Tag Archives: hypertonic saline

Salt Equivalents

As an exercise, I tried to figure out the equivalent amount of salt for 1 bullet of 23.4% (30mL) compared with the other hypertonic saline solutions.

 

23.4%:  30mL = 120 mEq Na Cl;

3%, 5%, 14.6% contain 0.51, 0.86, 2.5 mEq/mL of NaCl

3% 235 mL,

5% 140mL

14.6% 48mL

 

And came up with this table.

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XLS FILE (Old Table)

 

REVISED TABLE 05/03/2018

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PDF FILE (New Table)

DOC FILE (New Table)

XLS FILE (New Table)

References

Zakaria, Asma. Neurocritical Care Board Review. New York, NY: Demos Medical, 2014.

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Reflection Coefficient

Movement of solutes across the blood brain barrier depends on the reflection coefficient of the solute.  Reflection coefficient is defined as the selectivity of the blood brain barrier to a particular substance.  Molecules with a reflection coefficient of 1 are excluded by the blood brain barrier.  As shown in the table below, sodium chloride is effectively “reflected back” or excluded by the blood brain barrier compared to the other osmotic compounds listed.

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Reference:

Qureshi, Adnan I. and Jose I. Suarez. “Use Of Hypertonic Saline Solutions In Treatment Of Cerebral Edema And Intracranial Hypertension”. Critical Care Medicine 28.9 (2000): 3301-3313.

Hypertonic Solution as Treatment for ICP Crisis in ESRD

 

Transtentorial herniation:  acute unresponsiveness, decline in GCS >=2 pts with uni- or bilateral pupillary dilatation and loss of reactivity to light, and increase in ICP >20mmHg in acomatose patient x 5 mints +/- change in pupillary sie and reactivity.

Intervention:

  • 23.4% saline (30-60 mL bolus) over 5-10 minutes

– well-tolerated in renal failure, no observed pulmonary edema or overload despite high incidence of cardiovascular dysfunction in this population (small study)

 

Proposed Mechanism of Action: hypertonic saline causes osmolar gradient –> to fluid shifts, reduces brain mass, without significant diuresis

  • osmotic diuresis
  • vasoconstriction resulting in decreased cerebral volume
  • reduced blood viscosity
  • improved cerebral perfusion from volume expansion

 

Potential complications:

  1. hypotension – most common adverse event
  2. pulmonary edema
  3. arrhythmias
  4. coagulopathy
  5. hemolysis
  6. rebound ICP elevation

*mechanism for hypotension: ?not clarified yet, small animal study suggests may be mediated by sympathetic neural reflex and not a diuretic effect; others suggest may be due to vasodilatory effect; or maybe due to resolution of Cushing response

 

Reference:

Hirsch, Karen G. et al. “Treatment Of Elevated Intracranial Pressure With Hyperosmolar Therapy In Patients With Renal Failure”. Neurocritical Care 17.3 (2012): 388-394.

Hepatic Encephalopathy and 23.4% Hypertonic Solution (HTS)

Mechanism of Action of 23.4% HTS:  functional BBB allows an osmolar gradient to develop between blood and brain parenchyma, resulting in efflux of water from brain tissue with reduction in brain volume.  This allows displaced CSF to return from spinal subarachnoid space, and intracranial compliance improves.

Indications for 23.4% HTS in hepatic encephalopathy

  1. urgent treatment of life-threatening cerebral edema or intracranial hypertension (easily arousable or localizing excludes patient)
  2. cerebral herniation syndrome or other acute neurologic deterioration in context of existing severe hepatic encephalopathy and absence of more likely explanation (sepsis, seizure, medication toxicity)
  3. as an initial form of HTS therapy or added to ongoing infusion of 3% HTS
    • 23.4% HTS 30ml bolus over 30 minutes via central venous catheter, target acute serum sodium increase of 5 mEq/L
    • check Na 1 hour later, then serum Na q6h
    • continue 3% HTS infusion to maintain steady Na levels (acute decline may lead to rebound cerebral edema)

Displacement of CSF occurs before blood or brain displacement during pathologic processes.  Can changes in CSF volume be used to evaluate severity of cerebral edema?  See reference[1] for a retrospective study that looked into this clinical question.

Note: Change in CSF volume after 23.4% is associated with the magnitude of serum Na change but not with the total mEq of Na delivered.

Invasive ICP monitoring in hepatic encephalopathy:

  1. potential for hemorrhagic complications
  2. studies have not identified a survival benefit
  3. may be associated with worse outcomes for some patients
  4. may not accurately reflect compression of brain structures (thalami / brainstem)

West Haven Criteria

The severity of hepatic encephalopathy is graded with the West Haven Criteria.

  • Grade 1 Trivial lack of awareness; euphoria or anxiety; shortened attention span; impaired performance of addition or subtraction
  • Grade 2 Lethargy or apathy; minimal disorientation for time or place; subtle personality change; inappropriate behaviour
  • Grade 3 – Somnolence to semistupor, but responsive to verbal stimuli; confusion; gross disorientation
  • Grade 4 Coma

 

References

[1] Liotta, Eric M. et al. “23.4% Saline Decreases Brain Tissue Volume In Severe Hepatic Encephalopathy As Assessed By A Quantitative CT Marker”. Critical Care Medicine 44.1 (2016): 171-179. Web.

[2] Wikipedia,. “Hepatic Encephalopathy”. N.p., 2016. Web. 19 Feb. 2016.