Medicine Hack

The criteria for separating transudates from exudates were published in 1972 by Light and coworkers. They were based on the measurements of serum and pleural fluid protein and LDH.  The criteria are as follows: If at least one of the following 3 criteria is present, the fluid is virtually always an exudate and if none is present then the fluid is virtually always a transudate: 1)      Pleural fluid : Serum protein ratio > 0.5 2)      Pleural fluid LDH > 2/3 of the upper limit of the serum reference range 3)      Pleural fluid : Serum LDH ratio > 0.6 An exception to using Light’s criteria is in the setting of CHF treated with diuretics. Normally, in CHF, the effusions are due to an increased capillary hydrostatic pressure and are therefore transudates. But the use of diuretics has been shown to increase the pleural fluid protein and LDH concentrations. Thus we will have a false positive result making the fluid appear as an exudate. It is believed to be

Epidemiology:   Incidence of 3/1000 births.  4 times more in males.  Aetiology is unknown. In some cases there seems to be a familial association. In such families the mother has suffered from the condition in 50 per cent of cases. Characteristically it is a first-born male child that is most commonly affected. The condition is most commonly seen at 4 weeks after birth ranging from the third week to, on rare occasions, the seventh. Inexplicably, it is the time following birth that seems important and not the child’s gestational age. A premature infant will also develop the condition at about 4 weeks after birth. Pathology: Grossly hypertrophied musculature of the pylorus and adjacent antrum, the hypertrophy being maximum in the pylorus itself. The mucosa is compressed such that only a probe can be inserted. Clinical features : Vomiting is the presenting symptom that after 2—3 days becomes forcible and projectile. The child vomits milk and no bile is present. Immedi

It is at times difficult to interpret a PA chest X-ray as the amount of information present is huge. A systematic approach should always be done.  One should have the understanding of what is normal. This must include an evaluation of the  1) soft tissues,  2) bones and joints,  3) pleura, lungs, major airways and pulmonary vascularity,  4) mediastinum and its contents,  5) heart and its chambers, as well as  6) the areas seen below the diaphragm and above the thorax. The heart borders are explained in this post.  On the right side of the heart the following structures can be identified: 1) Az - Azygous vein 2) A - Ascending aorta 3) S - Superior vena cava 4) RA - Right atrium On the left side of the heart, we can identify the following: 1) SC - Subclavian artery 2) AA - Aortic arch 3) PA - Pulmonary artery 4) LB - Lower border of pulmonary artery 5) LA - Left atrial appendage 6) LV - Left ventricle The x-ray on the right side i.e. B shows the actual positio

The search for and use of an antidote should never replace good supportive care. Specific systemic antidotes are available for many common poisonings as shown in the table above. Inadequate availability of antidotes at acute care hospitals can complicate the care of a poisoned patient.  An evidenced-based consensus of experts has recommended minimum stocking requirements for 16 antidotes for acute care hospitals. These recommendations may provide guidance to pharmacy and therapeutics committees in establishing a hospital’s antidote needs. Drugs used conventionally for non-poisoning situations may act as antidotes to reverse acute toxicity, such as glucagon for β-adrenergic blocker or calcium channel antagonist overdose and octreotide for sulfonylurea-induced hypoglycemia. As our understanding of drug toxicity increases, antidotes may have applications beyond contemporary indications, such as for acetylcysteine, which has shown promise for treating approximately 25 different

A 78-year-old man is brought to hospital with an episode of dizziness. He was well until the last 6 months, since when he has had some falls, irregularly. On some occasions he lost consciousness and is unsure how long he has been unconscious. On a few occasions he has fallen, grazing his knees and on others he has felt dizzy and has had to sit down but has not lost consciousness. These episodes usually happened on exertion, but once or twice they have occurred while sitting down. He recovers over 10–15 min after each episode. Once, his wife was with him when he blacked out. Worried, she called an ambulance. He looked so pale and still that she thought that he had died. He was taken to hospital, by which time he had recovered completely and was discharged and told that he had a normal electrocardiogram (ECG) and chest X-ray. On examination He is pale with a blood pressure of 93/63 mm Hg.  The pulse rate is 35/min, regular.  There are no heart murmurs.  The jugular veno

HEPARIN-INDUCED THROMBOCYTOPENIA Drug-induced thrombocytopenia due to heparin differs from that seen with other drugs in two major ways. (1) The thrombocytopenia is not usually severe, with nadir counts rarely <20,000/L. (2) Heparin-induced thrombocytopenia (HIT) is not associated with bleeding and, in fact, markedly increases the risk of thrombosis. Pathology: HIT results from antibody formation to a complex of the platelet-specific protein platelet factor 4 (PF4) and heparin. The antiheparin/PF4 antibody can activate platelets through the FcRIIa receptor and also activate monocytes and endothelial cells. Many patients exposed to heparin develop antibodies to heparin/PF4, but do not appear to have adverse consequences. 1) A fraction of those who develop antibodies will develop HIT, and a portion of those (up to 50%) will develop thrombosis (HITT). 2) HIT can occur after exposure to low-molecular-weight heparin (LMWH) as well as unfractionated heparin (UFH), alt

Sick sinus syndrome is a term applied to a syndrome encompassing a number of sinus nodal abnormalities, including the following: (1) Persistent spontaneous sinus bradycardia not caused by drugs and inappropriate for the physiologic circumstance (2) Sinus arrest or exit block i.e. no P wave on ECG for > 2 s. (3) Combinations of SA and AV conduction disturbances and (4) Alternation of paroxysms of rapid regular or irregular atrial tachyarrhythmias and periods of slow atrial and ventricular rates (bradycardia-tachycardia syndrome). More than one of these conditions can be recorded in the same patient on different occasions, and their mechanisms often can be shown to be causally interrelated and combined with an abnormal state of AV conduction or automaticity. Incidence: 3 in every 10,000 persons are affected. Incidence increases with age, seen more after 65 years of age. Men and women are equally affected. Patients who have sinus node disease can be categorized