To restate:

35-year-old man admitted for worsening ascites. We know the patient because he had just left AMA 3 days before.  He had HIV with a low CD4 and did not take any anti-retrovirals.  He also had hep C cirrhosis with encephalopathy and worsening ascites.  He did take spironolactone and lactulose and the lactulose was causing diarrhea.

We go to the ED and find these labs:

Of course we need an ABG on room air

Interpretation:

The patient had respiratory alkalosis, likely secondary to hepato-pulmonary syndrome.

I find this quote on compensation:

Studies have shown an average 5 mmol/l decrease in [HCO3-] per 10mmHg decrease in pCO2 from the reference value of 40mmHg. This maximal response takes 2 to 3 days to reach.

This compensation seems appropriate.  Therefore a chronic respiratory alkalosis.

At morning report we had 3 guesses for normal gap acidosis.  The guesses included:

1. Type IV RTA secondary to spironolactone – the hyperkalemia always comes first, as the hyperkalemia leads to the decrease in NH₃ production
2. Diarrhea – the diarrhea must be a large volume.  Decreased GFR can make this more likely, but he did not have that.  Finally, his diarrhea would not be basic as he was taking lactulose which acidifies the stool
3. Distal RTA secondary to liver disease – I had not heard of that, so I looked up causes of distal RTA

Type I RTA is caused by a variety of conditions, including:

1. Amyloidosis
2. Fabry disease
3. Sickle cell disease
4. Sjogren syndrome
5. Systemic lupus erythematosus
6. Wilson disease
7. Use of certain drugs such as amphotericin B, lithium, and analgesics

To repeat a mantra – you should not assume a normal gap acidosis from the electrolyte panel (you can assume an increased anion gap acidosis).  Similarly when you see an elevated bicarbonate and the clinical situation does not fit metabolic alkalosis, you should think of the possibility of compensation for chronic respiratory acidosis.

I suspected respiratory alkalosis in this case because none of the potential causes of normal gap metabolic acidosis made sense.
 

35-year-old man admitted for worsening ascites. We know the patient because he had just left AMA 3 days before.  He had HIV with a low CD4 and did not take any anti-retrovirals.  He also had hep C cirrhosis with encephalopathy and worsening ascites.  He did take spironolactone and lactulose and the lactulose was causing diarrhea.

We go to the ED and find these labs:

I ask the team why the bicarbonate is low.  I presented this a morning report also and asked students, housestaff and applicants!

I looked at the old labs and this bicarbonate level was present on the previous admission and had remained stable.  What do you think?

Yesterday our team took call.  I saw patients both in the morning and the afternoon.  As I type this, I only know that we will have between 8 and 10 patients to see.  Yesterday I saw 3.

One raised some interesting questions.  This was the second patient I have seen in the past month with complications from a loop ileostomy.  In both patients, the daily output exceeds 3 liters.

Both patients have loop ileostomy for very good indications.  Both patients had lost their appetites – saying that they have lost their taste for food.  Both present with volume contraction.

The loop ileostomy patient has huge challenges.  Our goal today is to educate the patient, find a strategy for maintaining the patient's volume status, and trying to correct the ageusia.  We are trying zinc supplementation, which worked in the first patient splendidly.

Soon I will go to rounds as we do our best to get patients home for Christmas.  Fortunately today is Tuesday and we can get things done rather quickly.  The admission day of the week matters for length of stay.

A patient gets admitted for a COPD exacerbation.  The patient has right sided heart failure symptoms, so we continue the diuretic therapy.

The initial creatinine is 1.0, but the next day it goes to 1.3.  We blame the increase on over aggressive diuresis, and give some modest replacement.  The physical exam fits our hypothesis.

The patient's breathing continues to improve, but the 3rd day the creatinine is 2.0.

We have a long discussion of the possibilities.  While we doubt ATN, we must consider that possibility.  Volume contraction is possible, but we had treated for that possibility.  The urine output is 560 cc/24 hr.

We go to the bedside, and find a catheter, but looking under the sheets we find a condom catheter.

Now you can guess the answer.  A straight cath gets converted to a Foley – 1200 cc residual.

When the patient becomes oliguric or the creatinine rises (or both as in this patient) - 

RULE OUT OBSTRUCTION

RULE OUT OBSTRUCTION

50 something patient with combination of restrictive and obstructive disease.  This electrolyte panel caught everyone's attention.

ABG

What likely happened to this patient?  What do you want to do now?

Yesterday I started back on VA wards.  As I have done occasionally in the past, I will share some thoughts each day from my VA ward experience.

The patient of the day is one who has had repeated episodes of left leg cellulitis.  The patient has had osteomyelitis documented one time (3rd metatarsal).  

On physical exam the patient had lower leg cellulitis with apparent lymphedema.  Examination of the foot showed severe tinea pedis.  

The team had not thought to look for tinea pedis, not knowing how often tinea pedis provides the portal for infection.

So teaching point for day #1 – always look for tinea pedis in patients with lower leg cellulitis.

We have exciting news.  We are accepting applications for a new internal medicine residency.  We need 8 interns and 8 second year residents for July 2012.  UAB – Huntsville Regional Medical Campus Internal Medicine Residency – a brand new residency created in cooperation with Huntsville Hospital.

For many years I have written on this blog about the need for more residency slots.  We had an opportunity through the Affordable Care Act to apply for funding for a new residency.  The approval from CMS came through in the summer.  We also had to obtain Residency Review Committee approval.  This approval was granted in October.

We hope that some medical students will find us on ERAS.  We already have a significant number of applications, but we welcome more.

For interns at other programs who need to find a residency slot (for example, doing a preliminary year and the program has no internal medicine residency slots), we encourage you to contact our program. We had our first interviews today.

I am happy to answer any questions about the program, as are the program directors – Dr. Lourdes Corman and Dr. David Fahey.

Our excitement is palpable.  We look forward to greeting our new interns and residents in late June.  We promise to provide them a great education!

Now obviously this is my opinion, and other may differ.

We have an alcohol abusing woman who presented with a Na of 110 mEq/L and depressed mental status.  She awoke as saline increased her sodium quickly to 120 mEq/L.  This occurred because her urine osms of 150.

This patient admitted to a beer diet.  Her history fit beer potomania.  Normally the urine osms in beer potomania are less than 100, but she also presented with volume contraction from vomiting.  I suspect that she had some ADH from the volume contraction.

Given her dilute urine and underlying alcohol abuse, we worried that she had a predisposition for central pontine demyelination or an extra pontine demyelination syndrome.  Therefore the resident made the bold and correct decision to give vasopressin.  The idea behind giving vasopressin in this situation follows from an understanding of the true problem.  This patient would correct her sodium too quickly because she would excrete too much free water.  Therefore, the vasopressin would prevent the free water excretion and slow the sodium rise.

The vasopressin worked and the patient's sodium rose at a slow and desirable pace.

To recap:

47-year-old woman found stuporous and hypotensive.  She has known alcohol abuse and decreased LVEF around 30%.  

Her labs come back, and you should provide plausible reconstructions of these results.

Arterial Blood Gas on 2L nasal oxygen

What do you think her acid-base diagnosis is?  What additional information do you want (history, physical and/or labs)?