Hypertension in pregnancy
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Hypertension in pregnancy

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done by Al Yaqdhan Al Atbi

done by Al Yaqdhan Al Atbi

Sultan Qaboos university- Oman

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Hypertension in pregnancy Hypertension in pregnancy Presentation Transcript

  •  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.
  •  P/C Hx:  She complains of headache since 2 weeks which is bilateral, sharp in nature, 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, UTI symptoms). Bowel habits are normal. No vaginal discharge or leaking.
  •  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 she developed 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, all booking 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
  •  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 of smoking or Alcohol consumption. No history of contact with sick people.  Allergic Hx:  Unremarkable
  •  At admission:  Patient looks well oriented, alert, not in distress or pain.  Her vitals: pulse 84/min, BP 120/80, rechecked after 1 hr 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
  •  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: normal  ECHO: normal  Chest x-ray: normal 10 ug/L low
  •  Management:  Continue BP monitoring  Treat chest condition IV augmentin and regular 6hourly 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
  • Pregnancy Induced HTN
  •  In pregnancy  Increase Aldosterone increase blood volumes increase HR (15 beats/min more than usual), SV, CO (50%, mostly during the first trimester).  Increase progesteron smooth muscle relaxation and overall vasodilation systemic vascular resistance drops Diastolic BP decreases between 12–26 wks  Diastolic BP increases again to pre- pregnancy levels by 36 weeks
  •  Pregnancy-induced hypertension (PIH) is a syndrome 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 medical problem encountered during pregnancy, complicating 2-3% of pregnancies.
  •  Classification:  Gestational or transient HTN  Chronic HTN  Chronic HTN with superimposed preeclampsia  Preeclampsia/ eclampsia
  •  HTN without proteinuria first appears after 20 weeks of gestation or within 48-72 hour after delivery and resolves by 12 weeks Postpartum.  Is a retrospective diagnosis Thus, reassessment up to 12 weeks postpartum is necessary to establish a final definitive diagnosis.
  •      Most will have essential HTN but small percent will have secondary HTN due to renal, vascular and endocrine causes.
  •   
  •  Difficult to distinguish it from poorly controlled chronic HTN especially if women is not seen until after 20th wk of gestation  Carries a worse prognosis than does either condition alone.
  •  A syndrome unique to pregnancy where new HTN and 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
  •   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 urine dipstick +1.  Divided into mild and severe  Presence of one of the following considered as severe:
  • Classification
  • causes Enviromental Abnormal placental implantaion Maternal immunological intolerance Genetics CVS and inflammatory changes
  • 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
  • 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
  • Chronic HTN, immune mediate vascular damage, obesity, DM, dyslipidemia cause placental ischemia and hypoxia Release of toxins and Cytokines in the blood causing widespread of inflammatory process Endothelial dysfunction Occur due to imbalance between vasodilators (PGE, prostacysline, NO) and vasoconstrictors (PGF, trombaxan and endotheline I) Net results of this is vasoconstriction and increase PVR Systemic HTN, DIC, HELLP syndrome, and placental ischemia
  • Generalized vasospasm Lower renal flow and glomerular filtration rate Proteinuria oliguria Decreased cerebral blood flow Activation of coagulation system …. HELLP syndrome
  •  In most women, sign and symptoms first become apparent after 34 weeks of gestation  10 % of women, preeclampsia develop before 34 weeks of gestation  5 %, preeclampsia is first recognized postpartum usually within 48 hours of delivery
  • mild hypertension (≥140/90 and <160/110 mm Hg) and mild proteinuria (<5 grams in 24 hours), usually accompanied by peripheral edema.  Most patients have only  About 25 percent develop one or more of the following nonspecific findings:
  •  Severe hypertension (systolic blood pressure ≥160 mm Hg or          diastolic ≥110 mm Hg on two occasions at least six hours apart) Persistent and/or severe headache, Visual abnormalities (photophobia, blurred vision, or temporary blindness [rare]) Upper abdominal or epigastric pain Nausea, vomiting Oliguria Dyspnea, retrosternal chest pain Fetal growth restriction Oligohydramnios Altered mental status
  • Atypical presentation  include any of the following:  Onset of signs/symptoms at usuallyweeks of a complete or is <20 associated with partial molar pregnancy. gestation  Hypertension or proteinuria (but not both) with or without characteristic signs and symptoms of severe preeclampsia  Delayed postpartum onsetmay be observed in 15 percent of or exacerbation of patients with HELLP syndrome disease (>2 days postpartum) patients with eclampsia. and in some
  •   Vessels are less sensitive to angiotensine  Earliest sign of preclampsia   Occur due to endothelial dysfunction EVF accumulation  INF is low explain why diuretics are not indicated in preeclampsia  Hypovolemia and hemeconsentration
  •   Occur after days or weeks from onset of fluid retenstion  High diastolic usually due to increase PVR   Occur after days or weeks from onset of BP elevation  Occur due to afferent vasoconstriction damage to the capsular membrane.   Increase uric acid is the earliest sign of renal involvement
  •   Thrombocytopenia is the most common abnormality  DIC or HELLP syndrome may occur   Focal hemorrhages and infraction of liver may occur RUQ pain, elevated liver enzymes(AST & ALT) , epigastric pain  Haemolysis may increase bilirubin   Uteroplacental vasospasum and ischemia decrease blood perfusion IUGR, oligohydroamnious, fetal heart abnormalities  Placenta abruption or hemorrhage if extensive infraction   Visual disturbance blurred vision, spots  Hyperreflexia and irritability
  •  In general, clinical evaluation should include the mother and fetus   RUQ pain, headache and visual disturbances are potentially   •      ominous symptoms requiring immediate assessment -central nervous system headache -visual disturbances – blurring, scotomata tremulousness, irritability, -hyperreflexia Hematologic -bleeding, petechiae Hepatic -UQ or epigastric pain severe nausea and vomiting -urine output and colour : non-dependent edema (i.e. hands and face) •fetal movement •fetal heart rate tracing – NST •biophysical profile -ultrasound for growth -Doppler flow studies
  •  hemoglobin, platelets, blood film  PTT, INR, fibrinogen, D-dimer – especially if surgery or regional anesthetics are planned  ALT, AST, LDH, bilirubin  proteinuria, creatinine, uric acid  24-hour urine collection for total protein and creatinine clearance
  • Fetoplacental complications with preeclampsia:  IUGR  Oligohydroaminos.  Placental infarction.  Consequence of prematurity.  Uteroplacental insufficiency.  Perinatal death.
  • Maternal complications with preeclampsia: HELLP SYNDROME ABRUPTIO PLACENTAE PULMONARY OEDEMA ACUTE RENAL FAILURE CEREBRAL HAEMORRHAGE VISUAL DISTURBANCES & BLINDNESS DIC POSTPARTUM COLLAPSE
  •  Hemolysis, Elevated Liver enzymes, Low Platelets  Pathogenesis unknown   Affects 20% of women with severe preeclampsia  Presents >27 weeks GA (11% sooner)  up to 30% of cases present AFTER delivery and with no prevoius signs of hypertension   Epigastric, RUQ or chest pain, N/V, symptoms of preeclampsia (headache, blurred vision, thirst) ± jaundice Atypical presentations: asymptomatic reduction in platelet count, “flu-like” symptoms.
  •   AST (70-663 U/L), total bilirubin slightly increased, low platelet count (7-99), elevated LDH  elevated D-dimers,  tissue polypeptide antigen (TPA)  fragmented RBCs on smear  Liver biopsy (rarely done): periportal hemorrhage and fibrin deposition with periportal necrosis, macro- and microvesicular fatty deposits (NOT pericentral as in AFLP)   Supportive care (in ICU) and prompt delivery
  •  The definitive treatment of preeclampsia is delivery to prevent development of maternal or fetal complications from disease progression  Whether or not to deliver the fetus is based upon gestational age, the severity of preeclampsia, and maternal and fetal condition.
  •  Three important Qs, the clinician should ask:  The goal of management  
  •  Labour should be induced in the absence of obstetric indication for cessarian delivery  Continuous maternal-fetal monitoring  Seizure prophylaxis and control of hypertension  Other potenital maternal problems that may develop are oliguria, pulmonary edema, HELLP syndrome
  • Degree of hypertension Mild hypertension (140/90 to 149/ 99 mmHg) Moderate hypertension (150/100 to 159/ 109 mmHg) Severe hypertension (160/110 mmHg or higher) Admit to hospital yes yes yes Treat No, because it does not reduce or prevent progression of preeclampsia With oral labetalol With oral labetalol as first-line treatment to keep: diastolic blood pressure between 80–100 mmHg systolic blood pressure less than 150 mmHg as first-line treatment to keep: diastolic blood pressure between 80–100 mmHg systolic blood pressure less than 150 mmHg
  • Degree of Mild hypertension hypertensio (140/90 to 149/ n 99 mmHg) Moderate hypertension (150/100 to 159/ 109 mmHg) Severe hypertension (160/110 mmHg or higher) Measure blood pressure At least four times a day At least four times a day More than four times a day, depending on clinical circumstances Blood tests Monitor using the following tests twice a week: kidney function, electrolytes, full blood count, transaminases, bilirubin Monitor using the following tests three times a week: kidney function, electrolytes, full blood count, transaminases, bilirubin Monitor using the following tests three times a week: kidney function, electrolytes, full blood count, transaminases, bilirubin
  •  Manage pregnancy in women with pre-eclampsia conservatively until 34 weeks.  Offer birth to women with pre-eclampsia before 34 weeks, after discussion with neonatal and anaesthetic teams and a course of corticosteroids has been given if:  
  •  Recommend birth for women who have pre-eclampsia with severe hypertension after 34 weeks when their blood pressure has been controlled and a course of corticosteroids has been completed (if appropriate).  Offer birth to women who have pre-eclampsia with mild or moderate hypertension at 34+0 to 36 +6 weeks depending on maternal and fetal condition, risk factors and availability of neonatal intensive care.  Recommend birth within 24–48 hours for women who have pre-eclampsia with mild or moderate hypertension after 37 +0 weeks.
  •  Magnesium sulfate  Given during the intrapartum period and continued for about 24 hr after delivery  Unproved benefits for mild preeclampsia  Severe preeclampsia ….given on admission  If determined not to delivered …it can be stopped, restarted intrapartum and continued 24 hr postpartum or until there is evidence of resolution of the disease
  •  IV or IM Type of treatment IV IM Prophylactic loading 4 g over 15-20 min 5 g in 100 ml fluid Maintenance 2 g/hr 5 g /4 hr infusion
  •  It is excreted exclusively through the kidneys  Serial assessments of urine output, deep tendon reflexes and respirations are important for detecting signs of magnesium toxicity  every 6 hr  Toxicity can occur even in a patient with apparently normal renal function
  •  Toxicity is treated by stopping infusion and administering calcium gluconate, 10 ml of a 10 % solution, IV and resuscitative measures if necessary
  • Fluids:  Fluid balance should be monitored closely to avoid excessive administration  Maintenance fluids of 80 mL/hour are often adequate in the absence of ongoing fluid loss, such as bleeding. Antihypertensive medication:  Severe hypertension is treated with intravenous labetalol or hydralazine or oral nifedipine.
  •  On the basis of the recent evidence, nitric oxide agents may be beneficial in the prevention of preeclampsia. Randomized controlled trials initiated in the first trimester and using long-acting nitrates are needed in high-risk women to validate these findings.  Kalidindi M, Velauthar L, Khan K, Aquilina J. The role of nitrates in the prevention of preeclampsia: an update. Curr Opin Obstet Gynecol. 2012 Dec;24(6):361-7. doi: 10.1097/GCO.  Low-dose aspirin decreases the incidence of preeclampsia among nulliparous women, primarily through its effect in those who have elevated systolic blood pressure initially. This treatment does not decrease perinatal morbidity but increases the risk of abruptio placentae  Sibai BM, Caritis SN, Thom E, et al. Prevention of preeclampsia with low-dose aspirin in healthy, nulliparous pregnant women. The National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units .
  •  Obstetric emergency  Is the presence of tonic clonic seizures in a women with preeclampsia that cannot be attributed to other causes  Eclamptic seizures can also occur before the development of classic signs of preeclampsia   
  •  When evaluating cases of atypical eclampsia its important to consider other causes of seizures such as:  underlying seizure disorder hypertensive encephalopathy  metabolic abnormalities (hypoglycemia, hyponatremia)  CNS hemorrhage  Thrombosis  Mass  Infection
  •  IOL or cessarian birth during the acute phase may aggravate the disease  Stabilize the pt before delivery  Once hypoxia is corrected, convulsion controlled and diastolic blood pressure brought down to 90 to 100 mmHg, delivery should be expedited preferably by the vaginal route
  •  Gather equipment (airway, suction, mask and bag, oxygen) and give oxygen at 4-6 L per minute.  Protect the woman from injury  Start an IV line and infuse IV fluids (maintenance dose: 80 ml/hr or 1ml/kg/hr) after the convulsion.  Give anticonvulsive drugs (start a loading dose of magnesium sulphate by preparing 4 g of 50% magnesium sulphate solution given slowly IV over 10-15 minutes.
  •  If magnesium sulphate is not available, loading dose of diazepam can be given if convulsion recur, repeat the loading dose). her left side to reduce risk of aspiration of secretions, vomit and blood.  Position the woman on  Aspirate the mouth and throat as necessary.  Monitor vital signs (pulse, blood pressure, and respiration), reflexes and fetal heart rate hourly. emergency case to a secondary care institute.  Refer as an
  •  http://www.nice.org.uk/nicemedia/live/13098/5041      8/50418.pdf www.Uptodate.com www.medescape.com Hacker & More essentials of Obs& Gyne. 4th edition. www.moh.gov www.ncbi.nlm.nih.gov/pubmed
  • Thank you