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Einstein EM Case Presentation

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Presentation on theme: "Einstein EM Case Presentation"— Presentation transcript:

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…

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