• Aaron MD
    "Doctor, this patient wants to be seen by you". I was in the middle of clinic when the nurse barged in & dumped a giant set of notes on my desk. "Mrs Cook does not want to see the consultant". My consultant, nicknamed "Grumps", short for "Grumpy Old Man". He is not the most friendly of characters, to put it diplomatically.

    When I saw Mrs Cooks said, "I don't want to be seen by the consultant, because the last time I saw him, he hardly spoke to me". Mrs Cooks fumed, "He never asked me what I wanted & didn't listen when I told him I did not want to be investigated any further. I was examined & sent for 5 different tests including X-Rays, ultrasounds, blood tests & ECGs. I was here nearly 5 hours last time."

    I was not surprised by what I was hearing. I have seen how Grumps interacts with his patients. They are made to sit in the corner in silence whilst he pours through the notes. The atmosphere would be similar to a naughty pupil sitting in the headmaster's office. After a long deafening silence, he would instruct the patient to undress for examination. Without further explanation, the patient would then be sent on his or her way for an exhaustive battery of tests taking up to several hours. 

    After all the results are back, the patient would then be summoned back to Grump's room where he would pronounce his verdict & treatment plan. If the patient dared to as so much question him, he would give them a patronising look, simply repeat his verdict & treament plan without elaborating any further. At the end of the consultation, the patient would be dismissed with the phrase, "that will be all".

    Its absolutely embarassing to watch this display. I can't believe how little he communicates to the patient. Until then, I didn't realise that doctors like this existed anywhere except on television as caricatures.

    Grumps unfortunately, is a relic from a bygone era where patients were talked at, not talked to. He is an excellent, knowledgable clinician & even has many patients that adore him. But his clinical practice fails on the communication skills side. He gives doctors a bad name & lets patients down. Even to his fellow doctors, Grumps remains a poor communicator, in particular those junior to him. He is capable of communicating well with fellow consultants, so its because of a lack of will rather than a lack of ability. Grumps has been working in the same hospital for over 30 years. He is head of department & has many powerful allies.

    It will not be easy to change him. Suggestions anyone?
    Dr. Anmol
    Terrorism has no religion, but unfortunately it’s got a profession in India. Recently the doctors are being coined as ‘terrorists’ by a group of activists here. If you’re a doctor or you’ve one in your family,  you’ve been involved in terrorizing common people.
    ‘STOP Medical Terrorism: Justice for Dr. Anamika Ray’
    A growing community in Facebook, led by her husband Dr. Ankur Dutta for Dr. Anamika Ray  a ‘victim of medical negligence’ reportedly starts a nationwide movement named “STOP MEDICAL TERRORISM”.  It’s now being formally initiated by a group of victims of medical negligence and supporters of the cause under the platform of Dr. Anamika Ray Memorial Trust, Guwahati, demanding better health care services in India. The first advocacy meeting to combat medical terrorism and negligence was organised in Guwahati, where a large number of victims of medical negligence and supporters of this movement participated and prepared a road-map for a nationwide movement.
    The Data
    Around 52 lakh medical injuries are recorded in India each year, of which around 98,000 result in fatalities. It is a matter of serious concern for the entire nation that ten people fall victim to medical negligence every minute and more than 11 people die per hour in the country due to medical error and negligence. It is the eighth leading cause of death in the world. Approximately 30 lakh years of healthy life are lost in the country each year due to medical negligence.
    Confused?
    Are they doctors who are leading this ‘fight’ against the whole medical fraternity? No, they are PhD doctorates and not doctors.
    The Statistics
    Highly inflated, unauthenticated data to mislead common people. What is medical negligence? Is it dissatisfaction to patients? Every day, in my OPD I see approx. 200 patients (a central Govt. employee). I see them all, but satisfy none. Most of them are treated, some of them come back, and few are referred to higher medical echelon. I work like a robot, no time to pick up calls, no time to have a cup of coffee. I am aging fast, have no family life and often abused by people.  What do you expect more out of me? If 10 out of those dissatisfied patients call it medical negligence, I’m helpless. If I couldn’t cure someone, though I wanted to, is that medical negligence?
    In India, doctor patient ratio is 1: 1700. This ratio comes down further to 1: 11,528 for Govt. doctors (2015 statistics). Have you ever given a thought how many patients a doctor can handle in a day? In an average it’s 20-30. It depends on the doctors physical and mental abilities also. We’re humans too and don’t expect us to work alike machines.
    Environment
    As already mentioned, a doctor is not a manual labour. He has to work calm and quiet, to be able to judge the right decision for patients and to apply his best skills. Please give that much liberty to doctors. Do you think raising your tone on a doctor makes him give better treatment? If yes, you have grossly miss-leaded.  A doctor’s mind is no different from a common people. Abuses, harsh attire, physical strain, noise, news everything plays negative upon his mind. Result? Dissatisfied patients.
    The reaction:
    Indian Medical Council Assam Branch has expressed shock, dismay and indignation over the reported campaign against medical terrorism. In a statement by IMA Assam Branch secretary says that the initiative has been rather initiated to terrorize the common people against medical profession, trying to cause unrest among people to undergo tests and investigations and attempted to spill venom of mistrust between doctors and patients. IMA also demanded disclosure of the facts and data the trust has mentioned as around 52 lakh medical injuries are recorded in India each year, of which around 98,000 result in fatalities. It is a matter of serious concern for the entire nation that ten people fall victim to medical negligence every minute and more than 11 people die per hour in the country due to medical error and negligence
     
    The Sentiment
    I don’t deny few doctors are involved in malpractices. They are punished when it comes to criminal negligence from case to case basis. But generalizing medical practice as terrorism not only demotivates the other dedicated lot, also creates unnecessary mistrust between patient and doctor.  Such antisocial demonstrations must be handled carefully at its root.
    Mark Wallace, MD
    Specifically, does the protection of the first Amendment apply to doctors who espouse conservative beliefs in signs on their office windows? Florida urologist Jack Cassell when placed a sign on the window of his office that read, “If you voted for Obama … seek urologic care elsewhere. Changes to your healthcare begin right now, not in four years.”
    Of course, the liberal war machine when into high gear once word of this got out.
    To his credit, Dr. Cassell denies having abandoned or refused to treat patients based on their political views and denies even asking patients about their views or who they voted for as a
    The Oath: It's Greek to me.
    prerequisite for treatment.  Dr. Cassell’s sign is obviously a political statement and not a serious policy if considered in the context of the fact that voting remains by way of secret ballot in this country and that other then bumper stickers there is no way to identify the political affiliation or opinions of Americans.
    Rep. Grayson is right about one thing. Taking this sign seriously is about as “ridiculous” as literally believing the intentions of a doctor who puts up a sign stating their refusal to treat anyone who’s favorite color is blue.
    But don’t raise such practicalities of common sense with Mr. Grayson who has threatened to file a complaint against Dr. Cassell with the Florida Department of Health.  This is just another perfect example of why the first amendment continues to be so important (actual and real patient abandonment should be irrespective of the reasons for such ethics violations).
    This case does raise a troubling issue. Are physicians for all intents and purposes, stripped of their rights to political speech and political activity if such activity directly involves patient care? One of the letters to the editor of the Orlando Sentinel expressed disgust at Dr. Cassell’s mixing of politics and patient care while ironically stating her right to choose another physician if faced with a similar sign. Wait. Don’t doctors also have the right to choose to be politically active just as patients have the right to pick and change doctors?
    Though ivory tower bioethicists believe that the Hippocratic Oath binds physicians to an unbreakable doctor-patient relationship until death do us part or until the patient seeks care elsewhere, the fact is that there is nothing in the Oath that specifically forbids political activity by doctors nor compels them to treat a patient indefinitely irrespective of any reason to end the relationship. Practicalities take priority over idealism in common law.  Except for laws that bar discrimination, a physician is allowed to refuse service or to terminate services. In almost all cases, physician’s are allowed to end a professional relationship with a patient after giving appropriate notice and assistance as indicated to help the patient secure care elsewhere while being available for a practical time period to render emergency care as needed.
    Ideally, political activity should NOT impact or compromise patient care but sometimes a work stoppage (strike) and refusal to participate in the system is the only way to send an effective message. Nor should doctors be forced by some false interpretation of the Hippocratic Oath to continue to provide care within a health care system that they feel compromises their own economic stability and/or the ultimate care of their patients. In other words, do the ethical constraints of the Hippocratic Oath trump the Constitutional rights of physicians? Absolutely not. The Framers were well aware of the ancient Oath in their time and did not choose to make an exception in that the rights of patients for care would negate the speech and political rights of their physicians.
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    The Doc
    Always consider aortic dissection as the diagnosis if you hear aortic regurgitation, or a diastolic murmur
    Introduction
    Acute aortic dissection is a medical and surgical emergency - it is one of the critical causes of acute chest pain that must not be missed!   Aortic dissection now forms part of the ‘acute aortic syndrome’ The inner wall of the aorta is composed of the tunica intima and the tunica media Damage to the intimal layer generates a space for blood to enter.  This ‘dissection’ of the intima-media layer allows the entry and flow of blood along the path of the aorta Presentation may be acute: 2 months Type A aortic dissection prognosis is poor: 30% die immediately; 50% die <48h; 60% in-hospital mortality with medical management; 20-30% operative mortality; untreated, 1% die an hour, with 90% after 1 week In Type A dissection, 35% present with hypertension, 25% present with hypotension. In Type B, 70% present with hypertension, and 5% with hypotension 30% have acute aortic regurgitation A high index of suspicion is needed to diagnose in the emergency department; it is easily overlooked or misdiagnosed; it may mimic an MI Have a high index of suspicion in pregnant women presenting with chest pain What is aortic dissection

    Intimal damage resulting in generation of a false lumen within the aortic wall and propagation of blood along this space in either a forward or backwards direction Pathology
    Myxoid degeneration - loss of elastic fibres and replacement of musculo-elastic tissue with proteoglycan-rich matrix Cystic medial necrosis: may be associated with injury or occlusion of vasa vasorum Intimal tear - dissection propagates along plane that runs between inner 2/3 and outer 1/3 of media  Aortic Dissection Types
    Categorised anatomically, temporally (acute 2 months) or pathologically The aorta is divided into two parts, the thoracic and the abdominal aorta; the thoracic is further divided into the ascending part, the arch and the descending part The two commonly used anatomical classification systems are the Stanford and DeBakey systems (see figure below) Stanford: Type A and Type B:       Type A aortic dissection = ascending aorta affected       Type B aortic dissection = descending aorta affected DeBakey: Type I, II and III: Type I and II = ascending + descending aorta Type III = descending aorta Prognostically important, the Type A and Type I dissections carry the highest mortality and usually require acute surgical intervention  Epidemiology
    3-4 per 100,000 in UK/USA Male-to-female ratio is 2:1, to 5:1. Half in females before age 40y occur during pregnancy (typically in the 3rd trimester or early postpartum period) The peak age for Type A (proximal dissection) is 50-55 years, and that of Tyep B (distal dissection) is 60-70 years Classically at risk is a white, hypertensive man, age 50-70 years Risk factors of Dissecting Aortic Aneurysm
    Any process that weakens the wall of the aorta: Hypertension (70%) - leads to increased shearing forces across intima Traumatic injury to aorta (esp deceleration injury) Iatrogenic - surgery (eg AV replacement); cardiac catheterisation, aortic cannulation High cardiac output states: pregnancy Aortic disease: aortic aneurysm, anuloaortic ectasia, aortic arch hypoplasia, coarctation of the aorta, aortic arteritis (eg vasculitis (Giant cell, Takayasu's, Behcets), syphilis), bicuspid aortic valve Inherited defects    - Marfan's - 15q fibrillin defect. Marfan syndrome accounts for the majority of cases of aortic dissection in patients < 40 years of age   - Ehlers-Danlos - procollagen formation    - Pseudoxanthoma elasticum - fragmentation of elastic fibres in media   - Cardiac disease (bicuspid aortic valve)   - Turner's and Noonan's syndrome Age/sex; 50-70 years; male sex  Competitive weightlifting Smoking, cocaine use Pregnancy and Aortic Dissection Be highly suspicious of the diagnosis in a pregnant woman presenting with chest pain Any woman identified at risk (Marfans, coarctation, bicuspid AV and enlarged aorta, Ehlers Danlos Type IV etc) should have beta-blockade throughout pregnancy Patients with a known bicuspid aortic valve and enlarged aortic root should to be counselled like Marfan syndrome patients Normal sized patients with an aortic root size more than 4 cm (or smaller in patients with low BSA), or an increase of aortic root size during pregnancy, are at high risk for the occurrence of aortic dissection, mainly in the third trimester If possible, surgical repair of the enlarged aortic root should be done prepartum During pregnancy and during delivery, hypertension should be prevented Caesarean section under regional anaesthesia is recommended in all at risk patients. Then Aortic root surgery should be performed a few days after delivery, if it has not been performed prepartum In Type A dissection before 30 weeks of gestation immediate surgery should be performed, and after 30-weeks gestation caesarean section followed by cardiac surgery Close monitoring and the administration of beta-blocking agents is mandatory up to 3 months postpartum, as late dissections may occur in this time period Effects of Aoric dissection
    Propagation:
    Aortic ring - acute aortic regurgitation (30%) Coronary arteries - angina / MI Carotid arteries - stroke Abdominal aorta - gut ischaemia (if mesenteric vessels involved) Renal artery - ARF Intercostal / lumbar vessels - spinal cord ischaemia (loss of supply from arteria radicularis magna - great spinal artery of Adamkewicz) Rupture:
    Pericardium - tamponade Pleura - haemothorax Compression Trachea / oesophagus / SVC Double-barrelled lumen (if re-enters lumen through another intimal tear)  Aoric Dissection Symptoms
    Can be varied and non specific; usually always chest pain (1/10 do not have pain – commonly patients with diabetes) Classic presentation is sudden onset of severe ‘stabbing’ or ‘tearing’ chest pain, radiating to the interscapular region. Interscapular pain usually suggests Type A dissection Chest pain that moves suggests dissection American Heart Association suggests ‘PEP’:
    Pain character: sudden, tearing/stabbing pain in chest/back/abdomen Examination findings: pulse/BP asymmetry, hypovolaemic shock, focal neurology, new aortic regurgitation. Predisposing factors: Marfan’s, recent aortic surgery/procedure, thoracic aneurysm Of CCF (aortic regurgitation or MI) Other important features are a result of reduced perfusion:
    LOC/collapse Neurological focal deficit: dissection involving the carotids or low perfusion pressure Ischaemic limb Ischaemic end organ damage, eg ischaemic bowel, renal failure  Key Questions
    “Describe the nature of the pain” “How quickly did it start” Aortic Dissection Signs
    Shock, or hypertension (may have wide pulse pressure) New murmur (30% aortic regurgitation; early diastolic murmur) Of CCF (aortic regurgitation or MI) Cardiac tamponade Asymmetrical pulses (15-20%):
    Pulse or BP deficit deficit between upper limbs BP difference at upper and lower limbs NB: absent pulses may reappear as the blood flow swtiches from the false to the true lumen Neurological signs - stroke, cord features
    Bruits over peripheral arteries Note: examination may be normal Investigation for Aortic Dissection
    The key aim is to diagnose aortic dissection then assess its anatomy (Type A or B) Blood:
    FBC, U+E, LFT, Bone, Glucose, G&S CRP, ABG D-dimer (raised) Cardiac Troponin, if the patient presents > 6h after the onset of pain; may be raised if MI is diagnosis, or complication Other ECG
    Within 10 mins of presentation Rule out acute or evolving MI - complicated dissection can induce MI (dissection may involve the origin of the coronary vessels) May show LVH May be normal (30%)

    75% have classic changes including a wide mediastinum and prominent aortic knuckle; this is not a diagnostic sign, as many normal elderly patients have an unfolded aorta Left pleural effusion (20% Deviation of NG or tracheal to right Separation of two parts of wall of a calcified aorta by > 5mm ('calcium sign') May be normal (12%); or at least appear normal; with hindsight is almost always abnormal Compare with previous films Note widened mediastium and left pleural effusion  'Calcium sign' Key Investigations

    CT angiography is 100% sensitive, 98% specific and widely available  Transthoracic ECHO (if on-site cardiology available) to assess aortic root and valve in cases where type A is suspected (also to screen for pericardial effusion, aortic regurgitation; as this is quick and can be done at the bedside CT with contrast demonstrating aneurysmal dilation and a dissection of the ascending aorta (Type A Stanford) Specialist Investigations
    Transoesophageal echocardiography (TOE) MR angiogram may be better suited to monitoring established disease  Differential Diagnosis
    Any sudden onset of chest and/or back pain Cardiac (ACS, including acute MI, acute limb ischaemia) Respiratory (massive PE, pneumothorax) GI (peptic ulcer (+/-perforation), pancreatitis, mesenteric ischaemia, renal/ureteric colic) Neurovascular (e.g. stroke or cauda equina syndrome) Note: Neurovascular symptoms can also herald proximal aortic dissection Treatment of Aortic Dissection
    Type A dissection is usually treated surgically; Type B medically
    Resuscitate ABCDE Adequate oxygenation and ventilation, two large bore cannulae, adequate intravenous fluid resuscitation titrated to blood pressure, heart rate and urine output IV MORPHINE 2.5-5 mg and IV METOCLOPRAMIDE 10mg High flow OXYGEN NBM If hypertension severe, control SBP to 100-120mmHg: IV LABETOLOL (250mg/250mls 5% dextrose) at 2-8 mg/min, increasing every 15 mins to a maximum dose of 200mg; or IV SODIUM NITROPRUSSIDE (50mg/500 ml 5% GLUCOSE) at 10 mcg/min (6 ml/hr), increasing every 5 mins in steps of 10 mcg/min to a maximum of 75 mcg/min (45 ml/hr) Note: if these infusions are not available quickly, IV GTN infusion 10-200 mcg/min (start high), is a good drug to start with
    Urinary catheter Type A – emergency surgery: open repair = replacement of diseased segment of aorta with interpositional graft and re-implantation of coronary arteries if root involved +/- aortic valve replacement. Some centres use endovascular repair, or both
    Type B – classed as either complicated or uncomplicated
    Uncomplicated: medical treatment; control SBP to 100-120mmHg (as above)
    Complicated: co-incident rupture, ischaemia, uncontrolled pain or hypertension; for these patients intervention is with endovascular stent graft or open surgery
    Indications for Surgery
    Emergency: Acute type A dissection Urgent: Subacute type A dissection Elective: Chronic type A dissection Contraindications for Surgery
    Significant co-morbidity Chronic dementia Malignancy / terminal illness Irreversible profound brain injury  Supportive Measures
    Pain results in catecholamine release; these mediators increase the pulse and BP Use opiates to alleviate pain Key Management Decisions Intervention (surgical or endovascular) vs Medical Timing of Intervention – urgent vs chronic  Type A dissection is usually treated surgically; Type B medically (in absence of: malperfusion syndrome, ongoing pain, impending rupture or untreatable hypertension). Endovascular management should be considered in complicated type B dissection
    Complications
    Rupture of the aorta, with circulatory failure Stroke Visceral ischaemia, eg ischaemic bowel, limb or myocardial infarction Cardiac tamponade (secondary to rupture into pericardium)  Follow up
    Aneurysm, re-dissection, rupture and graft complications are all long-term risks Regular magnetic resonance angiography should be performed to monitor for progression and the patient treated with lifelong anti-hypertensives  Prognosis
    Type A have worse prognosis than Type B Type A prognosis is poor: 30% die immediately; 50% die <48h; 60% in-hospital mortality with medical management; 20-30% operative mortality; untreated 1% die an hour, with 90% after 1 week Of patients who make it out of hospital alive 30-60% survive ten years Secondary Prevention
    Lifelong antihypertensive therapy Don’t forget No individual symptom or sign is diagnostic Examination, ECG, CXR may be normal Compare CXR with previous ones 75% have widened mediastinum; ie 25% do not Request imaging ASAP As may mimic an MI, diagnosis requires a high index of suspicion. Thrombolysis not helpful Red Flags
    Type A dissection Severe hypo- or hypertension References:
    2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease. J Am Coll Cardiol, 2010; 55: 27-129 ESC/Diagnosis and management of aortic dissection. Recommendations of the Task Force on Aortic Dissection, European Society of Cardiology. Erbel R et al. European Heart Journal 2001; 22: 1642–1681
    Muhammad Mehtab
    Acne or acne vulgaris is an extremely common chronic inflammatory condition leading to pleomorphic pilosebaceous skin eruptions. Acne remains an enigma. Despite years of scientific research, we still lack answers to some of the most fundamental questions about this widespread problem.
    Peak incidence of Acne Vulgaris:
     Males      = 16 - 19 yrs  Females  = 14 - 17 yrs Normal sebaceous follicle:

    Etiopathogenesis
    1. Sebaceous gland hyperplasia + seborrhea
     Size of gland & number of lobules  per gland are increased increased circulating androgens end organ hyper-responsivenes Increased 5 alpha-reductase activity 2. Abnormal follicular desquamation
     hyperproliferation of keratinocytes shedding abnormal densely packed along with lipid   thinning & ballooning of follicle wall  microcomedo 3. Bacterial proliferation
     P.  acne colonisation Induces lesions by producing proteases chemotactic factors attracting, PMNLs and activated complement 4. Inflammation
     biologically active mediators  IL-1a, IL-1b, TNF CD4 lymphocytes invade follicle wall Disruption of follicle wall  Extravasation of lipids, corneocytes bacteria  inflammatory lesions Site of Acne Vulgaris :
    Face, back, chest, shoulders are commonly involved. Non inflammatory lesions are seen as open comedones and closed comedones. 
    Inflammatory lesions: It may be seen in any of the stages of  papules, pustules, nodules or cysts.
     Scars of Acne Vulgaris
        a) Ice-pick scars
        b) Box car scars
        c) Rolling scars
        d) Hypertrophic scars
        e) Atrophic scars
    Treatment of Acne Vulgaris:
         a)  Topical retinoids :  This is the first line therapy in all forms. In case of inflammatory lesions an antimicrobial is added.
     promotes normal desquamation decreases sebum production anti-bacterial  anti-inflammatory enhance penetration of other drugs maintain remission       Formulation
           Tretinoin 0.025%, 0.05%
          Side effects
    erythema, desquamation burning, pruritus photosensitivity    b) Antimicrobial therapy
    not to be used as monotherapy  rare instances of severe side effects  combine with topical retinoids      Role :
     Bactericidal for P.acne anti-inflammatory     Topical antimicrobials:
     slower acting, less effective. Commonly used  Clindamycin 1% and  Erythromycin 2%     Oral antibiotics
           Doxycycline, Minocycline and Erythromycin is used orally to control acne vulguris.
        Benzoyl peroxide  has bactericidal, anti-inflammatory mechanism. greatest advantage is that there is no resistance against it. 
        d) Oral retinoids  These are used only in 
     severe nodulocystic acne failure of conventional therapy nflammatory acne with scarring  frequently relapsing moderate and severe acne severe psychological distress     Dose   0.5 – 2 mg/kg
     Surgical therapy of Acne Vulgaris
    Comedo extraction Subcision Punch excision & closure Punch incision & elevation Punch excision & graft replacement Dermabrasion Laser resurfacing Cryoslush Soft tissue augmentation Hormonal therapy in Acne Vulgaris
          Indications : early use in females - moderate to severe acne, associated endocrine abnormalities,  late onset acne
     Goals of acne therapy
     controlling acne lesions  preventing new lesions  preventing scarring  minimizing morbidity  psychologic relief
    Dr Bilal
    Atrial Fibrillation With Rapid Ventricular Response ( Afib with RVR) or cardiac rvr is a condition where atrial fibrillation is described as rapid ventricular response if ventricular rate is more than 100 bpm. 
    What is Atrial Fibrillation (AFib) :
    Atrial Fibrillation is the most common sustained cardiac arrhythmia. SA node or Sinoatrial node is the dominant pacemaker in a healthy normal heart. When the normal atrial electrical impulses are overwhelmed by disorganized electrical impulses in the atria resulting in irregular rhythm, absence of p waves or fibrillatory waves.
    Atrial Fibrillation Pathophysiology:
    SA node or Sinoatrial node is the dominant pacemaker in a healthy normal heart. This structure lies at the junction of the superior vena cava and the right atrium. It works as an electrical impulse generator. The impulse travels down the atria and makes the right and left atria to contract.  Thus they pump blood to the ventricles. The electrical impulse also travel from the atria to the ventricles through the atrioventricular (AV) node. The optimal function of the heart is the resultant of the synchronized electrical activity between the atria and the ventricles. When there is a structural change in the atria, SA node or AV node and abnormal triggering of impulses occur, the electrical activity of the atria becomes uncoordinated. This chaotic, irregular atrial compressions ultimately results in Atrial Fibrillation. In recent studies, the pathogenesis of Atial Fibrillation is thought to involve an interaction between initiating triggers  the form of rapidly firing ectopic foci located inside one or more pulmonary veins, and an abnormal atrial tissue substrate capable of maintaining the arrhythmia. Although structural heart disease underlies many cases of AF, the pathogenesis of AF in apparently normal hearts is less well understood. Although there is considerable overlap, pulmonary vein triggers may play a dominant role in younger patients with relatively normal hearts and short paroxysms of AF.  Abnormal atrial tissue  may play important role in a patient with structural heart disease and persistent or permanent AF.
    Atrial Fibrillation Causes:
    Hypertension both pulmonary or systemic Atherosclerosis Coronary Artery Disease Cardiomyopathy  Valvular Heart disease Congenital heart disease Hyperthyroidism Pulmonary embolism  Chronic obstructive pulmonary disease (COPD) Pericarditis Pneumonia Asthma Pheochromocytoma Bronchogenic carcinoma Carbon monoxide poisoning etc Sleep Apnnea Diabetes Alcohol Caffein Amyloidosis Common Symptoms:
    Palpitations Chest discomfort Respiratory distress Hypotension Light-headedness Loss of consciousness Peripheral edema Jugular vein distention Pulmonary edema
    Image Credit: http://afib.utorontoeit.com/
    Dr. Anmol
    Femur Neck Fracture can be classified according to anatomical location, angle of fracture or displacement
    Classification Based on Anatomical Location: 
     Subcapital - Subcapital fracture occur just beneath the articular surface of the femoral head. Its usually along the old epiphyseal plate. Transcervical - Fracture runs across the femoral neck in between head and the greater trochanter Basicervical - This type of fracture is included in extracapsular intertrochanteric. Fracture Angle (Pauwel’s classification)
    The femur neck fracture can be classified based on angle of fracture as follows:

    Photo credit: Koraemed.org

    Pauwel’s angle is actually the angle formed by the line of fracture and horizontal plane.  Obliquity of the fracture line increases with femur neck fracture progression from type I to type III. Thus theoretically, the distracting sheer forces at the fracture site also increases.

    Femur Neck Fracture based on Displacement (Garden Classification)
     
     It is based on the degree of displacement associated with the fracture.  Displacement is determined by the irregular/abnormal shape of the bony outline &  trabecular line nonalignment in femoral head, neck              and  the acetabulum. Undisplaced fracture :  In Stage I  Femoral head trabeculae are normally aligned with acetabular trabeculae, though there is increased valgus with neck trabeculae. Stage II is complete fracture and full displacement. Trabeculae are essentially broken by a fracture line across the entire neck but all the three trabeculae (neck, head & acetabular) are in alignment.  Displaced  fracture:  Stage III    Complete fracture with partial  displacement  The trabecular pattern and femoral head does not align with  acetabulum & neck.  Stage IV   Complete fracture of femoral neck with full displacement of fractured part. Loss of contact between proximal & distal fracture fragments :  the proximal fragment lies free correctly with the the acetabulum. Trabeculae of head and acetabulum are aligned and the trabeculums of neck and head are not aligned with complete disruption.
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    • SERVICES IN the northern region’s premier health institute — PGIMER — were hit Monday as more than 1,200 resident doctors went on a flash strike after one of them was assaulted by a patient’s attendant. The patient, a 72-year-old woman from Ludhiana, died during treatment late Sunday evening.
      The strike affected thousands of patients who came to PGIMER OPDs from various states including Punjab, Haryana, Himachal Pradesh, Jammu and Kashmir.
      The situation looks set to continue as talks between hospital administration and doctors on Monday failed to end the strike. PGIMER has threatened to act against the doctors if they do not return to work on Tuesday.
      The hospital authorities announced that OPD registration would close at 9 am on Tuesday in view of the ongoing strike. On a normal day, OPD registration continues until 11 am.
      It was probably for the first time in the history of PGIMER that its main entrance gates were shut for more than two hours late Sunday night and patients were sent back by the resident doctors. However, some of them could gain access to PGIMER emergency from alternative entries. It was only when the doctors were persuaded back inside the emergency OPD for talks that the gates were opened.
      Besides a demand for their security, the resident doctors raised several other issues regarding their daily duties asking the PGI administration to implement all those demands instantly.
      “The strike continues because our demands have not been completely fulfilled. The administration has only given us assurances rather than fulfilling our demands,” said Dr Amit Sharma, vice-president, Association of Resident Doctors, PGIMER.
      There are nearly 1,500 resident doctors, both junior and senior in PGI. Barely 150 of them, mostly senior resident doctors, attended to patients throughout the day on Monday. Strengthening of security with a police post and armed security in emergency OPD, triage system to classify patients based on sickness levels, appointment of phlebotomists for sampling, alternative arrangement for report collections and limiting maximum number of patients admitted to emergency OPD and stopping unnecessary referrals were some of the prominent demands raised by the protesting doctors.
      After Sunday night’s chaos, patients who reached hospital early in the morning on Monday and stood in queues for OPD registration were informed that no registration cards shall be made after 8.30 am. Many of them had to return without treatment. “I left home at 6 am and I was not even aware that we will face such harassment,” said Sukhbir Singh, a Himachal Pradesh resident. Singh, who was lying on a stretcher near OPD block, had an appointment at the ortho department after he underwent a surgery last month.
      “How can the doctors act like uneducated people? They are beating plates which is very shocking,” said Kuldeep Singh, a resident of Ludhiana. “My mother is unwell. Who will be responsible if something happens to her?”
      PGIMER issued a statement in the evening that read, “Resident doctors went on indefinite flash strike on Monday, following which it was decided to reduce the OPD registration timings at the institute. Registration timings of Radiotherapy OPD dealing with cancer patients was not reduced. 4,110 patients were registered in different OPDs of the institute out of which 1,124 were new patients.” However, on average, PGIMER records around 10,000 patients in various OPDs on a daily basis.
      The PGI authorities added that ICU emergency and trauma services functioned normally on Monday.
      PGI campus is a “silence zone”. Showing no concern for thousands of patients, the doctors carried out a protest march on the roads of the campus, including outside cardiac centre, shouting anti-PGI administration slogans and beating steel utensils.
      Regarding inconvenience caused to thousands of patients in the last 24 hours, PGI director Yogesh Chawla said, “We shall investigate it. We shall see how many ambulances returned on Sunday night when the main gate of the institute was closed by the protesting doctors. The moment we came to know of it, we persuaded the protesting doctors not to indulge in such a thing and got the gates reopened.”
      Asked what action would be taken against the doctors for creating “indiscipline” inside the campus, head of the Medical Microbiology Department, PGI, Dr Arunaloke Chakrabarti, who was present with the director, blamed “few elements who are disturbing the area”. “We are trying to locate them. This is not PGI’s culture,” he said.
      Dr Chawla said if the residents continued the strike, “disciplinary action would be initiated as per rules”.
      Sources in the administration said all the heads of departments would meet on Tuesday morning to discuss the measures needed to be taken in view of the strike. A source said that the administration had also decided to deduct the salary of the protesting residents for the number of days they would not work.
      In a related development, the Chandigarh Police arrested Harpreet Singh, who had assaulted resident doctor Mani on Sunday night that led to this protest. However, Harpreet and his family have also lodged a formal complaint of medical negligence against Dr Mani and other doctors holding them responsible for his mother’s death. The police have lodged a DDR.
      The police also registered a case in another incident in which a resident doctor was allegedly beaten up by an attendant at PGI recently.
    • Can anyone explain the Guillain-Barré Syndrome Causes and the relation with zika virus infections? The recent studies seems to have established a good relation between the two. Any body with clearer view or reference?
    • I am surprised that this EKG doesn't show any escape beats. I mean, 4 dropped beats? That should induce at least Junctional Escape Beats or PJCs and more likely Ventricular Escape Beats or PVCs. So why are there no escape beats or premature beats in this sinus arrest? I also know that this EKG shows the first stage of a heart attack, the hyperacute phase where the only change is in the voltage and symmetry of the T wave(high voltage and symmetric vs normal low voltage and asymmetric).