Case of the Month – October 2017

 

Get your thinking caps ready folks, for it’s time for the newest edition of Case of the Month.

 

The patient is a 28-year-old man with a history of SLE complicated by lupus nephritis, who presents with pressure-like mid-back pain since last night. He experienced no relief with oral naproxen, resulting in his presentation to the emergency department.  His last bowel movement and urination were approximately 8 hours prior to presentation and normal.  He denies any trauma, focal weakness, new numbness or tingling, fevers/chills, N/V, or any bowel or bladder complaints.  He does admit to not taking his lupus medications for about a month.  His only recent travel was to Georgia two months ago and Florida four months ago.  His lupus was discovered when he had nephrotic syndrome as a child, and he has never had a lupus flare, and he has not been on corticosteroids for the last year.

 

No known drug allergies

Medications: hydroxychloroquine 200 mg twice daily, mycophenolate mofetil 1g twice daily

PMH/PSH: As above, pulmonary embolism at age 15; bilateral hip surgery for avascular necrosis secondary to chronic steroids

SH: No toxic habits; denies previous sexual activity

ROS: As per HPI.

 

Physical Exam:

Vitals: T 97.4 (F), HR 63/min RR 22/min BP 127/73 mm Hg, SaO2 100% on room air

General: Young man sitting in bed, in no acute distress

HEENT: Sclera anicteric, no oropharyngeal erythema or exudates, moist mucous membranes

CV: Normal S1S2; no murmurs, rubs, or gallops

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

Abdomen: Soft, mild/diffuse tenderness to palpation, dull to percussion

Rectal exam: Normal, no saddle anesthesia

Back: mild bilateral CVA tenderness

Neuro: CN2-12 intact.  Motor exam 5/5 bilateral upper and lower extremities; no sensory deficit; normal reflexes; no gait abnormality.

 

 

Labs:

Urinalysis: negative leukocyte esterase and nitrates, no WBCs or bacteria on micro

CMP: within normal limits

CBC: WBC 2.78 K/uL Hgb 13.5 g/dL Hct 39.2% Platelets 159 K/uL

 

EKG: Normal sinus rhythm, rate = 61/min

CXR: normal

Lumbar and Sacral Spine X-rays: Questionable L5 spondylolysis

 

After you give the patient APAP/oxycodone 5/325 mg once, he begins to complain of worsening weakness in his lower extremities, and requires assistance to walk to the bathroom. Once there, he finds he is unable to urinate.  A Foley catheter is placed, and he drains approximately 400 mL of urine. You order a CT of his head to rule out an acute stroke or intracranial hemorrhage.  Over the next three hours, the patient becomes unable to move his lower extremities, loses his bilateral patellar reflexes, and develops saddle anesthesia.  You consult neurology who recommend an MRI spine.  Over the following three hours, his paralysis rises to just below his xiphoid process.

 

Imaging

CT Head: No acute process

MRI Thoracic and Lumbar spine: No evidence of herniation, stenosis, or foramen narrowing.  Partially visualized high signal in the spinal cord to the level of the conus medularis which may represent demyelinating or inflammatory process, though primary vs metastatic malignancy cannot be excluded.

 

So…

  • What is your differential diagnosis for this patient?
  • Which, if any, further tests would you perform on this patient?
  • What therapeutic strategy would use for this patient?
  • What is his ultimate disposition? Is there any additional information that you need prior to making this disposition decision?

Good luck!

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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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