Case Presentation: A 27-year-old man with a history of malignant right coronary artery (RCA) malformation, paroxysmal supraventricular tachycardia (SVT), and depression presented to the emergency department with a 5 day history of progressively worsening ascending paresthesia, weakness, and numbness. His symptoms were preceded by a confirmed Group A Streptococcal oropharyngeal infection treated with amoxicillin-clavulanate. Neurologic examination demonstrated hyporeflexia, symmetric weakness in both upper and lower extremities, and mild facial weakness. Initial labs including complete blood count, basic metabolic panel, urinalysis, and non-contrast CT imaging, revealed no acute abnormalities. Same day lumbar puncture showed cerebrospinal fluid (CSF) protein within the normal range without other diagnostic abnormalities. Despite the absence of albuminocytologic dissociation (ACD), the patient’s recent infection and ascending sensorimotor deficits raised a high clinical suspicion for Guillain-Barré syndrome (GBS). Given the working diagnosis of GBS, intravenous immunoglobulin (IVIG) therapy was recommended. However, with the patient’s known RCA malformation the team elected to defer treatment until he is transferred to a quaternary care center capable of providing advanced cardiac monitoring with concerns of increased risk of complications during IVIG administration.
Discussion: GBS is an acute immune-mediated neuropathy with varied clinical presentations [1]. Although ACD is a classic CSF finding, it is not always present, especially earlier in the disease course [1]. Therefore, clinicians must rely on clinical suspicion rather than CSF findings, as illustrated in this case. Early initiation of IVIG is an effective treatment for GBS to prevent irreversible axonal injury and respiratory compromise [2]. The earlier the treatment, the better the prognosis [3]. While IVIG is generally safe, rare but serious complications like arrhythmias and myocardial infarction have been reported [4]. These risks were especially relevant for our patient with the history of SVT and the rare congenital RCA anomaly, a condition that inherently predisposes to ischemic and arrhythmogenic events [5]. Given the lack of advanced cardiac monitoring at the community hospital, initiating IVIG carried unacceptable risk, prompting the need for transfer in this case. This underscores a central challenge in hospital medicine – navigating competing risks in time-sensitive conditions when resource limitations intersect with patient specific hazards. Few reports describe the management of GBS in the setting of malignant coronary artery anomalies, and even fewer address the practical hospital medicine dilemma of balancing early immunotherapy with infusion-related cardiac risk. This vignette emphasizes the need for heightened clinical judgment, risk stratification, and inter-facility collaboration when standard therapy may be unsafe in the community hospital setting.
Conclusions: This case highlights the importance of prompt clinical recognition of GBS despite nondiagnostic early CSF findings without ACD. It also illustrates an under-recognized scenario in hospital medicine in which cardiac anomalies significantly alter the risk–benefit profile of time-sensitive neurologic treatment. The vignette emphasizes the critical role of the hospitalist in recognizing these challenges, coordinating multidisciplinary evaluation, and ensuring safe escalation of care.