Differential Diagnosis
Checklist:
Reference:
Andersen, Lars W. et al. “Etiology And Therapeutic Approach To Elevated Lactate Levels”. Mayo Clinic Proceedings 88.10 (2013): 1127-1140.
Month: June 2016
*clinical practice, uncertain of evidence – will have to investigate further.
- Labs
- CBC BMP CMP q6h or as needed
- P2Y12 levels
- Meds
- heparin drip x 24 hours then start heparin SQ q8h
- dexamethasone 2mg q8h x 1 day then dexamethasone 2mg q12h x 3 doses
- famotidine
- ASA/Plavix x 3 days?
- Safeguard x 4 hours
- Legs flat x 4 hours
- OOB / foley out 2 hours after heparin drip is stopped
- d/c A-line once heparin drip stopped unless with BP issues
Prior to Epidural Blood Patch:
FIRST 24 HOURS:
- Encourage PO fluid intake.
- Supine position
- Oral analgesics (NSAIDS / opioids)
SECOND 24 HOURS:
- Caffeine 500mg in 1L LR over 4 hours.
- Aminophylline 100 mg po BID.
THIRD 24 HOURS:
- consult anesthesiology or interventional radiology for possible epidural blood patch
Schematic section through the vertebral column, showing the cauda equina and its covering membranes with the dural leakage site before (A) and after (B) application of the epidural blood patch.
Post-blood patch orders:
- supine x2 hours
- no strenuous exercises x 3 weeks
- Watch out for:
- sciatica / immediate exacerbation of symptoms and radicular pain – PRN pain meds
- bowel and bladder dysfunction
- intracranial hypertension
If blood patch not an option: oral or IV caffeine 300-500mg OD or BID (therapeutic doses have been associated with CNS toxicity and atrial fibrillation
References
“Brain Sag”. Peripheral Brain. N.p., 2016. Web. 24 June 2016.
R Oedit et al. Efficacy of the epidural blood patch for the treatment of post lumbar puncture headache BLOPP: A randomised, observer-blind, controlled clinical trial. BMC Neurology 20055:12 DOI: 10.1186/1471-2377-5-12.
bedside clinical score for prediction of endocarditis in enterococcal bacteremia
NOVA:
- number of positive blood cultures [3/3 or the majority if more than 3], 5 points
- unknown origin of bacteremia, 4 points
- prior heart valve disease, 2 points
- auscultation of a heart murmur, 1 point
cutoff score <4 points suggested a very low risk for enterococcal IE
useful for avoiding unnecessary TEE in enterococcal bacteremia
Uptodate. http://www.uptodate.com/contents/treatment-of-enterococcal-infections?source=search_result&search=ENTEROCOCCUS+FAECALIS%5C&selectedTitle=1~37#H10055572. Accessed 06/22/2016
Treatment dose: amantadine 100 mg BID x 14 days; then 150 mg BID at week 3; then 200 mg BID at week 4; after week 4, taper over 2 to 3 days
Reference:
Giacino, Joseph T. et al. “Placebo-Controlled Trial Of Amantadine For Severe Traumatic Brain Injury”.New England Journal of Medicine 366.9 (2012): 819-826.
CT perfusion (CTP)
- repeated scanning of the same area of the brain during passage of contrast from arteries through capillaries to the veins and into the venous sinuses
- density curves are drawn for each pixel in the image, color-coded maps are derived from these curves
Parameters of CTP:
- Time to peak (TTP)
- shows the time to the apex of the time−density curve
- reflects the time it takes until the contrast bolus reaches the tissue
- the most sensitive marker for cerebral ischaemia
- TTP increased – longer time for contrast to reach ischaemic area
- Mean transit time (MTT)
- time from wash in to wash out of the contrast medium
- also prolonged in an ischaemic area
- Time to maximum (Tmax)
- flow-scaled residue function in the tissue
- prolonged in ischaemic lesion
- *widely used although physiological meaning is not well understood
- reflect delay, dispersion and to a lesser degree also MTT
- Cerebral blood volume (CBV)
- volume of blood present at a given moment in a distinct brain area
- calculated from area under the time−density curve
- Cerebral blood flow (CBF)
- blood supply to brain in a given time
- derived from the gradient of the wash in of the time−density curve
- relation between the parameters is described in this equation:
- MTT = CBV/CBF
Tissue at risk:
- goal is to assess ratio of infarct core (irreversibly damaged brain tissue) to penumbra, and identify ‘tissue at risk’
- penumbra
- critically hypoperfused, infarct core adjacent tissue
- still viable with reperfusion
- benign oligoaemia
- outside penumbra
- hypoperfused area to a lesser degree
- remains viable even if reperfusion fails
- penumbra
- approaches for estimating penumbra on CTP
- visible mismatch comparing CBV and CBF = penumbra
- presume that areas with significantly low CBV represent ischaemic core and areas with solely reduced CBF and/or TTP represent penumbra
- reduction of the CBF to 30%–50% relative to mean CBF in contralateral hemisphere
- most reliable predictor of infarct core
- visible mismatch comparing CBV and CBF = penumbra
The CTP Time-Density Curve:
Time−density curve on computed tomography perfusion.
- Time to peak (TTP) = time to apex of curve
- Mean transit time (MTT) = time from wash in to wash out of contrast agent
- Area under the curve = volume of blood (CBV) present at a given moment in a distinct brain area
- Cerebral blood flow (CBF) = gradient of wash in of time−density curve
Reference:
Kurz, K. D. et al. “Radiological Imaging In Acute Ischaemic Stroke”. Eur J Neurol 23 (2015): 8-17.
This blog describes the technique of FDG-PET in measuring brain metabolism in patients in the inter-ictal continuum..
- PET is co-registered to T1 MRI images.
- 10% color gradation (blue [hypo], green, yellow, red [hyper])
- cerebellum set to yellow
- measure maximum standardized uptake value (SUVmax)
- Regions:
- mesial temporal
- basal ganglia
- thalamic
- neo-cortex (frontal, temporal, parietal, occipital)
- SUVmax = voxel of highest SUV for a specified region
- SUV = ratio of radioactivity per voxel expressed as concentration (megaBeckquerel/Kg) divided by injected dose of radiation/Kg body mass
- Regions:
- Options for reference? (reference SUVmax or rSUVmax)
- internal control: 20% relative difference in SUVmax
- if focal: use contralateral homologous region
- cerebellum: compare to total cerebellar SUVmax
- if bilateral: 50% increase of SUVmax relative to cerebellum
- classify hyper- / hypometabolism as
- focal (single region)
- regional (extends to subcortical / adjacent)
- or diffuse (bilateral)
References
Renard, D. et al. “Teaching Neuroimages: FDG-PET In Progressive Supranuclear Palsy”. Neurology74.14 (2010): e60-e60.
Struck, Aaron F. et al. “Metabolic Correlates Of The Ictal-Interictal Continuum: FDG-PET During Continuous EEG”. Neurocritical Care 24.3 (2016): 324-331.
Transtentorial herniation: acute unresponsiveness, decline in GCS >=2 pts with uni- or bilateral pupillary dilatation and loss of reactivity to light, and increase in ICP >20mmHg in acomatose patient x 5 mints +/- change in pupillary sie and reactivity.
Intervention:
- 23.4% saline (30-60 mL bolus) over 5-10 minutes
– well-tolerated in renal failure, no observed pulmonary edema or overload despite high incidence of cardiovascular dysfunction in this population (small study)
Proposed Mechanism of Action: hypertonic saline causes osmolar gradient –> to fluid shifts, reduces brain mass, without significant diuresis
- osmotic diuresis
- vasoconstriction resulting in decreased cerebral volume
- reduced blood viscosity
- improved cerebral perfusion from volume expansion
Potential complications:
- hypotension – most common adverse event
- pulmonary edema
- arrhythmias
- coagulopathy
- hemolysis
- rebound ICP elevation
*mechanism for hypotension: ?not clarified yet, small animal study suggests may be mediated by sympathetic neural reflex and not a diuretic effect; others suggest may be due to vasodilatory effect; or maybe due to resolution of Cushing response
Reference:
Hirsch, Karen G. et al. “Treatment Of Elevated Intracranial Pressure With Hyperosmolar Therapy In Patients With Renal Failure”. Neurocritical Care 17.3 (2012): 388-394.
50% of patients in ICU may have low T3, T4 or TSH. These patients were previously thought to be “euthyroid,” and were thought to have euthyroid-sick syndrome. However, there is evidence that these patients may have acquired transient central thyroid dysfunction.
How to interpret TSH:
- low but detectable (0.05 to 0.3 mU/L) – will be euthyroid when reassessed after recovery
- undetectable (<0.01 mU/L) – 75% have hyperthyroidism
- high (up to 20 mU/L) – some hospitalized patients have transient elevations during recovery from nonthyroidal illness, few have hypothyroidismw hen re-evaluated after recovery
- very high (>20 mU/L) usually have permanent hypothyroidism
Graph below shows changes in thyroid function tests in nonthyroidal illness.
Thyroid function tests should not be measured on critically ill patients, unless thyroid dysfunction is suspected. When thyroid dysfunction is suspected, TSH is inadequate and all methods of assessing free T4 are unreliable in severe critical illness.
Patients who are critically ill with low T3 and T4 and no other clinical signs of hypothyroidism should not be treated with thyroid hormone replacement. Start thyroid replacement if there is evidence of hypothyroidism; in the absence of myxedema coma, start at half the expected full replacement dose.
TREATMENT: No benefit with hormone replacement.
TAKE HOME: Thyroid function should not be checked in critically ill patients unless you have a strong suspicion for thryoidal illness.
Reference:
“Thyroid Function In Nonthyroidal Illness”. Uptodate.com. N.p., 2016. 14 June 2016.
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.
