The story behind Hemocorr

Two deaths, and a question that would not go away

I met them both for the first time when I was eleven. One was my teacher. The other was a classmate. Both of them died of cancer, a few years back. I was with each of them as a friend and as a doctor until the end.

Both of them mattered in a special way. At eleven, I joined a residential school run by the army — I would call it home for the next seven years. There were fifty students in my batch. For better or worse, we were all together through our formative years. One of our teachers was Mr SSD. He taught us English. And he taught me, at least, a lot more than that.

He had a temper, was opinionated but flexible, accepted himself as he was, and neither cared for nor sought wider acceptance from people around him. What struck me was his brutal honesty. He would come to class and ask us to put any question to him, on any subject. A tall order. We would ask. Sometimes he answered. Other times he simply admitted he did not know — then read up, came back the next day, and answered.

Mr SSD did not have to do any of that. He was a fine English teacher. Why was he fielding questions from eighth-graders about physics, botany, biology, astronomy? Perhaps because we were too young to judge how right his answers were. But I think he was illustrating something else: that it is fine to extend yourself outside your field, and it is fine not to know. Just embrace your ignorance and mitigate as much of it as you can, by reading and thinking.

Throughout their illness, everyone from our batch chipped in to help. I, as a doctor, kept getting asked one question: what are the chances of — and the blank got filled in differently each time. Complete recovery. Getting better without full recovery. Survival. Survival for how long. I had nothing better to offer than "it depends," "we can't say," "no one can tell."

It wasn't that such questions had never been put to me before. But this time it was a group of people I had spent seven of the most important years of my life with, and every one of them was genuinely, desperately concerned. There was no escaping how profound the ignorance was. Not only could the questions that mattered most not be answered — nothing was really being done to answer them either. I started Project SSD360, 360 being my batchmate's roll number, not long after Mr SSD's death.

Their deaths made me stop and think — not in the way that loss usually makes you stop and think, but in a more specific way. Cancer was the cause of death. That part was straightforward. People with cancer die sooner or later; their life expectancy is shorter than someone without it. That much I could say with confidence.

But how, exactly, does cancer kill? What was happening inside their bodies — specifically, in quantitative terms — in the days and hours that led to death? Why did they die when they did, and not an hour before or an hour later? Many cancer patients show no detectable disease after surgery and chemotherapy. Some of them still die. What, precisely, pushed them over?

These are not questions about grief. They are questions about mechanism. And I found, when I looked for answers, that medicine does not really have them. We have causes of death. Mechanism — in the rigorous, quantitative sense I was after — is largely unexplored territory.

On reading widely — and why it matters

Before I get into the science, I want to explain something about how this whole line of thinking developed, because it did not come from pathology alone.

There is a book by Professor Jared Diamond called Guns, Germs and Steel. Diamond is a physiologist who is also an ornithologist, speaks multiple languages, and thinks across geography, history, botany, zoology and several other fields simultaneously. His central questions are large ones — why did global wealth and technology distribute the way they did? — and the only reason he can attempt answers is that he draws on many disciplines at once.

That book stayed with me. The lesson I took from it was not about colonialism or wealth. It was about the value of being willing to look at problems from outside your own field. If you are only trained to think within one discipline, there are whole categories of questions you will never be able to ask, let alone answer.

What pathology can — and cannot — tell you

My job as a pathologist is to look at tissue and report on its appearance. A biopsy arrives on my desk. I look at it under the microscope. I say whether it looks normal or abnormal. This is called morphological evaluation and it has been the basis of diagnostic pathology for well over a century.

It works. But it has a fundamental limitation that we do not often talk about directly: what something looks like is not the same as how it is functioning. An organ can appear entirely normal under the microscope — correct structure, no inflammation, no dead cells — and still have been working abnormally at the time the patient died. The appearance tells you one thing. The function is a different question entirely.

The organs looked normal. But someone had died.

I perform postmortems. I have a particular interest in autopsies of foetuses who die in the womb — lives that ended before they began, and that deserve the same careful attention as any other.

What struck me, again and again, was how often everything looked normal. The organs, the structure, the histology — normal. And yet the person had died. Something had failed. I just could not see it on the slide.

This led to an obvious next question: if the organs look normal but were not functioning normally, how would I know? The answer was to measure what they were actually producing — the hormones, the enzymes, the chemical output that tells you what an organ was actually doing.

We sometimes take blood samples right after death and run standard tests — kidney function, liver function, thyroid function — and if the results are within normal range, we conclude the organs were functioning normally. That is reasonable. But there is a catch: blood levels and organ levels are not necessarily the same thing. The concentration of a hormone in the blood may be normal while the concentration inside the organ that produces it is something quite different. And we have never, in any systematic way, actually measured what normal organ concentrations look like.

Functional autopsy: what I found when I looked

I decided to try, in a small study, to find out. I took adrenal glands from autopsies — glands that looked histologically normal — and measured the concentration of aldosterone, one of the principal hormones they produce. The results were not what I expected. Every single gland was different. The variation was not marginal; it was stark. I measured cortisol as well, and the ratio between aldosterone and cortisol varied just as widely.

I did the same with the pancreas, measuring insulin and glucagon. A few pancreases showed no detectable insulin at all. The rest showed wide variation. The corresponding blood values for all these hormones also varied substantially.

This was only ten individuals. I am aware of the limitations of a study that small. But the finding itself — that organs we routinely classify as normal are, at the molecular level, anything but uniform — had not been demonstrated before in this way.

I have taken to calling this approach functional autopsy: not just describing what the organ looks like, but asking what it was actually doing at the moment everything stopped.

To understand the dying, you have to watch the living

Functional autopsy can tell you something about organ function at the time of death. What it cannot tell you is the process that got there — the trajectory of the illness, the sequence of molecular events that led to that final state.

We know that organs communicate continuously with each other through molecules circulating in the blood. Nothing works in isolation. In health, these molecular levels stay within fairly narrow ranges. In serious illness — take a patient with diabetes, septicaemia, and multi-organ failure — they can swing dramatically within minutes, and the degree and frequency of those swings vary considerably from person to person.

The conclusion I arrived at was unavoidable: to understand what was happening, I needed to measure the levels of multiple circulating molecules while the patient was alive, continuously, for as long as they were critically ill. A few tests a day would not do it. The measurement had to be continuous.

Why so many molecules? Think about weather forecasting.

When I say multiple molecules, I mean dozens to hundreds. That sounds excessive until you think about weather forecasting.

A century ago, meteorologists tried to predict weather from a handful of readings — temperature, pressure, wind speed, humidity — taken in a limited number of places, a few times a day. They were mostly wrong, because the system they were trying to predict was far more complex than their data could capture. Today, thousands of sensors cover the land and sea and air. Satellites, commercial aircraft, ocean buoys — all feeding continuous data into supercomputers running AI-driven models that update in real time. Weather forecasting is now genuinely useful, because the data is finally comprehensive and continuous.

Thinking like a doctor would not help me get anywhere with this. I had to think like an engineer with at least a working acquaintance with chemistry, physics, electronics, mathematics, and systems biology. I work in a medical college with limited facilities, and I could not find a group of people to think through the problem with. The only person nearby with a similar wavelength was my brother — a community medicine specialist and faculty member — with whom I could talk for hours.

The blood loss problem

The obvious objection to continuous blood monitoring is simple: how do you keep testing blood without the patient running out of it? Even a single drop per minute adds up to 72 millilitres per day. A critically ill patient cannot spare that. Frequent discrete sampling was clearly not the answer.

There was a second issue that bothered me almost as much: most standard blood tests involve a chemical reaction that consumes the molecule being measured. If you are measuring something continuously for days, you are continuously removing a little of it. We do not fully understand the consequences of depleting certain molecules over extended periods. An ideal device should monitor without disturbing.

Sensors in blood vessels, or on the skin?

The alternatives to drawing blood samples are either to put sensors inside blood vessels or to use sensors applied to the skin.

Both approaches have serious limitations. Intravascular sensors carry infection risk and are prone to protein coating, which degrades their accuracy over time. More fundamentally, each sensor targets one molecule — so monitoring dozens of molecules means deploying dozens of sensors inside a patient's blood vessels, which is neither practical nor acceptable.

Sensors on the skin use optical and spectroscopic methods and are genuinely elegant in principle — we can determine the composition of Jupiter's atmosphere without sending anything inside it, using exactly these techniques. The problem is that skin and tissue between the sensor and the blood create interference that compounds with each additional sensor deployed. More sensors, more error.

Take the blood outside the body

The answer came from a different direction: take the blood outside the body.

If blood is flowing through an external channel beside the patient — exactly as in dialysis — you can place as many sensors as you want around that channel without any tissue interference, without any infection risk, without any of the biocompatibility constraints that limit in-vivo sensing. I talked to an astrophysicist and asked a single question: would something like this work in principle? He said yes.

The remaining challenge was the complexity of plasma itself. Even cell-free plasma contains thousands of different molecules, and sensors targeting specific analytes can be confused by the presence of others with similar properties. The solution was fractionation — dividing the plasma into sub-streams using semipermeable membranes, enriching the target molecule relative to potential interferents. Unlike dialysis, no bespoke dialysate is needed; ultrapure water is sufficient. The cells have already been returned to the patient, so there is no risk of osmotic damage.

That is where my focus originally stopped: a method for continuous, real-time, multi-analyte blood chemistry monitoring without blood loss and without consuming what was being measured.

Monitoring is not enough — correction without drugs

A conversation — I do not remember exactly with whom — made me realise the device should do more than monitor. There needed to be a way to correct abnormal levels as well.

The usual approach is drugs. But drugs come with adverse effects, and those effects are hardest to tolerate in the most seriously ill patients — the very ones who need correction most urgently. Dialysis can reduce concentrations of some molecules, but its membrane passes anything below a given size; it is not selective. An ideal correction device should remove only what needs to be removed, and leave everything else alone.

The dictum I kept coming back to: the biological system being monitored and corrected must be disturbed as minimally as possible. Do not remove something you did not intend to remove. Do not alter something whose consequences you do not fully understand.

One thing worth stating plainly: correction is a separable capability, addable per molecule, on the same architecture used for monitoring — not one fused step. A device built this way could watch a single molecule, or dozens, and it could stop at watching, without ever adding correction. The two capabilities scale independently.

Designer molecules: the capturing approach

The only solution consistent with that principle was purpose-designed molecules — engineered in a laboratory to react with one specific target and nothing else. Inject them into the external circuit. They find their target, bind to it, and then need to be removed before the plasma returns to the patient.

Several approaches work. The capturing molecule can be made very large — larger than anything else in the plasma — so that a membrane with an appropriate pore size will hold it back. It can be magnetised, so that an external magnetic field pulls the complex out of the plasma stream. Ideally both: large and magnetised, so the probability of it entering the patient's circulation is effectively zero. A catalyst tethered to the capturing molecule can speed the reaction. Multiple types of capturing molecules can be deployed simultaneously for multi-target correction.

I discovered, when I looked, that all the components I was describing already existed in validated laboratory or clinical use. Nobody had assembled them this way before.

Hemocorr, complete

The whole system came together through a process of asking simple questions and not getting distracted by the complexity of each answer. Take blood out. Return cells. Fractionate the plasma. Sense with multiple sensors. Correct with capturing molecules. Verify. Return. Repeat.

Will it be the ideal device I imagined? Almost certainly not — nothing is. But it is, I believe, the only architecture capable of meeting both mandates simultaneously: continuous multi-analyte monitoring without blood loss, and precise, selective, drug-free correction of abnormal levels.

Functional autopsy and Hemocorr together

Hemocorr generates quantitative blood chemistry data while the patient is alive. Functional autopsy generates quantitative data from organs after death. Together, for the first time, they would give us a complete picture of the molecular trajectory of a critical illness — from the living patient to the post-mortem findings — in hard numbers.

Without that, we cannot predict the efficacy of interventions. We cannot calculate the probability of survival in a given patient at a given moment. We cannot understand, in any rigorous sense, the mechanism by which a person died.

We, the doctors, are in the business of postponing death. To do that well, we need to understand life and death not in qualitative terms but in comprehensive quantitative ones. Thinking purely as a pathologist would never have produced Hemocorr. The idea demanded physics, chemistry, optics, engineering, systems biology, and mathematics — almost none of which belong to conventional medical training. That is not a criticism of medicine. It is just an observation about the kind of thinking certain problems require.

Trekking alone, and why that matters here

I wouldn't have had the guts to invent something like Hemocorr if I hadn't spent so much time trekking alone, deliberately, under difficult conditions. I like going to places hardly anyone else thinks of going — or going at the worst possible time to go there.

Trekking in perfect weather bores me. I go when conditions are bad — night, rain, snow, barely a trail, or none at all. It is panic-inducing to lose the trail, and exhilarating to find it again.

Carrying nearly thirty pounds over difficult terrain is close to meditation. Sometimes that meditation breaks, and I lose my footing and slide down a glacier in a way that is neither dignified nor pleasant. I accept that risk, because the payoff isn't there if you trek in good weather, at a good time, with a group.

Hemocorr was a place I wanted to reach. The terrain was intellectual — a web of thoughts pulling in different directions. But unlike the mountains, I wasn't entirely alone: I had my brother to think it through with, and my wife keeping an eye on me in case I took a serious fall.

Getting the patents — and what came after

I did not know anyone else who had conceptualised something like this. I found that doctors did not fully understand the engineering parts, and engineers had limited grasp of the medical applications. Even within their respective fields, most specialists had little understanding of anything outside their narrow domain. My functional autopsy work faced its own obstacles — repeated rejections from conventional pathology journals in India before eventually being accepted in a European specialist journal. The process left a bitter taste.

I found a patent agent with a doctorate in physics and mathematics, who grasped the concept quickly and drafted an application that captured the details of a genuinely complicated invention: parallel fractionation units that can be back-flushed while the other continues running; bifurcating sensor channels that average readings for greater accuracy; an architecture that was, as my agent put it, perhaps too complicated. The process took nearly six years. The patents were granted in India and in the United States almost simultaneously, in July 2025.

I thought I would feel settled after that. I did, briefly. Then came the more difficult part: how to reach the people who could turn this from a protected design into an actual device. I am not particularly patient with sustained social outreach — I can manage it in short bursts. A website seemed like the right answer.

Dr. Bal Chander
Professor of Pathology · Dr. RPG Medical College, Himachal Pradesh, India
AIIMS alumnus · bal@hemocorr.com · +91 70180 64940