Aim: To determine usefulness and safety of intravenous infusion of clonidine in critically-ill children.Methods: Prospective, single-centre observational study from January 2013 to December 2014. PICU of Hospital Sant Joan Déu.Results: 73 patients were enrolled. Median age 7.9 months. Reasons for admission: Respiratory failure (42.5%) and post-cardiac surgery (30.1%). Median PICU length of stay: 14 days. 72 patients were intubated. The median days of clonidine use was 4. Reason for choosing clonidine: To improve prior sedation. We found no major adverse effects but some asymptomatic bradycardia. Conclusions:Clonidine seems to be a good alternative for sedation in critically-ill children. KeywordsClonidine, Sedation, Critically-ill child Opioids and benzodiazepines are the most frequently administered, but long-term use of these drugs is associated with tolerance and withdrawal, suppression of respiratory drive with prolonged ventilation, constipation, and delayed enteric feeding [2,3].Clonidine is a mixed alpha-1 and alpha-2 adrenoceptor agonist with a predominant alpha-2 action [4]. It has a sedative effect mediated by binding to post-synaptic alpha-2 receptors in the pontine locus ceruleus, reducing noradrenergic output and thereby facilitating the firing of inhibitory neurones, mainly, the gamma-aminobutyric acid system. Clonidine has an analgesic action through binding to alpha-2 receptors in the dorsal horn and supra-spinal sites and thereby reduce the release of P substance [1,5,6]. It also causes peripheral vasodilatation and a decrease in systolic blood pressure, heart rate and cardiac output by decreasing sympathetic nervous system activity. Clonidine has varying degrees of affinity for other cellular components called Nonadrenergic Imidazoline Binding Sites (NAIBS). It seems that the hypotensive effect of clonidine would owe more to their affinity for one type of NAIBS, called I1 receptors [7].As clonidine is lipid soluble, it penetrates the bloodbrain barrier to reach the hypothalamus and medulla [5]. It does not require transformation in to another substance prior to its action and about 20-40% is bound to protein. 50% of the drug is metabolized in the liver to inactive metabolites which are excreted in the urine