Acquired Nevomelanocytic Nevi (aka moles)

nevomelanocytic-nevi

Nevi (or moles) are very, very common. They are generally well-circumscribed dark spots (or “papules” to use the dermatological terminology) that can appear at any time in someone’s life.

Histologically they are composed of groups of melanocytic nevus cells and can be found in the epidermis, dermis or both.

The problem with nevi is that they are pigmented and people tend to get worried about pigmented things on the skin (for good reason as melanoma can be a pretty scary disease).

Common acquired nevi are grouped into three categories (I’ll leave out congenital and dysplastic nevi for now)

  1. Junctional: the nevus cells are completely in the epidermis, just above the dermal-epidermal junction. Clinically they are <1 cm, flat or minimally elevated and dark in colour.
  2. Compound: the nevus cells are in both the epidermis and the papillary dermis (top layer of the dermis), and cross the basement membrane. Clinically they are raised, and a medium-brown colour.
  3. Dermal: the nevus cells are completely in the dermis. Clinically they are raised and almost always pigment less as the cells lose their capacity for melanization when in the dermis. They usually have telangectasia and may or may not have hair. They don’t tend to appear until the 2nd or 3rd decades of life.

Pierre-Robin Sequence

pierre-robin-sequence

Pierre-Robin Sequence is not a syndrome, it’s a sequence. While it is a collection of features, one happens because of the one that came before.

The features are:

  • Retrognathia/micrognathia (posterior mandible or very small mandible)
  • Glossoptosis (downwards/posterior displacement of the tongue due to the small mandible
  • Airway obstruction (because the tongue is in the way)

Pierre-Robin Sequence is associated with cleft palate (50% of children with the sequence have cleft palate). There are two proposed theories:

  1. The first is that the tongue simply gets in the way of the palate from fusing
  2. The second is that the tongue prevents the newly fused palate from staying fused (this is currently the more popular theory)

PRS, though not a syndrome itself, is associated with multiple syndromes including Stickler Syndrome, velocardiofacial syndrome, fetal alcohol syndrome and Treacher Collins Syndrome.

PHACE Syndrome (hemangiomas)

PHACE_syndromeThere are no shortage of congenital syndromes that are acronyms arranged into some sort of vaguely pronounceable word. There will be lots of doodles about these, but we’ll start off with a more uncommon one – PHACE Syndrome.

PHACE Syndrome is a collection of findings that go along with large infantile hemangiomas. They’re the more worrisome (but less obviously disfiguring) things you need to look for when you see a baby with a large hemangioma on the face or multiple hemangiomas.

  • Posterior fossa brain malformations
  • Hemangiomas
  • Arterial anomalies
  • Cardiac anomalies and coarctation of the aorta
  • Eye abnormalities
  • Sternal cleft

The most common symptom of PHACE is cerebrovascular abnormalities, followed by cardiac anomalies (coarctation, aortic arch anomalies, VSDs). If you suspect PHACE, do clinical exam of the skin and eyes and MRI of the head, neck and chest.

Other cool facts

  • PHACE occurs in full-term normal birth weight infants (other hemangiomas tend to occur in preterm infants)
  • Quite common, more girls than boys (8:1)
  • Don’t confuse it with Strurge-Weber (port wine stain, associated with the facial dermatomes)
    • Port wine stains don’t proliferate and then regress like an infantile hemangioma

Brachial Plexus Part 1 – anatomical relations

brachial_plexus

The brachial plexus is the bane of many med students’ existence during any sort of neuro block. So many nerves, so many connections, so many seemingly arbitrary names of different sections. It’s just a woven mess of misery. (especially when they start getting into the “where is the lesion” questions)

Thus I’ve decided to have a couple posts about the brachial plexus, hopefully demystifying it to some extent. This first doodle is about the brachial plexus and its anatomical relationship to some of the structures that show why anatomists who named the parts weren’t as crazy as they seem.

Important structures to remember because they explain why parts are named the way they are:

  1. Vertebrae
  2. Anterior and posterior scalene muscles
  3. Subclavian artery
  4. The arm (in its anatomical position)

Vertebrae: There are 7 cervical vertebrae and 12 thoracic vertebrae. To make things confusing the cervical spinal nerves exit ABOVE their named vertebrae (except for C8) while the thoracic, lumbar and sacral exit BELOW. This messes up the whole numbering system because there are SEVEN cervical vertebrae but there are EIGHT cervical spinal nerve roots. The brachial plexus generally includes the nerve roots C5-T1*
* I say generally because there’s are anatomical variations such as a “prefixed” plexus that goes from C4-C8 and a “postfixed” plexus that goes from C6-T2

Scalene Muscles: The brachial plexus is nestled between the scalenes in the neck. At this point the plexus is oriented up and down and therefore the trunks are superior (closest to your noggin), middle, and inferior.

Subclavian Artery/Anatomical Position: The artery is in front of the plexus at the level of the trunks and then the plexus starts to wrap around it (or at least seems to because we don’t keep our arms straight out to our sides in “anatomical position” at all times). The cords are named for their relationship to the artery. One is lateral (again, if the arm was held out to the side), one is posterior and one is medial (think closest to armpit).

 

Subdivisions of the Brachial Plexus

The parts are: Roots/Trunks/Divisions/Cords/Branches or, as I remember them being a classy east coast Canadian: Real/Truckers/Drink/Cold/Beer

Then you might think, “But how do I remember which of the terminal branches comes off where?” For that I think of the two “M” branches being on the M: Musculocutaneous, Median and (M)Ulnar and that the whole thing together can just be said as “MARMU” Pick the mnemonics you want, the brachial plexus is rife with them. I personally just like the sound of the word marmu.

Complex Regional Pain Syndrome

crps

Hypo/Hyperalgesia:Decreased/increased sensitivity to a usually-painful stimulus (e.g., pinprick).
Hypo/Hyperesthesia: Decreased/increased sensation to a usually-innocuous stimulus (e.g., light touch).
Allodynia: Sensation of pain from a usually-innocuous stimulus (e.g., light touch).

Chronic Regional Pain Syndrome (CRPS) refers to a chronic neuropathic pain condition with a broad and varied range of  clinical presentations. CRPS patients experience severe pain out of proportion to their original injury, and this may start at the time of injury or weeks later. The pain is described as deep-seated and burning/aching/shooting. Sesnory changes are common, including hypo/hyperesthesia, hypo/hyperalgesia, and allodynia. For instance, many patients describe not being able to tolerate the sensation of bedsheets on their painful limb.

In the affected area, there is often marked edema, temperature asymmetry (usually cooler), and sweating changes (usually increased). Loss of hair and nail growth is common, and disuse of the limb can result in weakness, muscle atrophy, and contractures.

The diagnosis is made clinically, using the Budapest Criteria. Some pain physicians use a nuclear medicine test, three-phase bone scintigraphy, for CRPS diagnosis but this test is becoming less popular, since it has a low positive predictive value.

Budapest Criteria

  1. Pain, ongoing and disproportionate to any inciting event
  2. Symptoms: at least one symptom in three of the four categories:
    • Sensory: reports of hyperesthesia and/or allodynia
    • Vasomotor: reports of temperature asymmetry and/or skin color changes and/or skin color asymmetr
    • Sudomotor/edema: reports of edema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  3. Physical Signs: at least one sign at time of evaluation in two or more categories:
    • Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or 
joint movement)
    • Vasomotor: evidence of temperature asymmetry and/or skin color changes and/or asymmetry
    • Sudomotor/edema: evidence of edema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  4. No other diagnosis better explains the signs and symptoms

CRPS is classified as Type I when there is no apparent history of nerve damage, and Type II when associated with definite peripheral nerve injury. CRPS most commonly occurs following fractures and immobilization, but can happen even with little to no trauma.The pathophysiology is thought to involve autonomic dysfunction and inflammation, but much is still unknown.

CRPS affects females about 2-4 times more often than males, and onset is usually in middle age (though there are rare pediatric cases reported). It is a progressive disease that can result in spread of pain, sensory disturbances, and physical changes to other limbs.

Treatment for CRPS may involve physiotherapy, complementary medicine (e.g., acupuncture, qi gong) psychological therapies, and a variety of pharmacologic (e.g., NSAIDs, anticonvulsants, antidepressants, opioids, ketamine, bisphosphonates) and interventional procedures (nerve blocks, sympathectomy, neurostimulators). As with all things CRPS, there isn’t great evidence for any particular intervention.

  • Harden RN, Bruehl S, Perez RSGM, Birklein F, Marinus J, Maihofner C, Lubenow T, Buvanendran A, Mackey S, Graciosa J, Mogilevski M, Ramsden C, Chont M, Vatine J-J. Validation of proposed diagnostic criteria (the “Budapest Criteria”) for Complex Regional Pain Syndrome. Pain; 150:268.
  • Hord E-D. Complex regional pain syndrome. In: Massachusetts General Hospital Handbook of Pain Management (Eds: Ballantyne JC, Fields HL). Lippincott Williams & Wilkins.
  • Moon JY, Park SY, Kim YC, Lee SC, Nahm FS, Kim H, Oh SW. 2012. Analysis of  patterns of three-phase bone scintigraphy for patients with complex regional pain syndrome diagnosed using the proposed research criteria (the ‘Budapest Criteria’). British Journal of Anesthesia; 108:655.
  • O’Connell NE, Wand BM, McAuley J, Marston L, Moseley GL. Interventions for treating pain and disability in adults with complex regional pain syndrome – an overview of systematic reviews. Cochrane Database of Systematic Reviews; 4:CD009416.
  • Schwartzman RJ, Erwin KL, Alexander GM. 2009. The natural history of complex regional pain syndrome. Clinical Journal of Pain; 25:273.
  • Smith H, Popp AJ. The patient with chronic pain syndromes. In: A Guide to the Primary Care of Neurological Disorders (Eds: Popp AJ, Deshaies EM). Thieme.
  • Tran DQH, Duong S, Bertini P, Finlayson RJ. Treatment of complex regional pain syndrome: a review of the evidence. Canadian Journal of Anesthesiology; 57:149.

Internuclear Opthalmoplegia

inoInternuclear opthalmoplegia (INO) is an impairment in lateral conjugate gaze (both eyes looking toward one side), caused by a lesion in the medial longitudinal fasciculus (MLF), and associated with multiple sclerosis.

Lateral conjugate gaze requires coordination of adduction (medial rectus muscle, CN III) in one eye and abduction (lateral rectus muscle, CN VI) in the other eye. These movements are coordinated by the paramedian pontine reticular formation (PPRF), also known as the pontine gaze centre. The pathway is as follows:

To look to the left, the right frontal eye field (FEF) sends a signal to the left PPRF. The left PPRF innervates 1) the left abducens (CN VI) nucleus, which controls the left lateral rectus muscle and causes the left eye to abduct (gaze to the left); and, 2) the right oculomotor (CN III) nucleus, which controls the right medial rectus muscle and causes the right eye to adduct (gaze to the left). The MLF is the tract connecting the PPRF to the contralateral CN III nucleus.

In INO, there is damage to the MLF, giving a deficit in adduction of the corresponding eye during conjugate lateral gaze, but convergence (eye crossing) is classically preserved because that is controlled by a different pathway. In very mild cases of INO, the only deficit is a slowed velocity of the affected eye. For naming, a right INO (as in the sketch) involves damage to the right MLF, which means that the right eye can’t adduct to look to the left, but can abduct to look to the right.

INO may also be associated with gaze abnormalities such as nystagmus, skew deviation, and even abduction or convergence deficits.

The causes of INO include: multiple sclerosis, pontine glioma, and stroke.

  • Flaherty AW, Rost NS. 2007. Eyes and vision. In: Massachusetts General Hospital Handbook of Neurology. Lippincott Williams & Wilkins.
  • Frohman EM, Frohman TC, Zee DS, McColl R, Galetta S. 2005. The neuro-opthalmology of multiple sclerosis. The Lancet Neurology; 4:111.
  • Ropper AH, Brown RH. 2005. Disorders of ocular movement and pupillary function. In: Adams and Victor’s Principles of Neurology. McGraw-Hill.
  • Wilkinson I, Lennox G. 2005. Cranial nerve disorders. In: Essential Neurology. Blackwell.

 

Monitoring Neuromuscular Blockade

nmb

As mentioned in a previous post, neuromuscular blocking drugs are used in anesthesia to ensure paralysis during surgery. The degree of neuromuscular block is assessed using nerve stimulation, where two electrodes impose a pulse of current on a peripheral nerve (e.g., ulnar n., facial n., posterior tibial n.) and induce muscle twitches which can then be monitored through the surgery. There are a few different ways to do nerve stimulation :

Tetany: A sustained stimulation (5 s)
Train-of-four (TOF): Four pulses in rapid succession
Double-burst stimulation (DBS): A series of 3 pulses followed after a pause by 2 or 3 pulses.
Post-tetanic potentiation: When a pulse is sent after a tetanic stimulation, it will bring on a stronger twitch than at first.

With non-depolarizing muscle blockers, there is a fade phenomenon where twitch amplitude decreases from the first stimulation. For instance, in a TOF each twitch is weaker than the last; the last twitch is the first to disappear with non-depolarizing blockade, while the first twitch is the last to disappear. This non-depolarizing fade is also seen in DBS and tetany, though there is still post-tetanic potentiation.

With a depolarizing muscle blockade, no fade will be seen. Instead, all twitches in response to stimulation will be uniformly decreased, and there is no post-tetanic potentiation. This pattern is known as a Phase I block. But, if there is a ton of succinylcholine or the blockade is of a long duration, the pattern of response will look like a non-depolarizing block. This would be a Phase II block.

Recovery of neuromuscular function
Throughout a surgery, the TOF ratio is often mentioned as a means of assessing neuromuscular blockade on an ongoing basis. This means dividing the amplitude of the fourth (and most influenced  by neuromuscular blockers) twitch in a TOF by the amplitude of the first (which is the least affected). In normal people, the 4:1 amplitude is the same, for a TOF ratio of 1. In a Phase I depolarizing block, the TOF ratio is also 1. The TOF ratio will be less than 1 in a non-depolarizing block (remember the fade?). It is commonly mentioned that a TOF ratio of 0.7 represents an full recovery of neuromuscular function, but these days it is thought that a TOF ratio of at least 0.9 is needed before extubation.

It is very hard to tell what the TOF ratio is by sight or feel alone! DBS ratio is more sensitive than TOF ratio for assessing neuromuscular block, and it’s easier to gauge by tactile evaluation than the TOF ratio. So, quantitative monitoring by electomyography (EMG), mechanomyography (MMG), or accelerometry is ideal!

  • Fuchs-Buder T. 2010. Neuromuscular monitoring in clinical practice and research. Springer.
  • McGrath CD, Hunter JM. 2006. Monitoring of neuromuscular block. Continuing Education in Anesthesia, Critical Care & Pain; 6:7.
  • Neuromuscular blocking agents. 2006. In: Clinical Anesthesiology (Eds: Morgan GE, Mikhail MS, Murray MJ). Lange.
  • Viby-Mogensen J. 2005. Neuromuscular monitoring. In: Miller’s Anesthesia (Eds: Miller RD, Erikkson LI, Fleisher LA, Wiener-Kronish JP, Young WL). Elsevier.

Types of sutures (and when to use them)

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

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

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.
Related Posts Plugin for WordPress, Blogger...