Renal electrolyte loss

Metolazone is effective when renal function is impaired. It potentiates the diuresis produced by frusemide and the combination can be effective in resistant oedema, provided the patient s fluid and electrolyte loss are carefully monitored. 

The efficacy and tolerability of amphotericin prepared in Intralipid 20% have been evaluated in 16 patients with HIV infection and esophageal candidiasis or cryptococcosis and compared with standard amphotericin in a matched group of 24 patients (44). While both formulations had apparently similar clinical and microbiological efficacy, fewer patients receiving the lipid emulsion formulation required premedication or symptomatic therapy for infusion-associated adverse events, and fewer patients were withdrawn because of adverse effects. Renal adverse effects (a rise in serum creatinine and/or electrolyte loss) were more common in patients who received the conventional formulation. 

As a consequence of the blockade of the Na, K, 2Cr-cotransporter, the diuresis produced by furosemide (frusemide) results in increased urinary excretion of sodium, potassium, chloride, calcium and magnesium ions. The losses of sodium, potassium and chloride are approximately 1750, 600 and 2150 mmol, respectively, after i.m. administration of furosemide (frusemide) at 1 mg/kg. Although these electrolyte losses are substantial, they are largely replaced (within the 24 h period following furosemide (frusemide) administration) by enhanced renal reabsorption as well increased ion absorption from the intestinal tract. In addition to this primary action, furosemide (frusemide) may have a lesser inhibitory effect on other chloride ion transporters and the drug can also inhibit carbonic anhydrase activity (Martinez-Maldonado Cordova 1990, Rose 1989,1991, Wilcox 1991). Finally, some of the renal and extrarenal effects of furosemide (frusemide) appear to be mediated through increased prostaglandin production. 

B. Diquat causes similar initial symptoms, but does not cause pulmonary fibrosis. Severe gastroenteritis and gastrointestinal fluid sequestration may cause massive fluid and electrolyte loss contributing to renal failure. Agitation, seizures, and coma have been described. Cerebral and brainstem hemorrhagic infarctions may occur. 

TH E PATIEN T WITH ED EM A. Fhtients with edema caused by heart failure or other causes are weighed daily or as ordered by the primary health care provider. A daily weight is taken to monitor fluid loss. Weight loss of about 2 lb/d is desirable to prevent dehydration and electrolyte imbalances. The nurse carefully measures and records the fluid intake and output every 8 hours. The critically ill patient or the patient with renal disease may require more frequent measurements of urinary output. The nurse obtains the blood pressure, pulse, and respiratory rate every 4 hours or as ordered by the primary health care provider. An acutely ill patient may require more frequent monitoring of the vital signs. 

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. 

In summary, the settings in which fluid replacement is used are hypovolemic patients (e.g., sepsis or pneumonia) hypervolemic patients [e.g., congestive heart failure (CHF), cirrhosis, or renal failure] euvolemic patients who are unable to take oral fluids in proportion to insensible losses (e.g., the perioperative period) and patients with electrolyte abnormalities (see below). 

Electrolytes are involved in many metabolic and homeostatic functions, including enzymatic and biochemical reactions, maintenance of cell membrane structure and function, neurotransmission, hormone function, muscle contraction, cardiovascular function, bone composition, and fluid homeostasis. The causes of electrolyte abnormalities in patients receiving PN may be multifactorial, including altered absorption and distribution excessive or inadequate intake altered hormonal, neurologic, and homeostatic mechanisms altered excretion via gastrointestinal and renal losses changes in fluid status and fluid shifts and medications. 

Electrolytes Daily doses based on daily maintenance requirements, renal function, gastrointestinal losses, acid-base status, concomitant drug therapy, nutritional and anabolic status Pa lion I has hyponatremia, hypokalemia, hypomagnesemia, and hypophosphatemia, also has low serum bicarbonate concentration, could be component of metabolic acidosis due to sepsis... 

Acute renal failure Sudden loss of the kidney s ability to excrete wastes, concentrate urine, and remove electrolytes. 

Chronic renal failure is a common consequence of diabetes but this case is complicated by the loss of fluid and electrolytes (sodium and potassium) due to diarrhoea and vomiting. Normally, the kidneys would respond to such a challenge and maintain homeostasis but Mrs Amin s kidneys were unable to do so. Mrs Amin was put on haemodialysis and treated to control the diabetes. 

Undesired effects. The magnitude of the antihypertensive effect of ACE inhibitors depends on the functional state of the RAA system. When the latter has been activated by loss of electrolytes and water (resulting from treatment with diuretic drugs), cardiac failure, or renal arterial stenosis, administration of ACE inhibitors may initially cause an excessive fall in blood pressure. In renal arterial stenosis, the RAA system may be needed for maintaining renal function and ACE inhibitors may precipitate renal failure. Dry cough is a fairly frequent side effect, possibly caused by reduced inactivation of kinins in the bronchial mucosa. Rarely, disturbances of taste sensation, exanthema, neutropenia, proteinuria, and angioneurotic edema may occur. In most cases, ACE inhibitors are well tolerated and effective. Newer analogues include lisinopril, perindo-pril, ramipril, quinapril, fosinopril, benazepril, cilazapril, and trandolapril. 

Signs of intoxication are (1) cardiac arrhythmias, which under certain circumstances are life-threatening, e.g., sinus bradycardia, AV-block, ventricular extrasystoles, ventricular fibrillation (ECG) (2) CNS disturbances — altered color vision (xanthopsia), agitation, confusion, nightmares, hallucinations (3) gastrointestinal — anorexia, nausea, vomiting, diarrhea (4) renal — loss of electrolytes and water, which must be differentiated from mobilization of accumulated edema fluid that occurs with therapeutic dosage. 

To eliminate the threat of shock, replenishment of the circulation is essential. With moderate loss of blood, administration of a plasma volume expander may be sufficient Blood plasma consists basically of water, electrolytes, and plasma proteins. However, a plasma substitute need not contain plasma proteins. These can be suitably replaced with macromolecules ( colloids ) that like plasma proteins, (1) do not readily leave the circulation and are poorly filtrable in the renal glomerulus and (2) bind water along with its solutes due to their colloid osmotic properties. In this manner, they will maintain circulatory filling pressure for many hours. On the other hand, volume substitution is only transiently needed and therefore complete elimination of these colloids from the body is clearly desirable. 

Fosfomycin (Monurol) [Antibiotic] Uses Uncomplicated UTl Action -1- CeU w l synth Dose 3 g PO in 90-120 mL of H2O single dose X in renal impair Caution [B, ] -t Absorption w/ antacids/Ca salts Contra Component sensitivity Disp Granules SE HA, GI upset Interactions X Effects W/ antacids, metoclopramide EMS Monitor ECG and BP for signs of hypovolemia and electrolyte disturbances d/t D OD May cause impaired coordination, hearing loss and bitt taste in mouth symptomatic and supportive... 

I.c.2.1. Fluid intake. This includes restriction of fluid intake to less than 1 liter per day if, as in oliguric renal failure, daily urine volumes are 500 ml or less and daily insensible losses are estimated to be 500-700 ml. In non-oliguric renal failure daily urine losses plus insensible losses may be in excess of 2 1/day and daily intake obviously has to be adjusted accordingly. Careful balance of intake and output of fluid and electrolytes is extremely important in ARF patients, both oliguric and non-oliguric. 

Urine volume, creatinine clearance, BUN, electrolytes, reduction in edema, increased diuresis, decrease in body weight, reduction in blood pressure, glucose, uricacid, serum calcium (tetany), tinnitus, vertigo, hearing loss (especiallyin those at risk for ototoxicity—IV doses > 120 mg concomitant ototoxic drugs renal disease)... 

Osmotic diuretics are non-electrolytes, freely filterable at the glomerulus, undergo limited reabsorption by the renal tubules. The amount of diuresis produced is proportional to the quantity of osmotic diuretic, therefore for more diuresis, a large quantity of osmotic diuretic should be given. The primary effect of osmotic diuretics involves an increased fluid loss caused by osmotically active diuretic molecule. This results in reduced reabsorption of sodium and water in proximal tubule and since the tubule is permeable to water, there is a passive back diffusion of water, such a process keeps the tubular fluid isotonic. 

Sodium phosphate is available as a nonprescription liquid formulation and by prescription as a tablet formulation. When taking these agents, it is very important that patients maintain adequate hydration by taking increased oral liquids to compensate for fecal fluid loss. Sodium phosphate frequently causes hyperphosphatemia, hypocalcemia, hypernatremia, and hypokalemia. Although these electrolyte abnormalities are clinically insignificant in most patients, they may lead to cardiac arrhythmias or acute renal failure due to tubular deposition of calcium phosphate (nephrocalcinosis). Sodium phosphate preparations should not be used in patients who are frail or elderly, have renal insufficiency, have significant cardiac disease, or are unable to maintain adequate hydration during bowel preparation. 

---