Diarrhea metabolic acidosis with

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. 

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. 

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. 

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,... 

Laboratory abnormalities such as increased packed red blood cell volume and total protein, magnesium, and calcium levels are a result of hemoconcentration. Hypoglycemia, seizures, fever, and mental alterations are seen more often in children, perhaps as a reflection of the greater degree of dehydration and electrolyte losses observed with diarrhea in children. Other complications include metabolic acidosis, prerenal azotemia, iatrogenic water intoxication from overrehydration, and aspiration pneumonia. Children, the elderly, and pregnant women are at an increased risk of complications due to cholera. 

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). 

IV. Diagnosis is usually based on a history of exposure combined with a typical pattern of multisystemic signs and symptoms. Suspect acute arsenic poisoning in a patient with abrupt onset of abdominal pain, nausea, vomiting, watery diarrhea, and hypotension, partiouiariy when followed by an evolving pattern of delayed cardiao dysfunction, panoytopenia, and peripheral neuropathy. Metabolic acidosis and eievated CPK may occur eariy in the course of severe cases. Some arsenic compounds, partiouiariy those of iower solubility, are radiopaque and may be visible on a plain abdominal x-ray. 

Diethylene glycol Highly nephrotoxic similar to ethylene glycol. Renal failure, coma, acidosis, and death have been reported In 5 patients with extensive burn Injuries after repeated dermal application. Vomiting, diarrhea, renal failure, metabolic acidosis, hepatitis, pancreatitis, coma, and death reported after Ingestion. Calcium oxalate crystals have been seen In animal studies. Molecular weight Is 106. Ethanol and fomepizole may be effective. 

If there is insufficient bicarbonate to compensate for the extra acid, acidosis can occur. Formally, acidosis is a significant decrease in pH of extracellular fluid. This condition can occur due to both respiratory and metabolic abnormalities. Respiratory acidosis occurs when breathing abnormalities result in CO2 retention and an elevation in Pco2 in alveoli and arterial blood (known as hypercapnia). The term Pco2 refers to the partial pressure of CO2 in the pulmonary alveoli during respiration. Retention of CO2 can result from inadequate ventilation during anesthesia, certain conditions that result from central nervous system disease, or from drug use, and it is observed with emphysema. Metabolic acidosis occurs with starvation, uncontrolled diabetes mellitus with ketosis, and with electrolyte and water loss due to diarrhea.il... 

Watson and his colleagues examined 50 autopsy reports of children poisoned with Impila [17]. Upon presentation to hospital, 80 % of patients showed a disturbed level of consciousness (confusion, stupor, or coma), and in 52 %, this was associated with convulsions. Other conmum symptoms included abdominal pain, vomiting and diarrhea. Hypoglycemia (blood glucose <2.5 mmol/L) was found in 93 % of cases, metabolic acidosis (serum bicarbonate <19 nunol/L) in 87 %, uremia (elevated blood urea >6.64 mmoI/L) in 60 %, hyperkalemia (serum potassium >5.3 mmol/L) in 63 %, hyponatremia (serum sodium <130 nunoI/L) in 45 %, and leukocytosis (total white cell count >11 x 10 /L) in 80 %. In patients who survived more than 24 h, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactic dehydrogenase (LDH) were elevated up to 5—10 times the normal levels, and the prothrombin time was elevated up to 50 % of upper limit of normal. In all cases documented to date, concomitant jaundice has rarely been observed in the patients with hepatotoxicity, and the progression to death was very rapid. 

Oral Treatment of hypokalemia in the following conditions With or without metabolic alkalosis digitalis intoxication familial periodic paralysis diabetic acidosis diarrhea and vomiting surgical conditions accompanied by nitrogen loss, vomiting, suction drainage, diarrhea, and increased urinary excretion of potassium certain cases of uremia hyperadrenalism starvation and debilitation corticosteroid or diuretic therapy. 

Adefovir dipivoxil is well tolerated. A dose-dependent nephrotoxicity has been observed in clinical trials, manifested by increased serum creatinine with decreased serum phosphorous and more common in patients with baseline renal insufficiency and those receiving high doses (60 mg/d). Other potential adverse effects are headache, diarrhea, asthenia, and abdominal pain. As with other NRTI agents, lactic acidosis and hepatic steatosis are considered a risk owing to mitochondrial dysfunction. No clinically important drug-drug interactions have been recognized to date. Pivalic acid, a by-product of adefovir dipivoxil metabolism, can esterify free carnitine and result in decreased carnitine levels. However, it is not felt necessary to administer carnitine supplementation with the low doses used to treat patients with HBV (10 mg/d). 

A. After an acute overdose, symptoms are typically delayed for 2-12 hours and include nausea, vomiting, abdominal pain, and severe bloody diarrhea. Shook results from depressed cardiac contractility and fluid loss into the gastrointestinal tract and other tissues. Delirium, seizures, or coma may occur. Lactic acidosis related to shock and inhibition of cellular metabolism is common. Other manifestations of acute colchicine poisoning include acute myocardial injury, rhabdomyolysis with myoglobinuria, disseminated intravascular coagulation, and acute renal failure. 

Chronic ipecac abuse by anorexic or bulimic individuals has been associated with cardiac toxicity characterized by PR prolongation, T-wave abnormalities, QRS abnormalities, congestive cardiomyopathy, and atrial and ventricular dysrhythmia. Generalized muscle weakness, myopathy, diarrhea, mild tremors, edema, dehydration, metabolic disturbances (hypokalemia, hypochloremic acidosis, elevation of creatinine phosphokinase), shock, and death have also been reported after chronic use (Manno and Manno 1977 Quang and Woolf 2000). 

---