Diarrhea metabolic acidosis

II. Toxic dose. Inhalation or ingestion of as little as 1 mg of fluoroacetate is sufficient to cause serious toxicity. Death is likely after ingestion of mote than 5 mg/kg. Clinical presentation. After a delay of minutes to several hours (in one report coma was delayed 36 hours), manifestations of diffuse cellular poisoning become apparent nausea, vomiting, diarrhea, metabolic acidosis, renal failure, agitation, confusion, seizures, coma, respiratory arrest, pulmonary edema, and ventricular arrhythmias may occur. One case series reported a high incidence of hypocalcemia and hypokalemia. 

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. 

Potassium is contraindicated in patients who are at risk for experiencing hyperkalemia, such as those with renal failure, oliguria, or azotemia (file presence of nitrogen-containing compounds in the blood), anuria, severe hemolytic reactions, untreated Addison s disease (see Chap. 50), acute dehydration, heat cramps, and any form of hyperkalemia Potassium is used cautiously in patients with renal impairment or adrenal insufficiency, heart disease, metabolic acidosis, or prolonged or severe diarrhea. Concurrent use of potassium with... 

Most healthy adults with diarrhea do not develop dehydration or other complications and can be treated symptomatically by self medication. When diarrhea is severe and oral intake is limited, dehydration can occur, particularly in the elderly and infants. Other complications of diarrhea resulting from fluid loss include electrolyte disturbances, metabolic acidosis, and cardiovascular collapse. 

The normal UAG ranges from 0 to 5 mEq/L (mmol/L) and represents the presence of unmeasured urinary anions. In metabolic acidosis, the excretion of NH4+ and concurrent CP should increase markedly if renal acidification is intact. This results in UAG values from -20 to -50 mEq/L (mmol/L). This occurs because the urinary CP concentration now markedly exceeds the urinary Na+ and K+ concentrations. Diagnoses consistent with an excessively negative UAG include proximal (type 2) renal tubular acidosis, diarrhea, or administration of acetazo-lamide or hydrochloric acid (HC1). Excessively positive values of the UAG suggest a distal (type 1) renal tubular acidosis. 

A 70-year-old man presents to the emergency department because of diffuse abdominal pain and nonbloody diarrhea. One day earlier he had been discharged from the hospital, where he had received ceftriaxone and levofloxacin for 7 days for an upper respiratory infection. Soon after going home, he passed numerous liquid brown stools. A few hours later, the patient became disoriented, and an ambulance was called. His medical history is unremarkable. Laboratory values White blood cell count 50,000 cells/mm3, hematocrit 43%, sodium 125 mmol/L, potassium 5.6 mmol/L, C02 14 mmol/L, and metabolic acidosis. An abdominal radiograph series show no evidence of obstruction. The patient was admitted to the hospital. 

Metabolic acidosis is characterized by decreased pH and serum HC03 concentrations, which can result from adding organic acid to extracellular fluid (e.g., lactic acid, ketoacids), loss of HC03 stores (e.g., diarrhea), or accumulation of endogenous acids due to impaired renal function (e.g., phosphates, sulfates). 

Two workers collapsed while inside a tank that was later found to contain a 0.1-0.3% EDB solution. Removed after 20-45 minutes in the tank, one man was intermittently comatose, and the other was delirious and combative. Both experienced vomiting, diarrhea, abdominal pain, and burning of the eyes and throat. Metabolic acidosis and acute renal and hepatic failure ensured. Death occurred 12 and 64 hours later, respectively, despite supportive measures. 

Special risk Use with caution in the presence of cardiac disease, particularly in digitalized patients or in the presence of renal disease, metabolic acidosis, Addison disease, acute dehydration, prolonged or severe diarrhea, familial periodic paralysis, hypoadrenalism, hyperkalemia, hyponatremia, and myotonia congenita. 

Prolonged use or overdose may result in electrolyte or metabolic disturbances (such as hypokalemia, hypocalcemia, and metabolic acidosis or alkalosis), as well as persistent diarrhea, vomiting, muscle weakness, malabsorption, and weight loss. 

Prolonged or excessive use may result in metabolic acidosis due to increased serum lactic acid concentrations. Metabolic acidosis may cause disorientation, fatigue, hyperventilation, headache, nausea, vomiting, and diarrhea. 

Transient diabetes and hyperlipidemia have been reported. Metabolic acidosis is probably a consequence of heavy, cholera-like diarrhea. Progressive reduction of libido was attributed to colchicine in patients with familial Mediterranean fever (312). 

Intoxication may present as inebriation and drowsiness similar to ethanol use. Other symptoms are vomiting, diarrhea, delirium and agitation, back and abdominal pain, and clammy skin. Toxic effects usually follow a latent period of several hours. Formate inhibits mitochondrial cytochromes resulting in neurotoxicity. Ocular signs include blurred vision, dilated pupils, and direct retinal toxicity with optic disc hyperemia and ultimately permanent blindness [91]. Cerebral hemorrhagic necrosis has been reported [92]. Severe poisoning may result in Kussmaul respiration, inspiratory apnea, coma, and death. Urine samples may have the characteristic smell of formaldehyde. An elevated serum osmolal gap from methanol will be evident early in presentation but may disappear after approximately 12 hours. At this time, an elevated anion gap metabolic acidosis from retained formate may be evident. 

Acute toxicity manifests primarily in the CNS, cardiovascular system, and gastrointestinal system. CNS signs include restlessness, tremor, nervousness, headache, insomnia, tinnitus, confusion, delirium, psychosis, and seizures. Cardiac manifestations of overdose include sinus tachycardia, various dysrhythmias, asystole, and cardiovascular collapse. Other findings include tachypnea, nausea, vomiting, hematemesis, diarrhea, and fever. Case reports also include rhabdomyolysis and pulmonary edema. Laboratory findings include metabolic acidosis, respiratory alkalosis, ketosis, hypokalemia, and hyperglycemia. The estimated lethal dose in adults is 150-200 mg kg whereas doses of 10-15mgkg ... 

If ingested (and depending on the amount), nausea, vomiting, and diarrhea are the most common manifestations of toxicity. Persistent effects rarely result but dehydration, electrolyte imbalance (most notable hypochloremic metabolic acidosis) have been reported. 

Diarrhea may cause acidosis as a result of loss of Na, Kfi and HCOJ. One of the primary exocrine functions of the pancreas is production of HCOs to neutralize gastric contents on entry into the duodenum. If the water, K", and HCO7 in the intestine are not reabsorbed, a hypokalemic, normal anion gap metabolic acidosis will develop. The resulting hyperchloremia is due to the replacement of lost bicarbonate with Cr to maintain electrical balance. 

Whenever possible, potassium supplementation should be administered by mouth. Three salts are available for oral potassium supplementation chloride, phosphate, and bicarbonate. Potassium phosphate should be used when patients are both hypokalemic and hypophosphatemic potassium bicarbonate is most commonly used when potassium depletion occurs in the setting of metabolic acidosis. Potassium chloride, however, is the primary salt form used because it is the most effective treatment for the common causes of potassium depletion (i.e., diuretic-induced and diarrhea-induced hypokalemia). Because diarrhea and diuretics such as hydrochlorothiazide and furosemide promote net potassium and chloride losses, supplementation with potassium chloride repletes both electrolytes. Potassium chloride can be administered in either tablet or liquid formulations (Table 50-4). The liquid forms are generally less expensive however,... 

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