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Emergency Medicine Clinics of North... Nov 2023Metabolic acid-base disturbances are frequently encountered in the emergency department, and many of these patients are critically ill. In the evaluation of patients... (Review)
Review
Metabolic acid-base disturbances are frequently encountered in the emergency department, and many of these patients are critically ill. In the evaluation of patients with these maladies, it is important for the emergency clinician to determine the cause, which can usually be elicited from a thorough history and physical examination. There are several mnemonics that can be used to form an appropriate list of potential causes. Most of the time, the management of these patients requires no specific treatment of the acid-base status but, rather, requires treatment of the underlying disorder that is causing the acid-base disturbance.
Topics: Humans; Acid-Base Imbalance; Acidosis; Alkalosis
PubMed: 37758428
DOI: 10.1016/j.emc.2023.06.008 -
Current Opinion in Nephrology and... Mar 2024Continuous renal replacement therapy (CRRT) is a vital medical intervention used in critically ill patients with acute kidney injury (AKI). One of the key components of... (Review)
Review
PURPOSE OF REVIEW
Continuous renal replacement therapy (CRRT) is a vital medical intervention used in critically ill patients with acute kidney injury (AKI). One of the key components of adequate clearance with CRRT is the use of anticoagulants to prevent clotting of the extracorporeal circuit. Regional citrate anticoagulation is the most often recommended modality. The term 'citrate toxicity' is used to describe potential adverse effects of accumulation of citrate and subsequent hypocalcemia. However, citrate is itself not inherently toxic. The term and diagnosis of citrate toxicity are questioned in this review.
RECENT FINDINGS
Citrate is being increasingly used for regional anticoagulation of the CRRT circuit. Citrate accumulation is infrequent and can cause hypocalcemia and metabolic alkalosis, which are potential adverse effects. Citrate itself, however, is not a toxic molecule. The term 'citrate toxicity' has been used to denote hypocalcemia and metabolic acidosis. However, citrate administration is well known to cause systemic and urinary alkalinization and under certain circumstances, metabolic alkalosis, but is not associated itself with any 'toxic' effects.We review the existing literature and debunk the perceived toxicity of citrate. We delve into the metabolism and clearance of citrate and question current data suggesting metabolic acidosis occurs as the result of citrate accumulation.
SUMMARY
In conclusion, this article calls into question prevailing concerns about 'citrate toxicity'. We emphasize the need for a more nuanced understanding of its safety profile. We recommend discarding the term 'citrate toxicity' in favor of another frequently used, but more meaningful term: 'citrate accumulation'.
Topics: Humans; Acidosis; Acute Kidney Injury; Alkalosis; Anticoagulants; Citrates; Hypocalcemia; Renal Replacement Therapy
PubMed: 37962170
DOI: 10.1097/MNH.0000000000000953 -
Seminars in Respiratory and Critical... Oct 2023Disorders of acid-base status are common in the critically ill and prompt recognition is central to clinical decision making. The bicarbonate/carbon dioxide buffer...
Disorders of acid-base status are common in the critically ill and prompt recognition is central to clinical decision making. The bicarbonate/carbon dioxide buffer system plays a pivotal role in maintaining acid-base homeostasis, and measurements of pH, PCO, and HCO are routinely used in the estimation of metabolic and respiratory disturbance severity. Hypoventilation and hyperventilation cause primary respiratory acidosis and primary respiratory alkalosis, respectively. Metabolic acidosis and metabolic alkalosis have numerous origins, that include alterations in acid or base intake, body fluid losses, abnormalities of intermediary metabolism, and renal, hepatic, and gastrointestinal dysfunction. The concept of the anion gap is used to categorize metabolic acidoses, and urine chloride excretion helps define metabolic alkaloses. Both the lungs and kidneys employ compensatory mechanisms to minimize changes in pH caused by various physiologic and disease disturbances. Treatment of acid-base disorders should focus primarily on correcting the underlying cause and the hemodynamic and electrolyte derangements that ensue. Specific therapies under certain conditions include renal replacement therapy, mechanical ventilation, respiratory stimulants or depressants, and inhibition of specific enzymes in intermediary metabolism disorders.
Topics: Humans; Acid-Base Imbalance; Hydrogen-Ion Concentration; Acid-Base Equilibrium; Acidosis; Alkalosis; Carbon Dioxide
PubMed: 37369215
DOI: 10.1055/s-0043-1770341 -
Journal of the Advanced Practitioner in... Jul 20235-fluorouracil (5-FU) is one of the most common adjuvant antineoplastic agents used in the treatment of localized and metastatic colon cancer. Frequent side effects of...
5-fluorouracil (5-FU) is one of the most common adjuvant antineoplastic agents used in the treatment of localized and metastatic colon cancer. Frequent side effects of 5-FU include myelosuppression, mucositis, nausea, vomiting, and diarrhea. However, hyperammonemic encephalopathy is a rare neurologic toxicity that can occur after 5-FU chemotherapy administration. Patients with 5-FU-induced hyperammonemic encephalopathy often exhibit symptoms of altered mental status with no radiologic abnormalities or laboratory abnormalities except for significantly elevated ammonia levels with occasional lactic acidosis and respiratory alkalosis. We report a case of a patient with stage IV colon adenocarcinoma who experienced altered state of consciousness due to hyperammonemia during the administration of palliative chemotherapy with 5-FU, bevacizumab, and leucovorin. On cycle 1 day 2 of chemotherapy, the patient became drowsy and confused at home, prompting a visit to the emergency department and ultimately hospital admission. Laboratory tests revealed an elevated blood ammonia level (838 μg/dL). After an extensive negative workup, his altered state of consciousness was thought to be secondary to 5-FU-induced hyperammonemia. Upon admission, 5-FU was immediately discontinued and the patient was treated with lactulose enemas, intravenous fluids, rifaximin, and continuous renal replacement therapy with gradual recovery to baseline mental status. It is crucial for advanced practitioners to be aware of this rare side effect to ensure prompt diagnosis and maximize treatment effectiveness.
PubMed: 37576363
DOI: 10.6004/jadpro.2023.14.5.6 -
Pflugers Archiv : European Journal of... Apr 2024Secretin is a key hormone of the intestinal phase of digestion which activates pancreatic, bile duct and Brunner gland HCO secretion. Recently, the secretin receptor... (Review)
Review
Secretin is a key hormone of the intestinal phase of digestion which activates pancreatic, bile duct and Brunner gland HCO secretion. Recently, the secretin receptor (SCTR) was also found in the basolateral membrane of the beta-intercalated cell (B-IC) of the collecting duct. Experimental addition of secretin triggers a pronounced activation of urinary HCO excretion, which is fully dependent on key functional proteins of the B-IC, namely apical pendrin and CFTR and the basolateral SCTR. Recent studies demonstrated that the SCTR knock-out mouse is unable to respond to an acute base load. Here, SCTR KO mice could not rapidly increase urine base excretion, developed prolonged metabolic alkalosis and exhibited marked compensatory hypoventilation. Here, we review the physiological effects of secretin with distinct focus on how secretin activates renal HCO excretion. We describe its new function as a hormone for HCO homeostasis.
Topics: Mice; Animals; Secretin; Cell Membrane; Sulfate Transporters; Biological Transport; Homeostasis; Bicarbonates
PubMed: 38221598
DOI: 10.1007/s00424-024-02906-3 -
Clinical Practice and Cases in... May 2024Diabetic ketoacidosis (DKA) is a common diagnosis in the emergency department (ED). However, one must consider other causes for acid-base disturbances when the pattern...
INTRODUCTION
Diabetic ketoacidosis (DKA) is a common diagnosis in the emergency department (ED). However, one must consider other causes for acid-base disturbances when the pattern is not consistent with typical presentation.
CASE REPORT
A 52-year-old female with a history of insulin-dependent diabetes mellitus type 2 presented to the ED with abdominal pain, nausea, and vomiting for three days. Her diagnostic workup revealed diabetic ketoacidosis but with concurrent metabolic alkalosis. Standard treatment for DKA was initiated, and there was improvement of her mentation and resolution of metabolic derangements.
CONCLUSION
Overlooking a diagnosis of DKA because of alkalosis on venous blood gas testing could lead to inappropriate treatment and, therefore, increased risk of morbidity and mortality in the affected patient.
PubMed: 38869331
DOI: 10.5811/cpcem.1389 -
BMJ Case Reports May 2024Bartter syndrome is a genetic disorder characterised by chloride-unresponsive metabolic alkalosis, hypokalaemia, hypomagnesaemia and hypercalciuria. While it commonly...
Bartter syndrome is a genetic disorder characterised by chloride-unresponsive metabolic alkalosis, hypokalaemia, hypomagnesaemia and hypercalciuria. While it commonly presents antenatally or in early infancy, sometimes, drugs can induce a state similar to Bartter syndrome in any age group, called acquired Bartter syndrome. Polymyxins and aminoglycosides are the most commonly implicated drugs. Polymyxin B and polymyxin E (popularly known as colistin) are the two chemically similar polymyxins that are commonly used clinically. While colistin is frequently associated with nephrotoxicity, polymyxin B is generally considered less nephrotoxic. This difference is due to the way these two drugs are handled by the kidneys. In this case report, we discuss a middle-aged male who developed Bartter syndrome due to polymyxin B, which resolved on discontinuation of the drug, and re-appeared after its re-introduction later. This case exemplifies the nephrotoxicity caused by polymyxin B and the need for vigilance when using this drug.
Topics: Humans; Male; Bartter Syndrome; Polymyxin B; Anti-Bacterial Agents; Middle Aged
PubMed: 38702070
DOI: 10.1136/bcr-2023-255242 -
International Journal of Molecular... Aug 2023The Cl-transporting proteins CFTR, SLC26A9, and anoctamin (ANO1; ANO6) appear to have more in common than initially suspected, as they all participate in the pathogenic... (Review)
Review
The Cl-transporting proteins CFTR, SLC26A9, and anoctamin (ANO1; ANO6) appear to have more in common than initially suspected, as they all participate in the pathogenic process and clinical outcomes of airway and renal diseases. In the present review, we will therefore concentrate on recent findings concerning electrolyte transport in the airways and kidneys, and the role of CFTR, SLC26A9, and the anoctamins ANO1 and ANO6. Special emphasis will be placed on cystic fibrosis and asthma, as well as renal alkalosis and polycystic kidney disease. In essence, we will summarize recent evidence indicating that CFTR is the only relevant secretory Cl channel in airways under basal (nonstimulated) conditions and after stimulation by secretagogues. Information is provided on the expressions of ANO1 and ANO6, which are important for the correct expression and function of CFTR. In addition, there is evidence that the Cl transporter SLC26A9 expressed in the airways may have a reabsorptive rather than a Cl-secretory function. In the renal collecting ducts, bicarbonate secretion occurs through a synergistic action of CFTR and the Cl/HCO transporter SLC26A4 (pendrin), which is probably supported by ANO1. Finally, in autosomal dominant polycystic kidney disease (ADPKD), the secretory function of CFTR in renal cyst formation may have been overestimated, whereas ANO1 and ANO6 have now been shown to be crucial in ADPKD and therefore represent new pharmacological targets for the treatment of polycystic kidney disease.
Topics: Humans; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Polycystic Kidney, Autosomal Dominant; Polycystic Kidney Diseases; Anoctamins; Membrane Transport Proteins; Sulfate Transporters; Antiporters
PubMed: 37686084
DOI: 10.3390/ijms241713278