Home About us Contact
|
Home About us Contact | ||
|
|
||
Metabolic Acidosis (metabolic + acidosis)
Kinds of Metabolic Acidosis Selected AbstractsBetter Correction of Metabolic Acidosis, Blood Pressure Control, and Phagocytosis with Bicarbonate Compared to Lactate Solution in Acute Peritoneal DialysisARTIFICIAL ORGANS, Issue 2 2001Visith Thongboonkerd Abstract: Lactate solution has been the standard dialysate fluid for a long time. However, it tends to convert back into lactic acid in poor tissue-perfusion states. The aim of this study was to evaluate the efficacy of magnesium (Mg)- and calcium (Ca)-free bicarbonate solution compared with lactate solution in acute peritoneal dialysis (PD). Renal failure patients who were indicated for dialysis and needed acute PD were classified as shock and nonshock groups, and then were randomized to receive either bicarbonate or lactate solution. Twenty patients were enrolled in this study (5 in each subgroup). In the shock group, there were more rapid improvements and significantly higher levels of blood pH (7.40 ± 0.04 versus 7.28 ± 0.05, p < 0.05), serum bicarbonate (23.30 ± 1.46 versus 18.37 ± 1.25 mmol/L, p < 0.05), systolic pressure (106.80 ± 3.68 versus 97.44 ± 3.94 mm Hg, p < 0.05), mean arterial pressure (80.72 ± 2.01 versus 73.28 ± 2.41 mm Hg, p < 0.05), percentages of phagocytosis of circulating leukocytes (65.85%± 2.22 versus 52.12%± 2.71, p < 0.05), and percentages of positive nitroblue tetrazolium (NBT) reduction test without and with stimulation (14.43 ± 1.93 versus 9.43 ± 2.12, p < 0.05 and 65.08 ± 6.80 versus 50.23 ± 4.21, p < 0.05, respectively) in the bicarbonate subgroup compared with the lactate subgroup. In the nonshock group, blood pH, serum bicarbonate, and phagocytosis assays in both subgroups were comparable. Lactic acidosis was more rapidly recovered and was significantly lower with bicarbonate solution for both shock and nonshock groups (3.63 ± 0.37 versus 5.21 ± 0.30 mmol/L, p < 0.05 and 2.92 ± 0.40 versus 3.44 ± 0.34 mmol/L, p < 0.05, respectively). Peritoneal urea and creatinine clearances in both subgroups were comparable for both shock and nonshock groups. There was no peritonitis observed during the study. Serum Mg and Ca levels in the bicarbonate subgroup were significantly lower, but no clinical and electrocardiographic abnormality were observed. We concluded that Mg- and Ca-free bicarbonate solution could be safely used and had better outcomes in correction of metabolic acidosis, blood pressure control, and nonspecific systemic host defense with comparable efficacy when compared to lactate solution. It should be the dialysate of choice for acute PD especially in the poor tissue-perfusion states such as shock, lactic acidosis, and multiple organ failure. [source] Bedside Detection of Urine ,-Hydroxybutyrate in Diagnosing Metabolic AcidosisACADEMIC EMERGENCY MEDICINE, Issue 8 2008Silas W. Smith MD Abstract Objectives:, While critically important, the rapid identification of the etiology of metabolic acidosis (MA) may be labor-intensive and time-consuming. Alcoholic, starvation, and severe diabetic ketoacidosis (AKA, SKA, and DKA, respectively) may produce ,-hydroxybutyrate (BOHB) in marked excess of acetone (ACET) and acetoacetate (AcAc). Unfortunately, current urine dipstick technology poorly detects ACET and cannot measure BOHB. The inability to detect BOHB might delay therapy for ketoacidoses or provoke unnecessary evaluation or empiric treatment of other causes of MA, such as toxic alcohol poisoning. The authors tested the previous assertion that commonly available hydrogen peroxide (H2O2) would improve BOHB detection. The effectiveness of alkalinization and use of a silver nitrate (AgNO3) catalyst was also assessed. Methods:, Control and urine test specimens containing from 0.5 to 800 mmol/L ACET, AcAc, and BOHB were prepared. Urine specimens were oxidized with H2O2 (3%) 1:9 (H2O2:urine), alkalinized with potassium hydroxide (KOH; 10%), exposed to AgNO3 sticks, or altered with a combination of these methods in a random fashion. Three emergency physicians (EPs) blinded to the preparation technique evaluated urine dipsticks (Multistix, Bayer Corp.) placed in the specimens for "ketones." Results:, Multistix detected AcAc appropriately; ACET was detected only at high concentrations of ,600 mmol/L. Multistix failed to measure BOHB at all concentrations tested. H2O2 improved urinary BOHB detection, although not to clinically relevant levels (40 mmol/L). Alkalinization and AgNO3 sticks did not improve BOHB detection beyond this threshold. Conclusions:, Addition of H2O2 (3%), alkalinization, or AgNO3 sticks did not improve clinically meaningful urine BOHB detection. Clinicians should use direct methods to detect BOHB when suspected. [source] Effect of selected alcohol dehydrogenase inhibitors on human hepatic lactate dehydrogenase activity , an in vitro studyJOURNAL OF APPLIED TOXICOLOGY, Issue 6 2005Jaroslaw Dudka Abstract Metabolic acidosis severely complicates methanol and ethylene glycol intoxications. Acidosis is caused by acid metabolites and can be intensified by lactate elevation. Lactate concentration depends on the NADH2/NAD ratio. Lactate dehydrogenase (LDH, E.C.1.1.1.27.) supplies more lactate when the level of NADH2 is elevated. The aim of the study was to evaluate the effect of alcohol dehydrogenase (ADH) inhibitors and substrates: cimetidine, EDTA, 4-methylpyrazole (4-MP), Ukrain and ethanol on LDH activity. The activity of LDH was determined spectrophotometrically in human liver homogenates incubated with cimetidine, EDTA, 4-MP and Ukrain at concentrations of 2 × 10,6, 10,5 and 5 × 10,5m as well as ethanol at concentrations of 12.50, 25.00, 50.00 mm. The LDH activity was significantly increased by 10,5 and 5 × 10,5m concentrations of cimetidine and 4-MP, and by all concentrations of ethanol. The most effective change of LDH activity of about 26% (P < 0.01) was observed at the highest concentration of ethanol. Ukrain inhibited LDH activity at both concentrations, i.e. 10,5 and 5 × 10,5m (P < 0.05). However, EDTA did not significantly influence LDH activity. The data showed that ethanol and 4-MP, the main antidotes in methanol or ethylene glycol poisoning, may increase liver LDH activity , an undesirable effect during the therapy of patients intoxicated with these alcohols. On the other hand, the decrease of LDH activity in the presence of Ukrain is a promising finding but definitely requires further investigation. Copyright © 2005 John Wiley & Sons, Ltd. [source] Metabolic Acidosis Stimulates RANKL RNA Expression in Bone Through a Cyclo-oxygenase-Dependent Mechanism,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2003Kevin K Frick Abstract Metabolic acidosis inhibits osteoblastic bone formation and stimulates osteoclastic resorption. To determine whether acidosis alters expression of RNA for the osteoclastic differentiation factor RANKL, mouse calvariae were incubated in neutral or physiologically acidic media. Acidosis resulted in a significant cyclo-oxygenase-dependent increase in RANKL RNA levels, which would be expected to induce the associated increase in bone resorption. Introduction: Metabolic acidosis increases net calcium efflux from bone, initially through physicochemical mechanisms and later through predominantly cell-mediated mechanisms. Acidosis decreases osteoblastic bone formation and increases osteoclastic resorption. The growth and maturation of osteoclasts, derived from hematopoietic precursors in the monocyte/macrophage lineage, are dependent on the interplay of a number of factors. Commitment of pre-osteoclasts to osteoclasts is induced by the interaction of the osteoclastic cell-surface receptor RANK with a ligand expressed by osteoblasts, RANKL. The RANK/RANKL interaction not only initiates a differentiation cascade that culminates in mature bone-resorbing osteoclasts but also increases osteoclastic resorptive capacity and survival. Methods: To test the hypothesis that metabolic acidosis increases expression of RANKL, we cultured neonatal mouse calvariae in acidic (initial medium pH ,7.1 and [HCO3,] ,11 mM) or neutral (initial medium pH ,7.5 and [HCO3,] ,25 mM) medium for 24 and 48 h. We determined the relative expression of RANKL RNA by reverse transcriptase-polymerase chain reaction (RT-PCR) and quantitated the expression by Northern analysis. Results: In this model of metabolic acidosis, there was significantly increased expression of RANKL RNA at both 24 (2-fold) and 48 h (5-fold) compared with respective controls. Net calcium efflux from bone was also increased in acidic medium compared with control medium. At 48 h, net calcium efflux correlated directly with RANKL expression (r = 0.77, n = 15, p < 0.001). Inhibition of prostaglandin synthesis with indomethacin blocked the acid-induced increase in RANKL RNA as well as the increased calcium efflux. Conclusions: Metabolic acidosis induces osteoblastic prostaglandin synthesis, followed by autocrine or paracrine induction of RANKL. This increase in RANKL would be expected to augment osteoclastic bone resorption and help explain the increase in cell-mediated net calcium efflux. [source] Assessment of acid-base status of cats with naturally occurring chronic renal failureJOURNAL OF SMALL ANIMAL PRACTICE, Issue 2 2003J. Elliott Metabolic acidosis is reported to be a common complication of feline chronic renal failure (CRF) but acid-base status of feline patients with this disease is rarely assessed by general practitioners. A cross-sectional study involving 59 cases of naturally occurring feline CRF was conducted to determine the prevalence of acid-base disturbances. Cases were categorised on the basis of their plasma creatinine concentrations as mild, moderate or severe. A group of 27 clinically healthy, age-matched cats was assessed for comparison. A low venous blood pH (<7·270) was found in 10 of the 19 severe cases (52·6 per cent), three of the 20 moderate cases (15 per cent) and none of the 20 mild cases. Acidaemia was associated with an increased anion gap contributed to by both low plasma bicarbonate and low chloride ion concentrations. Biochemical analysis of urine samples showed urine pH to decrease with increasing severity of renal failure. Urinary loss of bicarbonate was not associated with the occurrence of acidaemia and there was a tendency for urinary ammonium ion excretion to decrease as the severity of renal failure increased. Cats with naturally occurring CRF do not show plasma biochemical evidence of acid-base disturbances until the disease is advanced. [source] A fatal case of cutaneous zygomycosis in a patient with severe metabolic acidosisMYCOSES, Issue 4 2009C. Kosmidis Summary We present a case of cutaneous zygomycosis in a patient with an ureteroileostomy and severe metabolic acidosis, but without diabetes. The patient died despite multiple aggressive surgical interventions and antifungal therapy with liposomal amphotericin B. Ureteroileostomy-related acidosis can be a predisposing factor for zygomycosis. Metabolic acidosis can have a role in the severity of cutaneous disease. [source] Effect of Normal Saline Infusion on the Diagnostic Utility of Base Deficit in Identifying Major Injury in Trauma PatientsACADEMIC EMERGENCY MEDICINE, Issue 12 2006Richard Sinert DO Abstract Background Base deficit (BD) is a reliable marker of metabolic acidosis and is useful in gauging hemorrhage after trauma. Resuscitation with chloride-rich solutions such as normal saline (NS) can cause a dilutional acidosis, possibly confounding the interpretation of BD. Objectives To test the diagnostic utility of BD in distinguishing minor from major injury after administration of NS. Methods This was a prospective observational study at a Level 1 trauma center. The authors enrolled patients with significant mechanism of injury and measured BD at triage (BD-0) and at four hours after triage (BD-4). Major injury was defined by any of the following: injury severity score of ,15, drop in hematocrit of ,10 points, or the patient requiring a blood transfusion. Patients were divided into a low-volume (NS < 2L) and a high-volume (NS , 2L) group. Data were reported as mean (±SD). Student's t- and Wilcoxon tests were used to compare data. Receiver operating characteristic (ROC) curves tested the utility of BD-4 in differentiating minor from major injury in the study groups. Results Four hundred eighty-nine trauma patients (mean age, 36 [± 18] yr) were enrolled; 82% were male, and 34% had penetrating injury. Major-(20%) compared with minor-(80%) injury patients were significantly (p = 0.0001) more acidotic (BD-0 mean difference: ,3.3 mmol/L; 95% confidence interval [CI] =,2.5 to ,4.2). The high-volume group (n = 174) received 3,342 (±1,821) mL, and the low-volume group (n = 315) received 621 (±509) mL of NS. Areas under the ROC curves for the high-volume (0.63; 95% CI = 0.52 to 0.74) and low-volume (0.73; 95% CI = 0.60 to 0.86) groups were not significantly different from each other. Conclusions Base deficit was able to distinguish minor from major injury after four hours of resuscitation, irrespective of the volume of NS infused. [source] Topiramate-induced metabolic acidosis: report of two casesDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 10 2001Chun-hung Ko MRCP FHKAM Medical Officer Two children who presented with symptomatic metabolic acidosis after being put on topiramate (TPM) are reported. The first patient was an 11-year-old male with refractory complex partial epilepsy who was put on TPM for 13 months. He developed hyperventilation 1 week after increasing the dose to 300mg/day. Arterial blood gas revealed hyperchloraemic metabolic acidosis with partial respiratory compensation: pH 7.36, PCO2 27.2 mmHg, bicarbonate 14.9 mEq/L, base excess -8.9 mmol/L. Hyperventilation and acidosis resolved after administration of sodium bicarbonate and reduction of the dose of TPM. The second patient was a female who developed increasing irritability at age 16 months and 21 months, each time associated with introduction of TPM and resolved promptly upon withdrawal of the drug. Venous blood gas taken during the second episode revealed pH 7.34, PCO2 37.4 mmHg, bicarbonate 20.4 mEq/L, base excess -4.2 mmol/L. The predominant mechanism of TPM-induced hyperventilation involves inhibition of carbonic anhydrase at the proximal renal tubule, resulting in impaired proximal bicarbonate reabsorption. The occurrence of hyperpnoea or mental status change in any patient who is on TPM should prompt an urgent blood gas sampling, with correction of the acid-base disturbances accordingly. [source] Type 1 (distal) renal tubular acidosis in a patient with Type 1 diabetes mellitus,not all cases of metabolic acidosis in Type 1 diabetes mellitus are due to diabetic ketoacidosisDIABETIC MEDICINE, Issue 1 2008J. A. Dymot No abstract is available for this article. [source] General Anesthesia and the Ketogenic Diet: Clinical Experience in Nine PatientsEPILEPSIA, Issue 5 2002Ignacio Valencia Summary: ,Purpose: To determine if children actively on the ketogenic diet (KD) can safely undergo general anesthesia (GA) for surgical procedures. Methods: The records of children treated with the KD at Children's Hospital (Boston, Massachusetts) from 1995 to the present were reviewed. The charts of children who had received GA while on the diet were evaluated with regard to demographics, procedure information, anesthesia records, blood chemistries, and perioperative course. Of 71 children on the KD during the period of the study, nine (12.7%) had procedures requiring GA while on the diet. Results: Nine children received GA for surgical procedures ranging from central line placement to hemispherectomy while on the KD. At the time of GA, the children ranged from age 1 to 6 years, and had been on the KD for 2,60 months. The patients received carbohydrate-free intravenous solutions perioperatively. Anesthesia duration ranged from 20 min to 11.5 h; for longer procedures, serum pH, glucose, and electrolyte levels were monitored. Serum glucose levels remained stable in all patients, but serum pH typically decreased; the largest reduction was to 7.16. In three procedures, patients received intravenous bicarbonate because of level of acidosis. There were no perioperative complications. Conclusions: Children on the KD can safely undergo GA for surgical procedures. Although serum glucose levels appear to remain stable, serum pH or bicarbonate levels should be monitored because of the risk of metabolic acidosis. [source] Nitric oxide synthase inhibition in Thoroughbred horses augments O2 extraction at rest and submaximal exercise, but not during short-term maximal exerciseEQUINE VETERINARY JOURNAL, Issue S36 2006M. MANOHAR Summary Reason for performing study: Work is required to establish the role of endogenous nitric oxide (NO) in metabolism of resting and exercising horses. Objectives: To examine the effects of NO synthase inhibition on O2 extraction and anaerobic metabolism at rest, and during submaximal and maximal exertion. Methods: Placebo and NO synthase inhibition (with N,-nitro-L-arginine methyl ester [l -NAME] administered at 20 mg/kg bwt i.v.) studies were performed in random order, 7 days apart on 7 healthy, exercise-trained Thoroughbred horses at rest and during incremental exercise leading to 120 sec of maximal exertion at 14 m/sec on a 3.5% uphill grade. Results: At rest, NO synthase inhibition significantly augmented the arterial to mixed-venous blood O2 content gradient and O2 extraction as mixed-venous blood O2 tension and saturation decreased significantly. While NO synthase inhibition did not affect arterial blood-gas tensions in exercising horses, the exercise-induced increment in haemoglobin concentration and arterial O2 content was attenuated. In the l -NAME study, during submaximal exercise, mixed-venous blood O2 tension and haemoglobin-O2 saturation decreased to a greater extent causing O2 extraction to increase significantly. During maximal exertion, arterial hypoxaemia, desaturation of haemoglobin and hypercapnia of a similar magnitude developed in both treatments. Also, the changes in mixed-venous blood O2 tension and haemoglobin-O2 saturation, arterial to mixed-venous blood O2 content gradient, O2 extraction and markers of anaerobic metabolism (lactate and ammonia production, and metabolic acidosis) were not different from those in the placebo study. Conclusion: Endogenous NO production augments O2 extraction at rest and during submaximal exertion, but not the during short-term maximal exercise. Also, NO synthase inhibition does not affect anaerobic metabolism at rest or during exertion. Potential relevance: It is unlikely that endogenous NO release modifies aerobic or anaerobic metabolism in horses performing short-term maximal exertion. [source] Different pathophysiological mechanisms of intramitochondrial iron accumulation in acquired and congenital sideroblastic anemia caused by mitochondrial DNA deletionEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 2 2006Thomas Matthes Abstract:, Sideroblastic anemias (SA) are characterized by iron accumulation in the mitochondria of erythroblasts. Although we have evidence of mitochondrial gene alterations in sporadic congenital cases, the origin of acquired forms [refractory anemia with ring sideroblasts (RARS)], is still largely unknown. Here, we report the analysis of respiratory chain function in a patient with a large mitochondrial deletion and in patients with RARS. A young boy with SA showed symptoms typical of a mitochondrial disease with metabolic acidosis, muscle weakness and cerebral involvement. His bone marrow DNA was analyzed for the presence of mitochondrial deletions. We found a new mitochondrial (mt)DNA deletion spanning 3614 bp and including all the mt genes encoding complex IV, plus ATPase 6 and 8, and several transfer (t)RNAs. All tissues analyzed (liver, skeletal muscle, brain, pancreas) showed a heteroplasmic distribution of this mutant DNA. Bone marrow homogenates were obtained from five patients with RARS and from three patients with normal bone marrow and respiratory chain function assayed by spectrophotometric analysis. Cytochrome c oxidase (CCO) activity was greatly reduced in the patient's bone marrow. In contrast, CCO activity and global respiratory chain function were conserved in patients with RARS. We conclude that deficient CCO activity secondary to mtDNA deletions is related to intramitochondrial iron accumulation, as in our patient or in those with Pearson's syndrome, whereas other mechanisms, e.g. nuclear DNA mutations, have to be proposed to be involved in the acquired forms of SA. [source] Cutaneous and neurologic manifestations of biotinidase deficiencyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 5 2000Paloma Cornejo Navarro A male newborn with no obstetric or familial antecedents, except that his parents were cousins, developed hypotonia, lethargy, and feeding problems from birth. Analysis revealed a marked metabolic acidosis and hyperammonemia. Three weeks later, he was admitted to hospital in order to receive parenteral nutrition and to undertake a study for metabolic diseases. The boy did not improve in spite of the use of parenteral nutrition and began to present with inspiratory stridor and tachypnea. One week later, he presented with an erythematous scaling eruption, which was especially intense in the lumbosacral region ( Fig. 1a,b). The scalp was only slightly affected. Figure 1. Erythematous scaling eruption, more intense in the lumbosacral region Laboratory findings were compatible with biotinidase deficiency diagnosed by demonstrating absent enzyme activity. His parents were also studied and they were found to have partial biotinidase deficiency (30% of enzyme activity). After 37 days of life, the baby was given a treatment consisting of 20 mg of biotin per day intravenously. Biochemical and neurologic alterations improved quickly. Meckel's diverticulum and a duodenal membrane were detected at the second month of life after a gastroduodenal survey, and both were operated on. The skin lesions did not improve, however, and intravenous biotin had to be increased to 40 mg/day. The eruption disappeared after 10 days. On his first birthday, he remained asymptomatic with 40 mg of oral biotin. [source] Nursing and medical staff knowledge regarding the monitoring and management of accidental or exposure hypothermia in adult major trauma patientsINTERNATIONAL JOURNAL OF NURSING PRACTICE, Issue 6 2006Sharyn Ireland RN Dip.HSc B.Nurs CritCareCert ACCN M.Ed Recording a patient's vital signs is a basic requirement that in part informs clinical decision-making. Practice suggests that recording a trauma patient's temperature is occasionally overlooked in the emergency department. A staff survey was undertaken to gain an appreciation of knowledge and understanding of the issues that surround accidental or exposure hypothermia in trauma patients. Results demonstrate that nurses and doctors are unsure of how to define hypothermia and are not conversant with simple ways to prevent heat loss or rewarm patients. Complications from hypothermia such as coagulopathy and metabolic acidosis were seldom identified. Issues that limit staff recording temperature include patient access and acuity, lack of knowledge and confidence and access to temperature-measuring devices. These results emphasize the need for regular education. Implications for clinical practice were considered; an algorithm to guide staff on ways to improve the monitoring and management of temperature in trauma patients was developed. Opportunities for ongoing and further research were identified. [source] Metabolic Acidosis Stimulates RANKL RNA Expression in Bone Through a Cyclo-oxygenase-Dependent Mechanism,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2003Kevin K Frick Abstract Metabolic acidosis inhibits osteoblastic bone formation and stimulates osteoclastic resorption. To determine whether acidosis alters expression of RNA for the osteoclastic differentiation factor RANKL, mouse calvariae were incubated in neutral or physiologically acidic media. Acidosis resulted in a significant cyclo-oxygenase-dependent increase in RANKL RNA levels, which would be expected to induce the associated increase in bone resorption. Introduction: Metabolic acidosis increases net calcium efflux from bone, initially through physicochemical mechanisms and later through predominantly cell-mediated mechanisms. Acidosis decreases osteoblastic bone formation and increases osteoclastic resorption. The growth and maturation of osteoclasts, derived from hematopoietic precursors in the monocyte/macrophage lineage, are dependent on the interplay of a number of factors. Commitment of pre-osteoclasts to osteoclasts is induced by the interaction of the osteoclastic cell-surface receptor RANK with a ligand expressed by osteoblasts, RANKL. The RANK/RANKL interaction not only initiates a differentiation cascade that culminates in mature bone-resorbing osteoclasts but also increases osteoclastic resorptive capacity and survival. Methods: To test the hypothesis that metabolic acidosis increases expression of RANKL, we cultured neonatal mouse calvariae in acidic (initial medium pH ,7.1 and [HCO3,] ,11 mM) or neutral (initial medium pH ,7.5 and [HCO3,] ,25 mM) medium for 24 and 48 h. We determined the relative expression of RANKL RNA by reverse transcriptase-polymerase chain reaction (RT-PCR) and quantitated the expression by Northern analysis. Results: In this model of metabolic acidosis, there was significantly increased expression of RANKL RNA at both 24 (2-fold) and 48 h (5-fold) compared with respective controls. Net calcium efflux from bone was also increased in acidic medium compared with control medium. At 48 h, net calcium efflux correlated directly with RANKL expression (r = 0.77, n = 15, p < 0.001). Inhibition of prostaglandin synthesis with indomethacin blocked the acid-induced increase in RANKL RNA as well as the increased calcium efflux. Conclusions: Metabolic acidosis induces osteoblastic prostaglandin synthesis, followed by autocrine or paracrine induction of RANKL. This increase in RANKL would be expected to augment osteoclastic bone resorption and help explain the increase in cell-mediated net calcium efflux. [source] Coho salmon haematological, metabolic and acid-base changes during exercise and recovery in sea waterJOURNAL OF FISH BIOLOGY, Issue 5 2004J. J. Cech Jr. Cannulated, seawater-acclimated coho salmon Oncorhynchus kisutch were swum to exhaustion in a seawater tunnel (10° C, mean Ucrit 50 cm s,1), resulting in metabolic acidosis and increased plasma electrolyte and cortisol concentrations, which were corrected during a 4 h recovery. Because the swimming and physiological performance data were similar to those of other salmonids, it was concluded that life-history limitations, besides their exercise capabilities in upwelling zones, probably explain declining coho salmon populations. [source] Methanol outbreak in Norway 2002,2004: epidemiology, clinical features and prognostic signsJOURNAL OF INTERNAL MEDICINE, Issue 2 2005K. E. HOVDA Abstract. Objectives., Knowledge on methanol poisoning does mainly come from clinical studies. We therefore report epidemiological, clinical and prognostic features from the large methanol outbreak in Norway in 2002,2004 where the new antidote fomepizole was the primary antidote in use. Design and subjects., Combined prospective and retrospective case series study of 51 hospitalized patients who were confirmed poisoned with methanol, of whom nine died. In addition, eight patients died outside hospital. Most patients were admitted in a late stage and because of symptoms. Treatment consisted of alkali, fomepizole (71%) and haemodialysis (73%). Results., The median serum methanol was 25.0 mmol L,1 (80 mg dL,1) (range 3.1,147.0 mmol L,1), median pH was 7.20 (6.50,7.50), and median base deficit 22 mmol L,1 (range 0,31). The most frequent clinical features reported were visual disturbances (55%), dyspnoea (41%), and gastrointestinal symptoms (43%). Twenty-four per cent were comatose on admission, of whom 67% died. There was a trend towards decreasing pCO2 with decreasing pH amongst the patients surviving. The opposite trend was demonstrated in the dying; the difference was highly significant by linear regression analyses (P < 0.001). Conclusions., Methanol poisoning still has a high morbidity and mortality, mainly because of late diagnosis and treatment. Respiratory arrest, coma and severe metabolic acidosis (pH < 6.90, base deficit >28 mmol L,1) upon admission were strong predictors of poor outcome. Early admission and ability of respiratory compensation of metabolic acidosis was associated with survival. [source] Neonatal C-reactive protein value in prediction of Outcome of Preterm Premature Rupture of Membranes: Comparison of Singleton and Twin PregnanciesJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 4 2009Simin Taghavi Abstract Aim:, The clinical importance of preterm premature rupture of the membranes (PPROM) is its relationship to maternal and neonatal mortality and morbidity, especially in twin pregnancies. The aim of this study was to determine and compare the role of inflammatory factors as predictors of the PPROM outcome between singleton and twin pregnancies. Methods:, The medical records of 22 twins delivered between 28 and 34 weeks and complicated by PPROM were reviewed at the Al-Zahra Hospital in Tabriz, Iran. Also among singletons, 55 cases of matched gestational age were randomly selected as a control group. Three laboratory indices of neonatal white blood cell (WBC) count and C-reactive protein (CRP) in the two groups were measured immediately after delivery and the effects of two factors on neonatal outcome were assessed. Results:, In singletons, there was adverse relationship between the mean of WBC count and duration of latency (P = 0.007). Also, a positive relationship between the means of ventilation time and WBC count in second twins was found (P = 0.034). Positive CRP was the main predictor of neonatal intensive care unit admission in both singletons (odds ratio: 4.929, P = 0.042) and first twins (odds ratio: 9.000, P = 0.005). However, positive CRP did not influence the existence of metabolic acidosis or duration of latency in either of the two groups. Conclusion:, Neonatal WBC count was a predictor for the duration of latency in singletons and for ventilation time in twins. Positive neonatal CRP was an important factor for the prediction of neonatal intensive care unit admission in both types of pregnancy; its role in twins is clearer than in singletons. [source] Determining the contribution of asphyxia to brain damage in the neonateJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 4 2004James A. Low Abstract Studies in the research laboratory have demonstrated the complex relationship between fetal and newborn asphyxia and brain damage, a balance between the degree, duration and nature of the asphyxia and the quality of the cardiovascular compensatory response. Clinical studies would support the contention that the human fetus and newborn behave in a similar manner. An accurate diagnosis of asphyxia requires a blood gas and acid base assessment. The clinical classification of fetal asphyxia is based on a measure of metabolic acidosis to confirm that fetal asphyxia has occurred and the expression of neonatal encephalopathy and other organ system complications to express the severity of the asphyxia. The prevalence of fetal asphyxia at delivery is at term, 25 per 1000 live births of whom 15% are moderate or severe; and in the preterm, 73 per 1000 live births of whom 50% are moderate or severe. It remains to be determined how often the asphyxia recognized at delivery may have been present before the onset of labor. There is a growing body of indirect and direct evidence to support the contention that antepartum fetal asphyxia is important in the occurrence of brain damage. Although much of the brain damage observed in the newborn reflects events that occurred before delivery, newborn asphyxia and hypotension, particularly in the preterm newborn, may contribute to the brain damage accounting for deficits in surviving children [source] Acid-base balance of cats with chronic renal failure: effect of deterioration in renal functionJOURNAL OF SMALL ANIMAL PRACTICE, Issue 6 2003J. Elliott In a previous cross-sectional study of feline chronic renal failure (CRF), metabolic acidosis was identified in 52·6 per cent of animals with severe renal failure (plasma creatinine concentration > 400 umol/litre). The aim of this longitudinal study was to determine whether metabolic acidosis preceded or accompanied a deterioration in renal function in cats with CRF. Data were analysed from 55 cats with CRF that had been followed longitudinally for at least four months. Twenty-one cases showed deterioration in renal function over the period of the study, as evidenced by significant rises in their plasma creatinine concentrations and decreases in bodyweight. In five of the 21 cases, acidaemia accompanied the deterioration in renal function. Only one of these cats had evidence of metabolic acidosis before renal function deterioration. One other case developed metabolic acidosis without a rise in plasma creatinine concentration. These data suggest that biochemical evidence of metabolic acidosis does not generally occur until late in the course of feline CRF. [source] Grave acidosis after severe anaphylactic bronchospasm: friend or foe?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2007M. Pytte In a 20-year-old woman with known asthma, anaphylactic bronchospasm induced a grave combined respiratory and metabolic acidosis (pHa 6.66) with marked hypoxaemia (SaO2 45%). The beneficial effects of the rightward shift of the oxyhaemoglobin dissociation curve on tissue O2 unloading at such pH was more than offset by the negative effect on SaO2 at the reduced PaO2 (7.0 kPa) found in this patient. This case illustrates the detrimental effect of grave acidosis on arterial blood oxygen content at subnormal PaO2 values, the beneficial effect of a supranormal PaO2 on the SaO2 in such patients, and the rapid remission rate of life-threatening acidosis and blood lactate after adequate ventilation and tissue oxygenation were secured. The initial treatment of the patient and clinically relevant considerations are discussed. [source] Lactobacillus GG Does Not Affect D-Lactic Acidosis in Diarrheic Calves, in a Clinical SettingJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 3 2006Julia B. Ewaschuk D-lactate, produced by gastrointestinal fermentation, is a major contributor to metabolic acidosis in diarrheic calves. Lactobacillus rhamnosus GG survives gastrointestinal transit in the neonatal calf and does not produce D-lactate. To determine whether this probiotic reduces gastrointestinal D-lactate production or severity of diarrhea or both, 48 calves (mean, 11 days old; range, 2,30 days) admitted to the clinic for treatment of diarrhea were randomly allocated to 2 groups. The experimental group was given Lactobacillus rhamnosus GG (1×1011 cfu/d) PO, dissolved in milk or oral electrolyte solution, in addition to clinic treatment protocols; the other group served as a control. Serum and fecal samples were obtained at admission and at 24 and 48 hours after initial administration of Lactobacillus rhamnosus GG. All samples were analyzed for D-and L-lactate by using high-pressure liquid chromatography. Feces were also analyzed for pathogens, Lactobacillus rhamnosus GG recovery, and dry matter. D-lactic acidemia (>3 mmol/L) was present in 37/48 calves at admission. Lactobacillus rhamnosus GG was recovered in the feces of 13 experimental calves and 0 control calves 24 hours after administration. No difference in serum or fecal D- or L-lactate between the groups was detected at any time point. After therapy, D-lactic acidosis was absent at 48 hours in all but 1 calf. No relation between fecal pathogen (viral, bacterial, or protozoal) and degree of D-lactic acidosis was observed. The reduction in mortality and greater fecal dry matter in Lactobacillus rhamnosus GG-treated calves was not statistically significant. [source] A fatal case of cutaneous zygomycosis in a patient with severe metabolic acidosisMYCOSES, Issue 4 2009C. Kosmidis Summary We present a case of cutaneous zygomycosis in a patient with an ureteroileostomy and severe metabolic acidosis, but without diabetes. The patient died despite multiple aggressive surgical interventions and antifungal therapy with liposomal amphotericin B. Ureteroileostomy-related acidosis can be a predisposing factor for zygomycosis. Metabolic acidosis can have a role in the severity of cutaneous disease. [source] Glycosaminoglycans and the peritoneaumNEPHROLOGY, Issue 5 2002Susan YUNG SUMMARY: The introduction of peritoneal dialysis (PD) over two decades ago has allowed us to manipulate the peritoneal membrane to perform as a continuous dialysing organ. to maximize the efficacy of solute transport and waste removal, conventional PD fluids require unphysiological concentrations of glucose to provide the osmotic drive, lactate to alleviate metabolic acidosis, and a low pH to prevent the caramelization of glucose during the preparation of the solutions. These factors either alone or in combination, are irritants to the peritoneal membrane. Thus, continuous exposure of the peritoneum to PD solutions, together with frequent episodes of peritonitis confers a chronic inflammatory response within the peritoneum. It is, therefore, not unexpected that with time, long-term PD patients develop structural and functional changes within the peritoneum, which in many cases develop into peritoneal fibrosis of varying degrees and compromises the peritoneal membrane as a dialysing organ. to date, numerous studies have investigated methods to improve the efficiency of PD and preserve the structure of the peritoneal membrane. Recently, a number of reports have documented the beneficial effects of intraperitoneal administration of glycosaminoglycans (GAGs) on both the structural and functional qualities of the peritoneum. In this context, GAGs have been demonstrated to inhibit collagen synthesis within the peritoneum, decrease peritoneal advanced glycosylated end-products (AGE) deposition, and modulate cytokine and growth factor synthesis. This review will examine the available data with regards to the potential role of GAGs in maintaining ultrafiltration, solute transport and the structural integrity of the peritoneum. [source] Peritoneal mesothelial cells and the extracellular matrixNEPHROLOGY, Issue 6 2001Susan Yung SUMMARY: Continuous ambulatory peritoneal dialysis (CAPD) is an important treatment for patients with end-stage renal failure. Long-term success is dependent on the functional and structural integrity of the peritoneal membrane. Conventional peritoneal dialysis fluids are non-physiological. They contain glucose at high concentrations to provide the osmotic drive for ultrafiltration, lactate to correct the metabolic acidosis of renal failure, and a low pH to prevent caramelization of glucose during heat sterilization. These components, in isolation or acting together, exert adverse influences on both the resident cellular and extracellular elements of the peritoneal membrane, as well as phagocytic cells which infiltrate the peritoneum during inflammation, culminating in detrimental structural and functional effects, compromising the viability of the peritoneum during dialysis. Peritoneal biopsy studies of patients on long-term CAPD have demonstrated an intercellular space between adjacent mesothelial cells which allows the penetration of peritoneal dialysis fluid into the underlying submesothelium. This, together with episodes of peritonitis, can initiate a chronic inflammatory reaction within the peritoneum characterized by increased synthesis of matrix proteins. Perturbation of the regulatory mechanisms which govern the balance of synthesis and degradation of extracellular matrix can lead to progressive fibrosis. Human peritoneal mesothelial cells (HPMC) have been shown to synthesize fibronectin, laminin, collagens, proteoglycans and hyaluronan in vitro, and thus play a role in the pathogenesis of peritoneal fibrosis. This review will give an overview of extracellular matrix (ECM) synthesis by HPMC, how changes in the synthesis are affected by CAPD and postulate how these changes can compromise the dialytic properties of the peritoneum. [source] Death after re-exposure to propofol in a 3-year-old child: a case reportPEDIATRIC ANESTHESIA, Issue 3 2004Josef Holzki MD Summary This case report discusses the cause of death in a 3-year-old child who survived a high dose (20 mg·kg,1·h,1) of propofol, infused over a period of 15 h, following which the patient developed a combined respiratory and metabolic acidosis, the oxygenation remaining normal. Bronchospasm was assumed to be the cause of hypercapnia. At this time the doctors in charge did not think of a possible side-effect of propofol. The administration of propofol was interrupted, the patient recovered within 13 h from the acidosis, woke up and required further sedation. A supposedly entirely safe infusion of 4 mg·kg,1·h,1 propofol, as recommended in the literature for up to 48 h, was administered. After only 8 h intractable bradycardic dysrhythmias occurred. Although pharmacokinetic studies have pointed to a possible accumulation of propofol during continuous infusions, an interruption of an infusion for several hours has been considered sufficient for practically total clearance of the drug from the body. In this case re-exposure with a recommended dose of propofol was accompanied by bradycardia and dysrythmias that proved to be resistant to therapy and led to fatal cardiac insufficiency with a functioning artificial pacemaker in place. This case raises concerns about the safety of long-term infusions of propofol for sedation in children and possibly also in adults. [source] Acute Percutaneous Lactic Acid Poisoning in a ChildPEDIATRIC DERMATOLOGY, Issue 3 2006Manuela Esteban Ramírez M.D. We report a young girl with lamellar ichthyosis and symptoms of poisoning, with clinical signs of irritability, agitation, myoclonia, and difficulty in walking, accompanied by lactic acidosis as a result of the more frequent than recommended application of emollients containing lactic acid. The clinical symptoms resolved upon discontinuation of the topical treatment. Among the possible causes of metabolic acidosis, health care providers should be aware of the possibility of percutaneous poisoning. [source] Holocarboxylase Synthetase Deficiency Presenting as IchthyosisPEDIATRIC DERMATOLOGY, Issue 2 2006H. Alan Arbuckle M.D. Clinical manifestations usually present within the first few days of life and include severe acidosis, feeding difficulties, breathing abnormalities, vomiting, seizures, progressive loss of consciousness, coma, and death. Skin findings, when present, usually develop within the first weeks of life and are described as an erythroderma-like dermatitis involving the eyebrows, eyelashes, and scalp. We were asked to consult on a newborn with a collodion membrane and severe metabolic acidosis who was eventually diagnosed with holocarboxylase synthetase deficiency and ichthyosis. The diagnosis of holocarboxylase synthetase deficiency might be considered in a newborn with collodion membrane, ichthyosis, and acidosis. [source] Renal Fanconi syndrome and myopathy after liver transplantation: Drug-related mitochondrial cytopathy?PEDIATRIC TRANSPLANTATION, Issue 1 2008Umut Selda Bayrakci Abstract:, Advances in the field of transplantation provide a better quality of life and allow more favorable conditions for growth and development in children. However, combinations of different therapeutic regimens require consideration of potential adverse reactions. We describe a 15-yr-old girl who had orthotopic liver transplantation because of Wilson's disease. Tacrolimus, MMF, and steroids were given as immunosuppressant. Lamivudine was added because of de nova hepatitis B infection during her follow-up. Three yr after transplantation she developed renal Fanconi syndrome with severe metabolic acidosis, hypophosphatemia, glycosuria, and aminoaciduria. Although tacrolimus was suspected to be the cause of late post-transplant renal acidosis and was replaced by sirolimus, acidosis, and electrolyte imbalance got worse. Proximal muscle weakness has developed during her follow-up. Fanconi syndrome, as well as myopathy, is well recognized in patients with mitochondrial disorders and caused by depletion of mtDNA. We suggest that our patient's tubular dysfunction and myopathy may have resulted from mitochondrial dysfunction which is triggered by tacrolimus and augmented by lamivudine. [source] Liver transplantation for progressive familial intrahepatic cholestasis: Clinical and histopathological findings, outcome and impact on growthPEDIATRIC TRANSPLANTATION, Issue 6 2007Sema Aydogdu Abstract:, In this study, we analyze the demographic features, clinical and histopathological findings in patients who underwent liver transplantation for progressive familial intrahepatic cholestasis. We also analyze outcome and impact of liver transplantation on growth and bone mineral content. Most of the patients were presented with jaundice mainly beginning within the first six months. At the time of initial admission; eight patients had short stature (height SD score <2), and four patients had weight SD score <2. Liver transplantation were performed at the age of 43.2 ± 27 months (range 9 to 96 mfonths), 6.5 ± 3.5 months later after the first admission. Infection, surgical complications and osmotic diarrhea associated with severe metabolic acidosis were noted in 41.4%, 16.6% and 33.3%, respectively. One patient developed posttransplant lymphoproliferative disorder. Overall; 1 year graft and patient survival was 69.2% and 75%, respectively. At the end of the 1st year only 2 patients had height SD score <2. Linear regression of height gain against increase in total body BMD measured at the time of transplantation and 1 year after liver transplantation gave a coefficient r = 0.588 (p = 0.074). No correlation was found between the height gain and age and PELD score at time of transplantation, and no difference was noted between the sexes and donor type. Liver transplantation is effective treatment modality with good outcome and little morbidity, and increases the growth acceleration in patients with PFIC associated with cirrhosis. [source] | |||||||||||||||||||||||||||||||||||||