Overuse of cardiac telemetry monitoring in the inpatient setting is widespread, contributes to alarm fatigue, and is costly for health systems. We sought to quantify the rates of provider unawareness of ongoing telemetry use and to quantify the rate of appropriate monitoring compared to American Heart Association (AHA) guidelines using a survey design. Inpatient medical providers were questioned about the presence of telemetry for each of their patients. In the 870 inquiries, 47% of patients were receiving telemetry. Providers' awareness of whether their patient was receiving telemetry was inaccurate in 26% of assessments. A guideline-appropriate indication for telemetry use was provided in only 58% of assessments. Providers are often unaware of ongoing cardiac telemetry use in their patients, and may continue use despite the lack of a guideline-appropriate indication.
Objective: To report a case of peripheral and autonomic neuropathy following one cycle of bortezomib in a patient with newly diagnosed multiple myeloma. Case Summary: A 75-year-old male who was highly functional prior to therapy rapidly became bed-bound from hypotension, syncope, and peripheral neuropathy after initiating bortezomib. Orthostatic hypotension and syncope persisted despite exclusion of infection and endocrine derangements and his receiving adequate intravenous hydration. Five weeks after this single cycle, the patient had a complete treatment response, including undetectable M-spike, improved anemia, and return to baseline renal function. An objective causality assessment revealed that an adverse drug event was probable. Discussion: Although neurotoxicity is an adverse effect of bortezomib, a MEDLINE search revealed little evidence on autonomic neuropathy, such as orthostatic hypotension and syncope. Also unique is the patient's complete treatment response following this single cycle. One explanation for the toxicities and dramatic treatment response is increased bortezomib exposure due to decreased drug metabolism. Both drug interactions and genetic polymorphisms can reduce bortezomib metabolism via effects on cytochrome P450 enzymes. Our patient was concomitantly taking 4 CYP inhibitors; amiodarone and omeprazole were longstanding, and ciprofloxacin and fluconazole were recently initiated prior to chemotherapy. Of these, fluconazole inhibits CYP2C9, 2C19, and 3A4; amiodarone inhibits CYP3A4, 1A1, 1A2, 2B6, and 2D6; ciprofloxacin inhibits CYP1A2 and 3A4; and omeprazole inhibits CYP1A2, 2C19, 2C9, 2D6, and 3A4. Similarly, genetic variables affect CYP enzymes. Genetic testing can predict response to bortezomib therapy, but pretherapy testing is not standard practice due to availability and cost, as in our patient's case. Conclusions: CYP-inhibiting drugs and many genetic polymorphisms can reduce bortezomib metabolism and increase serum concentrations of the drug, but guidelines on drug-drug interactions, monitoring, and genetic testing prior to bortezomib toxicity are needed.
Background: Wernicke’s encephalopathy (WE) is a potentially fatal consequence of thiamine deficiency that must be considered in patients with poor nutrition and altered mentation. We report a case of a female with hyperemesis gravidarum (HG), nystagmus, clonus, and abnormal thyroid function tests associated with WE. Clinical Case: A 23 year-old healthy G2P0010 woman was admitted for rehydration at 15 weeks gestation after four weeks of intractable vomiting. She denied medications, supplements and alcohol use. Vitals were normal. Exam showed a fatigued ill appearing female with no thyromegaly, tremor, lid lag, or stare. She had a gravid uterus but otherwise normal exam. Fetal heart rate was normal. Laboratory findings included hyponatremia, hypokalemia, elevated creatinine and transaminases, and normocytic anemia. Hepatitis panel, vitamin B12, ammonia, urinalysis and ultrasound of the appendix and gallbladder were unremarkable. She was treated with intravenous fluids and potassium. Electrolyte abnormalities and renal dysfunction resolved. On hospital day three, she became lethargic, tachycardic, unable to follow commands, and exhibited nystagmus and clonus. Thyroid studies showed TSH 0.06 uIU/mL (0.34 - 5.66 µIU/mL), and free T4 3.59 ng/dL (0.52 - 1.21 ng/dL). Methimazole and propranolol were started while awaiting repeat thyroid studies. MRI brain was not obtained due to aspiration risk. EEG showed diffuse slowing but no epileptiform activity. She returned to baseline mentation within hours of intravenous thiamine, with resolution of dysphagia and nystagmus. Thiamine level returned low (51 nmol/l; normal 67–200 nmol/L). Methimazole and propranolol were stopped and thyroid function tests normalized. She was discharged and delivered a healthy baby at term. Conclusion: WE is an acute neuropsychiatric condition caused by thiamine deficiency. Early recognition and treatment are critical to prevent irreversible damage; the classic signs are ataxia, ophthalmoplegia, and encephalopathy. Historically considered in patients with a history of alcohol use, WE is increasingly recognized in other conditions associated with dietary deficiency, since body stores of thiamine last only 18 days. WE has been reported in HG due to prolonged vomiting and increased thiamine requirements in pregnancy. WE has been associated with thyrotoxicosis, possibly due to increased metabolic demands. Both gestational transient thyrotoxicosis and HG are associated with markedly elevated HCG and present in the first 16 weeks of pregnancy. Initial thyroid studies were concerning for thyrotoxicosis, but normal repeat studies argue against that as a contributor. WE is a life threatening complication of poor oral intake, which should be empirically treated with thiamine prior to glucose. WE may be associated with thyrotoxicosis.
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