infection by blood-borne pathogens, herpes simplex infection, and bacterial infections (eg, skin and soft-tissue infections, bacteremia). Animal bites are associated with a risk of bacterial infections, rabies, tetanus, hepatitis B virus, and monkeypox.⁵⁰

Rabies

Human rabies (Table 5) is almost always fatal. Essential factors in determining the need for postexposure prophylaxis include knowledge of the epidemiology of animal rabies in the area where the contact occurred and the species of animal involved, availability of the animal for observation or rabies testing, health status of the biting animal, and vaccination history of both the animal and exposed individual.⁶ Clinicians should seek assistance from public health officials for evaluating exposures and determining the need for postexposure prophylaxis in situations that are not routine.⁵¹

High-risk wild animals associated with rabies in North America include bats, raccoons, skunks, foxes, coyotes, bobcats, and woodchucks. Bats are the most common source of human rabies infections in the United States, and transmission can occur from minor, sometimes unnoticed, bites. The types of exposures that require postexposure prophylaxis include bites, abrasions, scratches, and contamination of mucous membranes or open wound with saliva or neural tissue of a suspected rabid animal.

Human-to-human transmission of rabies can rarely occur through exposure of mucous membrane or nonintact skin to an infectious material (saliva, tears, neural tissue), in addition to organ transplantation.⁶

Animal capture and testing is a strategy for excluding rabies risk and reducing the need for postexposure prophylaxis. A dog, cat, or ferret that bites a person should be confined and observed for 10 days without administering postexposure prophylaxis for rabies, unless the bite or exposure is on the face or neck, in which case this treatment should be given immediately.⁶ If the observed biting animal lives and remains healthy, postexposure prophylaxis is not recommended. However, if signs suggestive of rabies develop, postexposure prophylaxis should be given and the animal should be euthanized, with testing of brain tissue for rabies virus. Postexposure prophylaxis should be discontinued if rabies testing is negative.

The combination of rabies vaccine and human rabies immunoglobulin is nearly 100% effective in preventing rabies if administered in a timely and accurate fashion after exposure (Table 5).⁶

Tetanus

Tetanus transmission can occur through injuries ranging from small cuts to severe trauma and through contact with contaminated objects (eg, bites, nails, needles, splinters, neonates whose umbilical cord is cut with contaminated surgical instruments, and during circumcision or piercing with contaminated instruments).⁵

Tetanus is almost completely preventable with vaccination, and timely administration of postexposure prophylaxis (tetanus toxoid-containing vaccine, tetanus immune globulin) decreases disease severity (Table 5).^2,5,52