31 Labor Epidural with Unrecognized Dural Puncture, Causing High Sensory Block 237

Epidural
reduces
arterial
blood
pressure
Upper
body

Increased collateral
Compressed venous return to Compressed
IVC heart via lumbar aorta and iliac
and azygos system arteries

ACC
ACC
Uterine mass

Fetal
O2
supply

Uterine contractions Placental vascular disease

Fig. 31.5 When an epidural is administered in the setting of one or more preexisting threats to
fetal oxygenation, it can serve as the “straw that breaks the camel’s back” and lead to rapid deterio-
ration of the fetus—manifest as fetal bradycardia or loss of fetal HR variability. The anesthesiolo-
gist must be particularly vigilant of avoiding hypotension and ACC in patients who have preexisting
threats to fetal oxygenation, such as frequent uterine contractions or placental vascular disease
Chapter 32
Acute Pulmonary Dysfunction Immediately
After Cesarean Delivery Under General
Anesthesia

Thomas L. Archer

A 28-year-old woman, 65 in. tall and weighing 220 lb (BMI 37), gravida 3 para 1,
presented at 38 2/7 weeks estimated gestational age with a small amount of vaginal
bleeding. She had a primary cesarean section 4 years earlier for macrosomia,
received 14 units of blood for postpartum hemorrhage, and was diagnosed with von
Willebrand disease type 2b (L-1). Ten weeks prior to admission, prothrombin time
(PT), factor VIII, and von Willebrand factor (vWF) antigen were normal, but vWF
activity was low at 18 % of normal. Activated partial thromboplastin time (aPTT)
and Ivy bleeding time were prolonged at 43.1 s and greater than 20 min, respec-
tively (L-2). Automated platelet count was reported as “clumping.” The peripheral
smear revealed abundant platelet clumping in the feathered edge, with decreased
platelets in the regular part of the smear (L-3).
The morning before surgery, the patient received vWF/factor VIII concentrate
(Humate-P, 6,000 U), after which the vWF activity normalized. The decision was made
to proceed with cesarean section and to have blood and platelets available for transfusion.
General anesthesia was planned because of the decreased platelets seen on peripheral
smear and the history of hemorrhage. Physical examination was unremarkable.
A second IV was placed and during 3 h prior to surgery, the patient inadvertently
received 3 L of lactated ringers solution through the two IVs. She urinated three
times before going to the operating room. Despite this excessive fluid administra-
tion, the patient’s lungs were clear to auscultation immediately prior to induction,
she did not complain of any respiratory distress, and her oxygen saturation on room
air was 97 %. A Foley catheter was placed before induction of anesthesia and
drained 300 mL of pale urine. Cefazolin 2 g was administered and no rash or respi-
ratory symptoms were noted at that time. In addition to routine monitors, the
Aesculon Electrical Cardiometry system (Cardiotronic, Inc., La Jolla, California)
was applied.

T.L. Archer, MD, MBA

Department of Anesthesiology, University of California, San Diego, San Diego, CA, USA
e-mail: tarcher@ucsd.edu

J.L. Benumof (ed.), Clinical Anesthesiology, 239

DOI 10.1007/978-1-4614-8696-1_32, © Springer Science+Business Media New York 2014
240 T.L. Archer

140

120
HR

100

80

80
SI

60

40

6
CI

1315 I/I Del/oxy SpO2 80's, DA, Furosemide Improvement SpO2 100 % 1414

Wheezing, rales

Fig. 32.1 Hemodynamics of cesarean delivery under general anesthesia, complicated by sudden
hypoxemia and pulmonary edema. Intubation and incision (I/I) at 1325 are followed by delivery and
oxytocin administration (Del/oxy) at 1330. At 1336, hypoxemia, wheezing, and rales develop, associ-
ated with tachycardia and decreased stroke and cardiac indices, suggesting left ventricular failure. At
1338, anesthesia is deepened (DA) with fentanyl, propofol, and sevoflurane and muscle relaxation is
provided with vecuronium. Furosemide administered at 1342 is followed by diuresis, clinical improve-
ment, and increased stroke and cardiac indices. SI stroke index, CI cardiac index, HR heart rate

General anesthesia and muscle relaxation were induced with propofol 200 mg IV
and succinylcholine 140 mg IV. The trachea was intubated at 1325, with the tube
positioned at a depth of 18 cm at the teeth. Auscultation revealed normal breath
sounds bilaterally and the SpO2 was 100 %. Anesthesia was maintained with N2O
50 % in oxygen and sevoflurane 1 % inspired until a female infant was born with
Apgars of 6 and 9 at 1330. After delivery a bolus of oxytocin 2 U was given fol-
lowed by a “wide open” infusion of oxytocin 40 U/L of lactated ringers solution
(L-4). N2O was increased to 70 %, the sevoflurane was reduced to 0.2 % inspired,
and fentanyl 100 mcg and midazolam 2 mg were administered.
Six minutes after delivery (1336), the patient began to “buck” on the endotracheal
tube and the surgeon requested more relaxation. The chest was uncovered to better
observe chest movement and a blanching rash was noted. Also, the SpO2 had decreased
from 100 to 85 %. Blood pressure was 156/98 (L-5). Vecuronium 3 mg, propofol
80 mg, and fentanyl 100 mcg were administered to deepen anesthesia and facilitate
both surgery and ventilation. Auscultation of the lungs revealed diffuse, bilateral rales
32 Acute Pulmonary Dysfunction Immediately After Cesarean Delivery 241

140
120
MAP

100
80
60

600
500
SVRI

400
300
200
100

6
CI

1315 I/I Del/oxy SpO2 80’s, DA, Furosemide Improvement SpO2 100 % 1414
wheezing, rales

Fig. 32.2 Same case and time course as in Fig. 32.1, but here the upper two panels display mean
arterial pressure (MAP, by cuff) and systemic vascular resistance index (SVRI), as calculated from
CI and MAP. Pulmonary deterioration was associated with hypertension and high SVRI, consistent
with fluid overload and light anesthesia. Deepening of anesthesia (DA) was followed by an increase
in CI and furosemide was followed by an initial decrease in CI and a later, prolonged increase,
compatible with the patient’s clinical recovery. Other abbreviations as in Fig. 32.1

and wheezing. One-hundred percent oxygen was administered and the patient was
ventilated by hand with PEEP. Albuterol was administered into the endotracheal tube
because of a provisional diagnosis of bronchospasm of unknown etiology (L-6).
To further deepen anesthesia and provide bronchodilation, the sevoflurane was
briefly increased to 3 % inspired and then decreased to 1 %. The trachea was suc-
tioned for modest amounts of clear secretions.
At 1340 it was noted that the cardiac index (CI) and stroke index (SI) had decreased
somewhat compared to predelivery levels, as shown in Fig. 32.1 (L-7). Mean arterial
pressure and systemic vascular resistance index (SVRI) were high, as shown in
Fig. 32.2 (L-8), and coagulation in the surgical field appeared normal (L-8). These
facts, together with the timing of the hypoxemia and our knowledge of the previous
administration of a large amount of IV fluid, led to the tentative diagnosis of acute
volume overload heart failure, precipitated by autotransfusion and relief of vena caval
compression at delivery (L-9 and Figs. 32.3, 32.4, and 32.5). The patient received furo-
semide 40 mg IV at approximately 1342 and a brisk diuresis ensued. The fiber-optic
242 T.L. Archer

Rest of body

Compressed Compressed
IVC aorta and iliac
arteries

ACC
Uterine mass ACC

Pregnant
uterus
contains
substantial
blood volume

Fig. 32.3 Prior to delivery, venous return is limited by inferior vena cava (IVC) compression and
blood volume “stored” within uterus. ACC aortocaval compression

Excessive
IV fluid Rest of
Body

Compressed Compressed
IVC aorta and iliac
arteries

ACC Uterine mass ACC

Pregnant
uterus
contains
substantial
blood volume

Fig. 32.4 Iatrogenic fluid overload increases circulating blood volume, but patient is asymptom-
atic. ACC aortocaval compression
32 Acute Pulmonary Dysfunction Immediately After Cesarean Delivery 243

Heart
fails

Excessive
IV fluid

Rest of body
Uncompressed
Open aorta and iliac
IVC arteries
Relief of IVC compression at
delivery allows venous return to
reach heart

Uterine contraction at delivery

autotransfuses 500 mL blood into
maternal circulation

Fig. 32.5 Autotransfusion and relief of aortocaval compression overwhelm the heart with venous
return

bronchoscope revealed that the tip of the endotracheal tube was 4 cm above the carina
and that, despite copious watery secretions, there were no mucus plugs or foreign bod-
ies in the airway (L-10). Thereafter, during diuresis, CI increased as the SpO2 increased
and the lung auscultatory findings improved, as shown in Fig. 32.1 (L-11).
By the end of surgery at 1455, the lungs were clear and the SpO2 was 100 %. The
patient was extubated and recovered uneventfully. During surgery hemostasis was
normal. Estimated blood loss was 850 mL. Urine output from Foley placement until
the end of surgery was 2.5 L. By the end of the procedure, the rash on the chest had
disappeared.

Lessons Learned

L-1: von Willebrand disease

von Willebrand disease (vWD) is the most common inherited bleeding disorder and
affects approximately 1 % of the population. Patients with vWD may give a history
of easy bruising, nosebleeds, menorrhagia, and excessive bleeding after surgery.
von Willebrand factor (vWF) is a large multimeric glycoprotein which is made by
megakaryocytes and vascular endothelium and which has an affinity both for
244 T.L. Archer

disrupted vascular endothelium and for platelet receptors. Hence, vWF helps bind
platelets to disrupted vascular endothelium. vWF also carries factor VIII within it
and, thereby, physically maintains the coagulation activity of factor VIII close to the
disrupted vascular endothelium where it is needed.
vWD types 1 and 3 are due to a quantitative deficit of structurally and function-
ally normal vWF. Type 1 accounts for 70–80 % of patients with vWD, and in these
patients, the administration of desmopressin (DDAVP) causes normal vWF to be
released from vascular endothelium, thereby ameliorating the coagulation disorder.
DDAVP is not effective for treating vWD Type 2b, however, since this condition is
caused by a structurally and functionally abnormal vWF which binds with excessive
avidity to platelet receptors, causing platelet clumping and the destruction of both
platelets and the attached abnormal vWF. In vWD type 2b patients, it has been
thought that administration of DDAVP would be counterproductive, since it would
cause the release of additional abnormal vWF which would exacerbate thrombocy-
topenia and coagulopathy. Hence, vWD type 2b should be treated with exogenous,
functionally normal vWF/factor VIII complex, which is available as “Humate-P,” a
human plasma-derived preparation which has undergone viral inactivation treat-
ment. Cryoprecipitate also contains vWF/factor VII complex, but this product has
not undergone viral inactivation treatment.
The laboratory evaluation of vWD involves determination of both vWF “anti-
gen” and “activity” (also called ristocetin cofactor activity). vWD types 1 and 3 are
characterized by reductions in both vWF antigen and activity, whereas vWD type 2b
involves normal vWF antigen but abnormally low activity. Humate-P or cryopre-
cipitate can correct low activity.
Clinically important points to remember are:
(a) vWD type 1 is the commonest form and can usually be successfully treated with
DDAVP.
(b) DDAVP should probably not be used to treat vWD type 2b, which should be
treated with exogenous, normal vWF, either as vWF/factor VIII complex
(Humate) or as cryoprecipitate.
(c) vWD type 2b is often associated with thrombocytopenia.
L-2: PTT, PT, and bleeding time in von Willebrand disease
The aPTT is abnormal in about 25 % of patients with vWD type 2b. PT is normal,
since factor VIII is not involved in the “extrinsic pathway” of coagulation. The
bleeding time is seldom obtained in current perioperative practice since it is not very
sensitive or specific for any condition.
L-3: Platelet clumping
“Platelet clumping” can occur in vitro in many patients due to EDTA anticoagulant,
cold agglutinins, and for other reasons. Platelet clumping and destruction also occur
in vivo in vWD type 2b so that in this case the significance of platelet clumping on
the peripheral smear was not clear. We were prepared, however, to transfuse the
patient with red cells and platelets.
32 Acute Pulmonary Dysfunction Immediately After Cesarean Delivery 245

L-4: Intravenous oxytocin after delivery

We administered an oxytocin bolus in this case because we were concerned about
coagulopathy and we wanted the uterus to contract rapidly. Until recently, a 5-unit
bolus of oxytocin after delivery was fairly common, but many practitioners are cur-
rently using boluses much smaller than 5 units, if they use a bolus at all. Boluses of
oxytocin can cause arteriolar and venous dilation, hypotension, and decreased sys-
temic vascular resistance. Despite the venodilation due to oxytocin, cardiac output
usually increases at delivery due to relief of aortocaval compression and autotrans-
fusion. Oxytocin 40 U/L in lactated ringers is twice the usual infusion concentration
after delivery. The obstetricians had asked us to “double the oxytocin” because of
the history of bleeding.
L-5: When hypertension is associated with pulmonary dysfunction
The fact that the patient was hypertensive made us think that an anaphylactic reaction
or amniotic fluid embolus were less likely causes for the pulmonary dysfunction.
L-6: “All that wheezes is not asthma”
“All that wheezes is not asthma.” Our differential diagnosis at this point for acute
hypoxemia and wheezing during cesarean delivery under general anesthesia included:
(a) Incipient mainstem intubation with mechanical airway obstruction
(b) Acute fluid overload pulmonary edema due to excessive preoperative fluid infu-
sion and relief of aortocaval compression and autotransfusion
(c) Anaphylactic reaction with bronchospasm and increased alveolar capillary
permeability
(d) Aspiration of gastric contents, with mechanical airway obstruction and alveolar
capillary damage
(e) “Amniotic fluid embolism” (“anaphylactoid syndrome of pregnancy”)
L-7: Cardiac output increases after a normal delivery, due to relief of aortoca-
val compression, autotransfusion, and oxytocin administration
A decrease in cardiac output and stroke volume after delivery is highly abnormal.
Cardiac output normally increases 25–75 % immediately after delivery due to relief
of aortocaval compression, autotransfusion, and oxytocin administration.
L-8: Systemic vascular resistance
These facts made anaphylaxis or amniotic fluid embolus (AFE) less likely diagno-
ses, since both those conditions would have been associated with a low SVRI and a
low MAP. Also, an AFE is frequently associated with disseminated intravascular
coagulation (DIC).
Bolused oxytocin is a potent arteriolar dilator and usually decreases SVRI under
both neuraxial and general anesthesia (Fig. 32.6). Hence, the increase in SVRI after
delivery and oxytocin administration seen in this case was unusual and unexpected
and probably due to high sympathetic tone in the setting of light anesthesia. It may
well be that light general anesthesia postdelivery in this already volume-overloaded
patient was the event that precipitated the heart failure.
246 T.L. Archer

Cardiac output, L/min

20

10

Systemic vascular resistance, dyn s cm–5

1,000

500

0
Blood pressure, mmHg
150 3 4 5 6 7 8

100
50
0
Heart rate, beats/min and stroke volume (SV), mL SV
150
100
50
0
0 min Int Inc 8 Del Oxy3 12 16 min

Fig. 32.6 Normal hemodynamic response to delivery (Del) and oxytocin 3 unit bolus (Oxy3)
under general anesthesia, measured with LiDCO pulse contour analysis. Oxytocin bolus after
delivery increases stroke volume and cardiac output and decreases systemic vascular resistance
and blood pressure. Int intubation, Inc incision, SV stroke volume. Please note: this is not the case
described in the rest of the text

L-9: Cardiac output increases after delivery. Oxytocin dilates resistance arte-
rioles, thereby decreasing systemic vascular resistance
Delivery causes relief of aortocaval compression and uterine contraction causes
autotransfusion, both of which cause a sudden increase in venous return to the heart.
Oxytocin, besides contracting the uterus, decreases systemic vascular resistance
(SVR) and afterload by dilating resistance arterioles (0.1 mm in diameter and
smaller). If the heart is unable to “handle” this suddenly increased venous return by
increasing cardiac output, the heart can fail suddenly. Figures 32.3, 32.4, and 32.5
illustrate this pathophysiology. Examples of conditions in which the heart has trou-
ble increasing cardiac output would be mitral or aortic stenosis, cardiomyopathy, or
the high afterload accompanying light general anesthesia.
L-10: Misdiagnosis of “bronchospasm”
Partial or incipient mainstem intubation is often misdiagnosed as “bronchospasm”
under general anesthesia. This is particularly common when the patient is obese and
is placed into Trendelenburg position and when the anesthesiologist has not meticu-
lously avoided over-insertion of the endotracheal tube (ETT) during intubation. Use
of the fiber-optic bronchoscope (FOB) enables the anesthesiologist to definitively
exclude incipient mainstem intubation as a cause of “bronchospasm” and/or high
32 Acute Pulmonary Dysfunction Immediately After Cesarean Delivery 247

peak inspiratory pressures. Empirical withdrawal of an ETT which is probably well

placed runs the risk of accidental extubation. “Taking a look” with the FOB also
allows the rapid identification of aspirated stomach contents, mucus plugs, or for-
eign bodies in the airway.
L-11: Diuresis in heart failure due to fluid overload
Diuresis was accompanied by increased SpO2, improvement in breath sounds, and
by increasing CI, all of which was consistent with successful treatment of heart
failure due to fluid overload, although an allergic reaction was still a possible diag-
nosis in this case.