Sunday, August 19, 2007

Acute abdomen and other thoughts

Strange and unexpected findings in a ER case this week. A 45 year male with a history of mental retardation was transferred into the ER from an institutional facility because of "unusual breathing patterns". Apparently, he had been complaining of stomach pains and nausea for three or four days and then developed cold sweats and rapid breathing. I was called by the on-call hospitalist who sounded worried as hell about the guy. The patient wasn't much of a historian given the underlying mental retardation, but one glance was all it took to realize he was in some sort of trouble. You see enough critically ill people in surgery that one glance is usually all you need to tell if someone is "sick". And when a patient doesn't look good, I usually go into trauma mode. This means starting with the A,B,C's: airway, breathing, circulation. He was able to speak, so airway was patent, but his respirations were over 40/minute (the unusual breathing pattern, I guess) and his oxygen saturations were in the high 80's despite being on an high flow oxygen face mask. So breathing not so good. Circulation evaluation revealed a clammy, cool, pale middle aged male with a BP 80/40. I pushed the saline and did the rest of the exam. His abdomen was rigid and flat and peritoneal signs were evident on palpation. Plain films revealed some stacked loops of small bowel, but no free air. Then his labs started trickling back. WBC 38. Lactate 9.5. Bicarb 12. Hemoglobin 16. The metabolic acidosis and peritonitis had me worried about dead bowel, or some sort of intra-abdominal catastrophe. It was strange though; the guy was only 45 years old and had no history of heart disease, dysrhythmias, or otherwise. Perhaps it was a perforated ulcer and for some reason the free air wasn't showing on the films. Whatever was going on, it was apparent that definitve diagnosis and treatment would require a laparotomy. He stabilized hemodynamically after three quick liters of saline and his saturations improved with the non-rebreather mask.

After consent was obtained from a distant sister, we went straight to the OR. Upon entering his peritoneal cavity, I encountered liters of bloody/straw colored acites. Unexpectedly, however, the bowels looked perfectly pink and healthy from ligament of trietz to cecum. The colon seemed normal. There was no fecal or enteric contamination. I examined the stomach and duodenum closely, even doing a kocher maneuver, to identify any possible ulcer perforations. Nothing. The fluid seemed bloodier and darker from around the stomach, so I opened the lesser sac, in order to better evaluate the posterior gastric wall. And then boom, it was clear. Lying in the posterior retroperitoneum was a partially blackened, necrotic appearing pancreas with surrounding peripancreatic inflammation and necrosis: Necrotizing pancreatitis, every surgeon's nightmare. Severe pancreatitis leads to leakage of pancreatic enzymes around the pancreas which auto-digest the surrounding tissues and set off an inflammatory cascade known as S.I.R.S. (severe inflammatory response syndrome) which can manifest as respiratory failure, kidney failure, and cardiac dsyfunction. When the pancreatic inflammatory phlegmon gets infected, the only hope for survival is aggressive surgical debridement and washout. Usually though, surgery is delayed for 1-3 weeks after the onset of necrotizing pancreatits, which allows for better tissue demarcation and safer debridement. This was a very unusual situation I found myself in where I was operating acutely in new-onset pancreatitis. I started to debride some of the friable, blackened gunk (like the black, charred grit left on a grill after an afternoon of cooking) until I got into a little bit of bleeding. And by little bit, I mean half a liter in 30 seconds. There's a rich vascular network around the pancreas and millions of little branches to disturb. Tiger country, we call it. Not someplace you want to often be, even in the best of circumstances. In the setting of acute pancreatitis, with all the attendant inflammation and edema, this was like navigating a tight rope in the dark. A combination of sutures and clips were able to finally stem the ongoing exsanguination, allowing me to take a step back and make sure my boxers were still clean. So I got the hell away from there for a while and did a standard open cholecystectomy. His gallbladder was contracted and inflamed and full of marble sized stones. Severe pancreatitis is either a result of heavy drinking or gallstones passing near the pancreatic duct. So standard procedure is to remove the source of continuing irritation, in this case the gallbladder, presumably. I went back to the pancreas and debrided some more obvious loose necrosis near the body and tail and then washed everything out. Put a couple of sump drains in the lesser sac and closed the gastrocolic ligament. Finished it off with a feeding jejunostomy tube and closed him up. This was three days ago. He's now extubated and doing better. We'll see how it turns out in the end. In hindsight, perhaps I could have waited and obtained a CT scan and treated him conservatively. Or at least waited until clear cut infected pancreatic necrosis set in....

9 comments:

rlbates said...

Pancreatitis is nasty stuff. Sure hope your patient continues to improve. Lucky for him you didn't quit looking.

monash medical student said...

hi Buckeye Surgeon.

i am jeffrey, MS 2. i have submitted this post on your behalf to Surgexperiences 103 (a new surgical blog carnival) which will be hosted by Dr Jon at http://www.unboundedmedicine.com/

Look out for the release this week!

Buckeye Surgeon said...

Will do, Monash.

ahmed maasher said...

HI , I know its a nightmare for a surgeon to open for pancreatitis , but I am wondering since you are not sure about the diagnosis , did you ask for amylase and lipase first ?, retreospectively speaking , will you ask for CT abdomen before going to the OR ,
I hope your patient will go through it .

Buckeye Surgeon said...

The diagnosis was not definitely not in question. This was necrotizing pancreatitis. Amylase and lipase are very non-specific (not even a part of Ranson's criteria), so even if they are high, normal or low, it wouldn't change the clinical diagnosis. The reason I blogged about this case was the unusual presentation: severe metabolic acidodis, peritonitis, hypotension, leukocytosis.....

Sid Schwab said...

I'm thinking even if the CT had been done it might have been pretty hard to sit by with that level of acidosis and peritonitis. Tough call. Once there, you certainly did the right thing. One would expect another trip or two, but it sounds like a save...

Bongi said...

ct would have been good, but hindsight is so clear. i think i would have done what you did. by the way, i haven't seen too much success with this degree of pancreatitis.

Anonymous said...

From a lay reader... Can you give us a feel for how much alcohol consumption can lead to pancreatic problems?

Any guidelines or figures on daily intake, years of consumption, other mitigating effects?

Are there any reliable diagnostic tests to check
pancreatic and/or liver function to see if
alcohol is taking a toll on a person's organs, or if all is normal? Is blood workup sufficient, or is
imaging also required?

Spiral CTs for Kidney stones are available for the patient in the last month.

Would anything abnormal Panreatically or Liverly
show up in these scans, or would a different type of scan be required (such as w/ contrast agent or other xray exposure conditions for optimal organ
contrast)?

Thanks in advance if you can annswer these. Your Blog as well as the Blogs you have linked are absolutely fascinating, and I look forward to reading more!!

Buckeye Surgeon said...

Pancreatitis comes in 2 flavors: acute and chronic. Chronic Pancreatitis is a result of years and years of alcohol abuse (much like cirrhosis of the liver) Acute pancreatitis can happen to anyone subsequent to a single binge. HArd to put absolute number on the amount of ingested alcohol that will lead to such complications. Everyone is different. Genetics certainly play a role; not everyone metabolizes alcohol the same.

For necrotizing pancreatitis you look on CT scan for non-enhancement of pancreatic tissue, fluid collections, and air bubbles within the retroperitoneum.