{"title":"深静脉血栓。","authors":"Wilson Liang, Joy Amanda Moverley","doi":"10.1097/01.JAA.0000819540.23572.34","DOIUrl":null,"url":null,"abstract":"Deep vein thrombosis: case report A 67-year-old man developed deep vein thrombosis during treatment with prednisolone for AChr positive myasthenic gravis. The man had a history of AChr-antibody positive myasthenia gravis with ocular and oropharyngeal manifestations, hypertension and obstructive sleep apnoea. He also had urinary tract infection of an unknown aetiology, for which he was on ceftriaxone. He had been receiving prednisolone [route and initial dosage not stated], which was later increased to 30mg daily. Subsequently, he was admitted due to worsening of shortness of breath and generalised weakness for 3 days. He also had respiratory distress and decreased vital lung capacity. On hospitalisation, blood gas analysis showed hypoxia and hypocapnea, which was interpreted as hyperventilation compensating for hypoxaemia. On admission, an initial diagnosis of respiratory distress due to myasthenic crisis was made and the man received plasma exchange sessions. He was started on mycophenolate mofetil and pyridostigmine, and the dose of prednisolone was increased to 40mg daily. However, his respiratory symptoms persisted. The dose of prednisolone was later reduced to 30mg. Further, he showed worsening of dysponea along with pleuritic chest pain. The vital capacity decreased to <2L and peripheral oxygen saturation was 97% on oxygen nasal cannula. D-dimer was elevated. Arterial blood gas analysis revealed respiratory alkalosis without hypoxaemia. ECG and chest radiography was normal. Ultrasound revealed left proximal and deep vein thrombosis. Based on these findings, a final diagnosis of deep vein thrombosis associated with prednisolone was made [duration of treatment to reaction onset not stated]. A contrast CT scan of chest revealed extensive segmental and sub-segmental pulmonary emboli. He was started on enoxaparin and showed gradual improvement. It was concluded that the initial diagnosis of myasthenic crisis was a diagnostic error, and the final diagnosis was deep vein thrombosis.","PeriodicalId":520655,"journal":{"name":"JAAPA : official journal of the American Academy of Physician Assistants","volume":" ","pages":"61-62"},"PeriodicalIF":0.8000,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Deep vein thrombosis.\",\"authors\":\"Wilson Liang, Joy Amanda Moverley\",\"doi\":\"10.1097/01.JAA.0000819540.23572.34\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Deep vein thrombosis: case report A 67-year-old man developed deep vein thrombosis during treatment with prednisolone for AChr positive myasthenic gravis. The man had a history of AChr-antibody positive myasthenia gravis with ocular and oropharyngeal manifestations, hypertension and obstructive sleep apnoea. He also had urinary tract infection of an unknown aetiology, for which he was on ceftriaxone. He had been receiving prednisolone [route and initial dosage not stated], which was later increased to 30mg daily. Subsequently, he was admitted due to worsening of shortness of breath and generalised weakness for 3 days. He also had respiratory distress and decreased vital lung capacity. On hospitalisation, blood gas analysis showed hypoxia and hypocapnea, which was interpreted as hyperventilation compensating for hypoxaemia. On admission, an initial diagnosis of respiratory distress due to myasthenic crisis was made and the man received plasma exchange sessions. He was started on mycophenolate mofetil and pyridostigmine, and the dose of prednisolone was increased to 40mg daily. However, his respiratory symptoms persisted. The dose of prednisolone was later reduced to 30mg. Further, he showed worsening of dysponea along with pleuritic chest pain. The vital capacity decreased to <2L and peripheral oxygen saturation was 97% on oxygen nasal cannula. D-dimer was elevated. Arterial blood gas analysis revealed respiratory alkalosis without hypoxaemia. ECG and chest radiography was normal. Ultrasound revealed left proximal and deep vein thrombosis. Based on these findings, a final diagnosis of deep vein thrombosis associated with prednisolone was made [duration of treatment to reaction onset not stated]. A contrast CT scan of chest revealed extensive segmental and sub-segmental pulmonary emboli. He was started on enoxaparin and showed gradual improvement. It was concluded that the initial diagnosis of myasthenic crisis was a diagnostic error, and the final diagnosis was deep vein thrombosis.\",\"PeriodicalId\":520655,\"journal\":{\"name\":\"JAAPA : official journal of the American Academy of Physician Assistants\",\"volume\":\" \",\"pages\":\"61-62\"},\"PeriodicalIF\":0.8000,\"publicationDate\":\"2022-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"JAAPA : official journal of the American Academy of Physician Assistants\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1097/01.JAA.0000819540.23572.34\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"JAAPA : official journal of the American Academy of Physician Assistants","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/01.JAA.0000819540.23572.34","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Deep vein thrombosis: case report A 67-year-old man developed deep vein thrombosis during treatment with prednisolone for AChr positive myasthenic gravis. The man had a history of AChr-antibody positive myasthenia gravis with ocular and oropharyngeal manifestations, hypertension and obstructive sleep apnoea. He also had urinary tract infection of an unknown aetiology, for which he was on ceftriaxone. He had been receiving prednisolone [route and initial dosage not stated], which was later increased to 30mg daily. Subsequently, he was admitted due to worsening of shortness of breath and generalised weakness for 3 days. He also had respiratory distress and decreased vital lung capacity. On hospitalisation, blood gas analysis showed hypoxia and hypocapnea, which was interpreted as hyperventilation compensating for hypoxaemia. On admission, an initial diagnosis of respiratory distress due to myasthenic crisis was made and the man received plasma exchange sessions. He was started on mycophenolate mofetil and pyridostigmine, and the dose of prednisolone was increased to 40mg daily. However, his respiratory symptoms persisted. The dose of prednisolone was later reduced to 30mg. Further, he showed worsening of dysponea along with pleuritic chest pain. The vital capacity decreased to <2L and peripheral oxygen saturation was 97% on oxygen nasal cannula. D-dimer was elevated. Arterial blood gas analysis revealed respiratory alkalosis without hypoxaemia. ECG and chest radiography was normal. Ultrasound revealed left proximal and deep vein thrombosis. Based on these findings, a final diagnosis of deep vein thrombosis associated with prednisolone was made [duration of treatment to reaction onset not stated]. A contrast CT scan of chest revealed extensive segmental and sub-segmental pulmonary emboli. He was started on enoxaparin and showed gradual improvement. It was concluded that the initial diagnosis of myasthenic crisis was a diagnostic error, and the final diagnosis was deep vein thrombosis.