Hypertriglyceridemia: Difference between revisions

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==Background==
==Background==
*~5% of acute pancreatitis caused by high TGs<ref>Yadav D, Pitchumoni CS. Issues in hyperlipidemic pancreatitis. J Clin Gastroenterology 2003;36:54-62.</ref>
*~5% of acute [[pancreatitis]] caused by high triglycerides<ref>Yadav D, Pitchumoni CS. Issues in hyperlipidemic pancreatitis. J Clin Gastroenterology 2003;36:54-62.</ref>
*Etiologies
*Etiologies
**Familial hypertriglyceridemia, autosomal dominant with variable penetrance
**Familial hypertriglyceridemia, autosomal dominant with variable penetrance
**Secondary forms
**Secondary forms
***DM, obesity, EtOH, estrogen therapy
***[[DM]], obesity, [[EtOH]], estrogen therapy
***Hypothyroidism, ESRD, nephrotic syndrome, HIV, anti-HIV meds
***[[Hypothyroidism]], ESRD, nephrotic syndrome, [[HIV]], anti-HIV meds
*TG levels > 2000 mg/dL almost always have both secondary and genetic form<ref>Yuan et al. Hypertriglyceridemia: its etiology, effects and treatment. CMAJ 2007;176:1113-1120.</ref>
*TG levels > 2000mg/dL almost always have both secondary and genetic form<ref>Yuan et al. Hypertriglyceridemia: its etiology, effects and treatment. CMAJ 2007;176:1113-1120.</ref>
==Management of Pancreatitis==
*1.7% of US estimated to have [TG] between 500-2000<ref>Brown, Virgil W. Et al. “Clinical Lipidology Roundtable Discussion: Severe Hypertriglyceridemia.” Journal of Clinical Lipidology 2012; 6:397-408</ref>
*May present with normal serum lipase levels
 
===Pathophysiology===
*Excess TG hydrolyzed by increased concentration of pancreatic lipase
*Produces increased concentration of free fatty acids that exceeds binding capacity of albumin
*Micelles are formed that attack platelets, vascular endothelium and acinar cells
*Ischemia and pancreatic injury result
*An acidic environment potentiates free fatty acid toxicity
 
==Clinical Features==
===General===
[[File:Xanthoma.jpg|thumb|A pediatric patient's knee showing multiple xanthoma tuberosum (i.e. xanthoma located over a joint).]]
*Most are generally asymptomatic until sequelae present
*Eruptive xanthoma may be found on dermatologic exam
 
===Hypertriglyceridemic Pancreatitis===
''Signs/symptoms of pancreatitis''
*[[Epigastric pain|Pain]] is the most common symptom and is often characterized by:
**Persistent
**Localizes to epigastric area, around waist, RUQ, or occasionally LUQ
**Radiates to back
**The onset may be less abrupt and the pain poorly localized
*[[Nausea/vomiting]] noted in most
*Abdominal distention is frequent complaint
*[[Eponyms_(C-E)#Cullen.27s_sign|Cullen sign]] (ecchymosis of periumbilical region) - intrabdominal hemorrhage
*Turner sign (ecchymosis of flanks) - retroperitoneal hemorrhage
*Pulmonary Findings
**[[Hypoxemia]], [[ARDS]], tachypnea
**Indicates severe pancreatitis
***Diaphragmatic inflammation, pancreatico-pleural fistula
 
==Differential Diagnosis==
{{Abdominal Pain DDX Epigastric}}
 
 
==Evaluation==
[[File:hypertriglyceridemia_green_top.jpg|thumbnail]]
*Triglycerides; Severely elevated (at least >500 mg/dL, generally >1,000 mg/dL)
**Lipids in serum may interfere with other lab tests
***Falsely low Na+, amylase
 
===Pancreatitis workup===
*Rule out other causes of pancreatitis (e.g. [[gallstone pancreatitis]])
*In general, if triglycerides >1000, can assume this is cause of pancreatitis
*Lipase level >3x upper limit of normal
**Sensitivity 82-100%, specificity 82-100%<ref>Yadav D, Agarwal N, Pitchumoni CS. A critical evaluation of laboratory tests in acute pancreatitis. Am J Gastroenterol. 2002 Jun;97(6):1309-18.</ref>
**Negative lipase does not exclude pancreatitis in chronic/recurrent disease
**Absolute value not associated with prognosis or severity
*Characteristic findings on [[ultrasound]] or CT
 
 
==Management==
 
===Management of [[acute pancreatitis]] in the setting of hypertriglyceridemia===
*Evidence for management based on case series and reports<ref>Santana YR et al. Treatment of severe hypertriglyceridemia with continuous insulin infusion. Case Reports in Critical Care. June 2011.</ref><ref>Poonuru S et al. Rapid Reduction of Severely Elevated Serum Triglycerides with Insulin Infusion, Gemfibrozil and Niacin. Clin Med Res. 2011 Mar; 9(1): 38–41.</ref>
*Evidence for management based on case series and reports<ref>Santana YR et al. Treatment of severe hypertriglyceridemia with continuous insulin infusion. Case Reports in Critical Care. June 2011.</ref><ref>Poonuru S et al. Rapid Reduction of Severely Elevated Serum Triglycerides with Insulin Infusion, Gemfibrozil and Niacin. Clin Med Res. 2011 Mar; 9(1): 38–41.</ref>
*Insulin drip - most dramatic and rapid intervention, with reduction within 24 hrs
*[[Insulin]] drip - most dramatic and rapid intervention, with reduction within 24 hrs
**5-10 units/hr with dextrose infusion to maintain CBGs ~150 mg/dL
**Initiate at 0.1 units/kg/hr (similar to treatment for DKA)
**May require higher dosages for diabetics, 0.1 - 0.5 u/kg/hr
**Goal is to reduce triglycerides to < 500
*Heparin SC q8 5000 units
**Add D5NS if glucose drops < 200 <ref>Schaefer EW. Management of Severe Hypertriglyceridemia in the Hospital: A Review. Journal of Hospital Medicine Vol 7|No 5|May/June 2012.</ref>
*Niacin 500 mg qd
**Monitor BMP q2 hr
*Gemfibrozil or fenofibrate
**Manage potassium
*Diabetic diet, advanced slowly
***K < 3.2 stop insulin and replete K
*Follow TG levels, goal < 500 mg/dL by discharge
***K 3.3 to 5 add 20 mEq K/Lto IVF
***K > 5 no extra potassium
*IVF as for standard pancreatitis treatment, add potassium as per above
*Treat concurrent [[hypothyroidism]] if present
*Pain control
*[[Niacin]] 500mg QD
*[[Gemfibrozil]] or [[fenofibrate]]
*Max dose statin, 81mg [[ASA]]
*[[Heparin]] q8 SC, effect short-lived
*NPO initially
*May advance diet starting at TG level < 1000mg/dL with resolution of abdominal pain/pancreatitis symptoms
**No fat diet
**Low calorie diet
 
====[[Plasma exchange]]====
*Therapeutic plasma exchange, for 1-3 days (sickest patients)
**Generally indicated for hypocalcemia, persistent elevated lactic acidosis, other signs of worsening organ dysfunction
*For euglycemic patients, not routine first line
*Requires central venous access


==Disposition==
==Disposition==
*ICU for frequent labs, insulin drip
*Asymptomatic hypertriglyceridemia is treated as an outpatient
*For acute pancreatitis, ICU or step-down for frequent labs, insulin drip
 
==See Also==
*[[Acute pancreatitis]]
 
==External Links==
 


==Sources==
==References==
<references/>
<references/>


[[Category:GI]]
[[Category:GI]]

Latest revision as of 13:56, 2 June 2021

Background

  • ~5% of acute pancreatitis caused by high triglycerides[1]
  • Etiologies
    • Familial hypertriglyceridemia, autosomal dominant with variable penetrance
    • Secondary forms
  • TG levels > 2000mg/dL almost always have both secondary and genetic form[2]
  • 1.7% of US estimated to have [TG] between 500-2000[3]
  • May present with normal serum lipase levels

Pathophysiology

  • Excess TG hydrolyzed by increased concentration of pancreatic lipase
  • Produces increased concentration of free fatty acids that exceeds binding capacity of albumin
  • Micelles are formed that attack platelets, vascular endothelium and acinar cells
  • Ischemia and pancreatic injury result
  • An acidic environment potentiates free fatty acid toxicity

Clinical Features

General

A pediatric patient's knee showing multiple xanthoma tuberosum (i.e. xanthoma located over a joint).
  • Most are generally asymptomatic until sequelae present
  • Eruptive xanthoma may be found on dermatologic exam

Hypertriglyceridemic Pancreatitis

Signs/symptoms of pancreatitis

  • Pain is the most common symptom and is often characterized by:
    • Persistent
    • Localizes to epigastric area, around waist, RUQ, or occasionally LUQ
    • Radiates to back
    • The onset may be less abrupt and the pain poorly localized
  • Nausea/vomiting noted in most
  • Abdominal distention is frequent complaint
  • Cullen sign (ecchymosis of periumbilical region) - intrabdominal hemorrhage
  • Turner sign (ecchymosis of flanks) - retroperitoneal hemorrhage
  • Pulmonary Findings
    • Hypoxemia, ARDS, tachypnea
    • Indicates severe pancreatitis
      • Diaphragmatic inflammation, pancreatico-pleural fistula

Differential Diagnosis

Epigastric Pain


Evaluation

Hypertriglyceridemia green top.jpg
  • Triglycerides; Severely elevated (at least >500 mg/dL, generally >1,000 mg/dL)
    • Lipids in serum may interfere with other lab tests
      • Falsely low Na+, amylase

Pancreatitis workup

  • Rule out other causes of pancreatitis (e.g. gallstone pancreatitis)
  • In general, if triglycerides >1000, can assume this is cause of pancreatitis
  • Lipase level >3x upper limit of normal
    • Sensitivity 82-100%, specificity 82-100%[4]
    • Negative lipase does not exclude pancreatitis in chronic/recurrent disease
    • Absolute value not associated with prognosis or severity
  • Characteristic findings on ultrasound or CT


Management

Management of acute pancreatitis in the setting of hypertriglyceridemia

  • Evidence for management based on case series and reports[5][6]
  • Insulin drip - most dramatic and rapid intervention, with reduction within 24 hrs
    • Initiate at 0.1 units/kg/hr (similar to treatment for DKA)
    • Goal is to reduce triglycerides to < 500
    • Add D5NS if glucose drops < 200 [7]
    • Monitor BMP q2 hr
    • Manage potassium
      • K < 3.2 stop insulin and replete K
      • K 3.3 to 5 add 20 mEq K/Lto IVF
      • K > 5 no extra potassium
  • IVF as for standard pancreatitis treatment, add potassium as per above
  • Treat concurrent hypothyroidism if present
  • Pain control
  • Niacin 500mg QD
  • Gemfibrozil or fenofibrate
  • Max dose statin, 81mg ASA
  • Heparin q8 SC, effect short-lived
  • NPO initially
  • May advance diet starting at TG level < 1000mg/dL with resolution of abdominal pain/pancreatitis symptoms
    • No fat diet
    • Low calorie diet

Plasma exchange

  • Therapeutic plasma exchange, for 1-3 days (sickest patients)
    • Generally indicated for hypocalcemia, persistent elevated lactic acidosis, other signs of worsening organ dysfunction
  • For euglycemic patients, not routine first line
  • Requires central venous access

Disposition

  • Asymptomatic hypertriglyceridemia is treated as an outpatient
  • For acute pancreatitis, ICU or step-down for frequent labs, insulin drip

See Also

External Links

References

  1. ↑ Yadav D, Pitchumoni CS. Issues in hyperlipidemic pancreatitis. J Clin Gastroenterology 2003;36:54-62.
  2. ↑ Yuan et al. Hypertriglyceridemia: its etiology, effects and treatment. CMAJ 2007;176:1113-1120.
  3. ↑ Brown, Virgil W. Et al. “Clinical Lipidology Roundtable Discussion: Severe Hypertriglyceridemia.” Journal of Clinical Lipidology 2012; 6:397-408
  4. ↑ Yadav D, Agarwal N, Pitchumoni CS. A critical evaluation of laboratory tests in acute pancreatitis. Am J Gastroenterol. 2002 Jun;97(6):1309-18.
  5. ↑ Santana YR et al. Treatment of severe hypertriglyceridemia with continuous insulin infusion. Case Reports in Critical Care. June 2011.
  6. ↑ Poonuru S et al. Rapid Reduction of Severely Elevated Serum Triglycerides with Insulin Infusion, Gemfibrozil and Niacin. Clin Med Res. 2011 Mar; 9(1): 38–41.
  7. ↑ Schaefer EW. Management of Severe Hypertriglyceridemia in the Hospital: A Review. Journal of Hospital Medicine Vol 7|No 5|May/June 2012.
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