Other symptoms can be difficulty in breathing, snoring, day-time sleepiness and perspiration. The main causative agent of OSA is the [midface hypoplasia], which also poses a risk to the eyes that can be seen bulging out of the eye sockets. Other factors, such as a micrognathism and adenoid hypertrophy, are likely to contribute in causing OSA. The most common syndromic forms of craniosynostosis; i.e. Apert, Crouzon and Pfeiffer, have an increased risk of developing OSA. The children have nearly 50% chance of developing this condition.A theory regarding the involvement of OSA as a causative agent for elevated intracranial pressure suggests an association with the auto-regulation of blood flow in the brain. Certain cells in the brain respond specifically to an increase of CO2 in the blood. The response involves vasodilatation of the cranial vault blood vessels, increasing the volume of one of the elements in the Monro-Kellie doctrine. The increase of CO2 concentration in the blood is a consequence of impaired breathing, especially seen when the child with OSA is sleeping. It is well documented that the highest spikes in intracranial pressure often occur during sleep. Abnormalities in the skull base
Impaired venous outflow is often caused by a hypoplastic jugular foramen. This causes an increase in the intracranial blood volume, thereby causing an increase in intracranial pressure.This can be further complicated with a possible Arnold–Chiari malformation, which can partially obstruct the flow of cerebro-spinal fluid from the neurocranium to the spinal cord.
With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations. It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration. Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.In nephrotic syndrome, SBP can frequently affect children but only very rarely can it affect adults. Diagnosis
Infection of the peritoneum causes an inflammatory reaction with a subsequent increase in the number of neutrophils in the fluid. Diagnosis is made by paracentesis (needle aspiration of the ascitic fluid); SBP is diagnosed if the fluid contains neutrophils at greater than 250 cells per mm3 (equals a cell count of 250 x106/L) fluid in the absence of another reason for this (such as inflammation of one of the internal organs or a perforation).The fluid is also cultured to identify bacteria. If the sample is sent in a plain sterile container, 40% of samples will identify an organism, while if the sample is sent in a bottle with culture medium, the sensitivity increases to 72–90%. Prevention
All people with cirrhosis might benefit from antibiotics (oral fluoroquinolone norfloxacin) if:

Ascitic fluid protein <1.0 g/dL.