Hypercoagulable Panel

Checklist for hypercoagulable work-up

  • *Antithrombin III Activity
  • *Prothrombin Gene Mutation
  • *Factor V (5) Leiden Gene Mutation
  • Factor VIII (8) Activity
  • aPTT-LA (Lupus Sensitive Reagent)
  • Anticardiolipin Antibody (IgG, IgM, IgA)
  • Beta 2 glycoprotein
  • Russell Viper Venom Time (dilute)
  • *Homocysteine
  • *Protein C Activity
  • *Protein S Activity
  • ESR CRP ANA
  • MTHFR
  • SPEP
  • Lipoprotein A
  • Plasminogen activator inhibitor

*Shani list, also add Lupus anticoagulant, Vit B12 levels

Rarer causes:

  • Alpha-macroglobulin deficiency
  • Dysfibrinogenemia
  • Factor V deficiency, excess
  • Factor VII excess
  • Factor VIII excess
  • Factor XI excess
  • Heparin cofactor II deficiency
  • Hyperfibrinogenemia
  • PAI-1 excess
  • Plasminogen deficiency
  • tPA deficiency
  • TFPI deficiency
  • Thrombomodulin deficiency

 

References

“Hypercoagulability Panel – Machaon Diagnostics”. Machaon Diagnostics. N.p., 2016. Web. 30 Mar. 2016.

“Hypercoagulable States”. Clevelandclinicmeded.com. N.p., 2016. Web. 30 Mar. 2016.

Antiepileptic Medications

 

Antiepileptic Drug Absorption, Elimination Half-Life, FormulationsAEDAED2
Hepatic Metabolism, Enzyme Induction/Inhibition, Pharmacokinetic Interactions, and Protein Binding

AED3AED4

 

Established Efficacy of Antiepileptic Drugs by Seizure Type (FDA Indications and Class I-III Evidence)

AED5AED6

Key Known Antiepileptic Drug Mechanisms of Action

AED7AED8

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Table2

 

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Reference:

Daroff, Robert B et al. Bradley’s Neurology In Clinical Practice. London: Elsevier, 2016. Print.

 

 

SIADH

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  • Patients with severe symptoms or SAH at risk for vasospasm will receive hypertonic saline; otherwise the cornerstone of treatment for SIADH is fluid restriction.
  • Acute hyponatremia and/or severe symptoms should have 6 mmol/L corrected over 6 h or until severe symptoms improve.
  • The total correction of Na should not exceed 8 mmol/L over 24 h. Therefore, if 6 mmol/L is corrected in 6 h, the Na should not be increased more than 2 mmol/L in the following 18 h.
  • The total correction of Na is based on the Na deficit which is calculated conservatively with the formula depicted.
  • With improvement of symptoms, the patients can be moved to the less aggressive treatments in the algorithm, until Na reaches 131 mmol/L.

 

Reference

Layon, A. Joseph, Andrea Gabrielli, and William A Friedman. Textbook Of Neurointensive Care. Print.

CSW vs SIADH

Table compares clinical and laboratory findings in CSW vs SIADH.  Both conditions will present with low serum (osm and Na) and high urine (osm and Na).  The key to distinguishing between the two is extracellular fluid status (increased or normal in SIADH and decreased in CSW).

 

SIADH criteria proposed by Janicic and colleagues:

  1. Posm <275
  2. inappropriate urinary concentration (Uosm >100)
  3. clinical euvolemia (no orthostasis, tachycardia, dec skin turgor, dry mucous membranes or edema and ascites)
  4. elevated urinary Na excretion with normal salt and water intake
  5. absence of other causes of euvolemic hypoosmolality (hypothyroidism, hypocortisolism)

Bartter and Schwartz Criteria for SIADH: [Seay, et al]

Reference:

Layon, A. Joseph, Andrea Gabrielli, and William A Friedman. Textbook Of Neurointensive Care. Print.

Yuen, K., Ajmal, A., Correa, R. and Little, A. (2019). Sodium Perturbations After Pituitary Surgery. Neurosurgery Clinics of North America, 30(4), pp.515-524.

Seay, N., Lehrich, R. and Greenberg, A. (2019). Diagnosis and Management of Disorders of Body Tonicity—Hyponatremia and Hypernatremia: Core Curriculum 2020. American Journal of Kidney Diseases.

Prophylaxis for Acute Kidney Injury

Prevention of Acute Kidney Injury

  1. acetylcysteine 1,2000m g PO on day before and on the day of administration of the contrast agent, x 2 days PLUS
  2. saline 0.45% IV at 1ml/KgBW/h x12h before and 12h after administration of contrast agent
  3. for EMERGENCY procedures:  154 mEq/L NaHCO3 bolus of 3 ml/Kg/h x 1h before iopamidol contrast ffd by infusion of 1 ml/Kg/h x6h after procedure
  4. reduce contrast load

 

General Measures:

  1. maintain adequate BP
  2. optimize fluid balance
  3. adjust med dosage to renal function
  4. avoid NSAIDs

 

Reference:

Layon, A. Joseph, Andrea Gabrielli, and William A Friedman. Textbook Of Neurointensive Care. Print.

Antihypertensive Agents for Acute Stroke

Potential Approaches to Arterial Hypertension in Acute Ischemic Stroke Patients Who Are Candidates for Acute Reperfusion Therapy

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Eligible for tPA except BP 185/110 mmHg:

  • Labetalol 10–20 mg IV over 1–2 minutes, may repeat 1 time; or
  • Nicardipine 5 mg/h IV, titrate up by 2.5 mg/h every 5–15 minutes, maximum 15 mg/h; when desired BP reached, adjust to maintain proper BP limits; or
  • Other agents (hydralazine, enalaprilat, etc) may be considered when appropriate

BP not maintained </=185/110 mmHg, do not administer rtPA

Keep BP during and after tPA <= 180/105 mmHg:

  • Monitor BP from start of tPA
    • every 15 minutes x 2 hours
    • every 30 minutes x 6 hours
    • every hour x 16 hours

If systolic BP >180–230 mmHg or diastolic BP >105–120 mmHg:

  • Labetalol 10 mg IV followed by continuous IV infusion 2–8 mg/min; or
  • Nicardipine 5 mg/h IV, titrate up to desired effect by 2.5 mg/h every 5–15 minutes, maximum 15 mg/h

If BP not controlled or diastolic BP >140 mmHg, consider IV sodium nitroprusside

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Reference:

Jauch, E. C. et al. “Guidelines For The Early Management Of Patients With Acute Ischemic Stroke: A Guideline For Healthcare Professionals From The American Heart Association/American Stroke Association”. Stroke 44.3 (2013): 870-947. Web. 22 Mar. 2016.

Checklist: Immediate Diagnostic Studies for Evaluation of Suspected Acute Ischemic Stroke

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*Although it is desirable to know the results of these tests before giving intravenous recombinant tissue-type plasminogen activator, fibrinolytic therapy should not be delayed while awaiting the results unless (1) there is clinical suspicion of a bleeding abnormality or thrombocytopenia, (2) the patient has received heparin or warfarin, or (3) the patient has received other anticoagulants (direct thrombin inhibitors or direct factor Xa inhibitors).

 

 

 

References

Jauch, E. C. et al. “Guidelines For The Early Management Of Patients With Acute Ischemic Stroke: A Guideline For Healthcare Professionals From The American Heart Association/American Stroke Association”. Stroke 44.3 (2013): 870-947. Web. 22 Mar. 2016.

 

 

RIFLE Criteria for Acute Kidney Injury

The table below shows the RIFLE (Risk Injury Failure Loss End stage) classification scheme for acute kidney injury.

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This system has a separate criteria for creatinine and urine output.  If the patient’s condition falls under two different levels, then the worse classification should be used.

RIFLE-FC = denotes ‘acute-on-chronic’ disease.

RIFLE-FO = when RIFLE-F classification is reached by urine output criteria only

 

Checklist:  AKI work-up

  • Urinary sediment
  • Urinalysis
  • exclude obstruction
  • review of meds
  • rhabdomyolysis: creatine kinas, free myoglobin
  • vasculitis: CXR, blood smear, measurement of nonspecific inflammatory markers, specific antibodies (anti-GBM, ANCA, anti-DNA, anti-smooth muscle)
  • TTP: LDH, haptoglobin, unconjugated bilirubin, free hemoglobin
  • Cryoglobulins
  • Bence-Jones proteins
  • Renal biopsy

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References

Bersten, Andrew D, and Neil Soni. Oh’s Intensive Care Manual. London: Elsevier Health Sciences UK, 2013. Print.

EVD Management and Troubleshooting

CSF BASICS:

  • CSF production ~0.2–0.4 mL/min or 500–600 mL a day

 

MANAGEMENT OF EVD:

  • INITIAL SET UP
  • Determine height of EVD collecting system
  • Adjust height of EVD
    • pressure transducer in line with Foramen of Monro (external auditory meatus in supine and between eyebrows in lateral position)
    • Use Carpenter’s level or laser leveling device to zero drain
    • Unsecured aneurismal SAH
      • initial height set “high” so CSF not drained too quickly to avoid rapid change in transmural pressure across aneurism wall, which predisposes to rebleeding
      • Negative level of drainage may be encountered in negative pressure HCP or massive IVH
  • Set drainage
    • continuous set level
    • fixed volume per desired time
    • as needed according to ICP elevations
  • NOTES:
    • At prescribed height, CSF will drain whenever intraventricular pressure exceeds that set by the height of the collection system.
    • If transducer is above Foramen of Monro, falsely low ICP and insufficient drainage of CSF may occur, and intracranial hypertension would go undetected.
    • Clamp drain during transfer and transport.
  • Inspect ICP tracing.
    • If EVD is open with continuous drainage – turn stopcock at level of transducer “off” to drain and “open” to transducer. ICP waveform takes 30s to stabilize and should appear pulsatile.
    • Normal ICP waveform has 3 peaks, decreasing in height.
    • In intracranial HTN or failing compliance, amplitude of all 3 peaks increase followed by elevation of second over first.
  • ACCESSING EVD:
    • indications:
      • withdraw CSF for cultures or obtaining malignant cells
        • Do not collect samples from collection bag – rapid degradation of cellular components.
        • Aspirate from proximal port.
        • Aspirate slowly (no more than 1 ml/min). If resistance is met, abort procedure and inform MD.
      • instill medications
        • tPA for IVH or ABx for ventriculitis
        • clamp EVD x 1 hour.
  • Other nursing management:
    • 1. Monitoring for ICH
    • 2. Inspecting entire EVD systemand insertion site for CSF leak
    • 3. Noting quantity, color and clarity of CSF
      • increase in hourly output signals ICH
      • bright red bloody CSF indicate aneurysm rupture
      • cloudy CSF indicate presence of infection

 

TROUBLESHOOTING THE EVD:

  • Causes of obstruction of a ventriculostomy catheter
    • cellular debris, (blood clots / tissue fragments).
    • Mechanical kinking of tubing, failure of any part of the system, migration of EVD catheter
    • Physiologic factors such over drainage or tight ventricles or CSF leak
  • Technique:
    • FIXED OBSTRUCTION
      • clues:
        • Dampening of the ICP waveform
        • reduction or absence of CSF flow
        • lack of pulsation of the CSF meniscus in drain tubing with respiration
      • change EVD collection system
    • NO FIXED OBSTRUCTION
      • Lower drainage system briefly to see if CSF flow ensues (no fixed obs)
      • cellular debris = catheter irrigation with small volume (less than 2 ml) sterile isotonic normal saline
        • flush distal port first
        • flush proximal port (potentially result in increased ICP in patients with preexisting intracranial hypertension and/or poor intracranial compliance)

 

EVD RELATED INFECTION

  • Risk factors
    • systemic infection, depressed skull fracture, lack of tunneling of EVD catheter, site leak, catheter irrigation, frequency of CSF sampling and possibly duration of EVD placement
  • Techniques to reduce infection
    • Prophylactic IV antibiotics – develop resistant organisms
    • Antibiotic-impregnated and ionized silver particle coated EVD catheters – same, costly
    • Sample EVD only when infection suspected
    • Monitor EVD dressing site for CSF leak
    • Maintain collection system in upright position
    • Do not routinely change drain tubing

How to Sample CSF from EVD:

 

References:

Muralidharan, Rajanandini. “External Ventricular Drains: Management And Complications”. Surgical Neurology International 6.7 (2015): 271. Web.

Kiwon Lee, NeuroICU Book.