Heparin/temozolomide

Abstract

Various infections and heparin induced thrombocytopenia: case report A 53-year-old woman developed invasive cutaneous aspergillosis, pseudomonas infection, Stenotrophomonas maltophilia infection, Achromobacter xylosoxidans infection and Enterococcus casseliflavus infection during treatment with temozolomide for frontotemporal anaplastic astrocytoma. Additionally, she developed heparin-induced thrombocytopenia during treatment with heparin for saddle pulmonary embolism [dosages and routes not stated]. The woman was diagnosed with grade IV frontotemporal anaplastic astrocytoma. Therefore, she underwent surgery. After the surgery, she started receiving treatment with temozolomide along with radiotherapy. Later, she was admitted to hospital multiple times for adverse effects related to disease course and chemoradiotherapy. Subsequently, she suffered from saddle pulmonary embolism. Therefore, she started receiving treatment with heparin [unfractionated heparin] and respiratory support until her condition stabilised. Later, she presented to the emergency department with heparin-induced thrombocytopenia. Laboratory test revealed the following: platelet count 3000 /μL, leucopenia and neutropenia (WBC 1 and absolute neutrophil count 0.4). Her heparin treatment was stopped. Subsequently, she was admitted to the inpatient ward, as blood culture revealed Pseudomonas infection due to which she developed axillary cellulitis. Therefore, her treatment was started with aztreonam and vancomycin, which was shifted to cefepime. The woman’s temozolomide treatment was stopped. Two days later, she developed a lesion near the ala of left nostril and swelling of the left side of the cheek. Therefore, ENT team was consulted. Physical examination revealed a small lesion at the left nasal-alar crease, which was hyperemic, erythematous and tender about 1cm in size without any fluctuation. Nasal examination was limited due to tenderness elicited by examination maneuvers. It also showed clear discharge from the left nostril. CT scan of sinus with contrast revealed clear paranasal sinuses, partial opacification of the left maxillary, and ethmoidal sinuses with left facial edema without clear evidence of fungal sinusitis. Subsequently, she was treated with amphotericin-B-liposomal 3 mg/kg every 24 hours [liposomal amphotericin B]. Additionally, she was treated with empiric antimicrobial therapy with tigecycline and ciprofloxacin. However, no signs of improvement were noted, and the lesion evolved into the black lesion with central area of necrosis within 5 days. Biopsy was taken and culture growth revealed aspergillus flavis. Blood culture revealed Stenotrophomonas maltophilia, Achromobacter xylosoxidans and Enterococcus casseliflavus. Surgical debridement and endoscopic examination of paranasal sinuses was decided. However, electrolyte imbalance and abnormal coagulation profile was noted. Therefore, surgery was delayed until normalisation of laboratory parameters. She received Granulocyte Colony-Stimulating Factor and filgrastim for thrombocytopenia. However, platelet count was found to be 2000 /μL after filgrastim treatment. Therefore, she received six units of platelets daily for 5 days without any significant improvement in platelet count as it did not exceeded 40000 /μL. Ten days after appearance of primary lesion, she underwent surgery and nasal exploration, without any clear evidence of fungal sinusitis. Histopathology (biopsy and subsequent excision of the lesion) revealed widespread necrosis of the skin, with an extensive infiltration by numerous fungal organisms, composed of thin septate hyphae with branching at 45-degree angle. The morphological appearances were consistent with aspergillosis. Frontonasal flap was planned but postponded due to her abnormal coagulation profile. On the day of surgery, she received 10 units of platelet and empiric antibiotic therapy was continued along with unspecified fungal treatment and daily dressing on surgical site. Due to low platelet count, she tends to develop blood oozing from surgical site. Therefore, pressure dressing with haemostatic materials was applied. She had poor prognosis due to her disease. Based on these findings and clinical presentation it was concluded that she developed invasive cutaneous aspergillosis, pseudomonas infection, Stenotrophomonas maltophilia infection, Achromobacter xylosoxidans infection and Enterococcus casseliflavus infection associated with temozolomide [duration of treatment to reactions onsets not stated; not all outcomes stated]. Later, she died due to systemic complications of her primary disease [immediate cause of death not stated].