The dark side of cost-conscious medicine: Martin Samuels

Inflammatory markers in obese adolescents

Interesting read.

Hospitalization with infection as a particular risk factor for VTE

Highlights from a recent study:

Highlights

•Hospitalized infection appears to trigger VTE events.

•The triggering effect of infection on VTE decreases over time after an infection.

•VTE preventive measures may prevent VTE events in the peri-infection period.

•Hospitalized patients with an infection may be considered for VTE prophylaxis.

Having an ID doc involved in the ER management of severe sepsis and septic shock

It improved adherence to sepsis guidelines and mortality in this study.

GIK for myocardial infarction

We refuse to give up on it but haven’t quite found a way to make it work, and it’s been 40 years now. The latest? If you couple it with tight glycemic control in NSTEMI, then maybe.

Should drug eluting (as opposed to bare metal) stents be used in patients with atrial fibrillation?

Another way of asking this might be “how long do you want to subject a patient to triple anti-thrombotic therapy?”

There is not a clear evidence based answer. This study looked at practice patterns and there is considerable variation.

Cefepime neurotoxicity

Here’s a systematic review on this increasingly recognized problem.

Interatrial block aka Bayes syndrome: role in atrial fibrillation and stroke

Free full text review.

Interatrial block: diagnosis and clinical significance

Free full text review here.

Hypokalemia and supraventricular ectopy: risk factors for stroke

Reported here.

Hyperammonemic encephalopathy following bariatric surgery

You can add this one to two growing lists: bariatric surgery complications and non hepatic hyperammonemias. [1] [2]

Mechanisms? From the first reference:

The specific mechanisms driving the hyperammonemic state after RYGB may be multifactorial. As it has been almost exclusively observed in women, X-linked partial ornithine transcarbamylase (OTC) deficiency has been implicated (Figure 2). Previously asymptomatic heterozygous OTC-deficient women can present when faced with catabolic stressors, and biochemical profiling is consistent with impaired urea cycle function. Zinc deficiency has also been proposed to interfere with OTC function (5). Nongenetic mechanisms of increased ammoniagenesis have been considered, including portosystemic shunting, severe hepatic dysfunction, and overgrowth of intestinal flora. A profound catabolic state may also play a role, driving protein breakdown and accumulation of nitrogenous waste products.

HRCT scanning in the diagnosis of pulmonary diseases

In diffuse or multifocal parenchymal lung disease the HRCT may point to a specific diagnosis or place the disorder in a category, thus shortening the differential. Free full text review.

Hydrophilic polymer embolism

A newly appreciated complication of vascular access.

Hospitalists as housekeepers

Hospitalists write medication orders, take calls for “housekeeping” issues and do the discharge paperwork. With us, quality of care and patient satisfaction generally improve, and the surgeon isn’t being called at 2 a.m. with requests for Tylenol or laxatives. What’s not to like?

Plenty.

How did we get into this mess? By failing to set boundaries to limit the mission creep that moved us away from the original notion of hospitalists as clinicians within the original scope of their training, IMHO. Our professional organization didn’t help.

Histologic patterns and outcomes in hypersensitivity pneumonitis

From Chest, free full text.

The hospital of tommorrow

Hospitalists will be obsolete as the hospital care team continues home care via telemedicine and putting patients to death will be considered patient centered. Read the rest.

Clinical status before and outcomes after admission to hospice

From a report from last year:

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.

Hospitalists’ enthusiasm for MOC: less than overwhelming

Survey results.

Home NPPV

From JAMA:

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.

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.