Drug Safety - Case Reports最新文献

A 17-year-old male with history of neuromyelitis optica and seizures presented to the pulmonology clinic for evaluation of recurrent pneumonias. He had received rituximab for the past 6 years. Over the past 2 years, he experienced four episodes of pneumonia. In between these episodes, he would improve briefly but continued to have daily cough that was productive with yellow phlegm. He also had recurrent rhinitis and sinusitis despite multiple antibiotic courses. Review of chest X-rays revealed localized right middle lobe and right lower lobe infiltrates. An extensive workup was performed, including computed tomography (CT) of the chest and bronchoscopy to rule out congenital lesions of the right lung and foreign body aspiration. Chest CT showed right lower lobe bronchiectasis. Flexible bronchoscopy with bronchoalveolar lavage showed normal anatomy with thick mucus secretions in the right lower lobe. Immunologic evaluation was performed and revealed low levels of immunoglobulin (Ig)-G, IgM, and IgA, which had declined since initiation of rituximab. Lymphocyte subset testing was remarkable for low cluster of differentiation (CD)-19. He was referred to allergy and immunology and was initiated on immunoglobulin-replacement therapy (IGRT) for acquired hypogammaglobulinemia secondary to rituximab. There was marked clinical improvement after initiation of IGRT.

A 22-year-old man was admitted for an elective right-shoulder open subacromial decompression and distal clavicle excision. He received a single intravenous dose of fentanyl 50 μg for anesthesia. His procedure was completed without intra-operative complications; however, he developed post-operative respiratory depression in the setting of narcotic administration. He was given naloxone 0.2 mg intravenously once to reverse this effect, which subsequently led to acute hypoxic respiratory failure secondary to pulmonary edema shortly after administration of naloxone. His oxygen saturation was noted to be 50% on room air, he was tachypneic with a respiratory rate of 22, and his heart rate ranged from 89 to 104 beats per minute. His blood pressure remained within normal limits at 128/62. His chest X-ray was notable for patchy bilateral perihilar infiltrates and the patient was intubated postoperatively. An EKG revealed normal sinus rhythm, and cardiac enzymes were negative. He was diagnosed with naloxone-induced non-cardiogenic pulmonary edema supported by the temporal relationship of the causal drug and no other identifiable cause of his clinical picture. He received furosemide and underwent diuresis while intubated, with subsequent improvement in his oxygen requirements. His vitals remained stable and he was extubated 6 h later. A Naranjo assessment score of 6 was obtained, indicating a probable relationship between the patient's symptoms and the suspect drug.

Desmopressin, a synthetic vasopressin analog, is used to treat central diabetes insipidus, hemostatic disorders such as von Willebrand's disease, and nocturnal enuresis. We present the case of a 69-year-old man who developed severe hyponatremia during treatment with intranasal desmopressin at 10 µg twice daily for chronic polyuria and nocturia thought to be due to central diabetes insipidus. After 5 months of therapy, the patient noticed progressive fatigue, anorexia, dizziness, weakness, light-headedness, decreased concentration, and new-onset falls. At 6 months of therapy, the patient was brought to the emergency department for altered mental status and was found to be severely hyponatremic with a serum sodium level of 96 mmol/L, down from a value of 134 mmol/L at the initiation of therapy. The intranasal desmopressin was discontinued and the patient was admitted to the intensive care unit where the hyponatremia was slowly corrected over the next week to 132 mmol/L, never increasing by more than 8 mmol/L a day, with careful fluid management. This included infusion of over 11 L of 5% dextrose to account for a high urine output, which peaked at 7.4 L in 1 day. However, while the recommended rate for sodium correction was followed, the patient's magnetic resonance imaging of the brain obtained after discharge displayed evidence of central pontine myelinolysis. Despite this finding, the patient eventually returned to his baseline mental status with no permanent neurologic deficits.

In this case report, we describe a 66-year-old man who developed multiple adverse reactions beginning at age 56 after exposure to several azole antifungal drugs including ketoconazole and fluconazole. He also had a history of more than 40 years exposure to chemicals including pesticides, wood preservatives, fertilizers, and welding chemicals. His reactions involved dehydration (requiring several liters of intravenous fluids in less than an hour to alleviate this condition), angioedema, nausea, tinnitus, hypotension, and difficulty breathing. His acute adverse reactions were triggered by a wide range of chemicals including gasoline, diesel fuel, pesticides, chlorine, topical isopropyl alcohol, and paper mill emissions. His acute reactions were also triggered by a wide range of foods such as bananas, apples, milk, white potatoes, and processed sweets. A number of mechanisms could be responsible for his increased sensitivity to chemicals following exposure to fluconazole/ketoconazole, including inhibition of P450 and other detoxification enzymes, acetaldehyde buildup, and neurogenic sensitization.

Fluoroquinolones are usually well tolerated with a minimum of serious adverse effects; renal toxicity is uncommon. Apart from the renal side effects of ciprofloxacin, we aimed to highlight the renal impact of a ciprofloxacin overdose, and thus conducted a prospective study in the Department of Nephrology at La Rabta Hospital between 2010 and 2015. The cohort database was continually updated until the inclusion of five patients who were subjected to an overdose and who were initially admitted to the medical intensive care unit and then transferred to our department for acute renal failure (ARF) due to ciprofloxacin ingestion requiring urgent hemodialysis. All patients developed ARF after 12-36 h of ingestion. Renal ultrasound was normal in all cases. Twenty-four-hour proteinuria was present but not significant in one case, while microscopic hematuria was present in one case. Treatment consisted of supportive therapy and extrarenal purification by conventional intermittent hemodialysis. Four patients recovered normal renal function within 3 weeks and the remaining patient eventually had chronic kidney failure.

A 67-year-old male with history of well controlled type 2 diabetes mellitus and hypertension developed acute interstitial nephritis (AIN) with nephrotic-range proteinuria during treatment with cefazolin for methicillin-sensitive Staphylococcus aureus and Group B Streptococcus (GBS) bacteremia. The patient received intravenous cefazolin 2 g every 8 h for 4 weeks prior to presentation to the emergency department with abdominal distension, nausea, and vomiting. Investigations revealed a serum ascites albumin gradient of 1.0 with total protein of 1.8 g/dL suggestive of nephrotic syndrome, which was confirmed with a spot urine protein/creatinine ratio that estimated 7.95 g of protein per day. Serum creatinine was elevated compared with baseline. Urine studies showed sterile pyuria with 3+ protein and eosinophiluria. The patient was diagnosed with AIN with nephrotic-range proteinuria associated with cefazolin use. Cefazolin was discontinued and, within a couple of days, the patient's creatinine stabilized. He was discharged with prednisone 60 mg once a day for 10 days with a taper over 2 weeks for his AIN. The patient's creatinine and proteinuria slowly decreased over the next couple of weeks, however, did not recover to baseline. A Naranjo assessment score of 6 was obtained, indicating a probable relationship between the patient's AIN with nephrotic-range proteinuria and his use of cefazolin.

A 55-year-old male was admitted to the hospital with pneumonia. During an intubation procedure, the patient received an application of endobronchial lidocaine (4% gel). Within 2 h of intubation, the patient developed worsening hypoxia, and investigation of arterial blood gasses revealed a pH of 7.21, carbon dioxide partial pressure (PaCO₂) of 3.3 kPa, oxygen partial pressure (PaO₂) of 55.1 kPa, and measured oxygen saturation of 49%. Co-oximetry of this sample returned a methemoglobin level of 53%. Intravenous methylthioninium chloride (1% solution at 1 mg/kg) was delivered, and subsequent arterial blood gasses, at 30 min and 1 h post administration, showed methemoglobin levels of 12 and 9%, respectively, with return of oxygen saturation to > 90%.

A 66-year-old male patient with a 10-year course of Parkinson's disease (PD) was admitted for hallucination lasting a half a month. After treatment with levodopa/carbidopa, selegiline, and piribedil, the patient's motor symptoms were improved while no significant effects were observed on psychotic symptoms. A clinical pharmacist analyzed the pharmacologic and pharmacokinetic characteristics of selegiline and piribedil, summarized the scheme of PD with psychotic symptoms in the literature, and discovered that selegiline might potentiate psychotic side effects of piribedil, while the use of levodopa/carbidopa cannot be ruled out either. Finally, the clinical pharmacist proposed to reduce the dosage of levodopa/carbidopa, increase the dosage of selegiline and quetiapine, and discontinue piribedil. The clinician accepted this suggestion. After the adjustment of medication, the patient's motor symptoms were absolutely improved and the psychotic symptoms were notably improved. This case study suggests that long-term treatment with levodopa/carbidopa and piribedil, along with the progression of the disease itself, could contribute to the emergence of psychotic symptoms in PD. Additionally, selegiline could potentiate psychotic side effects of piribedil. Neurology clinical pharmacists should work alongside neurology clinicians at the bedside to optimize pharmacotherapy, improve patient safety, and contribute to scholarly efforts.

Medication errors remain among the major problems seen in hospitals. Such errors can relate to the prescription, dispensation, or administration of drugs. Human factors account for most of these mistakes, but other factors such as infusion pump programming defects should always be considered. Worldwide, medication errors have been reported to affect 2-30% of patients, depending on the institution. Intravenous lipid emulsion (ILE) infusion is frequently used as part of total parenteral nutrition in patients of all ages with feeding and gastrointestinal issues. ILE overdose has been previously reported, with variable clinical outcomes. We report a case of accidental ILE (Intralipid) overdose in a 3-month-old male infant who fully recovered after single-volume blood exchange transfusion. We also review reported cases and summarize potential solutions for ILE overdose. Our review indicates that ILE infusion is a high-risk medication, and opportunities for errors remain even in the best hospital set-ups. Attention should be directed towards proper prescription, dosing, dispensation, and administration. Most of the cases indicate the safety breach was at the nursing drug-administration level, with improper pump use or programming, together with other fluid infusion rate switching, being the main possible defects. Strategies targeting the areas of weakness in the drug-delivery pathway are needed. Special attention should be paid towards nursing duties and working hours. In addition, nursing staff should receive frequent education sessions and should be required to pass competency modules regularly. An error-prevention plan should be established and implemented. This plan needs full collaboration between physicians, pharmacists, and nursing staff.

Hyperprogressive disease (HPD) has been recently proposed as a new pattern of progression in patients treated with immune checkpoint inhibitors (ICIs). Until now, no biological marker has been found to predict this accelerated tumour growth. We describe the case of a 62-year-old women who experienced a marked increase in absolute eosinophil count (AEC) concurrently with a huge radiological progression after the first nivolumab dose in absence of other immune-related adverse events (irAEs). Further investigations are needed to establish the role of early hypereosinophilia as a marker of progression and to identify patients who might not benefit from ICI treatment.