28. Acute renal failure
Causes
- Prerenal: decreased effective arterial volume (hypovolemia, CHF, sepsis), ACE-I, NSAIDs
- Acute tubular necrosis (ATN): progression of prerenal state, drugs (aminoglycosides, ampho, cisplatin), myo- or hemoglobinuria, multiple myeloma. Sediment: muddy brown granular casts
- Contrast-induced acute renal failure: peaks in 3-5 days, resolves in 7-10 days
If high-risk: pre- and post- hydration and N-acetylcysteine 600 mg po bid on day prior to and day of contrast with iv hydration
- Acute interstitial nephritis (AIN): drugs (antibiotics, NSAIDs) or infection; sediment: WBC casts, WBCs, RBCs; may be associated with fever, rash, eosinophilia, and eosinophiluria
- Vascular: RAS (+ ACE-I), thrombosis, hypertensive crisis, scleroderma, cholesterol emboli, HUS/TTP, preeclampsia
- Acute glomerulonephritis: sediment may show dysmorphic RBCs and RBC casts
- Post-renal: obstruction (malignancy, BPH, bilateral stones), neurogenic bladder, anticholinergics
Workup
- Degree of and type of workup varies depending on history
- Examine urine sediment
- Determine if patient is oliguric/anuric (output <400 mL/24 hrs)
- Fractional excretion of sodium (FENa); refer to formulae section
<1% suggests prerenal, contrast, or pigment nephropathy
>1% suggests ATN
Diuretics may elevate FENa even if patient is prerenal
- Urine eosinophils (if AIN suspected)
- SPEP, urine for protein electrophoresis and Bence-Jones protein
- Glomerular disease suspected: ANCA, ANA, anti-GBM, ASLO, cryocrit
- C3, C4 to differentiate low-complement immune complex disease (endocarditis, SLE, MPGN, PSGN, cryoglobulinemia, visceral abscess) from normal complement immune complex disease (IgA nephropathy/HSP, fibrillary GN); complement levels can also be low in setting of cholesterol emboli
- Ultrasound useful in evaluating for hydronephrosis and determining chronicity of renal disease
- Biopsy may be needed if cause remains unclear
Management
- Optimize hemodynamic factors (fluids if hypovolemic, pressors if hypotensive, etc.)
- Avoid nephrotoxins (e.g. contrast, nephrotoxic drugs)
- Watch for and correct electrolyte (hyperkalemia, hyperphosphatemia) and acid/base disturbances
- Check medication dosing frequently and adjust for renal function
- Consider dialysis if refractory to medical management
- Specific treatments:
AIN: stop offending agent, consider steroids
Scleroderma renal crisis: ACE-I
HUS/TTP: plasma exchange
Glomerulonephritis: steroids, immunosuppressive drugs may be needed; discuss with renal fellow early if suspected
Postrenal: remove obstruction
MGH Medical Housestaff Manual1
29. Dialysis
Emergent indications
- Acidosis (refractory to medical management)
- Electrolyte imbalances (refractory to medical management), generally hyperkalemia, and hypercalcemia (Ca >18), tumor lysis syndrome (in settings of very high uric acid)
- Intoxications. Lithium, salicylates, theophylline, alcohols
- Overload (volume)
- Uremia (with complications, e.g. pericarditis)
Hemodialysis (HD)
- Principle. Blood flows along one side of a semipermeable membrane, dialysate along the other. Fluid removal occurs via pressure gradient. Solute removal occurs via concentration gradient, and in a manner inversely proportional to molecular size (effective at removing potassium, urea, creatinine but not very effective for removing PO4).
- Access. Double-lumen central catheter (tunneled or temporary), AV fistula, or AV graft
- Contraindications. Hemodynamic instability (see CVVH), arrhythmias, bleeding
- Complications. Hypotension (from ultrafiltration, medication, temperature of dialysate, bleeding, infection, arrhythmia, ischemia), arrhythmias, HIT, access complications
Continuous veno-venous hemofiltration (CVVH)
- Indications. Patients who are hemodynamically unstable and who are not likely to tolerate the large fluid shifts associated with HD
- Principle. Blood flows along one side of a highly permeable membrane and fluids and solutes pass by convection. Filtrate is discarded and fluid with plasma-like solute concentrations is infused. Fluid balance is precisely controlled by adjustment of the quantity of replacement fluid infused.
- Anticoagulation by citratev. heparin and bicarbonate. Citrate achieves regional anticoagulation by calcium chelation (metabolized in liver); contraindication is liver failure. Need to watch calcium levels and citrate toxicity (suggested by rising total calcium, falling ionized calcium, rising anion gap).
- Complications. Hypotension, hypophosphatemia, hypocalcemia, access complications
Peritoneal dialysis
- Principle. Gravity assisted infusion into peritoneum; control H2O and Na balance by adjusting the glucose concentration in the fluid; very long dwell times pull out less fluid as the glucose equilibrates
- Access. Catheter placed by transplant surgery generally.
- Contraindications. Recent abdominal surgery, infection, ileus
- Orders: PD fluid: 1.5%, or 2.5 %, or 4.25% dextrose (higher dextrose removes more fluid)
- Typical prescription. Volume 2 L, dwell time 6 hours, dextrose 1.5% for a total of 4 exchanges in 24 hour period. Prescription written generally by peritoneal dialysis nurse (PD unit 617-720-1317). PD nurse on call 24/7 for any issues.
- Complications
Infection: fairly common. Can occur at exit site, tunnel, and/or peritoneum. Catheter removal may be necessary especially if fungal infection. Diagnose by finding >100 WBC with >50% PMN in fluid. 50-60% infections are GPC, 15-20% GNR, remainder are fungal or no identifiable organism. Can treat with either intravenous or peritoneal antibiotics.
Hyperglycemia: exacerbated by inflammation, long dwell time, and higher dextrose concentrations. Treat by adding insulin sc
Clots: add heparin in first few infusions (but involve renal)
MGH Medical Housestaff Manual1
30. Acid-base
General considerations
- Determine if patient is alkalemic (pH>7.44) or acidemic (pH<7.36)
- Determine if process is metabolic or respiratory
- Acidemia
pCO2 >40 respiratory acidosis
HCO3 <24 metabolic acidosis
- Alkalemia
pCO2 <40 respiratory alkalosis
HCO3 >24 metabolic alkalosis
Metabolic acidosis
- Check the anion gap: Na – (Cl + HCO3). Normal is ~7 to 13
in hypoalbuminemia, “expected” AG lower by 2.5 for every 1 g/dL reduction in albumin.
- The diagnostic utility of a high AG is greatest when the AG is above 25 mEq/L
- If AG elevated, look for causes of AG acidosis: ketones, lactate, renal failure, methanol, ethylene glycol, ethanol, paraldehyde, salicylates
- Calculate ( anion gap/ HCO3), i.e. ratio of ∆AG (measured AG expected AG) to ∆HCO3 (24 HCO3).
If / = 1, suggests pure gap met acidosis (i.e. lactic acidosis)
If / <1, suggests mixed gap/non-gap metabolic acidosis
If / >1, suggests underlying metabolic alkalosis in addition to the metabolic acidosis
- If AG not elevated, check urine anion gap [Na + K – Cl].
In normal subjects, urine AG is positive or near 0
Positive urine AG suggests renal etiology, e.g. renal tubular acidosis type I or IV.
Negative urine AG, suggests diarrhea, recent saline administration, recently resolved respiratory alkalosis, RTA II, acetazolamide; rarely: ureteral diversions and pancreatic fistulas
Metabolic alkalosis
- Check urine Cl (avoid measuring while diuretics are active)
- UCl < 20 suggests saline-responsive metabolic alkalosis: prior diuretic use, volume depletion, vomiting, NGT drainage, villous adenoma, resolved respiratory acidosis
- UCl > 20 and euvolemia suggests saline-resistant metabolic alkalosis:
if hypertensive: hyperaldosteronism, Cushing’s syndrome, licorice ingestion, Liddle’s
if normotensive: extreme hypokalemia, exogenous alkali, Bartter’s, Gitelman’s
Respiratory acidosis
- CNS depression, especially from medications
- Airway disease: COPD, asthma, upper airway abnormalities
- Neuromuscular disease
- Parenchymal lung disease: pneumonia, pulmonary edema, restrictive lung disease
- Thoracic cage abnormalities: pneumothorax, kyphoscoliosis
Respiratory alkalosis
- Any cause of hypoxia causing increased respiratory drive (e.g. pneumonia, pulmonary embolism, pulmonary edema)
- Pain, anxiety
- Salicylates
- Pregnancy/progesterone
- Sepsis
- Liver failure
- Primary CNS disorder
MGH Medical Housestaff Manual1
31. Sodium disorders
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32. Potassium disorders
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33. Hyperkalemia treatment
EKG changes in hyperkalemia
- Patterns best seen in leads V4-5
- Correct diagnosis can usually be made when K > 6.7.
K / EKG changes
> 5.5 / peaking in T waves
> 6.5 / QRS widening
> 7 / P wave amplitude decreases, duration of P wave increases, prolongation of PR interval
> 8 / P wave disappears, auricular standstill
> 10 / ventricular rhythm may become irregular and may simulate atrial fibrillation
> 12-14 / asystole or ventricular fibrillation
General considerations
- Interpatient variability in effects of hyperkalemia, time course of hyperkalemia (e.g., end stage renal disease vs. acute tissue break down)
- K > 7, EKG changes, changes in muscle strength generally warrant immediate treatment
Therapy / Dose / Onset of effect / Duration of effect / Comments
Calcium / 10 mL (1 amp) of 10% calcium gluconate or calcium chloride solution infused over 2-3 min / 1-3 min / 30-60 min / Stabilizes cardiac membrane
Caution in patients taking digoxin as hypercalcemia can induce digitalis toxicity
Sodium bicarbonate / 1 mEq/kg iv bolus (1 amp of sodium bicarb ~45 mEq) / 5-10 min / 1-2 hours / K lowering most prominent in metabolic acidosis
Insulin and glucose / 10 U iv plus D50 1-2 amps (note more than 1 amp may be needed to prevent hypoglycemia) / 30 min / 4-6 hours / Enhances Na-K-ATPase pump in skeletal muscle
Causes 0.5-1.5 mEq/L fall in K
Albuterol, nebulized / 10-20 mg nebulized over 15 min / 15 min / 15-90 min / Drives potassium into cells by increasing Na-K-ATPase activity
Lowers K by 0.5-1
Kayexalate (Na polystyrene sulfonate) / 15-50 g po or pr, plus sorbitol / 1-2 hours / 4-6 hours / Binds K in gut and releases Na
Diuresis / Furosemide 40-80 mg iv
Dialysis / Consider dialysis when conservative measures fail, if hyperkalemia is severe, or if ongoing hyperkalemia a likely issue
MGH Medical Housestaff Manual1