Intravenous Administration Of Hypertonic Solutions Research Articles

Alterations in Metabolic Status and Headshaking Behavior Following Intravenous Administration of Hypertonic Solutions in Horses with Trigeminal-Mediated Headshaking.

Simple SummaryHorses with trigeminal-mediated headshaking syndrome suffer from pain and electric-shock-like sensation in the nerve that runs across their faces (trigeminal nerve), leading to violent head jerking that impairs their performance and quality of life. This condition has no curative treatments and often leads to euthanasia of the animal. Changes in blood components (pH, electrolytes) are known to affect nerve pain. To investigate this, three different kinds of fluids (with varying pH and electrolytes) were given in the vein to horses affected with trigeminal-mediated headshaking. The headshaking behaviors and changes in blood composition were assessed after each treatment. Changes in blood composition were transient, and there was a greater than 50% decrease in headshakes/minute with a high pH treatment. The limited effects following these fluids were likely due to normal mechanisms of regulation of blood levels of these salts and minerals. Further investigations of changes in electrolytes that might affect nerve firing should be explored.Trigeminal-nerve-mediated headshaking represents a major welfare challenge for owners and veterinarians and is caused by a low threshold firing of the trigeminal nerve resulting in pain manifested as violent head jerking that often terminates the horse’s career and life due to poor quality of life and suffering. As metabolic changes such as acid–base status and electrolytes play a role in nerve firing, this study sought to assess the effects following administration of hypertonic solutions on headshaking behavior in affected horses. This prospective randomized controlled crossover design utilized six horses affected with trigeminal-mediated headshaking and three treatment groups receiving intravenous administration of 5% dextrose solution at 2 mL/kg bwt (DS), NaCl 7.5% at 4 mL/kg bwt (HS), or NaHCO3 8.4% at 2 mmol/kg bwt (HB). Horses were assessed for headshaking behavior changes at times T0 (baseline, before infusion) and T15, 30, 60, 120 min post infusion. Venous blood variables: pH, HCO3−, standard base excess (SBE), Na+, Cl−, K+, Ca2+, Mg2+, total magnesium (tMg), glucose, and lactate were measured at T0 (baseline, before infusion) and T5, 15, 30, 60, 120 min post infusion. Strong ion difference (SID) and anion gap (AG) were calculated for each time point. With HB treatment, there was greater than 50% reduction in headshaking rate. There was an effect of time on increasing headshaking rate. There was an effect of breed on headshaking rate. Changes in blood parameters following DS were virtually absent. Infusion of HS caused mild changes and did not vary much from baseline except for SID and AG. Only infusion of HB caused blood pH and HCO3− to be outside of the physiologic range (alkalemia and metabolic alkalosis, respectively), SBE to double or triple, AG to decrease, and SID to increase compared to baseline. Infusion of DS was followed by increase in blood glucose and decrease in blood Na+. Infusion of HS was followed by increase in Na+ and Cl− and decrease in Mg2+. Infusion of HB was followed by decrease in Mg2+. Blood tMg, K+, and Ca2+ decreased slightly, but did not vary greatly from baseline following any of the treatments, remaining within physiologic ranges. Changes in blood composition were transient. Among all treatments, only HB had an effect on headshaking rate. The limited effects following these fluids were likely due to normal mechanisms of regulation of blood levels of pH and electrolytes. Further investigations of changes in electrolytes that might affect nerve firing should be explored.

Aggression to a foal after 4 months of nursing

A 4-month-old male Arabian foal was examined because of a kicking trauma to the right frontal region. The foal had been kicked by its dam when it was seeking the udder the previous day. Radiographic inspection of head and neck showed no defect or bone fracture. Treatment consisting of intravenous administration of hypertonic solution, dexamethasone, and furosemide improved the clinical signs temporarily; however, second head trauma due to falling of the standing foal resulted in deterioration of clinical condition and finally death. At necropsy, epidural, subdural, and subarachnoid hemorrhages, a hematoma at cerebrocerebellar fissure and cerebellar herniation were observed. Continuous assessment of foal rejection-related signs in susceptible mares should be considered until foal weaning.

Hyperosmolarity response of ocular standing potential as a clinical test for retinal pigment epithelium activity normative data

The standing potential of the eye is decreased by intravenous administration of hypertonic solutions. This hyperosmolarity-induced response has been recorded in normal subjects by the use of electro-oculography (EOG) in the dark. An intravenous administration of Fructmanit (1.4 X 10(3) mOsmol) (150 approximately 500 ml, 2.37 approximately 9.70 ml/kg, 0.08 approximately 0.36 ml/kg/min) was used to evoke the hyperosmolarity response. The amplitude of the response was expressed in percentage, V0-Vmin/V0 X 100, where V0 is the base value of the EOG before administration of the hypertonic solution and Vmin is a minimum EOG amplitude after administration. The distribution of the amplitude of the hyperosmolarity response was approximated by the normal distribution in normal subjects. The minimum, the maximum, the mean and the standard deviation of the amplitude of the hyperosmolarity response were respectively 34.2%, 52.3%, 42.6% and 4.6% in normal subjects. The normal range of the hyperosmolarity response would be 33.4 approximately 51.8% (M +/- 2SD). The hyperosmolarity response, which originates mainly in the retinal pigment epithelium, is a useful new quantitative and specific test of the activity of the retinal pigment epithelium in clinical practice.

The hypotensive response to rapid intravenous administration of hypertonic solutions in man and in the rabbit.

Transient hypotension has been observed in patients after rapid intravenous administration of mannitol, 25 per cent, in clinical doses. These studies were conducted to determine the mechanism for the hypotension, to determine dose and rate of injection response curves in rabbits, and to determine which vascular beds were most reactive. Studies in six patients showed mean decreases in blood pressure of 23 +/- 6.0 per cent (+/-SE) and in total peripheral resistance of 38 +/- 7 per cent after infusion of mannitol. Studies in 18 patients during cardiopulmonary bypass with mechanically fixed cardiac output demonstrated decreases in mean blood pressure of 30 +/- 5 to 40 +/- 3 per cent, depending on dose and rate of administration of mannitol. Patients not on bypass compensated for large decreases in total peripheral resistance by increases in cardiac output (3.6 +/- .4 at baseline to 4.4 +/- .4 l/min) during mannitol-induced hypotension with no change in heart rate. Serum osmolality increased as blood pressure decreased. Significant but clinically unimportant decreases in sodium and potassium ions, hemoglobin, pH, and base excess values were observed. Studies in 18 rabbits showed that the greater the dose or rate of injection of mannitol the greater the decrease in blood pressure. Injection of radiolabeled microspheres in rabbits demonstrated a near doubling of blood flow to skeletal muscle tissue during the hypotension. This occurred with both equiosmotic hypertonic glucose (17 +/- 3 to 32 +/- 7 per cent) and mannitol (17 +/- 1 to 31 +/- 5 per cent), but not after isotonic saline solution. Changes in blood flow to other organ beds were variable and unimportant. The results suggest that hypotension following the intravenous administration of hyperosmotic solutions is due primarily to vasodilation in skeletal muscle.

Parenteral and oral alimentation in the treatment of the nonspecific protracted diarrheal syndrome of infancy

Clinical experience in the management of 10 infants who had protracted diarrhea which started before 3 months of age is presented. The first 7 patients died; clearly identifiable pathologic entity was not established as a cause of the diarrhea, and treatment was ineffectual. The last 3 patients were initially evaluated in accord with a prearranged diagnostic protocol and then were started on a therapeutic regimen which included intravenous administration of hypertonic solutions of protein hydrolysate, dextrose, and alcohol and oral feedings of medium-chain triglycerides. This regimen could supply up to 400 calories per kilogram per day. The infants grew and developed while on this treatment and tolerated it for periods of up to 18 weeks without any serious problems. A specific cause for the diarrhea in the 3 infants who recovered could not be demonstrated. However, after recovery, each had an adverse reaction temporally associated with the change from Nutramigen to Enfamil or whole milk feedings, thus suggesting the presence of milk protein allergy.

Influence of blood osmolality on the concentration of protein and hexosamine in canine saliva.

In the present experiments, in an attempt to clarify the mechanism of the influence of the blood osmolality on the electrolyte concentration in saliva, the changes in concentration of the organic component, i. e., protein and hexosamine, in saliva resulting from the intravenous administration of hypertonic solution were studied.The results are as follows:1. Not only electrolyte concentration, but also protein and hexosamine concentration in saliva were increased after the intravenous administration of hypertonic glucose or NaCl.2. The reduction of salivary flow rate appeared together with the increase of blood osmolality, and the concentration of protein, and other constituents in saliva increased. The rate of increase of protein concentration can be explained by the reduction of salivary volume.3. From the relation between the salivary flow rate and the protein excretory rate, it is suggested that the increase of water reabsorption rate through the duct epithelium may play an important role in the increase of protein and hexosamine as well as electrolyte concentration in saliva.4. It was verified by the present experiment using RISA, that the protein was scarcely reabsorbed through the duct epithelium and protein contents in saliva was hardly influenced by the increase of blood osmolality.5. Thus, it is suggested that the previous hypothesis, which explains an increase of concentration of electrolyte in saliva at the state of hypertonicity of body fluid is due to a depressed reabsorption of electrolyte, should be revised.

Myocardial infarction resulting from intravenous administration of hypertonic solution of sodium chloride to patients with arteriosclerosis obliterans of the lower extremities: Borst, J. R., and Holleman, E. J. W.: Acta Med. Scandinav. 130:26, 1948

Myocardial infarction resulting from intravenous administration of hypertonic solution of sodium chloride to patients with arteriosclerosis obliterans of the lower extremities: Borst, J. R., and Holleman, E. J. W.: Acta Med. Scandinav. 130:26, 1948

HYPERLIPEMIA FOLLOWING INTRAVENOUS INFUSION OF HYPERTONIC SOLUTION OF SUCROSE

SEVERE hydropic degeneration of the kidneys, usually limited to the proximal convoluted tubules and the ascending loop of Henle, has been observed after intravenous administration of hypertonic solutions of sucrose in rabbits and men. Helmholtz 1 reported this condition first in 1933, and numerous investigators 2 subsequently confirmed his observations. Experimental evidence 3 has been obtained which suggests that impairment of function of the renal tubules in dogs, cats, rats and monkeys disturbs the balance of factors regulating the concentration of lipids in the blood. It was the object of this study to investigate whether hydropic degeneration of renal tubules, produced by intravenous and intraperitoneal administration of hypertonic solutions of sucrose, is followed by hyperlipemia. METHODS The chemical methods used in this study have been described previously. 3a Male dogs were maintained on a dog chow ration and were fed bones once a week. On the evening prior to the

RENAL LESIONS FOLLOWING ADMINISTRATION OF HYPERTONIC SOLUTIONS OF SUCROSE

Intravenous administration of hypertonic solutions of sucrose has become popular within recent years for the reduction of increased intracranial pressure. Bullock, Gregersen and Kinney 1 in 1935 showed that sucrose reduced cerebrospinal fluid pressure without a secondary rise, such as followed administration of dextrose or saline solutions. The usefulness of sucrose was confirmed by Masserman 2 and by Jackson, Dickerson and Gunther. 3 The injected sucrose did not appear to metabolize or to diffuse out into the cerebrospinal fluid. The sugar was rapidly excreted by the kidneys, with a marked diuresis amounting to about four times the amount of sucrose solution injected. Toxic effects noted were slight, although patients complained of malaise and muscle pain, and a moderate leukocytosis occurred. Helmholz 4 in 1933 noted that hypertonic solutions of sucrose given intravenously to rabbits produced marked renal lesions. One hour after a 20 per cent solution of sucrose was administered,

RENAL CHANGES FOLLOWING ADMINISTRATION OF HYPERTONIC SOLUTIONS (50 PER CENT SUCROSE, 50 PER CENT D-SORBITOL,* 50 PER CENT DEXTROSE AND 10 PER CENT SODIUM CHLORIDE)

Because of the widespread use of hypertonic solutions for intravenous administration in modern clinical practice we became interested in the question whether renal damage resulted from the employment of such solutions and, if so, what the nature and extent of this damage might be. In recent years the intravenous administration of hypertonic solutions of dextrose has become increasingly popular. Lately 50 per cent sucrose has gained wide vogue in the treatment of cerebral edema, glaucoma and retention of fluid resulting from a variety of causes. 1 This material has been rapidly replacing the older dextrose solution for this type of therapy. Helmholz 2 reported on a series of experiments on rabbits given single and multiple injections of 50 per cent solution of sucrose at various intervals and pathologic studies of the kidneys made at intervals of one to seven days after the final injection of the material. Included in his

DIURESIS PRODUCED BY INJECTION OF DEXTROSE

Induction of diuresis by the intravenous administration of hypertonic solutions of dextrose is a well recognized therapeutic measure for the relief of many forms of intoxication, especially for the form frequently accompanying infantile diarrhea. The effects on the circulation and the changes in the blood during and immediately following induction of diuresis have been amply studied in normal animals, but reports of prolonged observations following this procedure are not available in the literature. It was possible to obtain data on two normal infants to whom hypertonic solutions of dextrose had been administered intravenously and to follow the metabolism of fixed acids and bases in these subjects for periods of nine days following the initial diuresis. The main objects of this paper are to present data on: The immediate effect of dextrose diuresis on the body content of fixed acids and bases in normal infants. The time interval necessary

Effect of Hypertonic Solutions on Cerebrospinal Fluid Pressure with Special Reference to Secondary Rise and Toxicity.

The effect of hypertonic solution on the spinal fluid pressure is of vital importance from a clinical standpoint, since Weed and McKibben1 show that the cerebrospinal fluid volume could be reduced by intravenous injection of hypertonic solution. Cushing and Foley2 and Foley and Putnam3 applied this observation to clinical cases of increased intracranial pressure and it was immediately recognized of importance in the treating of head injuries. However, Browder4 among others pointed out from clinical observations: first, the toxicity of NaCl solution, and second, the occasional deaths that occur after a short period of clinical improvement after intravenous administration of hypertonic solution in cases of head injuries with symptoms of increased intracranial pressure.Our experiments were carried out on a series of 10 dogs and one man. We used various concentrations of NaCl and of glucose. The results were uniform. First, it was demonstrated that hypertonic saline has a definitely toxic effect, which in con...

REDUCTION OF INCREASED INTRACRANIAL PRESSURE

The old, empiric treatment for head injuries consisted of rest in bed, morphin and large doses of magnesium sulphate. The rationale of this not being evident, it was discarded in many clinics. However, experimental work by Weed and McKibben1demonstrated that cerebrospinal fluid pressure and brain volume were both reduced by the intravenous administration of hypertonic solutions of various salts and of glucose. Cushing and Foley2reported similar results through the ingestion of hypertonic solutions, and later Foley and Putnam3obtained like effects by intra-intestinal administration. Clinical application of these experimental findings was reported by a number of workers, particularly by Cushing and Foley,2Sachs and Belcher,4Ebaugh and Stevenson,5Hughson6and Fay.7Thus was the empiric administration of magnesium sulphate for traumatic intracranial lesions confirmed and its use reestablished. It has been shown that nearly identical results in the reduction of