If fragments of patella bone stick out from the skin it is known as an open patella fracture, and closed if the overlying skin is intact. Treatment
Treatment may be with or without surgery, depending on the type of fracture and whether the overlying skin is intact or broken. Conservative
Undisplaced fractures can usually be treated by casting. Even some displaced fractures can be treated with casting as long as the person can straighten their leg without help, thus confirming that the quadriceps mechanism of the leg is intact. In this case the leg is immobilized in a straight position for the first three weeks and then increasing degrees of bending are allowed as healing occurs. Surgery
Most patella fractures are transverse or comminuted, hence the quadriceps mechanism is disrupted and they are treated by a combination of wires in a tension band construct. This unites the fractured bones, reconstructing the straightening mechanism of the leg.If the patella is broken in several places, that is  comminuted, then traditionally a patellectomy (removal of the whole patella) is performed in order to reconstruct the extensor mechanism and prevent the onset of an extension lag at the knee joint, resulting in instability. Some surgeons however would rather opt for internal fixation. A partial patellectomy is removal of only a portion of the patella, and may be carried out if at least 60% of the patella can be maintained.Open fractures of the patella require emergency treatment with irrigation, debridement and fixation.
Antacids administered in a peptic ulcer regimen may decrease the AUC of a single dose of phenytoin. Patients should be cautioned against concomitant use of antacids and phenytoin. "Warfarin and trimethoprim increase serum phenytoin levels and prolong the serum half-life of phenytoin by inhibiting its metabolism. Consider using other options if possible. Pharmacology
Mechanism of action
Phenytoin is believed to protect against seizures by causing voltage-dependent block of voltage gated sodium channels. This blocks sustained high frequency repetitive firing of action potentials. This is accomplished by reducing the amplitude of sodium-dependent action potentials through enhancing steady-state inactivation. Sodium channels exist in three main conformations: the resting state, the open state, and the inactive state. Phenytoin binds preferentially to the inactive form of the sodium channel. Because it takes time for the bound drug to dissociate from the inactive channel, there is a time-dependent block of the channel. Since the fraction of inactive channels is increased by membrane depolarization as well as by repetitive firing, the binding to the inactive state by phenytoin sodium can produce voltage-dependent, use-dependent and time-dependent block of sodium-dependent action potentials.The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of post-tetanic potentiation at synapses which prevents cortical seizure foci from detonating adjacent cortical areas.