The clinical characteristics of SIADH caused by different drugs are comparable. Patients with SIADH treated with drugs from five common medication classes will probably be diagnosed with drug-induced SIADH. Physicians should be aware of the significance of these medication classes as SIADH aetiologies.
BackgroundAlthough medication induced syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common clinical entity, several issues remain unaddressed in the current literature. As most of the available data are derived from case reports and small case series, the distribution of the different medication classes as SIADH aetiologies is unknown. It is also not known whether different medication classes are associated with different severity and outcomes of SIADH. The percentage of patients with SIADH who take a suspected medication and are actually diagnosed with medication induced SIADH is unknown. Also, whether these patients can be differentiated by clinical parameters from those with SIADH due to other causes has not been studied.PurposeTo determine the distribution of aetiologies for medication induced SIADH in hospitalised patients, and to characterise them according to the different medication groups.Material and methodsA single centre retrospective study was conducted including all patients diagnosed with SIADH in a large community hospital and tertiary centre between 1 January 2007 and 1 January 2013 who were treated with medications known to be associated with SIADH. Two physicians reviewed every patient’s medical file for predetermined relevant clinical data.ResultsThe study cohort included 198 patients who had SIADH and received medications associated with SIADH. Most patients (146, 73.7%) were diagnosed with medication associated SIADH, while 52 (26.3%) were diagnosed with SIADH due to other aetiologies. The Naranjo algorithm differentiated well between the two groups (p<0.001). 5 medication classes, namely antidepressants, anticonvulsants, antipsychotics, cytotoxic agents and analgesics, were implicated in 82.3% of patients diagnosed with medication associated SIADH. Specific serotonin reuptake inhibitors and carbamazepine were commonly implicated. There were no clinically significant differences in characteristics or severity of SIADH according to medication class.ConclusionMedication induced SIADH is mostly caused by 5 medication classes. The Naranjo algorithm successfully differentiated between medication induced SIADH and SIADH due to other aetiologies in patients treated with these medications. Clinical characteristics were comparable between SIADH caused by different medications. Physicians should be aware of the high likelihood of medication induced SIADH among patients treated with the implicated medication classes.No conflict of interest
BackgroundLQTS, the long QT syndrome, is associated with an increased risk of ventricular arrhythmias, named torsades de pointes (TdP). TdP can result in ventricular fibrillation and sudden death. The incidence of such arrhythmia is often a result of polypharmacy and drug–drug interactions. Several studies have shown an advantage of pharmacist involvement in monitoring and reducing the risk.PurposeThe purpose of this study was to evaluate the potential role of a clinical pharmacist consult on monitoring and management of pharmacodynamic drug–drug interactions potentially causing QTc prolongation.Material and methodsThis was an observational and retrospective study. It included all admissions to a single 44 bed internal medicine department during 2013 for whom a ‘combination of drugs’ was prescribed. The ‘combination of drugs’ was defined as pharmacodynamic drug–drug interactions of major severity, potentially causing QTc prolongation. The study group, as opposed to the control group, received a clinical pharmacist consult and interventions. Demographic data and risk factors were collected and ECG records were obtained. Patients’ files were scanned for doctor’s mentioning of ECG results in the follow-up, and treatment interventions. The ECG records were read by an internal medicine resident. Evaluation of the impact of pharmacist consult on doctor’s follow up, and ECG records, was made. Factors affecting a doctor’s decision to intervene were identified.ResultsDuring the study period, pharmacist consultations were written in 643 electronic charts. About 6% of the total consultations involved QT prolonging interactions. Pharmacist consult resulted in higher ECG recordings (71.8% vs 39.2%; p=0.0004). In addition, the consult resulted in higher doctor’s attention to ECG findings in the follow-up (53.8% vs 5.7%; p<0.0001). Finally, a doctor’s decision to intervene in the treatment was influenced by the pharmacist consult (p=0.03). This decision was not influenced by the degree of QTc prolongation or the presence of risk factors. The most frequent intervention was drug discontinuation.ConclusionA clinical pharmacist has the ability to identify potentially dangerous drug combinations, increase medical awareness and monitoring where necessary. Most importantly, a pharmacist’s consult resulting in a doctor’s attention to ECG findings in the follow-up increases the probability of doctors’ interventions even in the absence of meaningful ECG changes.No conflict of interest
BackgroundHyperkalaemia is a common, potentially life threatening, disorder. Potassium binders (eg, sodium polystyrene sulfonate (Kayexalate)) are the mainstay of hyperkalaemia treatment regimens. However, there is no protocol for the use and monitoring of these drugs in our institution, nor did we find any published guidelines.PurposeTo evaluate the safety of non-protocol based treatment of hyperkalaemia using Kayexalate in internal medicine wards. Our hypothesis was that repeat administration of the drug is associated with higher toxicity than single administration and monitoring.Material and methodsThis was a retrospective observational study. The study included all patients treated with Kayexalate during 2013 in internal medicine wards. Patients receiving chronic Kayexalate treatment, and patients treated during anuric shock who died during treatment, were excluded. Patients were divided according to initial computerised treatment order: ‘once’ order (repeated according to laboratory results) or ‘constant’ order (x1/day, or x2/day, etc). Data collected included: pretreatment potassium level, number of doses given until normokalaemia, mean total doses given, hypokalaemia events (potassium levels <3.5 mEq/L), and time to first post-treatment laboratory results. Hypokalaemia was considered treatment related if it occurred during 48 hours post-treatment.ResultsA total of 696 treatment events met the inclusion and exclusion criteria of the study. We found significant inter- and intra-ward differences in preference of treatment regimens. Regimen choice of constant orders was associated with higher pretreatment potassium levels (p<0.0001). A total of 91 hypokalaemia events were documented. Hypokalaemia events were significantly more common in the constant versus the once treatment regimens (23.85% vs 6% respectively, p<0.0001). Mean time to first post-treatment laboratory assessment was 14.4 hours. Mean number of doses given until normokalaemia was 1.2 doses, while mean total number of doses was 3.9 doses.ConclusionLack of treatment protocol was associated with significant inter- and intra-ward differences in treatment and monitoring regimens. Treatment using constant regimens was significantly associated with superfluous doses and higher treatment related hypokalaemia. In light of these findings, we have developed and implemented an institutional treatment protocol. The post-intervention data are being processed—final results are pending. So far the results show a significant decrease in the number of treatment related hypokalaemia events.No conflict of interest
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