Patient-reported outcomes after acute carpal tunnel release in patients with distal radius open reduction internal fixation

Background

Acute carpal tunnel syndrome (CTS) is a complication that can develop after distal radius fractures. Our hypothesis tested whether patient-reported outcomes after acute carpal tunnel release (CTR) performed in combination with distal radius fracture open reduction internal fixation (ORIF) are worse than patient-reported outcomes with only elective CTR as measured by the symptom severity and functional status scales of the Boston carpal tunnel questionnaire (BCTQ).

Methods

A retrospective assessment identified 26 patients treated with acute CTR at the same time as distal radius ORIF, no history of pre-existing CTS or CTR, no other injuries, and >12 months follow-up. Sixteen of these patients (Group A) could be contacted and answered the BCTQ. Group A was age- and sex-matched to control patients (Group B) treated with only elective CTR. A case–control study was performed comparing outcomes of both groups.

Results

The average age of patients was 51 ± 15 years, with an average follow-up of Group A at 49 ± 21 months versus Group B at 55 ± 20 months. The mean symptom severity scale score for Group A was 1.4 ± 0.4 and for Group B was 1.4 ± 0.4. The mean functional status scale score for Group A was 1.4 ± 0.5 and for Group B was 1.3 ± 0.4. The mean total BCTQ score for Group A was 26.5 ± 7.5 and for Group B was 24.9 ± 7.5. There were no statistical or clinically significant differences between Group A and Group B for symptom severity, functional status, and total BCTQ scores.

Conclusions

Patients with acute CTR performed at the same time with distal radius ORIF do as well in the long-term as those patients with only elective CTR as measured by the BCTQ. Patients should expect similar recovery of subjective nerve function from acute median nerve dysfunction when CTR is performed with distal radius ORIF as patients with only elective CTR.     

Stimulation of bladder activity by volume, L-dopa and capsaicin in normal conscious rats - effects of spinal α1-adrenoceptor blockade

To study possible differences in α₁-adrenoceptor involvement in the spinal mechanisms mediating bladder activity induced by volume (bladder filling), central (L-dopa), and peripheral (capsaicin) stimulation, we investigated if these types of bladder activity were modified by intrathecal (i.t.) or intra-arterial (i.a.) administration of the α₁-adrenoceptor antagonist, indoramin. Indoramin is selective for the α_1A-adrenoceptor subtype, whereas most clinically used α₁-adrenoceptor antagonists, including doxazosin, have no subtype selectivity. The drug effects were studied by continuous cystometry in normal, conscious rats and rats with bladder activity evoked by intraperitoneal L-dopa (50 mg/kg after carbidopa pretreatment), or by intravesical capsaicin (30 μM). I.t. indoramin (50 nmol) significantly decreased micturition pressure, and increased bladder capacity and micturition volume. Dribbling incontinence due to urinary retention was observed in one of ten rats. L-dopa-stimulated bladder overactivity was significantly attenuated by i.t. or i.a. indoramin (50 nmol). Similar effects of i.t. and i.a. doxazosin (50 nmol) have been reported previously. Intravesical capsaicin (30 μM) caused bladder activity, which was attenuated by i.t. indoramin (50 nmol), but not by i.t. doxazosin (50 nmol). I.a. indoramin did not reduce capsaicin-induced bladder activity; doxazosin was moderately effective. The results suggest that the bulbospinal micturition reflex evoked by bladder filling and L-dopa involves a descending pathway where transmission is partly mediated by spinal α₁-adrenoceptors. Bladder overactivity evoked by intravesical capsaicin, which elicits a vesico-spinal-vesical reflex, was not affected by i.t. doxazosin in a dose that attenuates activity mediated through the bulbo-spinal pathway. This suggests less involvement of spinal α₁-adrenoceptors in the vesico-spinal-vesical than in the bulbo-spinal voiding reflex. Received: 29 November 1996 / Accepted: 3 March 1997     

Seasonal Variation of Alkaloids of Adhatoda vasica and Detection of Glycosides and N-Oxides of Vasicine and Vasicinone.

The distribution pattern of the alkaloids of A. VASICA has been studied with change of season. The study also resulted in the detection of glycosides and N-oxides of vasicine and vasicinone.     

An Unusual Cause of Dysphagia: Pericardial Effusion after Implantable Cardioverter-Defibrillator Placement

Background

Dysphagia is a known complication of pericardial effusions. Most cases of pericardial effusions are idiopathic, infectious, and neoplastic, but can also occur after cardiac procedures.

Objective

To report the case of a patient who developed dysphagia from a sub-acute pericardial effusion caused by the placement of an implantable cardioverter-defibrillator (ICD).

Case Report

A 62-year-old woman presented to the Emergency Department (ED) with a 2-day history of dysphagia. Imaging revealed a large pericardial effusion compressing the esophagus from the mid-thoracic level to the gastroesophageal junction. Ten days prior, a dual-chamber ICD with small-diameter active fixation leads was placed in the patient. There had been no apparent complications from the procedure, however, over this 10-day period she developed a sub-acute pericardial effusion from an incidental perforation during ICD lead placement that led to the extrinsic compression of the esophagus and her presenting symptom of dysphagia. The patient underwent pericardiocentesis for the pericardial effusion and she was discharged in stable condition.

Conclusion

This case report highlights the importance of recognizing a non-cardiac complaint such as dysphagia as the primary symptom of a critical cardiac condition. With an increase in cardiac procedures anticipated, clinicians should consider the possibility of a pericardial effusion as a cause of dysphagia, especially for those patients with recent cardiac procedures.     

Top advances of the year: Precision oncology

The advent of precision medicine has changed the landscape of oncologic biomarkers, drug discovery, drug development, and, more importantly, outcomes for patients with cancer. Precision oncology entails the genomic profiling of tumors to detect actionable aberrations. The advances in clinical next-generation sequencing from both tumor tissue and liquid biopsy and availability of targeted therapies has rapidly entered mainstream clinical practice. In this review, recent major developments in precision oncology that have affected outcomes for patients with cancer are discussed. Rapid clinical development was seen of targeted agents across various mutational profiles such as KRASG12C (which was considered “undruggable” for almost 4 decades), Exon 20 insertions, and RET mutations. Approaches to precision chemotherapy delivery by the introduction of antibody drug conjugates in the armamentarium against lung cancer has been appreciated.     

Myocardial Infarction Risk in Arthroplasty vs Arthroscopy: How Much Does Procedure Type Matter?

Background

This study aimed at assessing short-term risk of serious cardiac events after elective total joint arthroplasty (TJA) as compared to a less-invasive procedure, knee arthroscopy (KA).

CAPN1 mutations: Expanding the CAPN1-related phenotype: From hereditary spastic paraparesis to spastic ataxia

Aims and objectiveTo characterize the phenotype of CAPN1 (SPG76) mutations in patients diagnosed with hereditary spastic paraplegia (HSP).BackgroundThe CAPN1 gene, located on chromosome 11q13.1, is a protein-coding gene involved in neuronal plasticity, migration, microtubular regulation and cerebellar development. Several families with CAPN1 mutations have recently been reported to present with autosomal recessive (AR) HSP and/or ataxia.MethodPatients with HSP were identified through neurological and genetic clinics with detailed phenotyping. Whole exome sequencing revealed novel pathogenic CAPN1 mutations in four patients from 3 families.ResultsAffected families were of Turkish, Japanese, and Punjabi descent and all were consanguineous. Onset of spastic paraplegia in the four patients was between 20 and 37 years. Two also had mild ataxia. Three different novel, homozygous mutations in CAPN1 were found: c.2118+1G > T, c.397C > T, c.843+1G > C. The patient with the earliest onset also manifested profound muscle weakness, likely related to a second homozygous mutation in DYSF (dysferlinopathy).ConclusionsThe phenotype of AR CAPN1 mutations appears to be spastic paraplegia with or without ataxia; onset is most commonly in adulthood. Eye movement abnormalities, skeletal defects, peripheral neuropathy and amyotrophy can sometimes be seen. Occasionally, patients can present with ataxia, illustrating the genotypic and phenotypic overlap between HSP and spastic ataxia. With the advent of exome sequencing, mutations in more than one gene can be identified, which may contribute to the phenotypic variation, even within a family.