Doctors should stop wearing white coats – apron


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Bezold-Jarisch Reflex

Bezold-Jarisch Reflex

Eponym for a triad of responses (apnea, bradycardia, and hypotension)

A cardiovascular decompressor reflex involving a marked increase in vagal (parasympathetic) efferent discharge to the heart, elicited by stimulation of chemoreceptors, primarily in the left ventricle & hypopnea. This causes a slowing of the heart beat (bradycardia) and dilatation of the peripheral blood vessels with resulting lowering of the blood pressure.

Reflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, the Bezold–Jarisch reflex and neurocardiogenic syncope

The concept was originated by a German physiologist Albert von Bezold in 1867, later revised by an Austrian dermatologist Adolf Jarisch in 1937.

Miller’s Anesthesia 7 th Ed.p. 409

The Bezold-Jarisch Reflex responds to noxious ventricular stimuli sensed by chemoreceptors and mechanoreceptors within the LV wall by inducing the triad of hypotension, bradycardia, and coronary artery dilatation.  The activated receptors communicate along unmyelinated vagal afferent type C fibers.  These fibers reflexively increase parasympathetic tone.  Because it invokes bradycardia, the Bezold-Jarisch reflex is thought of as a cardioprotective reflex.  This reflex has been implicated in the physiologic response to a range of cardiovascular conditions such as myocardial ischemia or infarction, thrombolysis, or revascularization and syncope.  Natriuretic peptide receptors stimulated by endogenous ANP or BNP may modulate the Bezold-Jarisch reflex.  Thus, the Bezold-Jarisch reflex may be less pronounced in patients with cardiac hypertrophy or atrial fibrillation.

Stoelting’s Anesthesia and Co-Existing Disease 5 th Ed.p.74-5

The underlying mechanism responsible for bradycardia and asystole during spinal and epidural anesthesia is not known. Proposed theories include reflex-induced bradycardia resulting from decreased venous return and activation of vagal reflex arcs mediated by baroreceptors and stretch receptors in the sinus node resulting in a paradoxical Bezold-Jarisch response. Another possible mechanism is the unopposed parasympathetic nervous system activity that results from the anesthetic-induced sympathectomy. Blockade of cardiac accelerator fibers originating from thoracic sympathetic ganglia (T1-4) may alter the balance of autonomic nervous system input to the heart resulting in the emergence of relatively unopposed parasympathetic influences on the SA node and AV node. Secondary factors such as hypovolemia, opioid administration, sedation, hypercarbia, concurrent medical illnesses, and long-term use of medications that slow the heart rate could also contribute to development of bradycardia.The following source would not be used for board references, but is here to further illustrate the concept of the Bezold-Jarisch reflex.

British Journal of Anaesthesia 2001; volume 86; p. 859–68

Reflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, the Bezold–Jarisch reflex and neurocardiogenic syncope. The circulatory response changes from the normal maintenance of arterial pressure, to parasympathetic activation and sympathetic inhibition, causing hypotension. This change is triggered by reduced cardiac venous return as well as through affective mechanisms such as pain or fear. It is probably mediated in part via afferent nerves from the heart, but also by various non-cardiac baroreceptors which may become paradoxically active. This response may occur during regional anesthesia, hemorrhage or supine inferior vena cava compression in pregnancy; these factors are additive when combined. In these circumstances hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilation. Treatment includes the restoration of venous return and correction of absolute Blood volume deficits. Ephedrine is the most logical choice of single drug to correct the changes because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anesthesia.

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Targeted Anti-Anticoagulants

Four direct oral anticoagulants have been approved for use in many countries. These drugs are valuable alternatives to vitamin K antagonists, such as warfarin, for many patients requiring anticoagulation to prevent stroke due to nonvalvular atrial fibrillation and to treat and prevent venous thromboembolism. The mechanism of these agents is to selectively inhibit either thrombin or factor Xa, which are critical enzymes in the common pathway of blood coagulation. Dabigatran etexilate inhibits thrombin, whereas apixaban, edoxaban, and rivaroxaban inhibit factor Xa.

Direct oral anticoagulants have several pharmacologic advantages over vitamin K antagonists, including a wider therapeutic window, a rapid onset of action, and shorter half-lives that range between 7 hours and 14 hours in healthy persons. Direct oral anticoagulants are administered at fixed doses to adults without laboratory monitoring, which is more convenient than warfarin with its requirement for monitoring of the international normalized ratio and periodic dose adjustments. In randomized trials with good anticoagulation management (i.e., with international normalized ratios generally in the desired therapeutic range of 2 to 3 for >60% of the time), direct oral anticoagulants were noninferior, and in some cases superior, to dose-adjusted warfarin for the prevention and treatment of thrombosis. As compared with warfarin, direct oral anticoagulants reduced the rate of major bleeding by 28% and the rates of intracranial and fatal hemorrhage by 50%.1

Despite the better bleeding profile of direct oral anticoagulants, as compared with warfarin, some physicians and patients have been unwilling to consider these drugs in the absence of an established way to reverse their anticoagulant activity. Although the anticoagulant activity of warfarin can be reversed with vitamin K, fresh-frozen plasma, and prothrombin complex concentrates, major bleeding events that occur in patients taking this drug often lead to poor outcomes; approximately 10% of patients who are hospitalized with warfarin-related bleeding die within 90 days,2,3 and the mortality among patients with intracranial hemorrhage can be as high as 50%.4,5 The high mortality is attributable in part to coexisting conditions in this patient population. Experimental data suggest that nonspecific reversal agents such as prothrombin complex concentrates, activated prothrombin complex concentrates, or recombinant factor VIIa can reduce the anticoagulant effect of direct oral anticoagulants in vitro, in animal models, and in human volunteers.6 However, these agents are of unproven benefit in improving hemostasis in patients with bleeding related to direct oral anticoagulant use, and they carry a risk of thrombosis; thus, they are currently reserved for patients with severe bleeding who cannot be treated with supportive measures.

With the growing use of direct oral anticoagulants, it would be advantageous to have reversal agents that can rapidly and completely neutralize the anticoagulant activity of the drug and restore normal hemostasis. Specific reversal agents in clinical development include andexanet alfa, a recombinant factor Xa variant that specifically binds all the oral factor Xa inhibitors but lacks coagulant activity.7 There is also a nonspecific reversal agent in clinical development, PER977, which binds to several of the direct oral anticoagulants by means of electrostatic interactions.8 Given that there are no established reversal strategies for the direct oral anticoagulants, it is appropriate to undertake clinical trials of these agents without a control group.

Idarucizumab is a humanized monoclonal antibody fragment with high affinity for the oral direct thrombin inhibitor dabigatran that selectively and immediately neutralizes its anticoagulant activity.9 Pollack et al.10 now report in the Journal the results of an interim analysis of data from 90 patients who were taking dabigatran and who presented with either serious bleeding or the need for urgent surgery or intervention and received intravenous idarucizumab. This multicenter observational study evaluated the effect of a single 5-g dose of antibody in eligible patients who were judged by the treating clinician to require a reversal agent. The major end points of the study were pharmacodynamic assessments of the ability of idarucizumab to neutralize the anticoagulant activity of dabigatran. The data are convincing that the antidote effectively and immediately neutralized the activity of dabigatran with a satisfactory safety profile. Normal hemostasis was reported in more than 90% of the patients who underwent procedures after the administration of idarucizumab.

Without a control group, it is difficult to assess the clinical benefit that is conferred by the administration of idarucizumab in patients with dabigatran-related bleeding. The mortality in the study population was high at 20%; half the deaths occurred more than 96 hours after the administration of the antidote and were attributable to coexisting illness. Given that the half-life of dabigatran is 12 to 14 hours if renal function is normal, how important is it to be able to neutralize the anticoagulant activity of dabigatran rapidly in addition to providing supportive care measures? Major bleeding events in patients taking anticoagulants originate from anatomical lesions, and anticoagulation can lead to a rapid loss of blood from these sites. Thus, the location and size of the lesion along with the coexisting conditions of the patient may have a greater effect on prognosis than the ability to rapidly neutralize an anticoagulant that the patient is taking.

Laboratory measurements of the concentration of dabigatran were performed centrally in this study and were not used to guide therapy. The results of one of these tests, the dilute thrombin time, were normal on study entry in nearly one quarter of the study population. This group of patients had little or no circulating anticoagulant in their blood and would not be expected to benefit from the administration of idarucizumab. Thus, it will be useful to have activity measurements available for the various direct oral anticoagulants in real time to help guide the treatment of such patients and to prevent overutilization of what will surely be a costly medication.

The development of antidotes that are able to neutralize the activity of the various direct oral anticoagulants rapidly and completely is an important advance. When they become available, guidelines and clinical pathways will need to be developed to care effectively for patients with, or at risk for, major bleeding related to direct oral anticoagulant use. Additional studies, however, will be required to determine in which situations the antidotes improve clinical outcomes.

Source :
This article was published on June 22, 2015, at

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How can you confirm a CSF leak in a base of skull fracture?

How can you confirm a cerebrospinal fluid leak in a base of skull fracture?
Basilar skull fractures (i.e. base of skull fractures) have a high incidence of dural tears and thus a higher than average risk of meningitis – although it is controversial whether or not to give prophylactic antibiotics. The basics to know about this condition are as follows:

Firstly, skull X-rays are almost never of any help in diagnosing basilar skull fractures. You need to go by clinical signs.

Clinical signs include:

    Raccoon eyes – this refers to a periorbital (around the eyes) bruising, and is a result of blood tracking down from the skull fracture site to the soft tissue around the eyes.

    Battle’s sign – named after a guy (unsurprisingly) called Battle, this is bruising around the mastoid process (behind the ears). As with raccoon eyes, this bruising is due to blood tracking there from the skull fracture, not from damage directly to the mastoid process.

    Cerebrospinal fluid (CSF) otorrhoea -this is leakage of CSF out your ear, via a combination of a ruptured tympanic membrane and nearby basilar skull fracture.

    CSF rhinorrhoea – similar to the otorrhoea story, this is leakage of CSF out your nose. Usually (but not exclusively) the ethmoid cribriform plate is the part fractured.

    Cranial nerve palsies – many of the cranial nerves run nearby enough to be injured or compressed by a fractured base of skull.

A good question that might now arise is how you tell if fluid coming out the nose or ears is CSF – it could be pure blood, or (in the case of nasal discharge) it could be the normal nasal secretions. There are a number of tests you can do.

Firstly, CSF should have glucose in it, whereas this is unlikely in normal nasal secretions, and so measuring the glucose (initially on dipstix, and then formally) is helpful.

Secondly, if you are dealing with a bloody fluid, you could try to look for the halo sign (or ring sign). Get some of the blood on a tissue  If there is CSF mixed with the blood, it will move by capillary action further away from the centre than the blood will. You’ll get something like this:


These tests are helpful , but they aren’t accurate. If you want to be more sure, measure the level of beta-2-transferrin in the fluid. This protein is only found in CSF, so if you are finding it in fluid coming from the nose or ears, you have a CSF leak.

If you have any of these signs present, you may be dealing with a basilar skull fracture. To confirm your diagnosis, you need to organise a CT scan of the area. This is more or less the diagnostic procedure followed in most hospitals.

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Blood donation guidelines for thyroid & autoimmune diseases

Hypothyroid patients who are taking levothyroxine (i.e., Synthroid), Cytomel, Thyrolar, or natural thyroid products like Armour and are in the normal thyroid range can give blood if they don’t have any other precluding conditions.

Graves’ disease or hyperthyroidism patients who are on antithyroid medicines, or who are not currently in normal thyroid range, cannot give blood.

Anyone with any other autoimmune disease should not give blood, unless they are asymptomatic and off all medications for one month.

In thyroid patients, and some of the more common autoimmune disease, you specifically should NOT give blood if you have:

    Addison’s Disease
    Adrenal Disorders
    Sinus or respiratory infections, colds or flu symptoms
    Rheumatoid Arthritis, if you’re on steroids or immunosuppressive drugws
    Lupus, unless asymptomatic, and off all medication for at least a month
    Multiple sclerosis

Also, you can’t give blood if you:


Have ever used illegal intravenous drugs, even once
    Are a man who has had sex with another man since 1977, even once
    Are a hemophiliac
    Have had a positive HIV test
    Have had hepatitis any time after your eleventh birthday
    Have had cancer (except localized skin cancer)
    Have had a heart attack or stroke
    Have taken Tegison for psoriasis

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