Without proper management can lead to cardiac life-threatening conditions such as cardiopulmonary embolism, cardiac tamponade, and respiratory distress, depending on the volume of air trapped under the facial soft tissues. Infection
Infections can spread beyond their initial location, including lamina papyracea. Signs and Symptoms
The signs and symptoms of orbital emphysema vary depending on the original cause, but it is preliminary associated with swelling, bruising, and tenderness around the impacted eye. It may also involve proptosis or the deterioration of vision, typically diplopia. The entrapped air may cause an acute increase in the intraocular pressure or vascular compromise that restrict ocular motility, prohibit the closure of eyelids, and the loss of sensation over the upper cheek areas.Server entrapment in the soft tissues tends to stimulate oculocardiac reflex, which is likely to generate significant vagal responses including nausea, dizziness, vomiting, bradycardia, syncope and heart block. Without treating it promptly may subsequently result in compromisation of ocular function and visual impairment. Pathophysiology
Orbital emphysema occurs following forceful injection of air into the soft tissues of the orbit through a breach in one of the orbital walls which is typically associated with orbital fracture after blunt trauma, or less frequently with compressed air injuries, tumours and infections of the sinonasal region or complications after surgery.Orbital emphysema develops after an orbital fracture in a three-step process. After the fracture has occurred on one of the orbital walls, a sino-orbital communication is established.
Additionally, the study included a category for classifying "bizarre" answers, which included any answer that was far outside of the normal range of expected responses. WKS patients did give answers that could fall into such a category and these included answers such as 15s or 1 hour for the estimated length of a shower, or 4 kg or 15 tonnes as the weight of a car. Memory deficits
As mentioned previously, the amnesic symptoms of WKS include both retrograde and anterograde amnesia. The retrograde deficit has been demonstrated through an inability of WKS patients to recall or recognize information for recent public events. The anterograde memory loss is demonstrated through deficits in tasks that involve encoding and then recalling lists of words and faces, as well as semantic learning tasks. WKS patients have also demonstrated difficulties in perseveration as evidenced by a deficit in performance on the Wisconsin Card Sorting Test. The retrograde amnesia that accompanies WKS can extend as far back as twenty to thirty years, and there is generally a temporal gradient seen, where earlier memories are recalled better than more recent memories. It has been widely accepted that the critical structures that lead to the memory impairment in WKS are the mammillary bodies, and the thalamic regions. Despite the aforementioned memory deficits, non-declarative memory functions appear to be intact in WKS patients. This has been demonstrated through measures that assess perceptual priming.Other studies have shown deficits in recognition memory and stimulus-reward associative functions in patients with WKS.