Maternal Critical Illness Rapid Assessment
Urgent maternal stabilization, left uterine displacement, syndromic differentiation, and multidisciplinary escalation.
An educational representation of clinical reasoning, not a diagnostic algorithm or personalized medical advice — always apply clinical judgment and institutional protocols.
Caution
Escalate — Red Flags & Critical Warnings
- Performing CPR on a supine pregnant patient without Left Uterine Displacement reduces cardiac output by 40%.
- Delaying Resuscitative Hysterotomy beyond 4–5 minutes of cardiac arrest drastically reduces maternal and fetal survival.
Related Bedside Clinical Problems (24)
Bedside PresentationsBedside triage of acute desaturation: signal verification, immediate danger screening (DOPE / tension pneumothorax), oxygen escalation ladder, and mechanism-based differential.
Algorithmic troubleshooting of acute patient-ventilator collapse: the DOPE framework, peak vs plateau pressure differentiation, auto-PEEP evaluation, and manual bagging separation.
Airway preservation and bleeding localization: non-massive vs massive hemoptysis (> 100–200 mL/hr), lateral decubitus positioning, isolation of the bleeding lung, and endovascular/bronchoscopic intervention.
Linked Deep-Dive Topics (8)
Reference KnowledgeMaternal physiology, preeclampsia/eclampsia, HELLP vs AFLP, postpartum hemorrhage (MTP/TXA), peripartum cardiomyopathy, and arrest.
The trauma lethal diamond (hypothermia, acidosis, coagulopathy, hypocalcemia), 1:1:1 massive transfusion (PROPPR trial), early TXA (CRASH-2), and TEG/ROTEM algorithms.
Pulmonary vascular occlusion, acute RV pressure overload, ESC/AHA risk stratification, systemic thrombolysis, catheter-directed therapies, and hemodynamic support.
Life-threatening organ dysfunction caused by a dysregulated host response to infection — recognized by an acute rise in SOFA score, not by infection plus fever alone.
Primary pump failure, SCAI staging (A–E), PAC hemodynamics (CPO, PAPi), inotrope selection, emergent revascularization, and mechanical circulatory support.
Tissue-factor-driven coagulation activation, antithrombin/protein C depletion, PAI-1-associated fibrinolytic suppression, ISTH 2025 DIC assessment, comparison with TTP/HUS/HIT, and targeted replacement.
Hyperammonemia, cytotoxic cerebral edema, balanced coagulopathy, N-acetylcysteine, 3% saline neuroprotection, CRRT ammonia clearance, and King's College transplant criteria.
Multimodal resuscitation, post-cardiac arrest syndrome management, targeted temperature control, and delayed neuroprognostication.
Evidence status
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