Radiosurgery Based AVM Score (RBAS)

This score is used to predict outcomes following single or repeat LINAC (Linear Accelerator) radiosurgery in AVM.

  • Score is based on a validation cohort study of 403 patients with AVM treated with LINAC radiosurgery  and assigned an RBAS score


RBAS Score is calculated as:

               (0.1 × volume in cm3) + (0.02 × age in years) + (0.3 × location value)

  • location values
    • 0 = frontal/temporal
    • 1 = parietal/occipital/corpus callosum/cerebellar
    • 2 = basal ganglia/thalamus/brainstem


  • EXCELLENT Outcome = obliteration of AVM without deficit
    • RBAS <1 = 74%
    • RBAS 1-1.8 = 64%
    • RBAS 1.8-<2.5 = 50%
    • RBAS >=2.5 = 11%


Raffa, Scott J. et al. “Validation Of The Radiosurgery-Based Arteriovenous Malformation Score In A Large Linear Accelerator Radiosurgery Experience”. Journal of Neurosurgery 111.4 (2009): 832-839. Web.

Modified Ramsay Scale

The Modified Ramsay Scale:

  • first scoring system for evaluating sedation in mechanically ventilated patients
  • four levels of sedation (3-6) and one level of agitation (1)
  • lack of scientific validation, but used in many ICUs




Marino, Paul L, Kenneth M Sutin, and Paul L Marino. The Little ICU Book Of Facts And Formulas. Philadelphia: Wolter Kluwer Health/Lippincott Williams & Wilkins, 2009. Print.

The Anatomical Basis of Aphasia







aphasia algorithm



aphasia symptom chart


Types of Aphasia





authorSTREAM,. “ANATOMICAL BASIS Of APHASIA”. N.p., 2016. Web. 27 Feb. 2016.  Dr. Nazim Nasir Resident Department of Anatomy JNMCH,AMU, ALIGARH

Chapey, Roberta. Language Intervention Strategies In Aphasia And Related Neurogenic Communication Disorders. Philadelphia: Lippincott Williams & Wilkins, 2001. Print.

Anti-NMDA Encephalitis

Anti-NMDA receptor encephalitis 

  • autoimmune encephalitis, paraneoplastic encephalitis
  • associated with tumors in 60% of cases (usually ovarian teratoma)
  • first described in 2005, anti-NMDAR antibodies discovered in 2007

Anti-NMDA receptor encephalitis is an immune-mediated syndrome predominantly seen in young females.  Symptoms include psychiatric changes, autonomic dysfunction and other neurologic findings.  It is commonly associated with mature ovarian teratomas.

There is a need for increased awareness and diagnostic suspicion for anti-NMDA encephalitis in patients with suspected encephalitis of unknown etiology.  Early intervention significantly affects outcome.


  1. Prodromal – nonspecific (fever, headache, nausea)
  2. Psychotic – emotional disturbances, cognitive fluctuations, paranoia, delusions, amnesia, hallucinations
  3. Unresponsive / hyperkinetic – catatonia (cataplexy, mutism, rigidity), abnormal involuntary movements (orolingual dyskinesia), seizures, decreased level of consciousness, autonomic instability, sleep disturbances
  4. Recovery – gradual and usually complete

Treatment for this condition includes supportive care, considering surgical resection when appropriate and immune-modulating therapies.


This algorithm was taken from an abstract presented at the SCCM 45th Critical Care Congress by McLatchy, et al of Hofstra Northwell School of Medicine.

2016-02-24 07.27.46.jpg





Abstract.  Anti-N-methyl-D-aspartate Receptor Encephalitis: An underrecognized, Treatable Disease.  McLatchy, J. et al.  SCCM 2016 45th Critical Care Congress. February 19-24, 2016, Orlando, Florida.

Sepsis Redefined

New recommendations for sepsis was published in the February 2016 issue of JAMA and highlighted at SCCMs 45th Critical Care Congress in Orlando, Florida.

Sepsis is defined as life-threatening organ dysfunction due to a dysregulated host response to infection.  Septic shock is defined as a subset of sepsis in which profound circulatory, cellular and metabolic abnormalities substantially increase mortality.

The new definitions were suggested to reflect the advances made in the pathophysiology, management and epidemiology of sepsis.

The term “severe sepsis” has been removed to highlight the fact that sepsis, by itself, is already a severe condition, making the term severe sepsis redundant.

Organ dysfunction is a key part in the definition of sepsis, and it is the main consideration that elevates uncomplicated infection to sepsis.  Suspicion of infection should prompt a search for organ dysfunction, and organ dysfunction should prompt a search for a focus of infection.

A new diagnostic tool, quickSOFA or qSOFA, was recommended, which consists of 3 simple bedside tests to identify patients at risk for sepsis.  This tool directs physicians to look for these signs: a change in mental status, decrease in SBP <100mm Hg or a respiratory rate >22/min.  Patients with 2 or more of these conditions are at higher risk of prolonged ICU stay or to die in the hospital.  For these patients, clinicians should investigate further for organ dysfunction, initiate or escalate therapy, and consider referral to critical care or increase frequency of monitoring.

The task force identified two new clinical criteria that should be used in diagnosing septic shock:  persistent hypotension requiring vasopressors to maintain MAP>/=65mmHg and blood lactate >2mmol/L despite adequate volume resuscitation.

The report has been designated as “Sepsis-3” (the first two were proposed in 1991 an 2001)


TEG = thromboelastography

ROTEM = rotational thromboelastometry

Both TEG and ROTEM are methods of measuring coagulation and fibrinolysis.  In TEG, the “cup” of the machine rotates, whereas in ROTEM, it is the sensor shaft that rotates.

In thromboelastography, blood is rotated by 4`45″ 6x per minute to simulate sluggish blood flobe.  A wire probe is then used to measure the speed of coagulation and extent of fibrinolysis.

Thromboelastography measures 4 parameters of blood coagulation (reaction time, K value, alpha angle and maximum amplitude) and 2 parameters of clot lysis (estimated percentage of lysis and percent clot lysed after 30 minutes).  Two other values are calculated based on a proprietary formula from the company who created the machine (coagulation index).

The parameters for clot formation:

1.  Reaction time (R) – time to first clot detected, reflects coagulation factor activity

2.  K value (K) – time from (R) until clot reaches 20mm, reflects speed of clot formation

3.  alpha angle (A) – the tangent of the curve when K is reached, also reflects speed of clot formation; represents thrombin burst and conversion of fibrinogen to fibrin

4.  maximum amplitude (MA) – reflects clot strength; 80% is dervied fro platelet function and 20% from fibrin

The calculated parameters:


2.  G VALUE – log-derivation of MA, also represents clot strenght using dynes/sec as units;  rising levls may be seen in venous thromboembolic disease

The parameters for clot lysis:

1.  Estimated % lysis (EPL)

2.  % clot lysed after 30 minutes (LY30%)

Based on the TEG values, the following treatments may be given:

1.  Elevated R – give plasma

2.  decreased  alpha angle – give cryoprecipitate or large volume of plasma

3.  decreased MA – platelet transfusion or DDAVP

4.  increased EPL or LY30% – treat with antifibrinolytics (i.e. tranexamic acid or aminocaproic acid)

TEG Procedure:

1. Citrates blood introduced into the sample cup of the TEG machine

2. Cup oscillates around submerged torsion pin which is connected to a computer.

3. As coagulation occurs, pin adheres to clot and begins to move with it.

4. Magnitude of pin motion directly proportional to strength of the clot. Pin motion is displayed graphically by the computer. Torsion pin remains motionless until clotting begins.

5. Amplitude decreases as fibrinolysis begins and the pin begins to slip.

6. Graph analyzed and 5 parameters are measured.


1. R – time elapsed until first measurable clot forms. Impacted by coagulation factors.

2. K – time elapsed until clot reaches a fixed strength (20mm). Impacted by fibrinogen

3. Alpha angle – reflects speed of fibrin accumulation. Impacted by fibrinogen

4. MA – highest vertical amplitude of TEG tracing. Impacted by platelets.

5. LY30 – percentage of amplitude reduction 30 minutes after maximum. Measures fibrinolysis.

Interpretation of TEG:

R normal range is 5-10 minutes. Elevation represents deficient clotting factors and is treated with FFP.

K normal range is 1-3 units. Elevation represents deficient fibrinogen and is treated with cryoprecipitate.

Alpha angle normal is 53-72 degrees. A low value represents deficient fibrinogen and is treated with cryoprecipitate.

MA normal range is 50-70 mm. A low value represents deficient platelets and is treated with platelets.

LY30 normal range is 0-8%. A higher value indicates excess fibrinolysis and is treated with antifibrionlytics s.a. aminocaproic acid.


Another study uses the following normal parameters:

  1. R time 22-44 s
  2. k time 34-138s
  3. alpha angle 64-80 degrees
  4. MA 55-71mm
  5. LY30 0%



Martin, G., Shah, D., Elson, N., Boudreau, R., Hanseman, D., Pritts, T., Makley, A., Foreman, B. and Goodman, M. (2018). Relationship of Coagulopathy and Platelet Dysfunction to Transfusion Needs After Traumatic Brain Injury. Neurocritical Care.

YouTube. (2018). Thromboelastography. [online] Available at: [Accessed 2 Apr. 2018].

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



[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.