There was a time, not long ago, when the clinician diagnosed the condition the patient was suffering from entirely based on a detailed history, a thorough clinical examination and a few simple tests. The verdict was accepted without any questions. The possible expected course the disease would take and the expected outcome were discussed. Most of the time, the predictions came true. What was being practiced was "Experience based medicine". It was accepted and had stood the test of time. However when things went wrong, some disappointment was inevitable.Most of the time the turbulence settled down. Litigations were few and far between..
Somewhere in the 1990 s the experience based medicine gave way to evidence based medicine. Every disease entity was defined. There was a need to fulfil 'required' criteria to conclusively diagnose and start treating the same. Evidence therefore was needed to diagnose conclusively after ruling out other possible differential diagnoses; to know the stage, severity and extent of the disease and document the same; to prognosticate the outcome and if possible to help improve it. Diabetes mellitus is a case in point - hyperglycemia is a good pointer but exact sugar value gives a rough idea about the current severity. It is every doctor's observation that the patient either eats less or doubles the dose of the medicine on the day of check up to get a better blood sugar value to impress the doctor. Estimation of the glycosylated hemoglobin alerts the doctor as it is an average of 3 monthes' blood sugar values and cannot be 'doctored' by one day's efforts! Ketone bodies if present in blood and urine alert the doctor as the diabetic ketoaidosis is a serious life threatening complication.
Acute abdominal pain is another scenario - when the surgeon has ruled out all important surgical causes including gall stone colic, appendicitis, ureteric colic and when the physician has ruled out all important medical causes like diabetic ketoacidosis, acute pancreatitis, peritonitis, usually one has to think of acute intermittent porphyria a condition which can only be diagnosed by a simple urine test for porphobilinogen - a striking example where the evidence based laboratory medicine becomes indispensable. Even to diagnose acute peritonitis, one has to get values of serum amylase, serum lipase, serum calcium and other data. These also help in assessing the severity and prognosis (Ranson's criteria).
Imagine a scenario where a young athlete hits her head against a hard surface and loses consciuosness. There are no focal neurologic deficits. The CT scans are normal.. A clinical diagnosis of " concussion " is made. What is the evidence? Till recently, there were none. Now they are trying to correlate the values of
T- tau protein levels in CSF taken at serial intervals - immediately after the event, 12 hours later, 36 hours later. The first peak immediately seen after the concussion settles in 12 hours. The second peak comes between 12 and 36 hours. 1 hour values help to decide the time likely to be taken for the resolution of concussion and the time taken by the players to return to the game safely. Hence T - tau is an important' biomarker 'of concussion.
Then comes the most common and the most important scenario - acute chest pain. Acute myocardial infarction is the most important event to be excluded. There was a time ECG was enough. Then came the enzyme biomarkers. Enzyme CPK came just when I started to practice. It was a sensational discovery! It would not only help pick up the diagnosis but also would help us quantitate the extent of myocardial necrosis. I remember a particular patient referred by a psychiatrist saying "The ECG is normal. His CPK values are 2500. Where is the heart attack?" Truly, there was no heart attack - the extreme elevation was from the skeletal muscles - the patient had Myxedema (hypothyroidism). Soon Isoenzymes came and CPK MB was considered the most sensitive marker of a heart attack . Then came the Troponins - C, T and I of which T and I would help diagnose cardiac muscle necrosis. The problem however was that the elevation was seen even when the cardiac muscle got damaged due to non ischemic conditions as remote as a scorpion bite. Something more specific was obviously needed. Very recently, highly sensitive cardiac troponin T (hs cTnT) has become available and is now very helpful. The sad news though is that CPK MB has gone out of use and died a natural demise - most f the labs are not doing it any more - thereby showing that there is a 'shelf life' for these biomarkers!
I am sure, we have t understand that the EBLM (Evidene Based Laboratory Medicine) has come to stay. We cannot wish it away. The physicians have to extend an olive branch to the biochemists, use the EBLM and make the best use of the available options. It will help themselves and the patients.
Long live EBLM!
Somewhere in the 1990 s the experience based medicine gave way to evidence based medicine. Every disease entity was defined. There was a need to fulfil 'required' criteria to conclusively diagnose and start treating the same. Evidence therefore was needed to diagnose conclusively after ruling out other possible differential diagnoses; to know the stage, severity and extent of the disease and document the same; to prognosticate the outcome and if possible to help improve it. Diabetes mellitus is a case in point - hyperglycemia is a good pointer but exact sugar value gives a rough idea about the current severity. It is every doctor's observation that the patient either eats less or doubles the dose of the medicine on the day of check up to get a better blood sugar value to impress the doctor. Estimation of the glycosylated hemoglobin alerts the doctor as it is an average of 3 monthes' blood sugar values and cannot be 'doctored' by one day's efforts! Ketone bodies if present in blood and urine alert the doctor as the diabetic ketoaidosis is a serious life threatening complication.
Acute abdominal pain is another scenario - when the surgeon has ruled out all important surgical causes including gall stone colic, appendicitis, ureteric colic and when the physician has ruled out all important medical causes like diabetic ketoacidosis, acute pancreatitis, peritonitis, usually one has to think of acute intermittent porphyria a condition which can only be diagnosed by a simple urine test for porphobilinogen - a striking example where the evidence based laboratory medicine becomes indispensable. Even to diagnose acute peritonitis, one has to get values of serum amylase, serum lipase, serum calcium and other data. These also help in assessing the severity and prognosis (Ranson's criteria).
Imagine a scenario where a young athlete hits her head against a hard surface and loses consciuosness. There are no focal neurologic deficits. The CT scans are normal.. A clinical diagnosis of " concussion " is made. What is the evidence? Till recently, there were none. Now they are trying to correlate the values of
T- tau protein levels in CSF taken at serial intervals - immediately after the event, 12 hours later, 36 hours later. The first peak immediately seen after the concussion settles in 12 hours. The second peak comes between 12 and 36 hours. 1 hour values help to decide the time likely to be taken for the resolution of concussion and the time taken by the players to return to the game safely. Hence T - tau is an important' biomarker 'of concussion.
Then comes the most common and the most important scenario - acute chest pain. Acute myocardial infarction is the most important event to be excluded. There was a time ECG was enough. Then came the enzyme biomarkers. Enzyme CPK came just when I started to practice. It was a sensational discovery! It would not only help pick up the diagnosis but also would help us quantitate the extent of myocardial necrosis. I remember a particular patient referred by a psychiatrist saying "The ECG is normal. His CPK values are 2500. Where is the heart attack?" Truly, there was no heart attack - the extreme elevation was from the skeletal muscles - the patient had Myxedema (hypothyroidism). Soon Isoenzymes came and CPK MB was considered the most sensitive marker of a heart attack . Then came the Troponins - C, T and I of which T and I would help diagnose cardiac muscle necrosis. The problem however was that the elevation was seen even when the cardiac muscle got damaged due to non ischemic conditions as remote as a scorpion bite. Something more specific was obviously needed. Very recently, highly sensitive cardiac troponin T (hs cTnT) has become available and is now very helpful. The sad news though is that CPK MB has gone out of use and died a natural demise - most f the labs are not doing it any more - thereby showing that there is a 'shelf life' for these biomarkers!
I am sure, we have t understand that the EBLM (Evidene Based Laboratory Medicine) has come to stay. We cannot wish it away. The physicians have to extend an olive branch to the biochemists, use the EBLM and make the best use of the available options. It will help themselves and the patients.
Long live EBLM!
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