WELCOME TO THE FORUM
This is a place for any MDs/DOs/ from north of the Tobin bridge to make any comments . It could be about any thing under the sun. The MDs do not have to be associated with any of the hospitals in the area.
Comments may be of any nature about any thing. You can make anonymous comments on this blog.
The hope is whatever opinions you give will be for the good of our physician group or north shore of Boston or MA, or world at large. Be good please. Our time in this world is limited, make use of it.
KK
4 comments:
DID YOU KNOW THIS ? about Atenolol :
CAFE study in Circulation MARCH 7 2006 confirmed what LIFE study and ASCOT study had already shown. Atenolol is only slightly better than a placebo in cardiovascular outcome and lives saved. !!!!!!!
Atenolol decreases the BP but it does not decrease cardiovascular events
It does decrease brachial blood pressure but not intra-aortic blood pressure.
Vital organs including brain, heart and kidney respond to the intra-aortic BP and not brachial BP !!!!
It is now indisputable. Let me say this again Atenolol does not improve the outcome though it may improve the brachial BP.
Read on
ASCOT study- an Anglo-Scandinavian study of 20,000 people- was stopped prematurely because of the higher mortality in the Atenolol branch of the study- LANCET- 2005, 366: 895-906
Read on
All BP medications except Atenolol decreases brachial BP as much as intra-aortic BP. But not Atenolol. So this is not true of all beta blockers it is not a class action
In fact we think: if we knew , what we now know about Atenolol. it would not have been cleared for BP control at all. (the LANCET FEB 25, 2006 )
Mind you every thing I said above is for Atenolol and hypertension. Atenolol is still a good cardiac specific anti anginal drug.
Bottom line Atenolol is not a good BP medication at all though it decreases brachial BP( oxymoron) it does not save any lives.
This is specific comment on Atenolol ,not for all beta blockers. It still is a good cardiac medication. My challenge to you: how many of your patients are on Atenolol for hypertension, are you on it yourselves ?
KK
better yet, try to avoid/ minimize meds altogether by living well; exercise, don't smoke, eat a reasonable amount of food that is healthy for you, get enough sleep and minimize stress. life is not a dress rehersal!
DEPT OF ERROR
As a junior in the emergency department, I saw a 30-year-old man with severe numbness, tingling in the fingers and toes and perioral area, muscle cramps, and tetany; he had chronic hypoparathyroidism, due to thyroidectomy, which was being treated with oral replacement of thyroid hormones, calcium, and vitamin D. He had been unable to take his regular treatment over the past few weeks because of gastroenteritis.
Blood tests showed a low total calcium of 1•125 mmol/L ( ie equal to 4.4 mg/dl in American terms: kk)(free ionised portion 0•51 mmol/L), phosphate 1•8 mmol/L,creatinine 88•4 mol/L, urea 3•57 mmol/L, sodium139 mmol/L, potassium 4•5 mmol/L, blood bicarbonate29 mmol/L, and pH 7•4.
Because of the severe hypocalcaemia, I chose intravenous calcium replacement according to the formula: 1–2 mg/kg per h (body-weight 50 kg) of calcium. Using ampoules of 10 mL10% calcium gluconate, I assumed that each ampoule contained 1 g (1000 mg) of calcium. I diluted the 10 mL ampoule into 500 mL 5% dextrose, calculating that each mL of this solution contained almost 2 mg of calcium(1000 mg in 510 mL=1•96 mg/mL). The infusion was scheduled at 50 mL/h for the next 10 h, delivering 98 mg of calcium per h (1•96 mg/mL at 50 mL/h); this schedule met the requirement of 1–2 mg/kg per h, as the patient weighed 50 kg.
3 h later, my consultant took me to the patient’s bedside; the young man had complained of carpopedal spasm, laryngeal spasm, and bronchospasm, and 1 h earlier he had had other typical signs of hypocal-caemia—namely, a focal seizure, arrhythmia, and prolongation of the Q-T interval. His ionised calcium concentration had decreased further to 0•49 mmol/L.
Unfortunately, my calculation of calcium replacement had been incorrect: the replacement assumed that calcium gluconate was constituted only by elemental calcium; in the formula the replacement therapy is expressed as mg of elemental calcium and not mg of calcium salt. Calcium gluconate is the calcium salt of gluconic acid, and contains only 9 mg/mL elemental calcium (table). Therefore, each ampoule of 10%calcium gluconate contained 1000 mg of calcium gluconate, but only 90 mg of elemental calcium.
100–360 mg of elemental calcium should be given over5–10 min in cases of life-threatening hypocalcaemia(free ionised calcium 0•59 mmol/L), followed by a1–2 mg/kg per h of elemental calcium. This means that one to four 10 mL ampoules of 10% calcium gluconate should have been used in our patient, as this dose raises the concentration of ionised calcium by 0•5 mmol/L. We applied this dosing-schedule to our patient, followed by an infusion of 50 mL (five ampoules) of 10% calcium gluconate diluted in 500 mL 5% dextrose (450 mg elemental calcium); the 550 mL solution contained0•8 mg of elemental calcium per mL of solution.Therefore, an infusion of 100 mL/h provided 80 mg/h of elemental calcium—equivalent to 1•6 mg/h of elemental calcium for each kg of bodyweight.
IE: five ampoules in 500 ml to run 100 cc an hour that is how you treat life threatening hypocalcemia- kk-
The patient’s condition gradually improved over 24 h. Of note, calcium chloride salt is second line choice for treatment of hypocalcaemia, unless there is severe alka-losis, as it causes more tissue necrosis if extravasated.
My mistake will haunt me for the rest of my professional life. When replacing electrolytes, it is important to bear in mind the absolute need to understand basic chemistry, calculate replacement in Standard International Units, replace element and not salts, and to refer to the hospital formulary when in doubt. Lancet 2006; 367: 273
Nephrology andTransplantation, Departmentof Nephro-Urology, AmedeoAvogadro University, OspedaleMaggiore della Carità , CorsoMazzini 18, 28100 Novara,Italy (Prof P Stratta,V Morellini MD,E Lazzarich MD,M Brustia MD, M Quaglia MD,C Canavese MD); andDepartment of InternalMedicine, Section ofNephrology, University ofTorino, Molinette Hospital,Corso Bramante 88, 10126Torino (G Soragna MD, M Gai MD,D Motta MD)Correspondence to:Prof P Stratta strattanefro@hotmail.com
DEPT OF ERROR
DO YOU REALLY KNOW HOW TO TREAT SEVERE HYPOCALCEMIA WITH SEZURE.
MOST MDs THINK THEY DO. HOWEVER LET US LEARN FROM THE MISTAKES OF OTHERS.
FROM THE LANCET JAN.21, 2006
As a junior in the emergency department, I saw a 30-year-old man with severe numbness, tingling in the fingers and toes and perioral area, muscle cramps, and tetany; he had chronic hypoparathyroidism, due to thyroidectomy, which was being treated with oral replacement of thyroid hormones, calcium, and vitamin D. He had been unable to take his regular treatment over the past few weeks because of gastroenteritis.
Blood tests showed a low total calcium of 1•125 mmol/L ( ie equal to 4.4 mg/dl in American terms: kk)(free ionised portion 0•51 mmol/L), phosphate 1•8 mmol/L,creatinine 88•4 mol/L, urea 3•57 mmol/L, sodium139 mmol/L, potassium 4•5 mmol/L, blood bicarbonate29 mmol/L, and pH 7•4.
Because of the severe hypocalcaemia, I chose intravenous calcium replacement according to the formula: 1–2 mg/kg per h (body-weight 50 kg) of calcium. Using ampoules of 10 mL10% calcium gluconate, I assumed that each ampoule contained 1 g (1000 mg) of calcium. I diluted the 10 mL ampoule into 500 mL 5% dextrose, calculating that each mL of this solution contained almost 2 mg of calcium(1000 mg in 510 mL=1•96 mg/mL). The infusion was scheduled at 50 mL/h for the next 10 h, delivering 98 mg of calcium per h (1•96 mg/mL at 50 mL/h); this schedule met the requirement of 1–2 mg/kg per h, as the patient weighed 50 kg.
3 h later, my consultant took me to the patient’s bedside; the young man had complained of carpopedal spasm, laryngeal spasm, and bronchospasm, and 1 h earlier he had had other typical signs of hypocal-caemia—namely, a focal seizure, arrhythmia, and prolongation of the Q-T interval. His ionised calcium concentration had decreased further to 0•49 mmol/L.
Unfortunately, my calculation of calcium replacement had been incorrect: the replacement assumed that calcium gluconate was constituted only by elemental calcium; in the formula the replacement therapy is expressed as mg of elemental calcium and not mg of calcium salt. Calcium gluconate is the calcium salt of gluconic acid, and contains only 9 mg/mL elemental calcium (table). Therefore, each ampoule of 10%calcium gluconate contained 1000 mg of calcium gluconate, but only 90 mg of elemental calcium.
100–360 mg of elemental calcium should be given over5–10 min in cases of life-threatening hypocalcaemia(free ionised calcium 0•59 mmol/L), followed by a1–2 mg/kg per h of elemental calcium. This means that one to four 10 mL ampoules of 10% calcium gluconate should have been used in our patient, as this dose raises the concentration of ionised calcium by 0•5 mmol/L. We applied this dosing-schedule to our patient, followed by an infusion of 50 mL (five ampoules) of 10% calcium gluconate diluted in 500 mL 5% dextrose (450 mg elemental calcium); the 550 mL solution contained0•8 mg of elemental calcium per mL of solution.Therefore, an infusion of 100 mL/h provided 80 mg/h of elemental calcium—equivalent to 1•6 mg/h of elemental calcium for each kg of bodyweight.
(IE: five ampoules in 500 ml to run 100 cc an hour that is how you treat life threatening hypocalcemia- kk- )
The patient’s condition gradually improved over 24 h. Of note, calcium chloride salt is second line choice for treatment of hypocalcaemia, unless there is severe alka-losis, as it causes more tissue necrosis if extravasated.
My mistake will haunt me for the rest of my professional life. When replacing electrolytes, it is important to bear in mind the absolute need to understand basic chemistry, calculate replacement in Standard International Units, replace element and not salts, and to refer to the hospital formulary when in doubt. Lancet 2006; 367: 273
Nephrology andTransplantation, Departmentof Nephro-Urology, AmedeoAvogadro University, OspedaleMaggiore della Carità , CorsoMazzini 18, 28100 Novara,Italy (Prof P Stratta,V Morellini MD,E Lazzarich MD,M Brustia MD, M Quaglia MD,C Canavese MD); andDepartment of InternalMedicine, Section ofNephrology, University ofTorino, Molinette Hospital,Corso Bramante 88, 10126Torino (G Soragna MD, M Gai MD,D Motta MD)Correspondence to:Prof P Stratta strattanefro@hotmail.com
7:11 AM
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