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

2. 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

3. 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)

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

5. Labs & EKG
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. Hyperkalemia
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+.
Also Involved in Acid Base Balance (exchange of K+ for H+ is a buffer)
Intracellular shift can be seen in pts w/ uncontrolled diabetes
Look for dialysis signs (fistulas/grafts) - Three Main causes: 1) Excretion, 2) Excessive release from cells, 3) Excess intake

7. Signs & Symptoms 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**
Note, these symptoms are seen in mod. -> severe hyperkalemia. More milder cases may be asymptomatic
Hyperkalemia affects the kidneys ability to create ammonia and excrete H+ causing the hyperchloremic metabolic acidosis
T Waves follow K+

8. Treating Severe Hyperkalemia
Critical Care Medicine, 2008
Electrolyte levels should be repeated every 2-4 hours until normalized

9. Treatment Overview 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
Electrolyte levels should be repeated every 2-4 hours until normalized

10. 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
Paper, Winkler - Potassium increases resting membrane potential and inactivates some of the fast acting sodium channels
- CaCl can cause tissue necrosis - Repeat dose if no EKG effect seen

11. Potassium Redistribution
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
Insulin: - 10U of insulin
- Infusion given to prevent hypoglycemia at 60min
Albuterol:
- High Dose (10-20mg)
Tachycardia, avoid in CAD
Genetic component, possibly 40% of patients will not respond
Tertbutaline IM an option
Both:
Transient
Down side of shifting K+ into the cell is you reduce the amount excreted
Bicarb - Originally believed to shift via H+/K+ channels

12. 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 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

13. Treatment Summary
Diuretics - require the patient to be able to make urine

14. Our Patient
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
With good outpatient

15. Hyperkalemia Take-Aways
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
Suspect: fistula, graft sites etc…

16. References
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
Suspect: fistula, graft sites etc…