Platypnea-orthodeoxia is a relatively uncommon but striking clinical syndrome characterized by dyspnea and deoxygenation accompanying a change to a sitting or standing from a recumbent position. Since Burchell et al1 described this rare syndrome over half a century ago, no more than 50 cases have been reported in the literature.Platypnea-orthodeoxia has been described to occur in pulmonary arteriovenous shunts, pulmonary parenchymal shunts (as in the hepatopulmonary syndrome), or with intra-cardiac right-to-left shunts.
Two conditions must coexist to cause platypnea-orthodeoxia: an anatomical component in the form of an interatrial communication and a functional component that produces a deformity in the atrial septum and results in a redirection of shunt flow with the assumption of an upright posture. The former may be an atrial septal defect, a patent foramen ovale, or a fenestrated atrial septal aneurysm. The latter may be cardiac, such as pericardial effusion or constrictive pericarditis; pulmonary, such as emphysema, arteriovenous malformation, pneumonectomy, or amiodarone toxicity; abdominal, such as cirrhosis of the liver or ileus; or vascular, such as aortic aneurysm or elongation.2
Under normal conditions an interatrial communication allows blood to shunt from left to right due to a higher pressure in left atrium than right atrium and a greater compliance of the right ventricle than the left ventricle. Right-to-left interatrial shunting is usually associated with spontaneous or induced pulmonary hypertension and, therefore, in the absence of a right-to-left pressure gradient, what is the mechanism for a right-to-left shunt? Or put in another way, what causes water to flow uphill?2 A persistent Eustachian valve can cause interatrial right-to-left shunting with a normal right atrial pressure.3 Platypnea-orthodeoxia could be explained on the basis of positional modification of abnormal shunting. Standing upright could stretch the interatrial communication, be it a patent foramen ovale, an atrial septal defect, or a fenestrated atrial septal aneurysm, thus allowing more streaming of venous blood from inferior vena cava through the defect, whether or not a persistent Eustachian valve coexists.3 This redirection of flow caused by an anatomic distortion of the right atrium or the atrial septum also might occur from a loculated pericardial effusion, an aortic aneurysm, or aortic elongation.2
Platypnea-orthodeoxia
August 24, 2009
New breath holding test
this new test is useful in detecting early lung abnormalities in smokers and obese people..Read more...
Travel related VTE
Long distance travel is associated with increased risk of VTE. This meta analysis suggests 3 fold increase in VTE risk. Read More..
Subclinical Brain Embolization in Left-Sided Infective Endocarditis
The rue incidence of infective embolization in bacterial endocarditis is not known. This study looked at these patients using MRI.
Read the abstract of this article...
Drug Induced fibrotic Valve Diesase
Initial association between development of valvular heart disease and drugs based on 1960s use of methysergide and ergotamine for migraine prophylaxis
Currently implicated are the appetite suppressants fenfluramine and dexfenfluramine, the dopamine agonists pergolide and cabergoline, and the recreational drug ecstasy (MDMA)
ANCA of nembranous nephropathy
July 22, 2009
A landmark paper on membranous nephropathy was published by Beck et al in the most recent issue of NEJM. Ultimately we will have to see if the finding is reproducible, but based on the data presented this represents a major breakthrough in understanding the pathogenesis of membranous nephropathy and nephrotic syndrome.
There has long been strong evidence in support of a circulating factor which causes podocyte injury and resultant nephrotic syndrome. Additional evidence from the neutral endopeptidase story further suggested that an autoantibody directed again some podocyte antigen might be the culprit. In this issue, the researchers demonstrate that in 70% of patients with idiopathic membranous nephropathy (but 0% of patients with secondary membranous nephropathy or other forms of proteinuric kidney disease such as FSGS or diabetic nephropathy) contain an autoantibody against the podocyte antigen phospholipase A2 receptor. Furthermore, the autoantibody's presence appears to correlate with disease activity, suggesting a possible pathogenic role.
The work has a number of implications. First, it suggests that membranous nephropathy is indeed a separate disease than FSGS and other distinct forms of nephrotic syndrome. The common final pathway for proteinuria is the same (podocyte injury), but the ways in which to get there is likely different. Second, it suggests that detection of serum antibodies against phospholipase A2 receptor may be a useful part of the diagnostic workup for nephrotic syndrome--perhaps even making biopsies unnecessary--and perhaps could be used to follow disease activity in response to various therapeutic maneuvers. That is, this test may well become the "ANCA" of membranous nephropathy.
The Power of Pee?
Finally, I can sleep at night: scientists have discovered a way to turn urine into hydrogen. And you said I was crazy for collecting it in milk jugs!
From a group led by chemist Gerardine Botte of Ohio University comes a report (just published in the Royal Society of Chemistry's journal Chemical Communications) that hydrogen has been produced from urine.
According to a July 3, 2009 story on PhysOrg.com, "Urine's major constituent is urea, which incorporates four hydrogen atoms per molecule -- importantly, less tightly bonded than the hydrogen atoms in water molecules."
"Botte uses electrolysis to break the molecule apart, developing an inexpensive new nickel-based electrode to selectively and efficiently oxidise the urea. To break the molecule down, a voltage of 0.37V needs to be applied across the cell -- much less than the 1.23V needed to split water.
So, you know what this means, right? Wait for it....wait for it....the P-bomb. Thanks folks, I'll be here all week. Make sure to tip your bartender and maybe steal a bottle for me when they're not looking. *tap tap* Haha, is this still on?
Caveats for Using Renal Ultrasound to Diagnose Post-Renal Failure
Most would agree that the renal ultrasound is an invaluable tool in the workup of acute kidney injury. Although the renal ultrasound can give information regarding kidney echogenicity and presence of renal cysts, by and large its predominant utility is in determining the presence or absence of hydronephrosis, a marker for obstructive renal failure ("post-renal" failure when referring to the Holy Trinity of "pre-renal", "intrinsic renal", and "post-renal" categories of AKI).
However, there are important caveats to the use of the renal ultrasound to effectively rule-in or rule-out obstructive nephropathy. For instance, false-negatives (e.g., the renal ultrasound does not show hydronephrosis, but there actually is) can occur in the following scenarios:
1. very early obstruction: truly acute obstruction (e.g., with a kidney stone, for instance) may take some time to develop enough distension of the collecting system to detect with our current imaging tools.
2. obstruction in the setting of pre-renal failure: volume-depleted kidneys may not demonstrate significant hydronephrosis until after volume resuscitation, which expands the collecting system.
3. large retroperitoneal tumors: tumors which encase the kidneys may cause obstruction but not allow expansion of the collecting system enough to see hydronephrosis.
4. retroperitoneal fibrosis: this can occur in patients with past extensive GU surgery or prior chemotherapy or radiation therapy and can cause mechanical obstruction without allowing expansion of the collecting system.
In addition, false-positives (e.g., the renal ultrasound is read as "hydronephrosis" but this is probably not pathologic) can occur as well, most notably in pregnancy. It is also common that hydronephrosis detected on ultrasound is a chronic, long-standing issue and not the main culprit for the present episode of AKI.
This is taken from handout put up by Precious Body Fluids
Now a new study published in Circulation compared the blood pressure between individuals who ate vegetable protein (specifically glutamic acid along with 4 other amino acids which are relatively higher in vegetable than animal protein) with people who ate non-vegetable protein (read animal meat).
They found a difference of about -2.7/-2.0 mm Hg in blood pressure in people eating more vegetables. Although that may sound small, individual results may be different (and maybe higher for you).
H1N1 Death Rate Holds Steady
The latest update from the World Health Organization reveals the number of swine flu cases worldwide at 77,201—a nearly 50% increase from the June 22nd update. Deaths total 332 (up from 113) for an unchanged mortality rate of 0.43%.
H1N1 cases have now been reported in 120 countries or territories, and related deaths have occurred in 17. Countries disproportionately affected by new cases (where more than 500 cases have occurred) include Thailand, the United Kingdom, Brazil, Peru, and Spain. The number of swine flu deaths in the United States now surpasses those in Mexico.
Another Tool for anticoagulation
Medical management of T2DM
This review is a convenient reference and follows the “mainstream” recommendations. Note that the A1C target of 7%, which the authors advocate, is controversial number..
When will you request TEE in Ischemic Stroke?
June 14, 2009
The main reason for getting a TEE in a patient with ischemic stroke is to find out if that patient has an indication for warfarin anticoagulation. You can begin the selection process by excluding patients who already have an obvious indication for warfarin (e.g. atrial fibrillation) and those who have a contraindication for warfarin.
Among the remaining patients only those with cryptogenic stroke are likely to need a TEE. This is an old paper demonstrating a high yield for TEE in finding an indication for warfarin in such patients. Here is a new study documenting similar findings:
The TOAST classification may be helpful in the determination of cryptogenic stroke.
How well do you treat hypertension?
Not all docs are above average but, according to this study, most of us tend to think we do a better job of treating HT than we actually do. Moreover, when the patient doesn’t reach goal we blame it on “noncompliance.Read more..
The most forgotten Lead= aVR
The most neglected electrocardiographic lead may be the most important in some patients with ACS.Often relegated to the status of placeholder in the electrocardiogram, aVR may contain the critical data for the diagnosis of a number of conditions. A review in the American Journal of Emergency Medicine highlights pericarditis, left main coronary obstruction, orthodromic tachycardia and acute tricyclic antidepressant poisoning. From Medscape Emergency Medicine Viewpoints:
The takeaway point is simple: When patients with ACS, including non-STE ACS, demonstrate STE in lead aVR, the aggressiveness of early management must be
increased. These patients have more complex coronary lesions and will likely benefit from earlier invasive therapy.
Additional references:
ST elevation in aVR as a sign of left main coronary artery obstruction.
Review of electrocardiographic clues obtainable from aVR (JACC).
Classic paper on the electrocardiographic changes of pericarditis.
The electrocardiogram in non cardiac conditions..
