An 83 year-old female comes to the ED with burning epigastric pain, worse with an empty stomach, non-radiating, and non-exertional. It is not associated with nausea, vomiting or diaphoresis. She has not tried any remedies at home, but nothing makes the pain better. You start delving into her medical history and you find out the patient recently traveled from Haiti, was in the ED recently for a cough and cold, and started on moxifloxacin. The patient was discharged home, completed the course of antibiotics, but then developed fevers, night sweats and went to another hospital. There she was diagnosed with TB. She was started on appropriate 4-drug therapy with improvement and was eventually discharged home. She is now presenting to you 5 days after discharge and approximately 3 weeks after initial diagnosis .
PMH:HTN, dyslipidemia
PSH: None
Allergies: Seasonal allergies
Meds: INH, Rifampin, Ethambutol, Pyrazinamide, B6, amlodipine, simvastatin
Social: She lives with her niece and denies any drugs, alcohol or tobacco.
FH: none
PE:
HR 87, RR: 16, BP: 136/82, SPO2: 97%
GEN: Well appearing, comfortable, frequent audible belches
HEENT: Normal oropharynx, normal conjunctiva, normal sclera
PULM: Crackles at bases
CV: RRR, s1, s2, no r/m/g
ABD: +BS, soft, tender, no rebound or guarding. Palpable, tender liver 4cm below costophrenic angle
Ext: 2+ edema proximally to knees bilaterally. No warmth or erythema. Good distal pulses. No cyanosis or clubbing.
EKG: Normal sinus rhythm. Normal axis and intervals. No ST-segment changes. No T wave inversions. No signs of LVH
Labs:
Na – 121, K 4.5, Cl 87, HCO3: 16; BUN/Creatinine 35/.92 Glucose 69
Ca: 8.5; T Protein 7.3; Albumin 3.0; AST: 1793; ALT: 595; Alk Phos 474; T. bili 1.4; BNP: 2000;
INR 1.6
CBC: WBC 9.71; Hb: 9.1; Hct: 29.4%; Plt 230; Â MCV 86; RDW 19.9%
HIV: negative
Bedside sono: few B lines, mild to moderately reduced EF, no pericardial effusions. IVC plethora.
Think you know what is going on? Don’t forget to post your answers.
- You notice this patient is hyponatremic? Why might this be?
- What is your approach to a patient with abnormal liver function tests. How do you explain the tender, enlarged liver?
- The patient is coughing and has no sputum production. Does this patient need airborne isolation? Why or why not?
Steven Greenstein
Latest posts by Steven Greenstein (see all)
- Case of the Month 19: Inhaled Steroids for Asthma - March 16, 2017
- Case of the Month 19 - March 3, 2017
- Case of the Month 18: Refractory Epistaxis - February 13, 2017
4 Comments
Kaufman · September 3, 2016 at 3:51 pm
I’ll start this discussion up a bit 🙂
1- Pt appears hypervolemic, so hyponatremia likely from organ failure (heart in this case, also albumin is low likely poor nutrition) causing a low ECV and ADH release and change in free water. Start CHF tx with likely Lasix, ACEi
2- Statins AE: HMG (Hepatitis, Myositis, Gallstones). They are CYP cleared and INH and Rifampin alter that clearance, so RUQ US and medication changes may be in order, also a Hepatitis Panel (travel hx etc.), though AST > ALT doesn’t fit viral pattern
3- On 4 drug therapy, but without CXR or sputum tests for TB, unknown if active. Need sputum and a CXR to eval further, precautions for now I’d say
Tedward · September 3, 2016 at 7:37 pm
As an overall assessment, a patient who is actively being treated for TB diagnosed 3 weeks ago, is now presenting to the ED for abdominal pain, and found to have signs of pulmonary and peripheral edema and hepatomegaly, with otherwise normal exam and vitals. Workup was pertinent was hyponatremia (hypervolemic), AKI (pre-renal ratio) and elevated BNP. She also has broad increases in all LFTs, but most notably with an AST in the thousands, and a greater than 2:1 ratio of AST:ALT. Her gamma protein gap is elevated at 4.3. She has a normocytic anemia with a wide RDW. Bedside sono was consistent with mild pulmonary edema and reduced EF, and EKG was wnl.
The differential is potentially wide, but given her new onset heart failure and hepatomegaly/hepatitis, the most likely diagnoses would be constrictive pericarditis or restrictive myocarditis secondary to TB (given active infxn), with hepatic injury due to liver congestion (budd chiari syndrome). Although less likely here, given the patient’s age, wide gamma gap, and normocytic anemia, her symptoms could also reflect an infiltrative disease process, such multiple myeloma, affecting both heart and liver.
1. The patient has a hypervolemic hyponatremia, likely due to heart failure in this case. Hypervolemic hyponatremia suggests a dilutional effect due to water retention, resulting from increased ADH secretion triggered by intravascular depletion. Commonly seen in heart failure, cirrhosis, and nephrotic syndromes. Treat with diuretics like lasix, as the patient is whole body fluid overloaded.
2. LFTs can be broken down into 3 groups, reflective of the underlying mechanism of injury: acute hepatic cell injury (increased AST, ALT), impaired liver function (decreased albumin, prolonged coags), and intra- or extra-hepatic obstructive disease (increased bili and alk phos). This patient’s liver enlargement, tenderness, and injury profile are all likely due to vascular congestion resulting from constrictive pericarditis/restrictive myocarditis. Prolonged venous congestion would eventually cause decreased arterial perfusion, leading to subacute ischemic injury, which would give a primarily hepatocellular injury picture, as in this patient. The venous congestion would also cause liver distension and pain/tenderness (budd chiari syndrome). Nutmeg liver, anyone?
3. Although patients can generally be taken off iso following initiation of treatment if they have 3 negative AFB smears, we do not have access to this patient’s prior AFB smears or cultures. It is also possible that this patient with proven TB and active cough may have a strain of TB that is resistant to her current therapy. So even though the patient is actively being treated, if she develops a new cough or failed to have improvement of her prior symptoms, then she must be placed on airborne isolation until she has three negative AFB samples (via bronch if necessary) or is no longer symptomatic.
Lee · September 3, 2016 at 11:14 pm
The moxi was prescribed for a suspected CAP with a relatively high PSI score, I imagine. I am glad someone was able to catch her AFB+ because fluoroquinolones are shown to increase false negative sputum smears. Because of their activity against M. tuberculae, they should not be used in patients who may have TB (e.g.: anyone with AIDS who may need them as a 2nd line TB treatment). Hopefully we didn’t contribute to the MDRTB problem here.
1. I would guess the hyponatremia is 2/2 to an SIADH picture associated with her tuberculosis itself. I’d be curious how much lower it is than when she initially presented. She seems to have compensated (she doesn’t have neurologic manifestations, though a very careful exam is warranted including gait and cognition) so I’d be very cautious correcting it. 121 is pretty low, so if her serum osmols and urinary sodium are consistent (>40) with SIADH, let’s see how she does with some free water restriction (which will help her other issues as well) alone while we monitor her ins and outs. Any seizure and we can give a push of hypertonic saline (100mL) and probably some B6 until she returns to baseline. I’d be less concerned once it’s up to around 125-130. If free water restriction doesn’t work we can do salt tablets, maybe a loop diuretic.
2. I agree with Dr. Kauffman she’s earned a hepatitis panel and I’d do a RUQ ultrasound, but but our most likely culprit is the RIPE therapy itself (especially in an elderly female). I am glad she’s not febrile or with a raging leukocytosis. This is why patients need follow up in ID clinic are advised to completely abstain from EtOH even if just on INH alone. I see her h/o dyslipidemia and I am curious if she is on a statin (stop it!). She needs to stop all of her RIPE therapy because they created a synergistic fire ball of hepatotoxicity. This needs to monitored and if worsening, might be worth localizing your nearest liver transplant center. I suspect it will reverse with rearrangement of TB treatment regimen. She likely has congestion which is giving her a fluid overloaded state. If she is not having dyspea, let’s focus on the underlying cause.
In the meantime, let’s give her something for pain (not acetaminophen!) like small aliquots of morphine which may vasodilate her a touch and dull the edge of her sympathetic surge.
3. She needs isolation. Sorry Dr. Greenstein, I know you hate the excessive use of “maybe it’s TB!” isolation admissions. She has +AFB and is coughing. I am not sure when she started her RIPE treatment – if she were asymptomatic and 2-3+ weeks into therapy, she wouldn’t need it.
Ian deSouza · September 7, 2016 at 4:22 pm
Great, VERY comprehensive answers everyone. Nice work!