Uremia

Uremic platelet dysfunction - Decreased platelet factor 3 activity plus abnormal platelet adhesiveness and aggregation. For the actively bleeding patient, desmopressin (dDAVP) is first line — IV over 15 to 30 minutes or intranasally, effective in at least 50%, working within an hour and lasting 4 to 24 hours by releasing Factor VIII:von Willebrand factor multimers from endothelial stores. Tachyphylaxis appears after the second dose as those stores deplete.

Severe bleeding needs combination therapy - Desmopressin, cryoprecipitate, and packed red cells together, each addressing a different mechanism. Give platelets only alongside those, because transfused platelets turn dysfunctional soon after entering the uremic environment. Conjugated estrogens and erythropoietin are additional options.

Potassium before induction - Hyperkalemia is a medical emergency above 6.5 mEq/L and is worsened by acidosis and by potassium-sparing diuretics, ACE inhibitors, ARBs, beta blockers, and NSAIDs. Check a same-day potassium and an EKG.

Succinylcholine takes special consideration - It raises serum potassium by as much as 0.5 mEq/L, which matters in a patient with chronically elevated potassium. Avoid it if the potassium is high enough to produce EKG changes.

Don't strip the respiratory compensation - Impaired hydrogen ion secretion and ammonium excretion plus accumulated phosphate and organic acids produce anion-gap metabolic acidosis, which the patient offsets with hyperventilation. Match that minute ventilation on the vent; letting CO2 climb will drop the pH and worsen hyperkalemia. Acidosis itself causes lethargy, muscle weakness, and a blunted cardiac response.

Anemia is the baseline, not a surprise - Normocytic normochromic hypoproliferative anemia from lost erythropoietin, typically at GFR under 50 mL/min (under 60 in diabetics) or creatinine above 2 mg/dL. Iron and vitamin deficiency, hyperparathyroidism, and shortened red cell lifespan compound it.

Uremic pericarditis and effusion - Occurs in ESRD and severe azotemia, typically with BUN above 60 mg/dL. Listen for a friction rub and ask about chest pain that worsens lying flat; get an echocardiogram before induction if either is present, since effusions can progress to tamponade and the platelet dysfunction makes them hemorrhagic.

Cardiac reserve is limited - Uremic toxins and metastatic calcification contribute to hypertension, atherosclerosis, valvular stenosis and insufficiency, chronic heart failure, and angina. Suppressed myocardial contractility is part of the syndrome.

Uremic encephalopathy - Fatigue, muscle weakness, restless legs, headache, asterixis, polyneuritis, mental status change, seizures, stupor, and coma. Document a baseline neuro exam and mental status so you can interpret a slow wake-up rather than guess at it.

Subdural hematoma risk - BUN above 150 to 200 mg/dL raises the risk of spontaneous subdural hematoma. Any fall, head trauma, or unexplained mental status change earns a head CT.

GI symptoms and the airway - Nausea, vomiting, and anorexia are core uremic features, and occult GI bleeding from platelet abnormalities can present the same way. Plan the induction around a stomach you cannot assume is empty.

Insulin clearance falls - Declining renal function reduces insulin clearance, so antihyperglycemic doses come down. Watch for hypoglycemia in a diabetic whose control has "improved" as the kidneys failed.

Dialysis before the OR when it is a uremic emergency - Hyperkalemia, acidosis, symptomatic pericardial effusion, or uremic encephalopathy warrant emergent dialysis before an elective case. Dialysis is initiated gently to avoid dialysis disequilibrium syndrome — cerebral edema from too-rapid solute shifts.

Uremia is the clinical syndrome that appears when the failing kidney can no longer clear nitrogenous waste — literally "urine in the blood." Symptoms usually begin once creatinine clearance drops below 10-20 mL/min, though patients can be symptomatic at higher clearances when function is lost acutely. Urea is both directly and indirectly toxic; other putative toxins include parathyroid hormone, beta-2 microglobulin, and advanced glycosylation end products, and no single toxin explains the whole picture.

What you inherit at the board is a multi-system syndrome, not just a number: normocytic normochromic anemia from lost erythropoietin, anion-gap metabolic acidosis, hyperkalemia, platelet dysfunction with a bleeding diathesis, pericarditis and effusion, and encephalopathy — each with its own intraoperative consequence.