All posts by andersodav

Moffitt Pearls 3.23.18 – Chlamydia Proctitis and Syphilis

Thank you to Michelle for presenting the case of a young man presenting with symptomatic anemia found to have chlamydia proctitis and a positive RPR.

Key Pearls

  1. The diagnostic test of choice for chlamydial infection of the genitourinary tract is nucleic acid amplification testing (NAAT) of vaginal swabs for women or urine for men. Many laboratories have also validated NAAT on rectal swabs to diagnose chlamydial proctitis
  2. CDC recommended regimen for treatment of chlamydia proctitis is CTX 250 mg IM x1 PLUS Doxycyline 100 mg PO x 7 days
  3. In high risk patients diagnosed with chlamydia proctitis it is important to treat them for gonorrhea b/c of the risk of co-infections (hence the dual coverage above).
  4. Patients with severe proctitis may have lymphogranuloma venereum (LGV) which requires a full 3 weeks of therapy. See more info on LGV from prior blogs!
  5. As in this case, if the timing of syphilis is not known, late latent syphilis is presumed. Penicillin G IM once weekly for 3 weeks is the treatment of choice.



Inflammation of the lining of the rectum within 10-12 cm of the dentate line.

Differential Diagnosis:

# Infectious

  • Most commonly gonorrhea or chlamydia (including LGV strains with rq longer duration of therpay)
  • Other causes include HSV (more common in immunosuppressed patients), syphilis (usually secondary), C. difficile or parasites (amebiasis).

# Inflammatory

  • Crohn’s disease and Ulcerative colitis

# Ischemia

# Radiation or Chemical

# Trauma/instrumentation


Review of Syphilis and Therapy can be found in table form here.

See prior blog from the amazing Grant Smith for more on LGV


Moffitt Pearls 2.26.18 – Hypophosphatemia

Thank you, Matt, for presenting a case of an elderly woman with a history of recent diagnosis of lung cancer s/p chemo and XRT, weight loss, and multiple recent falls who presented after another mechanical fall with post-traumatic emesis.

Key Pearls:

    1. Check out this fantastic prior chief post from Christy that covers an approach to falls in the elderly. Christy also outlines how to perform and interpret the Get up and Go Test!
    2. Emesis after head trauma is an important historical feature. By some definitions, post-traumatic vomiting is diagnostic of concussion. Furthermore, in this case series of over 5000 adults and children presenting to the ED for head injury, post-traumatic vomiting was associated with a fourfold increase in the relative risk for a skull fracture.
    3. Undetectable phosphate?? What causes that? Big categories include poor nutrition or malabsorption, GI losses, cellular shifts, and renal losses. See more below.



Clinical manifestations of severe hypophosphatemia are widespread. They can include anorexia, muscle weakness, osteomalacia, progressive encephalopathy, seizures, coma, and death. Hematologic disturbances include hemolytic anemia, decreased release of O2 from Hb, and impaired leukocyte and platelet function.

Mechanisms for Hypophosphatemia

Less Coming In Cellular Shifts More Going Out
Poor Nutrition

–          alcoholics

Refeeding syndrome GI Losses

–          chronic diarrhea

–          chronic phosphate-binding aluminum (antacids)


–          short gut

–          Med effects: PPIs

Acid-base abnormalities

–          Severe respiratory alkalosis


Renal Losses

–          Fanconi syndrome (+/- Bcell neoplasm)

–          Hyper PTH (or PTHrP)

–          Diuretics

–          Vitamin D deficiency


Moffitt Pearls 2/14/18 – GI Report – Liver Masses

Thank you to Bennett and Scott for presenting the case of an middle aged man presenting from an outside hospital with RUQ pain found to have a rapidly growing hepatic mass (10 -> 20 cm in 6 weeks) extending into the R pleural cavity. We had a great discussion of possible liver lesions summarized below and are awaiting the pathology review from OSH biopsy. Given the rapid growth we discussed the possibility of a vascular component to this mass in addition to infectious causes (s/p biopsy) vs. lymphoma of the liver. Keep us updated!!

Key Pearls

  1. In the majority of patients (as Dr. Ostroff was alluding to), a proper diagnosis can be made based on the characteristics on imaging modalities.
  2. The majority of lesions < 1.0 cm are benign. Benign liver lesions are found in more than 20% of the general population[1], including haemangioma (4%), focal nodular hyperplasia (FNH, 0.4%) and hepatic adenomas (0.004%).
  3. Liver mets in a normal liver usually come from colon, stomach, lung and prostate. Importantly, mets are a rare finding in a cirrhotic liver.

Liver Lesions



Risk Factors Symptoms Dx Tx
Hepatic hemangioma Most common liver lesion; F>M Rarely causes pain US – well-circumscribed; peripheral enhancement None; no risk of bleed or CA
Cyst 5% of individuals; F>M Asx Rapid arterial uptake; hypodense lesions None
Focal Nodular Hyperplasia Hyperplastic growth around a preexisting arterial malformation Asx Solitary lesion None

Hepatic adenoma

Uncommon; M>F RUQ pain; palpable mass; fevers leukocytosis US or CT – no uptake with contrast Surgery (emergent if converts to bleeding)
Pyogenic Liver Abscess Ass w/ biliary stenting or acute ascending cholangitis; higher risk in DM Fevers, tender liver, leukocytosis Aspirate and Cx; US or CT; loculated single or multiple rim enhancement 4-6 weeks of abx


+/- Perc drainage

Amebic liver abscess Amoebiasis; endemic to Mexico Fevers, tender liver, leukocytosis Can’t culture; serology & empiric abx; Halo sign on CT “rim enhancement” Cholestatic LFTs; r/o IgG Echinococcal Metronidazole


If persistent then drain

Echinococcal cyst Ingestion of tapeworm eggs (fecal-oral); infected dogs/livestock If cysts rupture -> 2° echinococcis or anaphylactic shock Cholesttaic LFTs; eosinophilia; Test for IgG echinococcal Mebendazole


Avoid puncturing cyst



Malignant Risk Factors Symptoms Dx Tx
HCC Cirrhotics (EtoH, HBV, HCV, NASH…) Wt. loss, RUQ discomfort; HSM; jaundice; ascites – U/S or CT

-AFP – trend & prognosticate; -CEA (non-specific)

Resection, transplant, chemo
Biliary Tract Cancer CA of GB or intra-or extra hepatic biliary tract Abd pain, biliary obstruction, LFTs abnl Intrahepatic Ca; solid mass withing liver, Extra-hepatic: duct dilation, rim-enhancing (unlike HCC) Surgical resection, but often too large, embolization + chemo
Liver mets 20:1 more common than HCC, but uncommon in cirrhotic livers

-CRC, gastric, pancrearic, neuroendocrine

Looks for rise in CEA or LFTs in pt with hx of CRC or other CA CT or U/S Resection is confined to one lobe; radioablation
Heptic angiosarcoma 2% of primary liver cancers; Abd pain, weakness, wt loss, HSM, jaundice, CHF 31%; hepatic failure; intra-abd bleeding LFTs abnl

Ateriography “vascular lakes”

Mean life expectancy 6 months +/- chemo therapy or surgery
Lymphoma   B-symptoms, weight loss, fevers, RUQ abd pain Multiple, fast growing lesions Chemotherapy



Cardiology Report Pearls 2/13/18 – PD-1 Inhibitors and Myocarditis

Thank you, James, for presenting a case of an older male with history of metastatic squamous cell carcinoma s/p multiple round of chemotherapy now on pembrolizumab presenting with acute onset of dyspnea thought to be 2/2 to PD-1 myocarditis and less likely ACS w/ acute RV failure.

 Key Pearls:

  1. PD-1 Inhibitors, immune-check-point inhibitors that allow the patient’s own immune system to fight malignancy, have advanced our ability to control difficult-to-treat malignancies. It’s not all sunshine and roses though – PD-1 inhibitors have MANY toxicities! See below for more details.
  2. PD-1 inhibitor induced myocarditis and conduction abnormalities reported in literature at very low rate occurring in < 1% of patients in studies. See this study from NEJM with table below.
  3. External beam radiation can cause cardiac disease. Cardiac disease includes pericardial disease, cardiomyopathy, as well as accelerated coronary artery disease. Many of these adverse events don’t appear for up to 10 years!
  4. Acute RV failure DDx (large PE, acute mitral stenosis, RV infarct, myocarditis, ARDS) vs. Chronic RV failure DDx (chronic LV failure, pulmonary HTN, OSA, ASD or VSD, chronic mitral stenosis)
  5. Sometimes you can get information about the respiratory rate on the ECG!! Check out this example where you can see respiratory phasic variation that suggests significant tachypnea! Don’t get fooled in thinking this is electrical alternans, which would be more of a beat-to-beat variation.


PD-1 Myocarditis



Emerging data show that 20% of patients with melanoma treated with ipilimumab achieve long-term survival! See this associated review.

PD-1 (programmed cell death 1) and its association with the ligand (PD-L1) is a necessary step in stimulating apoptosis of T-cells, serving as an immune checkpoint. PD-L1 is generally expressed by native cells, signaling to the T-cell “I’m one of you! Don’t hurt me”.  Some tumors have been found to also express PD-L1, enabling them to evade destruction by T-cells.  In order to treat these malignancies, PD-1 inhibitors (pembrolizumab, nivolumab) serve to block the interaction between PD-1 and PD-L1, enabling T-cells to stay “programmed on”, and thus enable immune-mediated destruction of tumor.

Because of this mechanism of action, a common consequence is the upregulation of cell-mediated immunity and, unfortunately, inhibition of native tissues to turn off T-cells. As a result, we commonly see autoimmune-mediated inflammation manifested as new rash, diabetes, thyroid disease, pneumonitis, hepatitis, colitis, etc.

Common Immune-Mediated Toxicities Seen with Check-point Inhibition:


Organ System Manifestation Management
Skin & Mucosa Pruritic rash (most common!)




Topical corticosteroids

Oral antipruritics

Consider oral steroids

GI Tract Diarrhea/colitis – presents ~6wks into treatment R/O infxn

Anti-motility agents

Steroids if severe

Liver Hepatitis (rate <5%, severe toxicity very rare) Stop therapy if moderate-severe.

Steroids + mycophenolate given rarely.

Lung Pneumonitis – (rate <5%, but occasionally fatal) Steroids common. Infliximab, cyclophosphamide also used, though patients requiring therapy beyond steroids have nearly 100% mortality.
Endocrine Hypophysitis

Autoimmune thyroid disease

Adrenal Insufficiency T1 DM

Hormonal replacement



Less commonly reported immune-mediated adverse events include the following: acute renal injury, pancreatitis, neurotoxicity (GBS, myasthenia gravis, PRES, aseptic meningitis, autoimmune encephalitis), cardiotoxicity (myocarditis and complete HB reported in literature at very low rate occurring in < 1% of patients in studies), hematologic (cytopenias), and ocular inflammation.

Many of the adverse events described above can be managed with continued use of PD-1 inhibitors if mild. However, for severe adverse reactions, PD-1 inhibitors are withheld and potential discontinued permanently

Pulmonary Report Pearls – 2/12/18 – Pleural Effusions

Thank you to Max for presenting the case of a middle aged woman with history of SLE c/b Evans syndrome on steroids (20 grams x 2 weeks) re-presenting to medicine after treatment strep pneumonia on oral amox with recurrent cough, fevers and pleuritic chest pain. She was found to have a left sided effusion and will be evaluated today for drainage and possible chest tube (incomplete source control!!).

  • 15-20% of patients with Strep Pneumonia will have bacteremia. These patients should be continued on abx for 14 days and it is important to ensure there are no metastatic complications before abx are discontinued.
  • Remember wrong drug, wrong bug or incomplete source control in any patient presents with ongoing fevers. However, as we discussed other causes of ongoing fevers include failed immune system (immunosuppression preventing host from clearing an infection) and/or another problem (such as a rheum flare) driving fevers.
  • Pulmonary complications associated with strep pneumo bacteremia include empyema, necrotizing pneumonia, and lung abscess.
  • The main difference with a high resolution CT vs. standard CT at Moffitt is air dynamics – inspiration and expiration comes with HRCT. We no longer skip lesions with the high resolution CT. This is not true in the community…yet.
  • Effusions related to infection run on a spectrum from simple parapneumonic à complicated à empyema. See more details below on delineation and implications for management.
  • Never let the sunset on a pleural effusion without tapping it! In general, all parapneumonic effusions, EXCEPT those that are free flowing and layer less than 10 mm on a lateral decubitus film, should be sampled by thoracentesis.


The Gradient of Pleural Effusions

Stages Macro Appearance Pleural fluid characteristics Management
Simple Parapneumonic Clear Fluid pH > 7.2

LDH < 1000 IU/I

Glucose > 2.2 mmol/l

No organisms on culture or gram stain

Will resolve with abx alone

Chest tube for symptoms only

Complicated Parapneumonic Clear fluid or cloudy/turbid pH < 7.2

LDH > 1000

Glucose < 2.2 mmol/l

May be + organisms on gram stain/culture

Requires chest tube drainage
Empyema Frank pus May be + organisms on gram stain/culture Requires chest tube drainage
  • Other indications for drainage of an effusion include: large + free flowing ( > 1/2 the hemithorax), loculated effusions, or effusions with a thickened parietal pleura.

Moffitt Pearls 2/9/18 – DKA and NSTEMI

Thank you to Katie Sullivan for presenting the case of an elderly woman with history of type 1 diabetes and CAD s/p CABG presenting after colonoscopy with severe nausea/vomiting and diarrhea. The patient was found to be in DKA likely 2/2 to an NSTEMI with EKG changes suggestive of ischemia and a troponin of 25!

Key Pearls

  • Complications after colonoscopy are rare (approximately 3 per 1000 screening colonoscopies) and include complications of sedation, complications related to the preparation, bleeding, and perforation.
  • Never forget that Ischemia – acute MI – can precipitate DKA!! See the rest of the “I’s” below brought to you by our wonderful interns Noa and Hayley.
  • Any patient with ACS regardless of intervention (stent or no stent) should be treated with DAPT for 12 months b/c of improved cardiovascular outcome. Bleeding risk needs to be balanced against benefits and shorter durations are sometimes used. (See graph from the study)
  • Troponin elevation in the setting on non-ACS related demand is associated with worse f/u cardiac mortality in both low and high risk patients. In one study incidence of cardiovascular death or heart failure after adjusting for conventional risk factors (hazard ratio 1.84, 95% CI 1.30-2.61) [1].
  • Patient with the flu are at a much higher risk of ACS during and in the week after illness. A recent Canadian study in the NEJM showed that MI admissions were 6x more likely to occur in the week after a positive flu test!!

Remember the I’s for causes of DKA reviewed!!

  • Infection
  • Ischemia
  • Infant/pregnancy
  • Ingestion/intoxication
  • In-adherence to medications
  • Iatrogenic
  • (I)Other: hypercortisol and sympathetic surge

CURE trial



  1. Prognostic value of cardiac troponin I measured with a highly sensitive assay in patients with stable coronary artery disease. Omland T, Pfeffer MA, Solomon SD, de Lemos JA, RøsjøH,ŠaltytėBenth J, Maggioni A, Domanski MJ, Rouleau JL, Sabatine MS, Braunwald E, PEACE Investigators. J Am Coll Cardiol. 2013 Mar;61(12):1240-9. Epub 2013 Feb 13.

Morning Report 2/7/18 – Neutropenia, Fevers and Subdural Empyema

Thank you to Nadine for presenting a case of a young woman with very complex medical history including cryptogenic cirrhosis s/p TIPS, hepatic encephalopathy on lactulose and rifaximin listed for transplant, aplastic anemia, CAD s/p mid-LAD thrombectomy, LAD dissection, APS antibody positive on ASA, short telomere syndrome, who was admitted for neutropenic fever and evolution of spontaneous subdural hematomas in the setting of coagulopathy and thrombocytopenia. Wow!

Neutropenic Fever:

  • ANC <500 or <1000 with anticipated decline
  • Single temperature >38.3 or >38 sustained for more than 1 hour

When you think about empiric coverage, consider patients as either high risk or low risk. Here’s a breakdown of high vs. low from Medscape.

High-risk patients are those patients with any one of the following:

  • Anticipated, prolonged (>7-d duration), and profound neutropenia (ANC <100/µL) following cytotoxic chemotherapy
  • Significant medical comorbidities, including hypotension, pneumonia, new-onset abdominal pain, or neurologic changes

Low-risk patients are those with the following

  • Anticipated brief (<7-d duration) period of neutropenia
  • ANC greater than 100/µL and absolute monocyte count greater than 100/µL
  • Normal findings on chest radiograph
  • Outpatient status at the time of fever onset
  • No associated acute comorbid illness
  • No hepatic or renal insufficiency
  • Early evidence of bone marrow recovery
  • Most of the guidelines for neutropenia come from patients with chemotherapy induced neutropenia – these patients are at the highest risk for acute infection due to the combination of both low neutrophil count and mucositis.
  • However, patients with other causes of neutropenia who have had absolute low neutrophils for prolonged periods of time, may be at higher risk for indolent infections.

Infected Subdural Hematomas

  • As HH mentioned most subdural infections represent local extension of paranasal sinusitis or otitis, or are complication of intracranial surgery.
  • Infection of a subdural hematoma is a usual cause of subdural empyema with < 50 cases reported (see article below).
    • May transform in the setting of pre-existing subdural via hematogenous infection (concerning for our patient with new murmur and AMS).
    • Mostly seen in adults > 60 and immunolofic dysfunction (eg neutropenia).
    • Microbiology: Varied considerably. Of the 47 case reports 13 cases reported E. Coli (27%), 8 cases reported Salmonella (17%), Staph aureus in 6 cases (13%) and Streptococcus in 5 cases (10%). The rest were a mix of Klebsiella, Campylobacter or unknown.
  • Signs and symptoms are non-specific and include altered sensorium (depressed level of consciousness), fevers and focal deficits.
  • MRI has become the imaging modality of choice in patients with infected subdural hematoma. It is superior to CT scans for the demonstration of extra axial fluid and rim enhancement, and in the visualization of the presence of pus.
  • Definitive management is surgical: both burr hole and craniotomy.
  • The best surgical option is not well defined, however based on limited data the recurrence rate seems to be lower with craniotomy.

See the following review article for more information.