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Einstein EM Case Presentation

Einstein EM Case Presentation. - Kevin Carey 7/ 20. CC: 67yo male BIBEMS after a social worker visited him and reported he was acting lethargic

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Einstein EM Case Presentation

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  1. Einstein EM Case Presentation - Kevin Carey 7/20

  2. CC: 67yo male BIBEMS after a social worker visited him and reported he was acting lethargic HPI: - Pt speaks slowly and appears lethargic but is A&Ox3 and doesn’t understand why the social worker activated EMS. - Has been drinking beer and vodka and abusing cocaine for several days. - Reports: falling and hitting his head 2x, having abdominal pain and a single episode of chest pain. - Denies: Current chest pain, SOB, headaches, episodes of NV, weakness PMHx:- HTN, CKD, Gout- Current Meds unknown-Soc: Denies IVDU Case History

  3. V/S:- T: 97.2 HR: 105 BP: 79/53 RR: 15 O2: 99% on RA Exam:- Gen: Lethargic, slowly answers questions. Requires redirection- Neuro: A&O x 3, No focal deficits, gait not assessed- HENT: Dry mucus membranes, PERRL, EOMI-Cards: S1/S2, No MRG, No JVD- Pulm: CTAB- Abd: Soft, Non-tender, +BS- Ext: +1 Bilateral LE Edema, (No record of DTRs) Case Physical

  4. Differential

  5. Labs: WBC: 5.9H&H: 10.2/32.3Plts: 273 Na: 141K: 8.4Cl: 114CO2: 6.9BUN: 131Crea: 21 (Baseline 1.9)Glu: 120Gap: 20.1 LFTs: WNL UA: +Protein, - RBC, Nitrate LEFeNa: .5% Labs & EKG

  6. Brief Potassium Physiology:- Relative concentrations of intra/extracellular potassium are the major determinants of electrochemical gradients in all living cells - 98% of the body’s potassium is intracellular- Extracellular K+ tightly regulated between 3.5-5.0mEq/L- 90% is renally excreted Causes:- Most frequently seen in ESRD patients who have missed dialysis appointments and patients w/ acute renal failure. - DKA, Rhabdomyolysis (Crush/Burn injuries),Severe Acidosis*Laboratory Hemolysis is the most common cause of an abnormal K+. Hyperkalemia

  7. History: • Weakness, muscle cramps, paresthesias, N/V/D, & palpitations Physical: • Paresthesias, decreased strength, absence of DTRs • Audible arrhythmias • Hyperchloremic Metabolic Acidosis • EKG changes: • Typically occur at a plasma K > 6.5meq • Typical progression: 1) Peaked T-Waves (6.5 -7.5meq)2) Widening of the QRS (7.5 – 8.5meq)3) Loss of P Waves (7.5 – 8.5meq)4)Sine Waves / V-Fib (>10meq)5) Asystole **EKG changes can occur in any order and at varying potassium levels** Signs & Symptoms

  8. Critical Care Medicine, 2008 Treating Severe Hyperkalemia

  9. Who/When do we treat emergently? • Hemodynamically Unstable, EKG Changes or K+ > 6.5 • Suspected spike in K+: Crush injuries, tumor-lysis syndrome How do we treat? 1) Stabilization of the cardiac membrane 2) Redistribute extracellular K+ into cells 3) Eliminate K+ from the body Dispo: • Admission for cardiac and electrolyte monitoring and nephrology consult are required for moderate or severe cases • Home is only an option for mild cases where the patient is hemodynamically stable and has close outpatient follow-up Treatment Overview

  10. Calcium has NO effect on Extracellular K • Calcium Stabilizes Cardiac Myocytes by: 1) Increasing the Threshold Potential 2) Restoring contractility/Vmax 3) Increasing Ca+, increases SA/AV signal propagation • Dosing and Duration- 1 amp of CaGluconate is given over 10min - Effect is theoretically immediate with EKG changes within 3 min- Lasts 30-60min Calcium & Cardiac Stabilization

  11. Insulin-Effects seen within 20 min - Decreases K by 0.6-1.0 mEq/L for 4-6 hours-Given with a bolus of D50 in patients with a glucose < 250 Albuterol (Beta-Agonists)-Effects seen within 30min- Decreases K by 0.6-1.0 mEq/L for 2 hours*Albuterol and Insulin are synergistic and result in a reduction of ~1.2 - 1.5 mEq/L Bicarb- Not effective in reducing extracellular K+ - Should only be used to treat an underlying metabolic acidosis Potassium Redistribution

  12. Furosemide- Onset in ~30min- Patients must be able to make urine Kayexalate- Most common treatment- Cation exchange resin which binds K+ in the gut and releases Na+- 1-2 hours to initial onset with 12 hour fecal potassium output ~31meq Hemodialysis- Most effective treatment. Can remove 25-50 meq per hour- HD the patient if the measures above are insufficient or the hyperkalemia is severe Elimination of Potassium

  13. Treatment Summary

  14. Dx: - Acute on Chronic Kidney Injury 2/2 hypovolemia and cocaine use ED Tx: - Pt received 2L NS, Calcium, Insulin, Kayexalate and a Bicarb drip Outcome: • K was reduced to 6.0 by the time he was transferred to the floor • Pt course complicated by ATN & DTs Our Patient

  15. Who do we treat emergently? • Hemodynamically Unstable, EKG Changes, or K+ > 6.5 • Suspected spike in K+: Crush injuries, tumor-lysis syndrome What do we treat with? • Pneumonic: ABCDE • A: Albuterol • B: BiCarb • C: Calcium • D: Dextrose/Insulin, Diuretics, Dialysis • E: kayExalate Hyperkalemia Take-Aways

  16. Weisberg, L. "Management of severe hyperkalemia" Critical Care Medicine 2008; 36: 3246-3251. Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart Inst J. 2006;33:40–7. AllonM, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869. Mount, David B. Treatment and prevention of hyperkalemia. In: Up To Date, Travis, Anne. UpToDate, Waltham, MA 2012 References

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