Atrioventricular conduction abnormality and hyperchloremic metabolic acidosis in toluene sniffing


Hyperchloremic acidosis often occurs in the context of renal/tubular dysfunction. It is usually well tolerated, especially with adequate respiratory compensation. The prognosis largely corresponds to the underlying disease. Consider hypoaldosteronism (type 4 RTA) if accompanied by hyperkalemia, especially if diabetic. Consider RTA types 1 and 2 if hypokalemia persists. Arterial blood gas measurements are required to measure pH and determine if acidosis is of metabolic origin. The urinary anion gap is an important measure of hyperchloric acidosis to assess the status of urinary ammonium excretion, as described above. Distal tubular acidosis results in a urine pH greater than 5.3 and a positive urinary anion gap. In proximal renal tubular acidosis, the urine pH is usually below 5.3 and the urine anion gap is altered. In any case of hyperchloric acidosis, primary treatment aims to identify and treat the initiating event of the condition. If respiratory fatigue and respiratory failure occur, these patients must be intubated and mechanically ventilated. Hyperventilating the patient under ventilator control may help reduce the acid load. For gastrointestinal causes, patients are prone to dehydration from diarrhea and intestinal aspiration, so it is important to maintain fluid load with intravenous (IV) normal saline. Additionally, electrolytes should be monitored and replenished as needed. Potassium levels are especially important. Acidosis is relieved by adding bicarbonate to saline until the underlying medical condition resolves. Proximal renal tubular acidosis requires large doses of bicarbonate, vitamin D, and potassium. The usual dosage of bicarbonate is 5-15 mU/kg/day. In hypokalemic distal renal tubular acidosis, prolonged administration of sodium bicarbonate and alkali to supplement endogenous acid production. Calcium supplementation is also required. Obstructive uropathy should be identified in hyperkalemic distal renal tubular acidosis. If excessive fluid intake is a problem, diuretics with added potassium can be given with some benefit. Treatment-resistant acidosis may require dialysis therapy. As always, a variety of medications is known to induce hyperchloric acidosis and should be avoided or used with caution. Proximal tubular acidosis is associated with streptozotocin, lead, mercury, arginine, valproic acid, gentamicin, ifosfamide, and the use of tetracyclines, which are not recommended. If hyperchloremic acidosis is not corrected, acidosis can cause cardiac arrhythmias, be fatal and increase mortality. A pH below 7.2 may impair myocardial contractility and increase the risk of ventricular fibrillation and heart failure. Tachypnea can compensate for acidosis and cause respiratory muscle fatigue, which can lead to respiratory arrest if not corrected quickly. Hyperchloremic acidosis is treated by a multidisciplinary team of nephrologists, internists, endocrinologists, cardiologists, and pulmonologists. Acidosis causes many symptoms and can even lead to cardiac arrest and respiratory failure. The key lies in managing the main conditions that lead to hyperchloric acidosis. Patients with respiratory or cardiac symptoms should be monitored closely and acidosis may need to be reversed with bicarbonate. It is important to exclude drugs causing acidosis. For most patients, the prognosis is fair as long as the underlying disease is treated. Morbidity and mortality can be high if the underlying disease is not treated. Hyperchloremic metabolic acidosis is a pathological condition due to loss of bicarbonate rather than acid production or retention. The loss of bicarbonate (HCO3) leading to hyperchloremic metabolic acidosis occurs in several ways. Gastrointestinal (GI) cause’s renal causes and extrinsic causes. Gastrointestinal bicarbonate loss occurs with severe diarrhea, pancreatic fistula, nasojejunal aspiration from the duodenum, and chronic use of laxatives. Renal sources of hyperchloremic acidosis include proximal renal tubular acidosis, distal renal tubular acidosis, and long-term use of carbonic anhydrase inhibitors. Extrinsic causes include ingestion of acids such as ammonium chloride or hydrochloric acid and volumetric resuscitation with 0.9% saline.