Hypertriglyceridemia Induced Pancreatitis

Hypertriglyceridemia induced pancreatitis is relatively uncommon (about 8% of patients with pancreatitis). This is likely to become more of an increasing problem in the future due to growing rates of obesity.

 

Basic Pathophysiology:

·      Insulin promotes storage of triglycerides into adipose  if resistance or not enough insulin  lipolysis, releasing free fatty acids in circulation.

·      Many people have high triglyceride levels and don’t develop pancreatitis from it, so likely the toxicity causing pancreatitis comes from free fatty acids

·      It is difficult to measure free fatty acid levels, but we can easily measure triglyceride levels.

 

Risk Factors:

·      DM, Obesity

·      Hereditary hyperlipoproteinemia

·      Pregnancy

·      Hypothyroidism

·      Medications

Interesting Clinical Signs:

·      Xanthoma Tuberosum

o    Nontender, pink-yellow papules or nodules that occur on extensor surfaces, such as the elbows and knees, and on trauma-prone areas

·      Lipemia

o   White, milky, opaque serum on blood draw

Diagnosis:

·      Requires at least two:

o   Clinically significant history/physical (epigastric abdominal pain), CT demonstrating inflammation, or lipase >3 times upper limit of normal

o   Triglyceride level >1,000 (higher the level the more significant/ higher likelihood to be causing pancreatitis)

o   Must exclude other causes – gallstones, meds, etc.

 

Treatment:

·      *****Fluids*****

o   BE CAREFUL!!!! Overloading these patients is one of the worst things you can do for them. Don’t exceed >3-4 liters in the first

o   Lactated ringers (has been found to reduce inflammation compared to NS)

·      Vasopressors

o   Use early to prevent fluid overload

·      Pain control

o   Opioids can promote Ileus, try to avoid this class of medications as best as possible

o   Great time to use acetaminophen with pain-dose ketamine infusions (0.1-0.3mg/kg/hr)

·      Insulin

o   Appropriate dose is variable ranging from 0.1-0.3 U/kg/hr (dosage can vary based on history of diabetes or insulin resistance)

o   Monitor for hypokalemia, hypoglycemia

o   Likely to be best treatment

·      Plasmapheresis

o   Unclear if there is a large benefit to this

o   Invasive, requires large bore access catheter

o   Expensive, resource intensive, and not widely available

o   Heparin used during process can cause bleeding

·      Antibiotics

o   Generally, should be avoided with these exceptions:

§  Unclear diagnosis and have clinical suspicion for infection

§  Concern for coexisting ascending cholangitis

 

Complications:

            ARDS

            Infection

            Abdominal compartment syndrome

·      Increased intra-abdominal pressures

o   Pancreatic/peri-pancreatic inflammation

o   Ascites

o   Ileus (opioids)

o   Aggressive fluid resuscitation

o   Abdominal wall compliance (pain)

o   Pancreatic perfusion, worsens with intraabdominal hypertension  increases risk for pancreatic necrosis

 

Quick Tips:

·      Do not give too much fluid

·      Control pain with modalities other than opioids if possible

·      Insulin therapy is very effective, and plasmapheresis has not been shown to be more advantageous

·      Look for alternative causes before focusing solely on hypertriglyceride induced pancreatitis (consider ultrasound imaging and review patient medications)

 

 

References:

https://www.pancreapedia.org/reviews/management-of-abdominal-compartment-syndrome-in-acute-pancreatitis

https://emcrit.org/ibcc/hypertag/

https://wikem.org/wiki/Acute_pancreatitis

https://rebelem.com/acute-pancreatitis/

 

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