September 6, 2003

“If you love something, set it free. If it comes back to you, it is yours… If it doesn’t, it was never meant to be. But, if it just sits in your living room, messes up your stuff, eats your food, takes your money, and doesn’t appear to realize that you’ve set it free….. You either married it or gave birth to it.”

Summer passed by too quickly this year. We are experiencing a lovely fall day with temperatures hovering around 80 degrees. I spent some time Wednesday afternoon taking a video of my grandson and his friend skateboarding. After all was said and done I have 40 minutes of what could be the first movie of two famous skateboarders. Thursday evening it was my turn to take Grandson to hockey registration. Hockey camp begins on September 19th and the hockey season begins on October 14th.

I am still reading old lab reports and this morning came across the following Echocardiogram print out dated December 5, 2002.

Report: This study was performed to evaluate pulmonary hypertension. Image quantity was fair.
Interventricular septal thickness 1.2 cm.
Posterior left ventricular wall thickness 1.3 cm.
Left Ventricular end diastolic dimensions 5.3 cm.
Left Ventricular end systolic dimension 2.6 cm.
Left Ventricular ejection fraction 70%
Aortic root 2.9 cm.
Left Atrium 4.5 cm.

1. The left ventricular cavity size was normal. Wall thickness was mildly increased. Left ventricular systolic function was excellent. Diastolic function was essentially normal.
2. Normal right ventricular size and function.
3. Left atrial enlargement.
4. No significant valvular pathology was identified. An accurate estimate of pulmonary artery systolic pressure could not be made due to the presence of only trivial tricuspid regurgitation.

Impression: Preserved left ventricular systolic function. Mildly increased wall thickness.

This afternoon I spent some time going over the letter from the doctor at the sleep clinic I attended in February 2002. The observations and findings noted in the letter are as follows:

CPAP Therapy Start:

1. The amount of sleep and sleep continuity were adequate to assess sleep pathology. Technical quality of the study was adequate for interpretation.

2. Subject was started on CPAP at 4 cm and pressure increased mostly for arousals to 6 cm with reasonable control of her breathing including during REM, although she did not have any significant intervals of supine REM.

3. We did not see REM rebound.

4. She continued to have a large number of micro arousals at 35/hr not associated with respiratory events and not affected by changes in CPAP pressure.

5. She had increased transitions into stage 1 and wake. Very little slow wave sleep was seen. Sleep macrostructure was otherwise normal.

6. She had one interval of periodic limb movements with arousal ending with an awakening associated with a “jolt”.

7. Subjectively she tolerated CPAP reasonably well but did not note a dramatic change in her sleep quality.


1. Good control of mild, REM predominant sleep disordered breathing on a low-pressure CPAP.

2. Probable restless limb syndrome. Although she had only a brief interval of periodic limb movement during sleep it was clearly associated with a “jolt” awake strongly suggesting RLS/PLMD because of those symptoms.

3. Severe alpha intrusion.

Suggestions: I prescribed CPAP 7 cm. with a small Acclaim mask, and a heated humidifier. I remain pessimistic CPAP will alter her situation much.

Diagnostic Sleep Study:

1. Sleep onset was normal but difficult to score secondary to marked alpha intrusion. Overall sleep macrostructure showed increased fragmentation with increased transitions into Stage 1 and an interval of sleep maintenance insomnia. She had jolted awake without clear cause and was then quite restless. She settled with some reassurance and with one dose of Sinemet 100/25, although it is unclear if the drug did anything. No clear periodic limb movement was seen during sleep. Sleep microstructure showed marked alpha intrusion and increased arousals as 31/hr. Many of the arousals were associated with hypopneas although the events were relatively subtle. She snored occasionally and quietly and did not sound particularly obstructed. However, she had measurable hypopneas at 20/hr overall and 40/hr during REM. Events were not associated with significant desaturation and the overall mean saturation was 97% with her nadir at 89%.


1. Severe alpha intrusion

2. Mild, REM predominant hypopneas with associated sleep fragmentation.

3. “Jolt” awakenings not associated with evident cause. She was restless when awake and complaining of her legs but periodic limb movement was not seen during sleep. Overall I cannot draw a conclusion regarding restless leg syndrome.


1. She has sufficient sleep disordered breathing that a trial of therapy is warranted. With luck it will improve her fatigue and pain control, although I am not optimistic.


Pain in her hips, ankles and Achilles tendons.
Restlessness interfering with sleep maintenance, with restless crawling sensations in her legs and often with generalized restlessness.

Chronic fatigue; nonrestorative sleep with minimal daytime drowsiness.
She has had multiple problems since developing Graves’s disease treated with I-131 in 1998.

Concern regarding possible pulmonary hypertension and right sided heart failure caused by sleep apnea.


1. Restless limb syndrome. It remains unclear if this is related to her thyroid abnormalities or any other metabolic derangement. The lack of response to Sinemet and Pramipexole might have been from too low a dose. The RLS timing is slightly unusual in peaking around 0130 – 0230 rather than in the evening however the other features are typical.

2. The episodes where she “jolts awake” do not appear to be respiratory, but are accompanied by generalized restlessness and inability to lie still, although without crawling sensations in her legs. She relieves the restlessness by pacing. This is again suggestive of restless limb syndrome, although it is much less typical than the crawling sensations she describes on other nights. They do not suggest events from any respiratory disorder or other clear sleep apnea disorder. They may reflect an underlying anxiety disorder although she clearly states that her mind is calm and it is only her body that is restless.

3. She has mild REM predominant sleep disordered breathing. She does not have clinical features suggesting right-sided heart failure or pulmonary hypertension at this time. She has minimal daytime drowsiness despite her chronic fatigue. I am not optimistic that therapy of her REM predominant hypopneas will alter her symptoms much, but she has sufficient events to merit a trial of therapy. OSAS could contribute to peripheral edema.

4. Severe alpha wave intrusion during sleep. This is a non-specific marker but it is commonly associated with chronic pain and anxiety syndromes, nonrestorative sleep and fatigue. It is usually resistant to therapy.

5. Status post Graves’ disease treated with radioactive iodine, current thyroid status unclear. She has skin changes over her hands very suggestive of myxedema. She does not have clinical evidence of residual cardiomyopathy.

6. Recent episode of severe hypokalemia. This was possibly secondary to diuretics; however, she told me she was on amiloride which should induce hyperkalemia if anything, not hypokalemia.  If she was indeed profoundly hypokalemic and it cannot be explained clearly on potassium wasting diuretic therapy then she needs to be carefully assessed to ensure she doesn’t have hyperaldosteronism.  As well if she was hypokaemic she is at markedly increased risk of recurrent hypokalemia on her current furosemide without potassium supplement.

7. With her bone pain and history of hyperthyroidism she is at increased risk of osteoporosis.

8. I do not have an explanation of her bilateral Achilles tendon nodules.


1. I explained the mechanism of normal breathing, snoring and sleep apnea syndrome in detail. I discussed appropriate therapies and recommended a trial of CPAP. She is being titrated tonight. I will comment further after that study, but I am not optimistic CPAP will help much.

2. For her restless limb symptoms I suggest blood work to rule out metabolic causes including: hemoglobin; ferritin; Ca; Mg; Cr; TSH; folate and a WBC. Considering her recent electrolyte derangement I suggest following her Na, K and Cr closely while she is on any diuretic. Assessment for hyperaldosteronism should be considered.

3. It may be prudent to repeat bone density screening.

4. An electrocardiogram should be done if there was clinical suspicion of pulmonary hypertension.

5. For her restless leg syndrome and nocturnal jolts I suggest Pramipexole 0.5 qhs escalating immediately to 1.0 mg than 1.5 mg if the lower doses are ineffective. Response should be immediate. If this fails I would next try gabapentin escalating up to 400 mg qhs. I would next consider a narcotic such as codiene 30 – 90 mg at bedtime or during the night.

6. She might benefit from heel lifts for her Achilles tendons and local therapy from physio, and possibly from an NSAID or a COX2 inhibitor.

I read this report and shake my head. Squirt, my family doctor at the time, refused to follow any of these recommendations. When I asked him when he was going to request the recommended tests for me, Squirt asked me what I was talking about. I literally shoved his chair over, grabbed my chart off his desk and proceeded to show him the letter in my file from the sleep clinic doctor. My impression was that Squirt was ticked off that I had not received a firm diagnosis of sleep apnea. After all that is why he had sent me to the sleep clinic. It was also at this time that Squirt decided to close down his medical practice and I am sure that influenced his decision not to proceed with the recommended tests from the sleep clinic.

I will have to present this letter to the next doctor I see. Maybe, just maybe I will find a physician who will actually take the time to read it and follow it’s recommendations.

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