By differential diagnosis:
·
Pre-renal
-Hx: Decreased
po intake, over-diuresis, cardiomyopathy (decreased forward flow), sepsis,
hemorrhage, emesis, diarrhea. Increased NSAID use, ACE-I, etc.
-Dx: BUN/Crt
ratio >20, dark, concentrated urine on U/A (perhaps with hyaline casts), dry
on physical exam. Calculate FeNa,
particularly if oliguric. If FeNa
<1% suspect pre-renal. (Difficult to interpret FeNa if patient is on
diuretics)
-Tx: IV
fluids, and stop offending agents, it. NSAIDS and ACE Inh. May need vasopressors in cardiomyopaths.
·
Intrinsic
renal (vascular, glomerular, interstitial—most common are
ATN and AIN)
-Hx: Varies---may
include new medication, recent contrast exposure, or h/o DM, HTN, rheumatic ds
(ie Lupus), HIV etc, prolonged sedentary state (ie. in rhabdomyolysis)..
-Dx: Renal
ultrasound (may show “medical renal ds” or may have asymmetric kidneys), FeNa
(will be >1% in ATN), HIV Ab, C3/C4, RPR, ANA, ANCA, SPEP/UPEP, Hep B
serologies, HCV Ab, Urine Eosinophils (seen in AIN). Examine urine sediment for casts (can use Housestaff lab on
Nelson 4).
-Tx: Stop
offending agents (meds), treat underlying disease. Treat low bicarb with Bicitra or PO NaBicarb. Treat elevated Phos with Renagel with each
meal. Treat low Calcium (correct for
Albumin) with Calcium Carbonate.
-Indications for Emergent Dialysis: Severe Acidemia, Electrolyte abnormalities
not able to be controlled by other measures (kayexalate, etc), intoxications,
volume overload with hemodynamic or respiratory compromise, pericardial
friction rub, symptomatic uremia (ie.
Mental status change).
-When to Consult Renal team??: Consult
Renal if emergent dialysis thought to be necessary or if biopsy thought to be
required in order to make diagnosis.
It’s very helpful to the Renal team if you have all the aforementioned
labs ordered/pending and meds started before you consult them.
·
Post-renal
(BPH, prostate CA, pelvic mass, bladder mass or clot,
etc.)
-Hx: Oliguria
or anuria with elevated Crt and sensation of bladder fullness.
-Dx: Attempt
to pass a Foley catheter. May need to
compress the bladder to remove all the urine if the bladder is quite
distended. Renal Ultrasound.
-Tx: If
not able to get urinary flow after foley is passed, and ultrasound shows
obstruction, should consult Urology. They will definitely require that you
have attempted a foley catheter before they will come to see the patient. Patient may require further medical or
sometimes surgical management.
·
Respiratory
alkalosis: CNS disorders, hypoxia, pulmonary receptor
stimulation (asthma, pneumonia, pulmonary edema, PE), anxiety, drugs (ASA,
theo), liver failure, sepsis, recovery phase of met acidosis
Compensation: Acute: HCO3 decreases 2.0 for every
10mmHg change, in pCO2; Chronic: HCO3 decreases 4-5 for every 10mmHg change in
pCO2
Tx: Treat the
underlying condition (as noted above).
·
Respiratory
acidosis: respiratory center inhibition (opiates, myxedema, O2
in CO2 retainer), neuromuscular disorder (Guillain–Barré, myasthenia gravis,
botulism, hypokalemia), chest wall disorder, airway obstruction, acute and
chronic lung disease
Compensation: Acute:
HCO3 increases 1.0 for every 10mmHg change in pCO2; Chronic: HCO3 increases 3-3.5 for every 10 mmHg
change in pCO2
Tx: Treat
underlying condition. Often requires
Non-invasive ventilation (ie. BiPAP or CPAP) or Intubation.
·
Metabolic
alkalosis:
A. Chloride–responsive (urine
Cl– <10): vomiting, NG drainage, diuretics, post–hypercapneic, cystic
fibrosis, villous adenoma, congenital chloride diarrhea
B. Chloride–resistant (urine
Cl– >20): primary aldosteronism, secondary aldosteronism (CHF, cirrhosis
& ascites, Cushing’s, Bartter’s), congenital adrenal hyperplasia, Liddle’s,
licorice
C. Miscellaneous: poorly
resorbed anion (PCN, carbenicillin), refeeding alkalosis, administration of
alkali (e.g. antacids, overshoot from
Rx of acidosis, massive transfusions with citrate anticoagulant, milk alkali)
Compensation: Metabolic alkalosis: pCO2 increases
0.6-0.7 for each mmol/L change in HCO3
Tx: Treat
underlying condition. Chloride
responsive type is often responsive to IV fluids.
·
Metabolic
acidosis (gap):
Methanol, Uremia, Diabetic
ketoacidosis/starvation/EtOH ketoacidosis, Paraldehyde, INH, iron toxicity,
Lactic acidosis, Ethylene glycol, Rhabdomyolysis, Salicylates
D.
If an AG is present, calculate the gap-gap (delta-gap) = patient’s
anion gap – 12 (normal anion gap). Add this to the measured HCO3. If the result
is >30, then an additional metabolic alkalosis exists. If the result is
<23, then an additional non-gap metabolic acidosis exists.
DDx of low
AG: hypoalbuminemia, halide (Br-, I-) intoxication, severe hyperlipidemia,
multiple myeloma (via hyperparaproteinemia).
Compensation: pCO2 decreases 1.0-1.3 for each mmol/L change in HCO3, or pCO2 =
last two digits of pH
Tx: Treat
underlying condition. Discontinue the
offending agent.May require dialysis in some severe cases.
·
Metabolic
acidosis (nongap)
To differentiate between renal & extra-renal:
calculate the urine anion gap = UNa + UK – UCl. A negative UAG implies the
kidney is appropriately compensating for acidosis by secreting NH4+ (the
unmeasured cation), implying a nonrenal cause. A high UAG implies urinary loss
of unmeasured anion (RTA).
Renal causes (RTAs):
Type II varies proximal HCO3
reabs low/nl varies
Type IV <5.5 distal low
aldo high +
Type I RTA causes: drugs (ampho, Li), chronic
pyelonephritis, obstructive uropathy, nephrocalcinosis, autoimmune (SLE,
Sjogren’s, thyroiditis, cryoglobulinemia, chronic active hepatitis, PBC),
amyloidosis, myeloma. Tx: NaBicarb 1-3 mEq/kg/d
Type II RTA causes: primary (hereditary), myeloma,
amyloidosis, Sjogren’s, PNH, acetazolamide, hyperglobulinemia, heavy metals
(Pb, Cd, Hg, Cu, others). Tx: NaBicarb 10-15 mEq/kg/d
Type IV RTA causes: Addison’s dz, decreased aldo
synthesis heparin or LMWH, ACEI, ARB, CSA, critically ill patients, DM (most
common), NSAIDs, HIV, Aldo antagonists (spironolactone, TMP, pentamidine,
amiloride), obstructive uropathy, sickle cell disease, amyloidosis, AIN.
Tx: NaBicarb
1-3 mEq/kg/d (or correct hyperkalemia)
Nonrenal
causes of Non-gap Acidosis:
Bicarb wasting: GI (diarrhea, ileus, fistula, villous adenoma),
urinary tract diversions (ureterosigmoidostomy, ileal conduit), administration
of chloride-containing acid (HCl, TPN, cholestyramine), posthypercapnia
(transient)
Treatment of
Electrolyte Disorders
- Hypokalemia: keep K> or = 4.0. 10mEq KCL po/iv
increases serum K by 0.1. Replete IV or oral; 80 mEq max at a time per
pharmacy. IV K burns when infused; oral is a very large pill or a bad tasting
powder. Can request small 10 mEq pills from pharmacy. Replete Mg to 2.0 when K is low.
- Hyperkalemia: For K>5.0, kayexalate 15-30gm po
x1, second dose if no BM in 4hrs. For K>6.0, call lab to r/o hemolysis.
Check EKG. Temporize with D50 1amp IV x1, reg insulin 10u IV x1 (cellular
shift) and CaGluconate 1 amp IV x1 (cardioprotective), and albuterol MDI/neb
(cellular shift, via B agonism). Give Kayexalate, recheck potassium.
- Magnesium: keep Mg> or = 2.0; supposedly reduces
ectopy. MgSO4 4gm IV x1 if <1.4; 6-8gm if <1.0. MgOxide good for chronic
outpt repletion, although all PO Mag formulations act as laxatives.
- Calcium: keep Ca>8.5 (corrected for Albumin) or
iCa>1.0. CaGluconate 1-2amp IV; recheck. Also consider Ca carbonate 1300mg
po bid to tid. Ca x PO4 should be <70 to decrease risk of precipitation.
- Phosphate: PO4=1.5-1.9 give 0.125mmol/kg IVPB or Phospho-soda
5ml po bid-tid. PO4 1.0-1.4 give 0.25mmol/kg IVPB. PO4<1.0 give 0.375-0.5
mmol/kg; max 40mmol. For most
patients, 20 mmol of IV Phos will be sufficient to start with. PO formulations
also available as Neutra Phos and K Phos.
Can give 250 mg po tid x 3-6 doses.
Avoid giving Phos in severe hypocalcemia. Low PO4 impairs respiratory fxn.
In DKA replete only if < 1.