Malpractice Counsel

Aortic Rupture

A 59-year-old woman involved in a motor vehicle crash presented to the ED via emergency medical services. The patient had been the front-seat passenger and was wearing a seat belt. She complained of chest wall pain, but denied head injury, loss of consciousness, neck pain, abdominal pain, or shortness of breath. Her past medical history was unremarkable.

On physical examination, she was awake and alert but appeared pale. Her vital signs were: blood pressure (BP), 110/58 mm Hg; heart rate (HR), 112 beats/minute; respiratory rate, 20 breaths/minute; temperature, of 98.6^o F. Oxygen saturation was 97% on room air. She had no midline posterior cervical spine tenderness and her neurological examination was normal. She exhibited mild tenderness upon palpation of her chest wall, but had no crepitance or subcutaneous emphysema. Her lungs were bilaterally clear to auscultation. Examination of the heart revealed tachycardia and a regular rhythm without murmurs, rubs, or gallops. The remainder of the physical examination was normal.

A chest X-ray was performed and interpreted as normal by the attending radiologist. Laboratory studies were normal except for mild anemia. The patient was discharged from the hospital with a diagnosis of chest wall contusion. She died 36 hours later from a ruptured thoracic aorta. The family of the patient brought a malpractice suit against the emergency physician (EP) for failing to diagnose and treat acute aortic rupture. At trial, a defense verdict was returned.

Discussion

Aortic rupture from blunt trauma is a devastating injury. More than 90% of patients who have sustained this type of injury in a motor vehicle crash die at the scene.¹ For the remaining 10%, 50% die within the following 24 hours.¹ The injury occurs in the proximal descending aorta, secondary to the fixation of the vessels between the left subclavian artery and the ligamentum arteriosum; the cause in approximately 80% to 90% of cases is due to blunt trauma. Involvement of the ascending aorta is much less common. Many patients, such as the one in this case, exhibit no external physical findings of injury. Chest pain is the most frequent complaint, followed by dyspnea—both fairly nonspecific symptoms. Physical findings that should raise a suspicion for a thoracic aortic injury include hypotension, hypertension in the upper extremity and hypotension in the lower extremity, unequal BPs in the extremities, external evidence of chest wall trauma, and palpable fractures of the sternum and ribs.² While it is unclear if this patient had unequal extremity BPs, she did not have any of the other classic findings of aortic rupture. Associated neurological, abdominal, or orthopedic injuries are frequently present as well, and can mask the subtle signs of aortic rupture.

A chest radiograph is often the initial screening test used to evaluate for possible thoracic aortic injury. Suspicious findings include a widened mediastinum (greater than 8 cm), right-sided deviation of the esophagus, depression of the left mainstem bronchus, loss of the aortic knob, and an apical pleural cap. Unfortunately, chest X-ray can be normal, and a normal mediastinum on the radiograph does not exclude the diagnosis.

For patients with suspected thoracic aortic injury, helical computed tomography with angiography is the study of choice. It can accurately identify operative and nonoperative lesions, as well as associated injuries (eg, small pneumothorax, rib fractures). Magnetic resonance angiography provides similar sensitivity and specificity, but is not practical for the majority of trauma patients. Occasionally, aortography can be considered when the CT scan results are indeterminate and when thought to be needed to plan operative intervention. Finally, transesophageal echocardiography can be considered in hemodynamically unstable patients unable to be transferred to the radiology suite.

For most patients, immediate operative intervention is the definitive treatment. For patients with suspected thoracic aortic injury and hypertension, shear forces need to be decreased just as they are for patients with aortic dissection. A short-acting β-blocker like intravenous (IV) esmolol can be used initially to slow HR. Then, an IV arterial vasodilator can be given to decrease BP. To prevent rebound tachycardia and increased shear forces, the β-blocker should always be initiated before the vasodilator is given. Vital-sign targets include an HR of 60 beats/minute and a systolic BP in the range of 100 to 120 mm Hg.

This was a very atypical presentation of a devastating injury. Given the benign presentation, lack of associated injuries, and the normal chest X-ray, a defense verdict appears to be the correct one in this very unfortunate case.

 

Foot Drop

A 20-year-old woman presented to the ED complaining of severe numbness, tingling, and pain in her left calf. According to the patient, she had attended a New Year’s Eve party, where she spent much of the time dancing. She was awakened by calf pain on the following morning and sought treatment at the ED.

On physical examination, the patient’s vital signs were normal. Examination of the left calf revealed tenderness to palpation; no swelling was noted. The patient was unable to lift her left foot or bear weight on the left leg. She had normal dorsalis pedis and posterior tibial pulses in the affected leg. The remainder of her examination was normal and no testing was performed. The patient was diagnosed with “floppy foot syndrome” and discharged home with a prescription for a nonsteroidal anti-inflammatory drug.

The next day, the patient presented to a different ED because of worsening pain and swelling of the calf. She was admitted to the hospital and the orthopedic service was consulted. The patient was diagnosed with compartment syndrome; however, by that time her condition was complicated by rhabdomyolysis, resulting in acute renal failure.

The patient underwent a fasciotomy. After surgery, she required hemodialysis until her kidney function returned. She had damage to the nerves in her left calf and leg resulting in a permanent foot drop that required prolonged physical therapy following her hospitalization.

The patient sued the initial EP for failure to diagnose compartment syndrome, which resulted in permanent nerve damage and foot drop. A $750,000 settlement was reached.

Discussion

The EP did not appear to have taken this case seriously, as “floppy foot syndrome” is not a recognized diagnosis. No significance was attached to the presence of the foot drop, which is an objective and concerning physical finding.

The differential diagnoses of foot drop are relatively small: a nerve injury, which is the most common cause; a central nervous system event, such as a stroke; or a muscular disorder.³ An injury or problem with the peroneal nerve is the most common cause of foot drop.

While the patient’s history was not typical for the development of compartment syndrome, she potentially participated in strenuous physical activity, which can result in muscle swelling and subsequent compartment syndrome.⁴ The pain from compartment syndrome is typically described as out of proportion to physical findings; this seems to have been the case for this patient.

The symptoms and findings of compartment syndrome are classically taught as the five “Ps”: pain, paresthesias, paralysis, pallor, and pulselessness, with the symptoms typically presenting in this order. The patient had the first three symptoms, but they were not appreciated in the initial evaluation. Pulselessness is usually the last finding to develop, and tissue damage is frequently present at that point.

Interestingly, approximately 40% of compartment syndromes occur at the level of the tibia and fibula. The lower leg has four compartments: the anterior, which contains the anterior tibial artery and deep peroneal nerve; the lateral, which contains the superficial peroneal nerve; the superficial posterior, which contains the sural nerve; and the deep posterior, which contains the posterior tibial artery and nerve. 

As pressure within the enclosed space increases due to swelling, hemorrhage, fracture, etc, the blood supply as well as nerve and muscle functions become compromised. Left untreated, the increased pressure can result in permanent tissue and nerve damage. 

Compartment syndrome is a time sensitive diagnosis because of the need for surgical intervention to open the compartment. The EP can measure compartment pressures if he or she has the right equipment and training. A normal compartment pressure is less than 10 mm Hg. When the compartment pressure begins to exceed 30 mm Hg, tissue damage can occur. If unable to measure compartment pressure, an emergent orthopedic consult is indicated.

Aortic Rupture

A 59-year-old woman involved in a motor vehicle crash presented to the ED via emergency medical services. The patient had been the front-seat passenger and was wearing a seat belt. She complained of chest wall pain, but denied head injury, loss of consciousness, neck pain, abdominal pain, or shortness of breath. Her past medical history was unremarkable.

On physical examination, she was awake and alert but appeared pale. Her vital signs were: blood pressure (BP), 110/58 mm Hg; heart rate (HR), 112 beats/minute; respiratory rate, 20 breaths/minute; temperature, of 98.6^o F. Oxygen saturation was 97% on room air. She had no midline posterior cervical spine tenderness and her neurological examination was normal. She exhibited mild tenderness upon palpation of her chest wall, but had no crepitance or subcutaneous emphysema. Her lungs were bilaterally clear to auscultation. Examination of the heart revealed tachycardia and a regular rhythm without murmurs, rubs, or gallops. The remainder of the physical examination was normal.

A chest X-ray was performed and interpreted as normal by the attending radiologist. Laboratory studies were normal except for mild anemia. The patient was discharged from the hospital with a diagnosis of chest wall contusion. She died 36 hours later from a ruptured thoracic aorta. The family of the patient brought a malpractice suit against the emergency physician (EP) for failing to diagnose and treat acute aortic rupture. At trial, a defense verdict was returned.

Discussion

Aortic rupture from blunt trauma is a devastating injury. More than 90% of patients who have sustained this type of injury in a motor vehicle crash die at the scene.¹ For the remaining 10%, 50% die within the following 24 hours.¹ The injury occurs in the proximal descending aorta, secondary to the fixation of the vessels between the left subclavian artery and the ligamentum arteriosum; the cause in approximately 80% to 90% of cases is due to blunt trauma. Involvement of the ascending aorta is much less common. Many patients, such as the one in this case, exhibit no external physical findings of injury. Chest pain is the most frequent complaint, followed by dyspnea—both fairly nonspecific symptoms. Physical findings that should raise a suspicion for a thoracic aortic injury include hypotension, hypertension in the upper extremity and hypotension in the lower extremity, unequal BPs in the extremities, external evidence of chest wall trauma, and palpable fractures of the sternum and ribs.² While it is unclear if this patient had unequal extremity BPs, she did not have any of the other classic findings of aortic rupture. Associated neurological, abdominal, or orthopedic injuries are frequently present as well, and can mask the subtle signs of aortic rupture.

A chest radiograph is often the initial screening test used to evaluate for possible thoracic aortic injury. Suspicious findings include a widened mediastinum (greater than 8 cm), right-sided deviation of the esophagus, depression of the left mainstem bronchus, loss of the aortic knob, and an apical pleural cap. Unfortunately, chest X-ray can be normal, and a normal mediastinum on the radiograph does not exclude the diagnosis.

For patients with suspected thoracic aortic injury, helical computed tomography with angiography is the study of choice. It can accurately identify operative and nonoperative lesions, as well as associated injuries (eg, small pneumothorax, rib fractures). Magnetic resonance angiography provides similar sensitivity and specificity, but is not practical for the majority of trauma patients. Occasionally, aortography can be considered when the CT scan results are indeterminate and when thought to be needed to plan operative intervention. Finally, transesophageal echocardiography can be considered in hemodynamically unstable patients unable to be transferred to the radiology suite.

For most patients, immediate operative intervention is the definitive treatment. For patients with suspected thoracic aortic injury and hypertension, shear forces need to be decreased just as they are for patients with aortic dissection. A short-acting β-blocker like intravenous (IV) esmolol can be used initially to slow HR. Then, an IV arterial vasodilator can be given to decrease BP. To prevent rebound tachycardia and increased shear forces, the β-blocker should always be initiated before the vasodilator is given. Vital-sign targets include an HR of 60 beats/minute and a systolic BP in the range of 100 to 120 mm Hg.

This was a very atypical presentation of a devastating injury. Given the benign presentation, lack of associated injuries, and the normal chest X-ray, a defense verdict appears to be the correct one in this very unfortunate case.

 

Foot Drop

A 20-year-old woman presented to the ED complaining of severe numbness, tingling, and pain in her left calf. According to the patient, she had attended a New Year’s Eve party, where she spent much of the time dancing. She was awakened by calf pain on the following morning and sought treatment at the ED.

On physical examination, the patient’s vital signs were normal. Examination of the left calf revealed tenderness to palpation; no swelling was noted. The patient was unable to lift her left foot or bear weight on the left leg. She had normal dorsalis pedis and posterior tibial pulses in the affected leg. The remainder of her examination was normal and no testing was performed. The patient was diagnosed with “floppy foot syndrome” and discharged home with a prescription for a nonsteroidal anti-inflammatory drug.

The next day, the patient presented to a different ED because of worsening pain and swelling of the calf. She was admitted to the hospital and the orthopedic service was consulted. The patient was diagnosed with compartment syndrome; however, by that time her condition was complicated by rhabdomyolysis, resulting in acute renal failure.

The patient underwent a fasciotomy. After surgery, she required hemodialysis until her kidney function returned. She had damage to the nerves in her left calf and leg resulting in a permanent foot drop that required prolonged physical therapy following her hospitalization.

The patient sued the initial EP for failure to diagnose compartment syndrome, which resulted in permanent nerve damage and foot drop. A $750,000 settlement was reached.

Discussion

The EP did not appear to have taken this case seriously, as “floppy foot syndrome” is not a recognized diagnosis. No significance was attached to the presence of the foot drop, which is an objective and concerning physical finding.

The differential diagnoses of foot drop are relatively small: a nerve injury, which is the most common cause; a central nervous system event, such as a stroke; or a muscular disorder.³ An injury or problem with the peroneal nerve is the most common cause of foot drop.

While the patient’s history was not typical for the development of compartment syndrome, she potentially participated in strenuous physical activity, which can result in muscle swelling and subsequent compartment syndrome.⁴ The pain from compartment syndrome is typically described as out of proportion to physical findings; this seems to have been the case for this patient.

The symptoms and findings of compartment syndrome are classically taught as the five “Ps”: pain, paresthesias, paralysis, pallor, and pulselessness, with the symptoms typically presenting in this order. The patient had the first three symptoms, but they were not appreciated in the initial evaluation. Pulselessness is usually the last finding to develop, and tissue damage is frequently present at that point.

Interestingly, approximately 40% of compartment syndromes occur at the level of the tibia and fibula. The lower leg has four compartments: the anterior, which contains the anterior tibial artery and deep peroneal nerve; the lateral, which contains the superficial peroneal nerve; the superficial posterior, which contains the sural nerve; and the deep posterior, which contains the posterior tibial artery and nerve. 

As pressure within the enclosed space increases due to swelling, hemorrhage, fracture, etc, the blood supply as well as nerve and muscle functions become compromised. Left untreated, the increased pressure can result in permanent tissue and nerve damage. 

Compartment syndrome is a time sensitive diagnosis because of the need for surgical intervention to open the compartment. The EP can measure compartment pressures if he or she has the right equipment and training. A normal compartment pressure is less than 10 mm Hg. When the compartment pressure begins to exceed 30 mm Hg, tissue damage can occur. If unable to measure compartment pressure, an emergent orthopedic consult is indicated.

Aortic Rupture

A 59-year-old woman involved in a motor vehicle crash presented to the ED via emergency medical services. The patient had been the front-seat passenger and was wearing a seat belt. She complained of chest wall pain, but denied head injury, loss of consciousness, neck pain, abdominal pain, or shortness of breath. Her past medical history was unremarkable.

On physical examination, she was awake and alert but appeared pale. Her vital signs were: blood pressure (BP), 110/58 mm Hg; heart rate (HR), 112 beats/minute; respiratory rate, 20 breaths/minute; temperature, of 98.6^o F. Oxygen saturation was 97% on room air. She had no midline posterior cervical spine tenderness and her neurological examination was normal. She exhibited mild tenderness upon palpation of her chest wall, but had no crepitance or subcutaneous emphysema. Her lungs were bilaterally clear to auscultation. Examination of the heart revealed tachycardia and a regular rhythm without murmurs, rubs, or gallops. The remainder of the physical examination was normal.

A chest X-ray was performed and interpreted as normal by the attending radiologist. Laboratory studies were normal except for mild anemia. The patient was discharged from the hospital with a diagnosis of chest wall contusion. She died 36 hours later from a ruptured thoracic aorta. The family of the patient brought a malpractice suit against the emergency physician (EP) for failing to diagnose and treat acute aortic rupture. At trial, a defense verdict was returned.

Discussion

Aortic rupture from blunt trauma is a devastating injury. More than 90% of patients who have sustained this type of injury in a motor vehicle crash die at the scene.¹ For the remaining 10%, 50% die within the following 24 hours.¹ The injury occurs in the proximal descending aorta, secondary to the fixation of the vessels between the left subclavian artery and the ligamentum arteriosum; the cause in approximately 80% to 90% of cases is due to blunt trauma. Involvement of the ascending aorta is much less common. Many patients, such as the one in this case, exhibit no external physical findings of injury. Chest pain is the most frequent complaint, followed by dyspnea—both fairly nonspecific symptoms. Physical findings that should raise a suspicion for a thoracic aortic injury include hypotension, hypertension in the upper extremity and hypotension in the lower extremity, unequal BPs in the extremities, external evidence of chest wall trauma, and palpable fractures of the sternum and ribs.² While it is unclear if this patient had unequal extremity BPs, she did not have any of the other classic findings of aortic rupture. Associated neurological, abdominal, or orthopedic injuries are frequently present as well, and can mask the subtle signs of aortic rupture.

A chest radiograph is often the initial screening test used to evaluate for possible thoracic aortic injury. Suspicious findings include a widened mediastinum (greater than 8 cm), right-sided deviation of the esophagus, depression of the left mainstem bronchus, loss of the aortic knob, and an apical pleural cap. Unfortunately, chest X-ray can be normal, and a normal mediastinum on the radiograph does not exclude the diagnosis.

For patients with suspected thoracic aortic injury, helical computed tomography with angiography is the study of choice. It can accurately identify operative and nonoperative lesions, as well as associated injuries (eg, small pneumothorax, rib fractures). Magnetic resonance angiography provides similar sensitivity and specificity, but is not practical for the majority of trauma patients. Occasionally, aortography can be considered when the CT scan results are indeterminate and when thought to be needed to plan operative intervention. Finally, transesophageal echocardiography can be considered in hemodynamically unstable patients unable to be transferred to the radiology suite.

For most patients, immediate operative intervention is the definitive treatment. For patients with suspected thoracic aortic injury and hypertension, shear forces need to be decreased just as they are for patients with aortic dissection. A short-acting β-blocker like intravenous (IV) esmolol can be used initially to slow HR. Then, an IV arterial vasodilator can be given to decrease BP. To prevent rebound tachycardia and increased shear forces, the β-blocker should always be initiated before the vasodilator is given. Vital-sign targets include an HR of 60 beats/minute and a systolic BP in the range of 100 to 120 mm Hg.

This was a very atypical presentation of a devastating injury. Given the benign presentation, lack of associated injuries, and the normal chest X-ray, a defense verdict appears to be the correct one in this very unfortunate case.

 

Foot Drop

A 20-year-old woman presented to the ED complaining of severe numbness, tingling, and pain in her left calf. According to the patient, she had attended a New Year’s Eve party, where she spent much of the time dancing. She was awakened by calf pain on the following morning and sought treatment at the ED.

On physical examination, the patient’s vital signs were normal. Examination of the left calf revealed tenderness to palpation; no swelling was noted. The patient was unable to lift her left foot or bear weight on the left leg. She had normal dorsalis pedis and posterior tibial pulses in the affected leg. The remainder of her examination was normal and no testing was performed. The patient was diagnosed with “floppy foot syndrome” and discharged home with a prescription for a nonsteroidal anti-inflammatory drug.

The next day, the patient presented to a different ED because of worsening pain and swelling of the calf. She was admitted to the hospital and the orthopedic service was consulted. The patient was diagnosed with compartment syndrome; however, by that time her condition was complicated by rhabdomyolysis, resulting in acute renal failure.

The patient underwent a fasciotomy. After surgery, she required hemodialysis until her kidney function returned. She had damage to the nerves in her left calf and leg resulting in a permanent foot drop that required prolonged physical therapy following her hospitalization.

The patient sued the initial EP for failure to diagnose compartment syndrome, which resulted in permanent nerve damage and foot drop. A $750,000 settlement was reached.

Discussion

The EP did not appear to have taken this case seriously, as “floppy foot syndrome” is not a recognized diagnosis. No significance was attached to the presence of the foot drop, which is an objective and concerning physical finding.

The differential diagnoses of foot drop are relatively small: a nerve injury, which is the most common cause; a central nervous system event, such as a stroke; or a muscular disorder.³ An injury or problem with the peroneal nerve is the most common cause of foot drop.

While the patient’s history was not typical for the development of compartment syndrome, she potentially participated in strenuous physical activity, which can result in muscle swelling and subsequent compartment syndrome.⁴ The pain from compartment syndrome is typically described as out of proportion to physical findings; this seems to have been the case for this patient.

The symptoms and findings of compartment syndrome are classically taught as the five “Ps”: pain, paresthesias, paralysis, pallor, and pulselessness, with the symptoms typically presenting in this order. The patient had the first three symptoms, but they were not appreciated in the initial evaluation. Pulselessness is usually the last finding to develop, and tissue damage is frequently present at that point.

Interestingly, approximately 40% of compartment syndromes occur at the level of the tibia and fibula. The lower leg has four compartments: the anterior, which contains the anterior tibial artery and deep peroneal nerve; the lateral, which contains the superficial peroneal nerve; the superficial posterior, which contains the sural nerve; and the deep posterior, which contains the posterior tibial artery and nerve. 

As pressure within the enclosed space increases due to swelling, hemorrhage, fracture, etc, the blood supply as well as nerve and muscle functions become compromised. Left untreated, the increased pressure can result in permanent tissue and nerve damage. 

Compartment syndrome is a time sensitive diagnosis because of the need for surgical intervention to open the compartment. The EP can measure compartment pressures if he or she has the right equipment and training. A normal compartment pressure is less than 10 mm Hg. When the compartment pressure begins to exceed 30 mm Hg, tissue damage can occur. If unable to measure compartment pressure, an emergent orthopedic consult is indicated.