Urine anion gap can differentiate respiratory alkalosis from metabolic acidosis in the absence of blood gas results.

INTRODUCTION: Low plasma bicarbonate concentration due to chronic respiratory alkalosis may be misdiagnosed as metabolic acidosis and mistreated with administration of alkali therapy, particularly when arterial blood gas is not available. METHODS: We measured urine anion gap [urine (Na+ + K+ ) - (Cl- )], as a surrogate of renal ammonium excretion in 15 patients presenting with hyperventilation and low serum bicarbonate concentration to distinguish chronic respiratory alkalosis (CRA) from metabolic acidosis (MA) when blood gas was unavailable. RESULTS: Hyperventilation and low serum bicarbonate concentrations were associated with urine pH above 5.5 and positive urine anion gap in all, suggesting CRA. The diagnosis was later confirmed by obtaining capillary blood gas, which showed a decrease in PCO2 and high normal pH values. CONCLUSION: The use of urine anion gap can help to differentiate between chronic respiratory alkalosis and metabolic acidosis, especially when arterial blood gas is not obtained.

Acid-Base.

In clinical medicine, evaluation of acid-base balance can be a valuable diagnostic and monitoring tool. Blood gas machines need very small volumes of blood and provide immediate results, making them ideal for use in the emergency room and intensive care setting. This review outlines the stepwise approach to assessment of acid-base balance in dogs, common causes of acid-base abnormalities, and the general approach to treatment.

Acute Kidney Injury with Severe Metabolic Alkalosis Caused by Habitual Vomiting in an Alcohol Abuser with Pyloric Stenosis.

A 47-year-old man was complaining of consciousness disorder. He had acute kidney injury, hypokalemia, and severe metabolic alkalosis. Initial treatment using intravenous infusion of 0.9% saline and potassium chloride improved his consciousness. It was clarified that he was a severe alcohol abuser who habitually self-vomited. We diagnosed him with volume depletion and pseudo-Bartter's syndrome due to loss of chloride by habitual vomiting. Gastrointestinal endoscopy demonstrated pyloric stenosis, which was ameliorated by Helicobacter pylori eradication therapy. We should consider volume depletion and pseudo-Bartter's syndrome as differential diagnoses when we encounter patients with acute kidney injury and severe metabolic alkalosis.

Genetic diagnosis and treatment of hereditary renal tubular disease with hypokalemia and alkalosis.

Renal tubules play an important role in maintaining water, electrolyte, and acid-base balance. Renal tubule dysfunction can cause electrolyte disorders and acid-base imbalance. Clinically, hypokalemic renal tubular disease is the most common tubule disorder. With the development of molecular genetics and gene sequencing technology, hereditary renal tubular diseases have attracted attention, and an increasing number of pathogenic genes related to renal tubular diseases have been discovered and reported. Inherited renal tubular diseases mainly occur due to mutations in genes encoding various specific transporters or ion channels expressed on the tubular epithelial membrane, leading to dysfunctional renal tubular reabsorption, secretion, and excretion. An in-depth understanding of the molecular genetic basis of hereditary renal tubular disease will help to understand the physiological function of renal tubules, the mechanism by which the kidney maintains water, electrolyte, and acid-base balance, and the relationship between the kidney and other systems in the body. Meanwhile, understanding these diseases also improves our understanding of the pathogenesis of hypokalemia, alkalosis and other related diseases and ultimately promotes accurate diagnostics and effective disease treatment. The present review summarizes the most common hereditary renal tubular diseases (Bartter syndrome, Gitelman syndrome, EAST syndrome and Liddle syndrome) characterized by hypokalemia and alkalosis. Further detailed explanations are provided for pathogenic genes and functional proteins, clinical manifestations, intrinsic relationship between genotype and clinical phenotype, diagnostic clues, differential diagnosis, and treatment strategies for these diseases.

Acid-Base Disorders in the Critically Ill Patient.

Acid-base disorders are common in the intensive care unit. By utilizing a systematic approach to their diagnosis, it is easy to identify both simple and mixed disturbances. These disorders are divided into four major categories: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Metabolic acidosis is subdivided into anion gap and non-gap acidosis. Distinguishing between these is helpful in establishing the cause of the acidosis. Anion gap acidosis, caused by the accumulation of organic anions from sepsis, diabetes, alcohol use, and numerous drugs and toxins, is usually present on admission to the intensive care unit. Lactic acidosis from decreased delivery or utilization of oxygen is associated with increased mortality. This is likely secondary to the disease process, as opposed to the degree of acidemia. Treatment of an anion gap acidosis is aimed at the underlying disease or removal of the toxin. The use of therapy to normalize the pH is controversial. Non-gap acidoses result from disorders of renal tubular H + transport, decreased renal ammonia secretion, gastrointestinal and kidney losses of bicarbonate, dilution of serum bicarbonate from excessive intravenous fluid administration, or addition of hydrochloric acid. Metabolic alkalosis is the most common acid-base disorder found in patients who are critically ill, and most often occurs after admission to the intensive care unit. Its etiology is most often secondary to the aggressive therapeutic interventions used to treat shock, acidemia, volume overload, severe coagulopathy, respiratory failure, and AKI. Treatment consists of volume resuscitation and repletion of potassium deficits. Aggressive lowering of the pH is usually not necessary. Respiratory disorders are caused by either decreased or increased minute ventilation. The use of permissive hypercapnia to prevent barotrauma has become the standard of care. The use of bicarbonate to correct the acidemia is not recommended. In patients at the extreme, the use of extracorporeal therapies to remove CO 2 can be considered.

Acid-base disorders: A primer for clinicians.

An understanding of acid-base physiology is necessary for clinicians to recognize and correct problems that may negatively affect provision of nutrition support and drug therapy. An overview of acid-base physiology, the different acid-base disorders encountered in practice, a stepwise approach to evaluate arterial blood gases, and other key diagnostic tools helpful in formulating a safe and effective medical and nutrition plan are covered in this acid-base primer. Case scenarios are also provided for the application of principles and the development of clinical skills.

Metabolic Alkalosis Pathogenesis, Diagnosis, and Treatment: Core Curriculum 2022.

Metabolic alkalosis is a widespread acid-base disturbance, especially in hospitalized patients. It is characterized by the primary elevation of serum bicarbonate and arterial pH, along with a compensatory increase in Pco2 consequent to adaptive hypoventilation. The pathogenesis of metabolic alkalosis involves either a loss of fixed acid or a net accumulation of bicarbonate within the extracellular fluid. The loss of acid may be via the gastrointestinal tract or the kidney, whereas the sources of excess alkali may be via oral or parenteral alkali intake. Severe metabolic alkalosis in critically ill patients-arterial blood pH of 7.55 or higher-is associated with significantly increased mortality rate. The kidney is equipped with sophisticated mechanisms to avert the generation or the persistence (maintenance) of metabolic alkalosis by enhancing bicarbonate excretion. These mechanisms include increased filtration as well as decreased absorption and enhanced secretion of bicarbonate by specialized transporters in specific nephron segments. Factors that interfere with these mechanisms will impair the ability of the kidney to eliminate excess bicarbonate, therefore promoting the generation or impairing the correction of metabolic alkalosis. These factors include volume contraction, low glomerular filtration rate, potassium deficiency, hypochloremia, aldosterone excess, and elevated arterial carbon dioxide. Major clinical states are associated with metabolic alkalosis, including vomiting, aldosterone or cortisol excess, licorice ingestion, chloruretic diuretics, excess calcium alkali ingestion, and genetic diseases such as Bartter syndrome, Gitelman syndrome, and cystic fibrosis. In this installment in the AJKD Core Curriculum in Nephrology, we will review the pathogenesis of metabolic alkalosis; appraise the precipitating events; and discuss clinical presentations, diagnoses, and treatments of metabolic alkalosis.

[Analysis of acid-base disturbances in the emergency department]. / ABC om Syra­bastolkning på akuten.

The analysis of acid-base disturbances contributes to the diagnostic work-up of critically ill patients. Most emergency departments are equipped with blood gas point-of-care analyzers that quantify within minutes pH, pCO2, standard bicarbonate, standard base excess, sodium and chloride levels. This article provides a pragmatic stepwise approach to the analysis of acid-base disturbances in the emergency department. Standard base excess is used to assess the adequacy of the secondary (compensatory) response. Calculation of the anion gap based on the actual bicarbonate is used to identify the coexistence of metabolic acidosis and metabolic alkalosis. The delta anion gap allows for the identification of measurement errors, such as falsely elevated lactate and chloride values, which in turn may provide diagnostic clues.

Refractory hypokalaemia and hypertension with metabolic alkalosis: an acute presentation of Cushing's disease secondary to a pituitary macroadenoma.

A 68-year-old woman presented with right arm cellulitis, not responsive to oral antibiotics. Intravenous antibiotics were commenced, and an ultrasound scan confirmed a collection that was surgically drained. She developed refractory hypokalaemia with normal magnesium, no gastrointestinal losses and no iatrogenic cause. She was hypertensive, hyperglycaemic, alkalotic, clinically obese with proximal myopathy and skin bruising. These clinical findings and refractory hypokalaemic hypertension with metabolic alkalosis raised a suspicion of Cushing's syndrome (CS). 24-hour urinary free cortisol (24 hours) was grossly raised on two occasions. The adrenocorticotropic hormone (ACTH) was significantly raised at 154 ng/L, confirming ACTH-dependant CS. A CT scan of the thorax, abdomen and pelvis excluded an ectopic source of hypercortisolaemia. MRI pituitary revealed an invasive macroadenoma. Treatment with endoscopic debulking resulted in the resolution of hypokalaemia and metabolic alkalosis with significant improvement in hyperglycaemia and hypertension.