9/27/2023 0 Comments Oxygen decompressor![]() He was admitted and treated for an ischaemic stroke and meningitis with empirical antibiotics. After discussion with the diving medicine doctor, he was taken to a HBOC for the second time, but to no avail. He was haemodynamically stable and was commenced on 1000 ml of 0.9% sodium chloride over 1 h, followed by a maintenance of 3 L over 24 h. His haemoglobin was 222 g/L, haematocrit was 63%, white cells 28 × 10 9/L, neutrophils 23 × 10 9/L, C-reactive protein 81 mg/L, and a mild acute kidney injury. A computed tomography (CT) was conducted of the head. He was brought to the ED where his Glasgow Coma Score was 13 and he had a left upper limb weakness. ![]() The next morning, he became confused, agitated, feverish, and clammy. He was discharged home by the diving doctor requiring only some assistance with walking. He was taken to a hyperbaric oxygen recompression chamber (HBOC) in Rugby, after which he showed signs of improvement. Shortly after diving, within 30 min, he experienced symptoms of left arm weakness, confusion, pain in the left ear, and bilateral paraesthesia of the hands. A day prior to attending the ED, he had dived three times to depths of 40 m for 30 min each time in a quarry in the UK. He had 2 weeks ago been abroad scuba diving multiple times out at sea at depths of 40 m, after which he flew back to the United Kingdom (UK). He has a past medical history of depression, an ex-smoker, drinks 32 units of alcohol per week, in a same-sex marriage, and a body mass index of 39. Type 2 decompression sickness is the more severe form and includes neurological, respiratory, and cardiovascular symptoms.Ī 42-year-old male presented to the emergency department (ED) post-scuba diving in a quarry. Additionally, a patent foramen ovale allows arterial gas emboli to cause further harm. Conclusionsĭecompression illness results as a sudden decrease in pressures during underwater ascent it is caused by nitrogen bubbles forming in tissue. Through a diagnosis of exclusion, decompression sickness was the conclusive diagnosis. Symptoms had slowly improved but he was left with a left arm motor weakness, and the team was left puzzled as to what could have caused his signs and symptoms. A leptospirosis and a vasculitis screen were both negative. A bubble echo confirmed a patent foramen ovale. A magnetic resonance imaging of his head revealed some deep periventricular ischaemic changes, old and new, however no signs of gas embolism or poor flow. His saturation had dropped to 91% on room air, and a computed tomography pulmonary angiogram revealed no obvious cause. Upon admission, his blood showed polycythaemia. ![]() He had another session in the hyperbaric oxygen chamber but to no success. A computed tomography of the head showed no signs of intracranial pathology. He attended the hyperbaric decompression chamber before attending the emergency department but to no resolve. Post-diving, he displayed typical symptoms of decompression illness. We present the case of a 42-year-old male from the West Midlands, UK, who attended the emergency department post-scuba diving with confusion, light-headedness, left arm weakness, and bilateral paraesthesia of the hands. Learning points to take are that decompression illness can present atypically, but one must exclude other causes. It takes into account the thought process of multiple systems and a multidisciplinary team approach. ![]() The case reinforces the importance of stepping back and looking at every possibility along with multiple co-existing pathologies.
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