Archive for December, 2008

One of the important principles of medicine  is  “Diagnosis should  always precede treatment”

This quote , though appear reasonable , can not be practiced always especially in emergencies,  where we  have to first stabilise the patient   without a  prior diagnosis  .(Like administering IV fluids in hypotension , acetaminophen for fever , etc)

Modern medicine  considers treating a patient without a diagnosis as unscientific.

But,  it is a well recognised fact ,  millions  of decision in everyday medical practice is not based on scientific diagnosis  but on clinical acumen and empirical therapy . There are many  instances  wherein , we are never near the  diagnosis  even after exhaustive investigations. 


                       Ironically , in this era of evidence based medicine , when  we are  unable to  conclude ,  we are forced  to do the most  funniest  thing , namely converting patient’s symptom itself as disease entity and  be happy  in labelling them. Like , Motion sickness ,  poly-arthritis, , chronic fatigue syndrome, adult respiratory distress syndrome ,  pre mature ejaculation, fever of unknown origin  , attention deficit disorder , etc (The list is endless . . .)

               This happens because physicians always feel guilty if they are unable to label a patient with a disease entity.

Is the guilt  justified ?  Not necessarily so !  Symptomatic treatment without  diagnosis  is the most dominant theme even today (Fever, pain etc ).So don’t feel unduly negative* when one is not able to fit a patent’s  symptom into a disease entity  but ensure  he  gets relief from his symptom.

 *Except of course , one has to rule out a serious disorder.

 Comments welcome

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                                Hypertension is the most common clinical  cardiovascular entity.Left ventricular hypertrophy (LVH) is  an important consequence of  HT.In fact, it is considered as a end organ effect or damage. Others being brain, kidney, and peripheral vascular disease.Knowing about LVH is important because it has been linked to increased cardiovascular events.


                              Though LVH is considered  as a close companion of  HT  it is  surprising  only a minority (15-30%)  show evidence of LVH .Some  experienced clinicians (Level C evidence)  quote even lower < 10 %  .Traditionally LVH was detected by ECG and now it is replaced by echocardiography.

What determines the LVH ?

It will be suprising to note , answer to this question  is  still not  clear .

  • Is it the duration of elevated blood pressure ?
  •  Is it the absolute level of blood pressure ?
  • If so , is it  the systolic BP  , diastolic BP or the mean BP ?
  • Or is it related to the etiology of HT ?
  • There has been no significant correlation between the above parameters

When we don’t know  the answer to a question in medicine , the answer will  generally will be inside the genes !

So in HT also the major determinant of LVH is in the genes that determine the myosin heavy chain  response .

and also ACE gene polymorphism.ACE genes are involved in the expression of growth factors within the myocardium.

An excellent study  on the issue http://www.nature.com/jhh/journal/v17/n3/full/1001523a.html#tbl1

It implicates , gender, age, race etc in the genesis of LVH

Final message

So , the  myocardium does not respond with LVH   in all patients with HT.It happens only in a minority* .Duration of HT can be an important determinant , but  the major factor is  the alteration of genetic switches  within the myocytes How this switches are going to  behave ,  is largely inherited .Regression of LVH is also not uniform again implying lesser role for hemodynamics. (Some studies revealed ACEI have maximum regression  of LVH , later disputed )

*LVH is more consistently seen  in hypertension due to reno vascular  or parenchymal disorders .It is also an observed fact , a  combination of diabetes and HT is more likely to result in  LVH.

The other major issue  that needs explanation in HT/LVH  is   , how much of LVH is due to  myocyte hypertrophy perse  and how much is contributed by interstitial cell hypertrophy(Non myocytic hypertrophy)

This issue will be discussed soon

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This paper was presented in the just concluded 60th Annual scientific sessions of cardiological society of India , Chennai.India


Venkatesan  sangareddi , G.Gnanavelu, R.Alagesan,V.Jaganathan.

Department of cardiology, Madras Medical College, Chennai.


                          Radial  artery  has become the  major access  site for the interventional cardiologist in recent years. Radial approach has provided increased patient comfort and  less access site complication. Many  of  the   complications  are  unique to radial approach mostly due to  anomalies of origin, and course while others are  hardware related .Unlike femoral arterial access ,  compromise of blood supply to hand is never considered a  threat because of dual blood supply to hand  .But the fact  is that,  it  could be sub-clinical  and the hand is rarely assessed for vascular insufficiency after a radial procedure.

             The aim of the study is to assess the  impact of   radial  procedures  on the  blood flow  to  hand . 20 patients who had undergone routine  radial coronary  angiogram  formed the study population. All patients had negative Allen’s test prior to the procedure. The mean procedure time was   25mts (18-45) .Standard  hardwares were used. Difficulty in crossing at forearm and   subclavian   was observed in  4  patients. Extravasation of dye  in forearm was observed in two. Allen test  was  done 24 hours  after sheath removal and  repeated 48 hours after the procedure .  4 patients   showed positive Allen test  at 24hrs. One  patient   regained  Allen negativity at  48hours. The incidence of positive Allen test at  24 hours is 20%. The compromised blood flow was correlated with the  procedure time, and a difficult catheter course .

                 We propose,  radial procedures especially , when prolonged has a potential to compromise palmar arch flow .This phenomenon  is  either  permanent  or transient  and  may be attributable to enhanced  endothelial tone and sheath related injury. Irreversible  compromise  of blood flow to  palmar arch  may  also occur  in radial dominant hands. Further enhanced  sympathetic tone can  spill over to ulnar artery as well . 

             It is concluded, interventions through radial route has hitherto unreported adverse effect  of  “Post procedural  positive  Allen test”  . It  implies , radial  procedures  could  convert  a dual blood supply  pattern of the  hand to ulnar dependent  uni-modal  blood flow  in a significant  subset of patients. This is important   to recognise, as it   precludes further radial procedures in the same patient.


Final message

Hand function could be as vital as our heart’s ,   please handle with care to avoid this complication


Click on the slide to download PPT presentation


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