The present study aimed to evaluate the effect of dietary cation–anion difference (DCAD) on ruminal fermentation, total apparent digestibility, blood and renal metabolism of lactating dairy cows. Sixteen Holstein cows were distributed in four contemporary 4×4 Latin Square designs, which consisted of four periods of 21 days and four treatments according to DCAD: +290; +192; +98 and −71 milliequivalent (mEq)/kg dry matter (DM). Ruminal pH and concentrations of acetic and butyric acid increased linearly according to the increase of DCAD. Similarly, NDF total apparent digestibility linearly increased by 6.38% when DCAD increased from −71 to 290 mEq/kg DM [Y=65.90 (SE=2.37)+0.0167 (SE=0.0068)×DCAD (mEq/kg DM)]. Blood pH was also increased according to DCAD, which resulted in reduction of serum concentrations of Na, K and ionic calcium (iCa). To maintain the blood acid–base homeostasis, renal metabolism played an important role in controlling serum concentrations of Na and K, since the Na and K urinary excretion increased linearly by 89.69% and 46.06%, respectively, from −71 to 290 mEq/kg DM. Changes in acid–base balance of biological fluids may directly affect the mineral composition of milk, as milk concentrations of Na, K, iCa and chlorides were reduced according to blood pH increased. Thus, it can be concluded that the increase of DCAD raises the pH of ruminal fluid, NDF total apparent digestibility, and blood pH, and decreases the milk concentration of cationic minerals, as well as the efficiency of Na utilization to milk production.

Features consistent with the syndrome known as excited delirium (ExDS) have been associated with law enforcement restraint-related death. The pathophysiology and exact causative factors of restraint-related death associated with ExDS remain unclear. We present a case of successful field resuscitation of a man with ExDS who experienced cardiopulmonary arrest while being restrained by law enforcement officers. Despite the presence of a severe lactic acidosis on emergency department admission, the patient recovered following prehospital treatment with advanced cardiac life support measures and intravenous sodium bicarbonate, likely in part due to early recognition of the disease process.

Toluene sniffing, frequently described under the generic category of “glue sniffing,” is a potential cause of normal anion gap metabolic acidosis due to distal renal tubular acidosis. Urine anion gap is used to diagnose metabolic acidosis of a normal anion gap variety; however, pitfalls exist when using urine anion gap in the setting of toluene sniffing. We present the case of a young woman who had a normal anion gap metabolic acidosis due to toluene sniffing and an unexpectedly low urine anion gap. In such a scenario, the urine anion gap will underestimate the rate of ammonia excretion when the conjugate bases of acids other than HCl are excreted in large quantities. Estimation of the urine osmolal gap will provide a more accurate ammonia excretion rate in these circumstances. The challenges in interpretation of the urine anion gap and ammonia excretion in the setting of distal renal tubular acidosis due to toluene toxicity are discussed.

Salmeterol, a long-acting β2-adrenergic receptor agonist used for the treatment of asthma and chronic obstructive pulmonary disease, has an adverse effects profile that is similar to that of salbutamol and other β2-agonists. We report a sympathomimetic syndrome with metabolic acidosis and hyperlactatemia after intentional inhalation of salmeterol in a suicide attempt. A 16-year-old female patient was admitted to the emergency department approximately 2 hours after having inhaled 60 puffs of a combination of salmeterol xinafoate 25 μg and fluticasone propionate 50 μg. She presented in an anxious state with complaints of palpitations and chest pain. The electrocardiogram demonstrated sinus tachycardia and ST-segment depression in the inferior and anterolateral leads. Laboratory findings showed hypokalemia, hypophosphatemia, and lactic acidosis. Cardiac troponin I and creatine kinase MB remained within the normal range. Treatment was supportive and included intravenous fluids and cautious potassium supplementation. The next day, electrocardiographic and laboratory findings returned to normal. We hypothesize that stimulation of β2-adrenergic receptors by inhalation of salmeterol caused this patient's lactic acidosis. This observation is consistent with the hypothesis that the hyperlactatemia observed during asthma attacks is due in part to the administration of high doses of β2-agonists. Salmeterol overdose by inhalation appears to be sufficient to cause lactic acidosis.

A 36-year-old male with a history of chronic asthma presented to an emergency department with shortness of breath consistent with an asthma exacerbation. He had persistent tachypnea following inhaled bronchodilator treatment; thus, the workup and differential diagnosis were expanded. He was found to have a mixed respiratory alkalosis and metabolic acidosis with elevated serum lactate without an obvious cause and was admitted to hospital. His case was reviewed, and the lactic acidosis was thought to be caused by inhaled β2-agonist use. Emergency physicians should be aware of the potential side effects of inhaled β2-agonists as lactic acidosis may complicate clinical assessment and management of asthma exacerbations and lead to unnecessary and potentially dangerous escalations in therapy.

The workup of the emergency patient with a raised anion gap metabolic acidosis includes assessment of the components of “MUDPILES” (methanol; uremia; diabetic ketoacidosis; paraldehyde; isoniazid, iron or inborn errors of metabolism; lactic acid; ethylene glycol; salicylates). This approach is usually sufficient for the majority of cases in the emergency department; however, there are many other etiologies not addressed in this mnemonic. Organic acids including 5-oxoproline (pyroglutamic acid) are rare but important causes of anion gap metabolic acidosis. We present the case of a patient with profound metabolic acidosis with raised anion gap, due to pyroglutamic acid in the setting of malnutrition and chronic ingestion of acetaminophen.

The concept of diet-induced ‘acidosis’ as a cause of disease has been a subject of interest for more than a century. The present article reviews the history of our evolving understanding of physiological pH, the physiological support for the concept of ‘acidosis’, the causes of acidosis, how it is recognised, its short-term effects as well as the long-term clinical relevance of preventative measures, and the research support for normalisation of pH. Further, we suggest differentiation of the terms ‘acidosis’ and ‘acidaemia’ as a way to resolve the conflation of these topics which has led to confusion and controversy. The available research makes a compelling case that diet-induced acidosis, not diet-induced acidaemia, is a real phenomenon, and has a significant, clinical, long-term pathophysiological effect that should be recognised and potentially counterbalanced by dietary means.

The present review examines the importance of dietary organic anions in preventive nutrition. Organic anions are chiefly supplied by plant foods, as partially neutralised K salts such as potassium citrate, potassium malate and, to a lesser extent, oxalate or tartrate salts. Animal products may also supply K anions, essentially as phosphate, but also as lactate as a result of fermentative or maturation processes, but these K salts have little alkalinising significance. Citrate and malate anions are absorbed in the upper digestive tract, while a substantial proportion is probably metabolised in the splanchnic area. Whatever their site of metabolism, these anions finally yield KHCO3 which is used by the kidneys to neutralise fixed acidity. This acidity essentially reflects the oxidation of excess S amino acids to sulfate ions, which is mainly related to the dietary protein level. Failure to neutralise acidity leads to low-grade metabolic acidosis, with possible long-term deleterious effects on bone Ca status and on protein status. Furthermore, low-grade acidosis is liable to affect other metabolic processes, such as peroxidation of biological structures. These metabolic disturbances could be connected with the relatively high incidence of osteoporosis and muscle-protein wasting problems observed in ageing individuals in Europe and Northern America. Providing a sufficient supply of K organic anions through fruit and vegetable intake should be recommended, fostering the actual motivational campaigns ('five (or ten) per d') already launched to promote the intake of plant foods rich in complex carbohydrates and various micronutrients.

We have studied the acid-base equilibrium in 12 patients with end-stage renal failure (ESRF) during capnoretroperitoneoscopic nephrectomy. Bupivacaine (12 mL, 0.375%) and morphine (2 mg) were given in the lumbar epidural space, and fentanyl (0.5 μg kg−1) and midazolam (50 μg kg−1) were given intravenously. Anaesthesia was induced by thiopental, maintained with halothane carried by oxygen enriched air (inspired oxygen fraction = 0.35), and ventilation was achieved with a tidal volume of 10 mL kg−1 at a rate of 12 min−1. This procedure resulted in a mild degree of respiratory acidosis that was cleared within 60 min. We conclude that capnoretroperitoneoscopic nephrectomy can be performed in patients with end-stage renal failure with minimal transient respiratory acidosis that can be avoided by increased ventilation.