Cefoperazone/sulbactam/tigecycline
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Hypofibrinogenaemia, coagulopathy and off-label use: case report An 86-year-old man developed hypofibrinogenaemia and coagulopathy following off-label use of tigecycline for Acinetobacter baumannii infection. Additionally, cefoperazone/sulbactam contributed to the coagulopathy [not all dosages, duration of treatments to reaction onsets and outcomes stated; routes not stated]. The man was intubated and admitted to the ICU due to respiratory failure following a traffic accident. His history included hypertension and chronic kidney disease. At the time of admission, he was unconscious and displayed pinpoint-sized bilateral pupils. On day 3 of hospitalisation, he started to open his eyes in response to verbal command and was weakly responsive to external stimulation. However, he developed an infection and was initiated on empirical treatment with cefoperazone/sulbactam. Eventually, a significant drop in systemic inflammation markers was noted and his general condition improved. Twenty days after the initiation of treatment, he was awake and able to open his eyes autonomously. On day 28 of hospitalisation, he developed new onset of fever and was diagnosed with ventilator-associated pneumonia. Sputum culture workup was positive for Acinetobacter baumannii. Therefore, he was started on cefoperazone/sulbactam and high-dose off-label tigecycline 200mg loading dose followed by 100mg every 12 hours. Two days later, his fever resolved but his fibrinogen levels continued to decrease. Seven days after the initiation of cefoperazone/sulbactam and tigecycline treatment, his fibrinogen concentration dropped below the normal value. He was diagnosed with hypofibrinogenaemia. The man’s tigecycline treatment was discontinued on day 14 of its initiation. Subsequently, an improvement in fibrinogen concentration was noted. Also, no signs of hepatic dysfunction and bleeding were noted. Therefore, his cefoperazone/sulbactam treatment was switched to ceftizoxime and the inflammation improved. Within 5 days, his fibrinogen levels normalised. On day 41 of hospitalisation, he was transferred to the neurology department. Due to the cerebrovascular accident, he developed myasthenia of limbs and mild fever. After 9 days of treatment with ceftizoxime, his condition suddenly worsened and he developed hypotension and respiratory failure. Immediately, he was shifted to the ICU, reintubated and administered norepinephrine to maintain his BP. Additionally, his ceftizoxime treatment was stopped. The man was re-started on cefoperazone/sulbactam and high-dose tigecycline 100mg every 12 hour. At that time, his coagulation parameters were normal except for a slight elevation in fibrinogen level. Seven days after the re-initiation of treatment, a slow but progressive decrease in fibrinogen level was observed with elevation in prothrombin time (PT) and international normalised ratio (INR). His treatment with cefoperazone/sulbactam was suspected to have an effect on coagulation function. Hence, cefoperazone/ sulbactam was switched to piperacillin/taz
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