The ejection fraction in a patient with severe mitral regurgitation should be 65% or greater. If less than 65%, then left ventricular systolic dysfunction may be present, possibly due to the mitral regurgitation itself.
This past week we discussed about TB meningitis at Morning Report. Below are some key points about this disease and its management:
Diagnosis and Presentation
- Occurs when subependymal or subpial tubercles, also known as “Rich foci” seeded during bacillemia of primary infection or disseminated disease, rupture into the subarachnoid space
- Risk factors include travel to or residence in a country with high TB prevalence, elderly, alcoholism, HIV, drug abuse
- Presentation may be subacute or chronic as symptoms are variable and non-specific: unrelenting headache (28%), fever (13%), lethargy, confusion, seizures
- 25% of patients present with cranial nerve VI palsy (diplopia and medial strabismus)
- Hyponatremia due to SIADH is common
- Characteristic CSF findings: lymph-predominant pleiocytosis, elevated protein levels (100-500mg/dL), low glucose (<45mg/dL) or CSF:plasma ratio < 0.5, high opening pressure
- CSF samples sent for multiple tests increase sensitivity (smear, culture, PCR, adenosine deaminase)
- CXR: pulmonary TB seen in 25-55% of adults
- MRI/CT: may show leptominengeal enhancement, hydrocephalus, tuberculoma, or infarcts
- RIPE: If sensitive to isoniazid and rifampin, can narrow down to I+R after 2 months. Duration of 9-12 months.
- Steroids recommended for more severe disease: 12mg/day of dexamethasone for 3 weeks then taper for a total length of 6 weeks
1. Marx, et al. Tuber Res and Treat. 2011
2. Johns Hopkins ABX Guide
Sweet’s syndrome (the eponym for acute febrile neutrophilic dermatosis) is characterized by a constellation of clinical symptoms, physical features, and pathologic findings which include fever, neutrophilia, tender erythematous skin lesions (papules, nodules, and plaques), and a diffuse infiltrate consisting predominantly of mature neutrophils that are typically located in the upper dermis. Several hundreds cases of Sweet’s syndrome have been published.
Sweet’s syndrome presents in three clinical settings: classical (or idiopathic), malignancy-associated, and drug-induced. Classical Sweet’s syndrome (CSS) usually presents in women between the age of 30 to 50 years, it is often preceded by an upper respiratory tract infection and may be associated with inflammatory bowel disease and pregnancy. Approximately one-third of patients with CSS experience recurrence of the dermatosis.
The malignancy-associated Sweet’s syndrome (MASS) can occur as a paraneoplastic syndrome in patients with an established cancer or individuals whose Sweet’s syndrome-related hematologic dyscrasia or solid tumor was previously undiscovered; MASS is most commonly related to acute myelogenous leukemia. The dermatosis can precede, follow, or appear concurrent with the diagnosis of the patient’s cancer. Hence, MASS can be the cutaneous harbinger of either an undiagnosed visceral malignancy in a previously cancer-free individual or an unsuspected cancer recurrence in an oncology patient.
Drug-induced Sweet’s syndrome (DISS) most commonly occurs in patients who have been treated with granulocyte-colony stimulating factor, however, other medications may also be associated with DISS.
The pathogenesis of Sweet’s syndrome may be multifactorial and still remains to be definitively established. Clinical and laboratory evidence suggests that cytokines have an etiologic role.
Systemic corticosteroids are the therapeutic gold standard for Sweet’s syndrome. After initiation of treatment with systemic corticosteroids, there is a prompt response consisting of dramatic improvement of both the dermatosis-related symptoms and skin lesions. Topical application of high potency corticosteroids or intralesional corticosteroids may be efficacious for treating localized lesions. Other first-line oral systemic agents are potassium iodide and colchicine.
Second-line oral systemic agents include indomethacin, clofazimine, cyclosporine, and dapsone. The symptoms and lesions of Sweet’s syndrome may resolve spontaneously, without any therapeutic intervention; however, recurrence may follow either spontaneous remission or therapy-induced clinical resolution.
Sweet’s syndrome – a comprehensive review of an acute febrile neutrophilic dermatosis. By Philip R Cohen. Orphanet Journal of Rare Diseases 2007, 2:34 doi:10.1186/1750-1172-2-34
Case Challenge #1 presented a 32 year old male with AML s/p induction chemotherapy who presents with fever and a rash. The skin biopsy showed dense neutrophilic infiltrates without vasculitis and negative infectious stains. This patient has:
B) Sweet’s Syndrome
- General information:
- Classified as neutrophilic dermatosis
- Associated with heme malignancy, autoimmune disease or inflammatory bowel disease; onset described with marrow recovery from G-CSF
- Exam: Abrupt papulonodular lesions on face, neck, hands with antecedent fevers
- Biopsy: Neutrophilic infiltrates without organisms or vasculitis
- Rx: steroids
Look forward to a more extensive review of Sweet’s Syndrome. There will be a new case challenge next week – get ready for it!
Most of the fun in medicine is at the bedside. Try to get out from behind the computer as much as possible (there is little fun to be had there) and spend more time with the patients.
David Juurlink, Advice for Physicians in Training: 40 Tips From 40 Docs, The Winnower 2:e142006.67645 (2014). DOI: 10.15200/winn.142006.67645