1. A 36 year old leady from AL-Mabeala G8P7, LMP:15/5/2012 at 37weeks of gestation, EDD: 20/2/2013 referred from HC for evaluation of High blood pressure in the last 5 days, avg of BP 130/90 mmHg. K/C/O PIH on labetalol.

2. P/C Hx: She complains of headache since 2 weeks which is bilateral, sharp innature, progressive, intermittent, aggravated by waking, not relived by paracetamol, and it disturbing her daily activity. The headache associated with nausea, vomiting, dizzenss, palpitation, fatigability, labiality of mood. But there is no history of fall or visual disturbance or abnormal movements. She sleeps well. At the same episode she developed cough which was intermittent,continuous all the day, productive of yellow sputum, small amount, no blood, no foul smell. It is Associated with difficulty in breathing in exertion. No audible sounds or fever. Also she complains of abdominal pain and cramps (labour pain).And she noticed that her leg start to be swelling in the last two days markedly. She denied any urinary symptoms (pain, burning sensation, UTIsymptoms). Bowel habits are normal. No vaginal discharge or leaking. 3. OBS Hx: G8P7, all her previous pregnancies were uneventful (SVD,normal baby weight, no complications) except for the last pregnancy were she developed high BP at 37+ weeks of gestation and she was induced. After Last pregnancy shedeveloped low Hb post partum(Hb 6mg/dL with blood loss 100 mL) received 2 units of blood post delivery. Current pregnancy: all her antenatal scans were normal, allbooking investigations were normal. Booking Hb was 10,7 mg/dL; at 32-34 Hb was 8,8 mg/dL OGCT: 7.5 Anomaly scan normal Lat scan on 2/2/2013: cephalic, AFI: 12cm, Doppler normal, efw 3.2Kg 4. PMH/PSH: -she was admitted on 30/1/2013 due to leg pain, Doppler done normal,her Bp at that admission were normal -no HTN, DM -no surgery was done for her Mediaction Hx: PIH in labetalol Family Hx: No consanguinity ,Futher with HTN and DM, bronchial asthma (sister, and a brother) Social History: Housewife, husband is driver, good socioeconomic status, no history ofsmoking or Alcohol consumption. No history of contact with sick people. Allergic Hx: Unremarkable 5. At admission: Patient looks well oriented, alert, not in distress or pain. Her vitals: pulse 84/min, BP 120/80, rechecked after 1hr 140/87 mmHg, temp 36.8 General assessment: bilateral leg edema Chest Examination: chest with wheeze bilaterally, no crepition CVS: normal Abdominal examination: distended abdomen, abdominal wall thick uterus relaxed, cephalic presentation CTG: normal Scan: liquor normal, Doppler normal, AFI 12 cm, efw 3.2Kg 6. Blood tests: CBC: Hb (9.5 g/dL), Hcrts low, MCV low, platelet normal, WBC (14,5 high),neutophils(10.1 high) CRP:7.6 mg/L >>> high: low urea (2.2 mmol/L), Na, CL-, K+, creatinine are all normal U&E: normal enzymes, low albumin (25 g/L) LFT Uric acid: 190 normal Ferritin in serum/plasma (2/2/2013): Folate & vitB12:normalECHO: normalChest x-ray: normal10 ug/L low 7. Management: Continue BP monitoring Treat chest condition IV augmentin and regular6hourly salbutamol nebulizer Patient discharged after two days of admission with: Oral antibiotics (augmentin), Haematinic, and Methyldopa 250mg TID For admission on 12/2/2013 for IOL on 13/2/2013 Informed sos 8. Pregnancy Induced HTN 9. In pregnancy Increase Aldosterone increase bloodvolumes increase HR (15 beats/min more than usual), SV, CO (50%, mostly during the first trimester). Increase progesteron smooth musclerelaxation and overall vasodilation systemic vascular resistance drops Diastolic BP decreases between 1226 wks Diastolic BP increases again to pre-pregnancy levels by 36 weeks 10. Pregnancy-induced hypertension (PIH) is asyndrome of hypertension with or without proteinuria and edema, with the clinical manifestation usually occurring late in pregnancy and regressing after delivery of the conceptus. Hypertension is the most common medicalproblem encountered during pregnancy, complicating 2-3% of pregnancies. 11. Classification: Gestational or transient HTN Chronic HTN Chronic HTN with superimposedpreeclampsia Preeclampsia/ eclampsia 12. HTN without proteinuria first appears after 20 weeksof gestation or within 48-72 hour after delivery and resolves by 12 weeks Postpartum. Is a retrospective diagnosis Thus, reassessment upto 12 weeks postpartum is necessary to establish a final definitive diagnosis. 13. Most will have essential HTN but small percentwill have secondary HTN due to renal, vascular and endocrine causes. 14. 15. Difficult to distinguish it from poorly controlledchronic HTN especially if women is not seen until after 20th wk of gestation Carries a worse prognosis than does eithercondition alone. 16. A syndrome unique to pregnancy where new HTNand proteinuria developed in the latter half of gestation. More common in primigravida If occur in the early second trimester hydatidiform mole or chriocarcinoma should be considered 17. New development of HTN (sBP>=140mmHg,dBP>=90 mmHg) in previously normo-tensive women after 20 weeks of gestation New onset proteinuria after 20weeks of gestation(protein in urine > 0.3g in timed 24-hour urin collection Usually correlqted with urinanalysis >30mg/dL and urinedipstick +1. Divided into mild and severe Presence of one of the following considered assevere: 18. Classification 19. causes EnviromentalAbnormal placental implantaionMaternal immunological intoleranceGeneticsCVS and inflammatory changes 20. Maternal personal risk factors for preeclampsia First pregnancy New partner/paternity Age younger than 18 years or older than 35 years History of preeclampsia Family history of preeclampsia in a first-degree relative Black race Obesity (BMI 30) Interpregnancy interval less than 2 years or longer 21. Maternal medical risk factors for preeclampsia Chronic hypertension, especially when secondary to such disorders as hypercortisolism, hyperaldosteronism, or renal artery stenosis Preexisting diabetes (type 1 or type 2), especially with microvascular disease Renal disease Systemic lupus erythematosus Obesity Thrombophilia History of migraine Use of selective serotonin uptake inhibitor antidepressants (SSRIs) beyond the first trimester 22. Chronic HTN, immune mediate vascular damage, obesity, DM, dyslipidemia cause placental ischemia andhypoxia Release of toxins and Cytokines in the blood causing widespread of inflammatory processEndothelial dysfunction Occur due to imbalance between vasodilators (PGE, prostacysline, NO) and vasoconstrictors (PGF, trombaxan and endotheline I)Net results of this is vasoconstriction andincrease PVR Systemic HTN, DIC, HELLP syndrome, and placental ischemia 23. Generalized vasospasmLower renal flow and glomerular filtration rate Proteinuria oliguriaDecreased cerebral blood flowActivation of coagulation system . HELLP syndrome 24. In most women, sign and symptoms first becomeapparent after 34 weeks of gestation 10 % of women, preeclampsia develop before34 weeks of gestation 5 %, preeclampsia is first recognized postpartumusually within 48 hours of delivery 25. mild hypertension (140/90 and