Answer

PAINE PANCE Pearl – Endocrine



What are the indications for high-intensity statin therapy for hyperlipidemia?

New joint guidelines were released in 2013 by ACC/AHA on the management of hyperlipidemia.  In these guidelines, there are 3 criteria for high intensity statin therapy:

  1. Age < 75 years with a clinical Atherosclerotic Cardiovascular Disease (ASCVD):
    1. Acute coronary syndrome
    2. Myocardial infarction
    3. Stable or unstable angina
    4. Revascularization procedures
    5. Cerebrovascular disease
    6. Peripheral arterial disease
  2. LDL ≥ 190 mg/dL
  3. Age 40-75 years, with diabetes, LDL 70-189 mg/dL, and 10-year ASCVD risk > 7.5%
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2013 ACC/AHA Hyperlipidemia Guidelines


What are the drugs and dosing for high-intensity statin therapy?

There are only 2 medications that have been studied that are recommended for high-intensity statin therapy:

  1. Atorvastatin 40-80mg daily
  2. Rosuvastatin 20-40mg daily
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2013 ACC/AHA Hyperlipidemia Guidelines

2013-acc-hyperlipidemia-internal-medicine2-e1411205764336

Knowmedge


Reference

  1. Stone NJ, Robinson JG, Lichtenstein AH. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology. 63(25 Pt B):2889-934. 2014. [pubmed]
Wrinkled Parchment Paper

#18 – Benign Prostatic Hyperplasia



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Epidemiology

The prostate begins to enlarge in the 4th decade of life with a significant jump in the 6th decade of life.  Mean prostate weight in normal men < 30yo is around 20g and steadily increases after this.  Volume of the prostate also steadily increases after the 4th decade with symptoms typically starting to manifest once it reaches 30cc3.

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Up-To-Date. 2016


Risk Factors

  • Race
    • African Americans are at higher risk of requiring surgery
    • Asians have the lowest risk of requiring surgery
  • Prostatitis
    • Associated with increased risk of BPH

Pathogenesis of BPH

The main areas of the prostate that contribute to BPH are the periurethral (transitional zone) of the prostate and the hyperplastic nodules that develop are primarily comprised of stromal cells. The specific pathogenesis of BPH is still not completely understood and only 2 variables that have been identified as essential for BPH development: age and functioning Leydig Cells of the testes.  Androgens, estrogens, inflammation, genetics, and stromal growth factors have all been studied and have variable results.

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De Marzo. 2007.

 


Clinical Manifestations of BPH

The signs of symptoms of BPH can be broken down into 3 main categories:

  • Storage Symptoms
    • Urgency
    • Daytime frequency
    • Nocturia
    • Urgency incontinence
  • Voiding Symptoms
    • Slow, urinary stream
    • Splitting or spraying of the urinary stream
    • Intermittent urinary stream
    • Urinary hesitancy
    • Straining to void
    • Terminal dribbling
  • Post-micturition Symptoms
    • Incomplete bladder voiding
    • Post micturition dribble

Differential Diagnosis of BPH Symptoms

  • Urethral stricture or bladder neck contracture
    • Previous history of catheterization or instrumentation
    • Urethral trauma
    • Urethritis
  • Neurogenic bladder
    • Other signs and symptoms of neurologic disease
  • Bladder calculi
    • History of nephrolithiasis
  • Carcinoma of the bladder or prostate
    • Hematuria
    • Previous history of cancer
  • Urinary tract infection and prostatitis
    • Dysuria
    • Fever
  • Medications
    • Antcholinergics (decreases bladder function)
    • Sympathomimetics (increases outflow resistance)

International Prostate Symptom Score

The original AUA score was developed in 1992 and is used to assess the severity of symptoms of BPH, BUT NOT FOR DIFFERENTIAL DIAGNOSIS.  This is a seven-part questionnaire that evaluates symptoms on a 0-5 scale and then calculates the symptoms as mild, moderate, or severe.  An eight question was added to evaluate quality of life.

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International Prostate Symptom Score


Work-Up

  • Physical Exam
    • Digital Rectal Exam (DRE) should be performed to assess size, contour, regularity, and nodularity
    •  

  • Laboratory Testing
    • Urinalysis
      • Initial test to evaluate for microscopic hematuria and infection
    • Basic Metabolic Profile
      • BUN/Creatinine
        • Evaluate baseline renal function
      • Serum Prostate Specific Antigen (PSA)
        • PSA and prostate volume have a log-linear relationship
        • DOES NOT CORRELATE WITH CANCER
        • picture1
    • Uroflowmetry Study
      • Optional testing per AUA
      • Can evaluate maximal urinary flow rate
      • Patient voids with a full bladder (> 150cc)
      • < 15ml/s = outflow obstruction
      • picture1
      • picture1
    • Post-void Residual Urine Volume
      • Bladder scan is least invasive and most common
      • Normal men have < 12mL of residual urine post-void
      • picture1

Management

BPH can be managed by PCP if the patient has mild symptoms (low IPSS ≤ 7) and no complications.

Indications for urology referral are:

  • Symptoms with autonomic or peripheral neuropathy
  • Symptoms following invasive treatment of the urethra or prostate
  • Age < 45yo
  • Abnormality of prostate on DRE
  • Presence of hematuria in the absence of infection
  • Incontinence
  • Severe symptoms (IPSS ≥ 20)

Treatment

  • Medical
    • Alpha-1-adrenergic antagonists
      • Mechanism of Action
        • Relax smooth muscle of bladder neck, prostate capsule, and prostatic urethra
      • Side effects
        • Hypotension
      • Drugs
        • Terazosin (need to titrate)
        • Doxazosin (need to titrate)
        • Tamsulosin
    • 5-alpha-reductase inhibitors
      • Used if patients can’t tolerate hypotension of alpha-1-adrenergic antagonists
      • Need 6-12 months of treatment to see effects
      • Mechanism of Action
        • Reduce prostate size by preventing the conversion of testosterone to the more potent dihydrotestosterone
      • Drugs (no difference due to EPICS trial)
        • Finasteride
        • Dutasteride
    • Combination Alpha-1/5-Alpha Therapy
      • Indications
        • Severe symptoms (IPSS ≥ 20)
        • Large prostate (> 40cc)
        • Inadequate response to maximal monotherapy
      • Drugs
        • Doxazosin/finasteride
        • Tamsulosin/dutasteride
  • Surgical
    • Indications
      • Moderate/severe symptoms (IPSS ≥ 8) with high quality of life score (≥ 4)
      • Urinary retention refractory to medical therapy
      • Renal insufficiency secondary to BPH
      • Median lobe hypertrophy
    • Transurethral Procedures

Complications of Surgery

  • Bleeding
    • Higher in traditional TURP
  • Postprostatectomy Syndrome
    • Hyponatremia as a result of the systemic absorption of the hypotonic irrigation solution
  • Sexual Dysfunction
    • Ejaculatory Dysfunction
    • Erectile Dysfunction
  • Urethral Stricture
  • Urinary Incontinence

Cottage Physician

cottage-physician


References

  1. Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with age. The Journal of Urology. 1984;132(3):474-9. [pubmed]
  2. Bosch JL, Hop WC, Kirkels WJ, Schröder FH. Natural history of benign prostatic hyperplasia: appropriate case definition and estimation of its prevalence in the community. Urology. 1995;46(3 Suppl A):34-40. [pubmed]
  3. Sidney S, Quesenberry CP, Sadler MC, Guess HA, Lydick EG, Cattolica EV. Incidence of surgically treated benign prostatic hypertrophy and of prostate cancer among blacks and whites in a prepaid health care plan. American Journal of Epidemiology. 1991;134(8):825-9. [pubmed]
  4. Kang D, Andriole GL, Van De Vooren RC. Risk behaviours and benign prostatic hyperplasia. BJU International. 2004;93(9):1241-5. [pubmed]
  5. St Sauver JL, Jacobson DJ, McGree ME, Girman CJ, Lieber MM, Jacobsen SJ. Longitudinal association between prostatitis and development of benign prostatic hyperplasia. Urology. 2008;71(3):475-9; discussion 479. [pubmed]
  6. Rohr HP, Bartsch G. Human benign prostatic hyperplasia: a stromal disease? New perspectives by quantitative morphology. Urology. 1980;16(6):625-33. [pubmed]
  7. De Marzo AM, Platz EA, Sutcliffe S. Inflammation in prostate carcinogenesis. Nature Reviews. Cancer. 2007;7(4):256-69. [pubmed]
  8. Jones C, Hill J, Chapple C, . Management of lower urinary tract symptoms in men: summary of NICE guidance. BMJ (Clinical research ed.). 2010;340:c2354. [pubmed]
  9. Barry MJ, Fowler FJ, O’Leary MP. The American Urological Association symptom index for benign prostatic hyperplasia. The Measurement Committee of the American Urological Association. The Journal of Urology. 1992;148(5):1549-57; discussion 1564. [pubmed]
  10. McVary KT, Roehrborn CG, Avins AL. Update on AUA guideline on the management of benign prostatic hyperplasia. The Journal of Urology. 2011;185(5):1793-803. [pubmed]
  11. Roehrborn CG. The utility of serum prostatic-specific antigen in the management of men with benign prostatic hyperplasia. International Journal of Impotence Research. 2008;20 Suppl 3:S19-26. [pubmed]
  12. Oelke M, Bachmann A, Descazeaud A. EAU guidelines on the treatment and follow-up of non-neurogenic male lower urinary tract symptoms including benign prostatic obstruction. European Urology. 2013;64(1):118-40. [pubmed]
  13. Chapple CR. Pharmacological therapy of benign prostatic hyperplasia/lower urinary tract symptoms: an overview for the practicing clinician. BJU International. 2004;94(5):738-44. [pubmed]
  14. McVary KT, Roehrborn CG, Avins AL. Update on AUA guideline on the management of benign prostatic hyperplasia. The Journal of Urology. 2011;185(5):1793-803. [pubmed]
  15. Nickel JC, Gilling P, Tammela TL, Morrill B, Wilson TH, Rittmaster RS. Comparison of dutasteride and finasteride for treating benign prostatic hyperplasia: the Enlarged Prostate International Comparator Study (EPICS). BJU International. 2011;108(3):388-94. [pubmed]
  16. McConnell JD, Roehrborn CG, Bautista OM. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. NEJM. 2003;349(25):2387-98. [pubmed]
  17. Roehrborn CG, Siami P, Barkin J. The effects of combination therapy with dutasteride and tamsulosin on clinical outcomes in men with symptomatic benign prostatic hyperplasia: 4-year results from the CombAT study. European Urology. 2010;57(1):123-31. [pubmed]
  18. The Urology Book. urologybook.com. Accessed September 12, 2016.
  19. Gómez Sancha F, Bachmann A, Choi BB, Tabatabaei S, Muir GH. Photoselective vaporization of the prostate (GreenLight PV): lessons learnt after 3500 procedures. Prostate Cancer and Prostatic Diseases. 2007;10(4):316-22. [pubmed]

 

Answer Image

Answer to Genitourinary Question

22yo male presents to emergency department with a 2-hour history of increasingly intense testicular pain.  He reports being sexually active with multiple partners and intermittent condom use.  He is a very active person and completed a triathlon the day before presentation.  He denies dysuria, urethral discharge, or flank pain, but did have an episode of vomiting prior to arrival.  He is in visible distress and can not seem to get comfortable.  Evaluation of the scrotum reveals a tender, swollen left testicle.

  1. What are some bedside maneuvers you can perform to help with the differential?
    1. Epididymitis
      1. Point tenderness over the superior aspect of the testicle
      2. (+) Prehn Sign
        1. Manual elevation of the testicle improves pain
    2. Testicular Torsion
      1. High-riding and/or horizontal lie of testicle (“Bell Clapper Deformity)
      2. PMC2791735_wjem-10-281f2
      3. Absent cremesteric reflex
        1. Normal = pinching/stroking the thigh causes ipsilateral elevation of testicle
      4. (-) Prehn Sign
    3. Torsion of Appendix Testes
      1. More common in children
      2. 5940956_m
      3. (+) Blue Dot Sign
      4. Fig-1-'Blue-dot'-sign-in-patients-with-a-left-torted-hydatid-or-Mor-gagni

 

  1. What should be the initial management of this patient?
    1. If suspected epididymitis:
      1. Urinalysis, urine culture, and gonorrhea/chlamydia testing
      2. Antibiotics are directed towards:
        1. C. trachomatis or N. gonorrhoeae
          1. Ceftriaxone 250mg IM and doxycycline 100mg PO BID x 10 days
        2. Gram-negative enteric pathogens
          1. Levofloxacin 500mg PO daily x 10 days
    2. If suspected testicular torsion:
      1. Manual detorsion may be attempted
        1. 2/3 torse medially and detorsion is performed by rotating testicle outwards laterally
      2. Ultrasound may be performed if immediately available (this should not delay surgical consult or evaluation)
        1.  

        2.  

      3.  Surgical evaluation and management is the preferred initial management of patients with suspected testicular torsion
    3. If suspected torsion of appendix testes:
      1. Ultrasound is performed to rule-out other pathologies.
      2. Management is conservative with rest, ice, and NSAIDs.
      3. Surgical removal may be required if pain does not improve with conservative management.

 

Testicular Torision


References

  1. Tracy CR, Steers WD, Costabile R. Diagnosis and management of epididymitis. The Urologic Clinics of North America. 35(1):101-8; vii. 2008. [pubmed]
  2. Galejs LE. Diagnosis and treatment of the acute scrotum. American Family Physician. 59(4):817-24. 1999. [pubmed]
  3. Workowski KA, Bolan GA, . Sexually transmitted diseases treatment guidelines, 2015. MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports / Centers for Disease Control. 64(RR-03):1-137. 2015. [pubmed]
  4. Sessions AE, Rabinowitz R, Hulbert WC, Goldstein MM, Mevorach RA. Testicular torsion: direction, degree, duration and disinformation. The Journal of Urology. 169(2):663-5. 2003. [pubmed]
  5. Palestro CJ, Manor EP, Kim CK, Goldsmith SJ. Torsion of a testicular appendage in an adult male. Clinical Nuclear Medicine. 15(7):515-6. 1990. [pubmed]
question

Genitourinary Question

22yo male presents to emergency department with a 2-hour history of increasingly intense testicular pain.  He reports being sexually active with multiple partners and intermittent condom use.  He is a very active person and completed a triathlon the day before presentation.  He denies dysuria, urethral discharge, or flank pain, but did have an episode of vomiting prior to arrival.  He is in visible distress and can not seem to get comfortable.  Evaluation of the scrotum reveals a tender, swollen left testicle.

 

  1. What are some bedside maneuvers you can perform to help with the differential?
  2. What should be the initial management of this patient?

 

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Answer Image

Answer to Critical Care Question



This patient is ready for extubation.  Everyone has their own magic numbers they want to see on the vent before they think about extubating a patient, but mine are:

  • Pressure support mode
    • every breath is initiated by the patient and only supported by the vent
  • Pressure support ≤ 8 cmH2O
    • This will be enough support to overcome the resistance in the circuit.
  • PEEP ≤ 7 cmH2O
    • Physiologic PEEP of the epiglottis is 5 cmH2O
  • FiO2 ≤ 40%
    • No more supplemental oxygen than what would be given via nasal cannula or open face mask
  • Stable ABG on these settings for at least 2 hours
  • A&Ox3 and following commands
    • Patients need to be able to participate in pulmonary toilet after the tube comes out

These are basic principles and there are many variables that go into deciding to extubate a patient.  LITFL does a great review here and goes through a very systematic approach.

Once this is all good, then you can perform a few bedside tests or measurements that can help predict success of extubation.

  1. Rapid Shallow Breathing Index (RSBI)
    • Respiratory Rate / Vt (L)
    • < 105 predicts successful extubation
  2. Negative Inspiratory Force (NIF)
    • Measurement of the maximal inspiratory pressure
    • This is a great measurement of a patient’s ability to generate an adequate tidal volume once extubated.
    • > -20 cmH2O predicts successful extubation

Prediction of Successful Extubation. The ICU Book.

Prediction of Successful Extubation. The ICU Book.



Great post from Intensive Blog on “The Art and Science of Extubation



References

  1. http://lifeinthefastlane.com/ccc/spontaneous-breathing-trial/
  2. http://lifeinthefastlane.com/ccc/extubation-assessment/
  3. Fadaii, A.  Assessment of rapid shallow breathing index as predictor for weaning in a respiratory care unit.  Tanaffos.  2012;11(3):28-31.
  4. Yang KL, Tobin MJ. A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. N Engl J Med. 1991;324(21):1445–50. [PubMed]
index

#17 – Shock





Definition and Cellular Physiology of Shock

The definition of shock is a clinical state of cellular and tissue hypoxia/perfusion due to:

  1. Reduced oxygen delivery
  2. Increased oxygen consumption
  3. Inadequate oxygen utilization

It basically comes down to the ratio between oxygen delivery (DO2) and oxygen extraction (VO2).

Extraction Ratio (ER)

Extraction Ratio (ER)

Deranged Physiology

Deranged Physiology

Components of Oxygen Delivery

 

At the cellular level, shock hypoxemia causes cell membrane dysfunction leading to intracellular edema and leakage, as well inability to regulate cellular pH.  This causes progressive acidemia, which in turn, have severe systemic effects on multiple organ systems.

Kherallah M.

Kherallah M.


Pathophysiology of Shock

 

BP = (HR x SV) x SVR

 

Factors effecting HR:

  • Autonomic regulation
  • Hormones
  • Fitness levels
  • Age
  • Medications

Factors effecting SV:

  • Preload
  • Contractility
  • Afterload

Factors effecting SVR:

  • Vessel length
  • Vessel diameter
  • Blood viscosity

Signs and Symptoms of Shock

As perfusion decreases and hypoxia starts, the body begins to compensate and the signs and symptoms of shock are generally a result of this compensation.

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Classifications and Causes of Shock

UpToDate

UpToDate


How to Diagnose Shock

Laboratory studies should be performed very early in the screening process for a patient with suspected shock as it will help you determine the degree of end organ perfusion.  These include:

  • Lactate (> 2 mmol/L)
  • Creatinine
  • LFTs
  • ABG or VBG

 

There has been a tremendous amount of advancement in the diagnosis and management of patients in acute shock.  For years, the pulmonary artery catheter was the gold standard for critically ill patients admitted to the ICU.  It allowed for serial “measurements” of almost all the hemodynamic parameters you needed (PACWP, CO, CI, SVR, PAP, SvO2), but it was not without serious complications.  It still has it’s place for certain disease management, but it is no longer indicated for diagnosing the different types of shock.  I bring this up only because these parameters can be helpful when learning the different shock states as you can focus on 3 main variables: PACWP, CO/CI, and SVR.

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Point-of-Care ultrasonography (POCUS) has really become the test of choice for an undifferentiated shock patient, as it provides fast, vital information of the different causes of shock and allows for rapid rule-out of life-threatening conditions.  There are several different types of POCUS algorithms used depending on the history and clinical context of the patient.

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Rapid Ultrasound in Shock (RUSH) is used for undifferentiated patients. Scott Weingart does a great podcast on this technique here and Sinae EM Ultrasound did a step-by-step review here.

Picture1

 

Another approach to undifferentiated shock is the Abdominal and Cardiac Evaluation with Sonography (ACES) protocol.  It is used primarily in the UK and a good review can be found here.

ACES Exam

ACES Exam

 

Focus Assessed Transthoracic Echo (FATE) is a more detailed look at the heart to identify specific cardiac abnormalities.

Picture1

 

If you have a trauma patient, you would use the Focused Assessment with Sonography for Trauma (FAST) exam to rapidly identify traumatic causes for hemorrhage and need for operative intervention.

FAST Exam

FAST Exam



Really good paper in Critical Care that reviews echocardiography in shock management

http://ccforum.biomedcentral.com/articles/10.1186/s13054-016-1401-7


Management of Shock

Once you diagnose a patient with a specific type of shock, the management is pretty straight forward.  If the patient is in hypovolemic, distributive, or obstructive shock, IV fluids should be used to improve perfusion and hemodynamics.  The amount depends on the conditions, but usually starting with 1-2L of crystalloids is a good bet and then you can re-evaluate and repeat your ultrasound to look at the effects.  If you have a trauma patient, then blood products should be started early on in the course until definitive control can be performed.

 

If adequate fluid resuscitation has not improved the hemodynamics or clinical picture, then pharmacologic agents are needed to improve perfusion.  These can be broken down into vasopressors (increase vasomotor tone) and inotropes (increase contractility).

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UpToDate


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References

  1. Vincent JL, De Backer D. Circulatory shock. NEJM. 369(18):1726-34. 2013. [pubmed]
  2. Barber AE, Shires GT. Cell damage after shock. New horizons (Baltimore, Md.). 4(2):161-7. 1996. [pubmed]
  3. Deranged Physiology. The Relationship of Venous Oxygenation and Cellular Metabolism. Accessed 08/16/16. http://www.derangedphysiology.com/main/core-topics-intensive-care/arterial-blood-gas-interpretation/Chapter%208.0.1/relationship-venous-oxygenation-and-cellular-metabolism
  4. Kherallah M. Approach and Hemodynamic Evaluation of Shocks.  Accessed 08/16/16. http://slideplayer.com/slide/3900131/
  5. Gaieski DF, Mikkelsen ME. Definition, classification, etiology, and pathophysiology of shcok in adults.  In: UpToDate, Parsons PE (ed), UpToDate, Waltham, MA.  Accesed 08/17/2016. http://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults?source=search_result&search=shock&selectedTitle=1%7E150#H18097167
  6. Shah MR, Hasselblad V, Stevenson LW. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA. 294(13):1664-70. 2005. [pubmed]
  7. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in Shock in the evaluation of the critically lll. Emergency medicine clinics of North America. 28(1):29-56, vii. 2010. [pubmed]
  8. Weingart SD, Duque D, Nelson B. EmCrit Blog.  Rapid Ultrasound for Shock and Hypotension – the RUSH Exam.  Accessed 08/17/16.  http://emcrit.org/rush-exam/
  9. Labovitz AJ, Noble VE, Bierig M. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. Journal of the American Society of Echocardiography. 23(12):1225-30. 2010. [pubmed]
  10. Atkinson PR, McAuley DJ, Kendall RJ. Abdominal and Cardiac Evaluation with Sonography in Shock (ACES): an approach by emergency physicians for the use of ultrasound in patients with undifferentiated hypotension. Emergency medicine journal : EMJ. 26(2):87-91. 2009. [pubmed]
  11. AIUM practice guideline for the performance of the focused assessment with sonography for trauma (FAST) examination. Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine. 33(11):2047-56. 2014. [pubmed]
  12. Gaieski DF, Mikkelsen ME. Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock.  In: UpToDate, Parsons PE (ed), Waltham, MA.  Accessed on 08/17/16.  http://www.uptodate.com/contents/evaluation-of-and-initial-approach-to-the-adult-patient-with-undifferentiated-hypotension-and-shock?source=see_link#H87905481