Category Archives: Obs/Gyn

Types of sutures (and when to use them)

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sutures

There are many types of sutures and they differ by size, material and needle. I made this handy chart to help remember how long each type of material lasts in the body and what it’s commonly used for:

50% Strength Gone Reactivity Use
Ethibond
(coated polyethylene)		 indef n/an/a + Tendon
Mersilene
(uncoated polyethylene)		 indef n/a + Tendon
Nylon 20%/y n/a + Skin
Silk 1 year >2y ++++ Vessel ligation, drains
Prolene
(polypropylene)		 indef n/a – Skin
Steel indef n/a – Tendon, sternum
Fast Gut 6d 20d ++++ Skin
Plain Gut 7d 70d ++++ Skin
Chromic Gut 28d 90d ++++ Oral mucosa
Monocryl
(Poliglecaprone 25)		 7d 110d +++ Skin, subcuticular
PDS
(Polydioxanone)		 21d 100d ++ Internal organs, fascia
Vicryl
(Polyglactin 910)		 21d 90d ++ Skin, soft tissue

Key:
* Monofilament
* Braided

Approach to Secondary Amenorrhea

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amenorrhea-secondary

Whereas Primary Amenorrhea is defined as a lack of menses in a woman who had never previously menstruated, Secondary Amenorrhea is:

  • Cessation of menses for 6 months, in a female who was previously menstruating.

The causes of Secondary Amenorrhea are different from those causing Primary Amenorrhea:

  • Pregnancy, lactation, menopause: 95%
  • Other causes: 5%
    • ↓gonadotrophic ↓gonadism: 66%
      • (including hypothalamic abnormalities, PCOS)
    • ↑ PRL: 13%
    • Ovarian failure: 12%
    • Anatomic abnormality: 7%
    • ↑ androgens: 2%

To evaluate Secondary Amenorrhea, a thorough history and physical exam are of course of vital importance. Since these patients by definition have menstruated in the past, the overriding question to answer is, “what is now stopping this patient from having menses?” In the vast majority of cases, normal pregnancy or menopause drives the amenorrhea. Many of the topics to discuss are the same as in the assessment of Primary Amenorrhea, but also talk to the patient about:

  • Symptoms of menopause: hot flushing, vaginal dryness, poor sleep, decreased libido
  • Obs/Gyn history: past endometritis, D&C, significant hemorrhage. These factors may point to a diagnosis of Asherman’s syndrome (scarring of endometrium).
  • Pregnancy: Potential for pregnancy, currently breastfeeding
  • Lifestyle factors such as stress, nutrition, exercise, weight changes
  • Medication: THC, antipsychotics, or irradiation
  • Associated symptoms:
    • Hyperprolatinemia: galactorrhea
    • Hyperandrogenism: hair loss/excess, acne, voice change
    • CNS tumor: headaches, visual field deficits, polyuria/polydipsia
    • Family history: PCOS

physical exam

  • Vitals, height, weight
  • Breasts: galactorrhea?
  • Thyroid: exopthalmos, goiter, abnormal deep tendon reflexes
  • Hyperandrogenism: hirsuitism, acne, hair loss
  • Hypercortisolemia: striae, hyperpigmentation
  • Pelvic exam

The labs used to work up Secondary Amenorrhea can be quite informative:

  • βHCG: To rule out pregnancy.
  • TSH, PRL: To test for hypo/hyperthyroidism and hyperprolactinemia.
  • LH, FHS: For practicality’s sake, these would probably be ordered at the same time as TSH, PRL.
    • If levels are high may indicate premature ovarian failure.
    • If levels are very low, that may point to a sellar tumor, so obtain an MRI.
    • If levels are normal, there may be a functional hypothalamic cause for the amenorrhea (e.g., malnutrition).
  • +/- Androgens (testosterone, DHEAS, 17-alpha-hydroxyprogesterone): May indicate PCOS or androgen-secreting tumor
  • +/- Estradiol: These assays lack sensitivity, standardization, and only capture a single time point.
  • Progestin challenge: To test the patient’s estrogen status. Administer a course of progesterone (~ 7 days).
    • If this results in bleeding, there is evidence the patient is progesterone deficient, anovulatory, or has an androgen excess.
    • If there is a lack of withdrawal bleeding, there are still a few causes to examine, so try the estrogen/progesterone challenge.
  • Estrogen/progesterone challenge: Give a course of estrogen/progesterone.
    • If there is withdrawal bleeding, it is apparent the patient has an estrogen deficiency.
    • If there is no bleeding in response to the challenge, the suspicion for an anatomic abnormality is heightened, so visualization of the uterus is indicated (e.g., hysteroscopy).

Treatment goals

  • Treat underlying cause
    • Lifestyle
    • Discontinue offending medications
    • Surgery (e.g., lysis of intrauterine adhesions)
  • Preserve fertility
  • Reduce risk of complications
    • Young women with premature ovarian failure can take hormone replacement to protect against early bone loss, menopause symptoms, and improve sexual health. These benefits may outweigh the associated increase in risk of MI, stroke, or breast cancer.

Master-Hunter T, Heiman DL. 2006. Amenorrhea: evaluation and treatment; 73:1374.
The Practice Committee of the American Society for Reproductive Medicine. 2008. Current approach to amenorrhea. Fertility and Sterility;90:S219.
Welt CK, Barieri RL. Etiology, diagnosis, and treatment of secondary amenorrhea. In: UpToDate (Eds: Snyder PJ, Crowley Jr WF, Kirkland JL). Accessed 2013.10.05.

Approach to Primary Amenorrhea

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amenorrhea---primary

Primary Amenorrhea is defined as the absence of menses:

  • By age 13/14 without normal development of secondary sexual characteristics; OR,
  • By age 15/16, with normal secondary sexual characteristics.

In contrast, Secondary Amenorrhea refers to a loss of menses after it has already been established.

The causes of amenorrea are myriad, with an important one being pregnancy.

Causes of Amenorrhea
Hypothalamus Stress, malnutrition, exercise, lactation, immaturity, Kallmann syndrome
Pituitary Tumor, empty sella, apoplexy, hyperprolactinemia/prolactinoma
Ovaries Gonadal dysgenesis, premature ovarian failure, menopause, ovarian tumor, polycystic ovarian syndrome (PCOS), ovarian enzyme deficiency, chromosomal abnormalities (e.g., 45XO)
Uterus Intrauterine scarring, cervical agenesis, androgen insensitivity
Outflow Tract Imperforate hymen, transverse vaginal septum, cervical stenosis, Mullerian agenesis
Thyroid Hypo/hyperthyroidism
Pregnancy
Other Constitutional delay of puberty, hyperandrogenism, Cushing’s syndrome, medications

The most common pathologic causes of Primary Amenorrhea are:

  • Chromosomal abnormalities: 50%
  • Hypothalamic abnormalities: 20%
  • Mullerian agenesis: 5%
  • Pituitary abnormalities: 5%

Determining the etiology of Primary Amenorrhea depends on careful history-taking and a targeted physical exam. Key points to address in the history include:

  • Potential for pregnancy, current lactation
  • Develop of secondary sexual characteristics
    • On a side note, the general order of female sexual development is: breasts, pubic hair, growth spurt, menses; or, “boobs, pubes, grow, flow”
  • Lifestyle factors such as stress, nutrition, exercise, weight changes
  • Medication: THC, antipsychotics, or irradiation
  • Associated symptoms:
    • Hyperprolatinemia: galactorrhea
    • Hyperandrogenism: hair loss/excess, acne, voice change
    • CNS tumor: headaches, visual field deficits, polyuria/polydipsia
    • Family history: Does everyone have relatively late puberty?

In terms of physical exam:

  • Vitals, height, weight
  • Secondary sexual characteristics: breasts, pubic/axillary hair
  • Thyroid: exopthalmos, goiter, abnormal deep tendon reflexes
  • Hyperandrogenism: hirsuitism, acne, hair loss
  • Hypercortisolemia: striae, hyperpigmentation
  • Turner syndrome: webbed neck, low hair line, widely-spaced nipples, short stature
  • Pelvic exam: hymen, vaginal septum, ultrasound for uterine anatomy

Laboratory investigations can offer lots of insight:

  • βHCG: Gotta rule out this common reason first!
  • TSH, PRL: To test for hypo/hyperthyroidism and hyperprolactinemia.
  • LH, FHS: For practicality’s sake, these would probably be ordered at the same time as TSH, PRL.
  • +/- Androgens (testosterone, DHEAS, 17-alpha-hydroxyprogesterone): May indicate PCOS or androgen-secreting tumor, androhen insensitivity syndrome, or 5-alpha-reductase deficiency.
  • +/- Estradiol: These assays lack sensitivity, standardization, and only capture a single time point.

Since chromosomal abnormalities account for half of the pathologic cases of Primary Amenorrhea, karyotyping will be useful for patients who are found to have abnormal uterine anatomy on ultrasound or have elevated FSH, LH. Patients with an absent uterus may be worked-up for abnormal Mullerian development (46XX karyotype and normal female testosterone levels) versus a deficit in masculinization (i.e., androgen insensitivity syndrome, 5-alpha-reductase deficiency). There is a normal uterus, and LH and FSH are high, that means there is nothing feeding back to stop their release; karyotype may reveal Turner syndrome (45XO), while normal karyotype (46XX) may indicate Mullerian agenesis.

The over all treatment goals are to:

  • Treat underlying cause:
    • Lifestyle
    • Discontinue offending medications
    • Surgery
  • Preserve fertility
  • Reduce risk of complications (e.g., remove undescended tests in androgen insensitive patients to mitigate cancer risk).
  • Master-Hunter T, Heiman DL. 2006. Amenorrhea: evaluation and treatment; 73:1374.
  • The Practice Committee of the American Society for Reproductive Medicine. 2008. Current approach to amenorrhea. Fertility and Sterility;90:S219.
  • Welt CK, Barieri RL. Etiology, diagnosis, and treatment of primary amenorrhea. In: UpToDate (Eds: Snyder PJ, Crowley Jr WF, Kirkland JL). Accessed 2013.05.05.

Cytology of the Cervix and Testing for Abnormalities

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In the cervix there is a nice transition from the rough and tough squamous epithelial cells of the outside world (vagina) to the squishy secretory columnar epithelial cells of the inside (uterus). Over time the junction between these two cell types moves towards the inside (more squamous cells) and this is normal metaplasia. This is not to be confused with dysplasia, which is the transformation of normal squamous cells to less differentiated cells.

When women get colposcopies the examiner is looking for dysplasia, and two of the tricks they have up their sleeves to make the dysplasia more apparent are vinegar and iodine.

Both rely on the fact that dysplastic cells are more active and have a much larger nucleus:cytoplasm ratio.

  • When vinegar (acetic acid) is applied, the cells become dehydrated, and the nuclei reflect more light. This makes the cells with larger nuclei more prominent because they appear more white. This includes dysplastic cells and cells infected with HPV.
  • With an iodine solution (Lugol’s iodine) the iodine binds to glycogen in cells making them appear dark brown. Healthy columnar cells don’t have glycogen and due to their small amount of cytoplasm, dysplastic and HPV-infected cells don’t either.

Using these two techniques can help differentiate areas of dysplasia and guide sampling biopsies.

The Menstrual Cycle

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The menstrual cycle. What more of a classic drawing can you get? Though it has been done a million times over, here’s the Sketchy Medicine version of the classic hormonal interplay that allows for the endometrial lining to build up, shed, build up, shed, build up, shed…

The nice thing is the the pituitary hormones are aptly named so that FSH (follicle stimulating hormone) stimulates the follicle to grow and LH (luteinizing hormone) causes ovulation (the infamous LH surge) and subsequent corpus luteum development.

Meanwhile the developing follicle secretes estradiol which stimulates the proliferative phase of the cycle. Then the corpus luteum secretes estradiol and progesterone to kick things into high gear for the secretory phase.

You can now passively study this all the time (and keep your own notes) on a notebook or a mug. Nothing says “mmm, coffee” like the hormonal phases of the female reproductive system.

Signs of the 3rd Stage of Labour

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There are three stages of labour, even though most people just think of labour as what is technically just the first stage.

  1. Cervical dilatation (all the way to 10 cm): which is divided into three more stages, just to make things more complicated
    1. Latent: contractions start and the cervix kind of sort of changes (but slowly)
    2. Active: cervix gets its butt in gear (this starts once it’s 2-4 cm dilated),
    3. Descent: baby drops down, this part is on a blurred line between stages 1 and 2
  2. Delivery of the baby: pretty self-explanatory
  3. Delivery of the placenta: within 30 minutes after the baby, more than 60 minutes counts as a retained placenta

It’s very important to not try to yank the placenta out before having seen the signs of the third stage because chances are it has not separated from the endometrium and doing so will cause uterine inversion (it will be pulled inside out). And though you’d think that after the baby is out all the fun is over and the job is done, the 3rd stage is associated with significant potential morbidity such as hemorrhage, retained placenta (which can lead to hemorrhage) and the uterine inversion (and you guessed it, hemorrhage).

This is because the uterus is trying to contract down and squeeze off all the little blood vessels and having something in the way or being inside out prevents it from doing that properly.

Leopold Maneuvers

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Leopold Maneuvers are a slick series of abdominal palpations that let you determine which way the baby is facing in a pregnant woman.

It’s akin to palm reading, but cooler and more accurate. With the four maneuvers you can figure out which part of the baby is facing towards the pelvis (presentation aka bum first/breach or head first/cephalic), if it’s facing to the right or left and how far it is into the pelvis (engagement).

Skilled physicians can even estimate the weight based on Leopold maneuvers.

Direct and indirect antibody tests

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direct antibody Test

Looks for the presence of IgG and/or complement on the RBCs. This causes hemolysis and can be due to an autoimmune disease, transfusion reaction, etc.

Indirect antibody Test

This is used when cross-matching people for a blood transfusion. It tests patients for the presence of unexpected alloantibodies (anti-D, anti-E, anti-C, anti-Kell, anti-Duffy). This is just a screen, if it is positive, you can then test for specific antibodies and then only transfuse blood that is negative for those specific antigens.

* 19/06/2013 Please excuse the doodle for saying “agglutination” though it is testing by agglutinating, the “A” in DAT stands for antibody. Thanks Robina for pointing this out!

Placenta Previa

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Placenta previa isn’t generally something that is a concern in the western world, since prenatal ultrasounds are common practice, but in areas of the world where they’re not, it can be pretty devastating when the baby is being delivered.