CSI (Clinical Scenario Investigation): Hyperkalemia Alison Thomas, RN(EC), MN, CNeph(C) Ann Jones, RN(EC), MSN, CNeph(C) Joyce Hunter, RN, Vascular Access Co-ordinator Simcoe Muskoka Regional Kidney Care Program 12 th Annual Nephrology Education Day, April 27 th, 2011
CSI Objectives review the case of Ms. K., hemodialysis (HD) patient, with K + Examine the physical evidence (labs) Explore the contribution of all possible suspects (causes of K + ) Heighten awareness regarding the clinical importance of exploring all causes of K + in HD patients
Case Review Ms. K. is a 60 year old female with ESRD 2 DM AV fistula loves potatoes Despite dietary counseling, frequent lab results K + ~6.0 Presented to an ER after a fall at home
Physical Evidence: Labs Na 133 K >10 no hemolysis; repeated K = 8.0 HCO 3 21 Urea: 23.9 Creatinine 1074 Glucose, random 7.2 Albumin 38 Hgb 122 g/l WBC 5.78 Platelets 198 Troponin 0.06 range < 0.10 INR 1.03
Signs and Symptoms Weakness Depressed deep tendon reflexes Palpitations Bradycardia Sudden cardiac arrest Nausea Vomiting Paresthesias Generalized weakness Paralysis Fatigue
Normal ECG
K + = 9.4 ECG
K+ : The Suspects FALSE ELEVATIONS TRUE ELEVATIONS - Tight tourniquet - Sample hemolysis - Leukocytosis - Thrombocytosis Decreased or impaired potassium excretion - K + sparing diuretics High K + intake - Supplements, salt substitutes K + shifts out of cells to extracelluar space - Acidosis - Tissue trauma (rhabdomyolysis) - Malignant cell lysis
K + Management Strategies Severe life threatening emergency Protect the heart IV Calcium gluconate or calcium chloride Shift the K + into the cells Bicarbonate, Regular insulin, D50 Facilitate removal of K + from the body GI: cation exchange resin binders Caution: colonic necrosis Urine Hemodialysis Address the underlying cause
Potassium- Quick Review Major electrolyte in the intracellular space (98%); 1 muscle cells Remaining potassium is in the extracelluar fluid Constantly moving in and out of the cell via the Na-K pump Kidney excretes 90% to 95% of daily intake; GI the remainder ~5% http://www.daviddarling.info/encyclopedia/s/sodium-potassium_pump.html
Hemodialysis HD prescription: 1.0 K + dialysate, glucose 8.33 mmol/l, Ca 1.25, HCO 3-40, blood pump speed 400 ml/min Heparin 1000 u bolus; 1000 u/hr Dialyzed for 4 hours Circuit clotted twice Post dialysis lytes = K + 8.4, no hemolysis Why?
K + : The Suspects (Causes) Pseudohyperkalemia X Decreased potassium excretion X High K + intake X K + shifts out of cells X Pt fell; but no rhabdomyolysis no musculoskeletal injuries just dialyzed
Why is her K + still elevated? alarms during HD circuit clotted twice no known prolonged bleeding post HD no difficulty with cannulation What phenomenon should we suspect to be contributing to K +?
New Suspect: Recirculation Definition dialyzed blood returning through the venous needle re-enters the extracorporeal circuit through the arterial needle without returning to the systemic circulation
Hyperkalemia & AV Access AV Access: frequently overlooked as a cause of hyperkalemia Recirculation Stenosis Thrombosis
The Process: AV Access Surveillance Edema of the extremity with AV access Dynamic pressure monitoring Prolonged post venipuncture bleeding Failure of the vein to collapse with elevation of the AV access arm Changes in the thrill or pulse of the access
http://www.kidney.org/patients/plu/plu_online_images/hemodiagram.jpg Access recirculation
Assessing Recirculation Does blood appear to be concentrated/darker than usual during HD; clotted circuits? Flush saline through the circuit: Is saline being pulled in through the arterial access after it leaves the venous needle? Hydraulic compression between the 2 needles http://www.google.ca/imgres?imgurl=http://www.uninet.edu/cin2000/conferences/angoso/angosofig7.gif&imgrefurl=http://www.uninet.edu/cin2000/conferences/angoso/angoso.html&usg= UpXqcByiEEqmXCI60- ffqbish5s=&h=273&w=281&sz=15&hl=en&start=31&zoom=1&tbnid=1ldwkjqb69xy3m:&tbnh=111&tbnw=114&prev=/images%3fq%3dpictures%2bof%2bdialysis%2bav%2baccess%26start%3d20%26hl%3den%26sa%3dn %26tbs%3Disch:1&itbs=1
Hydraulic compression
AV Access Recirculation: Causes Inadequate arterial inflow High grade venous stenoses Improper needle placement Too close AV access flow is less than blood flow in the dialysis machine CSN Guidelines: Jindal, Chan, Deziel, et al., (2006)
20/20 Hindsight What would have been some cues signaling the occurrence of something going on with Ms. K s access prior to her visit to ER? Log sheets Dynamic pressure monitoring Kt/V, PRU
Dynamic Pressure Monitoring First 2 to 5 minutes Do not activate UFR Set blood flow rate 200 ml/min Goal to enable early identification of stenoses within the AV access
Dynamic Pressure Monitoring Review HD log sheet trends of arterial and venous pressures AP,VP ranges: depend on the needle gauge being used Must show a trend outside of the target range 3 times in succession
Needle Gauge and Dynamic Pressure Monitoring Needle Qb (ml/min) Range 14g 200 A= -50 to -70 V= 50 to 70 15g 200 A= -70 to -90 V=70 to 90 16g 200 A= -90 to -120 V= 90 to 120 17g 200 A= -120 to -150 V= 120 to -150
Log Sheet: Dynamic Pressure Monitoring Time BP Target Loss UF rate Total fld removed Blood Flow ml/min Arterial Pressures Venous pressures 200-10 110 0740 150/84 1.6 L 0.4-370 -70 200 0840 162/85 1.6 L 0.4-400 360-100 210 0940 155/85 1.6 0.4-800 360-120 230
Log Sheet: Dynamic Pressure Monitoring Time BP Target Loss UF rate Total fld removed Blood Flow ml/min Arterial Pressures Venous pressures 200 0 110 0805 142/84 2.6 L 0.65-370 -70 200 0905 126/71 2.6 L 0.65-700 360-100 210 1005 138/84 2.6 L 0.65-1300 360-80 240
Log Sheet: Dynamic Pressure Monitoring Time BP Target Loss UF rate Total fld removed Blood Flow ml/min Arterial Pressures Venous pressures 200-10 130 0800 137/74 2.4 L 0.6-370 -70 200 0900 139/69 2.4 L 0.6-600 360-100 210 1000 118/64 2.4 L 0.6 1200 340-90 240
Relationship between Access Flow and Venous and Arterial Pressures A V Blood flow Stenosis at arterial anastamosis Qb = 200 ml/min Expect to see high negative arterial pressures, low venous pressures
Relationship between Access Flow and Venous and Arterial Pressures A V Blood flow Stenosis risk of access thrombosis Qb = 200 ml/min in the first 2 to 5 minutes Expect to see normal or normal /low venous pressures Low (near zero) arterial pressures
Relationship between Access Flow and Venous and Arterial Pressures A V Blood flow Stenosis at venous outflow Qb = 200 ml/min Expect to see low (near zero) arterial pressures, high venous pressures
Impression and Plan K + secondary to access recirculation Cues were present with low AP and elevated VP over 3 consecutive HD sessions Angioplasty: multiple recurrent stenoses in venous outflow and at cephalic arch stent Follow-up access flows and recirculation ASAP post intervention Monthly access flows and recirculation studies
Final Thoughts RNs role is invaluable in early detection and early intervention of the potentially lethal impact of hyperkalemia With hyperkalemia, consider all potential sources: Intake Output Meds Dialysis Access Underlying medical condition
Final Thoughts Dialysis Access Evaluate trends in arterial and venous pressures at BPS 200 ml/min Follow-up reason for changes in PRU/Kt/V Check access flows and recirculation routinely, prn Become familiar with patient s access history, recurrent interventions, frequency of the interventions Do access flows ASAP after intervention Is it time to consider another access?
Final Thoughts Ongoing monitoring at the bedside, assessing trends in addition to correcting stenosis may : improve patency rates of the AV access reduce the risk of access thrombosis reduce rate of access failure (KDOQI, 2006)
References Jindal, K. Chan, C.T., Deziel, C., Hirsch, D, Soroka, S.D., Tonelli, M, Culleton, B. (2006). Candaian Society of Nephrology Clinical Practice Guidelines. Vascular Access. Journal of American Society of Nephrololgy, 17: S1 S27. National Kidney Foundation 2006 Updates Clinical Practice Guidelines and Recommendations. Vascular Access Guideline 4.
Acknowledgements St. Michael s Hospital : Hemodialysis nurses, physicians (Marc Goldstein and Sandra Donnelly) Multidisciplinary team