Penetrating injury

C i.e. Violating platysma

Penetrating neck trauma involves a gun shot or sharp object (stab, puncture wound & impalement injuries) penetrating the skin and volating the platysma layer of neckQ

A i.e. Penetrating injury to ciliary body

–       Sympathetic opthalmitis is B/L chronic granulomatous (non-suppurative) anterior uveitis Q (initially it is anterior uveitis may become panuveitis). So mutton fat keratic precipitates are seen prior to retrolental flareQ. (Don’t get confused about it).

–       Earliest symptom of sympathetic opthalmitis for which, the patient first seek advice are -photophobia & lacrimation or defective visionQ (due to loss of accommodation) in the uninjured eye. And the first sign may be presence of keratic precipitates on the back of corneaQ or the presence of retrolenticular flareQ and cells.

Sympathetic opthalmitis is a bilateral granulomatous (non-suppurative/plastic) panuveitis which almost always follows penetrating wound in the ciliary region (danger zone) with incarceration of ciliary body, iris (uveal tissue & vitreous) or lens capsule Q.

Ans is All 

• Most injuries to the esophagus are from penetrating trauma. Associated injuries are the rule.
• Symptoms include odynophagia (pain on swallowing foods or fluids), subcutaneous or mediastinal emphysema, pleural effusion, air in the retro-esophageal space and unexplained fever within 24 hours of injury. Mediastinal and deep cervical emphysema must be seen as evidence of an aerodigestive injury until proven otherwise.
• If the diagnosis is made early, primary surgical repair is generally possible. If the diagnosis is delayed for more than 24 hours, primary repair may be impractical, with diversion and drainage being the only alternative. The major morbidity and mortality associated with esophageal injuries are the result of delay in diagnosis, which underscores the necessity to aggressively exclude esophageal injury during the initial evaluation of a patient with neck injury. “The mortality rate rises exponentially if treatment is delayed for more than 12-24 hours.”- Bailey and Love
• Esophagoscopy can be performed to evaluate the esophagus, but injuries have been missed with this technique alone. Therefore patients at risk should also undergo a soluble contrast esophagram looking for extravasation of contrast. If no extravasation is seen, a barium esophagram should be performed for greater detail. Failure to identify esophageal injuries leads to fulminant mediastinitis that is often fatal.
• Treatment consists of early debridement, primary repair, and drainage if identified within 24 hours after injury. Injuries diagnosed after 24 hours with mediastinal contamination are treated by cervical esophagostomy and distal feeding access. Esophageal resection is rarely needed but may be indicated in patients with esophageal necrosis or severe mediastinitis.. A drain should be left in place after all esophageal repairs.

Ans. is b > a i.e. Small intestine > Liver

• Sabiston states “The small bowel is the most frequently injured organ for penetrating injuries”.
• Schwartz states “For penetrating trauma organs with the largest anterior surface area are most prone to injury i.e., the small bowel, liver and colon”.
• In Surgery pretest the answer is small intestine.

Ans is ‘a’ ie Tracheobronchial injury 

• Tracheobronchial injuries are so fatal that most pts. die at the scene or during transport as a result of poor ventilation.
• The other options are so easy to rule out as they are rarely the cause of death.
• I could not find the MC cause of death after penetrating injury but among the 4 options provided Tracheobronchial is definitely the right answer. No doubts about it.

Ans. A: Penetrating Injury of Ciliary Body

Sympathetic ophthalmitis or ophthalmia almost always results from a penetrating wound. others

Incarceration of the iris or lens capsule is more likely to set up sympathetic ophthalmitis than oers

Sympathetic ophthalmia/ SO

• It is a granulomatous uveitis of both eyes following trauma to one eye.
• It can leave the patient completely blind.
• Symptoms may develop from days to several years after a penetrating eye injury.
• Floating spots and loss of ^accommodation are among the earliest symptoms.
• The disease may progress to severe ^iridocyclitis with pain and photophobia.
• Commonly the eye remains relatively painless while the inflammatory may occur. disease spreads through the uvea, where characteristic focal infiltrates in the choroid named Dalen-Fuchs nodules can be seen.
• Papilledema, secondary glaucoma, vitiligo, and poliosis of the eyelashes may accompany SO.
• In approximately 80% of cases, the uveitis appears within 2-12 weeks after injury, and 90% occur within 1 year from the time of injury.
• Sympathetic ophthalmia is currently thought to be an autoimmune inflammatory response toward ocular antigens, specifically a delayed hypersensitivity to melanin-containing structures from the outer segments of the photoreceptor layer of the retina.
• The immune system, which normally is not exposed to ocular antigens, is introduced to the contents of the eye following traumatic injury.
• Once exposed, it senses these antigens as foreign, and begins attacking them.
• The onset of this process can be from days to years after the inciting traumatic event.

Diagnosis

• Diagnosis is clinical, seeking a history of eye injury.
• An important differential diagnosis is Vogt-Koyanagi-Harada syndrome (VKH), which is thought to have the same pathogenesis, without a history of surgery or penetrating eye injury.

Prevention and treatment

Definitive prevention of SO requires prompt (within the first 7 to 10 days following injury) enucleation of the injured eye.

Evisceration—the removal of the contents of the globe while leaving the sclera and extraocular muscles intact—is easier to perform, offers long-term orbital stability, and is more aesthetically pleasing.

• There is concern, however, that evisceration may lead to a higher incidence of SO compared to enucleation
• The first choice of treatment may not be enucleation or evisceration, especially if there is a chance that the injured eye may regain some function
• Immunosuppressive therapy is the mainstay of treatment for SO.
• Mild cases may be treated with local application of corticosteroids and pupillary dilators.
• More severe or progressive cases require high-dose systemic corticosteroids for months to years.

Patients who become resistant to corticosteroids or develop side effects of long-term corticosteroid therapy (osteoporosis and pathologic fractures, mental status changes, etc.), may be candidates for therapy with chlorambucil, cyclophosphamide, or ciclosporin.

Ans. Liver

Ans:B.)Copper.

The condition shown in the picture above represents  Chalcosis (Sunflower Catacract and Kayser-Fleischer ring)

Ans:A.)Deposited under the membraneous structures of the eye.

The condition shown in the picture above represents  Chalcosis (Sunflower Catacract and Kayser-Fleischer ring)

Some patient’s with Wilson’s disease will have copper deposition (chalcosis) in the lens. This is termed a “sunflower” cataract because of its appearance when fully developed. The copper deposits are in and beneath the lens capsule, usually on the anterior surface.

In chalcosis bulbi the electrolytically dissociated ions of copper are deposited under the membraneous structures of the eye.

Chalcosis

• It refers to the specific changes produced by the alloy of copper in the eye.
• Copper from the alloy are dissociated electrolytically and are deposited under the membranous structure of the eye. 
• Clinical manifestations of chalcosis includes:
  • Kayser Fleischer rings: due to deposition of copper under peripheral parts of Descement’s membrane.
  • Sunflower cataract: due to deposition of copper under the posterior capsule of the lens.
  • Deposition of golden plaques at the posterior pole of retina which reflects the light with a metallic sheen.