Objective To determine the optimal anticoagulation strategy in patients diagnosed with Lemierre Syndrome (LS). Data Sources A systematic review in accordance with PRISMA guidelines was conducted using PubMed, MEDLINE, Scopus, ProQuest, and CINAHL from January to April 2020. Search terms included “Lemierre Syndrome” AND “anticoagulation” NOT “prophylaxis” OR “atrial fibrillation,” in addition to a list of parenteral and oral anticoagulants. Adult patients who developed a clot and required systemic anticoagulation as a result of LS were included in this review. Study Selection and Data Extraction A total of 4180 records were initially identified, though following the removal of duplicates and nonrelevant entries, 216 full-text articles were reviewed for inclusion; 13 articles were ultimately included. Data Synthesis The majority (11/14) of patients developed thromboses of the internal jugular veins, which corresponds to the pathophysiology of LS. Anticoagulation strategies were varied in the included literature, though 12/14 patients initially received a parenteral product. Two patients received a direct-acting oral anticoagulant (DOAC) following either intravenous heparin or subcutaneous enoxaparin and had outcomes similar to patients transitioned to warfarin. Relevance to Patient Care and Clinical Practice Anticoagulation in LS is a clinical controversy because the thromboembolic events have rarely led to significant complications; thrombi typically resolve independently, and concerns for bleeding risks are well founded; however, this review indicates both the efficacy and safety of anticoagulation. Conclusions Anticoagulation is both efficacious and safe in LS, including treatment using a DOAC. Although further studies are needed, clinicians should consider a duration of anticoagulation of 6 to 12 weeks.
Objective: To review the efficacy and safety of medications used in the management of steroid-induced psychosis. Data Sources: A comprehensive literature search was conducted using PubMed, MEDLINE, ProQuest, and Scopus between May and October 2020 using the following search terminology: “steroid-induced psychosis” OR “corticosteroid-induced psychosis.” Study Selection and Data Extraction: Definitive cases, as defined by the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, were included in this review. Geriatric patients >65 years of age, those with a confounding neurological condition such as a traumatic brain or spinal cord injury, or those with active malignancy were excluded. Data Synthesis: A total of 13 patient cases were included in this review, representing 8 male patients and 5 female patients. The mean age at symptom presentation was 42.5 years. Six patients presented with delusions, 5 presented with hallucinations, and 2 presented with both manifestations; 12 patients were managed with an antipsychotic, with haloperidol being the most commonly prescribed, followed by risperidone. One patient was managed with lithium and clonazepam alone. All patients returned to their psychological baseline upon the discontinuation or decreased dose of steroids in combination with Pharmacological intervention, though the time to resolution of symptoms varied significantly. No notable adverse drug events associated with treatments were reported. Conclusions: Steroid-induced psychosis is a serious adverse effect of corticosteroid therapy; however, management strategies that combine a dose reduction or elimination of steroids, in combination with an antipsychotic medication, are effective in resolving this syndrome.
Objective: To determine the most appropriate thiamine replacement regimen by evaluating safety and efficacy of the drug specific to alcohol-induced Wernicke’s encephalopathy (WE). Data Sources: A comprehensive literature search was conducted using PubMed, MEDLINE, Scopus, and ProQuest between January and August 2020 using the following keyword and Boolean search terminology: “thiamine” AND “alcohol” AND (encephalopathy OR korsakoff). Study Selection and Data Extraction: Randomized control trials; prospective, observational, and retrospective cohort analyses; and case reports and series were included in this evaluation. A confirmed diagnosis of alcohol-induced WE and treatment with parenteral or intramuscular (IM) thiamine were required for inclusion. Data Synthesis: Six publications composed of 138 patients were evaluated in this review, in which a wide variety of thiamine supplementation strategies were employed. Clinical diagnostic criteria varied significantly between publications. Doses ranged from 100 to 1500 mg intravenous thiamine and up to 300 mg IM thiamine, with no apparent difference in patient outcomes. All patients who received thiamine experienced symptom improvement, and adverse drug events were minimal. Conclusions: Despite the clinical controversy regarding the appropriate thiamine supplementation regimen, the heterogeneity of published works combined with symptom resolution across the gamut of dosing strategies makes a definitive consensus elusive. Clinicians should continue to provide parenteral or IM thiamine in doses of ≥100 mg to patients with confirmed alcohol-induced WE.
Background: Health care providers routinely rely on tertiary drug information resources to affirm knowledge or proactively verify the safety and efficacy of medications. Though all patient care areas are affected, the reliability of these resources is perhaps nowhere as poignant as it is in high-acuity settings, including the emergency department and the intensive care unit. As providers seek to identify adjunctive analgesics for acute pain in these areas, they must be able to rely on the integrity to whichever resource their institution has granted access. Objective: To determine the congruency of drug-drug interaction information found on 3 tertiary drug resources. Methods: A drug-drug interaction analysis was conducted on Micromedex, Lexicomp, and Medscape. Adjunctive analgesics included dexmedetomidine and ketamine, which were compared with the intravenous opioid products morphine, fentanyl, and hydromorphone. Results: Significant discrepancies were appreciated with regard to the severity of drug-drug interactions. In addition, the heterogeneity in which reaction severity and likelihood are described by each respective resource makes direct comparisons difficult. Interaction warnings for dexmedetomidine and fentanyl included a “major interaction” from Micromedex, whereas Lexicomp did not identify a risk and Medscape only recommended increased monitoring on the grounds of respiratory and central nervous system depression. Conclusions: Health care providers must remain vigilant when reviewing tertiary drug information resources. Pharmacists possess the training and skills necessary to assist interdisciplinary medical teams in providing optimal patient care through evaluating and applying the information gleaned from these resources.
Objectives: To report an oxcarbazepine (OXC)-induced cutaneous reaction in a female of Mexican ancestry. Case Summary: A 60-year-old female of Mexican ancestry presented to clinic with a diffuse morbilliform rash, with erythema and eruptions of papules/pustules concentrated on her neck and torso. The rash appeared 1 week following the initiation of OXC for trigeminal neuralgia. Initially, the correlation between the reaction and initiation of OXC was not recognized by the provider. OXC was continued for a total of 4 weeks and several medical encounters transpired in the interim. Supportive therapy, in the form of oral antihistamines and oral/topical corticosteroids, failed to resolve the rash. A clinical pharmacist prompted the discontinuation of OXC due to suspicion that it incited the adverse reaction. Oral corticosteroid therapy was initiated and tapered over 2 weeks, with rash dissipation occurring in 1 month. Discussion: The association of OXC with the cutaneous eruption was classified as “probable” based on the Naranjo Scale. While financial resources were not available to perform genetic testing, it may be possible that the genetic status of this patient lent itself to greater potential for cutaneous reactions with OXC. Further research is needed to determine whether pharmacogenetic variables affiliated with pre-Columbian lineage may predispose individuals to specific adverse drug reactions. Conclusion: As regional genotypes disperse globally, it is imperative that clinicians are cognizant of risks regarding genetically implicated adverse drug reactions. While information is limited for certain ethnicities, it is essential that providers diligently monitor all populations for reactions characteristic to specific medications.
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