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No inadvertent permanent facial nerve paralysis occurred. The median operation time was 72 min (23-211). The average patient scores of satisfaction with the surgical scar and with the surgery were 9.54 and 9.72, respectively. CONCLUSIONS Individualized mini-Blair incision is feasible for benign as well as selected malignant parotid tumors. © 2020 S. Karger AG, Basel.In hypotonic hyponatremia, which is the most common form of hyponatremia, clinical manifestations are largely due to brain swelling caused by entry of water into the cells. In acute and severe hyponatremia, dramatic symptoms, such as seizures, acute psychosis, permanent brain damage, brain-stem herniation, leading to coma and death may occur. In chronic hyponatremia, symptoms are generally less dramatic and may include headache, nausea, vomiting, gait alterations, muscle cramps, restlessness, and disorientation. It has become evident in recent years that mild forms of chronic hyponatremia may also be associated with clinical signs, if carefully investigated. Several studies also reported an increased length of stay in the hospital of patients with hyponatremia in different clinical settings, leading to increased costs. Most important, this condition has been clearly associated with a significantly increased risk of death, even when serum [Na+] is slightly reduced. On the contrary, there is convincing evidence that the mortality risk is reduced when hyponatremia improves. © 2019 S. Karger AG, Basel.Exercise-associated hyponatremia (EAH) refers to below-normal serum sodium concentrations [Na+] that develop during exercise. The pathogenesis of EAH is best described as a spectrum ranging between profound polydipsia to modest sweat sodium losses with hypovolemia and relative dilution. Non-osmotic arginine vasopressin (AVP) remains the unifying pathogenic stimulus to abnormal renal water retention in acute symptomatic EAH. Cases of hyponatremia are mostly reported after endurance sports, but are also observed after shorter duration events and in team sport athletes. The signs and symptoms of EAH are vague, and include bloating, vomiting, headache, and altered mental status. A diagnosis of EAH can only be confirmed by a blood test, whereas signs/symptoms guide the most appropriate treatment strategy. Mild-to-moderate EAH (without encephalopathy) can be treated with either fluid restriction or an oral bolus of a hypertonic saline solution. Severe EAH (with encephalopathy) is a life-threatening emergency and should be urgently treated with intravenous 100 mL boluses of 3% saline until the resolution of encephalopathy symptoms. The prevention of EAH is evolutionarily rooted in preventing overdrinking during exercise. Drinking according to the dictates of thirst is the most individualized strategy to prevent life-threatening dysnatremia during exercise, regardless of sport. © 2019 S. Karger AG, Basel.BACKGROUND/AIM Few studies have examined the details of nutritional status in patients with unresectable hepatocellular carcinoma (u-HCC) undergoing systemic chemotherapy with lenvatinib. We evaluated the prognostic/predictive value of nutritional status using Onodera's prognostic nutritional index (O-PNI) for overall survival among patients with u-HCC treated with lenvatinib. METHODS Three-hundred and seventy-five u-HCC patients treated with lenvatinib were enrolled (median age 72 years; Child-Pugh class A/B/C n = 312/60/3; BCLC stage A/B/C/D n = 2/159/212/2). We examined median survival time (MST) and time to progression (TTP) in all patients (n = 375), prognosis according to the O-PNI (high/low >40/≤40) in 298 patients with lymphocyte findings, and the prognostic/predictive values of Child-Pugh stage, albumin-bilirubin (ALBI)/modified ALBI (mALBI) grade, and O-PNI for Chemotherapy grade (OPNIC grade 1/2/3 O-PNI >40/≤40 to >36/≤36). RESULTS The MST and TTP were 16.6 and 8.0 months, respectively. The MST andrger AG, Basel.Hyponatremia is a frequent occurrence in patients with neurosurgical disorders. Acute onset hyponatremia is particularly common in patients who have any type of cerebral insult, including traumatic brain injury, subarachnoid hemorrhage, and brain tumors. Furthermore, it is a common complication of intracranial procedures. Acute hyponatremia creates an osmotic gradient between the brain and the plasma, which promotes the movement of water from the plasma into brain cells, causing cerebral edema and neurological compromise. It is therefore far more likely to be symptomatic, and to have adverse outcomes, than chronic hyponatremia. Autophagy inhibitor Uncorrected acute hyponatremia with consequent cerebral edema may manifest through impaired consciousness level, seizures, elevated intracranial pressure, and, potentially, death due to cerebral herniation. The majority of cases of hyponatremia due to neurosurgical pathology are caused by the syndrome of inappropriate antidiuresis, but acute glucocorticoid insufficiency is increasingly being recognized as an important contributing factor. In this chapter, we summarize the existing literature on the clinical features and differential diagnosis of hyponatremia in the neurosurgical patient, and briefly discuss the management options. © 2019 S. Karger AG, Basel.Heart failure (HF) represents the most common cause of hypervolemic hyponatremia in current clinical practice. The presence of hyponatremia has been independently associated with worse outcomes in this patient population. The pathogenesis of hyponatremia in HF involves complex neurohormonal and cardio-renal interactions, including an increase in non osmotic secretion of arginine vasopressin (AVP) and insufficient tubular flow in the diluting segments of the nephron. The treatment of hyponatremia in HF involves decongestant therapy with diuretics, neurohormonal blockade and in certain occasions the use of AVP antagonists. The aim of this chapter is to summarize the pathophysiology, current evidence, and management recommendations for hyponatremia in patients with HF, with a specific focus on AVP homeostasis. © 2019 S. Karger AG, Basel.INTRODUCTION The ovine model is the gold standard large animal model of myelomeningocele (MMC); however, it has a high rate of fetal loss. We reviewed our experience with the model to determine risk factors for fetal loss. METHODS We performed a retrospective review from 2009 to 2018 to identify operative factors associated with fetal loss (early fetal demise, abortion, or stillbirth). Operative risk factors included gestational age at operation, operative time, reduction of multiple gestations, amount of replaced amniotic fluid, ambient temperature, and method of delivery. RESULTS MMC defects were created in 232 lambs with an overall survival rate of 43%. Of the 128 fetuses that died, 53 (42%) had demise prior to repair, 61 (48%) aborted, and 14 (11%) were stillborn. Selective reduction of multiple gestations in the same uterine horn was associated with increased fetal demise (OR 3.03 [95% CI 1.29-7.05], p = 0.01). Later gestational age at MMC repair and Cesarean delivery were associated with decreased abortion/stillbirth (OR 0.