Category Archives: Morning Report

Hepatitis B & HIV co-infection

We discussed a young male with past medical history of syphilis (incompletely treated) and recently diagnosed HIV (4 days prior to admission) who was admitted for elevated liver enzymes found incidentally. Liver enzymes consisted of mildly elevated alkaline phosphatase and bilirubin but extremely elevated AST/ALT in 4000s. Only a few entities cause elevation to the thousands. He was found to have acute co-infection of HIV and Hepatitis B. 

If AST/ALTs are in the thousands, there are only a few entities that can cause this:

  • Ischemia (shock liver)
  • Toxins (Tylenol is most common), Amanita aka magic mushrooms, herbal supplements (we don’t know what they put in these!)
  • Acute viral hepatitis (HAV, HBV, HCV, HEV, HSV, CMV, VZV, parvovirus)
  • Autoimmune hepatitis
  • Acute Budd Chiari
  • Reactivation HBV, HDV
  • HLH (we seem to see this a lot in this hospital for some reason?)
  • Malignant infiltration
  • HELLP
  • Wilsonian Crisis (severe hemolysis and impending acute liver failure in setting of Wilson’s)

According to the CDC, approx 10% of people with HIV in the US also have chronic or acute HBV. There is accelerated progression to liver disease and increased all cause mortality for HIV-HBV co-infection when compared to HIV mono infection. Monotherapy of HBV is not recommended in the HIV co-infected due to the evolution of HIV resistance. Recommended antiretroviral regimens for treating persons with HIV-HBV coinfection should include three medications that are active against HIV and two medications that are active against HBV.The preferred regimens include tenofovir alafenamide-emtricitabine, tenofovir DF-emtricitabine, or tenofovir DF plus lamivudine as part of a fully suppressive antiretroviral regimen.

Superior mesenteric artery syndrome

We discussed a case about a young woman with neuromyelitis optica, depression / anxiety, recent significant unintentional weight loss, who presented with acute abdominal pain (predominantly in the lower quadrants) and nausea (no vomiting). She was diagnosed with SMA syndrome. We reviewed the abdominal pain emergencies that should not be missed and discussed the pathophysiology + risk factors for + diagnosis + treatment of SMA syndrome.

What is SMA syndrome

  • Loss of mesenteric fat pad between the aorta and SMA -> compression of duodenum -> proximal intestinal obstruction

Risk factors

  • Significant weight loss due to medical / psychological disorders or surgery
  • Anatomic abnormalities (congenital vs acquired)

Diagnosis

  • Plain abdominal film, PO contrast studies, and/or CTA vs MRA

Imaging diagnostic criteria

  • Duodenal obstruction w/ abrupt cutoff in the 3rd portion and active peristalsis
  • Aortomesenteric artery angle of ≤25 degrees

Treatment

  • Conservative
    • GI decompression, correct electrolyte abnormalities (watch for refeeding!), nutritional support (for weight gain)
  • If conservative fails, surgical treatment
    • Strong’s procedure, gastrojejunostomy, duodenojejunostomy

Pulmonary emergencies featuring Dr. Halley Tsai

  1. Attached a good and recent NEJM review on supplemental O2. There’s an video too that has everything in the text: https://www.nejm.org/doi/full/10.1056/NEJMvcm2035240
  1. ABG interpretation, comprehensive chapter on CHEST: https://www.thoracic.org/professionals/clinical-resources/critical-care/clinical-education/abgs.php
  1. Attached the CHEST cheat-sheet quick ABG I had in my talk. If people want very easy one-look cheat-sheets like that, the “All Resources” section has great ones to click through if people have time: https://www.chestnet.org/topic-collections/covid-19/clinical-resources

DKA & acid-base analysis

We discussed a young male with no past medical history with 4 days of abdominal pain, nausea, vomiting, constipation found to be kussmaul breathing on physical exam. Patient presented with anion gap metabolic acidosis. 

Learn how to calculate acid base

  1. Anion gap = Na-Cl-bicarb
  2. Determine pH (7.35-7.45 is normal)
  3. Identify primary disorder (i.e. respiratory vs metabolic)
    • If metabolic: bicarb <22, think primary metabolic acidosis; if bicarb>28, think primary metabolic alkalosis
    • If respiratory: pCO2 <35, thik primary respiratory alkalosis; if pCO2>45, think primary respiratory acidosis
  4. To look for concomitant respiratory process on top of primary metabolic acidosis, calculate Winters Formula: expected pco2 = 1.5*(bicarb)+8
  5. To look for comitant metabolic process on top of primary metabolic process, calculate Delta gap:(patient’s AG – normal AG) – (patient’s bicarb-normal bicarb)
    • Delta gap>6 indicates metabolic alkalosis on top of AGMA 
    • Delta gap close to 0 is normal and indicates pure AGMA
    • Delta gap <-6 indicates NAGMA on top of AGMA  

Our patient had primary AGMA with metabolic alkalosis with superimposed respiratory acidosis. 

Learn differential for AGMA
GOLDMARK:

  1. Glycols – ethylene glycol/propylene glycol 
  2. Oxoproline (acetaminophen)
  3. L-lactate
  4. D-lactate
  5. Methanol
  6. Aspirin
  7. Renal Failure
  8. Ketoacidosis

Hyperkalemia

We discussed a case about a middle aged man with uncontrolled HTN and T2DM, presenting with subacute bilateral lower extremity edema and sacral edema, found to have Hyperkalemia likely due to CKD from uncontrolled HTN and T2DM. Teaching points focused on going over a framework to organize causes of hyperkalemia, EKG features of hyperkalemia, and treatment options for hyperkalemia.

EKG features of hyperkalemia

  • Tall peaked T waves, loss of P waves, widening QRS, sine wave / ventricular arrhythmia / asystole

Hyperkalemia tx (Check out the hyperkalemia order set!)

  • Calcium
    • Stabilize cardiac membrane action potential
    • Rapid onset (minutes); short duration (30-60 min)
    • Contraindicated in digoxin toxicity
  • Insulin + Dextrose
    • Intracellular shift of K via ↑ Na-K-ATPase
    • Rapid onset (10-20 min); lasts hours
  • NaHCO3-
    • Intracellular shifts of K
    • Rapid onset (minutes); short duration
  • Beta-2-adrenergic agonists
    • Intracellular shifts of K
    • Rapid onset (minutes)
    • Watch for tachycardia and angina
  • Loop diuretics
    • Excretion of K, prevention of K absorption
    • IV Lasix peak effect (30 min); IV Lasix duration (2hrs)
  • GI cation exchangers
    • Bind K in GI lumen -> excretion
    • Slow onset (many hrs); long duration (many hrs to days)
    • SPS (Kayexalate) associated w/ intestinal ischemia
  • Dialysis

Pulmonary embolism

We discussed a case of a middle aged woman who presented with subacute to acute shortness of breath on exertion. We discussed her EKG with S1Q3T3 findings which is not specific for PE but indicative of cor-pulmonale. The differential for cor-pulmonale is COPD, ARDS, PNA, Pneumothorax and PE. More specifically, her CTA showed bilateral pulmonary embolus and RV enlargement and her labs indicated elevation in BNP and troponin. Due to her hemodynamic stability but clear evidence of RV strain, troponin and BNP elevation – she was classified as submassive PE (these days known as intermediate high risk classification). In addition to starting heparin infusion, with all submassive PE, it is important to consider systemic thrombolysis (low dose vs high dose) AND catheter directed thrombolysis / thrombectomy. This will be a nuanced discussion but admission to ICU and early consults to IR, Cardiology and Pulmonology are required.

AML and leukostasis

We discussed a case of a man with weakness, found to have hyperleukocytosis. He was diagnosed with AML. There was a concern for leukostasis due to the tremendous amount of blasts on peripheral smear.We reviewed characteristics of AML vs ALL vs CML vs CLL and discussed four emergencies (TLS, DIC / bleeding, febrile neutropenia, and leukostasis), with a deeper discussion about leukostasis.

AML
– Adults (60s);  sxs: fatigue (anemia) + bleeding / bruising (thrombocytopenia) + infection (ineffective neutrophils);  dx by peripheral smear or bone marrow biopsy with >20% blasts;  Auer rods can be seen on smear

Leukostasis
– Hyperleukocytosis = total WBC > 50k to 100k
– Lots of blasts → ↑ blood viscosity → blockage/ischemia
– Respiratory distress and neurologic symptoms (eg stroke) are leading causes of early death
– Treatment: cytoreduction (chemotherapy, hydroxyurea, leukapheresis-controversial)

Serotonin syndrome

We discussed a case of a young male with complete C5/6 injury who presents with altered mental status and agitation. While in our rehab unit, he was on multiple medications for neuropathic pain and allodynia including Nortriptyline (started recently), Cymbalta, Morphine and Sudafed, Gabapentin, Baclofen and Lyrica. He had acute onset agitation (shaking his head right/left), fevers, diarrhea and horizontal roving eyes or opsoclonus /ocular clonus. The rest of his exam was non contributory as he suffered from flaccid paralysis below C5. He was diagnosed with serotonin syndrome. He was treated with Ativan and Cyproheptadine with significant improvement. It is important to realize that there are many mimickers of serotonin syndrome and that it is a fatal condition with 11% mortality. Think about this diagnosis when you see acute onset ocular clonus, tachycardia, fever, hypertension, diaphoresis and neuromuscular activation (hyperreflexia and tremor).  See attached case summary. 

GI Bleed

We discussed a case of a man who presented with coffee-ground emesis and melena in the setting of anticoagulation. He was diagnosed with upper GI bleed due to gastric and duodenal ulcers.
We reviewed characteristics that favor UGIB vs LGIB, etiologies of UGIB and LGIB, worrisome features of GI bleeds, and practical skills when managing GI bleeds.

Characteristics that favor UGIB

  • Melena (right-sided colonic bleed with slow transit can cause melena), Hematemesis, Coffee-ground emesis
  • BUN/Cr > 30
  • Hx UGIB

Characteristics that favor LGIB

  • Clots per rectum
  • Hematochezia (massive UGIB with rapid transit through the GI tract can cause hematochezia)
  • Hx of LGIB

Worrisome features

  • Comorbidities that increase risk of bleed (cirrhosis, hx AAA repair)
  • Symptoms: active bleeding, syncope / presyncope, tachycardia as an early sign of worsening bleed
  • Normal Hgb with unstable vital signs (drop in Hgb can lag despite severity of bleed)
  • Anemia that is unresponsive to transfusions