HELLP syndrome nursing: diagnosis, management, and NCLEX tips

LS
By Lindsay Smith, AGPCNP
Updated October 6, 2026

Reviewed for clinical accuracy · Methodology: NIH, NCBI, AANP guidelines

HELLP syndrome is a severe obstetric emergency defined by the triad of Hemolysis, Elevated Liver enzymes, and Low Platelets. It belongs to the preeclampsia–eclampsia spectrum, and ACOG describes it as one of the more severe forms of preeclampsia. HELLP occurs in about 0.5–0.9% of all pregnancies and in 10–20% of pregnancies with severe preeclampsia. In the largest US series (442 pregnancies), maternal mortality was 1.1%, while reported perinatal mortality ranges from 7.4% to 34%, driven mainly by gestational age at onset.

For labor and delivery nurses, HELLP is a condition where pattern recognition saves lives. Right upper quadrant pain in a third-trimester patient, a falling platelet count on a routine CBC, or a postpartum woman with flu-like symptoms the day after delivery can each be the first clue. This reference covers the pathophysiology, diagnostic criteria (ACOG, Tennessee, and Mississippi), nursing priorities, magnesium sulfate management, complications, and NCLEX high-yield points every nursing student should know.

What HELLP syndrome is

HELLP syndrome is a severe form of preeclampsia characterized by microangiopathic hemolytic anemia, hepatocellular injury, and thrombocytopenia. Louis Weinstein named it in 1982, describing it as “a severe consequence of hypertension in pregnancy” that may appear when the usual signs of severe preeclampsia are absent. Two classification systems followed: Sibai’s Tennessee system and Martin’s Mississippi triple-class system.

Points worth fixing in memory before you sit for NCLEX:

  • Timing: about 70% of cases present antepartum, most between 27 and 37 weeks’ gestation. The remaining ~30% are first expressed or progress after delivery, usually within 48 hours, although onset ranges from a few hours to 7 days postpartum.
  • It is a laboratory diagnosis. HELLP is confirmed by specific laboratory thresholds in a patient on the preeclampsia spectrum, after other causes of hemolysis and thrombocytopenia are ruled out.
  • Blood pressure can be normal. ACOG notes that up to 15% of patients lack either hypertension or proteinuria at presentation, so a normal blood pressure does not exclude HELLP.

Pathophysiology in one paragraph

The underlying process is endothelial dysfunction – the same vascular pathology that drives preeclampsia. Placental ischemia triggers release of anti-angiogenic factors (sFlt-1, soluble endoglin) that damage maternal endothelium. The damaged vessel walls activate and consume platelets, and red blood cells fragment as they pass through damaged, fibrin-lined small vessels. This produces the three hallmarks: hemolysis (schistocytes, elevated LDH, low haptoglobin), hepatocyte injury from sinusoidal fibrin deposition (elevated AST/ALT, RUQ pain from stretching of Glisson’s capsule), and thrombocytopenia from consumption.

Diagnostic criteria

ACOG Practice Bulletin No. 222 (reaffirmed 2026) states that many clinicians diagnose HELLP when all three of the following are present:

  • LDH 600 IU/L or more
  • AST and ALT elevated to more than twice the upper limit of normal
  • Platelets less than 100,000/µL

Two older research classifications remain in wide use, and NCLEX items may quote either one. The Mississippi system stratifies severity by the lowest platelet count reached at any point in the illness.

HELLP diagnostic criteria – Mississippi vs Tennessee classification
Parameter Mississippi Class 1 Mississippi Class 2 Mississippi Class 3 Tennessee (complete HELLP)
Platelets (nadir) ≤50,000/µL >50,000 to ≤100,000/µL >100,000 to ≤150,000/µL ≤100,000/µL
AST or ALT ≥70 IU/L ≥70 IU/L ≥40 IU/L AST ≥70 IU/L
LDH ≥600 IU/L ≥600 IU/L ≥600 IU/L ≥600 IU/L
Maternal risk Highest – about half had significant maternal morbidity in Martin's 777-patient series; 60% of the HELLP maternal deaths reviewed by Isler were Class 1 Intermediate Lowest, but treated as a clinically significant transitional group All three criteria present

Partial (incomplete) HELLP refers to patients meeting one or two of the three Tennessee criteria. Women with partial HELLP have fewer symptoms and complications than those with the complete syndrome, but they still need close surveillance as severe preeclampsia.

Supporting laboratory findings

  • Peripheral blood smear: schistocytes and burr cells reflect microangiopathic hemolytic anemia – the “H” in HELLP
  • Haptoglobin: low, because it binds free hemoglobin released by hemolysis
  • Total bilirubin: 1.2 mg/dL or higher (indirect predominant) is part of the Tennessee hemolysis definition
  • Fibrinogen: usually normal early; a falling fibrinogen signals evolving DIC, most often with placental abruption
  • Uric acid: often elevated; values above 7.8 mg/dL were among the thresholds linked to a high risk of serious maternal morbidity in the Mississippi data
  • Creatinine: rises with renal involvement

Laboratory trends matter as much as single values. ACOG notes that during worsening disease the platelet count falls by about 40% per day while liver enzymes rise, and that AST above 2,000 IU/L or LDH above 3,000 IU/L suggests an increased mortality risk. For a broader review of laboratory thresholds used in maternal care, see our nursing lab values cheat sheet.

Clinical presentation

Symptoms are nonspecific and frequently mistaken for gastroenteritis, viral illness, or gallbladder disease. ACOG reports that the main presenting symptoms are right upper quadrant pain and generalized malaise, in up to 90% of cases, with nausea and vomiting in about 50%.

Symptom or signFrequencyNursing note
RUQ or epigastric painUp to 90%From stretching of Glisson’s capsule over an edematous liver; may be fluctuating or colicky. Do not attribute it to GERD
Malaise / flu-like symptomsUp to 90%Often reported for several days before presentation; classic in postpartum HELLP. Do not reassure
Nausea and vomitingAbout 50%Easily mislabeled as a stomach virus
Headache30–60%May indicate central nervous system involvement
Visual disturbanceAbout 20%Scotomata, blurred vision
Hypertension or proteinuriaUsually presentUp to 15% of patients lack hypertension or proteinuria at presentation
EdemaCommonNonspecific in pregnancy and not a diagnostic criterion
JaundiceUncommonLate finding, concerning for advanced hepatic dysfunction

Key teaching point: a third-trimester patient reporting “I just don’t feel right” with a tender RUQ and a platelet count that dropped from 230,000 last week to 130,000 today needs an urgent CBC, smear, LDH, AST/ALT, and provider evaluation for HELLP.

Nursing assessment and priorities

HELLP management is time-critical. The nurse is the first line of surveillance – serial vitals, labs, fetal tracing, and deep tendon reflex checks detect deterioration before catastrophe. ACOG recommends that patients with HELLP remote from term receive care at a tertiary center with obstetric and neonatal intensive care available.

HELLP nursing assessment and intervention priorities
Priority Assessment Intervention
1. Maternal stability BP every 15 minutes until stable, then per protocol; HR, RR, SpO2; pain score; DTRs; strict intake and output with hourly urine output (report <30 mL/hr) Two large-bore IVs; type and screen, with crossmatch per protocol when bleeding risk is high or delivery is near; limit total IV fluids (NICE: maintenance fluids limited to 80 mL/hr in severe preeclampsia unless there are ongoing losses)
2. Fetal surveillance Continuous EFM; note decelerations, baseline changes, and variability Lateral positioning and other intrauterine resuscitation per protocol; notify the provider of Category II or III patterns. ACOG Clinical Practice Guideline No. 10 (2025) recommends against routine maternal oxygen for fetal indications – give oxygen for maternal hypoxia
3. Seizure prophylaxis Assess for headache, visual changes, clonus, hyperreflexia Magnesium sulfate 4–6 g IV loading dose over 20–30 minutes, then 1–2 g/hr maintenance, continued for 24 hours after delivery (ACOG PB 222)
4. Blood pressure control Systolic ≥160 or diastolic ≥110 mm Hg confirmed as persistent (15 minutes or more) = acute-onset severe hypertension Treat as soon as reasonably possible, within 30–60 minutes. PB 222 options: IV labetalol 10–20 mg, then 20–80 mg every 10–30 minutes (max 300 mg); IV hydralazine 5 mg, then 5–10 mg every 20–40 minutes (max 20 mg); or immediate-release oral nifedipine 10–20 mg, repeated in 20 minutes if needed
5. Fetal lung maturation Gestational age <34 weeks Betamethasone 12 mg IM every 24 hours x 2 doses. ACOG recommends steroids when delivery is indicated before 34 weeks, but delaying delivery to complete the course is not always advisable if mother or fetus deteriorates
6. Coagulation monitoring CBC with platelets, AST/ALT, LDH at least every 12 hours (ACOG), with PT/INR, PTT, and fibrinogen; watch for oozing from IV sites, petechiae, hematuria Blood products per institutional protocol – platelets for bleeding or a very low count before delivery (with a higher target before cesarean), and fibrinogen replacement for falling fibrinogen during hemorrhage
7. Delivery planning Gestational age, cervical exam, fetal status, maternal trajectory Delivery is the definitive treatment. Mode of delivery follows routine obstetric considerations (PB 222); vaginal birth is often possible, while cesarean becomes more likely at early gestational ages with an unfavorable cervix

Magnesium sulfate – the detail that shows up on NCLEX

Magnesium sulfate is given for seizure prophylaxis in preeclampsia with severe features, which includes HELLP. The usual US regimen is a 4–6 g IV loading dose over 20–30 minutes, followed by 1–2 g/hr. ACOG’s Table 2 lists the therapeutic range as 4–7 mEq/L (5–9 mg/dL).

Toxicity follows serum concentration in a predictable order, and DTRs are lost before respiratory depression – this is why every MgSO4 assessment includes reflexes (ACOG PB 222, Table 2):

  • Loss of patellar reflexes: above 7 mEq/L (above 9 mg/dL) – the first sign
  • Respiratory paralysis: above 10 mEq/L (above 12 mg/dL)
  • Cardiac arrest: above 25 mEq/L (above 30 mg/dL)

Antidote: calcium gluconate 10% solution, 10 mL (1 g) IV over 3 minutes. Stop the magnesium infusion, call for help, and support ventilation; intubation may be needed for respiratory depression.

Nursing monitoring during MgSO4:

  • DTRs every hour (patellar if no epidural; biceps or triceps if neuraxial anesthesia blunts leg reflexes)
  • Respiratory rate every hour; stop the infusion and notify the provider for respiratory depression or absent reflexes
  • Urine output every hour – magnesium is excreted almost entirely by the kidneys. ACOG advises reducing maintenance to 1 g/hr for mild renal impairment (creatinine 1.0–1.5 mg/dL) or oliguria (<30 mL/hr for more than 4 hours)
  • Serum magnesium every 4 hours when renal function is impaired; if the level exceeds 9.6 mg/dL (8 mEq/L), ACOG advises stopping the infusion and rechecking every 2 hours
  • Continuous fetal monitoring – magnesium is associated with a slightly lower FHR baseline and more minimal or absent variability without evidence of neonatal harm (Duffy 2012). Report minimal variability rather than assuming it is a drug effect, and evaluate it in the context of the whole tracing

For a broader review of electrolyte pharmacology, including magnesium, see our electrolyte imbalances nursing reference.

Complications

HELLP carries a high complication rate. In Sibai’s series of 442 pregnancies, 55% of patients needed blood or blood products. Every nurse working a high-acuity OB unit should recognize these before they declare themselves.

  • Disseminated intravascular coagulation (DIC): 21% in Sibai’s series, strongly associated with placental abruption. Fibrinogen normally rises in late pregnancy, so a value that looks normal for a nonpregnant adult may already be low. During postpartum hemorrhage, a fibrinogen of 2 g/L (200 mg/dL) or less predicted severe bleeding with a positive predictive value of 100% (Charbit 2007). Watch for oozing from IV sites, gum bleeding, petechiae, and hematuria.
  • Placental abruption: 16% in Sibai’s series. Sudden abdominal pain, vaginal bleeding (may be concealed), uterine tenderness or tetany, and fetal heart rate changes. See our placenta previa and abruption nursing reference for full assessment patterns.
  • Acute kidney injury: 7.7% in Sibai’s series. Rising creatinine and oliguria, more common with abruption and postpartum-onset HELLP.
  • Pulmonary edema: 6% in Sibai’s series, more common postpartum as fluid mobilizes. Dyspnea, crackles, falling SpO2. Strict fluid balance is essential.
  • Subcapsular liver hematoma and rupture: about 1% to less than 2% of HELLP cases. Presents with sudden severe epigastric or RUQ pain, shoulder pain, anemia, and hypotension. Diagnosis is by ultrasound, CT, or MRI, with immediate surgical consultation. In one series of 10 ruptures (9 treated surgically), maternal mortality was 10% and perinatal mortality 80% (Araujo 2006).
  • Stroke and eclamptic seizures: cerebral hemorrhage was the most common event among HELLP maternal deaths (45%) in the Isler review.
  • Postpartum hemorrhage: thrombocytopenia and coagulopathy increase bleeding risk. See our postpartum hemorrhage nursing reference.
  • Maternal death: 1.1% in Sibai’s US series. Delay in diagnosis was implicated in about half of the deaths Isler reviewed.

HELLP vs preeclampsia vs eclampsia

Students frequently confuse these three entities. The table below clarifies where HELLP sits on the preeclampsia spectrum.

Comparison of preeclampsia, eclampsia, and HELLP syndrome
Feature Preeclampsia Eclampsia HELLP
Onset 20 weeks of gestation or later; can also first appear postpartum During pregnancy, labor, or postpartum ~70% antepartum (most at 27–37 weeks); ~30% postpartum, usually within 48 hours
Blood pressure ≥140/90 (two readings at least 4 hours apart); ≥160/110 is severe range Typically elevated, but the seizure is the defining feature Usually elevated; up to 15% lack hypertension or proteinuria
Proteinuria ≥300 mg/24h or protein:creatinine ratio ≥0.3; in its absence, new hypertension with any severe feature also meets the definition Often present, but not required Often present, but not required
Laboratory changes Severe features include platelets <100,000, transaminases twice normal, creatinine >1.1 mg/dL or doubling Same as preeclampsia with severe features Defined by the lab triad: LDH ≥600 IU/L, AST and ALT more than twice normal, platelets <100,000 (ACOG)
Seizure No seizure (if seizure occurs, diagnosis becomes eclampsia) New-onset tonic-clonic, focal, or multifocal seizure with no other cause – defining feature Possible (HELLP with eclampsia); seizure prophylaxis with MgSO4 is standard
Definitive treatment Delivery; timing depends on severity and gestational age Stabilize, control seizures and blood pressure, deliver Delivery after maternal stabilization; before 34 weeks, a steroid course may be given first if mother and fetus are stable
Magnesium sulfate Recommended with severe features Recommended (load, then maintenance) Recommended

For a full review of preeclampsia assessment and management, see the preeclampsia nursing reference. For the broader picture of third-trimester complications, the obstetric nursing reference covers related conditions.

Delivery planning

Delivery is the only definitive treatment for HELLP syndrome. ACOG Practice Bulletin No. 222 lists HELLP among the conditions that preclude expectant management, and notes that many authors recommend delivery regardless of gestational age because of the risk of sudden deterioration.

  • 34 weeks or later: deliver after maternal stabilization. Delivery is not delayed for steroids in the late preterm period.
  • Before 34 weeks, mother and fetus stable: give betamethasone. PB 222 (Box 4) notes that a steroid course can be considered in some cases, depending on gestational age and maternal severity of illness, and in selected cases at a tertiary center delivery may be delayed 24–48 hours to complete it (Sibai 2004; Haram 2009). Expectant management beyond that window is not recommended.
  • Before viability: ACOG does not advise expectant management when neonatal survival is not anticipated; delivery follows maternal stabilization.
  • Deterioration at any gestational age: uncontrolled severe hypertension, eclampsia, pulmonary edema, DIC, suspected abruption, worsening renal function, stroke, hepatic hematoma or rupture, or abnormal fetal testing all call for delivery after stabilization.

Steroids are given for fetal lung maturity. High-dose dexamethasone was once used to raise maternal platelet counts. A Cochrane review of 11 trials found no difference in maternal death, severe maternal morbidity, or perinatal death, only a higher platelet count, and ACOG concluded the evidence does not support corticosteroids to attenuate HELLP. NICE advises against using dexamethasone or betamethasone to treat HELLP itself.

Route and anesthesia: mode of delivery follows routine obstetric indications. ACOG considers neuraxial anesthesia acceptable, with an exceptionally low epidural hematoma risk, when platelets are 70,000/µL or more and stable, with no other coagulopathy and no antiplatelet or anticoagulant therapy. A falling count can close this window, which is one reason the anesthesia team is involved early.

After delivery: HELLP often worsens before it improves. The lowest platelet count occurs a mean of 23 hours after delivery, and with supportive care 90% of patients have platelets above 100,000/µL and falling liver enzymes within 7 days. ACOG advises reassessing the diagnosis if platelets are still falling and enzymes still rising after 4 days postpartum.

NCLEX high-yield points

These are the points item writers love. Memorize them.

  1. RUQ or epigastric pain in a pregnant patient with hypertension equals HELLP until proven otherwise. Do not attribute it to GERD, gastritis, or gallbladder disease without a CBC, LFTs, and LDH.
  2. HELLP can occur without hypertension or proteinuria. Up to 15% of patients lack one or the other at presentation, so a normal BP does not exclude the diagnosis.
  3. The lab triad (ACOG): LDH ≥600 IU/L, AST and ALT more than twice the upper limit of normal, platelets <100,000/μL. Older items may quote the Tennessee AST cutoff of ≥70 IU/L or the Mississippi platelet classes.
  4. Schistocytes on peripheral smear indicate microangiopathic hemolytic anemia and confirm the “H” in HELLP. Low haptoglobin and elevated indirect bilirubin support the finding.
  5. Magnesium sulfate monitoring: DTRs are lost before respiratory depression (reflexes above 7 mEq/L, respiratory paralysis above 10 mEq/L). Absent DTRs or respiratory depression means stop the infusion and notify the provider; report falling urine output, because magnesium is renally excreted. The antidote is calcium gluconate 1 g (10 mL of 10%) IV over 3 minutes.
  6. Definitive treatment is delivery. At 34 weeks or later, or with maternal or fetal deterioration at any gestational age, delivery follows stabilization. A 24–48 hour delay for steroids applies only to a stable mother and fetus before 34 weeks at a tertiary center.
  7. Betamethasone before 34 weeks for fetal lung maturity (12 mg IM every 24 hours x 2 doses). Steroids do not treat HELLP itself, and delivery is not delayed for them if the mother deteriorates.
  8. Postpartum HELLP is real. About 30% of cases are first expressed or progress after delivery, usually within 48 hours but up to 7 days out. Do not dismiss a postpartum patient presenting with RUQ pain, malaise, and flu-like symptoms – draw a CBC and LFTs.
  9. Hepatic rupture is a surgical emergency. Sudden severe RUQ pain with shoulder pain and hemodynamic instability in a HELLP patient – call the surgical team, activate the massive transfusion protocol, and prepare for laparotomy.
  10. DIC risk tracks with abruption. DIC complicated 21% of HELLP pregnancies in Sibai’s series. Monitor fibrinogen (it should be high in late pregnancy, so a “normal-looking” value can be low), PT/INR, and clinical signs of bleeding (oozing IV sites, petechiae, hematuria).

Recurrence and counseling

In Sibai’s follow-up of 192 subsequent pregnancies in normotensive women with prior HELLP, recurrent HELLP occurred in 3%, preeclampsia in 19%, and preterm delivery in 21%. A history of preeclampsia, including HELLP, is a high-risk factor for which ACOG recommends low-dose aspirin (81 mg daily) in the next pregnancy, started between 12 and 28 weeks of gestation (optimally before 16 weeks) and continued until delivery. Women with any hypertensive disorder of pregnancy also carry roughly double the later risk of cardiovascular disease, so postpartum follow-up should include long-term blood pressure and cardiovascular risk screening.

References

  1. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia. Obstet Gynecol. 2020;135(6):e237–e260. doi:10.1097/AOG.0000000000003891 (Reaffirmed 2026.)
  2. Martin JN Jr, Rinehart BK, May WL, Magann EF, Terrone DA, Blake PG. The spectrum of severe preeclampsia: comparative analysis by HELLP (hemolysis, elevated liver enzyme levels, and low platelet count) syndrome classification. Am J Obstet Gynecol. 1999;180(6 Pt 1):1373–1384. doi:10.1016/s0002-9378(99)70022-0
  3. Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Obstet Gynecol. 2004;103(5 Pt 1):981–991. doi:10.1097/01.AOG.0000126245.35811.2a
  4. Haram K, Svendsen E, Abildgaard U. The HELLP syndrome: clinical issues and management. A review. BMC Pregnancy Childbirth. 2009;9:8. doi:10.1186/1471-2393-9-8
  5. Magpie Trial Collaborative Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002;359(9321):1877–1890. doi:10.1016/s0140-6736(02)08778-0
  6. Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol. 2003;102(1):181–192. doi:10.1016/s0029-7844(03)00475-7
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  8. Woudstra DM, Chandra S, Hofmeyr GJ, Dowswell T. Corticosteroids for HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome in pregnancy. Cochrane Database Syst Rev. 2010;(9):CD008148. doi:10.1002/14651858.CD008148.pub2
  9. Barton JR, Sibai BM. Diagnosis and management of hemolysis, elevated liver enzymes, and low platelets syndrome. Clin Perinatol. 2004;31(4):807–833. doi:10.1016/j.clp.2004.06.008
  10. Henderson JT, Vesco KK, Senger CA, Thomas RG, Redmond N. Aspirin use to prevent preeclampsia and related morbidity and mortality: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2021;326(12):1192–1206. doi:10.1001/jama.2021.8551
  11. Vigil-De Gracia P. Maternal deaths due to eclampsia and HELLP syndrome. Int J Gynaecol Obstet. 2009;104(2):90–94. doi:10.1016/j.ijgo.2008.09.014
  12. Isler CM, Rinehart BK, Terrone DA, Martin RW, Magann EF, Martin JN Jr. Maternal mortality associated with HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Am J Obstet Gynecol. 1999;181(4):924–928. doi:10.1016/s0002-9378(99)70343-1
  13. Abildgaard U, Heimdal K. Pathogenesis of the syndrome of hemolysis, elevated liver enzymes, and low platelet count (HELLP): a review. Eur J Obstet Gynecol Reprod Biol. 2013;166(2):117–123. doi:10.1016/j.ejogrb.2012.09.026
  14. Sibai BM, Ramadan MK, Usta I, Salama M, Mercer BM, Friedman SA. Maternal morbidity and mortality in 442 pregnancies with hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome). Am J Obstet Gynecol. 1993;169(4):1000–1006. doi:10.1016/0002-9378(93)90043-i
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  16. Weinstein L. Syndrome of hemolysis, elevated liver enzymes, and low platelet count: a severe consequence of hypertension in pregnancy. Am J Obstet Gynecol. 1982;142(2):159–167. doi:10.1016/s0002-9378(16)32330-4
  17. Sibai BM, Ramadan MK, Chari RS, Friedman SA. Pregnancies complicated by HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets): subsequent pregnancy outcome and long-term prognosis. Am J Obstet Gynecol. 1995;172(1 Pt 1):125–129. doi:10.1016/0002-9378(95)90099-3
  18. National Institute for Health and Care Excellence. Hypertension in pregnancy: diagnosis and management. NICE guideline NG133. Published June 25, 2019; last updated April 17, 2023. https://www.nice.org.uk/guidance/ng133
  19. Charbit B, Mandelbrot L, Samain E, et al. The decrease of fibrinogen is an early predictor of the severity of postpartum hemorrhage. J Thromb Haemost. 2007;5(2):266–273. doi:10.1111/j.1538-7836.2007.02297.x
  20. Duffy CR, Odibo AO, Roehl KA, Macones GA, Cahill AG. Effect of magnesium sulfate on fetal heart rate patterns in the second stage of labor. Obstet Gynecol. 2012;119(6):1129–1136. doi:10.1097/AOG.0b013e318257181e
  21. Araujo AC, Leao MD, Nobrega MH, et al. Characteristics and treatment of hepatic rupture caused by HELLP syndrome. Am J Obstet Gynecol. 2006;195(1):129–133. doi:10.1016/j.ajog.2006.01.016
  22. American College of Obstetricians and Gynecologists. ACOG Clinical Practice Guideline No. 10: Intrapartum Fetal Heart Rate Monitoring: Interpretation and Management. Obstet Gynecol. 2025;146(4):583–599. doi:10.1097/AOG.0000000000006049 (Replaces Practice Bulletins No. 106 and 116; source for the recommendation against routine maternal oxygen.)
  23. American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 743: Low-Dose Aspirin Use During Pregnancy. Obstet Gynecol. 2018;132(1):e44–e52. doi:10.1097/AOG.0000000000002708 (Reaffirmed 2023.)
  24. American College of Obstetricians and Gynecologists. Committee Opinion No. 713: Antenatal Corticosteroid Therapy for Fetal Maturation. Obstet Gynecol. 2017;130(2):e102–e109. doi:10.1097/AOG.0000000000002237 (Interim update; reaffirmed 2024.)

This article is for educational purposes and NCLEX preparation. It does not substitute for clinical training, facility protocols, or direct provider orders.