Morning Teaching Conference – AKI in Cirrhosis!

Hepatorenal syndrome: pathophysiology, diagnosis, and management | The BMJ

Today during Morning Teaching Conference at Hillcrest, one of our wonderful R1’s, Priyesha Bijlani, presented a “hot case” of a 74 year-old man with NASH cirrhosis and HFrEF who was admitted after he was found to have an AKI after a routine outpatient large-volume paracentesis. We discussed the diagnostic difficulties in this particular case, the differential for AKI (pre-renal due to poor PO intake, Hepatorenal Syndrome, and cardiorenal syndrome) as well as the diagnostic criteria and management of suspected hepatorenal syndrome. Ultimately, the patient’s AKI improved after albumin bolus and diuretic holiday, suggesting more likely a prerenal cause.

Key Learning Points:

1.) AKI in cirrhosis is usually due to volume depletion from prerenal causes (45%), ATN from hypotension or nephrotoxins (32%), or other (23%), which includes Hepatorenal Syndrome or abdominal compartment syndrome.

2.) Hepatorenal syndrome (HRS) is a process driven by portal hypertension, splanchnic vasodilation, decreased peripheral vascular resistance, all of which drive sympathetic activation and RAAS system activation, decreasing blood flow to the kidneys. It can be precipitated by bacterial infectious, GI bleeding, SBP, as well as acute fulminant hepatic failure. Type 1 HRS occurs more rapidly (doubling of Cr to >2.5 within 2 weeks) and can lead to end-stage kidney disease. Type 2 HRS occurs less rapidly.

3.) HRS is a diagnosis of exclusion. Because of this, other potential causes of AKI must be effectively ruled-out. Suggested diagnostic criteria include:

  • No response after 48h of withholding diuretic therapy and albumin 1g/kg/day.
  • No use of nephrotoxic medications
  • No evidence of structural renal disease: Proteinuria < 500 mg/day, no microhematuria, and no renal ultrasound findings suggestive of obstructive disease.

4.) The treatment for HRS is designed to maximize renal perfusion by elevating mean arterial pressure, increase splanchnic vasoconstriction. Midodrine/Octreotide/Albumin is an option for patients on the wards, and norepinephrine/Albumin is an option for patients in the ICU. Unfortunately, patients who progress to end-stage renal disease are only candidates for renal replacement therapy as a bridge to liver or liver/kidney transplantation.

Noon Conference 4/21 Colorectal Cancer Screening

Today Dr. Gupta, one of our amazing gastroenterologist, gave a very informative talk on colorectal cancer screening. Colorectal cancer is the 3rd most incident cancer for men and women and the 2nd leading cause of cancer deaths. He discussed risk factors for CRC including hereditary factors, modifiable risk factors and other factors as listed int the table above. Important to note that CRC risk is significantly increased in anyone with a first degree relative who had CRC regardless of age and increases as the number of family members with CRC increases. He reviewed the various modes we have for CRC screening include FIT, FIT-DNA, colonoscopy and sigmoidoscopy. All have a mortality benefit. He stated that the best test is the one that gets the screening done. He also reviewed guidelines for repeat screening pending results of colonscopy.

Grand Rounds 4/21

Grand Rounds today was given by Dr. Eliseo J. Perez-Stable the Director at the National Institute on Minority Health and Health Disparities. He gave a very insightful and important talk on Health Disparities and Health Equity Research in the Time of COVID.

He first defined populations with health disparities which include: racial/ethnic minorities defined by OMB, less privileged socioeconomic status, underserved rural residents, sexual and gender minorities. A health outcome that is worse in these populations compared to a reference group is defined as a health disparity. Social disadvantage that results in part from being subject to discrimination or racism and being underserved in health care. He discussed some statistics around this topic including that life expectancy in the US is decreased for both men an women in the black and latino population as compared to white population. Additionally all cause mortality is increased as annual household income level decreases. He then defined social determinants of health include demographics, urban or rural residence, geographic region, cultural identity, religiosity, spirituality, language proficiency, literacy and numeracy.

Dr. Perez-Stable then began to discuss the impact of COVID 19 on Racial and Ethnic Disparities. He discussed the disproportionate burden of COVID 19 among racial and ethnic minority populations that has persisted after 14 months. A lot of the underlying causes of this burden include long standing disparities and disadvantage, higher proportions of public facing jobs, crowded housing, higher rates of comorbid conditions, and less access to healthcare. This increased burden and disparity has also translated to the demographics of patients receiving COVID vaccines thus far. There is a Community Engagement Research Alliance Against COVID-19 Disparities that is trying to address these disparities and educate. He also discussed ways to help mitigate the effects of racism including supportive parenting, early childhood education, racial socialization and supportive relationships, social cohesion, interactions, religiosity, mediation and mindfullness, culture competence and patient centered medical home, and power and structure of institutions and policies. He also discussed the importance of patient centered communication and use of interpreters to help facilitate communication and improve outcomes.

Too much clotting hast thou, poor Thrombophilia

Today’s VA morning report was a rare case of mesenteric vein clotting in an otherwise healthy 38yo woman! This patient presented with abdominal pain and hematochezia, and was found to have ischemic colitis due to a thrombus in her inferior mesenteric vein! How weird! It was a great opportunity for us to review our thrombophilia workup, when to send it, what to send, and what to do with managing these conditions! Here are some pearls, including our first one on ischemic colitis since we have great colonoscopy pictures!

  1. Ischemic colitis is usually due to arterial insufficiency, but in our case the venous blockage led to the same pathology. Some ways to distinguish this from other types of colonic disease include:
    • distribution matching vascular supply
    • appearance on colonoscopy (friability, erythema, edema, patchy ulceration)
    • pathology on biopsy
  1. Okay now for the real meat of the case! That is who should we be sending a thrombophilia workup on? For these patients assume they have a new VTE and one of more of the following:
    • Family hx of clotting/inherited thrombophilia in 1st degree relative
    • Age <40 (men); <50 (women)
    • Arterial thrombosis
    • Rare sites of venous thrombosis: portal, hepatic, mesenteric, cerebral
      • You do NOT need to send a thrombophilia workup for provoked VTE, or patients with:
        • Cancer (active)
        • Trauma/Surgery (recent)
        • Pregnancy, Preeclampsia, Hormone supplementation, OCPs
        • Nephrotic Syndrome
        • Prolonged immobilization
        • IBD
        • HIT
        • A patient’s first unprovoked DVT in a common location
  2. When we do send a thrombophilia workup, there are 2 types of studies: inherited & acquired
    • Inherited: Factor V Leiden, Protein C & S deficiency, Antithrombin III deficiency
    • Acquired: JAK2 mutation, PNH flow cytometry, Antiphospholipid Syndrome serologies
  3. Finally, when it comes to management, the breakdown is easy!
    • Inherited: Treat like normal VTE when it comes to anticoagulation, DOACs are great!
    • Acquired:
      • JAK2 & PNH: Treat underlying disease process, otherwise treat like normal VTE
      • Antiphospholipid Syndrome: Treat with lifelong Warfarin, regardless of VTE status/history

Morning Teaching Conference – Autoimmune Polyglandular Syndrome Type 2!

Today during Hillcrest MTC, one of our amazing R2 Med/Peds residents, Cris Ebby, presented an 18 year-old woman who originally came to the emergency department with confusion four days after having vomiting and abdominal pain after having takeout food. She was found to be profoundly hypotensive to 60’s/20’s, have hyperpigmentation due to primary adrenal insufficiency (see photos above) and ultimately found to have hyponatremia, hyperkalemia, metabolic acidosis, hypoglycemia and AKI. On further endocrine workup, she was found to have abnormally low cortisol levels (0.2 at 1 pm), TSH to 59 and Free T4 of 0.2. Given her adrenal crisis (likely triggered by food poisoning) and hypothyroidism, she was diagnosed with autoimmune polyglandular syndrome type 2! Special thanks to our expert discussant, Dr. Vala Hamidi, who highlighted key management points for adrenal crisis, severe hypothyroidism, and walked us through the typical clinical presentation for autoimmune polyglandular syndrome (APS) type 2.

Key Learning Points:

1.) Adrenal crisis typically presents with hypotension, hyponatremia, hyperkalemia, metabolic acidosis, and hypoglycemia. It is critical to recognize this potential diagnosis early, obtain a random cortisol level if possible, and start stress-dose steroids and IV Fluid resuscitation immediately. IV Hydrocortisone at high doses provides both glucocorticoid and some mineralcorticoid activity but if using dexamethasone, don’t forget to add fludrocortisone (for mineralcorticoid activity!)

2.) Myxedema coma is an uncommon diagnosis in the era of easily-accessible TSH screening. It typically presents with lethargy, electrolyte abnormalities, psychomotor slowing, delayed reflexes, and in severe cases, can present with hypothermia and bradycardia. Since adrenal insufficiency is a common comorbid diagnosis, if myxedema coma is suspected, treat the patient with stress-dose steroids prior to initiating levothyroxine replacement to prevent a precipitation of adrenal crisis.

3.) Autoimmune Polyglandular Syndrome Type 2 (APS) manifests usually with dysfunction of at least two of three endocrine axes: adrenal (usually presenting as AI), thyroid (can present as autoimmune hyper or hypothryoidism), and DM type 1. It is associated with a host of other autoimmune-related diseases, including celiac disease, vitiligo, autoimmune hypoparathyroidism, pernicious anemia, and primary hypogonadism. It is important to continue to monitor for these conditions as they may present at any time after the initial endocrinopathies.

4.) Patients with adrenal insufficiency should have a Medi-Alert bracelet on discharge and should consider having an emergency hydrocortisone kit for use at home. They should be educated on sick-day rules to double or triple the dose of their baseline steroid.

VA Morning Report: Cholangiocarcinoma

Today, amazing PGY2 Sonya presented a case that she admitted last week of obstructive jaundice! Diagnosis…Cholangiocarcinoma!

Diagnostic Approach to Cholangiocarcinoma

CT A/P: First step to visualize obstruction and r/o other masses, including pancreatic cancer. CT will also provide more detail of regional LAD and extent of tumor

ERCP: Typically next step if intervention needed, such as biliary drainage and stent placement, or if CCA is high on the differential and tissue is needed. Usually combined with EUS (endoscopic US).

Cholangioscopy: Typically combined with ERCP when necessary. Unlike ERCP, this is better to directly visualize the biliary tree with a camera and endoscope! It can also be used to obtain intraluminal biopsy.

MRCP: Can be used to create 3D imaging of biliary system. It is non-invasive, so not the imaging modality of choice for for patients who require biliary drainage. It can be used if PSC is still high on the differential and you need to take a closer look at the biliary tree (both extra and intrahepatic).

Do you always need tissue to diagnose CCA? No, sometimes it can be done off imaging. Some lesions are hard to obtain tissue from, specifically perihilar lesions, therefore it may not be required if imaging suggests CCA. There is also a rare risk of seeding the biopsy tract with malignant cell therefore CT/MRI-guided biopsy is not recommended, and intraluminal biopsy is!

Random Pearls! (1) Normal CBD caliber is <6 mm however this increases with age, therefore you cannot definitively call CBD dilation unless it is >1 cm. (2) EUS does not predispose patients to the same complications as ERCP, which is most commonly pancreatitis (rectal indomethacin given to prevent this complication). (3) Tbili >4 and CBD dilation should get an ERCP.

Congratulations Dr. Jassal!

(Mr. Jaspering & Dr. Jassal @ his 100th Birthday Party–shared with permission & taken long before COVID)

Special Kudos to Dr. Simerjot Jassal, our fearless program director!

Philanthropist Ann Bedell Hunt has generously established The Bedell Family Endowed Medical Scholarship at UCSD in memory of her father, Omar Jaspering, and in honor of Dr. Jassal, Mr. Jaspering’s physician for many years. Dr. Jassal’s exemplary care for Mr. Jaspering and for all of her patients at the VA, regardless of background, has inspired generations of medical students and residents.

The Bedell scholarship carries forward this tradition by helping to remove financial barriers to medical education at UCSD, ensuring that the School of Medicine can continue to recruit outstanding minds from a diverse economic backgrounds.

See the full press release here!

Congratulations Dr. Jassal! Thank you for all that you do for the residency program and for medical education at UCSD!

Friday School 4/16

Today at Friday school we had some excellent discussions on the topics of both endocrinology and gastroentology.

We started out with an amazing session by Dr. Blumenthal one of our infectious disease physicians. She discuss transgender health disparities. She reminded the importance of addressing and recognizing proper pronouns with all our patients. She also discussed the increased rates of substance use, sexually transmitted infections and mental health disease in transgender patients and she gave us useful tools on how to best help our transgender patients feel more comfortable. We also had a patient panel where we got to talk to one of Dr. Blumenthal’s patients about their experience in the healthcare system.

Next we discussed management of elevated transaminases in the outpatient setting with Dr. Patton. We went over some real cases of LFT elevations in clinic encompassing diagnoses of hepatitis, NAFLD, hemochromatosis. We reviewed frequency of monitoring and following as well as imaging modalities. 

We then had amazing journal club session with Dr. Santos. We discussed two game changing articles regarding cardiac and renal benefits of SGLT2 inhibitors. Our amazing R3s Sophie Cannon and Mark Jiang led the discussion on these two ground breaking articles (EMPEROR Trial and DAPA Trial) posted below. It made us think about the wonderful benefits of SGLT2 inhibitors even in our non diabetes patients!!

Finally Dr. Santos led us in a discussion regarding diabetes medications. We worked though a worksheet posted above to help us characterize and understand the risks and benefits of various classes of DM medications. We then worked through cases to discuss the thought process behind adding various therapies to a DM regimen.

Look at me, I B D expert on IBD

Today at the VA we were lucky to have Dr. Anna Silverman give us an excellent talk on the management of IBD flares for the inpatient setting, with the help of GI expert Dr. Gobind Anand! Let’s check out some of Anna’s top pearls from the discussion!

  1. When a patient with IBD presents to the hospital, the top 5 labs to order are:
    • CBC (looking at Hgb level, signs of left shift for infection)
    • CMP (looking at Cr for potential AKI, albumin levels for protein loss, coinciding liver injury)
    • CRP (inflammation level compared to their baseline CRP for their disease)
    • Fecal Calprotectin (gut-specific inflammation)
    • C. diff (IBD patients have a ~5x increased risk of C. diff infection!)
  1. Patients admitted for IBD flares should always be started on DVT ppx (unless they are hemodynamically unstable from hemorrhagic shock). Even if there is hematochezia, as long as the Hgb is above the transfusion range and it’s not significant/life-threatening we STILL give DVT ppx due to the VERY high propensity for these patients to develop clots.
  2. Inpatient colonoscopy in these patients has 3 key functions:
    • Confirm diagnosis (many cases it’s not clear if the patient has UC or Crohn’s)
    • Establish the severity of inflammation
    • Obtain biopsies to confirm/rule out the presence of mimickers (like CMV colitis)
  1. Mainstay of flare treatment is going to be IV steroids. If these aren’t enough to turn things around, biologics are the next step (and ultimately what patients use for maintenance therapy).

That’s it for now! Great job Anna and Dr. Anand!! Thanks for teaching us so much!!

RACE Track Morning Teaching Conference – Abnormal Uterine Bleeding!

Today during Hillcrest MTC, one of our RACE Track R2’s, Alex Tong, presented a case of a 38 year old woman who presented to clinic with heavy menstrual bleeding that started two weeks prior. The patient ultimately was found to be pregnant and was sent to the ED for expedited workup of potential ectopic pregnancy. She was found ultimately to have a miscarriage with no retained products of conception. We discussed the key points for a gynecological history and exam for patients presenting with abnormal uterine bleeding. We discussed the differential for abnormal uterine bleeding, key clinical presenting factors for each cause, and further diagnostic imaging and workup. Finally, we discussed the diagnostic considerations and workup for suspected ectopic pregnancy.

Key Take-Away Points:

1.) A helpful pneumonic to organize the various causes of non-gravid abnormal uterine bleeding is PALM (structural)-COEIN (nonstructural): Polyps, Adenomyosis, Leiomyoma, Malignancy, Coagulopathy, Ovulatory, Endometrial, Iatrogenic, and Not otherwise classified.

2.) Depending on the suspected structural causes of abnormal uterine bleeding, workup should include transvaginal ultrasound, saline infusion sonogram. Pelvic MRI can be helpful to distinguish focal vs. diffuse adenomyosis. Hysteroscopy and biopsy may be necessary to work up suspected malignancy.

3.) For a patient with suspected ectopic pregnancy, a serum B-HCG is more sensitive than a urine B-HCG. If a transvaginal ultrasound does not reveal pregnancy, trending the B-HCG is the most important next step to differentiate ectopic pregnancy from a previous miscarriage without retained products of conception.