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Obstetric Anesthesia


  • Page extent: 992 pages
  • Size: 228 x 152 mm
  • Weight: 0.8 kg

Library of Congress

  • Dewey number: 617.9/682
  • Dewey version: 22
  • LC Classification: RG732 .O2634 2007
  • LC Subject headings:
    • Anesthesia in obstetrics--Handbooks, manuals, etc
    • Anesthesia, Obstetrical--methods--Handbooks
    • Pharmaceutical Preparations--Handbooks

Library of Congress Record


 (ISBN-13: 9780521709392)


Obstetric Anesthesia




■ Inherited disorder of bone metabolism that results in short stature, a small maxilla, large mandible & spinal abnormalities

■ Lumbar lordosis & thoracic kyphosis are increased.

■ The small vertebral pedicles & short anteroposterior & transverse diameters of the vertebral canal can result in spinal stenosis, which can worsen w/ age as scoliosis worsens & osteophytes form.


■ Physical exam

■ Lumbosacral spine films may add information.


■ Cervical mobility may be diminished; combined w/ other facial abnormalities, this may make intubation difficult.

■ Regional anesthesia may be technically difficult but is not contraindicated.

■ Because of the pt’s short stature & spinal stenosis, the dosage for a single-shot spinal may be difficult to estimate.

■ Insertion of an epidural or spinal catheter may be a better alternative to a single-shot spinal to allow careful titration of anesthetic.


■ Consider using an epidural or spinal catheter instead of a single-shot spinal, which may be difficult to dose appropriately.

■ Prepare for a difficult intubation if decreased cervical mobility or facial anomalies are present.


■ Physical exam, lumbosacral spine films





■ Rare disfiguring & disabling disease caused by growth hormone hypersecretion

■ Usually due to growth hormone-secreting anterior pituitary adenoma


■ Prevalence 50–60 cases per million population

■ Equal distribution btwn genders

■ Very rare for acromegalic women to become pregnant because of impaired gonadotropic axis; 60% of acromegalic women are amenorrheic

■ <100 pregnancies reported in women w/ acromegaly


■ Headache

■ Papilledema

■ Visual disturbances

■ Enlargement of tongue & epiglottis

■ Increased length of mandible

■ Overgrowth of soft tissues of upper airway

■ Hoarseness or change in voice

■ Stridor

■ Peripheral neuropathy

■ Diabetes mellitus

■ Systemic hypertension

■ Ischemic heart disease

■ Osteoarthritis/osteoporosis

■ Thick & oily skin

■ Skeletal muscle weakness

Changes Associated w/ Pregnancy

■ During early pregnancy, growth hormone (GH) is secreted by pituitary.

■ In 2nd trimester, placenta starts producing variant of GH.

GH levels continue to increase throughout pregnancy, peaking in 3rd trimester.

■ Placental GH induces maternal hepatic IGF-1 production, which inhibits pituitary GH secretion.

■ Serum IGF-1 levels increase in 2nd half of pregnancy.

■ Conflicting evidence that pregnancy worsens pituitary macroadenoma growth; some case reports of worsening of symptoms during pregnancy; others showed improvement.

■ In acromegalic women, pituitary GH secretion persists throughout pregnancy.

Maternal Complications

■ Diabetes mellitus

■ Hypertension

Fetal/Neonatal Complications

■ Newborns of untreated mothers have greater mean birthweights than newborns of treated mothers.


■ Plasma GH concentration >3 ng/mL

■ Failure of plasma GH concentration to decrease 1–2 hours after administration of 75–100 g glucose

■ Pituitary MRI w/ gadolinium for pituitary mass


■ Transsphenoidal surgical excision of pituitary adenoma is definitive treatment.

  ➢ May be required during pregnancy if pt has symptoms of tumor expansion or signs & symptoms not relieved by medical mgt

  ➢ Perform surgery in 2nd trimester: surgery in 1st trimester associated w/ increased risk of spontaneous abortion; surgery in 3rd trimester may cause premature labor

■ Medical mgt

  ➢ Dopamine agonists

   • Bromocriptine or Dostinex; however, dopamine agonist treatment is successful in only 10% of cases

   • Dopamine agonists are more effective on tumors w/ GH & prolactin co-secretion.

  ➢ Somatostatin analogs

   • Octreotide, octreotide LAR, lanreotide

   • Normalization of GH/IGF in 40–60% of pts

   • Limited experience during pregnancy

  ➢ GH receptor antagonists

   • Pegvisomant: no reported pregnancies on this medication

■ Radiotherapy

  ➢ Takes a long time to work

  ➢ High incidence of hypopituitarism

Anesthetic Management

■ Thorough evaluation of airway

  ➢ Acromegalic pts have higher incidence of difficult intubation.

  ➢ Distorted facial anatomy & increased length of mandible may lead to difficult mask airway.

  ➢ Enlargement of tongue & epiglottis & overgrowth of soft tissue in upper airway can lead to obstruction.

  ➢ Pt may require smaller endotracheal tube than normal because of subglottic narrowing & enlargement of vocal cords.

  ➢ Nasal turbinate enlargement may make nasal intubation difficult.

  ➢ Pt may require awake fiberoptic intubation.

■ Use non-depolarizing muscle relaxants sparingly, especially if skeletal muscle weakness exists.

■ Both regional anesthesia & general anesthesia can be used safely.

■ Anticipate difficulty placing epidural or spinal because of skeletal changes.

■ Document pre-op neuropathies & carefully pad all pressure points.

■ Carefully monitor blood glucose, especially if pt has diabetes mellitus or glucose intolerance.


■ Pt may have various airway issues; anticipate difficult intubation if general anesthetic is required.


■ Thorough preanesthetic evaluation, especially for hypertension, coronary artery disease, diabetes mellitus

■ Thorough airway evaluation

■ Anticipate difficult mask ventilation & intubation; may require fiberoptic bronchoscope.

■ Monitor blood glucose.





■ Approximate prevalence: 1/7,000 to 1/16,000 pregnancies

■ Disorder of late pregnancy, w/ most cases diagnosed btwn 35 & 37 weeks gestation


■ Exact causal mechanisms are unknown, but there seems to be an association of AFLP w/ maternal long-chain 3-hydroxyacyl CoA dehydrogenase deficiency (LCHAD).

  ➢ Long-chain 3-hydroxyacyl CoA dehydrogenase is an enzyme that is involved in mitochondrial beta-oxidation of fatty acids. It is thought that in mothers w/ this deficiency, fatty acid metabolites from the fetus & placenta can build up & overwhelm the mother’s mitochondrial oxidation pathways. These metabolites can be hepatotoxic, & their accumulation is thought to be a possible causative mechanism for AFLP.

■ Some evidence suggests a link between AFLP & pre-eclampsia.

  ➢ There can be hepatic involvement in pre-eclampsia (HELLP syndrome).

  ➢ Pre-eclampsia is often seen concurrently in pts w/ AFLP.

  ➢ Liver biopsies in pre-eclamptic women w/ & w/o liver dysfunction both show microvesicular fat infiltration, suggesting that AFLP may be at the severe end of a pathologic spectrum encompassing pre-eclampsia, HELLP syndrome & AFLP.

Clinical Manifestations

AFLP occurs late, near term in the 3rd trimester.

■ Symptoms of nausea, vomiting, lethargy, malaise & headache can be part of a prodromal period in AFLP.

■ Pt may report RUQ abdominal pain.

■ Jaundice or bleeding is sometimes the initial presentation.

■ Hepatic encephalopathy can be a late finding.

■ In contrast to intrahepatic cholestasis of pregnancy, pruritus is NOT a common symptom in AFLP.

■ Over half of pts w/ AFLP have pre-eclampsia as well during their course.

■ Coagulopathy & progression to DIC are possible in AFLP.


■ Diagnosis is usually made clinically through examination of symptoms & lab values (see “Studies”).

■ Work up the pt for pre-eclampsia & HELLP syndrome, since they are so often associated w/ AFLP.

  ➢ HELLP syndrome consists of hemolysis, elevated liver enzymes & low platelet count.

■ Imaging studies are not needed to diagnose AFLP but may be helpful to rule out other pathology, such as hepatic infarct or hematoma.


Laboratory Data & Studies

■ Serum transaminases are generally elevated in the neighborhood of 300–500 IU/L. Values may be as high as 1,000 but rarely exceed that.

■ Alkaline phosphatase levels are markedly elevated (can be 10× normal).

■ Leukocytosis w/ a left shift is a common but nonspecific finding.

■ Hypoglycemia is common secondary to impaired hepatic gluconeogenesis.

■ Acute renal failure may be a component of AFLP, w/ resultant rises in creatinine & BUN.

■ If there has been progression to DIC, then thrombocytopenia is seen, along w/ elevations in PT & aPTT & a decrease in fibrinogen.

■ Liver biopsy demonstrates microvesicular fatty infiltration of pericentral hepatocytes. There is also hepatocellular necrosis, portal inflammation & cholestasis. Biopsy is rarely needed to make the diagnosis & is in fact often contraindicated secondary to low platelets or abnormal coagulation studies.


■ The ultimate treatment for AFLP is fetal delivery as soon as safely possible. Prompt attention is necessary because progressive hepatic failure & fetal death can occur within days.

■ There is no evidence suggesting an advantage of cesarean delivery over prompt vaginal delivery.

■ Prior to delivery, the pt should be stabilized, w/ attention to correcting metabolic & coagulation abnormalities.

  ➢ Glucose infusion for hypoglycemia

  ➢ Correction of coagulopathy w/ FFP, platelets or cryoprecipitate as needed (to avoid massive intrapartum hemorrhage). This is particularly important if neuraxial spinal/epidural anesthesia is planned, because of the potential for a devastating epidural hematoma in a pt w/ coagulopathy &/or low platelets.

  ➢ If acute renal failure complicates the clinical picture, dialysis can be necessary.

■ Be aware of the renal status & potassium, & adjust your anesthetic plan accordingly (avoid potassium-containing replacement fluids if the pt is retaining K+, avoid succinylcholine if K+ is elevated).

■ In the case of hepatic encephalopathy, blood ammonia levels should be obtained & lactulose given if appropriate.

  ➢ If the encephalopathy is sufficiently bad to impair respiration, then mechanical ventilation in an ICU setting may be necessary.

■ For either vaginal delivery or cesarean delivery, establish large-bore IV access in anticipation of the need for fluid resuscitation & administration of blood products.

■ Be aware of intra-operative losses & have rapid access to appropriate replacement fluids & blood products.

■ An arterial line can be an appropriate monitor to assist in frequent sampling of blood for Hct & coagulation studies & also to provide close BP monitoring should vasopressors become necessary.

■ In the operating environment, especially if general anesthesia is required, it may be prudent to keep the pt warm to minimize coagulopathy.

■ Anesthetic mgt for AFLP, & indeed for all liver disease of pregnancy, should be guided by the symptoms & manifestations of the liver process. Various manifestations will have differing effects on physiology & choice of anesthetic technique.

  ➢ If pt is coagulopathic, see the section on “General Concepts.”

  ➢ If pt is cirrhotic, see sections on “General Concepts,” “Cirrhosis,” “Portal Hypertension,” “Ascites,” “Hepatic Encephalopathy.”

■ For general discussion of regional & general anesthesia considerations, see the section on “General Concepts.”


AFLP is a rare but potentially devastating disorder of pregnancy.

■ Presents in 3rd trimester

■ Lab abnormalities are prominently elevated alkaline phosphatase, w/ a less marked rise in serum transaminases. Coagulation studies may also be abnormal, w/ potential for DIC.

■ After diagnosis, treatment is maternal stabilization & delivery as soon as safely possible.

  ➢ Anesthetic mgt should be guided by OB criteria & physiologic manifestations of the disease process.

  ➢ Special attention to coagulation status, as it has important implications for regional anesthesia & peripartum hemorrhage

  ➢ The maternal condition usually improves within 24 hours of delivery, w/ continued recovery over the next week.

   • There is generally no long-term liver dysfunction for survivors.


■ Know OB plan.

■ Degree of pt’s compromise will dictate need for invasive monitoring, ICU care.

■ Beware of coagulopathy, renal failure.




■ Immunologic response to infection, usually group A beta-hemolytic streptococcal (although can be initiated by other bacterial or viral infections), that damages renal glomeruli

■ Acute glomerulonephritis is rare during pregnancy.

■ 3 urinary patterns are seen: focal nephritic, diffuse nephritic, nephrotic.


Lab tests commonly ordered to evaluate renal function in pregnancy include:

■ Creatinine


■ Electrolytes

■ Creatinine clearance


■ Urinalysis typically shows hematuria, proteinuria & red cell casts.

■ In addition, consider:

■ Renal biopsy

Focal nephritic

■ Inflammatory lesions in less than half of glomeruli

■ Urinalysis shows red cells, +/− red cell casts, & mild proteinuria.

Diffuse nephritic

■ Affects most or all glomeruli

■ Heavy proteinuria

■ +/− renal insuffiency


■ Heavy proteinuria

■ Few red cell casts


Medical/OB mgt of acute glomerulonephritis:

■ Treatment of acute glomerulonephritis depends on the underlying etiology.

■ For decreased renal function:

  ➢ Increased frequency of prenatal visits (q2 wks in 1st & 2nd trimesters, then q1 week)

  ➢ Monitoring: monthly measurements of serum creatinine, creatinine clearance, fetal development, BP

  ➢ Erythropoietin may be used for maternal anemia.

  ➢ Preterm delivery is considered for worsening renal function, fetal compromise or pre-eclampsia.

  ➢ Renal biopsy is considered if rapid deterioration in renal function occurs prior to 32 weeks gestation.

  ➢ If glomerulonephritis is responsive to steroids, these should be continued during pregnancy.

  ➢ See “Parturients on Dialysis” for dialysis mgt.

Anesthetic mgt of pts w/ acute glomerulonephritis


■ Evaluate degree of renal dysfunction & hypertension.

■ Evaluate for anemia & electrolyte abnormalities.

Intraoperative mgt

■ Monitors: standard monitoring + fetal heart rate (FHR) +/− arterial line +/− CVP

■ Limit fluids in pts w/ marginal renal function to prevent volume overload.

■ Use strict aseptic technique, as uremic pts are more prone to infection.

■ Careful padding/protection of dialysis access is important.

■ Consider promotility agents, as uremic pts may have impaired GI motility.

Regional anesthesia

■ Uremia-induced platelet dysfunction leads to increased bleeding time.

■ Pts may have thrombocytopenia from peripheral destruction of platelets.

■ Increased toxicity from local anesthetics has been reported in pts w/ renal disease, but amide & ester local anesthetics can be used safely.

■ Contraindications to regional technique: pt refusal, bacteremia, hypovolemia, hemorrhage, coagulopathy, neuropathy

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