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acidosis metabolic [keywords]
- Hypertriglyceridemia, Lipemia, and Elevated Liver Enzymes Associated With Prolonged Propofol Anesthesia for Craniotomy. [JOURNAL ARTICLE]
- Ther Drug Monit 2014 Oct; 36(5):556-559.
: Lipemic blood was noted in the surgical field by a neurosurgeon after 12.5 hours of anesthesia consisting of infusions of propofol (total dose, 14,956 mcg) and remifentanil (total dose, 25,091 mcg). For most of that time, the rate of propofol was 120-160 mcg·kg·min and never exceeded 160 mcg·kg·min. Lipemia was confirmed by allowing a sample of the patient's blood to settle in a syringe. The triglyceride concentration was 15.8 mmol/L. There was no metabolic acidosis or other indications of propofol infusion syndrome. Postoperatively, liver enzymes were elevated (peak aspartate aminotransferase, 420 units/L) but returned to nearly normal within 5 days. The patient recovered from surgery uneventfully. Reports of intraoperative lipemia during propofol anesthesia are very rare but raise concerns about the safety of prolonged propofol infusion.
- Lactic Acidosis as an Early Side Effect of Linezolid Therapy in Pediatric Patients. [JOURNAL ARTICLE]
- Pediatr Infect Dis J 2014 Aug; 33(8):890-891.
- A Case of Chronic Ethylene Glycol Intoxication Presenting without Classic Metabolic Derangements. [Journal Article]
- Case Rep Nephrol 2014.:128145.
Acute ethylene glycol ingestion classically presents with high anion gap acidosis, elevated osmolar gap, altered mental status, and acute renal failure. However, chronic ingestion of ethylene glycol is a challenging diagnosis that can present as acute kidney injury with subtle physical findings and without the classic metabolic derangements. We present a case of chronic ethylene glycol ingestion in a patient who presented with acute kidney injury and repeated denials of an exposure history. Kidney biopsy was critical to the elucidation of the cause of his worsening renal function.
- Acid-base disturbances in intensive care patients: etiology, pathophysiology and treatment. [REVIEW]
- Nephrol Dial Transplant 2014 Sep 11.
Acid-base disturbances are very common in critically ill and injured patients as well as contribute significantly to morbidity and mortality. An understanding of the pathophysiology of these disorders is vital to their proper management. This review will discuss the etiology, pathophysiology and treatment of acid-base disturbances in intensive care patients-with particular attention to evidence from recent studies examining the effects of fluid resuscitation on acid-base and its consequences.
- How an extended Perinatal Audit may improve Perinatal Policy. [JOURNAL ARTICLE]
- J Matern Fetal Neonatal Med 2014 Sep 12.:1-19.
Abstract Objective: A perinatal audit has the intention of quality of care improvement based on analysis of perinatal death, with our without analysis of maternal morbidity and/or mortality. Additional analysis of cases of intrapartum asphyxia could provide more insight into ways to improve quality of perinatal care. Methods: Analysis of cases of perinatal death and asphyxia in Jan Yperman Hospital, Ieper, Belgium, in 2012. Results: Three perinatal deaths occurred, none were preventable. Nineteen cases of proven metabolic acidosis have been identified. Three cases are considered possibly preventable, four cases are considered preventable. In three (possibly) preventable cases, fetal monitoring was absent during the active second stage of labour. In two preventable cases, intervention following a significant ST event in the second stage of labour was delayed. In one case intervention was delayed in the first stage of labour, while in another, indicated operative delivery in the second stage wasn't conducted. Conclusions: Integrating intrapartum asphyxia in the perinatal audit gives an opportunity to identify and eliminate weak points in the perinatal care chain, thereby optimizing quality of care. Lessons learned from our internal audit are the value of fetal monitoring and adequate action on significant ST events during second stage of labour.
- Dichloroacetate enhances apoptotic cell death via oxidative damage and attenuates lactate production in metformin-treated breast cancer cells. [JOURNAL ARTICLE]
- Breast Cancer Res Treat 2014 Sep 12.
The unique metabolism of breast cancer cells provides interest in exploiting this phenomenon therapeutically. Metformin, a promising breast cancer therapeutic, targets complex I of the electron transport chain leading to an accumulation of reactive oxygen species (ROS) that eventually lead to cell death. Inhibition of complex I leads to lactate production, a metabolic byproduct already highly produced by reprogrammed cancer cells and associated with a poor prognosis. While metformin remains a promising cancer therapeutic, we sought a complementary agent to increase apoptotic promoting effects of metformin while attenuating lactate production possibly leading to greatly improved efficacy. Dichloroacetate (DCA) is a well-established drug used in the treatment of lactic acidosis which functions through inhibition of pyruvate dehydrogenase kinase (PDK) promoting mitochondrial metabolism. Our purpose was to examine the synergy and mechanisms by which these two drugs kill breast cancer cells. Cell lines were subjected to the indicated treatments and analyzed for cell death and various aspects of metabolism. Cell death and ROS production were analyzed using flow cytometry, Western blot analysis, and cell counting methods. Images of cells were taken with phase contrast microscopy or confocal microscopy. Metabolism of cells was analyzed using the Seahorse XF24 analyzer, lactate assays, and pH analysis. We show that when DCA and metformin are used in combination, synergistic induction of apoptosis of breast cancer cells occurs. Metformin-induced oxidative damage is enhanced by DCA through PDK1 inhibition which also diminishes metformin promoted lactate production. We demonstrate that DCA and metformin combine to synergistically induce caspase-dependent apoptosis involving oxidative damage with simultaneous attenuation of metformin promoted lactate production. Innovative combinations such as metformin and DCA show promise in expanding breast cancer therapies.
- Differential uptake of Tc-99m DMSA and Tc-99m EC in renal tubular disorders: Report of two cases and review of the literature. [Journal Article]
- Indian J Nucl Med 2014 Jul; 29(3):160-2.
Tc-99m DMSA and Tc-99m EC studies are invaluable functional imaging modalities for renal structural and functional assessment. Normally, the relative renal function estimated by the two methods correlates well with each other. We here present two patients with renal tubular acidosis who showed impaired/altered DMSA uptake with normal EC renal dynamic study depicting the pitfall of DMSA imaging in tubular disorders. The two presented cases also depict distinct pattern of Tc-99m DMSA scintigraphic findings in patients with proximal and distal renal tubular acidosis, thus highlighting the factors affecting DMSA kinetics.
- Effects of metabolic acidosis on intracellular pH responses in multiple cell types. [JOURNAL ARTICLE]
- Am J Physiol Regul Integr Comp Physiol 2014 Sep 10.
Metabolic acidosis (MAc), a decrease in extracellular pH (pHo) caused by a decrease in [HCO3 (-)]o at a fixed [CO2]o, is a common clinical condition and causes intracellular pH (pHi) to fall. Although previous work suggests that MAc-induced decreases in pHi (ΔpHi) differ among cell types, what is not clear is the extent to which these differences are the result of the wide variety of methodologies employed by various investigators. In the present study, we evaluate effects of two sequential MAc challenges (MAc1 and MAc2) on pHi in 10 cell types/lines: primary-cultured hippocampal (HCN) neurons and astrocytes (HCA), primary-cultured medullary-raphé (MRN) neurons and astrocytes (MRA), CT26 colon cancer, the C2C12 skeletal muscles, primary-cultured bone marrow-derived macrophages (BMDM) and dendritic cells (BMDC), Ink4a/ARF-null melanocytes, and XB-2 keratinocytes. We monitor pHi using ratiometric fluorescence imaging of 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein while imposing MAc: lowering (pHo) from 7.4 to 7.2 by decreasing [HCO3 (-)]o from 22 to 14 mM at 5% CO2 for 7 min. After MAc1, we return cells to the control solution for 10 min and impose MAc2. Using our definition of MAc resistance [(ΔpHi/ΔpHo)≤40%], during MAc1, ~70% of CT26 and ~50% of C2C12 are MAc resistant, whereas the other cell types are predominantly MAc sensitive. During MAc2, some cells adapt [(ΔpHi/ΔpHo)2 < (ΔpHi/ΔpHo)1], particularly HCA, C2C12, and BMDC. Most maintain consistent responses [(ΔpHi/ΔpHo)2 ≈ (ΔpHi/ΔpHo)1], and a few decompensate [(ΔpHi/ΔpHo)2 > (ΔpHi/ΔpHo)1], particularly HCN, C2C12, and XB-2. Thus, responses to twin MAc challenges depend both on the individual cell and cell type.
- Update on volume therapy in obstetrics. [REVIEW]
- Best Pract Res Clin Anaesthesiol 2014 Sep; 28(3):297-303.
Symptomatic hypotension (maternal nausea, vomiting, dizziness and dyspnoea) during spinal anaesthesia for caesarean delivery remains a prevalent clinical problem. Severe and sustained hypotension can lead to impairment of uteroplacental perfusion, foetal hypoxia, acidosis, neonatal depression and further adverse maternal outcomes of unconsciousness, pulmonary aspiration, apnoea and cardiac arrest. Mechanical methods aimed at countering the effects of aortocaval compression do not reliably prevent maternal hypotension. Intravenous crystalloid preloading (given prior to administration of spinal anaesthesia) has poor efficacy, and focus has changed towards decreased use of crystalloid preload and ephedrine, to increased use of coload (given at the time of spinal administration) with colloids or crystalloids, and early use of phenylephrine. The recent multicentre, randomised, double-blinded CAESAR trial demonstrated the efficacy of a mixed 500 ml 6% hydroxyethyl starch (HES) 130/0.4 + 500 ml Ringer's lactate (RL) preload in significantly reducing hypotension, compared to a 1-l RL preload, without adverse effects on coagulation and neonatal outcomes in healthy parturients undergoing caesarean delivery under spinal anaesthesia.
- What's new in volume therapy in the intensive care unit? [REVIEW]
- Best Pract Res Clin Anaesthesiol 2014 Sep; 28(3):275-283.
The administration of intravenous fluid to critically ill patients is one of the most common but also one of the most fiercely debated interventions in intensive care medicine. During the past decade, a number of important studies have been published which provide clinicians with improved knowledge regarding the timing, the type and the amount of fluid they should give to their critically ill patients. However, despite the fact that many thousands of patients have been enrolled in these trials of alternative fluid strategies, consensus remains elusive and practice is widely variable. Early adequate resuscitation of patients in shock followed by a restrictive strategy may be associated with better outcomes. Colloids such as modern hydroxyethyl starch are more effective than crystalloids in early resuscitation of patients in shock, and are safe when administered during surgery. However, these colloids may not be beneficial later in the course of intensive care treatment and should best be avoided in intensive care patients who have a high risk of developing acute kidney injury. Albumin has no clear benefit over saline and is associated with increased mortality in neurotrauma patients. Balanced fluids reduce the risk of hyperchloraemic acidosis and possibly kidney injury. The use of hypertonic fluids in patients with sepsis and acute lung injury warrants further investigation and should be considered experimental at this stage. Fluid therapy impacts relevant patient-related outcomes. Clinicians should adopt an individualized strategy based on the clinical scenario and best available evidence. One size does not fit all.