Jump to content

Student case 3: Complications


Recommended Posts

The following case is for students and is based on real clinical problems. Unlike my last two cases, this case will "evolve" with new problems throughout the hospital stay (just like in real life) and it will be your job to manage the patient from admission to discharge. Questions are encouraged and all replies will be addressed by me. I encourage students to "follow" the case to the end and please feel free to join in late. Please give reasoning (brief or detailed) behind any testing or treatment you want.

 

You are a busy PA working a day shift on the in patient side of an over crowded hospital. After finally discharging your patient whom came in with his third case of endocarditis to an LTAC and recusitating your dehydrated CHF patient, you walk towards the coffee maker to take five minutes to unwind when your pager goes off again

 

It's the ER PA who informs you of a patient he needs you to admit. He tells you it's a fifties-looking "John Doe" who came in for AMS. EMS states a bystander called after the pt was found wandering around a convenience store, pulling items off the shelves.

 

His CBC is remarkable for Hb of 11 with MCV of 95, platelets of 115, otherwise the values fall within normal limits (WNL). His Tbili is 1.6, albumin is 3.0 and LFTs otherwiseare normal, his Cr is 1.4 and the remainder of his CMP is unremarkable. There is no family at bedside and the patient is without wallet or phone. He had a CT head which showed mild senescent changes but no acute disease.

 

On exam, he appears to be in his late 50s, has a disheveled appearance, but is otherwise resting in bed. His BP is 150/86, HR 88, normal respirations and 94% on room air (RA). Temperature is 98.0.

 

His heart and lung exam are normal. His stomach is distended. His legs have trace to no edema bilaterally. He denies being in pai. He knows the year and that he is in a hospital. When asked his name he just keeps saying "yes, uh-huh." He follows simple commands

 

What other exam findings do you want to know about?

What lab s and imaging do you want?

Do you start any empiric treatment?

What is your initial admitting diagnosis and your differential?

Link to comment
Share on other sites

BRAC and Drug UA: Would want to rule out intoxication. MRI and Thiamine level to rule out Wernicke's. Also blood lactate and would do a full cranial nerve exam. 

 

Stomach is distended but is it tender? I would probably order a standing abd XR or US abdomen. 

 

DDX: Intoxication, Wernickes encephalopathy with low suspicion for normal pressure hydrocephalus, meningitis, hyponatremia, or sepsis. 

Link to comment
Share on other sites

Stomach is non tender throughout both to light and deep palpating.

 

Good call on what I think you meant BAC or blood alcohol level. It returns as zero. You also check a UDS (urine drug screen) which is negative. Anyone who presents with AMS especially if no family is available for history - it is very reasonable to check UDS and blood ETOH level. If the ETOH level were high it might help to explain the etiology and also clue you into watching for ETOH withdrawal. In this case both were negative.

 

You consider ordering thiamine knowing it will take a while to get back. In this case we don't know if his AMS is acute or chronic. If he doesn't recover then wernickes is a fair diagnosis to consider.

 

Given his lab abnormalities, what other exam findings do you look for to help narrow his differential?

Link to comment
Share on other sites

I'll preface this with saying that I'm only in my 3rd week of clinical medicine class.

 

Further exam findings: is his distended Abdomen also rigid, which might suggest a bleed? Maybe a CT of his abdomen?

 

Lab studies: the HTN and mild elevation in creatinine put him at risk for anemia of chronic disease. I'd like to run an anemia panel and a serum B12, just in case his change in mental status is due to decreased cobalmin.

 

Other thoughts on his AMS change: possible drug/etoh use, so a tox screen?

Link to comment
Share on other sites

Would like to see a UA w/ Microscopy.  His bump in Cr and decreased albumin sparks my interest in kidneys being the etiology

Wanna get and EKG to see if he has an abnormal rhythm or not. 

Lets get a FOBT as well.....

You said LFTs are normal...Any signs of Jaundice? (Scleral or sublingual?) Any HSM on PE? or TTP? If any are present, possibly pull a Hepatitis panel 

 

Couple things that come to mind for a DDx

AKI

CKD....Uremic Encephalopathy?

UTI

GI Bleed

Anemia

Cardiac Arrhythmia 

Hepatitis

Hepatic encephalopathy 

Link to comment
Share on other sites

UA is unremarkable. Stomach is distended but neither rigid nor tender. He does not have an acute abdomen.

 

No CT just yet.

 

Review his abnormal lab findings. What are the major causes of encephalopathy (AMS) in someone with a negative CT head and negative UDS and ETOH level? There are some key exam findings here that haven't been found yet. These and his CBC/CMP abnormalities will give you his preliminary dx and tx plan. In fact PA2016 has it listed in the differential. There also is a key blood test that will confirm the initial dx however exam and basic labs alone would suffice for the astute clinician.

 

His BUN is not high enough to explain uremic encephalopathy.

EKG is NSR.

 

No jaundice. What is HSM?

FOBT is positive, but no gross blood.

You send off a chronic hepatitis panel (good call) and B12 and will get the results tomorrow. Please specify what you mean as "anemia panel" if you still want this.

 

Of note, with low albumin but normal UA, renal falls lower on the differential. He does have either AKI or CKD based on his high Cr.

Link to comment
Share on other sites

Okay good replies everyone.

 

While you can have altered DTRs in encephalopathy, they are typically non specific and not always terribly helpful except in certain neuromuscular disorders.

 

If he has hepatic encephalopathy (HE), which he does, then he obviously has cirrhosis. With longstanding cirrhosis, the LFTs are often normal or a bit high, but unless there is additional insult, often not above the low hundreds. (During earlier injury to the liver, LFTs would've been high.) This does not mean he will not have ascities. Alk phos is typically normal and Tbili is high - the higher it is, typically the more advanced (or more decompensated) the cirrhosis is. Albumin is almost always low, although less specific. Splenic sequestration also leads to low platelets (often in the 30-120 range - again, the more decompensated the liver is, the more pronounced the thrombocytopenia will be). Despite low platelets, cirrhotic patients are hypercoaguable. The ED PA didn't get the INR however you check it and it's 1.6.

 

So, low platelets and albumin with an elevated INR and Tbili - this is a picture of decompensated cirrhosis. Once someone becomes cirrhotic, they may be compensated (and spared of complications such as HE) for several years. Typically a PCP will be clued off on routine labs, but for patients who never go to the hospital or clinic, they often present with a complication, such as HE.

 

However you don't need labs to diagnose cirrhosis. What specific exam findings do you see in a pt with cirrhosis (whether they are encephalopathic or not) besides organomegaly and abdominal distension? Look it up online or in a textbook if you don' t know.

 

The other lab which can confirm HE is an elevated ammonia, but it isn't needed. However if it is negative, it is useful because that means it probably isn't HE but something else. In his case the ammonia was 84 (high). The degree of elevation of ammonia doesn't correlate well with the degree of HE (which is grades I-IV, from mild AMS to frank coma).

 

Low albumin can be seen in any state of chronic inflammation as well as a myriad of other issues such as nephrotic state, malignancy, cirrhosis, sepsis or severe malnutrition, just to name a few.

 

Dehydration and AKI are a common cause of HE. Anytime a cirrhotic patient presents with HE, it's the body's way of waving a red flag saying something is wrong. While the most common cause of HE is non compliance with the medication(s) that prevent and treat it, the differential is broad. What else might we worry about here?

 

If you want FENa, tell me what labs you want to order to calculate this. This can help separate out the causes of acute kidney injury (AKI, also sometimes called acute renal failure (ARF) in severe cases), eg < 1% pre renal and >1-2% intrinsic or post renal, it won't estimate the degree of AKI.

 

Which leads me to my next point. Cirrhotic patients have chronic muscle wasting and their Cr consequently runs low. In a healthy person a Cr of 1.4 might be mild AKI, but if his baseline Cr is 0.6, that would be more severe.

 

Great job on volume assessment. His mucous membranes are dry, his skin turgor is slow and his capillary refill is normal to slightly decreased. There is no fluid wave but mild dullness to percussion, leading you to believe he may have some minimal ascities DESPITE having intravascular dehydration. I rarely check orthostatics except during syncope work up but in this case he probably would've been positive.

 

He has an enlarged liver and spleen upon examination, or organomegaly as you said.

 

What exam findings are common in cirrhosis?

Besides non compliance and dehydration, what are common causes of HE?

Now that we diagnosed him with HE, what is the treatment?

 

Answer these and we'll move onto hospital day 2, when the real fun will begin.

Link to comment
Share on other sites

Also to earlier post: you decide against KUB as you have now diagnosed the pt with HE and abdominal auscultation revealed normoactive bowel sounds. Remember, a 40 year old guy with a big "beer belly" is distended (as an example) but does NOT have an acute abdomen.

 

U/S may be helpful here but first tell me why and what you're looking for.

Link to comment
Share on other sites

What exam findings are common in cirrhosis?

Besides non compliance and dehydration, what are common causes of HE?

Now that we diagnosed him with HE, what is the treatment?

 

Answer these and we'll move onto hospital day 2, when the real fun will begin.

Spider angiomas, caput medusa, positive fluid wave, jaundice, as mentioned encephalopathy, incidence of varices, increased portal hypertension, palmar erythema, scrotal atrophy, increased JVD and or positive hepatojugular reflex, many more...

 

As far as HE it's from the increased ammonia levels as far as I know. But anything that causes cirrhosis could induce that process. Things like Hep B and C, NASH, ASA-toxicity?, chronic ETOH abuse, hepatocellular carcinoma, not sure if Mirizzi syndrome can cause that, but one would guess if the obstruction persisted. 

 

Lactulose is the treatment for HE. It's a substance that goes undigested in the gut by us but the bacteria can and when they do they convert ammonia into ammonium and reduce the HE present. 

Link to comment
Share on other sites

Also to earlier post: you decide against KUB as you have now diagnosed the pt with HE and abdominal auscultation revealed normoactive bowel sounds. Remember, a 40 year old guy with a big "beer belly" is distended (as an example) but does NOT have an acute abdomen.

 

U/S may be helpful here but first tell me why and what you're looking for.

 

U/S Liver/Gallbladder possible fibroscan (if available) to check for progression of cirrhosis, fatty liver, or "goombas" (tumor). Evaluate function of hepatic portal vein? R/O vascular abnormality contributing to poor liver function

Link to comment
Share on other sites

For the FENa...Need a Urine Na, Urine Cr, Plasma Na, and Plasma Cr. 

 

FENa= (Urine Na/Plasma Na)(Urine Cr/Plasma Cr)

 

Would also like to add Hepatorenal Syndrome to the Ddx

 

Common caused of Cirrhosis: EtOH, Hepatitis, Metabolic Dz, NAFLD, and chronic acetaminophen use (That might be a stretch?)

Link to comment
Share on other sites

Dean - great job with exam findings. Hepatojugular reflex can be a helpful exam finding in real clinical practice, but remember this is seen in any form of volume overload, such as in an acute exacerbation of CHF. The same is true for JVD.

 

The scrotal atrophy, reduced chest and body hair (or "paucity of hair" as we say) comes from dysregulation of estrogen hormone in the body. The same is true for gynecomasty and some other exam findings. This is due to the livers role in estrogen production (look it up if you have time). Thus these findings, as well as to some extent ascities (quick note on this: while fluid wave is useful, a good exam including finding dullness to percussion on the flanks, often works just as well in practice) and the cirrhotic "body type" (distended belly, often scleral icterus and frank jaundice, thin limbs due to muscle wasting) will be a dead give away, even on an AMS "John Doe", that if such a patient presents encephalopathic (mentally altered), HE should immediately be on your differential.

 

Another clinically helpful exam finding is asterixis (or "liver flap" since the hands flap). Ask your patient to hold up both hands as if they are trying to stop traffic (palms facing you). Even altered patients that follow simple commands can often do this. You will see and never forget the distinct finding.

 

U/S is useful for all the above reasons you mentioned. Fibroscan is done in the clinic, I haven't seen it used on the in patient side.

 

The cause of cirrhosis is broad. This case is about a patient with chronic cirrhosis. You also can see acute liver failure in a myriad of clinical circumstances. For this case we are focusing on a patient with chronic cirrhosis. So what are the main causes of chronic cirrhosis? Your money should be on

1) chronic hepatitis C and/or B (in this case the patients panel came back positive for HCV)

2) alcoholism (3-5+ drinks a day for more than three years - not always the homeless blatant alcoholic, plenty of middle class patients have alcoholic cirrhosis)

 

Less common causes include NASH (common cause in your obese and diabetic patients), and to a lesser extent drugs, copper, genetic mutations, vasculitis or other systemic disorders. There are even other causes however the list would be quite long to get into that now.

 

Now let's review HE quickly. The liver breaks down ammonia, a natural toxin made in the body. When the liver fails (cirrhosis), ammonia builds up and causes the patient to become encephalopathic, either gradually or more acutely. The mainstay of treatment is lactulose. You often begin dosing it three times a day. The dose is increased until the patient has 3 bowel movements a day (how the ammonia is cleared), and/or decreased if having four or more. An up and coming second line treatment (which can be initiated with lactulose right off the bat, or added later for refractory treatment) is rifaximin. I encourage you to research the mechanism of action behind that drug if you have time.

 

A more aggressive approach is to dose lactulose every two hours until the patient has a BM. Then switch to the above dosing scheme. The risk of this is dehydrating your patient and throwing off their electrolytes if they have diarrhea. You may use an aggressive approach if the clinical case warrants it. In the obtunded or comatose patient it can be given as an enema and additionally through an NGT (nasogastric tube, or NG tube). In this patient, he can take pills and is dehydrated so you go with beginning the dose at three a day and ask the nurse to call you back if he has less or more than three BMS by the mid afternoon.

 

I will add one more section then get to hospital day 2. In the mean time think about what you want to do about his renal failure. He has an elevated but not markedly high BUN and his FENa returns 1.6%. Is this acute, chronic or acute on chronic renal failure? Remember he has some ascities and trace edema in both his legs. His albumin is low and Cr high, but you have no baseline labs to compare. What do you want to do?

Link to comment
Share on other sites

HE can occur due to natural progression of cirrhosis (when the patient gets worse despite treatment). However often there is a "trigger" for it so let's review the more common ones. Remember, in a patient with cirrhosis, finding them to be in hepatic encephalopathy is their body's way of waving a red flag to tell you something is wrong. Common triggers:

 

1) Spontaneous bacterial peritonitis (SBP) or other infection. They may or may not have a high WBC and fever. Thus we often screen with two sets of blood cultures, a UA, chest x Ray (CXR), and most importantly a good exam. Please review SBP on your own time.

2) Non compliance with lactulose. They couldn't get to the pharmacy. It tastes bad (quick tip - recommend your patients mix it with tea or juice). Et cetera.

3) dehydration and AKI. See above post. This is likely a factor in our case given he is dry on exam (dry membranes, poor turgor, etc).

4) bleeding (more on this later).

5) TIPS dysfunction (in patients whom had TIPS placed).

6) wide list of other causes but these are common ones.

 

So with this in mind, we admit and work up our patient. CXR returns and shows mild pleural effusion on the right. You order the U/S but know the results won't be back until tomorrow.

 

Someone (or everyone) tell me what to do with his renal failure (see above post). Then we will move on to hospital day two.

Link to comment
Share on other sites

I'd want an ABG to evaluate for acidosis if yes then start Bicarb. Patient is dry but has some evidence of fluid overload so this kind of has me stumped. 

 

Fluid resuscitation and monitor input/output. If reduced output I would US Kidney/Ureters to evaluate for obstruction. 

 

US Liver/Gallbladder should be able to identify a TIPS. 

Link to comment
Share on other sites

We're already getting an U/S to evaluate for ascities (which can be mild - seen only on U/S, moderate - apparent on careful exam, or severe - obvious on simple inspection and palpation alone and quite large/marked) since he falls between mild and moderate on exam, this will evaluate many other things including his kidneys.

 

He is dry on exam. He is in either acute, chronic or acute on chronic renal failure (what do you think? No right or wrong answer here). He also has some edema. And HRS is a diagnosis of exclusion but a possibility. This is a tough spot for pt and clinician alike, but we have to do something. What's it going to be? Fluid? Albumin? Diuretics? If you want fluids, how much?

 

I definitely agree with following I&O and also daily weights. This is a tough position in real clinical practice so feel free to chime in with best guesses. There is no easy or sure correct answer here, unlike in a written test. Such is the real life practice of medicine.

Link to comment
Share on other sites

I would still like an ABG. It would seem like the encephalopathy and osmolar balance are the immediate life threats, however they are being driven by the cirrhosis. I am concerned that fluids without addressing the etiology for the hypoalbuminemia will drive further fluid overload without addressing the distribution issue. I would start with lactulose (to address ammonia levels) and colloid fluids (to address hemodynamics and avoid acidosis, see ABG results hopefully). That said I am out of my depth with rate and dosing admittedly 

 

I am doing lots of reading on this one! Good case

 

I would like a GFR to work up chronic vs acute AKI...

Link to comment
Share on other sites

To address the above post: it is not unreasonable to get an ABG but remember the old adage: "before getting any test, consider how it's going to change your management - if it isn't, don't get it." He is oxygenating fine, following some commands, tolerating medication and liquids by mouth. His anion gap (which I didn't list) is normal. He is non toxic appearing (eg besides his encephalopathy, doesn't seem to have for example sepsis). At this point an ABG probably won't change your management much.

 

I'm not sure what you mean osmolar balance but perhaps you mean his dehydration and concurrent edema, in which case yes that and HE are his main problems.

 

GFR is helpful in certain instances. However the Creatinine (Cr) is a key part of the GFR calculation. You can NOT calculate a reliable GFR without a stable (or "steady state") Cr. He is clinically dry, based on his history he may have had poor PO intake (eg not drinking or eating much considering he's confused and without a wallet). His AKI is the most likely, obvious trigger for his HE. Thus he needs fluids especially until he wakes up more and can rehydrate orally.

 

You are right to be concerned that fluids will worsen his edema (eg peripheral and ascities). If his overall condition improves, it might not. Or he may get a little worse before he (hopefully) gets better. On the other hand, if we ignore his renal failure (which based on a lower BUN:Cr ratio and intermediate FENa you estimate is probably acute on chronic, meaning he has chronic kidney disease AND is in worse, acute renal failure on top of that because he's dehydrated). It's a tough call. In this case, I would rely on my good exam to see he is clearly hypovolemic and thus lean towards rehydrating and against diuresis for the time being. Things can change on a day to day basis, however.

 

HRS is an ominous finding in cirrhotic patients. The overall mortality is 50% in 2 years. These are very sick patients. But, HRS is a diagnosis of exclusion. First you decide to give a gentle "fluid challenge" of 1 L NS at 100 ml an hour. Albumin may help, but is expensive and not without its own risks. Still, you worry his ascities could worsen briskly given that he has some mild pleural effusion on CXR (likely secondary to his ascities). Thus, you order low dose albumin alongside the fluid. You know that eventually you may need to diurese him with aldactone and lasix, but for now you are more concerned for his kidneys. You also note that tomorrow you may need to get a diagnostic paracentisis if his U/S reveals a significant amount of ascities.

 

For his HE, you order lactulose TID and ask the nurse to to titrate it to 3 BMs a day. You also order rifaximin based off a small study showing it led to quicker resolution of HE and overall decreased length and cost of stay for hospitalized patients.

 

Satisfied, you finish your chart and get back to your other patients.

Link to comment
Share on other sites

Archived

This topic is now archived and is closed to further replies.

×
×
  • Create New...

Important Information

Welcome to the Physician Assistant Forum! This website uses cookies to ensure you get the best experience on our website. Learn More