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Two hypotheses have recently been raised to explain the metabolic acidosis (increased blood acidity) of severe malaria, and both are relevant to treatment. The first suggests that a decreased blood volume (hypovolaemia) has an important role in severe malaria; following this, treatment should be based on the current standard paediatric management of acidosis in children with features of cardiovascular compromise. The second hypothesis contends that acidosis in malaria has a metabolic cause and proposes treatment with dichloroacetate. Both hypotheses are plausible and are not mutually exclusive. In truth, the risks and benefits of either treatment are uncertain, and will remain so until large multicentre, randomised controlled trials provide appropriate supportive evidence. As both views involve complex physiological rationales, beyond the usual scope of this journal, I attempt here to present the largely academic aspects of these hypotheses within the practical and contextual aspects of childhood severe malaria.

Of 67 consecutive patients with spontaneous CSF hypovolemia (SCH), 11 (16.4%) had subdural hematoma (SDH). Patients with SDH were older (p = 0.005), more likely to be male (p = 0.035), and displayed longer time to diagnosis of SCH (p = 0.019) than those without SDH. All patients with SDH showed the findings of pseudo-subarachnoid hemorrhage on CT and responded favorably to epidural blood patches and neurosurgical drainage.

Study Objective: Survival from traumatic cardiac arrest is poor, and some consider resuscitation of this patient group futile. This study identified survival rates and characteristics of the survivors in a physician-led out-of-hospital trauma service. The results are discussed in relation to recent resuscitation guidelines., Methods: A 10-year retrospective database review was conducted to identify trauma patients receiving out-of-hospital cardiopulmonary resuscitation. The primary outcome measure was survival to hospital discharge., Results: Nine hundred nine patients had out-of-hospital cardiopulmonary resuscitation. Sixty-eight (7.5% [95% confidence interval 5.8% to 9.2%]) patients survived to hospital discharge. Six patients had isolated head injuries and 6 had cervical spine trauma. Eight underwent on-scene thoracotomy for penetrating chest trauma. Six patients recovered after decompression of tension pneumothorax. Thirty patients sustained asphyxial or hypoxic insults. Eleven patients appeared to have had "medical" cardiac arrests that occurred before and was usually the cause of their trauma. One patient survived hypovolemic cardiac arrest. Thirteen survivors breached recently published guidelines., Conclusion: The survival rates described are poor but comparable with (or better than) published survival rates for out-of-hospital cardiac arrest of any cause. Patients who arrest after hypoxic insults and those who undergo out-of-hospital thoracotomy after penetrating trauma have a higher chance of survival. Patients with hypovolemia as the primary cause of arrest rarely survive. Adherence to recently published guidelines may result in withholding resuscitation in a small number of patients who have a chance of survival.

Objective: The aim of this article is to extract from recent medical literature and nephrologic practice the facts and fallacies concerning the possible prophylaxis of contrast medium-induced nephropathy., Data Sources, Study Selection, and Data Extraction: A MEDLINE/PubMed search (1985 to January 2006) was conducted, including all relevant articles investigating the pathogenesis and prevention of contrast medium-induced nephropathy from a nephrologic critical point of view., Data Synthesis: Considerable efforts have been made to develop pharmacologic therapy for the prevention of contrast medium-induced nephropathy, especially in patients at risk, such as elderly subjects and those with preexisting renal impairment, hypovolemia, or dehydration. There is general consensus that hydration protocols implemented before and after imaging with contrast medium may be effective in preventing contrast medium-induced nephropathy. However, definitive and convincing data related to amounts to be infused, infusion timing, and type of solutions (half-isotonic, isotonic saline solution, or bicarbonate) are lacking. Forced diuresis with furosemide or mannitol and use of dopamine, together with concomitant hydration, have been proved to be ineffective or even more risky in the event of inadequate maintenance of euvolemia. Various direct or indirect vasodilators have been investigated (atrial natriuretic peptide, calcium channel blockers, angiotensin-converting enzyme inhibitors, and endothelin receptor antagonists), yet results have been inconsistent and inconclusive. Recent large meta-analyses concerning the protective role of antioxidant action of N-acetylcysteine have led to the conclusion that the statistical significance of the results is borderline. Preventive hemodialysis has not proved to be useful; on the contrary, it might worsen the clinical conditions by inducing hypotension. Hemofiltration, despite some positive studies, is too complex and cannot be used extensively., Conclusions: : It is believed that prevention is actually achieved by correcting hypovolemia, dehydration, or both. Normalization of body fluids is probably the true objective to be achieved by preventive measures in all patients, not only in those at risk. Because limited data have been collected in intensive care units, at present, no firm or specific recommendations can yet be provided for the critically ill.

A 42-year-old man was transferred to the Emergency Department after his friends had found him unresponsive and confused in his room. He had been experiencing upper abdominal complaints for a period of several months. He had taken large amounts of a calcium carbonate/magnesium subcarbonate preparation (Rennie) and had consumed at least 3 litres of dairy products per day. His behaviour was reported as being more and more abnormal during the previous few weeks. On admission he was confused and agitated and had involuntary movements of his limbs. Laboratory investigation indicated a triple acid base disorder, i.e. metabolic alkalosis, respiratory alkalosis and high anion gap metabolic acidosis, with severe dehydration. The metabolic alkalosis was caused by the intake of large amounts of dairy and antacids: milk-alkali syndrome. The metabolic acidosis was the result of hypovolaemia and pre-renal renal failure and the respiratory alkalosis was caused by hyperventilation due to the organic psychosyndrome. The patient was treated with volume expansion by isotonic saline and the administration of potassium and he was sedated with low-dose midazolam, which led to a full respiratory compensation of the metabolic alkalosis. A few days following admission, both the plasma calcium concentration and renal function returned to normal; the acid-base disorder completely normalized and the organic psychosyndrome disappeared. On gastroduodenoscopy a gastric ulcer was found; biopsies revealed a signet ring cell adenocarcinoma of the stomach.

Purpose: To study in rats the effect of S(+) ketamine on the renal histology after intraoperative hemorrhage., Methods: Twenty male Wistar rats, anesthetized with sodium pentobarbital, were randomly divided in 2 groups: G1 - control (n=l0) and G2 - S(+)-ketamine (n=10), both submitted to arterial hemorrhage of 30% of volemia in 3 moments (10% each 10 min) 60 min after anesthesia. G2 received S(+)-ketamine, 15 mg. kg-1, i.m., 5 min after anesthesia and 55 min before the 1st hemorrhage moment (Ml). Medium arterial pressure (MAP), rectal temperature (T) and heart rate were monitored. The animals were sacrificed in M4, 30 min after the 3rd hemorrhage moment (M3) and the kidneys and blood collected from hemorrhage were utilized for histological study and hematocrit (Ht) determination., Results: There were significant reduction of MAP, T, and Ht. The histological study verified G1 = G2 for tubular dilation, congestion, and necrosis. The total score addition were significantly different and G2 > G 1., Conclusion: Hemorrhage and hypotension determined changes in kidney histology. The rise in catecholamine blood concentration probably was the cause of S(+)-ketamine-induced higher score of histological changes.

We report an 88-year-old woman who developed a hemorrhagic venous infarction in the left cerebral hemisphere and brainstem, in association with left carotid-cavernous fistula (CCF). Without aura the patient noticed diplopia due to left abducens palsy, and exophthal mos and congestion of the left eye. Brain CT revealed extrusion of the left eye, and dilatation of left superior orbital vein and cerebral cortical veins. She received diagnosis of CCF. Brain CT also revealed a small mass in the left ethmoidal sinus, which was not attached to the CCF. Biopsy of the mass was done under local anesthesia. On the following she had high fever. Her consciousness level deteriorated and she developed right hemiparesis FLAIR images of MRI showed, extensive high signal lesions in the left frontal and temporal cortices, basal ganglia, thalamus, midbrain and pons. These findings were consisted with venous infarction, possibly associated with peri-operative infection and hypovolemia. Intracranial hemorrhage occur in 3% of cases with CCF, but venous infarction was much rarer. The patients with CCF, who show dilatation of cortical veins in CT or MRI, have a higher risk of cerebral hemorrhage or infarction, and should be carefully observed.

Background: The inspiratory impedance threshold device (ITD) has been shown to improve hemodynamic variables and survival outcomes during cardiopulmonary resuscitation in animals and humans. We hypothesized that use of an ITD, with a resistance of -10 cm H2O, will improve hemodynamics and short-term survival rates during hypovolemic hypotension in spontaneously breathing pigs., Methods: Female farm pigs ( approximately 26 kg) were intubated and anesthetized with propofol with the dose adjusted to permit spontaneous respirations. They were bled to 50% of calculated blood volume through an arterial catheter and then prospectively randomized to either treatment with an ITD or observation alone. Arterial and intratracheal pressures as well as arterial blood gases were measured. After 90 min the ITD was removed, normal saline was administered to all surviving animals, the anesthetic was discontinued, and animals were allowed to recover. Statistical analysis was performed with one-way repeated ANOVA and survival rates were calculated with Kaplan-Meier analysis., Results: Treatment with the ITD resulted in lower intratracheal inspiratory pressure in the treatment group (-11+/-0.4 mmHg versus -4+/-0.7 mmHg, respectively, P<0.005). Mean arterial pressure after 30 min of treatment with the ITD was higher in the treatment group (61.1+/-5.5 mmHg versus 37.4+/-2.1 mmHg, respectively, P<0.005). All pigs in the control group died within 65 min of the initial bleed, whereas 7/8 (87%) treated with an ITD survived for >90 min (P<0.001). During the recovery phase, 6/8 (75%) in the ITD group survived for >3h and awoke without neurological deficit; one surviving animal in the ITD group never woke up. Arterial oxygenation was not compromised in the ITD group., Conclusions: Use of an ITD improved blood pressure and short-term survival rates in a spontaneously breathing porcine model of hypovolemic hypotension.

The synthesis of arginine vasopressin (AVP) in the magnocellular neurons of the supraoptic (SON) and paraventricular nuclei (PVN) is physiologically regulated by plasma osmolality and volume. To clarify how the regulation of AVP gene transcription is affected by chronic dehydration, we examined changes in the transcriptional activities of AVP gene by plasma osmolality and volume in both euhydrated and dehydrated conditions. Euhydrated rats had free access to water, whereas dehydrated rats had been deprived of water for 3 days before experiments. Rats in both conditions were subjected to acute hypertonic stimuli or hypovolemia, and changes in AVP heteronuclear (hn)RNA levels, an indicator of gene transcription, in the SON and PVN were examined with in situ hybridization. The intraperitoneal (i.p.) injection (2% body wt) of hypertonic (1.5 M) saline increased plasma Na levels by approximately 40 meq/l in both euhydrated and dehydrated conditions. However, expression levels of AVP hnRNA in the SON and PVN were increased only in euhydrated, not dehydrated, rats. On the other hand, i.p. injection of polyethylene glycol decreased the plasma volume by approximately 16-20%, and AVP hnRNA levels in the SON and PVN were significantly increased in both conditions. Thus it is demonstrated that signaling pathways regulating AVP gene transcription in the magnocellular neurons were completely refractory to acute osmotic stimuli under the chronic dehydration and that AVP gene transcription could probably respond to acute hypovolemia through different intracellular signal transduction pathways from those for osmoregulation.

Background: Abdominal edema attacks in patients with hereditary angioedema are often extremely painful, associated with vomiting and diarrhea, and have a high potential for causing recurrent disability of the patient., Study Design and Methods: Intraindividual comparison of retrospective data in 75 hereditary angioedema patients comprising 4,834 abdominal attacks treated with C1 inhibitor concentrate versus 17,444 untreated abdominal attacks., Results: The mean duration of abdominal attacks was 92.0 hours (SD, 40.8 hr) when untreated compared to 39.9 hours (SD, 30.0 hr) when treated. Patients reported a mean maximal pain score of 8.6 (SD, 1.7; range, 1-10) for untreated attacks compared to 4.5 (SD, 2.9) when treated. Vomiting occurred in 83.3 percent of untreated attacks and in 6.0 percent of treated attacks, respectively. Diarrhea was reported in 41.8 percent of untreated attacks and in 11.0 percent of treated attacks, whereas cardiovascular collapse due to hypovolemia was observed in 3.5 percent of untreated attacks versus 0.1 percent in treated attacks. Mean time to relief of symptoms was 53.5 minutes when treated early compared to 114 minutes when treatment was delayed. No drug-related adverse or serious adverse events were observed as far as the injections were performed correctly., Conclusion: C1 inhibitor concentrate is highly effective and safe in treating abdominal attacks in patients suffering from hereditary angioedema.

Fluid management is a vital component of patient care within the critical care setting; it has a range of indications and applications, one of the most important being to maintain tissue perfusion and safeguard against single/multiple organ failure. Hypovolaemia is a commonly encountered condition within critical care and has the potential to jeopardize tissue perfusion and accelerate the risk of organ failure. In an attempt to optimize the fluid management of patients within the intensive therapy unit, this article outlines the development and implementation of a fluid prescription for ventilated patients with suspected hypovolaemia.

Gastric ulcers are an important cause of morbidity and mortality in the critically ill, especially those with CNS injury. We used cervical spinal cord transection (CCT) in the rat to model these ulcers and examined the effect of core body temperature and vascular volume on gastric ulcerogenesis. Hypothermia significantly increased ulcerogenesis compared to euthermia, while maintained euthermia produced ulcer indices not different from sham surgery. Hypovolemia (10% blood volume withdrawal) significantly increased ulcerogenesis compared to hypervolemia (10% of blood volume crystalloid infusion) or sham surgery. These results support crystalloid infusion and maintenance of core body temperature in the clinical setting.

We tested the hypothesis that women have blunted sympathetic neural responses to orthostatic stress compared with men, which may be elicited under hypovolemic conditions. Muscle sympathetic nerve activity (MSNA) and hemodynamics were measured in eight healthy young women and seven men in supine position and during 6 min of 60 degrees head-up tilt (HUT) under normovolemic and hypovolemic conditions (randomly), with approximately 4-wk interval. Acute hypovolemia was produced by diuretic (furosemide) administration approximately 2 h before testing. Orthostatic tolerance was determined by progressive lower body negative pressure to presyncope. We found that furosemide produced an approximately 13% reduction in plasma volume, causing a similar increase in supine MSNA in men and women (mean +/- SD of 5 +/- 7 vs. 6 +/- 5 bursts/min; P = 0.895). MSNA increased during HUT and was greater in the hypovolemic than in the normovolemic condition (32 +/- 6 bursts/min in normovolemia vs. 44 +/- 15 bursts/min in hypovolemia in men, P = 0.055; 35 +/- 9 vs. 45 +/- 8 bursts/min in women, P < 0.001); these responses were not different between the genders (gender effect: P = 0.832 and 0.814 in normovolemia and hypovolemia, respectively). Total peripheral resistance increased proportionately with increases in MSNA during HUT; these responses were similar between the genders. However, systolic blood pressure was lower, whereas diastolic blood pressure was similar in women compared with men during HUT, which was associated with a smaller stroke volume or stroke index. Orthostatic tolerance was lower in women, especially under hypovolemic conditions. These results indicate that men and women have comparable sympathetic neural responses during orthostatic stress under normovolemic and hypovolemic conditions. The lower orthostatic tolerance in women is predominantly because of a smaller stroke volume, presumably due to less cardiac filling during orthostasis, especially under hypovolemic conditions, which may overwhelm the vasomotor reserve available for vasoconstriction or precipitate neurally mediated sympathetic withdrawal and syncope.

Objective: To characterize use of volume infusion (VI) for infants who are > or =34 weeks' gestational age and receive intensive cardiopulmonary resuscitation (CPR; defined as >1 minute of positive-pressure ventilation and chest compressions, with or without the administration of medications) in the delivery room and are admitted to the NICU., Methods: A retrospective review of a resuscitation registry between January 1999 and June 2001 was conducted., Results: Of 37,972 infants, 23 received CPR, including 13 with VI. Ten of 13 received VI for persistent bradycardia despite CPR, and only 3 of 13 received VI for suspicion of hypovolemia with poor perfusion. More VI versus no VI infants had Apgar scores < or =2 at 5 and 10 minutes. VI versus no VI infants had lower cord arterial pH, had higher arterial partial pressure of carbon dioxide, had larger base deficit, required longer CPR, and required more epinephrine. On admission to the NICU, VI versus no VI infants had lower blood pressure and larger base deficit over the first 2 hours but did not differ in arterial pH, arterial partial pressure of carbon dioxide, heart rate, mortality, or use of additional VI or buffer., Conclusions: VI is rarely given for overt hypovolemia and more often for asphyxiated infants who are slow to respond to intensive CPR. Persistent postnatal hypotension in VI infants suggests that other factors, eg, myocardial dysfunction, may be important contributors to lack of response to CPR.

We undertook a study to investigate the short- and long-term outcomes of spontaneous CSF hypovolemia. Fifty-three consecutive patients with spontaneous CSF hypovolemia were included. Short-term outcome was assessed 4 weeks after the treatment in all patients. Long-term outcome after a mean follow-up of 61 months (range, 13-101 months) was evaluated in 26 patients. There were 18 men and 35 women (66%) with an age range of 22-64 years (mean 37 +/- 9.5). In assessing the short-term outcome of CSF hypovolemia, we found that complete headache relief was significantly higher in 43 patients who received epidural blood patch (EBP) than in 10 patients treated with supportive measures (p < 0.05). After a mean follow-up of 61 months, 25 (96%) of the 26 patients evaluated for long-term outcome had complete headache relief. These results suggest that EBP is safe and effective, resulting in excellent short- and long-term outcomes of CSF hypovolemia., ((c) 2005 S. Karger AG, Basel.)

We report a case of a 43-year-old man treated by craniotomy for chronical subdural hematoma (CSH) due to spontaneous intracranial hypovolemia. The patient complained of sudden onset severe headache. Initial CT scan showed normal brain structure, and his headache improved with bed rest in a few days. However, MR images obtained for vertigo one month later demonstrated bilateral subdural hygroma extending to the supracerebellar space and diffuse dural enhancement after gadolinium infusion. We diagnosed bilateral subdural hygroma due to spontaneous intracranial hypovolemia, and observed him conservatively. Four months after onset, he complained of severe headache again and MR images revealed enlargement of bilateral CSH with mass effect, which had heterogenous intensity on the right convexity. We evacuated hematoma on the right by craniotomy and aspirated the left side hematoma using a burr hole. His headache improved 2 weeks after the operation with strict bed rest. The follow-up MR images showed disappearance of abnormal meningeal enhancement and improvement of brain sagging.

Background: The mechanisms of simple faint remain elusive. We propose that postural fainting is related to excessive thoracic hypovolemia and splanchnic hypervolemia during orthostasis compared with healthy subjects., Methods and Results: We studied 34 patients 12 to 22 years old referred for multiple episodes of postural faint and 11 healthy subjects. Subjects were studied in the supine position and during upright tilt to 70 degrees for 30 minutes and subgrouped into S+, historical fainters who fainted during testing (n=24); S-, historical fainters who did not faint during testing (n=10); and control subjects. Supine venous occlusion plethysmography showed no differences between blood flows of the forearm and calf in S+, S-, or control. Cardiac index, total peripheral resistance, and blood volume were not different. Using impedance plethysmography, we assessed blood redistribution during upright tilt. This demonstrated decreased thoracic blood volume and increased splanchnic, pelvic, and leg blood volumes for all subjects. However, thoracic blood volume was decreased in S+ compared with control volume, correlating well with the maximum upright heart rate. Splanchnic volume was decreased in the S+ and S- groups, correlating with the change in thoracic blood volume. Pelvic and leg volume changes were similar for all groups and uncorrelated to thoracic blood volume., Conclusions: Enhanced postural thoracic hypovolemia and splanchnic hypervolemia are associated with postural simple faint.

The underfill and overflow hypotheses are usually held as mutually exclusive mechanisms for explaining sodium/water retention in nephrotic syndrome, but neither of them is entirely convincing. In this paper, we will briefly summarize the experimental and clinical evidence in favor of and against each hypothesis. Based on our personal observations, we propose a unifying hypothesis in which underfill and overflow are subsequent stages of the disease. In the transition, a central role is played by vasopressin, which is secreted in the two phases, respectively, by a volume and an osmotic stimulus; therefore, persistent sodium/water retention is maintained through the vascular and tubular effects of this peptide. In addition, we propose that vasodilation and sodium/water excretion could ensue when both stimuli for vasopressin release fade away, leading to the resolution of the syndrome.

Objectives: Although mnemonics are commonly used in medical education there are few data on their effectiveness. A RCT was undertaken to test the hypothesis that a new aide memoire, "EMD-aide", would be superior to the conventional "4Hs+4Ts" mnemonic in facilitating recall of causes of electromechanical dissociation (EMD) among house officers., Method: "EMD-aide", organises causes of EMD by frequency of occurrence and ease of reversibility: four groups organised by shape, colour, position, numbering, clockwise sequence, and use of arrows. Eight hospitals were randomised in a controlled trial and 149 house officers were then recruited by telephone. Baseline ability to recall causes of EMD was recorded at one minute and overall. House officers were then sent a copy of either "4Hs+4Ts" or "EMD-aide" according to randomisation group. Recall ability was retested at one month., Results: 68 of 80 and 51 of 69 house officers completed the study in the "4Hs+4Ts" and "EMD-aide" groups respectively (NS) with similar baseline recall. After intervention median number of recalled causes was greater in the "EMD-aide" group, eight compared with seven at one minute (p = 0.034) and eight compared with seven overall, p = 0.067. Recall of all eight causes was more common in "EMD-aide" group, 54% compared with 35%, p = 0.054, and these house officers spent longer examining their aide memoire, p<0.001., Conclusions: "EMD-aide" may be superior to "4Hs+4Ts" in facilitating the recall of the causes of electromechanical dissociation. Educational psychology of medical learning and the use of aide memoires in general are worthy of further study.

We report a patient with profound hypovolemia who developed dynamic left ventricular outflow tract obstruction and severe mitral regurgitation. Both the outflow tract obstruction and mitral regurgitation resolved with volume replacement. Unlike previous reports of dynamic left ventricular outflow obstruction and mitral regurgitation, the degree of mitral regurgitation was severe. Possible mechanisms are discussed.

Most African children with severe malaria who die do so on the day of admission as a result of the complications of falciparum malaria. We highlight the value of a rapid structured triage assessment to look for emergency signs that will prioritize initial management and implementation of basic life support. This can be delivered with few resources and by non-specialist medical personnel. Reduction in case fatality can only come through the wider appreciation of the need for and application of supportive therapies to treat the life-threatening complications. Hypovolaemia has emerged as a common feature of children presenting with severe malaria complicated by acidosis. Early recognition and prompt treatment may lead to improvements in outcome. We discuss the new evidence supporting the role of hypovolaemia in severe malaria and potential treatment options whilst awaiting the results of clinical trials.

The objective of this study is to investigate the effect of normovolaemic haemodilution (anaemia), haemoglobin level and replacement fluids on the survival of local flaps in rats. Fifty male Wistar rats were divided into four study groups and one control group (10 rats for each). In the study groups, 20% or 30% of blood was withdrawn and replaced by either Gelofusine or saline (0.9%). Single 1.5 cm x 3 cm cranially based dorsal random skin flaps consisting of skin and panniculus carnosus were elevated in all rats. No difference was determined between the control and 20% exsanguinated groups regarding flap survival area. There was a statistically significant difference between the flap survival areas of 20% exsanguinated groups and 30% exsanguinated groups. If the blood loss exceeds 30% of total volume and/or haemoglobin (Hb) level is lower than 10.72 g/dL, the risk of flap necrosis increases significantly.

A number of previous studies indicated that ischemia-reperfusion injury causes two distinct types of cell death--necrosis and apoptosis--in the central nervous system. It was also implicated that the intensity of injury can somehow affect the cell death mechanisms. By occluding the descending thoracic aorta with or without simultaneously induced hypovolemic hypotension in rats, we established a model of experimental spinal cord ischemia-reperfusion (I/R) in which the injury severity can be controlled. Recordings of carotid blood pressure (CBP) and spinal cord blood flow (SCBF) showed that aortic occlusion induced dramatic CBP elevation but SCBF drop in both the normotensive (NT) and hypotensive (HT) groups of rats. However, the HT group demonstrated significantly lower SCBF during aortic occlusion, and much slower elevation of SCBF after reperfusion, and extremely poor neurological performance. Spinal cord lesions were characterized by infarction associated with extensive necrotic cell death, but little apoptosis and caspase-3 activity. In contrast, in the NT group, I/R injury resulted in minor tissue destruction associated with persistent abundant apoptosis, augmented caspase-3 activity, and favorable functional outcome. The relative sparing of motoneurons in the ventral horns from apoptosis might have accounted for the minor functional impairment in the NT group. The severity of I/R injury was found to have substantial impact on the histopathological changes and cell death mechanisms, which correlate with neurological performance. Our results implicate that injury severity and duration after injury are two critical factors to be considered in therapeutic intervention.

Background: Proximal Femoral Fracture (PFF) or 'hip fracture' is a frequent injury, and adverse outcomes are common. Several factors suggest the importance of developing techniques to optimize intravascular fluid volume. These may include protocols that enhance the efficacy of clinicians' assessments, invasive techniques such as oesophageal Doppler or central venous pressure monitoring, or advanced non-invasive techniques such as plethysmographic pulse volume determination., Objectives: To determine the optimal method of fluid volume optimization for adult patients undergoing surgical repair of PFF. Comparisons of fluid types, of blood transfusion strategies or of pharmacological interventions are not considered in this review., Search Strategy: We searched CENTRAL (The Cochrane Library, issue 4, 2003), MEDLINE (1985 to 2003), EMBASE (1985 to 2003), and bibliographies of retrieved articles. Relevant journals and conference proceedings were handsearched., Selection Criteria: Randomized controlled studies comparing a fluid optimization intervention with normal practice or with another fluid optimization intervention, in patients following PFF undergoing surgery of any type under anaesthesia of any type., Data Collection and Analysis: Searches and exclusion of clearly irrelevant articles were performed by one reviewer. Two reviewers examined independently the remaining studies, extracting study quality and results data. A wide range of short- and long-term outcome data were sought. Studies were excluded if they did not meet selection criteria or if results were likely to be biased. Due to inconsistent data reporting, combination of data was not generally possible., Main Results: Searches identified four trials, of which two studies, randomizing a total of 130 patients, were of adequate quality and addressed the review question. Both studies were of invasive advanced haemodynamic monitoring, either oesophageal Doppler ultrasonography or central venous pressure monitoring, during the intraoperative period only. In both, invasive monitoring led to significant increases in fluid volumes infused and reductions in length of hospital stay. The pooled Peto odds ratio for in-hospital fatality was 1.44 (95% confidence interval 0.45-4.62). Neither study followed patients beyond hospital discharge or assessed functional outcomes. No serious complications were directly attributable to the interventions. There were no studies of protocol-guided fluid optimization or of advanced non-invasive techniques., Reviewer's Conclusions: Invasive methods of fluid optimization during surgery may shorten hospital stay, but their effects on other important, patient-centred, longer-term outcomes are uncertain. Adverse effects on fatality cannot be excluded. Other fluid optimization techniques have not been evaluated. The lack of randomized studies of adequate quality addressing this important question is disappointing. More research is needed.

The authors report the occurrence of sudden blindness in 5 children (mean age, 32 months; range, 11 to 60) during continuous peritoneal dialysis regimen. All children presented with loss of light perception, visual fixation and ocular pursuit, and bilateral mydriasis unreactive to bright light. Fundoscopic examination found signs of anterior ischemic optic neuropathy with disc swelling, edema, and hemorrhages. Whereas 1 patient was dehydrated, the 4 other patients appeared well and not dehydrated. Nevertheless, blood pressure was below the normal range in all of them. Therefore, hypovolemia is highly suspected to have been the cause of ischemic optic neuropathy in all cases. Treatment consisted of steroids (4 patients), anticoagulation or antiagregation drugs (3 patients), plasma or macromolecules infusions (2 patients), vasodilatators (2 patients), and transient dialysis interruption (1 patient). One child with hepatic cirrhosis died 4 days later of acute liver insufficiency owing to ischemic hepatic necrosis. The other children had only partial improvement of vision during the following months. Because the prognosis of ischemic optic neuropathy is very poor, diagnosis and treatment of chronic hypovolemia in children on continuous peritoneal dialysis is essential to prevent such a devastating complication.

Although volume expansion is liberally used in newborn intensive care, we know little about its effects on hemodynamics or outcomes. Given appropriately to a truly hypovolemic baby, it can be life-saving, but the clinical diagnosis of hypovolemia is probably very inaccurate. We know that volume expansion has less effect on blood pressure than dopamine, and although it seems to produce immediate increases in systemic blood flow, we do not know for how long these increases are sustained. There is evidence to show that the routine use of volume expansion in preterm babies has no effect on outcome, and there is little evidence to support its routine use during resuscitation or the treatment of metabolic acidosis. Whether crystalloids or colloids are preferable is also unclear in newborns. In situations of concern related to circulatory compromise, if possible, define the hemodynamics echocardiographically. Otherwise, if in doubt, some volume should be given, although it is probably unwise to keep expanding the volume if this is not improving physiologic (blood pressure and heart rate) or echocardiographic systemic blood flow parameters.

Most cases of ARF are secondary to volume depletion. In the literature, very few scientific publications address the problem of what to do when confronted with such a patient. As regarding the diagnosis of hypovolemia, an accurate history and physical examination can help to determine both the presence and etiology of volume depletion; postural hypotension (decrement in systolic blood pressure of more than 20 mmHg after standing from the supine position), associated with a pulse increment of 30 beats/min or more and dizziness are specific symptoms of hypovolemia. Laboratory indices are useful to diagnose volume depletion, but their interpretation is not simple, and they may not be available in the non-nephrologic environment. Fluid replacement therapy in hypovolemia is largely dependent upon the type of fluid that has been lost and concurrent electrolytic and acid-base disorders. Patients with hypernatremia and volume depletion should receive mild hypotonic solutions, whereas those with hyponatremia and hypovolemia should receive mild hypertonic solutions. The entity of reinfusion depends on daily losses. Conversely, monitoring of body weight can be considered an adequate index of fluid balance. Concerning the treatment of ARF, the use of loop diuretics in the early phases of pre-renal ARF decrease oxygen consumption in the tubular cells by inhibiting transcellular sodium transport, therefore preventing or limiting ischemic cell injury. The use of loop diuretics should also be evaluated in intermediate syndrome and ischemic NTA where diuretics can, respectively, reduce renal ischemia and convert oliguric ARF into the non-oliguric form.

Background: The role of volume resuscitation in severe Plasmodium falciparum malaria is controversial., Aim: To examine the role of hypovolaemia in severe childhood malaria., Study Design: Retrospective review., Methods: We studied 515 children admitted with severe malaria to a high-dependency unit (HDU) in Kilifi, Kenya. On admission to the HDU, children underwent a further assessment of vital signs and a standard clinical examination., Results: Factors associated with a fatal outcome included deep breathing or acidosis (base excess below -8), hypotension (systolic blood pressure <80 mmHg), raised plasma creatinine (>80 micro mol/l), low oxygen saturation (<90%), dehydration and hypoglycaemia (<2.5 mmol/l). Shock was present in 212/372 (57%) children, of whom 37 (17.5%) died, and was absent in 160, of who only 7 (4.4%) died (chi(2) = 14.9; p = 0.001)., Discussion: Impaired tissue perfusion may play a role in the mortality of severe malaria. Moreover, volume resuscitation, an important life-saving intervention in children with hypovolaemia, should be considered in severe malaria with evidence of impaired tissue perfusion.

Volume expansion is used commonly in preterm infants to treat presumed hypovolaemia. However, the amount that should be given is uncertain. We present data that were obtained from anonymised regional case notes of Project 27/28, a national case-controlled study run by the Confidential Enquiry into Stillbirths and Deaths in Infancy. Various clinical parameters were analysed, including the volume expansion administered during the first 48 h of life. All deaths in the first year of the study in the West Midlands (cases, n = 22) and matched regional controls (survivors, n = 29) were included. The primary outcome was death within 28 days. Sixteen of the 22 deaths were considered 'not inevitable' on the basis of the neonates' condition at birth. These newborns received on average more than twice the volume expansion compared with controls in the first 48 h of life (38.2 vs. 18.2 mL/kg, P = 0.007). There were no significant differences between the groups in lowest blood pressure or base deficit within the first 12 h of life. Newborns who received >or= 30 mL/kg volume expansion in the first 48 h of life were more likely to die than those who received < 30 mL/kg (OR 4.5 [95% CI 1.2, 17.2]). Our data suggest that administration of >or= 30 mL/kg volume expansion is associated with increased mortality in neonates of 27-28 weeks' gestation. Unless there is clear evidence of hypovolaemia, clinicians should exercise caution when prescribing volume expansion.

The syndrome of spontaneous intracranial hypotension is characterized by orthostatic headaches in conjunction with reduced cerebrospinal fluid (CSF) pressure or CSF volume, and characteristic magnetic resonance (MR) imaging findings. A 50-year-old man presented with a 1-year history of paroxysmal ataxia of gait and short attacks of blurred vision when he stood up from a recumbent position and began to walk. Orthostatic headache was not a feature of his clinical presentation. Magnetic resonance images of the brain revealed diffuse enhancement of the dura mater and hygromas over both cerebral convexities. Magnetic resonance images of the spine demonstrated dilated cervical epidural veins and dilation of the perimedullary veins. Radionuclide cisternography identified a CSF leakage that was localized to the T12-L1 level on subsequent myelograms and on computerized tomography scans obtained after the myelograms. An epidural blood patch was administered and visualized with tungsten powder. The patient's clinical symptoms and sites of disease on imaging completely resolved. The unusual clinical presentation in this case--paroxysmal ataxia of gait, lack of orthostatic headaches, and dilated epidural and perimedullary venous plexus--supports a recently noted broadening of both the clinical and imaging characteristics of spontaneous intracranial hypovolemia.

To monitor the ischemic and/or reperfusion injury after porta hepatis occlusion (Pringle maneuver) in livers subjected to hypotension, serum alanine amino transferase (ALT), liver malondialdehyde (MDA), and liver glutathione (GSH) levels were measured. MDA is a by-product of oxidant-induced lipid peroxidation, and GSH is an endogenous antioxidant. The effects of lactated Ringer's (LR) and hypertonic saline (7.5%)/Dextran (6%; HSD) resuscitation on liver injury, if any, was investigated. Rats in sham (S, n = 8) and five other groups (n = 8) underwent femoral artery and vein catheterization and laparotomy. The hemorrhage and ischemia (HI) group was bled 30% of their blood volume and had their porta hepatis occluded for 30 min. The HI, LR, and HSD groups underwent both hemorrhage and occlusion. Thirty minutes after hemorrhage, the LR and HSD groups received either LR (equivalent to three times the shed blood) or HSD (10 mL/kg) resuscitation over 30 min. Both LR and HSD resuscitation lowered the increased ALT and liver tissue MDA seen in the HI group. ALT was decreased from 348 +/- 93 IU/L in the HI group to 200 +/- 98 IU/L in the LR and 139 +/- 74 IU/L in the HSD groups. Liver tissue MDA was 353 +/- 22 nmol/g/tissue in the HI group and LR decreased it to 261 +/- 17 nmol/g/tissue, whereas HSD decreased it to 273 +/- 20 nmol/g/tissue. The decrease in ALT and the increase in liver GSH were more pronounced with HSD resuscitation (P < 0.05). HSD seems to be more effective than LR in decreasing the liver tissue damage produced by total hepatic inflow occlusion under hypovolemic conditions.

To investigate the role played by hypovolaemia in the mechanism of orthostatic intolerance, a mathematical model was developed. The model consisted of seven sub-models that describe: the redistribution of blood induced by lower body negative pressure (LBNP); filling of the left ventricle; contracting of the left ventricle; interaction between the left ventricle and peripheral circulation; and baroreflex regulation. The model was evaluated using experimental data. Using the model, computer simulations were performed to investigate the effects of hypovolaemia on the cardiovascular response to LBNP. The simulation results indicated that, first, when the blood loss is less than 5%, blood pressure can be maintained in the normal range by the baroreflex regulatory mechanism, even with high LBNP application; secondly, when the blood loss is between 15 and 20%, heart rate and blood pressure can be kept in the normal range if LBNP is not applied, but blood pressure falls sharply with LBNP application; and, thirdly, when the blood loss is 25%, the cardiovascular system is in an unstable state (heart rate: 116 beat min (-1), systolic blood pressure: 97 mmHg; diastolic blood pressure: 77 mmHg), even without any LBNP, and becomes more unstable with LBNP. The simulation results support the hypothesis that hypovolaemia is a cause of orthostatic intolerance.

The observations were carried out in 51 healthy volunteers (26 men and 25 women) who underwent passive orthotest with the registration of thoracic impedance (TI). It was found that women had a higher index of TI both in rest and in dynamics of the performance of the orthostatic test than men. In 10 subjects the increase of TI in orthostasis was higher than 15% that can be supposed to be a criterion of the pathological drop of the venous return. The TI dynamics in performing the orthotest was quicker than changes in AP and the appearance of complains can be taken for a preclinical symptom of latent volume disturbances in the orthostatic regulation that has an important diagnostic value.

Disorders of sodium and water metabolism are frequently encountered in hospitalized patients. Hyponatremia in critically ill patients can cause significant morbidity and mortality. Inappropriate treatment of hyponatremia can add to the problem. The diagnosis and management of salt and water abnormalities in critically ill patients is often challenging. The increasing knowledge about aquaporins and the role of vasopressin in water metabolism has enhanced our understanding of these disorders. The authors have outlined the general approach to the diagnosis and management of hyponatremia. A systematic approach by clinicians, using a detailed history, physical examination, and relevant diagnostic tests, will assist in efficient management of salt and water problems.

We describe a hypertensive patient who developed profound cardiogenic shock after treatment with nitrates and diuretics. Echocardiography revealed a marked left ventricular outflow tract obstruction with severe mitral regurgitation that were reversible after aggressive fluid therapy.

We retrospectively evaluated the phenomenon of arterial hypotension in peritoneal dialysis (PD) in a large cohort of 633 PD patients from two centers (Toronto Western Hospital, Toronto, Canada, and Division of Nephrology, Democritus University of Thrace, Greece), thus extending our previously reported experience for an additional 6 years (1995-2000). Together, the units had 81 hypotensive patients (12.8%), whose mean age was 63.8 +/- 14.2 years and whose mean duration of peritoneal dialysis was 49.3 +/- 30 months. Based on the underlying pathophysiology, the hypotensive PD patients were divided into four groups: (A) hypovolemia, 32 patients (39.5%); (B) congestive heart failure (CHF), 15 patients (18.5%); (C) receiving antihypertensive medications, 11 patients (13.6%); and (D) "unknown" etiology, 23 patients (28.4%). All patients in the hypovolemic and antihypertensive groups responded well to treatment (volume expansion and discontinuation of antihypertensive medication, respectively), but in the CHF and "unknown" groups, only 40% improved with the appropriate intervention. Patients in the latter two groups showed the poorest prognosis, with an approximate death rate of 65%. The hypovolemic group had better outcomes, which might reflect prompt response to fluid replacement in that group. We conclude that, in PD patients, careful use of antihypertensive medication, the right evaluation of target weight (especially in patients with cardiac failure), and judicious use of hypertonic exchanges may prevent the severe complication of arterial hypotension.

This patient had a complex presentation, with many potential causes for his shock status. He was obviously in shock, with many signs of poor perfusion. He presented with very rapid heart and respiratory rates, and poor skin perfusion and oxygenation. The clinical presentation of the patient prompted the EMS crew to consider electrical cardioversion in hopes of addressing the unstable tachycardic rate. However, the crew opted to consider the patient's past medical history--i.e., the diarrhea, vomiting and lack of fluid intake--and instead treat the patient for hypovolemia. The picture had not improved by arrival at the ED, and had not been corrected with a fluid bolus.

Hemodynamics was studied in 60 patients with pronounced initial hypovolemia, urgently operated on for acute gastrointestinal disease under conditions of 4 anesthesia. In contrast to traditional anesthesia, transcranial electric stimulation (TCES) as a component of anesthesia stabilized hemodynamics without increasing the rate and volume of intraoperative infusion therapy. This makes total anesthesia with TCES preferable in urgent operations, particularly in cases when hypovolemia cannot be properly corrected before surgery.