Friday, November 24, 2017

Clinical status before and outcomes after admission to hospice



Background

Prior work has shown that symptoms leading to restrictions in daily activities are common at the end of life. Hospice is a Medicare benefit designed to alleviate distressing symptoms in the last 6 months of life. The effect of hospice on the burden of such symptoms is uncertain.

Methods

From an ongoing cohort study of 754 community-dwelling older persons, aged greater than or equal to 70 years, we evaluated 241 participants who were admitted to hospice from March 1998 to December 2013. A set of 15 physical and psychological symptoms leading to restricted activity (ie, cut down on usual activities or spend at least half the day in bed) were ascertained during monthly telephone interviews in the year before and 3 months after hospice admission.

Results

The prevalence and mean number of restricting symptoms increased progressively until about 2 months before hospice admission, before increasing precipitously to a peak around the time of hospice admission. After the start of hospice, both the prevalence and the mean number of restricting symptoms dropped markedly. For several symptoms deemed most amenable to hospice treatment, including depression and anxiety, the prevalence dropped to levels comparable to or lower than those observed 12 months before the start of hospice. The trends observed in symptom prevalence and mean number of symptoms before and after hospice did not differ appreciably according to hospice admission diagnosis or sex. The median duration of hospice (before death) was only 15 days.

Conclusion

The burden of restricting symptoms increases progressively several months before the start of hospice, peaks around the time of hospice admission, and decreases substantially after the start of hospice. These results, coupled with the short duration of hospice, suggest that earlier referral to hospice may help to alleviate the burden of distressing symptoms at the end of life.

Thursday, November 23, 2017

Hospitalists’ enthusiasm for MOC: less than overwhelming


Wednesday, November 22, 2017

Home NPPV



Question Does the addition of home noninvasive ventilation to home oxygen therapy prolong time to readmission or death for patients with chronic obstructive pulmonary disease and persistent hypercapnia following a life-threatening exacerbation?

Findings In this randomized clinical trial of 116 patients, the addition of home noninvasive ventilation significantly prolonged time to readmission or death from 1.4 months to 4.3 months.

Meaning The addition of home noninvasive ventilation to home oxygen therapy may improve outcomes in patients with severe chronic obstructive pulmonary disease and persistent hypercapnia following hospital admission.

Tuesday, November 21, 2017

An attempted classification to encompass the diverse phenotypes of diabetes


The different forms of diabetes no longer lend them selves to two simple categories. Various efforts to refine the classification have been met with controversy and complicated by evolving understanding. Here is my attempt to summarize the current thinking.

Type 1: caused by complete autoimmune destruction of the beta cells. A good practical definition is that patients require exogenous insulin in order to stay alive. That is, they will invariably develop ketoacidosis (DKA) when deprived of insulin, even in the basal state. It is important to specify the basal state, because patients with other forms of diabetes can go into DKA as well, but only in the presence of some stressor such as sepsis, MI, stroke, etc. This designation has changed little in recent decades and remains useful, though it has seen some tweaks as noted below.



Type 1b aka 1.5: These designations are no longer very useful for a variety or reasons. They originally (especially 1b) referred to a group of patients in certain ethnic groups with phenotypic characteristics of both type 1 and type 2 diabetes who seemingly transitioned from type 1 to type 2 and/or back, due to a non autoimmune mechanism: intermittent reversible severe beta cell failure due to an exaggerated form of glucotoxicity. This group has subsequently been found to be more heterogeneous than previously thought, both in terms of ethnicity and pathogenesis. To confuse things further, these terms (especially 1.5) have also been used to denote late autoimmune diabetes of adulthood (LADA), an unrelated condition. The terms were partially replaced in popular usage with ketosis prone type 2 diabetes but that too has been waning in popularity, largely abandoned. The ADA, recognizing that there are patients who develop DKA but lack antibodies, created the category of “idiopathic type 1 diabetes.” A more recently proposed category recognizes the heterogeneity in these patients (and subclassifies them accordingly) and is known as ketosis prone diabetes (see below). To confuse things a bit, KPD also incorporates patients who do not fit this phenotype, in order to encompass all diabetic patients who go into ketoacidosis apart from some severe stress. (Note: a very early designation for patients seemingly transitioning between the phenotypes of DM 1 and 2 was Flatbush diabetes).



Ketosis prone diabetes (KPD): This is a proposed designation to replace the category immediately above and adds some other mechanisms, attempting to encompass all patients who spontaneously develop DKA. It recognizes the heterogeneity of the phenotype above, specifically the fact that some forms have an autoimmune pathogenesis. Its 4 categories are based on the presence or absence of beta cell reserve and the presence or absence of autoimmunity.



Type 2: DM 2 is pretty well defined and I will not spend a great deal of time here other than to caution against defining it as any case of diabetes that does not develop DKA in the basal state. That is to say that some forms of diabetes, that don’t invariably cause DKA in the basal state, are not appropriately classified as DM 2 as will be discussed below. Although DM 2 is itself heterogeneous the patients have in common insulin resistance, gradual beta cell fatigue and the metabolic syndrome.



Type 3: Here’s where it gets even more confusing. While often a wastebasket there are some forms of diabetes that rightfully belong in this category though in current literature they have varied and sometimes quite limited degrees of acceptance. There are numerous subcategories. Here they are.

Type 3, no letter designation: This is a theoretical construct that Alzheimer disease is essentially diabetes (insulin resistance) localized to the brain and might be effectively treated with insulin sensitizing agents.

Additional categories of DM 3, designated by letter, were taken from this site:

Type 3 A refers to genetic defects in beta cells, essentially MODY. Inheritance is monogenic autosomal dominant as opposed to the polygenic inheritance of DM 2.

Type 3 B refers to severe genetically determined insulin resistance as seen in Donohue syndrome and related disorders.

Type 3 C is a more accepted category and denotes diabetes due to damage to the pancreas as a whole, eg pancreatitis, pancreatic cancer or pancreatic trauma. [1] [2]. This is important because it is usually misdiagnosed as DM 2 yet has unique treatment implications.

Type 3 D is DM caused by other endocrinopathies eg Cushing’s.

Type 3 E refers to DM caused by drugs such as corticosteroids.

Type 3 F refers to DM caused by infection. In the cite referenced above congenital rubella was given as the example. Would Hep C fit in here?

Type 3 G refers to diabetes associated with unusual autoimmune diseases, eg stiff person syndrome.

Type 3 H refers to diabetes associated with Down’s syndrome.

Note: Although all the entities mentioned above under type 3 are real I could find little or no independent support in the literature for the nomenclature except for the one with no letter designation (Alzheimer disease) and type 3C.



Type 4 This is a theoretical construct based on an animal model, attempting to explain some instances of apparent DM 2 in lean adults. This may not be an important entity in man if it exists at all and might be confused with LADA.



Miscellaneous forms:

Latent autoimmune diabetes in adults (LADA). It is sometimes been referred to as DM 1.5.

Double diabetes. You could be unlucky and have both 1 & 2. Or, in DM 1, if you treat overeating with more and more and more insulin and thereby gain of sufficient weight the characteristics of DM 2 could develop secondarily.


Monday, November 20, 2017

Sunday, November 19, 2017

Saturday, November 18, 2017

Appropriate and inappropriate use of troponin assays



The article offers a useful perspective on troponin testing but, if I’m not mistaken (correct me if I’m wrong) starts out with an error:

Troponin is a protein in striated muscle that regulates excitation and contraction, and consists of 3 molecules: C, I, and T. Troponin I and T are specific to cardiac tissue…

I’m pretty sure skeletal muscle has troponin I and T.

At any rate, the key point of the article is that in the old days of the early generation troponins, any elevation meant the patient was having an acute MI, usually due to acute coronary syndrome. Several generations (and sensitivity improvements) later that is no longer the case. The problem is, too many of us apparently interpret troponins the way we did in those good old days. This, as the author points out, can lead to problems such as knee jerk anticoagulation.

The remedy for this, according to the author, is to do a history and physical before ordering a troponin. That’s easier said than done in the crazy environment of hospital medicine where time is of the essence and we often have to utilize a shotgun approach to very sick patients. The reality is that troponin positivity has now become much more complex and requires considerable skill in applying the result to the prevailing clinical context.