Lactic acidosis results from an acid-base balance disorder of the body due to an excess of lactic acid. It is frequently found in critically ill patients admitted to the intensive care. The most common cause is type A, found in pathologies such as cardiogenic, septic and hypovolemic shock, trauma and severe hypoxemia. The type B is less common and arises without evidence of tissue hypoperfusion or shock. Divers etiologies have been described for this type of hyperlactatemia: Grand Mal seizures, liver failure, hematologic malignancies, congenital enzyme deficiencies, thiamine deficiencies and diabetes mellitus and also alcohol abuse, which may induce a lactic acid under-use or an increased production. The authors describe a rare complication of type 1 Diabetes Mellitus (T1DM), leading to a major and persistent expression of a type B lactic acidosis during ketoacidosis.
Recently, with the advancement of techniques, endoscopic ultrasound-guided therapies have shown distinct advantages, especially in relieving benign and malignant gastric outlet obstruction (GOO), as well as in postoperative pancreaticobiliary diseases. Herein, we present five currently used approaches in endoscopic ultrasound-guided gastroenterostomy (EUS-GE) using lumenapposing biflanged metal stents (LAMS), along with several examples of LAMS-based EUS treatment of pancreaticobiliary diseases. Compared with traditional treatment methods, EUS-guided procedures have – to some degree – shown higher success rates, both technical and clinical. Moreover, EUS-guided therapies reduce the risk of multiple surgical adverse events, including delayed gastric emptying, prolonged hospital stay, increased costs, and delay in cancer treatment. Particularly in terms of postoperative pancreaticobiliary diseases, EUS-guided therapy has assumed an essential role as a treatment option in cases where traditional methods are difficult to perform. Nevertheless, EUS-guided gastrointestinal procedures are still relatively new, with some clinical failures, and additional prospective clinical trials are warranted.
High-dose colistin (COL) ensures adequate treatment of pneumonia caused by multidrug resistant gram-negative bacteria (MDR-GNB) but must be weighed against a higher risk of nephrotoxicity. Continuous veno-venous hemofiltration (CVVH) clears COL by filtering and membrane adsorption that permits to avoid dose accumulation and excessively high peak concentrations. We evaluated clinical/microbiological efficacy of the high-dose COL treatment under CVVH in patients with newly diagnosed MDR-GNB ventilator-associated pneumonia (VAP).
Observational cohort study in critically ill adult patients with MDR-GNB VAP. Colistimethate sodium (CMS) was administered as a 9 million international units (MIU) of loading dose followed by 3 × 4.5 MIU daily. CVVH was performed over a highly adsorptive membrane. Clinical and microbiological efficacies were assessed at the end of therapy. In survivors, serum creatinine level was evaluated before and at the end of therapy.
Fourteen patients (8 male patients, aged 57 ± 14 years) were consecutively included. Isolated pathogens were Pseudomonas aeruginosa in 7, Klebsiella pneumoniae in 5, and other Enterobacteriaceae in 2 patients. A favorable clinical response was observed in 9 patients (64%). Full and presumed microbiological eradication was observed in 12 patients (86%). Two patients were diagnosed with Stage 1 acute kidney injury.
In patients with MDR-GNB VAP, CVVH may represent an interesting option to enable effective high-dose COL treatment.
A young female presented to us with abdominal distension along with pedal edema. She had no prior medical or surgical history apart from a caesarean section done a few years prior. Initial workup showed low hemoglobin, low serum albumin and slight raised ESR. Her LFTs were slightly deranged. Ultrasound abdomen had evidence of portal hypertension along with splenomegaly. While ultrasound hepatic Doppler revealed a portosystemic shunt between the portal vein and the left hepatic vein, with a shunt ratio of 7.1%. CT scan abdomen confirmed these findings and a diagnosis of Type III intrahepatic portosystemic shunt and spleno-renal shunt was made. Since the patient was currently asymptomatic, she was advised regular follow-ups and was managed conservatively.
Significant rather than moderate coronary artery stenosis has been postulated to be the main substrate of plaque rupture in acute myocardial infarction (AMI). We evaluate if cavitation could influence the coronary artery plaque rupture contributing to the progression of thrombotic process.
We reconstructed a 3D model of the left anterior descending coronary artery (LAD) after reviewing the intravascular ultrasound (IVUS) data of 30 consecutive patients with mild to severe coronary artery disease.
Turbulent flow or cavitation occurs in both concentric and eccentric coronary artery stenosis (≥ 75% for the former and ≥ 50% for the latter). The analysis of vapor phase demonstrated that cavitation propagated downstream, creating microbubbles, which exploded when the fluid pressure was lower than the vapor pressure at a local thermodynamic state. The relative higher vorticity magnitude (as turbulent flow in vivo angiogram) observed on the distal cap of the atherosclerotic plaque created a higher turbulence, probably able to destabilize the plaque through a micro-erosion process.
Cavitation seems to be able to promote the thrombotic occlusion within the coronary vessels due the ‘constant injuries’ created by the micro-explosion of bubbles.
Calcium-sensing receptor (CaSR) is known to regulate hypoxia-induced pulmonary hypertension (HPH) and vascular remodeling via the phenotypic modulation of pulmonary arterial smooth muscle cells (PASMCs) in small pulmonary arteries. Moreover, autophagy is an essential modulator of VSMC phenotype. But it is not clear whether CaSR can regulate autophagy involving the phenotypic modulation under hypoxia.
The viability of human PASMCs was detected by cell cycle and BrdU. The expressions of proliferation protein, phenotypic marker protein, and autophagy protein in human PASMCs were determined by western blot.
Our results showed that hypoxia-induced autophagy was considerable at 24 h. The addition of NPS2390 decreased the expression of autophagy protein and synthetic phenotype marker protein osteopontin and increased the expression of contractile phenotype marker protein SMA-ɑ and calponin via suppressing downstream PI3K/Akt/mTOR signal pathways.
Our study demonstrates that treatment of NPS2390 was conducive to inhibit the proliferation and reverse phenotypic modulation of PASMCs by regulating autophagy levels.