Treatment is a relatively simple surgery in which excess skin of the outer lids is removed or tendons and muscles are shortened with one or two stitches. General anesthesia is sometimes used before local anesthetics are injected into the muscles around the eye. Prognosis is excellent if surgery is performed before the cornea is damaged.

@Congenital entropion:: may resolve with time ,or Hotz procedure

@Cicatricial entropion::

1 Anterior lamellar resection

2 Tarsal wedge resection

3 Transposition of tarso conjunctival wedge

4 Posterior lamellar graft

@Senile entropion::

1 Wies operation

2 Transverse everting suture

3 Quicker procedure

Entropion has been documented in most dog breeds, although there are some breeds (particularly purebreds) that are more commonly affected than others. These include the Akita, Pug, Chow Chow, Shar Pei, St. Bernard, Cocker Spaniel, Boxer, English Springer Spaniel, Welsh Springer Spaniel, Labrador Retriever, Cavalier King Charles Spaniel, Neapolitan Mastiff, Bull Mastiff, Great Dane, Irish Setter, Shiba Inu, Rottweiler, Poodle and particularly Bloodhound. The condition is usually present by six months of age. If left untreated, the condition can cause such trauma to the eye that it will require removal.

Entropion has also been seen in cat breeds. Typically it is secondary to trauma, or infection leading to chronic eyelid changes. It is also seen secondary to enophthalmos. Congenital cases are also seen with the brachicephalic breeds being over represented.

Upper lid entropion involves the eyelashes rubbing on the eye, but the lower lid usually has no eyelashes, so little or no hair rubs on the eye. Surgical correction is used in more severe cases. A number of techniques for surgical correction exist. The Hotz-Celsus technique involves the removal of strip of skin and orbicularis oculi muscle parallel to the affected portion of the lid and then the skin is sutured.

Alternative techniques such as the Wyman technique focus on tightening the lower eyelid, this technique is not as effective in cases of enophthalmos.

Shar Peis, who often are affected as young as two or three weeks old, respond well to temporary eyelid tacking. The entropion is often corrected after three to four weeks, and the sutures are removed.

In medicine, enophthalmia describes eyes that are abnormally sunken into their sockets. This condition usually affects elderly persons. Surgery can be done to correct it. Bilateral progressive enophthalmos may be the presenting sign of metastatic breast carcinoma even when local symptoms in the breast are absent.

Enophthalmos is the posterior displacement of the eyeball within the orbit due to changes in the volume of the orbit (bone) relative to its contents (the eyeball and orbital fat), or loss of function of the orbitalis muscle. It should not be confused with its opposite, exophthalmos, which is the anterior displacement of the eye.

It may be a congenital anomaly, or be acquired as a result of trauma (such as in a blowout fracture of the orbit), Horner's syndrome (apparent enophthalmos due to ptosis), Marfan syndrome, Duane's syndrome, silent sinus syndrome or phthisis bulbi.

All patients should follow-up with an ophthalmologist within 1 week of the fracture. To prevent orbital emphysema, patients are advised to avoid blowing of the nose. Nasal decongestants are commonly used. It is also common practice to administer prophylactic antibiotics when the fracture enters a sinus, although this practice is largely anecdotal. Amoxicillin-clavulanate and azithromycin are most commonly used. Oral corticosteroids are used to decrease swelling.

Medical management may involve immunosuppressive drugs such as methotrexate, corticosteroids, cyclophosphamide, and azathioprine. No randomized controlled trials have yet been conducted to evaluate such treatments, so the benefits have not been clearly established.

Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.

Surgery is indicated if there is enophthalmos greater than 2 mm on imaging, Double vision on primary or inferior gaze, entrapment of extraocular muscles, or the fracture involves greater than 50% of the orbital floor. When not surgically repaired, most blowout fractures heal spontaneously without significant consequence.

Surgical repair of a "blowout" is rarely undertaken immediately; it can be safely postponed for up to two weeks, if necessary, to let the swelling subside. Surgery to place an orbital implant leaves little or no scarring and the recovery period is usually brief. Hopefully, the surgery will provide a permanent cure, but sometimes it provides only partial relief from double vision or a sunken eye. Reconstruction is usually performed with a titanium mesh or porous polyethylene through a transconjunctival or subciliary incision. More recently, there has been success with endoscopic, or minimally invasive, approaches.

Horner's syndrome is a combination of symptoms that arises when a group of nerves known as the sympathetic trunk is damaged. The signs and symptoms occur on the same side as the lesion of the sympathetic trunk. It is characterized by miosis (a constricted pupil), partial ptosis (a weak, droopy eyelid), apparent anhidrosis (decreased sweating), with or without enophthalmos (inset eyeball).

The nerves of the sympathetic trunk arise from the spinal cord in the chest, and from there ascend to the neck and face. The nerves are part of the sympathetic nervous system, a division of the autonomic (or involuntary) nervous system. Once the syndrome has been recognized, medical imaging and response to particular eye drops may be required to identify the location of the problem and the underlying cause.

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.

Signs that are found in patients on the affected side of the face include

- partial ptosis

- upside-down ptosis (slight elevation of the lower lid)

- anhidrosis

- miosis

- pseudoenophthalmos (the impression that the eye is sunken, caused by a narrow palpebral aperture)

- pupillary dilation lag

- loss of ciliospinal reflex

- bloodshot conjunctiva, depending on the site of lesion.

- unilateral straight hair (in congenital Horner's syndrome); the hair on the affected side may be straight in some cases.

- heterochromia iridum (in congenital Horner's syndrome)

Interruption of sympathetic pathways leads to several implications. It inactivates the dilator muscle and thereby produces miosis. It inactivates the superior tarsal muscle which produces ptosis. It inactivates the orbitalis muscle which produces the effect of enophthalmos. It also reduces sweat secretion in the face.

Sometimes there is flushing on the affected side of the face due to dilation of blood vessels under the skin. The pupil's light reflex is maintained as this is controlled via the parasympathetic nervous system.

In children, Horner's syndrome sometimes leads to heterochromia, a difference in eye color between the two eyes. This happens because a lack of sympathetic stimulation in childhood interferes with melanin pigmentation of the melanocytes in the superficial stroma of the iris.

In veterinary medicine, signs can include partial closure of the third eyelid, or nictitating membrane.

In August 2016, researchers at the Instituto de Assistência dos Servidores do Estado do Rio de Janeiro used botulinum toxin as a method to block the acetylcholine release from the presynaptic neurons. Although they have seen a reduction in one sided flushing, sweating still occurs.

There have been case studies of individuals whom have experienced this syndrome after an operation. Two patients, a 37-year-old and 58-year-old female patients suffering from metastatic cancer were scheduled for placement of an intrathecal pump drug delivery system. After the intrathecal pump was placed, certain medications were given to the patients. Once the medications were administered, both patients had one sided facial flushes, closely resembling Harlequin Syndrome. Patients were given neurological exams to confirm that their nerves were still intact. An MRI was performed and showed no significant evidence of bleeding or nerve compression. After close observation for 16 hours, symptoms of the Harlequin syndrome was diminished and both patients did not have another episode.

Another case study was based on a 6-year-old male visiting an outpatient setting for one sided flushes during or after physical activity or exposed to heat. Vitals, laboratory tests, and CT scans were normal. Along with the flushes, the right pupil was 1.5 mm in size, while the left pupil was 2.5 mm in size; however, no ptosis, miosis, or enophthalmos was noted. The patient also had an MRI scan to rule out any lesion near the brain or spinal cord. No abnormalities were noted and the patient did not receive any treatments. The patient was diagnosed with idiopathic Harlequin syndrome.

Although the mechanism is still unclear, the pathophysiology of this condition, close monitoring, and reassurance are vital factors for successful management.

Management often includes the use of beta blockers such as propranolol or if not tolerated calcium channel blockers or ACE inhibitors.

Since angiotensin II receptor antagonists (ARBs) also reduce TGF-β, these drugs have been tested in a small sample of young, severely affected people with Marfan syndrome. In some, the growth of the aorta was reduced. However, a recent study published in NEJM demonstrated similar cardiac outcomes between the ARB, losartan, and the more established beta blocker therapy, atenolol.

There is no cure for Marfan syndrome, but life expectancy has increased significantly over the last few decades and is now similar to that of the average person. Regular checkups by a cardiologist are needed to monitor the health of the heart valves and the aorta. The syndrome is treated by addressing each issue as it arises and, in particular, preventive medication even for young children to slow progression of aortic dilation. The goal of treatment is to slow the progression of aortic dilation and damage to heart valves by eliminating arrythmias, minimizing the heart rate, and minimizing blood pressure.

Treatment is surgical, and usually is able to be performed once life-threatening injuries are stabilized, to allow the patient to survive the general anesthesia needed for invasive orthopedic restructuring. First a "frontal bar" is used, which refers to the thickened frontal bone above the frontonasal sutures and the superior orbital rim. The facial bones are suspended from the bar by open reduction and internal fixation with titanium plates and screws, and each fracture is fixed, first at its superior attachment to the bar, then at the inferior attachment to the displaced bone. For stability, the zygomaticofrontal suture is usually replaced first, and the palate and alveolar ridge are usually fixed last. Finally, after the horizontal and vertical maxillary buttresses are stabilized, the orbital fractures are fixed last.

Silent sinus syndrome is a spontaneous, asymptomatic collapse of the maxillary sinus and orbital floor associated with negative sinus pressures. It can cause painless facial asymmetry, diplopia and enophthalmos. Usually the diagnosis is suspected clinically, and it can be confirmed radiologically by characteristic imaging features that include maxillary sinus outlet obstruction, sinus opacification, and sinus volume loss caused by inward retraction of the sinus walls. Treatment is surgical involving making an outlet for mucous drainage from the obstructed sinus.

The treatment of a Pancoast lung cancer may differ from that of other types of non-small cell lung cancer. Its position and close proximity to vital structures (such as nerves and spine) may make surgery difficult. As a result, and depending on the stage of the cancer, treatment may involve radiation and chemotherapy given prior to surgery (neoadjuvant treatment).

Surgery may consist of the removal of the upper lobe of a lung together with its associated structures (subclavian artery, vein, branches of the brachial plexus, ribs and vertebral bodies), as well as mediastinal lymphadenectomy. Surgical access may be via thoracotomy from the back or the front of the chest and modifications

A Le Fort fracture of the skull is a classic transfacial fracture of the midface, involving the maxillary bone and surrounding structures in either a horizontal, pyramidal or transverse direction. The hallmark of Lefort fractures is traumatic "pterygomaxillary separation", which signifies fractures between the pterygoid plates, horseshoe shaped bony protuberances which extend from the inferior margin of the maxilla, and the maxillary sinuses. Continuity of this structure is a keystone for stability of the midface, involvement of which impacts surgical management of trauma victims, as it requires fixation to a horizontal bar of the frontal bone. The pterygoid plates lie posterior to the upper dental row, or alveolar ridge, when viewing the face from an anterior view. The fractures are named after French surgeon René Le Fort (1869–1951), who discovered the fracture patterns by examining crush injuries in cadavers.

Aside from cancer general symptoms such as malaise, fever, weight loss and fatigue, Pancoast tumour can include a complete Horner's syndrome in severe cases: miosis (constriction of the pupils), anhidrosis (lack of sweating), ptosis (drooping of the eyelid) and enophthalmos (sunken eyeball). In progressive cases, the brachial plexus is also affected, causing pain and weakness in the muscles of the arm and hand with a symptomatology typical of thoracic outlet syndrome. The tumour can also compress the recurrent laryngeal nerve and from this a hoarse voice and bovine cough may occur.

In superior vena cava syndrome, obstruction of the superior vena cava by a tumour (mass effect) causes facial swelling cyanosis and dilatation of the veins of the head and neck.

A Pancoast tumor is an apical tumour that is typically found in conjunction with a smoking history. The clinical signs and symptoms can be confused with neurovascular compromise at the level of the superior thoracic aperture. The patient's smoking history, rapid onset of clinical signs and symptoms and pleuritic pain can suggest an apical tumour. A Pancoast tumor can give rise to both Pancoast syndrome and Horner's syndrome. When the brachial plexus roots are involved it will produce Pancoast syndrome; involvement of sympathetic fibres as they exit the cord at T1 and ascend to the superior cervical ganglion will produce Horner's syndrome.