Platelet responses to focal hepatic necrosis were studied using spinning disk confocal intravital microscopy. Platelets instantly adhered to molecularly altered sinusoidal endothelium adjacent to the necrosis paving approximately 200 µm of vessels abutting the injury. Platelets remained accumulated around the necrosis for at least 4 hours but dissipated by 8 hours. GPIIbIIIa was the main adhesive mechanism; GPIb and GPVI were involved at later stages. Platelets did not cause by-stander injury and did not occlude the vessels. Endothelin-induced vasoconstriction via hepatic stellate cells and not the platelet accumulation or coagulation was responsible for temporarily restricted perfusion around the injury. Neutrophil recruitment over four hours to the sterile necrosis was platelet and GPIIbIIIa dependent. As platelets slowly dissipated neutrophil recruitment was also halted. Healing was delayed in GPIIbIIIa deficient mice. We conclude that in localized sterile injury platelets are essential for neutrophil recruitment and subsequent repair of the lesion.