Sudden cardiac death (SCD) represents a global emergency, with a high number of cases affecting all age groups every year. The prevention of these fatal events requires an accurate knowledge of etiology and pathogenesis, which can vary. Autopsy is an indispensable tool in cases of SCD for diagnostic purposes, as well as for judicial and preventive purposes for family members. Despite the completion of all routine post-mortem investigations, it is often complicated for the forensic pathologist to define the triggering cause of these events. The study of the proteome is proving to be extremely promising in the field of human cardiovascular disease. This paper aims to offer a literature review on the study of the proteome in post-mortem cadaveric biological samples obtained from SCD cases. The aim of this work is to outline the state of the art of the scientific advances that protein analysis can offer in the diagnosis of SCD and the limits that various studies have traced up to now. In conclusion, the work defines the future perspectives of this field in SCD, suggesting strategies to overcome the reported limits and improve the diagnostics of these events.

Exploring the Potential of Proteome Analysis as a Promising Tool for Evaluation of Sudden Cardiac Death (SCD) in Forensic Settings: A Literature Review

BACKGROUND: The multifocal acquired demyelinating sensory and motor neuropathy (MADSAM) is a rare adult onset subvariant of the chronic inflammatory demyelinating polyneuropathy (CIDP). The latter affects 1-9 cases per million adults and may pose a diagnostic challenge (antibody and electrophysiological overlap). The hallmark of the disease spectrum is an immune mediated structural myelin breakdown. Urgent differentiation of MADSAM from the other variants of CIDP is indicated due to its distinct pathogenesis, management, and long-term therapy response to immunomodulators. The disease presents with progressive asymmetrical motor and sensory deficits initially located typically in one limb. Rarely the disease manifests with cranial nerve involvement. The prognosis of patients suffering from MADSAM is reliant on rapid diagnosis and therapeutic response, but neurological deficits reside. Due to its rarity and diagnostic challenge, misdiagnosis is common.
THE CASE: A 84 years old Caucasian male diagnosed with multifocal acquired demyelinating sensory and motor neuropathy (MADSAM) presented to our department with progressive neurological deficits. His neurological examination and history revealed paresthesia, hypesthesia, diminished vibration sense (pallhypesthesia), distally pronounced paresis in the upper extremities with a wrist drop on the left hand. Gait examination exposed coordination deficits. The history of the patient and the initial presentation of the disease in 1998 exemplifies the diagnostic challenge of MADSAM, due its mimicry of other diseases, like multifocal motor neuropathy (MMN). The initial symptoms were asymmetrical motor and sensory deficit starting at the upper extremities. Before the patient presented to our facility, he was diagnosed with neuroborreliosis and treated accordingly. The correct diagnosis was set at our department according to clinical presentation, nerve conduction velocity parameters and conduction block during electroneurography, typical changes in nerve ultrasound suggesting an inflammatory neuropathy and fasciculations of the gastrocnemius muscle. After an ineffective steroid therapy and long standing intravenous immunoglobulins the patient is now on a therapeutic scheme of 1000mg Rituximab (CD20 Ab) every 6 months and 1000mg Mycophenolatmofetil. The patient subjectively reports improvement of his status and slower progression of the disease since the Rituximab paradigm. Furthermore, an evident atrophy of the orbicularis oculi muscle was now noted during follow up examination, which highlights facial nerve involvement.
CONCLUSION: This case exemplifies the challenge of diagnosing the multifocal acquired sensory and motor neuropathy, but prompt diagnosis and therapeutic intervention is associated with a better prognosis and slower progression of the disease in patients suffering from MADSAM.

Multifocal Acquired Demyelinating Sensory and Motor Neuropathy (MADSAM) with Cranial Nerve Involvement. Case Report

Lewis-Sumner syndrome (LSS) is a rare immune-mediated neuromuscular disorder. It shares some clinical and pathological features with chronic inflammatory demyelinating polyneuropathy (CIDP). We report on the anaesthetic management of a patient with LSS. There are several concerns when anaesthetizing patients with demyelinating neuropathies, the main ones being the post-operative worsening of symptoms and respiratory depression related to muscle relaxants. In our experience, the rocuronium effect was prolonged and an even lower dosage (0.4 mg/kg) was sufficient for intubation and maintenance. Sugammadex allowed total reversion of neuromuscular block and no respiratory complications occurred. In conclusion, the combination of lower dose rocuronium and sugammadex was safely used in a patient with LSS.

/pdf/perioperative-management-of-lewis-sumner-syndrome-2ahlny6j.pdf

Perioperative Management of Lewis-Sumner Syndrome.

Anesthetic Management of a Patient With Prinzmetal Angina

<h3>Background and Aims</h3> The main goals when managing patients with severe aortic stenosis are maintaining normal sinus rhythm and avoiding hypotension. Both general anesthesia and single-shot spinal are associated with significant hemodynamic changes, making them less than ideal options for these patients.<sup>1,2</sup> <h3>Methods</h3> We report the successful use of continuous spinal anesthesia in a frail patient with severe aortic stenosis waiting for Transcatheter Aortic Valve Implantation (TAVI). An 83-year-old woman, ASA IV, was scheduled for urgent non-cemented hip hemiarthroplasty due to a femoral neck fracture. Her medical history included severe aortic stenosis (valve area of 0.50 cm2, mean valve gradient of 33mmHg), heart failure, coronary artery disease, atrial flutter, hypertension, diabetes, bilateral carotid stenosis, COPD, and recent pneumonia. <h3>Results</h3> Once in the theatre, standard monitoring was started, and a brachial arterial line was placed. A femoral nerve block was performed with 0,5% ropivacaine (20 mL). An intrathecal catheter was placed and small doses of levobupivacaine 0,5% (up to 4mg) were administered (8,5mg total). A low-dose background infusion of phenylephrine was started at the time of intrathecal administration. The patient remained hemodynamically stable and comfortable throughout the procedure. The catheter was removed at the end of the surgery. Postoperative care continued in the level II unit for two days, with no complications. Postoperative pain was easily controlled with paracetamol and low-dose tramadol. <h3>Conclusions</h3> Patients with severe aortic stenosis remain a challenge for anesthesiologists when presenting for orthopedic surgery. Continuous spinal anesthesia with peripheral nerve block is a safe and effective technique for these patients. 

/pdf/b249-continuous-spinal-anaesthesia-and-peripheral-nerve-mermfm8j.pdf

B249 Continuous spinal anaesthesia and peripheral nerve block – a winning combination in severe aortic stenosis

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Perioperative Management of Lewis-Sumner Syndrome.

Anesthetic Management of a Patient With Prinzmetal Angina

B249 Continuous spinal anaesthesia and peripheral nerve block – a winning combination in severe aortic stenosis