Hypertension and Pregnancy [Power Point Presentation]

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  • All 3 cases illustrate headache as a symptom.
    Case 1 – postpartum with history of chronic HTN, significance of severe headache not appreciated
    Case 2 – intrapartum deterioration with low platelets and c/o headache (there is a 2nd case not presented with the same history and outcome)
    Case 3 – severe headache & delayed postpartum hypertension, no consultation with an obstetrician
  • Coagulopathy, intubation PO- difficult recognition of neurol complication
  • 5 d of HA, pt/family education
    Non-OB hospital
    5 d of HA, pt/family education
    Non-OB hospital
  • The focus of this talk is on ICH but there are many other types of CNS complications….with some shared pathophysiologic pathways
  • Etiology unknown : hypertensive encephalopathy ,vasospasm,hemorrhage,ischemia,edema .
    Dose of magnesium : 4-6 g IV over 20 minutes ,then continuous 2-3 g per hour .Repeat a 2g IV bolus if necessary .
    Diazepam : 1-10 mg . Anesthesia must be available .
    Phenytoin : load with 1000 mg followed by maintenance .
    Long term anticonvulsant therapy not necessary .
  • Hydralazine or Labetolol can be used as first line drugs .If one is ineffective , switcth to the other .
    If above 3 do not reduce B/P to safe level , NTG or Nitroprusside IV in ICU setting .
    Epidural anesthesia is beneficial and safe if preceded by volume loading .Shown to increase uterine blood flow .
    Induction in general anesthesia can increase systolic B/P by 50 points .
  • Multiple etiologies invoked …no reason to thoink threr is only one mechanism
    Endothelial damage: multiple mediators can be invoked; newest slant on this is the exploration of whether the antiangiogenic factors implicated in Preeclampsia may be involved in endothelial damage
  • ETIOLOGY : HIGH INTRAVASCULAR PRESSURE ,DAMAGE TO VASCULAR ENDOTHELIUM ,REDUCED PLASME COP CT :areas of low density
    MRI: index of water content
    Assisted hyperventilation reduces intracranial pressure . PCO2 at 25-30 mmHg .?role of hyperbaric O2
    Mannitol : increases serum osmolality ,draws water into vasc compartment .A 20 5 solution used as .5-1.0g /kg over 10 minutes ;serum osmolality goal 305-315 mosm
  • Associated with eclampsia,cavernous sinus thrombosis,encephalopathy
    -Cerebral edema if diagnosed should be treated accordingly .
  • This will be the focus of the remainder of the talk
    Etiology of the bleeding is likely multifactorial…there are reports of ischemia and vasospasm preceding hemorrhage. Hypertension is etiologic yet there remains considerable controversie s to what constitutes optimal control and what might be excessive control …concerns about the interplay between deficits in coagulation and thrombus formtion and bleeding, concerns about vascular integrity or damage…. As the etiology is better understood, one hopes for improved approaches to prediction , prevention and treatment
    All the risk discussion comes from the Bateman article in Neurology 2006 67 424-429 which Dr schumacher coauthored
    Multivariate odds ratio for intracranial hemorrhage 10.39 for PEC; 9.23 for PEC superimposed on chronic hypertension; 20.66 for coagulopathy
  • This will be the focus of the remainder of the talk
    Etiology of the bleeding is likely multifactorial…there are reports of ischemia and vasospasm preceding hemorrhage. Hypertension is etiologic yet there remains considerable controversie s to what constitutes optimal control and what might be excessive control …concerns about the interplay between deficits in coagulation and thrombus formtion and bleeding, concerns about vascular integrity or damage…. As the etiology is better understood, one hopes for improved approaches to prediction , prevention and treatment
    All the risk discussion comes from the Bateman article in Neurology 2006 67 424-429 which Dr schumacher coauthored
    Multivariate odds ratio for intracranial hemorrhage 10.39 for PEC; 9.23 for PEC superimposed on chronic hypertension; 20.66 for coagulopathy
  • Cerebral blood flow remains constant over a wide range of pressures in normotensive individuals .This is shifted to the right in chronic hypertensives .Cerebral autoregulation is lost when MAP exceeds 140 mm Hg.
  • Hydralazine or Labetolol can be used as first line drugs .If one is ineffective , switcth to the other .
    If above 3 do not reduce B/P to safe level , NTG or Nitroprusside IV in ICU setting .
    Epidural anesthesia is beneficial and safe if preceded by volume loading .Shown to increase uterine blood flow .
    Induction in general anesthesia can increase systolic B/P by 50 points .
  • We may want to blow this slide up into 3 separate slides if we have enough to say about each. I feel like these are sort of the main messages we wanted to get across and we ended up with very few slides specific to ICH (Dena)
  • Hypertension and Pregnancy [Power Point Presentation]

    1. 1. Complications of Hypertensive Disease: A Focus on Intracranial Hemorrhage
    2. 2. Safe Motherhood Initiative collaborative project of ACOG District II and New York State DOH • Initiated in 2001 • Voluntary Program • Onsite maternal mortality reviews – confidential, protected • Review of aggregate de-identified data • Educational programs
    3. 3. Results of 2008 Reviews Cause Preventable Hemorrhage 3 3 HTN with ICH 4 3 Cardiac 3 0 Sickle Cell 1 0 ICH/Aneurysm 2 0 TTP with CVA 1 0 Lung Ca 1 0 AIDS/PCP 1 0 Total 16 6/16 (37.5%)
    4. 4. Case 1 32 y/o Para 3 with chronic HTN c/o headache, vaginal bleeding at 31 wks with BP 205/100. Rx’d with hydralazine, MgSO4, and delivered POD#1 BP 126-150/75-85 POD#2 12pm c/o HA, BP 148/83 Rx’d with tylenol 4pm c/o pain in back of head BP 147/94 6pm pt unresponsive BP190/120, seizures. CT scan – ICH Brain Death
    5. 5. Case 2 31 y/o Para 1 at 33 wks admitted with BP 250/130 Rx with labetalol, MgSO4 BP’s 140-160/80-106. HELLP syndrome, platelets 44,0000 C/o headache, transfused platelets, cesarean delivery, GET Pt not responsive postop. CT scan – ICH, herniation Brain death
    6. 6. Case 3 26 y/o P1 2 wks postpartum from uncomplicated NSD BIBEMS with seizure at home, family reported 5 days of headache. 12 hours prior seen in ED of non OB hospital with high BP, given lasix and sent home CT – ICH, herniation Brain death
    7. 7. Hypertensive Disorders in Pregnancy Background Significant contributors to maternal morbidity and mortality Classification and Incidence: Preeclampsia (5-8% of pregnancies) Chronic HTN (3% of pregnancies) CHTN with superimposed Preeclampsia Gestational HTN (6% of pregnancies) Eclampsia (4 to 6 per 10,000 live births)
    8. 8. CNS Complications of Hypertensive Disorders in Pregnancy Can result in significant maternal morbidity and mortality Seen with increasing frequency in recent statewide maternal mortality reviews Learning objectives:  Raise awareness of potential CNS complications of hypertensive disorders in pregnancy  Improve prevention, early recognition, accurate diagnosis and prompt aggressive management of CNS emergencies.
    9. 9. Preeclampsia-Associated CNS Complications Eclampsia Intracranial hemorrhage Cerebral edema Encephalopathy Visual disturbances, usually transient Ischemia including ischemic stroke Vascular thrombosis
    10. 10. Eclampsia: Background Remains a leading cause of maternal mortality 4-6/10,000 live births Severity of preeclampsia is a predictor  0.5% of mild, 2% of severe preeclampsia Additional risk factors: Nonwhite, nulliparous, lower socioeconomic, teens Up to 1/3 unheralded by HTN or proteinuria Historically, 80% prior to delivery and 20% postpartum (up to 4 weeks) Recent data demonstrates increase in late postpartum eclampsia >48 hours after delivery Prodrome is common Opportunities for prevention:  Magnesium sulfate  Timely delivery
    11. 11. Eclampsia: Management  Prevent aspiration and injury  Maintain airway, oxygenation, lateral position  Do not need to try to stop 1st convulsion  Prevent recurrent seizure with Magnesium sulfate  10% will have 2nd seizure  Recurrent seizure first line is rebolus Magnesium sulfate (2g over 15-20 minutes)  Recurrent seizures refractory to Magnesium or Intractable seizure  use benzodiazepine, sodium amobarbital, phenytoin  Any of the following should raise suspicion of another process and prompt investigation with imaging:  Atypical presentation  Focal seizures  Postictal focal deficit  Failure to regain consciousness
    12. 12. Eclampsia: Medications Medication Indication Dosage Mg Sulfate Seizure prophylaxis IV: 4-6 g load IV over 15-20 min, then 2 g/hr maintenance IM: 5g into each buttock (10g) Recurrent seizure: rebolus 2g over 15-20 min Ca Gluconate Mg toxicity 1 g IV over 10 min Benzodiazepin e Intractable seizure, status eclampticus Ativan (lorazepam) 0.02-0.03 mg/kg IV (1-2 mg), allow 1 min to assess effect additional (up to a cumulative dose of 0.1 mg/kg) at a max rate of 2 mg/min Valium (diazepam) 0.1-0.3 mg/kg over 1 min, max cumulative dose 20 mg
    13. 13. Cerebral Edema: Background Proposed etiologies include Vasogenic Hyperperfusion from failure of autoregulation Ischemia related to vasospasm Endothelial damage Varying degrees of severity with predilection for occipital and posterior parietal lobes Explains prominence of visual symptoms Wide variety described : blurriness, scotomata, cortical blindness, more rarely distortions of size or color etc. Monocular deficits should prompt examination for ocular, retinal or CN II pathology
    14. 14. Cerebral Edema: Management Typically diagnosed based on imaging study obtained PRES Diagnose on CT or MRI Secondary to anoxia post eclamptic seizure Secondary to loss of cerebral autoregulation Treatment:  Aggressive blood pressure control  Preeclampsia management
    15. 15. Temporary Blindness Occurs in 1-3 % of preeclampsia/eclampsia Majority follow eclampsia Tends to resolve within 8 days Differential diagnosis:  retinal vasculature damage  retinal detachment  occipital lobe ischemia  occipital lobe edema Management:  Neurology consult  Ophthalmology consult  Image with CT or MRI
    16. 16. CNS Bleeding in Preeclampsia Variety of types of bleeding reported: Petechial hemorrhages without clinically notable bleeding are commonly seen in imaging studies, especially in areas of edema Subarachnoid hemorrhage and bleeding related to vascular anomalies reported Intracerecral hemorrhage=Intraparenchymal bleeding responsible for the majority of CNS mortality and morbidity Bateman,BT et al Neurology 2006;67:424
    17. 17. Bateman,BT et al Neurology 2006;67:424 Intracerebral hemorrhage: Risk factors Highest risks for intracerebral hemorrhage in pregnancy: Preeeclampsia with or without preexisting hypertension Coagulopathy Other risks include: advanced maternal age, chronic and gestational hypertension, tobacco abuse, African American race
    18. 18. Mechanisms for Increased Risk of Intracerebral Hemorrhage in Pregnancy, Pre-Eclampsia and Eclampsia Impaired cerebral autoregulation and alteration of the blood-brain barrier in pregnancy (animal data): Arterial vasoconstriction rather than vasodilatation in response to serotonin in pregnancy and post-partum Impaired arterial remodeling: lack of medial hypertrophy in pregnant females with chronic hypertension. Enhanced permeability of the blood-brain barrier with acute hypertension in pregnant females.
    19. 19. Copyright ©2007 American Heart Association Modified after Cipolla, M. J. Hypertension 2007;50:14-24 CBF autoregulatory curves (hypothetical) under various conditions Solid black line: normal CBF as a function of CPP. CBF remains relatively constant between 60 and 150 mm Hg of CPP, whereas above and below these limits, autoregulation is lost and CBF changes linearly with pressure. Solid red lines: chronic hypertension (chronic HTN). autoregulatory curve is shifted to the higher pressures. Solid blue line: potential shift in the autoregulatory curve during normal pregnancy. Dashed blue line: Loss of autoregulation in which CBF changes linearly with pressure and is thought to occur during eclampsia. The arrows point to pressures at which cerebral perfusion breakthroughs occur, demonstrating a large, steep increased in CBF.
    20. 20. Control of hypertension in obstetrics Due to the physiologic changes described, aggressive treatment of severe hypertension in pregnancy and postpartum is crucial and may reduce or prevent complications. When is medical management indicated? - Systolic blood pressure 160-180 - Diastolic blood pressure 105-110 - MAP>125
    21. 21. First Line Agents for Blood Pressure Control in Obstetrics Medication Indication Dosage Labetalol Severe HTN 10-20 mg IV q 10 min, then 40 mg, 60 mg, 80 mg IV q 10 min up to 300 mg total; IV gtt 1-2 mg/min Hydralazine Severe HTN 5-10 mg IV q 20 min up to 40 mg total; IV gtt 5-10 mg/hr
    22. 22. Neurological Warning Signs and Examination Warning signs Neurological examination Sudden confusion, trouble speaking or understanding • Level of consciousness • Language (fluency, comprehension, naming, repetition, reading, writing) Sudden weakness or numbness of the face, arm or leg, especially on one side of the body • Facial asymmetry • Muscle strength in arms and legs • Sensation (light touch, pin prick) Sudden trouble seeing in one or both eyes • Confrontational visual field testing of each eye individually Sudden trouble standing, walking, dizziness, loss of balance or coordination • Nystagmus • Romberg testing • Walking (including toe, heel, and tandem) • Finger-to-nose and heel-to-shin testing Sudden, severe headache with no known cause • Fundoscopy • Evaluate for nuchal rigidity
    23. 23. Immediate action to take when neurological warning signs or symptoms are identified Setting Action In-Hospital • Activate acute stroke page STAT or • Call neurology consult STAT Outpatient office • Call 911 Home • Call 911
    24. 24. ICH in the OB patient Principles: Recognition of the signs and symptoms by the obstetric team is crucial Prompt evaluation and consultation required Interdisciplinary management including: obstetrics, critical care, neurology, neurosurgery Guidelines exist for treating elevated blood pressure in spontaneous ICH Monitoring of intracranial pressure may be indicated Safe medication options exist for the antepartum patient ?maintain cerebral perfusion while prevention extension?
    25. 25. Summary: ICH in the OB Patient Prevention Recognize and optimally treat HTN Diagnose preeclampsia and institute seizure prophylaxis Recognize and optimally treat HTN Recognize and appropriately treat coagulopathy Recognition Patients and providers must appreciate the seriousness of neurologic warning signs Management Immediate evaluation of neurologic warning signs Immediate consultation with neurology Imaging
    26. 26. Decreasing Hypertensive CNS Complications in Pregnancy: Health Care Providers Recognize and optimize chronic hypertension, appropriate baseline work up to use for later comparison Screen for risk factors and consider increased surveillance Recognize abnormal blood pressure and/or proteinuria Appreciate trends: increasing bp, protein, excessive weight gain/edema Appreciate intrauterine growth restriction as an early sign Ask about signs and symptoms Be aware of atypical presentations Acknowledge persistent risk in the postpartum period Patient education
    27. 27. Decreasing Hypertensive CNS Complications in Pregnancy: Patients All pregnant patients should understand signs and symptoms of preeclampsia:  edema, nausea, epigastric or right upper quadrant pain  visual disturbances, headache, seizure, temporary blindness Signs and symptoms should be reviewed with all postpartum patients. Patients must understand that if symptoms present, need emergent evaluation.
    28. 28. Key Points Hypertensive disorders in pregnancy can lead to CNS complications which can result in significant morbidity and mortality. Improved patient and provider recognition of hypertension and preeclampsia may help to improve outcomes.
    29. 29. Key Points Preeclampsia and coagulopathy pose the highest risks of intracerebral hemorrhage in pregnancy. The presence of neurologic warning signs or symptoms in a pregnant patient requires immediate medical attention. Immediate evaluation by neurology/stroke service is indicated if neurologic warning signs are identified.

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