Fluid therapy clinical signs

Beclometasone dipropionate is the most widely dispensed inhaled anti-inflammatory agent for astfunatic human patients. Inhaled beclometasone dipropionate reduces inflammatory cell populations in bronchoalveolar lavage fluid, controls clinical signs of airway obstruction and improves parameters of pulmonary function in human asthmatics. Consequently, aerosolized beclometasone dipropionate is the first line of therapy for mod-erate-to-severe allergic airway disease in human patients. Aerosolized beclometasone does not cause adrenal suppression in asthmatic human patients at therapeutic dosages (800-1600 xg/day) and initiation of beclometasone therapy as a replacement for systemic corticosteroid administration permits recovery of the hypothalamic-pituitary-adrenal axis (Barnes et al 1998). 

The clinical scenario and the severity of the volume abnormality dictate monitoring parameters during fluid replacement therapy. These may include a subjective sense of thirst, mental status, skin turgor, orthostatic vital signs, pulse rate, weight changes, blood chemistries, fluid input and output, central venous pressure, pulmonary capillary wedge pressure, and cardiac output. Fluid replacement requires particular caution in patient populations at risk of fluid overload, such as those with renal failure, cardiac failure, hepatic failure, or the elderly. Other complications of IV fluid therapy include infiltration, infection, phlebitis, thrombophlebitis, and extravasation. 

The volume to be infused and rate of delivery are only part of the therapeutic plan for fluid therapy, albeit the most important in acute resuscitation. The electrolyte and acid-base status of the horse should also be considered and fluids chosen to help to correct physiological imbalances. Unfortunately, it is not possible to predict electrolyte and acid-base disturbances accurately based on clinical signs. Seemingly similar clinical presentations may have a quite different pathophysiology (Brownlow Hutchins 1982, Svendsen et al 1979). The recent availability of relatively inexpensive, portable blood gas and electrolyte measuring equipment (Grosenbaugh et al 1998) has made determining the acid-base status possible in ambulatory equine practice and allows the field veterinarian to monitor and treat these disturbances. As stated earlier, in the absence of specific laboratory information, fluid therapy should probably be limited to isotonic polyionic crystalloid fluids, possibly with the addition of 10-20 mEq/1 potassium chloride in the maintenance phase. 

Clinically, the animals do not show signs until 24-48 or more hours after ingestion of the bait. The affected animals are depressed, have reduced urine production, and the urine is of low specific gravity. Severely poisoned animals have hematemesis, azotemia, and cardiac arrhythmias. Animals with renal impairment are more susceptible to cholecalciferol poisoning than those with normal renal function. Cholecalciferol poisoning requires protracted treatment, which may require as long as 3 weeks in severe intoxications. Appropriate treatment consists of fluid therapy to assist the kidneys in removing the excess calcium, corticosteroids to minimize inflammation, and calcitonin to enhance calcium resorption into the bone. Pamidronate disodium is the new antidote for this poison. 

Appropriate follow-up care of patients with acute diarrhea is based on successful restoration of fluid losses. The clinical signs and symptoms (see Table 111-1) that led to the diagnosis also can indicate adequate rehydration and should be assessed frequently. Because oral rehydration therapy is now preferred, routine laboratory testing often is unnecessary. Electrolytes should be measured in those receiving parenteral fluids, when oral replacement fails, or when signs of hypernatremia or hypokalemia are present. Follow-up stool samples to ensure complete evacuation of the infecting pathogen may be necessary only... 

Patients with documented SBP, positive ascitic fluid cultures, or ascitic fluid PMN count >250 cells/mm, regardless of symptoms, should receive broad-spectrum empiric antibiotic therapy with cefotaxime 2 g every 8 hours, or a similar third-generation cephalosporin. Patients with ascitic fluid PMN counts <250 cells/mm , but with signs and symptoms of infection (abdominal pain, tenderness, fever, encephalopathy, renal failure, acidosis, or peripheral leukocytosis), should also receive empiric antibiotic treatment with cefotaxime 2 g every 8 hours, or a similar third-generation cephalosporin. Outpatient oral therapy of SBP with fluoroquinolones or amoxicillin-clavulanic acid awaits further clinical trials. Short-term inpatient quinolone therapy should be considered for the prevention of SBP in patients with low-protein ascites (<1 g/dL), variceal hemorrhage, or prior SBP. 

Edema is a common manifestation of volume overload and extracellular fluid volume expansion. Clinicians should evaluate patients for signs and symptoms of volume overload (e.g., pitting edema, rales, ascites, shortness of breath, and increased weight). Blood pressure monitoring in the clinic setting and at home if feasible to detect hypertension is also warranted. As kidney disease progresses dietary intervention and diuretic therapy (based on the degree of kidney function) will likely become necessary. 

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