Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
acidosis metabolic [keywords]
- 2014 Military Supplement: Comparison of Noninvasive pH and Blood Lactate as Predictors of Mortality in a Swine Hemorrhagic Shock with Restricted Volume Resuscitation Model. [JOURNAL ARTICLE]
- Shock 2014 Dec 18.
Recent clinical studies have demonstrated that high blood lactate in the pre-hospital setting and poor lactate clearance in the ED are predictive of in-hospital mortality. This analysis of data collected from a swine model of hemorrhage and restricted volume resuscitation, investigated the hypotheses that noninvasive muscle pH (pHm) and H clearance would predict mortality and the responses would be similar between pHm and lactate. Data from a set of 57 swine were analyzed over the first 2 hours after controlled hemorrhage and uncontrolled splenic bleeding. Surviving animals were ones that lived for the full 5 hour experimental period. Venous lactate was determined at baseline, shock, and 30, 60 and 120min after injury. Spectra were collected continuously from the posterior thigh using a prototype CareGuide 1100 Oximeter and pHm calculated from the spectra; H concentration was determined from pHm. Lactate clearance rate was calculated from the difference in lactate concentration at 120min and shock and H clearance was calculated in a similar manner. Comparison of the area under the ROC curves was used to compare prediction of survival at 5 hours after injury. At 120min after injury, lactate, lactate clearance, noninvasive pHm, and noninvasive H clearance were equivalent predictors of mortality each with an ROC area under the curve of 0.87. Thresholds for single lactate (<3.8 mmol/L) or pHm (>7.30) determinations were found to be consistent with a resuscitation goal targeted to reverse acidosis. Continuous, noninvasive pHm monitoring may provide a substitute for lactate measurement in trauma patients, particularly in the pre-hospital and ED settings.
- Functional outcome of supratrigonal cystectomy and augmentation ileocystoplasty in adult patients with refractory neurogenic lower urinary tract dysfunction. [JOURNAL ARTICLE]
- Neurourol Urodyn 2014 Dec 18.
To investigate the functional outcome after supratrigonal cystectomy and augmentation ileocystoplasty in adult patients with refractory neurogenic lower urinary tract dysfunction (NLUTD).Retrospective follow-up investigation in a single spinal cord injury rehabilitation center. In 29 patients, urodynamic data before and after supratrigonal cystectomy and augmentation ileocystoplasty, clinical outcome and post-operative complications were evaluated.The median age of the 29 patients at the time of surgery was 31 years, a median 14 years after NLUTD had occurred. At the last follow-up visit (median 2.4, range 0.4-9.0 years post-operatively), 20/29 patients (69%) were continent compared to 2/29 pre-operatively (P = 0.001). Furthermore, 16 patients required no or less detrusor relaxation therapy after augmentation ileocystoplasty. Augmentation cystoplasty resulted in a significant (P = 0.001) increase in the median bladder capacity (from 240 ml to 500 ml) and compliance (from 13 ml/cm H2 O to 50 ml/cm H2 O). The median maximum detrusor pressure had decreased significantly (P = 0.001) from 38 cm H2 O to 15 cm H2 O. Significantly (P = 0.001) fewer patients presented with a risk for renal damage (1 vs. 15 with maximum detrusor pressure >40 cm H2 O and 1 vs. 12 with detrusor compliance <20 ml/cm H2 O) at the last follow-up. The following complications were observed in 11/29 (38%) patients: paralytic and obstructive ileus, impaired bowel function, bladder stones, dehiscence, metabolic acidosis and autonomic dysreflexia.Protection of renal function, adequate bladder capacity and low detrusor pressure can be achieved using supratrigonal cystectomy and augmentation ileocystoplasty in patients suffering from refractory NLUTD. Neurourol. Urodynam. © 2014 Wiley Periodicals, Inc.
- Impaired expression of key molecules of ammoniagenesis underlies renal acidosis in a rat model of chronic kidney disease. [JOURNAL ARTICLE]
- Nephrol Dial Transplant 2014 Dec 18.
Advanced chronic kidney disease (CKD) is associated with the development of renal metabolic acidosis. Metabolic acidosis per se may represent a trigger for progression of CKD. Renal acidosis of CKD is characterized by low urinary ammonium excretion with preserved urinary acidification indicating a defect in renal ammoniagenesis, ammonia excretion or both. The underlying molecular mechanisms, however, have not been addressed to date.We examined the Han:SPRD rat model and used a combination of metabolic studies, mRNA and protein analysis of renal molecules involved in acid-base handling.We demonstrate that rats with reduced kidney function as evident from lower creatinine clearance, lower haematocrit, higher plasma blood urea nitrogen, creatinine, phosphate and potassium had metabolic acidosis that could be aggravated by HCl acid loading. Urinary ammonium excretion was highly reduced whereas urinary pH was more acidic in CKD compared with control animals. The abundance of key enzymes and transporters of proximal tubular ammoniagenesis (phosphate-dependent glutaminase, PEPCK and SNAT3) and bicarbonate transport (NBCe1) was reduced in CKD compared with control animals. In the collecting duct, normal expression of the B1 H(+)-ATPase subunit is in agreement with low urinary pH. In contrast, the RhCG ammonia transporter, critical for the final secretion of ammonia into urine was strongly down-regulated in CKD animals.In the Han:SPRD rat model for CKD, key molecules required for renal ammoniagenesis and ammonia excretion are highly down-regulated providing a possible molecular explanation for the development and maintenance of renal acidosis in CKD patients.
- Clinical experience with an active intravascular rewarming technique for near-severe hypothermia associated with traumatic injury. [Journal Article]
- J Intensive Care 2014; 2(1):11.
Hypothermia and acidosis are secondary causes of trauma-related coagulopathy. Here we report the case of a 72-year-old patient with severe trauma who suffered near-severe hypothermia despite the initiation of standard warming measures and was successfully managed with active intravascular rewarming. The patient was involved in a road traffic accident and was transported to a hospital. He was diagnosed with massive right-sided hemothorax, blunt aortic injury, burst fractures of the eighth and ninth thoracic vertebrae, and open fracture of the right tibia. He was referred to our hospital, where emergency surgery was performed to control bleeding from the right hemothorax. During surgery, the patient demonstrated progressive heat loss despite standard rewarming measures, and his temperature decreased to 32.4°C. Severe acidosis was also observed. A Cool Line® catheter was inserted into the right femoral vein and lodged in the inferior vena cava, and an intravascular balloon catheter system was utilized for aggressive rewarming. The automated target core temperature was set at 37°C, and the maximum flow rate was used. His core temperature reached 36.0°C after 125 min of intravascular rewarming. The severe acidosis was also resolved. The main active bleeding site was not identified, and coagulation hemostasis as well as rewarming enabled us to control bleeding from the vertebral bodies, lung parenchyma, and pleura. The total volume of intraoperative bleeding was 5,150 mL, and 20 units of red cell concentrate and 16 units of fresh frozen plasma were transfused. After surgery, he was transferred to the intensive care unit under endotracheal intubation and mechanical ventilation. His hemodynamic condition stabilized after surgery. The rewarming catheter was removed on day 2 of admission, and no bleeding, infection, or thrombosis associated with catheter placement was observed. Extubation was performed on day 40, and his subsequent clinical course was uneventful. He recovered well following rehabilitation and was discharged on day 46. These findings suggest that active intravascular rewarming should be considered as an aggressive, additional rewarming technique in patients with near-severe hypothermia associated with traumatic injury.
- Early administration of isosorbide dinitrate improves survival of cyanide-poisoned rabbits. [JOURNAL ARTICLE]
- Clin Toxicol (Phila) 2014 Dec 17.:1-6.
Context. More effective, rapidly delivered, safer antidotes are needed for cyanide poisoning. Previous study has demonstrated a beneficial effect of isosorbide dinitrate on the survival of cyanide-poisoned mice. Objective. To evaluate the effectiveness of isosorbide dinitrate compared with that of sodium nitrite in cyanide poisoning. Materials and methods. A comparative animal study was performed using 18 rabbits, randomized into 3 study groups. Animals were poisoned intravenously with potassium cyanide (1 mg/kg). The first group was not given any further treatment. The second and third groups were treated intravenously 1 min after poisoning with sodium nitrite (6 mg/kg) and isosorbide dinitrate (50 μg/kg), respectively. The primary outcome was short-term survival of up to 30 min. Secondary outcomes included time to death, a clinical score, mean blood pressure, pulse, blood pH, and lactate and methemoglobin levels. Results. Rabbits treated with isosorbide dinitrate or sodium nitrite survived while only one untreated rabbit survived. Median time to death of the 5 poisoned and untreated animals was 10 min. All the animals collapsed soon after poisoning, exhibiting rapidly disturbed vital signs and developed lactic metabolic acidosis; average peak blood lactate levels were 15.5-19.1 mmol/L at 10 min after poisoning. The treated animals improved gradually with practically full recovery of the clinical scores, vital signs, and blood gas levels. Sodium nitrite administration raised methemoglobin to an average peak of 7.9%, while isosorbide dinitrate did not change methemoglobin levels. Conclusion. Early administration of isosorbide dinitrate improved the short-term survival of cyanide-poisoned rabbits. Isosorbide dinitrate shows potential as an antidote for cyanide poisoning and may exert its effect using a nitric-oxide-dependent mechanism.
- [Growth retardation in children with chronic renal disease]. [English Abstract, Journal Article]
- Srp Arh Celok Lek 2014 Sep-Oct; 142(9-10):614-20.
Despite recent advances in the management of children with chronic renal disease (CRD), growth retardation remains its most visible comorbid condition. Growth retardation has adverse impact on morbidity and mortality rates, quality of life and education, and in adult patients on job family life, and independent leaving accomodation. Pathophysiology of impaired growth in CRD is complex and still not fully understood. The following complications are: anorexia, malnutrition, inflammation, decreased residual renal function, dialysis frequency and adequacy, renal anemia, metabolic acidosis, fluid/electrolyte imbalance, renal osteodistrophy, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) resistance. Malnutrition is most frequent and most important factor contributing to the degree of growth retardation in infancy. The degree of renal dysfunction is the major determinant of variability in growth from third year of age until puberty onset, while in puberty hypergonadotropic hypogonadism has negative effect. The main factors that influence growth after renal transplantation are the age of the recipient and glucocorticoid drugs dosage with negative effect and allograft function with positive effect. In order to improve growth in children with CRD it is necessary to include: diet with optimal caloric intake, correction of fluid/ electrolyte imbalance, correction of acidosis, renal osteodistrophy and anemia. If growth velocity is insufficient to normalize growth, it is necessary to start recombinant human GH (rhGH) therapy at 0.05 mg/kg per day (0.35 mg/kg per week or 28 IU/m2 per week) administered by subcutaneous injection.
- Prediction of mortality with unmeasured anions in critically ill patients on mechanical ventilation. [Journal Article]
- Vojnosanit Pregl 2014 Oct; 71(10):936-41.
Acid-base disorders are common within critically ill patients. Physicochemical approach described by Stewart and modified by Figge gives precise quantification method of metabolic acidosis and insight into its main mechanisms, as well as influence of unmeasured anion on metabolic acidosis. The aims of this study were to determine whether the conventional acid-base variables are connected with survival rate of critically ill patients at Intensive care unit; whether strong ion difference/strong ion gap (SID/SIG) is a better predictor of mortality rate comparing to conventional acid-base variables; to determine all significant predictable parameters for the 28-day mortality rate at intensive care units.This retrospective observational analytic study included 142 adult patients requiring mechanical ventilation, survivors (n = 68) and nonsurvivors (n = 74). Apparent strong ion difference (SIDapp), effective strong ion difference (SIDeff) and SIG values were calculated with the Stewart-Figge's quantitative biophysical method. Descriptive and analytical statistical methods were used in the study [t-test, Mann-Whitney U test, χ2-test, binary logistic regression, Reciever operating characteristic (ROC) curves, calibration].Age, Na+, acute physiology and chronic health evaluation (APACHE II), Cl-, albumin, SIG, SID app, SIDeff, and aninon gap (AG) were statistically significant predictors. AG represented a model with imprecise calibration, i.e. a model with little predictive power. APACHE II had p-value more than 0.05 if it was near it, and therefore it could be considered potentially unreliable for outcome prediction. SIDeff and SIG represented models with well-defined calibration. ROC analysis results showed that APACHE II, Cll-, albumin, SIDeff, SIG i AG had the largest area bellow the curve. By creation of logistic models with calibration methods, we found that outcome depends on SIG and APACHE II score.Based on our data, unmeasured anions provide prediction of mortality of critically ill patients on mechanical ventilation, unlike the traditional acid-base variables which are not accurate predictors of the 28-day mortality rate.
- Mutations in exons 3 and 7 resulting in truncated expression of human ATP6V1B1 gene showing structural variations contributing to poor substrate binding- causative reason for distal renal tubular acidosis with sensorineural deafness. [JOURNAL ARTICLE]
- J Biomol Struct Dyn 2014 Dec 17.:1-29.
Abstract Distal renal tubular acidosis (dRTA) is an Autosomal recessive syndrome results defect in either proximal tubule bicarbonate reabsorption or in distal tubule H(+) secretion and is characterized by severe hyperchloraemic metabolic acidosis in childhood. dRTA is associated with functional variations in the ATP6V1B1 gene encoding β1 subunit of H(+) -ATPase, key membrane transporters for net acid excretion of α-intercalated cells of medullary collecting ducts. In the present study a 13 year old male patient suffering with nephropathy and sensorineural deafness was reported in the Department of Nephrology. We predicted improper functioning of ATP6V1B1 gene could be the reason for diseased condition. Therefore, exon 3, 4 and 7 contributing active site of ATP6V1B1 gene was amplified and sequenced (Accession number: KF571726, KM222653). The obtained sequence was BLAST searched against the wild type ATP6V1B1 gene which showed novel mutations c.307 A > G, c.308 C > A, c.310 C > G, c.704 T > C, c.705 G > T, c.709 A > G, c.710 A > G, c.714 G > A, c.716 C > A, c.717delC, c.722 C > G, c.728insG, c.741insT, c.753G > C. These mutations resulted in the expression of truncated protein terminating at Lys 209. The mutated ATP6V1B1structure was superimposed with wild type showed extensive variations with RMSD 1.336 Å and could not bind to substrate ADP leading to non functional ATPase. These results conclusively explain these mutations in ATP6V1B1 gene resulted in structural changes causing accumulation of H(+) ions contributing to dRTA with sensorineural deafness.
- Rapid Reversal of Severe Lactic Acidosis After Thiamine Administration in Critically Ill Adults: A Report of 3 Cases. [JOURNAL ARTICLE]
- Nutr Clin Pract 2014 Dec 16.
Background: Thiamine plays a critical role in energy metabolism. Critically ill patients may have thiamine deficiency and increased mortality due to potentially irreversible consequences. The aim of this study was to show the impact of thiamine deficiency in a series of patients and the rapid response to thiamine replacement, showing the changes in clinical and metabolic conditions over time. Methods: We described 3 cases of hospitalized patients who had received parenteral nutrition (PN) without vitamin supplementation. All the patients were admitted to the ICU between 2010 and 2011 with a severe form of lactic acidosis, an unstable circulatory state, and a different neurological disorder (a lethargic state, a severe form of impaired near-coma consciousness, and Wernicke encephalopathy). Results: Intravenous (IV) administration of thiamine was associated with a rapid and marked restoration of acid-base balance, hemodynamic stability and the disappearance of neurological disturbances, and normalization of the clinical and biochemical conditions of all the patients within the following hours. Conclusions: The 3 cases demonstrated the rapidity of the reversal of severe thiamine deficiency, achieved by appropriate replacement in different hospitalized patients. The regression of clinical and biochemical disorders requires a prompt diagnosis and treatment based on the IV administration of thiamine and magnesium sulfate. In hospitalized patients at risk, thiamine deficiency is prevented by the integration of thiamine supplementation into PN and other forms of nutrition support.
- Low flow veno-venous extracorporeal carbon dioxide removal in the management of severe status asthmatics-A case report. [JOURNAL ARTICLE]
- Clin Respir J 2014 Dec 16.
Status asthmaticus is a life threatening condition that requires intensive care management. Most of these patients have severe hypercapnic acidosis that requires lung protective mechanical ventilation. A small proportion of these patients do not respond to conventional lung protective mechanical ventilation or pharmacotherapy. Such patients have an increased mortality and morbidity. Successful use of extracorporeal membrane oxygenation (ECMO) is reported in such patients. However the use of ECMO is invasive with its associated morbidity and is limited to specialised centres. In this report we report the use of a novel, minimally invasive, low flow extracorporeal carbon dioxide removal device in management of severe hypercapnic acidosis in a patient with life threatening status asthmaticus.