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A 73-year-old man participated in a charity cycle ride in Kenya. He was usually very fit and, despite coronary artery bypass grafting 12 years previously, had participated in several similar events. He rode the first 4 days in full, covering 40 miles, off road, in average daily shade temperatures of 34°C. On the fifth day, he had an episode of lightheadedness and was hypotensive, with a resting pulse of 28 beats/min. He rested in the shade, drank copious oral fluids and was given 1 litre of normal (0.9%) saline intravenously. He remained bradycardic and hypotensive for 8 h but was asymptomatic while resting, with no chest pain or breathlessness. His cardiac rhythm could not be determined. He was not taking β-blockers.
The following day, his pulse and blood pressure had returned to normal but he did not cycle. He was asymptomatic, walking, eating and drinking normally. The next day, he relaxed at a hotel complex, drinking normal fluids, ate a celebratory meal in the evening but did not consume alcohol. At 23:00, he developed dysarthria and I was asked to examine him. He had mild left-sided arm and leg weakness (drift, National Institute of Health Stroke Scale score 1), left-sided sensory loss, sensory inattention, left homonymous hemianopia and visual inattention. There were some word finding difficulties. The total National Institute of Health Stroke Scale score was 10. An ambulance was arranged to take him to Mombasa Hospital.
On arrival, his neurological signs were unchanged. I cautiously introduced myself as a doctor travelling with the group and said that I specialised in stroke. The emergency physician arranged a CT brain scan. During this, we had an informal discussion about stroke treatment and the possibility of thrombolysis, which had not previously been used in the city. Tenecteplase was available for myocardial infarction. There was no radiologist present to report the scan. It showed no haemorrhage and had an Alberta Stroke Program Early CT score of 10. The local specialist proposed conservative management as there was only barely detectable weakness. I suggested he might consider thrombolysis as there were other significant neurological signs and no contraindications. He agreed, and we decided to give the cardiac dose of tenecteplase 35 mg (body weight 67.5 kg). This was ordered verbally by the local specialist and given immediately as a single bolus. Onset to needle time was 90 min. The specialist wanted to give heparin and to insert a urinary catheter and nasogastric tube. I tactfully advised that these were not necessary. Routine blood tests available after thrombolysis showed that serum sodium was 135 mmol/l and serum urea was 23 mmol/l. Intravenous fluids were prescribed.
The patient improved. Nine hours later he was still dysarthric with some word finding problems but no weakness; his hemianopia, sensory loss and inattention had resolved. On day 2, all neurological signs had resolved. He flew back to England three days later. Brain MRI, carried out 11 days after treatment, showed localised swelling and signal abnormality within the right insular cortex and a further tiny focus within the lateral adjacent frontal cortex. The diffusion characteristics were in keeping with a subacute middle cerebral artery infarction, typically between 7 and 14 days old. Diffusion was not restricted within the lesion, and apparent diffusion coefficient characteristics were intermediate. There was a further focal signal abnormality within the splenium of the corpus callosum not showing restricted diffusion (figures 1 and 2). Renal function had returned to normal; echocardiography, carotid and renal ultrasound, and 24 h electrocardiogram were all normal.
The residual subacute ischaemic damage in the right insular and peri-insular cortex would be consistent with successful thrombolysis of what may well have been a more extensive initial region of middle cerebral artery territory ischaemia. The possibility of extrapontine myelinolysis as a result of his rehydration 2 days earlier was considered; however, there were no typical radiological features to support this, serum sodium was normal on admission and remained unchanged after overnight rehydration, and also the neurological signs largely resolved overnight. Nevertheless, this diagnosis still remains a possibility. It is also possible that this was cerebral ischaemia due to dehydration on a background of atherosclerotic small vessel disease, which was successfully treated by a combination of thrombolysis and rehydration.
Lesions such as that seen in the corpus callosum are most commonly associated with epilepsy but may also be seen in the context of acute illness and electrolyte disturbance, particularly in older people. The exact pathophysiology is not well understood and the diffusion characteristics of such lesions also vary but they are generally asymptomatic, self-limiting and frequently reversible. This would fit with this patient's clinical picture.
Dehydration became apparent only after thrombolysis had been given. This highlights one of the difficulties of having to make thrombolysis decisions rapidly. The evidence strongly supports early treatment but often the history and investigations are incomplete. It is impossible to be certain in retrospect whether thrombolysis in an individual has been effective, as the neurological signs may be short lived in stroke and its mimics. However, it is also important not to withhold potentially beneficial treatment. In this case the sudden onset of focal neurological symptoms in a patient with known vascular disease clearly came within the indications for thrombolysis.
Tenecteplase has a longer half life than alteplase. This means it can be given as a bolus without an infusion. It also has greater fibrin specificity and in studies in myocardial infarction it carried a lower risk of remote haemorrhage. There are reports of 200 stroke patients that have been treated with tenecteplase1 2 but a safe dosage has never been established and it has never been licensed for stroke. The challenge was to enable a treatment carrying significant risk, with which the local doctor was not familiar, to be given rapidly in a foreign country. I was fortunate to encounter a doctor who was sufficiently trusting and open minded to allow me, with no proof of who I was, to treat the patient. In the risk management culture of the UK I doubt this would have happened.
Others in this situation should be calm, allow the local doctors to make their own assessment and then to engage them in a professional conversation allowing your expertise to become apparent. It is also important to realise that standard procedures at home may not be known elsewhere. I had to detail the management of the patient after treatment to reduce risk and ensure adequate monitoring for neurological and haemodynamic deterioration. I was also reminded how doctors not trained or experienced in neurology fail to detect sensory, visual and cortical signs and therefore underestimate the seriousness of a stroke.
A copy of our thrombolysis protocol with details of the best available dosing data on tenecteplase has been sent to Mombasa, who have now adopted it for future use.
■ Chronic dehydration may be a cause of ischaemic stroke.
■ Extrapontine myelinolysis should be considered in the differential diagnosis of rapidly developing neurological symptoms.
■ Thrombolysis is possible outside stroke centres.
■ More research is needed on the risks or otherwise of thrombolysing potential stroke mimics.
■ When trying to get doctors you do not know to consider your advice:
■ Avoid being pushy
■ Establish friendly relationships and demonstrate your expertise by professional discussion
■ Recognise that modern treatment protocols include checks and balances that may not be routine elsewhere
■ Ensure you personally follow-up patients to avoid problems.
The author thanks Dr A Waldman for reporting the MR scan. This paper was reviewed by Tom Hughes, Cardiff, UK.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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