Persistent hyperammonia and altered concentrations of urea cycle metabolites in a 5-day swine experiment of sepsis

We measured plasma and cerebrospinal fluid (CSF) metabolite concentrations in a 5-day porcine sepsis model of fecal peritonitis. The objectives were: (i) to verify whether the expected pathways that had emerged in previous studies pertain only to the early inflammatory response or persist for the subsequent days; (ii) to identify metabolic derangements that arise later; (iii) to verify whether CSF metabolite concentrations were altered and if these alterations were similar to those in the blood or delayed. We observed an early response to inflammation and cytokine storms with alterations in lipid and glucose metabolism. The arginine/asymmetric dimethylarginine (ADMA) and phenylalanine/tyrosine balances changed 24 h after resuscitation in plasma, and later in CSF. There was a rise in ammonia concentration, with altered concentrations of metabolites in the urea cycle. Whether persistent derangement of these pathways have a role not only on short-term outcomes but also on longer-term comorbidities, such as septic encephalopathy, should be addressed in further studies.

Presentations and mechanisms of CNS disorders related to COVID-19

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the coronavirus disease 2019 (COVID-19) pandemic. In addition to severe respiratory symptoms, there are a growing number of reports showing a wide range of CNS complications in patients with COVID-19. Here, we review the literature on these complications, ranging from nonspecific symptoms to necrotizing encephalopathies, encephalitis, myelitis, encephalomyelitis, endotheliitis, and stroke. We postulate that there are several different mechanisms involved in COVID-19–associated CNS dysfunction, particularly activation of inflammatory and thrombotic pathways and, in a few patients, a direct viral effect on the endothelium and the parenchyma. Last, critically ill patients frequently present with protracted cognitive dysfunction in the setting of septic encephalopathy likely due to multifactorial mechanisms. Further studies are needed to clarify the relative contribution of each of these mechanisms, but available data suggest that CNS complications in COVID-19 are rare and probably not directly caused by the virus.

Differential diagnosis of atypical encephalopathy in critical care: a case report

Background A lower level of consciousness is a common presentation in critical care, with many different causes and contributory factors, of which more than one may be present concurrently. Case presentation We described a woman with poorly controlled diabetes and steroid-dependent asthma who presented in a deep coma. She was found to have Streptococcus intermedius bacteremia and pyogenic ventriculitis that originated from right middle lobe pneumonia. Also, multiple small parenchymal lesions were observed on brain magnetic resonance imaging and increased protein concentration was noted in cerebral spinal fluid. Initially, her coma was thought to be due to diabetic ketoacidosis and septic encephalopathy. However, her lowered level of consciousness was disproportionate to either diabetic ketoacidosis or septic encephalopathy, and her clinical course was not as expected for these two conditions. Treatment with antibiotic, corticosteroid and antihelminthic drugs was administered resulting in improving consciousness. The Streptococcus intermedius pneumonia progressed to form a large cavity that needed an early surgical lobectomy and resulted in the unexpected diagnosis of chronic cavitary pulmonary aspergillosus. Conclusions In critical care, a lowered level of consciousness may have many etiologies, and critical care clinicians should be familiar with the signs and symptoms of all possible causes to enable prompt diagnosis and appropriate treatment.

Medical conditions of Omer Seyfettin (1884–1920), the father of Turkish short stories, enshrined as a mystery

Born in 1884 in Balıkesir, Turkey, Ömer Seyfettin was a leading figure among modern Turkish short story writers whose death in 1920 at the age of 36 led to long-term speculations about his fatal illness. In order to pay homage to his memory in the centennial of his death and to shed light on his later medical condition, this paper seeks to reexamine his last days from a medico-historical perspective. Our findings indicate that there was a notable decline in his health occurring after 1917 when he was confined to social isolation. A carbuncle was diagnosed in his posterior neck when he was 35-years of age and not satisfactorily treated. In late February 1920, he developed progressive symptoms over two weeks consisting initially of a headache, followed by fever, delirium, hallucinations, and diplopia. These clinical signs and symptoms are clinically suggestive of a septic encephalopathy presumably caused by staphylococcus aureus infection secondary to the carbuncle, or perhaps by one of the myriad causes of viral meningoencephalitis.

Electroencephalographic Grading of Neuronal Dysfunction in Various Etiologies of Encephalopathy

Objective: The objective of this work was to study the electroencephalographic (EEG) grading of neuronal dysfunction in encephalopathy of various etiologies and assess their association with clinical outcomes. Subjects and Methods: This retrospective cross-sectional study was performed between June and November 2018 at the Neurology Department of King Fahd Hospital of University, Kingdom of Saudi Arabia (KSA) and involved a review and analysis of EEG and medical records pertaining to 222 patients in whom encephalopathy was diagnosed. Results: In patients suffering from encephalopathy, advanced age ( P = .01), low Glasgow Coma Scale (GCS) scores ( P = .00), and certain etiologies, namely hypoxic-ischemic encephalopathy (HIE) ( P = .00), septic encephalopathy ( P = .01), and other illnesses ( P = .00), were significantly associated with unfavorable clinical outcomes, whereas traumatic brain injury (TBI) ( P = .01) and GCS >7 ( P = .00) were associated with favorable outcomes. Among different etiologies, EEG grade I ( P = .02) and grade IV ( P = .04) neuronal dysfunction was significantly associated with TBI while grade III ( P = .05) and grade V ( P = .02) neuronal dysfunction was significantly associated with HIE. Grade I ( P = .03) neuronal dysfunction was mostly observed in septic encephalopathy cases, while patients suffering from other illnesses were also found to have grade I ( P = .04) and grade IV ( P = .05) neuronal dysfunction based on their EEG. Conclusion: EEG is being conducted routinely to determine the course and severity of various forms of encephalopathy. However, the clinical implications of EEG grading for neuronal dysfunction are largely dependent on underlying etiology and other clinical parameters, such as age and GCS score. Further larger prospective cohort studies involving other important prognostic parameters and continuous EEG monitoring are thus needed.