Journal of Emergencies, Trauma, and Shock

: 2020  |  Volume : 13  |  Issue : 4  |  Page : 237--238

What’s new in emergency trauma and shock? The choice of hyperosmolar agent in emergency department

Vivek Chauhan 
 Department of Medicine, IGMC, Shimla, Himachal Pradesh, India

Correspondence Address:
Dr. Vivek Chauhan
Department of Medicine, IGMC, Shimla, Himachal Pradesh

How to cite this article:
Chauhan V. What’s new in emergency trauma and shock? The choice of hyperosmolar agent in emergency department.J Emerg Trauma Shock 2020;13:237-238

How to cite this URL:
Chauhan V. What’s new in emergency trauma and shock? The choice of hyperosmolar agent in emergency department. J Emerg Trauma Shock [serial online] 2020 [cited 2021 Jan 17 ];13:237-238
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The acute cerebral insults start with a primary event such as trauma, hemorrhage, or infarct, which is invariably followed by secondary insult caused by the disruption in the blood–brain barrier and accumulation of protein and fluid in the extracellular space, resulting in vasogenic cerebral edema.[1] Secondary insult is more pronounced in the presence of hyperthermia, hypoglycemia, hyperglycemia, hypotension, coagulopathy, and dyselectrolytemia.

The current issue of Journal of Emergencies Trauma and Shock has an article by Busey et al., who have compared fixed dose versus weight-based dosing of 23.4% hypertonic saline (HTS) to reduce intracranial hypertension (ICH) in traumatic brain injury. Busey et al. Authors did not find a significant difference in any of the above approaches. Busey et al. HTS has also been compared by many authors with mannitol; however, according to a recent Cochrane meta-analysis, none was superior to the other in its efficacy in the reduction of ICH in traumatic brain injury patients.[2]

Monro in 1783 and Kellie in 1824 paved the way, through their experiments, for understanding of intracranial pressure (ICP) and is called the Monro–Kellie hypothesis.[3],[4] It states that the cranial compartment has a fixed volume because of its inelastic nature, and an increase in any one of the components of the cranial compartment, i.e., blood, cerebrospinal fluid (CSF), or brain parenchyma, will be compensated by the displacement of the other components; else, it will result in ICH.[5] Depending on the acuity of the problem, ICH will decrease in the cerebral perfusion pressure (CPP) of the brain tissue. CPP is derived by the following formula: CPP = Mean arterial pressure − ICP. CPP determines the cerebral blood flow and oxygenation, and thus, fall in CPP quickly results in coma.[5] Normal range for ICP is 3–15 mmHg, and sustained ICP >20 mm Hg is defined as ICH. The goal of treatment in ICH is to maintain ICP below 22 mmHg and to maintain CPP between 60 and 70 mmHg.[1] Patients with ICP over 40 mmHg have had more than 50% mortality, irrespective of the cause.[1]

Patients present to the emergency department (ED) with coma induced either by acute changes in ICP from head trauma, intracranial bleed, ischemic brain infarction, bacterial meningitis, high altitude cerebral edema, and hepatic encephalopathy or subacute change caused by intracranial space-occupying lesions and obstructive hydrocephalus.[5] ED physician must quickly diagnose and treat ICH in all such cases as mortality is directly proportional to the rise in the ICP. Presence of Cushing’s response (hypertension, bradycardia, and apnea) points toward extreme elevations of ICP.[5] The sequence of pupillary changes, pupillary reactivity, and presence of oculomotor palsies help in clinical monitoring the increasing ICH on the bedside.[6] Abnormal pupillary light reactivity precedes peak elevation in ICP by 15.9 h.[6] Another quick bedside tests of elevated ICP include optic nerve sheath diameter using an ultrasound.[7]

Hyperosmolar therapy has been the mainstay of therapeutic correction of ICH. The osmolarity of 20% mannitol, 3% saline, and 23.4% saline is 1098, 1026, and 8008 mOsm/L, respectively.[1] Due to its very high osmolality, 23.4% HTS should always be given through a central line, and the recommended dose is 30 mL bolus.[1] 3% HTS is preferred for hypotensive patients and is given in 250 mL boluses to correct both hypotension and ICH.[1] Mannitol, however, may cause acute kidney injury by inducing osmotic diuresis in these patients. Serum sodium needs to be measured in all patients on HTS therapy, and daily elevations in the sodium levels have to be restricted to less than 12 mEq/L to prevent central pontine myelinolysis.[1] While using mannitol for reducing ICP, osmolar gap should not exceed 20. Mannitol is preferred in patients where baseline cerebral hypoperfusion is present as it has been shown to increase cerebral perfusion.[1]

Equally important considerations are the protection of airway and prevention of secondary insults such as hypoglycemia, hyperglycemia, and hyperthermia in these patients. The head end must be kept in elevation by 30° with neck in a central position to allow venous drainage. Other treatments in use include decompression surgery, sedation, hypothermia induction, and barbiturate coma but with no clear reduction in mortality.[1] Hypotonic fluids such as dextrose solution and Ringer’s lactate should never be given to patients with ICH.[1] Hyperventilation is a temporizing measure that acts by reducing pCO2 and causing cerebral vasoconstriction and thus reducing vasogenic edema, but cerebral vasoconstriction in a patient with hypoperfused brain can be detrimental and is thus used only in extreme cases with marked elevation of ICP.[5] Surgical correction of underlying Pathology, if possible is the definitive method for ICP reduction.

To conclude, the hyperosmolar agent must be chosen carefully keeping in mind that both mannitol and HTS are in use for long, and there is no clear recommendation for use of either in preference over the other in ICH. Careful analysis of factors such as hypotension, volume status, cerebral perfusion, kidney injury, sodium levels, and type of venous access is helpful in choosing one over the other.


1NA Peters NF, JP Smith. Hyperosmolar Therapy for the Treatment of Cerebral Edema; 2018. Available from: [Last updated on 2018 Jan 19].
2Chen H, Song Z, Dennis JA. Hypertonic saline versus other intracranial pressure-lowering agents for people with acute traumatic brain injury. Cochrane Database Syst Rev 2020;1:CD010904.
3Monro A. Observations on the structure and functions of the nervous system, illustrated with tables. Lond Med J 1783;4:113-35.
4Kellie G. An account of the appearances observed in the dissection of two of three individuals presumed to have perished in the storm of the 3D, and whose bodies were discovered in the vicinity of Leith on the morning of the 4th, November 1821; with some reflections on the pathology of the brain: Part I. Trans Med Chir Soc Edinb 1824;1:84-122.
5Ropper AH. Hyperosmolar therapy for raised intracranial pressure. N Engl J Med 2012;367:746-52.
6Chen JW, Gombart ZJ, Rogers S, Gardiner SK, Cecil S, Bullock RM. Pupillary reactivity as an early indicator of increased intracranial pressure: The introduction of the neurological pupil index. Surg Neurol Int 2011;2:82.
7Chauhan V, Galwankar S. What’s new in emergencies trauma and shock; diagnosing intracranial hypertension. J Emerg Trauma Shock 2020;13:175-6.