We discussed a case about a young woman with hx of STIs (syphilis and chlamydia s/p treatment), subacute hx of migratory polyarthralgias, who presented with fevers and acute arthritis / tenosynovitis of her left index finger + thumb. She was found to have gram negative diplococci bacteremia and diagnosed with disseminated gonorrhea.
Framework for arthritis
Categorize differentials based on non-inflammatory vs inflammatory, as well as mono- / oligo- / polyarticular.
CDC screening recommendations
Men: those at high risk (MSM)
Women: can be asymptomatic -> complications of STIs (eg PID, infertility)
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!)
HLH (we seem to see this a lot in this hospital for some reason?)
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.
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
Anion gap = Na-Cl-bicarb
Determine pH (7.35-7.45 is normal)
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
To look for concomitant respiratory process on top of primary metabolic acidosis, calculate Winters Formula: expected pco2 = 1.5*(bicarb)+8
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.
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!)
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
Intracellular shifts of K
Rapid onset (minutes); short duration
Intracellular shifts of K
Rapid onset (minutes)
Watch for tachycardia and angina
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)
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.
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)
We discussed a middle aged man with heavy alcohol use presenting with jaundice found to have profound liver failure. It is important to note acute liver failure warrants consideration for transplant candidacy urgently. However, previous records revealed this patient had a history of cirrhosis and prior alcoholic hepatitis, this patient likely suffered from acute on chronic liver failure from alcoholic hepatitis. We reviewed the broad differential for jaundice and specifically for conjugated hyperbilirubinemia (attached). Alcoholic hepatitis may manifest as fever, jaundice, hepatomegaly and leukocytosis. Maddrey’s DF score is used to prognosticate. A score >32 warrants consideration of corticosteroids. STOPAH trial shows nonsigifnicant survival advantage at day 28 in patients with prednisolone vs no prednisolone.
We discussed a case of a young man who presented to the hospital after having a seizure. He had a history of neurocysticercosis complicated by seizures many years ago. His most recent seizure was in the setting of restarting albendazole.
We discussed how to come up with a broad and organized ddx for the cause of seizures using the MIST mnemonic, practical knowledge for acute seizure management, and highlights regarding the management and treatment of neurocysticercosis.
Acute seizure management
Check the patient’s ABCs and IV access
Check for hypoglycemia
Ativan 2-4 mg IV pushes x3
continuous seizure that lasts ≥5 min OR
≥2 discrete seizures w/out return to neuro baseline between seizures
Neuroimaging can definitely diagnose neurocysticercosis
Serologies can be helpful. The test of choice is enzyme-linked immunoelectrotransfer blot (EITB)
Antiparasitic therapy can cause degeneration of cysticerci -> inflammatory response.
In patients with ocular disease, the inflammatory response can cause edema and lead to blindness. Therefore, always consult ophthalmology to rule out ocular neurocysticercosis prior to starting antiparasitics.
In patients with CNS disease, the inflammatory response can cause edema and lead to seizures. Therefore, concomitant corticosteroids with antiparasitic medications (and AEDs) is recommended.