Absolute Obstetric Anesthesia Review

The Complete Study Guide for

Certification and Recertification
Cassandra Wasson
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Absolute Obstetric
Anesthesia Review

The Complete Study Guide for

Certification and Recertification
Cassandra Wasson
Albert Kelly
David Ninan
Quy Tran

123
Absolute Obstetric Anesthesia Review
Cassandra Wasson • Albert Kelly
David Ninan • Quy Tran

Absolute Obstetric
Anesthesia Review
The Complete Study Guide for
Certification and Recertification
Cassandra Wasson Albert Kelly
Riverside University Health System - Riverside University Health System -
Medical Center Medical Center
Moreno Valley, CA Moreno Valley, CA
USA USA

David Ninan Quy Tran

Riverside University Health System - Harbor–UCLA Medical Center
Medical Center Torrance, CA
Loma Linda, CA USA
USA

ISBN 978-3-319-96979-4    ISBN 978-3-319-96980-0 (eBook)

https://doi.org/10.1007/978-3-319-96980-0

Library of Congress Control Number: 2018957090

© Springer Nature Switzerland AG 2019

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of
the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation,
broadcasting, reproduction on microfilms or in any other physical way, and transmission or information
storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology
now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication
does not imply, even in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
The publisher, the authors, and the editors are safe to assume that the advice and information in this book
are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the
editors give a warranty, express or implied, with respect to the material contained herein or for any errors
or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims
in published maps and institutional affiliations.

This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
This book is dedicated to the Riverside
University Health System Anesthesia
Program and my classmates of the
anesthesia class of 2019 (Tyler Gouvea,
Kellie Morris, Devangi Patel, and Ngoc
Truong). Without the love and support of my
attendings, classmates, and staff at RUHS,
this book would not be possible.
Preface

The field of anesthesiology is ever expanding and the need for subspecializing is
becoming more and more common in order to provide the best care for the most
complex patients and improve patient safety and outcomes. With an increased num-
ber of high-risk patients (such as those congenital heart disease) becoming preg-
nant, the need for anesthesiologists subspecializing in obstetrics is growing.
Although the number of fellowships available for obstetric anesthesia is increas-
ing, the number of invaluable resources available to these trainees is not. Absolute
Obstetric Anesthesia Review was created to provide a concise, easy to follow outline
of obstetric anesthesia for anesthesiology residents, obstetric anesthesiology fel-
lows, and any anesthesiologist providing care to obstetric patients. It is written to
follow the outline set forth by the American Board of Anesthesiology (ABA) to be
an invaluable resource for in-service exam and board exams. It goes to a fellow-­
level depth of information. It provides testable information for the boards, as well as
practical tips for clinical practice.
We hope you find this book helpful, easy to use, and a quick read. It is small
enough to carry during your obstetric anesthesia rotation, rather than the larger text-
books that are over 1000 pages in length. We hope the concise nature of this book
allows you to cover more material in your limited time to study, allowing you more
time for the clinical aspects of obstetric anesthesia.

Moreno Valley, CA, USA Cassandra Wasson

Albert Kelly
Loma Linda, CA, USA David Ninan
Torrance, CA, USA Quy Tran

vii
Contents

Part I Maternal Physiology

1 Effects of Pregnancy on Uptake and Distribution. . . . . . . . . . . . . . .    3
2 Respiratory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .    5
3 Cardiovascular . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .    7
4 Renal. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .    9
5 Liver. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   11
6 Gastrointestinal. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   13
7 Hematology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   15
8 Placental O2 Exchange. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   17
9 Placental CO2 Exchange. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   19
10 Placental Blood Flow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   21
11 Barrier Function. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   23

Part II Maternal-Fetal Considerations

12 Pharmacology of Local Anesthetic Drugs. . . . . . . . . . . . . . . . . . . . . .   27
13 Pharmacology of Local Anesthetic Adjuvants. . . . . . . . . . . . . . . . . .   31
14 Pharmacology of Oxytocic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . .   35
15 Mechanisms of Placental Transfer, Placental Transfer of
Specific Drugs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   37
16 Fetal Disposition of Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   39
17 Drug Effects on Newborn. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   43
18 Amniotic Fluid. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   45
19 Antepartum Fetal Assessment and Therapy . . . . . . . . . . . . . . . . . . .   47

ix
x Contents

20 Systemic Medications: Opioids, Sedatives, Inhalational Agents. . . .   51

21 Epidural, Caudal, Spinal, Combined Spinal/Epidural. . . . . . . . . . .   53
22 Paracervical Block, Lumbar Sympathetic Block, Pudendal Block .   61
23 Complications of Labor Analgesia . . . . . . . . . . . . . . . . . . . . . . . . . . .   63
24 Influence of Anesthetic Technique on Labor. . . . . . . . . . . . . . . . . . .   73
25 Cesarean Delivery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   75

Part III Pathophysiology of Complicated Pregnancy

26 Anesthesia for Cerclage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   83
27 Anesthesia for Non-obstetric Surgery. . . . . . . . . . . . . . . . . . . . . . . . .   85
28 Ectopic Pregnancy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   87
29 Spontaneous Abortion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   89
30 Gestational Trophoblastic Disease (Hydatidiform Mole) . . . . . . . . .   91
31 Autoimmune Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   93
32 Diabetes Mellitus (DM). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   97
33 Thyroid Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
34 Pheochromocytoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103
35 Congenital Heart Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107
36 Valvular Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
37 Other Heart Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
38 Anemia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
39 Thrombocytopenic Coagulopathies. . . . . . . . . . . . . . . . . . . . . . . . . . . 119
40 Other Hematologic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
41 Hypertension (HTN). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123
42 Neurologic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
43 Asthma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
44 Other Respiratory Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
45 Renal Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
46 Human Immunodeficiency Virus (HIV) Infection. . . . . . . . . . . . . . . 141
Contents xi

Part IV Problems of Term and Delivery

47 Intrapartum Fetal Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
48 Supine Hypotensive Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
49 Embolic Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
50 Antepartum Hemorrhage. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153
51 Postpartum Hemorrhage. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
52 Cord Prolapse. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159
53 Dystocia, Malposition, and Malpresentation
(Breech, Transverse Lie). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161
54 Maternal Cardiopulmonary Resuscitation. . . . . . . . . . . . . . . . . . . . . 163
55 Fever and Infection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
56 Preterm Labor – Chapter 34 Chestnut’s . . . . . . . . . . . . . . . . . . . . . . 169
57 Vaginal Birth After Cesarean Section (VBAC). . . . . . . . . . . . . . . . . . 173
58 Multiple Gestation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175
59 Resuscitation of Newborn. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177
60 Intrauterine Surgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
 ppendix A: Management of Antithrombotic Therapy
A
for Neuraxial Procedures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  183
 Part I
Maternal Physiology
Effects of Pregnancy on Uptake
and Distribution 1

1. MAC for volatiles is decreased up to 40% in pregnancy

(a) Rate of induction is faster due to greater minute ventilation and reduced
functional residual capacity (FRC)
2. Pregnant women have a larger volume of distribution due to expanded extracel-
lular volume and total body water, so recovery from many anesthetic drugs is
faster
3. The potency of some medications is increased due to decreased levels of albumin
and alpha 1-acid glycoprotein for drug binding leading to more unbound drug
concentration in plasma

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Respiratory
2

Chapters 2, 16, and 17 Chestnut’s

1. Airway: increased edema, vascularity, and capillary engorgement of the larynx

and the nasal and oropharyngeal mucosa.
(a) Nasal breathing can be difficult
(b) Prone to epistaxis; avoid nasal intubation if possible
(c) Anticipate difficult oral intubation
(d) Smaller endotracheal tubes should be used
2. Respiratory changes during pregnancy compared to pre-pregnancy values:
(a) No change: FEV1, FVC, FEV1/FVC, peak expiratory flow, flow-volume
loop, closing capacity, pulmonary compliance, and diffusing capacity
(b) Decreased: pulmonary resistance and chest wall compliance
(i) Chest wall compliance is decreased because the ligamentous attach-
ments of the ribs are relaxed and the AP and transverse diameters of the
thoracic cage are increased due to the hormone relaxin
(ii) Total pulmonary and airway resistances decrease due to hormonal relax-
ation of tracheobronchial tree smooth muscles
(c) Increased: Diaphragm excursion (due to its higher resting position)
3. Respiratory physiology changes during pregnancy
(a) Increased: Dead space (+45%); inspiratory reserve volume (+5%); minute
ventilation (+45%); alveolar ventilation (+45%); tidal volume (TV) (+45%);
and inspiratory capacity (+15%)
(i) TV increases due to a decrease in expiratory reserve volume
(ii) Minute ventilation is increased due to an increase in tidal volume rather
than respiratory rate
1. Progesterone increases the sensitivity of the respiratory center to
CO2 leading to the increased minute ventilation

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6 2 Respiratory

(b) Decreased: expiratory reserve volume (−25%); residual volume (−15%);

FRC (−20%); and total lung capacity (−5%)
(i) FRC decreases due to the uterus expanding resulting in reduction of ERV
and RV
1. O2 reserve decreases and causes the potential for airway closure and
atelectasis
(c) Unchanged: respiratory rate and vital capacity
4. Pregnancy frequently causes respiratory alkalosis with a compensatory meta-
bolic acidosis
(a) The normal PaCO2 during pregnancy is 30 mmHg
(b) Normal blood gas during pregnancy: pH 7.44, PaCO2 30–34 mmHg, HCO3
20–22 mEq/L, PaO2 105 mmHg.
(c) Clinical implication: Maternal hyperventilation due to labor pain or anxiety
may cause fetal acidosis because further reduction in PaCO2 can lead to
decreased uteroplacental perfusion and a left shift of the maternal oxygen
dissociation curve
5. O2 consumption is increased
6. Changes during labor (mitigated by neuraxial anesthesia):
(a) Increased minute ventilation causes PaCO2 levels as low as 10–15 mmHg
(b) Increased O2 consumption due to the increased metabolic demands of hyper-
ventilation, uterine activity, and maternal expulsive efforts during the second
stage of labor, which leads to anaerobic metabolism and increased lactate
concentrations
Cardiovascular
3

Chapters 2, 16 and 17 Chestnut’s

1. EKG changes common during pregnancy: shortened PR and QT intervals; axis

shift (to the right during the first trimester and to the left during the third trimes-
ter); depressed ST segments; and low-voltage T waves
2. Echocardiography changes common during pregnancy: increase in end dia-
stolic volume of both left and right ventricles. Slight increase in mitral and tri-
cuspid annuluses causing regurgitations. Eccentric hypertrophy of left
ventricle
3. Hemodynamics observed during pregnancy
(a) Increased: cardiac output (+50%); stroke volume (+25%); heart rate
(+25%); left ventricular end-diastolic volume; ejection fraction (EF)
(b) Decreased: systemic vascular resistance (SVR) (−20%)
(c) Unchanged: left ventricular end-systolic volume; left ventricular stroke
work index; pulmonary capillary wedge pressure; pulmonary artery dia-
stolic pressure; central venous pressure
4. The greater blood volume of pregnancy causes cardiac eccentric hypertrophy
5. S1 is accentuated and S2 splitting is exaggerated
6. S3 is not pathologic during pregnancy
7. Systolic ejection murmur (grade II) is common during pregnancy due to aug-
mented blood flow from increased intravascular volume
(a) Diastolic murmurs are abnormal
8. MAP decreases with pregnancy

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8 3 Cardiovascular

9. Cardiac output is highest in the immediate postpartum period

(a) Due to relief of vena caval compression, contractions of the uterus (auto-
transfusion of blood into systemic circulation), decreased lower extremity
venous pressure, and reduced maternal vascular capacitance
(b) Cardiac output returns to prepregnancy levels between 12 and 24 weeks
postpartum
10. Aortocaval compression occurs after 18–20 weeks’ gestation
(a) Important to left tilt to maintain cardiac pre-load
Renal
4

Chapter 2 Chestnut’s

1. Kidneys enlarge by as much as 30%

2. Collecting system dilates; hydronephrosis is very common
3. Creatinine clearance increases and BUN decreases due to an increase in GFR
and renal plasma flow during pregnancy
(a) Normal Cr level during pregnancy is 0.5–0.6 mg/dL
(b) Normal BUN level during pregnancy is 8–9 mg/dL
4. Urinary protein, albumin, and glucose excretion are increased during pregnancy

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Liver
5

1. Liver size, morphology, and blood flow do not change

2. Bilirubin, ALT, AST, and lactic dehydrogenase are upper limits of normal during
pregnancy
3. ALP increases 2–4× due to production from placenta
4. Increased risk of gallbladder disease during pregnancy due to the inhibitory
effects of progesterone on GI smooth muscles, leading to gallbladder hypomotil-
ity and subsequent biliary stasis

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Gastrointestinal
6

1. Pregnancy compromises the integrity of the lower esophageal sphincter (LES),

alters the anatomic relationship of the esophagus to the diaphragm and stomach,
and raises intragastric pressure
(a) Stomach is displaced upward toward the left side of the diaphragm
(b) Decreased LES tone is likely due to smooth muscle relaxation properties of
progesterone
(c) Changes return to pre-pregnancy levels by 48 h post-partum
2. High rate of GERD during pregnancy. Risk factors include gestational age,
GERD prior to pregnancy, and multiparity
(a) Maternal age has an inverse correlation
3. Gastric acid pH and volume is unchanged in pregnancy
4. Rate of gastric emptying is unchanged during pregnancy, but significantly pro-
longed during labor
(a) Esophageal peristalsis and intestinal transit are slowed

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Hematology
7

1. RBC volume increases (~30%), but plasma volume increases more (~55%),
leading to a dilutional anemia “physiologic anemia of pregnancy” (normal
hemoglobin is 11.6 g/dL, hematocrit 35.5%)
(a) Plasma volume increases due to increased renin activity due to higher estro-
gen levels, which enhances renal sodium and water absorption
2. Lower hematocrit decreases blood viscosity and lowers resistance to blood flow,
which is essential to maintain the patency of the uteroplacental vascular bed.
3. Total blood volume increases (~45%), which allows delivery of nutrients to the
fetus, protects the mother from hypotension, and decreases the risks associated
with hemorrhage at delivery
4. Total plasma protein and albumin concentrations both decrease in pregnancy
5. Globulin levels increase, so albumin/globulin ratio decreases
6. Plasma cholinesterase concentrations decrease in pregnancy
7. Benign leukocytosis is common in pregnancy (WBC can rise to ~13,000/mm3
during labor)
8. Changes in coagulation and fibrinolytic parameters at term:
(a) Increased fibrinogen (a.k.a. factor I), factors VII, VIII, IX, X, and XII
(b) Decreased factor XI and XIII
(c) Factors II and V are unchanged
(d) PT and PTT are shortened
(e) Platelet count and function are changed, but bleeding time is unchanged
9. Enhanced platelet turnover, clotting, and fibrinolysis
(a) Normal D-dimer in pregnancy can be as high as 500–1700 ng/mL compared
to <500 ng/ml in nonpregnant adults

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Placental O2 Exchange
8

1. The placenta is the fetal “lung” and has a fifth of the O2 transfer efficiency of the
adult lung
2. Placenta provides ~8 mL O2/min/kg fetal body weight
3. Delivery of oxygen to the fetus is predominantly flow limited (i.e., maternal
delivery of blood to the uterus controls fetal oxygen transfer)
4. O2 transfer across the placenta depends on the O2 partial pressure gradient
between maternal blood and fetal blood
(a) O2 dissolved in plasma diffuses across the villous membranes and O2 bound
to hemoglobin (Hgb) is released and diffuses across the placenta
5. Factors favoring fetal oxygen uptake:
(a) Oxygen affinity: Fetal oxyhemoglobin (Hb F) dissociation curve is shifted
left (high oxygen affinity; P50: 19 mmHg) and maternal (Hb A) dissociation
curve is shifted right (P50: 27 mmHg), allowing greater O2 transfer to fetus
(b) Oxygen-carrying capacity: The hemoglobin concentration of fetal blood is
high 15 g/dL compared with the mother’s 12 g/dL
6. Bohr effect also enhances O2 transfer to fetus; fetal-maternal transfer of CO2
makes maternal blood more acidotic and fetal blood more alkalotic causing a
shift in maternal and fetal oxyhemoglobin dissociation curves favoring unload-
ing of maternal oxygen to fetus

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Placental CO2 Exchange
9

1. Transferred as dissolved CO2, carbonic acid, bicarbonate ion (predominant

form), carbonate ion, and carbaminohemoglobin
2. CO2 is 20× more diffusible than O2 and readily crosses the placenta
3. Only dissolved CO2 crosses the placenta. Carbonic anhydrase in RBCs convert
bicarbonate ion to CO2.
4. CO2 transfer is augmented by the Haldane effect (higher affinity for CO2 in
maternal deoxyhemoglobin than fetal oxyhemoglobin)

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Placental Blood Flow
10

1. Major determinant of oxygen and nutrient delivery to the fetus

2. Preeclampsia and intrauterine growth restriction (IUGR) are associated with
chronic placental insufficiency
3. Blood supply to the uterus is mainly from the uterine arteries (branch of the
anterior division of the internal iliac artery) and to a less extent the ovarian
arteries (branches off abdominal aorta)
4. Venous drainage of the uterus occurs via the uterine veins to the internal iliac
veins and the ovarian veins to the inferior vena cava on the left and the renal
vein on the right
5. Uterine blood flow increases during pregnancy from 50 to 100 mL/min prior to
pregnancy to 700–900 mL/min at term
6. Uterine blood flow exceeds the minimum required to satisfy fetal O2 demand,
causing a margin of safety
(a) Uteroplacental blood flow can decrease by 50% for limited periods before
fetal hypoxia and metabolic acidosis occurs
7. Uteroplacental circulation is a maximally dilated, low-resistance system with-
out autoregulation (i.e., perfusion is pressure dependent)
8. Placental perfusion decreases during contractions
(a) Inversely related to strength of contraction and rise in intrauterine
pressure
9. Uterine blood flow = (uterine perfusion pressure)/(uterine vascular resistance)
(a) Uterine perfusion pressure = uterine arterial pressure – uterine venous
pressure

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22 10 Placental Blood Flow

10. Causes of decreased uterine blood flow:

(a) Decreased perfusion pressure
(i) Decreased uterine arterial pressure (supine position (aortocaval com-
pression); hemorrhage/hypovolemia; drug-induced hypotension;
hypotension during sympathetic blockade)
(ii) Increased uterine venous pressure (vena caval compression; uterine
contractions; drug-induced uterine hypertonus (oxytocin, local anes-
thetics); skeletal muscle hypertonus (seizures, Valsalva maneuver))
(b) Increased uterine vascular resistance
(i) Endogenous vasoconstrictors (catecholamines (stress) and vasopressin
(released during hypovolemia))
(ii) Exogenous vasoconstrictors (epinephrine; vasopressors
(phenylephrine>ephedrine); and high concentrations of local anesthetics
11. Pregnancy causes a decreased response to endogenous and exogenous vasocon-
strictors due to increased levels of progesterone, prostacyclins, and nitric oxide.
12. Although Angiotensin II levels are increased 2–3× during pregnancy, it has lit-
tle effect on uterine vascular resistance.
13. Infusion of angiotensin II has minimal effect on uteroplacental blood flow
while increasing systemic blood pressure.
14. In contrast to angiotensin II, alpha-adrenergic agonists affect uterine circulation
more than systemic circulation
15. Angiotensin II affects systemic vascular resistance with little effect on uterine
vascular resistance causing an increase in uterine blood flow
16. Neuraxial anesthesia may increase or decrease uterine blood flow
(a) Decreased due to induced hypotension
(b) Increased uterine blood flow due to pain relief, decreased sympathetic
activity, and decreased maternal hyperventilation
(i) Hyperventilation causes vasoconstriction and may decrease uterine
blood flow
17. Agents commonly used to induce general anesthesia have minimal or no direct
adverse effect on uteroplacental blood flow.
(a) Uteroplacental perfusion may be affected indirectly by changes in blood
pressure and sympathetic response to laryngoscopy and endotracheal
intubation
18. Magnesium decreases uterine vascular resistance and increases uterine blood
flow
Barrier Function
11

1. The placenta is an imperfect barrier (allows many substances to cross)

2. Cytochrome P-450 isoenzymes are located in the placenta, and some may be
inducible
(a) These enzymes may metabolize agents and decrease fetal exposure
3. Placenta may also bind substances to minimize fetal exposure to and accumula-
tion of substances

© Springer Nature Switzerland AG 2019 23

C. Wasson et al., Absolute Obstetric Anesthesia Review,
https://doi.org/10.1007/978-3-319-96980-0_11
 Part II
Maternal-Fetal Considerations
Pharmacology of Local Anesthetic Drugs
12

1. All local anesthetics (except cocaine) contain a desaturated carbon ring and a
tertiary amine connected by an alkyl chain.
(a) The alkyl chain (ester vs. amide linkage) determines whether it is an amino-
ester or amino-amide.
(b) All local anesthetic are weak bases because the tertiary amine portion acts
as a proton acceptor.
2. Amino-amides (e.g., lidocaine, bupivacaine, ropivacaine) undergo hepatic
microsomal metabolism
3. Amino-esters (e.g., chloroprocaine, cocaine, tetracaine) are hydrolyzed by
pseudocholinesterase
4. When pH > pKa, more drug is ionized
(a) Un-ionized form is lipid soluble and diffuses through the cell membrane
(b) Ionized form is more active in blocking the Na+ channel
5. Mechanism of action of local anesthetics: interference with sodium-ion
conductance
6. 2-Chloroprocaine
(a) Hydrolyzed rapidly by plasma pseudocholinesterase
(b) Half-life: 11–21 s in plasma; 1.5–6.4 min epidural
7. Lidocaine
(a) Half-life ~114 min epidural
(b) Metabolized to two active compounds (glycinexylidide (GX) and
monoehylglycinexylidide (MEGX))
(c) Predominately bound to alpha-1-acid glycoprotein (AAG) in plasma.
Pregnancy has decreased AAG, causing an increased free plasma fraction
of lidocaine in pregnant women
8. Bupivacaine
(a) Half-life: 12–13 h plasma
(b) Highly binds to both AAG and albumin (96%).

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28 12 Pharmacology of Local Anesthetic Drugs

9. Ropivacaine
(a) Shorter half-life than bupivacaine (~5 h vs 12)
(b) Highly binds to albumin and AAG (92%)
10. H2 blockers (especially cimetidine) bind to cytochrome P-450, reducing hepatic
blood flow and renal clearance of local anesthetics
11. Pre-eclampsia decreases clearance of local anesthetics due to reduced hepatic
blood flow, abnormal liver function, and decreased intravascular volume
12. Local anesthetic toxicity signs/symptoms (earliest to latest) (affects CNS before
the CV system): numbness of tongue/lightheadedness/tinnitus, muscular
twitching, unconsciousness, convulsions, coma, respiratory arrest, cardiovas-
cular depression
(a) Convulsions are due to selective blockade of CNS inhibitory neurons, caus-
ing CNS excitation
(b) CNS depression/coma occurs due to reversible blockade of both inhibitory
and excitatory pathways
13. Local anesthetic CNS toxicity risk (greatest to least): bupivacaine > ropivacaine
> levobupivacaine > lidocaine > 2-chloroprocaine. Tetracaine, etidocaine, and
mepivacaine are rarely used in obstetric anesthetic practice
14. Treatment of local anesthetic systemic toxicity (LAST):
(a) Mild cases: discontinue drug, administer supplemental O2, maintain nor-
mal ventilation
(b) If signs of CNS excitation, small dose of thiopental (50 mg) or diazepam
(2.5–5 mg) or midazolam (1–2 mg) may prevent convulsions
(c) If active convulsions, maintain oxygenation and ventilation to prevent
hypoxemia, hypercarbia, and acidosis (as these may worsen local anes-
thetic toxicity)
(i) Intubate if necessary
(ii) Terminate convulsions with small dose of thiopental or diazepam
(iii) Maintain maternal circulation with left uterine displacement and vaso-
pressor as needed
(d) Treat cardiac arrest according to ACLS guidelines
(e) 20% Lipid emulsion therapy may be necessary for refractory cardiac arrest
due to local anesthetic toxicity
(i) Bolus 1.5 ml/kg (lean body mass) IV over 1 min. Repeat bolus once or
twice for persistent cardiovascular collapse
(ii) Continue infusion at 0.25 mg/kg/min, and double to 0.5 ml/kg/min if
blood pressure remains low.
(iii) Continue infusion for at least 10 min after cardiovascular stability is
achieved
(f) Avoid vasopressin, calcium channel blockers, beta-adrenergic blockers,
and local anesthetics.
(i) Amiodarone is first line for arrhythmias
(g) Reduce epinephrine doses to <1 ug/kg.
(h) Arrangement for cardiopulmonary bypass (CPB) for persistent cardiovas-
cular instability. CPB may be necessary while waiting for local anesthetic
to diffuse from cardiac receptors.
12 Pharmacology of Local Anesthetic Drugs 29

15. Tissue Toxicity

(a) Rare. Due to direct neural trauma, infection, injection of toxic dose of local
anesthetic, or the injection of the wrong drug
(b) Cauda equina syndrome, sacral nerve root deficits, or transient neurologic
toxicity can occur after subarachnoid injection of lidocaine
(c) Neurotoxicity of local anesthetics is concentration dependent
(d) Transient neurologic symptoms (TNS) is dyesthesia or low back pain radi-
ating to the buttocks, thighs, or calves that occurs after spinal anesthesia.
(i) Associated with lidocaine, and lithotomy position
(ii) Pregnancy may reduce the incidence of TNS
16. Allergic reactions
(a) True allergy to local anesthetic is rare
(b) Anaphylactic and anaphylactoid reactions may be due to additives in local
anesthetic (e.g. methylparaben and meta-bisulfite)
(c) Allergy: urticarial, bronchospasm, facial edema, and/or cardiovascular
collapse
(d) Pharmacologic management:
(i) Inhibition of mediator synthesis and release
(ii) Reversal of the effects of the mediators on target organs
(iii) Prevention of recruitment of other inflammatory processes
(iv) Drugs used: catecholamines (epinephrine (mainstay), norepinephrine,
or isoproterenol), phosphodiesterase inhibitors, antihistamines (diphen-
hydramine), and corticosteroids (hydrocortisone or methylprednisone).
Pharmacology of Local Anesthetic
Adjuvants 13

1. Opioids
(a) Neuraxial opioids cause analgesia without loss of sensation or proprioception
(b) 3 classifications:
(i) Naturally occurring (e.g. morphine, codeine, papaverine)
(ii) Semisynthetic (e.g. heroin, hydromorphone, oxymorphone, hydroco-
done, oxycodone, buprenorphine, nalbuphine)
(iii) Synthetic (e.g. meperidine, fentanyl, sufentanil, alfentanil, and
remifentanil)
1. Meperidine is unique in that it possesses weak local anesthetic
properties
(c) Produce analgesia by binding to G protein-coupled opioid receptors, which
inhibits both adenylate cyclase and voltage-gated calcium channels, causing
inhibition of release of excitatory afferent neurotransmitters (e.g. glutamate,
substance P, and other tachykinins)
(d) Parenteral opioids affect both spinal and supraspinal
(e) Neuraxial opioids bind presynaptic and postsynaptic receptor sites located at
substantia gelatinoa (rexed lamina II) in dorsal horn of spinal cord to block
transmission of pain-related information
(f) Four opioid receptors
(i) Mu – analgesia, miosis, bradycardia, sedation, respiratory depression,
decreased GI transit
(ii) Kappa – analgesia, sedation, respiratory depression, diuresis,
psychotomimesis
(iii) Delta – analgesia
(iv) Nociception/orphanin receptor – pain processing in spinal and supra-
spinal areas
(g) Onset and duration of analgesia and side effects of neuraxial opioid admin-
istration depend on the type of opioid receptor that is activated, the dose,
lipid solubility, and rate of movement and clearance of the opioid in the
cerebral spinal fluid (CSF)

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C. Wasson et al., Absolute Obstetric Anesthesia Review,
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Another random document with
no related content on Scribd:
Sayre places so much confidence in the power of this elastic tension to
overcome contractions that he rarely resorts to tenotomy in the treatment
of paralytic talipes. Hueter, however,180 considers tenotomy much the
speediest, and therefore the most desirable, way of removing
contractions.181
180 Loc. cit.

181 Loc. cit.

Seeligmüller quotes with approval Böttger's method for the treatment of

deformities, where the weight of the body is utilized to stretch the
retracted tendons. Thus, for talipes equino-varus an over-reduction is
effected under ether, and the foot forced into a position of moderate
calcaneo-valgus. In this position it is retained by the immediate
application of a plaster or silica bandage. After this has hardened the
child should be encouraged to walk in the mould, with the addition of felt
shoes having a slanting sole that is thickened like a wedge at the inner
side of the foot and strapped on like a skate. Then, during the act of
walking the body tends to constantly force down the heel and thus stretch
the retracted tendo Achillis, while the bandage and felt sole (acting like a
splint) prevent the inner side of the foot from slipping up.

For talipes valgus the method is analogous, but the foot is forced into an
equino-varus position, so that the tendo Achillis is artificially shortened,
and ultimately becomes a rigid band, capable, in spite of the sural
paralysis, of sustaining the heel.

A cause of relapse in talipes not unfrequently overlooked is the presence

of even slight contractions of the hip- and knee-joints. These by
shortening the limb tend to the production of equinus, since the foot
points itself in order to reach the ground. These contractions, whose
rigidity is far inferior to that induced by chronic arthritis, may be overcome
by forced extension under ether or gradually by manipulations, or by the
weight-and-pulley apparatus, applied in the recumbent position, as in
morbus coxarius. The obvious objection to the latter method is the
confinement in bed which it necessitates in a child enjoying at the time
perhaps robust general health.
The contraction once overcome, the limb must be placed in apparatus
which shall both maintain suitable extension and assist in supporting the
trunk during station and locomotion. The latter purpose is effected, as in
apparatus for chronic joint diseases, by transferring the weight of the
body to steel splints running up each side of the limb, the outer one as far
as a girdle which encircles the hips; the inner to a band surrounding the
upper part of the thigh. Thus is extended the support which in paralysis
limited to the leg-muscles is given by the steel splints inserted in the side
of the club-foot shoes.

In the simplest form of apparatus locomotion is expected to be

accomplished by the action of muscles inserted above the seat of the
paralysis. Thus, when the muscles passing over the ankle-joint are
paralyzed, the foot is moved as a dead weight by means of the
quadriceps extensor, popliteus, and hamstring muscles inserted at the
upper extremity of the leg. If the quadriceps cruris is paralyzed, the
rotators of the thigh, ilio-psoas, sartorius, and adductor muscles, passing
from the pelvis to the thigh, and which are so frequently intact in atrophic
paralysis, are enabled to move the limb if the weight of the body is borne
by steel splints, if these be light and properly jointed at the hip, knees,
and ankle.182
182 Or the joint of the knee may be kept locked while the patient walks, when extension of
the limb is mainly required, during both the active and passive movements of locomotion, the
necessary flexion being supplied at the hip and ankle. By means of a key the knee-joint can
be flexed during the sitting positions.

But an important aid to locomotion may be obtained from the artificial

muscles, whose elastic tension is of such value in overcoming
contractions. The quadriceps extensor, the most frequently paralyzed,
may be supplemented by an India-rubber band and chain passing down
the front of the thigh from a point on the pelvic girdle corresponding to the
anterior iliac spine to a point on a leg-band, imitating the tibial insertion of
the quadriceps tendon. Analogous bands stretched on the posterior
aspect of the thigh simulate the hamstring muscles. When the external
rotators are paralyzed, the artificial muscle must stretch from the pelvic
girdle to a band encircling the upper part of the thigh.

The action of these muscles, apart from their elastic tension of repose, is
thus explained by Duchenne: When any effort is made to move a
paralyzed limb, the intact antagonists to the paralyzed muscles contract;
thus, the flexors of the leg. But this contraction, being constantly opposed
by the elastic tension of the artificial quadriceps, is restrained and
gradual, instead of being brusque, jerking, and excessive, as it otherwise
would be. This is the first result obtained. In the second place, contraction
of the antagonist having ceased, the artificial muscle which has been
stretched returns upon itself in virtue of its elasticity, and restores the limb
to the position of normal equilibrium.

For the act of walking, however, the artificial quadriceps would require to
be made tense enough to resist flexion, and thus keep the limb in
extension. An artificial anterior tibial muscle, however, would require to
yield to the intact gastrocnemius while the heel was being raised from the
floor; then its elastic force should be sufficient to retract the point of the
foot in dorsal flexion during the pendulum movement which passively
swings the leg forward. The tension of the artificial muscle should
therefore be so adjusted that it can only be overcome by the active
contraction of the gastrocnemius, and at the moment of greatest tension,
immediately after stretching, it should be able to quite overcome the
gastrocnemius, then relatively183 relaxed.
183 We say relatively, believing that the simultaneous contraction of antagonist muscles has
been well established as a constant normal phenomenon.

The anterior tibial, gastrocnemius, and many other of the artificial muscles
devised by Duchenne are still in use in the modified form given to them by
Barwell. On the other hand, the action of the long peroneus in pronating
the foot, and which Duchenne imitated by an elaborate artificial tendon
following the exact course of the natural one, is to-day generally
supplemented by the jointed shoe and laced bandage.

In paralysis of all the muscles surrounding a joint, when the limb is placid
and no retractions by adapted atrophy have taken place, the artificial
muscles can only serve to oppose the malpositions which are threatened
from mechanical influences.

In the upper extremities prothetic apparatus has been principally used for
progressive muscular atrophy. Paralysis of the wrist extensors is perhaps
the only case in which the artificial muscle is required in anterior
poliomyelitis. A string may be necessary to support the arm in paralysis of
the deltoid, to avert luxation of the humerus.

Duchenne's ingenuity did not shrink from the difficult task of

supplementing the muscles of the trunk. This he did by inserting the
elastic spirals in corsets in a direction following that of the muscles
paralyzed. Thus, a unilateral paralysis of the sacro-lumbalis may be met
by a spiral splint running up one side of the spine; below, to the lateral
posterior portion of a pelvic girdle. In bilateral paralysis two springs are
used to antagonize the action of the abdominal muscles.

In Barwell's apparatus for the trunk184 India-rubber bands are again

substituted for spiral springs. No attempt is made to imitate the direction
of muscles, but the force is applied in any direction required to antagonize
the pressure producing the deformity.185
184 Especially designed for habitual scoliosis, but applicable also to the paralytic deformity.

185 Volkmann (loc. cit., p. 778) thinks that the force of Barwell's India-rubber straps, whether
for scoliosis or club-foot apparatus, is inadequate, and much inferior to metallic springs.

It is always important to remember the rarity of scoliosis caused by spinal

paralysis of the trunk-muscles, and the much greater frequency with
which this deformity occurs as a consequence of the paralytic shortening
of a leg. A high shoe, equalizing the length of the lower extremities, is
then the simple and efficient remedy.

In cases of long standing, even when the scoliosis is due to this cause,
certain muscles on the concave side of the curve may become so
retracted and rigid as to require tenotomy. Before this operation it is
necessary to put the rigid muscles on the stretch as much as possible;
and this may be done, if necessary, by means of Sayre's hanging
apparatus. After this operation the spine may be straightened out with
ease—an important distinction from advanced habitual scoliosis, where
the alteration in the shape of the vertebræ defeats all attempts at
rectification. The position may be maintained by elastic straps or corsets
and by removing the condition which has led to the deformity.

Seeligmüller criticises too unfavorably the entire system of elastic tension

in the prophylaxis and treatment of paralytic deformities. He quotes
Duchenne's admission, that in certain cases traction upon rigidly-retracted
tissues becomes insupportably painful, and must be abandoned. It is in
these cases that tenotomy becomes an indispensable preliminary to the
use of apparatus. Sayre insists that the necessity for tenotomy is
indicated when pressure on the rigid muscle is followed by instantaneous
spasmodic contraction in the affected or neighboring muscles. He
declares that such contractions indicate reflex irritations, show that the
muscle has undergone structural change, and that any attempt to stretch
or lengthen it would be followed by an excess of irritation and pain.

This explanation can hardly be accepted, since muscles, whether

imperfectly or not at all paralyzed, which from position and adapted
atrophy have become retracted, have necessarily undergone structural
changes. The greater these changes, the greater the diminution of reflex
excitability; and in any muscle completely paralyzed and degenerated this
is entirely lost. If, however, the afferent nerves retain enough vitality, if the
muscle be slightly paralyzed or altogether intact, then irritation of its
tendon by stretching may serve to excite contractions in the belly of the
muscle. The possibility of such spinal reflexes is demonstrated by the
now familiar phenomenon of the tendon reflex in various spinal
diseases.186 The contractions must be painful from the impediments
offered to the progress of the contracting nerve, and from the
exaggeratedly vicious position into which they tend to force the limb.
Under these circumstances prothetic apparatus must be deferred until
section of the tendons has been made.
186 “Passive muscular tension excites tonic contraction in a muscle, and this action may, in
abnormal conditions, be excessive, as in the myelitic contractions (so-called tendon
reflexes).... The afferent nerves commence in the fibrous tissues of the muscle, and seem to
be especially stimulated by extension” (Gowers, On Epilepsy, 1881, p. 97).

DISEASE OF ONE LATERAL HALF OF THE SPINAL

CORD.
 BY H. D. SCHMIDT, M.D.

SYNONYMS.—Unilateral lesion of the spinal cord; Spinal hemiplegia

and hemiparaplegia; Unilateral spinal paralysis.

INTRODUCTION.—This disease remained unnoticed until twenty years

ago, when Brown-Séquard, observing that certain lesions of the
spinal cord were accompanied by symptoms resembling those which
he witnessed in animals after section of one lateral half of the cord,
recognized it as a special affection. Although some of the
accompanying phenomena of such a section had likewise been
observed by Stilling, Budge, Eigenbrodt, Tuerk, Schiff, Von Bezold,
and Van Kempen,1 nevertheless this whole group of symptoms, as
belonging to the same disease, was first clearly recognized and
anatomically demonstrated by Brown-Séquard.2 According to this
physiologist, a section or a destruction of a small portion of a lateral
half of the spinal cord in its cervical region gives rise to the following
phenomena: namely, on the injured side is observed a paralysis of
voluntary motion, of the muscular sense, and of the blood-vessels;
the latter, manifesting itself by a greater supply of blood and a higher
temperature of the parts, may continue to exist for some years.
There is, furthermore, an increased sensibility of the trunk and
extremity to touch, prick, heat, cold, electricity, etc., owing to vaso-
motor paralysis, though in some cases a slight anæsthesia may exist
in a limited zone above the hyperæsthetic part, and also in certain
parts of the arm, breast, and neck. Besides these symptoms, vaso-
motor paralysis of the corresponding side of the face and of the eye,
manifested by an elevated temperature and sensibility, partial
closure of the eyelid, contracted pupil, slight contraction of some of
the muscles of the face, etc., may also be present. On the opposite
side of the injury an anæsthesia of all kinds of sensation, excepting
the muscular sense, is observed in both extremities; there is also an
absence of motor paralysis. The anæsthesia on this side is owing to
the decussation of the sensory nerves in the spinal cord.
1 Eckhard, “Physiologie des Nervensystems,” in Handbuch der Physiologie, edited by
L. Hermann, 2d part of vol. ii. p. 165.

2 “On Spinal Hemiplegia,” Lancet, Nov. 7, 21, and Dec. 12, 26, 1868, reported in
Virchow and Hirsch's Jahresbericht for the year 1868, vol. ii. p. 37.

If the hemisection of the cord is made in the dorsal region, the

functional disturbances are limited to that part of the body below the
point of division, and a hemiparaplegia, or paralysis of the
corresponding lower extremity, will be the result.

From these facts it will be readily understood that a lesion occurring

in any portion of one lateral half of the spinal cord of man must be
followed by some or all of the above-mentioned symptoms, and that
the phenomena produced by physiological experiments on animals
constitute, in reality, the pathological basis of unilateral spinal
paralysis in man. They will be more clearly understood by calling to
mind the course of the musculo-motor, vaso-motor, and sensitive
tracts in the spinal cord. Thus, the musculo-motor tracts, after having
descended to the crura cerebri, cross one another in the pyramids of
the medulla oblongata and adjoining upper portion of the spinal cord,
forming the so-called decussation of the pyramids; they then
descend through the spinal cord to supply the muscles of the same
side of the body.3 A section of one lateral half of the cord therefore
causes motor paralysis on the same side. The vaso-motor tracts
remain uncrossed, and pass, each, through one lateral half of the
cord to supply the vessels on the same side; some regions of the
body are stated to make an exception to this rule. According to
Brown-Séquard, the sensitive tracts conducting the different kinds of
sensation, with the exception of the muscular sense, on the contrary,
cross over to the opposite half of the spinal cord soon after their
entrance into it, and thence pursue their further course to the brain.
A section of one lateral half of the cord, therefore, will be followed by
a loss of sensation of touch, pain, heat, tickling, etc. on the other
side of the body.
 3 Though, in the majority of cases, a complete decussation of the motor tracts
probably takes place in the pyramids, the researches of Flechsig have shown (Die
Leitungsbahnen im Gehirn und Rückenmark des Menschen, p. 273) that there are a
number of others in which the decussation is not complete, but where a part of these
tracts passes to the spinal marrow uncrossed on the inner surface of the anterior
white columns.

The symptoms above mentioned must of course vary according to

the extent, the intensity, and the particular nature of the lesion, as
well as the height at which it is located in the spinal cord.

DEFINITION.—The chief characters of unilateral spinal disease are

motor paralysis, hemiplegia, or hemiparaplegia, paralysis of the
muscular sense and of the blood-vessels on the side of the lesion,
and paralysis of sensation with preservation of the muscular sense
on the other side of the body. These symptoms may vary, and be
accompanied by other phenomena according to the particular seat,
extent, and depth of the lesion.

SYMPTOMS.—According to the nature of the lesion, the symptoms of

unilateral disease of the spinal cord may be developed suddenly, as,
for instance, when caused by traumatic injuries; or in a gradual and
slow manner, when they may be preceded by premonitory
symptoms, such as vertigo, pain on the side of the lesion, etc. The
most prominent clinical phenomena, as before mentioned, are motor
paralysis on the side of the lesion, and anæsthesia on the opposite
side of the body. The motor paralysis on the side of the lesion may,
according to the seat of the latter, manifest itself in either the form of
a hemiplegia or hemiparaplegia, and even extend in a light form to
the opposite side of the body. In typical cases, however, in which the
injury or disease is strictly confined to one lateral half of the cord, the
motor power on the other side of the body remains entirely
undisturbed. At the same time, the muscular sense on the injured
side is paralyzed or considerably diminished, and in some cases
(Fieber, Lanzoni, Allessandrini) the electro-muscular excitability also
has been found lowered, while in others it has remained normal.
There is furthermore observed, on the side of the lesion, a vaso-
motor paralysis, manifesting itself by a greater supply of blood to,
and a higher temperature of, the paralyzed trunk and limbs, giving
rise to an increase of sensibility (hyperæsthesia) of touch, prick,
heat, cold, electricity, etc. in these parts. If the seat of the lesion is
sufficiently high up in the cord, this paralysis extends, moreover, to
the corresponding side of the face and eye, where it also causes an
elevation of temperature, increase of sensibility, partial closure of the
eyelid, contracted pupil, slight contraction of some of the muscles of
the face, etc. In a number of cases at the boundary of the
hyperæsthetic region a narrow anæsthetic zone is observed to exist
on the breast, neck, or arm. This anæsthesia is owing to the division,
at the level of the section, of some nerves of sensation on their way
to the other half of the spinal cord. An increase of the reflex irritability
of the tendons has in some cases (Erb, Schulz, Revillons) been
observed, while in one case (Glaeser) the reflex was found to be
absent. Swelling and œdema of the paralyzed limbs have also been
met with (Glaeser), and in one case (Allessandrini) even swelling
and pain in all the joints of the injured side were observed before
death, while masses of coagulated blood in these joints, particularly
in the knee, were revealed by the autopsy. The inflammatory
affection of the knee-joint of the paralyzed leg has, moreover, been
observed by Viguès, Joffroy, and Solomon.4 Frequently, atrophy of
the paralyzed muscles takes place, especially in chronic cases. In
one case (Fieber) even atrophy of the upper extremity of the
uninjured side of the body was observed.
4 Erb, “Diseases of the Spinal Cord, etc.,” Cyclopædia of the Practice of Medicine,
edited by H. v. Ziemssen, Amer. ed.

The most prominent symptoms observed on the side of the body

opposite to the seat of the lesion are anæsthesia of every kind of
sensation, preservation of the muscular sense, and absence of
motor paralysis. Reflex action and electro-muscular contractility
generally remain normal, though in one case (Fieber) the latter was
found increased. Although the anæsthesia of the skin generally
comprises every kind of sensation, three cases were observed
(Fieber) in which the sensation of heat remained unimpaired, while
the electro-cutaneous sensibility appeared to be lost. As a general
rule, there is no vaso-motor paralysis on the uninjured side, though
in some cases (Erb, Allessandrini) an elevation of temperature has
been observed.

Besides the above symptoms, some others, less characteristic in

nature, are now and then observed in individual cases. They are
painful sensations on one or the other side, or even simultaneously
on both sides of the body, and also a feeling of constriction at the
level of the lesion (Erb). Disturbances of the functions of the bowels
or bladder are also met with, though in other cases they are absent.

PATHOLOGICAL ANATOMY.—The pathological changes taking place in

the spinal cord of patients affected with unilateral spinal paralysis
must vary in different cases according to the particular nature of the
lesion giving rise to the characteristic symptoms. In those cases
reported to have terminated by a gradual disappearance of the
symptoms with or without therapeutic interference it is very probable
that the exciting cause was a hyperæmia or a myelitis of a small
portion of one lateral half of the spinal cord, sufficiently high in
degree to impair the conducting power of the nerve-fibres passing
through it. In some cases the myelitis may lead to a degeneration of
the nerve-fibres, or even extend to the other half of the cord, and by
calling forth additional symptoms render the case more complicated.
In syphilitic cases the disease depends upon syphilitic deposits or
neoplasms in the affected portion of the spinal cord; these cases,
however, generally yield to treatment. In the same manner may
circumscribed sclerosis give rise to the disease. Another cause may
be found in the compression of the cord caused by meningeal
tumors or by the fractured portions of some of the vertebræ. Chronic
disease of the vertebral bones themselves (Pott's disease) may also,
by encroaching upon the spinal cord, become an exciting cause.

The most typical cases, however, are those depending upon

traumatic injuries, by which one lateral half of the spinal cord is
forcibly divided. These lesions resemble in nature the division of the
cord in the physiological experiments on animals, and are most
frequently caused by a stab from a knife penetrating to the cord
through the intervertebral spaces.

DIAGNOSIS.—In those cases in which the symptoms of unilateral

spinal paralysis appear soon after an external injury to the spine, it
becomes obvious that the latter is the exciting cause. In cases of a
more chronic character, in which the symptoms appear gradually, the
nature of the exciting cause can only be correctly determined by the
observation of certain collateral symptoms characteristic of such
causes as might give rise to the symptoms of the disease in
question. As regards the diagnostic symptoms of unilateral spinal
paralysis themselves, they are sufficiently characteristic to be easily
distinguished from those of other forms of hemiplegia or
hemiparaplegia. Thus, cerebral hemiplegia may be distinguished
from the disease under discussion by the sensory disturbances
being either absent or on the same side as the paralysis;
furthermore, by the one-sided paralysis of the face and of the tongue
and by the affection of various cranial nerves. The hemiplegic form
of spasmodic spinal paralysis is distinguished by the absence of
sensory disturbance, etc. Lastly, hemiplegia depending upon lesion
of one side of the cauda equina is distinguished from unilateral
spinal disease by the paralysis and anæsthesia being confined to the
same side, and by generally affecting certain nervous districts of the
lower extremities.

PROGNOSIS.—In unilateral spinal lesions the prognosis depends

obviously on the particular nature and intensity of the exciting cause.
On the whole, there are quite a number of cases reported, even of
traumatic origin, which have terminated favorably.

TREATMENT.—The treatment of unilateral spinal paralysis depends,

like the prognosis, upon the nature of the exciting cause. The
principles upon which it is to be pursued of course are the same as
those upon which the treatment of the various lesions causing the
disease—such as hyperæmia, myelitis, sclerosis, wound of the
spinal cord, etc.—is based.
 PROGRESSIVE LABIO-GLOSSO-LARYNGEAL
PARALYSIS.

BY H. D. SCHMIDT, M.D.

SYNONYMS.—Chronic progressive bulbar paralysis; Progressive

muscular paralysis of the tongue, soft palate, and lips.

HISTORY.—Although the particular group of symptoms constituting

this disease must have been met with and known to the older
medical observers, they were nevertheless first recognized as a
special variety of paralysis in 1841 by Trousseau,1 who named the
affection labio-glosso-laryngeal paralysis. But as the memorandum
prepared by this distinguished physician at the time when, in
consultation with a medical colleague, he had observed the
particular symptoms of this affection, unfortunately remained
unpublished, twenty years more elapsed before the first accurate
and detailed description of the symptoms and progressive nature of
this disease under the name of progressive muscular paralysis of the
tongue, soft palate, and lips was rendered by Duchenne. The
writings of this author directed at once the attention of other medical
men to this disease, and since that time a large number of cases
have been reported and discussed,2 while the microscopical
examination accompanying the autopsies of many of them finally
revealed that the seat of the lesion giving rise to the phenomena of
this disease was to be sought in the nervous nuclei of the medulla
oblongata. Hence at the present time the pathology of this disease is
thoroughly understood.
1 Clinique médicale de l'Hôtel Dieu de Paris, vol. ii. p. 334.

2 A very considerable number of cases of this disease, and discussions thereon, will
be found reported in Virchow and Hirsch's Jahresbericht über die Leistungen und
Fortschritte der Gesammten Medizin, for the years 1866-80, vol. ii., section
“Krankheiten des Nervensystems.”

DEFINITION.—That form of labio-glosso-laryngeal paralysis to be

treated in the following pages is characterized by a progressive
paralysis and atrophy of the muscles of the tongue, lips, palate,
pharynx, and larynx, interfering in a greater or lesser degree with the
articulation of words and sounds and with the functions of
mastication and deglutition—affecting, furthermore, in the later
stages of the disease, the voice and the function of respiration. The
paralysis is caused by a progressive degeneration and atrophy of the
ganglion-cells of those nerve-centres in the medulla oblongata from
which the muscles of the above-named organs receive their supply
of nervous energy, though in most cases the pathological process
extends to, or even beyond, the roots of those nerves which
originate in these centres and terminate in the respective muscles. In
many cases the pathological process extends to the spinal marrow,
and there causes paralysis and atrophy of the muscles of the trunk,
and, generally, of the upper extremities. Almost in every case the
disease, as its name indicates, slowly progresses until it terminates
in death.

There are, however, a number of cases observed which, though

exhibiting the same or similar symptoms, do not, in reality, depend
upon a progressive degeneration and atrophy of the centres and
nerve-roots of the medulla, but, on the contrary, owe their symptoms
to other causes; as, for instance, to tumors, hemorrhages, syphilitic
neoplasms, etc., which, either by pressing upon the medulla from
without, or, if situated within, by deranging in various manners the
individual nervous elements of that part, may give rise to some or
even all of the symptoms of true labio-glosso-laryngeal paralysis.
These symptoms, however, according to the character of the lesion,
may, after remaining stationary for some time, retrograde, and even
disappear, as has been observed in syphilitic cases; or they may
progress, and finally end in death. In order to distinguish these cases
from the chronic or progressive bulbar paralysis some authors have
attached the term retrogressive to this form of the disease.

SYMPTOMS.—As the degeneration of the nerve-centres in the medulla

oblongata, upon which the disease depends, does not proceed in a
regular fixed order, the order in which the clinical symptoms
successively appear also varies in different cases. In the majority of
cases, however, the symptoms appear gradually, manifesting
themselves generally in the form of a greater or lesser impediment in
the articulation of certain sounds or letters depending upon the
movements of the tongue, such as e, i, k, l, s, and c, while at the
same time a difficulty of mastication and deglutition may be
experienced by the patient, due to the progressive development of
the paralysis, which deprives the tongue of its lateral and forward
movements. To this cause also, at this period, the apparently
increased secretion of saliva, running from the corners of the mouth,
must be attributed. With intelligent patients these symptoms are
rendered less prominent by the special effort which they make to
pronounce slowly for the purpose of hiding the deficiency in their
speech. But as the disease advances the difficulty of articulation
increases on account of the paralysis extending to the orbicularis
oris, thus affecting the mobility of the lips and interfering with the
pronunciation of the labial sounds p, b, f, m, and w. With the loss of
power of articulation the patient's speech becomes gradually
reduced to monosyllables, or even, finally, to incomprehensible and
inarticulated grunts, by which he expresses his wants to his friends.
In consequence of the paralysis of the lips the patient becomes
unable to whistle or blow or to perform any movement depending
upon these organs, while at the same time, through the disturbance
created in the co-ordination of the facial muscles by the paralysis of
the orbicularis oris, the mouth becomes transversely elongated and
drawn downward by the action of the remaining unparalyzed
muscles upon its angles. With the mouth partially open and the lower
lip hanging down, the face of the patient has a peculiar sad and
painful expression, while the voice assumes a nasal sound on
account of the paralysis of the palate.

After a while the difficulty of deglutition, caused by the inability of the

tongue to properly assist in the formation of the bolus of food and its
propulsion into the pharynx, increases on account of the paralysis
extending to the muscles of the pharynx. The failure of these
muscles in the performance of their special function of grasping the
food and carrying it to the œsophagus obliges the patient to push it
down the pharynx with his fingers. In some cases the difficulty of
swallowing rests with solids, in others with fluids. The defective
deglutition furthermore gives rise to spells of coughing and
suffocation by portions of food getting between the epiglottis and
larynx, while the paralyzed muscles of the palate allow the fluids to
pass through the nose and enter the posterior nares.

As the case slowly proceeds the symptoms grow worse. The

paralysis of the orbicularis oris reaches a point when this muscle is
no more able to close the oral cavity; the mouth of the patient
therefore remains open. The tongue, having now entirely lost its
lateral, forward, or upward movements, rests motionless upon the
floor of the mouth, evincing no other signs of life but occasional slight
muscular twitchings. In some cases a diminution of the sense of
taste, and also of that of touch in the tongue, pharynx, and larynx,
has been observed. Atrophy of the tongue and lips now sets in, and
the function of speech is almost entirely lost. The only letter which
the patient is still able to pronounce is a (broad); all other sounds are
indistinct and can hardly be understood. The paralysis of the tongue
and other muscles of deglutition gives rise, furthermore, to an
accumulation of the now excessively secreted saliva, which, being
retained in the oral cavity, assumes the form of a viscid mucous
liquid dripping from the mouth, extending, in the form of strings or
ribbons, between the surfaces of the lips. Finally, when, through the
progressive paralysis of the orbicularis oris, the patient can no more
close the lips, the flow of saliva from the mouth becomes continuous;
he is then seen engaged in the constant use of his handkerchief for
removing the secretion.

In the latter stages of the disease the pathological process extends

to the centres of respiration, paralyzing not only the muscles of
respiration, but diminishing at the same time the contractile power of
the lungs. A great difficulty of breathing—consisting not only in the
want of depth of the inspirations, but, moreover, in a feebleness of
expiration (manifested by weak, powerless coughing)—then ensues,
and the patient is no further able to blow his nose or clear his
bronchial tubes from the accumulating mucus. The paralysis of the
muscles of the larynx, also occurring at this stage, not only increases
the difficulties of deglutition, but most seriously affects the voice of
the patient by decreasing the innervation of the vocal cords; the
voice then becomes hoarse and weak, to be finally entirely lost.

The decrease in the innervation of the heart—which, lastly, also

occurs—gives rise to irregularities in the action of this organ,
followed by irregularity of the pulse, attacks of syncope, feelings of
extreme weakness, and fears of death; whilst simultaneously the
insufficient performance of the respiratory function renders the
breathing of the patient weaker and weaker. Feelings of great
oppression in the chest then arise, and the patient may die during
one of the now frequent attacks of dyspnœa and suffocation.

No fever or pain is observed during the course of this disease;

sensation remains unaffected and the mind is perfectly clear. It is
owing to these circumstances that frequently the patient walks about
and attends to the duties of life, until shortly before death he
becomes confined to bed by the great weakness caused by the want
of nutrition. The appetite also remains good, but, unfortunately, in
consequence of the difficulties attending the act of deglutition, the
patient cannot satisfy the demands of his stomach. In the latter
stages of the disease, therefore, when feeding can only be
accomplished by the aid of the stomach-tube, every attempt to
relieve the terrible gnawings and pains of hunger ends in a failure.
With starvation staring in his face, the unhappy victim of the disease
finally sinks into a state of extreme inanition, which, if life is not
suddenly extinguished by an attack of suffocation, slowly leads to
final dissolution.

The symptoms above described are those generally observed in

uncomplicated cases of labio-glosso-laryngeal paralysis. There are,
however, a number of cases reported in which the degenerative
process has passed from the medulla oblongata to the spinal cord,
and given rise to paralysis of the muscles of the neck, especially of
the trapezius, and to those of the shoulders, and even to those of the
upper extremities. Atrophy of the interosseus muscles of the hand,
with those of the ball of the thumb, is not unfrequently observed. In
other cases the disease has been found associated with progressive
muscular atrophy, and in others, again, with paralysis of the lower
extremities, accompanied by contractures and depending upon
amyotrophic lateral sclerosis.

Labio-glosso-laryngeal paralysis is, as before mentioned, slow but

progressive in its course, the duration of which is from one to three,
or even five, years. It always terminates in death within the limits of
this time, either from suffocation, inanition, paralysis of the heart, or
some other intercurrent disease.

PATHOLOGICAL ANATOMY.—The macroscopical and microscopical

examinations made during the last fifteen years of the cerebro-spinal
axis in quite a number of cases of progressive labio-glosso-laryngeal
paralysis show that this disease depends upon a degeneration of the
nervous elements of the nuclei or nerve-centres in the medulla
oblongata, involving also the roots of the nerves arising from the
latter, and supplying with nervous energy the muscles of the different
organs paralyzed in this disease. The exact nature of this
degeneration—that is, whether it represents the sequel of a
previously existing myelitis or originates in a so-called
parenchymatous inflammation—appears to be as yet not definitely
settled, though a number of pathologists entertain the view that it is
preceded by a chronic myelitis. This view appears to be corroborated
by the fact that frequently portions of the medulla oblongata and
cervical portion of the spinal cord are found in a state of sclerosis.
The uncertainty in the determination of the exact nature of the
pathological process here concerned chiefly depends upon the
diverse conditions in which the blood-vessels of the medulla are
found. For while, in some cases, perhaps the majority, they have
been found empty and in a normal condition, they have in others
been met with congested with blood—a condition pointing to a
chronic inflammatory process. In other cases, again, their walls have
been found thickened or undergoing fatty degeneration.

At any rate, whether inflammatory or not, the now numerous

microscopical examinations have revealed that the main features of
the process are a degeneration and atrophy, not only of the
ganglion-cells of the respective nervous nuclei with their plexuses,
but also of the fibres of the roots of the peripheral nerves arising
from these centres; frequently the degeneration extends to some
distance upon the nerves themselves. The microscopical changes in
the ganglion-cells consist of an increase of yellow pigment, a gradual
disappearance of their nuclei, terminating in an atrophy of the
ganglionic bodies themselves, the pathological process leaving,
finally, nothing but irregularly-shaped masses of pigment in the
places of these bodies. The degeneration of the nerve-fibres
appears to consist, as elsewhere, in a swelling of the axis-cylinder,
accompanied by atrophy of the medullary sheath—a condition which
finally leads to the complete destruction of these elements of the
nerve-fibres, so that, at last, the whole nerve is only represented by
the connective tissue of its neurolemma. Besides these changes,
certain pathological products, such as conglomerations of fatty
granules or globules, amylaceous bodies, etc., are also found in the
degenerated nerve-centres and nerve-fibres.

Although in different cases the route which the degenerative process

pursues is not the same, a certain general order, in which the nerves
and nerve-centres are successively affected, and corresponding to
the clinical symptoms, appears, nevertheless, to exist. It is thus that
the nucleus of the hypoglossus has been observed to degenerate
before the other nerve-centres. The nuclei of the spinal accessory
and pneumogastric nerves, and also that part of the facial nucleus
from which the inferior division of the facial nerve arises, appear to
be affected next. The glosso-pharyngeal nucleus appears not to be
affected in all cases, and still less frequently the nuclei and roots of
the abducens, auditory, and trifacial nerves. The fibres forming the
anterior pyramids have frequently been found degenerated
throughout the medulla oblongata and pons; sclerosis also has been
met with in this locality. In many cases, as has been remarked
before, the pathological process descends into the spinal cord. Here,
as in the medulla oblongata, the degeneration is principally confined
to the motor centres located in the anterior horns, while the posterior
horns, together with the lateral and posterior white columns, remain
free from disease. The degree of degeneration taking place in the
fibres of the respectively paralyzed muscles also corresponds to that
of the elements of the nerve-centres from which they are supplied.
The microscopical changes observed in the muscular fibres consist
in a decrease of their diameter, accompanied by an increase in the
number of their nuclei, as well as in the quantity of the connective
tissue surrounding the primary bundles; some authors have
observed amyloid degeneration of the muscular fibres.

ETIOLOGY.—The causes which give rise to the pathological process

above described are but little known. Nevertheless, in a number of
cases the disease has been traced back to taking cold, to physical
as well as cerebral over-exertion, mental excitement, sorrow caused
by misfortunes, poverty of nutrition, excessive use of tobacco, etc. In
some cases the disease commences in the spinal cord in the form of
progressive muscular atrophy or amyotrophic lateral sclerosis, and
gradually extends to the medulla oblongata; in many other cases no
particular cause can be found. The disease is rarely if ever met with
in persons under twenty years of age, but is confined to adult life and
old age. It occurs in both high and low walks of life, attacking more
frequently men than women.

DIAGNOSIS.—The symptoms of progressive labio-glosso-laryngeal

paralysis are so characteristic in themselves as to exclude any