Traumatic optic neuropathy.

Our concepts of optic nerve trauma and its treatment are evolving. Traditionally, optic nerve trauma was thought of as the syndrome of blunt force to the forehead causing visual loss, but iatrogenic injury is increasingly recognized as an important source of optic nerve trauma. Our understanding of this trauma as a type of brain injury is also evolving. For the past decade, it has been clinical dogma that high-dose methylprednisolone is beneficial in the treatment of optic nerve trauma. However, little clinical evidence has shown this to be the case, raising questions about whether methyprednisolone has any benefit in the treatment of optic nerve trauma. Increasingly, research in neuroprotection is thought to hold promise for the development of novel and effective treatments for optic nerve injury.

The endoscopic forehead lift.

Endoscopic techniques are being successfully applied to address eyebrow and forehead ptosis. The methods rely on extensive subperiosteal and subgaleal release of the forehead and scalp flap, allowing the elevation of soft tissues. Ablation of the depressor supercilli and procerus can be performed to address skin folding in the glabellar region. The mobilized frontotemporal flap is then elevated to the desired level and fixated with microscrews to the outer table of the skull. Laterally, the flap is fixed to the deep temporalis fascia. The technique relies upon a solid knowledge of the regional anatomy and the use of specialized instruments now available for dissecting under the flap. The endoscopic forehead lift can achieve results comparable to those obtained by the open coronal forehead lift while minimizing the incidence and extent of postoperative cutaneous anesthesia and telogenic hair loss, which frequently follows open coronal forehead surgery. In addition, the endoscopic technique is able to address eyebrow ptosis in the balding male without causing disfiguring scarring.

Extracranial optic canal decompression: indications and technique.

Optic canal decompression may be beneficial in cases of indirect optic nerve trauma, with or without canal fracture. Although no definitive data exist to clarify its role, several clinical series have reported on optic canal decompression for the treatment of intracanalicular optic nerve trauma, providing only limited information of the details of the procedure. We describe extradural optic canal decompression using a transethmoidal/transorbital approach. Removal of > 180 degrees of the bony canal is possible with this method. The technique can be accomplished by orbital surgeons familiar with orbital apical anatomy and orbital microsurgery. Experience with cadaver dissection of the orbital apex and cadaver surgery may be useful in that it provides confidence for the surgeon operating in this critical region. Careful exposure, microscopic visualization, delicate technique, and thorough anatomic knowledge minimize the risk of complications such as carotid artery penetration or dural laceration.

Management of exposed hydroxyapatite orbital implants.

BACKGROUND: Porous coralline hydroxyapatite orbital implants have gained significant popularity for use in anophthalmic sockets. Several reports have noted increased rates of early implant exposure. METHODS: Six patients with exposure complications of primary hydroxyapatite implants after enucleation or evisceration were studied. RESULTS: The hydroxyapatite implant exposures occurred 2 to 8 weeks after implantation. Magnetic resonance imaging scans with gadolinium enhancement obtained in two patients demonstrated a "cold" zone anteriorly with failure of fibrovascular ingrowth in the region of anterior exposure. Several different surgical procedures were used to regain implant coverage, including freshening the edge of the conjunctival defect and observing for spontaneous closure, burring away the anterior surface of the hydroxyapatite implant, and placing autogenous free tissue grafts of hard-palate mucosa or thin dermis-fat graft over the exposed hydroxyapatite. Repeated exposure after free graft was noted in several patients, and three of the six patients followed have an intact surface but very thin conjunctiva overlying hydroxyapatite spicules. CONCLUSION: Although small areas of hydroxyapatite exposure (< 3 mm) may close spontaneously, larger defects do not tend to close spontaneously and should be actively managed. Based on our experience, optimal results are obtained with free autogenous tissue grafts combined with burring of the anterior hydroxyapatite surface. Steps should be taken at the time of primary implantation to minimize implant exposure, including choosing appropriately sized implants and obtaining careful coverage with good vascularized tissue under minimal tension.

Traumatic optic neuropathy.

Knowledge concerning the pathophysiologic mechanisms of traumatic optic neuropathy is limited. The optic nerve is a tract of the brain. Therefore, the cellular and biochemical pathophysiology of brain and spinal cord trauma and ischemia provide insight into mechanisms that may operate in traumatic optic neuropathy. The dosage of methylprednisolone (30 mg/kg/6 hours) which was successful in the National Acute Spinal Cord Injury Study 2 (NASCIS 2) evolved from the unique pharmacology of corticosteroids as antioxidants. The management of traumatic optic neuropathy rests on an accurate diagnosis which begins with a comprehensive clinical assessment and appropriate neuroimaging. The results of medical and surgical strategies for treating this injury have not been demonstrated to be better than those achieved without treatment. The spinal cord is a mixed grey and white matter tract of the brain in contrast to the optic nerve which is a pure white matter tract. The treatment success seen with methylprednisolone in the NASCIS 2 study may not generalize to the treatment of traumatic optic neuropathy. Conversely, if the treatment does generalize to the optic nerve, NASCIS 2 data suggests that treatment must be started within eight hours of injury, making traumatic optic neuropathy one of the true ophthalmic emergencies. Given the uncertainties in the treatment, ophthalmologists involved in the management of traumatic optic neuropathy are encouraged to participate in the collaborative study of traumatic optic neuropathy.

A 16-year study of conjunctival dacryocystorhinostomy.

We reviewed a consecutive series of 79 conjunctival dacryocystorhinostomies performed over a 16-year period in 75 patients. Thirty-eight of 75 patients with canalicular blockage between the common canaliculus and the first 5 mm of the canaliculus as well as patients with common canalicular blockage who had failed previous dacryocystorhinostomy were treated with combined canalicular reconstruction, nasal lacrimal intubation, and conjunctival dacryocystorhinostomy. In 37 patients, less than 5 mm of proximal canaliculus remained open. These patients were treated with conjunctival dacryocystorhinostomy alone, including four patients who had bilateral procedures. Two of 38 patients who underwent combined canalicular and conjunctival procedures required further surgery for a successful outcome compared with 14 of 37 patients who underwent conjunctival dacryocystorhinostomy without canalicular reconstruction (P = .002). Overall, 71 of 74 patients (96%) had a successful outcome, and five patients were lost to follow-up.

Neuropathologic findings in the acquired immunodeficiency syndrome (AIDS).

The acquired immunodeficiency syndrome (AIDS) is characterized by a severe idiopathic deficiency in T-cell mediated immunity. Homosexuals, intravenous drug abusers and Haitians are predominantly affected, predisposing them to opportunistic infections and neoplasms. In this study, the central nervous system (CNS) was examined at autopsy in 29 AIDS patients. Significant CNS complications occurred in 55%, mainly related to opportunistic infections similar to those seen in patients with other causes of immunosuppression. Progressive multifocal leukoencephalopathy (three cases), cytomegalovirus (CMV) encephalitis (five cases), cryptococcal meningitis (four cases), Mycobacterium avium-intracellulare (three cases), and toxoplasmosis (one case) were found. Widespread microglial nodules were observed in 20 patients, 80% of whom had CMV inclusions elsewhere at autopsy. Primary cerebral lymphoma (one case) and lymphomatoid granulomatosis (one case) were present. Subarachnoid (five cases) and intraparenchymal (three cases) hemorrhage was seen although these were not usually clinically significant. A single case of embolic arterial obstruction with cortical infarction was due to non-bacterial thrombotic endocarditis.

Adrenal pathology in the acquired immune deficiency syndrome.

Adrenal pathology was examined in 41 autopsied patients with the acquired immune deficiency syndrome. This represents the largest series and the first study with quantitation of adrenal cortical necrosis. In 32 cases clinical data were analyzed for features of adrenal insufficiency. Common clinical findings included vomiting, diarrhea, fever, hypotension, and hyponatremia. None of the 32 patients showed characteristic skin hyperpigmentation. Two patients were suspected premortem to have adrenal insufficiency. In one of these patients, adrenocorticotrophic hormone (ACTH) stimulation resulted in an adequate rise in plasma cortisol values. In the other patient, the baseline plasma cortisol value was elevated and failed to rise significantly after ACTH stimulation. Pathologic findings included widespread lipid depletion, infection by cryptococcus, and acid-fast organisms consistent with Mycobacterium avium-intracellulare, involvement by Kaposi's sarcoma, and necrotizing adrenalitis due to cytomegalovirus (CMV). A point-counting method was used to quantitate adrenal cortical and medullary necrosis. Necrosis due to CMV was greater in the medulla than the cortex. The maximum amount of adrenal cortical necrosis in any case was 70%. The degree of cortical necrosis was less than that usually associated with adrenal insufficiency.

Central pontine myelinolysis in a child with the Shwachman-Diamond syndrome.

The first case of central pontine myelinolysis in a child with the Shwachman-Diamond syndrome is reported. Marked fluctuation of serum glucose and sodium levels, but no hyponatremia, was observed throughout the patient's hospital course. Both of these abnormalities may have contributed to the development of the lesion. Liver abnormalities, implicated in other pediatric cases of central pontine myelinolysis, were also observed.

Clinical and pathologic findings of the liver in the acquired immune deficiency syndrome (AIDS).

Clinical data and histologic sections of the liver, including immunohistochemical studies for hepatitis B surface and core antigens, were reviewed in 42 autopsy cases of the acquired immune deficiency syndrome (AIDS). Hepatomegaly, elevation of serum transaminases, and mild elevation of alkaline phosphatase were commonly observed clinical and biochemical abnormalities. Mildly elevated alkaline phosphatase and normal bilirubin levels were present in patients with Mycobacterium avium-intracellulare (MAI) infection, cytomegalovirus (CMV) infection, and Kaposi's sarcoma (KS). Histologic sections demonstrated liver involvement by MAI in eight cases; KS in six cases; cryptococcus in three cases; and CMV in two cases. One case of MAI infection was associated with marked central vein sclerosis, a finding previously unreported. Thirty-two (76%) of 42 cases had serologic or pathologic evidence of hepatitis exposure. Two patients had histologic evidence of chronic active hepatitis. The pathologic processes involving the liver appeared to be secondary to the infections and neoplasms for which this population is susceptible and did not significantly contribute to morbidity or mortality. No findings specific or pathognomic for AIDS were identified in the liver.