How much hypertonic solution?

To determine how much hypertonic solution to give a patient with hyponatremia:

  1.  calculate sodium deficit (mEq) = weight (kg) x 0.6 x (desired Na – actual Na)
    1. use 0.5 for females
    2. desired sodium in mEq/L
  2. calculate the safe rate of sodium correction for the patient in mEq/hr (0.5-1 mEq/L/hr) = weight (Kg) x 0.6 x 1.0 (rate of correction desired)
  3. 3% hypertonic saline contains 513 mEq/L; 2% contains 342 mEq/L; 1.5% contains 256 mEq/L and 0.9% contains 154 mEq/L
  4. desired rate = (safe rate of correction / 513) x 1000
  5. infusion time (hrs) = sodium deficit (mEq) / safe rate of correction (mEq/hr)

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Marino: estimate initial infusion rate of 3% NaCl by multiplying patient’s KgBW by the desired rate of increase in plasma Na. Example: 70Kg male, desired rise in plasma is 0.5 mEq/L per hour, then infusion rate = 70×0.5 = 35 ml/Hr

References

Globalrph.com,. “Sodium Chloride 3% –  Intravenous (IV) Dilution”. N.p., 2016. Web. 30 Jan. 2016.

Marino, 2014. The ICU Book.

Leukoaraiosis

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Leukoaraiosis:  

  • ischemic damage to the subcortical white matter
  • frequent complication of hypertension-related microvascular disease
  • contributes to the risk of stroke and vascular dementia
  • at greater risk of sICH and have a worse functional outcome after tPA treatment for acute ischemic stroke
  • Side Note:  other risk factors for sICH post-tPA:  age, stroke severity, DM, cardiac disease, elevated pre-treatment mean BP

 

Why is leukoaraiosis associated with greater risk of sICH after tPA?

Leukoaraiosis is a radiological marker for chronic ischemic damage of cerebral microcirculation, which worsens effects of acute ischemia and tPA at the BBB.

Pre-existing damage of cerebral microcirculation (including the endothelium) increases risk of vessel rupture and subsequent hemorrhage.   Stroke damages endothelium and astrocytes, weakening the BBB.  With tPA, further damage to BBB occurs.

Leukoaraiosis is likely a marker of increased susceptibility to hemorrhagic treatment complications, rather than a condition indicating a specific risk of thrombolytic treatment.

How is leukoaraiosis assessed?

For assessment of leukoaraiosis, studies used MRI with high-resolution T2-weighted sequence.

Sseverity of leukoaraiosis is rated using a visual rating scale proposed by Fazekas and Schmidt, with scores ranging from 0 to 3.  FLAIR sequence or high-resolution T2-weighted sequence for deep WM and periventricular WM was used to determine extent of leukoaraiosis.

Deep white matter lesions were scored as follows:

  • 0, no lesion
  • 1, punctuate foci
  • 2, beginning confluent foci
  • 3, confluent changes

Periventricular white matter lesions were scored as follows:

  • 0, no changes
  • 1, caps or a pencil-thin lining
  • 2, smooth halo
  • 3, irregular changes extending into deep white matter

 

See figure below for examples illustrating different degrees of leukoaraiosis in deep white matter (arrow) and periventricular areas (with identical scores for deep and periventricular changes).

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References

Ariës, M. J. H. et al. “Tpa Treatment For Acute Ischaemic Stroke In Patients With Leukoaraiosis”.European Journal of Neurology 17.6 (2010): 866-870. Web.

Neumann-Haefelin, T. et al. “Leukoaraiosis Is A Risk Factor For Symptomatic Intracerebral Hemorrhage After Thrombolysis For Acute Stroke”. Stroke 37.10 (2006): 2463-2466. Web.

Sph.umich.edu,. “Genetic Architecture Of Leukoaraiosis – Research – Kardia Lab – Genetic Epidemiology – Epidemiology – Faculty Research Projects – Faculty & Research – UM SPH”. N.p., 2016. Web. 29 Jan. 2016.

Debette, S. and Markus, H. The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: systematic review and meta-analysis. BMJ 2010; 341:c3666.

Ictal-Interictal Continuum

Which EEG patterns warrant treatment in the critically ill?

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The IIC graph modified by Struck, et al.

 

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Modification uses current ACNS terminology, with the addition of PET metabolism from hypometabolic (blue) to hypermetabolic (red).  X-axis = spectrum of cerebral dysfunction and Y-axis = neuronal damage

*SB suppression burst, RDA rhythmic delta activity, LPD lateralized periodic discharges, SW spike wave, GPD generalized periodic discharges, SIRPIDs stimulus-induced rhythmic, periodic, or ictal discharges, NCS non-convulsive seizures, GCSE generalized convulsive status epilepticus, NCSE nonconvulsive electrographic status epilepticus, EPC epilepsia partialis continua

 

 

  • strong correlation between PDs on the IIC and subsequent NCSZs or non-convulsive status epilepticus (NCSE)
  • link between PDs on the IIC and functional outcome remains less certain
  • link between interictal periodic patterns and secondary brain injury (as inferred by increased vasogenic or cytotoxic edema [8, 9] or increase in lactate-pyruvate ratio [10]), seen as similar sequelae to those resulting from NCSZs

References

Chong, Derek J., and Lawrence J. Hirsch. “Which EEG Patterns Warrant Treatment In The Critically Ill? Reviewing The Evidence For Treatment Of Periodic Epileptiform Discharges And Related Patterns”. Journal of Clinical Neurophysiology 22.2 (2005): 79-91.

 

Struck, Aaron F. et al. “Metabolic Correlates Of The Ictal-Interictal Continuum: FDG-PET During Continuous EEG”. Neurocritical Care 24.3 (2016): 324-331.

Risk of Rupture in SAH

Handy data for prognostication in SAH.

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SAH Prognosis

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References

Bhardwaj, Anish, and Marek Alexander Z Mirski. Handbook Of Neurocritical Care. New York: Springer, 2010. Print.

Wiebers, David O. “Unruptured Intracranial Aneurysms: Natural History, Clinical Outcome, And Risks Of Surgical And Endovascular Treatment”. The Lancet 362.9378 (2003): 103-110. Web.

How to:  Transthoracic Echo

The ultrasound machine is now becoming an indispensable tool for the (non-radiologist) doctor, providing real-time, clinically-relevant information at the bedside.  While this machine may not replace the reliable stethoscope any time soon, the ultrasound has certainly proven its utility, adding to the armamentarium of the modern physician.

Interpretation of ultrasound, just like interpretation of any radiologic modality, involves a certain learning curve.  It takes time and practice to be able to superimpose the anatomy of body organs on the low-resolution images, and derive some clinical information on the function of the insonated organ.  

The transthoracic echo in particular may be more challenging to interpret, because different views are used to slice the chambers of the heart in different planes.  The method of transthoracic echo is hard taught with words and pictures, but rather, time should be spent by the sonologist visualizing the ultrasound probe and the waves that emanate from the probe slicing through the cardiac chambers. 

Here are five videos from youtube, each one a little over a minute, that wonderfully illustrates how a picture (or in this case, a video) is worth a thousand words.  A novice would very well consider watching the videos over and over, until the the images are  ingrained in his memory.
Parasternal short axis – https://m.youtube.com/watch?v=_6Ltla3NL1k

Subcostal view – https://m.youtube.com/watch?v=oMwgUo6sbyY

Apical 4-chamber view – https://m.youtube.com/watch?v=5czv-c1uUnw

Parasternal long axis – https://m.youtube.com/watch?v=CIJewMLUQkU

IVC view – https://m.youtube.com/watch?v=McUUFvnFuJU

References

YouTube,. “How To Obtain: Apical 4 (Four) Chamber Ultrasound View- Training And Techniques – ICU”. N.p., 2016. Web. 25 Jan. 2016.

YouTube,. “How To Obtain: Inferior Vena Cava Ultrasound View- Training And Techniques – ICU”. N.p., 2016. Web. 25 Jan. 2016.

YouTube,. “How To Obtain: Parasternal Long Axis Ultrasound View – Training And Techniques – ICU”. N.p., 2016. Web. 25 Jan. 2016.

YouTube,. “How To Obtain: Parasternal Short Axis Ultrasound View – Training And Techniques – ICU”. N.p., 2016. Web. 25 Jan. 2016.

YouTube,. “How To Obtain: Subcostal Cardiac Ultrasound View – Training And Techniques – ICU”. N.p., 2016. Web. 25 Jan. 2016.

VASOGRADE

Patients are classically at risk of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage. We validated a grading scale—the VASOGRADE—for prediction of DCI.

 

vasograde

 

 

References

de Oliveira Manoel, Airton Leonardo et al. “The VASOGRADE”. Stroke 46.7 (2015): 1826-1831. Web.

NASAH – Nonaneurysmal Subarachnoid Hemorrhage

Checklist of DDx for NASAH:

  • perimesencephalic NASAH
  • occult aneurysm
  • intracranial or spinal vascular malformations
  • intracranial arterial dissection
  • sickle cell disease – can cause aneurysms, or SAH may result from fragile collateral vessels; recent transfusion and corticosteroid therapy may be risk factors
  • pituitary apoplexy – p/w sudden onset of headache and vomiting; heralded by vision change and accompanied by extraocular nerve palsy; MRI will demonstrate tumor
  • cocaine abuse – associated with both aSAH and NASAH; mechanism of latter unknown bur prob related to acute BP surge or underlying hypertensive or toxic vasculopathy
  • cerebral venous thrombosis – less abrupt than aneurysmal rupture, bleeding is localized and superficial; check for thrombosis on venous phase of DSA or on MRI
  • bleeding disorders / anticoagulant therapy – rare, systemic bleeding usually accompanies SAh if this is the primary cause, otherwise, assume an underlying aneurysm; PNSAH can have more extensive hemorrhage in the setting of reduced antiplatelet activity
  • traumatic SAH – if no clinical history available, radiologic clues [localized bleeding in superficial sulci, adjacent skull fracture, cerebral contusion, external evidence of trauma] is present
  • amyloid angiopathy – in older adults; restricted bleed, often to a single sulcus; microbleeds and/or superficial siderosis on MRI
  • spinal aneurysms – prominent neck or back pain and myeloradicular symptoms
  • brain or cervical tumors
  • Moyamoya disease – usually associated with aneurysms, but SAH can occur rarely due to rupture of fragile transdural anastomotic vessels
  • Other causes: cerebral vasculitis, reversible vasoconstriction syndrome, cerebral hyperperfusion syndrome after carotid endarterectomy, reversible posterior leukoencephalopathy syndrome

Diagnostic work-up:

  • emergent CT head
  • lumbar puncture [if CT head negative and suspicion high]
  • basic labs: CBC, CMP, coagulation studies, tox screen
  • baseline echocardiogram
  • conventional digital subtraction cerebral angiography [DSA] on all patients unless CT/CTA adequately defines the pathogenesis
  • repeat DSA within 4-14 days after an initial negative study  NOTE:  False negative rate of initial DSA in NASAH is ~7.1% [2]
  • MRI with gadolinium contrast of brain and spinal cord if angiography negative
  • some patients will not have an etiologic diagnosis after #6 and #7 – if rebleeding occurs, then option to repeat angio of brain and/or surgical exploration and/or surgical exploration

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NOTES:

  1. Initial DSA negative SAH ~15%
  2. Reasons for a negative DSA:
    1. a very small microaneurysm
    2. occult aneurysm concealed by hemorrhage or vasospasm
    3. hemorrhage from a venous system
    4. inadequate technique
  3. perimesencephalic NASAH (PN-SAH) – hemorrhage pattern restricted to perimesencephalic or prepontine cisterns, no aneurysms on DSA, low rates of rebleed and vasospasm, good recovery
    1. center hemorrhage located immediately in front of midbrain or within perimesencephalic, prepontine or medullary cisterns
    2. absence of IPH
    3. extension of blood into Sylvian fissure with no more than a minute amount of blood in the lateral Sylvian fissure
    4. absence of frank IVH
  4. Non-perimesencephalic SAH (NPN-SAH) – does not satisfy criteria above, but negative DSA
  5. As a general rule, in PNSAH, provided that the initial DSA was technically adequate and revealed no vasospasm, a repeat DSA might not be required.  However, in NPN-SAH, repeat DSA is necessary due to the possibility of aneurysmal SAH, even if the initial DSA is negative.
  6. DSA has high sensitivity and specificity for detection of cerebral aneurysms and is associated with some complications (SAH-specific mortality 0.17% of patients, neurological morbidity in 3.2% of patients, permanent disability in 0.04%)

References

[1] Uptodate. Nonaneurysmal subarachnoid hemorrhage, Farhan Siddiq, MD.  Accessed January 23, 2016.

[2] Yu, Dong-Woo et al. “Subarachnoid Hemorrhage With Negative Baseline Digital Subtraction Angiography: Is Repeat Digital Subtraction Angiography Necessary?”. Journal of Cerebrovascular and Endovascular Neurosurgery 14.3 (2012): 210. Web.

Density and Shape of ICH

Can hematoma shape or heterogeneity of hematoma density predict ICH growth?

A 2009 study published in stroke presented a new scale for categorizing ICH based on the shape and homogeneity of the intracerebral hematoma.  The study applied this novel 5-point categorical scale to randomly baseline CT images of ICH. Density and shape were defined as either homogeneous/regular (Category 1 to 2) or heterogeneous/irregular (Category 3 to 5).  The density and shape was then correlated to the risk of hematoma expansion.

Rationale:

A hematoma arising from a solitary focus will have a more regular shape, and a more homogeneous density of blood. Hemorrhage arising from multiple foci will have an irregular shape.  Heterogeneous CT density may reflect either 1.) active hemorrhage, 2.) more variable hemorrhagic time course, 3.) multifocality or multiple bleeding vessels.  Density of blood on CT in ICH is related to 1. age of blood, 2. time course, 3. number of foci of hemorrhage and 4. hematocrit.

In relation to time course:  liquid blood from active hemorrhage hypoattenuates on CT scans relative to surrounding brain or associated organized hyperattenuating thrombus.  As clot retracts, hypoattenuating serum is released.  As thrombi progressively liquefy into breakdown products, sites of hemorrhage become less dense on CT. Hypoattenuating edematous changes in perihematoma region evolve (in part) due to RBC hemolysate products such as thrombin and iron with associated BBB disruption.

 

Categorical Scales for shape (left) and density (right) of ICHF1.large

 

The 2 scales ranged from Category 1 (most regular shape and most homogeneous density) to Category 5 (most irregular shape and most heterogeneous density). Each progressive category added an extra lesion edge irregularity on the shape scale or degree of density variation on the density scale.

In cases of “satellite” bleeds, progressive irregularity and heterogeneity features could be joined or separate from the principal hemorrhage. Hematomas with more numerous lesion edge irregularities or more heterogeneous density than represented on the scale were assigned the maximum rating.

The study concluded that larger ICHs were significantly more irregular in shape, heterogenous in density and had greater growth.  Density heterogeneity independently predicted ICH growth.  Irregular shape was not identified as an independent ICH growth predictor.

 

References

Barras, C. D. et al. “Density And Shape As CT Predictors Of Intracerebral Hemorrhage Growth”. Stroke40.4 (2009): 1325-1331. Web.