done only if there is inadequate response to treatment or secondary
peritonitis is suspected. Albumin is recommended to decrease the incidence
of SBP-induced renal failure on day 1 (1.5 g/kg) and day 3 (1 g/kg) of
treatment in patients with Cr >1 mg/dL or total bilirubin >4 mg/dL.
WHAT DO I DO IF I’M CALLED ABOUT A
POSITIVE PERITONEAL CULTURE ON A PATIENT
SENT HOME?
Bacterascites is a term used to describe an ascitic fluid that is colonized with
bacteria (culture positive) but with a PMN count <250/mm3. The diagnosis is
delayed, usually 3 days after the original paracentesis when the culture
results become available. The current recommendations are to perform a
repeat paracentesis on day 3. Bacterascites is treated as SBP if, on the second
paracentesis, the PMN count is >250/mm3, or if the second culture is also
positive. If PMN count is <250/mm3 and cultures remain negative, no further
action is necessary.
KEY POINTS
SBP can present with vague complaints, not necessarily with
abdominal pain.
The leukocyte esterase test on urine dip allows for early diagnosis and
antibiotic administration.
Patients who have had one episode of SBP are at risk for another and
require lifelong prophylaxis.
Don’t mistake secondary peritonitis for SBP. If the ascitic fluid starts
to resemble pus (very high PMN count), a surgical emergency should
be considered.
SUGGESTED READINGS
Koulaouzidis A, Bhat S, Saeed AA. Spontaneous bacterial peritonitis. World J
Gastroenterol. 2009;15(9):1042–1049.
Lutz P, Nischalke HD, Strassburg CP, et al. Spontaneous bacterial peritonitis: The
clinical challenge of a leaky gut and a cirrhotic liver. World J Hepatol.
2015;7(3):304–314.
451
Wong CL, Holroyd-Leduc J, Torpe KE, et al. Does this patient have bacterial
peritonitis or portal hypertension? The rational clinical examination. JAMA.
2008;299:1166–1178.
452
87
ASCENDING CHOLANGITIS AKA
BILIARY SEPSIS AKA “THAT
OTHER PUS UNDER PRESSURE”
PRATHAP SOORIYAKUMARAN, MD
A classic “you’ll miss it if it’s not on your differential,” ascending
cholangitis refers to a bacterial infection of the biliary system, requiring both
obstruction and bacterial colonization of the biliary tract.
Normally, bile is sterile. Bile salts have bacteriostatic properties, and the
sphincter of Oddi controls the direction of bile flow, acting as a barrier
between the sterile bile duct and the bacteria-filled duodenum. Without
obstruction of the biliary system, ascending cholangitis does not occur. Even
bacterial colonization of the bile in the absence of obstruction does not
usually progress to clinical cholangitis. It’s still not always known how
bacteria enter an obstructed biliary system, but one clear way is when the
doctor does the dirty work by inadvertently interfering with the physiologic
barrier between the bile duct and the intestine via surgery, endoscopic
retrograde cholangiopancreatography (ERCP), or percutaneous transhepatic
cholangiography (PTC). Bacteria, of which the most common are
Escherichia coli, Klebsiella, Enterococcus, and Bacteroides, can also enter
the biliary system from the lymphatics or via portal vein blood. Once the
bacteria enter an obstructed bile duct, ascending cholangitis may result.
Who gets ascending cholangitis? You should think about it in any septic
patient who has signs and symptoms of biliary tract disease (often subtle),
especially if that patient is diabetic, elderly, or debilitated. Charcot was one
of the first physicians to describe cholangitis, or “hepatic fever” as he called
it, and he noted a constellation of symptoms that made up his triad:
453
intermittent fever with chills, right upper quadrant pain, and jaundice. Add
mental status changes and shock, and you get Reynolds pentad, which
confers a much graver prognosis without prompt decompression. The most
frequent symptoms with acute cholangitis are fever and abdominal pain
(approximately incidence of 80% in most reports). Clinical jaundice is less
frequently seen (~60% to 70%). Severe presentations (e.g., with shock and
altered mental status) are fortunately much less common (3.5% to 7.7%).
Cholangitis rarely presents classically, so it is an important consideration in
any septic patient without an obvious source. Importantly, the most severe
cases are often the most difficult to detect as the patient may be too sick to
help the clinician localize the infection of history and physical examination.
Bedside ultrasound examination may be particularly helpful in this scenario
as a screen for biliary pathology in the septic patient with altered mental
status.
The causes of biliary obstruction are many. Common causes are outlined
in Table 87.1.
TABLE 87.1 CAUSES OF BILIARY OBSTRUCTION
And don’t forget, kids can get ascending cholangitis too! Kids who have
undergone surgical Roux-en-Y procedures (such as the Kasai procedure for
biliary atresia) and those with indwelling catheters or failure to thrive are at
increased risk.
Once you suspect cholangitis, you’ll be tasked with differentiating it
from cholecystitis, both of which can present very similarly. An elevated
bilirubin is more characteristic of cholangitis. Ultimately, though, ultrasound
evidence of dilated common and intrahepatic bile ducts usually is required to
distinguish cholangitis from cholecystitis.
The keys to treatment include hemodynamic stabilization, broad-
spectrum antibiotics, admission to a monitored setting (ICU often), and
454
ultimately biliary tract decompression (surgery, interventional radiology,
gastroenterology). These patients are sick, and if you don’t make the
diagnosis, they will not do well!
KEY POINTS
Consider in any septic patient without another source.
Think of risk factors leading to obstruction of the biliary system, and
include cholangitis in your differential for septic kids too.
Differentiating cholangitis from cholecystitis: look for elevated
bilirubin and ultrasound evidence of biliary duct dilation in
cholangitis.
ERCP can be the cause and the cure!
SUGGESTED READINGS
Flemma RJ, Flint LM, Osterhout S, et al. Bacteriologic studies of biliary tract
infection. Ann Surg. 1967;166(4):563–572.
Kiriyama S, Takada T, Strasberg SM, et al. TG13 guidelines for diagnosis and
severity grading of acute cholangitis (with videos). J Hepatobiliary Pancreat
Sci. 2013;20(1):24–34.
Lai EC, Mok FP, Tan ES, et al. Endoscopic biliary drainage for severe acute
cholangitis. N Engl J Med. 1992;326:1582–1586.
Mosler P. Diagnosis and management of acute cholangitis. Curr Gastroenterol
Rep. 2001;13(2): 66–72.
455
88
ACALCULOUS CHOLECYSTITIS: NO
STONES, NO PROBLEMS?
CHRISTOPHER MARTIN, MD AND LAUREN LONGYEAR,
BS
The diagnosis and epidemiology of acute calculous cholecystitis have been
drilled into us since the early days of medical school. Every review book
ever published has the mnemonic: Fat, Fertile, Forty, Family history, and
Female. However, the discussion about acalculous cholecystitis has typically
been short and inadequately summarized by: “it’s an ICU diagnosis in the
critically ill.” The reporting and description of acalculous cholecystitis has
evolved along with the advancement of its care. Duncan initially described it
in 1844 in a patient who underwent a femoral hernia repair. Later, there was
increased reporting and awareness during the Vietnam War in soldiers
surviving sepsis and traumatic injuries. With the rise of intensive care units,
the prevalence of acalculous cholecystitis also grew. Now that modern
medicine allows patients to live longer with multiple comorbidities, we have
even seen this disease in the outpatient setting. The key to diagnosis starts
with an awareness of the unique set of risk factors these patients have (see
Table 88.1).
TABLE 88.1 RISK FACTORS ASSOCIATED WITH ACALCULOUS
CHOLECYSTITIS
456
Acalculous cholecystitis is a surgical emergency—a good prognosis
hinges on early recognition and appropriate surgical treatment. It is estimated
that acalculous cholecystitis comprises about 10% of all cholecystitis cases.
In one study, within a 7-year period, 77% of all patients identified with
acalculous cholecystitis presented in the outpatient setting. Importantly, 45%
of those patients were ultimately admitted without the diagnosis of
cholecystitis.1 If specific treatment is delayed, this disease has a mortality
rate as high as 65%, whereas, with early intervention, mortality is ~7%.2
Contrast this with commonly reported numbers of 1.5% to 3% mortality for
calculous cholecystitis.1 Acalculous cholecystitis is a rare entity, but it is
important to keep in mind in patients with sepsis due to an unclear source,
especially in the setting of abdominal pain.
The pathophysiology of acalculous cholecystitis is thought to start with
an acute or acute-on-chronic condition that leads to endothelial injury and
gallbladder ischemia. The lack of perfusion creates stasis in the gallbladder,
increased distention, and a localized inflammatory response. Some
hypothesize that the bile salts and their by-products are toxic to the
gallbladder when stasis occurs. Once cholecystitis has set in, a secondary
bacterial infection can occur, usually with coliforms and anaerobes
(commonly Escherichia coli and Klebsiella pneumoniae).2 The exact nature
and mechanism of the bacterial infection are not fully understood.
Nevertheless, antibiotics are still considered a mainstay of treatment.
The clinical presentation can be varied, but most commonly, it consists
of right upper quadrant abdominal pain, fever, jaundice, nausea, vomiting,
and occasionally septic shock. Physical examination may find a palpable
right upper quadrant mass and laboratory tests may show leukocytosis and
elevated liver enzymes. Inpatients are more apt to have the major identifying
risk factors: burns, trauma, nonbiliary surgeries, use of inotropes, mechanical
ventilation, or childbirth. It is most certainly more difficult to pick these
patients out in the outpatient and emergency department (ED) settings.
457
Acalculous cholecystitis is more common in males (1:1 to 2.8:1 male to
female predominance), advanced age (average age is in the 60s),
cardiovascular disease, diabetes, hypertension, peripheral vascular disease,
alcoholic liver disease, and COPD.1,2 These cases can be complicated by the
patient being demented or developmentally delayed, which may prevent an
adequate history and physical exam. In children, acalculous cholecystitis
may present as a complication of Epstein-Barr virus (EBV) infection.3
Patients with acquired immunodeficiency syndrome (AIDS) may also present
with a nonspecific infectious prodrome and upper abdominal pain with
acalculous cholecystitis secondary to an opportunistic infection, though it is
more common for these patients to have cholangitis.
Diagnostic imaging is critical in making the diagnosis early. One study
evaluating computed tomography (CT), ultrasound, and scintigraphy found
that ultrasound (sensitivity 92%, specificity 96%) and CT (sensitivity 100%,
specificity 100%) were both excellent diagnostic modalities but that
scintigraphy suffered from poor specificity (38%).4 Often, at the time of
diagnosis, the differential remains broad and a CT scan may offer further
diagnostic assessment for other possibilities on the differential.
On a positive note, once the diagnosis is made, the treatment remains
similar to that of calculous cholecystitis. Antibiotics should be initiated to
cover coliforms and anaerobes, typically a beta-lactam with a beta-lactamase
inhibitor. Surgical consultation is necessary to decide whether the patient
should be taken to the operating room for cholecystectomy versus an
interventional radiology–guided cholecystostomy.1 This decision usually
revolves around the patient’s comorbidities and perioperative risk.
Complications such as emphysematous cholecystitis and perforated
gallbladder can drastically alter the patient’s course and treatment plan,
further reinforcing the importance of early diagnosis in the ED.
KEY POINTS
Not all cholecystitis is caused by gallstones.
Many patients with acalculous cholecystitis may present from the
outpatient setting.
Once the diagnosis is made, initiate broad-spectrum antibiotics and
obtain early surgical consultation.
458
REFERENCES
1. Savoca PE, Longo WE, Zucker KA, et al. The increasing prevalence of
acalculous cholecystitis in outpatients. Results of a 7-year study. Ann Surg.
1990;211:433.
2. Wang AJ, Wang TE, Lin CC, et al. Clinical predictors of severe gallbladder
complications in acute acalculous cholecystitis. World J Gastroenterol.
2003;9:2821.
3. Yi DY, Kim JY, Yang HR. Ultrasonographic gallbladder abnormality of
primary Epstein–Barr virus infection in children and its influence on clinical
outcome. Celis MJC, ed. Medicine (Baltimore). 2015;94(27):e1120.
4. Mirvis SE, Vainright JR, Nelson AW, et al. The diagnosis of acute acalculous
cholecystitis: A comparison of sonography, scintigraphy, and CT. AJR Am J
Roentgenol. 1986;147:1171.
459
89
ANTICIPATE BLEEDING AND
REVERSE COAGULOPATHIES IN
PATIENTS WITH LIVER FAILURE
DEREK K. RICHARDSON, MD, MPH AND BARRY
SCHLANSKY, MD, MPH
Coagulopathy of liver disease leads to troubles as dramatic as large-volume
hematemesis in a resuscitation bay or as indolent and irritating as a slowly
oozing bleed around a central line on a boarded patient waiting for transfer
out of the emergency department (ED). By evaluating, anticipating, and
correcting bleeding diatheses when appropriate, the emergency physician
(EP) can help the patient achieve hemostasis and avoid these untoward
outcomes.
Blood clotting in the setting of chronic liver disease is complex and may
result in a net prothrombotic or antithrombotic state. Favoring bleeding are
reductions in hepatically produced procoagulant factors (II, VII, IX, and X)
and fibrinogen, as well as thrombocytopenia due to reduced thrombopoietin
production, splenic sequestration, and production of antiplatelet antibodies.
Favoring thromboses are reductions in a strong anticoagulant factor (protein
C) and increased platelet activation due to elevated von Willebrand factor
levels. Complicating this situation is the lack of accurate lab assays to
measure the net thrombotic state in liver disease patients. The international
normalized ratio (INR) was validated as a standardized measure of
anticoagulation for patients treated with Coumadin, but it is not calibrated to
assess coagulopathy in liver disease patients. Indeed, the risk of venous
thromboembolism in hospitalized chronic liver disease patients is higher than
for hospitalized patients without liver disease, indicating that a prothrombotic
460
state is also frequently present. Despite these issues, transfusion of blood
products to correct these coagulation abnormalities is recommended when
active bleeding is present.
EVALUATION OF COAGULOPATHY
Fortunately for the goal-oriented provider, a small number of crucial
laboratory tests are needed for rapid coagulopathy assessment in the ED. Any
patient with liver failure either actively bleeding or at risk of bleeding should
have the following tests sent: prothrombin time/INR, fibrinogen level, and
platelet count. A full battery of testing may help guide further evaluation and
management down the road, but acute interventions will focus on these three
tests.
ANTICIPATING NEED FOR CORRECTION
Patients with liver failure generally compensate for coagulopathy, and
corrective medications or blood products should not be administered to
patients without an active or anticipated source of bleeding, such as planned
invasive procedures. Acute correction is indicated for patients bleeding from
gastrointestinal, traumatic, or iatrogenic sources. Procedures with a high risk
of harmful bleeding include central lines, lumbar punctures, and intracranial
monitor placement; the urgency of these procedures must be weighed against
the risk of waiting for correction of coagulopathy. Lower-risk procedures
such as paracentesis and peripheral vascular access do not necessitate
correction.
APPROPRIATE SELECTION OF TREATMENT
Treatment based on laboratory abnormalities is summarized in Table 89.1.
TABLE 89.1 LABORATORY ABNORMALITIES AND TREATMENT
461
Interventions based on the fibrinogen level and platelet count are fairly
straightforward. If the fibrinogen level is under 100 mg/dL and the patient
warrants correction, cryoprecipitate should be given with weight-based
dosing. This is typically around ten units. If the platelet count is <50 × 109/L
during active or anticipated bleeding, 1 unit of platelets should be
administered. Certain very high-risk procedures, such as ICP monitor
placement, may warrant a higher platelet goal of >100 × 109/L. For patients
without active or anticipated bleeding, platelet transfusion should be
considered only for a platelet count of <10 × 109/L.
Treating coagulopathy based on INR is more complicated, due to the
multifactorial nature of delayed hemostasis and lack of consensus
recommendations. Fresh frozen plasma (FFP) is the frontline therapy for
active or anticipated bleeding with INR over 2.0. Of note, the large volume
of FFP required to treat coagulopathy may cause volume overload, which can
worsen portal hypertension and bleeding due to gastroesophageal varices.
Recombinant factor 7 may be considered in the case of life-threatening
bleeding, but outcome-based research remains limited and this agent is
extremely expensive. The role for other agents, including prothrombin
complex concentrates, is currently under investigation.
Although total vitamin K deficiency is not directly caused by chronic
liver disease, it frequently accompanies the malnourishment that occurs with
chronic alcohol abuse. Administration of parenteral (intravenous,
intramuscular, or subcutaneous) vitamin K should therefore be considered in
alcoholic patients with active bleeding when the INR is elevated, regardless
of whether liver disease is present.
Coagulopathy in patients with liver failure is complex due to imbalances
462
in both procoagulant and anticoagulant pathways. In the setting of active or
anticipated bleeding, the EP should evaluate the PT/INR, fibrinogen, and
platelet counts in these patients and prudently correct abnormalities based on
the clinical scenario and the severity of bleeding or anticipated procedural
risk.
KEY POINTS
If your patient has liver disease, anticipate both bleeding and clotting.
Check PT/INR, fibrinogen levels, and platelet count in all patients at
risk of bleeding.
Correct coagulopathies judiciously and with appropriate therapy.
SUGGESTED READINGS
Dasher K, Trotter JF. Intensive care unit management of liver-related coagulation
disorders. Crit Care Clin. 2012;28:389–398.
De Gasperi A, Corti A, Mazza E, et al. Acute liver failure: managing coagulopathy
and the bleeding diathesis. Transplantation Proceedings. 2009;41:1256–1259.
Munoz SJ, Stravitz RT, Gabriel DA. Coagulopathy of acute liver failure. Clin Liver
Dis. 2009;13:95–107.
Northup PG, Caldwell SH. Coagulation in liver disease: a guide for the clinician.
Clin Gastroenterol Hepatol. 2013;11:1064–1074.
463
90
BOERHAAVE SYNDROME: NOT ALL
LIFE-THREATENING CHEST PAIN
INVOLVES THE HEART AND LUNGS
CHRISTOPHER J. COYNE, MD, MPH
Boerhaave syndrome is a spontaneous rupture of the esophagus. It usually
results from barotrauma related to retching or any sudden increase in intra-
abdominal pressure against a closed glottis. Esophageal perforations are rare
and Boerhaave syndrome even rarer, accounting for only about 15% of cases.
However, the mortality from this disease varies from ~8% to 60% and
increases significantly if care is delayed. Although we have known about this
syndrome for over 200 years, its associated morbidity and mortality remain
high due to its nonspecific presenting symptoms and resulting delays in
diagnosis.
Classically, we associate Boerhaave syndrome with retrosternal chest
pain, vomiting, and subcutaneous emphysema (Mackler triad). Like with
many other difficult diagnoses, these classic symptoms seldom present all
together. Approximately 25% to 45% of patients have no history of
vomiting, and even fewer have subcutaneous emphysema. The diagnosis of
Boerhaave syndrome should be suspected in any patient who presents with
retrosternal chest pain, neck pain, or epigastric pain, especially if it began
after an episode of severe retching or bearing down against a closed glottis
(weight lifting, defecation, childbirth, etc.). The location of pain generally
correlates with the location of esophageal rupture, which most commonly
occurs in the distal left posterolateral portion. Be aware that the severity of
symptoms may vary widely depending on the time from the actual rupture,
ranging from simple retrosternal pain, to respiratory collapse, septic shock,
and multisystem organ failure.
464
The key to diagnosing Boerhaave syndrome is merely to consider the
diagnosis. Many cases, however, are diagnosed incidentally on chest
radiographs that reveal mediastinal air, subcutaneous emphysema, a
pneumothorax, or a pleural effusion. Although the gold standard of diagnosis
remains the contrast esophagram (with Gastrografin), computed tomography
(CT) has become more readily available, and a chest CT can often suggest an
esophageal perforation through the detection of esophageal edema,
periesophageal fluid, or air in the mediastinal or pleural spaces. Additionally,
if clinical suspicion is high, CT esophagography can be performed using
diluted oral contrast to allow visualization of the specific site of perforation.
Although endoscopy may aid in the diagnosis of Boerhaave syndrome, it is
generally not recommended due to the risk of extending the esophageal tear
through insufflation or direct trauma.
Once the diagnosis of Boerhaave syndrome is established, treatment
should proceed rapidly. Even if a patient initially looks stable,
decompensation may be rapid. Patients with Boerhaave syndrome should be
regarded as critically ill and be monitored closely, especially in regard to
their respiratory status. Many will present dehydrated and will require
intravenous fluids while remaining NPO (nothing by mouth). Broad-
spectrum intravenous antibiotics should be initiated early including coverage
of enteric organisms. Intravenous proton pump inhibitors may also be
considered, so as to decrease the severity of chemical mediastinitis and
pleuritis.
Ultimately, the definitive treatment of Boerhaave syndrome is rapid
surgical or endoscopic repair. A surgical consultation should be placed early
once the diagnosis is suspected, given that early repair has been shown to
decrease morbidity and mortality. Nevertheless, in certain subgroups of
esophageal perforation, such as cervical perforation, or contained perforation
with limited extraluminal extravasation of fluid, nonoperative management
may be considered.
KEY POINTS
Boerhaave syndrome is a rare disease that is almost universally fatal if
treatment is not performed.
Consider this syndrome in any patient that presents with retrosternal
pain.
Recognize that these patients are sick (or soon will be).
Initiate intravenous fluids and broad-spectrum antibiotics early in the
465
course of treatment.
Consult surgery as soon as the diagnosis is suspected for expedited
surgical or endoscopic repair.
SUGGESTED READINGS
Brinster CJ, Singhal S, Lee L, et al. Evolving options in the management of
esophageal perforation. Ann Thorac Surg. 2004;77(4):1475–1483.
Garas G, Zarogoulidis P, Efthymiou A, et al. Spontaneous esophageal rupture as
the underlying cause of pneumothorax: Early recognition is crucial. J Thorac
Dis. 2014;6(12):1655–1658.
Schweigert M, Beattie R, Solymosi N, et al. Endoscopic stent insertion versus
primary operative management for spontaneous rupture of the esophagus
(Boerhaave syndrome): An international study comparing the outcome. Am
Surg. 2013;79(6):634–640.
Tonolini M, Bianco R. Spontaneous esophageal perforation (Boerhaave syndrome):
Diagnosis with CT-esophagography. J Emerg Trauma Shock. 2013;6(1):58–60.
Wilson RF, Sarver EJ, Arbulu A, et al. Spontaneous perforation of the esophagus.
Ann Thorac Surg. 1971;12(3):291–296.
466
91
CAUSTIC INGESTIONS: DON’T
MAKE IT WORSE
ERIKA FLORES URIBE, MD AND
CHRISTOPHER R. PEABODY, MD, MPH
The 5,000 to 15,000 caustic ingestions (CI) per year in the United States
occur in both children and adults. Eighty percent of these ingestions occur
accidentally in children from 1 to 5 years old, and the rest typically occur
intentionally in adults greater than 21 years old. Serious ingestions can
immediately result in perforation, shock, and even death. Intentional
ingestions in adults tend to have more serious consequences. Long-term
complications can lead to strictures and an increased risk of esophageal
cancer. In the emergency department (ED), we need to be aware of the
atypical presentations of CI in children and be prepared for the immediate
resuscitation of high-volume ingestions in adults.
Caustic materials cause tissue injury by chemical reaction. These
materials are generally acidic or alkaline. The severity of tissue injury is
determined by pH, concentration, duration of contact, amount, and physical
form of the ingested substance. Acids cause coagulative necrosis, which
results in a self-limiting burn pattern, while alkaline materials induce
liquefactive necrosis with diffusion into deeper layers of the injured mucosa
(see Table 91.1). Even low concentrations of alkaline ingestion can cause
extensive injury.
TABLE 91.1 ALKALINE AND ACIDIC CAUSTIC INGESTIONS
467
CI can provoke injury from the mouth, the airway, down through the
esophagus to the small intestine. Depending on the quantity, intent, and
timing of the caustic ingestion, patients may present with a myriad of
symptoms. Obvious burns to the lips, mouth, and oropharynx may occur, but
do not be fooled if these signs are not present. Adults with intentional
ingestions without any oropharynx involvement may have significant
esophageal involvement (think about a fast intentional ingestion, where the
liquid does not burn the oropharynx). Furthermore, laryngeal or epiglottic
edema may present with stridor, dysphonia, hoarseness, dyspnea, and
drooling, leading to respiratory distress and impending airway obstruction.
Severe CI can cause esophageal perforation and may present with abdominal
pain, rigidity, substernal chest pain, or back pain.
While the diagnosis is obvious when the history is clear, there are case
reports of children presenting with symptoms of allergic reaction, being
treated as anaphylaxis and later found to have a CI. Thus, in children
presenting with allergic symptoms not improving with treatment, CI should
be considered in the differential, as the initial presentation is similar and
468
otherwise can be easily missed. Unfortunately, even if the clinician considers
CI, there is currently no definitive way to establish the diagnosis in the
emergent setting if the ingestion is not reported. Radiographs can help
provide information regarding perforation but are not always diagnostic.
Only through direct visualization (usually by endoscopy) can the definitive
diagnosis of CI be made. When performed within the first 72 hours after
ingestion, endoscopy stages pathology and identifies the need for further
intervention. If patients have any oropharyngeal injury, drooling, vomiting,
dysphasia, or pain, a high-grade injury is likely, and urgent endoscopy should
be performed to determine if surgical intervention is required.
The only management of CI that has reached consensus is to avoid
agents that induce vomiting, such as ipecac, as this can lead to esophageal
perforation. In the ED, the provider should attempt to identify the ingested
product and the concentration of active ingredients. Further injury can result
from attempting to neutralize the substance by using a weak acid or base and
should be avoided. Moreover, diluents should not be used with any caustic
ingestion. Because of poor adsorption and endoscopic interference, activated
charcoal is also not given in caustic ingestions.
When managing CI, remember to evaluate the patient’s airway first.
Equipment for endotracheal intubation and cricothyrotomy should be readily
available. If significant edema is present, consider fiberoptic-assisted
intubation. Always place the patient NPO (nothing by mouth) until the extent
of injury can be determined. If a suicide attempt is suspected, consider
ethanol, salicylate, and acetaminophen levels as well as a psychiatric
evaluation. In some cases, salicylate ingestion has been shown to
independently cause stricture formation. With large-volume liquid acid
ingestions, nasogastric tube suction may be beneficial, but its use needs to be
weighed against the risk of esophageal perforation. Aggressive hydration and
medications to decrease acid production are given to prevent reflux-
associated injury, while steroids remain controversial.
KEY POINTS
Do NOT induce emesis, use ipecac, give charcoal, or attempt to
neutralize the ingested substance by using a weak acid or base.
In children: consider CI in patients who present with symptoms of
anaphylaxis that do not improve with treatment.
Endoscopy is indicated within 24 to 48 hours for any patient who is
symptomatic (or asymptomatic with an alkali), children refusing to eat
469
or drink, or patients with altered mental status.
SUGGESTED READINGS
Bonnici KS, Wood DM, Dargan PI. Should computerised tomography replace
endoscopy in the evaluation of symptomatic ingestion of corrosive substances?
Clin Toxicol (Phila). 2014;52(9):911–925.
Lupa M, Magne J, Guarisco JL, Amedee R. Update on the diagnosis and treatment
of caustic ingestion. Ochsner J. 2009;9(2):54–59.
Sherenian MG, Clee M, Schondelmeyer AC, et al. Caustic ingestions mimicking
anaphylaxis: Case studies and literature review. Pediatrics.
2015;135(2):e547–e550.
Waasdorp Hurtado CE, Kramer RE. Salicylic acid ingestion leading to esophageal
stricture. Pediatr Emerg Care. 2010;26(2):146–148.
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92
INGESTED FOREIGN BODIES:
WHEN TO INTERVENE?
BRIAN DOANE, MD
Swallowed foreign body impaction occurs most commonly in children and
edentulous or otherwise impaired adults. In adults, by far and away the most
common foreign body ingestion is a meat bolus impacting a preexisting
anatomic structure, and in children, the most common foreign body ingestion
is coins. While most of these ingestions will pass spontaneously, nearly 20%
will require endoscopy and 1% will require surgical removal. The
manifestations are surprisingly broad and include the typical presentation of
dysphagia and neck tenderness after eating, but can also include choking,
wheezing, respiratory distress, or even a relatively asymptomatic patient. To
make matters worse, this is a patient population that quite often is not able to
provide an accurate history.
The esophagus naturally narrows at three places: the upper esophageal
sphincter, the aortic arch, and at the diaphragm. All of these sites are
common areas for impaction; however, many impactions, particularly
recurrent ones, are secondary to webs, strictures, or masses. While an acute
presentation is more common, partially obstructing lesions can present in a
delayed fashion (days later) and are at higher risk for esophageal perforation.
The clinical history is not always sufficient. These patients are often
elderly, are very young, or have a psychiatric diagnosis that would make
their clinical history less reliable. In the vast majority of cases, a screening
radiograph is appropriate. Be aware that many foreign bodies are not
radiopaque! These include fish bones, most pills, and meat boluses.
Therefore, a negative radiograph does not exclude a foreign body. In fact,
approximately two-thirds of ingestions are radiopaque. There are a few tricks
to reading these plain films that may be helpful:
471
Disk batteries often appear to be a double shadow or coin stack.
Tracheal foreign bodies are typically best seen on lateral projection.
Esophageal foreign bodies are better seen in a coronal view.
The timing of intervention will vary depending on the clinical scenario,
even with similar ingested objects (Table 92.1). The emergency medicine
mantra of “the ABCs” still reigns here, and as with any other case, airway
compromise is a true emergency. Other “hard signs” for emergent endoscopy
include inability to handle secretions, fever, crepitus, or free air on
radiograph. Furthermore, if the object is sharp, a disk battery, or a magnet,
endoscopy should not wait. Cases to consider urgent endoscopy (rather than
emergent) include large objects, inability to tolerate oral solids or liquids,
and foreign bodies in the esophagus longer than 24 hours.
TABLE 92.1 MANAGEMENT OF SPECIFIC INGESTIONS
Special consideration should be given to pediatric patients. Their
ingestions are often more insidious, and the history from caregivers is
paramount. A plain film is usually very helpful in these cases; however,
avoid oral contrast as it does not add much information and runs a high risk
of aspiration. Once the ingested foreign object has been localized and
identified, as long as it is not acutely dangerous, the child can be discharged
and followed with serial imaging from his or her pediatrician until passage.
Follow-up is recommended for anyone who has presented with this
complaint, as a thorough evaluation for the cause of the impaction will help
prevent recurrence and possibly other complications. In some cases, the
episode will lead to the unmasking of another more sinister diagnosis, such
as a malignancy, that requires prompt intervention. Ultimately, the goal is to
prevent perforation, which runs a considerable mortality risk, both acutely
472
and in the future.
KEY POINTS
Assess the airway first.
Localization and identification of the foreign object will guide
treatment.
Disk batteries, magnets, and sharp objects usually require immediate
intervention.
Get follow-up for these patients.
SUGGESTED READINGS
Ikenberry SO, Jue TL, Anderson MA, et al. Management of ingested foreign
bodies and food impactions. Gastrointest Endosc. 2011;73(6):1085.
Khan MA, Hameed A, Choudhry AJ. Management of foreign bodies in the
esophagus. J Coll Physicians Surg Pak. 2004;14:218.
Kramer RE, Lerner DG, Lin T, et al. Management of ingested foreign bodies in
children: A clinical report of the NASPGHAN Endoscopy Committee. J
Pediatr Gastroenterol Nutr. 2015;60:562.
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93
SEVERE ACUTE PANCREATITIS CAN
BE SNEAKY
DENNIS HSIEH, MD, JD
Acute pancreatitis is the leading cause of gastrointestinal (GI) related
hospitalizations in the United States, accounting for over 280,000
hospitalizations each year. One-fifth of these cases are considered severe,
carrying a mortality rate of around 10% or 25%, depending on whether these
cases are sterile or infected, respectively.
Recognition of severe acute pancreatitis (SAP) is tricky, as many of the
criteria, such as Ranson, Imrie-Glasgow, and APACHE II, are determined 24
to 48 hours after presentation. This renders them unhelpful in the emergency
department (ED) time frame. Meanwhile, the CT severity index/Balthazar
score is not available unless CT has been performed—and CT imaging early
on in patients with a straightforward diagnosis of pancreatitis is actually
discouraged (see Chapter 94). Finally, it should be noted that the degree of
lipase elevation itself is not helpful in predicting severity of acute
pancreatitis.
Early identification and aggressive management of SAP are linked
directly to improved survival, leading to the idea of the “golden hours” of
SAP, treating SAP similar to severe sepsis or a severe burn.
Two new scores have been proposed in recent years that are helpful in
the ED diagnosis of SAP. The first is the Bedside Index of Severity of Acute
Pancreatitis (BISAP) score, which consists of five factors: blood urea
nitrogen (BUN) >25 mg/dL, impaired mental status (Glasgow Coma Score
<15), presence of systemic inflammatory response syndrome (SIRS), age
>60 years old, and pleural effusion on imaging. Each variable, if present, is
worth 1 point. Scores of 3, 4, and 5 are reflective of in-hospital mortality
474
rates of 8.3%, 19.3%, and 26.7%, respectively. A BISAP score ≥3 is also
associated with an increased risk of developing organ failure, persistent
organ failure, and pancreatic necrosis.
A scoring system that excludes SAP is the harmless acute pancreatitis
(HAP) score. This score looks at three factors: hematocrit (Hct), serum
creatinine (Cr) >2.0 mg/dL, and rebound tenderness/guarding on exam.
Patients without any of the three are unlikely to develop SAP (sensitivity of
96%). Independently, Cr > 1.8 mg/dL is a predictor of poor prognosis in
SAP.
Using these scoring systems alongside clinical experience, one has a
better chance at identifying SAP. Severe acute pancreatitis can be a rapidly
progressive disease and thus requires aggressive initial management in the
ED even if a patient appears clinically well.
Fluid resuscitation and supportive care are the crux of early SAP
management.
Common pitfalls include insufficient fluid resuscitation and using the
wrong type of fluid. An initial bolus of 20 mL/kg followed by 3 mL/kg/h is
appropriate with a goal urine output of 0.5 to 1 mL/kg/h, heart rate <100,
systolic blood pressure >90, if there are no cardiac or pulmonary
contraindications. A reassessment of BUN, Cr, lactate, and Hct should be
performed in 6 to 8 hours, and at that time, the fluids should be decreased to
2 mL/kg/h if all the parameters are improving. Some evidence favors lactated
Ringer’s over normal saline, but this is an area of ongoing controversy.
Prophylactic antibiotics are no longer recommended. However, if the patient
has evidence of infection and/or meets SIRS criteria, empiric antibiotics are
indicated.
For SAP, ICU admission should be discussed. At a minimum, surgery
and GI should be consulted. RUQ ultrasound should be considered if
gallstone pancreatitis is suspected. A contrast CT of the abdomen/pelvis can
help further stage pancreatitis, but a CT is often more useful 48 to 72 hours
after the onset of symptoms, after a trial of medical management, to detect
surgical complications.
As fluid resuscitation continues, serial abdominal exams with
measurement of abdominal compartment pressure should be conducted to
ensure that abdominal compartment syndrome (ACS) does not develop. This
is defined as an intra-abdominal compartment pressure of >20 mm Hg
associated with new-onset organ failure. If ACS develops, initial (medical)
management includes
1) Decreasing intestinal volume: nasogastric/orogastric drainage,
475
promotility agents, rectal tubes, and, if necessary, endoscopic
decompression
2) Decreasing intra-/extravascular fluid: decreasing volume resuscitation
and, if volume overloaded, either ultrafiltration or diuretics
3) Medical abdominal wall expansion: analgesia and sedation to decrease
abdominal muscle tone and, if necessary, neuromuscular blockade
If these strategies fail, surgical decompression may be indicated.
However, new literature considers dialysis/hemofiltration as a less invasive
alternative. Early surgery and nephrology consultations will assist with
managing this insidious yet deadly complication.
In summary, SAP must be diagnosed early in the ED, treated
aggressively, and monitored closely to minimize morbidity and mortality
(see Table 93.1).
TABLE 93.1 APPROACH TO SEVERE ACUTE PANCREATITIS
KEY POINTS
Early identification and aggressive management of SAP are linked
directly to improved survival.
Patients with SAP may develop abdominal compartment syndrome,
infection, pseudocyst, and other life-threatening complications.
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SUGGESTED READINGS
Forsmark CE, Gardner TB, eds. Prediction and Management of Severe Acute
Pancreatitis. New York: Springer, 2015.
Lankisch PG, Weber-Dany B, Hebel K et al. The harmless acute pancreatitis score:
A clinical algorithm for rapid initial stratification of nonsevere disease. Clin
Gastroenterol Hepatol. 2009;7(6):702–705.
Working Group IPA/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based
guidelines for the management of acute pancreatitis. Pancreatology. 2013;13(4
Suppl 2):e1–e15.
Wu BU, Banks PA. Clinical management of patients with acute pancreatitis.
Gastroenterology 2013:144(4);1272–1281.
Wu BU, Johannes RS, Sun X, et al. The early prediction of mortality in acute
pancreatitis: A large population-based study. Gut 2008;57(12):1698–1703.
477
94
USE RESTRAINT WHEN IMAGING
PATIENTS WITH ACUTE
PANCREATITIS
DEREK K. RICHARDSON, MD, MPH AND BARRY
SCHLANSKY, MD, MPH
Acute pancreatitis is frequently encountered in the emergency department
(ED) and results in hospital admission around 65% of the time in the United
States. Many scoring systems have been developed to assess prognosis and
severity of acute pancreatitis, often incorporating CT and MR imaging of the
abdomen. However, this imaging is most beneficial later in the inpatient
hospitalization rather than during the acute ED evaluation, unless the
diagnosis is in question. Therefore, discretion should be used when ordering
abdominal imaging for patients with a secure diagnosis of acute pancreatitis
at the initial presentation.
PRESENTATION OF ACUTE PANCREATITIS
Acute pancreatitis is common in the ED, but the presentation may be
variable. Patients may suffer recurrent bouts and could be well known to ED
staff with loud complaints of unmanaged pain and nausea while eating
Flamin’ Hot Cheetos® in the waiting room. Other patients may suffer more
indolent symptoms that can be difficult to differentiate from dyspepsia.
Severe acute pancreatitis can mimic sepsis due to severe inflammation, and
patients may present with fever and shock due to extensive third spacing of
intravascular volume. The most common etiologies of acute pancreatitis,
gallstones, and alcohol consumption should be elicited as possible triggers.
478
UTILITY OF IMAGING FOR DIAGNOSIS
Serum lipase levels have excellent sensitivity and specificity for pancreatitis
in the acute phase of illness, approaching 95% in the first two days of
symptoms. However, this level becomes more unreliable in patients with
chronic or intermittent pancreatitis. In patients with typical symptoms and
diagnostic laboratory tests, CT or MR imaging is not required to confirm the
diagnosis of acute pancreatitis. Biliary imaging, typically by ultrasound, and
social history for alcohol use are critical first steps to determine the
underlying cause. When the diagnosis is unclear due to equivocal laboratory
findings and atypical presentation, CT imaging of the abdomen and pelvis
may be indicated to assess for nonpancreatitis causes of abdominal pain or to
verify pancreatic inflammation confirming an acute pancreatitis diagnosis.
UTILITY OF IMAGING FOR INTERVENTION AND
PROGNOSIS
CT or MR imaging for acute pancreatitis is primarily used to detect
complications such as pancreatic necrosis or fluid collections (pseudocysts)
that may warrant interventional drainage. However, these findings are
typically delayed by at least several days after the onset of symptoms.
Moreover, the initial management of pancreatitis is supportive. When
complications are detected on imaging, intervention is usually delayed until a
week or longer after diagnosis and is reserved for fluid collections with
mature cyst walls that do not resolve spontaneously or pancreatic necrosis
with associated infection. While the optimal timing of imaging is unclear, it
is generally recommended for patients with persistent symptoms or fever
after 48 to 72 hours of medical management. Boarding times in the ED
seldom approach these thresholds, so CT or MR imaging is not typically
indicated in the ED for the patient with an established diagnosis of acute
pancreatitis.
HAZARDS OF IMAGING
A recent retrospective study at an academic hospital found that over half of
all patients presenting to the ED with acute pancreatitis underwent CT
imaging in the first 24 hours of admission; the vast majority of these patients
had a clear diagnosis of acute pancreatitis without this imaging. Other studies
have also demonstrated increasing rates of early or ED-based imaging of
acute pancreatitis nationwide. Projections of radiation risk are dependent on
many factors, but modeling predicts a number needed to harm of roughly
479
1,000 abdomen/pelvis CT exposures in healthy 40-year-old patients for each
radiation-induced cancer. Detection of clinically insignificant lesions
elsewhere in the abdomen that require additional invasive testing or repeat
imaging (so-called incidentalomas) confers additional risk to the patient and
draws excess resources and cost from the health care system. While early CT
or MR imaging may be occasionally necessary in very ill patients or in cases
where there is diagnostic uncertainty, routine imaging is seldom useful and
potentially harmful. Be judicious with the radiation exposure risk of excess
CT imaging.
KEY POINTS
CT/MR imaging is not indicated for assessment of clear-cut
pancreatitis in the ED.
Excess imaging carries real risk to the patient.
Consider cross-sectional imaging if the diagnosis is unclear.
SUGGESTED READINGS
Bharwani N, Patel S, Prabhudesai S, et al. Acute pancreatitis: The role of imaging
in diagnosis and management. Clin Radiol. 2011;66:164–175.
Dachs RJ, Sullivan L. Does early ED CT scanning of afebrile patients with first
episodes of acute pancreatitis ever change management? Emerg Radiol.
2015;22:239–243.
Shinagare AB, Ip IK, Raja AS, et al. Use of CT and MRI in emergency department
patients with acute pancreatitis. Abdom Imaging. 2015;40:272–277.
Smith-Bindman R, Lipson J, Marcus R, et al. Radiation dose associated with
common computed tomography examinations and the associated lifetime
attributable risk of cancer. Arch Intern Med. 2009;169:2078–2086.
Tenner S, Baillie J, DeWitt J, et al. American College of Gastroenterology
guideline: Management of acute pancreatitis. Am J Gastroenterol.
2013;108:1400–1415.
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95
THE “PAIN” IN CHRONIC
PANCREATITIS
DELPHINE J. HUANG, MD, MS
Chronic pancreatitis occurs when there is irreversible and progressive
destruction of the pancreas.1 Patients frequently present with disabling
chronic abdominal pain with those with intractable pain requiring large doses
of pain medications.2,3 Due to the loss of pancreatic function, patients may
experience steatorrhea, malabsorption, weight loss, anorexia,
nausea,vomiting and diabetes mellitus.3
The transition from acute to chronic pancreatitis can be indistinct and
difficult to discern. Moreover, the clinical picture of chronic pancreatitis can
be highly variable.2,3 Clinicians frequently feel conflicted about doing a
detailed workup as many of these patients are frequent users of the
emergency department (ED) and may have opioid dependency issues.
Nonetheless, it is important to assess a patient’s abdominal pain, as well as
for complications of chronic pancreatitis.
In a patient with acute pancreatitis, lipase levels will most frequently be
elevated. These enzymes levels can normalize as the disease progresses. In
chronic pancreatitis, clinicians may be falsely reassured when they see a
normal lipase, despite true pancreatic functional burnout.2 Further, patients
who do not consume any alcohol and present with chronic pancreatitis
should be screened for gallstones and other toxic-metabolic, autoimmune,
and genetic etiologies. To confirm the diagnosis in those with suspicious
presentations, abdominal CT or MRI may be used to image the pancreas. In
some cases, patients may need referral for an endoscopic ultrasound (EUS)
or magnetic resonance cholangiopancreatography (MRCP), especially for
mild or early disease states.2 Once a diagnosis is established, however,
481
repeated imaging on subsequent presentations to the ED is not necessarily
indicated.
While it may be easy to dismiss patients with chronic pancreatitis as
“opiate seeking,” it is important to consider whether complications of this
disease may be contributing to their acute exacerbation. For example, are
there any new features, such as a change in the nature of the pain? Is a fever
present? Patients with intractable vomiting, or who are unable to tolerate any
food or fluids, may require further evaluation. Strictures of the pancreatic
ducts, pseudocysts, pancreatic stones, and fistulization are common in this
population. Fluid collections and pancreatic necrosis can develop into
infections or abscesses that require antibiotics or drainage.2 Diabetes
mellitus, secondary to a loss of islet cells, can manifest in the later stages of
disease. These patients may develop neuropathy and retinopathy and rarely,
may even develop diabetes ketoacidosis. Lastly, the risk of pancreatic cancer
is much higher in this population, especially in patients with hereditary
pancreatitis.1–3
The ED management of pancreatic pain can be very challenging as
therapeutic options may be limited. While the etiology of the pain is not well
understood, it is most likely due to chronic inflammation, altered
nociception, and tissue ischemia.1 Acetaminophen is considered to be a first-
line therapy, but by the time these patients arrive to the ED, they may require
or request opioid medications. Other nonnarcotic options are frequently used
in the outpatient setting. These include neuropathic pain modulators such as
antidepressants (e.g., cyclic antidepressants and serotonin reuptake
inhibitors), as well as, gabapentin. All have been shown to be effective.4
More recently, some success has been demonstrated with the use of oral and
intravenous ketamine, and this agent continues to be studied.5
Harm reduction counseling is extremely important. While not necessarily
reversible, alcohol abstinence has been shown to slow or halt disease
progression, which may improve chronic pain.3 Cigarette smoking is also a
major risk factor and contributor to the morbidity of chronic pancreatitis.
Patients can also diminish their pain by eating smaller, low-fat meals; adding
a proton pump inhibitor; and supplementing their diet with pancreatic
enzymes and micronutrients to improve digestion.1
In patients with intractable pain, referral for a nerve block, endoscopy, or
surgery should be considered.6 Ductal decompression, lithotripsy,
sphincterectomy, or pancreatectomy may all play a role in these cases to
improve pain control. Islet cell transplantation also has been shown to be
successful.2,3 Lastly, corticosteroid therapy for those with autoimmune
482
disease can be beneficial.1
KEY POINTS
Lipase levels may be normal, despite true functional pancreatic
burnout.
Remember to assess patients for complications if pain cannot be
controlled. These include pancreatic pseudocyst, necrosis, stricture,
and abscess.
If complications are not present and pain is not well controlled,
consider referring patients for specialist consultation with a
gastroenterologist, surgeon, or pain management specialist.
REFERENCES
1. Braganza JM. Chronic pancreatitis. Lancet. 2011;377:1184–1197.
2. Nair RJ. Chronic pancreatitis. Am Fam Physician. 2007;76:1679–1688.
3. Ahmed SA. Chronic pancreatitis: Recent advances and ongoing challenges.
Curr Probl Surg. 2006;43:127–238.
4. Puylaert M. Pain in chronic pancreatitis. Pain Pract. 2011;11:492–505.
5. Juel J. Study protocol for a randomised, double-blinded, placebo-controlled,
clinical trial of S-ketamine for pain treatment in patients with chronic
pancreatitis (RESET trial). BMJ Open. 2015;5:e007087.
6. Chauhan S. Pain management in chronic pancreatitis: A treatment algorithm.
Best Pract Res Clin Gastroenterol. 2010;24:323–335.
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96
ABDOMINAL PAIN IN
INFLAMMATORY BOWEL DISEASE:
A FLARE OR EMERGENT
COMPLICATION?
MARGARET HUANG, MD
Inflammatory bowel disease (IBD) includes Crohn disease (CD) and
ulcerative colitis (UC). Crohn’s disease is characterized by transmural bowel
wall inflammation that can occur anywhere throughout the gastrointestinal
tract. Normal mucosa surrounds diseased segments, resulting in characteristic
“skip lesions.” In contrast, ulcerative colitis is limited to the colon and
typically only involves the superficial mucosal layer, but with continuous
lesions starting from the rectum. In both CD and UC, fistulae, strictures, and
abscesses can develop, leading to complications such as intestinal
obstruction, perforation, infectious colitis, and toxic megacolon.
The exact pathophysiology of IBD is not well understood, but it is
thought to be multifactorial, with a combination of genetic, environmental,
and immune factors. In some cases, food-borne illnesses and increased
intestinal wall permeability have been identified as inciting factors. In
addition, bacterial, viral, or parasitic superinfections can trigger acute flares
in IBD patients.
Patients with IBD typically present to the emergency department with
abdominal pain and/or distention, along with bloody diarrhea. Fever, nausea,
vomiting, fatigue, and weight loss are also common presenting symptoms.
Symptoms may be acute and persistent (≥4 weeks) or recurrent (≥2 episodes
in 6 months).
484
An abdominal series x-ray can be a useful screening tool to rapidly
identify complications of IBD. The presence of free air, air-fluid levels,
and/or dilated bowel loops with a paucity of distal bowel gas should alert the
clinician to the possibility of bowel obstruction, perforation, and/or toxic
megacolon. In adults and children ≥10 years, acute dilatation of the
transverse colon to >5 to 6 cm with the loss of haustral folds is diagnostic for
toxic megacolon. In children <10 years, a transverse colonic diameter of >4
cm is suggestive. Toxic megacolon is a surgical emergency; it is associated
with an increased risk of intestinal perforation and hemorrhage, electrolyte
abnormalities, and sepsis.
In addition to plain x-ray, computed tomography (CT) imaging of the
abdomen should be considered to look for other complications, such as
abscess, stricture, and/or fistulae. CT imaging can also provide further details
on intestinal obstruction and the extent of colitis. In pediatric patients, both
ultrasound and magnetic resonance imaging are alternative imaging
modalities that can be used to avoid ionizing radiation exposure, although
such techniques are less well established and their use is limited by center-
specific availability and expertise.
It is often challenging to distinguish whether a patient is having an acute
flare or complications of IBD. Presenting symptoms are similar in both
cases, as are results from laboratory testing. Such common laboratory
abnormalities include thrombocytosis, anemia, and elevated inflammatory
markers (C-reactive protein and erythrocyte sediment rate). Additionally, the
use of corticosteroids or other immune modulators may potentially mask
signs and symptoms of an acute abdominal emergency, leading to delayed
diagnosis and treatment. A complication should be suspected in patients who
have unstable vital signs, escalating abdominal pain, a toxic appearance,
and/or signs of peritonitis.
Acute IBD flares require high-dose intravenous corticosteroids.
Methylprednisolone 1 mg/kg q12h (with a maximum of 30 mg q12h) is the
recommended first-line therapy. Patients should remain NPO for bowel rest,
and intravenous fluids should be initiated.
Antibiotics are indicated when infectious colitis, perforation, and/or toxic
megacolon are suspected. A combination of ciprofloxacin and metronidazole
is typically the first-line therapy, but the choice of antibiotics should be
tailored to the specific underlying infectious organism when results are
available. While ciprofloxacin is not routinely used in pediatric patients
younger than 12 years, it is an accepted alternative when no other effective
and safe therapies are available and benefits outweigh risks. In more severe
disease, surgical intervention may be indicated. Management decisions
485
should be made in consultation with gastroenterology and/or surgery.
As bacterial, viral, or parasitic superinfections can precipitate IBD flares,
a stool sample should be cultured for enteric pathogens, including
Campylobacter, C. difficile, cytomegalovirus, E. coli, Entamoeba, Giardia,
Salmonella, Shigella, and Yersinia spp. Among these enteric pathogens, C.
difficile is the most common and has been linked to worse outcomes.
The use of opioids is controversial in patients with IBD, as it has been
associated with intestinal perforation and toxic megacolon, particularly with
concurrent colitis. Other medications for pain management can be
considered; studies have shown that ketamine (0.1 to 0.5 mg/kg) provides
effective analgesia and decreases the opioid dose requirement.
Benzodiazepines have also been shown to be effective for pain relief in
patients with tenesmus.
KEY POINTS
Common complications of IBD include fistulae, strictures, abscesses,
intestinal obstruction, perforation, infectious colitis, and toxic
megacolon.
Abdominal series x-ray can rapidly identify many complications of
IBD and can be obtained prior to CT or other imaging modalities.
The use of corticosteroids or other immune modulators in patients
with IBD leads to immunosuppression and can obscure the diagnosis
of an acute abdominal emergency. Serial abdominal exam is crucial.
While antibiotics are only indicated in suspected infectious colitis,
perforation, and toxic megacolon, their administration should not be
delayed in toxic-appearing patients with escalating abdominal pain.
SUGGESTED READINGS
Anupindi SA, Janitz E, Darge K. Bowel imaging in children: A comprehensive
look using US and MRI. Semin Roentgenol. 2012;47:118–126.
Cosnes J, Gower-Rousseau C, Seksik P, Cortot A. Epidemiology and natural
history of inflammatory bowel diseases. Gastroenterology.
2011;140:1785–1794.
Sauer CG, Kugathasan S. Pediatric inflammatory bowel disease: Highlighting
pediatric differences in IBD. Med Clin North Am. 2010;94:35–52.
White M, Shah N, Lindley K, et al. Pain management in fulminating ulcerative
colitis. Paediatr Anaesth. 2006;16:1148–1152.
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97
NOT EVERY PREGNANT PATIENT
WITH VOMITING HAS
HYPEREMESIS GRAVIDARUM
ROLANDO G. VALENZUELA, MD, DTMH AND
WILLIAM K. MALLON, MD, FACEP, FAAEM, DTMH
Nausea and vomiting are common symptoms during pregnancy. It is
estimated that between 50% and 90% of women will experience nausea and
vomiting during their pregnancy, with 35% experiencing clinically
significant vomiting. Nausea and vomiting usually begin in the first trimester
and peak at 9 weeks of gestation, with more than 90% of cases resolving by
the 20th week of gestation; this appears to be related to human chorionic
gonadotropin and estradiol levels. Although common in otherwise normal
pregnancies, we need to resist the temptation to immediately attribute nausea
and vomiting to the physiology of pregnancy or to hyperemesis gravidarum.
We should maintain a cautious and thoughtful differential diagnosis.
Hyperemesis gravidarum is considered the extreme end of a spectrum of
nausea and vomiting in pregnancy. It is notable that hyperemesis gravidarum
is present in only 0.5% to 2% of all pregnancies. This diagnosis requires
exclusion of other causes and presents with a measure of actual starvation,
manifesting as large ketonuria. Patients may also have electrolyte imbalance
and dehydration and commonly have at least a 5% loss of prepregnancy
weight. Regardless of etiology, when severe, vomiting can itself result in
damage to both the mother and the fetus. Cases of splenic avulsion,
esophageal rupture, pneumothorax, acute tubular necrosis, Wernicke
encephalopathy, and central pontine myelinolysis have all been reported.
A careful history including a review of chronic medical conditions that
487
existed prior to the pregnancy, in addition to a targeted physical examination,
will yield important clues to potentially serious causes. It should be noted
that nausea and vomiting of pregnancy is rarely associated with other
concerning symptoms such as fever, headache, neurologic deficits,
abdominal pain, proteinuria, dysuria, hematuria, or flank pain. The presence
of any of these symptoms should prompt an aggressive search for another
etiology. Table 97.1 gives a differential diagnosis for nausea and vomiting in
pregnancy.
TABLE 97.1 DIFFERENTIAL DIAGNOSIS OF NAUSEA AND VOMITING IN
PREGNANCY
Adapted from Practice Bulletin No. 153: Nausea and Vomiting of
Pregnancy. Obstet Gynecol. 2015;126(3): 687–688.
Evaluation should include blood work to check for electrolyte
abnormalities as well as liver function tests, urinalysis, and a pelvic
ultrasound to exclude molar pregnancy. After serious conditions have been
excluded, the primary approach is to control symptoms through lifestyle and
diet interventions. Recommend avoiding triggers of nausea (i.e., strong
488
smells, fatty or spicy foods, iron tablets, etc.). Small meals should be eaten
frequently, and bland, dry, and high-protein diets appear to be better
tolerated. Ginger and pyridoxine (vitamin B6) have been shown to be more
effective than placebo. Both are considered safe in pregnancy and available
over the counter.
When lifestyle and dietary changes have failed and over-the-counter
therapies are ineffective, prescription medications can be considered. The
American College of Obstetrics and Gynecology (ACOG) recommendations
for initial management include pyridoxine hydrochloride 10 to 25 mg orally
three to four times daily and doxylamine succinate, an antihistamine, at a
dose of 12.5 mg orally three or four times daily. These are considered safe
for mother and fetus. Failing this, second-line agents include
diphenhydramine and/or promethazine. These are both antihistamines as
well, so beware of compounding doses with previously prescribed
doxylamine. Resistant cases can be treated with 5-HT3 antagonists
(ondansetron). Early studies have shown these agents to be generally safe in
pregnancy, though one retrospective study has shown an increased risk of
cardiovascular defects.
KEY POINTS
Although physiologic nausea and vomiting of pregnancy is common,
always consider other underlying causes.
Be familiar with lifestyle and dietary changes that may improve
nausea without pharmacologic treatment. These are first line.
Pyridoxine and doxylamine succinate are considered safe
pharmacologic interventions.
SUGGESTED READINGS
American College of Obstetrics and Gynecology. Practice Bulletin Summary No.
153: Nausea and vomiting of pregnancy. Obstet Gynecol. 2015;126:687–688.
Danielsson B, Wikner BN, Kallen B. Use of ondansetron during pregnancy and
congenital malformations in the infant. Reprod Toxicol. 2014;50:134–137.
Jarvis S, Nelson-Piercy C. Management of nausea and vomiting in pregnancy.
BMJ. 2011;342:d3606.
Matthews A, Haas DM, O’Mathuma DP, et al. Interventions for nausea and
vomiting in early pregnancy. Cochrane Database Syst Rev. 2015;9:CD007575.
Niebyl J. Clinical practice: Nausea and vomiting in pregnancy. N Engl J Med.
489
2010;363(16): 1544–1550.
Temming L, Franco A, Istwan N, et al. Adverse pregnancy outcomes in women
with nausea and vomiting of pregnancy. J Matern Fetal Neonatal Med.
2014;27(1):84–88.
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98
BEWARE OF THE PATIENT WITH
PAINLESS JAUNDICE
ANDRÉS GUZMÁN, MD AND
ROLANDO G. VALENZUELA, MD, DTMH
Jaundice is defined as a yellowish discoloration of the skin and mucosa. It is
the clinical manifestation of elevated serum bilirubin, which is largely the
product of degraded red blood cells. Hyperbilirubinemia can be due to
unconjugated bilirubin before it undergoes glucuronidation in the liver, or
conjugated bilirubin after it has undergone glucuronidation and is excreted in
stool (stercobilin) or urine (urobilinogen).
Important historical features in a patient with painless jaundice include
an occupational history, history of toxin exposures, overseas travel, family
history, a history of alcohol or intravenous (IV) drug abuse, or high-risk
sexual activity. Significant weight loss, fevers, night sweats, and increasing
abdominal girth can lead the physician to specific diagnoses such as parasitic
infections, autoimmune diseases, or neoplasm. Signs and symptoms of
anemia, a history of melena, and any other suggestion of gastrointestinal (GI)
bleeding are very important and should be sought in the history.
On physical examination, there are certain findings that, in conjunction
with jaundice, are concerning for an underlying emergent condition. These
include any vital sign abnormalities and anemia, easily determined by
bedside testing. Avoid the temptation to attribute abnormal vital signs to an
underlying chronic disease. Any degree of hypotension, for example, should
prompt an active search for a source of bleeding or infection.
Initial testing should include serum glucose, a complete blood count
(CBC), electrolytes, liver function tests (LFTs), type and screen, and fecal
occult blood. If the bilirubin level is abnormal, one must distinguish between
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conjugated (direct) and unconjugated (indirect) bilirubin. GI bleeding is a
critical consideration and should be recognized as quickly as possible; portal
hypertension due to liver dysfunction increases the risk of gastroesophageal
varices and ulcers that may manifest initially with hemorrhage (acute or
chronic).
Jaundice with unconjugated hyperbilirubinemia in the presence of
normal transaminases and alkaline phosphatase should raise concern for
hemolysis. This may be drug-induced, autoimmune, or due to an inherited
disorder (see Table 98.1). If hemolytic anemia is suspected, a peripheral
smear should be ordered as well as reticulocyte count, haptoglobin, and
lactate dehydrogenase (LDH). A hematologist should be consulted, and
admission is warranted.
TABLE 98.1 COMMON CAUSES OF HEMOLYTIC ANEMIA
Adapted from Approach to the diagnosis of hemolytic anemia in the adult.
UptoDate, 2015.
When direct hyperbilirubinemia is present a CBC with differential, LFTs,
and a prothrombin time (PT) will help identify the presence of primary
hepatic failure, primary intraductal or biliary tree disease, or the presence of
obstructive pathology. Painless jaundice with a posthepatic obstructive
source should prompt a search for primary or metastatic malignancies of the
liver, gallbladder, or pancreas. The presence of eosinophilia should raise
suspicion for a parasitic process.
Viral hepatitis will typically cause direct (conjugated) hyperbilirubinemia
along with transaminitis (with or without elevation of alkaline phosphatase),
indicating a primarily hepatocellular process. Viral hepatitis may develop
gradually, so that patients may only present when significant jaundice
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ensues. If a viral etiology is suspected, serologic studies should be
performed. If an autoimmune disease is suspected, relevant tests should be
ordered, though this may be done as an outpatient if close follow-up is
arranged.
Toxin exposure, both common and uncommon, can result in acute,
chronic, or acute-on-chronic liver failure. A careful occupational history may
reveal exposures to chemicals in the workplace (arsenic, carbon
tetrachloride, vinyl chloride). Acutely ingested or chronically used over-the-
counter medications (acetaminophen, NSAIDs), commonly prescribed
medications (isoniazid, amoxicillin–clavulanic acid, TMP-SMX, valproic
acid, nitrofurantoin, etc.), and complementary, alternative, or herbal
medications (ackee fruit, camphor, kava leaves, etc.) can all cause hepatic
failure. Subacute ingestion of plants or fungi (amanita mushrooms) can also
result in hepatic failure.
There are several imaging modalities used to evaluate the liver,
gallbladder, and biliary tree. Ultrasonography (US) is an excellent tool to
evaluate the presence of gallbladder stones and dilation of intrahepatic ducts,
but it is operator dependent and lacks the sensitivity and specificity of
endoscopic retrograde cholangiopancreatography (ERCP) in evaluating
extrahepatic and common biliary ductal etiologies. Nevertheless, US is
inexpensive and widely available and is the initial imaging study of choice.
Computed tomography (CT) does not identify gallstones as well as US or
ERCP; however, it has better sensitivity and specificity for hepatic abscess,
hepatic neoplasms (primary or secondary), and periampullary neoplasms and
masses. CT should be considered the modality of choice when suspicion is
high for malignancy in obstructive disease.
The disposition of the patient will depend on the suspected underlying
pathology as well as the patient’s clinical condition (vital signs, tolerance of
oral intake, overall appearance, etc.). The asymptomatic patient with
jaundice can be discharged safely home if acute and acute exacerbations of
chronic underlying processes are excluded; prompt ambulatory follow-up for
further evaluation should be arranged.
KEY POINTS
Painless jaundice may reflect ongoing GI bleeding. The initial
assessment should identify patients at risk for variceal bleeding and
ulcers.
Hemolytic anemia is another potentially life-threatening cause. It
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presents with unconjugated hyperbilirubinemia.
When studies suggest a posthepatic disease process, the differential
diagnosis should include primary or secondary malignancies as well
as parasitic infectious diseases (clues: travel history or eosinophilia).
Toxins (both common and uncommon) can produce liver failure with
jaundice. Asking about acetaminophen intake; use of complementary
and alternative remedies, teas, and plant-based medicines; and
workplace chemical exposures is important and often ignored.
SUGGESTED READINGS
Pappas G, Christou L, Akritidis NK, et al. Jaundice of unknown origin: Remember
zoonoses! Scand J Gastroenterol. 2006;41(4):505–508.
Patel SN, Baumann BM, Farmer MC. A rare incidental finding in a case of painless
jaundice. Am J Emerg Med. 2008;26(4):516.e1–2.
Reisman Y, Gips CH, Lavelle SM, et al. Clinical presentation of (subclinical)
jaundice—the Euricterus project in The Netherlands. United Dutch Hospitals
and Euricterus Project Management Group. Hepatogastroenterology.
1996;43:1190.
Rosenfeld GA, Nimmo M, Hague C, et al. Echinococcus presenting as painless
jaundice. Can J Gastroenterol. 2012;26(10):684–685.
Wheatley MA, Heilpern KL. Jaundice. In: Rosen’s Emergency Medicine. 8th ed.
Philadelphia, PA: Elsevier/Saunders, 2014:232–237.
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99
ERCP CAN CAUSE A LOT OF
COMPLICATIONS!
ABRAHAM FLINDERS, MD
Endoscopic retrograde cholangiopancreatography (ERCP) was developed in
the 1960s and is a diagnostic and therapeutic procedure for biliary and
pancreatic duct disease. It involves direct visualization of the stomach and
duodenum via endoscope with contrast capabilities to visualize the ductal
network. Instruments are used through the endoscope for biopsy, excision,
stone removal, and sphincterotomy. ERCP has many well-documented
complications. A survey of prospective studies that included approximately
17,000 patients reported a 6.5% incidence of complications. The most
common are pancreatitis, sepsis, perforation, and hemorrhage. As the
procedure has become more common, it has moved to the outpatient setting
where patients are monitored for a mere 4 to 6 hours postprocedure and then
deemed safe for discharge. Thus, emergency department (ED) providers
must be prepared to diagnose and treat complications of ERCP, which will
most frequently present with abdominal pain.
Acute pancreatitis is common in the ED and typically presents with
abdominal pain, nausea, and vomiting. The incidence is approximately 3% in
those undergoing ERCP. Any patient that presents with abdominal pain post
ERCP should have lipase levels drawn. The manipulation from ERCP alone
will elevate lipase somewhat, but usually less than three times the upper
limit, and it should clear by day 2 postprocedure. ERCP-induced pancreatitis
should be managed as any other case of pancreatitis but with a lower
threshold to pursue imaging as it can mimic other complications such as
perforation. If the patient is toxic appearing, admission (to an intensive care
unit) for intravenous (IV) hydration, bowel rest, and observation is indicated,
as is urgent evaluation by a general surgeon. In addition, empiric IV
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antibiotics are appropriate in this setting, as is computed tomography of the
abdomen and pelvis (CTAP) with IV contrast. Piperacillin-tazobactam or
imipenem can be used as monotherapy or, alternatively, a fluoroquinolone
combined with metronidazole.
Post-ERCP sepsis has an incidence of 0.5% to 2%. The most common
etiology is acute cholangitis/cholecystitis, but patients can also present with
sepsis due to liver abscess, infected pancreatic pseudocyst, viscus
perforation, and pancreatitis. Patients typically present with abdominal pain
and abnormal vitals including fever and shock. Suspect cholangitis when the
patient has the constellation of jaundice, right upper quadrant pain, and fever.
If the patient is stable, start with a right upper quadrant abdominal ultrasound
(US) but have a low threshold to order a CTAP with IV contrast. These
patients should be resuscitated with IV fluids, be started on broad-spectrum
antibiotics, have a surgical or gastroenterology consult, and be admitted to
the intensive care unit. The treatment often requires a repeat ERCP, so
contacting a consulting surgeon or gastroenterologist is key.
Another important differential diagnostic consideration in the patient
with post-ERCP abdominal pain is perforation. Perforation can present
dramatically with an esophageal free wall rupture and tension pneumothorax
or much more subtly with an asymptomatic collection of retroperitoneal free
air. An upright chest radiograph with a view of the diaphragms is a good
starting point if the patient presents with peritonitis, but the most sensitive
imaging modality is once again CTAP with IV contrast. If perforation is
suspected, patients should be made NPO and have nasogastric
decompression, IV antibiotics, and surgical consultation.
When patients present with shock post ERCP, hemorrhage should be
considered given the risk of bleeding from vascular injury. Most commonly,
this occurs after sphincterotomy, and it is generally not excessive. Rarely,
however, bleeding is severe, and it should be managed accordingly.
Evaluation and management include serial hemoglobin measurements, a type
and screen, and blood transfusion as needed. If the patient is stable for
imaging, CTAP with IV contrast can help localize the pathology.
Coagulopathy may be seen in patients with cirrhosis, and bleeding may also
occur and be difficult to control in anticoagulated patients. Reversal agents
should be considered in those who bleed severely and are not responsive to
blood transfusion. A surgeon or gastroenterologist should be consulted from
the ED since many of these bleeds are handled endoscopically or by
laparotomy, but some may require interventional radiology for embolization.
496
KEY POINTS
ERCP has revolutionized the diagnosis and treatment of patients with
biliary obstruction; however, it comes with a significant rate of
complications.
Acute pancreatitis, sepsis, perforation, and hemorrhage can all occur
post ERCP.
In ill-appearing patients, resuscitation with IV fluids, cross-sectional
imaging (e.g., with CTAP), empiric antibiotics, and early specialist
consultation are indicated.
SUGGESTED READINGS
Andriulli A, Loperfido S, Napolitano G, et al. Incidence rates of post-ERCP
complications: A systematic survey of prospective studies. Am J Gastroenterol.
2007;102(8):1781–1788.
Ferreira LE, Baron TH. Post-sphincterotomy bleeding: Who, what, when, and how.
Am J Gastroenterol. 2007;102(12):2850–2858.
Loperfido S, Angelini G, Benedetti G, et al. Major early complications from
diagnostic and therapeutic ERCP: A prospective multicenter study.
Gastrointest Endosc. 1998;48(1):1–10.
Masci E, Toti G, Mariani A, et al. Complications of diagnostic and therapeutic
ERCP: A prospective multicenter study. Am J Gastroenterol.
2001;96(2):417–423.
Paspatis GA, Dumonceau JM, Barthet M, et al. Diagnosis and management of
iatrogenic endoscopic perforations: European Society of Gastrointestinal
Endoscopy (ESGE) position statement. Endoscopy. 2014;46(8):693–711.
Sherman S, Lehman GA. ERCP and endoscopic sphincterotomy-induced
pancreatitis. Pancreas. 1991;6(3):350–367.
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100
DON’T BE AFRAID TO ORDER A
CT ON A PREGNANT PATIENT IF
SHE REALLY NEEDS IT
MARITA M. HARRIS-NADDELL, MD AND
MICHELLE D. LALL, MD, MHS, FACEP
Radiation exposure in pregnancy is a complex topic. Physicians remain
cautious when weighing the need to image a pregnant patient versus the
potential harm to an embryo or fetus. According to the American College of
Radiology (ACR), the low amount of radiation in a plain film does not cause
harm to a developing fetus. However, computed tomography (CT) studies
can vary in levels of exposure and should be used only after appropriate
risk/benefit analysis.
The ACR has released a practice parameter to guide clinicians in
determining which diagnostic studies to order when imaging pregnant or
potentially pregnant women with ionizing radiation. The American College
of Obstetricians and Gynecologists (ACOG) has also released guidelines for
imaging in pregnancy. According to ACOG, the possibility of radiation
exposure to a fetus should never prevent medically indicated imaging for a
pregnant patient. Both of these guidelines were most recently updated in
2014.
The ACR has summarized radiation effects based on gestational age. The
risk of radiation-induced central nervous system (CNS) effects is greatest at
8 to 15 weeks of gestation. At any gestational age, radiation exposure of <50
mGy has not been shown to cause harm. Imaging that delivers 50 to 100
mGy in patients >18 weeks pregnant has also not been shown to cause harm
to the developing fetus. Imaging with greater than 100 mGy may cause
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detrimental effects at all gestational ages. The ACR reports that a 20-mGy
dose of radiation to the fetus represents an additional lifetime cancer risk of
~0.8%. Table 100.1 shows radiation doses for common imaging studies.
TABLE 100.1 ESTIMATED FETAL EXPOSURE FROM SOME COMMON
RADIOLOGIC STUDIES
1 mGy = 0.1 rad; amount of energy deposited per kilogram of tissue.
Adapted from American College of Obstetrics and Gynecology. ACOG Committee on
Obstetric Practice. ACOG Committee Opinion. No. 299, September 2004 (replaces No.
158, September 1995). Guidelines for diagnostic imaging during pregnancy. Obstet
Gynecol. 2004;104(3):647–651.
Ultrasound (US) and magnetic resonance (MR) are the preferred
diagnostic modalities in pregnancy; however, MR is not always available.
CT should not be withheld if needed to make a critical diagnosis. In addition,
intravenous (IV) contrast should be ordered only if really necessary. There is
some concern that it may interfere with fetal thyroid function as IV contrast
does cross the placenta. Animal studies, however, have not shown
teratogenic effects. According to ACOG, contrast agents are unlikely to
cause harm.
Both the ACOG and the ACR recommend using imaging modalities that
are not associated with ionizing radiation, such as US and MR, if at all
possible. CT imaging of the abdomen and pelvis in pregnant patients is most
commonly ordered in the settings of suspected appendicitis and trauma.
When evaluating a pregnant patient with possible appendicitis, the most
common nonobstetric surgical emergency in pregnancy, US is the preferred
first-line imaging modality. If the US is nondiagnostic, MR is recommended
as the next best imaging study. If MR is unavailable, CT should be
performed. In a stable patient with blunt abdominal trauma, x-ray and US are
performed first. However, US has diagnostic limitations in the pregnant
trauma patient; CT remains the most accurate and cost-efficient tool when
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evaluating blunt abdominal trauma. Single-phase CT of the abdomen and
pelvis usually delivers less than 35 mGy, and with dose-sparing protocols,
the radiation dose is typically 10 to 25 mGy. There is no significant evidence
that a single CT of the abdomen and pelvis will be detrimental to a growing
embryo or fetus. However, dose-saving or adapted protocols should be used
whenever possible.
Informed consent should always be obtained, and every effort should be
made to decrease the amount of radiation required for the study. According
to the ACR, when obtaining patient consent, a realistic overview of the
limited risk and the beneficial role of the imaging should be explained to the
patient in understandable language. They state, “Conveying information in a
positive, rather than negative, format is useful in helping a patient understand
an accurate perspective of risk.” Informed consent should be documented in
the medical record.
KEY POINTS
Any diagnostic imaging required to make a critical diagnosis should
be ordered if the benefit to the mother outweighs the risk to the
embryo or fetus.
A single CT scan of the abdomen and pelvis is unlikely to cause fetal
harm.
SUGGESTED READINGS
American College of Obstetrics and Gynecology. ACOG Committee on Obstetric
Practice. ACOG Committee Opinion. No. 299, September 2004 (replaces No.
158, September 1995). Guidelines for diagnostic imaging during pregnancy.
Obstet Gynecol. 2004;104(3):647–651.
American College of Radiology. ACR Practice Guideline for Imaging Pregnant or
Potentially Pregnant Adolescents and Women with Ionizing Radiation. Reston,
VA: American College of Radiology, 2008: amended 2014. Available at:
http://www.acr.org/~/media/9e2ed55531fc4b4fa53ef3b6d3b25df8.pdf on
9/12/15.
Wieseler KM, Bhargava P, Kanal KM, et al. Imaging in pregnant patients:
Examination appropriateness. Radiographics. 2010;30(5):1215–1229.
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