Acute fatty liver of pregnancy (AFLP) is a rare microvesicular steatotic liver disease of late gestation, linked to impaired mitochondrial fatty acid β-oxidation, in which management centres on recognition and delivery before overt hepatic and multiorgan failure has developed. The Swansea criteria, which require six or more of fourteen features in the absence of an alternative explanation, define AFLP in guidelines and in most published cohorts. This narrative review examines how the criteria behave across the course of the illness and which markers might signal the disease earlier. The criteria are frequently fulfilled once AFLP is clinically established, but their accuracy against an independent reference standard derives from one small, high-prevalence biopsy series, and their specificity against haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome and other causes of acute liver failure appears limited. Because several criteria index established organ failure, the threshold may remain unmet earlier in the illness, a hypothesis consistent with limited retrospective evidence; to our knowledge, no study has evaluated the criteria prospectively at initial presentation. We relate each criterion to hepatic energy failure and appraise candidate early markers, including coagulation indices, antithrombin, conjugated hyperbilirubinaemia, hypocholesterolaemia, soluble fms-like tyrosine kinase-1 and metabolite-level signals of fatty acid oxidation failure; none has a validated early diagnostic threshold. We outline a conceptual, hypothesis-generating framework for prospective research that would complement, not replace, the Swansea case definition.

Chronic venous disease (CVD) in pregnancy is common, poorly codified, and interpreted with diagnostic thresholds, severity instruments and treatment algorithms all derived outside pregnancy. This narrative review synthesises the mechanistic, epidemiological, diagnostic and therapeutic literature, keeping pregnancy-specific evidence separate from evidence extrapolated from non-pregnant populations. Gestational change is characterised principally by increased venous capacitance and vein-wall distension; ambulatory venous hypertension was not demonstrated in the two pregnancy studies assessing it; and new reflux develops in a minority, undetectable postpartum in the one study reporting it. Physiological adaptation, CVD and thrombotic pathology overlap clinically, deep vein thrombosis and superficial vein thrombosis being at once the principal differential diagnoses and potential complications. Management is correspondingly conservative: compression relieves symptoms but has not been shown to prevent varicose veins, routine initiation of venoactive drugs is not supported, and intervention is deferred other than in exceptional circumstances. A venous finding first detected in pregnancy warrants postpartum reassessment before it is taken for established disease. A trimester-stratified framework spanning preconception to late postpartum reassessment is proposed; it is evidence-informed rather than prospectively validated, and is not a guideline.