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Final Case Study: Reproductive

Final Case Study: Reproductive. Sally Anderson Holly Cobb Christine Douglas Rachel Drosselmeyer Megan Reid. Patient History. OB History. Medications. Prenatal vitamins Tylenol for headache, prn. A.J. is a white, gravid 25 y.o. G8P4034 33 weeks gestation Breech presentation

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Final Case Study: Reproductive

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  1. Final Case Study: Reproductive Sally Anderson Holly Cobb Christine Douglas Rachel Drosselmeyer Megan Reid

  2. Patient History OB History Medications Prenatal vitamins Tylenol for headache, prn • A.J. is a white, gravid 25 y.o. • G8P4034 • 33 weeks gestation • Breech presentation • Oligohydramnios • H.A.’s last 2 months

  3. Patient History Medical History Surgical History D&C Lap salpinectomy • No allergies • 5’ 6 “, 135 lbs. • MRSA culture positive, 2006 • THC , last use 2005

  4. Psychosocial History • Married • Blended Family • Children with family members while mother in hospital • Patient unemployed-stay at home mom • Adequate support/resources • English speaking • Non-smoker

  5. Case Study Initial • From out of town • Reports migraine onset in a.m., unrelieved by Tylenol. • Denies visual disturbances • Severe RUQ and epigastric pain approx 1 hr after dinner. • Taken to local hospital by husband

  6. Clinical Findings at Local Hospital • BP 143/95 • FHR tracing “normal”, • No contractions • Morphine and Dilaudid for pain • Zofran and Phenergan for nausea • Cholelithiasas per abdominal U.S.

  7. Initial Working Diagnosis • Urinary tract infection • Cholelithiasis • ^ BP thought to be due to pain from UTI and gallstones.

  8. Alternative Diagnosis • Pregnancy Induced Hypertension (gestational hypertension)

  9. Initial Lab Results

  10. Initial Lab Results Treated with Rocephin 1 gm IV x1 dose for UTI

  11. Outlying Hospital Final Diagnosis Pregnancy induced hypertension: BP’s remained elevated despite: • Improved epigastric pain. • IV Labetalol 10 mg x 2 doses and then Labetalol 20 mg x 1 dose administered. Therefore decision made to transfer to tertiary care center. Magnesium sulfate drip started prior to transfer.

  12. Physical Exam Findings at Tertiary Center • LOC: sedated but responds appropriately to questions. • Reports headache/light sensitivity/no vision changes. • BP 165/120, 72, 18, SpO2 98%, • DTR’s: 2+ bilaterally/ clonus 1 beat on left, 2 beats on right. • Fetal heart tracing: absent variability, normal baseline. • Denies contractions, vaginal bleeding or leaking of amniotic fluid. • Foley catheter placed with return of small amount thick, brown urine.

  13. Plan • Continue magnesium sulfate for seizure prophylaxis. • PIH labs with 24 hr urine collection. • Antihypertensives • Corticosteroids (#2 of 2) for fetal lung maturity. • GBS culture • C/S for breech if indicated • MFM consultation in a.m.

  14. 1 Hour After Admission • C/S due to severe preeclampsia with HELLP Syndrome. • EBL: 1000 ml • Viable baby girl to NICU. • Apgars 7/8/8.

  15. 6 Hours After C/S • VS: 98.1 F, 106/69, 88, 18, 97% • Firm fundus • Bowels sounds x4 • Incision: clean/dry/intact, scant drainage on pressure bandage. • No edema in extremities • Patellar reflexes: 1+ • Brachoradialis reflexes: 2+

  16. 6 Hours After C/S

  17. Plan • Continue Magnesium Sulfate 2 gm/hr for 24 hours post-op. • Continue Fluid restriction with accurate I/O. • Continue close BP assessment. • Continue serial lab draws. • Monitor bleeding. • Continue antibiotics for UTI. • Continue PCA Morphine for post op pain.

  18. 11 Hours After C/S • VS: 117/76, 88, 16, 96% on 2 L. • Lethargic, slurred speech, appropriate responses, Glasgow Coma Score = 14. • Skin: yellow, dry and cool • DTR’s: Right patellar 3+/1 beat clonus; left patellar 2+ (slow and delayed reaction)/1 beat clonus.

  19. Labs: 11 Hours After C/S

  20. Are Findings from Morphine? From Magnesium ? From Worsening PIH? • Magnesium Sulfate stopped: patient more alert • Slurred speech improved

  21. Hospitalist Consult Exam Findings: • No SOB/chest pain/hemoptysis • Lethargic • Skin: pale/yellowish • Heart: RSR • Lungs: Clear bilaterally • Kidneys: No urine output, no peripheral edema • Abdomen: Fairly nontender. Questionable palpable liver edge. • Asymmetrical reflexes (right is areflexic, left is hyperreflexic).

  22. Exam Impression:

  23. Transfer to ICU Plan: • Magnesium level • Metabolic Panel • Possible hemodialysis (consult nephrology) • EKG • Administer Insulin, Bicarbonate, Calcium chloride, glucose

  24. Diagnosis • Working Diagnosis – Preeclampsia, HELLP syndrome, DIC • Alternative Diagnosis -Infection/sepsis, placenta abruption (ruled out) • Other Diagnosis- Cholilithiasis

  25. Diagnostics and Labs for Preeclampsia New onset of HTN and proteinuria after the 20th with BP greater than 140 mmHg systolic and/or greater than 90 mmHg diasystolic AND Proteinuria must also be present, .3 grams protein in 24hours or persistent 1+ on dipstick, 30 mg/dL Patient Findings on Arrival: BP- 143/95 164-120 Proteinuria- 75mg/dl 150mg/dl Does patient meet diagnostic criteria for preeclampsia? Yes Eclampsia –No, l presents of grand mal seizures.

  26. Diagnostics and Lab for HELLP Syndrome LabNormalHELLP AST 7-30 U/L -3 times above normal ALT 9-25U/L -3 times above normal Platelet 150-350/mm3 -under 150 Blood smear schistocytes present Patient Labs: AST 1216 1240 1264U/L ALT 357 453 305U/L Plts. 41 51 48/mm3 > D-Dimer 20 Does patient meet criteria for HELLP? YES!

  27. Diagnostic/labs for DIC Platelet count decreased Fibrin degradation product (FDP) increased Factor assay decreased Prothrombin time (PT) prolonged Activated PTT prolonged Thrombin time prolonged Fibrinogen decreased D-dimer increased Antithrombin decreased Not one specific test for DIC! Treat the Condition!

  28. Other Labs • Urine Analysis • Ultrasound • WBC DIFF • Comp Met Panel • Chest xray

  29. HELLP Syndrome H – hemolysis EL – elevated liver enzymes LP – low platelet count (PubMed Health, 2010)

  30. Etiology of HELLP Syndrome • Exact cause is unknown • Thought to be a variant of severe preeclampsia or eclampsia • Occurs in about 1 out of 1,000 births and in 10-20% of pregnant women with preeclampsia or eclampsia • Possible underlying coagulopathy • Developmental defect of the uterus or placental ischemia • Develops before the 37th week of pregnancy or within the week after pregnancy (Curtain & Weinstein, 1999; O’Hara Padden, 1999; PubMed Health, 2010)

  31. Mechanisms of Disease Genetic Factors Environmental Factors Poor prenatal care (National Institutes of Health website, 2010) • Believed to have a strong genetic component • Most cases are sporadic • Not fully understood

  32. Mechanism of Disease Maternal Characteristics • Preeclampsia • Hypertension • Multiparous • Maternal age >24 years • White race • Hx of poor pregnancy outcomes • Hx of autoimmune disease • Liver disease • Previous diagnosis or family history of HELLP Syndrome Clinical Manifestations • Malaise • Right upper quadrant pain • Headache • Nausea & vomiting • BP elevation • Hypertension • Edema • Proteinuria (Curtain & Weinstein, 1999; Henderson, 2010; O’Hara Padden, 1999)

  33. Normal Placental Development Uterine spiral arteries are transformed increasing uterine blood flow Trophoblast cells enter artery dilates, allowing for increased blood flow (Rogers & Dittus-Yaeger, 2006)

  34. Pathogenesis Artery remodeling is incomplete or absent, causing placental hypoxia and ischemia Platelet activation Thromboxane A and serotonin Vasospasm Further endothelial damage! (O’Hara Padden, 1999; Rogers & Dittus-Yaeger, 2006)

  35. Pathophysiology:Hemolysis • Microangiopathic hemolytic anemia • RBCs become fragmented Spherocytes Burr Cells Schistocytes (O’Hara Padden, 1999)

  36. Pathophysiology: Elevated Liver Enzymes Secondary to fibrin deposits in the sinusoids, obstructing hepatic blood flow Leads to periportal necrosis, intrahepatic hemorrhage, subcapsular hematoma formation or hepatic rupture (Curtain & Weinstein, 1999; O’Hara & Padden, 1999)

  37. Pathophysiology:Low Platelet Count • Thrombocytopenia • Increased consumption and/or destruction of platelets DIC!!!

  38. Pathology and the Patient • Preeclampsia • Hypertension • Multiparous • Maternal age >24 years • White race • Hx of poor pregnancy outcomes • Gestational age • Hemolytic anemia • Elevated liver enzymes • Low platelet count

  39. Disseminated Intravascular Coagulation (DIC) DIC is life threatening acquired disorder caused by an imbalance in the coagulation system. DIC is characterized by widespread coagulation and bleeding in the vascular department. (Kruger 2006, page 1)

  40. Etiology of DIC • Causes may be acute or chronic, systemic or localized, and may be a result of a single or multiple conditions • Severe Trauma • Hypothermia • Pregnancy complications • Malignancy • Liver disease • Vascular disease • Infection is most common cause (Kruger 2006, p. 31)

  41. Mechanism of Disease Genetic Factors Environmental Factors Heat Stroke Snake bites Trauma Hemolytic Transfusion reactions (Siminioni, Prandoni, Lennsing, Scudeller, Sardella, Prins, Villalta, Dazzi, Girolami, p. 1 2006). • Presence of Factor V Leiden • Activated C Protein Resistance

  42. Alteration in Defenses • Injury • Stress: inflammatory • Inflammation: cytokines • Immunity: innate • Neoplasia (Gando 2001)

  43. Pathogenesis of DIC (Porth 2009, p.275-276)

  44. Pathogenesis and Patient • S/P c/s of breach infant • Altered mental status • Respiratory failure • Acute Renal Failure • Elevated liver Enzymes • Anemia

  45. Treatment of Preeclampsia Preeclampsia: • Bed-rest with left side down • C-section (indicated >26 weeks) • Delivery is only cure • BP control for severe HTN (SBP >160; DBP >110) Goal: • Prevent cerebrovascular and cardiac complications • Maintain uteroplacental blood flow • Maintain BP around 140/90 • Hydralazine 5-10 mg IV q 20-30 min • Labetolol 20-80 mg IV bolus q 10 min or 0.5-2 mg/min IV gtt

  46. Treatment of Preeclampsia • Magnesium Sulfate • Loading dose of 4 g IV, followed by 1 to 2 gm/hr IV infusion • Stabilizes seizure threshold, reduces BP • Indicated in all patients with severe preeclampsia as prophylactic treatment • Minimize maternal risk, maximize fetal maturity • Fluid management • Avoid diuretics • Fluid restriction as possible (total 80 ml/hr or 1 ml/kg/h) • Careful measurement of I&O • Daily blood tests - LFTs, CBC, uric acid, LDH

  47. Treatment of HELLP • Delivery is critical – carried out in the most controlled situation possible • Strict bed rest with left lateral decubitus position • For <34 weeks, give MgSO4 and glucocorticoids • Plasmapheresis – improve platelet counts

  48. Treatment of DIC • Transfer to ICU (if not already) for close observation • Treat underlying disease – deliver appropriate obstetric care • Platelet and plasma transfusion • Should not be instituted based on lab results alone • Indicated in active bleeding and those requiring invasive procedure

  49. Treatment of DIC • Serial labs - coags, fibrinogen, CBC, CMP, LFT • If vitamin K deficiency – administer vitamin K • PRBC, FFP, plateletpheresis • Treat complications • Multisystem organ failure • Renal failure – hemodialysis • Respiratory failure, suspected ARDS – intubation

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