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Rectifying Inconsistent Data: A Case Report of Cardiac Tamponade
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A3518 - Rectifying Inconsistent Data: A Case Report of Cardiac Tamponade
Author Block: B. Aldrich1, P. Martin2; 1Bingham Memorial Hospital, Blackfoot, ID, United States, 2CCM, Portneuf Medical Center, Pocatello, ID, United States.
INTRODUCTION:
Patients are often admitted with incomplete or incorrect data. When data is inconsistent with received diagnoses, it is imperative that the clinician reconcile the inconsistencies. Failure to do so can result in significant morbidity and mortality.
DESCRIPTION:
44-year-old male with a history of traumatic brain injury four years prior. He is bedridden, aphasic and cared for by his family at home.
During the preceding week family noted dark urine with decreased output and received a prescription for antibiotics. Family brought him into the ED after his oxygen saturation dropped below normal. Initial vitals: Afebrile, 128/98, HR 84, RR 16. Physical exam: non-cachectic male, distended abdomen and Stage II sacral decubitus ulcers.
CXR showed ill-defined multi-lobar opacities and widened mediastinum. Significant labs: sodium 112, chloride 67, BUN 174, hemoglobin 5.6 and WBC 10.9. Family denied melena, hematochezia, hematemesis, jaundice, vomiting or diarrhea. He had not lost weight nor had his feeding regimen changed.
He rapidly developed shock physiology, excluding tachycardia. He was given a PRBC transfusion, aggressive volume resuscitation, broad-spectrum antibiotics, and hydrocortisone. When that failed to improve his blood pressure, he was initiated on norepinephrine. Unfortunately, his blood pressure remained low and his pulse normal.
Bladder scan revealed a distended bladder and a urethral stricture was identified and treated with dilation and a coudé catheter. Bladder decompression still did not alleviate the shock. His pressor requirement increased, but was still associated with a normal heart rate.
Pursuing the widened mediastinum, echocardiogram was performed. It revealed a pericardial effusion, with compression of the right atria and bilateral ventricles. Emergent pericardiocentesis was performed and approximately 700 ml blood was drained. Patient's pressor requirement decreased but did not disappear. Pulse remained normal.
Over the next 48 hours, the patient’s shock resolved. He was discharged home one week later.
DISCUSSION:
Identifying the source of the patient’s shock was challenging. Labs and history pointed to hypovolemia. Labs and exam suggested obstructive uropathy. His history and vital signs warranted antibiotics, even if he didn’t have a leukocytosis or tachycardia. His newly widened mediastinum warranted TTE, but in the absence of tachycardia, clinical suspicion for tamponade was low.
The foregoing case evinces the complexity of ICU medicine and the importance of pursuing explanations for all abnormalities. This patient had hypovolemic/hemorrhagic shock, septic shock with acute adrenal insufficiency, and obstructive shock. All complicated by the patient’s dysautonomia which prevented tachycardia, and thus, effectively caused cardiogenic shock.
.
Author Block: B. Aldrich1, P. Martin2; 1Bingham Memorial Hospital, Blackfoot, ID, United States, 2CCM, Portneuf Medical Center, Pocatello, ID, United States.
INTRODUCTION:
Patients are often admitted with incomplete or incorrect data. When data is inconsistent with received diagnoses, it is imperative that the clinician reconcile the inconsistencies. Failure to do so can result in significant morbidity and mortality.
DESCRIPTION:
44-year-old male with a history of traumatic brain injury four years prior. He is bedridden, aphasic and cared for by his family at home.
During the preceding week family noted dark urine with decreased output and received a prescription for antibiotics. Family brought him into the ED after his oxygen saturation dropped below normal. Initial vitals: Afebrile, 128/98, HR 84, RR 16. Physical exam: non-cachectic male, distended abdomen and Stage II sacral decubitus ulcers.
CXR showed ill-defined multi-lobar opacities and widened mediastinum. Significant labs: sodium 112, chloride 67, BUN 174, hemoglobin 5.6 and WBC 10.9. Family denied melena, hematochezia, hematemesis, jaundice, vomiting or diarrhea. He had not lost weight nor had his feeding regimen changed.
He rapidly developed shock physiology, excluding tachycardia. He was given a PRBC transfusion, aggressive volume resuscitation, broad-spectrum antibiotics, and hydrocortisone. When that failed to improve his blood pressure, he was initiated on norepinephrine. Unfortunately, his blood pressure remained low and his pulse normal.
Bladder scan revealed a distended bladder and a urethral stricture was identified and treated with dilation and a coudé catheter. Bladder decompression still did not alleviate the shock. His pressor requirement increased, but was still associated with a normal heart rate.
Pursuing the widened mediastinum, echocardiogram was performed. It revealed a pericardial effusion, with compression of the right atria and bilateral ventricles. Emergent pericardiocentesis was performed and approximately 700 ml blood was drained. Patient's pressor requirement decreased but did not disappear. Pulse remained normal.
Over the next 48 hours, the patient’s shock resolved. He was discharged home one week later.
DISCUSSION:
Identifying the source of the patient’s shock was challenging. Labs and history pointed to hypovolemia. Labs and exam suggested obstructive uropathy. His history and vital signs warranted antibiotics, even if he didn’t have a leukocytosis or tachycardia. His newly widened mediastinum warranted TTE, but in the absence of tachycardia, clinical suspicion for tamponade was low.
The foregoing case evinces the complexity of ICU medicine and the importance of pursuing explanations for all abnormalities. This patient had hypovolemic/hemorrhagic shock, septic shock with acute adrenal insufficiency, and obstructive shock. All complicated by the patient’s dysautonomia which prevented tachycardia, and thus, effectively caused cardiogenic shock.
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