Metabolic acidosis, management

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Metabolic acidosis in patients undergoing dialysis can often be managed by using higher concentrations of bicarbonate or acetate in the dialysate. 

Severe metabolic acidosis - Administer 90 to 180 mEq/L (approximately 7.5 to 15 g) at a rate of 1 to 1.5 L during the first hour. Adjust to patient s needs for further management. 

The answer is C. Ingestion of an acid or excess production by the body, such as in diabetic ketoacidosis, may induce metabolic acidosis, a condition in which both pH and HCOj become depressed. In response to this condition, the carbonic acid-bicarbonate system is capable of disposing of the excess acid in the form of CO2. The equilibrium between bicarbonate and carbonic acid shifts toward formation of carbonic acid, which is converted to COj and HjO in the RBC catalyzed by carbonic anhydrase, an enzyme found mainly in the RBC. The excess CO2 is then expired by the lungs as a result of respiratory compensation for the acidosis (Figure 1-2). The main role of the kidneys in managing acidosis is through excretion of H" rather than CO2. 

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... 

The cardiac arrhythmias are life-threatening, so the patient must be closely monitored, with facilities available for possible resuscitation. Drugs such as quinidine and procainamide are contraindicated, but lidocaine, propranolol, or phenytoin has been used safely and effectively. The arterial blood gas levels, pH, and electrolyte concentrations should be monitored so that metabolic acidosis or hypokalemia can be identified that would further aggravate the arrhythmias. Electrical pacing may be required if the antiarrhythmic drugs fail. Hyperpyrexia is treated by cooling. Seizures may be managed by intravenous doses of diazepam. 

It is critical that the blood methanol level be determined as soon as possible if the diagnosis is suspected. Methanol concentrations in excess of 50 mg/dL are thought to be an absolute indication for hemodialysis and ethanol treatment, though formate blood levels are a better indication of clinical pathology. Additional laboratory evidence includes metabolic acidosis with an elevated anion gap and osmolar gap (see Chapter 59 Management of the Poisoned Patient). A decrease in serum bicarbonate is a uniform feature of severe methanol poisoning. 

Prompt referral for liver transplantation is the therapy of choice for most patients with fulminant hepatic failure. Transplantation should be considered in all cases in which the patient demonstrates progressive clinical deterioration (encephalopathy, hypoglycemia, metabolic acidosis, renal failure, and coagulation defects)." Patients should be transferred at the first sign of altered mental status, because these patients often worsen very rapidly. One-year smvival rates with liver transplantation for fulminant hepatitis are 50% to 80% (as compared to <20% with medical management alone)."... 

In addition to CKD as a risk factor, other contributing factors should also be considered. This includes exposure to potassium-sparing diuretics -blockers, which work predominantly via 82-antagonistic effects to interfere with the extrarenal translocation of potassium into cells and ACEls, which may cause hyperkalemia by reducing aldosterone production. Polycitra, used for the treatment of metabolic acidosis, contains potassium citrate and should not be prescribed for patients with severe CKD. If hyperkalemia develops, management options are based on the degree to which potassium is elevated (see Chap. 50). 

Metabolic acidosis in both adult and pediatric patients undergoing dialysis can often be managed by using higher concentrations of bicarbonate or acetate in the dialysate (>38 mEq/L bicarbonate is safe and effective). Administration of oral bicarbonate salts as described above may also be necessary for some patients. 

The management of patients with life-threatening acute metabolic acidosis (plasma bicarbonate of 8 mEq/L and pH... 

Noncomphance with the infusion of appropriately prescribed fluids also can lead to dehydration. Patients who have SBS complicated by a pancreatic flsmla and severe diarrhea lose considerable potassium and bicarbonate and may develop metabohc acidosis. Patients with severe diarrhea who have an intact colon wiU conserve sodium and chloride, resulting in considerable loss of potassium and bicarbonate and the development of metabolic acidosis. Quantifying fluid losses with particular attention to the sources of loss wiU aid in the acid-base management of these patients (see Chap. 51). 

Ethanol is likely to be administered in management Metabolic acidosis is very likely Oxalate crystals may be present in the urine... 

Fluid management to reduce overload Treatment of metabolic acidosis... 

Drug overdose Of 16 796 toxic exposures to antiepileptic drugs (phenytoin, valproic acid, and carbamazepine) in the USA in 2006, 12 resulted in death, as reported by the US Toxic Surveillance System [67 ]. Some specific problems determined by overdose of some old and new antiepileptic drugs have been briefly reviewed. For example, topiramate can cause a significant metabolic acidosis, lamotrigine Stevens-Johnson syndrome, oxcarbazepine hyponatremia, and levetiracetam psychosis. Possible adoption of guidelines for critical care management of overdose are discussed. 

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