clinical pain management notes/ renal notes

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)