Hypertonic Saline Infusion Research Articles

Correlation of measured and calculated serum osmolality during mannitol or hypertonic saline infusion in patients after craniotomy: a study protocol and statistical analysis plan for a randomised controlled trial

IntroductionBrain oedema is a major complication after craniotomy. Hyperosmolar agents have been used as the medical treatment for this condition. Measurement and estimation of serum osmolality during hyperosmolar agent infusion...

The syndrome of inappropriate antidiuresis: a copeptin-based classification and identification of a novel subtype

Hyponatremia is the most frequent electrolyte disorder with the syndrome of inappropriate antidiuresis (SIAD) as its most common cause. However, comprehensive characterization of SIAD subtypes is still lacking, but may predict therapeutic success. Using hypertonic saline infusion, the osmoregulation in SIAD was studied in 50 patients with hyponatremia (serum sodium < 130 mmol/L) by serial measurements of serum osmolality, sodium, plasma arginine vasopressin (AVP), and copeptin concentrations. Sixty-eight healthy subjects served as controls showing a close correlation between plasma copeptin and osmolality with an osmotic threshold of 282 ± 4 mOsm/kg H2O. In SIAD, different types of altered AVP osmoregulation were identified: 10% of patients with grosly elevated copeptin concentrations independent of serum osmolality (type A); 14% with linear osmotic response to rising serum osmolality, but abnormally low osmotic threshold (type B); 44% of patients with a plateau-like copeptin secretion (type C); 12% with suppressed copeptin levels (type D). A novel SIAD subtype was discovered in 20% of patients, characterized by a plasma copeptin decrease with increasing osmolality during hypertonic saline infusion (type E or 'barostat reset'). The main alteration in SIAD is a partial or complete loss of AVP osmoregulation over the entire osmotic range. The novel subtype of 'barostat reset' is presumably caused by impaired non-osmotic inhibitory pathways in combination with an altered osmoregulation. Ectopic AVP secretion or AVP-independent antidiuresis has to be assumed in a subset of patients. We hypothesize that the different SIAD subtypes will affect treatment response and patient outcome.

Consistent interindividual increases or decreases in muscle sympathetic nerve activity during experimental muscle pain

We recently showed that long-lasting muscle pain, induced by intramuscular infusion of hypertonic saline, evoked two patterns of cardiovascular responses across subjects: one group showed parallel increases in muscle sympathetic nerve activity (MSNA), blood pressure, and heart rate, while the other group showed parallel decreases. Given that MSNA is consistent day to day, we tested the hypothesis that individuals who show increases in MSNA during experimental muscle pain will show consistent responses over time. MSNA was recorded from the peroneal nerve, together with blood pressure and heart rate, during an intramuscular infusion of hypertonic saline causing pain for an hour in 15 subjects on two occasions, 2-27 weeks apart. Pain intensity ratings were not significantly different between the first (5.8 ± 0.4/10) and second (6.1 ± 0.2) recording sessions. While four subjects showed significant decreases in the first session (46.6 ± 9.2% of baseline) and significant increases in the second (159.6 ± 8.9%), in 11 subjects, there was consistency in the changes in MSNA over time: either a sustained decrease (55.6 ± 6.8%, n = 6) or a sustained increase (143.5 ± 6.1%, n = 5) occurred in both recording sessions. There were no differences in pain ratings between sessions for any subjects. We conclude that the changes in MSNA during long-lasting muscle pain are consistent over time in the majority of individuals, reflecting the importance of studying interindividual differences in physiology.

Management of geriatric mania complicated by hyponatremia and psychogenic adipsic hypernatremia

A 70-year-old male presented with first episode mania and hyponatremia, which were later corrected with an infusion of hypertonic saline. His clinical condition deteriorated because of adipsic hypernatremia associated with hypokalemic periodic paralysis. Hypernatremia correction and potassium supplementation were started but could not be achieved because of manic symptoms as the patient's oral intake was poor. He was restarted on sodium valproate and olanzapine. Over the next few days, the patient's manic symptoms improved significantly and oral intake improved, which eventually led to correction of hypernatremia. Clinicians should evaluate the existence of electrolyte imbalance while dealing with a case of geriatric mania.

Hypertonic saline infusion during resuscitation from out-of-hospital cardiac arrest: A matched-pair study from the German Resuscitation Registry

AimSurvival rates after out-of-hospital-cardiac-arrest (OHCA) differ widely between EMS systems. Since hypertonic saline appears to improve long-term outcome after OHCA, some local EMS systems have included it in their treatment protocols for OHCA. Our first aim was to give a quality review of one of these protocols. Our second aim was to assess whether short-term survival improves when hypertonic saline is used in resuscitation after OHCA. MethodsMatched pairs were identified for the independent “return of spontaneous circulation (ROSC) after cardiac arrest” (RACA) score variables and for use of ACD-CPR, adrenaline, and amiodarone from the German Resuscitation Registry (GRR) for January 2000 to March 2011. Patients received either 2mlkg−1 hypertonic saline with hydroxyethyl starch (7.2% NaCl with 6% hydroxyethyl starch 200,000/0.5, HyperHAES® [HHS]) infused intravenously within 10min during CPR according to local treatment protocols or standard of care CPR (NON-HHS). The primary endpoint was admission to hospital rate (with spontaneous circulation); secondary endpoint was ROSC rate in relation to RACA score. Results322 matched pairs were defined for 14 variables. Predicted ROSC-rate using RACA-score was similar in HHS (44.63%) and NON-HHS (43.63%; p=0.440). In contrast, 190 (59.0%) HHS patients achieved ROSC compared with only 136 NON-HHS patients (42.2%; χ2: p<0.0001). Short term survival measured as rate of “admission to hospital with spontaneous circulation” was achieved in 169 HHS patients (52.5%) versus 108 NON-HHS patients (33.5%) (OR 2.19; 95%CI: 1.592–3.009; χ2: p<0.0001). ConclusionLocally implemented treatment protocols using hypertonic saline/HES after OHCA are safe and effective. Also, we verified that short-term survival rates were better in patients receiving HHS.

Treatment of Endocrine Disorders in the Neuroscience Intensive Care Unit

This review discusses concepts and treatments associated with the most clinically relevant areas of acute endocrine dysfunction amongst patients with common diseases in neuroscience intensive care units (Neuro ICUs). We highlight the following points:• While a thorough work-up for hyponatremia when it is present is always warranted, subarachnoid hemorrhage (SAH) patients who are in a time window concerning for cerebral vasospasm and who are hyponatremic with high urine output are generally thought to have cerebral salt wasting. These patients are typically treated with a combination of continuous hypertonic saline infusion and fludrocortisone.• Diabetes insipidus (DI) is often seen in patients fulfilling death by neurological criteria, as well as in patients with recent pituitary surgery and less often in SAH and traumatic brain injury patients who are not brain dead. Patients with DI in the Neuro ICU often cannot drink to thirst and may require a combination of desmopression/vasopressin administration, aggressive fluid repletion, and serum sodium monitoring.• Diagnosing adrenal insufficiency immediately following pituitary injury is complicated by the fact that the expected atrophy of the adrenal glands, due to lack of a stimulus from pituitary adrenocorticotropic hormone, may take up to 6weeks to develop. Cosyntropin testing can be falsely normal during this period.• Both hyperglycemia (glucose >200mg/dL) and hypoglycemia (glucose <50mg/dL) are strongly associated with neurological morbidity and mortality in ICUs and should be avoided. Glucose concentrations between 120-160mg/dL can serve as a reasonable target for insulin infusion protocols.• There is no data to suggest that treatment of abnormal thyroid function tests in nonthyroidal illness syndrome/sick euthyroid leads to benefits in either mortality or morbidity. True myxedema coma is a rare clinical diagnosis that is treated with intravenous levothyroxine accompanied by stress-dose steroids.

Median preoptic nucleus mediates the cardiovascular recovery induced by hypertonic saline in hemorrhagic shock.

Changes in plasma osmolarity, through central and peripheral osmoreceptors, activate the median preoptic nucleus (MnPO) that modulates autonomic and neuroendocrine adjustments. The present study sought to determine the participation of MnPO in the cardiovascular recovery induced by hypertonic saline infusion (HSI) in rats submitted to hemorrhagic shock. The recordings of mean arterial pressure (MAP) and renal vascular conductance (RVC) were carried out on male Wistar rats (250–300 g). Hemorrhagic shock was induced by blood withdrawal over 20 min until the MAP values of approximately 60 mmHg were attained. The nanoinjection (100 nL) of GABAA agonist (Muscimol 4 mM; experimental group (EXP)) or isotonic saline (NaCl 150 mM; control (CONT)) into MnPO was performed 2 min prior to intravenous overload of sodium through HSI (3 M NaCl, 1.8 mL/kg, b.wt.). Hemorrhagic shock reduced the MAP in control (62 ± 1.1 mmHg) and EXP (61 ± 0.4 mmHg) equipotently. The inhibition of MnPO impaired MAP (CONT: 104 ± 4.2 versus EXP: 60 ± 6.2 mmHg) and RVC (CONT: 6.4 ± 11.4 versus EXP: -53.5 ± 10.0) recovery 10 min after HSI. The overall results in this study demonstrated, for the first time, that the MnPO plays an essential role in the HSI induced resuscitation during hypovolemic hemorrhagic shock.

Effect of hypertonic saline on hypotension following induction of general anesthesia: A randomized controlled trial

Background:The aim of this study was to examine the effects of preoperatively administered i.v. hypertonic saline on hypotension following induction of general anesthesia.Materials and Methods:Fifty-four patients who scheduled for elective surgery were randomly allocated to two groups of 27 patients who received hypertonic saline 5% (2.3 ml/kg) or received normal saline (13 ml/kg). Infusion of hypertonic saline was done half an hour before induction of anesthesia during 30 minutes. Anesthesia was conducted in a standard protocol for all patients. Age, sex, body mass index (BMI), systolic and diastolic blood pressure (SBP, DBP), heart rate (HR) and mean arterial pressure (MAP) were assessed in all patients.Results:The mean age of patients was 36.68 ± 10.8 years. Forty percent of patients were male. The mean SBP at min 2 and min 5, mean of DBP at min 2, 5, and 15, mean of HR at all time points and mean of MAP at min 2 and 15 between groups were no significantly different (P > 0.05), but mean of SBP at min 10 and 15, mean of DBP at min 10, and mean of MAP at min 5 and 10 in hypertonic saline group was significantly more than the normal group (P < 0.05). Trend of SBP, DBP, HR and MAP between groups were not significantly different (P > 0.05).Conclusions:Infusion of hypertonic saline 5% (2.3 mg/kg) before the general anesthesia led to a useful reduction in MAP and reduced heart rate, with no episodes of severe hypotension.

Severe Hyponatremia Following Radioactive Iodine Therapy in Patients with Differentiated Thyroid Cancer

Symptomatic hyponatremia in association with radioactive iodine (RAI) therapy for differentiated thyroid cancer has rarely been reported. Due to the increasing incidence of thyroid cancer worldwide, more patients are now receiving postoperative RAI therapy. We report two cases of life-threatening severe hyponatremia in association with RAI therapy. Two elderly female patients who had bilateral thyroidectomies for their thyroid cancer underwent a low-iodine diet and levothyroxine withdrawal for two weeks prior to RAI therapy. Upon admission, the patients were given 130 mCi (4810 MBq) and 150 mCi (5550 MBq) of (131)I respectively, and oral hydration (two to three liters of water daily) to increase the frequency of emptying the bladder of RAI. Both patients completed their RAI therapy without significant complications and were discharged from hospital. Two days after discharge, both patients were admitted to the emergency room with complaints of severe nausea and dizziness. Initial laboratory tests revealed that they were in a hypothyroid state and had severe hyponatremia with a serum sodium level of 108 mEq/L. The symptomatic hyponatremia responded to intravenous hypertonic saline infusion and thyroid hormone replacement, and the patients made a full recovery. The low-iodine diet and hypothyroid state with overzealous hydration in the setting of RAI therapy may have provoked severe hypotonic hyponatremia. Hypothyroid patients after undergoing RAI therapy, especially the elderly, are at an increased risk for serious hyponatremia and should be monitored closely.

Circulating Levels of Human salusin-β,a Potent Hemodynamic and Atherogenesis Regulator

Using bioinformatics analysis, we previously identified salusin-β, an endogenous bioactive peptide with diverse physiological activities. Salusin-β is abundantly expressed in the neuroendocrine system and in systemic endocrine cells/macrophages. Salusin-β acutely regulates hemodynamics and chronically induces atherosclerosis, but its unique physicochemical characteristics to tightly adhere to all types of plastic and glassware have prevented elucidation of its precise pathophysiological role. To quantitate plasma total salusin-β concentrations, we produced rabbit and chicken polyclonal antibodies against the C- and N-terminal end sequences, circumvented its sticky nature, and successfully established a sandwich enzyme-linked immunosorbent assay (ELISA). Salusin-β was abundantly present in the plasma of healthy volunteers, ranging from 1.9 to 6.6 nmol/L. Reverse phase-high performance liquid chromatography analysis showed that a single immunoreactive salusin-β peak coincided with synthetic authentic salusin-β. Plasma salusin-β concentrations were unaffected by postural changes and by potent vasopressin release stimuli, such as hypertonic saline infusion or smoking. However, salusin-β concentrations showed significant circadian variation; concentrations were high during the daytime and reached the lowest concentrations in the early morning. Plasma salusin-β levels in subjects with diabetes mellitus, coronary artery disease, and cerebrovascular disease showed distinctly higher levels than healthy controls. Patients with panhypopituitarism combined with complete central diabetes insipidus also showed significantly higher plasma salusin-β levels. Therefore, the ELISA system developed in this study will be useful for evaluating circulating total salusin-β levels and for confirming the presence of authentic salusin-β in human plasma. The obtained results suggest a limited contribution of the neuroendocrine system to peripheral total salusin-β concentrations and a role for plasma total salusin-β concentrations as an indicator of systemic vascular diseases.

Effect of volume expansion with hypertonic- and isotonic saline and isotonic glucose on sodium and water transport in the principal cells in the kidney

BackgroundThe renal distal nephron plays an important role in the maintenance of sodium balance, extra cellular volume and blood pressure. The degree of water transport, via aquaporin2 water channels (AQP2), and sodium transport, via epithelial sodium channels (ENaC) in renal collecting duct principal cells are reflected by the level of urinary excretion of AQP2 (u-AQP2) and the γ-fraction of ENaC (u-ENaCγ). The effects of an acute intravenous volume load with isotonic saline, hypertonic saline and glucose on u-AQP2, u-ENaCγ and underlying mechanisms have never been studied in a randomized, placebo-controlled trial in healthy humans.MethodsWe studied the effects of 0.9% saline (23 ml/kg), 3% saline (7 ml/kg) and 5% glucose (23 ml/kg) on u-AQP2 and u-ENaCγ, fractional sodium excretion (FENa), free water clearance (CH2O), and plasma concentrations of vasopressin (AVP), renin (PRC), angiotensin II (ANG II) and aldosterone (Aldo) in a randomized, crossover study of 23 healthy subjects, who consumed a standardized diet, regarding calories, sodium and fluid for 4 days before each examination day.ResultsAfter isotonic saline infusion, u-AQP2 increased (27%). CH2O and u-ENaCγ were unchanged, whereas FENa increased (123%). After hypertonic saline infusion, there was an increase in u-AQP2 (25%), u-ENaCγ (19%) and FENa (96%), whereas CH2O decreased (-153%). After isotonic glucose infusion, there was a decrease in u-AQP2 (-16%), ENaCγ (-10%) and FENa (-44%) whereas CH2O increased (164%). AVP remained unchanged after isotonic saline and glucose, but increased after hypertonic saline (139%). PRC, AngII and p-Aldo decreased after isotonic and hypertonic saline infusion, but not after glucose infusion.ConclusionsVolume expansion with 3% and 0.9% saline increased u-AQP2, while isotonic glucose decreased u-AQP2. Infusion of hypertonic saline increased u-ENaCγ, whereas u-ENaCγ was not significantly changed after isotonic saline and tended to decrease after glucose. Thus, the transport of water and sodium is changed both via the aquaporin 2 water channels and the epithelial sodium channels during all three types of volume expansion to regulate and maintain water- and sodium homeostasis in the body.Trial registrationClinical Trial no: NCT01414088

A1 Noradrenergic Neurons Lesions Reduce Natriuresis and Hypertensive Responses to Hypernatremia in Rats

Noradrenergic neurons in the caudal ventrolateral medulla (CVLM; A1 group) contribute to cardiovascular regulation. The present study assessed whether specific lesions in the A1 group altered the cardiovascular responses that were evoked by hypertonic saline (HS) infusion in non-anesthetized rats. Male Wistar rats (280–340 g) received nanoinjections of antidopamine-β-hydroxylase-saporin (A1 lesion, 0.105 ng.nL−1) or free saporin (sham, 0.021 ng.nL−1) into their CVLMs. Two weeks later, the rats were anesthetized (2% halothane in O2) and their femoral artery and vein were catheterized and led to exit subcutaneously between the scapulae. On the following day, the animals were submitted to HS infusion (3 M NaCl, 1.8 ml • kg−1, b.wt., for longer than 1 min). In the sham-group (n = 8), HS induced a sustained pressor response (ΔMAP: 35±3.6 and 11±1.8 mmHg, for 10 and 90 min after HS infusion, respectively; P<0.05 vs. baseline). Ten min after HS infusion, the pressor responses of the anti-DβH-saporin-treated rats (n = 11)were significantly smaller(ΔMAP: 18±1.4 mmHg; P<0.05 vs. baseline and vs. sham group), and at 90 min, their blood pressures reached baseline values (2±1.6 mmHg). Compared to the sham group, the natriuresis that was induced by HS was reduced in the lesioned group 60 min after the challenge (196±5.5 mM vs. 262±7.6 mM, respectively; P<0.05). In addition, A1-lesioned rats excreted only 47% of their sodium 90 min after HS infusion, while sham animals excreted 80% of their sodium. Immunohistochemical analysis confirmed a substantial destruction of the A1 cell group in the CVLM of rats that had been nanoinjected withanti-DβH-saporin. These results suggest that medullary noradrenergic A1 neurons are involved in the excitatory neural pathway that regulates hypertensive and natriuretic responses to acute changes in the composition of body fluid.

Terlipressin-induced hyponatremic encephalopathy in a noncirrhotic patient

Terlipressin, an analogue of vasopressin, is frequently used for the management of esophageal varices bleeding and hepatorenal syndrome. Terlipressin therapy in portal hypertensive patients is frequently associated with hyponatremia, but is rarely accompanied with serious neurological manifestations. A 39-year-old female with pancreatic neuroendocrine tumor, liver metastasis, main portal vein thrombosis, and a history of esophageal varices presented to the emergency room because of hematemesis. Terlipressin was given with a loading dose of 2 mg followed by 1 mg every 6 hours. After a total of 6 mg terlipressin injection, she suffered from acute delirium. Pertinent examinations showed there was no gross brain lesion by computed tomography, whereas her serum sodium level dropped from baseline (136 mmol/L) to 116 mmol/L with a serum osmolality of 256 mOsm/kg. At that time, urine sodium and urine osmolality were 142 mmol/L and 488 mOsm/kg, respectively. Under the tentative diagnosis of terlipressin-induced hyponatremic encephalopathy, terlipressin was withheld and hypertonic saline infusion was given. Within 12 hours, her serum sodium level recovered to 130 mmol/L and she gradually regained her cognitive functions. Although symptomatic hyponatremic encephalopathy is a rare complication of terlipressin treatment, close monitoring of serum electrolyte level is warranted in patients receiving terlipressin.

Effect of experimental jaw muscle pain on EMG activity and bite force distribution at different level of clenching

Bite force at different levels of clenching and the corresponding electromyographic (EMG) activity in jaw-closing muscles were recorded in 16 healthy women before, during and after painful stimulation of the left masseter muscle. Experimental pain was induced by infusion of 5·8% hypertonic saline (HS), and 0·9% isotonic saline (IS) was infused as a control. EMG activity was recorded bilaterally from the masseter and temporalis muscles, and static bite force was assessed by pressure-sensitive films (Dental Pre-scale) at 5, 50 and 100% of maximal voluntary contraction (MVC) during each session. Visual feedback was applied by showing EMG activity to help the subject perform clenching at 5, 50 and 100% MVC, respectively. EMG activity at 100% MVC in left and right masseter decreased significantly during painful HS infusion (1·7-44·6%; P<0·05). EMG activity at 5% and 50% MVC was decreased during HS infusion in the painful masseter muscle (4·8-18·6%; P<0·05); however, EMG activity in the other muscles increased significantly (18·5-128·3%; P<0·05). There was a significant increase in bite force in the molar regions at 50% MVC during HS infusion and in the post-infusion condition (P<0·05). However, there were no significant differences in the distribution of forces at 100% MVC. In conclusion, experimental pain in the masseter muscle has an inhibitory effect on jaw muscle activity at maximal voluntary contraction, and compensatory mechanisms may influence the recruitment pattern at submaximal efforts.

Preliminary Experience with Low-dose Desmopressin Treatment and Urinary Arginine Vasopressin Concentration as a Response Predictor for Patients with Nocturia with Nocturnal Polyuria.

To assess whether urinary arginine vasopressin (AVP) concentrations adjusted for urinary creatinine (Cr) can predict responsiveness to low-dose desmopressin for nocturia with nocturnal polyuria (NP). Nine NP patients aged 64-84 years with ≥ 2 nocturnal voids received 2.5 µg of intranasal desmopressin for 4 weeks and were evaluated for its effectiveness. Prior to treatment, urinary AVP/Cr concentrations at first morning void and serum sodium and plasma natriuretic peptide (BNP) concentrations were measured, and all patients underwent 5% hypertonic saline infusion. Six responders to 2.5 µg desmopressin had average decreases in nocturnal frequency from 3.2 to 1.8 voids nightly and in nocturnal diuresis by 40%, without clinically significant adverse events. Non-responders remained unaffected even with dose escalation to 5.0 µg desmopressin. For responders, urinary AVP/Cr concentrations were less than 14 pg/mg · Cr, which is lower than in non-responders. Within a physiological range of plasma osmolality, plasma AVP release in response to 5% hypertonic saline infusion was less in responders than in non-responders. Blood pressure measurements and BNP concentrations were unchanged. Urinary AVP/Cr at first morning void may have potential clinical value as a predictor for responsiveness to low-dose desmopressin in nocturia with NP.

Complications Associated With Prolonged Hypertonic Saline Therapy in Children With Elevated Intracranial Pressure

Safe upper limits for therapeutic hypernatremia in the treatment of intracranial hypertension have not been well established. We investigated complications associated with hypernatremia in children who were treated with prolonged infusions of hypertonic saline. Retrospective chart analysis. PICU in university-affiliated children's hospital. All children from 2004 to 2009 requiring intracranial pressure monitoring (external ventricular drain or fiberoptic intraparenchymal monitor) for at least 4 days who were treated with hypertonic saline infusion for elevated intracranial pressure and did not meet exclusion criteria. Continuous hypertonic saline infusion on a sliding scale was used to achieve target sodium levels that would keep intracranial pressure less than 20 mm Hg once the conventional therapies failed. Eighty-eight children met inclusion criteria. Etiologies of elevated intracranial pressure included trauma (n = 48), ischemic or hemorrhagic stroke (n = 20), infection (n = 8), acute disseminated encephalomyelitis (n = 5), neoplasm (n = 2), and others (n = 5). The mean peak serum sodium was 171.3 mEq/L (range, 150-202). The mean Glasgow Outcome Score was 2.8 (± 1.1) at time of discharge from the hospital. Overall mortality was 15.9%. Children with sustained (> 72 hr) serum sodium levels above 170 mEq/L had a significantly higher occurrence of thrombocytopenia (p < 0.001), renal failure (p < 0.001), neutropenia (p = 0.006), and acute respiratory distress syndrome (p = 0.029) after controlling for variables of age, gender, Pediatric Risk of Mortality score, duration of barbiturate-induced coma, duration of intracranial pressure monitoring, vasopressor requirements, and underlying pathology. Children with sustained serum sodium levels greater than 165 mEq/L had a significantly higher prevalence of anemia (p < 0.001). Children treated by continuous hypertonic saline infusion for intracranial hypertension whose serum sodium levels exceeded certain thresholds experienced significantly more events of acute renal failure, thrombocytopenia, neutropenia, anemia, and acute respiratory distress syndrome than those whose sodium level was maintained below these thresholds.

Experimentally induced deep cervical muscle pain distorts head on trunk orientation

We wanted to explore the specific proprioceptive effect of cervical pain on sensorimotor control. Sensorimotor control comprises proprioceptive feedback, central integration and subsequent muscular response. Pain might be one cause of previously reported disturbances in joint kinematics, head on trunk orientation and postural control. However, the causal relationship between the impact of cervical pain on proprioception and thus on sensorimotor control has to be established. Eleven healthy subjects were examined in their ability to reproduce two different head on trunk targets, neutral head position (NHP) and 30° target position, with a 3D motion analyser before, directly after and 15min after experimentally induced neck pain. Pain was induced by hypertonic saline infusion at C2/3 level in the splenius capitis muscle on one side (referred to as "injected side"). All subjects experienced temporary pain and the head repositioning error increased significantly during head repositioning to the 30° target to the injected side (p=0.011). A post hoc analysis showed that pain interfered with proprioception to the injected side during acute pain (p<0.001), but also when the pain had waned (p=0.002). Accuracy decreased immediately after pain induction for the 30° target position to the side where pain was induced (3.3→5.3°, p=0.033), but not to the contralateral side (4.9→4.1°, p=0.657). There was no significant impact of pain on accuracy for NHP. A sensory mismatch appeared in some subjects, who experienced dizziness. Acute cervical pain distorts sensorimotor control with side-specific changes, but also has more complex effects that appear when pain has waned.

The timing of infusion of hypertonic saline to exert protective effect on intestinal barrier function in the rabbit with intestinal ischemia/reperfusion injury

To study the timing of infusion of hypertonic saline solution (HTS) to exert its protective effect on intestinal barrier function in rabbits with intestinal ischemia/reperfusion (I/R) injury. Seventy-two rabbits were randomly divided into four groups (each n=18): sham operation group, I/R group, HTS pretreatment group and HTS delayed treatment group. The intestinal I/R models were produced by blocking the superior mesenteric artery (SMA) for 1 hour followed by release of the SMA. 7.5% HTS (6 ml/kg) was infused in HTS pretreatment group 5 minutes before release of SMA, and HTS was infused in delayed treatment group 2 hours after reperfusion and finished in 5 minutes. Levels of D-lactic acid (D-Lac), lipopolysaccharide (LPS), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10) were determined before ischemia and 2, 4, 6 hours after reperfusion. The levels of malonaldehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO) in intestinal tissues of 8 rabbits in each group were measured at 6 hours after reperfusion. Meanwhile the intestinal morphological changes were observed, and the Chin score, which reflected the degree of injury to intestinal mucosa was calculated. Compared with sham operation group, D-Lac, LPS, TNF-α and IL-10 in I/R group were significantly increased from 2 hours after reperfusion (D-Lac: 18.91 ± 3.46 mg/L vs. 3.92 ± 0.61 mg/L, LPS: 869 ± 85 EU/L vs. 422 ± 27 EU/L, TNF-α: 23.80 ± 4.22 μg/L vs. 3.65 ± 0.51μg/L, IL-10: 8.90 ± 2.75 μg/L vs. 2.53 ± 0.80 μg/L, all P<0.05); MDA, MPO and Chiu score were significantly increased (MDA: 398 ± 28 nmol/mg vs. 173 ± 20 nmol/mg, MPO: 465 ± 52 mU/mg vs. 183 ± 25 mU/mg, Chiu score: 4.36 ± 0.52 vs. 0.38 ± 0.22, all P<0.05), while SOD decreased significantly (35 ± 9 U/mg vs. 52 ± 8 U/mg, P<0.05). Compared with I/R group, the levels of D-Lac, LPS, TNF-α, MDA, MPO and Chiu score in HTS pretreatment group were lower (D-Lac: 11.45 ± 0.92 mg/L vs. 18.91 ± 3.46 mg/L, LPS: 455 ± 114 EU/L vs. 869 ± 85 EU/L, TNF-α: 10.32 ± 2.11 μg/L vs. 23.80 ± 4.22 μg/L, MDA: 221 ± 21 nmol/mg vs. 398 ± 28 nmol/mg, MPO: 271 ± 20 mU/mg vs. 465 ± 52 mU/mg, Chiu score: 1.69 ± 0.24 vs. 4.36 ± 0.52, all P<0.05), while IL-10 and SOD were significantly increased (IL-10: 14.54 ± 2.02 μg/L vs. 8.90 ± 2.75 μg/L, SOD: 90 ± 14 U/mg vs. 35 ± 9 U/mg, both P<0.05). The levels of the above indexes in HTS delayed treatment group were similar to I/R group, and the effect was lower than that in HTS pretreatment group. HTS had the protective effect on intestine suffering from I/R injury. But the protective effect was time dependent, and early treatment shows protective effect.

Early Fluid Resuscitation With Hypertonic Solution in a Rat Crush Injury Model

The aim of the study was to evaluate the effects of bolus infusion of hypertonic hydroxyethyl starches (HHESs) and continuous infusion of hypertonic saline (HTS) in the early resuscitation in crush syndrome. A rat model of crush injury was established. Rats were randomly divided into five groups: (1) HHES group, (2) HTS group, (3) volume resuscitation group, (4) normal resuscitation (NR) group, and (5) sham group. Blood samples were collected 6 h after the crush period for biochemical evaluation. Blood pressure was monitored throughout this experiment. Muscles and kidneys were evaluated morphologically 24 h after reperfusion. Twenty rats in each group were taken for survival observation for 72 h. Compared with the NR and HTS groups, the HHES group had significantly increased the survival rate 72 h after release (P < 0.05). In the first 2 h after release, mean arterial blood pressure in the HHES group was significantly higher than in HTS, volume resuscitation, and NR groups (respectively, P < 0.05). Animals that received HHES infusion showed a better acid-base balance and renal function. However, there was no significant difference in survival rate between the HTS and NR groups. Furthermore, animals in the HTS group showed a bad acid-base balance and a higher serum sodium level. Bolus infusion of HHES combined with normal saline could be an effective therapy for crush syndrome in the early resuscitation period. However, continuous HTS injection was not seemed to be a suitable choice particularly in the absence of monitoring equipment for serum irons or blood gases (institutional protocol no. ZN5R20110016).

Hospitalizations for hyponatremia and syndrome of inappropriate antidiuretic hormone hypersecretion at the Policlinic of Modena, Italy from January 2006 to September 2008

Introduction: Hyponatremia is the most common electrolyte imbalance among hospitalized patients. The cause is not always identified, but 30-40% of cases are the result of the syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH). The aim of this study was to determine the frequency of hyponatremia in our hospital, its underlying causes (in particular the proportion of cases caused by SIADH), and approaches to treatment. Materials and methods: We retrospectively analyzed all nonpediatric hospitalizations occurring between 1 January 2006 and 30 September 2008 in which the discharge diagnosis was hyponatremia or SIADH. Results: A total of 64 cases were reviewed; 56 of the patients were aged &gt; 60. The hyponatremia was classified as severe (&lt; 125 mEq/L) in 36/64 cases (56%) (most involving patients aged &gt;70); moderate (129-125 mEq/L) in 22 (34%); and mild (134-130 mEq/L) in 6 (9%). Neurologic symptoms were present in 11 patients with severe hyponatremia (confusion, hallucinations, coma) and 9 with moderate hyponatremia (weakness, impaired memory). Thirteen had hypovolemic hypotonic hyponatremia, 16 had hypervolemic hypotonic hyponatremia, and 35 had normovolemic hypotonic hyponatremia, including 23 who met the criteria for SIADH: 5 patients with neoplastic disease, 6 with pulmonary disorders, 3 with drug-related hyponatremia (a selective serotonin reuptake inhibitor in 1 case, a tricyclic antidepressant in 1, carbamazepine in 1), 2 whose SIADH developed after surgery, 4 with head trauma, 1 receiving noninvasive ventilatory support, and 2 elderly patients whose SIADH appeared idiopathic. Thirteen patients had hyponatremia related to the use of diuretics (thiazides in 7 cases), and one other had long-standing untreated hypothyroidism. In most cases, treatment consisted of infusion of hypertonic saline (sometimes with fluid restriction and/or furosemide administration). Discussion: Over one third (36%) of the adults hospitalized in the Policlinic of Modena for hyponatremia during the 3-year study had SIADH, a figure that is consistent with literature data. In most cases, the cause of hyponatremia can be identified on the basis of simple laboratory tests and complete patient histories.