The case
A 61-year-old man comes to the ED with three days of sharp, intermittent pain in the left upper quadrant, a bloated and distended belly, and poor intake with on-and-off nausea, vomiting, and diarrhea. He had pancreatitis once, twenty years ago. Eventually it is found out that he drinks nearly a bottle of whiskey every two days; his last drink was about 24 hours ago. He is already on a fibrate and a statin for high cholesterol.
CT in the ED shows an edematous pancreas with a thickened duodenum and surrounding fat stranding. His first lipase is 236, with an AST of 188 and an ALT of 64. He gets IV fluids, an opioid, IV thiamine, and a proton-pump inhibitor, and is admitted. Then the triglyceride level comes back: 1380. He is moved to the ICU and started on an insulin infusion.
Overnight he starts to withdraw from alcohol: sinus tachycardia and anxiety, treated on a CIWA protocol. By morning the triglyceride drip is clearly working — triglycerides are down to the 260s — but he says he feels worse. His abdomen is rounded, distended, and taut, tender across the epigastrium and left upper quadrant, with bowel sounds that have gone nearly silent in all four quadrants. His pain needs keep climbing, and the nurse notes his urine output is trailing off.
- General: restless and anxious, awake and oriented
- Abdomen: rounded, distended, taut; mid-epigastric and LUQ tenderness; bowel sounds present but markedly hypoactive in all four quadrants
- Monitor: sinus tachycardia 105–120, blood pressure 166/102
- Triglycerides: 1380 on admission, now 262 on the drip
- Lipase: 236 in the ED, now 1065
- Kidneys: creatinine was 0.79 on arrival and has now climbed to 2.1; urine output is falling
The triglyceride number is getting better while the patient is getting worse. Is this just a stubborn ileus, or something you have to act on tonight? Commit to an answer, then work the questions.
| ED | Day 3 | |
|---|---|---|
| Triglycerides (mg/dL) | 1380 | 262 |
| Lipase (U/L) | 236 | 1065 |
| AST / ALT (U/L) | 188 / 64 | 96 / 38 |
| Glucose (mg/dL) | 148 | 171 |
| Creatinine (mg/dL) | 0.79 | 2.1 |
| Urine output | adequate | falling |
| Heart rate | 92 | 118, sinus |
| Blood pressure | 152/90 | 166/102 |
| Bladder (intra-abdominal) pressure | — | 39 mmHg |
Questions
Q1 His glucose is 171. Why is he on an insulin drip?
Not for the glucose — for the triglycerides. His triglyceride level of 1380 is the thing that drove his pancreatitis, and insulin is one of the fastest ways to bring a number that high down.
Insulin switches on lipoprotein lipase, the enzyme on the capillary wall that clears triglyceride-rich particles out of the blood, and at the same time it shuts down fat breakdown so fewer new triglycerides are shipped in. Both push the level down.
Because the target is the triglyceride and he is not meaningfully hyperglycemic, the drip runs with dextrose alongside it and a glucose check every hour, or you will drop his blood glucose. Trend the triglycerides and come off the drip once they fall below about 500, where the pancreatic risk eases. His were already in the 260s — that part of the plan worked.
Q2 The triglycerides are falling, but he is worse: taut belly, silent bowel, climbing pain, and now less urine with a creatinine up from 0.79 to 2.1. What are you worried about?
Stop looking at the triglyceride number. A tensely distended abdomen with new oliguria and a jump in creatinine is abdominal compartment syndrome until you have measured otherwise.
Most of that pressure is coming from the inflammation, not the ileus. Severe pancreatitis sets off a body-wide capillary leak, so fluid third-spaces into the bowel wall, the retroperitoneum, and the abdomen as ascites — and the liters of resuscitation fluid he needs leak right back out and add to it. The ileus stacks on top of all that edema and free fluid. Together they raise the pressure inside a closed abdominal cavity, and past a point it squeezes the veins and the kidneys: venous return drops, renal perfusion drops, and the urine follows.
Keep the differential open — worsening necrosis, a perforation, or bleeding can all look like this, and a CT helps. And since he is on insulin, recheck the glucose and keep his electrolytes corrected, because they feed the ileus. But the belly is the question now, so the next move is to put a number on it.
Q3 How do you actually confirm it at the bedside?
You do not eyeball a compartment syndrome — you measure it. The abdomen's pressure is read through the Foley catheter: you instill a small, fixed volume of saline into the empty bladder, connect a pressure transducer, zero it at the iliac crest in the midaxillary line, and read the pressure at end-expiration with the patient flat and relaxed. The bladder wall is floppy enough to pass the abdominal pressure straight to the transducer, so the number you get is the intra-abdominal pressure.
He was intubated and sedated before these readings, and that is part of why you can trust the number: the bladder only reports a true intra-abdominal pressure when the abdominal wall is relaxed. An awake patient who tenses or guards reads falsely high — so sedation, and paralysis if needed, is as much about getting an honest measurement as it is about treatment.
What the number means:
- Sustained above 12 mmHg is intra-abdominal hypertension — watch it, and start unloading the abdomen.
- Above 20 mmHg with new organ dysfunction — like his falling urine and climbing creatinine — is abdominal compartment syndrome.
It is cheap, fast, and repeatable, so trend it. A single reading is a snapshot; the trend tells you whether what you are doing is working.
Q4 His bladder pressure comes back at 39 mmHg, and the creatinine is still climbing. Now what?
That is abdominal compartment syndrome, and 39 is dangerously high with a kidney that is already failing. Work the ladder, quickly, while you line up the definitive fix:
- Decompress the bowel: an NG or OG tube to suction to empty what you can.
- Relax the wall: optimize analgesia and sedation, and consider neuromuscular blockade to drop the tension in the abdominal muscles.
- Fix the fluid balance: enough to perfuse, not so much that you add to the edema that is driving the pressure.
Re-measure the bladder pressure as you go. If it stays this high and the organ dysfunction persists, medical measures are not enough and the treatment is surgical: a decompressive laparotomy to open the cavity and release the pressure. Call surgery.
★ The reveal
He went for an emergent decompressive laparotomy. The abdomen was left open under a negative-pressure wound vac dressing, with a planned return to the OR for re-exploration and delayed closure once the swelling came down.
Opening the cavity dropped the pressure. His urine output picked up over the next several hours; the creatinine, which had climbed to 2.1, took a day or two to drift back down. Airway pressures and hemodynamics eased.
The insulin drip had already done its job on the triglycerides. The belly was the emergency — and the falling triglyceride number was never the thing to watch.
How an insulin drip clears triglycerides
Severe hypertriglyceridemia — usually a level above 1000 — can itself cause pancreatitis. This man was set up for it: he was already on a fibrate and a statin for high cholesterol, which tells you his triglycerides run high at baseline, and an alcohol binge tipped him over the edge.
The enzyme that does the clearing. Triglycerides travel in the blood inside large particles — chylomicrons and VLDL. The enzyme that pulls them apart is lipoprotein lipase, anchored to the lining of the capillaries. Insulin is its on-switch: it raises lipoprotein lipase activity, so the triglyceride-rich particles are hydrolyzed into free fatty acids and glycerol and taken out of circulation.
It also closes the tap. Insulin suppresses hormone-sensitive lipase in fat tissue, so stored fat is broken down more slowly and fewer new fatty acids are sent to the liver to be repackaged as triglyceride. One arm clears what is there; the other slows what is coming.
Why the dextrose matters. The goal is the triglyceride, not the glucose, and a patient like this is not very hyperglycemic to begin with. Run insulin hard enough to clear triglycerides and you will drive him hypoglycemic unless you give dextrose alongside it and check the glucose every hour. Trend the triglycerides and stop the drip when they drop below about 500.
The other options. Heparin also releases lipoprotein lipase into the blood, but the bump is short-lived and it can worsen bleeding, so many centers use insulin alone. For the sickest patients, plasma apheresis can strip the triglycerides out directly.
Bedside takeaway: in the right patient, an insulin drip is treating the triglycerides, not the glucose — it turns on lipoprotein lipase to clear them — so you run dextrose with it, check glucose hourly, and stop around 500.
Teaching points
- In pancreatitis, an insulin drip may be treating the triglycerides, not the glucose. Severe hypertriglyceridemia is a real cause of pancreatitis, and insulin clears it by switching on lipoprotein lipase.
- Run dextrose with it and check glucose hourly. The target is the triglyceride, the patient often is not hyperglycemic, and the drip will cause hypoglycemia if you forget. Trend triglycerides; come off around 500.
- Do not anchor on a number that is improving while the patient gets worse. Falling triglycerides did not mean he was getting better.
- A taut, distended abdomen with new oliguria and a rising creatinine is abdominal compartment syndrome until measured otherwise. Inflamed pancreas plus ileus plus resuscitation fluid is the classic setup.
- You can measure it at the bedside. Intra-abdominal pressure through the Foley: above 12 mmHg is intra-abdominal hypertension; above 20 mmHg with new organ dysfunction is ACS. His was 39.
- ACS has a ladder. Decompress the bowel, relax the wall, fix the fluid balance; if organ failure persists at a high pressure, the fix is a decompressive laparotomy and an open abdomen.
- Alcohol is a double hit. It drives both the pancreatitis and the high triglycerides, and the withdrawal you are treating overnight is a parallel emergency.
- Lipase and triglycerides move independently. His lipase climbed while his triglycerides fell. They answer different questions; do not read one as the other.
Who does what
Physician / APP
Recognizes severe hypertriglyceridemia as the driver and starts insulin with dextrose, reads the deteriorating abdomen as possible ACS, orders the bladder-pressure measurement, and calls surgery when it returns 39 with a rising creatinine.
RN
Hourly glucose and urine output, measures the bladder pressure through the Foley, tracks abdominal girth and the exam, runs the CIWA protocol and withdrawal meds, manages the PCA, and flags the trend early.
RT
Watches airway pressures and lung compliance — rising pressures are an ACS clue as the diaphragm is pushed up — and manages the ventilator once he is intubated for the OR.
Medic / flight
No bladder-pressure tool in the field. A rigid, tensely distended abdomen with shock and falling urine is the red flag. Avoid piling on fluid, support perfusion, and move fast to a surgical center.
References
- Tenner, S., Baillie, J., DeWitt, J., & Vege, S. S. (2013). American College of Gastroenterology guideline: Management of acute pancreatitis. The American Journal of Gastroenterology, 108(9), 1400–1415. https://doi.org/10.1038/ajg.2013.218
- Garg, R., & Rustagi, T. (2018). Management of hypertriglyceridemia induced acute pancreatitis. BioMed Research International, 2018, Article 4721357. https://doi.org/10.1155/2018/4721357
- Kirkpatrick, A. W., Roberts, D. J., De Waele, J., Jaeschke, R., Malbrain, M. L. N. G., De Keulenaer, B., Duchesne, J., Bjorck, M., Leppaniemi, A., Ejike, J. C., Sugrue, M., Cheatham, M., Ivatury, R., Ball, C. G., Reintam Blaser, A., Regli, A., Balogh, Z. J., D'Amours, S., Debergh, D., … Olvera, C. (2013). Intra-abdominal hypertension and the abdominal compartment syndrome: Updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Medicine, 39(7), 1190–1206. https://doi.org/10.1007/s00134-013-2906-z
Educational content only, not medical advice. Cases are drawn from clinical experience; details are changed so no patient can be identified. Medications are named without doses; follow your facility's protocols and your local medical direction.