Postpartum Hemorrhage

The high-yield in-house definition is unified across modes of delivery:

^[1][3][4]

Definition trap: Older teaching commonly used > 500 mL after vaginal delivery but > 1000 mL after Caesarean section. ^[2] Current in-house teaching uses > 500 mL after either mode of delivery. ^[1][3][4] ACOG instead uses >= 1000 mL or hypovolaemia within 24 hours regardless of delivery mode, so follow the named/local guideline in an exam. In practice, treat the patient, not the number.

^[1][2][3][4]

Primary PPH is often torrential and can cause shock and death within a short period of time. ^[3][4]

• 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]

1. 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.

2. 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.

3. 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]

4. 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.

5. 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 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.

Differential diagnosis including the 4 T's — Tone, Tissue, Trauma, Thrombin. ^[1][2]

This mnemonic is the backbone of your approach to PPH. Each "T" represents a category of cause, and they are listed roughly in order of frequency:

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.

"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)
• 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

Multiple T's often coexist — e.g., prolonged atony → massive blood loss → dilutional coagulopathy → DIC → further bleeding. Always systematically assess ALL four T's.

• 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

As detailed above: Tone, Tissue, Trauma, Thrombin.

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]

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.

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.

Monitoring and investigation should be performed alongside resuscitation. ^[5] The lecture notes on shock assessment ^[7][8] guide the core blood panel:

Interpreting the Clotting Profile — A Recap from First Principles [8]

Imaging is not first-line in acute primary PPH (this is a clinical and surgical diagnosis). However, imaging has specific roles:

• 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]

1. Volume replacement (e.g., giving intravenous fluids) to maintain an effective circulation
2. Red cell replacement (oxygen carriage)
3. Blood components replacement (platelet and FFP) to correct coagulation defect

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

• "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.

Blood components replacement (platelet and FFP) to correct coagulation defect. ^[5][6]

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.

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].

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:

• 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

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)

• 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: