How should I manage a 68‑year‑old man with daily cocaine use, intermittent dyspnea, normal vital signs, markedly elevated B‑type natriuretic peptide, metabolic acidosis, impaired renal function (estimated glomerular filtration rate 31 mL/min/1.73 m²), hypoalbuminemia, mildly elevated transaminases, subclinical hyperthyroidism, and modest hyperkalemia?

Management of a 68-Year-Old Man with Daily Cocaine Use and Multi-Organ Dysfunction

This patient requires immediate cardiac evaluation with ECG and consideration for coronary angiography given the markedly elevated BNP (1729 pg/mL), daily cocaine use, and dyspnea, while simultaneously addressing acute kidney injury, metabolic acidosis, and subclinical hyperthyroidism through a structured, prioritized approach.

Immediate Cardiac Assessment and Management

Primary Cardiac Evaluation

• Obtain a 12-lead ECG immediately to assess for ST-segment changes, as cocaine-induced acute coronary syndrome (ACS) requires specific management distinct from typical ACS 1.
• The markedly elevated BNP (1729 pg/mL) in the context of daily cocaine use suggests either cocaine-induced dilated cardiomyopathy or acute heart failure, both of which require urgent evaluation 2.
• Measure serial cardiac troponins at presentation and 3-6 hours later, as troponin I or T are more specific for myocardial injury than CK-MB in cocaine users (CK-MB can be elevated from rhabdomyolysis and skeletal muscle activity) 1, 3.

Cocaine-Specific Cardiac Management

If the ECG shows ST-segment elevation or depression:

• Administer sublingual or IV nitroglycerin AND IV or oral calcium channel blockers (e.g., diltiazem 20 mg IV) as first-line therapy 1, 3.
• Avoid beta-blockers entirely in the acute setting, as they worsen coronary vasoconstriction through unopposed alpha-adrenergic activity 1, 3.
• If ST-segments remain elevated after nitroglycerin and calcium channel blockers, proceed to immediate coronary angiography if available 1.

If the ECG shows normal or minimal ST-segment changes:

• Administer nitroglycerin or oral calcium channel blockers as beneficial therapy 1.
• The patient can be managed in a chest pain observation unit for 9-12 hours with serial troponins and continuous ECG monitoring 3.

Critical caveat: Combined alpha/beta blockers (e.g., labetalol) may only be considered if hypertension (>150 mmHg systolic) or tachycardia (>100 bpm) persists AND only after a vasodilator has been given within the previous hour 1.

Renal Management

Acute Kidney Injury Assessment

• The eGFR of 31 mL/min/1.73 m² with elevated creatinine (2.24 mg/dL) and BUN (30 mg/dL) indicates Stage 3b chronic kidney disease or acute-on-chronic kidney injury 1.
• Calculate creatinine clearance using the Cockroft-Gault formula (not MDRD) to guide medication dosing adjustments, as many cardiovascular drugs are renally cleared 1.
• The BUN/creatinine ratio of 13 suggests intrinsic renal disease rather than prerenal azotemia, consistent with cocaine-induced nephrotoxicity 4.

Cocaine-Related Renal Complications

• Cocaine can cause acute kidney injury through multiple mechanisms including rhabdomyolysis (check CPK levels), thrombotic microangiopathy, and direct nephrotoxicity 5, 4.
• Screen for rhabdomyolysis by measuring creatine phosphokinase (CPK), as cocaine-induced rhabdomyolysis commonly presents with elevated CPK, acute kidney injury, and metabolic acidosis 5, 4.
• If thrombocytopenia develops or worsens, measure ADAMTS13 activity immediately to exclude thrombotic thrombocytopenic purpura, which requires plasma exchange 6.

Medication Dosing Adjustments

• Adjust doses of all renally-cleared cardiovascular medications including antiplatelet agents, antithrombin agents (UFH, LMWH), and GP IIb/IIIa inhibitors based on Cockroft-Gault creatinine clearance to prevent excessive dosing and bleeding risk 1.

Metabolic Acidosis Management

Acidosis Evaluation

• The CO2 of 17 mEq/L indicates metabolic acidosis, likely from cocaine-induced lactic acidosis, renal dysfunction, or both 5.
• Calculate the anion gap using: Anion gap = Na - (Cl + CO2) = 139 - (110 + 17) = 12 mEq/L (normal to mildly elevated) 5.
• The metabolic acidosis combined with acute kidney injury suggests either Type B lactic acidosis from cocaine's sympathomimetic effects or uremic acidosis 5, 4.

Treatment Approach

• Address the underlying cause by ensuring adequate hydration, discontinuing cocaine use, and treating any concurrent rhabdomyolysis 5.
• Monitor serial arterial blood gases if acidosis worsens or if respiratory compensation is inadequate 5.
• Bicarbonate therapy is generally not indicated unless pH <7.1 or bicarbonate <10 mEq/L, as it may worsen intracellular acidosis 5.

Hyperkalemia Management

Potassium Assessment

• The potassium of 4.8 mEq/L is at the upper limit of normal but concerning in the context of eGFR 31 mL/min/1.73 m² and metabolic acidosis 1.
• Obtain an ECG to assess for hyperkalemic changes (peaked T waves, prolonged PR interval, widened QRS) even with modest elevation 1.

Monitoring and Prevention

• Avoid potassium-sparing diuretics, ACE inhibitors, and ARBs until renal function stabilizes and potassium normalizes 1.
• Recheck potassium within 24 hours and with any medication changes affecting renal function 1.

Hepatic Abnormalities

Liver Enzyme Evaluation

• The mildly elevated transaminases (ALT 72 U/L, AST 62 U/L) with AST/ALT ratio <1 suggest hepatocellular injury rather than alcoholic hepatitis 4.
• Cocaine can cause direct hepatotoxicity, ischemic hepatitis from demand ischemia, or congestive hepatopathy from heart failure 5, 4.
• The elevated alkaline phosphatase (126 U/L) with normal bilirubin (0.5 mg/dL) suggests cholestatic injury or bone source 4.

Management

• Monitor liver function tests serially to assess for progression or resolution 5, 4.
• The hypoalbuminemia (3.1 g/dL) and low total protein (5.1 g/dL) may reflect chronic liver disease, malnutrition, or protein-losing processes 1.

Subclinical Hyperthyroidism

Thyroid Assessment

• The low TSH (0.405 mIU/L) with high free T4 (1.39 ng/dL) indicates subclinical or overt hyperthyroidism 1.
• Hyperthyroidism increases myocardial oxygen demand and can precipitate angina even without significant coronary stenosis, particularly dangerous in cocaine users 1.

Thyroid Management

• Measure free T3 levels to determine if this is overt hyperthyroidism requiring immediate treatment 1.
• Consider beta-blockers for symptomatic hyperthyroidism only after cocaine has been metabolized (typically 4-6 hours after last use), as beta-blockers are contraindicated in acute cocaine toxicity 1.
• Refer to endocrinology for definitive management with antithyroid medications or radioactive iodine 1.

Substance Abuse Intervention

Cocaine Cessation

• Daily cocaine use is the primary driver of this patient's multi-organ dysfunction and must be addressed for any meaningful recovery 2.
• Cocaine-induced dilated cardiomyopathy is potentially reversible with sustained abstinence, as demonstrated by improved ejection fraction after 5 months of cessation 2.
• Refer to addiction medicine or psychiatry for medication-assisted treatment and behavioral therapy 2.

Urine Toxicology

• Urine toxicology for cocaine metabolites (benzoylecgonine) can be detected for 24-48 hours after use (up to 22 days in chronic heavy users) 7.
• However, management decisions should be based on clinical presentation and self-reported use rather than waiting for toxicology results 1, 7.

Critical Pitfalls to Avoid

• Never administer beta-blockers within 4-6 hours of cocaine exposure due to risk of unopposed alpha-adrenergic vasoconstriction and coronary spasm 1, 3.
• Do not rely on CK-MB for diagnosing myocardial infarction in cocaine users, as it is frequently elevated from rhabdomyolysis; use troponin instead 3, 6.
• Avoid excessive dosing of renally-cleared antiplatelet and antithrombotic agents in patients with eGFR <60 mL/min/1.73 m², as this significantly increases bleeding risk 1.
• Do not dismiss elevated BNP as solely due to renal dysfunction; this patient's BNP of 1729 pg/mL warrants echocardiography to assess for structural heart disease or heart failure 1, 2.
• If coronary stenting is required, ensure the patient understands the absolute necessity of dual antiplatelet therapy adherence, as cocaine users have substantial risk of in-stent thrombosis with non-adherence 1, 3.