Category Archives: General Internal Medicine

VA Ambulatory Report 2.21.18 – Sarcoid Diagnosis and Hematuria

We had two great case discussions today.

First Jeff presented an image of incidentally discovered pulmonary nodules and hilar lymphadenopathy.  The patient was diagnosed with sarcoid based on these imaging results alone.

Learning points:

  • How to diagnosis sarcoid:
    • If a patient is asymptomatic with characteristic radiographic findings – this is sufficient to make the diagnosis
    • For symptomatic patients, biopsy confirming noncaseating granulomas is required
  • For a new diagnosis of sarcoid monitor for complications and extrapulmonary involvement: EKG, eye symptoms, vitamin d levels, UA
  • In an asymptomatic patient with low grade radiologic changes, the management is observation only


Second, Akshai presented a patient seen in clinic the day prior with gross hematuria.

Learning points:

  • Gross hematuria should strongly increase your suspicion of malignancy. The incidence of malignancy in microscopic hematuria vs. gross hematuria  is ~2% vs. 20%.
  • Smokers are 4-7 times more likely to develop bladder cancer than non-smokers
  • CT Urography is the test of choice to evaluate for malignancy and nephrolithiasis.  CTU provides both functional and anatomic information about the kidney and ureter.  The pre-contrast phase evaluates for nephrolithiasis and hydronephrosis.  The post contrast phase evaluates renal and urothelial malignancies and can assess kidney function in the setting of obstruction.


Evernote link:


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



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.

Moffitt Pearls – 11/15/17 – VZV Encephalitis

Thank you to Andrew for presenting the case of an elderly man with recent CVA presenting with progressive encephalopathy 2/2 to VZV encephalitis.

Key Pearls

  • Acute toxic-metabolic encephalopathy (TME) is an acute condition of global cerebral dysfunction in the absence of primary structural brain disease
  • Acyclovir neurotoxicity should be considered with new neurological symptoms or encephalopathy 24 hours initiation of treatment, particularly in the presence of renal impairment.
  • Herpes zoster encephalitis (HZE) is an uncommon complication of herpes zoster with immunosuppression (HIV, immunosuppressive medications, increasing age) being the principal risk factor for the development of HZE.
  • Localized zoster can cause CSF pleocytosis and positive VZV PCR despite lack of active CNS infection -> this is b/c neurons are the primary site of latent virus
  • In suspected cases of zoster encephalitis send BOTH VZV PCR and Viral anti-body. The presence of one or both is evidence of small-vessel encephalitis due to VZV.
  • VZV encephalitis is rare and life-threatening-> Empirical treatment with IV Acyclovir 10-30 mg/kg per day for 10 days is currently recommended, however no RTCs have been performed.

The figure below outlines the disease pathology of VZV infection from primary infection to reactivation. See Dr. Gilden’s (a leader in the study of VZV) for an excellent review of VZV in the NEJM – “Neurologic Complications of the Reactivation of Varicella-Zoster Virus.”

VZV Encephalitis

Moffitt Pearls 11/7/17 – Cards Report – Vasopressors and PA Catheters

Thank you Matt H for your help with these PEARLS!!!

Thanks to Chloe for presenting a fascinating case of a 65 year old man with history of HOCM (w/o obstruction) who presented with acute onset shortness of breath, ultimately thought secondary to flash pulmonary edema from paroxysmal hypertension. We had a great discussion on vasopressors to use in different types of shock. Below is a summary of some of the more common vasopressors, as well as brief information on key considerations in their use. Finally, there is a bit of info on the ESCAPE trial that led to reductions in use of PA catheters in management of cardiogenic shock.

For more information, refer to the UCSF Hospitalist Handbook and the MGH CCU handbook.

Key Pearls

  • Dobutamine is considered a first line pressor in cardiogenic shock b/c it improves contractility and drops SVR (watch out for dropping BPs).
  • HOWEVER, never write for a MAP goal and titration parameters when using dobutamine as patients MAPs will sometimes drop with up titration (this is why we sometimes start this with norepinephrine).
  • The ESCAPE (2005) showed no improved 6 month mortality in patient with decompensated heart failure randomized to management with PA catheter monitoring vs. usual care. See indications for when to us a PA catheter below.

Vasoactive/Inotrope medications

Class Drug Dose Mechanism
Vasopressor Phenylephrine 0-200 mcg/min α-1 agonist
Vasopressin 0.04 units/min V-receptor agonist
Mixed Norepinephrine 1-20 mcg/min α-1, β-1 agonist
Epinephrine 1-20 mcg/min α-1, β-1, β-2 agonist
Dopamine 1-3 mcg/kg/min

2-10 mcg/kg/min

10-20 mcg/kg/min

D agonist

β-1, β-2 agonist

α-1 agonist

Inodilator Dobutamine 2-5 mcg/kg/min β-1 > β-2 agonist
Milrinone 0.375-0.75 mcg/kg/min PDE III inhibitor


Receptor Action
α-1 Vasoconstriction
β-1 Inotropy
β-2 Vasodilation, bronchodilation
D Splancnic vasodilation – increases renal blood flow
V Vasoconstriction

Quick info on selected vasoactive agents:

Norepinephrine: 1st line pressor for sepsis, cardiogenic shock, undifferentiated shock.

Vasopressin: Often 2nd line pressor in sepsis. Use caution in patients with coronary or peripheral vascular ischemia. Not affected by acidosis (many other pressors are less effective in this situation)

Phenylephrine: Useful for pure vasodilatory hypotension (e.g. sedation-related hypotension). Generally avoid in cardiac patients as can cause reflex bradycardia with decreased cardiac output. HOWEVER, can be useful in unstable arrhythmias when beta agonism may be undesirable. Also useful in HOCM with dynamic outflow obstruction (‘stents’ open the obstruction) or fixed obstruction in AS as it increases SVR without changing afterload felt by the heart.

Epinephrine: Primary use is in ACLS, though can also be used as 3rd pressor in refractory hypotension. Adverse effects include tachycardia/tacchyarrythmias, peripheral vasoconstriction and end-organ damage

Dobutamine: Increases contractility while reducing SVR. Often decreases blood pressure, therefore should not be thought of as a vasopressor, should also not be titrated to MAP goals. Risk of arrhythmia with higher doses, also risk of myocardial ischemia from increased oxygen demand.

Milrinone: PDE-3 inhibitor, inhibits cAMP breakdown. Similar to dobutamine, results in both inotropy and decreased SVR (perhaps more reduction in afterload, but also more risk of hypotension, than dobutamine). Requires dose-reduction in renal impairment.

Indications for PA Catheters

ESCAPE trial (2005) – randomized patients with acute decompensated heart failure to therapy guided by PA catheter vs no PA catheter. No difference in 6 month mortality or days out of the hospital. Based on this trial and meta-analysis, PA catheters are no longer used routinely. They still have a role in shock of uncertain etiology or when initial management is unsuccessful.

AHA guidelines on PA catheters (2013):

  • Recommended in patients with respiratory distress or evidence of impaired perfusion when intracardiac filling pressures can’t be determined by clinical assessment (class I, level C)
  • Can be useful in heart failure with persistent symptoms despite standard therapy if any of the following are present: (class IIa, level C):
    • Uncertain volume status, perfusion, SVR, PVR
    • Persistent hypotension
    • Worsening renal function despite initial therapy
    • Need for vasoactive agents
    • Anticipated need for mechanical cardiac support
  • Routine use not recommended in normotensive patients with acute decompensated heart failure responding to diuresis and afterload reduction (class III, level B)

Double Moffitt Pearls 11/3 & 11/6 – ALF, Toxic ingestions and Mesenteric Lymphadenopathy

Moffitt Pearls 11.3.17 – Saipan Case

Thank you to Amy for presenting a case from Saipan!! We learned about a middle-aged man presenting with encephalopathy and jaundice found to have acute liver injury and renal failure of unclear etiology. The leading thoughts were possibly leptospirosis vs biliary colic that self resolved. The patient was managed with IV abx and IVFs and improved over 2 weeks. We discussed the limitations of practicing in this setting and inability to transfer this patient to a center for transplant evaluation.

Key Pearls

  • EtoH Hepatitis: jaundice, anorexia, fever, and tender hepatomegaly. Labs: transaminases (typically less than 300 int. unit/mL), AST/ALT ratio > 2. Patients may also present with right upper-quadrant/epigastric pain, hepatic encephalopathy, and signs of malnutrition.
  • Acute liver failure is defined as the presence of coagulopathy (INR > 1.5), encephalopathy and no pre-existing liver disease. See more details below.
  • Leptospirosis has a broad range of manifestations, from subclinical illness or mild self-limited disease (approximately 90% of infections) to Weil’s syndrome (Weil’s disease), which is characterized by renal failure, jaundice, and hemorrhage and has a 5 to 15% mortality rate (1).
  • See this NEJM article where HH crushes the diagnosis in the first couple of sentences (it is related to this case)

Overview of Acute Liver Failure 

ALF = coaguapathy INR > 1.5, encephalopathy, and no signs of chronic liver disease

Key History: 

  • IVDU, travel, sexual, ingestions, Fmhx Wilson’s, (note: Hemochromatosis – no acute liver failure)

Physical Exam:  

  • Vitals, stigmata of liver disease, neuro exam, optho exam

Etiology of Acute Liver Failure

  • Ischemia*
  • Toxins* – Tylenol (most common cause in USA), Amanita
  • Acute viral hepatitis*
    • Professional: HAV, HBV, sometimes HCV, HEV
    • “Moonlighters”: HSV, CMV, VZV, parvovirus
  • Autoimmune Hepatitis
  • Acute Budd Chiari – esp if concomitant portal vein thrombosis
  • Reactivation of HBV or HDV on chronic HBV
  • Wilsonian crisis – often with concomitant hemolytic anemia
  • Malignant infiltration – breast, small cell lung, lymphoma, melanoma, myeloma
  • HLH
  • Heat stroke 
  • Remember -> NOT causes of acute liver failure – ETOH, NAFLD, iron overload, alpha-1 def, PSC, PBC
  • * denotes are most likely to cause AST/ALT in the 1000s


Moffitt Pearls 11/6 – Toxic Ingestions

Thank you to Tim for presenting a fascinating case of a young woman 9 weeks post-partum presenting with a profound gap acidosis and osm gap initially c/f ethylene glycol vs methanol ingestion found to have severe starvation ketosis. We discussed the evaluation of possible ingestions and treatment for suspected Ethylenel Glycol ingestion with fomepizole (below).

Thank you HH for presenting a mini-case of a young engineer returning from India p/w abdominal pain, n/v and mild hepatocellular transaminitis (300s) found to have mesenteric lymphadenopathy 2/2 hepatitis E!!

Key Pearls

  • Per EM guidelines send Serum Osm, Salicylates, APAP and EtoH levels in any suspected ingestion.
  • Fomepizole is used in ethylene glycol and methanol toxic ingestion. It is a competitive inhibitor of alcohol dehydrogenase and prevents formation of glycolic acid which is responsible for both the acidosis and oxalate crystal formation. See this NEJM article for more info.
  • We learned the ddx for mesenteric lymphadenopathy include hepatitis E in addition to those listed below!!

Effect of Fomepizole on Metabolism of Eythlene Glycol and Methanol (Brent J. N Engl J Med 2009;360:2216-2223)Picture1

Differential Diagnosis for Mesenteric Lymphadenopathy

  1. Malignancy – almost any intraabdominal malignancy and metastatic process can cause mesenteric lymphadenopathy, however the following are more common:
    1. Lymphoma
    2. Carcionid Tumors
    3. Kaposi Sarcoma
    4. Carcinoma of pancreas, colon or small bowel
  2. Infection
    1. TB or MAC
    2. Salmonella and Yersinia
    3. T. Whippelii
    4. Viral Infections –EBV and Hepatitis E
  3. Inflammatory