Delayed Iatrogenic Intracranial Hypotension After Thoracotomy.

We report a case of intracranial hypotension (IH) after thoracotomy. A 56-year-old woman presented 10 days after a left upper lobectomy with severe headache due to pneumocephalus and pneumorrhachis, which resolved on conservative treatment. Two months later, the patient was readmitted in an unconscious state with characteristics of IH and "sagging brain." Subsequent magnetic resonance imaging revealed a fistula at the level of the left Th5 pedicle. The patient underwent operation with closure of the fistula and recovered without complications. The presence of pneumocephalus and pneumorrhachis after thoracotomy should raise the suspicion of a persistent subarachnoid-pleural fistula to prevent IH and "sagging brain."

Duration of acute kidney injury in critically ill patients.

BACKGROUND: Duration of acute kidney injury (AKI) has been recognized a risk factor for adverse outcomes following AKI. We sought to examine the relationship of AKI duration and recurrent AKI with short-term outcomes in critically ill patients who were mechanically ventilated and met criteria for the acute respiratory distress syndrome. METHODS: Participants in the NHLBI ARDS Network SAILS multicenter trial who developed AKI were included in this analysis and divided into groups based on AKI duration. Differences in outcomes were evaluated using t test and Chi-square test. Competing risks regression and Cox regression were used to evaluate factors associated with resolving AKI and recurrent AKI. RESULTS: In total, 238 patients were included in the study. Seventy-seven patients had short duration AKI (1-2 days), 47 medium duration AKI (3-7 days), 87 persistent AKI (> 7 days) and 38 died during their AKI episode. Persistent AKI was associated with worse outcomes including increased ICU length of stay, time on the ventilator and days with cardiovascular failure. We found no clinical differences between patients with short and medium duration AKI, even when accounting for AKI severity and recurrent AKI. Patients with resolving AKI were less likely to have oliguria or moderate/severe ARDS on the day AKI criteria were met. Recurrent AKI was associated with poorer clinical outcomes. No baseline clinical factors were found to predict development of recurrent AKI. CONCLUSIONS: In critically ill patients with sepsis-associated ARDS and AKI, the impact of short and medium duration AKI on clinical outcomes was modest. Persistent and recurrent AKI were both associated with worse clinical outcomes, emphasizing the importance of identifying these patients, who may benefit from novel interventions.

The Apolipoprotein M/S1P Axis Controls Triglyceride Metabolism and Brown Fat Activity.

Apolipoprotein M (apoM) is the carrier of sphingosine-1-phosphate (S1P) in plasma high-density lipoproteins. S1P is a bioactive lipid interacting with five receptors (S1P1-5). We show that lack of apoM in mice increases the amount of brown adipose tissue (BAT), accelerates the clearance of postprandial triglycerides, and protects against diet-induced obesity (i.e., a phenotype similar to that induced by cold exposure or ß3-adrenergic stimulation). Moreover, the data suggest that the phenotype of apoM-deficient mice is S1P dependent and reflects diminished S1P1 stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.

[Limited evidence for monitoring and treatment of hypophosphataemia in critically ill patients]. / Begrænset evidens for monitorering og behandling af fosfatmangel hos kritisk syge patienter

Hypophosphataemia is a potentially hazardous metabolic disturbance which is common in critically ill patients. The condition is reported to be associated with severe complications and increased mortality. It is unknown, whether hypophosphataemia has a causal effect or reflects the severity of illness. There are no randomized clinical trials to support treatment of hypophosphataemia with intravenous phosphate substitution, which has resulted in large variations in monitoring and treatment of hypophosphataemia in the intensive care unit.