Dutch guideline for the management of hypertensive crisis -- 2010 revision.

Hypertensive crises are divided into hypertensive urgencies and emergencies. Together they form a heterogeneous group of acute hypertensive disorders depending on the presence or type of target organs involved. Despite better treatment options for hypertension, hypertensive crisis and its associated complications remain relatively common. In the Netherlands the number of patients starting renal replacement therapy because of 'malignant hypertension' has increased in the past two decades. In 2003, the first Dutch guideline on hypertensive crisis was released to allow a standardised evidence-based approach for patients presenting with a hypertensive crisis. In this paper we give an overview of the current management of hypertensive crisis and discuss several important changes incorporated in the 2010 revision. These changes include a modification in terminology replacing 'malignant hypertension' with 'hypertensive crisis with retinopathy and reclassification of hypertensive crisis with retinopathy under hypertensive emergencies instead of urgencies. With regard to the treatment of hypertensive emergencies, nicardipine instead of nitroprusside or labetalol is favoured for the management of perioperative hypertension, whereas labetalol has become the drug of choice for the treatment of hypertension associated with pre-eclampsia. For the treatment of hypertensive urgencies, oral administration of nifedipine retard instead of captopril is recommended as first-line therapy. In addition, a section on the management of hypertensive emergencies according to the type of target organ involved has been added. Efforts to increase the awareness and treatment of hypertension in the population at large may lower the incidence of hypertensive crisis and its complications.

[Acute renal failure following treatment with intravenously administered immunoglobulins]. / Acuut nierfalen na behandeling met intraveneus toegediende immunoglobulinen.

A 74-year-old woman with insulin-dependent diabetes mellitus type 2 developed severe, reversible renal failure due probably to the administration of high doses of intravenous immunoglobulins (IVIG) for Guillain-Barré syndrome. The preparation administered did not contain sucrose or mannitol as adjuvants. The risk factors for the development of acute renal failure include pre-existent diabetes mellitus, reduced renal function and advanced age. In approximately 150 case reports in the literature, acute renal failure developed mainly after the use of sucrose-containing IVIG preparations. The course of both the onset of and the recovery from the renal failure and the histopathological findings in the described patient were in accordance with these findings. Since other causes were unlikely and in view of the supportive finding of elevated colloid osmotic pressure, it was concluded that the renal failure in this case was probably mediated by the oncotic effect of the macromolecular immunoglobulin itself.

Unexpected survival from severe metformin-associated lactic acidosis.

Lactic acidosis is a recognised complication of the antihyperglycaemic biguanide agent metformin, especially in patients with renal failure. We report a case of severe lactic acidosis and hypothermia due to metformin treatment and renal impairment. The favourable outcome despite extremely unfavourable clinical signs and symptoms for survival after admission and initial treatment was unexpected. Specific aspects of the clinical course are addressed.

Lack of correlation between bronchoconstrictor response and bronchodilator response in a population-based study.

Bronchodilator and bronchoconstrictor responsiveness have been considered physiological opposites in patients with obstructive airways disease. Provocation challenges have been replaced by bronchodilator tests in the assessment of cases of severe airways obstruction. The aim of this study was to examine the relationship between bronchoconstrictor and bronchodilator responsiveness, and their supposed interchangeability, in a general population. From the Vlagtwedde-Vlaardingen follow-up study, 101 adults were recruited (mean (SD) age 55 (11) yrs, 67 males and 34 females, and 31 were smokers). All completed a questionnaire on airways symptoms. Bronchoconstrictor and bronchodilator responsiveness were assessed with cumulative dose-response curves, using histamine and terbutaline, respectively. Thus, it was possible to relate histamine sensitivity of the airways (the concentration of histamine, at which forced expiratory volume in one second (FEV1) falls by 10% (PC10)) to the maximal bronchodilator response (delta FEV1) and the sensitivity to the bronchodilator (cumulative dose of inhaled terbutaline at which FEV1 increases by 10% (RD10)). Subjects with a bronchoconstrictor response (PC10 < or = 16 mg x mL(-1); n=38) had more respiratory symptoms than those without (n=63) (40 versus 21%) and also lower baseline FEV1 values (90 versus 96% predicted), but had comparable bronchodilator responsiveness. Subjects with a bronchodilator response (delta FEV1 > or = 9% of the predicted value; n=13) did not differ from those without (n=88) for all parameters, including symptoms, allergy and pulmonary function. In those with a bronchoconstrictor response, there was a weak but significant correlation between the PC10 and RD10 (rho=-0.32), but not between PC10 and delta FEV1. This study suggests that bronchoconstrictor and bronchodilator responsiveness are not highly correlated, even in subjects with airways obstruction. Symptoms were associated with the presence of a bronchoconstrictor, but not a bronchodilator, response. We conclude that bronchoconstrictor and bronchodilator responsiveness are two different phenotypic markers that are not interchangeable in epidemiological studies.

Changes in respiratory symptoms and airway hyperresponsiveness after 27 years in a population-based sample of school children.

We wanted to test the hypothesis that childhood airway hyperresponsiveness, even in the absence of respiratory symptoms, is a risk factor for respiratory disease in adulthood. In a childhood survey of 1963, three groups of 20 children aged 8-11 yrs, were selected from a population sample: 1) a group with recurrent respiratory symptoms (symptomatic group); 2) a group with no symptoms but a positive family history of atopy; and 3) a control group. All children completed assessment of symptoms, atopy, lung function, and airway hyperresponsiveness. At the adulthood survey 27 yrs later, 85% of the original sample were reinvestigated. Only 10 out of 19 subjects (53%) of the original symptomatic group still had symptoms. The significant difference of forced expiratory volume in one second (FEV1) % predicted in childhood between the symptomatic and the control group had disappeared. The prevalence of airway hyperresponsiveness had decreased in all groups. In asymptomatic hyperresponders it had normalized at adult age. The asymptomatic hyperresponders in childhood had lower levels of lung function, both in childhood and in adulthood. In univariate and multivariate analyses, respiratory symptoms at adult age were related to childhood atopy. Results suggest that childhood atopy is a risk factor for respiratory symptoms in young adulthood, but that mild childhood airway hyperresponsiveness is not.