Chronic cardiac failure in children due to dilated cardiomyopathy: diagnostic approach, pathophysiology and management.

UNLABELLED: Dilated cardiomyopathy (DCM) is an important cause of chronic congestive cardiac failure (CCF) in infants and children. Although a variety of aetiological factors have been listed, most patients with echocardiographically documented DCM do not possess a demonstrable cause. Poor myocardial function in DCM triggers a sequence of compensatory mechanisms, mediated through the renin angiotensin system, the sympathetic system (neural and humoral) and a number of vasodilatory molecules. These favour myocardial and peripheral vascular remodelling by necrosis, fibrosis and apoptosis which ultimately does more harm than good. Management is essentially similar to that of CCF using a combination of diuretics, angiotensin converting enzyme inhibitors (ACEI) and digoxin. Use of additional diuretics, intravenous frusemide, dobutamine infusion and beta-adrenergic receptor blockers help to improve quality of life in resistant patients. ACEI, beta-adrenergic blockers and possibly aldosterone antagonists prolong survival. Compliance to medication can be enhanced by improving drug formulations and by assisting the family to choose the 'best-fit' regimen (concordance). At present, optimum management of end-stage CCF is cardiac transplant. CONCLUSION: Current understanding of the pathophysiology of chronic congestive cardiac failure resulting from dilated cardiomyopathy has shifted management strategy from steps that directly improve myocardial function to those that modulate the neuroendocrine profile and peripheral vascular reactivity. Similar advances in therapeutic applications would be assisted by controlled studies and full licensing of drugs for use in children. Medical intervention will remain the cornerstone of management until advances in surgical techniques become more widely available.

Infective endocarditis prophylaxis in children.

There has been no significant decrease in the incidence of infective endocarditis. Contributing factors include increased survival of susceptible patients, increased number of 'at risk' procedures and poor compliance with existing recommendations. This review highlights the scientific basis for prophylaxis, identifies patients and procedures at risk, and tabulates a simple protocol.

Symptomatic and prophylactic treatment of migraine: a critical reappraisal.

The pharmacologic management of migraine has traditionally focused on two approaches: symptomatic treatment and prophylactic therapy. The objective of symptomatic treatment is to reduce the intensity and duration of pain with its attendant symptoms and to optimize the patient's ability to function normally. The efficacy of most abortive antimigrainous drugs in probably related to their inhibitory effects on neurogenic inflammation mediated through serotoninergic control mechanisms. A variety of treatment strategies provide effective treatment for most attacks of moderate to severe migraine when utilizing one or a combination of the following classes of drugs: simple analgesics, nonsteroidal anti-inflammatory drugs, antiemetics, narcotic analgesics, ergot derivatives, and serotonin1-agonists. The choice of medication for an acute attack depends on factors such as the severity of the attack, the presence or absence of vomiting, time from onset of pain to peak pain level, rate of bioavailability of the drug, comorbid medical conditions, and the side effect profile of the drug. The major objective of prophylactic therapy is the reduction of frequency, duration, and intensity of attacks. Beta-blocking drugs without intrinsic sympathomimetic activity (such as propranolol), amitriptyline, flunarizine, serotonin antagonists (such as methysergide) and nonsteroidal anti-inflammatory drugs (such as naproxen) are the five main classes of drugs or agents that may be used as prophylactics.