#27 – Abnormal Uterine Bleeding – Definitions and Classifications

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History of FIGO

Because of confusing terminology and difficulty in translating to other languages, the International Federation of Obstetrics and Gynecology (FIGO) created a special task force in 2005 charged with clarifying the terminology and classifying the different causes.  This way clinicians, patients, and researchers throughout the world could be talking the same language.  Dysfunctional uterine bleeding (DUB) was replaced by abnormal uterine bleeding (AUB).. They also introduced a classification system to help sub-divide the causes of AUB.

 

But in order to define something as “abnormal”, they needed to define normality, which can obviously be very difficult when incorporating the world’s population. The consensus definitions were then agreed upon in 2015 to include the 5th to 95th percentiles form the available data.

 

The FIGO definition of AUB is any symptomatic variation from normal menstruation, with regards to frequency, regularity, duration, or volume.

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Classifications of Abnormal Uterine Bleeding

In 2011, FIGO created a classification system for the main causes of AUB.  It is broken down into 2 main categories based on whether or not the pathology can be seen on imaging or histopathology.  This also allows for subclassifications due to multiple etiologies.

  • Structural (PALM)
    • Polyps (AUB-P)
    • Adenomyosis (AUB-A)
    • Leiomyomas (AUB-L)
      • Hierarchy of classification
        • Primary
          • Presence or absence
        • Secondary
          • Submucosal
            • Abuts the endometrium or distorts the endometrial cavity
          • Other
            • Subserosal
          • Tertiary
            • 0-8 numbering system based on endometrial or serosal involvement
            • Hybrid (2-5)
              • Submucosal and subserosal
    • Malignancy and hyperplasia (AUB-M)
  • Non-structural (COEIN)
    • Coagulopathy (AUB-C)
      • Most commonly is von Willebrand disease
    • Ovulatory dysfunction (AUB-O)
      • At least one cycle that varies by more than 7 days in 12 months
    • Endometrial (AUB-E)
      • Category of exclusion
    • Iatrogenic (AUB-I)
      • Medications
        • Anticoagulants
        • Hormone therapies
      • IUDs
    • Not otherwise classified (AUB-N)

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Documentation

Very similar to the documentation for an OB patient (TPAL score), the documentation uses the PALM-COEIN scoring system for “simplicity”.  Example:

  • Patient with adenomyosis would be:
    • P0A1L0M0-C0O0E0I0N0
  • Patient with endometrial hyperplasia and a subserosal leiomyoma < 50% intramural would be:
    • P0A0L6M1-C0O0E1I0N0

References

  1. Fraser IS, Critchley HO, Munro MG, Broder M, . A process designed to lead to international agreement on terminologies and definitions used to describe abnormalities of menstrual bleeding. Fertility and Sterility. 2007; 87(3):466-76. [pubmed]
  2. Woolcock JG, Critchley HO, Munro MG, Broder MS, Fraser IS. Review of the confusion in current and historical terminology and definitions for disturbances of menstrual bleeding. Fertility and Sterility. 2008;90(6):2269-80. [pubmed]
  3. Fraser IS, Critchley HO, Munro MG, Broder M. Can we achieve international agreement on terminologies and definitions used to describe abnormalities of menstrual bleeding? Human reproduction (Oxford, England). 2007;22(3):635-43. [pubmed]
  4. Harlow SD, Lin X, Ho MJ. Analysis of menstrual diary data across the reproductive life span applicability of the bipartite model approach and the importance of within-woman variance. Journal of clinical epidemiology. 2000;53(7):722-33. [pubmed]
  5. Fraser IS, Critchley HO, Broder M, Munro MG. The FIGO recommendations on terminologies and definitions for normal and abnormal uterine bleeding. Seminars in reproductive medicine. 2011;29(5):383-90. [pubmed]
  6. Munro MG, Critchley HO, Broder MS, Fraser IS, . FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age. International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics. 2011;113(1):3-13. [pubmed]

Ep-PAINE-nym

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Chadwick Sign

 

Definition – Blue discoloration of the cervix and vaginal mucosa seen in early pregnancy.

Clinical Significance – Due to increased blood flow to support a newly implanted embryo and can be seen 6-8 weeks after conception.

History – Given to James R. Chadwick, an American gynecologist of the late 19th century, after he read a paper before the American Gynecologic Society in 1886, but 1st described by Etienne Jacquemin in 1836.  Dr. Chadwick did give appropriate recognition to Dr. Jacquemin during this presentation.

References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Gleichert JE. Etienne Joseph Jacquemin, discoverer of ‘Chadwick’s sign’. Journal of the history of medicine and allied sciences. 1971;26(1):75-80. [pubmed]

PAINE #PANCE Pearl – Cardiovascular

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82-year-old male, with a history of HTN, HLD, and CAD, presents to your clinic with a six-month history of dyspnea on exertion.  He states he is unable to walk as far as he used when exercising, and when he over exerts himself, he reports having some mild chest pain and feeling lightheaded.  This resolves with rest and he denies any syncope with these events.

 

Medications

Metoprolol 50mg daily

Lisinopril 10mg daily

Simvastatin 30mg daily

 

Vital Signs

BP – 158/97

HR – 62

RR – 13

O2% – 100%

 

Physical exam

General – WN/WD male in NAD

Pulmonary – CTA without adventitial breath sounds

CV – Soft S2 with murmur over right 2nd intercostal space

PV – carotid pulse is weak and has a slow rise, murmur is appreciated

Neuro – No focal deficits

 

EKG

lvh

 

This patient has aortic stenosis.  The suggestive parts of the H&P are:

  • History
    • The classic triad of aortic stenosis is chest pain, dyspnea, and syncope.
  • Aortic stenosis increases in prevalence with age
  • Cardiac Auscultation
    • Soft, single S2 since A2, which is due to aortic valve closure, is delayed and occurs with P2
    • Murmur
      • Systolic ejection murmur best heard over the right 2nd intercostal space
      • medicosnotes_heart-sounds-and-murmur-in-aortic-stenosis
      • Begins on S1 and ends before S2
      • May radiate to the carotids
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  • Peripheral Vascular
    • Carotid Palpation
    • Pulsus Parvus et Tardus (weak and late)
    • pulse-jvp-12-638
  • EKG
    • Shows LVH and strain pattern in precordial leads
  1. What is the next step in the management of this patient?
    1. Transthoracic echocardiography
  2. After the next step, what important variables must you specifically assess?
    1. Valvular anatomy and size
      1. Aortic valve surface area
    2. Valve hemodynamics
      1. Transvavular aortic velocity
      2. Mean transvalvular pressure
    3. LV size and ejection fraction
    4. Pulmonary artery pressure
    5. Other concomitant conditions

 

These variables will help with staging the severity of the stenosis, as well as determine need for operative intervention.

Ep-PAINE-nym

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Bainbridge Reflex

 

Other known aliases – Atrial Reflex

Definition – Compensatory increase in heart rate caused by a rise in right atrial pressure.  Opposite of carotid baroreceptors.

Clinical Significance – Respiratory sinus arrythmia.  Inspiration causes increased venous return.

History – Described by Francis Arthur Bainbridge in 1915

References

  1. Hakumäki MO. Seventy years of the Bainbridge reflex. Acta physiologica Scandinavica. 1987;130(2):177-85. [pubmed]
  2. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  3. http://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/bainbridge-reflex

PAINE #PANCE Pearl – Cardiovascular

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82-year-old male, with a history of HTN, HLD, and CAD, presents to your clinic with a six-month history of dyspnea on exertion.  He states he is unable to walk as far as he used when exercising, and when he over exerts himself, he reports having some mild chest pain and feeling lightheaded.  This resolves with rest and he denies any syncope with these events.

 

Medications

Metoprolol 50mg daily

Lisinopril 10mg daily

Simvastatin 30mg daily

 

Vital Signs

BP – 158/97

HR – 62

RR – 13

O2% – 100%

 

Physical exam

General – WN/WD male in NAD

Pulmonary – CTA without adventitial breath sounds

CV – Soft S2 with murmur over right 2nd intercostal space

PV – carotid pulse is weak and has a slow rise, murmur is appreciated

Neuro – No focal deficits

 

EKG

lvh

Questions

  1. What is the next step in the management of this patient?
  2. After the next step, what important variables must you specifically assess?

#26 – Pericardial Effusion and Cardiac Tamponade

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Anatomy

The pericardium consists of a double-layered semi-elastic sac that holds the heart in the mediastinum.  Basically, so the heart doesn’t flop around inside the thoracic cavity.  There should be a small amount of fluid (15-50mL) present to prevent adhesion of the pericardial sac to the heart.  It is then termed an effusion when it is more than the normal amount.  How much quantifies an effusion?  Doesn’t matter…. what does matter is how fast that fluid develops.  Because the pericardium is semi-elastic, it can accommodate and stretch over time if the accumulation is slow.  This would lead to a greater volume of fluid before symptoms occur.  If the fluid accumulates rapidly, less volume can produce profound effects due to the restrictive nature of the fibrous pericardium.

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Etiology

  • Infectious
    • Viral
    • Bacterial
    • Fungal
    • Parasitic
  • Non-infectious
    • Neoplastic
    • Autoimmune/inflammatory
    • Trauma
    • Cardiac
    • Radiation
    • Metabolic

Signs and Symptoms

There are no reliable historical clues or physical exam findings that are specific to pericardial effusions.  They are helpful, though, to sort out the cause of the effusion. Common findings include:

  • Fever
  • Dyspnea
  • Chest pain
  • Tachycardia
  • JVD
  • Hepatomegaly
  • Pulsus paradoxus
  • Ewart’s Sign
    • Dullness to percussion, egophony, and bronchial breath sounds over the inferior angle of the left scapula
  • Beck’s Triad
    • Hypotension
    • JVD
    • Muffled heart tones

Work-Up

  • EKG
  • Chest X-ray
    • Small effusions are generally not appreciated on radiography
    • Larger, chronic effusions may appear as an enlarged cardiac silhouette classically referred to as a “Water bottle heart”

    • pericardial-effusion-water-bottle-sign-1

      Radiopaedia

  • Echocardiogram
    • Looking for anechoic stripe around the heart
    • 2D Apical 4-chamber is my view of choice
    • Severity can also be assessed by looking for:
      • RV collapse during diastole
      • LV collapse with increased EF
      • IVC dilation and loss of respiratory variations

    •  

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Treatment

  • Pericardiocentesis with catheter placement

    •  

    • Three-way stopcock is used to measure pericardial pressure
    • Fluid is then sequentially removed and pressure re-measured until < 5mmHg during inspiration

    •  

  • Open surgical drainage via pericardial window if:
    • Fluid accumulates after catheter drainage
    • Effusion is loculated
    • Need for biopsy
    • Patient has coagulopathy

    •  

    •  

References

  1. Braunwald E. Pericardial Disease. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 19e. New York, NY: McGraw-Hill; 2015. http://accessmedicine.mhmedical.com/content.aspx?bookid=1130&Sectionid=79743215. Accessed January 12, 2017.
  2. Imazio M. Contemporary management of pericardial diseases. Current Opinion in Cardiology. 2012;27(3):308-17. [pubmed]
  3. Levy PY, Corey R, Berger P. Etiologic diagnosis of 204 pericardial effusions. Medicine. 2003;82(6):385-91. [pubmed]
  4. Permanyer-Miralda G. Acute pericardial disease: approach to the aetiologic diagnosis. Heart (British Cardiac Society). 2004;90(3):252-4. [pubmed]
  5. Bruch C, Schmermund A, Dagres N. Changes in QRS voltage in cardiac tamponade and pericardial effusion: reversibility after pericardiocentesis and after anti-inflammatory drug treatment. Journal of the American College of Cardiology. 2001;38(1):219-26. [pubmed]
  6. Sternbach G. Claude Beck: cardiac compression triads. The Journal of Emergency Medicine. 1989;6(5):417-9. [pubmed]
  7. Stanford University. Tamponade. Echocardiography in ICU. https://web.stanford.edu/group/ccm_echocardio/cgi-bin/mediawiki/index.php/Tamponade.
  8. Adler Y, Charron P, Imazio M. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal. 2015;36(42):2921-64. [pubmed]
  9. Gumrukcuoglu HA, Odabasi D, Akdag S, Ekim H. Management of Cardiac Tamponade: A Comperative Study between Echo-Guided Pericardiocentesis and Surgery-A Report of 100 Patients. Cardiology Research and Practice. 2011:197838. [pubmed]

PAINE #PANCE Pearl – Cardiovascular

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Question

What are the 3 eponymous physical exam findings in patients with bacterial endocarditis and who were they named after?

Answers

Osler Nodes

  • Painful, erythematous nodules of the hands and feet
  • Named after Sir William Osler in 1908.

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Janeway Lesions

  • Nontender, erythematous or hemorrhagic macular or nodular lesions on the palms or soles
  • Named after Theodore Caldwell Janeway in the late 1800s.

janeway-lesion-1

Roth Spots

  • Retinal hemorrhages with white or pale centers.
  • Named after Swiss pathologist Mortiz Roth in 1872

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References

  1. Osler W.  Chronic Infectious Endocarditis.  Quarterly Journal of Medicine.  1908;2:219-230.
  2. Ruiz-García J, Canal-Fontcuberta I. Diagnosis of Active Infective Endocarditis from Examination of the Toes and Soles. The American Journal of Cardiology. 2016;118(7):1094. [pubmed]
  3. Khanna N, Roy A, Bahl VK. Janeway lesions: an old sign revisited. Circulation. 2013;127(7):861. [pubmed]
  4. Sethi K, Buckley J, de Wolff J. Splinter haemorrhages, Osler’s nodes, Janeway lesions and Roth spots: the peripheral stigmata of endocarditis. British Journal of Hospital Medicine. 2013;74(9):C139-42. [pubmed]

#25 – Scabies

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Vector

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Sarcoptes scabiei

Scabies is caused by the mite Sarcoptes scabiei, which is a whitish-brown, eight-legged mite and it just barely visible by the naked eye at its largest size of 0.4×0.3mm.  Only the female mite causes the dermatologic manifestations seen in scabies, as it burrows into the epidermis down to the stratum granulosum layer to lay her eggs.

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The female mite can grow these burrows up to 2mm per day and lay 2-3 eggs, up to a total of 10-25 eggs.  These eggs hatch after 3-4 days, molt multiple times, and burrow to the surface to mate and then return to continue this viscous cycle.  Typically, incubation takes 3-6 weeks after infestations until symptoms present.

Transmission

Scabies are transmitted from direct contact with an infected person and most commonly is sexually acquired.  Although not as common, transmission has also been reported to occur through contaminated clothing or bedding as these mites can survive off a host for up to 24-36 hours.  Animals can contract scabies, but these rarely cause disease in humans, as they do not reproduce on human hosts.

Risk Factors

  • Colder temperatures
  • Higher humidity
  • Crowded areas with close contact

Signs and Symptoms

The typically manifestation of scabies is an intensely pruritic rash that is worse at night.  The lesions of the rash are small, erythematous, papules typically with an excoriated, hemorrhagic crust.  The burrows that may be seen are thin gray/brown/red lines up to 20mm in length.

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Areas most common infected are:screen-shot-2016-12-14-at-8-03-21-am

  • Webs of fingers
  • Flexor surface of wrist
  • Extensor surface of elbow
  • Axilliary folds
  • Peri-areolar
  • Periumbilical
  • Inguinal folds
  • Genital regions
  • Extensor surface of knees

 

Head, face, and back are not commonly seen and this is theorized to be due to the increased oil production in these areas.

Crusted (Norwegian) Scabies

Immunocomprimised, eldery, debilitated, or disabled patients are at increased risk of developing this severe form of scabies.  These mites are not more virulent, but because of their underlying medical conditions, the concentration of mites is much more numerous.  These patients develop thick crusts and are highly contagious due to the overwhelming contamination.

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Diagnosis

This should be a diagnosis of history and physical exam alone.  Skin scrapings can visualize the mites or eggs under the microscope.

Dermoscopy can be used to see the mite in burrow and is classically referred to as the “delta wing” sign, which is the dark head of the mite at the end of a burrow.

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“delta wing” sign

Treatment

  • Topical
    • Permethrin 5% cream
      • Apply from jaw line to the soles of feet
      • Leave overnight (8-14 hours) and washed off the next day
      • May be repeated 1-2 weeks later
      • Special populations
        • Category B in pregnancy
        • Safe in infants < 1 month
      • Crusted (Norwegian)
        • Daily application x 7 days, then 2x/wk until cured
  • Systemic
    • Ivermectin (3mg tabs)
      • 2 mg/kg single dose
        • Single dose not as effective as single application of permethrin
        • 2nd dose, 1 week later as effective as single application of permethrin
      • Recommended for large outbreaks, multiple infections in a single-household
      • Not recommended in pregnancy or children < 15kg
      • Crusted (Norwegian)
        • 2 mg/kg/dose given on day 1, 2, 8, 9, and 15
  •  Pruritus
    • Hydroxyzine 25mg q6hr
    • Mirtazapine 4.5-15mg qHS
    • Prednisone – 2-week taper starting at 60mg/day

Prevention of Re-infestation

Recommendations are for all close-contact household members to be treated simultaneously, even if asymptomatic, to prevent cross contamination and re-infestation.  Patients should be instructed to wash all clothing/bedding on the hot water cycle with high heat drying to kill any mites.  Stuffed animals, jackets, or any other objects not feasible to wash, can be isolated in a plastic bag for 3 days.  Fumigation is not necessary

References

  1. Romani L, Steer AC, Whitfeld MJ, Kaldor JM. Prevalence of scabies and impetigo worldwide: a systematic review. Lancet. Infectious diseases. 2015;15(8):960-7. [pubmed]
  2. Chosidow O. Clinical practices. Scabies. NEJM. 2006;354(16):1718-27. [pubmed]
  3. Heukelbach J, Feldmeier H. Scabies. Lancet. 2006;367(9524):1767-74. [pubmed]
  4. Johnston G, Sladden M. Scabies: diagnosis and treatment. BMJ. 2005;331(7517):619-22. [pubmed]
  5. Currie BJ, McCarthy JS. Permethrin and ivermectin for scabies. NEJM. 2010;362(8):717-25. [pubmed]
  6. Fuller LC. Epidemiology of scabies. Current Opinion in Infectious Diseases. 2013;26(2):123-6. [pubmed]
  7. Epidemiology and Risk Factors. Parasites – Scabies.  Centers for Disease Control.  Accessed December 14th, 2016. https://www.cdc.gov/parasites/scabies/epi.html
  8. Strong M, Johnstone P. Interventions for treating scabies. The Cochrane database of systematic reviews. 2007. [pubmed]
  9. Romani L, Whitfeld MJ, Koroivueta J. Mass Drug Administration for Scabies Control in a Population with Endemic Disease. NEJM. 2015;373(24):2305-13. [pubmed]
  10. Usha V, Gopalakrishnan Nair TV. A comparative study of oral ivermectin and topical permethrin cream in the treatment of scabies. Journal of the American Academy of Dermatology. 2000;42(2 Pt 1):236-40. [pubmed]
  11. Chambliss ML. Treating asymptomatic bodily contacts of patients with scabies. Archives of Family Medicine. 2000;9(5):473-4. [pubmed]