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1654058 tn?1407162666

Ammonia Levels & Lactulose

What levels are normal? I entered hospital last week w a 14. Leaving w 53 and they gave me an RX for lactulose. Reading all your posts on Dee's encouraged me. Bleed out, banding, n lactulose in 1 week is scary. I'm still posting on phone n can't reload long posts n messages.
How many are on something for HE? Also, would anyone who has been banded give a count?
I'm still pretty sore n on soft diet. How long does it take to heal?
Sry to be so jumbled. Maybe I shud make another post for banding.
Got my hgb up to 10 n platelets to 42. It dropped to 4 and 2dunn ER. Of course tx is over and I'm feeling better. Just learning about  new issues.
Confidence is not the lack of fear. It's moving forward in spite of it.
Love you guys. Thanks, xo Karen :)

9 Responses
1856046 tn?1330240845
Glad you are done with tx, are OK, and home Karen!

I have only had 1 episode of HE but I have been banded many times, usually every couple of years although this time around they did 2 sets of six bands (using a "six-shooter" attachment on the endoscope) pre-tx.

Mine heal in 2 weeks to a month and I have found the worst thing to eat was too big of a chunk of meat which has gotten stuck and took me some time to clear. Learned to eat with more awareness (translates as "slow down, take smaller bites,  chew your food, and learn to enjoy it"!)

Soft stuff is good!

Did you mean above that your hgb was 4 and your platelets were 2? If so, I am glad they took care of you as those are pretty low. My platelets dropped to 7 on my last round of tx ((using daily Infergen instead of the Peg) and they told me not to shave and to have someone else tie my shoes as they were afraid of me hemorrhaging.

I am on Promacta now to keep my platelets up during this round of triple w/Incivek.

446474 tn?1446351282
" I entered hospital last week w a 14. Leaving w 53 and they gave me an RX for lactulose."
14, 53 for what values?
Ammonia should be listed under ammonia on blood test result.
It is common for GI bleeding to exacerbate hepatic encephalopathy.

"• Gastrointestinal bleeding: Patients with cirrhosis frequently suffer from bleeding in the digestive tract, usually from dilated veins in the esophagus (esophageal varices).  Digested blood represents a large protein load in the gut which can lead to higher levels of ammonia and other toxins  and, not surprisingly, hepatic encephalopathy is frequent in this setting."
No variceal bleeding or banding. Nadolol is taken a a prophylaxis.
My meds for hepatic encephalopathy for the last 2-3 years:
* Lactulose 2 tablespoons by mouth once or twice a day
* Xifaxan 550 mg 2x per day
Ammonia Blood Levels

"The normal values listed here-called a reference range-are just a guide. These ranges vary from lab to lab, and your lab may have a different range for what’s normal. Your lab report should contain the range your lab uses. Also, your doctor will evaluate your results based on your health and other factors. This means that a value that falls outside the normal values listed here may still be normal for you or your lab.

Adults: 15-60 micrograms per deciliter (mcg/dL)

Ammonia levels do not always reflect the severity of a person's symptoms. For example, a person with severe cirrhosis may have only slightly elevated blood ammonia levels and yet may not be thinking clearly or may be sleepy or in a coma. Other people with very high ammonia levels may think and act normally."

446474 tn?1446351282
What is hepatic encephalopathy?

Hepatic encephalopathy is a potentially reversible disturbance of brain function due to liver (hepatic) failure. The syndrome is characterized by a broad spectrum of neuropsychiatric derangements including personality changes, intellectual impairment, and a depressed level of consciousness, and appears to be the result of neurotoxins that accumulate with liver failure.  Ammonia, which is usually metabolized by the liver, is a critical neurotoxin in the development of hepatic encephalopathy, but other toxins are also involved. The neuropsychiatric manifestations of hepatic encephalopathy are reversible with appropriate medical therapy, but the syndrome is a hallmark of advanced, decompensated liver disease and has an overall poor prognosis. Thus, certain patients with hepatic encephalopathy should be referred for liver transplantation.

Hepatic encephalopathy has a variety of symptoms, from very subtle cognitive impairment to full-blown coma. At the mild end of the spectrum, the term minimal encephalopathy refers to patients with cirrhosis who do not display clinically evident cognitive abnormalities, but who demonstrate cognitive impairments with formal neuropsychological testing. Despite its subtlety, minimal hepatic encephalopathy is an important diagnosis, as it has been associated with a reduced quality of life as well as impaired driving skill.

What causes hepatic encephalopathy?
The pathogenesis (cause) of hepatic encephalopathy is complex and not completely defined, but it is clear that nitrogenous wastes, particularly ammonia, derived from the gut play a major role in the observed disruptions of brain function. Bacteria residing in the large bowel (colon) produce ammonia that is absorbed into the bloodstream leading to the liver. Under normal circumstances, ammonia is efficiently detoxified in the liver so that relatively little escapes into the general circulation bathing the brain. However, with advanced liver disease, whether acute or chronic, the detoxification of ammonia and other toxins by the liver fails, and they accumulate in the blood and disturb brain function. This failure results in part from an inadequate mass of normally functioning liver cells (hepatocytes), and also from a propensity of blood to shunt (short circuit) around the liver with advanced liver disease, particularly cirrhosis.

Although the underlying pathogenesis of hepatic encephalopathy remains unclear, a number of precipitants (or triggers) that exacerbate underlying encephalopathy have been clearly defined. Such precipitants are important to rapidly identify and treat because without specific and effective intervention, the patient’s encephalopathy may not improve. Common precipitants that may trigger an episode of severe hepatic encephalopathy in patients with otherwise stable liver disease include:

• Constipation: Slow transit of stool through the gut appears to increase the time for bacteria digest foodstuffs and make ammonia and other toxins, potentially triggering hepatic encephalopathy.
• Infection: Although infection involving almost any site, including the urinary tract and lungs, many trigger hepatic encephalopathy in patients with advanced cirrhosis, infection of ascites (abdominal fluid) - called spontaneous bacterial peritonitis (SBP) - is one of the most frequent triggers of encephalopathy. Sampling ascites fluid using a needle, a procedure called paracentesis, is required to determine if SBP is present.
• Medications: Drugs that suppress the central nervous system, particularly opiate pain medications (e.g., codeine) and benzodiazepines (e.g. diazepam, lorazepam), may trigger hepatic encephalopathy.
• Electrolyte problems: Low serum sodium (hyponatremia) and potassium (hypokalemia) are common in cirrhotic patients treated with diuretics and both can worsen hepatic encephalopathy. Hypokalemia appears to exacerbate encephalopathy in part by stimulating ammonia production from the kidneys.
• Dietary indiscretion: Excessive consumption of protein, particularly from large red meat meals, seems to exacerbate hepatic encephalopathy in occasional patients, but this appears to represent a relatively rare trigger of severe encephalopathy.
• Kidney failure: Dehydration from diuretic therapy and diarrhea, infection, some medications, and progression of liver disease can all lead to kidney failure, which in turn leads to decreased clearance of urea, ammonia, and other toxins that can contribute to encephalopathy.
• Other factors: A rise of blood pH (alkalosis), which often results from diuretics and resulting dehydration, may facilitate entry of ammonia into the brain and exacerbate encephalopathy.

What are the symptoms of HE?

Patients suffering hepatic encephalopathy may come to the doctor with a spectrum of symptoms. In mild cases, called minimal hepatic encephalopathy, the patient may have no symptoms but have cognitive deficits revealed by formal neuropsychiatric testing (e.g., number connection tests, etc.). With more advanced hepatic encephalopathy, fatigue, and at least mild deficits of memory, concentration, and coordination may become apparent. At this stage, common complaints by the patient include:
- “I feel like my head is in the clouds.”
- “I’ll walk into a room and forget why I am there.”
- “I am always tired…but I can’t sleep.”
- “I often forget what to say in mid-sentence.”
- “My boss is telling me that my work is slipping.”
- “My handwriting has changed to scribble,”
- “My hands shake so much, I can’t hold my coffee cup without spilling it.”

Nighttime insomnia is a very common and troublesome symptom associated with hepatic encephalopathy. In fact, patients with encephalopathy may ultimately sleep more during the day, with fitful naps, than at night, and this “day-night reversal” is a hallmark of more advanced hepatic encephalopathy. Family and friends frequently notice a deterioration of the patient’s cognitive function as well as a change in the patient’s personality—with frequent irritability, bouts of anger, and loss of social graces. They may also witness firsthand deterioration of the patient’s driving skills (“He would have run off the road if I hadn’t grabbed the wheel!”).

Two of the most common physical (as opposed to subjective) manifestations of hepatic encephalopathy are asterixis and fetor hepaticus. Asterixis is a non-synchronous and coarse tremor– known colloquially as a “liver flap” – that is best elicited by asking the patient to outstretch the hands with straight elbows, wrists cocked at 90 degrees, and fingers spread apart, instructions easily communicated with the command, “Stop traffic!” Although such a tremor is not specific for hepatic encephalopathy (it can also be seen with renal failure and other conditions), it certainly suggests the diagnosis in patients with liver disease. Fetor hepaticus is a musty sweet odor that is usually evident by casually sniffing the patient’s breath.

When symptoms of hepatic encephalopathy progress, the patient may slip into a stupor or even comatose state and be virtually unarousable. Such situations are medical emergencies, and the patient should be brought to medical attention immediately.

Avatar universal
Hi Karen,
Sorry you are having so many complications.  I am praying that you recover quickly and remain UND.  Onward to SVR and a healthy liver with no more complications!  Remember, do whatever it takes to keep your health insurance.
Avatar universal
Karen thank you so much for the updates. I just want to let you know you are amazing :) I hope the lact. works well!!
Best wishes,
1652596 tn?1342015226
karen, i hope that you have a speedy recovery from this setback.  you are one of the strongest women on this forum.  i'm sending you some prayers.  best wishes on your health.  belle
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