A nursing shortage - a prospect of global and local policies.

AIM: The article addresses selected determinants of the nursing shortage in Poland and other countries in the face of employee ageing. BACKGROUND: Global demographic changes have led to a systematic increase in the elderly population and a decreasing number of births, which have impacted health policy and healthcare systems in various countries. Both processes necessitate transitions in global health care. Nursing care, which has faced a human resources crisis, is a strategic area within this context. SOURCES OF EVIDENCE: This study is based on national listings and strategic documents for nursing policy in Poland, including Increasing average age of nurses and midwives prepared by the Polish Main Council of Nurses and Midwives, the incorporation of big data, international reports and a literature review on nursing and healthcare challenges. DISCUSSION/CONCLUSIONS: This paper argues that the causes of the nursing shortage are multifaceted with no single global or local measure of its nature. An overview of the problem indicates ineffective planning and use of available nursing resources, poor recruitment or an undersupply of a new staff, and global demographic conditions. The overview highlights the fact that nursing shortages have reached a critical point for healthcare services on both the local and global levels. CONCLUSIONS FOR NURSING AND HEALTH POLICY: The general recommendations for nursing policy include the need to prepare and implement national social security agendas into services provided by nurses. Such a programme would include general issues: improving working and employment conditions, implementing mechanisms regulating salary and providing the possibility of lifelong learning with the incorporation of mobile and technological innovations as a sustainable solution.

Immunology of Helicobacter pylori infection.

We have tried to answer several questions in this article, dealing with: ontogenesis of the immune response, presentation of H. pylori antigens to immune cells, systemic vs local immune response, cytokine Th1/Th2 configuration, the role of cytokines, especially represented during H. pylori infection, mimicry phenomena, extragastroduodenal sites and manifestations and finally, vaccine development. The new achievements in the vaccine field, also of Polish groups, were underlined.

[Evaluation of the efficacy and safety of monotherapy for significant essential hypertension in adolescents with use of enalapril]. / Ocena skutecznosci i bezpieczenstwa monoterapii znamiennego nadcisnienia tetniczego u mlodziezy przy zastosowaniu enalaprylu.

Clinical evaluation of hypotensive effectiveness and the cardiovascular and side effects of enalapril monotherapy of significant essential hypertension (SEH) in adolescents was performed. The studied group included 30 pts., aged from 12 to 18 years. The mean enalapril dose was 0.22 mg/kg/24 hours. Significant decrease of systolic, diastolic and mean arterial blood pressure was observed. ECHO examination performed after 6 months of therapy demonstrated significant decrease of intraventricular septum thickness, cardiac index and percentage of LV fractional shortening. Only a few minor side effects involving the GI tract were observed during therapy. We conclude that enalapril monotherapy is effective in adolescents with SEH and exerts a beneficial influence on sodium and purine balance and no adverse effect on the lipid profile. It can therefore be safely used in hypertensive patients with hyperuricemia and hypercholesterolemia. It causes regression of LV hypertrophy and improves exercise capacity.

Effect of nifedipine on tubular handling of uric acid in transplanted kidney on cyclosporine A treatment.

Hyperuricemia resulting from tubular urate transport defects is a well-known nephrotoxic effect of cyclosporine A (CyA) on renal blood perfusion in organ recipients. The aim of this study was to define the mechanism of the tubular urate transport defect in hyperuricemic renal graft recipients on CyA and to evaluate the effect of nifedipine retard administration on this tubular dysfunction. Tubular uric acid transport was evaluated by the probenecid test in 17 hyperuricemic (group 1) and 6 normouricemic (group 2) renal graft recipients treated with CyA. Maximal urate excretion after probenecid administration was 25.5 +/- 4.6 versus 42.5 +/- 7.7% (p < 0.001) and postsecretory urate reabsorption was 79.2 +/- 8.3 versus 78.5 +/- 9.7% (NS), respectively. The effects of nifedipine retard on renal urate transport were evaluated in 6 hyperuricemic patients. Seven days of nifedipine therapy did not significantly decrease mean serum uric acid levels (7.7 +/- 1.6 to 7.1 +/- 1.1 mg/dl) nor increase urate clearance (3.8 +/- 1.3 to 4.7 +/- 1.6 ml/min/1.73 m2). The uricosuric effect of probenecid was manifested by an increase in tubular urate transport from 25.5 +/- 4.6 to 37.3 +/- 7.2%, p < 0.01, paralleled by an increase in postsecretory urate reabsorption from 20.5 +/- 3.7 to 31.4 +/- 5.7% (p < 0.003). Postsecretory reabsorption expressed as a percentage of secreted urate in both evaluations did not differ significantly (80.3 +/- 6.2 vs. 84.4 +/- 3.1%).(ABSTRACT TRUNCATED AT 250 WORDS)

The renin-angiotensin-aldosterone system and vasopressin in early-stage liver cirrhosis after HBV infection in children.

We evaluated the dynamic response of renin, aldosterone, and vasopressin to intravenous water loading (20 ml 5% glucose/kg b.w.) in 12 children (aged 7-18 years) with postinflammatory liver cirrhosis after hepatitis B virus (HBV) infection. All of the patients had early-stage liver cirrhosis; according to Child's classification, nine patients had group A; three, group B cirrhosis. A group of 17 children with chronic persistent hepatitis served as the control. The diagnoses were confirmed in all of the patients by liver biopsy. The patients followed a diet containing 3 mmol NaCl/kg/day, maximum 100 mmol per day for 6 days. Water loading was performed in recumbency over approximately 45 min. Renin, aldosterone, and vasopressin, assayed by radioimmunoassay (RIA), were determined before, 1 h, and 5 h after starting the water load. Prestudy hormone levels were within normal range in both groups. Renin and aldosterone concentration change patterns were similar in both groups and characterized by suppression of hormone activity caused by central volume expansion and recovery to prestudy levels after 5 h. However, the pattern of change of vasopressin concentrations differed in the control and study groups. In contrast to that of the controls, volume expansion did not suppress vasopressin in the group with liver cirrhosis. We conclude that failure to suppress vasopressin activity after central volume expansion may be one of the early mechanisms responsible for water-electrolyte imbalance in liver cirrhosis in children.

[Evaluation of the efficacy and tolerance of three antihypertensive agents used as single-drug therapy, nifedipine, prazosin and acebutolol in severe, idiopathic hypertension in adolescents]. / Evaluation de l'efficacité et de la tolérance de trois antihypertenseurs utilisés en monothérapie, nifédipine, prazosin et acébutolol dans l'hypertension idiopathique grave de l'adolescent.

The antihypertensive efficacy of single-drug therapy with nifedipine (N), prazosin (P), or acebutolol (A) and the influence of these agents on coronary risk factors including hypoglycemia, hyperuricemia, and hyperlipidemia, were studied in adolescents with hypertension. Ninety patients (73 girls and 17 boys) aged 14 to 18 years with idiopathic hypertension (IH) were randomized into three groups. Each group received N, P, or A as single-drug therapy for six months. Systolic and diastolic blood pressures fell in all three groups, from 152/90 mmHg to 127/70 mmHg* with N, from 150/90 mmHg to 121/70 mmHg* with P, and from 148/92 mmHg to 122/74 mmHg* mmHg with A. In 17% of cases, N failed to reduce blood pressures below the 90th centiles. Heart rate was not influenced by N or P but decreased from 84 to 75 bpm with A. Although none of the drugs modified serum uric acid levels, fractional uric acid secretion rose with P and A (from 4.1% to 6% with P; and from 4.4% to 6% with A). The lipid profile remained unchanged under N and P, whereas a decrease in serum LDL-cholesterol from 99.6 to 88.8% mg* was seen with A. Fasting serum glucose levels increased from 86.4 to 92.7 mg %* in the group given A. N, P, and A are suitable for single-drug therapy of IH in adolescents; the most appropriate drug should be selected on the basis of medical history.

Hypouricemia due to increased tubular secretion of urate in children with Amanita phalloides poisoning.

The tubular transport of urate was studied in 20 children poisoned with Amanita phalloides and in control group. The aim of this study was to investigate the cause of repeatedly observed episodes of hypouricemia in patients after A. phalloides poisoning. A significant negative correlation between serum uric acid concentration and fractional excretion of urate in poisoned and control groups (r = 0.73, p < 0.001) was found. The results of pyrazinamide and probenecid tests performed in patients after A. phalloides poisoning indicated that hyperuricosuria was most likely due to an increment in renal tubular urate secretion, and not due to decreased presecretory and postsecretory reabsorption of uric acid. These findings indicate that hypouricemia found after A. phalloides poisoning in children is of renal origin due to an increase in tubular urate secretion.

[Difficulties in the diagnosis of pheochromocytoma in children]. / Trudnosci diagnostyczne w rozpoznawaniu guza chromochlonnego u dzieci.

Pheochromocytoma was the cause of arterial hypertension observed in 0.9% of children treated in 1982-1989. Out of clinical features the most characteristic was sustained hypertension often complicated by the accelerated phase of malignant hypertension and encephalopathy. Sustained tachycardia was also found in all patients. Increased urinary excretion of catecholamines and its metabolites confirmed the diagnosis in all cases. The most sensitive and specific methods for tumor diagnosis were ultrasonography and computer tomography of the adrenals while scintigraphy with meta-iodobenzylguanidine+ labelled with iodine-131 radioisotope gave a high percentage of false negative results.

A single pediatric center experience with 1025 children with hypertension.

Between January 1982 and December 1989 1025 patients aged between one month and 18 years with increased blood pressure were referred for evaluation. Borderline hypertension was found in 389 children; 636 had sustained significant hypertension. In 351 patients, hypertension was secondary to a known disease. Renal parenchymal diseases were present in 68% of patients while renovascular and endocrine disorders were found in 10% and 11%, respectively. Of the 258 children aged less than 15 years, all but six children had known causes of hypertension, while 75% of adolescents had essential hypertension. In the 389 children with borderline hypertension, 65% developed fixed hypertension over a period of 2-3 years.

[Primary hyperaldosteronism suppressed after glucocorticoid administration]. / Pierwotny hiperaldosteronizm hamowany podawaniem glikokortykoidów.

Authors present a case of glucocorticoid suppressible hyperaldosteronism in 18 year old female. Unmeasurable low plasma renin activity and marked increase in aldosterone concentration was established. After administration of dexamethasone, normalization of aldosterone concentration and blood pressure has been observed.

Pheochromocytoma in children: difficulties in diagnosis and localization.

Surgically confirmed pheochromocytoma was the cause of arterial hypertension in 6 out of 668 (0.8%) children with significant hypertension admitted to Child Health Centre in Warsaw. Among clinical features most characteristic was sustained hypertension observed in all patients, often complicated by the accelerated phase of malignant hypertension and encephalopathy. Sustained tachycardia was also found in all patients. Elevated sedimentation rate and electrocardiographic changes were observed in each child while other abnormal laboratory findings such as hyperglycemia, etc. occurred at similar rate as in adults. Increased urinary excretion of catecholamines and their metabolites confirmed the diagnosis. In our study the most sensitive methods for tumor localization were ultrasonography and computed tomography of the adrenals while scintigraphy with iodo-131-metabenzylguanidine gave a high percentage of false negative results. Clinical presentation of pheochromocytomas in children is different than in adults and all pediatric patients with severe hypertension should be screened for this disease.

Characterization of the effect of nicotine on vasopressin and atrial natriuretic factor in the rabbit.

The effects of nicotine on the secretion of arginine vasopressin (AVP) and of the atrial natriuretic factor (ANF) were examined in conscious rabbits. Nicotine was shown to produce significant increases in plasma AVP from 1.7 +/- 0.4 to 75.3 +/- 35.1 pg/ml (P less than .05) and in plasma ANF levels from 39 +/- 11 to 121 +/- 52 pg/ml (P less than .05) within 5 min of an i.v. dose of 0.5 mg/kg. These nicotine-induced stimulations could not be inhibited by muscarinic (atropine), dopaminergic [(+/-)-sulpiride], alpha (phenoxy-benzamine) or beta adrenergic (propranolol) blockers or by a rapid infusion of fluids. Trimetaphan was ineffective in blocking the stimulation of AVP secretion but completely abolished the nicotine-induced secretion of ANF. The more lipophilic ganglionic blocker, mecamylamine, blocked the stimulation of the secretion of both peptides. The effect of nicotine on AVP production was confirmed in vitro using the rat hypothalamo-neurohypophysial system preparation where nicotine increased AVP secretion in a dose-dependent manner. This in vitro stimulation was blocked by the ganglionic blocker hexamethonium. The increase in ANF plasma concentrations was probably due to a primary response to nicotine, for although exogenous AVP (1 microgram i.v.) increased ANF levels by a factor of 3 (P less than .05), the AVP antagonist [-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2- (O-methyl)tyrosine]arginine vasopressin did not prevent the nicotine-induced increase in ANF. Thus, nicotine or its effects appear to stimulate the secretion of ANF and not AVP. It was concluded that nicotine stimulates the secretion of AVP by activating central nicotinic projections to the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)