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- Kevin Carey 7/20. CC: 67yo male BIBEMS after a social worker visited him and reported he was acting lethargic HPI: - Pt speaks slowly and appears lethargic.

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Presentation on theme: "- Kevin Carey 7/20. CC: 67yo male BIBEMS after a social worker visited him and reported he was acting lethargic HPI: - Pt speaks slowly and appears lethargic."— Presentation transcript:

1 - 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

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)

4 Cards: - Cocaine induce MI - Hypovolemia Metabolic: - Electrolyte abnormality - Toxic Alcohol Infectious: - SIRS Neuro: - Subdural Pulm: - PE GI: - Pancreatitis

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

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 mEq/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+.

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 ( meq) 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**

8 Critical Care Medicine, 2008

9 Who/When do we treat emergently? - Hemodynamically Unstable, EKG Changes or K+ > 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

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 Ca Gluconate is given over 10min - Effect is theoretically immediate with EKG changes within 3 min - Lasts 30-60min

11 Insulin - Effects seen within 20 min - Decreases K by 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 mEq/L for 2 hours *Albuterol and Insulin are synergistic and result in a reduction of ~ mEq/L Bicarb - Not effective in reducing extracellular K+ - Should only be used to treat an underlying metabolic acidosis

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 hours to initial onset with 12 hour fecal potassium output ~31meq Hemodialysis - Most effective treatment. Can remove meq per hour - HD the patient if the measures above are insufficient or the hyperkalemia is severe

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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

15 Who do we treat emergently? - Hemodynamically Unstable, EKG Changes, or K+ > 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

16 Weisberg, L. "Management of severe hyperkalemia" Critical Care Medicine 2008; 36: Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart Inst J. 2006;33:40–7. Allon M, 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


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