[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-study-detail:100653313":3},{"organization":4,"outcomesModule":7,"designInfo":30,"detailedDescription":38,"studyPopulation":11,"armGroups":39,"interventions":51,"overallOfficials":11,"centralContacts":61,"locations":71,"responsibleParty":87,"collaborators":11,"id":91,"slug":92,"hasResults":93,"nctId":94,"briefTitle":95,"officialTitle":96,"acronym":97,"eligibilityCriteria":98,"healthyVolunteers":93,"sex":99,"minAge":100,"maxAge":11,"enrollmentInfo":101,"targetDuration":11,"studyType":104,"phases":105,"briefSummary":107,"conditions":108,"keywords":112,"overallStatus":118,"whyStopped":11,"lastUpdateSubmitDate":119,"lastUpdatePostDateStruct":120,"startDateStruct":123,"completionDateStruct":125,"leadSponsor":127,"locationsCount":128},{"fullName":5,"class":6},"Assiut University","OTHER",{"primaryOutcomes":8,"secondaryOutcomes":13,"otherOutcomes":11},[9],{"measure":10,"description":11,"timeFrame":12},"Change in ONSD (mm) from baseline, after treatment (e.g., at 2 hour, 6 hours, and 24 hours).",null,"24 hours",[14,18,22,26],{"measure":15,"description":16,"timeFrame":17},"reduction of icp","1\\. Time to achieve target ICP reduction following administration of the hyperosmolar agent., hemodynamic stability and the frequency of secondary rebound hypertension during acute resuscitation.","1 hours, 6 hours, 24hours",{"measure":19,"description":20,"timeFrame":21},"GCS","Change in Glasgow Coma Scale (GCS) after treatment.","24HOURS",{"measure":23,"description":24,"timeFrame":25},"serum electrolyte","Changes in serum electrolyte. sodium and osmolarity","6hours, 24hours",{"measure":27,"description":28,"timeFrame":29},"surgery","Requirement for surgical intervention.","24hours",{"allocation":31,"interventionModel":32,"interventionModelDescription":11,"primaryPurpose":33,"observationalModel":11,"timePerspective":11,"maskingInfo":34},"RANDOMIZED","PARALLEL","TREATMENT",{"masking":35,"maskingDescription":11,"whoMasked":36},"SINGLE",[37],"CARE_PROVIDER","Introduction :- Traumatic brain injury (TBI) remains a primary driver of global trauma-related mortality and severe long-term neurological disability. The pathophysiological trajectory of severe TBI involves a primary mechanical insult followed by a complex cascade of secondary brain injury evolving over subsequent hours and days. Primary injury arises directly from mechanical forces-inducing focal contusions, lacerations, or diffuse axonal disruption. Secondary brain injury develops through cellular and metabolic dysfunction, characterized by blood-brain barrier (BBB) disruption, neuroinflammation, microvascular ischemia, cellular energy failure, and severe cytotoxic and vasogenic cerebral edema. Within the non-yielding osseous structure of the adult cranium, progressive cerebral edema and expanding traumatic lesions directly precipitate pathological elevations in intracranial pressure (ICP).\n\nThe volumetric dynamics of the cranium are governed by the Monro-Kellie doctrine, which dictates that the sum of brain tissue, blood, and cerebrospinal fluid (CSF) volumes within the intracranial vault remains constant. Because the intracranial volume is fixed, any increase in parenchymal or hemorrhage volume must be compensated by an equal reduction in CSF and venous blood volume. Once these physiological buffering mechanisms are exhausted, intracranial compliance drops sharply, causing exponential surges in ICP. Brain Trauma Foundation (BTF) guidelines define intracranial hypertension as sustained ICP elevations exceeding 22 mmHg. Sustained intracranial hypertension directly compromises cerebral perfusion pressure (CPP = MAP - ICP), precipitating secondary ischemic insults, tissue hypoxia, loss of cerebrovascular autoregulation, and life-threatening transtentorial or tonsillar herniation syndromes. Clinical evidence demonstrates a strong correlation between unmanaged intracranial hypertension and adverse outcomes; mortality rates increase significantly when ICP exceeds 20 mmHg and can surpass 50% when ICP rises above 40 mmHg.\n\nHyperosmolar therapy is the standard medical management strategy for ICH after supportive care which is most important for neuroprotection (sedation, analgesia, position, and so on). Currently, only 2 osmotic agents are utilized for this purpose: mannitol and HTS. Mannitol has been the primary hyperosmolar agent for nearly a century and remains a common treatment for ICH. Guidelines currently recommend mannitol as the mainstay in the treatment of ICH.\n\nHyperosmolar therapy, remains a cornerstone of ICP management . Mannitol, a 6 carbon inert sugar alcohol approved by the FDA, reduces ICP by increasing plasma osmolality and promoting water efflux. It is routinely used to treat cerebral edema following brain insults and neurosurgical procedures. Despite its widespread use, some concerns persist due to its systemic effects. Case reports and small clinical series have described complications such as transient heart failure triggered by rapid intravascular volume shifts, impaired cardiac function in the elderly, hypotension, dehydration, acute kidney injury, and hypernatremia. Mannitol-induced diuresis may also cause hypovolemia in vulnerable patients.\n\nFor several decades, 20% Mannitol has been the primary osmotic agent in neurocritical care. Mannitol is a sugar alcohol solution with an osmolarity of approximately 1098 mOsm\u002FL. Administered as intermittent IV boluses (0.5 - 1.0 g\u002Fkg), mannitol produces rapid intravascular volume expansion followed by pronounced renal osmotic diuresis. Although mannitol reduces ICP within 15 to 30 minutes, its diuretic mechanism can lead to systemic hypovolemia, arterial hypotension, hyperosmolality, electrolyte depletion, and acute tubular necrosis. Moreover, repeated dosing or continuous exposure can disrupt the blood-brain barrier, allowing mannitol to enter the brain parenchyma and induce rebound intracranial hypertension.\n\n3% Hypertonic Saline (HTS) provides an alternative hyperosmolar strategy that expands intravascular volume without causing systemic diuresis. is available from 2 to 23.4% and can be administered as a bolus alone or with mannitol. Concentrations of HTS greater than 7.5% should be given through a central venous catheter. Concentrations less than 7.5% can be bolused via a peripheral line; however, infusions should be given in a large vessel. Administered as boluses (3 mL\u002Fkg or 150 mL) or continuous infusions, 3% NaCl has an osmolarity of approximately 1026 mOsm\u002FL (513 mEq\u002FL Na+). Hypertonic saline enhances cardiac preload and maintains mean arterial pressure, offering hemodynamic benefits in trauma patients susceptible to hypotension or hemorrhagic shock. Furthermore, hypertonic saline maintains blood-brain barrier integrity more effectively than mannitol, producing sustained ICP reduction with a lower frequency of rebound spikes. Potential adverse risks include hypernatremia, hyperchloremic metabolic acidosis, fluid overload, and osmotic demyelination syndrome if serum sodium shifts are unmonitored.\n\nNeuromonitoring Modalities: Invasive Gold Standards and the Sonographic ONSD Window:\n\nAccurate measurement of ICP is fundamental to neurocritical care, guiding hyperosmolar therapy, adjusting ventilator parameters, and preventing secondary ischemic injury. Invasive intracranial monitoring-utilizing intraventricular catheters connected to external ventricular drains (EVD) or parenchymal strain-gauge microtransducers-remains the diagnostic gold standard. Intraventricular catheters provide continuous pressure monitoring alongside the unique capacity for therapeutic CSF drainage to manage acute ICP spikes. Nevertheless, invasive modalities involve substantial clinical challenges, including risks of intracranial hemorrhage, bacterial ventriculitis, localized brain parenchymal trauma, and technical malposition. Furthermore, invasive placement requires neurosurgical expertise and specialized critical care resources that are frequently unavailable in pre-hospital environments, low-resource regional hospitals, or remote emergency units.\n\nThese diagnostic limitations have driven the development of point-of-care ultrasound (POCUS) techniques, with measurement of the optic nerve sheath diameter (ONSD) emerging as a non-invasive surrogate for ICP monitoring. Anatomically, the optic nerve is an extension of the central nervous system, encased in a dural sheath that represents a direct continuation of the intracranial meninges. The subarachnoid space surrounding the optic nerve communicates directly with the intracranial subarachnoid cavity, allowing CSF to flow freely between the two regions. Increases in ICP transmit hydrostatic pressure through the subarachnoid CSF, expanding the retrobulbar optic nerve sheath. Because the dural sheath is most elastic and distensible 3 mm posterior to the eye globe, high-frequency ultrasonographic measurements taken at this specific landmark correlate closely with invasively measured ICP.\n\nClinical studies indicate that an ONSD cutoff between 4.8 mm and 5.5 mm reliably detects intracranial pressure exceeding 20 mmHg with high sensitivity and specificity . Sonographic ONSD assessment is non-invasive, cost-effective, rapidly repeatable at the bedside, and free from surgical risks.\n\nClinical literature directly comparing 3% Hypertonic Saline versus 20% Mannitol specifically in Traumatic Brain Injury (TBI) patients using bedside Optic Nerve Sheath Diameter (ONSD) ultrasonography in Egyptian medical centers is limited, primarily consisting of small, single-center pilot studies.",[40,46],{"label":41,"type":42,"description":43,"interventionNames":44},"Group M (Mannitol)","ACTIVE_COMPARATOR","used ultrasonography to assess the optic nerve sheath diameter from Baseline or Immediately before mannitol therapy.\n\nThen added mannitol with Follow-up ONSD, 2 hours, 6 hours,24 hours using 20% Mannitol Dose: 0.5-1 g\u002Fkg IV over 15-20 minutes.",[45],"Drug: Mannitol (20%)",{"label":47,"type":42,"description":48,"interventionNames":49},"Group H (Hypertonic Saline)","used ultrasonography to assess the optic nerve sheath diameter from Baseline or Immediately before hypertonic saline therapy.\n\nThen added hypertonic saline with Follow-up ONSD, 2 hours, 6 hours,24 hours used 3% Hypertonic saline at dose: 2-3 mL\u002Fkg IV over 15-20 minutes",[50],"Drug: Hypertonic Saline ( 3% Sodium Chloride Saline)",[52,57],{"type":53,"name":54,"description":55,"armGroupLabels":56,"otherNames":11},"DRUG","Mannitol (20%)","compare the efficacy of mannitol in reducing intracranial pressure, as assessed by serial optic nerve sheath diameter (ONSD) ultrasound measurements, in patients with traumatic brain injury.",[41],{"type":53,"name":58,"description":59,"armGroupLabels":60,"otherNames":11},"Hypertonic Saline ( 3% Sodium Chloride Saline)","compare the efficacy of hypertoic saline in reducing intracranial pressure, as assessed by serial optic nerve sheath diameter (ONSD) ultrasound measurements, in patients with traumatic brain injury.",[47],[62,67],{"name":63,"role":64,"phone":65,"phoneExt":11,"email":66},"Mostafa Hassan Abdellah, assisstant lecturer","CONTACT","00201552590309","mostafa.abdellah95@aun.edu.eg",{"name":68,"role":64,"phone":69,"phoneExt":11,"email":70},"Khaled Abd Elbaki Abd Elrahman, professor","00201008182061","khaledbaky@aun.edu.eg",[72],{"facility":73,"status":11,"city":74,"state":11,"zip":11,"country":75,"countryCode":76,"cosmosGeoPoint":77,"geoPoint":82,"contacts":83},"Assiut university","Asyut","Egypt","EG",{"type":78,"coordinates":79},"Point",[80,81],31.18368,27.18096,{"lat":81,"lon":80},[84],{"name":63,"role":64,"phone":85,"phoneExt":11,"email":86},"00201552090309","darsh.bash@gmail.com",{"type":88,"investigatorFullName":89,"investigatorTitle":90,"investigatorAffiliation":5,"oldNameTitle":11,"oldOrganization":11},"PRINCIPAL_INVESTIGATOR","Mostafa Hassan Mostafa Abdellah","doctor (assisstant lecturer)","100653313","comparison-of-hyperosmolar-agent-in-reduction-of-increased-intracranial-pressure-in-patients-with-traumatic-brain-injury-using-ultrasonography-100653313",false,"NCT07786324","Comparison of Hyperosmolar Agent in Reduction of Increased Intracranial Pressure in Patients With Traumatic Brain Injury Using Ultrasonography","Comparison of 3% Hypertonic Saline Versus 20% Mannitol in Reduction of Increased Intracranial Pressure in Patients With Traumatic Brain Injury Using Optic Nerve Sheath Diameter Measurements''","MHTS-ONSD","Inclusion Criteria:\n\n* • Age ≥18 years.\n\n  * Acute severe traumatic brain injury (TBI) (GCS 3-8) confirmed by CT brain.\n  * Elevated ONSD suggestive of raised ICP (ONSD cutoff value ≥5.6 mm ).(14)\n  * Initiation of hyperosmolar therapy within 24 hours of injury.\n\nExclusion Criteria:\n\n* • Penetrating head injury.\n\n  * Hypotension.\n  * Previous ocular trauma or orbital surgery.\n  * Glaucoma or optic nerve pathology.\n  * Bilateral ocular injuries preventing ultrasound assessment.\n  * Pregnancy.\n  * Chronic renal failure requiring dialysis.\n  * Initial serum sodium \\>150mmol\u002FL or Patients reaching a sodium level \\>160mmol\u002FL during hypertonic administration.\n  * Previous hyperosmolar therapy before enrollment.\n  * Refusal of consent by legal surrogate.","ALL","18 Years",{"count":102,"type":103},100,"ESTIMATED","INTERVENTIONAL",[106],"NA","The aim of this study to compare the efficacy of hypertonic saline and mannitol in reducing intracranial pressure, as assessed by serial optic nerve sheath diameter (ONSD) ultrasound measurements, in patients with traumatic brain injury.",[109,110,111],"TBI (Traumatic Brain Injury)","ICP (Intracranial Pressure) Increase","Optic Nerve Sheath Diameter Measurement",[113,114,115,116,117],"mannitol","hypertonic saline","ICP","ONSD","TBI","NOT_YET_RECRUITING","2026-08-21",{"date":121,"type":122},"2026-08-25","ACTUAL",{"date":124,"type":103},"2026-10-01",{"date":126,"type":103},"2029-09-30",{"name":5,"class":6},1]