Imaging

A 53-year-old Native American woman with a history of liver cirrhosis secondary to alcohol abuse presents to the emergency department after 2 days of diffuse abdominal pain and weakness. The pain was sudden in onset and has progressed relentlessly over the last day, reaching 9 on a scale of 10 in severity. Family members say that her oral intake has been decreased for the last 2 days, but she has had no fever, vomiting, change in bowel habit, blood in stool, or black stool. She has never undergone surgery, and has had one uncomplicated pregnancy.

Physical examination

Vital signs:

• Blood pressure 82/57 mm Hg
• Heart rate 96 beats per minute
• Temperature 37.3°C (99.1°F)
• Respiratory rate 16 per minute
• Oxygen saturation 92% while receiving oxygen at 2 L/minute.

The patient is somnolent and has scleral icterus. Her cardiopulmonary examination is normal. Her abdomen is tense, distended, and diffusely tender. She has bilateral +2 pitting edema in her lower extremities. She is oriented to person only and is noted to have asterixis. Her baseline Model for End-stage Liver Disease score is 18 points on a scale of 6 (less ill) to 40 (gravely ill).

Laboratory studies:

• Hemoglobin 9.8 g/dL (reference range 11.5–15.5)
• Platelet count 100 × 10⁹/L (150–400)
• White blood cell count 9.9 × 10⁹/L (3.7–11.0)
• Serum creatinine 1.06 mg/dL (0.58–0.96)
• Bilirubin 6.3 mg/dL (0.2–1.3)
• International normalized ratio of the prothrombin time 2.15 (0.8–1.2)
• Blood urea nitrogen 13 mg/dL (7–21)
• Serum albumin 2.7 g/dL (3.9–4.9).

Intravenous fluid resuscitation is initiated but the patient remains hypotensive, and on repeat laboratory testing 4 hours later her hemoglobin level has dropped to 7.3 mg/dL.

DIFFERENTIAL DIAGNOSIS

1. Which of the following are likely causes of this patient’s presentation?

• Splenic arterial aneurysm rupture
• Spontaneous bacterial peritonitis
• Variceal hemorrhage
• Portal vein thrombosis
• Abdominal aortic aneurysm rupture

Ruptured splenic artery aneurysm

Splenic artery aneurysms are the third most common intra-abdominal aneurysm, after those of the abdominal aorta and iliac artery.¹ They are often asymptomatic and are being detected more frequently because of increased use of computed tomography (CT).² Symptomatic splenic artery aneurysms may present with abdominal pain and have the potential to rupture, which can be life-threatening.^3,4

This patient may have a ruptured splenic artery aneurysm, given her hemodynamic shock.

Spontaneous bacterial peritonitis

Ten percent to 20% of hospitalized patients with cirrhosis and ascites develop spontaneous bacterial peritonitis. Patients may present with ascites and abdominal pain, tenderness to palpation, fever, encephalopathy, or worsening liver and renal function.

Diagnostic paracentesis is paramount to delineate the cause of ascites; one should calculate the serum-ascites albumin gradient and obtain a cell count and culture of the ascitic fluid. The diagnosis of spontaneous bacterial peritonitis can be made if the ascitic fluid polymorphonuclear cell count is 0.25 × 10⁹/L or higher, even if the ascitic fluid culture is negative.^5,6 Simultaneous blood cultures should also be collected, as 50% of cases are associated with bacteremia.

The in-hospital mortality rate of an episode of spontaneous bacterial peritonitis has been reduced to 10% to 20% thanks to prompt diagnosis and empiric treatment with third-generation cephalosporins.⁷

Five percent of cases of infected ascites fluid are due to secondary bacterial peritonitis from a perforated viscus or a loculated abscess, which cannot be differentiated clinically from spontaneous bacterial peritonitis but can be diagnosed with CT.⁸

This patient may be presenting with septic shock secondary to either of these causes.

Variceal hemorrhage

Half of patients with cirrhosis have gastroesophageal varices due to portal hypertension. Endoscopic surveillance is warranted, as the risk of hemorrhage is 12% to 15% per year, and the mortality rate approaches 15% to 20% with each episode. Prompt resuscitation, diagnosis, and control of bleeding is paramount.

Esophagogastroduodenoscopy is used for both diagnosis and intervention. Short-term prophylactic use of antibiotics improves survival by preventing infections in the event bleeding recurs.^9–11

Our patient may be presenting with hemodynamic shock from bleeding esophageal varices.

Portal vein thrombosis is a common complication of cirrhosis, occurring in 5% to 28% of patients. The risk increases with the severity of liver disease and in association with hepatocellular carcinoma.¹² Forty-three percent of cases are discovered incidentally in asymptomatic patients during ultrasonography, 39% present with upper gastrointestinal bleeding, and 18% present with abdominal pain.^13,14

Portal vein thrombosis is the complete or partial obstruction of blood flow due to a thrombus in the lumen of the portal vein. Contrast ultrasonography and CT can be used to establish the diagnosis.¹⁵

Anticoagulation is recommended in cases of complete thrombosis in candidates for living-donor liver transplant and for those at risk of mesenteric ischemia because of the thrombus extending into the mesenteric veins. In symptomatic patients, the decision to initiate anticoagulation should be made on a case-by-case basis after appropriate screening and management of varices.^16–18

Our patient’s thrombocytopenia reflects the severity of portal hypertension and increases her risk of portal vein thrombosis, but this is unlikely to be the sole cause of the hemodynamic compromise in this patient.

Ruptured abdominal aortic aneurysm

Rupture of an abdominal aortic aneurysm is a medical emergency, with a mortality rate approaching 90%. Risk factors for abdominal aortic aneurysms are smoking, male sex, age over 65, history of cardiovascular disease, hypertension, and a family history of abdominal aortic aneurysm, especially if a first-degree relative is affected.¹⁹ Endovascular repair is associated with lower rates of death and complications compared with open repair.²⁰

The patient does not have any of those risk factors, making this diagnosis less likely.

CASE CONTINUED: RUPTURED SPLENIC ARTERY ANEURYSM

Emergency CT of the abdomen and pelvis with contrast enhancement shows a large left intraperitoneal hematoma with active extravasation from a ruptured splenic artery aneurysm (Figure 1). The patient receives packed red blood cells and fresh-frozen plasma before being transferred to our hospital.

2. Which of the following is false regarding splenic artery aneurysms?

• They are the most common type of splanchnic arterial aneurysm
• True aneurysms are more common than pseudoaneurysms
• Asymptomatic aneurysms are discovered incidentally during assessment for other radiographic indications
• Splenic artery aneurysm in portal hypertension is the result of athero-sclerotic changes to the vascular intima

Splenic artery aneurysm in portal hypertension is not the result of atherosclerotic change to the vascular intima.

Splenic artery aneurysms are the most common type of splanchnic artery aneurysm.¹ True aneurysms involve all 3 layers of the arterial wall, ie, intima, media, and adventitia. Cirrhosis and portal hypertension are associated with true aneurysm formation. The proposed mechanism of aneurysm formation is increased splenic blood flow in response to portal congestion with resultant hemodynamic stress that disrupts arterial wall structure, leading to aneurysmal dilation.²¹

In earlier reports, the incidence of true splenic artery aneurysm in portal hypertension varied from 2.9% to 50%, the latter representing autopsy findings of small aneurysms that were found in the splenic hilum of patients with cirrhosis.^22–25 The incidence of clinically significant aneurysms in cirrhosis is unknown but incidental asymptomatic aneurysm is being detected more frequently on imaging studies pursued for screening purposes.²⁶

The risk of rupture is low, only 2% to 10% in older studies and likely even lower now due to increased incidental detection in asymptomatic patients.²⁷ However, emergent management of rupture at a tertiary care facility is paramount, as the mortality rate of ruptured splenic artery aneurysm is 29% to 36%.^1,26,28

Splenic artery pseudoaneurysm is rarer and has a different pathophysiologic process than true aneurysm. It usually arises in the setting of trauma, pancreatitis, or postsurgery.^29,30 Pseudoaneurysm is more likely to rupture, owing to compromise in the vascular wall integrity.^4,21,28 As a result, treatment is indicated for every pseudoaneurysm regardless of size.

RISK FACTORS FOR SPLENIC ARTERY ANEURYSM

3. Which of the following is true regarding our patient’s risk of splenic artery aneurysm?

• Liver cirrhosis and portal hypertension are her greatest risk factors for it
• Female sex and prior pregnancy are her greatest risk factors for it
• Being Native American makes it more likely that the patient has splenic artery aneurysm secondary to collagen vascular disease
• Her risk of rupture would diminish after receiving a liver transplant

Liver cirrhosis and portal hypertension are her greatest risk factors for splenic artery aneurysm.

Risk factors for true aneurysm include hypertension, atherosclerosis, portal hypertension with or without liver cirrhosis, liver transplant, third trimester of pregnancy, and multiparity.^1,4,26,28,31 Splenic artery aneurysm is  usually diagnosed in the sixth decade. It may be 4 times as common in women, given a hormonal influence.³² Cirrhosis is also associated with massive splenic artery aneurysm (≥ 5 cm). Although rare, massive splenic artery aneurysm is more frequent in men (the male-to-female ratio is 1.78:1) and has a heightened risk of rupture.²⁸ The incidence of rupture increases to around 3% to 4% after liver transplant.³³ Rare causes of true aneurysm include fibrodysplasia, collagen vascular disease (eg, Loeys-Dietz and type IV Ehler-Danlos syndromes), vasculitis (eg, polyarteritis nodosa due to amphetamine abuse), and mycotic aneurysms.^24,25,28,29

This patient’s age, sex, and history of cirrhosis puts her at increased risk of splenic artery aneurysm. The risk of rupture is highest in the peripartum period and in patients with cirrhosis who become pregnant. Although being Native American portends an increased risk for collagen vascular disease, the latter is unlikely to be a contributing factor.

4. Which of the following is false regarding treatment of splenic artery aneurysms?

• Aneurysms larger than 2 cm and those that are expanding require repair
• Treatment should be offered if the patient has symptoms attributable to the aneurysm
• Asymptomatic aneurysms in pregnant women can be followed with watchful waiting
• Minimally invasive therapies such as percutaneous embolization may be a good option in poor operative candidates

Asymptomatic aneurysms in pregnant women should not be followed with watchful waiting—they should be repaired, as rupture carries a maternal mortality rate of 75% and a fetal mortality rate of 95%.³⁴

Complications of splenic artery aneurysm depend on the type of aneurysm and its predisposing factors. Indications for treatment of true aneurysms include:

• Symptoms attributable to the aneurysm (hence, the second answer choice above is true)
• Diameter 2  cm or greater or enlarging diameter (hence, the first answer choice is true)
• Women of childbearing age in anticipation of pregnancy
• Need for surgical intervention such as portocaval shunt and liver transplant.

Conservative management is associated with a late mortality risk of 4.9%.² Interventional options include percutaneous embolization or stenting; or laparotomy with splenic artery ligation or excision with or without splenectomy.^1,28,35–37

Endovascular and open surgical repair have both been used to treat splenic artery aneurysms. The method used depends on the patient’s surgical history and aneurysm anatomy such as splenic artery tortuosity hindering passage of a catheter. Open surgery is associated with longer intraoperative time and length of hospital stay and higher rates of 30-day mortality and perioperative morbidity.^38–41 With endovascular repair, the complication of persistent or recurrent flow occurs in 3% to 5% of cases by 30 days; hence, postprocedural surveillance is recommended.^42–44 Endovascular repair has a higher reintervention rate but may still be more cost-effective than open surgical repair.

Because patients with cirrhosis have a higher risk of surgical complications,⁴⁵ elective endovascular treatment may be an option for patients with aneurysms at high risk of rupturing. Endovascular treatment of visceral aneurysms is associated with complications such as postembolization syndrome (fever, abdominal pain, pleural effusion, and pancreatitis), access site hematoma, splenic infarction, and persistent abdominal pain.⁴²

Patients with cirrhosis as the cause of splenic artery aneurysm tend to need longer hospitalization after endovascular treatment, but there is insufficient evidence to suggest that they are at higher risk of other complications.³⁷

CASE CONTINUED: SPLENIC ARTERY EMBOLIZATION

The patient undergoes emergency splenic artery embolization, performed by an interventional radiology team (Figure 2 and Figure 3). Over the next few days, her mental status improves and her abdominal pain resolves. Her hemoglobin level remains stable after the procedure.

The surgical and interventional radiology teams discuss the risk of repeat intervention with the patient and her family, who prefer a nonoperative approach. She is managed supportively in the intensive care unit and is finally discharged home in stable condition and is scheduled for outpatient follow-up.

SUSPECT THIS FATAL CONDITION

The low prevalence of ruptured splenic artery aneurysm may lead physicians to attribute septic shock to spontaneous bacterial peritonitis or hemorrhagic shock from gastroesophageal varices in patients with cirrhosis, but a high index of suspicion and early recognition of this rare disease can lead to timely diagnosis and treatment of this highly fatal complication.

KEY POINTS

• Splenic artery aneurysm is a common complication of cirrhosis, often diagnosed incidentally.
• Elective embolization should be considered for asymptomatic splenic artery aneurysms larger than 2 cm in diameter, clinically symptomatic aneurysms, women of childbearing age, and patients who are candidates for liver transplant.
• Although splenic artery aneurysm rupture is rare, it has a high mortality rate and warrants a high index of suspicion to institute prompt specialized intervention.
• We recommend that physicians consider splenic artery aneurysm rupture in their differential diagnoses in patients with liver cirrhosis presenting with abdominal pain, altered mental status, and hemodynamic shock.

A 53-year-old Native American woman with a history of liver cirrhosis secondary to alcohol abuse presents to the emergency department after 2 days of diffuse abdominal pain and weakness. The pain was sudden in onset and has progressed relentlessly over the last day, reaching 9 on a scale of 10 in severity. Family members say that her oral intake has been decreased for the last 2 days, but she has had no fever, vomiting, change in bowel habit, blood in stool, or black stool. She has never undergone surgery, and has had one uncomplicated pregnancy.

Physical examination

Vital signs:

• Blood pressure 82/57 mm Hg
• Heart rate 96 beats per minute
• Temperature 37.3°C (99.1°F)
• Respiratory rate 16 per minute
• Oxygen saturation 92% while receiving oxygen at 2 L/minute.

The patient is somnolent and has scleral icterus. Her cardiopulmonary examination is normal. Her abdomen is tense, distended, and diffusely tender. She has bilateral +2 pitting edema in her lower extremities. She is oriented to person only and is noted to have asterixis. Her baseline Model for End-stage Liver Disease score is 18 points on a scale of 6 (less ill) to 40 (gravely ill).

Laboratory studies:

• Hemoglobin 9.8 g/dL (reference range 11.5–15.5)
• Platelet count 100 × 10⁹/L (150–400)
• White blood cell count 9.9 × 10⁹/L (3.7–11.0)
• Serum creatinine 1.06 mg/dL (0.58–0.96)
• Bilirubin 6.3 mg/dL (0.2–1.3)
• International normalized ratio of the prothrombin time 2.15 (0.8–1.2)
• Blood urea nitrogen 13 mg/dL (7–21)
• Serum albumin 2.7 g/dL (3.9–4.9).

Intravenous fluid resuscitation is initiated but the patient remains hypotensive, and on repeat laboratory testing 4 hours later her hemoglobin level has dropped to 7.3 mg/dL.

DIFFERENTIAL DIAGNOSIS

1. Which of the following are likely causes of this patient’s presentation?

• Splenic arterial aneurysm rupture
• Spontaneous bacterial peritonitis
• Variceal hemorrhage
• Portal vein thrombosis
• Abdominal aortic aneurysm rupture

Ruptured splenic artery aneurysm

Splenic artery aneurysms are the third most common intra-abdominal aneurysm, after those of the abdominal aorta and iliac artery.¹ They are often asymptomatic and are being detected more frequently because of increased use of computed tomography (CT).² Symptomatic splenic artery aneurysms may present with abdominal pain and have the potential to rupture, which can be life-threatening.^3,4

This patient may have a ruptured splenic artery aneurysm, given her hemodynamic shock.

Spontaneous bacterial peritonitis

Ten percent to 20% of hospitalized patients with cirrhosis and ascites develop spontaneous bacterial peritonitis. Patients may present with ascites and abdominal pain, tenderness to palpation, fever, encephalopathy, or worsening liver and renal function.

Diagnostic paracentesis is paramount to delineate the cause of ascites; one should calculate the serum-ascites albumin gradient and obtain a cell count and culture of the ascitic fluid. The diagnosis of spontaneous bacterial peritonitis can be made if the ascitic fluid polymorphonuclear cell count is 0.25 × 10⁹/L or higher, even if the ascitic fluid culture is negative.^5,6 Simultaneous blood cultures should also be collected, as 50% of cases are associated with bacteremia.

The in-hospital mortality rate of an episode of spontaneous bacterial peritonitis has been reduced to 10% to 20% thanks to prompt diagnosis and empiric treatment with third-generation cephalosporins.⁷

Five percent of cases of infected ascites fluid are due to secondary bacterial peritonitis from a perforated viscus or a loculated abscess, which cannot be differentiated clinically from spontaneous bacterial peritonitis but can be diagnosed with CT.⁸

This patient may be presenting with septic shock secondary to either of these causes.

Variceal hemorrhage

Half of patients with cirrhosis have gastroesophageal varices due to portal hypertension. Endoscopic surveillance is warranted, as the risk of hemorrhage is 12% to 15% per year, and the mortality rate approaches 15% to 20% with each episode. Prompt resuscitation, diagnosis, and control of bleeding is paramount.

Esophagogastroduodenoscopy is used for both diagnosis and intervention. Short-term prophylactic use of antibiotics improves survival by preventing infections in the event bleeding recurs.^9–11

Our patient may be presenting with hemodynamic shock from bleeding esophageal varices.

Portal vein thrombosis is a common complication of cirrhosis, occurring in 5% to 28% of patients. The risk increases with the severity of liver disease and in association with hepatocellular carcinoma.¹² Forty-three percent of cases are discovered incidentally in asymptomatic patients during ultrasonography, 39% present with upper gastrointestinal bleeding, and 18% present with abdominal pain.^13,14

Portal vein thrombosis is the complete or partial obstruction of blood flow due to a thrombus in the lumen of the portal vein. Contrast ultrasonography and CT can be used to establish the diagnosis.¹⁵

Anticoagulation is recommended in cases of complete thrombosis in candidates for living-donor liver transplant and for those at risk of mesenteric ischemia because of the thrombus extending into the mesenteric veins. In symptomatic patients, the decision to initiate anticoagulation should be made on a case-by-case basis after appropriate screening and management of varices.^16–18

Our patient’s thrombocytopenia reflects the severity of portal hypertension and increases her risk of portal vein thrombosis, but this is unlikely to be the sole cause of the hemodynamic compromise in this patient.

Ruptured abdominal aortic aneurysm

Rupture of an abdominal aortic aneurysm is a medical emergency, with a mortality rate approaching 90%. Risk factors for abdominal aortic aneurysms are smoking, male sex, age over 65, history of cardiovascular disease, hypertension, and a family history of abdominal aortic aneurysm, especially if a first-degree relative is affected.¹⁹ Endovascular repair is associated with lower rates of death and complications compared with open repair.²⁰

The patient does not have any of those risk factors, making this diagnosis less likely.

CASE CONTINUED: RUPTURED SPLENIC ARTERY ANEURYSM

Emergency CT of the abdomen and pelvis with contrast enhancement shows a large left intraperitoneal hematoma with active extravasation from a ruptured splenic artery aneurysm (Figure 1). The patient receives packed red blood cells and fresh-frozen plasma before being transferred to our hospital.

2. Which of the following is false regarding splenic artery aneurysms?

• They are the most common type of splanchnic arterial aneurysm
• True aneurysms are more common than pseudoaneurysms
• Asymptomatic aneurysms are discovered incidentally during assessment for other radiographic indications
• Splenic artery aneurysm in portal hypertension is the result of athero-sclerotic changes to the vascular intima

Splenic artery aneurysm in portal hypertension is not the result of atherosclerotic change to the vascular intima.

Splenic artery aneurysms are the most common type of splanchnic artery aneurysm.¹ True aneurysms involve all 3 layers of the arterial wall, ie, intima, media, and adventitia. Cirrhosis and portal hypertension are associated with true aneurysm formation. The proposed mechanism of aneurysm formation is increased splenic blood flow in response to portal congestion with resultant hemodynamic stress that disrupts arterial wall structure, leading to aneurysmal dilation.²¹

In earlier reports, the incidence of true splenic artery aneurysm in portal hypertension varied from 2.9% to 50%, the latter representing autopsy findings of small aneurysms that were found in the splenic hilum of patients with cirrhosis.^22–25 The incidence of clinically significant aneurysms in cirrhosis is unknown but incidental asymptomatic aneurysm is being detected more frequently on imaging studies pursued for screening purposes.²⁶

The risk of rupture is low, only 2% to 10% in older studies and likely even lower now due to increased incidental detection in asymptomatic patients.²⁷ However, emergent management of rupture at a tertiary care facility is paramount, as the mortality rate of ruptured splenic artery aneurysm is 29% to 36%.^1,26,28

Splenic artery pseudoaneurysm is rarer and has a different pathophysiologic process than true aneurysm. It usually arises in the setting of trauma, pancreatitis, or postsurgery.^29,30 Pseudoaneurysm is more likely to rupture, owing to compromise in the vascular wall integrity.^4,21,28 As a result, treatment is indicated for every pseudoaneurysm regardless of size.

RISK FACTORS FOR SPLENIC ARTERY ANEURYSM

3. Which of the following is true regarding our patient’s risk of splenic artery aneurysm?

• Liver cirrhosis and portal hypertension are her greatest risk factors for it
• Female sex and prior pregnancy are her greatest risk factors for it
• Being Native American makes it more likely that the patient has splenic artery aneurysm secondary to collagen vascular disease
• Her risk of rupture would diminish after receiving a liver transplant

Liver cirrhosis and portal hypertension are her greatest risk factors for splenic artery aneurysm.

Risk factors for true aneurysm include hypertension, atherosclerosis, portal hypertension with or without liver cirrhosis, liver transplant, third trimester of pregnancy, and multiparity.^1,4,26,28,31 Splenic artery aneurysm is  usually diagnosed in the sixth decade. It may be 4 times as common in women, given a hormonal influence.³² Cirrhosis is also associated with massive splenic artery aneurysm (≥ 5 cm). Although rare, massive splenic artery aneurysm is more frequent in men (the male-to-female ratio is 1.78:1) and has a heightened risk of rupture.²⁸ The incidence of rupture increases to around 3% to 4% after liver transplant.³³ Rare causes of true aneurysm include fibrodysplasia, collagen vascular disease (eg, Loeys-Dietz and type IV Ehler-Danlos syndromes), vasculitis (eg, polyarteritis nodosa due to amphetamine abuse), and mycotic aneurysms.^24,25,28,29

This patient’s age, sex, and history of cirrhosis puts her at increased risk of splenic artery aneurysm. The risk of rupture is highest in the peripartum period and in patients with cirrhosis who become pregnant. Although being Native American portends an increased risk for collagen vascular disease, the latter is unlikely to be a contributing factor.

4. Which of the following is false regarding treatment of splenic artery aneurysms?

• Aneurysms larger than 2 cm and those that are expanding require repair
• Treatment should be offered if the patient has symptoms attributable to the aneurysm
• Asymptomatic aneurysms in pregnant women can be followed with watchful waiting
• Minimally invasive therapies such as percutaneous embolization may be a good option in poor operative candidates

Asymptomatic aneurysms in pregnant women should not be followed with watchful waiting—they should be repaired, as rupture carries a maternal mortality rate of 75% and a fetal mortality rate of 95%.³⁴

Complications of splenic artery aneurysm depend on the type of aneurysm and its predisposing factors. Indications for treatment of true aneurysms include:

• Symptoms attributable to the aneurysm (hence, the second answer choice above is true)
• Diameter 2  cm or greater or enlarging diameter (hence, the first answer choice is true)
• Women of childbearing age in anticipation of pregnancy
• Need for surgical intervention such as portocaval shunt and liver transplant.

Conservative management is associated with a late mortality risk of 4.9%.² Interventional options include percutaneous embolization or stenting; or laparotomy with splenic artery ligation or excision with or without splenectomy.^1,28,35–37

Endovascular and open surgical repair have both been used to treat splenic artery aneurysms. The method used depends on the patient’s surgical history and aneurysm anatomy such as splenic artery tortuosity hindering passage of a catheter. Open surgery is associated with longer intraoperative time and length of hospital stay and higher rates of 30-day mortality and perioperative morbidity.^38–41 With endovascular repair, the complication of persistent or recurrent flow occurs in 3% to 5% of cases by 30 days; hence, postprocedural surveillance is recommended.^42–44 Endovascular repair has a higher reintervention rate but may still be more cost-effective than open surgical repair.

Because patients with cirrhosis have a higher risk of surgical complications,⁴⁵ elective endovascular treatment may be an option for patients with aneurysms at high risk of rupturing. Endovascular treatment of visceral aneurysms is associated with complications such as postembolization syndrome (fever, abdominal pain, pleural effusion, and pancreatitis), access site hematoma, splenic infarction, and persistent abdominal pain.⁴²

Patients with cirrhosis as the cause of splenic artery aneurysm tend to need longer hospitalization after endovascular treatment, but there is insufficient evidence to suggest that they are at higher risk of other complications.³⁷

CASE CONTINUED: SPLENIC ARTERY EMBOLIZATION

The patient undergoes emergency splenic artery embolization, performed by an interventional radiology team (Figure 2 and Figure 3). Over the next few days, her mental status improves and her abdominal pain resolves. Her hemoglobin level remains stable after the procedure.

The surgical and interventional radiology teams discuss the risk of repeat intervention with the patient and her family, who prefer a nonoperative approach. She is managed supportively in the intensive care unit and is finally discharged home in stable condition and is scheduled for outpatient follow-up.

SUSPECT THIS FATAL CONDITION

The low prevalence of ruptured splenic artery aneurysm may lead physicians to attribute septic shock to spontaneous bacterial peritonitis or hemorrhagic shock from gastroesophageal varices in patients with cirrhosis, but a high index of suspicion and early recognition of this rare disease can lead to timely diagnosis and treatment of this highly fatal complication.

KEY POINTS

• Splenic artery aneurysm is a common complication of cirrhosis, often diagnosed incidentally.
• Elective embolization should be considered for asymptomatic splenic artery aneurysms larger than 2 cm in diameter, clinically symptomatic aneurysms, women of childbearing age, and patients who are candidates for liver transplant.
• Although splenic artery aneurysm rupture is rare, it has a high mortality rate and warrants a high index of suspicion to institute prompt specialized intervention.
• We recommend that physicians consider splenic artery aneurysm rupture in their differential diagnoses in patients with liver cirrhosis presenting with abdominal pain, altered mental status, and hemodynamic shock.

A 53-year-old Native American woman with a history of liver cirrhosis secondary to alcohol abuse presents to the emergency department after 2 days of diffuse abdominal pain and weakness. The pain was sudden in onset and has progressed relentlessly over the last day, reaching 9 on a scale of 10 in severity. Family members say that her oral intake has been decreased for the last 2 days, but she has had no fever, vomiting, change in bowel habit, blood in stool, or black stool. She has never undergone surgery, and has had one uncomplicated pregnancy.

Physical examination

Vital signs:

• Blood pressure 82/57 mm Hg
• Heart rate 96 beats per minute
• Temperature 37.3°C (99.1°F)
• Respiratory rate 16 per minute
• Oxygen saturation 92% while receiving oxygen at 2 L/minute.

The patient is somnolent and has scleral icterus. Her cardiopulmonary examination is normal. Her abdomen is tense, distended, and diffusely tender. She has bilateral +2 pitting edema in her lower extremities. She is oriented to person only and is noted to have asterixis. Her baseline Model for End-stage Liver Disease score is 18 points on a scale of 6 (less ill) to 40 (gravely ill).

Laboratory studies:

• Hemoglobin 9.8 g/dL (reference range 11.5–15.5)
• Platelet count 100 × 10⁹/L (150–400)
• White blood cell count 9.9 × 10⁹/L (3.7–11.0)
• Serum creatinine 1.06 mg/dL (0.58–0.96)
• Bilirubin 6.3 mg/dL (0.2–1.3)
• International normalized ratio of the prothrombin time 2.15 (0.8–1.2)
• Blood urea nitrogen 13 mg/dL (7–21)
• Serum albumin 2.7 g/dL (3.9–4.9).

Intravenous fluid resuscitation is initiated but the patient remains hypotensive, and on repeat laboratory testing 4 hours later her hemoglobin level has dropped to 7.3 mg/dL.

DIFFERENTIAL DIAGNOSIS

1. Which of the following are likely causes of this patient’s presentation?

• Splenic arterial aneurysm rupture
• Spontaneous bacterial peritonitis
• Variceal hemorrhage
• Portal vein thrombosis
• Abdominal aortic aneurysm rupture

Ruptured splenic artery aneurysm

Splenic artery aneurysms are the third most common intra-abdominal aneurysm, after those of the abdominal aorta and iliac artery.¹ They are often asymptomatic and are being detected more frequently because of increased use of computed tomography (CT).² Symptomatic splenic artery aneurysms may present with abdominal pain and have the potential to rupture, which can be life-threatening.^3,4

This patient may have a ruptured splenic artery aneurysm, given her hemodynamic shock.

Spontaneous bacterial peritonitis

Ten percent to 20% of hospitalized patients with cirrhosis and ascites develop spontaneous bacterial peritonitis. Patients may present with ascites and abdominal pain, tenderness to palpation, fever, encephalopathy, or worsening liver and renal function.

Diagnostic paracentesis is paramount to delineate the cause of ascites; one should calculate the serum-ascites albumin gradient and obtain a cell count and culture of the ascitic fluid. The diagnosis of spontaneous bacterial peritonitis can be made if the ascitic fluid polymorphonuclear cell count is 0.25 × 10⁹/L or higher, even if the ascitic fluid culture is negative.^5,6 Simultaneous blood cultures should also be collected, as 50% of cases are associated with bacteremia.

The in-hospital mortality rate of an episode of spontaneous bacterial peritonitis has been reduced to 10% to 20% thanks to prompt diagnosis and empiric treatment with third-generation cephalosporins.⁷

Five percent of cases of infected ascites fluid are due to secondary bacterial peritonitis from a perforated viscus or a loculated abscess, which cannot be differentiated clinically from spontaneous bacterial peritonitis but can be diagnosed with CT.⁸

This patient may be presenting with septic shock secondary to either of these causes.

Variceal hemorrhage

Half of patients with cirrhosis have gastroesophageal varices due to portal hypertension. Endoscopic surveillance is warranted, as the risk of hemorrhage is 12% to 15% per year, and the mortality rate approaches 15% to 20% with each episode. Prompt resuscitation, diagnosis, and control of bleeding is paramount.

Esophagogastroduodenoscopy is used for both diagnosis and intervention. Short-term prophylactic use of antibiotics improves survival by preventing infections in the event bleeding recurs.^9–11

Our patient may be presenting with hemodynamic shock from bleeding esophageal varices.

Portal vein thrombosis is a common complication of cirrhosis, occurring in 5% to 28% of patients. The risk increases with the severity of liver disease and in association with hepatocellular carcinoma.¹² Forty-three percent of cases are discovered incidentally in asymptomatic patients during ultrasonography, 39% present with upper gastrointestinal bleeding, and 18% present with abdominal pain.^13,14

Portal vein thrombosis is the complete or partial obstruction of blood flow due to a thrombus in the lumen of the portal vein. Contrast ultrasonography and CT can be used to establish the diagnosis.¹⁵

Anticoagulation is recommended in cases of complete thrombosis in candidates for living-donor liver transplant and for those at risk of mesenteric ischemia because of the thrombus extending into the mesenteric veins. In symptomatic patients, the decision to initiate anticoagulation should be made on a case-by-case basis after appropriate screening and management of varices.^16–18

Our patient’s thrombocytopenia reflects the severity of portal hypertension and increases her risk of portal vein thrombosis, but this is unlikely to be the sole cause of the hemodynamic compromise in this patient.

Ruptured abdominal aortic aneurysm

Rupture of an abdominal aortic aneurysm is a medical emergency, with a mortality rate approaching 90%. Risk factors for abdominal aortic aneurysms are smoking, male sex, age over 65, history of cardiovascular disease, hypertension, and a family history of abdominal aortic aneurysm, especially if a first-degree relative is affected.¹⁹ Endovascular repair is associated with lower rates of death and complications compared with open repair.²⁰

The patient does not have any of those risk factors, making this diagnosis less likely.

CASE CONTINUED: RUPTURED SPLENIC ARTERY ANEURYSM

Emergency CT of the abdomen and pelvis with contrast enhancement shows a large left intraperitoneal hematoma with active extravasation from a ruptured splenic artery aneurysm (Figure 1). The patient receives packed red blood cells and fresh-frozen plasma before being transferred to our hospital.

2. Which of the following is false regarding splenic artery aneurysms?

• They are the most common type of splanchnic arterial aneurysm
• True aneurysms are more common than pseudoaneurysms
• Asymptomatic aneurysms are discovered incidentally during assessment for other radiographic indications
• Splenic artery aneurysm in portal hypertension is the result of athero-sclerotic changes to the vascular intima

Splenic artery aneurysm in portal hypertension is not the result of atherosclerotic change to the vascular intima.

Splenic artery aneurysms are the most common type of splanchnic artery aneurysm.¹ True aneurysms involve all 3 layers of the arterial wall, ie, intima, media, and adventitia. Cirrhosis and portal hypertension are associated with true aneurysm formation. The proposed mechanism of aneurysm formation is increased splenic blood flow in response to portal congestion with resultant hemodynamic stress that disrupts arterial wall structure, leading to aneurysmal dilation.²¹

In earlier reports, the incidence of true splenic artery aneurysm in portal hypertension varied from 2.9% to 50%, the latter representing autopsy findings of small aneurysms that were found in the splenic hilum of patients with cirrhosis.^22–25 The incidence of clinically significant aneurysms in cirrhosis is unknown but incidental asymptomatic aneurysm is being detected more frequently on imaging studies pursued for screening purposes.²⁶

The risk of rupture is low, only 2% to 10% in older studies and likely even lower now due to increased incidental detection in asymptomatic patients.²⁷ However, emergent management of rupture at a tertiary care facility is paramount, as the mortality rate of ruptured splenic artery aneurysm is 29% to 36%.^1,26,28

Splenic artery pseudoaneurysm is rarer and has a different pathophysiologic process than true aneurysm. It usually arises in the setting of trauma, pancreatitis, or postsurgery.^29,30 Pseudoaneurysm is more likely to rupture, owing to compromise in the vascular wall integrity.^4,21,28 As a result, treatment is indicated for every pseudoaneurysm regardless of size.

RISK FACTORS FOR SPLENIC ARTERY ANEURYSM

3. Which of the following is true regarding our patient’s risk of splenic artery aneurysm?

• Liver cirrhosis and portal hypertension are her greatest risk factors for it
• Female sex and prior pregnancy are her greatest risk factors for it
• Being Native American makes it more likely that the patient has splenic artery aneurysm secondary to collagen vascular disease
• Her risk of rupture would diminish after receiving a liver transplant

Liver cirrhosis and portal hypertension are her greatest risk factors for splenic artery aneurysm.

Risk factors for true aneurysm include hypertension, atherosclerosis, portal hypertension with or without liver cirrhosis, liver transplant, third trimester of pregnancy, and multiparity.^1,4,26,28,31 Splenic artery aneurysm is  usually diagnosed in the sixth decade. It may be 4 times as common in women, given a hormonal influence.³² Cirrhosis is also associated with massive splenic artery aneurysm (≥ 5 cm). Although rare, massive splenic artery aneurysm is more frequent in men (the male-to-female ratio is 1.78:1) and has a heightened risk of rupture.²⁸ The incidence of rupture increases to around 3% to 4% after liver transplant.³³ Rare causes of true aneurysm include fibrodysplasia, collagen vascular disease (eg, Loeys-Dietz and type IV Ehler-Danlos syndromes), vasculitis (eg, polyarteritis nodosa due to amphetamine abuse), and mycotic aneurysms.^24,25,28,29

This patient’s age, sex, and history of cirrhosis puts her at increased risk of splenic artery aneurysm. The risk of rupture is highest in the peripartum period and in patients with cirrhosis who become pregnant. Although being Native American portends an increased risk for collagen vascular disease, the latter is unlikely to be a contributing factor.

4. Which of the following is false regarding treatment of splenic artery aneurysms?

• Aneurysms larger than 2 cm and those that are expanding require repair
• Treatment should be offered if the patient has symptoms attributable to the aneurysm
• Asymptomatic aneurysms in pregnant women can be followed with watchful waiting
• Minimally invasive therapies such as percutaneous embolization may be a good option in poor operative candidates

Asymptomatic aneurysms in pregnant women should not be followed with watchful waiting—they should be repaired, as rupture carries a maternal mortality rate of 75% and a fetal mortality rate of 95%.³⁴

Complications of splenic artery aneurysm depend on the type of aneurysm and its predisposing factors. Indications for treatment of true aneurysms include:

• Symptoms attributable to the aneurysm (hence, the second answer choice above is true)
• Diameter 2  cm or greater or enlarging diameter (hence, the first answer choice is true)
• Women of childbearing age in anticipation of pregnancy
• Need for surgical intervention such as portocaval shunt and liver transplant.

Conservative management is associated with a late mortality risk of 4.9%.² Interventional options include percutaneous embolization or stenting; or laparotomy with splenic artery ligation or excision with or without splenectomy.^1,28,35–37

Endovascular and open surgical repair have both been used to treat splenic artery aneurysms. The method used depends on the patient’s surgical history and aneurysm anatomy such as splenic artery tortuosity hindering passage of a catheter. Open surgery is associated with longer intraoperative time and length of hospital stay and higher rates of 30-day mortality and perioperative morbidity.^38–41 With endovascular repair, the complication of persistent or recurrent flow occurs in 3% to 5% of cases by 30 days; hence, postprocedural surveillance is recommended.^42–44 Endovascular repair has a higher reintervention rate but may still be more cost-effective than open surgical repair.

Because patients with cirrhosis have a higher risk of surgical complications,⁴⁵ elective endovascular treatment may be an option for patients with aneurysms at high risk of rupturing. Endovascular treatment of visceral aneurysms is associated with complications such as postembolization syndrome (fever, abdominal pain, pleural effusion, and pancreatitis), access site hematoma, splenic infarction, and persistent abdominal pain.⁴²

Patients with cirrhosis as the cause of splenic artery aneurysm tend to need longer hospitalization after endovascular treatment, but there is insufficient evidence to suggest that they are at higher risk of other complications.³⁷

CASE CONTINUED: SPLENIC ARTERY EMBOLIZATION

The patient undergoes emergency splenic artery embolization, performed by an interventional radiology team (Figure 2 and Figure 3). Over the next few days, her mental status improves and her abdominal pain resolves. Her hemoglobin level remains stable after the procedure.

The surgical and interventional radiology teams discuss the risk of repeat intervention with the patient and her family, who prefer a nonoperative approach. She is managed supportively in the intensive care unit and is finally discharged home in stable condition and is scheduled for outpatient follow-up.

SUSPECT THIS FATAL CONDITION

The low prevalence of ruptured splenic artery aneurysm may lead physicians to attribute septic shock to spontaneous bacterial peritonitis or hemorrhagic shock from gastroesophageal varices in patients with cirrhosis, but a high index of suspicion and early recognition of this rare disease can lead to timely diagnosis and treatment of this highly fatal complication.

KEY POINTS

• Splenic artery aneurysm is a common complication of cirrhosis, often diagnosed incidentally.
• Elective embolization should be considered for asymptomatic splenic artery aneurysms larger than 2 cm in diameter, clinically symptomatic aneurysms, women of childbearing age, and patients who are candidates for liver transplant.
• Although splenic artery aneurysm rupture is rare, it has a high mortality rate and warrants a high index of suspicion to institute prompt specialized intervention.
• We recommend that physicians consider splenic artery aneurysm rupture in their differential diagnoses in patients with liver cirrhosis presenting with abdominal pain, altered mental status, and hemodynamic shock.

A 64-year-old man with end-stage renal disease was evaluated in the pulmonary clinic for persistent abnormalities on axial computed tomography (CT) of the chest. He was a lifelong nonsmoker and had no history of exposure to occupational dust or fumes. His oxygen saturation was 100% on room air, and he denied any respiratory symptoms.

WHEN TO CONSIDER METASTATIC PULMONARY CALCIFICATION

The differential diagnosis for chronic upper-lobe-predominant ground-glass nodules is broad and includes atypical infections, recurrent alveolar hemorrhage, hypersensitivity pneumonitis, vasculitis, sarcoidosis, chronic eosinophilic pneumonia, occupational lung disease, and pulmonary alveolar microlithiasis. However, several aspects of our patient’s case suggested an often overlooked diagnosis, metastatic pulmonary calcification.

Metastatic pulmonary calcification is caused by deposition of calcium salts in lung tissue and is most commonly seen in patients on dialysis,^1,2 and our patient had been dependent on dialysis for many years. The chronically elevated calcium-phosphorus product and secondary hyperparathyroidism often seen with end-stage renal disease may explain this association.

Our patient’s lack of symptoms is also an important diagnostic clue. Unlike many other causes of chronic upper-lobe-predominant ground-glass nodules, metastatic pulmonary calcification does not usually cause symptoms and is often identified only at autopsy.³ Results of pulmonary function testing are often normal.⁴

Metastatic pulmonary calcification can appear as diffusely calcified nodules or high-attenuation areas of consolidation on CT. However, as in our patient’s case, CT may demonstrate fluffy, centrilobular ground-glass nodules due to the microscopic size of the deposited calcium crystals.¹ Identifying calcified vessels on imaging supports the diagnosis.⁴

Treatment of metastatic pulmonary calcification in a patient with end-stage renal disease is focused on correcting underlying metabolic abnormalities with phosphate binders, vitamin D supplementation, and dialysis.

A 64-year-old man with end-stage renal disease was evaluated in the pulmonary clinic for persistent abnormalities on axial computed tomography (CT) of the chest. He was a lifelong nonsmoker and had no history of exposure to occupational dust or fumes. His oxygen saturation was 100% on room air, and he denied any respiratory symptoms.

WHEN TO CONSIDER METASTATIC PULMONARY CALCIFICATION

The differential diagnosis for chronic upper-lobe-predominant ground-glass nodules is broad and includes atypical infections, recurrent alveolar hemorrhage, hypersensitivity pneumonitis, vasculitis, sarcoidosis, chronic eosinophilic pneumonia, occupational lung disease, and pulmonary alveolar microlithiasis. However, several aspects of our patient’s case suggested an often overlooked diagnosis, metastatic pulmonary calcification.

Metastatic pulmonary calcification is caused by deposition of calcium salts in lung tissue and is most commonly seen in patients on dialysis,^1,2 and our patient had been dependent on dialysis for many years. The chronically elevated calcium-phosphorus product and secondary hyperparathyroidism often seen with end-stage renal disease may explain this association.

Our patient’s lack of symptoms is also an important diagnostic clue. Unlike many other causes of chronic upper-lobe-predominant ground-glass nodules, metastatic pulmonary calcification does not usually cause symptoms and is often identified only at autopsy.³ Results of pulmonary function testing are often normal.⁴

Metastatic pulmonary calcification can appear as diffusely calcified nodules or high-attenuation areas of consolidation on CT. However, as in our patient’s case, CT may demonstrate fluffy, centrilobular ground-glass nodules due to the microscopic size of the deposited calcium crystals.¹ Identifying calcified vessels on imaging supports the diagnosis.⁴

Treatment of metastatic pulmonary calcification in a patient with end-stage renal disease is focused on correcting underlying metabolic abnormalities with phosphate binders, vitamin D supplementation, and dialysis.

A 64-year-old man with end-stage renal disease was evaluated in the pulmonary clinic for persistent abnormalities on axial computed tomography (CT) of the chest. He was a lifelong nonsmoker and had no history of exposure to occupational dust or fumes. His oxygen saturation was 100% on room air, and he denied any respiratory symptoms.

WHEN TO CONSIDER METASTATIC PULMONARY CALCIFICATION

The differential diagnosis for chronic upper-lobe-predominant ground-glass nodules is broad and includes atypical infections, recurrent alveolar hemorrhage, hypersensitivity pneumonitis, vasculitis, sarcoidosis, chronic eosinophilic pneumonia, occupational lung disease, and pulmonary alveolar microlithiasis. However, several aspects of our patient’s case suggested an often overlooked diagnosis, metastatic pulmonary calcification.

Metastatic pulmonary calcification is caused by deposition of calcium salts in lung tissue and is most commonly seen in patients on dialysis,^1,2 and our patient had been dependent on dialysis for many years. The chronically elevated calcium-phosphorus product and secondary hyperparathyroidism often seen with end-stage renal disease may explain this association.

Our patient’s lack of symptoms is also an important diagnostic clue. Unlike many other causes of chronic upper-lobe-predominant ground-glass nodules, metastatic pulmonary calcification does not usually cause symptoms and is often identified only at autopsy.³ Results of pulmonary function testing are often normal.⁴

Metastatic pulmonary calcification can appear as diffusely calcified nodules or high-attenuation areas of consolidation on CT. However, as in our patient’s case, CT may demonstrate fluffy, centrilobular ground-glass nodules due to the microscopic size of the deposited calcium crystals.¹ Identifying calcified vessels on imaging supports the diagnosis.⁴

Treatment of metastatic pulmonary calcification in a patient with end-stage renal disease is focused on correcting underlying metabolic abnormalities with phosphate binders, vitamin D supplementation, and dialysis.

To the Editor: We read with great interest the article by Patnaik et al¹ about a patient who had a cardiac metastasis of ovarian cancer, and we would like to raise a few points.

It is important to clarify that metastatic cardiac tumors are not necessary malignant. Intravenous leiomyomatosis is a benign small-muscle tumor that can spread to the heart, causing various cardiac symptoms.² Even with extensive disease, patients with intravenous leiomyomatosis may remain asymptomatic until cardiac involvement occurs. The most common cardiac symptoms are dyspnea, syncope, and lower-extremity edema.

Cardiac involvement in intravenous leiomyomatosis may occur via direct invasion or hematogenous or lymphatic spread of the tumor. In leiomyoma and leiomyosarcoma, cardiac invasion usually occurs via direct spread through the inferior vena cava into the right atrium and ventricle. Thus, cardiac involvement with these tumors (except for nephroma) was reported to exclusively involve the right side of the heart.

In 2014, we reported a unique case of intravenous leiomyomatosis that extended from the right side into the left side of the heart and the aorta via an atrial septal defect.² Intracardiac extension of intravenous leiomyomatosis may result in pulmonary embolism, systemic embolization if involving the left side, and, rarely, sudden death.²

In patients with malignancy, differentiating between thrombosis and tumor is critical. These patients have a hypercoagulable state and a fourfold increase in thrombosis risk, and chemotherapy increases this risk even more.³ Although tissue pathology examination is important for differentiating thrombosis from tumor, visualization of the direct extension of the mass from the primary source into the heart through the inferior vena cava by ultrasonography, computed tomography, or magnetic resonance imaging may help in making this distinction.²

To the Editor: We read with great interest the article by Patnaik et al¹ about a patient who had a cardiac metastasis of ovarian cancer, and we would like to raise a few points.

It is important to clarify that metastatic cardiac tumors are not necessary malignant. Intravenous leiomyomatosis is a benign small-muscle tumor that can spread to the heart, causing various cardiac symptoms.² Even with extensive disease, patients with intravenous leiomyomatosis may remain asymptomatic until cardiac involvement occurs. The most common cardiac symptoms are dyspnea, syncope, and lower-extremity edema.

Cardiac involvement in intravenous leiomyomatosis may occur via direct invasion or hematogenous or lymphatic spread of the tumor. In leiomyoma and leiomyosarcoma, cardiac invasion usually occurs via direct spread through the inferior vena cava into the right atrium and ventricle. Thus, cardiac involvement with these tumors (except for nephroma) was reported to exclusively involve the right side of the heart.

In 2014, we reported a unique case of intravenous leiomyomatosis that extended from the right side into the left side of the heart and the aorta via an atrial septal defect.² Intracardiac extension of intravenous leiomyomatosis may result in pulmonary embolism, systemic embolization if involving the left side, and, rarely, sudden death.²

In patients with malignancy, differentiating between thrombosis and tumor is critical. These patients have a hypercoagulable state and a fourfold increase in thrombosis risk, and chemotherapy increases this risk even more.³ Although tissue pathology examination is important for differentiating thrombosis from tumor, visualization of the direct extension of the mass from the primary source into the heart through the inferior vena cava by ultrasonography, computed tomography, or magnetic resonance imaging may help in making this distinction.²

To the Editor: We read with great interest the article by Patnaik et al¹ about a patient who had a cardiac metastasis of ovarian cancer, and we would like to raise a few points.

It is important to clarify that metastatic cardiac tumors are not necessary malignant. Intravenous leiomyomatosis is a benign small-muscle tumor that can spread to the heart, causing various cardiac symptoms.² Even with extensive disease, patients with intravenous leiomyomatosis may remain asymptomatic until cardiac involvement occurs. The most common cardiac symptoms are dyspnea, syncope, and lower-extremity edema.

Cardiac involvement in intravenous leiomyomatosis may occur via direct invasion or hematogenous or lymphatic spread of the tumor. In leiomyoma and leiomyosarcoma, cardiac invasion usually occurs via direct spread through the inferior vena cava into the right atrium and ventricle. Thus, cardiac involvement with these tumors (except for nephroma) was reported to exclusively involve the right side of the heart.

In 2014, we reported a unique case of intravenous leiomyomatosis that extended from the right side into the left side of the heart and the aorta via an atrial septal defect.² Intracardiac extension of intravenous leiomyomatosis may result in pulmonary embolism, systemic embolization if involving the left side, and, rarely, sudden death.²

In patients with malignancy, differentiating between thrombosis and tumor is critical. These patients have a hypercoagulable state and a fourfold increase in thrombosis risk, and chemotherapy increases this risk even more.³ Although tissue pathology examination is important for differentiating thrombosis from tumor, visualization of the direct extension of the mass from the primary source into the heart through the inferior vena cava by ultrasonography, computed tomography, or magnetic resonance imaging may help in making this distinction.²

The past 3 decades have seen an evolution in the understanding, diagnosis, and treatment of groin pain, both chronic and acute, in athletes and non-athletes alike. Groin pain and groin injury are common. Most cases are transient, with patients returning to their activities within weeks or months. There has also been increasing awareness of a definitive population of patients who do not get better, or who improve and plateau before reaching preinjury level of performance.^1-3 Several authors have brought more attention to the injury, introducing vocabulary, theories, diagnostic testing, and diagnoses, which now constitute a knowledge base.^1,3-5

As stated in almost every article on groin pain and diagnosis, lack of cohesive agreement and vocabulary, and consistent protocols and procedures, has abounded, making general understanding and agreement in this area inconsistent.^1,6-8In this article, members of a tertiary-care group specializing in chronic groin pain, athletic pubalgia (sports hernia), and inguinal herniorrhaphy outline their clinical examination, diagnostic algorithm, imaging protocol, treatment strategy, and outcomes for a population of patients referred by physicians and allied health professionals for a suspected diagnosis of athletic pubalgia.

Background

The pubic symphysis acts as a stabilizing central anchor with elaborate involvement of the anterior structures, including the rectus abdominis, adductor longus, and inguinal ligaments.^3,7,9 Literature from Europe, Australia, and the United States has described groin pain, mostly in professional athletes, involving these pubic structures and attachments. Several publications have been addressing chronic groin pain, and each has its own diagnostic algorithm, imaging protocol, and treatment strategy.^3,6,9-18

Terminology specific to groin pain in athletes is not new, and has a varied history dating to the early 20th century. Terms such as sportsman hernia¹⁹ and subsequently sports hernia²⁰, have recently been embraced by the lay population. In 1999, Gibbon²¹ described shearing of the common adductor–rectus abdominis anatomical and functional unit and referenced a 1902 anatomical text that describes vertical ligamentous fibers contiguous with rectus sheath and adductor muscles, both attaching to the pubis. Injury to this region is the basis of pubalgia, a term originally used in 1984 by Brunet to describe a pain syndrome at the pubis.²²

Many authors have proposed replacing sports hernia with athletic pubalgia.^{1,3,6,7,10,14,18,23} These terms refer to a group of musculoskeletal processes that occur in and around the pubic symphysis and that share similar mechanisms of injury and common clinical manifestations. The condition was originally described in high-performance athletes, and at one point the term sports hernia was reserved for this patient population.⁵ According to many authors, presence of an inguinal hernia excludes the diagnosis.^1,2,5Magnetic resonance imaging (MRI) has helped to advance and define our understanding of the injury.¹⁰ As the history of the literature suggests, earlier concepts of chronic pain focused either on the medial aspect of the inguinal canal and its structures or on the pubic attachments. Many specialists in the area have concluded that the chronic groin pain injury can and often does embody both elements.^3,9 Correlation with MRI findings, injury seen during surgical procedures, and cadaveric studies have directed our understanding to a structure, the pre-pubic aponeurotic complex (P-PAC), or rectus aponeurotic plate.^12,24,25 Anatomically, the P-PAC, which has several fascial components, attaches posteriorly to the pubic bone and, to a degree, the pubic symphyseal cartilaginous disc. Major contributions to the P-PAC are fibers from the rectus abdominis tendon, the medial aspect of the transversalis and internal oblique muscles (the conjoint tendon, according to some), the inguinal ligament, and the adductor longus tendon.²⁶When communicating with referring physicians, we use the term athletic pubalgia to indicate a specific injury. The athletic pubalgia injury can be defined as serial microtearing,¹ or complete tearing, of the posterior attachment of the P-PAC off the anterior pubis.^3,10 Complete tearing or displacement can occur unilaterally or across the midline to the other side. As athletic pubalgia is a specific anatomical injury rather than a broad category of findings, an additional pathologic diagnosis, such as inguinal hernia, does not exclude the diagnosis of athletic pubalgia. Unfortunately, the terms sports hernia and sportsman hernia, commonly used in the media and in professional communities, have largely confused the broader understanding of nuances and of the differences between the specific injuries and MRI findings.¹⁸

Our Experience

In our practice, we see groin pain patients referred by internists, physiatrists, physical therapists, trainers, general surgeons, urologists, gynecologists, and orthopedic surgeons. In many cases, patients have been through several consultations and work-ups, as their pain syndrome does not fall under a specific category. Patients without inguinal hernia, hip injury, urologic, or gynecologic issues typically are referred to a physiatrist or a physical therapist. Often, there are marginal improvements with physical therapy, but in some cases the injury never completely resolves, and the patient continues to have pain with activity or return to sports.

Most of our patients are nonprofessional athletes, men and women who range widely in age and participate casually or regularly in sporting events. Most lack the rigorous training, conditioning, and close supervision that professional athletes receive. Many other patients are nonprofessional but elite athletes who train 7 days a week for marathons, ultramarathons, triathlons, obstacle course races (“mudders”), and similar events.

Work-Up

A single algorithm is used for all patients initially referred to the surgeon’s office for pelvic or groin pain. The initial interview directs attention to injury onset and mechanism, duration of rest or physical therapy after surgery, pain quality and pain levels, and antagonistic movements and positions. Examination starts with assessment for inguinal, femoral, and umbilical hernias. Resisted sit-up, leg-raise, adduction, and hip assessment tests are performed. The P-PAC is examined with a maneuver similar to the one used for inguinal hernia, as it allows for better assessment of the transversalis fascia (over the direct space) to determine if the inguinal canal floor is attenuated and bulges forward with the Valsalva maneuver. Then, the lateral aspect of the rectus muscle is assessed for pain, usually with the head raised to contract the muscle, to determine tenderness along the lateral border. The rectus edge is traced down to the pubis at its attachment, the superolateral border of the P-PAC. Examination proceeds medially, over the rectus attachment, toward the pubic symphysis, continuing the assessment for tenderness. Laterally, the conjoint tendon and inguinal ligament medial attachments are assessed at the level of the pubic tubercle, which represents the lateral border of the P-PAC. Finally, the examination continues to the inferior border with assessment of the adductor longus attachment, which is best performed with the leg in an adducted position. In the acute or semiacute setting (pain within 1 year of injury onset), tenderness is often elicited. With long-standing injuries, pain is often not elicited, but the patient experiences pain along this axis during activity or afterward.

Patients with positive history and physical examination findings proceed through an MRI protocol designed to detect pathology of the pubic symphysis, hips, and inguinal canals (Figures 1A-1D).

Treatment

Patients who report sustaining an acute groin injury within the previous 6 months are treated nonoperatively. A combination of rest, nonsteroidal anti-inflammatory drugs, and physical therapy is generally recommended.^2,10 In cases of failed nonoperative management, patients are evaluated for surgery. No single operation is recommended for all patients.^1,6,14,27,28 (Larson²⁶ recently reviewed results from several trials involving a variety of surgical repairs and found return-to-sports rates ranging from 80% to 100%.) Findings from the physical examination and from the properly protocolled MRI examination are used in planning surgery to correct any pathology that could be contributing to symptoms or destabilization of the structures attaching to the pubis. Disruption of the P-PAC from the pubis would be repaired, for example. Additional injuries, such as partial or complete detachment of the conjoint tendon or inguinal ligament, may be repaired as well. If the transversalis fascia is attenuated and bulging forward, the inguinal floor is closed. Adductor longus tendon pathology is addressed, most commonly with partial tendinolysis. Often, concomitant inguinal hernias are found, and these may be repaired in open fashion while other maneuvers are being performed, or laparoscopically.

Materials and Methods

After receiving study approval from our Institutional Review Board, we retrospectively searched for all MRIs performed by our radiology department between March 1, 2011 and March 31, 2013 on patients referred for an indication of groin pain, sports hernia, or athletic pubalgia. Patients were excluded if they were younger than 18 years any time during their care. Some patients previously or subsequently underwent computed tomography or ultrasonography. MRIs were reviewed and positive findings were compiled in a database. Charts were reviewed to identify which patients in the dataset underwent surgery, after MRI, to address their presenting chief complaint. Surgery date and procedure(s) performed were recorded. Patients were interviewed by telephone as part of the in-office postoperative follow-up.

Results

One hundred nineteen MRIs were performed on 117 patients (97 men, 83%). Mean age was 39.8 years. Seventy-nine patients (68%) had an MRI finding of athletic pubalgia, 67 (57%) had an acetabular labral tear in one or both hip joints, and 41 (35%) had a true inguinal hernia. Concomitant findings were common: 47 cases of athletic pubalgia and labral tear(s), 28 cases of athletic pubalgia and inguinal hernia, and 15 cases of all 3 (athletic pubalgia, labral tear, inguinal hernia).

Use of breath-hold axial single-shot fast spin-echo sequences with and without the Valsalva maneuver increased sensitivity in detecting pathologies—inguinal hernia and Gilmore groin in particular. On 24 of the 119 MRIs, the Valsalva maneuver either revealed the finding or made it significantly more apparent.

Of all patients referred for MRI for chronic groin pain, 48 (41%) subsequently underwent surgery. In 29 surgeries, the rectus abdominis, adductor longus, and/or pre-pubic aponeurotic plate were repaired; in 13 cases, herniorrhaphy was performed as well; in 2 cases, masses involving the spermatic cord were removed.

The most common surgery (30 cases) was herniorrhaphy, which was performed as a single procedure, multiple procedures, or in combination with procedures not related to a true hernia. Eighteen patients underwent surgery only for hernia repair.

Of the 79 patients with MRI-positive athletic pubalgia, 39 subsequently underwent surgery, and 31 (79%) of these were followed up by telephone. Mean duration of rest after surgery was 6.2 weeks. Twelve patients (39%) had physical therapy after surgery, some as early as 4 weeks, and some have continued their therapy since surgery. Of the 31 patients who were followed up after surgery, 23 (74%) resumed previous activity levels. Return to previous activity level took these patients a mean of 17.9 weeks. When asked if outcomes satisfied their expectations, 28 patients (90%) said yes, and 3 said no.

Forty patients with MRI-positive athletic pubalgia were nonoperatively treated, and 28 (70%) of these patients were followed up. In this group, mean duration of rest after surgery was 6.9 weeks. Thirteen patients (46%) participated in physical therapy, for a mean duration of 10.8 weeks. Of the patients followed up, 19 (68%) returned to previous activity level. Twenty-one patients (75%) were satisfied with their outcome.

Discussion

Diagnosis and treatment of chronic groin pain have had a long, confusing, and frustrating history for both patients and the medical professionals who provide them with care.^3,6,7,10 Historically, the problem has been, in part, the lack of diagnostic capabilities. Currently, however, pubalgia MRI protocol allows the exact pathology to be demonstrated.³ As already noted, concomitant hip pathology or inguinal hernia is not unusual⁸; any structural abnormality in the area is a potential destabilizer of the structures attached to the pubis.¹⁸ Solving only one of these issues may offer only partial resolution of symptoms and thereby reduce the rate of successful treatment of groin pain.

Diagnostic algorithms are being developed. In addition, nonoperative treatments are being tried for some of the issues. Physicians are giving diagnostic and therapeutic steroid injections in the pubic cleft, along the rectus abdominis/adductor longus complex, or posterior to the P-PAC. Platelet-rich plasma injection therapy has had limited success.²⁹This article provides a snapshot of what a tertiary-care group of physicians specializing in chronic groin pain sees in an unfiltered setting. We think this is instructive for several reasons.

First, many patients in our population have visited a multitude of specialists without receiving a diagnosis or being referred appropriately. Simply, many specialists do not know the next step in treating groin pain and thus do not make the appropriate referral. Until recently, the literature has not been helpful. It has poorly described the constellation of injuries comprising chronic groin pain. More significantly, groin injuries have been presented as ambiguous injuries lacking effective treatment. Over the past decade, however, abundant literature on the correlation of these injuries with specific MRI findings has made the case otherwise.

Second, a specific MRI pubalgia protocol is needed. Inability to make a correct diagnosis, because of improper MRI, continues to add to the confusion surrounding the injury and undoubtedly prolongs the general medical community’s thinking that diagnosis and treatment of chronic groin pain are elusive. Our data support this point in many ways. Although all patients in this study were seen by a medical professional before coming to our office, none had received a diagnosis of occult hernia or attenuated transversalis fascia; nevertheless, we identified inguinal hernia, Gilmore groin, or both in 44% of these patients. These findings are not surprising, as MRI was the crucial link in diagnosis. In addition, the point made by other groin pain specialists—that a hernia precludes a pubalgia diagnosis^1,2,5—is not supported by our data. Inguinal hernia can and does exist in conjunction with pubalgia. More than half the patients in our study had a combined diagnosis. We contend that, much as hip labral pathology occurs concomitantly with pubalgia,²³ inguinal hernia may be a predisposing factor as well. A defect in the direct or indirect space can destabilize the area and place additional strain on the pubic attachments.

In our experience, the dynamic Valsalva sequence improves detection of true hernias and anterior abdominal wall deficiencies and should be included in each protocol for the evaluation of acute or chronic groin pain.

Shear forces and injury at the pubis can occur outside professional athletics. Our patient population is nonprofessional athletes, teenagers to retirees, and all can develop athletic pubalgia. Ninety percent of surveyed patients who received a diagnosis and were treated surgically were satisfied with their outcomes.

Am J Orthop. 2017;46(4):E251-E256. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

The past 3 decades have seen an evolution in the understanding, diagnosis, and treatment of groin pain, both chronic and acute, in athletes and non-athletes alike. Groin pain and groin injury are common. Most cases are transient, with patients returning to their activities within weeks or months. There has also been increasing awareness of a definitive population of patients who do not get better, or who improve and plateau before reaching preinjury level of performance.^1-3 Several authors have brought more attention to the injury, introducing vocabulary, theories, diagnostic testing, and diagnoses, which now constitute a knowledge base.^1,3-5

As stated in almost every article on groin pain and diagnosis, lack of cohesive agreement and vocabulary, and consistent protocols and procedures, has abounded, making general understanding and agreement in this area inconsistent.^1,6-8In this article, members of a tertiary-care group specializing in chronic groin pain, athletic pubalgia (sports hernia), and inguinal herniorrhaphy outline their clinical examination, diagnostic algorithm, imaging protocol, treatment strategy, and outcomes for a population of patients referred by physicians and allied health professionals for a suspected diagnosis of athletic pubalgia.

Background

The pubic symphysis acts as a stabilizing central anchor with elaborate involvement of the anterior structures, including the rectus abdominis, adductor longus, and inguinal ligaments.^3,7,9 Literature from Europe, Australia, and the United States has described groin pain, mostly in professional athletes, involving these pubic structures and attachments. Several publications have been addressing chronic groin pain, and each has its own diagnostic algorithm, imaging protocol, and treatment strategy.^3,6,9-18

Terminology specific to groin pain in athletes is not new, and has a varied history dating to the early 20th century. Terms such as sportsman hernia¹⁹ and subsequently sports hernia²⁰, have recently been embraced by the lay population. In 1999, Gibbon²¹ described shearing of the common adductor–rectus abdominis anatomical and functional unit and referenced a 1902 anatomical text that describes vertical ligamentous fibers contiguous with rectus sheath and adductor muscles, both attaching to the pubis. Injury to this region is the basis of pubalgia, a term originally used in 1984 by Brunet to describe a pain syndrome at the pubis.²²

Many authors have proposed replacing sports hernia with athletic pubalgia.^{1,3,6,7,10,14,18,23} These terms refer to a group of musculoskeletal processes that occur in and around the pubic symphysis and that share similar mechanisms of injury and common clinical manifestations. The condition was originally described in high-performance athletes, and at one point the term sports hernia was reserved for this patient population.⁵ According to many authors, presence of an inguinal hernia excludes the diagnosis.^1,2,5Magnetic resonance imaging (MRI) has helped to advance and define our understanding of the injury.¹⁰ As the history of the literature suggests, earlier concepts of chronic pain focused either on the medial aspect of the inguinal canal and its structures or on the pubic attachments. Many specialists in the area have concluded that the chronic groin pain injury can and often does embody both elements.^3,9 Correlation with MRI findings, injury seen during surgical procedures, and cadaveric studies have directed our understanding to a structure, the pre-pubic aponeurotic complex (P-PAC), or rectus aponeurotic plate.^12,24,25 Anatomically, the P-PAC, which has several fascial components, attaches posteriorly to the pubic bone and, to a degree, the pubic symphyseal cartilaginous disc. Major contributions to the P-PAC are fibers from the rectus abdominis tendon, the medial aspect of the transversalis and internal oblique muscles (the conjoint tendon, according to some), the inguinal ligament, and the adductor longus tendon.²⁶When communicating with referring physicians, we use the term athletic pubalgia to indicate a specific injury. The athletic pubalgia injury can be defined as serial microtearing,¹ or complete tearing, of the posterior attachment of the P-PAC off the anterior pubis.^3,10 Complete tearing or displacement can occur unilaterally or across the midline to the other side. As athletic pubalgia is a specific anatomical injury rather than a broad category of findings, an additional pathologic diagnosis, such as inguinal hernia, does not exclude the diagnosis of athletic pubalgia. Unfortunately, the terms sports hernia and sportsman hernia, commonly used in the media and in professional communities, have largely confused the broader understanding of nuances and of the differences between the specific injuries and MRI findings.¹⁸

Our Experience

In our practice, we see groin pain patients referred by internists, physiatrists, physical therapists, trainers, general surgeons, urologists, gynecologists, and orthopedic surgeons. In many cases, patients have been through several consultations and work-ups, as their pain syndrome does not fall under a specific category. Patients without inguinal hernia, hip injury, urologic, or gynecologic issues typically are referred to a physiatrist or a physical therapist. Often, there are marginal improvements with physical therapy, but in some cases the injury never completely resolves, and the patient continues to have pain with activity or return to sports.

Most of our patients are nonprofessional athletes, men and women who range widely in age and participate casually or regularly in sporting events. Most lack the rigorous training, conditioning, and close supervision that professional athletes receive. Many other patients are nonprofessional but elite athletes who train 7 days a week for marathons, ultramarathons, triathlons, obstacle course races (“mudders”), and similar events.

Work-Up

A single algorithm is used for all patients initially referred to the surgeon’s office for pelvic or groin pain. The initial interview directs attention to injury onset and mechanism, duration of rest or physical therapy after surgery, pain quality and pain levels, and antagonistic movements and positions. Examination starts with assessment for inguinal, femoral, and umbilical hernias. Resisted sit-up, leg-raise, adduction, and hip assessment tests are performed. The P-PAC is examined with a maneuver similar to the one used for inguinal hernia, as it allows for better assessment of the transversalis fascia (over the direct space) to determine if the inguinal canal floor is attenuated and bulges forward with the Valsalva maneuver. Then, the lateral aspect of the rectus muscle is assessed for pain, usually with the head raised to contract the muscle, to determine tenderness along the lateral border. The rectus edge is traced down to the pubis at its attachment, the superolateral border of the P-PAC. Examination proceeds medially, over the rectus attachment, toward the pubic symphysis, continuing the assessment for tenderness. Laterally, the conjoint tendon and inguinal ligament medial attachments are assessed at the level of the pubic tubercle, which represents the lateral border of the P-PAC. Finally, the examination continues to the inferior border with assessment of the adductor longus attachment, which is best performed with the leg in an adducted position. In the acute or semiacute setting (pain within 1 year of injury onset), tenderness is often elicited. With long-standing injuries, pain is often not elicited, but the patient experiences pain along this axis during activity or afterward.

Patients with positive history and physical examination findings proceed through an MRI protocol designed to detect pathology of the pubic symphysis, hips, and inguinal canals (Figures 1A-1D).

Treatment

Patients who report sustaining an acute groin injury within the previous 6 months are treated nonoperatively. A combination of rest, nonsteroidal anti-inflammatory drugs, and physical therapy is generally recommended.^2,10 In cases of failed nonoperative management, patients are evaluated for surgery. No single operation is recommended for all patients.^1,6,14,27,28 (Larson²⁶ recently reviewed results from several trials involving a variety of surgical repairs and found return-to-sports rates ranging from 80% to 100%.) Findings from the physical examination and from the properly protocolled MRI examination are used in planning surgery to correct any pathology that could be contributing to symptoms or destabilization of the structures attaching to the pubis. Disruption of the P-PAC from the pubis would be repaired, for example. Additional injuries, such as partial or complete detachment of the conjoint tendon or inguinal ligament, may be repaired as well. If the transversalis fascia is attenuated and bulging forward, the inguinal floor is closed. Adductor longus tendon pathology is addressed, most commonly with partial tendinolysis. Often, concomitant inguinal hernias are found, and these may be repaired in open fashion while other maneuvers are being performed, or laparoscopically.

Materials and Methods

After receiving study approval from our Institutional Review Board, we retrospectively searched for all MRIs performed by our radiology department between March 1, 2011 and March 31, 2013 on patients referred for an indication of groin pain, sports hernia, or athletic pubalgia. Patients were excluded if they were younger than 18 years any time during their care. Some patients previously or subsequently underwent computed tomography or ultrasonography. MRIs were reviewed and positive findings were compiled in a database. Charts were reviewed to identify which patients in the dataset underwent surgery, after MRI, to address their presenting chief complaint. Surgery date and procedure(s) performed were recorded. Patients were interviewed by telephone as part of the in-office postoperative follow-up.

Results

One hundred nineteen MRIs were performed on 117 patients (97 men, 83%). Mean age was 39.8 years. Seventy-nine patients (68%) had an MRI finding of athletic pubalgia, 67 (57%) had an acetabular labral tear in one or both hip joints, and 41 (35%) had a true inguinal hernia. Concomitant findings were common: 47 cases of athletic pubalgia and labral tear(s), 28 cases of athletic pubalgia and inguinal hernia, and 15 cases of all 3 (athletic pubalgia, labral tear, inguinal hernia).

Use of breath-hold axial single-shot fast spin-echo sequences with and without the Valsalva maneuver increased sensitivity in detecting pathologies—inguinal hernia and Gilmore groin in particular. On 24 of the 119 MRIs, the Valsalva maneuver either revealed the finding or made it significantly more apparent.

Of all patients referred for MRI for chronic groin pain, 48 (41%) subsequently underwent surgery. In 29 surgeries, the rectus abdominis, adductor longus, and/or pre-pubic aponeurotic plate were repaired; in 13 cases, herniorrhaphy was performed as well; in 2 cases, masses involving the spermatic cord were removed.

The most common surgery (30 cases) was herniorrhaphy, which was performed as a single procedure, multiple procedures, or in combination with procedures not related to a true hernia. Eighteen patients underwent surgery only for hernia repair.

Of the 79 patients with MRI-positive athletic pubalgia, 39 subsequently underwent surgery, and 31 (79%) of these were followed up by telephone. Mean duration of rest after surgery was 6.2 weeks. Twelve patients (39%) had physical therapy after surgery, some as early as 4 weeks, and some have continued their therapy since surgery. Of the 31 patients who were followed up after surgery, 23 (74%) resumed previous activity levels. Return to previous activity level took these patients a mean of 17.9 weeks. When asked if outcomes satisfied their expectations, 28 patients (90%) said yes, and 3 said no.

Forty patients with MRI-positive athletic pubalgia were nonoperatively treated, and 28 (70%) of these patients were followed up. In this group, mean duration of rest after surgery was 6.9 weeks. Thirteen patients (46%) participated in physical therapy, for a mean duration of 10.8 weeks. Of the patients followed up, 19 (68%) returned to previous activity level. Twenty-one patients (75%) were satisfied with their outcome.

Discussion

Diagnosis and treatment of chronic groin pain have had a long, confusing, and frustrating history for both patients and the medical professionals who provide them with care.^3,6,7,10 Historically, the problem has been, in part, the lack of diagnostic capabilities. Currently, however, pubalgia MRI protocol allows the exact pathology to be demonstrated.³ As already noted, concomitant hip pathology or inguinal hernia is not unusual⁸; any structural abnormality in the area is a potential destabilizer of the structures attached to the pubis.¹⁸ Solving only one of these issues may offer only partial resolution of symptoms and thereby reduce the rate of successful treatment of groin pain.

Diagnostic algorithms are being developed. In addition, nonoperative treatments are being tried for some of the issues. Physicians are giving diagnostic and therapeutic steroid injections in the pubic cleft, along the rectus abdominis/adductor longus complex, or posterior to the P-PAC. Platelet-rich plasma injection therapy has had limited success.²⁹This article provides a snapshot of what a tertiary-care group of physicians specializing in chronic groin pain sees in an unfiltered setting. We think this is instructive for several reasons.

First, many patients in our population have visited a multitude of specialists without receiving a diagnosis or being referred appropriately. Simply, many specialists do not know the next step in treating groin pain and thus do not make the appropriate referral. Until recently, the literature has not been helpful. It has poorly described the constellation of injuries comprising chronic groin pain. More significantly, groin injuries have been presented as ambiguous injuries lacking effective treatment. Over the past decade, however, abundant literature on the correlation of these injuries with specific MRI findings has made the case otherwise.

Second, a specific MRI pubalgia protocol is needed. Inability to make a correct diagnosis, because of improper MRI, continues to add to the confusion surrounding the injury and undoubtedly prolongs the general medical community’s thinking that diagnosis and treatment of chronic groin pain are elusive. Our data support this point in many ways. Although all patients in this study were seen by a medical professional before coming to our office, none had received a diagnosis of occult hernia or attenuated transversalis fascia; nevertheless, we identified inguinal hernia, Gilmore groin, or both in 44% of these patients. These findings are not surprising, as MRI was the crucial link in diagnosis. In addition, the point made by other groin pain specialists—that a hernia precludes a pubalgia diagnosis^1,2,5—is not supported by our data. Inguinal hernia can and does exist in conjunction with pubalgia. More than half the patients in our study had a combined diagnosis. We contend that, much as hip labral pathology occurs concomitantly with pubalgia,²³ inguinal hernia may be a predisposing factor as well. A defect in the direct or indirect space can destabilize the area and place additional strain on the pubic attachments.

In our experience, the dynamic Valsalva sequence improves detection of true hernias and anterior abdominal wall deficiencies and should be included in each protocol for the evaluation of acute or chronic groin pain.

Shear forces and injury at the pubis can occur outside professional athletics. Our patient population is nonprofessional athletes, teenagers to retirees, and all can develop athletic pubalgia. Ninety percent of surveyed patients who received a diagnosis and were treated surgically were satisfied with their outcomes.

Am J Orthop. 2017;46(4):E251-E256. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

The past 3 decades have seen an evolution in the understanding, diagnosis, and treatment of groin pain, both chronic and acute, in athletes and non-athletes alike. Groin pain and groin injury are common. Most cases are transient, with patients returning to their activities within weeks or months. There has also been increasing awareness of a definitive population of patients who do not get better, or who improve and plateau before reaching preinjury level of performance.^1-3 Several authors have brought more attention to the injury, introducing vocabulary, theories, diagnostic testing, and diagnoses, which now constitute a knowledge base.^1,3-5

As stated in almost every article on groin pain and diagnosis, lack of cohesive agreement and vocabulary, and consistent protocols and procedures, has abounded, making general understanding and agreement in this area inconsistent.^1,6-8In this article, members of a tertiary-care group specializing in chronic groin pain, athletic pubalgia (sports hernia), and inguinal herniorrhaphy outline their clinical examination, diagnostic algorithm, imaging protocol, treatment strategy, and outcomes for a population of patients referred by physicians and allied health professionals for a suspected diagnosis of athletic pubalgia.

Background

The pubic symphysis acts as a stabilizing central anchor with elaborate involvement of the anterior structures, including the rectus abdominis, adductor longus, and inguinal ligaments.^3,7,9 Literature from Europe, Australia, and the United States has described groin pain, mostly in professional athletes, involving these pubic structures and attachments. Several publications have been addressing chronic groin pain, and each has its own diagnostic algorithm, imaging protocol, and treatment strategy.^3,6,9-18

Terminology specific to groin pain in athletes is not new, and has a varied history dating to the early 20th century. Terms such as sportsman hernia¹⁹ and subsequently sports hernia²⁰, have recently been embraced by the lay population. In 1999, Gibbon²¹ described shearing of the common adductor–rectus abdominis anatomical and functional unit and referenced a 1902 anatomical text that describes vertical ligamentous fibers contiguous with rectus sheath and adductor muscles, both attaching to the pubis. Injury to this region is the basis of pubalgia, a term originally used in 1984 by Brunet to describe a pain syndrome at the pubis.²²

Many authors have proposed replacing sports hernia with athletic pubalgia.^{1,3,6,7,10,14,18,23} These terms refer to a group of musculoskeletal processes that occur in and around the pubic symphysis and that share similar mechanisms of injury and common clinical manifestations. The condition was originally described in high-performance athletes, and at one point the term sports hernia was reserved for this patient population.⁵ According to many authors, presence of an inguinal hernia excludes the diagnosis.^1,2,5Magnetic resonance imaging (MRI) has helped to advance and define our understanding of the injury.¹⁰ As the history of the literature suggests, earlier concepts of chronic pain focused either on the medial aspect of the inguinal canal and its structures or on the pubic attachments. Many specialists in the area have concluded that the chronic groin pain injury can and often does embody both elements.^3,9 Correlation with MRI findings, injury seen during surgical procedures, and cadaveric studies have directed our understanding to a structure, the pre-pubic aponeurotic complex (P-PAC), or rectus aponeurotic plate.^12,24,25 Anatomically, the P-PAC, which has several fascial components, attaches posteriorly to the pubic bone and, to a degree, the pubic symphyseal cartilaginous disc. Major contributions to the P-PAC are fibers from the rectus abdominis tendon, the medial aspect of the transversalis and internal oblique muscles (the conjoint tendon, according to some), the inguinal ligament, and the adductor longus tendon.²⁶When communicating with referring physicians, we use the term athletic pubalgia to indicate a specific injury. The athletic pubalgia injury can be defined as serial microtearing,¹ or complete tearing, of the posterior attachment of the P-PAC off the anterior pubis.^3,10 Complete tearing or displacement can occur unilaterally or across the midline to the other side. As athletic pubalgia is a specific anatomical injury rather than a broad category of findings, an additional pathologic diagnosis, such as inguinal hernia, does not exclude the diagnosis of athletic pubalgia. Unfortunately, the terms sports hernia and sportsman hernia, commonly used in the media and in professional communities, have largely confused the broader understanding of nuances and of the differences between the specific injuries and MRI findings.¹⁸

Our Experience

In our practice, we see groin pain patients referred by internists, physiatrists, physical therapists, trainers, general surgeons, urologists, gynecologists, and orthopedic surgeons. In many cases, patients have been through several consultations and work-ups, as their pain syndrome does not fall under a specific category. Patients without inguinal hernia, hip injury, urologic, or gynecologic issues typically are referred to a physiatrist or a physical therapist. Often, there are marginal improvements with physical therapy, but in some cases the injury never completely resolves, and the patient continues to have pain with activity or return to sports.

Most of our patients are nonprofessional athletes, men and women who range widely in age and participate casually or regularly in sporting events. Most lack the rigorous training, conditioning, and close supervision that professional athletes receive. Many other patients are nonprofessional but elite athletes who train 7 days a week for marathons, ultramarathons, triathlons, obstacle course races (“mudders”), and similar events.

Work-Up

A single algorithm is used for all patients initially referred to the surgeon’s office for pelvic or groin pain. The initial interview directs attention to injury onset and mechanism, duration of rest or physical therapy after surgery, pain quality and pain levels, and antagonistic movements and positions. Examination starts with assessment for inguinal, femoral, and umbilical hernias. Resisted sit-up, leg-raise, adduction, and hip assessment tests are performed. The P-PAC is examined with a maneuver similar to the one used for inguinal hernia, as it allows for better assessment of the transversalis fascia (over the direct space) to determine if the inguinal canal floor is attenuated and bulges forward with the Valsalva maneuver. Then, the lateral aspect of the rectus muscle is assessed for pain, usually with the head raised to contract the muscle, to determine tenderness along the lateral border. The rectus edge is traced down to the pubis at its attachment, the superolateral border of the P-PAC. Examination proceeds medially, over the rectus attachment, toward the pubic symphysis, continuing the assessment for tenderness. Laterally, the conjoint tendon and inguinal ligament medial attachments are assessed at the level of the pubic tubercle, which represents the lateral border of the P-PAC. Finally, the examination continues to the inferior border with assessment of the adductor longus attachment, which is best performed with the leg in an adducted position. In the acute or semiacute setting (pain within 1 year of injury onset), tenderness is often elicited. With long-standing injuries, pain is often not elicited, but the patient experiences pain along this axis during activity or afterward.

Patients with positive history and physical examination findings proceed through an MRI protocol designed to detect pathology of the pubic symphysis, hips, and inguinal canals (Figures 1A-1D).

Treatment

Patients who report sustaining an acute groin injury within the previous 6 months are treated nonoperatively. A combination of rest, nonsteroidal anti-inflammatory drugs, and physical therapy is generally recommended.^2,10 In cases of failed nonoperative management, patients are evaluated for surgery. No single operation is recommended for all patients.^1,6,14,27,28 (Larson²⁶ recently reviewed results from several trials involving a variety of surgical repairs and found return-to-sports rates ranging from 80% to 100%.) Findings from the physical examination and from the properly protocolled MRI examination are used in planning surgery to correct any pathology that could be contributing to symptoms or destabilization of the structures attaching to the pubis. Disruption of the P-PAC from the pubis would be repaired, for example. Additional injuries, such as partial or complete detachment of the conjoint tendon or inguinal ligament, may be repaired as well. If the transversalis fascia is attenuated and bulging forward, the inguinal floor is closed. Adductor longus tendon pathology is addressed, most commonly with partial tendinolysis. Often, concomitant inguinal hernias are found, and these may be repaired in open fashion while other maneuvers are being performed, or laparoscopically.

Materials and Methods

After receiving study approval from our Institutional Review Board, we retrospectively searched for all MRIs performed by our radiology department between March 1, 2011 and March 31, 2013 on patients referred for an indication of groin pain, sports hernia, or athletic pubalgia. Patients were excluded if they were younger than 18 years any time during their care. Some patients previously or subsequently underwent computed tomography or ultrasonography. MRIs were reviewed and positive findings were compiled in a database. Charts were reviewed to identify which patients in the dataset underwent surgery, after MRI, to address their presenting chief complaint. Surgery date and procedure(s) performed were recorded. Patients were interviewed by telephone as part of the in-office postoperative follow-up.

Results

One hundred nineteen MRIs were performed on 117 patients (97 men, 83%). Mean age was 39.8 years. Seventy-nine patients (68%) had an MRI finding of athletic pubalgia, 67 (57%) had an acetabular labral tear in one or both hip joints, and 41 (35%) had a true inguinal hernia. Concomitant findings were common: 47 cases of athletic pubalgia and labral tear(s), 28 cases of athletic pubalgia and inguinal hernia, and 15 cases of all 3 (athletic pubalgia, labral tear, inguinal hernia).

Use of breath-hold axial single-shot fast spin-echo sequences with and without the Valsalva maneuver increased sensitivity in detecting pathologies—inguinal hernia and Gilmore groin in particular. On 24 of the 119 MRIs, the Valsalva maneuver either revealed the finding or made it significantly more apparent.

Of all patients referred for MRI for chronic groin pain, 48 (41%) subsequently underwent surgery. In 29 surgeries, the rectus abdominis, adductor longus, and/or pre-pubic aponeurotic plate were repaired; in 13 cases, herniorrhaphy was performed as well; in 2 cases, masses involving the spermatic cord were removed.

The most common surgery (30 cases) was herniorrhaphy, which was performed as a single procedure, multiple procedures, or in combination with procedures not related to a true hernia. Eighteen patients underwent surgery only for hernia repair.

Of the 79 patients with MRI-positive athletic pubalgia, 39 subsequently underwent surgery, and 31 (79%) of these were followed up by telephone. Mean duration of rest after surgery was 6.2 weeks. Twelve patients (39%) had physical therapy after surgery, some as early as 4 weeks, and some have continued their therapy since surgery. Of the 31 patients who were followed up after surgery, 23 (74%) resumed previous activity levels. Return to previous activity level took these patients a mean of 17.9 weeks. When asked if outcomes satisfied their expectations, 28 patients (90%) said yes, and 3 said no.

Forty patients with MRI-positive athletic pubalgia were nonoperatively treated, and 28 (70%) of these patients were followed up. In this group, mean duration of rest after surgery was 6.9 weeks. Thirteen patients (46%) participated in physical therapy, for a mean duration of 10.8 weeks. Of the patients followed up, 19 (68%) returned to previous activity level. Twenty-one patients (75%) were satisfied with their outcome.

Discussion

Diagnosis and treatment of chronic groin pain have had a long, confusing, and frustrating history for both patients and the medical professionals who provide them with care.^3,6,7,10 Historically, the problem has been, in part, the lack of diagnostic capabilities. Currently, however, pubalgia MRI protocol allows the exact pathology to be demonstrated.³ As already noted, concomitant hip pathology or inguinal hernia is not unusual⁸; any structural abnormality in the area is a potential destabilizer of the structures attached to the pubis.¹⁸ Solving only one of these issues may offer only partial resolution of symptoms and thereby reduce the rate of successful treatment of groin pain.

Diagnostic algorithms are being developed. In addition, nonoperative treatments are being tried for some of the issues. Physicians are giving diagnostic and therapeutic steroid injections in the pubic cleft, along the rectus abdominis/adductor longus complex, or posterior to the P-PAC. Platelet-rich plasma injection therapy has had limited success.²⁹This article provides a snapshot of what a tertiary-care group of physicians specializing in chronic groin pain sees in an unfiltered setting. We think this is instructive for several reasons.

First, many patients in our population have visited a multitude of specialists without receiving a diagnosis or being referred appropriately. Simply, many specialists do not know the next step in treating groin pain and thus do not make the appropriate referral. Until recently, the literature has not been helpful. It has poorly described the constellation of injuries comprising chronic groin pain. More significantly, groin injuries have been presented as ambiguous injuries lacking effective treatment. Over the past decade, however, abundant literature on the correlation of these injuries with specific MRI findings has made the case otherwise.

Second, a specific MRI pubalgia protocol is needed. Inability to make a correct diagnosis, because of improper MRI, continues to add to the confusion surrounding the injury and undoubtedly prolongs the general medical community’s thinking that diagnosis and treatment of chronic groin pain are elusive. Our data support this point in many ways. Although all patients in this study were seen by a medical professional before coming to our office, none had received a diagnosis of occult hernia or attenuated transversalis fascia; nevertheless, we identified inguinal hernia, Gilmore groin, or both in 44% of these patients. These findings are not surprising, as MRI was the crucial link in diagnosis. In addition, the point made by other groin pain specialists—that a hernia precludes a pubalgia diagnosis^1,2,5—is not supported by our data. Inguinal hernia can and does exist in conjunction with pubalgia. More than half the patients in our study had a combined diagnosis. We contend that, much as hip labral pathology occurs concomitantly with pubalgia,²³ inguinal hernia may be a predisposing factor as well. A defect in the direct or indirect space can destabilize the area and place additional strain on the pubic attachments.

In our experience, the dynamic Valsalva sequence improves detection of true hernias and anterior abdominal wall deficiencies and should be included in each protocol for the evaluation of acute or chronic groin pain.

Shear forces and injury at the pubis can occur outside professional athletics. Our patient population is nonprofessional athletes, teenagers to retirees, and all can develop athletic pubalgia. Ninety percent of surveyed patients who received a diagnosis and were treated surgically were satisfied with their outcomes.

Am J Orthop. 2017;46(4):E251-E256. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

A 32-year-old man presented to the ED with acute onset of left testicular swelling and pain. He described the pain as severe, radiating to his lower back and lower abdomen. Regarding his medical history, the patient stated he had experienced similar episodes of significant testicular swelling in the past, for which he was treated with antibiotics.

Physical examination revealed mild enlargement of the left testis with tenderness to palpation. The right testis was normal in appearance and nontender. An ultrasound study of the testicles was ordered; representative images are shown (Figures 1a-1c).

What is the diagnosis?

The transverse image of both testes demonstrated an enlarged left testicle compared to the right testicle (Figure 2a). On color-flow Doppler ultrasound, spots of color within the testicle were noted within the right testicle only. The lack of blood flow was confirmed on the sagittal image of the left testicle, which also revealed a small hydrocele (white arrows, Figure 2b). A sagittal color Doppler image of the normal right testicle showed color flow (white arrows, Figure 2c) and normal vascular waveforms (red arrow, Figure 2c) within the testis, but no hydrocele, confirming the diagnosis of left testicular torsion. The Doppler ultrasound of the right testicle (white arrows, Figure 2c) further confirmed a normal right testicle but no evidence of flow in the left testicle. These findings were further consistent with the presence of left testicular torsion.

Answer

Testicular Torsion

Testicular torsion is a urological emergency that results from a twisting of the spermatic cord, cutting off arterial flow to, and venous drainage from, the affected testis. There are two types of testicular torsion depending on which side of the tunica vaginalis (the serous membrane pouch covering the testes) the torsion occurs: extra vaginal, seen mainly in newborns; and intravaginal, which can occur at any age, but is more common in adolescents.

“Bell clapper deformity” is a predisposing congenital condition resulting from intravaginal torsion of the testis in which the tunica vaginalis joins high on the spermatic cord, leaving the testis free to rotate.¹ Testicular torsion most commonly occurs in young males, with an estimated incidence of 4.5 cases per 100,000 patients between ages 1 and 25 years.²

Clinical Presentation

Patients with testicular torsion typically experience a sudden onset of severe unilateral pain often accompanied by nausea and vomiting, which can occur spontaneously or after vigorous physical activity or trauma. Associated complaints may include urinary symptoms and/or fever.³ The affected testis may lie transversely in the scrotum and be retracted, although physical examination is often nonspecific and unreliable. Since an absence of the cremasteric reflex is neither sensitive nor specific in determining the need for surgical intervention, further diagnostic testing is required.⁴

Doppler Ultrasound

Ultrasound utilizing color and spectral Doppler techniques is the imaging test of choice to evaluate for testicular torsion, and has a reported sensitivity of 82% to 89%, and a specificity of 98% to 100%.^5,6 Ultrasound findings include enlargement and decreased echogenicity of the affected testicle due to edema. Scrotal wall thickening and a small hydrocele also may be seen. Doppler imaging also typically demonstrates absence of flow, though hyperemia and increased flow may be present early in the disease process.

It is important to note that torsion may be intermittent; therefore, imaging studies can appear normal during periods of intermittent perfusion. If there is incomplete torsion and some arterial flow persists in the affected testis, comparison of the two testes using transverse views is very useful in making the diagnosis.⁷

With respect to the differential diagnoses, ultrasound imaging studies are also useful in diagnosing other conditions associated with testicular pain, including torsion of the appendix testis, epididymitis, orchitis, trauma, varicocele, and tumors.

Treatment

Rapid diagnosis of testicular torsion is important, as delay in diagnosis may lead to irreversible damage and loss of the testicle. Infertility can result even with a normal contralateral testis.⁸ When surgical intervention is performed within 6 hours from onset of torsion, salvage of the testicle has been reported to be 90% to 100%, but only 50% and 10% at 12 and 24 hours, respectively.³ The patient in this case was taken immediately for emergent surgical detorsion, and the left testicle was salvaged.

A 32-year-old man presented to the ED with acute onset of left testicular swelling and pain. He described the pain as severe, radiating to his lower back and lower abdomen. Regarding his medical history, the patient stated he had experienced similar episodes of significant testicular swelling in the past, for which he was treated with antibiotics.

Physical examination revealed mild enlargement of the left testis with tenderness to palpation. The right testis was normal in appearance and nontender. An ultrasound study of the testicles was ordered; representative images are shown (Figures 1a-1c).

What is the diagnosis?

The transverse image of both testes demonstrated an enlarged left testicle compared to the right testicle (Figure 2a). On color-flow Doppler ultrasound, spots of color within the testicle were noted within the right testicle only. The lack of blood flow was confirmed on the sagittal image of the left testicle, which also revealed a small hydrocele (white arrows, Figure 2b). A sagittal color Doppler image of the normal right testicle showed color flow (white arrows, Figure 2c) and normal vascular waveforms (red arrow, Figure 2c) within the testis, but no hydrocele, confirming the diagnosis of left testicular torsion. The Doppler ultrasound of the right testicle (white arrows, Figure 2c) further confirmed a normal right testicle but no evidence of flow in the left testicle. These findings were further consistent with the presence of left testicular torsion.

Answer

Testicular Torsion

Testicular torsion is a urological emergency that results from a twisting of the spermatic cord, cutting off arterial flow to, and venous drainage from, the affected testis. There are two types of testicular torsion depending on which side of the tunica vaginalis (the serous membrane pouch covering the testes) the torsion occurs: extra vaginal, seen mainly in newborns; and intravaginal, which can occur at any age, but is more common in adolescents.

“Bell clapper deformity” is a predisposing congenital condition resulting from intravaginal torsion of the testis in which the tunica vaginalis joins high on the spermatic cord, leaving the testis free to rotate.¹ Testicular torsion most commonly occurs in young males, with an estimated incidence of 4.5 cases per 100,000 patients between ages 1 and 25 years.²

Clinical Presentation

Patients with testicular torsion typically experience a sudden onset of severe unilateral pain often accompanied by nausea and vomiting, which can occur spontaneously or after vigorous physical activity or trauma. Associated complaints may include urinary symptoms and/or fever.³ The affected testis may lie transversely in the scrotum and be retracted, although physical examination is often nonspecific and unreliable. Since an absence of the cremasteric reflex is neither sensitive nor specific in determining the need for surgical intervention, further diagnostic testing is required.⁴

Doppler Ultrasound

Ultrasound utilizing color and spectral Doppler techniques is the imaging test of choice to evaluate for testicular torsion, and has a reported sensitivity of 82% to 89%, and a specificity of 98% to 100%.^5,6 Ultrasound findings include enlargement and decreased echogenicity of the affected testicle due to edema. Scrotal wall thickening and a small hydrocele also may be seen. Doppler imaging also typically demonstrates absence of flow, though hyperemia and increased flow may be present early in the disease process.

It is important to note that torsion may be intermittent; therefore, imaging studies can appear normal during periods of intermittent perfusion. If there is incomplete torsion and some arterial flow persists in the affected testis, comparison of the two testes using transverse views is very useful in making the diagnosis.⁷

With respect to the differential diagnoses, ultrasound imaging studies are also useful in diagnosing other conditions associated with testicular pain, including torsion of the appendix testis, epididymitis, orchitis, trauma, varicocele, and tumors.

Treatment

Rapid diagnosis of testicular torsion is important, as delay in diagnosis may lead to irreversible damage and loss of the testicle. Infertility can result even with a normal contralateral testis.⁸ When surgical intervention is performed within 6 hours from onset of torsion, salvage of the testicle has been reported to be 90% to 100%, but only 50% and 10% at 12 and 24 hours, respectively.³ The patient in this case was taken immediately for emergent surgical detorsion, and the left testicle was salvaged.

A 32-year-old man presented to the ED with acute onset of left testicular swelling and pain. He described the pain as severe, radiating to his lower back and lower abdomen. Regarding his medical history, the patient stated he had experienced similar episodes of significant testicular swelling in the past, for which he was treated with antibiotics.

Physical examination revealed mild enlargement of the left testis with tenderness to palpation. The right testis was normal in appearance and nontender. An ultrasound study of the testicles was ordered; representative images are shown (Figures 1a-1c).

What is the diagnosis?

The transverse image of both testes demonstrated an enlarged left testicle compared to the right testicle (Figure 2a). On color-flow Doppler ultrasound, spots of color within the testicle were noted within the right testicle only. The lack of blood flow was confirmed on the sagittal image of the left testicle, which also revealed a small hydrocele (white arrows, Figure 2b). A sagittal color Doppler image of the normal right testicle showed color flow (white arrows, Figure 2c) and normal vascular waveforms (red arrow, Figure 2c) within the testis, but no hydrocele, confirming the diagnosis of left testicular torsion. The Doppler ultrasound of the right testicle (white arrows, Figure 2c) further confirmed a normal right testicle but no evidence of flow in the left testicle. These findings were further consistent with the presence of left testicular torsion.

Answer

Testicular Torsion

Testicular torsion is a urological emergency that results from a twisting of the spermatic cord, cutting off arterial flow to, and venous drainage from, the affected testis. There are two types of testicular torsion depending on which side of the tunica vaginalis (the serous membrane pouch covering the testes) the torsion occurs: extra vaginal, seen mainly in newborns; and intravaginal, which can occur at any age, but is more common in adolescents.

“Bell clapper deformity” is a predisposing congenital condition resulting from intravaginal torsion of the testis in which the tunica vaginalis joins high on the spermatic cord, leaving the testis free to rotate.¹ Testicular torsion most commonly occurs in young males, with an estimated incidence of 4.5 cases per 100,000 patients between ages 1 and 25 years.²

Clinical Presentation

Patients with testicular torsion typically experience a sudden onset of severe unilateral pain often accompanied by nausea and vomiting, which can occur spontaneously or after vigorous physical activity or trauma. Associated complaints may include urinary symptoms and/or fever.³ The affected testis may lie transversely in the scrotum and be retracted, although physical examination is often nonspecific and unreliable. Since an absence of the cremasteric reflex is neither sensitive nor specific in determining the need for surgical intervention, further diagnostic testing is required.⁴

Doppler Ultrasound

Ultrasound utilizing color and spectral Doppler techniques is the imaging test of choice to evaluate for testicular torsion, and has a reported sensitivity of 82% to 89%, and a specificity of 98% to 100%.^5,6 Ultrasound findings include enlargement and decreased echogenicity of the affected testicle due to edema. Scrotal wall thickening and a small hydrocele also may be seen. Doppler imaging also typically demonstrates absence of flow, though hyperemia and increased flow may be present early in the disease process.

It is important to note that torsion may be intermittent; therefore, imaging studies can appear normal during periods of intermittent perfusion. If there is incomplete torsion and some arterial flow persists in the affected testis, comparison of the two testes using transverse views is very useful in making the diagnosis.⁷

With respect to the differential diagnoses, ultrasound imaging studies are also useful in diagnosing other conditions associated with testicular pain, including torsion of the appendix testis, epididymitis, orchitis, trauma, varicocele, and tumors.

Treatment

Rapid diagnosis of testicular torsion is important, as delay in diagnosis may lead to irreversible damage and loss of the testicle. Infertility can result even with a normal contralateral testis.⁸ When surgical intervention is performed within 6 hours from onset of torsion, salvage of the testicle has been reported to be 90% to 100%, but only 50% and 10% at 12 and 24 hours, respectively.³ The patient in this case was taken immediately for emergent surgical detorsion, and the left testicle was salvaged.

Concussion, also known as mild traumatic brain injury, affects more than 600 adults per 100,000 each year and is commonly treated by nonneurologists.¹ Public attention to concussion has been increasing, particularly to concussion sustained during sports. Coincident with this increased attention, the diagnosis of concussion continues to increase in the outpatient setting. Thus, a review of the topic is timely.

ACCELERATION OF THE BRAIN DUE TO TRAUMA

The definition of concussion has changed considerably over the years. It is currently defined as a pathophysiologic process that results from an acceleration or deceleration of the brain induced by trauma.² It is largely a temporary, functional problem, as opposed to a gross structural injury.^2–5

The acceleration of the brain that results in a concussion is usually initiated by a direct blow to the head, although direct impact is not required.⁶ As the brain rotates, different areas accelerate at different rates, resulting in a shear strain imparted to the parenchyma.

This shear strain causes deformation of axonal membranes and opening of membrane-associated sodium-potassium channels. This in turn leads to release of excitatory neurotransmitters, ultimately culminating in a wave of neuronal depolarization and a spreading depression-like phenomenon that may mediate the loss of consciousness, posttraumatic amnesia, confusion, and many of the other immediate signs and symptoms associated with concussion.

The sudden metabolic demand created by the massive excitatory phenomena triggers an increased utilization of glucose to restore cellular homeostasis. At the same time, cerebral blood flow decreases after concussion, which, in the setting of increased glucose demand, leads to an “energy crisis”: an increased need for adenosine triphosphate with a concomitant decreased delivery of glucose.⁷ This mismatch between energy demand and supply is thought to underlie the most common signs and symptoms of concussion.

ASSESSMENT

History

The history of present illness is essential to a diagnosis of concussion. In the classic scenario, an otherwise asymptomatic person sustains some trauma to the head that is followed immediately by the signs and symptoms of concussion.

Many of these signs and symptoms are nonspecific and may occur without concussion or other trauma.^8,9 Thus, the diagnosis of concussion cannot be made on the basis of symptoms alone, but only in the overall context of history, physical examination, and, at times, additional clinical assessments.

The symptoms of concussion should gradually improve. While they may be exacerbated by certain activities or stimuli, the overall trend should be one of symptom improvement. If symptoms are worsening over time, alternative explanations for the patient’s symptoms should be considered.

Physical examination

A thorough neurologic examination should be conducted in all patients with suspected concussion and include the following.

A mental status examination should include assessment of attention, memory, and recall. Orientation is normal except in the most acute examinations.

Cranial nerve examination must include careful assessment of eye-movement control, including smooth pursuit and saccades. However, even in patients with prominent subjective dizziness, considerable experience may be needed to actually demonstrate abnormalities.

Balance testing. Balance demands careful assessment and, especially for young athletes, this testing should be more difficult than the tandem gait and eyes-closed, feet-together tests.

Standard strength, sensory, reflex, and coordination testing is usually normal.

Any focal neurologic findings should prompt consideration of other causes or of a more serious injury and should lead to further evaluation, including brain imaging.

Diagnostic tests

Current clinical brain imaging cannot diagnose a concussion. The purpose of neuroimaging is to assess for other etiologies or injuries, such as hemorrhage or contusion, that may cause similar symptoms but require different management.

Several guidelines are available to assess the need for imaging in the setting of recent trauma, of which 2 are typically used^10–12:

The Canadian CT Head Rule¹⁰ states that computed tomography (CT) is indicated in any of the following situations:

• The patient fails to reach a Glasgow Coma Scale score of 15—on a scale of 3 (worst) to 15 (best)—within 2 hours
• There is a suspected open skull fracture
• There is any sign of basal skull fracture
• The patient has 2 or more episodes of vomiting
• The patient is 65 or older
• The patient has retrograde amnesia (ie, cannot remember events that occurred before the injury) for 30 minutes or more
• The mechanism of injury was dangerous (eg, a pedestrian was struck by a motor vehicle, or the patient fell from > 3 feet or > 5 stairs).

The New Orleans Criteria¹¹ state that a patient warrants CT of the head if any of the following is present:

• Severe headache
• Vomiting
• Age over 60
• Drug or alcohol intoxication
• Deficit in short-term memory
• Physical evidence of trauma above the clavicles
• Seizure.

Caveats: these imaging guidelines apply to adults; those for pediatric patients differ.¹² Also, because they were designed for use in an emergency department, their utility in clinical practice outside the emergency department is unclear.

Electroencephalography is not necessary in the evaluation of concussion unless a seizure disorder is believed to be the cause of the injury.

Concussion in athletes

Athletes who participate in contact and collision sports are at higher risk of concussion than the nonathletic population. Therefore, specific assessments of symptoms, balance, oculomotor function, cognitive function, and reaction time have been developed for athletes.

Ideally, these measures are taken at preseason baseline, so that they are available for comparison with postinjury assessments after a known or suspected concussion. These assessments can be used to help make the diagnosis of concussion in cases that are unclear and to help monitor recovery. Objective measures of injury are especially useful for athletes who may be reluctant to report symptoms in order to return to play.

Like most medical tests, these assessments need to be properly interpreted in the overall context of the medical history and physical examination by those who know how to administer them. It is important to remember that the natural history of concussion recovery differs between sport-related concussion and concussion that occurs outside of sports.⁸

The symptoms and signs after concussion are so variable and multidimensional that they make a generally applicable treatment hard to define.

Rest: Physical and cognitive

Treatment depends on the specifics of the injury, but there are common recommendations for the acute days after injury. Lacking hard data, the consensus among experts is that patients should undergo a period of physical and cognitive rest.^13,14 Exactly what “rest” means and how long it should last are unknown, leading to a wide variation in its application.

Rest aids recovery but also may have adverse effects: fatigue, diurnal sleep disruption, reactive depression, anxiety, and physiologic deconditioning.^15,16 Many guidelines recommend physical and cognitive rest until symptoms resolve,¹⁴ but this is likely too cautious. Even without a concussion, inactivity is associated with many of the nonspecific symptoms also associated with concussion. As recovery progresses, the somatic symptoms of concussion improve, while emotional symptoms worsen, likely in part due to prolonged rest.¹⁷

We recommend a period of rest lasting 3 to 5 days after injury, followed by a gradual resumption of both physical and cognitive activities as tolerated, remaining below the level at which symptoms are exacerbated.

Not surprisingly, many guidelines for returning to physical activity are focused on athletes. Yet the same principles apply to management of concussion in the general population who exercise: light physical activity (typically walking or stationary bicycling), followed by more vigorous aerobic activity, followed by some resistance activities. Mild aerobic exercise (to below the threshold of symptoms) may speed recovery from refractive postconcussion syndrome, even in those who did not exercise before the injury.¹⁸

Athletes require specific and strict instructions to avoid increased trauma to the head during the gradual increase of physical activities. The National Collegiate Athletic Association has published an algorithm for a gradual return to sport-specific training that is echoed in recent consensus statements on concussion.¹⁹ Once aerobic reconditioning produces no symptoms, then noncontact, sport-specific activities are begun, followed by contact activities. We have patients return to the clinic once they are symptom-free for repeat evaluation before clearing them for high-risk activities (eg, skiing, bicycling) or contact sports (eg, basketball, soccer, football, ice hockey).

Cognitive rest

While physical rest is fairly straightforward, cognitive rest is more challenging. The concept of cognitive rest is hard to define and even harder to enforce. Patients are often told to minimize any activities that require attention or concentration. This often includes, but is not limited to, avoiding reading, texting, playing video games, and using computers.¹³

In the modern world, full avoidance of these activities is difficult and can be profoundly socially isolating. Further, complete cognitive rest may be associated with symptoms of its own.^15,16,20 Still, some reasonable limitation of cognitive activities, at least initially, is likely beneficial.²¹ For patients engaged in school or academic work, often the daily schedule needs to be adjusted and accommodations made to help them return to a full academic schedule and level of activity. It is reasonable to have patients return gradually to work or school rather than attempt to immediately return to their preinjury level.

With these interventions, most patients have full resolution of their symptoms and return to preinjury levels of performance.

TREATING SOMATIC SYMPTOMS

Posttraumatic headache

Posttraumatic headache is the most common sequela of concussion.²² Surprisingly, it is more common after concussion than after moderate or severe traumatic brain injury.²³ A prior history of headache, particularly migraine, is a known risk factor for development of posttraumatic headache.²⁴

Posttraumatic headache is usually further defined by headache type using the International Classification of Headache Disorders criteria (www.ichd-3.org). Migraine or probable migraine is the most common type of posttraumatic headache; tension headache is less common.²⁵

Analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) are often used initially by patients to treat posttraumatic headache. One study found that 70% of patients used acetaminophen or an NSAID.²⁶

Treating early with effective therapy is the most important tenet of posttraumatic headache treatment, since 80% of those who self-treat have incomplete relief, and almost all of them are using over-the-counter products.²⁷ Overuse of over-the-counter abortive medications can lead to medication overuse headache, also known as rebound headache, thus complicating the treatment of posttraumatic headache.²⁶

Earlier treatment with a preventive medication can often limit the need for and overuse of over-the-counter analgesics and can minimize the occurrence of subsequent medication overuse headache. However, in pediatric populations, nonpharmacologic interventions such as rest and sleep hygiene are typically used first, then medications after 4 to 6 weeks if this is ineffective.

A number of medications have been studied for prophylactic treatment of posttraumatic headache, including topiramate, amitriptyline, and divalproex sodium,^28–30 but there is little compelling evidence for use of one over the other. If posttraumatic headache is migrainous, beta-blockers, calcium-channel blockers, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibtors, and gabapentin are other prophylactic medication options under the appropriate circumstances.^27,31,32 In adults, we have clinically had success with nortriptyline 20 mg or gabapentin 300 mg at night as an initial prophylactic headache medication, increasing as tolerated or until pain is controlled, though there are no high-quality data to guide this decision.

The ideal prophylactic medication depends on headache type, patient tolerance, comorbidities, allergies, and medication sensitivities. Gabapentin, amitriptyline, and nortriptyline can produce sedation, which can help those suffering from sleep disturbance.

If a provider is not comfortable prescribing these medications or doesn’t prescribe them regularly, the patient should be referred to a concussion or headache specialist more familiar with their use.

In some patients, even some athletes, headache may be related to a cervical strain injury—whiplash—that should be treated with an NSAID (or acetaminophen), perhaps with a short course of a muscle relaxant in adults, and with physical therapy.³²

Some patients have chronic headache despite oral medications.²⁶ Therefore, alternatives to oral medications and complementary therapies should be considered. Especially for protracted cases requiring more complicated headache management or injectable treatments, patients should be referred to a pain clinic, headache specialist, or concussion specialist.

Dizziness is also common after concussion. But what the patient means by dizziness requires a little probing. Some have paroxysms of vertigo. This typically represents a peripheral vestibular injury, usually benign paroxysmal positional vertigo. The latter can be elicited with a Hallpike maneuver and treated in the office with the Epley maneuver.³³

Usually, dizziness is a subjective sense of poor coordination, gait instability, or dysequilibrium. Patients may also complain of associated nausea and motion sensitivity. This may all be secondary to a mechanism in the middle or inner ear or the brain. Patients should be encouraged to begin movement—gradually and safely—to help the vestibular system accommodate, which it will do with gradual stimulation. It usually resolves spontaneously.

Specific treatment is unfortunately limited. There is no established benefit from vestibular suppressants such as meclizine. Vestibular rehabilitation may accelerate improvement and decrease symptoms.³³ Referral for a comprehensive balance assessment or to vestibular therapy (a subset of physical therapy) should be considered and is something we typically undertake in our clinic if there is no recovery from dizziness 4 to 6 weeks after the concussion.

Visual symptoms can contribute to dizziness. Convergence spasm or convergence insufficiency (both related to muscle spasm of the eye) can occur after concussion, with some studies estimating that up to 69% of patients have these symptoms.³⁴ This can interfere with visual tracking and contribute to a feeling of dysequilibrium.³⁴ Referral to a concussion specialist or vestibular rehabilitation physical therapist can be helpful in treating this issue if it does not resolve spontaneously.

Orthostasis and lightheadedness also contribute to dizziness and are associated with cerebrovascular autoregulation. Available data suggest that dysregulation of neurovascular coupling, cerebral vasoreactivity, and cerebral autoregulation contribute to some of the chronic symptoms of concussion, including dizziness. A gradual return to exercise may help regulate cerebral blood flow and improve this type of dizziness.³⁵

Sleep disturbance

Sleep disturbance is common after concussion, but the form is variable: insomnia, excessive daytime somnolence, and alteration of the sleep-wake cycle are all seen and may themselves affect recovery.³⁶

Sleep hygiene education should be the first intervention for postconcussive sleep issues. For example, the patient should be encouraged to do the following:

• Minimize “screen time” an hour before going to bed: cell phone, tablet, and computer screens emit a wavelength of light that suppresses endogenous melatonin release^37,38
• Go to bed and wake up at the same time each day
• Minimize or avoid caffeine, nicotine, and alcohol
• Avoid naps.³⁹

Melatonin is a safe and effective treatment that could be added.⁴⁰ In addition, some studies suggest that melatonin may improve recovery from traumatic brain injury.^41,42

Mild exercise (to below the threshold of causing or exacerbating symptoms) may also improve sleep quality.

Amitriptyline or nortriptyline may reduce headache frequency and intensity and also help treat insomnia.

Trazodone is recommended by some as a first-line agent,³⁹ but we usually reserve it for protracted insomnia refractory to the above treatments.

Benzodiazepines should be avoided, as they reduce arousal, impair cognition, and exacerbate motor impairments.⁴³

Emotional symptoms

Acute-onset anxiety or depression often occurs after concussion.^44,45 There is abundant evidence that emotional effects of injury may be the most significant factor in recovery.⁴⁶ A preinjury history of anxiety may be a prognostic factor.⁹ Patients with a history of anxiety or depression are more likely to develop emotional symptoms after a concussion, but emotional problems may develop in any patient after a concussion.^47,48

The circumstances under which an injury is sustained may be traumatic (eg, car accident, assault), leading to an acute stress reaction or disorder and, if untreated, may result in a more chronic condition—posttraumatic stress disorder. Moreover, the injury and subsequent symptoms may have repercussions in many aspects of the patient’s life, leading to further psychologic stress (eg, loss of wages or the inability to handle normal work, school, and family responsibilities).

Referral to a therapist trained in skills-based psychotherapy (eg, cognitive-behavioral therapy, exposure-based treatment) is often helpful.

Pharmacologic treatment can be a useful adjunct. Several studies have shown that selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants may improve depression after concussion.⁴⁹ The prescription of antidepressants, however, is best left to providers with experience in treating anxiety and depression.

As with sleep disorders after concussion, benzodiazepines should be avoided, as they can impair cognition.⁴³

Cognitive problems

Cognitive problems are also common after concussion. Patients complain about everyday experiences of forgetfulness, distractibility, loss of concentration, and mental fatigue. Although patients often subjectively perceive these symptoms as quite limiting, the impairments can be difficult to demonstrate in office testing.

A program of gradual increase in mental activity, parallel to recovery of physical capacity, should be undertaken. Most patients make a gradual recovery within a few weeks.⁵⁰

When cognitive symptoms cause significant school or vocational problems or become persistent, patients should be referred to a specialty clinic. As with most of the consequences of concussion, there are few established treatments. When cognitive difficulties persist, it is important to consider the complications of concussion mentioned above: headache, pain, sleep disturbance, and anxiety, all of which may cause subjective cognitive problems and are treatable.

If cognitive symptoms are prolonged despite improvement of other issues like headache and sleep disturbance, a low-dose stimulant medication such as amphetamine salts or methylphenidate may be useful for symptoms of poor attention.⁴⁹ They should be only a temporary measure after concussion to carry the patient through a cognitively challenging period, unless there was a history of attention-deficit disorder before the injury. A variety of other agents, including amantadine,⁵¹ have been proposed based on limited studies; all are off-label uses. Before considering these types of interventions, referral to a specialist or a specialty program would be appropriate.

With the interventions suggested above, most patients with concussion have a resolution of symptoms and can return to preinjury levels of performance. But some have prolonged symptoms and sequelae. Approximately 10% of athletes have persistent signs and symptoms of concussion beyond 2 weeks. If concussion is not sport-related, most patients recover completely within the first 3 months, but up to 33% may have symptoms beyond that.⁵²

Four types of patients have persistent symptoms:

Patients who sustained a high-force mechanism of injury. These patients simply need more time and accommodation.

Patients who sustained multiple concussions. These patients may also need more time and accommodation.

Patients with an underlying neurologic condition, recognized prior to injury or not, may have delayed or incomplete recovery. Even aging may be an “underlying condition” in concussion.

Patients whose symptoms from an apparently single mild concussion do not resolve despite appropriate treatments may have identifiable factors, but intractable pain (usually headache) or significant emotional disturbance or both are common. Once established and persistent, this is difficult to treat. Referral to a specialty practice is appropriate, but even in that setting effective treatment may be elusive.

PATIENT EDUCATION

Most important for patient education is reassurance. Ultimately, concussion is a self-limited phenomenon, and reinforcing this is helpful for patients. If concussion is not sport-related, most patients recover completely within 3 months.

The next important tenet in patient education is that they should rest for 3 to 5 days, then resume gradual physical and cognitive activities. If resuming activities too soon results in symptoms, then they should rest for a day and gradually resume activity. If their recovery is prolonged (ie, longer than 6 weeks), they likely need to be referred to a concussion specialist.

Concussion, also known as mild traumatic brain injury, affects more than 600 adults per 100,000 each year and is commonly treated by nonneurologists.¹ Public attention to concussion has been increasing, particularly to concussion sustained during sports. Coincident with this increased attention, the diagnosis of concussion continues to increase in the outpatient setting. Thus, a review of the topic is timely.

ACCELERATION OF THE BRAIN DUE TO TRAUMA

The definition of concussion has changed considerably over the years. It is currently defined as a pathophysiologic process that results from an acceleration or deceleration of the brain induced by trauma.² It is largely a temporary, functional problem, as opposed to a gross structural injury.^2–5

The acceleration of the brain that results in a concussion is usually initiated by a direct blow to the head, although direct impact is not required.⁶ As the brain rotates, different areas accelerate at different rates, resulting in a shear strain imparted to the parenchyma.

This shear strain causes deformation of axonal membranes and opening of membrane-associated sodium-potassium channels. This in turn leads to release of excitatory neurotransmitters, ultimately culminating in a wave of neuronal depolarization and a spreading depression-like phenomenon that may mediate the loss of consciousness, posttraumatic amnesia, confusion, and many of the other immediate signs and symptoms associated with concussion.

The sudden metabolic demand created by the massive excitatory phenomena triggers an increased utilization of glucose to restore cellular homeostasis. At the same time, cerebral blood flow decreases after concussion, which, in the setting of increased glucose demand, leads to an “energy crisis”: an increased need for adenosine triphosphate with a concomitant decreased delivery of glucose.⁷ This mismatch between energy demand and supply is thought to underlie the most common signs and symptoms of concussion.

ASSESSMENT

History

The history of present illness is essential to a diagnosis of concussion. In the classic scenario, an otherwise asymptomatic person sustains some trauma to the head that is followed immediately by the signs and symptoms of concussion.

Many of these signs and symptoms are nonspecific and may occur without concussion or other trauma.^8,9 Thus, the diagnosis of concussion cannot be made on the basis of symptoms alone, but only in the overall context of history, physical examination, and, at times, additional clinical assessments.

The symptoms of concussion should gradually improve. While they may be exacerbated by certain activities or stimuli, the overall trend should be one of symptom improvement. If symptoms are worsening over time, alternative explanations for the patient’s symptoms should be considered.

Physical examination

A thorough neurologic examination should be conducted in all patients with suspected concussion and include the following.

A mental status examination should include assessment of attention, memory, and recall. Orientation is normal except in the most acute examinations.

Cranial nerve examination must include careful assessment of eye-movement control, including smooth pursuit and saccades. However, even in patients with prominent subjective dizziness, considerable experience may be needed to actually demonstrate abnormalities.

Balance testing. Balance demands careful assessment and, especially for young athletes, this testing should be more difficult than the tandem gait and eyes-closed, feet-together tests.

Standard strength, sensory, reflex, and coordination testing is usually normal.

Any focal neurologic findings should prompt consideration of other causes or of a more serious injury and should lead to further evaluation, including brain imaging.

Diagnostic tests

Current clinical brain imaging cannot diagnose a concussion. The purpose of neuroimaging is to assess for other etiologies or injuries, such as hemorrhage or contusion, that may cause similar symptoms but require different management.

Several guidelines are available to assess the need for imaging in the setting of recent trauma, of which 2 are typically used^10–12:

The Canadian CT Head Rule¹⁰ states that computed tomography (CT) is indicated in any of the following situations:

• The patient fails to reach a Glasgow Coma Scale score of 15—on a scale of 3 (worst) to 15 (best)—within 2 hours
• There is a suspected open skull fracture
• There is any sign of basal skull fracture
• The patient has 2 or more episodes of vomiting
• The patient is 65 or older
• The patient has retrograde amnesia (ie, cannot remember events that occurred before the injury) for 30 minutes or more
• The mechanism of injury was dangerous (eg, a pedestrian was struck by a motor vehicle, or the patient fell from > 3 feet or > 5 stairs).

The New Orleans Criteria¹¹ state that a patient warrants CT of the head if any of the following is present:

• Severe headache
• Vomiting
• Age over 60
• Drug or alcohol intoxication
• Deficit in short-term memory
• Physical evidence of trauma above the clavicles
• Seizure.

Caveats: these imaging guidelines apply to adults; those for pediatric patients differ.¹² Also, because they were designed for use in an emergency department, their utility in clinical practice outside the emergency department is unclear.

Electroencephalography is not necessary in the evaluation of concussion unless a seizure disorder is believed to be the cause of the injury.

Concussion in athletes

Athletes who participate in contact and collision sports are at higher risk of concussion than the nonathletic population. Therefore, specific assessments of symptoms, balance, oculomotor function, cognitive function, and reaction time have been developed for athletes.

Ideally, these measures are taken at preseason baseline, so that they are available for comparison with postinjury assessments after a known or suspected concussion. These assessments can be used to help make the diagnosis of concussion in cases that are unclear and to help monitor recovery. Objective measures of injury are especially useful for athletes who may be reluctant to report symptoms in order to return to play.

Like most medical tests, these assessments need to be properly interpreted in the overall context of the medical history and physical examination by those who know how to administer them. It is important to remember that the natural history of concussion recovery differs between sport-related concussion and concussion that occurs outside of sports.⁸

The symptoms and signs after concussion are so variable and multidimensional that they make a generally applicable treatment hard to define.

Rest: Physical and cognitive

Treatment depends on the specifics of the injury, but there are common recommendations for the acute days after injury. Lacking hard data, the consensus among experts is that patients should undergo a period of physical and cognitive rest.^13,14 Exactly what “rest” means and how long it should last are unknown, leading to a wide variation in its application.

Rest aids recovery but also may have adverse effects: fatigue, diurnal sleep disruption, reactive depression, anxiety, and physiologic deconditioning.^15,16 Many guidelines recommend physical and cognitive rest until symptoms resolve,¹⁴ but this is likely too cautious. Even without a concussion, inactivity is associated with many of the nonspecific symptoms also associated with concussion. As recovery progresses, the somatic symptoms of concussion improve, while emotional symptoms worsen, likely in part due to prolonged rest.¹⁷

We recommend a period of rest lasting 3 to 5 days after injury, followed by a gradual resumption of both physical and cognitive activities as tolerated, remaining below the level at which symptoms are exacerbated.

Not surprisingly, many guidelines for returning to physical activity are focused on athletes. Yet the same principles apply to management of concussion in the general population who exercise: light physical activity (typically walking or stationary bicycling), followed by more vigorous aerobic activity, followed by some resistance activities. Mild aerobic exercise (to below the threshold of symptoms) may speed recovery from refractive postconcussion syndrome, even in those who did not exercise before the injury.¹⁸

Athletes require specific and strict instructions to avoid increased trauma to the head during the gradual increase of physical activities. The National Collegiate Athletic Association has published an algorithm for a gradual return to sport-specific training that is echoed in recent consensus statements on concussion.¹⁹ Once aerobic reconditioning produces no symptoms, then noncontact, sport-specific activities are begun, followed by contact activities. We have patients return to the clinic once they are symptom-free for repeat evaluation before clearing them for high-risk activities (eg, skiing, bicycling) or contact sports (eg, basketball, soccer, football, ice hockey).

Cognitive rest

While physical rest is fairly straightforward, cognitive rest is more challenging. The concept of cognitive rest is hard to define and even harder to enforce. Patients are often told to minimize any activities that require attention or concentration. This often includes, but is not limited to, avoiding reading, texting, playing video games, and using computers.¹³

In the modern world, full avoidance of these activities is difficult and can be profoundly socially isolating. Further, complete cognitive rest may be associated with symptoms of its own.^15,16,20 Still, some reasonable limitation of cognitive activities, at least initially, is likely beneficial.²¹ For patients engaged in school or academic work, often the daily schedule needs to be adjusted and accommodations made to help them return to a full academic schedule and level of activity. It is reasonable to have patients return gradually to work or school rather than attempt to immediately return to their preinjury level.

With these interventions, most patients have full resolution of their symptoms and return to preinjury levels of performance.

TREATING SOMATIC SYMPTOMS

Posttraumatic headache

Posttraumatic headache is the most common sequela of concussion.²² Surprisingly, it is more common after concussion than after moderate or severe traumatic brain injury.²³ A prior history of headache, particularly migraine, is a known risk factor for development of posttraumatic headache.²⁴

Posttraumatic headache is usually further defined by headache type using the International Classification of Headache Disorders criteria (www.ichd-3.org). Migraine or probable migraine is the most common type of posttraumatic headache; tension headache is less common.²⁵

Analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) are often used initially by patients to treat posttraumatic headache. One study found that 70% of patients used acetaminophen or an NSAID.²⁶

Treating early with effective therapy is the most important tenet of posttraumatic headache treatment, since 80% of those who self-treat have incomplete relief, and almost all of them are using over-the-counter products.²⁷ Overuse of over-the-counter abortive medications can lead to medication overuse headache, also known as rebound headache, thus complicating the treatment of posttraumatic headache.²⁶

Earlier treatment with a preventive medication can often limit the need for and overuse of over-the-counter analgesics and can minimize the occurrence of subsequent medication overuse headache. However, in pediatric populations, nonpharmacologic interventions such as rest and sleep hygiene are typically used first, then medications after 4 to 6 weeks if this is ineffective.

A number of medications have been studied for prophylactic treatment of posttraumatic headache, including topiramate, amitriptyline, and divalproex sodium,^28–30 but there is little compelling evidence for use of one over the other. If posttraumatic headache is migrainous, beta-blockers, calcium-channel blockers, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibtors, and gabapentin are other prophylactic medication options under the appropriate circumstances.^27,31,32 In adults, we have clinically had success with nortriptyline 20 mg or gabapentin 300 mg at night as an initial prophylactic headache medication, increasing as tolerated or until pain is controlled, though there are no high-quality data to guide this decision.

The ideal prophylactic medication depends on headache type, patient tolerance, comorbidities, allergies, and medication sensitivities. Gabapentin, amitriptyline, and nortriptyline can produce sedation, which can help those suffering from sleep disturbance.

If a provider is not comfortable prescribing these medications or doesn’t prescribe them regularly, the patient should be referred to a concussion or headache specialist more familiar with their use.

In some patients, even some athletes, headache may be related to a cervical strain injury—whiplash—that should be treated with an NSAID (or acetaminophen), perhaps with a short course of a muscle relaxant in adults, and with physical therapy.³²

Some patients have chronic headache despite oral medications.²⁶ Therefore, alternatives to oral medications and complementary therapies should be considered. Especially for protracted cases requiring more complicated headache management or injectable treatments, patients should be referred to a pain clinic, headache specialist, or concussion specialist.

Dizziness is also common after concussion. But what the patient means by dizziness requires a little probing. Some have paroxysms of vertigo. This typically represents a peripheral vestibular injury, usually benign paroxysmal positional vertigo. The latter can be elicited with a Hallpike maneuver and treated in the office with the Epley maneuver.³³

Usually, dizziness is a subjective sense of poor coordination, gait instability, or dysequilibrium. Patients may also complain of associated nausea and motion sensitivity. This may all be secondary to a mechanism in the middle or inner ear or the brain. Patients should be encouraged to begin movement—gradually and safely—to help the vestibular system accommodate, which it will do with gradual stimulation. It usually resolves spontaneously.

Specific treatment is unfortunately limited. There is no established benefit from vestibular suppressants such as meclizine. Vestibular rehabilitation may accelerate improvement and decrease symptoms.³³ Referral for a comprehensive balance assessment or to vestibular therapy (a subset of physical therapy) should be considered and is something we typically undertake in our clinic if there is no recovery from dizziness 4 to 6 weeks after the concussion.

Visual symptoms can contribute to dizziness. Convergence spasm or convergence insufficiency (both related to muscle spasm of the eye) can occur after concussion, with some studies estimating that up to 69% of patients have these symptoms.³⁴ This can interfere with visual tracking and contribute to a feeling of dysequilibrium.³⁴ Referral to a concussion specialist or vestibular rehabilitation physical therapist can be helpful in treating this issue if it does not resolve spontaneously.

Orthostasis and lightheadedness also contribute to dizziness and are associated with cerebrovascular autoregulation. Available data suggest that dysregulation of neurovascular coupling, cerebral vasoreactivity, and cerebral autoregulation contribute to some of the chronic symptoms of concussion, including dizziness. A gradual return to exercise may help regulate cerebral blood flow and improve this type of dizziness.³⁵

Sleep disturbance

Sleep disturbance is common after concussion, but the form is variable: insomnia, excessive daytime somnolence, and alteration of the sleep-wake cycle are all seen and may themselves affect recovery.³⁶

Sleep hygiene education should be the first intervention for postconcussive sleep issues. For example, the patient should be encouraged to do the following:

• Minimize “screen time” an hour before going to bed: cell phone, tablet, and computer screens emit a wavelength of light that suppresses endogenous melatonin release^37,38
• Go to bed and wake up at the same time each day
• Minimize or avoid caffeine, nicotine, and alcohol
• Avoid naps.³⁹

Melatonin is a safe and effective treatment that could be added.⁴⁰ In addition, some studies suggest that melatonin may improve recovery from traumatic brain injury.^41,42

Mild exercise (to below the threshold of causing or exacerbating symptoms) may also improve sleep quality.

Amitriptyline or nortriptyline may reduce headache frequency and intensity and also help treat insomnia.

Trazodone is recommended by some as a first-line agent,³⁹ but we usually reserve it for protracted insomnia refractory to the above treatments.

Benzodiazepines should be avoided, as they reduce arousal, impair cognition, and exacerbate motor impairments.⁴³

Emotional symptoms

Acute-onset anxiety or depression often occurs after concussion.^44,45 There is abundant evidence that emotional effects of injury may be the most significant factor in recovery.⁴⁶ A preinjury history of anxiety may be a prognostic factor.⁹ Patients with a history of anxiety or depression are more likely to develop emotional symptoms after a concussion, but emotional problems may develop in any patient after a concussion.^47,48

The circumstances under which an injury is sustained may be traumatic (eg, car accident, assault), leading to an acute stress reaction or disorder and, if untreated, may result in a more chronic condition—posttraumatic stress disorder. Moreover, the injury and subsequent symptoms may have repercussions in many aspects of the patient’s life, leading to further psychologic stress (eg, loss of wages or the inability to handle normal work, school, and family responsibilities).

Referral to a therapist trained in skills-based psychotherapy (eg, cognitive-behavioral therapy, exposure-based treatment) is often helpful.

Pharmacologic treatment can be a useful adjunct. Several studies have shown that selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants may improve depression after concussion.⁴⁹ The prescription of antidepressants, however, is best left to providers with experience in treating anxiety and depression.

As with sleep disorders after concussion, benzodiazepines should be avoided, as they can impair cognition.⁴³

Cognitive problems

Cognitive problems are also common after concussion. Patients complain about everyday experiences of forgetfulness, distractibility, loss of concentration, and mental fatigue. Although patients often subjectively perceive these symptoms as quite limiting, the impairments can be difficult to demonstrate in office testing.

A program of gradual increase in mental activity, parallel to recovery of physical capacity, should be undertaken. Most patients make a gradual recovery within a few weeks.⁵⁰

When cognitive symptoms cause significant school or vocational problems or become persistent, patients should be referred to a specialty clinic. As with most of the consequences of concussion, there are few established treatments. When cognitive difficulties persist, it is important to consider the complications of concussion mentioned above: headache, pain, sleep disturbance, and anxiety, all of which may cause subjective cognitive problems and are treatable.

If cognitive symptoms are prolonged despite improvement of other issues like headache and sleep disturbance, a low-dose stimulant medication such as amphetamine salts or methylphenidate may be useful for symptoms of poor attention.⁴⁹ They should be only a temporary measure after concussion to carry the patient through a cognitively challenging period, unless there was a history of attention-deficit disorder before the injury. A variety of other agents, including amantadine,⁵¹ have been proposed based on limited studies; all are off-label uses. Before considering these types of interventions, referral to a specialist or a specialty program would be appropriate.

With the interventions suggested above, most patients with concussion have a resolution of symptoms and can return to preinjury levels of performance. But some have prolonged symptoms and sequelae. Approximately 10% of athletes have persistent signs and symptoms of concussion beyond 2 weeks. If concussion is not sport-related, most patients recover completely within the first 3 months, but up to 33% may have symptoms beyond that.⁵²

Four types of patients have persistent symptoms:

Patients who sustained a high-force mechanism of injury. These patients simply need more time and accommodation.

Patients who sustained multiple concussions. These patients may also need more time and accommodation.

Patients with an underlying neurologic condition, recognized prior to injury or not, may have delayed or incomplete recovery. Even aging may be an “underlying condition” in concussion.

Patients whose symptoms from an apparently single mild concussion do not resolve despite appropriate treatments may have identifiable factors, but intractable pain (usually headache) or significant emotional disturbance or both are common. Once established and persistent, this is difficult to treat. Referral to a specialty practice is appropriate, but even in that setting effective treatment may be elusive.

PATIENT EDUCATION

Most important for patient education is reassurance. Ultimately, concussion is a self-limited phenomenon, and reinforcing this is helpful for patients. If concussion is not sport-related, most patients recover completely within 3 months.

The next important tenet in patient education is that they should rest for 3 to 5 days, then resume gradual physical and cognitive activities. If resuming activities too soon results in symptoms, then they should rest for a day and gradually resume activity. If their recovery is prolonged (ie, longer than 6 weeks), they likely need to be referred to a concussion specialist.

Concussion, also known as mild traumatic brain injury, affects more than 600 adults per 100,000 each year and is commonly treated by nonneurologists.¹ Public attention to concussion has been increasing, particularly to concussion sustained during sports. Coincident with this increased attention, the diagnosis of concussion continues to increase in the outpatient setting. Thus, a review of the topic is timely.

ACCELERATION OF THE BRAIN DUE TO TRAUMA

The definition of concussion has changed considerably over the years. It is currently defined as a pathophysiologic process that results from an acceleration or deceleration of the brain induced by trauma.² It is largely a temporary, functional problem, as opposed to a gross structural injury.^2–5

The acceleration of the brain that results in a concussion is usually initiated by a direct blow to the head, although direct impact is not required.⁶ As the brain rotates, different areas accelerate at different rates, resulting in a shear strain imparted to the parenchyma.

This shear strain causes deformation of axonal membranes and opening of membrane-associated sodium-potassium channels. This in turn leads to release of excitatory neurotransmitters, ultimately culminating in a wave of neuronal depolarization and a spreading depression-like phenomenon that may mediate the loss of consciousness, posttraumatic amnesia, confusion, and many of the other immediate signs and symptoms associated with concussion.

The sudden metabolic demand created by the massive excitatory phenomena triggers an increased utilization of glucose to restore cellular homeostasis. At the same time, cerebral blood flow decreases after concussion, which, in the setting of increased glucose demand, leads to an “energy crisis”: an increased need for adenosine triphosphate with a concomitant decreased delivery of glucose.⁷ This mismatch between energy demand and supply is thought to underlie the most common signs and symptoms of concussion.

ASSESSMENT

History

The history of present illness is essential to a diagnosis of concussion. In the classic scenario, an otherwise asymptomatic person sustains some trauma to the head that is followed immediately by the signs and symptoms of concussion.

Many of these signs and symptoms are nonspecific and may occur without concussion or other trauma.^8,9 Thus, the diagnosis of concussion cannot be made on the basis of symptoms alone, but only in the overall context of history, physical examination, and, at times, additional clinical assessments.

The symptoms of concussion should gradually improve. While they may be exacerbated by certain activities or stimuli, the overall trend should be one of symptom improvement. If symptoms are worsening over time, alternative explanations for the patient’s symptoms should be considered.

Physical examination

A thorough neurologic examination should be conducted in all patients with suspected concussion and include the following.

A mental status examination should include assessment of attention, memory, and recall. Orientation is normal except in the most acute examinations.

Cranial nerve examination must include careful assessment of eye-movement control, including smooth pursuit and saccades. However, even in patients with prominent subjective dizziness, considerable experience may be needed to actually demonstrate abnormalities.

Balance testing. Balance demands careful assessment and, especially for young athletes, this testing should be more difficult than the tandem gait and eyes-closed, feet-together tests.

Standard strength, sensory, reflex, and coordination testing is usually normal.

Any focal neurologic findings should prompt consideration of other causes or of a more serious injury and should lead to further evaluation, including brain imaging.

Diagnostic tests

Current clinical brain imaging cannot diagnose a concussion. The purpose of neuroimaging is to assess for other etiologies or injuries, such as hemorrhage or contusion, that may cause similar symptoms but require different management.

Several guidelines are available to assess the need for imaging in the setting of recent trauma, of which 2 are typically used^10–12:

The Canadian CT Head Rule¹⁰ states that computed tomography (CT) is indicated in any of the following situations:

• The patient fails to reach a Glasgow Coma Scale score of 15—on a scale of 3 (worst) to 15 (best)—within 2 hours
• There is a suspected open skull fracture
• There is any sign of basal skull fracture
• The patient has 2 or more episodes of vomiting
• The patient is 65 or older
• The patient has retrograde amnesia (ie, cannot remember events that occurred before the injury) for 30 minutes or more
• The mechanism of injury was dangerous (eg, a pedestrian was struck by a motor vehicle, or the patient fell from > 3 feet or > 5 stairs).

The New Orleans Criteria¹¹ state that a patient warrants CT of the head if any of the following is present:

• Severe headache
• Vomiting
• Age over 60
• Drug or alcohol intoxication
• Deficit in short-term memory
• Physical evidence of trauma above the clavicles
• Seizure.

Caveats: these imaging guidelines apply to adults; those for pediatric patients differ.¹² Also, because they were designed for use in an emergency department, their utility in clinical practice outside the emergency department is unclear.

Electroencephalography is not necessary in the evaluation of concussion unless a seizure disorder is believed to be the cause of the injury.

Concussion in athletes

Athletes who participate in contact and collision sports are at higher risk of concussion than the nonathletic population. Therefore, specific assessments of symptoms, balance, oculomotor function, cognitive function, and reaction time have been developed for athletes.

Ideally, these measures are taken at preseason baseline, so that they are available for comparison with postinjury assessments after a known or suspected concussion. These assessments can be used to help make the diagnosis of concussion in cases that are unclear and to help monitor recovery. Objective measures of injury are especially useful for athletes who may be reluctant to report symptoms in order to return to play.

Like most medical tests, these assessments need to be properly interpreted in the overall context of the medical history and physical examination by those who know how to administer them. It is important to remember that the natural history of concussion recovery differs between sport-related concussion and concussion that occurs outside of sports.⁸

The symptoms and signs after concussion are so variable and multidimensional that they make a generally applicable treatment hard to define.

Rest: Physical and cognitive

Treatment depends on the specifics of the injury, but there are common recommendations for the acute days after injury. Lacking hard data, the consensus among experts is that patients should undergo a period of physical and cognitive rest.^13,14 Exactly what “rest” means and how long it should last are unknown, leading to a wide variation in its application.

Rest aids recovery but also may have adverse effects: fatigue, diurnal sleep disruption, reactive depression, anxiety, and physiologic deconditioning.^15,16 Many guidelines recommend physical and cognitive rest until symptoms resolve,¹⁴ but this is likely too cautious. Even without a concussion, inactivity is associated with many of the nonspecific symptoms also associated with concussion. As recovery progresses, the somatic symptoms of concussion improve, while emotional symptoms worsen, likely in part due to prolonged rest.¹⁷

We recommend a period of rest lasting 3 to 5 days after injury, followed by a gradual resumption of both physical and cognitive activities as tolerated, remaining below the level at which symptoms are exacerbated.

Not surprisingly, many guidelines for returning to physical activity are focused on athletes. Yet the same principles apply to management of concussion in the general population who exercise: light physical activity (typically walking or stationary bicycling), followed by more vigorous aerobic activity, followed by some resistance activities. Mild aerobic exercise (to below the threshold of symptoms) may speed recovery from refractive postconcussion syndrome, even in those who did not exercise before the injury.¹⁸

Athletes require specific and strict instructions to avoid increased trauma to the head during the gradual increase of physical activities. The National Collegiate Athletic Association has published an algorithm for a gradual return to sport-specific training that is echoed in recent consensus statements on concussion.¹⁹ Once aerobic reconditioning produces no symptoms, then noncontact, sport-specific activities are begun, followed by contact activities. We have patients return to the clinic once they are symptom-free for repeat evaluation before clearing them for high-risk activities (eg, skiing, bicycling) or contact sports (eg, basketball, soccer, football, ice hockey).

Cognitive rest

While physical rest is fairly straightforward, cognitive rest is more challenging. The concept of cognitive rest is hard to define and even harder to enforce. Patients are often told to minimize any activities that require attention or concentration. This often includes, but is not limited to, avoiding reading, texting, playing video games, and using computers.¹³

In the modern world, full avoidance of these activities is difficult and can be profoundly socially isolating. Further, complete cognitive rest may be associated with symptoms of its own.^15,16,20 Still, some reasonable limitation of cognitive activities, at least initially, is likely beneficial.²¹ For patients engaged in school or academic work, often the daily schedule needs to be adjusted and accommodations made to help them return to a full academic schedule and level of activity. It is reasonable to have patients return gradually to work or school rather than attempt to immediately return to their preinjury level.

With these interventions, most patients have full resolution of their symptoms and return to preinjury levels of performance.

TREATING SOMATIC SYMPTOMS

Posttraumatic headache

Posttraumatic headache is the most common sequela of concussion.²² Surprisingly, it is more common after concussion than after moderate or severe traumatic brain injury.²³ A prior history of headache, particularly migraine, is a known risk factor for development of posttraumatic headache.²⁴

Posttraumatic headache is usually further defined by headache type using the International Classification of Headache Disorders criteria (www.ichd-3.org). Migraine or probable migraine is the most common type of posttraumatic headache; tension headache is less common.²⁵

Analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) are often used initially by patients to treat posttraumatic headache. One study found that 70% of patients used acetaminophen or an NSAID.²⁶

Treating early with effective therapy is the most important tenet of posttraumatic headache treatment, since 80% of those who self-treat have incomplete relief, and almost all of them are using over-the-counter products.²⁷ Overuse of over-the-counter abortive medications can lead to medication overuse headache, also known as rebound headache, thus complicating the treatment of posttraumatic headache.²⁶

Earlier treatment with a preventive medication can often limit the need for and overuse of over-the-counter analgesics and can minimize the occurrence of subsequent medication overuse headache. However, in pediatric populations, nonpharmacologic interventions such as rest and sleep hygiene are typically used first, then medications after 4 to 6 weeks if this is ineffective.

A number of medications have been studied for prophylactic treatment of posttraumatic headache, including topiramate, amitriptyline, and divalproex sodium,^28–30 but there is little compelling evidence for use of one over the other. If posttraumatic headache is migrainous, beta-blockers, calcium-channel blockers, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibtors, and gabapentin are other prophylactic medication options under the appropriate circumstances.^27,31,32 In adults, we have clinically had success with nortriptyline 20 mg or gabapentin 300 mg at night as an initial prophylactic headache medication, increasing as tolerated or until pain is controlled, though there are no high-quality data to guide this decision.

The ideal prophylactic medication depends on headache type, patient tolerance, comorbidities, allergies, and medication sensitivities. Gabapentin, amitriptyline, and nortriptyline can produce sedation, which can help those suffering from sleep disturbance.

If a provider is not comfortable prescribing these medications or doesn’t prescribe them regularly, the patient should be referred to a concussion or headache specialist more familiar with their use.

In some patients, even some athletes, headache may be related to a cervical strain injury—whiplash—that should be treated with an NSAID (or acetaminophen), perhaps with a short course of a muscle relaxant in adults, and with physical therapy.³²

Some patients have chronic headache despite oral medications.²⁶ Therefore, alternatives to oral medications and complementary therapies should be considered. Especially for protracted cases requiring more complicated headache management or injectable treatments, patients should be referred to a pain clinic, headache specialist, or concussion specialist.

Dizziness is also common after concussion. But what the patient means by dizziness requires a little probing. Some have paroxysms of vertigo. This typically represents a peripheral vestibular injury, usually benign paroxysmal positional vertigo. The latter can be elicited with a Hallpike maneuver and treated in the office with the Epley maneuver.³³

Usually, dizziness is a subjective sense of poor coordination, gait instability, or dysequilibrium. Patients may also complain of associated nausea and motion sensitivity. This may all be secondary to a mechanism in the middle or inner ear or the brain. Patients should be encouraged to begin movement—gradually and safely—to help the vestibular system accommodate, which it will do with gradual stimulation. It usually resolves spontaneously.

Specific treatment is unfortunately limited. There is no established benefit from vestibular suppressants such as meclizine. Vestibular rehabilitation may accelerate improvement and decrease symptoms.³³ Referral for a comprehensive balance assessment or to vestibular therapy (a subset of physical therapy) should be considered and is something we typically undertake in our clinic if there is no recovery from dizziness 4 to 6 weeks after the concussion.

Visual symptoms can contribute to dizziness. Convergence spasm or convergence insufficiency (both related to muscle spasm of the eye) can occur after concussion, with some studies estimating that up to 69% of patients have these symptoms.³⁴ This can interfere with visual tracking and contribute to a feeling of dysequilibrium.³⁴ Referral to a concussion specialist or vestibular rehabilitation physical therapist can be helpful in treating this issue if it does not resolve spontaneously.

Orthostasis and lightheadedness also contribute to dizziness and are associated with cerebrovascular autoregulation. Available data suggest that dysregulation of neurovascular coupling, cerebral vasoreactivity, and cerebral autoregulation contribute to some of the chronic symptoms of concussion, including dizziness. A gradual return to exercise may help regulate cerebral blood flow and improve this type of dizziness.³⁵

Sleep disturbance

Sleep disturbance is common after concussion, but the form is variable: insomnia, excessive daytime somnolence, and alteration of the sleep-wake cycle are all seen and may themselves affect recovery.³⁶

Sleep hygiene education should be the first intervention for postconcussive sleep issues. For example, the patient should be encouraged to do the following:

• Minimize “screen time” an hour before going to bed: cell phone, tablet, and computer screens emit a wavelength of light that suppresses endogenous melatonin release^37,38
• Go to bed and wake up at the same time each day
• Minimize or avoid caffeine, nicotine, and alcohol
• Avoid naps.³⁹

Melatonin is a safe and effective treatment that could be added.⁴⁰ In addition, some studies suggest that melatonin may improve recovery from traumatic brain injury.^41,42

Mild exercise (to below the threshold of causing or exacerbating symptoms) may also improve sleep quality.

Amitriptyline or nortriptyline may reduce headache frequency and intensity and also help treat insomnia.

Trazodone is recommended by some as a first-line agent,³⁹ but we usually reserve it for protracted insomnia refractory to the above treatments.

Benzodiazepines should be avoided, as they reduce arousal, impair cognition, and exacerbate motor impairments.⁴³

Emotional symptoms

Acute-onset anxiety or depression often occurs after concussion.^44,45 There is abundant evidence that emotional effects of injury may be the most significant factor in recovery.⁴⁶ A preinjury history of anxiety may be a prognostic factor.⁹ Patients with a history of anxiety or depression are more likely to develop emotional symptoms after a concussion, but emotional problems may develop in any patient after a concussion.^47,48

The circumstances under which an injury is sustained may be traumatic (eg, car accident, assault), leading to an acute stress reaction or disorder and, if untreated, may result in a more chronic condition—posttraumatic stress disorder. Moreover, the injury and subsequent symptoms may have repercussions in many aspects of the patient’s life, leading to further psychologic stress (eg, loss of wages or the inability to handle normal work, school, and family responsibilities).

Referral to a therapist trained in skills-based psychotherapy (eg, cognitive-behavioral therapy, exposure-based treatment) is often helpful.

Pharmacologic treatment can be a useful adjunct. Several studies have shown that selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants may improve depression after concussion.⁴⁹ The prescription of antidepressants, however, is best left to providers with experience in treating anxiety and depression.

As with sleep disorders after concussion, benzodiazepines should be avoided, as they can impair cognition.⁴³

Cognitive problems

Cognitive problems are also common after concussion. Patients complain about everyday experiences of forgetfulness, distractibility, loss of concentration, and mental fatigue. Although patients often subjectively perceive these symptoms as quite limiting, the impairments can be difficult to demonstrate in office testing.

A program of gradual increase in mental activity, parallel to recovery of physical capacity, should be undertaken. Most patients make a gradual recovery within a few weeks.⁵⁰

When cognitive symptoms cause significant school or vocational problems or become persistent, patients should be referred to a specialty clinic. As with most of the consequences of concussion, there are few established treatments. When cognitive difficulties persist, it is important to consider the complications of concussion mentioned above: headache, pain, sleep disturbance, and anxiety, all of which may cause subjective cognitive problems and are treatable.

If cognitive symptoms are prolonged despite improvement of other issues like headache and sleep disturbance, a low-dose stimulant medication such as amphetamine salts or methylphenidate may be useful for symptoms of poor attention.⁴⁹ They should be only a temporary measure after concussion to carry the patient through a cognitively challenging period, unless there was a history of attention-deficit disorder before the injury. A variety of other agents, including amantadine,⁵¹ have been proposed based on limited studies; all are off-label uses. Before considering these types of interventions, referral to a specialist or a specialty program would be appropriate.

With the interventions suggested above, most patients with concussion have a resolution of symptoms and can return to preinjury levels of performance. But some have prolonged symptoms and sequelae. Approximately 10% of athletes have persistent signs and symptoms of concussion beyond 2 weeks. If concussion is not sport-related, most patients recover completely within the first 3 months, but up to 33% may have symptoms beyond that.⁵²

Four types of patients have persistent symptoms:

Patients who sustained a high-force mechanism of injury. These patients simply need more time and accommodation.

Patients who sustained multiple concussions. These patients may also need more time and accommodation.

Patients with an underlying neurologic condition, recognized prior to injury or not, may have delayed or incomplete recovery. Even aging may be an “underlying condition” in concussion.

Patients whose symptoms from an apparently single mild concussion do not resolve despite appropriate treatments may have identifiable factors, but intractable pain (usually headache) or significant emotional disturbance or both are common. Once established and persistent, this is difficult to treat. Referral to a specialty practice is appropriate, but even in that setting effective treatment may be elusive.

PATIENT EDUCATION

Most important for patient education is reassurance. Ultimately, concussion is a self-limited phenomenon, and reinforcing this is helpful for patients. If concussion is not sport-related, most patients recover completely within 3 months.

The next important tenet in patient education is that they should rest for 3 to 5 days, then resume gradual physical and cognitive activities. If resuming activities too soon results in symptoms, then they should rest for a day and gradually resume activity. If their recovery is prolonged (ie, longer than 6 weeks), they likely need to be referred to a concussion specialist.

We well recall, back in the day, getting our “bell rung” from some form of sports-related head contact. If we could count the coach’s fingers clearly, run fast and straight, and know the plays, we could happily go back into the game. There was little additional thought given to short-term or lasting effects. I recall hearing tales from my grandfather, a boxing enthusiast, of retired punch-drunk fighters working as bouncers and greeters at sports-focused restaurants and clubs. I certainly didn’t draw any link to a few episodes of personally feeling spacey or dizzy after playing football.

But now, as parents, we are all highly tuned in to the issue of wrongly minimized “minor” head contact and concussion in our children playing sports. There is a growing research-based understanding of the mechanisms of concussion, which remains a clinical syndrome diagnosed on the basis of symptoms and sometimes subtle objective findings that occur in the appropriate environmental context. Intracranial brain impact sets the stage for locally spreading firing of neurons outside their usual pattern. This can result in a diffuse jamming of some normal electrochemical pathways of cognitive function, as well as create additional mismatch between neuronal metabolic needs and the local blood flow providing oxygen and nutrients. This disruption in autoregulation of blood flow sets the stage for enhanced brain sensitivity to any second injurious event, even a minimal one. Hence the aggressive implementation of enforced rest and recovery time for athletes and others with concussion.

It is critical to realize that the patient may not have had a loss of consciousness. Equally important is to consider the need for imaging and protection of patients who are not recovering as expected in 7 to 10 days, as well as for initial imaging of those with severe head impact or baseline neurologic disease, the aged, and those on anticoagulation.

We well recall, back in the day, getting our “bell rung” from some form of sports-related head contact. If we could count the coach’s fingers clearly, run fast and straight, and know the plays, we could happily go back into the game. There was little additional thought given to short-term or lasting effects. I recall hearing tales from my grandfather, a boxing enthusiast, of retired punch-drunk fighters working as bouncers and greeters at sports-focused restaurants and clubs. I certainly didn’t draw any link to a few episodes of personally feeling spacey or dizzy after playing football.

But now, as parents, we are all highly tuned in to the issue of wrongly minimized “minor” head contact and concussion in our children playing sports. There is a growing research-based understanding of the mechanisms of concussion, which remains a clinical syndrome diagnosed on the basis of symptoms and sometimes subtle objective findings that occur in the appropriate environmental context. Intracranial brain impact sets the stage for locally spreading firing of neurons outside their usual pattern. This can result in a diffuse jamming of some normal electrochemical pathways of cognitive function, as well as create additional mismatch between neuronal metabolic needs and the local blood flow providing oxygen and nutrients. This disruption in autoregulation of blood flow sets the stage for enhanced brain sensitivity to any second injurious event, even a minimal one. Hence the aggressive implementation of enforced rest and recovery time for athletes and others with concussion.

It is critical to realize that the patient may not have had a loss of consciousness. Equally important is to consider the need for imaging and protection of patients who are not recovering as expected in 7 to 10 days, as well as for initial imaging of those with severe head impact or baseline neurologic disease, the aged, and those on anticoagulation.

We well recall, back in the day, getting our “bell rung” from some form of sports-related head contact. If we could count the coach’s fingers clearly, run fast and straight, and know the plays, we could happily go back into the game. There was little additional thought given to short-term or lasting effects. I recall hearing tales from my grandfather, a boxing enthusiast, of retired punch-drunk fighters working as bouncers and greeters at sports-focused restaurants and clubs. I certainly didn’t draw any link to a few episodes of personally feeling spacey or dizzy after playing football.

But now, as parents, we are all highly tuned in to the issue of wrongly minimized “minor” head contact and concussion in our children playing sports. There is a growing research-based understanding of the mechanisms of concussion, which remains a clinical syndrome diagnosed on the basis of symptoms and sometimes subtle objective findings that occur in the appropriate environmental context. Intracranial brain impact sets the stage for locally spreading firing of neurons outside their usual pattern. This can result in a diffuse jamming of some normal electrochemical pathways of cognitive function, as well as create additional mismatch between neuronal metabolic needs and the local blood flow providing oxygen and nutrients. This disruption in autoregulation of blood flow sets the stage for enhanced brain sensitivity to any second injurious event, even a minimal one. Hence the aggressive implementation of enforced rest and recovery time for athletes and others with concussion.

It is critical to realize that the patient may not have had a loss of consciousness. Equally important is to consider the need for imaging and protection of patients who are not recovering as expected in 7 to 10 days, as well as for initial imaging of those with severe head impact or baseline neurologic disease, the aged, and those on anticoagulation.

On examination, her lung fields were clear, with no audible murmurs, and she had no lower-extremity edema. Her oxygen saturation was 98% on room air.

BREAST CALCIFICATIONS CAN MIMIC PULMONARY NODULES

Diffuse bilateral calcifications on mammography are typically benign and represent either dermal calcification (spherical lucent- centered calcification that develops from a degenerative metaplastic process) or fibrocystic changes.¹ Up to 10% of women have fibroadenomas, and 19% of fibroadenomas have microcalcifications.^2–4 Therefore, given the high prevalence, calcified breast masses should be considered in the differential diagnosis when evaluating initial chest radiographs in women.

Calcifications in the breast can overlie the lung fields and mimic pulmonary nodules. When assessing pulmonary nodules, prior imaging of the chest should always be assessed if available to determine if a lesion is new or has remained stable.

Given our patient’s age and 35-pack-year history of smoking, apparent pulmonary lesions caused concern and prompted chest CT to clarify the diagnosis. However, if the patient has no risk factors for lung malignancy, it can be safe to proceed with mammography.

By including breast calcifications in the differential diagnosis of apparent pulmonary nodules on chest radiography, the clinician can approach the case differently and inquire about a history of fibroadenomas and prior mammograms before pursuing a further workup. This can avoid unnecessary radiation exposure, the costs of CT, and apprehension in the patient raised by unwarranted concern for malignancy.

On examination, her lung fields were clear, with no audible murmurs, and she had no lower-extremity edema. Her oxygen saturation was 98% on room air.

BREAST CALCIFICATIONS CAN MIMIC PULMONARY NODULES

Diffuse bilateral calcifications on mammography are typically benign and represent either dermal calcification (spherical lucent- centered calcification that develops from a degenerative metaplastic process) or fibrocystic changes.¹ Up to 10% of women have fibroadenomas, and 19% of fibroadenomas have microcalcifications.^2–4 Therefore, given the high prevalence, calcified breast masses should be considered in the differential diagnosis when evaluating initial chest radiographs in women.

Calcifications in the breast can overlie the lung fields and mimic pulmonary nodules. When assessing pulmonary nodules, prior imaging of the chest should always be assessed if available to determine if a lesion is new or has remained stable.

Given our patient’s age and 35-pack-year history of smoking, apparent pulmonary lesions caused concern and prompted chest CT to clarify the diagnosis. However, if the patient has no risk factors for lung malignancy, it can be safe to proceed with mammography.

By including breast calcifications in the differential diagnosis of apparent pulmonary nodules on chest radiography, the clinician can approach the case differently and inquire about a history of fibroadenomas and prior mammograms before pursuing a further workup. This can avoid unnecessary radiation exposure, the costs of CT, and apprehension in the patient raised by unwarranted concern for malignancy.

On examination, her lung fields were clear, with no audible murmurs, and she had no lower-extremity edema. Her oxygen saturation was 98% on room air.

BREAST CALCIFICATIONS CAN MIMIC PULMONARY NODULES

Diffuse bilateral calcifications on mammography are typically benign and represent either dermal calcification (spherical lucent- centered calcification that develops from a degenerative metaplastic process) or fibrocystic changes.¹ Up to 10% of women have fibroadenomas, and 19% of fibroadenomas have microcalcifications.^2–4 Therefore, given the high prevalence, calcified breast masses should be considered in the differential diagnosis when evaluating initial chest radiographs in women.

Calcifications in the breast can overlie the lung fields and mimic pulmonary nodules. When assessing pulmonary nodules, prior imaging of the chest should always be assessed if available to determine if a lesion is new or has remained stable.

Given our patient’s age and 35-pack-year history of smoking, apparent pulmonary lesions caused concern and prompted chest CT to clarify the diagnosis. However, if the patient has no risk factors for lung malignancy, it can be safe to proceed with mammography.

By including breast calcifications in the differential diagnosis of apparent pulmonary nodules on chest radiography, the clinician can approach the case differently and inquire about a history of fibroadenomas and prior mammograms before pursuing a further workup. This can avoid unnecessary radiation exposure, the costs of CT, and apprehension in the patient raised by unwarranted concern for malignancy.

Acute pancreatitis accounted for more than 300,000 admissions and $2.6 billion in associated healthcare costs in the United States in 2012.¹ First-line management is early aggressive fluid resuscitation and analgesics for pain control. Guidelines recommend estimating the clinical severity of each attack using a validated scoring system such as the Bedside Index of Severity in Acute Pancreatitis.² Clinically severe pancreatitis is associated with necrosis.

Acute pancreatitis results from inappropriate activation of zymogens and subsequent auto­digestion of the pancreas by its own enzymes. Though necrotizing pancreatitis is thought to be an ischemic complication, its pathogenesis is not completely understood. Necrosis increases the morbidity and mortality risk of acute pancreatitis because of its association with organ failure and infectious complications. As such, patients with necrotizing pancreatitis may need admission to the intensive care unit, nutritional support, antibiotics, and radiologic, endoscopic, or surgical interventions.

Here, we review current evidence regarding the diagnosis and management of necrotizing pancreatitis.

PROPER TERMINOLOGY HELPS COLLABORATION

Managing necrotizing pancreatitis requires the combined efforts of internists, gastroenterologists, radiologists, and surgeons. This collaboration is aided by proper terminology.

A classification system was devised in Atlanta, GA, in 1992 to facilitate communication and interdisciplinary collaboration.³ Severe pancreatitis was differentiated from mild by the presence of organ failure or the complications of pseudocyst, necrosis, or abscess.

The original Atlanta classification had several limitations. First, the terminology for fluid collections was ambiguous and frequently misused. Second, the assessment of clinical severity required either the Ranson score or the Acute Physiology and Chronic Health Evaluation II score, both of which are complex and have other limitations. Finally, advances in imaging and treatment have rendered the original Atlanta nomenclature obsolete.

In 2012, the Acute Pancreatitis Classification Working Group issued a revised Atlanta classification that modernized the terminology pertaining to natural history, severity, imaging features, and complications. It divides the natural course of acute pancreatitis into early and late phases.⁴

Early vs late phase

In the early phase, findings on computed tomography (CT) neither correlate with clinical severity nor alter clinical management.⁶ Thus, early imaging is not indicated unless there is diagnostic uncertainty, lack of response to appropriate treatment, or sudden deterioration.

Moderate pancreatitis describes patients with pancreatic necrosis with or without transient organ failure (organ dysfunction for ≤ 48 hours).

Severe pancreatitis is defined by pancreatic necrosis and persistent organ dysfunction.⁴ It may be accompanied by pancreatic and peripancreatic fluid collections; bacteremia and sepsis can occur in association with infection of necrotic collections.

Interstitial edematous pancreatitis vs necrotizing pancreatitis

The revised Atlanta classification maintains the original classification of acute pancreatitis into 2 main categories: interstitial edematous pancreatitis and necrotizing pancreatitis.

Necrotizing pancreatitis is further divided into 3 subtypes based on extent and location of necrosis:

• Parenchymal necrosis alone (5% of cases)
• Necrosis of peripancreatic fat alone (20%)
• Necrosis of both parenchyma and peripancreatic fat (75%).

Peripancreatic involvement is commonly found in the mesentery, peripancreatic and distant retroperitoneum, and lesser sac.

Of the three subtypes, peripancreatic necrosis has the best prognosis. However, all of the subtypes of necrotizing pancreatitis are associated with poorer outcomes than interstitial edematous pancreatitis.

Fluid collections

Acute pancreatic fluid collections contain exclusively nonsolid components without an inflammatory wall and are typically found in the peripancreatic fat. These collections often resolve without intervention as the patient recovers. If they persist beyond 4 weeks and develop a nonepithelialized, fibrous wall, they become pseudocysts. Intervention is generally not recommended for pseudocysts unless they are symptomatic.

Radiographic imaging is not usually necessary to diagnose acute pancreatitis. However, it can be a valuable tool to clarify an ambiguous presentation, determine severity, and identify complications.

The timing and appropriate type of imaging are integral to obtaining useful data. Any imaging obtained in acute pancreatitis to evaluate necrosis should be performed at least 3 to 5 days from the initial symptom onset; if imaging is obtained before 72 hours, necrosis cannot be confidently excluded.⁸

COMPUTED TOMOGRAPHY

CT is the imaging test of choice when evaluating acute pancreatitis. In addition, almost all percutaneous interventions are performed with CT guidance. The Balthazar score is the most well-known CT severity index. It is calculated based on the degree of inflammation, acute fluid collections, and parenchymal necrosis.⁹ However, a modified severity index incorporates extrapancreatic complications such as ascites and vascular compromise and was found to more strongly correlate with outcomes than the standard Balthazar score.¹⁰

Contrast-enhanced CT is performed in 2 phases:

The pancreatic parenchymal phase

The pancreatic parenchymal or late arterial phase is obtained approximately 40 to 45 seconds after the start of the contrast bolus. It is used to detect necrosis in the early phase of acute pancreatitis and to assess the peripancreatic arteries for pseudoaneurysms in the late phase of acute pancreatitis.¹¹

Pancreatic necrosis appears as an area of decreased parenchymal enhancement, either well-defined or heterogeneous. The normal pancreatic parenchyma has a postcontrast enhancement pattern similar to that of the spleen. Parenchyma that does not enhance to the same degree is considered necrotic. The severity of necrosis is graded based on the percentage of the pancreas involved (< 30%, 30%–50%, or > 50%), and a higher percentage correlates with a worse outcome.^12,13

Peripancreatic necrosis is harder to detect, as there is no method to assess fat enhancement as there is with pancreatic parenchymal enhancement. In general, radiologists assume that heterogeneous peripancreatic changes, including areas of fat, fluid, and soft tissue attenuation, are consistent with peripancreatic necrosis. After 7 to 10 days, if these changes become more homogeneous and confluent with a more mass-like process, peripancreatic necrosis can be more confidently identified.^12,13

The portal venous phase

The later, portal venous phase of the scan is obtained approximately 70 seconds after the start of the contrast bolus. It is used to detect and characterize fluid collections and venous complications of the disease.

Drawbacks of CT

A drawback of CT is the need for iodinated intravenous contrast media, which in severely ill patients may precipitate or worsen pre-existing acute kidney injury.

Further, several studies have shown that findings on CT rarely alter the management of patients in the early phase of acute pancreatitis and in fact may be an overuse of medical resources.¹⁴ Unless there are confounding clinical signs or symptoms, CT should be delayed for at least 72 hours.^9,10,14,15

MAGNETIC RESONANCE IMAGING

Magnetic resonance imaging (MRI) is not a first-line imaging test in this disease because it is not as available as CT and takes longer to perform—20 to 30 minutes. The patient must be evaluated for candidacy, as it is difficult for acutely ill patients to tolerate an examination that takes this long and requires them to hold their breath multiple times.

MRI is an appropriate alternative in patients who are pregnant or who have severe iodinated-contrast allergy. While contrast is necessary to detect pancreatic necrosis with CT, MRI can detect necrosis without the need for contrast in patients with acute kidney injury or severe chronic kidney disease. Also, MRI may be better in complicated cases requiring repeated imaging because it does not expose the patient to radiation.

On MRI, pancreatic necrosis appears as a heterogeneous area, owing to its liquid and solid components. Liquid components appear hyperintense, and solid components hypointense, on T2 fluid-weighted imaging. This ability to differentiate the components of a walled-off pancreatic necrosis can be useful in determining whether a collection requires drainage or debridement. MRI is also more sensitive for hemorrhagic complications, best seen on T1 fat-weighted images.^12,16

Magnetic resonance cholangiopancreatography is an excellent method for ductal evaluation through heavily T2-weighted imaging. It is more sensitive than CT for detecting common bile duct stones and can also detect pancreatic duct strictures or extravasation into fluid collections.¹⁶

SUPPORTIVE MANAGEMENT OF EARLY NECROTIZING PANCREATITIS

In the early phase of necrotizing pancreatitis, management is supportive with the primary aim of preventing intravascular volume depletion. Aggressive fluid resuscitation in the first 48 to 72 hours, pain control, and bowel rest are the mainstays of supportive therapy. Intensive care may be necessary if organ failure and hemodynamic instability accompany necrotizing pancreatitis.

Prophylactic antibiotic and antifungal therapy to prevent infected necrosis has been controversial. Recent studies of its utility have not yielded supportive results, and the American College of Gastroenterology and the Infectious Diseases Society of America no longer recommend it.^9,17 These medications should not be given unless concomitant cholangitis or extrapancreatic infection is clinically suspected.

Early enteral nutrition is recommended in patients in whom pancreatitis is predicted to be severe and in those not expected to resume oral intake within 5 to 7 days. Enteral nutrition most commonly involves bedside or endoscopic placement of a nasojejunal feeding tube and collaboration with a nutritionist to determine protein-caloric requirements.

Compared with enteral nutrition, total parenteral nutrition is associated with higher rates of infection, multiorgan dysfunction and failure, and death.¹⁸

Necrotizing pancreatitis is a defining complication of acute pancreatitis, and its presence alone indicates greater severity. However, superimposed complications may further worsen outcomes.

Infected pancreatic necrosis

Infection occurs in approximately 20% of patients with necrotizing pancreatitis and confers a mortality rate of 20% to 50%.¹⁹ Infected pancreatic necrosis occurs when gut organisms translocate into the nearby necrotic pancreatic and peripancreatic tissue. The most commonly identified organisms include Escherichia coli and Enterococcus species.²⁰

This complication usually manifests 2 to 4 weeks after symptom onset; earlier onset is uncommon to rare. It should be considered when the systemic inflammatory response syndrome persists or recurs after 10 days to 2 weeks. Systemic inflammatory response syndrome is also common in sterile necrotizing pancreatitis and sometimes in interstitial pancreatitis, particularly during the first week. However, its sudden appearance or resurgence, high spiking fevers, or worsening organ failure in the later phase (2–4 weeks) of pancreatitis should heighten suspicion of infected pancreatic necrosis.

Imaging may also help diagnose infection, and the presence of gas within a collection or region of necrosis is highly specific. However, the presence of gas is not completely sensitive for infection, as it is seen in only 12% to 22% of infected cases.

Before minimally invasive techniques became available, the diagnosis of infected pancreatic necrosis was confirmed by percutaneous CT-guided aspiration of the necrotic mass or collection for Gram stain and culture.

Antibiotic therapy is indicated in confirmed or suspected cases of infected pancreatic necrosis. Antibiotics with gram-negative coverage and appropriate penetration such as carbapenems, metronidazole, fluoroquinolones, and selected cephalosporins are most commonly used. Meropenem is the antibiotic of choice at our institution.

CT-guided fine-needle aspiration is often done if suspected infected pancreatic necrosis fails to respond to empiric antibiotic therapy.

Debridement or drainage. Generally, the diagnosis or suspicion of infected pancreatic necrosis (suggestive signs are high fever, elevated white blood cell count, and sepsis) warrants an intervention to debride or drain infected pancreatic tissue and control sepsis.²¹

While source control is integral to the successful treatment of infected pancreatic necrosis, antibiotic therapy may provide a bridge to intervention for critically ill patients by suppressing bacteremia and subsequent sepsis. A 2013 meta-analysis found that 324 of 409 patients with suspected infected pancreatic necrosis were successfully stabilized with antibiotic treatment.^21,22 The trend toward conservative management and promising outcomes with antibiotic therapy alone or with minimally invasive techniques has lessened the need for diagnostic CT-guided fine-needle aspiration.

Hemorrhage

Spontaneous hemorrhage into pancreatic necrosis is a rare but life-threatening complication. Because CT is almost always performed with contrast enhancement, this complication is rarely identified with imaging. The diagnosis is made by noting a drop in hemoglobin and hematocrit.

Hemorrhage into the retroperitoneum or the peritoneal cavity, or both, can occur when an inflammatory process erodes into a nearby artery. Luminal gastrointestinal bleeding can occur from gastric varices arising from splenic vein thrombosis and resulting left-sided portal hypertension, or from pseudoaneurysms. These can also bleed into the pancreatic duct (hemosuccus pancreaticus). Pseudoaneurysm is a later complication that occurs when an arterial wall (most commonly the splenic or gastroduodenal artery) is weakened by pancreatic enzymes.²³

Prompt recognition of hemorrhagic events and consultation with an interventional radiologist or surgeon are required to prevent death.

Inflammation and abdominal compartment syndrome

Inflammation from necrotizing pancreatitis can cause further complications by blocking nearby structures. Reported complications include jaundice from biliary compression, hydronephrosis from ureteral compression, bowel obstruction, and gastric outlet obstruction.

Abdominal compartment syndrome is an increasingly recognized complication of acute pancreatitis. Abdominal pressure can rise due to a number of factors, including fluid collections, ascites, ileus, and overly aggressive fluid resuscitation.²⁴ Elevated abdominal pressure is associated with complications such as decreased respiratory compliance, increased peak airway pressure, decreased cardiac preload, hypotension, mesenteric and intestinal ischemia, feeding intolerance, and lower-extremity ischemia and thrombosis.

Patients with necrotizing pancreatitis who have abdominal compartment syndrome have a mortality rate 5 times higher than patients without abdominal compartment syndrome.²⁵

Abdominal pressures should be monitored using a bladder pressure sensor in critically ill or ventilated patients with acute pancreatitis. If the abdominal pressure rises above 20 mm Hg, medical and surgical interventions should be offered in a stepwise fashion to decrease it. Interventions include decompression by nasogastric and rectal tube, sedation or paralysis to relax abdominal wall tension, minimization of intravenous fluids, percutaneous drainage of ascites, and (rarely) surgical midline or subcostal laparotomy.

The treatment of necrotizing pancreatitis has changed rapidly, thanks to a growing experience with minimally invasive techniques.

Indications for intervention

Infected pancreatic necrosis is the primary indication for surgical, percutaneous, or endoscopic intervention.

In sterile necrosis, the threshold for intervention is less clear, and intervention is often reserved for patients who fail to clinically improve or who have intractable abdominal pain, gastric outlet obstruction, or fistulating disease.²⁶

In asymptomatic cases, intervention is almost never indicated regardless of the location or size of the necrotic area.

In walled-off pancreatic necrosis, less-invasive and less-morbid interventions such as endoscopic or percutaneous drainage or video-assisted retroperitoneal debridement can be done.

Timing of intervention

In the past, delaying intervention was thought to increase the risk of death. However, multiple studies have found that outcomes are often worse if intervention is done early, likely due to the lack of a fully formed fibrous wall or demarcation of the necrotic area.²⁷

If the patient remains clinically stable, it is best to delay intervention until at least 4 weeks after the index event to achieve optimal outcomes. Delay can often be achieved by antibiotic treatment to suppress bacteremia and endoscopic or percutaneous drainage of infected collections to control sepsis.

Open surgery

The gold-standard intervention for infected pancreatic necrosis or symptomatic sterile walled-off pancreatic necrosis is open necrosectomy. This involves exploratory laparotomy with blunt debridement of all visible necrotic pancreatic tissue.

Methods to facilitate later evacuation of residual infected fluid and debris vary widely. Multiple large-caliber drains can be placed to facilitate irrigation and drainage before closure of the abdominal fascia. As infected pancreatic necrosis carries the risk of contaminating the peritoneal cavity, the skin is often left open to heal by secondary intention. An interventional radiologist is frequently enlisted to place, exchange, or downsize drainage catheters.

Infected pancreatic necrosis or symptomatic sterile walled-off pancreatic necrosis often requires more than one operation to achieve satisfactory debridement.

The goals of open necrosectomy are to remove nonviable tissue and infection, preserve viable pancreatic tissue, eliminate fistulous connections, and minimize damage to local organs and vasculature.

Minimally invasive techniques

Video-assisted retroperitoneal debridement has been described as a hybrid between endoscopic and open retroperitoneal debridement.²⁸ This technique requires first placing a percutaneous catheter into the necrotic area through the left flank to create a retroperitoneal tract. A 5-cm incision is made and the necrotic space is entered using the drain for guidance. Necrotic tissue is carefully debrided under direct vision using a combination of forceps, irrigation, and suction. A laparoscopic port can also be introduced into the incision when the procedure can no longer be continued under direct vision.^29,30

Although not all patients are candidates for minimal-access surgery, it remains an evolving surgical option.

Endoscopic transmural debridement is another option for infected pancreatic necrosis and symptomatic walled-off pancreatic necrosis. Depending on the location of the necrotic area, an echoendoscope is passed to either the stomach or duodenum. Guided by endoscopic ultrasonography, a needle is passed into the collection, allowing subsequent fistula creation and stenting for internal drainage or debridement. In the past, this process required several steps, multiple devices, fluoroscopic guidance, and considerable time. But newer endoscopic lumen-apposing metal stents have been developed that can be placed in a single step without fluoroscopy. A slimmer endoscope can then be introduced into the necrotic cavity via the stent, and the necrotic debris can be debrided with endoscopic baskets, snares, forceps, and irrigation.^9,31

Similar to surgical necrosectomy, satisfactory debridement is not often obtained with a single procedure; 2 to 5 endoscopic procedures may be needed to achieve resolution. However, the luminal approach in endoscopic necrosectomy avoids the significant morbidity of major abdominal surgery and the potential for pancreaticocutaneous fistulae that may occur with drains.

In a randomized trial comparing endoscopic necrosectomy vs surgical necrosectomy (video-assisted retroperitoneal debridement and exploratory laparotomy),³² endoscopic necrosectomy showed less inflammatory response than surgical necrosectomy and had a lower risk of new-onset organ failure, bleeding, fistula formation, and death.³²

Selecting the best intervention for the individual patient

Given the multiple available techniques, selecting the best intervention for individual patients can be challenging. A team approach with input from a gastroenterologist, surgeon, and interventional radiologist is best when determining which technique would best suit each patient.

Surgical necrosectomy is still the treatment of choice for unstable patients with infected pancreatic necrosis or multiple, inaccessible collections, but current evidence suggests a different approach in stable infected pancreatic necrosis and symptomatic sterile walled-off pancreatic necrosis.

The Dutch Pancreatitis Group²⁸ randomized 88 patients with infected pancreatic necrosis or symptomatic walled-off pancreatic necrosis to open necrosectomy or a minimally invasive “step-up” approach consisting of up to 2 percutaneous drainage or endoscopic debridement procedures before escalation to video-assisted retroperitoneal debridement. The step-up approach resulted in lower rates of morbidity and death than surgical necrosectomy as first-line treatment. Furthermore, some patients in the step-up group avoided the need for surgery entirely.³⁰

Necrosis significantly increases rates of morbidity and mortality in acute pancreatitis. Hospitalists, general internists, and general surgeons are all on the front lines in identifying severe cases and consulting the appropriate specialists for optimal multidisciplinary care. Selective and appropriate timing of radiologic imaging is key, and a vital tool in the management of necrotizing pancreatitis.

While the primary indication for intervention is infected pancreatic necrosis, additional indications are symptomatic walled-off pancreatic necrosis secondary to intractable abdominal pain, bowel obstruction, and failure to thrive. As a result of improving technology and inpatient care, these patients may present with intractable symptoms in the outpatient setting rather than the inpatient setting. The onus is on the primary care physician to maintain a high level of suspicion and refer these patients to subspecialists as appropriate.

Open surgical necrosectomy remains an important approach for care of infected pancreatic necrosis or patients with intractable symptoms. A step-up approach starting with a minimally invasive procedure and escalating if the initial intervention is unsuccessful is gradually becoming the standard of care.

Acute pancreatitis accounted for more than 300,000 admissions and $2.6 billion in associated healthcare costs in the United States in 2012.¹ First-line management is early aggressive fluid resuscitation and analgesics for pain control. Guidelines recommend estimating the clinical severity of each attack using a validated scoring system such as the Bedside Index of Severity in Acute Pancreatitis.² Clinically severe pancreatitis is associated with necrosis.

Acute pancreatitis results from inappropriate activation of zymogens and subsequent auto­digestion of the pancreas by its own enzymes. Though necrotizing pancreatitis is thought to be an ischemic complication, its pathogenesis is not completely understood. Necrosis increases the morbidity and mortality risk of acute pancreatitis because of its association with organ failure and infectious complications. As such, patients with necrotizing pancreatitis may need admission to the intensive care unit, nutritional support, antibiotics, and radiologic, endoscopic, or surgical interventions.

Here, we review current evidence regarding the diagnosis and management of necrotizing pancreatitis.

PROPER TERMINOLOGY HELPS COLLABORATION

Managing necrotizing pancreatitis requires the combined efforts of internists, gastroenterologists, radiologists, and surgeons. This collaboration is aided by proper terminology.

A classification system was devised in Atlanta, GA, in 1992 to facilitate communication and interdisciplinary collaboration.³ Severe pancreatitis was differentiated from mild by the presence of organ failure or the complications of pseudocyst, necrosis, or abscess.

The original Atlanta classification had several limitations. First, the terminology for fluid collections was ambiguous and frequently misused. Second, the assessment of clinical severity required either the Ranson score or the Acute Physiology and Chronic Health Evaluation II score, both of which are complex and have other limitations. Finally, advances in imaging and treatment have rendered the original Atlanta nomenclature obsolete.

In 2012, the Acute Pancreatitis Classification Working Group issued a revised Atlanta classification that modernized the terminology pertaining to natural history, severity, imaging features, and complications. It divides the natural course of acute pancreatitis into early and late phases.⁴

Early vs late phase

In the early phase, findings on computed tomography (CT) neither correlate with clinical severity nor alter clinical management.⁶ Thus, early imaging is not indicated unless there is diagnostic uncertainty, lack of response to appropriate treatment, or sudden deterioration.

Moderate pancreatitis describes patients with pancreatic necrosis with or without transient organ failure (organ dysfunction for ≤ 48 hours).

Severe pancreatitis is defined by pancreatic necrosis and persistent organ dysfunction.⁴ It may be accompanied by pancreatic and peripancreatic fluid collections; bacteremia and sepsis can occur in association with infection of necrotic collections.

Interstitial edematous pancreatitis vs necrotizing pancreatitis

The revised Atlanta classification maintains the original classification of acute pancreatitis into 2 main categories: interstitial edematous pancreatitis and necrotizing pancreatitis.

Necrotizing pancreatitis is further divided into 3 subtypes based on extent and location of necrosis:

• Parenchymal necrosis alone (5% of cases)
• Necrosis of peripancreatic fat alone (20%)
• Necrosis of both parenchyma and peripancreatic fat (75%).

Peripancreatic involvement is commonly found in the mesentery, peripancreatic and distant retroperitoneum, and lesser sac.

Of the three subtypes, peripancreatic necrosis has the best prognosis. However, all of the subtypes of necrotizing pancreatitis are associated with poorer outcomes than interstitial edematous pancreatitis.

Fluid collections

Acute pancreatic fluid collections contain exclusively nonsolid components without an inflammatory wall and are typically found in the peripancreatic fat. These collections often resolve without intervention as the patient recovers. If they persist beyond 4 weeks and develop a nonepithelialized, fibrous wall, they become pseudocysts. Intervention is generally not recommended for pseudocysts unless they are symptomatic.

Radiographic imaging is not usually necessary to diagnose acute pancreatitis. However, it can be a valuable tool to clarify an ambiguous presentation, determine severity, and identify complications.

The timing and appropriate type of imaging are integral to obtaining useful data. Any imaging obtained in acute pancreatitis to evaluate necrosis should be performed at least 3 to 5 days from the initial symptom onset; if imaging is obtained before 72 hours, necrosis cannot be confidently excluded.⁸

COMPUTED TOMOGRAPHY

CT is the imaging test of choice when evaluating acute pancreatitis. In addition, almost all percutaneous interventions are performed with CT guidance. The Balthazar score is the most well-known CT severity index. It is calculated based on the degree of inflammation, acute fluid collections, and parenchymal necrosis.⁹ However, a modified severity index incorporates extrapancreatic complications such as ascites and vascular compromise and was found to more strongly correlate with outcomes than the standard Balthazar score.¹⁰

Contrast-enhanced CT is performed in 2 phases:

The pancreatic parenchymal phase

The pancreatic parenchymal or late arterial phase is obtained approximately 40 to 45 seconds after the start of the contrast bolus. It is used to detect necrosis in the early phase of acute pancreatitis and to assess the peripancreatic arteries for pseudoaneurysms in the late phase of acute pancreatitis.¹¹

Pancreatic necrosis appears as an area of decreased parenchymal enhancement, either well-defined or heterogeneous. The normal pancreatic parenchyma has a postcontrast enhancement pattern similar to that of the spleen. Parenchyma that does not enhance to the same degree is considered necrotic. The severity of necrosis is graded based on the percentage of the pancreas involved (< 30%, 30%–50%, or > 50%), and a higher percentage correlates with a worse outcome.^12,13

Peripancreatic necrosis is harder to detect, as there is no method to assess fat enhancement as there is with pancreatic parenchymal enhancement. In general, radiologists assume that heterogeneous peripancreatic changes, including areas of fat, fluid, and soft tissue attenuation, are consistent with peripancreatic necrosis. After 7 to 10 days, if these changes become more homogeneous and confluent with a more mass-like process, peripancreatic necrosis can be more confidently identified.^12,13

The portal venous phase

The later, portal venous phase of the scan is obtained approximately 70 seconds after the start of the contrast bolus. It is used to detect and characterize fluid collections and venous complications of the disease.

Drawbacks of CT

A drawback of CT is the need for iodinated intravenous contrast media, which in severely ill patients may precipitate or worsen pre-existing acute kidney injury.

Further, several studies have shown that findings on CT rarely alter the management of patients in the early phase of acute pancreatitis and in fact may be an overuse of medical resources.¹⁴ Unless there are confounding clinical signs or symptoms, CT should be delayed for at least 72 hours.^9,10,14,15

MAGNETIC RESONANCE IMAGING

Magnetic resonance imaging (MRI) is not a first-line imaging test in this disease because it is not as available as CT and takes longer to perform—20 to 30 minutes. The patient must be evaluated for candidacy, as it is difficult for acutely ill patients to tolerate an examination that takes this long and requires them to hold their breath multiple times.

MRI is an appropriate alternative in patients who are pregnant or who have severe iodinated-contrast allergy. While contrast is necessary to detect pancreatic necrosis with CT, MRI can detect necrosis without the need for contrast in patients with acute kidney injury or severe chronic kidney disease. Also, MRI may be better in complicated cases requiring repeated imaging because it does not expose the patient to radiation.

On MRI, pancreatic necrosis appears as a heterogeneous area, owing to its liquid and solid components. Liquid components appear hyperintense, and solid components hypointense, on T2 fluid-weighted imaging. This ability to differentiate the components of a walled-off pancreatic necrosis can be useful in determining whether a collection requires drainage or debridement. MRI is also more sensitive for hemorrhagic complications, best seen on T1 fat-weighted images.^12,16

Magnetic resonance cholangiopancreatography is an excellent method for ductal evaluation through heavily T2-weighted imaging. It is more sensitive than CT for detecting common bile duct stones and can also detect pancreatic duct strictures or extravasation into fluid collections.¹⁶

SUPPORTIVE MANAGEMENT OF EARLY NECROTIZING PANCREATITIS

In the early phase of necrotizing pancreatitis, management is supportive with the primary aim of preventing intravascular volume depletion. Aggressive fluid resuscitation in the first 48 to 72 hours, pain control, and bowel rest are the mainstays of supportive therapy. Intensive care may be necessary if organ failure and hemodynamic instability accompany necrotizing pancreatitis.

Prophylactic antibiotic and antifungal therapy to prevent infected necrosis has been controversial. Recent studies of its utility have not yielded supportive results, and the American College of Gastroenterology and the Infectious Diseases Society of America no longer recommend it.^9,17 These medications should not be given unless concomitant cholangitis or extrapancreatic infection is clinically suspected.

Early enteral nutrition is recommended in patients in whom pancreatitis is predicted to be severe and in those not expected to resume oral intake within 5 to 7 days. Enteral nutrition most commonly involves bedside or endoscopic placement of a nasojejunal feeding tube and collaboration with a nutritionist to determine protein-caloric requirements.

Compared with enteral nutrition, total parenteral nutrition is associated with higher rates of infection, multiorgan dysfunction and failure, and death.¹⁸

Necrotizing pancreatitis is a defining complication of acute pancreatitis, and its presence alone indicates greater severity. However, superimposed complications may further worsen outcomes.

Infected pancreatic necrosis

Infection occurs in approximately 20% of patients with necrotizing pancreatitis and confers a mortality rate of 20% to 50%.¹⁹ Infected pancreatic necrosis occurs when gut organisms translocate into the nearby necrotic pancreatic and peripancreatic tissue. The most commonly identified organisms include Escherichia coli and Enterococcus species.²⁰

This complication usually manifests 2 to 4 weeks after symptom onset; earlier onset is uncommon to rare. It should be considered when the systemic inflammatory response syndrome persists or recurs after 10 days to 2 weeks. Systemic inflammatory response syndrome is also common in sterile necrotizing pancreatitis and sometimes in interstitial pancreatitis, particularly during the first week. However, its sudden appearance or resurgence, high spiking fevers, or worsening organ failure in the later phase (2–4 weeks) of pancreatitis should heighten suspicion of infected pancreatic necrosis.

Imaging may also help diagnose infection, and the presence of gas within a collection or region of necrosis is highly specific. However, the presence of gas is not completely sensitive for infection, as it is seen in only 12% to 22% of infected cases.

Before minimally invasive techniques became available, the diagnosis of infected pancreatic necrosis was confirmed by percutaneous CT-guided aspiration of the necrotic mass or collection for Gram stain and culture.

Antibiotic therapy is indicated in confirmed or suspected cases of infected pancreatic necrosis. Antibiotics with gram-negative coverage and appropriate penetration such as carbapenems, metronidazole, fluoroquinolones, and selected cephalosporins are most commonly used. Meropenem is the antibiotic of choice at our institution.

CT-guided fine-needle aspiration is often done if suspected infected pancreatic necrosis fails to respond to empiric antibiotic therapy.

Debridement or drainage. Generally, the diagnosis or suspicion of infected pancreatic necrosis (suggestive signs are high fever, elevated white blood cell count, and sepsis) warrants an intervention to debride or drain infected pancreatic tissue and control sepsis.²¹

While source control is integral to the successful treatment of infected pancreatic necrosis, antibiotic therapy may provide a bridge to intervention for critically ill patients by suppressing bacteremia and subsequent sepsis. A 2013 meta-analysis found that 324 of 409 patients with suspected infected pancreatic necrosis were successfully stabilized with antibiotic treatment.^21,22 The trend toward conservative management and promising outcomes with antibiotic therapy alone or with minimally invasive techniques has lessened the need for diagnostic CT-guided fine-needle aspiration.

Hemorrhage

Spontaneous hemorrhage into pancreatic necrosis is a rare but life-threatening complication. Because CT is almost always performed with contrast enhancement, this complication is rarely identified with imaging. The diagnosis is made by noting a drop in hemoglobin and hematocrit.

Hemorrhage into the retroperitoneum or the peritoneal cavity, or both, can occur when an inflammatory process erodes into a nearby artery. Luminal gastrointestinal bleeding can occur from gastric varices arising from splenic vein thrombosis and resulting left-sided portal hypertension, or from pseudoaneurysms. These can also bleed into the pancreatic duct (hemosuccus pancreaticus). Pseudoaneurysm is a later complication that occurs when an arterial wall (most commonly the splenic or gastroduodenal artery) is weakened by pancreatic enzymes.²³

Prompt recognition of hemorrhagic events and consultation with an interventional radiologist or surgeon are required to prevent death.

Inflammation and abdominal compartment syndrome

Inflammation from necrotizing pancreatitis can cause further complications by blocking nearby structures. Reported complications include jaundice from biliary compression, hydronephrosis from ureteral compression, bowel obstruction, and gastric outlet obstruction.

Abdominal compartment syndrome is an increasingly recognized complication of acute pancreatitis. Abdominal pressure can rise due to a number of factors, including fluid collections, ascites, ileus, and overly aggressive fluid resuscitation.²⁴ Elevated abdominal pressure is associated with complications such as decreased respiratory compliance, increased peak airway pressure, decreased cardiac preload, hypotension, mesenteric and intestinal ischemia, feeding intolerance, and lower-extremity ischemia and thrombosis.

Patients with necrotizing pancreatitis who have abdominal compartment syndrome have a mortality rate 5 times higher than patients without abdominal compartment syndrome.²⁵

Abdominal pressures should be monitored using a bladder pressure sensor in critically ill or ventilated patients with acute pancreatitis. If the abdominal pressure rises above 20 mm Hg, medical and surgical interventions should be offered in a stepwise fashion to decrease it. Interventions include decompression by nasogastric and rectal tube, sedation or paralysis to relax abdominal wall tension, minimization of intravenous fluids, percutaneous drainage of ascites, and (rarely) surgical midline or subcostal laparotomy.

The treatment of necrotizing pancreatitis has changed rapidly, thanks to a growing experience with minimally invasive techniques.

Indications for intervention

Infected pancreatic necrosis is the primary indication for surgical, percutaneous, or endoscopic intervention.

In sterile necrosis, the threshold for intervention is less clear, and intervention is often reserved for patients who fail to clinically improve or who have intractable abdominal pain, gastric outlet obstruction, or fistulating disease.²⁶

In asymptomatic cases, intervention is almost never indicated regardless of the location or size of the necrotic area.

In walled-off pancreatic necrosis, less-invasive and less-morbid interventions such as endoscopic or percutaneous drainage or video-assisted retroperitoneal debridement can be done.

Timing of intervention

In the past, delaying intervention was thought to increase the risk of death. However, multiple studies have found that outcomes are often worse if intervention is done early, likely due to the lack of a fully formed fibrous wall or demarcation of the necrotic area.²⁷

If the patient remains clinically stable, it is best to delay intervention until at least 4 weeks after the index event to achieve optimal outcomes. Delay can often be achieved by antibiotic treatment to suppress bacteremia and endoscopic or percutaneous drainage of infected collections to control sepsis.

Open surgery

The gold-standard intervention for infected pancreatic necrosis or symptomatic sterile walled-off pancreatic necrosis is open necrosectomy. This involves exploratory laparotomy with blunt debridement of all visible necrotic pancreatic tissue.

Methods to facilitate later evacuation of residual infected fluid and debris vary widely. Multiple large-caliber drains can be placed to facilitate irrigation and drainage before closure of the abdominal fascia. As infected pancreatic necrosis carries the risk of contaminating the peritoneal cavity, the skin is often left open to heal by secondary intention. An interventional radiologist is frequently enlisted to place, exchange, or downsize drainage catheters.

Infected pancreatic necrosis or symptomatic sterile walled-off pancreatic necrosis often requires more than one operation to achieve satisfactory debridement.

The goals of open necrosectomy are to remove nonviable tissue and infection, preserve viable pancreatic tissue, eliminate fistulous connections, and minimize damage to local organs and vasculature.

Minimally invasive techniques

Video-assisted retroperitoneal debridement has been described as a hybrid between endoscopic and open retroperitoneal debridement.²⁸ This technique requires first placing a percutaneous catheter into the necrotic area through the left flank to create a retroperitoneal tract. A 5-cm incision is made and the necrotic space is entered using the drain for guidance. Necrotic tissue is carefully debrided under direct vision using a combination of forceps, irrigation, and suction. A laparoscopic port can also be introduced into the incision when the procedure can no longer be continued under direct vision.^29,30

Although not all patients are candidates for minimal-access surgery, it remains an evolving surgical option.

Endoscopic transmural debridement is another option for infected pancreatic necrosis and symptomatic walled-off pancreatic necrosis. Depending on the location of the necrotic area, an echoendoscope is passed to either the stomach or duodenum. Guided by endoscopic ultrasonography, a needle is passed into the collection, allowing subsequent fistula creation and stenting for internal drainage or debridement. In the past, this process required several steps, multiple devices, fluoroscopic guidance, and considerable time. But newer endoscopic lumen-apposing metal stents have been developed that can be placed in a single step without fluoroscopy. A slimmer endoscope can then be introduced into the necrotic cavity via the stent, and the necrotic debris can be debrided with endoscopic baskets, snares, forceps, and irrigation.^9,31

Similar to surgical necrosectomy, satisfactory debridement is not often obtained with a single procedure; 2 to 5 endoscopic procedures may be needed to achieve resolution. However, the luminal approach in endoscopic necrosectomy avoids the significant morbidity of major abdominal surgery and the potential for pancreaticocutaneous fistulae that may occur with drains.

In a randomized trial comparing endoscopic necrosectomy vs surgical necrosectomy (video-assisted retroperitoneal debridement and exploratory laparotomy),³² endoscopic necrosectomy showed less inflammatory response than surgical necrosectomy and had a lower risk of new-onset organ failure, bleeding, fistula formation, and death.³²

Selecting the best intervention for the individual patient

Given the multiple available techniques, selecting the best intervention for individual patients can be challenging. A team approach with input from a gastroenterologist, surgeon, and interventional radiologist is best when determining which technique would best suit each patient.

Surgical necrosectomy is still the treatment of choice for unstable patients with infected pancreatic necrosis or multiple, inaccessible collections, but current evidence suggests a different approach in stable infected pancreatic necrosis and symptomatic sterile walled-off pancreatic necrosis.

The Dutch Pancreatitis Group²⁸ randomized 88 patients with infected pancreatic necrosis or symptomatic walled-off pancreatic necrosis to open necrosectomy or a minimally invasive “step-up” approach consisting of up to 2 percutaneous drainage or endoscopic debridement procedures before escalation to video-assisted retroperitoneal debridement. The step-up approach resulted in lower rates of morbidity and death than surgical necrosectomy as first-line treatment. Furthermore, some patients in the step-up group avoided the need for surgery entirely.³⁰

Necrosis significantly increases rates of morbidity and mortality in acute pancreatitis. Hospitalists, general internists, and general surgeons are all on the front lines in identifying severe cases and consulting the appropriate specialists for optimal multidisciplinary care. Selective and appropriate timing of radiologic imaging is key, and a vital tool in the management of necrotizing pancreatitis.

While the primary indication for intervention is infected pancreatic necrosis, additional indications are symptomatic walled-off pancreatic necrosis secondary to intractable abdominal pain, bowel obstruction, and failure to thrive. As a result of improving technology and inpatient care, these patients may present with intractable symptoms in the outpatient setting rather than the inpatient setting. The onus is on the primary care physician to maintain a high level of suspicion and refer these patients to subspecialists as appropriate.

Open surgical necrosectomy remains an important approach for care of infected pancreatic necrosis or patients with intractable symptoms. A step-up approach starting with a minimally invasive procedure and escalating if the initial intervention is unsuccessful is gradually becoming the standard of care.

Acute pancreatitis accounted for more than 300,000 admissions and $2.6 billion in associated healthcare costs in the United States in 2012.¹ First-line management is early aggressive fluid resuscitation and analgesics for pain control. Guidelines recommend estimating the clinical severity of each attack using a validated scoring system such as the Bedside Index of Severity in Acute Pancreatitis.² Clinically severe pancreatitis is associated with necrosis.

Acute pancreatitis results from inappropriate activation of zymogens and subsequent auto­digestion of the pancreas by its own enzymes. Though necrotizing pancreatitis is thought to be an ischemic complication, its pathogenesis is not completely understood. Necrosis increases the morbidity and mortality risk of acute pancreatitis because of its association with organ failure and infectious complications. As such, patients with necrotizing pancreatitis may need admission to the intensive care unit, nutritional support, antibiotics, and radiologic, endoscopic, or surgical interventions.

Here, we review current evidence regarding the diagnosis and management of necrotizing pancreatitis.

PROPER TERMINOLOGY HELPS COLLABORATION

Managing necrotizing pancreatitis requires the combined efforts of internists, gastroenterologists, radiologists, and surgeons. This collaboration is aided by proper terminology.

A classification system was devised in Atlanta, GA, in 1992 to facilitate communication and interdisciplinary collaboration.³ Severe pancreatitis was differentiated from mild by the presence of organ failure or the complications of pseudocyst, necrosis, or abscess.

The original Atlanta classification had several limitations. First, the terminology for fluid collections was ambiguous and frequently misused. Second, the assessment of clinical severity required either the Ranson score or the Acute Physiology and Chronic Health Evaluation II score, both of which are complex and have other limitations. Finally, advances in imaging and treatment have rendered the original Atlanta nomenclature obsolete.

In 2012, the Acute Pancreatitis Classification Working Group issued a revised Atlanta classification that modernized the terminology pertaining to natural history, severity, imaging features, and complications. It divides the natural course of acute pancreatitis into early and late phases.⁴

Early vs late phase

In the early phase, findings on computed tomography (CT) neither correlate with clinical severity nor alter clinical management.⁶ Thus, early imaging is not indicated unless there is diagnostic uncertainty, lack of response to appropriate treatment, or sudden deterioration.

Moderate pancreatitis describes patients with pancreatic necrosis with or without transient organ failure (organ dysfunction for ≤ 48 hours).

Severe pancreatitis is defined by pancreatic necrosis and persistent organ dysfunction.⁴ It may be accompanied by pancreatic and peripancreatic fluid collections; bacteremia and sepsis can occur in association with infection of necrotic collections.

Interstitial edematous pancreatitis vs necrotizing pancreatitis

The revised Atlanta classification maintains the original classification of acute pancreatitis into 2 main categories: interstitial edematous pancreatitis and necrotizing pancreatitis.

Necrotizing pancreatitis is further divided into 3 subtypes based on extent and location of necrosis:

• Parenchymal necrosis alone (5% of cases)
• Necrosis of peripancreatic fat alone (20%)
• Necrosis of both parenchyma and peripancreatic fat (75%).

Peripancreatic involvement is commonly found in the mesentery, peripancreatic and distant retroperitoneum, and lesser sac.

Of the three subtypes, peripancreatic necrosis has the best prognosis. However, all of the subtypes of necrotizing pancreatitis are associated with poorer outcomes than interstitial edematous pancreatitis.

Fluid collections

Acute pancreatic fluid collections contain exclusively nonsolid components without an inflammatory wall and are typically found in the peripancreatic fat. These collections often resolve without intervention as the patient recovers. If they persist beyond 4 weeks and develop a nonepithelialized, fibrous wall, they become pseudocysts. Intervention is generally not recommended for pseudocysts unless they are symptomatic.

Radiographic imaging is not usually necessary to diagnose acute pancreatitis. However, it can be a valuable tool to clarify an ambiguous presentation, determine severity, and identify complications.

The timing and appropriate type of imaging are integral to obtaining useful data. Any imaging obtained in acute pancreatitis to evaluate necrosis should be performed at least 3 to 5 days from the initial symptom onset; if imaging is obtained before 72 hours, necrosis cannot be confidently excluded.⁸

COMPUTED TOMOGRAPHY

CT is the imaging test of choice when evaluating acute pancreatitis. In addition, almost all percutaneous interventions are performed with CT guidance. The Balthazar score is the most well-known CT severity index. It is calculated based on the degree of inflammation, acute fluid collections, and parenchymal necrosis.⁹ However, a modified severity index incorporates extrapancreatic complications such as ascites and vascular compromise and was found to more strongly correlate with outcomes than the standard Balthazar score.¹⁰

Contrast-enhanced CT is performed in 2 phases:

The pancreatic parenchymal phase

The pancreatic parenchymal or late arterial phase is obtained approximately 40 to 45 seconds after the start of the contrast bolus. It is used to detect necrosis in the early phase of acute pancreatitis and to assess the peripancreatic arteries for pseudoaneurysms in the late phase of acute pancreatitis.¹¹

Pancreatic necrosis appears as an area of decreased parenchymal enhancement, either well-defined or heterogeneous. The normal pancreatic parenchyma has a postcontrast enhancement pattern similar to that of the spleen. Parenchyma that does not enhance to the same degree is considered necrotic. The severity of necrosis is graded based on the percentage of the pancreas involved (< 30%, 30%–50%, or > 50%), and a higher percentage correlates with a worse outcome.^12,13

Peripancreatic necrosis is harder to detect, as there is no method to assess fat enhancement as there is with pancreatic parenchymal enhancement. In general, radiologists assume that heterogeneous peripancreatic changes, including areas of fat, fluid, and soft tissue attenuation, are consistent with peripancreatic necrosis. After 7 to 10 days, if these changes become more homogeneous and confluent with a more mass-like process, peripancreatic necrosis can be more confidently identified.^12,13

The portal venous phase

The later, portal venous phase of the scan is obtained approximately 70 seconds after the start of the contrast bolus. It is used to detect and characterize fluid collections and venous complications of the disease.

Drawbacks of CT

A drawback of CT is the need for iodinated intravenous contrast media, which in severely ill patients may precipitate or worsen pre-existing acute kidney injury.

Further, several studies have shown that findings on CT rarely alter the management of patients in the early phase of acute pancreatitis and in fact may be an overuse of medical resources.¹⁴ Unless there are confounding clinical signs or symptoms, CT should be delayed for at least 72 hours.^9,10,14,15

MAGNETIC RESONANCE IMAGING

Magnetic resonance imaging (MRI) is not a first-line imaging test in this disease because it is not as available as CT and takes longer to perform—20 to 30 minutes. The patient must be evaluated for candidacy, as it is difficult for acutely ill patients to tolerate an examination that takes this long and requires them to hold their breath multiple times.

MRI is an appropriate alternative in patients who are pregnant or who have severe iodinated-contrast allergy. While contrast is necessary to detect pancreatic necrosis with CT, MRI can detect necrosis without the need for contrast in patients with acute kidney injury or severe chronic kidney disease. Also, MRI may be better in complicated cases requiring repeated imaging because it does not expose the patient to radiation.

On MRI, pancreatic necrosis appears as a heterogeneous area, owing to its liquid and solid components. Liquid components appear hyperintense, and solid components hypointense, on T2 fluid-weighted imaging. This ability to differentiate the components of a walled-off pancreatic necrosis can be useful in determining whether a collection requires drainage or debridement. MRI is also more sensitive for hemorrhagic complications, best seen on T1 fat-weighted images.^12,16

Magnetic resonance cholangiopancreatography is an excellent method for ductal evaluation through heavily T2-weighted imaging. It is more sensitive than CT for detecting common bile duct stones and can also detect pancreatic duct strictures or extravasation into fluid collections.¹⁶

SUPPORTIVE MANAGEMENT OF EARLY NECROTIZING PANCREATITIS

In the early phase of necrotizing pancreatitis, management is supportive with the primary aim of preventing intravascular volume depletion. Aggressive fluid resuscitation in the first 48 to 72 hours, pain control, and bowel rest are the mainstays of supportive therapy. Intensive care may be necessary if organ failure and hemodynamic instability accompany necrotizing pancreatitis.

Prophylactic antibiotic and antifungal therapy to prevent infected necrosis has been controversial. Recent studies of its utility have not yielded supportive results, and the American College of Gastroenterology and the Infectious Diseases Society of America no longer recommend it.^9,17 These medications should not be given unless concomitant cholangitis or extrapancreatic infection is clinically suspected.

Early enteral nutrition is recommended in patients in whom pancreatitis is predicted to be severe and in those not expected to resume oral intake within 5 to 7 days. Enteral nutrition most commonly involves bedside or endoscopic placement of a nasojejunal feeding tube and collaboration with a nutritionist to determine protein-caloric requirements.

Compared with enteral nutrition, total parenteral nutrition is associated with higher rates of infection, multiorgan dysfunction and failure, and death.¹⁸

Necrotizing pancreatitis is a defining complication of acute pancreatitis, and its presence alone indicates greater severity. However, superimposed complications may further worsen outcomes.

Infected pancreatic necrosis

Infection occurs in approximately 20% of patients with necrotizing pancreatitis and confers a mortality rate of 20% to 50%.¹⁹ Infected pancreatic necrosis occurs when gut organisms translocate into the nearby necrotic pancreatic and peripancreatic tissue. The most commonly identified organisms include Escherichia coli and Enterococcus species.²⁰

This complication usually manifests 2 to 4 weeks after symptom onset; earlier onset is uncommon to rare. It should be considered when the systemic inflammatory response syndrome persists or recurs after 10 days to 2 weeks. Systemic inflammatory response syndrome is also common in sterile necrotizing pancreatitis and sometimes in interstitial pancreatitis, particularly during the first week. However, its sudden appearance or resurgence, high spiking fevers, or worsening organ failure in the later phase (2–4 weeks) of pancreatitis should heighten suspicion of infected pancreatic necrosis.

Imaging may also help diagnose infection, and the presence of gas within a collection or region of necrosis is highly specific. However, the presence of gas is not completely sensitive for infection, as it is seen in only 12% to 22% of infected cases.

Before minimally invasive techniques became available, the diagnosis of infected pancreatic necrosis was confirmed by percutaneous CT-guided aspiration of the necrotic mass or collection for Gram stain and culture.

Antibiotic therapy is indicated in confirmed or suspected cases of infected pancreatic necrosis. Antibiotics with gram-negative coverage and appropriate penetration such as carbapenems, metronidazole, fluoroquinolones, and selected cephalosporins are most commonly used. Meropenem is the antibiotic of choice at our institution.

CT-guided fine-needle aspiration is often done if suspected infected pancreatic necrosis fails to respond to empiric antibiotic therapy.

Debridement or drainage. Generally, the diagnosis or suspicion of infected pancreatic necrosis (suggestive signs are high fever, elevated white blood cell count, and sepsis) warrants an intervention to debride or drain infected pancreatic tissue and control sepsis.²¹

While source control is integral to the successful treatment of infected pancreatic necrosis, antibiotic therapy may provide a bridge to intervention for critically ill patients by suppressing bacteremia and subsequent sepsis. A 2013 meta-analysis found that 324 of 409 patients with suspected infected pancreatic necrosis were successfully stabilized with antibiotic treatment.^21,22 The trend toward conservative management and promising outcomes with antibiotic therapy alone or with minimally invasive techniques has lessened the need for diagnostic CT-guided fine-needle aspiration.

Hemorrhage

Spontaneous hemorrhage into pancreatic necrosis is a rare but life-threatening complication. Because CT is almost always performed with contrast enhancement, this complication is rarely identified with imaging. The diagnosis is made by noting a drop in hemoglobin and hematocrit.

Hemorrhage into the retroperitoneum or the peritoneal cavity, or both, can occur when an inflammatory process erodes into a nearby artery. Luminal gastrointestinal bleeding can occur from gastric varices arising from splenic vein thrombosis and resulting left-sided portal hypertension, or from pseudoaneurysms. These can also bleed into the pancreatic duct (hemosuccus pancreaticus). Pseudoaneurysm is a later complication that occurs when an arterial wall (most commonly the splenic or gastroduodenal artery) is weakened by pancreatic enzymes.²³

Prompt recognition of hemorrhagic events and consultation with an interventional radiologist or surgeon are required to prevent death.

Inflammation and abdominal compartment syndrome

Inflammation from necrotizing pancreatitis can cause further complications by blocking nearby structures. Reported complications include jaundice from biliary compression, hydronephrosis from ureteral compression, bowel obstruction, and gastric outlet obstruction.

Abdominal compartment syndrome is an increasingly recognized complication of acute pancreatitis. Abdominal pressure can rise due to a number of factors, including fluid collections, ascites, ileus, and overly aggressive fluid resuscitation.²⁴ Elevated abdominal pressure is associated with complications such as decreased respiratory compliance, increased peak airway pressure, decreased cardiac preload, hypotension, mesenteric and intestinal ischemia, feeding intolerance, and lower-extremity ischemia and thrombosis.

Patients with necrotizing pancreatitis who have abdominal compartment syndrome have a mortality rate 5 times higher than patients without abdominal compartment syndrome.²⁵

Abdominal pressures should be monitored using a bladder pressure sensor in critically ill or ventilated patients with acute pancreatitis. If the abdominal pressure rises above 20 mm Hg, medical and surgical interventions should be offered in a stepwise fashion to decrease it. Interventions include decompression by nasogastric and rectal tube, sedation or paralysis to relax abdominal wall tension, minimization of intravenous fluids, percutaneous drainage of ascites, and (rarely) surgical midline or subcostal laparotomy.

The treatment of necrotizing pancreatitis has changed rapidly, thanks to a growing experience with minimally invasive techniques.

Indications for intervention

Infected pancreatic necrosis is the primary indication for surgical, percutaneous, or endoscopic intervention.

In sterile necrosis, the threshold for intervention is less clear, and intervention is often reserved for patients who fail to clinically improve or who have intractable abdominal pain, gastric outlet obstruction, or fistulating disease.²⁶

In asymptomatic cases, intervention is almost never indicated regardless of the location or size of the necrotic area.

In walled-off pancreatic necrosis, less-invasive and less-morbid interventions such as endoscopic or percutaneous drainage or video-assisted retroperitoneal debridement can be done.

Timing of intervention

In the past, delaying intervention was thought to increase the risk of death. However, multiple studies have found that outcomes are often worse if intervention is done early, likely due to the lack of a fully formed fibrous wall or demarcation of the necrotic area.²⁷

If the patient remains clinically stable, it is best to delay intervention until at least 4 weeks after the index event to achieve optimal outcomes. Delay can often be achieved by antibiotic treatment to suppress bacteremia and endoscopic or percutaneous drainage of infected collections to control sepsis.

Open surgery

The gold-standard intervention for infected pancreatic necrosis or symptomatic sterile walled-off pancreatic necrosis is open necrosectomy. This involves exploratory laparotomy with blunt debridement of all visible necrotic pancreatic tissue.

Methods to facilitate later evacuation of residual infected fluid and debris vary widely. Multiple large-caliber drains can be placed to facilitate irrigation and drainage before closure of the abdominal fascia. As infected pancreatic necrosis carries the risk of contaminating the peritoneal cavity, the skin is often left open to heal by secondary intention. An interventional radiologist is frequently enlisted to place, exchange, or downsize drainage catheters.

Infected pancreatic necrosis or symptomatic sterile walled-off pancreatic necrosis often requires more than one operation to achieve satisfactory debridement.

The goals of open necrosectomy are to remove nonviable tissue and infection, preserve viable pancreatic tissue, eliminate fistulous connections, and minimize damage to local organs and vasculature.

Minimally invasive techniques

Video-assisted retroperitoneal debridement has been described as a hybrid between endoscopic and open retroperitoneal debridement.²⁸ This technique requires first placing a percutaneous catheter into the necrotic area through the left flank to create a retroperitoneal tract. A 5-cm incision is made and the necrotic space is entered using the drain for guidance. Necrotic tissue is carefully debrided under direct vision using a combination of forceps, irrigation, and suction. A laparoscopic port can also be introduced into the incision when the procedure can no longer be continued under direct vision.^29,30

Although not all patients are candidates for minimal-access surgery, it remains an evolving surgical option.

Endoscopic transmural debridement is another option for infected pancreatic necrosis and symptomatic walled-off pancreatic necrosis. Depending on the location of the necrotic area, an echoendoscope is passed to either the stomach or duodenum. Guided by endoscopic ultrasonography, a needle is passed into the collection, allowing subsequent fistula creation and stenting for internal drainage or debridement. In the past, this process required several steps, multiple devices, fluoroscopic guidance, and considerable time. But newer endoscopic lumen-apposing metal stents have been developed that can be placed in a single step without fluoroscopy. A slimmer endoscope can then be introduced into the necrotic cavity via the stent, and the necrotic debris can be debrided with endoscopic baskets, snares, forceps, and irrigation.^9,31

Similar to surgical necrosectomy, satisfactory debridement is not often obtained with a single procedure; 2 to 5 endoscopic procedures may be needed to achieve resolution. However, the luminal approach in endoscopic necrosectomy avoids the significant morbidity of major abdominal surgery and the potential for pancreaticocutaneous fistulae that may occur with drains.

In a randomized trial comparing endoscopic necrosectomy vs surgical necrosectomy (video-assisted retroperitoneal debridement and exploratory laparotomy),³² endoscopic necrosectomy showed less inflammatory response than surgical necrosectomy and had a lower risk of new-onset organ failure, bleeding, fistula formation, and death.³²

Selecting the best intervention for the individual patient

Given the multiple available techniques, selecting the best intervention for individual patients can be challenging. A team approach with input from a gastroenterologist, surgeon, and interventional radiologist is best when determining which technique would best suit each patient.

Surgical necrosectomy is still the treatment of choice for unstable patients with infected pancreatic necrosis or multiple, inaccessible collections, but current evidence suggests a different approach in stable infected pancreatic necrosis and symptomatic sterile walled-off pancreatic necrosis.

The Dutch Pancreatitis Group²⁸ randomized 88 patients with infected pancreatic necrosis or symptomatic walled-off pancreatic necrosis to open necrosectomy or a minimally invasive “step-up” approach consisting of up to 2 percutaneous drainage or endoscopic debridement procedures before escalation to video-assisted retroperitoneal debridement. The step-up approach resulted in lower rates of morbidity and death than surgical necrosectomy as first-line treatment. Furthermore, some patients in the step-up group avoided the need for surgery entirely.³⁰

Necrosis significantly increases rates of morbidity and mortality in acute pancreatitis. Hospitalists, general internists, and general surgeons are all on the front lines in identifying severe cases and consulting the appropriate specialists for optimal multidisciplinary care. Selective and appropriate timing of radiologic imaging is key, and a vital tool in the management of necrotizing pancreatitis.

While the primary indication for intervention is infected pancreatic necrosis, additional indications are symptomatic walled-off pancreatic necrosis secondary to intractable abdominal pain, bowel obstruction, and failure to thrive. As a result of improving technology and inpatient care, these patients may present with intractable symptoms in the outpatient setting rather than the inpatient setting. The onus is on the primary care physician to maintain a high level of suspicion and refer these patients to subspecialists as appropriate.

Open surgical necrosectomy remains an important approach for care of infected pancreatic necrosis or patients with intractable symptoms. A step-up approach starting with a minimally invasive procedure and escalating if the initial intervention is unsuccessful is gradually becoming the standard of care.

Study Title

The impact of a High Value Care curriculum on rate of repeat of trans-thoracic echocardiogram ordering among medical residents

Background

There is little data to confirm the impact of a High Value Care curriculum on echocardiogram ordering practices in a residency training program. We sought to evaluate the rate of performance of repeat transthoracic echocardiograms (TTE) before and after implementation of a High Vale Care curriculum.

Methods

A High Value Care curriculum was developed for the medical residents at Griffin Hospital, a community hospital, in 2015. The curriculum included a series of lectures aimed at promoting cost-conscious care while maintaining high quality. It also involved house staff in different quality improvement (QI) projects aimed at promoting high value care.

A group of residents decided to work on an initiative to reduce repeat echocardiograms. Repeat echocardiograms were defined as those performed within 6 months of a previous echocardiogram on the same patient. Only results in our EHR reflecting in-patient echocardiograms were utilized.

We retrospectively examined the rates of repeat echocardiograms performed in a 6 month period in 2014 before the High Vale Care curriculum was initiated. We assessed data from a 5 month period in 2016 to determine the rate of repeat electrocardiograms ordered at our institution.
 

Results

A total of 1,709 echocardiograms were reviewed in both time periods. Of these, 275 were considered repeat. At baseline, or before the implementation of a High Value Care curriculum, we examined 908 echocardiograms that were ordered, of which 21% were repeats.

After the implementation of a High Vale Care curriculum, 801 echocardiograms were ordered. Only 11% of these were repeats. This corresponds to a 52% reduction in the rate of repeated ordering of echocardiograms.

Discussion

The significant improvement in the rate of repeat echocardiograms was noted without any initiative directed specifically at echocardiogram ordering practices. During the planning phases of the proposed QI initiative to reduce repeat echocardiograms, house staff noted that their colleagues were already being more selective in their echocardiogram ordering practices because of the impact of the-cost conscious care lectures they had attended, as well as hospital-wide attention on the first resident-driven QI initiative that was aimed at reducing repetitive daily labs.

As part of the reducing repetitive labs QI, house staff had to provide clear rationale for why they were ordering daily labs. The received regular updates about their lab ordering practices and direct feedback if they consistently did not provide clear rationale for ordering daily labs.

Conclusion

Our study clearly showed a greater than 50% reduction in the ordering of repeat echocardiograms because of a High Value Care curriculum in our residency training program.

The improvement was brought on by increased awareness by house staff regarding provision of high quality care while being cognizant of the costs involved. The reduction in repeat echocardiograms resulted in more efficient use of a limited hospital resource.

Dr. Arole is chief of hospital medicine at Griffin Hospital, Derby, Conn. Dr. Zyed is in the department of internal medicine at Griffin Hospital. Dr. Njike is with the Yale University Prevention Research Center at Griffin Hospital.

Study Title

The impact of a High Value Care curriculum on rate of repeat of trans-thoracic echocardiogram ordering among medical residents

Background

There is little data to confirm the impact of a High Value Care curriculum on echocardiogram ordering practices in a residency training program. We sought to evaluate the rate of performance of repeat transthoracic echocardiograms (TTE) before and after implementation of a High Vale Care curriculum.

Methods

A High Value Care curriculum was developed for the medical residents at Griffin Hospital, a community hospital, in 2015. The curriculum included a series of lectures aimed at promoting cost-conscious care while maintaining high quality. It also involved house staff in different quality improvement (QI) projects aimed at promoting high value care.

A group of residents decided to work on an initiative to reduce repeat echocardiograms. Repeat echocardiograms were defined as those performed within 6 months of a previous echocardiogram on the same patient. Only results in our EHR reflecting in-patient echocardiograms were utilized.

We retrospectively examined the rates of repeat echocardiograms performed in a 6 month period in 2014 before the High Vale Care curriculum was initiated. We assessed data from a 5 month period in 2016 to determine the rate of repeat electrocardiograms ordered at our institution.
 

Results

A total of 1,709 echocardiograms were reviewed in both time periods. Of these, 275 were considered repeat. At baseline, or before the implementation of a High Value Care curriculum, we examined 908 echocardiograms that were ordered, of which 21% were repeats.

After the implementation of a High Vale Care curriculum, 801 echocardiograms were ordered. Only 11% of these were repeats. This corresponds to a 52% reduction in the rate of repeated ordering of echocardiograms.

Discussion

The significant improvement in the rate of repeat echocardiograms was noted without any initiative directed specifically at echocardiogram ordering practices. During the planning phases of the proposed QI initiative to reduce repeat echocardiograms, house staff noted that their colleagues were already being more selective in their echocardiogram ordering practices because of the impact of the-cost conscious care lectures they had attended, as well as hospital-wide attention on the first resident-driven QI initiative that was aimed at reducing repetitive daily labs.

As part of the reducing repetitive labs QI, house staff had to provide clear rationale for why they were ordering daily labs. The received regular updates about their lab ordering practices and direct feedback if they consistently did not provide clear rationale for ordering daily labs.

Conclusion

Our study clearly showed a greater than 50% reduction in the ordering of repeat echocardiograms because of a High Value Care curriculum in our residency training program.

The improvement was brought on by increased awareness by house staff regarding provision of high quality care while being cognizant of the costs involved. The reduction in repeat echocardiograms resulted in more efficient use of a limited hospital resource.

Dr. Arole is chief of hospital medicine at Griffin Hospital, Derby, Conn. Dr. Zyed is in the department of internal medicine at Griffin Hospital. Dr. Njike is with the Yale University Prevention Research Center at Griffin Hospital.

Study Title

The impact of a High Value Care curriculum on rate of repeat of trans-thoracic echocardiogram ordering among medical residents

Background

There is little data to confirm the impact of a High Value Care curriculum on echocardiogram ordering practices in a residency training program. We sought to evaluate the rate of performance of repeat transthoracic echocardiograms (TTE) before and after implementation of a High Vale Care curriculum.

Methods

A High Value Care curriculum was developed for the medical residents at Griffin Hospital, a community hospital, in 2015. The curriculum included a series of lectures aimed at promoting cost-conscious care while maintaining high quality. It also involved house staff in different quality improvement (QI) projects aimed at promoting high value care.

A group of residents decided to work on an initiative to reduce repeat echocardiograms. Repeat echocardiograms were defined as those performed within 6 months of a previous echocardiogram on the same patient. Only results in our EHR reflecting in-patient echocardiograms were utilized.

We retrospectively examined the rates of repeat echocardiograms performed in a 6 month period in 2014 before the High Vale Care curriculum was initiated. We assessed data from a 5 month period in 2016 to determine the rate of repeat electrocardiograms ordered at our institution.
 

Results

A total of 1,709 echocardiograms were reviewed in both time periods. Of these, 275 were considered repeat. At baseline, or before the implementation of a High Value Care curriculum, we examined 908 echocardiograms that were ordered, of which 21% were repeats.

After the implementation of a High Vale Care curriculum, 801 echocardiograms were ordered. Only 11% of these were repeats. This corresponds to a 52% reduction in the rate of repeated ordering of echocardiograms.

Discussion

The significant improvement in the rate of repeat echocardiograms was noted without any initiative directed specifically at echocardiogram ordering practices. During the planning phases of the proposed QI initiative to reduce repeat echocardiograms, house staff noted that their colleagues were already being more selective in their echocardiogram ordering practices because of the impact of the-cost conscious care lectures they had attended, as well as hospital-wide attention on the first resident-driven QI initiative that was aimed at reducing repetitive daily labs.

As part of the reducing repetitive labs QI, house staff had to provide clear rationale for why they were ordering daily labs. The received regular updates about their lab ordering practices and direct feedback if they consistently did not provide clear rationale for ordering daily labs.

Conclusion

Our study clearly showed a greater than 50% reduction in the ordering of repeat echocardiograms because of a High Value Care curriculum in our residency training program.

The improvement was brought on by increased awareness by house staff regarding provision of high quality care while being cognizant of the costs involved. The reduction in repeat echocardiograms resulted in more efficient use of a limited hospital resource.

Dr. Arole is chief of hospital medicine at Griffin Hospital, Derby, Conn. Dr. Zyed is in the department of internal medicine at Griffin Hospital. Dr. Njike is with the Yale University Prevention Research Center at Griffin Hospital.