Situation: A 55-year-old man with chronic kidney disease (CKD) stage G5 caused by diabetes starts hemodialysis (HD) in a hospital dialysis unit. His access is an arteriovenous (AV) fistula in his left forearm, created 4 months ago. Before his first session, his blood urea nitrogen (BUN) is 128 mg/dL (45.7 mmol/L). During the last hour of his first 4-hour session, he becomes restless and confused and complains of a severe headache and nausea. His blood pressure is 156/92 mmHg (160/94 mmHg before dialysis), pulse 88/min, respirations 18/min, and oxygen saturation 97%; he has no chest pain. His capillary blood glucose is 142 mg/dL (7.9 mmol/L). Which complication do these findings MOST likely represent?

Disequilibrium syndrome occurs during or soon after the first sessions, when urea leaves the blood faster than the brain, so water moves into brain tissue and causes cerebral edema with headache, nausea, restlessness, confusion, and sometimes seizures. His very high starting BUN raises the risk, and his normal glucose, stable blood pressure, normal saturation, and absence of chest pain point away from the other causes. The nurse slows or stops the treatment and notifies the physician; early sessions are made shorter and slower to prevent it.

What the findings point to

This patient’s presentation during the last hour of his first hemodialysis session — new-onset restlessness, confusion, severe headache, and nausea — is the classic neurologic cluster of dialysis disequilibrium syndrome (DDS). The timing matters: DDS typically appears during or shortly after dialysis, especially in the first sessions when the blood is still markedly uremic ^[3][4]. His starting BUN of 128 mg/dL places him in a high-risk, hyperosmolar uremic state, which is precisely the setting in which rapid solute removal triggers the syndrome ^[3].

Why the brain swells

The underlying problem is an osmotic gradient between plasma and brain tissue. During hemodialysis, urea is cleared from the blood much faster than it can move out of the brain’s intracellular and interstitial compartments. The brain is left relatively hyperosmolar compared with the now-diluted plasma, so water shifts down the osmotic gradient into brain cells, producing cerebral edema and increased intracranial pressure ^[2][4]. The resulting symptoms range from mild restlessness and headache to confusion, seizures, and coma ^[2]. In this patient, the severe headache, nausea, and acute confusion are consistent with early but significant cerebral edema.

Why the other options do not fit

Finding	Hypoglycemia	Air embolism	Cardiac tamponade
Expected clue	Low capillary glucose, diaphoresis, tremor, altered consciousness	Chest pain, dyspnea, cough, hypotension, cyanosis, “mill-wheel” murmur	Beck triad: hypotension, muffled heart sounds, distended neck veins; chest pain, dyspnea
This patient	142 mg/dL — normal, not hypoglycemic	No chest pain, SpO₂ 97%, stable respirations	No chest pain, BP 156/92 mmHg — not hypotensive, no muffled sounds described

The capillary glucose of 142 mg/dL effectively excludes hypoglycemia as the cause of his confusion. The absence of chest pain, dyspnea, or oxygen desaturation makes air embolism unlikely. Cardiac tamponade would present with hypotension and signs of impaired cardiac filling, not a blood pressure of 156/92 mmHg with isolated neurologic symptoms.

Clinical recognition and risk factors

DDS is a diagnosis of exclusion in a uremic, hyperosmolar patient whose neurologic symptoms emerge during or just after rapid renal replacement therapy ^[3]. The syndrome is most commonly described with hemodialysis, although it can occur with continuous renal replacement therapy in acute kidney injury as well ^[3]. Because the presentation overlaps with other neurologic emergencies, the nurse must first rule out stroke, hypoglycemia, subdural hematoma, and electrolyte disturbances — but in this vignette, the first-session timing, extreme starting BUN, and normal glucose and vital signs point strongly to DDS.

Key point! The highest-risk window is the first few hemodialysis sessions in a patient with severe azotemia. A very high pre-dialysis BUN, new-onset headache or confusion during treatment, and normal glucose should immediately raise suspicion for DDS.

What the nurse does

Once DDS is suspected, the priority is to reduce the osmotic gradient and prevent worsening cerebral edema. The nurse should slow or stop the dialysis session, keep the patient safe from falls or seizures, and notify the physician promptly. Prevention for future sessions includes shorter, slower initial treatments with lower blood flow rates and reduced dialysate flow, sometimes with a smaller dialyzer, so that urea clearance is more gradual ^[2][4]. Because treatment of established DDS is rarely successful once severe neurologic injury has developed, prevention is the central strategy ^[2].

Why this matters for licensure exams

This question tests the ability to distinguish DDS from other dialysis-related complications using the pattern of findings. The key discriminators are the timing (first session, late in treatment), the neurologic symptom cluster (headache, nausea, restlessness, confusion), the very high starting BUN, and the normal glucose and stable cardiopulmonary status. When a dialysis patient develops acute confusion with headache and nausea, the nurse should not assume hypoglycemia or a cardiac event without checking glucose and vital signs — and in the first-session setting, DDS must be at the top of the differential ^[3].