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Drugs may be effective against hematologic, other cancers
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.”
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.”
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.”
Shoulder Dislocations
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.
1. Omoumi P, Teixeira P, Lecouvet F, Chung CB. Glenohumeral joint instability. J Magn Reson Imaging. 2010;33(1):2-16.
2. Rouleau DM, Hebert-Davies J. Incidence of associated injury in posterior shoulder dislocation: systematic review of the literature. J Orthop Trauma. 2012;26(4):246-251.
3. Sachit M, Shekhar A, Shekhar S, Joban SH. Acute spontaneous atraumatic bilateral anterior dislocation of the shoulder joint with Hill-Sach’s lesions: a rare case. J Orthop Case Rep. 2015;5(1):55-57.
4. Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann R Coll Surg Engl. 2009;91(1):2-7.
5. Magee DJ. Orthopedic Physical Assessment. 5th ed. St. Louis, MO. Saunders Elsevier; 2008.
6. Greenspan A. Orthopedic Imaging: A Practical Approach. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
7. Karimi-Nasab MH, Shayesteh-Azar M, Sajjadi-Saravi M, Mehdi Daneshpoor SM. Anterior shoulder dislocation and ipsilateral humeral shaft fracture. Iran J Med Sci. 2012; 37(3):202-204.
8. Robinson CM, Aderinto J. Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am. 2005; 87(3):639-650.
9. Cacioppo E, Waymack JR. Bilateral inferior shoulder dislocation. West J Emerg Med. 2015;16(1):157.
10. Tiamkao S, Shorvon SD. Seizure-related injury in an adult tertiary epilepsy clinic. Hong Kong Med J. 2006;12(4):260-263.
11. Shaw JL. Bilateral posterior fracture-dislocation of the shoulder and other trauma caused by convulsive seizures. J Bone Joint Surg Am. 1971;53(7):1437-1440.
12. Lawn ND, Bamlet WR, Radhakirshnan K, et al. Injuries due to seizures in persons with epilepsy: a population-based study. Neurology. 2004;63(9):1565-1570.
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.
1. Omoumi P, Teixeira P, Lecouvet F, Chung CB. Glenohumeral joint instability. J Magn Reson Imaging. 2010;33(1):2-16.
2. Rouleau DM, Hebert-Davies J. Incidence of associated injury in posterior shoulder dislocation: systematic review of the literature. J Orthop Trauma. 2012;26(4):246-251.
3. Sachit M, Shekhar A, Shekhar S, Joban SH. Acute spontaneous atraumatic bilateral anterior dislocation of the shoulder joint with Hill-Sach’s lesions: a rare case. J Orthop Case Rep. 2015;5(1):55-57.
4. Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann R Coll Surg Engl. 2009;91(1):2-7.
5. Magee DJ. Orthopedic Physical Assessment. 5th ed. St. Louis, MO. Saunders Elsevier; 2008.
6. Greenspan A. Orthopedic Imaging: A Practical Approach. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
7. Karimi-Nasab MH, Shayesteh-Azar M, Sajjadi-Saravi M, Mehdi Daneshpoor SM. Anterior shoulder dislocation and ipsilateral humeral shaft fracture. Iran J Med Sci. 2012; 37(3):202-204.
8. Robinson CM, Aderinto J. Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am. 2005; 87(3):639-650.
9. Cacioppo E, Waymack JR. Bilateral inferior shoulder dislocation. West J Emerg Med. 2015;16(1):157.
10. Tiamkao S, Shorvon SD. Seizure-related injury in an adult tertiary epilepsy clinic. Hong Kong Med J. 2006;12(4):260-263.
11. Shaw JL. Bilateral posterior fracture-dislocation of the shoulder and other trauma caused by convulsive seizures. J Bone Joint Surg Am. 1971;53(7):1437-1440.
12. Lawn ND, Bamlet WR, Radhakirshnan K, et al. Injuries due to seizures in persons with epilepsy: a population-based study. Neurology. 2004;63(9):1565-1570.
1. Omoumi P, Teixeira P, Lecouvet F, Chung CB. Glenohumeral joint instability. J Magn Reson Imaging. 2010;33(1):2-16.
2. Rouleau DM, Hebert-Davies J. Incidence of associated injury in posterior shoulder dislocation: systematic review of the literature. J Orthop Trauma. 2012;26(4):246-251.
3. Sachit M, Shekhar A, Shekhar S, Joban SH. Acute spontaneous atraumatic bilateral anterior dislocation of the shoulder joint with Hill-Sach’s lesions: a rare case. J Orthop Case Rep. 2015;5(1):55-57.
4. Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann R Coll Surg Engl. 2009;91(1):2-7.
5. Magee DJ. Orthopedic Physical Assessment. 5th ed. St. Louis, MO. Saunders Elsevier; 2008.
6. Greenspan A. Orthopedic Imaging: A Practical Approach. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
7. Karimi-Nasab MH, Shayesteh-Azar M, Sajjadi-Saravi M, Mehdi Daneshpoor SM. Anterior shoulder dislocation and ipsilateral humeral shaft fracture. Iran J Med Sci. 2012; 37(3):202-204.
8. Robinson CM, Aderinto J. Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am. 2005; 87(3):639-650.
9. Cacioppo E, Waymack JR. Bilateral inferior shoulder dislocation. West J Emerg Med. 2015;16(1):157.
10. Tiamkao S, Shorvon SD. Seizure-related injury in an adult tertiary epilepsy clinic. Hong Kong Med J. 2006;12(4):260-263.
11. Shaw JL. Bilateral posterior fracture-dislocation of the shoulder and other trauma caused by convulsive seizures. J Bone Joint Surg Am. 1971;53(7):1437-1440.
12. Lawn ND, Bamlet WR, Radhakirshnan K, et al. Injuries due to seizures in persons with epilepsy: a population-based study. Neurology. 2004;63(9):1565-1570.
Pleth Variability Index shows promise for asthma assessments
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.
Setting: A 137-bed, tertiary-care children’s hospital.
Synopsis: Over a 6-month period on weekdays, researchers enrolled patients aged 1-18 years evaluated in the ED for asthma exacerbations or reactive airway disease. ED staff diagnosed patients clinically, and other patients with conditions known to affect PP – such as dehydration, croup, and cardiac disease – were excluded. PVI was calculated by measuring the minimum perfusion index (PImin) and the maximum perfusion index (PImax) using the following formula:
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).
Of the 117 patients who were analyzed after application of exclusion criteria, 48 were discharged to home, 61 were admitted to a general pediatrics floor, and eight were admitted to the PICU. The three groups were found to be demographically similar. Researchers found a significant difference between the PVI of the three groups, but pairwise analysis showed no significant difference between the PVI of patients admitted to the general pediatrics floor versus discharged to home (see Table 2).
Bottom line: PVI shows promise as a tool to rapidly assess disease severity in pediatric patients being evaluated and treated for asthma, but further studies are needed to validate this in the ED and hospital setting.
Citation: Brandwein A, Patel K, Kline M, Silver P, Gangadharan S. Using pleth variability as a triage tool for children with obstructive airway disease in a pediatric emergency department [published online ahead of print Oct. 6, 2016]. Pediatr Emerg Care. doi: 10.1097/PEC.0000000000000887.
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.
Setting: A 137-bed, tertiary-care children’s hospital.
Synopsis: Over a 6-month period on weekdays, researchers enrolled patients aged 1-18 years evaluated in the ED for asthma exacerbations or reactive airway disease. ED staff diagnosed patients clinically, and other patients with conditions known to affect PP – such as dehydration, croup, and cardiac disease – were excluded. PVI was calculated by measuring the minimum perfusion index (PImin) and the maximum perfusion index (PImax) using the following formula:
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).
Of the 117 patients who were analyzed after application of exclusion criteria, 48 were discharged to home, 61 were admitted to a general pediatrics floor, and eight were admitted to the PICU. The three groups were found to be demographically similar. Researchers found a significant difference between the PVI of the three groups, but pairwise analysis showed no significant difference between the PVI of patients admitted to the general pediatrics floor versus discharged to home (see Table 2).
Bottom line: PVI shows promise as a tool to rapidly assess disease severity in pediatric patients being evaluated and treated for asthma, but further studies are needed to validate this in the ED and hospital setting.
Citation: Brandwein A, Patel K, Kline M, Silver P, Gangadharan S. Using pleth variability as a triage tool for children with obstructive airway disease in a pediatric emergency department [published online ahead of print Oct. 6, 2016]. Pediatr Emerg Care. doi: 10.1097/PEC.0000000000000887.
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.
Setting: A 137-bed, tertiary-care children’s hospital.
Synopsis: Over a 6-month period on weekdays, researchers enrolled patients aged 1-18 years evaluated in the ED for asthma exacerbations or reactive airway disease. ED staff diagnosed patients clinically, and other patients with conditions known to affect PP – such as dehydration, croup, and cardiac disease – were excluded. PVI was calculated by measuring the minimum perfusion index (PImin) and the maximum perfusion index (PImax) using the following formula:
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).
Of the 117 patients who were analyzed after application of exclusion criteria, 48 were discharged to home, 61 were admitted to a general pediatrics floor, and eight were admitted to the PICU. The three groups were found to be demographically similar. Researchers found a significant difference between the PVI of the three groups, but pairwise analysis showed no significant difference between the PVI of patients admitted to the general pediatrics floor versus discharged to home (see Table 2).
Bottom line: PVI shows promise as a tool to rapidly assess disease severity in pediatric patients being evaluated and treated for asthma, but further studies are needed to validate this in the ED and hospital setting.
Citation: Brandwein A, Patel K, Kline M, Silver P, Gangadharan S. Using pleth variability as a triage tool for children with obstructive airway disease in a pediatric emergency department [published online ahead of print Oct. 6, 2016]. Pediatr Emerg Care. doi: 10.1097/PEC.0000000000000887.
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.
Embrace change as a hospitalist leader
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.
Trending at SHM
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.
January 2017: Click for Credit
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?
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 rbarbieri@frontlinemedcom.com. 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 rbarbieri@frontlinemedcom.com. 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 rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.
Removal of wrong ovary?
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 rbarbieri@frontlinemedcom.com. 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 rbarbieri@frontlinemedcom.com. 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 rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.
Whether to anticoagulate: Toward a more reasoned approach
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.
BETTER RISK PREDICTORS ARE NEEDED
Prediction tools are available for estimating the risk of stroke in patients with atrial fibrillation without anticoagulation2,3 and to estimate bleeding risk from anticoagulation4–7 (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-BLED5,6 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-BLED5,6 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.
- Hagerty T, Rich MW. Fall risk and anticoagulation for atrial fibrillation in the elderly: a delicate balance. Cleve Clin J Med 2017; 84:35–40.
- Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001; 285:2864–2870.
- Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the Euro Heart Survey on atrial fibrillation. Chest 2010; 137:263–272.
- Fang MC, Go AS, Chang Y, et al. A new risk scheme to predict warfarin-associated hemorrhage: the ATRIA (Anticoagulation and Risk Factors in Atrial Fibrillation) study. J Am Coll Cardiol 2011; 58:395–401.
- Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest 2010; 138:1093–1100.
- Lip GY, Frison L, Halperin JL, Lane DA. Comparative validation of a novel risk score for predicting bleeding risk in anticoagulated patients with atrial fibrillation: the HAS-BLED (Hypertension, Abnormal Renal/Liver Function, Stroke, Bleeding History or Predisposition, Labile INR, Elderly, Drugs/Alcohol Concomitantly) score. J Am Coll Cardiol 2011; 57:173–180.
- Gage BF, Yan Y, Milligan PE, et al. Clinical classification schemes for predicting hemorrhage: results from the National Registry of Atrial Fibrillation (NRAF). Am Heart J 2006; 151:713–719.
- Fang MC, Chang Y, Hylek EM, et al. Advanced age, anticoagulation intensity, and risk for intracranial hemorrhage among patients taking warfarin for atrial fibrillation. Ann Intern Med 2004; 141:745–752.
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.
BETTER RISK PREDICTORS ARE NEEDED
Prediction tools are available for estimating the risk of stroke in patients with atrial fibrillation without anticoagulation2,3 and to estimate bleeding risk from anticoagulation4–7 (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-BLED5,6 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-BLED5,6 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.
BETTER RISK PREDICTORS ARE NEEDED
Prediction tools are available for estimating the risk of stroke in patients with atrial fibrillation without anticoagulation2,3 and to estimate bleeding risk from anticoagulation4–7 (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-BLED5,6 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-BLED5,6 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.
- Hagerty T, Rich MW. Fall risk and anticoagulation for atrial fibrillation in the elderly: a delicate balance. Cleve Clin J Med 2017; 84:35–40.
- Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001; 285:2864–2870.
- Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the Euro Heart Survey on atrial fibrillation. Chest 2010; 137:263–272.
- Fang MC, Go AS, Chang Y, et al. A new risk scheme to predict warfarin-associated hemorrhage: the ATRIA (Anticoagulation and Risk Factors in Atrial Fibrillation) study. J Am Coll Cardiol 2011; 58:395–401.
- Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest 2010; 138:1093–1100.
- Lip GY, Frison L, Halperin JL, Lane DA. Comparative validation of a novel risk score for predicting bleeding risk in anticoagulated patients with atrial fibrillation: the HAS-BLED (Hypertension, Abnormal Renal/Liver Function, Stroke, Bleeding History or Predisposition, Labile INR, Elderly, Drugs/Alcohol Concomitantly) score. J Am Coll Cardiol 2011; 57:173–180.
- Gage BF, Yan Y, Milligan PE, et al. Clinical classification schemes for predicting hemorrhage: results from the National Registry of Atrial Fibrillation (NRAF). Am Heart J 2006; 151:713–719.
- Fang MC, Chang Y, Hylek EM, et al. Advanced age, anticoagulation intensity, and risk for intracranial hemorrhage among patients taking warfarin for atrial fibrillation. Ann Intern Med 2004; 141:745–752.
- Hagerty T, Rich MW. Fall risk and anticoagulation for atrial fibrillation in the elderly: a delicate balance. Cleve Clin J Med 2017; 84:35–40.
- Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001; 285:2864–2870.
- Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the Euro Heart Survey on atrial fibrillation. Chest 2010; 137:263–272.
- Fang MC, Go AS, Chang Y, et al. A new risk scheme to predict warfarin-associated hemorrhage: the ATRIA (Anticoagulation and Risk Factors in Atrial Fibrillation) study. J Am Coll Cardiol 2011; 58:395–401.
- Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest 2010; 138:1093–1100.
- Lip GY, Frison L, Halperin JL, Lane DA. Comparative validation of a novel risk score for predicting bleeding risk in anticoagulated patients with atrial fibrillation: the HAS-BLED (Hypertension, Abnormal Renal/Liver Function, Stroke, Bleeding History or Predisposition, Labile INR, Elderly, Drugs/Alcohol Concomitantly) score. J Am Coll Cardiol 2011; 57:173–180.
- Gage BF, Yan Y, Milligan PE, et al. Clinical classification schemes for predicting hemorrhage: results from the National Registry of Atrial Fibrillation (NRAF). Am Heart J 2006; 151:713–719.
- Fang MC, Chang Y, Hylek EM, et al. Advanced age, anticoagulation intensity, and risk for intracranial hemorrhage among patients taking warfarin for atrial fibrillation. Ann Intern Med 2004; 141:745–752.