Category Archives: Morning Report

Approach to Abdominal pain, and Acute Pancreatitis

Thank you Max for presenting an interesting case of an elderly woman with h/o CVA, CAD, DM2 who presented with vomiting and epigastric abdominal pain, found to have acute pancreatitis, likely 2/2 gallstones.

Very Basic Approach to Abdominal Pain:

The history and physical exam are great tools to help clarify a diagnosis in abdominal pain, but it is less reliable if:

  • Older age (>50)
  • Immunosuppresion (prednisone can easily mask intra-abdominal catastrophes)
  • Neurologic disease

Typically, we approach anatomically, but first consider:

  • Surgical emergencies: If the patient has an acute abdomen, call surgery! Obstruction, perforation, appendicitis (may be higher risk for perforation with normal WBC in immunosuppressed patients)
  • Vascular emergencies: Do a vascular exam in every patient with abdominal pain! Think about AAA rupture, ischemia (arterial or venous), splenic rupture

Consider causes adjacent to the abdomen:

  • Thoracic:
    • Cardiac: MI, pericarditis
    • Pulmonary: Lower lobe PNA, sub-diaphragmatic empyema, PE
  • Skin/MSK: Herpes zoster rash, rib fractures, costochondritis
  • Retroperitoneal: RP bleed
  • GU: Kidney stone, renal abscess
  • Pelvic: PID, ectopic pregnancy, ovarian torsion, cervicitis, endometriosis, ovarian cyst rupture, ovarian abscess
  • Diaphragm: Sub-diaphragmatic abscess
  • Spleen: Infarction, hematoma, splenomegaly

Abdominal pain by GI organ:

  • Stomach: GERD, gastritis, peptic ulcer disease, lymphoma
  • Small bowel: Infectious (enteritis), inflammatory (IBD), obstruction, ischemia
  • Large bowel: Infectious (diverticulitis, typhlitis – in neutropenic patients, HIV+), inflammatory (IBD), obstruction (constipation, mass, stricture), ischemia
  • Hepatobiliary disease
    • Portal vein
      • Thrombosis
      • Septic thrombophlebitis
    • Hepatic Parenchyma
      • Congestive
      • Inflammatory
      • Infiltrative
    • Liver capsule disease
      • Fitz Hugh Curtis
      • HELLP
      • Subcapsular hematoma
    • Biliary disease
      • Stone disease
      • Biliary perotinitis
    • Pancreas: Pancreatitis


Alternatively, it can be useful to think by abdominal quadrant too, so here’s my typical list:

















Ruptured AAA


Splenic infarct Splenic rupture

Splenic abscess


Gastric ulcer







Inguinal hernia

Ectopic pregnancy






Early appendicitis


Bowel obstruction

Ruptured AAA





Inguinal hernia

Ectopic pregnancy




Diffuse: Gastroenteritis, mesenteric ischemia, SBO, IBS/IBD, peritonitis, diabetes, Familial Med Fever, metabolic dx, psych

Chronic Upper: Ulcer, dyspepsia, reflux, biliary colic, chronic pancreatitis, IBS/IBD, cancer (stomach, pancreas, liver)

Chronic Lower: IBS/IBD, diverticulitis, lactose intolerance dysmenorrhea, endometriosis, hernia, cancer (colonic, pelvic)



CBC, BMP, Liver panel, INR, lactate, lipase, UA, Urine pregnancy


  • Bladder scan
  • KUB: Upright and left lateral decubitus
  • Consider pelvic ultrasound, renal ultrasound, RUQ ultrasound
  • CT Abd/pelvis: Given the expense, radiation and risk of incidental findings, careful consideration of this tool is important. Abdominal CTs are typically more useful if done with contrast, if the patient’s GFR is high enough


And then a few pearls about Acute Pancreatitis 

  • Pathophysiology:
    • Premature activated pancreatic digestive enzymesà Pancreatic tissue autodigestion
  • Causes:
    • “GET SMASHED”: Gallstones (40-50%) EtoH (30-40%) Trauma (blunt, kids) Scorpion Mumps Autoimmune Steroids Hyper-trygliceridemia (>1000)/Hypercalcemia, ERCP (post-procedure) Drugs- sulfonamides, thiazides, lisinopril, lasix, HIV meds
    • Note: Gallstones + EtOH make up about 90% of cases! The rest are much more rare. See here for a prior blog post that discusses the differential for rare causes of pancreatitis:
  • Symptoms:
    • Abdominal pain that radiates to back, often worse after meals. N/V, fever
    • If hemorrhagic, a few physical exam findings that you may see: 1. Grey Turner (flank ecchymosis) 2. Cullen (periumbilical ecchymosis) 3) Fox (inguinal lig ecchymosis)
  • Diagnosis:
    • Elevated lipase!
    • In patients with acute pancreatitis, an >3 fold elevation in ALT is very specific for gallstone pancreatitis! (though not sensitive, so only about 50% of patients with gallstone pancreatitis will actually have an elevated ALT). Check out this paper!
    • May get hypocalcemia bc fat sponoificaiton (perioral tingling)!
  • Prognostic tools:
    • BISAP: 5pt score- BUN >25, GCS <15, SIRS, Age >60, Pleural effusion
    • Ranson’s Criteria: Admission labs vs. 48hrs
  • Treatment:
    • NPO, aggressive IVF (250-500cc/hr), electrolytes, pain control
    • Typically NO antibiotics needed for acute pancreatitis alone (except in cases like this when you’re also concerned about cholangitis)
    • Gallstone pancreatitis:
      • Do urgent ERCP if the patient has 1) moderate-severe pancreatitis by Randon score, and 2) High suspicion for a retained stone. Patients that get ERCP in this setting benefit from early ERCP, so consult hepatobiliary! If they don’t meet the above criteria, you can actually worsen someone’s pancreatitis by doing ERCP
      • These patients should also get a cholecystectomy prior to discharge
  • Complications:
    • Pancreatic necrosis: Sterile– monitor closely in ICU, antibiotics controversial. Infected – Surgical debridement, antibiotics
    • Pancreatic pseudocyst: Fluid collection 2-3 weeks after acute attack, no epithelial lining. Risk rupture, infxn, obstruction. Tx: Cyst <5cm: observe Cyst >5cm: drain percutaneously or surgically.
    • Hemorrhagic pancreatitis: Cullen’s (periumbilical), Grey Turner’s (flank), Fox’s ecchymosis. Dx: CT w/ contrast
    • Other: ARDS, pancreatic ascites, pleural effusion, ascending cholangitis, ileus, renal failure, pancreatic abscess



HHS and Osmolol Gap

Endocrine report

Thank you to Santo for coming to morning report on his last morning of intern year and presenting a case of a woman with AMS found to have hyperglycemia and non-gap metabolic acidosis with osmolol gap. Pearls below!

The amount of insulin required to control hyperglycemia can be 10 times higher than the amount needed to suppress ketogenesis, hence many of the differences below between DKA and HHS.


Differential Dx for Metabolic Acidosis with Osmolol Gap

With Anion Gap •       Ketoacidosis

•       Ingestions: Ethylene glycol, methanol, propylene glycol, paraldehyde

•       Lactic Acidosis

Without Anion Gap •       Ingestions: Ethanol, isopropanol

•       Medications: Mannitol


Syndromes of ingestion:

Methanol: Ocular findings, cherry red macula

Ethylene glycol: Crystaluria, acute renal failure

Isoprolol alcohol: can be associated with some ketosis


Tx: Fomepizole (alcohol dehydrogenase inhibitor) or dialysis



ZSFG AM Report 6/18/2018: Vulnerable Patients – Unmet Social Needs

Shout out to our awesome crew of ZSFG students & residents at “Caring for Vulnerable Patients” report this AM. We learned about a tough case of a homeless/marginally housed man who presented with heart failure exacerbation and was found to have very limited writing and numeric literacy.  We discussed ways of counseling this patient as well as discharge options, including Medical Respite. Also, check out this amazing Unmet Social Needs Decision Tool, developed by two outstanding R3s – Drs. Jessica Wang and Emily Thomas, to help navigate potential resources for our most vulnerable patients.


Scleroderma basics! And a few pearls about immunosuppression and infections

Thank you to Megan for presenting an interesting case of a middle-aged woman with scleroderma who presented with pulmonary nodules of unclear etiology. Our rheumatology discussant, Dr. Sarah Goglin, helped us review the clinical manifestations of scleroderma, and treatment options depending on the organ systems involved. Remember that scleroderma renal crisis is a medical emergency requiring hospital admission for IV ACE inhibitors! And then also see a few pearls from Harry about infections that have increased risk with patients on immunosuppression.

❤ TLC (Tim and Laura, your Chiefs)


Scleroderma Basics

  • Etiology: Cytokines stimulate fibroblasts to increase collagen deposition, causing fibrosis
  • Prevalence: 1/10,000- so fairly rare, but can be devastating clinical manifestations, so we see these patients in medical care more frequently
  • Categories: These terms JUST refer to the amount of skin involvement but both can have internal manifestations.
    • Limited (80%): Skin manifestations = Elbows, knees, face (spares trunk). Pulm HTN more common. Anti-centromere ab.
    • Diffuse (20%): ANY skin involvement, ILD more common in diffuse patients
  • Diagnosis:
    • Most have +ANA (70%)
    • Anti-centromere antibody associated with limited scleroderma
    • Anti-SCL70 and anti-topoisomerase antibody associated with diffuse scleroderma
  • Clinical:
    • Raynaud’s present in almost all patients
    • Derm: Cutaneous fibrosis – tight skin, sclerodactyly
    • Cardiac: Myocarditis, arrhythmias (screen with EKG annually), pericardial effusions
    • Pulm: ILD (esp in diffuse), pulmonary HTN (esp in limited, screen with TTE annually)
    • GI: GERD, dysmotility, GAVE (“watermelon stomach” – usually found bc pts have iron deficiency anemia)
    • Renal: Scleroderma Renal Crisis – this is an EMERGENCY! More prevalent in patients that have RNA polymerase 3 ab. Can be precipitated by steroid use. Clinical: Rapid onset hypertension. Work-up: Check a SMEAR- look for schistocytes.
  • Treatment: Depends on the organs involved! Call rheum! But some general pearls from Dr. Goglin:
    • Raynauds: CCB (amlodipine) first line, avoid beta blockers bc can worsen vasospasm. Second line – sildenafil. Some data for use of aspirin as well, so often started for these patients
    • Derm: Mycophenylate if catch in early inflammatory state
    • ILD: Mycophenylate the treatment of choice depending on ILD severity.
    • Myocarditis: Steroids
    • Scleroderma renal crisis: No role for immunosuppression as vasculopathy. Admit to the hospital – IV ACE inhibitors. No prophylaxis with ACEi is indicated though.


Immunosuppression and Infections?

  • Amaaaaazing pearl from Harry: Patients on exogenous steroids have increased risk for these infections in particular:
    • PCP
    • Aspergillus
    • Nocardia
    • Mycobacteria
    • Legionella
    • Cryptococcus
  • PCP prophylaxis: We generally recommend PCP prophylaxis for patients on 15-20mg prednisone for more than two weeks. Another great pearl from Dr. Goglin: Patients with lupus are less likely to get PCP per a recent review of UCSF data, so rheum providers have a different prophylaxis algorithm for these patients.


To pace or not to pace?

Andrew presented a great case of an older woman with a history of bradycardia who presented with symptomatic bradycardia due to sick sinus syndrome.

  • There are a couple way to think about it bradycardia. Andrew and Ann offered a great example of intrinsic vs extrinsic causes (see bradycardia in AgileMD). Luke suggested thinking about a framework based on the EKG and need for intervention aka pacing.
    • Don’t forget ischemia as a cause!


  • Immediate management branch point: unstable vs stable, aka ACLS or not. Start ACLS for unstable bradycardia if unstable which includes transcutaneous or transvenous pacing immediately if unstable
  • After immediate management, you are thinking about the next management branch point: permanent pacemaker vs not.
  • Pacemaker indications
    • Dysfunction at or above AV node = Sinus node dysfunction. Pauses > 3 seconds (or >5 w/ intermittent A.Fib).
      • Sick sinus, sinus arrest: Not sinus bradycardia i.e. no P waves before every QRS complex.
      • Sinus bradycardia in which symptoms are clearly related to the bradycardia (usually in patients with a heart rate below 40 beats per minute or frequent sinus pauses). Pacemaker use for this indication is rare.
    • Dysfunction below AV node = at or below Bundle of His
      • Type II second degree block (look for intermittently dropped beats)
      • Third degree (complete) heart block: Total AV node dissociation

Other Pearls:

  • Beware of AFib with a regular rhythm. This is not good = complete heart block until proven otherwise. It is a junctional escape and because none of the atrial impulses are getting to the ventricles i.e. complete heart block.
  • Dysfunction below the AV node are unlikely to respond to atropine.

Late Presentation of HIV

6/12/18: Ellie shared a fascinating case of a 30yo man with no past medical history except one incidence of IVDU and frequent crack cocaine use who presented with neck pain and swelling, fever, oral thrush, and seb derm found to have multiple large abscesses, new HIV diagnosis with a CD4 count of 84, persistent MRSA bacteremia, and positive serum CRAG. Dr. Goosby joined us to offer many learning pearls. The most high yield from the case are highlighted below.

  • Given this patient presented with evidence of profound immunosuppression with oral thrush and a CD4 count of 84 at the time of diagnosis, this is considered a presentation of advanced HIV/AIDS.
  • Patients presenting with neck swelling should be assessed both with history and exam for airway compromise and be admitted to the unit for closer monitor if concern exists.
  • Cryptococcal infection moves from peripheral to central. Dissemination from the lungs to the central nervous system (CNS) in immunocompetent patients is rare, and routine lumbar puncture to evaluate for cryptococcal meningoencephalitis is generally not necessary with no CNS symptoms and low serum cryptococcal antigen titer (<1:512). However, lumbar puncture is warranted for patients with neurologic symptoms, an underlying condition that predisposes to dissemination like HIV/AIDS, and immunocompetent patients with a very high serum cryptococcal antigen titer (>1:512); such patients appear to have a higher burden of infection with risk for extrapulmonary spread and seeding of the central nervous system.
  • Oropharyngeal findings in HIV/AIDS: Pharyngitis in acute HIV, oral thrush CD4 <50, hairy oral leukoplakia CD4 < 50.
  • Consult the PHAST team! The PHAST team consists of a part time registered nurse, part time nurse practitioner and full time social worker. This team supports over 500 patients at risk for poor linkage to care and who are primarily persons of color with high rates of homelessness, mental illness and active substance use.
  • 4th generation HIV tests like those at ZSFGH detect both HIV Ab and HIV p24 Ag and have an 11 day window for acute HIV infection. Per algorithm, if negative but concern remains, send HIV RNA.

HIV algorithm



Syncope in a young person, Brugada pattern vs. syndrome

Thank you to Jessie Fitzpatrick and Max Kinet for presenting two EKG mini cases today! In the first case, we discussed syncope in a relatively young person with concern for possible Brugadda pattern on ECG, so see some relevant pearls below! And then related to the second case this morning, please find the Rational Clinical Exam article for likelihood of MI.

❤ TLC (Tim & Laura, your Chiefs!)

Framework for cardiac syncope in a young person:

— History is the most important diagnostic tool

— It is helpful to differentiate whether the patient has a structurally normal vs. abnormal heart

  • Structurally abnormal heart
    • Hypertrophic cardiomyopathy (HOCM): Autosomal dominant trait attributed to mutations in genes that encode for sarcomere proteins
    • Arrhythmogenic Right Ventricular Dysplasia  (ARVD): Hereditary condition w progressive fibrofatty replacement of cardiac myocytes
    • Dilated cardiomyopathies, infiltrative disease (sarcoid, amyloid)
    • Congenital heart conditions, anomalous origin of the coronary artery
    • Valvular pathology – mitroal valve prolapse or aortic stenosis
  • Structurally normal heart
    • Channelopathies: Long QT, short QT, Brugada
    • Conduction system abnormalities: Wolf-Parkinson White
    • Catecholaminergic polymorphic VT
    • Electrolyte disturbances


Brugada Pattern on EKG:

  • The right precordial leads, V1 to V3, display a positive deflection (R’ or prominent J wave) followed by an elevated down-sloping ST segment elevation and a negative T wave with a normal or even short QT interval.
  • QRS is normal but QT dispersion between V2 and V6 is larger than normal (120 ms)


Brugada Pattern vs. Syndrome:

  • Patients with typical EKG features who are asymptomatic and have no other clinical criteria have Brugada pattern
  • Patients with typical EKG features who have experienced sudden cardiac death, documented VT/VF, family history of sudden cardiac death <45 years old, syncope, inducible VT, or ventricular tachyarrhythmia have Brugada syndrome
    • Pathogenesis: An autosomal dominant disorder with variable expression – gene mutations in SCN genes (subunits of a cardiac sodium channel)
    • Epidemiology: Rare with prevalence of 0.1-1% of the general population, M > F
    • AFib risk: Incidence of Afib is ~10-20% in patients with Brugada syndrome
    • Risk stratification: After identifying a patient with Brugada syndrome, further diagnostic testing is needed:
      • Genetic testing for SCN mutations and family screening/genetic counseling
      • Raising V1 and V2 to the 2nd intercostal spaces increases the sensitivity of detection of Brugada pattern on EKG – great clinical pearl.
      • Consider EP testing and consideration for ICD implantation based on specific criteria
      • However, no treatment is recommended for asymptomatic patients w/ Brugada pattern on EKG but no Brugada syndrome