How does hypertonic saline decrease intracranial pressure? Hypertonic saline and mannitol
Mannitol
Mannitol is a type of sugar alcohol, used as a sweetener and medication. As a sweetener it is used in diabetic food as it is poorly absorbed from the intestines. As a medication, it is used to decrease pressure in the eyes, as in glaucoma, and to lower increased intracranial pressure. Medical…
Does hypertonic saline affect intracranial pressure after traumatic brain injury?
Objective: Hypertonic saline is emerging as a potentially effective single osmotic agent for control of acute elevations in intracranial pressure (ICP) caused by severe traumatic brain injury. This study examines its effect on ICP, cerebral perfusion pressure (CPP), and brain tissue oxygen tension (PbtO2).
What is the role of hypertonic saline in the ICU?
Patients in the Neuro ICU are frequently given hypertonic saline for brain injuries when there is significant cerebral edema, elevated intracranial pressure or due to processes that lower Na+. Hyponatremia can worsen cerebral edema and hypernatremia has been shown to lower intracranial pressure.
What is hypertonic saline made of?
Hypertonic Saline (3% Sodium Chloride) Hypertonic Saline (3% Sodium Chloride) Hypertonic saline is an osmotic agent uses to reduce the effects of secondary brain injury in patients with traumatic brain injury (TBI). It is known as hypertonic saline because its concentration of sodium is higher than the physiologic concentration of plasma (0.9%).
How does hypertonic saline work in hypovolemic shock?
Resuscitation of patients with hypovolemic shock. Mechanism of action of hypertonic saline. Hypertonic saline works principally by exerting an osmotic effect. Due to its higher concentration of sodium and lower concentration of water when compared to plasma, it draws fluid out of the swollen (edematous) cerebral tissue.
What is hypertonic saline used for?
What is hyperosmolar therapy?
Does mannitol help with dehydration?
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Does hypertonic saline reduce ICP?
Hypertonic saline was associated with decreased ICP, whereas hypertonic saline and mannitol had similar observed effectiveness for CPP. Meaning This study of children with severe traumatic brain injury found that bolus administration of hypertonic saline was associated with superior ICP and CPP outcomes.
Why is a hypertonic IV solution used to reduce brain swelling?
It draws fluid out of edematous cerebral tissues because it has a higher concentration of sodium and a lower concentration of water than blood.
How does NaCl reduce intracranial pressure?
Giving saline with a NaCl concentration far in excess of the plasma sodium will exert an osmotic effect that will help shift fluid out of the cranial vault – overcoming this baseline lack of permeability. This, can lower intracranial pressure.
How does hypertonic saline work?
Hypertonic saline requires less overall volume administered to achieve similar plasma volumes as larger volumes of normal saline. [6] Hypertonic saline stimulates vasopressin release from the pituitary gland, which decreases water loss through the kidneys.
Why is hypertonic saline better than mannitol?
Hypertonic saline is superior to mannitol for the combined effect on intracranial pressure and cerebral perfusion pressure burdens in patients with severe traumatic brain injury.
Why use hypertonic saline for cerebral edema?
Our experience, and that of others, suggests that hypertonic saline solution therapy reduces intracranial pressure and lateral displacement of the brain in patients with cerebral edema. This therapy appears most promising in patients who have head trauma or postoperative cerebral edema.
What relieves rapidly increasing intracranial pressure?
Cerebrospinal fluid drainage CSF drainage lowers ICP immediately by reducing intracranial volume and more long-term by allowing edema fluid to drain into the ventricular system. Drainage of even a small volume of CSF can lower ICP significantly, especially when intracranial compliance is reduced by injury.
How does hyperosmolar therapy reduce ICP?
Hyperosmolar solutions are effective in reducing elevated intracranial pressure through 2 distinct mechanisms: plasma expansion with a resultant decrease in blood hematocrit, reduced blood viscosity, and decreased cerebral blood volume; and the creation of an osmotic gradient that draws cerebral edema fluid from brain ...
How do you lower intracranial hypertension?
Treatments for chronic intracranial hypertensionlosing weight if you're overweight. ... stopping any medicine that may be causing your symptoms, including contraception methods. ... medicine to remove excess fluid from the body (diuretics)medicine to reduce the production of cerebrospinal fluid in your brain.More items...
What happens when you give a patient a hypertonic solution?
When infused, hypertonic fluids cause an increased concentration of dissolved solutes in the intravascular space compared to the cells. This causes the osmotic movement of water out of the cells and into the intravascular space to dilute the solutes in the blood.
What happens when you inject a hypertonic solution?
Intravenous injection of hypertonic NaCl solution evokes reflex bradycardia and hypotension, effects thought to result from stimulation of afferent vagal endings in the lungs.
Does hypertonic saline cross the blood brain barrier?
Hypertonic saline has a reflection coefficient of 1.0, meaning that it does not readily cross the blood-brain barrier (Rockswold et al., 2009).
What kind of IV solution would you use to help reduce brain swelling?
Mannitol, a hypertonic crystalloid solution, is commonly used to decrease brain water content and reduce intracranial pressure (ICP). Hypertonic saline solutions also decrease brain water and ICP while temporarily increasing systolic blood pressure and cardiac output.
What IV solution is used for cerebral edema?
Osmotherapy agents such as hypertonic saline (HTS) are currently used in the treatment of patients with post-traumatic cerebral edema and raised ICP resulting from TBI [51]. It is believed to have a particularly useful role in the treatment of ICP whilst administering small volume fluid resuscitation [52].
What kind of solution should be given to a patient with swollen brain tissues?
Osmotherapy When your brain swells, it accumulates excess fluid. Osmotherapy is a technique meant to draw water out of the brain. This is done using osmotic agents such as mannitol, or high-salt saline. Osmotic therapy also helps improve blood circulation.
How do they relieve swelling on the brain?
Usually, swelling happens quickly and is simple to treat with some combination of rest, ice, elevation, medication, or removal of excess fluid. Your brain can also swell as a result of injury, illness, or other reasons.
Hypertonic Saline Versus Mannitol for Traumatic Brain Injury: A ...
Background: Mannitol and hypertonic saline are widely used to treat raised intracranial pressure (ICP) after traumatic brain injury (TBI), but the clinical superiority of one over the other has not been demonstrated. Methods: According to the PRISMA statement, this meta-analysis reports on randomized controlled trials investigating hypertonic saline compared with mannitol in the treatment of ...
Peripheral 3% Hypertonic Saline is Safe - EMCrit Project
Peripheral Hypertonic Saline There are still pharmacies that believe that 3% Hypertonic Saline can only be given through a central line. The evidence would go against this assertion: Brenkert TE et al. Intravenous Hypertonic Saline Use in the Pediatric Emergency Department (Pediatr Emer Care 2013;29: 71Y73) Bulger, Eileen M, Susanne May, Karen J Brasel, Martin […]
Hypertonic Saline is Superior to Mannitol for the Combined ... - PubMed
Background: Hypertonic saline (HTS) and mannitol are effective in reducing intracranial pressure (ICP) after severe traumatic brain injury (TBI). However, their simultaneous effect on the cerebral perfusion pressure (CPP) and ICP has not been studied rigorously. Objective: To determine the difference in effects of HTS and mannitol on the combined burden of high ICP and low CPP in patients with ...
Hypertonic saline in critical care: a review of the literature and ...
Hypertonic saline solutions have been in experimental and clinical use since the early 1900s [].Weed and McKibben published work on brain volume reduction with hypertonic saline as early as 1919 [].Experimental work on compartmental fluid shifts in animals [] confirmed hypertonic saline produced haemodynamic changes and its use in many different clinical settings has followed.
Hypertonic saline in critical care | Deranged Physiology
Hypertonic saline is a tool with numerous uses, among which is the replacement of sodium (and not water) to correct hypervolaemic hypoosmolar hyponatremia, osmotherapy for raised intracranial pressure, resuscitation of hypotensive patients where a small fluid volume is desirable, and increased sputum clearance when given via a nebuliser. Unfortunately, for many of these indications there is ...
Neurocritical Care Protocol for Hypertonic Saline
< 50 kg: 210 ml/hr -- round to 200 ml over 1 hour 51-100 kg: 375 ml/hr – round to 400 ml over 1 hour >100 kg: 625 ml/hr – round to 600 ml over 1 hour
What is hypertonic saline used for?
Hypertonic saline for the management of raised intracranial pressure after severe traumatic brain injury
What is hyperosmolar therapy?
Hyperosmolar agents are commonly used as an initial treatment for the management of raised intracranial pressure (ICP) after severe traumatic brain injury (TBI). They have an excellent adverse-effect profile compared to other therapies, such as hyperventilation and barbiturates, which carry the risk of reducing cerebral perfusion.
Does mannitol help with dehydration?
While mannitol can cause dehydration over time, HTS helps maintain normovolemia and cerebral perfusion, a finding that has led to a large amount of pilot data being published on the benefits of HTS, albeit in small cohorts. Prophylactic therapy is not recommended with mannitol, although it may be beneficial with HTS.
Why is hypertonic saline used?
Hypertonic saline was first reported for the treatment for alteration of brain bulk by Weed and McKibben.[3] Because of its effect of reducing I CP, hypertonic saline has become more and more widely used in clinical practice.
Is 20% mannitol better than 3% saline?
The main findings are as follows: For patients with intracranial hypertension, 20% mannitol was slightly more effective than 3% hypertonic saline in reducing ICP. In the aspect of increasing CPP, both 20% mannitol and 3% hypertonic saline had the effect of increasing CPP, and 3% hypertonic saline perform better.
Is mannitol superior to hypertonic saline?
Evaluation of the prognosis of children after treatment with hypertonic saline and mannitol requires a randomized study with adequate power and a reasonable follow-up period to confirm that hypertonic saline is superior to mannitol in patient-centered outcomes.
Why is hypertonic saline used?
Hypertonic saline is an osmotic agent uses to reduce the effects of secondary brain injury in patients with traumatic brain injury (TBI). It is known as hypertonic saline because its concentration of sodium is higher than the physiologic concentration of plasma (0.9%). This solution is given during the acute phase of the management ...
Why is hypertonic saline used in hemodynamic stabilization?
Hypertonic saline is an effective plasma expander therefore it is used in hemodynamic stabilization of patients with hypovolemia. Volume expansion improves blood pressure and cerebral perfusion pressure leading to better brain oxygenation and reduced risk for secondary damage.
What happens to the brain after traumatic brain injury?
Brain hyponatremia results after traumatic brain injury can lead to cerebral edema, ischemia and extracellular volume depletion. The edema can all result in dangerous increases in intracranial pressure. Hypertonic saline (HTS) helps to counteract the effects of hyponatremia by increasing serum sodium levels.
What is the goal of continuous HTS?
The main objective of continuous HTS therapy is to provide an optimal osmolar gradient while avoiding the dangerous effects of hypernatremia. Maintaining serum sodium levels of 145 to 155 mmol/L is likely to achieve this goal.
What is secondary injury?
Secondary injury can lead to development of cerebral edema and intractable increased intracranial pressure (ICP). The resultant cerebral edema is treated with surgery and medications (osmotic agents such as mannitol and hypertonic saline).
How much sodium does 3ml of 3% saline increase?
When 3mls/kg of 3% saline are used, there will be an increase plasma sodium by approximately 2-3 mmol/L but the increase may be greater if a large diuresis occurs and whenever in doubt you will need to check plasma sodium.
How long does it take to take a syringe for cerebral oedema?
In the management of cerebral oedema due to traumatic brain injury or DKA, the standard dose is 3-5 mls/kg infused over 10–20 minutes.
What is the treatment for cerebral edema?
This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of cerebral edema. Clinicians must be able to select appropriate therapies for initial cerebral edema management based on available evidence while balancing efficacy and safety.
How much NaCl should I use for SAH?
In a prospective study, Al-Rawi et al. administered 2 ml/kg of 23.5% NaCl to 44 patients with poor-grade SAH [14]. Patients who demonstrated a robust and durable response to the NaCl infusion were more likely to have a favorable outcome (mRS < 4). Bentsen and colleagues published three studies using 7.2% NaCl with 6% HES, a formulation which is currently not available in the USA, in patients with SAH [11–13]. One of these was a prospective, randomized, placebo-controlled trial of 22 patients that found modest reductions in ICP using 7.2% HTS/6% HES compared to placebo [11]. The other studies were of lower quality with similar results [12, 13].
What is cerebral edema?
Cerebral edema is a non-specific pathological swelling of the brain that may develop in a focal or diffuse pattern after any type of neurological injury. The underlying cause of this brain swelling is highly variable and relates to multiple physiological cellular changes. The simplest description of cerebral edema is an accumulation of excessive fluid within either brain cells or extracellular spaces. Cerebral edema can be secondary to disruption of the blood brain barrier, local inflammation, vascular changes, or altered cellular metabolism. The identification and treatment of cerebral edema is central to the management of critical intracranial pathologies. Measurement of cerebral edema is indirect and generally relies on surrogate markers seen on imaging studies, such as tissue shifts or structural changes, or via intracranial pressure (ICP) monitoring devices. It is considered one of the more common contributors to elevated ICP, which has been identified as a predictor of poor outcome in patients with TBI, stroke, and other intracranial pathologies [1, 2]. The literature describes multiple treatment modalities including hyperosmolar therapy, acute hyperventilation, temperature modulation, diversion of CSF, surgical decompression, and metabolic suppression [3]. These treatments are often administered without consideration of the underlying disease process, when in fact their efficacy may hinge upon the pathophysiology at hand. Recent guidelines for the management of AIS, ICH, and TBI, among others, discuss the treatment of cerebral edema. However, practical recommendations regarding the selection and monitoring of therapies for optimal efficacy and safety are generally lacking [3–6].
What is the grade methodology used in Cochrane?
The panel used the GRADE methodology to evaluate the quality of evidence as high, moderate, low, or very low [7]. These designations denote the degree of certainty that the estimate of effect in each study approximates the true effect. Recommendations generated from this literature review and the subsequent quality of evidence rating accounted for efficacy, risks, potential sources of bias, and treatment effect. The Cochrane Risk of Bias Assessment tool was used to evaluate bias in sequence generation, allocation, blinding, missing outcome data, selective outcome reporting, and other sources of bias. The panel classified recommendations as strong (“We recommend”) when they are the preferred treatment for most patients and should be adopted as policy in the majority of situations. Conditional recommendations (“We suggest,” “Clinicians should consider”) should be further considered based upon the clinical scenario and carefully evaluated by stakeholders before being implemented as policy. Areas where there is insufficient evidence to support recommendations are identified, and, in some instances, “good practice statements” are provided. These statements are meant to state guidance where there may be a lack of published evidence, but the practice is commonly accepted as beneficial.
Is HTS as effective as mannitol?
In making this recommendation, the panel felt that while the quality of evidence was low, the consistency of the literature suggested HTS was at least as safe and effective as mannitol. In addition, the panel agreed that the putative advantages of HTS over mannitol for fluid resuscitation and cerebral perfusion justified the suggestion to use HTS over mannitol. Although treatment effect of these agents on elevated ICP or cerebral edema may be expected based on the literature, neither agent has been demonstrated to improve neurological outcomes.
Can you use mannitol over hypertonic sodium?
We suggest that neither HTS nor mannitol be used with the expectation for improving neurological outcomes in patients with TBI (conditional recommendation, low-quality evidence).
Does HTS help with ICP?
While the overall quality of the evidence in this area is very low, the panel felt there was enough consistency across the published studies to suggest symptom-based bolus dosing of HTS as an effective means of reducing ICP and cerebral edema in patients with SAH. In addition, HTS bolus administration may also raise serum sodium, improve brain pH, and increase brain tissue oxygenation [17, 18]. At present, there are insufficient data to support the use of HTS to improve neurological outcome, regardless of the administration strategy. We did not identify any substantial evidence to support targeting a specific serum sodium concentration in order to reduce ICP or improve neurological outcome in patients with SAH, demonstrating the need for future research regarding the impact of specific sodium targets on ICP and neurological outcomes.
How many tiers of ICP elevation?
Treatment for ICP elevation can be loosely divided into three rough tiers, depending on how aggressive the treatments are (table below). Please note, however, that this is intended only as a rough cognitive rubric. It will often be appropriate to mix treatments from different tiers.
Why is noncommunicating hydrocephalus easier to diagnose?
Noncommunicating hydrocephalus is therefore easier to diagnose based on CT scans, because pressure differentials will cause shifts in brain tissue visible on CT.
How does fever affect ICP?
A fever increases ICP by increasing the brain’s metabolic demands and need for arterial blood supply.
What causes CSF to accumulate in the lateral and third ventricles?
For example, obstruction of the fourth ventricle will cause CSF to accumulate in the lateral and third ventricles. Alternatively, a single lateral ventricle may become obstructed (“trapped”), causing it to expand.
What causes cytotoxic edema in MRI?
MRI features: cytotoxic edema causes diffusion restriction, which leads to hyperintensity on DWI sequences and hypointensity on ADC sequences. Causes: Cytotoxic edema is caused most notably by ischemic stroke.
Is papilledema accurate for ICP elevation?
Papilledema may be less accurate for immediate-onset intracranial hypertension, because it takes some time to develop. Papilledema may be useful for identifying ICP elevation in cases where the nerve sheath is borderline (e.g., between 5-6 mm wide). More on this here.
Does volume increase pressure?
Initially, changes in volume cause relatively little increase in pressure (e.g., due to displacement of blood from the venous sinuses, and of CSF out of the skull). Beyond a certain point, the pressure will rapidly increase. The clinical significance of this is that in some situations, relatively small shifts in intracerebral volume may cause large ...
How does hypertonic solution affect ICP?
One proposed mechanism for the ICP-decreasing action of hypertonic solutions is by means of dehydration and shrinkage of cerebral tissue. Wisner et al. ( 7) assessed the effects of HTS on cerebral water content after head injury in rats, comparing 6.5% HTS to lactated Ringer’s solution. Brain water content was reduced in both the noninjured animals and in the uninjured hemisphere of the injured animal. Water content was increased in the injured brain to a similar extent in both groups. Similar conclusions were drawn by Shackford et al. ( 6) when comparing hypertonic Ringer’s lactate solution (500 mOsm/L) with hypotonic Ringer’s lactate solution (270 mOsm/L) in a porcine model of focal cryogenic brain injury. Ramming et al. ( 39) used a cryogenic porcine model of TBI to examine the relationship between fluid administration, free water, sodium, and ICP. There was a significant positive correlation between the amount of fluid administered, fluid balance, free water, and ICP and a significant negative correlation between serum osmolarity and ICP. These studies suggest the following ideas: hypertonic fluid improves intracranial compliance and CBF by dehydrating uninjured cortex, an intact BBB is required for osmotherapy to be effective, and excess free water and hypervolemia should be avoided.
What is the pathophysiology of intracranial hypertension?
The pathophysiology of intracranial hypertension is complex, and it depends on the mechanism of cerebral edema, volume of intracranial components, integrity of the blood/brain barrier (BBB), and cerebral perfusion pressure (CPP).
How much HTS is used for TBI?
( 17 ). They compared a 250-mL bolus of 7.5% HTS with lactated Ringer’s solution in 229 head-injured and hypotensive patients. Paramedics at the scene of the accident initiated allocation and treatment. Resuscitation was rapid, and both groups were normotensive by the time they arrived at hospital. Despite a small but statistically significant difference in sodium concentration on admission (148 versus 143 mmol/L; P < 0.001), outcome measures were equal. The ICP and CPP in the control group compared with the interventional group were 10 mm Hg versus 15 mm Hg ( P = 0.08) and 73 mm Hg versus 69 mm Hg ( P = 0.40), respectively. The duration of CPP < 70 mm Hg was 9.5 h compared to 17 h ( P = 0.06). All survival data including admission, 6 mo, and discharge from hospital were equal in both groups. They concluded that routine use of HTS in prehospital treatment of TBI has no advantage over resuscitation with Ringer’s lactate solution.
How does HTS affect TBI?
HTS administration produces an osmotic gradient between the intravascular and intracellular/interstitial compartments, leading to shrinkage of brain tissue (where BBB is intact) and therefore a reduction in ICP. The reflection coefficient (selectivity of the BBB to a particular substance) of NaCl is more than that of mannitol, making it potentially a more effective osmotic drug ( 21,22 ). HTS augments volume resuscitation and increases circulating blood volume, mean arterial blood pressure (MAP), and CPP ( 23 ). Other beneficial effects include restoration of the neuronal membrane potential, maintenance of the BBB integrity, and modulation of the inflammatory response by reducing adhesion of leukocytes to endothelium ( 24–26 ).
What is the recommended infusion of 3% NaCl for TBI?
The guidelines recommend a continuous infusion of 3% NaCl ranging between 0.1 and 1.0 mL·kg −1 ·h −1, administered on a sliding scale allowing serum osmolarity to reach 365 mOsm/L if required ( 71 ).
What are the adverse effects of HTS?
These include the potential for renal failure, osmotic demyelination syndrome (ODS), a rebound increase in ICP, and various systemic complications including coagulopathies, volume overload, and electrolyte abnormalities.
Does hypertonic saline affect blood flow?
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.
What is hypertonic saline used for?
Hypertonic saline for the management of raised intracranial pressure after severe traumatic brain injury
What is hyperosmolar therapy?
Hyperosmolar agents are commonly used as an initial treatment for the management of raised intracranial pressure (ICP) after severe traumatic brain injury (TBI). They have an excellent adverse-effect profile compared to other therapies, such as hyperventilation and barbiturates, which carry the risk of reducing cerebral perfusion.
Does mannitol help with dehydration?
While mannitol can cause dehydration over time, HTS helps maintain normovolemia and cerebral perfusion, a finding that has led to a large amount of pilot data being published on the benefits of HTS, albeit in small cohorts. Prophylactic therapy is not recommended with mannitol, although it may be beneficial with HTS.