A Seat Belt Injury Causing a Large Breast Hematoma: A Case Report

Seat belts with shoulder restraints have decreased the frequency of life-threatening severe chest trauma caused by car accidents. However, the introduction of seat belt legislation has led to an increase in a specific pattern of blunt trauma known as seat belt syndrome, which includes rib, clavicle, spine, and sternum fractures, as well as rupture of hollow pelvic and abdominal viscera, mesenteric tears, and major vessel injuries. The shoulder restraint part of the three-point seat belt commonly rests near or over the female and male breast. A 54-year-old female presented to our emergency department complaining of swelling and pain in her left breast immediately after a traffic accident. The patient had used a seat belt with a shoulder restraint. Bruising was noted along her chest where there had been seat belt contact. Her breast hematoma was most likely caused by breast tissue compression between her rib and the seat belt. Contrast-enhanced computed tomography demonstrated a sizable breast hematoma with active arterial contrast material extravasation, as well as multiple left rib fractures. The patient was conservatively treated with analgesic and anti-inflammatory drugs. Complete resolution was achieved, and her breast returned to its normal appearance. Although endovascular treatment and surgical hemostasis have been proposed for the treatment of breast injuries with active bleeding, conservative treatment such as compression hemostasis may be feasible

Association between emergency medical service transport time and survival in patients with traumatic cardiac arrest: a Nationwide retrospective observational study

Background Patients with traumatic cardiac arrest (TCA) are known to have poor prognoses. In 2003, the joint committee of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma proposed stopping unsuccessful cardiopulmonary resuscitation (CPR) sustained for > 15 min after TCA. However, in 2013, a specific time-limit for terminating resuscitation was dropped, due to the lack of conclusive studies or data. We aimed to define the association between emergency medical services transport time and survival to demonstrate the survival curve of TCA. Methods A retrospective review of the Japan Trauma Data Bank. Inclusion criteria were age >= 16, at least one trauma with Abbreviated Injury Scale score (AIS) >= 3, and CPR performed in a prehospital setting. Exclusion criteria were burn injury, AIS score of 6 in any region, and missing data. Estimated survival rate and risk ratio for survival were analyzed according to transport time for all patients. Analysis was also performed separately on patients with sustained TCA at arrival. Results Of 292,027 patients in the database, 5336 were included in the study with 4141 sustained TCA. Their median age was 53 years (interquartile range (IQR) 36-70), and 67.2% were male. Their median Injury Severity Score was 29 (IQR 22-41), and median transport time was 11 min (IQR 6-17). Overall survival after TCA was 4.5%; however, survival of patients with sustained TCA at arrival was only 1.2%. The estimated survival rate and risk ratio for sustained TCA rapidly decreased after 15 min of transport time, with estimated survival falling below 1%. Conclusion The chances of survival for sustained TCA declined rapidly while the patient is transported with CPR support. Time should be one reasonable factor for considering termination of resuscitation in patients with sustained TCA, although clinical signs of life, and type and severity of trauma should be taken into account clinically

MOLECULAR CONSTANTS OF SO IN THE 1Δ^{1}\Delta STATE BY A COMBINED USE OF GAS PHASE EPR AND MICROWAVE ROTATIONAL SPECTRA

Author Institution: Sagami Chemical Research CenterThe rotational transition $J=3\leftarrow 2$ of SO in the a $^{1}\Delta$ state has been detected at $127770.45\pm 0.15$ MHz with microwave spectroscopy. This is the first observation of microwave rotational transition for a molecule in an electronically excited state. The rotational constant was found to be $B_{o}=21295.1 \pm 0.7$ MHz and the dipole moment obtained was $1.336 \pm 0.045$ D. Gas-phase EPR spectroscopy at 4460 MHz in the C-band region has revealed five lines of the six allowed transitions for the rotationally excited J = 3 level of SO in the $^{1}\Delta$ state besides four lines for the J = 2 ground level. The use of the C band in place of the X band (ca. 9 GHz) conventionally employed doubles the measurable resonance region and hence enables one to determine molecular constants more precisely. The analysis of the EPR spectra has resulted in the l-uncoupling constant $\Sigma_{\Pi}/(E_{\Pi}-E_{\Delta}) =0.60 \pm 0.11\times 10^{-4}$, using the theoretical values of $g_{L} = 1,00000$ and $g_{z}^{N} = -0.00027$, as well as the rotational constant $B_{o}$ determined above, and assuming finite perturbations only from the $^{1}\Pi$ states. If only one $^{1}\Pi$ state contributes dominantly to the perturbation, the perturbing state lies $12000 cm^{-1}$ above the $^{1}\Delta$ state under pure precession hypothesis

Updates for Cardio‐Kidney Protective Effects by Angiotensin Receptor‐Neprilysin Inhibitor: Requirement for Additional Evidence of Kidney Protection

The incidence of heart failure and chronic kidney disease is increasing, and many patients develop both diseases. Angiotensin receptor‐neprilysin inhibitor (ARNI) is a promising therapeutic candidate for both diseases. ARNI has demonstrated superior cardioprotective effects compared with renin–angiotensin system inhibitors (RAS‐Is) in large clinical trials such as the PARADIGM‐HF (Prospective Comparison of ARNI With ACEI [Angiotensin‐Converting Enzyme Inhibitor] to Determine Impact on Global Mortality and Morbidity in Heart Failure) trial. It has also been suggested that ARNI can provide renoprotective effects beyond those of RAS‐Is in patients with HF. ARNI might have beneficial effects on the kidneys because of its ability to improve cardiac function in patients with heart failure and affect renal hemodynamics by enhancing the effects of hormones such as natriuretic peptide. In contrast, in the PARADIGM‐HF trial, ARNI was associated with more albuminuria compared with RAS‐I; thus, it is unclear whether long‐term ARNI therapy has renoprotective effects. Additionally, ARNI did not provide renoprotective effects beyond RAS‐I in patients with chronic kidney disease in the UK HARP‐III (United Kingdom Heart and Renal Protection‐III) trial. In other words, the patient population in which ARNI is more renoprotective than RAS‐I might be limited. Collectively, ARNI may have renoprotective effects in addition to cardioprotective effects, but the evidence to date is applicable only to heart failure. Theoretically, given the molecular mechanism of ARNI, it could also be renoprotective in conditions such as nephrosclerosis, which has low risks of albuminuria and reduced kidney perfusion, but the evidence for such effects is lacking. Further research is needed to clarify whether ARNI therapy is an acceptable treatment strategy for renal protection