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Electrolyte and Acid-Base Disturbances
Published in John K. DiBaise, Carol Rees Parrish, Jon S. Thompson, Short Bowel Syndrome Practical Approach to Management, 2017
Lingtak-Neander Chan, Berkeley N. Limketkai
Acid-base disturbances in SBS depend largely on stool output. In the setting of significant mal-absorption and large-volume diarrhea, metabolic acidosis can occur through similar mechanisms of HCO3- loss as described with other severe diarrheal diseases. In addition, relative carbohydrate malabsorption in SBS patients leads to fermentation by colonic bacteria into l- and d-isomers of lactic acid [9,12]. While humans can rapidly metabolize l-lactic acid, metabolism for d-lactic acid occurs more slowly and is then allowed to accumulate in the bloodstream, thus further contributing to metabolic acidosis. Lactic acidosis can also arise from vascular hypoperfusion in severe volume depletion. A fourth mechanism for potential acid-base imbalance in SBS is iatrogenic metabolic acidosis or alkalosis through the provision of excessive amount of chloride or acetate in parenteral nutrition.
Acid/base balance
Published in Bernie Garrett, Fluids and Electrolytes, 2017
Acidosis and alkalosis may result from a wide variety of acute or chronic disorders, and can be categorized as metabolic or respiratory, depending on their primary cause. For example, acid accumulation in the blood caused by acute respiratory failure and insufficient clearance of CO2 is known as an acute respiratory acidosis, whereas an excess loss of HCl due to vomiting would cause an acute metabolic alkalosis. See Table 5.1 for a summary of the most common causes of acid/base imbalance.
Practice Paper 5: Answers
Published in Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar, Get ahead! Medicine, 2016
Anthony B. Starr, Hiruni Jayasena, David Capewell
The pH is 7.31 (an acidosis). The bicarbonate is normal but the carbon dioxide is high, so it must be this that is contributing to the acid–base imbalance (respiratory acidosis). Since there is no effort at compensation by bicarbonate, this is an uncompensated respiratory acidosis and could be due to an underlying chest infection.
Lethal toxicity induced by combined ingestion of dietary acetic acid and carbamazepine
Published in Drug and Chemical Toxicology, 2023
Iuliu Fulga, Oana-Maria Dragostin, Carmen Chitescu, Ioana Irimia, Alin Pîrăianu, Elena Stamate, Ana Fulga
The 52-year-old female patient is brought to the Emergency Department of the Medical-Social Unit for suspicion of acetic acid ingestion. From the reports of the medical staff, recorded that the patient did not show up at breakfast, being later found in the ward, with an empty bottle of food acetic acid next to her, saying she was feeling unwell. From her personal pathological history, the diagnosis of ‘dementia’ is remembered, being under treatment with carbamazepine. Upon the arrival of the ambulance crew, the patient presents with the Glasgow Score = 3p, Rr = 14 breaths/min, Pulse = 80 bpm, BP left hand = 83/55 mmHg, BP right hand = 60/27 mmHg, SatO2 below 50%, glycemia = 164 mg/dL, the crew intervenes with ALS (advanced life support) maneuvers which are without any result, the patient died shortly after admission. Following the arterial blood gas (ABG) test, an acid–base imbalance is detected, manifested in the form of severe respiratory acidosis with a pH of 6758; P CO2 = 80.3 mmHg, HCO3– = 10.7 mmol/L.
Efficacy and safety of nafamostat mesilate anticoagulation in blood purification treatment of critically ill patients: a systematic review and meta-analysis
Published in Renal Failure, 2022
Yao Lin, Yiming Shao, Yuchun Liu, Ruoxuan Yang, Shuanglin Liao, Shuai Yang, Mingwei Xu, Junbing He
In the 2012 Kidney Disease Improving Global Outcome (KDIGO) Clinical Practice Guidelines, regional citrate anticoagulation is recommended internationally for acute kidney injury (AKI) patients with bleeding tendencies [45], but the conclusion was drawn from several clinical studies showing the advantages of citrate in the aspect of lower risk of circuit loss, filter failure and bleeding in comparison to heparin [47–49]. Comparative studies on the treatment of NM and citrate for BPT patients are lacking; only one study presented available data in our meta-analysis, and no significant difference in bleeding risk was found between the NM and citrate groups [30]. Furthermore, critically ill patients who undergo BPT with citrate usually have liver dysfunction or other conditions that result in impaired citrate metabolism [50]. Citrate accumulation might cause metabolic complications such as acid-base imbalance, electrolyte abnormalities, hypotension and arrhythmia, while these potential side effects did not exist in anticoagulation with NM [51].
Proteomic profiling of carbonic anhydrase CA3 in skeletal muscle
Published in Expert Review of Proteomics, 2021
Paul Dowling, Stephen Gargan, Margit Zweyer, Hemmen Sabir, Dieter Swandulla, Kay Ohlendieck
Rhabdomyolysis is a serious muscle-associated syndrome that is characterized by the unregulated release of intracellular components through the damaged sarcolemma membrane. Secondary disturbances of the heart, kidneys, and body-wide electrolyte homeostasis can cause potentially life-threatening cardiac arrhythmias, renal failure, and acid–base imbalance due to the accumulation of muscle-derived electrolytes and excess muscle proteins in the systemic circulatory system [107]. Patients suffering from an acute episode of rhabdomyolysis may experience myalgia and contractile weakness to a different degree, as well as myoglobinuria that usually presents itself as darkly stained urine. Triggering factors of rhabdomyolysis may include traumatic reasons (such as severe skeletal muscle damage through crushing injury, third-degree burns or electric shock injury), or nontraumatic reasons (such as unusual strenuous exercise, excess alcohol abuse in association with binge drinking, certain medicines, toxins, infections, or sepsis). Established serum biomarkers of rhabdomyolysis and the general disintegration of sarcolemmal structure are creatine kinase, myoglobin, troponins, the FABP3 isoform of fatty acid-binding protein, and myosin light-chain MYL3, as well as an elevated concentration of muscle-specific CA3 [105,108].