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1/73. hypertensive encephalopathy in a patient with neonatal thyrotoxicosis.

    Neonatal hyperthyroidism may give rise to serious cardiovascular complications. A girl with severe thyrotoxicosis in whom hypertensive encephalopathy developed is described. CONCLUSION: Neonatal thyrotoxicosis can give rise to hypertension and may lead to hypertensive encephalopathy. ( info)

2/73. hypertensive encephalopathy in a patient with retroperitoneal fibrosis.

    A patient presented with retroperitoneal fibrosis but without any ureteric obstruction. The diagnosis was made by an abdominal CT scan and also at laparotomy. Post-operatively, she developed hypertensive encephalopathy. An isotope renogram with captopril was abnormal but not diagnostic of renal artery stenosis. The patient's condition improved with steroid and antihypertensive treatment. A follow-up CT scan showed complete resolution of peri-aortic thickening. A causative link is postulated between retroperitoneal fibrosis, trauma during laparotomy, and onset of acute hypertension. ( info)

3/73. Unusual MR findings of the brain stem in arterial hypertension.

    MR imaging findings have been reported in only a few cases of severe arterial hypertension. We report two cases of severe paroxysmal arterial hypertension associated with unusual brain stem hyperintensity. The lesions improved dramatically after stabilization of blood pressure, suggesting that edema could be the main cause of the MR imaging-observed hyperintensity. ( info)

4/73. hypertensive encephalopathy: complication in children treated for myeloproliferative disorders--report of three cases.

    We routinely perform echo-planar diffusion-weighted sequences in all brain magnetic resonance (MR) imaging studies. When three children undergoing chemotherapy for acute leukemia presented with seizures, conventional MR images demonstrated what appeared to be acute, posterior, parasagittal infarcts. However, diffusion-weighted images were normal. These MR imaging findings were consistent with those of hypertensive encephalopathy. Early recognition and treatment of minimal hypertension in these patients allows reversal of encephalopathy. ( info)

5/73. Functional recovery despite prolonged bilateral loss of somatosensory evoked potentials: report on two patients.

    A bilateral loss of short latency somatosensory evoked potentials (SSEPs) after head trauma or non-traumatic brain damage is normally associated with a deleterious neurological outcome. An adequate recovery in reported in two deeply comatose patients with head trauma or severe hypertensive encephalopathy despite prolonged bilateral loss of SSEPs over days, found in repeated recordings. Hence, a bilateral loss of SSEPs should not be considered alone for prediction of outcome in cerebral injury. ( info)

6/73. Low doses of liquorice can induce hypertension encephalopathy.

    Prolonged ingestion of liquorice is a well-known cause of hypertension due to hypermineralocorticoidism. We describe 2 cases of hypertension encephalopathy (in addition to the classical symptoms of hypertension, hypokalemia and suppression of the renin-aldosterone system) which resulted in pseudohyperaldosteronism syndrome due to the regular daily intake of low doses of liquorice. Glycyrrhizic acid, a component of liquorice, produces both hypermineralocorticism and the onset of encephalopathy through the inhibition of 11beta-hydroxysteroid dehydrogenase. hypertension encephalopathy due to the daily intake of low doses of liquorice, however, has not been previously documented. It is proposed that some people could be susceptible to low doses of glycyrrhizic acid because of a 11beta-hydroxysteroid dehydrogenase deficiency. ( info)

7/73. Hypertensive crisis and myocardial infarction following massive clonidine overdose.

    OBJECTIVE: To describe a patient who experienced a hypertensive crisis and myocardial infarction following a massive dose of parenteral clonidine. CASE SUMMARY: A 62-year-old white woman with stage 3 breast cancer metastatic to the spine and a history of hypertension received a combined injection of hydromorphone 48.3 mg and clonidine 12.24 mg subcutaneously in an attempt to refill an implanted epidural infusion pump. She promptly developed mental deterioration, blurred vision, worsening respiration, tachycardia, and hypertension. She was immediately treated with naloxone, but subsequently experienced hypertensive urgency, a short-duration tonic-clonic seizure, and an anteroseptal myocardial infarction. cardiac catheterization showed no arteriolar narrowing or blockage, but an anterior infarct was confirmed. DISCUSSION: clonidine is a commonly used alpha-adrenergic agonist. At usual oral doses of 0.2-2 mg/d, it acts centrally to produce hypotensive effects; at doses >7 mg/d, it acts peripherally to stimulate alpha1- and alpha2-adrenergic receptors, leading to vasoconstriction and increased blood pressure. These effects are not easy to control by standard medical therapies and can cause significant morbidity. CONCLUSIONS: clonidine, although a safe medication with usual dosages, must be used with caution when given in injectable form. An overdose of this alpha-adrenoreceptor agonist can produce significant vasospasm and hypertensive emergency. Drugs used to treat overdose, such as naloxone, can potentiate clonidine's adverse effects, leading to further morbidity. ( info)

8/73. The hyponatraemic hypertensive syndrome in a 2-year-old child with behavioural symptoms.

    In this case report we present a 2-year-old girl with the classical signs of the hyponatraemic hypertensive syndrome. She initially presented with a history of behavioural abnormalities and hyponatraemia (126 mmol/l) and her blood pressure was as high as 220/160 mmHg. After admission, somnolence developed. Intravenous anti-hypertensive therapy was started immediately. The hyponatraemia was treated with i.v. sodium supplementation. The cause of this syndrome proved to be fibromuscular dysplasia of the left renal artery. Finally, a left nephrectomy was performed. With this therapy, blood pressure and serum sodium normalised and the girl promptly regained normal consciousness and behaviour. CONCLUSION: Behavioural abnormalities in the history of a child without any other neurological symptoms might be one of the first signs of hypertensive encephalopathy. In combination with hyponatraemia, these symptoms should alert the physician to consider the hyponatraemic hypertensive syndrome. ( info)

9/73. hepatitis b-associated polyarteritis nodosa and hypertensive encephalopathy.

    The case of a two-year-old boy with hypertensive encephalopathy secondary to hepatitis b-associated polyarteritis nodosa is presented. polyarteritis nodosa is a rare condition in children and its association with hepatitis b viral infection is also rare. ( info)

10/73. Takayasu's arteritis and tuberculosis: a case report.

    The aetiology of Takayasu's arteritis is unknown, but an association with tuberculosis has been reported. We report the case of a 12-year-old-boy with Takayasu's arteritis: his blood pressure was 150/90 mmHg and fundoscopic examination showed grade I hypertensive changes. A tuberculin test was positive and acid-fast bacteria were seen in the urine. angiography revealed involvement of the descending aorta, thoracic aorta and upper abdominal aorta, with fusiform enlargement and no filling of the left renal artery. He was started on prednisolone therapy, with cyclophosphamide being added subsequently. Despite vigorous treatment, including three courses of nitroprusside infusion, the severe hypertension persisted and his blood pressure became regulated only after left nephrectomy. Acid-fast bacteria were seen in the nephrectomy material. The exact role of mycobacterium tuberculosis in the pathogenesis of Takayasu's arteritis is still unknown. In this patient the tuberculin test was positive and acid-fast bacteria were seen in both the urine and nephrectomy material. This finding is suggestive of the association between tuberculosis and the disease process. ( info)
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