{'fraction_non_alphanumeric': 0.018329938900203666, 'fraction_numerical': 0.0047522063815342835, 'mean_word_length': 5.353448275862069, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Sonography of the Optic Nerve: a New Bedside Tool in Intensive Care?]

History and clinical findings Here, we present the case history of a 76-year old man with out-of-hospital cardiac arrest due to a cardiogenic shock and a consecutive no-flow-time of approximately 10 minutes. After 25 minutes of resuscitation procedures a spontaneous return of circulation could be established. The patient was admitted to our center for emergency coronary angiography. After coronary stenting the patient was admitted to our intensive care unit and treated in accordance with the guidelines on cardiogenic shock due to myocardial infarction. Therapy and course After therapeutic hypothermia and subsequent termination of analgosedation a delayed wake-up reaction could be remarked. In the laboratory chemistry the initial parameter of neuron-specific enolase, a marker for cerebral hypoxia, was increased. Measurement of the optic nerve sheath diameter with a maximum diameter of 7 mm indicated an increased intracranial pressure. In the subsequent CT scan of the brain signs of hypoxic encephalopathy with breakup of grey and white matter differentiation were present. Conclusions In case of clinical and/or laboratory-chemical indications for hypoxic encephalopathy and/or increased intracranial pressure the bedside-based sonography examination at the intensive care unit should imply an evaluation of the optic nerve in order to initiate early apparative neurological diagnostics.