A pilot study to standardize and peer-review shift handoffs in an academic internal medicine residency program: The DOCFISH method.

With increased oversight of residency work hours, there has been an increase in shift handoffs, which are prone to medical errors. To date, there are no evidence-based recommendations on essential elements of shift handoffs. We implemented a standardized shift-handoff rubric at an academic medicine residency program. Compliance, resident/faculty perceptions, and surrogate markers of patient safety were measured.Shift-handoff documents were collected January-February 2016 (control) April-June 2016 (intervention). Signouts were scored based on inclusion of seven elements: Daily events, Overnight events, Code status, Follow up tasks, If/then statements, 'sick or stable' and History present illness. The mnemonic 'DOCFISH' was taught in a grand-rounds forum then embedded into a shift-handoff tool within our electronic health record (EHR). Senior residents were assigned to supervise/provide feedback on shift handoffs from April-June 2016. Faculty and resident perceptions regarding quality of shift handoffs was measured by the annual ACGME (Accreditation Council Graduate Medical Education) program survey.Patient safety was measured by number of rapid-response teams (RRT) initiated for unstable vital signs. Handoffs were 74% complete in intervention group and 60% in control group (p < .0001). Median DOCFISH features present in patients that required RRT was 3 of 7 whereas, total post-intervention group had 5 of 7 (p < .001). 'Daily events' and 'follow -up tasks' were less frequent in patients that required RRT (20%, 67% respectively, p < .001).Academic medical centers can implement standardized shift handoffs by embedding high-yield information in an EHR with peer-review. Information during shift changes that may have significant improvement on patient safety includes: 'daily events' and 'follow -up tasks.'

Expression of TPM1κ, a Novel Sarcomeric Isoform of the TPM1 Gene, in Mouse Heart and Skeletal Muscle.

We have investigated the expression of TPM1 α and TPM1 κ in mouse striated muscles. TPM1 α and TMP1 κ were amplified from the cDNA of mouse heart by using conventional RT-PCR. We have cloned the PCR amplified DNA and determined the nucleotide sequences. Deduced amino acid sequences show that there are three amino acid changes in mouse exon 2a when compared with the human TPM1 κ . However, the deduced amino acid sequences of human TPM1 α and mouse TPM1 α are identical. Conventional RT-PCR data as well as qRT-PCR data, calculating both absolute copy number and relative expression, revealed that the expression of TPM1 κ is significantly lower compared to TPM1 α in both mouse heart and skeletal muscle. It was also found that the expression level of TPM1 κ transcripts in mouse heart is higher than it is in skeletal muscle. To the best of our knowledge, this is the first report of the expression of TPM1 κ in mammalian skeletal muscle.