Monthly Archives: December 2015

Anticoagulation Reversal Agents

Reversal Agents (click to access pdf)

Reference: accessed 12/30/2015 7:09 a.m.

AED Therapeutic Drug Levels

The concept of critical values for drug levels was originally developed by the late Daniel M. Baer, MD, and first published in the April 1982 issue of MLO. This table was taken from an expanded version of that publication and newly revised for 2011-2012 by Yashpal Agrawal, MD, PhD; Department of Pathology and Laboratory Medicine, New York Presbyterian Hospital-Cornell Campus, New York, NY.

therapeutic drug levels.jpg

NSUH VTE Prophylaxis Guidelines

DVT / VTE prophylaxis guidelines at NSUH.



NSUH VTE Prophylaxis Guidelines Summary Table (Kapinos)

Antibiotics for CNS Infections




Gilbert, David N. The Sanford Guide To Antimicrobial Therapy 2010. Sperryville, VA: Antimicrobial Therapy, 2010. (2018). UpToDate. [online] Available at: [Accessed 12 Jul. 2018].

Manhasset Antibiogram






Comparison of Antibacterial Spectra

Imaging in Vasogenic Edema

Pathophysiology:  disturbance of vascular permeability –> plasma fluid and protein escapes –> increase in extracellular space volume

  • Vasogenic edeme represents reactive changes rather than permanent cell damage, and are therefore reversible.

Peritumoral edema:  nonenhancing area of abnormality surrounding enhancing tumor core

  • mets or noninfiltrative primary tumors (meningiomas) – peritumoral edema is synonymous with vasogenic edema (no tumor cells are present)
  • Gliomas – peritumoral edema better referred to as infiltrative edema because it represents both vasogenic edema and infiltrating tumor cells behing the BBB and invading the white matter tracts

CT Scan:

  • brain tumors identified by abnormal density +/- distortion of adjacent structures
  • tumor-induced vasogenic edema extends along white matter extracellular fluid spaces and appear hypodense
  • contrast enhancement: defines the tumor border (if tumor is contrast enhancing)

Noncontrast CT showing vasogenic edema surrounding a brain tumor.


  • T1-weighted with contrast – edema may be subtle
  • T2-weighted – edema readily apparent
  • FLAIR – CSF signal suppressed to make lesions adjacent to ventricles more conspicuous
  • DWI – differentiates cytotoxic edema from vasogenic edema

F6.large.jpegA = noncontrast T1W;  B = T1W with contrast; C=T2W; D= FLAIR



Esquenazi, Y., V. P. Lo, and K. Lee. “Critical Care Management Of Cerebral Edema In Brain Tumors”.Journal of Intensive Care Medicine (2015): n. pag. Web.

Herniation Syndromes

Types of Herniation

  1. Subfalcine herniation
    • supratentorial mass lesions may lead to cingulate gyrus hernation
    • often in supratentorial metastasis, low- or high-grade gliomas
    • pericallosal branches of ACA along free edge of falx may be compressed leading to infarction
  2. Uncal herniation
    • most common type
    • presents as: impaired consciousness, fixed dilated ipsilateral pupil, hemiparesis contralaterally
    • uncus herniates over tentorial edge, compresses CN III
    • uncus can also herniate into midbrain and into posterior fossa, compressing corticospinal tract
    • PCA may be compressed between uncus and midbrain causing occipital lobe infarct
  3. Central herniation
    • generalized cerebral mass effect
    • entire mid-brain herniates downward
    • presentation: obtunded with altered breathing pattern, pinpoint pupils, loss of upward gaze
  4. Tonsillar herniation:
    • infratentorial tumors cause cerebellum to herniate through foramen magnum compressing the medulla
    • presentation:  cardiorespiratory dysfunction, altered breathing patterns, impaired consciousness


  1. positioning:  elevate head 30° (decrease CSF hydrostatic pressure, facilitate venous drainage), head facing straightforward (decrese IJ vein compression), remove constricting garments or devices around neck
  2. avoid hypoxia and hypercapnia – target PaCO2 35-40 mm Hg, intubate if declining neurologic status or GCS <8 or requiring sedation / GA for ICP control
  3. hemodynamic support – maintain euvolemia (use isotonic fluids); avoid CPP<50mm Hg; initiate treatment if CPP fall <60 to avoid CPP<50mm Hg; vasopressors, avoid vasodilators (nitroglycerine and nitroprusside – exacerbates cerebral edema through cerebral hyperemia)
  4. avoid fever, hypothermia may be effective in lowering ICP but long-term outcome still unclear; target normothermia for now
  5. anticonvulsants – seizures affect airway, increases PaCO2, exacerbates cerebral edema and ICP; seizure prophylaxis after crani for tumor resection still unclear but prudent to start prophylaxis for supratentorial brain tumors; prefer newer generation anticonvulsants
  6. Mannitol 25% at 0.5-1.5 g/Kg – reduces ICP, peak effect 15-35 mins after infusion, duration several hours; osmotic diuresis may lead to hypovolemia and electrolyte imbalance (check q6-8h); given peripheral or through central IV catheter over 10-20minutes;  high osmotic levels may produce renal damage; upper limit to safely administer mannitol is 320 mOsm/L; may leak into brain parenchyma and exacerbate vasogenic edema if used over sustained time
  7. hypertonic saline – continuous infusion (2-3%) or bolus (23.4%); central venous catheter needed for concentrations 3% or higher; complications include fluid overload (CHF); do not abruptly stop infusion to avoid rebound ICP; wean over 12-24h
  8. Steroids – reduces permeability of tumor capillaries, dexamethasone is drug of choice (low index of Na and water retention, long half life, low mineralocorticoid activity, low tendency to induce psychosis, controls tumor-associated pain, limits n/v, improves appetite in cancer); 10-20mg IV x1 if with acute nruologic symptoms, maintenance dose of oral or IV 4-24mg in divided doses; expect improvement in 48 hours, use lowest effective dose; use GI prophylaxis
  9. Surgery – resection, intraventricular catheterization

Future Therapies

  1. inhibition of VEGF – SU5416 (semaxanib), AZD2171
  2. COX-2 inhibitors – inhibits production of prostaglandins involved in inducing cerebral edema, also found to induce apoptosis and prevent anigogenesis; SC-236, rofecoxib, PPAR-γ



Esquenazi, Y., V. P. Lo, and K. Lee. “Critical Care Management Of Cerebral Edema In Brain Tumors”.Journal of Intensive Care Medicine (2015): n. pag. Web.