Obstetric Anesthesia
992
Obstetric Anesthesia
992Paperback
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Overview
Product Details
| ISBN-13: | 9780521709392 |
|---|---|
| Publisher: | Cambridge University Press |
| Publication date: | 08/13/2007 |
| Series: | Cambridge Pocket Clinicians |
| Pages: | 992 |
| Product dimensions: | 5.00(w) x 6.93(h) x 1.61(d) |
Read an Excerpt
Cambridge University Press
978-0-521-70939-2 - Obstetric Anesthesia - Edited by May C. M. Pian-Smith and Lisa Leffert
Excerpt
PART ONE
Obstetric Anesthesia
ACHONDROPLASIA
STEPHEN PANARO, MD
EDWARD MICHNA, MD
FUNDAMENTAL KNOWLEDGE
■ 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.
STUDIES
■ Physical exam
■ Lumbosacral spine films may add information.
MANAGEMENT/INTERVENTIONS
■ Cervical mobility may be diminished; combined w/ other facial abnormalities, this may make intubation difficult.
■ Regional anesthesia may be technically difficult but is notcontraindicated.
■ 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.
CAVEATS/PEARLS
■ 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.
CHECKLIST
■ Physical exam, lumbosacral spine films
ACROMEGALY
GRACE C. CHANG, MD, MBA; ROBERT A. PETERFREUND, MD, PHD; AND STEPHANIE L. LEE, MD, PHD
FUNDAMENTAL KNOWLEDGE
Definition
■ Rare disfiguring & disabling disease caused by growth hormone hypersecretion
■ Usually due to growth hormone-secreting anterior pituitary adenoma
Epidemiology
■ 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
Signs/Symptoms
■ 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.
STUDIES
■ 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
MANAGEMENT/INTERVENTIONS
■ 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.
CAVEATS/PEARLS
■ Pt may have various airway issues; anticipate difficult intubation if general anesthetic is required.
CHECKLIST
■ 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.
ACUTE FATTY LIVER OF PREGNANCY (AFLP)
LAWRENCE WEINSTEIN, MD DOUG RAINES, MD
FUNDAMENTAL KNOWLEDGE
Epidemiology
■ Approximate prevalence: 1/7,000 to 1/16,000 pregnancies
■ Disorder of late pregnancy, w/ most cases diagnosed btwn 35 & 37 weeks gestation
Pathogenesis
■ 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
■ 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.
STUDIES
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.
MANAGEMENT/INTERVENTIONS
■ 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.”
CAVEATS/PEARLS
■ 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.
CHECKLIST
■ Know OB plan.
■ Degree of pt’s compromise will dictate need for invasive monitoring, ICU care.
■ Beware of coagulopathy, renal failure.
ACUTE GLOMERULONEPHRITIS
JOSHUA WEBER, MD
PETER DUNN, MD
FUNDAMENTAL KNOWLEDGE
■ 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.
STUDIES
Lab tests commonly ordered to evaluate renal function in pregnancy include:
■ Creatinine
■ BUN
■ Electrolytes
■ Creatinine clearance
■ CBC
■ 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
Nephrotic
■ Heavy proteinuria
■ Few red cell casts
MANAGEMENT/INTERVENTIONS
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
Pre-op
■ 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
© Cambridge University Press