Thanks to Dr. Tracy Lin for an excellend case of newly diagnosed HIV presenting as PCP Pneumonia!

Learning Points:

-HIV often presents with opportunistic infections, including PCP pneumonia. PCP pneumonia in an HIV positive patient typically takes an indolent course with weeks to months dyspnea on exertion, fever, and dry cough. PCP pneumonia presents as a more acute and severe infection in immunocompetent patients.

-Findings suggestive of PCP pneumonia include and elevated LDH, diffuse interstitial infiltrates on CXR and patchy GGO on CT. Definitive diagnosis requires a bronchoscopy or BAL with staining or DFA.

– Click Here to read a Cochrane Review describing indications for corticosteroids in addition to Bactrim in severe cases of PCP Pneumonia.

Thanks to Dr. Duminda Suraweera for an excellent review of UGIB management

Learning points:
• Triage:
– SDU vs ICU depending on etiology of upper GI bleed, BP, HR, mental status, ability to protect airway and continued active bleeding
• Immediate interventions:
– Resuscitate, resuscitate AND resuscitate with IVFs
– Transfuse pRBCs to keep Hg>7 as per guidelines published in NEJM
– Transfuse FFP and give vitamin K to reverse coagulopathy and maintain INR<1.5
– Transfuse platelets to keep levels >50K
– Start PPI gtt vs intermittent PPI therapy to promote platelet aggregation and clot formation
– Start Octreotide gtt to decrease portal hypertension via vasoconstriction of splanchnic circulation
– Start short course of Ceftriaxone or Norfloxacin in cirrhotic patients with UGIB in an effort to decrease risk of SBP

Click on this great review article for more learning on variceal hemorrhage

Thank you Dr. Caspian Oliai for a great case of symptomatic pulmonary hypertension!

Teaching Points:

–Classification by the World Health Organization (WHO):

• Group 1 – PAH
• Group 2 – PH due to left heart disease
• Group 3 – PH due to chronic lung disease and/or hypoxemia
• Group 4 – Chronic thromboembolic pulmonary hypertension (CTEPH)
• Group 5 – PH due to unclear multifactorial mechanisms

–EKG clues of right ventricular strain: RVH, RAD, S1Q3T3 pattern, atrial arrhythmias, new incomplete RBBB, ST-segment changes and T-wave inversions in the right precordial leads (V1-3) ; repolarization abnormalities

–Patients’ fluid status can be tenuous, and much caution should be taken when administering fluids and/or diuretics

Great AM report by Dr. Liza Buchbinder! Today we presented a patient who was found to have an anterior mediastinal mass and multiple cavitary pulmonary lesions.

Learning points:

• There is a broad differential for multiple pulmonary nodules, which may be narrowed based on CT characteristics.
• When describing lung lesions on imaging, consider the following characteristics:
  • Pattern: reticular, nodular, or reticulonodular
  • Density of lesions: hypodense (COPD vs. cysts) vs. hyperdense (ground-glass vs. airspace consolidation)
  • Distribution: Central vs. peripheral, upper vs. lower
  • Relationship to secondary lobule: Are lesions perilymphatic, centrilobular, or random?
• A nice primer on reading CTs
• Specifically for cavitary lung lesions, consider:
  • Infection: bacterial abscess, fungal disease (mycobacterial, cocci, histo), septic emboli
  • Malignancy:  lymphoproliferative, SCC, angiosarcoma, Kaposi’s Sarcoma
  • Collagen vascular disease: GPA.

Have a great weekend and continue the great work!

Thank you Dr. Duminda Suraweera for a great and unique case and presentation of GPA presenting as subacute limb ischemia.
 
Learning points:
–Vasculitides are commonly classified by vessel size (small, medium, large). The diagram below is also a great visual way to think about working up vasculitis when it is suspected
–Common clinical presentations of GPA include constitutional symptoms, and disorders of the upper and lower respiratory tract (e.g., sinusitis, hemoptysis) and renal disease (e.g.,glomerulonephritis).
–Click here for a great article on the most recent literature on systemic vasculitides

Thanks to Dr. Diana Sarkisyan for an outstanding case and presentation of likely NMO presenting as acute persistent vision loss.

Learning Points:

– Etiology of acute persistent vision loss can be divided into three broad categories: problems involving the media (keratitis, uveitis, vitreous hemorrhage), retina (CRAO, CVAO, retinal detachment) or optic nerve (ischemia, optic neuritis, or NMO).

-Neuromyelitis optica is an inflammatory disorder of the optic nerves and spinal cord which is distinct from optic neuritis. Diagnosis is made by MRI of brain and spine and seropositivity for NMO-IgG. Treatment includes high dose IV steroids and plasmapheresis for refractory cases.

– Click here for an article describing conditions requiring an emergent ophthalmologic consultation.

Sagittal and diagrammatic views of the musculature involved in enacting oropharyngeal swallowing.

Thanks to Dr. Elliot Ho for discussing a case of dysphagia secondary to gastric adenocarcinoma of the GE junction.

Learning points:
— Nomenclature:

• Dysphagia: difficulty with swallowing
• Odynophagia: pain with swallowing
• Aphagia: inability to swallow
• Phagophobia: fear of swallowing

— There is a broad, but a structured differential can be created with the following categories:

• Oropharyngeal vs. esophageal
• Mechanical vs. motor
• Extrinsic vs. intrinsic.

— History is key:

• Dysphagia to solids + liquids suggests motor
• Dysphagia to solids progressing to liquids suggestive mechanical.
• Screen associated sx for possible neuromuscular, malignant, or infectious source.
• Ferrous sulfate + alendronate frequent cause of pill esophagitis

— Barium swallow may be better than EGD for webs, rings, and linitis plastica.

Phlegmasia cerulea dolens. From PMID: 17229945

Thanks to Dr. van den Burg and Julien Nguyen, PGY2 for a comprehensive introduction to lower extremity DVT management!

Learning points from today:

• When to treat?
  • Assess for contraindications.
  • No bleeding risk score developed specifically for anticoagulation in VTE, but for HASBLED score is being used for anticoagulation in atrial fibrillation. (PMID: 20299623)
  • All proximal DVT should be treated (popliteal, femoral, iliac vein)
  • Symptomatic distal DVT generally treated.
  • Asymptomatic distal DVT may undergo serial U/S surveillance.
• For how long do we treat?
  • 3 months for active episode of VTE.
  • Treating beyond 3 months (i.e., indefinitely) is for “secondary prevention,” typically done if active cancer or 2+ unprovoked VTE.
  • See this great Blood article for a great review of the literature regarding treatment duration. (PMID: 24497538)
• Treatment options
  • Factor Xa inhibitors:
    • Parenteral: Some LMWH (enoxaparin, dalteparin, tinzaparin, nadroparin)
    • Oral: rivaroxaban, apixaban, edoxaban.
  • Direct thrombin inhibitors (No “x” in generic name):
    • Parenteral: bivalirudin, argatroban, desirudin.
    • Oral: dabigatran.
  • Coumadin
• Idarucizumab as a reversal agent for dabigatran is undergoing expedited FDA approval.  (PMID:  26095746, 26095632)
• Consider IR and/or vascular surgery consult for catheter-directed thrombolysis or thrombectomy if evidence of ischemia due to decreased venous outflow (e.g., phlegmasia cerulea dolens, phlegmasia alba dolens).