RESUMEN
It is rare for quadriparesis to manifest as a symptom of tropical illnesses. With a history of only one fever episode one week prior, our patient, a 48-year-old male with obesity and prediabetes, who was also known to have ankylosing spondylitis, presented with acute onset flaccid quadriparesis. He did not exhibit any additional symptoms of dengue, such as bleeding tendencies, petechial rashes, thrombocytopenia, or febrile episodes. Upon examination, it was discovered that he had extremely low serum potassium levels and was dengue non-specific antigen 1 (NS1) positive. His hyperinsulinemia, as seen by elevated C peptide levels, most likely caused a transcellular shift that was then triggered by the dengue infection, leading to hypokalemic paralysis.
RESUMEN
BACKGROUND: Procalcitonin (Pct) is a common biomarker in clinical practice, especially in the era of coronavirus disease 2019 (COVID-19) infection. Although it is frequently used for the diagnosis and prognostication of bacterial infections or sepsis, it is also elevated in a few other conditions, including medullary thyroid carcinoma (MTC). CASE SUMMARY: A 43-year-old female presented with moderately severe COVID-19 pneumonia in April 2021. She gradually recovered clinically; however, despite normalization of other inflammatory markers, Pct levels remained persistently elevated. Further workup identified the cause as left lobe MTC with locoregional metastasis. Calcitonin levels were high, and carcinoembryonic antigen levels were normal. The patient underwent total thyroidectomy and neck dissection, which was followed by another radical neck dissection due to residual disease. Currently, she is doing well, nearly having completed her course of external beam radiotherapy with no recurrence. Pct is well documented as a screening tool for MTC, especially because of its stable nature compared to calcitonin in the community settings. It is important to keep in mind the differential diagnosis of MTC in patients with persistently elevated Pct levels despite normal levels of other acute phase reactants. To the best of our knowledge, this is the first report from Asia of such an incidental diagnosis of MTC due to persistently elevated Pct levels in a patient with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. CONCLUSION: Persistently elevated Pct levels can occur in any pro-inflammatory state including infections, sepsis, or acute respiratory distress syndrome. In the current setting, SARS-CoV-2 infection is one such clinical scenario, and in rare situations of persistent elevation, MTC may need to be ruled out.
RESUMEN
A 41-year-old lady who presented with sudden-onset severe headache diagnosed to have ruptured supraclinoid internal carotid artery (ICA) aneurysm. Her cardiac echocardiography showed features of Takotsubo cardiomyopathy. After stabilizing her cardiac condition, she underwent craniotomy and clipping of aneurysm. Both cardiac and neurological catastrophes were managed by the joint team with excellent outcome. This paper emphasizes the need for high-quality combined care. HOW TO CITE THIS ARTICLE: Tripathy LN, Rana I, Saha A, Dixit R. Takotsubo Cardiomyopathy Secondary to Ruptured Supraclinoid Internal Carotid Artery Aneurysm. Indian J Crit Care Med 2020;24(5):363-364.
RESUMEN
The introduction of antipsychotics in the 1950s revolutionised the treatment of schizophrenia, but it soon became apparent that a substantial number of patients demonstrated a suboptimal response to these antipsychotics. Clozapine proved to be beneficial in patients whose symptoms were treatment resistant, but it too had limitations, with as many as 40-70% of those treated with clozapine demonstrating inadequate response to this drug as well. The availability of other 'atypical' antipsychotics offers options, but clozapine appears to remain the most effective option in treatment-resistant schizophrenia. This, of course, raises the question of what to do when clozapine is only partially effective. To address the issue of treatment in patients who have demonstrated a suboptimal response to clozapine, efforts have focused on a variety of augmentation strategies, including numerous medications and electroconvulsive therapy. The current body of evidence consists largely of data from smaller open trials and case series/reports, although data from a limited number of controlled studies are now available. Not surprisingly, the evidence drawn from the former is more supportive of augmentation strategies, although the controlled trials are not without positive findings. The available information is certainly not so overwhelming as to endorse any single augmentation approach. Indeed, it argues for more controlled data and cautions us regarding the cost-benefit ratio in adopting this strategy. Over and above the added adverse effects of another treatment, there is evidence to indicate that actual clinical worsening can occur. Without compelling evidence, clinicians must resort to guiding principles. The potential benefits of augmentation cannot be ruled out, but it should be approached with caution and in a systematic fashion. Factors compromising clozapine response should first be ruled out, and any augmentation trials should be guided by existing evidence and a treatment plan that incorporates a clear understanding of target symptoms. A means of evaluating outcome effectively needs to be in place, and the trial should be circumscribed to prevent needless polypharmacy. A priori, an endpoint needs to be established and the trial discontinued unless results firmly support added benefits.
