7/18/16 AM Report: Disseminated Histoplasma

Remember the different dimorphic fungi:

  • Histoplasma capsulatum
  • Blastomyces dermatitidis
  • Coccidioides immitis
  • Paracoccidiodies brasiliensis
  • Sporothrix schenckii

Histoplasma infection route: spores are inhaled (remember the association with bats and caves), enter the lungs and travel to the alveolar spaces where immune cells trap them.  The spores are then spread through the lymph system to mediastinum where they can enter your blood stream.

Picture1

Think of histoplama when a patient presents with symptoms after traveling to an endemic area:

Picture2

Disseminated histoplasma can affect various systems:

GI: approximately 70% have GI involvement at autopsy, but manifestations occur in <10% of patients.  Can cause HSM, but typically results in ulcers/polypoid masses in the colon and ilium.

Skin: reported in 10-15% of disseminated histoplasma; more common in patients with AIDs.  Lesions typically include nodules, papules, plaques, ulcers, vesicles, and generalized dermatitis.

Adrenal: common (80-90%) of autopsy cases, but overt adrenal insufficiency is rare – <10% of cases.

CNS: occurs in 5-20% of patients with disseminated histoplasma; more common in immunosuppressed individuals.

*Be able to recognize blastomyces (broad based budding yeast) and cocciodioidomycosis (thick walled spherules with endospores) on histology.

Treatment:

Amphotericin B (lipid formulation): recommended for patients sufficiently ill to require hospitalization; itraconaozle not recommended because it does not eradicate fungemia as rapidly.

Itraconazole: treatment of choice for mild/moderate symptoms and as step-down for people improving on amphoterician B.

7/27/16 AM Report: Thyrotoxic periodic paralysis

Epidemiology:

-95 % of cases occur in men, usually young age (~20-39)
-Highest incidence in Asian descent but also seen in those of American Indians and Hispanic descent
-Any etiology of hyperthyroidism can be involved, but most commonly it is Grave’s disease
-Also exists in familial form (familial periodic paralysis)

Pathogenesis

-Thought to be a “channelopathy ” and thyroid hormone increases Na/K ATPase activity in skeletal muscle, driving potassium into the cell.
-High carb meals (more insulin release==>more shift of potassium into cells), ethanol, and over-exertion can trigger attack

Lab/Clinical features

-Proximal muscle weakness, with LE weakness>UE weakness, commonly presents in AM with inability to move lower extremities!
-Varying degrees of hypokalemia
-Mild hypomagnesemia, hypophosphatemia
-Elevated FT4, low TSH
-Elevated CK
-EKG with sinus tachycardia and often U waves (from hypokalemia)

DDX

1)Myasthenia Gravis (more sub-acute/chronic symptoms, more ptosis, bulbar weakness)
2)Botulism (hx of IVDU, black tar heroin, descending paralysis with CN paralysis and eye involvement)
3)GBS (2-4 weeks after GI illness, also ascending paralysis but with paresthesias and bulbar signs

Treatment

1)do NOT over-correct potassium as it can lead to rebound hyperkalemia!
2)Correct with ~10 meQ q1h KCL, check chem 7 q4h and MAX of 90 meQ/24 hour period
3)Treatment of Thyrotoxicosis with MMI and Propranolol (watch for agranulocytosis with MMI!)

7/19/16 AM Report: Cholangitis

Cholangitis=bacterial infection in patient with biliary obstruction and stasis (eg: stones-most common, stenosis, malignancy)- high mortality if not treated!

What is Charcot’s Triad and Reynolds’ Pentad?

Charcot’s Triad: Fever, RUQ, Jaundice, ~50-75 % of patients
Reynold’s Pentad: Fever, RUQ, Jaundice, AND hypotension, AMS

Workup

Abdominal ultrasound/MRCP to evaluate for biliary dilation
Blood cultures
CBC (elevated leukocytosis), LFT (cholestatic pattern of injury)

What is a normal CBD diameter?

~4-6 mm,normal range can slightly increase in later decades of life

Most common etiologies of cholangitis

1)E.coli (25-50 %)
2)Klebsiella (15-20 %)
3)Enterobacter (5-10 %)
4)Enterococcus (10-20 %)
5)Anaerobes (usually mixed)

Treatment

1)Empiric antibiotics choices

a)Beta lactam/Beta Lactamase inhibitor (eg: Zosyn)
b)CTX/Flagyl
c)Cipro/Flagyl
d)Carabapenem

2) ERCP within 24-48 hours for endoscopic sphincterotomy with stone extraction and/or stent insertion- can be both diagnostic and therapeutic!

 

7/14/16 AM Report: Insulinoma

Whipple’s Triad:

  1. Symptoms consistent with hypoglycemia
  2. Documented low plasma glucose when symptoms present
  3. Relief of symptoms following resolution of hypoglycemia

Physiological response to hypoglycemia:

hypo1a

Endogenous Insulin Synthesis:

biosynthesis-of-insulin

  • Endogenous insulin is formed as two insulin chains (A & B) linked by C-peptide.  Measurement of C-peptide can help distinguish from endogenous versus exogenous insulin.

Causes of Hypoglycemia:

  1. Drugs (insulin, sulfonylureas, alcohol)
  2. Critical illness (hepatic failure, sepsis, etc.)
  3. Hormone deficiency (cortisol, glucagon, etc.)
  4. Non-islet cell tumor ~ increased production of IL-GF2 resulting increased glucose utilization
  5. Endogenous insulin
    • Insulinoma
    • Non-insulinoma Pancreatogenous Hypoglycemic Syndrome (NIPHS)
    • Post-gastric bypass hypoglycemia
    • Antibody to insulin / Antibody to insulin receptor

Interpretation of 72 hour glucose fast data:

Capture

*Remember the only way to distinguish between insulinoma, NIPHS, PGBH and a sulfonylurea ingestion is with a urine sulfonylurea toxicity screen!

07/13/16 AM Report-Digoxin toxicity

What is Digoxin and how does it work?

  • Cardiac glycoside extracted from the Foxglove plant (Digitalis Lanata)
  • Blocks the Na+/K+ ATPase in the myocardium

Potential uses of digoxin

  • Atrial fibrillation(lowers heart rate by increasing refractory period
  • Heart failure (due to + Inotropy)

Digoxin toxicity

Check Digoxin level
GI: N/V/anorexia/diarrhea
Visual: blurred vision, yellow/green discoloration (Xanthopsia), haloes
CV: palpitations, syncope, dyspnea
CNS: cofusion/dizziness/fatigue/delirium

Most common EKG findings of Digoxin use 

  • PVC (most common finding)
  • Heart block
  • U Waves
  • Scooped ST-depressions (the Salvador Dali mustache)
  • Combo of SVT with slow ventricular response (eg: atrial tachycardia with block)

*From Rapid Interpretation of EKG’s copyright © 2016 COVER Publishing Co. Inc.

Treatment

  • Discontinue Digoxin!
  • Dig fab fragments (Digibind) if life threatening/HD unstable arrthymia,
  • hyperkalemia (K>5.5), or end-organ damage from hypoperfusion (eg: renal failure/AMS)
  • Remember that HYPOkalemia worsens toxicity (less potassium=more digoxin binding at Na/K ATPase) and digoxin toxicity causes HYPERkalemia (if Na/K+ ATPase not working, cant pump potassium into the cell)

7/12/16 AM Report – Pancreatitis

Remember the common (and not so common) causes of pancreatitis (I GET SMASHED):

Idiopathic

Gallstones
ETOH
Trauma

Steroids
Mumps
Autoimmune
Scorpion stings (species found on the island of Trinidad)
HyperTG/Ca2+
ERCPs
Drugs
* Gallstones and alcohol account for approximately 80% of all cases in the US

Diagnosis of pancreatitis (requires 2 of 3):

  1. Typical clinical symptoms
  2. Elevated Lipase > 3 x the ULN
  3. Imaging findings consistent with pancreatitis

Clinical predictors of worse prognosis:

  • Older age (usually 55-75 years old)
  • Alcohol – increased risk for pancreatic necrosis and need for intubation
  • Obesity (BMI > 30) OR 2.9
  • Multiple medical co-morbidities

Management Principles:

  1. Fluid Replacement
    • 5-10 mL/kg/hr of isotonic crystalloid solution unless contraindicated 
    • Avoid LR in patients with hypercalcemia since it contains calcium
    • Re-evaluate frequently in the first 6 hours and adjust rate as necessary
  2. Pain Management
    • Typically IV opiates in PCA form
    • Dilaudid/fentanyl are good choices; morphine has been shown to increase sphincter of Oddi pressure, but no studies exist to suggest worse outcomes
  3. Nutrition
    • Oral feeds can be resumed in mild pancreatitis as soon as pain controlled/patient hungry
    • Enteral feeds are preferred over parental feeds; place NJ tube beyond ligament of Trietz if possible – but NG preferred to NPO
  4. Antibiotics
    • prophylactic antibiotics are not recommended regardless of the type (interstitial/narcotizing) or severity (mild/moderate/severe)

07/11/16 AM REPORT – STICKY KLEB

Sticky Klebsiella (Hypermucoid variant) 

Diagnosis of Hypermucoid variant Klebsiella (Hypermucoviscosity phenotype) 

String test done in lab after identifying Klebsiella pneumoniae, + test is >5 mm viscous string from the colony on an agar plate

FIG. 1.

(c) Andres Rivero et al. J. Clin. Microbiol. 2010;48:639-641

Risk factors for KLA (Klebsiella Liver Abscess)

DMII (poor neutrophil control impairs neutrophil phagocytosis of capsular subtypes)
Asian descent (especially Taiwan)
Prior antibiotic use

Clinical manifestations

Fever (93 %)
RUQ tenderness (71 %)
N/V/diarrhea
Leukocytosis

Complications (in addition to liver abscess)

Endolphalmitis (ask about ocular symptoms daily!)
Meningitis, Brain Abscess

Treatment

Drainage of liver abscess
Cephalosporins (commonly CTX), can add Flagyl if anaerobic coverage needed, plan for     4-6 weeks antibiotic course depending on resolution of abscess