Situation: A 47-year-old woman is in the intensive care unit (ICU) with acute kidney injury after severe sepsis. Her blood pressure is now stable without vasopressors. She receives intermittent hemodialysis (HD) through a temporary dialysis catheter and parenteral nutrition (PN) by infusion pump through a dedicated lumen of a central venous catheter. During her first HD session, 2.5 hours into the treatment, she reports headache, nausea and mild leg cramps, then becomes restless and confused. Findings: - Blood pressure 114/72 mmHg (130/80 mmHg before dialysis) - Heart rate 94/min; oxygen saturation by pulse oximetry 97%; no chest pain or cough - Capillary blood glucose 142 mg/dL (7.9 mmol/L) - Blood urea nitrogen before dialysis 148 mg/dL (52.8 mmol/L) Which problem do these findings MOST likely indicate?

In the first sessions, when blood urea is very high, rapid urea removal makes the plasma less concentrated than brain tissue; water shifts into the brain and causes cerebral edema, with headache, nausea, restlessness, confusion and possibly seizures. Her blood pressure is lower but not hypotensive, her oxygenation is normal without chest pain, and her glucose is normal, so the neurologic picture points to disequilibrium. The nurse slows or stops the treatment and notifies the provider.

Core Pathophysiology
During the first hemodialysis session, the blood urea nitrogen is markedly elevated at 148 mg/dL. Urea is an effective osmole that normally contributes to plasma osmolality. When dialysis removes urea from the extracellular space rapidly, plasma osmolality falls faster than the osmolality inside brain cells. Because urea crosses the blood–brain barrier more slowly than water, a transient osmotic gradient develops: water moves from the relatively hypotonic plasma into brain cells, producing cerebral edema and elevated intracranial pressure. The neurologic symptoms of headache, nausea, restlessness, and confusion during or shortly after the first dialysis session reflect this acute osmotic shift into brain tissue. This clinical picture is termed dialysis disequilibrium syndrome (DDS) ^[1][2][3][4].

Why the Other Options Are Less Likely
The patient’s blood pressure is 114/72 mmHg, which is lower than her predialysis value of 130/80 mmHg but does not meet a definition of intradialytic hypotension. She has no chest pain, cough, or oxygen desaturation, making air embolism unlikely; air embolism would typically present with sudden dyspnea, chest pain, hypotension, or a machinery-like murmur, not isolated neurologic symptoms. Capillary blood glucose is 142 mg/dL, which is normal and rules out hypoglycemia as the cause of her confusion ^[1][2].

Clinical Recognition and Risk Factors
DDS is most common when dialysis is first initiated in patients who are markedly uremic and hyperosmolar. The first session is the highest-risk period because the urea reduction is greatest relative to baseline. Symptoms range from mild restlessness and headache to seizures, coma, and death in severe cases ^[2][4]. The diagnosis is clinical and is made after excluding other causes of neurologic deterioration during dialysis, such as hypotension, hypoglycemia, electrolyte abnormalities, and intracranial bleeding. In this patient, the normal oxygenation, stable blood pressure, normal glucose, and absence of chest symptoms support DDS as the most likely explanation ^[1][2][3].

Nursing Priorities During the Session
When DDS is suspected, the immediate nursing actions are to slow or temporarily stop the dialysis treatment, maintain the patient’s airway and hemodynamic stability, and notify the provider. The goal is to reduce the rate of further osmotic shift. Key point! Slowing the blood flow rate or stopping ultrafiltration reduces the rate of urea removal and allows brain osmolality to equilibrate more gradually. Watch out! Do not confuse the mild blood pressure drop with hypovolemia requiring a fluid bolus; giving fluid rapidly can worsen cerebral edema if intracranial pressure is already elevated ^[2][3][4].

Prevention in Future Sessions
For subsequent dialysis treatments in high-risk patients, preventive strategies include reducing the efficiency of the first few sessions, using a smaller dialyzer surface area, lowering the blood flow rate, shortening the session duration, and adding an osmotically active agent such as mannitol or hypertonic saline to the dialysate or infusion. The overarching principle is to lower urea gradually rather than rapidly, allowing the brain to adapt its intracellular osmolality without a steep osmotic gradient. Continuous renal replacement therapy may be preferred over intermittent hemodialysis in some hemodynamically unstable or severely uremic patients with acute kidney injury ^[2][3][4].

Finding	DDS	Intradialytic hypotension	Air embolism	Hypoglycemia
Headache, nausea, confusion	Typical, due to cerebral edema	Possible from cerebral hypoperfusion	Possible if cerebral air emboli	Possible from neuroglycopenia
Blood pressure	Mild decrease or stable	Marked drop below baseline	Sudden severe hypotension	Usually unchanged
Oxygenation and chest symptoms	Normal, no chest pain	May have dizziness, no chest pain	Dyspnea, chest pain, desaturation	Normal, no chest pain
Glucose	Normal	Normal	Normal	Low
Predialysis urea	Very high, first session	Variable	Variable	Variable

The neurologic presentation in the setting of a very high predialysis urea concentration and the first hemodialysis session is most consistent with dialysis disequilibrium syndrome caused by rapid urea removal and the resulting osmotic water shift into brain cells ^[1][2][3][4].