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Status Panicus

May 31, 2008





The other night we had a 36 year old woman come in for shortness of breath when I was about to leave my JPMC clinic. She had just had a typical fight with husband.. Of course I imagine there was quite a lot of drama as there tends to be with nearly any argument between partners.


However, in this case I was pretty impressed. Not with the details of the argument but with the numbers she was able to achieve (as we will see below). She came in breathing at about 50 times a minute! Her oxygenation was normal and her heart rate was slightly tachycardic. However, we decided to get some labs and do a CXR on her just to be safe (also I think to appease the parents a little). Her HCO3- (bicarb level) was pretty low (16) so we thought of acidosis. However, why would she be acidotic? Made no sense. So, we got an arterial blood gas. Would you believe her Ph was 7.71!!!!! (normal is 7.42) I have never seen such an alkalotic patient. Her bicarb repeated was 11 and her PCO2 was 14! She was hyperventilating so much that her body began to dump bicarbonate to try to bring the Ph back down! I can’t believe she did not pass out. We gave her 2 doses of ativan and told her to breath into a bag. When my shift was over, I signed her out still breathing about 30 into the bag! She needed more ativan I think!

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Neurogenic Orthostatic hypotension

A 65-year-old man reports a 6-month history of dizziness, light-headedness, weakness, and fatigue while upright. He takes no medication and has no personal or family history of neurologic disease. On physical examination, his supine blood pressure is 160/100 mm Hg, with a heart rate of 72 beats per minute; on standing, his blood pressure falls to 70/40 mm Hg, with no change in heart rate. The results of the remainder of the examination, including neurologic examination, are normal. How should he be evaluated and treated?

This patient s symptoms are consistent with neurogenic orthostatic hypotension. Read more here.

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Liver induced pulmonary disorder

Hepato pulmonary syndrome has three components

  • Liver disease
  • Pulmonary vascular dilatation
  • Defect in oxygenation
Usually patients have signs of chronic liver disease and signs of pulmonary syndrome such as cynaosis, finger clubbing, orthodeoxia. If you want to see a image of such a patient click here.

This is a review article published in NEJM.

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Only a Hammer

May 30, 2008

One of my favorite quotes comes from Abraham Maslow - "If you only have a hammer, you tend to see every problem as a nail."
Recently I saw a 74 year old man admitted for a GI bleed. We appropriately got a GI consult. The consultant scheduled a colonoscopy, but called (without letting us [...]

Read more here.


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Unstable angina and STEMI guideline made simple

2007 ACC duideline for management of Unstable angina and STEMI is large and complex for simple minded. You don't believe me you can read this pages ( flow charts) guideline here. In USCF conference in Hospital medicine Dr McNulty decided to simplify the guideline.

Compressing the guidelines there are three take home points.

  • a)Which patients should be admitted?
  • b)What anticoagulation strategy should physicians use for non- STEMI or unstable angina patients?
  • c)And when should doctors ship patients to the cath lab vs. taking a more conservative approach and ordering additional tests?

You can read the article in Todays Hospitalist here.

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New MDS classification

  • The WHO classification is as follows:
    • Refractory anemia with or without ringed sideroblasts (erythroid dysplasia only, marrow blasts <5%)
    • RA with multilineage dysplasia (blasts <5%)
    • 5q- syndrome (blasts <5%,>
    • RAEB (blasts 5-20%)
    • Myelodysplasia syndrome unclassified (does not fit into the above groups)



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Illustrated guide to Tube Thoracostomy

Whether the fluid accumulation in the pleural cavity is the result of rapid traumatic filling or insidious malignant seepage, the placement of a chest tube allows for continuous, large volume drainage until the underlying pathology can be more formally addressed.

You can read the guide here.

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Per-oral suturing as a potential treatment for adolescent obesity

May 29, 2008

I think it is a great way to deal with teen obesity. This was only a pilot trial done on 12 patients. There was over 60% weight loss over 6 months. More studies are needed soon. You can read report published as an abstract in DDW.



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PCI in modern cardiology: a shift from chronic stable patients to acute coronary syndromes.

Natural course of Chronic stable angina is generally good and also there are no culprit lesions to treat. hence PCI does not improve prognosis. On the other hand PCI can improve prognosis in Acute coronary syndromes because culprit lesion can be identified.PCI centers should fcus on treating acute coronary syndromes. Want to know more about COURAGE and MASS II trails you can click here.

Lessons to be learned

* PCI centers should focus its resources (both human and financial) mainly on the treatment of acute coronary syndromes, where PCI was clearly shown to improve the patients outcomes
* Patients with chronic stable coronary artery disease should be initially treated medically and PCI should be performed upon patient’s request (when medical therapy failed) to aleviate the symptoms (patients should be informed, that PCI will not prolong their life in this setting)
* The proportion of acute / elective PCI cases can be used to evaluate the effectivity of health care systems (regional, national, local): PCI for acute coronary syndromes should exceed 50% of all PCI workload (probably should be around 60-70%) in a modern PCI center.
* Bypass surgery remains a viable alternative for chronic stable patients with multivessel coronary artery disease.


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Latest anatomical Tattoos!


My favourite Anatomical tattoo. There is another one if you want!

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8 drugs even doctors dont take!

Well now, here’s something you don’t see every day: an article stating the names of meds that doctors wouldn’t take. Yikes. These must be really nasty then, eh?

Well, we make no claims as such, but there surely is fair enough warning against them that we thought we’d pass ‘em along to you. For the hows and whys, read the entire article. But for now, here’s a quick look. Here is the list.

1. Advair

2. Avandia

3. Celebrex

4. Ketek

5. losec

6. Nexium

7. Visine Original

8. Pseudoephedrine

I have taken some of these medications myself and I guess you too.

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Heart failure guidelines ignored?

Heart failure guidance ‘ignored’

Many GPs, and even some hospital specialists, are failing to follow guidelines for managing heart failure, a Europe-wide survey suggests.

British GPs frequently did not use recommended tests or drugs, which the researchers said could be unsafe.

The European Heart Journal report said the results were "very worrying".


However, one specialist GP disputed whether the survey answers were clear evidence of poor practice among family doctors in the UK.

I have several thoughts about this article. I know of subspecialists publishing guidelines and then criticizing generalists for not following the guidelines. Many guidelines have conflicts with other guidelines. So I usually recoil from such proclamations.

On the other hand, the measures that this guideline proposes are reasonable and logical. They are not controversial. Every clinical diagnosis of heart failure should require an echocardiogram. I teach that we find 5 features of the echocardiogram which can change our approach to the patient:

1. Left ventricular ejection fraction - treating patients with decreased ejection fractions is different from patients with normal left ventricular function
2. Occult valvular disease - including IHSS or HOCUM
3. Regional wall motion abnormalities - suggesting significant CAD
4. Occult pericardial effusion
5. Pulmonary hypertension with normal LVEF

I see all these results.

I would make this suggest to cardiologists and heart failure experts - understand how to help generalists learn these important concepts. Publishing a guideline is somewhat self serving. I agree with the standards that they advocate. They have the responsibility to learn how to positively influence practice. This should be an active event not a passive publication.

Syndicated from Original Article.

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ACE, ARB or Both for pateints with proteinuria

Progression from proteinuria to CKD can be prevented by giving ACE inhibitors and we know ARB also effective. This meta analysis compares effects of ACE inhibitors and ARB on proteinuria and also looks at efficacy and clinical safety of combining these two drugs. This meta anlysis is published in Annals of Internal Medicine.

The final pool of available trials included 49 trials involving a total of 6181 patients. The agents used in the studies are summarized below:

* 12 studies compared ARBs with placebo;

* 9 studies compared ARBs with calcium channel blockers;

* 23 studies compared ARBs with ACE inhibitors; and

* 16 studies compared ARBs with combinations of ARB plus ACE inhibitor.

Conclusion from this study is combination of an ACEI and an ARB may be
considered for individual patients, particularly for those who are not receiving significant benefit from monotherapy targeting proteinuria and who are at a low risk for possible adverse events.



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Hyperglycemia and STEMI

Hyperglycemia is well recognized as being associated with extended hospital stays, negative postdischarge outcomes, significant morbidity and mortality, and exorbitant medical costs. In acute myocardial infarction (MI), hyperglycemia adversely affects the outcomes of patients with or without diabetes. Plasma glucose level at hospital admission is an independent predictor of death in patients with acute MI. Moreover, fasting glucose level on the day after hospital admission, and failure of an elevated glucose level on admission to fall within 24 h, have been shown to be better predictors of early mortality in patients with acute MI than is glucose level on admission.

Taken from Nature Clinical Practice Cardiovascular Medicine


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Head Positional Maneuvers for Benign Vertigo

May 28, 2008



Almost like wet dogs shaking their heads, patients with benign paroxysmal positional vertigo are resolving dizziness by a series of directed movements to remove loose calcium crystals from semicircular canals in the ear.The quick head-positioning treatment was effective for relieving vertigo especially in patients with loose calcium crystals (otoliths) in the posterior-canal, a common form of the disorder, Terry D. Fife, M.D., of the University of Arizona, and colleagues reported in treatment guidelines in the May 27 issue of Neurology.


The most common form of vertigo occurs when a patient looks up or bends over so that otoliths from the macula of the utricle fall into a semicircular canal. Now referred to as canaliths, they move in the semicircular canal eventually deflecting the cupula, resulting in a burst of vertigo and nystagmus.

All of the repositioning maneuvers move these ectopic canaliths from the semicircular canal into the vestibule of the ear where they are absorbed.

There are a number of repositioning maneuvers in use, said Dr. Fife and colleagues, but they lack standardization, the guidelines authors wrote.

So they reviewed all relevant articles from 1996 to June 2006. These included, for example, treatment for posterior-canal disorder and horizontal-canal and anterior-canal disorder.

Among various maneuvers reviewed, the investigators found that for the common posterior-canal disorder, the canalith repositioning maneuver (also called the Epley maneuver) is safe and effective and should be offered to patients of all ages with this form of benign positional vertigo.

The Semont maneuver is "possibly effective," they said, but received only a low recommendation on the basis of a single study.

The relapse rate and second occurrence rate are not fully established, the guideline writers said. Short-term relapse rates range from 7% to nearly 23% within a year of treatment, but long-term recurrences may approach 50%, depending on the age of the patients.

As an example of the positional treatment, the canalith maneuver for right-sided disorder begins with the patient sitting up on a bed or table.

Then, while lying down, the patient's head is held by the therapist in the right head-hanging position for 20 to 30 seconds (steps one and two). In step three, the therapist turns the head 90 degrees toward the unaffected side.

The head is held this way for 20 to 30 seconds before being turned another 90 degrees so that it is nearly in the face-down position (step four).

After 29 to 30 seconds the patient is brought to the sitting up position (step five).

Although the therapist guides the patient through these steps, the patient's head position is key to successful treatment, the investigators said.

The guidelines also evaluated whether activity restriction is needed following treatment and concluded that five of six studies showed no added benefit for post-treatment activity or position restriction, such as sleeping upright and wearing a cervical collar.

For patients treating themselves, home exercises seemed to pose little risk, but evidence was insufficient to show that it is as effective as maneuvers done by a physician or other therapist.

Turning to the efficacy of medication treatment, the investigators said that in the absence of randomized controlled trials, there is no evidence to support a recommendation of any medication in the routine treatment of this form of benign vertigo.

Lack of evidence precluded recommendations for surgical treatment for refractory disorder, they added.

Future studies, they concluded, are needed to clarify the best treatments for the horizontal-canal form of the disorder, they concluded.


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Intensive Insulin Therapy for newly diagnosed T2DM

I always believed insulin is the right treatment for declining beta cell dysfunction though OHA are used as first line . This  review article published in Lancet  confirms my view.
The natural history of type 2 diabetes is characterised by worsening hyperglycaemia and progressive deterioration in function of the insulin-secreting pancreatic β cells. Despite intense investigative efforts, the pathophysiological basis underlying β-cell dysfunction (and the concomitant loss of β-cell mass) remains unclear

Nevertheless, the central importance of declining β-cell function in type 2 diabetes is underscored by its correlation with a progressive loss of glycaemic control, which typically occurs over time. Although β-cell dysfunction contributes to worsening glycaemia, hyperglycaemia itself further undermines β-cell function. This so-called glucotoxicity is apparent in the observation that the first-phase component of normal biphasic insulin secretion is abolished when the blood glucose concentration exceeds 6·4 mmol/L. Accordingly, early in the course of type 2 diabetes (ie, when sufficient residual β-cell mass still exists), the glucose-lowering effect of antidiabetic therapy can be amplified by improved endogenous insulin secretion secondary to the elimination of hyperglycaemia. Unfortunately, however, this effect is ultimately transient, because no oral antidiabetic agent has yet been shown to profoundly change the inexorable β-cell deterioration and worsening glycaemia in type 2 diabetes.

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Liver puzzle answered

NO one gave any suggestion so far for the recent puzzle.. I am giving away the correct answers.



The liver tests did not support primary liver disease. The albumin was low but not what we would expect with cirrhosis. The other liver tests were remarkably normal.
We obtained an echocardiogram which showed severe pulmonary hypertension and pure right sided dilation and heart failure. I will followup on the pulmonary consultation. I suspect that the patient has obstructive sleep apnea, and possibly also COPD.
This patient represents a fascinating cognitive issue. He presented with ascites and anasarca. The SAAG was consistent with portal hypertension. Assuming primary liver disease was the natural error. This presentation requires further thought. His lab values were not consistent with that clinical assumption, so we reconsidered our assumptions. This reconsideration allowed us to hone in on the correct explanation.

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Hyponatremia

May 27, 2008


When a patient gets admitted with hyponatremia, you need to ask following questions:-
1) What is his volume status?
2) Is the hyponatremia chronic? any previous results available?
3) Any history of vomiting or diarrhoea?
4) Any history of renal, heart failure, cirrhosis or nephrotic syndrome?
5) any history or symptoms of hypothyroidism or adrenal insufficiency?


6) Is patient taking medications that could cause low sodium?
7) Does patient suffer from any pulmonary disease or CNS disease?
8) Is there history suggestive of neoplasm?
9) is there history suggestive of hyperlipaedemia or hyperproteinemia?
10) Is the lab value correct?



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Does this patient With Diabetes Have Osteomyelitis of the Lower Extremity? Rational

May 25, 2008

The most recent installment in JAMA’s Rational Clinical Exam Series seeks to determine the accuracy of the history, physical exam, radiology and laboratory in making the diagnosis of osteomyelitis in diabetics.


This is relevant given its frequency of occurrence and its cost and since the gold standard for diagnosis, namely a bone biopsy and culture, is less than optimal for a variety of reasons.Less than 10% of the nearly 300 articles reviewed were included for review by the authors and of the 10%, most were graded in the mid categories for quality. Nonetheless, some important findings were reported (highlighted in green).
Finding Likelihood Ratio Negative Likelihood Ratio
Ulcers >2 cm2 7.2 (CI 1.1-49) 0.48 (CI 0.31-.076)
Positive “probe to bone” test* 6.4 (CI 3.6-11) 0.39 (CI 0.20-0.76)
ESR >70 11 (CI 1.6-79) 0.34 (CI 0.06-1.9)
Abnormal plain X-ray** 2.3 (CI 1.6-3.3) 0.63 (CI 0.51-0.78)
Abnormal MRI 3.8 (CI 2.5-5.8) 0.14 (CI 0.08-0.26)
*Probe to bone test: the examiner gently and in a sterile fashion, probes the ulcer with a steel probe to determine if the probe can advance to bone

**abnormal X-Ray findings include: focal loss of trabecular pattern, periosteal reaction, and frank bone destruction. 2 or 3 views can be selected

For example, the interpretation is as follows:

The LR (sensitivity/1-specificity) tells you how much the odds of a disease will increase based on a positive result.

So, if you determine the pre-test probability to be 15% and the patient has an ulcer >2.0cm2 then the post-test probability would rise to 56%.

Remember:

Pre-test odds = pre-test probability /(1-pre-test probability)= 0.15/0.85=0.18 Post-test odds=pre-test odds * LR = 0.18 * 7.2 = 1.3
Post-test probability = post-test odds / (post test odds+1) = 1.3/2.3= 0.56 = 56%

or, more simply, use a Likelihood ratio nomogram.

Similarly, a negative LR (1-sensitivity/specificity) tells you how much the odds of a disease decrease based on a negative test rest. So, for a patient whose pre-test probability is 15%, a normal MRI (ie a negative result), would change the post-test probability to 2.4%.

The article specifically noted that the studies that exist have not studied the significance of multiple findings in a patient. (As a personal commentary, I believe that it stands to reason that multiple positive findings would make a diagnosis of osteomyelitis more likely.)

Of note, there are no features of the medical history or other elements of the physical which were found to be helpful in the diagnosis, including presence of pain, fever or other systemic signs. Because it is established that diabetic ulcers tend to occur in patients with more advanced and poorly controlled diabetics, a history focusing on the diabetes history, including the presence of retinopathy, neuropathy, and nephropathy would be appropriate.

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Roziglitazone still alive?

Bad press and a flawed meta-analysis helped to eliminate the use of rosiglitazone in the management of diabetes late last year. I have found this drug to be very useful in some patients who don't manage to put on weight. In this month’s issue of Gastroenterology, however, a new life for rosiglitazone is born as a possible therapeutic addition for active ulcerative colitis.

A randomized, double-blinded,
placebo-controlled trial involving 105 patients with mild to moderately active ulcerative colitis showed significant differences in the rates of clinical response and remission in those treated with 4mg of rosiglitazone twice daily for twelve weeks compared to placebo. The patients were allowed to be on other UC medications during the study that could not be adjusted during the study period. While the sample size was small and the treatment duration short, no significant differences in the rate of cardiovascular adverse events were seen!

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Universal screening for MRSA? not primetime Yet

Recently, there has been a lot of coverage in press about the “recent” epidemic of methicillin-resistant Staph Aureus (MRSA) infections. In reality, we know that the MRSA epidemic really isn’t new, but it is a huge problem that isn’t improving on its own. So what is the most effective way to reduce MRSA infections?

A study from Northwestern published in the
Annals of Internal Medicine examined the outcomes of instituting a comprehensive MRSA screening in a large academic medical system. Starting in Arpil 2004, all patients admitted to an ICU had nasal swabs to test for MRSA colonization (74% adherence). Patients that were positive based on PCR testing were placed on contact isolation. After 12 months of this protocol, the surveillance program was expanded to the entire hospital system. During this phase of the study, patients that tested positive underwent decolonization with muciporin and a chlorhexidine wash/shower (how clean!). The study found a decrease in the incidence of MRSA disease by 70%. Most notably, while there was decreased MRSA surgical site and UTI, there was no statistically significant decrease in MRSA bacteremia with universal surveillance. Also since MRSA is associated with higher mortality, it’s odd that this study did not try to observe for decreased mortality. These results contradict the findings of a recent study published in JAMA  that did not find any significant reduction in surgical site infections with universal screening. While this study does not absolutely prove universal MRSA surveillance is ready for primetime, it is a significant step in creating a robust and sensible system to improve our detection and containment of MRSA transmission.

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It is quality not quantity

We knew all the time that  “newer blood” might be safer than “older blood.” There has been evidence to suggest that during storage, red blood cells undergo functional and structural changes which impair RBC function (termed “storage lesion”).

A retrospective study from
Cleveland Clinic published in the NEJM examined outcomes of patients given red-cell transfusions during CABG surgery. Blood stored for more than 14 days prior to transfusion was considered “older blood” and blood stored less than 14 days was considered “newer blood.” Patients who received older blood had increased perioperative complications (25.9% vs. 22.4%), higher in-hospital mortality (2.8% vs. 1.7%), and decreased survival at one year. In recent years, there have been several studies that found improvement and benefit with conservative strategies of blood transfusions. An incremental increase of adverse outcomes has been observed with each additional unit of PRBC transfused. This new study suggests that it may not only be quantity, but the quality of blood we should be concerned with as well.

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Guidelines for the evaluation of fever in the ICU

May 24, 2008

America and the Society of Critical Care Medicine, is available here and represents the first revision in 10 years. Points of interest follow:
A new fever should trigger a clinical assessment rather than automatic orders for laboratory and radiographic testing.
Blood cultures, however, are indicated in all patients except those in whom the clinical assessment strongly indicates a non-infectious source of fever. Paired cultures rather than single cultures are recommended.
A clear approach to fever in patients with central venous lines is outlined.

Consider chest CT scanning in patients with negative plain chest x rays who are suspected of having pulmonary infections, particularly if immunocompromised.
Don’t forget nosocomial sinusitis.
“Catheter-associated bacteriuria or candiduria usually represents colonization, is rarely symptomatic…” .
Information on post operative fever and empiric antibiotic therapy is presented.

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What is Sezary syndrome?

Case Presentation: 83 year old with a past medical history of hypertension noted erytematous plaques with scale about 1 year ago. The rash was associated with diffuse pruritis at that time. The patient subsequently underwent several inconclusive biopsies. She was eventially diagnosed with mycosis fungoides and treated with UV therapy. Her rash progressed to a diffuse pruritic erythema covering the vast majority of her body, including palms and soles. (erythroderma). She was noted to have Sezary cells on peripheral smear and diagnosed with Sezary syndrome. She was now admitted to TH with fevers likely secondary to cellulitis on her lower extremities, the site of significant skin breakdown. The patient is improving on treatment with IV antibiotics and interferon alpha.

Teaching Points:

1. What is Mycosis fungoides:Extranodal Non-Hodgkins lymphoma of T-cell origin, with primary involvement of the skin

What is Sezary Syndrome:

  • Generalized erythroderma
  • Lymphadenopathy
  • Atypical T- cells (Sezary cells) in the peripheral blood

2. Tumor grades

  • T1 Limited patch/plaque (<>
  • T2 Generalized patch/plaque (>10 percent of total skin surface)
  • T3 Tumors
  • T4 Generalized erythroderma

These four tumor grades correlate with median survivals approximately 30 years, 12 years, 5 years, 4 years, respectively. Note that T1 and T2 are usually not dying of the disease while T3 and T4 are.

3. Therapy-correlates with prognosis. T1 and T2 will receive almost exclusively topical therapy with nitrogen mustard, UVA, UVB and Electron beam therapy. T3 and T4 will likely require topical and systemic medications, immunomodulators and chemotherapy.

Sezary syndrome powerpoint presentation

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Hit the Dot

Surfing the internet and I found this game to be quite a challenge. Really got my heart pumping as I got further up in the levels.

Give it a try. See if your mouse skills are great?

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Treating ICH with rTPA?

May 23, 2008

Can you believe you would treat Intra Cranial hemorrhage with Thromolytics. Bleed  on CT scan is one of the contraindications for giving rTPA in stroke. If you don't believe me you can see this guideline. It will make them bleed more.


This study is published in Medscape that low dose rTPA safe and effective in treating Intra ventricular hemorrhage, The researchers developed a system where tPA could be delivered directly to the site of the clot with a catheter placed by a neurosurgeon. When patients with intraventricular hemorrhage were given 1mg tPA every 8 hours for 4 days (usual dose for treating ischemic strokes is 100 mg over 90 minutes), their mortality rate dropped from 80% to 15%! In other words, before researchers tried this therapy, 8 out of 10 patients died from intraventricular bleeding. In this study less than 2 out of 10 patients died from intraventricular hemorrhage. In addition, the functional outcomes of the survivors was significantly better (i.e. less people had long-term disability).
More information for the study can be found on the Johns Hopkins web site. The information on inclusion and exclusion criteria is here. Obviously this therapy isn’t ready for prime-time yet, but there’s a lot of promise here.

It must have taken a lot of bravery  to give the first patient with recent onset brain bleeding a dose of a thrombolytics, but that type of “outside the box” thinking will save a lot of lives and prevent a lot of disability.

Amazing!!



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Classical cardiovascular risk factors according to fasting plasma glucose levels.

BACKGROUND: To compare the prevalence of classical cardiovascular risk factors (CVRF) and metabolic syndrome (MetS) in our population according to fasting plasma glucose levels (FPG). METHODS: We have studied 344 subjects between 20-70 years of age, recruited in a Primary Care Clinic. Subjects were divided into four groups according to their fasting plasma glucose (FPG) values: normal plasma glucose (NG) when FPG<5.6>/=7 mmol/L or previous diagnosis of diabetes. Cardiovascular risk factors (hypertension, TC/HDL-C index and Apo B values), presence of the MetS and indirect measure of insulin resistance (HOMA) were analyzed. RESULTS: Subjects with FPG2 have a prevalence of classic CVRF and MetS similar to that observed in subjects with type 2 diabetes mellitus (T2DM). The TC:HDL-C index>/=5 in 56% and 57%, Apo B>/=1.2 g/L in 59% and 57%, hypertension in 60% and 54% of FPG2 and T2DM subjects, respectively. MetS was diagnosed in 79% of FPG2 and 80% of T2DM. We found significant differences with FPG1 group who presented low CVRF and MetS proportion. CONCLUSION: In our population FPG2 and T2DM subjects show a similar cardiovascular risk profile. On the other hand, such risk is significantly lower in subjects with FPG between 5.6-6.0 mmol/L. These results might have practical implications.
Source: European journal of Internal Medicine

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Coronary Heart Disease and White Coat Hypertension

May 22, 2008

White Coat hypertension was considered benign for so long and now e know it is not so. Read my previous post here on WCH.

Coronary disease may be more severe among patients with WCH than among those without. In this group, data from myocardial and carotid ultrasound may help to estimate coronary artery disease.

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Early repolarization syndrome and Brugada syndrome: are they relatives?


Early repolarization syndrome (ERS) is characterized by the presence, in most cases in mid-to-lateral precordial leads, of a J wave on the downsloping portion of the QRS complex, followed by an elevation of the ST-segment with upward concavity. ERS is considered a benign electrocardiographic pattern of ventricular repolarization and, thus far, clinical interest in this syndrome has been confined to its differential diagnosis from myocardial infarction and pericarditis. Brugada syndrome (BS), an inherited cardiac disease first described in 1992, exhibits a characteristic electrocardiographic pattern consisting of a J wave mimicking a right bundle branch block with typical ST-segment elevation in the right precordial leads. Believed to be a normal repolarization variant for more than three decades, the syndrome is now known instead to be associated with a high incidence of life-threatening ventricular tachyarrhythmias and is responsible for a number of sudden deaths in young adults worldwide. Although clinical findings seem to differentiate the two syndromes, similarities between BS and ERS in terms of response to heart rate, pharmacologic agents, and neuromodulation could suggest a linkage in their pathophysiological mechanism. The authors review the clinical and experimental data in order to test this hypothesis. 

In May NEJM sudden death with repolarization is described. Worth reading the editorial in the same journal.

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Acute worsening of pulmonary fibrosis

Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) is a clinical entity defined by rapid deterioration of IPF during the course of the disease that is not due to infections, pulmonary embolism, or heart failure. The condition needs to be differentiated from acute interstitial pneumonia (or Hamman-Rich syndrome), which occurs in patients with no underlying lung disease. The exact etiology and pathogenesis remain unknown, but the condition is characterized by diffuse alveolar damage (on a background of IPF) that probably occurs as a result of a massive lung injury due to some unknown etiologic agent. High-resolution computed tomography can help in prognostication and management of this condition. Once infections and other causes of worsening have been excluded, treatment involves enhanced immunosuppression with pulse doses of methylprednisolone and cytotoxic agents. Our systematic review shows that the outcome, however, is poor, with 1-month and 3-month mortality around 60% and 67%, respectively. Few studies have shown beneficial effects of cyclosporine, pirfenidone, and anticoagulants in the management and prevention of AE-IPF. The etiology, risk factors, pathogenesis, therapy, prognosis, and predictors need to be studied and the potential role of newer agents in the management and prevention of AE-IPF needs to be further clarified.by 

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Pill that monitors if you took them!


I have been waiting for such an advance.  You can read my previous post here.

Compliance with taking medications is a huge problem in medicine. Studies show more than half of all prescriptions are either not filled or not taken. Everyone is familiar with how easy it is to forget to take medications. This problem becomes overwhelming in complex diseases such as cancer or Diabetes where patients are on rigorous schedules throughout the day. Even worse is the situation where the

patient may have compromised cognitive abilities.

A new development is a chip containing networked pill that reports back on medication taking and the dissolution of the pill as reported by MIT technology review.

The company behind the technology, Proteus Biomedical, of Redwood City, CA, calls its technology the Raisin system. Read more here.

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Rifampicin for Staph aureus infection: a review

Background  Staphylococcus aureus causes severe life-threatening infections and has become increasingly common, particularly methicillin-resistant strains. Rifampin is often used as adjunctive therapy to treat S aureus infections, but there have been no systematic investigations examining the usefulness of such an approach.

Methods  A systematic review of the literature to identify in vitro, animal, and human investigations that compared single antibiotics alone and in combination with rifampin therapy against S aureus.

Results  The methods of in vitro studies varied substantially among investigations. The effect of rifampin therapy was often inconsistent, it did not necessarily correlate with in vivo investigations, and findings seemed heavily dependent on the method used. In addition, the quality of data reporting in these investigations was often suboptimal. Animal studies tended to show a microbiologic benefit of adjunctive rifampin use, particularly in osteomyelitis and infected foreign body infection models; however, many studies failed to show a benefit of adjunctive therapy. Few human studies have addressed the role of adjunctive rifampin therapy. Adjunctive therapy seems most promising for the treatment of osteomyelitis and prosthetic device–related infections, although studies were typically underpowered and benefits were not always seen.

Conclusions  In vitro results of interactions between rifampin and other antibiotics are method dependent and often do not correlate with in vivo findings. Adjunctive rifampin use seems promising in the treatment of clinical hardware infections or osteomyelitis, but more definitive data are lacking. Given the increasing incidence of S aureus infections, further adequately powered investigations are needed.

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Marker for first atrial fibrillation

LA emptying fraction  was associated with risk for first AF or atrial flutter after adjusting for baseline clinical risk factors for AF or atrial flutter, left ventricular ejection fraction, diastolic function grade, and LA volume.

 In conclusion, reduced LA reservoir function markedly increases the propensity for first AF or atrial flutter, independent of LA volume, left ventricular function, and clinical risk factors.
Says study published from Mayo clinic.

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Interpreting data

The Happy Hospitalist: "It's situations like this where it never ceases to amaze me how two people can look at the same data and one be so right and one be so wrong. This isn't a matter of walking the fine line of too wet or too dry. This is life and death."


i can only laugh when i read this post and i am not surprised this happens all over.

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Extra intestinal manifestations of Crohn's disease

A case report of uveitis as the as the presenting manifestation is presented, along with a review of extraintestinal manifestations if IBD and differential diagnostic considerations.

Via Nature Clinical Practice Gastroenterology and Hepatology.

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Liver puzzle

55 year old man admitted to our service for ascites and anasarca (massive scrotal and leg edema.)  The patient had large volume paracentesis.  The SAAG (serum ascites albumin gradient) was 1.8 - consistent with portal hypertension.  He had no evidence for spontaneous bacterial peritonitis.  His serum ammonia was normal.

Later that evening he becomes hypoxic and is transferred to intensive care.  He is placed on a 50% rebreathing mask.

In reviewing his lab data we find:

 

Liver tests
 shows:
 AST 34 alk phos 98 albumin 2.7 ALT 27 T. Bili. 0.8 INR1.3

His ABG the next morning on 50% O2

Arterial Blood Gas - 50% oxygen
pH 7.115 pCO2 91 pO2 90

 

When he was admitted he had a serum bicarbonate of 31.

He has cardiomegaly on chest xray.

Questions:

1. What liver diseases might he have - what is your best guess?

2. What other tests would you order?

3. Why is his pCOso high?

I will provide some answers and a strong hypothesis.

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Interesting Articles: A Weekly Review of the "Big Five" Medical Journals

May 21, 2008

This is a collection of articles I have found interesting in the weekly editions of the "big five" medical journals: NEJM, JAMA, Annals, Lancet and BMJ.

Stents versus Coronary-Artery Bypass Grafting for Left Main Coronary Artery Disease: No Difference.
NEJM, 04/2008.

There was no significant difference in the risk of death, Q-wave myocardial infarction, or stroke between patients receiving stents and those undergoing CABG. However, stenting, even with drug-eluting stents, was associated with higher rates of target-vessel revascularization than was CABG.
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Home Use of Automated External Defibrillators for Sudden Cardiac Arrest: Not Helpful.
NEJM, 04/2008.

The most common location of out-of-hospital sudden cardiac arrest is the home, consequently, home use of an automated external defibrillator (AED) might offer an opportunity to improve survival. In this study of survivors of anterior-wall myocardial infarction, access to a home AED did not significantly improve overall survival.
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Carotid bruits as a prognostic indicator of cardiovascular death and myocardial infarction: a meta-analysis. The Lancet 2008; 371:1587-1594.

The rate of myocardial infarction in patients with carotid bruits was 3·69 per 100 patient-years compared with 1·86 per 100 patient-years in those without bruits. Yearly rates of cardiovascular death were also higher in patients with bruits than in those without (2·85 per 100 patient-years vs 1·11 per 100 patient-years). In the four trials in which direct comparisons of patients with and without bruits were possible, the odds ratio for myocardial infarction was 2·15 and for cardiovascular death 2·27. Auscultation for carotid bruits in patients at risk for heart disease could help select those who might benefit the most from an aggressive modification strategy for cardiovascular risk.
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Use of Multiple Biomarkers to Improve the Prediction of Death from Cardiovascular Causes: Useful.
NEJM, 05/2008.

The combination of biomarkers reflects myocardial cell damage, left ventricular dysfunction, renal failure, and inflammation (troponin I, N-terminal pro–brain natriuretic peptide, cystatin C, and C-reactive protein). In elderly men (mean age 71), the simultaneous addition of several biomarkers of cardiovascular and renal abnormalities improves the risk stratification for death from cardiovascular causes beyond that of a model that is based only on established risk factors.
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Cardiac Troponin and Outcome in Acute Heart Failure: Positive troponin predicts worse outcome.
NEJM, 05/2008.

Patients who were positive for troponin had lower systolic blood pressure on admission, a lower ejection fraction, and higher in-hospital mortality (8.0% vs. 2.7%) than those who were negative for troponin. The odds ratio for death in the group of patients with a positive troponin test was 2.55.

In conclusion, in patients with acute decompensated heart failure, a positive cardiac troponin test is associated with higher in-hospital mortality.
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Efficacy and Safety of Recombinant Activated Factor VII for Acute Intracerebral Hemorrhage: No Clinical Difference.
NEJM, 05/2008.

Intracerebral hemorrhage is the least treatable form of stroke. This trial did not confirm a previous NEJM study in which recombinant activated factor VII (rFVIIa) improved survival and functional outcomes. Factor VII still reduced growth of the hematoma though, it just did not make a clinical difference.

The growth in volume of intracerebral hemorrhage was reduced by 2.6-3.8 ml. The frequency of thromboembolic adverse events was similar in the 3 groups; however, arterial events were more frequent in the group receiving 80 µg of rFVIIa than in the placebo group (9% vs. 4%, P=0.04).

Hemostatic therapy with rFVIIa reduced growth of the hematoma but did not improve survival or functional outcome after intracerebral hemorrhage.

Etiquette-Based Medicine. NEJM, 05/2008.

This is a possible checklist for the first meeting with a hospitalized patient:

1. Ask permission to enter the room; wait for an answer.
2. Introduce yourself, showing ID badge.
3. Shake hands (wear glove if needed).
4. Sit down. Smile if appropriate.
5. Briefly explain your role on the team.
6. Ask the patient how he or she is feeling about being in the hospital.
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Effect of Folic Acid and B Vitamins on Risk of Cardiovascular Events and Total Mortality Among Women at High Risk for Cardiovascular Disease: Not Useful.
JAMA, 05/2008.

After 7.3 years of treatment and follow-up, a combination pill of folic acid, vitamin B6, and vitamin B12 did not reduce a combined end point of total cardiovascular events among high-risk women, despite significant homocysteine lowering.

The Polypill proposed by BMJ should not include folic acid after all. In the light of recent evidence, it looks like we should skip the beta-blocker too.

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Life Hacks For Doctors

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Therapy for Helicobacter pylori

May 20, 2008

Sequential therapy for Helicobacter pylori refers to the idea of adding more antibiotics to the treatment regimen but giving them in sequence rather than giving all 4 drugs together. This editorial is published in Annals of Internal Medicine.
If you want to read the original meta analysis click here.

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Overconfidence as a Cause of Diagnostic Error in Medicine

May 19, 2008


 I consider making the proper diagnosis the epitome of internal medicine (as well as many other specialties.)  We know that we often miss diagnoses, but we often do not know why.  This article gives a classic example of medical error.

If you see nothing wrong, try again. It took us several tries.

This case is an example of  “a horse masquerading as a zebra.” Why didn’t we see the horse? To help answer the question, Dr. Ginsberg uses  this picture of how the mind may not perceive a visual abnormality.

The current American Journal of Medicine has an interesting article on diagnostic error -Overconfidence as a Cause of Diagnostic Error in Medicine.  This article is long and detailed.  I recommend it only for those who want to study this problem in depth.

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Why Are Hypotonic Parenteral Fluids Still Being Used?

May 18, 2008

Hospital-acquired hyponatremia can be lethal. There have been multiple reports of death or permanent neurological impairment in both children and adults. The main factor contributing to the development of hospital-acquired hyponatremia is routine use of hypotonic fluids in patients in whom the excretion of free water, which is retained in response to excess arginine vasopressin (AVP), might be impaired. The practice of administering hypotonic parental fluids was established over 50 years ago, before recognition of the fact that there are numerous potential stimuli for AVP production in most hospitalized patients. Virtually all neurological morbidity resulting from hospital-acquired hyponatremia has been associated with administration of hypotonic fluids. Multiple prospective studies have shown that 0.9% NaCl is effective prophylaxis against hyponatremia. There is not a single report in the literature of neurological complications resulting from the use of 0.9% NaCl in non-neurosurgical patients. Patients at greatest risk of developing hyponatremic encephalopathy following hypotonic fluid administration are children, premenopausal females, postoperative patients, and those with brain injury or infection, pulmonary disease or hypoxemia. When hyponatremic encephalopathy develops, immediate administration of 3% NaCl is essential. In this Review, authors discuss the question of why administering hypotonic fluids is unphysiologic and potentially dangerous, the settings in which isotonic fluids should be administered to prevent hyponatremia, and the appropriate treatment of hyponatremic encephalopathy.

Clinical pearls:

Several key points that added to my knowledge:

1. Premenopausal women are more likely to develop hyponatremic encephalopathy - probably secondary to the effect of estrogen on astrocytes - therefore increased cerebral edema for the same level of hyponatremia

2. The cerebral edema can cause non-cardiogenic pulmonary edema - and thus hypoxemia.

3. When hypoxemia occurs, then cerebral blood flow decreases, with potential disastrous results.

4. Author  argues passionately against the routine use of hypotonic parenteral fluids 

5. Author  argues that the treatment for hyponatremic encephalopathy is 100 cc of hypertonic saline (3%) push, with transfer to the ICU and careful frequent monitoring of sodium levels.  Pulmonary edema is not a contraindication to hypertonic saline if the patient has normal heart size.

This was truly an excellent review on an infrequent but potentially lethal condition.  Author included in the discussion the consideration of marathon runners.  He now recommends that marathon runners to present with altered mental status should receive 100 cc of 3%NS bolus. 

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Schzophrenia


 


Why people become like this ? visit Pizzimentiart here.

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Lipid management at a glance

This is what you need to do in your clinical practice. You can read here.

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Cardiovascular risk assessment in the metabolic syndrome


 

Prospective Cardiovascular Münster (PROCAM) Study, a prospective study of men and women at work in the northwest of German is published. Men who were classified as having the metabolic syndrome  were 2.59-fold more likely to experience a major coronary event within 10 years of follow-up than men not having the metabolic syndrome.

You can click here for online triology of primary care risk calculators.

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Acute heart failure: how to cut down on "frequent flyers"


If you find that many of your acute heart failure patients are being re-admitted, you’re not alone. “We are not doing a very good job of taking care of these patients.”5% of these patients return to the hospital within 30 days for heart failure, and 50% are back within six to 12 months .

We can help reduce these numbers by better differentiating the type of heart failure; knowing what tests to use and what drugs and devices do or don’t work; and doing a better job educating and treating patients on discharge.

If we need more information read this document.

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Interventions for enhancing medication adherence

May 17, 2008

This review article brings out the difficulties we face in making our patients take their medications.

Pearls for Practice
  • Many reasons exist for nonadherence to medical regimens, including problems with the regimen (such as adverse effects), poor instructions, poor provider-patient relationship, poor memory, patients' disagreement with the need for treatment, or patients' inability to pay.
  • For short-term treatments, several quite simple interventions increased adherence and improved patient outcomes, but the effects were inconsistent from study to study, with less than half of studies showing benefits. Current methods of improving adherence for chronic health problems are mostly complex and are not very effective.
  • This review is published in cochrane review

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