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2.2 Perioperative Medications
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2.2.2 Pain Management
2.2.2.1 NSAIDs
The use of NSAIDs during the second and third
trimesters is associated with oligohydramnios and
anuria. After 30weeks of gestation, it is associated with an increased risk of premature closure
of the fetal ductus arteriosus (Botalli’s duct), with
subsequent pulmonary hypertension, intracranial
hemorrhage, and necrotizing enterocolitis [79–
84]. After appendectomy with CS, all classes of
medications could be used as in nonpregnant
patients unless contraindicated for maternal
reasons.
NSAIDs were the rst-choice treatment for
symptomatic relief, but the risk of miscarriage
was the highest with NSAID use around conception and increased with NSAID use for longer than a week [85–87]. Prostaglandins are
needed to successfully implant an embryo into
the uterus wall [88] and play an important role
in human ovulation and implantation through
their effect and interaction with platelet-activating factors and cytokines, both in the uterus and
in the embryo [89, 90]. Suppression of prostaglandin biosynthesis by NSAIDs could lead to
abnormal implantation with a predisposition for
miscarriage [87]. There are also differences in
transplacental pharmacokinetic parameters
between different NSAIDs. The results suggest
that the fetal risk of diclofenac is higher than
salicylic acid and antipyrine [91]. If indicated,
ibuprofen is the preferred agent. Unfortunately,
selective NSAIDs (cyclo-oxygenase 2 inhibitors) are classied in FDA category C because
of increased peri-implantation and postimplantation losses and reduced fetal survival in rats
and rabbits.
NSAIDs and aspirin should be given in
pregnancy only if the maternal benets out-
weigh the potential fetal risks, at the lowest
effective dose, and for the shortest duration
(less than a week) with avoidance during
conception and ideally after 30 weeks of
pregnancy.
2.2.2.2 Paracetamol
Paracetamol, which shares many indications with
NSAIDs,did not affect the risk of miscarriage.
NSAIDs and aspirin inhibit prostaglandin biosynthesis in most organ systems, whereas
paracetamol inhibits prostaglandin biosynthesis
only in the central nervous system [86].
During pregnancy, paracetamol is the drug
of choice for analgesic, anti- inammatory,
and antipyretic action.
2.2.2.3 Opioids
Weak opioids such as codeine may be used as
additional treatments to help control the pain.
They are also helpful if NSAIDs are not tolerated
or are contraindicated. Morphine analgesia and
its derivatives should be avoided, as they may
cause spasms of the sphincter of Oddi. This
spasm may exacerbate an already painful acute
cholecystitis or biliary obstruction.
2.2.2.4 Local Anesthesia
Long-acting local anesthesiautilized in laparoscopic port sites or laparotomy wound improves
postoperative analgesia, minimizing postoperative narcotic requirements.
2.2.3 Thromboprophylaxis
andAnticoagulation
2.2.3.1 General Recommendations
The annual frequency of deep venous thrombosis
(DVT) in the general population is 0.16–1% [92,
93], of which 2% are pregnancy-related [94].
Therefore, the risk of athromboembolic event,
either DVT or pulmonary embolism (PE), during
pregnancy and puerperium is estimated to be tenfold higher, reaching 2% [92, 95–98]. Gestational
hormones, particularly estrogen, contribute to
mild hypercoagulability during pregnancy by
increasing the synthesis of clotting factors [99].
Thromboembolic phenomena are also promoted
by intra-abdominal vascular stasis resulting from
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Table 2.4 Risk factors for thrombosis during pregnancy [92, 93, 95, 96, 101]
Thrombophilic disorders Causes related to pregnancy General risk factors
Antithrombin deciency Immobility Age >35years
Factor V Leiden
Antiphospholipid
Antibodies
Hyperhomocysteinemia Weight gain >21kg Smoking
Protein C deciency Diabetes mellitus
Homozygous MTHFR
C677T
Protein S deciency Preeclampsia
Prothrombin gene
Mutation
Plasminogen activator
Inhibitor-1 (PAI-1) 4G/5G
Parity ≥3
Multiple gestations History of deep vein thrombosis
Prolonged labor >12h Major abdominal surgery for >30min
(emergency) cesarean section Anemia
Blood loss (>1l)/ blood transfusion Black race
Preterm delivery Dehydration
Mid-cavity instrumental delivery Infections
Hyperemesis Severe varicose veins
Assisted reproductive techniques Systemic lupus erythematosus
2 Anesthetic andPerioperative Management
Body mass index >30
compression by the enlarged gravid uterus. The
risk may increase exponentially throughout the
pregnancy [100]. Puerperium is the period with
the highest venous thromboembolism (VTE)
risk, up to 25-fold higher than that in nonpregnant women [92, 96, 98, 101]. Around 43–60%
of pregnancy-related PE episodes occur during
puerperium [92, 95]. Approximately 80% of
thrombotic events occur in the rst 3–4weeks
after delivery and are explained by the immobility and the trauma of pelvic vessels at delivery,
leading to endothelial damage [102].
Hypercoagulability during the obstetric period
is explained by many factors, including abnormalities in coagulation proteins (increased levels
of factors II, V, VII, VIII, X, XII, and von
Willebrand factor, and decreased levels of protein
S and activated protein C) and abnormalities in
the brinolytic system (low plasma brinolytic
activity during pregnancy, labor, and delivery)
with decreased activity of tissue plasminogen
activator. The most signicant changes occur in
factor VIII and brinogen levels, each of which
increases two to threefold [103, 104].
Pregnant women undergoing nonobstetric
surgery should be screened for venous throm-
boembolism risk and should have the appro-
priate perioperative prophylaxis administered.
(ACOG Committee opinion 2019 [1])
Risk factors for thrombosis during pregnancy
are listed in Table2.4. The American College of
Chest Physicians Evidence-Based Clinical
Practice Guidelines 2012 is the most comprehensive thromboprophylaxis guideline for the pregnant population [97].
• Low-molecular-weight heparin
(LMWH) is recommended for the prevention and treatment of VTE instead of
unfractionated heparin (UFH),
• For women receiving anticoagulation
for the treatment of VTE who become
pregnant, LMWH is recommended over
vitamin K antagonists,
• The use of fondaparinux and parenteral
direct thrombin inhibitors should be
limited to those with severe allergic
reactions to heparin (e.g., HIT) who
cannot receive danaparoid,
• Avoid the use of oral direct thrombin
(e.g., dabigatran) and anti-Xa (e.g., rivaroxaban, apixaban) inhibitors,
• For lactating women using warfarin,
acenocoumarol, or UFH who wish to
breastfeed, continuing the use of warfarin, acenocoumarol, or UFH is
recommended,
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• For lactating women using LMWH,
danaparoid, or r-hirudin who wish to
breastfeed, a continuation of LMWH,
danaparoid, or r-hirudin is
recommended,
• For breastfeeding women, alternative
anticoagulants rather than fondaparinux
are recommended,
• For breastfeeding women, alternative
anticoagulants rather than oral direct
thrombin (e.g., dabigatran) and factor
Xa inhibitors (e.g., rivaroxaban, apixaban) are recommended,
• For lactating women using low-dose
aspirin for vascular indications who
wish to breastfeed, a continuation of this
medication is recommended,
• For women undergoing assisted reproduction, routine thrombosis prophylaxis
is not recommended,
• For women undergoing assisted reproduction who develop severe ovarian
hyperstimulation syndrome, thrombosis
prophylaxis (prophylactic LMWH) for
3months postresolution of clinical ovarian hyperstimulation syndrome is
recommended,
• For all pregnant women with prior VTE,
postpartum prophylaxis for 6 weeks
with prophylactic- or intermediate-dose
LMWH or vitamin K antagonists targeted at INR 2.0-3.0 is recommended,
• For pregnant women at low risk of
recurrent VTE (a single episode of VTE
associated with a transient risk factor
not related to pregnancy or use of estrogen), only clinical vigilance antepartum
is recommended,
• For pregnant women at moderate to high
risk of recurrent VTE (single unprovoked
VTE, pregnancy- or estrogen- related
VTE, or multiple prior unprovoked VTE
not receiving long- term anticoagulation),
antepartum prophylaxis with prophylactic- or intermediate-dose LMWH is
recommended,
• For pregnant women receiving longterm vitamin K antagonists, an adjusted
dose of LMWH or 75% of a therapeutic
dose of LMWH throughout pregnancy
followed by resumption of long-term
anticoagulants postpartum is
recommended,
• For pregnant women with no prior history of VTE who are known to be homozygous for factor V Leiden or the
prothrombin 20210A mutation and have
a positive family history of VTE, antepartum prophylaxis with prophylacticor intermediate-dose LMWH and
postpartum prophylaxis for 6 weeks
with prophylactic- or intermediate-dose
LMWH or vitamin K antagonists targeted at INR 2.0-3.0 is recommended,
• For pregnant women with all other
thrombophilias and no prior VTE who
have a positive family history of VTE,
antepartum clinical vigilance and postpartum prophylaxis with prophylacticor intermediate-dose LMWH or, in
women who are not protein C or S decient, vitamin K antagonists targeted at
INR 2.0-3.0 are recommended,
• For pregnant women with no prior history of VTE who are known to be homozygous for factor V Leiden or the
prothrombin 20210A mutation and who
do not have a positive family history of
VTE, antepartum clinical vigilance and
postpartum prophylaxis for 6 weeks
with prophylactic- or intermediate-dose
LMWH or vitamin K antagonists targeted at INR 2.0-3.0 are recommended,
• For pregnant women with all other
thrombophilias and no prior VTE who
do not have a positive family history for
VTE, antepartum and postpartum clinical vigilance are recommended,
• For women with recurrent early pregnancy loss (three or more miscarriages
before 10weeks of gestation), screening
for APLAs is recommended,
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• For women with a history of pregnancy
complications, no screening for inherited thrombophilia is recommended,
• For women who fulll the laboratory
criteria for APLA syndrome and meet
the clinical APLA criteria based on a
history of three or more pregnancy
losses, antepartum administration of
prophylactic- or intermediate-dose UFH
or prophylactic LMWH combined with
low-dose aspirin, 75–100 mg/d is
recommended,
• For women with inherited thrombophilia and a history of pregnancy complications, antithrombotic prophylaxis
is not recommended,
• For women considered at risk for preeclampsia, low-dose aspirin throughout
pregnancy, starting from the second
trimester,is recommended,
• For women with two or more miscarriages but without APLA or thrombophilia, antithrombotic prophylaxis is not
recommended,
• For pregnant women with mechanical
heart valves: (a) adjusted-dose bid
LMWH throughout pregnancy to
achieve the manufacturer’s peak anti-Xa
LMWH 4h postsubcutaneous injection,
or (b) adjusted-dose UFH throughout
pregnancy administered subcutaneously
every 12h in doses adjusted to keep the
mid-interval aPTT at least twice control
or attain an anti-Xa heparin level of
0.35–0.70 units/mL, or (c) UFH or
LMWH (as above) until the 13th week,
with substitution by vitamin K antagonists until close to delivery when UFH
or LMWH is resumed.
2.2.3.2 Low-Risk Surgery
Many factors can alter postoperative coagulation.
These include the type of operation [105] and
anesthesia [106]. Postoperative changes in cytokine levels are affected by even more factors: the
2 Anesthetic andPerioperative Management
type of the procedure and the anesthetic technique or anesthetic agent [107], the duration of
the operation [108], and the use of autologous or
allogenic transfusion [109].
Open surgery (OS), compared with laparoscopic surgery (LS), leads to activation of the clotting system to a higher degree, implying a greater
thromboembolic risk. Subclinical brinolysis is
also more profound with OS.Although of a lower
degree, hypercoagulability is observed in patients
undergoing LS. This fact, combined with the
pneumoperitoneum-induced venous stasis of the
legs, explains the reduced, but not negligible,rate
of thromboembolic complications after
LS. Therefore, routine thromboembolic prophylaxis (subcutaneous LMWH, elastic compression
stockings, intraoperative pneumatic stockings, and
early postoperative patient mobilization) should
be considered for LS [110]. Gestational hormones,
particularly estrogen, contribute to mild hypercoagulopathy during pregnancy by increasing the
synthesis of clotting factors [99]. If a laparotomy
can be avoided, recovery time is greatly reduced;
thus, postoperative complications due to immobilization, such as DVT and PE, are less likely.
Prophylaxis with pneumatic compression devices,
both intraoperatively and postoperatively, and
early postoperative ambulation are recommended.
No recommendations for thromboprophylaxis
exist for low-risk groups (appendectomy via laparoscopy or gridiron incision, isolated Fallopian
tube torsion, and (ruptured) ectopic pregnancy).
The use of calf-length sequential pneumatic compression stockings increases venous return and
prevents the risk of VTE [111]. Early ambulation
further minimizes or eliminates the VTE risk.
2.2.3.3 Elective Cholecystectomy
A marked hypercoagulable state after LC is seen
by an increase in the thromboelastographic index
on the rst postoperative day compared to preoperative values [105]. Reports have documented a
reduction in postoperative hypercoagulability
after LS compared to OS [112, 113]. A signicant increase in prothrombin fragment F1 + 2
levels after LC is found, but these levels were signicantly lower than those after OC [113].
Conversely, others have not found a difference in
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postoperative hemostasis between LC and OC
[114, 115]. Fibrinogen levels increased and
reached maximum levels at 72h, but signicantly
less after LC than after OC.In contrast, plasminogen levels decreased postoperatively without a
signicant difference between groups [116]. LC
is associated with a lesser degree of thromboembolic complications despite pneumoperitoneum,
which, by reducing venous inow toward the
heart, promotes venous stasis of the legs and predisposes to DVT [117, 118]. TAT, F1, FIB, soluble brin, and D-dimer plasma levels until 72h
after surgery were signicantly higher in the OC
group than in the LC group, implying signicantly higher activation of coagulation and brinolysis in the OC group [116]. The levels of
coagulation factors and cytokines were,on average, two times higher in the OC group. Other
nonrandomized studies found insignicant differences in brinolytic activity between OC and
LC groups [114, 115, 119]. Postoperative DVT is
additionally reduced after LC due to the early
mobility of such patients.
2.2.3.4 Emergent Cholecystectomy
The emergent LC carries a better fetal prognosis
than delayed cholecystectomy (see Sect.
16.1.8.4). Still, there are several issues. First is
coagulation and brinolysis mechanisms during
pregnancy complicated with acute cholecystitis.
Second is the question of coagulation during the
complete process of cholecystitis as a disease. Is
it better to perform emergent cholecystectomy
with initially increased coagulation or to start
medical management, which, due to inammation, also increases coagulation? Moreover, coagulation is also increased in the second phase of
the treatment process when delayed elective cholecystectomy is performed. There are no recommendations for additional thromboprophylaxis in
acute cholecystitis during pregnancy.
IVF Pregnancy
Currently, there is only one case report of LC due
to acute cholecystitis during pregnancy [99].
Thromboprophylaxis should be recommended in
dosage for IVF pregnancy due to its higher risk for
VTE.Prospective studies should solve this issue.
2.2.3.5 General IBD Patients (ECCO
Consensus)
IBD patients in general, particularly those hospitalized with theactive disease, are at increased
risk for VTE [120, 121]. Hospitalized pregnant
IBD patients have an increased risk of VTE compared to non-IBD pregnant controls, for CD an
OR 6.12 and UC an OR 8.44. LMWH in a prophylactic dose reduces VTE risk in medical and
surgical patients by 60–70%.
LMWH is safe and effective in the pregnant
population [122]. Therefore, prophylactic
LMWH in pregnant IBD patients experiencing a
relapse or being admitted to the hospital is recommended. Women should undergo a documented assessment of risk factors for VTE in
early pregnancy or before pregnancy. This assessment should be repeated if the woman is admitted
to the hospital and again after delivery.
Pregnant women with IBD are at increased
risk of vitamin D insufciency compared with
those without IBD. The current guidelines for
vitamin D supplementation (400IU/day) may be
inadequate for pregnant women with IBD [123].
2.2.3.6 Cesarean Section
The VTE incidence rate following CS is 1.78%,
with an odds ratio of 2 [95]. Thromboprophylaxis
guidelines from the American College of Chest
Physicians Evidence-Based Clinical Practice
Guidelines 2012 for women undergoing CS are
presented [97]:
• For women undergoing CS without
additional thrombosis risk factors,
thromboprophylaxis is not recommended other than early mobilization,
• For women at increased risk of VTE
after CS because of the presence of one
major or at least two minor risk factors,
pharmacologic thromboprophylaxis
(prophylactic LMWH) or mechanical
prophylaxis (elastic stockings or intermittent pneumatic compression) in
those with contraindications to antico-
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2 Anesthetic andPerioperative Management
agulants while in hospital following
delivery is recommended,
• For women undergoing CS who are
considered to be at very high risk for
VTE and who have multiple additional
risk factors for thromboembolism that
persist in the puerperium, prophylactic
LMWH should be combined with elastic stockings or intermittent pneumatic
compression,
• For selected high-risk patients in whom
signicant risk factors persist following
delivery, extended prophylaxis (up to
6 weeks after delivery) following discharge from the hospital is
recommended.
2.2.3.7 Torsion oftheGravid Uterus
Several cases of PE after uterine detorsion [124,
125] exist. Therefore, LMWH (enoxaparin 20mg
once a day) for 6weeks to prevent VTE is recommended [126].
2.2.3.8 Venous Thromboembolism
Therapeutic recommendations for VTEduring
pregnancy from the American College of Chest
Physicians Evidence-Based Clinical Practice
Guidelines 2012 are presented [97]:
• For pregnant women with acute VTE,
adjusted-dose subcutaneous LMWH
over adjusted-dose UFH is
recommended,
• For pregnant women with acute VTE,
LMWH over vitamin K antagonist treatment antenatally is recommended,
• For pregnant women with acute VTE,
anticoagulants should be continued for
at least 6weeks postpartum (for a minimum total duration of therapy of
3months),
• For pregnant women receiving adjusteddose LMWH therapy and where delivery is planned, discontinuation of
LMWH at least 24h before induction of
labor or CS (or expected time of neuraxial anesthesia) rather than continuing
LMWH up until the time of delivery is
recommended.
Mesenteric Vein Thrombosis
Guidelines for the duration of anticoagulation
after pregnancy for mesenteric vein thrombosis
(MVT) do not exist, and decisions on a case-bycase basis need to be taken by hematologists
[127]. In the general population, anticoagulation
with low-molecular-weight heparin should be
initiated as soon as the diagnosis is made, including when the diagnosis is delayed until surgery
[128]. Although maintenance anticoagulation
therapy is recommended for at least 6 months
after diagnosis to prevent the recurrence of the
thrombosis, its benet was questioned during
pregnancy [129]. Lifelong anticoagulation is
warranted with inherited hypercoagulable disorders (i.e., protein S, protein C, antithrombin III
deciencies, and factor V Leiden mutation). For a
general population with reversible predisposing
causes, at least 6 months of anticoagulation is
recommended [130].
Guidelines for anticoagulation management
strategies exist for various clinical situations
before and after controlled ovarian stimulation
[131, 132]. A history of prior MVT should be
placed in the clinical classication of the previous episode(s) of venous thromboembolism
receiving long-term anticoagulation. It is recommended to switch from oral anticoagulants
to LMWH therapy (e.g., enoxaparin 1 mg/kg
every 12h) before controlled ovarian stimulation and continue throughout pregnancy [131,
132]. The recommendation is to refrain from
administering LMWH for 24 h before egg
retrieval and restart therapeutic anticoagulation
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3h after egg retrieval [131, 132]. Without large
studies, IVF associated with MVT indicates
lifelong oral anticoagulation in patients at low
risk for bleeding and full anticoagulation with
LMWH per the above protocol during repeat
IVF cycles. However, controversy in preventing
venous thrombosis exists after delivery, especially if no risk factors were detected [133].
Though the induction of oral anticoagulation in
protein C deciency has been widely used, it
carries signicant risks in patients with esophageal varices and thrombocytopenia [134].
2.3 Perioperative Management
Surgery should be done at an institution with neonatal and pediatric services.
(ACOG Committee opinion 2019 [1])
An obstetric care provider with cesarean delivery
privileges should be readily available.
(ACOG Committee opinion 2019 [1])
2.3.1 Fetal Heart Rate Monitoring
If the fetus is considered previable, it is generally
sufcient to ascertain the fetal heart rate by
Doppler before and after the procedure.
(ACOG Committee opinion 2019 [1])
At a minimum, if the fetus is considered to be viable, simultaneous electronic fetal heart rate and
contraction monitoring should be performed
before and after the procedure to assess fetal wellbeing and the absence of contractions.
(ACOG Committee opinion 2019 [1])
There are two principal types of FHR monitoring: internal and external (Fig. 2.2). When
emergency abdominal conditions are considered,
only the external type is used. FHR, after
16weeks of pregnancy, should be monitored preand postoperatively in the setting of urgent
abdominal surgery during pregnancy (Evidence
level III) [135, 136]. In specic circumstances,
intraoperative electronic fetal monitoring can be
appropriate but is never practiced in emergency
abdominal surgery in pregnancy [1]. Indirect
(transabdominal) intraoperative FHR (every
5min in the lower left quadrant without disination) resembles external FHR monitoring
(Fig.2.3a) to detect fetal distress and is used during laparoscopy. No intraoperative FHR abnormalities have been reported [137, 138]. Direct
(transuterine) FHR monitoring is performed during laparotomy (Fig. 2.3b). Three methods of
intraoperative FHR monitoring include (1) cardiotocography, (2) ultrasonography with a transesophageal echocardiographyprobe, and (3)
point-of-care ultrasound [139, 140]. One of the
limitations of point-of-care ultrasound is that it
cannot always serve as a continuous monitoring
tool because of interference from the pneumoperitoneum. External monitors of uterine contractions are variably effective in the insufated
abdomen [141].
The effects of general anesthesia on cardiotocography result in a reduction of beat-to-beat
variation with normal baseline frequency. The
decreased variability can persist until 90min in
the postoperative course due to the residual
effects of anesthetic agents on the fetus. Also,
preoperative anxiety and stress can further
increase catecholamine levels. This could be misinterpreted as fetal distress, leading to an emergency delivery and adding to fetal morbidity and
mortality [143]. Additional factors that can inuence intraoperative beat-to-beat variations are
surgical manipulation, especially of the pregnant
uterus, primary inammatory process, or bleeding. Transvaginal sonography should be used
during the procedure because the signals from
transabdominal ultrasound would be lost during
insufation [144–146]. This has led some to recommend only pre-, and postoperative monitoring
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Scalp electrode
Intrauterine
catheter
Fig. 2.2 Internal and external types of fetal heart rate monitoring. (Reproduced with permission from [142])
2 Anesthetic andPerioperative Management
Contraction
monitor sensor
Fetal heart
Fig. 2.3 Intraoperative fetal monitoring. (a) Indirect during laparoscopy in advanced pregnancy. (b) Direct fetal moni-
toring during laparotomy
of the FHR as no increased fetal morbidity has
been reported [60, 135].
Special monitoring precautions beyond those
usually employed during general anesthesia—
continuous maternal pulse oximetry, end-tidal
There are fewer derangements in maternal and
fetal physiology without CO
pneumoperito-
2
neum. Moreover, it is possible to perform surgical procedures under locoregional (peridural or
spinal) rather than general anesthesia.
CO2, monitoring, electrocardiography, and pulse
rate measurements, combined with frequent
blood pressure measurements—have generally
2.3.2 Perioperative Nutrition
not been employed. Also, in women predisposed
to signicant hypercarbia, changes in end-tidal
CO
may lag signicantly behind maternal
2
2.3.2.1 Total Parenteral Nutrition
andRefeeding Syndrome
PaCO2. Frequent direct measurements of
maternal PaCO2 via an arterial catheter may be
warranted [146].
Some faults of pneumoperitoneum can be
avoided with the use of gasless laparoscopy.
Pathophysiology
Refeeding syndrome was rst recognized during
World War II when returning prisoners of the
Japanese who had been starved rapidly devel-
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oped neurological and cardiovascular abnormalities after the institution of a normal diet [147].
level of consciousness, seizures, cardiac or respi-
ratory depression) and potentially death [148].
The pathophysiology of refeeding syndrome
relates to the rapid rise in insulin production following a carbohydrate or protein shock when
protein calories are administered at a rate above
which the patient can tolerate. This can occur in
those receiving moderate dietary intake depending on their underlying nutritional, metabolic, or
physical condition and may arise with glucose
administration alone. This insulin release, associated with possible increased insulin sensitivity,
leads to increased cellular uptake of glucose,
uid, and electrolytes with associated altered
plasma availability of electrolytes.
Refeeding syndrome can manifest as either
metabolic changes (hypokalemia, hypophosphatemia, hypomagnesemia, altered glucose metabolism, and uid balance abnormalities) or
physiological changes (i.e., arrhythmias, altered
Table 2.5 Initial management of refeeding syndrome
1. Identication and Treatment of Sepsis
• May not be clinically apparent but may explain an acute deterioration
• Low threshold for septic screen
• Low threshold for broad-spectrum antibiotics (orally or via NG tube if possible)
2. Fluid Resuscitation and Monitoring Fluid Balance
• Assess and carefully restore circulatory volume, monitor pulse rate, uid intake, and output
• Malnourished patients have a reduced tolerance of intravenous uids in moderate to high intakes
(>2L/24h),which can lead to heart failure
• Administration of intravenous uids may be necessary for the initial 72h until sufcient oral intake is
achieved
• Evidence of dehydration—for careful rehydration, i.e., 1–2L in the rst 24h, depending on response.
Greater volumes only if severely dehydrated
• Total uid intake (including intravenous, enteral, and oral) should aim for a maximum of 30mL/kg per day
(≤1.5L)
• At least 6 hourly monitoring of blood pressure, pulse,and respiratory rate is necessary to detect evidence of
heart failure or inadequate intravascular volume
3. Correction of Electrolyte Abnormalities
• Ensure recent (last 48h) electrolyte levels are available. These should include: urea and electrolytes,
phosphate, calcium, magnesium (add to standard blood prole), liver function tests, full blood count
• If electrolytes are deranged, consider and treat possible causes
• Perform ECG if Potassium is less than 3.5mmol/L or Phosphate is less than 0.80mmol/L
• Organize supplementation if: Phosphate <0.8mmol/L, K<3.5mmol/L, Mg <0.5mmol/L or adjusted Ca
<2.0mmol/L
• Caution should be used in renal patients due to the reduced excretion of these electrolytes
• If very low plasma electrolyte values are demonstrated, e.g., Phosphate <0.32mmol/L
• K<2.5mmol/L, Mg <0.5mmol/L, then the institution of feeding or nutritional support may result in a
further drop of these electrolytes to possibly critical levels. Electrolyte correction with oral or intravenous
supplementation is required to achieve levels above these thresholds before the institution of feeding
Total Parenteral Nutrition inPregnancy
Total parenteral nutrition has been used successfully in pregnant women with hyperemesis gravidarum, postintestinal surgery, and acute
pancreatitis [149]. The maternal and neonatal
outcomes measured by adequate maternal weight
gain and fetal growth are not compromised by
total parenteral nutrition [150]. The average daily
intake through total parenteral nutrition in pregnant women should be 2430kcal [151]. However,
it is better to increase daily calories to avoid
refeeding syndrome.
Algorithms for initial management (Table2.5)
and monitoring (Table2.6) of the refeeding syndrome from the Drug Therapy Guideline No:
46.00 Issued: 10.10.07 Refeeding Syndrome
Guideline (NHS trust)are presented:
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Table 2.5 (continued)
4. Correction of Hypoglycemia/Blood Sugar Control
• Monitor blood glucose once to twice daily unless more frequent tests are indicated (i.e., for those patients
with known diabetes or IGT)
• If hypoglycemic, replace IV uids with 5% glucose
5. Management of Hypothermia
• Monitor body temperature and, if necessary, the core temperature at least daily
• Hypothermia is commonly associated with malnutrition. Its correction should be simultaneous with uid
rehydration and can include the provision of heated drinks and blankets
6. Correction/Prevention of Micronutrient Deciencies
• Administer Thiamine 100mg orally or crushed via feeding tube three times daily for 10days or until
recommended feeding rate is reached, with the rst dose being administered at least 30min before instituting
feeding
• If an enteral route is not available, the patient has anorexia nervosa or has chronic alcoholism; administer
Pabrinex IVHP—1 pair of ampoules 30minutes before instituting feeding and then daily until recommended
feeding rate reached
• Administer vitamin B compound strong (one tablet three times daily) and Sanatogen Gold (one tablet daily)
orally or crushed via a feeding tube
2 Anesthetic andPerioperative Management
Table 2.6
proven refeeding syndrome (minimum 72h)
Monitor until levels are in the reference range or the
patient is on a stable feeding regimen:
Clinical deterioration may reect rapid overfeeding.
Too little is always safer than too much, half the rate
of feeding and observe
Monitoring of patients with suspected or
• Serum urea and electrolytes, adjusted calcium,
phosphate, and liver function tests at least daily
• Serum magnesium; baseline, every 3days and then
weekly once stable
• Fluid balance daily
• Blood glucose once to twice daily unless more
frequent tests are indicated
• Temperature, pulse, respiration, heart rate; daily
• Blood pressure 6 hourly
• ECG if abnormal heart rate or pulse. The patient
will require cardiac monitoring if there is evidence
of cardiac abnormalities on assessment or during
refeeding. If necessary, transfer to the appropriate
ward
Early parenteral nutrition in Crohn’s disease
maintains normal maternal metabolism and normal fetal development in patients with the operation and complicated perioperative courses. Early
parenteral nutrition should be considered in acute
pancreatitis due to a protracted course with disease ares.
2.3.2.2 Perinatal Outcome
Symptomatic cholelithiasisor cholecystitis in
pregnant women could be associated with a
higher risk of neonatal neural tube defects [152].
Confounding factors for preterm labor should be
considered. An association exists between neural
tube defects or other congenital anomalies and
high fever during the critical period [153]. The
hypothesis for the association between symptomatic cholelithiasis or cholecystitis and neural tube
defects is based on a frequently present fever. It is
a single factor that may play a role in the origin of
neural tube defects (see Sect. 4.7.3). Thus, periconceptional folic acid/multivitamin supplementation in pregnant women with symptomatic
cholelithiasis or cholecystitis is recommended
[152, 153] and other abdominal conditions when
the caloric intake is diminished. Folic acid and
folic acid-containing multivitamins were less frequent in the symptomatic cholelithiasis or cholecystitis group, partly due to a higher rate of
anorexia or vomiting. No association between the
bacterial causes of cholecystitis and neural tube
defects has been proven [154]. The drugs used to
treat symptomatic cholelithiasis or cholecystitis
have no role in the origin of neural tube defects.
Recommended prenatal vitamin supplementation
is based on the inverse relationship of the B
vitamins (i.e., folate, vitamins B1, B2, B6, and
B12), minerals, and vitamin E with CDH in newborns [155].
Dietary supplementation of ω-3 has been suggested as secondary prevention of all-cause spontaneous preterm delivery, implying that ω-3 fatty
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