Prolonged Delirium During Alcohol Withdrawal: A Case of Delirium Tremens Lasting 25 Days and a Review of Related Reports

Dear Editor,

Delirium tremens (DT) is a severe and potentially life-threatening complication of alcohol withdrawal. Although its prevalence is only 2% in individuals with alcohol dependence, it carries a mortality risk of about 30%. ¹ It is a “short-lasting condition with a usual duration of 3–4 days.” ¹ A few rare ones, though, are prolonged, especially in the presence of multiple medical and surgical comorbidities. ² We present a unique case who had a 25-day “prolonged DT” despite having no obvious comorbidities for the most part. We provide a detailed description of the case to illustrate the management challenges and results of a literature review of 35 reported “prolonged DT” cases to explore underlying factors in the discussion.

Case Report

A 41-year-old married male, a fruit seller, with no significant past or family history and no medical comorbidity, was brought by his family members with disorientation and agitation for the past one day. He had a 20-year history of alcohol consumption in a dependence pattern with a current average daily intake of 720 mL of whiskey and 1 L of “kallu/toddy,” a form of country-made liquor (CML). He also has a history of chewing tobacco in a dependence pattern. Last use of both alcohol and tobacco was five days prior to the onset of symptoms. Upon examination, the patient had exhibited coarse tremors with constant agitation, disorientation to time, place, person, decreased attention span, Clinical Institute Withdrawal Assessment for Alcohol-revised (CIWA-Ar), ³ scale score of 13, Richmond Agitation-Sedation Scale (RASS), ⁴ score of +2. Patient was diagnosed with alcohol induced delirium and nicotine dependence, according to International Classification of Diseases–11th Revision (ICD-11). ⁵

He was admitted, and all routine investigations, including a complete blood count, liver and renal function tests, serum electrolytes, and electrocardiography (ECG), were within normal limits (Table S3). Detoxification was initiated with lorazepam along with thiamine supplementation and nicotine replacement therapy (NRT). A summary of the treatment course is given in Table 1 . The dose of lorazepam was escalated (from 12–20 mg) as per the symptom-triggered approach using serial CIWA-Ar scores, which increased from 13 to 20 by day 3 of admission. As agitation escalated (RASS +4), parenteral haloperidol 5mg was initiated on day 3, and the patient was transferred to the intensive care unit. Physical restraints were applied after obtaining written informed consent from the wife. Dexmedetomidine augmentation was given on day 4 of admission. The patient experienced a drop in oxygen saturation after one of the doses of lorazepam. Considering issues such as limited ventilator availability, a consultation–liaison was done with the anesthesia team, and a joint decision was made to augment with dexmedetomidine instead of further increasing the dose of lorazepam. Dexmedetomidine infusions were repeated on days 6 and 7, along with the replacement of lorazepam with diazepam, as he continued to be delirious and agitated (CIWA-Ar- 22). A bolus dose of propofol was given on day 8. As the ECG showed prolonged QTc, haloperidol was switched to olanzapine. Melatonin as an augment was also initiated. During this time, serial monitoring of liver functions, serum electrolytes including calcium and magnesium, and vitamin D and B12 showed no abnormalities.

A magnetic resonance imaging (MRI) of the brain was performed to rule out any organic causes of prolonged delirium, which showed no abnormality. He was maintained on the same regimen for the next 10 days. On day 18, during an episode of aggression, he pulled out the urinary catheter, leading to urethral rupture and subsequent fever spikes, which were medically managed over the next five days. The CIWA-Ar scores gradually started declining from day 23. Diazepam was tapered and discontinued over the next 11 days. Motivational enhancement therapy and baclofen 40mg as an anticraving agent was initiated before being discharged, as the patient declined disulfiram and could not afford naltrexone or acamprosate. Consent for the publication of this report was obtained from the patient.

Table 1.

Summary of Overall Treatment Course.

Mode	Day 1–5	Day 6–10	Day 11–15	Day 16–20	Day 21–25
Benzodiazepines	IV lorazepam 12–20 mg	IV lorazepam 20 mg (on day 6 and 7) IV diazepam 80 to100 mg (day 7–10)	IV diazepam 100 mg	IV diazepam 100 mg	IV diazepam 100 mg (tapered from day 22, discontinued over 11 days)
Adjunct	Dexmedetomidine 0.4 mg/kg/hr infusion (on day 4)	Dexmedetomidine repeated infusions (0.3 mg/kg/hr ® 0.2 mg/kg/hr) given on day 6 and 7 Propofol 50 mg bolus + 5 mL/hr infusion on day 8
Antipsychotics	IV haloperidol 5 mg (day 3)	T. Olanzapine 5 mg (IV haloperidol 5mg discontinued due to QT prolongation)	T. Olanzapine 5 mg	T. Olanzapine 5 mg
Augment		T. Melatonin 10 mg	T. Melatonin 10 mg	T. Melatonin 10 mg	T. Melatonin 10 mg
Thiamine supplementation	IV thiamine 1200 mg	IV thiamine 1200 mg	IV thiamine 1200 mg	IV thiamine 1200 mg	T. Thiamine 600 mg
Nicotine replacement	Nicotine patch 14 mg (24 hourly)	Nicotine patch 14 mg (24 hourly)	Nicotine patch 14 mg (24 hourly)	Nicotine patch 14 mg (24 hourly)	Nicotine patch 14 mg (24 hourly)
Additional drugs				T. Nitrofurantoin 200 mg and T. Paracetamol 1500 mg (for urethral rupture and fever spikes)

IM: Intramuscular, IV: Intravenous, T: Tablet.

Discussion

This report highlights a case of “prolonged DT” who required management with multiple pharmacological interventions, beyond the routine benzodiazepine-based detoxification, like most cases reported in the literature.

A literature review (see supplementary material; Table S1 and S2) revealed 35 reported cases of prolonged DT, lasting from 8 to 147 days. Most reported cases of prolonged DT are associated with comorbidities such as aspiration pneumonia, alcoholic hepatitis, pancreatitis, hyponatremia, hypomagnesemia, central pontine myelinolysis, seizures, and rhabdomyolysis (Sl. Nos. 6-35 in Table S2), offering important insights into the condition’s complexity and guiding clinicians on what to monitor when DT is prolonged. In contrast, five cases (Sl. nos. 1–5 in Table S2) attributed prolongation to individual vulnerability in the absence of comorbidities—similar to our patient. In our case, although no comorbidities were initially present, the contribution of inflammation from a later urethral rupture to further prolongation cannot be ruled out; this underscores the need for rigorous monitoring and proper restraint. Additionally, the benzodiazepine doses we administered were lower than those reported in many cases, this may also have contributed to prolongation, reinforcing the recommendation that higher doses should be used whenever tolerated to reduce this risk. As suggested previously, ⁶ one reason for prolongation could be attributed to the type of alcohol (i.e., CML) consumed and its distinct effects on the nervous system, and its impact on the duration of DT. However, it is difficult to comment as most papers do not report it (Table S2). Another important consideration is the use of NRT for nicotine withdrawal during DT. With no standard guidelines available, evidence remains conflicting—a review ⁷ on NRT in terminally ill delirious patients found few studies showing reduction in agitation and delirium and few showing worsening—highlighting the need for further research.

Overall, there is also a need for the standardization of definitions and treatment protocols corresponding to the duration and severity of DT use, taking into account comorbidities.

Supplemental Material

Supplemental material for this article available online.

Supplemental Material

Supplemental material for this article available online.