A concept and design for a revolutionary medical device aimed at critically ill patients
Hemocorr — a clinical brief
A patented concept and design for a platform that would give intensivists what they have never had: continuous, real-time, multi-analyte blood chemistry — glucose, electrolytes, lactate, inflammatory and coagulation markers — and selective, drug-free correction of derangements, simultaneously, in a single closed-loop extracorporeal circuit.
Sources: peer-reviewed critical care pharmacology, glycaemic-control, and epidemiological literature cited throughout.
We monitor the heart continuously. We barely monitor the blood at all.
Bay four — septicaemic, post-operative, insulin-dependent — was haemodynamically stable two hours ago. Now lactate is climbing, MAP is trending down, and the picture you're working from is a chemistry panel drawn four hours earlier.
This is an information failure, not a clinical one. Every bed runs continuous ECG, arterial pressure, and SpO₂ monitoring — but blood chemistry is still point-in-time: a sample drawn, sent, and reported in arrears. In a patient whose physiology can decompensate within minutes, results already lag the true state by the time they return.
A working Hemocorr would deliver a continuous, real-time, multi-analyte panel — glucose, lactate, electrolytes, cytokines, coagulation factors — without interruption, closing that lag entirely.
Monitored continuously today
Heart rhythm · Blood pressure · SpO₂ — three cardiovascular parameters.
Checked by laboratory draw (1–3× daily)
Glucose, lactate, electrolytes, creatinine, cytokines, coagulation factors, liver enzymes, hormones — results in arrears.
What Hemocorr would provide
Continuous real-time monitoring of all of the above simultaneously — and drug-free correction of any that go abnormal.
What every ICU already watches — and what falls through
Beyond the three continuously monitored cardiovascular parameters, blood chemistry is checked intermittently by laboratory draw — point-of-care or blood-gas glucose at best hourly, most other analytes far less often.
25–35 medications per ICU stay. The paradox is built in.
Glycaemic control illustrates the gap well. Dysglycaemia has been proposed as a "fifth vital sign" in critically ill patients, yet ICU point-of-care and blood-gas glucose measurement — however accurate — is still intermittent, at best hourly. Subcutaneous continuous glucose monitors validated in ambulatory diabetes care are being trialled in the ICU, and early closed-loop insulin studies have shown significantly more time in target range than sliding-scale protocols — but interstitial lag and single-analyte scope limit them to one variable among dozens that matter.
Critically ill patients also face pharmacokinetic and pharmacodynamic derangement — altered volume of distribution, hypoalbuminaemia, capillary leak, hepatic and renal dysfunction — that shifts drug and electrolyte handling hour to hour, while confirmatory chemistry still arrives on a laboratory's schedule, not the patient's.
Polypharmacy is compounded by altered pharmacokinetics in organ dysfunction, making dosing and drug selection genuinely difficult — and drug-drug interactions in the ICU are not merely theoretical: they carry documented links to adverse events, therapeutic failure, and prolonged stay.
For biochemical derangements — hyperglycaemia, electrolyte imbalance, cytokine excess, elevated lactate — Hemocorr offers a drug-free alternative: capturing molecules in the external circuit bind one target and are removed by a magnetic field before return, leaving pharmacokinetics elsewhere in the system undisturbed.
Where a drug genuinely is indicated, continuous chemistry would finally support therapeutic drug monitoring and model-informed precision dosing in real time, rather than titration against hours-old levels.
The architecture is a closed-loop control system
Closed-loop control is already established in critical care physiology: pressure-regulated ventilator modes respond to respiratory mechanics breath by breath, and fully automated closed-loop insulin delivery — using continuous subcutaneous glucose values to drive a model-predictive control algorithm — has been trialled in ICU patients with meaningfully more time in target glycaemic range than protocolised sliding-scale insulin.
Hemocorr's architecture is already the same control topology: sensor array feeding a correction actuator through a defined algorithm. Full automation is the natural extension — set target ranges, let the sensor array supply continuous state data, let the controller trigger the capture cycle.
A fully automated Hemocorr would monitor, correct, and verify continuously, without staff manually charting results or titrating replacement/correction doses at the bedside.
ICU physicians spend only around 9% of clinical time in direct patient contact, and patients may go unobserved for the majority of an admission. Automating this monitor-correct loop redirects clinical attention to the judgement calls that genuinely require a physician — goals-of-care, ventilator weaning, source control — with a biochemical consistency no rota can sustain over a multi-day admission.
The architecture — eight steps, continuously repeating
Two non-negotiable requirements: continuous multi-molecule monitoring and correction, without blood loss or disturbing non-target molecules. Both require an extracorporeal circuit.
Scalable and stageable. Hemocorr can be configured to target a single analyte or scaled up to many, on the same validated architecture. Correction is a separable capability, addable per analyte — so a clinical deployment can begin as monitoring-only, for one analyte or several, with drug-free correction layered in as the same design matures.
Blood routed to an external channel — no tissue interference, no thrombosis risk
Clinical rationale
Skin sensors suffer tissue interference and spectral overlap; subcutaneous sensors add a 4–15 minute lag and infection risk; intravascular sensors foul and clot, each targeting only one analyte. Moving measurement outside the body removes all these constraints at once.
Mechanism
Blood is drawn continuously via peristaltic pump into an external circuit — the same routing principle used in dialysis and plasmapheresis for decades.
Cellular fraction separated and returned immediately — zero haematological loss
Clinical rationale
Erythrocytes dominate whole blood's optical profile, and platelets foul direct-contact sensors. Removing the cellular fraction resolves both; returning it immediately keeps haematological loss at zero — essential for continuous operation over days to weeks.
Mechanism
Continuous centrifugal separation, standard apheresis technique. Cells return directly to the patient; plasma continues through the device.
From separation to sensing — combined view
Multi-analyte sensor array reads simultaneously in real time — no patient-side constraints
Clinical rationale
One sensor detects one analyte. In the extracorporeal channel, sensors work free of tissue interference, biocompatibility limits, or implantation risk — count is limited only by cost-benefit, and calibration is consistent across patients.
Mechanism
Optical and electrochemical sensors ring the external channel, each targeting a specific analyte — read simultaneously for a continuous multi-analyte profile.
Plasma fractionation — minimise inter-analyte interference, maximise sensor accuracy
Clinical rationale
Even cell-free plasma holds thousands of molecules that can interfere with target sensors. Fractionation enriches the target relative to interferents, improving signal-to-noise without removing anything from the patient's plasma.
Mechanism
Semipermeable membranes fractionate plasma by molecular-weight cut-off. Unlike dialysis, ultrapure water — not a bespoke dialysate — runs the permeate side; the goal is enrichment, not isolation.
Chemical capture — precise, selective, drug-free correction. Superior to dialysis and adsorption columns.
Clinical rationale
The biological system must be disturbed minimally — no non-target molecule removed or altered. Dialysis removes by size; adsorption columns bind non-specifically. Chemical capture is one molecule, one confirmed target — and can add a deficit as well as remove an excess.
Mechanism
Target-specific capturing molecules, potentially magnetised or catalyst-tethered, are injected into the plasma stream; a magnetic field removes the complex entirely. Molecules are sized so systemic entry into the patient is effectively zero.
Capture and verification — combined view
Post-correction verification — second sensor pass before anything is returned to the patient
Clinical rationale
The built-in quality-control step — equivalent to checking post-administration drug levels, but automated and immediate. Nothing returns to the patient until levels are confirmed in range.
Mechanism
Plasma passes the sensor array again; anything still out of range routes back to Step 5 until confirmed.
Corrected plasma returned to the patient — zero net blood loss throughout
Clinical rationale
Zero blood loss is a design requirement — even small repeated losses accumulate unacceptably over a multi-day admission in a compromised patient.
Mechanism
Standard extracorporeal reinfusion, as in plasmapheresis. Combined with Step 2's returned cells, full circulating volume is restored each cycle.
Continuous cycling until clinical stability — the entire blood volume monitored and corrected
Clinical rationale
A single pass can't cover the whole blood volume. Continuous cycling processes it multiple times per hour, and each pass adds to the continuous record that outcome models and AI tools will need.
Mechanism
The circuit returns to Step 1 automatically and runs until the clinical team ends monitoring. Full automation — target ranges triggering correction without manual input — is the natural next step.
Cause of death is the easy part. Mechanism is the hard one.
We name causes of death confidently on a death certificate — arrhythmia, refractory shock, multi-organ dysfunction syndrome (MODS). What we can't state in quantitative terms is the mechanism: the precise biochemical cascade and timing that connected the underlying disease to the terminal event.
Non-linear, mutually dependent variables converging on a single fatal endpoint is the rule in critical illness, not the exception. We can't characterise that trajectory quantitatively because we only have serial snapshots — not a continuous physiological signal.
A working Hemocorr would produce that continuous signal: minute-by-minute chemistry across dozens of analytes — electrolytes, lactate, cytokines, coagulation factors, hormones — over hours or days.
For the first time, the precise biochemical trajectory to organ failure could be traced — sequence, timing, and each variable's relative contribution to the terminal cascade.
Over time, that would let quantitative models fit real clinical data — with AI, individualised prognosis: an actual, continuously updated probability of deterioration, not just a qualitative impression that a patient is trending the wrong way.
A granted patent awaiting its engineering team
What exists
- US Patent 12,350,039 B2 (granted July 8, 2025) and Indian Patent 567865
- 41 of 44 EPO claims found novel and inventive — "does not appear to be disclosed nor hinted at in the prior art"
- A complete architecture built from validated component technologies
- Clear clinical rationale grounded in published critical care science
- Sole inventor and owner — no licensees, no co-owners, no funding obligations
What is needed
- Engineering and fabrication of the integrated prototype
- Bench and preclinical validation
- Regulatory strategy (FDA / CDSCO / EMA as applicable)
- Clinical trial design and execution
- Manufacturing scale-up and commercialisation
- Industry partners, research collaborators, and/or investors
A direct appeal to fellow doctors
I am a pathologist. It was in the postmortem room — measuring hormone concentrations in histologically normal organs and finding variation that no antemortem chemistry panel would have captured — that the idea for Hemocorr began.
I could establish cause of death, not mechanism — the biochemical sequence that led there. That continuous physiological record doesn't exist anywhere in medicine; building a device to generate it became a conviction, then a patent, then this brief.
I've done this alone, with no funding, and I cannot build it alone. If this makes clinical sense to you, I'd welcome any engagement — a conversation, a connection, a referral.
Dr. Bal Chander · AIIMS alumnus · Professor, Dept. of Pathology · Dr. RPG Medical College, H.P., India