By SAURABH JHA

Though the exact cost of Modicare, the government’s extension of health insurance for poor people, estimated at one lakh crore (a trillion U.S. dollars), is open for debate, what is not disputable is that the cost of insuring India’s poor won’t fall with time. A sure way of accelerating healthcare inflation, that is speeding the rate of increase of healthcare costs, is by subsidizing or paying for health insurance. Insurance is like Newton’s Second Law of Motion – the velocity keeps increasing as long as the force is applied.

Healthcare is a peculiar industry. Cars get cheaper but medical care doesn’t. The Maruti eventually became cheaper than the Ambassador, and more aesthetically pleasing than its Neanderthalic predecessor. Medical care doesn’t get cheaper because a life saved from cancer is a life waiting to be killed by another disease, which needs treating, too. Survivors of cancer get heart attacks and survivors of heart attacks get cancer, and survivors of both get dementia.

It’s like a restaurant where you can’t just pay for lunch – if you pay for lunch you have to pay for breakfast and dinner and may be a few samosas in between the meals. But unlike eating, consumption of medical care is not guarded by satiety. The insatiable medical sciences keep delivering even more expensive ways death can marginally be deferred. For example, the once dreaded stroke which leads to paralysis is now treatable. However, the treatment is not cheap and comprises clot busters, dangerous drugs with fatal side effects. Further, to treat stroke you need rapid diagnosis by modern imaging – that is you need CAT scans and radiologists. If penicillin for pneumonia is like eating at a roadside dhaba, treatment for acute stroke is fine dining at the Taj.

Continue reading…

By ANISH KOKA

The year was 1965, the place was Boston Children’s and a surgery resident named Robert Bartlett took his turn at the bedside of a just born baby unable to breathe.  This particular baby couldn’t breathe because of a hole in the diaphragm that had allowed the intestines to travel up into the thoracic cage, and prevent normal development of the lungs.  In 1965, Robert Bartlett was engaged in the cutting edge treatment of the time – squeeze a bag that forced oxygenated air into tiny lungs and hope there was enough functioning lung tissue to participate in gas exchange to allow the body to get the oxygen it needed.  Bartlett persisted in ‘bagging’ the child for 2 days.  As was frequently the case, the treatments proved futile and the baby died.

The strange part of the syndrome that had come to be known as congenital diaphragmatic hernia was that repairing the defect and putting the intestines back where they belonged was not necessarily curative.  The clues to what was happening lay in autopsy studies that demonstrated arrested maturation of lung tissue in both compressed and uncompressed lung.  Some systemic process beyond simple compression of one lung must be operative.  It turns out that these little babies were blue because their bodies were shunting blood away from the immature lungs through vascular connections that normally close off after birth.  Add abnormally high pressures in the lungs and you have a perfect physiologic storm that was not compatible with life.

Pondering the problem, Bartlett wondered if there was a way to artificially do what the lungs were supposed to do – oxygenate.  Twelve years later in 1977, while most pediatric intensive care units were still figuring out how to ventilate babies, a team lead by Bartlett was using jerry rigged chest tube catheters to bypass the lungs of babies failing the standard treatments of the day.  In a series of reports that followed, Bartlett described the technique his team used in babies that heretofore had a mortality rate of 90%.  A home made catheter was placed in the internal jugular vein and pumped across an artificial membrane that oxygenated blood before it was returned via a catheter to the carotid artery.  The usual hiccups ensued.  The animal models didn’t adequately model the challenges of placing babies on what has come to be known as ECMO (Extra Corporeal Membrane Oxygenation).

Patient 1 developed a severely low platelet count, hemorrhaged into the brain and died. Patient 2 survived but was on a ventilator for 7 weeks.  Patient 3 developed progressive pulmonary hypertension and died.  Patient 4 died because of misplacement of one of the ECMO catheters.

The team improved, and mortality in this moribund population improved to 20%.  The pediatric journals of the day refused to publish the data because they felt ECMO for neonates was irresponsible.  Once published, the neonatology community came out in force against ECMO, and some penned editorials implying the children only became supremely ill because Bartlett’s team was incompetent.  The team persisted, as is anyone that is driven by the desperate need of patients.  None of this should be surprising.  The constant battle between skeptics and proponents is a recurring theme known to anyone with even a limited understanding of  medical history.  But this is where the story goes off the rails.Continue reading…

By ANISH KOKA

The phone rings.  It’s not supposed to be ringing.  It’s 2 am.   The voice on the other line is from an apologetic surgery resident.

Resident: There is this patient..

Me: Yes, go ahead. Please.

Resident: He’s tachycardic.

Me: How fast?

Resident: 160 ?

Me: What’s the blood pressure?

Resident: 130/90

Me: Rhythm?

Resident: An SVT I think.. I gave adenosine.  Nothing happened

Me: Audibly groaning.  I’ll be in..

Forty five minutes later I’m at the bedside of a decidedly ill appearing man.

I want to be triumphant that his heart rate is only 145, and a quick glance at the telemetry monitor above his bed uncovers juicy p waves in a cadence that suggests this is no primary electrical arrhythmia.

Something is very wrong somewhere – the heart in this case is an innocent bystander being whipped into a frenzy to compensate for something.

At the moment the whip is a norepinephrine infusion being used to keep his blood pressure up.

I ask the nurse if the amount of norepinephrine infusing has been stable.  She replies that his dose has been slowly escalating.

Eureka! I think – the heart rate response in this case is being driven by the norepinephrine – a powerful adrenaline that acts on beta receptors and alpha receptors within the body that increase heart rate and constrict the blood vessels to raise blood pressure.  Fix the cause of the low blood pressure, come down on the norepinephrine, and perhaps the heart rate would be better.

But it turns out this particular post surgical patient doesn’t have a medical cause of low blood pressure I can find.  I cycle through cardiac ultrasounds, blood gases, steroid and volume challenges, and try inching down on the norepinephrine.

All of it is to no avail.  I’m growing more and more convinced this problem is surgical in nature. Perhaps an infarcted piece of bowel?  All I know is that the man acts like he has no peripheral vascular tone.

An interesting thing happens shortly after.  The norepinephrine drip runs out.

As one nurse runs to get another bag from the pharmacy – a quick cascade of events unfolds.

The brisk upstroke from the arterial line that marks the pressure wave generated with every beat of the heart starts to dampen.  The color seems to visibly drain from the patients face, and he begins to complain that his vision is getting blurry.  His systolic blood pressure is 70 – an almost forty point drop within a minute of the norepinephrine running out.

Continue reading…