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TMP/SMX-induced severe thrombocytopenia [Meeting Abstract]

Jacobs, R; Toklu, B
LEARNING OBJECTIVE 1: Recognize that TMP/SMX can induce a severe, potentially life-threatening, isolated thrombocytopenia. CASE: A 50-year-old healthy female without significant medical history presented with a day history of non-pruritic red rash on her torso. The patient was in her usual state of good health until three days prior to admission when she starting trimethoprim/sulfamethoxazole (TMP/SMX) for a possible dental infection. Except TMP/SMX, she was not taking any other prescribed or over the counter medication. Two days after starting taking TMP/SMX, she noticed the rash and presented to the hospital. On initial physical examination, the patient noted to have scattered nonblanching red petechial rash over her torso extending down to the bilateral lower extremities. The rest of her physical exam and review of systems were unremarkable. Her initial complete blood count (CBC) revealed an isolated thrombocytopenia with a platelet count of 4.000/mm3. The rest of her blood work including chemistry, coagulation, liver function and hemolysis panels were all within normal range. A subsequent peripheral smear confirmed thrombocytopenia with large platelets, but otherwise was normal. Bactrim was held off as a possible causative agent, and the patient was being evaluated for possible idiopathic thrombocytopenic purpura (ITP). Patient's platelet count responded poorly to the first unit of single donor platelets (SDP) transfusion, while a second unit of SDP tranfusion led to appropriate increase in platelet count. Within 36 hours of her hospital stay, the platelet count recovered to a normal range without any further transfusion requirement or glucocorticoids for initially presumed ITP. This led to a diagnosis of TMP/SMX-induced severe thrombocytopenia. Her presenting petechial rash also gradually resolved over hospital course. Patient was discharged on hospital day 3 with a platelet count of 202.000/ mm3. A week after discharge, her repeat platelet count was 425.000/mm3. DISCUSSION: Based on the N!
EMBASE:71297393
ISSN: 0884-8734
CID: 783142

Lemierre's syndrome: Recalling the "forgotten disease" [Meeting Abstract]

Jacobs, R; Toklu, B
LEARNING OBJECTIVE 1: Distinguish clinical clues to assess for Lemierre's Syndrome. LEARNING OBJECTIVE 2: Manage Lemierre's Syndrome when appropriate anaerobic antibiotics are not sufficient. CASE: A 24-year-old healthy female was admitted after presenting with fever, sore throat, neck and pleuritic chest pain that started 3 days prior to admission. On physical examination, the patient appeared in mild respiratory distress requiring supplemental oxygen, and noted to have swelling and tenderness along the left sternocleidomastoid muscle with associated left tonsillar exudate and bibasilar pulmonary rales. Her initial complete blood count revealed isolated mild thrombocytopenia and a bandemia of 79%. A rapid strep test returned negative and a rapid influenza A/B RNA test also was negative. Following admission, a CT scan of the neck with contrast showed left peritonsillar abscess extending into the hypopharyngeal region with extensive lymphadenopathy. The patient was subsequently started on piperacillin-tazobactam and metronidazole after her admission blood culture began growing gram-negative anaerobes, which later speciated as Fusobacterium necrophorum. As the patient continued to spike high grade fevers, metronidazole was switched to intravenous sulbactam-ampicillin. On appropriate antibiotic coverage, the patient continued to complain of worsening dyspnea requiring increased supplemental oxygen by nasal cannula. A CT scan of the chest then showed multifocal pneumonia and multiple lung nodules concerning for septic emboli. In search for the source of her septic emboli, an echocardiogram showed normal findings, while a repeat CT of the neck with contrast revealed new findings of multiple necrotic lymph nodes and left internal jugular vein thrombus leading to a diagnosis of Lemierre's Syndrome. Subsequently, given clinical deterioration, patient was initiated on intravenous anticoagulation and the left internal jugular vein was resected. Over the ensuing several days, the patient's clinical pictur!
EMBASE:71297300
ISSN: 0884-8734
CID: 783162