There is no excerpt because this is a protected post.
Thank you to Dr Patel for joining us at Jacobs Oncology Conference today and reviewing colon cancer screening!
Increased Incidence in Colon Cancer Diagnosis in Ages <50 years! Left-sided colorectal cancer rates have been increasing in the population less than 50 years, therefore some new guidelines suggest starting screening at 45 years of age. The incidence is increasing every year. This is not completely understood, however many environmental factors may be contributing to this increase!
Environmental Risk Factors for Colorectal Cancer: Red meat intake (RR 1.5), Obesity (RR 1.5), Alcohol consumption >4 drinks/week (RR 1.4), Cigarette use (RR 1.5)
Screening Modalities: FOBT/FIT testing (quick to use, no dietary restrictions, inexpensive, however lacks sensitivity for early disease, requires annual administration and a positive results needs a colonoscopy), Stool DNA Tests (non invasive, 90% sensitive, however requires 24 hours stool collection and may still lead to false negatives), Flex sigmoidoscopy, and colonoscopy (can detect AND remove precancerous growths, less frequent testing, but more invasive, resource intensive, and completion is low)
SCREENING: AVERAGE RISK patient should be screened from ages 50-75 years
-Annual Screening with high-sensitivity FOBT/FIT (low sensitivity)
-Annual Screening with stool DNA tests (Cologuard)
-Sigmoidoscopy every 5 years, high sensitivity FOBT every 3 years
-Screening colonoscopy every 10 years
SCREENING: POSITIVE FAMILY HISTORY (first degree relative or multiple second degree relatives)
-Colonoscopy every 5 years starting at age 40 ears or ten years before the youngest case in the immediate family
This morning, Jerry Lipinski, one of our stellar R2s presented an interesting patient he recently took care of at the VA: a 53-year-old woman with a history of Rheumatoid Arthritis who presented with acute bloody diarrhea. Her initial presentation was notable for sinus tachycardia, LLQ tenderness, leukocytosis. We used the opportunity to work through our differential diagnosis and discuss the work-up to obtain.
A CT scan of the abdomen showed non-specific inflammation of the colon in the splenic flexure and adjacent bowel. We highlighted some of the common findings on imaging – mucosal thickening, edema, fat stranding, and “thumbprinting” (haustra of the large bowel becoming thickened and projecting into the intestinal lumen at regular intervals). The patient then underwent colonoscopy which showed patchy erythematous, edematous, and friable mucosa consistent with ischemic colitis. We were very lucky to have Dr. Cynthia Hsu, an alumnus of our residency and current GI fellow as a discussant to walk us through the findings.
We then talked about the causes of ischemic colitis, which can broadly be divided into occlusive and non-occlusive etiologies. We also discussed one common reason to have ischemia in “watershed” areas of the colon – episodic hypoperfusion. The exact cause of ischemic colitis in any given patient is often difficult to find, and in this case, there was reason to suspect that the patient’s TNF-alpha inhibitor (adalimumab) for RA was the culprit. This adverse event has been described in the literature for biologic agents. Additionally, the patient had been transitioned from etanercept to adalimumab two years prior due to colitis that at the time was not further specified.
Our surgical colleagues were consulted, but the patient did not require intervention and improved over several days of conservative management. She was treated for 5-day course of antibiotics – the routine use of antibiotics is not necessary, but this patient’s clinical status was concerning (rising leukocytosis and extensive colonic involvement on endoscopy) that the team needed to treat potential bacterial gut translocation.
A special thank you to Dr Hsu for all her high-yield clinical pearls!
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.
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 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.
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!
- 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
- 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
- A patient’s first unprovoked DVT in a common location
- You do NOT need to send a thrombophilia workup for provoked VTE, or patients with:
- 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
- Finally, when it comes to management, the breakdown is easy!
- Inherited: Treat like normal VTE when it comes to anticoagulation, DOACs are great!
- JAK2 & PNH: Treat underlying disease process, otherwise treat like normal VTE
- Antiphospholipid Syndrome: Treat with lifelong Warfarin, regardless of VTE status/history
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.
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.
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!