Diarrhea fluid loss from

Augmenting antidepressants with lithium has repeatedly been shown to be effective. But lithium is a difficult medication to take. It is very dangerous in overdose and can quickly reach toxic levels due to fluid loss from diarrhea, profuse sweating, or high fevers. Even at treatment levels, lithium can produce unpleasant side effects such as dizziness, frequent urination, and tremors. Despite all its problems, lithium... 

The child s estimated blood volume is 80 mL/kg, which is larger than an adult s on a milliliter per kilogram basis. Therefore, small amounts of blood loss can impair perfusion and decrease circulating blood volume. Children have greater cardiac reserves and catecholamine responses compared with adults, allowing them to compensate for fluid losses from hemorrhage, diarrhea, or lack of oral intake. However, shock and cardiopul-... 

Treat fluid loss from vomiting or diarrhea with intravenous crystalloid fluids (P 16). 

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. 

Lithium toxicity can occur as a result of intentional overdose therefore, care must be taken when administering lithium to potentially suicidal patients with BPAD. Inadvertent lithium toxicity may also occur. For example, diuretics and nonsteroidal anti-inflammatory drugs such as ibuprofen (Advil, Motrin) slow the excretion of lithium and can lead to accidental toxicity. Consequently, the patient should be advised not to take such commonly available medications while treated with lithium. In addition, dehydration resulting from varied causes such as diarrhea, vomiting, and profuse sweating can lead to accidental lithium toxicity. One should advise the patient who takes lithium to be careful to remain well hydrated at all times and to contact his/her physician if any medical condition arises that may cause rapid fluid losses (e.g., stomach virus, high fevers). 

Reported reference intervals for the serum of adults vary from 3.5 to 5.1 and 3.5 to 5.0mmol/L, and 3.7 to 5.9 for newborns. For plasma, frequently cited intervals are 3.5 to 4.5 and 3.4 to 4.8mmol/L for adults. Cerebrospinal fluid concentrations are -70% of plasma. Urinary excretion of K varies with dietary intake, but a typical range observed in an average diet is 25 to 125 mmol/day. Gastric juice contains IC at lOramol/L. Fecal excretion has been reported as 18.2 2.5 mmol/day in one instance and 5 mmol/day in another. In severe diarrhea, gastrointestinal loss maybe as much as 60 mmol/day. 

V. cholerae is a gram-negative baciUus sharing similar characteristics with the family Enterobacteriaceae. Most pathology of cholera results from an enterotoxin (cholera toxin) produced by the bacteria. Conditions that reduce gastric acidity, such as the use of antacids, histamine-receptor blockers, or proton pump inhibitors or infections with Helicobacter pylori, increase the risk for clinical disease. Cholera toxin stimulates adenylate cyclase, which increases intracellular cAMP and results in inhibition of sodium and chloride absorption by microvillli and promotes the secretion of chloride and water by crypt cells. The toxin likely acts along the entire intestinal tract, but most fluid loss occurs in the duodenum. The net effect of the cholera toxin is isotonic fluid secretion (primarily in the small intestine) that exceeds the absorptive capacity of the intestinal tract (primarily the colon). This results in the production of watery diarrhea with electrolyte concentrations similar to that of plasma. 

Dennis Veere has become dehydrated because he has lost so much water through vomiting and diarrhea (see Chapter 4). Cholera toxin increases the efflux of sodium and chloride ions from his intestinal mucosal cells into the intestinal lumen. The increase of water in his stools results from the passive transfer of water from inside the cell and body fluids, where it is in high concentration (i.e., intracellular Na+ and Cl concentrations are low), to the intestinal lumen and bowel, where water is in lower concentration (relative to high Na+ and Cl ). The watery diarrhea is also high in K+ ions and bicarbonate. All of the signs and symptoms of cholera generally derive from this fluid loss. 

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. 

A. Phosphorus is highly corrosive and is also a general cellular poison. Cardiovascular collapse occurring after ingestion probably results not only from fluid loss owing to vomiting and diarrhea but also from direct toxicity on the heart and vascular tone. 

Ingestion of the toxin produces fever, severe stomach cramps, vomiting, and diarrhea. There is marked fluid loss that can lead to death from dehydration and hypovolemic shock. Within 3 to 12 hours of inhalation of SEB, patients will develop high fever, headache, myalgias, and nonproductive cough. The more severe cases will develop midstemal chest pain and dyspnea. 

After an incubation period of 12 to 72 hours, the disease suddenly presents with abdominal cramping and then painless, profuse rice water diarrhea (5—10 liters per day). Some patients may also have vomiting, weakness, and headache. Fever, if present, is low-grade. The response to infection varies greatly. Many patients have few or no symptoms (400 1 ratio of asymptomatic to symptomatic) others lose massive amounts of fluids and develop hypovolemic shock. As with other diseases, cholera is worse in the very young and very old. Deaths are from fluid loss and electrolyte abnormalities. 

The disease usually lasts from 2 to 7 days. The mainstay of treatment is fluid and electrolyte replacement. This can be done orally for those patients who are not vomiting (3.5 g NaCl, 2.5 g NaHGOs, 1.5 g KGl, 20 g glucose per hter). Some patients will lose fluid so rapidly that they require oral and IV replacement. Antibiotics (doxycychne 100 mg BID for 3 days or ciprofloxin 500 mg BID for 3 days) shorten the diarrhea and thus decrease fluid loss. 

Hypernatremia, that is, sodium levels of 146 mEq/L (146 mmol/L) or higher, results from excessive sodium intake or sodium retention with excessive loss of water owing to diarrhea, diurehc medicahon use, vomiting, sweating, heavy respirahon, or severe bums. Therefore, these pahents are at highest risk and should be monitored closely. Elderly hospitalized pahents should be watched most carefully because many have chronic diseases that may be fatal in combinahon with excessive sodium and fluid loss. 

Receiving updated medical information about the patient s condition or new medicines. Symptom assessment such as cramps, prolonged bleeding from puncture sites, or fluid loss due to diarrhea. If the patient complains of cold fingers on the side of the access, a glove should be used during the winter. 

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). 

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