Hiteshi K.C. Chauhan

Piperacillin and vancomycin induced severe thrombocytopenia in a hospitalized patient

In hospitalized patients with complex medical problems on numerous drugs, thrombocytopenia may have a multiple confounding etiology. Keeping this in mind, it is of utmost importance to monitor the platelet count regularly during hospitalization and on subsequent follow-up visits, even after the most probable etiology has been identified/most likely causative drug has been withdrawn. Isolated thrombocytopenia with no evidence of microangiopathic hemolysis on the peripheral blood smear in an acutely ill hospitalized patient implicated sepsis, disseminated intravascular coagulation and drugs as the most probable causes. Our patient represents an uncommon case of antibiotic-induced severe immune thrombocytopenia, as he developed both vancomycin-dependent and piperacillin-dependent antibodies, while being treated for cellulitis (vancomycin-specific antibodies of the IgG isotype, and both IgG and IgM antibodies specific for piperacillin were identified in laboratory testing). Vancomycin was stopped before the reports were available. Following this, the patients platelet count showed a transient upward trend, but then the thrombocytopenia worsened drastically reaching a nadir of 10,000/µL. The platelet count returned to normal only after piperacillin/tazobactam was stopped after a week, thus establishing it as the cause of the more severe thrombocytopenia, which occurred later on; this was subsequently confirmed by the laboratory results. Vancomycin is an established cause of drug-induced immune thrombocytopenias, especially in acutely ill, hospitalized or elderly patients, whereas incidents of piperacillin/tazobactam-induced immune thrombocytopenia are uncommon. In case clinical suspicion is high, workup should include immunoprecipitation and flow cytometry studies to confirm antiplatelet antibodies.

Diabesity – The ‘Achilles Heel’ of our modernized society

Diabesity – a term coined by Dr. Francine Kaufman to cover a constellation of signs, including obesity, insulin resistance, metabolic syndrome, and diabetes – is ready to become the largest rapidly escalating pandemic in human history. The statistics are grim and shocking – diabesity affects more than one billion people worldwide, including 100 million Americans, and 50% of Americans over the age of 65. Mortality from diabetes stands at approximately 4.6 million people per year worldwide. More than 366 million people are currently affected by this disease. According to current statistics, by the year 2020 diabesity will be the leading cause of chronic disease and death in the world. The “sugar disease” has evolved from merely affecting rich, industrialized countries to the status of a global economic and chronic disease catastrophe in the making. The World Health Organization (WHO) predicts that, by 2030, developing countries will have three-fourths of the world’s estimated 900 million diabetics . The conventional way to see developing countries was to observe the ‘want’ – for food, for money, for life – with millions struggling below the poverty line. But now the other side of the coin tells the story of their newfound excesses. The mantra is: make good money, buy cars, buy houses, eat out, get obese, get diabetes. According to the latest United Nations (UN) statistics, there are more patients overweight than undernourished. Both India and China are already home to more diabetics than any other country. Forsaking paddy fields for a city lifestyle clearly has a downside, especially in populations with a pronounced genetic vulnerability to the disease. These populations contract the disease ten years earlier than people in developed countries. The future of diabetes in ‘young’ countries such as India, where half the population is under 25, is chilling. The pressing and urgent is that we put a HALT to this rapidly evolving sinister scenario by finding the answers for a few simple questions. 1. What is the ROOT cause of the current diabesity epidemic? 2. Why are our current approaches to treat it failing miserably? 3. What new initiatives do we need to implement to more effectively treat the problem? In our viewpoint, we are trying to mop up the floor while the sink overflows. It is as important, if not more, to treat the root causes of diabesity as it is to treat the mere symptoms and risk factors. The diabesity complex originates from the interaction of our modern western sedentary lifestyle, dietary and environmental toxins, micronutrient deficiencies, chronic stress, and altered gut microflora with our unique genetic susceptibilities. These root causes are intricately interlinked to each other. The best news they are 100% preventable and in most cases, entirely reversible. Research should focus on the underlying environmental and genetic risk factors for diabetes and obesity worldwide, especially in susceptible populations. A greater focus on epigenetics and early life risk factors such as maternal nutrition may lead to more effective strategies to curb diabesity. Developmental plasticity, fetal programming, and intergenerational risk means that a stimulus applied in utero establishes a permanent response in the fetus, leading to enhanced susceptibility to later diseases such as type 2 diabetes and CVD. We are sure that not a single person reading this editorial has been left untouched by the effects/consequences of the ‘diabesity poison’, either directly or indirectly. Our focus needs to encompass ‘PREVENTION’ rather than just ‘CURE’, by educating the masses about comprehensive diet/lifestyle change programs, developing research programs to analyze the environmental-gene interactions leading to diabesity, and by initiating an intense unified global initiative to target this pandemic. Isn’t it about time we took steps to turn the faucet off before this diabesity storm drowns the world?

A tale of early Reel syndrome caused by an over-enthusiastic masseuse.

Twiddler syndrome is a form of pacemaker lead dislocation caused by the coiling of the pacemaker leads due to pulse generator rotation on its long axis. Similar to Twiddler syndrome, Reel syndrome occurs due to rotation of the pulse generator on its transverse axis, leading to lead dislocation or fracture, followed by clinical symptoms of dislodged leads. We report a case of 75 years old woman with Reel syndrome presenting with syncope.

PCI in a case of dual (type IV) LAD with anomalous origin of the LCx from RCA

Dual left anterior descending coronary artery (LAD) originating from the left main stem and the right coronary artery (type IV LAD) is a rare congenital anomaly. Its association with an anomalous origin of the left circumflex (LCx) from RCA is even rarer. We describe a patient presenting with acute inferior wall myocardial infarction, who was subsequently found to have this coronary anomaly. He underwent staged PCI of the dominant RCA and anomalous LCx successfully through the radial route. We conclude that anomalous coronaries can be safely and successfully treated through the radial route after careful evaluation of origin and course of the anomalous vessels. CT coronary angiography is extremely useful in delineating the vessel course and particularly their relation to great arteries.

Collateral approach for LV lead implantation in a case with abnormal venous anatomy.

A 75-year-old man, 8 years after CABG, with ischemic cardiomyopathy underwent cardiac resynchronization therapy (CRT) for refractory heart failure. Retrograde occlusion venography revealed absence of lateral vein. A functionally occluded middle cardiac vein with branch to anterolateral vein was used for left ventricular lead implantation. Using a collateral route for left ventricular lead implantation is a new technique. Lead position was stable with excellent threshold. Follow-up at 6 months reveals continued stable lead position.