final case study: reproductive sally anderson holly cobb christine douglas rachel drosselmeyer megan...

Final Case Study: Reproductive

Sally AndersonHolly Cobb

Christine DouglasRachel Drosselmeyer

Megan Reid

Patient History

OB History

• A.J. is a white, gravid 25 y.o.

• G8P4034• 33 weeks

gestation• Breech

presentation• Oligohydramnios• H.A.’s last 2

months

Medications• Prenatal vitamins• Tylenol for

headache, prn

Patient History

Medical History• No allergies• 5’ 6 “, 135 lbs.• MRSA culture

positive, 2006• THC , last use

2005

Surgical History• D&C • Lap salpinectomy

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

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

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.

Initial Working Diagnosis

• Urinary tract infection

• Cholelithiasis• ^ BP thought

to be due to pain from UTI and gallstones.

Alternative Diagnosis

• Pregnancy Induced Hypertension (gestational hypertension)

Initial Lab Results

Labs Results

WBC 9.6

Hgb 12.6

Platelets 212,000

Creatinine 0.73

AST 22

ALT < 6

Amylase 56

Lipase 69

Initial Lab ResultsUrinalysis Results

Protein 75, 150

WBC 31-50

RBC 4-8

Bacteria Present

Treated with Rocephin 1 gm IV x1 dose for UTI

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.

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.

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.

Labs Results

Hgb 11.6

Platelets 60,000, 50,000

ALT 453

Creatinine 0.8

Uric Acid 5.2

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.

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+

6 Hours After C/S Intake 500 ml

Output 99 ml

Net 401 ml

Labs Results

Hgb 9.4

HCT 26.9

Platelets 41,000

WBC 11.7

AST 1216

ALT 351

Creatinine 0.9

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.

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.

Labs: 11 Hours After C/S

Labs Results

AST 1264

ALT 305

Platelets 48,000

Hgb 6.5

Albumin 2.7

Creatinine 1.5

Sodium 133

Calcium 7.7

Potassium 6.6

Co2 20

Are Findings from Morphine? From Magnesium ? From

Worsening PIH?• Magnesium Sulfate stopped: patient

more alert• Slurred speech improved

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).

Exam Impression:

Transfer to ICU

Plan:• Magnesium level• Metabolic Panel• Possible hemodialysis (consult

nephrology)• EKG• Administer Insulin,

Bicarbonate, Calcium chloride, glucose

Diagnosis

• Working Diagnosis – Preeclampsia, HELLP syndrome, DIC

• Alternative Diagnosis -Infection/sepsis, placenta abruption (ruled out)

• Other Diagnosis- Cholilithiasis

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 diasystolicAND

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.

Diagnostics and Lab for HELLP Syndrome

Lab Normal HELLPAST 7-30 U/L -3 times above normalALT 9-25U/L -3 times above normalPlatelet 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!

Diagnostic/labs for DIC

Platelet count decreasedFibrin degradation product (FDP)increasedFactor assay decreasedProthrombin time (PT) prolongedActivated PTT prolongedThrombin time prolongedFibrinogen decreasedD-dimerincreasedAntithrombin decreased 

Not one specific test for DIC! Treat the Condition!

Other Labs

• Urine Analysis

• Ultrasound

• WBC DIFF

• Comp Met Panel

• Chest xray

HELLP Syndrome

H – hemolysisEL – elevated liver

enzymesLP – low platelet

count(PubMed Health, 2010)

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)

Mechanisms of Disease

Genetic Factors• Believed to have a

strong genetic component

• Most cases are sporadic

• Not fully understood

Environmental Factors• Poor prenatal care

(National Institutes of Health website, 2010)

Mechanism of DiseaseMaternal

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

ClinicalManifestations

• Malaise• Right upper quadrant

pain• Headache• Nausea & vomiting• BP elevation• Hypertension• Edema• Proteinuria

(Curtain & Weinstein, 1999; Henderson, 2010; O’Hara Padden, 1999)

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)

Pathogenesis

Artery remodeling is incomplete or absent, causing placental hypoxia and ischemia

Platelet activation

Thromboxane A and serotonin

VasospasmFurther endothelial damage!

(O’Hara Padden, 1999; Rogers & Dittus-Yaeger, 2006)

Pathophysiology:Hemolysis

• Microangiopathic hemolytic anemia

• RBCs become fragmentedSpherocytes

Burr Cells

Schistocytes

(O’Hara Padden, 1999)

Pathophysiology: Elevated Liver Enzymes

Secondary to fibrin deposits in the sinusoids, obstructing hepatic blood flow

Leads to periportalnecrosis, intrahepatic hemorrhage, subcapsular hematoma formation or hepatic rupture

(Curtain & Weinstein, 1999; O’Hara & Padden, 1999)

Pathophysiology:Low Platelet Count

• Thrombocytopenia– Increased consumption and/or

destruction of platelets

DIC!!!

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

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)

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)

Mechanism of Disease

Genetic Factors

• Presence of Factor V Leiden

• Activated C Protein Resistance

Environmental Factors

• Heat Stroke• Snake bites• Trauma• Hemolytic

Transfusion reactions

(Siminioni, Prandoni, Lennsing, Scudeller, Sardella, Prins,

Villalta, Dazzi, Girolami, p. 1 2006).

Alteration in Defenses

• Injury• Stress: inflammatory • Inflammation: cytokines • Immunity: innate• Neoplasia

(Gando 2001)

Pathogenesis of DIC

(Porth 2009, p.275-276)

Pathogenesis and Patient

• S/P c/s of breach infant– Altered mental status– Respiratory failure – Acute Renal Failure – Elevated liver Enzymes– Anemia

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

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

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

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

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

ReferencesBecker, J. (2011). Disseminated

intravascular coagulation in emergency medicine. Retrieved from http://emedicine.medscape.com/article/779097-overview

Curtain, W. M. & Weinstein, L. (1999). A review of HELLP syndrome. Journal of Perinatology, 19(2), 138-143.

Gando, S. (2001). Disseminated intravascular coagulation in trauma patients. Seminars in Thrombosis and Hemostasis, 27, (6), p. 585-592

Henderson, T. (2010). HELLP syndrome in pregnancy and premature delivery. http://trilby-henderson.suite101.com/hellp-syndrome-in-pregnancy-and-premature-delivery-a236464.

Hypertension in pregnancy. (n.d.). In Skyscape ipad application.

Kruger. D. (2006). Acute Systemic disseminated intravascular coagulation: Managing a complex medication condition. Journal of the American Academy of Physicians Assistants, 19, (5), p 28-32.

Lim, K. (2011). Preeclampsia. Retrieved from http://emedicine.medscape.com/article/1476919-overview

National Institutes of Health website. (2010). HELLP syndrome. Genetic and Rare Diseases Information Center. http://rarediseases.info.nih.gov/GARD/Condition/8528/QnA/25433/HELLP_syndrome.aspx

O’Hara Padden, M. 1999. HELLP syndrome: Recognition and perinatal management. Journal of the American Academy of Family Physicians, 60(3). Retrieved from http://www.aafp.org/afp/1999/0901/p829.html

Porth, C., Matfin, G. (2009). Pathophysiology: Concepts of altered health states. Philadelphia, PA: Lippincott Williams & Wilkins.

Portis, R, Jacobs, M. A., Skerman, J. H. & Skerman, E. B. (1997). HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) pathophysiology and anesthetic considerations. Journal of the American Association of Nurse Anesthetists, 65(1), 37-47.

PubMed Health website. 2010. HELLP syndrome. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001892/

ReferencesRogers, N. & Dittus-Yaeger, L. (2006).

Preeclampsia: Behind the scenes [PowerPoint slides]. Retrieved from faculty.alverno.edu/bowneps/MSN621/.../Preeclampsia.ppt

Simioni, P., Prandoni, P., Lensing, A., Scudeller, A., Sardella, C., Prins, M.,… Girmlami, A. (2006). The risk of recurrent venous thromboembolism in patients with an Arg 506 G1n mutation in the gene for factor V (Factor V Leiden). British Journal of Hematology, 336, (6), p. 336- 403.