CCRN · Endocrine, Hematology/Immunology, GI, Renal/GU, Integumentary · 8 min read
Dialysis, CRRT, CKD and Urosepsis
- Differentiate continuous renal replacement therapy modalities, circuit pressures, and regional citrate anticoagulation management in unstable adult patients.
- Identify and manage acute complications associated with intermittent hemodialysis, vascular access, and chronic kidney disease uremic syndromes.
- Formulate critical care nursing priorities for early recognition, diagnostic sampling, and protocolized resuscitation in acute pyelonephritis, urosepsis, and septic shock.
Indications for RRT and CRRT Modalities and Mechanics
Urgent renal replacement therapy is indicated when life-threatening disturbances cannot be corrected with medical therapy alone. In the intensive care unit, key indications for urgent initiation include refractory metabolic acidosis, life-threatening hyperkalemia, selected dialyzable drug toxicities, refractory fluid overload, and symptomatic uremia. While intermittent hemodialysis clears solutes rapidly, continuous renal replacement therapy is preferred for critically ill patients experiencing hemodynamic instability because it removes fluid and solutes gradually, minimizing sudden shifts in intravascular volume and osmolality.
Continuous modalities vary in their primary mechanisms of clearance and fluid movement. Slow continuous ultrafiltration removes plasma water via hydrostatic pressure gradients without utilizing dialysate or replacement fluid. Continuous veno-venous hemofiltration clears solutes primarily by convection; clearance of middle molecules depends on the membrane, whereas clearance of large molecules is limited. Continuous veno-venous hemodialysis clears small molecular weight solutes primarily through diffusion driven by a countercurrent dialysate flow. Continuous veno-venous hemodiafiltration combines both convection and diffusion by utilizing dialysate fluid and replacement fluid simultaneously.
The location of replacement fluid administration profoundly impacts both circuit longevity and clearance efficacy. Administering replacement fluid pre-filter dilutes blood entering the hemofilter, which prolongs filter life but reduces solute clearance efficiency. Conversely, administering replacement fluid post-filter maximizes solute clearance efficiency but increases blood viscosity within the circuit, raising the risk of circuit clotting. Because extensive solute removal occurs during continuous therapies, the critical care nurse must monitor for severe hypophosphatemia and hypokalemia caused by excessive clearance into the effluent fluid.
Continuous monitoring of circuit pressures is vital to anticipate filter failure and circuit disruption. A rising transmembrane pressure at unchanged flow settings may suggest reduced filter permeability from protein deposition or clotting; assess pressure trends and circuit settings rather than attributing the change to one cause. A rising filter pressure drop at a stable blood-flow rate suggests increasing resistance within the hemofilter, often from clotting, and warrants prompt circuit assessment. Pressure trends can suggest access or circuit problems: a more negative access pressure may indicate impaired inflow, and a falling venous return pressure may indicate a disconnection or leak; because alarms may not detect every disconnection, inspect the circuit and patient promptly. The nurse must assess the circuit and the patient promptly whenever these alarms occur.
| Modality | Primary Clearance Mechanism | Dialysate Fluid | Replacement Fluid |
|---|---|---|---|
| Slow Continuous Ultrafiltration (SCUF) | Hydrostatic pressure gradient (ultrafiltration only) | None | None |
| Continuous Veno-Venous Hemofiltration (CVVH) | Convection (middle molecule clearance membrane-dependent) | None | Required (pre-filter or post-filter) |
| Continuous Veno-Venous Hemodialysis (CVVHD) | Diffusion (countercurrent flow for small molecules) | Required | None |
| Continuous Veno-Venous Hemodiafiltration (CVVHDF) | Combined convection and diffusion | Required | Required |
Common mistakes
- Assuming normal platelet counts rule out uremic bleeding; retained uremic toxins impair platelet adhesion and aggregation, causing bleeding despite normal platelet numbers.
- Delaying broad-spectrum antimicrobial administration while waiting to collect blood and urine cultures in suspected urosepsis.
- Assuming that a low urine output (below 0.5 mL/kg per hour) in sepsis always indicates fluid responsiveness rather than assessing for hypoperfusion, acute kidney injury, or obstruction.
- Administering oral phosphate binders between meals rather than with meals, which prevents them from binding dietary phosphorus within the gastrointestinal tract.
Key points
- Indications for urgent renal replacement therapy include refractory metabolic acidosis, life-threatening hyperkalemia, selected dialyzable drug toxicities, refractory fluid overload, and symptomatic uremia.
- Continuous renal replacement therapy is preferred over intermittent hemodialysis in hemodynamically unstable patients; CVVH relies primarily on convection, CVVHD on diffusion, and CVVHDF on both.
- Regional citrate anticoagulation binds ionized calcium in the circuit; a rising total-to-ionized calcium ratio, particularly above 2.5, suggests citrate accumulation, which may increase calcium requirements and cause systemic ionized hypocalcemia or metabolic acidosis.
- Vascular access must be protected: assess arteriovenous fistulas and grafts every shift for a thrill and bruit, avoid blood pressures or punctures on the access extremity, and report acute loss of bruit or thrill immediately.
- Uremic pericarditis may cause positional or pleuritic chest pain and a pericardial friction rub, but these findings and classic diffuse ST-segment elevation may be absent; suspected cases require urgent provider evaluation for renal replacement therapy.
- Septic shock resuscitation includes about 30 mL/kg of balanced crystalloid within three hours, titrating norepinephrine as the first-line vasopressor to a mean arterial pressure of at least 65 mm Hg, and considering vasopressin at a fixed dose of 0.03 units per minute.
- Urine output below 0.5 mL/kg per hour in sepsis demands comprehensive evaluation for acute kidney injury, hypoperfusion, or obstruction rather than an assumption of fluid responsiveness.
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