DIFFERENTIAL DIAGNOSIS

Appendicitis, Acute

Obstruction of the appendiceal lumen is the primary cause of appendicitis. An anatomic blind pouch,
obstruction of the appendiceal lumen leads to distension of the appendix due to accumulated intraluminal fluid.
Ineffective lymphatic and venous drainage allows bacterial invasion of the appendiceal wall and, in advanced cases,
perforation and spillage of pus into the peritoneal cavity.
Sex
The incidence of appendicitis is approximately 1.4 times greater in men than in women. The incidence of
primary appendectomy is approximately equal in both sexes.
Age
 Incidence of appendicitis gradually rises from birth, peaks in the late teen years, and gradually declines in
the geriatric years. The median age at appendectomy is 22 years.
 Although rare, neonatal and even prenatal appendicitis have been reported.
 The emergency department clinician must maintain a high index of suspicion in all age groups.

Patients with many other disorders present with symptoms similar to those of appendicitis. Examples include the
following:
o Pelvic inflammatory disease (PID) or tubo-ovarian abscess
o Endometriosis
o Ovarian cyst or torsion
o Ureterolithiasis and renal colic
o Degenerating uterine leiomyomata
o Diverticulitis
o Crohn disease
o Colonic carcinoma
o Rectus sheath hematoma
o Cholecystitis
o Bacterial enteritis
o Mesenteric adenitis
o Omental torsion

 The classic history of anorexia and periumbilical pain followed by nausea, right lower quadrant (RLQ) pain,
and vomiting occurs in only 50% of cases.
 Migration of pain from the periumbilical area to the RLQ is the most discriminating feature of the patient's
history. This finding has a sensitivity and specificity of approximately 80%. Positive likelihood ratio is 3.18
(2.41-4.21), and negative likelihood ratio is 0.5 (0.42-0.59).2
 When vomiting occurs, it nearly always follows the onset of pain. Vomiting that precedes pain is suggestive
of intestinal obstruction, and the diagnosis of appendicitis should be reconsidered.
 Nausea is present in 61-92% of patients; anorexia is present in 74-78% of patients. Neither finding is
statistically different from findings in ED patients with other etiologies of abdominal pain.
 Diarrhea or constipation is noted in as many as 18% of patients and should not be used to discard the
possibility of appendicitis.
 Duration of symptoms is less than 48 hours in approximately 80% of adults but tends to be longer in elderly
persons and in those with perforation. Approximately 2% of patients report duration of pain in excess of 2
weeks.
 A history of similar pain is reported in as many as 23% of cases. A history of similar pain, in and of itself,
should not be used to rule out the possibility of appendicitis.
 An inflamed appendix near the urinary bladder or ureter can cause irritative voiding symptoms and
hematuria or pyuria. Cystitis in male patients is rare in the absence of instrumentation. Consider the
possibility of an inflamed pelvic appendix in male patients with apparent cystitis.
 Also consider the possibility of appendicitis in pediatric or adult patients who present with acute urinary
retention.3
Physical
 RLQ tenderness is present in 96% of patients, but this is a nonspecific finding. Rarely, left lower quadrant
(LLQ) tenderness has been the major manifestation in patients with situs inversus or in patients with a
lengthy appendix that extends into the LLQ.
 The most specific physical findings are rebound tenderness, pain on percussion, rigidity, and guarding.
  Ovarian Cysts
An ovarian cyst is a fluid-filled sac in an ovary. They can develop from the neonatal period to postmenopause. Most
ovarian cysts occur during infancy and adolescence, which are hormonally active periods of development. Most are
functional in nature and resolve with minimal treatment. However, ovarian cysts can herald an underlying malignant
process or, possibly, distract the emergency clinician from a more dangerous condition, such as ectopic pregnancy,
ovarian torsion, or appendicitis. When ovarian cysts are large, persistent, or painful, surgery may be required,
sometimes resulting in removal of the ovary. With the more frequent use of ultrasonography in recent years, the
diagnosis of ovarian cysts has become more common.
Abdominal pain in the female can be one of the most difficult cases to diagnose correctly in the emergency
department (ED). The spectrum of gynecological disease is broad, spanning all age ranges and representing various
degrees of severity, from benign cysts that eventually resolve on their own to ruptured ectopic pregnancy that causes
life-threatening hemorrhage.
When presented with this scenario, the goal of the emergency physician is to rule out acute causes of abdominal pain
associated with high morbidity and mortality, such as appendicitis or ectopic pregnancy, to assess for the possibility
of neoplasm or malignancy, and either to refer the patient to the appropriate consultant or to discharge them with a
clear plan for follow-up with an obstetrician/gynecologist.
Pathophysiology
The median menstrual cycle lasts 28 days, beginning with the first day of menstrual bleeding and ending just before
the subsequent menstrual period. The variable first half of this cycle is termed the follicular phase and is
characterized by increasing follicle-stimulating hormone (FSH) production, leading to the selection of a dominant
follicle that is primed for release from the ovary. In a normally functioning ovary, simultaneous estrogen production
from the dominant follicle leads to a surge of leuteinizing hormone (LH), resulting in ovulation and release of the
dominant follicle from the ovary and commencing the leuteinizing phase of ovulation.
After ovulation, the follicular remnants form a corpus luteum, which produces progesterone. This, in turn, supports the
released ovum and inhibits FSH and LH production. As luteal degeneration occurs in the absence of pregnancy, the
progesterone levels decline, while the FSH and LH levels begin to rise before the onset of the next menstrual period.
Different kinds of functional ovarian cysts can form during this cycle. In the follicular phase, follicular cysts may result
from a lack of physiological release of the ovum due to excessive FSH stimulation or lack of the normal LH surge at
mid cycle just before ovulation. Hormonal stimulation causes these cysts to continue to grow. Follicular cysts are
typically larger than 2.5 cm in diameter and manifest as pelvic discomfort and heaviness. Granulosa cells that line the
follicle may also persist, leading to excess estradiol production, which, in turn, leads to decreased frequency of
menstruation and menorrhagia.1
In the absence of pregnancy, the lifespan of the corpus luteum is 14 days. If the ovum is fertilized, the corpus luteum
continues to secrete progesterone for 5-9 weeks until its eventual dissolution in 14 weeks time, when the cyst
undergoes central hemorrhage. Failure of dissolution to occur may result in a corpus luteal cyst, which is arbitrarily
defined as a corpus luteum that grows to 3 cm in diameter. The cyst can cause dull, unilateral pelvic pain and may be
complicated by rupture, which causes acute pain and possibly massive blood loss.
Theca lutein cysts are caused by luteinization and hypertrophy of the theca interna cell layer in response to excessive
stimulation of beta-human chorionic gonadotropin (bhCG). This type of cyst can occur in the setting ofgestational
trophoblastic disease, multiple gestation, or exogenous ovarian hyperstimulation. These cysts are associated with
maternal androgen excess in up to 30% of cases but usually resolve spontaneously as the bhCG level falls. Theca
lutein cysts are usually bilateral and result in massive ovarian enlargement, a condition termed hyperreactio
luteinalis.2
Ovarian cysts are extremely prevalent, affecting an estimated 7% of premenopausal and postmenopausal woman.
Furthermore, up to 4% of women will be admitted to the hospital with a primary diagnosis of ovarian cysts3 ; 1%-4% of
pregnant women are diagnosed with an adnexal mass, with ovarian cysts accounting for most.4 Ovarian cysts are the
most common fetal and infant tumor, with a prevalence exceeding 30%.5
Mortality/Morbidity
 Ovarian cysts can result in pain and other morbidity, including menorrhagia, an increased intermenstrual
interval, dysmenorrhea, pelvic discomfort, and abdominal distention.
 Approximately 3% of theca lutein cysts are complicated by torsion or hemorrhage, and approximately 30%
of these cysts can cause maternal androgen excess.2
 Follicular cysts can cause excess estradiol production, leading to metrorrhagia and menorrhagia.
 Ovarian cysts, and more specifically corpus luteal cysts, can rupture, causing hemoperitoneum,
hypotension, and peritonitis. This can be exacerbated in women with bleeding dyscrasias, such as those
with von Willebrand disease and those receiving anticoagulation therapy.
 Ovarian torsion can complicate ovarian cysts and can result in ovarian infarction, necrosis, infertility,
premature ovarian menopause, and preterm labor.6
Race No racial discrepancies regarding ovarian cysts are reported in the literature. This disease affects all racial
groups. Age Ovarian cysts affect all age ranges of females, from those in utero to postmenopausal women. Even
benign-appearing ovarian cysts in postmenopausal patients may require aggressive treatment owing to the increased
risk of malignancy in this population.
Clinical
History
 Most ovarian cysts are asymptomatic and are discovered incidentally during ultrasonography or routine
pelvic examination.
o Most symptomatic ovarian cysts produce a transient dull, vague, unilateral sensation of pelvic pain
or heaviness.
o Some patients may experience tenesmus or dyspareunia.
o The intermenstrual interval may be prolonged, followed by menorrhagia.2
o Cyst rupture is characterized by sudden, unilateral, sharp pelvic pain. This can be associated with
trauma, exercise, or coitus.3,7
o Cyst rupture can lead to peritoneal signs, abdominal distention, and bleeding that is usually self
limited.
o Theca lutein cysts are commonly bilateral and thus can cause bilateral, dull pelvic pain.2 Theca
lutein cysts may be associated with excess stimulation, as is seen in pregnancy (in particular
twins), a large placenta, and diabetes. Newborns may also develop theca lutein cysts due to the
effects of maternal gonadotropins. In rare cases, these cysts may develop in the setting
ofhypothyroidism owing to similarities between the alpha subunit of thyroid-stimulating hormone
(TSH) and bhCG.1,2
Physical
 Hemorrhage due to cyst rupture may lead to tachycardia and hypotension. Blood pressure monitoring may
show orthostatic hypotension.
 Some complications of ovarian cysts, such as ovarian torsion, may result in hyperpyrexia.3
 Examination reveals moderate-to-severe unilateral or bilateral lower abdominal tenderness in some women
with an ovarian cyst.
 Some complications of ovarian cysts may result in adnexal tenderness or cervical motion tenderness.
However, pelvic examination reveals that up to 88% of ovarian cysts are benign.8
 Ovarian cysts may be palpable on abdominal or bimanual examination. An examiner may also palpate large
ovaries in a patient with hyperreactio luteinalis.
 If hemorrhage or peritonitis ensues, the patient may present with a diffusely tender abdomen with rebound
tenderness and guarding; in addition, a distended abdomen may be found on abdominal examination.
Causes
 Factors that can increase the risk for ovarian cysts include disorders that increase ovarian stimulation, such
as gestational trophoblastic disease, multiple gestation pregnancies, and exogenous ovarian stimulation.
 In pregnant women, ovarian cysts may form in the second trimester, when bhCG levels peak.2
 Because of similarities between the alpha subunit of TSH and bhCG, hypothyroidism may stimulate ovarian
and cyst growth.1
 The transplacental effects of maternal gonadotropins may lead to the development of neonatal and fetal
ovarian cysts.9
 The risk of functional ovarian cysts is increased with cigarette smoking and possibly increased further with a
decreased body mass index (BMI).10,11
 Functional cysts have been associated with tubal ligation sterilizations.12
 There may be an inverse relationship between ovarian cysts and breast cancer.13,14

Endometriosis
Background
Endometriosis is the presence of endometrial-like tissue outside the uterine cavity, which induces a chronic
inflammatory reaction. It can occur in various pelvic sites such as on the ovaries, fallopian tubes, vagina, cervix, or
uterosacral ligaments or in the rectovaginal septum. It can also occur in distant sites including laparotomy scars,
pleura, lung, diaphragm, kidney, spleen, gallbladder, nasal mucosa, spinal canal, stomach, and breast.
This condition is often associated with pelvic pain and infertility, but it is most often asymptomatic. It is a frequently
encountered gynecologic disorder in the emergency department (ED) as well as in the outpatient setting. Because it
is enigmatic, endometriosis can present as a diagnostic and therapeutic challenge for emergency physicians in their
approach to the female patient with pelvic pain.
Pathophysiology
The exact cause and pathogenesis of endometriosis is unclear. Several theories exist that attempt to explain this
disease though none have been entirely proven.
Previous theories suggest that endometriosis results from the transport of viable endometrial cells through retrograde
menstruation. Cells flow backwards through the fallopian tubes and deposit on the pelvic organs where they seed and
grow. A population of cells reside in the endometrium, which retain stem cell properties. It may be these properties
that allow these cells to survive in ectopic locations.
Retrograde menstruation is a common physiologic event. Diagnostic laparoscopy during the perimenstrual period has
shown that as many as 90% of women with patent fallopian tubes have bloody peritoneal fluid. Since most women do
not have endometriosis, perhaps immunologic or hormonal dysfunction leaves some women predisposed.
Recent research has suggested involvement of the immune system in the pathogenesis of endometriosis. Women
with this disorder appear to exhibit increased humoral immune responsiveness and macrophage activation while
showing diminished cell-mediated immunity with decreased T-cell and natural killer cell responsiveness.
Transtubal dissemination is the most common route, although other routes have been observed. These include
lymphatic and vascular channels. This may explain how endometrial tissue can be found at distant locations in the
body.
Metaplasia, or the changing from one normal type of tissue to another normal type of tissue, is another theory. The
endometrium and the peritoneum are derivatives of the same coelomic wall epithelium. Peritoneal mesothelium has
been postulated to retain its embryologic ability to transform into reproductive tissue. Such transformation may occur
spontaneously, or it may be facilitated by exposure to chronic irritation by retrograde menstrual fluid.
Another theory states that remnant mullerian cells may remain in the pelvic tissues during development of the
mullerian system. Under situations of estrogen stimulation, they may be induced to differentiate into functioning
endometrial glands and stroma.
Finally, iatrogenic deposition of endometrial tissue has been found in some cases following gynecologic procedures
and cesarean sections.
Some women may have a genetic predisposition to endometriosis. Studies have shown that first-degree relatives of
women with this disease are more likely to develop it as well. The search for an endometriosis gene is currently
underway.
Many theories exist as to why endometriosis occurs, and it is likely a combination of these factors that cause and
determine severity of disease.
Frequency
United States
The incidence of endometriosis has not increased in the last 30 years. The prevalence is approximately 6-8% but
estimates vary. It is usually diagnosed during laparoscopic surgery for evaluation of pelvic pain. Most prevalence
studies are based on a surgical population in which the likelihood of disease is greater. Of the surgical population,
endometriosis was diagnosed in 25% of women who had a laparoscopy for pelvic pain and in 20% of women who
underwent surgery for infertility. No large-scale laparoscopic evaluation of asymptomatic women has been
undertaken.
Mortality/Morbidity
Mortality is negligible.
 Acute or chronic pelvic pain is common in patients with endometriosis.
 Infertility is also common. Thirty to forty percent of women with endometriosis will be subfertile.
 Cases have been reported of extrapelvic involvement in virtually every other organ system including the
central nervous system (CNS), lungs, pleura, kidney, and bladder. The gastrointestinal (GI) tract is the most
common extrapelvic site of endometriosis, and symptoms include bowel obstruction, rectal bleeding, and
constipation. Symptoms in other locations are related to the site and size of endometrial implants.
Race
Most research and case studies have been performed in white populations; however, no difference appears to exist
among ethnic or social groups.
Sex
Endometriosis occurs in women. Rare reports of endometriosis have been documented in men undergoing estrogen
therapy.
Age
Pelvic endometriosis typically occurs in women aged 25-30 years. Extrapelvic manifestations of this disorder occur in
woman aged 35-40 years. Women younger than 20 years with this disease often have anomalies of the reproductive
system. Endometriomas and symptoms related to them regress significantly after menopause.
Clinical
History
 Patients with endometriosis present with a variety of symptoms including the following:
o Dysmenorrhea
o Heavy or irregular bleeding
o Pelvic pain
o Lower abdominal or back pain
o Dyspareunia
o Dyschezia (pain on defecation) often with cycles of diarrhea and constipation
 o Bloating, nausea, and vomiting
o Inguinal pain
o Pain on micturition and/or urinary frequency
o Pain during exercise
 The most common symptom is dysmenorrhea, which may precede the onset of menstruation. In addition to
pain, patients present with nonspecific symptoms of fatigue, generalized malaise, and sleep disturbances.
 Intensity of pain and discomfort does not correlate with extent of disease because the location and depth of
endometrial implants affect the symptomatology. Pain is thought to be related to the degree of peritoneal
inflammation rather than the volume of implants. Associated intrapelvic/intra-abdominal adhesions are also
important determinants of the degree of pain experienced. 
 Ureteral obstruction and hydronephrosis can result from endometrial implants on the ureter or mass effect
from an endometrioma.
 Extra-abdominal manifestations can include cyclical hemoptysis and pneumothorax (catamenial).
 Symptoms usually improve during pregnancy and after menopause. They can recur postpartum or with
postmenopausal hormone replacement therapy.
 In 15% of cases of pelvic pain, endometriosis is the underlying cause. It should be considered in women
with chronic pelvic pain who do not respond to standard NSAID or oral contraceptive therapy.
 One third of women with endometriosis are asymptomatic.
Physical
The physical examination usually correlates with the extent of disease.
 The most common finding is nonspecific pelvic tenderness. In one study, 22% of adolescents had abnormal
physical findings consistent with anatomic lesions found during surgery.
 The hallmark finding on examination is the presence of tender nodular masses along thickened uterosacral
ligaments, the posterior uterus, or the posterior cul-de-sac.
 Ovarian involvement may present with adnexal tenderness or masses.
 Obliteration of the cul-de-sac in conjunction with fixed uterine retroversion implies extensive disease.
 Rupture of an ovarian endometrioma may present as an acute abdomen.
 Extensive involvement of the rectum and other areas of the GI tract may cause adhesions and obstruction.
 Examination should include evaluation for cervicitis, abnormal discharge, and sexually transmitted diseases
(STDs).
Causes
Refer to Pathophysiology for more detail.
 Retrograde menstruation
 Lymphatic/vascular metastases
 Coelomic metaplasia
 Remnant mullerian cells induced by estrogen
 Direct implantation
 Genetic predisposition
 Risk factors
o Family history of endometriosis
o Early age of menarche
o Short menstrual cycles (<27 d)
o Long duration of menstrual flow (>7 d)
o Heavy bleeding during menses
o Inverse relationship to parity
o Delayed childbearing
o Defects in the uterus or fallopian tubes
o Hypoxia and iron deficiency may contribute to the early onset of endometriosis

Gastroenteritis
astroenteritis is a nonspecific term for various pathologic states of the gastrointestinal tract. The primary manifestation
is diarrhea, but it may be accompanied by nausea, vomiting, and abdominal pain. A universal definition of diarrhea
does not exist, although patients seem to have no difficulty defining their own situation. Although most definitions
center on the frequency, consistency, and water content of stools, the author prefers defining diarrhea as stools that
take the shape of their container.
The severity of illness may vary from mild and inconvenient to severe and life threatening. Appropriate management
requires extensive history and assessment and appropriate, general supportive treatment that is often etiology
specific. Diarrhea associated with nausea and vomiting is referred to as gastroenteritis.
Diarrhea is one of the most common reasons patients seek medical care. In the developed world, it is the most
common reason for missing work, while in the developing world, it is a leading cause of death. In developing
countries, diarrhea is a seasonal scourge usually worsened by natural phenomena, as evidenced by monsoon floods
in Bangladesh in 1998. An estimated 100 million cases of acute diarrhea occur every year in the United States. Of
these patients, 90% do not seek medical attention, and 1-2% require admission. Diarrheal diseases can quickly reach
epidemic proportions, rapidly overwhelming public health systems in even the most advanced societies.
Pathophysiology
Infectious agents usually cause acute gastroenteritis. These agents cause diarrhea by adherence, mucosal invasion,
enterotoxin production, and/or cytotoxin production.
These mechanisms result in increased fluid secretion and/or decreased absorption. This produces an increased
luminal fluid content that cannot be adequately reabsorbed, leading to dehydration and the loss of electrolytes and
nutrients.
Diarrheal illnesses may be classified as follows:
 Osmotic, due to an increase in the osmotic load presented to the intestinal lumen, either through excessive
intake or diminished absorption
 Inflammatory (or mucosal), when the mucosal lining of the intestine is inflamed
 Secretory, when increased secretory activity occurs
 Motile, caused by intestinal motility disorders
The small intestine is the prime absorptive surface. The colon then absorbs additional fluid, transforming a relatively
liquid fecal stream in the cecum to well-formed solid stool in the rectosigmoid.
Disorders of the small intestine result in increased amounts of diarrheal fluid with a concomitantly greater loss of
electrolytes and nutrients.
Microorganisms may produce toxins that facilitate infection. Enterotoxins are generated by bacteria (ie,
enterotoxigenic Escherichia coli, Vibrio cholera) that act directly on secretory mechanisms and produce typical,
copious watery (rice water) diarrhea. No mucosal invasion occurs. The small intestines are primarily affected, and
elevation of the adenosine monophosphate (AMP) levels is the common mechanism.
Cytotoxin production by bacteria (ie, Shigella dysenteriae, Vibrio parahaemolyticus, Clostridium
difficile, enterohemorrhagic E coli) results in mucosal cell destruction that leads to bloody stools with inflammatory
cells. A resulting decreased absorptive ability occurs.
Enterocyte invasion is the preferred method by which microbes such as Shigella and Campylobacter organisms and
enteroinvasive E coli cause destruction and inflammatory diarrhea. Similarly, Salmonella and Yersinia species also
invade cells but do not cause cell death. Hence, dysentery does not usually occur. However, these bacteria invade
the bloodstream across the lamina propria and cause enteric fever such as typhoid.
Diarrheal illness occurs when microbial virulence overwhelms normal host defenses. A large inoculum may
overwhelm the host capacity to mount an effective defense. Normally, more than 100,000 E coli are required to cause
disease, while only 10 Entamoeba or Giardia cysts may suffice to do the same. Some organisms (eg, V
cholera,enterotoxigenic E coli) produce proteins that aid their adherence to the intestinal wall, thereby displacing the
normal flora and colonizing the intestinal lumen.
In addition to the ingestion of pathogenic organisms or toxins, other intrinsic factors can lead to infection. An
alteration of normal bowel flora can create a biologic void that is filled by pathogens. This occurs most commonly
after antibiotic administration, but infants are also at risk prior to colonization with normal bowel flora.
The normally acidic pH of the stomach and colon is an effective antimicrobial defense. In achlorhydric states (ie,
caused by antacids, histamine-2 [H2] blockers, gastric surgery, decreased colonic anaerobic flora), this defense is
weakened.
Hypomotility states may result in colonization by pathogens, especially in the proximal small bowel, where motility is
the major mechanism in the removal of organisms. Hypomotility may be induced by antiperistaltic agents (eg, opiates,
diphenoxylate and atropine [Lomotil], loperamide) or anomalous anatomy (eg, fistulae, diverticula, antiperistaltic
afferent loops) or is inherent in disorders such as diabetes mellitus or scleroderma.
The immunocompromised host is more susceptible to infection, as evidenced by the wide spectrum of diarrheal
pathogens in patients with AIDS.
The exact mechanism of vomiting in acute diarrheal illness is not known, although serotonin release has been
postulated as a cause, stimulating visceral afferent input to the chemoreceptor trigger zone in the lower brainstem.
Preformed neurotoxins produced by Staphylococcus aureus and Bacillus cereus, when ingested, can cause severe
vomiting.
Mortality/Morbidity
 Estimates for mortality and morbidity widely vary. In the United States, 210,000 pediatric hospitalizations
occur yearly, with as many as 10,000 deaths.
 Internationally, the mortality rate is 5-10 million deaths each year.
Age
 Pediatric gastroenteritis is discussed in Pediatrics, Gastroenteritis.
 Gastroenteritis may occur at any age. Morbidity and mortality are much higher in the very young and the
very old.
Clinical
History
A well-taken history, considering important epidemiologic factors, can help to identify not only the cause of diarrhea
but also the patient at risk for complications. History in infectious cases and food poisoning varies depending upon
the agent with variation in the onset; the frequency and nature of the stools; and the presence or absence of blood
and mucus, vomiting, cramps, and fever. The history should also identify risk factors for unusual causes of acute
gastroenteritis and possible reasons to suspect noninfectious etiologies. Indications of dehydration or sepsis should
also be sought. As an example, norovirus is usually diagnosed by history. The incubation period for the norovirus is
between 12 and 48 hours. Some of the early symptoms include nausea, a sudden onset of vomiting, moderate
diarrhea, headache, fever (~50%), chills, and myalgia and will last 12-60 hours. The clinical factors suggestive of
norovirus include the patient's presentation and the sudden onset of symptoms, with uncontrolled vomiting being a
classic sign. Usually, more vomiting than diarrhea occurs. The natural course of this illness usually provides
resolution within 36 hours.
 Duration of illness
o Duration and rapidity of symptom onset are important in determining the incubation period and
possible infecting organism and in directing further care.
o Diarrhea that lasts longer than a month requires consideration of a different spectrum of etiologic
factors than diarrhea that lasts less than 1-2 weeks.
 Fever: The presence of fever (with or without chills) generally suggests that an invasive organism is the
cause of diarrhea, although many extraintestinal illnesses can present with both fever and diarrhea,
especially in children.
 Vomiting
o Vomiting, a symptom common to a host of illnesses, implies proximal bowel involvement, especially
with preformed neurotoxin, as elaborated by S aureusand B cereus.
o Vomiting is a leading symptom of intestinal obstruction, usually coupled with distention; however,
distention may not be significant if the obstructing lesion is very proximal. Vomiting without diarrhea
must always prompt a search for noninfectious causes and cannot be referred to as gastroenteritis.
 Pain
o The location and character of pain may be indicative of the area of infection because colonic
involvement is usually associated with tenesmus and pain in either of the lower quadrants or the
lower back, whereas jejunoileal infection may result in periumbilical pain.
o Cramps may be caused by an electrolyte imbalance.
o Pain, especially in patients older than 50 years, should raise the suspicion of an ischemic process.
 Stools
o Ask about frequency, nature (amount, color, watery, semisolid, odor), and presence of blood and/or
mucus.
o Large volumes of stool are usually associated with enteric infection, whereas colonic infection
results in many small stools.
o The presence of blood indicates colonic ulceration (bacterial infection, inflammatory disease,
ischemia).
o White bulky feces that float (high fat content) are due to a small bowel pathology that leads to
malabsorption.
o Copious (rice water) diarrhea is a hallmark of cholera.
 Extraintestinal causes
o A history of other nonintestinal illnesses that can lead to diarrhea may be obtained. Vomiting and/or
diarrhea may be a manifestation of that illness or a result of its treatment. Obtaining a history of
recent surgery or radiation, food or drug allergies, and endocrine or gastrointestinal disorders is
extremely important. The patient should always be questioned regarding prior episodes.
o Malaria, Whipple disease, irritable bowel, incomplete bowel obstruction, inflammatory disease,
nutritional disease, and carcinoid and malabsorption syndromes can result in diarrhea.
o Drugs such as colchicine, quinidine, antimicrobials, cancer chemotherapeutic agents, and
magnesium-containing antacids frequently cause diarrhea.
 Dehydration
 o Orthostasis, lightheadedness, diminished urine formation, and a change in mentation herald
marked dehydration and electrolyte loss, requiring aggressive treatment.
o These symptoms are particularly important in elderly patients, a group that is most at risk from
diarrhea.
 Epidemiologic factors
o A number of historical questions may provide clues to the etiology of the illness, including foreign
travel, recent camping, recent antibiotic use, daycare attendance, and/or ingestion of raw, possibly
spoiled, or new marine products, as well as similar illnesses in family, friends, or contacts.
o An epidemiologic factor may be travel to developing countries where bacterial or parasitic agents
can cause infection or to campgrounds in developed regions, where agents such as Giardia
lamblia, Aeromonas, and Cryptosporidium can contaminate untreated water.
o Enterotoxigenic E coli is the most frequent cause of traveler's diarrhea. Symptoms usually begin
within days of arrival in the region and can last from 5 days to 2 weeks.
o Vibrio species are more common in Asia, although epidemics have occurred in Central America
within the last 10 years.
o As many as 12% of diarrheal illness cases may be caused by rotavirus in travelers to Asia, Africa,
and South America.
o Men who are homosexual are more prone to infection by usual pathogens via the fecal-oral route
(ie, Shigella, Campylobacter jejuni, Salmonella, protozoalike Entamoeba). Anal receptive
intercourse may result in the direct inoculation of Neisseria gonorrhoeae, Chlamydia trachomatis,
Treponema pallidum, and herpes simplex virus. Severely immunocompromised states (CD4 cell
count <200) increase the risk of infection by agents such as Mycobacterium aviumcomplex,
microsporidia, cytomegalovirus (CMV), and Isospora belli.
o Recent use of antimicrobial drugs increases the risk of C difficile infection.
o A common source outbreak from contaminated water and food may cause gastroenteritis either by
infection (C jejuni, G lamblia) or by ingestion of a preformed toxin (E coli O157:H7, scombroid,
ciguatera).
o Infections via the fecal-oral route are prevalent in children who attend daycare centers. Rotavirus
has an infection rate of nearly 100% in exposed children younger than 2 years. Other family
members are also at risk for infection.
Physical
A thorough physical examination is essential to assess the general state of hydration and nutrition and to exclude
extraintestinal causes of diarrhea. Often, the cause of diarrhea cannot be determined based on the physical findings
present, which may be scarce.
 The most important element of the physical examination is the assessment of the patient's hydration status.
(Dehydration in children, for example, is classified according to the degree of hydration/percentage deficit as
<3%, none; 3-6%, mild; 6-9%, moderate; and >10%, severe.) Additionally, signs of bacteremia or sepsis
should be sought. Patients with chronic diarrhea may need an evaluation of their nutritional status.
 A rectal examination should be performed, involving checking for blood and mucus. Rectal examination may
reveal abscesses, fistulae, and fissures, which may indicate inflammatory bowel disease. A partially
obstructing tumor or a fecal impaction may be discovered as a cause of diarrhea. Finally, the stool can be
examined for the presence of blood and pus.
 Hydration and nutritional status
o Diminished skin turgor, weight loss, resting hypotension and tachycardia, dry mucus membranes,
decreased frequency of urination, changes in mental status, and orthostasis can be used to gauge
dehydration.
o In children, the absence of tears, poor capillary refill, sunken eyes, depressed fontanelles,
increased axillary skin folds, and dry diapers all may reflect a dehydrated state.
o Muscle wasting and signs of neural dysfunction due to nutritional depletion may be observed in
patients with chronic diarrhea.
 Abdominal examination
o A careful abdominal examination is necessary to exclude causes of diarrhea that may require
surgical intervention, such as pelvic abscesses close to the rectosigmoid that are causing
tenesmus.
o The examiner should look for signs of an acute abdomen, listening for bowel sounds, determining
the location of any tenderness, and palpating for masses or organomegaly.
o Appendicitis in children may manifest as diarrhea.
Causes
 Viral (50-70%)
o Norovirus
  This is the leading cause of viral gastroenteritis in the United States. Noroviruses (formerly
known as Norwalk virus in the United States and as small round structured virus [SRSV] in
the United Kingdom), along with the sapoviruses (formerly known as Sapporo-like
viruses), are members of the Caliciviridae family of viruses. The norovirus is a small, 26-
40 nm, nonenveloped, single-stranded RNA virus classified as a Calicivirus. Sapoviruses,
a cause of gastroenteritis, predominantly in children, are also in the Caliciviridae family.
Five norovirus genogroups have been identified: GI, GII, GIII, GIV, and GV; 27 clusters
(genotypes) have also been identified. In 2006, the land-based experience was slightly
busier than usual. The dominating strain was GII-4 (Bristol).
 It is a highly infectious virus—with as few as 10-100 particles necessary for transmission
—and is quite resistant to quaternary ammonia compounds, alcohol, detergent-based
compounds, freezing, and heat (to 60o C). It is a very difficult virus to culture and measure;
thus, studies on norovirus are limited, with researchers using a "surrogate," nonenveloped
virus, Feline Calicivirus (FCV), to assess the efficacy of disinfectants and other mitigation
strategies. Recently, some researchers have questioned the use of FCV as a surrogate
since FCV is a respiratory virus and norovirus is a GI virus and likely is more resilient than
FCV due to the need for norovirus to survive in the hostile environment of the gut.
Therefore, the results of testing performed to validate the efficacy of disinfectants and
hand sanitizers possibly overestimate the actual effectiveness of these products on
human norovirus.
 Various modes of transmission exist including fecal-oral transmission (predominant),
person to person, fecal contamination of food and/or water, fomite transmission, and
airborne spread when in close proximity of someone vomiting, as the virus is easily
aerosolized.
 Between January 1996 and November 2000, 348 outbreaks of norovirus were reported to
the CDC. Out of these, 54% patients were contaminated by food, 17% by person to
person, 4% by water, and 25% by unidentified sources. Most of the food sources
responsible were identified as oysters, salads, salad dressing, sandwiches, deli meats,
cake and frosting, raspberries, drinking water, and ice. Shellfish have been implicated in
some outbreaks, but it is not a frequent source on cruise ships, where the predominant
mode of infection is believed to be fecal-oral and person to person from individuals who
come onto the ships ill and do not report the illness or quarantine themselves in their
cabins. The same study reveals that 39% contracted the disease in restaurants, 30% in
nursing homes, 12% at school, 10% on vacation, and 9% remain unidentified.
 The incubation period for the norovirus is between 12 and 48 hours. Some of the early
symptoms include nausea, a sudden onset of vomiting, moderate diarrhea, headache,
fever (~50%), chills, and myalgia and will last 12-60 hours. The clinical factors suggestive
of norovirus include the patient's presentation and the sudden onset of symptoms, with
uncontrolled vomiting being a classic sign. Usually, more vomiting than diarrhea occurs.
The virus is noninvasive of the colon; therefore, WBCs are not seen in the stool, and
hematochezia is rare.
 The natural course of this illness usually provides resolution within 36 hours. Unless the
patient is very young, very old, debilitated with severe underlying disease, or
immunocompromised, they usually do very well with this self-limited illness responding to
oral rehydration and a rapid return to normal diet once the vomiting has ceased. The only
therapy is oral and/or intravenous hydration with occasional need for antiemetics. The
usual cautions concerning the use of antiemetics in very young patients apply. Although
viral shedding has been reported for up to 2 weeks, the polymerase chain reaction (PCR)
testing used to determine this may just be detecting inactivated RNA.
 There are many norovirus strains with no cross-immunity, so repeat infections are
possible throughout one's lifetime.
Pregnancy, Ectopic
Introduction
Background
An ectopic pregnancy is any implantation of a fertilized ovum at a site other than the endometrial lining of the uterus.
Virtually all ectopic pregnancies are considered nonviable and are at risk of eventual rupture. Rupture of an ectopic
pregnancy and resulting hemorrhage is one of the leading causes of first-trimester maternal death in the developed
world; therefore, early diagnosis and treatment (before rupture) is important to prevent morbidity and mortality.[1 ]
Pathophysiology
The faulty implantation that occurs in ectopic pregnancy occurs because of a defect in the anatomy or normal
function of either the fallopian tube (as in surgical or infectious scarring), the ovary (as in women undergoing fertility
treatments), or the uterus (as in cases of bicornuate uterus, cesarean delivery scar).
 
Reflecting this, about 95% of ectopic pregnancies occur in the fallopian tube — 70% in the ampulla; 12%, isthmus;
11.1%, fimbria; and 2.4%, interstitium (or cornual region of the uterus). Some ectopic pregnancies implant in the
cervix (<1%), in prior cesarean delivery scars, or in a rudimentary uterine horn; although these may be technically in
the uterus, they are not considered normal intrauterine pregnancies. About 3.2% of ectopic pregnancies occur in the
ovary, and 1.3% occur in the abdomen.[2 ]About 80% of ectopic pregnancies are found on the same side as the
corpus luteum (the old ruptured follicle), when present.[3 ]In the absence of modern prenatal care, abdominal
pregnancies can present at an advanced stage (>28 wk) and have the potential for catastrophic rupture and bleeding.
[4 ]

Race In the United States from 1991-1999, ectopic pregnancy was the cause of 8% of all pregnancy-related deaths
of African American women compared with 4% for white women.[12 ]
Sex Any woman with functioning ovaries can potentially have an ectopic pregnancy.
Age Any woman from the age of menarche until menopause can potentially have an ectopic pregnancy. Women
older than 40 years were found to have an adjusted odds ratio of 2.9 (95% confidence interval [CI], 1.4-6.1) for
ectopic pregnancy.[14 ]
Clinical
History
The classic triad of symptoms in ectopic pregnancy is abdominal pain, amenorrhea, and vaginal bleeding, but fewer
than half of patients present with all 3 symptoms. In one case series of ectopic pregnancies, abdominal pain
presented in 98.6%, amenorrhea in 74.1%, and irregular vaginal bleeding in 56.4%.[15 ]These symptoms overlap with
those of spontaneous abortion; a prospective consecutive case series found no statistically significant differences in
the presenting symptoms of patients with unruptured ectopic pregnancies versus those with intrauterine pregnancies.
[16 ]

In first-trimester symptomatic patients, pain as the presenting symptom is associated with an odds ratio of 1.42 (95%
CI, 1.06-1.92), and moderate-to-severe vaginal bleeding at presentation is associated with an odds ratio of 1.42 (95%
CI, 1.04-1.93) for ectopic pregnancy.[17 ]In one study, 9% of patients with ectopic pregnancy presented with painless
vaginal bleeding.[18 ]

Other presenting complaints may be nonspecific such as painful fetal movements (in the case of advanced abdominal
pregnancy), dizziness or weakness, fever, flu-like symptoms, vomiting, syncope, or cardiac arrest. Shoulder pain may
be reflective of peritoneal irritation.

In a review of deaths from ectopic pregnancy in Michigan, 44% were either found dead at home or were dead on
arrival at the emergency department.[19 ]
Physical
The physical examination of patients with ectopic pregnancy is highly variable and often unhelpful. Patients frequently
present with benign examination findings, and adnexal masses are rarely found. Patients in hemorrhagic shock from
ruptured ectopic may not be tachycardic.[20 ]

Some physical findings that have been found to be predictive (although not diagnostic) for ectopic pregnancy were
the presence of peritoneal signs, cervical motion tenderness, and unilateral or bilateral abdominal or pelvic
tenderness. However, midline abdominal tenderness or a uterine size of greater than 8 weeks on pelvic examination
decreases the risk of ectopic pregnancy.[21 ]

The presence of uterine contents in the vagina, which can be caused by shedding of endometrial lining stimulated by
an ectopic pregnancy, may lead to a misdiagnosis of an incomplete or complete abortion and therefore a delayed or
missed diagnosis of ectopic pregnancy.
Causes
An ectopic pregnancy requires the occurrence of 2 events: fertilization of the ovum and abnormal implantation. Many
risk factors affect both events; for example, history of major tubal infection decreases fertility and increases abnormal
implantation. Major risk factors include previous ectopic pregnancy, previous tubal surgery, documented tubal
pathology, and maternal in utero DES exposure.

Previous treatment of pelvic infections (whether documented or not), 2 or more years of infertility (whether treated or
not), and multiple sexual partners were associated with mildly elevated risk.[22 ]A large case-control study in France
found that about one third of cases could be attributed to smoking (presumably by impairing tubal motility), one-third
to infectious history and prior tubal surgery (considered together), 18% to a history of infertility, and 14% to maternal
age (although this is not an independent risk factor); 24% had no attributable risk factors.[14 ]Women using assisted
reproduction seem to have a doubled risk of ectopic pregnancy (to 4%), although this is mostly due to the underlying
infertility.[23 ]

All contraceptive methods lead to an overall lower risk of pregnancy, and therefore also an overall lower risk of
ectopic pregnancy. However, among cases of contraceptive failure, women at increased risk of ectopic pregnancy
compared with pregnant controls include those using progestin-only oral contraceptives, progestin-only implants, or
intrauterine devices (IUDs), and those with a history of tubal ligation.[24 ]In one study, 33% of pregnancies occurring
after tubal ligation were ectopic; those who underwent electrocautery and women younger than 35 years were at
higher risk.[25 ]Emergency contraception (levonorgestrel, or Plan B) does not appear to lead to a higher-than-expected
rate of ectopic pregnancy.[26 ]A recent literature review found 56 reported cases of ectopic pregnancy (by definition)
after hysterectomy, dating back to 1937.[27 ]

Other causes of ectopic pregnancy include anatomic abnormalities of the uterus such as a bicornuate uterus, fibroids
or other uterine tumors, or endometriosis; or abnormalities of the tubes such as salpingitis isthmica nodosa or tubal
ligation reversal. Appendicitis has also been found to be a risk factor for ectopic pregnancy.[14 ]
Urinary Tract Infection, Female
David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine,
University of Chicago/Pritzker School of Medicine
Updated: Nov 20, 2009
Introduction
Background
Urinary tract infection (UTI) is defined as significant bacteriuria in the presence of symptoms. This common clinical
entity accounts for a significant number of emergency department (ED) visits. It affects an estimated 20% of women
at some time during their lifetimes.
Successful emergent management includes proper specimen collection, use of immediately available laboratory
testing for presumptive diagnosis, appreciation of epidemiological and host factors that may identify patients with
clinically inapparent upper UTI, and selection of appropriate antimicrobial therapy with recommendations for follow-up
care.
Pathophysiology
The urinary tract is normally sterile. Uncomplicated UTI involves the urinary bladder in a host without underlying renal
or neurologic disease. The clinical entity is termed cystitis and represents bladder mucosal invasion, most often by
enteric coliform bacteria (eg, Escherichia coli) that inhabit the periurethral vaginal introitus and ascend into the
bladder via the urethra.
Sexual intercourse may promote this migration, and cystitis is common in otherwise healthy young women. Urine is
generally a good culture medium; factors unfavorable to bacterial growth include a low pH (5.5 or less), a high
concentration of urea, and the presence of organic acids derived from a diet that includes fruits and protein. Organic
acids enhance acidification of the urine.
Frequent and complete voiding has been associated with a reduction in the incidence of UTI. Normally, a thin film of
urine remains in the bladder after emptying, and any bacteria present are removed by the mucosal cell production of
organic acids. If the mechanisms of the lower urinary tract fail, upper tract or kidney involvement occurs and is termed
pyelonephritis. Host defenses at this level include local leukocyte phagocytosis and renal production of antibodies
that kill bacteria in the presence of complement.
Complicated UTI occurs in the setting of underlying structural, medical, or neurologic disease. Patients with a
neurogenic bladder or bladder diverticulum and postmenopausal women with bladder or uterine prolapse have an
increased frequency of UTI due to incomplete bladder emptying. This eventually allows residual bacteria to
overwhelm local bladder mucosal defenses. The high urine glucose content and the defective host immune factors in
patients with diabetes mellitus also predispose to infection.
Frequency
United States
UTI accounts for over 6 million patient visits to physicians per year in the United States. Approximately one fifth of
those visits are to EDs.
International
As 1 in 5 adult women experience UTI at some point, it is an exceedingly common, clinically apparent, worldwide
patient problem.
Mortality/Morbidity
 Although simple lower UTI (cystitis) may resolve spontaneously, effective treatment lessens the duration of
symptoms and reduces the incidence of progression to upper UTI.
 Pyelonephritis is associated with substantial morbidity, including systemic effects such as fever, vomiting,
dehydration, and loss of vasomotor tone resulting in hypotension. Complications include acute papillary
necrosis with possible development of ureteral obstruction, septic shock, and perinephric abscess. Chronic
pyelonephritis may lead to scarring with diminished renal function.
  Younger patients have the lowest rates of morbidity and mortality. Unfortunately, despite appropriate
intervention, 1-3% of patients with acute pyelonephritis die. Factors associated with unfavorable prognosis
are general debility and old age, renal calculi or obstruction, recent hospitalization or instrumentation,
diabetes mellitus, sickle cell anemia, underlying carcinoma, intercurrent chemotherapy, or chronic
nephropathy.
Race
No racial predilection exists.
Sex
The natural history of UTI varies with sex and age.
 Of neonates, boys are slightly more likely than girls to present with UTI as part of a gram-negative sepsis
syndrome. The incidence in preschool children is approximately 2% and is 10 times more common in girls.
Five percent of school-aged girls experience UTI. It is rare in school-aged boys.
 The largest group of patients with UTI is adult women. The incidence increases with age and sexual activity.
Rates of infection are high in postmenopausal women because of bladder or uterine prolapse causing
incomplete bladder emptying; loss of estrogen with attendant changes in vaginal flora; loss of lactobacilli,
which allows periurethral colonization with gram-negative aerobes, such as E coli; and higher likelihood of
concomitant medical illness, such as diabetes.
 UTI is unusual in males younger than 50 years, and symptoms of dysuria and frequency are usually due to
urethral or prostatic infection. In older men, however, the incidence of UTI rises because of prostatic
obstruction or subsequent instrumentation.
Clinical
History
 The classical symptoms of UTI in the adult are primarily dysuria with accompanying urinary urgency and
frequency.
 A sensation of bladder fullness or lower abdominal discomfort is often present.
 Bloody urine is reported in as many as 10% of cases of UTI in otherwise healthy women; this condition is
called hemorrhagic cystitis.
 Fevers, chills, and malaise may be noted, though these are associated more frequently with upper UTI (ie,
pyelonephritis).
 Because of the referred pain pathways, even simple lower UTI may be accompanied by flank pain and
costovertebral angle tenderness. In the ED, assume that the presence of these symptoms represents upper
UTI.
 A history of vaginal discharge suggests that vaginitis, cervicitis, or pelvic inflammatory disease is responsible
for symptoms of dysuria; therefore, a pelvic examination must be performed.
 Important additional information includes a history of prior sexually transmitted disease (STD) and multiple
current sexual partners.
Physical
 Most adult women with simple lower UTI have suprapubic tenderness with no evidence of vaginitis,
cervicitis, or pelvic tenderness (eg, cervical motion tenderness, which suggests pelvic inflammatory
disease).
 The patient appears uncomfortable but not toxic.
 The patient with pyelonephritis usually appears ill and, in addition to fever, sweating, and prostration, is
found to have costovertebral angle (flank) tenderness in the majority of cases.
 The clinician may appreciate signs of dehydration, such as dry mucous membranes and tachycardia, as well
as poor vascular tone due to gram-negative bacteremia, which may be manifested by clammy extremities
and profound orthostatic hypotension.

Abortion, Complications
Background
Complications of spontaneous miscarriages and therapeutic abortions include the following: 

 Complications of anesthesia  
 Postabortion triad (ie, pain, bleeding, low-grade fever)
  Hematometra
 Retained products of conception
 Uterine perforation
 Bowel and bladder injury
 Failed abortion
 Septic abortion
 Cervical shock
 Cervical laceration
 Disseminated intravascular coagulation (DIC)

The term "septic abortion" refers to a spontaneous miscarriage or therapeutic/artificial abortion

complicated by a pelvic infection.

Pathophysiology
Postabortion complications develop as a result of 3 major mechanisms as follows: incomplete evacuation
of the uterus and uterine atony, which leads to hemorrhagic complications; infection; and injury due to
instruments used during the procedure.

In septic abortion, infection usually begins as endometritis and involves the endometrium and any
retained products of conception. If not treated, the infection may spread further into the myometrium and
parametrium. Parametritis may progress into peritonitis. The patient may develop bacteremia and sepsis
at any stage of septic abortion. Pelvic inflammatory disease (PID) is the most common complication of
septic abortion.

Frequency
United States

Frequency of complications depends on gestational age (GA) at the time of miscarriage or abortion and
method of abortion. Complication rates according to gestational age at the time of abortion are as
follows: 

 8 weeks and under - Less than 1% 

 8-12 weeks - 1.5-2% 
 12-13 weeks - 3-6%
 Second trimester - Up to 50%, possibly higher

Mortality/Morbidity
Mortality and morbidity depend on gestational age at the time of miscarriage or abortion. In the United
States, mortality rates per 100,000 abortions are as follows: fewer than 8 weeks, 0.5%; 11-12 weeks,
2.2%; 16-20 weeks, 14%; and more than 21 weeks, 18%.

Septic abortion was once the leading cause of maternal death around the world. The condition remains a
primary cause of maternal mortality in the developing world, mostly as a result of illegal abortions.
According to the World Health Organization, about 68,000 women die each year due to complications
from unsafe abortions, with sepsis as the main cause of death. [1 ]In the United States in 2005, 7 women
reportedly died from complications of legal induced abortion. [2 ]
In the United States, mortality from septic abortion rapidly declined after legalization of abortion. Death
now occurs in less than 1 per 100,000 abortions. Figures for most European countries are similar to US
rates.

The risk of death from septic abortion rises with the progression of gestation.

Clinical

History
Presentation depends on the type of complication the patient develops. Intraoperative and early
postoperative complications are rarely seen in the ED, but some patients develop these types of
complications and present to the ED for treatment. Complications include the following:

 Local anesthesia: Paracervical block is a common method of anesthesia for therapeutic abortion.
Accidental intravascular injection of anesthetic is a potentially life-threatening complication of this
method that could lead to seizure, cardiopulmonary arrest, and death.
 General anesthesia: Complications with general anesthesia may lead to uterine atony with severe
hemorrhage.
 Cervical shock: Vasovagal syncope produced by stimulation of the cervical canal during dilatation
may occur. Rapid recovery usually follows.
 Postabortion triad: Pain, bleeding, and low-grade fevers are the most common presenting
complaints. Postabortion triad usually is caused by retained products of conception.
 Hemorrhage: Excessive hemorrhage during or after abortion may signify uterine atony, cervical
laceration, uterine perforation, cervical pregnancy, a more advanced gestational age than
anticipated, or coagulopathy.
 Hematometra: Also known as post abortion syndrome, this is the result of retained products of
conception or uterine atony for other causes. The endometrium is distended with blood, and the
uterus is unable to contract to expel the contents. Patients usually present with increasing lower
midline abdominal pain, absent or decreased vaginal bleeding, and, at times, hemodynamic
compromise. This may develop immediately after miscarriage or abortion, or it may develop
insidiously.
 Perforation: Patients with uterine perforation missed during the procedure usually present to the
ED with increased abdominal pain, bleeding (possibly ranging from very mild to absent), and
fever. If perforation results in injury to major blood vessels, patients may present in hemorrhagic
shock.
 Bowel injury: This may accompany uterine perforation. If initially unrecognized, patients present
with abdominal pain, fever, blood in the stool, nausea, and vomiting.
 Bladder injury: This occurs as a result of uterine or cervical perforation. Patients present with
suprapubic pain and hematuria.
 Septic abortion: This is endometritis. Patients present with fever, chills, abdominal pain, vaginal
discharge, vaginal bleeding, and history of recent pregnancy.
 Failed abortion (continued intrauterine or ectopic pregnancy): Failure to terminate the pregnancy
is relatively common with very early abortions (<6 wk gestational age). Such patients may present
to the ED with symptoms of continuing pregnancy such as hyperemesis, increased abdominal
girth, and breast engorgement. In addition, an unrecognized ectopic pregnancy in the
postabortion period presents in the usual manner.
  Disseminated intravascular coagulation: Suspect DIC in all patients who present with severe
postabortion bleeding, especially after midtrimester abortions. Incidence is approximately 200
cases per 100,000 abortions; this rate is even higher for saline instillation techniques (660 per
100,000 abortions).

Physical

 Vital signs 
o Monitoring of vital signs is essential for patients with postabortion complications.
o Increasing fever could be a sign of progressing infection.
o Tachycardia and hypotension may be signs of severe hemorrhage or septic shock.
 Abdominal examination 
o Suprapubic tenderness is common in the postabortion period. Severe tenderness is
unusual and may be a sign of hematometra, bladder perforation, or bowel injury.
o Tenderness in other areas of the abdomen (eg, rebound tenderness, guarding) strongly
indicates instrumental injury complications (eg, perforation, bowel injury, bladder injury).
o A tender mass in the suprapubic area suggests hematometra.
o Diminished or absent bowel sounds are a sign of developing peritonitis.
 Vaginal examination 
o Assess the quantity and rate of hemorrhage. 
 Look for possible vaginal or cervical injury.
 Identify the source of bleeding (eg, uterine; cervical os; lesions of the vulva,
vagina, or vaginal portion of cervix).
o Cervical motion tenderness on bimanual examination may be suggestive of pelvic
infection or ectopic pregnancy.
o A large tender uterus may be a sign of hematometra.
o Adnexal tenderness or masses may suggest ectopic pregnancy, pelvic inflammatory
disease (PID), cyst, or hematoma.
 Rectal examination 
o A rectal examination must be performed if bowel injury is suspected.
o The presence of rectal tenderness and blood (or guaiac-positive stool) makes the
diagnosis of bowel injury almost certain.

Causes
Two major factors contribute to the development of septic abortion: retained products of conception and
infection introduced into the uterus.

 Retained products of conception due to incomplete spontaneous miscarriage or therapeutic

abortion
 Introduction of infection into the uterus: Pathogens causing septic abortion usually are mixed and
derived from normal vaginal flora and sexually transmitted bacteria. These organisms include the
following: 
o Escherichia coli and other aerobic, enteric, gram-negative rods
o Group B beta-hemolytic streptococci[3 ]
o Staphylococcal organisms[4 ]
o Bacteroides species
o Neisseria gonorrhoeae
o Chlamydia trachomatis
o Clostridium perfringens
o Mycoplasma hominis
o Haemophilus influenzae