# Massive Transfusion Protocol

> Massive transfusion protocol for NEET-PG Surgery: definitions, 1:1:1 component ratios, tranexamic acid, calcium and temperature targets, and monitoring.

- Canonical URL: https://prepelephant.com/topics/neet-pg/surgery/massive-transfusion-protocol
- Exam / course: NEET-PG · Subject: Surgery
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Massive Transfusion Protocol", PrepElephant, https://prepelephant.com/topics/neet-pg/surgery/massive-transfusion-protocol

## Direct answer

Ten units of packed red cells within 24 hours — the classical definition of massive transfusion — is too slow a trigger to wait for. A modern massive transfusion protocol (MTP) is activated on predictive criteria such as four units of red cells within one hour, ongoing blood loss exceeding about 150–200 mL/min, or shock plus a positive FAST, and it delivers blood components in balanced "boxes" (red cells, fresh frozen plasma and platelets in roughly 1:1:1) until haemorrhage is controlled. Alongside component issue, the protocol mandates tranexamic acid, calcium replacement, active warming, and laboratory or viscoelastic monitoring, because the patient dies as often from iatrogenic coagulopathy, hypocalcaemia and hyperkalaemia as from the original wound.

## What you must remember

- Definitions: 10 or more units of red cells in 24 hours (classical), or 4 units in 1 hour with ongoing need, or replacement of one blood volume within 24 hours.
- Balanced resuscitation aims for a plasma:platelets:red cell ratio near 1:1:1; PROPPR (commonly quoted) found haemostasis achieved more often (about 86% versus 78%) and fewer exsanguination deaths at 24 hours with 1:1:1 versus 1:1:2.
- Tranexamic acid 1 g bolus plus 1 g over 8 hours, only within 3 hours of injury (CRASH-2).
- Complications to anticipate and prevent: hypocalcaemia from citrate (keep ionised calcium above about 1.1 mmol/L), hyperkalaemia from stored red cells, hypothermia ("blood is warm when it leaves the donor — it must be warm when it enters the patient"), dilutional coagulopathy, and transfusion-related acute lung injury.
- Fibrinogen is the first factor to fall: replace with cryoprecipitate or fibrinogen concentrate when levels drop below about 1.5–2 g/L; platelet target above 50 × 10^9/L (100 in active bleeding with brain injury, per common practice).
- Monitoring: repeat arterial blood gases, ionised calcium, potassium, and full blood count plus ROTEM/TEG-guided component therapy where available.
- Blood group O negative red cells for the first packs in women of childbearing age is standard practice; switch to group-specific blood as soon as possible.

## A typical protocol walked through

A 35-year-old man arrives after a road traffic accident with a systolic of 70 and a positive FAST. The trigger is physiological, not a laboratory number: the trauma surgeon activates the MTP by a single phone call, and the blood bank issues the first cooler without waiting for results — say 6 units of red cells, 6 of fresh frozen plasma and one apheresis platelet pack (the "1:1:1 box" approximation). Meanwhile the team gives tranexamic acid, sets up a rapid infuser with a blood warmer, and sends baseline bloods including calcium and fibrinogen along with a crossmatch sample.

For every one to two boxes issued, the protocol demands a reassessment checkpoint: ionised calcium replaced with calcium chloride or gluconate, potassium checked and hyperkalaemia treated if the ECG shows peaked T waves, core temperature kept above 35 degrees C, and acidosis tracked by lactate and base deficit. Component therapy is then finessed by ROTEM/TEG: low fibrinogen on the trace (FIBTEM) brings cryoprecipitate; prolonged clotting times bring more plasma; low platelet count after several boxes brings platelets. Once surgical or angiographic control is achieved and the patient stabilises, the protocol is formally stood down with a documented decision — continuing to transfuse by protocol after control is reached is how circulatory overload and TRALI happen.

## Where students slip

The favourite error is quoting "10 units in 24 hours" as if it were the activation trigger. It is a retrospective definition; activation is prospective and based on predicted need — examiners specifically reward that distinction. The second slip is forgetting calcium: candidates list hypothermia and dilution but miss that citrate toxicity produces both myocardial depression and further coagulopathy, and that calcium chloride through a central line is the standard replacement in massive transfusion. Third, O negative blood: many candidates answer "O positive" for the emergency packs — acceptable in males in some protocols, but O negative is the default taught answer, and mandatory for women of childbearing potential.

## Frequently asked questions

### What criteria activate a massive transfusion protocol?
Commonly used triggers include expected replacement of one blood volume, four or more red cell units within an hour with ongoing haemorrhage, shock with a positive FAST, or blood loss over 150 mL/min; activation is a clinical phone call, not a laboratory result.

### Why is 1:1:1 preferred over red-cell-only transfusion?
Plasma and platelets prevent dilutional coagulopathy; the PROPPR trial showed better early haemostasis and fewer exsanguination deaths with balanced ratios, and component-only resuscitation reproduces the "bloody vicious cycle".

### Which electrolyte disturbance kills fastest during massive transfusion?
Hypocalcaemia from citrate anticoagulant (with hyperkalaemia close behind) — ionised calcium should be monitored and replaced during ongoing transfusion.

### What is the role of ROTEM or TEG in massive transfusion?
Viscoelastic testing gives real-time clot kinetics, allowing targeted replacement of fibrinogen, platelets and factors instead of formula-driven transfusion, and reducing total component usage.

### When is O negative blood used?
As the immediate-issue option in exsanguinating patients before a sample is processed, and specifically for women of childbearing age to avoid Rh D sensitisation; group-specific blood follows within about 15–30 minutes.