The importance of monitoring magnesium levels in alcohol withdrawal delirium

INTRODUCTION

Alcohol withdrawal, as classified by the Diagnostic and Statistical Manual of Mental Disorders-5, is the most severe manifestation of alcohol withdrawal, commonly presenting with altered mental status and autonomic hyperactivity, which, if not managed promptly, can be fatal.^[1] Electrolyte abnormalities, particularly hypomagnesemia, are often seen in individuals with alcohol withdrawal and can aggravate neurological problems, complicating management. Studies have underlined the frequency of hypomagnesemia in critical care environments and its correlation with negative consequences.^[2,3] This case report emphasizes the need to monitor and correct magnesium levels in alcohol withdrawal. It addresses the inadvertent discovery of a cerebral arteriovenous malformation (AVM) during the patient’s assessment.^[2-5]

CASE REPORT

A 49-year-old married man, a manual laborer from a low socioeconomic background, presented to the emergency department with seizures following a 1-day period of alcohol abstinence. He had a 10-year history of hypertension and consumed 500–750 mL of brandy daily, had a history of hypertension, and was on irregular medications for the same. He had experienced a similar seizure episode 2 months earlier but had not sought medical care.

The patient’s vital signs at admission were notable for hypertension (170/100 mmHg). Laboratory investigations revealed hypomagnesemia (serum magnesium: 1.3 mg/dL; reference range: 1.8–2.6 mg/dL) and increased liver enzymes (serum glutamicoxaloacetic transaminase/serum glutamate pyruvate transaminase: 95/56 U/L). Levels of serum lipase and amylase were normal. The computed tomography (CT) scan of the brain was initially unremarkable; abdominal ultrasonography revealed a Grade 1 fatty liver.

The patient was initially treated with lorazepam (10 mg in divided doses), high-dose intravenous thiamine, amlodipine for hypertension, and oral magnesium oxide for hypomagnesemia. He was transferred to the de-addiction ward for further management of alcohol withdrawal seizures.

During hospitalization, he was disoriented, had memory impairment, gait instability, and sleep disturbances. A magnetic resonance imaging of the brain and CT angiography were performed, revealing a cerebral AVM with arterial feeders from the right middle cerebral artery and posterior cerebral artery, emptying into superficial veins classified as Spetzler-Martin grade 2. Neurology and interventional radiology consultations recommended conservative management with periodic follow-up.

Despite continued treatment with oral magnesium and other drugs, the patient’s neuropsychiatric symptoms persisted. A repeat serum magnesium test on day 14 showed persistently low levels (1.3 mg/dL). Medicine consultation was sought, and a single dose of 1 g of intravenous magnesium sulfate was administered, leading to significant clinical improvement, including better recent memory, normalized sleep patterns, and improved orientation to time, place, and person.

He was discharged with a treatment plan that included lorazepam 2 mg, thiamine 200 mg, magnesium oxide 800 mg, amlodipine 10 mg, and quetiapine 25 mg, with regular follow-ups scheduled.

DISCUSSION

Hypomagnesemia is common in individuals with alcohol use disorder. Research suggests that low magnesium levels can exacerbate neuropsychiatric symptoms such as delirium and seizures, reinforcing the importance of regular electrolyte monitoring in alcohol withdrawal management.^[6]

In this case, persistent hypomagnesemia correlated with sustained neuropsychiatric symptoms despite conventional treatment of alcohol withdrawal, thereby stressing the importance of routine magnesium monitoring and correction.^[2,3] Magnesium plays an important role in neuromuscular function, enzymatic activity, and neurotransmitter modulation. Chronic alcohol consumption significantly contributes to magnesium depletion through poor dietary intake, gastrointestinal (GI) losses, renal wasting, and redistribution from extracellular to intracellular compartments.^[7]

Historically, routine assessment of serum magnesium was a cornerstone of detoxification protocols for alcohol use disorders. However, over the years, this practice has gradually faded from standard treatment procedures despite its proven clinical relevance.^[8] This decline in routine evaluation should be revisited, as subclinical magnesium deficits are common in alcohol-dependent individuals and may complicate withdrawal management.

Magnesium deficiency is prevalent in 30–60% of chronic alcohol users.^[9] It exacerbates symptoms of alcohol withdrawal, such as seizures, irritability, tremors, and delirium tremens, due to destabilization of neuronal membranes and antagonism of N-methyl-D-aspartate receptors.^[10] Hypomagnesemia can worsen neuromuscular excitability and potentiate complications of withdrawal, including arrhythmias and refractory seizures.^[11]

Failure to assess and correct magnesium levels can result in increased severity of withdrawal symptoms,^[12] higher risk of seizures and delirium tremens,^[10] cardiac arrhythmias, particularly in patients with concurrent hypokalemia,^[13] adverse clinical outcome, and prolonged hospitalization. Magnesium deficiency should be suspected in alcohol withdrawal if symptoms such as refractory seizures despite benzodiazepine treatment, persistent tremors or neuromuscular irritability, and hypokalemia or hypocalcemia are not responding to supplementation, prolongation or ventricular ectopy on electrocardiogram, muscle cramps, weakness, or altered mental status^[10,13] are present.

Although not universally emphasized in guidelines, targeted magnesium evaluation is advocated by several expert groups, such as the American Society of Addiction Medicine, which recommends monitoring and correcting electrolytes, including magnesium, in patients with moderate to severe alcohol withdrawal.^[14] The British Association for Psychopharmacology includes electrolyte assessment in the comprehensive management of withdrawal states.^[15] Suggested protocol for magnesium evaluation in alcohol withdrawal delirium includes a baseline assessment, serum magnesium (preferably ionized mg if available) on admission.

Follow-up testing every 24–48 h in patients with moderate-to-severe withdrawal, seizures, or ongoing GI/renal losses is also recommended. Magnesium supplementation is recommended if serum magnesium levels are <1.7 mg/dL or symptomatic and in high-risk patients, even with normal serum values, due to poor sensitivity of total magnesium tests.^[9]

Furthermore, the inadvertent discovery of a cerebral AVM in this patient emphasizes the significance of comprehensive neurological examination in people presenting with seizures and altered mental states, particularly when symptoms persist despite appropriate management.^[16]

While many AVMs remain asymptomatic, their presence may contribute to neurological complications, necessitating careful assessment and individualized management strategies.^[6] Although the AVM was hemodynamically stable, its presence could have influenced the patient’s clinical presentation and posed additional risks such as hemorrhage and progressive neurological deficits, necessitating long-term neurological follow-up.^[16]

This case highlights the importance of electrolyte monitoring, particularly magnesium levels, in individuals with alcohol withdrawal. Prompt correction of hypomagnesemia can significantly improve therapeutic outcomes and reduce the risk of complications. Patients with unusual presentations or refractory symptoms warrant a thorough neurological assessment to rule out underlying abnormalities such as cerebral AVMs.

CONCLUSION

Effective management of alcohol withdrawal depends on the vigilant monitoring and correction of magnesium levels. Persistent hypomagnesemia can exacerbate neuropsychiatric symptoms and delay recovery. In addition, incidental findings, such as cerebral AVMs, highlight the importance of comprehensive neurological evaluations in patients with atypical or refractory symptoms.