Guillain-Barre syndrome (GBS) is an acute autoimmune demyelinating polyradiculoneuropathy that presents with rapidly progressive ascending muscle weakness. GBS typically follows a respiratory or gastrointestinal infection. Early detection and treatment can improve recovery rate [1]. We present a case of GBS induced by varicella zoster virus (VZV) reactivation in a patient receiving treatment for multiple myeloma. CASE PRESENTATION:A 68-year-old male with a history of multiple myeloma, abdominal aortic aneurysm with repair and hypertension initially presented to the emergency department (ED) with fever and altered mental status. In the ED, his blood pressure was initially 210/134 and remained elevated despite intravenous (IV) administration of labetalol. The patient was started on empiric therapy with IV vancomycin, acyclovir, ceftriaxone, and ampicillin for possible meningitis. It was found that the patient had previously received an autologous stem cell transplantation, as well as treatment with bortezomib, lenalidomide, and low-dose dexamethasone, with only partial response. The patient was started on an escalated regimen with daratumumab one week prior to admission. The patient was transferred to the intensive care unit (ICU) and placed on an IV esmolol drip for hypertensive emergency. The next day, the patient developed bilateral lower extremity areflexia and motor weakness. IV immunoglobulin (IVIg) was initiated for presumed GBS. Cerebrospinal fluid (CSF) results were significant for positive VZV-PCR and elevated protein. Magnetic resonance imaging (MRI) of the brain showed a linear enhancement in the cauda equina that was consistent with GBS. The patient continued to receive acyclovir and IVIg with clinical improvement.DISCUSSION: GBS induced by reactivation of latent VZV is rare. Prompt initiation of empiric treatment is imperative to prevent further complications and decrease time to recovery. Patients may also present with labile blood pressures or arrhythmias due to dysautonomia and should be monitored closely for cardiovascular and respiratory stability. Daratumumab is an IgG1 subtype human monoclonal antibody directed against CD38, a cell surface glycoprotein that is highly expressed in myeloma cells. Previous studies have noted infection complications of daratumumab [2-5], including reactivation of a viral infection. Further studies investigating the role of prophylaxis and screening in individuals who begin immunomodulatory therapies should be considered. CONCLUSIONS:In an immunocompromised patient presenting with bilateral lower extremity areflexia and motor weakness, GBS should be considered with prompt initiation of appropriate therapy. This case report highlights the importance of a thorough history, prompt treatment, and close follow-up to avoid adverse outcomes.
INTRODUCTION:Severe hyponatremia presents with nausea and vomiting, which progresses to lethargy, seizures, coma, and respiratory arrest as hyponatremia advances. Focal neurological deficits (FND) are uncommonly reported. Here we present a case of reversible FND in a patient with severe hyponatremia. CASE PRESENTATION:An 84-year-old female with hypertension and anxiety presents with stroke-like symptoms. She had several months of frequent falls and 2 weeks of word-finding difficulties, with progressive confusion, lethargy, slurred speech, and facial droop in the past week. Of note, she takes hydrochlorothiazide and was started on citalopram one week prior to presentation. On admission, blood pressure was 155/82 mmHg. Exam revealed aphasia, confusion, right-sided facial droop, and right-sided extremity weakness. Labs included sodium of 117 mEq/L, glucose of 160 mg/dL, urine osmolality of 450 mOsm/kg, and urine sodium of 105 mEq/L. Computed Tomography (CT) Brain was negative and CT angiography Head and Neck incidentally found a 1.5 cm spiculated nodule in the left upper lobe. Patient was admitted to the Intensive Care Unit (ICU) and received hypertonic saline. Hyponatremia was deemed secondary to Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH) secretion from thiazide and citalopram use, and likely malignancy. Fluids were restricted and she was given salt tablets. Sodium levels improved and her neurological deficits completely resolved.DISCUSSION: Symptoms of hyponatremia traditionally include nausea, vomiting, gait instability, and coma. FND secondary to hyponatremia occur in only 5% of severe hyponatremia cases. While the relationship between FND and hyponatremia is poorly understood, FND are typically associated with intracranial bleeding, which was not seen in our patient. FND are often seen in cases of head trauma, tumors, stroke, meningitis, or encephalitis. In cases of hyponatremia where these conditions are not seen, hyponatremia-induced FND should be strongly considered. CONCLUSIONS:Severe hyponatremia may present with focal neurological deficits that resolve as sodium levels improve.
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