Case of the Month – July 2017 – Answer

We had three wonderful answers to last month’s COTM, but Dr. Segarra’s comprehensive response takes the cake.

 

For a complete review of the case, please click here.

 

Just to recap:

 

50-year-old woman with DM2, HTN, GERD, recently completed 6 months of TB therapy, presented with abdominal pain, N/V, weight loss, and anorexia. Her exam was notable for a diffusely tender abdomen, most pronounced in the right lower quadrant, and bilateral costovertebral angle tenderness. Labs were notable for a leukocytosis and bandemia of 11%, thrombocytopenia, hyponatremia of 116 (uncorrected), anion gap of 17 (20 when corrected for Albumin of 2.8), hyperglycemia of 526, creatinine of 3.23, large leukocyte esterase in the urine. CT imaging was notable for massively enlarged kidneys, ascites, hepatomegaly, and a large bulky uterus. The patient was initially tachycardic and hypotensive but after a 2L bolus, the hemodynamics improved, creatinine decreased to 2.89, glucose decreased to 435, and sodium decreased to 107 (uncorrected).

 

What is your differential diagnosis for the patient’s presentation?

Dr. Segarra gave a wide differential diagnosis and went through the process of paring down the possibilities. For this patient, labs ruled out DKA (no ketonemia), and CT excluded appendicitis, pancreatitis, hepatitis, cholecystitis, and bowel obstruction. The remaining diagnoses included sepsis (patient had a leukocytosis/bandemia and tachycardia), hematologic disorders, endocrine disorders such as SIADH and adrenal insufficiency, and infiltrative diseases. All of our respondents included extra-pulmonary tuberculosis as part of their differential diagnosis. The treatment regimen for drug-susceptible renal and disseminated tuberculosis is the same as for pulmonary tuberculosis, and as such, our patient had recently completed treatment (Nahid, 2016).

 

What antibiotics would you choose?

It all depends on what is being treated and which organisms may be responsible. Piperacillin/tazobactam was the initial choice in the ED based on the suspicion for an intra-abdominal infection as it offers coverage for both Gram negatives and anaerobic organisms (in addition to pseudomonas which was not likely to be a culprit in this case). The only risk factor that she had for TB is her previous infection; otherwise, she had no previous history of incarceration (recall that she works in the police department), and she had been adherent to her therapy (this was confirmed by the medicine team with the DOH). So, her risk for multidrug resistant TB was deemed to be low. Nevertheless, in such patients, the use of a fluoroquinolone, despite its broad-spectrum activity, would be controversial as it also is effective against Mycobacteria species and is generally given as part of a multi-drug regimen to avoid development of resistance. Piperacillin/tazobactam is an acceptable choice, but ceftriaxone with metronidazole would be most appropriate for the treatment of community-acquired intra-abdominal sepsis.

Does this patient need to be on isolation?

Based on CDC guidelines, respiratory isolation is not required. The patient had very recently completed a treatment regimen and did not have any respiratory symptoms.

How would you characterize the sodium disturbances, both on initial presentation and after the initial interventions?  How would you address them?

The sodium derangements are somewhat masked by the hyperglycemia. Her initial value indicates some degree of pseudohyponatremia, with the corrected value being either 123 or 126 depending on whether you use 1.6 or 2.4 as your correction factor. That the serum sodium decreased to 107 (112 or 115 depending again on choice of correction factor) despite infusion of crystalloid containing 154 mmol/L indicates that she is suffering from either too much free water retention or from too much loss of salt. Her corrected values still represent hyponatremia, but it is important to recognize that the concomitant hyperglycemia has an impact.

As Dr. Segarra noted, it’s helpful to break down hyponatremia based on serum osmolality and then on volume status (Spasovski, 2014). Calculation of this patient’s serum osmolarity would be affected by her hyperglycemia, but her downtrending creatinine (3.23 to 2.89 after 2L of fluids), and initial vital sign abnormalities all point towards an initial hypovolemic state. The resolution of her tachycardia/hypotension and downtrending creatinine also indicate that her initial hypovolemia had improved, and she was now closer to a euvolemic state. Euvolemic hyponatremia is usually caused by endocrine derangements such as hypothyroidism, adrenal insufficiency, and syndrome of inappropriate antidiuretic hormone (SIADH).

Further diagnostic work-up for the exact etiology of her hyponatremia would likely include serum cortisol, serum TSH, serum osmolarity, urine electrolytes, urine osmolarity, and urine creatinine. However, much of this work-up typically continues after the patient has left the ED.

Treatment of hyponatremia requires assessing whether the patient is symptomatic, characterizing the time-course during which it had developed, and clarifying the underlying etiology. Acute (e.g. developing within 48 hours) severe (Na < 125 mmol/L) hyponatremia has severe complications including altered mental status, hallucinations, seizures, coma, decerebrate posturing, respiratory arrest, and ultimately, death (Berl, 2007). While the available information does not definitively tell us how long the patient’s hyponatremia had been present, the lack of any of these signs/symptoms points towards a more chronic picture. Chronic hyponatremia may cause milder or even no neurologic symptoms (like our patient).

Assessment of time-course and presence (or absence) of symptoms will determine the treatment plan (Berl, 2007). A patient with documented acute (e.g. <48 hours) severe hyponatremia or chronic severe hyponatremia with symptoms, should received 3% hypertonic saline at 2 mL/kg/hr and IV furosemide, with a goal of 2 mmol/L/hr increase in serum sodium (Berl, 2007). Spasovski et. al describes alternative dosing regimens for treatment of symptomatic severe hyponatremia.  Patients may require ICU level of care for monitoring and administration of hypertonic saline (Berl, 2007).

 

A patient with an unclear time-course and moderate symptoms (symptoms not including coma or seizures) should get 0.9% saline with IV furosemide, with a goal of 0.5-2 mmol/L/hr increase and a goal of 8-10 mmol/L increase in serum sodium in the first 24 hours (Berl, 2007). Alternatively, the patient may receive a single bolus of 2 mL/kg 3% hypertonic saline over 20 minutes, cause-specific therapy, and discontinuation of any inciting factors (Spasovski, 2014).

An asymptomatic patient should have fluid restriction with dietary salt or urea (at 0.25-0.5 g/kg). Use of ADH antagonists is controversial, and based on 2014 European guidelines, it is not recommended due to the fear that it may increase the rate of sodium correction (via free water excretion) beyond a safe level (Spasovski, 2014).

In the event of overcorrection of serum sodium (e.g. a rise in >10 mmol/L during the first 24 hours, or >8 mmol/L in any 24 hour period afterwards), the saline treatment should be discontinued, and the prospect of starting D5W at 10 mL/kg over 1 hour should be discussed (Spasovski, 2014).

 

Fluid restriction would be appropriate for treatment of our asymptomatic patient’s hyponatremia. However, this creates a dilemma because she also has an AKI (suggested by the fact that her creatinine is downtrending after the initial 2L bolus). As such, it may also be reasonable to give 0.9% saline as detailed above, withholding the furosemide (which would counteract the goal of increasing her intravascular volume). The key is to avoid over-correction as it can cause Osmotic Demyelination Syndrome.

What is the ultimate disposition for this patient?

Ultimately the disposition depends on the treatment plan. Continuous administration of 3% hypertonic saline would likely require placement of a central line and close observation that would only be possible in an ICU. If treatment is fluid restriction, then a stepdown unit (as we have at UHB) would be appropriate as it would allow for closer observation than a floor bed, in case the patient then develops the significant symptoms of hyponatremia.

 

Clinical Course

This patient was admitted to the stepdown unit and initially treated with maintenance normal saline.  After approximately 12 hours, her sodium decreased to 114 (corrected). Her treatment was switched to fluid restriction and oral salt, and her home insulin regimen was restarted. The Department of Health reported that she had drug-susceptible TB and corroborated that she had completed antimycobacterial therapy. Urine AFBs were negative. Urine studies were indicative of a pre-renal etiology behind her AKI, and ruled out renal sodium loss as the etiology behind her hyponatremia. Renal, Hematology/Oncology, and Infectious Diseases were consulted. Her hyponatremia was attributed to SIADH; her leukocytosis/bandemia and initial hemodynamic instability was attributed to sepsis. Urine and blood cultures ended up growing ESBL E. coli, and her antibiotics were switched to IV meropenem. After approximately 48 hours of fluid restriction and oral salt, the serum sodium increased to 120 mmol/L (corrected). Maintenance fluid was restarted and oral salt continued, and after one week, the sodium was 130 mmol/L and remained stable until discharge.

The patient experienced dramatic improvement in her urine output during her hospitalization, and an abdominal ultrasound done prior to discharge demonstrated marked reduction (but not resolution) of her ascites. There were 24-hour intervals during which maintenance fluids were discontinued, but it was quickly restarted after the patient experienced a rise in her creatinine. Eventually, her serum creatinine decreased and remained stable at 1.5. The patient was discharged home after completion of her antibiotic course.

Unfortunately, the ultimate etiology behind the patient’s enlarged kidneys, organomegaly, and ascites was never fully elucidated during her hospitalization. Therefore, the patient was discharged with follow up appointments with gynecology (for further characterization of her large bulky uterus), nephrology (for possible biopsy of her massively enlarged kidneys), and hepatology (for her hepatomegaly and ascites).

Thanks to our respondents!  Stay tuned for the next installment of Case of the Month!

 

References:

https://www.cdc.gov/tb/publications/factsheets/prevention/ichcs.htm

Berl, D. E. (2007). The Syndrome of Inappropriate Antidiuresis. New England Journal of Medicine, 1064-1072.

Nahid, D. A. (2016). Official American Thoracic Society/CDC/IDSA Clinical Practice Guidelines: Treatment of Drug-Susceptible Tuberculosis. Clinical Infectious Diseases, e147-e195.

Spasovski, V. (2014). Clinical Practice Guidelines on Diagnosis and Treatment of Hyponatraemia. Nephrology Dialysis Transplantation, 1-39.

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Case of the Month – July 2017

 

After a two-month hiatus, Case of the Month returns!

Get your thinking caps on for July’s Edition…

 

The patient is a 50-year-old woman with a previous history of type II diabetes, and recently completed a 6-month course of treatment for tuberculosis, presenting with 5-6 days of worsening lower abdominal pain, back pain, nausea, non-bloody non-bilious emesis, and anorexia. She is adamant about compliance with her insulin regimen. She notes 40-lb. weight loss over the past year but denies any cough or night sweats. She has no fevers/chills, change in bowel habits, recent travel, or CP/SOB. She was placed on observation one month ago for hyperglycemia and vomiting and was discharged after 1 day.

No known drug allergies

Meds:

Insulin glargine 14U every night

Insulin aspart 5U three times daily with meals

PMH/PSH: No history of abdominal surgeries

SH: Denies toxic habits; works for the police department

Physical Exam:

VS: T 98.6 HR 111 RR 18 BP 99/54 SaO2 100% (room air)

General: Uncomfortable woman lying in stretcher

HEENT: No conjunctival pallor or scleral icterus, slightly dry mucous membranes

CV: Tachycardia; normal S1S2; no murmurs, rubs, or gallops

Pulm: Clear to auscultation bilaterally; no wheezes, rales, rhonchi or crackles

Abd: Soft, diffusely tender to palpation, most pronounced in RLQ without rebound or guarding; bilateral CVA tenderness.

Ext: No C/C/E

Skin: No changes noted on limbs, trunk, palms, or soles

 

ECG: Sinus Tachycardia, no other abnormalities

Labs:

CBC:

46.22>12.1|37.2<125 (11% bands)

CMP:

Na 116 K 5.2 Cl 79 CO2 20 BUN 88 Cr 3.23 Calcium 8.4 Glucose 526

Protein 5.8 Albumin 2.77 AST 10 ALT 14 Alk Phos 145 Bili 0.8

Lipase 35

Acetone negative

VBG pH:7.37 Lactate 1.9 Na 108

Troponins negative

Urinalysis: Large leukocyte esterase, >500 Glucose

Urine culture: pending

 

Imaging

CT Abdomen/Pelvis: Massively enlarged kidneys, hepatomegaly, large bulky uterus, ascites

CXR: No airspace opacity

 

You give 2L NS, 4 mg morphine, regular insulin 10U, antibiotics

After a couple of hours, your patient’s vitals are:

HR 106 BP 150/99 RR 20 SaO2 100%

A repeat VBG after the 2L bolus shows sodium of 107, glucose 435, Cr 2.89.

 

So…

  • What is your differential diagnosis for the patient’s presenting chief complaint?
  • What antibiotics would you choose?
  • Does this patient need to be on isolation?
  • How would you characterize the sodium disturbances, both on initial presentation, and after the initial interventions? How would you address it?
  • What is the ultimate disposition for this patient?

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Case of the Month April 2017 – Answer

Both of this month’s responses hit the diagnosis square on the head: Dr. Schnitzer’s succinct reply with the differential, work-up, and disposition, and Dr. Hernandez’s expanded (and entertaining) discussion.

Click here to review the case.

A quick recap:

A 15 year-old boy presents with chest pain, decreased oral intake, cough, and fatigue in the setting of a recent upper respiratory infection. He is found to be febrile, tachycardic, and in respiratory distress on exam. Labs show leukocytosis; ECG demonstrates decreased voltage, and CXR with bilateral pleural effusions.

 

What is in the differential diagnosis?  What diagnosis is most likely and which is less likely?

The chest pain, shortness of breath, fatigue (worsening dyspnea?) with exertion, and the time-course are all clues that he is suffering from symptoms of acute heart failure. The presence of sinus tachycardia and low voltage QRS complexes are also additional clues. In a pediatric patient, this raises the possibility of a structural or congenital heart defect, idiopathic dilated cardiomyopathy, or an intrinsic cardiac infection such as myocarditis, endocarditis, and pericarditis. However, as Drs. Schnitzer and Hernandez noted, he could be suffering from Rheumatic fever, or, as Dr. Schnitzer’s work-up correctly alluded to, his symptoms could be a result of severe sepsis from an alternate infection

The key here is to always have a high index of suspicion. This case had several clues pointing towards acute heart failure, but patients can present with such non-specific symptoms as fever, lethargy, decreased PO intake, lethargy, pallor, dyspnea, chest pain, or even abdominal pain. Given how non-specific the symptoms can be, myocarditis is often initially misdiagnosed and may require numerous evaluations by a healthcare provider before being definitively identified. Ultimately, myocarditis is a clinical diagnosis and then is either supported or refuted by additional testing.

 

What further tests would you do?

In the ED, laboratory tests like cardiac enzymes and BNP may be helpful with differentiating myocarditis from dilated cardiomyopathy. But, troponin T only has a sensitivity of 71% for myocarditis in pediatric patients with limited data supporting a cut-off of 0.052 ng/mL.2

A bedside echo can be helpful with characterizing the contractility, the presence or absence of wall motion abnormalities, or valvular dysfunction, though again, there are no echocardiographic findings that are specific to myocarditis.

However, the greatest utility of the echo is the differentiation between acute and fulminant myocarditis. In acute myocarditis, the patient will demonstrate decreased wall motion and EF; in fulminant myocarditis (often with symptoms of cardiogenic shock), the left ventricle will demonstrate normal diastolic dimensions and increased septal thickness. Differentiating between the two may confer some prognostic value; counterintuitively, patients with fulminant myocarditis have better long-term prognosis. This may be due to their presentation being more obvious, so that they receive more rapid/aggressive care.

Obviously, sending autoimmune markers and anti-Streptolysin O could clue you in as to the etiology of the patient’s myocarditis, and blood cultures would clue you in to whether or not the patient’s symptoms are simply due to severe sepsis, but these won’t come back while he is in the ED.

According to the textbooks, the gold standard for diagnosis is still an endomyocardial biopsy, but this is beyond ED management and can produce false negatives if the biopsied portion does not happen to be inflamed. Cardiac MRI has been shown to increase the sensitivity of a biopsy when used as an adjunct to identify areas of inflammation to guide the biopsy.

 

What is your therapeutic plan?

The same as the therapeutic plan for every patient: ABCs, IV, O2 (for hypoxemia), monitor….

Seriously though, the key is to treat any dysrhythmias and provide cardiac support. Medications may include inotropic/vasopressor agents and general heart failure medications (diuretics, aldosterone inhibitors, afterload reducing agents). Until the definitive diagnosis is identified, start broad-spectrum antibiotics to account for severe sepsis. Consider intubation and mechanical ventilation depending on the patient’s clinical picture, as it may reduce his work of breathing and overall metabolic demands. Immunomodulating drugs such as steroids or IVIG have also been tested as adjunctive therapies for myocarditis. A Cochrane review from 2013 demonstrated LVEF improvement with corticosteroid therapy in viral myocarditis, particularly with analysis of a pediatric subgroup, but the trials were deemed low-quality, and results were thus inconclusive. Similarly, the data is limited for the use of IVIG. One study6 involving 46 patients (21 receiving IVIG and 25 controls) suggesting improved survival over 1 year, and another study7 involving 216 patients showed no survival benefit.

 

What is the ultimate disposition for this patient?

At the very least, the patient warrants a cardiac consultation and admission to the PICU, but given the severity of his symptoms, he may ultimately benefit from transferring to a facility with the capability to perform ECMO or cardiac transplantation.

 

References

  1. Allan, Catherine, and David Fulton. “Treatment and Prognosis of Myocarditis in children.”  09 March 2017. Uptodate. Web
  2. Durani, Yamini; Giordano, Katie, and Brett Goudie. “Myocarditis and Pericarditis in Children.” Pediatric Clinics of North America.  57:6, 1281-1303, December 2010
  3. Quiñones, Casandra, and Beth Bubolz. “Cardiac Emergencies.” Fleisher & Ludwig’s Textbook of Pediatric Emergency Medicine. Philadelphia: Lippincott Williams, 2016. 651. Print.
  4. Allen, Catherine, and David Fulton. “Clinical manifestations and diagnosis of myocarditis in children.” Uptodate. N.p., 23 Nov. 2015. Web.
  5. Chen HS, Wang W, Wu SN, Liu JP. “Corticosteroids for viral myocarditis.” Cochrane Database Syst Rev. 2013;
  6. Drucker NA, Colan SD, et Al. “Gamma-globulin treatment of acute myocarditis in the pediatric population.” Circulation. 1994;89(1):252.
  7. Klugman D, Berger JT, et Al. “Pediatric patients hospitalized with myocarditis: a multi-institutional analysis.”  Pediatric Cardiology.  2010; 31(2):222

 

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