Familial hyperlipidemia syndromes Type I and V causes severe hypertriglyceridemia enough to cause spontaneous pancreatitis while Type IV usually requires a secondary factor such as alcohol, diabetes mellitus, obesity or thyroid dysfunction to cause the disease [17].
Secondary causes of hypertriglyceridemia Non-insulin dependent diabetes mellitus is a well-known cause of hypertriglyceridemia and is the most common cause of hypertriglyceride-induced pancreatitis [1]. Initial treatment Initial treatment of hypertriglyceride-induced pancreatitis is no different from treating other causes of pancreatitis bowel rest, aggressive intravenous hydration, pain control and anti-emetics. Apharesis Apheresis is capable of rapidly lowering markedly elevated triglyceride levels, clear prancreatic enzymes, and provides symptom relief from pancreatitis within 2.
Prevention Prevention of initial and recurrent pancreatitis from hypertriglyceridemia should be emphasized.
Conclusion In conclusion, we provide an evidence based algorithm to summarize the approach to the etiology of hypertriglyceride-induced pancreatitis. Am J Gastroenterol GastroenterolClin North Am Nordic Federation of Societies of Obstetrics and Gynecology — World J Gastroenterol Relationship with etiology, onset, and severity of the disease.
Int J Pancreatol Mayo ClinProc Lancet JAMA Ann Surg Pancreas All rights reservsms of pancreatitis: current opinion. J GastroenterolHepatol Surgery Gastroenterol Res Pract BMC Gastroenterol Arch Intern Med ClinChimActa Ann Intern Med Evidence for enhanced lipoprotein assembly, reduced intracellular ApoB degradation, and increased microsomal triglyceride transfer protein in a fructose-fed hamster model. J BiolChem : Arch Med Res Van de Wiel A The effect of alcohol on postprandial and fasting triglycerides.
Int J Vasc Med : Brunzell JD Clinical practice. N Engl J Med Pancreatology 5: Effects of long-term fenofibrate therapy on cardiovascular events in people with type 2 diabetes mellitus the FIELD study : randomised controlled trial.
Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation Intensive Care Med Dig Dis Sci The American Journal of Emergency Medicine A multifunctional enzyme relevant to common metabolic diseases.
Isolation and characterization of the enzyme from normal rat heart. J BiolChem J Am CollNutr J Lipid Res Nephrol Dial Transplant Use vasopressors e. This may reduce the amount of fluid given, thereby reducing the risk of abdominal compartment syndrome more on this below.
Be careful about the use of fluid-responsiveness in these patients. Even if the patient is fluid-responsive, administered fluid will rapidly leak out of the vascular space. Pancreatitis patients will often be fluid-responsive regardless of how much fluid they are given.
Patients will often develop renal failure due to acute tubular necrosis. This doesn't respond to additional fluid administration. Not only is this wrong, it's probably backwards. Reduced hospital length of stay. Decreased gastrointestinal symptoms. Cessation of oral fat intake may be important to help triglyceride levels fall. Thus, a truly non-fat diet might be beneficial initially.
For nonintubated patients, this could include foods such as fruit and pasta which are extremely low in fat. For intubated patients, modular protein supplementation could be provided in addition to intravenous dextrose. This may be observed for a couple days. If the patient still isn't eating after days, a small-bore nasal feeding tube may be placed to provide nutrition. It is controversial whether to feed the stomach e. RCTs show no differences in outcome: either route is fine.
Among intubated patients it's usually easier to place an orogastric tube, so this route is often used initially. If the patient has problems with gastroparesis or vomiting, then switching to a post-pyloric tube may be helpful.
This has been shown to increase the risk of infected pancreatic necrosis and multi-organ failure. Most patients will need some amount of opioid, but this should be kept to a minimum. Pain-dose ketamine infusions e. Among patients with cirrhosis or severe alcoholism, this should probably be reduced to a dose of two grams daily e. Epidural analgesia may be considered if available. For more on analgesia in critical care, see the chapter here. These will cause the pancreatitis patient to look infected upon arrival e.
However, this is generally a reflection of sterile inflammation rather than true infection. Historically there was a concept that prophylactic antibiotics could prevent the development of infected pancreatic necrosis. This has been debunked and should not be used.
Up-front antibiotics will select out resistant organisms, which cause problems later on when true infection actually does occur. Antibiotics should generally be avoided during the first week, with the following exceptions: a The diagnosis of pancreatitis is unclear and there is concern for septic shock with a focus of infection elsewhere.
Infectious complications of pancreatitis e. During this time frame, inflammatory symptoms e. The classic presentation would be a patient who initially improves, but subsequently deteriorates with worsening sepsis.
Investigation typically begins with repeat CT scan. Occasionally, radiologic features may be diagnostic e. Fine-needle aspiration to determine whether infection is present is routinely used at some centers and recommended in the Canadian guidelines for acute pancreatitis. However, other antibiotics also penetrate the pancreas well e.
A team approach is required for these stubborn problems, including pancreatic surgeons, interventional radiologists, and invasive gastroenterologists. J Biomed Inform. The Scottish Government. Scottish Index of Multiple Deprivation. Accessed May 18, Lipid-modifying therapies and risk of pancreatitis: a meta-analysis. Save Preferences. Privacy Policy Terms of Use. This Issue. Views 12, Citations View Metrics. Twitter Facebook More LinkedIn. Research Letter.
Michael J. Back to top Article Information. Conflict of Interest Disclosures: None reported. Access your subscriptions. Access through your institution. Add or change institution. Hurtado Andrade, M. However, these are extremely rare disorders, including lipoprotein lipase deficiency, which has an estimated prevalence of one in a million. Secondary exacerbating factors in patients with an underlying lipid disorder, often polygenic, are more commonly responsible for hypertriglyceridemic pancreatitis.
It is therefore very important to seek and address these secondary causes for elevated TG, which include uncontrolled diabetes, alcohol use, weight gain, and high intake of saturated fats and refined carbohydrates. Drug-induced hypertriglyceridemia is another important cause for acute pancreatitis.
The list of offending agents includes estrogen, retinoic acid derivatives, sirolimus, L-asparaginase, capecitabine, protease inhibitors and propofol. Tiffany M. Cortes, M. The NPO state not only helps decrease pancreatic secretion and inflammation but also decreases further generation of chylomicrons.
Pharmacotherapy to lower serum TG with fibrates is unlikely to be beneficial in the initial stages, and attention has focused on other measures to achieve this.
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