Postpartum Hemorrhage
Postpartum hemorrhage is excessive blood loss after delivery, defined as more than 500 mL after vaginal or caesarean delivery, or symptoms and signs of shock regardless of measured loss.
Definition
Postpartum haemorrhage (PPH) — let's break the name down: "post" = after, "partum" = delivery/childbirth, "haemorrhage" = heavy bleeding. So it literally means heavy bleeding after childbirth.
PPH is one of the major causes of direct maternal death worldwide. [1][2][3] In Hong Kong, maternal mortality from obstetric haemorrhage has dramatically fallen — 17 women died from haemorrhage of pregnancy and childbirth in 1961; by 2000, only one woman died from this cause — but it remains a leading killer globally, particularly in resource-limited settings. [3][4]
The high-yield modern definition is unified across modes of delivery:
| Definition element | Threshold |
|---|---|
| Quantified blood loss | >= 1000 mL cumulative blood loss within 24 hours after delivery |
| Clinical trigger | Signs or symptoms of hypovolemia within 24 hours after delivery, even if measured blood loss is below the numeric threshold |
Some lecture/source notes still use the older practical trigger of > 500 mL after vaginal delivery or Caesarean section to encourage early recognition. The SketchEase memory palace uses the >= 1000 mL or hypovolemia definition; in practice, treat the patient, not the number.
Clinical Pearl
For clinical purposes, even if the estimated blood loss is below the numeric threshold, treatment should be initiated if the patient has symptoms or signs of shock. [3][4] Accurate estimation of blood loss is notoriously difficult — visual estimation consistently underestimates true loss by 30–50%. Always treat the patient, not the number.
| Grade | Blood Loss | Clinical Significance |
|---|---|---|
| Minor postpartum bleeding | 500–1000 mL | May be well-compensated in healthy women; monitor closely and treat if symptomatic |
| Major PPH | >= 1000 mL | Requires urgent intervention |
| Massive PPH | > 2000 mL or haemodynamic instability | Life-threatening; activate massive transfusion protocol |
Why do sources use different thresholds?
Historically, a higher threshold (> 1000 mL) was used for CS because operative blood loss is generally greater at baseline (~500–700 mL for an uncomplicated CS vs ~200–300 mL for a normal vaginal delivery). Some teaching notes lowered the trigger to > 500 mL for any delivery to encourage earlier recognition. The modern SketchEase anchor is >= 1000 mL or hypovolemia, regardless of mode of delivery.
- Global incidence: Primary PPH complicates approximately 5–10% of all deliveries worldwide; severe PPH (> 1000 mL) occurs in 1–3%.
- Maternal mortality: PPH accounts for approximately 25–30% of all maternal deaths globally (WHO). The vast majority of these deaths are in sub-Saharan Africa and South Asia.
- Hong Kong context: With modern obstetric care, the case fatality rate is extremely low, but morbidity (ICU admission, massive transfusion, hysterectomy, Sheehan syndrome) remains clinically significant. The incidence of PPH in Hong Kong tertiary centres is approximately 5–8% depending on definition used.
- Trend: Rates of PPH are actually increasing in many developed countries over the past two decades — likely due to rising CS rates, increasing maternal age, rising rates of obesity, and more induced/augmented labours.
Risk Factors
Risk factors essentially map onto the "4 T's" causes (discussed below in Aetiology), but let's lay them out as the lectures present them:
Risk factors for PPH can be classified into: [1]
- Overdistension of uterus (multiple pregnancy, polyhydramnios, large-for-gestational-age baby > 3800 g)
- Insensitivity to oxytocin (grand multiparity — defined as ≥ 5 births (live or stillborn) at ≥ 20 weeks of gestation; "great grand multiparity" defined as ≥ 10 births)
- Abnormal myometrium (fibroid, previous surgery on uterus)
Complete list of risk factors from the lectures:
| Risk Factor | Mechanism |
|---|---|
| Antepartum haemorrhage (placenta praevia, abruption) | Abnormal placentation / disrupted placental bed |
| Previous history of manual removal of placenta, PPH, precipitated labour, repeated suction evacuation | Scarred/damaged endometrium → abnormal placental attachment or poor contractility |
| Previous surgery on uterus (Caesarean section, myomectomy) | Scar tissue in myometrium impairs coordinated contraction; risk of placenta accreta spectrum at scar site |
| Grand multiparity | Myometrial fibres become less responsive to oxytocin after repeated stretching |
| Anaemia (Haemoglobin < 10 g/dL) at onset of labour | Poor physiological reserve; even modest blood loss causes decompensation |
| Large for gestational age baby (> 3800 g) | Overdistension of uterus → poor contraction after delivery |
| Multiple pregnancy | Overdistension + larger placental bed |
| Polyhydramnios | Overdistension of uterus |
| Induced or augmented labour | Oxytocin receptor desensitisation from prolonged exogenous oxytocin; also prolonged labour → uterine fatigue |
| Bleeding tendencies | Coagulopathy (inherited or acquired, e.g. vWD, thrombocytopenia, anticoagulant use) impairs haemostasis at placental site |
| Low-lying placenta | The placental bed is where the uterus is very vascular; since this is the lower part of the uterus, it does not contract very well → blood vessels are not controlled → massive bleeding |
Additional risk factors to be aware of (not on lecture slide but clinically important):
- Prolonged labour (uterine fatigue)
- Chorioamnionitis / intra-amniotic infection (endotoxins impair myometrial contractility)
- Retained placenta / placenta accreta spectrum (especially with prior CS)
- Obesity (BMI > 35) — poor uterine tone, difficult bimanual compression
- Advanced maternal age (> 35 years)
- Asian ethnicity — some studies suggest higher baseline risk, though data are mixed
- Use of tocolytics (e.g., MgSO₄ for pre-eclampsia → relaxes myometrium)
- General anaesthesia (volatile agents like sevoflurane cause uterine relaxation)
High Yield Exam Point
Upper segment of the uterus is the main contraction force → hence a low segment Caesarean section (LSCS) is NOT a contraindication for future vaginal delivery, whereas high segment (classical CS) has ~10% rupture risk for subsequent vaginal delivery. [1] This is because the lower segment is relatively passive and thin — a scar here does not significantly weaken the contractile upper segment.
Anatomy and Physiology of Uterine Haemostasis
Understanding why the uterus normally stops bleeding after placental separation is critical — because PPH occurs when any step in this process fails.
- The uterus is supplied by the uterine arteries (branches of the internal iliac arteries) and has collateral supply from the ovarian arteries.
- During pregnancy, the uterine arteries undergo massive remodelling: the spiral arteries in the decidua are invaded by trophoblast, losing their smooth muscle layer and becoming wide, low-resistance conduits → this allows the massive blood flow needed to support the placenta (~500–700 mL/min at term, which is about 15–20% of cardiac output).
- The branches of the mother's blood vessels supplying the placenta implantation site course through the uterine muscles. [3][4]
After delivery of the baby, the uterus decreases rapidly in size and this causes the separation of the placenta from the uterus. [3][4]
-
Placental separation: As the uterus contracts after delivery of the baby, the placental bed surface area shrinks dramatically. Since the placenta cannot shrink (it's a fixed-size disc), shearing forces at the decidua basalis cause it to separate.
-
Exposure of raw placental bed: The raw area left by the placenta in the uterus is very vascular and the bleeding from this area is heavy. [3][4] The opened spiral arteries at the placental site are essentially "bare pipes" that would bleed freely.
-
Myometrial contraction — the "living ligature": In normal situations, the uterus rapidly contracts. Strong contraction of these muscles will occlude these vessels and the normal amount of bleeding from the uterus is around 200 to 300 mL. [3][4]
- The myometrium is uniquely structured with a criss-cross lattice of smooth muscle fibres (the "figure-of-eight" arrangement, particularly in the upper uterine segment). When these fibres contract, they physically compress and kink the spiral arteries running between them — acting like a biological tourniquet.
- This is why the upper segment of the uterus is the main contraction force. [1]
-
Coagulation cascade: Simultaneously, the normal clotting cascade activates at the placental site — platelet plugs and fibrin mesh seal the torn vessels. Pregnancy is a hypercoagulable state (↑ fibrinogen, ↑ factors VII, VIII, X, vWF) which facilitates this.
-
Retraction: Unlike contraction (which is temporary), retraction means the muscle fibres do not return to their original length — the uterus stays small, maintaining vessel occlusion.
The Three Pillars of Postpartum Haemostasis
- Myometrial contraction (the dominant mechanism — the "living ligature")
- Blood coagulation at the placental bed
- Intact genital tract (no tears/lacerations diverting blood loss)
PPH occurs when one or more of these pillars fails. The 4 T's classification maps directly onto these pillars.
The placental bed is where the uterus is very vascular. Since this is the lower part of the uterus, it does not contract very well → hence, the blood vessels are not controlled, resulting in massive bleeding. [1]
The lower uterine segment is:
- Thinner, with fewer muscle fibres
- Derived from the isthmus, which is not designed for powerful contraction
- Therefore, when the placenta implants in the lower segment (placenta praevia), the "living ligature" mechanism is much less effective → this is why placenta praevia is a major risk factor for PPH.
Aetiology and Pathophysiology
1. TONE — Uterine Atony (~70–80% of PPH)
"Atony" = a (without) + tonos (tension/tone) → the uterus lacks muscle tone and fails to contract.
This is the single most common cause of PPH because, as we explained above, myometrial contraction is the dominant haemostatic mechanism.
When the myometrium fails to contract adequately after placental separation:
- The criss-cross muscle fibres do not compress the spiral arteries
- The "living ligature" is lost
- The open spiral arteries at the placental bed bleed freely — at a rate of up to 500–700 mL/min (the full uteroplacental blood flow!)
- This explains why uterine atony can cause life-threatening haemorrhage within minutes
| Mechanism | Specific Causes |
|---|---|
| Overdistension of uterus | Multiple pregnancy, polyhydramnios, macrosomia/LGA baby (> 3800 g) [1][5] — overstretched myometrial fibres cannot contract efficiently |
| Uterine fatigue | Prolonged labour, precipitate labour, induced/augmented labour (oxytocin receptor downregulation) |
| Insensitivity to oxytocin | Grand multiparity (≥ 5 births) [1] — repeated pregnancies → myometrial fibre replacement by connective tissue → less responsive to oxytocin |
| Abnormal myometrium | Fibroids (leiomyomata), previous surgery on uterus (CS scar, myomectomy scar) [1] — disrupt coordinated contraction |
| Infection | Chorioamnionitis — bacterial endotoxins directly inhibit myometrial smooth muscle contraction |
| Drug-induced relaxation | Tocolytics (MgSO₄, nifedipine, terbutaline), volatile anaesthetic agents (sevoflurane, halothane), nitroglycerine |
| Functional | Full bladder (prevents uterine contraction by displacement — always catheterise!) |
When the whole placenta is attached to the uterus and has not yet separated, there is no bleeding and there is no hurry to deliver the placenta. If attempts are made to deliver the placenta e.g. by pulling on the umbilical cord before the placenta has separated, the placenta separates partially. This exposes part of the placental site while the uterus cannot contract well. This causes heavy bleeding. [3][4]
Occasionally, the uterus comes out like a reversed pocket with the attached placenta (uterine inversion), again causing heavy bleeding. [3][4]
Therefore, do not attempt to deliver a placenta which has not separated from the uterine wall yet if there is little bleeding. [3][4]
Critical Safety Point
Never pull on the umbilical cord to force delivery of an unseparated placenta. This can cause:
- Partial placental separation → exposed placental bed bleeds while the still-attached portion prevents uterine contraction → massive PPH
- Uterine inversion → the fundus turns inside-out through the cervix → profound neurogenic shock (vagal stimulation) + haemorrhage
Both are obstetric emergencies. Signs that the placenta has separated include: uterus becomes firm and globular, a gush of blood, cord lengthening, and the uterus rises in the abdomen.
2. TISSUE — Retained Placental Tissue (~10–20% of PPH)
Why does retained tissue cause PPH? The uterus cannot fully contract if something is inside the cavity. Retained tissue acts as a "wedge" that prevents the myometrial walls from coapting — the "living ligature" is incomplete.
| Type | Explanation |
|---|---|
| Retained placental fragments | Cotyledons or membranes left behind — most common "tissue" cause; always inspect the placenta after delivery for completeness |
| Retained whole placenta (> 30 minutes after delivery = "retained placenta") | The placenta has not separated or has separated but is trapped |
| Succenturiate lobe | An accessory lobe of the placenta connected by vessels through the membranes — easy to miss, as it is separate from the main disc |
| Placenta accreta spectrum (PAS) | Abnormally adherent placenta — trophoblast invades beyond the decidua basalis into the myometrium (accreta), through the myometrium (increta), or through the serosa (percreta). Cannot separate normally → massive haemorrhage when attempted |
| Blood clots in the uterine cavity | A large intrauterine clot can prevent contraction — evacuation of the clot restores tone |
- Rising incidence due to ↑ CS rates worldwide (including HK)
- The strongest risk factor is placenta praevia overlying a previous CS scar (the risk of PAS is ~3% with one prior CS + praevia, rising to ~60–70% with ≥3 prior CS + praevia)
- Pathophysiology: deficient decidua basalis at the CS scar → trophoblast has no "stop signal" and invades deeper into the myometrium
- Classification:
- Accreta (78%): adherent to myometrium but does not invade
- Increta (17%): invades into myometrium
- Percreta (5%): penetrates through myometrium and serosa, may invade adjacent organs (bladder most commonly)
Any laceration or injury to the genital tract creates a bleeding source independent of uterine contraction. Even with a well-contracted uterus, a woman can bleed to death from an unrecognised cervical tear.
| Type | Mechanism / Risk Factors |
|---|---|
| Vaginal / perineal tears | Especially 3rd/4th degree tears; instrumental delivery (forceps > vacuum), macrosomia, precipitate delivery |
| Cervical tears | Rapid cervical dilatation, instrumental delivery, pushing before full dilatation |
| Uterine rupture | Previous surgery on uterus (especially classical/high-segment CS — 10% rupture risk in subsequent vaginal delivery) [1]; obstructed labour; excessive oxytocin use; grand multiparity |
| Uterine inversion | Excessive cord traction on an unseparated placenta (iatrogenic); fundal placentation; short cord |
| Episiotomy / surgical site bleeding | Especially if extension occurs during delivery |
| Broad ligament haematoma | Concealed bleeding — may present with shock without visible blood loss |
"Thrombin" here is a catch-all for clotting disorders. Even if the uterus is well-contracted and the tract intact, failure to form stable clot leads to ongoing oozing.
Coagulopathy in PPH can be:
A. Pre-existing (before delivery):
- Inherited bleeding disorders: von Willebrand disease (most common inherited bleeding disorder — prevalence ~1%), haemophilia A carrier, platelet function disorders
- Acquired: thrombocytopenia (ITP, gestational thrombocytopenia), anticoagulant therapy, liver disease
- Bleeding tendencies [5]
B. Acquired during/after delivery:
- Disseminated intravascular coagulation (DIC) — the most feared coagulopathy in obstetrics
- Obstetric causes of DIC (from senior notes [6][7]):
- Amniotic fluid embolism (triggers massive coagulation cascade activation)
- Abruptio placentae (retroplacental blood releases tissue factor)
- Eclampsia / HELLP syndrome (endothelial damage)
- Septic abortion / chorioamnionitis
- Intrauterine fetal death (retained dead fetus releases tissue factor over days–weeks)
- Pathophysiology of DIC [6][7]: release of procoagulant materials (especially tissue factor) into the maternal circulation → widespread intravascular thrombosis → consumption of platelets and clotting factors ("consumption coagulopathy") + secondary fibrinolysis → paradoxical bleeding
- Lab features of acute DIC: ↓ platelets, ↑ PT, ↑ aPTT, ↓ fibrinogen, ↑ D-dimer, schistocytes on PBS (MAHA)
- Obstetric causes of DIC (from senior notes [6][7]):
- Dilutional coagulopathy — from massive fluid resuscitation without blood products; fibrinogen is the first factor to reach critically low levels
- Massive transfusion-related coagulopathy — stored packed RBCs contain no functional platelets or clotting factors; transfusing large volumes without FFP/cryoprecipitate → coagulopathy
Why Is Fibrinogen So Important in PPH?
Fibrinogen (Factor I) is the substrate for fibrin clot formation. In pregnancy, fibrinogen levels are physiologically elevated (~4–6 g/L vs normal 2–4 g/L). During PPH, fibrinogen is consumed rapidly. A fibrinogen level < 2 g/L during PPH is a strong predictor of progression to severe haemorrhage. This is why early cryoprecipitate or fibrinogen concentrate is critical.
| "T" | Cause | Frequency | Primary Mechanism |
|---|---|---|---|
| Tone | Uterine atony | ~70–80% | Failure of myometrial contraction → spiral arteries remain open |
| Tissue | Retained products | ~10–20% | Prevents uterine wall coaptation; retained tissue = wedge preventing full contraction |
| Trauma | Genital tract injury | ~5–10% | Direct vascular injury independent of uterine tone |
| Thrombin | Coagulopathy | ~1–2% | Failure to form/maintain stable clot at placental bed or injury site |
Multiple T's often coexist — e.g., prolonged atony → massive blood loss → dilutional coagulopathy → DIC → further bleeding. Always systematically assess ALL four T's.
Classification
- Primary PPH: within 24 hours (90% of cases)
- Secondary PPH: > 24 hours to 6–12 weeks postpartum
- Causes differ: most commonly endometritis, retained products of conception, subinvolution of placental site, rarely choriocarcinoma
| Category | Blood Loss | Notes |
|---|---|---|
| Minor | 500–1000 mL | Monitor closely; may not need transfusion in healthy women |
| Major (non-massive) | 1000–2000 mL | Activate PPH protocol |
| Major (massive/life-threatening) | > 2000 mL or rate > 150 mL/min, or haemodynamic instability despite resuscitation | Activate massive transfusion protocol; multidisciplinary team |
As detailed above: Tone, Tissue, Trauma, Thrombin.
Clinical Features
This section covers what you will see and hear at the bedside. I'll separate symptoms (what the patient tells you) from signs (what you find on examination), with pathophysiological explanations inline.
| Symptom | Pathophysiological Basis |
|---|---|
| Heavy vaginal bleeding (the cardinal symptom) | Direct blood loss from the uterine placental site (atony, retained tissue) or from genital tract lacerations |
| Passage of blood clots | When blood pools in the uterus/vagina, it clots; passage of large clots suggests significant ongoing haemorrhage |
| Dizziness / lightheadedness | ↓ circulating volume → ↓ cerebral perfusion → pre-syncope |
| Feeling faint / wanting to lie down | Baroreceptor-mediated; the body compensates by wanting to assume a supine position to improve venous return |
| Palpitations | Sympathetic activation → tachycardia to maintain cardiac output despite ↓ preload |
| Breathlessness | ↓ oxygen-carrying capacity (anaemia) + metabolic acidosis from tissue hypoperfusion → stimulates respiratory centre |
| Anxiety / "sense of doom" | Catecholamine surge; also seen in amniotic fluid embolism |
| Abdominal pain (suggests specific cause) | Uterine rupture → sudden severe pain; inverted uterus → acute lower abdominal pain; abruptio placentae → constant, tender uterus |
| Urge to push / feeling of "something coming down" | Uterine inversion → the inverted fundus descends through the cervix into the vagina → sensation of a mass |
| May be asymptomatic initially in young healthy women | Young women have excellent cardiovascular reserve; they may lose 1000–1500 mL before showing obvious haemodynamic compromise — then decompensate suddenly |
Beware the 'Well-Compensated' Young Woman
A healthy 25-year-old parturient can maintain a normal blood pressure despite losing 15–20% of blood volume (~1000–1500 mL in a pregnant woman with expanded blood volume of ~6–7L). The first sign may be subtle tachycardia. Do NOT wait for hypotension — by the time she is hypotensive, she has lost > 30–40% of her blood volume and is in Class III/IV shock.
Signs
These signs correlate with the classification of haemorrhagic shock [8]:
| Class | Blood Loss | Heart Rate | BP | Other Signs |
|---|---|---|---|---|
| I | < 750 mL (< 15%) | Normal or mildly ↑ | Normal | Minimal symptoms |
| II | 750–1500 mL (15–30%) | 100–120 | Normal (maintained by ↑ SVR) | Anxiety, delayed cap refill, pallor |
| III | 1500–2000 mL (30–40%) | 120–140 | ↓ Systolic | Confusion, marked tachycardia, ↓ urine output, cold clammy skin |
| IV | > 2000 mL (> 40%) | > 140 or bradycardia (preterminal) | Severe ↓ | Obtunded, anuria, imminent cardiac arrest |
Specific signs of hypovolaemia [8]:
- Tachycardia: earliest compensatory sign — sympathetic activation → ↑ HR to maintain cardiac output (CO = HR × SV)
- Hypotension: late sign — means compensatory mechanisms are overwhelmed
- Pallor: sympathetic vasoconstriction shunts blood from skin to vital organs
- Cold, clammy extremities: peripheral vasoconstriction + sweating from sympathetic activation
- Delayed capillary refill (> 2 seconds): poor peripheral perfusion
- Collapsed / empty peripheral veins: ↓ circulating volume
- Oliguria (< 0.5 mL/kg/hr): renal hypoperfusion → ↓ GFR → ↓ urine output
- Altered mental status: confusion → drowsiness → unconsciousness as cerebral perfusion falls
- Tachypnoea: metabolic acidosis (lactic acid from anaerobic tissue metabolism) → respiratory compensation
| Sign | What It Tells You | Pathophysiology |
|---|---|---|
| Soft, "boggy," enlarged uterus (above the umbilicus) | Uterine atony — the #1 cause | The uterus has not contracted; it is distended with blood. Normally, the postpartum uterus should be firm, globular, and at or below the umbilicus. A boggy uterus = the "living ligature" is not working. |
| Firm, well-contracted uterus but still bleeding | The bleeding source is NOT atony → think Trauma or Thrombin | If the uterus is hard and contracted, the spiral arteries should be compressed. Ongoing bleeding must come from a genital tract laceration or coagulopathy. |
| Uterine fundal height rising | Blood is collecting inside the uterus (concealed haemorrhage) | The uterus fills with clot and blood; it may appear to contract but is actually distending |
| Tender, rigid uterus (Couvelaire uterus) | Placental abruption | Retroplacental haemorrhage infiltrates the myometrium → woody hard uterus that does not relax between contractions |
| Uterus not palpable abdominally + mass in vagina | Uterine inversion | The fundus has inverted through the cervix; the "dimple sign" (absent fundus on abdominal palpation) is pathognomonic |
| Sign | Significance |
|---|---|
| Continuous bright-red bleeding despite a well-contracted uterus | Genital tract trauma (cervical/vaginal tear) — must examine under adequate light and analgesia |
| Visible perineal / vaginal tear | Trauma — classify degree (1st–4th) |
| Cervical tear (seen on speculum examination) | Often at 3 or 9 o'clock position; can extend into the lower uterine segment |
| Foul-smelling discharge, fever (in secondary PPH) | Endometritis / retained infected products |
| Non-clotting blood | Coagulopathy — blood that oozes and doesn't form clots at IV sites, wound edges, or from the vagina suggests DIC or severe hypofibrinogenaemia |
| Cause | Specific Signs |
|---|---|
| Amniotic fluid embolism | Sudden cardiovascular collapse, respiratory distress, DIC, seizures — often during or shortly after delivery; extremely high mortality |
| Uterine rupture | Sudden severe abdominal pain, loss of fetal station, cessation of contractions, easily palpable fetal parts abdominally, haematuria (if bladder involved) |
| Uterine inversion | Neurogenic shock (vagal — bradycardia + hypotension out of proportion to blood loss), mass protruding from vagina, fundus not palpable abdominally |
| DIC | Oozing from IV sites, bruising, petechiae, haematuria, non-clotting blood |
| Broad ligament haematoma | Shock with minimal visible blood loss ("concealed haemorrhage"), unilateral pelvic mass, lateral deviation of uterus |
Concealed vs Revealed Haemorrhage
Not all PPH is visible. Blood can collect in:
- The uterus (atony with cervical/lower segment clot obstruction)
- The broad ligament (haematoma)
- The peritoneal cavity (uterine rupture)
Always correlate the degree of shock with the visible blood loss. If the patient looks worse than the blood loss suggests → think concealed haemorrhage.
High Yield Summary
Definition: PPH = blood loss >= 1000 mL or signs/symptoms of hypovolemia within 24 hours after delivery, regardless of mode of delivery. Treat if symptomatic/shocked regardless of measured loss. [1][2][3]
Classification: Primary (within 24 hours, 90% of cases) vs Secondary (> 24 hours). [1][2]
Aetiology — 4 T's (in order of frequency): Tone (~70–80%), Tissue (~10–20%), Trauma (~5–10%), Thrombin (~1–2%). [1][2]
Key Mechanism: The "living ligature" — criss-cross myometrial fibres compress spiral arteries at the placental bed. Failure of this mechanism (uterine atony) is the #1 cause of PPH.
Risk Factors: Overdistension (multiple pregnancy, polyhydramnios, macrosomia), grand multiparity, abnormal myometrium (fibroids, previous uterine surgery), induced/augmented labour, low-lying placenta, bleeding tendencies, anaemia, antepartum haemorrhage.
The upper segment is the main contractile force; low-segment CS does NOT contraindicate future vaginal delivery; classical CS carries ~10% rupture risk. [1]
Never pull on the umbilical cord of an unseparated placenta — causes partial separation (PPH) or uterine inversion. [3][4]
Clinical Features: Boggy, atonic uterus → atony; firm uterus + continued bleeding → trauma or coagulopathy; non-clotting blood → DIC/thrombin; absent fundus + vaginal mass → uterine inversion. Beware concealed haemorrhage and the "well-compensated" young woman who decompensates suddenly.
Active Recall - Postpartum Haemorrhage (Definition, Epidemiology, Aetiology, Clinical Features)
[1] Lecture slides: Block C - Postpartum Haemorrhage.pdf (definition, risk factors, 4T classification, summary) [2] Lecture slides: PPH for teaching (20210716)v6.pdf (definition, risk factors, summary) [3] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (introduction, definition, causes of primary PPH, iatrogenic causes) [4] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf (introduction, definition, causes of primary PPH, iatrogenic causes) [5] Lecture slides: PPH for teaching (20210716)v6.pdf p6 (risk factor list) [6] Senior notes: Maksim Medicine Notes.pdf p165 (DIC pathophysiology, obstetric causes, lab features) [7] Senior notes: Ryan Ho Haemtology.pdf p136–138 (DIC causes, pathogenesis, acute vs chronic DIC, management) [8] Senior notes: Ryan Ho Critical Care.pdf p21 (hypovolaemic shock causes, clinical features, management)
Differential Diagnosis of Postpartum Haemorrhage
When a woman is bleeding after delivery, you don't just shout "PPH!" — you need to identify the specific cause because the management differs radically for each. A boggy atonic uterus needs uterotonics; a cervical tear needs suturing; DIC needs blood products. The wrong treatment for the wrong cause wastes precious minutes and can kill.
Differential diagnosis including the 4 T's — Tone, Tissue, Trauma, Thrombin. [1][2]
The 4 T's framework is not just an aetiology list — it is your systematic diagnostic algorithm at the bedside. You work through them in order of frequency, systematically excluding each one.
Key Diagnostic Principle
The single most important bedside manoeuvre is to palpate the uterine fundus. If it is soft and boggy → uterine atony (the #1 cause, ~70–80%). If it is firm and well-contracted but bleeding continues → you MUST look elsewhere: trauma, retained tissue, or coagulopathy. Multiple T's can coexist — always check all four systematically.
Detailed Differential Diagnosis by Category
| Differential | Key Distinguishing Features | Why It Causes Bleeding |
|---|---|---|
| Uterine atony (primary/idiopathic) | Soft, boggy, enlarged uterus palpable above umbilicus; often with identifiable risk factors (overdistension, grand multiparity, prolonged labour) | The "living ligature" fails — myometrial fibres don't compress the spiral arteries at the placental bed → free-flowing haemorrhage from open vessels |
| Drug-induced uterine relaxation | History of MgSO₄ (for pre-eclampsia/eclampsia), volatile GA agents (sevoflurane), tocolytics (nifedipine, terbutaline) | These agents directly relax smooth muscle → same mechanism as atony above; the pharmacological effect opposes myometrial contraction |
| Full bladder | Distended bladder palpable suprapubically; uterus deviated to one side | A full bladder mechanically displaces and prevents the uterus from contracting effectively; simple catheterisation may resolve the "atony" — always catheterise first! |
The lecture slide exam question [M27_R1(23)_Q2] identifies twin pregnancy and uterine fibroids as risk factors for PPH in a case of uterine atony — both cause overdistension and abnormal myometrium respectively. [3]
| Differential | Key Distinguishing Features | Why It Causes Bleeding |
|---|---|---|
| Retained placental fragments / cotyledons | Placenta inspection shows missing cotyledon(s) or ragged membranes; uterus may be suboptimally contracted | Retained tissue acts as a physical "wedge" preventing complete uterine contraction + the retained vascular tissue itself continues to bleed from exposed maternal vessels at the attachment site |
| Retained whole placenta (> 30 min post-delivery) | Placenta has not delivered; cord may be visible at introitus; no signs of separation (no gush of blood, no cord lengthening, no fundal rise) | If the whole placenta is still attached, it's usually not bleeding yet (vessels still compressed by intact attachment). But if partially separated → exposed bed bleeds while the remaining attached portion prevents contraction |
| Succenturiate lobe | Main placenta appears complete but there is a separate accessory lobe connected by membrane vessels; inspect membranes for torn vessels at the margin (suggests a missing accessory lobe) | Same mechanism — retained vascular tissue in the cavity |
| Placenta accreta spectrum (accreta / increta / percreta) | Failure to separate despite controlled cord traction; manual removal attempts encounter a plane-less attachment; history of prior CS with anterior low-lying placenta | Trophoblast has invaded through deficient decidua basalis into myometrium → no natural cleavage plane → attempted removal causes massive haemorrhage from torn myometrial vessels |
| Intrauterine blood clots | Uterus appears large/boggy but expels large clots on massage; may be confused with atony | Large clots filling the uterine cavity prevent wall coaptation → the clot itself acts as retained "tissue" preventing contraction → vicious cycle |
This category is the key differential when the uterus is firm and well-contracted but bleeding continues — the bleeding source must be somewhere other than the placental bed.
| Differential | Key Distinguishing Features | Why It Causes Bleeding |
|---|---|---|
| Vaginal / perineal lacerations | Visible tear on inspection; bright red bleeding; history of instrumental delivery, macrosomia, precipitate delivery | Direct vascular injury — torn vessels bleed independently of uterine tone |
| Cervical tear | Well-contracted uterus + ongoing bright red bleeding; found on speculum examination (classically at 3 or 9 o'clock); often after rapid cervical dilatation or instrumental delivery | The cervix is highly vascular during pregnancy; tears can extend into the lower uterine segment and involve branches of the uterine artery → arterial-type bleeding |
| Uterine rupture | Sudden severe abdominal pain (may have preceded delivery), maternal tachycardia/shock, easily palpable fetal parts through abdomen, haematuria; history of previous surgery on uterus (classical CS has ~10% rupture risk) [1]; may see cessation of contractions | Full-thickness myometrial tear → blood flows into the peritoneal cavity (often concealed) and/or through the vagina → haemorrhagic shock |
| Uterine inversion | Uterus comes out like a reversed pocket [4][5]; fundus not palpable abdominally ("dimple sign"); fleshy mass in vagina; neurogenic (vagal) shock with bradycardia and hypotension disproportionate to blood loss | The inverted fundus drags the placental bed surface outside-in → exposed vessels bleed; simultaneously, traction on the peritoneum and round ligaments triggers a profound vasovagal response |
| Episiotomy extension / haematoma | Localised swelling, pain, discolouration at episiotomy site; may be vulval, paravaginal, or retroperitoneal | Unrecognised bleeding vessel at the surgical site; paravaginal haematoma can be concealed and massive |
| Broad ligament haematoma | Shock disproportionate to visible blood loss; unilateral pelvic mass on examination; lateral deviation of uterus | Concealed haemorrhage — blood tracks into the broad ligament from uterine/cervical vessel injury |
The exam question [M27_R1(22)_Q3] presents a patient after twin CS with total blood loss 2.6L, complete placenta, well-contracted uterus, but profuse vaginal bleeding in recovery → answer is Coagulopathy (A) — demonstrating that when Tone and Tissue are excluded, you must consider Trauma and Thrombin. In that case, massive blood loss likely caused dilutional/consumptive coagulopathy. [3]
Coagulopathy should be suspected when blood is non-clotting, there is oozing from IV sites or wound edges, and the other 3 T's have been addressed. It can be pre-existing or develop secondary to massive haemorrhage from any cause.
| Differential | Key Distinguishing Features | Why It Causes Bleeding |
|---|---|---|
| DIC (most feared obstetric coagulopathy) | Clinical setting: amniotic fluid embolism, placental abruption, eclampsia/HELLP, sepsis, IUFD; Lab: ↓ platelets, ↑ PT, ↑ aPTT, ↓ fibrinogen, ↑ D-dimer, schistocytes on PBS [6][7] | Release of procoagulant material (tissue factor from placenta/amniotic fluid) → widespread intravascular coagulation → consumption of platelets and clotting factors → paradoxical bleeding ("consumption coagulopathy") + secondary fibrinolysis [6][7] |
| Dilutional coagulopathy | Occurs after massive crystalloid/colloid resuscitation without balanced blood product replacement; fibrinogen is the first factor to fall critically | Large-volume fluid replacement dilutes circulating clotting factors and platelets below the haemostatic threshold → cannot form stable clots |
| Massive transfusion coagulopathy | After > 10 units pRBC without FFP/cryoprecipitate/platelets; stored pRBCs contain no functional platelets or clotting factors | Same dilutional mechanism + citrate in stored blood chelates calcium (Ca²⁺ is Factor IV, essential for coagulation cascade) → further impairment |
| Pre-existing bleeding disorders | History of easy bruising, menorrhagia, family history; vWD (most common inherited bleeding disorder, ~1% prevalence, AD/AR), haemophilia carriers | Impaired primary haemostasis (vWD, platelet disorders) or secondary haemostasis (factor deficiencies) → cannot form adequate plug/clot at placental bed [8] |
| HELLP syndrome | Haemolysis (↑ LDH, ↑ bilirubin, schistocytes), Elevated Liver enzymes, Low Platelets; in the context of pre-eclampsia; RUQ pain, nausea | Secondary TMA with endothelial damage → thrombocytopenia (consumption in microvasculature) → both thrombotic and bleeding tendency [7][9] |
| Acquired factor deficiencies | Rare; autoantibodies against clotting factors (most commonly Factor VIII — "acquired haemophilia A"); classically described postpartum or with autoimmune disease [10] | Autoantibodies neutralise clotting factors → factor activity drops → bleeding from deep tissues, retroperitoneal haematoma, surgical sites |
| Anticoagulant use | History of LMWH, warfarin, DOACs for conditions like mechanical heart valve, VTE prophylaxis | Pharmacological inhibition of coagulation cascade → impaired clot formation |
Acquired Haemophilia A — A Rare But Important Postpartum Diagnosis
Acquired haemophilia A (autoantibodies against Factor VIII) is classically described as postpartum or associated with autoimmune disease [10]. It typically presents days to weeks after delivery with unexpected deep tissue bleeding (retroperitoneal haematoma, compartment syndrome) rather than the typical mucocutaneous bleeding of platelet disorders. Suspect it when aPTT is prolonged, does not correct with mixing study, and Factor VIII activity is very low. It is rare but carries high morbidity if missed.
| Feature | Tone (Atony) | Tissue (Retained) | Trauma (Injury) | Thrombin (Coagulopathy) |
|---|---|---|---|---|
| Uterine fundus | Soft, boggy, enlarged | May be soft (retained tissue prevents contraction) or subinvoluted | Firm, well-contracted | Usually firm (unless concurrent atony) |
| Blood character | Dark red, gushing, with clots | Similar to atony; may see tissue fragments | Bright red, continuous stream | Non-clotting blood; generalised ooze |
| Placenta inspection | Complete | Incomplete; missing cotyledon or ragged membranes | Complete | Complete |
| Genital tract exam | No tears | No tears | Visible tear / laceration | No tears (unless combined) |
| Bleeding from other sites | No | No | No | Yes — IV sites, wound edges, mucosal surfaces |
| Response to uterotonics | Improves (at least transiently) | Partial/no response until tissue removed | No response | No response |
| Lab findings | Normal clotting initially | Normal clotting | Normal clotting | ↓ Plt, ↑ PT/aPTT, ↓ fibrinogen, ↑ D-dimer |
When bleeding occurs > 24 hours after delivery, the differential shifts. The 4 T's still apply conceptually, but the relative frequencies change:
| Cause | Features | Why |
|---|---|---|
| Endometritis (most common cause of secondary PPH) | Fever, uterine tenderness, cervical excitation, foul-smelling lochia; temperature 38°C, cervical excitation and uterine tenderness on pelvic examination [3] | Infected uterine cavity → inflammation prevents involution → subinvolution of placental bed vessels → late bleeding; infection also breaks down early clot at placental site |
| Retained products of conception | Incomplete involution, ongoing bleeding, USS showing echogenic material in cavity | Same as primary — tissue prevents full contraction and acts as a nidus for infection |
| Subinvolution of the placental site | Prolonged lochia beyond expected, no fever, USS may show enlarged uterus with abnormal vascularity | The spiral arteries at the placental bed fail to undergo normal thrombosis and fibrosis → they remain patent and continue to bleed |
| Gestational trophoblastic disease (rare) | Persistently elevated β-hCG after delivery; USS shows abnormal uterine echogenicity | Residual trophoblastic tissue remains vascular and continues to grow |
| Pseudoaneurysm of uterine artery (rare) | Intermittent heavy bleeding; diagnosed on Doppler USS | Post-traumatic (CS or instrumentation) → weakened arterial wall forms pseudoaneurysm → ruptures intermittently |
The exam question [M27_R1(23)_Q7] presents a patient 5 days post-CS with increased vaginal bleeding, temperature 38°C, cervical excitation and uterine tenderness → most likely diagnosis is Endometritis (secondary PPH). [3]
Primary vs Secondary PPH — Quick DDx Rule
- Primary PPH (within 24h): Tone > Tissue > Trauma > Thrombin (the classic 4 T's in order of frequency)
- Secondary PPH (> 24h): Endometritis > Retained products > Subinvolution > Rare causes (GTD, pseudoaneurysm)
Don't confuse them in exam scenarios! Pay close attention to the timing stated in the question stem.
Let me walk you through the reasoning process the lectures expect, using actual exam questions:
Scenario 1 [3]: 38-year-old G1P0, elective CS for twins, delivered uneventfully, total blood loss 2.6L requiring transfusion. Twin 1: 2.3 kg, Twin 2: 2.4 kg. Placenta checked and complete. Subsequently develops profuse vaginal bleeding in recovery. Uterus well-contracted.
Step-by-step reasoning:
- Tone? → Uterus well-contracted → Atony excluded
- Tissue? → Placenta checked and complete → Retained products excluded
- Trauma? → Possible but this was a CS (no vaginal instrumentation) and delivery was uneventful → less likely as primary cause
- Thrombin? → She lost 2.6L (massive haemorrhage!) requiring transfusion → massive blood loss causes dilutional and consumptive coagulopathy → Answer: Coagulopathy (A)
Scenario 2 [3]: 20-year-old with PPH due to uterine atony. Given syntometrine, IV oxytocin, IV tranexamic acid, PR misoprostol, two doses IM carboprost. Uterine contraction improved but ongoing slow vaginal bleeding.
Reasoning:
- Atony has been treated — contraction improved
- But still bleeding → Must exclude Tissue and Trauma
- Next step: Examination under anaesthesia in theatre (A) — to inspect the genital tract for lacerations and explore the uterine cavity for retained tissue [3]
Scenario 3 [3]: 38-year-old G1P0 with twin pregnancy and uterine fibroids (6 cm anterior wall), emergency LSCS for breech, uterine atony with 1000 mL blood loss. Which are risk factors for PPH?
- Twin pregnancy → overdistension [1]
- Uterine fibroids → abnormal myometrium [1]
- Answer: Twin pregnancy and uterine fibroids (B) [3]
- Note: PPROM and advanced maternal age are NOT established risk factors for uterine atony specifically (though age is a general PPH risk factor)
| Condition | Why It Mimics PPH | How to Differentiate |
|---|---|---|
| Concealed abruption (if occurs before delivery) | Shock without proportionate visible bleeding | Woody-hard, tender uterus; fetal distress; often coexists with DIC |
| Amniotic fluid embolism | Sudden cardiovascular collapse ± DIC during or after delivery | Acute onset dyspnoea, hypoxia, cardiovascular collapse, seizures → then DIC develops; diagnosis of exclusion |
| Uterine artery pseudoaneurysm | Intermittent heavy vaginal bleeding post-CS | Delayed presentation; Doppler USS diagnostic |
| Return of menses (vs secondary PPH) | Vaginal bleeding weeks postpartum | Normal lochia pattern has resolved and then recurs cyclically; no fever, no tenderness; β-hCG negative |
High Yield Summary
The 4 T's are both the aetiological framework AND the diagnostic algorithm for PPH:
- Tone (70–80%) → Soft, boggy uterus → Uterotonics
- Tissue (10–20%) → Incomplete placenta → Manual removal / Evacuation
- Trauma (5–10%) → Firm uterus + bright red bleeding → Inspect genital tract → Surgical repair
- Thrombin (1–2%) → Non-clotting blood, oozing from multiple sites → Blood products
The key bedside manoeuvre: Palpate the uterine fundus. Soft/boggy = atony. Firm = look for trauma or coagulopathy.
When uterus is well-contracted, placenta is complete, but bleeding continues → think Trauma and Thrombin. Massive blood loss from any cause can lead to secondary coagulopathy (dilutional + consumptive) → always check clotting.
Secondary PPH (> 24 hours): Think endometritis first (fever + uterine tenderness + cervical excitation), then retained products, then subinvolution.
Multiple T's coexist — always check ALL four systematically, even if you find one cause.
Active Recall - Differential Diagnosis of PPH
References
[1] Lecture slides: Block C - Postpartum Haemorrhage.pdf (4T classification, risk factor classification, upper/lower segment physiology) [2] Lecture slides: PPH for teaching (20210716)v6.pdf (summary, 4T classification) [3] Lecture slides: OBGYN Clinical Test By Topic.pdf p11–12 (exam questions on PPH differential diagnosis, coagulopathy, endometritis, risk factors) [4] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (uterine inversion, iatrogenic causes) [5] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf (causes of primary PPH, uterine inversion) [6] Senior notes: Maksim Medicine Notes.pdf p165 (DIC aetiology, pathophysiology, lab features) [7] Senior notes: Ryan Ho Haemtology.pdf p136–138 (DIC causes, pathogenesis, acute vs chronic DIC, MAHA/TMA terminology) [8] Senior notes: Maksim Medicine Notes.pdf p160–161 (platelet vs clotting disorder differentiation, clotting cascade interpretation) [9] Senior notes: Ryan Ho Haemtology.pdf p137 (HELLP as secondary TMA) [10] Senior notes: Ryan Ho Haemtology.pdf p123 (acquired haemophilia A — classically postpartum)
Diagnostic Criteria and Algorithm for Postpartum Haemorrhage
Unlike many medical conditions (e.g., SLE with ACR/EULAR criteria, or DIC with ISTH scoring), PPH does not have a formal "diagnostic criteria" scoring system. The diagnosis is made on the basis of:
- Quantitative blood loss exceeding the threshold
- Clinical assessment of haemodynamic status
- Systematic identification of the cause using the 4 T's
This makes sense from first principles: PPH is an emergency. You cannot wait for lab results or imaging to make the diagnosis — a woman can exsanguinate in minutes from uterine atony. The diagnosis is made at the bedside, with your hands and eyes, and treatment begins simultaneously with investigation.
PPH is defined as blood loss >= 1000 mL or signs/symptoms of hypovolemia within 24 hours after delivery, regardless of mode of delivery. [1][2]
For clinical purposes, even if the estimated blood loss is below the numeric threshold, treatment should be initiated if the patient has symptoms or signs of shock. [3][4]
Treat the Patient, Not the Number
Visual estimation of blood loss underestimates true loss by 30–50%. A soaked maternity pad holds ~100 mL; a soaked surgical drape can hide over a litre. Quantitative blood loss measurement (QBL) — using graduated drapes, weighing swabs (1 g = 1 mL blood) — improves accuracy but is not universally practiced. In practice, if the patient looks shocked, treat as PPH regardless of the estimated volume.
The lecture notes lay out a clear, stepwise approach to identifying the source of bleeding [5]:
Identifying the source of bleeding: [5]
- Palpate the uterus to check if it is contracting well.
- Vaginal examination systematically from cervix down to introitus to identify lower genital tract bleeding (local, regional or general anaesthesia).
- Check the placenta for completeness (if it has been delivered).
- Arrange emergency operation for examination under anaesthesia. Explore the inside of the uterus to check for retained placenta, rupture of the uterus (usually done through the cervix, does not require laparotomy, but regional or general anaesthesia required).
- Laparotomy is required in exceptional circumstances when the source of bleeding cannot be identified or to stop the bleeding.
(Always do 1–3. Do 4 if 1–3 fail to identify the source of bleeding and the bleeding persists. 4 is seldom needed and when needed, is more often for stopping the bleeding.) [5]
This is the core diagnostic algorithm for your exam. Notice it follows the 4 T's in order: Tone → Trauma → Tissue → then EUA/Laparotomy for deeper causes.
Key Exam Point — The Stepwise Approach
Always do Steps 1–3 (fundal palpation, genital tract inspection, placenta check). Step 4 (EUA) is performed if Steps 1–3 fail to identify the source and bleeding persists. Step 5 (laparotomy) is seldom needed and is more often for stopping the bleeding than for diagnosis. [5]
In the exam question where a patient has had all uterotonics but still has ongoing slow bleeding with improved uterine contraction, the next most appropriate action is Examination Under Anaesthesia in theatre (EUA) — to systematically inspect the cervix, vagina, and explore the uterine cavity. [6]
Investigation Modalities
Investigations in PPH serve three purposes simultaneously:
- Assess the severity of blood loss and haemodynamic compromise
- Identify the cause (which T?)
- Monitor response to resuscitation and treatment
Investigations run in parallel with resuscitation — never delay treatment to wait for results.
| Investigation | Key Findings | Interpretation / Why We Do This |
|---|---|---|
| Uterine fundal palpation | Soft/boggy vs firm/contracted | THE most important bedside test — distinguishes atony (70–80% of PPH) from other causes in seconds. A boggy fundus = failure of the "living ligature" |
| Placenta inspection | Complete vs missing cotyledon/ragged membranes | A missing cotyledon means retained tissue in the uterine cavity → this tissue prevents full contraction and continues to bleed. Inspect both maternal surface (cotyledons) and fetal surface (membranes, vessels for succenturiate lobe) |
| Genital tract inspection | Perineal/vaginal/cervical tears | Requires adequate lighting, analgesia (often regional/GA), and systematic approach: cervix (speculum) → vaginal walls → perineum. A cervical tear missed at the bedside is a classic cause of "unexplained" ongoing PPH |
| Vital signs monitoring | BP, HR, SpO₂, RR, temperature, GCS | Tachycardia is the earliest sign of haemorrhage — appears before hypotension. Remember: young healthy women compensate well → a normal BP does NOT exclude significant blood loss [7] |
| Urine output (Foley catheter) | Oliguria < 0.5 mL/kg/hr | Renal hypoperfusion → ↓ GFR → ↓ UO. Also, emptying the bladder is therapeutic — a full bladder prevents uterine contraction! Two birds with one catheter. [7] |
| Quantitative blood loss (QBL) | Weigh swabs, graduated drapes, suction volume | More accurate than visual estimation. 1 g weight gain = 1 mL blood. Cumulative blood loss guides transfusion decisions |
| Bedside clot test | Place 5 mL blood in a red-top tube → observe at 7–10 minutes | If the blood fails to clot, or clots then lyses within 30 min → suggestive of coagulopathy/DIC/hypofibrinogenaemia. A rapid, no-cost bedside screen — especially useful in resource-limited settings |
Monitoring and investigation should be performed alongside resuscitation. [5] The lecture notes on shock assessment [7][8] guide the core blood panel:
| Investigation | Key Findings in PPH | Interpretation |
|---|---|---|
| CBC/FBC | ↓ Hb, ↓ Hct; ↓ platelets (if DIC or dilutional) | Hb may be initially normal in acute haemorrhage! Why? Because both red cells and plasma are lost proportionally — the Hb concentration doesn't change until compensatory haemodilution occurs (fluid shifts from interstitium to intravascular, or IV fluids are given). A "normal" Hb in the first hour does NOT exclude major blood loss. Serial Hb at 2–4 hours is more informative. Thrombocytopenia suggests DIC or dilutional effect [8][9] |
| Group and Screen / Type and Screen | ABO group, Rh type, antibody screen | Essential for blood product availability. In an emergency, give O-negative pRBCs if crossmatch not yet available. Always send this EARLY — crossmatching takes 45–60 minutes |
| Crossmatch | Prepare compatible pRBC units | Request 4–6 units initially for major PPH; activate massive transfusion protocol (MTP) if massive PPH |
| Coagulation profile: PT, aPTT, fibrinogen | ↑ PT, ↑ aPTT → consumed clotting factors; ↓ fibrinogen → critical predictor | Fibrinogen < 2 g/L is the strongest single predictor of progression to severe PPH (sensitivity ~100%). In pregnancy, normal fibrinogen is 4–6 g/L; a level of 2 g/L that would be "normal" in a non-pregnant patient is actually dangerously low in a parturient [8][9] |
| D-dimer | ↑↑ (if DIC) | D-dimer is a fibrin degradation product. In DIC, widespread clotting → widespread fibrinolysis → massively elevated D-dimer. However, D-dimer is physiologically elevated in pregnancy and post-delivery, so it is less specific — interpret alongside other clotting parameters |
| Blood film / PBS | Schistocytes (fragmented RBCs) | Schistocytes = microangiopathic haemolytic anaemia (MAHA) → suggests DIC, TTP, HELLP. The RBCs are sheared as they pass through fibrin strands deposited in small vessels [9][10] |
| Renal function tests (RFT: urea, creatinine, electrolytes) | ↑ Urea/Creatinine → AKI; ↑ K⁺ | Hypovolaemic shock → renal hypoperfusion → pre-renal AKI. Also needed as baseline before potential massive transfusion (citrate in stored blood binds Ca²⁺; K⁺ leaks from stored RBCs) [7] |
| Liver function tests (LFT) | ↑ ALT/AST → shock liver or HELLP; ↑ LDH → haemolysis | "Shock liver" = acute hepatic hypoperfusion → transaminase rise. In HELLP: elevated LDH (haemolysis marker) + elevated AST + low platelets. Always check LFT to exclude HELLP as the underlying cause [7] |
| Venous/Arterial blood gas + Lactate | Metabolic acidosis (↓ pH, ↓ HCO₃⁻, ↑ lactate); ↓ base excess | Lactate rises when tissues switch to anaerobic metabolism due to poor oxygen delivery → lactic acidosis. Lactate > 4 mmol/L in the context of PPH indicates severe tissue hypoperfusion and impending decompensation. Serial lactate measurements guide resuscitation adequacy [7] |
Interpreting the Clotting Profile — A Recap from First Principles [8]
| PT | aPTT | What It Means | PPH Context |
|---|---|---|---|
| ↑ | Normal | Extrinsic pathway defect (Factor VII) | Early DIC (Factor VII has shortest half-life ~6h, so is consumed first) |
| Normal | ↑ | Intrinsic pathway defect (Factors VIII, IX, XI, XII) | vWD, haemophilia carrier, lupus anticoagulant, heparin effect |
| ↑ | ↑ | Common pathway (Factors V, X, II) or multiple pathway defect | Established DIC, massive transfusion dilution, severe liver disease |
| Normal | Normal | Normal coagulation — but doesn't exclude platelet dysfunction or fibrinolytic disorders | Quantitative platelet and fibrinogen levels are needed separately |
The DIC Lab Pattern — 'Full House' Clotting
DIC classically shows 'full house' clotting parameters: ↓ platelet, ↑ PT/aPTT, ↑ D-dimer, ↓ fibrinogen [9][10], but seldom all present simultaneously. In the obstetric setting, the ISTH DIC scoring system can be used:
| Parameter | 0 points | 1 point | 2 points |
|---|---|---|---|
| Platelet count | > 100 | 50–100 | < 50 |
| D-dimer | No increase | Moderate increase | Strong increase |
| Prolonged PT | < 3 sec | 3–6 sec | > 6 sec |
| Fibrinogen | > 1 g/L | < 1 g/L | — |
Score ≥ 5 = compatible with overt DIC. Repeat daily. In pregnancy, use the modified obstetric DIC score as pregnancy physiologically alters these values (↑ fibrinogen, ↑ D-dimer).
| Test | What It Tells You | Why It's Valuable in PPH |
|---|---|---|
| Thromboelastography (TEG) / Rotational thromboelastometry (ROTEM) | Viscoelastic assessment of whole blood clot formation and lysis in real-time; measures clot initiation, propagation, strength, and fibrinolysis | Provides a functional, real-time picture of the coagulation status within 10–15 minutes — much faster than conventional lab clotting times (which take 30–60 min). Guides targeted blood component therapy: low clot strength → give fibrinogen/cryoprecipitate; evidence of fibrinolysis → give TXA; prolonged initiation → give FFP |
| Point-of-care Hb (HemoCue) | Rapid bedside Hb estimation | Useful for immediate triage; however, same caveat — initial Hb may not reflect acute blood loss |
| iSTAT / blood gas analyser | Rapid lactate, pH, base excess, ionised Ca²⁺, K⁺ | Ionised Ca²⁺ is critical: citrate in transfused blood chelates calcium → hypocalcaemia → impaired coagulation (Ca²⁺ is required for multiple steps in the clotting cascade) AND impaired cardiac contractility |
ROTEM/TEG in Massive Obstetric Haemorrhage
Modern obstetric haemorrhage protocols increasingly incorporate ROTEM/TEG-guided transfusion. The key advantage is speed and specificity:
- FIBTEM A5 < 12 mm → give fibrinogen concentrate or cryoprecipitate (low functional fibrinogen)
- EXTEM CT > 75 sec → give FFP (prolonged clot initiation)
- EXTEM ML > 15% → give tranexamic acid (hyperfibrinolysis)
This replaces the "blind" empirical approach of giving FFP:pRBC at fixed ratios and allows targeted, faster correction.
Imaging is not first-line in acute primary PPH (this is a clinical and surgical diagnosis). However, imaging has specific roles:
| Modality | Indication | Key Findings |
|---|---|---|
| Transabdominal ultrasound (TAUS) | Suspected retained products; unclear uterine contents; secondary PPH evaluation | Echogenic/heterogeneous material within the uterine cavity suggests retained tissue. A "normal" empty cavity with thin endometrial stripe makes retained products unlikely. Endometrial thickness > 10 mm post-delivery is suggestive |
| Transvaginal ultrasound (TVUS) | Better resolution for retained products, subinvolution, uterine artery pseudoaneurysm | More sensitive than TAUS for small retained fragments; Colour Doppler shows vascularity of retained tissue (feeding vessels = PAS/accreta) or swirling "yin-yang" pattern of pseudoaneurysm |
| Colour Doppler ultrasound | Suspected placenta accreta spectrum (antenatal); uterine artery pseudoaneurysm (postnatal) | Antenatal: loss of clear retroplacental zone, "Swiss cheese" lacunae in placenta, myometrial thinning, bladder wall interruption. Postnatal: pseudoaneurysm shows to-and-fro flow |
| CT angiography (CTA) | Haemodynamically stable patient with ongoing bleeding from uncertain source; suspected broad ligament haematoma; retroperitoneal bleeding | Active contrast extravasation ("blush") identifies the bleeding point — guides interventional radiology embolisation. Useful for concealed bleeding (broad ligament haematoma, retroperitoneal haematoma) that cannot be seen on vaginal exam |
| MRI pelvis | Rarely used acutely; antenatal planning for suspected PAS; secondary PPH evaluation | Superior soft tissue contrast for mapping depth of placental invasion in PAS (accreta vs increta vs percreta). Not practical in acute emergency |
| Procedure | Indication | Key Findings |
|---|---|---|
| Examination Under Anaesthesia (EUA) in theatre | When Steps 1–3 fail to identify the source and bleeding persists [5][6] | Allows thorough cervical and vaginal inspection under optimal conditions (good light, relaxation, retractors). Manual exploration of the uterine cavity can identify: retained tissue (felt as rough/spongy areas vs smooth myometrium), uterine rupture (finger passes through myometrial defect into peritoneal cavity), placenta accreta (no cleavage plane) |
| Laparotomy | Required in exceptional circumstances when the source of bleeding cannot be identified or to stop the bleeding [5] | Direct visualisation of uterus, adnexae, broad ligament → identify uterine rupture site, broad ligament haematoma, bleeding vessels. Also the route for definitive surgical management (B-Lynch suture, uterine artery ligation, hysterectomy) |
| Interventional radiology angiography | Haemodynamically stable or stabilised patient with ongoing bleeding; complements or replaces laparotomy in selected cases | Fluoroscopy-guided selective catheterisation of uterine/internal iliac arteries → identifies active extravasation ("blush") → allows therapeutic embolisation in the same session [11] |
4 major principles in the management of PPH: [5]
- Communication with all relevant professionals
- Resuscitation
- Monitoring and investigation
- Arresting the bleeding
This should be monitored with blood pressure, pulse rate, urine output, central venous pressure, laboratory haematology tests. [5]
The key concept is parallelism — you do NOT investigate first then treat. You resuscitate AND investigate AND treat concurrently:
Since the diagnosis of PPH hinges on a quantitative threshold, accurate blood loss estimation matters. Here are the approaches:
| Method | Description | Accuracy |
|---|---|---|
| Visual estimation | Clinician eyeballs the blood on drapes, pads, floor | Underestimates by 30–50%; very poor for large volumes |
| Gravimetric (weighing) | Weigh soaked swabs/drapes; subtract dry weight; 1 g = 1 mL | More accurate; the RCOG and WHO recommended standard |
| Volumetric (calibrated drapes) | Blood collects in a graduated pouch under the patient | Good for vaginal delivery; less practical for CS |
| Shock Index (SI) | Heart rate ÷ systolic BP; normal = 0.5–0.7 | SI > 0.9 suggests significant haemorrhage even if BP is "normal"; SI > 1.7 suggests massive haemorrhage needing activation of MTP |
| Haemoglobin drop | Post-delivery Hb minus antenatal Hb | Useful retrospectively; each 1 g/dL drop ≈ 500 mL blood loss (very rough). Remember Hb is unreliable acutely |
The Shock Index — A Vital Bedside Tool
Shock Index = Heart Rate / Systolic Blood Pressure
- Normal: 0.5–0.7
- 0.9–1.1: Mild shock (~1000 mL loss)
- 1.2–1.5: Moderate shock (~1500–2000 mL loss)
-
1.5: Severe shock (> 2000 mL loss)
This is better than relying on BP alone because it incorporates the compensatory tachycardia. A patient with HR 110 and BP 100 systolic has SI = 1.1 — this is NOT "stable," this is significant haemorrhage despite the "normal" BP.
For bleeding > 24 hours post-delivery, the investigation approach shifts:
| Investigation | Purpose | Key Findings |
|---|---|---|
| CBC, CRP, blood cultures | Assess for infection (endometritis — the most common cause) | ↑ WCC, ↑ CRP, positive blood cultures → endometritis/sepsis |
| Pelvic ultrasound (TAUS ± TVUS) | Assess for retained products, subinvolution | Echogenic material in cavity → retained products; enlarged uterus with abnormal vascularity → subinvolution |
| β-hCG | Exclude gestational trophoblastic disease | Persistently elevated or rising β-hCG after delivery → GTD (molar remnant, choriocarcinoma) |
| Coagulation screen | Exclude coagulopathy | Usually normal in secondary PPH unless sepsis-related DIC |
| Endometrial biopsy/histology (if evacuation performed) | Confirm retained products vs GTD vs endometritis | Chorionic villi = retained products; hydropic villi = molar pregnancy; acute inflammatory infiltrate = endometritis |
| Timing | Investigation | Purpose |
|---|---|---|
| Immediate (0–5 min) | Fundal palpation, genital tract inspection, placenta check, vital signs, Foley catheter | Identify cause (4 T's); assess shock severity |
| Early (5–15 min) | CBC, group & screen/crossmatch, coagulation profile (PT/aPTT/fibrinogen), RFT, LFT, VBG with lactate | Baseline severity; guide transfusion; detect DIC |
| Ongoing (15–60 min) | Serial vitals q5min, repeat Hb/coag at 30–60 min, ROTEM/TEG if available, bedside USS | Monitor response to treatment; detect evolving coagulopathy |
| If bleeding persists | EUA in theatre, CT angiography (if stable), interventional radiology | Identify occult source; plan surgical/IR intervention |
| Secondary PPH | CBC, CRP, blood cultures, pelvic USS, β-hCG, ± endometrial biopsy | Different DDx: endometritis, retained products, GTD |
High Yield Summary
PPH is a clinical diagnosis — defined by blood loss >= 1000 mL OR presence of haemodynamic compromise regardless of measured loss.
The diagnostic algorithm follows the 4 T's systematically [5]:
- Palpate fundus (Tone)
- Inspect genital tract (Trauma)
- Check placenta completeness (Tissue)
- Check coagulation (Thrombin)
- EUA in theatre if source unidentified + bleeding persists
- Laparotomy in exceptional circumstances
Key lab investigations: CBC, coag profile (PT/aPTT/fibrinogen), D-dimer, group & crossmatch, VBG with lactate, RFT, LFT. Fibrinogen < 2 g/L is the strongest predictor of severe PPH progression. Initial Hb may be normal — it is a lagging indicator.
Point-of-care: ROTEM/TEG guides targeted blood product therapy in real time. Shock Index (HR/SBP) is a better indicator of haemodynamic compromise than BP alone.
Imaging: USS for retained products/PAS; CTA for concealed haemorrhage; MRI for antenatal PAS planning. Imaging is NOT first-line in acute primary PPH.
Active Recall - PPH Diagnosis and Investigations
References
[1] Lecture slides: Block C - Postpartum Haemorrhage.pdf (definition, 4T classification, summary) [2] Lecture slides: PPH for teaching (20210716)v6.pdf (definition, summary) [3] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (definition, clinical purposes note on estimated blood loss) [4] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf (definition, clinical purposes note) [5] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf p5 (management principles, identifying source of bleeding algorithm, monitoring) [6] Lecture slides: OBGYN Clinical Test By Topic.pdf p12 (EUA exam question — M27_R1(22)_Q8) [7] Senior notes: Ryan Ho Critical Care.pdf p17 (shock evaluation: ECG, CBC, RFT, LFT, ABG, clotting, D-dimer) [8] Senior notes: Maksim Medicine Notes.pdf p161 (clotting cascade interpretation, PT/aPTT patterns) [9] Senior notes: Ryan Ho Haemtology.pdf p136–138 (DIC pathogenesis, full-house clotting, ISTH scoring, lab features) [10] Senior notes: Maksim Medicine Notes.pdf p165 (DIC aetiology, lab features — obstetric causes) [11] Senior notes: Ryan Ho Diagnostic Radiology.pdf p85 (uterine artery embolisation for PPH)
Management of Postpartum Haemorrhage
The management of PPH follows 4 major principles: [5][6]
- Communication with all relevant professionals
- Resuscitation
- Monitoring and investigation
- Arresting the bleeding
Similar to the management of heavy bleeding elsewhere, the principles are to replace the blood loss to reverse or prevent shock while efforts are made to identify and stop the source of bleeding. [5][6]
The lecture notes draw an explicit analogy: Compare and contrast the management of severe haemorrhage in general, bleeding oesophageal varices versus primary PPH to see if the same principles apply. These include tension, pressure, balloon, medication, embolization and surgery. [5][6]
This is a brilliant teaching point. Whether it's a bleeding varix, a trauma patient, or a postpartum uterus, the management toolkit is the same: compress it (pressure/tamponade), constrict it (medication), block it (embolisation), or cut/remove it (surgery).
PPH is a team sport. A single doctor cannot manage it alone. The moment PPH is recognised:
| Who to Call | Why |
|---|---|
| Senior obstetrician / MO on call | Decision-making for surgical intervention; the exam answer to "who to call first when you're an intern suspecting retained placenta" is the Medical Officer [7] |
| Anaesthetist | Airway management, haemodynamic resuscitation, GA if needed for EUA/surgery, massive transfusion protocol activation |
| Midwives / nursing staff | IV access, drug administration, vital sign monitoring, uterine massage, blood loss quantification |
| Laboratory / Blood bank | Urgent crossmatch, release of emergency blood products, massive transfusion protocol |
| Haematologist | Guidance on blood product therapy if coagulopathy |
| Interventional radiologist | If uterine artery embolisation (UAE) anticipated |
| Porters / extra hands | Rapid transfer to OT if needed |
Communication is Examinable
In OSCE/clinical test scenarios, failure to call for help early is marked down. The very first action when PPH is recognised should be calling for senior help, even before you start examining the patient. Delegate tasks — you cannot put in IV access, give drugs, examine the genital tract, and call blood bank simultaneously as one person.
Principle 2: Resuscitation
This follows standard hypovolaemic shock management [8], adapted for the obstetric setting.
- High-flow oxygen 15 L/min via non-rebreather mask with reservoir bag
- Why? Even before Hb drops significantly, tissue oxygen delivery is compromised by ↓ cardiac output from hypovolaemia. Supplemental O₂ maximises the oxygen-carrying capacity of the remaining circulating haemoglobin
Replacement of blood loss: [5][6]
- Volume replacement (e.g., giving intravenous fluids) to maintain an effective circulation
- Red cell replacement (oxygen carriage)
- Blood components replacement (platelet and FFP) to correct coagulation defect
| Step | Detail | Rationale |
|---|---|---|
| 2× large-bore IV access (14G or 16G, antecubital fossa) [8] | Take bloods simultaneously: CBC, coagulation profile, group & crossmatch, RFT, LFT, VBG with lactate | Large-bore cannulae allow rapid infusion rates (flow ∝ r⁴ / length — Poiseuille's law: a 14G cannula delivers ~300 mL/min vs ~60 mL/min for a 20G) |
| Rapid crystalloid bolus 500–1000 mL over 5–10 min [8] | Warmed Hartmann's / Ringer's lactate preferred over normal saline (NS causes hyperchloraemic metabolic acidosis in large volumes) | Expands intravascular volume immediately; warm fluids prevent hypothermia (hypothermia impairs coagulation → the "lethal triad": hypothermia + acidosis + coagulopathy) |
| Reassess q5min → repeat bolus if not responding [8] | Target: SBP > 90 mmHg, HR < 100, UO > 0.5 mL/kg/hr, improving lactate | Up to 2L crystalloid; beyond this, you are diluting clotting factors → transition to blood products |
| Foley catheter | Empty bladder (a full bladder prevents uterine contraction!) + monitor UO hourly | Therapeutic (restores uterine tone) AND diagnostic (UO reflects renal perfusion = adequacy of resuscitation) |
| Product | Trigger / Indication | Content & Dose | Mechanism |
|---|---|---|---|
| Packed Red Blood Cells (pRBC) | Hb < 7–8 g/dL OR ongoing massive haemorrhage regardless of Hb; use O-negative if crossmatch not available | 1 unit ≈ raises Hb by ~1 g/dL | Restores oxygen-carrying capacity — each gram of Hb carries 1.34 mL O₂ |
| Fresh Frozen Plasma (FFP) | PT/aPTT > 1.5× normal + active bleeding; massive transfusion protocol; DIC [12] | 2–4 units adult; 12–15 mL/kg [12]; contains ALL soluble plasma proteins and clotting factors | Replaces consumed/diluted clotting factors — fibrinogen, Factors II, V, VII, X, etc. |
| Cryoprecipitate | Fibrinogen < 2 g/L (critical threshold in obstetric haemorrhage) [12] | 10 units/dose for adults; 1 unit contains fibrinogen 150–300 mg + FVIII 80–120 U + vWF [12]; standard dose raises fibrinogen by ~1 g/L | Concentrated source of fibrinogen (much higher concentration per mL than FFP — gives more fibrinogen in less volume → less fluid overload) |
| Platelet concentrate | Platelets < 50 × 10⁹/L with active bleeding; < 75 × 10⁹/L if ongoing haemorrhage [12] | 1 adult therapeutic dose (pool of 4 units or 1 apheresis unit) | Replaces consumed platelets to enable primary haemostasis at the bleeding site |
| Fibrinogen concentrate (Riastap) | Alternative to cryoprecipitate for fibrinogen < 2 g/L; faster to prepare, no thawing needed | 2–4 g IV; dose-adjusted by ROTEM/Clauss fibrinogen | Purified fibrinogen — bypasses the volume and time limitations of cryoprecipitate |
Massive Transfusion Protocol (MTP)
When blood loss is > 2000 mL or ongoing at > 150 mL/min, or the patient is in Class III/IV shock:
- Activate MTP → blood bank releases products in pre-set packs
- Ratio-based approach: pRBC : FFP : Platelets = 1 : 1 : 1 (or 4:4:1 units) — this is based on trauma literature (PROPPR trial) extrapolated to obstetric haemorrhage
- Monitor ionised Ca²⁺ and replace with calcium gluconate 10 mL of 10% IV — stored blood contains citrate anticoagulant which chelates Ca²⁺; hypocalcaemia impairs coagulation (Ca²⁺ = Factor IV) AND cardiac contractility
- Keep patient warm — use fluid warmers, forced-air warming blankets; hypothermia < 35°C worsens coagulopathy and reduces uterotonic effectiveness
The 'Lethal Triad' of Massive Haemorrhage
Hypothermia + Acidosis + Coagulopathy form a vicious cycle:
- Hypothermia → slows enzymatic clotting cascade → coagulopathy → more bleeding
- Acidosis (from lactic acid due to hypoperfusion) → impairs clotting factor function
- Coagulopathy → more bleeding → more shock → more acidosis and hypothermia
All three must be actively corrected simultaneously. This is why warm fluids, active warming, aggressive correction of acidosis (via perfusion restoration), and early blood products are critical.
- "Trans" = across; "examic" = from amino + hexanoic acid — it's a synthetic lysine analogue
- Mechanism: competitively blocks the lysine-binding sites on plasminogen, preventing plasmin from binding to and degrading fibrin → anti-fibrinolytic → stabilises existing clots
- WOMAN Trial (2017): landmark RCT showing TXA 1g IV given within 3 hours of PPH onset reduces death from bleeding (OR 0.81) with no increase in thrombotic events
- Dose: 1g IV over 10 minutes, as soon as possible, ideally within 3 hours of delivery; can repeat a second 1g dose if bleeding continues after 30 minutes
- Key point: TXA does NOT cause uterine contraction — it is an adjunct to uterotonics, not a replacement
The exam question specifically tests this: for uterine atony, the answer is "Uterotonic agent" (D), NOT tranexamic acid (C), NOT blood transfusion (A). [7] TXA supports haemostasis but does not treat the underlying cause of atony.
TXA in PPH — Timing Is Everything
The benefit of TXA diminishes rapidly after 3 hours. The WOMAN trial showed no benefit when given > 3 hours after PPH onset. In practice, give TXA early alongside uterotonics — don't wait for the coagulation results to come back. It is safe, cheap, and widely available.
This should be monitored with blood pressure, pulse rate, urine output, central venous pressure, laboratory haematology tests. [5][6]
| Parameter | Frequency | Target |
|---|---|---|
| BP, HR, SpO₂ | q5 min during active bleeding, q15 min once stable | SBP > 90, HR < 100, SpO₂ > 95% |
| Urine output | Hourly (Foley in situ) | > 0.5 mL/kg/hr |
| Temperature | q30 min | > 36°C (prevent hypothermia) |
| CBC, Coag profile, fibrinogen | q30–60 min during active management | Hb > 8, Plt > 50, fibrinogen > 2 g/L, PT/aPTT < 1.5× |
| VBG with lactate | q30–60 min | Lactate < 2, pH > 7.35, BE > −6 |
| Ionised Ca²⁺ | With each VBG (especially during massive transfusion) | iCa > 1.0 mmol/L |
| ROTEM/TEG | If available: q30 min during active haemorrhage | Guides targeted blood product therapy |
Principle 4: Arresting the Bleeding — Cause-Specific Treatment
This is the core of PPH management. Treatment is directed by the identified cause (4 T's).
A. Management of TONE — Uterine Atony (The Stepwise Escalation)
This is the most common cause and the one with the most detailed management pathway. The approach is stepwise escalation: simple and conservative measures first → escalating to progressively more invasive interventions if bleeding persists.
| Intervention | Technique | Why It Works |
|---|---|---|
| "Rub up" the fundus / Uterine massage | Place one hand on the abdominal surface over the fundus and massage firmly in a circular motion | Direct mechanical stimulation of the myometrium triggers reflex contraction; also expels clots from the cavity that may be preventing contraction |
| Bimanual uterine compression | One hand inside the vagina (fist in the anterior fornix pushing the uterus anteriorly), other hand on the abdomen compressing the fundus posteriorly → the uterus is "sandwiched" between two hands | Directly compresses the uterine body → physically occludes the spiral arteries (mimicking the "living ligature" externally) while uterotonics take effect; buys time |
| Empty the bladder (Foley catheter) | Insert urinary catheter | A distended bladder displaces the uterus and prevents effective contraction — this simple act alone may restore tone |
Step 2: Pharmacological — Uterotonic Agents
This is the most high-yield section for exams. The lecture Appendix I provides the exact dosing regimens used at QMH/HKU:
For prevention of primary postpartum haemorrhage: [9][10]
a) At low risk of developing postpartum haemorrhage: [9][10]
- (i) Syntometrine® 1 mL (ergometrine 0.5 mg and oxytocin 5 units) IMI after delivery of fetal head
- (ii) Use oxytocin instead if Syntometrine® is contraindicated (hypertension, heart disease)
b) At high risk of postpartum haemorrhage: [9][10]
- (i) Oxytocin 5 units IVI after delivery of fetal shoulder, followed by IV infusion of oxytocin 40 units in 500 mL of normal saline over 4 hours
- (ii) Carbetocin 100 micrograms IV bolus for Caesarean section with high risk for PPH
For treatment of primary postpartum haemorrhage due to uterine atony: [9][10]
- (i) Oxytocin 10 units IVI followed by infusion 10 units per hour
- (ii) Carboprost (a prostaglandin) 250 micrograms IMI, can be repeated at 15 minutes later, up to maximum of 2 mg (8 doses)
- (iii) Misoprostol 800–1000 micrograms per rectal or sublingual
Now let me explain each drug from first principles:
| Drug | Class | Mechanism | Dose & Route | Contraindications | Side Effects |
|---|---|---|---|---|---|
| Oxytocin (Syntocinon) | Synthetic oxytocin analogue | Binds oxytocin receptors on myometrial smooth muscle → ↑ intracellular Ca²⁺ → muscle contraction. "Oxy" = quick/sharp, "tocin" = relating to birth | Prevention: 5 IU IVI; Treatment: 10 IU IVI bolus → 10 IU/hr infusion [9][10] | Few absolute CIs; caution with rapid IV bolus in cardiac disease (transient hypotension, tachycardia from vasodilation) | Water retention (ADH-like effect at high doses) → hyponatraemia; hypotension (especially with rapid IV bolus) |
| Ergometrine (Methergin) | Ergot alkaloid | Acts on smooth muscle α-adrenergic AND serotonin receptors → sustained tonic uterine contraction (not rhythmic like oxytocin) | 0.25–0.5 mg IM or slow IV | Contraindicated in HYPERTENSION, pre-eclampsia, heart disease [9][10] — causes systemic vasoconstriction → dangerously ↑ BP; also CI in Raynaud's, peripheral vascular disease | Nausea/vomiting (5-HT effect), hypertension, vasospasm, rarely coronary artery spasm |
| Syntometrine® | Combination: ergometrine 0.5 mg + oxytocin 5 IU | Combines the rapid onset of oxytocin (2–3 min) with the sustained action of ergometrine (up to 2–3 hours) → quick AND prolonged contraction | 1 mL IMI after delivery of fetal head [9][10] | Same CIs as ergometrine: hypertension, heart disease [9][10] | Same as ergometrine |
| Carboprost (Hemabate, 15-methyl PGF₂α) | Prostaglandin F₂α analogue | Potent stimulator of myometrial contraction via PGF₂α receptors → ↑ intracellular Ca²⁺; also causes bronchospasm and GI smooth muscle contraction | 250 μg IMI; can repeat q15 min; max 2 mg (= 8 doses) [9][10] | Asthma (causes bronchospasm — PGF₂α contracts bronchial smooth muscle); active cardiac, pulmonary, renal, or hepatic disease | Diarrhoea, vomiting, bronchospasm, fever, hypertension |
| Misoprostol (Cytotec, PGE₁ analogue) | Prostaglandin E₁ analogue | Binds EP receptors on myometrium → stimulates contraction; also softens cervix | 800–1000 μg per rectal or sublingual [9][10] | Few absolute CIs; generally safe in asthma (PGE₁ is bronchodilatory, unlike PGF₂α) | Diarrhoea, fever/shivering (dose-related thermoregulatory effect), nausea |
| Carbetocin (Pabal) | Long-acting oxytocin analogue | Same mechanism as oxytocin but with longer half-life (~40 min vs ~3 min for oxytocin) → sustained contraction from single dose | 100 μg IV bolus; used for CS with high risk for PPH [9][10] | Same cautions as oxytocin (cardiac disease) | Similar to oxytocin but generally better tolerated |
Key Contraindication Pair for Exams
- Ergometrine / Syntometrine® → Contraindicated in HYPERTENSION and HEART DISEASE (causes vasoconstriction → ↑ BP → stroke / MI risk)
- Carboprost → Contraindicated in ASTHMA (PGF₂α causes bronchospasm)
- Misoprostol → Safe in asthma (PGE₁ is actually a bronchodilator)
These are among the most commonly tested contraindications in O&G exams.
If uterotonics fail to control atony:
- What: A balloon (Bakri balloon, Sengstaken-Blakemore tube, or condom catheter) is inserted into the uterine cavity and inflated with 300–500 mL warm saline
- Mechanism: Direct mechanical compression of the uterine walls → compresses the open spiral arteries at the placental bed from the inside; same principle as a Sengstaken tube for oesophageal varices or nasal packing for epistaxis — tension, pressure, balloon [5][6]
- Why it's placed before surgery: It's less invasive, buys time, can be performed at the bedside/labour ward, and is effective in ~80% of atony cases; it serves as a "tamponade test" — if bleeding stops, surgery can be avoided
- Monitoring: A drain catheter below the balloon allows ongoing blood loss to be measured — if > 200 mL/hr drains, the tamponade has failed → proceed to surgery
- Remove: Usually after 12–24 hours once haemostasis is established; deflate gradually
These are performed via laparotomy:
| Procedure | Description | Mechanism | When to Use |
|---|---|---|---|
| B-Lynch suture (uterine compression suture) | A continuous suture is placed around the uterus in a "braces" (suspender) pattern, compressing the anterior and posterior walls together | Mechanically compresses the uterine walls → closes the uterine cavity → compresses spiral arteries (same principle as bimanual compression, but surgical and sustained) | First-line surgical option for atony unresponsive to uterotonics and tamponade; preserves fertility |
| Uterine artery ligation (bilateral) | Surgical ligation of the ascending branches of the uterine arteries at the level of the lower uterine segment | ↓ arterial inflow to the uterus → ↓ pulse pressure at the placental bed → promotes haemostasis; collateral supply from ovarian arteries maintains uterine viability | If B-Lynch insufficient; can be combined with B-Lynch; preserves fertility |
| Internal iliac artery ligation (bilateral) | Surgical ligation of the anterior division of the internal iliac arteries | Reduces pulse pressure to the pelvis by ~85% → converts arterial flow to venous-type flow → promotes clot formation; does NOT fully stop blood flow (extensive collaterals exist) | Technically demanding; requires surgical expertise; may be attempted before hysterectomy |
| Hysterectomy (subtotal or total) | Removal of the uterus — the definitive, last-resort procedure | Removes the bleeding source entirely | When all other measures have failed; placenta accreta spectrum with uncontrollable bleeding; uterine rupture not amenable to repair. This is the "nuclear option" — it ends future fertility but saves the mother's life |
Fertility-Preserving Approach
The stepwise escalation is designed to exhaust all fertility-preserving options before proceeding to hysterectomy. B-Lynch sutures, artery ligations, and even balloon tamponade all allow future pregnancies. Hysterectomy is performed ONLY when the mother's life is at immediate risk and all other measures have failed. Never delay a life-saving hysterectomy for the sake of preserving fertility.
Uterine artery embolization (UAE) for post-partum haemorrhage [11]
- Technique: Fluoroscopy-guided selective catheterisation of both uterine arteries (via femoral artery access) → injection of embolic agents (Gelfoam, PVA particles, coil, glue [11]) to block blood flow
- Mechanism: Occludes the uterine arterial supply at the level of the bleeding source → promotes haemostasis; Gelfoam is temporary (resorbed in 2–4 weeks → allows recanalisation → preserves fertility)
- Indication: Haemodynamically stabilised or borderline-stable patient with ongoing bleeding refractory to uterotonics; particularly useful when surgical expertise is limited or anatomy is complex (pelvic haemorrhage preferred over surgery due to complex anatomy [11])
- Contraindication: Haemodynamically unstable patient who cannot be transferred to IR suite (the IR suite is typically NOT in the labour ward — patient needs transport)
- Success rate: ~85–95% for PPH
- Advantage: Fertility-preserving; avoids laparotomy
| Scenario | Management | Details |
|---|---|---|
| Retained placenta (not delivered > 30 min) | Manual removal of placenta under regional or general anaesthesia | The operator's hand enters the uterine cavity, identifies the cleavage plane between the placenta and decidua, and sweeps the placenta off the uterine wall. This requires anaesthesia (uterine relaxation, pain control). Start IV oxytocin infusion simultaneously to prevent atony after removal |
| Retained placental fragments / incomplete placenta | Surgical evacuation of uterus (suction curettage or digital/sponge-forceps evacuation) under USS guidance | Performed in OT under anaesthesia; USS guidance reduces risk of perforation; always send tissue for histology |
| Placenta accreta spectrum | Do NOT attempt forcible manual removal — will cause catastrophic haemorrhage; proceed to hysterectomy (usually planned electively if diagnosed antenatally); if unexpected, may attempt conservative management with the placenta left in situ in selected cases | The trophoblast has invaded into the myometrium — there is no cleavage plane. Tearing it off avulsions myometrial vessels. Antenatal diagnosis by USS/MRI allows planned CS-hysterectomy with multidisciplinary team |
| Injury | Management |
|---|---|
| Perineal / vaginal tears | Systematic inspection under good light + anaesthesia → primary surgical repair with absorbable sutures (Vicryl); ensure haemostasis of each vessel; classify degree (1st–4th) and repair accordingly |
| Cervical tears | Identified on speculum examination; grasp the cervix with ring forceps and systematically inspect all 360° → suture the tear with continuous absorbable suture. Deep tears extending into the lower segment may require EUA |
| Uterine rupture | Laparotomy → repair of the rupture site if feasible; if repair impossible (extensive rupture, PAS) → hysterectomy |
| Uterine inversion | Immediate manual replacement (Johnson manoeuvre): push the inverted fundus back through the cervix with steady pressure using the palm of the hand. If the cervix has contracted (making replacement impossible) → uterine relaxation with IV MgSO₄, terbutaline, or GA with volatile agents → then manual replacement. Do NOT remove the placenta before replacing the uterus (removing it increases bleeding). If manual replacement fails → surgical (Haultain's procedure at laparotomy: incise the constriction ring posteriorly, replace the fundus, then close) |
| Broad ligament haematoma | Small/stable: conservative management with monitoring; Large/expanding: surgical exploration at laparotomy, evacuate haematoma, ligate bleeding vessels |
Blood components replacement (platelet and FFP) to correct coagulation defect. [5][6]
| Condition | Management | Key Points |
|---|---|---|
| DIC | Treat underlying cause (most important [12][13]); replace consumed components: FFP (PT/aPTT > 1.5× with bleeding), cryoprecipitate (fibrinogen < 2 g/L), platelet transfusion (Plt < 50 with active bleeding); TXA for fibrinolysis [12][13] | In DIC: AVOID PCC (promotes thrombosis); heparin is controversial (may reduce thrombin but increases bleeding) [13] |
| Dilutional coagulopathy | Balanced blood product transfusion (MTP with 1:1:1 ratio); cryoprecipitate to maintain fibrinogen > 2 g/L | Fibrinogen is the first factor to fall critically in dilution — target replacement early |
| Pre-existing bleeding disorders (e.g., vWD) | Factor-specific replacement: DDAVP (desmopressin) for mild vWD Type 1; vWF/FVIII concentrate for severe cases; cryoprecipitate as alternative [12] | Should have been identified antenatally and a delivery plan made with haematology input |
| HELLP syndrome | Deliver the baby (definitive treatment); supportive care; MgSO₄ for seizure prophylaxis; platelet transfusion if Plt < 50 + bleeding or < 20 + no bleeding | DIC may complicate HELLP — manage both simultaneously |
Prevention is always better than cure. AMTSL reduces PPH by ~60%:
| Component | What | Why |
|---|---|---|
| Prophylactic uterotonic at delivery | Syntometrine® 1 mL IMI after delivery of fetal head (low risk) [9][10]; Oxytocin 5 IU IVI (if Syntometrine CI) [9][10] | Promotes immediate uterine contraction → the "living ligature" activates early |
| Controlled cord traction (Brandt-Andrews technique) | Gentle, sustained traction on the cord with counter-pressure on the uterus suprapubically (guarding against inversion) | Facilitates delivery of the separated placenta; must only be performed after signs of placental separation |
| Early cord clamping (within 1–3 minutes) | Clamp and cut cord | Reduces feto-maternal transfusion; though delayed clamping (1–3 min) now preferred for neonatal benefit (↑ iron stores), this is balanced against PPH risk in high-risk patients |
| Uterine massage after placental delivery | Firm massage of the uterine fundus | Stimulates contraction; expels any residual clots |
| Intervention | Detail |
|---|---|
| Antibiotics (first-line for endometritis) | Broad-spectrum IV antibiotics (e.g., IV amoxicillin + metronidazole + gentamicin, or piperacillin-tazobactam) — endometritis is the most common cause |
| Ultrasound-guided surgical evacuation | If retained products confirmed on USS → evacuate under GA with USS guidance |
| Uterotonics | Oxytocin infusion if uterine atony contributing |
| Resuscitation | Same principles as primary PPH if bleeding is significant |
| Investigation for rare causes | β-hCG (GTD), Doppler USS (pseudoaneurysm, AVM), endometrial biopsy |
The exam question [M28_R1(?1)_Q4]: G5P0 with multiple surgical TOPs, delivered 3.0 kg baby by SVD, heavy vaginal bleeding, BP 80/40, pulse 120 → most appropriate IMMEDIATE management? [7]
- A. Emergency manual removal of placenta
- B. IV fluid resuscitation ✓
- C. IV oxytocin
- D. IV TXA
Answer: B. IV fluid resuscitation — The patient is in haemorrhagic shock (hypotensive, tachycardic). The immediate priority is to restore circulating volume to prevent cardiovascular collapse. Uterotonics and cause-specific treatment come immediately after (or simultaneously), but the very first action for a shocked patient is volume resuscitation. You cannot give uterotonics to a dead patient.
The exam question [M27_R1(23)_Q6]: 22-year-old with uterine atony → what should be given for treatment? [7] Answer: Uterotonic agent (D) — NOT blood transfusion, NOT pethidine, NOT TXA. The specific treatment for atony is uterotonics. TXA is an adjunct; blood transfusion treats anaemia/hypovolaemia but doesn't address the cause.
High Yield Summary
4 major principles of PPH management: Communication, Resuscitation, Monitoring and Investigation, Arresting the bleeding. [5][6]
Resuscitation: Volume replacement → Red cell replacement → Blood components replacement [5][6]. 2× large-bore IV, rapid crystalloid, pRBC if needed, FFP/cryoprecipitate/platelets for coagulopathy. Warm fluids. Monitor q5min.
Uterotonics (in order of use):
- Oxytocin 10 IU IVI + 10 IU/hr infusion (first-line treatment)
- Carboprost 250 μg IM q15min, max 8 doses (CI: asthma)
- Misoprostol 800–1000 μg PR/SL (safe in asthma)
- Ergometrine 0.5 mg IM (CI: hypertension, heart disease)
Stepwise escalation for refractory atony: Massage + empty bladder → Uterotonics → Intrauterine balloon tamponade → Surgical (B-Lynch, artery ligation) → UAE or Hysterectomy (last resort).
Syntometrine® is contraindicated in hypertension and heart disease; use oxytocin instead. [9][10]
TXA 1g IV within 3 hours — adjunct, not replacement for uterotonics.
Immediate management of a shocked PPH patient = IV fluid resuscitation. [7]
Treatment for uterine atony = uterotonic agent (not blood transfusion, not TXA alone). [7]
Active Recall - PPH Management
References
[5] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf p5 (4 principles of PPH management, replacement of blood loss, identifying source of bleeding algorithm) [6] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf p5 (4 principles, replacement of blood loss, identifying source algorithm) [7] Lecture slides: OBGYN Clinical Test By Topic.pdf p12–15 (exam questions: immediate management of shocked PPH, uterotonic for atony, call MO for retained placenta, atonic uterus as cause) [8] Senior notes: Ryan Ho Critical Care.pdf p21 (hypovolaemic shock management: large bore IV, crystalloid bolus, reassess q5min, Foley, RBC transfusion) [9] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf p7 (Appendix I: dosage and route of oxytocic agents — prevention and treatment) [10] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf p7 (Appendix I: dosage and route of oxytocic agents — prevention and treatment) [11] Senior notes: Ryan Ho Diagnostic Radiology.pdf p85 (transcatheter embolization, UAE for PPH, embolic agents, pelvic haemorrhage) [12] Senior notes: Ryan Ho Haemtology.pdf p144 (FFP content/indications/dosing, cryoprecipitate content/indications/dosing, PCC) [13] Senior notes: Maksim Medicine Notes.pdf p165 (DIC management: treat cause, supportive, avoid TXA/PCC in DIC, ?heparin)
Complications of Postpartum Haemorrhage
PPH is one of the major causes of direct maternal death. [1][2][3][4] But even when the mother survives, PPH can leave a devastating trail of complications — from organ damage caused by hypovolaemic shock, to complications of the treatment itself (massive transfusion, surgery), to long-term endocrine and psychological consequences. Understanding these complications requires tracing the pathophysiological cascade from blood loss through to its downstream effects on every organ system.
Whatever the initial cause of bleeding, the patient can develop blood coagulation defects after heavy bleeding, and this causes more bleeding. [14][15] — This single sentence from the lecture notes captures the vicious cycle that underpins the most dangerous acute complications.
A. Acute / Immediate Complications
This is the direct consequence of the massive blood loss and the most lethal immediate complication.
Pathophysiology from first principles:
Blood loss → ↓ circulating volume → ↓ venous return → ↓ preload → ↓ stroke volume → ↓ cardiac output → ↓ tissue oxygen delivery → tissue hypoxia → anaerobic metabolism → lactic acidosis → cellular injury → organ failure.
The body compensates initially through:
- Sympathetic activation → tachycardia, vasoconstriction (shunting blood from skin/gut/kidneys to brain/heart)
- ADH/aldosterone release → water/sodium retention
- Transcapillary fluid shift (interstitial fluid moves into intravascular space)
But these mechanisms have limits. Once compensation is overwhelmed (typically at > 30–40% blood volume loss), decompensated shock ensues — BP falls precipitously and organ damage begins.
| Organ | Mechanism of Injury | Clinical Manifestation |
|---|---|---|
| Kidneys | Renal hypoperfusion → ↓ GFR → acute tubular necrosis (ATN) from prolonged ischaemia | Acute kidney injury (AKI): oliguria → anuria; ↑ creatinine, ↑ urea, ↑ K⁺; may require renal replacement therapy (dialysis) |
| Liver | Hepatic hypoperfusion → centrilobular hepatocyte necrosis ("shock liver" / ischaemic hepatitis) | ↑↑ transaminases (ALT/AST can reach thousands), ↑ bilirubin, ↑ INR; usually reversible if perfusion restored |
| Lungs | Endothelial injury from shock + massive transfusion → capillary leak → pulmonary oedema; also TRALI from blood products | Acute respiratory distress syndrome (ARDS): bilateral pulmonary infiltrates, hypoxaemia refractory to supplemental O₂; PaO₂/FiO₂ ratio < 300 |
| Brain | Cerebral hypoperfusion → watershed infarction; severe cases → diffuse hypoxic-ischaemic encephalopathy | Confusion → obtundation → coma; seizures; may have permanent neurological deficit |
| Heart | Myocardial ischaemia from ↓ oxygen delivery to the myocardium (especially if pre-existing coronary disease) | Chest pain, ST changes on ECG, ↑ troponin; arrhythmias; cardiogenic shock (secondary) |
| GI tract | Splanchnic vasoconstriction (blood shunted away from gut) → mucosal ischaemia | Ileus, mucosal sloughing, stress ulceration; potential translocation of gut bacteria → secondary sepsis |
| Adrenal glands | Bilateral adrenal haemorrhage/infarction in the setting of DIC and shock (Waterhouse-Friderichsen-like syndrome) | Acute adrenal insufficiency: refractory hypotension despite fluids/vasopressors, hypoglycaemia, ↓ Na⁺, ↑ K⁺ |
The Lethal Triad — Revisited
In massive PPH, three physiological derangements reinforce each other in a lethal positive feedback loop:
- Hypothermia (exposure, cold fluids, massive transfusion) → slows enzymatic clotting cascade
- Acidosis (lactic acid from hypoperfusion; citrate from transfused blood) → impairs clotting factor function and cardiac contractility
- Coagulopathy (consumption + dilution + hypothermia/acidosis) → continued bleeding → more shock → more hypothermia and acidosis
Breaking this triad is the central goal of resuscitation — warm fluids, early blood products (not just crystalloid), and aggressive source control.
Whatever the initial cause of bleeding, the patient can develop blood coagulation defects after heavy bleeding, and this causes more bleeding. [14][15]
DIC is both a cause of PPH (e.g., amniotic fluid embolism, abruption) and a complication of PPH (secondary to massive haemorrhage from any cause).
Why does PPH cause DIC?
- Massive tissue trauma (delivery, especially instrumental/operative) releases tissue factor (TF) into the circulation
- Hypotension and acidosis cause endothelial damage → further TF exposure
- Massive transfusion with stored blood (which contains activated procoagulant debris) contributes
- The combination triggers widespread intravascular coagulation → consumption of clotting factors and platelets → paradoxical bleeding [14][15][16][17]
Clinical features: Non-clotting blood, oozing from IV sites/wound edges/mucosal surfaces, worsening haemorrhage despite mechanical haemostasis
Lab picture: ↓ platelets, ↑ PT/aPTT, ↓ fibrinogen, ↑ D-dimer, schistocytes on PBS ("full-house" clotting) [16][17]
Management: Treat the underlying cause + replace consumed components (FFP, cryoprecipitate, platelets) [17]
PPH is one of the major causes of direct maternal death. [1][2] When resuscitation fails, cardiac arrest and death result from:
- Severe hypovolaemia → pulseless electrical activity (PEA) or asystole
- Massive DIC → uncontrollable haemorrhage
- Multi-organ failure
Importantly, most PPH deaths are preventable — delays in recognition, treatment, and escalation are the leading modifiable factors (the "Three Delays" model). This is why communication with all relevant professionals is the first principle of PPH management [5][6].
B. Subacute / Early Complications (Hours to Days)
Even after bleeding is controlled, the patient may be left profoundly anaemic:
- Mechanism: Direct loss of red blood cells + haemodilution from fluid resuscitation
- Impact: Fatigue, dyspnoea, tachycardia, impaired lactation, delayed recovery, poor wound healing, difficulty bonding with the baby
- Management: Oral or IV iron supplementation (IV iron preferred if Hb < 7–8 g/dL or intolerance of oral iron); continued blood transfusion if symptomatic or Hb critically low
When a patient receives > 10 units pRBC (or > 1–2× blood volume in 24 hours) [18][19], specific transfusion-related complications arise:
| Complication | Mechanism | Prevention/Treatment |
|---|---|---|
| Hyperkalaemia | Stored RBCs leak intracellular K⁺ over time (haemolysis during storage); rapid transfusion delivers a potassium load | Monitor K⁺ with serial VBGs; use fresher units if available; treat hyperkalaemia with calcium gluconate, insulin-dextrose, nebulised salbutamol [18][19] |
| Hypocalcaemia (citrate toxicity) | Stored blood contains citrate anticoagulant which chelates ionised Ca²⁺; Ca²⁺ is Factor IV — essential for multiple steps in the clotting cascade AND cardiac muscle contraction | Monitor ionised Ca²⁺; replace with 10 mL of 10% calcium gluconate IV for every 4 units pRBC; signs: prolonged QT, tetany, worsening coagulopathy, cardiac dysfunction [18][19] |
| Hypothermia | Cold stored blood (4°C) is infused rapidly → core body temperature drops | Use fluid warmers for ALL blood products; forced-air warming blankets; hypothermia worsens coagulopathy and cardiac function [18][19] |
| Dilutional coagulopathy / thrombocytopenia | pRBCs contain no functional platelets or clotting factors; massive crystalloid dilutes existing factors | Balanced transfusion (pRBC:FFP:Plt = 1:1:1); cryoprecipitate if fibrinogen < 2 g/L; ROTEM-guided if available [18][19] |
| Transfusion-related acute lung injury (TRALI) | Donor antibodies (anti-HLA or anti-neutrophil) activate recipient neutrophils in the pulmonary vasculature → capillary leak → non-cardiogenic pulmonary oedema | Occurs within 6h of transfusion; presents like ARDS; supportive management; use male-only plasma donors (↓ anti-HLA antibodies) [19] |
| Transfusion-associated circulatory overload (TACO) | Rapid fluid administration exceeds cardiac capacity → hydrostatic pulmonary oedema | Diuretics; slower transfusion rate; upright positioning; more common in patients with cardiac comorbidity |
| Febrile non-haemolytic transfusion reaction (FNHTR) | Recipient antibodies react with donor leucocyte antigens → cytokine release → fever/rigors | Paracetamol; leucocyte-reduced blood products [19] |
| Allergic reactions | IgE-mediated reaction to donor plasma proteins | Antihistamines ± steroids; anaphylaxis protocol if severe [19] |
| Metabolic alkalosis | Citrate is metabolised to bicarbonate in the liver after transfusion → delayed alkalaemia | Usually self-correcting; monitor ABGs [18] |
| Procedure | Specific Complications |
|---|---|
| Peripartum hysterectomy | Permanent loss of fertility; bladder/ureteric injury (especially with PAS involving the bladder); haemorrhage; infection; VTE; prolonged recovery; psychological impact |
| B-Lynch suture | Uterine necrosis (rare — if suture too tight); pyometria (intrauterine infection trapped by compressed cavity); adhesions |
| Uterine artery ligation | Generally well-tolerated; rare: broad ligament haematoma, ureteric injury |
| Internal iliac artery ligation | Technically difficult; risk of injury to internal iliac vein (torrential venous haemorrhage), ureteric injury; buttock claudication (rare — usually adequate collaterals) |
| UAE | Post-embolisation syndrome (pain, fever, nausea — self-limiting); uterine necrosis/infection (rare); non-target embolisation (ovarian artery → ovarian failure); femoral artery access site complications (haematoma, pseudoaneurysm) |
- Why: The uterine cavity is exposed and potentially contaminated after delivery; retained products, instrumentation (manual removal, EUA), and surgical procedures all increase risk; PPH itself impairs immune function (hypoperfusion, transfusion-related immunosuppression)
- Presentation: Fever, uterine tenderness, offensive lochia, tachycardia; can progress to sepsis
- Management: Broad-spectrum IV antibiotics; evacuate any retained products; rarely, drainage of pelvic abscess
- Why: Pregnancy is already a hypercoagulable state (↑ fibrinogen, ↑ factors VII/VIII/X/vWF, ↓ protein S); PPH compounds this with immobilisation, dehydration, surgical intervention, DIC (which paradoxically causes both bleeding AND thrombosis), and post-transfusion procoagulant state
- Risk: Highest in the 6 weeks postpartum; PPH with surgical intervention significantly increases risk
- Prevention: Early mobilisation; mechanical thromboprophylaxis (TED stockings, pneumatic compression); pharmacological thromboprophylaxis (LMWH) once haemostasis is secure — typically started 6–12 hours after bleeding is controlled
C. Late / Long-term Complications
This is the classic long-term complication of severe PPH and is highly examinable.
- Etymology: Named after Harold Sheehan (1937) who described pituitary necrosis following postpartum haemorrhage
- Pathophysiology: During pregnancy, the anterior pituitary gland doubles in size (hyperplasia of lactotroph cells to prepare for lactation). This enlargement outpaces its blood supply — the pituitary is supplied by the portal venous system from the hypothalamus, which has low perfusion pressure. When severe PPH causes prolonged hypotension, the enlarged anterior pituitary is exquisitely vulnerable to ischaemic necrosis because:
- The gland is enlarged but its vascular supply has not proportionally increased
- It sits in the rigid sella turcica → swelling from ischaemia causes further compression
- The portal system is low-pressure and easily compromised
- Result: Partial or complete destruction of the anterior pituitary → panhypopituitarism (deficiency of all anterior pituitary hormones)
| Hormone Lost | Clinical Consequence | Why / When It Manifests |
|---|---|---|
| Prolactin (first to manifest) | Failure of lactation (agalactia) — often the earliest sign | Prolactin is needed to initiate and maintain milk production; damaged lactotrophs cannot produce it; presents within days of delivery |
| GH (most common deficiency) | Fatigue, loss of muscle mass, central obesity, ↓ quality of life | GH deficiency is the most common single deficiency in Sheehan syndrome; manifests over weeks–months |
| FSH / LH (gonadotropins) | Amenorrhoea (failure to resume menstruation), loss of axillary/pubic hair, vaginal atrophy, loss of libido, infertility | Loss of gonadotropins → secondary hypogonadism → ↓ oestrogen; often the presenting complaint months–years later |
| ACTH | Secondary adrenal insufficiency: fatigue, weight loss, hypoglycaemia, inability to mount a stress response; can be life-threatening | Unlike primary adrenal insufficiency (Addison's), aldosterone is preserved (RAAS-dependent, not ACTH-dependent) → less hyperkalaemia; but ↓ cortisol is dangerous |
| TSH | Secondary hypothyroidism: cold intolerance, fatigue, weight gain, constipation, bradycardia, dry skin | T4 and T3 production ↓ due to lack of TSH stimulation |
Sheehan Syndrome — The Classic Exam Scenario
A woman with a history of severe PPH presents months to years later with:
- Failure to lactate (earliest clue)
- Amenorrhoea (never resumed menses after delivery)
- Loss of pubic/axillary hair
- Features of hypothyroidism and adrenal insufficiency
Diagnosis: MRI pituitary (empty sella or atrophied gland) + hormonal profile (low anterior pituitary hormones with low/inappropriately normal target gland hormones)
Treatment: Lifelong hormone replacement — cortisol first (before thyroxine, because giving T4 without cortisol cover increases cortisol metabolism and can precipitate adrenal crisis), then T4, then oestrogen/progesterone, then GH.
- What: Formation of scar tissue (synechiae) within the uterine cavity
- Why it happens after PPH: Aggressive uterine curettage for retained products, manual removal of placenta, or intrauterine instrumentation damages the endometrial basalis layer → healing by fibrosis rather than regeneration → adhesions form between opposing uterine walls
- Presentation: Secondary amenorrhoea or hypomenorrhoea (reduced menstrual flow), cyclical pain (haematometra if outflow obstructed), infertility, recurrent miscarriage
- Diagnosis: Hysteroscopy (gold standard — direct visualisation of adhesions); USS may show thin endometrium; HSG shows filling defects
- Treatment: Hysteroscopic adhesiolysis (cutting the adhesions) + oestrogen therapy to promote endometrial regeneration + intrauterine balloon/stent to prevent re-adhesion
- Following peripartum hysterectomy: permanent, absolute loss of uterine fertility
- Following UAE: usually fertility-preserving (Gelfoam is temporary), but rare cases of ovarian failure (non-target embolisation), uterine necrosis, or Asherman syndrome can impair future reproduction
- Following bilateral uterine artery ligation: usually preserves fertility (ovarian collateral supply maintained), but there is a small risk of uterine ischaemia
These are underappreciated but extremely common:
| Condition | Prevalence Post-PPH | Mechanism / Features |
|---|---|---|
| Post-traumatic stress disorder (PTSD) | ~5–15% after severe PPH | The traumatic experience of life-threatening haemorrhage, emergency surgery, ICU admission → intrusive memories, flashbacks, avoidance behaviours, hyperarousal |
| Postnatal depression (PND) | Increased risk after PPH | Multifactorial: physiological (anaemia, hormonal disruption, fatigue), psychological (trauma, separation from baby during resuscitation, failure to breastfeed due to Sheehan), social (prolonged hospital stay) |
| Tokophobia | Variable | "Tokos" = childbirth, "phobia" = fear → pathological fear of future pregnancy/childbirth; may lead to avoidance of future pregnancies or request for elective CS |
| Impaired bonding / attachment | Common in early period | Separation from baby during resuscitation/ICU; inability to breastfeed; maternal fatigue and anaemia |
| Timing | Complication | Key Mechanism |
|---|---|---|
| Immediate (minutes–hours) | Hypovolaemic shock → multi-organ failure | ↓ Cardiac output → ↓ tissue O₂ delivery → organ ischaemia |
| DIC / consumptive coagulopathy | Tissue factor release + endothelial damage → consumption of clotting factors → paradoxical bleeding | |
| Cardiac arrest / maternal death | End-stage of unresuscitated shock | |
| Early (hours–days) | Anaemia / iron deficiency | Direct blood loss + haemodilution |
| Complications of massive transfusion | HyperK⁺, hypoCa²⁺, hypothermia, dilutional coagulopathy, TRALI, TACO | |
| Surgical complications | Hysterectomy (loss of fertility, organ injury); B-Lynch (uterine necrosis); UAE (post-embolisation syndrome) | |
| Endometritis / sepsis | Contamination of open uterine cavity; instrumentation; immunosuppression | |
| VTE | Hypercoagulable state + immobility + surgery | |
| Late (weeks–years) | Sheehan syndrome | Ischaemic necrosis of enlarged anterior pituitary → panhypopituitarism |
| Asherman syndrome | Intrauterine adhesions from curettage/instrumentation → amenorrhoea, infertility | |
| Loss of fertility | Post-hysterectomy; post-UAE ovarian failure (rare); Asherman | |
| Psychological (PTSD, PND, tokophobia) | Trauma of life-threatening event; separation; inability to breastfeed; hormonal disruption |
High Yield Summary
Acute complications follow the pathophysiology of hypovolaemic shock: ↓ perfusion → multi-organ failure (AKI, shock liver, ARDS, DIC). The patient can develop blood coagulation defects after heavy bleeding, which causes more bleeding [14][15] — this vicious cycle of bleeding → coagulopathy → more bleeding is the central lethal mechanism.
The lethal triad (hypothermia + acidosis + coagulopathy) must be actively broken by warming, balanced transfusion, and early blood products.
Complications of massive transfusion: hyperkalaemia, hypocalcaemia (citrate toxicity), hypothermia, dilutional coagulopathy, TRALI, TACO.
Sheehan syndrome is THE classic long-term complication — ischaemic necrosis of the enlarged anterior pituitary from prolonged hypotension → failure of lactation (earliest sign), amenorrhoea, panhypopituitarism. Treat with cortisol first (before T4).
Asherman syndrome — intrauterine adhesions from instrumentation → secondary amenorrhoea, infertility; diagnosed by hysteroscopy; treated by adhesiolysis.
Psychological sequelae (PTSD, PND, tokophobia) are common and underdiagnosed — screen actively.
Active Recall - Complications of PPH
References
[1] Lecture slides: Block C - Postpartum Haemorrhage.pdf p1 (PPH as major cause of direct maternal death, definition) [2] Lecture slides: Block C - Postpartum Haemorrhage.pdf p32 (summary: obstetric emergency, major cause of direct maternal death) [3] Lecture slides: PPH for teaching (20210716)v6.pdf p2 (definition, major cause of direct maternal death) [4] Lecture slides: PPH for teaching (20210716)v6.pdf p37 (summary) [5] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf p5 (4 principles of PPH management) [6] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf p5 (4 principles of PPH management) [14] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf p4 (coagulation defects after heavy bleeding causing more bleeding; DIC in pregnancy complications) [15] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf p4 (coagulation defects after heavy bleeding; DIC in pregnancy complications) [16] Senior notes: Maksim Medicine Notes.pdf p165 (DIC pathophysiology, lab features, management — avoid TXA/PCC in DIC) [17] Senior notes: Ryan Ho Haemtology.pdf p138 (DIC: acute vs chronic, lab features, management: treat underlying cause, supportive, blood products) [18] Senior notes: Ryan Ho Critical Care.pdf p20 (massive transfusion: risks including hypothermia, coagulopathy, hyperK, citrate toxicity/hypoCa, metabolic alkalosis; pRBC:FFP:PLT = 1:1:1) [19] Senior notes: Maksim Medicine Notes.pdf p184 (complications of massive transfusion: hyperK, hypoCa, acidosis, hypothermia, dilutional coagulopathy; complications of long-term transfusion)
High Yield Summary
Definition: PPH = blood loss >= 1000 mL or signs/symptoms of hypovolemia within 24 hours after delivery, regardless of mode of delivery. Treat if symptomatic or shocked regardless of measured loss — visual estimation underestimates by 30–50%.
Classification: Primary (within 24 hours, ~90%) vs Secondary (> 24 hours to 6–12 weeks). Severity: minor 500–1000 mL, major > 1000 mL, massive > 2000 mL or haemodynamic instability.
Aetiology — 4 T's (in order of frequency): Tone (~70–80%), Tissue (~10–20%), Trauma (~5–10%), Thrombin (~1–2%). Multiple T's often coexist.
Key mechanism: The "living ligature" — criss-cross myometrial fibres compress spiral arteries at the placental bed after separation. Failure of contraction (atony) is the #1 cause. Lower uterine segment contracts poorly → low-lying placenta is a major risk factor.
Risk factors: Overdistension (twins, polyhydramnios, macrosomia > 3800 g), grand multiparity (≥ 5 births), abnormal myometrium (fibroids, prior uterine surgery/CS), induced/augmented labour, antepartum haemorrhage, anaemia (Hb < 10 g/dL), bleeding tendencies.
Critical safety points: Never pull on the umbilical cord before placental separation (partial separation → PPH; uterine inversion). Upper segment is the main contractile force — low-segment CS does NOT contraindicate future VBAC; classical CS carries ~10% rupture risk.
High Yield Summary
The 4 T's as diagnostic algorithm:
- Tone: Soft, boggy, enlarged uterus → uterine atony → uterotonics + bimanual compression
- Tissue: Incomplete placenta / retained fragments / accreta spectrum → manual removal or evacuation
- Trauma: Firm uterus + bright red bleeding → inspect genital tract (cervical tear at 3 or 9 o'clock, perineal tear, rupture, inversion)
- Thrombin: Non-clotting blood, oozing from IV sites → DIC, dilutional or massive transfusion coagulopathy
Key bedside manoeuvre: Palpate the fundus first. Soft/boggy = atony. Firm + ongoing bleeding = trauma or coagulopathy.
When uterus is well-contracted and placenta is complete but bleeding continues → think Trauma and Thrombin. Massive blood loss from any cause causes secondary coagulopathy.
Secondary PPH (> 24 hours): Endometritis first (fever + uterine tenderness + cervical excitation), then retained products, subinvolution, rarely GTD or uterine artery pseudoaneurysm.
Obstetric causes of DIC: Amniotic fluid embolism, placental abruption, eclampsia/HELLP, septic abortion, intrauterine fetal death — tissue factor release → consumption coagulopathy → paradoxical bleeding.
High Yield Summary
PPH is a clinical diagnosis — resuscitate and investigate simultaneously; never delay treatment for labs.
Diagnostic algorithm (always do Steps 1–3; EUA if source unidentified + bleeding persists):
- Palpate uterus for contraction (Tone)
- Inspect genital tract cervix to introitus under adequate light/anaesthesia (Trauma)
- Check placenta completeness (Tissue)
- Check coagulation profile (Thrombin)
- EUA in theatre to explore uterine cavity
- Laparotomy in exceptional circumstances
Key investigations: CBC, coagulation (PT/aPTT/fibrinogen), D-dimer, group & crossmatch, VBG with lactate, RFT, LFT. Fibrinogen < 2 g/L is the strongest predictor of severe PPH progression. Initial Hb may be normal in acute haemorrhage — it is a lagging indicator.
Shock Index = HR / SBP. Normal 0.5–0.7; > 0.9 suggests significant haemorrhage even with "normal" BP. Better than BP alone in young, well-compensated women.
Point-of-care: ROTEM/TEG guides targeted blood product therapy. Bedside clot test: blood failing to clot suggests coagulopathy.
High Yield Summary
4 major principles: Communication, Resuscitation, Monitoring and Investigation, Arresting the bleeding.
Resuscitation: 2× large-bore IV (14/16G), high-flow O₂, rapid crystalloid bolus 500–1000 mL (warmed Hartmann's), Foley catheter (empty bladder + monitor UO), blood products as needed. Replace: volume → red cells → clotting components (FFP, cryoprecipitate if fibrinogen < 2 g/L, platelets if < 50 × 10⁹/L with active bleeding). MTP ratio pRBC:FFP:Platelets = 1:1:1 for massive PPH.
Uterotonics for atony (treatment, in order):
- Oxytocin 10 IU IV bolus → 10 IU/hr infusion (first-line)
- Carboprost 250 μg IM q15 min, max 8 doses (CI: asthma)
- Misoprostol 800–1000 μg PR/SL (safe in asthma)
- Ergometrine / Syntometrine® 0.5 mg IM (CI: hypertension, heart disease — use oxytocin instead)
Prevention (AMTSL): Syntometrine® 1 mL IMI after delivery of fetal head (low risk); oxytocin 5 IU IVI if Syntometrine CI; carbetocin 100 μg IV for high-risk CS.
TXA 1 g IV within 3 hours (WOMAN trial) — adjunct to uterotonics, NOT a replacement.
Stepwise escalation for refractory atony: Massage + bimanual compression + empty bladder → uterotonics + TXA → intrauterine balloon tamponade → surgical (B-Lynch, uterine artery ligation, internal iliac ligation) → UAE or peripartum hysterectomy (last resort).
Immediate management of shocked PPH patient = IV fluid resuscitation before or alongside cause-specific treatment.
High Yield Summary
Acute complications: Hypovolaemic shock → multi-organ failure (AKI/ATN, shock liver, ARDS, cerebral hypoperfusion). Vicious cycle: bleeding → coagulopathy (DIC) → more bleeding. Lethal triad: hypothermia + acidosis + coagulopathy — break with warm fluids, balanced transfusion, and source control.
Massive transfusion complications: Hyperkalaemia (stored RBCs), hypocalcaemia/citrate toxicity (replace Ca²⁺), hypothermia, dilutional coagulopathy, TRALI, TACO.
Sheehan syndrome (classic long-term complication): Ischaemic necrosis of the enlarged anterior pituitary from prolonged hypotension → failure of lactation (earliest sign), amenorrhoea, loss of pubic/axillary hair, panhypopituitarism. Replace cortisol before thyroxine to avoid adrenal crisis.
Asherman syndrome: Intrauterine adhesions from curettage/instrumentation → secondary amenorrhoea, infertility; diagnosed by hysteroscopy; treated by adhesiolysis.
Other late complications: Loss of fertility (post-hysterectomy), VTE (hypercoagulable state + immobility + surgery), endometritis, psychological sequelae (PTSD, PND, tokophobia).
Memory palace hooks for Postpartum Hemorrhage
How to Use This Memory Palace
Each numbered symbol is a recall hook mapped back to this page's own notes. The Note concept column is the source of truth; the symbol logic explains why the visual cue should trigger that concept.
This first pass maps the symbols supplied for labels 1-52. Any additional labels visible in the image should be added only after they are tied back to the MBBSPedia note sections.
Definition Guardrail
This page uses the SketchEase anchor definition: PPH is blood loss >=1000 mL or symptoms/signs of hypovolemia within 24 hours after delivery, regardless of mode of delivery. Some source notes use >500 mL as an early practical trigger; treat shock immediately regardless of measured volume.
| No. | Symbol | Source tab | Note concept | Etymology / symbol logic |
|---|---|---|---|---|
| 1 | 1000 mL red paint can | Summary / Dx | PPH is blood loss >=1000 mL or signs/symptoms of hypovolemia within 24 hours after delivery. | Red paint stands for blood loss; the 1000 mL label marks the formal threshold. |
| 2 | Sun on red paint can | Summary / Dx | The definition applies within the first 24 hours after delivery, and shock should be treated regardless of exact measured volume. | The sun cues the first day after birth. |
| 3 | Sun painting in primary colors | Summary / Etiology | Primary PPH occurs within 24 hours of delivery. | "Primary" colors plus a single-day sun cue the first 24 hours. |
| 4 | Secondary artwork of three moons | Summary / Etiology | Secondary PPH occurs after 24 hours and up to 6-12 weeks postpartum. | Moons cue later nights after delivery; "secondary" artwork separates it from the primary sun. |
| No. | Symbol | Source tab | Note concept | Etymology / symbol logic |
|---|---|---|---|---|
| 9 | Red splatter painting on a floppy canvas | Etiology | Uterine atony is the most common cause of PPH; the boggy uterus fails to contract and loses the "living ligature." | A floppy canvas lacks tone, just like an atonic uterus. |
| 10 | Thick glob of paint stuck to the splatter painting | Etiology / Dx | Retained placental tissue prevents full uterine contraction and causes ongoing bleeding. | A stuck glob inside the scene represents tissue left behind in the uterine cavity. |
| 11 | Inverted painting | Etiology / Dx | Uterine inversion can follow excessive cord traction and causes haemorrhage plus shock. | The painting turned inside-out mirrors the uterus turning inside-out. |
| 12 | Plate stuck to muscle painting | Etiology / Dx | Placenta accreta spectrum is abnormally adherent placenta, often with no safe cleavage plane. | The plate stuck to muscle cues placenta attached to myometrium. |
| 13 | Slash through muscle painting | Etiology / Dx | Trauma causes PPH through cervical, vaginal, perineal, periurethral, rectal, uterine, or broad-ligament injury. | A slash is the laceration/trauma hook. |
| 14 | Wet red paint dripping down the canvas | Etiology / Dx | Thrombin causes include inherited bleeding tendency, thrombocytopenia, DIC, dilutional coagulopathy, and massive transfusion coagulopathy. | Paint that will not clot or dry cues non-clotting blood. |
| 15 | Woman with large waist | Etiology | Obesity and uterine overdistension increase atony risk. | A stretched body silhouette cues poor tone from distension. |
| 16 | Woman with multiple children | Etiology | Grand multiparity reduces myometrial responsiveness and increases atony risk. | Many children cue repeated pregnancies and reduced uterine tone. |
| 17 | Multiple buns in the uterus bag | Etiology | Multiple pregnancy overdistends the uterus and increases atony risk. | Multiple buns cue multiple fetuses in one uterus. |
| 18 | Water coming out of the uterus bag | Etiology | Polyhydramnios overdistends the uterus and increases atony risk. | Water escaping the bag cues excess amniotic fluid. |
| 19 | Big bun in the uterus bag | Etiology | Macrosomia / large-for-gestational-age baby overdistends the uterus and increases atony risk. | One oversized bun cues one oversized fetus. |
| 20 | History exhibition catalog | Etiology | Previous PPH, manual removal of placenta, precipitated labour, or repeated suction evacuation increase risk. | A history catalog cues important obstetric history. |
| 21 | Art history book with palette knife | Etiology | Prior uterine surgery, Caesarean section, myomectomy, or uterine instrumentation increase risk of poor contraction and accreta-spectrum disease. | A knife on the art-history book cues prior surgical injury to the uterus. |
| 22 | Ox sculpture with long horns | Etiology | Induced or augmented labour can cause oxytocin receptor desensitisation and uterine fatigue. | The ox cues oxytocin; long horns cue prolonged exposure. |
| 23 | Latex balloons on fire | Etiology | Prolonged labour and chorioamnionitis impair myometrial contraction. | Inflamed balloons cue an infected, inflamed intra-amniotic environment. |
| 24 | Smoke detector abrupting out of the wall | Etiology / Complications | Placental abruption is an antepartum haemorrhage risk factor and an obstetric trigger for DIC. | The detector abruptly coming off the wall cues abruption and alarm-level bleeding. |
| 25 | "As seen in ART MAG" poster | Etiology | Magnesium sulphate and other tocolytic/relaxing drugs can worsen uterine atony. | "MAG" cues magnesium; the poster is a medication-risk hook. |
| 26 | "No pain, no gain" sign | Etiology | General anaesthesia and volatile agents relax uterine smooth muscle and increase atony risk. | "No pain" cues anaesthesia; relaxed muscle loses contractile gain. |
| 27 | Wet red paint titled "War is Hell" | Etiology / Dx | Bleeding tendencies, anticoagulants, HELLP/eclampsia, abruption, sepsis, and amniotic fluid embolism can drive Thrombin problems. | War-like uncontrolled red paint cues coagulopathic bleeding. |
| 28 | Vacuum near lacerated painting | Etiology / Dx | Operative vaginal delivery and macrosomia raise laceration risk. | The vacuum cues assisted delivery; the slash cues genital tract trauma. |
| 29 | Inverted painting hanging from a short tense cord | Etiology | Do not pull on the umbilical cord before placental separation; excessive traction can cause partial separation, PPH, or inversion. | A short tense cord pulling the painting inward cues cord traction. |
| 30 | Spilled fluid on wet paint painting | Etiology / Dx | Amniotic fluid embolism is an obstetric cause of DIC and severe PPH. | Spilled fluid mixing with wet paint cues amniotic fluid triggering coagulopathy. |
| No. | Symbol | Source tab | Note concept | Etymology / symbol logic |
|---|---|---|---|---|
| 31 | Man fainting with raised heart watch | Dx / Complications | Tachycardia is early; hypotension is late. Shock index HR / SBP >0.9 suggests significant haemorrhage. | The heart watch cues pulse; fainting cues decompensated shock. |
| 32 | Kid holding a floppy canvas | Dx | Palpate the fundus first: soft, boggy, enlarged uterus means Tone / uterine atony. | The floppy canvas recalls the boggy uterus in your hands. |
| 33 | Slashed painting | Dx | Firm uterus plus bright red ongoing bleeding should trigger systematic genital tract inspection for lacerations. | The slash cues Trauma as the bleeding source. |
| 34 | Globe light by inverted painting | Dx | Look for a globular mass at the introitus when uterine inversion is suspected. | "Globe" cues the rounded mass produced by an inverted uterus. |
| 35 | Sonar waves next to a thick stripe | Dx | Ultrasound can support retained-products diagnosis; an endometrial thickness >10 mm or echogenic intrauterine material is suspicious. | Sonar waves cue ultrasound; the thick stripe cues endometrial thickness. |
| 36 | Four T's on the pedestal | Summary / Dx | Use the 4 T's diagnostic algorithm: Tone, Trauma, Tissue, Thrombin. | The four block letters are the organizing scaffold for the whole case. |
| 37 | "1" labels beside primary-cause paintings | Summary / Etiology | Primary PPH causes include atony, retained tissue/accreta, genital tract trauma, uterine inversion, rupture, and coagulopathy. | "1" cues primary PPH in the first 24 hours. |
| 38 | "2" labels beside retained tissue and wet paint | Summary / Etiology | Secondary PPH: endometritis first, then retained products, subinvolution, and less commonly GTD, pseudoaneurysm, or coagulopathy. | "2" cues secondary PPH after the first day. |
| No. | Symbol | Source tab | Note concept | Etymology / symbol logic |
|---|---|---|---|---|
| 39 | Bartender with ivy bracelets | Mx | Start resuscitation immediately: call for help, high-flow oxygen, two large-bore IVs, fluids, bloods, monitoring, Foley catheter. | Ivy sounds like IV; bracelets cue vascular access. |
| 40 | Drinks sponsored by the Blood Bank | Mx | Alert the blood bank, crossmatch early, transfuse red cells and components as needed, and activate MTP for massive PPH. | The bar sponsor turns the scene into a transfusion station. |
| 41 | Bartender massaging a drink with two purple-gloved hands | Mx | Uterine massage and bimanual compression are first-line mechanical measures for atony. | Two gloved hands squeezing the drink cue bimanual uterine compression. |
| 42 | Yellow drink spilling through a straw | Mx | Empty the bladder with a Foley catheter; this both improves uterine tone and monitors urine output. | Yellow liquid through a tube cues urine drainage. |
| 43 | Gin and tonic on the bar menu | Mx | Uterotonic agents are first-line pharmacologic treatment for uterine atony. | "Tonic" cues uterotonic treatment. |
| No. | Symbol | Source tab | Note concept | Etymology / symbol logic |
|---|---|---|---|---|
| 44 | Ox statue | Mx | Oxytocin is first-line for prevention and treatment of atony-related PPH. | Ox cues oxytocin. |
| 45 | Morning glory flowers | Mx | Ergometrine / Syntometrine causes sustained uterine contraction but is contraindicated in hypertension and heart disease. | Morning glory seeds are associated with ergot-like alkaloids, cueing ergometrine. |
| 46 | Pro Slugger bat in "Fake alphaRT" box | Mx | Carboprost is a prostaglandin F2-alpha analogue; it is contraindicated in asthma. | The pro-staglandin slugger and alpha cue PGF2-alpha; the bat also cues bronchospasm/asthma risk. |
| 47 | Missed throw of an empty "E" bottle | Mx | Misoprostol is a prostaglandin E1 analogue; fever and shivering are common side effects. | The "E" bottle cues PGE1; the missed throw cues misoprostol. |
| 48 | Art EXAM packet | Mx | Tranexamic acid is an anti-fibrinolytic adjunct given early, ideally within 3 hours; it stabilises clot and does not replace uterotonics. | "EXAM" cues tranEXAMic acid. |
| 49 | Bakery balloon compressing pastries | Mx | Intrauterine balloon tamponade is the next escalation for refractory atony. | Bakery/Bakri and compression cue the Bakri balloon. |
| 50 | Suspenders on the bartender | Mx | B-Lynch compression suture is a surgical uterus-sparing escalation. | Suspenders brace and compress like a B-Lynch suture. |
| 51 | Bartender applying whipped-cream foam beside two red straws | Mx | Surgical devascularisation or uterine/internal iliac artery ligation can arrest bleeding; UAE is an option when stable and available. | Foam and red straws cue blocking or ligating bleeding vessels. |
| 52 | Bartender throwing away uterus-shaped glass spilling red wine | Mx | Peripartum hysterectomy is the last resort for uncontrollable life-threatening haemorrhage. | Throwing away the uterus-shaped glass cues removing the uterus to save the patient. |
| No. | Symbol | Source tab | Note concept | Etymology / symbol logic |
|---|---|---|---|---|
| 5 | Dice keychain on the art critic | Complications | DIC and dilutional/massive-transfusion coagulopathy create a vicious cycle of bleeding -> coagulopathy -> more bleeding. | Dice sounds like DIC and cues the loss of clotting control. |
| 6 | Cracked kidney earring on the art critic | Complications | Hypovolaemic shock can cause AKI/ATN and renal failure. | The cracked kidney cues renal hypoperfusion injury. |
| 7 | Shark shoes on the art critic | Complications | Hypovolaemic shock can progress to multi-organ failure, ARDS, cerebral hypoperfusion, and death. | Shark sounds like shock and makes the danger memorable. |
| 8 | Ms. Sheehan with pituitary purse and skulls | Complications | Sheehan syndrome is ischaemic anterior pituitary necrosis after prolonged hypotension; failure of lactation is the earliest sign. | The named art critic anchors Sheehan; the pituitary purse identifies the injured gland. |
Antepartum Hemorrhage
Antepartum hemorrhage is bleeding from the genital tract from 24 weeks of gestation until delivery, most commonly caused by placenta praevia or placental abruption.
Pre-eclampsia
Pre-eclampsia is a pregnancy-specific multisystem disorder occurring after 20 weeks, characterised by new-onset hypertension with end-organ involvement, and may progress to eclampsia.