Metabolic acidosis correction

Salicylates Confusion, lethargy, coma, seizures, hyperventilation, hyperthermia, dehydration, hypotelemia. anion gap metabolic acidosis Correct acidosis and fluid and electrolyte imbalance. Provide alkaline diuresis or hemodialysis to aid elimination... 

Metabolic Effects. Severe metabolic acidosis with high anion gap and hyperglycemia was reported in humans after acute poisoning with endosulfan (Blanco-Coronado et al. 1992 Lo et al. 1995). In five of the six cases reported by Blanco-Coronado et al. (1992), the metabolic acidosis was corrected with gastric lavage with activated charcoal and intravenous sodium bicarbonate and diazepam. No further information regarding metabolic effects in humans after exposure to endosulfan was located. 

Monitor serum electrolytes and arterial blood gases regularly. Correct metabolic acidosis slowly to prevent the development of metabolic alkalosis or other electrolyte abnormalities. 

Pierce NF, Fedson DS, Brigham KL, et al. The ventilatory response to acute base deficit in humans. Time course during development and correction of metabolic acidosis. Ann Intern Med 1970 72 633-640. 

The primary treatment of metabolic acidosis is to correct the underlying disorder. Additional treatment depends on the severity and onset of acidosis. 

Management of methanol and ethylene glycol poisoning is similar. Symptomatic support of respiration and circulation is augmented by correction of metabolic acidosis with intravenous bicarbonate infusion, and control of seizures with diazepam. Ethanol inhibits the metabolism of methanol and ethylene glycol to the toxic metabolites, and can give time for further treatment. The goal is to maintain blood ethanol concentrations between 100 and 150 mg per decilitre, sufficient to saturate alcohol... 

Roderick P, Willis NS, Blakeley S, Jones C, Tomson C. Correction of chronic metabolic acidosis for chronic kidney disease patients. Cochrane Database Syst Rev 2007. 

During or after giving anaesthesia, to correct metabolic acidosis which results from disturbed respiration. 

Electrolytes and other fluids to correct metabolic acidosis and hypotension. 

Correction of the metabolic acidosis with intravenous bicarbonate. This will also increase urine flow and cause it to become more alkaline (alkaline diuresis) and therefore facilitate excretion of salicylic acid and its conjugated metabolites. As the blood pH rises, the ionization of the salicylic acid increases, causing a change in the equilibrium and distribution of salicylate, which diffuses out of the CNS (Fig. 7.59). 

Secondly, i.v. sodium bicarbonate is given for correction of the metabolic acidosis. Hemodialysis may be used in very serious cases. 

Death. Aluminum is not thought to be life-threatening to healthy humans. Studies of people receiving extremely high doses of oral aluminum in antacids have not shown any human deaths from aluminum. However, in the past, aluminum-related deaths have been reported for persons with renal disease dialyzed with aluminum -containing solutions, uremic patients exposed to dietary aluminum hydroxide to treat hyperphosphatemia and sodium citrate to correct metabolic acidosis (Kirschbaum and Schoolwerth 1989), and workers exposed by inhalation to fine powders of aluminum metal. Only very large doses (hundreds of mg/kg) of aluminum cause death in laboratory animals. 

Phosphate An intracellular shift of phosphate occurs along with potassium as fluid rehydration commences.The phosphate deficit can also be worsened with correction of the metabolic acidosis. Controlled, randomized studies have shown that routine phosphate repletion is not necessary, but some practitioners think it prudent to provide supplemental phosphate if serum phosphate levels are less than 1 mEq/L, potentially reducing the risk of seizure or tissue ischemia. During intravenous phosphate administration, serum calcium concentrations should be monitored carefully to avoid hypocalcemia and tetany (Fisher and Kitabchi, 1983). 

Bicarbonate Current guidelines state that acidosis need not be corrected using exogenous bicarbonate therapy. Intravenous administration of fluids and insulin are sufficient to correct the metabolic acidosis and to regenerate bicarbonate. Some practitioners believe, however, that bicarbonate repletion should be provided in the setting of severe acidosis with pH less than 6.9. 

At presentation, the patient was hemodynami-cally unstable. She had a rapid heart rate and exhibited orthostatic hypotension (a fall in blood pressure on assuming an upright posture) and slow mentation. Her fluid deficit was greater than 4 L. Her lab work revealed hyponatremia (low serum sodium), hyperkalemia (high serum potassium), and a severe anion gap metabolic acidosis with dehydration. Her anion gap was 28, and her corrected serum Na+ was 135 mEq/L. 

Metabolic acidosis involves a build-up of hydrogen ions in the blood, thus lowering blood pH. Under normal physiological conditions, the kidneys excrete excess hydrogen ions, and release more bicarbonate ions into the bloodstream to buffer the excess acid. However, in renal failure, or in diabetic ketoacidosis, this mechanism either fails, or is unable to compensate to an adequate extent. Hence, metabolic acidosis is usually treated with sodium bicarbonate, either intravenously (1.26% or 8.4% i.v. solution) or orally (typically 1 g three times a day). Sodium bicarbonate 1.26% intravenous solution is isotonic with plasma (and with sodium chloride 0.9%), so may be given in large volumes (1-2 L) by peripheral venous catheter to correct metabolic acidosis and provide fluid replacement at the same time. Sodium bicarbonate 8.4% may only be given by central venous catheter. 

Ventilation needs should be assessed, if necessary supported by blood gas analysis. A mixed respiratory and metabolic acidosis is common. Hypoxia may be corrected by supplementing the inspired air with oxygen but mechanical ventilation is necessary if the PaCOj exceeds 6.5 kPa. 

Treatment consists of completely avoiding fructose and, if necessary, in correcting metabolic acidosis, electrolytes and blood sugar values. 

A 76-year-old woman developed quadriparesis associated with hyperkalemia after taking diclofenac lOOmg/day for 10 months for gouty arthritis. She had a metabolic acidosis with a normal anion gap and mild renal impairment. Her weakness resolved after withdrawal of diclofenac and correction of the hyperkalemia. 

In 18 children with nalidixic acid intoxication, most of whom were aged under 1 year, the clinical effects were neurological disorders of alertness, hjrpertensive cranial syndrome, and neuronal damage some had a metabolic acidosis (30). Treatment included gastric lavage, correction of acid-base balance, and control of convulsions. 

Hemodialysis corrects any metabolic acidosis while removing methanol and formate [97] and should be considered with evidence of organ toxicity, presence of acidosis, and methanol levels greater than 50 mg/ dL. Fomepizole is dialyzable (see next section). Closure of the osmolal gap correlates with methanol removal and can be followed if methanol levels are unavailable or... 

Treatment should include correction of metabolic acidosis, inhibition of ethylene glycol metabolism and if necessary, extracorporeal elimination of the parent alcohol and metabolites. Acidemia likely increases tissue penetration of toxic metabolites and hinders renal clearance. Although evidence is lacking, bicarbonate administration should be given to correct acidemia. Although more expensive, fomepizole is preferred to ethanol for ADH inhibition due to proven efficacy, predictable pharmacokinetics, and lack of adverse effects [105]. Inhibition of ADH with fomepizole prevents formation of toxic metabolites and renal injury, and improves add-base status [106]. Elimination half-life of ethylene glycol with fomepizole in patients with preserved renal function is approximately 20 hours [107]. Pyridoxine and thiamine should be administered to promote glyoxyhc add conversion less toxic metabolites than oxalate [108]. 

Ekblad H, Kero P, Takala J. Slow sodium acetate infusion in the correction of metabolic acidosis in premature infants. Am ] Dis Child 1985 139(7) 708-710. 

Sodium bicarbonate (8.4%, 5% and 1.25% (isotonic)) has been advocated for the correction of metabolic acidosis in horses (Table 17.7) (Divers 1998, Johnson 1995). However, the cause of the... 

Bjerneroth G, Sammeli 0, Li Y-C et al 1994 Effects of alkaline buffers on cytoplasmic pH in lymphocytes. Critical Care Medicine 22 1550-1556 Boilaert P E, Levy B, Nace L et al 1995 Hemodynamic and metabolic effects of rapid correction of hypophosphatemia in patients with septic shock. Chest 107 1698-1701 Bonagura J D, Reef V B 1998 Cardiovascular diseases. In Reed S M, Bayly W M (eds) Equine internal medicine. Saunders, Philadelphia, PA, pp. 290-370 Bonventre J V, Cheung J Y 1985 Effects of metabolic acidosis on viability of cells exposed to anoxia. 

There is no specific antidote. Supportive care should be instituted for all patients with history of serious boric acid exposure. Substantial recent ingestions may benefit from administration of activated charcoal. Fluid and electrolyte balance, correction of acid/base disturbance, and control of seizures are essential to therapy. Hemodialysis has been successfully used to treat acute boric acid poisoning. Sodium bicarbonate may be used for any metabolic acidosis. 

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