A case of spinal epidural abscess concealed by delirium in a young man.

Spinal epidural abscess is a rare but serious condition with poor outcomes. It's classic triad of new back pain, neurological deficit and fever is only present in 15% of cases at presentation and is initially misdiagnosed in 75-89%.6,7 Delaying treatment is associated with worse outcomes. Delirium is itself a risk factor for mortality but the disturbance in cognition and memory can also complicate clinical assessment.1-5 We present a case of delirium caused by, and obscuring, a spinal epidural abscess. This case highlights the difficulties in diagnosing spinal epidural abscesses, the need for a high index of suspicion for the condition and timely action to minimise morbidity. In addition, it demonstrates the value of treating unexplained delirium as an emergency and the danger of diagnostic premature closure. Finally, the importance of persistent clinical examination of the confused and non-cooperative patient.

Multiple Organ Dysfunction Secondary to Herpes Simplex Virus -1 Reactivation After Treatment With Dexamethasone and Sarilumab for Covid-19 Disease.

Introduction: The immunological response to the SARS-CoV-2 virus and the treatment of COVID-19 disease present a potential susceptibility to viral reactivation, particularly Herpes simplex virus-1 (HSV-1). Case Presentation: A 49-year-old female presented to hospital with severe COVID-19 pneumonitis and was given sarilumab and dexamethasone. She was intubated and ventilated in the intensive care unit (ICU) and initially demonstrated biochemical and clinical evidence of improvement. This was followed by a severe acute deterioration in respiratory, renal, and cardiovascular function, accompanied by a vesicular rash on the face. Polymerase chain reaction confirmed HSV-1 reactivation and treatment with acyclovir was commenced. After 49 days in ICU the patient was successfully weaned from all organ support, and she made a satisfactory recovery. Conclusions: HSV-1 reactivation is common in COVID-19 and likely contributes to poorer clinical outcomes. The mechanism causing susceptibility to viral reactivation is not clearly defined, however, the development of critical illness induced immunosuppression via dysfunction of interferon and interleukin pathways is a likely mechanism. This effect could be perpetuated with immunosuppressant medications, although further research is needed to characterise this phenomenon.

Full neurological recovery following tricyclic overdose associated with absent brainstem reflexes.

We report the case of an 18-year-old gentleman who presented to the emergency department following a large overdose of amitriptyline. He was comatose on admission but his neurology further deteriorated to global loss of brainstem reflexes. He made a full but slow neurological recovery. First signs of improving neurology were seen on day 3 of admission; he was extubated on day 6 and discharged home on day 9. There is limited recent literature to help guide prognostication in this group of patients.

Risk of thromboembolism in patients developing critical illness-associated atrial fibrillation.

Although common, the long-term significance of -developing atrial fibrillation (AF) during a period of critical illness is unclear. We undertook a retrospective cohort analysis to -assess the rate of thromboembolism (TE) in patients -developing atrial fibrillation de novo during admission to our intensive care unit. In total, 1,955 patients were followed up (-maximum follow-up 1,276 days) for the occurrence of TE, of which 220 (11.3%) had developed AF or atrial flutter during their critical care admission. There were 11 TE events among the patients with new AF (0.053 events per patient-year), compared with 18 in the non-AF group (0.0059 events per patient-year). The unadjusted hazard ratio for TE in patients developing new AF compared with those not developing AF was 8.09 (95% CI 3.08-17.19, p<0.001). In patients admitted to critical care, the development of AF appears to be associated with a significantly increased risk of subsequent thromboembolism.

Plasma CC16 levels are associated with development of ALI/ARDS in patients with ventilator-associated pneumonia: a retrospective observational study.

BACKGROUND: Despite consensus criteria, diagnosing acute lung injury, or its more severe form acute respiratory distress syndrome (ALI/ARDS) remains challenging. Adding objective measures, such as plasma levels of biological markers could facilitate recognition of ALI/ARDS. This study was designed to assess and compare the diagnostic accuracy of biological markers for ALI/ARDS with ventilator-associated pneumonia (VAP). METHODS: We performed serial measurements of Clara cell protein (CC16), soluble receptor for advanced glycation end products (sRAGE), surfactant protein D (SP-D) and Krebs von den Lungen (KL-6) in plasma of patients with VAP and mechanically ventilated control patients without VAP. ALI/ARDS was diagnosed using the criteria of the North-American European consensus conference. RESULTS: Thirty-seven patients were enrolled - 22 patients with VAP and 15 control patients. Ten patients with pneumonia met the ALI/ARDS consensus criteria. Control patients never met these criteria. Plasma CC16 had a good diagnostic capacity for ALI/ARDS as shown by the receiver operating characteristic curve with an area under the curve of 0.91 (95% confidence interval (CI) 0.79 - 1.00; p < 0.001). Identification of ALI/ARDS patients by sudden increases in plasma CC16 of 30% or more yielded a sensitivity of 90% and a specificity of 92%. Of note, levels of CC16 increased 2 days before ALI/ARDS diagnosis. A cut-off level of 50 ng/ml SP-D yielded a specificity of 100% while the sensitivity was 70%. The area under the curve for SP-D was 0.80 (95% CI 0.58 - 1.00; p = 0.02). The diagnostic accuracies of KL-6 and sRAGE were low. CONCLUSION: Plasma CC16 seems a potential biological marker for ALI/ARDS in patients with VAP. Plasma levels of sRAGE, SP-D and KL-6 have limited discriminative power for diagnosing ALI/ARDS in VAP.