Check back with Clinical Correlations for another post detailing the general management of hypertriglyceridemia…. References: 1. Yadav D. Gan S. Kasper D. Alagozlu H.
Thanks, now that that question was answered, I am curious how beta-blockers and TSH may cause pancreatitis…. I would actually consider chylomicronemia syndrome in this case given the normal amylase and list pancreatitis as a differential.
High serum triglyceride levels interfere with the assays for serum amylase and lipase, therefore the amylase result for this patient is uninterpretable. A better test would be urinary amylase in a case like this. This is extremely helpful. After being hospitalized for 3 times in the past for pancreatitus, — , the Hospital lab never ever knew the reason why. I guess it was before this research. 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.
Ideally this should be managed at a large center which offers a range of minimally invasive debridement techniques. Although procalcitonin is often conceptualized as a test for bacterial sepsis, it can be elevated in pancreatitis as well as might be expected based on similarities between these two conditions. Procalcitonin may potentially be used for two purposes: 1 Risk stratification Greater procalcitonin elevation reflects more severe inflammation, which may predict a more severe disease course.
Therefore, a markedly elevated procalcitonin level e. The value of procalcitonin for infected pancreatic necrosis is likely as a rule-out test e. This might be useful in avoiding unnecessary antibiotic courses or invasive procedures in patients at low risk for true infection. Further prospective evidence is needed to validate this. This is largely an iatrogenic complication, due to the use of excessive volumes of crystalloid.
As we are moving away from large-volume resuscitation of pancreatitis, this seems to be less of a problem. This ought to drop the serum level of free fatty acids within a few hours although direct proof of this is lacking in hypertriglyceridemic pancreatitis.
The goal of the insulin infusion is not necessarily to reduce the triglyceride level since the best available evidence suggests that insulin is ineffective for this, as explored above. The dose of insulin required to shut off fatty acid production isn't known.
However, this is probably similar to the dose required to treat diabetic ketoacidosis since, in both cases, we are aiming to shut down the metabolic conversion of fats into fatty acids. This is unknown. Most studies have reported use of an insulin infusion at 0. Perhaps most importantly, there probably is no single appropriate dose of insulin for all patients. Rather, the amount of insulin required will vary widely depending on how insulin-resistant any individual patient is. Patients with greater insulin resistance e.
Patients who are insulin naive will require less insulin. The goal of the insulin infusion is to establish an anabolic state i.
Clinically, we can tell that the patient is in an anabolic state if we are giving them dextrose and they aren't becoming hyperglycemic. This implies that the appropriate dose of insulin may be whatever dose is required to prevent hyperglycemia in the face of a significant dextrose administration. Below is a simple protocol for achieving this. There is no prospective evidence supporting this protocol.
Continue D10W infusion at a fixed rate. If the patient has central access, then D20W or D50W may be used at a lower volume, but establishing central access solely for this purpose shouldn't generally be needed. Typically, the insulin infusion will run at rates around 0. Maintenance 1 Follow electrolytes including magnesium and phosphate q6hr.
On the other hand, excessive alcohol intake can cause hypertriglyceridemia even in a fasting state because it promotes the synthesis of large VLDL particles in the liver. Furthermore, alcohol increases the synthesis of large VLDL particles in the liver, which is the main source of triglycerides in the hypertriglyceridemia associated with chronic excessive alcohol intake.
In case of chronic consumption, lipoprotein lipase activity seems to adapt itself. In an animal study comparing the triglyceride levels after acute and chronic ingestion of alcohol, it was shown that the increase in triglyceride levels were less pronounced in rats subjected to chronic alcohol intake in a non-fasting state, confirming that chronic alcohol intake stimulates the production of extrahepatic lipoprotein lipase in response to the increased triglyceride concentration.
In some cases, acute alcohol intake may cause significantly elevated triglyceride levels with an increased risk of pancreatitis, especially patients with metabolic syndrome[26]. Medications such as estrogen, estradiol, glucocorticoids, thiazide diuretics, beta blockers, sertraline, protease inhibitors, valproate and related drugs, and isotretinoin can cause severe hypertriglyceridemia and the chylomicronemia syndrome in patients with inherited lipid metabolic syndromes Table 2 [27].
These drugs reduce lipoprotein lipase and hepatic triglyceride lipase activity [28]. Oddly, fenofibrates, which decrease triglyceride levels, causes an increased risk of pancreatitis among patients with type 2 DM[29]. Table 2. Causes of Sever Hypertriglyceridemia that maybe associated with pancreatitis [41]. Table 2 shows a list of genetic and acquired cause of severe hypertriglyceridemia that maybe associated with pancreatitis.
This was adopted from a scientific statement by the American Heart Association on triglycerides and cardiovascular disease [30]. 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. A recent study shows that goal-directed hemodynamic management guided by functional hemodynamic parameters such as stroke volume variation, compared to CVP-guided therapy, led to a significantly improved survival, tissue oxygenation, and microcirculatory perfusion, as well as less histopathologic damage in porcine model of severe acute pancreatitis[31].
There are still no randomized studies that compare the efficacy of the different treatment regimens used in the management of this disease.
Insulin may be considered the first choice with or without heparin in patients with concomitant hyperglycemia, but appears to be slower in action compared with apheresis, which decreases serum triglycerides and decrease symptoms in a very short period of time [34]. Intravenous insulin and heparin administration should be considered in patients with concomitant hyperglycemia[32]. Insulin activate lipoprotein lipase which degrade chylomicrons into glycerol and free fatty acids resulting in rapid reduction of triglyceride levels [35,36].
Subcutaneous regular insulin dosed at 0. Intravenous insulin is more efficacious than subcutaneous insulin for treating hypertriglyceride-induced pancreatitis. While insulin has been shown to be effective when used as monotherapy [37], intravenous heparin does not. Heparin stimulates the release of endothelial lipoprotein lipase and causing an initial rise of the circulating enzyme but is immediately followed by its degradation in the liver resulting in its further depletion and recurrence of hypertriglyceridemia [38].
That is why heparin is recommended only as an adjunct treatment to insulin. A single bolus of low molecular weight heparin Dalteparin was found to deplete lipoprotein lipase similarly to unfractionated heparin [39].
Apheresis is capable of rapidly lowering markedly elevated triglyceride levels, clear prancreatic enzymes, and provides symptom relief from pancreatitis within 2. Several studies have shown that apheresis can significantly decrease serum triglycerides and cause both clinical and laboratory improvement when conservative treatment with diet and pharmaceutical drugs fail.
All these studies also stress the importance of performing apheresis as soon as possible to maximize therapeutic benefit. Its limiting factor is, however, its availability and very high cost.
Prevention of initial and recurrent pancreatitis from hypertriglyceridemia should be emphasized. However, drug treatment with fenofibrates or niacin of asymptomatic persons with high triglyceride levels, particularly those less than Lastly, Pancreatic enzyme therapy has been shown to alleviate abdominal symptoms [49]. Risk factors for hypertriglyceridemia such as insulin resistance and alcoholism should be assessed in this setting as these are correctible factors that can be treated to avoid future bouts of pancreatitis in patients with occult hereditary lipid metabolism disorders.
Epidemiologic reports have shown the glycemic index of foods has a direct correlation to triglyceride levels [50]. In conclusion, we provide an evidence based algorithm to summarize the approach to the etiology of hypertriglyceride-induced pancreatitis. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Gastroenterol Hepatol Endosc1: doi Home Contact Us. About us About Us Providing cutting-edge scholarly communications to worldwide, enabling them to utilize available resources effectively Read More.
Open Access News and events Contact Us. For Authors We aim to bring about a change in modern scholarly communications through the effective use of editorial and publishing polices. Read More. Special Issues Frequently Asked Questions. Links Advanced knowledge sharing through global community… Read More. Take a look at the Recent articles. Key words acute pancreatitis, hypertriglyceridemia, algorithm, hypertriglyceride induced pancreatitis Introduction Hypertriglyceride-induced pancreatitis is the third most common cause of pancreatitis after gallstones and alcohol [1,2].
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