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A Patient with Anaplasmosis and Subsequent Spontaneous Splenic Rupture
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A5300 - A Patient with Anaplasmosis and Subsequent Spontaneous Splenic Rupture
Author Block: A. S. Ray1, H. C. Cain2; 1Yale University School of Medicine, New Haven, CT, United States, 2VA Connecticut Healthcare System, West Haven, CT, United States.
Introduction: Human Granulocytic Anaplasmosis (HGA) is a tick-borne human pathogen primarily found in the Northeastern and Midwestern United States with increasing incidence in recent years. Fever, constitutional symptoms, leukopenia, and thrombocytopenia are common findings. Splenic involvement has not been reported before with HGA, though it has been reported with Babesia infection before.
Case: A 68 year-old White female with a complex past medical history presented to the emergency department (ED) with 1 week of fevers, malaise, and fatigue. She was admitted, found to be orthostatic and had an acute kidney injury (AKI). She was given intravenous (IV) fluids and an initial infectious work-up revealed no pathogens. She was discharged after 2 days. Her fevers persisted and she had worsening abdominal pain, fatigue, dysuria, nausea and returned to the ED after 5 days. Her initial laboratory studies found to have an AKI and hypokalemia. Initial blood, urine, and sputum cultures were nondiagnostic. She developed worsening abdominal pain on hospital day 3 and had a CT chest, abdomen, pelvis with abnormalities of a splenic infarct and colitis. Subsequently, she was placed on IV ceftriaxone, metronidazole for colitis and doxycycline over concern for tick-borne illnesses. Her anaplasma smear returned positive on hospital day 4. On the night of hospital day 4, she developed progressive hypotensive unresponsive to large volume intravenous crystalloid replacement and was start on vasopressor agents which rapidly escalated in dose. Initial laboratory studies revealed a lactic acidosis, stable hemoglobin of 10 g/dl and an elevated d-dimer. In this context, bedside echocardiogram revealed new RV enlargement as compared to before. Given her persistent shock and possibility of pulmonary embolism, she was given empiric IV TPA. Laboratory testing after 3 hours revealed a hemoglobin of 7 g/dl. Packed RBCs were ordered, however the patient quickly expired. Autopsy revealed splenic rupture and hemoperitoneum.
Discussion: There are no reports of either splenic infarct or rupture associated with HGA. Given her clinical course, it is likely that her splenic rupture preceded thrombolysis. Her RV enlargement is likely attributable to large volume fluid resuscitation in a patient with a history of congestive heart failure. There was no history of trauma and she received no other medications associated with splenic rupture. This case demonstrates that splenic pathology is a possible sequelae of HGA.
Author Block: A. S. Ray1, H. C. Cain2; 1Yale University School of Medicine, New Haven, CT, United States, 2VA Connecticut Healthcare System, West Haven, CT, United States.
Introduction: Human Granulocytic Anaplasmosis (HGA) is a tick-borne human pathogen primarily found in the Northeastern and Midwestern United States with increasing incidence in recent years. Fever, constitutional symptoms, leukopenia, and thrombocytopenia are common findings. Splenic involvement has not been reported before with HGA, though it has been reported with Babesia infection before.
Case: A 68 year-old White female with a complex past medical history presented to the emergency department (ED) with 1 week of fevers, malaise, and fatigue. She was admitted, found to be orthostatic and had an acute kidney injury (AKI). She was given intravenous (IV) fluids and an initial infectious work-up revealed no pathogens. She was discharged after 2 days. Her fevers persisted and she had worsening abdominal pain, fatigue, dysuria, nausea and returned to the ED after 5 days. Her initial laboratory studies found to have an AKI and hypokalemia. Initial blood, urine, and sputum cultures were nondiagnostic. She developed worsening abdominal pain on hospital day 3 and had a CT chest, abdomen, pelvis with abnormalities of a splenic infarct and colitis. Subsequently, she was placed on IV ceftriaxone, metronidazole for colitis and doxycycline over concern for tick-borne illnesses. Her anaplasma smear returned positive on hospital day 4. On the night of hospital day 4, she developed progressive hypotensive unresponsive to large volume intravenous crystalloid replacement and was start on vasopressor agents which rapidly escalated in dose. Initial laboratory studies revealed a lactic acidosis, stable hemoglobin of 10 g/dl and an elevated d-dimer. In this context, bedside echocardiogram revealed new RV enlargement as compared to before. Given her persistent shock and possibility of pulmonary embolism, she was given empiric IV TPA. Laboratory testing after 3 hours revealed a hemoglobin of 7 g/dl. Packed RBCs were ordered, however the patient quickly expired. Autopsy revealed splenic rupture and hemoperitoneum.
Discussion: There are no reports of either splenic infarct or rupture associated with HGA. Given her clinical course, it is likely that her splenic rupture preceded thrombolysis. Her RV enlargement is likely attributable to large volume fluid resuscitation in a patient with a history of congestive heart failure. There was no history of trauma and she received no other medications associated with splenic rupture. This case demonstrates that splenic pathology is a possible sequelae of HGA.
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