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Introduction Vitamin B12 (VitB12) deficiency rarely manifests with visual symptoms. Optic nerve damage in VitB12 deficiency is thought to be via degeneration. However, optic neuritis, though infrequent, has been reported secondary to VitB12 deficiency. Material and methods We conducted a systematic review of all the reported cases of VitB12 deficiency with optic nerve involvement in Pubmed, Cochrane, and Google Scholar any date up to September 6, 2020. We have discussed the findings and compiled the available information on ophthalmological manifestations of VitB12 deficiency. We aim to provide a unified knowledge about the evidence related to types of optic neuropathies reported to date secondary to VitB12 deficiency. We also present a case of bilateral optic neuritis secondary to VitB12 deficiency. Presentation of case We present a 29-year-old previously healthy male with progressive, painful, bilateral, but asymmetric visual deterioration for forty-five days. A detailed history, examination, and laboratory workup were carried out. He was diagnosed as having optic neuritis secondary to VitB12 deficiency. He showed partial improvement with the replacement of VitB12. Conclusion We suggest promptly identifying and replacing VitB12 in patients with optic neuritis with proven VitB12 deficiency to prevent permanent damage to the optic nerve. Patients with VitB12 deficiency should have a baseline fundoscopic exam to rule out subclinical optic nerve damage. Moreover, patients who present with visual disturbances should be screened for VitB12 deficiency, especially the vegan population.

Background Tolosa Hunt syndrome (THS) is a rare disease that manifests mainly as painful unilateral ophthalmoplegia. It is caused by an inflammatory process of unknown aetiology within the cavernous sinus with a rare intracranial extension. The International Classification of Headache Disorders (ICHD)- 3 diagnostic criteria aids in its diagnosis. There is limited literature on its varied presentations, diagnosis, and management. Steroids are used in the treatment of THS with varied success. Methods We conducted a single-center-retrospective-study and included all patients admitted with a diagnosis of THS from January 2015 to December 2020. Descriptive and summary statistics were used to describe the study cohort's socio-demographic parameters. Results Among 31 THS patients (predominantly Asians (18) and Arabs (9)), visual disturbance was commonest presenting complaint. Third-nerve paralysis was seen in 70.9% cases. Magnetic-resonance-imaging (MRI) was abnormal in 64.5%. 93.5% patients received steroids, with a response-rate of 70.9% and a recurrence-rate of 9.7%. A previous history of THS and female gender were associated with recurrence ( p -value 0.009 and 0.018). Recurrence was seen in 66.7% fully recovered and 33.3% partially recovered cases (p-value 0.04). Among the benign and inflammatory subtypes of THS, the ICHD-3 criteria were applicable in 85% of inflammatory THS. Conclusions THS is a rare disease with ethnic variation in presentation and response to treatment. In our cohort female gender and a previous history of THS were associated with recurrence. ICHD-3 diagnostic criteria had a higher validity in our patients compared to prior studies, especially among the inflammatory THS.

Rationale: BRASH syndrome is a relatively unknown medical entity in which there is a combination of bradycardia, renal injury, hypoperfusion, and hyperkalemia. It is clinically essential to take these manifestations as a syndrome rather than isolated findings because they are interrelated and have synergistic effects. Bradycardia can result in hypoperfusion, which can cause renal injury. The resultant renal injury causes hyperkalemia (which can also be the initial trigger), which potentiates the bradycardia. Deteriorating patients with the syndrome usually do not respond to regular Advanced Cardiac Life Support resuscitation protocols. Treatment focused on the timely replacement of fluids and electrolytes gives better outcomes. It is vital to keep BRASH syndrome in diagnostic possibilities while seeing patients with refractory bradycardia, hyperkalemia, and renal injury, especially when other diagnoses are ruled out. Patient concerns: In this report, we present a 64-years-old gentleman who came with generalized fatigue, non-bloody diarrhea, vomiting, and low oral intake for the past 5 days. Diagnoses: The patient was diagnosed with BRASH syndrome. Interventions: The patient received intravenous fluids, 2 doses of atropine 0.5 mg and received dextrose 50 percent with insulin regular 10 units, and salbutamol 5 mg for hyperkalemia. He was intubated due to a low Glasgow Coma Scale and received dialysis for resistant hyperkalemia. A transvenous pacemaker was inserted due to bradycardia. Outcomes: The patient had 2 cardiac arrests and could not survive the second. Lessons: BRASH is a life-threatening yet largely underdiagnosed condition. Physicians should keep a high index of suspicion for BRASH while seeing patients with resistant and self-potentiating bradycardia, hyperkalemia, and renal failure, as a timely diagnosis is crucial in the management. Variable clinical presentations and limited literature create a diagnostic challenge. Further studies are warranted to understand the pathophysiology and develop better and accurate management algorithms. Patients’ risk of developing BRASH syndrome should be considered while prescribing causative medications (Atrioventricular nodal blocking drugs such as beta-blockers) in hospitals and outpatient settings.

The co‐occurrence of acute hemolysis and methemoglobinemia secondary to favism in G6PD deficient individuals is rare. Identifying it promptly is of high clinical significance as treating methemoglobinemia (with methylene blue) can worsen hemolysis.

We report a 56-year-old man with methemoglobinemia and hemolytic anemia, secondary to fava bean ingestion. Methylene blue administration worsened the hemolysis as he was G6PD deficient but not diagnosed before. We have discussed the mechanism of hemolysis in such patients and the management of such cases.Hemolytic anemia, a form of anemia that causes premature rupture of erythrocytes, accounts for five percent of anemias. 1 Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a well-known cause of hemolysis and currently affects around 400 000 000 individuals globally. It has a notable prevalence in African, Asian, and Mediterranean countries. 2 Favism is a common trigger of oxidative stress in G6PD deficient people, which can lead to hemolysis. Additionally, fava bean ingestion can cause methemoglobinemia. 3 Methemoglobin is an abnormal variation in the hemoglobin in which the ferrous (Fe2 + ) iron in heme is oxidized to the ferric (Fe3 + ) state. The condition is usually acquired, secondary to oxidative stress in the body such as favism or infections, but can rarely be congenital. 4 The first-line treatment for methemoglobinemia is methylene blue. However, in G6PD deficient patients, methylene blue can potentiate hemolysis because of its oxidative effects. 3 It is vital to take a detailed history of patients presenting with hemolysis to identify the potential causes and avoid any additional oxidative stress.

After a complete symptomatic recovery after COVID-19 pneumonia, the second phase of desaturation is a new phenomenon that is being increasingly observed. Two possible mechanisms behind it can be a continued subclinical infection and lung fibrosis. We have presented a case with the former mechanism, who responded well to steroids.