Rapid ACTH Stimulation Test

Popular but often unnecessary test

  • – perform at any time of day or night
  • – obtain blood sample for baseline (random) plasma cortisol level
  • – give synthetic ACTH IV (Cosyntropin) 250 ug X11
  • – repeat plasma cortisol 1 hour after injection

 

ADRENAL SUPPRESSION:

  1. Random cortisol <10 ug/dL OR
  2. Increment in plasma cortisol <9 ug/dL after ACTH

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APPROACH

  • – check random plasma cortisol
  • – if >=35 ug/dL – likely normal or adequate adrenal function
  • – if <10 ug/dL – evidence of adrenal suppression
  • – if 10-34 ug/dL – do rapid ACTH stim test as above

** In septic shock, do not check cortisol levels – trial of IV hydrocortisone is recommended if hypotension refractory to volume resuscitation.

 

Reference:

Marino, P. (n.d.). The ICU book.

Checklist: Autoimmune Encephalitis Work-up

Serum studies:

  • ESR CRP
  • C3 C4 CH50
  • ANA
  • RF
  • sjogren’s SSA SSB
  • SPEP
  • Thyroid peroxidase, thyroglobulin antibody
  • Glutamic acid-decarboxylase antibody
  • paraneoplastic panel (includes VGKC and NMDA)

 

MRI brain w/wo con
CTA head/neck

 

Lumbar Puncture

  • opening pressure
  • CSF protein, glucose, cell count
  • CSF IgG index, oligoclonal bands (check in serum as well)
  • CSF myelin basic protein
  • Gram stain and bacterial culture
  • Fungal culture

*withdraw at least 30 cc of CSF and save extra for additional studies if necessary

 

 

CSF WBC Correction for Traumatic Tap

If peripheral WBC is normal, then use ratio of 1:500 or 1:750.

If peripheral WBC abnormal, then use the following formula:

  • WBCcsf = WBCblood x RBCcsf / RBCblood
  • or  WBCc * RBCb = WBCb*RBCc
  • or WBCc/RBCc = WBCb/RBCb

The result is the number of artificially introduced WBCs.

True WBCcsf is then calculated by subtracting the artificially introduced WBCs from the actual WBCcsf

Reference:

“WBC Correction For Traumatic Tap – Labce.Com, Laboratory Continuing Education”. Labce.com. N.p., 2016. Web. 17 Aug. 2016.

Interpretation of Hepatitis B Serologic Test Results

Capture

 

Hepatitis B surface antigen (HBsAg):

  • protein on surface of virus
  • high levels during acute or chronic infection
  • indicates that person is infectious

Hepatitis B surface antibody (anti-HBs)

  • indicates recovery and immunity
  • also develops in a person successfully vaccinated, persists for life

Anti-HBc

  • indicates previous or ongoing infection in an undefined time-frame
  • IgM antibody core antigen indicates recent infection (<6 months) – indicates acute infection.

 

References

2016. Web. https://www.cdc.gov/hepatitis/hbv/pdfs/serologicchartv8.pdf 11 June 2016.

Platelet Response / ARU / PRU

VerifyNow for Clopidogrel:

  • Values less than 194 PRU are specific evidence of a P2Y12 inhibitor effect

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VerifyNow for Aspirin:

  • ≤ 549: Evidence of platelet dysfunction due to aspirin
  • > 550: No evidence of aspirin-induced platelet dysfunction

 

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ASA-specific VerifyNow uses arachidonic acid as an agonist for platelet aggregation onto fibrinogen-coated beads.

VerifyNow (P2Y12) uses adenosine diphosphate and is more commonly utilized to detect platelet dysfunction due to clopidogrel.

Degree of platelet aggregation is recorded as aspirin reaction units (ARUs) or P2Y12 reaction units (PRUs).

Abnormally functiong platelets are defined as ARU <550 or PRU 208 (U of Cincinnati lab normal value, cutoff not universally defined).

 

VerifyNow Reference Guide

Clinical Value of the VerifyNow System

 

REFERENCES:

Click to access mvn0005_-_verifynow_pocket_guide_1.pdf

Click to access CLMA_Educ_Day_Presentation_-VerifyNow_2-18-14.pdf

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.

 

Interpreting Procalcitonin Values

Units:  ng/mL (normal <0.10)

Interpretation:

1. predicting progression to severe sepsis / septic shock (taken on D1 ICU admission)

  • >2 = high risk
  • <0.5 = low risk

2. As guide to Abx therapy in respiratory infections

  • <0.1 = ABx not needed
  • >0.5 = ABx needed

PCT-Algorithms-1 PCT-Algorithms-2 PCT-Algorithms-3 PCT-Algorithms-4bild_15_pct_04_06 procalcitonin-img Procalcitonin for diagnosis Figure 2

Basics:

  • precursor of calcitonin
  • produced by parafollicular cells of thyroid gland and neuroendocrine cells of lung / intestine / other tissues in response to inflammation, esp bacterial.
  • serum values correlate with severity of sepsis, recede with improvement, worsen with exacerbation.

Test performance:

  • Bacteremia (Sn 76%, Sp 70%)
  • systemic inflammatory response syndrome (SIRS)
  • sepsis
  • septic shock.

A/G Ratio

Total Protein Levels

  • Low = liver disorder, kidney disorder, malabsorption of kidney; malnutrition
  • High = chronic inflammation, infections (viral hepatitis or HIV), bone marrow diseases, multiple myeloma

A/G Ratio (normally, there is a little more albumin than globulins, so slightly >1)

  • Low = decreased albumin (cirrhosis, nephrotis syndrome) or increased globulins (MM, autoimmune diseases)
  • High = increased albumin <?> or decreased globulin (leukemias, genetic deficiencies)

Next tests: liver enzyme tests, SPEP

NOTE:  plasma expansion decreases total protein but A/G ratio will be normal because both albumin and globulin will be diluted to the same extent


Vitamin K Cycle and Coumadin

Explanation of Vitamin K Cycle from NEJM  (N Engl J Med 2013; 369:2345-2346December 12, 2013DOI: 10.1056/NEJMe1313682)

Vitamin K plays a single role in human biology — as a cofactor for the synthesis of γ-carboxyglutamic acid. 


Importance of γ-carboxyglutamic acid?

1.  component of at least 14 proteins (factor IX, factor VII, factor X, and prothrombin, protein C and protein S)

2. critical for the physiologic function of these proteins


We do not synthesize vitamin K, we ingest it in our diet. 


Vit K Cycle:

1. vitamin K quinone reduced to the semiquinone –> cofactor required for conversion of glutamic-acid residues on the vitamin K–dependent proteins to γ-carboxyglutamic acid by vitamin K–dependent carboxylase

2.  reaction produces Vitamin K epoxide –>  converted back to vitamin K quinone by VKOR (vitamin K epoxide reductase)


Warfarin inhibits VKOR –> post-translational modification of the vitamin K–dependent blood-coagulation proteins is impaired –>  reduced function of factors 10, 9, 7, 2 leads to delayed coagulation


Simplified Diagram:


Where the Protein products come in the cycle:

A more complicated diagram to illustrate the Vit K cycle:

Illustration showing where warfarin works in the Vit K cycle: