Clinical Case Scenario
A 63-year-old woman with diabetes mellitus, hypertension, coronary artery disease (status post PCI), and end-stage kidney disease on twice-weekly maintenance hemodialysis presented with sudden-onset breathlessness after missing one dialysis session. On examination, she was in hypertensive pulmonary edema with BP 230/110 mmHg, HR 135/min, RR 35/min, and SpO₂ 100% on a non-rebreather mask (15 L/min).
Investigations showed:
Dialysis initiation was delayed because the dialysis machine and water distribution loop were undergoing the scheduled disinfection cycle. She was started on non-invasive ventilation (NIV), intravenous nitroglycerin (NTG) infusion, and diuretics while awaiting urgent hemodialysis. Subsequently, the patient underwent hemodialysis (Qb 250 mL/min, Qd 500 mL/min, UF target 2 L, Dialysate K+: 1 mEq/L, Dialysate bicarbonate: 35 mEq/L & Dialysate Na: 135 mEq/L). After 2.5 hours of dialysis and removal of 1.5 L ultrafiltrate, pulmonary edema improved and NIV was discontinued.
Shortly thereafter, she again desaturated. NIV was restarted (FiO₂ 100%), but SpO₂ remained at 84%.
Despite severe desaturation, the patient remained comfortable. Point-of-care lung ultrasound demonstrated an A-profile bilaterally with only minimal pleural effusion.
Arterial blood gas showed PaO₂ 180 mmHg despite SpO₂ 84%.
Wrong Answer: ❌ A. Continue dialysis with additional ultrafiltration Pulmonary edema had already improved clinically and on lung ultrasound. Continuing dialysis risks further exposure to the offending oxidizing agent.
Wrong Answer: ❌ B. Stop NTG infusion and continue dialysis Although NTG can rarely cause methemoglobinemia or pulmonary shunting, the duration of infusion was insufficient to explain the presentation. Continuing dialysis fails to address the likely source.
Right Answer: ✅ C. Discontinue dialysis, continue 100% oxygen and NTG infusion, and send blood for co-oximetry.
Key Learning Point The differential diagnosis of sudden hypoxemia during haemodialysis include: • Refractory pulmonary edema • Cardiogenic shock • Pulmonary embolism • Dialyzer reaction/anaphylaxis • Pneumothorax • Dyshemoglobinemia The diagnostic clue in this case is the saturation gap: • SpO₂: 84% • PaO₂: 180 mmHg A saturation gap (markedly reduced SpO₂ despite a high PaO₂) should immediately raise suspicion for dyshemoglobinemia, particularly methemoglobinemia. In this patient, desaturation occurred despite resolution of pulmonary edema, normal lung ultrasound, and excellent arterial oxygen tension suggests dyshemoglobinemia. Dialysis should be stopped immediately to eliminate ongoing exposure to the suspected oxidizing agent. NTG-induced methemoglobinemia is possible but unlikely after such a short duration of infusion. Recent dialysis water-loop disinfection makes dialysis-related oxidant exposure the most likely etiology. Dialysis-Induced Methemoglobinemia Dialysis-associated methemoglobinemia occurs when oxidizing agents convert hemoglobin iron from the ferrous (Fe²⁺) to the ferric (Fe³⁺) state, producing methemoglobin, which is incapable of binding oxygen and thereby impairs tissue oxygen delivery. It occurs through two main mechanisms: 1. Dialysate contamination: Oxidizing agents, like Chloramines in the dialysate can oxidize hemoglobin, although this is now uncommon due to modern multistage water purification and robust quality control. 2. Residual hydrogen peroxide/silver-ion disinfectants: Water distribution loops and reverse osmosis (RO) systems are periodically disinfected to eradicate bacterial biofilms. If flushing is inadequate after the required dwell time, residual hydrogen peroxide may contaminate the dialysate and oxidize hemoglobin, resulting in methemoglobinemia. In the present case, dialysis was initiated shortly after routine water-system disinfection, making residual oxidant exposure the most likely cause. Methemoglobin absorbs both red (660 nm) and infrared (940 nm) light almost equally. Consequently, pulse oximeters characteristically display SpO₂ of approximately 85%, irrespective of the true arterial oxygen tension, producing the classic saturation gap (or cyanosis–saturation gap). Symptomatic or severe methemoglobinemia requires treatment which includes- stopping the offending agent, 100% High flow Oxygen, methylene blue 1-2mg/kg IV (contraindicated in G6PD deficiency), alternatives including intravenous vitamin C, exchange transfusion, or hyperbaric oxygen therapy. CLINICAL PEARLS 💎 Low SpO₂ with a high PaO₂ = Think saturation gap. 🎯 SpO₂ ~85% despite FiO₂ 100% + PaO₂ >150 mmHg → Think methemoglobinemia. 🎯 During hemodialysis, unexplained hypoxemia should prompt consideration of dialysis-related oxidant exposure. 🎯 Confirm the diagnosis with co-oximetry—not pulse oximetry alone.
Wrong Answer: ❌ D. Urgent CT pulmonary angiography The patient had no clinical, echocardiographic, or ultrasonographic evidence of pulmonary embolism. The marked saturation gap strongly favours methemoglobinemia, making immediate CTPA unnecessary.
