Monthly Archives: August 2014

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Hypertonic Saline

HYPERTONIC SALINE

  • Brain Trauma Foundation – start treatment for increased ICP at pressures >20mm Hg
  • Hyperosmolar therapy:
    1. Mannitol vs HTS
      1. Mannitol
        • BTF recommends mannitol as mainstay in management of intracranial HTN
        • Considered first choice in immediate treatment of increased ICP
        • Even for cases requiring emergent surgery, mannitol is a good temporizing choice
        • Is the standard treatment of choice, so any Level 1 evidence should compare HTS to mannitol
      2. HTS
        • 2%-23.5%
        • More effective than mannitol for reduction of ICP
  • Side effect profile of HTS more favorable
    • Mannitol causes delayed hypovolemia due to diuretic effect (not good in trauma patients); hypotension due to osmotic diuresis, compromises renal function
    • Mannitol may exacerbate cerebral edema if administered late after cerebral injury due to disrupted BBB
    • HTS improves MAP and increases circulating blood volume
  1. Mechanism of action
    1. Classic theory: reduced brain water content through osmotic effects
      • Na has reflection coefficient of nearly 1 (with intact BBB, very little Na crosses barrier, pulls fluid out of interstitial space)
      • BUT
        • studies show equal decrease in ICP in those with and without a decrease in brain volume after HTS treatment
        • studies show sustained decrease in ICP even at serum Na levels that will not have osmotic effect
  1. Other mechanisms:
    • VASOCONSTRICTION: Early after administration, HTS reduces blood viscosity, increases rheological properties, improves CBF and cerebral oxygenation causing autoregulatory vasoconstriction, reduced ICP.
    • ENDOTHELIAL SHRINKAGE: HTS induces endothelial cell shrinkage, improves circulation
    • IMMUNOMODULATORY ROLE?
    • REDUCED CSF PRODUCTION?
  • Cerebral edema:
Type Mechanism Conditions Timing Notes
Cytotoxic Cellular swelling due to ischemic or toxic injury Trauma Minutes to hours Resistant to treatment
Vasogenic Extracellular edema due to capillary disruption / breakdown of BBB Trauma, tumors, abscess Hours to days

 

  • Questions:
    1. What is the role of HTS in intracranial hypertension due to trauma, SAH, mass lesions? HTS appears to have a favorable outcome in all types of intracranial hypertension, no matter the origin
    2. What is the most optimal concentration for HTS? There is no consensus on the most optimal concentration – all concentrations appear to have favorable effects on ICP
    3. Is there an advantage of continuous drip or bolus administration? Meta analysis shows more favorable short term ICP outcome for HTS, regardless of concentration or administration mode (continuous drip or bolus)
    4. What is the optimal length of treatment? Is there a rebound effect with HTS? Studies looking into rebound risk of HTS are lacking. The few studies that mentioned rebound phenomenon have inadequate monitoring
  • Take home:
    1. Decreasing ICP: HTS is superior to mannitol
    2. Neurological outcome: no clear benefit, but positive trend for HTS

Mortazavi, Martin M, Andrew K Romeo, Aman Deep, Christoph J Griessenauer, Mohammadali M Shoja, R Shane Tubbs, and Winfield Fisher. 2012. ‘Hypertonic Saline For Treating Raised Intracranial Pressure: Literature Review With Meta-Analysis: A Review’. Journal Of Neurosurgery 116 (1): 210–221.

Dictations

NORMAL SYSTEMIC PHYSICAL EXAMINATION
Vital signs as follows: BP HR RR Temp sats
General: awake, not in distress
Heart: normal S1 S2, no MRG, NRRR, peripheral pulses 2+ bilaterally, no edema
Lungs: clear to auscultation bilaterally, no wheezes, rales, rhonchi, no accessory muscle use
Abdomen: soft, nontender, nondistended, bowel sounds normal, no palpable masses
 
NORMAL NEURO DICTATION
Mental Status, patient is awake, alert, oriented to person place and time, normal affect;  Attention, can spell WORLD backwards, good attention span; speech is fluent without paraphasic errors, able to repeat, name objects, read and write; memory is good, calculation is good, no left-right confusion; Praxis: able to mimic blowing out match with either hand.
Cranial nerve exam:  II, III pupils equal and briskly reactive to light; visual acuity, visual fields full by confrontation, III IV VI EOM intact without nystagmus, no ptosis; V sensation intact to light touch, masseters strong symmetrically, VII face symmetric without weakness; VIII hearing grossly intact; IX X palate elevates symmetrically XI good shrug XII tongue protrudes midline, no atrophy or fasciculation.
DTRs: normoreflexive – bilateral biceps, brachioradialis, patellar and Achilles reflexes
MMT, strength is 5/5 on all 4s.  Sensory testing intact to light touch, pinprick, temperature, vibration and joint position intact.  No evidence of extinction.  Coordination: able to do rapid alt and point-to-point movements.  
Gait posture, stance, stride and arm swing normal.
 
CORE MEASURES:
NIHSS in ED
If no tPA given, why?
If Afib – on AC? If no AC, reason / plan
Meds listed out
Lipid panel, A1C Carotids (Doppler, CTA, angio), Echo
On statin, if not, why?
ASA & PLavix
PT/OT, if no PT/OT why?
Modified Rankin Scale

Phenytoin

Phenytoin has significant protein binding, so hypoalbuminemia will lead to increased free phenytoin.
Adjust for hypoalbuminemia using the following formula = Total Phenytoin Level / [(0.2*albumin)+0.1]
*0.2 is a correction factor

In renal failure, aside from hypoalbuminia leading to increased free phenytoin, phenytoin binding is further reduced, and this formula will tend to underestimate the free phenytoin levels.  To correct for this, use 0.1 as correction factor if GFR is <10 ml/min.

 

Drug monitoring: (http://emedicine.medscape.com/article/2090306-overview#a2)

  • loading doses should be checked 1 hour after IV load and 24 hours after oral loading
  • long term phenytoin therapy generally do not need to be monitored at intervals <3-12 months after steady state reached unless clinically indicated
  • reference range is 10-20 ug/mL – although half of patients’ seizures are controlled at values lower and higher than therapeutic range
  • adverse effects related to serum levels
    • nystagmus if >20 ug/mL
    • slurreg speech, movement disorders (tremor, choreoathetosis, orofacial dyskinesia) if >30 ug/mL
    • lethargy, stupor, confusion if >40 ug/mL

 

Intracerebral Hemorrhage (ICH)

How to measure hematoma volume (ABC/2 method) where:
A = greatest diameter of the largest hemorrhage slice
B = diameter perpendicular to A
C = approx # of axial slices with hemorrhage multiplied by the slice thickness

Ventilator Settings

1. Mode of ventilation – start with A/C mode, SIMV if tachypneic
2. Tidal Volume – use 8ml/Kg of predicted BW then reduce to 6ml/Kg over next 2 hours
**Monitor peak alveolar pressure (goal </=30cmH20)
**Inspiratory Flow Rate – set at 60mL/min; higher (>/=80mL/min) if respiratory distress or high MV (>/=10L/min)
**I:E ratio – normally >/=1:2, if <1:2 then inc IFR or dec TV or dec RR
3. Respiratory Rate – set at patient’s MV prior to intubation, not to exceed 35 /min; check PCO2 after 30 minutes
4. PEEP – initial PEEP at 5 cmH20
**If with occult PEEP, then increase I:E ratio or ad extrinsic PEEP
5. FiO2