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Love ’ s Labour ’ s Lost

Love ’ s Labour ’ s Lost. CCM Inter-Hospital Grand Round 13 Nov 2012 SK Yung Chairman: Dr Osburga Chan Queen Elizabeth Hospital. Case 3. F/25, Indian Para 0, Gestation 31 weeks Good past health Attended AED 19/2/2011 for acute onset of headache and epigastric pain ~ 2 hours. Case 3.

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Love ’ s Labour ’ s Lost

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  1. Love’s Labour’s Lost CCM Inter-Hospital Grand Round 13 Nov 2012 SK Yung Chairman: Dr Osburga Chan Queen Elizabeth Hospital

  2. Case 3 • F/25, Indian • Para 0, Gestation 31 weeks • Good past health • Attended AED 19/2/2011 for acute onset of headache and epigastric pain ~ 2 hours

  3. Case 3 • Tympanic temp 370C • BP/P 141/70, 71/min • Developed generalized tonic convulsion ~ 1 min aborted by valium 5mg IM in AED cubicle • Post ictal drowsiness • Transferred to the resuscitation room for further management

  4. Case 3 • BP/P 180/110, 76/min • Urine multistix Alb 4+, RBC 3+ • Hstix 4.7 • MgSO4 4g loading then 1g/hour • Obstetric and anesthetic colleagues informed • 2 more short lasting seizures aborted by valium

  5. Case 3 • P/E Uterus size 32 weeks, cephalic above brim • USG : Single fetus, Fetal heart rate ~ 160/min • GCS E3V3M5. SaO2 by pulse oximetry not measured well as patient struggling • Decided for intubation before transfer to operation theatre for emergency LSCS

  6. Case 3 • Intubated by RSI. Grade 1 larynx • Post intubation BP/P 166/79, 115/min, SaO2 100% • Proceeded to emergency LSCS • Female baby, Apgar score satisfactory • Intraop blood loss 400ml • Post op not extubated and transferred to ICU

  7. Case 3 • On arrival to ICU • BP high side 151/101, 90/min • SaO2 100% on FiO2 0.4 • BP under control with labetalol infusion •  CT Brain (plain) • No abnormalities detected

  8. Case 3 • AN in QEH since 13 weeks • G2P0 (history of surgical TOP in 2005) • Husband : Indian • Obesity BMI ~ 34 . OGTT : no GDM • Otherwise AN unremarkable • Last seen 10 days before admission (31 weeks) • BP 150/85, recheck 123/65 • Urine x albumin -ve

  9. Case 3 • Hb cancelled a few times (haemolyzed), recheck = 12.4 • Plt66, WCC 15.6, Blood smear not available (Saturday) • Clotting profile normal • Na 136, K cancelled, Ur 5.1, Cr 77 • ABG pH 7.24, pCO2 4.4, pO2 15, HCO3 14, BE -12.5 • ALT 121, ALP 117, Bilirubin 4 • Urate 0.43

  10. Case 3 • CXR enlarged cardiac silhouette ? related to supine film, not congested, no consolidation • ECHO showed good EF, no RWMA, no pericardial effusion • Treated as eclampsia, suspected HELLP • BP stabilized with oral methyldopa and nifedipine SR, weaned off labetalol infusion, seizure free • Metabolic acidosis improved, fully conscious • Extubated on the next day

  11. Case 3 • Hb 12.4 (19/2)  9.1 (20/2)  9.9 (21/2) • Plt 68 (19/2)  26 (20/2)  21 (21/2) • Clotting profile normal • Cr 77 (19/2)  183 (20/2)  280 (21/2) • Remained oliguric despite cautious fluid challenge • Urine x Haemoglobin 3+. CK mildly elevated ~ 300 • LDH 2748 (19/2)  2507 (20/2)  1288 (21/2)

  12. Case 3 • ALT 121 (19/2)  370 (20/2)  240 (19/2) • AST 517 (20/2) • ALP 117 (19/2)  86 (20/2)  98 (21/2) • GGT 16 (20/2) • Bilirubin 4 (19/2)  37 (20/2)  25 (19/2) • Direct bili 13, indirect bili 23 (20/2) • Haptoglobin < 0.08 • Ammonia not elevated

  13. Case 3 • Blood smear 21/2/2011 • A few schizocytes • Impression ? HELLP ? TTP • Plasmapheresis (replacement with cryo-reduced plasma) since 21/2/2011 • Haemofiltration since 22/2/2011 for oliguric renal failure and pulmonary congestion

  14. Case 3 • HbsAg –ve , HIV -ve • USG abdomen 22/2/2011 • Unremarkable except small right pleural effusion • Autoimmune markers including ANA, AntiENA, ANCA, Anti-cardiolipin Ab all -ve

  15. Case 3 • Seen by Haematology colleagues: • Lots of overlap between HELLP and TTP • Checking ADAMTS-13 level after plasmapheresis renders the interpretation difficult • ADAMTS-13 checked 25/2/2012 • Level = low (245.1, reference 253- 2238) • Antibody +ve • Comment • Borderline decrease of ADAMTS 13 NOT consistent with TTP • The Antibody result probably spurious, may represent cross reaction

  16. Case 3 • Platelet improved to 120 & LDH 239 • Plasmapheresis stepped down from daily to alternate day regime after 8 days • Then stopped 4 days later when platelet count normalized (266) • Dialysis independent 9 days since commencement • Wean off antihypertensives • RFT and Platelet count normalized on subsequent follow ups • Patient defaulted after 2 OPD sessions

  17. Pre-eclampsia and related complications

  18. Definitions • Eclampsia = to shine forth in Greek • “Ek” = out • “Lampein” = shine • Pre-eclampsia = the state before eclampsia

  19. Definitions • New onset hypertension after 20 weeks of pregnancy with significant proteinuria (NICE guideline ‘Hypertension in pregnancy’ Aug 2010) • Hypertension • Mild 140/90 – 149/99 • Moderate 150/100 – 159/109 • Severe >= 160/110 • Significant proteinuria • Urinary protein: creatinine ratio > 30mg/mmol OR • A validated 24 hour urine collection > 300mg protein • (Concerning the reagent-strip testing, it is recommended to be read by an automated reading device and if result >= 1+, use a spot urinary protein: creatinine ratio or 24 hour urine collection to quantify proteinuria)

  20. Definitions • SEVERE pre-eclampsia = pre-eclampsia with severe hypertension and/or with symptoms, and/or biochemical and/or haematologic impairment

  21. Definitions • HELLP (Hemolysis, elevated liver enzymes, low platelets) • Variable and inconsistent diagnostic criteria • Definition by UKOSS (UK Obstetric surveillance system) in 2011 • All pregnant women with new onset of • Elevated liver enzymes (AST >= 70 U/L orGGT >= 70U/L or ALT >= 70U/L) AND • Platelet count < 100 x 109/L AND • Haemolysis defined by abnormal blood smear or serum LDH >= 600 U/L or total bilirubin >= 20.5μmol/L) OR • Hypertension (SBP >= 140mmHg or DBP >= 90mmHg) OR • Proteinuria 1+ (0.3 g/l) or more on dipstick testing, a protein:creatinine ratio of 30 mg/mmol or more on a random sample, or a urine protein excretion of 300 mg or more per 24 hours

  22. Definitions • Eclampsia = A convulsive state associated with pre-eclampsia

  23. Risk factors High risk Moderate risk Age >= 40 Nulliparity Pregnancy interval of more than 10 years Family history of pre-eclampsia BMI >= 30kg/m2 Multiple pregnancy • Previous history of pre-eclampsia • Preexisting vascular disease e.g. hypertension • Preexisting renal disease • Type 1 / 2 DM • Autoimmune disease e.g. SLE / APS (NICE guideline ‘Hypertension in pregnancy’ Aug 2010)

  24. Epidemiology • Exact incidence unknown • In developed countries e.g. UK/US, quoted to be around • 5% for overall incidence • 0.5% for severe disease • 0.05% for eclampsia • HKCOG audit 2004 • 2.5% for overall incidence of hypertensive disorder in pregnancy • 0.7% for severe disease • 0.035% for eclampsia

  25. Pathophysiology • Abnormal placentation • Pre-eclampsia reported in pregnancy without uterus (abdominal pregnancy) and pregnancy without fetus (molar pregnancy) • Characteristic pathology = shallow cytotrophoblast invasion and restricted endovascular remodeling • ? Immunological/genetic factors contributing to the development of abnormal placenta • ?? Ischemic placenta liberates factors into maternal circulation leading to generalized endothelial dysfunction and exaggerated inflammatory response • Elevated levels antiangiogenic molecules e.g. sFLT-1 documented The origins and end-organ consequence of pre-eclampsia. G. Eastabrook et al. Best Practice & Research Clinical Obstetrics and Gynaecology 2011;25:435-447

  26. Pathophysiology • Systemic endothelial dysfunction/ exaggerated inflammatory response with • Capillary leakage and reduction of effective circulating volume • Platelet activation, intravascular thrombosis and platelet consumption • Vasoconstriction with enhanced response to vasoactive substances e.g. angiotensin II • Patients with pre-existing vascular/ renal disease particularly prone to develop superimposed pre-eclampsia • Multiple end organs can be involved to variable extents • Severe damage can occur without significant hypertension The origins and end-organ consequence of pre-eclampsia. G. Eastabrook et al. Best Practice & Research Clinical Obstetrics and Gynaecology 2011;25:435-447

  27. Renal • One of the most vulnerable organs in pre-eclampsia • Characteristic lesion = ‘glomeular endotheliosis’ • Endothelial cell swelling, obliteration of endothelial fenestrate, occlusion of capillary lumens • Relative VEGF deficiency ? related to excessive sFlt-1 with disruption of glomerular endothelium leading to proteinuria • Oliguria and raised Ur/Cr related to renal vasoconstriction and reduced effective circulating volumes, correlates with severe disease • Raised uric acid level ?due to increased reabsorption (with sodium retention) , also increased production from trophoblast The origins and end-organ consequence of pre-eclampsia. G. Eastabrook et al. Best Practice & Research Clinical Obstetrics and Gynaecology 2011;25:435-447

  28. Hepatic • ? Hepatic sinusoids blocked by intravascular fibrin deposition with ischaemia • Clinically manifesting as epigastric/ right upper quadrant pain, elevated transaminases / coagulopathy • At extremes, can have subcapsular haematoma/ liver rupture The origins and end-organ consequence of pre-eclampsia. G. Eastabrook et al. Best Practice & Research Clinical Obstetrics and Gynaecology 2011;25:435-447

  29. Haematological • Microvascular endothelial dysfunction • Platelet activation and fibrin deposition leading to turbulent blood flow • Red blood cells became fragmented when subjected to shear stress -> haemolytic anaemia • Thrombocytopenia due to accelerated consumption The origins and end-organ consequence of pre-eclampsia. G. Eastabrook et al. Best Practice & Research Clinical Obstetrics and Gynaecology 2011;25:435-447

  30. Neurological • 2 theories trying to explain cerebral abnormalities in pre-eclampsia/ eclampsia with endothelial dysfunction having a central role • 1. Vasospasm (cerebral overregulation in response to raised CPP/ hypertension with ischaemia and cytotoxic edema) • 2. Hyperperfusion with breakdown of blood brain barrier with leakage of plasma/RBC with vasogenic edema (autoregulatory capacity of cerebral circulation exceeded with regions of vasoconstriction and forced vasodilatation) • The latter one is more favoured and known as PRES (Posterior Reversible Leucoencephalopathy Syndrome) Neurological complications of pre-eclampsia GG. Zeeman Seminars in perinatology 2009;33:166-172

  31. Neurological • The posterior circulation is particularly vulnerable because of less sympathetic innervation and lower ability to respond to elevated blood pressure • Maybe complicated with intracranial haemorrhages / cerebral infarction • Most common clinical manifestations • Headache • Seizures • Visual disturbance • Altered mental state Neurological complications of pre-eclampsia GG. Zeeman Seminars in perinatology 2009;33:166-172

  32. Neurological • Note: despite the name of posterior reversible leucoencephalopathy syndrome, the deficit is not necessarily reversible and residual lesions have been reported in follow up MRI up to 7 years post insult Neurological complications of pre-eclampsia GG. Zeeman Seminars in perinatology 2009;33:166-172

  33. Neurological imaging • CT scan • Localized hypodense lesions at gray white matter junction in parieto-occipital lobes. Less commonly in frontal, inferior temporal lobes, basal ganglia and thalamus • Intracranial haemorrhages usually at the striatocapsular area, thalamus, cerebellum and brain stem Neurological complications of pre-eclampsia GG. Zeeman Seminars in perinatology 2009;33:166-172

  34. Neurological imaging • MRI • Much more effective than CT • T2 hyperintense signals at parieto-occipital and temporal lobes, occasional involvement of basal ganglia and/or brainstem • ‘New’ MRI techniques for better characterization / differentiating from other causes • E.g. diffusion weighted imaging and apparent diffusion coefficient mapping (ADC) Neurological complications of pre-eclampsia GG. Zeeman Seminars in perinatology 2009;33:166-172

  35. Cardiopulmonary • Increase demand on cardiac function, increased capillary permeability and lowered oncotic pressure • Prone for development of pulmonary edema especially if iatrogenically volume overloaded The origins and end-organ consequence of pre-eclampsia. G. Eastabrook et al. Best Practice & Research Clinical Obstetrics and Gynaecology 2011;25:435-447

  36. Complications Preeclampsia B Sibai et al. Lancet 2005; 365: 789-99

  37. Peripartum management • Treatment of acute hypertension • Prevention and control of eclampsia • Fluid management • In women with severe pre-eclampsia, limit maintenance fluid 80ml/hour unless there are other ongoing fluid losses e.g. haemorrhage (NICE guideline ‘Hypertension in pregnancy’ Aug 2010) • Thromboembolism prophylaxis • Close monitoring of fetal condition before delivery

  38. Treatment of acute hypertension • Why is it important? • How should the BP be measured? • How should the BP be controlled?

  39. Why is it important? One of the top ten recommendations in CEMACE 2003-2005

  40. Why is it important? • ‘The single most serious failing in the clinical care provided for mothers with pre-eclampsia was the inadequate treatment of their systolic hypertension. In several cases this resulted in a fatal intracranial haemorrhage….’ • 14 women died from preeclampsia related complications and 9 were intracranial haemorrhages

  41. Why is it important? One of the top ten recommendations in CEMACE 2006-2008

  42. Why is it important? • ‘It is disappointing that in this triennium, as flagged up in the last report, the single most serious failing in the clinical care provided for mothers with pre-eclampsia was the inadequate treatment of their systolic hypertension. In several women, this resulted in a fatal intracranial haemorrhage…’ • 19 women died from preeclampsia related complications and 9 were intracranial haemorrhages • History keeps repeating itself

  43. Why emphasizing so much on treating systolic hypertension? • Obstet Gynecol 2005;105:246–54 • Retrospective review of 28 women with severe pre-eclampsia and stroke (26 cases were haemorrhagic) • 24 women treated immediately before their stroke, 23 had a SBP >= 160mmHg, DBP more variable, only 3 >= 110 • Conclusion : A paradigm shift is needed toward considering antihypertensive therapy for severely pre-eclamptic and eclamptic patients when SBP >= 155–160 mm Hg

  44. BP measurement • Invasive BP monitoring is theoretically most accurate (with appropriate calibration and damping) and provide real time measurement • If non invasive BP measurement • Appropriate cuff size • Brachial artery at the level of the heart • Korotkoff 5 should be used for diastolic BP for sphygmomanometer measurement • If an automated BP monitor is used, it should be a validated one for use in pregnancy and preferably in preeclampsia

  45. Automated BP machine tend to underestimate systolic pressure in preeclampsia • J villar et al. International journal of Gynaecology and Obstetrics 85 Supp 1 2004:S28-S41

  46. How should the blood pressure be controlled? NICE Guideline 2010

  47. How should the blood pressure be controlled? • ACOG committee opinion for emergent therapy for acute onset severe hypertension with pre-eclampsia or eclampsia 2011 • The goal is not to normalize BP but to achieve a range of 140-160/90-100 • 1st line therapy • IV labetalol and hydralazine are both considered 1st line medications • Less information available for the use of calcium channel blockers • MgSO4 is NOT recommended as an antihypertensive

  48. How should the blood pressure be controlled? • ACOG committee opinion for emergent therapy for acute onset severe hypertension with preeclampsia or eclampsia2011 • E.g. Labetalol as first line • 20mg IV over 2 mins, repeat BP measurement in 10 minutes • 40mg IV over 2 minsif target not achieved, repeat BP measurement in 10 minutes • 80mg IV over 2 mins, if target not achieved, repeat BP measurement in 10 minutes • Hydralazine 10mg IV over 2 mins if target not achieved • Note: Parental labetalol can cause neonatal bradycardia and should be avoided in women with asthma/ heart failure. Hydralazine may increase the risk of maternal hypotension (SBP < 90)

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