Thank you Dr. Shah for an excellent case of Stress-Induced Cardiomyopathy!

Learning Points:

• Pathophysiology: not well understood, however postulated mechanisms include catecholamine excess, coronary artery spasm and microvascular dysfunction
• Mostly associated with physical or emotional stress preceding onset of chest pain
• Clinical presentation: most common symptom is acute substernal chest pain followed by dyspnea, syncope, heart failure, malignant arrhythmias and cardiogenic shock
• Diagnostic criteria:
  • 1) transient hypokinesis, akinesis or dyskinesia of the LV mid segments with or without apical involvement
  • 2) no obstructive CAD or acute plaque rupture
  • 3) new EKG abnormalities or troponin elevation
  • 4) no pheochromocytoma or mypcarditis

• Workup: serial troponins, BNP, EKG, 2D echo, cardiac MRI, radionuclide myocardial perfusion imaging study
• Treatment: generally a transient disorder  thus requires only supportive therapy, however standard management for heart failure, cardiogenic shock or other complications

Click here for a great review of Takotsubo Cardiomyopathy

Thank you Dr. Walter Igawa-Silva for a great atypical presentation of Vertebral Osteomyelitis!

Teaching Points:

• Clinicians should suspect the diagnosis of native vertebral osteomyelitis in patients with new or worsening back or neck pain and fever  AND in patients with new or worsening back pain or neck pain and elevated ESR/CRP (IDSA; strong recommendation, low-quality evidence).
  • Clinical Features: Back pain (most common); Fever may not always be present
  • ESR/CRP have high sensitivity
• Pathophysiology: Hematogenous seeding> Direct innoculation or contiguous spread
• Obtaining blood cultures is crucial!
  • Positive culture may preclude more invasive procedures (ie bone biopsy)
  • S. aureus = most common pathogen
• MRI has high accuracy (90%) and assesses for abscess while ruling out herniated disk

IDSA Clinical Diagnostic Recommendations for Vertebral Osteomyelitis

Orchid announcement: Please order AFB rule-outs using the “MED Tuberculosis TB AFB Sputum bundle” shown below.

Thank you Dr. Sarkisyan for an excellent case of CAPS on 11/20/15!

Teaching Points:

• CAPS: The most severe form of APS, an acute biologic process that leads to occlusion of vessels of multiple organs.
  • Clotting gone wild!
  • MUST NOT MISS Diagnosis: High mortality rate (30-50%)
• Diagnosis requires acute (<1 week) onsets of symptoms, 3 or more organ involvement, APL antibodies, and biopsy confirmation of small vessel occlusion
• Infections are most common precipitating factors
• Think about this dx in any patient p/w anemia and thrombocytopenia (MAHA) with evidence of end organ dysfunction (ie. Chest pain, SOB, AKI, HTN, Stroke, DVT/PE, etc)
• Treatment: Anticoagulation, High-dose glucocorticoids, Plasma exchange

Thanks to Dr. Nicole Mandich for an excellent presentation on Idiopathic Intracranial Hypertension

Learning Points:

• Predominantly seen in young, obese females of child bearing age
• Classic presentations include headaches, papilledema, sixth nerve palsy , visual disturbances (including diplopia, photopsia and sustained visual loss), pulsatile tinnitus
• Predisposing factors include obesity, OCPs, tetracylines, hypervitaminosis A
• DDx: intracranial masses, obstruction of venous outflow, hydrocephalus, increased CSF production, decreased CSF resorption, malignant HTN, dural vein thrombosis

Click here to review the Idiopathic Intracranial Hypertension Treatment Trial

Thanks to Dr. Patrick Poquiz for an outstanding presentation of AIDS related pulmonary Kaposi sarcoma.

Learning Points:

• Pulmonary Kaposi sarcoma (KS) can present shortness of breath, fever, cough, and hemoptysis. The incidence of KS increases as CD4 count decreases, and KS may be associated with Immune Reconstitution Inflammatory Syndrome (IRIS).
• Diagnosis of KS is definitively made by biopsy, however a presumptive diagnosis can be made by presence of characteristic cutaneous, mucosal, or visceral lesions.
• The mainstay of treatment of KS include highly active antiretroviral therapy, but systemic chemotherapy with daunorubicin or doxorubicin may be required with widespread disease.
• Click here for a NEJM review article on KS.

Thanks to Dr. Jarred Reed for an excellent presentation on workup and management of hypercalcemia

Learning Points:

• Clinical manifestations of hypercalcemia include GI (anorexia, N/V), Neuro (weakness, AMS), Renal (polyuria, nephrocalcinosis), and MSK (fractures, osteopenia) symptoms. Causes may be broken down to PTH-mediated and PTH-independent causes.
• Excess PTHrP (also called humoral hypercalcemia of malignancy) is the most common cause of hypercalcemia with non-metastatic solid tumors, and will result in a low or inappropriately normal PTH level.
• The mainstay of management includes aggressive IVF but may require bisphosphonates, calcitonin, and corticosteroids. Use of Lasix is controversial but should largely be utilized to avoid fluid overload.
• Denosumab may be used for refractory cases of hypercalcemia. Denosumab works on the OPG-RANK-RANKL pathway and prevents bone resorption by limiting RANKL driven osteoclast activity.

Thank you Dr. Julien Nguyen for an excellent presentation on herpes zoster and indications for IV treatment

Teaching Points: 

• Herpes Zoster is a reactivation of VZV in ganglia, leading to acute neuritis with a dermatomal rash, sometimes followed by post-herpetic neuralgia in 10% of patients
• Goal is to initiate treatment within 72 hrs of onset with an antiviral
• Indications for IV tx:
  • Disseminated zoster
  • Severe immunocompromised state
  • Herpes zoster ophthalmicus
  • CNS involvement
  • Significant bacterial superinfection
  • Failed PO therapy
• The Shingles Prevention Study demonstrated that HZ vaccine significantly reduced the morbidity due to HZ and PHN in older adults. Read more from the Journal of Infectious Disease

Thank you Dr. Betty Lai for a great case of hypercalcemia on 10.7.15  presenting as altered mental status!

Learning Points:

• The first diagnostic test to workup hypercalcemia should be PTH
• • Hypercalcemia is due to elevation of ionized or free calcium
  • 40-45% of calcium in serum is bound to protein, mainly albumin.
  • Calcium = serum calcium + 0.8 x (normal albumin – patient albumin)
• >90% of cases of hypercalcemia are either from primary hyperparathyroidism vs. malignancy
• Tx: Only for severe hypercalemia (Ca>14) or for symptomatic cases
  • Acutely (quick onset of of action): IVF; Calcitonin; Dialysis; Loop diuretics
  • Long term: Bisphosphonates

Acute transverse myelitis after DTP vaccine.
T2-weighted MRI showing diffuse cord edema, signal hyperintensity (C3-T6).
From PMID: 16317420.

Thanks to Dr. Nguyen-Fa for a great presentation on transverse myelitis!

Learning points:

• Ddx for upper + lower motor neuron symptoms includes ALS, MS, transverse myelitis, ADEM, compressive myeloradiculopathy, HIV, B12 deficiency, WNV
• Proposed diagnostic criteria of acute transverse myelitis (PMID: 12236201):
  • Sensory/motor/autonomic dyusfunction attributable to spinal cord
  • Bilateral s/s
  • Clearly defined sensory level
  • No compressive cord lesion
  • CSF pelocytosis OR elevated IgG index OR gadolinium enhancement
  • Progression to nadir between 4h – 21 d.
• Treated with steroids +/- plasmapharesis +/- cyclophosphamide

Thanks to Dr. John Feng for a great presentation on severe hypothyroidism

Learning Points:

• Symptoms include: fatigue, cold intolerance, constipation, depression, weight gain, dry skin, hair thinning or loss and memory impairment
• Exam findings include: bradycardia, diastolic HTN, coarse facies, delayed relaxation phase of deep tendon reflexes, non-pitting edema (myxedema), dry skin, hypoactive bowel sound
• Treatment: start IV levothyroxine when there is concern for gut edema (most commonly seen in myxedema crisis) and transition to po levothyroxine at 1.6ug/kg. Please note, start at lower doses in elderly and cardiac patients.

Click on this great article to learn more about hypothyroidism