The pressure will be transmitted to orbital tissues and then to the globe, resulting in an increase in intraocular pressure which may cause visual loss when the nutrient vessels supplying the optic nerve are compressed. Stage IV
Stage IV orbital emphysema develops when the intraorbital air mass  results in an intraocular pressure of more than 60 to 70 mmHg. The significantly elevated intraocular pressure will lead to central retinal artery occlusion, which may result in permanent and irreversible damage to the retina. Clinical Diagnosis
The diagnosis of orbital emphysema is usually made by physical examination of the eyelids, and, or by computer tomography (CT). Physical examination
Physical examination of the eyelid can be done by the palpation for the pathognomonic cracking, crepitation, and tense tissue on the upper and lower eyelids. The findings of the examination are supported with the medical history of the patient and confirmed with orbital CT.

Computed tomography (CT)
Computed tomography is effective and sensitive in the diagnosis of orbital emphysema, as it can confirm the anatomical location and size of air, bony defects, indentation of the eyeball, and the condition of the optic nerve, as well as the presence of any extraocular muscle entrapment and herniation of preorbital fat into the sinus cavities. The location of the orbital emphysema is present near the site of the fracture. The scans are usually taken along the transverse plane. Transverse images allow the evaluation of fractures in medial and lateral orbital walls.
Furthermore, approximately 20% of those with CPVT have a slow resting heart rate known as a sinus bradycardia. Mechanism
Excitation-contraction coupling
The arrhythmias that those with CPVT experience are caused by abnormalities in the way that cardiac muscle cells control their levels of calcium. Calcium interacts with the protein fibres or myofibrils inside the cell that allow the cell to contract, and the concentration of calcium within each cell needs to be tightly regulated. During each heartbeat, the concentration of calcium must rise to allow the muscle to contract and then fall to allow the muscle to relax, a process achieved by using a store within the cell known as the sarcoplasmic reticulum. At the start of each heartbeat, calcium is released from the sarcoplasmic reticulum through specialised channels known as ryanodine receptors. Ryanodine receptors open when the concentration of calcium near the channel increases. This happens when, in response to an electrical signal from the cell membrane called an action potential, a small amount of calcium flows across the cell membrane into the cell through L-type calcium channels, many of which are located on specialised inpouchings of the membrane called T-tubules designed to bring these surface ion channels close to the sarcoplasmic reticulum.The increase in calcium concentration triggers ryanodine receptors on the sarcoplasmic reticulum to release a puff of calcium known as a calcium spark. Each spark triggers the release of further sparks from neighbouring ryanodine receptors to create an organised rise of calcium throughout the cell known as a calcium transient.