Determination of cerebral water content by magnetic resonance imaging after small volume infusion of 18% hypertonic saline solution in a patient with refractory intracranial hypertension

Abstract

Hypertonic saline solution (HSS) has been investigated in the treatment of intracranial hypertension (ICH) in a limited number of studies, usually after failure of conventional treatment. HSS, used in concentrations that vary from 3% to 23.4%, seems to be effective in reducing refractory ICH and to be devoid of adverse effects. We treated a patient with refractory ICH with a small-volume infusion of 18% HSS, and performed magnetic resonance imaging (MRI) before and after HSS infusion. MRI showed a marked reduction in cerebral water content 1 h after the infusion. To our knowledge, this is the first MRI study in a patient with brain injury to evaluate the effect of HSS on brain water content. Further studies are necessary to test HSS efficacy and to identify, through MRI or computed tomography (CT) scan imaging, a subgroup of patients with brain injury who would be best treated with HSS.

Role of Hypertonic Saline for the Management of Intracranial Hypertension After Stroke and Traumatic Brain Injury

“…57 Future studies are necessary to directly compare these therapies in a head-tohead trial (using identical osmolar loads) powered to detect differences in clinical outcome. 61 hydroxyethyl starch 250 ml Prospective, 42 a 10% NaCl 100 ml Mean ICP ↓ of 43% (to 18 mm Hg) lasting a observational study 69 mean of 93 min Prospective, 34 1.6% NaCl infusion vs No significant difference between groups in ICP randomized study 46 Ringer' s lactate solution control; hypertonic saline group had higher number of ICP interventions (↑ severity of illness) Retrospective, 82 2% or 3% NaCl-sodium acetate No significant difference in number of case-control study 67 (1:1) infusion, 250-ml bolus interventions required vs control (normal if needed; target serum saline); in hypertonic saline group, higher sodium concentration in-hospital mortality rate and more penetrating 145-155 mEq/L injuries and mass lesions on CT scans Prospective, 14 7.2% NaCl 1.5-ml/kg bolus ↓ ICP, ↑ CPP, no change in mean arterial observational study 65 if ICP > 15 mm Hg pressure; inverse correlation between ICP and osmolarity Case report 68 1 18% NaCl 1.5-ml/kg bolus ↓ cerebral edema per MRI, ↓ ICP; peak serum sodium concentration 161 mEq/L Prospective, 20 7.5% NaCl 2 ml/kg bolus Lower ICP spikes and clinical failure with randomized study 71 vs 20% mannitol 2 ml/kg hypertonic saline; no significant difference in number of infusions required for either group Prospective, 9 20% mannitol 20 ml vs Greater ↓ in ICP in hypertonic saline group; randomized, controlled, 7.5% NaCl-dextran 100 ml maximum serum sodium concentration was crossover study 57 156.3 mEq/L in the NaCl-dextran group vs 151 mEq/L in the mannitol group Retrospective study 72 13 23.4% NaCl 30-ml bolus, No significant difference in ICP; hypertonic if no response to mannitol saline group had a longer duration of reduced ICP Prospective, 18 3% NaCl 300-ml bolus ↓ ICP at 20 and 60 min; ↓ serum potassium observational study 62 concentration at 20 min but returned to baseline at 60 min Prospective, 14 20% NaCl 40 ml Hypertonic saline ↑ volume of contused area, observational study 64 ↓ volume of noncontused area Pediatric population Double-blind, 18 3% NaCl vs 0.9% NaCl With 3% NaCl, ICP ↓ significantly and maximum crossover study 60 serum sodium concentration was 151.8 ± 4.8 at 30 min Prospective, 32 1.7% NaCl infusion vs Correlation between serum sodium concentration randomized study 70 Ringer' s lactate solution and ICP in hypertonic saline group; Ringer' s lactate group required ↑ number of ICP interventions, had longer ICU stays, and had ↑ mortality rate Prospective, 10 3% NaCl infusion to increase ↓ ICP with ↑ serum sodium concentration; mean observational study 63 serum sodium concentration sodium 170.7 mEq/L; sustained hypernatr...…”

“…13 However, as shown in Table 5, several reports have demonstrated hypertonic saline as an effective osmotic agent after both bolus and continuous infusion. 46,[57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72] Table 6 lists several reports that include various types of neurologic injury, from traumatic brain injury to elective craniotomy. [73][74][75][76][77][78][79] One group of authors evaluated the use of 23.4% sodium chloride administered as a 30-ml bolus over 15-20 minutes for 20 episodes of refractory intracranial pressure in eight patients.…”

“…A group of authors reported one patient in whom magnetic resonance imaging, performed before and after 18% hypertonic saline infusion, showed a marked reduction in cerebral water content 1 hour after hypertonic saline infusion. 68 The use of functional imaging is a tool that should be explored to evaluate who might benefit from hypertonic saline.…”

Hypertonic saline: First-line therapy for cerebral edema?

“…Presently, the effect of HS solutions on cerebral water content in clinical TBI is not well studied. A case report of a patient with TBI (multiple hemorrhagic contusions) and refractory intracranial hypertension to mannitol treated with a small volume infusion (1.5 mL/kg) of 18% HS demonstrated that cerebral water content was dramatically reduced on MRI in both healthy and edematous brain regions following treatment, and associated with ICP reduction of 109% lasting approximately 6 h [53].…”

Resuscitation of Hypotensive Head-Injured Patients: Is Hypertonic Saline the Answer?

“…After brain injury, edema of injured as well as uninjured cerebral tissue may follow, often reaching a maximal extent within 48 to 72 hours. 18 Hypertonic crystalloid administered early in TBI appears to decrease this tissue water accumulation, particularly in uninjured tissue. 18,19 Although the exact mechanism by which HTS reduces ICP is not clearly known, the ability of HTS to osmotically extract water from brain tissue into the vascular space explains, at least in part, its beneficial effects in neurotrauma.…”