Category Archives: Uncategorized

Hypothermia

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hypothermiaHypothermia is when you get really cold. Generally, hypothermia is defined as a core temperature less than 35C (95F). The Swiss staging system is fairly commonly used for correlating core temperature and clinical signs:

  • Stage I (35 – 32C; 90 – 95F): conscious, shivering
  • Stage II (28 – 32C; 82 – 90F): altered mental status, not shivering
  • Stage III (24 – 28C; 75 – 82F): unconscious, not shivering, vital signs present
  • Stage IV (< 24C; < 75F): apparent death (but resuscitation possible!)
  • Stage V (< 13.7C; < 58F): death due to irreversible hypothermia

Healthy people have fairly effective mechanisms for maintaining a normal temperature (37C; 99F) (e.g., shivering, peripheral vasoconstriction) but these can be overwhelmed by extreme cold (Primary Hypothermia). Some comorbid patients can develop hypothermia even in a warm environment (Secondary Hypothermia). For instance, severely-burned patients can have increased heat loss, while acute spinal cord injury can impair peripheral thermoregulation.

For the development of hypothermia, it is sometimes helpful to remember that heat can be lost by 4 physical mechanisms:

  • Radiation: heat exchange by infrared electromagnetic radiation
  • Evaporation: molecules converting from liquid to gas phase (e.g., sweat)
  • Convection: heat exchange by air/fluid currents
  • Conduction: heat exchange by direct contact with a colder surface
  • Brown DJA, Brugger H, Boyd J, Paal P. 2012. Accidental hypothermia. NEJM; 367:1930.
  • Zafran K, Mechem CC. 2017. Accidental hypothermia in adults. In: UpToDate.

Amyotrophic Lateral Sclerosis (ALS) & the corticospinal tract

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corticospinal_tract

Amyotrophic Lateral Sclerosis (ALS) is a degenerative disease of the motor neurons in the brain and spinal cord. It progressively affects all the muscles in the body but there is no known cause and no treatment. Only about 5-10% of cases are inherited while the rest are sporadic.

The neurons ALS affects are primarily the upper motor neurons. These are the ones that originate in the brain and travel down the spinal cord. These neurons then synapse with the lower motor neurons in the ventral horn, and it is the lower motor neurons that go directly to the muscles.

In ALS there are both upper motor neuron and lower motor neuron symptoms. As the neurons die, a constellation of symptoms including numbness, weakness and paralysis emerge. Eventually the paralysis progresses leading to inability to speak, swallow and breath. There is no cure for ALS and treatments only help with the symptoms, they do not slow the progression of the disease.

So you may have seen a lot of ice bucket challenges over the last few weeks but please support this cause as it is a horrible disease that up until now had almost no recognition or support. So please donate to The ALS Association (alas.org).

And in case you get tired or jaded seeing your social media full of these videos, watch this one of my father doing it. He’s not an emotional guy, but he has lost more than his fair share of friends to this disease.

donate to help fund ALS research and support from Ali & Mike on Vimeo.

Monitoring Neuromuscular Blockade

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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.

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.

Acute Limb Ischemia

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acute limb ischemia

Acute limb ischemia is a sudden decrease in limb perfusion that can potentially threaten limb viability, in patients presenting within 2 weeks of symptom onset (it is considered chronic if more than 2 weeks have passed). The common causes of limb ischemia are:

  • Arterial embolism (80% of cases)
  • Thrombus (usually from site of atherosclerotic plaque)
  • Arterial trauma (e.g., after interventional catheterization procedures)

The symptoms can come on over a period of hours or days. It is important to recognize this condition, in order to improve the chance of limb preservation. Acute limb ischemia is characterized by the 6 P’s:

  • Pain
  • Paresthesia
  • Polar/Poikylothermia (affected extremity is cool on palpation)
  • Pallor
  • Paralysis
  • Pulselessness

If no pulse is palpable, then assessment of perfusion with a Doppler ultrasound is the next step. Note that acutely ischemic limbs may not always appear pale; the extremity may progress to a blue or mottled appearance as the ischemia continues. The most reliable symptoms are paresthesias, which will progress to complete loss of sensation, and paralysis, which may indicate the limb is no longer viable.

Once acute limb ischemia is identified, intravenous heparin is administered. Surgical or endovascular revascularization is the definitive treatment for acute limb ischemia, though these interventions should be performed within 6 hours of symptom onset to improve the probability of limb salvage.

  • Callum K and Bradbury A. 2000. ABC of arterial and venous disease: acute limb ischemia. British Medical Journal; 320:764.
  • Creager MA, Kaufman JA, and Conte MS. 2012. Acute limb ischemia. New England Journal of Medicine; 366:2198.
  • Mitchell ME, Mohler III ER, and Carpenter JP. Acute arterial occlusion of the lower extremities (acute limb ischemia). In: Uptodate (Eds: Clement DL, Hoekstra J, and Collins KA). Accessed 2013.08.24.