CASE REPORT cardiac tamponade; hernia, traumatic diaphragmatic
Delayed Traumatic Intrapericardial Diaphragmatic Hernia Associated With Cardiac Tamponade We describe a case of delayed presentation of traumatic intrapericardial diaphragmatic hernia associated with cardiac tamponade. A 71-year-old woman presented to our emergency department complaining of epigastric and midabdominal pain one month after hospitalization for multiple injuries suffered in an automobile accident. Chest radiograph showed a diaphragmatic hernia. In the ED, the patient became hypotensive and tachycardic with elevated central venous pressure. A t surgery, she was found to have o m e n t u m and transverse colon herniated into the pericardial sac causing cardiac tamponade. The defect was repaired, and her postoperative course was uncomplicated. Cardiac tamponade should be included in the differential diagnosis of hypotension in patients with radiographic evidence of diaphragmatic hernia. [Girzadas D V Jr, Fligner DJ: Delayed traumatic intrapericardial diaphragmatic hernia associated with cardiac tamponade. Ann Emerg Med November 1991;20:1246-I247.]
INTRODUCTION Patients with delayed diaphragmatic hernias often present with pain, respiratory complaints, or gastrointestinal symptoms. 1 Rarely does the clinical picture include hypotension.2, 3 Reported causes of hemodynamic instability resulting from delayed diaphragmatic hernia include tension pneumothorax, tension viscerothorax, bowel strangulation, or perforation with secondary sepsis and hypovolemiaA,4,s With our case report, we add cardiac tamponade secondary to intrapericardial diaphragmatic hernia (IDH) to the differential diagnosis.
Daniel V Girzadas, Jr, MD Denise J Fligner, MD, FACEP Oak Lawn, Illinois From the Emergency Medicine Residency Program and the Department of Emergency Medicine, Christ Hospital and Medical Center, Oak Lawn, Illinois. Received for publication November 26, 1990. Revision received May 13, 1991. Accepted for publication June 20, 1991. Address for reprints: Patricia Deacetis, Department of Emergency Medicine, Christ Hospital and Medical Center, 4440 West 95th Street, ©ak Lawn, Illinois 6O465.
CASE REPORT A 71-year-old woman presented to our ED with a complaint of severe midabdominal and epigastric pain that began suddenly 30 minutes after she had eaten dinner. She characterized the, pain as a constant ache radiating to the back that improved with sitting. The pain was accompanied by nausea but not emesis. She had experienced mild diarrhea for the previous four days but otherwise had felt well. She denied chest pain, diaphoresis, and shortness of breath. The patient had been hospitalized at our institution four weeks earlier for acute injuries sustained in an automobile accident. At that time, she had been treated for a pubic ramus fracture, multiple rib fractures, and pulmonary contusion; her therapy included endotracheal intubation and assisted ventilation. She had been asymptomatic at the time of discharge. She had no other significant medical history, was receiving no medications, and had no drug allergies. Physical examination revealed an obese woman who was pale and mildly dyspneic. The patient was alert but appeared uncomfortable and frequently moved about on the cart. Vital signs were blood pressure of 150/68 mm Hg; pulse, 132; respirations, 24; and temperature, 36.8 C. There were no significant orthostatic changes in pulse or blood pressure. Cardiopulmonary examination was normal, although the neck veins could not be assessed secondary to adiposity. The abdomen was obese, without scars, soft, and nontender; bowel sounds were high pitched. There was no palpable organomegaly and no masses. The aorta was not palpable. Rectal examination was normal except for trace occult blood in the stool.
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Annals of Emergency Medicine
20:11 November 1991
HERNIA Girzada & Fligner
An arterial blood gas drawn during the initial examination showed pH 7.49; Pco2, 27 m m Hg; Po2, 79 m m Hg; HCO3, 21 mmol/L; base excess, - 1 mmol/L; and oxygen saturation, 96% on room air. An ECG was interpreted as sinus tachycardia at 117 beats per minute with lateral nondiagnostic ST depression. A peripheral IV line was started, and the patient was sent for chest and abdominal radiographs. On returning from the radiology suite, she was profusely diaphoretic. She appeared to be in more distress and complained of increased epigastric pain. Systolic blood pressure was 112 m m Hg by Doppler, and pulse was 128. A second peripheral IV line was started, and a 300-mL bolus of normal saline was infused. Oxygen was given by nasal cannula, and a nasogastric tube was placed. Gastroccult testing of nasogastric aspirate was negative. After the initial fluid challenge, blood pressure dropped to 80 m m Hg systolic. Both IV line sites were increased to the maximal flow rate. The chest and abdominal examinations remained unchanged despite worsening symptoms. The chest radiograph showed an air-filled mass over the heart shadow that had not been present on chest radiographs from the previous hospitalization. A portable ultrasound of the abdomen at this time showed no evidence of abdominal aortic aneurysm. Laboratory results revealed hemoglobin of 14.8 g/dL; WBC count of 12.9/mm 3 with 81% neutrophils; and creatine kinase of 21 units/L. Electrolytes, blood urea nitrogen, creatinine, amylase, and coagulation studies were otherwise within normal limits. Urinalysis was remarkable for 20 RBCs per high-power field. A repeat arterial blood gas showed an increasing metabolic acidosis: pH 7.4; Pco2, 26 m m Hg; Po2, 161 m m Hg; HCO3, 16 m m o l / L ; and base excess, - 7 mmol/L. Surgical consultation was obtained for a presumptive diagnosis of diap h r a g m a t i c h e r n i a w i t h probable bowel strangulation. Myocardial is-
20:11 November 1991
chemia was again considered, and the patient was given sublingual nitroglycerin with no relief of her pain; a repeat ECG was unchanged. After receiving 2,000 mL of normal saline over 20 minutes, the patient's diaphoresis, dyspnea, and pain continued to worsen even as her blood pressure increased to 90/70 m m Hg and her pulse decreased to 110. A central venous catheter was introduced; central venous pressure measured 27 m m H20. Despite physician uncertainty regarding the patient's hemodynamic instability, she was taken to the operating room for emergency reduction of the h e r n i a t e d bowel and repair of the diaphragmatic rupture. Intraoperatively, not only was the diaphragm torn but the pericardium had a defect as well. Omentum and transverse colon had herniated into the pericardial space and were causing cardiac tamponade. Only minor necrosis of the omentum was present; the transverse colon remained viable. After reduction of the bowel, the patient's h e m o d y n a m i c status improved. The pericardium and diaphragm were repaired, and the patient recovered w i t h o u t complications. DISCUSSION There is an approximately 5% to 8% incidence rate of diaphragmatic tears in patients undergoing emergency surgery for blunt and penetrating trauma J, 6 The majority of tears are l o c a t e d in the left h e m i d i a phragm, whereas the pericardial portion of the diaphragm, which is often referred to as the central tendon of the diaphragm, is only rarely injured. In a review of 324 diaphragmatic injuries from six series between 1976 and 1987, seven injuries were noted to extend into the central tendon from a n o t h e r d i a p h r a g m a t i c site, whereas only two ruptures were located exclusively in the pericardial portion of the diaphragm.I, 7 Pericardial diaphragmatic injuries may result acutely in herniation of the heart into the abdominal cavity or more often later herniation of abdominal vis-
Annals of Emergency Medicine
cera into the pericardial sac. 8 Pericardial diaphragmatic injuries may be classified according to the time elapsed between injury and recognition. Acute injuries are most often recognized as incidental findings at surgery for other injuries. If undiagnosed during this period, a latent period ensues during which the patient may be only mildly symptomatic. An acute complication, usually visceral strangulation or obstruction, ends the latent period and brings the patient to medical attention. 9 Our case is unique because of the delay between injury and presentation. In our review of the literature, we found no previous reports of delayed IDH associated with hemodynamically significant cardiac tamponade. SUMMARY The case of a patient with delayed presentation of traumatic IDH associated with hemodynamically significant cardiac tamponade is described. Chest radiography was crucial to making the diagnosis and differentiating this condition from other complications of delayed diaphragmatic hernias. The clinical presentation of IDH with h e m o d y n a m i c instability should suggest cardiac tamponade and requires emergency operative intervention for reduction of the hernia and repair of the injury. REFERENCES 1. Laws HL, Hawkins ML: Diaphragmatic injury. Adv Trauma 1987;2:207-228. 2. Saber WL, Moore EE, Hopeman AR, et aI: Delayed presentation of traumatic diaphragmatic hernia. J Emerg Med 1986;4:i-7. 3. Bematz PE, Burnside AF Jr, Clagett OT: Problem of the ruptured diaphragm. JAMA 1958;168:8774881. 4. Skinner EF, Cart D, Duncan JT, et al: Strangulated diaphragmatic hernia. J Thorac Surg 1958;36:102q11. 5. Kanowitz A, Marx JA: Delayed traumatic diaphragmatic hernia simulating acute tension pneumothorax. J Emerg Med 1989;7:619-622. 6. Waldschmidt ML, Laws HL: Injuries of the diaphragm. J Trauma 1980~20:587-592. 7. Rodriguez-Morales G, Rodriguez A, Shatney CH: Acute rupture of the diaphragm in blunt trauma: Analysis of 60 patients. J Trauma 1986~26:438-444. 8. Clark DE, Wiles CS, Lira MK, et al: Traumatic rup ~ ture of the pericardium. Surgery 1983;93:495-503. 9. Grimes OF: Traumatic injuries of the diaphragm: Diaphragmatic hernia. Am J Surg 1974;128:175-181.
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Delayed Traumatic Intrapericardial Diaphragmatic Hernia Associated With Cardiac Tamponade We describe a case of delayed presentation of traumatic intrapericardial diaphragmatic hernia associated with cardiac tamponade. A 71-year-old woman presented to our emergency department complaining of epigastric and midabdominal pain one month after hospitalization for multiple injuries suffered in an automobile accident. Chest radiograph showed a diaphragmatic hernia. In the ED, the patient became hypotensive and tachycardic with elevated central venous pressure. A t surgery, she was found to have o m e n t u m and transverse colon herniated into the pericardial sac causing cardiac tamponade. The defect was repaired, and her postoperative course was uncomplicated. Cardiac tamponade should be included in the differential diagnosis of hypotension in patients with radiographic evidence of diaphragmatic hernia. [Girzadas D V Jr, Fligner DJ: Delayed traumatic intrapericardial diaphragmatic hernia associated with cardiac tamponade. Ann Emerg Med November 1991;20:1246-I247.]
INTRODUCTION Patients with delayed diaphragmatic hernias often present with pain, respiratory complaints, or gastrointestinal symptoms. 1 Rarely does the clinical picture include hypotension.2, 3 Reported causes of hemodynamic instability resulting from delayed diaphragmatic hernia include tension pneumothorax, tension viscerothorax, bowel strangulation, or perforation with secondary sepsis and hypovolemiaA,4,s With our case report, we add cardiac tamponade secondary to intrapericardial diaphragmatic hernia (IDH) to the differential diagnosis.
Daniel V Girzadas, Jr, MD Denise J Fligner, MD, FACEP Oak Lawn, Illinois From the Emergency Medicine Residency Program and the Department of Emergency Medicine, Christ Hospital and Medical Center, Oak Lawn, Illinois. Received for publication November 26, 1990. Revision received May 13, 1991. Accepted for publication June 20, 1991. Address for reprints: Patricia Deacetis, Department of Emergency Medicine, Christ Hospital and Medical Center, 4440 West 95th Street, ©ak Lawn, Illinois 6O465.
CASE REPORT A 71-year-old woman presented to our ED with a complaint of severe midabdominal and epigastric pain that began suddenly 30 minutes after she had eaten dinner. She characterized the, pain as a constant ache radiating to the back that improved with sitting. The pain was accompanied by nausea but not emesis. She had experienced mild diarrhea for the previous four days but otherwise had felt well. She denied chest pain, diaphoresis, and shortness of breath. The patient had been hospitalized at our institution four weeks earlier for acute injuries sustained in an automobile accident. At that time, she had been treated for a pubic ramus fracture, multiple rib fractures, and pulmonary contusion; her therapy included endotracheal intubation and assisted ventilation. She had been asymptomatic at the time of discharge. She had no other significant medical history, was receiving no medications, and had no drug allergies. Physical examination revealed an obese woman who was pale and mildly dyspneic. The patient was alert but appeared uncomfortable and frequently moved about on the cart. Vital signs were blood pressure of 150/68 mm Hg; pulse, 132; respirations, 24; and temperature, 36.8 C. There were no significant orthostatic changes in pulse or blood pressure. Cardiopulmonary examination was normal, although the neck veins could not be assessed secondary to adiposity. The abdomen was obese, without scars, soft, and nontender; bowel sounds were high pitched. There was no palpable organomegaly and no masses. The aorta was not palpable. Rectal examination was normal except for trace occult blood in the stool.
106/1246
Annals of Emergency Medicine
20:11 November 1991
HERNIA Girzada & Fligner
An arterial blood gas drawn during the initial examination showed pH 7.49; Pco2, 27 m m Hg; Po2, 79 m m Hg; HCO3, 21 mmol/L; base excess, - 1 mmol/L; and oxygen saturation, 96% on room air. An ECG was interpreted as sinus tachycardia at 117 beats per minute with lateral nondiagnostic ST depression. A peripheral IV line was started, and the patient was sent for chest and abdominal radiographs. On returning from the radiology suite, she was profusely diaphoretic. She appeared to be in more distress and complained of increased epigastric pain. Systolic blood pressure was 112 m m Hg by Doppler, and pulse was 128. A second peripheral IV line was started, and a 300-mL bolus of normal saline was infused. Oxygen was given by nasal cannula, and a nasogastric tube was placed. Gastroccult testing of nasogastric aspirate was negative. After the initial fluid challenge, blood pressure dropped to 80 m m Hg systolic. Both IV line sites were increased to the maximal flow rate. The chest and abdominal examinations remained unchanged despite worsening symptoms. The chest radiograph showed an air-filled mass over the heart shadow that had not been present on chest radiographs from the previous hospitalization. A portable ultrasound of the abdomen at this time showed no evidence of abdominal aortic aneurysm. Laboratory results revealed hemoglobin of 14.8 g/dL; WBC count of 12.9/mm 3 with 81% neutrophils; and creatine kinase of 21 units/L. Electrolytes, blood urea nitrogen, creatinine, amylase, and coagulation studies were otherwise within normal limits. Urinalysis was remarkable for 20 RBCs per high-power field. A repeat arterial blood gas showed an increasing metabolic acidosis: pH 7.4; Pco2, 26 m m Hg; Po2, 161 m m Hg; HCO3, 16 m m o l / L ; and base excess, - 7 mmol/L. Surgical consultation was obtained for a presumptive diagnosis of diap h r a g m a t i c h e r n i a w i t h probable bowel strangulation. Myocardial is-
20:11 November 1991
chemia was again considered, and the patient was given sublingual nitroglycerin with no relief of her pain; a repeat ECG was unchanged. After receiving 2,000 mL of normal saline over 20 minutes, the patient's diaphoresis, dyspnea, and pain continued to worsen even as her blood pressure increased to 90/70 m m Hg and her pulse decreased to 110. A central venous catheter was introduced; central venous pressure measured 27 m m H20. Despite physician uncertainty regarding the patient's hemodynamic instability, she was taken to the operating room for emergency reduction of the h e r n i a t e d bowel and repair of the diaphragmatic rupture. Intraoperatively, not only was the diaphragm torn but the pericardium had a defect as well. Omentum and transverse colon had herniated into the pericardial space and were causing cardiac tamponade. Only minor necrosis of the omentum was present; the transverse colon remained viable. After reduction of the bowel, the patient's h e m o d y n a m i c status improved. The pericardium and diaphragm were repaired, and the patient recovered w i t h o u t complications. DISCUSSION There is an approximately 5% to 8% incidence rate of diaphragmatic tears in patients undergoing emergency surgery for blunt and penetrating trauma J, 6 The majority of tears are l o c a t e d in the left h e m i d i a phragm, whereas the pericardial portion of the diaphragm, which is often referred to as the central tendon of the diaphragm, is only rarely injured. In a review of 324 diaphragmatic injuries from six series between 1976 and 1987, seven injuries were noted to extend into the central tendon from a n o t h e r d i a p h r a g m a t i c site, whereas only two ruptures were located exclusively in the pericardial portion of the diaphragm.I, 7 Pericardial diaphragmatic injuries may result acutely in herniation of the heart into the abdominal cavity or more often later herniation of abdominal vis-
Annals of Emergency Medicine
cera into the pericardial sac. 8 Pericardial diaphragmatic injuries may be classified according to the time elapsed between injury and recognition. Acute injuries are most often recognized as incidental findings at surgery for other injuries. If undiagnosed during this period, a latent period ensues during which the patient may be only mildly symptomatic. An acute complication, usually visceral strangulation or obstruction, ends the latent period and brings the patient to medical attention. 9 Our case is unique because of the delay between injury and presentation. In our review of the literature, we found no previous reports of delayed IDH associated with hemodynamically significant cardiac tamponade. SUMMARY The case of a patient with delayed presentation of traumatic IDH associated with hemodynamically significant cardiac tamponade is described. Chest radiography was crucial to making the diagnosis and differentiating this condition from other complications of delayed diaphragmatic hernias. The clinical presentation of IDH with h e m o d y n a m i c instability should suggest cardiac tamponade and requires emergency operative intervention for reduction of the hernia and repair of the injury. REFERENCES 1. Laws HL, Hawkins ML: Diaphragmatic injury. Adv Trauma 1987;2:207-228. 2. Saber WL, Moore EE, Hopeman AR, et aI: Delayed presentation of traumatic diaphragmatic hernia. J Emerg Med 1986;4:i-7. 3. Bematz PE, Burnside AF Jr, Clagett OT: Problem of the ruptured diaphragm. JAMA 1958;168:8774881. 4. Skinner EF, Cart D, Duncan JT, et al: Strangulated diaphragmatic hernia. J Thorac Surg 1958;36:102q11. 5. Kanowitz A, Marx JA: Delayed traumatic diaphragmatic hernia simulating acute tension pneumothorax. J Emerg Med 1989;7:619-622. 6. Waldschmidt ML, Laws HL: Injuries of the diaphragm. J Trauma 1980~20:587-592. 7. Rodriguez-Morales G, Rodriguez A, Shatney CH: Acute rupture of the diaphragm in blunt trauma: Analysis of 60 patients. J Trauma 1986~26:438-444. 8. Clark DE, Wiles CS, Lira MK, et al: Traumatic rup ~ ture of the pericardium. Surgery 1983;93:495-503. 9. Grimes OF: Traumatic injuries of the diaphragm: Diaphragmatic hernia. Am J Surg 1974;128:175-181.
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