Animal reproductive studies have not yet been conducted with benzonatate to evaluate its teratogenicity. Benzonatate should only be given to a pregnant woman if it is clearly needed.It is not known whether benzonatate is excreted in human milk. It is recommended to exercise caution when benzonatate is given to a nursing woman. Overdose
Benzonatate is chemically similar to other local anesthetics such as tetracaine and procaine, and shares their pharmacology and toxicology.Benzonatate overdose is characterized by symptoms of restlessness, tremors, seizures, abnormal heart rhythms (cardiac arrhythmia), cerebral edema, absent breathing (apnea), fast heart beat (tachycardia), and in severe cases, coma and death. Symptoms develop rapidly, typically within 1 hour of ingestion. Treatment focuses on removal of gastric contents and on managing symptoms of sedation, convulsions, apnea, and cardiac arrhythmia.Despite a long history of safe and appropriate usage, the safety margin of benzonatate is reportedly narrow. Toxicity above the therapeutic dose is relatively low and ingestion of a small handful of pills can cause symptoms of overdose. Children are at an increased risk for toxicity, which have occurred with administration of only one or two capsules.Due to increasing usage of benzonatate and rapid onset of symptoms, there are accumulating cases of benzonatate overdose deaths, especially in children. Pharmacology
Benzonatate is chemically similar to other local anesthetics such as tetracaine and procaine, and shares their pharmacology. Mechanism of action
Similar to other local anesthetics, benzonatate is a potent voltage-gated sodium channel inhibitor.
Primary juvenile glaucoma is glaucoma that develops due to ocular hypertension and is evident either at birth or within the first few years of life. It is caused due to abnormalities in the anterior chamber angle development that obstruct aqueous outflow in the absence of systemic anomalies or other ocular malformation. Presentation
The typical infant who has congenital glaucoma usually is initially referred to an ophthalmologist because of apparent corneal edema. The commonly described triad of epiphora (excessive tearing), blepharospasm and photophobia may be missed until the corneal edema becomes apparent. Systemic associations
Two of the more commonly encountered disorders that may be associated with congenital glaucoma are Aniridia and Sturge-Weber syndrome. Genetics
JOAG is an autosomal dominant condition. The primary cause is the myocilin protein dysfunction. Myocilin gene mutations are identified in approximately 10% of patients affected by juvenile glaucoma. Diagnosis
The diagnosis is clinical. The intraocular pressure (IOP) can be measured in the office in a conscious swaddled infant using a Tonopen or hand-held Goldmann tonometer. Usually, the IOP in normal infants is in the range of 11-14 mmHg. Buphthalmos and Haabs striae can often be seen in case of congenital glaucoma. Differential diagnosis
Corneal cloudiness may have myriad of causes. Corneal opacity that results from hereditary dystrophies is usually symmetric. Corneal enlargement may result from megalocornea, a condition in which the diameter of the cornea is larger than usual and the eye is otherwise normal. Treatment
The preferred treatment of congenital glaucoma is surgical, not medical.