The authors declare no conflicts of interest regarding the publication of this paper.
Delirium is a common and serious neuropsychiatric syndrome characterized by an acute onset, fluctuating course, inattention, and global cognitive dysfunction. It is associated with increased morbidity, mortality, prolonged hospitalization, and long-term cognitive decline, particularly in older adults and patients with chronic medical conditions [
Diabetic ketoacidosis (DKA) is an acute and potentially life-threatening complication of diabetes mellitus, defined by hyperglycemia, ketosis, and metabolic acidosis. Neurological manifestations such as confusion, agitation, and decreased level of consciousness are frequently observed in severe cases and are mediated by osmotic shifts, dehydration, electrolyte disturbances, and inflammatory pathways [
Benzodiazepine withdrawal is also a recognized cause of delirium, particularly after abrupt cessation in patients receiving long-term therapy. Clinical manifestations may include agitation, tremor, autonomic instability, anxiety, and confusion, creating significant diagnostic overlap with metabolic causes of delirium [
This overlap may result in anchoring bias, particularly in psychiatric settings where substance-related etiologies are initially prioritized. We report a case illustrating this diagnostic challenge, where DKA-related delirium was initially misdiagnosed as benzodiazepine withdrawal.
A 58-year-old woman with a 12-year history of type 2 diabetes mellitus was admitted for acute behavioral disturbance characterized by psychomotor agitation, insomnia, and incoherent speech evolving over three days.
Collateral history revealed abrupt discontinuation of lorazepam, prescribed at 2 mg/day for approximately 18 months for anxiety symptoms. There was no documented history of dose escalation, misuse, or prior withdrawal episode. The last dose was taken approximately 72 hours before admission.
On admission, the patient exhibited marked disorientation in time, place, and situation. She was unable to correctly identify the date or location and demonstrated impaired recognition of family members, suggesting significant perceptual and cognitive dysfunction. Immediate memory was severely impaired, with inability to retain simple information beyond short intervals.
Speech was incoherent, with frequent derailment, tangentiality, and incomplete sentences. Psychomotor behavior fluctuated between agitation and periods of reduced motor activity. Attention was globally impaired, with inability to maintain focus during clinical interaction. Based on this presentation, a provisional diagnosis of benzodiazepine withdrawal delirium was initially considered.
Vital signs revealed tachycardia at 110 beats per minute and tachypnea at 28 breaths per minute. Blood pressure was 140/85 mmHg and temperature was 37.9˚C. Clinical examination showed clear signs of dehydration, including dry mucous membranes and decreased skin turgor.
Neurological assessment revealed fluctuating consciousness with preserved arousability. No focal neurological deficit was identified. The presence of tachypnea and dehydration raised early suspicion of metabolic decompensation.
Laboratory evaluation showed marked hyperglycemia at 2.55 g/L and significant ketonuria (3+) with glycosuria. HbA1c was elevated at 12.1%, indicating chronic poor glycemic control. Leukocytosis and elevated C-reactive protein (18 mg/L) suggested an inflammatory response. Proteinuria was also noted, consistent with dehydration-related renal stress.
Arterial blood gas analysis, serum bicarbonate, anion gap calculation, serum
Although full biochemical confirmation was unavailable, diabetic ketoacidosis was considered the most probable diagnosis based on significant hyperglycemia (2.55 g/L), marked ketonuria (3+), clinical dehydration and tachypnea, rapid response to insulin and fluid therapy, and absence of alternative toxic or neurological explanation. These findings were considered sufficient in a resource-limited context to justify immediate treatment rather than delayed confirmatory testing.
The clinical course began approximately three days prior to admission with progressive insomnia, increasing psychomotor agitation, and incoherent speech. On the day of admission, the patient was initially evaluated in a psychiatric context, and benzodiazepine withdrawal was suspected due to the history of abrupt lorazepam discontinuation. Within the first hours of hospitalization, physical examination revealed signs suggestive of a metabolic disorder, including tachypnea and dehydration. During the first 24 hours, laboratory investigations demonstrated significant hyperglycemia and ketonuria, leading to the diagnosis of diabetic ketoacidosis and initiation of intravenous fluid resuscitation and insulin therapy. Over the subsequent 24 to 48 hours, there was a marked reduction in agitation and progressive improvement in orientation and cognitive function. By the fourth day of hospitalization, the patient had achieved full recovery of baseline mental status with complete resolution of delirium.
An etiological assessment was performed to identify precipitating factors. No clear infectious focus was identified clinically, although inflammatory markers were mildly elevated. The patient reported reduced oral intake due to agitation and insomnia in the days preceding admission. There was also suspicion of suboptimal adherence to antidiabetic treatment during the same period.
No corticosteroid use, sympathomimetic exposure, or other hyperglycemic drugs were identified. The most plausible contributors were dehydration, reduced oral intake, and possible treatment non-adherence in a background of poorly controlled diabetes.
Treatment consisted of intravenous isotonic fluid resuscitation and continuous insulin infusion, following standard DKA management principles. Electrolytes were monitored and corrected as permitted by available resources.
Clinical evolution was rapidly favorable. Psychomotor agitation decreased within 48 hours, with progressive restoration of orientation and cognitive clarity. By day four, the patient had fully recovered baseline mental status with no residual confusion.
Delirium is a medical emergency requiring immediate identification of underlying causes. Failure to recognize metabolic etiologies may lead to inappropriate psychiatric management and delayed life-saving interventions [
DKA is increasingly recognized as a cause of neuropsychiatric syndromes, including delirium and acute confusional states. Hyperosmolarity, metabolic acidosis, electrolyte imbalance, and systemic inflammation contribute to neuronal dysfunction and acute brain failure [
In this case, diagnostic difficulty was amplified by the presence of abrupt benzodiazepine discontinuation, which strongly biased initial clinical reasoning toward withdrawal delirium, illustrating a classical anchoring bias.
The clinical overlap between metabolic delirium and benzodiazepine withdrawal delirium is substantial. However, DKA is more commonly associated with dehydration, tachypnea, and metabolic abnormalities, whereas benzodiazepine withdrawal is characterized by tremor, marked autonomic hyperactivity, and anxiety. The main differential features between DKA-related delirium and benzodiazepine withdrawal delirium are summarized in
| Feature | DKA (Metabolic Delirium) | Benzodiazepine Withdrawal |
| Onset | Progressive | Rapid after discontinuation |
| Context | Diabetes, metabolic stress | Drug cessation |
| Consciousness | Fluctuating | Hypervigilance |
| Neurological signs | Confusion, possible coma | Tremor, anxiety |
| Respiratory pattern | Kussmaul breathing | Normal |
| Autonomic signs | Moderate | Marked |
| Blood glucose | Elevated | Normal |
| Ketones | Positive | Negative |
| Acidosis | Present | Absent |
| Biology | Electrolyte imbalance | Usually normal |
| Treatment | Insulin + fluids | Benzodiazepines |
| Outcome | Rapid if treated | Variable |
This case illustrates anchoring bias, emphasizing the importance of prioritizing reversible medical causes before psychiatric diagnoses.
Systematic evaluation of delirium must include vital signs, metabolic screening, medication history, and physical examination. International guidelines emphasize delirium as a medical emergency requiring urgent etiological assessment [
DKA-related delirium resolves with correction of metabolic abnormalities. Psychotropic medications should not be used without addressing the underlying cause.
Limitations include absence of arterial blood gas, serum ketones, electrolyte panels, and standardized delirium assessment tools.
Other causes include hypoglycemia, hyperosmolar state, CNS infections, electrolyte disorders, and intoxications.
DKA-related delirium may mimic psychiatric disorders and substance withdrawal syndromes. Delirium should always be considered of organic origin until proven otherwise.
Written informed consent was obtained from the patient.