Facilitation Of Donation After Circulatory Death

 

A previously fit and well 45 year old man presented to the emergency department with a two-hour history of a sudden onset severe headache associated with weakness, vomiting and photophobia. He had a normal breathing pattern and oxygen saturations of 96% in air. He was hypertensive with a non-invasive blood pressure of 220/115mmHg and a pulse rate of 85 beats/minute in sinus rhythm. Neurological examination revealed a Glasgow Coma Scale (GCS) of 14/15 with a dense hemiparesis, with hemisensory neglect and dysarthria.

He deteriorated and dropped his GCS to 5/15. He was intubated and an urgent computed tomographic (CT) brain scan was performed that revealed a large right-sided intraparenchymal haemorrhage with 4mm of midline shift. Blood tests including full blood count, urea and electrolytes and clotting screen were normal.

He was discussed with the neurosurgeons who felt transfer to institute intracranial pressure monitoring or surgical intervention was not indicated. His blood pressure was managed with a labetalol infusion aiming for a target systolic blood pressure of ≤ 160mmHg. Seizure activity was managed with a 15mg/kg loading dose of phenytoin followed by a maintenance dose of 300mg once daily nasogastrically. Sodium levels were monitored closely and hypotonic fluids avoided.

By day 5 he was making spontaneous respiratory effort, and his pupils were equal and sluggishly reactive. His GCS remained 3/15. A repeat CT was performed on day 9 due to no improvement in his clinical condition and revealed extension of the intraparenchymal haemorrhage with 8mm midline shift, effacement of the ventricles and loss of sulcal definition. A discussion regarding end of life care was held with his family who raised the possibility of organ donation. In agreement with his family, end of life care was instituted and he became an organ donor after circulatory death was confirmed.

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Thrombotic Thrombocytopaenic Purpura

A previously fit and well 64 year old gentleman presented to the acute medical unit with a two-week history of lethargy, bruising, dark urine and an episode of transient facial numbness, blurred vision and dysarthria lasting 30 minutes. Clinical examination revealed mild jaundice, multiple bruises and a palpable liver edge but was otherwise normal. His respiratory rate was 14 breaths/minute with normal oxygen saturations. He was in sinus rhythm with a pulse of 68 beats/minute and non-invasive blood pressure was 130/70. He was GCS 15 and was apyrexial.

His full blood count revealed a haemoglobin of 94 g/L, platelets 9 x109/L, and white cell count 9 x109/L. A blood film showed red cell fragmentation, spherocytes, polychromasia, poikilocytosis and no platelet clumps. Reticulocytes and lactate dehydrogenase were raised at 168.6 x 109/L and 3027 iu/L respectively. Liver function tests revealed a bilirubin of 49 µmol/L but were otherwise normal. A liver ultrasound showed fatty infiltration. Clotting was normal and direct antiglobulin test negative. Urea and electrolytes were normal, creatinine 80 µmol/L and the C reactive protein was 37. ADAMTS13 assay showed complete absence of activity. CT brain was normal.

He was reviewed by the haematologists who diagnosed thrombotic thrombocytopenic purpura and referred him to the intensive care unit for plasma exchange. He received a three-day course of methylprednisolone, was intubated due to agitation, received plasma exchange with octaplas replacement that increased from 2 litre to 5 litre exchanges, and rituximab 750mg.

He deteriorated progressively with: vomiting, anaemia requiring blood transfusions, worsening thrombocytopenia, acute kidney injury with a peak creatinine of 457 µmol/L, an inferior ST elevation myocardial infarction, and a posterior cerebral artery territory infarct.

On day 5 he developed fixed and dilated pupils. Mannitol 1g/kg was administered and an urgent CT brain performed. This revealed multiple infarcts in both cerebral hemispheres and right cerebellum, loss of grey-white differentiation, 5mm midline shift and low cerebellar tonsils.

After discussion with the neurosurgeons it was decided this was an unrecoverable injury. In agreement with his family, end of life care was instituted and he died within 24 hours.

Describe the management of Thrombotic Thrombocytopaenic Purpura.Read More »