random clinical notes from pain management and renal service
Epidural steroid injection
methylprednisolone or triamcinolone - less post injection flare
dilute w/local anesthetic for less atrohpy/rupture
3 causes of lumbar stenosis
1. ligamentum flavum hypertrophy
2. disc bulge
3. facet hypertrohpy/osteophyte
chief complaint: i have back pain.
clinical question: should you image?
in light of data indicating false positive findings on normals, one should image only in cases of:
history of trauma
unexplained weight loss
fever
immunosuppression
h/o neoplasm
steroid use
age >70
intravenous drug use
definite change in neurological status
chronic pain -76.2 million people in US
20% of outpatient office visits
12% of prescriptions
untreated pain estimated economic impact ~$100 billion/year
pain categories by etiology
nociceptive (somatic, visceral) - this pain is adaptive (keep you out of trouble)
musculoskeletal/inflammatory/mechanical
neuropathic - (this pain no longer helpful, lingers, remains past point of being informative)
sympathetically mediated
peripheral (post herpetic neuralgia, neuromas)
central (post stroke, phantom limb)
nociceptive afferents come in two categories
peptidergic - calcitonin gene related peptide (CGRP), somatostatin, trkA, trpV1
non-petidergic -purinergic ligand gated ion (Ca++) channels, scn9A (sodium channel)
ascending signals are subject to descending modulation from the following neuroanatomical structures
somatosensory cortex, hypothalamus, peri-aqueductal grey, pons, prefrontal, anterior cingulate, - these descend by DLF (dorsal longitudinal fasciculus)
COMPLEX REGIONAL PAIN SYNDROME
type 1 - RSD - reflex sympathetic dystrophy, no evidence of actual tissue damage
type 2 -causalgia - has an identifiable etiology
treatment - sympathetic block and PT/OT.
a sympathetic block is determined to be successful in the the ipsilateral the skin temperature increases >1 degree C in the distrubution of the nerve. the temperature increases presumably because sympathetics are responsible for sweat, which cool the body by transfer of heat to H2O. side effect - horners syndrome
cervical blocks be aware - 0.5cc of of local into the vertebral artery is all that it takes to cause a seizure
don't do b/l cervical blocks because you can knock out the phrenic nerve
3 things to do to decrease ICP
1. hyperventilate
2. mannitol
3. steroids
acute increased in ICP only 1/3-1/2 will get papilledema
old tenet in medicine, "the real problem is greater than the potential problem"
i don't know if i agree with this all the time!
RENAL STUFF
PTH - catabolic for cortical bone, anabolic for trabecular
osteocalcin - blast marker
c-telopeptide - breakdown product of collagen, an osteoclast marker
alk phos - blast product (marker of mineralization) not metabolized by kidney
SIADH
A - erratic, greatly increased levels of ADH
B- constant ADH leak
C - osmostat reset
D -genetic increase in V2 aquaporin
etiologies of SIADH
cns - stroke, hemorrhage, infection, trauma, psychosis
malignancy - ectopic ADH secretion (usually in small cell lung ca) - a neuroendocrine tumor
drugs - carbamazepine, cyclyophosphamide, SSRI, valproate, ecstasy, interferons
surgery - 2/2 pain, can see triphasic presentation 1. polyuria, 2. siadh, 3. diabetes insipidus
pulmonary - pneumonia (viral bacteria tb)
hormone def - adrenal insufficiency and hypothyroid!!
hiv
treatment
free water restrict
salt tabs and furosemide (to wash out intramedullary gradient and prevent the ability to concentrate urine)
hypertonic saline (only in emergency hyponatremia)
classic blunder: giving IVF to siadh patient, anything fluid given is hypotonic to the patient's urine will only exacerbate free water retention
tolvaptan - V2 receptor antagonist
potent pimpable!
what is the differential diagnosis for increased BUN in the setting of normal GFR?
prerenal
catabolic process
high protein diet
GI bleed or other hemorrhage - (tissue destruction)
glucocorticoids (increases tissue destruction)
tetracycline therapy (decreasing tissue anabolism)
cystatin - a ubiquitous cysteine protease inhibitor looking to challenge creatinine as clinical measure of GFR
patient all of the sudden gone into A-FIB? don't forget about PE on your differential.
40 & 5, 40% O2 and 5cm PEEP - lowest vent settings (either coming off or going on)
