Gout: A Rapid Review of Presentation, Diagnosis and Management.

Gout is inflammatory arthritis caused by monosodium urate crystal deposition in articular and non-articular structures. Acute gout flares are often monoarticular/polyarticular involving lower extremity joints characteristically involving 1st metatarsophalangeal joint. However, gout flares can also be polyarticular, involving upper extremity joints, especially in patients with multiple comorbidities and contraindications to urate-lowering therapies (ULT). Risk factors exacerbating gout flares include obesity, high alcohol and purine-rich food consumption, and the use of diuretics. Diagnosis requires synovial fluid analysis with direct visualization of monosodium urate crystals. Acute flares are managed with steroids, non-steroidal anti-inflammatory drugs, or colchicine. Long-term management includes lifestyle modifications including a heavy emphasis on weight loss, avoidance of alcohol, purine-rich foods, and diuretics. ULT is indicated in patients with 2 or more gout flares/year, tophi, or radiographic evidence of gouty arthropathy. Although allopurinol is the first-line ULT agent, it does carry a risk of inducing severe cutaneous adverse reactions, especially in patients with chronic kidney disease and patients harboring the HLA-B*5801 allele. Other ULT agents include febuxostat and probenecid. ULT is usually titrated to achieve goal serum uric acid (SUA) levels below 6 mg/dL. However, in patients with tophi, a lower SUA target of less than 5 mg/dL should be implemented for prompt urate crystal dissolution.

Crowned Dens Syndrome: A Challenging Diagnosis in Older Adults Presenting With Acute Neck Pain.

Crowned dens syndrome (CDS) is a rare syndrome of calcium pyrophosphate dihydrate (CPPD) deposition on the odontoid process of the second cervical vertebra leading to unique clinical presentation and radiographical findings. Symptoms usually overlap with more common etiologies, including meningitis, stroke, and giant cell arteritis. Thus, patients struggle with extensive evaluation before diagnosing this uncommon condition. There are few case reports and case series of CDS in the literature. Patients respond well to treatment, but unfortunately, there is a high rate of relapse. Here we present an interesting case of a 78-year-old female patient who presented with acute onset headache and neck pain.

A Unique Case of Community Acquired Proteus mirabilis Meningitis.

Proteus mirabilis, a gram-negative bacterium commonly known for causing urinary tract infections (UTI) can rarely present with central nervous system (CNS) infections. Proteus mirabilis CNS infections are usually encountered in the neonatal and infantile period and occasionally cause brain abscesses. It is an uncommon cause of adult CNS infection. We report the first case of a community-acquired Proteus mirabilis meningitis (PMM) in a patient with Proteus mirabilis UTI, urolithiasis, and bacteremia. Risk factors for gram-negative bacillary meningitis (GNBM) include extremes of age, cancer history, diabetes mellitus, UTI, and nosocomial exposure, with the latter being a more prominent cause of PMM. Compromise of the anatomical defense against CNS infections whether accidental or neurosurgical is another important cause, and approximately two-thirds of reported cases of PMM have occurred after neurosurgical procedures. PMM patients develop fever, altered consciousness, and have an acute clinical course. Antimicrobials that can be used for treatment include third-generation cephalosporins, ciprofloxacin, imipenem/ cilastatin, aztreonam, and intraventricular aminoglycosides. Despite appropriate antibiotic therapy outcomes are poor with severe neurological deficit and death commonly resulting. Nosocomial infections can be drug-resistant and multiple antibiotics should be started while awaiting culture results. Literature review reveals that treatment with intraventricular aminoglycosides when attempted has shown bacteriological cure indicating this can be an important treatment approach. Due to the acute clinical course and high morbidity and mortality, we recommend starting multiple antibiotics with different mechanisms of action as soon as the disease is suspected. Our patient was initially started on ceftriaxone, vancomycin, acyclovir, and ampicillin for UTI and meningoencephalitis. The antibiotics were later consolidated to cefepime based on blood, urine and, cerebrospinal fluid cultures growing pan-sensitive Proteus mirabilis. Her clinical condition continued to worsen and ciprofloxacin was added. However, due to the progressive decline in her condition, the family elected for inpatient hospice care and intraventricular aminoglycosides were not attempted.

Hantavirus Cardiopulmonary Syndrome and Diffuse Alveolar Hemorrhage in the Era of COVID-19.

Hantavirus Cardiopulmonary Syndrome (HCPS) can occur after infection with Hantavirus which can occur by inhaling aerosolized rodent urine, feces, and saliva contaminated with the virus. It presents with the rapid development of pulmonary edema, respiratory failure, and cardiogenic shock with the hallmark being microvascular leakage. We report a patient with a history of alcohol abuse and recent exposure to mice and sick kittens who presented with cough with sputum production, shortness of breath, orthopnea, and new-onset lower extremity edema. Imaging revealed bilateral infiltrates more common on the left with an unremarkable echocardiogram. Testing for COVID-19, Human Immunodeficiency Virus (HIV), influenza, bacterial pneumonia including tuberculosis and methicillin-resistant Staphylococcus aureus (MRSA), aspergillosis, histoplasmosis, Blastomyces, and Coccidiodes was negative. Bronchoscopy and bronchoalveolar lavage revealed diffuse alveolar hemorrhage (DAH) and were negative for acid-fast bacilli and Nocardia cultures. He was further tested for Hantavirus, Q fever, leptospirosis, toxoplasmosis, and empiric treatment with doxycycline initiated. His Hantavirus IgM antibody came back positive. Human Hantavirus infection occurs after inhalation of infected rodent excreta; fortunately, human-to-human transmission has not been documented. HCPS most commonly occurs due to the Sin Nombre virus (SNV), has a case fatality rate of 50%, and is a notifiable disease in the United States. It has 3 distinct phases, prodromal, cardiopulmonary, and convalescent/recovery. The cardiopulmonary phase occurs from increased permeability of pulmonary capillaries and in severe cases can progress to cardiogenic shock. Diagnosis is based on the presence of IgM and IgG Hantavirus antibodies. Treatment is mainly supportive; however, patients are usually treated with broad-spectrum antibiotics while workup is underway. In animal models, ribavirin and favipiravir are only effective when administered in the prodromal phase. If suspicion of Hantavirus infection exists, early mobilization to the intensive care unit for treatment is recommended. Extracorporeal membrane oxygenation (ECMO) has been suggested to improve outcomes in severe HCPS with refractory shock.