Congenital trigger thumb is a trigger thumb in infants and young children. Triggering, clicking or snapping is observed by flexion or extension of the interphalangeal joint (IPJ). In the furthest stage, no extension is possible and there is a fixed flexion deformity of the thumb in the IPJ. Cause, natural history, prognosis and recommended treatment are controversial. Signs and symptoms
Besides the clicking, snapping or triggering, a characteristic Notta nodule is commonly found on the palmar side at the metacarpophalangeal (MCP) joint. This nodule can be found by palpation. Children can also present a thumb which they cannot extend actively due to entrapment of the nodule to the A1 pulley. Some may even present with a fixed flexion deformity of the IPJ where no extension is possible. Cause
It is unclear whether the cause of the trigger thumb is congenital or acquired. The occurrence of bilateral incidence and trigger thumbs in both children of twins are an indication for a congenital cause. Trigger thumb in children is also associated with trisomy of chromosome 13. For these reasons it was assumed that trigger thumbs in children are to be of congenital cause. However, more and more evidence which point towards an acquired cause have been found in recent studies. Therefore, the name pediatric trigger thumb is also widely used (and currently preferred by some) for the same disorder. Diagnosis
Diagnosis of a trigger thumb is solely made by these clinical observations and further classified into four stages:

Treatment
There are several types of treatment for congenital trigger thumb, conservative and surgical.
Pharmacology
Mechanism of action
Alvimopan is a competitive antagonist of the μ-opioid receptors (MOR) in the gastrointestinal tract, with a Ki of 0.2 ng/mL. Activation of these receptors by endogenous or exogenous agonists reduces gastrointestinal motility, and alvimopan blocks this effect. Like most other peripherally-selective MOR antagonists, such as naloxegel and methylnaltrexone, alvimopan is selective for peripheral receptors because is effluxed by P-glycoprotein, which  reduces its ability to cross the blood-brain barrier and affect the central nervous system. Pharmacokinetics
Absorption
Peak plasma concentration (Cmax) of alvimopan is reached approximately 2 hours after oral dosing, while the Cmax for metabolite occurs 36 hours after an oral dose. Alvimopans high affinity for the peripheral μ-receptor results in an absolute bioavailability less than 7%. Distribution
80% to 90% of systemically available alvimopan is bound to plasma protein. At steady state, the volume of distribution is approximately 30 liters. Metabolism
Alvimopan undergoes no significant hepatic metabolism, but is metabolized by intestinal flora. Gut metabolism produces an active metabolite with no clinically significant contribution to drug effect. Elimination
Alvimopan undergoes 35% renal excretion and greater than 50% biliary excretion. Drug metabolized by intestinal flora is excreted in the feces. Alvimopans half-life of elimination is 10 to 17 hours, while that of the gut metabolite is 10 to 18 hours. Dosing and administration
Alvimopan is required by the FDA to participate in Risk Evaluation and Mitigation Strategy (REMS) to ensure safe use. Alvimopan is only approved for short term use of no more than 15 doses.