Volume replacement with lactated Ringer's or 3% hypertonic saline solution during combined experimental hemorrhagic shock and traumatic brain injury

BACKGROUND: The devastating effects of hypotension on head-trauma-related mortality are well known. This study evaluates the systemic and cerebral hemodynamic responses to volume replacement with 3% hypertonic saline (HSS) or lactated Ringer's solution (LR), during the acute phase of hemorrhagic shock (HS) associated with traumatic brain injury (TBI). METHODS: Fifteen dogs were assigned to one of three groups (n = 5, each) according to the volume replacement protocol, infused after TBI (brain fluid percussion, 4 atm) and epidural balloon to an intracranial pressure (ICP) higher than 20 mm Hg and HS, induced by blood removal to a mean arterial pressure (MAP) of 40 mm Hg in 5 minutes: Group HS+TBI+HSS (8 mL/kg of 3% HSS), HS+TBI+LR (16 mL/kg LR), and Group HS+TBI (controls, no fluids). We simulated treatment during prehospital and early hospital admission. Groups HS+ TBI and HS+TBI+LR received shed blood infusion to a target hematocrit of 30%. Measurements included shed blood volume, fluid volume infused to restore MAP, MAP, cardiac output, cerebral perfusion pressure, cerebral and systemic lactate, and oxygen extraction ratios. RESULTS: Fluid replacement with HSS 3% or LR promoted major hemodynamic benefits over control animals without luids. Cerebral perfusion pressure was higher than controls and similar between treated groups; however, HSS 3% infusion was associated with lower ICP during the "early hospital phase" and a higher serum sodium and osmolarity. CONCLUSION: In the event of severe head trauma and hemorrhagic shock, the use of HSS 3% and larger volumes of LR promote similar systemic and cerebral hemodynamic benefits. However, a lower ICP was observed after HSS 3% than after LR.     

Effect of intracranial pressure and cerebral perfusion pressure on outcome prediction of severe traumatic brain injury

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Effects of hypertonic saline versus lactated Ringer's solution on cerebral oxygen transport during resuscitation from hemorrhagic shock

Hypertonic saline successfully restores systemic hemodynamics in dogs and humans with severe hemorrhagic shock and, in contrast to lactated Ringer's solution, does not increase intracranial pressure (ICP). This study compares cerebral oxygen delivery in 12 dogs subjected to hemorrhagic shock by the rapid removal of blood (mean arterial pressure of 40 mm Hg maintained for 30 minutes), and then resuscitated with lactated Ringer's solution (six dogs) or 7.5% saline solution (six dogs) to restore systolic arterial pressure. Both solutions effectively restored systemic hemodynamic stability, increasing cardiac output and systolic blood pressure while decreasing mean and diastolic arterial pressure and systemic vascular resistance. The ICP was significantly lower after resuscitation in the hypertonic saline group (p less than 0.05), but cerebral blood flow, which had decreased during shock, was not restored by either fluid, and cerebral oxygen transport fell further secondary to a hemodilutional reduction of hemoglobin. Although hypertonic saline may improve systemic hemodynamics and maintain a low ICP during resuscitation, it fails, as does Ringer's solution, to restore cerebral oxygen transport to prehemorrhagic shock levels.     

Positive end-expiratory pressure alters intracranial and cerebral perfusion pressure in severe traumatic brain injury

BACKGROUND: Optimizing intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is important in the management of severe traumatic brain injury (TBI). In trauma patients with TBI and respiratory dysfunction, positive end-expiratory pressure (PEEP) is often required to support oxygenation. Increases in PEEP may lead to reduced CPP. We hypothesized that increases in PEEP are associated with compromised hemodynamics and altered cerebral perfusion. METHODS: Twenty patients (mean Injury Severity Score of 28) with TBI (Glasgow Coma Scale score < 8) were examined. All required simultaneous ICP and hemodynamic monitoring. Data were categorized on the basis of PEEP levels. Variables included central venous pressure, pulmonary artery occlusion pressure, cardiac index, oxygen delivery, and oxygen consumption indices. Differences were assessed using Kruskal-Wallis analysis of variance. RESULTS: Data were expressed as mean +/- SE. As PEEP increased from 0 to 5, to 6 to 10 and 11 to 15 cm H O, ICP decreased from 14.7 +/- 0.2 to 13.6 +/- 0.2 and 13.1 +/- 0.3 mm Hg, respectively. Concurrently, CPP improved from 77.5 +/- 0.3 to 80.1 +/- 0.5 and 78.9 +/- 0.7 mm Hg. As central venous pressure (5.9 +/- 0.1, 8.3 +/- 0.2, and 12.0 +/- 0.3 mm Hg) and pulmonary artery occlusion pressure (8.3 +/- 0.2, 11.6 +/- 0.4, and 15.6 +/- 0.4 mm Hg) increased with rising levels of PEEP, cardiac index, oxygen delivery, and oxygen consumption indices remained unaffected. Overall mortality was 30%. CONCLUSION: In trauma patients with severe TBI, the strategy of increasing PEEP to optimize oxygenation is not associated with reduced cerebral perfusion or compromised oxygen transport.     

Monitoring intracranial pressure in traumatic brain injury

Increased intracranial pressure (ICP) is an important cause of secondary brain injury, and ICP monitoring has become an established component of brain monitoring after traumatic brain injury. ICP cannot be reliably estimated from any specific clinical feature or computed tomography finding and must actually be measured. Different methods of monitoring ICP have been described but intraventricular catheters and microtransducer systems are most widely used in clinical practice. ICP is a complex variable that links ICP and cerebral perfusion pressure and provides additional information from identification and analysis of pathologic ICP wave forms. ICP monitoring can also be augmented by measurement of indices describing cerebrovascular pressure reactivity and pressure-volume compensatory reserve. There is considerable variability in the use of ICP monitoring and treatment modalities among head injury centers. However, there is a large body of clinical evidence supporting the use of ICP monitoring to detect intracranial mass lesions early, guide therapeutic interventions, and assess prognosis, and it is recommended by consensus guidelines for head injury management. There remains a need for a prospective, randomized, controlled trial to identify the value of ICP monitoring and management after head injury.     

Limited resuscitation with hypertonic saline, hypertonic sodium acetate, and lactated Ringer's solutions in a model of uncontrolled hemorrhage from a vascular injury

BACKGROUND: Hypertonic sodium acetate-dextran solution (HAD) causes vasodilatation and buffers metabolic acidosis. In controlled hemorrhage models, HAD in small volumes increases cardiac output without increasing blood pressure, thus creating a "high flow-low pressure" state. The objective of this study was to determine whether limited resuscitation of uncontrolled hemorrhage with HAD solution improves gut perfusion as measured by intestinal mucosal tonometry. METHODS: Three groups of 10 swine were bled 25 mL/kg by means of a femoral artery catheter to produce a mean blood pressure of 30 mm Hg. A 4-mm abdominal aortic laceration was then produced by pulling out a preimplanted wire loop. Groups were then randomly assigned to be resuscitated with either lactated Ringer's solution, a hypertonic saline-dextran solution or HAD solution sufficient to maintain a mean blood pressure of 45 mm Hg for 5 hours or until death. Outcomes were measured by survival, intraperitoneal blood loss, hemodynamic monitoring, and ileal mucosal tonometry. RESULTS: HAD infusions caused transient worsening of hypotension and were associated with increased mortality (p = 0.038). Blood loss and volumes required for resuscitation were significantly increased in the lactated Ringer's solution group. HAD showed significant buffering effect against metabolic acidosis in arterial blood only, but intestinal ileal mucosal tonometry was not different among the groups. CONCLUSION: HAD did not improve gut perfusion despite buffering the systemic acidosis of shock and caused increased mortality. Limited resuscitation with any of these solutions is associated with significant mucosal acidosis.     

A model for studies of intracranial volume pressure dynamics in traumatic brain injury

The present study was undertaken to establish an experimental trauma model where it was possible to alter intracranial pressure (ICP) dynamics without raising intracranial pressure to abnormal levels and monitor metabolic disturbances with microdialysis. Thirty rats were intubated and mechanically ventilated before and after trauma. ICP was measured in the left ventricle. A weight-drop technique (21 g from 35 cm) with a brain compression of 1.5 mm was used to produce the injury. Intracranial compensatory volume was decreased 20 or 60 microL by placement of rubber film between the dura mater and bone. A bolus injection technique was used for the pressure volume response. ICP remained within normal limits for 2 h after trauma irrespective of the reduction in compensatory intracranial volume. Pressure-volume index decreased from 0.0825 +/- 0.009 to 0.0779 +/- 0.011 mL in the sham trauma and from 0.0871 +/- 0.018 to 0.0748 +/- 0.017 mL in the trauma groups (p < 0.015) when the intracranial volume was reduced by 60 microL. Intracranial compliance was not affected significantly. The present study shows that it is possible to vary ICP dynamics in a traumatic brain injury model without causing pathological increases in baseline ICP. This model may be used to study the effects of secondary insults (i.e., hypotension, hypoxia, hypercarbia, and hyperthermia) on the injured brain when ICP is normal but intracranial compensatory volume is impaired.     

The effects of aortic crossclamping and resuscitation on intracranial pressure, cerebral blood flow, and cerebral water content in a model of focal brain injury and hemorrhagic shock

Aortic crossclamping (AOXC) is performed frequently in hypotensive trauma patients who may have had a head injury. The effect of AOXC on the injured brain is unknown. We studied the effect of AOXC on mean arterial pressure (MAP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral perfusion pressure (CPP), and cerebral water content in a porcine model of focal cryogenic brain injury. Four groups of animals were studied: Group I--brain injury only; Group II--brain injury and AOXC; Group III--brain injury with hemorrhage and AOXC; and Group IV--AOXC only. Focal cryogenic grain injury increased the ICP in Groups I-III. Aortic crossclamping increased MAP, CBF, ICP, and CPP after hemorrhage in Group III. Following declamping and resuscitation there were no differences between the groups in any studied variable. Cerebral water content at the site of the focal brain injury was greater than in nonlesioned cortex but there was no significant difference between groups despite a greater positive fluid balance in hemorrhaged animals. AOXC improved perfusion to the injured brain without a significant increase in ICP. Increased MAP induced by AOXC and large fluid resuscitation appeared to have no detrimental effect on ICP, CBF, cerebral water content, or CPP in this model of brain injury.     

Effect of decompressive craniectomy on intracranial pressure and cerebrospinal compensation following traumatic brain injury

OBJECTIVE: Decompressive craniectomy is an advanced treatment option for intracranial pressure (ICP) control in patients with traumatic brain injury. The purpose of this study was to evaluate the effect of decompressive craniectomy on ICP and cerebrospinal compensation both within and beyond the first 24 hours of craniectomy. METHODS: This study was a retrospective analysis of the physiological parameters from 27 moderately to severely head-injured patients who underwent decompressive craniectomy for progressive brain edema. Of these, 17 patients had undergone prospective digital recording of ICP with estimation of ICP waveform-derived indices. The pressure-volume compensatory reserve (RAP) index and the cerebrovascular pressure reactivity index (PRx) were used to assess those parameters. The values of parameters prior to and during the 72 hours after decompressive craniectomy were included in the analysis. RESULTS: Decompressive craniectomy led to a sustained reduction in median (interquartile range) ICP values (21.2 mm Hg [18.7; 24.2 mm Hg] preoperatively compared with 15.7 mm Hg [12.3; 19.2 mm Hg] postoperatively; p = 0.01). A similar improvement was observed in RAP. A significantly lower mean arterial pressure (MAP) was needed after decompressive craniectomy to maintain optimum cerebral perfusion pressure (CPP) levels, compared with the preoperative period (99.5 mm Hg [96.2; 102.9 mm Hg] compared with 94.2 mm Hg [87.9; 98.9 mm Hg], respectively; p = 0.017). Following decompressive craniectomy, the PRx had positive values in all patients, suggesting acquired derangement in pressure reactivity. CONCLUSIONS: In this study, decompressive craniectomy led to a sustained reduction in ICP and improvement in cerebral compliance. Lower MAP levels after decompressive craniectomy are likely to indicate a reduced intensity of treatment. Derangement in cerebrovascular pressure reactivity requires further studies to evaluate its significance and influence on outcome.     

Comparative study on the effects of acetated Ringer's solution,lactated Ringer's solution,Ringer's solution,and 5% glucose-acetated Ringer's solution on canine hemorrhagic shock

The abilities of acetated Ringer's solution (AR), lactated Ringer's solution (LR), Ringer's solution (R), and 5% glucose-acetated Ringer's solution (AR-D) to improve canine hemorrhagic shock were investigated. All solutions studied were infused at 1 ml·kg⁻¹·min⁻¹ for 90 min after base excess (BE) reached about −13 mEq·l⁻¹ by maintaining the mean blood pressure (MBP) at 40 mmHg. MBP, renal blood flow (RBF), vertebral blood flow (VBF), and urinary output significantly increased after the start of infusion of AR, LR, R, and AR-D. The VBF and urinary output were particularly improved with AR-D. The arterial blood level of HCO ₃ ⁻ and BE were also increased after the start of infusion of AR, LR, and AR-D but not of R. AR infusion improved BE more effectively than LR. Although AR-D, AR, and LR increased HCO ₃ ⁻ , the blood pH did not increase in AR-D. The value of plasma acetate increased after the start of infusion of AR and AR-D but not of LR, and R. On the other hand, plasma lactate and pyruvate levels were higher with LR than with AR. The increase in the lactate/pyruvate ratio induced by LR was larger than that by AR. The plasma norepinephrine and epinephrine levels decreased after the start of all infusions. Plasma insulin and glucose levels were markedly increased after the start of AR-D infusion but were not affected by AR, LR, and R. These results indicate that the effectiveness of various infusion solutions such as AR, LR, R, and AR-D during canine hemorrhagic shock varies. AR-D may be useful for increasing both peripheral blood flow and urine output. AR may also be useful for improvement in metabolic acidosis and surgical diabetes induced by hemorrhagic shock.     

Prospective, randomized trial of hypertonic sodium lactate versus lactated Ringer's solution for burn shock resuscitation

We prospectively randomized 51 adult burned patients on admission to study fluid, electrolyte, and physiologic parameters during burn resuscitation with the use of hypertonic saline (HSL, Na 250 mEq/L, 514 mOsm) or lactated Ringer's solution (LR, Na 130 mEq/L, 268 mOsm). Patients suffered at least 20% total body surface area burns (BSA); the mean BSA injury was 36.7% BSA, with a range of 20 to 74% BSA. All patients were admitted to our Burn Center within at least 12 hours of injury. Laboratory studies included frequent determinations of serum chemistries including osmolalities, and continuous 24-hour urine collections for electrolytes and osmolality determinations. Fluid requirements (cc/kg/% BSA), urine output (cc/kg/hr), sodium intake and excretion (mEq/kg/% BSA), serum and urine osmolality (mOsm/kg), serum creatinine (mg/dl), body weight (kg), and enteral intake (cc/24 hrs and calories/24 hrs) were analyzed for comparison at 24-hour intervals following burn injury. Using Student's t-test, significance was attributed to a p less than 0.05. Nonparametric methods were used to compare non-normalized data. Regression analysis was used to compare sodium intake (mEq/kg) and fluid intake (cc/kg) between the HSL and the LR groups in relation to % BSA. Our data show no advantage of HSL over conventional therapy with LR for burn resuscitation. We were not able to demonstrate decreased fluid requirements, improved tolerance of feedings, or decrease in per cent weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)     

Treatment of raised intracranial pressure following traumatic brain injury

Appropriate treatment of raised intracranial pressure (ICP) after traumatic brain injury (TBI) remains a controversial topic in neurotraumatology. Several techniques are employed clinically, which include vasopressors, osmotically active substances, hyperventilation, and decompressive surgery. This article reviews six recent papers that have examined alternative methods of treating elevated ICP. The first two papers consider a new and controversial alternative to cerebral perfusion pressure (CPP) management, which involves mild hypotension coupled with pre-capillary vasoconstriction using dihydroergotamine. The authors claim success with this treatment, and although the patient numbers are small, there is no evidence that they fare any less well than patients treated with conventional techniques. The third and fourth papers consider hypertonic saline (HTS) as a possible osmotic treatment for raised ICP. The third examines HTS given as a 23.4% bolus and found beneficial effects. The fourth examines HTS as a 1.6% constant infusion for fluid replacement and found that patients fared less well. The reason for this difference between the results for the two administration methods is unknown, although it may relate to the triggering of body homeostatic mechanisms in the case of constant infusion. The fifth paper compares glycerol and mannitol as osmotic ICP agents and found no significant differences between them. The final study reports for the first time a series of patients treated for refractory elevations in ICP with bifrontal craniectomy. They report good results, and suggest that this therapy should be formalized as a treatment option for severely elevated ICP. The pathophysiological mechanisms underlying the generation of a raised ICP belie the use of one therapy to treat all cases. Analysis of these studies demonstrates how problematic heterogeneity in the injury population can be for the assessment of possible treatments. It is clear, therefore, that effective analysis of treatments for raised ICP requires appropriate subdivision of the injured population into common pathophysiological processes and, furthermore, that the future of clinical TBI management may well require a similar stratification in order to tailor treatments for the individual patient.     

Clinical applications of intracranial pressure monitoring in traumatic brain injury

Background

Intracranial pressure (ICP) monitoring has been for decades a cornerstone of traumatic brain injury (TBI) management. Nevertheless, in recent years, its usefulness has been questioned in several reports. A group of neurosurgeons and neurointensivists met to openly discuss, and provide consensus on, practical applications of ICP in severe adult TBI.

Methods

A consensus conference was held in Milan on October 5, 2013, putting together neurosurgeons and intensivists with recognized expertise in treatment of TBI. Four topics have been selected and addressed in pro-con presentations: 1) ICP indications in diffuse brain injury, 2) cerebral contusions, 3) secondary decompressive craniectomy (DC), and 4) after evacuation of intracranial traumatic hematomas. The participants were asked to elaborate on the existing published evidence (without a systematic review) and their personal clinical experience. Based on the presentations and discussions of the conference, some drafts were circulated among the attendants. After remarks and further contributions were collected, a final document was approved by the participants.

Summary and conclusions

The group made the following recommendations: 1) in comatose TBI patients, in case of normal computed tomography (CT) scan, there is no indication for ICP monitoring; 2) ICP monitoring is indicated in comatose TBI patients with cerebral contusions in whom the interruption of sedation to check neurological status is dangerous and when the clinical examination is not completely reliable. The probe should be positioned on the side of the larger contusion; 3) ICP monitoring is generally recommended following a secondary DC in order to assess the effectiveness of DC in terms of ICP control and guide further therapy; 4) ICP monitoring after evacuation of an acute supratentorial intracranial hematoma should be considered for salvageable patients at increased risk of intracranial hypertension with particular perioperative features.     

The use of hypertonic saline for treating intracranial hypertension after traumatic brain injury

The past decade has witnessed a resurgence of interest in the use of hypertonic saline for low-volume resuscitation after trauma. Preliminary studies suggested that benefits are limited to a subgroup of trauma patients with brain injury, but a recent study of prehospital administration of hypertonic saline to patients with traumatic brain injury failed to confirm a benefit. Animal and human studies have demonstrated that hypertonic saline has clinically desirable physiological effects on cerebral blood flow, intracranial pressure, and inflammatory responses in models of neurotrauma. There are few clinical studies in traumatic brain injury with patient survival as an end point. In this review, we examined the experimental and clinical knowledge of hypertonic saline as an osmotherapeutic agent in neurotrauma.     

Slope of the intracranial pressure waveform after traumatic brain injury

BACKGROUND: The measurement and treatment of ICP within the management of TBI generally focuses on keeping the mean ICP to less than 20 mm Hg. More sophisticated analysis of the intracranial pressure waveform has yielded important relationships, but those methods have not gained widespread use. Prior analysis of the slope of the ICP waveform during inspiration and expiration in patients with hydrocephalus has provided valuable information that has never been applied to patients with TBI. This study used digital methods to examine ICP and the slope of the ICP waveform in relation to the respiratory cycle in subjects with TBI. METHODS: Intracranial pressure was monitored in 6 randomly selected patients admitted with acute TBI. In the first 3 subjects, a single 5-minute recording was analyzed. In 3 subsequent subjects, 4 nonsequential 5-minute epochs were analyzed during periods of varying ICP. The systolic slope of the ICP waveform was compared during inspiration and expiration, and then evaluated in relation to simultaneous mean ICP. RESULTS: The slope of the systolic ICP waveform was significantly greater during inspiration than during expiration (P < .0001 for 5 subjects and P < .03 for 1 subject). Within each subject, the ICP slope was positively correlated with simultaneous ICP (P < .0001 in all 6 cases). CONCLUSION: Greater systolic ICP waveform slope during inspiration has not been described previously after TBI and is consistent with prior observations in subjects with hydrocephalus. The strong correlation between ICP slope and simultaneous mean ICP suggests that increasing ICP slope might indicate loss of intracranial compliance after TBI.     

Comparison between hypertonic saline and mannitol in the reduction of elevated intracranial pressure in a rodent model of acute cerebral injury

Clinically both mannitol and hypertonic saline (HTS) have been used successfully to treat elevated intracranial pressure (ICP), although which therapy is superior is yet unclear. Most experimental data have been derived from animal models of brain injury using general anesthesia, which may not be applicable under other conditions. Our laboratory compared the efficacy of single, equi-osmolar bolus doses of HTS and mannitol in reducing elevated ICP in a lightly sedated, unrestrained rodent model of acute brain injury. Sprague-Dawley rats were mask anesthetized for craniectomy and placement of invasive monitors. Following emergence from anesthesia, continuous sedation was provided (0.25% halothane in oxygen). A focal, liquid nitrogen cold lesion was introduced to the right parietal cortex. Animals were continuously monitored and then treated with a single bolus of 0.9% saline (control group) or 11.0 mOsm/kg equivalents of either mannitol or HTS (experimental groups) at time of maximal ICP increase (60 minutes). Both mannitol and HTS reduced ICP, but HTS was more effective-53.9% reduction versus 35.0% (P < .01). The therapeutic action of HTS was also more durable, lasting up to 500 minutes whereas the mannitol treated animals were observed to return to, and overshoot the baseline elevated ICP by 10% to 25% by 120 minutes following dosing (P < .01). Despite these differences, brain water content was similar between groups. We conclude that HTS was more effective in reducing elevated ICP in this awake model of traumatic brain injury.