Bilateral Adie’s Pupil following Laser Treatment of the Ischemic Peripheral Retina for Uveitis: A Case Report

Adie’s pupil is a neurological condition of unknown origin with unusual, asymmetric presentation known as anisocoria with the enlarged pupil failing to react to light. It is believed that this pupillary abnormality results from damage to the ciliary ganglion or postganglionic short ciliary nerves. Affected individuals (usually female) may be symptomatic with photophobia or difficulty reading in the diseased eye. Although most Adie’s pupil cases are idiopathic, previous studies have associated photocoagulation and uveitis with symptom onset. To the best of our knowledge, there have been no reports of specific means of preventing Adie’s pupil. We describe a patient who experienced varying severities of Adie’s pupil after separate laser treatments of the ischemic peripheral retina for uveitis. Fluorescein angiography revealed peripheral retinal nonperfusion in the bilateral eyes of a 37-year-old Japanese female who had been suffering from posterior uveitis. To avoid proliferative changes, 360° laser photocoagulation of the retinal nonperfusion region located in the far periphery was first delivered to the left eye over 2 sessions. Soon after treatment, the patient complained of acute photophobia and blurred vision in the treated eye. Ocular examination revealed left pupil dilation and poor light sensitivity, although the pupil was reactive to a close stimulus. The left pupil also displayed positive denervation sensitivity based on the dilute pilocarpine (0.125%) test. Adie’s pupil was diagnosed based on these observations. Three months later, similar, albeit milder, findings were observed in her right eye after 360° peripheral laser photocoagulation that was more conservatively performed over 4 sessions. Four months after the first treatment, her subjective visual function had improved, and the pupil diameter had decreased to a normal size in both eyes without additional treatment. We encountered a patient whose severity of Adie’s pupil was apparently reduced by more conservative laser photocoagulation of the ischemic peripheral retina.

Bilateral Severe Mydriasis Due To Escitalopram

A 22 year old male student was seen by a psychiatrist for the complaint of having no interest in studying for his final college examination accompanied with loss of appetite and sleep disturbance. Upon taking psychiatric history, his symptoms were: diminished interest in daily activities of three months duration, fatigue, insomnia of sixth months duration, anorexia of two months duration and feelings of worthlessness. His physical examination and laboratory tests were normal with no abnormality. Thus, the diagnosis of major depressive disorder was made based on the psychiatric evaluation and he was prescribed Escitalopram 10 mg daily. On the third day of the Escitalopram therapy, bilateral severe mydriasis was observed by the patient, after contacting the psychiatry department, he was referred for ophthalmological examination. Upon ophthalmological examination, his examination revealed a right pupil diameter of 8 mm and a left pupil diameter of 8 mm with room light. Pupillary responses were equal with light exposure. The ophthalmological examination was reported as normal except for the unexplained bilateral mydriasis that was not ophthalmological in origin.

Adie’s tonic pupil presenting with unilateral photophobia successfully treated with dilute pilocarpine

A 40-year-old healthy man presented with a 4-month history of photophobia, blurred vision and a right dilated pupil. Examination revealed a right pupil that was not reactive to light but constricted strongly to a near target and slowly redilated when he looked back in the distance. Pharmacological testing with dilute pilocarpine 0.1% resulted in constriction of the right pupil but no change in the left pupil. This also resulted in resolution of his photophobia and blurry vision. Neurological examination was otherwise normal, and a diagnosis of Adie’s tonic pupil was made. The main differential diagnosis to consider for a large pupil is a third nerve palsy, pharmacological mydriasis, tonic pupil and local iris processes, such as iris sphincter tears from trauma. Knowledge of the key features of these conditions can avoid wasted resources from unnecessary testing. Dilute pilocarpine 0.1% three times a day can be considered as a pharmacological therapy for symptomatic relief.

Isolated invasive fungal sphenoid sinusitis – a case study

Invasive fungal sphenoid sinusitis is a rare and potential life threating disease. An incidence rate of fungal sphenoiditis among patients with isolated sphenoid disease varies from 4.5% to 26.8%. Generally the symptoms of sphenoid sinusitis are non-specific and include headaches, visual disorder, post nasal drip, nasal obstruction and paralysis or paresis of single or multiplicitous cranial nerves. In this study, a case of isolated invasive fungal left sphenoiditis in immunocompetent 56-year-old woman is described. The first sinus computed tomography (CT) examination revealed complete opacification of the left sphenoid sinus, she second CT scans showed also erosions of the sphenoid sinus bony walls. Endoscopic sinus surgery was performed and intraoperatively fixed and dilated left pupil was observed thus surgery team decided to finish an operation immediately. Ophthalmologist diagnosed the left oculomotor nerve paresis. Pathologic analysis demonstrated fungal hyphae morphologically identical to Aspergillus spp. Due to suspicion of cerebrospinal fluid (CSF) leak, increasing pneumocephalus and manifestation of mental changes in our subject, endoscopic reoperation with CFS fistula closure was done nine days after the first operation. The patient was treated with intravenous voriconazole and ceftriaxone for one month, and after discharge with itraconazole for 3 months. The full recovery of the left oculomotor nerve function ensued 4 months after surgery and no signs of recurrence of the fungal disease were present up to date.

Large Vertex Epidural Hematoma: Case Report and Review of Surgical Approaches

Vertex epidural hematomas (VEHs) are a special clinical entity due to their clinical presentation, vascular etiology and options of surgical approach. The clinical suspicion involves recognizing the mechanism of the injury and the correct visualization of the hematoma in computed tomography (CT) coronal sequences. In the present article, we describe a case of a very large (146 mL) VEH with central brain herniation, and provide a technical note on the surgical planning and treatment. A 34-year-old male patient was admitted to the hospital after an injury on the left superior parietal region. The Glasgow coma scale score was 6, and the left pupil of the patient was dilated. The CT scan showed a large epidural hematoma on the vertex between the coronal e lambdoid sutures, and a fracture over the sagittal suture. During the surgery, multiple burr holes were made laterally to the sagittal suture, and after inspection and no visualization of bleeding in the superior sagittal sinus (SSS), we performed a standard biparietal craniotomy. The patient was discharged three days after the surgery without any deficits. Currently, with the improvement in imaging modalities, more cases of VEH are being identified. Identifying the etiology prior to the craniotomy is challenging in severe cases. Tears in the SSS can bleed profusely, and they demand strategies during the craniotomy. With multiple burr holes parallel to the sagittal suture, we can visualize whether there is bleeding in the SSS and design a craniotomy with or without a central osseous bridge to anchor the dura. Neurosurgeons must be prepared to plan a surgical strategy in cases of large VEHs. Due to its rare frequency and bleeding risks, VEHs are considered challenging.

Severe cerebral edema following nivolumab treatment for pediatric glioblastoma: case report

Nivolumab is an immune checkpoint inhibitor (ICI) currently undergoing Phase III clinical trials for the treatment of glioblastoma. The authors present the case of a 10-year-old girl with glioblastoma treated with nivolumab under compassionate-use guidelines. After the first dose of nivolumab the patient developed hemiparesis, cerebral edema, and significant midline shift due to severe tumor necrosis. She was managed using intravenous dexamethasone and discharged on a dexamethasone taper. The patient's condition rapidly deteriorated after the second dose of nivolumab, demonstrating hemiplegia, seizures, and eventually unresponsiveness with a fixed and dilated left pupil. Computed tomography of her brain revealed malignant cerebral edema requiring emergency decompressive hemicraniectomy. Repeat imaging demonstrated increased size of the lesion, reflecting immune-mediated inflammation and tumor necrosis. The patient remained densely hemiplegic, but became progressively more interactive and was ultimately extubated. She resumed nivolumab several weeks later, but again her condition deteriorated with headache, vomiting, swelling at the craniectomy site, and limited right-sided facial movement following the sixth dose. MRI demonstrated severe midline shift and uncal herniation despite her craniectomy. Her condition gradually declined, and she died several days later under “do not resuscitate/do not intubate” orders. To the authors' knowledge, this represents the first case of malignant cerebral edema requiring operative intervention following nivolumab treatment for glioblastoma in a pediatric patient.

Unilateral Dilated Pupil and Spontaneous Cardiac Arrest with Successful Bystander Resuscitation

A 75-year-old man collapsed on a golf course and received cardiopulmonary resuscitation from a bystander, including the use of a public automated external defibrillator (AED). The AED was discharged once, with return of spontaneous circulation. An air ambulance crew found the patient haemodynamically stable, with no acute abnormalities on a 12-lead ECG. He had reduced consciousness and a dilated left pupil. On contacting the patient’s wife by telephone, she said that he had fallen and hit his head earlier that day. The crew decided to convey the patient to a Major Trauma Centre that had both neurosurgical and cardiology specialist services (rather than the nearest hospital) so that both traumatic brain injury and cardiac pathologies could be addressed if required. A head CT was normal, but coronary angiography demonstrated occlusion of two coronary arteries. These were successfully treated with stenting, and the patient went home two weeks later. He informed medical staff that his left pupil has been permanently dilated since he was a boy following a traumatic ocular injury. This case illustrates the utility of early deployment of an AED as well as the importance of an accurate history and emergency decision-making by prehospital personnel.

Unilateral Adie's tonic pupil and viral hepatitis: Report of two cases

Introduction. Adie?s (tonic) pupil is a neuro-ophthalmological disorder characterized by a tonically dilated pupil, which is unresponsive to light. It is caused by damage to postganglionic fibers of the parasympathetic innervation of the eye, usually by a viral or bacterial infection. Adie?s syndrome includes diminished deep tendon reflexes. Outline of Cases. We report data of a 59-year-old female with unequal pupil sizes. She complained of blurred vision and headache mainly while reading. She had a 35-year history of hepatitis B and liver cirrhosis. On exam, left pupil was mydriatic and there was no response to light and at slit lamp we saw segments of the sphincter constrict. We performed 0.125% pilocarpine test and there was a remarkable reduction of size in the left pupil. The second case is a 55-year-old female who was referred to the University Eye Clinic because of a headache and mydriatic left pupil. She had diabetes mellitus type 2, as well as hepatitis A virus 20 years earlier. On exam, the left pupil was mydriatic, with no response to light. Test with diluted pilocarpine was positive. Neurological examinations revealed no abnormality in either case so we excluded Adie?s syndrome. Conclusion. Adie?s tonic pupil is benign neuro-ophthalmological disorder of unknown etiology. Most patients commonly present no symptoms and anisocoria is noticed accidentally. Although the etiology is unknown, there are some conditions that cause tonic pupil. It may be a part of a syndrome in which tonic pupil is associated with absent deep tendon reflexes.

Republished: Intracranial pseudoaneurysm after intracranial pressure monitor placement

Traumatic intracranial pseudoaneurysms are a rare but severe complication following arterial injury. Pseudoaneurysm formation can occur secondary to blunt or penetrating trauma or iatrogenic injury. We report a case of traumatic pseudoaneurysm secondary to placement of an intracranial pressure (ICP) monitor. A 27-year-old man was involved in a motorcycle accident resulting in multiple intracranial hemorrhages. The patient underwent craniectomy and placement of an ICP monitor. 17 days later he developed dilation of his left pupil, with imaging demonstrating a new hemorrhage in the vicinity of the previous ICP monitor. A cerebral angiogram confirmed a left-sided distal M4 pseudoaneurysm which was treated by n-butyl cyanoacrylate embolization. Intracranial pseudoaneurysm formation following neurosurgical procedures is uncommon. Delayed intracranial hemorrhage in a region of prior intracranial manipulation, even following a procedure as ‘routine’ as placement of an ICP monitor, should raise the suspicion for this rare but potentially lethal complication.

Intracranial Haemorrhage due to Minor Trauma in a Patient with Idiopathic Thrombocytopenic Purpura- A Case Report

Introduction: Intracranial haemorrhage (ICH) is a rare but the most dangerous complication of idiopathic thrombocytopenic purpura (ITP) which is usually fatal. ITP is caused by autoantibodies to platelet which can be demonstrated in plasma. Case-Report: A 32 years old male patient sustained minor trauma around his head, following which he developed features of raised intracranial pressure including headache, vomiting and loss of consciousness. On examination Glasgow Coma Scale was 7/15 (E2, M3, V2), left pupil was moderately dilated, there was bilateral papilloedema and haemorrhagic spots on the left sided retina. CT scan of the head showed significant intracranial haemorrhage. Laboratory investigation showed anaemia and thrombocytopenia with platelet count 40X109/L. All the relevant causes of thrombocytopenia were excluded and the diagnosis of ITP was established. Intracranial haemorrhage was managed conservatively without surgical intervention. ITP was managed with splenectomy on 12th day following a period of therapy with steroids, transfusion of packed cell and platelet concentrates. DOI: http://dx.doi.org/10.3329/jafmc.v9i1.18740 Journal of Armed Forces Medical College Bangladesh Vol.9(1) 2013: 115-117