BackgroundNutrition has been widely recognized to influence the risk of kidney stone formation. Therefore the aim of our study was to assess: a) whether usual diet of women with idiopathic calcium nephrolithiasis (ICN) living in Parma (Northern-Italy) is different compared to healthy controls, b) how their diet differs from Italian National guidelines and c) whether it is related to nephrolithiasis clinical course.Methods143 women with recurrent ICN (mean age 43 ± 13 ys) and 170 healthy women (mean age 42 ± 11 ys) were enrolled. All women completed a food frequency questionnaire for the last 60-days and a 3-day dietary diary analysed with a dedicated software.ResultsStone formers showed a higher consumption of sausages, ham, meat and sweets than healthy controls (43.1% vs 11.1%, 29.4% vs 13.9%, 21.6% vs 4.2%, 66.7% vs 18.1%, p < 0.001). The 3-day diary analysis showed an intake of calories, carbohydrates, lipids and non-discretionary sodium about 10% higher than healthy controls (p < 0.001). Finally, after dividing the population into 3 age groups (≤30, 31-40, > 40 years), the differences described above were amplified in the class ≤30 years, where nephrolithiasis presented a more serious course (shorter recurrence interval, greater stone-rate). In this age group the intake of fruit and vegetables was notably lower than guideline recommendations.ConclusionsWe conclude that the usual diet of women with recurrent ICN is different from controls and characterized by low intake of fruits and vegetables and higher consumption of simple sugars and foods with high protein and salt content. This dietary imbalance could play a role in the ICN pathogenesis, especially in younger women.This work was financed by grants from Italian Ministry of University and Research as part of a larger project about the prevention of kidney stones (PRIN 2005063822) and by Fondazione per la Ricerca Scientifica Termale (FoRST). No potential conflict of interest relevant to this paper was reported.

SummaryBackground and objectives Obesity is associated with a higher risk of nephrolithiasis. However, it is not known whether higher body fat mass or abnormal fat distribution influences stone risk independent of dietary factors.Design, setting, participants, & measurements In this cross-sectional study, non-stone-forming men with no known kidney disease and with a wide range of body weight collected a 24-hour urine specimen while consuming a fixed metabolic diet. They underwent dual-energy x-ray absorptiometry to assess body composition and fat distribution. Urinary risk factors for nephrolithiasis and urine saturation with respect to calcium oxalate and uric acid (assessed as supersaturation index [SI]) were correlated with various measures of adiposity.Results Study participants included 21 men with a mean age of 52.1 years, mean weight of 91.1 kg, and mean total fat mass of 24.3 kg. Twenty-four-hour urine pH and SI uric acid were more closely correlated with fat mass than with lean mass or total body weight. Both 24-hour urine pH and SI uric acid were also significantly correlated with truncal fat mass but not with leg fat mass. Moreover, there was a significant negative correlation between truncal/leg fat mass and NH 4 + /net acid excretion ratio (R=20.62; P=0.009). However, there was no significant association between SI calcium oxalate and body weight, lean mass, fat mass, trunk fat mass, or leg fat mass. ConclusionsThe association between 24-hour urine pH and SI uric acid and various measures of adiposity suggest that total body fat and trunk fat are more strongly associated with risk factors for uric acid stone formation than are total body weight and lean body mass. Under a controlled metabolic diet, adiposity is not associated with risk factors for calcium oxalate stones. Further studies are needed to confirm these findings in larger populations that include women and patients who form stones.

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The neuroleptic malignant syndrome (NMS) is an uncommon, but potentially fatal adverse event of neuroleptic medications, mainly described in polytherapy psychiatric patients.Although initially described mostly with typical neuroleptics, many atypical ones have also been associated with this syndrome more recently.An NMS is neither dose dependent nor related to the duration of the therapy. The recognized risk factors are: dehydration, stress, concomitant use of lithium, anticholinergic agents or some antidepressants. A very important and dangerous NMS complication is acute renal failure.We report an unusual case of NMS, in the absence of concomitant schizoaffective disorders.Mr. G, an otherwise healthy 86-year-old man was admitted to our department for acute nocturnal onset dyspnea.On admission, he was alert and cooperative, afebrile, tachycardic (110 beats per min), and tachypnoic (25 breaths/ min); the blood pressure was 160/110 mmHg, The BNP was high (3,029 pg/ml), serum creatinine was 1.6 mg/dl. Physical examination revealed a 4/6 systolic murmur and pulmonary rales.The patient denied any pharmacologic therapy, except from taking antihypertensive medication (ramipril).The chest X-ray study showed pulmonary oedema, and diuretic therapy was rapidly started, resulting in prompt resolution of the clinical picture. The day after, an echocardiogram revealed global hypokinesia with an ejection fraction of 40% and a severe aortic stenosis.During hospitalisation the patient developed sudden psychomotor agitation and was treated with 40 mg of intramuscular clotiapin. He had no documented history of psychiatric disorders, although occasional nocturnal altered sensorium episodes were reported by his wife.A psychiatrist was consulted, who prescribed oral olanzapine 2.5 mg by mouth for the first day, and up to 5 mg from the second day on.Within 2 days of the onset of neuroleptic therapy, the patient developed drowsiness and fever, labile blood pressure control, followed by muscle rigidity, oliguria with a urine output of 200 ml/day and acute renal failure, with consensual increase of creatine kinases, myoglobin levels and myoglobinuria (Fig. 1).Laboratory results showed an elevated white blood cell count (14,000/mm 3 ), increased serum creatinine (5.4 mg/dl), abnormal BUN (100 mg/dl), elevated creatine kinase (4,559 U/l), increased serum myoglobin (3,512 mg/ml) and myoglobinuria (1,200 ng/ml).An NMS presenting with acute renal failure was then hypothesized and olanzapine immediately stopped, along with forced hydration and urine alkalinization. These measures rapidly solved the acute renal failure (serum creatinine 1.5 mg/dl at discharge), but rigidity and altered sensorium persisted until discharge.Other possible causes of this clinical picture were excluded by urine culture, blood culture, chest X-ray study, EEG and brain CT, all of which were normal.Many cases of NMS due to typical neuroleptics have been described so far, whereas cases of NMS related to the

Cement extravasation is a rather common complication of vertebroplasty, which can be observed in up to 30-40% of patients undergoing this procedure, further associated with venous leakage occurring in up to 24% of cases. Pulmonary embolism may eventually develop once the cement migrates within the pulmonary artery, and is the most common complication of cement extravasation (involving ~4.6% of patients). Intra-cardiac cement embolism is considerably less frequent, but is a potentially fatal complication, mostly managed with cardiac surgery. We describe here a rare case of near-fatal cardiac cement embolism, with a large fragment perforating the right ventricle and reaching the pericardium, who presented to the Emergency Department (ED) for syncope. The patient, who displayed this severe complication after a vertebroplasty procedure performed for osteoporotic compression fracture, needed cardiac surgery.

Post-traumatic haemorrhage is the leading cause of death in trauma patients. The development of coagulopathy substantially contributes to bleeding severity and to the ensuing unfavourable outcome. Trauma-induced coagulopathy (TIC) can be seen in 10-25% of patients with major trauma, and its early and appropriate therapeutic management leads to considerable reduction of mortality risk. Due to the extreme complexity of TIC pathophysiology, the limitations of conventional coagulation tests (CCTs) have become evident in recent years. Unlike these routine tests, point of care viscoelastic tests (VET) such as thromboelastogram (TEG) or rotational thromboelastography (ROTEM) provide valuable clinical information by real time assessment of changes in viscoelastic properties of blood throughout clot formation. This review was aimed to collect and discuss available evidence on goal-directed hemostatic resuscitation, based on TEG or ROTEM data. We included studies with patients aged 18 years or older, major trauma, and needing massive transfusions. Overall, 6 studies totalling 1533 patients were finally included. A total number of 288 patients died, 98 of whom in the TEG- or ROTEM-guided cohorts (i.e., intervention groups). A 36% reduction of death was observed in the intervention groups (relative risk, 0.641; 95% CI 0.517-0.795; P<0.001). Our results show that VET-guided management is effective to reduce mortality compared to conventional management with CCTs. Except for mortality, all others endpoints were heterogeneous across the studies. This emphasize the need of scheduling new and well-designed trials, aimed to better define the optimal strategy for TIC management.

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The authors report neuropsychological and PET data for a patient in the acute (early recovery) phase of a period of transient global amnesia (TGA). The PET scan revealed a reduction in cerebral blood flow and oxygen consumption over the entire right lateral frontal cortex, with some ipsilateral thalamic and lentiform nucleus metabolism but sparing of the hippocampal area. Three months post TGA this had resolved. It is suggested that right prefrontal metabolic depression may be the underlying mechanisni for the TGA seen in this patient. This explanation is consistent with the emerging involvement of the prefrontal cortex in strategies or control of memory trace retrieval. The authors conclude that TGA may be a core syndrome with several possible foci of dysfunction along the neuronal networks that subserve explicit memory. 0 Right prefrontal metabolic depression, perhaps secondary to thalamic dysfunction. may be the underlying mechanism for TGA in this case. 0 TGA may be a core syndrome with several possible foci of dysfunction along the neuronal networks that subserve explicit memory. AbstractSPECT and neuropsychological tests are reported for a patient during an attack of transient global amnesia (TGA) as well as at two days and seven weeks after the attack. During the attack the patient experienced profound anterograde amnesia but limited remote memory loss. The most dramatic impairment was a deficit in personal episodic memory. Personal and general semantic information, however, were less impaired. After the attack the patient's anterograde and retrograde memory had returned to normal. A SPECT scan during TGA revealed a bilateral focal reduction in cerebral perfusion in the postero-medial-temporal lobes. This had resolved after seven weeks.