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Table of Contents
                            Critical Care Obstetrics
	Contents
	List of Contributors
	1: Epidemiology of Critical Illness in Pregnancy
	2: Organizing an Obstetric Critical Care Unit
	3: Critical Care Obstetric Nursing
	4: Pregnancy-Induced Physiologic Alterations
	5: Maternal–Fetal Blood Gas Physiology
	6: Fluid and Electrolyte Balance
	7: Cardiopulmonary Resuscitation in Pregnancy
	8: Neonatal Resuscitation
	9: Ventilator Management in Critical Illness
	10: Vascular Access
	11: Blood Component Replacement
	12: Hyperalimentation
	13: Dialysis
	14: Cardiopulmonary Bypass
	15: Non-Invasive Monitoring
	16: Pulmonary Artery Catheterization
	17: Seizures and Status Epilepticus
	18: Acute Spinal Cord Injury
	19: Pregnancy-Related Stroke
	20: Cardiac Disease
	21: Thromboembolic Disease
	22: Etiology and Management of Hemorrhage
	23: Severe Acute Asthma
	24: Acute Lung Injury and Acute Respiratory Distress Syndrome (ARDS) During Pregnancy
	25: Pulmonary Edema
	26: The Acute Abdomen During Pregnancy
	27: Acute Pancreatitis
	28: Acute Renal Failure
	29: Acute Fatty Liver of Pregnancy
	30: Sickle Cell Crisis
	31: Disseminated Intravascular Coagulopathy
	32: Thrombotic Thrombocytopenic Purpura,Hemolytic–Uremic Syndrome, and HELLP
	33: Endocrine Emergencies
	34: Complications of Pre-eclampsia
	35: Anaphylactoid Syndrome of Pregnancy (Amniotic Fluid Embolism)
	36: Systemic Lupus Erythematosus and Antiphospholipid Syndrome
	37: Trauma in Pregnancy
	38: Thermal and Electrical Injury
	39: Overdose, Poisoning and Envenomation During Pregnancy
	40: Hypovolemic and Cardiac Shock
	41: Septic Shock
	42: Anaphylactic Shock in Pregnancy
	43: Fetal Considerations in the Critically Ill Gravida
	44: Fetal Effects of Drugs Commonly Used in Critical Care
	45: Anesthesia Considerations for the Critically Ill Parturient with Cardiac Disease
	46: The Organ Transplant Patient in the Obstetric Critical Care Setting
	47: Ethics in the Obstetric Critical Care Setting
	48: Acute Psychiatric Conditions in Pregnancy
	49: Fetal Surgery Procedures and Associated Maternal Complications
	50: Cancer in the Pregnant Patient
	51: Pregnancy in Women with Complicated Diabetes Mellitus
	52: Biological, Chemical, and Radiological Attacks in Pregnancy
	Index
                        
Document Text Contents
Page 381

c27f002.eps


Acute Pancreatitis

369

cysts, hemorrhage, thrombophlebitis, and abcess formation [36]
and provide guidance for directed sampling of abscess cavities
(Figures 27.1 & 27.2 ). CT is also useful in differentiating pancre-
atitis from other intra - abdominal pathologies.

The role of ultrasound is typically quite limited in the initial
evaluation of patients who have pancreatitis, because the pan-
creas often is obscured by bowel gas. Additionally, the pancreas
may have an entirely normal sonographic appearance in the acute
phase. In patients suspected of having acute pancreatitis, the
primary role of ultrasound is to assess for gallstones and biliary
obstruction [36] .

Differential d iagnosis
Abdominal complaints in pregnancy present unique diagnostic
challenges (Table 27.3 ). Non - obstetric conditions include acute

rated these fi ndings, noting no difference in amylase activity
related to pregnancy. Lipase levels were also studied, and no
signifi cant difference was found between the second and third
trimesters or compared with non - pregnant controls, although
one study noted a lower lipase level in the fi rst trimester [34] .
Mean values of lipase in 175 women were approximately 12 IU/L,
with none exceeding 30 IU/L.

As a screening tool for acute pancreatitis, urinary trypsino-
gen - 2 has also been evaluated in the general population. Using a
dipstick test for urinary trypsinogen - 2, Kemppainen et al. [35]
evaluated 500 consecutive patients presenting to the emergency
room with abdominal pain. The authors found 94% sensitivity
and 95% specifi city in detecting acute pancreatitis. While requir-
ing further study, the 99% negative predictive value achieved with
this urinary dipstick test may prove a useful adjunctive test to
standard serum evaluation of amylase and lipase.

Leukocytosis, hyperglycemia, hyperbilirubinemia, abnormal
coagulation tests, and elevated liver enzymes may also be present.
Although other diseases can result in abnormal values, amylase
and lipase remain the cornerstone of diagnosis. These values are
typically elevated more than threefold over normal.

Radiologic e valuation
While the diagnosis of acute pancreatitis is based on clinical sus-
picion, physical examination, and elevated amylase and lipase,
radiologic tests aid in the confi rmation of acute pancreatitis and
can be used to monitor the development and progression of
complications. A plain fi lm of the abdomen may show dilation
of an isolated loop of intestine (sentinel loop) adjacent to the
pancreas. Pleural effusions may be detected on chest X - ray.

Computed tomography (CT) is considered the radiographic
procedure of choice for determining the extent or the severity of
the pancreatitis [36] . Since CT is unhindered by bowel gas pat-
terns, CT scans can demonstrate pancreatic necrosis, pseudo-

L

Figure 27.1 Computed tomography scan demonstrating necrosis in the head
of the pancreas (curved arrow) and free fl uid in the anterior pararenal space
(straight arrow). (Courtesy of Dr Paula Woodward.)

Figure 27.2 Computed tomography scan demonstrating pseudocyst in the tail
of the pancreas (arrow). (Courtesy of Dr Paula Woodward.)

Table 27.3 Differential diagnosis of acute pancreatitis.

Non - obstetric conditions
Acute cholecystitis
Appendicitis
Biliary colic
Intestinal obstruction
Duodenal ulcer
Splenic rupture
Mesenteric vascular occlusion
Perinephric abscess
Pneumonia
Pulmonary embolus
Myocardial infarction
Diabetic ketoacidosis

Obstetric conditions
Pre - eclampsia
Ruptured ectopic pregnancy
Hyperemesis gravidarum

Page 382

Chapter 27

370

atitis. Utilizing color charts, Mayer and McMahon [43] identifi ed
90% of the patients who subsequently died and 72% of patients
with severe morbidity.

Biochemical indicators that have been evaluated as predictors
of severity of disease include C - reactive protein [44 – 46] , tryp-
sinogen activation peptide [47 – 49] , procalcitonin [50,51] , throm-
bomodulin [45] , and serum amyloid A [46] . Only C - reactive
protein is currently used clinically, but is limited in that it is
predictive only after 48 – 72 hours following onset of symptoms.
While interleukin - 6, trypsinogen activation peptide and granulo-
cyte nuclear elastase all show promise in acutely identifying
patients destined for a severe clinical course, they await confi rma-
tory trials and widespread acceptance into routine clinical use.

Compared with scoring systems and laboratory markers, con-
trast - enhanced CT scans offer broader information regarding
intra - abdominal anatomy. Location and extent of necrosis are
identifi ed and can be serially evaluated (see Figure 27.1 ). Infection
within pseudocysts is suggested by evidence of gas production.
This test, however, may be limited in its availability and is diffi cult
to obtain in severely ill patients.

cholecystitis, duodenal ulcer (including perforation), appendici-
tis, splenic rupture, perinephric abscess, mesenteric vascular
occlusion, pneumonia, diabetic ketoacidosis, biliary colic, and
intestinal obstruction. In the pregnant patient, pre - eclampsia,
hyperemesis gravidarum, and ruptured ectopic pregnancy must
be added to the differential diagnosis.

Preeclampsia may mimic pancreatitis with upper abdominal
pain, nausea, and vomiting. Concomitant hypertension, protein-
uria, and edema, however, will usually be present. Hyperemesis
gravidarum most often affects patients in the fi rst trimester,
without a signifi cant component of pain. Ruptured ectopic preg-
nancy may produce symptoms similar to those seen in acute
pancreatitis. Hemoperitoneum can occur with either and may
require laparotomy for diagnosis. But ruptured ectopics are not
typically associated with an elevated lipase.

Prognostic i ndicators

Several methods utilizing clinical and laboratory data have been
developed to indicate the severity of acute pancreatitis and allow
refi nement of prognosis [37 – 39] . The most widely used criteria
were developed by Ranson (Table 27.4 ). The number of criteria
met correlates with the mortality risk for the individual. For non -
gallstone pancreatitis, patients with fewer than three signs have
rates of mortality less than 3% and morbidity less than 5%.
Patients with three or more positive signs carry a 62% mortality
rate and a 90% morbidity rate. Utilizing a modifi ed set of criteria
for gallstone pancreatitis, individuals with fewer than three signs
have a 1.5% mortality rate, while those with three or more signs
demonstrate a 29% mortality rate. Critics of this system cite poor
sensitivity, specifi city, delayed assessment (due to the labs
required at 48 hours), and inability to perform repeated assess-
ments as major deterrents to its usefulness.

Another method of clinically evaluating the severity of several
types of critical illnesses, including pancreatitis, is the Acute
Physiology and Chronic Health Evaluation (APACHE) III criteria
[40] . Unlike Ranson ’ s criteria [37 – 39] , the APACHE assessment
[40] can be updated and the patient ’ s course monitored on a
continuing basis. This system evaluates several variables, both
biochemical and physiologic, and calculates scores based on devi-
ation from normal values. A 5 - point increase in score is indepen-
dently associated with a statistically signifi cant increase in the
relative risk of hospital death within a specifi c disease category.
Within 24 hours of admission, 95% of patients admitted to the
intensive care unit could be given a risk estimate for death within
3% of that actually observed [40] . Although more complex and
computer dependent, the APACHE scoring system appears more
accurate than Ranson ’ s criteria in predicting morbidity [41] . The
addition of body mass index seems to improve prediction as
obesity predicts severity [42] . Several single prognostic indicators
have been investigated in order to achieve early identifi cation of
pancreatic necrosis. Paracentesis can be performed; return of
dark, prune - colored fl uid is characteristic of necrotizing pancre-

Table 27.4 Clinical indicators of poor prognosis: Ranson ’ s criteria [36 – 38] .

Non - gallstone pancreatitis
On admission
Age > 55 y
WBC > 16 000/mm 3
Glucose > 200 mg/dL
LDH > 350 IU/L
AST > 250 IU/L

Within 48 h
Decrease in hematocrit > 10%
Increase in BUN > 5 mg/dL
Calcium < 8 mg/dL
P a O 2 < 60 mmHg
Base defi cit > 4 mmol/L
Fluid defi cit > 6 L

Gallstone pancreatitis
On admission
Age > 70 y
WBC > 18 000/mm 3
Glucose > 220 mg/dL
LDH > 400 IU/L
AST > 250 IU/L

Within 48 h
Decrease in hematocrit > 10%
Increase in BUN > 2 mg/dL
Calcium < 8 mg/dL
Base defi cit > 5 mmol/L
Fluid defi cit > 4 L

AST, aspartate amino transferase; BUN, blood urea nitrogen ; LDH, lactic
dehydrogenase.

Page 761

Index

749

stroke volume index 34
strychnine poisoning 527
subarachnoid hemorrhage 241–4

aneurysm 245

arteriovenous malformations 245–6

clinical presentation 242

diagnosis 242–3

during pregnancy 241–2

imaging 243

laboratory evaluation 243

management 243–4

intracranial pressure 244

mannitol 244

nimodipine 243–4

surgical 244

neurologic status 242, 242
prognosis 244

subclavian vein, cannulation 158–9, 159

substituted judgement 666

suicidality 687–9

assessment and management 688–9

pregnancy and postpartum 689

risk factors 687
self-injurious behavior 688

sulfi ting agents, anaphylaxis 598
supine hypotensive syndrome 37

surfactant therapy 344

sympathomimetics, overdose 522
synchronized intermittent mandatory ventilation

132, 132

systemic infl ammatory response syndrome 571–2,

573
systemic lupus erythematosus 475–9

aetiology 475

diagnosis 477–8, 477
exacerbation during pregnancy 475–6

neonatal 476–7

obstetric complications 476

treatment 478–9

fl ares 479, 479
glucocorticoids 478

hydroxychloroquine 478

immunosuppressants 478

NSAIDs 478–9

systemic vascular resistance 34, 38, 39, 258, 258
pregnancy adaptations 35–6, 36

systolic hypertension, severe 237–8

T-tube 129
tachycardia, fetal 606–8, 607, 608

tacrolimus 658
tension pneumothorax 497

terbutaline 331

tetralogy of Fallot 264–5, 642

theophylline

asthma 331

overdose 524
thermal management

post-resuscitation 120

pre-resuscitation 112–13, 114

thermal/electrical injury 508–13

classifi cation 508–9

chemical burns 509

electrical burns 509

thermal burns 508, 509, 509

complications

fetal 512–13

maternal 511–12

fetal distress 617–18, 617, 618
management 510–11

infl ammation-infection period 511

postresuscitation period 510–11

rehabilitation 511

resuscitation period 510

maternal concerns 509–10

cardiovascular system 509

respiratory system 509–10

skin 510

rule of nines 508, 509
thiamine, overdose 521
thrombasthenin 286

thrombin 286

thrombin-antithrombin 401
thromboembolic disease 283–301

anticoagulant therapy 293–300, 293
antepartum management 297–8, 298
heparin 293–4, 293
intrapartum management 298–9

low molecular weight heparin 294–5, 294
postpartum management 299

prophylaxis 299–300

selective factor Xa inhibitors 297

warfarin 296–7, 296, 297
incidence and risk factors 283–5, 284, 284, 285,

285
surgical intervention 301

thrombolytic therapy 300–1, 300
thrombophilias 287–8

see also deep venous thrombosis; pulmonary

embolism

thromboembolism 138–9

thrombolytic therapy 103, 240

fetal effects 633

ischemic stroke 246

thromboembolic disease 300–1, 300
thrombophilias 287–8

thromboplastin 286

thrombosis, catheter-related 176–7

thrombotic thrombocytopenic purpura 381, 407–16

causes and pathophysiology 408–13

von Willebrand factor and ADAMTS-13

408–12, 409–11, 412
clinical features 407

differential diagnosis 415–16

laboratory fi ndings 407, 408

obstetric issues 415

treatment 413–15, 413
types 407–8, 408

thromboxane A2 286

thyroid dysfunction 428–31

hyperthyroidism 428–30, 429
hypothyroidism 430–1

thyroid gland, pregnancy adaptations 45–6

thyroid storm 431
thyroxine, fetal effects 634

tiagabine hydrochloride 223
tidal volume ventilation 115

tissue plasminogen activator 286

tocolytics, pulmonary edema 341

total body water 69

total lung capacity 42
total parenteral nutrition 184

complications 186
monitoring 186, 186

toxins/chemicals 735

transfusion see blood component transfusion

transfusion reactions 173–7

acute 173–6, 174, 175
allergic reactions 174–5

bacterial contamination 176

extravascular hemolytic reactions 174

febrile non-hemolytic 174

hemolytic reactions 173–4, 174
transfusion-related acute lung injury 176

delayed 176–7

graft-vs-host disease 177

hemolytic reactions 176–7

post-transfusion purpura 177

transfusion-related acute lung injury 176

transmissible spongiform encephalopathies, blood

transmission 178

transplant patients 656–63, 657
bone marrow transplantation 398, 661–2

cardiac transplantation 276, 277, 652–3, 661

fetal/neonatal welfare 662–3

immunosuppression 657–9, 658
labor and delivery 662

liver transplantation 660–1

lung transplantation 661

obstetric emergencies 662

pancreas transplantation 660

pregnancy outcome 660
prenatal care 656–7

prepregnancy evaluation 656, 657
renal transplantation 659–60, 659, 721

transposition of great vessels 265–6

transtracheal cannula 129
trauma 487–504

blunt abdominal 493–5

evaluation 493–4, 494, 495

fetal manifestations 493

motor vehicle accidents 493

uterine rupture 494–5

chest 496–8

airway management 497

blunt cardiac injury 498

cardiac tamponade 497–8

classifi cation 496–7, 497
fl ail chest 498

hemothorax 497

open pneumothorax 497

tension pneumothorax 497

head 499–503

brain injury mechanism 499

cerebral autoregulation 499

classifi cation 500
delivery considerations 502–3

diffuse brain injury 500

focal brain injury 500–1

general principles 501–2, 502

primary management 499–500

skull fractures 501

management 487, 488, 489–92

fetal evaluation 490–1

fetal patient 491

Page 762

Index

750

investigations 490

perimortem cesarean section 492, 492

primary survey 487, 489–90, 489
secondary survey and treatment 490

volume resuscitation 491–2

maternal physiologic adaptations 487,

488
orthopedic 503

penetrating abdominal 495–6

direct uterine injury 496

gunshot wounds 495–6

stab wounds 496

spinal 503–4

thermal/electrical see thermal/electrical injury

tricuspid regurgitation 267
tricuspid stenosis 267
Trousseau’s sign 83

tubular necrosis 378–9

twin-twin transfusion syndrome 701

ultrasound, spinal injury 230

uterine artery ligation 316–17, 316

uterine atony, treatment 312–14

emergency procedures 312–13

methylergonovine/ergometrine 313

misoprostol 314

oxytocin 313

prostaglandins 313–14

uterine contractions, during cardiopulmonary

bypass 199–200

uterine devascularization 315–16

uterine rupture 309–11

traumatic 494–5

uterine tamponade 315

uterine trauma 496

uteroplacental perfusion, and cardiopulmonary

bypass 198–9, 199, 200

uterus

Couvelaire 309

inversion 312

valproic acid 223
vancomycin, prophylaxis 641
vascular access 152–63

advantages of 153
arterial 159–61

axillary artery 161

brachial artery 161

dorsalis pedis artery 161

femoral artery 161

radial artery 159–61

catheter type 152–4, 153, 154
catheterization techniques 154–5, 156

complications 155–7, 156

catheter malposition 155–6

embolism 157

thrombosis, stenosis and occlusion 156–7

indications 153
preparation for catheter insertion 154

sites of

cephalic vein 159

external jugular vein 158

femoral vein 159, 160

internal jugular vein 157–8, 157, 158

subclavian vein 158–9, 159

skin preparation 154

vasodilators, fetal effects 632–3

vasopressin 100

vecuronium 143, 144
fetal effects 629

venous access systems, totally implantable 153

ventilation 24–9, 25, 26, 26, 28, 28, 124–47
acute lung injury/acute respiratory distress

syndrome 342–3

asthmatic patients 143–4

continuous positive airway pressure 128

extracorporeal membrane oxygenation 135–6

intubation 130

lung protective 136–7

neonate 111, 114–18, 117

continuous positive airway pressure 115–16

endotracheal intubation 117–18, 118
mask CPAP 116

positive end-expiratory pressure 115

positive-pressure ventilation 116–17, 117
resuscitation devices 116

room air vs 100% oxygen 118

tidal volume 115

pain control, sedation and paralysis 142–3

positive-pressure ventilation

neonate 116–17, 117
non-invasive 128–9, 129

in pregnancy 129–30

prolonged 120

prone 135

special considerations 137–42

cardiovascular complications 141

critical illness polyneuropathy and myopathy

138

fl uid balance 141–2

gastrointestinal haemorrhage 138

nutritional implications 140–1

oxygen toxicity 137

permissive hypercapnia 137–8

renal complications 139

thromboembolic complications 138–9

ventilator-associated pneumonia 139–40

ventilator-induced lung injury 137

weaning from 144–6

failure of 145–7, 146
prediction of outcome 145, 145
techniques 145

ventilation-perfusion lung scan 291–2, 292

ventilation/perfusion mismatch 124–5

ventilator modes 130–5

airway pressure release ventilation 133, 134

assist control 130–1, 131

controlled mechanical ventilation 130

high-frequency oscillatory ventilation 133–4

inverse ratio ventilation 132–3

positive end-expiratory pressure 134–5, 135
pressure support ventilation 132

pressure-regulated volume control ventilation

132

synchronized intermittent mandatory ventilation

132, 132

ventilator-associated pneumonia 139–40

ventilator-induced lung injury 137, 342

ventimask 129
ventricular arrhythmias 493

ventricular septal defect 260–1

vesicants 735

viral hemorrhagic fevers 734

virtual obstetric intensive care unit 14

vital capacity 42
vitamins 186
volume expanders, neonatal resuscitation

119

volume expanding agents 70–3, 70, 71
colloid solutions 72–3

crystalloid solutions 70–2, 70
von Willebrand disease 320–1

von Willebrand factor, thrombotic

thrombocytopenic purpura 408–12, 409–11,

412

warfarin 293
antidotes 526
drug interactions 297
fetal effects 633

side effects 296
thromboembolic disease 296–7, 296, 297

weight gain 182

Wernicke’s encephalopathy 75

West Nile virus 165

white cell count, pregnancy adaptations 45,

45
whole blood 71

transfusion 167

zafi rlukast 332

zileuton 332

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