MATERNAL HEMORRHAGE

SCF ENCYCLOPEDIA ENTRY

MATERNAL HEMORRHAGE

SCF-RDOS Obstetric Blood Loss, Maternal Hemodynamic Failure & Maternal–Fetal Perfusion Disorders Registry

Disease Classification:

Obstetric Emergency / Maternal Vascular Disorder / Hemodynamic Instability Syndrome / Pregnancy-Associated Hemorrhagic Disease / Maternal–Fetal Critical Care Condition

Master Registry Code:

SCF-MH-0001

I. DEFINITION

Maternal Hemorrhage refers to excessive blood loss occurring during pregnancy, labor, delivery, or the postpartum period that threatens maternal physiologic stability and fetal well-being.

Maternal hemorrhage remains one of the leading causes of maternal mortality worldwide and may result in:

Hypovolemic shock
Disseminated intravascular coagulation (DIC)
Multiorgan failure
Maternal death
Fetal hypoxia
Fetal death

Within the Synergistic Compatibility Framework (SCF), maternal hemorrhage is modeled as a:

Maternal perfusion collapse syndrome
Obstetric vascular integrity failure disorder
Maternal–fetal oxygen transport disruption architecture
Hemodynamic decompensation cascade

II. CORE SCF ETIOPATHOGENIC PRINCIPLE

Central SCF Thesis

Maternal hemorrhage develops when disruption of vascular integrity, uterine hemostasis, placental attachment, coagulation systems, or reproductive tract structures results in blood loss exceeding physiologic compensatory capacity, leading to impaired tissue perfusion and systemic shock.

This propagates through:

Vascular injury or bleeding source
Progressive blood loss
Reduced circulating volume
Hemodynamic instability
Tissue hypoperfusion
Organ dysfunction
Maternal and fetal compromise

III. MAJOR MATERNAL HEMORRHAGE REGISTRY

A. ANTEPARTUM HEMORRHAGE

Occurs before delivery.

Major causes:

Placenta previa
Placental abruption
Uterine rupture
Vasa previa

Associated with:

Placental Abruption

B. INTRAPARTUM HEMORRHAGE

Occurs during labor.

Associated with:

Uterine rupture
Cervical trauma
Operative delivery complications

C. POSTPARTUM HEMORRHAGE (PPH)

Most Common Form

Defined clinically as significant blood loss following delivery.

Major causes include:

Uterine atony
Retained placental tissue
Genital tract trauma
Coagulopathy

Associated with:

Postpartum Hemorrhage

D. MASSIVE OBSTETRIC HEMORRHAGE

Life-threatening blood loss requiring:

Massive transfusion
Intensive care
Surgical intervention

IV. ETIOLOGIC DOMAINS

A. UTERINE ATONY

Most common cause of postpartum hemorrhage.

Results from:

Failure of uterine contraction
Inadequate vessel compression

B. PLACENTAL DISORDERS

Includes:

Placenta previa
Placenta accreta spectrum
Placental abruption

Associated with:

Placenta Accreta Spectrum

C. TRAUMA

Includes:

Cervical lacerations
Vaginal lacerations
Uterine rupture

D. COAGULOPATHY

Includes:

DIC
Inherited bleeding disorders
Severe preeclampsia complications

Associated with:

Disseminated Intravascular Coagulation

E. RETAINED PRODUCTS OF CONCEPTION

Causes:

Persistent bleeding
Failure of uterine involution

V. SCF MULTI-OMIC PATHOGENESIS

A. VASCULAR INTEGRITY LAYER

Normal pregnancy requires:

Stable maternal vasculature
Controlled placental attachment

Failure causes:

Vessel disruption
Active hemorrhage

B. HEMOSTATIC CONTROL LAYER

Involves:

Platelets
Coagulation factors
Fibrin stabilization

Disruption promotes:

Persistent bleeding

C. HEMODYNAMIC FAILURE LAYER

Blood loss results in:

Reduced preload
Decreased cardiac output
Compensatory tachycardia

D. OXYGEN TRANSPORT LAYER

Hemorrhage reduces:

Hemoglobin delivery
Tissue oxygenation

E. ORGAN HYPOPERFUSION LAYER

Targets include:

Brain
Kidneys
Liver
Heart
Placenta

F. FETAL COMPROMISE LAYER

May produce:

Hypoxia
Acidosis
Fetal distress

Associated with:

Fetal Distress

VI. SCF FAULT-TIER ARCHITECTURE

SCF Tier	Maternal Hemorrhage Fault
Tier I	Vascular or placental injury
Tier II	Active blood loss
Tier III	Hemodynamic instability
Tier IV	Organ hypoperfusion
Tier V	Shock and systemic failure

SCF fault progression models maternal hemorrhage as escalation from localized bleeding into systemic perfusion collapse.

VII. MAJOR CLINICAL MANIFESTATIONS

A. EARLY FINDINGS

Includes

Vaginal bleeding
Tachycardia
Pallor
Anxiety

B. PROGRESSIVE FINDINGS

Includes

Hypotension
Dizziness
Oliguria
Altered mental status

C. SEVERE FINDINGS

Includes

Hypovolemic shock
Organ failure
Cardiovascular collapse

VIII. FETAL CONSEQUENCES

Acute

Fetal hypoxia
Fetal bradycardia
Emergency delivery

Severe

Intrauterine fetal demise
Neonatal encephalopathy

Associated with:

Hypoxic-Ischemic Encephalopathy

IX. MAJOR COMPLICATIONS

Maternal

Shock
Acute kidney injury
DIC
Multiorgan failure

Associated with:

Acute Kidney Injury

Endocrine

Severe hemorrhage may cause:

Pituitary infarction

Associated with:

Sheehan Syndrome

Reproductive

May result in:

Hysterectomy
Future fertility impairment

X. SCF RHENOVA INTERPRETATION

Within the SCF–RHENOVA model, maternal hemorrhage represents:

Hemodynamic bioenergetic variance collapse
Oxygen transport insufficiency
Perfusion network failure

Key RHENOVA Signatures

Hypovolemia
Mitochondrial stress
Tissue hypoxia
Endothelial injury
Organ ischemia

XI. SCF DBI INTERPRETATION

Under the SCF Decentralized Biological Intelligence (DBI) framework, maternal hemorrhage disrupts:

Circulatory communication networks
Oxygen-distribution systems
Maternal–fetal resource allocation pathways
Tissue survival signaling
System-wide adaptive response architectures

This transforms blood loss into distributed physiologic information-processing failure.

XII. QUANTUM & PERFUSION-HOMEOSTASIS INTERPRETATION

Within SCF Quantum Medicine:

Blood functions as the body’s primary transport medium for oxygen, nutrients, immune mediators, and signaling molecules.
Maternal hemorrhage represents catastrophic loss of transport-network integrity.
Clinical manifestations emerge when compensatory mechanisms fail to preserve systemic perfusion coherence.

XIII. DIAGNOSTIC ARCHITECTURE

Clinical Assessment

Includes

Quantification of blood loss
Vital signs monitoring
Obstetric examination

Laboratory Evaluation

Core Studies

Complete blood count
Coagulation profile
Fibrinogen
Blood type and crossmatch

Imaging

May include:

Ultrasound
Placental evaluation
Identification of retained products

XIV. SCF PCR MODEL (PREVENTATIVE–CURATIVE–RESTORATIVE)

A. PREVENTATIVE

Risk Identification

Includes:

Placenta previa screening
Accreta risk assessment
Hemorrhage preparedness planning

B. CURATIVE

Immediate Stabilization

Airway support
Oxygen administration
Large-bore IV access
Fluid resuscitation

Uterotonic Therapy

Common agents include:

Oxytocin
Methylergonovine
Carboprost

Hemostatic Therapy

May include:

Tranexamic Acid

Blood Product Support

Includes:

Packed red blood cells
Plasma
Platelets
Cryoprecipitate

Surgical Intervention

When necessary:

Uterine balloon tamponade
Arterial embolization
Hysterectomy

C. RESTORATIVE

Recovery Phase

Anemia correction
Nutritional rehabilitation
Endocrine evaluation
Psychological support

XV. ORIGIN-OF-DISEASE & CYTOGENESIS PROGRESSION TIMELINE

Stage	Cytogenic Event	Clinical Consequence
Stage 1	Vascular or placental disruption	Active bleeding
Stage 2	Progressive blood loss	Hypovolemia
Stage 3	Reduced perfusion	Organ stress
Stage 4	Tissue hypoxia	Functional impairment
Stage 5	Shock physiology	System failure
Stage 6	Recovery or decompensation	Long-term outcome

Cytogenesis Loci

Primary loci:

Uterus
Placenta
Uterine arteries
Cervix
Vaginal tissues

Secondary loci:

Heart
Brain
Kidneys
Liver
Maternal–fetal circulation

XVI. REGULATORY & CLINICAL MANAGEMENT FRAMEWORK

Relevant clinical domains:

Obstetrics
Maternal–Fetal Medicine
Critical Care Medicine
Transfusion Medicine
Emergency Medicine

Therapeutic development requires:

Hemodynamic outcome monitoring
Maternal survival assessment
Fetal outcome surveillance
Long-term reproductive follow-up

XVII. SCF API DISCOVERY & THERAPEUTIC PRIORITIES

Potential Therapeutic Domains

Rapid hemostatic biologics
Uterine contractility optimization agents
Endothelial stabilization therapies
Precision hemorrhage-control systems
Maternal–fetal perfusion preservation technologies

Safety Requirements

All interventions require:

Maternal cardiovascular monitoring
Coagulation surveillance
Organ-function assessment
Maternal and neonatal outcome tracking

XVIII. SCF SUMMARY

Maternal Hemorrhage = Maternal Perfusion and Hemostatic Synchronization Failure Syndrome

Within SCF:

Maternal hemorrhage is a major obstetric emergency resulting from excessive blood loss before, during, or after delivery.
Uterine atony, placental disorders, trauma, and coagulopathy are the principal causes.
Progressive blood loss impairs oxygen transport, tissue perfusion, and maternal–fetal stability.
Rapid recognition, hemostatic intervention, transfusion support, and source control are essential for survival.
Future therapeutic strategies focus on precision hemorrhage prevention, rapid hemostatic restoration, uterine contractility enhancement, and preservation of maternal–fetal perfusion networks.

MASTER REGISTRY INDEX

SCF-MH-0001 — Maternal Hemorrhage

SCF-MH-VASC-0002 — Vascular Integrity Failure Layer

SCF-MH-HEMO-0003 — Hemodynamic Collapse Layer

SCF-MH-PLACENTA-0004 — Placental Hemorrhage Module

SCF-MH-SHOCK-0005 — Hypovolemic Shock Layer

SCF-MH-RHENOVA-0006 — Perfusion Bioenergetic Variance Layer

SCF-MH-DBI-0007 — Maternal–Fetal Resource Allocation Failure Layer

SCF-MH-PCR-0008 — Preventative–Curative–Restorative Management Framework