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Abstract: A 46-year-old middle-aged man with epigastric pain after drinking alcohol came to the hospital to have his blood drawn and found that his blood turned into a milk-like color. After examination, it turned out that there was too much oil in the blood, which the body could not metabolize, causing hypertriglyceridemia and even inducing acute pancreatitis.
Basic information】Male, 46 years old
Disease Type】 Hyperlipidemia, very severe hypertriglyceridemia, acute pancreatitis
Hospital】Beijing Hospital
Date of Consultation】June 2020
Treatment plan] Gastrointestinal decompression + medication (ustekin injection + octreotide acetate for injection + ornidazole injection + moxifloxacin hydrochloride sodium chloride injection + esomeprazole sodium for injection + fenofibrate extended release capsule + fat milk injection (C14-24) + compound amino acid injection (18AA) + pushen capsule) + lipid adsorption treatment
[Treatment period] 14 days of hospitalization, 2 months of outpatient follow-up
Treatment effect】The condition has been controlled and all indicators are improving
I. Initial consultation
The patient was a 46-year-old middle-aged man with epigastric pain without fever, nausea and vomiting after drinking alcohol the day before he was admitted to the hospital. He had a history of mixed hyperlipidemia for 10 years, mainly elevated triglycerides, and was treated with oral medication, but his lipids were not well controlled. He had a history of smoking and drinking for more than 20 years. On examination, he was in good general condition, with a BMI of 27.69 kg/m^2, stable vital signs, no significant positive cardiac or pulmonary signs, and mild pressure pain in the middle and upper abdomen, without rebound pain. Emergency blood tests (celiac) leukocytes 13.64×10^9/L, neutrophils 75%, total cholesterol 8.41mmol/L (celiac), triglycerides 55.43mmol/L (celiac), HDL-C 0.32mmol/L (celiac), ALT 45U/L (celiac), blood amylase 318U/L (celiac), FPG 9.47 mmol/L, Ca ion concentration 1.84 mmol/L, prothrombin time 13.2s (celiac), C-reactive protein 118mg/L (celiac), and normal total bilirubin. Abdominal ultrasound showed fatty liver. abdominal plain film showed no abnormality. CT scan of the abdomen showed blurred fat around the pancreatic head area, and pancreatitis could not be excluded. He was diagnosed with hyperlipidemia, very severe hypertriglyceridemia and acute pancreatitis and was admitted to the hospital.
II. Treatment history
After admission, the patient was given fasting, gastrointestinal decompression, ustekin injection and octreotide acetate for injection to inhibit pancreatic enzyme secretion, as well as ornidazole injection and moxifloxacin hydrochloride sodium chloride injection for anti-infection, and esomeprazole sodium for injection to inhibit gastric acid secretion. As the patient’s blood lipids, especially triglycerides, were significantly elevated, lipid adsorption treatment was given once after explaining the patient’s condition to the patient and family members and signing the informed consent form for rapid lipid lowering.
After treatment, the triglycerides decreased to 16.92 mmol/L. On the next day, the triglycerides were 24.56 mmol/L. Lipid adsorption therapy was administered once again, and the triglycerides decreased to 6.54 mmol/L. Oral fenofibrate extended-release capsules were given for lipid regulation. During the fasting period, fat milk injection (C14-24) and compound amino acid injection (18AA) were given for intravenous nutritional support. After 3 days of treatment, the abdominal pain disappeared, and after 5 days of treatment, the nasal feeding diet was gradually opened.
III. Treatment effect
After 14 days of hospitalization, the patient’s abdominal pain disappeared, and thereafter no abdominal pain occurred again until he resumed normal diet, and he was discharged. The patient continued to receive oral lipid-lowering treatment with fenofibrate extended-release capsules and busulfan capsules. 2 months later, the patient was seen at the outpatient clinic with stable disease control and no uncomfortable symptoms.
IV. Notes
We are glad that the patient’s condition was controlled. Improvement of lifestyle should be the first treatment option for hypertriglyceridemia. Patients need to be advised to focus on lifestyle changes.
1, reasonable diet: limit carbohydrate and fat intake, less greasy food, the amount of staple food should also be controlled, increase the intake of vegetables and high-quality protein, eat more green leafy vegetables, appropriate lean meat, fish, etc..
2, limit alcohol consumption: long-term alcohol consumption will affect liver function, affecting the liver’s ability to metabolize fat and aggravate triglyceride elevation.
3, appropriate moderate intensity aerobic exercise can help reduce weight, weight loss is conducive to improving multi-organ function and vascular health.
4, Quit smoking can significantly reduce the overall risk of cardiovascular disease in patients.
V. Personal insights
Hypertriglyceridemia is an important cause of acute pancreatitis. The mechanism by which it causes pancreatitis may be due to increased blood viscosity in such patients, fat particles and free fatty acids causing local microthrombosis and capillary damage, blocking pancreatic vessels, leading to pancreatic hemorrhage and necrosis, which in turn induces acute pancreatitis.
In this case, the patient had a history of long-term hypertriglyceridemia, which was not regularly treated, and a small amount of alcohol was consumed before the onset of the disease. The condition of acute pancreatitis changes rapidly and can worsen rapidly and may even be life-threatening, therefore, treatment related to acute pancreatitis needs to be given immediately. At the same time, active measures should be taken to remove hypertriglyceridemia as the cause of the disease to avoid the progression to life-threatening severe pancreatitis.