Rule of 30 to asses obstestric haemorrhage

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Rule of 30 obstetric haemorrhage assessment clinical

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"rule of 30" postpartum hemorrhage

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https://pmc.ncbi.nlm.nih.gov/articles/PMC9313855

Here is a full clinical breakdown of the Rule of 30 for assessing obstetric haemorrhage.

Rule of 30 - Obstetric Haemorrhage

What is it?

The Rule of 30 is a bedside mnemonic and clinical decision-support tool used to identify when a woman has lost approximately 30% of her circulating blood volume - the threshold at which haemodynamic compensation begins to fail and clinical deterioration accelerates. It is particularly useful because visual estimation of blood loss is notoriously inaccurate and typically underestimates true loss.

The Four Components

Parameter	Change indicating ~30% blood loss
Systolic Blood Pressure	Falls by 30 mmHg
Heart Rate	Rises by 30 beats per minute
Haematocrit	Falls by 30%
Haemoglobin	Falls by 30% (approximately 3 g/dL)

How to Calculate 30% Blood Loss

Blood volume in pregnancy is approximately 100 mL/kg (versus 70 mL/kg in a non-pregnant adult).

Example: A woman weighing 70 kg has an estimated blood volume of 7,000 mL. A 30% loss = 2,100 mL.

So for any given patient:

30% blood loss = patient's weight (kg) × 100 × 0.30 mL

Why the Rule of 30 Matters in Obstetrics

Healthy postpartum women have significant physiological compensation - the cardiovascular adaptations of pregnancy (increased blood volume, cardiac output, heart rate) mean vital signs can remain near-normal even after substantial haemorrhage exceeding 1,000 mL. By the time a systolic BP drop becomes clinically obvious, the patient may already be in decompensated shock.

The Rule of 30 helps identify this critical threshold before obvious clinical deterioration, prompting earlier intervention.

Shock Index (SI) - a Complementary Tool

The Shock Index (SI = Heart Rate / Systolic BP) is used alongside the Rule of 30:

Normal non-pregnant adult: 0.5 - 0.7
Standard obstetric range: 0.7 - 0.9 (higher due to pregnancy physiology)
SI ≥ 0.9 is associated with increased mortality
SI > 1 increases the likelihood of requiring blood transfusion

The SI is particularly useful because heart rate rises before systolic BP falls, giving an early warning of haemodynamic compromise.

Limitations

Vital signs lag behind blood loss - especially in young, fit women whose compensatory mechanisms are strong. A woman can lose >1,000 mL before showing any change in BP or heart rate.
The 30% threshold is approximate - it does not replace quantitative blood loss measurement.
Gravimetric measurement is preferred - weighing all soiled linen and pads is more accurate than visual estimation. Any measured liquor should be subtracted from the total.
Lab values (Hb, haematocrit) are delayed - they may not reflect acute blood loss until haemodilution has occurred. Do not wait for lab results before treating haemodynamically unstable patients.
Chronic anaemia baseline - a woman who is already anaemic will reach critical haemoglobin thresholds at a smaller absolute volume of blood loss.

Putting it Together Clinically

When assessing an obstetric patient with haemorrhage:

Estimate blood volume: weight (kg) × 100 mL
Calculate 30% threshold: to set your alarm threshold
Monitor vital signs: rising HR is the earliest sign - use Shock Index
Apply Rule of 30: any one of the four parameters crossing the 30-unit mark signals ~30% loss
Quantify blood loss: gravimetric (weigh pads/linen) + direct collection where possible
Do not wait for labs to resuscitate - clinical parameters come first

Classification of Haemorrhagic Shock (for context)

Class	Blood loss	HR	SBP	Signs
I	<15%	<100	Normal	Minimal
II	15-30%	100-120	Normal/slightly ↓	Anxiety, delayed cap refill
III	30-40%	120-140	↓	Confusion, pallor
IV	>40%	>140	Very ↓	Lethargy, cold/clammy

The Rule of 30 specifically flags the Class II-III transition - the critical point at which intervention must not be delayed.

Source: FIGO 2022 PPH Management Recommendations; SA Health PPH Guideline

Falls by 30 mmhg means

It means the systolic blood pressure drops by 30 mmHg from the patient's own baseline.

Example

Situation	Systolic BP
Patient's normal/baseline BP	120 mmHg
After ~30% blood loss	90 mmHg
Difference	30 mmHg fall

Key Points

It is not a fixed absolute number like "BP falls to 90 mmHg"
It is a relative drop from that individual's baseline
This matters because a woman who normally runs 150 mmHg systolic (e.g. with chronic hypertension) would still read 120 mmHg after significant haemorrhage - which looks "normal" on a chart but actually represents a 30 mmHg fall and is clinically significant
Conversely, a woman with a baseline of 100 mmHg systolic reaching 70 mmHg has crossed the same threshold

Why this is important in obstetrics

Pregnant and postpartum women typically have lower baseline BP than non-pregnant adults due to the vasodilatory effects of progesterone. So even a reading of 90/60 mmHg might not trigger alarm unless you know her booking BP was 120/80 mmHg.

Always document baseline BP early in labour or on admission so you have a reference point to detect this 30 mmHg fall.

Finding Sources

Investigations in Obstetric Haemorrhage

Bedside / Immediate (done simultaneously with resuscitation)

Investigation	What you're looking for
Vital signs (HR, BP, RR, SpO₂, temp)	Haemodynamic compromise - apply Rule of 30 and Shock Index
Urine output (catheterise)	Target ≥ 30 mL/hour - reflects end-organ perfusion
Capillary refill, skin colour/temp	Peripheral shutdown in shock

Haematological

Test	Relevance
FBC (Full Blood Count)	Haemoglobin, haematocrit (note: may be normal early - haemodilution takes time), platelet count
Blood group & crossmatch	Essential - request 4-6 units packed red cells in major haemorrhage
Coagulation screen - PT, APTT, fibrinogen	Detect coagulopathy/DIC which complicates major PPH
Fibrinogen level	Low fibrinogen (<2 g/L) predicts severity; <1 g/L = critical, give cryoprecipitate/fibrinogen concentrate
D-dimer	Elevated in DIC
Thromboelastography (TEG) / ROTEM	Point-of-care viscoelastic test - gives real-time picture of clot formation and lysis; guides blood product therapy

Biochemical

Test	Relevance
U&E / Renal function	Baseline + monitor for acute kidney injury (AKI)
LFTs	Relevant if HELLP syndrome or liver trauma is suspected
Serum lactate	Marker of tissue hypoperfusion/anaerobic metabolism - rising lactate = inadequate resuscitation
ABG (Arterial Blood Gas)	pH, base deficit, lactate, haemoglobin - rapid bedside assessment of metabolic acidosis and oxygen-carrying capacity

Imaging

Modality	Indication
Ultrasound (USS) - bedside	Retained products of conception (RPOC), uterine atony assessment, intra-abdominal free fluid (FAST scan in trauma), placenta accreta complications
CT Angiography	Identify source of bleeding for embolisation; used in stable or stabilised patients
MRI	Rarely used acutely; useful for placenta accreta spectrum pre-delivery

In DIC / Massive Haemorrhage - Targeted

Fibrinogen - most important single coagulation test in PPH
Platelet count - transfuse if <50 × 10⁹/L in active bleeding
PT ratio / INR - guide FFP use
Repeat FBC and coags every 30-60 minutes during active major haemorrhage

Practical Note

Do not delay treatment to wait for results. Resuscitation runs in parallel with investigations. In massive haemorrhage, activate the major haemorrhage protocol and transfuse on clinical grounds if crossmatched blood is not yet available (use O-negative packed red cells).

Why we asses it

Great question - this gets to the "why bother" behind the whole Rule of 30 framework.

Why We Assess Obstetric Haemorrhage

1. Visual Estimation is Unreliable

Blood loss is consistently underestimated by eye - studies show clinicians underestimate by 30-50% on average. A soaked pad looks like 50 mL but may contain 150 mL. Without a structured assessment tool, you miss the true magnitude of loss.

2. The Body Compensates - and Fools You

This is the most important reason.

Pregnant and postpartum women are young, fit, and have expanded blood volume (up to 50% above normal). Their cardiovascular system can compensate silently for large blood losses:

A woman can lose 1,000-1,500 mL and still have a normal BP and only mildly raised HR

By the time vital signs deteriorate visibly, she is already in decompensated shock - and the window for easy reversal has passed.

The Rule of 30 catches the warning signs before collapse.

3. To Quantify Severity and Guide Treatment

Assessment tells you which stage of shock the patient is in, which directly drives management:

Severity	Action
Minor loss, no haemodynamic change	Oxytocin, monitor closely
Rule of 30 triggered	IV access × 2, fluids, bloods, escalate
Class III shock	Blood transfusion, surgical intervention
Class IV / DIC	Massive haemorrhage protocol, ICU

Without assessment, you cannot match the intensity of response to the severity of bleeding.

4. To Prevent the Lethal Triad

Unassessed/undertreated haemorrhage leads to:

Hypothermia (tissue hypoperfusion)
Acidosis (anaerobic metabolism, rising lactate)
Coagulopathy (consumption of clotting factors, DIC)

These three form a self-reinforcing cycle - each makes the others worse, and together they make haemorrhage increasingly difficult to control. Early, structured assessment breaks this cycle before it starts.

5. Obstetric Haemorrhage is a Leading Cause of Maternal Death

Globally, PPH accounts for approximately 27% of maternal deaths - the single largest cause. In many of these cases, death is preventable with timely recognition and response.

Structured assessment tools like the Rule of 30 exist precisely because delayed recognition is the most common failure point.

In Summary

We assess because:

We cannot trust our eyes to estimate blood loss
The patient's body hides the true picture until it is too late
Assessment drives the right level of response
Early intervention prevents irreversible shock and death

The Rule of 30 is not just a number - it is a safety net for the gap between what we can see and what is actually happening.

I mean for each investigation I need justification for why we doing this ix

Here is every investigation with its specific justification:

Investigations in Obstetric Haemorrhage - With Justification

Bedside / Immediate

Investigation	Why we do it
Vital signs (HR, BP, RR, SpO₂)	HR rises before BP falls - earliest sign of haemodynamic compromise. Allows application of Rule of 30 and Shock Index to quantify severity in real time
Urine output (catheterise)	Kidneys are the first organ to show hypoperfusion. Output <30 mL/hr = inadequate end-organ perfusion = still in shock despite normal-looking BP
Capillary refill / skin	Peripheral vasoconstriction is an early compensatory response - cold, pale, clammy peripheries indicate the body is shunting blood to vital organs

Haematological

Investigation	Why we do it
FBC	Haemoglobin and haematocrit confirm the degree of blood loss (Rule of 30: Hb falls ~3 g/dL, haematocrit falls 30%). Platelet count detects thrombocytopaenia which worsens bleeding. Caveat: in acute haemorrhage, Hb may be normal initially because haemodilution has not yet occurred - do not be falsely reassured
Blood group & crossmatch	You need compatible blood ready before the patient deteriorates further. In massive haemorrhage every minute counts - this must be sent immediately, not when the patient is already in crisis
Coagulation screen (PT, APTT)	Major haemorrhage consumes clotting factors. Prolonged PT/APTT signals coagulopathy or early DIC - you cannot control bleeding without functioning clotting
Fibrinogen	The single most important coagulation test in PPH. Fibrinogen is consumed rapidly in PPH. Level <2 g/L predicts progression to severe PPH. Level <1 g/L = critical - replace immediately with cryoprecipitate or fibrinogen concentrate. Normal pregnancy fibrinogen is 4-6 g/L so "normal" non-pregnant ranges are misleading
D-dimer	Elevated in DIC due to fibrin degradation. Confirms consumptive coagulopathy when combined with low fibrinogen and prolonged clotting times
TEG / ROTEM	Standard coagulation tests take 45-60 minutes. TEG/ROTEM gives a real-time, whole-blood picture of clot formation, strength, and lysis within minutes. Tells you exactly which component is failing - red cells, platelets, fibrinogen, or fibrinolysis - so you give the right blood product rather than guessing

Biochemical

Investigation	Why we do it
U&E / Renal function	Establishes baseline kidney function. Prolonged hypoperfusion causes acute tubular necrosis (ATN) and AKI - serial measurements track whether kidneys are recovering or failing
LFTs	If HELLP syndrome, liver capsule haematoma, or hepatic trauma is a possible cause of haemorrhage, LFTs identify liver involvement. Also important before giving drugs metabolised hepatically
Serum lactate	Lactate rises when tissues switch to anaerobic metabolism due to inadequate oxygen delivery. A rising lactate despite fluid resuscitation means the patient is not adequately perfused - your treatment is not working. Target lactate <2 mmol/L
ABG (Arterial Blood Gas)	Gives you five critical pieces of information simultaneously and immediately: pH (acidosis = severity of shock), base deficit (quantifies metabolic derangement), lactate (perfusion), HCO₃ (compensation), and haemoglobin (oxygen-carrying capacity). Faster and more comprehensive than waiting for lab results

Imaging

Investigation	Why we do it
Bedside USS	Identifies retained products of conception (a cause of ongoing bleeding), assesses uterine tone, detects intra-abdominal free fluid (haemoperitoneum after uterine rupture or trauma), and evaluates for placenta accreta complications. Done at the bedside without moving an unstable patient
CT Angiography	Identifies the precise arterial source of bleeding so interventional radiology can perform uterine artery embolisation (UAE) - a uterus-sparing alternative to surgery. Only used in haemodynamically stable or stabilised patients
MRI	Not used acutely. Used antenatally to characterise placenta accreta spectrum (depth of invasion) to plan delivery. Occasionally post-operatively to assess complications

The Underlying Logic Across All Investigations

Every investigation answers one of four questions:

How much has she bled? (FBC, ABG, vital signs)
Can her blood still clot? (fibrinogen, coags, TEG/ROTEM)
Are her organs still perfused? (lactate, urine output, renal function)
What is the source / can we stop it? (USS, CT angiography)

Prophylactic oxytocis means

Prophylactic Oxytocin

Prophylactic means given before bleeding occurs - as a preventive measure, not as a treatment for haemorrhage that has already started.

What it means in practice

Oxytocin is given routinely to every woman at the time of delivery of the baby (or with delivery of the anterior shoulder), regardless of whether she is bleeding or not, to:

Stimulate uterine contraction
Prevent uterine atony - the most common cause of PPH (~70-80% of cases)
Reduce blood loss during the third stage of labour

This is the "Active Management of the Third Stage of Labour" (AMTSL)

Prophylactic oxytocin is the core component of AMTSL, which includes:

Component	Purpose
Oxytocin 10 IU IM (or IV infusion) given at/after birth	Prevent atony - this is the prophylactic part
Controlled cord traction	Deliver placenta quickly and cleanly
Uterine massage (in some guidelines)	Sustain contraction

Why at that specific timing?

Given with delivery of the anterior shoulder or immediately after birth
At this point the baby is out but the placenta has not yet delivered
The uterus needs to contract firmly to shear off the placenta and compress the open blood vessels at the placental site
Without a contraction, those vessels bleed freely = atony = PPH

Contrast with Therapeutic Oxytocin

	Prophylactic	Therapeutic
When given	Before bleeding, routinely at delivery	After PPH has already occurred
Purpose	Prevent atony	Treat atony that has happened
Dose	10 IU IM single dose	Higher doses, IV infusion
Goal	Primary prevention	Stop active haemorrhage

Key Point for Exams

Prophylactic oxytocin is the single most effective intervention for preventing PPH and is recommended for all women at every delivery by WHO, FIGO, and RCOG - regardless of risk level.

Uterotonic agent

Uterotonic Agents

A uterotonic is any drug that causes the uterus to contract. Used both prophylactically and therapeutically in obstetric haemorrhage.

1. Oxytocin

Feature	Detail
Class	Synthetic posterior pituitary hormone
Mechanism	Binds oxytocin receptors on myometrium → increases intracellular Ca²⁺ → uterine contraction
Dose (prophylactic)	10 IU IM at delivery of anterior shoulder
Dose (therapeutic)	20-40 IU in 500 mL Normal Saline IV infusion
Onset	IM: 3-5 min / IV: immediate
Side effects	Hypotension (especially IV bolus), tachycardia, nausea, water retention (antidiuretic effect)
Contraindications	Avoid large IV bolus in cardiac disease
First line	YES - first line for both prevention and treatment of PPH

2. Ergometrine (Ergonovine)

Feature	Detail
Class	Ergot alkaloid
Mechanism	Acts on α-adrenergic and serotonin receptors → sustained tonic uterine contraction
Dose	0.2-0.5 mg IM or slow IV
Onset	IM: 2-5 min / IV: immediate
Side effects	Hypertension, nausea, vomiting, coronary vasospasm
Contraindications	Hypertension, pre-eclampsia, cardiac disease - causes vasoconstriction systemically
Note	Often combined with oxytocin as Syntometrine (oxytocin 5 IU + ergometrine 0.5 mg IM)

3. Carboprost (15-methyl PGF₂α)

Feature	Detail
Class	Prostaglandin F₂α analogue
Mechanism	Binds prostaglandin receptors on myometrium → strong sustained contraction
Dose	250 mcg IM, can repeat every 15-90 min, max 8 doses (2 mg total)
Side effects	Bronchospasm, diarrhoea, vomiting, flushing, hypertension
Contraindications	Asthma - causes bronchospasm
Use	Second line when oxytocin fails

4. Misoprostol

Feature	Detail
Class	Prostaglandin E₁ analogue
Mechanism	Binds PGE receptors → uterine contraction
Dose	600-1000 mcg - sublingual, oral, or rectal
Side effects	Shivering, pyrexia, diarrhoea
Contraindications	Few - no significant cardiovascular effects
Advantage	Stable at room temperature, cheap, no injection needed - ideal for low-resource settings and home deliveries
Use	Alternative first line where oxytocin unavailable; also used rectally in unconscious patients

5. Carbetocin

Feature	Detail
Class	Long-acting oxytocin analogue
Mechanism	Same as oxytocin but longer duration of action
Dose	100 mcg IV or IM single dose
Duration	Single dose lasts ~1 hour (vs oxytocin needing infusion)
Advantage	Heat-stable formulation now available (WHO recommended) - useful in resource-limited settings
Use	Prophylaxis at caesarean section particularly

Quick Comparison Table

Drug	Route	Contraindication	Key Advantage
Oxytocin	IV/IM	Avoid IV bolus in cardiac disease	First line, safest
Ergometrine	IM/IV	Hypertension, pre-eclampsia	Sustained tonic contraction
Syntometrine	IM	Hypertension	Combined effect
Carboprost	IM	Asthma	Powerful, second line
Misoprostol	SL/oral/rectal	Few	No injection, heat stable
Carbetocin	IV/IM	-	Long acting, single dose

Step-Up Approach in PPH (Uterotonic Escalation)

Oxytocin (first line)
        ↓ fails
Ergometrine or Syntometrine
        ↓ fails
Carboprost (if no asthma)
        ↓ fails
Misoprostol (if not already given)
        ↓ fails
Surgical / interventional options

Memory Aid

Oxytocin - Ergometrine - Carboprost - Misoprostol "Only Ever Consider More" when the previous one fails

photo-1783913276054.jpg

Management

Your image shows the HAEMOSTASIS mnemonic for PPH management. Here is a full explanation of each step:

HAEMOSTASIS - Management Algorithm for PPH

H - Ask for HELP and Hand on uterus

Call the entire team immediately - obstetrician, anaesthetist, midwives, haematologist
Bimanual uterine massage - one hand on the abdomen, one hand in the vagina compressing the uterus
Stimulates contraction mechanically while other steps are initiated
Do this while everything else is being organised - it is immediate and costs nothing

A - Assess and Resuscitate

Apply Rule of 30, Shock Index
2 large bore IV cannulae (14-16G)
Send bloods (FBC, coags, fibrinogen, crossmatch, ABG, lactate)
IV fluids - crystalloid first, then blood products
Oxygen, catheterise (monitor urine output ≥30 mL/hr)
Position: lie flat, keep warm (prevent hypothermia)

E - Establish Aetiology, Ensure blood available

Find the cause using the 4 T's:

T	Cause	Frequency
Tone	Uterine atony	70-80%
Tissue	Retained placenta/clots	~10%
Trauma	Lacerations, uterine rupture	~10%
Thrombin	Coagulopathy/DIC	~1%

Contact blood bank - activate Major Haemorrhage Protocol
Ensure crossmatched blood is on its way

M - Massage Uterus

Sustained uterine massage - encourages tonic contraction
Bimanual compression continued
Expel any clots from the uterine cavity (clots inhibit contraction)
Check uterine tone regularly

O - Oxytocin

First line uterotonic
10 IU IM or 5 IU slow IV bolus
Followed by 20-40 IU in 500 mL saline infusion over 4 hours
If fails → escalate to ergometrine, carboprost, misoprostol (as discussed previously)
Tranexamic acid 1g IV also given here - inhibits fibrinolysis, reduces death from PPH (within 3 hours of delivery)

S - Shift to Theatre

If bleeding not controlled with above measures
Move to operating theatre for examination under anaesthesia (EUA)
Allows proper inspection for:
- Cervical/vaginal lacerations
- Uterine rupture
- Retained products
Better lighting, instruments, anaesthetic support available

T - Tamponade Balloon / Packing

Bakri balloon or Sengstaken-Blakemore tube inserted into uterine cavity
Inflated with 300-500 mL saline → applies pressure to bleeding sinuses from inside
Tamponade test - if bleeding stops with balloon in = no need for surgery
Uterine packing with gauze is an alternative if balloon unavailable
Buys time and may avoid surgery

A - Apply Compression Sutures

Surgical step - done in theatre
B-Lynch suture - brace suture compresses the uterus like a corset
Other types: Hayman, Cho (square) sutures
All work by physically squeezing the uterus to reduce blood flow to placental bed
Uterus-conserving procedure

S - Systematic Pelvic Devascularisation

Surgical ligation of blood vessels supplying the uterus, step by step:
1. Uterine artery ligation (O'Leary sutures)
2. Ovarian artery ligation
3. Internal iliac (hypogastric) artery ligation - reduces pulse pressure to uterus by 85%
Each step reduces blood flow - try in sequence before hysterectomy

I - Interventional Radiology - Uterine Artery Embolisation (UAE)

Radiologist passes a catheter via femoral artery → selectively blocks uterine arteries with gelfoam particles
Uterus-conserving, minimally invasive
Requires a haemodynamically stable patient - cannot be done if she is crashing
Future fertility can be preserved
Very effective in slow/ongoing haemorrhage after delivery or caesarean

S - Subtotal / Total Abdominal Hysterectomy

Last resort - when all else has failed
Life-saving - do not delay if the patient is dying
Subtotal (remove uterine body, leave cervix) - faster, less risk to bladder/ureters
Total (remove uterus + cervix) - if cervical/lower segment bleeding
Ends fertility permanently - but saves the patient's life

Summary Ladder

CONSERVATIVE (bedside)
H → A → E → M → O
         ↓
SURGICAL (theatre)
S (shift) → T → A → S (devascularisation)
         ↓
RADIOLOGICAL
I (UAE)
         ↓
DEFINITIVE SURGERY
S (Hysterectomy)

The principle is escalate stepwise but do not delay the next step if a measure is clearly failing. In a rapidly deteriorating patient, move faster through the algorithm.

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