Paraparesis, Urinary Dysfunction, and Acute, Therapy-Resistant Heart Failure in a Previously Healthy Patient Should Not Remain Unexplained

Letter to the Editor

We read with interest the article by Ramcharan et al. about a 61-year-old, previously healthy man who developed treatment-resistant heart failure following a mild respiratory infection, followed by urinary retention and lower extremity paraparesis, which was interpreted as Guillain-Barré syndrome (GBS). ¹ Despite extensive diagnostic efforts and guideline-compliant therapy, the patient died. ¹ The study is compelling but requires further discussion.

First, the patient was not tested for the causative agent of the infectious disease after the onset of motor symptoms. Identifying the trigger of GBS is crucial, as not only the neurological complications but also the underlying infection must be treated appropriately. Since the patient had elevated CRP and erythrocyte sedimentation rate (ESR) levels upon admission, it is conceivable that the causative agent could still have been identified. Common pathogens of respiratory infections and GBS include Epstein-Barr virus, cytomegalovirus, influenza virus, HIV, and Mycoplasma pneumoniae. ² Was any of these pathogens detected in the patient, either directly or indirectly? At the very least, a viral panel should have been performed to determine whether one of these common viruses was the causative agent.

Second, myocarditis as a cause of the heart failure was not ruled out. ¹ Since the patient had an infection prior to the onset of heart failure, exclusion of myocarditis by cardiac MRI or endomyocardial biopsy would have been necessary. In myocarditis, contrast-enhanced cardiac MRI typically shows myocardial enhancement. ³

Third, Takotsubo syndrome (TTS) as a cause of the heart failure was not adequately ruled out. ¹ Since there are different types of TTS, it is crucial to consider not only the classic distal type (apical ballooning), which is the most common, but also the rarer types. These include the midventricular, basal, and global types. ⁴ If the heart failure was not caused by myocarditis, the global TTS type should be considered. To diagnose TTS according to the Mayo Clinic criteria, proof of patent coronary arteries in coronary angiography would have been required.

The fourth point is that the patient did not undergo an MRI of the lumbar nerve roots. ¹ In GBS, the nerve roots typically appear as swollen and contrast-enhancing structures on MRI. ⁵

The fifth point is that the cause of the urinary dysfunction was not identified. ¹ Was an MRI of the spine performed to rule out myelitis? Even with normal CSF, infectious or inflammatory myelitis cannot be excluded. Myelitis can be associated with radiculopathy. At the very least, a viral panel should have been performed on serum and CSF.

The sixth point is that reference ranges were not provided for some of the reported laboratory parameters. ¹ This is particularly problematic for the CSF cell count. What was the upper reference range for the CSF cell count? Does a CSF cell count of 10/3 represent a normal value or an elevated cell count? Furthermore, it should be specified whether these cells are lymphocytes, monocytes, granulocytes, or a mixture of two or three of these cell types.

Finally, the patient did not undergo an autopsy. An autopsy would have been helpful in determining the cause of the acute heart failure, cardiogenic shock, urinary retention, and lower extremity paraparesis.

ORCID iD

Josef Finsterer https://orcid.org/0000-0003-2839-7305