Category Archives: M&M

Bonus M&M pearls 5/4! Decompensated cirrhosis, cryptococcal meningitis

 

Huge thanks to Varun, Andy, and Brian for these pearls!!

LTU pearls

  • Decompensated cirrhosis = immunosuppressed!!
    • Infection is a key case of early death in patients with cirrhosis, precipitating 50% of hospital admissions (and among these, 15-35% develop a nosocomial infection) (Fernandez et al. Hepatology, 2012)
    • Sepsis and requirements for multi-organi support in the ICU is associated with a 65-90% mortality in this population (O’Brien et al. Intensive Care Med, 2012)
  • HCC and cirrhosis:
    • remember that HCC can give you MELD exception points to help get you listed for transplant. Transplant hepatologists use the Milan Criteria to determine suitability for liver transplant in these patients (people who don’t meet these criteria are at high risk of recurrent HCC post-transplant)
      • Single tumor <5cm in diameter, or up to 3 tumors, each < 3cm
      • No extrahepatic involvement
      • No major vessel involvement
    • Sometimes, patients’ tumors are too big and may benefit from locoregional treatment to reduce size of tumors. Options include:
      • Transarterial chemoembolization (TACE)
      • Local ablation (percutaneous ethanol injection, radiofrequency, microwave, cryo)
      • Radioembolization/radiation (Yitrium-90, SBRT)
      • Deciding among these many options is largely driven by how sick a patient is
    • Liver transplant is potentially curable for HCC (much moreso than resection or ablation)

 

Neuro/ID pearls

  • Low CSF glucose (<40% of serum): think of 5 things on your ddx:
    • Bacterial
    • TB
    • Carcinoma/lymphoma
    • Sarcoid
    • Fungal
  • Low CSF WBC in bacterial meningitis portends a poorer prognosis
  • Cryptococcal meningitis
    • AIDs is the number 1 risk factor for cryptococcal meningitis (unadjusted OR 1118.8). Decompensated cirrhosis is #2 (OR 6.5) (Lin et al. Plos One. 2015)
    • Cryptococcal meningitis in decompensated cirrhosis has a poor prognosis
    • Can see low CSF WBC
    • CrAg titers
      • Specific but not sensitive!
      • Can see low titers in: capsule-deficient crypto, specific species of crypto, or prozone phenomenon. Doesn’t change management!
      • Trending titers is not helpful because it stays positive for a while!
  • Complications of meningitis
    • Stroke (eg from surrounding inflammation à vasculitis)
    • Hydrocephalus
    • Seizure
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Moffitt BONUS M&M PEARLS 9/23: Acute liver failure

Acute liver failure:

  • 3 criteria for diagnosis:
    • INR >1.5 (new)
    • Encephalopathy (usually last)
    • No pre-existing liver disease (look on exam for stigamata of liver dz, careful history)
  • Most common cause of death is neurological complications (edema and herniation). Hyperammonemia crosses the BBB and gets stuck, pulls in fluid and causes cerebral edema. Should go to the ICU for q1-2hr neuro checks, may need hypertonic saline and mannitol (targeted to Na 145 or Serum osm 320)
  • Differential for ALT >1000 is short with three main things: toxin (Tylenol, mushroom), ischemia, viral hepatitis

Ammonia:

  • Useless in end stage liver disease for hepatic encephalopathy. Must be made as a clinical diagnosis
  • In acute liver failure, ammonia can predict prognosis (cerebral edema). Cutoff of >100 suggests poor prognosis.

NAC:

  • Good for almost every cause of ALF except drug-induced. Most data for Tylenol but growing evidence for other causes of ALF. Mostly harmless therapy but should be aware of the following:
    • Volume considerations (often cerebral edema etc, so if no benefit then may not want the extra volume)
    • Infusion-related (vasodilation, pulm edema)

VA M&M Pearl: An approach to proteinuria

Pearl: There are four basic types of proteinuria.

  1. Glomerular
  2. Tubular
  3. Overflow
  4. Reactive/Post-Renal

Hi Everyone!

Yesterday at M&M, nephrologist Dr. Lowell Lo was at it again – dropping serious knowledge. He presented his basic approach to finding protein in the urine. He said that his first step in evaluating proteinuria is to consider which of the four types he is dealing with.

The four basic types of proteinuria are:

Glomerular:

  • caused by increased filtration of macromolecules (e.g. albumin) across the glomerular capillary wall
  • examples: primary glomerular disease, diabetic nephropathy, hypertensive nephrosclerosis, benign causes including orthostatic and exercise-induced proteinuria
  • degree of proteinuria: variable, can reach nephrotic range

Tubular:

  • in a normal kidney, low-molecular-weight proteins (smaller than albumin) get filtered across the glomerulus and are largely reabsorbed in the proximal tubule (examples include immunoglobulin light chains, beta-2-microglobulin)
  • diseases that cause tubulointerstitial damage limit reabsorption of these proteins in the proximal tubule, leading to proteinuria
  • increased excretion of these smaller proteins is often not detected on urine dipstick
  • the increased excretion of tubular proteins (e.g. polyclonal immunoglobulin light chains) is not injurious to the kidney
  • examples: autoimmune or allergic interstitial inflammation, medication-induced interstitial injury
  • degree of proteinuria: < 3g per day

Overflow:

  • caused by increased excretion of low-molecular-weight proteins in setting of overproduction, leading to increased filtration and excretion
  • the filtered load exceeds the proximal tubule’s normal reabsorptive capacity!
  • examples: multiple myeloma (monoclonal light chains), hemolysis (hemoglobinuria), rhabdomyolysis (myoglobinuria)
  • degree of proteinuria: variable, can sometimes reach nephrotic range

Reactive/Post-renal 

  • inflammation of the urinary tract can give rise to increases in urinary protein excretion (mechanism unknown)
  • examples: UTI, nephrolithiasis, genito-urinary tumor
  • degree of proteinuria: <1 g per day

References:

Rovin BR. “Assessment of urinary protein excretion and evaluation of non-nephrotic proteinuria in adults.” UpToDate.