Search

Highlights • Femoral herniation of transplanted ureter is a rare occurrence and has not been documented in the literature to date. • Such patients may present with transplant kidney failure due to obstructive uropathy. • Diagnosis includes physical exam, transplant kidney ultrasound or CT of abdomen and pelvis. • Treatment should include urgent repair of hernia to salvage the transplant ureter and kidney., Introduction Herniation of the ureter after kidney transplant is a rare and under documented event. Many of these herniations are due to abdominal wall defects or ureteral redundancy. After an extensive review of available literature, there has not been a reported case of a femoral herniation of ureter after kidney transplant. We report a case of late allograft renal transplant failure due to ureteral obstruction secondary to femoral herniation of the ureter. Case presentation We report a case of 64 year old male with a history of kidney transplant, who was found to have an inguinal bulge. He was diagnosed with a femoral hernia containing transplant ureter using transplant kidney ultrasound and CT of the abdomen and pelvis. Subsequently he developed transplant kidney failure due to obstructive uropathy from the femoral hernia. The patient underwent a femoral hernia repair with biologic mesh. Compromised ureter was excised and a neoureterocystostomy was created. Post operatively his creatinine returned to baseline. Discussion In our literature search there are two types of inguinal ureteral hernias described. Paraperitoneal, which makes up the majority of the cases, and extraperitoneal. There are no classifications for ureteral femoral hernias. We may extract these definitions to femoral hernias, as evidenced by our case where we encountered a paraperitoneal femoral hernia containing transplant kidney ureter. Conclusion To the best of our knowledge this is the first reported case of a femoral ureter hernia. Due to its rarity in the literature, an understanding of management is critical to patient outcome.

Background In pharmacologic management of fetal supraventricular tachycardia (SVT), antiarrhythmic agents are administered to the pregnant patient serving as a vehicle of transplacental delivery to the fetus. Given that antiarrhythmic therapy can have profound maternal adverse effects, administration of initial loading and dose adjustments should involve deliberate attention to pharmacologic principles with close maternal monitoring for adverse effects. We reviewed current monitoring practices and maternal complications of transplacental antiarrhythmic therapy for fetal SVT. Methods A query of the Embase database for search terms ”Fetal” or ”Foetal” and ”Supraventricular Tachycardia” or ”SVT” yielded 93 titles, of which 19 articles detailing the modalities of therapy for Fetal SVT were reviewed. Results The 19 articles represented 565 cases of fetal SVT, 111 of which had developed hydrops fetalis. Of these cases, 184 received a course of digoxin alone and 33, 56, and 5 cases received a combination therapy of digoxin with flecainide, sotalol, or amiodarone. Flecainide, Sotalol, and amiodarone were given as monotherapy in 89, 77, and 6 cases, respectively. Maternal monitoring information was available in 15 studies. Investigators performed electrocardiograms (EKGs) at baseline and during follow-up in 12 studies, and monitored electrolytes in five. Two studies reported a mandatory cardiologist consultation for all mothers and two studies considered performing echocardiography in select mothers. Digoxin and flecainide levels were measured in eight and four studies, respectively. Toxicity was reported in 5 patients: two on digoxin monotherapy, two on flecainide monotherapy, and one on combination of digoxin and flecainide. Conclusion Pharmacologic management of fetal SVT is generally safe for mothers with normal baseline cardiac assessments and close monitoring of symptoms, EKG, electrolytes, and/or drug levels. Future prospective studies on the treatment of fetal SVT should also include a systematic monitoring strategy for mothers, with consistent reporting of adverse reactions.

Ghrelin receptors are expressed by key components of the arousal system. Exogenous ghrelin induces behavioral activation, promotes wakefulness and stimulates eating. We hypothesized that ghrelin-sensitive mechanisms play a role in the arousal system. To test this, we investigated the responsiveness of ghrelin receptor knockout (KO) mice to two natural wake-promoting stimuli. Additionally, we assessed the integrity of their homeostatic sleep-promoting system using sleep deprivation. There was no significant difference in the spontaneous sleep-wake activity between ghrelin receptor KO and wild-type (WT) mice. WT mice mounted robust arousal responses to a novel environment and food deprivation. Wakefulness increased for 6 h after cage change accompanied by increases in body temperature and locomotor activity. Ghrelin receptor KO mice completely lacked the wake and body temperature responses to new environment. When subjected to 48 h food deprivation, WT mice showed marked increases in their waking time during the dark periods of both days. Ghrelin receptor KO mice failed to mount an arousal response on the first night and wake increases were attenuated on the second day. The responsiveness to sleep deprivation did not differ between the two genotypes. These results indicate that the ghrelin-receptive mechanisms play an essential role in the function of the arousal system but not in homeostatic sleep-promoting mechanisms.