A skull fracture is a break in one or more of the eight bones that form the cranial portion of the skull, usually occurring as a result of blunt force trauma. If the force of the impact is excessive, the bone may fracture at or near the site of the impact and cause damage to the underlying structures within the skull such as the membranes, blood vessels, and brain. While an uncomplicated skull fracture can occur without associated  physical or neurological damage and is in itself usually not clinically significant, a fracture in healthy bone indicates that a substantial amount of force has been applied and increases the possibility of associated injury. Any significant blow to the head results in a concussion, with or without loss of consciousness. A fracture in conjunction with an overlying laceration that tears the epidermis and the meninges, or runs through the paranasal sinuses and the middle ear structures, bringing the outside environment into contact with the cranial cavity is called a compound fracture. Compound fractures can either be clean or contaminated. There are four major types of skull fractures: linear, depressed, diastatic, and basilar. Linear fractures are the most common, and usually require no intervention for the fracture itself. Depressed fractures are usually comminuted, with broken portions of bone displaced inward—and may require surgical intervention to repair underlying tissue damage. Diastatic fractures widen the sutures of the skull and usually affect children under three. Basilar fractures are in the bones at the base of the skull.
Combination with other agents
One strategy for reducing harm done by acetaminophen overdoses is selling paracetamol pre-combined in tablets either with an emetic or an antidote. Paradote was a tablet sold in the UK which combined 500 mg paracetamol with 100 mg methionine, an amino acid formerly used in the treatment of paracetamol overdose. There have been no studies so far on the effectiveness of paracetamol when given in combination with its most commonly used antidote, acetylcysteine.Calcitriol, the active metabolite of vitamin D3, appears to be a catalyst for glutathione production. Calcitriol was found to increase glutathione levels in rat astrocyte primary cultures on average by 42%, increasing glutathione protein concentrations from 29 nmol/mg to 41 nmol/mg, 24 and 48 hours after administration; it continued to have an influence on glutathione levels 96 hours after administration. It has been proposed that co-administration of calcitriol, via injection, may improve treatment outcomes. Paracetamol replacements
Paracetamol ester prodrug with L-pyroglutamic acid (PCA), a biosynthetic precursor of glutathione, has been synthesized to reduce paracetamol hepatotoxicity and improve bioavailability. The toxicological studies of different paracetamol esters show that L-5-oxo-pyrrolidine-2-paracetamol carboxylate reduces toxicity after administration of an overdose of paracetamol to mice. The liver glutathione values in mice induced by intraperitoneal injection of the ester are superimposable with the GSH levels recorded in untreated mice control group. The mice group treated with an equivalent dose of paracetamol showed a significative decrease of glutathione of 35% (p<0.01 vs untreated control group).