- Kevin Carey 7/20

*Einstein EM Case Presentation

*Case History

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 Physical

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)

*Differential

Cards:- Cocaine induce MI- HypovolemiaMetabolic:- Electrolyte abnormality- Toxic AlcoholInfectious:- SIRS

Neuro:- SubduralPulm:- PEGI:- Pancreatitis

*Labs & EKG

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%

*HyperkalemiaBrief 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+.

*Signs & SymptomsHistory:

- 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**

*Treating Severe HyperkalemiaCritical Care Medicine, 2008

*Treatment OverviewWho/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

*Calcium & Cardiac Stabilization- 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

*Potassium RedistributionInsulin

- 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

*Elimination of Potassium 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

*Treatment Summary

*Our PatientDx: - 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

*Hyperkalemia Take-AwaysWho 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

*ReferencesWeisberg, 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.

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