52 year old man is brought to the hospital by ambulance. He has been camping in the mountains for three days and his family noticed that he had been getting progressively more confused. The day before he had tried to put his pants on his arms, put dishes in the dryer and tried to use the telephone to change channels on the TV. His family called the ambulance the next day when he wouldn't wake up. His past medical history was significant for chronic renal insufficiency (kidney failure), cirrhosis, Hepatitis C and hypertension. He was also a recovering alcoholic and claimed (in his previous medical records) he had been on the wagon for several years.
On exam he appeared to be sleeping quietly. Noxious stimuli (pressing a pen firmly across his fingernail) did not cause him to stir. His breathing was steady, his EKG was good, but his fingernails looked pale (a sign of anemia). He had no signs of trauma, and his family told the paramedics they weren't aware of any recent drug or alcohol use. His abdomen was distended and moderately firm. He would occasionally stir and groan, shifting his arms and legs. His pupils were dilated, but would react sluggishly to light. Because all of his limbs were moving and his pupils reacted, it was unlikely that he had suffered a stroke. he had shit himself at some point, and his poop smelled foul. The particular odor produced indicated blood in his poop. When I checked him (put finger up his butt to check for fresh blood/hemorrhoids/fissures -- none found) I also tested his poop which was indeed positive for blood. That finding, coupled with his apparent anemia meant that he was probably bleeding somewhere in his gastroinstestinal tract. I had the lab tech draw blood, I ordered labs, and did what I usually do in the ER: sit and wait. The ER nurses almost immediately began to badger me about what to do next. They felt that I should be doing more to bring him out of his unconscious state. I asked them for suggestions.
"It looks like an overdose. We should give him Narcan (naloxone)." Narcan is used to reverse narcotic overdose. I reminded them that with narcotics, the pupils get small, not large.
"We should give him IV fluids; he looks dehydrated." I reminded them that he had kidney failure, and if we overload him on fluids, his lungs would fill with water and he'd drown.
"We should give him insulin, it's probably his diabetes." His blood sugar was mildly elevated at 210 and we had nothing to indicate that he was diabetic. You don't go into a diabetic coma until your sugars get up around 500. Giving insulin to someone who is not diabetic can have unpredictable results like dropping their sugars so low that their brain stops working.
The nurses continued to fret, but stopped pestering me to "just do something." I continued to wait, and wait some more. The lab as the hospital is infamously slow. I've worked in lots of ERs and most labs will come back in about ten to fifteen minutes if the techs hurry. In this hospital, best case scenario is thirty minutes, but it can take much, much longer. I've been told that there is an old cranky tech that is nearing retirement that is the cause; I suspect that it's due to the lab equipment that was purchased from the Soviets in the 1940s.
On the up side, because the labwork was taking so long, the guy began to come around a little. He only said two words, "God Damn!" Over and over and over, and he was screaming. He drifted back to sleep for awhile, then opened his eyes a little, tried to focus, and would yell, "God Damn!" This was a good sign in that he was able to speak, sort of.
The labs finally came back and this guy is fucked. His liver and kidney function is all screwed up, and he is terribly anemic. On the bright side he had no infection. The reason for his stuporous state seemed to be his ammonia level which was more than double what is considered high (normal is 10 - 30, his was 70). His brain is pickled in ammonia, which is why he was unconscious. Now I knew what he had. It's called hepatic encephalopathy. Here's a little excerpt from Wikipedia that explains in nicely.
Although the onset of hepatic encephalopathy may simply reflect worsening of underlying liver disease, it may also be due to a number of independent factors, each treatable in its own right. In fact, studies have shown that the majority of cases are due to one (or more) of such precipitation factors. It is critical, then, that a search for possible precipitants be conducted in patients with new-onset hepatic encephalopathy, and specific treatment initiated if such a precipitant is discovered.
Virtually any metabolic disturbance may precipitate hepatic encephalopathy. Common culprits are hyponatremia (often arising as a result of diuretic treatment or simply as a complication of the edema typically found in advanced cirrhosis), hypokalemia (again, often as a result of diuretic use), alkalosis, dehydration, hypoglycemia (a condition to which people with cirrhosis are susceptible), and renal failureof even mild degree.
Likewise, there are several medications the use of which may bring on hepatic encephalopathy. These include benzodiazepines (e.g., diazepam, lorazepam), narcotics, and diuretics. Alcohol ingestion, whether or not it was the cause of the patient's liver disease, may also precipitate hepatic encephalopathy.
Infection is an important precipitant of hepatic encephalopathy. In some cases, the only clinical manifestation of the infection is the development of the encephalopathy. In fact, this is a frequent phenomenon in patients whose ascites has become infected (i.e., spontaneous bacterial peritonitis).
Sometimes, hepatic encephalopathy arises as a result of patient non-compliance with dietary protein restriction. Indeed, given the general lack of palatability of low-protein diets, non-compliance is common and, hence, so is its effect to precipitate encephalopathy.
Bleeding into the stomach or small intestine (both of which occur with increased frequency in people with liver disease and/or portal hypertension) may also lead to hepatic encephalopathy. Blood contains large quantities of protein in the form of plasma proteins and hemoglobin. Hence, the presence of blood in the stomach or small intestine represents a protein load which, as a result of bacterial metabolism in the lumen of the gut, is converted to potentially toxic products such as ammonia.
Certain surgical procedures employed to treat portal hypertension commonly lead to the development of hepatic encephalopathy. For example, operations to relieve pressure in the portal vein by connecting it to the splenic vein or other systemic venous vessels, have the effect of diverting incoming intestinal venous blood away from the liver. This means that such ammonia-carrying blood will not be able to be "purified" by the liver. Encephalopathy can result. In a similar manner, the more-recently-developed "TIPS" procedure (transjugular intrahepatic portosystemic shunt) often precipitates hepatic encephalopathy (~30 percent of patients undergoing it).
Once I saw the lab work, I tried to find somebody who might know the patient so I can get more history. I tracked down his sister, who told me that he had not been taking his medications. The main medication that was important for this guy to take was Lactulose, which is an osmotic laxative. It helps by moving protein out of the gut before bacteria can produce ammonia from it, and change the acidity of the intestines which helps to convert ammonia into ammonium which is less easily absorbed by the bloodstream. It also turned out that despite the initial story I had heard, he was indeed drinking again. This is a no-no for someone with cirrhosis (not to mention Hepatitis C) because it further inflames the liver, which further impairs its function.
So I had a few things to figure out:
1. how to reverse the elevated ammonia levels
2. how to reverse his anemia
3. how to do one and two without further inflaming his liver
4. how to do one and two without worsening his kidney failure
5. figure out exactly why he was anemic, and how to fix it
Luckily, by the time I get all the lab work back, the guy had had come around enough that he could drink fluids without choking to death. If asked him his name, he could answer correctly. He still has no idea where he was or how he got here, he can't tell me his last name, doesn't know what city he's in but he is able to ask for one thing, "I need a beer! Get me a beer!" Priorities.
I get him started on drinking some Lactulose, 45 ml every hour until his ammonia level starts to improve toward normal. This means lots of urgent bowel movements will be coming soon. His lab work also showed that he had been anemic for some time. His hemoglobin was 8.7, and at 8.5 you start giving somebody packed red blood cells. His oxygen saturation was still very good at 97%. Because he was still getting oxygen to his body (and brain) I could wait to correct the anemia. His most serious problem was his pickled brain. However, it was important to figure out from where he was bleeding. It was clear he had a gastrointestinal bleed somewhere, which interestingly, was feeding his encephalopathy. As mentioned above, blood is a source of protein that the gut digests, which in turn increases the ammonia levels. The most likely place for this guy to be bleeding is from his esophagus. I knew this because when you have cirrhosis bad enough it causes a backflow of the blood coming from the gut, that reverse pressure often causes varices in the esophagus. A varice is like a varicose vein, swollen and saggy and chock full of blood. Lucky for him veins are on the low pressure side of our vascular system, so he's slowly leaking as opposed to gushing. But in order to find out, we would have to shove an endoscope down his neck.
While we were working on getting the Lactulose into him, his hemoglobin level dropped below 8.5, and he was given 2 units of packed red blood cells. Unfortunately, this did not raise his hemoglobin. That means he's bleeding out faster than we can replace his blood. That's bad. He was then sent to a larger hospital because his problems were becoming more than our little rural hospital could handle.
It turned out that he did indeed have varices in his esophagus, and he was bleeding from them. It was a nice, steady leak. Think back to those educational films you saw in grade school about how a leaky faucet and can lose gallons of water per day and you'll understand why this guy's little leak was a serious problem. They gave him some medication that would lower the portal hypertension (back flow of blood from the liver) and continued to feed him Lactulose. Last I heard, he was having lots of diarrhea and bugged everyone at the hospital to bring him a beer. A lifetime of bad habits, which he is doomed to continue, are going to lead to a very ugly end.
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