Unknown Pleural Effusion

Today at Parkland Morning Report we talked about what to do when a patient presents with a persistent unilateral pleural exudative effusion and the initial tests are unremarkable. This is a follow up to an earlier post regarding pleural effusions. Below are some key points:

  • Up to 25% of pleural effusions will remain undiagnosed after the 1st diagnostic thoracentesis. (1)
  • Malignant pleural effusions are diagnosed only 60-65% of the time on cytology alone. Repeat thoracentesis and cytology may increase the yield. (2)
  • Sensitivity of pleural fluid cytology in malignant pleural effusions range from 40 to 87%. (3)
  • CT chest with pleural fluid enhancement is recommended in all patients with undiagnosed pleural effusion. Can identify optimal sites for CT guided needle biopsy and invasion from underlying structures that would suggest malignancy.
  • Pleural biopsy follows CT scan if pleural effusion remains undiagnosed. Pleural biopsy can be achieved by the following techniques:
    • Percutaneous – Ultrasound or CT guided needle biopsy
    • Thorascopic – Useful when percutaneous is negative, no visible mass on CT, or patchy disease is suspected
    • Open biopsy has fallen out of favor since the growing use of thorascopic

Check out the references below to learn more:

1. Venekamp, et al. Respirology. 2005

2. Garcia LW, et al. Modern Pathology. 1994

3. BTS guidelines for the investigation of a unilateral pleural effusion in adults. 2003

Legionellosis

We had TWO very interesting cases today at VA morning report….one of which is still in the diagnostic stage so stay tuned…

Our second case today was Legionella Pneumonia. Here’s some highlights and a review article to help you be aware of when to think about it.

  • Diagnosed initially in 1976 at the American Legion Convention in Philadelphia
  • Classically thought of as an outbreak, legionella is also an important cause of CAP and nosocomial pna
  • Incidence of legionella as a cause of sporadic CAP in those that require hospitalization varies from 2-15%
  • Transmission occurs by inhalation of aerosols containing legionella or microaspiration of water contaminated with legionella (linked to cooling towers, respiratory therapy equipment and whirlpools)
  • Risk factors: smoking, chronic lung disease, immunosuppression (especially steroids), surgery (especially transplants). Interestingly the incidence of legionnaires’ disease with AIDS is low
  • Pathogens: L. pneumonphilia causes 90% with serotype 1 accounting for 70% of all strains
  • Clinical manifestations: Pneumonia is the predominant clinical syndrome (ranging from mild cough to respiratory failure), constitutional early sx (malasise, anorexia, body aches), fever often exceeds 40 C, watery diarrhea (20-40%), hyponatremia (Na <130)
  • Extra-pulmonary manifestations are rare but can cause sinusitis, cellulitis, pancreatitis, peritonitis, pyelonephritis from dissemination due to bacteremia
  • Lab tests:
    • Sputum cx sensitivity 80%, specificity 100% –> requires buffered charcoal yeast extract agar
    • Urinary antigen assay sensitivity 70%, specificity 100% –> only tests for serogroup 1
    • IgM, IgG serology tests 50% sensitive, 96% specific
  • Treatment:
    • Azithromycin/Clarithromycin
    • Levaquin/Ciprofloxacin
    • Treat with IV until clinical response then switch to po for 10-14 d course (21 d if imunosuppressed)
  • See full NEJM review article here:
  • http://www.nejm.org/doi/pdf/10.1056/NEJM199709043371006

Classic Text for Abdominal Pain

Today at Parkland Morning Report, Dr. Paulk mentioned “Cope’s Early Diagnosis of the Acute Abdomen”, a medical text that is often referred to and beloved by physicians in how to approach a patient with abdominal pain. Dr. Zachary Cope was a physician from Great Britain who wrote the first edition in 1921, currently in its 22nd edition. Check out the link below.

http://www.amazon.com/Copes-Early-Diagnosis-Acute-Abdomen/dp/0199730458

“Dislocation, Italy Style”

Funny article from The New York Times titled, “Dislocation, Italy Style”, as it’s written by Holly Brubach (American) who experiences a hip fracture while visiting Italy. She comments on some differences between US and international care from a patient’s perspective. Check out the link below:

http://www.nytimes.com/2014/07/19/opinion/sunday/dislocation-italian-style.html

Ankylosing spondylitis and IBD

VA morning report had a great case yesterday of a young patient with back pain and GI bleeding that was found to have Anklyosing Spondylitis and associated IBD! Thanks to Dr Bhushan, we have a great review article to share with you all. Here are some highlights:

  • 5-10% of patients with Ankylosing Spondylitis are associated with IBD (either Crohn’s or UC)
  • Inflammation of the axial skeleton is the major hallmark of AS, occuring in more than 90% of patients and is typically characterized by inflammatory low back pain and morning stiffness due to sacroilitis or spondylitis
  • AS can also exhibit peripheral synovitis +/- enthesitis. Peripheral joint involvement is generally oligo-articular and asymmetric and is generally non-erosive, self-resolving joint pain
  • Although 75-90% of AS patients have associated HLA-B27 molecule, only 50-70% of AS and IBD patients are HLA-B27 positive
  • Although 5-10% of AS patients have overt IBD, up to 40-60% of AS patients have subclinical gut inflammation – current guidelines do not recommend screening asymptomtic patients with colonoscopy
  • The clinical implications of this fact are that NSAID therapy can pose a severe problem in AS patients with underlying IBD (the mainstay of medical therapy in AS is NSAIDs)
  • Treatment options for AS asscociated with IBD include physiotherapy, local corticosteroids and anti-TNF agents
  • Unfortunately, conventinoal disease-modifying anti-rheumatic drugs such as MTX, azathioprine or sulfasalazine (all effective for IBD) do not show improvement in axial AS symptoms
  • Anti-TNF agents such as infilximab and etanercept are highly effective in treating active AS and are recommended for patients with active AS that cannot tolerate NSAIDs
  • Interestingly, only inflximab has been showed to have clinical efficacy in IBD sx (not etanercept). The mechanism for this difference is unclear.
  • Check out the whole article here!

http://ac.els-cdn.com/S1521694206000404/1-s2.0-S1521694206000404-main.pdf?_tid=0c85de70-0eb2-11e4-b9ab-00000aab0f6c&acdnat=1405712040_28c88288a53b5c3fb5813a9087aa7bcc

DRESS Syndrome

Over at the University, we discussed the variety of drug-related reactions, particularly DRESS Syndrome. Take a look, it may come up in potpourri some day!

Basics:

  • Drug Reaction with Eosinophilia and Systemic Symptoms
  • <1/100,000 people in the general population
  • Highly variable clinical presentation
  • No strict diagnostic criteria

Culprits:

  • Antiepileptic agents (eg, carbamazepine, lamotrigine, phenytoin, phenobarbital)
  • Allopurinol
  • Sulfonamides (particularly sulfasalazine)
  • Dapsone, minocycline, and vancomycin
  • HLA-B 5801: allopurinol
  • HLA-A 3101: carbamazepine

Drug Rash:

  • Initially presents as a morbilliform eruption
  • Face and upper part of the trunk and extremities are involved initially
  • Progresses to a diffuse, confluent, and infiltrated erythema with follicular accentuation
  • Often involves more than 50 percent of the BSA – extent of involvement suggests severity
  • Can progress to exfoliative dermatitis, vesicles, pustules

Eosinophilia:

  • Leukocytosis with eosinophil counts >700/microL (in 50 to 90 percent of cases)
  • Atypical lymphocytosis with large activated lymphocytes, lymphoblasts, or mononucleosis-like cells (in 30 to 70 percent of cases)
  • Increased serum ALT (in up to 80 percent of cases)
  • HHV-6 infection (in 40 to 60 percent of tested patients)

Systemic Symptoms:

  • Fever, malaise, lymphadenopathy
  • Liver: mild transaminitis to frank hepatitis and acute liver failure. Severe hepatitis is responsible for the majority of deaths associated with DRESS.
  • Kidney (acute interstitial nephritis)
  • Lungs (eos on BAL, interstitial pneumonitis)
  • Heart (eosinophilic myocarditis, pericarditis)
  • Gastrointestinal tract (diarrhea, mucosal erosions, bleeding)
  • Pancreas (pancreatitis)
  • Thyroid (autoimmune thyroiditis, appearing often late, as a sequel of DRESS)
  • Brain (encephalitis, meningitis)
  • Muscle (myositis)
  • Peripheral nerves (polyneuritis)
  • Eye (uveitis)

Management: 

  • Mainstay: withdrawal of the offending drug
  • Exfoliative dermatitis: fluids, electrolytes, and nutritional support
  • High potency topical corticosteroids for symptomatic management
  • Supportive care of organ involvement
  • Usually resolves in 6-9 weeks, but can last up to 6 months

 

Is my patient at risk for MRSA pneumonia?

Today at Parkland Morning Report we talked about selection of antibiotics for suspected pneumonia and when to cover for MRSA. There are several studies that have looked at risk factors for MRSA pneumonia, but there is no general consensus. This seems to imply that risk factors depend on the location of the community and hospital. Below are some risk factors associated with MRSA pneumonia (includes HAP/HCAP and community acquired):

  • Immunocompromised
  • Active or post-influenza infection
  • Recent antibiotic use (particularly cephalosporins and fluoroquinolones)
  • Multilobar infiltrate – cavitary and necrotic lesions
  • IV Drug Use
  • Pleural Effusion
  • Dialysis patient

Check out this interesting case-control study from 2013 in Respiratory Medicine that looked at risk factors for MRSA pneumonia at an academic university hospital. The study looked at risk factors associated with MRSA pneumonia, both hospital/health care and community acquired forms.

Risk factors for methicillin-resistant Staphylococcus aureus in patients with community-onset and hospital-onset pneumonia

Enter your publications, presentations, or abstracts!

Have you published an article, abstract, or manuscript recently? Have you presented at a local, state, or national conference? If so, send us the information below! We want to know all of the amazing things you have done and let the rest of the program know as well!

Does my patient still need bladder cancer surveillance?

At VA morning report today we had a patient who was >10 years out from TURBT for his bladder cancer and so we asked “does this patient still need surveillance?” As internists, we share the responsibility of cancer surveillance post treatment so this is an important question to ask!

  • GU cancers account for 22% of new cancer cases in the US (in 2000)
  • For non-muscle invasive bladder cancers the treatment is TURBT +/- intravesicular therapy (often BCG)
  • Bladder cancer patients are at risk for recurrance in organs that share the genitourinary epithelium such as renal pelvis, ureter, prostate, bladder
  • For follow up, the recommendations are to perform cytoscopy and urine cytology starting 3 m after therapy and q 3 months for two years, then q 6 m for two years. After that the recommendation is for yearly cytoscopy and urine cytology lifelong
  • Three studies have looked at the need for lifelong follow up with data showing that there is a high rate of recurrance early on with significant decline in risk as time progresses (eg one study looked at 86 pts with high risk bladder cancer and found 31% had progression at 5 years and 5% had progression at 10 yrs)
  • The AUA guidelines however currently support lifelong follow up:
  • The high frequency of local recurrence and the potential for stage progression especially for high-risk disease highlights the importance of vigilant surveillance with cystoscopy for patients with nonmuscle invasive bladder cancer. Furthermore the potential for disease recurrence and progression even in the long term typically requires and necessitates lifelong follow-up
  • Check out this article that summarizes follow up  for bladder cancer, prostate cancer, RCC and testicular cancer:
  • http://onlinelibrary.wiley.com/doi/10.1002/cncr.10525/pdf
  • Full AUA guidelines:

Eculizumab – When is it used?

Today at Parkland Morning Report we discussed about the utility of the medication, eculizumab, for hemolytic uremic syndrome. Below are some interesting articles regarding treating thrombotic thrombocytopenic purpura, hemolytic uremic syndrome (HUS), and eculizumab. Key points below:

  • Eculizumab is a recombinant, humanized, monoclonal anti-C5 antibody. It binds to C5 which halts the complement cascade and inhibits production of protein complexes that kill cells.
  • Blocks terminal complement activation, thus patients may have higher risk to infections from encapsulated bacteria such as Neisseria meningitides, Haemophilus influenzae and pneumococci as vaccination is recommended.
  • Used to treat paroysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS).
  • Atypical HUS is distinguished from classic HUS in that it primarily involves the kidneys and seems to have a clear link to dysregulation of the complement system.
  • In regards to administration, patients typically receive 4 weekly IV doses for induction, then a maintenance dose every 2 weeks for aHUS. Duration is unclear as some patient remain on therapy indefinitely. Alternative therapy is plasma therapy.
  • Eculizumab side effects include constipation, nausea, vomiting, tachycardia, fever.
    How I treat thrombotic thrombocytopenic purpura and atypical haemolytic uraemic syndrome
    Update on hemolytic uremic syndrome: Diagnostic and therapeutic recommendations
    http://www.nlm.nih.gov/medlineplus/druginfo/meds/a612024.html#side-effects

UTSW Internal Medicine

%d bloggers like this: