Extremely Preterm (23 Weeks) Vaginal Cephalic Delivery En Caul and Subsequent Postpartum Intraventricular Hemorrhage and Respiratory Distress: A Teaching Case.

En caul deliveries are defined as a fetus that is delivered completely contained within an amniotic sac and are considered to be less common than 1 in 80,000 live births. Vaginal en caul births compared to abdominal or cesarean are the rarest subtype. Most en caul births are associated with prematurity and low gravida. The combination of prematurity, high gravida, vaginal en caul birth, and severe postpartum complications has not previously been described. We report a woman with gravida of 12 delivering vaginally a neonate female en caul at the extremely preterm gestational age of 23 weeks. The neonate subsequently decompensated, underwent respiratory distress, and was diagnosed with a bilateral intraventricular hemorrhage. Owing to deteriorating status, supportive care was removed and the infant was pronounced dead 5 days after delivery

Acute carotid thrombosis and ischemic stroke following overdose of the synthetic cannabinoid K2 in a previously healthy young adult male

With the popularity of synthetic cannabinoid street drugs such as “K2 and Spice,” a number of serious neurologic adverse events are coming to light. This case is a 36-year-old African American man, with no significant medical history, who presented with extensive left cervical and intracranial internal carotid artery occlusion and subsequent ischemic stroke. The patient endorsed smoking K2—a synthetic cannabinoid (SC) with structural similarity to cannabis. The mechanism by which SC abuse induces a prothrombotic state leading to ischemic neurovascular sequelae is currently unclear, although a temporal association in the absence of other stroke risk factors suggests a causal relationship. Our case highlights the need for emergent neuroimaging upon suspected SC overdose. Practitioners should be vigilant in recognizing that ischemic stroke and unexplained neurologic deficit can arise after SC abuse, especially in younger populations with few stroke risk factors and who are prone to chronic cannabis use. Keywords: Synthetic cannabinoid, K2, Thrombosis, Stroke, CV

Relationships Between Serum and Urine Phosphorus With All-Cause and Cardiovascular Mortality: The Osteoporotic Fractures in Men (MrOS) Study

BACKGROUND: Serum phosphorus is associated with cardiovascular disease (CVD) in the general population but may not comprehensively reflect phosphorus homeostasis. Whether urine phosphorus/creatinine ratio (UPi/UCr, a marker of intestinal absorption) or urine fractional excretion of phosphorus (FePi, a marker of urinary phosphorus handling) is associated with risk of mortality or CVD is uncertain. STUDY DESIGN: Prospective observational study. SETTING AND PARTICIPANTS: 1,325 community-dwelling men aged ≥65 years. PREDICTORS: Serum phosphorus, UPi/UCr, and FePi. OUTCOMES: All-cause and CVD death. RESULTS: Mean age was 74±6 years, eGFR was 75±16 ml/min/1.73m(2), and serum phosphorus was 3.2±0.4 mg/dL. During 9.3 years median follow-up, there were 364 deaths (120 CVD deaths). After adjustment for demographics, CVD risk factors, and kidney function, the risks of all-cause death in the highest quartiles of serum phosphorus (≥3.6 mg/dL), UPi/UCr, and FePi were 1.63 (95% CI 1.23-2.17), 1.22 (95% CI 0.90-1.65), and 0.88 (95% CI 0.64-1.23), respectively. Results were similar for CVD death. Results were also similar irrespective of eGFR above or below 60 ml/min/1.73m(2). LIMITATIONS: Older, all male cohort. Few had advanced CKD. Specimens were collected in the morning after an overnight fast. CONCLUSIONS: In community-living older men, higher serum phosphorus is associated with all-cause and CVD death. In contrast, UPi/UCr and FePi were not. These findings do not support using UPi/UCr or FePi as adjuvant measures to predict risk of mortality or CVD in the general population

The sodium chloride cotransporter SLC12A3: new roles in sodium, potassium, and blood pressure regulation

SLC12A3 encodes the thiazide-sensitive sodium chloride cotransporter (NCC), which is primarily expressed in the kidney, but also in intestine and bone. In the kidney, NCC is located in the apical plasma membrane of epithelial cells in the distal convoluted tubule. Although NCC reabsorbs only 5 to 10 % of filtered sodium, it is important for the fine-tuning of renal sodium excretion in response to various hormonal and non-hormonal stimuli. Several new roles for NCC in the regulation of sodium, potassium, and blood pressure have been unraveled recently. For example, the recent discoveries that NCC is activated by angiotensin II but inhibited by dietary potassium shed light on how the kidney handles sodium during hypovolemia (high angiotensin II) and hyperkalemia. The additive effect of angiotensin II and aldosterone maximizes sodium reabsorption during hypovolemia, whereas the inhibitory effect of potassium on NCC increases delivery of sodium to the potassium-secreting portion of the nephron. In addition, great steps have been made in unraveling the molecular machinery that controls NCC. This complex network consists of kinases and ubiquitinases, including WNKs, SGK1, SPAK, Nedd4-2, Cullin-3, and Kelch-like 3. The pathophysiological significance of this network is illustrated by the fact that modification of each individual protein in the network changes NCC activity and results in salt-dependent hypotension or hypertension. This review aims to summarize these new insights in an integrated manner while identifying unanswered questions