Renal: Treatments Flashcards
hypovolemia
goal=hemodynamic stability
- treat underlying problem
- treat volume deficit
- address ongoing losses
- be aware of co-morbidities
- 0.9% NaCL 1st line– to expand ECF—- ONE LITER WILL INCR PLSAMA VOLUME BY 200 mL while the rest goes interstitially
- blood/products
* ***multiple studies show no benefit to albumin/colloids vs NSS
hypervolemia
fix underlying problem
- restrict salt and fluids
- diuresis if volume is causing significant clinical problems–> SOB for ex
hypotonic hypovolemic hyponatremia
volume replacement–>NSS 0.9% IV and tx undrelying cause
hypotonic hypervolemic hyponatremia
. volume removal–>diruetics, sodium + water restriction
hypotonic isovolemic hyponatremia
water restriction
fix underlying cause
SIADH
3% NSS
Severe hyponatremia
IV HYPERtonic saline + furosemide
-be so so so cautious about rate to avoid cerebral pontine myelinolysis
symptomatic hyponatremia without severe s/s
serum NA not raised >4-6 mEq/L in 24 hours
- rate no greater than 0.5 mEq/hr
- fluid restriction
symptomatic hyponatremia with severe s/s
100 mL bolus or 2ml/kg bolus infusion of 3% NSS at a rate of 1-2 ml/hr/kg
rate should not be greater than 1 mEq/hr
chronic symptomatic hyponatremia
TX
-no greater than 8 mEq/24 hours
hypernatremia
- Hypotonic fluids–>pure water PO, D5W, 0.45% NS, 0.2% saline
* pref route is PO or tube feeding - isotonic fluids if hypovolemic—- NSS or LR
* then switch to hypotonic fluids to correct hyponatremia once volume is repleated
**8Rapid correction (>0.5 mEq/L/hr) can result in cerebral edema
tx goals for HYPERVOLEMIC
-gradually correct hyperNA using NA restriction, diuresis (loops), water replacement or hemodyalysis
tx goals for HYPOVOLEMIC
- significant volume depletion ie shock–>isotonic NaCl at rate no more than 10mEq/24 hrs
- rate of correction 0.5 mEq/Hr
- fluids to use: D5W, 0.2% NACL or 0.45% NACL
DI
central
nephrogenic
- volume replacement
- central: DDAVP
- nephrogenic: thiazides and salt restriction, amiloride for lithium pt, and NSAIDs
pseudohyperkalemia
no tx
-re-do sample
hyperkalemia
- stabilize cardiac membrane
* IV Calcium gluconate (or Calcium chloride)—.CONTRAINDICATED WITH DIGOXIN TOXICITY
* does not lower K+ but protects against arrhythmias - Drive K+ back into cell:
* IV insulin with glucose
* high dose beta 2 agonists–albuterol nebs
* Bicarb if patient is acidotic
* Resin Binder–>K+ removal
* diuretics–loop and thiazides if kidney function normal
* Sodium Polysteryene sulfonate—removes K from body via bowel movement
* DIALYSIS IS FASTEST AND MOST EFFECTIVE
hypokalemia
STOP THE LOSSES
- for each decrease of 1.0 mEq/L there is a K+ deficit of approx 100 mEq/L
1. Asympto/mild–>PO K+
- SEVERE:
* SLOW IV potassium chloride (usually 10-20 mEq/L/hr)
* peripheral infusions >40 mEq/L/hr can lead to burning, sclerosis or phlebitis - if patietns dont respond– always check the mag
- montor cardiac status
*do not add glucose or sodium bicarb to solutions initially bc they cause intracellular intake of K+
Metabolic acidosis
ECLS
Emergency
- assess need for ventilation or cardiopulmonary resusitation
- check electrolyte abnormalities—HYPERK ***
Cause
- tx underlying cause
1. lactic acidosis—tx the sepsis
2. DKA–tx diabetes and check for causes like infection
3. ETOH ingestion/poisoning–ethanol/methanol
4. Uremia–tx renal failure
5. salicylate OD–>alkalinize urine +/- hemodialysis
Losses
- repalce fluid and electorlyte losses
- remember giving bicarb not always necessary
Specifics
*tx specific problems to underlying cause
when would you give biacarb for metabolic acidosis
ESRD—CKD stages 2-4
DKA–only for extreme cases
Lactic acidosis with pH < 7.0
IGA nephropathy
ACEI, ARGS
- lipid lowering therapy
- corticosteroids 6 MO
post infectious GN
- manage the renal effects—renal insuff, HTN (Nifedipine)
- ABX –>PCN for strep
- NO STEROIDS
- referral to nephrology might need HD
MPGN
- underlying cause— HEP C etc
- monoclonal gammopathy
- ACEI
Wegenrs aka Granulomatosis Polyangiitis
- steroids alone–mild
- moderate-severe: steroids + immune modulators
- severe pulmonary hemorrahge/renal dz or not respoidng to above tx–> Plasma exchange
Goodpastures
- plasmaphoresis + prednisone
* anti-GBM abs
general tx for nephrotic syndome
-1st line tx for minimal change dz
- immunosupresive therapy
* steroids
* immunomodulators - PU
* goal=lower intra glomerular pressure–>reduction in protein excretion
* ACEI* or ARBS
* want efferent arteriolar diltion–>reduces renal blood flow, GFR and protein loss - Hyperlipidemia
* diet mod
* statins - Edema
* thiazides or loops
* 1 liter fluid and NA restriction
MINIMAL CHANGE
1st line=glucocorticoids—prednisone
FSGS
-steroids—prenisone 1st line
ACEI to reduce PU
membranous nephropathy
Patients at moderate to high risk should be treated with a combination of glucocorticoids and cytotoxic therapy (cyclophosphamide). Those at low risk can be treated with ACE-Is. Lipid-lowering agents should be used in cases of persistent nephrotic syndrome.
RAS
- MEDS FIRST
1. ACEI or ARB - ->contra for bilateral RAS or if PT with a solitary kidney
2. Add on tx= thiazides, long acting CCB, mineralcorticoid receptor angatonist - SURGICAL
1. revascularization definitive tx—angioplasty or bypass
2. can also do a stent
