Your Family Physician

Progesterone treatment may not prevent early preterm birth in twin pregnancy, according to the results of a randomized, double-blind, placebo-controlled study and meta-analysis reported in the June 11 Online First issue of The Lancet.

"Women with twin pregnancy are at high risk for spontaneous preterm delivery," write Jane E. Norman, MD, from the University of Edinburgh, United Kingdom, and colleagues from STudy Of Progesterone for the Prevention of Preterm birth In Twins (STOPPIT). "Progesterone seems to be effective in reducing preterm birth in selected high-risk singleton pregnancies, albeit with no significant reduction in perinatal mortality and little evidence of neonatal benefit. We investigated the use of progesterone for prevention of preterm birth in twin pregnancy."

Between 2004 and 2008 at 9 UK National Health Service clinics specializing in the management of twin pregnancy, 500 women were recruited and randomly assigned to receive daily vaginal progesterone gel 90 mg (n = 250) or placebo gel (n = 250) for 10 weeks beginning at 24 weeks' gestation. Assignment was by permuted blocks of randomly mixed sizes. Analysis was by intent-to-treat, and the main endpoint of the study was delivery or intrauterine death before 34 weeks' gestation.

To assess the efficacy of progesterone in preventing early (<>

In each group of the randomized trial, 3 women were lost to follow-up. The combined proportion of intrauterine death or delivery before 34 weeks of pregnancy was 24.7% (61/247) in women receiving progesterone vs 19.4% (48/247) in women receiving placebo (odds ratio [OR], 1.36; 95% confidence interval [CI], 0.89 - 2.09; P = .16). Both groups had similar rates of adverse events.

Similarly, progesterone did not appear to prevent early preterm birth in women with twin pregnancy, based on results of the meta-analysis (pooled OR, 1.16; 95% CI, 0.89 - 1.51).

"Progesterone, administered vaginally, does not prevent preterm birth in women with twin pregnancy," the study authors write. "The biological mechanism by which preterm delivery occurs might be different in twin and singleton pregnancy, and this hypothesis merits further study. Perhaps stretching of uterine muscle has a substantial role in preterm labour in twin pregnancy, and infection and inflammation a role in singletons."

Limitations of this study include participation rate of only 40% of eligible women and performance of the study mostly in tertiary referral centers.

In an accompanying comment, Lex W. Doyle, from the University of Melbourne in Melbourne, Australia, notes that progesterone might be beneficial in multiple pregnancies even if delivery is not delayed.

"Magnesium sulphate, which is not successful as a tocolytic despite being widely used for that purpose, improves neurological outcome for the preterm infant," Dr. Doyle writes. "Other trials in progress should continue to completion, survivors of all trials should be followed up into childhood, and data pooled to establish the balance between long-term benefits and risks of progesterone to prevent preterm delivery, of both singletons and multiple births."

The Chief Scientist Office of the Scottish Government Health Directorate supported this study. Some of the study authors have disclosed various financial relationships with government and charitable organizations for research into understanding the mechanism of term and preterm labor and investigating treatments, a small drug company that was considering developing treatments of preterm labor, and/or the pharmaceutical industry. One study author has been named as an inventor on patent applications for 2 compounds potentially useful in preterm labor prevention, and another was chair of the Data Safety and Monitoring Board.

Dr. Doyle has disclosed no relevant financial relationships.

Lancet. Published online June 11, 2009.

Clinical Context

Study Highlights

• Women with ongoing twin pregnancies were recruited from 9 UK National Health Service hospitals, with gestation and chorionicity established by scan before 20 weeks' gestation.
• Excluded were women with pregnancies complicated by structural or chromosomal abnormalities, planned cervical suture, planned elective delivery before 34 weeks, and planned intervention for twin-twin transfusion before 22 weeks.
• Women were recruited at booking and at 22 weeks and were randomly assigned to either progesterone gel 90 mg or identical-appearing placebo gel for intravaginal insertion from 24 weeks.
• The progesterone was delivered via an applicator with a twist-off top for single use by self-insertion.
• The applicator contained 1.45 g and delivered 1.125 g of gel with 8% progesterone or excipients.
• The primary outcome was delivery or intrauterine death before 34 weeks and 0 days.
• Delivery of the first twin was used to define time of delivery.
• The gestational age was calculated from the ultrasound scan done before 20 weeks.
• Maternal secondary outcomes were gestation at delivery, method of delivery, and duration of stages of labor.
• Neonatal secondary outcomes were admission to the neonatal unit and duration of neonatal care.
• A meta-analysis was performed of similar studies, with outcome of delivery before 34 weeks' gestation using search of PubMed and the Cochrane Controlled Trials register and the Jadad criteria for quality of studies.
• In the randomized trial, mean age of women was 33 years, 12% to 18% were current smokers, 71% to 72% currently used alcohol, and 48% to 49% were multiparous.
• 3 patients from each randomized group were lost to follow-up.
• The proportion of women delivering or with an intrauterine death before 34 weeks was 24.7% in the progesterone group vs 19.4% in the placebo group (OR, 1.36; P = .16).
• Progesterone did not reduce the incidence of preterm delivery or death before 34 weeks.
• Subgroup analysis suggested that progesterone may increase preterm delivery or intrauterine death in women with dichorionic pregnancies, but this was not statistically significant.
• For maternal outcomes, the only differences were reduced odds of cesarean delivery (OR, 0.53; P = .006), operative delivery (OR, 0.42; P = .013), and nausea (OR, 0.43; P = .035) in the progesterone group, but the authors attributed the reduction in cesarean delivery and operative delivery to chance.
• The rate of adverse effects such as vaginal discharge, irritation, discomfort, itching, nausea, fluid retention, and breast tenderness did not differ between the 2 groups.
• The meta-analysis generated 198 results, of which only 2 met criteria for inclusion.
• Both studies had high Jadad scores for quality, and the pooled OR for preterm delivery or intrauterine death before 34 weeks was 1.16 (not significant) for progesterone.
• The authors concluded that use of intravaginal progesterone from 24 weeks in women with twin pregnancies was not associated with a reduction in preterm delivery or intrauterine death before 34 weeks.

Clinical Implications

• Use of intravaginal progesterone in women with twin pregnancies is not associated with a reduction in preterm delivery or intrauterine death before 34 weeks' gestation.
• Use of intravaginal progesterone in women with twin pregnancies is not associated with increased adverse events.

Source : http://cme.medscape.com/viewarticle/704610?sssdmh=dm1.488649&src=nldne

Changes in natriuretic-peptide levels over the first five days of hospitalization for acute decompensated heart failure (ADHF) significantly and independently predict both short- and intermediate-term survival, probably better than mere baseline biomarker levels, conclude researchers, on the basis of their post hoc analysis of a randomized trial [1].

The group reviewed in-hospital changes in levels of brain-type natriuretic peptide (BNP) in the Survival of Patients With Acute Heart Failure in Need of Intravenous Inotropic Support (SURVIVE) trial and compared them with all-cause mortality at one and six months in the study's patients as a whole, rather than by treatment group. SURVIVE was a randomized comparison of levosimendan (Simdax, Orion) vs dobutamine in ADHF patients in need of inotropic support [2].

The authors, led by Prof Alain Cohen-Solal (Hôpital Lariboisière, Université Denis Diderot, Paris, France), found significant independent associations between mortality and change in BNP from baseline to days 1, 3, and 5. A >30% BNP decline or an absolute drop of at least 800 pg/mL by day 5 provided the best prediction, according to their report in the June 23, 2009 issue of Journal of the American College of Cardiology.

"Such early and reliable prediction information offers the advantage of achieving early optimization of treatment," according to the group. "Consistent with our current findings in patients hospitalized with ADHF, we hypothesize that survival can be improved when the in-hospital treatment algorithm is aimed at decreasing BNP" by at least 30% or 800 pg/mL over five days, they write, cautioning that the strategy remains to be tested in prospective trials.

BNP: Biomarker, But Also Mortality Surrogate?

An accompanying editorial accepts that in-hospital BNP reductions seemed to predict one- and six-month mortality in the analysis but is skeptical of the group's resulting hypothesis that therapy aimed at BNP-lowering in the first days of ADHF hospitalization might improve later survival [3].

"Although the authors clearly state that this requires confirmatory testing, such a hypothesis has important implications for clinical practice and clinical trials in acute heart-failure syndromes because the number of patients hospitalized with heart failure continues to grow," according to Drs Mihai Gheorghiade and Peter S Pang (Northwestern University Feinberg School of Medicine, Chicago, IL).

Most patients with ADHF "appear to improve" during hospitalization with available treatments, yet they still have a high risk of rehospitalization, and their 60-day mortality "can be as high as 30% to 40%," they write. "Attempts to improve clinical outcomes with novel therapies have largely failed in terms of efficacy and/or safety." A surrogate marker for outcomes would in fact be welcome, they say, considering the difficulty and cost of conducting large mortality trials in ADHF.

But neither SURVIVE nor the levosimendan studies before it, write Gheorghiade and Pang, support the idea that "reductions in BNP are a reliable surrogate for postdischarge mortality as a result of early therapeutic optimization." A lot of data, in fact, suggest that "decreases in BNP may be associated with no benefit or even worse outcomes."

Commenting to heartwire , Cohen-Solal called the editorial "unfair" for its focus on his group's "hypothesis" that BNP reductions might lead to improved outcomes, while their analysis and actual conclusions were limited to the predictive value of BNP changes.

SURVIVE had randomized 1327 ADHF patients to receive infusions of either levosimendan, a calcium-sensitizing agent with both inotropic and vasodilating properties, or the familiar inotrope dobutamine. Entry to the study required an LVEF <30%>heartwire , the two groups fared the same with respect to the primary end point of all-cause mortality at 180 days; the rates were 26% and 28%, respectively.

Levosimendan is marketed in Europe and Latin America, but plans to gain approval in the US were abandoned following completion of SURVIVE [4].

In the current analysis, patients with >30% drop in BNP levels over five days had a 67% reduction in adjusted risk of death from any cause over the next month and a 47% decrease over the next six months. The risk reductions were independent of randomization group as well as such baseline features as BNP level, systolic and diastolic blood pressures, use of ACE inhibitors and beta blockers, and creatinine.

Rates and Hazard Ratios (Responders vs Nonresponders) for All-Cause Mortality at 31 and 180 Days

End point	Responders (%)	Nonresponders (%)	HR (95% CI)	p
31-d mortality	4.6	13.1	0.33 (0.21–0.52)	0.001
180-d mortality	17.9	30.3	0.53 (0.41–0.68)	0.001

*Responders defined as those with >30% BNP decrease from baseline at day 5 (of the trial's 1038 patients with available day-5 BNP levels).

On the other hand, the group writes, mortality at 31 days was tripled in patients with increased BNP levels from baseline to day 5, compared with those with a >30% decrease. The latter group, compared with those without a >30% BNP decrease, had significantly less cardiogenic shock and ventricular tachycardia over 180 days and similar rates of ACS, hypertension, renal failure, and acute MI.

BNP-Guided Therapy in Context

"There have been a lot of trials in chronic heart failure looking at whether tailoring therapy to reduce BNP levels would improve outcomes, but they used proven therapies like ACE inhibitors and beta blockers," Dr Monica R Shah (National Heart, Lung, and Blood Institute, Bethesda, MD) told heartwire . Some of those trials suggested that BNP-guided therapy was an improvement over standard management and some, like the STARBRITE trial for which Shah was principal investigator, showed no difference.

In ADHF, "a 30% decrease in BNP may just mark patients who are going to do better," she said. It may be possible to improve outcomes by pushing BNP down that far over five days, "but it's also a possibility that patients more likely to get better are also going to have a 30% decrease in their BNP simply because their disease isn't as advanced. Patients who are sicker may not be able to lower their BNP by that much regardless of the therapy used."

And if treatment with a drug actually does seem to lower biomarker levels, it could also have detrimental effects. "A drug may reduce BNP levels but may also increase the risk for ventricular arrhythmias and sudden death. That was the case with inotropes," Shah said.

"We all know that BNP is a good prognostic marker for outcomes. But we really don't have a marker that totally captures all of the effects of any drug."

Gheorghiade and Pang point out that in another levosimendan trial called REVIVE, which had a placebo control but enrollment criteria similar to those of SURVIVE, patients who received the active drug showed short-term BNP reductions but also more ventricular tachycardia, atrial fibrillation, and hypotension and a trend of increased mortality in the first five days. "It should be pointed out that the analysis by Cohen-Solal et al excluded the 69 patients (5.2%) who died within the first five days," they write. And in neither trial did five-day reductions in BNP with levosimendan translate into improved outcomes.

"We're not saying that we should aim to decrease BNP whatever the method used," said Cohen-Solal, who freely acknowledged that levosimendan was not associated with improved survival compared with dobutamine in SURVIVE. "We are saying that, overall, an early decrease in BNP is a very, very important predictor of outcome," whereas BNP as a treatment target was just a proposal for future research. There is now justification, he said, for a prospective trial comparing standard management with one in which "you do everything to decrease BNP by more than 30% by day 5."

SURVIVE was funded by Abbott Laboratories and Orion. The report discloses that coauthors Drs Bidan Huang and Danlin Cai are Abbott employees. Cohen-Solal and coauthors Dr Markku S Nieminen (University Central Hospital, Helsinki, Finland) and Dr Alexandre Mebazaa (Hôpital Lariboisière, Université Denis Diderot) report receiving honoraria from Abbott; Nieminen reports being a consultant for Orion; and Dr Damien Logeart (Hôpital Lariboisière, Université Denis Diderot) reports receiving fees from Biosite and Roche Diagnostics. Gheorghiade "is or has been a consultant for and/or received honoraria" from Abbott, Astellas, Bayer, AstraZeneca, Corthera, DebioPharm, Erre-Kappa Terapeutici, EKR Therapeutics, GlaxoSmithKline, Johnson & Johnson, Medtronic, Merck, Nile Therapeutics, Novartis, Otsuka, PeriCor Therapeutics, PDL BioPharma, Scios, Solvay Pharmaceuticals, and SigmaTau. Pang "is or has been a consultant" to Astellas, Bayer, the Medicines Company, Otsuka, Nile Therapeutics, PDL BioPharma, Pericor Therapeutics, and Solvay Pharmaceuticals; has received honoraria from Biogen Idec, Corthera, EKR Therapeutics, and Palatin Technologies; and has received research support from Corthera, Merck, and PDL BioPharma. Shah said she has no conflicts.

Source : http://www.medscape.com/viewarticle/704586?sssdmh=dm1.487338&src=nldne

Introduction

Background

Sleep disorders are among the most common clinical problems encountered in medicine and psychiatry. Sleep problems can be primary or result from a variety of psychiatric and medical conditions. Inadequate or nonrestorative sleep can markedly impair a patient's quality of life.¹

Primary sleep disorders result from an endogenous disturbance in sleep-wake generating or timing mechanisms, often complicated by behavioral conditioning. Primary sleep disorders are subdivided into parasomnias and dyssomnias. Parasomnias are unusual experiences or behaviors during sleep and include sleep terror disorder and sleepwalking (which occur during Stage 4 sleep) and nightmare disorder (which occurs during REM sleep). Dyssomnias are characterized by abnormalities in the amount, quality, or timing of sleep. These include primary insomnia and hypersomnia, narcolepsy, breathing-related sleep disorder (ie, sleep apnea), and circadian rhythm sleep disorder.

Assessing if a sleep disorder is primary or secondary is important. At times, assessing if anxiety and depression are causing sleep problems or if the anxiety and depression are secondary to a primary sleep problem is difficult. See Medscape's Anxiety Disorders and Depression Resource Centers.

Primary insomnia is the general term for difficulty in initiating or maintaining sleep. Because sleep requirements vary from individual to individual, insomnia is considered clinically significant when a patient perceives the loss of sleep as a problem. Insomnia may be characterized further as acute (transient) or chronic.

Pathophysiology

Rapid eye movement and nonrapid eye movement

Sleep is divided into 2 categories, rapid eye movement (REM) and nonrapid eye movement (NREM). Each of these sleep states is associated with distinct central nervous system activity.

NREM sleep is further divided into 4 progressive categories, termed stages 1-4 sleep. The arousal threshold rises with each stage of sleep, with stage 4 (delta) being the sleep state from which a person is least able to be aroused, characterized by high-amplitude slow waves.

REM sleep is characterized by muscle atonia, episodic REMs, and low-amplitude fast waves on electroencephalogram (EEG) readings. Dreaming occurs mainly during REM sleep.

Disturbances in the pattern and periodicity of REM and NREM sleep are often found when people aver to experiencing sleep disorders.

Sleep-wake cycles

Sleep-wake cycles are governed by a complex group of biological processes that serve as internal clocks.

The suprachiasmatic nucleus, located in the hypothalamus, is thought to be the body's anatomic timekeeper, responsible for the release of melatonin on a 25-hour cycle.

The pineal gland secretes less melatonin when exposed to bright light; therefore, the level of this chemical is lowest during the daytime hours of wakefulness.

Multiple neurotransmitters are thought to play a role in sleep. These include serotonin from the dorsal raphe nucleus, norepinephrine contained in neurons with cell bodies in the locus ceruleus, and acetylcholine from the pontine reticular formation. Dopamine, on the other hand, is associated with wakefulness.

Abnormalities in the delicate balance of all of these chemical messenger systems may disrupt various physiologic, biologic, behavioral, and EEG parameters responsible for REM (ie, active) sleep and NREM (slow-wave) sleep.

Frequency

United States

Approximately one third of all Americans have sleep disorders at some point in their lives. Approximately 20-40% of adults report difficulty sleeping at some point each year. Approximately 17% of adults consider the problem to be serious. Sleep disorders are a common reason for patient visits throughout medicine. Approximately one third of adults have insufficient sleep syndrome. Twenty percent of adults report chronic insomnia.

Mortality/Morbidity

• Chronic insomnia is associated with an increased risk of depression and accompanying danger of suicide, anxiety, excess disability, reduced quality of life, and increased use of health care resources.
• Insufficient sleep can result in industrial and motor vehicle crashes, somatic symptoms, cognitive dysfunction, depression, and decrements in daytime work performance owing to fatigue or sleepiness.

Sex

• Primary insomnia is more common in women, with a female-to-male ratio of 3:2. Hormonal variations during the menstrual cycle or during menopause may cause disruptions in sleep.
• Obstructive sleep apnea is more common in men (4%) than in women (2.5%).

Age

• Increasing age predisposes to sleep disorders (5% in persons aged 30-50 y and 30% in those aged 50 y or older).
• People who are elderly experience a decrease in total sleep time, with more frequent awakenings during the night.
• People who are elderly have a higher incidence of general medical conditions and are more likely to be taking medications that cause sleep disruption.

Clinical

History

Insomnia may present as decreased sleep efficiency or decreased total hours of sleep, with some associated decrease in productivity or well-being. Sleep quality is more important than the total number of hours slept because sleep requirements vary from person to person. Compare the total number of hours slept with each individual's lifelong normal night sleep time.

• Initial insomnia is characterized by difficulty falling asleep, with increased sleep latency (time between going to bed and falling asleep). Initial insomnia is frequently related to anxiety disorders.
• Middle insomnia refers to difficulty maintaining sleep. Decreased sleep efficiency is present, with fragmented unrestful sleep and frequent waking during the night. Middle insomnia may be associated with medical illness, pain syndromes, or depression.
• In terminal insomnia, also referred to as early morning wakening, patients consistently wake up earlier than needed. This symptom is frequently associated with major depression.
• Alterations of the sleep-wake cycle may be a sign of circadian rhythm disturbances, such as those caused by jet lag and shift work.
• Hypersomnia, or excessive daytime sleepiness, is often attributable to ongoing sleep deprivation or poor quality sleep for reasons ranging from sleep apnea to substance abuse or medical problems.
• In delayed sleep phase syndrome, the patient is unable to fall asleep until very early morning. As time progresses, the onset of sleep becomes progressively delayed.
• Sleepwalking, also called somnambulism, refers to episodes of complex behaviors during NREM sleep (stages 3 and 4) of which the patient is amnestic afterward.
• Nightmares are repeated awakenings from sleep caused by vivid and distressing recall of dreams. Nightmares usually occur during the second half of the sleep period. Upon wakening from the dream, the person rapidly reorients to time and place.
• Night terrors are recurrent episodes of abrupt awakening from sleep characterized by a panicky scream, with intense fear and autonomic arousal. The individual usually has no recall of the details of the event and is unresponsive during the episode. Night terrors occur during the first third of the night, during stages 3 and 4 of NREM sleep.
• The bed partner of patients who snore may provide a history of snoring. Such a history may help identify whether a patient experiences obstructive sleep apnea.

Physical

• Hypertension (can be caused by sleep apnea)
• Disturbed coordination (caused by sleep deprivation)
• Drowsiness
• Poor concentration
• Slowed reaction time
• Weight gain

Causes

The major causes of insomnia may be divided into medical conditions, psychological conditions, and environmental problems.

• Medical conditions
  • Cardiac conditions include ischemia and congestive heart failure.
  • Neurologic conditions include stroke, degenerative conditions, dementia, peripheral nerve damage, myoclonic jerks, restless leg syndrome, hypnic jerk, and central sleep apnea.
  • Endocrine conditions affecting sleep are related to hyperthyroidism, menopause, the menstrual cycle, pregnancy, and hypogonadism in elderly men.
  • Pulmonary conditions include chronic obstructive pulmonary disease, asthma, central alveolar hypoventilation (the Ondine curse), and obstructive sleep apnea syndrome (associated with snoring).
  • Gastrointestinal conditions include gastroesophageal reflux disease.
  • Hematological conditions include paroxysmal nocturnal hemoglobinuria, which is a rare, acquired, hemolytic anemia associated with brownish-red morning urine.
  • Substances that may result in insomnia include stimulants, opioids, caffeine, and alcohol, or, withdrawal from any of these also may cause insomnia.
  • Medications implicated in insomnia include decongestants, corticosteroids, and bronchodilators.
  • Other conditions include fever, pain, and infection.
• Psychiatric conditions: Bear in mind that the major psychiatric conditions now are known to have a biological basis and constitute a subset of medical conditions.
  • Depression may cause alterations in REM sleep. As many as 40% of people with depression have insomnia.
  • Posttraumatic stress disorder (PTSD) can produce vivid and terrifying nightmares.
  • Anxiety disorders predispose to insomnia. The most common of these are generalized anxiety disorder, panic disorder, and anxiety disorders not otherwise specified.
  • Thought disorders and misperception of sleep state are other potential states that cause insomnia.
  • Psychotropic medications, such as antidepressants, may interfere with normal REM sleep patterns.
  • Rebound insomnia from benzodiazepines or other hypnotic agents is common.
• Environmental problems
  • Stressful or life-threatening events (eg, bereavement, PTSD) may cause insomnia.
  • Shift work may disturb the sleep cycle, as might jet lag or changes in altitude.
  • Sleep deprivation may occur as a result of an overly warm sleeping environment, environmental noise, or frequent intrusions (such as in an intensive care unit setting).

Differential Diagnoses

Alcoholism	Emphysema
Anxiety Disorders	Hyperthyroidism
Bipolar Affective Disorder	Hypoparathyroidism
Breathing-Related Sleep Disorder	Obstructive Sleep Apnea-Hypopnea Syndrome
Chronic Obstructive Pulmonary Disease	Opioid Abuse
Depression	Posttraumatic Stress Disorder

Other Problems to Be Considered

Stimulant abuse (eg, amphetamine abuse)

Workup

Laboratory Studies

Lab studies appropriate for those with sleep disorders include the following:

• Hemoglobin and hematocrit
• Arterial blood gases
• Thyroid function tests
• Drug and alcohol toxicology screening

Imaging Studies

Although no imaging studies are indicated directly for the workup of insomnia, underlying medical conditions require appropriate investigation using suitable studies.

Other Tests

• Oximetry may be performed during sleep to examine blood oxygen levels for clinically important desaturations suggestive of sleep apnea or other sleep-disordered breathing.
• A Beck Depression Index or similar clinical screening tool may be used to detect an underlying depressive illness as a contributing factor in insomnia.
• An Epworth Sleepiness Score or other objective measure of daytime sleepiness may lead to clues of another underlying sleep disorder. For example, approximately 20% of patients with sleep apnea present with a history of nighttime insomnia; however, patients are excessively sleepy by day and have an abnormal score on the Epworth Sleepiness Scale.

Procedures

• Subjective measures of sleep are obtained by means of a sleep journal.
  • A sleep journal kept for approximately 2 weeks may help determine the extent of the sleep disturbance.
  • Patients should record the total hours slept per night, frequency of nighttime awakenings, and level of restfulness provided after sleep.
  • Further objective history might be available if patients have a sleep partner who keeps a 2-week journal or provides history.
• Objective measures of sleep may be obtained using EEG monitoring or polysomnography.
  • Monitored polysomnography is the criterion standard for evaluating measures of sleep. This study includes measures of multiple channels of electroencephalogram (EEG), electrooculogram (EOG), chin and leg electromyogram, nasal and oral airflow, oximetry, abdominal and chest movements, and ECG. Monitored polysomnography can help the physician discriminate between REM and NREM sleep, as well as causes of sleep arousal.
  • Polysomnogram may be useful in determining the etiology of the sleep disturbance.
  • These studies may be helpful in determining sleep and wakefulness in the intensive care unit or in the sleep laboratory.
  • Patients with chronic medical conditions, such as fibromyalgia or anxiety disorders, often have characteristic alpha brain-wave activity that intrudes into the deeper stages of sleep. This activity can readily be seen on the EEG during the polysomnogram (PSG).
  • Patients with insomnia often have some degree of sleep-state misperception, wherein they perceive and believe that they achieve significantly less sleep than they actually do. This can be documented by correlating the EEG findings from the PSG with patient subjective reports of sleep duration and onset.
  
  

Treatment

Medical Care

Evaluate patients for other primary sleep disorders (eg, sleep apnea); the impact of prescribed medication; and underlying medical, psychiatric, and substance abuse disorders. Teach good sleep hygiene. If necessary, consider medication.

• Educating the patient on good sleep hygiene is the center of treatment.
  • Use the bed for sleep and sex only (no television watching or reading in bed).
  • Avoid caffeine, especially late in the day. Avoid activities that will get you stimulated and upset late in the day. Practice relaxation techniques before bedtime.
  • Exercise each day.
  • Maintain a regular schedule for bedtime and wakening; avoid naps.
  • Do not watch the clock while in bed. Avoid struggling to fall asleep in bed. Instead, get up and spend quiet time out of bed until sleep comes.
• Sleep apnea can be helped by losing weight, the use of continuous positive airway pressure, and sometimes surgery.
• If someone sleep walks you may need to take steps to prevent them from accidentally hurting themselves at night by walking into things or out of the house.
• Light-phase shift therapy is useful for sleep disturbances associated with circadian rhythm abnormalities. Patients may be exposed to bright light, from either a light box or natural sunlight, to help normalize the sleep schedule.
• Cognitive behavioral therapy (CBT) and hypnotic medications are efficacious for short-term treatment of insomnia, but few patients achieve complete remission with any single treatment. Morin et al studied 160 adults with persistent insomnia and demonstrated that CBT used singly or in combination with zolpidem produced significant improvements in sleep latency, time awake after sleep onset, and sleep efficiency during initial therapy (all P <0.001). p =" .05).">2

Surgical Care

Surgical referral may be indicated to correct some underlying medical conditions that cause insomnia, such as for palate surgery in some cases of sleep apnea.

Consultations

Consultation can help evaluate patients for medical (including psychiatric) causes of insomnia. The evaluation team optimally should include a psychiatrist, neurologist, pulmonologist, sleep medicine specialist, and dietitian.

Diet

• No special diet is needed to treat insomnia, but large meals and spicy foods should be avoided in the 3 hours before bedtime.
• Patients should avoid sleep-disturbing substances such as alcohol, nicotine, and caffeine. Alcohol creates the illusion of good sleep, but sleep architecture is affected adversely. Nicotine and caffeine are stimulating and should be avoided in the second half of the day, from late afternoon on.
• Consumption of tryptophan-containing foods may help induce sleep. The classic example is warm milk.

Activity

• Strenuous exercise during the day may promote better sleep, but this same exercise during the 3 hours before bedtime can cause initial insomnia.
• Stimulating activities should be avoided 3 hours before bedtime. Examples include tense movies, exciting novels, thrilling television shows, arguments, and vigorous physical exercise other than coitus.

Medication

Many agents are useful in treating insomnia. Short-term drug therapy is preferred to restore a normal sleep pattern. Generally, hypnotic drugs are approved for 2 weeks or less of continuous use. In chronic insomnia, longer courses may be indicated, which require long-term monitoring to ensure ongoing appropriate use of the medication.

Barbiturates and chloral hydrate are seldom used now because of safety concerns related to their undesirably low therapeutic indexes.

Drugs that block the histamine type 1 receptor are used primarily in over-the-counter preparations, are inexpensive, and are helpful to some patients. However, in view of the anticholinergic properties of these agents, caution should be exercised in their use with older patients and with those who have disorders such as prostatic hypertrophy, cognitive disorders, and constipation. In addition, most of these drugs have a long duration of action, and their sedative effects may persist well into the following day.

Zolpidem (Ambien) and zaleplon³ (Sonata) are the newest and, arguably, the safest agents that are US Food and Drug Administration (FDA) approved for short-term hypnotic use. Zolpidem (Ambien CR) has recently released an extended-release version that lasts slightly longer than the original preparation. In addition, the FDA recently approved the new agent eszopiclone (Lunesta) as the first agent for long-term use in the management of chronic insomnia.

Benzodiazepines

Benzodiazepine receptor agonists are the mainstay in treatment of insomnia. Flurazepam, temazepam, quazepam, estazolam, and triazolam are the benzodiazepines that are approved by the US Food and Drug Administration as hypnotics.

These drugs bind to a special benzodiazepine site on the GABA receptor complex, enhancing activity of this neurotransmitter. All have variable half-lives and different metabolites that affect their onset and duration of action. This class of drugs suppresses REM sleep and reduces stages 3 and 4 sleep while increasing stage 2 sleep. The drug described here, temazepam, is only one example of this class of medications. A more detailed discussion of the other agents in this class can be found elsewhere in the text.

Temazepam (Restoril)

Intermediate rate of absorption and duration of action make this drug useful for treating initial and middle insomnia. Has no active metabolite, which reduces cognitive impairment and grogginess the following day.

Imidazopyridine

Zolpidem is the sole member of this class of medications. It binds at a benzodiazepine receptor subtype (omega I). Found more in CNS more than in peripheral nervous system, which helps to account for hypnotic effect with no significant muscle-relaxant properties. Unlike benzodiazepines, normal sleep architecture not suppressed.

Zolpidem (Ambien)

Rapidly absorbed, with fast onset (20-30 min) of action, which makes this a good drug for sleep induction. Decreases sleep latency and increases duration of sleep.

Pyrazolopyrimidine

Zaleplon is the sole agent in this class of nonbenzodiazepine hypnotics.

Zaleplon (Sonata)

Not structurally related to benzodiazepines, barbiturates, or other drugs with known hypnotic properties. Interacts with GABA-benzodiazepine receptor complex, causing effects in sedation. Should be taken immediately before bedtime.
Decreases time to sleep onset. Shorter onset of action means peak serum concentrations achieved within 1 h of administration. This may account for lower incidence of daytime grogginess and less withdrawal rebound insomnia.

Pyrrolopyrazine

This is another nonbenzodiazepine sedative/hypnotic drug class indicated to improve sleep onset and maintenance.

Eszopiclone (Lunesta)

Nonbenzodiazepine hypnotic pyrrolopyrazine derivative of the cyclopyrrolone class. The precise mechanism of action is unknown but is believed to interact with GABA-receptor at binding domains close to or allosterically coupled to benzodiazepine receptors. Indicated for insomnia to decrease sleep latency and improve sleep maintenance. Short half-life of 6 h. Higher doses (ie, 2 mg for elderly adults and 3 mg for nonelderly adults) are more effective for sleep maintenance, whereas lower doses (ie, 1 mg for elderly adults and 2 mg for nonelderly adults) are suitable for difficulty in falling asleep.
Decreases sleep latency and improves sleep maintenance.

Melatonin receptor agonist

Ramelteon is the first and only nonscheduled insomnia medication with a novel mechanism of action.

Ramelteon (Rozerem)

Melatonin receptor agonist with high selectivity for human melatonin MT₁ and MT₂ receptors. MT₁ and MT₂ are thought to promote sleep and be involved in maintenance of circadian rhythm and normal sleep-wake cycle. Indicated for insomnia characterized by difficulty with sleep onset.

Antidepressants

Although no antidepressants are approved specifically for use in the treatment of sleep disorders, a cyclic antidepressant, trazodone (Desyrel), is used routinely for this purpose.

Trazodone (Desyrel)

Mechanism of action not fully understood. Thought to selectively inhibit serotonin uptake by brain synaptosomes and potentiate behavioral changes induced by serotonin precursor, 5-HT. Major adverse effect is sedation.

Follow-up

Further Inpatient Care

Inpatient care is rarely, if ever, required for treatment of insomnia. Only a severe underlying medical, psychiatric, or substance abuse disorder would warrant inpatient care.

Further Outpatient Care

Multiple possible medical etiologies of sleep disorders make them difficult to diagnose and necessitate regular appropriate follow-up care until final diagnosis has been made and successful treatment has been implemented. Several medical specialists may be needed for care and consultations and can be coordinated by the patient's internist, personal physician, or medical sleep specialist.

Inpatient & Outpatient Medications

Regular follow-up care, even if infrequent, is necessary once appropriate medication is successfully in use. (However, medication may be unnecessary.)

Deterrence/Prevention

• In addition to specific treatment for diagnosed sleep disorders, good sleep hygiene should be taught to every patient (and this information should be publicly available). Just as with dental hygiene, appropriate sleep habits should be cultivated by all individuals at all times.
• See Medical Care for more information.

Complications

Mood and anxiety disorders may develop from untreated sleep disturbances, and current medical literature supports the theory that these brain-based mental status changes are risk factors for morbidity and mortality from a host of medical conditions (eg, cardiovascular disease).

Prognosis

The prognosis varies widely depending on the etiology of the insomnia or other sleep disorder. For example, insomnia due to obstructive sleep apnea resolves with successful treatment of the apnea, while insomnia due to refractory major depression is itself refractory until a successful treatment can be found for the depression.

Patient Education

• All individuals should be taught and encouraged to practice good sleep hygiene, as outlined in Medical Care.
• Educating the patient's family about proper sleep hygiene is imperative, especially because the patient's spouse can be adversely affected by sleep disorders such as sleep apnea.
• Use the bed for sleep and sex only (no television watching or reading in bed).
• For excellent patient education resources, visit eMedicine's Mental Health and Behavior Center and Sleep Disorders Center. Also, see eMedicine's patient education articles Disorders That Disrupt Sleep (Parasomnias), Insomnia, Primary Insomnia, REM Sleep Behavior Disorder, Understanding Insomnia Medications, Sleep Disorders in Women, Sleep Disorders and Aging, and Sleeplessness and Circadian Rhythm Disorder.

Miscellaneous

Medicolegal Pitfalls

• Patients should be warned to not drive or operate machinery while taking sedative-hypnotic medications. Document these admonitions clearly in the medical record.
• Caution is advised in the treatment of patients who are elderly and others who may be at increased risk for falls.

Source : http://emedicine.medscape.com/article/287104

Abstract

The patient-centered medical home (PCMH) is emerging as a potential catalyst for multiple health care reform efforts. Demonstration projects are beginning in nearly every state, with a broad base of support from employers, insurers, state and federal agencies, and professional organizations. A sense of urgency to show the feasibility of the PCMH, along with a 3-tiered recognition process of the National Committee on Quality Assurance, are influencing the design and implementation of many demonstrations. In June 2006, the American Academy of Family Physicians launched the first National Demonstration Project (NDP) to test a model of the PCMH in a diverse national sample of 36 family practices. The authors make up an independent evaluation team for the NDP that used a multimethod evaluation strategy, including direct observation, in-depth interviews, chart audit, and patient and practice surveys. Early lessons from the real-time qualitative analysis of the NDP raise some serious concerns about the current direction of many of the proposed PCMH demonstration projects and point to some positive opportunities. We describe 6 early lessons from the NDP that address these concerns and then offer 4 recommendations for those assisting the transformation of primary care practices and 4 recommendations for individual practices attempting transformation.

Introduction

The patient-centered medical home (PCMH) is rapidly becoming a powerful engine for multiple reform efforts related to health care delivery, reimbursement, and primary care.^[1-13] During the next few years, we can expect thousands of primary care practices to attempt to convert their offices into PCMHs. Demonstration projects are underway in numerous states and supported by amazingly diverse constituencies that include professional organizations, major employers, insurers, Medicare, state governments, not-for-profit foundations, and others. These diverse and rapidly growing efforts are being initiated based on an appealing idea but with little direct empirical support.^[4,5] The PCMH represents an innovative and exciting national conversation that melds core primary care principles, relationship-centered patient care, reimbursement reform, new information technology, and the chronic care model. Unfortunately, the rush to demonstrate operational and financial feasibility of the PCMH, proceeding apace with the recognition process of the National Committee for Quality Assurance (NCQA)^[14] risks premature closure of the larger PCMH conversations and potentially stifles evolution of the PCMH to meet important patient, practice, and system needs.

The "Future of Family Medicine" report^[15] was published in 2004 and detailed the "New Model of Family Medicine."^[16] This report helped to initiate the national conversations leading to the PCMH. The National Demonstration Project (NDP) was launched in June 2006 by the American Academy of Family Physicians^[17] to test this new model and was updated to be consistent with the emerging consensus principles of the PCMH.^[10] Thirty-six family practices were selected from 337 practices completing a well-publicized, comprehensive on-line application. Practice selection attempted to maximize a diversity of geography, size, age, and ownership arrangements. For the most part, the participating practices were highly motivated to test the new models of care and in many cases had begun a local process of innovation.

Practices were randomized into either facilitated or self-directed groups. Facilitated practices received ongoing assistance from a change facilitator, as well as on-going consultation from a panel of experts in practice economics, health information technology, quality improvement, and discounted software technology, training, and support. They were also involved in 4 learning sessions and regular group conference telephone calls. Self-directed practices were given access to Web-based practice improvement tools and services, but they did not have on-site assistance. They self-organized their own learning session halfway through the 2-year project and participated in the final learning session.

The NDP officially concluded, after 2 years, in June 2008. The authors of this report make up an independent evaluation team that designed and is continuing to analyze a multimethod assessment of the NDP. The evaluation addresses both the effect of the PCMH model on patient and practice outcomes and the effectiveness of the facilitated intervention in bringing about transformation.

Even though analysis of the NDP is not yet complete, we feel compelled to share early lessons in advance of more-exhaustive mixed methods research reports planned for early next year. As close observers of these practices for 2 years, we have gained a perspective on the implementation process that we feel deserves attention and public discussion even before the final outcome analysis is completed. In the process of working with these practices, our team has seen the day-to-day reality of changing community-based practices into the current idealized model of the PCMH. We have already learned enough from the NDP to identify some potentially dangerous red flags fluttering over the demonstrations just getting underway. Our early analysis raises concerns that current demonstration designs seriously underestimate the magnitude and time frame for the required changes, overestimate the readiness and expectations of information technology, and are seriously undercapitalized. We fear that with current assumptions, many demonstrations place participating practices at substantial risk and may jeopardize the evolution of the PCMH as unrealistic expectations set up demonstrations and evaluations for failure.

The lessons described below arise from both the real-time or "live" qualitative analysis conducted during the NDP and the in-depth and comprehensive analysis currently underway. The live analysis included real-time reading of all data and multidisciplinary analysis team discussion in biweekly conference calls, quarterly reports to the NDP board,^[18] site visits by a member of the evaluation team, 3 analytic retreats, and member checking with NDP facilitators and practice participants to both expand understanding and seek disconfirming data. This special report, based on our ongoing analysis, raises timely concerns and opportunities. The pressure toward widespread adoption of this is model is gaining momentum so rapidly that we feel compelled to share our observations and summarize the early process-evaluation lessons. We describe 6 critical lessons, suggest 4 recommendations for health policy and 4 for practices, and raise hopeful warnings at this critical juncture for primary care reform.

Initial Lessons Learned

Becoming a PCMH Requires Transformation

Change is hard enough; transformation to a PCMH requires epic whole-practice reimagination and redesign. It is much more than a series of incremental changes. Since the early 1990s, theories of quality improvement emphasizing sequential plan-do-study-act cycles have dominated change efforts within primary care practices.^[19] Many NDP practices initially chose to take this incremental approach -- literally checking off each model component as completed. They were soon overwhelmed with complications. Whereas the traditional quality improvement model works for clearly bounded clinical process changes, the NDP experience suggests that transformation to a PCMH requires a continuous, unrelenting process of change. It represents a fundamental reimagination and redesign of practice, replacing old patterns and processes with new ones. Transformation includes new scheduling and access arrangements, new coordination arrangements with other parts of the health care system, group visits, new ways of bringing evidence to the point of care, quality improvement activities, institution of more point-of-care services, development of team-based care, changes in practice management, new strategies for patient engagement, and multiple new uses of information systems and technology.

These multiple components of a PCMH are highly interdependent.^[20] Each component, when implemented, ripples throughout the practice, affecting all other work processes and individual roles. Prior changes require adjustment as new ones are made and practice systems and relationships begin to operate in different ways. Roles of individuals and the practices, sense of identity, and imagination about the meaning of patient care are changed. Most current practice models are designed to enhance physician workflow. The PCMH should be designed to enhance the patient experience. This shift requires a transformation, not an incremental change.

Technology Needed for the PCMH Is Not Plug and Play

Although most participating practices had an electronic medical record (EMR) at the beginning of the project, an initial strategy of the NDP was to implement further technological enhancements supporting a PCMH (eg, registries, e-prescribing, patient portals, etc) and to use them to reconfigure work patterns. These added features included a range of components, some of which were enhancements to EMR.^[17] New technology implementation was more difficult and time consuming than originally envisioned. The hodgepodge of information technology marketed to primary care practices resembles more a pile of jigsaw pieces than components of an integrated and interoperable system. A function as seemingly simple as a disease registry was either absent from EMR systems or extremely awkward to activate and required complicated workarounds. Even with discounted pricing and more than usual technical support from vendors, the challenges proved daunting. Making the tasks more difficult was the need to redefine work processes before implementation rather than after. Technology often foundered on the shoals of practice work redesign. This lesson resonates well with the emerging research literature about the EMR in primary care practices.^[21-24]

Transformation to the PCMH Requires Personal Transformation of Physicians

Transformation to a PCMH requires not only implementing new, sophisticated office systems, but also adopting substantially different approaches to patient care. Such a fundamental shift nearly always challenges doctors to reexamine their identity as a physician. For example, transformation involves a move from physician-centered care to a team approach in which care is shared among other adequately prepared office staff.^[25] To function in this team-based environment, physicians need facilitative leadership skills instead of the more common authoritarian ones. A PCMH requires expanding the clinical focus from 1 patient at a time to a proactive, population-based approach, especially for chronic care and preventive services.^[26,27] In addition, physician-patient relationships need to shift toward a style of working in relationship-centered partnerships to achieve patients' goals rather than merely adhering to clinical guidelines.^[28-30]

Change Fatigue Is a Serious Concern Even Within Capable and Highly Motivated Practices

The magnitude and pace of change required to transform into a PCMH produced change fatigue midway through the first year. Transformation occurs, not at a steady and predictable pace, but in fits and starts. After the strenuous task of implementing a particular PCMH component, the practice had to simultaneously manage the ripple effects, maintain the change, and prepare for the next. The work is daunting and exhausting and occurring in practices that already felt as if they were running as fast as they could. This type of transformative change, if done too fast, can damage practices and often result in staff burnout, turnover, and financial distress. Fortunately, we saw several instances in which the arduous effort of change was punctuated by a breakthrough, a glimmer of insight, and new energy as process change became connected to personal change and to a renewed sense of meaning and purpose. Learning sessions became important opportunities for practice leaders to reenergize through sharing experiences and providing support. Nevertheless, participants found it challenging to pass this energy on to colleagues when they returned home.

Transformation to a PCMH Is a Developmental Process

As the NDP progressed, we began to see a distinction between what we have named the practice's "core structure" and its "adaptive reserve." Core structure includes capabilities to manage basic finances and clinical and practice operations during times of stability and modest change. A practice's ability to keep pace with rapid development and change, however, was largely a function of the practice's adaptive reserve. A strong adaptive reserve includes such capabilities as a strong relationship system within the practice, shared leadership, protected group reflection time, and attention to the local environment.^[31] In the beginning of the NDP, practices varied considerably in their adaptive reserve, and that capability was a major determinant of a practice's initial progress. None of the practices, at baseline, had a systematic change management process in place, and few preserved time for planning and reflection. In many practices, change began as an initial flurry of physician-led, just-do-it, top-down actions. Although initially successful in some practices, this approach proved ineffective in the long-term. The intense pace and magnitude of change soon revealed and exacerbated deeper dysfunction within the relationship infrastructure of practices, including tension among physicians and among practice staff, ineffective communication patterns, and avoidance of potential conflict and difficult conversations that produced stalemate. Transformation toward a PCMH appears to require a strategic developmental approach that starts with assuring a strong structural core, and then implements smaller changes that help to build the adaptive reserve. Only then can larger, more complex changes begin. Such transformation takes more time than the 2 years allocated to the NDP.

Transformation Is a Local Process

We observed multiple pathways toward the PCMH, each highly dependent on initial conditions at the local practice, health care system, and community level. Even among the highly motivated NDP practices (both facilitated and self-directed) there was considerable variation in need for assistance, depending on specific challenges and previous experience with change. Facilitated practices received a spectrum of assistance, including a combination of consultation (providing specific information), coaching (assisting physicians and others in personal transformation), and facilitation (addressing a practice's adaptive reserve.) Among the self-directed practices, some believed they would have benefited from assistance but varied in describing what might have helped. Others reported they did better plotting their own course and time frame with reinforcement from their learning session. Practices with strong adaptive reserve were especially able to develop and implement PCMH components that made sense in the context of their unique characteristics and circumstances.

Recommendations for Supporting PCMH Practice Transformation

Health Policy Recommendations

1. Assure Adequate Financial Resources. Transforming to a PCMH costs dollars, as well as time and effort, and currently available funds and reimbursements are likely to be inadequate for the transitional costs. We are encouraged by the many diverse pilot funding programs, but more will be necessary. Pilot programs should include up-front capital dollars to help purchase and implement new information technologies and additional ongoing operational dollars to support the personnel changes needed to implement better care management. All the well-supported NDP-facilitated practices were challenged financially by the project.

2. Tailor the Approach to the Practice. There are many ways to create a PCMH and many different forms a PCMH may take. Either over-specification of the model or prescribing the pathway for achieving it can be counterproductive, frustrate practice participants, and exacerbate change fatigue. Respect the practice's responsibility for its own destiny. Practices may need assistance, but decisions of what and how and when to change must be theirs. Facilitation, consultation, coaching, learning sessions, and use of Web resources, all have roles. Practices must remain full partners in their learning and development process.

3. Assist Physicians With Their Personal Transformation. A substantial barrier to conversion to a PCMH is the need for most individual physicians to change their professional identity and the socialized ways they currently deliver primary care. It is important for professional organizations that promote PCMH development to understand their role as much more than advocating for a new reimbursement structure; they should embrace with equal enthusiasm and dedication the need to promote new approaches to doctoring and managing practices and transformation. This endeavor requires new tools, workshops, and other learning and personal development formats to help physicians transform within themselves and in their relationships with their practice partners, patients, health care systems, and communities. Some new doctoring skills required for the PCMH include working in practice teams, managing chronic care using the chronic care model, incorporating population management, using evidence at the point of care, facilitating leadership skills, integrating change management, training staff as peers (ie, adult learning), patient partnering, and thinking outside the examination room.

4. National Committee for Quality Assurance Should Modify its PCMH-Recognition Process. For most practices, full transformation to a PCMH is likely to require more than the 3 years of the NCQA process. Even in the NDP, with highly motivated and capable practices, full transformation to a PCMH was not achieved within the 2 years of the project because of the multiple challenges of transforming personal, developing teams, recreating job descriptions and work flow, implementing multiple technologies, building adaptive reserve, accommodating change fatigue, adjusting for problems, learning along the way, and maintaining financial integrity. For most practices, this transformation is likely to require an ongoing process.

Practice transformation is a developmental process; recognition and certification should encourage and support a developmental approach. The NCQA has taken the lead in defining some essential components and creating a 3-tiered, implementation process for recognizing a PCMH.^[14] We fear the details of the recognition process may have reached premature closure,^[4,5] however, before the rich data have emerged from the NDP and other current demonstrations. The experience from the NDP clearly suggests becoming a PCMH necessitates that practices work on leadership development, relationship and communication improvements, and other aspects of building adaptive reserve to achieve sustainable success and to avoid unintentional harm to practice, staff, and patients. As further information on the change process becomes available, we strongly encourage the NCQA to reevaluate its PCMH-recognition process and landmarks to encourage and support a more developmental approach at the practice level. Finally, there is need to incorporate more measures of patient engagement and patient-centeredness.

Practice Recommendations

1. Establish Realistic Initial Expectations for Time and Effort Required. Practices should not underestimate the difficulty they face. Practice transformation is a lengthy process, and at times practices will feel like quitting. They should recognize early the need to build better communications, trust, and relationships so the adaptive reserve for change will be up to the challenges. Having an adaptive reserve is paramount to transformation success and may require months or years of hard work to create a strong communication and relationship infrastructure. Whole-practice redesign is different from incremental quality improvement, although reflection on the effect of individual changes and willingness to make further modification are essential. Finally, it is important protect regular time to reflect and learn as a practice. Transformation to a PCMH will require that everyone in the practice to be engaged in the transformation process.

2. Develop a Practice Technology Plan, Be Flexible and Reflective. Implementing technology support for a PCMH consumes an inordinate amount of time, energy, and dollars. Given this level of investment and the interdependencies of the technology components, practices should develop their own plan that projects which technology components they will implement and in what sequence to achieve the care capabilities they desire. Because the technology landscape is changing so rapidly, the plan should be revisited and updated frequently, with reflection incorporated on the experience thus far. For example, it is possible and sometimes preferable to implement e-prescribing, local hospital system connections, evidence at the point of care, disease registries, and interactive patient Web portals without an EMR.

3. Monitor Change Fatigue. It will be important for the practice and its external change agents to monitor closely to avoid or detect early any unfortunate change casualties. In the NDP, periodic learning sessions provided an opportunity to reenergize and motivate participants. In some practices a whole-practice retreat addressing and naming what was happening substantially enabled supportive relationships to develop. Do not be surprised if the situation seems worse after the first 6 months to a year; the experience of benefits often takes at least 2 years.

4. Learn to Be a Learning Organization. Observations in the NDP practices suggest transformation is more about learning how to become a learning organization, which co-creates an emergent future, than it is about learning from experts on how to build something already known. There is no expert who knows what a PCMH actually looks like. We are all learning together as thoughtful practices around the country transform in their own way and at their own pace. This learning organization model differs appreciably from the conventional expert model and challenges a medical community expecting consultants to come with external expertise and simply fix problems.

Hopeful Warnings

In the headlong rush for widespread implementation of the PCMH, it will be important to continue to learn from the change process and how it evolves in diverse local environments and a rapidly changing national context. Is the PCMH the new managed care of the mid-90s, a new savior of primary care that will be implemented in such a way as to undermine and weaken it? What if the technology isn't ready? What if the endeavor is undercapitalized and underreimbursed? What if the insurers continue to hold all the cards? What if disease management indices and short-term costs are measured and promoted over relationships and health status and value? What if, in the name of economy of scale, the scale of implementation at the local level is too big for real personalization of care? What if, in the guise of efficiency and safety, standardization overwhelms the particular? What if the timeline of expectations is too short? Beyond the skeleton of the Joint Principles,^[10] is there even a shared understanding of what the heart and soul of a PCMH really is?

Part of the PCMH's strong appeal, and also what creates confusion, is that it potentially unites 4 compelling areas of health care reform activity.^[5] These areas include research on primary care's value, improved approaches to chronic care, consumerism, and new health care-related information and communication technology. There is mounting evidence showing primary medical care's value in assuring a health care system of higher quality at lower cost and with more equity.^[32,33] The primary care and practice characteristics associated with this evidence are first-contact care with easy access, comprehensive care (degree to which primary care clinician provides a broad range of services), sustained partnerships or longitudinal care, coordinated care, and personal or patient-focused care with family and community orientation.^[34,35] In addition, there is growing support for the use of the chronic care model in health systems and primary care practices.^[26,27] These core primary care features and the chronic care model constitute core elements of the medical home concept.

At the same time, consumer-related groups are advocating for better service, partnership, and transparency in health care. Consumers of health care services want the care they want and need when and how they want and need it, as well as access to information necessary to make appropriate choices. This consumerism track informs the patient-centered part of the medical home.^{[13,29,30,36,37]} New Web-based technologies, electronic clinical information systems, and telecommunications are finally nearing accessibility and utility for both health systems and primary care practices.^[22-24,38] They offer an opportunity for integrating primary care with the rest of our fragmented health care system and for facilitating more engagement of patients in their own care. Future PCMH recognition and certification processes should focus more on patient-centered attributes and the proven, valuable key features of primary care^[32] than on the disease management and information technology features of the PCMH. The PCMH represents the essentials for better primary care, improved delivery of chronic care, and active partnership with an informed patient synergized by appropriate use of information and communications' technology.

The PCMH represents a pivotal turning point for the restoration of a healthy primary care foundation and better health for our nation. Everyone should have a PCMH, and it should be developed primarily to improve health care; payment reform should remain an important secondary goal.^[2,3] In the spirit of seizing this historical moment, we close with some reminders and hopeful warnings. The PCMH will need adequate capital funding from a combination of federal, state, local, insurance industry, and health systems' participation. Having practices front the cost of transformation with the hope of more appropriate reimbursement in the future is unlikely to succeed. We will need more transparency and negotiation of the many hidden agendas, especially among insurers and physicians. We should be wary of industrial-like schemes and excessive use of the language of productivity and efficiency. Primary care, like healthy food, works best at a local and personal level. What is waste on an assembly line is not necessarily waste in a healing relationship; allow for appropriate variability. Stewarding patients toward healthier lives is a deliberate process -- stewarding practices toward health and toward becoming a PCMH is also.

To read commentaries or to post a response to this article, see the online version at
http://www.annfammed.org/cgi/content/full/7/3/254.

Source : http://www.medscape.com/viewarticle/703460